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100 Cards in this Set

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What is mechanism of action of phenoxybenzamine?
irreversibly blocks alpha 1 and alpha 2 adrenergic receptors non-competitively.
1) irreversible
2) non-competitive.

Use pre-operatively in pheochromocytoma.
What is mechanism of action of phentolamine?
1) reversible
2) competitive

Blcoks alpha-1 and alpha 2 receptors.
What is mechanism of action of propranolol in HTN?
Decreases BP by decreasing CO
What is mechanism of action of propranolol in angina pectoris?
Decreases HR, decreases contractility, so decreases O2 demand of the myocardium.
What is mechanism of action of propranolol in CHF?
Blcoking beta receptors allow the myocardium to remodel and limits stress by preventing myotoxicity caused by chronic high doses of catecholamines.
What is mechanism of propranolol in supraventricular cardiac arrythmias?
Slows AV nodal conduction velocity.
What is MOA of propranolol on migraines?
Blocks catecholamine induced vasodilation in cerebral vasculature.
Why should propranolol be used with caution in diabetics?
These drugs inhibit glucagon secretion from pancreatic islet cells and attenuate normal physiological response to hypoglycemia!!

1) inhibit glucagon secretion
2) attenuate normal physiological response.
Note:
Beta blockers can block renin release.
What are the adverse effects of hydrochlorothiazides in use of HTN?
1) Hypokalemia
2) Hyperglycemia
3) Hyperlipidemia
4) Hyperuricemia
5) Hypercalcemia
What are the adverse effects of loop diuretics?
Potassium wasting

Metabolic alkalosis

Hypotension

Ototoxicity.
What is side effect of clonidine?
1) Alpha-2-agonist.
By fooling the brain into believing that catecholamine levels are higher than they really are, clonidine causes the brain to reduce its signals to the adrenal medulla, which in turn lowers catecholamine production and blood levels.

Side effects: SEVERE REBOUND HYPERTENSION!! Dry mouth
What is side effect of methyldopa?
Also activates alpha-2

Sedation
Positive Coombs' test
What is mechanism of hexamethonium?
is an nAch receptor antagonist which acts in autonomic ganglia by preventing the acetylcholine molecules from binding to the site of the cholinergic receptor. It has no effect on the muscarinic acetylcholine receptors, or mAChRs.
What are side effects of hexamethonium?
Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction.
How does reserpine work?
Blocks transports of amines from the cytoplasm into the vesicle: so MAO can break it down in the vesicle.
What are side effects of reserpine?
Sedation, depression, nasal stuffiness, diarrhea (block sympathetics). Nasal stuffiness b/c block action on alpha-1 adrenergic.
What is mechanism of action of guanethidine?
Orthostatic and exercise hypotension, sexual dysfunction, and diarrhea.

Blocks storage and release of catecholamines!!!
What is mode of action of prazosin?
Alpha-1-antagonist. So it decreases TPR
What are side effects of prazosin?
1st dose orthostatic hypotension --> so make sure first dose is given at night when patient is sleeping so patient no fall down.
What are the side effects of beta blockers?
Impotence
Asthma
bradycardia, CHF, AV block
CNS: sedation, sleep alterations.
What is mechanism of hydralazine?
Increases cGMP

Causes smooth muscle relaxation

Vasodilates arterioles>veins

Afterload reduction!!!
What is the uses of hydralazine?
Severe hypertension, CHF
What is the toxicity of hydralazine?
Compensatory tachycardia, fluid retention, lupus-like sndrome, salt retention, reflex tachycardia.
what is mechanism of minoxidil?
Vasodilator;
What are side effects of minoxidil?
Hypertrichosis (excessive body hair), pericardial effusion, reflex tachycardia, salt retention.
What are the side effects of captopril?
Hyperkalemia
Cough
Angioedema
Proteinuria
Taste Changes
Hypotension
Pregnancy Problems
Rash
Increased renin
Lower angiotensin II.
What is side effect of losartan?
Fetal renal toxicity
hyperkalemia.
What are some examples of calcium channel blockers?
nifedipine, verapamil, and diltiazem.
What is action of nifedipine, verapamil, and diltizaem?
Blocks voltage dependent L-type calcium channels of CARDIAC AND SMOOTH MUSCLE and so reduces muscle contractility.
Which calcium channel blockers have greatest effect on smooth muscle?

heart muscle?
Smooth: nifedipine > diltiazem > verapamil

Heart: verapamil > diltiazem > nifedipine.
What are the clinical uses of calcium channel blockers?
hypertension, angina,

arrythmias (verapamil)
What are the side effects of calcium channel blockers?
Dizziness, flushing, constipation (verapamil), and nausea.
What is side effect of nitroprusside?
cyanide toxicity (releases CN).
Which drugs are first line agents for angina?
Beta-blockers in px with chronic angina (except acebutolol and pindolol) b/c they have intrinsic sympathomimetic activity and can exacerbate symptoms of angina.
What is action of labetolol?
Alpha 1 blocker
B blocker

