Contraction/conduction and cardiac glycosides Flashcards

Question

ACE inhibitors: - suffix - admin - metabolism - Side effects - DDIs - miscellaneous

Answer 1

* -pril * inhibits ACE * Admin: Oral * except enalaprilat * don't have to have food in system when you take * Metabolism: * excreted renally * Advise to take at night before bed to reduce risk of hypotension and maximize effictiveness * Side effects: * **COUGH** * iron supplement dampens this effect * Angioneurotic edema * more common in african americans * Hyperkalemia * applies to B-blockers, ARBS, DRIs * Acute renal failure in the presence of renal artery stenosis * Skin rash; abnormal taste sensation (iron) * Fetal harm due to exposre to ace inhibitors during 1st trimester * Never use any of the RAAS inhibitors * DDIs: * Diuretics * potassium sparing diuretics * Potassium supplements * Lithium * ACEI can raise lithium levels * NSAIDS * can inhibit antiHTN effects by retention of salt and water * Additional Benefits: * slow the progression of: * diabetes-induced nephropathy (proeinuria\>300mg/day) * diabetes-induced retinopathy _independent of BP lowering bc:_ * __Diabetes causes Increased VEGF * Angiotensin II interacts with VEGF=retinopathy

Answer 2

* ACEIs and ARBS are the drugs of choice to prevent long-term cardiac remodeling * Use DRIs if side effects are not tolerated

Answer 3

* -sartan/artan * MOA: * Angiotensin Type 1 antagonists (AT1 antagonists) * Blocks AT1 receptor * works similar to ACEI but: * ACEIs are decreasing Ang II * Block AT1 receptor where Ang II would bind * Downstream effects: * dilation of arterioles and veins * reduce excretion of K+ * decrease release of aldosterone * Increase renal excreetion of Na+ and Water follows * Do not inhibit ACE * DO not increase levels of Bradykinin * Side effects: * **NO COUGH-biggest advantage over ACEIs** * same as ACEIs * DDIs: * Same as ACEIs * **Losartan (Cozaar**

Answer 4

Direct Renin Inhibitor=Aliskerin * Admin: Oral * MOA: Binds to the active site on renin * No cough * angioedema * NOT 1st line agent * Newer drug and more expensive * use if patient has side effects with angioedema from ARBs & ACEIs

Answer 5

* Aka Calcium channel antagonists * Slow calcium blockers * Calcium entry blockers * Calcium channels * critical role in the function of vascular smooth muscle and heart * 2 main groups * Nodihydropyridines: Verapamil & Diltiazem * acts on both VSM and heart * Dihydropyridines: Nifedipine * act on VSM only * MOA: * prevent calcium ions from entering the cell * greatest effect on heart and blood vessels * effective in low renin HTN * Physiologic fxns and consequences of blockade * VSM * regulate contraction= Decrease sensitivity of constriciton of vessels * CCBs act selectively on arterioles and arters, and arterioles of heart * no significant effect on veins * Heart: * Myocadrium: Ca2+ increases Contractility * inotropy * SA node: Decrease HR * AV node: decrease velocity of conduction * coupling Calcium channels to Beta1-adrenergic receptors * when B1 is activated, calcium influx is increased * Adverse effects: * **Constipation** * dizziness * facial flusing * headache * edema of ankles and feet * heart block-can report a heart attack on ECG * DDI: * Beta-adrenergic blocking agents * synergistic effect * Food * grape fruit juice (anything citrisy) * CYP3A4 * Digoxin * Toxicity: * severe hypotension * Bradycardia and AV block * Ventricular tachydysrhytmias=Fatal heart syndrome

Answer 6

Have same effects: * Reduce force of contraction * slow HR * suppress conduction through AV node **DO NOT GIVE IN COMBO=SYNERGISTIC EFFECT** **-can introduce new arrythmias**

Answer 7

* Type of CCB * Verapamil & Diltizaem * Admin: * oral or IV * Metabolism: Extensive 1st pass metabolism * MOA-act on VSM and heart * blacks Ca2+ channels * Both drugs act like one another=hemodynamic effects * vasodilation * reduced arterial pressure * increased coronary perfusion * Major therapeutic uses * angina pectoralis * essential HTN * cardiac dysrhythmias

Answer 8

Type of CCB * Nifedipine/Amlodipine * -dipine * MOA: Acts on VSM * Blocks Ca2+ channels * Hemodynamic effect * lowers BP * increases HR and contractile force * Therapeutic use: * angina pectoralis * HTN * relieve migraine headache * suppress preterm labor * Adverse effects: * **gingival hyperplasia** * **reflex tachycardia** * DDI * Beta-adernergic blockers (Beta blockers) * **often combined with beta-blocker to reduce** **reflex tachycardia** * **Long-acting Nifedipine reduces reflex tachycardia and is more useful in treating essential HTN than original short-acting**

Answer 9

* Primarily target the alpha 2 receptors (Adrenergic 2) in the CNS * inhibit SNS * CNS receptors: * B1 (Beta 1) * increases SNS activity=vasoconstriction * alpha 2 (a2) * inhibits SNS activity=vasodilation * Outcome: * reduciton in postganglionic nerve activity (NE) and adrenal medulla (NE/E) * leads to a reduction in vascular resistance (BP * Positive and Negative Feedback control of NE release @ sympathetic nerve termina * NE binds A2 and inhibits teh SNS * Negative feedback * NE binds to Beta receptors=Increase SNS activity * positive feedback

Answer 10

Aka Beta Blockers * -olol * Slows HR and Lowers BP * MOA: Block B1 adrenoreceptor (B1 receptor antagonist) * Heart=Reduce CO and HR * Kidney (B1)=reduced renin * CNS: inhibits SNS * BLood Vessels: Enhance endothelial synthesis of DGI2 * Adverse effects: * Adverse lipid profile * can mask or induce diabetes * Hyperglycemia * can mask or induce diabetes * Excessive bradycardia (such as AV block), arrythmyia * combo with CCBs * Hyperkalemia * Fatigue, depression, insomnia, CNS effects * Contraindications: * Asthma * don't use non-cardioselective B-Blcokers * can use cardioselective-hopefully only selects B1 * Diabetes * Peripheral artery disease-challenged by Nebivolol/metoprolol * DDIs: * NSAIDs * K-sparing diuretics * CCBs--\> nonodihydropyridine * can use with Nifediipine * Reasons: * reduced hypotensive actions=inhibits PGI2 produciton * Hyperkalemia * bradycardia * AV block