Cardiovascular Pharmacology

Front 1

What is mechanism of action of phenoxybenzamine?

Back 1

irreversibly blocks alpha 1 and alpha 2 adrenergic receptors non-competitively.
1) irreversible
2) non-competitive.

Use pre-operatively in pheochromocytoma.

Front 2

What is mechanism of action of phentolamine?

Back 2

1) reversible
2) competitive

Blcoks alpha-1 and alpha 2 receptors.

Front 3

What is mechanism of action of propranolol in HTN?

Back 3

Decreases BP by decreasing CO

Front 4

What is mechanism of action of propranolol in angina pectoris?

Back 4

Decreases HR, decreases contractility, so decreases O2 demand of the myocardium.

Front 5

What is mechanism of action of propranolol in CHF?

Back 5

Blcoking beta receptors allow the myocardium to remodel and limits stress by preventing myotoxicity caused by chronic high doses of catecholamines.

Front 6

What is mechanism of propranolol in supraventricular cardiac arrythmias?

Back 6

Slows AV nodal conduction velocity.

Front 7

What is MOA of propranolol on migraines?

Back 7

Blocks catecholamine induced vasodilation in cerebral vasculature.

Front 8

Why should propranolol be used with caution in diabetics?

Back 8

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.

Front 9

Note:

Back 9

Beta blockers can block renin release.

Front 10

What are the adverse effects of hydrochlorothiazides in use of HTN?

Back 10

1) Hypokalemia
2) Hyperglycemia
3) Hyperlipidemia
4) Hyperuricemia
5) Hypercalcemia

Front 11

What are the adverse effects of loop diuretics?

Back 11

Potassium wasting

Metabolic alkalosis

Hypotension

Ototoxicity.

Front 12

What is side effect of clonidine?

Back 12

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

Front 13

What is side effect of methyldopa?

Back 13

Also activates alpha-2

Sedation
Positive Coombs' test

Front 14

What is mechanism of hexamethonium?

Back 14

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.

Front 15

What are side effects of hexamethonium?

Back 15

Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction.

Front 16

How does reserpine work?

Back 16

Blocks transports of amines from the cytoplasm into the vesicle: so MAO can break it down in the vesicle.

Front 17

What are side effects of reserpine?

Back 17

Sedation, depression, nasal stuffiness, diarrhea (block sympathetics). Nasal stuffiness b/c block action on alpha-1 adrenergic.

Front 18

What is mechanism of action of guanethidine?

Back 18

Orthostatic and exercise hypotension, sexual dysfunction, and diarrhea.

Blocks storage and release of catecholamines!!!

Front 19

What is mode of action of prazosin?

Back 19

Alpha-1-antagonist. So it decreases TPR

Front 20

What are side effects of prazosin?

Back 20

1st dose orthostatic hypotension --> so make sure first dose is given at night when patient is sleeping so patient no fall down.

Front 21

What are the side effects of beta blockers?

Back 21

Impotence
Asthma
bradycardia, CHF, AV block
CNS: sedation, sleep alterations.

Front 22

What is mechanism of hydralazine?

Back 22

Increases cGMP

Causes smooth muscle relaxation

Vasodilates arterioles>veins

Afterload reduction!!!

Front 23

What is the uses of hydralazine?

Back 23

Severe hypertension, CHF

Front 24

What is the toxicity of hydralazine?

Back 24

Compensatory tachycardia, fluid retention, lupus-like sndrome, salt retention, reflex tachycardia.

Front 25

what is mechanism of minoxidil?

Back 25

Vasodilator;

Front 26

What are side effects of minoxidil?

Back 26

Hypertrichosis (excessive body hair), pericardial effusion, reflex tachycardia, salt retention.

Front 27

What are the side effects of captopril?

Back 27

Hyperkalemia
Cough
Angioedema
Proteinuria
Taste Changes
Hypotension
Pregnancy Problems
Rash
Increased renin
Lower angiotensin II.

Front 28

What is side effect of losartan?

Back 28

Fetal renal toxicity
hyperkalemia.

Front 29

What are some examples of calcium channel blockers?

Back 29

nifedipine, verapamil, and diltiazem.

Front 30

What is action of nifedipine, verapamil, and diltizaem?

Back 30

Blocks voltage dependent L-type calcium channels of CARDIAC AND SMOOTH MUSCLE and so reduces muscle contractility.

Front 31

Which calcium channel blockers have greatest effect on smooth muscle?

heart muscle?

Back 31

Smooth: nifedipine > diltiazem > verapamil

Heart: verapamil > diltiazem > nifedipine.

Front 32

What are the clinical uses of calcium channel blockers?

Back 32

hypertension, angina,

arrythmias (verapamil)

Front 33

What are the side effects of calcium channel blockers?

