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161 Cards in this Set
- Front
- Back
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Digoxin
(Mechanism) |
Method: Na/K ATPase inhibitor --> increased Ca in cells. Sympatholytic, decreased plasma noradrenaline, decreased RAAS activity, increased vagal tone, normalizes arterial baroreceptors. Increased filtering effect on AV node.
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What is secreted by normal endothelial cells?
Injured endothelial cells? |
Normal: PGI2, NO
Injured: Decreased PGI2 and NO, Endothlin increased |
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Digoxin
(Effect) |
Effect: Increased CO (from dec LVEDP, inc. natriuresis), decreased HR.
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Syphilis affects which layer of the vessel wall?
How does this affect the aorta? What is the hallmark of a syphilitic lesion? |
Vaso vasorum in adventitia (endarteritis obliterans) --> marked thickening and narrowing in the lumen of v.v. --> aortic wall becomes ischemic, undergoes necrosis --> collagen replaces dead tissue, no recoil --> aneurysm
Plasma cell inflammation |
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Digoxin
(Adverse reactions) |
ADR: Ventricular arrhythmias, SVT (PAT), heart block & bradyarrhythmias, nausea, vomit, vision
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What gives the inside of the aorta a treebark appearance?
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Syphilis
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Digoxin
(indications and contraindications) |
Indications: CHF w/atrial fib
Contraindications: kidney failure, low K or Mg, diuretics, quinidine, antibiotics, cholestyramine, amiodarone, verapamil |
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What is the histology of Giant Cell Arteritis?
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In temporal artery (and others in head and neck):
Inflammation of all layers. Giant cell reaction to internal elastic lamina |
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Amrinone
(method) |
Phosphodiesterase inhibitor --> inhibits inactivation of cAMP --> increased Ca in --> increased contractility
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What is the pathogenesis of GCA?
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T-cell response to blood vessel antigen, attract macrophages
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Amrinone
(Effect) |
Increased CO (contractility, not HR)
Vasodilates Decreased LA pressure |
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What vessels does Takayasu's Arteritis affect?
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Aortic arch and ostia of branches - thickening
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Amrinone
(Adverse reactions) |
Long-term toxicity
Arrhythmias Thrombocytopenia Abnormal LFTs |
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What disease of the vessels is related to smoking (other than atherosclerosis)?
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Buerger's disease (thromboangiitis obliterans)
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Amrinone
(Indications) |
Short term use in refractory CHF
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What is the pathology of Buerger's Disease?
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Segmental thrombosing inflammation of distal limb arteries, full of neutrophils, granulomatous inflammation.
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Milrinone
(Method) |
Phosphodiesterase inhibitor --> inhibits inactivation of cAMP --> increased Ca in --> increased contractility
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What vessels does Henoch-Schonlein Purpura affect?
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Post-capillary venules
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Milrinone
(Effect) |
Increased CO
Vasodilates Decreased LA pressure |
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What is present in Henoch-Shonlein Purpura lesions?
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Deposition of IgA, fibrin, C3
Nuclear fragments Thrombi Neutrophilsx |
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Milrinone
(ADRs) |
Long term toxicity
Thrombocytopenia Abnormal LFTs Arrhythmias |
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What vasculitis is associated with crescenteric necrotizing glomerulonephritis?
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Henoch-Schonlein Purpura
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Milrinone
(Indications) |
Short term use in refractory CHF
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What are symptoms of HSP?
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Palpable purpura
Arthralgia Abdominal pain Hematuria |
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Milrinone
(compared to dobutamine) |
More effective vasodilator, longer acting, no tolerance buildup.
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What are the symptoms of Polyarteritis Nodosa?
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Fever, weight loss, malaise
Widespread vascular inflammation --> infarcts Leads to renal problems, HTN, hematuria, protinuria, neuropathy, GI bleeding |
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Dobutamine
(Method |
B1 agonist --> increased synthesis of cAMP
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What is the pathology of polyarteritis nodosa?
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Fibrinoid necrosis
Internal elastic lamina is disrupted Aneurysms |
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Dobutamine
(Effect) |
Increased CO, increased HR, decreased LA pressure
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What is the genetic cause of Hereditary hemorrhagic telangiectasia?
