First Aid Cv - Pharm

Front 1

Clonidine is what type of drug and what are its adverse effects

Back 1

a2 agonist; dry mouth, sedation, severe rebound hypertension

Front 2

a2 agonist; side effects: dry mouth, sedation, severe rebound HTN

Back 2

Clonidine

Front 3

Methyldopa is what type of drug and what are its adverse effects

Back 3

a2 agonist: sedation, positive Coombs' test

Front 4

Reserpine: mechanism and SE

Back 4

promote NE degradation; sedation, depression, nasal stuffiness, diarrhea

Front 5

Guanethidine: mechanism and SE

Back 5

inhibit release of NE by replacing it in vesicles; orthostatic and exercise hypotension, sexual dysfunction, diarrhea

Front 6

Prazosin: mechanism and SE

Back 6

a1 blocker; 1st dose orthostatic hypotension, dizziness, headache

Front 7

Side effects of beta blockers

Back 7

Impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)

Front 8

Nitroprusside toxicity

Back 8

Cyanide toxicity

Front 9

Diazoxide toxicity

Back 9

Hyperglycemia (reduces insulin release, hypotension)

Front 10

ACE inhibitor toxicities

Back 10

Hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increased renin

Front 11

Losartan toxicities

Back 11

Fetal renal toxicity, hyperkalemia

Front 12

Hydralazine mechanism

Back 12

Increased cGMP leads to smooth muscle relaxation Vasodilates arterioles > veins; AFTERLOAD reduction

Front 13

Clinical use of hydralazine

Back 13

Severe hypertension, CHF. First lien therapy for hypertension in pregnancy, with methyldopa

Front 14

Increased cGMP leads to smooth muscle relaxation Vasodilates arterioles > veins; AFTERLOAD reduction

Back 14

Hydralazine

Front 15

toxicity of hydralazine

Back 15

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus like syndrome

Front 16

Mechanism of Minoxidil

Back 16

K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle.

Front 17

Clinical use of minoxidil

Back 17

Severe HTN

Front 18

Toxicity of Minoxidil

Back 18

Hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention

Front 19

Vasodilator. K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle.

Back 19

Minoxidil

Front 20

Name 3 commonly used calcium channel blockers

Back 20

Nifedipine, verapamil, diltiazem

Front 21

Mechanism of action for Nifedipine

Back 21

Block voltage dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility for VESSELS mainly (not really heart)

Front 22

What are the clinical uses of Nifedipine, Verapamil, and diltiazem

Back 22

HTN, angina, arrhythmias (notnifedipine), Prinzmetal's angina, Raynaud's

Front 23

Toxicities of nifedipine

Back 23

Peripheral edema, flushing, dizziness, and constipation

Front 24

Toxicities of verapamil and diltiazem

Back 24

Cardiac depression, flushing, dizziness, and constipation

Front 25

Mechanism of Nitroglycerin

Back 25

Vasodilate by releasing NO in smooth muscles, increasing cGMP and smooth muscle relaxation. Dilate veins >> arteries decreasing preload.

Front 26

Clinical uses of Nitroglycerin or isosorbide dinitrate

Back 26

Angina, pulmonary edema. also used as an aphrodisiac and erection enhancer

Front 27

"Monday disease" in indusrial exposure - development of tolerance during work week and loss of tolerance over weeend resulting in tachycardia, dizziness, and headache on reexposure. what drug?

Back 27

Nitroglycerin or Isosorbide dinitrate

Front 28

Three treatments for malignant hypertension

Back 28

Nitroprusside, Fenoldopam, Diazoxide

Front 29

Mechanism of action of Nitroprusside

Back 29

Short acting, increases cGMP via direct release of NO

Front 30

Mechanims of action of Fenoldopam

Back 30

Dopamine D1 receptor agonist - relaxes renal vascular smooth muscle

Front 31

Dopamine D1 receptor agonist - relaxes renal vascular smooth muscle

Back 31

Fenoldopam

Front 32

Diazoxide mechanism

Back 32

K+ channel opener - hyperpolarizes and relaxes vascular SM

Front 33

K+ channel opener - hyperpolarizes and relaxes vascular SM

Back 33

Diazoxide

Front 34

Which beta blockers are also parital B agonists and contraindicated in angina

Back 34

Pindolol and acebutolol

Front 35

Side effects of HMG-CoA reductase

Back 35

Reversible increase in LFTs, rhabdomyolisis

Front 36

Simvastatin inhibits the formation of what cholesterol precursor?

Back 36

Mevalonate

Front 37

Which lipid lowering agent has the highest effect in raising HDL?

Back 37

Niacin

Front 38

What is the mechanisms of action of niacin?

Back 38

Inhibit lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

Front 39

Cholestyramine and colsevelam are examples of

Back 39

Bile acid resins

Front 40

Which lipid lowering agent is contraindicated in pts with gallstones?

Back 40

Cholestyramine, colestipol (bile acid resins)

Front 41

What are the side effects of colestipol, cholestyramine?

