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IPFC-3: Dyslipidemia > Dyslipidemia: Patho > Flashcards

Dyslipidemia: Patho Flashcards

(75 cards)

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1
Q

What is atherosclerosis

A

pathological disease of coronary, cerebral + peripheral arteries
—- marked thickening of arterial walls due to increase in plaque/hardening

** normally causes decrease in BP (ischemic) + plaque rupture (ACS)

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2
Q

What is ischemia

A

reduced BF to part of body caused by BV constriction

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3
Q

What is IHD

A

insufficient BF to heart (blockage of coronary artery)

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4
Q

What is CVD

A

point when atherosclerosis causes S+S —— MI, stroke, CHD, TIA or PAD

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5
Q

What is CHD

A

coronary heart disease - includes CAD + CHD + IHD
—- defined as when not enough supply of O2 + blood to myocardium

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6
Q

What is the main symptom of CHD

A

angina/chest pain —- 3 types of

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7
Q

What are the different types of angina and their differences

A

Stable: predictable chest pain (ex// after PA)
unstable: changes in patterns + severity (normally result of clot) ;; platelet rich plaque w/ no tissue damage
variant: vasospam (not caused by atherosclerosis)

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8
Q

What are the main contributors to ASCVD

A

dyslipidemia + HTN
- other factors include: obesity, smoking, genetics

** work together to cause plaque growth

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9
Q

What are the types of ACS that can result from unstable plaque

A

STEMI: fibrin rich clot; total occlusion —- necrosis
NSTEMI: platelet rich clot w/ tissue injury
unstable angina : platelet rich clot w/out tissue injury

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10
Q

What causes stable angina

A

ASCVD —- stable plaque/fiborous cap
—- stable ischemia w/ decreased BF

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11
Q

What causes ACS

A

unstable plaque (normally have no to thin cap): can rupture + form clot on top

** plaque growth again result of HTN + dyslipidemia

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12
Q

T or F: ALL ACS can lead to afib + HF

A

T— ACS can lead to these; not all afib + HF are a result of ACS though (can get due to other CV risk)

** Afib + HF can cause each other as well

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13
Q

What can afib lead to

A

stroke

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14
Q

T or F: variant angina is a result of atherosclerosis (HTN + dyslipidemia)

A

F - dyslipidemia is not a RF
unsure of RF but do include smoking
—- result of vascular SM hyperactivity

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15
Q

Primary CVD prevention

A

delaying /preventing onset of CVD

— has no S+S of CVD or experienced CVD event

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16
Q

What is secondary prevention of CVD

A

prevention of progression (had CVE already)
—- use more aggressive therapy

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17
Q

Is stable angina considered primary or secondary CVD prevention

A

primary normally
— you have plaque + BV narrrowing but no CVE

** some studies include it as 2nd though

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18
Q

What is the role of lipids in the body

A

fatty acids (energy), cholesterol (building block of steroid hormones, bile acids, cell membranes), phospholipids

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19
Q

T or F: lipids need to be bound by lipoproteins in order to go into circulation because they are lipophilic

A

T

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20
Q

What are the 2 components of a lipoproteins

A

Lipid component: esterified or unesterified lipids (cholesterol, TG, phospholipids) — ester ones in core, unesterified on outside

Protein: found on surface (help ID lipoprotein + help with fins)

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21
Q

A more dense lipoprotein has more______ component

A

protein

  • density: relative to content of lipids + proteins (F:P); more fat —- lighter + less dense
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22
Q

What are the 5 different types of lipoproteins

A

Chylomicrons

VLDL

IDL

LDL

HDL

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23
Q

Which lipoprotein in the lightest but biggest ? Which is the densest?

A

lightest— chylomicrons (mostly fat)

