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PHARMACOLOGY > DRUGs ACTING ON THE CARDIOVASCULAR SYSTEM > Flashcards

DRUGs ACTING ON THE CARDIOVASCULAR SYSTEM Flashcards

1
Q

7 Drugs acting on the cardiovascular system

A

Anti-hypertensive drugs
Cardiotonic agents
Antiarrhythmic agents
Antianginal agents
Lipid lowering agents
Drugs affecting blood coagulation
Drugs used to treat anemia

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2
Q

Since the underlying cause of hypertension is
usually unknown (essential hypertension),
altering the body’s regulatory mechanisms is
the best treatment available. These
drugs work by altering the normal reflexes that
control blood pressure.

A

Anti-hypertensive drugs

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3
Q

4 subclasses of Antihypertensive drugs

A
  1. AngIOtenSIn-COnVertIng-EnZYMe (ACE)InHIBItOrS
  2. AngIOtenSIn II ReCePtOr BLOCKerS (ARBS)
  3. CaLCIuM-CHanneL BLOCKerS
  4. VaSODILatOrS
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4
Q

act in the lungs to prevent ACE from converting
angiotensin I to angiotensin II, a powerful vasoconstrictor and stimulator
of aldosterone release.

A

ACE INHIBITORS

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5
Q

Drugs under ACE INHIBITORS

A

Ends with Pril
Benazepril

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6
Q

selectively bind with the angiotensin II receptors in vascular smooth
muscle and in the adrenal cortex to block vasoconstriction and the release of
aldosterone.

A

ARBS

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7
Q

Drugs under ARBS

A

ending with Tan
losartan

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8
Q

inhibit the movement of calcium ions
across the membranes of myocardial and arterial muscle cells,
altering the action potential and blocking muscle cell contraction.

A

Calcium channel blockers

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9
Q

drugs under calcium channel blockers

A

ending with pine
amlodipine

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10
Q

act directly on vascular smooth muscle to cause muscle
relaxation, leading to vasodilation and drop in BP.

A

vasodilators

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11
Q

drugs under vasodilators

A

Diazoxide (Hyperstat)
• Hydralazine (Apresoline)
• Minoxidil (Loniten)
• Nitroprusside (Nitropress)

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12
Q

a common, often asymptomatic disorder in which systolic blood
pressure persistently exceeds 140 mm Hg and/or diastolic pressure exceeds 90mmhg

A

hypertension

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13
Q

sustained blood pressure above normal limits with no
discernible underlying cause.

A

Essential hypertension

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14
Q

sustained blood pressure that is lower than that required to
adequately perfuse all of the body’s tissues.

A

hypotension

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15
Q

force that resists the flow of blood through the vessels,
mostly determined by the arterioles, which contract to increase resistance;
important in determining overall blood pressure

A

peripheral resistance

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16
Q

drugs used to increase
the contractility of the heart muscle for patients
experiencing heart failure.

A

cardiotonics

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17
Q

2 subclasses of cardiotonics

A

CarDIaC
GLYCOSIDe
PHOSPHODIeSteraSe
InHIBItOrS

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18
Q

originally derived from
the foxglove or digitalis plant. These plants were once
ground up to make digitalis leaf. indicated for treating heart
failure and irregular heartbeats.

A

cardiac glycoside

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19
Q

drugs under cardiac glycoside

A

digoxin- brand name called Lanoxin. Most
frequently it is used for atrial fibrillation, atrial flutter,
and heart failure it is one of the oldest
medications used in the field of cardiology
digitoxin- cardiac glycoside used for the
treatment of heart failure and certain kinds of heart
arrhythmia. It is a phytosteroid and is similar in
structure and effects to digoxin.

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20
Q

belong to a second class
of drugs that act as cardiotonic (inotropic) agents. These
include inamrinone (Inocor) and milrinone (Primacor).
Approved only for use in patients with HF who does not
have been responsive to digoxin, diuretics, or
vasodilators.
● Short-term management of HF in adults receiving digoxin
and diuretics

A

Phosphodiesterase inhibitor

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21
Q

enlargement of the heart, commonly seen with chronic
hypertension, valvular disease, and heart failure

A

cardiomegaly

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22
Q

disease of the heart muscle that leads to an enlarged heart
and eventually to complete heart muscle failure and death

A

cardiomyopathy

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23
Q

discomfort with respirations, often with a feeling of anxiety and
inability to breathe, seen with left-sided heart failure.

