M2255p (patho conc.2) PDF - Pathophysiology Past Paper

Questions for pathophysiology Semester 6. 2nd totalisation (2024-2025) 1. What are manifestations of humoral syndrome in acute renal failure? a) [x] hyperazotemia b) [x] hyperhidratation c) oliguria d) [ ] anemia e) [ ] alcalosis or hyperhydration...

Questions for pathophysiology Semester 6. 2nd totalisation (2024-2025) 1. What are manifestations of humoral syndrome in acute renal failure? a) [x] hyperazotemia b) [x] hyperhidratation c) oliguria d) [ ] anemia e) [ ] alcalosis or hyperhydration in oligoanuric phase hyponatremia in oligoanuric phase hyperkalemia hyponatremia caused by hemodilution 2. What are pathogenetic mechanisms for changes of diuresis in hyperglycemia? Osmotic diuresis: Hyperglycemia can cause osmotic diuresis, which is an increase in urine production due to the presence of excess glucose in the urine. Alterations in kidney function: Hyperglycemia can also impair kidney function by damaging the small blood vessels in the kidneys and reducing blood flow to the glomeruli, the filtering units of the kidneys. Neurogenic mechanisms: Hyperglycemia can also stimulate the release of certain hormones, such as vasopressin, Sodium and water balance: Hyperglycemia can also disrupt the balance of sodium and water in the body, leading to alterations in urine output 3. How diuresis is changed in obstruction of urinary pathways? Increased pressure Impaired filtration Backflow of urine Hormonal changes 4. What are manifestations of clinical syndrome in chronic renal failure? Osteoporosis iron deficiency anemia secondary hyperparathyroidism osteodystrophy 5. What are prerenal causes of acute renal failure? systemic vasodilation in spinal shock heart failure high level of catecholamines in the blood  6. What are the consequences of reduced glomerular filtration? Fluid and electrolyte imbalance Waste product accumulation Hypertension Anemia Bone disease Cardiovascular disease 7. What are the consequences of urinary pathway obstruction? Hydronephrosis Renal failure Urinary tract infections Stone formation Pain and discomfort Urinary incontinence 8. What are the pathogenetic mechanisms of enhanced blood pressure in glomerulopathy with nephritic syndrome? Activation of RAAS Increased extracellular fluid volume Endothelial dysfunction Inflammation Genetic factors 9. What is the mechanism of coagulopathy in nephrotic syndrome? Loss of anticoagulant proteins Increased level of procoagulant factors Endothelial dysfunction Hyperlipidemia 10.How does glomerular filtration rate (GFR) change in hypovolemia? 1. GFR is reduced, caused by reduced effective pressure of filtration 2. GFR is reduced caused by diminished hydrostatic pressure in glomerular capillaries 3. GFR is reduced, caused by enhanced osmotic pressure in primary urine 4. GFR is reduced, caused by reduced permeability of renal filter 5. GFR is reduced, caused by reduced tubular water resorption 11.What are pathogenetic mechanism of nephritic renal edema? Increased permeability of the glomerular capillary wall: Sodium retention Activation of the renin-angiotensin-aldosterone system (RAAS) Decreased clearance of water and solutes: 12.What are the consequences of disturbances in hormone inactivation in the kidney in patients with chronic kidney disease? decreased inactivation of parathyroid hormone (PTH) can lead to secondary hyperparathyroidism, which can cause bone disease and calcification of soft tissues. Additionally, impaired inactivation of insulin-like growth factor-1 (IGF-1) can cause growth abnormalities and increased risk of cancer. The accumulation of vasopressin can also cause water retention and hyponatremia, while the decreased inactivation of erythropoietin can lead to anemia 13.What is pathogenesis of tertiary hyperthyroidism? Increased TRH 14.What is the cause of primary hyperaldosteronism? Hormone-secretory tumor from the glomerular layer of adrenal gland aldosterone-producing adrenocortical neoplasm, usually an adenoma, or by primary adrenocortical hyperplasia.  