i^Me iUV jSS!;;;;;-.'-;<;;a ■^AS'r"-'i:'*~'-"^'i Cornell University Library The original of tiiis bool< is in tine Cornell University Library. There are no known copyright restrictions in the United States on the use of the text. http://www.archive.org/details/cu31924012514067 Syllabus of general pathology. 3 1924 012 514 067 □lit) I'f^iJi SYLLABUS OF GENERAL PATHOLOGY. BY \'» . J. M. VAN COTT, M. D. >, j:; '. Professor of Pathology and Bacteriology at the Long Island College Hospital, Brooklyn, New York. Pathologist to Long Island College Hospital, Brooklyn Hospital, and Kings County Hospital. 1900 V. New York : Press of I^ouGHLiN Bros., 126 Maiden I^ane. MCM. PREFACE. The aim of this Syllabus is to place in the hands of my Class at the Long Island College Hospital, a digest of the fundamen- tal principles of the Science of Pathology, presented in such a manner as not only to stimulate a desire for acquiring knowl- edge in a branch of the Medical Science which must always be the bed-rock of the whole, but also in such a way as to help the studpnt to classify the facts involved to the best advantage, with a ininimum of application. The' method adopted to attain this end is the result of ten years' experience as student and teacher of Pathology, and is calculated to form a foundation upon which the student is to build- his own individual superstructure. The typography, punctuation and syntax are all adapted to this end, i. e., to emphasize each fact in proportion to its relative importance ; and for this reason, grammar and diction have not been regarded beyond the bare requirements of correct language. It is earnestly hoped that the wofk may prove a source of benefit and guidance to those whom it is intended to assist. J. M. VanCott, M. D., 123 Joralemon Street, Brooklj'n, New York 1894. PREFACE TO SECOND EDITION, The first edition of this Syllabus' having, after a lapse of five years, become exhausted, and having stood the test of time as to its utility, this new edition has been prepared for the Class in Pathology, with the hope that it still may be found useful. The Chapter on Neoplasms has been entirely reconstructed, eliminating all hieroglyphics ; and many other errors itx the con- text, the result of the failure of the printer to take notice of his proof corrections, have been corrected.' Effort has been made to, bring the Syllabus up to date. Only those more modern discoveries have been omitted -which might be regarded as yet moot points. My warmest thanks are due Mr. John J. O'Reilly, of the Class of 1901, for his untiring and invaluable assistance in preparing this second edition. J. M. VanCott, M. D., 188 Henry Street, Brooklyn, New York. January, 1900. INDEX. OHAPTBB PAGE Preface to 1894 Edition 3 Preface to 1900 Edition 4 I. Genebal Pathology 9 II. Blood, Changes in Quantity of 17 ni. Inflammation 30 IV. Blood, Pathology of 25 V. Vasoulae Appabatus, Pathology of 37 VI. Bactbbia 46 VII. Bbspieatoby Appabatus, Pathology op 48 VIII. Neoplasms 57 IX. Ueinaby Appabatus, Pathology of 75 PAGE Abscess • •• • 32 Actinomycosis 32, 56 Adenoma 69 .aitiology 11 Amyloid Degeneration (Eenal) . . 91 Anaemia 34 Angioma 67 Anthraoosis 56 Antitoxines 47 Arteries 17, 43 Anomalies of 43 AtSophy, Eenal 94 Atrophy, Senile (Eenal) 94 Bacteria 46 Culture of 47 Experiments -with 47 Staining of 47 Bladder 99 Anomalies of 100 Circulatory disturbances of .. . 100 General Morphology of 99 Blood, CO 3 poisoning 36 Change in quantity of 17 Histology of 35 Micro-organisms in 36 Morphology of 36 Pathology of 25,32 Physiology of 35 Plasmodium Malarise 36 Preparation of 28 Staining of 39 Bronchi 52 Anomalies of 52 Capillaries 18, 44 Carcinoma 71 . PAGE Cardiac Degeneration 42 Cardiac Hypertrophy 42 Caseation 24 Cell, the 12 Cellular Pathology 12 Cirrhosis, Eenal 86 Color Picture 16 Corpuscle counting 27 Cystic Haemorrhage 103 Cystic Neoplasms 102 Cystitis 100 Cystitis, Tubercular 101 Cystoma 73 Deciduoma 73 Degeneration, Cardiac 42 Cell 15 Formsof 15 Eesults of 15 Tissue 14 Disease 9 Classification of ll Echinococcus 56 Eclampsia 83 Emphysema 56 Enchondroma 64 Endocarditis 41 Endothelioma 73 Epithelioma 71 Erythrocytes 35, 32 Fatty Degeneration, Eenal. . Fibroma Gangrene Glioma Granuloma 93 63 33 33 PAGE Hsematuria 103 HsBmoglobin , 28 HsBmoglobinaemia 36 Hsemonieter, Fleisohel's 38 HsBmorrhage, Cystic 103 Kinds of 19 Nomenclature 19 Benal 103 Heart 17,37,39 Anomalies of 40 Circulatory disturbances of . . . 40 Hydrops Pericardii 38 Hypersemia 18 Acnte 30 Chronic 20 Cohnheim's observations 20 Inflammation 10, 30 Actinomycosis 22 etiology of '. 34 Chronic 33 Coccidiosis 22 Croupous 31 Diffuse 24 Diphtheritic 21 Interstitial 34 Lepra 32 Mixed 24 Nomenclature 31 Parenchymatous 34 Results of 31 Tubercular 31 Sequsele of 32 Specific forms of 21 Sub Acute 33 Syphilitic •. . . 33 Systemic complications of 24 Karyokinesis 13, 16 Kidney 75 Anomalies of 76 Circulatory disturbances of . . . 76 General Morphology of 75 Large, White, 84 Laryngitis, Chronic Productive 51 Prom Lupus 51 From Syphilis 51 Tubercular 51 Typhoid 51 Larynx 50 PAGE Lesions, forms of,. 14 Functional 41 Valvular 41 Vascular 43 Leucaemia 35 Pseudo 36 Leucocytes 36, 33 Leucocytosis 85 Lipoma 64 Lung 53 Anomalies of 53 Atrophy of 56 Degenerations of 56 Lymphangioma 68 Lymphatics 44, 45 Lymphoma 68 MelansBmia 36 Micro-organisms 47 Myocardium 39, 41 Myoma 67 Myxoma 61 Nares 48 Neoplasms. 57 etiology 57, 59 Age at which likely to occur. . . 60 Anatomic Classification 57 Anatomy of 60 Behavior of 58 Combinations of 61 Complications of 61 Consistence of 60 Cystic 103 Histology of 60 Homology of 58 Key to classification of 58 Laryngeal 51 Location of 60 Lung 56 Mode of growth of 59 Nomenclature of 57 Originof 61 Progression of 61 Quality of 60 Eegression of 61 Benal 98 Specific varieties of 59 PAGE Nephritis, Acute Diffuse 80 Acute Parenchymatous 77 Chronic Diffuse, non-indurative 84 Chronic Glomerulo 86 Chronic Parenchymatous 84 Chronic Parenchymatous with Chronic Glomerulo 85 Chronic Productive Indurative 86 Chronic Productive Interstitial 86 Puerperal 82 , Scarlatinal 80 Suppurative 89 Neuroma 66 Odontoma 65 Oligsemia 18 Organs 14 Osteoma 65 Papilloma 70 Pathologic Anatomy, classifi- cation of ' 10 Pathology, scope of 9 Pericarditis 38 Phlegmon 23 Placques. 27 Pleura 56 Pneumonia, Apostematous 56 Foreign Body .' 56 Purulent •• 55 Splenic 56 Stone-cutters' 56 Syphilitic 56 PAGE Pneumonitis 54 Acute Lobar 54 Catarrhal 55 Croupous 54 Frank 54 Tubercular ". 56 Psammoma 73 Pus 22 Pyaemia 23 Pyelitis 96 Benal Abscess 89 Amyloid degeneration.. 91 Atrophy, simple non-inflam- matory 94 Cirrhosis 86 Fatty degeneration 93 Hsemorrhage 103 Pelvis 95 Anomalies of 95 Circulatory disturbances of 96 General morphology of 95 Tuberculosis 98 Tumors 98 Bhinitis 49 Ssemiology 11 Sarcoma 62 Stroma 13 Thoma-Zeiss apparatus 28 Trachea 51 Ulceration 23 Ureters ". : 99 Vascular apparatus : . . 17, 37 Veins 18,44,45 Page Line 29 12 35 33 35 34 53 33 83 5 85 11 88 36 ERRATA. CORRECTION Nigrosinor should be Nigrosin or Fever- should be Fever, Rheuma, should be Rheuma- Peri-evascular should be Peri- vascular Comma bet-ween Pericardium and Endocardium occur should be occur Eliminate dash after " this" SYLLABUS OF GENERAL PATHOLOGY. Chapter I. PATHOLOGY. DISEASE : Morbid Processes. Morbid Anatomy. Morbid Phys- iology. Deviations of Form, Location, Function, beyond tbeir normal limits. DISEASE IS : Disturbed Anatomy and Physiology. KINDS OF DISEASE : Hereditary. Acquired, ) &■ g-, Acute. Sub-acute. Chronic. \ Syphilis. External. Internal. General. Local. TERMINATIONS OF DISEASE : Recovery, complete. Recovery, incomplete. Death. DEATH : Cessation of all function. SCOPE OF PATHOLOGY : 1. General. Fundamental principles of disease. 2. Special. Appli cation of these principles to specific organs, RELATION OF NORMAL STANDARDS TO PATHOLOGY : Difficulty of fixing normal standards. 10 SYLLABT78 OF GENERAL PATHOLOGY. DIVISION OF DISEASE ACCORDING TO LIFE PERIODS. Anaplasia. Metaplasia. Kataplasia. Professor Armour's Life Line : Metaplasia. PATHOLOGY STUDIED FROM THREE STANDPOINTS Gross Pathology or Pathologic Anatomy. Microscopio Pathology or Pathologic Histology, a. h. c. 3. Pathologic Physiology or Pathologic Chemistry and Function. ULTIMATE AIM OF PATHOLOGY : a. Diagnosis, b. Aetiology. CLASSIFICATION IN PATHOLOGIC ANATOMY : Anatomic changes in disease processes. 1. Aplasia or Hypolasia. Lack of, or incomplete development. Regression or Retrogression (Degeneration.) Defective structure through degeneration of parts already formed. Progression or Hyperplasia. Excessive formative action. Increase in sub- stance by numerical increase in elements. Hypertrophy. Increase in size of already formed elements Increase in substance vsrithout numerical in- crease in elements. 5. Regeneration. EestituttQ ad mtegrvm of parts destroyed. 6. Metaplasia. Transformation of one tissue into another tissue, usually of a lower grade. 7. Inflammation. The process by means of which Nature en- deavors to nd the tissues of noxious elements. 8. Neoplasms. New growths. 4. 11 SYLLABUS OF GENEBAL PATHOLOGY. CLASSIFICATION OF DISEASES : 1. External. 2. Internal. 3. Functional or intangible. 4. Organic or tangible. 5. General or systemic. 6. Circumscribed or local. 7. Parasitic, resulting from the invasion of an indi- vidual by other living beings. 8. Contagious. Transmission of disease through contact of one individual with another. Immediate transmission. 9. Infectious. Transmission of disease through the medium of the earth, air, water, etc. Intermediate transmission. (No strict line of demarcation between Contagion and Infection.) SEMIOLOGY : Science of Symptomatology. Can only be correctly acquired in conjunction with Pathological studies. DIAGNOSIS : That branch of the Science which determines the nature of a given disease. ETIOLOGY : Doctrine of the causation of disease. CLASSIFICATION OF iETIOLOGICAL FACTORS IN DISEASE : 1. Physical, a. Heat. External. b. Cold, External. c. Chemical substances which are ex- ternal and internal. 3. Nutrition disturbances. 3. Parasites. 18 SYLLABUS OF GENEBAL PATHOLOGY, CELLULAR PATHOLOGY. COMPONENTS OF ALL TISSUES : a. Cells. b. Stroma. TISSUE CHARAOTEKISTICS : Governed by Cells and Stroma and their ratio and re- lations to each other. TISSUE FUNCTION : a. Elaborate active function, i. e., secretion, con- traction, etc. b. Simple passive function, support. a. THE CELL. MORPHOLOGICALLY : A minute mass of protoplasm with a nucleus. PHYSIOLOGICALLY : A Microscopic mass of nitrogenous material having certain properties called " vital." CELL COMPONENTS : 1. Protoplasm, a. Hyaloplasm. 6. Spongioplasm. c. Attraction spheres. d. Centrosomes. e. Microsomes. 2. Nucleus. a. Chromatin. b. Achromatin. 3. Cell wall, not constant. 4. Nucleolus, not constant. SIZE OF CELLS : jsW to rh inch. 13 SYLLABUS OF GENEBAL PATHOLOGY. CELL PROPERTIES, (i. e., VITAL) : 1. Reproductive. Virchow's maxim: " Omnis Cel- lula e Celluta." 2. Nutritive. a. Ingestion. b. Digestion, c. Egestion. 3. Automatism, a. Intrinsic motion. b. Irritability. c. Chemical action. 4. Functional activity, specific work of specific cell. REPRODUCTION : 1. Direct Fission. 2. Fragmentation. 3. Budding. 4. Indirect Nuclear division, — Earyokinesis or Karyo- mitosis. EARYOKINESIS IN PATHOLOGIC PROCESSES : 1. As a measure of growth. 2. Heredity. (Vide : Minot & Weissman's theories. C. Hertwig's " Die Zelle," '93, S-aiO. Wilson, "The Cell in Development and Inheritance," '96, sqq. 133.) MORPHOLOGY : Constant relation of form to function. Co-relation of cells to each other and to the intercellular substance to form a harmonious whole. STROMA. 1. Nature. 2. Location. 3. Distribution. 4. Function, 5. Various structure and amount. SYNONYMS OF (&) STROMA : Connective tissue. Intercellular substance. 14 SYLLABUS OF GENERAL PATHOLOGY. ORGANS. ESSENTIAL COMPONENT ELEMENTS a. Parenchyma. ] Definite ratio between these four 6. .Stroma. esssential to normal function. Disturbance of this ratio results in some Pathologic process. e. Vessels d. Nerves. THE TERM LESION : I Any morbid change in : The exercise of function. Dynamic The texture of the organ. Morphologic (Really disease or degeneration.) DIFFERENT FORMS OF LESION : 1. Parenchymatous. 2. Interstitial. 3. Diffuse. 4. Vascular. 5. Trophic. TISSUE DEGENERATIONS : 1. Parenchymatous. Depending upon degeneration of cells. 2. Interstitial. Depending upon degeneration of stroma. 3. Diffuse. Depending upon degeneration of cells and stroma. (All governed by Vascular or Trophic changes or both.) 4. Vascular. a. Depends upon changes in the blood or lymph. b. Depending upon changes in the blood or lymph vessels. c. Depends upon changes in both a and b. 5. Trophic. Depends upon neuroses. 15 SYLLABUS OF GENEBAL PATHOLOGY. CELL DEGENERATIONS. NATURE OF THESE : Chemical — Vital. Not exactly understood in point of mode of origin or progress. Really molecular recon- struction. MORPHOLOGIC LIMITS : Produce form changes only to a certain extent. MICRO-CHEMIC REACTIONS : Change regarding behaviour of nucleus and body toward stains. FORMS OF DEGENERATION : (Lukjanow's classification. 1. Granular- Albuminous (Cloudy swelling. 2. Mucous. 3. Colloid. 4. Amyloid. 5. Waxy. 6. Reticular- Albuminous. 7. Coagulation Necrosis. 8. Hyaline. 9. Fatty. 10. Carbohydrate. 11. Horny. (Keratinoid.) 12. Pigmenty. 13. Calcareous. 14. Serous-Oedema. 15. Atrophy. 16. Intra-cellular Parasitismus. 17. Changes in reproduction. (Karyokinesis.) EFFECT OF THESE CHANGES UPON ORGANS : 1. Size. 2. Consistence. 3. Color. 4. Weight. 5. Functional activity. (Extent of cell degeneration necessary to exterminate all function is unknown.) 16 SYLLABUS OF GENEKAL PATHOLOGY. IMPORTANCE OF THE " COLOR PICTURE ": The " Color Picture " resultant from Chemical and Morphologic changes in the cells and intercellular sub- stances, e. fir., fat granules, dullness, yellowness, opacity, etc., etc. CELL DIVISION AND MULTIPLICATION UNDER PATH- OLOGIC CONDITIONS : 1. Karyokinesis. 3, Fragmentation. 3. Direct Division. 4. Endogenous cell multiplication (Giant Cell.) DEATH ; 1. Somatic or Physiologic. 2. Death from disease. 17 SYLLABUS OF GENEBAL PATHOLOGY. Chaptee II. BLOOD. CHANGES IN THE QUANTITY OF BLOOD IN THE VESSELS : 1. 2. 3. Oligsemia. Hypereemia. Heemorihage. COMPONENT PARTS OF THE VASCULAR AF 1. Heart. , 2. Arteries. 3. 4. Capillaries. Veins. HEART : 1. 2. Myocardium. Vessels. 3. Nervous endowment. a. Extrinsic. b. Intrinsic. c. Accelerators. d. Inhibitors. e. Strengtheners, /. Weakeners. ARTERIES J . Varieties in point of size. 2. Histology. 3. Vaso-motor apparatus, muscularis, vaso-dilatoVs and vaso-constrictors. 4. Vascular calibration and tension. 18 SYLLABUS OF GENEBAL PATHOLOGY. CAPILLARIES : VEINS : 1. Histology. 2. Intimate relation with oelis . 3 . Constant calibre. 4. Function. 1. Histology. 3. Mechanism. 3. Carrying capacity. 4. Function. OLIGiEMIA (MECHANICAL) : Lack of bloood in the vessels. 