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PMCOL 303 > Cardiotoxicology > Flashcards

Cardiotoxicology Flashcards

1
Q

what is direct cardiovascular toxicity

A

direct effects on the myocardium

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2
Q

what is indirect cardiovascular toxicity

A

indirect effects through vasculature

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3
Q

what is the pathophysiology of non reversible damage

A

cell loss (necrosis, apoptosis)

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4
Q

what is the diagnosis of non reversible damage (3)

A

injury marker release, progressive contractile dysfunction, cardiac remodelling

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5
Q

what is the diagnosis of reversible damage (3)

A

no injury marker release, reversible contractile dysfunction, reversible arterial hypertension

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6
Q

what is the pathophysiology of reversible damage

A

cellular dysfunction

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7
Q

what is the manifestation of non reversible cardiovascular toxicity (3)

A

cardiomyopathy, MI, thrombosis

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8
Q

what is the manifestation of reversible cardiovascular toxicity (3)

A

temporary contractile dysfunction, vasoplastic angina, arterial hypertension

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9
Q

what happens to electricity of heart in cardiotoxicity

A

cardiac conduction and dysrhythmias - abnormalities in repolarization

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10
Q

what happens to ventricles of heart in cardiotoxicity

A

systolic/diastolic dysfunction - reduction in ventricular ejection

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11
Q

what happens to structure of heart in cardiotoxicity (2)

A

cardiac structural remodeling, fibrosis

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12
Q

what happens to function of heart in cardiotoxicity (2)

A

cardiomyopathies, heart failure

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13
Q

what happens to vasculature of body in cardiotoxicity

A

systemic and pulmonary vascular dysfunction and altered hemodynamics

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14
Q

what happens to blood of body in cardiotoxicity

A

hemostasis and thrombosis

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15
Q

what are the primary contractile cells

A

cardiomyocyte

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16
Q

what are cardiomyocytes

A

the primary contractile cells

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17
Q

can cardiomyocytes be replaced

A

no

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18
Q

what are the 4 main cells of the heart

A

cardiomyocytes, endothelial cells, epicardial cells, fibroblasts

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19
Q

which cell type is promoted with injury

A

fibroblasts

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20
Q

what are 3 ways to tell if you have cardiotoxicity

A
  • changes in myocardial strain and biomarkers
  • assessment of cardiac function
  • determination of coronary blood flow reserve, stroke work, VO2 max
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21
Q

what is the most useful tool/machine to diagnose cardiac injury

A

echocardiography

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22
Q

why is echocardiography the best

A

safe, availability, reliability and low cost

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23
Q

what are 5 ways to diagnose cardiac injury (5)

A

MRI, ECG, echocardiography, SPECT, ultrasound

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24
Q

what are 4 markers of cardiac injury

A

CK-MB: creatine kinase
TnT or I-troponin
LDH (lactate dehydrogenase)
BNP B-type natriuretic peptide

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25
Q

when is CK-MB: creatine kinase released

A

lysis of cell

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26
Q

what does BNP B-type natriuretic peptide release cause

A

release water from water from body, vasodilation

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27
Q

which markers are more specific to the heart

A

TnT or I-troponin

and BNP B-type natriuretic peptide

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28
Q

which markers are less specific to the heart

A

CK-MB: creatine kinase

LDH (lactate dehydrogenase)

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29
Q

what is the most common way to test for ejection fraction

A

echocardiogram

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30
Q

what are 3 ways to test for ejection fraction

A

echocardiogram, MRI, nuclear medicine scan

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31
Q

what is left ventricular ejection fraction

A

the measure of % blood is being ejected from the left ventricle (% of blood leaving heart each time it contracts)

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32
Q

what are 6 examples of changes to vital signs that can happen in toxic syndromes

A

BP HR RR temp pupils skin (wet dry)

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33
Q

what can cause bradycardia (what are 7 places that are affected)

A

affects on the CNS or PNS, pacemaker cells or conduction system, changes to sympathetic outflow, enhanced vagal tone, altered Ca++ handling

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34
Q

what is the most common type of tachycardia

A

sinus

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35
Q

what does atropine do to HR

A

rise HR without inhibitory effect of vagal influence

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36
Q

what are direct effects that cause tachycardia

A

beta-adrenergic agonism

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37
Q

what are indirect effects that cause tachycardia

A

response to hypotension, hypoxia

38
Q

what is an important channel for cardiotoxic events

A

hERG

39
Q

what does the hERG gene do

A

encodes pore forming usbunit of the rapidly activating delayed rectifier cardiac K+ channel

