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GIR Test 3 > B5.047 Renal Pharmacology > Flashcards

B5.047 Renal Pharmacology Flashcards

1
Q

4 main drug classes acting on the kidney

A

diuretics
B blockers
SGLT2 inhibitors
uricosuric drugs

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2
Q

how much plasma do kidneys filter per day

A

180 L

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3
Q

average urine production per day

A

1.5 L

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4
Q

how does NaCl movement influence water movement

A

by increasing or decreasing Na+ reabsorption the kidney increases or decreased body fluid volume

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5
Q

4 main classes of diuretics

A
  1. carbonic anhydrase inhibitors
  2. loop diuretics
  3. thiazide diuretics
  4. K+ sparing agents (Na+ channel inhibitors or mineralcorticoid receptor antagonists)
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6
Q

2 other classes of diuretics, less common

A
  1. ADH antagonists: vaptans

6. osmotic diuretics

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7
Q

can you get diuresis due to glomerular action?

A

no

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8
Q

site of CA inhibitors action

A

proximal tubule

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9
Q

site of loop diuretic action

A

thick ascending loop of henle

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10
Q

site of thiazide diuretics

A

distal tubule

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11
Q

site of K+ sparing agents

A

collecting ducts

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12
Q

main clinical applications for diuretics

A

acute and chronic heart failure (loop)
hypertension (thiazide)
acute and chronic renal failure (loop)
nephrotic syndrome/ cirrhosis (loop)

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13
Q

oral CA inhibitors

A

acetazolamide
dichlorphenamide
methazolamide

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14
Q

ophthalmic preparations of CA inhibitors

A

brinzolamide

dorzolamide

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15
Q

mechanism of action of CA inhibitors

A

blocks NaHCO3 reabsorption

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16
Q

CA inhibitor pharmacokinetics

A

well absorbed after oral admin
effectiveness diminishes over several days because bicarb depletion enhances NaCl reabsorption by remainder of the nephron

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17
Q

primary use of CA inhibitors

A

glaucoma

rarely used as a diuretic

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18
Q

why do CA inhibitors work in glaucoma?

A

ciliary body secretes bicarb into the aqueous humor

inhibition of CA decreases aqueous humor formation which reduces intraocular pressure

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19
Q

other uses of CA inhibitors

A

urine alkalization
correction of metabolic alkalosis
prevention of acute mountain sickness

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20
Q

possible toxicities associated with CA inhibitors

A

hyperchloremic metabolic acidosis
renal stones
renal potassium wasting
drowsiness and paresthesias with large doses
nervous system toxicity in renal failure due to accumulation

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21
Q

why do CA inhibitors cause renal stones

A

calcium phosphate salts are less soluble at alkaline pH

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22
Q

why do CA inhibitors cause renal K+ wasting

A

more Na+ reaches the collecting duct so more K+ is secreted

combine with K+ sparing diuretic

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23
Q

loop diuretic drugs

A

furosemide
bumetanide
torsemide
ethacrynic acid

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24
Q

mechanism of action of loop diuretics

A

selective inhibitors of NKCC co-transporter, decreases NaCl reabsorption
decreases potential difference generated by recycling of K+ which normally drive divalent reabsorption
leads to increased excretion of Ca2+ and Mg2+

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25
Q

characteristics of loop diuretics

A 
"high ceiling" = most effective
sulfonamide derivatives (except ethacrynic acid)
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26
Q

pharmacokinetics of loopmdiuretics

A 
oral, IV, or IM
rapidly absorbed
eliminated by tubular secretion and filtration
t1/2 depends on renal function
NSAIDs can interact for secretion
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27
Q

electrolyte imbalances caused by loop diuretics

A

hypokalemia : increased Na+ delivery to distal tubule = enhanced H+ and K+ secretion
reduced Ca2+ reabsorption in the loops normally no problem bc it can be reabsorbed in distal tubule
hypomagnesemia: increase in Mg2+ excretion

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28
Q

discuss the pathway by which loop diuretics can stimulate renin release

A

reduced NaCl absorption > lower intracellular [Na] > reduced [NaCl] > increased secretion of prostaglandins > increased renin secretion

