Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PED2007 > hyperlipidaemia and lipid lowering drugs > Flashcards

hyperlipidaemia and lipid lowering drugs Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is excess cholesterol excreted

A

trapped in GIT then excreted via faeces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are lipoproteins

A

breaks off proteins combining cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the cause of primary dyslipidaemia

A

combination of dietary and genetic factors - familial hypercholesteolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the cause of of secondary dsylipidaemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the non-pharmacological treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how many types of hyperlipidaemia are there

A

I, IIa, IIb, III, IV, V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what types of hyperlipidaemia is chylomicrons levels elevated

A

Type I and Type V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of hyperlipideamia is beta very low density lipoproteins elevated

A

Type III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of hyperlipideamia is LDL elevated

A

Type IIa, IIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which two types of hyperlipideamia has high atherosclerosis

A

IIa and IIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which type of hyperlipidaemia has the highest levels of triglycerides

A

Type I - Chylomicrons elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which type of hyperlipideamia can be treated with statins

A

type IIa, IIb, V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which type of hyperlipideamia can be treated with fibrates

A

IIb,III,IV,V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which type of hyperlipideamia can be treated with ezetimibe

A

IIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which type of hyperlipideamia can be treated with nicotinic acid

A

IIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which type of hyperlipideamia isn’t treated with parmaceutical

A

Type I

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

A

1/250

25
Q

what is the lipid profile of FH

A

elevated LDL, Cholesterol , triglycerides

26
Q

what are the physical signs of FH

A

-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
Q

what is Niacin an example of

A

Nicotinic acid

28
Q

what is the effect of Niacin

A
  • 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
Q

what are the indications for niacin

A

Hypercholesterolaemia
Hypertriglycidemia with low level of HDL

30
Q

what are the adverse effect of the nicotinic acid

A

Cutaneous flushing
-Pruirtus & palpiattion
-dose dependant nausea + abdominal discomfort
- moderate incraese of liver enzymes to severe hepatoxicity
-hyperuricemia in 20% of patients

31
Q

what decreases the adverse effects of Niacin

A

pretreatment with aspirin + NSAIDs

32
Q

how does ezetimibe work ?

A

-Inhibits intestinal absorption of cholesterol by interfering with Neimann-Pick C1-Like 1 (NPC1L1) transport protein
-Decreases LDL and VLDL

33
Q

hows does Colestipol/Cholestyramine work and how is it administered

A

-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
Q

what are the adverse effects of Ezetimibe

A

diarrohoea, abdominal pain, headache (mild), rash, angioedema

35
Q

what are the adverse effects of Colestipol/Cholestyramine

A

constipation, bloating, malabsorption of Vitamin K/folic acid/ascorbic acid
- disrupts absorption of digitalis, thiazides, warfarin and iron

36
Q

what are Colestipol/Cholestyramine’s clinical uses

A

-primary hypercholesterolemia, when statins are contraindicated
-pruitus associated with bilarily obstruction
-bile acid diarrhoea

37
Q

who cant take ezetimibe

A

breastfeeding mothers

38
Q

which other lipid lowering drug is used with ezetimibe to treat hyperlipideamia

A

statins

39
Q

ezetimbe is metabolised into an active metabolites - true or false

A

true

40
Q

what is an example of a fibrate and what is the mechanism of action

A

Fenofibrate
-agonist at peroxisome proliferator-activated receptor (PPAR-a) nuclear receptor that regulate lipid metabolism

41
Q

how does fibrates effects lipid metabolism

A

-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
Q

what are the adverse effects of fibrates

A

Common = Rash, GI disturbance
Rhabdomyolysis = smooth muscle degradation which causes renal failure by effecting glomerulus filtering
Clofibrate may cause gall stones

43
Q

what are the clinical uses of fibrates

A

hypertriglyceridemia
mixed hyperlipidaemia

44
Q

what types of patient cant take fibrates

A

-Allergies
-Diabetes
-people with Gall bladder, liver and kidneys conditions

45
Q

give an example of statins

A

atorvastatin (long acting), lovastatin (short acting)

46
Q

what is the mechanism of action for statins

A

-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
Q

what is the cellular effect of statins

A

Endothelial function improves
Improved vascularisation of ischaemic tissue
Atherosclerotic plaque stabilisation
Reduces vascular inflammatory response
Reduced platelet activation
Enhanced fibrinolysis
Antithrombotic

48
Q

what are the adverse effects of statins

A

normally well tolerated
may have muscle pain, GI disturbance, insomnia, rash
Rarely myositis and angiodema

49
Q

when is statins not suitable

A

it patients have severe liver disease

50
Q

when are statins used (3)

A

-primary hyperlipidaemia
-secondary hypercholesteroleamia
-secondary prevention of MI and Stroke

PED2007 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions