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Pharm Exam 3 > Drennan 1 > Flashcards

Drennan 1 Flashcards

1
Q

Factors affecting CO

A

SV*HR

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2
Q

Consequenes of reduced CO

A
  • Tachycardia
  • Cardiomegaly
  • Arrhythmia
  • Fatigue
  • SOB
  • Pulm edema
  • Cyanosis
  • Orthopnea
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3
Q

Key thing that happens in CHF

A

reduction in CO

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4
Q

Decrease in preload leads to

A

decrease in O2 consumption

Increase in myocardial perfusion

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5
Q

Decrease in afterload leads to

A

decrease in O2 consumption

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6
Q

Decreased HR will

A

increase coronary perfusion

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7
Q

Afterload definition

A

Force distributed in ventricular wall during systole

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8
Q

Limit of starling relationship

A

Stretching passes a certian point >> actin and myosin are not properly aligned >> no further increase in force can be generated

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9
Q

Optimal length of overlap

A

2 to 2,2 microns

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10
Q

In Frank Starling curve, increasing contraction will shift the curve ___

A

upward

(increased SV per a certain EDV)

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11
Q

____ and _____ are inversely related.

What relationship is this?

A

Stroke volume and Afterload

The force-tension relationship

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12
Q

Failing hearts start to show signs of…

A

higher sensitivity to afterload for a given stroke volume

Increases in afterload will shift SV down further than normally

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13
Q

Progessive CHF is a disease of:

A

compensation and decompensation

Compensation = Stable patient, normal activity

Decompensated = acute worsening of CHF

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14
Q

Type of CHF with thin/dilated heart

A

Systolic failure

(Deficit in contraction)

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15
Q

Thick/stiff walls can’t relax in which type of CHF

A

Diastolic failure

(Deficit in filling)

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16
Q

afterload, SV, and preload in early heart failure

A

afterload = high

SV = reduced somewhat

Preload = starts to increase –> drop off normal curve

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17
Q

Compensation for maintaining SV in early HF

A

Increased Sy

Increased volume (RAAS)

Cardiac remodeling

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18
Q

AT2 effects

A
  1. Vasoconstriction
  2. Stimulates remodeling
  3. Induces aldosterone
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19
Q

Increased CT in cardiac remodling is due to

A

cell death and replacement of dead myocytes with fibroblasts

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20
Q

Increased ____ in remodeling with CHF

A
  • Increase in Ca2+ cycling
  • Increase in response to Calcium (Ca sensors that will go and mediate Calcium-dependnt genes that play role in hypertrophic response)
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21
Q

CHF drug strategies (and dothey improve mortality)

A

Manipulate hemodynamics (NO)

Inhibit compensation (YES)

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22
Q
A

Vasodilators

Diuretics

Angiotensin Inhibitors

Inotropic agents

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23
Q

Inotropic agents

A

Cardiac glycosides

PDE inhibitors

B adrenergic agonists

24
Q

Chronic therapy inotropic agent

A

Cardiac glycosides

25
Q

Acute therapy inotropic classes

A

PDE inh

B agonists

26
Q

B agonists (inotropic agents)

A

dobutamine, DA

27
Q

Pumps calcium into SR lumen

A

SERCA

28
Q

Two mechanisms to get calcium out of the cell

A
  1. Ca2+ ATPase
  2. NCX exchanger = 3 Na in, Ca2+ out
29
Q

Manipulation of _____ enhances cardiac contractility

A

Na+ gradient

30
Q

PDE inhiitor risk

A

arrhythmia (long term)

31
Q

Beta agonists long term AE

A

desensitzation

32
Q

Ca2+ overload is

A

pro-arrhythmic

e.g. overdoses of digoxin

33
Q

digoxin MOA

A
  1. Inhibit Na/K+ ATPase
  2. sodium builds up in cell
  3. Low Na+ gradient
  4. NCX is less functional at exchanging Na+ for Ca++
  5. Increases cytoplasmic levels of Ca++
34
Q
A

Increases = Contractility and AV node refraction

Decreases = HR (indirect via Vagus) and vascular tone

35
Q

Glycosides common toxicities

A
  1. Psych
  2. GI (N/V, pain)
  3. Resp (Increased response to hypoxia)
  4. Cardiovascular - Arrhyth., AVBlock
36
Q

Digoxin interactions

A
  • BB and CCBs depress heart and digoxin action
  • Kaliuretic diuretics promote digoxin action (via decrease in K+), which raises risk for arrhytmia
37
Q

PDE3 inhibitors

A

Milrinone

Amrinone

38
Q

PDE inhibitors risk

A

Pro arrhyth.

Decrease survival

39
Q

Beta AR agonists risks

A

prone to desensitization

cause hypertension

40
Q

PDE antagonists block

A

cAMP–> AMP

41
Q

Drugs that act by Inhibiting compensation

A

RAAS inhibition

Aldosterone antagonist

BB’s

42
Q

RAAS inhibitors reduce

A

preload and afterload

43
Q

Agents for RAAS inhibition

A

ACEi’s (enalapril)

AT2R blockers

Aliskiren

44
Q

Aldosterone antagonist that acts as a potassium sparing diuretic

A

Spironolactone

45
Q

Arrhythmogenesis and risk of sudden cardiac death

A

K and Mg loss

46
Q

Aldosterone effects (6)

A
  1. Increase Na/water retention
  2. K+ and Mg2+ loss
  3. Reduced myocardial NE uptake
  4. Reduced baroreceptor sensitivity
  5. Myocardial fibrosis, FB proliferation
  6. Change Na+ channel expression (related to arrhythmias)
47
Q

B-AR blockers are useful in normalizing..

A

the hyperadrenergic state in CHF

48
Q

B-AR effect on after/pre load

A

reduce afterload

may increase preload

49
Q

AT2 stimulates…

effects?

A

Vasopressin secretion

(Water retention, Vasoconstrict, enhanced PLATELET aggreg., VSM and myocyte proliferation)

50
Q

VR antagonists in CHF

A

Tolvaptan

Conivaptan

51
Q

Indications for tolvaptan and conivaptan

A

Tx for hyponatremic state in SIADH and HF

Acute care setting

52
Q

VR antagonists AE’s and interactions

A

HoTN, osmotic demyelination

CYP3A substrate

53
Q

Neprilysin MOA

A

terminates the action of naturetic peptides (neutral endopeptidase)

Degrades Naturetic peptides, bradykinin, adrenomedullin

54
Q

Neprilysin inhibition results in…

This Counters…

A

increased vasoactive peptides

counters neurohumoral vasoconstriction, Na+ retention, remodeling

55
Q

Human Type B naturetic peptide

A

Activates membrane-bound guanylate cyclase in VSMC and endothelial cells

Increased cGMP –> dephosphorylate MLC –> Vascular smooth muscle relaxation

56
Q

Inotropic agents help with…

A

low output symptoms but not congestive symptoms

57
Q

ACE inhibitors reduce

A

both preload and afterload

  • Preload via volume reduction*
  • Afterload via BP reduction*

Pharm Exam 3 (11 decks)

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