hyperlipidaemia and lipid lowering drugs Flashcards

(50 cards)

1
Q

what is the two function of cholesterol

A

-give cell rigidity (becomes a problem is cell is too rigid)
-importance component in bile acids which allows recirculation of cholesterol

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2
Q

how is excess cholesterol excreted

A

trapped in GIT then excreted via faeces

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3
Q

what are lipoproteins

A

breaks off proteins combining cholesterol

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4
Q

what is the difference between high density (HDL) and low density lipoproteins (LDL)

A

HDL = has more protiens, mops up cholesterol from various organs and walls of arteries (slows athersceolosis)
LDL = deposits cholesterol into tissues

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5
Q

what is the cause of primary dyslipidaemia

A

combination of dietary and genetic factors - familial hypercholesteolaemia

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6
Q

what is the cause of of secondary dsylipidaemia

A

consequence of other condition
-diabetes melitius
-alcoholism
-renal disease

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7
Q

what is the non-pharmacological treatment

A

-cardioprotective diet
-weight loss
-physical activity (increases HDL)
-decrease alcohol consumption
-smoking cessation

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8
Q

when would pharmacological treatment be used to treat dyslipidaemia

A

-only if there is a history/family history of CV disease
-many risk factors
-poor lipid profile

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9
Q

how many types of hyperlipidaemia are there

A

I, IIa, IIb, III, IV, V

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10
Q

what types of hyperlipidaemia is chylomicrons levels elevated

A

Type I and Type V

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11
Q

What type of hyperlipideamia is beta very low density lipoproteins elevated

A

Type III

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12
Q

What type of hyperlipideamia is LDL elevated

A

Type IIa, IIb

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13
Q

what is the difference between Type IIa and Tyoe IIb hyperlipidaemia

A

In both LDL is elevated, in IIb VLDL is elevated also

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14
Q

which two types of hyperlipideamia has high atherosclerosis

A

IIa and IIb

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15
Q

which type of hyperlipidaemia has the highest levels of triglycerides

A

Type I - Chylomicrons elevated

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16
Q

which type of hyperlipideamia can be treated with statins

A

type IIa, IIb, V

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17
Q

which type of hyperlipideamia can be treated with fibrates

A

IIb,III,IV,V

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18
Q

which type of hyperlipideamia can be treated with ezetimibe

A

IIa

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19
Q

which type of hyperlipideamia can be treated with nicotinic acid

A

IIb

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20
Q

which type of hyperlipideamia can be treated with niacin & fish oil

A

V

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21
Q

which type of hyperlipideamia isn’t treated with parmaceutical

22
Q

which type of hyperlipideamia has the highest levels of cholesterol

A

IIa, IIb, III

23
Q

What is familial hypercholesterolaemia (FH) and how is it caused

A

The reduction in receptor mediator clearance of LDL
Due to mutation of LDLR, APOB or PCSK9 gene
autosomal co-dominant

24
Q

what is the risk of developing FH

25
what is the lipid profile of FH
elevated LDL, Cholesterol , triglycerides
26
what are the physical signs of FH
-Cholesterol deposits in the eyes (Xanthelasmas) -white, blue or grey crescent shape made of lipid (fatty) deposits that curves around the outer edge of the cornea -tendon xanthomas - slowly enlarging subcutaneous nodules usually found attahced to the Achilles tendon/tendon over knuckles -homozygous also have planal digital and natal cleft, cutanous xanthomas, Aortic stenosis
27
what is Niacin an example of
Nicotinic acid
28
what is the effect of Niacin
- liver = decrease VLDL synthesis + decrease VLDL & LDL levels - Adipose = decrease sensitive lipase activity, decreased Triglycerides levels - Decrease catabolic rate of HDL - increases HDL - Increase clearance of VLDL by activating lipoprotein lipase
29
what are the indications for niacin
Hypercholesterolaemia Hypertriglycidemia with low level of HDL
30
what are the adverse effect of the nicotinic acid
Cutaneous flushing -Pruirtus & palpiattion -dose dependant nausea + abdominal discomfort - moderate incraese of liver enzymes to severe hepatoxicity -hyperuricemia in 20% of patients
31
what decreases the adverse effects of Niacin
pretreatment with aspirin + NSAIDs
32
how does ezetimibe work ?
-Inhibits intestinal absorption of cholesterol by interfering with Neimann-Pick C1-Like 1 (NPC1L1) transport protein -Decreases LDL and VLDL
33
hows does Colestipol/Cholestyramine work and how is it administered
-Binds bile acid (BA) in gut, prevents reabsorption, diverting hepatic cholesterol to BA synthesis, upregulates LDL receptors -increasing LDL removal from the blood -orally as they stay in the GIT
34
what are the adverse effects of Ezetimibe
diarrohoea, abdominal pain, headache (mild), rash, angioedema
35
what are the adverse effects of Colestipol/Cholestyramine
constipation, bloating, malabsorption of Vitamin K/folic acid/ascorbic acid - disrupts absorption of digitalis, thiazides, warfarin and iron
36
what are Colestipol/Cholestyramine's clinical uses
-primary hypercholesterolemia, when statins are contraindicated -pruitus associated with bilarily obstruction -bile acid diarrhoea
37
who cant take ezetimibe
breastfeeding mothers
38
which other lipid lowering drug is used with ezetimibe to treat hyperlipideamia
statins
39
ezetimbe is metabolised into an active metabolites - true or false
true
40
what is an example of a fibrate and what is the mechanism of action
Fenofibrate -agonist at peroxisome proliferator-activated receptor (PPAR-a) nuclear receptor that regulate lipid metabolism
41
how does fibrates effects lipid metabolism
-increase synthesis of lipoprotein lipase by adipose tissue -stimulates fatty acid oxidation in liver -increase expression of apoA-1 & apoA5 -increase hepatic LDL uptake =Marked reduction circulating VLDL and TG Modest reduction in LDL
42
what are the adverse effects of fibrates
Common = Rash, GI disturbance Rhabdomyolysis = smooth muscle degradation which causes renal failure by effecting glomerulus filtering Clofibrate may cause gall stones
43
what are the clinical uses of fibrates
hypertriglyceridemia mixed hyperlipidaemia
44
what types of patient cant take fibrates
-Allergies -Diabetes -people with Gall bladder, liver and kidneys conditions
45
give an example of statins
atorvastatin (long acting), lovastatin (short acting)
46
what is the mechanism of action for statins
-decrease synthesis of cholesterol (HMG CoA Reductase inhibitors) -increase uptake of LDL (secondary) by increases LDL receptor synthesis which incraeses clearance of LDL by the liver
47
what is the cellular effect of statins
Endothelial function improves Improved vascularisation of ischaemic tissue Atherosclerotic plaque stabilisation Reduces vascular inflammatory response Reduced platelet activation Enhanced fibrinolysis Antithrombotic
48
what are the adverse effects of statins
normally well tolerated may have muscle pain, GI disturbance, insomnia, rash Rarely myositis and angiodema
49
when is statins not suitable
it patients have severe liver disease
50
when are statins used (3)
-primary hyperlipidaemia -secondary hypercholesteroleamia -secondary prevention of MI and Stroke