What's its other name? |
Endoglin gene mutation --> responses to TGF-B are impaired --> vascular dysplasia
Osler-Weber-Rendu disease |
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Dobutamine
(Adverse reactions) |
Arrhythmias, tolerance buildup.
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Dobutamine
(Indications) |
Short term use in severe CHF
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Dopamine
(Method) |
Low dose --> renal vasodilation
High dose --> B agonist and vasoconstriction |
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Dopamine
(Effect) |
High dose increases CO
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Dopamine
(Adverse reactions) |
Tachycardia
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Dopamine
(Indications) |
Short term use for patients with pulmonary congestion and peripheral hypoperfusion (and poor renal perfusion).
Shock --> increases BP |
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Furosemide
(brand name and method) |
Lasix.
Loop diuretic --> decreased Na and H20 retention |
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Furosemide
(Effect) |
Decreases ventricular preload
Neurohormonal activation (sympathetic and RAAS) |
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Furosemide
(Adverse reactions) |
Increases TG > LDL
Lose K and Mg Azotemia (inc urea in blood) Blood dyscrasia Hyperglycemia Gout Deafness |
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Furosemide
(Indications) |
CHF with volume overload
Do not use as monotherapy. |
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Spironolactone
(Method) |
Aldosterone antagonist
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Spironolactone
(Effect) |
Diuresis with K+ sparing
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Spironolactone
(Adverse reactions) |
Gynecomastia
Hyperkalemia |
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Spironolactone
(Indications) |
CHF with volume overload
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ACE inhibitors
Two names and methods |
Captopril and enalapril
Prevents conversion of Angiotensin I --> II Results in decreased aldosterone, decreased vasoconstriction, decreased cell growth. |
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ACE inhibitors
(Effect) |
Decreased PA pressure, LA pressure, LVEDP.
Decreased systemic vascular resisistance and BP. Increased CO Increased renal, cerebral, and coronary perfusion Increased diuresis and natriuresis Inhibit breakdown of bradykinins --> increased prostaglandin release --> vasodilation |
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ACE inhibitors
(Adverse reactions) |
Cough
Increased K+ Hypotension Angioneurotic edema Renal insufficiency Dysgeusia Neutropenia Thrombocytopenia |
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ACE inhibitors
(indications and contraindications) |
+Congesive heart failure
+Post-AMI +Hypertension -Smoker -Spironolactone (hyperkalemia) -Renal insufficiency |
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Losartan
(Method) |
Binds to angiotensin 1 receptor, inhibiting aldosterone production, vasoconstriction, and cell growth.
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Losartan
(Effect) |
Decreased BP
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Losartan
(Indications) |
Better tolerated than ACE-inhibitors (less cough)
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Nesiritide
(Method) |
Binds to guanylate cyclase receptor of vascular smooth muscle and endothelial cells --> increased intracellular concentrations of cGMP and smooth muscle cell relaxation
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Nesiritide
(Effect) |
Potent, dose-related vasodilation that is rapid in onset and sustained for the duration of drug infusion.
No effects on cardiac contractility |
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Nesiritide
(indications and contraindications) |
Acute treatment of decompensated CHF (elevated PCWP)
Doesn't cause arrhythmias. Don't use with patients w/hypotension or shock, caution with renal insufficiency. |
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Atenolol + Metoprolol
(Mechanism) |
Beta blocker (B1 selective)
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Beta blockers
(Effect) |
Neg. chronotrope
Neg. inotrope Inc. diastole duration Dec. BP (esp for a1 blockers labetalol and carvedilol). Attenuate exercise mediated HR/contractility inc Suppress ventricular arrythmias by prolonging refractory period of AV nodal cells. |
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Beta blockers
(Adverse reactions) |
Bronchospasm
claudication fluid retention sinus bradycardia and AV block Depression, impotence Masks diabetic hypoglycemia |
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Beta blockers
(indications) |
CHF: use ACE-inhib and diuretics first
Anti-arrhythmic - prevent AV nodal reentry, slow ventricular rate during A-fib, prevent V-fib |
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Which beta blocker is safe/effective for CHF?
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Carvedilol
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Propranalol
(mehod) |
Non-selective B-blocker
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Labetalol and Carvedilol
(Method) |
a1 and B blocker --> decrease peripheral resistance
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Hydralazine
(effect) |
Vasodilation of arterioles --> antihypertensive
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Hydralazine
(Adverse effects) |
Tachyphylaxis
Reflex tachycardia and inc. sympathetic tone --> may worsen LVH |
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Hydralazine
(indications) |
CHF (along with isosorbide dinitrate) when ACE inhibitor is contraindicated.
