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37 Cards in this Set
- Front
- Back
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What is the MOA of alpha-2A agonists?
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inhibit sympathetic outflow from cardiovascular control centers of the brain (the NTS and RVLM) by:
a) inhibiting presynaptic Ca2+ channels -> ↓ NE release **b) opening postsynaptic K+ channels -> K+ efflux -> hyperpolarization Net effect: ↓ peripheral resistance, HR and CO with ↑ vagal tone |
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Guanfacine
Methyldopa Clonidine |
alpha 2A agonists
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CAUTION: Discontinue slowly to avoid rebound sympathetic activity that can lead to a hypertensive crisis, tachycardia or an arrhythmia
SIDE EFFECTS: a) dry mouth b) sedation c) Constipation d) sexual dysfunction in males (interferes w/ ejaculation) |
clonidine
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chronic use can cause a (+) Coomb’s test for autoantibodies vs the Rh locus on RBCs
hemolytic anemia proven safe to use during pregnancy |
methyldopa
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What is the MOA of alpha antagonists?
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↓ BP by inhibiting vasoconstriction, not by causing vasodilation
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What class are drugs that end in "zosin"?
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alpha antagonists
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What is the “1st Dose Effect” caused by alpha antagonists?
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characterized by postural hypotension & syncope
a) 30-90 minutes after the 1st dose b) after a rapid ↑ in dose c) after adding another antihypertensive medication to the regimen MECHANISM: results from delayed baroreflex compensation for the ↓ BP leading to an exaggerated postural hypotension effect & some tachycardia |
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What is the MOA of beta blockers?
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net effect is a ↓ in BP from combined (-) inotropic effects and inhibition of renin release.
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What class of drugs end in "olol" or "alol"
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Beta blockers
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Why should you use caution in diabetics with beta blockers?
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By blocking β receptors, you inhibit glycogenolysis -> ↓ blood sugar.
In diabetics on β blockers, when the next dose of insulin or oral hypoglycemic is due, blood sugar will ↓ even further and the patient can become hypoglycemic. Beta blocker will block tachycardia response normally seen in hypoglycemia MONITOR BLOOD GLUCOSE CAREFULLY! |
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high intrinsic sympathomimetic activity (ISA). It therefore does not decrease BP & HR as much as other β blockers. This can be useful in hypertensive patients with bradycardia
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pindolol
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a) block α1 -> vasodilation -> ↓ BP
b) block β1 -> ↓ HR & BP c) stimulates β2 -> vasodilation -> ↓ BP NET EFFECT: ↓ BP with little or no significant increase in HR |
labetalol
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approved for CHF
rare, but serious hypersensitivity reactions |
carvedilol
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CAUTION if pregnant. Can decrease placental perfusion
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betaxolol
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What are the side effects of beta blockers?
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bradycardia
fatigue-hypokalemia in muscle increased plasma lipids |
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What is the mechanism of Ca channel blockers?
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block L-type Ca2+ channels. On T tubules, this site is sometimes called the DHP receptor (DHP = dihydropyridine)
net effect-decrease afterload |
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What class of drugs end in "dipine"?
Verapamil Diltiazem |
Ca channel blockers
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1. in decreased liver function-hypotensive episodes from excessive vasodilation or cardiodepressant effects
2. In patients with CHF, iIf you add a vasodilator, the heart could go into decompensation 3. Do not take with grapefruit juice-contains furanocoumarins that inhibit the metabolism--> ↑ Rx levels and side effects. |
CAUTIONS FOR Ca2+ CHANNEL BLOCKERS
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What do you know about renin?
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Synthesized in renal J-G cells of afferent arterioles; a drop in arterial presssure stimulates its release; Renin converts angiotensinogen into ANG I. Angiotensin converting enzyme (ACE) converts ANG I into ANG II
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What are the effects of ANG II?
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a) ↑s total peripheral resistance by constricting arterioles and venules.
b) ↑ aldosterone release-->**Increases Na resorption in excahange for K** c) releases ADH-->Retain H2O d) releases NE from sympathetic nerve endings -> potentiation of vasoconstriction by Ang II. e) ↑s sympathetic outflow from CNS f) causes remodeling (proliferation and hypertrophy of vascular smooth muscle and cardiac myocytes) |
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What is the MOA of ACE inhibitors?
