Diseases associated with Lipids Flashcards
Dyslipidaemia occurs when the
??? lipids are in the abnormal range
plasma/serum
when the disorder is not due to an
identifiable underlying disease- is this primary or secondary dyslipidaemia?
primary
when the disorder is a manifestation of some other disease. It is acquired via another cause or disease- is this primary or secondary dyslipidaemia?
secondary
TRUE or FALSE: Post menopausal women have a hgiher TC (LDL-C) than males
TRUE
Males have higher or lower (?) TG and lower HDL-C than females
higher
Oestrogen increases LDL receptor activity and increases or decreases (?) the synthesis of Apo A-1
increases
Oestrogens lower LDL-C and raise HDL-C whereas androgens have the opposite or same (?) effect
opposite
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
does not change
HDL-C is inversely correlated with ???
adiposity
Alcohol increases HDL-C (cholesterol inside HDL) and LPL activity which then increases catabolism of VLDL and generates surface constituents to form ???
HDL
HDL-C is inversely correlated with plasma ???
TGs
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
TRUE
No beneficial effects of reducing ??? fat intake on CVD and total mortality.
saturated
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.
GI tract
TRUE or FALSE: Smoking reduces nitric oxide, but nitric oxide is crucial to maintain normal vascular tone
TRUE
Nitric oxide (NO)
1. decreases or increases (?) leucocyte adhesion to endothelial cells, decreases expression of VCAM & ICAM, inhibits monocyte chemotactic protein-1 (MCP-1)
DECREASES
Nitric Oxide (NO)
2. decreases or increases (?) endothelial permeability to lipoproteins & other atherogenic macromolecules
decreases
nitric oxide (NO)
3. decreases or increases vascular smooth muscle cell proliferation & migration from internal elastic
lamina to the intima
decreases
Nitric Oxide prevents platelet adhesion & aggregation, inhibits platelet hyperactivity or hypoactivity (?)
hyperactivity
Primary or secondary (?) causes for Hypertriglyceridaemia:
Type I, IV and V
primary
Primary or secondary (?) causes for Hypercholesterolaemia:
Type IIa
primary
Primary or secondary (?) causes for Combined Hyperlipidaemia:
Type IIb, III
primary
familial hyperchylomicronaemia is genetic type I: Reduced levels of
functional LPL/Inability to synthesise
apo-??? (LPL cofactor)
apo C-II
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
unable
what is the treatment for Type I – familial hyperchylomicronaemia?
very low fat diet
Type IV - Familial hypertriglyceridaemia: an increase or decrease (?) in VLDL as well as synthesis of VLDL & also reduced
catabolism
increase
treatment for Type IV - Familial
hypertriglyceridaemia: diet, ideal body weight, avoid ??? & alcohol increase exercise, possibly drugs
sucrose
which types of WHO classifications are at risk of pancreatitis?
Types I IV and V
Type V – Familial hypertriglyceridaemia AKA Mixed hyperlipidaemia: mutation in the apo-??? gene causes increased VLDL production and reduced LPL
mutation in apo C-II gene
treatment of type V is ??? such as fibrates and niacin
drugs
Both chylomicrons and VLDL are
triglyceride rich and therefore people with Type I, IV and V have
??? looking plasma
cloudy/creamy
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.
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.
which type of dyslipidaemia primarily has high chylomicrons?
Type I
which type of dyslipidaemia primarily has high VLDL?
Type IV
which type of dyslipidaemia primarily has high VLDL and chylomicrons?
Type V because of Mutation in apo C-II gene
which type of dyslipidaemia primarily has high LDL?
Type IIa heterozygous and even more homozygous
which type of dyslipidaemia primarily has high LDL and VLDL?
Type IIb because of low LDL
receptor and high apo B
which type of dyslipidaemia primarily has high chyloremnants and high IDL?
Type III because of Mutation in
apo E gene
