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PHA 222 > cholesterol > Flashcards

cholesterol Flashcards

1
Q

what does high plasma LDL levels mean?

A

high risk of CHD

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2
Q

Why do humans need cholesterol?

A

synthesis of: cell membranes/ steroid hormones/bile acids

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3
Q

what are the two major sources of cholesterol?

A

Exogenous–dietarysupply,e.g.eggs,shellfish

Endogenous–denovo synthesis in organs&tissues e.g.liver,intestines,ovaries,adrenals

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4
Q

is cholesterol water soluble?

A

no, it is water insoluble

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5
Q

what is cholesterol transported as?

A

water-soluble cholesterol lipoproteins

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6
Q

what makes up the inner fatty hydrophobic core?

A

cholesterol / cholesterol esters

triglycerides/free fatty acids(FFAs)

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7
Q

what makes up the outer hydropillic coat?

A

apolipoproteins
phospholipid
cholesterol

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8
Q

what are the key functions of Apolipoproteins?

A

Lipoprotein assembly & transport
Maintenance of structural integrity of lipoproteins Enzyme activation & inhibition
Cellular receptor binding

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9
Q

what are the 5 classes of lipoproteins?

A

VLDL/IDL/HDL/LDL/ CHYLOMICRONS

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10
Q

what are all the types of Apolipoproteins?

A

apoA, apoB-100, apoB-48, ApoA-1,apoA2, apoC

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11
Q

what are the 3 Pathways of Plasma Lipid Transport and Metabolism?

A

Exogenous (Intestinal) Pathway
Endogenous (Hepatic) Pathway
Reverse Cholesterol Transport

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12
Q

what are the pathways co-ordinated by?

A

the liver- to ensure balance

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13
Q

what happens in the exo-intestinal pathway?- in intestine walll

A

Lipid (cholesterol) synthesis in the intestinal wall
Dietary & biliary cholesterol -absorbed into enterocytes via the Niemann-Pick C1-Like 1 (NPC1L1) transporter
Esterified through acyl-coenzyme A:cholesterol acyltransferase (ACAT)
Packaged into apoB-48 containing & triglyceride-rich chylomicrons (CMs) by microsomal triglyceride transfer protein (MTP)

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14
Q

what happens in the exogenous pathway?- in blood

A

Lipid (cholesterol) transport in the blood
Triglyceride-rich CMs leave the intestine via lymphatic system & enter blood stream
Triglycerides in CM core are hydrolysed by endothelial lipoprotein lipase (LPL) to release free fatty acids (FFAs), as CMs pass through capillaries in muscle & adipose tissue
FFAs utilised for energy in muscle cells, or stored as fat in adipose tissue
Resulting chylomicron remnant particles are removed from plasma by the liver, viaapo
Ebinding to the remnant receptor (LRP) or LDL receptor (LDLR), for further metabolism

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15
Q

what happens in the Endogenous (Hepatic) Pathway?

A

Once inside hepatocytes, CM remnants are packaged with more cholesterol, cholesteryl esters & ApoB100 to form triglyceride-rich
VLDLVLDL particles are released into circulation & triglycerides in the core are hydrolysed by LPL to release FFAs, to be utilised for energy in muscle cells, or stored as fat in adipose tissue
The resulting IDL is either taken up directly by the liver or converted to LDL-C by hepatic lipase (HL)LDL-C is then taken up by peripheral tissues via the LDLR to meet local cholesterol needs
Any left-over LDL-C particles are finally removed by the liver via the LDLR

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16
Q

what happens in the reverse transport?

A

Return of excess LDL-C from peripheral cells to the liver by HDL
Nascent or pre-HDL (rich in apoA-I) particles, secreted directly from the gut and liver or generated from LPL-mediated lipolysis of triglyceride-rich CM & VLDL, enters the circulation
Remove free cholesterol from deposits in peripheral tissues via the ATP-binding cassette A1 (ABCA1)
Plasma lecithin-cholesterol acyltransferase (LCAT) converts free cholesterol in pre-HDL to cholesteryl ester (CE), resulting in mature a-HDL
a-HDL cholesterol is transported to the liver by a director indirect pathway

17
Q

what happens in the direct pathway?

A

hepatocytes selectively take up cholesteryl ester from a-HDL via the scavenger receptor, class B, type 1 (SR-B1)

18
Q

what happens in the indirect pathway?

A

a-HDL cholesteryl ester is exchanged for triglycerides in apoB-rich VLDL & LDL via the cholesteryl-ester-transfer protein (CETP)

19
Q

what are the first generating agents?

A

Bile acid sequestrants
Fibric acid derivatives
Nicotinic acid group

20
Q

what do bile acid seq do?

A

Bind bile acids & prevent enterohepatic cycling
dec Hepatic cholesterol levels
inc LDL-R expression- inc hepatic cholesterol uptake

21
Q

what are the adverse effects of bile acid seq?

A

GIT interactions

pharmacokinetics

22
Q

what do fibric acid derivatives do?

A

Effects mediated viaPPAR-receptoractivation
inc Uptake & b-oxidation of FFAin liver & muscle cells
inc Lipoprotein lipase activity incTG hydrolysis in VLDL & CM incelimination of TG-rich particles

23
Q

what do nicotinic acids do?

A

decrease FFA mobilisation from peripheral tissues
dec TG synthesis &VLDL secretion
dec plasma LDL
dec apoA-I uptake by liver inc HDL & reverse cholesterol transport

24
Q

what are the second gen agents?

A

statins

Selective cholesterol absorption inhibitors

25
Q

how do statins work?

A

Cholesterol lowering effects inhibit HMG-CoA reductase - decrease hepatic cholesterol synthesis

26
Q

what are the side effects of statins?

A

Myalgia-muscle aches, soreness or weakness
Myopathy-myalgia and serum CK levels (10,000 U/L
Rhabdomyolysis acute destruction of skeletal muscle (with myoglobinaemia & myoglobinuria))

27
Q

how do Selective cholesterol absorption inhibitors work?

A

Inhibit uptake of intestinal cholesterol into enterocytes
dec Intestinal delivery of cholesterol to the liver
inc Expression of hepatic LDL receptors
inc HDL-C clearance from circulation

28
Q

What are the newer agents used?

A

Proprotein convertase subtilisin/kexintype 9 (PCSK9) inhibitors
Apolipoprotein B synthesis inhibitors
Microsomal triglyceride transfer protein (MTP) inhibitors

29
Q

how do Proprotein convertase subtilisin/kexintype 9 (PCSK9) inhibitors work?

A

Binds to the LDL receptor and targets it for lysosomal degradation -inhibition of LDL receptor recycling & dec expression of hepatic LDL receptors inc LDL-C clearance from circulation incplasma LDL-C levels

30
Q

how does Apolipoprotein B synthesis inhibitors work?

A

Reduce LDL cholesterol through reduction of apoB-100 synthesis & VLDL production

31
Q

how does Microsomal triglyceride transfer protein (MTP) inhibitors work?

A

Reduce LDL cholesterol through reduction of VLDL production

32
Q

where is MTP found?

A

within the endoplasmic reticulum in enterocytes & hepatocytes

PHA 222 (41 decks)

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