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ZZ3 Clinical Pharma > Lesson 4 > Flashcards

Lesson 4 Flashcards

1
Q

have a resting membrane potential of - 90 mV

A

fast response fibers

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2
Q

impulse conduction of slow response fibers

A

0.1 - 1 m per sec

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3
Q

impulse conduction of fast response fibers

A

0.3 - 3 m per sec

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4
Q

resting membrane potential of slow response fibers

A

negative 60 mV

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5
Q

produce rapid upstroke (phase 0) of action potential when depolarized

A

fast response fibers

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6
Q

produce slower upstroke of action potential

A

slow response fibers

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7
Q

The more negative the RMP, results to?

A

greater the rise of phase 0 and faster is the rate of impulse

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8
Q

sequence of voltage changes occurring as a result of changes in ionic conductances across cell membrane

A

action potential

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9
Q

fast channels are activated in what mV

A

negative 70 to negative 50 mV

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10
Q

fast channels during phase 0 or depolarization is inactivated for how many milliseconds

A

0.5 milliseconds

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11
Q

reactivation of voltage-dependent sodium channels occur in what phase

A

phase 3

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12
Q

slow component of depolarization is mediated by inward movement of

A

calcium

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13
Q

phase caused by calcium influx and partially potassium efflux

A

limited repolarization or phase 1

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14
Q

plateau is caused by the inward movement of this important ion

A

calcium

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15
Q

it is due to algebraic sum of the inward calcium and outward potassium current

A

phase 2 or plateau

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16
Q

due to time dependent outward current of potassium and sodium channels are reactivated

A

phase 3 or repolarization

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17
Q

the restored intracellular potassium concentration caused by sodium potassium ATPase pump

A

phase 4 or diastole

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18
Q

frequency of discharge of action potential is determined by

A
  1. distance between the maximal diastolic potential and threshold potential; 2. slope of diastolic depolarization
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19
Q

inability of an excitable tissue to respond to elicit action potential

A

refractory period

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20
Q

absolute refractory period mV

A

0 to -60 mV

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21
Q

relative refractory period mV

A

negative 60 to negative 90 mV

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22
Q

refractory period which refers to a minimal interval between two propagating impulses

A

effective refractory period

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23
Q

refractory period in which premature stimuli will elicit action potentials with slow response characteristics

A

relative refractory period

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24
Q

a refractory period wherein premature stimuli will not elicit action potential

A

absolute refractory period

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25
Q

drugs used for treatment of CHF

A

cardiac glycoside or digitalis glycosides

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26
Q

active glycosides of digitalis purpuria

A

Digitoxin, gitoxin, and gitalin

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27
Q

active glycosides of lanata

A

Digitoxin, digoxin, and gitoxin

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28
Q

active glycosides of strophantus kombe

A

strophantin

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29
Q

active glycosides of gratis

A

ouabain

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30
Q

contain cardioactive poisons similar to cardiac glycosides

A

skin glands of toads

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31
Q

a positive inotropic effect of glycosides

A

direct action

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32
Q

direct action is not dependent upon adrenergic stimulation but rather of

A

consequence of inhibition of the sodium pump

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33
Q

increased inward calcium current occurs at this phase of myocardial action potential

A

phase 2 or plateau

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34
Q

made through the parasympathetic autonomic nervous system that influence EXCITABILITY and AUTOMATICITY of cardiac tissues

A

indirect action

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35
Q

magnitude of an electric impulse required in producing an action potential

A

excitability

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36
Q

reduced RMP results to?

A

decreased amplitude of action potential or rate of rise of action potential, and reduced conduction velocity

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37
Q

behavior by which cardiac tissues spontaneously generate action potential

A

automaticity

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38
Q

the EXTRACELLULAR concentration of this ion influences the action of cardiac glycosides on automaticity

A

potassium

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39
Q

low concentration of potassium influence glycosides to?

