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DEMS > Lipoprotein physiology > Flashcards

Lipoprotein physiology Flashcards

1
Q

What are the 2 main lipid species that are transported in lipoproteins?

A
  • The insoluble ones

* Cholesterol esters and triglycerides

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2
Q

How does the body get rid of cholesterol?

A
  • Remember that cholesterol is not able to be oxidized in fatty acid oxidation.
    • Instead, it is secreted as bile salts and excreted in the stool (at least the bit that isn’t reabsorbed in the terminal ileum)
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3
Q

What are the 5 general classes of lipoprotein particles?

A
  • Chylomicrons
    • VLDL - very low density lipoproteins
    • Remnant particles and Intermediate Density lipoproteins
    • (LDL) - Low Density Lipoproteins
    • (HDL) - High Density Lipoproteins
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4
Q

What are chylomicrons?

A
  • Responsible for rise of Tg levels after a meal
    • Made from GI tract from dietary fat
    • Physically large and have far more triglyceride than cholesterol (10:1)
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5
Q

What’s up with the VLDL?

A
  • Source of basal triglyceride production
    • Made by the liver
    • 5:1 Tg to cholesterol
    • Deliver triglyceride to peripheral tissues between meals
    • Made at lower levels in the post-meal period
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6
Q

What makes up an HDL?

A
  • These are the trash trucks of lipid metabolism
    • Collect cholesterol from peripheral tissues
    • Transport cholesterol back to liver
    • Provide a reservoir of phospholipids for other lipoprotein particles
    • Exchange triglyceride and apo-proteins with other particles in the circulation
    • Higher HDL means less atherosclerotic risk
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7
Q

What makes up an LDL?

A
  • Produced from metabolism of VLDL
    • More cholesterol than Tg
    • VERY atherogenic
    • Less Tg means smaller and more dense
    • Small, dense LDL are espcecially aterogenic
    • Cleared from circulation by liver
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8
Q

What makes up an IDL?

A
  • Metabolic byproducts of the metablosim of chylomicrons and VLDL
    • As Tg rich lipoproteins deliver Tg to peripheral tissues they become physically smaller
    • They also become more cholesterol enriched as they lose Tg
    • Mid-sized and about 50/50 Tg/cholesterol
    • These are ATHEROGENIC
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9
Q

Describe in general the chylomicron pathway

A

• This pathway is how the body handles dietary fats
• Chylomicros are mostly triglyceride with some cholesterol, but most diets have way more triglyceride than cholesterol
• In the intestine, dietary triglyceride is hydrolyzed to monoacylglycerol and free fatyy acids through the action of pancreatic lipase
• The lipids and free fatty acids diffuse across the intestinal wall
• Once intracellular, they are rebuilt into triglycerides and packaged into chylomicrons
• APOPROTEIN B48 is the important protein here intracellularly
• The chylomicrons pick up C-2 and E (other apo-proteins) in the central circulation
○ Pick these up from HDL particles
• C-2 is a co-factor for LPL
○ LPL = lipoprotein lipase
• LPL is what breaks down the triglycerides in the chylomicron and if this can’t interact with C-2 there is hypertryglyceridemia
• Remnant particles of chylomicron breakdown are taken up by the liver
• Not normally present when taken in the fasting state
• This is why we ask patients to fast before we check lipid levels

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10
Q

What are the really important apo-proteins in the chylomicron pathway

A
  • APOPROTEIN B48 is the important protein here intracellularly - it is the scaffold on which the reassembled triglycerides from the diet are built into the chylomicron
  • C-2 - important item picked up by the chylomicron in the central circulation FROM HDL - an important cofactor for LPL (lipoprotein lipase) and degradation of chylymicron to get triglycerides into tissues
  • E - the other protein picked up in circulation from HDL
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11
Q

Describe in general the VLDL pathway

A
  • VLDL is a triglyceride rich lipoprotein synthesized by the liver
    • 50% triglyceride, 10% cholesterol
    • B100 is the all-important apoprotein here
    • Full length gene produce, B48 in chylomicron pathway is a PTM shortened version
    • Like the chylomicron pathway, VLDL will pick up C-2 and E apo-lipoproteins from HDL in the circulation
    • LPL is responsible for degradation of VLDLs just like chylomicron pathway
    • Degradation product here is LDL
    • LDL is 45% cholesterol (enriched for cholesterol)
    • LDL particles are taken out of circulaiton mostly by the liver though all tissues have LDL receptors
    • Problems in LDL receptor means high LDL levels and high risk for atherogenesis
    • LDL uptake in liver is what regulates cholesterol synthesis pathway
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12
Q

What are the important proteins in the VLDL pathway?

