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161 Cards in this Set

  • Front
  • Back
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.
What is secreted by normal endothelial cells?
Injured endothelial cells?
Normal: PGI2, NO

Injured: Decreased PGI2 and NO, Endothlin increased
Digoxin
(Effect)
Effect: Increased CO (from dec LVEDP, inc. natriuresis), decreased HR.
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
Digoxin
(Adverse reactions)
ADR: Ventricular arrhythmias, SVT (PAT), heart block & bradyarrhythmias, nausea, vomit, vision
What gives the inside of the aorta a treebark appearance?
Syphilis
Digoxin
(indications and contraindications)
Indications: CHF w/atrial fib
Contraindications: kidney failure, low K or Mg, diuretics, quinidine, antibiotics, cholestyramine, amiodarone, verapamil
What is the histology of Giant Cell Arteritis?
In temporal artery (and others in head and neck):
Inflammation of all layers.
Giant cell reaction to internal elastic lamina
Amrinone
(method)
Phosphodiesterase inhibitor --> inhibits inactivation of cAMP --> increased Ca in --> increased contractility
What is the pathogenesis of GCA?
T-cell response to blood vessel antigen, attract macrophages
Amrinone
(Effect)
Increased CO (contractility, not HR)
Vasodilates
Decreased LA pressure
What vessels does Takayasu's Arteritis affect?
Aortic arch and ostia of branches - thickening
Amrinone
(Adverse reactions)
Long-term toxicity
Arrhythmias
Thrombocytopenia
Abnormal LFTs
What disease of the vessels is related to smoking (other than atherosclerosis)?
Buerger's disease (thromboangiitis obliterans)
Amrinone
(Indications)
Short term use in refractory CHF
What is the pathology of Buerger's Disease?
Segmental thrombosing inflammation of distal limb arteries, full of neutrophils, granulomatous inflammation.
Milrinone
(Method)
Phosphodiesterase inhibitor --> inhibits inactivation of cAMP --> increased Ca in --> increased contractility
What vessels does Henoch-Schonlein Purpura affect?
Post-capillary venules
Milrinone
(Effect)
Increased CO
Vasodilates
Decreased LA pressure
What is present in Henoch-Shonlein Purpura lesions?
Deposition of IgA, fibrin, C3
Nuclear fragments
Thrombi
Neutrophilsx
Milrinone
(ADRs)
Long term toxicity
Thrombocytopenia
Abnormal LFTs
Arrhythmias
What vasculitis is associated with crescenteric necrotizing glomerulonephritis?
Henoch-Schonlein Purpura
Milrinone
(Indications)
Short term use in refractory CHF
What are symptoms of HSP?
Palpable purpura
Arthralgia
Abdominal pain
Hematuria
Milrinone
(compared to dobutamine)
More effective vasodilator, longer acting, no tolerance buildup.
What are the symptoms of Polyarteritis Nodosa?
Fever, weight loss, malaise
Widespread vascular inflammation --> infarcts
Leads to renal problems, HTN, hematuria, protinuria, neuropathy, GI bleeding
Dobutamine
(Method
B1 agonist --> increased synthesis of cAMP
What is the pathology of polyarteritis nodosa?
Fibrinoid necrosis
Internal elastic lamina is disrupted
Aneurysms
Dobutamine
(Effect)
Increased CO, increased HR, decreased LA pressure
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
Dobutamine
(Adverse reactions)
Arrhythmias, tolerance buildup.
Dobutamine
(Indications)
Short term use in severe CHF
Dopamine
(Method)
Low dose --> renal vasodilation
High dose --> B agonist and vasoconstriction
Dopamine
(Effect)
High dose increases CO
Dopamine
(Adverse reactions)
Tachycardia
Dopamine
(Indications)
Short term use for patients with pulmonary congestion and peripheral hypoperfusion (and poor renal perfusion).
Shock --> increases BP
Furosemide
(brand name and method)
Lasix.
Loop diuretic --> decreased Na and H20 retention
Furosemide
(Effect)
Decreases ventricular preload
Neurohormonal activation (sympathetic and RAAS)
Furosemide
(Adverse reactions)
Increases TG > LDL
Lose K and Mg
Azotemia (inc urea in blood)
Blood dyscrasia
Hyperglycemia
Gout
Deafness
Furosemide
(Indications)
CHF with volume overload
Do not use as monotherapy.
Spironolactone
(Method)
Aldosterone antagonist
Spironolactone
(Effect)
Diuresis with K+ sparing
Spironolactone
(Adverse reactions)
Gynecomastia
Hyperkalemia
Spironolactone
(Indications)
CHF with volume overload
ACE inhibitors
Two names and methods
Captopril and enalapril
Prevents conversion of Angiotensin I --> II
Results in decreased aldosterone, decreased vasoconstriction, decreased cell growth.
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
ACE inhibitors
(Adverse reactions)
Cough
Increased K+
Hypotension
Angioneurotic edema
Renal insufficiency
Dysgeusia
Neutropenia
Thrombocytopenia
ACE inhibitors
(indications and contraindications)
+Congesive heart failure
+Post-AMI
+Hypertension
-Smoker
-Spironolactone (hyperkalemia)
-Renal insufficiency
Losartan
(Method)
Binds to angiotensin 1 receptor, inhibiting aldosterone production, vasoconstriction, and cell growth.
Losartan
(Effect)
Decreased BP
Losartan
(Indications)
Better tolerated than ACE-inhibitors (less cough)
Nesiritide
(Method)
Binds to guanylate cyclase receptor of vascular smooth muscle and endothelial cells --> increased intracellular concentrations of cGMP and smooth muscle cell relaxation
Nesiritide
(Effect)
Potent, dose-related vasodilation that is rapid in onset and sustained for the duration of drug infusion.

