Exam 4 Pharm Flashcards

Question

Statins

Answer 1

Anti-hyperlipidemics MOA: Competitively inhibits HMG-CoA Reductase leading to decreased endogenous cholesterol synthesis, up regulates expression of LDL-R leading to decreased LDL levels AE: Rhabdomyolosis Do not use w/ Gemfibrozil (competes for OATP2 transporter leading to increase in Statin serum levels and subsequent rhabdomyolysis) Pravastatin is the safest statin b/c dual renal/hepatic elimination. Not dependent on CYP3A4 for elimination like other statins. Cyclosporin is a CYP3A4 inhibitor

Answer 2

Bile-Acid Resins MOA: Inhibit reabsorption of Bile acids in small intestine leading to use of LDL to create more bile acids. More LDL-R and increased LDL clearance AE: Can potential increase VLDL levels, Contraindicated in Type III Dysbetalipoproteinemia and high triglycerides

Answer 3

Cholesterol absorption inhibitor MOA: Decrease dietary and biliary absorption of cholesterol in the small intestine, raises LDL-R Does not raise VLDL levels like bile acid resins

Answer 4

PCSK9-Inhibitors MOA: Inhibit PCSK9, which normally targets LDL-R for lysosomes. Increased LDL-R expression and clearance.

Answer 5

MOA: Increases HDL, decreases VLDL production, Increases VLDL clearance, Decreases risk of thrombosis, Decreases recruitment of monocytes to atherosclerotic lesions, AE: Gout, Peptic ulcer disease, Skin Flushing (prostaglandin mediated, can prevent with NSAIDS, aspirin)

Answer 6

MOA: Decrease VLDL, increase HDL via gene expression change of lipoproteins AE: Do not use Gem with Statins, risk of rhabdomyolysis Contraindicated in severe Renal/Hepatic disease

Answer 7

Viagra | MOA: Phosphodiesterase Inhibitor, prevents degradation of NO

Answer 8

Class 1A Na+-Channel Blocker MOA: Slows AP upstroke and conduction, depresses SA Rate and AV rate, Prolongs QRS, 2nd/3rd choice for Atrial and ventricular arrhythmias, AE: Metabolite (NAPA) can cause torsades des points, hypotension, anti-cholinergic, ganglion-blocking

Answer 9

Class 1A Na+-channel blocker MOA: Same as procainamide AE: Same as procainamide but worst

Answer 10

Class 1 B Na+-channel blocker MOA: Selectively slows conduction in ischemic/infarcted cells V-Tach/V-Fib in the setting of ischemia/infarction (#1 choice) AE: Least cardiotoxic of class 1 drugs, hypotension at high doses, neurologic effects

Answer 11

Class 1 B Na+-channel blocker MOA: Selectively slows conduction in ischemic/infarcted cells V-Tach/V-Fib in the setting of ischemia/infarction, Offlabel chronic pain use AE: Hypotension at high doses, neurologic effects

Answer 12

Class 1C Na+ Channel Blocker MOA: Blocks Na+ and K+ channels Indicated for Supraventricular Arrhythmias in pts w/ healthy hearts AE: mortality in pts w/ other heart problems

Answer 13

Class 1C Na+ Channel Blocker MOA: Blocks Na+ channels, Blocks K+ channels, Weakly blocks B-receptors Indicated for Supraventricular Arrhythmias in pts w/ healthy hearts AE: mortality in pts w/ other heart problems, B-Blockade, sinus bradycardia, bronchospasm, metallic taste

Answer 14

Non-selective B-blocker MOA: blocks sympathetic effects on cardiac electrical activity, slows conduction velocity, slows hr, decreases contractility, depresses SA automaticity, decreases catecholamine-induced DADs and EADs Indicated for recurrent infarction/sudden death after MI, exercised induced arrhythmias, A-Fib/Flutter, AV-nodal re-entry AE: bradycardia, reduced exercise capacity, HF, hypotension, AV-block, bronchospasm, MASKS TACHYCARDIA DUE TO HYPOGLYCEMIA IN DIABETICS. B1 blockers lower HR, B2 blockers lower plasma glucose

Answer 15

Cardio-selective B1 blocker MOA: Blocks symp. effects on cardiac electrical activity: slows conduction velocity, slows HR, decreases contractility, depresses SA automaticity, decreases catecholamine-induced DADs and EADs Indicated for recurrent infarction/sudden death after MI, exercise-induced arrhythmias, A-fib/flutter, AV-nodal re-entry AE: Bradycardia, bronchospasms, hypotension, reduced exercise capacity, heart failure, MASKS TACHYCARDIA DUE TO HYPOGLYCEMIA IN DIABETIC PATIENTS, B1-blockers lower HR, B2-blockers lower plasma glucose,

