Digestion Past Paper PDF

Visual. Hypersthenics / Endomorphic Horn-shaped or transverse appear more rounded and wider due to its transverse orientation Normosthenics / Mesomorphic / Average Build Oblique 24-48 hours Hook-shaped or vertical...

Visual. Hypersthenics / Endomorphic Horn-shaped or transverse appear more rounded and wider due to its transverse orientation Normosthenics / Mesomorphic / Average Build Oblique 24-48 hours Hook-shaped or vertical Asthenics / Ectomorphic / Slender build Smooth convex curve Achalasia  Upright position Left anterior oblique (LAO) position. Trendelenburg position Double-contrast technique Longitudinal ridges. Longitudinal folds Concave  Duodenal bulb or second part of the duodenum Gastric polyp. Irregular, lobulated mass extending into the gastric lumen. Large filling defect with irregular contours Anechoic (dark) with well-defined borders and posterior acoustic enhancement. Anechoic with a thin capsule Hypo- or hyperdense mass, often with irregular borders and possible contrast enhancement. Calcification is present. hypoechoic, exogenous Homogeneous with fine granular echotexture hourglass shape near narrow side  Anatomy Pathology Answers (Based on Strukov & Cepos) 1. 1. Local complications of acute pancreatitis: Edema, fat necrosis, hemorrhages, suppuration, pseudocysts, sequestration. Shock, peritonitis, abscess 2. 2. Localization of the initial damage in chronic pancreatitis: Initial damage occurs in pancreatic ducts and acinar cells, leading to fibrosis and atrophy. 3. 3. Clinical and morphological forms of viral hepatitis: Acute cyclic (icteric), anicteric, fulminant (necrotic), cholestatic, chronic. 4. 4. Main etiological factors leading to liver cirrhosis: Viral hepatitis, alcohol abuse, biliary obstruction, metabolic disorders, toxins, chronic 1) infectious (viral hepatitis, parasitic liver diseases, biliary tract infections); 2) toxic and toxic-allergic (alcohol, venous congestion.industrial and food poisons, drugs, allergens); 3) biliary (cholangitis, cholestasis of various nature:); 4) metabolic- alimentary (deficiency of proteins, vitamins, lipotropic factors, accumulation cirrhosis in hereditary metabolic disorders); 5) circulatory (chronic venous congestion in the liver); 6) cryptogenic cirrhosis 5. 5. Pathogenetic moment in the development of biliary cirrhosis: Chronic bile duct obstruction and autoimmune reactions. obstruction of the extrahepatic biliary tract (stone, tumor), which leads to cholestasis (cholestatic cirrhosis) 6. 6. Macroscopic signs of alcoholic (portal) cirrhosis: Nodular liver surface, small regenerative nodules, fibrosis, shrunken liver. 7. 7. Macroscopic characteristics of viral (postnecrotic) cirrhosis: Large regeneration nodules, fibrous septa, shrunken and deformed liver. macronodular cirrhosis 8. 8. Histological signs of acute alcoholic hepatitis: Hepatocyte necrosis, Mallory bodies, neutrophilic infiltration, perivenular fibrosis. ballooning 9. 9. Types of dystrophy in viral hepatitis: Ballooning degeneration, hydropic dystrophy, fatty degeneration, necrosis. 10. 10. Diseases causing large nodular (postnecrotic) cirrhosis: Viral hepatitis, toxic liver damage, massive liver necrosis. Chronic viral hepatitis leads to cirrhosis, toxic liver dystrophy, viral hepatitis with extensive necrosis, rarely alcoholic hepatitis. 11. 11. Liver disease characterized by dystrophy and necrosis:of hepatic parenchyma : Acute toxic liver dystrophy. Postnecrotic cirrhosis 12. 12. Form of viral hepatitis depending on the etiological factor: Hepatitis A (fecal-oral), Hepatitis B/C/D (parenteral), Hepatitis E (waterborne). 13. 13. Cause of rupture of esophageal veins in cirrhosis: 13.The death of a 43-year-old man suffering from cirrhosis of the liver was caused by bleeding from the veins of the esophagus. The cause of rupture of esophageal veins : decompensated portal hypertension  Portal hypertension leading to variceal dilation and rupture. 