Chapters 42-49 Flashcards

(123 cards)

1
Q

resting phase of the heart, blood is returned to the heart during this phase

A

Diastole

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2
Q

contracting phase of the heart; blood is pumped out of the heart during this phase

A

Systole

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3
Q

a period of cardiac muscle relaxation followed by a period of contraction in the heart

A

Cardiac Cycle

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4
Q

Route of deoxygenated blood?

A

right atrium through tricuspid valve through pulmonary valve to the lungs

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5
Q

Route of oxygenated blood?

A

through the pulmonary veins to the left atrium through the mitral valve to the left ventricle, through the aortic valve to the aorta

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6
Q

refers to the difference in charge between the inside and outside of a neuron, which is created due to the unequal distribution of ions on both sides of the cell

A

Membrane potential

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7
Q

refers to the electrical signaling that occurs within neurons

A

Action potential

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8
Q

what are the drugs in Class 1 - Na+ Channel Blocker 1a (moderate)

A

Quinidine, Procainamide

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9
Q

Class 1 - Na+ channel blocker 1b (weak)

A

Lidocaine, Phenytoin

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10
Q

Class 1 - Na+ channel blocker 1c (strong)

A

Flecainide, Propafenone

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11
Q

what are the drugs involved in Class 4 - Ca2+ channel blocker?

A

Verapamil, Diltiazem

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12
Q

what are the drugs involved in Class 3 - K+ channel blocker

A

Amiodarone, Sotalol

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13
Q

what are the drugs involved in Class 2 - Beta Blocker

A

Propranolol, Metoprolol

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14
Q

functional unit of a muscle cell

A

Sacromere

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15
Q

Sacromere is composed of?

A

actin and myosin molecules arranged in layers to give the unit a striped or striated appearance

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16
Q

thin filament that makes up a sacromere

A

Actin

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17
Q

thin filament with projections that makes up a sacromere

A

Myosin

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18
Q

chemical in heart muscle that prevents actin and myosin from reacting, leading to muscle relaxation

A

troponin

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19
Q

troponin is inactivated by ___________ during muscle stimulation to allow actin and myosin to react, causing muscle contraction

A

calcium

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20
Q

antihypertensions

A
  • diuretics
  • beta blockers
  • alpha and beta blockers
  • alpha adrenergic blockers
  • alpha1 blockers
  • alpha 2 agonists
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21
Q

They block a chemical reaction in your body where angiotensin I is turned into angiotensin II.

A

Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors)

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22
Q

normally makes your blood vessels tighten (vasoconstrict) and causes your body to hold on to salt and water, which raises blood pressure.

A

Angiotensin II

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23
Q

ACE Inhibitor leads to a decrease in blood pressure and in aldosterone secretion with a resultant slight increase in serum ____________ and a loss of serum ________________________

A

potassium, sodium and fluid

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24
Q

Selectively bind with angiotensin II receptor sites in vascular smooth muscle and adrenal gland to block vasoconstriction and the release of aldosterone.

A

Angiotensin II Receptor Blockers (ARB)

