Cardiology Exam > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

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1
Q

chylomicrons - apolipoproteins, origin, and cargo

A

*apolipoproteins: Apo-B48, Apo-C-II, and Apo-E
*origin: small intestine → lymphatics
*cargo: triglycerides > cholesterol

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2
Q

VLDL - apolipoproteins, origin, and cargo

A

*apolipoproteins: Apo-B100, Apo-C-II, Apo-E
*origin: liver
*cargo: triglycerides > cholesterol

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3
Q

IDL - apolipoproteins, origin, and cargo

A

*apolipoproteins: Apo-B100, Apo-C-II, Apo-E
*origin: liver (more so a remnant of VLDL after it unloads some of its triglycerides)
*cargo: triglycerides/cholesterol

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4
Q

LDL - apolipoproteins, origin, and cargo

A

*apolipoproteins: Apo-B100
*origin: liver
*cargo: cholesterol

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5
Q

HDL - apolipoproteins, origin, and cargo

A

*apolipoproteins: Apo-A-1, Apo-C-II, Apo-E
*origin: liver
*cargo: cholesterol

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6
Q

apolipoprotein A-1 (Apo A-I)

A

*structural protein for HDL
*activates LCAT enzyme

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7
Q

apolipoprotein B-48 (Apo-B48)

A

*structural protein for chlyomicrons

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8
Q

apolipoprotein B-100 (Apo-B100)

A

*structural protein for VLDL, IDL, LDL
*binds LDL receptor

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9
Q

apolipoprotein C-II (Apo C-II)

A

*co-factor for LPL (lipoprotein lipase)
*Apo C-II enables LPL to unload triglycerides to tissues that need it for energy

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10
Q

apolipoprotein E (Apo-E)

A

*ligand for binding to LDL receptor & LDL-like receptors
*helps particles get back to the liver to be broken down and remade into VLDL

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11
Q

lipoprotein lipase (LPL)

A

*AN ENZYME THAT PRODUCES HYDROLYSIS IN LOW-DENISTY LIPOPROTEINS TO TURN THEM INTO GLYCEROL TO BE RELEASED IN THE MUSCLE
*expressed on endothelial cells in the heart, muscle, and adipose tissue
*has dual functions of triglyceride hydrolase and ligand/bridging factor for receptor-mediated lipoprotein uptake
*LPL isozymes are regulated differently depending on the tissue:
-the form that is in adipocytes is activated by insulin
-the form that is in muscle & myocardium is activated by glucagon & adrenaline

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12
Q

exogenous cholesterol pathway (how we absorb & use dietary fats, lipids, and cholesterol)

A

*dietary fats are absorbed from the intestines & packaged into chylomicrons, which enter the circulation through the thoracic duct
*chylomicrons help to deliver triglycerides to tissues for energy

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13
Q

lifecycle of chylomicrons

A
  1. dietary fats are absorbed in the small intestine and packaged into chylomicrons (Apo-B48 is attached)
  2. HDL in the bloodstream donates Apo-E and Apo-CII to the chylomicron
  3. mature chylomicrons travel through circulation and deposit triglycerides to muscles & adipose tissue to use for energy
  4. after delivering a significant amount of triglycerides, the chylomicron remnant returns to the liver
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14
Q

how do chylomicrons deliver triglycerides to muscle, myocardium, and adipose tissue?

