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Pharm II > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Ch. 22: Atrial Fibrillation

A

A common cardiac dysrhythmia involving atrial contractions that are so rapid that they prevent full depolarization of myocardial fibres between heart beats

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2
Q

Ch. 22: Automaticity

A

A property of specialized excitable tissue that allows self-activation through the spontaneous development of an action potential, as in the pacemaker cells of the heart

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3
Q

Ch. 22: Cardiac Glycosides

A

Glycosides (carbohydrates that yield a sugar and a non sugar upon hydrolysis) that are derived from the plant species Digitalis Purpurea and are used in the treatment of heart disease

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4
Q

Ch. 22: Chronotropic Drugs

A

Drugs that influence the rate of the heartbeat

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5
Q

Ch. 22: Dromotropic Drugs

A

Drugs that influence the conduction of electrical impulses

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6
Q

Ch. 22: Ejection Fraction

A

The proportion of blood that is ejected during each ventricular contraction compared with the total ventricular filling volume

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7
Q

Ch. 22: Heart Failure

A

An abnormal condition in which cardiac pumping is impaired as the result of myocardial infarction, ischemic heart disease, or cardiomyopathy

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8
Q

Ch. 22: Inotropic Drugs

A

Drugs that affect the force or energy of muscular contractions, particularly contraction of the heart muscle

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9
Q

Ch. 22: Left Ventricular End-Distolic Volume (LVEDV)

A

The total amount of blood in the ventricle before it contracts, or the preload

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10
Q

Ch. 22: Phosphodiesterase Inhibitors

A

A group of inotropic drugs that work by inhibiting the enzyme phosphodiesterase

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11
Q

Ch. 22: Refractory Period

A

The period during which a pulse generator (e.g., the sinoatrial node of the heart) is unresponsive to an input signal of specified amplitude and it is impossible for the myocardium to respond

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12
Q

Ch. 22: Therapeutic Window

A

The range of drug levels in the blood that is considered beneficial as opposed to toxic or ineffective

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13
Q

Ch. 22: What percentage of the general population does heart failure affect?

A

Heart failure affects 1% to 2% of the general population, or approximately 450,000 Canadians

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14
Q

Ch. 22: Signs and Symptoms of Left Ventricle Heart Failure

A

Producing pulmonary edema and symptoms of dyspnea or cough

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15
Q

Ch. 22: Signs and Symptoms of Right Ventricle Heart Failure

A

Producing symptoms such as pedal edema, jugular venous distention, ascites, and liver congestion

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16
Q

Ch. 22: What is the normal ejection fraction?

A

Approximately 65% (0.65) of the total volume in the ventricle

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17
Q

Ch. 22: What does increased hydrostatic pressure from the left ventricle lead to?

A

Pulmonary congestion

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18
Q

Ch. 22: What does increased hydrostatic pressure from the right ventricle lead to?

A

Systemic venous congestion and peripheral edema

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19
Q

Ch. 22: What are the two types of physical defects producing heart failure?

A
  1. A heart defect (myocardial deficiency such as myocardial infarction or valve insufficiency), which leads to inadequate cardiac contractility and ventricular filling
  2. A defect outside the heart (e.g., systemic defects such as coronary artery disease, pulmonary hypertension, or diabetes), which results in an overload on an otherwise normal heart
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20
Q

Ch. 22: What are the common causes of Inadequate Contractility?

A

Cardiomyopathy
Coronary artery disease
Infection
Myocardial infarction

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21
Q

Ch. 22: What are the common causes of Inadequate Filling?

A

Atrial fibrillation
Infection
Ischemia
Tamponade

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22
Q

Ch. 22: What are the common causes of Pressure Overload?

A

Hypertension

Outflow Obstruction

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23
Q

Ch. 22: What are the common causes of Volume Overload?

A

Anemia
Congenital abnormalities
Hypervolemia
Thyroid disease

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24
Q

Ch. 22: What is the most frequently prescribed cardiac glycoside?

