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342 > advances cardiovascular > Flashcards

advances cardiovascular Flashcards

1
Q

drugs used (10)

A

lipid lowering drugs - targets hypercholesterolemia

organic nitrates - cardiac output

beta blockers/ beta adrenoreceptor antagonists - hypertension

calcium ion channels - hypertension

thienopyridines - antiplatelet

COX inhbititors - antiplatelet

positive ionotropes - heart contractivity

anti arrhythmic or ace inhibitors - multiple targets

arbs

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2
Q

lipid lowering drug example

A

atorvastatin

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3
Q

organic nitrates drug example

A

nitroglycerin

fast acting

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4
Q

beta adrenoreceptor antagonist example

A

atenolol

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5
Q

calcium channel blocker example

A

verapamil

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6
Q

thienopyridines example

A

clopidogrel

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7
Q

COX inhibitor example

A

naproxen, aspirin

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8
Q

positive ionotropes

A

digoxin

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9
Q

anti arrhythmic III drug example

A

amiodarone

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10
Q

ACE inhibitor example

A

captopril

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11
Q

ARB drug example

A

candesartan

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12
Q

novel cardiovascular therapies in lipid lowering drugs - 3

A

mipomersen

lomitapide

PCSK9 inhibitors

manage atheromatous disease

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13
Q

novel cardiovascular therapies in anginal therapies - 3

A

ivabradine

nicorandil

trimetazidine

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14
Q

novel cardiovascular therapies in heart failure therapies - 2

A

tolvaptan

cardiotrophin-1

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15
Q

novel cardiovascular therapies in hypertension therapies - 2

A

aminopeptidase A inhibitors

diminazene

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16
Q

what do lipid lowering drugs do

A

dec plasma ldl

offer endothelial protection so are prophylactic

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17
Q

nutraceuticals

A

small group of cells associated with diet, found naturally e.g. oats, yeast, rice

has some effect in dec cardiovascular risk

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18
Q

what is mipomersen/ mechanism of action

A

antisense oligonucleotide to ApoB mRNA, binds and promotes mRNA degradation

targets apolipoprotein B-100 (ApoB) which is a component of LDL and VLDL synthesis (bad cholesterol)

reduced formation of ApoB, reduced synthesis of bad cholesterol

dec of 25-40% of circulating LDL in patients

not commonly used

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19
Q

what does mipomersen target

A

liver - significant in managing plasma cholesterol level

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20
Q

mipomersen administration frequency

A

weekly injection

at lipid lowering clinic

21
Q

mipomersen side effects

A

injection site reactions

hepatic steatosis/ fatty liver due to accumulation

22
Q

lomitapide mechanism of action

A

inhibits microsomal triglyceride transfer protein (MTP) enzyme (endoplasmic reticulum of hepatocytes)

reduction in VLDL-C, LDL-C, chylomicrons

reduction in LDL-C in plasma circulation by more than 40%

23
Q

microsomal triglyceride transfer protein (MTP)

A

linked to ApoB assembly and release

24
Q

VLDL-C, LDL-C, chylomicrons

A

plasma cholesterol precursors

25
Q

lomitapide administration

A

oral, uninvasive

not with food, with low fat diet

in clinic

starts 5mg per day, up to 20 mg per day

not commonly used

26
Q

PCSK9 or proprotein covertase subtilisin/ kexin 9 inhibitors

A

inhibit the PCSK9’s inhibitory impact on LDL receptors

dec LDL-C by 60%

27
Q

where is PCSK9 or proprotein covertase subtilisin/ kexin 9 found

A

liver- found in all people but at differing levels
amount found correlates to cardiovascular risk in many

28
Q

PCSK9 or proprotein covertase subtilisin/ kexin 9 - how does it work normally

A

binds to LDL receptor and inhibits it, thus reduced LDL recycling in liver cells

29
Q

LDL receptor role

A

take in low density lipoproteins from blood via endocytosis, break it down via lysosomal degradation

