FUNDAMENTALS OF PATHOLOGY FUNDAMENTALS 
OF 
PATHOLOGY 
FOR STUDENTS AND GENERAL PRACTITIONERS OF 
MEDICINE AND DENTISTRY AND FOR NURSES 
IN TRAINING SCHOOLS 
BY 
PAUL G. WOOLLEY, B.S., M.D. 
04 
PROFESSOR OF PATHOLOGY, THE UNIVERSITY OF CINCINNATI; DIRECTOR OF THE 
PATHOLOGIC INSTITUTE OF THE CINCINNATI GENERAL HOSPITAL, 
CINCINNATI, OHIO. 
EIGHTY-ONE ILLUSTRATIONS, INCLUDING ONE 
COLOR PLATE 
ST. LOUIS 
C. V. MOSBY COMPANY 
1916 Copyright, 1916, by The C. V. Mosby Company. 
Press of 
The C. V. Mosby Company 
St. Louis PREFACE 
This volume makes no pretense of being either complete 
or perfect. All that it pretends to do is to make it pos- 
sible for certain groups of students of one or another 
aspect of medicine to get a bird's-eye view of the prob- 
lems of pathology, and of the methods of disease. 
There is a rapidly growing need among the students of 
dentistry for something more than the often superficial 
and somewhat disconnected accounts of the basic prin- 
ciples of their art. More and more the dentist is realizing 
that his problems and those of the physician are very 
close together; so close that it seems that dentistry will 
no longer be looked upon as essentially separate from 
medicine and surgery. There is, then, every reason why 
the dentist should be provided with a systematic treatise, 
which, while it is not applied specifically to his work, will 
form a basis for closer relationships with his fellow stu- 
dents in medicine. 
P. G. W. 
Cincinnati, Ohio. CONTENTS 
CHAPTER I. 
Introduction 17 
PART L^GENERAL PATHOLOGY. 
CHAPTER II. 
Health and Disease 22 
CHAPTER III. 
The Causes of Disease 26 
Physical Causes 27 
Physico-Chemical Causes 30 
Chemical Causes 34 
Infection 36 
Sociologic Causes of Disease 39 
Intestinal Intoxications 40 
CHAPTER IV. 
Disturbances of Metabolism 43 
Anomalies of Metabolism 47 
High Temperature 48 
The Internal Secretions ' 53 
The Thyroid and Parathyroid Glands 58 
The Thymus 61 
The Pituitary Gland 62 
The Adrenals 66 
The Pancreas 69 
The Pineal Body 69 
CHAPTER V. 
Growth and Overgrowth 71 
CHAPTER VI. 
Degeneration-Pigmentation-Calcification 78 
Degeneration 78 
Pigmentation 81 
Calcification 82 
11 12 
CONTENTS 
CHAPTER VII. 
Inflammation 83 
Repair and Regeneration 95 
Types of Inflammation 97 
CHAPTER VIII. 
Tumors 99 
PART II.-SYSTEMIC PATHOLOGY. 
CHAPTER IX. 
The Cardiovascular System 109 
The Blood 109 
Hyperemia 109 
Anemia 114 
Edema 115 
Thrombosis and Embolism 116 
The Heart 118 
The Blood Vessels 124 
CHAPTER X. 
The Urinary System 130 
The Nephroses 130 
The Simple Nephroses 131 
The Atrophies 132 
The Nephritides 134 
Classification 139 
Urinary Changes in the Nephroses 139 
CHAPTER XI. 
The Respiratory System 141 
CHAPTER XII. 
Gastrointestinal System 149 
CHAPTER XIII. 
The Nervous System 164 
CHAPTER XIV. 
The Hemopoietic System 172 
CHAPTER XV. 
The Supporting and Locomotory System 174 ILLUSTRATIONS 
Fig. Page. 
1. Diagrammatic representation of cell structure 19 
2. Continuous fever 48 
3. Remittent fever 49 
4. Intermittent fever 50 
5. Goiter • 58 
6. A case of congenital myxedema 59 
7. A case of hypophyseal destrophy in hypopituitarism 60 
8. A chondrodystrophic dwarf 62 
9. A case of giantism, a hypophyseal dwarf, and a normal man . . 63 
10. Example of enamel defect in case of tetany 65 
11. Same as Fig. 10 65 
12. A case of mongolism standing beside a healthy child .... 66 
13. The facial expression in mild myxedema 67 
14. Showing some idea of the expression and position of the fingers 
in tetany 68 
15. Cell degeneration 79 
16. Formation of new blood vessels, as seen in the tail of a tadpole . 84 
17. A section of an area in the liver which is the seat of a tuberculous 
process 90 
18. A photograph of granulation about an area of chronic tuber- 
culosis : 91 
19. Acute catarrhal colitis 92 
20. An abscess of the liver 93 
21. An appendix vermiformis which has been the seat of an inflam- 
matory process 95 
22. An epithelioma of the hand 99 
23. Mucous papilloma of bladder 100 
24. Photograph of a bit of skin sent to the laboratory because there 
was a suspicion of malignancy in the case 100 
25. Squamous papilloma, showing thickened skin epithelium, covering 
a branching vascular connective core 101 
26. Epithelioma of the lip 103 
27. Adenocarcinoma of the cervix uteri 103 
28. Sarcoma . . .................. 104 
29. Same as Fig. 28 104 
30. Same as Fig. 28 104 
31. Fibrolipoma 105 
32. Small polyp of the mucous membrane of the small intestine . . 105 
33. An angioma 106 
34. Schematic representation of the varieties of cancer which may 
arise from glandular epithelium 107 
13 14 
ILLUSTRATIONS 
Fig, Page. 
35. Abdominal arteries in a ease of double iliac thrombosis of typhoid 
origin 112 
36. Diagram illustrating the establishment of collateral circulation in 
obstruction of a vein. (Color Plate) Facing 118 
37. Diagram illustrating the formation of a hemorrhagic infarct. 
(Color Plate) - . . . Facing 118 
38. A schematic representation of the general circulation of the body 122 
39. Section of the blood vessel which is the seat of an obliterating 
endarteritis 123 
40. Myocardial fibrosis 125 
41. Atrophy of elastic tissue in wall of the aorta in atheroma . . . 126 
42. In the kidney depicted in the illustration there are several infarcts 
of the white variety 131 
43. An example of "chronic parenchymatous nephritis" .... 132 
44. A specimen of acute nephritis associated with multiple fine hem- 
orrhages 133 
45. Secondary contraction 134 
46. The so-called "embolic kidney" 135 
47. Chronic interstitial nephritis 136 
48. Arteriosclerotic kidney 137 
49. Schematical illustration of blood supply of the kidney .... 138 
50. Schematical illustration of respiratory tract 143 
51. Lung 145 
52. Lung 146 
53. Schematic sketch to illustrate the arrangement of the bile pas- 
sages 153 
54. Section of a bit of " fatty liver" 155 
55. Tuberculous ulcers of the small intestine 156 
56. Tuberous tubercles following the lymph-vessels at the bottom of 
a tuberculous ulcer of the small intestine 157 
57. An alveolar abscess at the root of an upper molar discharging 
into the maxillary sinus 158 
58. An acute alveolar abscess from the buccal root, and a chronic 
one from the lingual root of an upper molar 158 
59. Alveolar abscess from buccal roots of an upper molar discharging 
on the face 158 
60. Scar remaining from a sinus following an alveolar abscess . . 158 
61. Acute alveolar abscess from a lower incisor "pointing" on the 
gum 160 
62. Acute alveolar abscess from a lower incisor forming a pocket be- 
neath the periosteum 160 
63. Chronic alveolar abscess at the root of a lower incisor with a sinus 
opening on the gum 160 
64. Chronic abscess with sinus opening through the skin beneath the 
chin 160 ILLUSTRATIONS 
15 
Fig. Page. 
65. Chronic abscess which has involved the maxilla and finally pene- 
trated it and the skin beneath the chin 160 
66. A photograph from a smear preparation from material beneath 
an apparently perfect crown on a bicuspid tooth 162 
67. Diagram to illustrate afferent systems to cerebrum and cerebellum 164 
68. Schema of course taken by chief descending tracts of brain stem 165 
69. Diagram of ascending tracts between the spinal cord and brain 166 
70. Secondary descending degeneration 167 
71. Amyotrophic lateral sclerosis . . . 167 
72. Showing the fibers in certain sensory (ascending) nerve tracts 
which degenerate in tabes dorsalis (locomotor ataxia) . . 168 
73. Appearance in the spinal cord when both ascending (sensory) 
and descending (motor) tracts are affected 168 
74. Section of a brain showing an area of softening resulting from 
a brain hemorrhage 170 
75. Coronal section through the cranium and brain of a case of 
a brain hemorrhage 170 
76. A case of rickets 174 
77. Same as Fig. 76 175 
78. Same as Fig. 76 176 
79. Same as Fig. 76 177 
80. Showing extreme case of bow-legs 178 
81. Extreme rickety deformities of the femur and the tibia . . . 179 FUNDAMENTALS OF PATHOLOGY 
CHAPTER I. 
INTRODUCTION. 
It is of course realized that the body is a composite 
organism, i. e., that it is composed of organs, and that 
the organs are composed of cells. It follows from this 
that the various functions of the body depend upon the 
activities of the cells. As Guyer has expressed it, "Ev- 
ery biological manifestation of function and process 
from the flow of thought to the pathology of cancer re- 
solves itself in last analysis into a problem of the liv- 
ing cell." It is exactly the same with us whether we 
deal with a single cell like a bacterium or an ameba, an 
organ like the liver or the whole human body, with this 
exception,-that in the first cases we deal with single 
cells which constitute the whole organism, while in the 
latter cases we deal with groups of cells-cells which 
act together in harmony. 
Even in the smallest of the unicellular organisms the 
cell body is not homogeneous but shows certain struc- 
tures which are known as primitive organs. In some 
cases we recognize only a nucleus; sometimes not even 
that. In other cases, we find other things than the 
nucleus, for instance, a contracting vacuole, which is 
an excretory organ. These organs are parts of the cell 
body which have been differentiated from the rest of 
the protoplasm and set apart to do certain specific things. 
The cytoplasm, for instance, may be largely responsible 
for the ingestion and assimilation of food, while the 
17 18 
FUNDAMENTALS OF PATHOLOGY 
nucleus lias rather to do with functions of reproduc- 
tion and growth. 
These primitive organs therefore play a part in the 
lower organisms which the more complex organs play 
in the human. They are parts of the living organism 
which perform certain tasks which no other part can 
do so well, and often cannot do at all. They are not, 
however, independent of the body as a whole but are 
carefully coordinated in the organism and depend for 
their activities upon one another. Remove the nucleus 
from a cell and that cell no longer grows. Remove the 
liver from the man and he dies. In the lower organisms 
the correlation is relatively simple. In the higher forms 
of life it becomes more and more complicated as the 
conditions of life become more and more complex. 
So long as the coordination remains relatively undis- 
turbed, i. e., not affected beyond certain limits, health 
results. When these limits are passed, disease is pro- 
duced. Health then depends upon cellular and organic 
coordination; disease upon lack of coordination. 
In the lower forms of life, as in the ameba, the cor- 
relation between different parts of each cell is the im- 
portant thing. In more advanced forms, it exists be- 
tween cells. In the still higher forms, groups of cells 
are involved. Such groups of cells may form large or- 
gans as, for instance, the liver, or pancreas, or, on the 
other hand, may be merely a part of an anatomical or- 
gan as illustrated in the medulla of the adrenal or the 
cells of the respiratory center. 
The cells of the body are composed, we are told, of 
protoplasm. The protoplasm is divided according to its 
varying chemical structure into cytoplasm and nuclear 
material. Roth are albuminous in constitution. Besides 
these substances there are others which also are present 
in all cells; for instance, fats, lipoids (such as choles- 
terin and lecithin), glycogen; and still others which are INTRODUCTION 
19 
present in only certain types of cells, such as keratin in 
epithelial cells, pigments in some epithelial cells, in the 
retina cells, in certain nerve cells and their derivatives, 
and in the corpus luteuni of the ovary. The bodies 
which are present in all cells are spoken of as primary 
constituents; those present only in certain types of cells, 
as secondary constituents. It is the latter which often 
help us in deciding what type of cells we are dealing 
Fig. 1.-Diagrammatic representation of cell structure, a, Cell-wall or membrane; 
b, Cytoreticulum or spongioplasm, containing the hyaloplasm in its meshes; c, Endo- 
plasm; d, Plastids or protoplasts; e, "Vacuole;" e, Digestive "Vacuole," containing par- 
tially digested cell inclusion; f, Metaplasm (granules of pigment, ingested food, etc.); 
h, Nuclear membrane; i, "Net-knot" or karyosome; j, k, Nuclear network, consisting 
of chromatin and linin, and enclosing in its meshes the nuclear hyaloplasm or karyo- 
lymph; I, Nucleolus or plasmosome; m, Astral system, containing divided centrosome. 
(After Wilson, from Beattie and Dickson.) 
with and perhaps whether or not, if we know the type 
of cell, what abnormal process is affecting the cells. The 
presence of a certain substance (melanin) in cells when 
no melanin is present under normal conditions, is evi- 
dence of a pathologic process. The same thing may be 20 
FUNDAMENTALS OF PATHOLOGY 
said of enzymes. The presence of pepsin in the kidney 
would be just as abnormal as the absence of it in the 
stomach. It is interesting to know that the secondary 
constituents depend upon the activities of the primary 
ones. 
One of tlie most important constituents of all proto- 
plasm is water. Were it not for this substance, life could 
not exist, for without it solutions of food substances and 
salts could not be made in the body,-and the cells all 
depend upon solutions for their nourishment. In the 
gastrointestinal tract the foodstuffs are changed by 
means of ferments from insoluble states to soluble ones. 
Albumins become changed into peptones and amino-acids 
and these absorbed into the tissues, are again built up 
into relatively insoluble combinations. And it is mainly 
nitrogenous substances (proteins), the carbohydrates 
(sugars), and the fats, which serve as foods. For them 
the water is a vehicle of transmission from one part of 
the body to another. The salts, on the other hand, prob- 
ably have no nutritive value, but are effective in mod- 
ifying the protoplasm so that it has greater affinity for 
water in which the nutritive substances are dissolved. 
Protoplasm is a substance which belongs to the same 
physical category as glue, and gelatine, i. e., it is a col- 
loid,-a nitrogenous colloid. When a salt in solution 
conies in contact with a colloid of the type of protoplasm, 
the colloid gives up water. When it comes in contact 
with an acid is takes up water. 
In the body, the tissues are normally neutral. But 
whenever they are active they tend to be split up into 
simpler chemical substances which invariably are acid 
in character. Under these circumstances the cells ab- 
sorb water with its dissolved substances, foodstuffs and 
salts. When the concentration of salts reaches a certain 
point, water absorption ceases. W hen it passes that 
point, water and dissolved substances are given up by INTRODUCTION 
21 
the protoplasm (excretion), and since the blood serum 
is always, though very little, more acid than the tissues, 
because of the presence of acid excretions (carbonic acid 
and other substances), the tendency is for substances in 
solution to continually pass out of the cells into the 
serum. At the same time actively functionating cells con- 
stantly produce acids and so there is the constant ten- 
dency for cells to take up water and dissolved substances. 
It is therefore upon local variations in acidity and al- 
kalinity that absorption and secretion depend. 
So pathology while it is, as the word signifies, the study 
of disease, it is also fundamentally a study of the physics 
and chemistry of the body colloids, particularly the ni- 
trogenous colloids. We shall, however, in the following 
chapters not make a fundamental study of the facts of 
disease, but will devote ourselves to a more superficial 
view of the problems of disease. 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Alsberg: Mechanisms of Cell Activity. Science, New York, 1911, 
xxxiv, 97. 
Bechhold: Die Kolloide in Biologie u. Medizin. Dresden, 1912. 
Guyer: Trans. Amer. Microscopical Soc. 1911, xxx, 145. 
Henderson: The Fitness of the Environment. New York, 1913. 
Ostwald: Grundriss u. Kolloidchemie. Dresden, 1911. 
Schaefer: The Nature, Origin and Maintenance of Life. Science, New 
York, 1912, xxxvi, 289. 
Vaughan: The Physical Basis of Life. Science, New York, 1909, xxix, 
799. 
Wells: Chemical Pathology. Phila., 1914. PART 1-GENERAL PATHOLOGY 
CHAPTER. II. 
HEALTH AND DISEASE. 
As we have said, health depends upon coordination of 
cellular processes: disease depends upon a lack of such 
coordination. If we accept this conception then we see 
that health and disease depend upon two things; the 
structure of the cells of the body and the reaction of 
them to influences without the cells. 
Were the cells constant in structure and were the en- 
vironment constant, then cellular disease would not exist. 
Were the body constructed in a constant fashion, and 
were the surroundings of the body constant, then dis- 
ease of the body would not exist. So disease of the body 
depends upon (1) the structure of the body and (2) the 
environment. 
We may illustrate this in the following ways: 
I. Suppose we consider a normal human being. His 
digestion is perfect. His temperature is normal. He 
is happy and contented, and is free from any annoyance, 
however petty. Suppose he take by mistake a solution 
of bichloride of mercury, thinking it water. Suppose in 
place of the corrosive sublimate, the water contains ty- 
phoid bacilli, or cholera spirilla. Suppose he is struck 
by a falling object. In either case damage to the body 
results. He is poisoned, we say in the first case. He 
becomes infected, in the second. He receives a trauma, 
in the third. He is upset. No longer are the functions 
of the body carried out in a normal fashion. His peace 
22 HEALTH AND DISEASE 
23 
of mind is lost. He is sick. He serves us as an example 
of an organism, internally perfect, to start with, which 
has suffered from abnormal conditions in the environ- 
ment. 
II. Suppose, again, we take a case in which the sur- 
roundings of the individual are almost perfect-let us 
make them perfect. Let us say that the water supply 
is absolutely clean, the food supply fresh, the cuisine un- 
excelled, the surroundings normally sterile. And yet the 
individual whom we are considering does not behave in 
a normal fashion. Perhaps he has some "nervous" con- 
dition ; perhaps he passes too much sugar in his urine; 
perhaps he reacts toward stimuli which come from his 
surroundings in a totally strange manner. He weeps at 
small things; he raves at objects; he has maniacal at- 
tacks ; perhaps he is depressed. He does not easily with- 
stand changes of temperature. Evidently something is 
the matter inside the body. The cells do not respond 
to stimuli as they should. He is phlegmatic we say, or 
he shows spleen, he has a bad disposition, or a weak 
constitution. Here we have an example of the effect of 
a normal environment on a body which is constructed 
badly. 
III. Suppose still again, we consider an individual 
who because of improper care has become run down, we 
say,-anemic, tired, worn out. He has allowed a per- 
fectly good environment to play havoc with his body. 
The internal arrangements have been damaged so that 
while others in the same environment preserve their 
health, he becomes tuberculous, let us say. Because he 
is "run down" he becomes infected. He is careless of 
chill and fatigue and "takes" pneumonia. He allows 
his tonsils or teeth to get into a bad state of repair, and 
develops rheumatism and its attendant states. He is al- 
lowed or forced by parents or society to think and feel 
and behave in wrong directions and, following false gods, 24 
FUNDAMENTALS OF PATHOLOGY 
lie becomes a criminal. Here we have had under con- 
sideration the results to be expected from combinations 
of internal abnormalities together with bad surround- 
ings. 
There are then three points-categories into which we 
may classify disease: 
J. Those in which there is a primary external ab- 
normality. 
II. Those in which there is a primary internal ab- 
normality. 
III. Those in which both internal and external ab- 
normalities play a part. 
Sometimes we say that a disease, or a tendency is in- 
herited or congenital. What do we mean by that? An 
inherited disease is one which appears in similar form 
in several generations of individuals of the same family. 
A congenital disease is one which appears at birth. Such 
a disease may be therefore also inherited. 
Inherited diseases are the evidence of some permanent 
variation of the cellular correlations of the body, and 
being permanent the variation tends to reappear in suc- 
ceeding generations. A congenital disease is, on the 
other hand, oftentimes a temporary variation, or an iso- 
lated example of disease appearing at birth. Perhaps 
we should be safe in saying that a congenital abnormality 
is one which is acquired during the intrauterine period 
of life, while inherited is applied to conditions which 
depend upon permanent changes in the germinal plasm. 
Suppose we illustrate this in the following ways: 
I. Take an individual who after birth exhibits cer- 
tain abnormalities which were characteristics of his fa- 
ther, and of his grandfather, and great grandfather. We 
would say that he was the subject of an inherited con- 
dition. Take an example such as color-blindness which 
is transmitted from generation to generation, chiefly in HEALTH AND DISEASE 
25 
the men of a family, or hemophilia, a condition which 
characterizes "bleeders." Evidently in these cases the 
fundamental qualities of the germinal protoplasm have 
suffered a change. 
II. On the other hand, take the case of an apparently 
healthy mother who, just previous to conception, or af- 
ter conception, while the fetus is developing in the uterus, 
becomes intoxicated, let us say with alcohol (alcohol is 
perhaps the best example we can choose). The ger- 
minal plasm (the ovum) or the embryo (fetus) is affected 
by the poison so that after it is born it shows or de- 
velops abnormalities which are completely foreign in 
the family of mother or father. The child is the subject 
of a congenital condition or perhaps disease. It is apt 
to be less stable mentally ("neurotic") than an otherwise 
normal child. Its general mental condition is apt to be 
below the normal average (deficient), or it may be far 
below the average (idiocy, feeble-mindedness). If such 
a child reaches maturity it may become an alcoholic, and 
then certain persons speak of it as having an "heredi- 
tary craving" for alcohol, whereas it is merely congen- 
itally mentally unstable. If, again, such a child reaches 
maturity, and has children and those children are also 
mentally unstable, then we may say that they show an 
hereditary taint, or hereditary mental instability. 
Perhaps a mother, during the period of gestation, be- 
comes infected with one or another disease. If the child 
at birth has the same disease, that disease is congenital, 
not inherited. The infectious diseases are not heredi- 
tary, whether we speak of syphilis, gonorrhea, tubercu- 
losis, or measles. On the other hand, diseases of the 
mother which do not directly affect the child in utero 
may produce immunity to the maternal diseases, and so 
we have congenital immunity to disease. If the condi- 
tions which produce immunity affect permanently the 
germinal tissues, hereditary immunity may result. CHAPTER III. 
THE CAUSES OF DISEASE. 
Regardless of whether the basis of disease rests on in- 
trinsic or extrinsic variations, we can divide the causes 
into four great groups; namely, physical, physico-chem- 
ical, chemical, sociologic. These we will discuss in the 
order in which they have been named. This classifica- 
tion is of course arbitrary, and is made for convenience 
sake, for, with few exceptions, all injuries produce chem- 
ical damage within the body. That is to say, they lead 
to internal disorders of a chemical nature in the absence 
of which they would be of little or no importance, so far 
as the life or death of the whole organism is concerned. 
A cut or a bruise is of relatively small importance un- 
less infection occurs or severe hemorrhage takes place. 
In the first instance, the tissues are prepared for the 
growth of bacteria; in the second, the tissues do not re- 
ceive an adequate supply of oxygen because the oxygen 
carrying material of the blood has been lost. 
It is of course evident that the mechanical and phys- 
ical causes of disease are very commonly primary, but 
it is the secondary effects which are of greatest signifi- 
cance. The symptoms of disease following mechanical 
or physical insults are the expressions (for the most 
part) of these secondary effects. Both pressure and ten- 
sion act in producing variations in the nutritive activities 
of cells, and no matter whether these forces are exerted 
upon normal or abnormal cells, tissues or organs, 
changes are inaugurated which express themselves in 
various directions, such as hypertrophy, atrophy, degen- 
erations, or necrosis (of which more later), which are 
26 THE CAUSES OF DISEASE 
27 
the results of interference with nutritive (chemical) ac- 
tivities. 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Aschoff: Pathologische Anatomie. Jena, 1913. 
Encyclopaedia Britannica: Articles on "Pathology, "" Health" and 
"Disease. " 
Pembrey and Ritchie: General Pathology. New York, 1913. 
Physical Causes. 
The physical causes, as we shall group them, are pre- 
dominantly mechanical ones, and their effects are spoken 
of as traumas (or traumata). In this group are (1) 
pressure, (2) tension (or strain), and (3) combinations 
of pressure and tension. 
It must be evident to everyone, even if he has only 
a butcher-shop acquaintance with anatomy, that pressure 
is an important factor in producing the characteristic 
form of organs. One need only mention the lungs, the 
brain, the liver, to call attention to this factor. Were 
it not for the pressure exerted upon solid organs they 
would probably all be round. This is illustrated in the 
case of accessory spleens and livers which are not firmly 
attached, but hang more or less loosely in the body cav- 
ity and which are always round, quite unlike the larger 
fixed organs. The markings (grooves) on the surfaces 
of bones macle by blood vessels, the very surfaces them- 
selves, are examples of similar effects of normal pres- 
sures on normal organs. 
In the category of phenomena resulting from abnor- 
mal pressures on normal organs, there are many every- 
day illustrations. Among them are corns, calluses, in- 
growing toe nails. In former times, the days of tight 
lacing, the weird corset-liver was not infrequent. More 
important than these changes in form, are the symptoms 
produced by pressures, symptoms which indicate inter- 
ference with function. In this connection one recalls 28 
FUNDAMENTALS OF PATHOLOGY 
the " going-to-sleep " (anesthesia) of a foot from pres- 
sure upon a nerve trunk; the headache caused by a too 
tight collar; the bed-sores (decubitus) and "pressure 
spots" on the backs of bed-ridden patients; the swelling 
of the feet and appearance of varicose veins from tight 
garters. Also, in this group belong the erosions of bone 
caused by the intermittent pressure of aneurisms, the 
blistering of the hands by unusual manual work; the 
smothering (asphyxia) brought about by the pressure 
of tumors on the trachea; the difficulty in swallowing 
(dysphagia) caused by pressure upon the esophagus, 
and, an extremely frequent occurrence, the appearance 
of hemorrhoids (piles) from internal pressure in the 
bowels (constipation). 
When normal or abnormal pressures act upon ab- 
normal organs, the consequences are often still more se- 
vere. In this group we note the curvatures,-exemplified 
in knock-knees and bow-legs,-in rickets, as well as the 
spontaneous fractures of bones which have been affected 
by primary diseases of the bone. In these the bones 
are so weakened that even normal pressures warp and 
bend them and even cause them completely to give way. 
Internal pressures (distention) also produce, not 
merely changes of form but also, symptoms. A too 
great quantity of blood within the heart embarrasses it. 
An accumulation of fluid in the ventricles of the brain 
causes a gradual disappearance (atrophy) of the brain 
substance, caught as it is between the fluid and the bony 
skull. 
The effects of pressures depend largely upon the dur- 
ation and continuity of action. Continuous pressure of 
moderate or extreme intensity may produce death (ne- 
crosis) of tissue while one of great intensity, acting in- 
termittently, may produce only growth of tissue (hyper- 
trophy) as in calluses. Obviously the continuous pres- 
sures are of most serious import. THE CAUSES OF DISEASE 
29 
It must be apparent that the place of action of a phys- 
ical force and the character of the agent must be im- 
portant items in considering the effects of a trauma. 
An incision made with a clean sharp knife may be of no 
more than very transient importance and may have no 
appreciable effect upon the economy provided it does 
not open a large vessel or injure a vital organ. A lacer- 
ation produced by a dull dirty knife is more serious. A 
clean punctured wound may do no essential damage or 
it may cause death. A black eye (contusion) is rarely 
of importance, while a lacerated contusion is more im- 
mediately serious and potentially dangerous. A con- 
cussion may be either temporarily or permanently evil, 
depending upon the degree of force and the condition 
of the organs which are affected. 
All these types of damage (traumas) produce tissue 
destruction. Disorganized tissue is an excellent culture 
medium, and so, since bacteria are constantly present on 
and in the skin, and frequently in the blood, traumas 
tend to be complicated by infections. Moreover traumas 
may leacl to dislocations of cells, and such cells growing 
and reproducing in abnormal positions may produce 
fumors. 
Tension produces frequent disorders, some of them 
of considerable significance, some of them rarely even 
recognized. Physiologically strain is the important 
cause of strengthening of the fibrous unions of muscle 
and bone. It accounts in a large measure for the pres- 
ence of the tuberosities and other points of attachments 
of muscles. How it does this, is not definitely under- 
stood, but it is possible that the stretching of the tissues 
acts as a stimulus to the cells and so they make better 
use of the normal supply of food, or that intermittent 
application of the force increases the supply of food 
(blood) carried to the cells, much as happens during 
massage. 30 
FUNDAMENTALS OF PATHOLOGY 
The effects of severe strain are well known in sprains 
of various sorts, as well as in the less severe strains. In 
the latter the tendons or their attachments are but mod- 
erately damaged. In the former they are often rup- 
tured. In the case of muscular strain, whether of the 
skeletal muscles or of the eye muscles-for instance, eye- 
strain, fatigue is produced, with subsequent loss of 
power, and even atrophy or wasting. 
Physico-Chemical Causes. 
In this group we deal with such influences as atmos- 
pheric pressure, electricity, x-rays, radium, light and 
light waves, heat and cold, all of which are physical 
agents which produce both physical and chemical changes 
in the body, but of which the chemical effects are most 
important. They form a boundary group of influences 
standing between the more purely physical and the more 
purely chemical. In some instances the distinction is 
very little evident. For instance, the effects of sudden 
changes of atmospheric pressure such as occur in cais- 
son disease are quite different from those of the grad- 
ual changes which occur when a person goes from one 
altitude to another. In the first instance, the blood ab- 
sorbs more than a normal amount of atmospheric gases 
(oxygen and nitrogen chiefly), and this, when the pres- 
sure is suddenly removed, is set free in the blood and 
the bubbles of gas plug the small blood vessels. The 
phenomenon is quite similar to that observed in uncork- 
ing a soda water bottle. In the latter case, the decreased 
pressure apparently acts as a stimulant to the blood 
producing organs, and this results in a large number of 
blood cells. 
Electric currents act upon the tissues of the body much 
as they do upon materials in a test tube. A current 
passed through a solution is modified so that certain par- 
ticles pass to one pole while others pass to the other THE CAUSES OF DISEASE 
31 
(ions; electrolytic dissociation). In the body a similar 
process occurs only it is more complex. When such dis- 
sociation affects intensively such parts of the body as 
the respiratory center, death is immediate. 
The method of action of the x-rays and radium we do 
not understand. Depending, however, upon the time of 
exposure, or the intensity of the rays, perhaps also upon 
the quality of the rays (the proportion of alpha, beta 
and gamma rays) cells may either be destroyed and so 
produce x-ray or radium burns, or may undergo hyper- 
trophy, and ultimately give rise to x-ray cancers. 
