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1st Year Med > Cardiac Diseases > Flashcards

Cardiac Diseases Flashcards

1
Q

what is angina pectoris?

A

chest pain due to myocardial ischaemia
due to buildup of metabolites (lactate, K+)
ischaemia due to increased myocardial O2 demand which is not met

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2
Q

describe stable angina

A

attacks predictable situations (exercise, stress)
caused by occlusive coronary artery disease (atherosclerosis)

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3
Q

describe unstable angina

A

attacks unpredictable situations
coronay artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque

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4
Q

describe variant angina

A

attacks unpredictable situations
coronary artery occlusion caused by vasospasm

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5
Q

what is coronary steal?

A

dangerous dilation of coronary arteries
vessel dilation sends more blood to well vascularised areas)

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6
Q

what is the general solution to all angina types?

A

decreasing myocardial O2 demand

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7
Q

how can myocardial O2 demand be reduced?

A

beta blockers (propranolol/atenolol)
lowering HR

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8
Q

explain the mechanisms of ivabradine

A

anti anginal
blocks Na currents contributing to SA node depolarisation
decreases HR (not force)

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9
Q

what is the effect of vasodilator drugs in arteries?

A

reduces myocardial work and O2 demand

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10
Q

what are the effects of vasodilator drugs on veins?

A

reduces:
venous return
preload
ventricular/atrial stretch
contraction strength
myocardial work
myocardial O2 demand

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11
Q

what is the bainbridge reflex and what does it do?

A

sympathetic reflex caused by increased blood in atria
causes SA node stimulation which stimulates baroreceptors in atria causing increased sympathetic stimulation

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12
Q

what is GTN and how is it administered?

A

glycerol trinitrate is a nitrovasodilator
taken as sub-lingual tablet or spray as it inst orally active

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13
Q

what are the uses of nitrovasodilators in angina?

A

prophylaxis in stable angina
rapid relief of ongoing angina

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14
Q

describe pro-drugs and give an example

A

nitrovasodilators are pro drugs
lipophilic (enter smooth muscle cells and reduced to NO)
mimics action of endothelium derived NO

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15
Q

what does NO do in the heart?

A

activates soluble guanylate cyclase (sGC) which is a cytoplasmic enzyme
NO binds to haem receptor increasing enzyme activation
this converts GMP to cGMP causing vasodilation

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16
Q

what are the side effects of nitrovasodilators?

A

headache (cerebral artery dilation)
tolerance at prolongued use

17
Q

describe L-type blockers and their mechanism of action, and give examples

A

dilates arteries (reduces TPR)
anti angilans as lowered TPR reduces afterload and CO (reduces myocardial O2 demand)

examples: verapamil, diltiazem, nifedipine

18
Q

describe T-type (transient) channel blockers and give and example

A

ethosuxamide

present in pacemakers and smooth muscle
blocks Ca channels to thalamocortical (TC) neurons to treat absense seizures

19
Q

describe K+ activators, give and example and state their advantages

A

nicorandil
venodilating properties
no tolerance built up over time and potent cardioprotective action

20
Q

describe what heart failure is physiologically

A

inability of the heart to pump sufficient oxygenated blood to metabolising tissues despite adequate filling pressure

21
Q

what are the causes of heart failure?

A

dysfunctional stenotic valve (most common)
genetics
congenital heart disease
endocrine dysfunction

22
Q

what are the cardinal symptoms of heart failure?

A

breathlessness
ankle swelling
fatigue

23
Q

what are the physical signs of heart failure?

A

sinus tachycardia
atrial fibrillation
BP changes
raised JVP
oedema
pleural effusion
displaced apex beat
murmurs

24
Q

explain what can occur after myocardial remodelling

A

ventricular function and CO decrease causing overactivation of neurohormonal signalling pathways

25
Q

what can neurohormonal signalling overactivation cause?

A

vasoconstriction, apoptoses, hypertrophy/fibroses increasing cardiac afterload
or
Na/water retention and increase in intravascular volume, increasing cardiac preload

26
Q

what neurohormonal activations occur after a delay in the ventricular systolic function?

A

SNS through epinephrine and norepinephrine (a1, b1, b2)

natriuretic peptide system through NPRs to neuropeptide receptors

RAAS through angiotensin II to angiotensin II type 1 receptors

27
Q

what does vasoconstriction by the SNS increase?

A

RAAS/vasopressin activity
HR
contractility

28
Q

what does RAAS system cause and what does this increase?

A

causes vasoconstriction
increases:
BP
sympathetic tone
aldosterone
hypertrophy
fibrosis

29
Q

what does the natriuretic peptide system cause and what does this decrease?

A

causes vasodilation
decreases:
BP
sympathetic tone
diuresis/natriuresis
vasopressin/aldosterone activity
hypertrophy
fibrosis

30
Q

name investigations in blood tests for heart failure

A

urate
electrolytes
liver function (LFT)
thyroid function (TFT)
creatine kinase (CK)
iron
BNPs (natriuretic function)
full blood count (FBC)

31
Q

name routine investigationd for heart failure and what it may show

A

chest x-ray, ECG, ECHO, cardiac MRI, endomyocardial biopsy

can show wall dysfunction, valvular dysfunction or dilated chambers

32
Q

what are the goals of heart failure treatment?

A

releive symptoms
prevent premature death
avoid admission/readmission

33
Q

what are the common medications administered for heart failure and what do they do?

A

beta blockers (inhibit SNS)
neprilysin inhibitors (inhibit natriuretic peptide system)
ACE inhibitors (inhibit RAAS)

34
Q

describe the mechanism of action of SGLT2 inhibitors

A

inhibit proximal tubular glucose reabsorption
causes diuresis and natriuresis
lowers BP and weight

35
Q

what drugs aggrevate the symptoms of heart failure?

A

NSAIDs
Ca antagonists
anti-arrythmics
tricyclic antidepressants
corticosteroids

36
Q

what do implantable cardioverter defibrillators (ICDs) do?

A

inserted into heart with a transvenous lead, chocking coils, pectoral device and endocardial sensor
defibrillates heart in emergencies

37
Q

describe the intra-aortic balloon pump

A

used for cardiogenic shock
causes diastolic augmentation of aortic pressure
increases coronary perfusion, reduces afterload anf improves CO

38
Q

what is the function of an LVAD (LV assisting device)?

A

pumps blood for heart reducing cardiac work
short temp VAds used to pump blood outside body before bringing it back in

often used as bridge treatment in organ failure

1st Year Med (52 decks)

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