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29
Q

clinical uses of loop diuretics

A

most common for relief of pulmonary edema & hypercalcemia
others:
hypertension if thiazides don’t work
severe hyperkalemia (+ NaCl and water)
acute renal failure (to convert oliguric to nonoliguric failure when GFR is low)

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30
Q

adverse effects of loop diuretics

A

dehydration & hyponatremia leading to hypotension, circulatory collapse, reduced GFR, and thromboembolic episodes
hypokalemia > cardiac arrhythmias
ototoxicity > reversible dose related hearing impairments, more common with ethacrynic acid
hyperuricemia & gout attacks > due to hypovolemia associated with increased uric acid reabsorption in proximal tubule
allergic reactions w sulfonamides

31
Q

thiazides

A 
bendroflumethiazide
chlorothiazide
hydrochlorothiazide
hydroflumethiazide
methylclothiazide
polythiazide
trichlormethiazide
32
Q

thiazide like drugs

A

chlorthalidone
indapamide
metolazone
quinethazone

33
Q

thiazide mechanism of action

A

inhibitors of Na+/Cl- cotransport by blocking NaCl transporter in the distal convoluted tubule (inhibit NaCl reabsorption from the lumen)
enhances Ca2+ reabsorption because of the increased Na+ gradient across the basolateral membrane (increased Na+/Ca2+ counter co-transport)

34
Q

characteristics of thiazides

A

sulfonamides
more effective as antihypertensives in AAs and the elderly
only moderately effective in increasing NaCl excretion (90% has already been reabsorbed by this point)
ineffective when GFR is low

35
Q

electrolyte imbalances caused by thiazides

A

hyperuricemia : are secreted by organic acid secretory systems that also handle uric acid, this induces competition
hypokalemia: increased K+ secretion in collecting duct
reduce Ca2+ excretion

36
Q

clinical uses of thiazides

A

hypertension at low dose (chlorthalidone is preferred)
CHF at higher dose, second to loop diuretics
nephrolithiasis due to hypercalciuria, reduced urinary calcium
nephrogenic diabetes insipidus to reduce polyuria and polydipsia

37
Q

adverse effects of thiazides

A

hypokalemic metabolic alkalosis
hyperuricemia
hypercalcemia
hyperglycemia/ impaired glucose tolerance due to decreased pancreatic insulin release and decreased glucose utilization
hyperlipidemia (5-15% increased in total cholesterol)
hyponatremia from combo of elevated ADH, reduce renal diluting capacity, and increased thirst

38
Q

discuss allergic toxicities of thiazides

A

photosensitivity and dermatitis rare

serious allergic reactions rare but include hemolytic anemia, thrombocytopenia, and acute necrotizing pancreatitis

39
Q

2 types of K+ sparing agents

A

aldosterone antagonists

Na+ channel blockers

40
Q

aldosterone antagonists

A

eplerenone

spirinolactone

41
Q

Na+ channel blockers

A

amiloride

triamterene

42
Q

mechanism of action of aldosterone antagonists

A

aldosterone binding to its receptors increases Na+ reabsorption and K+ and H+ secretion
opposite effects when blocked by aldosterone antagonists

43
Q

mechanism of action of Na+ channel blockers

A

block apical Na+ channels to cause loss of potential (decreases the driving force for K+ secretion) and reduce K+ and H+ secretion

44
Q

uses of K+ sparing agents

A

weak diuretics, seldom used alone
counteract hypokalemia caused by loop or thiazide diuretics
eplerenone: reduced mortality rate in pts with HF after MI
primary mineralcorticoid hypersecretion (Conn’s syndrome or ectopic ACTH production)
secondary aldosteronism due to CHF, cirrhosis, or other associated w salt retention and reduced fluid volume

45
Q

toxicities associated with K+ sparing agents

A

hyperkalemia- mild, moderate, or life threatening
hyperchloremic metabolic acidosis due to inhibition of H+ secretion with reduced K+ secretion
gynecomastia due to steroid chemical structure

46
Q

triamterene specific toxicities

A

acute renal failure when combined with indomethacin

kidney stones due to poor solubility

47
Q

ADH antagonists

A

conivaptan (IV)

tolvaptan (oral)

