10/02 Flashcards

1
Q

beta 1 and 2 __________ cyclic AMP and acetylcholine _______ cyclic AMP

A

increases
decreases

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2
Q

cyclic AMP activates

A

protein kinase A

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3
Q

protein kinase A binds to the ______ which then releases _______. This in turn increases the force of ________

A

sarcoplasmic reticulum
calcium
contraction

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4
Q

in pacemaker cells, the role of norepinephrine is to

A

increase the heart rate and increase the force of contraction

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5
Q

acetylcholine ____ the rate and force of a heart beat

A

decreases

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6
Q

in the underlying endothelial cells of the vasculature, we have norepinephrine being released and it binds to alpha 1 and to some extent to alpha 2. What is the effect?

A

alpha 1gq increases IP3= contraction

alpha 2inhibitory deceases cyclic AMP= contraction

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7
Q

if we give an alpha 2 agonist in the setting of HTN, it is primarily going to work by _______

A

stimulating parasympathetic outflow and inhibiting the sympathetic outflow

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8
Q

what is an alpha 2 antagonist that is not used clinically? This drug works on which neuron?

A

yohimbine
the presynaptic neuron to increase blood pressure by blocking the negative feedback loop

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9
Q

what can, over time, lead to things like arrhythmias, heart failure, and cardiac death?

A

scar tissue on the heart from things like MI’s. cardiac myocytes don’t proliferate

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10
Q

what are non cardiac related heart failure examples?

A

graves disease
beriberi- thiamine deficiency

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11
Q

when do we start using the word “congestive” when talking about heart failure?

A

when fluid starts leaving the heart and going into the lungs or into the periphery

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12
Q

How are the heart walls in systolic failure

A

thin

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13
Q

How are the heart walls in diastolic failure

A

thick

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14
Q

systolic heart failure reduces cardiac ________. This is more acute or chronic?

A

function
acute

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15
Q

diastolic heart failure reduces cardiac ________. This is more acute or chronic?

A

filling
chronic

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16
Q

what is the most common precipitating factor for heart failure?

A

coronary artery disease

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17
Q

what is the first and last line of defense in systolic heart failure?

A

first: diuretic
last: inotropic drugs

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18
Q

what are the 4 factors that affect cardiac performance?

A

preload
afterload
contractility
heart rate

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19
Q

what is blood pressure largely determined by?

A

the contraction of the left ventricle

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20
Q

in the heart, the more stretch we have, the more

A

forceable the contraction there will be

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21
Q

what is preload?

A

the measure of stretch of the heart

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22
Q

what is the blood that’s left in the heart after every systole called?

A

end systolic volume

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23
Q

what contributes to end diastolic volume?

A

passive filling
atrial contraction
end systolic volume

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24
Q

left ventricle ESV equation

A

passive filling (65mL)+atrial contraction (25mL)= ESV 50mL

25
Q

Stroke volume = what minus what?

A

EDV-ESV

26
Q

what is the normal end diastolic range?

A

4-12mmHg

27
Q

what contributes to altered preload?

A

increase in EDV, increase in blood volume or increase in venous tone

28
Q

What can reduce preload?

A

salt restriction
diruetics
venodilation

29
Q

what is afterload?

A

BP. the force the heart has to pump against

30
Q

what leads to diastolic heart failure?

A

increased afterload

31
Q

as output decreases, the body increases

A

afterload which decreases output

32
Q

what may be more useful for long-term treatment of heart failure?

A

non-cardiac targets
ACE inhibitors
ARB’s
Aldosterone receptor antagonists
vasodilators

33
Q

List the steps of heart muscle contraction

A

AP depolarizes the cell
trigger Ca++ comes in and binds to the Ryr receptors
Ryr opens on the sarcoplasmic reticulum releasing stored Ca++
Ca++ bathes the troponin tryptomysin complex which dissociates from actin.
actin then can interact with myosin.
With the help of ATP we have contraction.

to reset SERCA pumps Ca++ back into the SR
trigger Ca++ is exchanged via the Na+/Ca++ exchanger (3Na+1Ca++)
Na+/Ca++ pump (3Na+2K+)

34
Q

How does Digoxin work?

A

it blocks the Na+/K+ pump.
More Na+ in the cell= the Na+/Ca++ exchanger stops working= more Ca++ in the cell= more Ca++ release from the SR=increased inotropy

35
Q

what is another name for the Na+/Ca++ exchanger in pharm

A

Na+/Ca++ antiporter

36
Q

digitalis increases the _____ of the heart

A

force of contraction

37
Q

where does digitalis come from?

A

foxglove plant

38
Q

Why is digoxin so dangerous?

A

it has a very narrow therapeutic index, it causes arrhythmias

39
Q

what is the only oral positive inotropic agent for heart failure?

A

digoxin

40
Q

what are the electrical effects of digoxin?

A

Increases PR
decreases QT

41
Q

What is the EKG characteristic of digoxin therapy?

A

a downward “schwoop” between the S and T.
Called the digitalis effect
compared to the mustache of famous painter Salvador Dali

42
Q

What is the Therapeutic index of Digoxin?

A

2

43
Q

What are the little depolarizations that happen before we are out of the absolute refractory period?

A

early or delayed after depolarizations. Can lead to Vtach or Vfib

44
Q

Digoxin is a ___________ of potassium

A

competitive inhibitor

45
Q

How does Digoxin induce arrhythmias?

A

Hypercalcemia d/t it blocking the Na+/K+ pump

Hypomagnesium, not sure how

46
Q

what is the IV positive inotrope?

A

milrinone
only one available in the US

47
Q

What does Milrinone target?

A

PDE3- normally this degrades cAMP to AMP= relaxation. Milrinone blocks it so there’s increased cAMP=increased force of contraction

48
Q

What does PDE stand for?

A

phosphodiesterase

49
Q

beta one selective agonists have an effect on the heart, but do not effect the ______

A

blood pressure

50
Q

what drugs are more widely used compared to Digoxin for their positive inotropic effects? What class of drug are these?

A

Dopamine
Dobutamine (most widely used)

beta adrenergic stimulants

51
Q

What drugs reduce compensatory responses to failure by decreasing afterload?

A

ACE
ARBs

52
Q

How do vasodilators help in heart failure?

A

decreases preload and afterload

53
Q

What drug is never indicated for acute heart failure, but can be added to the patient’s ACE and ARBS regimens for chronic heart failure, and why?

A

Beta Blockers
this reduces the stress on the heart by decreasing the HR and decreasing the force of contraction

54
Q

meds to avoid in heart failure

A

NSAIDS
Thiazolidinediones
Metformin

55
Q

What is stage A heart failure?

A

high risk with no symptoms- lifestyle changes

56
Q

What is stage B heart failure?

A

structural heart disease, no symptoms- start on ACE

57
Q

What is stage C heart failure?

A

structural disease with symptoms- start on ACE and B blockers

58
Q

What is stage D heart failure?

A

refractory symptoms requiring special intervention- Digoxin,Transplantation, ventricular assistive device, CABG

59
Q

IV treatment for Acute heart failure

A

diuretics
dobutamine
vasodilators