diuretics and anti-HTN meds Flashcards Preview

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Flashcards in diuretics and anti-HTN meds Deck (49):
1

Diuretics that act in proximal tubule

mannitol and acetazolamide

2

Mannitol MOA

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

3

Mannitol uses

elevated intracranial pressure, gluacoma, prevention of acute kidney injury

4

Acetazolamide MOA

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

5

Acetazolamide uses

glaucoma and prevention/treatment of high altitude sickness

6

Diuretics that act at loop of Henle

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

7

Loop diuretics MOA

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

8

Loop diuretics uses

Volume overload, Heart failure, BP reduction, Pulmonary edema

9

Loop diuretics adverse effects

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

10

Diuretics that act at distal convoluted tubule

Thiazide diuretics (HCTZ, chlorthalidone, metolazone)

11

Thiazide diuretics MOA

•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

12

Thiazide diuretics adverse effects

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)

13

compare half lives of chlorothalidone vs HCTZ

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

14

Thiazide altered responses with chronic kidney disease

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

15

Diuretics that act at distal tubule/collecting duct

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

16

Aldosteron antagonists MOA

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.

17

Aldosterone antagonists uses

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

18

Na Channel blockers MOA

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

19

ACE Inhibitors examples

Lisinopril, benazepril, captopril, enalapril, ramipril

20

Angiotensin II actions

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

21

Angiotensin II role in kidney disease

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

ACEI MOA

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

ACEI adverse effects

cough, hyperkalemia, mild increase in serum creatinine, angioedema

24

ARBs examples

Losartan, irbesartan, candesartan, valsartan

25

ARBs MOA

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

26

ARBs adverse effects

hyperkalemia, rise in serum creatinine, angioedema

27

ACEI and ARB uses

HTN, CKD, Heart Failure, Diabetic nephropathy

28

List calcium channel blockers

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

29

Calcium channel blockers MOA

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

Calcium channel blockers side effects

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

31

Calcium channel blocker uses

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

32

Calcium channel blockers drug interactions

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

Beta blocker examples

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

Beta blocker MOA

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

Beta blocker side effects

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

36

Beta blockers route of elimination

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

37

Beta blocker uses

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

38

List direct vasodilators

hydralazine, minoxidil

39

Vasodilators MOA

–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

Vasodilators side effects

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

41

List Alpha-1 receptor blockers

terazosin, doxazosin, prazosin

42

Alpha-1 receptor blockers MOA

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

Alpha-1 receptor blockers side effects

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

44

Alpha-1 receptor blockers uses

Benig prostatic hypertrophy

45

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

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

46

Lis alpha-2 receptor agonists

Clonidine, methyldopa

47

Alpha-2 receptor agonist MOA

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

48

Alpha-2 receptor agonist side effects

•dry mouth, depression, lipid abnormalities, sedation

49

Alpha-2 receptor agonist uses

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