Questions for pathophysiology- 2nd Concluding (Answers Got Completely From Pdf) 15. What pathogenetic factors contribute to reduced glomerular filtration rate in nephritic syndrome? - decreased glomerular membrane permeability and has manifestations related to decreased GFR, - fluid retention and accumulation of nitrogenous waste products; 16. A distinctive clinical sign for primary hipocorticism is skin hyperpigmentation. What is pathogenesis? - Diminished negative feedback from cortisol lead to massive rise in the synthesis of Proopiomelanocortin -> MSH/ACTH INCREASES -> melanotropic effect -> brown discolouration of the skin. 17. Accumulation of what metabolic products explain metabolic acidosis in liver failure? (Same ans as qn-18) 18. Accumulation of what metabolic products explain metabolic acidosis in liver failure? a. ẞ-hydroxybutyric acid b. acetoacetic acid c. CO2 d. Oxaloacetate e. Acetic acid 19. How are gastric tone and motility of stomach disturbed in hyperchlorhydria? a. hypotonia b. hypertonus c. accelerated evacuation d. chymostasis in the stomach e. vomit 20. How are gastric tone and motility of stomach disturbed in hypochlorhydria? a. hypotonia b. hypertonicity c. accelerated evacuation d. chemostasis in the stomach e. vomit 21. How can digestion be disturbed due to pancreatic exocrine deficiency? a. maldigestion of polysaccharides b. protein maldigestion c. lipid maldigestion d. improving intestinal digestion e. cellulose maldigestion 22. How carbohydrate metabolism in affected in hepatocyte in liver failure? a. increased glucose level after meal b. reduced glucose level in fasting c. development of fructosemia d. reduced glycogen storages in the liver e. increased glycogen storages in the liver 23.How change the level of branched aminoacids and aromatic aminoacids in the blood in patients with liver failure? - Increased branched amino acid due to their increased breakdown in pheripheral tissue (muscular and adipose tissue ) - Increased aromatic amino acid due to their decreased breakdown in liver 24. How does acid-base balance change in patients with type I diabetes mellitus? A. metabolic acidosis caused by increased level of CO2 B. metabolic acidosis caused by accumulation of acetylacetic acid C. excretory acidosis with accumulation of acids D. metabolic acidosis caused by accumulation of oxaloacetate E. lactoacidosis 25. How does blood hormones concentration change in primary hypothyroidism? a. low thyroid-releasing hormone, low thyrotropin, low thyroid hormones b. low thyroid-releasing hormone, high thyrotropin, decreased thyroid hormones c. increased thyroid-releasing hormone, increased thyrotropin, low thyroid hormones d. low thyroid-feleasing hormone, low thyrotropin, raised thyroid hormones e. increased thyroid-releasing hormone, low thyrotropin, low thyroid hormones 26. How does blood hormones concentration change in secondary hypothyroidism? a. low thyroid-releasing hormone, low thyrotropin, low thyroid hormones b. low thyroid-releasing hormone, high thyrotropin, decreased thyroid hormones c. increased thyroid-releasing hormone , increased thyrotropin , low thyroid hormones d. low thyroid-releasing hormone, low thyrotropin, raised thyroid hormones e. increased thyroid-releasing hormone, low thyrotropin, low thyroid hormones 27. How does blood hormones concentration change in tertiary hyperthyroidism? a. increased thyroid-releasing hormone, increased thyrotropin , low thyroid hormones b. increased thyroid-releasing hormone , low thyrotropin, raised thyroid hormones c. low thyroid-releasing hormone, high thyrotropin, raised thyroid hormones d. low thyroid-releasing hormone, low thyrotropin, raised thyroid hormones e. increased thyroid-realising hormone, increased thyrotropin, raised thyroid hormones 28. How does body weight change in diabetes mellitus type I? a. increases due to reduced lypolysis in lack of insulin b. increases due to sodium retention and water caused bu insulin deficiency c. increase caused by enhanced lipogenesis in lack of insulin d. decreases due to reduced appetite and reduced food intake e. decreases due to enhanced lypolysis which is the effect of glucocorticoids  Questions for pathophysiology Semester 6. 