Light rays are antagonistic to life if they are suffi- 
ciently concentrated. Even diffused light is harmful to 
some forms of life. This is especially true of certain 
of the lower forms of life, particularly of the bacteria. 
It is not true of man. 
Light is undoubtedly a stimulus to the chemical ac- 
tivities of cells, just as it accelerates many chemical re- 
actions outside the body (silver salts in photography), 
and it may be true that light is more destructive to the 
bacteria because it is able more readily and thoroughly 
to penetrate their bodies and so start processes which 
result in self-destruction. In the large organisms, such 
as man, growth is favored by light. Metabolism is ab- 
normally slow in darkness. Children of the light are 
physically larger than "basement children." These ef- 
fects are in part due to the heat producing rays (red 
and infra-red); in part to the stimulant rays (violet and 
ultra-violet). 
We know better the effects of the heat producing rays. 
We know the reddening of the skin with the subsequent 
soreness and blistering (vesiculation, sunburn), and the 
also subsequent increase of pigment in the skin (pig- 
mentation, tanning). We also know the condition called 
sunstroke (insolation). Sunstroke is a condition which 
is caused indirectly by the action of the red and infra- 32 
FUNDAMENTALS OF PATHOLOGY 
red (heat) waves of light. It is the result of insuffi- 
cient elimination of heat from the body. When the body 
retains its heat, the chemical processes within it are ac- 
celerated, exactly as the chemical processes in a test 
tube mixture are hastened by waving over the flame. The 
result of this is that poisonous products of metabolism 
are more rapidly produced than at normal temperature, 
too rapidly to be excreted,-and the body suffers. If 
the heat of the body is not so extreme and if its action 
is spread out over a longer time, the organism loses wa- 
ter, by perspiration, in abnormal amount, and so the 
main solvent of the substances in the body is lost to an 
extent that the poisonous products of metabolism accu- 
mulate. This produces heat exhaustion. 
Heat produces the effects which are generally known 
as burns. In the case of a slight burn (burn of the first 
degree) the skin is reddened, swells, and is painful. If 
the burn is slight and the action continued for some time, 
the skin is apt to become pigmented as in sunburn. If 
the burn is of a more severe character, the skin is not 
merely reddened, swollen and painful, but shows the 
presence of blisters, large or small (burns of the second 
degree). If the burn is still more severe the whole thick- 
ness of the skin may be affected. It is killed (undergoes 
necrosis) by the heat; the protoplasm of the cells and 
of the blood is coagulated, and the dead tissue sloughs 
away and leaves ulcers (burns of the third degree). In 
still more severe cases the skin is charred (carbonized) 
and we speak of burns of the fourth degree. 
The effects of burns upon the whole organism depen a 
upon the extreme pain, the absorption of dead materials 
from the skin, the infection of the burned areas, and the 
formation of disfiguring scars. 
The effects of cold are, in some respects similar to 
those caused by heat. That is to say, cold may produce 
death of tissues by blocking the blood vessels. In se- THE CAUSES OF DISEASE 
33 
vere cases this is brought about by rapid thawing of the 
frozen tissue. In the course of freezing the water of 
the tissue solidifies in crystalline form, in other words, 
it is partially separated from the rest of the constituents. 
During rapid thawing the water is set free and not 
enough time is given it to reunite with the other sub- 
stances. The result is blocking of the blood vessels and 
death of tissue. 
REFERENCES. 
Light. 
Arons: Investigations on the Action of the Tropical Sun on Man and 
Animals. Philippine Jour. Sc., 1911, vi, 101. 
Bovie: A Preliminary Note on the Coagulation of Proteins by Ultra- 
violet Light. Science, New York, 1913, xxxvii, 24. 
Houghton and Davis: A Study of the Germicidal Action of the Ultra- 
violet Rays. Am. Jour. Public Health, 1914, iv, 224. 
MacDougal: Light and the Rate of Growth. Science, New York, 1915, 
xli, 467. 
Verhoeff: Ultraviolet Light as a Germicidal Agent, etc. Jour. Am. 
Med. Assn., 1914, Ixii, 762. 
Verhoeff and Bell: The Alleged Dangers to the Eye from Ultraviolet 
Radiation. Science, New York, 1914, xl, 452. 
Woolley: Insolation. Forchheimer's Therapeusis of Internal Diseases, 
1913, iv, 672; New York Med. Jour., 1914, xcix, 1165. 
Electricity. 
Cleaves: The Destructive and Lethal Effects of High Pressure Cur- 
rents. Ref. Handb. Med. Sc., 1913, iii, 876. 
Heat and Cold. 
Csillag: Beitraege zur Klinik der Erfrierung. Wien. med. Wchnschr., 
1914, xxvii, 1275. 
Lee and Scott: On the Action of Temperature and Humidity on the 
Organism. Proc. Soc. Exper. Biol, and Med., 1914-15, xii, 10. 
Pfeiffer: Das Problem des Verbruehungstodes. Studien zur Pathologie 
und Pathogenese der thermische Allgemeinschaedigung. Wien., 1913. 
Puppe: Das Problem des Verbrennungstodes. Jahresb. f. aerztl. Fort- 
bild., 1914, ix, 32. 
Air Pressures. (Caisson Disease; High Altitudes.) 
Bassoe: The Late Manifestations of Compressed Air Disease. Am. 
Jour. Med. Sc., 1913, cxlv, 526. 
Bornstein: Physiologic Und Pathologie des Lebens in verdichter Luft. 
Berl. klin. Wchnschr., 1914, li, 923. 
Editorial: Anglo-American Expedition to Pike's Peak. Jour. Am. 
Med. Assn., 1912, lix, 449. 
X-Rays and Radium. 
Clunet: Histological Changes Produced by X-Rays in Animal Tissues, 
etc. Jour. Roentgen Soc. Lond., 1914, x, 29. 34 
FUNDAMENTALS OF PATHOLOGY 
Eden: Neuere Versuehe zur biologische Wirkung der Roentgenstrahlen. 
Munchen, med. Wchnschr., 1914, Ixi, 2010. 
Grunbaum: Some Effects of Radium on Various Tissues. Jour. Path, 
and Bacterio!., 1911, xv, 356. 
Keetman: Die Absorption der .... und Roentgenstrahlen imm Gewebe. 
Berl, klin., Wchnschr., 1914, li, 739. 
Lazarus-Barlow: Discussion on the Action of Radiations on Cells and 
Fluids. Brit. Med. Jour., 1914, ii, 708. 
Rowntree and Baetjer: Radium in Internal Medicine; Its Physiological 
and Pharmacological Effects. Jour. Am. Med. Assn., 1913, Ixi, 1438. 
Chemical Causes. 
The body may be affected by the most various sub- 
stances, some of which produce very apparent gross ef- 
fects, as, for instance, sulphuric acid, caustics of various 
sorts; some of which produce no obvious gross effect, as, 
for instance, poisonous gases, and the toxins produced 
by bacteria. These substances poison the body, some of 
them locally, some of them generally (intoxication). 
Many of them are products of living organisms, such as 
bacteria (bacterial toxins), many the product of unor- 
ganized chemical action (the caustics, acids, organic and 
inorganic poisons), and some of them are the products 
of the body itself. The fact that some are produced by 
the body while some are produced outside of it, allows us 
to classify them as exogenous and endogenous, while the 
fact that some are the products of living bodies, chiefly 
parasites, allows us to group them also as parasitic and 
non-parasitic. We make, therefore, the following 
schema: 
A. Intoxications of exogenous and non-parasitic ori- 
gin. 
B. Intoxications of exogenous and parasitic origin 
(infections). 
C. Intoxications of exogenous and saprophytic origin 
(meat poisonings, etc.). 
D. Intoxications of endogenous and non-parasitic ori- 
gin. THE CAUSES OF DISEASE 
35 
Iii the first group which concerns itself with exogenous 
and non-parasitic intoxications, belong the effects pro- 
duced by the chemical substances,-strong acids, mineral 
or organic, silver nitrate, carbolic acid and the like. These 
as a rule act by killing the cells (coagulating their proto- 
plasm) upon which they act. Sometimes, however, the 
local action is less important than the general action, or 
the action in other organs, than the one upon which the 
substance acted primarily. This is true of certain gases, 
for instance hydrocyanic acid gas, which, breathed into 
the lungs, causes death by its action upon the central ner- 
vous system. Carbolic acid likewise, if introduced into 
the body in dilute solutions, does less damage in the gas- 
trointestinal tract than in the kidneys. Examples could 
be multiplied, and may be found in any pharmacology. 
Alcohol is the most useful example perhaps, because of 
its local, general and social effects. It may be useful to 
call to mind the so-called selective action of poisonous 
substances, illustrated by strychnine which affects the 
spinal cord; carbon dioxide which affects the respiratory 
center; and barium chloride which affects the muscle of 
the blood vessels. 
The second group, that in which the exogenous para- 
sitic intoxications belong, is concerned mainly with mat- 
ters which are studied in bacteriology. They comprise 
the infections, which, though in certain cases the symp- 
toms are due to the presence of the parasites themselves, 
are as a rule the result of the chemical action of the sub- 
stances elaborated by the bacteria (see p. 41). 
The exogenous saprophytic intoxications are ones 
caused by what are ordinarily called non-pathogenic or- 
ganisms. They are the result of poisoning with sub- 
stances produced by the microorganisms during splitting 
up of food materials. Such substances are the various 
amines, formed from proteins during putrefaction. A 
connecting link between this group and the previous ones 36 
FUNDAMENTALS OF PATHOLOGY 
are the gastrointestinal intoxications or toxemias, often 
erroneously called autointoxications (see p. 149). 
The last group comprises a series of metabolic disturb- 
ances which are coming to be of greater and greater sig- 
nificance, namely, the disturbances which result from im- 
perfect correlation of function of physiologically associ- 
ated organs, chiefly those called the glands of internal 
secretion, or the ductless glands (see p. 53). 
Infection. 
By infection we mean the entrance of living organisms 
(bacteria, protozoa, metazoa) into the bodies of other ani- 
mals. In certain instances, the penetrating organisms 
are confined to the skin (acarus, itch mites) where they 
live and cause disturbances which are largely irritations, 
and which are not followed by the general reaction called 
immunity. In other cases organisms (intestinal worms) 
enter the gastrointestinal tract where they live and cause 
disturbances which are, in part, irritative, in part, toxic. 
Evidence of the toxic effects are given by changes in the 
structure of the blood (eosinophilia, etc.). In still an- 
other group of cases, the parasites penetrate into the tis- 
sues (bacteria, metazoa) where they reproduce and by 
their toxins give rise to local and general effects, which 
in some instances are so characteristic that we speak of 
definite disease. Tn some such cases the growth of the 
parasites in the body is followed by immunity (bacterial 
diseases, infectious diseases), in others, it is not (infec- 
tions with such parasites as tapeworms, trichina, filaria, 
etc.). 
Bacteria enter the body constantly, even during health. 
They also enter the tissues to which they are carried from 
the intestinal tract or infected tonsils or teeth, sometimes 
by leucocytes which have engulfed them, sometimes by 
their own activities. As a rule (in health) they are de- 
stroyed. When they succeed in living and multiplying THE CAUSES OF DISEASE 
37 
tliey cause infectious diseases, the symtoms of which may 
be due to mechanical effects, such as plugging of vessels, 
to toxic (chemical) effects or to both. 
Normally, that is, in the state of health, the body can 
withstand the attacks of its bacterial foes, but a damaged 
body is not so resistant. For instance, it is well known 
that bacteria are commonly present, not only on the skin, 
but in it and yet these bacteria do but little damage. Bpt 
after a cut or a bruise, "festering" is quite common. Of- 
ten this is due to bacteria introduced during the cutting. 
Often it is due to the bacteria of the skin which are able 
to grow in damaged tissue. "Stitch abscesses" arise in 
the same way. A person with a normally acid gastric 
juice is infected with difficulty with cholera. But let 
him neutralize the acid juice with alkali and then he be- 
comes very susceptible. In many conditions (for exam- 
ple, after using alcohol) the gastric contents are neutral 
or alkaline. 
But beside such things, the resistance of the body de- 
pends upon many other factors, such as species, age, phys- 
ical condition, nutritive conditions, on the one hand, and 
upon the virulence of the bacteria on the other. In brief, 
infection is determined by the relative virulence of the 
infecting organisms. 
What is often called predisposition to infection is a real 
enough thing provided we use the term broadly. "Pre- 
disposition to tuberculosis" is however not a valuable 
phrase. An individual who is little resistant to infection 
is prone to acquire the frequent diseases, i. e., those from 
which many of his fellow beings are infected. The op- 
portunities for infection with tuberculosis are legion. 
"Predisposition to tuberculosis" then is no more than a 
lack of resistance on the part of the individual to many 
infections, coupled with multiplied exposition to tuber- 
culosis. The factor of exposition is probably the impor- 
tant one in the notable incidence of certain diseases in 38 
FUNDAMENTALS OF PATHOLOGY 
children at the time when they begin to creep and to be 
handed from relative to relative. They begin to be ex- 
posed more systematically to infection. In creeping they 
soil their hands, and every object of interest is carried 
to the mouth for experimentation. They are kissed by 
every chance acquaintance. Tuberculosis is frequent in 
children in the early years of life. 
Susceptibility to infection is another matter, and de- 
pends upon presence or absence of immunity and upon 
the relative resistance of the body, which latter may be 
lowered by various effects, such as fatigue, hunger, cold, 
intoxications (especially alcohol), by previous infections, 
and by secondary simultaneous infections. 
Immunity results from the ability of the cells of the 
body to chemically fix or modify toxic substances which 
are brought to them by the blood, and is a quality which 
is sometimes inherited. It may also be the result of the 
inability of the cells of the body to make any use what- 
ever of the toxins. 
The effects of fatigue, hunger and cold are frequently 
seen in cases of "taking cold" [nasal infections (coryza); 
pneumonia]. 
The effects of intoxications we have already called at- 
tention to in speaking of alcohol and cholera. 
The effects of previous infections are seen in cases, 
which, having had measles, develop tuberculosis or pneu- 
monia: of simultaneous infection as to the appearance of 
tuberculosis during whooping cough. 
Local infections produce local inflammation (boils, ab- 
scesses, furunculosis). General infections (bacteremia, 
septicemia) produce general effects, such as various types 
of tissue degenerations, fever, and other disorders of met- 
abolism which are grouped under the term, the effects of 
intoxications. 
Certain infective agents remain localized and produce 
general effects by means of soluble toxins (diphtheria, THE CAUSES OF DISEASE 
39 
tetanus) which effects we refer to toxemia as opposed to 
septicemia. 
Sometimes bacteria localized at first, enter the blood 
stream and form new foci of growth as in furunculosis. 
This process of distribution from a primary focus we call 
metastasis: the condition is often called pyemia, or sep- 
ticopyemia. 
In latent infections, the bacteria remain in an inactive 
state in the tissues (tuberculosis). 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Browning: Pembrey and Ritchie's General Pathology. New York, 1913. 
Vaughan: Jour. Am. Aled. Assn., 1914, Ixii, 583. 
Walker: Pembrey and Ritchie's General Pathology. 
Zinsser: Infection and Resistance. New York, 1914. 
Sociologic Causes of Disease. 
Very possibly it will seem strange and out of place 
in a volume of this sort to even mention social surround- 
ings as a factor in disease. Nevertheless there is very 
probably no more important aspect of disease than the 
social. The character of associates, parents, and rela- 
tives; the formation of habits because of special associa- 
tions; the growth of imitations of other individuals; the 
character of instruction in educational institutions; and 
the possibility of permanence of early impressions re- 
ceived in the juvenile or even in the infantile period of 
life,-all are entirely worthy of the attention they are 
only beginning to receive. It is in this field that the ap- 
plication of experimental psychology is beginning to 
prove of the utmost value, and it is here that medicine 
appears as a territory standing between sociology and 
normal psychology. In this field the benefits of prevent- 
ive medicine will, in the future, be as striking and as val- 
uable as they have shown themselves to be in the bet- 
ter known and perhaps more obvious fields of hygiene. 40 
FUNDAMENTALS OF PATHOLOGY 
It will perhaps be discovered that what we call heredi- 
tary, in certain and very frequent instances, is not that, 
but is in reality social in a broad sense. The most valua- 
ble materials for the study of these sociological factors 
in disease are to be found in the records and reports of 
the Hospital Social Service Associations and in such vol- 
umes as Cabot's Social Service and Art of Healing, the 
Journal of Abnormal Psychology, and the like. 
There are, beside the above mentioned aspects, others 
which are associated with industrial surroundings. In 
this group belong the subjects of industrial poisonings, 
vocational morbidity and mortality, and diseases of oc- 
cupation. One thinks in such a connection with the al- 
lied problems of vocational guidance which are ones deal- 
ing, in part, at least, with the placing of individuals in 
industries, or divisions of industries, suited to their phys- 
ical and mental make-up, for it is obvious that a person 
may be either physically or mentally harmed if he is 
placed at work for which he is not fitted. With this is 
again associated problems of the effects of fatigue as in- 
fluenced by interest and pleasure, as well as those of 
mental retardation, and deficiency and moral delinquency. 
REFERENCES. 
Bertillon: Vocational Mortality. Jour. Am. Med. Assn., 1913, Ixi, 1388. 
Cabot: Social Service and Art of Healing. New York, 1909. 
Cabot: What Men Live By. New York. 
Freud-Brill: Psychopathology of Everyday Life. New York, 1914. 
Goldmark: Fatigue and Efficiency. New York, 1912. 
Oliver: Diseases of Occupation. 
Rambousek: Industrial Poisonings. New York, 1913. 
Intestinal Intoxications. 
The term intestinal intoxication is one which has, at 
the present time, more clinical significance than patho- 
logic. To the clinician the term means a series of symp- 
toms which are associated with gastrointestinal abnor- 
malities of almost any kind. It is a term which occupies THE CAUSES OF DISEASE 
41 
a place similar to that held, in the minds of many, by 
neurasthenia. In other words its significance varies with 
the physician or surgeon, and perhaps the point of view 
of the individual clinician is based upon his belief that 
the symptoms are due to the following: 
1. The toxic effects of poisonous substances produced 
in the intestine and thence absorbed into the system. It 
may be said that this is a possibility although there is 
no definite experimental evidence. It is true that in the 
process of digestion of foodstuffs, especially the proteins, 
that poisonous materials are produced. These however 
are as a rule neutralized or inactivated by chemical com- 
binations in the tissues during the process of absorption. 
2. The toxic effects of poisonous substances produced 
by bacterial activity in the intestines. Such substances, 
for example, the ptomains, are extremely toxic. The 
amines also are exceedingly active poisons, and such aro- 
matic substances as indol and skatol have been credited 
with grave disorders. As a rule, however, these sub- 
stances are produced in too small amounts to be serious 
menaces, or, like indol and skatol, are chemically com- 
bined, inactivated and excreted. It may, however, hap- 
pen that in occasional instances, as in ptomain poisoning, 
such substances found completely without the body, are 
introduced in sufficient amount to produce disease. It 
may also happen that chemical combination does not oc- 
cur in the body. 
3. The symptoms may be due to the action of endo- 
toxins or exotoxins of the intestinal bacteria, which may 
be found within the intestinal canal and from there ab- 
sorbed. 
4. The symptoms may be due to the penetration of 
bacteria themselves which gain entrance to the tissues 
from the intestines. 
As a rule the effects produced by the factors men- 
tioned in groups 1 and 2 cannot be separated, nor can 42 
FUNDAMENTALS OF PATHOLOGY 
tliose indicated in groups 3 and 4, because in the first in- 
stance bacteria are constantly present in the intestines 
and carry on their work ot* splitting the foods while the 
normal ferments are carrying on theirs, and, in the sec- 
ond instance, toxins are absorbed from the intestinal 
tract and cause changes in the organs, while in occasional 
instances, the bacteria also enter through the walls of 
the tract and are engulfed by the cells of the tissues 
where the endotoxins are set free and there they produce 
their pathologic effects. This is illustrated in the severe 
clinical complex called typhoid fever. In many cases of 
intestinal intoxication the symptoms are produced by or- 
ganisms which are of less pathologic significance, for in- 
stance, the colon bacillus, and perhaps other bacterial 
forms. To such conditions Adami applies the useful 
term sub-infection. 
REFERENCES. 
Adami: Principles of Pathology. 
Adami: Chronic Intestinal Stasis. Brit. Med. Jour., Jan. 24, 1914. 
Herter: Bacterial Infections and the Digestive Tract. Lond. and New 
York, 1907. 
Metchnikoff: Poisons Intestinaux et scleroses. Ann. de 1'Inst. Pasteur, 
1910, xxiv, 755. 
Metchnikoff: The Prolongation of Life. Putnam Science Series, New 
York. 
Woolley: Intestinal Stasis and Intestinal Intoxications: A Critical 
Review. Jour. Lab. and Clin. Med., 1915, i, 45 (Literature). CHAPTER IV. 
DISTURBANCES OF METABOLISM. 
By metabolism we mean the sum of the chemical 
changes taking place in the tissues of an organism. One 
phase, which is concerned with ingestion and assimila- 
tion of food materials is known as anabolism. The other, 
concerned with the breaking down excretion and elimina- 
tion is known as katabolism. 
Metabolism is modified in either or both its phases by 
the quality and the quantity of the food, and also by con- 
ditions within the body which influence the cells and tis- 
sues in such a way that they are less able or more able 
than normal to make use of food. For instance, the quan- 
tity of food which is necessary to keep the body in a nor- 
mal state of nutrition depends upon age, muscular activ- 
ity, and climate, and upon certain other conditions some 
of which are inherited, some of which are acquired. Also 
some of the individual conditions are transient, some are 
permanent. 
It is quite evident from superficial observation that a 
child uses more food compared with its weight than an 
adult. It is just as evident that an old man uses less than 
an adult in the prime of life. These variations are de- 
pendent upon the activities of the cells of the organism. 
In the infant and during childhood, growth is rapid, the 
individual is very active, and food is used rapidly, both 
for the production of heat and for the growth of the tis- 
sues. As age increases, the activities of cells, and of 
the organism itself, decreases, and not only is less food 
necessary, but less food can be utilized. 
It is a matter of everyday experience that the active 
43 44 
FUNDAMENTALS OF PATHOLOGY 
person needs more food (other things being equal) than 
lie who is sedentary. During muscular activity, more 
food is used in the production of heat. In the absence of 
muscular activity, the food that might merely be burnt 
becomes unnecessary, and therefore we may say, in a 
very general sort of way, that the needs of the body de- 
pend upon the amount of muscular activity. Of course 
this is not entirely true but it is sufficiently true to make 
a point of it. The food needs of the body are modified by 
age, and this depends in part at least upon muscular ac- 
tivity. They are also modified by the external tempera- 
ture which surrounds the body. 
Other influences which affect the use to which food is 
put within the body are (1) individual differences, which 
are difficult of description for obvious reasons, and (2) 
the influence of the ductless glands, which are only now 
beginning to be understood. It is perhaps true that the 
so-called individual differences are expressions of vary- 
ing activities of the ductless glands. 
We all know that some individuals eat very large 
amounts of food and remain slender, while others take 
small quantities of food and become excessively stout. 
In part such phenomena depend upon muscular activity; 
in part, upon certain not-understood conditions within 
the body which allow of storage of large amounts of 
fats. In some instances one or another mental type is 
associated with the physical condition. In some cases 
we believe that the internal arrangements within the or- 
ganism are not properly balanced, and in some such 
cases we have reason to believe that the derangements 
are associated with more or less definite lesions, that is 
to say, with abnormal activities, of certain of the or- 
gans of internal secretion; for instance, the pituitary 
gland, the genital glands, the thymus, the thyroid, the 
adrenals and the pancreas. 
When a person becomes stout, when he increases in DISTURBANCES OF METABOLISM 
45 
weight, it is obviously because lie assimilates and holds 
a larger proportion of his food than he uses up in produc- 
ing heat and other forms of energy. If he loses weight, 
it is because he uses up more food than he retains. Some 
individuals will do one or the other of these things, re- 
gardless of the amount of food taken. But the normal 
individual who holds his weight upon a normal diet can 
be made to increase in weight by increasing his food or 
by decreasing his muscular activity. He may also be 
made to lose weight by decreasing the food or by increas- 
ing his activity. He will also lose weight if he is not con- 
tented, if he is worried. Hence, the saving, "laugh and 
grow fat." 
But aside from the question of quantity of food there 
is the very important factor of the quality of food. We 
know from our studies in physiology that a normal diet 
must be more or less balanced in its content of protein, 
fats and carbohydrates, salts and water, and we know that 
absence of any one of these constituents will produce 
greater or less change, or even damage to the organism, 
depending upon the length of time the lack is continued. 
So much for the general external conditions of meta- 
bolism. Beside these there are the general internal con- 
ditions of metabolism which have been touched upon in 
the section on Intestinal Intoxications. 
We know that during metabolism many substances are 
formed within the body-in the cells, and given to the 
blood-which if they were permitted to remain unmodi- 
fied in the body would be extremely poisonous. We know 
that as a rule these substances are disposed of by excre- 
tion in the urine, feces, sweat, etc., usually after they 
have been chemically combined in such a way as to make 
them physiologically innocuous. We also know that cer- 
tain-perhaps all-the cells of the body produce sub- 
stances (internal secretions,-hormones) which serve a 
physiologic purpose, but which also, when they are pro- 46 
FUNDAMENTALS OF PATHOLOGY 
duced in more than normal amounts, lead to serious dis- 
orders. It will be obvious that if such substances when 
produced in normal amounts serve a physiologic purpose, 
then the body will suffer as it is not supplied with ade- 
quate amounts. Here then, as in the case of food, we 
have disorders due to too much, and too little, internal 
secretion. 
There is a final possibility that abnormal substances 
may be formed within the body, as a result of prevented 
activity of the cells. As a rule such substances are not of 
serious import. 
It appears that disturbances of metabolism are the re- 
sults of interruptions in the chain of physiologic trans- 
formation of foodstuffs and that these interruptions are 
the results of modifications of cellular activities which 
are, except in rare instances, the results of variations in 
the environment of the organism which result in certain 
instances in what we call hereditary, or congenital, indi- 
vidual differences. 
According to the foregoing remarks, pathologic condi- 
tions the body may result from the following: 
1. Failure of elimination. 
2. Failure of one tissue to make physiologic use of the 
products of metabolism of other tissues. 
3. Failure of chemical combinations. 
4. Excessive production of otherwise physiologic ma- 
terials. 
5. Insufficient production of otherwise physiologic 
materials. 
6. Combinations of two or more of the previous fac- 
tors. 
During metabolism, the constituents of the tissues are 
broken down into simpler compounds, many of which are 
acids. In the presence of a sufficient supply of oxygen 
these acids are present only transiently and are rapidly DISTURBANCES OF METABOLISM 
47 
decomposed or combined, and so become harmless. In 
the absence of a sufficient supply of oxygen they persist. 
When this happens a condition arises which we call acid- 
osis. 
Acidosis is present in greater or less degree in diabetes, 
anemia, starvation, inanition, and cachexia, fatigue (mus- 
cular or mental), following anesthetics, during preg- 
nancy and fevers, and in uncompensated cardiac and re- 
spiratory diseases. 
In certain abnormal circumstances, a condition of acid- 
osis is associated with certain acids, particularly those 
belonging to the group of amino-acids. Such conditions 
are uremia, eclampsia, acute yellow atrophy and chloro- 
form necrosis. 
Anomalies of Metabolism. 
Anomalies, as we usually use the word, are varia- 
tions from normal which have no detrimental effect upon 
the organism. In the realm of the anatomic we speak of 
the presence of six fingers, or six toes, for instance, as 
anomalies. They interfere not at all with the health and 
life of the organism, although they may be inconvenient. 
In the same way, when we speak of anomalies of meta- 
bolism, we mean chemical phenomena as they occur in 
the organism which, though they do not appear in the 
perfectly normal individual, yet do not act to the essen- 
tial disadvantage of the organism. Such anomalies are 
alkaptonuria, cystinuria, pentosuria. The former is char- 
acterized by the excretion in the urine of a substance 
(homogentisic acid) which normally is not present in the 
urine. Upon exposure to the air and light such urines 
become quite dark in color, even almost black. Cystinuria 
is characterized by the excretion in the urine of a sulphur 
containing material called cystin, which can be recognized 
by the microscope. Pentosuria depends upon the excre- 
tion in the urine of a pentose, a sugar, which may be rec- 
ognized by chemical methods. 48 
FUNDAMENTALS OF PATHOLOGY 
Somewhat analogous to these conditions is albinism, in 
which the body, even the hair, appears to be completely 
devoid of pigment. The causes of this lack of pigment 
we do not know. 
High Temperature. 
The regulation of the temperature of the body depends 
mainly upon two factors-physical and chemical. The 
Fig. 2.-Continuous fever. 
physical factor has to do with heat elimination and is 
largely bound up with the circulation and secretion from 
the skin. The chemical factor has to do with heat produc- 
tion within the body and is an affair of combustion (ox- 
idations) of foodstuffs within the body. If heat produc- 
tion rises without a corresponding activity in the organs 
of elimination, the body temperature rises. The body 
temperature therefore depends upon the balancing of 
heat production and heat elimination. DISTURBANCES OF METABOLISM 
49 
Every activity of the body increases, temporarily, its 
temperature. Muscular exercise is especially active in 
this respect. During exercise more fuel is burned, and 
more heat is produced and must be eliminated, and so the 
blood vessels of the skin dilate, the face is flushed, and 
perspiration is increased. In this way heat is eliminated 
from the body and the temperature tends to keep its nor- 
mal level. During such work, the rectal temperature may 
reach 38.3° (101°) without any evidence of discomfort. 
Fig. 3.-Remittent fever. 
It is probable that the normal temperature curve owes 
its form to the effects of rest and activity. 
Even after a hearty meal the temperature may rise to 
a slight degree. Hot and cold drinks of course modify 
the temperature. 
More important perhaps than any other factors than 
exercise, are external temperature, humidity and breeze. 
These influence heat elimination chiefly for very obvious 
reasons. If the temperature surrounding the body is 50 
FUNDAMENTALS OF PATHOLOGY 
high, less heat can be given off in a unit of time and so the 
body temperature tends to rise. This is especially true 
if the humidity is high, for the moisture on the surface 
of the body will not evaporate rapidly and so the cooling 
effect of evaporation is lost. If, on the other hand, a 
breeze fans the body, evaporation is more rapid. It has, 
for instance, been shown by workers in the tropics that 
Fig 4.-Intermittent fever. 
the effect of even light breezes may counteract the other- 
wise almost intolerable heat of the glaring days. 
