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DRUGS > CVD Drugs > Flashcards

CVD Drugs Flashcards

1
Q

what is angina

A

heart temporarily deprived of oxygen

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2
Q

what is a heart attack

A

heart deprived of oxygen (muscle death)

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3
Q

what is dysrhythmia

A

heart rhythm disturbed

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4
Q

what is heart failure

A

heart does not pump properly

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5
Q

how many people in the UK have had a heart attack

A

1.5 million

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6
Q

how many people have CHD and angina

A

2.3 million have CHD and 2 million have angina

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7
Q

what are lipoproteins composed of

A
  1. lipids (triglycerides or cholesterol esters)

2. phospholipids, cholesterol and proteins

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8
Q

what lipoproteins have the lowest density of all

A

chylomicrons

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9
Q

what is synthesised in the hepatocytes

A

cholesterol

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10
Q

increased risk of atherosclerosis diagram

A
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11
Q

how does HDL decreased risk of atherosclerosis

A

increases fibrinolysis - helps break down blood clots and increases fibrin degradation
increase prostacyclin formation - decrease aggregation

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12
Q

what is familial hypercholesterolaemia

A

defect in LDL receptor or ApoB protein

autosomal dominant

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13
Q

what is the main component in plaque

A

foam cells (they are dark areas where the nucleus is)

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14
Q

what is an example of a statin

A

atorvastatin

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15
Q

how does atorvastatin reduce LDL

A
  • competitively inhibits HMG-CoA reductase, rate limiting enzyme in production of cholesterol
  • similar in structure
  • recuses liver production of cholesterol
  • lowered cholesterol leads to more LDL receptors
  • increased removal of LDL from plasma
  • also increased HDL and lower triglycerides
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16
Q

mevalonate pathway

A
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17
Q

problems with statins

A
  • myositis - muscle inflammation
  • rhabdomyolysis - muscle breakdown causes dark coloured urine
  • myoglobin is being reduced fro muscle and released in urine
  • altered liver function tests
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18
Q

percentage of population taking statins in 2013

A

13%

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19
Q

what is the NHS tool to see your own cardiovascular risk

A

QRISK3

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20
Q

what does the QRISK3 do

A

calculates risk that you will have a heart attack or stroke in net 10 years

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21
Q

what factors does the QRISK3 use

A

age, sex, ethnicity and weight

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22
Q

what is the cut off for statin treatment for primary prevention

A

10% It was 20%

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23
Q

how does exzetimibe work

A

inhibits intestinal cholesterol absorption

inhibits specific cholesterol transporter in gut

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24
Q

what does ezetimibe result in

A

reduced LDL

reduced total cholesterol

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25
Q

when is ezetimibe used

A

in patients who cannot tolerate statins

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26
Q

cholesterol absorption in the intestine and how ezetimibe inhibits it diagram

A
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27
Q

how do anion exchange resins work

A

sequester bile acids in the gut, increased usage of cholesterol

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28
Q

how do fibrates work

A

agonists at a receptor called PRAR alpha

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29
Q

what is olestra

A

fat substitute
cannot be absorbed by the GI tract
Mal-absorption of fat-soluble vutamus

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30
Q

acute coronary syndromes

A

1 unstable angina
2 non ST elevated myocardial infarction NSTEMI
3 ST elevated myocardial infarction STEMI

