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Cardiology (small) > Pathophysiology of cardiac disease (Yr 3) > Flashcards

Pathophysiology of cardiac disease (Yr 3) Flashcards

1
Q

what is backwards heart failure also known as?

A

congestive heart failure

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2
Q

what is heart failure?

A

clinical syndrome caused by heart disease resulting in systolic/diastolic function severe enough to overwhelm the normal compensatory mechanisms resulting in poor cardiac output and reduced perfusions (forward) or oedema and effusions (congestive)

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3
Q

what are the possible results of heart failure?

A

poor cardiac output and reduced peripheral perfusion (forwards)
elevated filling pressures, oedema, effusions (backwards)

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4
Q

what are the major consequences of congestive heart failure?

A

oedema and effusions
peripheral vasoconstriction
tachycardia/arrhythmias
remodelling/fibrosis of myocardium

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5
Q

when there is a drop in cardiac output and blood pressure which is detected by the baroreceptors, what happens to sympathetic drive?

A

increased sympathetic drive causing vasoconstriction and increased heart rate and contractility
renin release

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6
Q

what receptors are stimulated to cause vasoconstriction?

A

alpha adrenoreceptors

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7
Q

what receptors are stimulated to cause increased heart rate?

A

beta receptors

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8
Q

when is the RAAS stimulated?

A

decreased glomerular perfusion, which is sensed by the juxtaglomerular apparatus

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9
Q

what happens with RAAS activation?

A

renin is release
angiotensinogen is converted to angiotensin 1 in the liver
ACE catalyses angiotensin 1 converting to angiotensin 2 in the lungs
angiotensin 2 triggers aldosterone release from adrenal cortex
aldosterone acts on distal convoluted tubules and collecting duct to cause sodium/water retention

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10
Q

what are the effects of angiotensin 2?

A

causes aldosterone release
causes vasoconstriction
increases sympathetic drive
causes vasopressin release
triggers endothelin

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11
Q

what effects does vasopressin have?

A

cause water retention
causes vasoconstriction

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12
Q

what substances causes remodelling and fibrosis in congestive heart failure?

A

angiotensin 2
aldosterone
endothelin

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13
Q

what are the endogenous counteractions of RAAS?

A

atrial natiuretic peptide
brain natiuretic peptide

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14
Q

what causes atrial natiuretic peptide release?

A

atrial stretch

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15
Q

what causes brain natiuretic peptide release?

A

increase ventricular pressure (released from ventricles)

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16
Q

what effects do atrial/brain natiuretic peptides have?

A

vasodilators
natiuretics/diuretics

17
Q

why would natriuretic peptides be measured in congestive heart failure?

A

it is a test for wall stretch (diagnostic for congestive heart failure)

18
Q

what natriuretic peptide is used to test for congestive heart failure?

A

NT-pro-BNP

19
Q

what is the function of peripheral vasoconstriction of CHF?

A

arterioconstriction to maintain blood pressure
venoconstricition to increase preload

20
Q

what are the mediators of vasoconstriction in CHF?

A

alpha 1 receptors (sympathetic nervous system)
angiotensin 2
reduced bradykinin levels (ACE breaks down bradykinin)
vasopressin
endothelin

21
Q

how does angiotensin 2 help to control glomerular filtration?

A

constricts the efferent arteriole more than the afferent

22
Q

what are the effects of ACE inhibitors?

A

reduce aldosterone release
reduce glomerular capillary pressure
prevent angiotensin 2 mediated remodelling/fibrosis
reduced vasopressin and endothelin release

23
Q

what drug can be used as an aldosterone antagonist?

A

spironolactone

24
Q

what is the main cause of tachycardia in CHF?

A

elevated catecholamine levels
increased sympathetic drive
reduced vagal tone

25
Q

how do cardiomyocytes replicate in concentric hypertrophy?

A

in parallel (wall thickness increases)

26
Q

how do cardiomyocytes replicate for eccentric hypertrophy?

A

in series (wall stays the same thickness)

Cardiology (small) (14 decks)

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