SRI VENKATESWARAA MEDICAL COLLEGE HOSPITAL & RESEARCH CENTRE.

DEPARTMENT OF BIOCHEMISTRY
I-MBBS (2024-25)
THEORY MODEL EXAMINATION – PAPER II

Date: 23.07.2025 Maximum: 100 marks Time: 03.00 hours

I. MCQ: (20 × 1 = 20 marks)

II. ESSAY: (1×10 = 10marks)

1. A 50 year old male was admitted to hospital with a complaint of persistent vomiting. On
examination, he was found dehydrated and his respiration was shallow. He had a past history of
dyspepsia. Investigation reports are as follows:
Blood pH – 7.7
Plasma HCO3- - 45 mmol/L
pCO2 – 60 mmHg
Na+ - 140 mEq/L
K+ - 2.5 mEq/L (2+4+4)
(a) What is the probable diagnosis? Justify
(b) Name four causes for the above acid base disorder
(c) Write about renal regulation of acid base balance

III. SHORT NOTES (APPLIED): (4X5 = 20 marks)

2. A 21 yr boy experienced severe worsening abdominal pain following consumption of beer in his
birthday party. He also had nausea, vomiting, was anxious with hallucinations. His blood
pressure and heart rate was increased and peripheral neuropathy was observed. Laboratory
investigations showed increased serum and urine aminolevulinic acid (ALA) and
porphobilinogen (PBG). What is the diagnosis? Write about the biochemical defect and
management of the disease? (2+2+1)

3. A 25-year-old athlete presented with tiredness, inability to move his arms and legs and
palpitations. He gives a history of diuretic intake before the competition. He was diagnosed with
hypokalemia. What is the normal level of serum potassium? List the causes of hypokalemia
(1+4)

4. A 4 yr old boy presented with features of iron overload. He gave history of repeated blood
transfusions and was a known case of Thalassemia.
What is the biochemical basis, clinical features, laboratory investigations and management of
Thalassemia? (1+2+1+1)

5. A 2.5 yr girl child presented with complaints of edema on legs & hands, poor growth and frequent
diarrhea. Mother said the child was breastfed till 2 yrs and was now receiving diluted buffalo milk
 and rice with dhal. Child looked weak, pale had discolored skin and hair, distended abdomen with
hepatomegaly. Laboratory results showed
Hemoglobin 6.5 g/dl
Total protein 4h g/dl
Serum albumin 2 g/dl
What is the diagnosis? Write about the biochemical basis and clinical features

IV. SHORT NOTES: (7X5 = 35 marks)

6. Hybridoma technology and its importance (4+1)
7. Write a note on classification and functions of lipoproteins.
8. Tumor markers and the diagnostic importance (3+2)
9. Describe the synthesis and functions of Prostaglandins. Mention a drug which inhibits the
prostaglandins. (2+2+1)
10. Describe the secondary structure of proteins
11. Dietary fiber and its importance? (2+3)
12. Describe the roles of a physician

V. REASONING TYPE QUESTIONS: (5X3 = 15 marks)

13. Why carnitine is supplemented in preterm babies?
14. Why haem is given for porphyria treatment?
15. Why there is hyperkalemia in severe diabetes mellitus?
16. Why peripheral cell membrane proteins and extracellular domains of integral proteins are
glycosylated?
17. Why serum potassium should be analyzed immediately after sample collection?

Answers

1. Essay

Question Analysis – 50 year old male – persistent vomiting – clue- loss of gastric contents- loss of
HCl . Past history of dyspepsia- peptic ulcer.
Blood pH - 7.7 (7.35- 7.45) Increased – alkalosis.
Plasma bicarbonate – 45 mmol/l ( 22-28 mmol/l) – Increased, so metabolic alkalosis
pCO2 – 60 mm of Hg (35-45 mm of Hg) - Increased – respiratory acidosis but it is compensation by
respiratory system because blood pH is alkaline and there is loss of acid causing alkalosis.
Answer

Diagnosis – Metabolic alkalosis with compensatory respiratory acidosis

Justification- Blood pH - 7.7 (7.35- 7.45) Increased – Alkalosis
Plasma bicarbonate – 45 mmol/l ( 22-28 mmol/l) – Increased so metabolic alkalosis
pCO2 – 60 mm of Hg (35-45 mm of Hg) - Increased – respiratory acidosis but it is
due to compensation by respiratory system because blood pH is alkalotic. (partially
compensated metabolic alkalosis)
Due to loss of HCl in the gastric juice

Causes for metabolic alkalosis

 Excess loss of hydrogen ions
1. Vomiting – loss of HCl
2. loss of H+ ions- in use of diuretics
3. Hyperaldosteronism – Increased reabsorption of sodium in exchange for H+ ions
4. Hypokalemia – Normally Sodium is reabsorbed in exchange for H+ and K+ ions. In
hypokalemia, to conserve K+ ions, more H+ ions are excreted.
Excess gain of Bicarbonate
5. Excessive intake of antacids
6. Excessive intake of milk- Milk alkali syndrome

Renal regulation of acid base balance

1. Excretion of Hydrogen ions
2. Reabsorption of bicarbonate

Reabsorption of bicarbonate involves the reabsorption of bicarbonate filtered without

excretion of H+ ions.

