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Drugs: From molecules to man > Angina and Acute Coronary Syndromes > Flashcards

Angina and Acute Coronary Syndromes Flashcards

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Organic Chemistry 101 flashcards
1
Q

what is the purpose of lipoproteins?

A

to transport lipids in plasma

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2
Q

what are lipoproteins composed of?

A

Lipids (triglyceride or cholesterol esters)
phospholipids
cholesterol
proteins

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3
Q

in what form are dietary cholesterol and fats taken up into the blood stream?

A

chylomicrons

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4
Q

What happens to fats/cholesterol in the peripheral tissues?

A

they are broken down into fatty acids (which are taken up by tissues) and glycerol by lipoprotein lipase
the chylomicron remnants are then taken up by the liver and the cholesterol they contain is added to the cholesterol that the liver has synthesised
the liver then secretes cholesterol and newly formed triglycerides in the form of VLDL

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5
Q

how is VLDL converted into LDL?

A

by the absorption of fatty acids in the peripheral tissues

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6
Q

how do HDLs arise?

A

from the recycling of cholesterol (cell breakdown) in peripheral tissues

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7
Q

How are bile acids formed?

A

from the oxidation of cholesterol

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8
Q

what happens to bile acids?

A

they are secreted into the GI tract, mixed with cholesterol

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9
Q

what do bile acids do?

A

emulsify fats

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10
Q

what happens to bile after use?

A

it’s returned to the liver via the portal vein

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11
Q

what do LDL and VLDL do in the plasma? (why are they bad?)

A

involved in the formation of fatty streaks
inhibit fibrinolysis (fibrin breakdown)
activate platelets- which increases the risk of atherosclerosis

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12
Q

What do HDLs do in the plasma? (why are they good?)

A

increase fibrinolysis
decrease aggregation
reduces the risk of atherosclerosis

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13
Q

what are Hyperlipidaemias?

A

elevated LDL/VLDL/cholesterol levels

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14
Q

what are the 2 main methods for controlling hyperlipidaemias?

A

lifestyle changes

lipid- lowering drugs

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15
Q

Give three lifestyle changes to treat Hyperlipidaemias

A
  • reduce sat fats
  • increase unsat fats
  • increase fibre
  • avoid trans fats
  • avoid hydrogenated fats
  • increase exercise
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16
Q

what do lipid-lowering drugs do?

A

reduce LDL and raise HDL levels

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17
Q

what drugs tend to be given to treat hyperlipidaemia? (2)

A

Statins and Ezetimibe

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18
Q

what sort of genetic defect can cause hyperlipidaemia? (2)

A

defect in the LDL receptor or ApoB protein

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19
Q

What sort of mutation is that that causes hyperlipidaemia?

A

Autosomal dominant

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20
Q

what proportion of the UK population are heterozygous for familial hyperlipidaemia?

A

1:500

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21
Q

How does being heterozygous for familial hyperlipidaemia affect the individual?

A

tends to develop CVD by the age of 40-50 years

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22
Q

What proportion of the UK population are homozygous for familial hyperlipidaemia?

A

1:1000000

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23
Q

How does being homozygous for familial hyperlipidaemia affect the individual?

A

tends to develop severe CVD in childhood

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24
Q

How is familial hyperlipidaemia primarily treated?

A

statins

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25
Q

give an example of a widely used statin

A

Atorvostatin

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26
Q

what do statins do?

A

competitively inhibit HMGCoA reductase (the rate limiting enzyme in production of cholesterol (similar structure to cholesterol)
reduces liver prouduction of cholesterol leading to more LDL receptors, therefore increased removal of LDL from plasma
increases HDL and lowers triglycerides

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27
Q

how is cholesterol produced?

A

when HMGCoA allows AcetylcoA to be converted to mevalonate.

Mevalonate then is converted to Cholesterol

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28
Q

give side effects of statins (4)

A
  • Myositis (muscle inflammation)
  • rhabdomyolysis (muscle breakdown)
  • altered liver function
  • altered kidney function
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29
Q

why are statins controversial?

A

many statins are prescribed and used when lifestyle changes could be made (which would be more effective and safer)

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30
Q

what 4 other drug classes can be used to lower cholesterol?

A

Anion exchange resins
Fibrates
Nicotinic acid
Fish oils

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31
Q

what do anion exchange resins do?

