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HESI RN Advanced Pathophysiology
Study Questions and verified answers
Graded A+
CARDIOVASCULAR PATHOPHYSIOLOGY
1. What is the primary pathophysiological mechanism in systolic heart
failure?
Answer: Decreased contractility of the left ventricle leading to reduced ejection fraction (<40%). The heart cannot pump blood effectively, causing backup into pulmonary circulation.
2. Which compensatory mechanism in heart failure leads to increased
preload?
Answer: Activation of the renin-angiotensin-aldosterone system (RAAS), causing sodium and water retention, increasing blood volume and venous return.
3. What causes the S3 gallop sound in heart failure?
Answer: Rapid ventricular filling during diastole due to increased preload and decreased ventricular compliance, creating turbulent blood flow.
4. In myocardial infarction, what is the difference between STEMI and
NSTEMI?
Answer: STEMI involves complete coronary artery occlusion with full-thickness myocardial damage and ST elevation. NSTEMI involves partial occlusion with subendocardial damage and no ST elevation.
5. What is the Frank-Starling mechanism?
Answer: The relationship between ventricular stretch (preload) and contractile force. Increased preload stretches myocardial fibers, leading to stronger contraction up to an optimal point.
6. Why does hypertension cause left ventricular hypertrophy?
Answer: Chronic increased afterload forces the left ventricle to work harder, causing compensatory muscle fiber thickening to maintain cardiac output.
7. What causes the murmur in aortic stenosis?
Answer: Turbulent blood flow through the narrowed aortic valve during systole, creating a harsh, crescendo-decrescendo murmur.
8. How does atherosclerosis develop?
Answer: Endothelial injury โ lipid accumulation โ inflammatory response โ plaque formation with fibrous cap โ potential rupture and thrombosis.
9. What is the pathophysiology of atrial fibrillation?
Answer: Multiple chaotic electrical impulses in the atria cause irregular, rapid atrial contraction without effective pumping, leading to irregular ventricular response.
Answer: Narrowed airways create turbulent airflow, producing the characteristic musical sound during expiration.
16. What causes acute respiratory distress syndrome (ARDS)?
Answer: Diffuse alveolar damage from various triggers causing increased capillary permeability, protein-rich pulmonary edema, and severe hypoxemia.
17. How does pneumonia affect ventilation-perfusion matching?
Answer: Infected alveoli fill with inflammatory exudate, creating areas of perfusion without ventilation (shunt), leading to hypoxemia.
18. What is the difference between Type I and Type II respiratory failure?
Answer: Type I: Hypoxemic failure (PaO2 <60 mmHg) with normal/low CO2. Type II: Hypercapnic failure with elevated CO2 (>50 mmHg) and hypoxemia.
19. Why does pulmonary embolism cause right heart strain?
Answer: Blocked pulmonary vessels increase pulmonary vascular resistance, forcing the right ventricle to work harder against increased afterload.
20. What causes clubbing in chronic respiratory disease?
Answer: Chronic hypoxemia stimulates vascular proliferation and connective tissue growth in fingertips, causing characteristic bulbous appearance.
NEUROLOGICAL PATHOPHYSIOLOGY
21. What is the pathophysiology of ischemic stroke?
Answer: Arterial occlusion causes tissue hypoxia, leading to cellular energy failure, membrane depolarization, and neuronal death within the infarct core.
22. What is the penumbra in stroke?
Answer: The area of brain tissue around the infarct core that is hypoperfused but potentially salvageable if reperfusion occurs quickly.
23. How does increased intracranial pressure develop?
Answer: Brain swelling, mass lesions, or CSF accumulation increase pressure within the rigid skull, potentially causing brain herniation.
24. What is the Cushing's triad?
Answer: Hypertension, bradycardia, and irregular respirations - late signs of severely increased intracranial pressure.
25. What causes seizures at the cellular level?
Answer: Abnormal, excessive, synchronous neuronal discharges due to imbalance between excitatory and inhibitory neurotransmitters.
26. What is the difference between focal and generalized seizures?
Answer: Autoimmune destruction of pancreatic beta cells leads to absolute insulin deficiency and inability to regulate blood glucose.
32. What is insulin resistance in Type 2 diabetes?
Answer: Cells become less responsive to insulin, requiring higher levels to achieve glucose uptake, eventually leading to beta cell exhaustion.
33. Why do diabetic patients develop polyuria?
Answer: Hyperglycemia exceeds renal glucose threshold, causing osmotic diuresis as glucose acts as an osmotic agent in urine.
