diuretics and anti-HTN meds Flashcards

1
Q

Diuretics that act in proximal tubule

A

mannitol and acetazolamide

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2
Q

Mannitol MOA

A

Non metabolized, non- reabsorbed osmotic diuretic: draws free water out of the tissue and into the circulation, where it is excreted by the kidneys

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3
Q

Mannitol uses

A

elevated intracranial pressure, gluacoma, prevention of acute kidney injury

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4
Q

Acetazolamide MOA

A

Carbonic Anhydrase Inhibitor: CA converts CO2 and water into bicarb (or vice versa). By blocking this process, bicarb is lost in the tubular fluid and a metabolic acidosis results. Loses effectiveness when metabolic acidosis develops

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5
Q

Acetazolamide uses

A

glaucoma and prevention/treatment of high altitude sickness

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6
Q

Diuretics that act at loop of Henle

A

Furosemide(la SIX), bumetanide, torsemide, ethacrynic acid

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7
Q

Loop diuretics MOA

A

Inhibits Na/K/2Cl transporter in thick ascending limb. Decrease tonicity of medullary interstitium and therefore inhibit reabsorption of water in collecting duct (i.e., inhibit concentration of urine). Lead to excretion of 15-25% of filtered sodium

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8
Q

Loop diuretics uses

A

Volume overload, Heart failure, BP reduction, Pulmonary edema

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9
Q

Loop diuretics adverse effects

A

Decreased K/Mg, hypocalcemia, precipate gout attack (uric acid retention), metabolic alkalosis, hearing loss

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10
Q

Diuretics that act at distal convoluted tubule

A

Thiazide diuretics (HCTZ, chlorthalidone, metolazone)

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11
Q

Thiazide diuretics MOA

A
  • Inhibit Na/Cl cotransporter in distal tubule, causing moderate diuresis since only about 5% of filtered sodium is reabsorbed in this location. Antihypertensive effect secondary to dec plasma volume and dec CO, plus mild vasodilation
  • Inhibit Na/Cl cotransporter in distal tubule, causing moderate diuresis since only about 5% of filtered sodium is reabsorbed in this location. Antihypertensive effect secondary to dec plasma volume and dec CO, plus mild vasodilation
  • Inhibit Na/Cl cotransporter in distal tubule, causing moderate diuresis since only about 5% of filtered sodium is reabsorbed in this location. Antihypertensive effect secondary to dec plasma volume and dec CO, plus mild vasodilation
  • Inhibit Na/Cl cotransporter in distal tubule, causing moderate diuresis since only about 5% of filtered sodium is reabsorbed in this location. Antihypertensive effect secondary to dec plasma volume and dec CO, plus mild vasodilation
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12
Q

Thiazide diuretics adverse effects

A

Hyperuricemia (inhibits uric acid secretion), hypokalemia (increases K secretion at collecting tubule), metabolic alkalosis (increased H excretion due to K/H co transporters), hyperglycemia (decreases insulin secretion into blood from pancreas)

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13
Q

compare half lives of chlorothalidone vs HCTZ

A

Chloro has half life of 40-60 hrs. HCTZ has half life of 2.5hrs

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14
Q

Thiazide altered responses with chronic kidney disease

A

Lose efficacy in later stages of CKD as less drug reaches site of action as kidney fails. More efficacious Loop Diuretic necessary at GFR < 30 ml/min. Resistance can occur at later stages of CKD- overcome with synergistic combo of Loop + Metalozone
Lose efficacy in later stages of CKD as less drug reaches site of action as kidney fails. More efficacious Loop Diuretic necessary at GFR < 30 ml/min. Resistance can occur at later stages of CKD- overcome with synergistic combo of Loop + Metalozone
Lose efficacy in later stages of CKD as less drug reaches site of action as kidney fails. More efficacious Loop Diuretic necessary at GFR < 30 ml/min. Resistance can occur at later stages of CKD- overcome with synergistic combo of Loop + Metalozone
Lose efficacy in later stages of CKD as less drug reaches site of action as kidney fails. More efficacious Loop Diuretic necessary at GFR < 30 ml/min. Resistance can occur at later stages of CKD- overcome with synergistic combo of Loop + Metalozone

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15
Q

Diuretics that act at distal tubule/collecting duct

A

K sparing diuretics: Aldosterone Antagonist (Spironolactone, eplerenone) and Sodium channel blockers (Triamterene, Amiloride)

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16
Q

Aldosteron antagonists MOA

A

Competitively inhibit the mineralocorticoid receptor (eplereonone is more specific) and block binding of Aldosterone. This decreases activity of Na/K exchanger Reducing the reabsorption of sodium and secretion/excretion of potassium.

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17
Q

Aldosterone antagonists uses

A

resistant HTN, heart failure, hyperaldosteronism (use with other diuretics to preserve K)

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18
Q

Na Channel blockers MOA

A

block luminal sodium channels and decrease the driving force for potassium secretion/excretion. Also indirectly decrease hydrogen ion secretion.