Back 33

Dizziness, flushing, constipation (verapamil), and nausea.

Front 34

What is side effect of nitroprusside?

Back 34

cyanide toxicity (releases CN).

Front 35

Which drugs are first line agents for angina?

Back 35

Beta-blockers in px with chronic angina (except acebutolol and pindolol) b/c they have intrinsic sympathomimetic activity and can exacerbate symptoms of angina.

Front 36

What is action of labetolol?

Back 36

Alpha 1 blocker
B blocker

Decreases HR, CO, and TPR!!

Front 37

What is mechanism of action of nitroglycerin, isosorbide dinitrate?

Back 37

Vasodilate by releasing NO in smooth muscle.
1) causes increase in cGMP
2) increases smooth muscle relaxation
3) Dilate veins >>arteries
4) Decrease preload.

Front 38

What is the clinical use of nitroglycerin, isosorbide dinitrate?

Back 38

Used for angina, pulmonary edema. Also used as aphrodisiac and erection enhancer!

Front 39

What is side effects of nitroglycerin and isosorbide dinitrate?

Back 39

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.

Front 40

What are the goals of antianginal therapy?

Back 40

Reduce myocardial oxygen consumption, by decreases 1 or more of the determinants of myocardial oxygen consumption: EDV, blood pressure, HR, contractility, and ejection time

Front 41

What are the determinants of myocardial oxygen consumption?

Back 41

1) End diastolic volume
2) Blood pressure
3) Contractility
4) HR
5) Ejection time

Front 42

What effect does nitrates have on heart?

Back 42

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!

Front 43

What effect does Beta-blockers have on myocardial O2 consumption?

Back 43

1) Increases EDV
2) Decreases BP
3) Decreases contractility
4) Decreases HR
5) Increases ejection time
6) Decreases O2 consumption.

Front 44

Beta blockers vs nitrates?

Back 44

beta blockers decreases afterload

nitrates decrease preload!

Front 45

What is the effect of nitrates and beta blockers combined?

Back 45

1) No effect on EDV
2) Decrease BP
3) No effect on contractility
4) Decrease HR
5) Decrease O2 consumption!!

Front 46

Key points of Nitrates

Back 46

1) Decrease preload
2) Decreas EDV
3) increase contrac + HR

Front 47

Key points of beta-blockers?

Back 47

1) increase EDV (decrease afterload so more blood comes back)
2) Increase ejection time.

Front 48

Which calcium channel blocker is most similar to nitrates?

Back 48

Nifedipine

Front 49

Which calcium channel blocker is most similar to beta blockers?

Back 49

Verapamil.

Front 50

What is the action of digoxin?

Back 50

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.

Front 51

What are the side effects of digoxin?

Back 51

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)

Front 52

Whats the antidote for digoxin?

Back 52

slowsly normalize K+, lidocaine, anti-dig Fab fragments.

Front 53

What are the pharmacological properties of digoxin/

Back 53

75% bioavailability
20-40% protein bound
half life = 40 hours.

Front 54

What are the clinical uses of digoxin?

Back 54

1) CHF (increase contracility)
2) atrial fibrillation (decreases conduction at AV node).

Front 55

What are some EKG changes that can be seen with digoxin use?

Back 55

1) Increases PR
2) Decreased QT
3) Scooping of ST segment
4) T wave inversion of EKG.

Front 56

What are the classes of antiarrythmics for Na+ channel blockers?

Back 56

1) Class IA
2) Class IB
3) Class IC

Front 57

What is the mechanism of class I Na+ channel blocker antiarrythmics?

Back 57

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).

Front 58

What are the class I antiarrythmics?

Back 58

Quinidine, Amiodorone, Procainamide, Disopyramide.

"Queen Amy Proclaims Diso's Pyramid"

Front 59

What is the effect of quinidine, amiodorone, procainamide, and disopyramide?

Back 59

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.

Front 60

What effect does amiodorone, procainamide, and disopyramide have on Pacemaker Cells?

Back 60

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!!

Front 61

What effect does quinidien, amiodorone, and procainamide, and disopyramide have on ventricular cells/atrial cells?

Back 61

1) Increases AP Duration
2) Increases effective refractory period
3) Increases QT interval
4) Use in atrial/ven fibrillation!

Front 62

What is the toxicity of quinidine?

Back 62

Class IA antiarrythmic

Cinchonism: headache, tinnitus, and thrombocytopenia

Increases QT interval: torsades de points

Front 63

What os toxicity of procainamide?

Back 63

Reversible SLE like syndrome.

Front 64

What is toxicity of amiodorone?

Back 64

Pulmonary fibrosis
Corneal deposits (very prominent)
Smurf syndrome: blue gray discoloration of skin.

