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 ACE inhibitor  




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Author8 Posts
  #1

A 77-year-old man, with a history of hypertension and a recent myocardial infarction, is given an angiotensin converting enzyme (ACE) inhibitor as part of his therapy. One week later, he reports feeling unwell and is found to have elevated blood urea nitrogen (BUN) and elevated plasma creatinine concentration. Which of the following changes in glomerular filtration rate (GFR) and filtration fraction (FF) have most likely resulted from treatment with an ACE inhibitor in this patient?


Answer Choices Correct answer Your answer
A. GFR decreased, FF decreased
B. GFR decreased, FF increased
C. GFR decreased, FF unchanged
D. GFR increased, FF decreased
E. GFR increased, FF increased
F. GFR increased, FF unchanged




  #2

A


  #3

plz explain your answer.



  #4

Angiotensin II constricts the efferent arteriole and lower RPF, rise GFR and FF. ACEI inhibits formation of Angiotensin II that means dilate efferent arteriole, rise RPF, lower GFR, and lower FF (FF=GFR/RPF).


  #5

vanilla is right :

Afferent art = PGs open them (NSAIDs close them)
Efferent art = Angiotensin closes them (ACE-I open them)



  #6

thanx vallia and dragonfly.

Option A (GFR decreased, FF decreased) is correct. Elevated BUN and elevated creatinine indicates low GFR. Angiotensin II preferentially constricts the efferent arteriole. ACE inhibitors therefore cause efferent arteriole dilation. Glomerular capillary hydrostatic pressure may fall, decreasing GFR. A fall in renal vascular resistance increases renal blood flow. Filtration fraction is the ratio of GFR to renal plasma flow rate. A rise in blood flow, with a fall in GFR, reduces FF






  #7

Hello, I have read on High-Yield Histopathology, that angiotensin II constrics both afferent and efferent arteriols and decreases GFR. Any ideas?


  #8

fiance13 you are right but the effect on efferent arterioles is greater than on afferent.





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