1. General. due to 2. Local. due to 3. Partial. due to 4. Total. due to 5. Collateral, due to a. Hypolasia Cordis. b. Diminished cardiac ac- tion. c. Haemorrhage. a. Vasomotor action. 6. Arterial obstruction. a. Hypolasia Cordis. b. Diminished cardiac ac- tion. 0. Haemorrhage. d. Vaso-motor action. e. Arterial obstruction. Complete arterial obstrucr tion : a. From without. b. From within. Is General or Local. HYPEREMIA (CONGESTION) : Hyperasmia of other ities (Ischaemia.) Pressure. Sclerosis. Thrombosis. Embolism. local- Excess of blood in a part. 1. Active, arterial or acute. 3. Passive, venous, chronic or mechanical. ETIOLOGY. a. -Chemical. 6. Mechanical. Effect of Hy{)eraemia on Vascular apparatus: Active, causes vascular paralysis. Passive, causes induration of vascular areas. 19 SYLLABUS OF GENERAL PATHOLOGY. HAEMORRHAGE : Escape of blood from vascular channels. Heemorrhage by : a. Rhexis. b. Diapedesis. Varieties. a. Arterial . b. Capillary. c. Venous. d. Suggillation. e. PeteccMse. /. Haematocele. LOCATION OF HEMORRHAGE : 1. Intra-cranial, - (Apoplexy.) 3. Epistaxis. 3. Hsemotliorax. 4. Hsemopericardium. 5. Hsemoptysis. 6. Hsematemesis. 7. HaBmoperitoneum 8. Hsematuria. 9. Metrorrhagia. 10. Heematocele. 30 SYLLABUS OF GENEEAL PATHOLOGY. Chaptee III. INFLAMMATION. DEFINITION: Result of congestion. Increased blood in the part, hence: 1. Swelling . 2. Heat, ^ Redness. 4. Pain. 5. Modified function. ACUTE HYPEREMIA : Behavior of vessels under prolonged acute Hyperaemia. 1. Vascular spasm, a. Vascular paresis, 3. Dilatation. 4. Increased speed of blood current, followed by: 5. Stasis. MICROSCOPIC CHANGES CAPABLE OF ACCURATE STUDY : Cohnheim's observations : Behavior of 1. Blood current. 2. Blood corpuscles, 3. Transudate. 4. Exsudate, 5. Diapedesis. 6. Emigration. 7. Cloudy swelling of Parenchyma- tous and other elements. 8. Phagocytosis (MetschnikofE's the- ory). CHRONIC HYPEREMIA : Venous congestion. 1. Mechanical nature of. 2. Aetiology. 3. Ultimate effect on the tissues. 31 SYLLABUS OF GENEBAL PATHOLOGY. RESULTS OF INFLAMMATION : 1. Resolution. 2. Inflammatory products. NOTE:— The real difference in these j products is only ^ in their varying proportion, e x - ^ cepting/. a. Serum. b. Pus. c. Fibrin. d. Various combina tions of Serum Pus and Fibrin. e. Membranous ex sudate. /. New formed fi brous connective tissue. NOMENCLATURE : 1. Serous. 2. Purulent. 3. Fibrinous. 4. Serous, Purulent, Fibrinous in various combina tions. 5. Croupous. 6. Productive. Rule for designation : Add " itis " to nam( of the part affected, e. g., Pneumonitis, Cyst itis, Nephritis, etc., etc. SPECIFIC FORMS OF INFLAMMATION : 1. Septicaemia. 2. Pyaemia. 3. Catarrhal. 4. Croupous, 5. Diphtheritic. 6. Tubercular. 7. Syphilitic, etc. CROUPOUS INFLAMMATION: Nature of products. Extent of exsudate. Essentially superficial. Aetiology. DIPHTHERITIC INFLAMMATION : Nature of products . Extent of exsudate. Essentially deep seated Aetiology. TUBERCULAR INFLAMMATION : Nature and cause. SYLLABUS OP GENERAL PATHOLOGY. SYPHILITIC INFLAMMATION : Nature and cause. OTHER SPECIFIC FORMS OF INFLAMMATION Lepra. Actinomycosis. Coccidiosis. CERTAIN OP THE SEQUtELE OF INFLAMMATION. PUS; Constituent elements : 1. Liquor puris. 2. Certain salts. 3. Albumin. 4. Leucocytes. 5. Usually Micro-organisms. 6. Granular detritus. 7. Blood. 8. Ptomaines, etc. Variable in quality, i. e.: 1. Laudable. 2. Sanious. 3. Ichorous. Color. Odor. Reaction. ABSCESS— ETIOLOGY— MODE OF ORIGIN : 1. Acute. Intense local inflammation. Pressure effects in area involved. Tissue ne- crosis, synchronously small round cell infiltration. Advent of Leucocytes 3. Chronic. 3. Cold abscess. Cause and nature. Abscess usually results from Microbi( infection : may result from trauma oi from Chemical irritation. 33 SYLLABUS OF GENERAL PATHOLOGY. ULCERATION : Superficial solution in continuity of the soft parts . Aetiology. Specific Forms: 1. Tubercular. 2. Syphilitic. 3. Varicose Ulcer, depending upon Aetiology. PY^^MIA— NATURE— VARIETIES : 1. Superficial. 2. Deep. 3. Empyema. PHLEGMON : Purulent infiltration of tissues. GANGRENE : Death en masse of the tissues. Aetiology: a. Infectious. b. Local. c. Oligsemia from endarteritis, atheroma, etc. d. Hypersemia from venous ob- struction. Varieties: 1. Moist or acute. 2. Dry, slow or senile. GRANULOMA : Histology. Vascularity, absence of nerves. Varieties. 1. Granuloma Simplex. 2. Specific (infectious) Granuloma; charac- teristic changes in perivascular spaces SUB-ACUTE INFLAMMATION : Cause and nature. CHRONIC INFLAMMATION ; Aetiology. 1, Chronic irritation . 2. Chronic Hypersemia. Results in induration. Permanent effects of Chronic Irritation is on the Stro- ma, and of the Chronic Hypersemia on the Parenchyma, 24 SYLLABUS OF GENEBAL PATHOLOGY. PARENCHYMATOUS INFLAMMATION : 1. Nature. 2. Location. 3. Acute. 4. Chronic. 5. Aetiology. Largely a nutrition disturbance due to : a. Organic intoxicants.as Ptomaines, deficient blood either in quantity or quality. 6. Inorganic intoxicants, as Phos- phorous, Arsenic, etc. INTERSTITIAL INFLAMMATION : Restricted, as a process, to the stroma of the tissue.' DIFFUSE INFLAMMATION : Involves, synchronously, Parenchyma and Stroma. ETIOLOGY OF INFLAMMATION— SYSTEMIC COM- PLICATIONS. CASEATION : How difEerent from abscess. Granular, albuminous and fatty degeneration of all the tissue elements involved in the lesion. Microscopic findings. Cause. — Complete occlusion of trophic vessels. MIXED INFLAMMATION : One variety may be superinduced by another, e. g. Typhoid Lymphadenitis, perforation of intestin( resulting in Septic Purulent Peritonitis, or Tuberculai Pneumonia, pulmonary cavity filled with pus anc septic organisms, resulting in Pyssmia. ^TIOLOGIC FACTORS IN INFLAMMATION : 1. Extremes of o. Cold. b. Heat. 2. Inorganic Chemical substances: acids, poisonou salts and metals. 3. Organic Chemical substances: ptomaines, toxa] bumins. 25 SYLLABUS OF GENEEAL PATHOLOGY. Chapter IV. PATHOLOGY OF THE BLOOD. (Normal Data.) PHYSIOLOGY : Color : 1. Arterial Blood, the light red of Oxyhsemoglobin 3. Venous Blood, dichroio, due to MetlisemoglobiE (Lenhartz). a. Dark red by transmitted light. b. ■ Green by reflected light. Reaction': Intra-vitam, normally always alkaline. Method of de- termining reaction. Specific Gravity varies, according to Landois, be- tween 1045 and 1075, and, according to Lloyd Jones, between 1035 and 1068 ; von Jaksch says that it is lower in females than in males. Method of determining Specific Gravity. Quantity, one-thirteenth of body weight. Other phenomena: coagulability, etc. HISTOLOGY : 1. Stroma or Plasma. a. Water. b. Albumins and fats. c. Salts. d. Ferments. 2. Parenchyma or Corpuscles, a. Red. b. White. c. Placques. Red Corpuscles or Er-xthrocytes : Bi-concave, circular discs, composed of albuminous Stroma and Haemoglobin . y^ inch m diameter. 26 SYLLABUS OF GENERAL PATHOLOGY. Haemoglobin composed of an Albumin nearly re- lated to Globulin and a coloring matter containing Iron — Hsematin. Hsematin plus Cblorine makes Hsemin. Spectrum Analysis (Sorby-Browning Microspectro- scope). 1. Oxyhaemoglobin. 2. Free reduced Haemoglobin. 3. Methsemoglobin. Red corpuscles are freely soluble in Ether and Chloro- form. Origin of red corpuscles, for the most part, the bone marrow. White Coepuscles or Leucocytes : Of these there are five principal varieties according to origin and structural elements. Ehrlich's classification is as foUo-ws : 1. a. Granules or Eosinophiles. — Coarse granules _ which take only the acid color from the neutral stain. In suckling animals originate principally from the bone marrow. 3. h. Granules or Amphophiles. — Fine granules originating in the human marrow, 3. c. Granules (Mastzellen) Basophiles, which are stained only by basic analine dyes. 4. d. Granules or Basophiles.— Mostly found in Mon- onuclear cells. 6. e. Granules or Neutrophiles. — Commonest of all the forms. Always found to take from the color mixture only the neutral stains. Classification According to Morphology : 1. Eosinophile. — Are various in structure. The cell- body varies in size between that of the small Lymphocyte and the larger cells. The so called " marrow cells " can also be Eosinophiles. Nucleus not regular in structure, the majority being polymorphous. The Granules may show transition forms between the a and 6 granules. According to Zappert these vary, normally, between .67^ and 11^ of the total White Coi'- puscles or 55,784 per cubic millimeter. These cells are regularly increased in Bronchial Asthma and diminished even to total absence in Croupous Pneumonia,. 27 SYLLABUS OF GENERAL PATHOLOGY. 2. NeutropMles. — Size of body and form of nuclei vary greatly. Body averages the diameter of tl Erythrocyte. Nucleus generally Polymorpliou Transition forms usually possess a single nuclei constricted in one or more places. These eel multiply in the majority of the so called Leucoc^ toses. They are also Phagocytes. 70 to 80 per cent, of the White Corpusolei normally, and form the most of the cells i theexsudate fluids.e.g., Pus, and in Leucsemii 3. Basophiles. — Usually small, not exceeding the d ameter of the Erythrocyte. One round nuclei; and relatively coarse granules, never as coarsi however, as those of the Eosinophiles. According to Cannon, always present in th blood of healthy and sick children. Accorc ing to Ehrlich and von Limbeck, never no: mally present in adults and only present i Leucaemia. 4. Mastsellen. Mdrphologically mostly transitio forms. Found in Leuceemia. 5. So called "Marrow Cells," — Mostly very larg cells whose nuclei very nearly fill the body c the cell and are poor in Chromatin. Placques : Nature. Origin. Size, etc. ENUMERATION OF CORPUSCLES : 1. Red. — Methods of Vierordt; Welcker, et al, consis in the proportional dilution of a definite quantit of blood in suitable fluid media, and the countin of the number of corpuscles in a given space, e. g. Sodii Snlphatis 5.0 cc Sodii Chloratis 2.0 oc Hydrargyri Chloridum Corrosivum . . . 0. 5 c Aqua Destillata 200.0 c M. Sig.—Hayem's Fluid. Sanguinis 1.0 cc Solutio Hayem's . 100.0 cc M. Sig.— For numerical estimates, th blood is to solution as 1 is t 100. 28 SYLLABUS OF GENEEAL PATHOLOGY. 3. White.— Use a pipette witli larger calibre. Solution of Acetic Acid i to i per cent., wliicli dissolves tlie red corpuscles. 1 to 20, 1 to 35 or 1 to 50 of blood and solution, as above described, depending upon the number of white corpuscles. 0,000 to 10,000. Average for adults, 8,000; aver- age for children, 9,500 in 1 cubic millimeter. (Rieder, Lenhartz.) 3. Placques. — No exact method is kuown for count- ing the placques. THOMA-ZEISS APPARATUS : Used for the enumeration of both white and red cor- puscles. Each quadrate formed by the rulings has a square surface of ^fir sq. m.m. The height of the chamber is -j^ m.m. The cubic capacity of each com- partment is, therefore, ^^^^ cubic millimeter. Example : If in 128 quadrates there are 1580 red cells, in a solution of blood 1 to 100, there would be in one compartment y^5 of 1580 or 13.3 cells. Each compartment has a cubic capacity of ^^^ cubic milli- meter, hence one cubic millimeter or f|^ would con- tain 13.3x4000 or 49,300.0- cells, and, since this is a 1 to 100 solution which is being examined, the un- diluted blood would contain 100x49,300 or 4,930,000 red corpuscles in one cubic millimeter. The normal average is 5,000,000. ESTIMATION OF HEMOGLOBIN : Pleischel's Hsemometer, Normal Haemoglobin equals 14 grammes to 100 c.c. of blood. Since percentage equals part in a hundred, a specimen of blood which is shown, bjr Fleischel's Hae- mometer, to contain 75^ haemoglobin, will yield tVo of 14 or 10.5 grammes of Haemoglobin in 100 c.c. of blood. METHOD OF PREPARING BLOOD : Dry preparation.— Smear the cover j;lass. Dry in the air. Fix in the Bunsen flame or in absolute alcohol or in absolute alcohol and ether, equal parts. (If in alcohol leave it for i to 1 hour.) Schwarze's copper plate may be used for fixing. 29 SYLLABUS OF GENEEAL PATHOLOGY. STAINING 1. 0.1 to 0.5 per cent. Aqueous solution of Eosin from 10 to 20 minutes. Wash in water. Dry. Mount in Xylol Balsam. Red cells take intense, even red. Protoplasm of white cells, faintly tinted. Eosinophile granules appear as unusually strongly stained spherules .- 2. Triple Glycerine Mixture : 5 Eosin ) Aurantia [■ aa 2.0 Nigrosinor Indulin. ) Glycerine 30.0 M, Sig. — Stain 16 to 24 hours. Copious wash- ing in water. Dry. Xylol Balsam. Red cells, orange. Bodies of Leucpcytes, dirty gray ; nuclei darker. Eosinophile granules, intense red". 3. Hsematoxylin and Eosin Solution (Ehrlich's. ) 5 Aqua destillata ... ) Alcohol y.&a, 100.0 Glycerine ) Hsematoxylin 4.0 to 5.0 Acid Acetic, Glacial 20.0 Alum in excess. M. Sig. — Let stand 4 to 6 weeks in the sun and then add 1 per cent, of Eosin. Stain in covered dishes in the sun. Dry. Xylol Balsam. Red cells, strawberry red, sometimes orange ; if nucleated, nuclei dark, black. Bodies of Leucocytes, light ; nuclei, dark lilac. Eosinophile granules, intense red. Lymphocytes, protoplasm scarcely stained; nuclei, blackish or shade lighter than those of erythrocytes. 4. Ehrlich's Tri-acid. Solution : a. 5 Aqua Destillata 100.0 Orange G 135.0 Acid Fuchsin 65.0 ft. Aqua Destillata 100.0 Alcohol, Absolute 100.0 Methyl-green 126.0 30 SYLLABUS OP GENERAL PATHOLOGY. c. Aqua Destillata 100.0 Alcohol, Absolute 100.0 Glycerine 100.0 Mix the three solution^ slowly together and allow them to stand for several weeks before using. Stain two, six or eight minutes. Finish as before. Erythrocytes, golden; their nuclei, green blue;' Leucocytes appear mostly as neutrophile, fine violet granula ; nuclei, grfeenish blue." Eosinophile granula, light red. 6. Chenzinsky — Plehn Solution : Concentrated Aqueous Solution Methyl Blue, 40.0 .5^ solution of Eosin iu 70^ Alcohol ... ..^0.0 Aqua Destillata 40.0 M. Sig. — Stain cold 24 hours, hot fifteen minutes. Mount as before. Red cells, eosin red. Eosinophile cells, light red. Nuclei , blue. 6 . Ehrlich's Neutral Stain 5 Saturated Solution Acid Fuchsin 5.0 Concentrated Aqueous Sol. of Methyl Blue, . .1.0 M. Sig. — Mix Methyl slowly with Fuchsin under constant agitation. Let stand for several days. Stain five to twenty minutes. Red cells, strong acid fuchsin red. Nuclei of those and of white cells, sharp black or light blue. Eosinophile and Neutrophile, violet ; granula very clear with oil immersion lens. 7. 5 Concentrated Aqueous Sol. Methylene Blue, 40.0 .5^ Eosin in 70^ Alcohol »0.0 Glycerine 20.0 Aqua Destillata 20.0 M.Sig. — Staining requires 12 to 24 hours and the solution easily deteriorates. 31 SYLLABUS OF GENEBAL PATHOLOGY. 5 Eosin (Crystals) 5 Hsematoxylin 2.0 Absolute Alooliol ... J Aqua Destillata >■ aa 100.0 Glycerine ) Acid Acetic, Glacial 10.0 Add Alum in excess. This colors in the course of ^ to 1 hour. This gives a splendid nuclear stain, while the neutrophile cell granules are not specifically stained. Ehrlich's Mixture: 9. ^ Orange G 13.0 to 14.0 Acid Fuchsin 6.0 to 7.0 Aqua Destillata 15.0 Alcohol 15.0 Methylene Green 12.5 " Alcohol 10.0 Glycerine lo.O For the demonstration of proportions. — The- cell elements appear beautifully and distinct- ly colored. This tri-color used iu saturated aqueous solution, which is colored by long standing. The materials are measured out into the same measure glass in the order given above' and thoroughly shaken. The mixture keeps well and colors in from 5 to 15 minutes. 