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Here are the answers to all visible questions:
Q5. The filtration barrier includes all EXCEPT: C. Collecting duct
  • The filtration barrier = fenestrated endothelium + basement membrane + podocytes (slit diaphragm). The collecting duct is not part of it.
Q6. The main function of podocytes is: A. Slit diaphragm formation
  • Podocytes extend foot processes that form the slit diaphragm, the final barrier to protein filtration.
Q7. Glomerular filtration is prevented mainly by: C. Negative basement membrane charge
  • The GBM carries a strong negative charge that repels negatively charged proteins (especially albumin), preventing their filtration.
Q8. Which drug acts on the afferent arteriole? A. NSAIDs
  • Prostaglandins normally dilate the afferent arteriole. NSAIDs block prostaglandin synthesis, causing afferent constriction and reduced GFR.
Q9. NSAIDs decrease GFR by inhibiting: B. Prostaglandins
  • NSAIDs inhibit COX, reducing prostaglandin synthesis. Prostaglandins maintain afferent arteriolar dilation; their inhibition causes afferent constriction and drops GFR.
Q10. Proximal tubule mainly reabsorbs: A. Sodium, glucose, amino acids
  • The PCT reabsorbs ~67% of filtered Na+, nearly 100% of glucose and amino acids, and significant bicarbonate and water.
Q11. Descending limb of loop of Henle is permeable to: C. Water
  • The thin descending limb is highly permeable to water (via aquaporin-1) but impermeable to solutes like Na+ and Cl-.
Q12. Thick ascending limb function is mainly: C. Na-K-2Cl reabsorption
  • The TAL actively reabsorbs Na+, K+, and 2Cl- via the NKCC2 cotransporter. It is impermeable to water ("diluting segment").
Q13. Thiazide diuretics act on: D. Distal convoluted tubule
  • Thiazides block the NCC (Na-Cl cotransporter) in the DCT.
Q14. Aldosterone increases: C. Na+ reabsorption
  • Aldosterone acts on the DCT/collecting duct to increase Na+ reabsorption (and secondarily K+ excretion and water retention).
Q15. ADH acts on: C. Collecting duct
  • ADH (vasopressin) inserts aquaporin-2 channels in the collecting duct principal cells, increasing water reabsorption.
Q16. RAAS is activated by: B. Low BP
  • Low renal perfusion pressure triggers renin release from juxtaglomerular cells, initiating the RAAS cascade.
Q17. Angiotensin II causes: A. Efferent vasoconstriction
  • Ang II preferentially constricts the efferent arteriole, maintaining GFR even when systemic BP is low.
Q44. Pre-renal AKI BUN:Cr ratio: C. >20:1
  • In pre-renal AKI, reduced tubular flow allows more urea reabsorption, raising BUN disproportionately. A ratio >20:1 is the hallmark.
Q45. Post-renal AKI cause: C. Prostatic hypertrophy
  • Post-renal = obstruction below the kidney. BPH is the classic cause. ATN is intrinsic renal, GN is intrinsic renal, hypovolemia is pre-renal.
Q46. ATN is caused by: C. Ischemia or toxins
  • Acute tubular necrosis results from ischemic injury (shock, hypoperfusion) or nephrotoxins (aminoglycosides, contrast, myoglobin).
Q47. ATN urine finding: C. Muddy brown casts
  • ATN produces "muddy brown" granular casts from sloughed tubular epithelial cells - the pathognomonic finding.
Q48. Loop diuretics act on: D. Thick ascending limb
  • Furosemide and other loop diuretics block the NKCC2 cotransporter in the TAL of the loop of Henle.
Q49. ACE inhibitors cause: A. Efferent dilation
  • ACE inhibitors block Ang II production. Since Ang II constricts the efferent arteriole, ACE inhibitors cause efferent dilation, dropping intraglomerular pressure. This is protective in diabetic nephropathy.
Q50. ARBs block: D. Angiotensin II receptor
  • ARBs (e.g., losartan, valsartan) directly block the AT1 receptor for angiotensin II, unlike ACE inhibitors which prevent Ang II formation.
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