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BIOCHEMISTRY

OBJECTIVES
Format of biochemistry Important questions Practical

FORMAT
TOTAL MARKS: 150 marks 1. MIDYEAR a) 25 marks b) Format: -MCQ -Cross match -Complete sentences 2. FINAL a) 125 marks b) Division: -MCQ (25 marks) -Written (50 marks) -Oral (25 marks) -Practical (20 marks) -Logbook (5 marks)

MID YEAR

MCQ

WRITTEN

BIOLOGICAL OXIDATION LIPID METABOLISM GENERAL PROTEIN INDIVIDUAL METABOLISM

4 6 4 4 8

4 10 3 8

CHO METABOLISM MINERAL METABOLISM


HAEM METABOLISM MECHANISM OF HORMONAL REACTION METABOLIC CORRELATION NUCLEOTIDE METABOLISM

10 3
2 3 2 4

10 3
2 3 3 4

CARBOHYDRATE

GLYCOGENESIS & GLYCOGENOLYSIS

OXIDATION OF GLUCOSE
1. MAJOR - Glycolysis
- Oxidative decarboxylation of pyruvic acid to acetyl coa NADH.H - Complete oxidation of acetyl coa in kreb's cycle 2. MINOR - Hexose Monophosphate Pathway - Uronic Acid Pathway

1. GLYCOLYSIS

2. Oxidative decarboxylation of pyruvic acid to acetyl coa NADH.H

3. KREB'S CYCLE

TOTAL ENERGY PRODUCED


Glycolysis = 6@8 ATP Pyruvic acid to acetyl coa = 6 ATP Kreb's Cycle = 24 ATP TOTAL = 36@38 ATP

PROTEIN

PROTEIN ABSORPTION

UREA BIOSYNTHESIS

LIPIDS

Past years
6/2009 (How acetyl coA is converted to B(OH) Butyric acid ? (pg 120 : Ketogenesis)
2 acetyl coA thiolase coASH Aceto acetyl coA deacyclase coASH Aceto acetate

synthase

Acetyl coA

HMGcoA

lyase Aceto acetate

Acetyl CoA

B-OH Butyric acid

Role of eicosapentanoic acid in preventing heart disease(pg 109)


**Fatty acids are effective in preventing heart disease because: 1)they lead to formation of more TXA3, relative to TXA2 and more PGI3 relative to PGI2 2)TXA3 is less effective in stimulating platelets aggregation than TXA2 3)PGI3 is more potent as antiaggregation of platetelets than PGI2 Thus, the balance of activity is shifted toward nonaggregation.

Increased intracellular cholestrol content can be regulated by different methods. Comment


(pg 92)

If the cell contain oversupply of cholestrol from LDL, HDL, or chyclomicron remnant, cholestrol can be decreased by : Oversupply of cholestrol inhibit HMG coA necluctase enzyme so cholestrol synthesis is decreased Oversupply of cholestrol stimulates acyl CoA. Cholestrol acyl coA (ACAT), which transfers FA from acyl coAto cholestrol to form cholestrol ester that can be stored in the cell Oversupply of cholestrol inhibits synthesis of new LDL receptor, so further entry of LDL cholestrol into the cell is limited.

Lipotropic factors (pg 141)-last page of lipid met

9/2009
Illustrate by diagram only biosynthesis of eicosanoids from cell membrane phospholipids with the effect of corticosteroids & aspirin(pg 107)
Phospholipids(from cell membrane) Phospholipase A2 Arachidonic acid 5-lipooxygenase 5-HPETE PGG2 cyclooxygenase

Corticosteroids eg:cortisol

LTA4

PGH2

LTB4

LTC4

LTD4

LTE4

PGI2 PGE2 PPGF2

TXD2 PGD2

Role of insulin on adipose tissue met(pg 138)


Insulin reduces the output FFA from adipose tissue by : How? (see text book) Insulin enhances lipogenesis and synthesis of trigylcerides by : How?