10. For the staining of Blood Placques, Eabl recom- mends the following procedure : The preparation is: a. Fixed in Physiological Salt Solution (.75^), saturated with sublimate for i to i hour. b. Washed in distilled water. c. Placed for a half hour in Mor daunt consisting of a 1,S^ solution of Iron-Alum with equal parts of water. d. Put for from i hour to 1 hour in fresh saturated solution of Hsemotoxylin. e. Again into the Mordaunt, diluted. The Red Corpuscles are then decolorized and the Blood Placques are dark black-blue. 32 SYLLABUS OF GENERAL PATHOLOGY. 11. Widal's reaction. — This observer has shown that if the blood of a typhoid patient be withdrawn a week after the onset of the fever, and mixed in the proportion of one part of blood to one-hundved parts of a Bouillon culture of the typhoid bacillus, there is a tendency for the Bacilli to lose their motility, partially at first and then completely, while at the same time they collect in clumps. If the hanging drop of such a mixture be examined with an oil immersion lens these phenomena are directly observed to occur within the space of a half hour. A control experiment should be made with the Bouillon culture to determine the motility of the organisms. The theory of this reaction is based upon the supposition that, as the disease progress- es in the system, the serum of the blood acquires germicidal properties ; in other words, becomes an antitoxin. PATHOLOGIC DATA. PARENCHYMA, MORPHOLOGIC CHANGES : 1. Red Cells : a. Poikilocytosis (Quinke). Schistocytosis (Ehrlich). Size greater; shape altered;, numbers di- minished. Possible relation to respiration (Lenhartz) . •h. 1. Normoblasts ; nucleated red cells, nor- mal size. 2. Megaloblasts or Gigantoblasts ; nucleat- ed red cells three to five times larger than normal. Possible relation of Normoblasts to regenerative process. Definite relation of Megalo and Gigantoblasts to Pernicious An- Eemia. 33 SYLLABUS OF GENEBAL PATHOLOGY. e. Megaloc'ytesj giant red cells J often con- tain increase of Haemoglobin; regarded as criterium for Pernicious Anaemia (Laache). Seen sometimes in Chlorosis, d. Microcytes; small spherical Hsemoglo- binated bodies, supposed to be new- formed corpuscles (Gram). Most often seen after acute Haemorrhagic Olig- semia. €. Ansemic degeneration (Lenhartz). Red cells react feebly to stains. Evidence of rapid degeneration of fresh elements from bone marrow, hence of severe gen- eral lesions of pernicious type. /. HsemoglobiniRemia (Ehrlich). Triple glycerine stain reveals bright red bodies within the erythrocytes. 2. Leucocytes : a. Purely Morphologic relations. Size, fine and coarser gianulation ; various form of nucleus. h. Probably duplex origin from (l) Lymph Glands and (2) Spleen (Max Schultze, Virchow, Ehrlich, et al). Ehrlich's color analysis : 1. Eosinophile Cells. 2. Neutrophile Cells. 3. Mastzellen or Basophile Gran- ules. . Percentage ofl, 2 and 3 in the Blood. c. Lymphocytes, 25?^ ; Polynuclear Cells, 7S^. Of these latter, .12 to 4^ Eosinophile ; scarcely .5^ Basophile ; remainder, Neutro- phile granules. d. Eosinophile cells must be studied, for diag- nostic purposes, with dry preparations, stained. Diagnostic interest lies in the presence in the blood of Eosinophile cells, nor- mally found only in bone marrow. See Leucaemia. Mastzellen. Origin from fixed connective tissue corpuscles (Ehrlich) also in part from spleen. Common in Leucaemia, also in spu- tum of Asthma. 34 SYLLABUS OF GENEBAL PATHOLOGY. THE BLOOD IN SPECIAL DISEASES. a. AN^.MIA. 1. Simple, primary. 2. Simple, secondary. 3. Severe, pernicious. 1 . Simple primary (CMorosis) : Color paler ; hsemoglobin, SO to 40 and even to 10^. Specific Gravity often markedly diminished. Ery- throcytes usually normal in number and form. Leucocytes not increased ; occasional per c&nt. in- crease of Eosinophile cells. Severe cases (see 3) Haemoglobin, 15 to 20^. Specific Gravity, 1033 ; Erythrocytes sink to 3,500,000 or 3,000,000. Exquisite Poikilocy- tosis or Schistocytosi§. 2. Simple, secondary Ansemia : Blood changes depend usually on form and duration of primary disease, e. g. Tuberculosis, Carcinoma, Syphilis, Nephritis Chronica. Erythrocytes reduced in number and per cent, of Hsem'oglobin; not usually changed in form. Leu- cocytes relatively, sometimes actually, increased in numbers. Occasionally Poikilocytosis, Normoblasts, etc. Possible Primary Anaemia, when these latter are present. Hypeririosis. May merge into the pernicious form . 3. Progressive Pernicious Anaemia : Color normal ; pale, occasionally dark, thin cq^ee or tea color. Often vei^ fluid. Erythrocytes amazingly reduced in numbers. Exquisite Poikilocytosis, Micro and Megalocytosis. Placques greatly reduced in number (?) (Hayem). Hypinosls. Total absence of Eosinophile cells regarded as an evil circumstance (Ehrlich, Lenhartz). Reason for this. 35 SYLLABUS OF GENEKAL PATHOLOGY. b. LEUC^MIA: Necessity for corpuscle counting, and dried stained prepa- rations. Leucocj^tes greatly increased in number ; may reach one to eight, ten or twenty of red cells ; even one to two or more (Fleischer, Penzoldt). DiPFEEBNTIAL DIAGNOSIS OF DIFFERENT FORMS : 1. Lymphatic Leucaemia. Increase in number of those Leucocytes resembling in size Erythrocytes (Basophiles). 3. Increase in larger Leucocytes. a. Marrow form. When large mono-nuclear leucocytes. b. When large cells with highly refractive granules are present. Large mono-nuclear cells particularly diagnostic of Leucaemia. .Advantages of Ehrlich's differential stains. c. LEUCOCYTOSIS : Transient increase in the number of white cells. 1. Physiologic form,— Digestion, Pregnancy, Infan- tile. 3. Pathologic form,— Chronic Cachectic lesions, severe exsanguination, shortly ante-mortem. Hydraemia, 20,000 to 30,000 Leucocytes in 1 cubic millimeter of blood. Various cell forms indifferently increased. Polynuolear cells particularly abund- ant in Carcinoma cachexia. 3. Inflammatory Leucocytosis,-7-Differential diag- nostic and prognostic value. Present in Penumonitis, Scarlatina, Pri- mary Meningitis, Sepsis, Puerperal Fever- Erysipelas, Acute Articular Rheuma, tism. Diphtheria, Febris Recurrens, Osteo- myelitis. Absent in Tubercular Meningitis, Measles, Pleuritis, Peritonitis-, Typhus Abdominalis. 36 SYLLABUS OF GENEBAL PATHOLOGY. d. PSEUDO-LEUC^MIA. Microscopic findings negative in spite of glandular en- largement, etc. e. HJEMOGLOBIN^MIA. f. MELAN^MIA. S'. CARBON-DIOXIDE POISONING. h. MICRO-ORGANISMS. Plasmodium Malaria : Discovered, 1880, by A. Laveraii. Place in Zoological system disputed. Sporozoon and Coccidia according to Metsch- nikoff and Mannaberg. Rbizopodia, i. e., Amoeba according to Autolisi, Grassi and Feletti. Three principal forms : a. Spheres. h. Flagellate bodies. c. Crescentic forms. During some period of their existence these parasites usually contain a pigment derived from the Erythro- cytes which they regularly infest. Four species generally recognized : 1. Parasite of typical quartana. 2. Parasite of typical tertiana. 3. Parasite of pernicious quotidiana. 4. Parasite of malignant Tertiana. Mixed infections with these parasites may occur. OTHER BLOOD PARASITES : Recurrent fever, Spirochaeta Obermeieri. Filaria Sanguinis Hominis. Distoma Haematobium (Bilharzia Hsema- tobia.) For accurate descriptions of blood parasites, consult Stengel, Cabot, ■i;. Limbeck, -y. Jacksch, Ehrlich, etal. 37 SYLLABUS OF GENEEAL PATHOLOGY. Chapter V. PATHOLOGY OF THE VASCULAR APPARATUS. a. HEART. b. ARTERIES. c. CAPILLARIES, VEINS, LYMPHATHICS. a. HEART. NORMAL DATA: Pathological changes in organs depend upon the Patho- logical changes common to the elementary tissues which compose them. Heart is the size' of the fist ; weight, 12 ounces ; average thickness of left ventricular wall, f inch to | inch; of right ventricular wall, -J- inch to i inch. HISTOLOGY: 1. Three Coats : a. Pericardium. b. Myocardium. c. Endocardium. 3. Vascularization 3. Coronary Vessels. 4. Intrinsic Cardiac Circulation. 5. Nerves. a. Intrinsic. b. Extrinsic. Terminal nature of the Coronary Arteries. Vital import of Intrinsic Cardiac Ganglia. 38 • SYLLABUS OP GENEBAL PATHOLOGY., PATHOLOGY: (PiiRICARDIUM.) 1. Hypoplasia. Dystociee. 2. Hyperaemia. a. Simple. Difference in vascularity between the visceral per- icardium and the epicar- diumj the epicardium much more vascular. b. Inflammatory. 3. Haemorrhage, a, Punctiform, usually parietal near base of heart ; seen in Scorbutus ; cerebral lesions ; Anaemia; Leucaemia ; Morbus Maculosus ; Phosphorous pois- oning ; Sepsis ; Tuberculosis ; Murder, especially in infants (Orth). b. Profuse. From lesions or tra- uma of the great vessels and Tuberculosis ; also Myocardial softening from Coronary em- HYDROPS PERICARDII : ^°^^'^ °' endarteritis. Oedema proper^never present. Marked transudate not in- frequent. May occur during or just after the death agony. Effect on 1. Sac. 3. Lungs. 3. Heart. ./Etiology 1. Circulatory disturbances. 3. Alterations in blood. 3. Hydrops ex vacuo (?) (Orth). Hydrops may amount to one litre or more, in which case, pericardial disten- sion and atrophy (gelatinous) of epicar- dial fat (Orth). ' f PERICARDITIS : 1. Serosa. Inflammatory Hydropericardium. Fluid usually small. May be large in amount, say one litre or more. 2. Sero-Fibrinosa. Fibrin in and on pericardium. 3. Pibrinosa-sicca. Always marked Hyperaemia and cell infiltration. May result in re- sorption, or organization with per- manent adhesion of parietal and visceral portions. a. Distension a.nd compromise of cardiac cycle. h. Congestion and compro- mise of function, especially of the left lung. Miiologj, microbio infection. 39 SYLLABUS OF GENERAL PATHOLOGY. 4. Productiva. 5. Purulenta. Absence of Endothelium, yellow elastic tissue the boundary layer. Process either general or local . Effect of fluid, — synechia, adhesion ; Vascularization with new form^d connectire tissue, — permanent adhesion. Other sequsele, — Pus, Haemorrhage. These usually due to progression in continuity of other structures. Secondary nature of pericarditis, — Articular Rheumatism, Pleuritis, Pneumonitis, Peritonitis, Infectious disease in general, Nephritis. Generally combined with Fibrinosa- sioca; may be pure or in combination with Pericarditis Productiva, which will be after a crisis and with chronicity as a result. Findings in Pericardium ; an- alysis of Pus. Etiology, —the general causes of purulent inflammation, i. e. , microbic infection. 6. Tuberculosa, a. Acute 6. Chronic c. Miliary d. Diffuse Differences due to differ- ence in mode of invasion. Tubercle bacilli travel through vessels, or, by continuity, through the tissues ; is Primary or Secondary. Primary is the younger and Secondary is the older. Hydropericardium is particularly apt to be present in diituse tubercular pericarditis. 7. Syphilitica. Exceedingly rare. 8. Progressive nutrition disturbances. 9. Adipose Metaplasia. 10. Neoplasms. 11. Regressive nutrition disturbances. PATHOLOGY (MYOCARDIUM AND ENDOCARDIUt): GENERAL PATHOLOGICAL DATA: Myocardium and Endocardium considered together. Le- sions those of any organ with Parenchyma and Stroma. Specific peculiarity of the heart as an organ,— contractility, vascularization, nervous endowment. Lesions ultimately effect both quantity and quality of blood supply to the tissues, hence general nutrition. 40 SYLLABUS OF GENERAL JPATHOLOGY. HYPOPLASIA CORDIS (Foerster's classification) : 1. Diefective arterial arches. 2. Transposition of great trunks. 3 . Patency of Fcetal apertures. 4. Atresia. a. Deficient valves. b. Ectopia cordis. c. Dexio-cardia. CIRCULATORY DISTURBANCES : Difficulty of determining Myocardial blood contents ; Rigor Mortis ; Pigment. Oligsemia. 1. Partial. 2. Severe. 3. Chronic. When Chijonic, combined with other changes : o. Regressive degenerations. 6. Rupture. c. Fatty degeneration. Sudden syncope from acute local Oligsemia. Hydro-pericardium, — embolism, coronary atheroma. HYPERJEMIA : Difficulty of recognition, T- sought for on anterior aspect of organ. Chronic Venous Hypersemia,— inevitable sequsele are : a. Venous dilatation. 6. Diapedesis and migration. c. Peri-vascular induration. CONGESTIVE HYPEREMIA. Causes: 1. Original vaso-motor relations. 2. Theoretic Hypersemia in Goitre Exohpthal- mus. 3. Infectious diseases. 4. Increased Cardiac activity. 5. Penetrating endocardial lesions. There is no Endocardial Hypersemia, for the reason that the Endocardium has no blood supply. The exception to this is in Endocarditis Productiva. 41 SYLLABUS OF GENBBAL PATHOLOGY. HEMORRHAGE : Severe. From wound or rupture. From general blood changes. From Pathological changes in intracardiac vessels. Venous congestion. Arterial pressure, Ecchymoses. Thrombosis, Embolism. MALIGNANT EMBOLISM : Multiple abscess, etc. HEMORRHAGIC INFARCT. CEDEMA. MYOCARDIUM AND ENDOCARDIUM : 1. Myocarditis Degenerativa seu Parehchymatosa, simi- lar in all respects to other parenchymatous inflam- mation. 2. Myocarditis Purulenta ; localized or disseminated ; metastatic or by continuity. 3. Myocarditis Productiva. i. Myocarditis Interstitialis Chronica. 5. Myocarditis Papillaris ; Conus Stenosis ; Cardiac aneurysm from cicatrization. 6. Myocarditis Tuberculosa. 7. Myocarditis Syphilitica. ENDOCARDITIS : 1. Verrucosa. Ultimate result, thickening and con- traction. 2. Productiva. a. Granulating. b. Fibrous. 3. Chordalis Chronica. 4. Ulcerosa Atheromatosa. 5. Ulcerosa Malignans. FUNCTIONAL LESIONS OF VALVES FROM ENDO- CARDITIS : 1. Mitral insufficiency : a. From valve perforation, — chord rupture. b. Through cardiac dilatation ; left ventricular hypertrophy; capillary stasis; dilatation with hypertrophy of left ventricle. 42 SYLLABUS OF GENEBAL PATHOLOGY. 2. Mitral Stenosis. — Commonest with Hyperplasia and thickening of valve ; calcification of flaps and chords. Nature of secondary degenerations depends upon pre- ponderance of stenosis or regurgitation. Dilatation of left Auricle ; Vascular stasis. 3. Tricuspid insufficiency from vascular stasis ; hyper- trophy and dilatation of right ventricle. AORTIC CUSPS. INSUFFICIENCY: Ulceration ; Rupture ; Perforation ; Retraction ; Marked hypertrophy -with dilatation of the left ventricle ; Pa- pilliary muscles often markedly flattened. Dilatation of Aorta from great volume of blood with each systole ; Stasis in capillaries. STENOSIS OF AORTIC ORIFICE : Hyperplasia ; Calcification of cusps ; Thrombosis ; Marked left ventricular hypertrophy and dilatation ; ultimate in- volvment of pulmonary circulation. TRICUSPID INSUFFICIENCY : Seldom primary; secondary to right auricular and right ventricular dilatation. TRICUSPID STENOSIS : Very seldom ; sometimes congenital; commonest as com- plication with left valvular lesions. PULMONIC INSUFFICIENCY: Very seldom ; occasionally through rupture of valves or aneurysms. A secondary lesion in twenty-five per cent, of all cases. May be Embryonic in origin. PROGRESSIVE NUTRITION DISTURBANCES : Hypertrophy. Causes ; Nature ; end result if progressive. REGRESSIVE NUTRITION DISTURBANCES : Brown Atrophy. Fatty Degeneration. Fatty Infiltration. Necrotic Degenerations. Waxy Degenerations. Hyaline Degenerations. Amyloid Degenerations. Anaemia. Co- agulation Necrosis, results in Cicatrix, Rupture, Calci- fication. 