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Therapeutics 3 Kappa Epsilon > Exam 1 - Wendt (Ischemia) > Flashcards

Exam 1 - Wendt (Ischemia) Flashcards

1
Q

Angina Pain occurs when there is decreased ________ or increased _________

A

decreased coronary blood flow

increased oxygen consumption

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2
Q

what things my lead to decrease coronary blood flow

A

blockages (vasospasm, fixed stenosis, thrombus)

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3
Q

what things may lead to increased oxygen consumption

A

increased heart rate
increase contractility
increased afterload
increased preload

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4
Q

what are the risk factors for angina pectoris

A
  • age (> 55 - men; > 65 - women)
  • cigarette smoking
  • diabetes
  • HTN
  • Kidney disease
  • obesity
  • sedentary lifestyle
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5
Q

Preload is seen as a _______ vs Afterload is _______

A

Preload - volume

afterload - pressure/force

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6
Q

Preload _______ when veins are dilated

A

decreased

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7
Q

Afterload is _______ when arteries are dilated

A

decreased

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8
Q

preload decreases when _____ are dilated

A

veins

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9
Q

afterload decreases when ______ are dilated

A

arteries

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10
Q 
Pre-Load or After-Load:
Which one (when decreased) will cause an increase in myocardial perfusion
A

Preload

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11
Q

What are the 3 hemodynamic factors that influence the O2 supply/demand ratio

A

Preload
afterload
Heart rate

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12
Q

Chronotropic or Inotropic?

will change heart rate or rhythm

A

chronotropic

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13
Q

Chronotropic or Inotropic?

will change the strength of contractility

A

Inotropic

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14
Q

3 types of angina?

A
  • Printzmetal;s/Variant Angina (Vasospasm)
  • Chronic Stable Angina (fixed stenosis)
  • Unstable Angina (thrombus)
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15
Q

which angina is known as vasospasm

A

Printzmetal/Variant Angina

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16
Q

when does printzmetal usually occur

A

night/at rest

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17
Q

which angina is known as fixed stenosis

A

chronic stable angina

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18
Q

which angina is known as thrombus

A

unstable angina

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19
Q

which angina is known as supply ischemia

A

vasospasm/printzmetal/variant
AND
unstable/thrombus

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20
Q

which angina is known as demand ischemia

A

chronic stable ischemia

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21
Q

which angina is an emergency

A

unstable/thrombus… (possible MI on the way)

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22
Q

which angina is normally occurring during exertion/after eating/due to heightened emotional states

A

chronic/stable

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23
Q

2 main causes of Stable/Classic Angina

A
  • Atherosclerosis

- Chronic yet stable obstruction of coronary arteries

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24
Q

With Stable/Classic Angina - the ____ demand exceeds supply due to inadequate _______

A

O2; perfusion

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25
Q

What commonly triggers vasospasm/printzmetal/variant angina

A

atherosclerotic damage to endothelium

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26
Q

What agents are used to increase O2 Supply (general terms/drug classes)

A

vasodilators (CCBs and nitrodilators)
statins
antithrombotics (antiplatelets and anticoagulants)

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27
Q

What agents are used to decrease O2 demand (general terms/drug classes)

A

Beta adrenergic antagonists
Ca2+ entry blockers
Organic nitrates
HCN channel inhibitor

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28
Q

Treatment Goals for Angina:

A

Dilate coronary arteries
decrease O2 demand
decrease preload and afterload

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29
Q

MOA for Organic Nitrates:

A

the nitrates become NO (nitric oxide)

Activation of guanylate cyclase

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30
Q

Organic Nitrates:

dilate (arteries or veins?)

A

VEINS

very very very minor artery dilation…

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31
Q

Organic Nitrates:

decrease (preload or afterload)

A

preload (because they dilate veins)

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32
Q

How does NO lead to relaxation/dilation?

A

NO –> activates soluble GC –> GTP to cGMP –> increase activity of PKG (protein kinase G) –> activates MLCP (myosin light chain phosphotase) –> dephosphorylation of MLC/detachment of myosin from actin

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33
Q

NO has short or long half life – and why?