Hypertensive emergency |
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Isosorbide dinitrate
(onset and duration) |
onset: 15-30 min
duration: 3-6 hours |
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Isosorbide mononitrate
(onset and duration) |
onset: 30 min
duration: 6-8 hours |
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Nitrates
(Method) |
Degrade to NO --> activate SMC guanylyl cyclase --> cGMP depohosphorylates myosin light chain --> inactivates myosin-actin interaction
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Nitrates
(Effect) |
Venodilator > arteriodilator
Decrease blood return to heart Attenuate coronary vasospasm Decreased BP Improved collateral blood flow |
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Nitrates
(adverse reactions) |
Headaches
Orthostatic hypotension Reflex tachycardia Tolerance possible |
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Nitrates
(indications) |
CHF w/ischemia and good BP
Angina (esp Prinzmetal's vasospastic) |
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Calcium channel blockers
(method) |
Blockade voltage sensitive L type Ca channel --> reduce Ca influx
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Calcium channel blockers
(effect) |
Arteriodilator > venodilator
Decreased BP Coronary artery dilation Negative inotropy, chronotropy Block conductance at AV and sinus nodes Improve oxygen delivery to the myocardial tissue, decrease total peripheral resistance, decrease systemic blood pressure, and decrease afterload. |
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Calcium channel blockers for SVT
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Verapamil, diltiazem
(more action on AV node) |
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Calcium channel blocker
(Common adverse reactions) |
Headaches
Lower extremity edema |
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Nifedipine
(Adverse reactions) |
Common rxns
Reflex tachycardia, dizziness |
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Nifedipine
(Indications) |
Rarely used due to hypotension
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Amlodipine
(Adverse reactions) |
Well-tolerated
(2nd generation dihydropyridine) |
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What CCB is safest for CHF?
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Amlodipine.
Use when other drugs won't work (persistent high BP and afterload) |
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Diltiazem
(Adverse reactions) |
Excessive sinus bradycardia and AV block.
CHF exacerbation! |
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Diltiazem
(indications, interactions) |
Control ventricular rate in A-fib
Don't use with beta-blocker (hypotension) |
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Verapamil
(Adverse reactions) |
Common + constipation
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Verapamil
(indications and interaction) |
Anti-arrhythmic for SVT (prevents AV nodal re-entry)
Vasospastic angina Don't use with digoxin (raises dig levels) |
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What CCB is a potent negative chronotrope?
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Verapamil
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Fibrinolytics
(method) |
Activate plasminogen into plasmin --> lyse clots
Administer with aspirin and IV heparin |
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Which fibrinolytic is most associated with cerebrovascular accident?
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human t-PA
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Fibrinolytics
(indications and contraindications) |
+Chest pain under 6 hours long
+ECG change (2 consec ST elevations), new LBBB -altered consciousness -internal bleeding or recent trauma/surgery -persistent hypertension -pregnancy -Aortic dissection -Peptic ulcer |
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Name 4 calcium channel blockers
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Nifedipine
Amlodipine Diltiazem Verapamil |
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Name 6 anti-platelet drugs
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Aspirin
Ticlopidine Clopidogrel Abciximab Tirofiban Eptifibatide |
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Aspirin
(Method) |
Irreversible acetylation and inactivation of COX --> no TXA2 --> inactivates platelets
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Aspirin
(adverse reactions) |
GI bleeding
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Aspirin
(indications and contraindications) |
+Secondary prevention of MI
+Stroke prevention in low risk A-fib -surgery coming in a week or less |
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Ticlopidine
(Method) |
ADP receptor antagonist
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Ticlopidine
(Effect) |
Prevents recruitment of circulating platelets
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Ticlopidine
(Adverse reactions) |
Nausea/vomitting, dizziness, gastric irritation
Leukopenia TTP |
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Ticlopidine
(indications) |
Secondary stroke prevention
Post coronary stent Irreversible |
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Clopidogrel
(Method) |
ADP receptor antagonist
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Clopidogrel
(Effect) |
Prevents recruitment of circulating platelets
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Clopidogrel
(Adverse reactions) |
Minimal
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Clopidogrel
(indications) |
Secondary stroke prevention
Post coronary stent |
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Abciximab
(Method) |
Platelet GP IIb/IIIa receptor antagonist
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Abciximab
(Effect) |
Most potent platelet antagonist
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GP IIb/IIIa receptor antagonists adverse reactions
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Excessive bleeding
Allergic reaction Thrombocytopenia |
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GP IIb/IIIa receptor antagonists
(Indications) |
Treatment of acute coronary syndromes
High risk PCTA, stents |
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Abciximab versus tirobfiban/eptifibatide
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Abcix: Longer acting, reversible w/platelet transfusion, must be used with heparin. Binds tightly.