No effects on cardiac contractility
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.
Atenolol + Metoprolol
(Mechanism)
Beta blocker (B1 selective)
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.
Beta blockers
(Adverse reactions)
Bronchospasm
claudication
fluid retention
sinus bradycardia and AV block
Depression, impotence
Masks diabetic hypoglycemia
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
Which beta blocker is safe/effective for CHF?
Carvedilol
Propranalol
(mehod)
Non-selective B-blocker
Labetalol and Carvedilol
(Method)
a1 and B blocker --> decrease peripheral resistance
Hydralazine
(effect)
Vasodilation of arterioles --> antihypertensive
Hydralazine
(Adverse effects)
Tachyphylaxis
Reflex tachycardia and inc. sympathetic tone --> may worsen LVH
Hydralazine
(indications)
CHF (along with isosorbide dinitrate) when ACE inhibitor is contraindicated.
Hypertensive emergency
Isosorbide dinitrate
(onset and duration)
onset: 15-30 min
duration: 3-6 hours
Isosorbide mononitrate
(onset and duration)
onset: 30 min
duration: 6-8 hours
Nitrates
(Method)
Degrade to NO --> activate SMC guanylyl cyclase --> cGMP depohosphorylates myosin light chain --> inactivates myosin-actin interaction
Nitrates
(Effect)
Venodilator > arteriodilator
Decrease blood return to heart
Attenuate coronary vasospasm
Decreased BP
Improved collateral blood flow
Nitrates
(adverse reactions)
Headaches
Orthostatic hypotension
Reflex tachycardia
Tolerance possible
Nitrates
(indications)
CHF w/ischemia and good BP
Angina (esp Prinzmetal's vasospastic)
Calcium channel blockers
(method)
Blockade voltage sensitive L type Ca channel --> reduce Ca influx
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.
Calcium channel blockers for SVT
Verapamil, diltiazem
(more action on AV node)
Calcium channel blocker
(Common adverse reactions)
Headaches
Lower extremity edema
Nifedipine
(Adverse reactions)
Common rxns
Reflex tachycardia, dizziness
Nifedipine
(Indications)
Rarely used due to hypotension
Amlodipine
(Adverse reactions)
Well-tolerated
(2nd generation dihydropyridine)
What CCB is safest for CHF?
Amlodipine.
Use when other drugs won't work (persistent high BP and afterload)
Diltiazem
(Adverse reactions)
Excessive sinus bradycardia and AV block.
CHF exacerbation!
Diltiazem
(indications, interactions)
Control ventricular rate in A-fib