43 SYLLABUS OP GENERAL PATHOLOGY. 6. ARTERIES. VASCULAR LESIONS AFFECT : 1. Resiliency. 2. Contractility. 3. Carrying capacity. ■ 4. Osmotic properties of vessels, hence ultimate nutri- tion of vessels and tissues generally. CLASSIFIED LESIONS: 1. HypoplasisB. Small calibres, anomalous origin and distribution. 2. Changes in blood current : a. Of Vasomotor origin. Neuroses. 6. Thrombus and Embolus. Benign. Septic. c. Productive Inflammation. ■ Non-specific. Specific. 3. Inflammations. t a. Periarteritis. b. Mesarteritis. c. Endarteritis. d. Arteritis DifEusa. e. Arteritis Acuta. /. Arteritis Chronica. ■ g. Arteritis Tuberculosa. h. Arteritis Syphilitica. 4. Progressive and Regressive Nutrition Disturbances in: a. Periarteritis. b. Mesarteritis. c. Endarteritis. d. Arteritis Diffusa. e. Arteritis Acuta. /. Arteritis Chronica. g. Arteritis Tuberculosa. h. Arteritis Syphilitica. i. Atrophy. j. Dilatation. Etc. 44 SYLLABUS OF GENEBAL PATHOLOGY. 5. Degenerations. a. Amyloid. 6. Hyaline. c. Fatty. d. Atheromatous. 6. Aneurysm. Nature. Origin. Varieties : a. Cylindrical. b. Fusiform. c. Saccular or Sacculated. d. Cirsoid. e. Dissecting. f. Miliary. g. Venous Varix, or Phlebectasia. h. Varicose. i. Aneurysmal Varix. True and false Aneurysm, differential points. CAPILLARIES, VEINS, LYMPHATICS. CAPILLARIES : In acute exsudate inflammation, productive inflammation, Telangiectasis,— Simple degeneration, Patty, Chalky, Hy- aline, Amyloid. Lesions resulting in Haemorrhage by (a) Diapedesis and by (6) Rhexis. Fatty degeneration. Pernicious Ansemia. Leucaemia. Infection. Miliary Aneurysm. CAPILLARY CONTENTS: Thrombus, Embolus. Degeneration of capillary contents largely dependent upon lesions of capillary walls. Vast import of septic embolus. Parasitismus in general. Relation to metastasis of neoplasms. 45 SYLLABUS OF GENERAL PATHOLOGY. VEINS : Hypoplasia of minor interest. Circulatory lesions similar to those of arteries, but com- moner. Inflammation, — Phlebitis Exsudativa. Phlebitis Septica. Phlebitis Productiva. Phlebitis Tuberculosa. Phlebitis Sjrphilitica. Thrombosis. Organization of clot. Progressive nutrition disturbances, — Hyperplasia through increased activity in Angioma Cavernosa. Neoplasms, Primary and Secondary, commoner than in arteries. Regressive nutrition disturbances, — Atrophy; Fatty, Amyloid, Hyaline, Calcareous degenerations. LYMPHATICS : Same as Veins. 46 SYLLA.BUS OF GENEEAL PATHOLOGY." Chaptee VI. BACTERIA. MICRO-ORGANISMS IN DISEASE. CARL FRAENKEL'S HYPOTHESIS : "The Bacteria are, in the truest sense, members of the plant world, nearly related to the lower Algse. They fall in a series of well circumscribed species, different from each other in behavior and form, and not merging into each other." The forms in which Bacteria present themselves are: Sphero-Bacteiia or Micrococci; Rod Bacteria or Ba- cilli ; Screw Bacteria or Spirillse. Bacteria are cells, but have no nucleus ; have cell contents and membranes ; Capsules. Varieties : Diplococci. Strepto-cocci. Staphylococci. Zooglea masses. Motility by means of Flagellse or Cilise. Spore formation : a. Arthrospores, , b. Endos pores. Spores, the permanent form of some species. SAPROPHYTES, PARASITES, FACULTATIVES : Influence of temperature; of Oxygen. Aerobes and Anaerobes. Facultative AnaSrobes. 47 SYLLABUS OF GENEEA.L PATHOLOGY. PRODUCTS OF BACTERIA : Ptomaines. Fermentation. Putrefaction. Liquefaction of Gelatin or peptonization. Pigment formation. Gas formation. Induction of infectious disease. Pathogenic organisms. TECHNICAL METHODS : Microscope. Immersion lenses. Abbe illuminator. Dia- phragms, etc. The " Hanging Drop." STAINING METHODS : ' In general the basic analine dyes, carbolic acid, analine oil, etc. Dyes: Fuchsin, Methyl Blue, Gentian Violet, Bismarck Brown. Cover glass preparations : Koch's i fixation methods. Flaming. Staining, Differential stains, spores and rods. Tubercle, etc. CULTURE METHODS: Nutrient materials : Bouillon, Gelatin, Agar- Agar, Blood, Serum, Potatoes. Isolation of col- onies. Pure cultures: Plate method (Koch). Roll Tubes (Esmarch). Petri dishes. Sternberg's bulbs. In- oculation methods. Thermostats, Anaerobic cultures. Sterilization : 1. Heat continuous, dry. Steam, discontinuous. Formalin and steam. 2. Chemicals,— Corrosive Sublimate, Car bolic Acid, etc. EXPERIMENTAL METHODS : Treatment of animals. Septic, Pyogenic, Specific organisms. MICRO-ORGANISMS IN ETIOLOGY. ANTITOXINES : Diphtheria, Tetanus, Hydrophobia. 48 SYLLABUS OF GENERAL PATHOLOGY. Chapter VII. PATHOLOaY OP THE RESPIRATORY APPARATUS. a. NARES. b. LARYNX. c. TRACHEA AND BRONCHI. d. LUNGS. NORMAL DATA: Accurate gross anatomy and histology essential to the study of Respiratory Pathology. Arrangement of Bones, cartilages, sub-mucosa, mucosa, vascularity. Difficulties at hand because of few post-mortems. a. NARES. 1. Constituent parts. 2. Hypoplasia. Asymmetry, septal deviations, cleft palate, complete and incomplete. Absent septum. Hypoplas- tic ethmoid and nasal bones. Atresia Naris posterius. 3. Circulatory lesions. Chronic Hyperaemia, of cardiac and pulmonary origin. Local Hypersemia from press- ure. Acute Hypersemia, various causes. 4. Epistaxis occurs readily. Causes: Fracture, Typhoid, Vicarious Menstruation, Ansemia, Chlorosis, Heemo- philia. 6. CEdema is common, often sudden ; usually of inflam- matory origin ; may be neurotic. 49 SYLLABUS OF GENEEAL PATHOLOGY. 6. Inflammation, all known forms. Serous ; Purulent ; Fibrinous ; Serous, Purulent and Fibrinous in various combinations ; Croupous ; Productive. 7. JEtiologic factors the same as those of Inflammation : a. Extremes of, — Cold ; Heat. 6. Inorganic chemical substances, — acids, poison- ous salts and metals. c. Organic chemical substances, — Ptomaines, Tox- albumins. RHINITIS : 1. Purulenta. Superficial. Deep. Empyema of Antra and of frontal sinuses. etiology: Dental caries; Gonococcus ; Rotz. Scarlatina. Small Pox. Diphtheria. 2. Croupous. Seldom primary; is secondary to similar le- sions in mouth by continuity. Nature of associated Rhinitis. 3. Diphtheritic. Seldom primary; is secondary to sim- ilar lesions in mouth by continuity. Nature of associ- ated Rhinitis. Recurrent Diphtheritic Rhinitis. 6. Chronica. From Primary Rhinitis Purulenta. Re- gressive tendency. Progressive atrophy. CEzena. Exact findings. 5. Productiva. May involve, also, adjacent cavities, as the Antra, frontal sinuses, etc. Hydrops Antra High- morii is a misnomer. Periostitis. Perichrondritis. Osteitis with caries. 6. Tuberculosa." 7. Syphilitica. 8. Rhinoscleroma : Frisch's oi-ganism. Histology. 9. Lepra. 10. Progressive nutrition disturbances.— Polyp. Cyst. Cyst-adenoma. Fibroma. Myxoma. Enchondroma! Osteoma. Sarcoma. Carcinoma. 11. Perforating Ulcus Septi. Foreign bodies. Rhinoliths. 12. Parasites. 50 SYLLABUS OF GENERAL PATHOLOGY. i. LARYNX. NORMAL DATA. HISTOLOGY : Abundant sub-muoosa in spots. Practical absence in others. Great vascularity. Abundant glands in mu- cosa. Solitary Lymph Nodes. Nerves. Epithelium. Difference between Mucosa Naris and Mucosa Laryngis. HYPOPLASIA : Aplasia complete. Hypoplasia in varying degrees. CIRCULATORY LESIONS : 1. Haemorrhage. Profuse not common. Petecchial very common in acute specific disease and trauma from cough. 3. CEdema. The most important circulatory disturbance. QEdema- Laryngis. CEdema Glottidis. Laryngismus Stridulus. 3. Hydrops Laryngis. Cachectic Hydrsemia. Cardiac, renal and chronic 'stasis. CEdema in loco, froni press- ure of neoplasms. Chronicity of all these. 4. Inflammatory CEdema. Difference from other forms. Extent. Location. Color Picture. Origin. 5. CEdema Circumscripta. Around chronic ulcer. INFLAMMATION : 1. Catarrhal. 2. Fibrinous, a. Croupous. 6. Diphtheritic. Differential points between Crou- pous and Di^theritic. -iEtiology not simple. 3. Laryngitis Phlegmonosa. Nature. Closely allied to . Inflammatory CEdema. Effect on tissues involved. 4. Perichrondritis Purulenta (or Angina Ludovici). Usu- ally a secondary lesion, complicating all infectious diseases. May follow with abscess, fistula, total thy- roid necrosis, etc. True also of Laryngitis Phlegm- onosa. 51 SYLLABUS OF GENERAL PATHOLOGY. LARYNGITIS CHRONICA PRODUCTIVA : New connective tissue. Hyperplasia of portions of vocal apparatus. LARYNGITIS TUBERCULOSA : Usually local. Progress and effects, — ulceration, second- ary sepsis, paresis, aphonia, tendency to involve lungs. LUPUS, SYPHILIS, TYPHOID: Laryngitis from Syphilis presents few anatomicalj char- acteristics; usually originates from some lesion in Pharynx. When diffuse, is superficial, and when deep-seated is gummatous. Produces circumscribed ulcers. Condy- loma. Discrete Adenitis, ) Catarrh, >■ from Typhoid. Secondary Necrosis, ) NEOPLASMS : Papilloma, Papillary Fibroma. Epithelioma. Fibroma. Myxoma. Angioma. Lymphangioma. Enchondroma, Cysts. Sarcoma. Carcinoma. c- TRACHEA. NORMAL DATA: Submucosa. Mucous follicles. HYPOPLASIA : a. Total aplasia. b. Atresia. c. Too few cartilages. d. Length. e. Fistula, — complete, incomplete or CEsophago-tracheal. /. Cysts. g. Diverticula (Third bronchial tube). h. DystocisB. Situs inversus; telescoping cartilages. CIRCULATORY DISTURBANCES: Similar to Larynx (q.v.). INFLAMMATION : Similar to Larynx (q.v.). Stenosis from Trachitis H yper- trophioa Chronica, usually of syphilitic origin. 53 SYLLABUS OF GENEEAL PATHOLOGY. REGRESSIVE NUTRITION DISTURBANCES: Senile changes. Necrosis. Calcification. Amyloid de- generation, etc. Simple ulcer, perforation. PROGRESSIVE NUTRITION DISTURBANCES : Seldom observed. Cyst. Cyst-adenoma. Exostosis. Oste- oma. Fibroma. Pibro-sarcoma. Sarcoma rare and usually metastatic. Carcinoma, primary, very rare; secondary is common. c. BRONCHI. NORMAL DATA: Exceedingly important. Difference in structure between larger bronchi, medium bronchi and bronchioles. Note particularly peri-bronchial lymph follicles in smaller bronchi, also muscularis. Nerves. HYPOPLASIA: Total aplasia. Third bronchus. Ectasia, universalis and telangiectatica. Atresia with atelectasis pulmonalis. CIRCULATION DISTURBANCES: Hyi)er8Bmia (a) active and (6) passive. Cardiac Ecchy- moses. Relation to coloration of sputa. Haemoptysis. Haemophilia. In marked haemorrhage always ulceration of Pul- monary artery or vein, especially in "Phthisical Initial Haemorrhage; " also rupture of branch of Pulmonary artery or vein ; perforation of pul- monary aneurysm, and less [ frequently Aortic aneurysm. Difference from Parenchymatous pulmonary Haemorrhage. INFLAMMATION : Exceedingly common, seldom invades all the tubes at once. Upper tube, with larynx and trachea in adults. Lower tubes with lungs in children . 53 SYLLABUS OF GENEBAL PATHOLOGY. Varieties: Serous. 1 Purulent. Fibrinous. Combinations of Serous, Purulent and Fibrinous. Croupous. Productive. Superficial. Deep Peri-broncMtis : Blen- orrnea, — stinking purulent sputum. Ori- gin specific and non-specific. Schizo- mycetes or mycosis. General findings: — Effect on pul- monary function: Pus; Stagnation of Bronchial secretions; BroncMtis; Exhudativa Asthmatica; Curshman's spirals ; Bronchitis Pseudomem- branosa (descending in children and ascending [chronic] in adults); also in acute Lobar Pneumonia; Chronic Fibrinous Bronchitis ; Chronic Ca- tarrhal Bronchitis. The two latter, with altered secretions, become pro- ductive. Embryonic Metaplasia. ' Bronchiectasis. d. LUNGS. NORMAL DATA : Histologic relation to epithelial glands, — Different from those in ultimate structure and function. Enormous vas- cularity. Relation of vessels to Parenchyma. Nature of Parenchyma. Nature of Stroma. Abundance of yellow elastic tissue. Three-fold nature of connective tissue, — interstitial, peri-bronchial and peri-evascular. Lesions of lungs coi'respondingly different from those of other organs. Analogy between Pulmonic Parenchyma and cutaneous, or, better, serous surfaces. The acinus. The lobule. Location of bronchial vessels. Relation of heart to pul- monary blood vessels. 54 SYLLABUS OF GENERAL PATHOLOGY. HYPOPLASIA : Aplasia, complete or partial. Hypoplasia circumscripta. Congenital Bronchiectasis. Hydrothorax. Hernia Dia- phragmatica. Importance of these partial anomalies. Often predisponents of other lesions. Dystocise lobse, pure secondary lungs. CIRCULATORY DISTURBANCES : Relation to cardiac conditions, — Various, often profound; are primarily (a) Arterial, (b) Venous. Similar ultimate lesions may result from either Arterial or Venous. Hy- persemia,— acute, chronic, general, local, and Arterial or Venous, or both. (Edema, — Pneumonia Hypostatica. Oligsemia from general Oligsemia or intra-pleural pressure or emphysema. Oligsemia of apices and Hypersemia of bases. Mechanical ^Etiology. The color picture, — Important as predisponent to Tuberculosis (Rhindfleisch). Grave nuti'ition dis- turbances of circulatory origin not common. Reason for this, — Dual circulation. Qualification of this, — Oligeemia from pressure. INFLAMMATION— PNEUMONITIS : True Parenchynlatous (?) alveolar lesions may be discrete; usually associated with stroma lesions. Lobar Pneumonia. Lobular Pneumonia. etiology various, — Air the common carrier. Bronchial tubes the passages of entrance. Blood next to air as car- rier. Contiguity as a factor. Duration short or . long, depending upon cause and nature. Importance of mor- phology of inflammatory product. Varieties, — Cellular. Catarrhal. Purulent. Desquam- ative or caseous. Croupous. Tubercular. Syphilitic. Fibrous. ACUTE LOBAR PNEUMONITIS ; FRANK PNEUMON- ITIS ; CROUPOUS PNEUMONITIS : " ^Etiology, — Stages: 1. Hypersemia. — Findings macroscopic and microscopic. Its non-spe- cific nature. 2. Exsudative, — Red hepatization. Find- ings macroscopic and mi- croscopic. 55 SYLLABUS OF GENERAL PATHOLOGY. , 3. ExsTidate disintegrates, — Gray hepatiza- tion. Findings macroscop- ic and microscopic. 4. Eesolution, — Resorption by (a) Blood vessels and (6) Lymphat- ics and (c) expectoration, •which begins at sixth day and lasts for d ays. R6le of Lymphatics is extension ; may retard resorption. Atypical courses. Incomplete. Hilus Pneumonia. Apex Pneumonia. Disseminated Pneu- monia. Caseation. Organization . Abscess. Gangrene. Effect on other lung. Effect on Spleen. Effect on Heart. ■ Effect on Kidneys. Effect on Blood. Hyperinosis. Leucocytosis. CATARRHAL PNEUMONITIS : Superficial character, usually Lobular, usually secondary. Acute and Chronic. Uni-lateral and Bi-lateral. Typical in Scarlatina, Measles, etc. Gross appearance of lung. Consistence ; color ; effect of pressure on cut surface. Findings macroscopic and microscopic of exsudate and sections. Fibrin present at times in the alveoli ; always insignificant; Transition forms in children,— Atelectasis, through stenosis and occlusion. Plugs as factors of inflam- mation. Inflammation by continuity. Discontinuous. Cattarrhal Broncho-Pneumonia. Findings, — Oldema. Cardiac Pneumonia. PURULENT PNEUMONIA: etiology, — Findings macroscopic and mioroscopic. 