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Basic Concepts-I

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1. Pathology- Etiology + Pathogenesis + Lesions + Symptoms + Result
2. Altered structures- lesions
3. Disorganized functions- symptoms
4. Button ulcers in large intestine- swine fever
5. Punched out ulcers in abomasum- theileriasis

6. Negri bodies in hippocampus and cerebellum- Rabies
7. Gr. Clinics= Klinike = bed
8. Diagnosis = Dia(through)+gnos (to know)
9. Invalidism-incomplete recovery of body (JD, TB)
10. Necropsy- PM in animals and birds

11. Autopsy- PM in humans
12. Biopsy- tissue examination  during life
13. Morbid changes- changes at PM
14. Intrinsic cause= endogenous cause= predisposing factors
15. Extrinsic cause= exogenous cause

16. Brain tumors – bulldog, boxer
17. Tumors- older animals (DNA repair capacity got reduced over age)
18. Strangle- young horse
19. Caecal coccidiosis– chicks
20. Nephritis- more in male dogs

21. Nephritis- more in female cattle
22. Idiosyncrasy- unusual reaction to some substances (drugs)
23. Melanoscarcoma- more in white and gray horses
24. Cohneheim and Metchnikoff- cellular and vascular changes
during inflammation
25. Father of Medicine- Hippocrates

26. Father of Veterinary Medicine- Renatus Vegetius
27. Humoral theory of disease- Hippocrates
       a. Blood- warm and moist like air
b. Phlegm- cold and moist like water
       c. Yellow bile- warm and dry like fire
d. Black bile- cold and dry like earth
28. Originator of anatomy and physiology- Aristotle
29. Father of Anatomy- Claudius Galen
30. Cardinal signs of inflammation- Cornelius Celsus

31. Book of the veterinary art- Renatus Vegetius
32. Father of pathological anatomy- Antonio Benivieni
33. First modern dissector- Leonardo da Vinci
34. Century of anatomy- 16th century
35. Discovery of blood circulation- William Harvey

36. Discovery of capillaries, erythrocytes, Malpighian layer of skin- Marcello Malpighi
37. Invention of Microscope- Hans and Zacharias Jannsen
38. First to see protozoa under microscope- Leeuwenhoek
39. First textbook of pathology- Jean Fernel
40. Anatomical concept in Medicine- Morgagni

41. Father of Histology – Bichat
42. Histology term coined by- Bichat
43. Father of Immunology- Edward Jenner
44. First modern veterinary college- @ Lyon, France by Claude Bourgelat
45. First experimental pathologist- John Hunter

46. Originator of modern experimental pathology- Julius Cohnheim
47. Supreme descriptive pathologist- Carl Rokitansky
48. Father of modern/cellular pathology- Rudolph Virchow
49. Embolism, thrombosis, fatty degeneration amyloidosis coined by- Rudolph Virchow
50. Germ theory of disease- Louis Pasteur

51. Vaccination against rabies, anthrax, Pasteurellosis- Louis Pasteur
52. Discovery of tubercle bacilli- Robert Koch
53. Phagocytosis, macrophage, microphage- Elie Metchnikoff
54. Discovery of lysosomes- Cristian de Duve
55. Lysosomes= suicide bags

56. Prions- Stanely Prusiner(1997 Noble prize for this)
57. Hypertrophy- increase in size only 
58. Hyperplasia- increase in both size and number
59. Atrophy- decrease in size and function
60. Hypoxia- lack of oxygen

61. Ischaemia- lack of blood and oxygen (so, faster injury)
62. Sickle cell anemia- glutamic acid alters valine
63. Myelin figures- phospholipids
64. Critical step in cell death- membrane damage
65. Important mediator of cell death- Calcium ion

66. Free radical scavengers- Vit E, A, C, beta carotene
67. First reaction to cell injury- cellular swelling
68. Chediak Higashi syndrome- microtubule polymerization defect
69. Mallory bodies- in alcoholic liver, humans
70. Heat shock proteins- Chaperons