Now, inasmuch as temperatures as high as 38.8° (101°) 
may be considered as falling within physiologic limits, 
and inasmuch as the normal range of body temperature 
in a healthy person lies between 96.8° (36°) and 99.5° 
(37.5°), and inasmuch as these upper figures are some- 
times called fever temperature, we wish to know what 
"fever" is. Perhaps we might say that fever is a condi- 
tion of abnormal temperature variation during which the DISTURBANCES OF METABOLISM 
51 
mean temperature of the body is raised. The mean daily 
temperature is about 37° (98.6°), or we may say that 
"fever is a term to include all conditions in which the 
normal temperature of the animal body is markedly ex- 
ceeded for any length of time." 
But fever relates to more than temperature alone. 
The person who works, physically, until his temperature 
reaches 101° (38.3°) does not feel any discomfort. The 
person who has a fever of 101° (38.3°) does feel discom- 
fort. "The elevation of the temperature of the body is 
one of the usual signs of fever, but is not an essential one. 
As a matter of fact, fever as a rule is the result of infec- 
tion by bacteria, and is a complex thing, associated with 
chills, headaches, feelings of malaise, nausea, vomiting, 
pains in the limbs and muscles, dizziness, and often with 
a rise of temperature (pyrexia). It is quite different 
in all its appearance from the rise of temperature (hy- 
perthermia) caused by external heat (sunstroke-insola- 
tion), lesions of the nervous system, and poisonous drugs. 
In speaking of the temperature during fever, the fol- 
lowing terms which are sometimes used, are illustrative: 
Slight fever 100.°-101.12° F. (38-38.4° C.). 
Moderate fever 101.3°-102.2° F. (38.5°-39° C.) in the morning, rising 
to 103.1° (39.5°) in the evening. 
Considerable fever 103.1° (39.5°) in the morning, and 104° (40°) in 
the evening. 
High fever 103.1° (39.5°) in the morning, and 104.9° (40.5°) in the 
evening. 
Hyperpyrexia 107.6° (42°) or more. 
Fever is divided into three stages, the initial or pyro- 
genic stage; the fastigium or fastigial stage; and the def- 
ervescence or defervescent stage. The first stage may 
he short or long; an hour or two-malaria, or lasting one 
or several days as in typhoid. The second stage may be 
very brief or very long. The third stage also may be 
quite short (crisis) or the fall of temperature may occur 
gradually (lysis). 
A continued fever, as one in which the daily tempera- 52 
FUNDAMENTALS OF PATHOLOGY 
ture changes, although they occur at a higher level, are 
little or not at all greater than in health. (Typhoid, pneu- 
monia.) 
A remittent fever is one in which the temperature 
changes are exceedingly irregular, and during its course 
the normal line may be touched (suppurations; pyemia, 
tuberculosis with secondary infection). 
Intermittent and recurrent fevers are characterized by 
series of initial fastigial and defervescent stages as in ma- 
laria, relapsing fever, etc. 
In the first or initial stage, the patient complains of 
cold, and suffers a chill. Uis skin feels cold and clammy 
though the thermometer introduced in the rectum will 
show that the internal temperature is above the normal. 
The onset may be rapid or slow, and the duration of the 
rigor may be brief or prolonged. Often, at the onset of 
a fever, there is no chill but merely a period of depression 
during which the temperature rises. The feeling of cold, 
in spite of these increased temperatures depends upon the 
fact that the sensations of heat and cold arise in the skin, 
at the onset of a fever the surface temperature commonly 
falls. 
In the second stage, into which the initial one merges, 
the skin becomes hot and Hushed, and instead of feeling- 
cold the patient feels hot, and correspondingly thirsty. 
The third stage, as has been said, may he short (crisis) 
or prolonged (lysis). In this first case the temperature 
falls very rapidly and the fall is accompanied by profuse 
perspiration. 
Fever, we believe, is due to the production of too much 
heat in the body and is caused by the action of bacteria 
or their products. It is a compound of heat accumula- 
tion by over-production, and intoxication by poisonous 
substances. 
In sunstroke (insolation) on the other hand, the cause 
of the symptoms is the heat rays acting upon the body. DISTURBANCES OF METABOLISM 
53 
These rays act first by healing the body so that its chem- 
ical processes are quickened and more heat is therefore 
produced to the point where elimination by evaporation 
or radiation is no longer possible, or to the point when 
the water supply of the body is so depleted that the skin 
is no longer capable of secretions for evaporation. When 
the air is hot, still and humid, the body cannot lose its 
heat, and then if physical exercise is persisted in, the in- 
ternal temperature of the body may rise to very high 
points. It is possible that heat exhaustion is due to grad- 
ual depletion of the water of the body without equiva- 
lent loss of heat, and that heat stroke is due rather to 
rapid accumulation of heat with or without water loss.* 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Barbour: Die Wirkung unmittelbarer Erwarmung u. Abkahlung der 
Warmzentre, etc. Arch. f. exper. Path. u. Pharmakol., 1912, Ixx, 1; 
Abst. Jour. Am. Aled. Assn., Feb. 15, 1913. 
Garrod: Inborn Errors of Metabolism. 1909. 
Garrod: Anomalies of Metabolism. Pembrey and Ritchie's General 
Pathology, 1913. 
Howland and Marriott: A Discussion of Acidosis. Bull. Johns Hopkins 
Hosp., 1916, xxvii, 63. 
Lusk: The Fundamental Basis of Nutrition. New Haven, 1914. 
Mendel: Newer Points of View Regarding the Part Played by Differ- 
ent Food Substances in Nutrition. Jour. Am. Med. Assn., 1914, Ixiii, 
819. 
Opie and Alford: Influence of Diet on the Toxicity of Substances 
which Produce Lesions of the Liver or the Kidney. Jour. Am. Med. 
Assn., 1914, Ixiii, 136. 
Opie and Alford: The Influence of Diet in Hepatic Necrosis and the 
Toxicity of Chloroform. Jour. Am. Aled. Assn., 1914, Ixii, 895. 
Pembrey: Pembrey and Ritchie's General Pathology. New York, 1913. 
Vaughan: Protein Split Products. Phila., 1913. 
Vernon: Intracellular Enzymes. Lond., 1908. 
Willis: Chemical Pathology. Phila., 1914. 
The Internal Secretions. 
The organs of the body are very commonly looked upon 
as independent of one another, each doing its own work 
with no other than an anatomic relation to the others, or 
*For a discussion of the effects of drugs on the temperature, see Pembrey and 
Ritchie's General Pathology, p. 534. 54 
FUNDAMENTALS OF PATHOLOGY 
only related by means of the nervous system. How in- 
complete such a conception must be one may readily ap- 
preciate if he remembers that the function of the vascu- 
lar system makes it fully as vital a correlating mechan- 
ism as is the nervous system. The blood vessels are chan- 
nels by which food is carried to the various cells of the 
body, but they are likewise, in a sense at least, channels 
by which cellular wastes are carried away, in whatever 
way we may interpret the word wastes, the conception 
does not necessarily mean that such materials are value- 
less in the general economy. What is waste to one organ 
may he food for another. A waste may be a serious mat- 
ter only when some group of cells which make physio- 
logic use of it are absent. It therefore is evident that 
each organ is apt to have an influence on other organs 
through its metabolic products which are secreted (or 
excreted) into the venous blood or into the lymphatics. 
There are many evidences of the truth of these state- 
ments, but they are most frequently studied in connection 
with the ductless glands,-the glands of internal secre- 
tion. In the secretion of these organs there appear to be 
particular chemical substances (one of which, adrenalin, 
has been isolated, and even synthetically prepared) that 
produce characteristic physiologic effects. These sub- 
stances are the hormones. They are parts of the chemical 
coordinating system of the body. This system deter- 
mines the direction of reactions. The nervous system de- 
termines the speed. Each system modifies the other. 
If these secretions are of such importance it might be 
expected that the systemic effects of increased or de- 
creased activity of the organs of internal secretion would 
be striking, and it is true that they are. Such effects may 
he the results of excess or loss of the specific materials 
of the secretions, or they may be due to the lack or modi- 
fication of a specific substratum upon which to act. There 
is evidence in experimental work that the effects are not DISTURBANCES OF METABOLISM 
55 
simple, i. e., that they are not the result of damage to one 
organ, and modification of its secretion, but the result of 
interference with the interrelated activities of such or- 
gans. As yet we know next to nothing of the methods of 
interference, or of the conditions upon which these gland- 
ular effects depend, whether in antecedent metabolic dis- 
turbances, infections, intoxications, or in primary de- 
rangements of the central nervous system. "In the case 
of the thyroid, for example, exophthalmic goiter with its 
outspoken nervous and psychic manifestations was for- 
merly regarded as essentially a sympathicogenic or psy- 
chogenic disorder, and among others Biedl has again 
come to support this view as opposed to Moebius. Un- 
questionably the mental repose of successful psychother- 
apy on the one hand, and on the other, such a radical 
measure as the blocking of secretory impulses to the gland 
by cervical sympathectomy, have both served in many 
cases almost as effectively as the now popular extirpation 
of the hyperplastic gland itself." It is in connection with 
studies of the effects of nervous impulses in the produc- 
tion of secretory effects that we need to recall the older 
expression "phlegmatic and nervous disposition, or di- 
athesis, or constitution." These same peculiarities ap- 
pear now as sympathetico-tonic and vago-tonic, and indi- 
cate the same old misunderstood fact that one individual 
reacts with abnormal quickness to an impulse, particular- 
ly an emotional one, while another reacts less quickly than 
normal. On the other hand there seems to be no doubt 
that certain intoxications produce important effects upon 
certain, at least, of the ductless glands. In such cases 
we may perhaps search for the causes of vago-tonicity 
or sympathetico-tonicity in infections or gastrointestinal 
intoxications. Schiefferdecker goes to the extreme in 
saying: ' ' Internal secretion determines the effects which 
the products of metabolism excreted by the nerve cells 
during the simple processes of nutrition, will exercise 56 
FUNDAMENTALS OF PATHOLOGY 
upon other nerve cells and the end organ, such activity 
being called 'trophic.' It also determines the effect 
which the products of metabolism excreted in the course 
of specific activity will produce, and this effect is known 
as 'irritation' or 'stimulus'." Whatever one may think 
of such a statement it indicates, as Biedl says, the trend 
toward the ultimate explanation of physiologic and path- 
ologic correlationships in terms of chemistry, and it also 
indicates the value and extraordinary interest which is 
attached to the glands of internal secretion. 
It will be noted that the internal secretory organs are 
in a triple alliance. One other member, the nervous sys- 
tem, we have mentioned. The other is the sexual system. 
During normal growth there are certain psychic events 
which accompany sexual development. Morphologic and, 
certainly, secretory changes in the ductless glands occur 
during the same period. It is no more than one might ex- 
pect, then, that experimental work indicates a chemical 
connection between these three systems, and that while 
the reproductive organs exercise an influence upon the 
nervous system, other organs which also influence that 
system may affect the reproductive glands. There is an 
interlocking directorate, and it seems "probable that a 
disorder primarily involving any member of the ductless 
glands series, leads not only to peculiar somatic altera- 
tions but also to an accompanying and characteristic 
mental change," with, frequently, a sexual phase. So, 
says Cushing, "it is quite possible that the psychopath- 
ology of everyday life hinges largely upon the effect of 
the ductless gland discharges upon the nervous system." 
But, we may add, these effects may lie in an increased 
stimulability on the part of the tissues toward nervous 
impulses, or an increased susceptibility of the elements of 
the nervous system to otherwise subliminal or unproduc- 
tive stimuli. 
"It is more or less customary, largely because of their DISTURBANCES OE METABOLISM 
57 
effects upon metabolism, to classify the internal secre- 
tions as inhibitory (or assimilative) and stimulant (or 
disassimilative), the one influencing the anabolic phase of 
metabolism, the other the katabolic. They are also re- 
ferred to as growth producing and growth retarding. In 
certain cases the effects of these secretions are felt 
throughout the whole span of life; in others they play 
but a transient part, at one or another age or period. Not 
infrequently their influence is shown by special effects 
on certain organs; again they modify general nutrition; 
or in still other cases they produce purely psychic ef- 
fects." 
In the foregoing paragraphs the emphasis has been 
placed upon the idea that the effects produced by disor- 
ders of the organs of internal secretion are the results of 
overabundance or lack of the specific chemical products 
of these organs. This is not the only tenable point of 
view. 
It is believed by many that these organs have also what 
is called a detoxicating action, and that in cases in which 
there is insufficiency the effects produced in the organism 
are rather the result of the action of toxic substances 
which, normally, are destroyed or modified by these or- 
gans. This idea is applied chiefly in the case of the thy- 
roid. In this connection it may merely be suggested that 
local detoxication is rendered doubtful by the fact that 
in mammals the effects of thyroidectomy may be removed 
partially by feeding of desiccated gland substance. There- 
fore it seems more plausible to conceive that action of the 
secretion of the thyroid is effective, in a general meta- 
bolic way, in increasing the activities of the other organs 
and tissues of the body to a point where toxic substances 
are cared for. 
However, so far as we know, the main feature of all 
disturbances of the glands of internal secretion is that 
they are not simple. The effects as shown in symptoma- 58 
FUNDAMENTALS OF PATHOLOGY 
tology are the results of the action of what has been called 
the "interlocking glandular directorate which profound- 
ly influences metabolism and the mental and sexual life" 
(Dunn). Therefore it may be said that while it is sim- 
plest to discuss the effects of the organs of internal secre- 
tion under the heads of the different organs, it is to be 
remembered that the complexes associated with these ef- 
fects are, as a rule, polyglandular ones. 
Fig. 5.-Goiter. 
The Thyroid and Parathyroid Glands. 
There seems to be no conclusive evidence at present 
that there is any essential difference between thyroid and 
parathyroid tissue, for it has been shown that all morpho- 
logical transitions occur between the two. In speaking 
of the thyroid gland we therefore mean to include the 
parathyroids. 
The internal secretion of the thyroid acts chiefly as a DISTURBANCES OF METABOLISM 
59 
dissimilatory hormone insofar as it increases katabolism 
and therefore tends to accentuate normal function. This 
effect is seen in various activities-in protein metabol- 
ism, in the effect upon cardiac activity, and especially, 
perhaps, upon other internal secretory organs (hypophy- 
sis, adrenals). Certain phenomena suggest that the thy- 
Fig. 6.-A case of congenital myxedema. (After Kassowitz.) 
roid secretion also possesses an inhibitory function, and 
that therefore it contains an assimilatory hormone. The 
promotion of skeletal growth, the development of the 
sexual glands, the limitation of the internal secretion of 
the pancreas, are evidences of such activity. 
The experiments of Gudernatsch indicate that "the 60 
FUNDAMENTALS OF PATHOLOGY 
thyroid has the power to excite differentiation, but it 
lacks the power to cause growth." At the same time it 
does not seem to have the power of preventing growth. 
If these experimental results, which were acquired by 
Fig. 7.-A case of hypophyseal destrophy in hypopituitarism. Froehlich's type of 
dystrophia adiposo-genitalis. Caused, it is believed, by lack of pituitary secretion. 
(After Falta.) 
work in tadpoles, be true for the human being, then the 
effects which are referred to as inhibitory are not thyroid 
effects, but effects resulting from the action of the secre- DISTURBANCES OF METABOLISM 
61 
tion of the thyroid on other organs. It is believed by 
some upon very good evidence that the parathyroids are 
concerned in calcium metabolism, and that they are re- 
sponsible for the symptom-complex known as tetany. 
Diseases of the thyroid are associated with: 
Graves' disease (exophthalmic goiter). 
Cretinism. 
Infantilism (infantilismus myxedematosus, Bris- 
saud). 
Delayed maturity. 
Achondroplasia (fetal rickets). 
Myxedema. 
Tetany. 
The Thymus. 
It seems possible that the thymus exercises, through its 
internal secretion, important effects upon growth and 
that it has an inhibitory influence upon the development 
of the genital glands. Appearances seem to indicate that 
involution of the thymus is consequent upon sexual ma- 
turity. The work of Gudernatsch suggests that the thy- 
mus has the power to stimulate growth, but lacks the 
power to excite differentiation and not only that, but thy- 
mus feeding seems to suppress differentiation. 
Lesions of the thymus are associated with: 
Status thymico-lymphaticus 
Precocious adiposity 
Certain cachectic states 
Exophthalmic goiter 
Skeletal changes (rickets?) 
Dwarfism 
Achondroplasia 62 
FUNDAMENTALS OF PATHOLOGY 
The Pituitary Gland. 
The pituitary gland has effects upon general processes 
which in some respects are quite similar to those associ- 
ated with the thyroid gland. In young animals suppres- 
sion of function is manifested in an increase in the body 
fat together with hypoplasia of the sexual glands, and 
arrested development. The influence upon the sexual 
Fig. 8.-A chondrodystrophic dwarf. (After Falta.) 
glands is seen also in older animals in which partial de- 
struction of the anterior lobe is followed by atrophy of 
the genitalia. It seems evident that "the pituitary body 
and the germinal glands are protagonistic. Hypophyseal 
insufficiency and lowering of the activity of the repro- 
ductive functions go hand in hand," and also "a libidi- DISTURBANCES OF METABOLISM 
63 
Fig- 9.-A case of giantism, a hypophyseal dwarf, and a normal man. (After Falta.) 64 
FUNDAMENTALS OF PATHOLOGY 
nous tendency often accompanies states of secretory hy- 
perplasia." 
Lesions of the hypophysis are associated with: 
Acromegaly 
Gigantism 
Diabetes insipidus 
Diabetes mellitus 
Infantilism 
Dystrophia adiposo-genitalis (Froehlich). 
Cachexia hypophyseopriva. 
Jt is to be recalled that lesions of the thymus are apt 
to be associated with dwarfism, while those of the pitui- 
tary and thyroid are associated with infantilism. These 
two conditions are frequently confounded. The impor- 
tant difference is that mental changes are not associated 
with the former. Dwarfism is a defect of size and ap- 
pears because growth ceases at some stage of develop- 
ment. A child may be normal at birth and then growth 
may cease (nanosomia infantilis), or it may be defective 
as to size from the start (nanosomia primord ialis). The 
term infantilism, as defined by Laseigue, "is a disturb- 
ance of development, the salient feature of which is the 
persistence in both the mental and physical state, of in- 
fantile characters." In the term, however, has been in- 
cluded certain cases in which arrested development has 
resulted from nutritional derangements, and from disease 
of the blood vessels, brain, etc. This form is known as 
infant ilismus dystrophicus of Lorrain. It may appear as 
the result of hypoplasia of the vascular system, in heredi- 
tary syphilis, after alcoholism and other forms of chronic 
poisoning in the parents; in primary cerebral disease, 
as a result of infectious diseases contracted in early life 
(tuberculosis, pellagra); metabolic derangements (chlo- 
rosis) ; cardiac diseases (pulmonary and mitral insuffi- 
ciency) ; and finally as the result of unhygienic surround- 
ings and insufficient nourishment in early childhood. DISTURBANCES OF METABOLISM 
65 
From the fact that lesions of numerous glands of internal 
secretion are associated with infantilism it is probable 
that this complex is associated with lesions of more than 
Fig. 10. 
Fig. 11. 
Figs. 10 and 11.-Examples of enamel defects in cases of tetany. 
(After Falta and Phelps.) 66 
FUNDAMENTALS OF PATHOLOGY 
one gland and that the distinguishing characters of vari- 
ous forms of the complex are connected with single 
glands. Infantilism is therefore a polyglandular affec- 
tion. 
The Adrenals. 
The adrenals like the pituitary are composed of two 
functional parts. These are the medulla and the cortex. 
Fig. 12.-A case of mongolism standing beside a healthy child. (After Falta.) 
The medulla is the chromaffin portion of the organ and 
is closely associated with the sympathetic nervous sys- 
tem. The cortex is quite similar in structure and ap- 
pearance to the corpus luteum, and seems to be closely 
related, functionally, to the sexual glands. The medulla DISTURBANCES OF METABOLISM 
67 
is a part of the chromaffin system of the body, and is the 
portion of the gland which (like the other chromaffin tis- 
sues) produces a vasoconstricting substance known as 
adrenalin. Variations in its activity have been associated 
with Addison's disease, with conditions of low vascular 
tension, on the side of insufficiency; and with glycosuria, 
arteriosclerosis, cardiac hypertrophy and conditions 
characterized by high vascular tension, on the side of hy- 
peractivity. Cortical variations have been found in as- 
sociation with periods of heat and rut, sexual precocity 
Fig. 13.-The facial expression in mild myxedema. (After Falta.) 
and with defective sexual development. There is reason 
to believe that a close relation exists between the adre- 
nals, pancreas, thyroid, pituitary and sexual glands. In 
the fact that the internal secretory activity of the pan- 
creas is inhibited by adrenalin lies an intensely interesting 68 
FUNDAMENTALS OF PATHOLOGY 
application of the ideas of Eppinger and Hess, for the 
pancreas is under the nervous influence of the vagus, 
while the adrenals are under sympathetic influence. The 
fact that adrenalin increases thyroid activity while at 
Fig. 14.--To give some idea of the expression and position of the fingers in tetany. 
Tetany is supposed to be associated with disturbances of the parathyroid glands. (After 
Falta, i 
the same time it decreases that of parathyroids, suggests, 
following the same reasoning, that the latter are under 
the influence of the vagus. DISTURBANCES OF METABOLISM 
69 
The Pancreas. 
The internal secretion of the pancreas seems to be an 
important factor in carbohydrate metabolism, though 
just what part it plays is by no means certain. It is pos- 
sible that this secretion contains a substance or sub- 
stances which make it possible for the tissues to use 
sugar. Stanley calls attention to the fact that an iso- 
lated heart from a diabetic animal, when perfused with 
blood plus glucose, is unable to consume the glucose; but 
in adding an extract of fresh pancreas, the sugar is con- 
sumed. How this happens we do not know. Biedl says 
the most probable assumption is that the active substance 
is ferment, which inhibits the diastotic conversion of 
glycogen into sugar, though it does not prevent the stor- 
ing of glycogen. Absence of the hormone permits un- 
checked splitting of glycogen. 
The Pineal Body. 
Of this gland we know too little. It seems to be true 
however that whatever changes occur must present them- 
selves during the period during which the gland is ac- 
tive, for it, like the thymus, undergoes early retrogres- 
sive changes. Lesions in it have been associated with 
obesity and macrogenitosomia precox. Recent experi- 
mental work of Dandy indicates that the pineal body 
(epiphysis) has no physiologic importance. 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Auer: Tne Physical Manifestations of Diseases of the Glands of In- 
ternal Secretion. Am. Jour. Insanity, 1914, 405. 
Biedl: Internal Secretory Organs. New York, 1913. 
Cannon: Bodily Changes in Pain, Hunger, Fear and Rage. New York 
and Lond., 1915. 
Capelle u. Bayer: Beitr. z. klin. Chir., 1913, Ixxxvi. 
Cushing: Psychic Disturbances Associated With Ductless Glands. Am. 
Jour. Insanity, 1913, Ixix, 965. 
Dandy: Jour. Exper. Med., 1915, xxii, 237. 
Editorial: Jour. Am. Med. Assn., 1914, Ixiii, 322 (literature). 70 
FUNDAMENTALS OF PATHOLOGY 
Editorial: Newer Views of the Functions of the Adrenals. Jour. Am. 
Med. Assn., 1914, Ixiii, 322. 
Eppinger and Hess: Die Vagotonie. Berlin, 1910. 
Falta: The Ductless Glandular Diseases (Trans, by Meyers). Phila., 
1915. 
Gies: Studies of Internal Secretions, etc. Dental Cosmos, 1915, Ivii, 276. 
Goetsch: The Influence of Pituitary Feeding Upon Growth and Sexual 
Development. Bull. John Hopkins Hosp., 1916, xxvii, 29. 
Halsted: The Significance of the Thymus Gland in Graves' Disease. 
Bull. Johns Hopkins Hosp., 1914, xxv, 223. 
Handbuch der Neurologic, edited by Lewandowsky: Bd. iv. Spezielle 
Neurologic III, Berlin, 1913. 
Kendall: The Isolation in Crystalline Form of the Compound Contain- 
ing Iodine, which Occurs in the Thyroid. Jour. Am. Med. Assn., 
1915, Ixiv, 2042. 
Launoy: L'appareil thymo-thyroidien. Paris, 1914. 
Major: The Pathological Anatomy of the Pancreas in Diabetes. Jour. 
Med. Research, 1914, xxxi, 313. 
Marine: The Evolution of the Thyroid Gland. Bull. Johns Hopkins 
Hosp., 1913, xxiv, 135. 
Marine and Lenhart: Pathologic Anatomy of the Thyroid. Arch. Int. 
Med., 1911. 
McCord: The Pineal Gland in Relation to Somatic, Sexual, and Mental 
Development. Jour. Am. Med. Assn., 1914, Ixiii, 232. 
Pappenheim: Further Experiments Upon the Effects of Extirpation of 
the Thymus in Rats. Jour. Exper. Med., 1914, xx, 477. 
Pembrey: "Metabolism." Pembrey and Ritchie's General Pathology, 
New York, 1913. 
Vincent: Internal Secretion and the Ductless Glands. London, 1912. CHAPTER V. 
GROWTH AND OVERGROWTH. 
Growth, overgrowth, and atrophy are chemical prob- 
lems. They are problems of metabolism. Later we shall 
see that the degenerations and death are similar prob- 
lems, but before we attack these latter let us study for 
a while some other problems-such, for instance, those 
which have to do with the quality and quantity of food, 
which are also problems of metabolism and which there- 
fore influence growth and function. 
All of these problems are ones which involve the con- 
stitution of the apparatuses which are employed by the 
organs in making use of food. The food reaches the cells 
by way of the blood from which it passes (is it excreted? 
or is it secreted?) through the endothelium directly into 
the cells, or first into lymph spaces and then to the cells. 
The composition of the blood will have an effect upon 
the cells, will modify their functions. Sometimes it will 
stimulate, sometimes paralyze, sometimes kill. Some- 
times we see one effect, sometimes another in the same 
individual under apparently similar circumstances. Do 
the cells take everything that comes to them and discard 
what they do not need? Or do they select what they de- 
sire and reject what they do not like? 
The fact that any substance enters a cell depends upon 
physico-chemical conditions which we do not thoroughly 
understand. Perhaps it is easy to say why substances in 
watery solutions are absorbed, but if we use the current 
hypothesis, that involving semi-permeability, we cannot 
explain the entrance of water-insoluble substances. How- 
ever, we know all these things go in in one or another 
form. Normal constitution brings about normal absorp- 
71 72 
FUNDAMENTALS OF PATHOLOGY 
tion, and this depends upon certain physico-chemical con- 
ditions. Abnormal constitution will just as surely bring 
about abnormal absorption, and, perhaps, what was not 
absorbed yesterday will be absorbed today and illness 
will result. Normal constitution of cells and organs de- 
pends upon normal activity, and so, as Cohnhein said, 
"The regular circulation of blood of normal quality and 
the physiologic activity of the organs are equally nec- 
essary. ' ' 
The quality of the blood we wish to discuss in relation 
to physiologic activity. The regularity of the circula- 
tion we shall discuss at another time. But first it will 
be useful to say some words concerning the quantity of 
food. 
As you know from your consideration of growth, quan- 
tity of food may mean two things. It may mean the 
quantity available, or the quantity needed. Atrophy, 
you remember, may occur in the presence of an abundant 
supply of normal blood, providing the cells are inactive 
-which is to say, are in a condition (physico-chemical) 
which makes them unable to take food. On the other 
hand, atrophy will just as surely occur in the absence of 
a sufficient supply of foodstuffs. 
The quantity of food needed by an organism depends, 
other things being equal, upon activity. It is for this 
reason more than any other, that the normal necessary 
amount varies with age, and climate. In growth the 
whole organism is active; the food is rapidly consumed 
and transformed into heat and other forms of energy and 
the supply must be frequently replenished. In old age, 
the opposite is true, the individual is less active; combus- 
tion is slower, and therefore less is needed. A cold cli- 
mate tends to increase activity, and therefore the food 
demands are increased. Hot climate conduces to inac- 
tivity and to decreased demands, even though it hastens 
combustion. GROWTH AND OVERGROWTH 
73 
And yet we hear it said frequently enough that we eat 
too much, or we eat too little. Why do we eat too much, 
or too little, and what happens when we do either? 
Sometimes we eat too much because we haven't anything 
else to do and because we like the taste of food-or of 
some foods. Sometimes, because we are completely, 
mentally, contented, and being contented we are inactive. 
Nothing stimulates us to activity. Sometimes there is 
something wrong in our physiologic make-up, so that we 
experience the feeling of hunger when we should not. 
But sometimes we eat too little because we are discon- 
tented and the taste of food is unpleasant, or because we 
cannot have pleasant food. We may be worried, and 
being either discontented or worried, our appetites are 
small and our activity increased. We are restless and 
burn more food than we otherwise would. Sometimes, 
again, our physiologic make-up is deranged and we have 
no desire for food, or desiring it, cannot use it or, some- 
times, retain it. 
And then, in either case, what happens? We "laugh 
and grow fat" as the saying is, or we "worry ourselves 
to a skeleton." We become obese, or poorly nourished, 
or in the end we starve. 
There are two main types of obesity-physiologic and 
pathologic. The former is seen in infants, and in youth 
just before the time of puberty. The latter occurs as a 
result of lack of exercise-of physical inactivity, and as 
a result of disturbances of the function of one or more of 
the ductless glands. It is quite possible that the obesity 
that precedes or accompanies puberty is due to internal 
secretory activities. Certain types of familial and ra- 
cial obesity may be either physiologic or pathologic,- 
which, we do not know. All, however, of whatever type, 
depends upon a storage of fats in the tissues and this in 
time may be due to deficient powers of oxidation within 
the body or to the presence, along with ordinary food- 74 
FUNDAMENTALS OF PATHOLOGY 
stuffs, of more easily oxidizable materials, such, for in- 
stance, as alcohol. Opposite to obesity is emaciation, 
malnutrition, undernourishment, and starvation, due not 
merely to the using up of the transient supplies, but also 
of that other source of heat and energy that should be 
used only in occasional times of need,-the fats and pro- 
teins of the body. Poorly nourished children may grow 
in stature though not in weight, and during such abnor- 
mal growth the bones grow at the expense of the internal 
organs. It is only in the last stages of emaciation that 
growth stops in children, but even then the power of 
growth is not lost but returns with proper feeding 
(Arons: Jour. Am. Med. Assn., 1911, Ivii, 1619). But 
under certain circumstances growth is retarded, though 
mental development proceeds-a condition we call in- 
fantilism, and this leads us to call attention to the inter- 
esting fact that in starvation the vital organs are spared 
at the expense of the other organs. The brain even at 
the last shows little or no change. 
Finally, in this connection, let me emphasize that either 
overeating or the refusal of food is not important. It 
is the cause of either. 