A

Digoxin is the most fequenly prescribed cardiac glycoside and the only one currently available in Canada

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25
Q

Ch. 22: Data recently released on the use of cardiac glycosides

A

Digoxin therapy as a first line treatment of heart failure did not improve mortality rates. Angiotensin-converting enzyme (ACE) inhibitors and diuretics were recommended as the key drugs to offer therapeutic benefit

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26
Q

Ch. 22: What are the primary beneficial effects of a cardiac glycoside?

A

The primary beneficial effect f a cardiac glycoside is thought to be an increase in myocardial contractility. This occurs secondary to the inhibition of the sodium-potassium ATPase pump

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27
Q

Ch. 22: Digoxin…

A

Digoxin also auguments (cholinergic or parasympathetic) vagal tone, resulting in increased diastolic filling between heartbeats secondary to reduced heart rate. This further enhances cardiac efficiency and output

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28
Q

Ch. 22: What are the dramatic inotropic, chronotropic, dromotropic, and other heart effects that digoxin produces?

A
  • A positive inotropic effect, resulting in an increase in the force and velocity of myocardial contraction without a corresponding increase in oxygen consumption
  • A negative chronotropic effect, producing a reduced heart rate
  • A negative dromotropic effect that decreases automaticity at the SA node, decreases AV nodal conduction, reduces conductivity at the bundle of His, and prolongs the atrial and ventricular refractory periods
  • An increase in store volume
  • A reduction in heart size during diastole
  • A decrease in venous blood pressure and vein engorgement
  • An increase in coronary circulation
  • Promotion of dieresis as the result of improved blood circulation
  • Palliation of exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis
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29
Q

Ch. 22: What is the primary use of Cardiac Glycosides?

A

Cardiac glycosides are used primarily in the treatment of heart failure and supra ventricular dysrhythmias
Cardiac glycosides are also effective in the treatment of supraventricular dysrhythmias such as atrial fibrillation and atrial flutter because of their negative chronotropic and negative dromotropic actions

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30
Q

Ch. 22: What are the contraindications to the use of cardiac glycosides?

A

Known drug allergy, may include second- or third- degree heart block, atrial fibrillation, ventricular tachycardia or fibrillation, heart failure resulting from diastolic dysfunction, and subaortic stenosis

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31
Q

Ch. 22: What are the common adverse effects of cardiac glycosides?

A

Any type of dysrhythmia including bradycardia or tachycardia. Headache, fatigue, malaise, confusion, convulsions. Coloured vision, halo vision, or flickering lights. Anorexia, N/V/D

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32
Q

Ch. 22: What are some of the possible interactions of cardiac glycosides?

A

Bran, taken in large amounts, may decrease the absorption or oral digitalis drugs.
Hawthorne (herbal supplement) can reduce the effectiveness of cardiac glycosides.
The consumption of excessive amounts of potassium-rich foods can decrease its therapeutic effect whereas the consumption of excessive amounts of liquorice can increase digoxin toxicity as the result of the hypokalemia produced. St. John’s wort (Hypericum perforatum) may interfere with intestinal digoxin absorption, resulting in low serum concentrations of digoxin

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33
Q

Ch. 22: What are Phosphodiestrerase Inhibitors?

A

Phosphodiesterase Inhibitors are a group of inotropic drugs that work by inhibiting an enzyme called phosphodiesterase. The inhibition of this enzyme results in two beneficial effects in an individual with heart failure: a positive inotropic response and vasodilation.

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34
Q

Ch. 22: What is the sole phosphodiesterase inhibitor available in Canada?

A

Milrinone

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35
Q

Ch. 22: How does Milrinone work?

A

Milrinone works by selectively inhibiting phosphodiesterase type III, which results in more calcium for the heart to use in muscle contraction. The increased calcium in heart muscle contraction. The increase calcium in heart muscle is also taken back up into its storage sites in the sacroplasmic reticulum at a much faster rate than normal. As a result, the heart muscle relaxes and is more compliant.

