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Pharmacology > Diuretics 2 > Flashcards

Diuretics 2 Flashcards

1
Q

Adenosine receptors

A

increase Na reabsorption at proximal tubule

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2
Q

Adenosine A1 receptor antagonists

A

Vasomotor effects on renal vasculature
blunt proximal tubule and collecting duct NaCl reabsorption
Do not affect K absorption

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3
Q

Caffeine

A

Weak adenosine receptor blocker–mild diuretic

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4
Q

Natriuretic peptides

A

ANP, BNP, CNP, urodilatin

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5
Q

BNP

A

Nesiritide–used for heart failure

Vascular and sodium transport effects

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6
Q

Urodilatin

A

effects kidney. made in distal tuble. Blunts sodium reabsorption.
Vascular effects: decrease afferent tone and increases efferent tone, increases GFR

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7
Q

Carbonic anhydrase inhibitors

A

Inhibit formation of H and bicarb from H20 and CO2
Increase excretion of Na, bicarb, K
Water reabsorption decreased
Urine volume increased
Urine becomes alkaline
Agents: Acetazolamide, dichlorphenamide, methazolamide, dorzolamide, brinzolamide. work at proximal tuble

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8
Q

Acetazolamide

A

Carbonic anhydrase inhibitor
Results in up to 85% inhibition of Na bicarb reabsorption–compensated be reabsorption later in tuble. net effect–45%.
RESULTS IN HYPERCHLOREMIC METABOLIC ACIDOSIS
PO is dosed 2-3x/d
Use: acute high altitude sickness, start 24 hrs prior, 250mg-1g daily

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9
Q

Dichlorphenamide

A

Carbonic anhydrase inhibitor

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10
Q

Methazolamide

A

Carbonic anhydrase inhibitor

Reduce formation of aqueous humor, lowering IO pressure

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11
Q

Dorzolamide

A

CAI. 2% ophthalmic solution
Reduce formation of aqueous humor, lowering IO pressure
Used for glaucoma

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12
Q

Brinzolamide

A

CAI. 1% ophthalmic solution used for glaucoma

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13
Q

CAI Anticonvulsant effects

A

transports HCO3 from blood to CSF (opposite of kidney)

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14
Q

CAI uses

A

Glaucoma
edema
Metabolic alkalosis
Acute high altitude sickness

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15
Q

CAI ADEs

A 
Hypokalemia
hypercholoremic metabolic acidosis
hyperglycemia and glucosuria
drowsiness, h/a, depression, paresthesias,
SULFA hypersensitivities
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16
Q

Loop diuretic agents

A

Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)
Ethacrynic acid (Edecrin)

17
Q

Loop diuretics

A

Inhibit NaCl reabsorption in thick ascending limb
Most efficacious diuretics–no limit d/t acidosis
Increases renal prostaglandin synthesis

18
Q

Loop diuretic uses

A

Edema d/t CHF, pulm edema, nephrotic syndrome, cirrhosis, HTN (when thiazides can no longer be used)
Acute renal failure to control volume and enhance K excretion.
Tx of severe hypercalcemia (given w/ saline)
Mild hyperkalemia
Anion overdose

19
Q

Loop diuretic ADE

A 
Orthostatic hypotension
Hypokalemic metabolic alkalosis
Mg loss (check K and Mg), Ca loss
Increased uric acid--gout
Otic effects
Sulfa hypersensativities
20
Q

Loop diuretics DIs

A

Other diuretics
Hypotensive agents
DIGOXIN–hypokalemia increases risk of toxicity
Ototoxic drugs: amino, erythro
Indomethacin–effects of loop decreased
Bile acid sequestrients–absorption of furosemide decreased by cholestyramine

21
Q

Thiazide diuretics

A 
Agents: Chlorothiazide (.5-1gm bid)
Chlorthalidone (50-100mg qd)
Hydrochlorothiazide (12.5-50mg qd)
Indapamide (2.5-10mg qd)
Metolazone (2.5-10mg qd)
Inhibit NaCl reabsorp and enhance Ca reabsorp in distal convuluted tubule
Increase renal prostaglandin production
22
Q

Chlrothalidone

A

Thiazide diuretic
90% bound to RBC, long half life (40 hours)
Primarily renal elimination