Don't use with beta-blocker (hypotension)
Verapamil
(Adverse reactions)
Common + constipation
Verapamil
(indications and interaction)
Anti-arrhythmic for SVT (prevents AV nodal re-entry)
Vasospastic angina

Don't use with digoxin (raises dig levels)
What CCB is a potent negative chronotrope?
Verapamil
Fibrinolytics
(method)
Activate plasminogen into plasmin --> lyse clots
Administer with aspirin and IV heparin
Which fibrinolytic is most associated with cerebrovascular accident?
human t-PA
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
Name 4 calcium channel blockers
Nifedipine
Amlodipine
Diltiazem
Verapamil
Name 6 anti-platelet drugs
Aspirin
Ticlopidine
Clopidogrel
Abciximab
Tirofiban
Eptifibatide
Aspirin
(Method)
Irreversible acetylation and inactivation of COX --> no TXA2 --> inactivates platelets
Aspirin
(adverse reactions)
GI bleeding
Aspirin
(indications and contraindications)
+Secondary prevention of MI
+Stroke prevention in low risk A-fib

-surgery coming in a week or less
Ticlopidine
(Method)
ADP receptor antagonist
Ticlopidine
(Effect)
Prevents recruitment of circulating platelets
Ticlopidine
(Adverse reactions)
Nausea/vomitting, dizziness, gastric irritation
Leukopenia
TTP
Ticlopidine
(indications)
Secondary stroke prevention
Post coronary stent

Irreversible
Clopidogrel
(Method)
ADP receptor antagonist
Clopidogrel
(Effect)
Prevents recruitment of circulating platelets
Clopidogrel
(Adverse reactions)
Minimal
Clopidogrel
(indications)
Secondary stroke prevention
Post coronary stent
Abciximab
(Method)
Platelet GP IIb/IIIa receptor antagonist
Abciximab
(Effect)
Most potent platelet antagonist
GP IIb/IIIa receptor antagonists adverse reactions
Excessive bleeding
Allergic reaction
Thrombocytopenia
GP IIb/IIIa receptor antagonists
(Indications)
Treatment of acute coronary syndromes
High risk PCTA, stents
Abciximab versus tirobfiban/eptifibatide
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.
Tirofiban and eptifibatide
(Method)
GP IIb/IIIa receptor antagonist
Warfarin
(Method)
Blocks carboxylation of clotting factor precursors --> prevents reduction of inactive vitamin K to active KH2
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)
Warfarin
(Adverse reactions)
Bleeding w/long term therapy
Teratogenic
Hemorrhagic skin necrosis for Protein C and S deficient pts
Alcohol can cause over-anticoagulation
Warfarin
(indications)
Mechanical heart valve prosthesis
Atrial fib in high risk (> 65)
DVT
Recent anterior wall MI
Heparin
(method)
binds/activates antithrombin III
Heparin
(effect)
inhibited thrombin and Xa
Enhanced Tissue Factor Pathway Inhibitor activity
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.
Heparin
(indications)
Initiation of warfarin
Acute coronary syndromes
Acute MI
Catheterization, surgery
Cholestyramine
(method)
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
Colestipol
(Method)
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
Colesevelam
(Method)
Bile acid sequestrant - exchange Cl ion for negatively charged bild acid --> resin binds to bile acid and can't be reabsorbed
Bile acid sequestrant
(Effect)
Compensatory increase in liver LDL receptors --> lowers circulating LDL levels

