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Cardio Exam 2 > Lect 2- Disorders of Lipoprotein Metabolism > Flashcards

Lect 2- Disorders of Lipoprotein Metabolism Flashcards

1
Q

lipoprotein definition

A

transport hydrophobic lipids (TG, chol, fat-soluble vitamins)
2 functions:
1.) absorption of dietary chol, long-chain fatty acids, and fat-soluble vitamins
2.) transport from liver to peripheral tissues and vice versa

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2
Q

What is in the core of lipoproteins?

A

Cholesterol esters and TGs

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3
Q

Which parts of the lipoprotein are hydrophilic?

A

Protein, cholesterol, phospholipids (some can be modified and moved inside the core)

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4
Q

HDL

A

very tiny and very dense

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5
Q

LDL

A

low density lipoproteins
Little bit larger but less dense than HDL
Bad guys= strong clinical evidence that correlates w/ increased risk of atherosclerosis and other CV diseases

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6
Q

IDL

A

intermediate density lipoproteins

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7
Q

VLDL

A

very low density lipoproteins

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8
Q

chylomicrons

A

largest
Big diff b/w these and all other lipoproteins b/c these are involved in absorption of dietary lipids
Carry all these lipids from gut to other tissues

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9
Q

Which lipoproteins transport TGs?

A

chylomicrons and VLDLs

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10
Q

Which lipoproteins transport cholesterol and cholesterol esters?

A

LDLs, HDLs

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11
Q

Apolipoproteins

A

activate enzymes important in lipoprotein metabolism

ligands for cell surface receptors

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12
Q

ApoB-48

A

synthesized in ONLY intestine

part of chylomicrons

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13
Q

ApoB-100

A

synthesized in liver (liver makes VLDL and IDL and LDL originate from VLDL)
on VLDL, IDL, LDL

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14
Q

ApoE

A

ligand for VLDL receptors

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15
Q

Which apolipoprotein does not transfer b/w lipoproteins?

A

ApoB

Lipoproteins normally interact w/ each other and exchange substances (lipids and proteins)

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16
Q

ApoC

A

important in lipoprotein lipase (LPL) rxn

on chylomicrons, VLDL, IDL

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17
Q

lipoprotein lipase

A

Enzyme to digest TG which are inside the chylomicron (hydrolysis rxn)
Responsible for hydrolysis of TG into glycerol and FA’s which can be used as energy

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18
Q

hepatic lipase

A

makes IDL into LDL

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19
Q

transport of lipids

A

LOOK AT SLIDE W/ PICTURE

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20
Q

ApoA-1

A

on HDL

made in liver or small intestine

21
Q

LCAT

A

makes cholesterol into cholesterol esters so they can be moved into the core of HDL

22
Q

CETP (cholesterol ester transport protein)

A

Moves esters from HDL to chylomicrons and VLDL

23
Q

HDL metabolism and reverse chol transport

A

LOOK AT PICTURE ON SLIDE

24
Q

amts of chol in chylomicrons

A

low levels of TC, high levels of TGs

25
Q

high amts of LDL results in __ amts of TC

A

high

26
Q

Which cholesterol is high in pancreatitis?

A

chylomicrons

27
Q

Which cholesterol is high in coronary atherosclerosis?

A

very high levels of LDL!

28
Q

primary disorders in lipoprotein metabolism

A

genetic
abnormalities in lipoprotein metabolism is a starting point
Ex. familial hypercholesterolemia

29
Q

secondary disorders in lipoprotein metabolism

A

assoc with other comorbidities (obesity, DM, alcohol, etc)

more common than primary

30
Q

Which genetic hyperlipoproteinemia is most common?

A

familial hypercholesterolemia

31
Q

familial hypercholesterolemia

A

autosomal codominant disorder
increased levels of LDL-C
normal TGs, tendon xanthomas, premature coronary atherosclerosis
higher levels of LDL in homozygotes than heterozygotes

32
Q

What is mutated in familial hypercholesterolemia?

A

• Lot of mutations in LDL receptor gene

○ Don’t have proper pickup of LDL → buildup → excess can go to tissues and cause increased risk of atherosclerosis

33
Q

Homozygotes vs heterozygotes in familial hypercholesterolemia

A

• Homozygous= chol levels can be 500-1,000
• Heterozygous= chol levels can be 200-400
○ Much lower
• Direct link b/w affected # of alleles affected and function of receptor and severity of disease/ level of chol (homo has disability and death in childhood)

34
Q

Diagnosis of homozygotes in familial hypercholesterolemia

A
  • Family history
  • skin biopsy
  • flow cytometry analysis of LDL receptor density
  • DNA sequencing
35
Q

Obesity

A

increased amts of FFAs are delivered to the liver from adipose tissue (massive amts of VLDLs which can be converted to LDLs)
often assoc w/ insulin resistance

36
Q

Role of HDL

A

• HDL is important b/c it is removing cholesterol from the tissues and taking it to the liver to be metabolized
○ Want to reduce the level of LDL and maintain/increase level of HDL in your pts

37
Q

Type I DM

A

usually w/o hyperlipidemia if glycemia is under control
Have no prob with lipid metabolism unless they are in ketoacidosis (hypertriglyceridemia due to an increased hepatic FFAs influx from adipose tissue)

38
Q

Type II DM (high insulin and insulin resistance)

A
  • decreased LPL activity
  • increased release of FFAs from adipose tissue
  • increased synthesis of FAs in the liver
  • increased hepatic prod of VLDLs
39
Q

Type II DM (lipid abnormalities)

A
  • elevated levels of TGs from VLDL
  • increased LDL
  • decreased HDL-C
40
Q

Hypothyroidism

A

inc LDL-C (due to reduction in activity of LDL receptor)
inc circulating IDL
sometimes mild high TG
ALL pts presenting w/ inc plasma levels of LDL-C, IDL, or TGs should be screened!

41
Q

nephrotic syndrome

A

increased hepatic prod and decreased clearance of VLDLs w/ increased LDL prod
Set of clinical features which are assoc with kidney abnormalities

42
Q

ESRD

A 
end stage renal disease
mild hyperTGemia (<300) due to accumulation of VLDLs and remnant lipoproteins in the circulation
43
Q

renal transplants

A

pts with these usually have increased lipid levels due to the effect of the drugs required for immunosuppression

44
Q

hepatitis

A

increased VLDLs and mild-mod hyperTGemia

45
Q

severe hepatitis and liver failure

A

reduced plasma chol and TG

46
Q

cholestasis

A

hypercholesterolemia
free chol, coupled w/ phopholipids, is secreted in plasma as constituent of LP-X and can deposit in skin folds and prod xanthomas

47
Q

alcohol

A

increased plasma TGs
increased hepatic secretion of VLDLs
regular consumption of HDL-C

48
Q

screening

A

all adults >20 should have TC, TG, LDL-C, HDL-C measured after 12 hour overnight fast

49
Q

diagnosis

A

determine class/cause of altered lipoproteins
rule out 2’ causes (2’ causes of hyperlipidemia= easier to treat the underlying prob than the lipid problem directly)
fasting glucose= to see if they have DM or not
liver function tests

Cardio Exam 2 (7 decks)

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