diuretics and anti-HTN meds Flashcards
(49 cards)
Diuretics that act in proximal tubule
mannitol and acetazolamide
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
Mannitol uses
elevated intracranial pressure, gluacoma, prevention of acute kidney injury
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
Acetazolamide uses
glaucoma and prevention/treatment of high altitude sickness
Diuretics that act at loop of Henle
Furosemide(la SIX), bumetanide, torsemide, ethacrynic acid
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
Loop diuretics uses
Volume overload, Heart failure, BP reduction, Pulmonary edema
Loop diuretics adverse effects
Decreased K/Mg, hypocalcemia, precipate gout attack (uric acid retention), metabolic alkalosis, hearing loss
Diuretics that act at distal convoluted tubule
Thiazide diuretics (HCTZ, chlorthalidone, metolazone)
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
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)
compare half lives of chlorothalidone vs HCTZ
Chloro has half life of 40-60 hrs. HCTZ has half life of 2.5hrs
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
Diuretics that act at distal tubule/collecting duct
K sparing diuretics: Aldosterone Antagonist (Spironolactone, eplerenone) and Sodium channel blockers (Triamterene, Amiloride)
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.
Aldosterone antagonists uses
resistant HTN, heart failure, hyperaldosteronism (use with other diuretics to preserve K)
Na Channel blockers MOA
block luminal sodium channels and decrease the driving force for potassium secretion/excretion. Also indirectly decrease hydrogen ion secretion.
ACE Inhibitors examples
Lisinopril, benazepril, captopril, enalapril, ramipril
Angiotensin II actions
vasoconstriction. Salt/water retention, growth stimulation, disease progression
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
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
ACEI adverse effects
cough, hyperkalemia, mild increase in serum creatinine, angioedema
ARBs examples
Losartan, irbesartan, candesartan, valsartan