71. Fatty liver – cattle- yellow
                             cat- white
                             horse- orange
72. Phosphorus poisoning- small and numerous fat droplets in hepatocytes
73. Foam cells- macrophages full of lipid debris
74. Russel bodies- plasma cells
75. Glycogenoses= glycogen storage disease

76. Melas- black
77. Acanthosis nigricans- accumulation of melanin in skin (dog)
78. Albinism- complete absence of melanin
79. Albinism- deficiency of tyrosinase
80. Leukoderma- local loss of pigments

81. Vitiligo– Partial or complete loss of melanocytes in epidermis
82. Fuscus– brown
83. Lipochrome= wear and tear pigment= ageing pigment
84. Brown atrophy- large accumulates of autophagus vacuoles of lipofuschin within cells
85. Ferittiniron protein complex

86. Hemosiderin- large aggregates of ferittin micelle
87. Hemosiderin- greatest in spleen of horse and least in dog
88. Biliverdin- green bile
89. Bilirubin- yellow bile
90. Hemosiderin- golden yellow color

91. Hemochromatosis– excessive accumulation of iron
92. Equine infectious anemia- hemosiderin in kidneys
93. Heart failure cells- hemosiderin laden macrophages
94. Brown enduration- pulmonary change in hemosiderosis
95. Bilirubin to biliverdin- mononuclear cells of spleen

96. Birds lack biliverdin reductase
97. Screla of eye contains more elastin which has affinity to bilirubin
98. Brain and spinal cord- do not change in color in jaundice
99. Hemolytic= pre-hepatic jaundice
100. Toxic= intrahepatic jaundice

101. Obstructive= post hepatic jaundice
102. Hemolytic- all the causes that lead to breakdown of rbc
103. Erythroblastalis fetalis– mother rh –ve, father rh +ve
104. Hemolytic jaundice- unconjugated hyperbilirubinemia
105. Toxic jaundice –conjugated and non-conjugated hyperbilirubinemia

106. Post hepatic– only conjugated hyperbilirubinemia
107. Xanthomas- macrophages laden with cholesterol in skin
108. Van den Bergh reaction
        a. Hemolytic J- indirect (unconjugated bilirubin)
        b. Toxic J- biphasic (both conjugated and unconjugated bilirubin)
         c. Obstructive J- direct (conjugated bilirubin)
109. Pneumoconiosis- dust particles
110. Anthracosis– carbon or coal

111. Tattooing- localized pigmentation in skin
112. Siderosis- iron
113. Silicosis- silicon dioxide=stone dust=silicon
114. Plumbism- lead+H2S
115. Lead line- on gums

116. Chalicosis- calcium carbonate (chalk)
117. Asbestosis- asbestos
118. Argyrosis- silver compound
119. Mucin- precipitate with acetic acid
120. Psuedomucin- does not precipitate with acetic acid (bcoz its pseudo)

121. Hyperkeratosis- chlorinated naphthalene poisoning
122. Epithelial pearls- squamous cell carcinoma
123. Corpora amylacea= starch bodies=brain sand
124. Autolysis- lysosomes from dead cells itself
125. Hetorolysis-lysosomes from infiltrating leukocytes

126. Karyolysis- fading of basophilia of chromatin
127. Karyorrhexis- fragmentation
128. Pyknosis- shrinkage leading to increased basophilia
129. Protein denaturation- coagulative necrosis
130. Enzymatic digestion- liquefactive necrosis

131. Coagulative N- architectural details lost but cellular details preserved
132. Liquefactive necrosis- both architectural and cellular details are lost
133. Coagulative necrosis cant occur in brain
134. Caseous N- TB, lymphadenitis/oesophagostomiasis in sheep
135. Critical life or death switch (apoptosis)- TP53 gene