Decreases HR, CO, and TPR!!
What is mechanism of action of nitroglycerin, isosorbide dinitrate?
Vasodilate by releasing NO in smooth muscle.
1) causes increase in cGMP
2) increases smooth muscle relaxation
3) Dilate veins >>arteries
4) Decrease preload.
What is the clinical use of nitroglycerin, isosorbide dinitrate?
Used for angina, pulmonary edema. Also used as aphrodisiac and erection enhancer!
What is side effects of nitroglycerin and isosorbide dinitrate?
Tachycardia, hypotension, headache.

"Monday disease" in industrial exposure, development of tolerance for vasodilating activity during the work week and loss of tolerance over the weekend, causing tachycardia, dizziness, and headache.
What are the goals of antianginal therapy?
Reduce myocardial oxygen consumption, by decreases 1 or more of the determinants of myocardial oxygen consumption: EDV, blood pressure, HR, contractility, and ejection time
What are the determinants of myocardial oxygen consumption?
1) End diastolic volume
2) Blood pressure
3) Contractility
4) HR
5) Ejection time
What effect does nitrates have on heart?
1) Decreases EDV (dilate veins)
2) Decreases B.P. (dilate arteries)
3) Increase contractility (reflex response)
4) Increases HR (reflex response)
5) Decrease ejection time
6) Decreases O2 consumption!
What effect does Beta-blockers have on myocardial O2 consumption?
1) Increases EDV
2) Decreases BP
3) Decreases contractility
4) Decreases HR
5) Increases ejection time
6) Decreases O2 consumption.
Beta blockers vs nitrates?
beta blockers decreases afterload

nitrates decrease preload!
What is the effect of nitrates and beta blockers combined?
1) No effect on EDV
2) Decrease BP
3) No effect on contractility
4) Decrease HR
5) Decrease O2 consumption!!
Key points of Nitrates
1) Decrease preload
2) Decreas EDV
3) increase contrac + HR
Key points of beta-blockers?
1) increase EDV (decrease afterload so more blood comes back)
2) Increase ejection time.
Which calcium channel blocker is most similar to nitrates?
Nifedipine
Which calcium channel blocker is most similar to beta blockers?
Verapamil.
What is the action of digoxin?
Inhibits the Na+/K+ ATPase of cell membrane, causing increases intracellular Na+. The Na+-Ca+ antiport doesnt function as well, so Calciumi increases intracellularly causing positive inotropy.
What are the side effects of digoxin?
nausa, vomiting, diarrhea. blurry yellow vision. Arrythmia. Toxicities of digoxin are increased by renal failure (decreased excretion), hypokalemia (potentiates drugs effects), and quinidine (decreases digoxin clearance)
Whats the antidote for digoxin?
slowsly normalize K+, lidocaine, anti-dig Fab fragments.
What are the pharmacological properties of digoxin/
75% bioavailability
20-40% protein bound
half life = 40 hours.
What are the clinical uses of digoxin?
1) CHF (increase contracility)
2) atrial fibrillation (decreases conduction at AV node).
What are some EKG changes that can be seen with digoxin use?
1) Increases PR
2) Decreased QT
3) Scooping of ST segment
4) T wave inversion of EKG.
What are the classes of antiarrythmics for Na+ channel blockers?
1) Class IA
2) Class IB
3) Class IC
What is the mechanism of class I Na+ channel blocker antiarrythmics?
1) Local anasthetics
2) Decrease conduction (especially in depolarized cells)
3) Decrease slop of phase 4 depolarization of pacemaker cells, so increase threshold for firing in abnormal pacemaker cells.
4) Are state dependent (selectively depress tissue that is frequently depolarized, fast tachycardia).
What are the class I antiarrythmics?
Quinidine, Amiodorone, Procainamide, Disopyramide.

"Queen Amy Proclaims Diso's Pyramid"
What is the effect of quinidine, amiodorone, procainamide, and disopyramide?
1) Increases AP duration of AP
2) Increases effective refractory period of AP
3) Increases QT interval (risk of torsades)
4) Affect BOTH atrial and ventricular arrythmias.
What effect does amiodorone, procainamide, and disopyramide have on Pacemaker Cells?
Pacemaker:
1) block conduction in depolarized cells especially!
2) Decrease slope of phase 4 depolarization
3) Increases threshold for firing in abnormal pacemaker cells.
4) State dependent: depress tissue that is frequently depolarized!!
What effect does quinidien, amiodorone, and procainamide, and disopyramide have on ventricular cells/atrial cells?
1) Increases AP Duration
2) Increases effective refractory period
3) Increases QT interval
4) Use in atrial/ven fibrillation!
What is the toxicity of quinidine?
Class IA antiarrythmic

Cinchonism: headache, tinnitus, and thrombocytopenia

Increases QT interval: torsades de points
What os toxicity of procainamide?
Reversible SLE like syndrome.
What is toxicity of amiodorone?
Pulmonary fibrosis
Corneal deposits (very prominent)
Smurf syndrome: blue gray discoloration of skin.