23
Q

Indapamide

A

Thiazide diuretic

extensive liver metabolism

24
Q

Thiazide diuretic uses

A

HTN: long term control d/t vasodilation. reduces BP and mortality
HF: EARLY HF for control fluid overload, sx relief only. Ineffected with reduced renal fx
Diabetes insipidus: fall in GFR = greater reabsorption of NaCl at proximal tubule = less fluid delivered to diluting segments
Prophylaxis of renal calculus formation associated with hypercalciuria
Osteoporosis

25
Q

Thiazaide ADEs

A

Hypokalemia (THEY MUST WATCH SODIUM INTAKE)
Hypokalemia metabolic alkalosis
Hyponatremia
Hyperuricemia
Hypercalcemia–rare
Hyperglycermia, hyperlipidemia (not w/ indapamide)
Orthostatic HoTN, rash, SJS, impotenence

26
Q

Thiazide diuretic DI

A

Other diuretics, other hypotensives, digoxin, other drugs causing K loss, indomethacin, bile acids sequest
Lithium
Calcium salts

27
Q

Potassium sparing diuretics

A

Inhibit Na reabsorption at distal tubule
Agents: triamterene, amiloride (inhibit Na flux thru ion channels of the principal cell in luminal membrane
spironolactone, eplernone (aldosterone antagonist; aldoesterone enhances Na/K/ATPase and Na/K channel activity)
Depend on prostaglandin production

28
Q

Potassium-sparing diuretics Use

A

Primary hyperaldosteronism: Conn’s syndrome
Secondary hyperaldosteronism:
HF-spironolactone reduces mortality, eplerenone; edema d/t cirrhosis and nephrotic syndrome; HTN in combo with thiazides to spare K, avoid in renal insuff.

29
Q

Potassium sparing diuretic ADEs

A

Hyperkalemia! use in caution in renal dz, ACE I, ARBs, betablockers, NSAIDs, potassium supplements
Hyperchloremic metabolic acidosis: inhibit K and H secretion
Spironolactone: gynecomastia, impotence, BPH, rash

30
Q

Potassium sparing diuretic DI

A

ACEI, ARB, renin inhibitors, potassium supplements, NSAIDs, antihypertensives, eplernone

31
Q

Osmotic diuretics

A

Mannitol 5-25% solution, IV only
Not metabolized, handled by GFR
prevents normal reabsoption of water via osmotic force
Increased urine flow reduces contact time and decreases Na reabsorption

32
Q

Mannitol uses

A

Oliguric renal failure
Reduction of intracranial pressure
Reduction of IOP

33
Q

Mannitol ADEs

A

If inadequate urine output–> expansion of extracellular fluid and circulatory overload –> pulm edema, CHR. Give test dose to see if urine volume increases in 3 hours
H/A, N/V
dehydration, hypernatremia, hyponatremia in renal insuff in not cleared

34
Q

ADH agonist

A

Vasopressin (IV or IM) and desmopressin (PO, IV, IN SubQ)
Vasoconstriction, increased water perm
Use: diabetes insipidus, enuresis, esophageal variceal bleeding
ADE: h/a, n, abd cramping, agitation

35
Q

ADH antagonists

A

Conivaptan
Arginine vasopressin
Indications: SIADH, heart failure, hyponatremia with normal ECF volume
ADE: hypertension, otho HoTN, hypokalemia, c/d/ha

36
Q

Demeclocycline and Lithium

A

ADH antagonists
Non-specific agents
Used to tx SIADH
can causes nephrogenic diabetes insipidus–severe hypernatremia

37
Q

Uses for diuretics

A

HF: decrease cardiac output, decrease BP and renal blood flow–> sensed as hypovolemia –> renal retention Na and water
HTN: primarily thiazides
Kidney dz: retention of Na and water by kidney. Diabetic kidney dz often associated with hyperkalemia–avoid k-sparing.
Hepatic cirrhosis: spironolactone
Ca phosphate or Ca oxalate nephrolithiasis–thiazides
Hypercalcemia–loop with saline
Diabetes insipidus–thiazides reduce plasma volume –> reduce GFR —> greater Na/water reabsorption –> less fluid presents to collecting tube

Pharmacology (10 decks)

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