Pharm Module 3 Flashcards

1
Q

the drugs associated with AIN include

A
  • penicillins
  • cephalosporins
  • ciprofloxacin
  • vancomycin
  • rifampin
  • omeprazole
  • lansoprazole

PCC LOVR

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2
Q

the drugs associated with ATN include

A
  • aminoglycosides
  • amphotericin B
  • radiocontrast dyes (iohexol)
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3
Q

the drugs associated with RTA Type 4 include

A
  • ACE inhibitors
  • ARBs
  • cyclosporin
  • tacrolimus

CATA

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4
Q

the drugs that can induce both AIN and RTA include

A
  • trimethoprim

- NSAIDs

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5
Q

acute kidney injury is characterized by

A
  • sudden loss of kidney function
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6
Q

prerenal AKI is caused by

A
  • reduced blood flow to the kidneys
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7
Q

renal/intrinsic AKI is caused by

A
  • direct damage to the tissues of kidneys themselves
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8
Q

post renal Aki caused by

A
  • urinary tract obstruction downstream of the kidneys
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9
Q

drug induced AKI is almost always of which type

A
  • intrinsic/renal type
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10
Q

damage to the interstitium is called

A
  • acute interstitial nephritis
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11
Q

damage to the glomerulus is called

A
  • glomerulonephritis
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12
Q

damage to the tubular epithelium is called

A
  • acute tubular necrosis
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13
Q

75% of cases of acute interstitial nephritis is caused by

1/3 of it is caused by

the other 2/3 caused by

A
  • adverse reactions to drugs
  • antibiotics
  • NSAIDs and proton pump inhibitors
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14
Q

how drugs cause inflammatory immune response known as AIN

A

1) drug is recognized as a distinct antigen that the immune system hasn’t recognized before
2) drug structurally similar to authentic antigen to which immune system has already been exposed
3) non-immunogenic drug may bind to endogenous host protein, creating an immunogenic molecular structure (haptenization)

  • activate dendritic cells that patrol kidney which initiates inflammatory response
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15
Q

other immune reactions of AIN

A
  • rash
  • fever
  • eosinophilia
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16
Q

nephrotoxic ATN causes death of

A
  • epithelial cells in PT and thick ascending limb of LOH
17
Q

how do ahminoglycosides cause nephrotoxic ATN

A
  • positive charges cause them to bind negative charged lipids in tubular cells
  • accumulate in tubular epithelial cells
  • disrupt cell processes and kill the cell
18
Q

example of an ahminoglycoside that causes nephrotoxicin ATN

A
  • gentamicin
19
Q

the relative renal toxicities of different aminoglycosides correlate with

A
  • their affinity for membrane phospholipids
20
Q

which aminoglycoside has the highest affinity and highest toxicity

A
  • neomycin
21
Q

which aminoglycoside has the lowest affinity and lowest toxicity

A
  • streptomycin
22
Q

how does amphotericin B cause nephrotoxic ATN

A
  • binds to membrane cholesterol instead of ergosterol

- damages renal epithelial cells

23
Q

how do iodinated radio contrast dyes cause ATN

A
  • concentrates in tubular epithelial cells and can lead to their death
24
Q

what causes type 4 renal tubular acidodis

A
  • defect in aldosterone signaling to the kidney
25
Q

type 4 RTA characterized by

A
  • hyperkalemia

- mild acidosis

26
Q

what is type 4 RTA also called

A
  • hypoaldosteronism
27
Q

which drugs reduce aldosterone production

A
  • ACE inhibitors
  • ARBs
  • NSAIDs
28
Q

which drugs block the effect of aldosterone on the kidneys

A
  • cyclosporin
  • tacrolimus
  • trimethoprim
29
Q

role of ACE inhibitors

A
  • block production of AgII

- block AgII vasoconstriction of efferent arteriole

30
Q

role of ARBs

A
  • block AgII from inducing aldosterone secretion from adrenal cortex
31
Q

role of NSAIDs

A
  • block secretion of renin and AgII-induced release of aldosterone
  • block prostaglandins and cause afferent arteriole vasoconstriction
32
Q

role of trimethoprim

A
  • directly inhibits ENaC
33
Q

role of cyclosporin/tacrolimus

A
  • reduce levels of aldosterone receptor
34
Q

how do ACE inhibitors exacerbate reduction of glomerular BP caused by bilateral renal artery stenosis

A
  • renal blood flow in bilateral renal artery stenosis is low due to atherosclerotic plaques in afferent arterioles
  • ACE inhibitors increase efferent dilation which increases blood flow away from glomeruli.