denser: HDL (half protein

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24
Q

Which lipoproteins carry mostly TG

A

chylomicrons — 80-95% TG

VLDL - 55-85%

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25
Which lipoproteins have more cholesterol component in comparison to the others?
LDL - 6-8% cholesterol HDL : 3-5%
26
What the main apolipoproteins on chylomicrons
A1, B48 + CII
27
Main apolipoproteins on VLDL
B100 + CII
28
Main apolipoproteins on IDL
B100
29
Main apolipoproteins on LDL
B100
30
Main apolipoproteins on HDL
A1 + CII —- no B100: pathologic one
31
Which lipoproteins have larger protein content
LDL - 18-22% HDL - 45-55%
32
Most plasma TG are carried by ____ and ____ lipoproteins at a ratio of 4:1
Chylomicrons + VLDL — can estimate VLDL levels by taking TG/5 if TG < 250
33
What are apolipoproteins
protein component of the lipoproteins (hydrophilic)
34
Fxn of apolipoproteins
-physical structural base of lipoproteins - ligands for cell surface receptors (allow them to get into places) - cofactors for enzyme activity
35
What apolipoprotein is linked to increase morbidity
B100— pathologic one - found in VLDL, IDL, LDL
36
A1: fxn
cofactor for the LCAT enzyme —- converts free cholesterol into esters that can be taken in by chylomicrons — enzyme that transfers cholesterol from peripheral tissues into HDL (fills HDL with cholesterol; ligand for HDL receptor to allow cholesterol ) ** in chylomicrons + HDL
37
AIV: fxn
activates LPL + LCAT - LCAT: lecithin-cholesterols acteyltransferase - LPL: helps with release of FFA from chylomicrons ** found in chylomicrons
38
B100: fxn
ligand for the LDL receptor (allows lipoprotein to be taken/get into the liver) ** also needed to make VLDL, IDL
39
B48 fxn
Helps with production + secretion of chylomicrons from SI (containing dietary cholesterol)
40
CI fxn
- cofactor of LCAT again (enzyme that makes cholesterol esters + helps with filling HDL with cholesterol from periphery) - found in chylomicrons, VLDL, HDL
41
CII fxn
activator of LPL (release of FFA from TG) —- happens with chylomicrons , VLDL, HDL
42
E fxn
ligand for LDL + LDL related proteins - remnant receptor; helps with CL
43
Where does the exogenous pathway start
in intestinal cells ( intake of cholesterol from food/outside the body) —- rate of A of dietary cholesterol not understood (what controls the extent)
44
Once into the intestinal cells, what happens to dietary cholesterol
TG produced from glycerol + FA (using DGAT enzyme) cholesterol esters produced from cholesterol
45
What is packaged into chylomicrons
cholesterol esters + TG produced in intestinal cells packaged into ceylon’s using B48 apolipoprotein ( helps with assembly + secretion)
46
What happen to chylomicrons once in circulation
They lose some of their FFA via the LPL enzyme (activated by AIV + CII) — CII: activates LPL to cause the release of FFA into the periphery to be used as energy source of stored in adipose ** release of energy from the food we just ate - during rxn: also releases some apolipoproteins into plasma: A1 (LCAT cofactor), AII + AIV ** what remains are the chylomicrons remnants
47
T or F: during the release of FFA from chylomicrons, there is a transfer of some apolipoproteins to HDLs
T - transfer of CI (LCAT cofactor) , CII (LPL), CIII + PL
48
What happens to the chylomicrons remnants
they go to liver + are taken up via Apo-E (binds to LDL-R)
49
Where is most cholesterol made in the body
liver — made internally in hepatocytes to produce VLDL —- regulated by diet + hormones
50
How is cholesterol released from liver
in VLDLs —- contain mostly TGs + B100 ** leave as immature VLDL
51
How do VLDLs become mature
become mature with the transfer of Apo A, CII, CIII + E from HDL (some of these stolen originally from chylomicrons ) —— CII: LPL —- E: LDL R for CLearance
52
What happens to VLDL in the periphery
binds to LPL via CII to cause the release of FFA to the periphery (SAME PROCESS AS CHYLOS) —- CII activates LPL to cause energy release to periphery ** what is leftover is the VLDL remnants (AKA IDL)
53
What can IDL do
they can bind to LDL R on liver, converted to LDL and be cleared (B100). OR be taken up by the liver + converted to LDLs + put out into circulation — LDLs go out into circulation and can go to periphery or if excess can
54
What converts IDLs to LDLs
hepatic lipase (VLDLs originate from liver; made from leftovers of VLDL/IDLs)
55
How does the liver clear/get rid of IDL/VLDL leftovers
bind to liver via E, converted to LDL —- converted to bile acids that are then secreted into intestinal lumen
56
