Diseases associated with Lipids Flashcards

1
Q

Dyslipidaemia occurs when the
??? lipids are in the abnormal range

A

plasma/serum

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2
Q

when the disorder is not due to an
identifiable underlying disease- is this primary or secondary dyslipidaemia?

A

primary

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3
Q

when the disorder is a manifestation of some other disease. It is acquired via another cause or disease- is this primary or secondary dyslipidaemia?

A

secondary

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4
Q

TRUE or FALSE: Post menopausal women have a hgiher TC (LDL-C) than males

A

TRUE

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5
Q

Males have higher or lower (?) TG and lower HDL-C than females

A

higher

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6
Q

Oestrogen increases LDL receptor activity and increases or decreases (?) the synthesis of Apo A-1

A

increases

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7
Q

Oestrogens lower LDL-C and raise HDL-C whereas androgens have the opposite or same (?) effect

A

opposite

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8
Q

However, Japanese have higher HDL-C than those found in Western countries. This does or doesn’t (?) change if westerners live in Japan proving there is some genetic incfluence

A

does not change

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8
Q

HDL-C is inversely correlated with ???

A

adiposity

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8
Q

Alcohol increases HDL-C (cholesterol inside HDL) and LPL activity which then increases catabolism of VLDL and generates surface constituents to form ???

A

HDL

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9
Q

HDL-C is inversely correlated with plasma ???

A

TGs

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10
Q

TRUE or FALSE: Coffee (boiled) increases cholesterol minimally (does not occur with tea or instant coffee), therefore appears to be caused by a lipid-rich constituent of coffee extracted by
boiling

A

TRUE

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11
Q

No beneficial effects of reducing ??? fat intake on CVD and total mortality.

A

saturated

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12
Q

20g per day of plant sterols/stanol esters reduces LDL-C by 10% because they reduce the absorption of cholesterol in the ??? = reduced amount of cholesterol going to liver
which responds by increasing LDL receptors and takes up more LDL particles from the bloodstream, reducing LDL-C.

A

GI tract

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13
Q

TRUE or FALSE: Smoking reduces nitric oxide, but nitric oxide is crucial to maintain normal vascular tone

A

TRUE

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14
Q

Nitric oxide (NO)
1. decreases or increases (?) leucocyte adhesion to endothelial cells, decreases expression of VCAM & ICAM, inhibits monocyte chemotactic protein-1 (MCP-1)

A

DECREASES

15
Q

Nitric Oxide (NO)
2. decreases or increases (?) endothelial permeability to lipoproteins & other atherogenic macromolecules

A

decreases

16
Q

nitric oxide (NO)
3. decreases or increases vascular smooth muscle cell proliferation & migration from internal elastic
lamina to the intima

A

decreases

17
Q

Nitric Oxide prevents platelet adhesion & aggregation, inhibits platelet hyperactivity or hypoactivity (?)

A

hyperactivity

17
Q

Primary or secondary (?) causes for Hypertriglyceridaemia:
Type I, IV and V

A

primary

17
Q

Primary or secondary (?) causes for Hypercholesterolaemia:
Type IIa

A

primary

18
Q

Primary or secondary (?) causes for Combined Hyperlipidaemia:
Type IIb, III

A

primary

18
Q

familial hyperchylomicronaemia is genetic type I: Reduced levels of
functional LPL/Inability to synthesise
apo-??? (LPL cofactor)

A

apo C-II

19
Q

Apo C-II deficiency = apo C-II is a cofactor for LPL, hence LPL is able or unable (?) to function normally, therefore unable to hydrolyse TG within chylomicrons

A

unable

20
Q

what is the treatment for Type I – familial hyperchylomicronaemia?

A

very low fat diet

21
Q

Type IV - Familial hypertriglyceridaemia: an increase or decrease (?) in VLDL as well as synthesis of VLDL & also reduced
catabolism

A

increase

22
Q

treatment for Type IV - Familial
hypertriglyceridaemia: diet, ideal body weight, avoid ??? & alcohol increase exercise, possibly drugs

A

sucrose

23
Q

which types of WHO classifications are at risk of pancreatitis?

A

Types I IV and V

24
Q

Type V – Familial hypertriglyceridaemia AKA Mixed hyperlipidaemia: mutation in the apo-??? gene causes increased VLDL production and reduced LPL

A

mutation in apo C-II gene

25
Q

treatment of type V is ??? such as fibrates and niacin

A

drugs

26
Q

Both chylomicrons and VLDL are
triglyceride rich and therefore people with Type I, IV and V have
??? looking plasma

A

cloudy/creamy

27
Q

why acute pancreatitis in types I, IV, V?
Hint: when TGs exceed normal amounts, chylomicrons are… They are large and may obstruct blood vessels = …= exposure of TGs to … = TG degradation …= further local injury that increases … = pancreatitis.

A

They are large and may obstruct blood vessels = local ishcemia = exposure of TGs to pancreatic lipases = TG degfradation can lead to cytotoxic injury = further local injury that increases inflammatory mediators and free radicals = pancreatitis.

28
Q

which type of dyslipidaemia primarily has high chylomicrons?

A

Type I

29
Q

which type of dyslipidaemia primarily has high VLDL?

A

Type IV

30
Q

which type of dyslipidaemia primarily has high VLDL and chylomicrons?

A

Type V because of Mutation in apo C-II gene

31
Q

which type of dyslipidaemia primarily has high LDL?

A

Type IIa heterozygous and even more homozygous

32
Q

which type of dyslipidaemia primarily has high LDL and VLDL?

A

Type IIb because of low LDL
receptor and high apo B

33
Q

which type of dyslipidaemia primarily has high chyloremnants and high IDL?

A

Type III because of Mutation in
apo E gene