30
Q

examples of PCSK9 inhibitors - 2

A

alirocumab

evolocumab

31
Q

PCSK0 inhibitor administration

A

lipid clinic

biweekly or bi monthly administration

subcutaneous injection

32
Q

PCSK0 inhibitor side effects

A

injection rash

monoclonal antibody so minor side effects

33
Q

novel anti-angina therapies - 3

A

ivabradine, nicorandil, trimetazidine

often coadministered, additive effect

34
Q

ivabradine mechanism of action

A

last resort

targets If “funny current” in diastole/ pacemaker SA node

blocks/ reduces this, thus reduces heart rate and contractivity and pressure of heart

selective to cardiac muscle

35
Q

nicorandil mechanism of action

A

dual action

activates ATP-sensitive potassium channels causing blood vessel dilation

has nitrate group - causes systemic vasodilation

reduces preload and cardiac work, increases myocardial perfusion

reduces major cardiovascular events e.g. cardiovascular death, unstable angina

36
Q

nicorandil side effects - 2

A

flushes due to systemic vasodilation

GI system upset/ vomiting

37
Q

trimetazidine mechanism of action

A

modulates metabolism of cells prone to ischemic/ hypoxic conditions

in ischaemia, metabolism is shifted to free fatty acids, inhibits glucose metabolism and oxidation. free fatty acid metabolism needs more oxygen than glucose metabolism

trimetazidine inhibits free fatty acid metabolism, and activates glucose metabolism so less oxygen is used by cells

reduced angina pain

38
Q

aims of treating heart failure - 4

A

inc cardiac output by increasing contractility

decrease pre-load by dec blood pressure

decrease water retention and BP by increasing natriuresis

inc tissue perfusion by inc vasodilation

39
Q

novel drugs used to treat heart failure examples - 2

A

tolvaptan

cardiotrophin-1 or CT-1

40
Q

what is tolvaptan/ mechanism of action

A

vasopressin receptor 2 V2 antagonist

decreases expression of aquaporin - 2

so we do not rely on electrolyte excretion

less reuptake of water, less blood volume, dec pressure

dec heart failure symptoms e.g. dyspnoea

41
Q

cardiotrophin-1 or CT-1 mechanism of action

A

cytokine, level of IL-6 family

binds to Gp-130 pro survival receptors

stimulates physiological cardiac muscular hypertrophy and vessels

inc cardiac output when patients cannot exercise for this effect

still in studies

42
Q

cardiotrophin-1 or CT-1 side effects

A

correlation with myocardial fibrosis

43
Q

aminopeptidase A inhibitors mechanism of action

A

inhibit metabolism of angiotensin II to angiotensin III

reduces APase aminopeptidease

downregulates vasopressin release

can improve and inc diuresis - removal of water from blood

improves vasodilation

reduces pressure on heart via SA node

44
Q

aminopeptidase A inhibitor example

A

in clinical trials

RB150

well tolerated prodrug

CNS side effects, not fully understood

inc in angiotensin II despite angiotensin III not being activated, but no effect

45
Q

ACE-2 activator

A

can convert angiotensin I and II to cardioprotective peptides

via Mas GPCR

counteracts angiotensin II and AT1R effects

already used in protozoal treatment

reduces blood pressure by inc vasodilation

46
Q

pharmacogenomic considerations - 4

A

HLA variants - link to ADRs

drug metabolism

genes encoding drug targets

combined - metabolism and target can be changed by genetics

47
Q

example of drug metabolism being relevant in pharmacogenomics

A

drugs with single CYP metabolism

varied metabolism and plasma drug conc

e.g. clopidogrel

48
Q

variants of CYP2C19 (2) and effects on clopidogrel metabolism

A

loss of function CYP2C19*2 and *3 - poor metabolism, so still high risk of ischaemic events

gain of function CYP2C19*17 - extensive metabolism, inc bleeding as inc platelet inhibition

342 (20 decks)

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