Partial 4 - Lipoproteins

Question 1

Lipoproteins consist of

Answer 1

nonpolar lipid core of TAGs, cholesteryl esters, then monolayer of amphipathic lipids such as phospholipids and two types of proteins

Question 2

Apo A-I

Answer 2

is the principal protein in HDL and activates LCAT

Question 3

Apo A-II

Answer 3

occurs as dimer mainly in HDL and enhances hepatic lipase activity

Question 4

Apo B-48

Answer 4

is found only in chylomicrons, enhances chylomicron secretion from intestine, lacks the LDL receptor binding domain in Apo B-100

Question 5

Apo B-100

Answer 5

is the principal protein in LDL that binds to LDL receptor

Question 6

Apo C-I

Answer 6

is found in Chylomicrons, VLDL, and HDL and may also activate LCAT

Question 7

Apo C-II

Answer 7

is found in chylomicrons, VLDL, and HDL and activates lipoprotein lipase

Question 8

Apo C-III

Answer 8

is found in chylomicron, VLDL, IDL, and HDL and inhibits lipoprotein lipase by inhibiting Apo C-II

Question 9

Apo D

Answer 9

is found in HDL and is also called cholesterol ester transfer protein (CETP)

Question 10

Apo E

Answer 10

is found in chylomicron, VLDL, IDL, and HDL and binds to LDL receptor and chylomicron remnant receptor in liver

Question 11

Apo H

Answer 11

is found in chylomicrons and is also known as β-2-glycoprotein I and is involved in TAG metabolism

Question 12

Apo E4

Answer 12

is implicated in Alzheimer`s disease and other neurological conditions.

Atherosclerosis, impaired congnitive function, reduced hippocampal volume, HIV, ischemic cerebrovascular disease, faster progression in Multiple Sclerosis, Sleep apnea

Question 13

All apoproteins are found in chylomicrons except

Answer 13

B-100 and D

Question 14

Which LDL values are desirable, borderline high and high

Answer 14

Desirable: <130 mg/dl
Borderline high 130-159 mg/dl
High: >160 mg/dl

Question 15

HDL are composed of

Answer 15

They are mainly composed of proteins (50%) and cholesteryl esters (20%).

Question 16

HDL is formed

Answer 16

in liver and intestine where it interacts with chylomicron remnants and LCAT to form HDL3 by taking up cholesterol from peripheral tissues via a lipid transporter called ABCA1 (ATP-binding cassette transporter)

Question 17

Lipoproteins (a) - Lp (a)

Answer 17

They are altered form of LDL that contains apoB-100 covalently linked to apo A, and is considered to be an independent risk factor for the development of atherosclerosis.

Question 18

Lp (a) mechanism

Answer 18

enhances cholesterol delivery to injured blood vessels, suppresses the generation of plasmin, and promotes smooth muscle proliferation

Question 19

The primary and secondary bile acids are reabsorbed from

Answer 19

Almost exclusively in the ileum returning to the liver by way of the portal circulation (enterohepatic circulation)

Question 20

HLP Type I

Answer 20

Familial lipoprotein lipase deficiency (Type I hyperlipoproteinemia) is a rare disorder caused by deficiency of lipoprotein lipase or its coenzyme, apolipoprotein C-II. There is also reduced HDL. The result is fasting chylomicronemia and hypertriacylglycerolemia.

Question 21

HLP Type II-A

Answer 21

A deficiency of functional LDL receptors (thus LDL catabolism) causes a significant elevation in plasma LDL and, therefore, of plasma cholesterol. Patients with such deficiencies have Type II hyperlipidemia (familial hypercholesterolemia, FH) and premature atherosclerosis, with xanthomas of skin and tendons

Question 22

HLP Type II-B

Answer 22

Defect in HMG-CoA reductase. Increased production of VLDL and impaired LDL catabolism leads to raised VLDL and LDL. There is also often reduced HDL.

Question 23

HLP Type III

Answer 23

Defective recognition of apo E2 which causes deficiency in clearance of IDL. These individuals have familial Type III hyperlipoproteinemia (dysbetalipoproteinemia), with hypercholesterolemia, Triglycerides and premature atherosclerosis (formerly known as broad beta disease).

