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Renal 2 Final - Pharm > Kruse - Diuretics > Flashcards

Kruse - Diuretics Flashcards

1
Q

What is the fxn of a diuretic

A
  • increase Na excretion + urine production by kidney

- adjust volume/composition of body fluids

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2
Q

What is fxn of natriuretic

A
  • Increase in renal sodium excretion
  • Diuretic = increase urine volume
  • Natriuretic called diuretic sometimes because it inevitably increases urine volume
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3
Q

Where are diuretics usually delivered?

A

To the luminal side of the tubule

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4
Q

What is reabsorbed at the thin descending limb of the loop of henle? Ions or water?

A

Water = descending loop

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5
Q

What is reabsorbed at the thick ascending limb of the Loop of Henle

A

25% of filtered Na+

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6
Q

Which transporter maintains the ion concentration gradient in the interstitium?

It is located in the TAL

A

NaK2Cl cotransporter

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7
Q

What is the fxn of NaK2Cl cotransporter?

A
  • Creates increase in intracellular K+
  • reabsorbs 25% Na
  • this drives K+ to diffuse back into lumen to create a + potential
  • Mg, Ca+ ions in the lumen diffuse from lumen into blood paracellulary to escape the + potential created by K+

***blocking this transporter results in excretion of many ions in urine

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8
Q

What happens at the DCT?

A
  • 10% of NaCl is reabsorbed = dilutes tubular fluid
  • impermeable to H20
  • NaCl transported via thiazide-sensitive NaCl cotransporter
  • Ca+ is passively reabsorbed by calcium channesl (PTH sensitive)
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9
Q

Function of the Collecting Duct

A
  • reabsorbs 2-5% of NaCl via ENaC
  • most important site of K secretion
  • secrete H+ into lumen = acidic urine
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10
Q

Diuretics that act upstream of the CD, will ______ Na delivery to the CD and _____K+ secretion

A

Increase; enhance

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11
Q

What is the fxn of aldosterone?

A
  • Increases the expression of both the ENaC on luminal side = Na reabsorption into cell
  • increase in basolateral Na+ K+ ATPase = increased Na reabsorption + K+ secretion = increase bp
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12
Q

Fxn of ADH (vasopressin)?

A
  • control permeability of CD to H20
  • controls aquaporin-2 channels at apical membrane

Without ADH = CD impermeable to H20 = dilute urine

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13
Q

How does alcohol affect ADH release?

A

Alcohol DECREASES ADH release and increases urine production

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14
Q

Prototype of Carbonic Anhydrase Inhibitor?

A

Acetazolamide

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15
Q

Acetazolamide

Metabolism and excretion?

A
  • well absorbed after oral intake
  • excreted by secretion in PCT —- need to reduce dose if renal insufficiency
  • no hepatic metabolism/breakdown
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16
Q

MOA of Acetazolamide (CA Inhibitor)

A
  • inhibits membrane bound + cytoplasmic CA = no NaHCO3 reabsorption in PCT
  • decreased NHE3 (Na/H exchanger) activity = increased diuresis because more sodium left in lumen
  • 45% more bicarb excreted = blood acidosis

Note
- within few days, drug efficacy decreases b/c rest of nephron makes up for lack of Na reabsorption at PCT by reabsorbing at other spots in nephron

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17
Q

How long before urine alkalosis seen when using a CA inhibitor

A

Within 30 minutes

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18
Q

Adverse effects of CA Inhibitor?

A
  • metabolic acidosis
  • bicarbonaturia
  • Renal stones because calcium salts are more insoluble at basic urine pH
  • potassium wasting (hypokalemia) = increase Na in CCT increases K+ secretion
  • sleepy + tingling @ large doses
  • Hypersensitivity rxn = rare
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19
Q

Contraindications of CA I

A

Patients with cirrhosis
- increase. Urine pH due to CAI = decrease urine excretion of ammonia –> hyperammonemia + hepatic encephalopathy

Patients with hyperchloremic acidosis or severe COPD
- CA I = makes metabolic or respiratory acidosis worse

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20
Q

Clinical indications for CAI

A
  • rarely used as diuretics
  • used for glaucoma = common
  • reduces aqueous humor formation + decrease intraocular pressure
  • acute mountain sickness
  • adjuvants in epilepsy
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21
Q

How are CA I used to help excrete uric acid, cystine, and other weak acids?

