Pharmocology Test 3

Front 1

back up of blood into the venous side of the heart. This leads to liver enlargement and edema in the lower extremeties...

Back 1

Right-sided heart failure

Front 2

This leads to back up of blood into the lungs and results in pulmonary edema

Back 2

left-sided heart failure

Front 3

Diuretics, cardiac glycosides, ACE inhibitors, and vasodialtors

Back 3

Drugs used to treat congestive heart failure (CHF)

Front 4

Digitalis and digoxin (Lanoxin)

Back 4

Cardiac glycosides

Front 5

Dobutamine, dopamine, amiodarone

Back 5

Inotropic drugs

Front 6

Atropine

Back 6

Anticholinergics

Front 7

nitroglycerin (Nitro-Bid) isosorbide dinitrate (Isordil)

Back 7

Nitrates

Front 8

Ability of cardiac glycosides to slow the heart rate. cardiac glycosides cause the release of acetylcholine which depresses the SA node and slows electrical conduction.

Back 8

negative chronotropic effect

Front 9

This referes to the ability of cardiac glycosides to increase the strength of contractions

Back 9

Positive inotropic effect

Front 10

This drug has a low therapeutic index,
meaning the margin of safety between the
effective dose and the toxic dose is very
narrow

Back 10

Digitalis Toxicity

Front 11

remove excess fluid. for CHF

Back 11

Diuretics

Front 12

which are also used in the
treatment of hypertension) decrease the resistance to blood flow by inducing vasodilation.
captopril (Capoten)
enalapril (Vasotec)

Back 12

ACE Inhibitors

Front 13

(most of which should be used with caution in patients with CHF) slow the heart rate (negative chronotropy) and causes some vasodilation, (which helps to “unload”the heart)
verapamil (Calan)
nifedipine (Procardia)

Back 13

Calcium Channel Blockers

Front 14

is reversible heart pain due to lack of oxygen

Back 14

Angina Pectoris (usually just called Angina

Front 15

cause vasodilation throughout the circulatory system making more blood (and O2 ) available to the heart muscle

Back 15

Nitrates

Front 16

These drugs lower the heart rate which dramatically decreases the heart muscle’s need for O2

propanolol(Inderal)

Back 16

Beta blockers

Front 17

was the first β-blocker, developed in the late 1970’s, and has found use in treating angina, arrhythmias, migraine headaches, and hypertension

Back 17

propanolol(Inderal)

Front 18

decrease blood pressure, decrease heart rate, and increase coronary blood flow - all of which improve myocardial O2 supply vs. O2 demand

Back 18

Ca-channel blockers

Front 19

used to inhibit a clot, or “bust” the clot in a clogged coronary artery. Aspirin is the first thing administered in acute MI to restore blood flow (inhibit platelet aggregation and the formation of an obstructing blood clot)

Back 19

Anticoagulant or Thrombolytic Drugs

Front 20

when given within 24 hours of an MI can increase survival rates

Back 20

ACE Inhibitors

Front 21

abnormal patterns of electrical conduction in the heart, including bradycardias (slow heart rates), tachycardias (fast heart rates), fibrillation (a disorganized pattern), and irregular heart rates

Back 21

Dysrhythmias

Front 22

slow heart rates

Back 22

bradycardias

Front 23

fast heart rates

Back 23

tachycardias

Front 24

a disorganized pattern

Back 24

fibrillation

Front 25

atropine, which blocks parasympathetic nerve fibers to the SA node (the heart’s normal pacemaker)

Back 25

Drugs used to treat bradycardia

Front 26

verapamil (Calan), a Ca-blocker

Back 26

Drugs used to treat atrial dysrhythmias

Front 27

lidocaine (Xylocaine), procainamide (Pronestyl), and quinidine (Quinaglute) block fast sodium channels in the heart

Back 27

Drugs used to treat ventricular dysrhythmias

Front 28

are used to control a variety of
dysrhythmias by slowing the heart rate

Back 28

β-blockers

Front 29

some are used more than others when it comes to controlling abnormal rhythms.
verapamil (Calan) instead of, say, nifedipine (Procardia), which is more often used in the treatment of angina

Back 29

Calcium channel blockers

Front 30

digoxin is used to control (Blank)because it causes a release of ACh which will slow down the SA node

Back 30

tachycardias

Front 31

is broadly
defined as a BP>135/90

Back 31

Hypertension

Front 32

historically been the first-line drugs for treatment of uncomplicated, “essential” HTN