56 SYLLABUS OF GENEBAL PATHOLOGY. SPLENIC PNEUMONIA: Hypostasis, etiology, — Findings macroscopic and mi- croscopic. FOREIGN BODY PNEUMONIA: -Etiology, — Findings macroscopic and microscopic. Diphtheritic Pneumonia. Aspiration Pneumonia. APOSTEMATOUS PNEUMONIA. STONE-CUTTERS' PNEUMONIA. SYPHILITIC PNEUMONIA. ANTHRACOSIS. PROGRESSIVE ATROPHY: Anatomy, — Color picture, etc. Effects. EMPHYSEMA : JEtiology, — Findings; Varieties. Macroscopic and mi- croscopic. DEGENERATIONS : Amyloid. Fatty. Calcareous. NEOPLASMS : Fibroma. Myxoma. Lipoma. Enchrondroma. Aden- oma. Carcinoma, priinary and secondary. Sarcoma very rare as primary and infrequent as secondary. TUBERCULAR PNEUMONITIS : Acute. Chronic. Miliary or disseminated. Localized, apex usually, etiology, — Anatomy macroscopic and microscopic. Double nature of process, — destructive and productive. Importance of mixed infection. Sequsele. Cavity, Induration. Cicatrix. Perforation. Haemorr- hage. Empyema. Pysemia. Gastric Ssemiology. Gen- eral effect on organs at large. OTHER PARASITES: Actinomycosis. Echinococcus, etc. PLEURA : Lesion based on Histology. Pleuritis. Varieties of ,— (a) Acute, (6) Chronic. Empyema. Neoplasms. 57 SYLLABUS OF GENERAL PATHOLOGY. Chapter VIII. NEOPLASMS. DEFINITION ; A new growth. A tumor. A local abnormal development of Histologic elements. ETIOLOGY : Often obscure. Cobnlieim's embryonic theory. Hans-, mann's theory of Asymmetric Karyomitosis ; Parasitic theories. Trauma. • GENERAL FINDINGS : Tumors are : Diffuse ; Circumscribed ; Encapsulated. Sessile ; Pedunculated. Nodular J Lobular, Solid ; Semi-solid ; Cystic ; Mixed. Primary ; Secondary, Benign ; Malignant. ANATOMIC CLASSIFICATION: Neoplasms are susceptible of arrangement into groups ac- cording to the tissues which compose them, for the reason that these component tissues are analagous to normal His- tologic types of tissue. Classification is, therefore, based upon the normal tissue types, e. g. , Fibroma, Myoma, Lip- oma, etc. (see reference key) . NOMENCLATURE : "Oma" added to the predominant Histologic element or elements, e, g., Fibroma, Myxo-Sarcoma. 58 SYLLABUS OP GENER.^L PATHOLOGY. HOMOLOGY OR HETEEOLOGY : Neoplasms composed of tissues similar to the tissues in wliich they exist are Homologous. Those composed of tissues dissimilar to the tissues in which they exist are Heterologous. Teratoid Neoplasms, BEHAVIOR OP NEOPLASMS : 1. Nutrition disturbances in the patient : a. Cachexia. h. Local tissue destruction through pressure ef- fects,' etc. 2. Regressive nutrition disturbances in the Neoplasm. Necrosis : a. Central. &. Peripheral. Pigmentation. Degeneration a. Colloid. 6. [Amyloid. c . Hyaline. Etc., etc. 3. Metaplasia. 4. Metastasis : a. Through the blood vessels. b. Through the Lymphatics. 5. Malignancy : a. Through the blood vessels. 6. Through the Lymphatics. c. Through pressure effects. KEY TO CLASSIFICATION OF NEOPLASMS. In the consideration of the Neoplasms, the use of the capital letters A to iV inclusive will be substituted for the cap- tion which each is intended to represent, as follows : A. Specific Varieties. Etiology. B. C. Mode of growth. D. Consistence. E. Location. F. Anatomy. a. Histology, H. Quality. I. Age at which likely to occur. J. Progression. K. Combinations. L. Regression. M. Complications. N. Origin. 59 SYLLABUS OF GENEBAL, PATHOLOGY. {A) SPECIFIC VARIETIES : Neoplasms : Homologub : 1. Myxoma Embryonic connective tissue, 2. Sarcoma Immature fibrous tissue. 3. Fibroma '- .Adult connective tissue. 4. Lipoma Adipose connective tissue. 5. En chondroma Cartilage. 6. Osteoma Bone. 7. Odontoma Dentine. 8. Glioma Neuroglia. 9. Neuroma Nerve. 10. Myoma ... Muscle. 11. Angioma Blood vessels. 12. Lymphangioma.. Lymph vessels. 13. Lymphoma Lymph glands. Adenoma Glands. 14. 15. Papilloma Epithelium. 16. Epithelioma Epithelium. 17. 18, Endothelioma . . . Endothelium. 19. Psammoma. 20. Cystoma. 21. Deciduoma. (B) ETIOLOGY : 1. Obscure. 2. Hereditary. 3. Acquired. 4. Congenital. 5. Specific. 6. Non-Specific. 7. Mechanical. 8. Physical. 9. Chemical . 10. Inflammatory. 11. Bacteria. 12. Aniifaal Parasites. (C) MODE OF GROWTH : 1. Continuous. 2. Discontinuous. 3. Centric. 4. Eccentric. 5. Single. 6. Multiple. 60 SYLLABUS OF GENERAL PATHOLOGY. (D) CONSISTENCE: 1. Soft or MoUusca. 2. Medium. 3. Hard or Dura. 4. Fluctuating. (E) LOCATION: 1. Skin, 2. Sub-cutaneous tissue. 3. Connective tissue. 4. General connective tissue. 6. Particular connective tissue. 6. Stroma. 7. Muscles. 8. Nerves. 9. Epithelium. 10. Vessels, 1 1. Glands. 12. Sub-mucosa. 13. Organs. {F) ANATOMY: 1. Diffuse. 2. Circumscribed, 3. Sessile. 4. Pedunculated. 5 . Nodiilar. 6. Encapsulated, 7. Lobular. (G) HISTOLOGY: 1. Structure. 2. Metaplasia. 3. Metastasis : a. By Lymphatics. h: By Blood Vessels. c. By both Blood and Lymph Vessels. {H) QUALITY : 1. Benign. 2. Malignant. (I) AGE AT WHICH LIKELY TO OCCUR: 1. Congenital. 2. Up to 30th year. 3. From 30th to 70th year and over. 4. All ages. 61 SYLLABUS OF GENERAL PATHOLOGY. (J) PROGRESSION: 1. Rapid.) 2. Slow. 3. Either rapid or slow. (K) COMBINATION : With one or more of the specific varieties enumerated in group {A.) {L) REGRESSION: 1. Necrosis. 2. Central Necrosis. 3. Peripheral Necrosis. 4. Pigmentation. 5. Colloid, 6. Amyloid, 7. Hyaline, 8. Calcareous, }■ Degenerations. 9. Mucous, 10. Fatty, 11. Cheesy, (M) COMPLICATIONS : 1. Disturbed Function. 2. Sepsis. 3. Pyaemia. 4. Pain. 5. Haemorrhage. (N) ORIGIN : 1. Primary. 2. Secondary. 3. Primary or Secondary. CLASSIFICATION OF NEOPLASMS. (^-1) MYXOMA: Seldom a pure tumor. B. Entirely obscure, but mayocour as a congenital growth. C. Usually continuous and single. May be discontinuous and multiple. D. Soft. E. Skin. Subcutaneous tissue. Connective tissue. Also certain glands. «2 SYLLABUS OF GENEEAL PATHOLOGY. F. Circumscribed, except where it is in combination, when it may be diffused through the tumor mass. G. Mucous tissue. H. Usually benign. I. Usually before the 30th year. May grow at any time. J. Usually slow. May be rapid. K. Is found in combination with Sarcoma, Fibroma, Lijjoma, Enchondroma, Osteoma, and in Carcinoma as in Carcinoma-Myxomatodes. Occasionally is a de- generated process of Adenomata. L. May become Necrotic. M. Pyaemia. N. Usually primary. Often secondary as a degenerative process in other tumors. {A-%). SARCOMA: B. Often congenital. Possibly parasitic, and possibly as the result of inflammatory irritation. C. May be continuous, discontinuous; centric, eccentric; single or multiple. D. When pure, is soft. E. Any portion of the body where connective tissue is found. F. May be diffuse, circumscribed ; sessile, pedunculated; nodular, encapsulated or lobular. O. Structure generally that of a seven months' umbilical cord: An intimate association of cells, with a fine reticulated stroma containing atypical blood vessels. The cells are either round or spindle in shape, either of these varieties being small or large ; sometimes multi- nuclear giant cells, the nuclei showing a definite ten- dency to mass in the centre of the cell body. May probably degenerate into myxomatous tissue. Metastasis, as a rule, by the blood vessels; occasionally lymphatic. Some sarcomata are alveolar and pig- mented; these kinds are highly malignant. 63 SYLLABUS OF GENERAL PATHOLOGY. H. Benign when encapsulated. Most malignant when cells are small and round or when involving bony structures as in the Myeloid variety, but is always malignant when not encap- sulated. When alveolar, highly malignant. /. Usually in the early ages, up to 30". Has been seen at 80. J. Rapid as a rule when not encapsulated. May remain dormant for years when encapsulated. K. In combination with every variety of tumor, except the Odontoma. Note particularly Glio-Sarcoma. L. May show a central necrosis ; sometimes peripheral as a result of infection. M. Pyaemia. Pain from pressure. Haemorrhage . N. May be primary or secondary. (^-3) FIBROMA : B. Obscure. C. Continuous, discontinuous; centric, eccentric; single, multiple. D. Soft, hard. May be medium when mixed. E. Airy place where connective tissue is found, but usually the skin, subcutaneous tissue and the uterus. F. May be diffuse, circumscribed ; sessile, pedunculated; nodular, encapsulated, lobular. Q: The soft variety is a loose, wavy connective tissue, in the meshes of which are "fixed" connective tissue cells. May be myxomatous or sarcomatous. Metastasis not recorded. //. Benign, usually. Malignant only when location pro- duces pressure effects on vital parts, or through metaplasia. I. All ages. ■ J. Usually slow. In special varieties, as in the Uterus, may suddenly grow rapidly. K. In combination with Myxoma, Sarcoma, Lipoma and Mammary Adenoma. 64 SYLLABUS OF GENEKAL PATHOLOGY. L. Central Necrosis. Hyaline or Calcareous Degene- ration. M, Often becomes infected. May induce Pysemia. Often induces excessive Metrorrhagia. N. Primary, except in Mammary Adenomata. (J. -4) LIPOMA : B. Obscure. Really caused by hyperplasia of adipose tissue. C. Centric, eccentric. Single as a rule. D. Soft. E. SJjin. Subcutaneous tissue. F. Almost invariably sessile. Encapsulated. Circum- scribed. 0. Adipose tissue. Metaplasia into Myxoma, occasionally Sarcoma. Metastasis not observed. H. Beni'gn.' Malignant occasionally from pressure on vital parts. 1. Any period of life. J. Usually slow. K. Combination witli Myxoma or Sarcoma. L. Central necrosis. Peripheral necrosis from infection. M. Pain. Sepsis. N. Primary. (^-5) ENCHONDROMA: B. Obscure, C. Continuous. Eccentric. £>. Hard. E. Usually where cartilage occurs. Sometimes in the skin and subcutaneous tissues, as in Teratoma. E. Diffuse or circumscribed. G. Hyaline cartilage. Metaplasia to Myxoma or Sarcoma. Metastasis through blood or lymph vessels. H. Benign. Malignant only in Multiple Pulmonary En-, chondromata. I. Usually in old age. 65 SYLLABUS OF GENEEAL PATHOLOGY. 7. Rapid in Multiple Pulmonary Enohondromata. Slow usually. K. In combination with Myxoma, Sarcoma, Osteoma, Fibroma, L. Calcareous degeneration. M. May complicate mobility of joints. N. Primary. (^-6) OSTEOMA: (Two varieties : Typical and Atypical bone.) B. Obscure. Inflammation possibly in some cases. C. Continuous. Eccentric. Single or multiple. D. Hard. E. Always the bones. F. Diffuse or circumscribed. G. That of bone, but in the Atypical variety there is no regular canalization. Lacunae are distributed around irregular spaces, communicating with them by means of canaliculi. Metastasis not observed. H. Benign. I. Any age. J. Slow. K. In combination with Sarcoma, Chondroma ; also found in Teratomata. L. No regression. M. Immobilization of joints. Pain. Rarely they produce disturbances in the central nervous system through pressure, as in Osteomata of the skull, N. Primary. U-7) ODONTOMA: Exceedingly rare. B. Obscure. O. Consists of Hyperplasia of the Dentine. K. No combination. M. No complications. ' 66 SYLLABUS OF GENEEAL PATHOLOGY. (^-8) GLIOMA: B. Obscure. C. Continuous usually. Ecoeutric. Occasionally multiple. D. Soft E. The particular connective tissue of the Choroid and the brain (Neuroglia.) F. Diffuse usually. (?. Closely allied to Sarcoma. The tissue consists of a deli- cate connective tissue stroma, in which are multi-polar 'cells having a spider-like appearance. Highly metastatic by the blood vessels or the lymphatics. H. Highly malignant. I. Usually young people, below the age of 30. J. Rapid usually. K. Combination with Sarcoma. L. Often melanotic. M. Produce ocular and cerebral complications- N. Primary. (^-9) NEUROMA: B. Obscure. C. Usually multiple and continuous D. Medium. E. Peripheral nerves. F. Circumscribed. Sessile. Nodular. G. Two varieties : a. True Neuroma, a Hyperplasia of the nerve fibre. &. The false variety, a Hyperplasia of the peri- and endoneurium. H. Benign, J. Any period of life. J. Slow, usually. K. None. L. None. 67 SYLLABUS OP GENEBAL PATHOLOGY. M. Produces exquisite pain from pressure on nerve ends. N. Primary, and usually in amputation stumps. (^-10) MYOMA : Two varieties : (a) Strio-cellulare and (fe) Leio-cellulare. a. Strio-cellulare. These growths are congenital and are found in the Testicle, the Ovary, and the Kidney. 6. Leio-cellulare, as follows. B. Obscure. C. Continuous. Eccentric. May be single or multiple. D. Medium. E. Anywhere in the body. Principally the Uterus. ' F. Sessile as a rule. Nodular often. Encapsulated often. Lobular sometimes, G. Non-striated muscular fibre. Seldom pure. Meta- stasis by the Uterine Veins. H. Usually benign. May become malignant through size, and pressure on pelvic organs. I. Begins to grow in the early periods of adult life, J. May be very slow. Not infrequently rapid. K. Usually associated with fibroma ; sometimes with myxoma. L. Central Necrosis. Hyaline and Calcareous degenera- tion. Pigmentation by haemorrhage. M. Not infrequently sepsis. Produces pain from press- ure. Produces metrorrhagia. N. Primary. (^-11) ANGIOMA : Two varieties : (a) Cavernosa and (6) Telangiectoides. B. Obscure. C. Continuous. Single. D. Soft. E. Skin. Subcutaneous tissue. Liver. C8 SYLLABUS OF GENEEAL PATHOLOGY. F. Diffuse usually. Occasionally circumscribed. Ses- sile. G. Cavernosa consists of large, dilated veins, surrounded by connective tissue. Telangiectoides consist of irregularly dilated, hyperplastic capillaries. H. Sometimes malignant, but may be benign, usually in tlie Liver. /. Early periods of life ; under 30 years. J. May be either rapid or slow. K. In combination with Sarcoma. L. None, M. Haemorrhage. N. Primary.. (A-12) LYMPHANGIOMA : Simply a circumscribed dilatation of Lymphatics. (4-13) LYMPHOMA: B. Obscure. C. Eccentric. Diffuse. Usually multiple. May be single. D. Medium. E. Lymphatic glands. F. Circumscribed. Usually encapsulated. Maybe nodular. ' G. Hyperplasia of Lymphatic tissue. H. Malignant. I. May grow at any age. Usually before 24. J. Usually rapid. May be slow. K. Sarcoma. L. May undergo central necrosis. M. Systemic complications. N. Primary. SYLLABUS OF GENERAL PATHOLOGY. (A-U) ADENOMA: B. Sometimes congenital as in the kidney where multiple cyst-ademoma involves usually both organs, the cysts being relatively small and very numerous. In adults the tumor is one often resulting from stenosis of gland ducts, which stenosis may affect one gland, with single cyst, or many glands, with multiple cysts. Otherwise, the gland tumors occur as adenomata from unknown causes, presumably irritant, which are probably in the nature of parasites. C. Continuous. Sometimes discontinuous. May be single, in which case the whole tumor may be formed of one cyst, or an enlarged cyst whose walls contain many smaller cysts. Or there may be more than one distinct cyst. Or the growth may be diffuse as in the En- dometrim in Adenomatous degeneration. Usually centric. Usually multiple, may be single. D. Usually a soft, highly vascular tumor. E. In the skin and mucous membranes generally and in glands. It is most common in the skin near the alse nasi and in the Stomach, Rectum, Uterus, Ovaries and Liver. F. Often Diffuse. Frequently sessile. May be pedunc- ulated in the Uterine Polypi. When multiple are nodular. Frequently encapsulated. G. The structure varies with the gland in which located; The structure is that of an aborted gland formation . the distinguishing feature is that, while the glands are irregular, tortuous, dilated and often telescoped, they always retain their membrana propria and do not show regularly asymmetric Karyokinesis. The cells are of cuboidal or columnar variety; often greatly elongated, frequently being seen in thick strata. A stroma is present which may be dense 'and firm, or loose and soft, and contains many blood vessels. The stroma may undergo myxomatous de- generation, or sarcomatous degeneration. Metastasis is not present in the pure or benign. H. When pure, benign. 