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pharm
HTN diuretics
| Question | Answer |
|---|---|
| HTN | BP >130/80 mmHg, or receiving antihypertensive therapy |
| prevalence of HTN | 45-50% of US adults ( around 115 million) |
| how many adults have their BP controlled | <25% (<130/80 mmHg) |
| BP calculation | BP= CO x TPR (total peripheral resistence) |
| primary HTN | unknown cause, referred to as essential HTN >90% of HTN dx |
| possible cause of primary HTN | many theories of structure, neural, or hormonal factors genetic basis: likely multiple genes sodium balance or other BP regulating pathways |
| secondary HTN | comorbid condition or drug induced 10% of HTN remove or treat cause |
| most common cause of secondary HTN | renal dysfunction from severe CKD or renovascular disease |
| drugs associated with HTN | vasoconstrictors abruptly stopping meds |
| Normal BP | <120/<80 |
| elevated | 120-129 / <80 |
| stage 1 | 130-139 / 80-89 |
| stage 2 | >140/ |
| cardiovascular risk pearls | starting BP at 115/75, risk doubles with every 20/10 increase SBP increases are stronger predictors in adults >50yo |
| why control BP? | stroke death by 50-60 % CAD related death by 40-50% heart failure by 50% |
| isolated systolic hypertension | SBP >130 mmHg and normal DBP |
| wider pulse pressure reflects | extent of atherosclerotic disease and arterial stiffness |
| diuretics | loop* thiazide* potassium-sparing* carbonic anhydrase inhibitors * most often used* |
| aldosterone binds to what | mineralocorticoid receptor, making Na channels available body holds onto Na (and water) |
| blocking aldosterone | leads to fewer channels, less Na+ absorbed, and then K+ is not eliminated in exchange (ex:spironolactone) |
| Loop diuretics examples | furosemide, bumetanide, torsemide, ethacrynic acid |
| loop diuretics- site of action | thick ascending loop of henley blocks Na+/K+/2Cl- transporter |
| loop diuretics- adverse effect | decreases K+ and Na+ (may need to take K) dehydration hypotension (check for dizziness) uric acid (gout) |
| loop diuretics- clinical uses | heart failure or other conditions with volume overload |
| thiazide diuretics examples | hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide, Metolazone |
| thiazide diuretics- site of action | distal convoluted tubule blocks Na+/Cl- transporter doesn't move fluid out as quickly |
| thiazide diuretics- adverse effects | decrease in K+ and decrease in Na+ dehydration hypotension increase uric acid (gout) |
| thiazide diuretics- clinical used | HTN in combination with other classes (ex: K+ sparing diuretic), adjunct to loop diuretic for HF |
| potassium sparing diuretics- site of action | collecting duct |
| potassium sparing diuretics- adverse effects | increased K+ and decreased Na+ |
| potassium sparing diuretics- clinical used | myocardial infarction (MI) HF HTN in combo with other classes |
| aldosterone antagonist diuretics- examples | spironolactone, eplerenone, finerenone |
| aldosterone antagonist diuretics- site of action | prevent aldosterone from causing Na+ reabsorption by binding to mineralocorticoid receptor |
| aldosterone antagonist diuretics- adverse effects | increased K+ and decreased Na+ androgenic effects with spironolactone due to non-selectivity of effect |
| aldosterone antagonist diuretics- clinical uses | myocardial infarction (MI) HF HTN in combo with other classes chronic kidney disease/diabetes (finerenone) primary aldosteronism; acne (spironolactone) |
| sodium blockers diuretics- examples | amiloride, triamterene *combination with HCTZ (dyazide, maxzide) |
| sodium blockers diuretics- site of action | inhibits epithelial Na+ channels |
| sodium blockers diuretics- adverse effects | increased K+ and decreased Na+ |
| sodium blockers diuretics- clinical uses | HTN in combination with thiazide diuretics |
| carbonic anhydrase inhibitor diuretics- examples | acetazolamide, dorzolamide |
| carbonic anhydrase inhibitor diuretics- site of action | inhibit carbonic anhydrase in the proximal tubule |
| carbonic anhydrase inhibitor diuretics- adverse effects | decrease Na+, decrease HCO3- dehydration hypotension increased uric acid (gout) |
| carbonic anhydrase inhibitor diuretics- clinical uses | glaucoma (decrease in intraocular pressure) acute mountain sickness metabolic alkalosis |
| other agents with diuretic-like properteries | sodium glucose co-transporter 2 inhibitors (SGLT2i) not a diuretic but same effect work in the proximal tubule prevent reabsorbtion of glucose, salt, and water |
| SGLT2 inhibitors examples | dapagliflozin empagliflozin |
| SGLT2 inhibitors site of action | inhibits SGLT2i in proximal tubule |