Tiro&Eptif: Shorter acting irreversible until metabolized, fewer side effects. Binds loosely. |
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Tirofiban and eptifibatide
(Method) |
GP IIb/IIIa receptor antagonist
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Warfarin
(Method) |
Blocks carboxylation of clotting factor precursors --> prevents reduction of inactive vitamin K to active KH2
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Warfarin
(effect) |
Takes 2 days
Clotting factors not activated. Proteins C and S synthesis inhibited (these proteins inactivate factor Va, which is necessary for thrombosis) |
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Warfarin
(Adverse reactions) |
Bleeding w/long term therapy
Teratogenic Hemorrhagic skin necrosis for Protein C and S deficient pts Alcohol can cause over-anticoagulation |
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Warfarin
(indications) |
Mechanical heart valve prosthesis
Atrial fib in high risk (> 65) DVT Recent anterior wall MI |
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Heparin
(method) |
binds/activates antithrombin III
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Heparin
(effect) |
inhibited thrombin and Xa
Enhanced Tissue Factor Pathway Inhibitor activity |
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Heparin
(adverse reactions) |
Bleeding
Osteoporosis (long term) Rebound hypercoagulable period Heparin induced thrombocytopenia (diffuse thrombosis caused by activated platelets) Alopecia Thromboembolic disease LMWH has less non-specific protein binding --> more reliable, doesn't have to be monitored. |
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Heparin
(indications) |
Initiation of warfarin
Acute coronary syndromes Acute MI Catheterization, surgery |
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Cholestyramine
(method) |
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
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Colestipol
(Method) |
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
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Colesevelam
(Method) |
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
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Bile acid sequestrant
(Effect) |
Compensatory increase in liver LDL receptors --> lowers circulating LDL levels
BAD: induces HMG-CoA reductase activity |
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Bile acid sequestrants
(Adverse reactions) |
Mild rise in TG
Bloating, constipation Interfere with absorption of fat-soluble vitamins and drugs (e.g. digitalis, thiazides, warfarin, aspirin) |
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Bile acid sequestrants
(indications) |
Reduce LDL
(Adjunctive therapy with statins or nicotinic acid) |
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Ezetemibe
(Method) |
Localizes on brush border, inhibits absorption of Ch.
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Ezetimibe
(Adverse reactions) |
NONE!