This may all be epitomized as follows: 
1. Normally anabolism should equal katabolism. 
2. When anabolism is greater than katabolism, obes- 
ity results. 
3. When katabolism is greater than anabolism, wast- 
ing, emaciation, inanition and starvation result. 
Beside obesity there are more serious things which 
happen as a result of overeating. Various sorts of gas- 
trointestinal disturbances are not infrequent. The over- 
loading and distention of the stomach, together with the 
irritant effects of much food; the continuous or overstim- 
ulation of the gastric secretory apparatus; the fermenta- 
tive changes in the food which, in large quantity, is with 
difficulty saturated and sterilized by the normally pro- GROWTH AND OVERGROWTH 
75 
tective acid gastric juice; and similar effects in the in- 
testines. All of these result in symptoms which are 
grouped together under "gastrointestinal autointoxica- 
tions" or mere "indigestion." Such conditions are ex- 
pressions of irritation of the gastrointestinal organs, of 
subsequent and consequent inflammations, and of the ab- 
sorption of abnormal products or products abnormal in 
quantity, which may act as poisons when carried to other 
organs. We shall speak of these conditions at another 
place (see Intoxications). Faber, as an example of what 
one may think of the importance of too much food, says, 
regarding overeating, that he is convinced that many of 
the morbid conditions credited to the "uric acid diathe- 
sis" are in reality the effects of overeating. He has tab- 
ulated a large number of corpulent and normally nour- 
ished individuals and calls attention to the preponder- 
ance in the former group of certain types of rheumatism, 
lumbago, varices and constipation. The mortality from 
apoplexy, heart and kidney disease, is also higher in this 
group. He calls attention to the particular value of re- 
stricting the diet in such individuals. 
While the quantity of food needed by the body is im- 
portant, the quality of the food is still more important. 
We are told that to continue in health, the body needs 
proteins, carbohydrates and fats, and that these serve in 
part for tissue building, i. e., growth (proteins), and as 
sources of energy (carbohydrates and fats). In a way 
this is true, but in the past few years Osborne and Men- 
del especially have shown that mixtures of chemically 
pure proteins, carbohydrates and fats, together with the 
normal salts and water, while they will sustain life, are 
not able to promote growth. Osborne and Mendel found 
the necessary stimulus for growth in milk whey, and in 
extracts of tissues, and, they found that these materials 
would be effective in such small amounts that their ac- 
tion could not be accounted for on the basis of oxidations. 76 
FUNDAMENTALS OF PATHOLOGY 
More recently Funk, studying the tropical disease beri- 
beri and its congeners, has extracted similarly effective 
substances from yeast, rice, etc., and the extract he calls 
vitamin. Not only have these things been discovered, 
but Osborne and Mendel have found that proteins of dif- 
ferent origins have different nutritive values. So you 
see the quality of food is really decidedly important. 
Perhaps it is the quality of boiled milk and not the di- 
gestive variations in children which causes rickets and 
scurvy. Pasteurized and boiled milk are not as safe as 
uncooked milk, and yet all the original constituents are 
present. Holst and Froehlich fed guinea pigs with only 
cereals or bread, and produced scurvy in the animals. If 
fresh carrots and cabbage were fed, the animals remained 
well, and these vegetables acted in curative fashion if 
fed to scorbutic pigs. If, however, the vegetables were 
cooked at 110-120°, the curative power was lost. 
There is a great group of diseases-i. e., clinical com- 
plexes-which seem to be due to qualitative changes- 
the diet. Beri-beri, scurvy, and rickets have already been 
mentioned. Goiter, pellagra, certain forms of neuritis, 
and gout, are possibly other members of the group. Per- 
haps certain of the anemias also are. In the case of beri- 
beri it is interesting to recall that the complete removal 
of the husks in the process of polishing the grains pro- 
duces a grain which used as an exclusive article of diet 
results in the disease. It has been noticed that the daily 
use of milk has been reported as useful in preventing pel- 
lagra; that fruit acids and salts prevent the occurrence, 
and hasten the cure of scurvy. 
Schaumann calls attention to the minute amount of 
certain necessary substances in the diet. He says that 
they are present in most articles of diet but are readily 
removed and destroyed. Pice and other cereals lose 
them by polishing, and they are destroyed in other ar- 
ticles of food by heating above a certain temperature, or GROWTH AND OVERGROWTH 
77 
by long cooking, sometimes by desiccation and by pick- 
ling, by boiling in alkalin water, by moulds and even in 
some cases, by the intestinal bacteria. The disturbances 
following loss of these materials, he says, differ in differ- 
ent organisms. Herbivora develop scurvy; omnivora, 
scurvy and neuritis; and goats, monkeys, fowls and pig- 
eons, multiple neuritis. The practical conclusions are 
that the diet of man must comprise, beside the classical 
protein, fat and carbohydrates, salts and water, these un- 
isolated substances. The protein must be one which con- 
tains tryptophan. As Osborne and Mendel have shown, 
a protein cannot be called a nutritive one if it lacks 
tryptophan (gelatin, zein). Tryptophan, Mendel says, 
is indispensable for life; lysine, for growth. 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910, i, 98. 
Gudernatsch: Feeding Experiments on Tadpoles. Am. Jour. Anat., 
1914, xv, 431. Arch. f. Entwcklngsmechn d. Organ., 1912, xxxv, 457. 
Friedenthal: Allgemeine und spezielle Physiologic der Menschen- 
wachstums. Berlin, 1914. 
Ritchie: Pembrey and Ritchie's General Pathology, New York, 1913, 
217. 
Sabatini: Il Policlinico, Dec. 13, 1914. (Rev. Jour. Am. Med. Assn., 
1915, Ixiv, 378.) 
Thoma: Pathology and Pathological Anatomy (Trans, by Bruce). 
London, 1896, 448. 
White: The Pathology of Growth, etc. New York, 1913. 
Woolley: Growth and Overgrowth. New York Med. Jour., 1915, ci, 
656. CHAPTER VI. 
DEGENERATION-PIGMENTATION 
-CALCIFICATION. 
Degeneration. 
When we speak of degenerations we have reference to 
a group of phenomena which characterize the presence 
of abnormal amounts of normal substances, the presence 
of normal substances in abnormal physical conditions, or 
the presence of abnormal substances within cells. 
Fat is a common constituent, and a normal one, of all 
cells. In most cells it is not visible even under the mi- 
croscope, This is true, for example, of heart muscle cells 
and kidney cells. In some cells it is commonly and nor- 
mally visible, for example, in liver cells, and in the ordi- 
nary fat cells of the subcutaneous tissue. When fat ap- 
pears in such a form or amount in kidney or heart cells, 
so that it can be seen, we speak of fatty degeneration. 
When it appears in the liver cells so that there seems to 
be more than a normal amount of visible fat we speak 
of fatty infiltration. Fatty degeneration then applies to 
the occurrence of fat where no fat should be visible, and 
fatty infiltration means an increase of fat where some 
fat might be expected. Fat appears in cells and tissues 
when the oxidations of the body are not sufficient to burn 
it, which may be the result of too great a supply of fat, 
or it may be due to deficient activities of the cells. 
There is a certain condition which we call cloudy sivell- 
ing on account of the fact that tissues so affected are 
swollen, and at the same time are not as clear, or trans- 
lucent as they are under normal conditions. Such tis- 
sues have a "boiled appearance,"-they resemble, in a 
78 DEGENERATION 
79 
way, a piece of tissue which has been dropped into hot 
water. Under the microscope the protoplasm of such 
tissues has a finely granular appearance, which is due to 
the fact that certain of the proteins which compose pro- 
toplasm have coagulated and appear as granules, solu- 
ble in dilute acids, or alkalies, in the otherwise clear pro- 
toplasm. From the fact that very small amounts of di- 
lute acids will produce cloudy swelling we may argue 
Fig. 15.-Cell degeneration. 1-3, Karyolysis; 4-7, Pyknosis, hyperchromatosis, and 
karyorrhexis; 8-10, Karyorrhexis. Cloudy swelling is present in all of these cells. 
(Beattie and Dickson.) 
that under certain conditions in the body acids accumu- 
late, cause the protoplasm to take up water (swelling) 
and, at the same time, cause some of the proteins to co- 
agulate. 
Like cloudy swelling, the appearance we call hyalin, 
colloid, and amyloid, in cells and tissues, are also due to 
abnormal states of the proteins in the tissues. Connect- 
ive tissues may appear hyaline (translucent); if it be also 
viscid or gluey, we speak of colloid; if it gives certain of 80 
FUNDAMENTALS OF PATHOLOGY 
the starch reactions we call it amyloid. Tissues are said 
to undergo hyalin, colloid, or amyloid degeneration when 
they answer to these descriptions. 
When cells or tissues die we speak of necrosis. Some- 
times cells die as a whole, sometimes all the cells in a 
tissue die, and sometimes only part of a cell dies. When 
a group of cells die leaving their ferments still active so 
that the tissue is more or less softened or digested, we 
speak of autolysis. It is autolysis which goes on in 
pneumonia when the exudate of cells in the alveoli of the 
lungs is softened. It is autolysis which causes the cen- 
tral part of an abscess to soften so it can he squeezed out. 
When autolysis does not occur the material from the 
dead tissue may become somewhat dry and granular like 
cottage cheese. Then we speak of caseation. When a 
whole part of the body dies as a whole-like a hand or 
a leg, we speak of gangrene (because of the color) though 
the process is still necrosis. If the gangrenous part be- 
comes dry and mummified, because the moisture is evap- 
orated from it, we speak of "dry gangrene." If it re- 
mains moist, and becomes infected, we speak of "wet 
gangrene." Death of bone is commonly called "caries." 
There are other forms of degeneration which are as- 
sociated with abnormal amounts of certain substances 
within the cells. For instance we speak of mucoid degen- 
eration and mean that more mucin is present than should 
normally be. When tumors show a high degree of mu- 
coid degeneration or infiltration we call them myxomas; 
when, as in certain forms of disease such as those due 
to interference with the thyroid gland, the connective 
tissues, particularly the subcutaneous tissues, contain too 
much mucin, we speak of myxedema. In the one case 
the mucin is of epithelial origin, in the other of connec- 
tive tissue origin. Glycogenic degeneration occurs when 
more than the usual amount of glycogen appears in cells; 
soapy degeneration when soaps appear; and myelinic or PIGMENTATION 
81 
lipoid degeneration when the lipoid or the myelins of the 
nerves or central nervous system undergo retrogressive 
transformations. 
Pigmentation. 
Under certain conditions foreign substances enter the 
body, are taken up by the cells and held in the tissues 
which are colored by reason of these substances. A per- 
son who lives in a dirty atmosphere, one like that of a 
large city, breathes into his lungs the small particles of 
carbon that are always present in the smoke which min- 
gles with the air. These particles enter the lungs and 
are taken up by the cells of the tissue, the phagocytic 
cells, which carry them sometimes to the neighboring lym- 
phatic glands, sometimes only into the neighboring con- 
nective tissue. The result of this is that the lungs be- 
come permanently blackened by the insoluble carbon. 
This condition is one of the conioses, or "granule dis- 
eases," and is specially known as anthracosis. In work- 
ers in iron, particles of that metal take the place of the 
carbon, and we speak of siderosis. In workers in clay, 
particles of that substance enter the tissues and we have 
silicosis or chalicosis. Pigmentation with silver, from 
overuse of silver salts, is called argyria, and pigmenta- 
tion with lead occurs in plumbism. 
In another group of circumstances the pigmentation 
is the result of excessive production, beyond the possi- 
bility of excretion from the body of pigmented bodies 
which stain the tissues. Sometimes the staining is due 
to interference with the excretory pathways, as in jaun- 
dice of the ordinary "yaller janders" type. According 
to the process such forms of pigmentation as melanosis 
appear, due to the deposition of melanin in the skin. 
The pigmentation of sunburn is due to localization of 
melanin. The color of freckles also is due to melanin. 
Generalized jaundice we speak of as icterus; jaundice 82 
FUNDAMENTALS OF PATHOLOGY 
due to breaking up of the blood pigment is hematogenous 
jaundice. 
Calcification. 
Calcification under pathologic conditions is analogous 
to that which occurs under normal conditions, for in- 
stance in the calcification of membranes to form the flat 
bones of the skull. 
When tissues die (undergo necrosis) several things 
may happen. The dead tissue may become liquefied and 
be removed or it may be replaced by fluid which remains 
as a cyst. The dead tissue may become infected by bac- 
teria and an abscess results, or in the dead tissue lime 
salts may be deposited. This is what happens very fre- 
quently in tuberculous lesions, in various organs, espe- 
cially in the lymph glands and in the lungs. Such areas 
are calcified. Sometimes dead bones are completely or- 
ganized and scars are formed, and sometimes the scar tis- 
sue becomes calcified. Sometimes as organization of 
dead tissue goes on, calcification accompanies it, and the 
process goes on in such a fashion that bone is formed, and 
then we speak of ossification. 
REFERENCES. 
Addis: A Working Hypothesis of Hemoglobin Pigment Metabolism. 
Jour. Int. Med., 1915, xv, 413. 
Beddard and Plumtre: Ochronosis Associated with Carboluria. Quart. 
Jour. Med., 1912, v, No. 20. 
Dyson: An Investigation on Cutaneous Pigmentation in Normal and 
Pathological Conditions. Jour. Path, and Bacteriol., 1911, xv, 298. 
King, Bigelow and Pearce: Experimental Obstructive Jaundice. Jour. 
Exper. Med., 1911, xiv, 159. 
Landois: Zur Kenntnis der Ochronosis. Virchow's Arch., 1908, cxciii, 
275. 
Thayer and Morris: Two Cases of Congenital Haemolytic Jaundice, etc. 
Bull. Johns Hopkins Hosp., 1911, xxii, 85. 
Wells: Chemical Pathology. 
Whipple and King: The Pathogenesis of Jaundice. Jour. Exper. Med., 
1911. CHAPTER VII. 
INFLAMMATION. 
Every one knows something about inflammation. Ev- 
ery one knows, for instance, that a conjunctiva that is in- 
tensely congested, that is painful, that produces a more 
or less serous discharge, is inflamed. Every one knows 
that a "boil," otherwise technically known as a furun- 
cle, is the seat of a localized inflammatory process, and 
when one knows this he is immediately aware of the car- 
dinal symptoms of inflammation, which Celsus, perhaps, 
first wrote down for others to read, namely, heat, red- 
ness, pain and swelling-calor, rubor, dolor and tumor. 
One is also aware that, because these four cardinal symp- 
toms are present, something must be wrong with the parts 
of the affected tissues. With normal blood vessels there 
should not be this increase of redness and of heat. With 
normal tissues and normal processes there should be no 
pain and swelling. Something else is wrong. The func- 
tion of the parts is abnormal. And so a fifth symptom 
has been added to those of Celsus, namely, disturbance 
of function-functio kesa. 
Inflammation is a process by which the body reacts to 
injury. It is best described by Cohnheim in the follow- 
ing paragraphs. 
"If you withdraw a loop in intestine from the abdomen 
of a rabbit and expose it to the air, it, together with the 
vessels, ultimately perishes, but death is far from instan- 
taneous-rather a comparatively long interval must 
elapse before this point is reached, and during it the dis- 
organization of the tissues and vessels progresses little 
by little till they finally die. If you cut off the circulat- 
83 84 
FUNDAMENTALS OF PATHOLOGY 
ing blood from a part and its vessels, necrosis sets in, but 
here again, as you know, a very considerable period 
passes during which the tissues, in specie the vessel walls, 
become gradually disorganized. At a temperature of 
from 36° to 38° C., the life and function of the blood ves- 
sels are regular and normal, at one of say 60° C. they are 
certainly destroyed. Now, if you expose a vascular part 
to a temperature somewhere between these extremes, 
though it does not die, the heat is not without its effect 
on the constitution of the vessel walls. Lastly, in order 
Fig. 16.-Formation of new blood vessels, as seen in the tail of a tadpole, a, Capil- 
lary vessel extending by means of a terminal protoplasmic filament (&); c and d, Proto- 
plasmic filaments or offshoots by which a capillary reticulum will eventuallj' be formed. 
(Arnold.) 
to kill a part with its vessels by the action of sulphuric 
acid, the latter must have a certain concentration; a 
weaker solution is, however, far from innocuous, although 
it does not instantaneously destroy the vitality of the ves- 
sel walls. These examples will, I think, explain the drift 
of my thoughts, for they show that alterations in the con- 
stitution of the vessel walls, for which the term molecular 
just now appears to be the most suitable designation, are 
called forth by a number of influences of the most differ- 
ent kinds. But if such alterations occur we are justified INFLAMMATION 
85 
in asking, What effect have they upon the circulation? 
"Yet however natural this question, it is impossible to 
answer it a priori; the direct observation of appropriate 
cases is necessary, and it will be best, with this end in 
view, to have recourse to express experiment. This may 
be carried out without any difficulty. You need only ex- 
pose the vessels of a part to the air by removing its pro- 
tective coverings, when, if you have selected a transpar- 
ent tissue, there is nothing to hinder microscopic obser- 
vation. The simplest method is to draw out the intestine 
of a curarized frog through a laterally placed opening- 
in the abdominal wall, and to bring the mesentery under 
the microscope, after having carefully spread it out on a 
slide adapted to the purpose.". . . "The first thing 
you notice in the exposed vessels is a dilatation which 
occurs chiefly in the arteries, then in the veins, and least 
of all in the capillaries. With the dilatation which is grad- 
ually developed, but which, during the space of fifteen to 
twenty minutes, has usually attained considerable propor- 
tions (often exceeding twice the original diameter) there 
immediately sets in in the mesentery an acceleration of 
the blood stream, most striking again in the arteries, 
but very apparent in the veins and capillaries also. Yet 
this acceleration never lasts long; after half an hour or 
an hour, or sometimes after a shorter or longer interval, 
it invariably gives place to a decided retardation, the ve- 
locity of the stream falling more or less below the normal 
standard, and so continuing as long as the vessels occupy 
their exposed position. Such is the course of events in 
the mesentery experiment, in which not only the vessels 
of the mesentery, but their terminal ramifications in the 
intestine, are laid bare. In the wound of the (frog's) 
tongue, on the other hand, the acceleration is often alto- 
gether absent; and from the first there is associated with 
the dilatation a retardation of the stream, which increases 
as the dilatation increases. 86 
FUNDAMENTALS OF PATHOLOGY 
"This stage having been reached, the vessels are seen 
to be all of them very wide; a multitude of capillaries 
which, even formerly, were hardly perceptible, can now 
be clearly distinguished; pulsation is usually conspicuous 
mi into the finest ramifications of the arteries; while the 
How is everywhere slower than normal, so that the indi- 
vidual corpuscles may easily be recognized not only in 
the capillaries, but also in the veins, and during diastole 
in the arteries. In consequence of the tardy, forward 
movement the corpuscles accumulate in large numbers in 
the capillaries, so that the latter appear redder than us- 
ual, and therefore fuller, more voluminous; yet their 
cross section, as just stated, is only very inconsiderably 
enlarged. But it is the veins rather than the capillaries 
that attract the notice of the observer; for slowly and 
gradually there is developed in them an extremely char- 
acteristic condition; the originally plasmatic zone be- 
comes filled with innumerable colorless corpuscles. The 
plasmatic zone of the veins, you will remember, is always 
occupied by scattered colorless blood corpuscles which, 
owing to their globular form and low specific gravity, 
are driven into the periphery of the stream, and whose 
adhesiveness makes it difficult for them to escape from 
the wall once they have come into contact with it. It is 
obvious that this difficulty will be enhanced in proportion 
to the slowness of the blood stream; and thus it is not 
surprising that a gradual accumulation of large numbers 
of colorless corpuscles should take place in the peripheral 
zone, and here come to be comparatively motionless. For 
that a state of absolute rest, an actual standstill is out of 
the question, 1 need hardly mention expressly; the color- 
less cells of the plasmatic layer remain stationary at most 
for a time, they then advance a little, and perhaps make 
another short halt, and so on. Yet this does not lessen 
the striking contrast presented by the central column of 
red blood corpuscles, flowing on in an uninterrupted INFLAMMATION 
87 
stream of uniform velocity, and the peripheral layer of 
resting colorless cells; the internal surface of the vein ap- 
pears paved with a single but unbroken layer of colorless 
corpuscles without the interposition at any time of a sin- 
gle red one. It is the separation of the white from the 
red corpuscles that gives the venous stream in these cases 
that characteristic appearance, anything analogous to 
which you will look for in vain in the other vessels. For 
in the capillaries, although large numbers of colorless 
blood corpuscles adhere to the walls, there is always an 
admixture of red cells, or rather these are very decidedly 
in the majority. Lastly, in the arteries there is seen dur- 
ing diastole, almost at the moment of exit of the wave, a 
number of colorless blood corpuscles rolling straight to- 
wards the periphery; yet these are always swept into the 
stream at the next systole, so that the development of a 
resting peripheral layer is here altogether out of the 
question. 
"But the eye of the observer hardly has time to catch 
all the details of the picture before it is fettered by a very 
unexpected occurrence. Usually it is a vein with the 
typical peripheral arrangement of the white corpuscles, 
but sometimes a capillary, that first displays the phenom- 
ena. A pointed projection is seen in the external con- 
tour of the vessel wall; it pushes itself further outwards, 
increases in thickness, and the pointed projection is trans- 
formed into a colorless rounded hump; this grows longer 
and thicker, throws out fresh points, and gradually with- 
draws itself from the vessel wall, with which at last it 
is connected only by a long thin pedicle. Finally, this 
also detaches itself, and now there lies outside the ves- 
sel a colorless, faintly glittering, contractile corpuscle 
with a few short processes, and one long one, of the size 
of a white blood cell, and having one or more nuclei; in 
a word, a colorless blood corpuscle. While this is taking 
place at one spot, the same process has been carried on 88 
FUNDAMENTALS OF PATHOLOGY 
in other portions of the veins and capillaries. Quite a 
large number of white blood cells have betaken them- 
selves to the exterior of the vessels, and these are con- 
stantly followed by fresh one, whose place in the periph- 
eral layer is immediately occupied by others. Like 
every stage of the entire process on from the time of ex- 
posure, these phenomena may develop either rapidly or 
slowly; at one time the earliest emigration very quickly 
succeeds the pavementing; at another, an hour or more 
may pass without anything happening to draw the at- 
tention to the contour of a single vein or capillary. In 
any case the final result, after six or eight or more hours 
have elapsed, will be the enclosure of all the veins, small 
and large, of the mesentery or wound of the tongue with 
several layers of colorless blood corpuscles. These fence 
in the veins, in the interior of which the previously de- 
scribed conditions continue, namely, the peripheral ar- 
rangement of the colorless cells and the central unbroken 
flow of red blood corpuscles. Nothing analogous has oc- 
curred in connection with the arteries, their contour has 
remained smooth as before, nor can a solitary corpuscle, 
red or white, be discovered on their outer surfaces, ex- 
cept, of course, such as may have reached them from the 
neighboring veins. On the other hand, the capillaries 
take, as already mentioned, a very active part in the pro- 
cess; yet these and the capillary veins differ remarkedly 
from the veins proper in that not merely colorless, but 
red corpuscles, emigrate from them. This result is com- 
pletely in harmony with the condition of the stream in 
these vessels, for I have already called your attention to 
the fact that in the veins only white corpuscles, in the 
capillaries both varieties, are in contact with the vessel 
wall, so that whether a preponderance of white or of red 
corpuscles passes out of a given capillary depends solely 
on the numerical relations of the cells accumulated in 
its interior. INFLAMMATION 
89 
"Keeping pace with this exodus, emigration, or, as it 
is also called, extravasation of corpuscular elements, 
there occurs an increased transudation of fluid, in conse- 
quence of which the meshes of the mesentery, or the tis- 
sues of the tongue, are infiltrated and swell. But this is 
not all. The extravasated colorless corpuscles distribute 
themselves, in proportion as their numbers increase, over 
a larger area, forsaking the neighborhood of the vessels 
from which they are derived. The tissues become more 
and more densely packed with them, while the red cells, 
which have not the power of independent locomotion, re- 
main seated in the vicinity of their capillaries; yet these 
also may be carried off by the stream of transudation. 
Soon a moment must arrive when the products of exuda- 
tion and transudation can no longer be accommodated in 
the tissues. They now gain the free surface of the 
mesentery, and should the transuded fluid coagulate, as 
is the rule here, the final result of the process just de- 
scribed will be the deposition on the mesentery, as well 
as on the intestine, of a fibrinous pseudo-membrane, 
densely packed with colorless blood corpuscles, and in- 
terspersed with isolated red cells." 
Inflammation then is a process characterized chiefly 
by vascular changes. Its chief phenomena are vascular 
dilatation, slowing of the blood stream, perivascular 
edema, emigration and diapedesis. In situations where 
the blood vessels are absent, as in the cornea, the essen- 
tial phenomenon is leucocytic migration. In either case 
the tendency is to healing or repair of the lesion. 
Very many inflammations are the result of infection 
with bacteria (septic inflammations). In these the pro- 
cess is generally the same so far as the fundamental tis- 
sue and vascular changes are concerned. The following 
description is taken from Adami's book on "Inflamma- 
tion," a book which every student will be interested to 
read. In it he summarizes the observations of Hohnfeldt 90 
FUNDAMENTALS OF PATHOLOGY 
on abscess development through the agency of staphy- 
lococcus pyogenes aureus: "He inoculated small quan- 
tities of pure cultures of the microbe subcutaneously into 
rabbits. Four hours after inoculation the vessels of the 
region were found densely filled with corpuscles, and in 
them a commencing margination of the white corpuscles 
was discernible. Leucocytes were present within the tis- 
Fig. 17.-A section of an area in the liver which is the seat of a tuberculous 
process. In this instance the infection is in the tissue about a bile vessel. Note the 
giant cell. 
sue in numbers greater than normal; although compared 
with later stages they were infrequent. They were of 
two kinds-the mononuclear in the majority, the poly- 
morphonuclear in lesser numbers; both forms were con- 
gregated mainly around the line of entrance of the in- 
jecting needle. Many of the connective tissue cells were 
so swollen as to be rounded rather than flattened. The INFLAMMATION 
91 
injected cocci, lying in the lymph-spaces, were scattered 
through the tissue; in part free, in part already ingested 
by cells, not only by the leucocytes, but also by the con- 
nective tissue cells, the number within leucocytes being 
not inconsiderable. Preparations made at the end of ten 
hours showed the same conditions, but more distinctly. 
There was ample evidence of migration of the leucocytes; 
Fig. 18.-A photograph of granulation about an area of chronic tuberculosis. This 
' illustrates well why such areas have been called granulomas. 
margination in the congested vessels, various stages of 
passage through the vascular walls, and large collections 
of cells in the perivascular lymph spaces; from these they 
spread into the spaces between the bundles of connective 
tissue fibrils. The cocci lay in the lymph spaces in in- 
creased numbers, and the massing of leucocytes corre- 
sponded in position to the accumulation of microbes. In 92 
FUNDAMENTALS OF PATHOLOGY 
these regions the leucocytes were mainly polymorphonu- 
clear, but in the boundary zone away from the cocci the 
mononuclear form predominated. At the end of twenty 
hours there was further accentuation of these condi- 
tions. As yet an abscess proper had not been formed, 
but there were enormous numbers of leucocytes and also 
of micrococci; the fibrilla? of connective tissue were widely 
separated by the collections of leucocytes, which clus- 
Fig. 19.-Acute catarrhal colitis. The epithelium of the tubular glands, especially 
near their mouths, is forming an excessive amount of mucus with destruction and ex- 
foliation of the cells. The tubules are dilated with mucus which covers the surface. 
The mucosa at the right is necrotic and forms the edge of an ulcerated area. (Dela- 
field and Prudden.) 
tered round and hid the connective tissue cells. With the 
completion of forty-eight hours a well-defined abscess had 
formed, separated sharply from the surrounding healthy 
tissue. The center of the abscess was seen to consist of 
densely packed leucocytes mingled with large growths of 
cocci. These leucocytes were almost entirely polymor- 
phonuclear; and in this central area the nuclei of some 
showed fragmentation. (Such a matrix constitutes pus.) INFLAMMATION 
93 
Neither leucocytes nor connective tissue cells showed the 
slightest indication of mitosis. In the central area all 
traces of the previous capillaries had disappeared; in the 
peripheral zone they were easily recognized, being fully 
injected; and showing a marginal disposition of their leu- 
cocytes, many of which could be seen (in osmic acid prep- 
arations) fixed in the process of migration. The major- 
Fig. 20.-An abscess of the liver. The central part is composed of leucocytes, some 
■of them apparently living and some of them dead. There are fragmented cells and 
parts of cells lying in the more fluid portion of the mass. This whole central area is 
what is known as pus. About the abscess the liver tissue is compressed and infiltrated 
with leucocytes, some of them on their way into the abscess to act as scavengers 
(phagocytes), some of them on their way out of the abscess carrying off dead material. 
ity of the cocci lay in these leucocytes. Even where the 
colonies of the microbes were thickest, there the majority 
were intracellular. Passing toward the periphery the 
number of cocci became smaller and smaller. At the 
periphery they could be seen not only to be intracellular, 
but also free in the lymph spaces; and Hohnfeldt, with 94 
FUNDAMENTALS OF PATHOLOGY 
other observers, saw them definitely grouped within the 
endothelial cells of the peripheral vessels. Thus it may 
be noted that, at this stage, the proliferating microbes 
extended into the healthy tissues outside the abscess. In 
the center of the abscess the original tissue had wholly 
disappeared; nearer the periphery light streaks and bun- 
dles of the disintegrating fibrillae could be recognized 
between the leucocytes. Not until the tenth day did new 
growth of tissue begin to show itself. During the preced- 
ing six days there had been mere breaking down of the 
polymorphonuclear cells, characterized by fragmentation 
of the nuclei and by fatty degeneration of the cell sub- 
stance. But by the tenth day the periphery had begun 
to assume the appearance of granulation tissue; it con- 
tained numerous, capillaries and new-formed connective 
tissue with characteristic epithelioid cells or fibroblasts 
possessing larger, oval, pale-staining nuclei. In these 
cells, as in the connective tissue cells of the surrounding 
tissue, the numerous steps of indirect cell division could 
be made out. In this granulation tissue cocci were ab- 
sent and leucocytes were infrequent." 
Such is the typical picture of abscess formation and 
the progress up to the commencement of healing. The 
fact should be mentioned here that, at almost any stage 
of this process, the bacteria may enter the blood stream 
and be distributed to the rest of the body. Then one of 
two things may happen; either the bacteria may prolif- 
erate exclusively in the blood and overwhelm the infected 
organism, a condition which we know as septicemia, or 
they may become located in other organs or tissues and 
there proliferate and produce other secondary or meta- 
static abscesses, a condition known as septicopyemia. It 
is also possible that the bacteria without of necessity en- 
tering the blood stream spread in an apparently unhin- 
dered and unlocalized way in the tissues, and so produce 
a diffuse reaction (cellulitis; phlegmon). INFLAMMATION 
95 
Repair and Regeneration. 