| SGLT2 inhibitors adverse effects | UTI, genital yeast infection dehydration hypoglycemia diabetic ketoacidosis (rare) (T1DM) |
| SGLT2 inhibitors clinical uses | HF diabetes mellitus (DM) |
| diuretic effects of BP- dec ECF | decreased amount of ECF volume is inverse with urine volume |
| diuretic effects of BP- volume loss | volume loss = RAAS system activated to increase BP |
| renin-angiotensin-aldosterone system (RAAS) | angiotensinogen -> renin -> angiotensin I -> ACE ->angiotensin II ->aldosterone release and vasoconstriction -> Na reabsorption, increased blood volume, and INC BP |
| ACE inhibitors | stop the conversion of angiotensin I to angiotensin II '-pril' |
| ACE inhibitors examples | captopril, benazepril, enalapril, fosinopril,lisinopril, moexipril, quinapril, ramipril |
| ACE inhibitors mechanism of action | bind to and inhibit ACE and prevent formation of angiotensin II from angiotensin I |
| ACE inhibitors adverse effects | increased K increase serum creatinine; caution w advanced CKD and AKI cough decreased BP angioedema (rare) |
| ACE inhibitors clinical uses | HTN HF MI CKD with or without DM (can use with stable CKD, not advanced) |
| angiotensin receptors blockers (ARBs)- examples | Losartan, Candesartan, Eprosartan, Irbeesartan, Telmisartan, Valsartan, Olmesartan, Azilsartan |
| angiotensin receptors blockers (ARBs)- mechanism of action | bind to and inhibit angiotensin II from binding to its receptor |
| angiotensin receptors blockers (ARBs)- adverse effects | increased potassium increase serum creatinine, caution with advanced CKD and avoid AKI decreased BP |
| angiotensin receptors blockers (ARBs)- clinical uses | HTN HF MI CKD (with or without DM) *often used as an alternative to an ACEi in patients who experience cough or angioedema |
| direct renal inhibitor- example | Aliskiren |
| direct renal inhibitor- mechanism of action | bind to and inhibit renin from binding to angiotensinogen |
| direct renal inhibitor- adverse effects | increased potassium increased creatinine, caution with advanced CKD and avoid AKI decreased BP |
| direct renal inhibitor- clinical uses | HTN only |
| angiotensin receptor-Neprilysin inhibitor (ARNi)- examples | sacubitril |
| angiotensin receptor-Neprilysin inhibitor (ARNi)- mechanism of action | -angiotensin receptor-Neprilysin inhibitor -ARB (valsartan) with a neprilysin inhibitor (sacubitril) -Neprilysin is an enzyme that degrades vasoactive peptides -Sacubitril leads to increased in important vasodilators (but also some vasoconstricts) |
| angiotensin receptor-Neprilysin inhibitor (ARNi)- adverse effects | increased potassium inreased creatinine, caution with advanced CKD and avoid AKI decreased BP cough angioedema (rare) |
| RAAS inhibitors effects on BP | all lower BP. vasodilators. block aldosterone, less Na and water reabsorbed |
| beta blockers suffix | '-lol' |
| beta one selective (cardio-selective)- examples | metoprolol tartrate, metoprolol succinate, atenolol, bisoprolol, esmolol |
| beta one selective (cardio-selective)- site of action | block B1 receptors on heart leading to decrease HR and SV which lowers CO |
| beta one non-selective- examples | propanolol, timolol, nadolol |
| beta one non-selective- site of action | blocks B1 and B2 receptors |
| non selective with alpha 1 antagonism- examples | labetalol, carvedilol |
| non selective with alpha 1 antagonism- site of action | blocks B1 and B2 receptors block A1 receptors on the arteries (vasorelaxation) |
| cardio-selective with nitric oxide (NO)- mediated vasodilation examples | nebivolol |
| cardio-selective with nitric oxide (NO)- mediated vasodilation site of action | block B1 receptors increased No effects (vasorelaxation) |
| beta blockers adverse effects | decreased HR heart block (slows AV node conduction) fatigue dizziness bronchospasm (avoid w asthma) sedation, disturbed sleep, depression sexual dysfunction avoid abrupt withdrawal due to rebound HTN (need time to replenish beta blockers) |
| beta blockers clinical uses | MI chronic stable angina HF HTN many "off label" uses (migraine, tremors, anxiety, hyperthyroidism) |
| Alpha receptor blockers suffix | '-zosin' |
| alpha receptor blockers examples | prazosin, terazosin, doxazosin |
| alpha receptor blockers site of action | block alpha 1 receptors on the arteries and veins (vasorelaxation) |
| alpha receptor blockers - adverse effects | first does hypotension/ orthostasis dizziness |
| alpha receptor blockers - clinical uses | HTN (adjunct) benign prostatic hypertrophy (men w enlarged prostate) |
| centrally active agents- examples | clonidine, methyldopa alpha 2, decrease adrenalin out of the brain |
| centrally active agents- site of action | bind to and stimulate alpha 2 receptors in the brain (medulla) leading to decreased sympathetic outflow to body |