A

dyspnea

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24
Q

condition in which the heart muscle fails to adequately pump
blood around the cardiovascular system, leading to a backup or congestion of
blood in the system

A

heart failure

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25
Q

blood-tinged sputum, seen in left-sided heart failure when blood
backs up into the lungs and fluid leaks out into the lung tissue

A

hemoptysis

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26
Q

getting up to void at night, reflecting increased renal perfusion with fluid
shifts in the supine position when person has gravity-dependent edema related to
heart failure; other medical conditions, including urinary tract infection, increase
the need to get up and void

A

nocturia

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27
Q

difficulty breathing when lying down, often referred to by the
number of pillows required to allow a person to breath comfortably

A

orthopnea

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28
Q

effect resulting in an increased force of contraction

A

positive inotropic

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29
Q

severe left-sided heart failure with backup of blood into the
lungs, leading to loss of fluid into the lung tissue

A

pulmonary edema

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30
Q

rapid and shallow respirations, seen with left sided heart failure

A

tachypnea

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31
Q

also known as
cardiac dysrhythmia medications, are a
group of pharmaceuticals that are used to
suppress abnormal rhythms of the heart
(cardiac arrhythmias), such as atrial
fibrillation, atrial flutter, ventricular
tachycardia, and ventricular fibrillation.

A

antiarrhythmic agents

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32
Q

subclasses of antiarrhythmic agents

A

calsses 1
classes 2
classes 3
classes 4

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33
Q

are fast sodium channel blockers. These drugs preferable in conditions such as tachycardia,
in which the sodium gates are open frequently

A

class 1 anti arrythmics

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34
Q

are conventional beta blockers competitively block
beta-receptor sites in the heart and kidneys.
● These drugs are indicated for the treatment of
supraventricular tachycardias and PVCs.

A

class 2 antiarrhythmic

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35
Q

act by blocking depolarizing currents and thereby prolonging the
effective refractory period of the myocardium. block potassium channels and slow the outward
movement of potassium during phase 3 of the action potential, prolonging it.

A

class 3 antiarrhythmic

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36
Q

slow non-dihydropyridine calcium channel blockers. block the movement of calcium ions across the
cell membrane, depressing the generation of action potentials and delaying
phases 1and 2 of repolarization, which slows automaticity and conduction.

A

class 4 antiarrhythmic

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37
Q

slower-than-normal heart rate (usually less than60 beats/min).

A

bradycardia

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38
Q

the amount of blood the heart can pump per beat; influenced by the
coordination of cardiac muscle contraction, heart rate, and blood return to the heart

A

cardiac output

39
Q

large research study run by the National
Heart and Lung Institute that found that long-term treatment of arrhythmias may have
a questionable effect on mortality, and in some cases actually lead to increased cardiac
death; basis for the current indication for antiarrhythmics (short-term use to treat

A

CAST cardiac arrhythmia suppression test

40
Q

blocks to conduction of an impulse through the cardiac conduction
system; can occur at the atrioventricular node, interrupting conduction from the
atria into the ventricles, or in the bundle branches within the ventricles,preventing
the normal conduction of the impulse.

A

heartblocks

41
Q

study of the forces moving blood throughout the cardiovascular

A

hemodynamics

42
Q

used to reduce ischemia by increasing the
delivery of oxygen-rich blood to cardiac tissues or by
reducing oxygen consumption by the coronary vessels.
Either of these mechanisms can reduce ischemia and
lead to a decrease in anginal pain.

A

antianginal agents

43
Q

subclasses of antianginal agents

A

nitrates and nitrites
beta blockers
calcium channel blockers

44
Q

work mainly by decreasing venous return to
the heart (preload) and decreasing systemic vascular resistance
(afterload).

A

nitrates and nitrites

45
Q

help by slowing the heart rate and decreasing
contractility, thereby decreasing oxygen demands.

