Diuretics Flashcards

1
Q

what type of drug do you use in heart failure

A

loop

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2
Q

what drug do you use in hypertension

A

thiazide

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3
Q

acetazolamide

A

CA inhibitor

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4
Q

brinzolamide

A

CA inhibitor

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5
Q

dichlorphenamide

A

CA inhibitor

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6
Q

Dorzolamide

A

CA inhibitor

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7
Q

Methazolamide

A

CA inhibitor

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8
Q

Bumetanide

A

Loop

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9
Q

Furosemide

A

loop

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10
Q

ethacrynic acid

A

loop

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11
Q

torsemide

A

loop

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12
Q

amiloride

A

K sparing

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13
Q

eplerenone

A

K sparing

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14
Q

spironolactone

A

K sparing

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15
Q

triamterene

A

K sparing

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16
Q

bendroflumethiazide

A

thiazide

17
Q

chlorothiazide

A

thiazide

18
Q

hydrochlorothiazide

A

thiazide

19
Q

hydroflumethiazide

A

thiazide

20
Q

methylclothiazide

A

thiazide

21
Q

polythiazide

A

thiazide

22
Q

trichlormethiazide

A

thiazide

23
Q

chlorthalidone

A

thiazide like agent

24
Q

indapamide

A

thiazide like agent

25
Q

metolazone

A

thiazide like agent

26
Q

quinethazone

A

thiazide like agent

27
Q

dapagliflozin

A

SGLT2 inhbitor

28
Q

canagliflozin

A

SGLT2 inhbitor

29
Q

empagliflozin

A

SGLT2 inhibitor

30
Q

mannitol

A

osmotic diuretic

31
Q

conivaptan

A
32
Q

tolvaptan

A
33
Q

carbonic anhydrase inhibitors

A
  • Carbonic anhydrase inhibitors
    • Oral preparations
      • Acetazolamide
      • Dichlorphenamide
      • Methazolamide
    • Ophthalmic preparations
      • Brinzolamide
      • Dorzolamide
    • mech
      • Blocks Na and HCO3 reabsorption (co transporter so when you block HCO3 you block Na)
    • uses
      • Used for glaucoma - the ciliary body secretes bicarb into aq humor - water follows - inhibit the secretion = less humor
      • Other uses: urinary alkalization, correction of metabolic alkalosis, prevention of mountain sickness - CSF formation involves bicarb secretion
    • Tox
      • Hyperchloremic metabolic acidosis
      • Remal stones - calcium phosphate salts are less soluble in alkaline pH
      • Renal K wasting - whenever there is more Na delivery to collecting duct it absorbs Na while excreting K -> more K in the urine
34
Q

Sodium glucose cotransporter 2 (SGLT2) inhibitors

A

not used as diuretics

  • Dapagliflozin, canagliflozin, empagliflozin
  • Used in third line therapy for DM type 2
  • Block Na and glucose transporter = excrete more glucose in the urine = less glucose in the blood
35
Q

loop diuretics

A
  • sulfonamides
    • Furosemide
    • Bumetanide
    • Torsemide
  • Ethacrynic acid - use if pt is allergic to sulfonamides
  • Mech
    • Inhibits NKCC transporter = decresaed in Na Cl reabsorption (because there is more Na in the lumen when it gets to collecting ducts you lose K)
    • Decreases the potential diff generated by recycling K = less divalent reabsorption (increased excretion of Ca and Mg
    • It is excreted by the same transporters that excrete NSAIDs - taking these may interact with secretion = longer HL
    • Direct vascular effects due to increased prostaglandin synthesis may increase renal blood flow
    • Powerful stimulators of renin - the mac dense uses the same NKCC transporter - so it can’t sense the Na = thinks there is no Na = increased secretion of prostaglandins on JG cells = more renin
  • Uses
    • Relief of pulm edema (usually assoicated with heart failure)
    • Other uses
      • Hypertension if thiazides don’t work
      • Severe hyperkalemia
      • Acute renal failure - can convert oliguric to nonoliguric failure
        • Can secrete water from the tubules (even if GFR is down you can still get volume excretion)
  • AE
    • Dehydration/hyponatremia
    • Hypokalemia
    • Ototoxicity - usually reversible
      • NKCC is used in endolymph production
    • Hyperuricemia and gout attacks - due to hypovolemia = increased Uric acid concentration
    • Allergic reactions - more common in sulfonamides than with ethacrynic acid
36
Q

thiazide diuretics (and thiazide like agents)

A
  • Basics
    • All are sulfonamides
  • drugs
    • Thiazides (end in thiazide)
      • Chlorothiazide
      • Hydrochlorothiazide
      • Methyclothiazide
      • Polythiazide
      • Trichlormethiazide
    • Thiazide like drugs
      • Chlorthalidone
      • Indapamine
      • Metolazone
      • Quinethazone
  • Mech
      • Inhibitors of Na Cl transport
    • Enhanced Ca reabsorption because of increased Na gradient basolaterally (no Na in the cell) - so the Na Ca exchanger works well
    • More Na in collecting ducts = more K excretion
    • Only moderatley effective in increaseing NaCl excretion (most has already been reabsorbed before it reaches the tubule)
  • Uses
    • Used to be first line agents for hypertension
      • Still used at a low dose
      • Can be used at high dose for CHF
    • Neophrolithiasis - reduces urine Ca concentration so stones may disolve
    • Neophrogenic diabetes insipidus - reduce polyuria and polydipsia
      • This is counterintuititve - we don’t know why it works (we thing because it decreases reabsorption of Na = less Na = less blood vol = decrease GFR = increased Na reabsorption in prox tubule ) - we really just don’t know
    • Works better in african americans and elderly
    • Not effective when GFR is low (unlike loops)
  • AE
    • Excreted by organic acid secretory system (also excretes uric acid) = hyperuricemia
    • Hypokalemia
    • Reduced Ca excretion (opposite of loops)
    • Hyperglycemia - decreases pancreatic release of insulin and diminished tissue utilization of glucose
    • Hyperlipidemia - increase total serum cholesterol (may return to normal after prolonged use)
    • Allergic reactions (sulfonamides)
    • ED (probably due to volume depletion)
37
Q

K sparing agents

A
  • Drugs
    • Aldosterone antagoinsts
      • Eplerenone, pironolactone
      • Blocks aldosterone (normally makes more ENAC )
    • Na channel blockers
      • Amiloride, triameterene
      • Blocks the ENAC itself
  • mech
      • Both drugs decrease the amount of Na absorbed - therefore less K gets excreted
  • Uses
    • These are generally weak diruetics - seldom used alone but used to counteract hypokalemia in loop or thiazide diuretics
    • Primary mineralocorticoid hypersecretion (as in conns syndrome or ectopic ACTH production) - in this case you have too much aldosterone
    • Secondary aldosetonism - due to congestive HF, heptic cirrhosis, nephrotic syndrome, and other conditions assoicated with salt tertention and reduced fluid volume
  • Tox
    • Hyperkalemia
    • Hyperchloremic metabolic acidosis - inhibition of H+ secretion with reduced K secretion
    • Gynecomastica - due to steroid chemical structure of spironolactone
    • Acute renal failure may occur when triamterene is combined with indomethacin
    • Kidney stones may occur with triamterene which is poorly soluble
38
Q

vaptans

A

ADH antagonists

  • Drugs
    • Conivaptan - IV
    • Tolvaptan - oral
  • Mech
      • Blocks ADH receptors = less aquaporin 2 = collecting tubule not perm to water
  • Use
    • Manage syndrome of inappropriate ADH secretion (SIADH) when water restriction can’t correct the abnormality
    • Congestive heart failure when ADH is elevated due to low blood volume (helps you not retain water)
    • Need to monitor serum Na to look out for hypernatremia and nephrogenic diabetes insipidus
39
Q

osmotic diuretics

A
  • Mannitol
  • Filtered by glom but not reabsorbed - increased osmolarity of the inter tubular fluid - less reabsorption
  • Used primarily for rapid (emergency) reduction in intracranial pressure (pulls fluid into the BV and then transports it to kidney)
  • Poorly absorbed orally - can cuase osmotic diarrhea