A

Because it causes urinary alkalinization

*basic urine decreases excretion of NH4 (basic)

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22
Q

Prototypes of loop diuretics?

A

Furosemide + ethacrynic acid

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23
Q

Metabolism of loop diuretics (furosemide + ethacrynic acid)

A
  • rapidly absorbed after oral administration
  • can be taken IV for some
  • eliminated by kidney
  • secreted into lumen at PCT, acts on luminal side of nephron — halflife related to kidney fxn
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24
Q

Why is coadministering loop diuretics with other weak acids (Ex. NSAIDs) bad?

A

Can cause reduced loop diuretic secretion into lumen = less effect

B/c competition for secretion of other weak acids

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25
Q

MOA of loop diuretics (furosemide + ethacrynic acid)

A
  • inhibit NaK2CL cotransporter in TAL
  • ion transport in TAL pretty much stops because lumen-positive potential is not created, so Mg + Ca are not reabsorbed
  • more Na delivered to DCT/CD, so more K and titratable acid is excreted as Na is reabsorbed into body to make up for lack of Na reabsorption at TAL
  • H+ released into lumen as well (3 Na taken in, 2 K pumped out, so maybe secrete H+ to balance out?)
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26
Q

Loop diuretics induce the production of _____

A

Renal PG (prostaglandins)

Note: NSAID reduce loop diuretics ability to make PG

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27
Q

Loop diuretics can be weak inhibitors of

A

Carbonic anhydrase

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28
Q

Loop diuretics increase

A

RBF (renal blood flow) via PG-mediated vasodilation

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29
Q

Too much loop diuretics (toxicity) can cause:

A
  • depletion of total-body Na+ = hyponatremia, decreased GFR, circulatory collapse, thrombohemolytic episodes, hepatic encephalopathy in pts with liver disease
  • hypokalemic metabolic alkalosis
  • hyperuricemia = gout b/c too much uric acid reabsorbed at PCT
  • ototoxicity*
  • hypomagnesemia
  • allergic rxn
  • dehydration
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30
Q

When is loop diuretics contraindicated?

A
  • Bad for pts with hepatic cirrhosis, borderline renal failure, HF
  • postmenopausal women b/c of hypocalcemia = osteoporosis
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31
Q

Which 3 loop diuretics should not be used b/c they may cause allergic rxns in pts with sulfonamide sensitivity?

A

Furosemide
Bumetanide
Torsemide

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32
Q

What drugs do loop diuretics interact with?

A

Aminoglycosides
Lithium
Digoxin

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33
Q

Clinical indications for loop diuretics

A
  • most efficient diuretic
  • acute pulmonary edema
  • HTN + heart failure
  • tx for hyperkalemia b/c loop diuretics promote K+ excretion
  • anion overdose
  • hypercalcemia
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34
Q

Prototype for thiazide diuretics

A

Hydrochlorothiazide

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35
Q

thiazides are given ______.

Which thiazide is not lipid soluble?

A
  • given orally

- Chlorothiazide = not lipid soluble — so give in large doses

36
Q

Which thiazide is the longest acting thiazide?

A

Chlorthalidone

47 hours = halflife

37
Q

Where are thiazides secreted?

A

PCT by organic acid secretory system

  • competes with secretion of uric acid …so may get increased uric acid in blood
38
Q

MOA

Thiazides Inhibit ______ cotransporter
Thiazides increase _____ reabsorption. Why?