A
  • B100 is the all-important apoprotein here
  • Full length gene product, B48 in chylomicron pathway is a PTM shortened version
  • Like the chylomicron pathway, VLDL will pick up C-2 and E apo-lipoproteins from HDL in the circulation
  • LPL is responsible for degradation of VLDLs just like chylomicron pathway
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13
Q

Describe in general the HDL pathway

A

• This is the more complicated pathway because it interacts with so many other particles
• There are also several functions of the HDL in which molecules are transferred
• Think of it as a trash truck that collects cholesterol and Tg from the periphery and takes back to the liver
• Nascent HDL contains the main structural apo-protein apo-A1
○ Key protein = apo-A1
• These are synthesized in the liver and secreted into blood stream
• In circulation they pick up free cholesterol from peripheral tissues via diffusion and faciliated transport
○ ABC-A1 cassette is what is actively transporting cholesterol in circulation into the HDL particle
• Free cholesterol is “trapped” into the particle by conversion to cholesterol ester, which is performed by LCAT
○ Key enzyme = LCAT = lecithin cholesterol acyltransferase
○ Transfers a fatty acid from phospholipid onto free cholesterol to trap it in the HDL particle
• Maturing (as opposed to nacent or mature) HDL = HDL3
○ In circulation and involved in the transfer of cholesterol esters to VLDL in exchange for triglycerides through CETP
○ CETP = cholesterol ester transfer protein
○ KEY PROTEIN = CETP
• Mature HDL = HDL2
○ Taken up by liver

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14
Q

What are the important proteins and enzymes in the HDL particle?

A

*Apo-A1 is the scaffold protein made by the liver on which the whole complex is built

○ ABC-A1 cassette is what is actively transporting cholesterol in circulation into the HDL particle

○ Key enzyme = LCAT = lecithin cholesterol acyltransferase
○ Transfers a fatty acid from phospholipid onto free cholesterol to trap it in the HDL particle

*CETP = cholesterol ester transfer protein
○ used in the maturing HDL3 lipoprotein
*In circulation and involved in the transfer of cholesterol esters to VLDL in exchange for triglycerides through CETP

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15
Q

What is important about ABC A1?

A

• ATP binding cassette (ABC) transporter
• Very important in the transport of cholesterol from periphery to apo-A1
• Tangiers disese = deficiency in ABC A1
○ Unable to remove cholesterol from peripheral tissues
○ Low levels of HDL and have premature atherosclerosis
○ ORANGE TONSILS - classic finding
○ Accumulation of cholesterol in lymphatic tissues

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16
Q

What is • Tangiers disease?

A

• Tangiers disease = deficiency in ABC A1
○ Unable to remove cholesterol from peripheral tissues
○ Low levels of HDL and have premature atherosclerosis
○ ORANGE TONSILS - classic finding
○ Accumulation of cholesterol in lymphatic tissues

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17
Q

What is important to know about the LCAT enzyme?

A

• LCAT = lecithin cholesterol acyl transferase
• AKA = PCAT
• Catalyses the transfer of a fatty acid from the phospholipid lecithin to un-esterified cholesterol
• The product of this reaction is cholesterol ester, more non-polar and more tightly bound to HDL particle
○ “trapped” for transport to the liver
• Deficiency in this enzyme means low HDL levels
• COMPLICATIONS = corneal opacities, reanal insufficiency and hemolytic anemia due to the accumulation of un-esterified cholesterol in tissues
• Renal failure is main problem here
• Atherosclerosis is NOT as big a problem as you would expect
• Look for “fish eye disease” or cholesterol deposition in the eye causing corneal opacities

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18
Q

What is important about CETP?