A

beta blockers

46
Q

decrease calcium influx into the smooth
muscle, causing vascular relaxation. considered first-line
drugs for the treatment of such conditions as angina, hypertension, and
supraventricular tachycardia.

A

calcium channel blockers

47
Q

Chest pain that occurs when the heart’s supply of blood
carrying oxygen is insufficient to meet the demands of the he

A

angina pectoris

48
Q

common form of arteriosclerosis involving deposits of fatty,
cholesterol-containing material (plaques) within arterial walls

A

atherosclerosis

49
Q

Chest pain that is primarily caused by atherosclerosis,
which results in a long-term but relatively stable level of obstruction in one or
more coronary arteries. (p. 369)

A

chronic stable angina

50
Q

Arteries that deliver oxygen to the heart muscle.

A

coronary arteries

51
Q

Any one of the abnormal conditions that can
affect the arteries of the heart and produce various pathological effects,
especially a reduced supply of oxygen and nutrients to the myocardiu

A

coronary artery disease CAD

52
Q

Poor blood supply to an organ. (p.

A

ischemia

53
Q

Poor blood supply to the heart via the coronary arteries

A

ischemic heart disease

54
Q

Necrosis of the myocardium following interruption of
blood supply; it is almost always caused by atherosclerosis of the coronary
arteries and is commonly called a heart attack

A

myocardial infarction

55
Q

A rapid heartbeat caused by a variety of autonomic nervous
system effects, such as blood pressure changes, fever, or emotional stress

A

reflex tachycardia

56
Q

Early stage of progressive coronary artery disease.

A

unstable angina

57
Q

Ischemia-induced myocardial chest pain caused by spasms
of the coronary arteries; also referred to as Prinzmetal or variant angina. (p. 369)

A

vasospastic angina

58
Q

lower serum levels of
cholesterol and various lipids. l

A

lipid lowering agents

59
Q

subclasses of lipid lowering agents

A

bile acid sequestrants
HMG-COA reductase inhibitors/statins
cholesterol absorption inhibitor

60
Q

prevent the reabsorption of bile salts, which
are very high in cholesterol. Consequently, the liver will pull
cholesterol from the blood to make new bile acids, lowering the
serum cholesterol level.

A

BILe ACIDSequeStrantS

61
Q

block the
enzyme HMG-CoA reductase, resulting in lower serum
cholesterol levels, a resultant breakdown of LDLs, and a
slight increase in HDLs

A

HMG-COAREDuCtaSe
InHIBItOrS/ StatInS

62
Q

works in the brush
border of the small intestine to prevent the absorption of dietary
cholesterol, which leads to increased clearance of cholesterol by
the liver and a resultant fall in serum cholesterol.
· Change in diet and increased exercise are very important parts of
the overall treatment of a patient receiving a cholesterol
absorption inhibitor.

A

CHOLeSterOLABSOrPtIOn InHIBItOr

63
Q

general term used for drugs used to lower lipid levels
in the blood.

A

Antihyperlipidemic agents

64
Q

cholesterol-containing acids found in the bile that act like detergents
to break up fats in the small intestine.

A

bile acids

65
Q

necessary component of human cells that is produced and
processed in the liver, then stored in the bile until stimulus causes the
gallbladder to contract and send the bile into the duodenum via the common
bile duct;

A

cholesterol

66
Q

carrier for lipids in the bloodstream, consisting of proteins, lipids,
cholesterol, and so forth.

A

chylomicrons

67
Q

endogenous substances that activate nervous system
receptors that are important in the regulation of appetite, food intake, and
metabolism.

A

endocannabinoid

68
Q

loosely packed chylomicron containing fats, able
to absorb fats and fat remnants in the periphery;

A

HDL

69
Q

A (HMG-CoA) reductase: enzyme that
regulates the last step in cellular cholesterol synthesis.

A

hydroxymethylglutaryl-coenzyme

70
Q

increased levels of lipids in the serum, associated with increased
risk of coronary artery disease development.

A

hyperlipidemia

71
Q

tightly packed fats that are thought to contribute
to the development of coronary artery disease when remnants left over from
the LDL are processed in the arterial lining.

A

LDL

72
Q

a collection of factors, including insulin resistance,
abdominal obesity, low high-density lipoprotein and high triglyceride levels,
hypertension, and proinflammatory and prothrombotic states, that increase the
incidence of coronary artery disease.

A

metabolic syndrome

73
Q

factors that have been identified as increasing the risk of the
development of a disease; for coronary artery disease, risk factors include
genetic predisposition, gender, age,

A

risk factors

74
Q

some of the most
dangerous drugs used today, and numerous factors
can affect their action. These drugs are among the
most commonly associated with adverse drug
reactions.

A

drugs affecting blood coagulation

75
Q

sublasses of drugs affecting blood coagulation

A

anticoagulants
antiplatelet drugs
thrombolytic drugs

76
Q

drugs that interfere with the normal coagulation process
by interfering with the clotting cascade and thrombin formation.

A

anticoagulants

77
Q

decrease the formation of the platelet plug by decreasing the
responsiveness of the platelets to stimuli that would cause them to stick and
aggregate on a vessel wall.

A

antiplatelEt drugs

78
Q

break down the thrombus that has been formed by
stimulating the plasmin system. thrombus has already formed in a vessel (e.g., during an
acute MI), it may be necessary to dissolve that clot to open the
vessel and restore blood flow to the dependent tissue.

A

thrombolytic agents

79
Q

drugs that block or inhibit any step of the coagulation process,
preventing or slowing clot formation

A

anticoagulants

80
Q

drugs that interfere with the aggregation or clumping of
platelets to form the platelet plug

A

antiplatelet agent

81
Q

the process of blood’s changing from a fluid state to a solid state
to plug injuries to the vascular system

A

coagulation

82
Q

drugs that lyse, or break down, a clot that has formed;
these drugs activate the plasminogen mechanism to dissolve fibrin threads

A

thrombolytic agents

83
Q

7th drug class

A

drugs used to treat anemia

84
Q

subclasses of drugs used to treat anemia

A

ErYtHrOPOIeSIS
StIMuLatIng
AgentS
AgentS uSeD FOr
IrOn-DeFICIenCY AneMIa
AgentS USeD
FOrOtHer aneMIaS

85
Q

substance that stimulates the bone marrow to
make more red blood cells.

A

ErYtHrOPOIeSIS StIMuLatIng AgentS

86
Q

Indicated for the treatment of iron-deficiency anemias and may also
be used as adjunctive therapy in patients receiving an
erythropoiesis-stimulating drug

A

AgentS uSeD FOrIrOn-DeFICIenCY aneMIa

87
Q

treated with folic acid and vitamin B12 tissue. Folic
acid and vitamin B12 are essential for cell growth and division and for the
production of a strong stroma in RBCs.

A

MegaLOBLaStIC aneMIaS
l

88
Q

treated with antibiotics to help
fight the infections that can occur when blood flow is decreased to any
area; with pain-relieving activities to help alleviate the pain associated
with the anoxia to tissues, which can range from heat applied to the
area to over-the-counter pain medications to prescription opioids; and
now, for adults, with hydroxyurea (Droxia).

A

sickle cell anemia

89
Q

disorder involving too few red blood cells (RBCs) or ineffective RBCs that can
alter the blood’s ability to carry oxygen

A

anemia

90
Q

RBCs, responsible for carrying oxygen to the tissues and removing
carbon dioxide; they have no nucleus and live approximately 120 days

A

erythrocytes

91
Q

process of RBC production and life cycle; formed by megaloblastic
cells in the bone marrow, using iron, folic acid, carbohydrates, vitamin B12, and amino
acids; they circulate in the vascular system for about 120 days and then are lysed and
recycled

A

erythropoiesis

92
Q

glycoprotein produced by the kidneys, released in response to
decreased blood flow or oxygen tension in the kidney; controls the rate of RBC
production in the bone marro

A

erythropoietin

93
Q

RBC count with low iron available because of high
demand, poor diet, or poor absorption; treated with iron replacement

A

iron deficiency anemia

94
Q

anemia caused by lack of vitamin B12 and/or folic acid, in which
RBCs are fewer in number and have a weak stroma and a short lifespan; treated by
replacement of folic acid and vitamin B12

A

megaloblastic anemia

PHARMACOLOGY (3 decks)

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