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ENDO > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

0
Q

lipid circuit

A

fat from food–>small intestine–>cylomicrons–>blood–>meet LPL (stimulated by insulin)–>release FFA from chylomicron–>chylo get smaller until picked up by liver as VLDL

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1
Q

lipids by size

A

chylomicron>VLDL>IDL>LDL>HDL
increase desnity and protein
decrease in size and TG

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2
Q

circuit to deliver fat frm stores

A

fasting–>liver exports TG and cholesterol as VLDL–>LPL in blood chews it up–>becomes LDL and HDL

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3
Q

apoplipoproteins function

A

structure
activation of enzymes
ligands for recepotrs

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4
Q

apoB100

A

interacts wtih B receptor

useful marker for atherogenic risk

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5
Q

where is LPL made?

A

liver, localized to endothelium

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6
Q

function of LPL

A

when stimulated by insulin apoC2, hydrolyzes TGs to phospholipids and glycerol

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7
Q

Hepatic Lipase

A

acts ike LPL but only in liver

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8
Q

LCAT

A

interacts wtih apoA1 on HDL-creates cholesterol esters so cholesterol is easier to carry around

function is HDL maturation, does this by transferring acyl group from lecithin to chlesterol–>choelsterol ester

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9
Q

CETP

A

cholesterol esterase transfer protein

converts cholesterol esters back to cholesterol for delivery to liver

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10
Q

blocking CETP

A

increases HDL levels

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11
Q

SCAP

A

SREBP cleaving protein
sensor for lower intracellular sterol
if low–>binds SREBP2–>allows cleavage and activation–>brings in more LDL

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12
Q

what activates SCAP

A

low cholesterol diets and meds that decrease cholesterol production (niacin, statins) making cells take more cholesterol in

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13
Q

SREBP2

A

a TF activated by SCAP in response to low cholesterol–>increases HMGCOA expression–>increases cholseterol in LDL form–>the cell takes up more LDL

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14
Q

ABC1

A

transfers cholesterol to cell membrane to interact with apo1 on HDL for pickup by HDL

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15
Q

LDLR

A

LDL receptor on hepatocytes

interacts with apoB100 to pick cholesterol from blood into hepatocyte –> then recycles it back to its surface

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16
Q

PCSK9

A

secreted protein that binds LDLR and targets it for removal

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17
Q

blocking pCSK9

A

increases LDLR–>decreases cholseterol

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18
Q

PPARa

A

TF that upregulates genes involved in FA uptake and oxidation, a key determinant of VLDL synthesis

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19
Q

total cholesterol=

A

LDL cholesterol + VLDL cholesterol (aka TG/5) + HDL cholesterol

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20
Q

total cholesterol calculation only works if

A

relatively normal TF levels, so need to do it in fasting state

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21
Q

measuring LDL does nto require

A

fasting- more direct measurement

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22
Q

LDL cholesterol estimated=

A

total-HDL-TG/5 (as long as TG <250)

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23
Q

as TG go up..

A

moer get carried by non-CLDL particles, so VLDL does not equal TG/5

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24
Q

atherogenic cholesterol calculation

A

non-hdl cholesterol=total-HDL cholesterol

*includes VLDL LDL & apoB lipoproteins

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25
Q

fasting is only required for measuring

A

triglycerids

26
Q

total cholesterol

A

<180

27
Q

HDL chol

A

> 46

28
Q

LDL chols

A

<130

29
Q

chilled tube test and fasting

A

will remove chylomicrons unless patient has a disease that cant remove chylomicrons

30
Q

types of primary hyperlipidemias

A 
chylomicron excess
VLDL excess
ILDL excess
LDL excess
HDL deficiency
Lipoa excess
31
Q

chylomicron excess

A

chylomicrons that you eat do not clear

LPL deficiency & apoCII def

32
Q

clinical consequences of chylomicron excess

A

TG>1000
pancreatitis
eruptive xnathomas

33
Q

VLDL excess diseases

A

familial hypertgemia

familial comvined hyperlipidemia

34
Q

familial hyperTGemia

A

TG 250-1000
pancreatitis
increased hepatic production of VLDL OR LPL def
decreases LDL, so total cholesterol not high

NOT associated with ASCVD

35
Q

familial combined hyperlipidemia

A

increased total cholesterol (TG, LDL, VLDLetc) decreased HDL
eruptive and tuberous xanthomas, ASCVD
decreased LDLR or increased apoB

36
Q

ILDL excess

A

familial dys-beta-lipproteinemia

37
Q

familial dysbetalipoproteinemia

A 
must have 2 ApoE genes
remnant removal disorder- very rare
cholesterol = TG
palmar and tuberous xanthomas
ASCVD
38
Q

4 types of LDL excess diseases

A

familial hypercholesterolemia-LDLR def
familial defective ApoB100-defective protein
familial combined hyperlipidemia- clearing issues (LDL R)
polygenic hypercholesterolemia- high fat diet

39
Q

clinical pictures of LDL excess

A

NO pancreatitis
LDL accumulates in extensor tendons
cholesterol between 350-550
**ASCVD

40
Q

if patient lacks both LDL R

A

doesnt survive past teens

41
Q

HDL deficiency diseases

A

tangier’s

ABC1 def

42
Q

Tangier’s disease

A

very rare decrease in HDL, ASCVD, tangier’s tonsils

43
Q

ABC1 def

A

can’t get cholesterol out of cels

44
Q

Lipoa excess

A

LDL molecule with a moiety on it-atherogenic marker

45
Q

increased VLDL and ILDL can cause

A

fatty liver

46
Q

secondary hyperlipidemias

A

chylomicron excess
VLDL excess
LDL excess
atherosclerosis

47
Q

chylomicron excess results from

A

(increased TG)

chronic renal failure

48
Q

VLDL excess results from

A

(increased TG and cholesterol)–alcohol, CHO inducisble, uncontrolled DM, HAART, nephrotic syndrome, estrogens

49
Q

LDL excess

A 
(increased cholesterol)
hypothyroidism
nephritic syndrome
obstructive liver disease
high cholesterol diet
50
Q

atherosclerosis is associated wtih

A

increased LDL, ILDL, and small desnse VLDL

NOT associated with normal VLDL or chylomicrons

51
Q

treatment hyperlipidemia

A

best is statins + PCSK9 antibodies

52
Q

goal for statin therapy

A

reduce cholesterol to <100 mg/dl

53
Q

statins

A

stabilize plaque

54
Q

start therapy for high rsk patients (>20% 10 year risk for CHD)

A

when LDL-C exceeds ~115 mg/dl

55
Q

tx chylomicron excess

A

restrict fats and alcohol

56
Q

CLDL excess

A

restrict diet, drugs
PPAR a agonists - gemifibrizol, fenofibrate
Niacin

57
Q

ILDL excess

A

same as VLDL excess

58
Q

LDL excess

A

diet-reduce CHO and staurated fats

drugs

59
Q

drugs for LDL excess

A

bile acid sequestrants
HMGcoa reductase inhibitors
cholesterol transport inhibition

60
Q

cholestyramine, Welchol

A

bile acid sequesterants

61
Q

Statins

A

HMGcoa reducatse inhibitors

62
Q

ezetemibe

A

cholesterol transport inhibition
–taken up by intestinal BB–>liver activates–>excreted in bile–>acts as BB to block cholesterol and bile salt uptake

decreases intrahepatic cholesterol–>increases expression of LDLR

63
Q

fish oil

A

good for TG but not LDL

ENDO (5 decks)

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