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25
Indicated to be used alone or in combination therapy for the treatment of hypertension
ARB
26
Inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction; depressing myocardial contractility, slowing cardiac impulse formation in the conductive tissues, and relaxing and dilating arteries, causing a fall in blood pressure and a decrease in venous return
Calcium Channel Blocker
27
Calcium in indicated for treatment of
hypertension and angina (chest pain or reduced blood flow to the heart)
28
act directly on vascular smooth muscle to cause muscle relaxation, leading to vasodilation and drop in blood pressure
Vasodilator
29
Vasodilators are indicated for the treatment of
severe hypertension that has not responded to other therapy
30
Antihypotensive agents are
sympathetic adrenergic agonists
31
example of an antihypotensive agent?
Midodrine
32
a 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
Congestive Heart Failure (CHF)
33
severe left-sided congestive heart failure with backup of blood into the lungs, leading to loss of fluid into the lung tissue
Pulmonary Edema
34
are medicines that change the force of your heart's contractions.
Inotropic agents, or inotropes
35
2 kinds of inotropes
positive inotropes and negative inotropes.
36
inotropes that strengthen the force of the heartbeat.
Positive
37
inotropes that weaken the force of the heartbeat.
Negative
38
These are effects that change the heart rate
Chronotropic effects (from chrono-, meaning time, and tropos, "a turn")
39
Effects of digitalis glycosides?
1. positive inotropic effect - increase in myocardial contractility associated with a prolongation of relaxation period. 2. negative chronotropic - lower the heart rate. 3. negative dromotropic - impede stimulus conduction. 4. positive dromotropic - promote myocardial excitablity
40
Affects the speed of electrical signal conduction in the heart
Dromotropic
41
Influences the strength of heart muscle contractions
Inotropic
42
Changes the heart rate
Chronotropic
43
These increase intracellular calcium and allow more calcium to enter myocardial cells during depolarization
Cardiac Glycosides
44
Cardiac Glycosides effects?
1. increased force of myocardial contraction 2. increased cardiac output and renal perfusion 3. slowed heart rate by slowing the rate of cellular repolarization 4. decreased conduction velocity through the AV node
45
Phosphodiesterase Inhibitor block the enzyme phosphodiesterase leading to :
an increase in myocardial cell cAMP which increases calcium levels in the cell
46
Increased calcium levels in the cell leads to what?
stronger contraction and prolonged effects of sympathetic stimulation, leading to vasodilation, increased oxygen consumption and arrythmias
47
Phosphodiesterase inhibitors is indicated for the short-term treatment of?
CHF patients who are not responding to digoxin or diuretics
48
Premature atrial contractions (PACs) is caused by?
an ectopic focus in the atria stimulating an atrial response.
49
an ectopic focus in the ventricles stimulating the cells and causing an early contraction
Premature ventricular contractions (PVCs)
50
What are the causes of cardiac arrhythmias?
1. electrolyte disturbances 2. decreases in the oxygen delivered to the cells 3. structural damage 4. acidosis or the accumulation of waste products
51
drugs that can affect the action potential of cardiac cells and are used to treat arrhythmias and return normal rate and rhythm
Antiarrhythmics
52
tending to cause arrhythmias
proarrhythmics
53
it is used short-term to treat life threatening ventricular arrhythmias, not long-term
Cardiac Arrhythmia suppression Trial (CAST)
54
1 small box = ?
0.04 s
55
1 big box = ?
0.20 s
56
fatty tumors in the intima of the vessels
Atheromas
57
narrowing of the arteries caused by build up of atheromas, welling and accumulation of platelets, leads to a loss of elasticity and responsiveness to normal stimuli
Atherosclerosis
58
"suffocation of the chest"
Angina Pectoris
59
Angina pectoris is a pain in the chest caused by the imbalance between??
oxygen being supplied to the heart and muscle and demand for oxygen by the heart muscle
60
this is the end result of vessel blockage in the heart, leads to ischemia and then necrosis of the area cut off from the blood supply
Myocardial Infarction
61
characterized by drop in blood flow through the coronary arteries caused by a vasospasm in the artery, not by atherosclerosis
Prinzmetal's Angina
62
causes direct relaxation of smooth muscle with a resultant decrease in venous return and decrease in arterial pressure, which reduces cardiac workload and decreases myocardial oxygen consumption
Nitrates
63
Nitrates are indicated for?
the prevention and treatment of attacks of angina pectoris
64
Nitrates adverse effects:
vasodilation and decrease in blood flow
65
Competitively block beta-adrenergic receptors in the heart and juxtaglomerular apparatus
Beta blockers
66
effects of beta blockers?
1. decreasing the influence of the sympathetic nervous system on these tissues 2. decreasing the excitability of the heart, cardiac output, and cardiac oxygen compensation 3. lowering blood pressure
67
Beta blockers are indicated for :
the long-term management of angina pectoris caused by atherosclerosis
68
Adverse effects of beta blockers are related to ?
The blockade of the sympathetic nervous system
69
Inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction
Calcium Channel Blockers
70
Calcium channel blocker is Indicated for the treatment of
Prinzmetal's angina, chronic angina, effort-associated angina, and hypertension
71
Adverse effects of calcium channel blockers are related to
their effects on cardiac output and on smooth muscle
72
what are the risk factors of coronary artery disease?
Unmodifiable and modifiable Risk factors
73
Unmodifiable risk factors inclue:
genetic predispositions, age, gender
74
Modifiable Risk Factors include?