A

• Cholesterol ester transfer protein = CETP
• Catalyzes the exchange of the non-polar lipids
○ Cholesterol esters and triglycerides
• The transfer is between lipoprotein particles of different class
• Normally the CE from HDL is exchanged for Tg present in VLDL and remnants
○ This is an alnernative Tg clearance pathway
• As HDL is more Tg enriched it is taken out of circulation (leading to lower HDL levels)
• If you have low amounts of this protein, you have high HDL levels, and patients live longer than average
○ BUT medically interfering with this as of now has unforseen CV risk.
○ Thus, we don’t know all that much about the reverse transport pathway

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19
Q

What does apoC3 do?

A
  • Inhibits LPL and as a result high apoC3 means high triglyceride levels and increased risk for CV disease
    • Inhibition of apoC3 for treatment of hypertriglyceridemia is under investigation
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20
Q

What is the ligand for the remnant receptor?

A
  • apoE

* Deficiency predisposes to CV disease because of reduced clearance of remnant particles

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21
Q

What is the ligand for the LDL receptor?

A

• apoB100

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22
Q

what marker is best for cardiovascular disease risk stratification among patients?

A
  • there is a substantial body of data that risk stratifying patients based on their LDL-C level and treating this marker (with statins) has beneficial effects on CVD risk.
  • For this reason, LDL-C levels are the focus of most lipid evaluation and treatment strategies.
  • The level of LDL cholesterol is closely related to CVD risk and is amenable to treatment. Thus, LDL is the most important lipid parameter to address clinically.
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23
Q

what is the Friedwald formula?

A
  • method of calculating LDL cholesterol levels from total cholesterol measurement
  • HDL is easier to measure, total cholesterol is easier to measure, triglycerides is easier to measure
  • in a fasting state you shouldn’t see chylomicrons, remnants, or IDLs
  • also, the Tg/5 assumption only works if there is less than 400mg/dL triglycerides when no chylomicrons are present

*LDL-C = Total Cholesterol – HDL-C – (Triglycerides ÷ 5)

24
Q

What are the risk factors for CVD that add to LDL-c level specific risk?

A 
Age, (males > than females)
Caucasian vs. African American 
Higher total cholesterol
Lower HDL-C
Current cigarette smoking
Systolic BP >140 or on antihypertensive medications
Diabetes
25
Q

The “classic” risk factors are the only ones that go into the online risk estimator. But, technically, what are other risk factors for CVD?

A

There are other known but less established risk factors for CVD:

  • life-habit risk factors
    • obesity, insulin resistance, sedentary lifestyle, atherogenic diet, and psychosocial factors.
  • emerging risk factors:
    • apo B, LDL particle number, lipoprotein (a), high sensitivity C - reactive protein (hsCRP), pro-thrombotic factors, and evidence of ‘subclinical’ atherosclerosis
26
Q

What are secondary causes of hypercholesterolemia and how do you screen for them?

A

Secondary causes of increased LDL-C:
*diets high in saturated and trans fat, hypothyroidism, nephrotic syndrome, obstructive liver disease and cyclosporine.

*screening = HandP and send the following lab tests: serum TSH, a urine dipstick for protein and liver function tests

27
Q

What are the only 2 general causes for increased LDL-C?

A

too much production, or not enough catabolism

28
Q

what might lead to increased LDL production?

A

a. Increased LDL-C Production:
* When increases in VLDL particle number ± the triglyceride content of VLDL ensue, increases in plasma apo B are typically present.
* In this setting (high VLDL and high apoB) increases in LDL-C relate to the conversion of the increased number of VLDL particles to LDL by the lipoprotein lipase reaction in tissues.

29
Q

what might lead to decreased LDL catabolism as the cause for LDL hypercholesterolemia?

A

Familial Hypercholesterolemia (FH).

