1. Describe the role of bile salts in the digestion and absorption of lipids.
2. What is steatorrhea? What are the conditions that can cause it and what is the outcome?
3. Discuss the steps of beta oxidation of a fatty acid with 16 carbon atoms. What will be the net energy yield per mole upon its complete oxidation?
4. How is fatty acid oxidation switched off when the active synthesis of fatty acid is in process?
Or
5. Discuss the regulation of fatty acid oxidation.
6. Which process out of fatty acid synthesis or fatty acid oxidation would predominate during starvation? Discuss the steps,energetics and regulation of that pathway?
7. Give a brief account of Alpha oxidation of fatty acids. What is its biological or clinical significance?
8. If a person fails to metabolize Phytanic acid which is a normal component of dairy products and green vegetables, what could be the possible defect? What would be the clinical manifestations and how can this defect be treated?
or
9. Discuss the causes, consequences,laboratory diagnosis and treatment of Refsum disease.
10. What is the role played by Carnitine in mitochondrial oxidation of long chain fatty acids?
11. What is the cause of non ketotic hypoglycemia in Carnitine deficiency?
12. Discuss the causes, consequences and laboratory diagnosis of-
i)Jamaican sickness ii) Sudden cot death syndrome iii) Zellwegar syndrome
13.-What is ketosis ? Outline the steps of formation and utilization of ketone bodies.
14.- Why it is said that ketone bodies are synthesized in liver and utilized in the peripheral tissues?
15- Give a flow chart representation of biochemical basis of ketosis in starvation and Diabetes mellitus.
16. What are the clinical features,laboratory findings and possible treatment of Ketosis?
17-Discuss the steps of de novo biosynthesis of fatty acids. How is this pathway regulated?
18- Give a diagrammatic representation of fatty acid synthase complex.
19- Discuss the regulation of fatty acid synthesis in the presence of i) Excess of citrate ii) Palmitic acid and describe the long term control of fatty acid synthesis if a person has developed a compulsive urge to eat carbohydrate rich diet.
20- De novo Fatty acid synthesis is a cytoplasmic process while its precursor Acetyl co A is present in the mitochondrion,how is that transported out in to the cytoplasm ?
21- “Fatty acid oxidation is not simply a reversal of fatty acid synthesis”, justify the statement giving the details of differences.
22- Discuss the steps and regulation of denovo synthesis of cholesterol.
23- Discus the significance of reactioncatalyzed by HMG Co A reductase.
24- What is the normal level of serum total cholesterol? What are the different conditions in which variations of serum total cholesterol level are observed?
25 Differentiate between LCAT (LecithinCholesterol Acyl Transferase) and ACAT (Acyl cholesterol acyl transferase) by giving at least three points of differences.
26- Discuss the steps of formation of bile acids. How is this pathway regulated?
27- How do bile acid sequestrants help in lowering serum total cholesterol levels?
28- Why it is said that equimolar amount of bile salts and phospholipids are needed during excretion of cholesterol in bile? What will happen if the bile salts or phospholipids are deficient?
29- What do you understand by cholelithiasis? What is the biochemical defect and what are the clinical manifestations in the affected patients?
30- What are lipoproteins? Discuss the general structure and classification of lipoproteins.
31- Discuss the functions of different apo-proteins giving examples.
32- What is meant by down regulation of LDLreceptors? What is the clinical significance associated with it?
33- Discuss the role of lipoprotein lipase in the metabolism of lipoproteins. What is clearing factor? What will be the clinical outcome if lipoprotein lipase is deficient?
34- Give a detailed account of hyperlipidemia. What is the possible line of treatment for this group of disorders?
35.- Discuss the central role of Acetyl coA giving the details of its sources andchannels of utilization.
36- Give a brief account of hypolipidemic drugs.
37- How do polyunsaturated fatty acids help in lowering serum total cholesterol levels?
38- Give a brief account of metabolism of HDL highlighting the process of reverse cholesterol transport.
39- Why is LDL called a bad cholesterol while HDL a good cholesterol?
40- What is Lp (a) ? Discuss its clinicalsignificance?
41- Outline the reaction catalyzed by each of the following enzymes-
i) Acetyl co A carboxylase
ii) HMG Co A reductase
iii) Thiokinase
iv) Thiophorase
v) Thiolase
vi) 7-Alpha hydroxylase
vii) Acyl co A dehydrogenase
42-What is fatty liver? Enlist the causes and discuss the role of lipotropic agents.
43- What is the product of oxidation of a fatty acid with odd number of carbon atoms?
44- Why it is partly correct to say that fats can not be converted to glucose?
45- What is Atherosclerosis? Discuss in detail the causes, pathogenesis, laboratory findings and its possible treatment.
------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------
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