2nd totalisation (2024-2025) 29..How does carbohydrate metabolism change in GH hypersecretion in children? a. hyperglycemia caused by enhanced glycogenogenesis with insulin-resistence b. hyperglycemia caused by enhanced glycogenolysis with insulin-resistence c. hyperglycemia caused by enhanced gluconeogenesis from free fatty acids released in the result of enhanced lipolysis d. hyperglycemia caused by enhanced gluconeogenesis from glycerol released in the result of enhanced lipolysis e. hyperglycemia caused by enhanced gluconeogenesis from amonoacids released in the result of enhanced proteolysis 30.How does energy metabolism change in hypothyroidism? a. reduced oxidation processes with conservation of heat due to vasoconstriction b. decreased basal metabolism caused by decoupling of oxidative phosphorilation c. decreased basal metabolism caused by increased oxidative phosphorilation d. decreased basal metabolism caused by reduced oxidative phosphorilation e. reduced oxidation processes with loss of energy in form of heat due to vasodilation 31.How does glomerular filtration rate (GFR) change in hypervolemia? 32.How does lipid metabolism change in hypothyroidism? a. reduced lypolisis with decreased level of free fatty acids in the blood b. hypercholesterolemia with HDL without atheromatosis c. hypercholesterolemia with fractions VLDL, LDL and HDL d. reduced lypolisis with increased level of glycerol in the blood e. hypercholesterolemia with reduced cholesterol metabolism 33.How does metabolism change in diabetes mellitus type I? a. increased lypolysis with enhanced oxidation of glycerol b. increased lypolysis with enhanced oxidation of FFA c. reduced lypolysis caused by excess of glucocorticosteroids d. increased lypolysis due to low level of glucagon e. increased lypolysis due to low level of catecholamines or a. reduced catabolism due to insulin lack b. increased lypogenesis due to excess of glucagon c. reduced proteolysis caused by excess of glucocorticosteroids d. excessive proteolysis caused by excessive glucagon e. increased anabolism due to insulin deficiency or a. increased lypolysis with enhanced oxidation of glycerol b. increased lypolysis with enhanced oxidation of FFA c. reduced lypolysis caused by excess of glucocorticosteroids d. increased lypolysis due to low level of glucagon e. increased lypolysis due to low level of catecholamines or a. reduced lypolysis and proteolysis caused by insulin lack b. increased proteolysis and lypolisis caused by catecholamine deficiency c. enhanced proteolysis and lypolysis caused by deficiency of glucocorticosteroids d. increased anabolism due to excess of glucagon e. increased lypolysis and proteolysis caused by excess of catecholamines 34.How does metabolism change in diabetes mellitus type I? 35.How does protein metabolism change in GH hypersecretion in children? a. intensifies deamination of amino acids and increased their uptake from the blood with enhanced proteosynthesis b. intensifies transamination of amino acids and increased their uptake from the blood with enhanced proteosynthesis c. increase peripheral use of aminoacids leading to high level of ammonia in the blood d increased aminoacids uptake from the blood with enhanced proteosynthesis e. increases peripheral use of aminoacids leading to high level of urea in the blood 36.How does protein metabolism change in patients with type I diabetes mellitus? a. reduced lypolysis and proteolysis caused by insulin lack b. increased proteolysis and lypolisis caused by catecholamine deficiency c. enhanced proteolysis and lypolysis caused by deficiency of glucocorticosteroids d. increased anabolism due to excess of glucagon e. increased lypolysis and proteolysis caused by excess of catecholamines 37.How is explained hemorrhagic syndrome in patients with hepatic and posthepatic jaundice? Due to increased concentration of biliary acid in the blood (cholalemia) that binds to the calcium ions. Decreased synthesis of clotting factor in the liver 38.How is explained hemorrhagic syndrome in patients with hepatic and posthepatic jaundice? 