Answer 16

K+ Channel blocker MOA: Block's outward K+ current, delays depolarization thus prolonging AP, QRS, QT. Also blocks Na+ and Ca2+ channels. Indication: Oral- Recurrent V-tach/Fib IV - Out of hospital: Cardiac Arrest, V-tach/fib More effective at slower HRs AE: Hyperthyroid/Hypothyroid, Bradycardia, Heart Block, Pulm toxicity/fibrosis, Hepatic toxicity, Photodermatitis = blue man, corneal micro-deposits,

Answer 17

K+ channel blocker/ analogous to amiodarone MOA: Blocks K+ Channel, prolonging AP, QRS, QT. Blocks Na+, and Ca2+ channels as well. Indicated: A-Fib More effective at slower HRs AE: bradycardia, heart block, photo dermatitis, corneal micro-deposits. CONTRAINDICATED IN MODERATE-SEVERE CHF due to decreased contractility effects of b-blocking and Ca2+ channel blocking

Answer 18

Non-dihydropyridines Ca2+ Channel blocker, selective for SA/AV slow Ca2+ channels MOA: blocks Ca2+ channels, primarily in slow response tissue. SA/AV nodal tissues. Increases refractoriness, slows down SA automaticity. Slows HR, prolongs PR-interval, Inhibits CA2+ in VSM causing vasodilation Indicated: Supraventricular Arrhythmia (#1 CHOICE!), AV-Re-entry; AV-tachycardia, A-Fib/Flutter, uncomplicated HTN AE: vasodilation, negative inotropic effects, AV-block, constipationg, nervousness, peripheral edema, Bradycardia, transient headaches Contraindicated: Ventricular Tachycardia, LV dysfunction, B-blockers will cause heart block, chronic HTN, patients w/ conduction disturbances

Answer 19

Similar action to Ach MOA: Increases K+-conduction, hyper polarizing cells, inhibits Ca2+-currents slowing conduction. Hyper polarization causes transient cardiac arrest. Decreased atrial contraction, AV-node conduction, Av-node refractoriness. Indicated: Paroxysmal Supraventricular Tachycardia (#1 Choice). Converts to normal sinus rhythm AE: Flushing, Sinus bradycardia, sinus pauses, AV-block, hypotension

Answer 20

Dihydropyridines, CA2+ Channel blocker MOA: Inhibits CA2+ in VSM -> Vasodilation AE: acute Tachy, peripheral edema, transient headache

Answer 21

Vasodilator MOA: Small vessel vasodilation - mainly arterioles Indicated: Drug-resitant HTN AE: Reflex tachycardia via baroreceptors, angi aggravation - reduced venous return, edema

Answer 22

Vasodilator MOA: Small vessel vasodilation - mainly arterioles Indicated: Drug-resitant HTN AE: Reflex tachycardia via baroreceptors, angina aggravation, edema, hypertrichosis

Answer 23

Vasodilator MOA: small vessel vasodilation - mainly arterioles Indicated: EMERGENCIES, causes both venous and arterial dilation AE: CYANIDE POISONING!!, nausea, vomiting, muscle twitch

Answer 24

ACEi MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics AE: Hyperkalemia, dry cough (bradykinin), angioedema Contraindication: pregnancy, bilateral renal artery stenosis Short half life

Answer 25

ACEi MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics AE: Hyperkalemia, dry cough (bradykinin), angioedema Contraindication: pregnancy, bilateral renal artery stenosis Longer half life

Answer 26

ACEi MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics AE: Hyperkalemia, dry cough (bradykinin), angioedema, Contraindication: pregnancy, bilateral renal artery stenosis Longer half life

Answer 27

AT2-Receptor Blocker (ARBs) MOA: Inhibits AT-2, more Na+ secretion, decreased vasoconstriction AE: Hyperkalemia Contraindications: Hyperkalemia, pregnancy, causes fetal renal failure

Answer 28

Thiazide diuretic MOA: Inhibits NaCL-symporter in DCT, vasodilation (via PGs) AE: Metabolic alkalosis, hyponatremia, hypokalemia, Hypercalcemia, hyperglycemia, hyperlipidemia, Contraindicated: Hypokalemia due to K+ wasting, pregnancy