48
Q

mechanism of ADH antagonists

A

nonpeptide ADH receptor antagonists that inhibit effects of ADH in collecting tubule
reduce water reabsorption and dilute urine

49
Q

uses of ADH antagonists

A

syndrome of inappropriate ADH secretion when water restriction cannot fully correct
CHF when ADH is elevated due to low blood volume

50
Q

adverse effects of ADH antagonists

A

potential hypernatremia and nephrogenic diabetes insipidus

51
Q

example of osmotic diuretic

A

mannitol 5, 10, 15, 20, or 25% for injection

52
Q

mechanism of mannitol

A

filtered by glomerulus but not reabsorbed > increase osmolarity of ultrafiltrate and prevent water reabsorption > promote water diuresis
greatest effect in proximal tubule and descending limb of henle bc they are freely permeable to water

53
Q

uses of mannitol

A

emergency reduction of intracranial pressure

fall in 60-90 minutes

54
Q

adverse effects of mannitol

A 
poor oral absorption, diarrhea
severe dehydration
loss o f free water
hypernatremia
headache
nausea and vomiting
55
Q

how do diuretics work in heart failure

A

reduce extracellular fluid volumes > reduce preload > reduce cardiac work

56
Q

specific drug choices for heart failure

A

1st choice: loop, furosemide
thiazides for mild HF
spironolactone and eplerenone reduce mortality and are often added
concurrent treatment with vasodilator may reduce renal blood flow and inhibit diuretic effectiveness

57
Q

treatment of hypertension with diuretics

A

thiazides used at low doses (12.5-25 mg)
recommended for monotherapy of mild to moderate HTN
-lower BP in 40-60% of pts
-can enhance efficacy of other antihypertensives
-can be given as a single daily dose

58
Q

who are thiazides more effective in for HTN?

A

AA
elderly
GFR > 30

59
Q

B1 selective blockers

A

atenolol
betaxolol
bisoprolol
metoprolol

60
Q

B1 selective and vasodilatory B blockers

A

nebivolol

NO production

61
Q

non selective N blockers

A

nadolol

propranolol

62
Q

B blockers with intrinsic sympathomimetic activity

A 
B2 agonists:
acetbutolol (B1 selective)
penbutolol (non selective)
pindolol (non selective)
NO producer:
carteolol (non selective)
63
Q

b blockers with combined a blocking effects

A

carvedilol (a1 antagonist, blocks Ca2+ entry)

labetalol (a1 antagonist)

64
Q

how do B blockers work on the kidney

A

inhibit renin secretion
used with other antihypertensives to counteract:
-increased renin secretion in thiazides and loop diuretics
-reflex tachy caused by vasodilators

65
Q

how do B blockers reduce BP

A

block B adrenergic receptors in:

  • heart to reduce CO
  • ridneys to reduce renin secretion
  • CHS to reduce sympathetic vasomotor tone
66
Q

who are B blockers most effects in

A

Caucasians

young people

67
Q

adverse effects of B blockers

A 
can worsen symptoms in pts with:
-reduced myocardial reserve
-asthma
-peripheral vascular insufficiency
-diabetes
predispose to atherogenesis (increase TGs and decrease HDLs)
delays recovery of normoglycemia bc inhibits hyperglycemic response
risk of new onset diabetes
68
Q

abrupt cessation of B blockers

A 
tachycardia
hypertension
angina
MI
worse CV outcomes than recommended drug classes
69
Q

SGLT2 inhibitors

A

dapagliflozin
canagliflozin
empagliflozin

70
Q

mechanism and use of SGLT2 inhibitprs

A

3rd line therapy of DM2
block glucose reabsorption so 30-50% of filtered glucose gets excreted
weight loss

71
Q

mechanism of uricosuric drugs

A

increase excretion of uric acid in the urine
reduce concentration of uric acid in the blood plasma
inhibits uric acid reabsorption channels in the proximal tubule

72
Q

URAT1 inhibitors

A

probenecid
sulfinpyrazole
lesinurad

73
Q

uses of uricosuric drugs

A

used in gout patients with underexcretion of uric acid

74
Q

adverse effects of uricosuric drugs

A

formation of renal stones is augmented

maintain high urine volume and keep urine pH >6 to prevent

GIR Test 3 (19 decks)

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