If, as the result of a trauma only a few cells are dam- 
aged (as illustrated in the lesion produced by a sharp 
knife or a pin prick), and the edges of the wound remain 
in apposition or very close together, healing takes place 
very rapidly. There is little dead material to be re- 
moved, and a few phagocytes can do the necessary work 
quickly. The blood or serum which is present below the 
Fig. 21.-An appendix vermiformis which has been the seat of an inflammatory 
process. The lumen of the appendix has been filled with an exudate which instead 
of being absorbed has been organized. (Delafield and Prudden.) 
edges of the wound coagulates and glues them together 
and the fibrin formed during coagulation forms a network 
upon which the cells for either side can be supported 
in their growth. The result is that the capillary loops 
send their sprouts across the wound: the fibroblasts, few 
in number, grow with the capillaries and form a perma- 
nent binding of the tissue. At the same time the epithe- 
lium of the surface grows across the wound and covers it. 96 
FUNDAMENTALS OF PATHOLOGY 
At the end of a few days the healing is complete and 
strong. This we call "healing by first intention," and 
it is what the surgeon strives for in approximating the 
edges of the wounds he makes with his sharp instruments. 
Tearing of tissues tends to destroy more cells and delay 
healing. 
In healing by second intention or healing by granula- 
tion one of two things has happened: either the space to 
be tilled with tissue is too wide for rapid tilling with liv- 
ing cells, or infection has occurred. If a wound is filled 
with sterile blood clot, healing will occur especially by 
means of organization of the blood clot; if the wound or 
the blood clot is infected (stitch abscesses for instance) 
then the process of healing is analogous to that already 
described in the formation and healing of abscesses. 
Such healing results in the formation of much fibrous tis- 
sue, which tends to produce a scar and scar tissue, espe- 
cially when it replaces muscle, and tends to stretch. 
Fibrous tissue is the tissue with which all other tissues 
are apt to be replaced if healing is not rapid. Many tis- 
sues do not regenerate save only very slowly. Fibrous 
tissue grows rapidly and hence tends to replace the "no- 
bler" tissues. The more highly developed a tissue is the 
less power it has of regeneration. Complex tissues never 
undergo complete regeneration. The nearest approach to 
it is seen in per primam healing. 
In healing of wounds in bone the process is much the 
same as in other situations. It is only modified by the fact 
that the fibroblasts play a role which is supplemented 
by osteoblasts, which are merely modified fibroblasts. 
After a fracture there is a certain amount of hemorrhage 
which fills in the spaces between and around the broken 
ends of the bones. Associated with this there is exuda- 
tion of cells and serum. Soon the blood clot which is 
formed begins to organize and the whole mass forms 
what is known as the callus. This callus is finally, in INFLAMMATION 
97 
part, replaced by osteoblastic tissue, and finally by bone, 
and is in part absorbed. Sometimes it is not replaced, 
but remains fibrous and then we speak of "fibrous union 
of bones. ' ' This is what is apt to happen in old persons, 
in persons whose bones are not well "set" or approxi- 
mated, and in those in whom the bones are not kept sol- 
idly in place during healing. 
Types of Inflammation. 
Inflammations are classified according to the time dur- 
ing which they have existed, or according to the morpho- 
logic characters of the exudates. For instance they are 
called acute if they appear and develop within a very 
short time or last but a short time; they are called chronic 
if they develop slowly or last a long time. One remem- 
bers the acute coryzas which appear almost in a minute, 
last a few days and disappear, or the acute tonsillitis 
which acts in the same way. A boil is an acute inflam- 
mation. One also remembers the "colds" that last all 
winter; the bronchitis of old people, which lasts for years 
as is shown by the '"chronic" cough, and the pulmonary 
tuberculosis with which some individuals live for years. 
On the other hand one recalls the terms "membranous 
croup" (which we now know is diphtheria), which re- 
ferred to the membrane found in the larynx. A mem- 
brane is an exudate formed almost purely of fibrin, with 
sometimes a few leucocytes. An abscess is a purulent 
form of inflammation, for purulent refers to pus. A se- 
rous inflammation is characterized by the predominance 
of serum; a hemorrhagic inflammation, by the presence of 
numbers of blood cells. A catarrhal inflammation is one 
whose exudate contains much mucus (a mucous inflamma- 
tion). Also there are serofibrinous inflammations; sero- 
purulent; fibropurulent, and other inflammations,-terms 
which explain themselves. Suppuration is a term which 98 
FUNDAMENTALS OF PATHOLOGY 
means the same thing as purulent. Any of these forms 
of inflammations may be acute or chronic. 
An abscess is a localized purulent inflammation in a 
tissue. An ulcer is a localized purulent inflammation 
upon a surface. A sinus is a localized inflammatory tract 
connecting two surfaces. 
The types of inflammation depend upon the nature of 
the tissue affected; upon the nature of the irritant; and 
upon the intensity and duration of the irritant action. 
For instance, the skin of the hands is less easily affected 
by heat and cold than the skin of the body. Dilute car- 
bolic acid placed upon the surface of the body does no 
damage, while strong carbolic acid will produce local 
death of cells. Heat of great intensity will do no dam- 
age if it be applied momentarily to the skin, but if a mod- 
erately hot object be left in contact with the skin for a 
certain length of time it may produce a burn. Under 
certain conditions a hot water bottle placed upon a pa- 
tient will burn, while under other conditions of health 
and resistance it would do no damage. So, there enters 
into the question the problem of individual resistance. 
It is this relationship that accounts for the fact that cer- 
tain bacteria produce no effects in one person and disease 
in another. 
REFERENCES. 
Adami: Inflammation. Principles of Pathology, Vol. I, 1810. 
Adami: Inflammation. New York and Lond., 1909. 
Cohnheim: Lectures on General Pathology, Vol. I, London, 1889. 
Vaughan: Protein Split Products (Fever), 1913. 
Vaughan: The Protein Poison and Its Relation to Disease, Jour. Am. 
Med. Assn., 1913, lxi., 1761. 
Walker: Inflammation. Pembrey and Ritchie's General Pathology, 
1913. 
Wells: Chemical Pathology, 1907. 
Woolley: Inflammation. Lancet-Clinic, Apr. 5, 1913. 
Woolley: The Factors Governing Vascular Dilatation and Slowing of 
the Blood-Stream in Inflammation. Jour. Am. Med. Assn., 1914, Ixiii, 
2279. CHAPTER VIII. 
TUMORS. 
In the old sense of the word the expression tumor was 
applied to swellings of any sort (hematoma, tuberculoma, 
syphiloma). Usage in that sense is no longer proper and 
now the word is applied to certain types of hyperplastic 
tissue growths, which are more or less autonomous. The 
term neoplasm is still better, because it is a more concise 
Fig. 22.-An epithelioma of the hand. 
one and implies, through usage, independence and hy- 
perplasia. 
"A tumor proper," says C. P. White, liis a mass of 
cells, tissues, or organs resembling those normally pres- 
ent, but arranged atypically. It grows at the expense 
of the organism without at the same time subserving any 
useful function. ' ' 
The ordinary tumors which are seen in the wards of 
hospitals belong to a group known as the blastomas. 
They are derived from but a single tissue in each instance 
and according to the tissue from which they originate 
their names arise. For instance a tumor growing from 
99 100 
FUNDAMENTALS OF PATHOLOCxY 
Fig. 23.-Mucous papilloma of bladder, composed of long slender branching processes 
with delicate vascular core covered by proliferated transitional epithelium-the so-called 
Villous Papilloma. (x200.) 
Fig. 24.-Photograph of a section of a bit of skin sent to the laboratory because 
there was a suspicion of malignancy in the case. There is nothing malignant to be 
seen, but the section illustrates the earliest histologic tendency in the direction of in- 
vasion (infiltration) of the subcutaneous tissues by the epithelium. Note the small 
downgrowths. TUMORS 
101 
epithelium is called an epithelioma; from fibrous tissue a 
fibroma; from bone, an osteoma, etc. There are also a 
certain group of tumors which arise from more than one 
tissue and these are the teratoblastomas or ordinary 
Fig. 25.-Squamous papilloma, showing thickened skin epithelium, covering a branching 
vascular connective tissue core. (x38.) 
mixed tumors which are frequently encountered in the 
parotid region of the body. 
Depending upon the course which the growth of a 
tumor takes we speak of benign and malignant neoplasms. 
The former is one which is not incompatible with health; 
the latter is a menace to existence. 
The following table will indicate the commoner termi- 
nology as well as the origin of the tumors: 102 
FUNDAMENTALS OF PATHOLOGY 
SOURCES 
BENIGN 
MALIGNANT 
Epithelium (skin) 
Epithelium (glands) 
Mammary gland 
Epithelium of intes- 
tine, liver, pancreas, 
etc. 
Benign epithelioma1 
Papilloma (warts, 
corns) 
Adenoma 
Adenoma 
Papilloma; Polyps. 
Epithelioma; (Skin 
cancers) 
Carcinoma (Adenocar- 
cinoma) 
Carcinoma (Adenocar- 
cinoma) 
Carcinoma 
Connective tissue 
Fibrous tissue 
Fatty tissue 
Bone tissue 
Cartilage 
Muscle 
Fibroma 
Lipoma 
Osteoma 
Chondroma 
Myoma 
Sarcoma 
Fibrosarcoma 
Liposarcoma 
Osteosarcoma 
Chondrosarcoma 
Myosarcoma 
Nervous system 
Neuroglia 
Glioma 
Gliosarcoma 
Endothelium 
Blood vessels 
Endothelioma 
Angioma 
Endothelioma 
Angiosarcoma 
The main differences between benign and malignant 
tumors is shown in the following table: 
BENIGN. 
MALIGNANT. 
Slow growing 
Circumscribed (Encapsulated) 
Do not metastasize 
Do not interfere with health 
Rapidly growing 
Not encapsulated (infiltrating) 
Metastasize 
Produce evident interference with 
health by pressure upon other 
organs, by producing anemia, 
cachexia, etc. 
Sarcomas are more frequent in young individuals. 
Carcinomas are more frequent in older individuals. 
Tumors are apt to be most frequent at places in the 
body where there is continued irritation. Such irritation 
may be due to bacteria, to toxins, to other chemical irri- 
tants, or to mechanical influences. Just why tumors 
start to grow no one knows. TUMORS 
103 
Fig. 26.-Epithelioma of the lip. 
Fig. 27.-Adenocarcinoma of the cervix uteri. Almost the entire field is made up 
of the main trunks a and b, which send off many branches, a' and b'. c indicates 
cross sections of terminal outgrowths. The stroma g consists of elongate cells with 
spindle-shaped nuclei. Covering the outer surfaces of the main and terminal branches 
are layers of epithelium, a single layer at e, several at d. (Cullen.) 104 
FUNDAMENTALS OF PATHOLOGY 
Fig. 28.-Sarcoma. 
Fig. 29. 
Fig. 30. 
Figs. 29 and 30.-Sarcoma. TUMORS 
105 
Tumors spread in two ways by infiltration, i. e., by di- 
rect growth into other tissues, which are destroyed; and 
by metastasis either by the lymphatic vessels or the blood 
vessels. Sarcomas are more apt to follow the blood ves- 
sels; carcinomas to follow the lymphatics. 
No one knows what the cause of tumors is, and there- 
fore no one knows how to prevent them, or in many cases, 
Fig. 32.-Small polyp of 
the mucous membrane of the 
small intestine. (Delafield 
and Prudden.) 
Fig. 31.-Fibrolipoma. 
to cure them. All that is certain, therefore, is that the 
most certain cure is to remove them completely. With 
benign tumors this is usually easy. With malignant ones 
it becomes increasingly difficult, the longer the tumor has 
been allowed to persist, though it is true that in a few 
instances spontaneous healing has occurred. There is 
some hope at the present time that x-rays and radium 
emanations may have a beneficial influence in the treat- 
ment of tumors. 106 
FUNDAMENTALS OF PATHOLOGY 
REFERENCES. 
General. 
Adami: Principles of Pathology. Phila., 1910. 
Cohnheim: Lectures on General Pathology. New Sydenham Soc. Ed., 
Vol. 2. London, 1889. 
Ribbert: Das Karzimon. Bonn, 1911. 
Ritchie: Pembrey and Ritchie's General Pathology. New York, 1913. 
Rous: Jour. Am. Med. Assn., 1911, Jan. 21, 198. 
Rous and Murphy: Jour. Exper. Med., 1914, xix, 52. 
Fig. 33.-An angioma, i. e., a tumor composed entirely of blood vessels. There are 
two sorts of angiomas; one composed as in this case of blood capillaries (hemangioma); 
the other composed of lymphatic vessels (lymphangioma). 
Animal Parasites and Cancer. 
Editorial: Jour. Am. Med. Assn., 1913, Mar. 22, 948. 
Fibiger: Berl. klin. Wchnschr. 1913, 1, 289. 
Latency of Cancer. Spontaneous Healing. 
Graham: Surg., Gynec. and Obst., June 1907, 701. (Lit.) 
McConnell: Internal. Clin., Ser. xx, vol. 2. TUMORS 
107 
Heredity and Cancer. 
Slye: Ztschr. f. Krebsforsch., 1913, xiii, 500. 
Slye: Jour. Med. Research, 1914, xxx, 281. 
Slye, Holmes and Wells: Ibid, 417. 
Cancer in Plants. 
Smith: Bull. 213 Bureau of Plant Industry, Washington, D. C., 1911. 
Smith: Bull. 255, ibid, 1912. 
Smith: Proc, xvii Intern. Cong. Medicine, Aug., 1913. 
Transmissible Tumors. Filterable Viruses. 
Rous: Jour. Am. Med. Assn., 1910, Iv, 1805; Jour. Exper. Med., 1910, 
xii, 696; Jour. Am. Med. Assn., 1911, Ivi, 198. 
Fig. 34.-Schematic representation of the varieties of cancer which may arise from 
glandular epithelium. (After Beattie and Dickson.) 
A. Transverse section of Normal Gland Acinus consisting of regular epithelium 
upon a basement membrane, surrounded by a connective tissue stroma containing 
nutrient vessels. This may give rise to any of the following types of new growth. 
B. Malignant Adenoma, with irregularity in shape of acini, the lumen of which 
persists. Absence of basement membrane. Irritation giving rise to proliferative over- 
growth, etc., of stroma. 
C. Scirrhus or Hard Cancer, in which solid clumps of cells are formed, and give 
rise to dense fibrous tissue overgrowth. 
D. Encephaloid or Soft Cancer, which may arise directly, or may supervene upon 
the harder variety, the two resembling one another in being composed of solid clumps 
of cells. 
E. Colloid Cancer, which may arise directly from the normal gland type, or may 
supervene upon any of the other forms. 108 
FUNDAMENTALS OF PATHOLOGY 
Rous and Murphy: Jour Am. Med. Assn., 1911, Ivi, 741; ibid, 1912, 
Iviii, 1938; Jour. Exper. Med., 1914, xix, 52. 
Rous, Murphy and Tytler: Jour. Am. Med. Assn., 1912, Iviii, 1751; ibid, 
1912, lix, 1793. 
Miscellaneous. 
Davis: Paraffin Cancers. Jour. Am. Med. Assn., 1914, Ixii, 1716. 
Diet and Cancer. 
Fleischer and Loeb: Jour. Exper. Med., 503. 
Fleischer, Vera and Loeb: Ibid., 522. 
Leighton: Ibid., 542. 
Rous: Ibid., 1914, xx, 433. 
Woglom: Ibid., 1915, xxii, 766. PART II-SYSTEMIC PATHOLOGY 
CHAPTER IX. 
THE CARDIOVASCULAR SYSTEM. 
The Blood. 
Normally the body contains a certain average amount 
of blood, including certain fairly definite properties of 
fluid (plasma), and the cells (red cells, leucocytes and 
platelets). In disease these proportions vary. Accord- 
ing to the type of variation we speak of general hyper- 
emia or general anemia. Also under normal circum- 
stances the distribution of the blood in the body remains 
constant. In disease the distribution varies and we 
speak of local hyperemia or local anemia, as the case 
may be. 
Depending upon the constituent of the blood which is 
increased, there are certain terms in use. For instance, 
a general increase in the total blood is spoken of as 
plethora; increase of the fluid constituents, as hydremia; 
of the red elements, as polycythemia; of the leucocytes, as 
leukemia. The term anemia covers a large field but 
most frequently has reference to diminuation of the hemo- 
globlin concentration of the blood. Decrease of the 
leucocytes is called leucopenia. Total decrease of blood 
we call oligemia; of fluids only, anhydremia. 
Hyperemia. 
Hyperemia may be, as we have indicated, general or 
local, arterial or venous. Normally there is in the human 
body about one-twentieth its weight of blood. In infants 
109 110 
FUNDAMENTALS OF PATHOLOGY 
Abnormally small-Microcytes-Pernicious anemia. 
Abnormally large-Macrocytes and megaloblasts-Pernicious anemia. 
Physiologic-infancy. 
Pathologic-Lymphatic leucemia. 
Infection-Helminthiasis 
Trichiasis. 
Uncinariasis. 
Physiologic-post prandial. 
Pathologic-infection. 
Cells abnormal in the blood-Myelocytes-myelogenous leucemia. 
Absolute deficiency of hemoglobin-Chlorosis. 
Absolute increase of hemoglobin-Pernicious anemia. 
In structure-Nucleated-Megaloblasts-Pernicious anemia. 
In shape-Poikilocytes-Pernicious anemia. 
Physiologic-infancy. 
In staining-Polychromatophilia-Pernicious anemia. 
Pathologic 
Polymorphonuclear 
Lymphocytes 
Lymphocytosis. 
Eosinophiles 
Eosinophilii 
the BLOOD corpuscles. (After McFarland.) 
Cells normal to 
the blood. 
Deficient-anemia. 
I ncreased-Polycythemia. 
Deficient-Leucopenia. 
In size 
In color 
Increased- 
Leucocytosis. 
Peculiar 
Erythrocytes 
measure 7.5^. • 
5,000,000 per 
c.mm. 
Leucocytes 
measure 7 to 
. 7,500 per 
c.tnm. 
Absolutely increased 
polycythemia. 
Absolutely decreased 
oligocythemia 
Corpuscles THE CARDIOVASCULAR SYSTEM 
111 
there is more, in old persons less. This weight or volume 
of blood can be increased temporarily by injecting fluids 
into the body, particularly by the intravenous route, but 
the fluid so injected, unless it be held by a colloid, as, for 
instance, gelatine, is very rapidly eliminated. Neverthe- 
less under certain abnormal circumstances the whole vol- 
ume of blood increases, or in other cases one of its con- 
stituents becomes augmented. Plethora is uniformly 
associated with either polycythemia or with one or an- 
other type of anemia. 
In local hyperemias, however, things are different. 
When the hyperemia (or congestion) is the result of ar- 
terial activity, when it is produced by the presence of ar- 
terial blood, we speak of active congestion; when it re- 
sults from decreased drainage of the blood through the 
venous channels, we call it passive congestion. When for 
any reason the arteries or arterioles are dilated, whether 
by nervous impulses, or by chemical causes, more arterial 
blood rushes into the affected part. This we call arterial 
(or active) hyperemia, or congestion. If, on the other 
hand, without any participation on the part of the arter- 
ies, blood is prevented from leaving an organ, we call it 
venous (or passive) hyperemia or congestion. Active 
(arterial) hyperemia is the cause of the very well known 
blush or flush. It is also the phenomenon which accounts 
for the increase of blood in a functionally active organ, 
like a muscle, or the stomach. It is the cause of the red- 
ness that appears during inflammation. Passive conges- 
tion, on the other hand, results from increased venous 
pressure and may be cause by blocking of a vein from 
within or from without. When the heart is so damaged 
that blood is prevented from entering it at a normal rate 
because of disease of the tricuspid valve, the liver be- 
comes the seat of a passive congestion. When the mitral 
valve is damaged so that the blood coming from the lungs 
cannot pass through it rapidly enough, the lungs become 112 
FUNDAMENTALS OF PATHOLOGY 
Fig. 35.--Abdominal arteries in a case of double iliac thrombosis of typhoid origin. 
(Thayer.) 
passively congested. The pressure of fluid in the pleural 
cavities may so affect the circulation of blood that the 
circulation from the right to the left heart is impeded 
and the organs of the abdominal cavity become passively THE CARDIOVASCULAR SYSTEM 
113 
congested. Air in the pleural cavity, or tumor growths, 
may produce the same effects, and very similar ones fol- 
low the accumulation of large amounts of fluid in the 
pericardial cavity. 
The arterial hyperemias are as a rule transient ones, 
and are in physiologic circumstances associated with 
transient increase of function. When a muscle is exer- 
cised, more blood is carried to it, and with the blood more 
food. Functional activity and increased food lead to 
growth. The venous hyperemias, on the contrary, tend 
to be more permanent-chronic, we call them, and these 
chronic passive congestions lead to the opposite changes 
to those which follow arterial hyperemias. The dam- 
ming back of venous blood prevents the arterial blood 
reaching the parts. The venous blood, which is poor in 
oxygen and other foods, accumulates and the functional 
cells of the affected tissue tend to undergo atrophy, while 
the fibrous tissue becomes richer. In the liver, for in- 
stance, the cells affected by the passive congestion do not 
receive oxygen enough and commence to degenerate. 
More than a normal amount of fat appears in them; they 
shrivel, become atrophic and disappear. At the same 
time the fibrous tissue is accentuated by loss of liver cells 
and also undergoes increase and the organ becomes 
fibrous-cirrhotic. And also because the venous blood 
(some of it) cannot get out of the tissue, the blood cells 
die, the pigment is set free and stains the tissue. The 
gross result is that the liver takes on an appearance that 
resembles the cut surface of a nutmeg and the organ is 
known as the nutmeg liver. Much the same thing hap- 
pens in the lungs. They become fibrous-indurated, and 
pigmented, but some of the pigment and some of the 
blood passes into the air spaces and is coughed up. When 
free blood is present the sputum is tinged with red; when 
only pigment is present, the sputum is "rusty." 114 
FUNDAMENTALS OF PATHOLOGY 
Anemia. 
Anemia, like hyperemia, may he general or local. Gen- 
eral anemia may be caused by large single losses of blood 
as from large hemorrhages, or by many small losses. Se- 
vere grades of anemia may be caused by the small fre- 
quent hemorrhages from hemorrhoids. More frequently, 
however, severe anemia is the result of intoxication with 
substances which cause destruction of the red blood cells. 
The so-called pernicious anemias, or primary anemias, 
are almost certainly of infectious origin, although there 
is the possibility that some forms may he the result of 
wearing out of the blood forming tissue of the body. 
The primary anemias are those whose causes we have 
not discovered. The secondary anemias are those the 
causes of which are known. 
Local anemias are as a rule the result of interference 
with the blood How. Such interference may take place 
within the vessels or by pressure from without. One of 
the best examples is a bed sore which is the direct effect 
of extravascular pressure. When the blood supply of a 
part is cut off, that part dies. In the case of the bed sore 
(decubitus) the area is usually circular, and corresponds 
to the pressure. In the case of gangrene of a leg pro- 
duced as a rule by intravascular disturbances, all the tis- 
sues, whose blood supply is cut off, die. 
Sometimes it happens that the blood supply of a part 
is interrupted for hut a short time. In most instances 
only temporary effects are produced. In other cases the 
interference is permanent but because of collateral path- 
ways blood still reaches the part in sufficient amounts to 
prevent death or necrosis. As time goes on these collat- 
erals become more and more sufficient until they are com- 
pletely able to satisfy the needs of the tissues. It also 
is true that sometimes the collaterals are sufficient pro- 
vided the blood supply is not shut off too suddenly. If 
blockage occurs slowly enough, the collaterals may ac- THE CARDIOVASCULAR SYSTEM 
115 
commodate themselves whereas if the main current is 
suddenly shut off they are not sufficient. It therefore hap- 
pens that the effects of a local anemia will vary with the 
rate of its production and the degree of its completeness. 
Edema. 
When we speak of edema we mean a condition which 
results from the presence of too much water in the tissues. 
Hence the term hydrops. It is a symptom which is asso- 
ciated with kidney disease, heart disease, lung disease, 
and general anemias. It is encountered during preg- 
nancy, during the latter part of which the feet and legs 
often swell. It appears in the hands and fingers after se- 
vere and unaccustomed manual exercise, or even after 
long walks. The palms swell after catching a haseball- 
especially early in the season, or after rowing a boat. 
Moreover swelling is a symptom of inflammation. Under 
these circumstances the water is held in the cells and tis- 
sues of the body. When it is general, we speak of 
anasarca or general dropsy; otherwise it is known as 
edema. Sometimes fluid appears in the cavities of the 
body. When the abdominal cavity is affected we speak 
of ascites. In other cases we speak of pleural or peri- 
cardial effusions, or of hydrothorax, or hydropericardium, 
if the pleural or pericardial cavities are involved; of 
hydrocephalus, if the ventricles of the brain are affected. 
Edema is the result of the presence of too little oxygen 
in the tissues. If we give an animal a poison which re- 
duces oxidation in the body-which makes it impossible 
for the tissues to use oxygen-and which at the same time 
will not cause the death of the animal or tissue, the tis- 
sues swell. If we interfere with the blood stream so that 
the blood current is slowed and too little oxygen reaches 
the tissues, they swell. If we decrease that part of the 
blood which carries oxygen to a point where there is not 
enough to carry a sufficient amount of oxygen to the tis- 116 
FUNDAMENTALS OF PATHOLOGY 
sues, they swell. In pregnancy the fetus in utero presses 
upon the great veins which supply the legs of the moth- 
er with blood. The blood How is decreased and the feet 
and legs become swollen,-"dropsical." Tight garters 
will do the same thing and produce the same result. In 
severe anemia, in chlorosis or pernicious anemia there is 
not enough hemoglobin, or not enough red blood cells, 
or both, to carry sufficient oxygen to the tissues, and the 
feet and legs swell-become puffy, so that the shoes are 
too tight. In heart disease when the blood does not cir- 
culate rapidly enough through the lungs, especially when 
the arterial blood How is interfered with, the lungs be- 
come edematous. 
The reason seems to be this: when the substance of the 
tissues (the protoplasm) is broken down to furnish 
energy, acids are produced. AVe know, for instance, that 
during muscular activity, lactic acid is formed in the 
muscles. If the blood supply is good, enough oxygen is 
furnished to oxidize the lactic acid and split it until the 
acid part is represented by carbonic acid which is ab- 
sorbed by the blood and excreted as carbon dioxide. If 
not enough oxygen is present, then part at least of the 
lactic acid remains as such. It has been found that any- 
thing in the nature of protoplasm,-gelatin, fibrin, egg 
albumen-takes up or absorbs water when it is placed in 
very dilute acids. So it happens that when not enough 
oxygen is carried to the tissues by the blood, the acids 
accumulate and the tissues absorb water from the blood, 
and swell. The swelling we call edema. 
Thrombosis and Embolism. 
Local anemia is very frequently the result of the block- 
ing of blood vessels from within. Such blocking may oc- 
cur as the result of thrombosis or embolism. 
Thombosis is the process which results in the forma- THE CARDIOVASCULAR SYSTEM 
117 
tion of a clot within a blood vessel during life. It may 
be the result of one or both of two factors. 
1. Injury to the vessel wall by toxins or other poisons, 
or by traumata. When a vessel wall, especially the 
intimal cells, are injured, a substance called fibrin fer- 
ment is set free, which acts upon the blood and causes it 
to clot. The process of clotting begins in the immediate 
region of the cellular damage and so the clot remains ad- 
herent to the wall. It then proceeds to enlarge by pro- 
gressive clotting until the lumen of the vessel is filled. 
2. Changes in the constitution of the blood itself. 
Certain substances cause the cells of the blood to break 
up or to change the physical character of the blood, and 
so make it more easily able to clot. From the cells of 
the blood itself fibrin ferment may be set free and then, 
particularly if the blood is more viscid than usual, or is 
flowing more slowly, it may form a clot. 
In either case a thrombus is formed. 
The result, thrombosis, is of course local anemia be- 
yond the thrombus, and if this anemia is complete, then 
local death or necrosis follows. If the trombus is in an ar- 
tery of an organ like the kidney or lungs, the death is as 
a rule more rapid, and also the area that undergoes death 
has a tendency to be wedge-shaped, with the apex of the 
wedge at the thrombus. If the thrombus is in a vein, the 
tissue death is apt to be slower though the area is still 
wedge-shaped. In either case we speak of infarction. 
An infarct is a wedge-shaped (as a rule) area of com- 
plete local anemia in an organ and is caused by sudden 
interruption of the blood supply. 
It not infrequently happens that a thrombus is formed 
within a vessel which supplies a tissue whose collateral 
circulation is sufficient to prevent death. Sometimes, 
however, from such a thrombus a piece breaks off and 
proceeds in the blood stream until finally it reaches an- 
other smaller vessel which it plugs. Such a free bit of 118 
FUNDAMENTALS OF PATHOLOGY 
thrombus is called an embolus. All emboli are, however, 
not formed in this manner. A clump of bacteria, a bub- 
ble of air, a group of fat cells from the medulla of a frac- 
tured bone, a group of tumor cells, or a few placental 
cells, may be set free in the blood stream and produce 
embolism. An embolus is a foreign body which blocks 
completely or incompletely, from within, a blood vessel. 
The commonest examples of emboli are fragments of val- 
vular cardiac vegetations which are broken off and are 
carried to the coronary arteries or brain, where they pro- 
duce sudden death; or to the lungs, kidney or spleen 
where they produce infarcts. Infarcts may be produced 
by thrombi or emboli. 
The Heart. 
The heart is a series of chambers that have developed 
by dilation of a certain part of the vascular system. Its 
walls are fibromuscular, and its chambers are separated 
by valves which are merely reduplications of the endo- 
cardium. The movements of the heart are influenced by 
a conducting mechanism which is composed of muscle 
fibers of an embryonic type, and by a system of nerves 
belonging to the vago-sympathetic system. The nervous 
mechanism modifies the contractions of the muscles by 
producing changes which result in increased or decreased 
irritability of the myocardium. 
The chambers of the heart serve as containers of 
blood; the muscles act in moving the blood; and the 
valves serve to direct the flow of the blood. 
Pathologic changes in the heart are the results of proc- 
esses which affect the muscles, the valves, the conduction 
system or the nervous system. 
Leaving out of consideration the developmental de- 
fects, we may say that the conditions of the chambers of 
the heart are the results of (1) the amount of blood the 
heart must receive, and this depends upon the conditions Fro. 36.-Diagram Illustrating the Establishment of Collateral Circulation in 
Obstruction of a Vein. (After Ribbert, from Delafield and Prudden.) 