Liver hepatitis.
What are some Class IB antiarrythmics?
Lidocaine, tocainide, and mexilteine.
What is mechanism of lidocaine and tocainide?
1) Slow or block conduction in depolarized cells
2) Decrease slope of phase 4 depolarization
3) Selectively depress tissue that frequently depolarizies.
4) DECREASES AP DURATION
5) AFFECT ISCHEMIC OR DEPOLARIZED PURKINJE AND VENTRICULAR TISSUE
What is the clinical use of lidocaine and tocainide?
1)Acute vent. arrythmias post MI
2) Digoxin induced arrythmias
What is toscitiy of lidocaine and tocainine and mexiletine?
Local anasthetic
CNS stimulation/depression
What are the class IC antiarrythmics?
Flecainide, encainide, propafenone.
what is action of flecainide?
No effect on AP duration
When is flecainie and encainide used?
V-tachs that progress to VF
Intractable Supraventricular tachycardias.
What is toxicity of flecainide and encainide?
proarrythmic (especially post MI), so contraindicated!!!
What are class II antiarrythmics?
Beta blockers such as propranolol, esmolol, metoprolol, atenolol, and timolol.
What is mechanism of class II antiarythmics?
1) Decrease cAMP
2) Decrease Calcium currents
3) Decrease slope of phase 4
4) AV node is particulary sensitive!! Blocks AV node: so increase PR interval!!!
What is toxicity of b-blocker antiarrythmics?
Impotence
Exacerbation of asthma
Sedation, sleep alterations.
Can mask hypoglycemia
What are the class III antiarrythmics?
K+ channel blockers
SIBA

Sotalol
Ibutilide
Bretylium
Amiodoron
What is action of class III antiarrythmics?
Increases AP Duration
Increases ERP
Increases QT interval.
What is the toxicity of sotalol?
Torsades de points
What is toxicity of ibutilide?
Torsades de pointes
What is toxicity of bretylium?
New arrythmias
Hypotension.
What is toxicity of amiodorone?
Corneal deposits
PULMONARY FIBROSIS!
Hepatotoxicity.
Skin deposits causing photodermatitis
Constipation
HYPOTHYROIDISM/HYPERTHYROIDISM
What must you check with amiodorone?
Pulmonary function tests
Liver function tests
Thyroid function tests
What are the class IV anitarrythmics?
Verapamil and diltiazem.
What effect does verapamil and diltiazem have on arrythmias?
1) Affect AV nodal cells
2) Decrease conduction velocity
3) Increase ERP
4) Increase PR interval
What is toxicity of verapamil and diltiazem?
Constipation
Flushing
CHF
AV block
sinus node depression.
What action does adenosine have on arrythmias?
Drug of choice to abolish AV nodal arrythmias!!
What action does K+ have on arrythmias?
Depresses ectopic pacemakers, especially in digoxin toxicity.
What action does Mg+ have on arrythmias?
Use in torsades

Use in digoxin toxicity.
What are some HMG-cOA reductase inhibitors?
Lovastatin
Pravastatin
Simvastatin
Atorvastatin
What effect does statins have?
1) Decrease LDL!!
2) Increase HDL slightly
3) Decrease TG solightly
What are the side effects of statins?
Expensive
Reversible Increase in LFTs
Myositis
Rhabdomyolysis
What is the effect of niacin?
1) Decreases LDL
2) Increases HDL!!
3) Decreases LDL slightly
What are the side effects of niacin?
1) Red, flushed face
2) Can decrease this by use of aspirin
What are examples of bile acid resins?
Cholestyramine
Colestipol
What is MOA of cholestyramine and colestipol?
1) Decrease LDL
2) No effect on HDL
3) SLIGHTLY INCREASES TG!!
What is side effect of cholestyramine?
1) Tastes horrible
2) Gauses GI discomfort
What are the cholesterol absorption blockers?
Ezetimbie
What effect does ezetimibe have?
1) Decreases LDL

2) No effect on HDL or TG
What are fibrates?
Gemfibrozil
Clofibrate
Benzafibrate
Fenofibrate
What is action of fibrates: gemfibrozil, clofibrate, bezafibrate?
1) Decreases LDL
2) Increases HDL
3) Main action DECREASES TG!!