136. Dry gangrene- body extremities
137. Wet gangrene- internal organs
138. Tophi- large crystalline aggregates of monosodium urate in joints
139. Poultry- lack uricase enzyme
140. Visceral gout in poultry- dehydration

141. Amyloid- protein
142. Amyloidosis- spleen, liver, kidneys
143. Primary A- immunological origin
144. Secondary A- chronic inflammation

145. Bence Jones proteins- urine in amyloidosis
146. Lardaceous/sago spleen- amyloidosis
147. Amyloidosis- glomerulus of kidneys affected mainly
148. Amyloid deposition is permanent change
149. Rigor mortis-
        a. appears 1 to 8 hrs after death
        b. disappears 24 to 36 hrs after death

150. Acute inflammation- edema and neutrophils
151. Chronic inflammation- fibrosis and lymphocyte, macrophages
152. Cardinal signs of inflammation- Given by Cornelius Celsus
       a. Rubor- redness
       b. tumor- swelling
       c. Calor- heat
       d. Dolor- pain
153. Fifth sign- functio-laesa given by Rudolf Virchow
154. Quantitation of vascular permeability-
       a. Dye technique- gross and microscopic
       b. Colloidal carbon technique- microscopic
155. Inflammatory exudate- accumulated plasma outside the vessel

156. Diapedesis- RBCs leaving from intact blood vessel
157. Rhexis- RBCs leaving from ruptured intact blood vessel
158. Triple response- given by Sir Thomas Lewis (1927), (to suggest role of chemical mediators in inflammation)
       a. Erythema- within seconds, dull red line along the point of stroke
       b. Flare- brite red hallow around the stroke
       c. Weal- swelling of stroke mark
159. Role in increasing vascular permeability-
       a. Bradykinin
       b. C3a
       c. C5a
160. Emigration=transmigration=diapedesis

161. Main events in acute inflammation
       a. First 6 to 24 hrs- neutrophils predominate
       b. 24 to 48 hrs- replaced by monocytes
162. Boyden’s micropore filter technique- to demonstrate chemotaxis
163. Chemotactic agents
       a. Endogenous- complement system, cytokines, leukotriene B4
       b. Exogenous- soluble bacterial products (n formyl methionine terminal amino acids)
164. Phagocytosis- taking particulate matter
165. Pinocytosis- taking fluid

166. Regurgitation during feeding- phagocytic vacuole remains open to the outside before complete closure of phagolysosome, escaping lysosomal hydrolases
167. Frustrated phagocytosis= reverse endocytosis- neutrophils are exposed to indigestible material on flat surface, lysosomes are released outside
168. Granules in neutrophils
       a. Primary- azurophils-hydrolase, peroxidase, muramidase
       b. Secondary- smaller and specific- lactoferrins, lysozymes
169. Catarrhal inflammation/mucous inflammation- mucus is the main component of exudate
170. Serous inflammation- clear watery fluid

171. Fibrinous inflammation- more violent injury
172. Pus= neutrophils+ necrotic cells+ serus
       a. In cattle, corynobacteria– greenish pus
       b. Canine pus– watery (more lysosomal enzymes, more proteolysis)
       c. Bovine pus- viscid
       d. Avian pus- dry and caseous (bcoz anti enzymes are present)
173. Giant cells
       a. Foreign type- Langhans giant cells- horseshoe nuclei at periphery, TB, JD, actinomycosis, blastomycosis (chronic conditions)
       b. Tumor type- in malignant cells
174. Epithelioid cells- activated macrophages (granulomatous inflammation)
175. Avian inflammation- eosinophils are absent in allergic and parasitic inflammations

176. Avian phagocytic cells
       a. Heterophils
       b. Monocytes
       c. Basophiles
d. Thrombocytes
177. Mast cells are absent in granulomatous tissue of avian inflammation (present in mammals)

The secret of getting ahead is getting started. Mark Twain

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