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Ezetemibe
(Indications) |
Reduce LDL
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Nicotinic acid
(effects) |
Decreased LDL
INCREASED HDL and decreased catabolism of it Decreased prodction of VLDL, enhanced clearance (enhanced lipoprotein lipase activity) |
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Nicotinic acid
(Adverse reactions) |
Flushing
Pruritis (both mediated by prostaglandins --> treat w/aspirin) Hepatic toxicity Glucose intolerance Elevated uric acid |
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Nicotinic acid
(indications and contraindications) |
Decrease LDL, increase HDL, lower Lp(a)
-Gout, pregnancy |
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Name two fibric acid derivatives
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Gemfibrozil
Fenofibrate |
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Gemfibrozil
(effect) |
Decreases TG
Increases HDL Decreases LDL (lesser effect) |
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Gemfibrozil
(Adverse reactions) |
Gallstones
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Gemfibrozil
(indications and contraindications) |
Elevated TG
LOW HDL - hepatic or renal dysfunction |
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Fenofibrate
(effect) |
Decreased TG
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Fenofibrate
(Indications and contraindications) |
No current incications in CAD
- Pts with severe hyperTGemia at risk of pancreatitis |
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Name 4 statins
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Lovastatin
Simvastatin Atorvastatin Pravastatin |
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Statins
(method) |
Competitive inhibition of HMG-CoA
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Statins
(effect) |
increase liver LDL receptors, decrease LDL
Moderate decrease in TG Small increase in HDL |
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Statins
(adverse reactions) |
Liver dysfunction (elevated aminotransferase)
Skeletal muscle pain (myopathy and elevated CK) CYP 450 metabolism (except pravastatin) |
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Statins
(indications and contraindications) |
High LDL
-liver disease and alcohol abuse |
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Name 4 sodium channel blockers
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Type 1A: quinidine, procainamide
Type 1B: lidocaine Type 1C: Flecainide |
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Name 2 potassium channel blockers
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Sotalol
Amiodarone (also blocks Na and Ca, beta) |
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Quinidine
(method) |
Type 1A sodium blocker (has some K blockade)
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Quinidine and Procainamide
(effect) |
Atrial and ventricular muscles
Prolong action potential duration (QT interval, via K blockade) Slows Phase 0 depolarization |
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Quinidine and Procainamide
(Adverse reactions) |
Tinnitus, GI upset, thombocytopenia
PRO-ARRHYTHMIA (Torsade de Pointes) from AP prolongation and early afterdepolarization) Procainamide: also causes a lupus-like syndrome |
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Quinidine and Procainamide
(indications) |
V-tach, SVT, prevents V-fib and ventricular premature beats
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Lidocaine
(method) |
Type 1B sodium channel blocker
Binds best to ischemic cells |
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Lidocaine
(effect) |
Slows Phase 0 depolarization
Suppress ventricular arrhythmia, little atrial effect Decreased automaticity of ectopic pacemakers due to decreased phase 4 depolarization. |
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Lidocaine
(Adverse reactions) |
CNS toxicity
Dizziness Seizures |
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Lidocaine
(Indications) |
Acute MI/ischemia to suppress ventricular arrhythmia.
Also prevents digitalis v-arrhythmia. Preferred for managing nonsustained ventricular tachycardia and frequent premature ventricular beats (>6/minute), and for use as an adjunct to defibrillation and CPR in patients with ventricular tachycardia and/or fibrillation. |
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Flecainide
(method) |
Type 1C Na blocker
Potent! |
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Flecainide
(effect) |
Slows conduction (QRS prolongation)
Prolongs refractory period in AV node |
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Flecainide
(adverse reactions) |
Significant pro-arrhythmic risk
Bradycardia CHF |
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Flecainide
(indications) |
Not used very much -- too toxic
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Beta blockers
(mechanism and effect in anti-arrhythmia) |
Reduce cAMP --> reduce Na and Ca current --> prolongs refractory period of AV nodal cells
Prevents extra beats by enhancing filter of AV node. Mild anti-arrhythmic in all settings |
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Sotalol
(method) |
K+ blocker
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K+ blocker
(effect) |
Act on atria and ventricle
Prevent atrial premature depolarization QT prolongation --> prolonged refractory periods in AV node Widened QRS Vasodilator |
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K+ blockers
(Adverse reactions) |
QT prolongation and Torsade de Pointes in some pts
Amiodarone only: Pumonary inflammation and fibrosis Hypo/hyperthyroidism Skin discolorization Liver effects GI effects Corneal opacities Photodermatitis |
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Sotalol
(indications) |
Severe ventricular and atrial arrhythmias
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Amiodarone
(indications) |
Almost all arrhythmias
Ventricular tachy Bypass tract paroxysmal SVT Atrial fib and flutter |
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Digoxin as anti-arrhythmic
(method and indication) |
Activates vagal nuclei --> acts on nodes --> slows conduction, prolongs refractory period by interfering with K channel)
Blocks re-entry, enhances AV filter Good for a-fib (controls ventricular response to A-fib) |
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Adenosine
(method) |
acts on G-protein coupled adenosine receptors, which reduce Ca influx
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Adenosine
(effect and use) |
terminate AV nodal re-entry immediately
Block AV conduction Used only to identify atrial arrhythmia and WPW re-entrant paroxysmal SVTs |
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AV filter enhancers
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Digitalis
CCB Beta-blockers |
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Atrial fibrillation drugs
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Digitalis
Beta-blockers Calcium Channel Blockers K+ blocker |
