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Pharmacology Test 3 > Renal > Flashcards

Renal Flashcards

1
Q

What is the primary determinant of body water load?

A

body sodium load

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2
Q

importance of location of nephron

A

medulla provides a high-salt (high osmotic) environment for loop of Henle

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3
Q

glomerular filtration rate

A

tells how well the initial filter is working; the amt of fluid filtered by the kidney over time; self-limiting process

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4
Q

physiology of glomerulus

A

surrounds a capillary bed fed by renal arterioles; size-based filter; slurry of high-osmotic fluid exits here

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5
Q

physiology of proximal tubule

A

permeable to water & most salts; fluid is iso-osmotic with blood; site of 65% of water/K/Na/bicarb reabsorption; 2nd site of entry into nephron; primary site at which highly protein-bound molecules can gain entry

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6
Q

function of Na/K ATP basolateral antiporter pump in the proximal tubule

A

pushes Na out of cytoplasm & brings K in; sets up Na conc gradient; drives import of organic acids

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7
Q

function of Na/H+ antiporter in luminal membrane in the proximal tubule

A

takes up Na from luminal space & exchanges Na for a proton; proton gradient drives organic bases into luminal space

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8
Q

physiology of loop of Henle

A

fluid becomes concentrated as it flows through medullary space; descending thin limb & ascending thick limb are key areas

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9
Q

thin descending limb

A

highly permeable to water; impermeable to salts/urea; concentrating action

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10
Q

thick ascending limb

A

impermeable to water; highly permeable to NaCl; end w/ small volume of very dilute fluid

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11
Q

osmolality of loop of Henle

A

increased osmolality as you descend; decreased osmolality as you ascend; active transport of NaCl out of ascending limb feeds high salt interstitial envir. (drives water absorption in descending loop); Na/K pumps in basolateral membranes of epithelial cells

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12
Q

physiology of vasa recta

A

highly permeable to salt & water to reclaim what is removed by loop of Henle and deliver it back to circulation; salt picked up by descending vasa recta; water picked up by ascending vasa recta

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13
Q

physiology of the macula

A

specialized epithelial cells at the distal end of the ascending thick limb; sense osmolality of urine; reduces flow in afferent arteriole (constricts) if NaCl is too high in urine

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14
Q

tubuloglomerular feedback (TGF)

A

reduces the amt of fluid that enters the tubular network; makes nephron less effective & lessens the material presented for elimination; preserves the organism from Na loss (Na diuresis is self-limiting d/t TGF)

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15
Q

physiology of distal convoluted tubule

A

actively transports out NaCl but not water; fluid here is hypotonic urine relative to circulatory fluid

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16
Q

physiology of collecting tubules

A

water pores responsive to ADH; vasopressin opens pores to reabsorb water; distal ducts permeable to urea (adds to medullary salt gradient)

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17
Q

What is the major site of bicarbonate reabsorption and acidification?

A

proximal tubule

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18
Q

Where is acid secretion inhibited?

A

proximal tubule & distal collecting duct

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19
Q

carbonic anhydrase

A

speeds up the equilibrium of H2CO3CO2 + H2O

involves Na/K ATPase, Na/bicarbonate ion symporter, Na/H antiporter; *read through this

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20
Q

mechanism of action of carbonic anhydrase inhibitors

A

interfere w/ the reabsorption of bicarbonate ion; mess up the cyclical exchange that provides the proton for the antiporter; reduces import of Na across the membrane; increases urine pH and decreases circulating pH

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21
Q

effects of carbonic anhydrase inhibitors

A

5% increase of Na excretion; modest diuretic effects; increase in K secretion; cause metabolic acidosis d/t loss of circulating bicarbonate (base)

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22
Q

If you deliver Na late in the distal tubules…

A

you will increase K and H excretion

*except for carbonic anhydrase inhibitors

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23
Q

Which medication is used in combination with a diuretic to counter metabolic alkalosis?

A

Acetazolamide (Diamox)

24
Q

mechanism of action of osmotic diuretics

A

act on tissues by drawing water into the blood to increase circulatory volume; dilutes & reduces circulatory viscosity; act on kidney by increasing renal blood flow and washing out medullary salt gradient; increased excretion of higher volume/higher salt conc fluid

25
Q

The reduced medullar salt gradient created by osmotic diuretics…

A

affects the ability of ADH to act to reclaim water during dehydration.

26
Q

sites of action of osmotic diuretics

A

loop of Henle (vasa recta); proximal convoluted tubule

27
Q

dialysis disequilibrium syndrome

A

results when solutes are removed too rapidly during dialysis

28
Q

mechanism of action of loop diuretics

A

inhibit Na/K/2Cl symporter in thick ascending limb of loop of Henle; enter urine via organic ion transporters in proximal tubules b/c they’re highly protein-bound; K wasting

29
Q

explain the Na/K/2Cl symporter

A

transports 2Cl with every 1Na & 1K into the epithelial space (sets up negative potential); K enters lumen via channel to hyperpolarize the luminal membrane; Cl enters interstitial space to depolarize the basolateral membrane; positive potential in luminal space drives transport of positively charged Ca+2 and Mg+2 into intracellular space

30
Q

effects of loop diuretics

A

Na/Cl/K stay in thick ascending limb with water so increased flow of concentrated urine is created; accounts for 25% of NaCl excretion

31
Q

How is uric acid secretion affected by loop diuretics?