A
  1. when one of these tissues is in need of energy, it expresses lipoprotein lipase (LPL) on its endothelial cells
  2. chylomicrons have Apo C-II, which interacts with the LPL receptors
  3. this interaction allows the chylomicrons to donate triglycerides to that tissue
  4. once the chylomicron has used up its reserve of Apo C-II, the chylomicron remnant uses Apo-E to return to the liver
  5. the chylomicron remnant is repackaged in the liver as VLDL
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15
Q

endogenous cholesterol pathway (how the liver packages lipids & cholesterol)

A

*liver produces VLDL, which delivers triglycerides to tissues
*as triglycerides are delivered to tissues, the particles get much smaller
*when the particle contains almost all cholesterol and few little triglyceride, it has become an LDL particle

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16
Q

VLDL (Apo-B100) lifecycle

A
  1. tissues in need of energy express lipoprotein lipase (LPL) on their surface
  2. VLDL particles have Apo C-II, which interacts with LPL receptors
  3. this interaction allows VLDL particles to donate triglycerides to that tissue
  4. as the VLDL particle donates triglycerides, it becomes IDL
  5. IDL continues to donate triglycerides until it has used up its Apo C-II and no more triglycerides are left to donate
  6. at this point, the particle is LDL (contains only cholesterol & only has Apo B100)
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17
Q

LDL receptor - overview

A

*LDL particle binds to LDL-receptor → receptor-mediated endocytosis (brings the LDL particle into the cell)
*inside the cell, endosomes combine and break down the lipid particles
*the receptor itself is recycled and returns to the cell surface, where it can bind another LDL particle

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18
Q

LDL receptor & PCSK-9

A

*if the cell does not need any more cholesterol, it produces & secretes PCSK-9
*PCSK-9 binds to the cell’s LDL receptors
*when the LDL particles bind to the PCSK-9-bound LDL receptors, they are brought into the cell via receptor-mediated endocytosis (like normal)
*however, the LDL receptors are then BROKEN DOWN (not recycled to the cell surface) so that there are no more LDL receptors on the cell surface

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19
Q

classical LDL receptor

A

*located on cell membranes of most tissues in the body, but the MAJORITY ARE FOUND IN THE LIVER
*binds apolipoprotein B-100 and Apo-E
*Apo-E binds LDL receptors with 20x affinity than Apo-B100
*therefore, it is more difficult for the LDL particles (which only have Apo-B100) to return to the liver compared to VLDL and IDL particles (which also have Apo-E)

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20
Q

LDL-related protein-1 (LRP-1)

A

*acts as a scavenger receptor for remnant lipid particles
*binds Apo-E
*located in liver & nervous system

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21
Q

reverse cholesterol transport (how free cholesterol finds its way back to the liver) - detailed

A
  1. HDL has Apo-A1, which activates the enzyme LCAT
  2. LCAT (lecithin-cholesterol acyltransferase) CONVERTS FREE CHOLESTEROL INTO CHOLESTERYL ESTER (a more hydrophobic form of cholesterol), which is then sequestered into the core of a lipoprotein particle, particularly HDL
  3. CETP (cholesteryl ester transfer protein) facilitates transport of cholesteryl esters & triglycerides between lipoproteins:
    -CETP enables HDL to give its cholesterol to lipoproteins that will go back to the liver (VLDL, IDL)
    -this enables HDL to remain in the periphery & scavenge more free cholesterol
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22
Q

reverse cholesterol transport (SIMPLE)

A
  1. HDL uses Apo-A1 to activate LCAT
  2. LCAT converts free cholesterol into cholesteryl ester
  3. HDL takes up the free cholesterol
  4. CETP (activated by LCAT) transfers cholesterol from HDL to VLDL and IDL
  5. VLDL & IDL return the cholesterol to the liver, while HDL remains in the periphery to scavenge for more free cholesterol
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23
Q

inhibition of HMG-CoA reductase (part of the cholesterol synthesis pathway)

A

results in:
1. a build-up of HMG-CoA (the substrate of the enzyme)
AND
2. a decrease in mevalonic acid (the product of the enzyme)

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24
Q

hyperlipidemia - defined

A

*an increase in lipids in the blood
*hypercholesterolemia is a type of hyperlipidemia, but not all hyperlipidemias have increased LDL cholesterol