A

sequester bile acids in gut

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32
Q

what do fibrates do?

A

they are agonists are PPARa receptor

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33
Q

What do Nicotinic acids (vitamin B3) do?

A

reduce cholesterol, however mechanism not well understood

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34
Q

What do fish oils do?

A

fish are rich in omega 3 fatty acids which are linked with a decreased CVD risk by reducing platelet aggregation and decreasing fibrinogen
little evidence supporting fish oils as a treatment
reduce plasma lipids but increase cholesterol

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35
Q

define angina

A

chest pain caused by reduced blood flow, therefore reduced oxygen supply to the heart. (an imbalance in supply and demand of oxygen in the heart)

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36
Q

what are the 2 types of angina?

A

stable and Acute Coronary Syndrome (ACS)

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37
Q

what is stable angina also known as?

A

Angina of effort

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38
Q

which is the most common form of angina?

A

stable

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39
Q

what is the primary cause of stable angina?

A

atherosclerosis of the coronary artery

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40
Q

what triggers stable angina pains? (3)

A

exercise, excitement, cold weather

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41
Q

How is stable angina released?

A

rest

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42
Q

which is the least serious/ dangerous form of angina?

A

stable

43
Q

Is ACS resolved with rest?

A

no

44
Q

how many components of ACS?

A

3

45
Q

what are the 3 components of ACS?

A

unstable angina, non- ST elevated myocardial infarction (NSTEMI) (HA) and ST elevated myocardial infarction (STEMI) (HA)

46
Q

How do organic nitrates treat angina?

A

they reduce cardiac work by reducing preload and afterload
large doses of nitrates cause arteriolar dilation and hence a fall in peripheral resistance
also improve coronary heart supply by dilating collateral vessels

47
Q

which organic nitrate is commonly used to treat angina?

A

Glycerol Trinitrate (GTN)

48
Q

Why is GTN commonly used?

A

cheap and easy to use

49
Q

can GTN be taken orally? and why?

A

no- due to its short duration of action

50
Q

can Isosorbide dinitrate be taken orally?

A

yes

51
Q

on what does the activity of isosorbide dinitrate depend?

A

metabolism to yield mononitrate

52
Q

How can Isosorbide dinitrate be given? (give 3)

A
  • subligual tabelets
  • buccal sprays (mouth spray)
  • sustained release tablets
  • transdermal sprays (skin spray)
  • i.v. injection
53
Q

How long is the duration of isosorbide dinitrate from sustained release tablets?

A

up to 12 hours

54
Q

What does nicorandil do?

A

activates K+ ATP channels and is also an NO donor

Dilates arteries and veins

55
Q

is nicorandil a nitrate?

A

no

56
Q

give 3 side effects of organic nitrates

A
  • flushing of skin
  • sweating
  • headache
  • orthostatic hypotension (fainting)
  • reflex tachycardia
57
Q

why are the side-effects of organic nitrates tolerable?

A

due to the short duration of action- they don’t last long

58
Q

what 3 other drugs are given to treat Angina?

A

beta blockers, Verapamil (calcium channel blocker) and Amlodipine (calcium channel blocker)

59
Q

what do Beta-blockers do for angina?

A

reduce cardiac workload
less O2 required
improve cornary blood supply by increasing diastole
slows HR

60
Q

give 3 main examples of beta blockers used for angina

A

atenolol, bisoprolol and metoprolol

61
Q

what does verapamil do for angina?

A

affects heart more potently than vascular system
Ca2+ channel blockade in myocardium reduces HR and CO
dilates arterioles to reduce cardiac output
cardiac workload + O2 demand are reduced

62
Q

What does Amlodipine do for angina?

A

more potent in vascular system than heart
dilates arterioles to reduce afterload
dilates capitance veins to reduce reload
cardiac output and O2 demand reduced

63
Q

what are the 2 surgical options to treat angina?

A

Bypass or Angioplasty

64
Q

what does Bypass surgery do?

A

a BV is grafted from another part to the body to allow blood to bypass area of stenosis (narrowed vessel)

65
Q

what does Angioplasty surgery do?

A

dilates BV using a stent

66
Q

what are the risks of surgery to treat angina?

A

risk of embolism and decline in mental function

67
Q

How are Acute Coronary Syndromes characterised? (in terms of symptoms)

A

severe chest pain radiating to left arm and jaw- not relieved by rest and last more than a few minutes

68
Q

what do all 3 types of ACS involve?