What can LDL do out in circulation (instead of being converted into bile acids)
Good uses: used for hormone production, cell membrane synthesis or storage BAD USES: can be out in periphery oxidized in the walls of BVs into pathologic form which attracts monocytes to form foam cells (pathologic) —- eventually leads to plaque formation
57
Why is LDL bad cholesterol
transfers cholesterol made in liver into the periphery ( cholesterol originally came from VLDL—- IDL) B100: used to bind to LDL R on liver
58
What regulates LDL R levels on liver
regulated by the internal cholesterol synthesis balance (how much cholesterol is made/stored in the liver) —— cholesterol production in liver occurs via HMG-CoA reductase — level of R on liver that can be used to uptake LDL depends on cholesterol levels already in the liver (higher cholesterol level in liver — less R; lower cholesterol - up regulate R to take in more )
59
In what condition do you find an Absence of LDL-R
familial hypercholesterolemia — increase in LDL in circulation can’t be taken up by liver
60
What does HDL do
brings cholesterol back from periphery TO the liver (reverse cholesterol transport)
61
Where does HDL come from
made + excreted by liver + gut in the form of immature HDL —- picks up apolipoprotein from chylomicrons + interacts with VLDL (drops off the apos)
62
How does HDL pick up cholesterol
picks up peripheral cholesterol; activates LCAT by AI to product cholesterol esters — once picked up — mature now - once have the cholesterol— can transfer them to VLDL (IDL — LDL for excretion) or to chylos vis CETP enzyme ** once empty of cholesterol : HDL interacts with liver to be cleared
63
Primary vs secondary lipoprotein metabolism: what are the differences
primary: inherited or polygenic secondary: caused by disease or meds
64
what is the most common cause of dyslipidemia
polygenic : combination of genes + environment
65
What is the fredrickson classification
classifications of the different phenotypes of dyslipidemia based on the lipoprotein that is elevated
66
Fredrickson class: IIa vs IIb
IIA - increase LDL IIb - increase LDL + VLDL
67
Fredrickson class: IV vs V
IV- VLDL V - VLDL + chylos
68
What is FH IIa hyperlipidemia
autosomal dominant genetic disease with 85-90% mutations in LDL-R gene resulting in super high LDL - can be homo (HoFH IIa): super rare 1/1000000+ causes super high LDL (early CVD risk) - hetero: more common (1/500), smaller increase in LDL
69
T or F: with FH IIa hyperlipidemia; you have have physical signs of increased LDL
T - increase risk of LDL oxidation — can get deposits of cholesterol in vascular sites (lumps) - tendinous xanthomas: thickening of lateral border of Achilles - Xanthelasmas: cholesterol deposits in eyelids - Acrus cornealis: deposits in corenal rim
70
What is FH IV hyperlipidemia
- autosomal dominant disorder with mutation in LDL gene (causes an increase in VLDL) —- increase in TG —- LPL: removes FFA from TG from VLDL ** not sure impact of high TG on CVD — but increased risk of acute pancreatitis
71
T or F: with polygenic hypercholesterolemia, you will have physical findings of the increase in cholesterol
F- no physical findings disorder with multiple abnormalities in geno + phenotype of LDL metabolism (multiple defects in LDL-R/fxn, flawed B100, increase in apo B synthesis + other E phenotypes — interaction of diet + PA causing a slight increae in LDL usually have FH of early onset of CVD (D > 55, M> 65)
72
What are some secondary disease causes of dyslipidemia
anorexia, hypo, obesity, Cushings, DM, renal/hepatic disorders, sedentary
73
Secondary drugs causes of dyslipidemia
HIV, cyclosporine, carbemazepine —- increase LDL glucocorticoid thiazide diuretics +BB
74
Patho of Atherosclerosis / formation of plaque
increase in LDL + endothelial damage —- LDL go into BV walls + gets oxidized (inflammation —- recruit monocytes to the area — engulf LDL to form foam cells (eventually leads to plaque formation under endothelial layer) —- fatty streak —- foam cells cause SM migration + proliferation + fiborous capsule forms on top of plaque —- narrows BV — increase in BV to this area (Vasa vasorum - micro vessels that supply outer layer of the wall)
75
When do we start screening people for dyslipidemia
M >/=40 + W>/= 40 or postemopausal —- if certain conditions , increased risk of condition, so screen no matter age - clinical evidence of atherosclerosis - DM HTN current smokers FH of premature CVD CKD obese IBD HIV infection ED COPD

IPFC-3: Dyslipidemia (5 decks)

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