Pharm. Cardio
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| Things that determine O2 demand | heart rate, myocardial contractility, intramyocardial wall tension (preload and afterload)
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| Things that determine O2 supply | myocardial blood flow (can increase flow or increase blood oxygen content- Hgb)
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| 2 Goals of drug therapy for angina | 1) Prevention of MI and death
2) Prevention of ischemia and pain
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| Drugs used to prevent MI and death for angina patients (CV prophylaxis) | antilipemics and antiplatelets, ACE inhibitors
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| Drugs used to prevent ischemia and pain for angina patients | nitrates, beta blockers, calcium channel blockers
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| Stable angina | usually triggered by physical activity, emotional excitement, large meal, cold exposure. CAD is underlying cause; partial obstruction (>70%) deposition of fatty plaque in arterial wall. coronary arteries cant dilate during exertion b/c of plaque.
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| Therapy for Stable Angina | Reduce oxygen demand by decreasing HR, contractility, afterload and preload. 1) Organic Nitrates 2) Beta Blockers 3) Calcium Channel blockers 4) Renolazine (Ranexa)
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| Ranolazine (Ranexa) | blocks late sodiun (and K+ and Ca2+), weak alpha and beta antagonist activity (antiarrythmic qualities), increases exercise performance and reduces angina frequency
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| Adverse effects of Ranolazine (Ranexa) | prolongs QT interval
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| Unstable Angina | medical emergency! Angina at rest, ne onset exertional angina, intensification of existing angina. Plaque rupture leads to platelet aggregation and thrombus formation = severe stenosis
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| treatment of unstable angina | anti-ischemic therapy AND antiplatelet therapy AND anticoagulant therapy
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| Antiischemic therapy for unstable angina | (NTG, betablocker, supplemental O2, IV morphine sulfate)
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| antiplatelet therapy for unstable angina | aspirin, clopidogrel (Plavix), GP IIb-IIa antagonists (abciximab, integrilin, aggrastat)
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| anticoagulant therapy for unstable angina | heparin or LMWH
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| Variant Angina (prinzmetals/vasospastic) | caused by coronary artery spasm; pain not exertion related
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| treatment of variant angina | calcium channel blockers and nitrates
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| CABG | more expensive than PCI, longer hospital stay, slower recovery but better coronary blood flow, angina relief, exercise tolerance. Should consider for multivessel disease
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| PCI | usually balloon angioplasty- higher initial reperfusion, less residual stenosis, lower reccurence rates, no intracranial bleeding. Use heparin, antiplatelets, for adjuncts
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| 3 major vasodilator classes | ACE inhibitors/ARBs, nitrates, Calcium Channel Blockers
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| Adverse effects of vasodilators | postural hypotension, reflex tachycardia, increase blood volume??
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| Nitrates (Nitroglycerin)- MOA | in endothelium, NTG is denitrated and nitric oxide is released. NO stimulates guanylyl cyclase to produce cGMP, dephosphorylation of myosin, relaxation of vascular smooth muscle and vasodilation
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| Nitroglycerin for use during stable angina | decreases oxygen demand by reducing preload - primary effect is on VEINS
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| Nitroglycerin for use during variant angina | increases cardiac O2 supply by dilating arterioles
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| Adverse effects of nitroglycerin | secondary to vasodilation: headache, orthostatic hypotension, reflex tachycardia
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| Drug interactions of NTG | other hypotensive drus, especially sildenafil
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| tolerance of nitroglycerin | rapid- within a day complete tolerance or tachyphylaxis can occur
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| prevention of tolerance to NTG | low dose, long acting formulations, intermittent schedule that allows 8 drug free hours every day; can also withhold nitrates for a while
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| sublingual NTG | rapid onset, short duration
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| transmucosal (buccal) tablets of NTG | rapid onset, long duration (3-5 hours)
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| transdermal patches of NTG | slow onset, long duration (24 hr)
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| oral NTG | sustained release, taken q 6-12 h (dont take at night to avoid tolerance)