The veins a and b at A are connected by a slender trunk, c. If a in B is occluded, 
as by a thrombus, the blood cannot all pass out of the territory drained by a, so that 
the vessels here are dilated-congestion. If, however, the small anastomosing trunk 
widens as at c, the congestion is relieved by the conveyance away of the blood through 
the vein b 
Fig. 37.-Diagram Illustrating the Formation of a Hemorrhagic Infarct. 
(After Ribbert, from Delafield and Prudden.) 
The artery, A, plugged by an embolus or thrombus, E, is a terminal artery, but it 
has abundant capillary anastomoses, so that while the territory deprived of blood is not 
sufficiently nourished and its tissues die; but from the abundant capillary anastomoses 
from the artery B, and from the vein C, a certain amount of blood enters the infarct 
area, which thus becomes hemorrhagic. THE CARDIOVASCULAR SYSTEM 
119 
existing in the peripheral vessels, and in the blood itself 
(caliber of the vessels, elasticity, viscosity, resistance), 
and upon the condition of the valves (efficiency); and (2) 
upon the amount of blood they can contain and this de- 
fends upon the condition of the musculature. 
The musculature of the heart is influenced by but two 
sorts of influences, i. e., mechanical and chemical, if we 
class nutritional disturbances as chemical, as we should. 
We may properly say, then, that the musculature of 
the heart is modified by (1) the mechanical conditions 
under which it acts, which means, the work it has to do, 
and (2) the chemical conditions under which it acts. A 
heart doing a normal amount of work, that is one which 
is working within physiologic limits, has, other things 
being equal, a normal musculature. The walls of such 
a heart are of characteristic thickness and structure. A. 
heart doing increased work either because of increased 
blood or increased work either because of increased blood 
or increased arterial pressure, however, behaves differ- 
ently. Provided the food supply is sufficient it undergoes 
hypertrophy, as we say. The walls become thicker, the 
muscle fibers become larger and more numerous, while 
the cavities remain of normal relative size. But if the 
supply of food is not sufficient to meet the increased de- 
mands, the compensatory hypertrophy is not as marked 
and the cavities become larger, both relatively and abso- 
lutely. (Ju the other hand, if the amount of work ac- 
complished is small in amount, or if the food supply is 
but moderately insufficient, as is true in cases of under- 
nutrition, in cachexia, etc., then atrophy results, and 
atrophy of the myocardium is apt to be accompanied by 
at least a moderate degree of dilatation. We may con- 
sider that we are dealing with work, increased, overwork, 
and lack of work in these cases. It is only when a heart 
is overworked that dilatation of clinical importance 
occurs, that is, only when the food supply is insufficient 120 
FUNDAMENTALS OF PATHOLOGY 
to meet the demand of increased activity. In such cases 
we are dealing with muscular fatigue, with the accumu- 
lation of the chemical products of metabolism which can- 
not be removed rapidly enough to allow normal meta- 
bolism to proceed. Tone is lost, the muscles do not con- 
tract in a normal manner, and the cavities of the heart 
become larger and are less promptly and completely 
emptied. The chemical cardiac intoxications, such as we 
find in the anemias, and those produced by toxins, and 
poisons of other sorts, produce similar changes except 
that the pure work element, hypertrophy, is absent, for 
the reason that in these the active agents do not act as 
stimulants of the muscle, do not increase the work of the 
muscle, but act from the first by decreasing the ability 
to do work, and so they bring about from the start proto- 
plasmic changes which are found only in cases of chronic 
overwork. If the substances acting upon the muscle are 
in dilute solution the changes are slow, and progression 
occurs from edema to fatty degeneration, atrophy, and 
necrosis. If the solutions are concentrated the gradua- 
tions are absent. In pernicious anemia, the heart muscle 
is cloudy and fatty; in sudden local anemia, as in in- 
farction, the muscle undergoes necrosis. In certain in- 
toxications, diphtheria for instance, the heart may do 
very well provided no burden is thrown upon it. But 
place a sudden strain upon it, even that due to sitting up 
in bed, and what was normal work becomes overwork, 
because of the damaged muscle and its inability to use 
the materials present in the blood. Overwork depends, 
therefore, on the condition of the muscle at the time the 
strain is put upon it. 
When a heart becomes tired out so that it no longer 
does its work easily, it undergoes degeneration-usually 
fatty degeneration. Also at the same time some of the 
fibers disappear and their place is taken by adipose or 
fat tissue or fibrous tissue. In the one case we speak of THE CARDIOVASCULAR SYSTEM 
121 
a fatty heart, in the other of fibrous myocarditis which 
is often a misnomer for myocardial (or cardiac) fibrosis. 
But fibrous tissue may be increased in the heart as a re- 
sult of inflammation, and then we may properly speak of 
myocarditis. Under these conditions, bacteria gain ac- 
cess to the myocardium and by their growth and activity 
kill, or cause to degenerate, the muscle fibers. Also, at 
the same time, exudation occurs between the muscle 
fibers. According to the character of the exudate, we 
speak of a suppurative myocarditis or hemorrhagic serous 
myocarditis. Usually we speak merely of an acute in- 
terstitial myocarditis. As the inflammatory lesions heal, 
fibrous tissue is produced and so the healed heart will 
have scars in it just as any other organ may have, but 
since during the inflammation some muscle has been de- 
stroyed, and since muscular tissue does not regenerate 
easily, the heart is weaker than a. normal one. 
Strain and infection may also affect the heart valves. 
Of the two processes the second is by far the more im- 
portant. The bacteria which cause the infection may 
lodge upon the valves from the general circulation or 
may reach the interior of the valves by way of the small 
vessels which supply them. Since the latter method is 
more frequent and since the valvular vessels are more 
numerous in infants and young persons, it follows that 
acute valvular endocarditis is more frequent in young 
people and that the "valvular heart disease" of adults 
is more apt to be chronic. 
When bacteria arrive upon or in a valve, the cells of 
the endocardium are sooner or later damaged and from 
them fibrin ferment is set free. Then, just as happens 
in a blood vessel, a thrombus is formed, and is usually 
called a vegetation. Hence we speak of vegetative en- 
docarditis. The things which may happen to such vege- 
tations are the same things which may happen to any 
thrombus: it may be organized; it may soften and rup- Cerebral 
circulation. 
Pulmonary 
circulation. 
Pulmonary 
valve. 
' V £ a/ p £ r 
Tricuspid 
valve. 
AO ATA 
Mitral valve. 
- Aortic valve. 
Visceral 
circulation. 
Peripheral 
circulation. 
Fig. 38.-A schematic representation of the general circulation of the body. The 
blood leaves the left ventricle (LF) and enters the aorta through which it passes to 
the visceral and peripheral vessels to supply the abdominal organs and the limbs. 
It leaves the aorta and through the carotids and vertebrals supplies the brain. After 
passing through the various organs it is collected into the two cavas and is returned to 
the heart which it enters through the right auricle (RA). From there it passes to 
the right ventricle (RR). From the right ventricle it is carried to the lungs by the 
pulmonary artery (PA), and it then reaches the left auricle (LA) through the pul- 
monary veins (PR). The pulmonary vein carries arterial blood. Suppose the mitral 
valve is so affected by disease that it is no longer able to prevent the blood from being 
forced back into the left auricle during ventricular systole (insufficiency), at every beat 
of the heart some of the blood which should be sent into the aorta is pushed back into 
the auricle and eventually into the lungs. The lungs become the seat of a "passive 
congestion." Eventually the back pressure effects the right side of the heart also so 
that the right chambers become dilated and after a time the tricuspid valve becomes 
unable to prevent reflux of blood (insufficiency). Then, of course, the liver and other 
viscera will become passively congested. If there are clots or grow'ths (vegetations) 
upon the mitral valve, as in rheumatic fever, and one or more of these are broken off 
and become free in the blood stream, they will be carried with the blood until they 
become caught in some small blood vessel (artery or arteriole) which will be plugged 
(infarction). THE CARDIOVASCULAR SYSTEM 
123 
ture or remain cystic; or it may be infected and break 
down. When the last thing happens we speak of an ul- 
cerative (or malignant) endocarditis. Bits of the in- 
fected material carried away in the blood stream, cause 
infected infarcts in other organs-embolic infarcts, they 
are often called. If the bits of vegetations are not in- 
fected they form bland emboli and cause infarcts which 
are not infected. When organization of a vegetation oc- 
Fig. 39.-Section of a blood vessel which is the seat of an obliterating endarteritis. 
The intima of the vessel has undergone hyperplasia to the point of almost complete 
closure. Such a process in the vessels (arteries) of a limb leads to death of the limo 
(gangrene). This section was taken from the tissues of the hand from a case of Ray- 
naud's disease. 
curs, the number of capillaries in it is increased, and so 
as it heals there is increased opportunity for a second in- 
fection when bacteria are present in the blood. This ac- 
counts for the fact that a person who has had an acute 
endocarditis, is apt to have new attacks of the same 
disease. If reinfection does not occur, then the valves 
come to have more than normal fibrous tissue in them 124 
FUNDAMENTALS OF PATHOLOGY 
which makes them rigid, and as it contracts, pulls them 
out of shape so that the valve no longer holds the blood- 
is no longer competent. It produces valvular insuffi- 
ciency or incompetency. Later, when the contraction 
has gone so far as to obstruct the flow of blood, we have 
produced a valvular stenosis. 
When blood is hindered in passing through the heart 
it tends to be dammed back into the organs behind the 
valve. For instance, if the mitral valve is stenotic, then 
the left auricle is apt to be dilated; and the lungs will 
be the seat of a passive congestion, and also because the 
left auricle will do more work in pushing the blood past 
the mitral valve, it will undergo hypertrophy. The 
series of events applies in the case of each valve. When 
incompetency of a valve occurs much the same things 
occur. If the aortic valve is incompetent at each systole, 
some blood flows back to the heart from the aorta. The 
left ventricle consequently has more work to do, and this 
it meets by hypertrophy. Then it becomes fatigued in 
the long run and undergoes dilatation. Still later, the 
mitral becomes incompetent because of the ventricular 
dilation and then the series of changes occurs in the left 
auricle-and so on. 
The Blood Vessels. 
The blood vessels are the organs through which food 
(including oxygen) is carried to the various parts of 
the body. They are elastic tubes composed of layers 
of muscular, elastic, and white fibrous tissue, and are 
lined with endothelium. The smaller vessels, the capil- 
laries, are composed only of an endothelial membrane. 
So far as they can be separated from the blood itself, 
they are functionally important mainly because of their 
elasticity. This physical condition is dependent upon 
the quality of the blood, and modifications of it are THE CARDIOVASCULAR SYSTEM 
125 
probably invariably of toxic (organic or inorganic) and 
most frequently, infectious, origin. 
The musculature of the blood vessels is automatic in 
exactly the same way, though not in the same degree 
as is the cardiac muscle. Also it is affected in a similar 
way by the vasomotor system, which corresponds to the 
vagosympathetic system of the heart. 
So long as the quality of the blood is normal, the con- 
Fig. 40.-Myocardial fibrosis. The figure shows the presence of increased amount 
of fibrous tissue between the muscle fibers of the heart. When it is realized that prac- 
tically all of the area included in the photograph should be composed of muscle it will 
be seen to what an extreme degree the efficiency of the heart is decreased by loss of 
functional tissue. When so much of the muscle is lost the rest of the myocardium 
must do additional work to make up for the loss (hypertrophy), and when this remainder 
becomes overworked the heart fails, is less able to contract, and the cavities are 
dilated. 
dition of the musculature remains normal, and the blood 
pressure is preserved at a normal level. But let the 
quality of the blood vary and immediately the condition 
of the muscles is modified so that either it responds to 
otherwise inefficient stimuli, and contracts, or fails to 
respond even to normal stimulation and relaxes. In the 
first case the blood pressure rises and increased work is 126 
FUNDAMENTALS OF PATHOLOGY 
thrown upon the heart. In the second case the blood 
pressure falls, and again increased work is thrown upon 
the heart, or, the extreme may happen, all incentive to 
work is removed from the heart and it ceases. 
A consistently high pressure produces one or two ef- 
fects. It leads to cardiac hypertrophy and it leads, if it 
persists, in hypertrophy of the muscular coats of the ar- 
teries (so long as the supply of food is sufficient), or to 
degeneration and atrophy of the muscular coats (if the 
food supply is not equal to the demands). 
Tn toxic conditions the same things are true but are 
Fig. 41.-Atrophy of elastic tissue in wall of the aorta in atheroma. The elastic tissue 
is replaced by dense fibrous tissue. (Delafield and Prudden.) 
merely modified by the abnormal conditions which bring 
it about that fatigue of the muscles occurs earlier, and 
the gross lesions are more apt to be focal, particularly 
in those of infectious origin. 
When the muscle of the vascular system is damaged 
so that strain of the walls occurs, the stimulus of the 
strain is felt by the fibrous elements. The results of 
this in the vessels is the same as in other tissues, namely, 
fibrous hyperplasia, and since fibrous tissue is not elas- 
tic in the sense that either muscle tissue or elastic tis- 
sue is, the vessels become permanently inelastic. THE CARDIOVASCULAR SYSTEM 
127 
Even, however, with a comparatively high grade of 
inelasticity, the circulation may be maintained at a level 
consistent with the nutrition of the tissue. But let the 
lumens of vessels be diminished in caliber and the nutri- 
tion of the tissue suffers. Diminution of caliber occurs 
when there is a diffused toxic substance present in the 
blood; for instance, in lead poisoning. In this and sim- 
ilar conditions the vascular effect tends to be general- 
ized in the smaller vessels. 
In the great vessels the lesions tend rather to be focal 
than general, for the reason that the toxic effects tend 
to be produced first in the neighborhood of the vasa 
vasorum, in and about which the lesions are similar to 
those which occur in the smaller vessels, especially the 
arterioles, elsewhere. 
In old individuals, and in the absence of infection ar- 
teriosclerosis tends to appear as a combination of de- 
generative process, which involves the muscularis, asso- 
ciated with fibrosis. In such cases the lesion is a senile 
one. But the more serious form is that which occurs in 
younger persons and which is associated with, and char- 
acterized by, the changes we call inflammatory. This 
form is characterized by the very common syphilitic 
aortitis. 
Arteriosclerosis: 
Infections- (aortitis, arteritis). 
Noninfectious-senile arteriosclerosis. 
It is in arterial conditions that are characterized by 
focal degeneration and inflammation that abnormalities 
of the normal form of the lumen, such as dilatations, tend 
to appear. Such dilatations are called aneurysms. Such 
abnormalities occur also as a result of trauma, which 
produce localized weakening or breaks of continuity of 
the vessel walls. When the vessel wall forms the wall 
of an aneurysm, we speak of a true aneurysm. When it 
does not, we speak of a false aneurysm. 128 
FUNDAMENTALS OF PATHOLOGY 
It has been claimed by many that in the production 
of aneurysm, strain is the most important factor. This 
has been said because aneurysms tend to occur in indi- 
viduals who do heavy work. It seems however that 
strain is entirely secondary; that it is active only be- 
cause preceding it the vessel wall has been damaged so 
that a sudden increase in blood pressure is able to over- 
come the resistance at a diseased part. 
The blood vessels may also be affected by the inflam- 
matory process (arteritis, phlebitis), which do not lead 
to sclerosis. In some instances the vascular involvement 
follows a perivascular disease, in others it commences 
intravascularly (septicemia, septico-pyemia, embolism, 
etc.). Such inflammatory conditions result very com- 
monly in interruption of the blood flow. 
REFERENCES. 
Blood. 
Adami: Principles of Pathology. Phila., 1910. 
Aschoff: Thrombosis. Arch. Int. Med., November, 1913. 
Hunter: Severest Anaemias. London, 1909. 
Jores: Anatomische Grundlagen wichtiger Krankheiten. Berlin, 1913. 
Klemensiewicz: Die Pathologie d. Lymphstrbmung. Krehl u. March- 
land's Handb. d. allg. Pathologic, iii, 1, 1912. 
Krehl-Hewlett: Clinical Pathology. Phila., 1907. 
Marchand: Die Storung d. Blutvertheilung. Krehl u. Marchland's 
Handb. d. allg. Pathologie, iii, 1, 1912. 
Miller: Normal Differential Leucocyte Count. Bull. Johns Hopkins 
Hosp., 1914, xxv, 317. 
Paltauf, Freund u. Sternberg: Die Pathologie des Blutes. Krehl u. 
Marchland's Handb. d. allg. Pathologie, iii, 1, 1912. 
Trotter: Embolism and Thrombosis of the Mesenteric Vessels. Cam- 
bridge, 1913. 
Whipple: Haemorrhagic Diseases. Arch. Int. Med., Dec., 1913. 
Heart. 
Barach and Marks: Blood Pressures: Their Relation to Each Other and 
to Physical Efficiency. Arch. Int. Med., 1914, xiii, 648. 
Editorial: Auricular Fibrillation and the Changes in the Sinus Node. 
Jour. Am. Med. Assn., 1915, Ixiv, 911 (Literature). 
Fleisher and Loeb: Experimental Myocarditis. Centr. f. allg. Path., 
1909, xx, 104. 
Hedinger: Ueber Herzbefunde bei Arrhythmia perptua. Frankf. 
Ztschr. f. Path., 1910, v. THE CARDIOVASCULAR SYSTEM 
129 
Hirschfelder: Diseases of the Heart and Aorta. Phila., 1913 (Litera- 
ture). 
Krehl-Hewlett: Clinical Pathology. Phila., 1907. 
Lewis: The Mechanism of the Heart Beat. 1911. 
McKenzie: Diseases of the Heart. New York, 1910. 
Thalheimer and Rothschild: Experimental Focalized Myocardial Le- 
sions, etc. Jour. Exper. Med., 1914, xix, 429. 
Thorel: Pathologic der Kreislauforgane des Menschen. Ergeb. d. allg. 
Path. (Lubarsch-Ostertag), 1915, (17 Abth. 2) 90. (Sammelreferat.) 
Ritchie: The Action of thp Vagus on the Human Heart. Quart. Jour. 
Med., 1912, vi, 47. 
Warthin: Congenital Syphilis of the Heart. Am. Jour. Med. Sc. 
Wiggers: Does Cardiac Rhythm Alone Determine Human Blood Pres- 
sure Variations? Jour. Exper. Med., 1914, xix, 1. 
Woolley: The Fundamental Factors in Cardiac Conditions. Ohio State 
Med. Jour., 1912. 
Blood Vessels. 
Adami: Principles of Pathology. Phila., 1912. 
J ores: Anatomische Grundlagen wichtiger Krankheiten. Berlin, 1913. 
Kaufmann: Spezielle pathologische Anatomic. Berlin, 1911. 
Klotz: Arteriosclerosis. Publications of the University of Pittsburgh 
Medical School, Lancaster, 1911. 
Krehl-Hewlett: Clinical Pathology. Phila., 1907. 
Minervini: Ueber die Neubildung von Blutgefassen. Virchow's Arch., 
1911, cciv, 75. 
Moritz u. Tabora: Die allg. Pathologic d. Herzens und d. Gefasse. 
Krehl u. Marchand's Handb. d. allg. Pathologic, ii, Abth. 2, 1913. 
Thoma: Ueber die Histomechanic des Gefass-systems und die Patho- 
genese der Angiosklerose. Virchow's Arch., 1911, cciv, 1. 
Verszpremi: Ueber die Periarteritis nodosa. Zieg. Beitr., 1912, lii, 476. CHAPTER X. 
THE URINARY SYSTEM. 
This system is composed of the kidneys, the ureters, 
the urinary bladder and the urethra. In the kidneys 
the wastes of the body (free water, salts, and various 
other substances) are separated from the blood, and 
passed into the ureters and bladder and thence into the 
external world through the urethra. Lesions of the kid- 
ney result in retention of toxic materials in the blood. 
Lesions of the other parts of the tract cause interference 
with the discharge of urine. 
The Nephroses. 
The term nephrosis is an inclusive one. It includes 
all the diseases except tumors from which the kidneys 
suffer, from mere edema to the true inflammations, 
whether suppurative or non-suppurative. It therefore 
includes what we speak of a-s nephritis, or Bright's dis- 
ease. 
The term nephritis includes two conceptions: one of 
them clinical, the other histologic, or if you please ana- 
tomic. Clinically it means the presence of certain qual- 
itative or quantitative urinary variations, which are, 
generally speaking, increase or decrease of the total 
amount of urine and the presence of albumin and casts 
in the urine. In the anatomic sense it means this and 
something more. It means inflammation, which is to say 
the kidney is the seat of certain vascular and perivascu- 
lar changes which we associated with a very distinct his- 
tologic picture, in which vascular dilatation, congestion. 
130 THE URINARY SYSTEM 
131 
and exudation are in the foreground. Albumin and casts 
in the urine may be produced by any process which dis- 
turbs sufficiently the nutrition (or metabolism) of the 
renal cells. Inflammation is one such process. 
There are three main types of renal lesions. The sim- 
ple nephroses, including simple edema and simple ne- 
crosis; the nephritides or inflammatory nephroses; and 
the renal atrophies, including the arteriosclerotic and 
diffuse nephroses. 
Fig. 42.-In the kidney depicted in the illustration there are several infarcts of the 
white variety. These lesions if they are infected may undergo suppuration. If on the 
other hand they are "bland" they tend to heal by granulation and organization. 
The Simple Nephroses. 
This group is one which is fundamentally the most 
important. In it are included all those types of renal 
disturbance which are the result of partial or complete 
lack of oxygen, from the edema of the athlete, and that 
of the soldier on the march, both of which are benign 
and transient, to the sudden complete necrosis of in- 
farction. In it belong the toxic necrotic conditions which 
are the result of the action of organic or inorganic poi- 
sons. In all these albumin and casts appear in the urine; 
in all the quantity of urine is diminished. The main dif- 132 
FUNDAMENTALS OF PATHOLOGY 
ference that needs mention in discussing these simple 
nephroses, is that in the kidney, of edema, the organ may 
return to a completely normal condition very rapidly; 
in the toxic degenerated and in the infarcted kidney, the 
chances are that this does not occur, but that an increase 
of scar tissue is found as a part of a secondary inflam- 
matory process. In the case of the infarcts, the scar- 
ring is localized; in cases of certain chemical intoxica- 
tions, it is diffuse. 
Fig. 43.-An example of "chronic parenchymatous nephritis.'' Note that it is larger 
than normal and that it is exceedingly pale. 
The Atrophies. 
Similar in some respects to the simple nephroses are 
the atrophies. These, like the former, depend for their 
urinary phenomena upon lack of oxygen, hut the cause 
in this instance lies not in the composition of the blood, 
but in the condition of the blood vessels, which have been 
so changed by one or another factor, that the blood, qual- 
itatively perfect though it be, does not reach the cells in 
sufficient amounts over long periods of time to keep them 
at a physiologically active level. What happens to the THE URINARY SYSTEM 
133 
kidney in arteriosclerosis is exactly what would happen 
to the kidney of a modern simple edema, provided the 
edema were chronic, which is to say, provided the cir- 
culatory conditions remained the same. In the renal 
edema of the sprinter, the oxygen supply in the blood is 
not quite sufficient for the cells of the kidney. In the 
arteriosclerotic kidney, the oxygen in the blood is suffi- 
cient but it cannot reach the cells rapidly enough. The 
Fig. 44.-A specimen of acute nephritis associated with multiple fine hemorrhages. 
Note how diffusely the kidney is affected. It is also evidently swollen. Such an organ 
will obviously lead to a decreased output of urine. 
result of this decreased access of the cells to oxygen is 
that they undergo atrophy, become smaller, and some of 
them disappear, or if the progress of the vascular dis- 
ease is somewhat more rapid they undergo degeneration 
and disappear, and in vanishing leave the stroma of the 
organ apparently more abundant, relatively increased, 
and this tends to produce the appearance of sclerosis or 
fibrosis in the organ. Actually such an atrophic organ 134 
FUNDAMENTALS OF PATHOLOGY 
contains no more fibrous tissue than a normal organ,-it 
merely possesses less parenchyma. 
The Nephritides. 
This group of the nephroses is characterized, so far 
as the renal parenchyma is concerned, by all the ana- 
tomic changes which are present in the former groups, 
and by certain other features, which are clearly inflam- 
Fig. 45.-As time goes on with a chronic diffuse nephritis, there is a gradual de- 
crease in the amount of parenchyma and an increase in fibrous tissue. The organ 
becomes smaller and more or less distorted in shape. Such an organ is referred to as 
one of "secondary contraction." 
matory. In all the types one phenomenon dominates the 
picture, and that is the one we term exudation which 
may or may not be associated with fibrosis. It is from 
the obviousness of the associated fibrosis that we are 
led to speak of an acute or a chronic inflammation. 
Fibrosis in the absence of exudation does not spell in- 
flammation, though it may be a sequel of it. A sclerotic 
kidney is not necessarily one of interstitial nephritis. 
It has been customary to speak of parenchymatous and THE URINARY SYSTEM 
135 
interstitial nephritis, and of hemorrhagic and suppura- 
tive, and as glomerular, tubal, and diffuse, and further 
as acute and chronic. These terms are however merely 
helpful in characterizing nephritides from the stand- 
point of general extent. The process in all the cases is 
the same. It varies only in the extent to which it af- 
fects the kidney, in the type of exudation, and the rapid- 
Fig. 46.-The so-called "embolic kidney." The lesions are due to the presence of 
small pieces of infected material which have reached the kidney from some other part 
of the body. Not infrequently this material comes from vegetations on the heart valves. 
The lesions are small abscesses. 
ity of its development. All forms of inflammation are 
essentially interstitial in type, and the peculiar and some- 
times characteristic changes which one observes in the 
parenchyma are secondary ones due to disturbances of 
metabolism resulting from poisons which reach the cells 
from foci of inflammation, or from lack of oxygen which 
is the result of perivascular conditions. There are times 
when these secondary changes dominate the picture; 
when the parenchyma has undergone fatty or soapy de- 136 
FUNDAMENTALS OF PATHOLOGY 
generation, as, for example, in the "large white kidney.'' 
Under such circumstances we have been in the habit of 
speaking of a chronic parenchymatous nephritis, a desig- 
nation which we may preserve provided we realize that 
it is but a type of interstitial nephritis with abundant 
secondary degeneration-a diffuse nephritis. This is 
very reasonable, because if we study the other classical 
type of kidney, the "small red" one, we find similar 
changes, though not so evident. In this the focal in- 
flammatory fibrosis dominates the picture, and obscures 
the parenchymatous changes. In all nephritides paren- 
chyma and interstitial tissue are both affected, but in 
Fig. 47.-When the smaller blood vessels of the kidney are generally affected by the 
arteriosclerotic process, or when there is in the kidney a chronic interstitial inflamma- 
tory process going on, the kidney becomes generally contracted and finely granular as 
to its surface. Such an organ is called that of "chronic interstitial nephritis." 
one the degenerative changes predominate; in the other, 
the productive. Perhaps it is best to speak of diffuse 
and focal nephroses. All of these remarks apply equally 
to the suppurative and tuberculous kidneys. In these 
the only difference is that the lesions tend to be more 
obviously and completely focal than even in the inter- 
stitial form, and therefore they acquire specific char- 
acteristics. 
Now this would all be very simple were the forms of THE URINARY SYSTEM 
137 
nephroses simple, which, as a rule, they are not. As a 
rule they are combined, at least this is apt to be almost 
completely true except in cases in which death has been 
produced suddenly by trauma. That the conditions ex- 
isting in the kidneys may undergo sudden changes is 
shown in many clinical cases. For instance, a person 
who has a well developed interstitial type of nephrosis 
does very well for long periods of time. The vascular 
and perivascular changes have advanced to such a stage 
Fig. 48.-When the larger vessels of the kidney are affected by the arteriosclerotic 
process and when this process is not as diffuse as in the former type, the kidney 
becomes focally affected and contracted. It is then known as the "arteriosclerotic 
kidney." 
that the compensatory powers of the organ are quite 
limited. Much of the parenchyma has disappeared, but 
the portion which remains is physiologically active and 
produces a normal amount of fluid, with little or no al- 
bumin and few or no casts. If at such a time he meets 
a sudden traumatic death, the kidney would appear as a 
' ' small red kidney, ' ' a primarily contracted kidney. But 
let him suffer an attack of enteritis; let him absorb a 138 
FUNDAMENTALS OF PATHOLOGY 
few more colon bacilli; a too large quantity of poison- 
and lie dies in uremia and the kidney at postmortem is 
apt to be gray and then we are apt to say that it is a 
"secondarily contracted kidney," or small gray kidney. 
And it is quite probable that under such conditions un- 
less he makes use of the clinical details, the pathologist 
may insist that what he finds tells the whole story. 
CORTEX. 
-Artery 
- VEirV 
MEDULLA 
Fig. 49.-This illustrates very schematically the blood supply of the kidney. It 
shows that the colateral blood supply between the anatomic parts of the organ is a 
very slender one-that the arteries of the kidney like those of the spleen, lungs, in- 
testine, heart, and brain, are functional or physiological end-arteries. From the stand- 
point of vascular disturbances, this means that a sudden blocking of one of the end 
arteries (embolism) will result in death of the tissue in the area supplied by the ob- 
structed vessel (infarction), and that gradual closing of the vascular lumen (arterio- 
sclerosis, or thrombosis) will lead rather to atrophy of the tissue. Atrophy of this 
area will lead eventually to decrease in volume while adjacent areas will retain their 
size, or, because of the additional work thrown upon them, will become somewhat larger 
(compensatory hypertrophy). The result will be a surface with a depression for each 
area of atrophy (granular kidney). THE URINARX SYSTEM 
139 
Classification. 
It would seem then that for the sake of simplicity the 
following classification would be serviceable: 
A. The diffuse nephroses-(acute intoxication). 
Simple edema, and necrosis. 
Acute diffuse nephritis (acute Bright's). 
Glomerular nephritis. 
Hemorrhagic nephritis. 
Chronic passive congestion. 
Chronic diffuse nehpritis (chronic parenchyma- 
tous nephritis). 
Glomerular nephritis. 
B. The focal nephroses-(vascular or infective). 
Infarction. 
Arteriosclerosis. 
Acute interstitial (septic or simple) nephritis. 
Chronic interstitial nephritis. 
C. Combinations of focal and diffuse forms. 
Such a classification has one value, if no other, namely, 
that it allows of a better understanding of the urinary 
findings, that is to say it permits the clinician and the 
pathologist to stand a little closer together. 
Urinary Changes in the Nephroses. 
i. Diffuse nephroses-(acute and chronic). 
Decrease of urine. 
Casts present. 
Albumin in very noticeable amounts. 
ii. Focal nephroses- 
A. Acute- 
Urine may be decreased depending upon 
the number and extent of the lesions. 
Casts present. 