A

enhance automaticity

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40
Q

cause the appearance of after-depolarization, or depolarization appearing immediately following repolarization

A

administration of glycosides with normal or high potassium concentration

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41
Q

appears as subthreshold depolarization early during phase 4

A

after-depolarization

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42
Q

the beat outside of normal cardiac rhythm

A

ectopic beat

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43
Q

Give one cause of ectopic beat

A

after-depolarization

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44
Q

normal or high concentration of potassium effect on automaticity of the heart

A

leads to after-depolarization

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45
Q

clinically important effects of a digitalis glycoside on the rate of formation of impulses by the SA and AV nodes are due to its

A

indirect VAGAL action

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46
Q

common effect of digitalis glycosides on the electrical activity of the SA and AV nodes

A

increase in the REFRACTORY period; decrease in the CONDUCTION velocity

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47
Q

digitalis glycosidesalso influence on atria and ventricles also leads to

A

decreased contractility

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48
Q

overshadows the indirect negative inotropic effects on atria and the ventricles

A

direct positive inotopic effect

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49
Q

commonly used as indicator of adequate blood levels o digitalis in patients

A

gut disturbances

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50
Q

glycosides effect on kidney when edema is present

A

diuresis, due to failing heart and not direct action to kidney

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51
Q

these glycosides are commonly administered orally in clinical setting

A

digoxin an digitoxin

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52
Q

on set of action of ouabain and peak action

A

3-10 mins and 0.5-2 hours, respectively

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53
Q

(blank) is more readily absorbed from the gut than (blank)

A

digitoxin, digoxin

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54
Q

onset of action and peak action of digoxin tablets

A

15-30 mins an 6-8 hrs, respectively

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55
Q

peak action of alcohol or elixir digoxin

A

1-2 hours

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56
Q

digitoxin is bound to plasma protein to about 5 times greater than digoxin in these species

A

dogs

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57
Q

human elimination of digoxin is through

A

direct renal excretion

58
Q

human elimination of digitoxin

A

hepatic metabolism

59
Q

in dogs, digitoxin are eliminated through

A

renal excretion and hepatic metabolism

60
Q

an important part of therapy of CHF or DILATED CARDIOMYOPATHY (DCM)

A

cardiac glycoside or digitalis glycosides

61
Q

Why are glycosides a drug of choice for cardiac arrhythmias

A

because it BLOCKS OR REDUCES IMPULSES conducted in AV node, causing less number of impulses reaching the ventricles than are produced in atria

62
Q

Digitalis is beneficial in the treatment of ventricular associated with congestive heart failure by improving?

A

coronary artery perfusion and oxygenation

63
Q

dose for digitalization is about (blank) of the lethal dose

A

40 percent

64
Q

most severe toxic effect of glycosides

A

cardiac arrhythmias, especially fibrillation

65
Q

a common side effect of digitalis

A

hypokalemia

66
Q

Digitalization is usually accomplished in

A

7-14 days

67
Q

dose of digitalis glycosides may be based on

A

body surface area in meters

68
Q

loading dose of digoxin for dogs

A

0.66 mg per meter

69
Q

maintenance dose of digoxin in dogs

A

0.22 mg

70
Q

first ACE inhibitor to be developed

A

captopril

71
Q

most commonly ACE inhibitor usesd in animals

A

enalapril

72
Q

ACE which are not prodrugs and are therefore directly acting

A

captopril and lisinopril

73
Q

ACE inhibitor now available

A

lisinopril, ramipril, perindropril, trandolapril

74
Q

prodrug that is converted which competes with Angiotensin I for ACE

A

enalapril

75
Q

onset of action of enalapril as well as duration time

A

4-6 hours (onset), 12-14 hrs (duration)

76
Q

enalapril is used for treatment of HEART FAILURE and HYPERTENSION in

A

dogs, not to be given to cats

77
Q

deviation from the normal heart rate and rhythm

A

arrhythmia

78
Q

general classification of arrhythmias

A

supraventricular, ventricular

79
Q

listening to body sounds with stethoscope

A

auscultation

80
Q

most specific way to diagnose cardiac arrhythmias

A

electrocardiography

81
Q

in screening for arrhythmia, a jugular pulse indicates

A

abnormality

82
Q

a heart beat should have this pulse

A

femoral

83
Q

feature common to all cardiac conduction and related to the slow inward movement of calcium ions

A

automaticity

84
Q

characterized by enhanced responsiveness to catecholamines, which then increase calcium conductance during diastole

A

enhancd normal automaticity

85
Q

altered automaticity wherein after-depolarization reaching threshold potential which result in repetitive firing of the cell

A

triggered activity

86
Q

an altered automaticity wherein vagal activity increase potassium conductance which repolarizes the cell

A

sick-sinus syndrome

87
Q

progression movement of an action potential from on area of myocardium to another