Answer 29

Loop diuretic MOA: Inhibits NAKCL-symporter in TAL, venous dilation via PGs. Most potent diuretic AE: Hyponatremia, hypokalemia, hyperglycemia (impaired diabetes control), hyperlipidemia (^ LDL, ^HDL), metabolic alkalosis, hypomagnesia, hypocalcemia, Ototoxicity

Answer 30

K+ sparing diuretic MOA: Inhibits aldosterone receptor, also blocks DHT receptors AE: Hyperkalemia, gynecomastia (DHT receptor) Never double up on drugs that target RAAS

Answer 31

K+ sparing diuretic, same as spironolactone via adverse effects on testosterone synthesis MOA: Inhibits aldosterone receptor AE: Hyperkalemia Never double up on drugs that target RAAS

Answer 32

K+ sparing diuretic MOA: Inhibits Na channel resorption, lumen more (+) K+ no longer secreted along electrical gradient AE: Hyperkalemia Contraindications: ACEi, AT2 Receptors antags. Never double on RAAS inhibitors

Answer 33

K+ sparing diuretic MOA: Inhibits Na channel resorption, lumen more (+) K+ no longer secreted along electrical gradient AE: Hyperkalemia Contraindications: ACEi, AT2 Receptors antags. Never double on RAAS inhibitors

Answer 34

Sympatholytic MOA: Blocks VMAT (vesicular transport of monoamines) decreased D/NE/E Decreased vasoconstriction, CO, Renin release. AE: Depression, suicide, nasal congestion, sedation Drug interactions: MAO-I, CNS depressants

Answer 35

Sympatholytic MOA: Brain: A2-R agonist -> reduces tonic sympathetics Vessels: A2-R agonist -> early vasoconstriction that goes away Decreased vasoconstriction, CO, renin release AE: Sedation, dy mouth, dermatitis, rebound HTN if withdrawn too fast. Guanfacine was made to have longer half life and limit rebound HTN

Answer 36

Sympatholytic MOA: A2-R agonist -> reduce tonic sympathetics Decreased vasoconstriction, CO, renin release AE: Sedation Drug interactions: Levodopa Contraindicated in liver disease

Answer 37

Non-selective A1-A2-antagonist Used in Pheochromocytoma Effects: A1 block, -> vasoconstriction, A2 block -> decreased sympathetic tone, decreased D/NE/Ea AE: Tachycardia

Answer 38

Selective A1 antagonist blocks vasoconstriction Effects: A1 block, -> vasoconstriction, A2 block -> decreased sympathetic tone, decreased D/NE/Ea AE: Tachycardia, Hypotension (1st dose)

Answer 39

B Non-selective Blocker MOA: decreased cardiac contractility, decreased CO, decreased Renin Propanolol: Adjunct to other vasodilators to prevent tachycardia, lipophilic Nadolol: longer half-life AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics, bronchospasm Contraindicated: Ca2+ channel blockers, cariogenic shock, sinus bradycardia, asthma, severe/uncompensated heart failure

Answer 40

Cardio B1 selective Blockers MOA: decreased cardiac contractility, decreased CO, decreased Renin Atenolol: Hydrophilic, excreted by kidney Metoprolol: Crosses BBB, less side effects AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics

Answer 41

partial antagonist, partial beta blocker Less bradycardia than others MOA: decreased cardiac contractility, decreased CO, decreased Renin AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics,

Answer 42

A/B non selective blockers Lipophilic

Answer 43

A/B non selective blockers Vasodilator Lipophilic

Answer 44

NO Donor Effect on Veins>Arteries Coronaries: Dilate Systemic arteries: Dilate Veins: Dilate Decreasing after load and preload (decreased wall tension decreases O2 demand), decreased venous return allows for better coronary perfusion gradient (***most important mechanism) MOA: NO-mediated vasodilation independent of endothelium Indicated: Stable, unstable, prinzmetal angina, HTN emergencies, CHF AE: Orthostatic hypotension, Reflex tachy, headache, nitrate tolerance

Answer 45

BRAND NEW ANGINA DRUG MOA: Inhibition of FA oxidation increased PDH leading to increased glucose-metabolism, leads to decreased glycolysis, decreased lactate, decreased acidosis, decreased ischemic response

Answer 46

"Funny" Na+ inhibitor Inhibits phase 4 depol MOA: Inhibition of funny NA+ channels, blocks phase 4 depolarization in pacemaker cells Indicated; Stable angina (patients who cannot use B blockers), off label: Sinus Tachy AE: luminous phenomena (everything appears brighter), bradycardia, AV-Block

Exam 4 Pharm Flashcards

(70 cards)