Albumin in moderate amounts. 140 
FUNDAMENTALS OF PATHOLOGY 
B. Chronic- 
Little or no decrease of urine. 
Few or no casts (these come from the dis- 
eased foci). 
Little or no albumin. 
in. Combination forms- 
The urinary changes vary. 
REFERENCES. 
Barker: The Commoner Forms of Renal Disease, etc. Am. Jour. Med. 
Sc., January, 1913. 
Brewer: Hematogenous Infection of the Kidneys. New York Med. 
Jour., 1915, ci, 556. 
Bright: Clinical Lectures on Abdominal Tumors and Intumescence. 
London, 1860, Sydenham Soc. Ed., 198 et seq. 
Cohnheim: Lectures on General Pathology. New Sydenham Soc. Ed., 
1890, iii. 
Councilman: Med. and Surg. Reports, Boston City Hospital. Boston, 
1897. 
Councilman: The Pathology of the Kidney. Jour. Am. Med. Assn., 
1906, xlvi, 81. 
Fischer: Oedema and Nephritis. New York, 1915. 
Hewitt: Necrosis of the Epithelium in the Kidney in Infections and 
Intoxications. Bull.' Johns Hopkins Hosp., 1906, xvii, 272. 
Osler: Practice of Medicine. 
Volhard and Fahr: Die Brightsche Nierenkrankheit. Berlin, 1913. CHAPTER XI. 
THE RESPIRATORY SYSTEM. 
The respiratory tract is a system of organs by means 
of which the oxygen of the air is taken into the body and 
so distributed that it can be absorbed into the blood. It 
also acts as the means by which the body is able to rid 
itself of a certain proportion of the gases formed with- 
in the body and held in the blood. This interchange of 
gases takes place in the alveoli of the lungs from which 
there is a clear passageway to the exterior of the body. 
Any lesion which disturbs this interchange is important 
because it interferes with the ventilation of the body. 
External respiration may be disturbed by limiting the 
amount of air which can be inspired, or by limiting the 
ability to inspire. In the first case we must consider 
the quantity of air surrounding the body. In the second 
case we have to deal with effects which prevent expan- 
sion or contraction of the normal lungs or with changes 
in elasticity in abnormal lungs. On the one hand the 
lungs are unable to expand because of extrinsic difficul- 
ties ; on the other, because of intrinsic ones. 
Extrinsic conditions-(exclusive of qualitative or quan- 
titative variations in the surrounding air). 
Any extrapulmonary pressure. 
Fluid in the pleural cavities. 
Air in the pleural cavities. 
Pleural adhesions. 
Paralyses of the respiratory muscles. 
Intrinsic conditions- 
Acute inflammations. 
141 142 
FUNDAMENTALS OF PATHOLOGY 
Pulmonary fibrosis (chronic inflammations; kon- 
ioses). 
Edema. 
Emphysema. 
Bronchial inflammations. 
Muscular contraction of bronchial muscle (asthma). 
Tumors. 
Internal respiration (gaseous interchange) is modified 
by variations in the quantity and quality of the blood 
which passes through the pulmonary and bronchial ves- 
sels and by variations in the area of the respiratory sur- 
face. The rate of the blood flow is an important factor 
in internal respiration, since when the blood flow is slow, 
as in chronic congestions, carbon dioxide tends to accu- 
mulate in the blood just as surely as though respirations 
were partially suspended. When such a condition arises 
a secondary condition of edema tends to be produced 
which has a direct effect upon external respiration. On 
the other hand, when the respiratory surface is dimin- 
ished as is the case in the pulmonary consolidations, the 
air has not the normal access to the walls of the alveoli 
where the gaseous interchange takes place. 
Blood and vascular conditions- 
Slowing of the pulmonary circulation. 
Chronic passive congestion. 
Arteriosclerosis. 
Interference with the bronchial circulation. 
Edema. 
Pulmonic conditions- 
Consolidations. 
Bronchial obstruction. 
The most frequent abnormal pulmonary conditions are 
infectious in origin and although they are preeminently 
toxic in their effects on the body as a whole, they also 
produce mechanical difficulties which result from the ef- THE RESPIRATORY SYSTEM 
143 
fects upon respiratory surfaces, that is to say, from 
the edemas and the frequently associated inflammatory 
changes. 
The mechanical effects follow several sorts of causes, 
chief among which are the obstructions, complete and in- 
complete. Among the latter are the stenoses. The chem- 
ical effects are illustrated in the infections, particularly 
in cases in which less than half the pulmonary tissue is 
involved, or in other cases, like diphtheria, in which there 
Fig. 50.-This illustrates schematically the respiratory tract with the two nares (1); 
the mouth (2) ; the pharynx and larynx, the trachea (3); the main bronchi (4), and 
the terminal bronchi. If the nares are obstructed, respiration is carried on through 
the mouth. In the upper respiratory tract there are therefore alternative pathways 
for the air. If, however, the trachea is obstructed, the entrance of air tends to be 
completely cut off. At the epiglottis an edema of comparatively slight degree may 
produce asphyxiation. The farther one proceeds out in the respiratory tract, the less 
danger is there of asphyxiation. The small rounded area illustrates what is meant by a 
locus of lobular pneumonia (bronchopneumonia). The larger area is intended to repre- 
sent an area of lobar pneumonia. 
may be no hindrance to inspiration or expiration. Since 
it has been shown that a gradual reduction of the pul- 
monary tissue to one-sixth the normal amount is com- 
patible with life, it will be apparent that the majority 
of pulmonary lesions are important rather from the 
chemical than the mechanical point of view, and that 144 
FUNDAMENTALS OF PATHOLOGY 
except for a relatively small group of cases, most of the 
lesions of the respiratory tract are of vital importance 
because of the chemical conditions that develop. 
If we consider the anatomic arrangement of the re- 
spiratory tract we find that it is composed of three an- 
atomically (mechanically) important parts-the nasal 
part, the tracheal part, and the bronchial part. 
The nasal portion forms the normal entrance for air. 
It serves as a warming oven, and as a filter. It is only 
when it is damaged in one or another way that the ac- 
cessory path (the oral) is used. When this accessory 
path is used the air is not sufficiently warmed or filtered, 
and the opportunities for irritation and infection of the 
pharynx, trachea, bronchi and the lungs themselves are 
multiplied. One of the most frequent causes of disease 
of the nasal passages is adenoid growths in the pharynx; 
another is inflammation of the mucous membrane of the 
nasal cavities with consequent swelling of the tissue 
(coryza). 
The tracheal portion of the tract is a single pathway. 
It therefore is that part of the respiratory system in 
which a mechanical defect produces the most serious re- 
sults. External pressure of enlarged adjacent organs, 
such as the thymus or lymph glands, often produces the 
most serious effects, as illustrated in edema of the glot- 
tis and inflammations, often producing effects upon the 
respiration altogether out of proportion to the size and 
extent of the lesion. 
The bronchial portion of the tract begins as a double 
pathway, which rapidly breaks up into many fine sub- 
divisions, the bronchioles, which terminate in the infun- 
dibula and air vesicles. In this part of the tract there 
are many opportunities for damage which may produce 
little or no general disturbance. This is especially true 
of the mechanical effects. It makes a great deal of dif- 
ference, however, whether an obstruction occurs in one THE RESPIRATORY SYSTEM 
145 
of the main bronchi or in one of the small bronchi be- 
cause the nearer to the trachea an obstruction exists the 
greater the area of respiratory surface which is affected. 
Fig. 51.-Lung. Subacute tuberculosis with some fibrous overgrowth towards upper 
part of lung, and showing acute peribronchial spread into the lower lobe. (Edinburgh 
University Anatomical Museum. Catalogue No. R.C.e.6.) (Beattie and Dickson.) 146 
FUNDAMENTALS OF PATHOLOGY 
The rapidity with which an obstruction develops is a 
very important item in the production of symptoms, for 
whereas five-sixths of the lung tissue may be eliminated 
Fig. 52.-Lung. Chronic phthisis, showing a large irregular cavity in the upper 
lobe. In the lower lobe there are scattered acute nodules grouped in clusters around 
the small bronchi; and also several small more acute cavities. The bronchial glands 
are enlarged and caseous. (Edinburgh University Anatomical Museum. Catalogue No. 
R.C.g. 10.) (Beattie and Dickson.) THE RESPIRATORY SYSTEM 
147 
it* this be done only gradually, a sudden obstruction 
which involves less than one-half of this same tissue may 
and not infrequently does prove fatal. In certain cases 
of pulmonary tuberculosis one finds that at least three- 
fourths of the respiratory surface has become valueless, 
functionally, before death has occurred, but a perfora- 
tion of the pleura which allows air to enter the pleural 
cavity (pneumothorax) and compress one lung, may 
prove fatal. 
The causes of respiratory insufficiency are as follows: 
I. Physical-(disturbances of ventilation). 
Obstructions to entrance and exit of air: 
Nasal-Hyperemia, including the inflamma- 
tory type, septal deformities, turbinate de- 
formities, foreign bodies, tumors. 
Pharynx-Adenoid growths, edemas, periton- 
sillar and peripharyngeal inflammations, tu- 
mors. 
Larynx-Edema of the glottis, acute inflam- 
mations, tumors, paralyses. 
Trachea-Inflammations, external pressure 
(thymus, thyroid, lymph glands), foreign 
bodies, paralyses. 
Bronchi-Inflammations, muscular spasm (us- 
ually associated with edema), foreign bod- 
ies, pressure of enlarged lymph glands 
(tumors, inflammation). 
Lungs-Edema, chronic congestion, infarc- 
tion (embolism), inflammations, tumors. 
Loss of elasticity including increased external 
pressure (limitation of expansion). 
Pulmonary fibrosis (anthracosis, chronic pas- 
sive congestion). 
Emphysema, pneumothorax, hydrothorax. 148 
FUNDAMENTALS OF PATHOLOGY 
The chemical factors in pulmonary disease are, as a 
rule, associated with abnormal physical conditions. 
II. Toxic-(disturbances of metabolism). 
Bacterial-The inflammations, pneumonias, 
bronchitides, laryngitides, tracheitides. 
Irritating gases-Ammonia, chlorine, sul- 
phurous acid, etc. 
REFERENCES. 
Adami: Principles of Pathology. 1909, ii, 237. 
Alwens and Frick: Ueber die Localization von Embolien in der Lunge. 
Frankf. Zeits. f. Path., 1915, xxvi, 12. 
Fischer: Pulmonary Oedema. Oedema and Nephritis, 1914. 
Haldane: Pembrey and Ritchie's General Pathology. 1913, 432. 
Kaufmann: Lehrbuch d. Spezielle Pathologic. 
Kline and Winternitz: Studies upon Experimental Pneumonia in Rab- 
bits. Jour. Exper. Med.. 1915, xxi, 304. 
Miller and Matthews: Experimental Acute Pulmonary Edema. Arch. 
Int. Med. 
Minkowski u. Bittorf: Krehl u. Marchand's Handb. u. Allg. Pathologic, 
1912, ii, 456. 
Moncreeberg: Zur pathologischen Anatomic d. Bronchialasthmas. Ver- 
handl. d. deutsch. path. Gesellsch, 1909, p. 173. 
Neusser: Dyspnoea and Cyanosis. New York, 1907. 
Starling: Human Physiology. 1912, 979. CHAPTER XII. 
GASTROINTESTINAL SYSTEM. 
What we call gastrointestinal diseases are expressions 
of alterations of function in one or more parts of the 
gastrointestinal system. They are commonly confused 
with symptoms, such as hyperacidity, hypoacidity, hy- 
permotility and hypomotility, which are not diseases, 
but symptoms of disease. Sometimes they are associated 
with symptoms in other parts of the body than the gastro- 
intestinal tract, and such symptoms call attention to the 
fact that the various organs of the body are not truly 
separated or independent, but that they are actually de- 
pendent upon one another. So with gastrointestinal up- 
sets the nervous system may be affected, or the urinary 
system, and it is from these distance effects that we have 
come to make so much of a group of symptoms, which 
may be combined into different complexes, in different 
individuals, which we call, comprehensively, gastrointes- 
tinal intoxications or, also, autointoxication. 
In order to be clear in our conceptions we should con- 
sider first of all the functions of the organs comprising 
this tract or system. 
The function of the stomach and of the intestines also 
is to contain and retain food for a certain period of time 
during which the food is chemically changed by means 
of ferments. In order to fulfill this function it must be 
capable of expansion, and, in order to expel the contents 
at the proper time it must be capable of returning to its 
original size. In other words, it must be elastic and 
contractile, and the elasticity and contractility are chiefly 
the result of the condition of the musculature. The func- 
149 150 
FUNDAMENTALS OF PATHOLOGY 
tion of the intestine is to carry the food from the stom- 
ach to the external world and at the same time to allow 
time for absorption of foodstuffs into the body. This 
function depends upon elasticity and contractility and 
here again the contractility is mainly dependent upon 
the condition of the musculature. In other words, the 
function of the gastrointestinal tract, so far as motility 
(contractility) is concerned, is dependent upon the con- 
dition of the muscularis, and so disease tends to be pro- 
duced by variation in the elasticity and •motility of the 
various portions of the gastrointestinal tract. 
It is these qualities of elasticity and contractility which 
present stasis in the intestinal tract. Normally the va- 
rious segments of the tract act in such harmony that 
the contents are gradually pushed along to their nor- 
mal destination in a certain normal time. A healthy 
bowel will not permit of stasis but will carry on its 
motor functions with ease and regularity. To assist 
in this function there must be a coordinating or regulat- 
ing mechanism. This Keith believes he has found in 
the myenteric (Auerbach's) plexus. He finds that at 
certain points this plexus is concentrated to form masses 
(or nodes) which correspond to the nodes in the con- 
ducting tissue of the heart, and that at these nodes new 
rates of peristalsis are inaugurated and persist through- 
out the segment to which they belong. Evidently disease 
of the gastrointestinal tract may occur because of in- 
terference with, or damage to, the myenteric coordinat- 
ing system. 
In order that the food shall be properly prepared for 
absorption, the necessary kinds and amounts of ferments 
must be secreted by the glands of the gastrointestinal 
tract and by the accessory glands, and in order that these 
shall act properly the contents of the tract must have 
the proper chemical reaction. In the stomach the reac- 
tion must be acid; in the intestine it must be alkaline. GASTROINTESTINAL SYSTEM 
151 
Therefore variations in the quantitative secretion of the 
various digestive fluids and in the qualitative composi- 
tion of them, tends to produce disease. 
Gastrointestinal disease arises from abnormal changes 
in elasticity, motility (contractility), segmental coordi- 
nation, secretion of ferments, and (chiefly) chemical re- 
action. 
When we consider these four groups we find that we 
can most usefully combine them into two large groups, 
for we find that changes in elasticity and motility are 
apt to occur together; and that changes in production 
of ferments and the chemical reaction of the juices are 
apt to be combined. Also we discover that each of these 
groups are interwoven to such an extent that it is not 
possible to separate them completely. 
The normal course of events in gastric digestion is 
briefly as follows: 
Food enters the stomach and is there kneaded and 
thoroughly mixed with gastric juice so that the ferments, 
chiefly pepsin, may act upon the proteins. For the fer- 
ment action, a certain degree of acidity is necessary. 
After a certain time the partially digested food is ex- 
pelled through the pylorus and enters the duodenum. 
What we call gastric indigestion may depend upon a 
break at any point in this process, i. e., the muscular 
movements of the stomach may not be sufficiently active 
to produce thorough mixture of the food and the gas- 
tric juice; the gastric juice may not contain sufficient 
pepsin to accomplish a normal result; the acid content 
of the gastric juice may be below or above normal, and 
then in either case the food may be held too long in the 
stomach and then undergo abnormal changes which lead 
to more or less disturbing symptoms or distress. 
How shall we account for variations in gastric motil- 
ity? There is a variation that occurs normally and 
which depends upon the nature of the ingested food. 152 
FUNDAMENTALS OF PATHOLOGY 
For instance, carbohydrate foods pass through the stom- 
ach most rapidly, proteins are next and fats are slow- 
est. We can say at once then, that a diet very rich in 
fats will hinder the passage of foods through the stom- 
ach. Moreover the ingestion of oils decreases the 
amount of gastric juice, while ingestion of proteins in- 
creases it, and carbohydrates (bread) produce a juice 
of greatest digestive power. These facts account for 
the ordinary effects of dietary indiscretions which are 
commonly transient, but which may persist, if the indis- 
cretions are persisted in, and produce other less tran- 
sient effects resulting in structural changes. 
Now it is quite possible that these normal variations 
in motility are the result of modification in the acid con- 
tent of the gastric juice. We know the opening and clos- 
ing of the pylorus are due to the reaction of the food- 
i. e., they depend upon the presence of a certain amount 
of free acid. We know that ingestion of carbohydrates 
produces an abundant active secretion, and we know that 
carbohydrates are less active in neutralizing the acid (by 
chemical combination) than the proteins which also pro- 
duce an abundant secretion. We would expect then, that 
the carbohydrates would pass through the stomach more 
rapidly because they permit the acid to accumulate, and 
that the proteins would remain longer in the stomach be- 
cause in combining with the acid they reduce the acidity 
of the gastric contents. Fats and oils, on the other hand, 
reduce the quantity of juice and therefore the acid is 
slow in accumulating. 
When the emptying of the stomach is unduly impeded, 
there is opportunity for fermentation to occur in the con- 
tents. We constantly swallow bacteria with our food, 
but commonly these organisms are rendered harmless 
because their activities are hindered by the hydrochloric 
acid. With a decrease of acid they are allowed to act 
upon the food, and in doing this they produce abnor- GASTROINTESTINAL SYSTEM 
153 
mal acids and gases. The former act upon the mucous 
membrane producing inflammatory effects; the latter 
produce distention or "bloating." 
Immediately inflammation is produced, an increased 
amount of mucus is produced, and mucus, being alkaline 
in reaction, neutralizes more hydrochloric acid, and 
therefore assists in hindering the passage of food into 
the intestine. The same stimulation which produces the 
increase in mucus, irritates the functional cells, so that 
eventually they become fatigued and produce- less secre- 
L IV£|> . 
He h 0.1^ 
' 3uc.r 
B/adLdQj^ - 
CysT.c 
3u<r- 
Ofv>m oh 
■Zk> cT* 
t«n Clre 
Qu ct - 
Th T^T<n». 
Fig. 53.-This is a schematic sketch to illustrate the arrangement of the bile passages 
and the effects of lesions in them. Bile formed in the liver is stored in the gall bladder 
from which as occasion demands, it passes into the small intestine. An obstruction in 
the cystic duct does two things; it prevents the storage of bile, and it prevents what 
bile happens to be in the bladder from reaching the intestine. No clinical symptoms 
follow either of these eventualities. On the other hand an obstruction in either the 
hepatic duct or in the common duct prevents the bile from reaching the intestine and 
jaundice (icterus) results. Blocking of the pancreatic duct hinders the pancreatic secre- 
tion from the intestine and so leads to a certain type of indigestion. If an obstruc- 
tion occurs in the common duct below the entrance of the pancreatic duct, bile may 
be forced into the latter and cause pancreatic disease. 
tion. The result of this is that further fermentations 
are assisted and so (the disease we call it) becomes 
chronic. When this stage is reached-when inflamma- 
tion has become chronic, fibrous tissue is produced in 
the wall of the stomach, the functional cells atrophy and 
disappear, the mucous membrane becomes thin and grad- 154 
FUNDAMENTALS OF PATHOLOGY 
ually becomes less and less able to produce the neces- 
sary amount of acid or ferments. When this stage is 
reached, an incurable condition has been produced. Be- 
fore it is reached, there is no incurable stage,-only 
each more advanced stage is less easily remedied. 
But oftentimes it is not so much the relative amounts 
of carbohydrates, proteins, or fats that is the original 
cause of indigestion. More frequently it is the quality 
of the food or other substances that gain entrance to 
the stomach. Very hot food or drink, very cold drinks, 
alcoholic beverages, highly spiced foods-all are far 
more frequent causes. These act by the virtue of their 
irritative action on the mucous membrane. They pro- 
duce hypersecretion of mucus and the related stages of 
fermentation that have already been mentioned, or they 
cause hypersecretion of gastric juice with subsequent 
atrophy or hypertrophy of the mucous membrane, re- 
sulting on the one hand in absence of secretion or, on 
the other, in more or less permanent hypersecretion. 
What has been said concerning the stomach applies 
with very few variations to the intestines. Changes in 
motility, in secretion and absorption depend largely up- 
on factors which are introduced from without, and very 
commonly are associated with gastric disturbances. Gas- 
tric fermentations are prone to lead to intestinal dis- 
ease, and variations in gastric acidity lead to modifica- 
tions in the production of pancreatic ferments. In the 
course of these general modifications which result from 
gastrointestinal disease then are produced the most va- 
rious diseased conditions in other organs which cause the 
symptoms which belong to what we often call the gastro- 
intestinal intoxications. 
But all gastrointestinal disease does not depend upon 
abnormal processes which are primary in the stomach 
and intestines. Some are the results of changes which 
are primary in the liver or in the pancreas. As a result GASTROINTESTINAL SYSTEM 
155 
of certain changes, quantitative or qualitative varia- 
tions in the secretions of these organs are produced, 
and these variations are of far reaching importance. 
It will be remembered that all the above-mentioned 
juices are poured into the intestine, immediately after 
the entrance of the acid gastric chyme into the duode- 
num, apparently as a result of the action of the acid. 
All the intestinal secretions are alkaline. They there- 
Fig. 54.-Section of a bit of "fatty liver." Note that there is fully as much fat, 
which appears as clear space in the photograph, as active liver tissue. Such changes 
occur either because the organ is not able to burn the fat brought to it or because too 
much fat reaches it by way of the blood stream. 
fore tend to neutralize the acid of the gastric juice and 
therefore they produce the conditions which are neces- 
sary for opening of the pylorus. So long as the duode- 
nal contents are acid, the pylorus remains closed. An 
insufficient amount of alkaline juice from the digestive 
glands tends to produce disease. 
The activity of the pancreatic juice depends upon the 156 
FUNDAMENTALS OF PATHOLOGY 
activation of its proteolytic pro-enzymes by enterokinase 
which exists in the succus entericus, which is caused to 
How by the presence of pancreatic juice in the intestines. 
Absence of enterokinase tends to produce disease. 
The flow of all the intestinal juices, pancreatin, bile 
and succus entericus, is brought about by the action of 
the secretion (produced in the cells of the intestines by 
the action of the acid gastric chyme) upon the cells of 
the pancreas, liver, and intestinal glands. Absence of 
sufficient acid in the gastric juice tends to produce lack 
of intestinal secretion, and hence to produce intestinal 
disease. 
If the pancreatic juice is not activated, proteolytic 
Fig. 55.-Tuberculous ulcers of the small intestine. Showing the extension of the 
ulcers in a direction transverse to the axis of the gut. (Delafield and Prudden.) 
digestion suffers. If the bile is not present in sufficient 
amounts, the utilization of the fats of the food is re- 
duced or hindered. The conditions produced in this way 
are ones that result from insufficient preparation and 
absorption of food. The insufficient preparation allows 
of increased bacterial activity and tends to the produc- 
tion of abnormal substances, or substances in abnormal 
amounts, which, being absorbed, may give rise to intoxi- 
cations, providing they are not neutralized. 
But aside from these there are changes which occur 
in the glandular organs themselves which produce sim- 
ilar effects. Diseases of the liver, of the pancreas, of 
the wall of the intestines, produce the same effects. In GASTROINTESTINAL SYSTEM 
157 
this group we have the fibroses of the liver and the bile 
passages which decrease the flow of bile and produce 
qualitative changes in it. Inflammation of the pancreas 
or its ducts produces quantitative and qualitative effects 
upon the pancreatic juice and similar changes in the wall 
of the intestines tend to reduce the formation of entero- 
kinase and secretin. 
Just as gastrointestinal disease may have its starting- 
point outside that tract, in the accessory glands in the 
abdominal cavity, so also it may have its origin in the 
mouth. The mouth is the most important portal of in- 
Fig. 56.-Subserous tubercles following the lymph-vessels at the bottom of a tuberculous 
ulcer of the small intestine. (Delafield and Prudden.) 
fection of the body, and is perhaps more prone, espe- 
cially in the years after the first decennium, to infection 
than any other part of the body. Moreover diseases of 
the mouth, especially those in which the teeth are in- 
volved, are every day assuming greater importance in 
medicine. It is becoming more and more evident that 
the lesions of many accepted clinical complexes are sec- 
ondary to primary infections of the oral cavity and also 
that many obscure symptoms are the sequels of chronic 
focal infections which in very many cases are located 
in the teeth or in their surrounding tissues. Hence it 158 
FUNDAMENTALS OF PATHOLOGY 
is that pyorrhea alveolaris and peridental and dental 
abscesses are becoming of as great importance to the 
physician as to the dentist, and that there is every rea- 
son to believe that, in certain directions at least, the 
Fig. 57.-An alveolar abscess at the root of an upper molar discharging into the 
maxillary sinus, a, Abscess cavity; b, Mouth of sinus in the floor of the antrum; 
c, Pus in the antrum; d, Nasal cavity; e, Tooth; f, Tissues of the cheek. (After 
Black.) 
Fig. 58.-An acute alveolar abscess from the buccal roots and a chronic one from 
the lingual root of an upper molar, a, Cavity of acute abscess in the bone; b, Pus 
cavity between bone and periosteum; c, Tissue of cheek; d, Tooth; e, Maxillary sinus; 
f, Nasal cavity; g, Malar process; h, Chronic abscess discharging at i. (After Black.) 
Fig. 57. 
Fig. 58. 
Fig. 59. 
Fig. 60. 
Fig. 59.-Alveolar abscess from buccal roots of an upper molar discharging on the 
face, a, Abscess cavity in bone; b, Sinus opening on the face; c, Maxillary sinus; 
d, Nasal cavity; e, Tooth, f, Tissues of the face. (After Black.) 
Fig. 60.-Scar remaining from a sinus following an alveolar abscess. (After Black.) GASTROINTESTINAL SYSTEM 
159 
practice of dentistry will have to be revolutionized even 
as medical views concerning the importance of the mouth 
as a source of generalized disease are being changed. It 
is coming to be realized that foci of infection in or about 
the mouth may be the starting points of such so-called 
diseases as rheumatism, endocarditis, appendicitis, gall- 
bladder disease, gastric ulcer, osteomyelitis, hay fever, 
asthma, urticaria, and even certain goiters. When we 
say in or about the mouth we have reference to the ton- 
sils, the nasal sinuses and antra, as well as the teeth and 
peridental tissues. 
The reason why the mouth is so apt to be a primary 
source of trouble is that it, more than almost any other 
part of the body, is exposed to the action of external 
injuries, and that modern habits of eating and drinking 
produce conditions which, without proper precautions, 
lay the foundations for various sorts of local and gen- 
eral trouble. Too hot or too cold foods taken into the 
mouth do two things-they injure the epithelial sur- 
faces and so predispose to infection, and they tend to 
damage the teeth and make them more easily attacked 
by bacteria. Food which is too carefully chosen for 
tenderness and easy mastication, or which is finely di- 
vided, tends to collect between the teeth or along the 
margins of the gums, and there ferment. Thereupon 
inflammations or caries, or both, result. The more an- 
tique habit of not eating hash but of exercising the teeth 
and gums on the food made the toothbrush less essen- 
tial for health than it now is. Cattle which are fed on 
soft food,-as, for instance, still slops,-almost ex- 
clusively, have dental trouble that animals under normal 
circumstances never have. It is exercise which keeps 
the teeth and gums in good condition and if this can- 
not be accomplished by means of the food, some other 
agent is required and this is usually the toothbrush as- 
sisted too frequently by the dentist's drill. Dental floss 160 
Fundamentals of pathology 
Fig. 61. 
Fig. 62. 
Fig. 61.-Acute alveolar abscess from a lower incisor "pointing" on the gum. 
(After Black.) 
Fig. 62.-Acute alveolar abscess from a lower incisor forming a pocket beneath the 
periosteum. (After Black.) 
Fig. 63.-Chronic alveolar abscess at the root of a lower incisor with a sinus opening 
on the gum. 
Fig. 64.-Chronic abscess with sinus opening through the skin beneath the chin. 
Fig. 65.-Chronic abscess which has involved the maxilla and finally penetrated it 
and the skin beneath the chin. 
Fig. 63. 
Fig. 64. 
Fig. 65. GASTROINTESTINAL SYSTEM 
161 
takes the place of the older meat fibers which stuck be- 
tween the teeth and had to be picked out after the pran- 
dial exercises (or even sometimes during them). In 
this process the spaces between the teeth were cleaned. 
From the standpoint of dentistry it is important to 
remember that crowns and bridge-work, as they are too 
commonly applied, while they may be something of a 
convenience, are nevertheless a very real danger in pro- 
ducing focal and general infections and intoxications. 
To the truth of this x-ray pictures of the teeth will tes- 
tify. Any apparatus which tends to produce mechanical 
irritation is a dangerous one, for while it is true that 
foreign bodies may produce little or no damage pro- 
vided they exist in aseptic surroundings, yet in the 
presence of infective organisms they act invariably to 
intensify the reaction between tissue and germ. A bridge 
which offers opportunity for the collection of food and 
bacteria about it; a crown or a bridge which is attached 
to or which covers a tooth whose nerve has been killed 
(by which procedure the tooth itself has been made a 
foreign body), especially if complete sterilization has 
not been carried out, is a menace to the general health 
of the patient, who had far better have fewer teeth than 
such an appliance. A little macerated pulp at the bot- 
tom of root canal and one living bacterium buried at the 
bottom of a root canal under an impervious cap or fill- 
ing, is not to be preferred to a vacant space in the tooth 
line. It is under such conditions that root and alveolar 
abscesses develop and remain for long periods of time 
affecting the health of the individual by producing bac- 
teria and toxins to enter the blood stream by which they 
are carried to the heart, central nervous system, mus- 
cles, bones, or other tissues and organs. 
Recent studies of the teeth make it increasingly evi- 
dent that to care for these instruments, especially with 
regard to the root canals, is extremely difficult for me- 162 
FUNDAMENTALS OF PATHOLOGY 
chanical reasons if for no others. As long as it was be- 
lieved that each tooth had a single pore at the tip of 
each root it seemed simple enough to completely remove 
the dead nerve and its surrounding tissue. But when, 
as Cassidy has shown, there may be, not merely several 
terminal pores, but also lateral canals and pores, then 
indeed is the problem accentuated, for there is little 
chance that an instrument can be devised to enter these 
lateral passages. And evidently the dead tissue should 
be completely removed. Dead tissue is always a source 
of danger, offering as it does a favorable medium for 
bacterial growth, and even small remnants of such nutri- 
Fig. 66.-A photograph from a smear preparation from material beneath an ap- 
parently perfect crown on a bicuspid tooth. In this case there was absolutely no visible 
defect in either tooth or crown. (Photo by Goosmann.) 
ent material may lead to the production of a focus of 
infection which may have a tremendous influence on the 
body as a whole. Such things as these emphasize the 
necessity of perfect aseptic (and antiseptic) technic in 
operations upon the teeth no less than in surgical opera- 
tions upon other parts of the mouth. 