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31
Q

what is angina pectoris

A

crushing pain in chest that may radiate to arm, neck or jaw

the pain results from cardiac schema

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32
Q

what substrates are released as an example of referred pain

A

k+ , h+ and bradykinin

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33
Q

types of angina

A

stable and unstable

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34
Q

what are types of angina when vessels constrict/spasm

A

prizmental’s angina

microvascular angina

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35
Q

what is stable angina caused by

A

atherosclerosis of coronary arteries

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36
Q

what is unstable angina

A

atherosclerosis and a blood clot

with higher risk of MI

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37
Q

NICE care pathway for stable angina

A
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38
Q

what do short acting nitrates do

A

relieve an attack

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39
Q

what does optimising angina drugs do

A

prevents further attacks

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40
Q

what do secondary prevention drug do

A

prevent progression of atherosclerosis

41
Q

what is the surgical approach to angina

A

revasularisation

42
Q

aspirin as an organic nitrate treatment

A

prevents platelet aggregation

43
Q

first pass metabolism diagram

A
44
Q

organic nitrate list

A

glyceryl trinirate
amylnitrate
isosorbide denigrate
nicroandil

45
Q

what are pro drugs

A

drugs that have to be metabolised before becoming effective

46
Q

where do organic drugs get metabolised

A

at their site of action and not in the liver

47
Q

vasodilation pathway induced by an organic nitrate (prodrug)

A
48
Q

how do nitrates relieve an attack of angina

A
  • by dilating coronary arteries although less important as coronary arteries already maximally dilated by metabolises from ischaemic myocardium
  • by reducing cardiac work and hence reducing the cardiac O2 demand - nitrates reduce cardiac work by reducing preload (principal effect) and after load
49
Q

how is cardiac workload reduced

A
  • dilation of peripheral blood vessels - capacitance veins
  • heart does not have to push so hard
  • less blood returned to the heart ; lower force of contraction.
50
Q

sequence of events leading to angina

A
51
Q

what do large doses of nitrates cause

A

arteriolar dilation
fall in peripheral resistance
reduce in cardiac after load
reduces cardiac work

52
Q

improved coronary blood supply

A
53
Q

nicorandil mechanism of action

A
  • activator of K+ ATP channels and NO donor
  • dilates both arteries and veins
  • effects vs angina similar to nitrates
54
Q

what are the unwanted effects of nicorandil

A

headache, flushing, hypotension, nausea and vomiting

55
Q

reducing cardiac workload : beta blockers diagram

A
56
Q

binding sites for verapamil and amlodipine

A
57
Q

mechanism of vearpamil in stable angina

A
  • blockade of Ca2+ channels in use-dependent
  • more potent on heart than vascular smooth muscle
  • Ca2+ channel blockade in cardiac tissue reduces heart rate and cardiac output
  • dilation of orioles reduces cardiac after load
  • cardiac work and O2 demand are reduced
58
Q

amlodipine in stable angina

A
  • blockade of Ca2+ channels and is NOT use dependent
  • more potent on vascular smooth muscle than the heart
  • dilatation of arteries reduces cardiac after load
  • dilatation of capacitance veins reduced cardiac preload
  • cardiac work and O2 demand are reduced
59
Q

when are surgical approaches used for treating angina

A

if the drug options have not Brough the angina under control.

60
Q

how does a coronary artery angioplasty work

A

a catheter is introduced into a large vessel in the groin or arm and is treated into the heart and guided to the place where the artery is blocked. the journey of the catheter to the blocked artery can br visualised by injection a dye out of the catheter into the blood vessel and following it using an Xray machine.
when the catheter reaches the blockage, a balloon at its tip is inflated, which opens the artery and also pushes open a metal mesh tube, called a stent. the stent will keep the artery open once the balloon is delated and the catheter is removed. stents can be either bare stainless steel or impregnanted with drugs designed to reduce inflammation

61
Q

what are stents with drugs in them called

A

drug eluting stents

62
Q

when is an angioplasty used

A

to treat angina that has not been controlled by drugs. it is also used as an emergency treatment in patients who have had a heart attack. in angina it can be used to reduce the frequency of angina attacks and give better control than drug treatment but t does not reduce the chance of death or of another heart attack in the usurer.

63
Q

what are the adverse effects of an angioplasty

A

stroke and myocardial infarction due to the angioplasty either triggering the formation of a blood clot or dislodging one that has already formed which travels through the blood to a smaller vessel and blocks it. (embolism)

64
Q

what is re closing of the artery called

A

restenosis

65
Q

what is a coronary artety bypass graft

A

it is open heart surgery. it removes a non-essential blood vessel from another part of the body and uses it to restore blood flow to the part of heart in which the blood supply is compromised.