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25
causes of hyperlipidemia
*diet *hypothyroidism *nephrotic syndrome *anorexia nervosa *obstructive liver disease *obesity *diabetes mellitus *pregnancy *acute hepatitis *SLE *AIDS (protease inhibitors)
26
Friedewald Equation for measuring LDL levels
*LDL = (total cholesterol - 0.2) x (triglycerides - HDL) *LDL is not directly measured, but rather it is calculated *note - cannot calculate LDL if triglycerides are > 400 mg/dl
27
appearances of various increased lipoproteins in serum
*increased chylomicrons → creamy top layer *increased LDL → clear *increased VLDL/IDL → turbid
28
type I hyperlipoproteinemia (familial hyperchylomicronemia)
*defects can be any of the following: -lipoprotein lipase (LPL) deficiency -familial Apo-CII deficiency -circulating inhibitor of LPL *increased particle = CHYLOMICRONS *lab finding = increased triglycerides *look out for pancreatitis!
29
type I hyperlipoproteinemia (familial hyperchylomicronemia) - pathophysiology
*by inhibiting LPL, the chylomicron is unable to unload its triglyceride-rich content *the VLDL which is made also cannot unload its triglycerides *result = INCREASED CHYLOMICRONS & INCREASED TRIGLYCERIDES
30
type IIa hyperlipoproteinemia (familial hypercholesterolemia)
*defect: defective LDL receptor *increased particle = LDL *lab findings = increased LDL, normal triglycerides
31
type IIa hyperlipoproteinemia (familial hypercholesterolemia) - pathophysiology
*by having a defective LDL receptor, LDL builds up *note that VLDL and IDL do not build up because hepatic lipase converts them to LDL
32
dermatologic manifestations of hypercholesterolemia (type IIa hyperlipoproteinemia)
*xanthelasmas *tendinous xanthomas *corneal arcus
33
xanthelesmas
*plaques or nodules composed of lipid-laden histiocytes in the EYELIDS *associated with FAMILIAL HYPERCHOLESTEROLEMIA (type IIa hyperlipoproteinemia)
34
tendinous xanthomas
*lipid deposits in tendons, especially Achilles tendon & finger extensors *associated with FAMILIAL HYPERCHOLESTEROLEMIA (type IIa hyperlipoproteinemia)
35
corneal arcus
*lipid deposits in corneas *common in older adults (arcus senilis) but appears earlier in life with hypercholesterolemia *associated with FAMILIAL HYPERCHOLESTEROLEMIA (type IIa hyperlipoproteinemia)
36
type IIb hyperlipoproteinemia (familial combined hypercholesterolemia / hyperlipidemia)
*defect: defective/inhibited LDL receptor WITH increased apolipoprotein B100 production *increased particles = LDL and VLDL *lab findings = increased LDL and increased triglycerides
37
type IIb hyperlipoproteinemia (familial combined hypercholesterolemia / hyperlipidemia) - pathophysiology
*by having a defective LDL receptor & increased Apo-B100, the VLDL, IDL, and LDL all build up *VLDL/IDL build up because hepatic lipase is overwhelmed and can't keep up in converting them to LDL
38
type III hyperlipoproteinemia (familial dysbetalipoproteinemia)
*defect: defective apolipoprotein E related to larger particles *increased particles = IDL, VLDL, and chylomicrons *lab findings = increased triglycerides, increased total cholesterol
39
dermatologic manifestations of dysbetalipoproteinemia (type III hyperlipoproteinemia)
*tubo-eruptive xanthomas *palmar xanthomas
40
tubo-eruptive xanthomas
*reddish bunos that appear suddenly over elbows, forearms, trunk, legs, extensor digitorum tendons, or buttocks *associated with FAMILIAL DYSBETALIPOPROTEINEMIA (type III hyperlipoproteinemia)
41
palmar xanthomas
*soft yellow plaques/nodules containing deposits of lipoproteins on the creases of the PALMS *associated with FAMILIAL DYSBETALIPOPROTEINEMIA (type III hyperlipoproteinemia)
42
type IV hyperlipoproteinemia (familial hyperlipidemia)