REFERENCES. 
Bass and Johns: Pyorrhoea Dentalis and Alveolaris. Jour. Am. Med- 
Assn., 1915, Ixiv, 553. 
Billings, Mayo and Rosenow: Mouth Infection as a Source of Systemie 
Disease. Jour. Am. Med. Assn., 1914, Ixiii, 2024-2027. GASTROINTESTINAL SYSTEM 
163 
Bunting and Rickert: Dental Caries. Jour. Natl. Dent. Assn., 1914, 
i, 16. 
Cannon: The Mechanical Factors of Digestion. New York, 1911. 
Collins: The Possible Relationship of Organic Disease of the Nervous 
System to Rigg's Disease. Trans. Assoc. Amer. Phys., 1913, xxviii, 87. 
Craig: Peridental Infection as a Causative Factor in Nervous Diseases. 
Jour. Am. Med. Assn., 1914, Ixiii, 2027. 
Davis: Intestinal Obstruction: Formation and Absorption of Toxin. 
Bull. Johns Hopkins Hosp., 1914, xv, 33. 
Evans and Middleton: Endamebic Pyorrhoea and Its Complications. 
Jour. Am. Med. Assn., 1915, Ixiv, 442. 
Gies: Dental Cosmos, 1915 Ivii, 276. 
Gies: Further Nutrition Studies of Dentition. Jour. Allied Dent. Soc., 
1916, ix, 47. 
Gilmer and Moody: A Study of the Bacteriology of Alveolar Abscess 
and Infected Root Canals. Jour. Am. Med. Assn., 1914, Ixiii, 2023. 
Hartzell, Henrici and Leonard: Report of the Mouth Infection Research 
Corps. Jour. Natl. Dent. Assn., 1914, 48. 
Hunter: Severest Anaemias; Their Infectious Natures, etc. London, 
1909. 
Hunter: Oral Sepsis. Brit. Jour. Dent. Sc., 1914, Ixii, 833. 
Keith: Lancet, London, 1915, ii, 371; Brit. Jour. Surg., 1915, ii, 576. 
Krehl-Hewlett: Clinical Pathology. Phila., 1907. 
Pavlov: The Work of the Digestive Glands. London, 1910. 
Price and Bensing: Are Endomoebae Important in the Etiology of 
Pyorrhoea? Jour. Natl. Dent. Assn., 1915, ii, 143. 
Starling: Human Physiology. Phila., 1912. 
Thoma: Oral Abscesses. Jour. Allied Dent. Soc., 1916, ix, 95. 
Turner: Dental Sepsis. Brit. Med. Jour., 1914, i, 1244; 1301. CHAPTER XIII. 
THE NERVOUS SYSTEM. 
The nervous system is the chief mechanism in bring- 
ing about the adjustments of the organism to its environ- 
ment, and therefore upon it depends in a very large 
measure the preservation of the species. It consists of 
a mechanism which receives stimuli and transmits im- 
pulses, a mechanism for adjusting reactions to stimuli, 
Part of Gower's tract 
entering cerebrum by 
superior cerebellar 
peduncle 
Dentate nucleus ■■ 
Tactile 
-Gracilis - cuneate nuclei 
Direct cerebellar- 
Pain, heat, and cold 
Tactile 
(discrimination) 
Joint and 
muscle senses 
(sense of position) 
- Tactile receptor 
Non-sensory receptoi 
(Clarke's column) 
Pain receptor 
■ Heat receptor 
• Cold receptor 
Deep sensation 
Superficial sensation . 
Fig. 69.-Diagram to illustrate afferent systems to cerebrum and cerebellum. 
(After Mott and Sewell.) 
164 THE NERVOUS SYSTEM 
165 
and a mechanism for preserving and correlating impres- 
sions. By means of these, stimuli are localized and re- 
sponses coordinated, and, in some manner which we do 
not understand, associations are formed upon which are 
Optc i 
Thalamus] 
Internal I 
Capsule J 
-Chustfum 
Lenticular i 
Nucleus , 
Substantia Ni^ra 
Red Nucleus 
Rubro-Spinal Tract 
- Pyramidal Tract 
Deiters Nucleus - 
- Dentate Nucleus 
_ Inferior 011 vt 
VcSfibulo Spinal Tract. 
Crossed Pyramidal Tract 
x Direct Pyramidal Tract 
oescertoiNG ncrve 
TRACTS 
Fig. 67.-Schema of course taken by chief descending tracts of brain stem. (Gordon 
Holmes.) The tract in red, to the right of the rubro-spinal tract, includes the posterior 
longitudinal bundle, together with the fibers of the thalamo-spinal and tecto-spinal tracts. 
(After Mott and Sewell.) 166 
FUNDAMENTALS OF PATHOLOGY 
founded memory, thought, will, judgment, and the emo- 
tions. 
Interference with conduction in any part of the sys- 
tem leads to variations in the status of the organism by 
Corpus Callosum . 
V- ThAlamo Cortical f ibr/S 
L .Clau strum 
'■Lenticular Nucleus 
Red Nucleus 
\Sylvian Iter. 
: Median Fillet 
SubsUnt.6 Nigra 
Pf dune Ie 
Ct rebel I urn ; 
LDentate Nucleus 
Spmo-Cercbellar 
Tracts 
(Co-ordination 
Muscular Tone / 
•^Crossed Sensory fibres 
//Pain. Heat & Cold \ 
' (Touch & Pressure / 
Pyramid 
Deep Arcuate Fibre$_ 
--Inferior Olive 
Dorsal Column (direct) 
/sense of position 1 
\ - - movement/ 
/ASCENDING- NERVE 
TRACTS. 
Spinal Ganglion _ 
Spmal Nerve _ 
Fig. 68.-Diagram of ascending tracts between the spinal cord and brain (Gordon 
Holmes), with the probable path of sensory impulses. (After Mott and Sewell.) THE NERVOUS SYSTEM 
167 
causing abnormal responses to stimuli. In some indi- 
viduals conduction is slow; in others, it is rapid, but in 
either it may become slower or more rapid depending 
Fig. 70.-Secondary descending degeneration. When a lesion is produced in the 
brain the nerve fibers below the lesion degenerate and it is this which causes the 
paralysis. This figure shows the area of degenerated fibers in the spinal cord after 
a hemorrhage into the internal capsule. (Delafield and Prudden.) 
Fig. 71.-Amyotrophic lateral sclerosis. Sometimes all of the motor fibers of the 
spinal cord degenerate and lead to a progressively developing muscular paralysis. This 
figure illustrates the appearances of the spinal cord under such conditions. The pale 
areas are the degenerated ones. (Delafield and Prudden., 168 
FUNDAMENTALS OF PATHOLOGY 
upon the sort of influence which acts upon the system 
as a whole or upon any part of it. 
The cells of which the nervous system is composed 
are perpetual cells in the sense that in the course of de- 
Fig. 72.-In tabes dorsalis (locomotor ataxia) it is the fibers in certain sensory 
(ascending) nerve tracts which degenerate. The appearances are shown in this figure. 
(Delafield and Prudden.) 
velopment they have lost the power of reproduction. 
They are therefore incapable of regeneration and so 
when a cell or a group of cells have undergone necrosis 
they are completely lost to the organism, and their place 
Fig. 73.-When both ascending (sensory) and descending (motor) tracts are affected, 
the appearances in the spinal cord are a composite of those shown in Figs. 94 and 95. 
This figure illustrates this. (Delafield and Prudden.) THE NERVOUS SYSTEM 
169 
is taken by an overgrowth of glia cells, which, although 
they are of the same embryonic origin as the nerve cells, 
have preserved the power of growth and reproduction. 
Gliosis in the nervous system is the analogue of fibrosis 
in other organs. 
Lesions of the nervous system may be divided into 
those which involve inhibition, loss, or intensification of 
the power of receiving impulses, of transmitting im- 
pulses (afferently or efferently), or of making associa- 
tions. 
1. Disturbances of the receiving and afferent trans- 
mitting mechanism (sensory). 
Anesthesias 
Paresthesias 
Hyperesthesias 
Ataxias (?) 
2. Disturbances of the efferent transmitting mechan- 
ism (motor). 
Paralyses 
Tonic contractions (tetanic) 
Clonic contractions 
Ataxias and choreas (?) 
3. Disturbances of the associative mechanism. 
Mental dissociation and abnormal associations. 
1 lallucinations Amnesias Hysterias 
Amentia Aboulia 
Dementia Delusions 
4. General disturbances of the nervous system. 
1. Intoxications 
Delirium 
Coma 
Convulsions 
2. Defective development 
Idiocy 
Imbecility 
"Mental debility" 170 
FUNDAMENTALS OF PATHOLOGY 
Fig. 74.-Section of a brain showing an area of softening resulting from a brain 
hemorrhage (apoplexy) in the thalamus and the internal capsule. Through the internal 
capsule the motor fibers to the muscles of the body pass. Destruction of these fibers 
lead to paralysis on the opposite side of the body. If the hemorrhage is on the left 
side the paralysis will be on the right. 
Fig. 75.-Coronal section through the cranium and brain of a case of chronic hydro- 
cephalus, showing extreme distension of the lateral ventricles. (From the Pathological 
Museum, University of Sheffield.) (Beattie and Dickson.) THE NERVOUS SYSTEM 
171 
REFERENCES. 
Adami: Principles of Pathology. Phila., 1910. 
Bing: Gehirn u. Riickenmarksdiagnostik. Berlin, 1911. 
Cushing: Studies in the Cerebrospinal Fluid. Jour. Med. Research, 
1914, xxxi, 1. 
Frazier and Others: The Cerebrospinal Fluid in Health and Disease. 
Proc. N. Y. Acad, of Med. Jour. Am. Med. Assn., 1915, Ixiv, 934. 
Hoche: Die Storungen d. psychischen Funktionen. Krehl u. Marchand's 
Handb. d. allg. Pathologic. Bd. II Abth. 2, Leipzig, 1913. 
Lewandowsky: Handbuch der Neurologic. Berlin, 1912-1914. 
Paton: Psychiatry. Phila., 1905. 
Sherrington: Integrative Action of the Nervous System. 
Villiger: Gehirn u. Riickenmark. Leipzig, 1910. CHAPTER XIV. 
THE HEMOPOIETIC SYSTEM. 
This system is composed of the lymph glands, spleen 
and bone marrow, and is named hemopoietic because 
of the fact that one of the functions of each of these or- 
gans is the production of the cells of the circulating 
blood, of the adult organism. As a matter of fact, the 
blood cell producing function is more closely associated 
with the bone marrow, and perhaps, under certain con- 
ditions, with the hemolymph glands. The spleen and 
lymph nodes are, on the other hand, of value rather as 
filters than as producers of cells. The hemolymph glands 
stand midway between lymph nodes and bone marrow. 
The general structure of all these organs is much the 
same, so that there is some reason to conclude that there 
is something common in their functions, a conclusion 
that seems to be justified in experience with clinical cases 
such as myelogenous leukemia, in which the whole sys- 
tem is, as a rule, changed. 
The bone marrow is the chief blood cell producing tis- 
sue and, like other tissues, undergoes hyperplastic and 
retrograde changes. In certain types of disease, as in 
aplastic anemia, it seems to be completely fatigued so 
that it no longer produces. In less severe cases, as in 
the usual pernicious anemia, and the leukemias, it pro- 
duces activity. There is evidence that in anemia from 
any cause the bone marrow increases in activity more 
or less in proportion to the circulatory losses. 
The spleen, though it is a producer of cells, seems 
to be rather more important as a reduction plant when 
broken down cells, especially senile red cells, are filtered 
172 THE HEMOPOIETIC SYSTEM 
173 
out of the blood stream and prepared for re-using in 
the body. It is perhaps because of its reduction func- 
tion that it may play a part in the neutralization of tox- 
ins which come to it bound to the cellular proteins. 
When the spleen is removed its functions are apparently 
assumed by the bone marrow and lymph glands. Evi- 
dence is accumulating that it is more commonly the seat 
of infections than was formerly supposed. 
The lymph glands are of two indistinct orders: one, 
the ordinary lymph nodes, and, second, the hemolymph 
glands. Their importance resides in their filtration ac- 
tivities which are similar in some respects to those of 
the spleen, but which are devoted to the periphery of 
the body and with the lymphatic fluids rather than with 
the blood. Their especial value seems to be in combat- 
ting infections, during which they filter out and hold in- 
fectious organisms. They also furnish, especially un- 
der such conditions as exist in lymphatic leukemia, and 
in certain infections, small mononuclear cells (lympho- 
cytes) to the blood. 
REFERENCES. 
Arndt: Diseases and New-Growths of Lymphatic Origin. Jour. Am. 
Med. Assn., 1914, Ixiii, 1268. 
Bunting and Yates: Hodgkin's Disease. Arch. Int. Med., Aug. 1913; 
Jour. Am. Med. Assn., 1914, Ixiii, 2225. 
King: The Pathology of the Spleen. Arch. Int. Med., 1914, xiv, 145. 
Maclachlan: Tonsillitis: A Histo-Pathological Study. Publication from 
the University of Pittsburgh School of Medicine, 1912. 
Meyer: The Supposed Experimental Production of Hemolymph Nodes 
and Accessory Spleens. Jour. Exper. Zool., 1914, xvi, 241. 
Robertson: The Anatomy and Physiology of the Tonsil. Jour. Am. Med. 
Assn., 1901, liii, 684. 
Warthin: The Changes Produced in the Hemolymph Glands of the Sheep 
by Splenectomy, Hemolytic Poisons, and Haemorrhages. Jour. Med. 
Research, 1902, ii, 435. 
Warthin: A Contribution to the Normal Histology and Pathology of 
the Hemolymph Glands. Jour. Med. Research, July, 1901. 
Woolley: The Function of the Spleen. Jour. Lab. and Clin. Med., 1915, 
i, 75. CHAPTER XV. 
THE SUPPORTING AND LOCOMOTORY 
SYSTEM. 
This system includes the bones, joints, muscles, ten- 
dons, and ligaments. The bones are of importance be- 
cause they give rigidity to the body; the joints, because 
Fig. 76.-A case of rickets 
they allow of a certain degree of flexibility; the muscles, 
because of their contractility, make motion possible; the 
tendons and ligaments preserve the positions of the 
174 THE SUPPORTING AND LOCOMOTORY SYSTEM 
175 
bones, and determine the amount and direction of move- 
ment at the joints. 
The structure and composition of bone accounts for 
Fig. 77.-A case of rickets. 
its rigidity, and therefore variations in structure and 
composition will modify the normal rigidity. 
Physical causes- 
Trauma (fractures). 176 
FUNDAMENTALS OF PATHOLOGY 
Metabolic causes- 
Hyperplasias (tumors). 
Atrophy (halisteresis, osteomalacea). 
Inflammation (osteomyelitis). 
Fig. 78.-A case of rickets. 
Necrosis (metallic poisons). 
Metaplasia (osteitis deformans). 
The joints depend for their function upon the synovial 
membranes, and upon the ligaments and tendons, and so, THE SUPPORTING AND LOCOMOTORY SYSTEM 
177 
variations in structure and composition of these tissues 
will modify the effectiveness of a joint. 
Physical causes- 
Trauma (dislocations). 
Metabolic causes- 
Inflammations (arthritis). 
Toxic arthritis (gout). 
Fig. 79.-A case of rickets. 
Lesions of nervous system (?). 
Metaphasia (arthritis deformans) (?). 
The functions of the tendons and ligaments depend 
upon their tensile strength and this upon their struc- 
ture. Therefore variations in the structures of these 
tissues will modify their function. 
Physical causes- 
Trauma (rupture, strain, sprain). 178 
Metabolic causes- 
Inflammations (tendinitis; tenosynovitis). 
The muscles determine the movements of the body, 
and movement is the expression of contractility. Varia- 
tions in contractility of the muscles will modify in greater 
or less degree the movements of the body. 
Physical causes- 
Trauma (rupture). 
FUNDAMENTALS OF PATHOLOGY 
Metabolic causes- 
Inflammation (myositis). 
Atrophy. 
Necrosis. 
Intoxications (fatigue, anemia). 
Tumors. 
Lesions of nervous system (paralyses, spasms). 
Fig. 80.-Showing extreme case of bow-legs. THE SUPPORTING AND LOCOMOTORY SYSTEM 
179 
Fig. 81.-Extreme rickety deformities of the femur and the tibia. Note the flattening 
of the shafts of the deformed bones. (Edinburgh University Anatomical Museum 
Catalogue No. OS.D.i.8.) (Beattie and Dickson.) 180 
FUNDAMENTALS OF PATHOLOGY 
REFERENCES. 
Mayer and Wehner: An Experimental Study of Osteogenesis. Am. Jour. 
Orthop. Surg., 1914, xii. 
Moschowitz: The Relation of Angiogenesis to Ossification. Bull. Johns 
Hopkins Hosp., 1916, xxvii, 71. 
Phemister: The Fate of Transplanted Bone. Surg. Gynec. and Obst., 
1914, xix, 303. 
COLLATERAL REFERENCE BOOKS. 
Bechhold: Die Kolloide in Biologie und Medizine. Dresden, 1912. 
Broman: Normale und abnonnale Entwicklung des Menschen. Wies- 
baden, 1911. 
Charcot: Lectures on Senile Diseases. London, 1881. 
Conklin: Heredity and Environment in the Development of Men. 
Princeton, 1915. 
Freudenthal: Allgemeine u. Spez. Physiologic des Menschenwachstums. 
Berlin, 1914. 
Henderson: The Fitness of the Environment. New York, 1913, 
Herter: Bacterial Infections of the Digestive Tract. New York, 1907. 
Herter: Biological Aspects of Human Problems. New York, 1911. 
Hoeber: Physicalische Chemie der Zelle und Gewebe. Leipzig, 1906. 
.Tores: Anatomisehe Grundlagen wichtiger Krankheiten. Berlin, 1913. 
Loeb: The Mechanistic Conception of Life. Chicago, 1912. 
Mallory: Principles of Pathological Histology. Phila., 1914. 
Mallory and Wright: Pathological Technique. Phila., 1913. 
Oppenheimer: Handbuch der Biochemie des Menschen und der Thiere. 
Jena, 1909. 
Orth: Pathologisch-Anatomische Diagnostic. Berlin, 1909. 
Ostwald: Grundriss der Kolloidchemie. Dresden, 1911. 
Parmelee: The Science of Human Behavior. New York, 1913. 
Hibbert: Geschwulstlehre. Bonn, 1904. 
Vaughan: Protein Split Products. Phila., 1913. 
Vernon: Intracellular Enzymes. London, 1908. 
Verworn: Irritability. New Haven, 1913. 
White: The Pathology of Growth: Tumors. New York, 1913. 
Zinsser: Infection and Resistance. New York, 1914. INDEX 
Abscess, alveolar, 158, 160, 161 
defined, 98 
formation, 89 
of the liver, 93 
Acidosis, 47 
Achrondroplasia, associated with, 
diseases of the thyroid, 61 
diseases of the thymus, 61 
Acromegaly, associated with lesions 
of the hypophysis, 64 
Adenocarcinoma of cervix uteri, 103 
Adrenals, 66 
Albinism, 48 
Amyloid degeneration, 79 
Anabolism, 43, 74 
Anasarca, 115 
Anemia, general, 109, 114 
local, 109, 114 
Aneurysm, 127 
Anhydremia, 109 
Anomalies of metabolism, 47 
Anthracosis, 81 
Aortitis, 127 
Arteriosclerosis, 127 
Arteritis, 127, 128 
Argyria, 81 
Ascites, 115 
Atmospheric pressure as physical 
cause of disease, 30 
Atrophies, 132 
Atrophy, 71 
Autointoxications, 36, 149 
Autolysis, 80 
Bacteria, 34, 36, 41, 90, 121, 152 
in health, 36 
Bacterial toxins, 34 
Blastomas, 99 
Blood, 109 
changes in constitution of, 117 
circulation of body, 122 
clot in blood vessels, 117 
corpuscles, 110 
in heart, 118 
Blood vessels, aneurysm, 127 
arteriosclerosis, 127 
arteritis, 128 
defined, 124 
embolism, 116, 118 
formation of clot in, 117 
inflammation, 127 
infarction, 117, 118 
in tail of tadpole, 84 
musculature, 125 
phlebitis, 128 
Blood vessels--Cont'd 
section of, 123 
thrombosis, 117 
Bone marrow, 172 
Bones, 174 
Bow-legs, extreme case of, 178 
Brain, section of, 170 
Bright's disease, 130 
Bridge-work, producing infection, 
161 
Burns, 32 
Cachexia hypophyseopriva, asso- 
ciated with lesions of the 
hypophysis, 64 
Calcification, 82 
Cancer, varieties, illustrated, 107 
Carcinoma, 102 
Cardiovascular system, 109 
anemia, 114 
blood, 109 
blood vessels, 124 
edema, 115 
embolism, 116 
heart, 118 
hyperemia, 109 
thrombosis, 116 
Caries, 80 
Caseation, 80 
Causes of disease, 26 
chemical, 34 
classification, 34 
classification, 26 
infections, 36 
physical, 26, 27 
sociologic, 39 
Cell degeneration, 79 
Cells of the body, 17 
composition of, 18 
structure of, 17, 19 
Cellulitis, 94 
Chalicosis, 81 
Cholesterin, 18 
Circulation of the body, 122 
Cloudy swelling, 78 
Cold, as physico-chemical cause of 
disease, 32 
Colloid degeneration, 79 
Congenital diseases, 24 
Conioses, 81 
Cretinin, associated with disease 
of the thyroid, 61 
Crowns, producing infection, 161 
Cystinuria, 47 
Cytoplasm, 18 
181 182 
INDEX 
Degeneration, 78 
amyloid, 79 
autolysis, 80 
caries, 80 
caseation, 80 
colloid, 79 
gangrene, 80 
glycogenic, 80 
hyalin, 79 
lipoid, 81 
mucoid, 80 
myelenic, 80 
myxedema, 80 
necrosis, 80 
of cells, illustrated, 79 
soapy, 80 
Diabetes insipidus, associated with 
lesions of the hypophysis, 
64 
Diabetes mellitus, associated with 
lessions of the hypophysis, 
64 
Diet in disease, 76 
Diseases of the body, 22 
causes, 26 
classification, 24 
congenital, 24 
inherited, 24 
Disturbances of function, 83 
Disturbances of metabolism, 43 
Dwarfism, associated with disease 
of the thymus, 61 
defined, 64 
Dystrophia adipose-genitalis, asso- 
ciated with lesions of the 
hypophysis, 64 
Edema, 115 
Electric currents, effect on bodv, 
30 
Electricity, as physico-chemical 
cause of disease, 30 
Electrolytic dissociation, 31 
Emaciation, 74 
Embolism, 118 
Enamel defects in tetany, 65 
Endocarditis, acute, 123 
ulcerative, 123 
vegetative, 121 
Endogenous non-parasitic intoxica- 
tions, 34, 36 
Exogenous, non-parasitic intoxica- 
tions, 34, 35 
parasitic intoxications, 34, 35 
saprophytic, 34, 35 
Exophthalmic goiter, associated 
with diseases of the thy- 
mus, 61 
Fat, 78 
Fatty degeneration, 78 
infiltration, 78 
Fever, charts, 48, 49, 50 
continuous, 48, 51 
defervescence or defervescent 
stage, 51 
defined, 50 
fastigium or fastigial stage, 51 
initial or pyrogenic stage, 51 
intermittent, 50, 52 
recurrent, 52 
remittent, 49, 52 
temperature, relation to, 51 
Food, effect of, on the body, 43, 49 
quality, needed by body, 72 
quantity, needed by body, 75 
Function, disturbance of, 83 
Gangrene, 80 
Gastrointestinal autointoxication, 
75, 149 
Gastrointestinal intoxications, 36 
Gastrointestinal tract, 149 
diseases, 150, 151 
functions, 149 
gastric digestion, 151 
secretion of glands, 150 
Giantism, illustrated, 63 
associated with lesions of the 
hypophysis, 64 
Glycogen, 18 
Glycogenic degeneration, 80 
Goiter, 58 
Graves' disease, 61 
Growth, 71 
Harmones, 54 
Health and disease, 22 
Heart, 118 
fatty degeneration of, 120 
infection, 121 
strain, 121 
Heat, as physico-chemical cause of 
disease, 31 
Heat exhaustion, 53 
Heat producing rays, 31 
Hemolymph glands, 173 
Hemopoietic system, 172 
bone marrow, 172 
lymph glands, 173 
spleen, 172 
High temperature, 48 
Hyalin degeneration, 79 
Hydremia, 109 
Hydrocephalus, 115 
Hydrops, 115 
Ilydropericardium, 115 INDEX 
183 
Malnutrition, 74 
Melanin, 19 
Melanosis, 81 
Metabolism, acidosis, 47 
adrenals, 66 
anomalies, 47 
defined, 43 
disturbances of, 43 
food, effect of, 43 
high temperature, 48 
internal secretions, 45, 53 
pancreas, 69 
parathyroid glands, 58 
parathyroids in, 61 
pineal body, 69 
pituitary glands, 62 
result of, 46 
thymus, 61 
thyroid glands, 58 
Metastasis, defined, 39 
Mouth, as portal of infection, 157 
Mucoid degeneration, 80 
Muscles, 174 
Myelinic degeneration, 80 
Myocarditis, 121 
Myxedema, associated with dis- 
eases of the thyroid, 61 
defined, 80 
facial expression in, 67 
illustrated, 59 
Nanosomia infantilis, 64 
Nanosomia primordialis, 54 
Necrosis, 80, 82 
Neoplasm, 99 
Nephritides, 134 
Nephritis, 130 
Nephroses, 130 
classification, 139 
urinary changes in, 139 
Nervous system, 164 
cells, 168 
lesions, 169 
Obesity, 73, 74 
Oligemia, 109 
Ossification, 82 
Overeating, results of, 74 
Overgrowth, 71 
Overwork, 120 
Pancreas, 69 
Parathyroid glands, 58 
Pathology, defined, 21 
Pentosuria, 47 
Phlebitis, 128 
Phlegmon, 94 
Physical causes of disease, 27 
pressure, 27 
strain, 30 
Hydrothorax, 115 
Hyperemia, general, 109 
local, 109 
Hyperthermia, 51 
Hypophysis, lesions of, 64 
Immunity from infection, 38 
Indigestion, 75 
Infantilism, associated with disease 
of the thyroid, 61 
associated with lesions of the 
hypophysis, 64 
defined, 64 
Infantilismus dystrophicus, 64 
Infarction, 117, 122, 123 
Infection, defined, 36 
immunity from, 38 
local, 38 
predisposition to, 37 
susceptibility to, 38 
Infectious causes of diseases, 36 
Inflammation, 83 
degeneration, 95 
repair, 95 
septic, 89 
types, 97 
Inherited diseases, 24 
Ions, 31 
Internal secretions, 53 
Intestinal intoxications, 40 
symptoms of, due to, 41 
Intoxications, 34 
intestinal, 40 
of endogenous non-parasitic ori- 
gin, 34, 36 
of exogenous non-parasitic ori- 
gin, 34, 35 
of exogenous parasitic origin, 
34, 35 
of exogenous saprophytic origin, 
34, 35 
Joints, 174 
Katabolism, 43, 74 
Kidneys, 130 
blood supply of, 138 
Lecithin, 18 
Leucopenia, 109 
Leukemia, 109 
Ligaments, 174 
Light, as physico-chemical cause 
of disease, 31 
Light rays, 31 
Lipoid degeneration, 81 
Liver, section of area of, 90 
Lymph glands, 173 
Lysis, 52 184 
INDEX 
Physical causes of disease-Cont'd 
tension, 29 
Physico-chemical causes of disease, 
30 
atmospheric pressure, 30 
cold, 32 
electricity, 30 
heat rays, 31 
light, 31 
light rays, 31 
radium, 31 
x-ray, 31 
Pigmentation, 31, 81 
anthracosis, 81 
argyria, 81 
chalicosis, 81 
icterus, 81 
melanosis, 81 
silicosis, 81 
siderosis, 81 
Pineal body, 69 
Pituitary gland, 62 
Plethora, 109 
Polycythemia, 109 
Precocious adiposity, associated 
with disease of the thy- 
mus, 61 
Predisposition, to infection, 37 
to tuberculosis, 37 
Pressure, as physical cause of dis- 
ease, 27 
Protoplasm, 18, 20 
Pyemia, defined, 39 
Pyorrhea alveolaris, 158 
Pyrexia, 51 
Radium, as physico-chemical cause 
of disease, 31 
Regeneration of tissue, 96 
Repair and regeneration, 95 
Respiration, external, 141 
internal, 142 
Respiratory insufficiency, 147 
Respiratory system, 141 
Respiratory tract, anatomical ar- 
rangement, 144 
bronchial portion, 144 
illustrated, 143 
nasal portion, 144 
tracheal portion, 144 
Rickets, 174, 175, 176, 177 
Sarcomas, 102, 104 
Secretions, internal, 53 
Septicemia, 94 
Septicopyemia, 39, 94 
Siderosis, 81 
Sinus, defined, 98 
Soapy degeneration, 80 
Soeiologic causes of disease, 3!) 
Spleen, 172 
Starvation, 74 
Stitch abscesses, 37, 96 
Stomach, function of, 149 
gastric digestion, 151 
Strain, as physical cause of dis- 
ease, 30 
Sub-infection, 42 
Sunburn, 31 
Sunstroke, 31, 52 
Supporting and locomotory system, 
174 
Teeth, as focus of infection, 161 
Temperature of the body, 48 
charts of, 48, 49, 50 
exercise, effect of, 49 
high, 48 
relation to fever, 51 
Tendons, 174 
Tension, as physical cause of dis- 
ease, 29 
Tetany, associated with disease of 
the thyroid, 61 
illustrated, 68 
Thrombosis, 116, 117 
Thymus, 61 
Thyroid glands, 58 
internal secretions of, 59 
Tissue, fibrous, 96 
Toxemias, 36 
Tuberculosis, in children, 38 
predisposition to, 37 
Tumors, 99 
benign, 101 
cause, not known, 105 
differentiation of benign and 
malignant, 102 
malignant, 101 
original, 102 
site of predilection, 102 
terminology, 102 
Ulcer, defined, 98 
Undernourishment, 74 
Ureters, 130 
Urethra, 130 
Urinary system, 130 
Vesiculation, 31 
Vitamin, 76 
Wastes, 54 
X-rays, as physico-chemical causes 
of disease, 31