66
Q

what are the most common blood vessels used in a CABG

A

internal mammary artery and the great saphenous vein from the leg

67
Q

how long to CABG last

A

15 years and then need to be replaced

68
Q

ACS classification and ECG readings

A
69
Q

what is the pain treatment given in ACS

A

opioids

70
Q

platelet activation and aggregation

A
71
Q

what are platelets derived from

A

megakaryocytes (bone marrow cells)

72
Q

what are the stimuli for platelet aggregation/activation

A
  • thrombin
  • ADP
  • TxA2
73
Q

TxA2 mechanism

A

synthesised from arachidonic acid by cycle-oxygenase (COX)
platelets syntheses TxA2 when activated
TxA2 is released from platelets
enhances expression of glycoprotein IIB/IIa receptors

74
Q

how do platelets link together

A

through binding to fibrinogen and it is a chain reaction

75
Q

what stops the chain reaction of platelet activation from happening

A

prostacyclin is released which stops the chain reaction from speeding.
demo the cells adjacent to the damage
synthesised from membrane lipids
inhibits platelet activation

76
Q

formation of TxA2 and PGI2

A

thromboxane and prostacyclin

77
Q

what is the COX1 gene

A

‘housekeeping gene’. expressed in most cells and is involved in the synthesis of thromboxane A2 and prostacyclin.

78
Q

what is the COX2 gene

A

mainly expressed in inflamed tissues and is the target of non-steroidal anti-inflammatory drugs (NSAIDS) like ibuprofen

79
Q

what is the COX3 gene

A

frameshift mutation and does not produce active enzymes

80
Q

NSAID effect on COX

A

NSAIDS produce their anti-inflammatory effects by acting on. COX2, most of them also have actions at COX1 and it is these COX1 effects that produce many of the side effects of NSAIDS.

81
Q

aspirin mechanism

A

irreversibly blocks platelet COX enzyme, reducing TxA2 synthesis
low doses of aspirin used to avoid reducing enzyme in endothelium (source of prostacyclin)
aspirin alters the balance between platelet TxA2 and endothelial prostacyclin

82
Q

unwanted effects of aspirin as an anti-platelet drug

A

extended bleeding time
indigestion
allergy
provoke asthma attacks - involves diverting membrane derived acid into pro0inflammatory signally molecules

83
Q

what is Reye’s syndrome

A

under 16s - liver and brain damage when aspirin is used during a viral illness

84
Q

what is anti-platelet drug action via

A

modulation expression of glycoprotein IIb/IIa receptors

85
Q

an example of an anti platelet drug and its mechanism

A

clopidogrel - inhibits glycoprotein IIb/IIa receptor expression on platelets by blocking the ADP receptor irreversibly

86
Q

what does ticagrelor do

A

allosterically inhibits the ADP receptor

87
Q

what does allosterically mean

A

In biochemistry, allosteric regulation is the regulation of an enzyme by binding an effector molecule at a site other than the enzyme’s active site. The site to which the effector binds is termed the allosteric site or regulatory site.

88
Q

what is the PLATO trail

A
89
Q

clopidogrel and ticagrelor unwanted effects

A
  • extended bleeding time
  • GI tract problems
  • headaches and dizziness
  • gout
  • breathlessness
    bottom two are only ticagrelor
90
Q

what is dipyridamole

A

phosphodiesterase inhibiter. prevents the breakdown of cAMP in platelets

91
Q

mechanism diagram for dipyridamole

A
92
Q

dipyridamole unwanted effects

A 
GI tract problems 
headaches 
muscle pain 
feeling hot (vasodilation) 
worsen angina 
decrease the flow in stenosed vessel
93
Q

examples of thrombolytic drugs

A

reteplase
alteplase
streptokinase

94
Q

mechanism diagram for thrombolytic drug

A
95
Q

thrombus maturation –>

A

4.5 hour treatment window before it changes shape

96
Q

PCI vs Thrombolysis for MI

A
97
Q

what procedure has a risk of haemorrhage

A

thrombolysis

98
Q

are there more PCI or thrombolysis centres

A

PCI centres

DRUGS (4 decks)

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