gout, cigarette smoking, sedentary lifestyle, high stress levels, hypertension, obesity, diabetes, bacterial infections
75
these are cholesterol-containing acids found in the bile, which act like detergents to break up fats in the small intestine
bile acids
76
a necessary component of human cells and the formation of steroid hormones; produced in the body and found in dietary fats
cholesterol
77
carrier for lipids in the blood stream, consist of proteins and lipids, cholesterol, and so forth
chylomicron
78
tightly packed fats that are thought to contribute to the development of CAD when remnants left over from the LDL are processed in the arterial lining
Low density lipoproteins (LDL)
79
loosely packed chylomicron containing fats, able to absorb fats and fat remnants in the periphery; thought to have a protective effect, decreasing development of CAD
High density lipoproteins
80
an enzyme that regulates the last step in cellular cholesterol synthesis
HMG CoA reductase
81
this bind with bile acids in the intestine to form a complex that is excreted in the feces
bile acid sequestrants
82
used to reduce serum cholesterol in patients with primary hypercholesterolemia (with high LDLs) as an adjunct to diet and exercise
bile acid sequestrants
83
adverse effects of bile acid sequestrants include:
direct GI irritation, including nausea, constipation that may lead to fecal impaction
84
this block the formation of cellular cholesterol
HMG CoA reductase inhibitors
85
effects of HMG CoA reductase inhibitors?
decrease in serum cholesterol and LDLs, with a slight increase or no change in the levels of HDLs
86
HMG CoA reductase inhibitor is indicated as adjuncts with diet and exercise for the treatment of:
elevated cholesterol and LDL levels in patients unresponsive to dietary restrictions alone. it also slows the progression of CAD and prevent MI
87
the most common adverse effect of HMG CoA reductase inhibitor is associated with
the GI system
88
inhibits liver synthesis of LDL and cholesterol, lowers serum lipids and has an antiplatelet effect
clofibrate
89
inhibits triglyceride synthesis in the liver, resulting in the reduction of LDLs; increases uric acid secretion and may stimulate triglyceride breakdown
Fenofibrate
90
inhibits peripheral breakdown of lipids, reduces triglyceride production and LDL production and increases HDL concentrations
Gemfibrozil
91
inhibits the release of free fatty acids from adipose tissue, increases the rate of triglyceride removal from plasma, and generally reduces LDL and triglyceride levels and increases HDL levels
Vitamin Niacin
92
the zymogen form of factor XIa, one of the enzymes of the coagulation cascade
Factor XI or plasma thromboplastin antecedent
93
a blood test that measures the time it takes your blood to clot.
Partial thromboplastin time (PTT)
94
can be used to check for bleeding problems. Blood clotting factors are needed for blood to clot (coagulation)
PTT
95
The reference range of the aPTT is
30 - 40 s
96
The reference range of the PTT is
60-70 s
97
In patients receiving anticoagulant therapy, the reference range is
1.5 - 2.5 times the control value in seconds
98
measures how quickly your blood clots, sometimes call a PT or pro time test
99
uses a sample of your blood
Prothrombin time test
100
Prothrombin is a protein produced by?
the liver
101
what is the term for the result of a prothrombin time test?
International Normalized Ratio (INR)
102
If you are not taking blood thinning medicines, such as warfarin, the normal range for your PT results is:
11 to 13.5 seconds
103
this inhibit platelet adhesion and aggregation by blocking receptor sites on the platelet membrane, preventing platelet-platelet interaction
Antiplatelet Drugs
104
Antiplatelet drugs are used to:
decrease the risk of fatal MI, to prevent reinfarction after MI, to prevent thromboembolic stroke and to maintain the patency of grafts
105
most common adverse effects seen with antiplatelet drugs is:
bleeding
106
this interfere with the normal cascade of events involved in the clotting process
anticoagulants
107
anticoagulants are used to treat thromboembolic disorders such as?
atrial fibrillation, MI, pulmonary embolus, evolving stoke and to prevent the formation of thrombi
108
Oral anticoagulant
warfarin
109
parenteral anticoagulant
heparin: low molecular weight
110
Antiplatelets include:
ASA, also called acetylsalicylic acid (Aspirin, Asaphen, Entrophen, Novasen) Clopidogrel (Plavix) Prasugrel (Effient) Ticagrelor (Brilinta)
111
this agents work by activating plasminogen to plasmin, which in turn break down fibrin threads in a clot to dissolve a formed clot
Thrombolytic agents
112
Thrombolytic agents are indicated for:
the treatment of acute MI, pulmonary emboli, ischemic stroke and to open clotted IV catheters
113
Most common adverse effect of Thrombolytic agents?
bleeding
114
Thrombolytic agents drugs?
Eminase (anistreplase) Retavase (reteplase) Streptase (streptokinase, kabikinase) t-PA (class of drugs that includes Activase) TNKase (tenecteplase) Abbokinase, Kinlytic (rokinase)
115
what are some bleeding disorders?
hemophilia, liver disease, bone marrow disorders
116
Drugs used to control bleeding?
antihemophilic agents, systemic hemostatic agents, topical hemostatic agents
117
Hemostatic Agents
Aminocaproic. Antifibrinolytic Agents. Estrogens, Conjugated (USP) Hemostatics. Tranexamic Acid. Aprotinin. Deamino Arginine Vasopressin.
118
the liquid part of blood?
plasma
119
bone marrow contains a large number of large, immature RBCs
megaloblastic anemia
120
gastric mucosa cannot produce intrinsic factor and vitamin B12 cannot be absorbed
Pernicious anemia
121
acts like natural glycoprotein to stimulate the production of RBC in the bone marrow
erythropoietin
122
erythropoietin is indicated for the:
treatment of anemia associated with renal failure or for patients on dialysis
123
Megaloblastic Anemia Treatments
folic acid derivatives and vitamin B12