Case of crash Dieter Flashcards
lipoproteins?
lipid with amphipathic molecules surrounding (phospholipids) and apoliproteins so can float around in plasma
Classes of Lipoprotein?
chylomicron
VLDL
IDL
LDL
HDL
A1/2 role?
transfer of cholesterol from periphery to liver
endogenous lipid cycle in fasting ?
liver produces VLDL, which is broken down by lipoprotein lipase into free fatty acids and glycerol so IDL. then free fatty acids stored into fat tissue and the IDL is back in liver to be disposed of or moved into LDL to peripheral tissues
endogenous lipid cycle in fasting ?
liver produces VLDL, which is broken down by lipoprotein lipase into free fatty acids and glycerol so IDL. then free fatty acids stored into fat tissue and the IDL is back in liver to be disposed of or moved into LDL to peripheral tissues
role of the liver in endogenous?
triglyceride synthesis
export as VLDL
take up particles when triglyceride removed
LDL delivers cholesterol to peripheral cells
cholestrol is produced from?
acetate converted by HMG- CoA reductase
statins inhibit?
HMG coA reductase
when free cholesterol is low in cell?
N-SREBP transcription factor is switched on and the LDL receptor gene codes for LDL receptor protein
endogenous pathway, HDL particles produced from liver, what do they do?
absorb cholesterol from cells in the vascular endothelium and recycle it back to liver as LDL
exogenous pathway?
from dietary lipids- chylomicron particle are absorbed and broken down by lipoprotein lipase into free fatty acids and glycerol which then stored in adipose tissue
the remaining chylomicron is transported to liver
cholesterol and fatty acid in the gut are?
absorbed into intestinal mucosa cells and the reesterified to cholestrol ester and triglyceride and packaged with phospholipids and lipoproteins. they are then secreted into lymphatic vessels as chylomicrons
what happens to glycerol?
it is processed in liver to form more triglycerides or converted to glucose
what happens to the chylomicron remenant?
taken up by LDL receptors in liver
hepatic lipase features?
no cofactor,
substrate is IDL, HDL and LDL
present in liver, adrenal and endocrine
lipoprotein lipase features?
cofactor- ApoCII
substrate- CM and VLDL
tissues- adipose and skeletal muscle
regulation in feeding fasting and exercise
normal serum lipid concentration?
should be less than 5mmol/L
upper limit of normality for fasting triglycerides?
1.7mmol/L
HDL levels
above 0.9 mmol/l in men and 1.2 mmol/l
FH?
autosomal dominant disorder of lipid metabolism, usually hetereogenous
occurs in 1 in 270 people, raised cholestrol specifically LDL cholestrol
tendon and skin xanthomata
pathognomic for hypercholesterolaemia?
corneal arcus before age of 40
mutations of FH found?
ApoB
PCSK9
LDLR
causes of hypertriglyceridaemia?
obesity, DM, excess alcohol, renal failure, gout, drug treatment, thiazides, beta blockersm retinoic acid derivatives, oestrogen therapy
causes of hypercholestrolemia?
hypothyroidism, nephrotic syndrome, high saturated fat diet, cholestatic liver disease, anorexia nervosa
obesity?
over 30
normal weight?
18.5-24.9
as obesity increases so does?
insulin resisitance
metabolic/ X syndrome?
reduced glucose tolerance, hyperinsulinaemia, hypertension, visceral obesity, homeostatic disorder, lipid disorder (high triglycerides, low HDL, normal or elevated LDL)
clinical identification metabolic syndrome
waist circumference:
men> 94cm
women> 80 cm
plus any 2 of
fasting triglycerides over 1.7
HDL men less than 1.03
women less than 1.29
blood pressure over 130/85
fasting glucose over 5.6
dying of cardiovascular disease in UK?
1: 3
Q Risk score?
age, cholestrerol, RA, renal, AF, sex, smoking status, FH, BMI, systolic blood pressure, left ventricular hypertrophy, T2DM
PCSK inhibitors?
block PCSK 9 protein which is responsible for degrading cholesterol receptors thus preventing removal of LDL from blood
Metabolic adaptation?
decreased energy expenditure, decreased satiety, improving metabolic efficiency, increased cues for energy intake