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PBL SEM 2 > PBL 5 - PHARMACOLOGY - drugs used in CHD > Flashcards

PBL 5 - PHARMACOLOGY - drugs used in CHD Flashcards

1
Q

what is it when ischaemia of cardiac tissue from CAD is temporary?

A

angina

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2
Q

what does thrombus formation on an atherosclerotic plaque lead to?

A

permanently occludes the artery —> heart attack

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3
Q

what is coronary artery disease?

A

the process by which coronary arteries become clogged by atherosclerotic plaques

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4
Q

what is coronary heart disease?

A

the consequences of coronary artery disease

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5
Q

angina vs. heart attack

A
  • angina = heart temporarily deprived of oxygen — not immediately fatal — heart attack in waiting
  • heart attack = heart deprived of oxygen — muscle death —much more serious
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6
Q

why are people with angina or heart attack open to the development of dysrhythmias?

A

heart muscle becomes ischaemic and so it can’t maintain its resting membrane potential so easily

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7
Q

when do dysrhythmais occur?

A

when you get inappropriate firing of APs in the heart so you get disturbance of rhythm

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8
Q

how do dysrhythmias lead to pumping inefficiencies? the same pumping inefficiencies can also occur due to what?

A

they disturb the electrical rhythm of the heart but also the mechanical rhythm

the same pumping inefficiencies can also occur because of muscle death that you see inMI

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9
Q

when does HF come about?

A

when the heart can’t pump enough blood around to supply the body

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10
Q

what is primary vs secondary prevention of CHD?

A
  • primary = stopping it happening

- secondary = stopping it recurring or worsening (after angina, HA, stroke)

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11
Q

what is the link between exercise and heart disease?

A

people with an active lifestyle have a lower BP, are less likely to be obsese — had a much lower risk of CHD (independent of their physiology)

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12
Q

describe lipoproteins role and structure

A
  • transport lipids in plasma
  • cholesterol and triglycerides in core
  • phospholipid monolayer on outside — fatty acid tails facing the hydrophobic core
  • apolipoproteins — can be recognised by receptors in tissue
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13
Q

how do we classify lipoproteins?

A

via DENSITY

  • HDL
  • LDL
  • VLDL
  • chylomicrons (have the lowest density of them all)
  • there are also intermediates between LDL and VLDL
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14
Q

where is cholesterol synthesised?

A

hepatocyte = liver cell (major drug target)

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15
Q

cholesterol is used by the liver to make what?

A

bile acids

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16
Q

what happens to bile acids in the liver?

A
  • secreted into the GI tract and act as a detergent, emulsifies dietary cholesterol and fats, and enables it to be taken up
  • bile acids are recycled back to the liver
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17
Q

what happens to the dietary fats emulsified by bile acids?

A

dietary fats are taken up from the GI tract into chylomicrons

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18
Q

what do chylomicrons do?

A

transport fats to the tissue

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19
Q

what happens to the chylomicron remnant?

A

taken up by the liver where it delivers cholesterol

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20
Q

after the chylomicron remnant delivers cholesterol, what 2 kinds of lipoprotein does the liver produce?

A
  • VLDL

- HDL

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21
Q

what happens to the VLDL?

A
  • released into circulation
  • delivers more fats to the tissues
  • converted to LDL
22
Q

what does LDL do?

A

delivers cholesterol to tissues

23
Q

what does HDL do?

A

takes up cholesterol from the tissues and delivers it to VLDL

24
Q

tissue takes up fatty acids after breaking down fats using what?

A

lipoprotein lipase

25
Q

what does the liver do when it needs more cholesterol?

A

recognises and takes up LDL

26
Q

what are LDL and VLDL and what do they do?

A

= ”bad cholesterol”

  • involved in formation of fatty streaks and promote atherosclerosis
  • inhibit fibrinolysis (breakdown of blood clots) by preventing fibrin breakdown
  • activate platelets by increasing aggregation — increase likelihood of blood clot

INCREASE RISK OF ATHEROSCLEROSIS

27
Q

what do LDL and VLDL also increase the risk of?

A

angina, HA and stroke

28
Q

what is the mechanism for HA and ischaemic stroke?

A
  • plaque is a weak point in vessel wall so it can rupture
  • causes formation of blood clot over plaque
  • can block the vessel in place or detach and travel in blood steam and block a smaller vessel elsewhere in the body
29
Q

what roles does HDL have?

A
  • increase fibrinolysis (helps breakdown blood clots) by increasing fibrin degradation
  • may also increase prostacyclin (platelet inactivator and vasodilator) formation by decreasing aggregation

LOWERS RISK OF ATHEROSCLEROSIS

30
Q

what is hyperlipidaemia?