A
  • Inhibits Na/Cl cotransporter in luminal side in DCT
  • increase Ca reabsorption to bring more Na into epithelial cell (Na/Ca antiporter on basolat side) = HELP STOP STONES
  • NaCl not reabsorbed from the luminal side
39
Q

Thiazides are a weak inhibitor of

A

Carbonic anhydrase

40
Q

Too much thiazides = toxicity

Symptoms are:

A
  • Hypokalemic metabolic alkalosis + hyperuricemia (like loop diuretics)
  • Decreased glucose tolerance = hyperglycemia
  • hyperlipidemia
  • Hypnatremia
  • hypercalcemia + hyperuricemia
  • weakness
  • fatigue
  • Paresthesias (tingling)
  • allergic rxn
  • impotence
  • sulfonamide hypersensitivity
41
Q

Thiazides can diminish effects of?

A

Anticoagulants
Agents used to treat gout
Insulin

42
Q

Thiazides increase the effect of

A

Loop diuretics

43
Q

Use thiazides with caution if patient has

A

Diabetes

B/c thiazides cause hyperglycemia by decreasing glucose tolerance

44
Q

Taking thiazides with _____ + _______ decreases thiazide efficacy

A

NSAID + COX2 inhibitor (b/c inhibit PG synthesis)

45
Q

Use thiazides to treat:

A
  • HTN + HF
  • nephrolithiasis (renal stones) by decreasing hypercalciuria
  • nephrogenic diabeties inspidus (intense thirst and heavy urination)
46
Q

Potassium sparing diuretics

Mineralocorticorticoid receptor (aldosterone) antagonist prototype is:

A

Spironolactone

47
Q

Potassium sparing diuretics

Na channel inhibitor prototype:

A

Amiloride

48
Q

How are spironolactone + EPLERENONE inactivated

A
  • Inactivated in liver after several days

- both given orally

49
Q

What is eplerenone

A

Analog of spironolactone with greater selectivity for MR

50
Q

Amilordie + triamterene are given

A

Given orally

51
Q

How is triamterene and amiloride metabolized ? What type of diuretic are they?

A

Potassium sparing - renal Na channel inhibitor

Taken orally

Triamterene metabolized by liver and has shorter half life
Amiloride not metabolized

52
Q

MOA of spironolactone + eplerenone (Aldosterone antagonists - potassium sparing diuretic)

A

MR antagonists = synthetic steroids that act as competitive inhibitors of aldosterone binding MR

MR antagonist reduces NA reabsorption in CD = less K secretion

53
Q

Which diuretic is the only on that doesnt need access to tubular lumen to induce diuresis?

A

MR antagonist

54
Q

What does MR regulate?

A 
Na channel (ENaC)
Na/K ATPase in DT + CD
55
Q

MOA of amiloride + triamterene

A

Inhibit Na reabsorption by blocking EnaC in apical membrane of CD = less K secretion

56
Q

Excessive potassium sparing diuretics results in

A
  • hyperkalemia
  • metabolic acidosis b/c increased H+ secretion
  • gynecomastia, impotence, BPH (since MR antagonists are steroids that can react with other hormone receptors)
57
Q

Triamterene __________ in the urine and can cause _______.

When combined with ______, it can cause kidney failure

A

Precipitates; kidney stones

Indomethacin

58
Q

What increases risk of hyperkalemia

A

Renal disease or use of b-blockers, NSAIDS (reduce renin) or AngII activity (ACEI, or ARBs)

59
Q

Contraindications for potassium sparing diuretics

A
  • pts with chronic renal insufficiency
  • vulnerable to fatal hyperkalemia
  • using K sparing diuretics with b-blockers, NSAD, ACEI, ARBs
  • pts wtith liver disease = impaired metabolism of spironolactone + amterene
  • inhibitors of CYP3A4 = increase blood levels of eplerenone
60
Q

Clinical indications to use K sparing diuretics

A
  • hyperaldosteronism
  • thiazides + loop diuretics cause secondary hyperaldosteronism = renal wasting of K+ ….so use K sparing drugs to prevent wasting of K
  • treat heart failure
61
Q

Agents that alter water excretion

A

Osmotic agents, ADH antagonist, ADH, agonists

62
Q

Example of osmotic agent

A

Mannitol

  • absorbed poorly, so give it via IV
  • not metabolized
  • excreted in GFR within 30-60 min, but not reabsorbed = promotes water diuresis
63
Q

Osmotic agents MOA

A
  • Increases osmotic pressure of glomerular filtrate = inhibits tubular reabsorption of H20 + electrolytes = increased urine output
  • opposite ADH effect in CD
64
Q

What does increased water diuresis by osmotic diuretics do?