Biosynthesis of sphingolipids(pg 129)

(sphinganine)

7/2010 Mention the biochemical lesion of the following


-type ii hyperbeta lipoproteinemia (pg 79) **caused by reduced LDL metabolism due to defective LDL receptors

Comment on the following


(a) acetyl coA carboxylase : catalytic activity, regulation &sources of its substrates

(Pg 114) Acetyl coA

Acetyl coA carboxylase

Malonyl coA

Mn++

CO2 ATP

Biotin

ADP+Pi

Regulation (pg 117) Source substrate[acetyl coA](pg 112) :excess acetyl coA from oxidation of glucose

(b)Glucocorticoids are better anti-inflammatory agent than aspirin like drugs. Explain (pg 108)
* Glucocorticoids inhibit activity of phospholipase A2, thus the precursor of the prostaglandins(arachidonic a)is not available. As a result, the synthesis of prostaglandins and leukotrienes are decreased and the inflammatory response is reduced * While aspirin only block activity of cyclooxygenase which only inhibit formation of prostaglandins and do not effect synthesis of leukotrienes. * thats why glucocorticoids are better anti inflammatory agent than aspirin.

Biosynthesis of HMG coA(beta hydroxylmethyl glutaryl coA) and its fates

8/2010
Mention the biochemical lesion of the following : b)type 1 lipoproteinemia (pg 95) ** due to deficiency of lipoprotein lipase enzyme

Comment on the following : a) causes &prevention of fatty liver(pg 140) b) Ketosis(def, mech, causes and effect)[pg125126] c) Biosynthesis of mevalonic acid from active acetate .(pg 132-134) Explain how this pathway is controlled. [show/draw pathway] **Step 1: Ketogenensis(2 active acetate forming HMGCoA) **Step 2 : HMGCoA forming mevalonic acid (cholestrol synthesis)

Must do!
1)Question banks(from department) 2)Past 5 years Questions

PRACTICAL

1. Colour - yellowish (glucose/acetone/protein) - greenish yellow (bile) - reddish (blood)

2. Odour - odourless (glucose) - specific (protein/blood/bile) - acetone odour


3. Aspect - clear (glucose/acetone) - turbid (blood/protein/bile) 4. Reaction to L.P - acidic (blue - red) - alkaline (red - blue) - neutral (no change) 5. Volume : of given sample 6. Specific gravity - reading SG (R) ..... by urinometer - temp (T) ..... by thermometer - corrected SG R+[(T-15)/3]

TEST

OBSERVATION

COMMENT - urine sample contains reducing sugar - urine sample doesn't contain reducing sugar

detection of reducing sugar: fehling test

2ml urine+2ml fehling, boil

- red colour and ppt - no red colour and precipitate

detection of heat coagulable protein: heat couagulation test

- cloudness at the upper part 10 ml urine, boil - no cloudness at the the upper part upper part

- urine sample contains heat coagulable protein - urine sample doesn't contain heat coagulabe protein

detection of blood: benzidine test

1ml benzidine+1ml hydrogen peroxide+1ml urine

- deep blue colour - no deep blue colour

- urine sample contains blood - urine sample doesn't contain blood

detection of ketone bodies - rothera test - gerhard test (--)

10ml urine, saturate with ammonium sulfate crystals +3 drops of sodium nitroprusside+3 ml ammonium hyroxide conc

- permanganate colour - no permnganate colour - no red colour

- urine sample contains acetone and/or AAA - urine sample doesn't contain acetone or AAA - urine sample doesn't contain AAA

detection of bile salts: hay's sulfur test

5ml urine+sulfur powder

- sinking of sulfur powder to the bottom of tube - floating of sulfur powder on surface of urine

- urine sample contains bile salts - urine sample doesn't contain bile salts

detection of bile pigments: modified gmelin test

10 ml urine+5 drops saturated mg sulphate+3ml barium chloride, boil then cool under tap water, pour supernatant, take ppt in cone shaped filter paper, dry it close to fire + drops of nitric acid on the edge of paper

- coloured rings (red-green-blue) at the edge of ppt - no coloured rings at the edge of ppt

- urine sample contains bile pigments - urine sample doesn't contain bile oigments

Conclusion: urine sample contains ..... and doesn't contain


Comment: (possible causes) ....