A

= too much lipid in blood

  • number of different forms
  • classified according to which lipoprotein is disturbed or which type of lipid you have too much of
  • different disturbances in LDL, VLDL, cholesterol etc
  • treated differently
31
Q

describe familial hypercholesterol

A
  • very high risk of having atherosclerosis
  • defect in LDL receptor (the receptor that recognises LDL and allows it to be taken up by the liver)
  • or ApopB protein mutation
  • autosomal dominant — heterozygous not as bad as homozygous
  • 1:500 in UK heterozygotes — CVD by age 30-40
  • 1:1000000 homozygous — severe CVD in childhood
32
Q

what is familial hypercholesterolaemia treated using?

A

statins but other drugs may be added too

33
Q

describe the formation of a plaque due to hyperlipidaemia

A
  • excess LDL in circulation enters the intima of a blood vessel
  • monocytes migrate to the intima and transform into macrophages
  • macrophages take up oxidised LDL and transform into foam cells
  • foam cells attach to the endothelium and form the fatty streak
  • foam cells release cytokines and other growth factors that recruit smooth muscle cells
  • migrating smooth muscle cells thicken the streak into a stable plaque
34
Q

what are the aims of statins and other lipid lowering drug?

A

reduce LDL/VLDL and increase HDL

35
Q

name a statin

A

atorvastatin

36
Q

how do statins work?

A
  • completely inhibit HMG-CoA reductase = rate limiting enzyme in production of cholesterol in the liver
  • have a similar structure to the substrate for this enzyme, HMG-CoA
  • reduces liver production of cholesterol
  • more LDL receptors
  • increased removal of LDL from plasma
  • also increased HDL and lowered triglycerides
37
Q

what does lowered cholesterol (due to statins) lead to?

A
  • more LDL receptors — liver takes more LDL out of circulation so it produces more receptive on its surface to recognise the apolipoproteins on LDL and remove it from circulation
38
Q

how is cholesterol formed from Acetyl-coenzyme A?

A

acetyl-coenzyme A —> HMG-CoA —(HMGCoA reductase)—> mevalonate —> cholesterol

39
Q

what are some problems with statins?

A
  • myosotis = muscle inflammation
  • rhabdomyolysis = muscle breakdown (causes dark coloured urine — myoglobin released = toxic for kidneys = kidney failure)
  • altered liver function tests
  • complications very rare but lots of people are taking them
40
Q

what is QRISK3? cut off for statin treatment?

A

calculates risk that you will have a HA or stroke in the next 10 years

  • uses age, ethnicity, weight, other illnesses to assess risk
  • cut off for statin treatment for primary prevention is 10%
  • also used for secondary prevention
41
Q

what is ezetimibe?

A
  • inhibits intestinal cholesterol absorption
  • inhibits specific cholesterol transporter in the gut
  • results in reduced LDL and reduced total cholesterol
42
Q

who might use ezetimibe?

A
  • can be used in patients who do not tolerate statins
  • co-administered with statins in resistant cases or familial hyperlipidaemia — gives dual inhibition of cholesterol absorption and synthesis
43
Q

what are anion exchange resins?

A
  • drugs that sequester bile acids in the gut (bind to bile acids in gut and stop them from being reabsorbed)
  • very large volumes required to unpleasant to take
44
Q

what are fibrates?

A
  • agonists at a receptor called PRARa
  • may be used with elevated VLDL
  • commonly produce muscle problems
45
Q

what about vitamin B3?

A
  • mechanism not well understood

- very high doses required

46
Q

what about fish oils?

A
  • cold water fish rich in poly unsaturated fatty acids
  • omega 3 fatty acids
  • consuming such fish is associated with lower risk of CVD
  • reduces plasma triglycerides, increases cholesterol
  • appears to reduce platelet aggregation and reduce fibrinogen (mechanism not understood)
  • NICE concludes there is little evidence to support use
47
Q

what is a micronutrient that can have beneficial effects on plasma lipid levels if used in gramme quantities?

A

vitamin B3

48
Q

how does ezetimibe reduce risk of HA or stroke?

A

blocks GI cholesterol transporters — lowers LDL levels and this reduces risk

49
Q

what is rhabdomyolysis? what can it cause and why? what drugs can cause it?

A

when skeletal muscle breaks down rapidly — the breakdown products are toxic to the kidney and can cause kidney failure

some statins produce rhabdomyolysis as an unwanted effect

50
Q

name 3 lipid lowering drugs

A
  • statins eg atorvastatin
  • ezetimibe
  • fibrates

PBL SEM 2 (44 decks)

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