70 SYLLABUS OF GENEKAL PATHOLOGY. I. The earlier periods of life, excepting in Endometrial tumors, which may occur at any time. J. Either rapid or slow; usually rapid. K. Most frequently with Myxoma, Sarcoma, and in retro- grading tumors of carcinoma. Some adenomatous tumors originate from the breast glands in common with a large development of fibrous tissue and are called Intra-canalicular- fibro-adenomata. L. May undergo necrosis or any of the degenerations ; most frequently mucous or colloid degeneration. Pig- mentatioa occurs as the result of haemorrhage. M. May produce either or all of the necroses, and in certain locations show distinct tendency to malignant retro- gression. ZV. Primary as a rule ; may be secondary to inflammation. (^-15) PAPILLOMA: B. Usually an irritant. Probably parasitic. May occur as the result of syphilis. C As a rule is a single eccentric growth; may be mul- tiple, as in Condylomata. D. Soft or medium, E. Skin. Prima Vise. Uterine Mucosa. Also the nose and pharynx and the upper respiratory tract. F. Circumscribed. Usually sessile. May be nodular. Never encapsulated. G. They are outward growths of the epithelium of a part, the epithelium surrounding arms or branches of connective tissue ; the epithelium always remaining superficial. There is no tendency of the Rete Malpig- hii to develop inwards into the subcutaneous or sub- mucous tissue. H. Benign. I. All ages. J. Usually slow. K. None. L. May become malignant when it would be a Carcinoma or Epithelioma. M. None. N. Primary. 71 SYLLABUS OP GENEBAL PATHOLOGY. (4-16) EPITHELIOMA: B. Some form of irritation; probably parasitic. C. Continuous, eccentric growth. D. Hard, usually. .May be soft. E. Skin and Mucous Membranes generally. F. Sessile. Diffuse. 6r. Three varieties: a. Simple, flat epithelial cell. 6. Flat cell with "Pearls." c. Glandular variety. Metastasis by the lymphatics and occasionally through the blood vessels. It is an inward growth, into the subcutaneous or submucous tissues, of the cells of the Stratum Mal- pighii, excepting in the glandular variety which is a diffuse, honeycomb growth of glands. H. Malignant tendency depending upon metastasis. Is benign if ablated early and thoroughly. I. The later periods of life. J. May be either rapid or slow. Usually slow. K. None, excepting where papillomata have undergone degeneration. L. In the flat-celled variety ulceration is extremely frequent. M. Pain. Sepsis. N. Primary, excepting in degenerated Papilloma. (4-17) CARCINOMA : (The Epitheliomata are properly [classed with Carcino- mata as flat-cell Carcinoma.) B. Is often called flat-celled carcinoma, but the main form of carcinoma consists in the lawless growth of epithelial cells whose origin is in the gland structures. Here the glands lose their membrana propria and the cells assume or acquire various shapes. The cause of this lawless growth of cells has been assumed by Cohnheim and his school to be due to a sudden growth of dormant • embryonic elements which have for some time rested in an inactive state in such tissues as the skin or breasts or other glands. By a' more recent school it is believed to be due to the presence, either in or near the cell, of a specific micro-organism. 72 SYLLABUS OF GENEEAL PATHOLOGY. C. Oontmuous or disoontimious. Both single and multiple, tlie primary tumor is single. D. Soft in the Enoephaloid and hard in the Scirrhous variety. E. It is primary in all structures containing epithelium. It may be anywhere in the body as the result of meta- stasis. F. Diffuse. Sessile. May be lobular or nodular. G. The Enoephaloid carcinoma consists of a very large mass of cells contained in large irregular cavities and surrounded by a moderate amount of a stroma of con- nective tissue fairly rich in blood vessels. The Scirrhous variety consists of small masses of epithelial cells contained in small irregular spaces or alveoli, surrounded by a dense, firm, con- nective tissue and with a moderate blood supply. Oftentimes areas of adipose tissue are found in- cluded within the areas of the tumor ti ssne and this is regarded as, in a measure, diagnostic of the tumor, it differing in this respect from the Enoephaloid. When the Carcinoma is purely of glandular origin, it is usually possible to discover gland structure in adenomatous degeneration in some portions of the tumor. Metastasis is by lymphatics as a rule, and sometimes by the blood vessels. H. Always malignant. I. Usually found after 40 years. Has been seen as early as three years. J. It may be rapid, as in the Enoephaloid variety, or very slow as in some varieties of the Scirrhous. K. With Adenoma ; Sarcoma ; Myxoma, as in Carcinoma- Myxomatodes. L. May undergo peripheral or central necrosis.- Is Melan- otic occasionally. May undergo colloid degeneration, commonly in the Om.entum and Rectum. May also .un- dergo hyaline, waxy and calcareous degeneration, and frequently is hsemorrhagio in areas. M. Pain. Sepsis, Pysemia occasionally. Malnutrition and cachexia. N. Primary, excepting where adenomata or papillomata have degenerated. SYLLABUS OF GENERAL PATHOLOGY. (J-18) ENDOTHELIOMA: B, Closely allied to Sarcoma, some authorities disputing any difference in origin between the two, but recent ob- servers are increasingly of the opinion that true endothe- lioma is a tumor whose origin is in the Endothelial cells of blood and lymphatic capillaries and lymphatic spaces. There are two varieties of this tumor ; one is com- monly found in the Dura and the Pia Mater and originates from the Lymph spaces and consists of strings of endothelial cells presenting a lawless growth through the lymphatic system. The second variety is mostly found in the cervix uteri, and in the nasal passages and consists of a lawless growth of endothelial cells in the peri-vascular spaces, around the venules and arterioles. Here cells are found surrounding the blood vessels. • Both of these tumors are malignant, but grow more slowly than the Carcinomata. The malignancy of such tumors is- not so much from their tendency to undergo met- astasis as because of their usual location in the membranes of the brain or in the inop- erable portions of the nasal passages. In the uterus it is benign, if the uterus be removed before the extension of the growth into the pelvic tissues has oc- curred. (^-19) PSAMMOMA : This is a peculiar occurrence of connective tissue surround- ing spaces which contain a material which has been termed "brain sand." This "brain sand" is found in the brain and the testicle. (JL-20) CYSTOMA : This is a tumor which is formed as a result of the closure of the mouth of a duct by inflammatory processes, such as Bteno's duct, or the ducts of the other Salivary glands, or Gaertner's duct, etc. {A--Z1) DECIDUOMA: This neoplasm was first described by the author. It con- sists in a hyperplasia of portions of the Decidua Serotina which have remained after the expulsion of the Secundines. 74 SYLLABUS OF GENERAL PATHOLOGY. This retained placental tissue becomes organized, and may follow one of two courses; either it will induce a Chronic Productive Endometritis, or the Decidual cells will take on sudden activity and assume the properties or character- istics of a malignant growth; this will invade the wall of thei uterus, may become generalized in the pelvic tissues, or be carried to distant organs by metastasis; the original tumor never acquires much size. The diagnosis is made on the finding of the placental elements; namely, portions of the Villi lined with the characteristic cells, or so-called decidual cells. The malignant form is differentially diagnosticat- ed from the benign and from the mere products of an abortion by the peculiar arrangement of the de- cidual elements which behave in a manner closely resembling the growth of Carcinoma. 75 SYLLABUS OF GENERAL PATHOLOGY. CHAPTER IX. URINARY TRACT. a. KIDNEY. b. BLADDER AND URETERS. a. KIDNEYS. GENERAL MORPHOLOGY: Adult Kidney, — Length, 4imclies; width, 2 inches; thick- ness, 1^ inches; volume, 8 + cubic inches; average weight, 4f ounces. Left always heavier than the right. , Both organs stripped, in the male, about 10 ounces ; in the female, 9^ ounces. Relation of total Renal weight to body weight as 1 is to 100 ; relation of total Renal weight to that of the heart, in the 20th to 25th . year, as 1 is to ]^ (Thoma). Daoble function of elimination of water ^nd poisonous salts fromthe body. 1. Peculiar structure to accomplish this. 2. Peculiarity of the vascular appar- atus. 3. General arrangement of the par- enchymatous tissues. n. Of the Renal cortex. b. Of the Pyramidal tissue. c. Of the Pelvis. 76 SYLLABUS OF GENEEAL PATHOLOGY ANOMALIES: Absence of one or both kidneys. General Hypoplasise. Congenital cystic kidney. Horseshoe kidney. Dystocia, both kidneys right or left. Floating kidney. One or both kidneys in the pelvis ; corre- sponding anomalous distribution of the renal vessels. Two or more renal arteries. Two or more renal veins. Double ureters. Persistent congenital furrows. CIRCULATORY DISTURBANCES: Oligsemia : General, from general causes; namely, Systemic oligsemia, or obstruction of the main renal artery, — this may be uni- or bi-lateral; Hydro- and Pyo-nephrosis. Local, from arterial thrombosis or embolism. Hypersemia : Acute or Arterial : Of vaso-motor origin. Of inflammatory origin. Is general or local, depending upon cause. Chronic or Venous : From local pressure on renal veins. From Cardio-vascular lesion. Infarction: The renal arteries are terminals in all their branches, hence infarction, as a rule, is white. The exception to this is where the infarcted area is ti-aversed by a peri-capsular artery, when the infarction is hsemorr- hagic. Explanation of this diiference. 77 SYLLABUS OF GENERAL PATHOLOGY. NEPHRITIS, ACUTE PARENCHYMATOUS : Etiology, — Febrile Forms : 1. Scarlatina. 3. Influenza. 3. Diphtheria. 4. Weil's disease. 5. Pneumonia. 6. Articular Rheumatism. 7. Typhus Abdominalis. 8. Sepsis. 9. Pyaemia. 10. Erysipelas. IL Measles. 13. Variola. 13. Epidemic Parotitis. 14. Malaria. 15. Syphilis. 16. Toxines: Auto-intoxicants, as Bile, Gallic Acid, Urotoxin, Acetone, Haemolysis, etc. 17. Medicinal Agents i] Acids, — Sulphuric, Oxalic and Carbolic. Chloroform. Ether. Hydrargyrum. Glycerine. Oleum TerebinthinsB. Arsenic. Phosphorous. Kali-Chloricum, etc. 18. Organic substances : Mustard. Pepper. Alcohol. Cythsemolysis. 19. Pus products. 30. Cold and burns. 31. Gravidity. Of acute nephritis following infection with fever: a. In part the toxic process per se. b. In part the toxic nature of the in- fection. Scarlatinal Nephritis, early Glom- erulo Nephritis with ultimate Tu- bular Nephritis. 78 SYLLABUS OF GENERAL PATHOLOGY. Pathologic Anatomy 1. Gross findings, — Gross appearances vary, de- pending upon vascular conditions, namely : a. OligBBmia. fe. Hypersemia. c. Both,— Mottled Kidney. Size and weight increased ; consistence elastic; capsule tense, thin and non- adherent ; surface smooth, dark red or grey red, flecked and striped. On gross section, cortex' regularly swollen; dull, with exaggerated markings. 2. Microscopic findings, — Cortical changes promi- nent ; principally and most marked in : a. Malpighian corpuscles, — Glomerulo ne- phritis. h. Tubular epithelium, —Tubular nephritis. c. Both parenchyma and stroma, — Diffuse nephritis . (Irregularly disseminated in all the pro- cesses.) 3. Epithelium of convoluted tubules : a. "Cloudy swelling. ft. Granular fatty degeneration. c. Plasmolysis. d. Coagulation necrosis. e. Here and there fibrillation of cells. /. Vacuolation with net formation. rj. Bristle processes not seen. h. Gathering and enlargement of Altmaun's granules, according to Bernsteiner, the first change to occur. i. Karyolysis, which follows liberation of nuclei. i. Tubules of the Labyrinth,— Dilated through swelling of epithelium. Contain finely granu- lar coagulated albumin in cylinders ; also hyaline cylinders; erythrocytes; a few leu- cocytes; fat. 79 S"SLLABUS OF GBNEEAL PATHOLOGY. 5. The deeper tubules, — epithelium normal ; lu- men widened;' cast material; often desquam- ated epithelium descended from above. Normal condition of parenchyma of deeper tubules would indicate restriction of process to the convoluted tubules. 6. Malpighian corpuscles : a. Mild cases, — Only a small quantity of coagulated albumin in capsule. b. Severe cases, — Glomeruli engorged with blood, often contain collections of leuco- cytes. Marked nuclear growth; desqua- mation of capsular and glomerular epithelium; deposit of erythrocytes; co- agulum of transuded albumin which distends the capsules and compresses the glomeruli; this afEects the elimination of ■Vyater. 7. Stroma, — Not involved, or oedematous; thick- ened;showssmallroundeell infiltration, which is greatest where the tubular changes are most marked and very commonly around the vasa afferentia and extending around the capsules. This must be regarded as a localized diffuse nephritis. 8. Vessels,— Usually no very marked changes. In Scarlatina and Diphtheria hyaline degenera- tion of intima, swelling of muscularis and adventitia; smull, round cell infiltration and deposit of fibrinous masses around the tissues. 9. Hsemorrhage, — Intra-capsular; Intra-tubular; Interstitial; Mild or severe. May not occur in tubular nephritis, constant in diffuse forms. 10. Hsemoglobinuria : Supervenes through : General blood changes. Local blood changes from action of renal tissues. Is primary and induces Nephritis. (The Kidneys in these cases are swollen, dark red or grey-red with flecks and stripes.) 1 1 . Microscopic findings,— As in other forms plus the staining of cast material. Interstitial hsemorrhage and small, round cell infiltration. 