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cardiovascular system current treatments Flashcards

1
Q

how many deaths worldwise are attributable to cardiovascular disease

A

approx 1 in 3

best prevented through lifestyle changes

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2
Q

what is CVD

A

multifactorial with risk factors including hyperlipidaemia, hypertension, obesity

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3
Q

drugs used to treat CVD - (5)

A

anticoagulant drugs

lipid lowering drugs

angina treatments

antihypertensive drugs

heart failure

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4
Q

examples of anticoagulant drugs

A

aspirin, warfarin, clopidogrel

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5
Q

example of lipid lowering drugs

A

statins

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6
Q

example of angina treatments

A

nitroglycerin

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7
Q

examples of antihypertensive drugs

A

beta blockers, calcium channel blockers

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8
Q

examples of heart failure drugs

A

digoxin, amiodarone, candesartan, captopril

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9
Q

where does digoxin come from

A

foxglove plant

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10
Q

what do most CVD trugs target

A

the adrenergic GPCRs

aka adrenoreceptors

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11
Q

what are adrenergic receptors endogenously activated by

A

adrenaline/ epinephrine

noradrenaline/ norepinephrine

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12
Q

adrenoreceptors can be divided into two groups. what are they called

A

alpha adrenoreceptors

beta adrenoreceptors

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13
Q

alpha adrenoreceptors are subdivided into two groups. what are they called

A

alpha 1 and alpha 2

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14
Q

alpha 1 adrenoreceptors are ____ ____

A

Gq linked

interact with PIP2, increase PKC, CamK2

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15
Q

alpha 2 adrenoreceptors are ____ ____

A

Gi linked

dec cAMP

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16
Q

beta 1-3 adrenoreceptors are ____ ____

A

Gs linked

stimulate cAMP

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17
Q

adrenoreceptors have differential expression and function based on

A

where they are expressed

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18
Q

alpha 1 adrenoreceptors in smooth muscle

A

constrict blood vessels and bronchi

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19
Q

beta 1 adrenoreceptors in the heart

A

inc heart rate and force of contraction

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20
Q

beta 2 adrenoreceptors in the heart

A

increase heart rate and force of contraction

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21
Q

beta 2 adrenoreceptors in smooth muscle

A

dilate blood vessels and bronchi

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22
Q

in the heart, activation of beta 1/2 adrenoreceptors

A

increase levels of intracellular cAMP as they are Gs linked

inc PKA intracellularly

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23
Q

in the heart, activation of beta 1/2 adrenoreceptors causes inc PKA intracellularly. what does this cause

A

activation of ryanodine receptor 2 (RyR2) and L-type calcium ion channel (LTCC)

release of calcium activates calmodulin

this activates myosin light chain kinase MLCK

MLCK can phosphorylate myosin filaments (interaction between myosin and actin is phosphate dependent, allowing for contraction)