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36
Q

Ch. 22: What are the indications of Milrinone?

A

Milrinone is primarily used as an indicator for the short-term management of heart failure.
Traditionally, a PDI is administered to patients who can be closely monitored and who have not responded adequately to digoxin, diuretics, or vasodilators.
Many hospitals that treat large numbers of patients with heart failure now treat those experiencing end-stage heart failure with weekly 6-hour infusions of milrinone. This has been shown to increase patients’ quality of life and decrease the number of re-admissions to the hospital for exacerbations of heart failure

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37
Q

Ch. 22: What are the contraindications of PDIs?

A

Known drug allergy, and may include the presence of severe aortic or pulmonary valvular disease and heart failure resulting from diastolic dysfunction

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38
Q

Ch. 22: What are the adverse effects seen with milrinone therapy?

A

Primary adverse effects are ventricular dysrhythmia, occurring in approximately 12% of patients treated with this drug, hypotension (3.1%), headache (2.4%), angina, pectoris, and chest pain (1.4%), hypokalemia (0.7%), tremor (0.5%), and thrombocytopenia (0.5%)

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39
Q

Ch. 22: What is the toxicity and management of overdose for milrinone?

A

No specific antidote exists for an overdose f milrinone

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40
Q

Ch. 22: What are some of the interactions seen with PDIs (milrinone)?

A

Concurrent administration of diuretics may cause significant hypovolemia and reduced cardiac filling pressure. Also, additive inotropic effects may be seen with coadministration of digoxin. Furosemide must not be injected into IV lines of milrinone because it will precipitate immediately

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41
Q

Ch. 23: Action potential

A

Electrical activity consisting of a self-propagating series of polarizations and depolarizations that travel across the cell membrane of a nerve fibre during the transmission of a nerve impulse and across the cell membrane of a muscle cell during contraction or other activity of the cell

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42
Q

Ch. 23: Action potential duration (APD)

A

For a cell membrane, the interval beginning with baseline (resting) membrane potential followed by depolarization and ending with depolarization to baseline membrane potential

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43
Q

Ch. 23: Arrhythmia

A

Literally “no rhythm,” meaning absence of a heartbeat rhythm. More commonly used in clinical practice to refer to any variation from the normal rhythm of the heartbeat

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44
Q

Ch. 23: Cardia Arrhythmia Suppression Trial (CAST)

A

The name of the major research study conducted by the National Heart, Lung, and Blood Institute to investigate the possibility of eliminating sudden cardiac death in patients with asymptomatic, non-life threatening ectopy that has arisen after a myocardial infarction

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45
Q

Ch. 23: Depolarization

A

The movement of positive and negative ions on either side of a cell membrane across the membrane in a direction that tends to bring the net charge to zero

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46
Q

Ch. 23: Dysrhythmia

A

Any disturbance or abnormality in the rhythm of the heartbeat

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47
Q

Ch. 23: Effective refractory period (ERP)

A

The period after the firing of an impulse during which a cell may respond to a stimulus but the response will not be passed along or continued as another impulse

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48
Q

Ch. 23: Internodal pathways (Bachmann’s bundle)

A

Special pathways in the atria that carry electrical impulses spontaneously generated by the sinoatrial node. These impulses cause the heart to beat

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49
Q

Ch. 23: Relative Refractory Period (RRP)

A

The time after generation of an action potential during which a nerve fibre will show a (reduced) response only to a strong stimulus

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50
Q

Ch. 23: Resting membrane potential (RMP)

A

The transmembrane voltage that exists when cell membranes of heart muscle (or other muscle or nerve cells) are at rest

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51
Q

Ch. 23: Sodium-potassium adenosine triphosphatase (ATPase) pump

A

A mechanism for transporting sodium and potassium ions across the cell membrane against an opposing concentration gradient

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52
Q

Ch. 23: Sudden cardiac death

A

Unexpected, fatal cardiac arrest

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53
Q

Ch. 23: Threshold potential (TP)

A

The critical state of electrical tension required for spontaneous depolarization of a cell membrane

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54
Q

Ch. 23: Vaughan Williams Classification

A

The system most commonly used to classify antidysrhythmic drugs

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55
Q

Ch. 23: How many major classes of drugs does the Vaughan Williams classification identify?

A

4

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56
Q

Ch. 23: What are the four major classes of antidysrhythmic drugs?

A

Class I antidysrhythmics are considered membrane-stabilizing drugs, but they are further divided into Ia, Ib, and Ic drugs.
Class II drugs are B-blockers that depress phase 4 depolarization.
Class III drugs primarily prolong depolarization during phase 3.
Class IV drugs depress phase 4 depolarization during phases 1 and 2

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57
Q

Ch. 23: What is the gradual trend with the use of class Ia drugs?

A

There is a gradual current trend away from the use of class Ia drugs

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58
Q

Ch. 23: Which class Ic drug was removed?

A

The formerly available class Ic drug ecainide was removed from the market after research indicated that its risk of inducing fatal cardiac dysrhythmias overshadowed its dysrhythmia suppression effects. For similar reasons, the other two class Ic drugs, flecainide and propafenone, are generally used only in patients intolerant of other drugs

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59
Q

Ch. 23: Which are the most widely used antidyshrythmics?

A

Class III drugs

60
Q

Ch. 23: Which class has limited usefulness in tachydysrhythmias?

A

Class IV

61
Q

Ch. 23: What is the mechanism of action and drug effects of class I drugs?

A

Class I drugs exert their actions on the sodium channels

62
Q

Ch. 23: What is the mechanism of action and drug effects of class Ia drugs?

A

Class Ia drugs block the sodium channels; more specifically, they delay reolarization and increase the APD

63
Q

Ch. 23: What is the mechanism of action and drug effects of class Ib drugs?

A

Class Ib drugs also block the sodium channels, but unlike class Ia drugs, they accelerate depolarization and decrease the APD. Phenytoin is more commonly used as an anticonvulsant than as an antidysrhythmic

64
Q

Ch. 23: What is the mechanism of action and drug effects of class Ic drugs?

A

Class Ic drugs have a more pronounced effect on the blockade of sodium channels but have little effect on depolarization or the APD

65
Q

Ch. 23: What is the mechanism of action and drug effects of class II drugs?

A

Class II drugs are B-adrenergic blockers commonly used as antianginal drugs and as antihypertensives. They work by reducing or blocking sympathetic nervous system stimulation to the heart and, consequently, the transmission of impulses in the heart’s conduction system

66
Q

Ch. 23: What is the mechanism of action and drug effects of class III drugs?

A

Class II drugs increase the APD by prolonging depolarization in phase 3. They affect fat tissue and are most commonly used to manage dsrhythmias that are difficult to treat

67
Q

Ch. 23: What is the mechanism of action and drug effects of class IV drugs?

A

Class IV drugs are the calcium channel blockers, and are also used as antianginals and antihypertensives. They act specifically by inhibiting the channel pathways, reducing the influx of calcium ions during action potentials

68
Q

Ch. 23: What are some of the contraindications to the use of antidysrhythmic drugs?

A

Known drug allergy
May include second- or third-degree AV block, bundle branch block, cardiogenic shock, sick sinus syndrome, or any other major ECG changes
All antidysrhythmic drugs are potentially dysrhythmogenic and can therefore worsen existing dysrhythmias. This risk of such an effect is greater in patients with structural heart damage (MI)

69
Q

Ch. 23: What are some of the common adverse effects to the use of antidysrhythmic drugs?

A

Hypersensitivity reactions, N/V/D, dizziness, headache, and blurred vision

70
Q

Ch. 23: What is the toxicity and management of overdose to the use of antidysrhythmic drugs?