A

acute increase of secretion; decrease in secretion if used chronically

32
Q

Why is furosemide good for heart failure and pulmonary edema?

A

It acutely increases systemic venous capacitance that reduces pressure behind the left ventricle and relaxes the vasculature.

33
Q

Why are loop diuretics not limited by TGF (tubuloglomerular feedback)?

A

They block salt transport into the macula.

34
Q

How does the action of loop diuretics lead to volume depletion?

A

Their action collapses the medullar gradient, eliminating the ability to reclaim water from the collecting ducts.

35
Q

How do NSAIDs affect diuretic activity?

A

NSAIDs reduce GFR, which antagonizes diuretic activity and reduces efficacy. (loop & thiazides)

36
Q

How does Probenecid affect diuretic activity?

A

It may increase the effective dose needed. It competes for the transporter. (loop & thiazides)

37
Q

mechanism of action of thiazide diuretics

A

block Na/Cl symport but not K; enter the urine via organic ion transporters in proximal tubules b/c they’re protein-bound; act in the late distal convoluted tubule; K wasting

38
Q

Does the Na/Cl symporter affect the medullary gradient?

A

No, because the distal tubule resides in the cortex. (thiazide diuretics)

39
Q

How do thiazide diuretics affect Ca reabsorption?

A

High Na conc in the interstitial space drives the Na/Ca antiporter in the basolateral membrane. This increases Ca reabsorption and decreases elimination.

40
Q

Why are thiazide diuretics safer than loop diuretics?

A

They act distal to the macula so are not limited by tubuloglomerular feedback. This maintains the ability to reabsorb water from the collecting ducts.

41
Q

Which diuretic is best for HTN and why?

A

thiazides: no risk of hypovolemia (don’t affect water reabsorption and urine conc in the collecting tubules)

42
Q

effect of renal Na channel inhibitors

A

act on distal convoluted tubule and collecting duct; cause small increases in NaCl excretion; block K excretion in combo w/ other diuretics; K sparing

43
Q

function of renal Na channels

A

Na channels on luminal membranes of epithelial cells in the late distal tubules; ATPase brings Na into the cell which depolarizes the membrane and increases negative potential in the lumen; drives K secretion out of cell; the more Na in the lumen, the more depolarization and K excretion occurs

44
Q

mechanism of action of renal Na channel inhibitors

A

block luminal Na channels which lowers K secretion; inhibits H secretion by raising intra-luminal positive potential

45
Q

What is Liddle’s syndrome?

A

It is a mutation in renal Na channels; causes channel stabilization; hypokalemia w/ HTN

46
Q

Which diuretic is best for African Americans with HTN and why?

A

renal Na channel inhibitors b/c they have a polymorphism in the ENaC beta subunit (target of these drugs)

47
Q

How do mineralocorticoids function in renal physiology?

A

Mineralocorticoids (aldosterone) are secreted by the adrenal glands. They cause retention of salt and water, while increasing excretion of K and protons.

48
Q

mechanism of action of mineralocorticoid antagonists

A

receptors in distal convoluted tubule & collecting duct; act the same as renal Na channel blockers; act in the nucleus to change DNA expression of aldosterone-induced proteins; increase transport of K and H out of lumen; K sparing

49
Q

Which 2 types of diuretics function in the same way?

A

renal Na channel blockers & mineralocorticoid antagonists

50
Q

function of aldosterone-induced proteins (AIPs)

A

activate previously silent Na channels and pumps; increase expression and deposition of channels & increase ATPase activity; promotes Na (& water) reabsorption

51
Q

What affects the efficacy of mineralocorticoid antagonists?

A

how much aldosterone-mediated Na channel activity is occurring in these cells

52
Q

diuretic summary

A

carbonic anhydrases: weak, counteract alkalosis
osmotic agents: very effective, collapse medullar salt gradient & inactivate loop of Henle
loop diuretics: most effective, collapse medullar salt gradient & inactivate macula to reduce feedback
thiazides: not much Na left to act upon so not efficacious
mineralocorticoids: least efficacious, reverse increased K excretion of other agents

53
Q

V1 effects of antidiuretics

A

reduce medullary blood flow; increase medullary salt gradient; water reabsorption from distal tubules & collecting ducts

54
Q

V2 effects of antidiuretics

A

stimulate production of aquaporins in the epithelium for more water reabsorption; more aquaporins in apical membrane d/t recycling, more permeability of distal duct to urea, increased activity of Na/K/2Cl symporter in thick ascending limb

55
Q

receptors & functions for antidiuretics

A

V1: pressor effects, increase vascular constriction to reduce medullar blood flow
V2: renal antidiuretic effects

56
Q

Explain the biphasic effect of uricosuric agents.

A

first cause decreased excretion of uric acid; once in the lumen, inhibit urate reabsorption and increase excretion

57
Q

mechanism of action of probenecid

A

competes w/ urate for access to antiporter that brings urate back into the epithelia cell; increases urate excretion; block export of urate from epithelial cells back into tubular lumen so increases hyperuricemia acutely

Pharmacology Test 3 (10 decks)

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