| centrally active agents- adverse effects | sedation dry mouth sudden withdrawal can lead to hypertensive crisis lactation (methyldopa) due to increased prolactin |
| centrally active agents- clinical uses | HTN (adjunct/refractory) many "off-label" uses for clonidine (ex analgesics, withdrawal) |
| calcium channel blockers (CCBs): Dihydropyridines (DHPs) examples | amlodipine, felopdipine, nifedipine, isradipine, nimodipine (-dipine) |
| calcium channel blockers (CCBs): Dihydropyridines (DHPs) site of action | reduce contractile state of vascular smooth muscle cells binding to L-type calcium channels (vasorelaxation of arterioles) |
| calcium channel blockers (CCBs): Dihydropyridines (DHPs) adverse effects | peripheral edema constipation increased HR (reflex tachycardia) dizziness |
| calcium channel blockers (CCBs): Dihydropyridines (DHPs) clinical uses | HTN chronic stable angina |
| calcium channel blockers (CCBs): NON-Dihydropyridines (non-DHPs) examples | Diltiazem, verapamil |
| calcium channel blockers (CCBs): NON-Dihydropyridines (non-DHPs) site of action | -reduce contractile state of vascular smooth muscle cells binding to L-type calcium channels (vasorelaxation of arterioles) -this sub-class also decreases HR and SV, which lowers CO |
| calcium channel blockers (CCBs): NON-Dihydropyridines (non-DHPs) adverse effects | decreased HR heart block (slows AV nodal conduction) hypotension fatigue dizziness |
| calcium channel blockers (CCBs): NON-Dihydropyridines (non-DHPs) clinical uses | slows heart rate in atrial arrythmias such as Afib HTN *avoid in HF* |
| calcium channel blockers (CCBs) are | ALL vasodilators prevents Ca from entering the cell |
| direct acting vasodilators | hydralazine, minoxidil |
| hydralazine site of action | interferes with the release of calcium from the sarcoplasmic reticulum in vascular smooth muscle (arterial vasorelaxation) |
| hydralazine adverse effects | Increased HR rash/ lupus-like syndrome: joint pain, butterfly rash |
| hydralazine clinical uses | HTN (adjunct/ refractory) HF (used as an alternative to RAAS inhibitor in certain pts) |
| minoxidil site of action | binds to and stimulates potassium channels in vascular smooth muscle (arterial vasorelaxation) |
| minoxidil adverse effects | increased HR hair grow (hypertrichosis) |
| minoxidil clinical uses | HTN (adjunct/ refractory) |
| nitrates: examples | isosorbide mononitrate ER, isosorbide mononitrate IR, isosorbide dinitrate, nitroglycerin (MI, unstable angina) transdermal, sublingual, spray, IV |
| nitrates: mechanism of action | metabolism leads to intracellular production of nitric oxide (NO) venodilator |
| nitrates adverse effects | headaches dizziness hypotension |
| nitrates clinical uses | CAD (chronic stable angina) acute coronary syndrome (ACS) |
| nitroprussides example | sodium nitroprusside IV |
| nitroprusside- sodium nitroprusside mechanism of action | metabolism lads to intracellular production of NO and cyanide potent arterial and venous vasodilator |
| nitroprusside- sodium nitroprusside adverse effects | -cyanide and thiocyanate toxicity with high doses or prolonged use (confusion, metabolic acidosis, bradycardia, seizures, low O2) -hypotension |
| nitroprusside- sodium nitroprusside clinical uses | hypertensive emergency |
| nursing considerations for anti-hypertensives: | do not abruptly discontinue monitor BP, weight, edema, labs (BUN, Cr, K+) positional changes (orthostasis) |
| best proven non-pharmalogical ways to prevent and treat HTN | weight loss, healthy diet, reduced sodium intake, enhanced intake of dietary potassium |
| Tx for stage 1 HTN | ACEi, ARB, OR thiazide diuretic only one |
| Tx for stage 2 HTN | two drug combo ACEi or ARB with CCB ...or... ACEi or ARB with thiazide diuretic |
| why dont we give ACEi and ARB together | they do the same thing |
| Tx of HF with reduced ejection fraction (HFrEF) standard pharmacotherapy (first line) | ACEi or ARB then add beta blocker; diuretic to control edema |
| Tx of HF with reduced ejection fraction (HFrEF) add-on after standard pharmacotherapy | mineralocorticoid receptor antagonist |
| Tx of HF with preserves ejection fraction (HFpEF) | beta blocker or ACEi or ARB; diuretic if edema is present |
| Tx of stable ischemic heard disease standard pharmacotherapy (first line) | beta-blocker, then add ACEi or ARB |
| Tx of stable ischemic heard disease add-on after standard pharmacotherapy | CCB (if angina) thiazide or mineralocorticoid receptor antagonist |
| Tx of diabetes mellitus | ACEi, ARB, CCB, or thiazide |
| Tx of CKD | ACEi or ARB |
| Tx of secondary stroke prevention | thiazide or thiazide with ACEi |
Created by:
ago24