A

The main toxic effects of the antidysrhythmics involve the heart, circulation, and CNS. Specific antidotes are not available, and the management of an overdose involves maintaining adequate circulation and respiration using general support measures and any required symptomatic treatment

71
Q

Ch. 24: Acute coronary syndrome (ACS)

A

A group of clinical symptoms compatible with acute myocardial ischemia

72
Q

Ch. 24: Angina pectoris

A

Chest pain occurring when the heart’s supply of blood carrying oxygen and energy-fish nutrients is insufficient to meet the demands of the heart

73
Q

Ch. 24: Atherosclerosis

A

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

74
Q

Ch. 24: Chronic Stable Angina

A

Chest pain that occurs from atherosclerosis that results in long-term but relatively stable level of obstruction in one or more coronary arteries

75
Q

Ch. 24: Coronary arteries

A

Arteries that deliver oxygen to the heart muscle

76
Q

Ch. 24: Coronary Artery Disease (CAD)

A

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

77
Q

Ch. 24: Ischemia

A

Inadequate blood supply to an organ

78
Q

Ch. 24: Ischemic Heart Disease

A

Inadequate blood supply to the heart via the coronary arteries

79
Q

Ch. 24: Myocardial infarction (MI)

A

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

80
Q

Ch. 24: Reflux tachycardia

A

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

81
Q

Ch. 24: unstable angina

A

Early stage of progressive coronary artery disease

82
Q

Ch. 24: Vasospastic angina

A

Ischemia-induced myocardial chest pain caused by spasms of the coronary arteries

83
Q

Ch. 25: a1- blockers

A

Drugs that primarily cause arterial and venous dilation through their action on peripheral sympathetic neurons

84
Q

Ch. 25: Antihypertensive Drugs

A

Drugs used to treat hypertension

85
Q

Ch. 25: Cardiac Output

A

The amount of blood ejected from the left ventricle. measured in litres per minute.

86
Q

Ch. 25: Centrally acting adrenergic drugs

A

Drugs that modify the function of the sympathetic nervous system in the brain y stimulating a2-receptors, which has a revere sympathetic effect causing a decrease in blood pressure

87
Q

Ch. 25: Essential hypertension

A

An elevated systemic arterial pressure for which no cause can be found and which is often the only significant clinical finding; also called primary or idiopathic hypertension

88
Q

Ch. 25: Ganglionic blocking drugs

A

Drugs that prevent nerves from responding to the action of acetylcholine by occupying the receptor sites for acetylcholine (i.e., nicotinic receptors) on sympathetic and parasympathetic nerve endings

89
Q

Ch. 25: Hypertension

A

A common, often asymptomatic disorder in which blooc pressure persistently exceeds 140/90 mm Hg

90
Q

Ch. 25: Idiopathic hypertension

A

Hypertension with no known primary cause; also called primary hypertension

91
Q

Ch. 25: Nicotinic receptor

A

The receptor and site of action for acetylcholine in both the parasympathetic and sympathetic nervous systems

92
Q

Ch. 25: Orthostatic hypotension

A

A common adverse effect of adrenergic drugs involving a sudden drop in blood pressure when patients change position, especially when rising from a seated or horizontal position

93
Q

Ch. 25: Prodrug

A

A drug that is inactive in its administered form and must be biotrasformed in the liver to its active form

94
Q

Ch. 25: Secondary hypertension

A

High blood pressure known to be associated with a primary disease, such as kidney, pulmonary endocrine, or vascular disease

95
Q

Ch. 26: Afferent Arterioles

A

The small blood vessels branching from the renal artery approaching the glomerulus (proximal part of the nephron)

96
Q

Ch. 26: Aldosterone

A

A mineralcorticoid steroid hormone produced by the adrenal cortex that mediates the actions of the renal tubule in the regulation of sodium and potassium balance in the blood

97
Q

Ch. 26: Ascites

A

An abnormal intraperitoneal accumulation of fluid (defined as a volume of 500ml or greater) containing large amounts of protein and electrolytes

98
Q

Ch. 26: Collecting duct

A

The most distal part of the nephrons between the distal convoluted tubule and the ureters, which lead to the urinary bladder