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24
Q

where is the ryanodine receptor 2 (RyR2) located

A

sarcoplasmic reticulum

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25
where is the L-type calcium ion channel (LTCC) located
on the cell membrane
26
beta blockers
beta adrenoreceptor competitive antagonists bind to orthosteric site
27
examples of beta blockers
propanolol beta 1 selective beta blockers
28
what is propanolol
non selective antagonist, so interacts with both beta 1 and beta 2 adrenoreceptors - binds to all in the body i.e. in lungs too
29
beta 1 selective beta blocker examples - 3
are cardioselective: atenolol bisoprolol metoprolol
30
what are beta blockers used to treat
angina, heart failure, atrial fibrillation, after heart attack, tachycardia recently, propanolol used as anti anxiety med to control inc heart rate symptoms
31
tolerability of beta blockers
generally well tolerated but, dose dependent side effects inc low blood pressure causing postural hypotension at high doses esp in elderly patients
32
propanolol is a non selective beta blocker. what does this mean clinically
should be avoided in asthmatic patients as they prevent bronchodilation
33
asthma patients treatment
cardio selective beta blocker - only affects B1 receptor so doesnt impact B2 binding of SABAs
34
atherosclerosis
ateries become clogged with fatty substances called plaques or atheroma plaques harden and increase risk of blood clots that block blood flow to heart (heart attack) or brain (stroke) constrict blood flow, increases blood pressure
35
how do blood clots in atherosclerosis occur
blood vessels lining smooth endothelial cells can rupture resulting in a rough surface. this exposes collagen and tissue factors, promoting activation of platelets and coagulation cascade this forms thrombus (blood clot) formation - termed atherothrombosis this blocks blood flow
36
thromboembolism
formed thrombus can break off from initial site and travel around the body lodge elsewhere, blocks blood flow can cause ischemia depending on where embolus gets stuck
37
ischemia
blood clot embolism leading to lack of blood reaching tissues
38
hypercholestrolemia
inc cholesterol in blood which can contribute to atheroma formation
39
HDL
high density lipoprotein good cholesterol absorbs cholesterol, carries back to liver
40
LDL
low density lipoproteins bad cholesterol contributes to atheroma
41
what is used to treat hypercholesterolemia
statins
42
statins are structurally related to ___ which is the substrate of ____
HMG-CoA HMG-CoA reductase
43
statins have a ___ bioavailability as they have
low extensive first pass metabolism and short half life
44
examples of prodrug statins
simvastatin lovastatin these are used to use first pass metabolism to our advantage - increases bioavailability
45
statins act on the same pathway as the nitrogen containing bisphosphonates used in ____
skeletal pharmacology
46
HMG-CoA is converted to ____ through HMG-CoA reductase
mevalonate which can go on to produce cholesterol
47
statins interact with ___, inhibiting production of ___
HMG-CoA reductase mevalonate
48
bisphosphonates are not front line therapies for hypercholesterolaemia. why
inhibits conversion of mevalonate via FDDP synthase due to their impact on skeletal system
49
aspirin is also known as
acetylsalicylic acid
50
when is aspirin used
once atheroma has formed to prevent platelet aggregation anti platelet therapy also can use warfarin
51
standard dose of aspirin to prevent heart attack or stroke
75mg once a day if previously patient has had stroke/ heart attack, this can be increased up to 300mg daily
52
standard dose of aspirin for pain relief
300 mg daily
53
metabolic pathway of aspirin
aspirin - inhibits platelet aggregation undergoes phase 1 hydrolytic event, acetyl group removed forming salicylic acid no platelet inhibition, but anti inflammatory futher phase 2 metabolism to form glucoronide conjugate inactive
54
why does the conversion from aspirin to salicylic acid cause anti inflammation
aspirin inhibits cyclooxygenase-1 (COX-1) which is constitutively expressed this eventually inhibits formation of thromboxane A2/ platelet activation and aggregation salicylic acid instead binds to COX-2, which is upregulated/ expressed only during inflammation, inhbiting production of pro-inflammatory prostaglandin
55
role of cyclooxygenase-1 COX-1
metabolise arachidonic acid into prostaglandin G2 which is then converted to prostaglandin H2 in platelets, can be then metabolised to thromboxane A2, which activates and aggregrates platelets
56
prostaglandin G2
short lived
57
salicylic acid has also been shown to inhibit COX-2 __ __
gene transcription so reduces expression during inflammation, can be taken prophylactically
58
warfarin
anticoagulant prevents clotting events like aspirin but varies in therapeutic window between patients so difficult to dose correctly, also subject to changes in diet
59
warfarin mechanism of action
competitively inhibits vitamin k epoxide reductase complex 1 (VKORC1) prevents reduction of oxidised vitamin k, thus cant be reused, vitamin k dependent carboxylase is inhibited, clotting is inhibited
60
vitamin k epoxide reductase complex 1 (VKORC1)
activates vitamin K for body - which allows for clotting events including healthy clotting events and preventing haemorrhage reduces oxidised vitamin k to reduced vitamin k1, allowing it to be oxidised again to form clotting factors
61
vitamin k dependent carboxylase
converts hypofunctional factors into functional factors aka into able to clot dependent on oxidising vitamin k
62
clopidogrel
prodrug, targets platelet activation and aggregation via inhibiting binding of ADP to P2Y12 receptor
63
__% of clopidogrel is converted into inactive metabolites by __
85 carboxylesterases
64
__% of clopidogrel undergoes first pass metabolism in the __ to active metabolite by conversion to __ , the active metabolite
15 2-oxo-clopidogrel
65
P2Y12
GPCR expressed on platelets purinergic relevant in aggregration
66
P2Y12 is endogenously activated by __ causing
ADP activation of COX-1, fibrinogen binding, clotting cascade
67
2-oxo-clopidogrel irreversibly binds to the
P2Y12 receptors strong as contains thiol group which binds to free cysteine - high affinity inhibits activation via ADP
68
how long does 2-oxo-clopidogrel effect last
platelets are effected for entire lifespan of approx 7-10 days as irreversible only change when new P2Y12 formed via new platelets
69
angina
results from formation of atherosclerosis plaques in vessel walls, limits coronary blood flow and oxygen supply to myocardium causes heavy weight feeling and pressure on chest
70
angina treatment
vasodilators
71
vasodilators example
glyceryl trinitrate or nitroglyceryin
72
glyceryl trinitrate or nitroglyceryin work on the same pathway as
sildenafil/ viagra and amyl nitrites
73
nitric oxide
gaseous signalling molecule
74
vasodilators mechanism of action
nitric oxide crosses membrane effectively as gas binds to guanylate cyclase converts GTP to cGMP reduces intracellular calcium ion stores causes smooth muscle relaxation via myosin light chain phosphatase increases blood flow cGMP converted to GMP via phosphodiesterase activation of phosphodiesterase shuts off cGMP, no more relaxation, cycles to GTP, cycle starts again glyceryl trinitrate or nitroglyceryin is converted to nitric oxide, starts this system and leads to inc blood flow
75
glyceryl trinitrate or nitroglyceryin is converted to nitric oxide via
mitochondrial aldehyde dehydrogenase
76
how is glyceryl trinitrate or nitroglyceryin administered - 2
sublingual tablets or sprays under tongue to inc vascularisation and alleviate symptoms reaches heart faster in angina attack
77
clinical issues we gaf ab - 6
cvd which include/ contributed to by thromboembolism (which can cause ischemia) hypercholestrolemia (can cause atheroma) atheroma blood clotting atherosclerosis (can cause angina)
78
drugs used to treat
anticoagulant drugs - aspirin, warfarin, clopidogrel lipid lowering drugs (for hypercholestrolemia)- prodrug statins (simvastatin, lovastatin) angina treatments - nitroglycerin vasodilator antihypertensive drugs - beta adrenoreceptor competitive antagonists (propanolol (atenolol, bisoprolol, metoprolol are cardioselective), calcium channel blockers heart failure drugs - digoxin, amiodarone, candesartan, captopril

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