A

SHORT(bc high affinity for hemoglobin)

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34
Q

what are the nitrate compounds mentioned in lecture?

A

glyceryl trinitrate (GTN)
Isosorbide Mononitrate
Isosorbide Dinitrate

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35
Q

which nitrate is used strictly for attacks

A

GTN (glyceryl trinitrate)

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36
Q

which nitrate has the shortest half life?

A

GTN (~ 5 mins)

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37
Q

Bioactivation of organic nitrates occurs mainly by ______ in the ______ of target cells

A

ALDH2; mitochondria

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38
Q

why does tolerance occur for organic nitrates?

A

ALDH2 is needed to convert nitrates to NO — ALDH2 needs time to regenerate

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39
Q

CCBs dilate (arteries or veins)

A

arteries

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40
Q

CCBs have a greater effect on (preload or afterload)

A

AFTERLOAD (bc does artery dilation)

41
Q

CCBs MOA:
Decrease influx of _______
and
decrease ________ in nodal cells

A

Ca2+ (duh…); chronotropy

42
Q

Why does decreasing Ca2+ influx work on causing relaxation?
Because normally….
Ca2+ comes in through ____ Ca2+ channels and Ca2+ binds to ________ for its secondary effects and it also binds to _______ on _______ and all this crap leads to contraction

A

through L-type; binds to Calmodulin (CM) for secondary; binds to troponin on actin

43
Q

Beta Blockers:

Block what?

A

block epinephrine stimulatin of myocardium

44
Q

Beta blockers _______ inotropic and _____ chronotropic effects

A

decrease; decrease

45
Q

Beta Blockers _____ heart rate which ______ coronary perfusion

A

LOWER HR: INCREASE coronary perfusion

46
Q

Beta blockers have negative inotropic and chronotropic effects by block _______ in myocytes and nodal cells (respectively)

A

block cAMP signaling

47
Q

Coronary perfusion increases with beta blockers because why?

A

decrease HR = more filling time aka more time in diastole (diastole is only time myocardium can be perfused)

48
Q

Beta Adrenergic Receptors when stimulated in VSM do what? and via what pathway?

A

cause RELAXATION (relax arteries and bronchioles)

pathway: G(alpha)S - cAMP - PKA - inhibit MLCK = relaxation

49
Q

Beta Adrenergic Receptors when stimulated in cardiocytes do what? and via what pathway?

A

cause contraction! (why we use beta blockers….)

pathway: cAMP - PKA - phosphorylate Ca2+ channels = contraction

50
Q

what are the cardioselective beta blockers

A

atenolol
metoprolol
acebutolol

51
Q

what are the non-selective beta blockers

A

propranolol
carvedilol
pindolol
labetalol

52
Q

which drug classes used for angina can cause reflex tachycardia?

A

Nitrates and CCBs( mainly DHPs)

53
Q

which CCB is benzothiazopine

A

diltiazem

54
Q

which CCB is phenylalkylamine

A

Verapamil

55
Q

how do we compensate for the reflex tachycardia for nitrates and CCBs?

A

beta blockers

56
Q

beta blockers increase ____load

A

pre

57
Q

beta blockers increase preload which can be problematic because why?

A

too much filling can stress the heart tf out

58
Q

how do compensate for beta blockers increasing preload

A

nitrates!

59
Q

why do nitrates work to compensate for beta blockers increasing preload

A

nitrates dilate veins aka return reduce venous return and preload!

