Lipoproteins

Question 1

ApoB-100 Abnormality

Answer 1

High blood levels of LDL

Question 2

Apo E Deficiency or Less Activity

Answer 2

accumulation of IDL and Chylomicron remnants in the blood

Question 3

ApoC-II Deficiency

Answer 3

elevated levels of chylomicrons and VLDL in the blood

Question 4

Where is HDL filled with cholesteryl esters?

Answer 4

in the blood

Question 5

CETP

Answer 5

Connects HDL and VLDL and allows for interchange of totally non polar lipids in the blood. Protein that provides a blood bridge between VLDL and HDL and forms a hydrophobic channel. Allows for movement of cholesterol esters from HDL into VLDL in exchange for TAGs.

Question 6

Hypoalphalipoproteineimia (low HDL)

Hypolipidemia

Answer 6

characterized by very low HDL-C levels below 35 mg/dl and low Apo A-1 levels. Hereditary: Tangier disease. May be acquired and related to obesity, smoking, and some medical drug treatment

Question 7

Abetalipoproteinemia (now or low LDL)

Hypolipidemia

Answer 7

rare hereditary disease caused by an abnormal MTP (microsomal TAG transfer protein)

Question 8

Tangier Disease

Answer 8

rare hereditary disease. Indicated by orange colored tonsils, common symptoms are peripheral neuropathy and premature MI. There is an accumulation of cholesteryl esters found in the tonsils, liver, spleen, and sometimes the corneal opacities

Question 9

How does a defective ABC-transporter lead to Tangier Disease?

Answer 9

It leads to less substrate for LCAT and to early degradation of the lipid poor apoA-1 in the blood. This results in very low HDL levels

Question 10

Clinical Features of Abetalipoproteinemia

Answer 10

Fat malabsorption with severe neonatal steatorrhea, failure to thrive, TAG accumulation in liver and intestine. retinitis pigmentosa, progressive blindness, and peripheral neuropathy

Question 11

What are the two types of hyperlipidemias?

Answer 11

Hypertriacyglycerolemia (high TAGs) and hypercholesterolemia (high cholesterol)

Question 12

Friedwald Equation

Answer 12

[LDL-C]=[total C]-([HDL-C]+[TAG:5])

Question 13

What values are measured and used to calculate LDL-C in the Friedewald equation?

Answer 13

HDL-C and VLDL-TAGS are measured

Question 14

Fredericton Classification

Answer 14

Way to classify hyperlipidemia which described their abnormal pattern of blood lipoproteins

Question 15

Type I: Familial Hyperchylomicronemia

Answer 15

Rare disease characterized by high chylomicron levels after an overnight fast. Can be grouped into Type Ia (deficiency of LPL), type Ib (deficiency of apoC-II), and Type Ic (inhibitor protein for LPL). Onset in childhood, often abdominal cholic.

Question 16

Eruptive Xanthomas

Answer 16

Occur in clusters on the skin of the trunk, buttock, or extremities. Result of familiar hyperchylomicronemia.

Question 17

Type IIa: Familiar Hypercholesterolemia

Answer 17

Common disease characterized by high LDL levels and normal VLDL levels. Autosomal dominant disease with a defective LDL receptor. Adult onset with risk of coronary heart disease. Treated with statins and other drugs.

Question 18

Type IIb: Familiar Combined Hyperlipidemia

Answer 18

Common diseased characterized by high LDL levels and also high VLDL levels. Overproduction of apoB-100 and VLDL, and defective clearance of LDL. Puberty onset, risk of coronary heart disease.

Question 19

Type III: Dysbetalipoproteinemia

Answer 19

rare disease characterized by high remnant levels and abnormal beta-VLDL. High blood cholesterol levels mainly from IDL. Results from app E deficiency. Homozygous for the inefficient apoE-2 and lack the normal apoE-3. Xanthomas on the palms, elbows, and knees. Adult onset with accelerated atherosclerosis.

Question 20

Type IV: Familial Hyperprebetalipoproteinemia

Answer 20

High VLDL due to a specific LPL deficiency or from overproduction of VLDL. High serum TAGs increases the risk of pancreatitis.

Question 21

Type V: Familial Mixed Hypertriacylglycerolemia

Answer 21

High chylomicron microbe and high VLDL levels. Leads to elevated levels of both TAG-rich lipoproteins. Patients blood is characterized by a creamy layer on top and in addition to a turbid lower part due to high VLDL

Question 22

What do statins competitively inhibit?

Answer 22

HMG CoA reductase

Question 23

Treatments of Hyperlipidemia

Answer 23

Reception of free hepatic cholesterol or reduction of VLDL in the serum

Question 24

Ezetimbie

Answer 24

Reduction of dietary uptake of cholesterol

Question 25

Cholestyramine

Answer 25

reduced hepatic cholesterol by bile acid binding and excretion

Question 26

Statins

Answer 26

Inhibition of cholesterol synthesis, target organ is the liver

Question 27

Niacin

Answer 27

Reduces TAGs and LDL-cholesterol and raises HDL. Side effects are flushing and nausea. Treatment for Type IIb.

Question 28

Fibrates

Answer 28

Lowers VLDL in blood via decreased VLDL synthesis and increased LPL activity. Inhibit app C-III synthesis in hepatocytes. Increase HDL via apoA synthesis in hepatocytes.