Liver hepatitis.

Front 65

What are some Class IB antiarrythmics?

Back 65

Lidocaine, tocainide, and mexilteine.

Front 66

What is mechanism of lidocaine and tocainide?

Back 66

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

Front 67

What is the clinical use of lidocaine and tocainide?

Back 67

1)Acute vent. arrythmias post MI
2) Digoxin induced arrythmias

Front 68

What is toscitiy of lidocaine and tocainine and mexiletine?

Back 68

Local anasthetic
CNS stimulation/depression

Front 69

What are the class IC antiarrythmics?

Back 69

Flecainide, encainide, propafenone.

Front 70

what is action of flecainide?

Back 70

No effect on AP duration

Front 71

When is flecainie and encainide used?

Back 71

V-tachs that progress to VF
Intractable Supraventricular tachycardias.

Front 72

What is toxicity of flecainide and encainide?

Back 72

proarrythmic (especially post MI), so contraindicated!!!

Front 73

What are class II antiarrythmics?

Back 73

Beta blockers such as propranolol, esmolol, metoprolol, atenolol, and timolol.

Front 74

What is mechanism of class II antiarythmics?

Back 74

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!!!

Front 75

What is toxicity of b-blocker antiarrythmics?

Back 75

Impotence
Exacerbation of asthma
Sedation, sleep alterations.
Can mask hypoglycemia

Front 76

What are the class III antiarrythmics?

Back 76

K+ channel blockers
SIBA

Sotalol
Ibutilide
Bretylium
Amiodoron

Front 77

What is action of class III antiarrythmics?

Back 77

Increases AP Duration
Increases ERP
Increases QT interval.

Front 78

What is the toxicity of sotalol?

Back 78

Torsades de points

Front 79

What is toxicity of ibutilide?

Back 79

Torsades de pointes

Front 80

What is toxicity of bretylium?

Back 80

New arrythmias
Hypotension.

Front 81

What is toxicity of amiodorone?

Back 81

Corneal deposits
PULMONARY FIBROSIS!
Hepatotoxicity.
Skin deposits causing photodermatitis
Constipation
HYPOTHYROIDISM/HYPERTHYROIDISM

Front 82

What must you check with amiodorone?

Back 82

Pulmonary function tests
Liver function tests
Thyroid function tests

Front 83

What are the class IV anitarrythmics?

Back 83

Verapamil and diltiazem.

Front 84

What effect does verapamil and diltiazem have on arrythmias?

Back 84

1) Affect AV nodal cells
2) Decrease conduction velocity
3) Increase ERP
4) Increase PR interval

Front 85

What is toxicity of verapamil and diltiazem?

Back 85

Constipation
Flushing
CHF
AV block
sinus node depression.

Front 86

What action does adenosine have on arrythmias?

Back 86

Drug of choice to abolish AV nodal arrythmias!!

Front 87

What action does K+ have on arrythmias?

Back 87

Depresses ectopic pacemakers, especially in digoxin toxicity.

Front 88

What action does Mg+ have on arrythmias?

Back 88

Use in torsades

Use in digoxin toxicity.

Front 89

What are some HMG-cOA reductase inhibitors?

Back 89

Lovastatin
Pravastatin
Simvastatin
Atorvastatin

Front 90

What effect does statins have?

Back 90

1) Decrease LDL!!
2) Increase HDL slightly
3) Decrease TG solightly

Front 91

What are the side effects of statins?

Back 91

Expensive
Reversible Increase in LFTs
Myositis
Rhabdomyolysis

Front 92

What is the effect of niacin?

Back 92

1) Decreases LDL
2) Increases HDL!!
3) Decreases LDL slightly

Front 93

What are the side effects of niacin?

Back 93

1) Red, flushed face
2) Can decrease this by use of aspirin

Front 94

What are examples of bile acid resins?

Back 94

Cholestyramine
Colestipol

Front 95

What is MOA of cholestyramine and colestipol?

Back 95

1) Decrease LDL
2) No effect on HDL
3) SLIGHTLY INCREASES TG!!

Front 96

What is side effect of cholestyramine?

Back 96

1) Tastes horrible
2) Gauses GI discomfort

Front 97

What are the cholesterol absorption blockers?

Back 97

Ezetimbie

Front 98

What effect does ezetimibe have?

Back 98

1) Decreases LDL

2) No effect on HDL or TG

Front 99

What are fibrates?

Back 99

Gemfibrozil
Clofibrate
Benzafibrate
Fenofibrate

Front 100

What is action of fibrates: gemfibrozil, clofibrate, bezafibrate?

Back 100

1) Decreases LDL
2) Increases HDL
3) Main action DECREASES TG!!