A
  • increase urine flow rate
  • decrease contact time btw fluid + tubular epithelium = less Na reabsorption

Note: natriuresis is less than water diuresis = too much water lost + too much sodium in body (hypernatremia)

65
Q

too much mannitol causes

A

Extracellular volume expansion

  • b/c too much water extracted from cells
  • dehydration
  • hyperkalemia
  • hypernatremia
66
Q

When is mannitol contraindicated

A

Severe renal disease (anuria)
Severe dehydration
Severe pulmonary edema or congestion

67
Q

When to use mannitol? (Osmotic diuretics)

A
  • increase/maintain urine volume

- reduce intracranial/intraocular pressure

68
Q

ADH agonist causes:

A
  • increased water reabsorption
  • vasoconstriction
  • increase H20 permeability + reabsorption in CD
69
Q

ADH agonists are used for?

A 
Pituitary diabetes inspidus
Polyuria
Polydipsia
Hypernatremia
Nocturnal enuresis (urinating)
70
Q

ADH agonists names

A

Vasopressin

Desmopressin

71
Q

ADH antagonist prototype

Given via? Half life?

A

Conivaptan

  • given via IV
  • half life is 5-10 hours
72
Q

ADH antagnoist used for?

A
  • to treat medical conditions (ex. Heart failure, SIADH) that cause water retention b/c too much ADH == hyponatremia
73
Q

MOA of ADH antagonist

A

Antagonist of ADH receptors in CD

74
Q

ADH antagonist toxicity can cause

A

Hypernatremia

nephrogenic diabetes inspidus

75
Q

Why would you combine Loop agents + thiazides ..what does it do

A
  • helps diuresis If usual dose of loop diuretics dont work
76
Q

Why would one diuretic be not as effective as two diuretics?

A
  • Na/H20 reabsorption in TAL (blocked by loops) or DCT (blocked by thiazides) can increase when other is blocked
  • inhibiting both = diuresis
  • thiazides produce slight natriuresis in PCT that is masked by increased absorption in TAL
  • combo drugs can inhibit Na reabsorption at PCT, TAL, DCT
77
Q

Why should not use loops and thiazides as outpatient

A
  • significant diuresis!

- K wasting is common

78
Q

Effect of K sparing + loop/thiazides?

A

To treat hypokalemia (by preventing K secretion) which is a side effect of loop/thiazides as Na is reabsorbed

Hypokalemia initially managed by restricting NaCl or KCl suppplementation

79
Q

When should K sparing diuretics + loops be avoided?

A

For pts with renal insufficiency and ppl getting Ang antagonists

80
Q

Common use for diuretics

A

Reduce peripheral or pulm edema

Tx for heart failure, kidney disease + hepatic cyrrhosis

81
Q

How does pulm or interestial edema occur due to heart failure?

A

HF decrease CO = decreased bp + decreased RBF = kidney wants to retain Na + H20 = pulm + intersitial edema

82
Q

When do diuretics help and NOT HELP if pt has kidney disease?

A

Loss of renal fxn = decreased GFR = natriuresis doesnt occur, so diuretics cant help

  • diuretics help with glomerular diseases (SLE or DM) where renal H20/Na occurs
83
Q

Loop + thiazides are helpful for ppl with ________ when they also have early stage renal failure

A

Hyperkalemia

84
Q

When to not use aggressive diuretics?

A

Liver disease (hepatic cirrhosis)

  • though diuretics can help with edema + ascites
85
Q

Nonedematous conditions when diuretics are used

A
  • HTN = thiazides, loops
  • Nephrolithiasis = thiazides
  • Hypercalcemia = loops + saline
  • Diabetes Insipidus = ADH agonist for central DI, thiazides for central + nephrogenic DI

Renal 2 Final - Pharm (4 decks)

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