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| intravenous infusion of NTG | short half life; rarely used for angina, may be used for MI or acute HTN
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| Beta Blockers- MOA | used for stable angina (not effective for variant) reduce angina pain by decreasing O2 demand via blockade of B1 receptors in heart, decreasing HR and contractility. Also decrease arterial pressure (dec. afterload), increase O2 supply
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| adverse effects of beta blockers | bradycardia, AV block, bonchoconstriction, CNS effects (insomnia, bizarre dreams, depression, sexual dysfunction)
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| Calcium channel blockers | decreased calcium influx inhibits smooth muscle contraction in vessel, diltiazem and verapamil also decrease heart rate and contractility [decrease O2 demand by dilating arterioles]--- used to treat variant angina (works on arterioles)
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| calcium channel blockers- dihydropyridines | nifedipine and amlodipine; act on smooth muscle of arterioles, no conduction effects
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| calcium channel blockers- non dihydropyridines | verapamil, diltiazem; act on aretrioles and on heart, lowers HR, decreases AV conduction, decreases force of contraction
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| adverse effects of calcium channel blockers | cardiac depression (arrest, bradycardia, AV block), reflex tachycardia with nifepidine
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| Myocardial Infarction- STEMI | complete interruption of regional blood flow to myocardium, ST elevation. Cell death within 20 minutes, scar formation by 4-6 weeks. Injury triggers ventricular remodeling, which increases risk of heart failure and death- Troponin I/T and CPK-MB
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| 7 drug classes for treatment of MI | oxygen, aspirin, IV morphine sulfate, beta blockers, NTG, ACE inhibitors, thrombolytics
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| Purpose of oxygen therapy in MI tx | increases oxygen supply
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| purpose of aspirin in tx of MI | suppresses platelet aggregation, producing antithrombotic effect
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| purpose of IV MS in tx of MI | for pain, modest arterial and venous dilation so improves preload and afterload to lower oxygen demand
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| purpose of beta blocker in tx of MI | reduce short term mortality rate and infarct size, also long term survival
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| purpose of NTG in tx of MI | does not reduce mortality, but offers hemodynamic properties and relieves pain
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| purpose of ACE inhibitors in tx of MI | decrease short term mortality in MI and decrease long term mortality if reduced LV function
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| purpose of thrombolytics in tx of MI | if present early (3 hours or less after signs and symptoms of MI)
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| Heart Failure | progressive disorder characterized by left ventricular dysfunction, decreased cardiac output, decreased tissue perfusion and s/s of intravascular and interstitial volume overload
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| 4 things the body does to adapt to reduced CO in heart failure | 1) cardiac dilation, 2) increased sympathetic tone, 3) water retention and increased blood volume, 4) natriuretic peptides
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| HF compensation- Cardiac dilation | heart expands, initially improves cardiac output (contractility increases), BUT maximal contractile force of failing heart not enough to drive new muscle mass (causes further decrease in CO)
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| HF compensation- Increased Sympathetic tone | heart failure causes decrease in arterial pressure, so baroreceptor reflex increases sympathetic output to heart and arterioles - increased HR, increased contractility, increased venous tone, increased arteriolar tone
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| problem with increased heart rate during HF | if Hr increases too much, there will be insufficient time for complete ventricular filling and CO will fall
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| problem with increased contractility in HF | increases myocardial oxygen demand
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| problem with increased venous tone in HF | increases venous pressure, which increases ventricular filling, which increases stroke volume, preload. If venous pressure is excessive, blood will back up behind failing ventricle, causing edema.
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| problem with increased arteriolar tone in HF | increased arteriolar pressure increases perfusion of organs, BTU heart must pump against greater resistance
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| HF compensation- Water Retention and Increased blood volume | reduction in renal blood flow and glomerular filtration causes activation of RAA, which promotes water retention.