A

Ischemia (and may involve tissue damage)

69
Q

what causes ACS?

A

coronary artery thrombosis

70
Q

how is ACS diagnosed?

A

using an ECG

71
Q

using an ECG, how would an NSTEMI be diagnosed?

A

if the ST segment is inverted/depressed and blood markers are present

72
Q

using an ECG, how would unstable angina be diagnosed?

A

if the ST segment is inverted/depressed and blood markers aren’t present

73
Q

using an ECG, how would STEMI be diagnosed?

A

if the ST segment is elevated

74
Q

define thrombosis

A

a pathological blood clot

75
Q

what can thrombosis cause? (3)

A

embolism, stroke, Heart Attack

76
Q

define Thrombus

A

an insoluble fibrin framework which forms a mesh/web, trapping other blood cells
attached to vessel wall
impedes BF and reduces tissue perfusion

77
Q

what’s the main cause of venous thrombosis?

A

coagulation

78
Q

what’s the main cause of arterial thrombosis?

A

platelet aggregation

79
Q

what’s an embolus?

A

fragment of/ whole thrombus that’s detached from vessel wall and travels through vessels until it reaches a narrow vessel- blocking it

80
Q

what can an embolus cause? (4)

A

Pulmonary embolism (blocked blood supply to lungs)
HA
stroke
limb infarction (blocked blood supply to limb)

81
Q

flow chart of the coagulation cascade

A

damage to the vessel –> activates clotting cascade –> many factors interact –> prothrombin converted to thrombin –> thrombin allows fibrinogen to convert to fibrin –> fibrin forms a net/mesh trapping blood cells –> clot formed

82
Q

what’s the role of Vitamin K in blood clotting?

A

several proteins/ factors are dependent on vitamin K (Factors II, VII, IX and X)

83
Q

How does tissue damage trigger platelet aggregation?

A

the tissue damage exposes glycoproteins that aren’t normally on the BV lining.
Receptors on platelets recognise these proteins and start the platelet activation process (shape change)
acitvated platelets release chemical signals (TXA2 and ADP) that trigger the activation of other platelet
chain reaction

84
Q

what inhibits platelet aggregation?

A

Prostacylin released from the endothelium

85
Q

name 4 antiplatelet drugs

A
  • Aspirin
  • Ticagrelor
  • Clopidogrel
  • Dipyridamole
86
Q

what does Aspirin do?

A

irreversibly blocks platelet COX enzyme, reducing TxA2 synthesis
alters balance between platelet TxA2 and endothelial prostaglycin

87
Q

what does Ticagrelor do?

A

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

88
Q

What does dipyridamole do?

A

it’s a Phosphodiesterase inhibitor that prevents the breakdown of cAMP in platelets- raises cAMP levels, prevents aggregation

89
Q

what do fibrinolytic drugs do?

A

help to breakdown clots once they’ve formed
fibrinolytic drugs speed up the conversion of plasminogen to plasmin, thereby accelerating the rate at which thrombi breakdown

90
Q

give 3 examples of fibrinolytic drugs

A

Alteplase, Streptokinase, Reteplase

91
Q

what’s the risk with fibrinolytic drugs?

A

haemorrhage/ embolism

92
Q

What is Heparin?

A

A naturally occurring sulphated mucopolysaccharide, used to prevent blood clotting.

93
Q

How does Heparin work?

A

Binds to antithrombin III, and increases binding of different components of the clotting cascade

94
Q

How is Heparin given?

A

By injection

95
Q

What can Heparin OD cause?

A

Haemorrhage

96
Q

What is Warfarin?

A

an analogue of vitamin K

97
Q

how does Warfarin work?

A

inhibits vitamin K reductase and reduces plasma vitamin K levels. This reduces clotting as Vitamin K is needed for clot formation

98
Q

How is Warfarin given?

A

orally

99
Q

What can Warfarin OD cause?

A

Haemorrhage

100
Q

Why can’t Warfarin be given to pregnant women?

A

Can cause birth-defects

101
Q

What is enoxoparin?

A

a low molecular weight heparin

102
Q

what does enoxoparin do?

A

increases the affinity for antithrombin III for factor Xa

103
Q

The primary molecular site of action of dipyridamole is

A

an enzyme

Drugs: From molecules to man (10 decks)

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