Question 24

HLP Type IV

Answer 24

(Familial combined hyperlipidemia) Hyperprebetalipoproteinemia is due to impaired VLDL catabolism and thus associated with raised levels of VLDL (and thus TAG levels) and often reduced HDL.

Question 25

HLP Type V

Answer 25

Hyperlipoproteinemia type V, also known as mixed hyperlipoprotenemia is very similar to type I, but with high VLDL in addition to chylomicrons. It happens due to decreased lipoprotein lipase (Apo C-II deficiency), in addition to VLDL hypersecretion. This leads to raised levels of chylomicrons and VLDL.

Question 26

In atherogenesis endothelial dysfunction leads to

Answer 26

decreased synthesis of vasodilators and increased synthesis of vasoconstrictors, as well as it leads to increased flux of LDL into arterial wall

Question 27

Macrophages recognize oxidized lipoproteins through

Answer 27

Scavanger receptors, where they engulf them and become foam cells

Question 28

What other cells then macrophages can become foam cells?

Answer 28

Smooth muscle cells

Question 29

Two most common causes of endothelial dysfunction

Answer 29

Hemodynamic disturbances and hypercholesterolemia

Question 30

Hemodynamic disturbances means

Answer 30

where the is turbulent blood flow (ostia of vessels, at branch points, along posterior wall of the abdominal aorta etc.)

Question 31

Mediators commonly seen in atherosclerotic lesions

Answer 31

Monocyte chemoattractant protein 1 (MCP-1)
Tumor necrosis factor alpha (TNFa)
Intracellular adhesion molecule 1 (ICAM-1)
Vascular cell adhesion molecule (VCAM-1)

Question 32

Lipid profile

Answer 32

Total cholesterol level should be lower than 200 mg/dl
LDL-cholesterol should be lower than 100 mg/dl
HDL-cholesterol should be higher than 60 mg/dl
TAGs should be lower than 150 mg/dl.

Question 33

Metabolic syndrome is characterized by

Answer 33

central obesity (more than 40 inches in men and 35 in women), insulin resistance (fasting glucose 110-125 mg/dL), hypertension (blood pressure 130/85), dyslipidemia HDL cholesterol in men less than 40 mg/dL and less than 50 mg/dL in women, and TAGs more than 150 mg/dL), hypercoagulability, and a proinflammatory state.

Question 34

Primary dyslipidemias include

Answer 34

Chylomicronemia, hypercholesterolemia, dysbetalipoproteinemia, hypertriglyceridemia, mixed hyperlipoproteinemia, and combined

Question 35

Secondary dyslipidemias is caused by other diseases such as

Answer 35

Diabetes mellitus, pancreatitis, renal disease, hypothyroidism

Question 36

Primary (genetic) causes of low HDL

Answer 36

(1) Tangier disease
(2) Familial hypo-α-lipoproteinemia
(3) Apo A-I deficiency
(4) LCAT deficiency
(5) CETP deficiency leading to increased apo A-I, HDL- C enriched in CE
(6) Hepatic lipase deficiency

Question 37

Tangier disease

Answer 37

defects in ABCA1 transporter which promotes movement of cholesterol from peripheral cells to the lipid-poor HDL cholesterol, and is characterized by accelerated atherosclerosis and little or no HDL cholesterol, as well as accelerated catabolism of apo A-I + II, and cholesterol accumulation leads to enlarge orange tonsils, hepatosplenomegaly, and peripheral neuropathy

Question 38

Two forms of LCAT deficiency

Answer 38

Familial LCAT deficiency (complete) or partial LCAT deficiency (Fish-eye disease)

Question 39

Chylomicron function

Answer 39

carry dietary TAGs, cholesterol, Fat-soluble vitamins, and cholesteryl esters to the peripheral tissues

Question 40

Where is lipoprotein lipase most abundant?

Answer 40

Cardiac muscle

Question 41

Abetalipoproteinemia

Answer 41

Abetalipoproteinemia is a rare hypolipoproteinemia caused by a defect in microsomal triacylglycerol transfer protein (MTP), leading to an inability to load apo B with lipid. As a consequence, no VLDL or chylomicrons are formed, and triacylglycerols accumulate in the liver and intestine.

Question 42

What levels of triglyceride levels are classified as abnormal

Answer 42

> 200 mg/dL are classified as abnormal
150-200 mg/dL is borderline high
<150 mg/dL is normal