*defect: decreased removal of VLDL/excess VLDL production *increased particle = VLDL *lab finding = increased triglycerides
43
type V hyperlipoproteinemia (familial hypertriglyceridemia)
*defect: increased VLDL production & decreased LPL activity *increased particles = VLDL & chylomicrons *lab findings = increased triglycerides *look out for pancreatitis!
44
apolipoprotein B48 defects
*if impairs production of chylomicrons, then leads to fat/cholesterol absorption problems: -steatorrhea -failure to thrive -muscle wasting -neurological issues/coordination -fat soluble vitamin deficiencies
45
apolipoprotein B100 defects
*if significant impairment of B100's ability to bind LDL receptor, then may mimic familial hypercholesterolemia with high levels of LDL
46
CETP (cholesterol ester transfer protein) defects
*rare mutations leading to reduced function of CETP have been linked to accelerated atherosclerosis *a CETP inhibitor (Ancetropib) causes substantial increase in HDL and modest decline in LDL *trans fats increase CETP activity
47
LCAT (lecithin-cholesterol acyltransferase) defects
*impairment of LCAT leads to cholesterol deposits in the corneas, kidney, and other tissues and organs *decreased LCAT concentration and activity are associated with decreased HDL levels but not with increased atherosclerosis
48
LDL levels and risk of MI/CAD
*LOWER LDL levels are BETTER *increasing LDL levels are associated with increased risk for MI and CAD
49
LDL particle size & risk of atherosclerosis
*among individuals with the same LDL levels, the number of LDL particles and the size vary *SMALLER LDL PARTICLES are associated with MORE ATHEROSCLEROSIS (it is easier for these particles to enter the arterial lining following injury)
50
HDL levels & risk of MI
*individuals with high LDL PLUS LOW HDL are at the highest risk of developing an MI
51
lipoprotein(a)
*sits on the surface of the LDL particle *associated with a significantly INCREASED risk of atherosclerosis and coronary artery disease *Lp(a) contributes to the process of atherogenesis: because of its structural similarity to plasminogen & tPA, competitive inhibition leads to reduced fibrinolysis *must be very aggressive in lowering LDL
52
statins - site of action
*competitive inhibition of HMG-CoA REDUCTASE in the liver (part of the cholesterol synthesis pathway) *2 groups: hydrophilic and lipophilic
53
effects of statins on LDL receptors & plasma LDL levels
*statins inhibit cholesterol synthesis → liver perceives a deficiency and expresses MORE LDL RECEPTORS to obtain cholesterol *by increasing LDL receptors, LDL binds to the receptors and goes into the liver → LOWER PLASMA LEVELS OF LDL CHOLESTEROL
54
atorvastatin
*example of LIPOPHILIC statin
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rosuvastatin
*example of HYDROPHILIC statin
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pleiotropic effects of statins
*increased platelet function *decreased coagulation *decreased inflammation *decreased free radicals *increased endothelial function *increased collagen *DECREASED LDL *INCREASED HDL
57
PCSK-9 inhibitors - MOA
*inhibition of PSCK-9 → LDL receptors return to the cell surface, rather than being degraded by lysosomes *hence, LDL receptors increase → LDL levels DECREASE *example = evolocumab
58
bempedoic acid - MOA
*a first-in-class small molecular inhibitor of ATP-citrate lyase (which produces acetyl-CoA)
59
non-pharmacologic considerations to lower lipids: DIETARY FAT/CHOLESTEROL
*monounsaturated fats: lowers LDL, raises HDL *polyunsaturated fats: lowers LDL, raises HDL *saturated fats: raises both LDL and HDL *trans fats: raises LDL
60
non-pharmacologic considerations to lower lipids: EXERCISE
*exercise is one of the few ways to RAISE HDL
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