A

conduction

88
Q

Class of membrane stabilization drugs

A

Class I

89
Q

give the subclass IA drugs which reduces the inward current of sodium

A

quinidine, procainamide, disopyramide

90
Q

give the members of subclass IB which increase the outward current of potassium

A

lidocaine, phenytoin, tocainide, mexiletin, aprindin

91
Q

antiarrhythmic effect of this group results from a selection beta adrenergic blocking action

A

Class II

92
Q

give examples of class which can decrease velocity, block automaticity, increase effectivity refractory period

A

propranolol, timolol, alprenolol, pindolol, metotrolol

93
Q

Membrane of this class have action and effects as those in subclasses IA and IB but with very little effect on refractoriness and on action potential duration

A

Subclass 1C

94
Q

Their major effect is to lengthen action potential duration and refractory period primarily in the Purkinje fibers and ventricular myocardium

A

Class III

95
Q

Give examples of Class III

A

bretylium, amiodarone, sotalol

96
Q

give examples of Subclass 1C

A

encainide, lorcainide, flecainide, propafenone

97
Q

Class of antiarryhthmitic drugs which block the calcium entry

A

Class IV

98
Q

members of Class IV

A

verapamil, nifedipine, diltiazem

99
Q

it has little antiarrhythmic affect and is also used as antifungal agent in humans

A

diltiazem

100
Q

A dextro-stereoisomer o quinine, an antimalarial drug

A

quinidine sulfate

101
Q

half life of quindine in dogs

A

6 hours

102
Q

half life of quindine in cats

A

19 hrs

103
Q

half life of quindine in pony

A

4 hrs

104
Q

quinidine is rapidly absorbed in how many minutes

A

60 to 90 mins

105
Q

Clinical use of quinidine sulfate

A

atrial fibrillation in dogs and horses, and ventricular premature beats

106
Q

has direct action similar to quindine but controlling ventricular arrhythmias

A

procainamide

107
Q

clinically used for ventricular ectopic beats or ventricular tachyarrhythmias

A

procainamide

108
Q

drug of choice for digitalis-induced ventricular arrhythmias

A

phenytoin (diphenyldantoin)

109
Q

clinical uses of propanolol

A
  1. for severe atrial fibrillation unresponsive to digitalis
  2. sinus tachycardia associated with anesthesia
  3. ventricular arrhythmias
  4. hypertrophic cardiomyopathy
110
Q

has direct antiarrhythmic action due to adrenergic blocking effect (decreased spontaneous firing in SA node)

A. Phenytoin
B. Propranolol
C. Lidocaine
D. both a and c
E. Quindine sulfate

A

B. Propranolol

111
Q

What are the antiarrhythmic drugs proven useful in veterinary medicine?

A
  1. QUINDINE SULFATE
  2. PROCAINAMIDE
  3. LIDOCAINE (without epinephrine)
  4. PHENYTOIN (Diphenyldantoin)
  5. PROPRANOLOL
112
Q

An anti-arrhythmic drug dangerous to use in heart congested heart failure

A. Quindine sulfate
B. Phenytoin
C. Procainamide
D. Propranolol

A

D. Propranolol

113
Q

an anti-arrhythmic drug not effective for controlling supraventricular arrhythmias

A. Lidocaine
B. Phenytoin
C. Procainamide
D. Propranolol

A

A. Lidocaine

114
Q

Subclass 1A members

A
  • Quinidine
  • Procainamide
  • Disopyramide
115
Q

Subclass 1B members

A
  • Lidocaine
  • Phenytoin
  • Tocainide
  • Mexiletin
  • Aprindin
116
Q

3 Supraventricular (atrial, AV nodal) arrhythmias

A
  • Paroxysmal atrial tachycardia
  • Atrial flutter
  • Atrial fibrillation
117
Q

3 ventricular arrhythmias

A
  • Premature ventricular contraction
  • Ventricular tachycardia
  • Ventricular fibrillation
118
Q

Adverse reactions to enalapril include

A
  • GI distress (anorexia, vomiting, and diarrhea)
  • Lethargy
  • Hypotension
  • Anemia
  • Angioedema, and
  • Vasculitis
119
Q

mechanism of the indirect vagal action of digitalis

A
  1. Direct stimulation of the centers in the brain
  2. Sensitization of the carotid sinus baroreceptors to changes in blood pressure
  3. Enhancement at the myocardial level of the response to acetylcholine
120
Q

Which ion is primarily responsible for repolarization of myocardial cells?

A

Potassium ions (K⁺)

121
Q

What can cause a shift from fast-response to slow-response behavior in myocardial fibers?