99
Q

Ch. 26: Distal convoluted tubule

A

The part of the nephrons immediately distal to the ascending loop of Henle and proximal to the collecting duct

100
Q

Ch. 26: Diuretics

A

Drugs or other substances that tend to promote the formation and excretion of urine

101
Q

Ch. 26: Efferent arterioles

A

The small blood vessels exiting the glomerulus. At this point, blood has completed its filtration in the glomerulus

102
Q

Ch. 26: Filtrate

A

The material that passes through a filter. In the kidney, the filter is the glomerulus, and the filtrate is the extracted material from the blood (normally liquid) that ultimately becomes urine

103
Q

Ch. 26: Glomerular capsule

A

The open, rounded, and most proximal part of the proximal convoluted tubule that surrounds the glomerulus and receives the filtrate from the blood

104
Q

Ch. 26: Glomerular Filtration Rate (GFR)

A

The volume of ultra filtrate extracted per unit of time from the plasma flowing through the glomeruli of the kidney

105
Q

Ch. 26: Glomerulus

A

The cluster of kidney capillaries that mars the beginning of the nephron and is immediately proximal to the proximal convoluted tubule

106
Q

Ch. 26: Loop of Henle

A

The part of the nephrons that is immediately distal to the proximal convoluted tubule

107
Q

Ch. 26: Nephron

A

The microscopic functional filtration unit of the kidney consisting of (in anatomical order from proximal to distal), the glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule, and the collection duct, which empties urine into the ureters. There are approximately one million nephrons in each kidney

108
Q

Ch. 26: Open-angle glaucoma

A

Elevated pressure in an eye because of obstruction of the outflow of aqueous humour, but access to the trabecular meshwork remains open

109
Q

Ch. 26: Proximal convoluted tubule

A

The part of the nephron that is immediately distal to the glomerulus and proximal to the loop of Henle

110
Q

Ch. 26: Ultrafiltration

A

Filtration at a microscopic level, the term is often used to describe the filtration function of the kidneys, with the filtrate referred to more specifically as ultrafiltrate

111
Q

Ch. 28: Anticoagulant

A

A substance that prevents or delays coagulation of the blood

112
Q

Ch. 28: Antifibrinolytic drug

A

A drug that promotes formation of clots through prevention of the lysis of fibrin

113
Q

Ch. 28: Antiplatelet drug

A

A drug that prevents platelet plugs from forming; this effect can help prevent cardiovascular disease such as MI and strokes

114
Q

Ch. 28: Antithrombin III (AT-III)

A

A substance that inactivates three major activating factors of the blotting cascade: activated II (thrombin), activated X, and activated IX

115
Q

Ch. 28: ß-Hemolytic streoptococci (group A)

A

The pyogenic streptococci of group A that cause hemolysis of red blood cells in blood agar in the laboratory setting

116
Q

Ch. 28: Clot

A

Insoluble solid elements of blood (cells, fibrin threads, etc.) that have chemically separated from the liquid (plasma) component of the blood

117
Q

Ch. 28: Coagulation

A

The sequential process by which the multiple coagulation factors of the blood interact in the coagulation cascade, ultimately forming an insoluble fibrin clot

118
Q

Ch. 28: Coagulation cascade

A

The series of steps beginning with the intrinsic or extrinsic pathways of coagulation and proceeding through the formation of a fibrin clot

119
Q

Ch. 28: DVT

A

The formation of a thrombus in one of the deep veins of the body, most commonly the iliac and femoral veins

120
Q

Ch. 28: Embolus

A

A blood clot (thrombus) that has been dislodged form the wall of the blood vessel and is travelling throughout the blood stream

121
Q

Ch. 28: Fibrin

A

A stringy, insoluble protein produced by the action of thrombin on fibrinogen during the clotting process; a major component of blood clots or thrombi

122
Q

Ch. 28: Fibrinogen

A

A plasma protein that is converted into fibrin by thrombin in the presence of calcium ions

123
Q

Ch. 28: Fibrinolysis

A

The continual process of fibrin decomposition produced by the actions of the enzymatic protein fibrinolysin

124
Q

Ch. 28: Fibrinolytic system

A

An area of the circulatory system undergoing fibrinolysis

125
Q

Ch. 28: Fibrin-specificity

A

Property of newer thrombolytic drugs to activate plasminogen to plasmin in the presence of established clots having fibrin threads

126
Q

Ch. 28: Hemorheological drug

A

A drug that alters the function of platelets without compromising their blood-clotting properties

127
Q

Ch. 28: Hemostasis

A

Arrest of bleeding, either by the physiological properties of vasoconstriction and coagulation, or by mechanical, surgical, or pharmacological means

128
Q

Ch. 28: Hemostatic

A

A procedure, device, or substance that arrests the flow of blood

129
Q

Ch. 28: Plasmin

A

The enzymatic protein that breaks down fibrin into fibrin degradation products; it is derived from plasminogen

130
Q

Ch. 28: Plasminogen

A

A plasma protein that is converted to plasmin

131
Q

Ch. 28: Pulmonary embolus (PE)

A

The blockage of a pulmonary artery by foreign matter such as fat, air, tumour, or a thrombus that usually arises from a peripheral vein

132
Q

Ch. 28: Stroke

A

Occlusion of the blood vessels of the brain by an embolus, thrombus, or cerebrovascular hemorrhage, resulting in schema of the brain tissue

133
Q

Ch. 28: Thromboembolic event

A

An event in which a blood vessel is blocked by an embolus carried in the blood stream from the site of its formation

134
Q

Ch. 28: Thrombolytic drug

A

A drug that dissolve thrombi by functioning similarly to tissue plasminogen activator

135
Q

Ch. 28: Thrombus

A

Technical term for a blood clot (thrombi); an aggregation of platelets, fibrin, clotting factors, and the cellular elements of the blood that is attached to the interior wall of a vein or artery, sometimes occluding the lumen of the vessel;

136
Q

Ch. 28: Tissue plasminogen activator

A

A naturally occurring plasminogen activator secreted by vascular endothelial cells in the walls of the blood vessels. Thrombolytic drugs are based on this blood component

137
Q

Ch. 29: Antilipemic

A

A drug that reduces lipid levels

138
Q

Ch. 29: Apolipoprotein

A

The protein component of a lipoprotein

139
Q

Ch. 29: Cholesterol

A

A fat-soluble crystalline steroid alcohol that is found in animal fats and oils and egg yolk and wifely distributed in the body, especially in bile, blood, brain tissue, liver, kidneys, adrenal glands, and myelin sheaths of nerve fibres

140
Q

Ch. 29: Chylomicrons

A

Minute droplets of lipoproteins; the forms in which dietary fats are absorbed from the small intestine

141
Q

Ch. 29: Exogenous lipids

A

Lipids originating outside the body or an organ or produced as the result of external causes, such as disease caused by a bacterial or viral drug foreign to the body

142
Q

Ch. 29: Foam Cells

A

The characteristic initial lesion of atherosclerosis, also known as the fatty streak

143
Q

Ch. 29: HMG-CoA reductase inhibitors

A

A class of cholesterol-lowering drugs that act by inhibiting the rate-limiting step in cholesterol synthesis; also commonly referred to as statins

144
Q

Ch. 29: Hypercholesterolemia

A

A condition in which greater-than-normal amounts of cholesterol are present in the blood

145
Q

Ch. 29: Lipoprotein

A

Conjugated protein in which lipids form an integral part of the molecule

146
Q

Ch. 29: Statins

A

A class of cholesterol-lowering drugs more formally known as HMG-CoA reductase inhibitors

147
Q

Ch. 29: Triglycerides

A

A compound consisting of a fatty acid (oleic, palmitic, or stearic) and a type of alcohol known as glycerol

Pharm II (5 decks)

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