LIPID TRANSPORT AND ATHEROSCLEROSIS

Question 1

STATE THE SUBSTANCES THAT CONTAIN IN THE NASCENT CHYCLOMICRONS (NC).

Answer 1

1. TG
2. CE
3. FAT SOLUBLE VITAMIN (A, D, E, K)
4. APO B-48

Question 2

WHERE DOES THE NC SYNTHESISED?

Answer 2

IN THE INTESTINE

Question 3

DESC THE TRANSPORT OF NC TO THE PRERIPHERAL TISSUES.

Answer 3

1. AFTER A MEAL, A NC IS SYNTHESISED BY THE INTESTINE. IN THE NC, THERE IS TG, CE, FAT SOLUBLE VITAMINS AS WELL AS APO B-48.
2. IN THE PLASMA, THIS NC WILL RECEIVE APO-E AND APO-Cii FROM THE HDL. THIS CAUSES THE NC TO BECOME A MATURE AND FUNCTIONAL CHYCLOMICRON (CM)
3. IN THE CAPILLARY WALL THERE IS LPL THAT IS NOT ACTIVATED. THIS LPL WILL BECOME ACTIVATED DUE TO THE PRESENCE OF APO Cii IN THE CM. AS A RESULT, DEGRADATION OF TG INTO FA AND GLYCEROLS THAT IS CATALYSED BY THE LPL OCCURED. FA WILL BE USED AGAIN TO RESYNTHESIS TG AND STORED IN THE ADIPOSE TISSUE OR BE USED AS ENERGY. AS FOR THE GLYCEROLS, IT WILL BE USED TO SYNTHESISED LIPIDS OR FOR GLUCONEOGENESIS IN THE KIDNEY OR LIVER.
4. THE CM WILL REDUCED IN SIZE AND IT WILL RETURN THE APO Cii TO THE HDL. NOW THE CM BECOME A CM REMNANT.
5. THE CM REMNANT WILL BE ENDOCYTOSED IN THE LIVER VIA THE APO E MEDIATED PROCESS IN WHICH THE CM WILL BE DEGRADED INTO FREE CHOLESTEROLS AND FA, AND AMINO ACIDS.

Question 4

DESC THE TRANSPORT OF VLDL TO THE PERIPHERAL TISSUES.

Question 5

DESC THE TRANSPORT OF CHOLESTEROL TO LIVER AND EXTRAEPATIC TISSUE BY THE LDL.

Question 6

DESC THE REVERSE CHOLESTEROL TRANSPORT BY THE HDL

Question 7

STATE THE FUNCTION OF THE HDL.

Answer 7

1. RESERVOIR FOR APO Cii
2. UPTAKE OF THE UNESTERIFIED/ FREE CHOLESTEROL FROM PERIPHERAL TISSUES TO LIVER
3. ESTERIFICATION OF CHOLESTEROL
4. REVERSE CHOLESTEROL TRANSPORT

Question 8

STATE THE DEFECT THAT CAN BE FOUND IN TYPE
1. TYPE I
2. TYPE IIa
3. TYPE IIb
4. TYPE III
5. TYPE IV
6. TYPE V

Answer 8

TYPE
1. TYPE I - LPL
2. TYPE IIa - LDL-R
3. TYPE IIb - APO-B RECEPTOR AND HDL DEFICIENCY
4. TYPE III - APO E
5. TYPE IV - VLDL OVERPRODUCTION
6. TYPE V - APO Cii

Question 9

STATE THE RF OF ATHEROSCLEROTIC PLAQUE FORMATION.

Answer 9

1. HYPERLIPIDEMIA
2. HYPERTENSION
3. GENETIC FAMILY HISTORY OF ATHEROSCLEROSIS
4. CIRCULATION OF ROS
5. CHRONICALLY ELEVATED BLOOD GLUCOSE

Question 10

STATE THE SEQUENCE OF EVENTS LEADING TO THE FORMATION OF ATHEROSCLEROSIS.

Answer 10

KEYPOINTS!
1. ENDOTHELIAL INJURY
2. INFLAMMATORY RESPONSE
3. RELEASED CELL SURFACE ADHESION MOLECULES
4. PENETRATION OF MONOCYTE AND T LYMPHOCYTE INTO THE SUIBENDOTHELIAL
5. MONOCYTE -> MACROPHAGE, RELEASE CYTOKINE
6. LDL HIGH, INFILTRATIONS AND RETAINED IN THE INTIMA LAYER, OXIDISED
7. MACROPHAGE ENGULF, FOAM CELL ACCUMULATION
8. UNDERGOES APOPTOSIS, LIPID IN THE INTIMA -> FATTY STREAK
9. T- LYMPHOCYTE -> CYTOKINE, SMC MIGRATE AND PROLIFERATE
10. ACCUMULATION OF SMC AND LIPIDS IN THE INTIMA, RAISE THE INTIMA, ENCROACH THE LUMEN, ATHEROSCLETIC PLAQUE
11. RUPTURE, TRIGEGER ACUTE TROMBOSIS

Question 11

STATE THE MUTATION THAT OCCUR IN FH.

Answer 11

MUTATION IN:
1. LDLR GENE
2. APO B100
3, PCSK9 GENE