A) Increased oxygen supply
B) Hyperkalemia
C) Hypocalcemia
D) Hypoxia

A

Hypoxia

122
Q

What is the primary mechanism by which sodium ions enter myocardial cells during depolarization?

A) Diffusion through leak channels
B) Active transport by sodium-potassium pump
C) Opening of voltage-gated sodium channels
D) Binding to potassium ions

A

Opening of voltage-gated sodium channels

123
Q

How do fast-response fibers differ from slow-response fibers in myocardial cells?

A) Fast-response fibers have higher resting membrane potentials
B) Slow-response fibers have faster action potential durations
C) Fast-response fibers respond more quickly to depolarization
D) Slow-response fibers have greater sodium permeability

A

Fast-response fibers respond more quickly to depolarization

124
Q

Which condition is associated with an increased risk of altered resting membrane potential in cardiac cells?

A) Hypocalcemia
B) Hypernatremia
C) Hyperkalemia
D) Hypomagnesemia

A

Hyperkalemia

125
Q

What is the significance of the threshold potential in cardiac cells?

A) Initiates sodium influx
B) Triggers potassium outflow
C) Leads to depolarization
D) Maintains the resting membrane potential

A

Leads to depolarization

126
Q

How does the sodium-potassium pump contribute to maintaining the electrochemical gradient in cardiac cells?

A) By pumping in sodium and potassium ions simultaneously
B) By pumping out more sodium ions than potassium ions
C) By exchanging sodium ions for chloride ions
D) By modulating calcium influx

A

By pumping out more sodium ions than potassium ions

127
Q
A
128
Q

What role does calcium play in myocardial cell function?

A) Initiates depolarization
B) Triggers potassium outflow
C) Stimulates contraction
D) Inhibits sodium influx

A

Stimulates contraction

129
Q

How does hypoxia affect myocardial fibers?

A) Converts fast-response fibers to slow-response fibers
B) Converts slow-response fibers to fast-response fibers
C) Has no effect on myocardial fibers
D) Increases sodium influx

A

Converts fast-response fibers to slow-response fibers

130
Q

What is the main function of the sodium-potassium pump in myocardial cells?

A) Maintain calcium homeostasis
B) Generate action potentials
C) Control the resting membrane potential
D) Regulate pH balance

A

Control the resting membrane potential

131
Q

Which ion primarily contributes to depolarization in myocardial cells?

A

Sodium ions (Na⁺)

132
Q

What are the usual intracellular and extracellular concentrations of potassium ions (K⁺) in myocardial cells?

A) [K⁺]ᵢ = 4 mM, [K⁺]ₒ = 150 mM
B) [K⁺]ᵢ = 150 mM, [K⁺]ₒ = 4 mM
C) [K⁺]ᵢ = 40 mM, [K⁺]ₒ = 100 mM
D) [K⁺]ᵢ = 100 mM, [K⁺]ₒ = 40 mM

A

[K⁺]ᵢ = 150 mM, [K⁺]ₒ = 4 mM

133
Q

What is the role of potassium (K⁺) leak channels in myocardial cells?

A) Allow K⁺ to flow inward
B) Prevent K⁺ from leaving the cell
C) Facilitate K⁺ outflow
D) Maintain K⁺ concentration gradient

A

Facilitate K⁺ outflow

134
Q

How does the membrane become partially depolarized in myocardial cells?

A) Decreased potassium outflow
B) Increased potassium outflow
C) Influx of sodium ions
D) Activation of calcium channels

A

Influx of sodium ions

135
Q

What triggers the opening of sodium channels in myocardial cells?

A) Decrease in potassium outflow
B) Increase in potassium outflow
C) Depolarization to threshold potential
D) Hyperpolarization

A

Depolarization to threshold potential

136
Q
A
137
Q

What is the function of the sodium-potassium pump in myocardial cells?

A) Pump out 3 sodium ions in exchange for 2 potassium ions
B) Pump in 3 sodium ions for every 2 potassium ions
C) Pump out potassium ions only
D) Pump in sodium ions only

A

Pump out 3 sodium ions in exchange for 2 potassium ions

138
Q

time course for inactivation for the fast channels during phase 0

A

0.5 milliseconds

139
Q

time course for inactivation of calcium channels during phase 3

A

50 milliseconds

140
Q

voltage – dependent activated at -40 mV

A

calcium channels

ZZ3 Clinical Pharma (11 decks)

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