14. 14. Clinical and morphological form of viral hepatitis: Icteric, anicteric, cholestatic, fulminant, chronic. 15.Characteristics of the height of the stage of yellow dystrophy of progressive massive liver necrosis 15. 15. Characteristics of progressive massive liver necrosis (yellow dystrophy stage): Diffuse hepatocyte necrosis, jaundice, hemorrhagic diathesis. intense jaundice, hepatic encephalopathy, coagulopathy, hepatic failure 16. 16. Cause of progressive massive liver necrosis: Viral hepatitis, toxic damage, severe ischemia. exogenous (food poisoning, fungi, heliotrope, phosphorus, arsenic) endogenous (pregnancy toxicosis, thyrotoxicosis) intoxications, Allergic and autoallergic factors 17. 17. Characteristics of liver steatosis: Fat accumulation in hepatocytes, ballooning degeneration, perisinusoidal fibrosis. 18. 18. Most common cause of death in serum hepatitis: Liver failure, hepatic coma. hepatocellular carcinoma Cirrhosis or liver Failure 19. 19. Characteristics of pre-jaundice period of viral hepatitis: Malaise, fever, nausea, anorexia, dark urine. 20. 20. Characteristics of viral hepatitis A: Acute, self-limiting, fecal-oral transmission, no chronicity. Benign, Self-limiting – Type A resolves without chronic issues (infectious hepatitis) (epidemic hepatitis) 21. 21. Liver in primary biliary cirrhosis: Intrahepatic bile duct destruction, periportal fibrosis, nodular liver. liver in primary biliary cirrhosis is enlarged, dense, gray-green in section, its surface smooth or fine grained 22. 22. Manifestation of decompensated portal hypertension: Ascites, esophageal varices, splenomegaly, hepatic encephalopathy. hemorrhoidal plexus and bleeding from these veins. 23. 23. Morphological sign of jaundice form of hepatitis: Hepatocyte necrosis, bile plugs in canaliculi, Kupffer cell proliferation. 24. 24. Liver changes in fulminant hepatitis:of viral hepatitis: Massive hepatocyte necrosis, hemorrhages, microvesicular steatosis. atrophy 25. 25. Disease complicated by fatty hepatosis: Diabetes mellitus, alcoholism, metabolic syndrome. obesity 26. 26. Histological diagnosis of acute viral hepatitis: Hyperemia, hepatocyte swelling, lymphocytic infiltration in portal tracts. 27. 27. Main histological sign of viral hepatitis: 26.Histological examination of the liver shows marked hyperemia and swelling of the tissue, granular dystrophy of hepatocytes, and histiolymphocytic infiltration of the portal tracts. Your diagnosis Acute viral hepatitis  Lobular inflammation, periportal necrosis, ballooning degeneration. 28. 28. Diagnosis for a small, nodular, fibrotic liver: 28.Macroscopically: the liver is dense, reduced in size, with large nodules. The incision shows wide Micronodular cirrhosis (portal cirrhosis). gray layers dividing the liver into lobules. Your diagnosis Postnecrotic cirrhosis 29. 29. Structural changes in pancreas in diabetes mellitus: Islet cell destruction, fibrosis, hyalinization of islets. Sclerotic changes - lead to impaired patency of the ducts, the formation of cysts., Atrophic processes, Cicatricial deformity, Calcification of pancreatic tissue In chronic pancreatitis, manifestations of diabetes mellitus 30. 30. Types of pancreatic necrosis: Hemorrhagic, fat necrosis, mixed necrosis. Purulent necrosis 31. 31. Forms of acute focal gastritis: Catarrhal, hemorrhagic, fibrinous, phlegmonous. Erosive gastritis 32. 32. Morphological forms of acute gastritis: Superficial, deep, necrotizing.1) catarrhal (simple); 2) fibrinous; 3) purulent (phlegmous); 4) necrotic (corrosive). 33. 33. Variants of acute fibrinous gastritis: Croupous, diphtheritic. croupous (superficial necrosis) and diphtheria (deep necrosis) 34. 34. Consequences of cicatricial stenosis of gastric pylorus:in peptic ulcer disease: Gastric retention, vomiting, metabolic alkalosis. Pyloric obstruction 35. 