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| benefits of water retention and increased blood volume in HF | increased blood volume increases venous pressure and venous return- ventricular filling increases and SV increases. increases CO and tissue perfusion
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| harms of water retention and increased blood volume | increased blood volume= increased venous pressure= blood back up and edema
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| HF compensation- Natriuetic Peptides | in response to stretching of fibers and dilation, heart releases atrial natriuetic peptide and B natriuetic peptide to promote dilation of arterioles and veins and to promote loss of Na+ and H20 to counterbalance SNS and RAA effects
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| 5 drug classes for treatment of heart failure | 1) diuretics 2) ACE inhibitors 3) aldosterone antagonists 4) Beta blockers 5) Digoxin
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| Diuretics for HF | reduce blood volume, decrease arterial pressure (preload), edema, cardiac dilation. Thiazides, Loop, and K+ sparing (spironolactone prolongs survival by blocking recpetors for aldosterone)
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| ACE inhibitors for HF | blocks conversion of AT1-AT2. Dilates arterioles and veins and decreases aldosterone release. Dilation counteracts sympathetic outflow, increases CO, and decreases edema. Aldosterone suppression= less sodium and water retention, decreases preload
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| Adverse effects of ACE inhibitors | hypotension, hyperkalemia, dry cough, angioedema
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| aldosterone anatgonists for HF | Spironolactone and Inspra. Reduce symptoms, decreased hospitalizations, prolong life. Block aldosterone receptors: supress cardiac remodeling and fibrosis, prevents SNS activation, prevents vascular fibrosis
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| Beta Blockers for HF | contraindicated until 1990s because they reduce contractilit. Now: can improve LV ejection fraction, increase exercise tolerance, slow progression, decrease hospitalization, and prolong survival
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| Digoxin- MOA | cardiac glycoside, increases contractility and CO by inhibition of Na+/K+ ATPase (sodium potassium pump)
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| Normal Action of the Na+K+ATPase pump | during action potential, Na+ and Ca++ enter the cardiac cell and K+ exits. Following the action potential, Na+K+ATPase pumps Na+ out of cell and takes up K+ to restore ion concentrations. Ca+ leaves the cell in exchange for uptake of Na+
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| Inhibition of Na+K+ATPase by digoxin | digoxin prevents extrusion of Na+ from cell and take up of K+ to restore balance after AP. Na+ accumulates inside cell. Calcium cant be exported outside cell b/c theres too much sodium inside(no way to exchange). Result = increase in calcium concentration
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| Pharmacokinetics fo Digoxin | enterohepatic circulation contributes to long half life (50 hr), but 2/3 excreted unchanged by kidney. Loading dose usually given b/c of long half life. Narrow therapeutic range
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| Electrical Effects of Digoxin | resting membrane potential reduced(less k+ inside due to sodium pump inhibition) eventually leading to premature depolarization. May lead to arrythmia
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| neurohormonal effects | decreased sympathetic tone, increased renal blood flow and urine output, decreased renin release
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| Adverse Effects of Digoxin | arrythmias (caused by hypokalemia), GI, CNS (fatigue, visual disturbances)
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| digoxin- K+ levels | K+ levels must be kept within physiologic range because K+ competes with digoxin for binding to the ATPase. too much K+ interferes with digoxin efficacy and too low K+ can cause dig toxicity
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| Digoxin Toxicity | diarrhea, loss of appetite, nausea, vomiting, headache, visual disturbances, or cardiac dysrhythmia
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| Reversing Digoxin toxicity | IV antidigoxin fab fragments (total neutralization not necessary
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| which classes have been shown to prolong survival in heart failure patients? | ACE Inhibitors, aldosterone antagonists, Beta Blockers
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| Nesiritide (Natrecor)- MOA | recombinant form of BNP (hormone secreted from ventricles in response to inc. volume and pressure overload)- vasodilation via increased cGMP in smooth muscle and decreases venous and arterial tone and diuresis, suppress RAA, suppress sympathetic outflow
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| Nesiritide (Natrecor)- Uses | addition to standard care for decompensated heart failure, more rapid and sustained hemodynamic actions compared to NTG/dobutamine/milrinone; effective IV when patient has dyspnea at rest
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| sildenafil- MOA | inhibits breakdown of cGMP by phosphodiesterase (5), resulting in vasodilation.Relaxation of smooth muscle of corpus cavernosa, fills with blood= erection. NO/nitrates activate guanylyl cyclase, increase cGMP and cause vasodilation too- dont take together
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| Arrhythmia | abnormality in site of origin of impulse, its rate or regularity or its conduction
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| refractory period | lenght of time between phase 0 and sufficient recovery of Na+ channels to permit a new propagated response (cell will not respond to stimulus)
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| P wave | atrial depolarization
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| QRS | ventricular depoolarization
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| T wave | ventricular repolarization
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| Phase 0 | rapid rise that represents depolarization following rapid sodium entry into cell
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| Phase 1 | overshoot; early fast repolarization as sodium gates inactivate
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| Phase 2 | plateau; slower calcium current- calcium enters cell and promotes contraction of atrial and ventricular muscle (drugs that reduce calcium entry during phase 2 dont influence cardiac rhythm, but reduce contractility)
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| Phase 3 | repolarization, completion of Na and Ca channel inactivation and increase K permeability (K+ leaves cell)- can be delayed by drugs that block calcium channels(prolongs AP duration and prolongs effective refractory period)
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| Phase 4 | membrane potential may remain stable or membrane can undergo spontaneous depolarization (phase 0 starts, starting new AP= automaticity) - pathological conditions, membrane may depolarize spontaneously and initiate dysrhythmia
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| how do dysrhythmias form? | 1) disturbances in impulse FORMATION (automaticity) and 2) disturbances of impulse CONDUCTION
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| Disturbances of Automaticity | 1) Cell normally capable of automaticity (SA/AV/HIS/ purkinje)produce dysrhytmias if normal rate of discharge changes
2) dysrhythmias occurif tissues that dont normally express automaticity (atria/ventricle muscle) develop spontaneous phase 4 dep.