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19
Q

ACE Inhibitors examples

A

Lisinopril, benazepril, captopril, enalapril, ramipril

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20
Q

Angiotensin II actions

A

vasoconstriction. Salt/water retention, growth stimulation, disease progression

21
Q

Angiotensin II role in kidney disease

A

A-II causes small amount of afferent arteriole constriction and a large amount of efferent arteriole constriction. This increases pressure load and wall tension rises. Growth and destruction occur, leading to end stage renal failure

22
Q

ACEI MOA

A

blocks the conversion of angiotensin I to angiotensin II, preventing angiotensin II-mediated vasoconstriction and stimulation of aldosterone release. Blocks degradation of bradykinin. Bradykinin (along with Substance P) cause bronchoconstriction and stimulate irritant receptors

23
Q

ACEI adverse effects

A

cough, hyperkalemia, mild increase in serum creatinine, angioedema

24
Q

ARBs examples

A

Losartan, irbesartan, candesartan, valsartan

25
Q

ARBs MOA

A

Irreversibly blocks the actions of angiotensin II at AT1 receptor. Prevents angiotensin II-mediated vasoconstriction, aldosterone release

26
Q

ARBs adverse effects

A

hyperkalemia, rise in serum creatinine, angioedema

27
Q

ACEI and ARB uses

A

HTN, CKD, Heart Failure, Diabetic nephropathy

28
Q

List calcium channel blockers

A

Dihydropyridines (DHP): amlodipine, nislodipine, nifedipine, felodipine. Non-dihydropyridines (NDHP): diltiazem, verapamil

29
Q

Calcium channel blockers MOA

A

Cause arterial vasodilation and lower peripheral vascular resistance by blocking L-type calcium channels. Dihydropyridines are selective for blood vessels, while non-DHP bind equally to cardiac (decrease conduction, negative chronotropy and inotropy) and vasculature.

30
Q

Calcium channel blockers side effects

A

DHP: peripheral edema, increased HR, gingival hyperplasia. Non-DHP: constipation, bradycardia, nausea

31
Q

Calcium channel blocker uses

A

DHP: HTN (african americans and elderly), migraine prophylaxis. Non-DHP: angina, rate control for atrial fibrillation, migraine prophylaxis, HTN

32
Q

Calcium channel blockers drug interactions

A

DHP and non-DHP to a small extent, are inhibitors of CYP450 3A4 and caution should be used with statins, immunosuppressants, warfarin, grapefruit juice.

33
Q

Beta blocker examples

A

Selective beta 1 (cardio) receptor blockers: atenolol, metoprolol. Non-selective beta 1 and beta 2 (located in bronchial and vascular system) blockers: propranolol, timolol. Beta and alpha blocker: carvedilol, labetalol

34
Q

Beta blocker MOA

A

Beta-1 selective beta-adrenergic receptor blocking agents compete with catecholamines at peripheral adrenergic neuron sites, block cardiac receptors to decrease cardiac output, and suppress renin activity

35
Q

Beta blocker side effects

A

•decrease libido, bradycardia, bronchospasm, glucose/lipid changes

36
Q

Beta blockers route of elimination

A

metoprolol- renal and hepatic elimination. Atenolol- renal elimination.

37
Q

Beta blocker uses

A

Post MI/CAD (ist line), heart failure, HTN, angina, migraine prophylaxis

38
Q

List direct vasodilators

A

hydralazine, minoxidil

39
Q

Vasodilators MOA

A

–Increase intacellular cGMP > relaxation of arterial smooth muscle > decrease systemic pressure and contractility. This causes increased heart rate, stroke volume and CO. Renin secretion increases causing stimulation of aldosterone and sodium reabsorption

40
Q

Vasodilators side effects

A

•edema, tachycardia, lupus rash (hydralazine), neuropathy, hair growth (minoxidil)

41
Q

List Alpha-1 receptor blockers

A

terazosin, doxazosin, prazosin

42
Q

Alpha-1 receptor blockers MOA

A

Selectively block alpha-1 adrenergic receptors. This causes a reduction in systemic vascular resistance, thus causing an antihypertensive effect. Also decreases urethral resistance and may relieve the obstruction and improve urine flow and BPH symptoms

43
Q

Alpha-1 receptor blockers side effects

A

•: postural hypotension, dizziness, somnolence, nasal congestion/rhinitis, and impotence

44
Q

Alpha-1 receptor blockers uses

A

Benig prostatic hypertrophy

45
Q

Compare relative action on arteries vs veins for direct vasodilators, calcium channel blockers, ACEI, alpha blockers

A

Direct: A»V. CCB: A»V. ACEI: A>V. Alpha blockers: A+V

46
Q

Lis alpha-2 receptor agonists

A

Clonidine, methyldopa

47
Q

Alpha-2 receptor agonist MOA

A

stimulate presynaptic alpha 2 receptor >decrease sympathetic tone > decrease PVR and CO

48
Q

Alpha-2 receptor agonist side effects

A

•dry mouth, depression, lipid abnormalities, sedation

49
Q

Alpha-2 receptor agonist uses

A

Methyldopa is used during pregnancy. Clonidine off label for smoking cessation, ADHD. Both are 3/4th line HTN treatment