Back 41

Patients hate it - tastes bad and causes GI discomfort, decreased absorption of fat-soluble vitamins

Front 42

Name of cholesterol absorption blocker

Back 42

Ezetimibe

Front 43

Toxicity of ezetimibe

Back 43

Rare incrase in LFTs

Front 44

Mechanism of ezetimibe

Back 44

Prevent cholesterol reabsorption at small intestine brush border

Front 45

Fenofibrate, clofibrate mechanims

Back 45

Upregulate LPL causing increased TG clearance

Front 46

Side effects of gemfibrozil, bezafibrate

Back 46

Myositis, increased LFTs

Front 47

B1 receptors on cardiac cells are what G protein motif which end up doing what

Back 47

Gs, activate PKA and phosphorylates L-type Ca2+ channels and phospholamban, both of which increase intracellular Ca2+ druing contraction

Front 48

Mechanism of action of digoxin

Back 48

Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. Increased Ca results in positive inotropy. Also stimuates vagus nerve

Front 49

Clinical uses of digoxin

Back 49

CHF (Increase contractility) and AFib (Decrease conduction at AV node and depression of SA node)

Front 50

Toxicity of digoxin seen on eCG

Back 50

Increased PR, Dec QT, scooping ST segment, T wave inversion on ECG

Front 51

What increases the toxicities of digoxin?

Back 51

Renal failure (Decreased excretion), hypokalemia (digoxin competes with K+ at binding site in Na+/K+ ATPase so decreased K+ means increased digoxin biding and effect), and quinidine (decreased digoxin clearance, displaces digoxin from tissue binding sites)

Front 52

Antidote for digoxin poisoning

Back 52

Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+

Front 53

AP length effect on Class IA, IB, IC antiarrythmics

Back 53

1A: Increase 1B: Decrease 1C: No effect

Front 54

What class antiarrhythmic is Disopyramide?

Back 54

IA

Front 55

Class 1A antiarrythmics are used for what abnormalities?

Back 55

Atrial and ventricular arrhythmias, esp reentrant and ectopic supraventricular and ventricular tachycardia

Front 56

Toxicity of quinidine

Back 56

Cinchonism - headache, tinnitus, thrombocytopenia; Torsades de pointes due to increased QT interval

Front 57

Toxicity of procainamide

Back 57

Reversible SLE-like syndrome

Front 58

What are the Class 1B antiarrythmics?

Back 58

Lidocaine, Mexiletine, Tocainide

Front 59

What abnormalities does Mexiletine and it's class correct?

Back 59

Affects ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythmias (esp post M!) and in digitalis induced arrhythmias NO EFFECT on atrial arrythmias

Front 60

Toxicities of Class 1B antiarrhythmics

Back 60

Local anesthetic, CNS stimulation/depression, cardiovascular depression

Front 61

What are the class 1C antiarrythmics

Back 61

Flecainide, encainide, propafenone

Front 62

What are Class 1C antiarrhythmics used for?

Back 62

V-tachs that progress to VF and in intractable SVT. usually used only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities

Front 63

Toxicities of Class 1C antiarrhythmics

Back 63

Proarrhythmic, esp post-MI (contraindicated), significantly prolongs refractory period in AV node

Front 64

What causes increased toxicity for all class I drugs?

Back 64

Hyperkalemia

Front 65

What is the mechanism of Class II antiarrhythmics?

Back 65

B-blockers - decrease cAMP, decrease Ca2+ currents. Suppress abnomral pacemakers by decreasing slope of phase 4. AV node particularly sensitive increasing the PR interval.

Front 66

Which of the Class II antiarrhythmics are the shortest acting?

Back 66

Esmolol

Front 67

What are the clinical uses for metoprolol, esmolol, etc.?

Back 67

V-tach, SVT, slowling ventricular rate during Afib and A. flutter

Front 68

What is a toxicity particular to metoprolol

Back 68

Dyslipidemia

Front 69

Name 4 commonly used Class III antiarrhthmics

Back 69

Sotalol, ibutilide, amiodarone, dofetilide

Front 70

What is the mechanism of action of Class III antiarrythmics?

Back 70

Increase AP duration, increase effective refractory period. Increases QT interval

Front 71

Which class of antiarrhythmics is state dependent?

Back 71

Class I (selectively depress tissue that is frequently depolarized)

Front 72

When is Class III antiarrhythmics used?

Back 72

When other antiarrhythmics fail

Front 73

Toxicity of sotalol

Back 73

Torsades de pointes, excessive B block (sotalol is a racemic mixture with class III and beta-blocker)

Front 74

What is the toxicity of ibutilide?

Back 74

Torsades de pointes

Front 75

Toxicities of amiodarone?

Back 75

Pulmonary fibrosis, corneal depsoits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, CV effects(bradycardia, heart block, CHF), hypothyroidism/hyperthyroidism

Front 76

What needs to be checked when using amiodarone?'

Back 76

TFTs, PFTs, LFTs

Front 77

What class of antiarrythmics have Torsades as potential toxicity?

Back 77

Class III, Class 1A (Increased QT intervals)

Front 78

Name the two Class IV antiarrhythmics commonly used

Back 78

Verapamil, diltiazem

Front 79

Mechanism of Class IV antiarrythmics

Back 79

Ca2+ channel blockers. Primarily affect AV cells. Decrease condiction velocity, Inc ERP, Inc PR interval, used in prevention of nodal arrhythmias (SVT)

Front 80

Which two class of antiarrythmics primarily affect AV nodal cells?

Back 80

Class II and Class IV

Front 81

Toxicities of Class IV antiarrythmics

Back 81

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

Front 82

Mechanism of Adenosine as an antiarrythmic

Back 82

Increase K+ out of cells, hyperpolarizing cell and decreasing Ca+

Front 83

What is the drug of choice in diagnosing/abolishing AV nodal arrythmias?

Back 83

Adenosine

Front 84

What are the toxicities of adenosine

Back 84

Flushing, hypotension, chest pain

Front 85

K+ is used as an antiarrhythmic how?

Back 85

Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)

Front 86

What is Mg2+ used for as an antiarrythmic

Back 86

Torsades de pointes and digoxin toxicity