  • FH is an autosomal dominant disorder that is a partial (heterozygote) or complete (homozygote) absence/defectiveness of the LDL receptor.
  • Approximately 50% of these patients are LDL receptor-negative; the other 50% are LDL receptor-defective (defects in receptor function).
  • LDL-C levels are 2-3 times normal (200-300 mg/dl) in heterozygotes and 5-8 fold elevated (500-800 mg/dl) in homozygotes.
  • Premature death from atherosclerosis is common in both forms, occurring often before age 20 in homozygotes.

*Other causes include mutations in the genes for apolipoprotein B, PCSK9 and G5G8 that mediates plant sterol absorption in the intestine.

30
Q

What is FH (when talking about cholesterol)

A

Familial Hypercholesterolemia (FH).

  • FH is an autosomal dominant disorder that is a partial (heterozygote) or complete (homozygote) absence/defectiveness of the LDL receptor.
  • Approximately 50% of these patients are LDL receptor-negative; the other 50% are LDL receptor-defective (defects in receptor function).
  • LDL-C levels are 2-3 times normal (200-300 mg/dl) in heterozygotes and 5-8 fold elevated (500-800 mg/dl) in homozygotes.
  • Premature death from atherosclerosis is common in both forms, occurring often before age 20 in homozygotes.
31
Q

How would a defect in affect LDL levels?

A

•PCSK9 is an important regulator of LDL receptor degradation, because binding of PCSK9 to the LDL receptor results in degradation of the receptor, thereby preventing LDL receptor recycling.

  • Loss of function mutations of PCSK9 are associated with increased LDL receptor function, low LDL-C, and reduced ASCVD,
  • however, gain of function mutations of PCSK9 may lead to clinical FH, because PCSK9 reduces hepatic LDL receptor activity, the site of over 70% of LDL clearance.
32
Q

What physical exam findings make you think inherited cholesterol (LDL) problems?

A

• In genetic forms of LDL-C, arcus cornealis, xanthelasma and/or tendinous xanthomata can be seen on physical exam.

33
Q

what are normal fasting triglyceride levels?

A

Normal fasting triglyceride levels are crudely defined as <150 mg/dl.

34
Q

when do you start running into immediate problems with hypertriglyceridemia?

A

When triglyceride concentrations are >500-1000 mg/dl, the clearance of chylomicrons approaches saturation kinetics
*>1000 mg/dl means a predictable pathophysiology

  • Consequently, the serum becomes lipemic (looks like milk), and other manifestations including pancreatitis can occur.
35
Q

What physical exam findings scream really bad hypertriglyceridemia?

A

Physical manifestations of severe hypertriglyceridemia, most typically seen with more severe chylomicronemia, include

  • lipemia retinalis (fatty serum in the small vessels of the retina),
  • eruptive xanthomas (small yellowish papules on the extensor surfaces of the arms and also on the abdomen and back), and
  • hepatosplenomegaly (from triglyceride infiltration).
36
Q

What drugs can cause secondary hypertriglyceridemia

A

including thiazides, beta-blockers, glucocorticoids, protease inhibitors, oral estrogens and retinoids).

37
Q

What medical conditions can cause secondary hypercholesterolemia?

A
  • poorly controlled DM
  • central obesity
  • alcohol use,
  • nephrotic syndrome,
  • renal failure,
  • hepatitis
38
Q

what can cause increased triglyceride production?

A

a. Increased VLDL Production:
• Increases in VLDL production are most commonly a result of insulin resistance. insulin has a profound anti-lipolysis effect, so in states of insulin resistance there is increased free FA floating back to the liver
• Drugs, e.g. protease inhibitors (used to treat HIV infection), oral estrogens, nephrotic syndrome and chronic renal failure may also contribute to this pathophysiology.
• Alcohol partially inhibits VLDL secretion (which can result in fatty liver), but also enhances fatty acid production from the ethanol derived carbons; in many people hypertriglyceridemia can result.

39
Q

What can cause decreased triglyceride catabolism and thus hypertriglyceridemia?

A

Decreased triglyceride is a problem with lipoprotein lipase (LPL) or its activity.
• Primary defects can be a result of LPL deficiency, deficiency of apo C2 (the specific apoprotein activator of LPL),
*can also be a problem with the GPI-anchoring of LPL to the endothelium
• Familial Dysbetalipoproteinemia (described below)
• Secondary disorders such as diabetes, alcohol and chronic renal failure can also reduce triglyceride-rich lipoprotein catabolism by decreasing LPL.