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| Sinus tachycardia | excessive discharge of sympathetic neurons that innervate the SA node can augment automaticity to such a degree that tachycardia results (inc. sympathetic stimulation= sinus bradycardia)
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| Disturbances of Conduction | AV block, Reentry
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| Atrioventricular Block | impaired conduction through the AV node produces varying degrees of AV block
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| First degree AV block | if impulse conduction is delayed (but not prevented completely)
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| Second degree block | if some impulses pass through the node, but others do not
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| third degree AV block | if all traffic throguht he AV node stops
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| Reentry (Recirculating Activation) | causes dysrhythmias by establishing a localized, self sustaining circuit capable of repetitive cardiac stimulation
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| Normal Conduction | impulses from purkinje fiber stimulates the strip of ventricular muscle in 2 places. Within the muscles, waves of excitation spread from both points of excitation, meet between the purkinje fibers, and cease further travel
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| One Way Block | strip of muscle excited at only one location. impulses spreading from this area meet no impulses from other side, can travel to stimulate other branch of purkinje fiber. Stimulation passes back up fiber, past block, then stimulate first branch again
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| Drugs for One way Block (reentrant conduction) | 1) convert unidirectional block to bidirectional
2) improve conduction in block (eliminate block)
3) increase refractory period
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| 4 antidysrhythmic classes | 1) Sodium Channel Blockade
2) Beta Blockers
3) Action potential blocking agents
4) Calcium Channel Blockers
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| Class IA Antidysrhythmics | Quinidine, Disopyramide, Procainamide
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| Quinidine (class IA)- MOA | blocks sodium channels- slows impulse conduction in atria, ventricles, and HIS/Purkinje system. Also delays repolarization.
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| Quinidine (class IA)- Uses | broad spectrum use against supraventricular and ventricular dysrhythmias. Long term suppression of dysrhythmias
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| Quinidine (Class IA) Adverse Effects | diarrhea, GI upset, cinchonism, cardiotoxicity, arterial embolis,
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| Class 1B antidyrhythmics | Lidocaine
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| Lidocaine (class IB)- MOA | blocks sodium channels and reduces automaticity, accelerates repolarization; no effects on EKG
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| Lidocaine (class IB)- uses | short term treatment of ventricular dysrhythmias, local anesthetic
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| Lidocaine (class IB)- Adverse Effects | generally well tolerated, may cause CNS effects (drowsiness, confusion, paresthesias), toxic doses can cause convulsions and respiratory arrest
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| Class IC Antidyrhythmics | Propafenone (Rhythmol), Flecainide (Tambocor)
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| Class IC (flecainide/propafenone) - MOA | block Na channels and delay ventricular repolarization (increases effective refractory period)
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| Flecainide (uses and warnings) | twofold increase in mortality for asymptomatic ventricular tachycardia after Mi, reserved fro severe refractory ventricular dysrhythmias
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| Class II Antidysrhytmics | Beta Blockers
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| Beta Blockers (Class II) | reduce calcium entry and depress phase 4 depolarization, reduce automaticity, slow conduction velocity, reduce contracitlity
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| Class III Antidyrhythmics | Action Potential Prolonging Agents (AMIODARONE)
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| Amiodarone (Class III)- MOA | K+ channel blocker that delays repolarization, but also blocks inactivated sodium channel and is a weak adrenergic and Ca++ channel blocker
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| Effects of Amiodarone (class III) | slowed HR, AV conduction, QT prolongation
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| Amiodarone (Class III)- uses | highly effective for atrial and ventricular dysrhytmias, only used/approved for refractory life threatening ventricular dysrhythmias
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| Amiodarone (class III)- adverse effects | Pulmonary toxicity, hepatic function must be monitored, corneal microdeposits, photophobia, blurred vision, photosensitivity, blue gray discoloration of the skin, CYP interactions
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| Class IV Antidysrhythmics | Calcium Channel Blockers
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| Effects of Calcium Channel blockers | reduce automaticity in SA node, delay conduction throguh AV node, reduction of myocardial contractility