34. What causes diabetic ketoacidosis (DKA)?
Answer: Insulin deficiency forces fat metabolism, producing ketones that accumulate and cause metabolic acidosis.
35. How does hyperthyroidism affect metabolism?
Answer: Excess thyroid hormones increase metabolic rate, protein synthesis, and sympathetic nervous system activity.
36. What causes the exophthalmos in Graves' disease?
Answer: Thyroid-stimulating immunoglobulins cause inflammation and tissue expansion behind the eyes, pushing them forward.
37. What is the pathophysiology of Addison's disease?
Answer: Adrenal cortex destruction leads to deficiency of cortisol and aldosterone, causing hypotension, hyperkalemia, and hypoglycemia.
38. Why does Cushing's syndrome cause central obesity?
Answer: Excess cortisol promotes fat deposition in truncal areas while causing muscle wasting in extremities.
39. What causes the symptoms of diabetes insipidus?
Answer: ADH deficiency (central) or kidney resistance (nephrogenic) leads to inability to concentrate urine, causing massive water loss.
40. How does hyperparathyroidism affect calcium homeostasis?
Answer: Excess PTH increases bone resorption, kidney calcium reabsorption, and intestinal calcium absorption, leading to hypercalcemia. RENAL PATHOPHYSIOLOGY
41. What is the difference between acute kidney injury (AKI) and chronic
kidney disease (CKD)?
Answer: AKI is rapid loss of kidney function (hours to days) that may be reversible. CKD is progressive, irreversible loss over months to years.
42. What causes prerenal AKI?
Answer: Block sodium-potassium-chloride cotransporter in ascending limb of Henle, preventing sodium reabsorption and causing diuresis.
49. Why do patients with kidney stones develop severe pain?
Answer: Stones cause ureteral spasm and obstruction, leading to increased pressure in the renal pelvis and intense visceral pain.
50. What causes uremic syndrome?
Answer: Accumulation of uremic toxins in severe kidney failure affects multiple organ systems, causing neurological, GI, and other symptoms. GASTROINTESTINAL PATHOPHYSIOLOGY
51. What is the pathophysiology of peptic ulcer disease?
Answer: Imbalance between aggressive factors (H. pylori, NSAIDs, acid) and protective factors (mucus, bicarbonate) leads to mucosal erosion.
52. How does H. pylori cause gastric ulcers?
Answer: Bacterial infection causes chronic inflammation, disrupts mucus production, and increases acid secretion, leading to mucosal damage.
53. What causes the pain pattern in appendicitis?
Answer: Visceral pain from appendiceal inflammation initially causes periumbilical pain, then shifts to RLQ as parietal peritoneum becomes involved.
54. What is the pathophysiology of inflammatory bowel disease?
Answer: Abnormal immune response to intestinal bacteria causes chronic inflammation, leading to mucosal damage and systemic symptoms.
55. How does liver cirrhosis develop?
Answer: Chronic liver injury causes hepatocyte death, fibrosis, and regenerative nodules, leading to altered liver architecture and function.
56. Why do cirrhotic patients develop ascites?
Answer: Portal hypertension, hypoalbuminemia, and sodium retention cause fluid accumulation in the peritoneal cavity.
57. What causes hepatic encephalopathy?
Answer: Liver failure allows ammonia and other toxins to reach the brain, causing altered mental status and neurological symptoms.
58. What is the mechanism of cholestasis?
Answer: B12 deficiency impairs DNA synthesis, causing production of large, immature red blood cells with shortened lifespan.
64. What is the pathophysiology of hemophilia?
Answer: Deficiency of clotting factors (VIII in A, IX in B) impairs secondary hemostasis, leading to prolonged bleeding.
65. Why do patients with thrombocytopenia develop petechiae?
Answer: Low platelet count impairs primary hemostasis, causing small capillary bleeds that appear as pinpoint hemorrhages.
66. What causes disseminated intravascular coagulation (DIC)?
Answer: Widespread activation of coagulation cascade consumes clotting factors and platelets while forming microthrombi.
67. How does chronic lymphocytic leukemia progress?
Answer: Accumulation of mature but non-functional B lymphocytes in blood, bone marrow, and lymphoid organs impairs immune function.
68. What is tumor lysis syndrome?
Answer: Rapid cancer cell destruction releases intracellular contents, causing hyperkalemia, hyperphosphatemia, and acute kidney injury.