35. Inflammatory complications of peptic ulcer:of the stomach and duodenum: Perigastritis, periduodenitis, adhesions. Perforation, hemorrhage, and penetration 36. 36. Most common location of stomach cancer: Pyloric region, lesser curvature. Antrum 37. 37. Types of hepatocyte dystrophy in viral hepatitis: Ballooning, hydropic, fatty dystrophy. 38. 38. Exacerbation of stomach ulcer is characterized by: Necrosis, hemorrhage, infiltration. 39. 39. Immediate cause of death in viral cirrhosis: Hepatic coma, variceal bleeding. Gastrointestinal bleeding (Hemorrhage) 40. 40. Precancerous condition in stomach: Chronic atrophic gastritis, intestinal metaplasia. 41. 41. Form of acute gastritis: 42.Histological examination of the liver shows marked hyperemia and swelling of the tissue, granular dystrophy of hepatocytes, and histiolymphocytic infiltration of the portal tracts. What is your diagnosis? Acute viral hepatitis  Catarrhal, hemorrhagic, fibrinous, phlegmonous. 42. 42. Histological diagnosis of viral hepatitis: Hyperemia, hepatocyte swelling, lymphocytic infiltration in portal tracts. 43. 43. Form of gastritis with metaplasia and inflammatory infiltrates: 43.A form of gastritis characterized by microscopic changes in the mucous Chronic atrophic gastritis. membrane: moderate dystrophy and restructuring of the integumentary pit epithelium (metaplasia). Inflammatory infiltrates in the superficial parts of the mucous membrane (less often in the entire thickness): Chronic superficial gastritis 44. 44. Precancerous gastritis: Chronic atrophic gastritis with intestinal metaplasia. 45. 45. Bottom of a chronic gastric ulcer in remission: Fibrous tissue, hyperplastic mucosa, capillary proliferation. Smooth, fibrous, with a scarred appearance 46. 46. Cause of death in toxic liver dystrophy: Hepatic coma, renal failure. postnecrotic cirrhosis of the liver, acute liver or kidney failure (hepatorenal syndrome) 47. 47. Diagnosis for black, flabby vermiform appendix: 47.A vermiform appendage of flabby consistency, black in color. Histologically: the Gangrenous appendicitis. layers are indistinguishable, homogeneous pink in color, with diffuse leukocyte infiltration. Your diagnosis: 48. 48. Complications of gastric ulcer: Perforation, bleeding, penetration, malignancy. 1)ulcerative-destructive (bleeding, perforation, penetration); 2) inflammatory (gastritis, duodenitis, perigastritis, periduodenitis) 49. 49. Penetration of stomach ulcers: Ulcer extends into adjacent organs (pancreas, liver, colon). [Penetration of an ulcer is called its penetration beyond the walls of the stomach or duodenum into neighboring organs] 50. 50. Diagnosis for a small, nodular, fibrotic liver: Micronodular (portal) cirrhosis. 50.During a macroscopic examination of the liver, it was noted that the organ was reduced in size, dense in consistency, and the surface was finely rounded. On the incision, connective-woven layers divide the liver into lobules. Your diagnosis: postnecrotic cirrhosis  Physio Test questions for integrated midterm control on the topic «Pathophysiology of Digestive system» for the 2024-2025 academic year PREPARED BY SYED EESHAAN 347B 1. Which diseases are characterized by the appearance of bilirubin in the urine: (hepatitis cirrhosis, liver tumor) jaundice 2. Cholemia syndrome is caused by a pathogenic effect:(presence of bile in blood ) 3. Bleeding with prolonged subhepatic jaundice occurs due to:(due to absence of clotting factor (vitamin K) 4. Neurotic anorexia is observed when: ( 5. Occurs with insufficiency of the esophago-gastric sphincter:(GERD) 6. Malabsorption syndrome is characterized by impaired absorption of nutrients: (fat soluble vit (B12 ADEK) 7. The accumulation of ammonia in liver failure is especially toxic to... (brain) 8. Factors contributing to the development of peptic ulcer disease include: (alcohol, H pylori infection, smoking, NSAID) 9.