40
Q

any triglyceride concentration over 1,000mg/dL will cause the blood to look milky and all sorts of problems. What could ever make it so a patient has 30,000mg/dL?

A

*essentially several hits from several angles to the pathway of LDL metabolism
(Severe Hypertriglyceridemia):
*Since LPL-mediated triglyceride removal is a saturable enzyme system and both chylomicrons and VLDL compete for LPL, severe hypertriglyceridemia is possible when several disorders of lipoprotein triglyceride synthesis and/or catabolism are simultaneously present and fat remains in the diet.

*Patients with absolute LPL deficiency or two or more disorders of triglyceride metabolism (e.g. genetic disorder of overproduction of VLDL + an acquired disorder), may have fasting triglyceride levels that exceed 1000 mg/dl and sometimes reach levels of 30,000 mg/dl.

41
Q

What estimates CVD risk better than LDL-C levels?

A

Non-HDL-C levels (total cholesterol - HDL) correlate closely with obesity, especially central or visceral obesity and are a strong predictor of ASCVD events and death.

  • Some studies have found this parameter to be a better predictor of mortality than LDL-C.
  • Elevated non-HDL-cholesterol can be associated with high levels of LDL and/or VLDL and is also commonly associated with the “metabolic dyslipidemia” seen in insulin resistant states and the metabolic syndrome.
  • The metabolic dyslipidemia is manifest by increased triglycerides, low HDL-C, and small dense LDL. Small dense LDL is more likely to be oxidized which may relate to atherosclerosis development.
42
Q

What’s up with FD? (in the discussion of lipoprotein level disorders)

A

• Familial Dysbetalipoproteinemia (FD or broad beta disease)

  • is due to disturbances in IDL and remnant catabolism.
  • FD is manifest by an approximately equivalent increase in both total cholesterol and triglycerides. (remnants contain a relative balance between Tg and cholesterol)
  • FD most often occurs due to genetic variation in Apo E, with the ApoE2 isoform conferring increased risk of abnormal triglyceride-rich lipoprotein metabolism.
  • This is a consequence of defective binding of apo E2 to hepatic receptors that recognize VLDL and chylomicron remnants.
  • Planar xanthomata, usually on the palms or soles, are characteristic of this condition.
  • Premature atherosclerosis is common.
43
Q

What are the indications for statin therapy?

A

Indications for Statin Therapy

  • Secondary prevention - clinical ASCVD
  • LDL–C >190 mg/dL, Age >21 years
  • Primary prevention – Diabetes: Age 40-75 years, LDL–C 70-189 mg/dL
  • Primary prevention - No Diabetes: ≥7.5% 10-year ASCVD risk (online calculator that plugs in the major risk factors), Age 40-75 years, LDL–C 70-189 mg/dL‡
44
Q

What are the three general classes of statin therapy and what can you expect them to do to LDL-C levels?

A

*Think high intensity when you see this (50% reduction)
Atorvastatin
Rosuvastatin

*think moderate intensity when you see this (30-50% reduction)
simvistatin

*think low intensity when you see these (less than 30% reduction)
pravistatin
lovastatan

45
Q

When should you use the high, moderate, or low statin therapy?

A 
Not recommended to use low intensity
use high intensity:
* ANY secondary prevention 
*and in primary prevention when LDL-C >190 mg/dL
*when diabetes is present (period)

Use moderate-intensity statin:
*when the 10-year ASCVD risk is ≥7.5%.

46
Q

statins are interesting in that they reduce LDL-C levels more through a mechanism NOT their primary target/mechanism of action. What is that all about?

A

Although the primary mechanism of action for the statins is to inhibit the enzyme HMG CoA reductase, the primary means by which they lower LDL-C is by increasing the number of intra-hepatic LDL receptors and increasing the subsequent uptake and catabolism of circulating LDL.

47
Q

What are the adverse effects of statin therapy?