60
Q

what is the most common combo for angina

A

nitrates and beta blockers

61
Q

what two drug combos are NEVER used for stable angina due to codepression of pacemaker cells

A

Verapamil and Beta blockers

62
Q

why is verapamil and beta blockers NOT used together for stable angina

A

they cause codepression of pacemaker cells

63
Q

step wise process for Angina (what drug combos do we do in what order

A

1 - always nitrates and beta blockers
2 - CCB + beta blockers OR nitrates + CCBs
3- last line = all 3 (nitrates, CCBs, beta blockers)

64
Q

Side Effects of Beta blockers

A
  • bronchoconstrictor
  • Bradycardia/AV block
  • LV dysfunction
  • minor GI distress
65
Q

Side effects of Nitrates

A
  • Hypotension/Flushing/headaches (v common)
66
Q

Side effects of Diltiazem

A

All “minor”

  • hypotension/flushing/HAs
  • LV dysfunction
  • Bradycardia/AV block
67
Q

Side effects of DHPs

A
  • Hypotension/Flushing/headaches (v common)
68
Q

Side effects of Verapamil

A

Lots of GI distress and Bradycardia/AV block

  • LV dysfuntion (medium)
  • Hypotension/Flushing/headaches (minor)
69
Q

HCN Channels are regulators of _______

A

heart rate

70
Q

HCN channels are regulated by ______ and are sensitive to _______

A

cAMP; transmembrane voltage

71
Q

for HCN channels are more open when they are _______

A

hyperpolarized/negative

72
Q

HCN is sensitive to cAMP and thus is regulated by _______

A

catecholamines (NE, E, dopamine)

73
Q

HCN channels are only found in ______ cells in cardiac cels

A

Nodal cells (AV and SA)

74
Q

you can slow heart rate down by slowing down ______ when it comes to HCN channels

A

the rate of action potential generation

75
Q

HCN channels usually flux what things?

A

Na+ and Ca2+ (shocker)

76
Q

what drug is a HCN channel inhibitor

A

Ivabrandine

77
Q

Ivabrandine is a ________ inhibitor

A

HCN channel

78
Q

Ivabradine reduces ______ _______ current

A

diastolic depolarization

79
Q

Ivabradine _______ heart rate

A

slows

80
Q

Ivabradine ______ diastole and thus _______ ventricular filling

A

prolongs diastole; improves filling

81
Q

T or F: Ivabradine has NO hemodynamic or conduction abnormalities

A

TRUE!

82
Q

what channel has importance during the ischemia cycle? (Wendt mentioned a “vicious cycle of ischemia”)

A

NCX channel

83
Q

“Vicious” Cycle of Ischemia:
Normally the NCX channel ______ Ca2+ but during ischemia Ca2+ ______ instead (this happens because Na+ levels get out of wack)

A

normally Ca2+ gets kicked out of cell; Ca2+ starts to come in during ischemia to make everything worse..

84
Q

what drug blocks the NCX channel

A

Ranolazine (Ranexa)

85
Q

how does Ranolazine work

A

it blocks NCXS channel — aka will help prevent ischemia

86
Q

side effects of Ranolazine

A

Dizziness; QT prolongation

87
Q

what statins are prodrugs

A

lovastatin and simvastatin

88
Q

treatment goals for unstable angina

A
  • block thrombus formation

- dissolve existing thrombi

89
Q

drugs used for unstable angina

A

aspirin; heparin; P2Y12 antagonists

90
Q

Aspirin inhibits what?

A

platelet activation

91
Q

P2Y12 antagonists inhibit what?

A

platelet activation

92
Q

GPIIb/IIIa antagonists block what?

A

platelet aggregation

93
Q

Heparin inhibits what?

A

thrombin formation

94
Q

what is aspirins MOA?

A

it irreversibly acetylates COX-1 platelets –> reduces TXA2 production (TXA2 is major for platelet aggregation)

95
Q

what drugs are P2Y12 inhbitors

A 
clopidogrel
prasugrel (effient)
ticagrelor (Brlinta)
96
Q

Heparin binds to _______ which ends up inactivating what things?

A

AT-III (antithrombin)

inactivates thrombin; factor Xa

97
Q

which drugs are LMW heparins (low molecular weight)

A

enoxaparin
dalteparin
tinzaparin

98
Q

T or F: Warfarin and direct Xa inhibitors are not indicated for angina

A

truueee

99
Q

what drugs are GPIIa/GPIIIa inhibitors

A

tirofiban
abciximab
eptifibatide

Therapeutics 3 Kappa Epsilon (20 decks)

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