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prevents ACE from converting ANG I into ANG II, therefore inhibiting all of the effects of ANG II
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What class of drugs ends in pril?
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ACE inhibitors
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1. 1st dose effect
2. DRY COUGH –Referred to as the bradykinin cough b/c ACEIs ↑ bradykinin levels. Bradykinin is a vasodilator and releases histamine -> fluid accumulation in the lungs 3. HYPERKALEMIA 4. ANGIOEDEMA –Rapid swelling in the nose, throat, mouth, glottis, larynx, lips & tongue. AFRICAN-AMERICANS are at greater risk 5. FETAL TOXICITY – Pregnancy category D: (+) evidence of human fetal risk but benefits might outweigh risks in life-threatening situations |
Side effects of ACE Inhibitors
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What are factors that increase the risk of hyperkalemia?
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a) renal insufficiency
b) adding a K+-sparing diuretic c) K+ supplements d) NSAIDS-inhibit synthesis of PGs--> Na+/H2O retention-->less Na+ is presented to the distal tubules where it is normally exchanged for K+. (By not reabsorbing as much Na+, you are not excreting as much K+ -> hyperkalemia) e) β blockers – inhibits K+ from going into the tissues |
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What drugs enhance ACEI's and why?
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Diuretics enhance natriuresis (Na excretion into urine); ACEIs decrease aldosterone
BETA BLOCKERS-Inhibit renin release (watch for hypokalemia) |
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What is the MOA of Angiotensin II Receptor Blockers (ARBS)?
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Blocking AT-1 receptors; should be more effective that ACEIs b/c Ang II can be synthesized from angiotensinogen by other enzymes
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They are in pregnancy category D
Hyperkalemia-common if decreased renal function or taking K+ sparing diuretics. |
side effects of ARBs
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What class of drugs ends in "sartan"?
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ARBs
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prodrug that's other use is for prophylaxis against migraine
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candesartan
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RENIN INHIBITOR
Given 1x/day. Side effects: diarrhea, cough, rash. Do not use if pregnant |
ALISKIREN
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MOA-Relaxes arteriolar smooth muscle by:
a) ↓ IP3-mediated release of Ca2+ from the SR b) opens ATP-dependent K+ channels (K+ATP) -> hyperpolarization This causes a dramatic increase in sympathetic activity resulting in: a) ↑ HR & contractility b) ↑ plasma renin c) fluid retention from ↑ renin Side effects: Strong baroreflex can cause myocardial ischemia which could precipitate an angina attack Lupus syndrome Symptoms resembling serum sickness |
hydralazine
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hydralazine + isosorbide: Promoted for African-Americans who don’t respond well to β blockers, ACEIs or ARBs.
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BIDIL
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metabolized to nitric oxide in vascular smooth muscle; Dilates arteries and veins. Given by IV infusion. Light sensitive - the IV bag and line must be wrapped in foil.
Onset within 30 seconds. Nitric oxide is metabolized to cyanide which in turn is metabolized to thiocyanate for excretion; accumulation of cyanide or thiocyanate -> toxicity (thiocyanate: nausea, disorientation, spasms, convulsions, psychosis). |
NITROPRUSSIDE
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MOA:
Stimulates dopamine D1 receptors in coronary, renal & mesenteric arteries CAUTION if: a) using with a Beta blocker -> highly increases hypotension b) glaucoma -> increases intraocular pressure c) allergic to sulfas-Contains sulfite |
FENOLDOPAM
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MOA:
Activates K+ channels -> relaxation of vascular smooth muscle. It dilates arteriolar resistance vessels with no significant effect on venous capacitance. It elicits a strong baroreflex increasing in CO, stimulates renin release & causes fluid retention. Side effects: It can flatten & invert T-waves & cause pericardial effusions -> tamponade. Chronic use can cause hypertrichosis (hair growth); used in male pattern baldness |
MINOXIDIL
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Iloprost
Bosentan Epoprostenol Ambrisentan Treprostinil |
Drugs for pulmonary hypertension
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MOA: Antagonist at endothelin-1 (ET-1) receptors ETA & ETB. ET-1 is a powerful vasoconstrictor whose levels in the pulmonary artery are elevated in PAH.
CAUTION: a) liver toxicity b) teratogenic in animals so be careful if pregnant. c) potential to ↓ sperm count. |
BOSENTAN
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