A

Overall statins are very well tolerated.
*The major serious adverse effects are rare and include hepatic transaminase elevation >3x normal in <0.3% and rhabdomyolysis in 0.01% of patients.

*In primary care settings myopathy defined as myalgias and/or elevations in CPK occurs in ~10-20% of statin-treated patients.

  • There is a higher risk of these complications when a statin is combined with other lipid lowering medications such as fibrates or niacin.
  • Additionally, combining a statin with drugs that inhibit their metabolism, e.g. CYP3A4 inhibitors such as ketoconazole, protease inhibitors, or large consumptions of grapefruit juice can increase the risk of adverse events including myopathy.
  • Other conditions including chronic renal insufficiency or hypothyroidism increase the risk of myopathy with statins.

*Finally, statins are also associated with a ~10% risk of new-onset type 2 diabetes. Preexisting glucose intolerance or a positive family history of diabetes predispose to this outcome. Despite new-onset diabetes, these patients also benefit from statin therapy and CVD risk reduction, and therefore if indicated a statin should still be prescribed.

48
Q

When should bile acid sequestrants be used as a monotherapy?

A

Hardly ever, except for specific special circumstances. they just don’t work as well
* Thus, presently bile acid sequestrants are an add-on therapy and only appropriate to consider as monotherapy if statins are not tolerated, or during pregnancy.

49
Q

How do bile acid sequestrants work and how much of a reduction in LDL-C can you expect with their use?

A

MOA= reduce the enterohepatic circulation of bile acids.
*Because bile acids are synthesized in the liver from cholesterol, bile acid sequestrants produce a reduction in the intra-hepatic pool size of cholesterol and reduce circulating LDL-C by increasing intra-hepatic LDL receptors.
*Sequestrants reduce LDL-C by 10-30%.
The side effects are primarily GI and include nausea, bloating and constipation.

50
Q

What is Ezetimibe?

A

(cholesterol drug)
Ezetimibe lowers cholesterol by selectively inhibiting cholesterol absorption.
* Because less cholesterol reaches the liver, the LDL-C lowering effect is via increases in the LDL receptor.
*Like the bile acid sequestrants, ezetimibe should not be used as monotherapy in the prevention or treatment of ASCVD but the drug may be beneficial in combination with statins to further reduce CVD risk in high risk patients with inadequate lowering of LDL-C with statins.
*The IMPROVE-IT Trial whereas in ezetimibe vs. placebo lowered LDL-C by ~20% in addition to simvastatin reduced major CVD events.
*Ezetimibe has no side effects.

51
Q

If a patient is just not getting their LDL-C levels down to your satisfaction, can you combine your cholesterol medications?

A

Although all 3 classes of cholesterol-lowering drugs work through the intra-hepatic LDL receptor, their effects are additive.

52
Q

What humanized antibodies can be used to lower LDL-C levels in a hurry?

A

PCSK9 Inhibitors: lowers LDL-C by up to 60%
*alirocumab and evolocumab have been approved as adjuncts to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C.

53
Q

gemfibrozil and fenofibrate are what type of drug? What are the indications for use?

A

These are fibrates

  • use in secondary prevention of events when added to a statin in patients with diabetes or with existing ASCVD who are hypertriglyceridemic and have lower levels of HDL-C.
  • they work by Fibrates lower TG by 20-40%, and also raise HDL-C by 5-15%.
54
Q

What can you expect addition of fibrates to your statin therapy to do?

A

Fibrates lower TG by 20-40%, and also raise HDL-C by 5-15%.

55
Q

What does Niacin do?

A

Niacin or nicotinic acid lowers LDL-C and TG, and raises HDL-C.

  • evidence is shaky on the benefit though
  • Moreover, niacin is associated with many side effects including flushing, rash, GI distress, hepatotoxicity, myopathy, glucose intolerance, hyperuricemia and gout. .
  • Niacin decreases synthesis of VLDL and secondarily LDL and also increases HDL by decreasing the catabolism of apo AI.
  • Niacin lowers LDL-C by 5-25%, decreases TG by 15-35%, and raises HDL-C by10-30%.

DEMS (30 decks)

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