40
Q

what kind of channel does the hERG code for

A

voltage gated potassium channel

41
Q

what is the role of the voltage gated potassium channel

A

contributes to repolarization of cardiac action potential

42
Q

what is the common cause of withdrawal or restriction of drugs with the hERG

A

prolongation of the QT interval

43
Q

what is the major effect of drugs that interact with this channel

A

blocks the channel so there is a loss of function

44
Q

what is torsades de pointes + what causes it

A

lethal arrhythmia, often caused by drugs that block the hERG K+ channel

45
Q

besides long QT, what can blocking of the hERG K+ channel lead to

A

early after depolarization

46
Q

what are the 3 main mechanisms that xenobiotics cause hypertension

A
  • CNS sympathetic over activity
  • increased myocardial contractility
  • increased peripheral resistance
47
Q

what are the 4 main mechanisms that xenobiotics cause hypotension

A
  • decreased peripheral resistance
  • decreased myocardial contractility
  • depletion of intravascular volume
  • dysrhythmias
48
Q

what are 3 general things that xenobiotic impact on cardiac contractility can result in changes to

A
  • ejection fraction
  • cardiac output
  • blood pressure
49
Q

what is afterload

A

the force that you have to push against in the arterial system

50
Q

what is preload

A

the amount you have before pump, volume

51
Q

do we often know the mechanisms of toxicity

A

no, often multiple factors

52
Q

is ventricular or atrial fibrillation worse

A

ventricular

53
Q

why can opioid receptor stimulation affect the heart

A

because OPR stimulation can inhibit B1 and B2 adrenergic receptor activity in cardiomyocytes

54
Q

what are the physical effects of OPR stimulation on heart physiology

A

restrict inotropic and chronotropic effects, interfering with excitation-contraction coupling

55
Q

what is infarction

A

dead tissue

56
Q

what is ischemia

A

low oxygen or low blood flow

57
Q

what are 2 main things that cocaine do to oxygen

A

increase demand decrease supply

58
Q

how does cocaine decrease oxygen supply

A

by increasing thrombosis and vasoconstriction

59
Q

how does cocaine increase oxygen demand

A

increasing HR BP contractility

60
Q

what are the 2 major pathways that cocaine affects CVS

A

sympathetic output and local anesthetic effect

61
Q

what can cocaine do to fat

A

it can accelerate atherosclerosis

62
Q

what are 3 things that consequences of cannabis toxicity may stem from

A
  • inhalation of combustion products
  • direct THC effects
  • indirect THC effects (acute anxiety, hallucinations, psychosis)
63
Q

what are CB 1 receptors most associated with

A

adverse effects

64
Q

what are CB 2 receptors most associated with

A

beneficial effects, anti inflammation

65
Q

what is bad about lots of chemo agents

A

they have cardio toxic effects

66
Q

what is doxorubicin

A

quinone containing anthracycline antibiotic

67
Q

which is one of the most effective and commonly used anti cancer drugs

A

doxorubicin

68
Q

what is a bad thing about doxorubicin

A

associated with increased risk of cardiomyopathy or congestive heart failure

69
Q

what is the mechanism of doxorubicin anti tumor properties

A

inhibits topoisomerase and DNA synthesis

70
Q

what can happen to HR with doxorubicin

A

tachycardia

71
Q

what can happen to T wave with doxorubicin

A

flat

72
Q

what can happen to voltage with doxorubicin

A

decrease

73
Q

what can happen to myofibrils with doxorubicin

A

loss

74
Q

what can happen to cytoplasm with doxorubicin

A

vacuolization

75
Q

what can happen to mitochondria with doxorubicin

A

damage

76
Q

what are 3 main things that COX makes

A

PGE2
PGI2
TXA2

77
Q

what does PGE2 do

A

inflammatory response

78
Q

what does PGI2 do

A

inhibits platelet adhesion, vasodilator

79
Q

what does TXA2 do

A

vasoconstrictor, inflammatory response

80
Q

how did COXIB cause thrombosis

A

promotes thrombosis by inhibiting COX-2 derived PGi2

81
Q

how did COXIB cause platelet aggregation

A

inhibit COX2 block suppression of thrombin - augment platelet activation

82
Q

overall, what does inhibition of COX-2 derived metabolites cause

A

augment response to thrombotic and hypertensive stimuli

83
Q

which COX does COXIB inhibit

A

only COX 2

84
Q

what is the effect of only inhibiting COX-2 with COXIB

A

TXA2 effects are exaggerated (Vascular tone, reduced cardioprotection)

85
Q

what does COXIB do gradually

A

constant inhibition of neutrophils and platelets, promotes initiation and early progression of atherosclerosis

86
Q

what is the 1 major problem with linking cause and effect

A

there is no ethical way to get human volunteers

87
Q

what are 4 problems with using human volunteers (besides ethics)

A
  • effect may not occur at the time of exposure
  • variability in response (age gender health)
  • complications of combined effects (like many drugs they may be taking)
  • detailed toxicological information may not be available
88
Q

what do outcomes depend on

A

reversibility of injury

89
Q

what is our understanding of mechanisms like

A

limited but rapidly increasing

90
Q

what is the hard thing to balance

A

cardioprotective response and adverse effect

91
Q

what will comprehensive understanding of cardiotoxicity do

A

enhance therapy

92
Q

what direction of K+ transport does the hERG channel move it

A

outside of the cell (repolarization, make more -ve)

PMCOL 303 (25 decks)

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