MOD 6 part 1 Flashcards
Ace-Inhibitors
-e.g. Lisinopril
-MOA: Reducing levels of angiotensin II (through inhibition of ACE) and increase levels of bradykinin (through inhibition of kinase II)
-Block production of angiotensin II
-Indications: Treat HTN, HF, diabetic nephropathy, MI
-Adverse Effects: cough, angioedema, first dose hypotension, hyperkalemia, renal failure
-Do not use in 2nd + 3rd trimesters can cause fetal injury
-Monitor BP + renal function
-Evidence shows decrease in cardiovascular morbidity and mortality
Angiotensin II Receptor Blockers (ARBS)
-e.g. Losartan (approved for diabetic nephropathy in pts w/ type II DM)
-8 ARBS approved for HTN, Losartan and Candesartan are approved for HF; these meds should be reserved for patients who do not tolerate ACEI d/t limited availability
-MOA: block action of Angiotensin II–>cause dilation of arterioles and veins. Heart prevents angiotensin II from inducing pathologic changes in cardiac structure. Adrenals decrease release of aldosterone and can increase renal excretion of sodium and water.
-DO NOT inhibit kinase II and DO NOT increase bradykinin in the lung (low risk for cough)
-Indications: Treatment for HTN, HF, diabetic nephropathy. Prevention of MI, stroke, death in people at high risk for cardiac events
-Side effects: hypotension if given w/ other antihypertensives, dose adjustment may be needed
-Well tolerated, but like ACEI can cause angioedema-withdraw ARBS–severe cases treated w/ subcu epi
-Monitor in renal failure
-Low risk for hyperkalemia/cough
-ACEI prefered over ARBS, but if pt can’t tolerate ACEI, ARBS are 2nd choice.
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Beta Blockers
Indications (cardiac): HF through decreasing contractility and when added w/ other therapy can improve LV EF, angina pectoris, HTN, cardiac dysrhythmias, MI
MOA: bloackade of beta 1 receptors in heart leads to decrease HR, reduced force of contraction, and reduced velocity through the AV node
Adverse effects: bradycardia, reduced cardiac output, precipitation of HF, AV heart block, rebound cardiac excitation
-Most adverse effects are actually caused by nonselective beat adrenergic receptor blockade, not the cardioselective beta blocker
Loop Diuretics
-Most effective diuretics available
-E.g. Furosemide-prevents passive resorption of water
-Adverse effects: dehydration, hyponatremia, hypokalemia, hypotension, ototoxicity
-All loop diuretics can cause profound diuresis w/ water and electrolyte depletion: hypovolemia or severe dehydration
-Thiazide diuretics: Hydrochlorothiazide (moderate diuresis) Only used with minimum edema
-Potassium sparing diuretics: Sprionolactone
Ca channel Blockers
E.g. verapamil, diltiazem, nifedipine
-drugs that prevent calcium ions from entering blood vessels and heart
-Therapeutic uses: angina pectoris, HTN, cardiac dysrhythmias
Adverse effects: constipation, dizziness, facial flushing, headache, edema of ankles and feet
Interacts w/ grapefruit juice, beta blockers, digoxin
Can cause chronic eczematous rash in elderly
Cardizem
Digoxin
-increase myocardial contractile force and cardiac output
-neurohormonal benefits
Indications: positive inotrope, 2nd line for CHF
Actions: Inhibits enzyme sodium-potassium adenosine triphosphate, calcium accumulation within monocytes causing increase contractile force
-Adverse effects: dysrhythmias, anorexia, N/V, fatigue, visual disturbances (yellow tinge, halos around dark objects).
-Use with caution d/t toxicity risk
-Goal range .5-.8 mg/ml
Discuss the RASS system as it relates to regulation of blood pressure
-RASS supports arterial pressure by causing:
1) constriction of arterioles and veins and retention of water by kidneys
2) vasoconstriction is mediated by a hormone (angiotensin II)
-Vasoconstriction happens within minutes-hours of activating the system, hence can raise blood pressure quickly
What pathologic effects does Angiotensin II have on the body
-Angiotensin II participates in all processes regulated by RASS
-Prominent actions: vasoconstriction + stimulation of aldosterone release (both actions raise BP)
-Angiotensin II can act on the heart and blood vessels to cause pathogenic changes in their structure and function
Identify first line agents in treating HTN. How do these differ based on race
Pharmacological
Diuretics- first choice in african americans
Vasodilators
CCB-effects for african americans
aldosterone antagonist
ACE/ARB-beta blockers and ACEI used w/ comorbidities. Monotherapy w/ beta blockers is less effective
Non pharm
-First recommend lifestyle modifications then if no improvement start single drug
-if inadequate response or poorly tolerated, then add or transition to a new agent
-lifestyle modifications: exercise, dietary changes, weight loss, low Na diet
How does hydralazine work.
Vasodilator-acts directly on smooth muscle in arterioles and veins to produce vessel relaxation
-Readily absorbed after oral admin
-used in treatment of HTN (used in combo w. beta blockers)
-Adverse effects: postural hypotension
Role of Atrial Natriuretic peptide in blood pressure regulation
-promote arteriole and vein dilation
-promote loss of Na and water via kidneys
-helps balance vasoconstriction by SNS and angiotensin II caused by RAAS, but eventually become overwhelmed as CHF progresses
-lower is better outcomes
-an increase in ANP/BNP leads to decresed blood pressure, natriuresis, and diuresis
