Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GIR Test 3 > B5.047 Renal Pharmacology > Flashcards

B5.047 Renal Pharmacology Flashcards

(74 cards)

Start Studying
1
Q

4 main drug classes acting on the kidney

A

diuretics
B blockers
SGLT2 inhibitors
uricosuric drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how much plasma do kidneys filter per day

A

180 L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

average urine production per day

A

1.5 L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does NaCl movement influence water movement

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

2 other classes of diuretics, less common

A
  1. ADH antagonists: vaptans

6. osmotic diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

can you get diuresis due to glomerular action?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

site of CA inhibitors action

A

proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

site of loop diuretic action

A

thick ascending loop of henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

site of thiazide diuretics

A

distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

site of K+ sparing agents

A

collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

oral CA inhibitors

A

acetazolamide
dichlorphenamide
methazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ophthalmic preparations of CA inhibitors

A

brinzolamide

dorzolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

mechanism of action of CA inhibitors

A

blocks NaHCO3 reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

primary use of CA inhibitors

A

glaucoma

rarely used as a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

other uses of CA inhibitors

A

urine alkalization
correction of metabolic alkalosis
prevention of acute mountain sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why do CA inhibitors cause renal stones

A

calcium phosphate salts are less soluble at alkaline pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

loop diuretic drugs

A

furosemide
bumetanide
torsemide
ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
characteristics of loop diuretics
``` "high ceiling" = most effective sulfonamide derivatives (except ethacrynic acid) ```
26
pharmacokinetics of loopmdiuretics
``` oral, IV, or IM rapidly absorbed eliminated by tubular secretion and filtration t1/2 depends on renal function NSAIDs can interact for secretion ```
27
electrolyte imbalances caused by loop diuretics
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
28
discuss the pathway by which loop diuretics can stimulate renin release
reduced NaCl absorption > lower intracellular [Na] > reduced [NaCl] > increased secretion of prostaglandins > increased renin secretion
29
clinical uses of loop diuretics
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)
30
adverse effects of loop diuretics
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
thiazides
``` bendroflumethiazide chlorothiazide hydrochlorothiazide hydroflumethiazide methylclothiazide polythiazide trichlormethiazide ```
32
thiazide like drugs
chlorthalidone indapamide metolazone quinethazone
33
thiazide mechanism of action
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
characteristics of thiazides
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
electrolyte imbalances caused by thiazides
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
clinical uses of thiazides
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
adverse effects of thiazides
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
discuss allergic toxicities of thiazides
photosensitivity and dermatitis rare | serious allergic reactions rare but include hemolytic anemia, thrombocytopenia, and acute necrotizing pancreatitis
39
2 types of K+ sparing agents
aldosterone antagonists | Na+ channel blockers
40
aldosterone antagonists
eplerenone | spirinolactone
41
Na+ channel blockers
amiloride | triamterene
42
mechanism of action of aldosterone antagonists
aldosterone binding to its receptors increases Na+ reabsorption and K+ and H+ secretion opposite effects when blocked by aldosterone antagonists
43
mechanism of action of Na+ channel blockers
block apical Na+ channels to cause loss of potential (decreases the driving force for K+ secretion) and reduce K+ and H+ secretion
44
uses of K+ sparing agents
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
toxicities associated with K+ sparing agents
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
triamterene specific toxicities
acute renal failure when combined with indomethacin | kidney stones due to poor solubility
47
ADH antagonists
conivaptan (IV) | tolvaptan (oral)
48
mechanism of ADH antagonists
nonpeptide ADH receptor antagonists that inhibit effects of ADH in collecting tubule reduce water reabsorption and dilute urine
49
uses of ADH antagonists
syndrome of inappropriate ADH secretion when water restriction cannot fully correct CHF when ADH is elevated due to low blood volume
50
adverse effects of ADH antagonists
potential hypernatremia and nephrogenic diabetes insipidus
51
example of osmotic diuretic
mannitol 5, 10, 15, 20, or 25% for injection
52
mechanism of mannitol
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
uses of mannitol
emergency reduction of intracranial pressure | fall in 60-90 minutes
54
adverse effects of mannitol
``` poor oral absorption, diarrhea severe dehydration loss o f free water hypernatremia headache nausea and vomiting ```
55
how do diuretics work in heart failure
reduce extracellular fluid volumes > reduce preload > reduce cardiac work
56
specific drug choices for heart failure
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
treatment of hypertension with diuretics
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
who are thiazides more effective in for HTN?
AA elderly GFR > 30
59
B1 selective blockers
atenolol betaxolol bisoprolol metoprolol
60
B1 selective and vasodilatory B blockers
nebivolol | NO production
61
non selective N blockers
nadolol | propranolol
62
B blockers with intrinsic sympathomimetic activity
``` B2 agonists: acetbutolol (B1 selective) penbutolol (non selective) pindolol (non selective) NO producer: carteolol (non selective) ```
63
b blockers with combined a blocking effects
carvedilol (a1 antagonist, blocks Ca2+ entry) | labetalol (a1 antagonist)
64
how do B blockers work on the kidney
inhibit renin secretion used with other antihypertensives to counteract: -increased renin secretion in thiazides and loop diuretics -reflex tachy caused by vasodilators
65
how do B blockers reduce BP
block B adrenergic receptors in: - heart to reduce CO - ridneys to reduce renin secretion - CHS to reduce sympathetic vasomotor tone
66
who are B blockers most effects in
Caucasians | young people
67
adverse effects of B blockers
``` 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
abrupt cessation of B blockers
``` tachycardia hypertension angina MI worse CV outcomes than recommended drug classes ```
69
SGLT2 inhibitors
dapagliflozin canagliflozin empagliflozin
70
mechanism and use of SGLT2 inhibitprs
3rd line therapy of DM2 block glucose reabsorption so 30-50% of filtered glucose gets excreted weight loss
71
mechanism of uricosuric drugs
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
URAT1 inhibitors
probenecid sulfinpyrazole lesinurad
73
uses of uricosuric drugs
used in gout patients with underexcretion of uric acid
74
adverse effects of uricosuric drugs
formation of renal stones is augmented | maintain high urine volume and keep urine pH >6 to prevent

GIR Test 3 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions