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Renal 2 > PostMT Diuretics > Flashcards

PostMT Diuretics Flashcards

1
Q

What is reacsorbed in PCT?

A

65% of Na, K, water
85% NaHCO3
100% of glucose and amino acids

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2
Q

What is reabsorbed in thick ascending LoH?

A

Impermeable to water.

25% of filtered Na reabsorbed

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3
Q

What establishes the cortex and medulla concentration gradient?

A

The Na/K/2Cl cotransporter in the thick ascending limb.

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4
Q

What drives Mg and Ca paracellular reabsorption?

A

The diffusion of K back into the lumen due to the incrased intracellular concentration gradient that creates an ELECTROPOSITIVE status in the lumen.

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5
Q

What % of Na is reabsorbed in DCT?

A

10%

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6
Q

What is Ca reabsorption regulated by in the DCT?

A

PTH

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7
Q

What is Ca reabsorption regulated by in the thick ascending limb?

A

electropositive gradient produced by K

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8
Q

Where does K balance and seretion primarily occur?

A

CCT

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9
Q

What are Aldosterone’s action?

Physiological results?

A

Na reabsorption
H+ expelled
K+ expelled
Results in increased water retention&raquo_space; increased blood volume&raquo_space; increased BP

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10
Q

What regulates ADH levels?

What does alcohol do?

A

serum osmolarity and volume

Alcohol decreases ADH release and increases urine production.

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11
Q

What two drug classes decrease body pH?

A

CAi’s (decrease bicarb formation in cytosol of PCT cells = decrased bicarb into interstitum&raquo_space; less to body)
K-sparing (block Na channels, so Na cannot leave lumen = lumen remains more electropositive)

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12
Q

What two diuretic classes increase NaCl urinary content the most?

A

Loops and even greater, Loops + thiazides
Loops = block Na/K/2Cl
Thiazides = block Na/Ca cotransporter

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13
Q 
What diuretic class increases urinary NaHCO3 most?
What has no effect on NaHCO3 urinary levels?
A

CAi’s

Loops

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14
Q

What increases urinary K most?

A

Loops + thiazides

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15
Q

CAi

A

acetazolamide

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16
Q

CAi location of action and MOA

A

PCT

abolition of NaHCO3 reabsorption

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17
Q

Urinary and body result of CAi

A

DECREASED body pH (due to less bicarb reabsorbed).
INCREASED urinary pH (due to more NaHCO3).
Bicarb-esis, natriuresis, diuresis

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18
Q

How fast to CAi’s work?

Efficacy short or long course of admin?

A

Apparent within 30 min.

Significant loss of efficacy after several days of use.

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19
Q

CAi toxicity

A
  • Metabolic acidosis.
  • Ca2+ stones due to pH alkalinization (decreased calcium salt solubility)
    Paresthesia, sulfonamide hypersensitivity
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20
Q

Cirrhosis is a contraindication for use of what diuretic? Why?

A

CAi use.

1. alkalinization of urine results in hyperammonemia and hepatic encephalipathy

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21
Q

What three things are contraindications of CAi’s?

A

Cirrhosis, severe COPD, hyperchloremic acidosis

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22
Q

Clinical indications of CAi’s?

What’s it rarely used for?

A

glaucoma,
urinary alkalinization or metabolic alkalosis
ACUTE MOUNTAIN SICKNESS

Rarely used as antiHTN.

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23
Q

Loop Diuretics
Names
Best used for what?

A

furosemide and ethacrynic acid

Most efficacious diuretic/volume depletion class.

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24
Q

Metabolism of CAi’s

A

excreted unchanged - no hepatic metabolism

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25
Q

Loop half life is correlated with what? Why?

A

Correlated with kidney function because it works on luminal side of tubule at Na/K/2Cl cotransport.

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26
Q

Co-administration of NSAIDS with a Loop (esp in a person with cirrhosis or nephritic syndrome) could result in what?

A

Reduction of loop secretion due to competition for weak acid secretion.
NSAIDs interfere because they reduce PG synthesis.

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27
Q

What do Loops cause?

A

uresis of Mg, Ca, Na, K, and water
Synthesis of PGs
Increasein renal blood flow to vascular beds
Weak inhibitors of CAi’s

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28
Q

Loop toxicity

A

hyponatremia (hepatic enceph in liver diseased patients)
hypokalemia, Mg, uricemia
ototoxicity (associated with renal dysfunction)
hyperuricemia

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29
Q

Contraindications of Loops

A

furosemide, bumetanide, torsemide may cause sulfa allergic reactions
HEPATIC CIRRHOSIS, HF, or renal failure
post-menopausal osteopenic women

30
Q

Clinical indications of Loops

A

pulm edema, HTN, HF,
hyperK
Anion overdose - coadmin loop and saline
hypercalceimic states

31
Q

Thiazide diuretic

A

hydrochlorothiazide

32
Q

Half life of HCTZ

MOA

A

47 hours

block Na/Cl in DCT

33
Q

HCTZ toxicity

A 
hypokalemic metabolic alkalosis and hyperuricemia
*HYPERGLYCEMIA and UNMASK DIABETES
*HYPERLIPIDEMIA
hypoNa, hyperCa, hyperUrecemia
Sulfonamide hypersensitivity
34
Q

HCTZ contraindications

A

Will decrease effectiveness of anticoags for gout, insulin, loops
*DIABETIC PATIENTS
NSAIDs and COX-2 inhibitors
Hepatic cirrhosis, renal failure, HF

35
Q

Clinical indications of HCTZ

A

HTN, HF
Nephrolithiasis due to hypercalcinuria
NEPHROGENIC DI

36
Q

K Sparing Diuretics

A

Mineralicorticoid receptor (MR) antagonist prototype - SPIRONOLACTONE&raquo_space; eplerenone (analog)

Na channel inhibitor prototype: AMILORIDE and triamterene

37
Q

Eplerenone inactivation location

38
Q

What is a spironolactone analog with greater MR selectivity?

A

eplerenone

39
Q

What Na-channel inhibitor do you give if you want less frequent dosing?

40
Q

MOA of MR antagonists

A

They are synthetic steroids that are competitive inhibitors of aldosterone binding to the MR (a nuclear hormone).

41
Q

What is MR?

A

A nuclear hormone

42
Q

What is unique about MR antagonists?

A

Only diuretic that does not require access to tubular lumen to induce diuresis.
*Reduce mortality in HF!!

43
Q

MOA of amiloride and triamterene

A

directly inhibit Na entry to DCT principle cells though Na channels

44
Q

Toxicity of K-sparindg diuretics

A

extreme hyperK - esp use of renin-reducing agents like B-blockers
met acidosis
BPH, impotence

45
Q

Stones can be caused especially by what K-sparing diuretic?

A

triamterene

46
Q

Contraindications of K-sparine

A

chronic renal insuff

B-blockers, NSAIDS, ACEis, ARBs

47
Q

Clinical inidcations of K-sparing?

A

hyperaldosteronism or MC excess

thiasizeds and loops

48
Q

What are osmotic agents that alter water excretion?
Administration route?
Metabolized?

A

Mannitol
given parenterally
Not metab. Excreted within 30-60min

49
Q

MOA of mannitol

REsutls in what?

A

increase osmotic pressure of glom filtrate&raquo_space; inhibit tubular reabsorption of wtaer&raquo_space; decrease urine
REsults in Natriuresis and diuresis

50
Q

Mannitol opposes what effects in CCT?

51
Q

Mannitol toxicity

A

EC volume expansion and hyponatriemai

52
Q

Contrainidications of mannitol

A

dehyrdation, hyperK, hyperNa

53
Q

Mannitol clinical indications

A

increase urine volume

REDUCE ICP OR INTRAOCULAR PRESSURE

54
Q

What are effects of ADH agonists that alter water excretion?

A

Increased water reabs in CCT

55
Q

ADH agonist are treatment of choice in what disease?

A

Pituitary DI

56
Q

What is a ADH antagonist that alters water excretion? What do you use it to avoid?

A

Conivaptan

Use because you want to avoid hyponatremia caused by ADH excess

57
Q

Conivaptan admin route

A

parenterally

58
Q

Toxicity of Conivaptan

A

hyperNa

nephrogenic DI

59
Q

When do you use Loops and thiazides?

A

When you want to block Na reabsorption from all three segments.
Loops - block in thick ascending limb
Thiazides - block in DCT and cause mild natriuresis in PCT

60
Q

Adverse effect of loops and thiazides

61
Q

What edematous states are treated with diuretics?

A

HF
Kidney disease/renal failure
Hepatic cirrhosis

62
Q

What nonedematous states are treated with diuretics?

A

HTN
Nephrolithiasis
HyperCa
DI

63
Q

Why does HF cause an edematous state?

A

Decreased CO&raquo_space; decreased BP sensed leads to retention of Na and water&raquo_space; unecessary retention of water&raquo_space; pulm or interstital edema result

64
Q

Why does kidney disease cause an edematous state?

A

Renal disease = retention of salt and water, sometimes K = diruetics useful

65
Q

When should diuretics be used in hepatic cirrhosis-caused edema?

A

Useful for when edema and ascites become severe due to liver disease.
DO NOT USE aggressively in patients wtih liver disease….

66
Q

What diuretics are used in HTN (nonedematous state)?

A

Thiazides or loops, combo with vasodilator (bc cause signif salt and water rentention)

67
Q

What diuretics are used in nephrolithiasis (nonedematous state)?

A

Thaizide to reduce urinary Ca concentration and enhance Ca reabsorption

68
Q

What diuretics are used in hypercalcemia (nonedematous state)?

A

Loops coadmin with saline to maintain effective Ca diuresis without volume contraction.

69
Q

What diuretics are used in DI (nonedematous state)?

A

Supplementary ADH only useful when it’s central DI.
Thiazides reduce polyuria and polydypsia in both nephrogenic DI (inadequate responsiveness to ADH) and neurogenic/central DI (deficient ADH production)

70
Q

Membrane transport protein diuretics

A

lops
thiazides
K-sparing

71
Q

Enzyme diuretics

72
Q

Hormone receptor diuretics

A

MR (K-sparing)

Renal 2 (12 decks)

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