drugs and the kidney Flashcards

1
Q

what is best predictor of kidney functions

A

GFR

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2
Q

what is GFR

A

sum of filtration across all the nephrons (ml/min)

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3
Q

what is perfect way to measure GFR

A

give substance that is not secreted or reabsorbed and measure output in urine

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4
Q

what are problems with using Crr

A
  • can have slight variations despite stable GFR
  • different assays give slightly different results
  • actives SECRETED from proximal tubule
  • tied to muscle mass
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5
Q

2 uses of Cr

A
  1. use to measure clearance
    - 24 hours
  2. used to estimate GFR or clearance
    - equations for both
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6
Q

what is equation for clearance and issues

A

cockroft gault

  • overestimate GFR when severely impaired
  • imprecise when near normal
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7
Q

4 variables used in estimating GFR

A
  1. age
  2. sex
  3. serum Cr
  4. race
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8
Q

what is key to GFR estimation

A

need to be in steady state

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9
Q

3 general classes of drugs that have a renal effect

A
  1. RAAS
  2. diuretics
  3. ADH
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10
Q

3 main outcome of RAAS activation

A
  1. incr. aldosterone
  2. vasocontriciton
  3. increase Na reabsorbtion
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11
Q

4 main drugs that affect the RAAS

A
  1. renin inhibitors
  2. ACEi
  3. ARB
  4. blockers of aldo - spironoloactone
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12
Q

what are 4 main classes of diuretics

A
  1. carbonic anhydrase inhibs
  2. loops
  3. thiazide
  4. K sparing
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13
Q

main actions of diuretics

A
  • reduce Na content - reduce ECF
  • increase Na excretion
  • if proximal to CCD - K wasting
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14
Q

action of carbonic anhydrase

A
  • weak
  • block in brush border of proximal tubule
  • also excrete bicarb
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15
Q

action of loops

A
  • most potent
  • can work with thiazides
  • block reabsorbtion of Na in thick ascending loop
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16
Q

action of thiazides

A

block reabsoption at distal collecting duct

17
Q

4 important SE of thiazides

A
  1. dydlipidemia
  2. hyponatremia
  3. hyperuricemia
  4. hypercalcermia
18
Q

2 main actions of K-sparing

A
  1. block aldo from binding

2. bind to the eNaC channel

19
Q

what is ADH

A

vasopressin

  • inserts aquaporin channels in the medulary collecting duct
  • VAPTANS compete for binding with ADH sites
20
Q

3 drugs associatied with pre-renal AKI

A
  1. diuretics
    - increase Na loss
  2. RAAS blockade
    - block ang2
    - results in efferect vasodilation and decreased pressure
  3. NSAIDS
    - inhib. prostaglandins
    - neeeded to vasodilate afferent arterioles
21
Q

drugs that can cause tubular necrosis

A
  • aminoglycosides
  • amphoceterin
  • cisplatin
  • IV contrast
22
Q

** what is clinical picture of drug induced AIN

A

AKI 7-10 days aftere

- WBC casts

23
Q

3 options of dose adjustments in renal patients

A
  1. none
  2. increase dosing interval
  3. reduce dose
24
Q

what does dose adjustment rely on

A
  1. extent it is renally cleared

2. degree of renal impairment

25
Q

7 step approach to drug dosing in renal disease

A
  1. what is GFR (>60 not a prob)
  2. is the drug effective in low GFR
  3. is the drug safe in CKD
  4. is the drug nephrotoxic
  5. is immediate effect needed to desired
    - loading - same
    - maintenance - may need to adjust
  6. is the drug extensively elimnationed by kidney
  7. does the drug have an active/toxic metabolite that is renally excreted