80 SYLLABUS OF GENERAL PATHOLOGY. 12. Urine: a. Febrile forms, — Urinary changes legs iu this class. ' 'Febrile Albuminuria," — Albumin is min- imum. Urine spare. High color. Strongly- acid. High specific gravity. A little sedi- ment which contains a few hyaline casts. b. Acute parenchymatous nephritis; quantity diminished. Occasionally normal; color darker; often brown, red and opalescent, (reason for this, — sediment contains renal epithelium; epithelial and hyaline casts, the latter often containing fat) . Red blood corpuscles, single or as casts; granular detritus; often Uric or Oxalic Acid in Crystals; leucocytes in small numbers. Albumin scantyin pure Tubular form with but slight haemorrhage. Associated Lesions, — CEdema, Serous inflammations. Cardiac dilatation ; Left ventricular hypertrophy in Scarlatinal Nephritis. Resolution : a. Complete, as in acute lobar Pneumonia. b. Incomplete, with permanent loss of function. (Note, — Parenchymatous nephritis, particularly the tubular, obtains with most infectious pro- cesses at the acme of the fever.) NEPHRITIS, ACUTE DIFFUSE, e.g., Scarlatinal Nephritis : Exhibits, usually, a much severer lesion with multiform symptom-complex. Etiology : ToxiaemisB (see -.Etiology, page 77). Pathologic Anatomy : 1. Gross findings, — Practically those of acute ne- phritis, excepting that the surface of the organ presents a more varied color picture, hsemorrhagic areas often being seen. 81 SYLLABUS OF GENEEAL PATHOLOGY. 2. The two phenomena most prominent are: a. Urinary changes. b. (Edema. Urine, almost without exception, diminished in quantity ; very com- monly the first indication. Reduction to 100 c. c. or to Anuria. Darker, smutty brown to chocolate ; increased specific gravity in ratio wiih diminution. Blood regularly present and is in microscopic quantity, or large and accompanied by Haemoglobinuria, Albumin constant, namely, — Serum Albumin, Globulin, and, when an abundance of cells, Nuc- leo-albumin; also, often, albumose. "Proteoses and Propeptone" (Bartley). Albumose may alone be present and account for absence of reaction with boiling. Albumin present in inverse ratio with quantity of urine ; may reach 1^ or more. Sediment; constantly ery- throcytes, well preserved or washed out; leucocytes, principally mono-nuclear, less often poly-nuclear. Re- nal epithelia single or in clumps; casts of every de- scription. With haemo- globinuria, staining of all these elements. Micrococci sometimes due to contamination. These changes readily explained by the Anatomical lesions. Urea, Sodium Chloride, and Phosphates are di- minished; Uric acid may not be diminished and Xanthin bases are in- creased. 83 SYLLABUS OF GENEEAL PATHOLOGY. b. (Edema : (1) Skin ; (3) Auasaica. Eesults from lesions of blood vessels of skin, serous and mucous membranes. Associated Lesions,— Inflammation of internal organs common; Pleura, Pericardium Endocardium; Re- tinitis Apoplectica. NEPHRITIS, PUERPERAL : Appears in the second half of the gravid state; never be- fore the third month. Youth and twin pregnancies pre- dispose. Etiology : According to some Pathologists, from pressure eif ects; according to others, from blood conditions. Rayer, of Paris, (1840,) first called attention to the condition. Pressure produces Nephritis Simplex; cold pro- duce Nephritis Albuminurica. Blood Conditions : According to Virchow, inflammation analagous to Puerperal Hepatitis and Splenitis. Embolism of fat and placental elements common with Puerperal Eclampsia. According to Rosenstein, increase of intra- abdominal pressure produces Nephritis, and alterations in cerebral circulation produces Eclampsia, There is Oligaemia with or without CEdema. Pathologic Anatomy : ]. Gross-findings, —Differ in different cases, depend- ing upon the severity of the lesion. There may be congestion more or less marked ; Oligeemia more common. Organ regularly swollen and the capsule not adherent. Surface somewhat pale. Slightly yellow, of a grey -yellow or brown- yellow color. 83 SYLLABUS OF GENERAL PATHOLOGY. 2. Microscopic findings, — By common consensus, ul- timate changes confined to parenchyma; stroma intact. Malpighian corpuscles frequently may show fatty degeneration of Glomerular Endothelium (Leyden). Parenchymatous elements reveal those changes common to : (a) CEdema, (6) Altered blood properties. Fatty degeneration of epithelium principally confined to the primary and secondary convoluted tubules. 3. Urine, — Quantity diminished. Specific gravity in- creased. Albumin usually abundant. Deposit presents variety of findings dependent upon in- tensity of process. (Findings do not afford certain evidence of condition.) Hsematuria occasionally marked; usually ab- sent. Mono-nuclear leucocytes ; erythrocytes ; hyaline, granular, fatty Casts ; Hsema- toidin crystals. Renal epithelium in various stages of degeneration. Eclampsia : May occur without Albuminuria or other find- ings. May not occur with all other findings pres- ent. Usually fatal. At least 50^ of cases (Sen- ator). Latest researches tend to show ; (a) That the characteristic pathological Anatomic findings in Puerperal Eclampsia obtain ; (6) Eclampsia caused by auto-intoxication from various sources ; (c) The Nephritis itself of toxic origin. Associated Lesions: a. Usually progressive CEdema. Anasarca. b. Less frequently serous effusions; most often Hydro-thorax. c. Retinitis Albuminurica. d. Marked Cardiac Hypertrophy. (This is physiological in pregnancy. ) 84 SYLLABUS OF GENERAL PATHOLOGY. Differential Diagnosis : a. Clironic Cardio- Vascular Hypereemia; here the Heart, Lungs and general findings characteristic; also the microscopic findings. fe. Ancient Nephritis ; here, possibly, ancient Retinitis Albuminurica. c. Subsequent history: In Puerperal Nephritis the recedence is almost invariably rapid, rarely merges into the chronic lesion. NEPHRITIS, CHRONIC: Four principal forms, according to the Histologic changes: . A. Chronic Parenchymatous Nephritis, — The degenera- tive changes principally in the epithelium of the primary and secondary convoluted tubules. B. Chronic Parenchymatous Nephritis -with Chronic GIo- merulo Nephritis. C. Chronic Glomerulo Nephritis, — This variety only recog- nized, with certainty, microscopically. D. Chronic productive interstitial Nephritis, —Here the parenchyma and glomeruli are regularly involved in the lesion. {A) NEPHRITIS, CHRONIC PARENCHYMATOUS: Synonyms, — Large white Kidney; Chronic Diffuse Non- iudurative Nephritis (Senator). Etiology: Exposure to cold. •Toxic Substances: a. Organic, — Scarlatina, Syphilis, etc. b. Inorganic, — Lead, Mercury, etc. Pathologic Anatomy: 1. Gross findings, — Increase in size and weight. Con- sistence, "doughy." Capsule tense, not adherent. Surface smooth and dull; gray, yellow or mottled in color. Stellate veins often injected. Gross section, — Cortex swollen, dull and glisten- ing, with yellowish and transparent gray stripes. Malpighian pyramids, dark red. 2. Microscopic findings, — Fatty degeneration of epithe- lium in" convoluted tubules. CEdema of peri- tubular connective tissue in the Pyramids of Ferrein. 85 SYLLABUS OF GENERAL PATHOLOGY. Glomeruli, irregularly but always, degenerated. Dilatation of some tubules, -wliioh. -are filled with the products of parenchymatous degeneration, erythrocytes and leucocytes. Others collapsed, with productive inflammation of connective tissue which shows small, round cell infiltration and contains fat granules. There may be multiple disseminated haemorr- hage, — mottled variety. These changes never universally distrib- uted through the cortex, but occur as more or less patchy conditions . Close resemblance between the large mottled kidney and that of Acute Diffuse Nephritis, the difference being in greater thickness and density of the former. 3. Urine,— Quantity diminished. Usually dark; occas- ionally light. Specific gravity slightly increased. Reaction acid. Albumin constant, usually consider- able. Deposits marked. Microscopic findings.— These of Acute Diffuse Nephritis, (q.v.) Associated Lesions, — Anasarca. Pneumonia. Cardiac hypertrophy. Note:— This form of Nephritis usually, ultimately results in contraction of the organ, which now more closely resembles the Chronic Indurative Nephritis. Kidneys, in this middle stage of degeneration, are regularly smaller, firmer, with non-adherent cap- sule; nodular surface distinctly mottled. The nodules represent those areas of tissue in which no collapse of tubules, and relatively little hyperplasia of connective tissue are seen . The darker, depressed areas, present the re- verse of these findings. (B) NEPHRITIS, CHRONIC PARENCHYMATOUS, WITH CHRONIC GLOMERULO NEPHRITIS. The only difference between this and the preceding lesion is in the more universal involvement of the Glomeruli, which are the seat of degenerative changes involving all structural elements. Desquamation and hyperplasia of SYLLABUS OF GENERAL PATHOLOGY. epithelium. Small, round ceil infiltration; fatty, hya- line and amyloid degenerations of capsules, together with exsudate albumin and sometimes diapedesis of erythro- cites into the capsule of Bowman. Etiology, — The same as Chronic Parenchymatous Nephritis. (C) NEPHRITIS, CHEONIC GLOMERULO : Presents changes, principally, in the capsules of Bowman and, when pure, yields no gross findings diagnostic of the condition. In the great majority of these cases other cortical change^ are present, similar to those already described, the poin* of interest being the large preponderance of Glomerular degeneration. Etiology, — The same as Chronic Parenchymatous Nephritis. (D) NEPHRITIS, CHRONIC PRODUCTIVE INTER- STITIAL: Synonyms, — Chronic Productive Indurative Nephritis ; Renal Cirrhosis. JEtiology : Chronic Toxaemias, Chronic Malnutrition, Chronic Alcoholism, Chronic general Vascular Lesions. Pathologic Anatomy : J. Gross findings, — Essentially a connective tissue hyperplasia with synchronous parenchymatous atrophy. Organs decreased in size. Greatly increased in density and firmness. Capsule regul arly adherent. Surface finely granular. Is dark or light and shows many Malpighian tufts. Cysts commonly seen between and in ele- vations on surface, which vary in size from a pin head to a cherry. The surface often mottled, greyish red. These changes in proportion to the duration of the process. 87 SYLLABUS OF GENEEAL PATHOLOGY. Gross section, — Cut surface shows cortex irregu- larly thin, in advanced cases almost obliterated; the color picture that of the surface. Markings obliterated. Surface dull. Malpighian pyramids usually congested. Renal pelvis occasionally dilated. Renal artery, large branches and Arterial Arcade commonly rigid and patent. Veins proportionately wide. CaCOj infarcts not uncommon in tubules of Labyrinth, also in ducts of Bertini, especially in old people. Microscopic findings, — Clearly demonstrate the preponderance of the lesion in the cortex rather than the medulla. Various conditions irregularly disseminated throughout the cortex. (Compare this with disseminated Pneumonia.) Areas corresponding to the surface elevations reveal relatively normal structure. Those cor- responding to the depressions reveal dense con- nective tissue with fat, remains of tubules and Malpighian tufts, small round cell infiltration and cicatrization around the malpighian cor- puscles and between the tubules. Obliteration of Nuclei; dilatation of tubules with corresponding epithelial changes, i. e., desquam- ation and total necrosis. Malpighian tufts, — In contracted areas reduced to small lamellated bodies, poor in nuclei and huddled together ; in other portions actually separate from the Glomerulus, the latter being impervious, homogeneous; here the capsule is normal or thickened, stratified. In less involved areas nor- mal, remarkably rich in nuclei, with swollen capsule ; swelling and hyperplasia of capsular epi- thelium which desquamates. Intra-capsular exsudate ; small round cell in- filtration. In areas showing fresher inflammation, tubular changes similar to those in Chron- ic Diffuse Non-Indurative Nephritis, but in far less degree, namely, fatty degene- ration much less marked. SYLLABUS OF GENEBAL PATHOOLGY. 6. Vascular changes, — In cicatrized areas intra-tubn- lar capillaries for most part obliterated ; occasion- ally dilated. Arteries reveal thickened adventitia, which is fused with surrounding connective tissue. Intima and Media commonly also in- volved. Veins show regularly no change, or adventitious thickening. 7. Non-cicatrized areas reveal no general abnormal relations ; merely enlarged Malpighian corpuscles with engorged gomeruli, which, with capsules, are otherwise normal. 8. Uriniferous tubules in part normal and in part dilated, with normal or hypertrophied epithelium, which, in places, is flattened or in moderate fatty degeneration. This compensatory hypertrophy can progress to the formation of small Adenomata, seen occasionally as minute white granules on renal surface. (Saborin.) 9. Urine, — Hegularly increased, light in color; opal- escent. Low Specific Gravity. Albumin absent or in traces. Deposit very slight Microscopic findings, — Of ten "nil; "there may 'be a few mono-nuclear leucocytes and a few hyaline cylinders. We find the urine often practically normal until the latter stage of the disease when Albuminuria is more or less marked, with considerable cast material. Associated Lesions, — All determinable lesions slowly progressive. a. Hsemorrhage, — Cerebral, epistaxis, metrorr- hagia, etc. b. Common disposition to catarrhal inflamma- tion of the entire respiratory tract. c. Retinitis Albuminurica commonest in this- form of Nephritis ; occasionally the first symptom to appear, and may be severe. d. Left Ventricular Hypertrophy. e. Gastro-intestinal catarrh. /. Neuritis, with intense neuralgia. g. CEdema, seldom present. h. General obliterating endarteritis a common complication. 89 SYLLABUS OF GENERAL PATHOLOGY. DiFFEKENTIAL DIAGNOSIS : a. Diabetes Insipidus, — Absence of sugar and al- bumin; very low specific gravity. h. Diabetes Mellitus, — Relatively Mgh specific gravity, absence of albumin; presence of glu- cose. c. Absence in both the above (a and b) of cardiac hypertrophy. d. Arterio-Sclerotic Cirrhosis assumable where predisposing causes to this vascular lesion, as senility,conditions of debility and syphilis, are found, and where cardiac asthma obtains. Note :— Great practical importance of diag- nosis before the characteristic phenomena of advanced cirrhosis obtain ; is only possible with prolonged observation. Initial Cirrhosis can be confounded with (a) acute and sub-acute Nephritis or with the characteristic urine of cirrhosis and (6) with mild but insidious development, absence of cardiac hypertrophy, properties of urine, observations of other organs and systemic findings, NEPHRITIS, SUPPURATIVE : (Renal Abscess.) Described by Hippocrates, Rufus, Galen, Aetius, et al. Aretaus first separated Acute from Chronic forms and described the often fatal cerebral phenomena consequent upon diminished urine. Friedrich Hoffman (1761) first attempted to differentiate Suppurative Nephritis, according to the location of pus, and described (a) Superficial, benign suppuration, and (6) . Deep, extensive, purulent infiltration. Suavages, particularly (1768), differentiated Purulent Nephritis as : Vera, Calculosa, and Arthritica. R. Virchow's investigations of embolism and metastasis and the parasitic nature of suppuration, first Ijrought out the true conception of this lesion. JEtiology : Infection by pathogenic micro-organ ism s. Four chan- nels of infection ; a. Direct, local (traumatic infection). b. Secondary to suppuration in peri-renal tissues. c. Genito-Urinary canal. d. Blood and Lymph channels. 