HCTZ prevents re-absorption of Na+ in the distal tubules of the kidneys

Back 32

Diuretics

Front 33

block both the β1&β2Rc

Back 33

Non selective Beta Blockers

Front 34

block mainly β1while sparing the β2Rc. This group has less undesirable effects on bronchial airways, e.g. atenolol (Tenormin)

Back 34

Cardioselective Beta Blockers

Front 35

relax the smooth muscle of blood vessels causing them to dilate (thus lowering BP)

verapamil (Calan), and nifedipine (Procardia)

Back 35

Ca++ channel blockers

Front 36

Both the vasoconstriction effects of Angiotensin II, and the Na+ resorption effects of aldosterone promote HTN.

Back 36

ACE Inhibitors

Front 37

captopril (Capoten) and enalapril (Vasotec)

Back 37

ACE Inhibitors

Front 38

All of these drugs have the ending “sartan”-losartan (Cozaar), valsartan (Diovan)

Back 38

Angiotensin II Blockers

Front 39

Some (like hydralazine) inhibit flow of Ca++in smooth muscle (but not by the same mechanism as Ca++ channel Blockers) while others (diazoxide –pg 167) open potassium channels in vascular smooth muscle. They all cause vascular resistance to decrease and blood vessels to dilate

Back 39

vasodilators

Front 40

hydralazine (Apresoline)
•
minoxidil (Loniten) - which is used to increase blood flow to the scalp to treat baldness

Back 40

vasodilators

Front 41

Tenoretic (Tenormin + HCTZ)

Back 41

A diuretic + β-blocker

Front 42

Capozide (captopril + HCTZ)

Back 42

A diuretic + ACE inhibitor

Front 43

This drug stimulates the opening of K+ channels and stabilizes the cell membrane potential at resting levels

Back 43

diazoxide (Hyperstat—I.V.)

Front 44

treated with platelet inhibiting drugs (drugs which have the same effect on platelets
as aspirin) and with Vasodilator
Drugs like the Ca-Blockers

Back 44

Peripheral Vascular Disease PVD

Front 45

a “good”lipid which carries wayward fats
from blood vessels back to the liver

Back 45

HDL

Front 46

a lipid which carries cholesterol to cells. It is only “bad”when there is too much of it

Back 46

LDL

Front 47

most of our triglycerides are carried here, and are considered to be “bad”when found in excess

Back 47

VLDL

Front 48

called Statins
for short. They block the production of LDL while increasing HDL

Back 48

HMG Co-A Reductase Inhibitors

Front 49

currently the most widely used lipid lowering drugs because they have a good side effect profile (however, liver and muscle function
must be monitored)

atorvastatin (Lipitor)

simvastatin (Zocor)

Back 49

Statins

Front 50

activate an enzyme that speeds the breakdown of triglycerides in the blood. Not used as much since the Statins came along

gemfibrozil (Lopid)

Back 50

Fibrates

Front 51

cholestyramine (Questran)

Back 51

Bile Sequestrants

Front 52

Some Uses for Anticoagulants

Back 52

prevent deep venous thrombosis (DVT)

prevent pulmonary embolisms (related to DVT formation);

provide anticoagulation during hemodialysis and cardiopulmonary bypass;

prevent stroke or the recurrence of stroke;

prevent Myocardial Infarction or the recurrence of MI

treat acute MI or stroke

Front 53

reduce the ability of platelets to aggregate and help form a clot

Back 53

Platelet Inhibitors

Front 54

enoxaparin (Lovenox)

Back 54

low molecular weight heparins (LMWH)

Front 55

inhibit vitamin K which is essential for clotting factors II, V, VII and X to function

Back 55

Oral Anticoagulants

Front 56

“rat poison”, is one of the most complex drugs that a physician can employ

Back 56

warfarin (Coumadin

Front 57

inhibit the ability of thrombin to activate fibrinogen (fibrinogen is cleaved to form fibrin, one of the last steps in the clotting process)

Back 57

Direct Thrombin Inhibitors

Front 58

bivalirudin (Angiomax)

Back 58

Direct Thrombin Inhibitors

Front 59

Are used to lyse (break apart or “bust”) a clot that has already formed. They work by converting plasminogen to plasmin (an enzyme which breaks apart the fibrin strands in a clot).

Back 59

Thrombolytic Drugs

Front 60

Tissue Plasminogen Activators, or t-PA’s are the most common

Back 60

thrombolytics