39.How is hyperaldosteronism manifested? A. increased resistance of peripheral vessels B. excretory acidosis C. urine hyperosmolarity D.urine hypoosmolarity E.excretory alkalosis. or A. muscle hypotonus caused by hypercloremia B. muscle hypotonus caused by hypernatremia C. muscle hypotonus caused by hypercalcemia D.muscle hypotonus caused by hypokalemia E. muscle hypotonus caused by hyperkalemia or A. arterial hypertension which is in relation with izotonic hyperhydration B. arterial hypertension which is in relation with hypotonic hyperhydration C. arterial hypertension due to increased sensibility of the heart to catecholamines D.arterial hypertension which is in relation with hypertonic hyperhydration 40.How is hypoaldosteronism manifested? A.arterial hypotension caused by hypoosomolar dehydration B. arterial hypotension caused by hyperosmolar dehydration C.hyperosmolarity of the urine D. hypoosomolarity of the urine E. cell dehydration Or A. arterial hypotension caused by reduced sensitivity of the heart and blood vessels to catecholamines B.arterial hypotension caused by hypoosmolar dehydration C. arterial hypotension caused hyperosmolar dehydration D. arterial hypotension caused by izoosmolar dehydration E.arterial hypotension caused by decreased preload 41.How the diuresis is changed in hypoproteinemia? 42.How will change the biliary pigment metabolism in haemolytic jaundice? *Increased unconjugated bilirubin in blood *Increased conjucated bilirubin in liver *Increased urobilinogen in small intestine *Increased urobilinoid bodies(stercobilin &urobilin) in urine(dark colour of urine ) *Increased stercobilinogen &stercobilin (feces overcolourated 43. In what disorders can be attested lipiduria? Compensatory Hyperlipidemia(liver) caused by Nephrotic syndrome, and familial hypercholesterolemia. Nephrotic syndrome caused by liver lipoprotein lipase synthesis inhibition Lipoid nephrosis (minimal change disorder) Diabetic nephropathy Renal tubular disorder (Fanconi syndrome) 44. Level of what biological active substances is enhanced locally in toxic and ischemic kidney injury? Reactive oxygen species (ROS): Cytokines: Inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha). Chemokines: monocyte chemoattractant protein-1 (MCP-1), CCL5 and interleukin-8 (IL-8) can be upregulated, leading to the recruitment of inflammatory cells to the kidney. - Growth factors: Growth factors, such as transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF), connective tissue growth factor, FGF (all causes increased extracellular matrix proliferation, thus sclerosis/fibrosis.) - Adhesion molecules: Adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), 45. One severe medical emergency in absolute insulin deficiency is ketoacidotic coma. What is pathogeny? Deviations from normal dietary intake, unusual physical activity, infection, or any other forms of stress, these all lead to exacerbation of absolute insulin deficiency. Leads to two pathogenic manifestations. (a) Insulin deficiency is exacerbated by catecholamine action of blocking any residual insulin action and stimulates the secretion of glucagon. this severe hyperglycemia causes an osmotic diuresis and dehydration characteristic of the ketoacidotic state. (b) Increased lipolysis causes increased free fatty acids and it causes excessive formation of ketone bodies (acetone, acetoacetate, B- hydroxybutyric acid)—ketonemia, ketonuria with water excretion, thus dehydration---metabolic keto-acidotic state. (c) Ketogenic protein lysis also increases ketone bodies. 46. One severe medical emergency in absolute insulin deficiency is ketoacidotic coma. What is pathogeny?  Refer qn 45……deficiency of oxalacetate and inability of acetyl-CoA to be involved in the Krebs cycle, as well as inability to use Acetyl-CoA in resynthesis of fatty acids increase ketone bodies. 47. What are the consequences of renin activation? It causes systemic hypertension due to vasoconstrictive action of angiotensin and also aldosterone helps in sodium and water retention, increasing blood volume. Water retention causes local or generalized edema. Hypernatremia, hypokalemia Hydrogen excretion increases causing metabolic alkalosis. 48. What are the causes of galactosemia in liver failure? In liver failure conversion of galactose to glucose in the liver is impaired, leading to galactosemia and galactosuria. 