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cardio and antihtn 2

pharm exam 2

QuestionAnswer
beta blockers site of action -Block β1 receptors on the heart leading to ↓ heart rate (HR) & stroke volume (SV) which lowers cardiac output (CO)
beta blockers adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Fatigue -Dizziness -Bronchospasm (avoid in asthma) -Sedation, disturbed sleep, depression -Sexual dysfunction -Avoid abrupt withdrawal due to rebound HTN
beta blockers clinical uses -MI -Chronic stable angina -HF -HTN -many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism)
beta - one selective (cardio selective) (beta blocker) examples Metoprolol tartrate (Lopressor), Metoprolol succinate (Toprol XL), Atenolol (Tenormin), Bisoprolol (Zebeta), Esmolol (Brevibloc)
beta - one selective (cardio selective) (beta blocker) site of action -Block β1 receptors on the heart leading to ↓ heart rate (HR) & stroke volume (SV) which lowers cardiac output (CO)
beta - one selective (cardio selective) (beta blocker) adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Fatigue -Dizziness -Bronchospasm (avoid in asthma) -Sedation, disturbed sleep, depression -Sexual dysfunction -Avoid abrupt withdrawal due to rebound HTN
beta - one selective (cardio selective) (beta blocker) clinical uses -MI -Chronic stable angina -HF -HTN -many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism)
non-selective beta blockers examples Propranolol (Inderal), Timolol, Nadolol
non-selective beta blockers site of action Block β1 and β2 receptors
non-selective beta blockers adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Fatigue -Dizziness -Bronchospasm (avoid in asthma) -Sedation, disturbed sleep, depression -Sexual dysfunction -Avoid abrupt withdrawal due to rebound HTN
non-selective beta blockers clinical uses -MI -Chronic stable angina -HF -HTN -many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism)
non-selective beta blockers with alpha-one antagonism examples Labetalol, Carvedilol (Coreg)
non-selective beta blockers with alpha-one antagonism site of action Block β1 and β2 receptors -Block α-1 receptors on the arteries (vasorelaxation)
non-selective beta blockers with alpha-one antagonism adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Fatigue -Dizziness -Bronchospasm (avoid in asthma) -Sedation, disturbed sleep, depression -Sexual dysfunction -Avoid abrupt withdrawal due to rebound HTN
non-selective beta blockers with alpha-one antagonism clinical uses -MI -Chronic stable angina -HF -HTN -many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism)
cardio-selective beta blockers with nitric oxide (NO)- mediated vasodilation examples Nebivolol (Bystolic)
cardio-selective beta blockers with nitric oxide (NO)- mediated vasodilation site of action --Block β1 receptors -↑ NO effect (vasorelaxation)
cardio-selective beta blockers with nitric oxide (NO)- mediated vasodilation adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Fatigue -Dizziness -Bronchospasm (avoid in asthma) -Sedation, disturbed sleep, depression -Sexual dysfunction -Avoid abrupt withdrawal due to rebound HTN
cardio-selective beta blockers with nitric oxide (NO)- mediated vasodilation clinical uses -MI -Chronic stable angina -HF -HTN -many “off-label” uses (i.e., migraine prophylaxis, essential tremor, anxiety, hyperthyroidism)
ideal beta blocker beta one selective (cardio selective)
beta blockers end in? -lol
what beta blocker is used commonly for HF carvedilol
what happens if you block B2 receptors? risk for bronchospasm
beta blocker effects on BP decreases CO and TPR
alpha receptor blockers examples Prazosin (Minipress), Terazosin (Hytrin), Doxazosin (Cardura),
alpha receptor blockers site of action -Block α-1 receptors on the arteries and veins (vasorelaxation)
alpha receptor blockers adverse effects -First-dose hypotension/ orthostasis -Dizziness
alpha receptor blockers clinical uses -HTN (adjunct) -Benign prostatic hypertrophy
what do alpha receptor blockers end in? -zosin
why do alpha receptor blockers cause first dose hypotension/ orthostasis? baroreceptors can't compensate because receptors are blocked
alpha blockers effects on BP decreased CO and TPR
how do alpha blockers decrease CO blockade of alpha-one receptors in the veins prevents the vasoconstrictive effects of NE released from sympathetic neurons innvervating the veins causing venous dilation-> decreased venous return
how do alpha blockers decrease TPR blockade of alpha-one receptors in the arteries prevents the vasoconstrictive effects of NE released from sympathetic neurons innervating arteries
centrally active agents examples Clonidine (Catapres), Methyldopa
centrally active agents site of action Bind to and stimulate α-2 receptors in the brain (medulla) leading to ↓ sympathetic outflow to body
centrally active agents adverse effects -Sedation -Dry mouth -Sudden withdrawal can lead to hypertensive crisis -Lactation (methyldopa) due to ↑ prolactin
centrally active agents clinical uses -HTN (adjunct/refractory) -many “off-label” uses for clonidine (i.e., analgesic, withdrawal)
where do centrally active agents work? medulla in the brain
how do centrally active agents decrease CO decreased sympathetic tone to veins-> venous dilation-> decreased venous return
how do centrally active agents decrease TPR? decreased sympathetic tone to arteries
calcium channel blockers site of action -Reduce contractile state of vascular smooth muscle cells by binding to L-type calcium channels (vasorelaxation of arteries)
CCBs adverse effects -Peripheral edema -Constipation -↑ HR (reflex tachycardia) -Dizziness
CCBs clinical uses -HTN -Chronic stable angina
dihydropyridines- DHPs (CCBs)- examples Amlodipine (Norvasc), Felodipine, Nifedipine (Procardia, Adalat), Isradipine, Nimodipine