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| Prodysrhytmics effects | all antidyrhythmic drugs can worsen existing dysrhythmias and generate new ones
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| Supraventricular Dysrhythmias | arise in areas of the heart above the ventricles (atria, SA node, AV node)- includes atrial fibrillation, atrial flutter, sustained supraventricular tachycardia
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| Atrial fibrillation | multiple ectopic foci fire randomly and stimulates a small area of atrial muscle. Highly abnormal atrial rhythm but rapid or normal ventricular rate. Sometime benign
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| Main risk with Atrial fibrillation | STROKE- blood can be trapped in atria, permitting formation of a clot. when normal sinus rhythm is restored, the clot may become dislodged and can travel to brain
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| Treatment goals of Atrial fibrillation | 1) improvement of ventricular pumping
2) prevention of stroke
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| 1) Improvement of ventricular pumping in A Fib | 1) restoring normal sinus rhythm (DC cardioversion, short term tx with drugs, RF ablation of dydrhythmic source)
2) Slowing ventricular Rate: beta blocker, cardioselective CCB
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| 2) Prevention of Stroke in A Fib | Warfarin therapy or new oral agent dabigatrin (pradaxa)
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| What do you treat infrequent episodes of A Fib with? | PRN flecainide or propafenone, "pill in pocket"
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| Atrial Flutter | caused by an ectopic atrial focus discharging at a rate of 250-350 times per minute. Ventricular rate is slower (~150) because AV node cant transmit impulses at such a high rate (creates saw tooth pattern)
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| Treatment of choice for atrial flutter | DC cardioversion
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| Long term therapy of atrial flutter | class IC (flecainide or propafenone) of Class II (amiodarone)
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| Alternatives to cardioversion for atrial flutter | RF ablaiton of focus, ventricular rate control (beta blocker, cardioselective CCB)
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| supraventricular tachycardia | usually caused by an AV nodal reentrant circuit; HR increases to 150-250 bpm
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| Interventions (non pharmacological) for Supraventricular tachycardia | interventions that increase vagal tone= carotid sinus massage or Valsava maneuver). Catheter ablation of focus (transect reentrant circuit)
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| Drugs for Supraventricular tachycardia | IV beta blocker or calcium channel blocker to slow the rate, IV adenosine for paroxysmal SVT
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| Ventricular dysrhythmias | NOT benign, affect cardiac output, common cause of sudden cardiac death, may be paroxysmal
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| sustained ventricular tachycardia | arises from single, rapidly firing ventricular ectopic focus, typically located at the border of an old infarction. Focus drives ventricles at a rate of 150-250 bpm
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| Treatment of choice for ventricular tachycardia | cardioversion
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| What do you give a patient in V Tach if Cardioversion fails? | IV amiodarone (lidocaine and procainamide are alternatives)
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| long term management of Ventricular tachycardia | amiodarone, sotalol OR implantable cardio defibrillator (ICD)
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| Ventricular Fibrillation | asynchronous discharge of multiple ventricular foci- localized twitching all over ventricles. Pumping of heart stops, patient becomes unconscious and cyanotic, death follows if heartbeat is not restored quickly
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| Immediate treatment for Ventricular Fibrillation | electrical countershock (defibrillation)
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| Drugs to enhance effects of defibrillation in V Fib | IV lidocaine, procainamie, bretylium
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| Long term suppression of ventricular fibrillation | amiodarone, ICD
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| Tosades de Pointes | caused by prolonged prolongation of QT interval by a variety of drugs (Class 1A and II)
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| High Risk Patients: LDL goals | has CAD or CAD risk equivalents, 10 year risk >20%. GOAL: <100 mg/dL. DRUG THERAPY if LDL >130
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| Moderate Risk Patients: LDL goals | has 2 or more risk factors, doesn’t have CAD yet, 10 year risk is <10%
o Goal is <130 mg/dL
o Start therapeutic lifestyle changes if 10 year risk 10-20%, or LDL >130
o Start drug therapy if LDL >160
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| Low to Moderate Risk Patients: LDL goals | has 0-1 risk factor
o goal is <160
o TLCs at >160
o Drug therapy at >190
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| Lipoproteins (Chylomicrons) | serve as carriers for transporting triglycerides and cholesterol in blood (hydrophobic core of TG/cholesterol and hydrophilic shell of phospholipids)