49. What are the causes of secondary endocrine disorders? adenohypophysis disorders, problems at the level of pituitary gland. (tumor, radiation, surgery, ischemia)..) THE PROBLEMS CAN BE HYPERSECRETORY OR HYPOSECRETORY 50. What are the causes of tertiary endocrine disorders? Disorders of endocrine hypothalamus (LIBERINS RELIES DISORDERS)…..problems at the level of hypothalamus. (tumor, radiation, surgery, ischemia etc.) THE PROBLEMS CAN BE HYPERSECRETORY OR HYPOSECRETORY 51. What are changes of the stool are attested in patients with posthepatic jaundice? Lack of bile in feces(acholia), thus stool is not colored, Feces are discoloured and fatty in appearance (steatorrhea). Normal free bilirubin but icreased conjucated bilirubin 52. What are clinical manifestations related to deficiency of liposolubile vitamin D in liver failure? Bone and muscle weakness (osteoporosis) Hypokalaemia Impaired immune system Mood change (depression, anxiety Increased cardiovascular disease, diabetes , cancer (ie, chronic disorders). Impaired wound healing 53. What are clinical manifestations related to deficiency of liposolubile vitamin A in liver failure?  imparied vision (keratinomalacia) Xerophthalmia , nightblindness Epithelium changes Immune deficiency Hyperplasia and hyperkeratinization Urinary stones and squamous cell metaplasia of git, ugt and resp.tract. 54. What are clinical manifestations related to deficiency of liposolubile vitamin D in liver failure? Same as qn no.52 55. What are consequences of disaccharide maldigestion? intestinal distension and flatulence. isotonic dehydration osmotic diarrhea, dehydration (hypovolemia) hypoglycemia pancreatic insufficiency (maldigestion, which causes flatulence and distention) 56. What are consequences of disaccharide maldigestion? Same as qn 55  QUESTIONS FROM 57 – 70 57. What are electrolytic disturbances triggered by secondary hyperaldosteronism in liver failure? 58. What are electrolytic disturbances triggered by secondary hyperaldosteronism in liver failure? a. Hypernatremia: Excessive sodium retention due to high aldosterone levels leads to increased sodium levels in the blood. This can cause intracellular hyperosmolarity, leading to a shift of water into the cells and resulting in cell swelling or intracellular edema, including in endothelial cells, which narrows the vascular lumen. b. Hypokalemia: Potassium excretion is increased, leading to low potassium levels in the blood.Hypokalemia causes clinical manifestations such as heart arrhythmias, muscular weakness, and paresthesia. c. Metabolic Alkalosis: Hydrogen ion excretion is increased, leading to an alkaline state in the blood. d. Decreased Urine Osmolarity and pH: Secondary hyperaldosteronism is associated with oliguria (reduced urine output), decreased urine osmolarity, and a lower pH. OR 1. Hypernatremia * 2. Metabolic alkalosis * 3. Metabolic acidosis 4. Hyperkalemia 5. Lactacidemia 59. What are endocrine functions of the kidneys? a. local activation of kallikrein system b. paracrine secretion of vasodilator prostaglandins c. production of calcitriol 60. What are features of hepatocyte apoptosis? 61. What are features of hepatocyte apoptosis? a. Hepatocyte Shrinkage: The affected hepatocyte becomes smaller in size. b. Nuclear Chromatin Condensation (Pyknosis): The chromatin within the nucleus condenses and becomes more compact. c. Nuclear Fragmentation (Karyorrhexis): The nucleus fragments into smaller pieces. d. Cellular Fragmentation into Acidophilic Apoptotic Bodies: The cell breaks into smaller, acidophilic (staining pink with eosin dye) fragments known as apoptotic bodies.  These processes are characteristic of "programmed" cell death in the liver and are a hallmark of hepatocyte apoptosis in liver diseases. Apoptotic hepatocytes in yellow fever are called Councilman bodies 62. What are features of hepatocyte necrosis? a. Cell Swelling: Due to defective osmotic regulation, sodium ions accumulate within the cell, leading to intracellular hyperosmolarity. Fluid flows into the cell, causing it to swell. b. Rupture of the Cell: The swollen cell eventually ruptures, releasing its contents into the extracellular compartment. c. Formation of Membrane Blebs: Before rupture, membrane blebs form and release cytoplasmic contents (without organelles) into the extracellular space. d. Macrophage Activity: Macrophages cluster at the sites of injury to remove cellular debris and mark areas of hepatocyte necrosis. e. Confluent Necrosis: Widespread loss of hepatocytes, often seen in acute toxic or ischemic injuries or severe viral/autoimmune hepatitis. Begins around the central vein with a zone of hepatocyte dropout filled with cellular debris, macrophages, and remnants of the reticulin meshwork. f. Bridging Necrosis: Zones of necrosis link central veins to portal tracts or connect adjacent portal tracts. g. Parenchymal Extinction: Large areas of contiguous hepatocyte death due to vascular insults like inflammation or thrombosis. 63. What are hematological changes in hypersplenism which can develop in liver failure? 64. What are hematological changes in hypersplenism which can develop in Anemia: A reduction in red blood cell count due to decreased lifespan and increased removal of red blood cells in the enlarged spleen Thrombocytopenia: A reduction in platelet count caused by increased sequestration and destruction of platelets. Leukopenia: A decrease in white blood cell count due to excessive removal of leukocytes in the spleen.iver failure? 65. What are manifestations of clinical syndrome in chronic renal failure? 1. Fluid and Electrolyte Imbalances Edema Hyperkalemia Hyponatremia Metabolic Acidosis 2. Neurological Complications a. Uremic Encephalopathy: Symptoms include confusion, lethargy, and in severe cases, seizures or coma. b. Peripheral Neuropathy: Tingling, numbness, and motor weakness in extremities. c. Restless Legs Syndrome: Discomfort and urge to move the legs, especially at night. 3. Cardiovascular Disorders a. Hypertension: Due to fluid retention and activation of the renin- angiotensin-aldosterone system. b. Left Ventricular Hypertrophy (LVH): Caused by chronic hypertension and volume overload. c. Heart Failure: Resulting from increased cardiac workload and electrolyte disturbances. d. Accelerated Atherosclerosis: Due to dyslipidemia and oxidative stress. e. Pericarditis: Uremic toxins can cause inflammation of the pericardium, presenting as chest pain and pericardial effusion. 4. Gastrointestinal Manifestations a. Nausea and Vomiting: Resulting from increased urea and toxins affecting the gastrointestinal tract. b. Anorexia: Reduced appetite, contributing to malnutrition. c. Uremic Fetor: Ammonia-like odor on the breath caused by breakdown of urea in saliva. 5. Hematologic and Immune System Disorders a. Anemia: Due to decreased erythropoietin production by the kidneys and hemolysis caused by uremic toxins. b. Coagulation Abnormalities: Platelet dysfunction leading to increased bleeding risk. c. Increased Susceptibility to Infections: Impaired immune system function due to uremic toxins and malnutrition. 6. Endocrine and Metabolic Changes a. Impaired Vitamin D Synthesis: Leading to hypocalcemia, secondary hyperparathyroidism, and renal osteodystrophy. b. Hyperphosphatemia: Resulting in calcium-phosphate deposits in tissues. c. Dyslipidemia: Increased triglycerides and altered lipid metabolism. 7. Dermatologic Manifestations a. Pruritus: Severe itching due to uremic toxins and secondary hyperparathyroidism. b. Uremic Frost: Deposition of crystallized urea on the skin in severe cases. c. Pallor: Caused by anemia.  d. Dry, Scaly Skin: Related to dehydration and toxin accumulation. 8. Musculoskeletal Disorders a. OSTEODYSTROPHY - Bone pain, fractures, and deformities due to altered calcium-phosphate metabolism and vitamin D deficiency. b. Muscle Weakness: From electrolyte imbalances and malnutrition. 9. Immune Dysfunction a. Impaired response to infections due to inflammation, malnutrition, and the effects of uremic toxins. 10. Oxidative Stress and Toxin Effects a. Retention of Uremic Toxins: (e.g., dimethyl-arginine, methylglyoxal, phenols) leads to systemic oxidative injuries b. Increased Blood Pressure: Due to dimethyl-arginine's inhibition of nitric oxide synthesis. c. Cellular Damage: Methylglyoxal contributes to cell lysis and leukocyte dysfunction. d. Protein Destabilization: High urea levels cause protein denaturation. 66. What are manifestations of urinary syndrome in acute renal failure? 1. Diuresis Disorders: a. Oliguria: Urine output