dihydropyridines- DHPs (CCBs) site of action -Reduce contractile state of vascular smooth muscle cells by binding to L-type calcium channels (vasorelaxation of arteries)
dihydropyridines- DHPs (CCBs) adverse effects -Peripheral edema -Constipation -↑ HR (reflex tachycardia) -Dizziness
dihydropyridines- DHPs (CCBs) clinical uses -HTN -Chronic stable angina
non- dihydropyridines- DHPs (CCBs) examples Diltiazem (Cardizem), Verapamil (Calan, Isoptin)
non- dihydropyridines- DHPs (CCBs) site of action In addition to above effect on vasculature, this sub-class also ↓ HR & SV, which lowers CO
non- dihydropyridines- DHPs (CCBs) adverse effects -↓ HR -Heart block (slows AV nodal conduction) -Hypotension -Fatigue -Dizziness
non- dihydropyridines- DHPs (CCBs) clinical uses -Slow heart rate (rate control) in atrial arrhythmias such as Afib -HTN
when to avoid non- dihydropyridines- DHPs (CCBs)? in HF
what do dihydropyridines end in? -ipine
what are non-dihydropyridines used more for? slow HR in atrial arrythmias-> rate control
CCBs all vasodilators, prevent CA from entering cells
CCBs effect on BP decrease TPR- bind to Ca channels, reduce intracellular calcium, reduced contraction
direct acting vasodilators hydralazine, minoxidil
hydralazine site of action -Interferes with release of calcium from the sarcoplasmic reticulum in vascular smooth muscle (arterial vasorelaxation)
hydralazine adverse effects -↑ HR -Rash/lupus-like syndrome
hydralazine clinical uses -HTN (adjunct/refractory) -HF (used with nitrate as an alternative to RAAS inhibitor in certain patients)
minoxidil site of action Binds to and stimulates potassium channels in vascular smooth muscle (arterial vasorelaxation)
minoxidil adverse effects -↑ HR -Hair growth (hypertrichosis)
minoxidil clinical uses -HTN (adjunct/refractory)
when is minoxidil used? when truly refractory HTN
nitrates and nitroprusside examples Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate-release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin - transdermal, sublingual, spray, IV; Sodium nitroprusside - IV
Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate-release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin - transdermal, sublingual, spray, IV- mechanism of action Metabolism leads to intracellular production of nitric oxide (NO) -Venodilator
Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate-release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin - transdermal, sublingual, spray, IV- adverse effects -headache -dizziness -hypotension
Isosorbide mononitrate extended-release (Imdur), isosorbide mononitrate immediate-release (Ismo, Monoket), isosorbide dinitrate (Isordil), nitroglycerin - transdermal, sublingual, spray, IV- clinical uses -CAD (chronic stable angina) -Acute coronary syndrome (ACS)
Sodium nitroprusside - IV mechanism of action -Metabolism leads to intracellular production of NO and cyanide -Potent arterial and venous vasodilator
Sodium nitroprusside - IV- adverse effects -cyanide and thiocyanate toxicity with high doses or prolonged use (confusion, metabolic acidosis, bradycardia, seizures, low oxygen) -hypotension
Sodium nitroprusside - IV- clinical uses Hypertensive emergency
what do you need when receiving sodium nitroprusside? good liver and kidney function to clear out cyanide
Nursing Considerations: Anti-hypertensives Do not discontinue abruptly Monitor BP, weight, edema, labs (BUN, SCr, K+) Positional changes (orthostasis)
Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertension* weight loss, healthy diet, reduced intake of dietary sodium, enhanced intake of dietary potassium
weight loss for htn Best goal is ideal body weight, but aim for at least a 1-kg reduction in body weight for most adults who are overweight. Expect about 1 mm Hg for every 1-kg reduction in body weight.
weight loss approximate impact on sbp htn- -5mmHg normotension- -2/3mmHg
healthy diet for htn Consume a diet rich in fruits, vegetables, whole grains, and low-fat dairy products, with reduced content of saturated and total fat.
healthy diet approximate imapct on sbp htn- -11mmHg normotension- -3mmHg
reduced intake of dietary sodium for htn Optimal goal is <1500 mg/d, but aim for at least a 1000-mg/d reduction in most adults.
reduced intake of dietary sodium impact on sbp htn- -5/6 mmHg normotension- -2/3mmHg
enhanced intake of dietary potassium for htn Aim for 3500–5000 mg/d, preferably by consumption of a diet rich in potassium.
enhanced intake of dietary potassium impact on sbp htn- -4/5mmHg normotension- -2mmHg
what to do for normal BP promote optional lifestyle habits, reassess in 1 year
what to do for elevated BP lifestyle modifications, reassess in 3-6 months
what to do for stage one htn- clinical ASCVD, diabetes, CKD, or 10yr ASCVD risk score >10% lifestyle modifications and medication, if no compelling indication: monotherapy with and ACEi, ARB, CCB, or thiazide; reassess in 1 month
what to do for stage one htn- no clinical ASCVD, diabetes, CKD, or 10yr ASCVD risk score >10% lifestyle modifications, reassess in 3-6 months
what to do for stage 2 hypertension lifestyle modifications and medications; if no compelling indication: two drug combination using an ACEi or ARB with CCB or ACEi or ARB with thiazide, reassess in 1 month
treatment HF rEF ACEi or ARB then add beta blocker, diuretic to control edema
treatment HFpEF beta blocker, or ACEi or ARB, diuretic if edema present
treatment stable ischemic heart disease beta blocker, then add ACEi or ARB- can add on CCB if angina, thiazide or mineralcorticoid receptor agonist
treatment DM ACEi, ARB, CCB, or thiazide
treatment ckd ACEi or ARB
treatment secondary stroke prevention thiazide or thiazide with ACEi
Created by: camrynfoster
 

 



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