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| Apolipoprotein | constitute protein in lipoprotein. Serve as recognition sites for cell receptors and allow cells to bind with and ingest lipoproteins, activate enzymes that metabolize lipoproteins, increase structural stability of lipoproteins
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| Apolipoprotein B-100 | lipoproteins that deliver triglycerides and cholesterol to nonhepatic tissues contain B-100
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| Apolipoprotein A-I | Lipoproteins that transport lipids from nonhepatic tissues to liver contain A-1
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| LDL | contain cholesterol as primary core lipid and account for 70% cholesterol in blood. Deliver cholesterol to nonhepatic tissues(cells use receptor mediated endocytosis by binding to B-100 apolipoprotein)
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| HDL | contain cholesterol as primary core lipis and account for 20-30% of blood cholesterol. carry cholesterol form peripheral tissues back to liver and promote cholesterol removal from blood. Contain apolipoprotein AI and A-II
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| Antilipemic Therapy classes (4) | Statins, Niacin, Fibric Acid Derivatives, Bile Acid binding resins
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| Statins- MOA | competitive inhibition of HMG CoA reductase (enzyme that catalyzes hepatic cholesterol synthesis). Causes hepatocytes to synthesize more LDL receptors so they are able to remove more LDL from blood. Also decrease production of apolipoprotein B-100
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| statins- effects | Raises HDL by 5-22%, Reduce LDL by 25-63%. Promote plaque stability, reduce inflammation, improve endothelial function, enhance dilaiton, lower the risk of AF, reduce risk of thrombosis, increase bone formation
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| Statins- Indications | hypercholesteorlemia, primary and secondary prevention of CV events, post MI therapy, diabetes
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| Statins- drugs | Lovastatin, Simvastatin (prodrugs), Atorvastatin, Fluvastatin, Rosuvastatin - given at night b/c cholesterol biosynthesis is at night, contraindicated in pregnancy and children
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| Statins- Adverse effects | myopathy, rhabdomyolysis, liver injury, CYP3A4 Inhibitors raise statin levels (grapefruit juice)
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| Niacin - MOA | inhibits VLDL production, which decreases LDLs (byproducts of VLDL degradation)
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| Niacin- effects | decreases LDL by 14-17% alone, but 40-60% when combined with a resin. Triple combination of niacin/statin/bile resin can lower LDL by 70% or more. Most effective for increasing HDL (combo with statin raises by 41%)
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| Adverse effects of Niacin | harmless cutaneous vasodilation and headache (flushing of face, neck, ears), Hepatotoxic
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| what should you do to reduce flushing with use of niacin? | pretreatment with aspirin 325 mg or 200 mg ibuprofen. tolerance also helps
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| Fibric Acid Derivatives (Fibrates)- MOA | increase lipolysis via Lipoprotein lipase (LPL) and decrease VLDL secretion
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| Fibric Acid- effects | lower levels of triglycerides by 50% or more, raises HDL, little effect on LDL
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| Fibric Acid Derivatives- drugs | Gemfibrozil, Fenofibrate
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| Fibric Acid Derivatives- Indications | useful in hypertriglyceridemia when VLDL predominates, also useful for increased triglycerides from viral protease inhibitors
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| Fibric Acid derivatives- adverse effects | well tolerated, rash and GI disturbances, can cause gallstones, myopathy, and liver injury
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| Bile Acid Binding Resins- MOA | bind bile acids in intestine and prevent reabsorption and reuse. Liver must increase cholesterol uptake from plasma, so plasma LDL decreases
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| Bile Acid Binding Resins- drugs | Colesevelam (Welchol)- produces 20% reduction in LDL, 50% in combo with statin
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| Bile Acid Binding Resins- indications | hypercholesterolemia
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| Bile Acid Binding Resins- adverse effects | constipation and bloating, interfere with absorption of other drugs (give 1 hr before or 2 hr after resins)
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| Ezetimibe (zetia) | inhibits intestinal absorption of cholesterol, 18% avg. cholesterol reduction, decreases LDL by 25% beyond statin alone (synergistic) --> Vytorin= simvastatin+zetia
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| Fish Oil | omega 3 fatty acids- decrease risk for CHD and thrombotic stroke
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| Lovaza | : contains a combination of EPA and DHA. Approved as adjunct to dietary measures to reduce triglycerides (can decrease by 20-50%)
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