69. Why do patients with polycythemia vera have increased thrombosis risk?
Answer: Elevated red blood cell count increases blood viscosity and promotes sluggish flow, predisposing to clot formation.
70. What causes splenomegaly in portal hypertension?
Answer: Increased portal pressure causes splenic congestion and enlargement, leading to sequestration of blood cells. MUSCULOSKELETAL PATHOPHYSIOLOGY
71. What is the pathophysiology of osteoporosis?
Answer: Imbalance between bone resorption and formation leads to decreased bone density and increased fracture risk.
72. How does rheumatoid arthritis cause joint destruction?
Answer: Autoimmune inflammation creates pannus tissue that releases enzymes, destroying cartilage and bone.
73. What causes the morning stiffness in rheumatoid arthritis?
Answer: Overnight accumulation of inflammatory mediators in joints causes stiffness that improves with movement and activity.
74. What is the difference between osteoarthritis and rheumatoid arthritis?
Answer: Chronic synovial inflammation weakens joint structures, allowing tendons and ligaments to shift and create deformities. IMMUNE SYSTEM PATHOPHYSIOLOGY
81. What is the difference between Type I and Type IV hypersensitivity?
Answer: Type I: immediate IgE-mediated (anaphylaxis). Type IV: delayed T-cell mediated (contact dermatitis, taking 24-72 hours).
82. How does anaphylaxis cause cardiovascular collapse?
Answer: Massive histamine and mediator release causes vasodilation, increased capillary permeability, and distributive shock.
83. What is molecular mimicry in autoimmune disease?
Answer: Foreign antigens share structural similarities with self-antigens, causing immune system to attack both foreign and self tissues.
84. How does HIV cause immunodeficiency?
Answer: Virus targets CD4+ T helper cells, gradually depleting them and impairing both cellular and humoral immunity.
85. What causes transplant rejection?
Answer: Recipient's immune system recognizes donor tissue as foreign due to HLA differences, mounting immune attack against graft.
86. Why do immunocompromised patients get opportunistic infections?
Answer: Weakened immune system cannot control normally harmless organisms that take advantage of reduced host defenses.
87. What is the pathophysiology of systemic lupus erythematosus?
Answer: Type III hypersensitivity with immune complex deposition in multiple organs causes widespread inflammation.
88. How does complement activation contribute to inflammation?
Answer: Complement cascade produces mediators that cause vasodilation, increase vascular permeability, and attract neutrophils.
89. What causes the symptoms of allergic rhinitis?
Answer: IgE-mediated mast cell degranulation releases histamine and leukotrienes, causing nasal congestion, rhinorrhea, and sneezing.
90. Why do autoimmune diseases often affect women more than men?
Answer: X-linked immune genes, hormonal influences (estrogen), and epigenetic factors may predispose women to autoimmunity.
96. How do oncogenes contribute to cancer development?
Answer: Mutated genes that normally promote cell growth become overactive, driving uncontrolled cell proliferation.
97. What is the role of tumor suppressor genes?
Answer: These genes normally prevent cancer by controlling cell division; their loss or mutation removes growth constraints.
98. How does hypoxia affect cellular metabolism?
Answer: Oxygen lack forces cells to use anaerobic glycolysis, producing less ATP and potentially toxic lactate accumulation.
99. What causes cellular aging?
Answer: Telomere shortening, accumulated DNA damage, mitochondrial dysfunction, and protein aggregation contribute to senescence.
100. How do growth factors regulate cell proliferation?
Answer: Extracellular signals bind receptors, activating intracellular pathways that control cell cycle progression and division.
ACID-BASE AND ELECTROLYTE DISORDERS
101. What is the difference between respiratory and metabolic acidosis?
Answer: Respiratory: CO2 retention (pHโ, PCO2โ). Metabolic: bicarbonate loss or acid gain (pHโ, HCO3-โ).
102. How does the body compensate for metabolic acidosis?
Answer: Hyperventilation to blow off CO2 (respiratory compensation) and kidney hydrogen excretion/bicarbonate retention.
103. What causes hyperkalemia in kidney failure?
Answer: Reduced renal potassium excretion and metabolic acidosis cause potassium to shift from cells to extracellular fluid.
104. Why is severe hyperkalemia dangerous?
Answer: Elevated potassium affects cardiac conduction, potentially causing fatal arrhythmias and cardiac arrest.
105. What causes hyponatremia in SIADH?
Answer: Inappropriate ADH secretion causes excessive water retention, diluting serum sodium concentration.