BAD: induces HMG-CoA reductase activity
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)
Bile acid sequestrants
(indications)
Reduce LDL
(Adjunctive therapy with statins or nicotinic acid)
Ezetemibe
(Method)
Localizes on brush border, inhibits absorption of Ch.
Ezetimibe
(Adverse reactions)
NONE!
Ezetemibe
(Indications)
Reduce LDL
Nicotinic acid
(effects)
Decreased LDL
INCREASED HDL and decreased catabolism of it
Decreased prodction of VLDL, enhanced clearance (enhanced lipoprotein lipase activity)
Nicotinic acid
(Adverse reactions)
Flushing
Pruritis (both mediated by prostaglandins --> treat w/aspirin)
Hepatic toxicity
Glucose intolerance
Elevated uric acid
Nicotinic acid
(indications and contraindications)
Decrease LDL, increase HDL, lower Lp(a)

-Gout, pregnancy
Name two fibric acid derivatives
Gemfibrozil
Fenofibrate
Gemfibrozil
(effect)
Decreases TG
Increases HDL
Decreases LDL (lesser effect)
Gemfibrozil
(Adverse reactions)
Gallstones
Gemfibrozil
(indications and contraindications)
Elevated TG
LOW HDL

- hepatic or renal dysfunction
Fenofibrate
(effect)
Decreased TG
Fenofibrate
(Indications and contraindications)
No current incications in CAD

- Pts with severe hyperTGemia at risk of pancreatitis
Name 4 statins
Lovastatin
Simvastatin
Atorvastatin
Pravastatin
Statins
(method)
Competitive inhibition of HMG-CoA
Statins
(effect)
increase liver LDL receptors, decrease LDL
Moderate decrease in TG
Small increase in HDL
Statins
(adverse reactions)
Liver dysfunction (elevated aminotransferase)
Skeletal muscle pain (myopathy and elevated CK)
CYP 450 metabolism (except pravastatin)
Statins
(indications and contraindications)
High LDL

-liver disease and alcohol abuse
Name 4 sodium channel blockers
Type 1A: quinidine, procainamide
Type 1B: lidocaine
Type 1C: Flecainide
Name 2 potassium channel blockers
Sotalol
Amiodarone (also blocks Na and Ca, beta)
Quinidine
(method)
Type 1A sodium blocker (has some K blockade)
Quinidine and Procainamide
(effect)
Atrial and ventricular muscles
Prolong action potential duration (QT interval, via K blockade)
Slows Phase 0 depolarization
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
Quinidine and Procainamide
(indications)
V-tach, SVT, prevents V-fib and ventricular premature beats
Lidocaine
(method)
Type 1B sodium channel blocker
Binds best to ischemic cells
Lidocaine
(effect)
Slows Phase 0 depolarization
Suppress ventricular arrhythmia, little atrial effect
Decreased automaticity of ectopic pacemakers due to decreased phase 4 depolarization.
Lidocaine
(Adverse reactions)
CNS toxicity
Dizziness
Seizures
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.
Flecainide
(method)
Type 1C Na blocker
Potent!
Flecainide
(effect)
Slows conduction (QRS prolongation)
Prolongs refractory period in AV node
Flecainide
(adverse reactions)
Significant pro-arrhythmic risk
Bradycardia
CHF
Flecainide
(indications)
Not used very much -- too toxic
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
Sotalol
(method)
K+ blocker
K+ blocker
(effect)
Act on atria and ventricle
Prevent atrial premature depolarization
QT prolongation --> prolonged refractory periods in AV node
Widened QRS
Vasodilator
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
Sotalol
(indications)
Severe ventricular and atrial arrhythmias
Amiodarone
(indications)
Almost all arrhythmias
Ventricular tachy
Bypass tract paroxysmal SVT
Atrial fib and flutter
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)
Adenosine
(method)
acts on G-protein coupled adenosine receptors, which reduce Ca influx
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
AV filter enhancers
Digitalis
CCB
Beta-blockers
Atrial fibrillation drugs
Digitalis
Beta-blockers
Calcium Channel Blockers
K+ blocker