90 SYLLABUS OF GENERAL PATHOLOGY. Pathologic Anatomy : 1. Gross findings : a. Traumatic cases usually uni-lateral. ,The kidney is bathed in pus and hsemorrhage- b. In suppuration of peri-renal tissues, findings similar to the above, without the evidence of trauma. c. Primary suppurative lesion either in renal pel- vis, ureter or bladder, or all. d. Metastatic renal suppurative processes almost always bi-lateral. Here abscess is single or multiple and orig- inates in the cortex or medulla or both, depending upon the location of emboli. The abscesses vary in size depending upon the age of the process. Where the process is due to Pyelitis, puru- lent infiltration generally may obtain. The pelvis contains pus and often one or more calculi, and, depending upon the age of the process, is dilated; its membrana propria is destroyed, the renal tissue be- coming thin in proportion to the dilatation. Where this form of lesion is uni-lateral, hypertrophy of the other kidney occurs. 3. Microscopic findings, are those of suppurative conditions of any tissue. 3. Urine; contains pus, blood, necrotic tissue, patho- genic micro-organisms. Associated Lesions : Where primary to kidney ; the general pthenomena of septic infection with, sometimes, peritonitis. Where secondary ; the primary condition is (e.g.) Endocarditis Ulcerosa Malignans, Cystitis. Differential Diagnosis : Metastatic renal suppuration can not be certainly diag- nosticated ; but is assumed when, in course of Sepsis, or Pyaemia or Endocarditis, a sudden Albuminuria with Pyuria occurs. 91 SYLLABUS OF GENERAL PATHOLOGY. la the other varieties, — History, local findings on i palpation, Pyuria together with microscopic evi- dence, in the urine, of renal necrosis. Note, — Exit of pus from Ureter into the blad- der often seen with the Cystosoope. Resolution : In some rare cases, where single abscess occurs, with relatively mild infection, the process may subside with final formation of cicatrix which replaces the pus. Note, — Bacteriological examination of urinary deposit usually determines pathogenic micro- organism present in a given case. RENAL AMYLOID DEGENERATION : Etiology : Essentially Toxaemia : This varies with cause : a. Chronic Pulmonary Tuberculosis. 6. Chronic suppuration. c. Constitutional Syphilis. d. Severe Malarial cachexia, c. Carcinoma. Rapidity of development 2^ to 6 months (Cohnheim, Litten). Pathologic Anatomy : Characteristic Macroscopic and Microscopic appearances no absolute proof ; Only chemical reaction certain. 1. Gross findings, — When marked, two principal forms : o. Resembling large White Kidney. Great en- largement. Capsule thinned, not adherent. Organ usually white, heavy. Surface smooth, shiny, waxy or butter yellow. Gross section, — Cortex thickened. More exact inspection reveals Malpighian tufts as brilliant "dew drops," which react to stains. Medulla more or less enlarged, usually dark blue red. u 92 SYLLABUS OF GENEEAL PATHOLOGY. b. So called Amyloid-Renal- Cirrhosis : Presents cirrhosis and amyloid with regularly less con- traction. Greater paleness. Enlarged. More prominent Malpighian tufts which react char- acteristically. c. All degrees of intermediate variety- 2. Microscopic findings, — In early cases no regular- ity of distribution save primary vascular involve- ment. Parenchyma of convoluted tubules usually in fatty degeneration. Usually small round cell infiltration of stroma. Occasionally haemorrhage. 3. Vascular changes, — This lesion attacks the vessels first, principally, and often, only the Glomeruli ; here all degrees of change to vascular obliteration. , Vasa afi'erens first and commonly involved ; later primary inter-tubular arteries and capil- laries ; Vasse Rectse later. In large majority of cases, lesion restricted to vascular appar- atus. 4. Uriniferous tubules, — Occasionally, particularly in the medulla, involved, with thickening and characteristic reaction of membrana propria to stains, epithelium being fused with it, or desquam- ated, forming homogeneous mass, often reacting to stains. 5. Capsular and interstitial changes in advanced cases. 6. Urine, — Quantity regularly markedly increased. Specific gravity diminished, 1012 — 1006 (Senator). Albumin, marked quantity. Deposit none or very slight, reveals microscopically a few hyaline or fatty casts, leucocytes, rarely red corpuscles, rarely renal epithelium. Fatty spherules (Senator). Associated Lesions: The primary cause. Various forms of Nephritis. Often amyloid of Spleen and Liver. Commonly ex- tensive general vascular amyloid. DiFFEBENTIAL DIAGNOSIS : Not al ways possible. Only certain with characteristic urinary findings together with definite cause. as SYLLABUS OF GENERAL PATHOLOGY. RENAL FATTY DEGENERATION : Fat obtains in organs whicli do not normally contain it in three ways : a. Fatty infiltration. b. Fatty degeneration. c. Fatty embolism. Etiology : a. Renal Fatty Infiltration in Hsematogenous Lipuria ; here fat not in parenchyma but] in glomeruli, whence it passes into Urine. b. Fatty degeneration results from all conditions re- ducing the supply of oxidized blood to tissues in general, short of absolute suppression of oxidation; This occasioned by : Renal Oligsemia, inadequate flow of blood to kidney. General Oligaemia, pernicious anaemia, etc. , here the fatty degeneration of paren- chyma of convoluted tubules. c. Fatty embolism occasionally from fractures of bones. Pathologic Anatomy : I. Gross findings,— Kindey large. Pale yellow. ' "Doughy." Non -adherent capsule. Gross section,— Cortex thickened, gray yellow, opaque with spare red striae and points. Medulla more commonly in less degree. ;>. Microscopic findings, — Epithelium universally in fatty degeneration to absolute disintegration. Glomeruli mostly normal, rarely in fatty degene- ration ; the same holds for inter-tubular vessels. Renal fatty embolism uni-lateral or bi-lateral and rare. Produces no marked renal lesion; always secondary. :^. Urine,— In grave cases, spare, dark, albuminous, contains peptone. Sediment contains fatty granules from epithelium; fatty epithelium; hyaline and finely granular casts ; a few erythrocytes and leucocytes. 94 SYLLABUS OF GENERAL PATHOLOGY. Albumiu originates from serum albumin, glo- bulin, nucleo-albumin , derived partly from the blood and lympb, partly from degenerated epithelium. Urinary findings in proportion to parenchy- matous degeneration. Diagnosis based on causation. Associated Lesions : Vascular changes already stated. Blood degeneration. Chronic disease with advanced cachexia. Acute yellow atrophy of the liver. SIMPLE NON-INFLAMMATORY RENAL ATROPHY: Commonest form Senile Atrophy, here lessened energy and arterio-sclerosis particularly of renal arteries. jEtiology : All conditions inducing oligsemia; Congenital smallness of arterial system in general, more rarely of the renal arteries ; or inherent constriction of the arteries. Diminution in actual quantity of blood, e.g., grave ansemia. Improper nutrition, e.g., persistent each exise. Pathologic Anatomy: 1. Gross findings, — Organ red or gray red ; appreci- ably reduced in size, never to the degree of chronic indurative variety. Capsule thickened, usually non-adherent. Surface smooth or granular, often exhibits isolated cysts. Gross section, — Cut surface reveals thinner cortex with relatively distinct markings. 2. Microscopic findings, — Malpighian tufts more or less destroyed, in spots nearer each other than normal. Capillary loops lack nuclei, are at first hyaline, ultimately reduced to homogeneous opaque masses, showing here and there a nucleus. . Capsular epithelium absent and capsule crumpled or in hyaline degeneration, invariably thickened and ultimately fused with glomerulus, forming a homogeneous sphere, smaller than normal. 95 SYLLABUS OF GENEBAL PATHOLOGY. Tubules around these atrophic tufts in various degrees of atrophy, being dimin- ished in size, with flattened epithelium, which latter finally disappears, with tubular collapse and formation into strands. Other tubules dilated and here and there cystic, with colloid contents. Endarteritis obliterans with atresia of smaller vessels. Stroma unchanged, either no small round cell infiltration or insignifi- cant. . Tissue relations differ some- what from those in the rare cases of atrophy due to trophic changes with vascular sclerosis, e. g,, marked Anaemia or Cach- exia. Exact diagnosis intra vitam impossible. (a) RENAL PELVIS. GENERAL MORPHOLOGY: Practically the upper, dilated extremity of the Ureter. Is a thin fibrous membrane which forms the hilus of the kidney, and passes upward in the form of infundibula, which are sleeve-like processes surrounding the lower portion of the Malpighian pyramids whose papillse punc- ture these sleeves. It is covered with a layer of stratified epithelium, the outer cells of which are irregularly shaped and more angular than those of the Bladder. The membrane is crossed by blood, vessels, lymphatics, nerves, and a limited amount of non- striated muscular fibres and, aroun d the m embran a propria, there is oftentimes a considerable amount of fat. ANOMALIES: In a few instances the pelvis contains a membranous septum, dividing it into two parts, both of which com- municate with the ureter. 96 SYLLABUS OF GENERAL PATHOLOGY. Occcasionally there are double pelves with double ureters, Oocasionaily, also, the ureters being atresic, con- genital Hydro-nephrosis obtains, in which instance the whole kidney may be converted practically into a cyst with thinning and obliteration of the true renal substance. CIRCULATORY DISTURBANCES: 1. Hyperasmia is .(a) Acute or (6) Chronic: a. Where Acute, may be synchronous with general renal hypersemia, or as a direct result of local irritant in the pelvis, such as calculi or pathogenic micro-organisms. It may also be circumscribed, and depend upon ulcerative lesions. b. Chronic Hypersemia is due to those causes pro- ducing a similar condition in the kidney. 2. Haemorrhage in renal pelvis usually acute as a result of trauma, from calculus or the etching of ulcers. May be considerable or very slight. PYELITIS: Usually uni-lateral j may be bi-lateral, especially when of cystic origin. Etiology: Renal calculus. Infection from the bladder or from the vascular channels, e.gr., Tuberculosis, Pus organ- isms. Pathologic Anatomy: Pyelitis is of all grades, depending upon cause; from a simple inflammatory hypersemia with desquamation of epithelium, to Phlegmon with necrosis and for- mation of pus. In the former case the Pathologic Anatomy is that of such conditions in tissues generally. In the latter, the destruction of tissue is irregular and accompanied by ulceration and granulation, and often a deposit of urinary salts on the surface of the pelvis. Where the inflammatory change is specific, as in Tuberculosis, single or multiple foci are seen, with typical tubercular ulceration, which is often complicated by deposit of urinary salts. SYLLABUS OF GENERAL PATHOLOGY. Urine, — Often increased from reflex irritation. Contains albumin, from traces to considerable, the amount depending upon tbe severity of the lesion. Usually pale in color, with diminished specific ' gravity and acid or alkaline reaction. Sediment varying in degree from practically none to large quantities of pus and detritus which, microscopically, will present character- istics in keeping with the nature of the pro- cess : a few pelvic epithelial cells, erythrocytes and leucocytes ; or vast numbers of leucocytes and numerous erythrocytes ; all layers of epithelium; shreds of necrotic connective tissue ; shales of calculous material and bac- teria. • Three principal forms of calculus: a. Oxalic Aoid, j Commoner where caloyli !.. Uric Acid, ■i-a-*'';^™-'''- r Commoner where inflam- c. phophatic, ] sf lar^MK [-line Cystitis. Associated Lesions: Often Pyo- and Hydro-nephrosis. Conditions arising from occulsion or atresia of ureter due to inflammatory change, or blocking of uretral entrance with necrotic tissue or calculi or inspissated pus. In these cases the pelvis becomes eventually dilated, somewhat spherical, and the renal tissue is compressed and, in advanced stages, very much thinned, the cortex often being obliter- ated and the Malpighian pyramids flattened. Where the Pyelitis is of secondary origin, as in ascendiilg inflammatory conditions beginning in the Bladder, these occur first and often persist. Not infrequently peri-renal inflammatory lesions and sometimes peritonitis with or without per- foration are the direct outcome of Septic Pyelitis. Occasionally Uretritis and Cystitis are secoiid- dary to Pyelitis. 98 SYLLABUS OF GENERAL PATHOLOGY. Differential Diagnosis : Pyelitis is differentiated by the clinical phenomena of pain and the Urseinic symptoms, together with local tumor and passage of pus aiid other morphologic ele- ments, depending upon the exact nature of the Pye- litis, from the Ureter into the Bladder. These are seen in the urinary sediment, or, directly observed, with the Cystoscope. Where mild Pyelitis occurs, exact differential di- agnosis impossible, owing to the very great mor- phologic similarity between the epithelial struc- tures of the Pelvis, Ureter and Bladder. Resolution : Occurs in those cases where lesion is mild, and pri- mary cause disappears, but doubtful in severe forms with pus, calculi and considerable tissue necrosis. RENAL TUMORS: Adenoma, — May be congenital. Occasionally in child- hood. Adeno-Cakoinoma, — In adults. Rhabdo-Myoma, — Purely congenital and very rare. Of no Pathologic significance. Sarcoma, — In youth ; rare. Fibroma i ^^ *^® Pelvis; rather rare. RENAL TUBERCULOSIS: General, in Acute Miliary Tuberculosis. Tubercles being everywhere disseminated throughout the Renal tissues. Discrete rarely ever : metastasis in which one kidney alone is usually affected. Is secondary, and perhaps more commonly, re- sulting from Tubercular Cystitis and Uretritis; here, also, usually uni-lateral. Diagnosis on general findings, together with evidence in the urinary deposit of renal ne- crosis and, finally, the finding of tubercle bacilli in the sediment. Note, — Danger of confounding Smegma Bacillus with B. Tuberculosis, the for- mer taking the same differential stain; the only safe conclusion made by in- oculation of guinea pig with urinary sediment.