Excretion of H+ ions
Here there is net gain of bicarbonate for each H+ excretion. As the H+ ion excretion increases,
the excretion of H+ against concentration gradient becomes difficult. So, in the distal
convoluted tubules, urinary buffers buffer the free H+ ions.
Two important urinary buffers are:
1. Phosphate buffer
2. Ammonia
The maximum limit of acidification of urine is 4.5.
Acid base balance has two components.

CA- Carbonic anhydrase

Normal arterial blood pH- 7.35 -7.45
pCO2- 35-45 mm of Hg
bicarbonate- 22-28 mmol/l
pO2- 80-100 mm of Hg

2. A 21 yr boy experienced severe worsening abdominal pain following consumption of beer in his
birthday party. He also had nausea, vomiting, was anxious with hallucinations. His blood pressure
and heart rate was increased and peripheral neuropathy was observed. Laboratory investigations
showed increased serum and urine aminolevulinic acid (ALA) and porphobilinogen (PBG).
What is the diagnosis? Write about the biochemical defect and management of the disease?

Analysis- Severe abdominal pain, peripheral neuropathy, anxiety , BP and tachycardia,

hallucinations ( seeing or hearing something that is not there really).
Serum and urine delta ALA and porphobilinogen (PBG) were increased.
Delta ALA is the first compound formed in the heme synthesis pathway.
Second compound formed is porphobilinogen. No photosensitivity.
Hence it is a case of porphyria.
The compounds formed after porphobilinogen is not found. Hence the enzyme involved in the third
step must be involved. That is porphobilinogen deaminase (or hydroxymethylbilane synthase or
uroporphyrinogen I synthase deficiency )
Clinically Acute abdominal pain, neuropsychiatric symptoms were present.

So, it is a case of acute intermittent porphyria.

Answer-

Diagnosis-

Acute intermittent porphyria - Autosomal dominant

Biochemical defect-

Porphobilinogen deaminase or hydroxymethylbilane synthase deficiency.

Management-

Glucose infusion, heme infusion , liver transplantation.

Avoiding precipitating factors such low carbohydrate diet, starvation.

Barbiturates will precipitate acute attacks because they induce ALA synthase.
3. 25 year old athlete presented with tiredness, inability to move his arms, legs and palpitations. He
gives a history of diuretic intake before the competition. He was diagnosed with hypokalemia.
What is the normal level of serum potassium? List the causes of hypokalemia.

Serum potassium – 3.5 -5.0 mmol/l

Hypokalemia causes

1. Less intake - Poor nutrition, poor diet.

2. Increased excretion- Certain diuretics, Mineralocorticoid excess – Eg: Primary

or secondary hyperaldosteronism, increased urine flow ( osmotic diuresis)
Gastrointestinal losses – loss of electrolytes - diarrhoea
Vomiting, or nasogastric suctioning- Alkalosis occurs. To retain H+ ions,
potassium is excreted for sodium reabsorption.
3. Extracellular/intracellular shift
Potassium shifts back to intracellular compartment s in acute insulin therapy for
hyperglycemia.

4. 4 yr old boy presented with features of iron overload. He gave history of repeated blood
transfusions and was a known case of Thalassemia. What is the biochemical basis, clinical features,
laboratory investigations and management of Thalassemia? (1+2+1+1)

Since the RBC life span is limited and Iron is an one way mineral, repeated blood transfusion for
the management of Thalassemia results in iron overload.

Biochemical basis

Thalassemias are inherited disorders of reduced synthesis of normal hemoglobin.

5. A 2.5 yr girl child presented with complaints of edema on legs & hands, poor growth and frequent
diarrhoea. Mother said the child was breastfed till 2 yrs and was now receiving diluted buffalo
milk and rice with dhal. Child looked weak, pale had discolored skin and hair, distended abdomen
with hepatomegaly. Diarrhoea is due to infection. Laboratory results showed
Hemoglobin 6.5 g/dl
Total protein 4h g/dl
Serum albumin 2 g/dl
What is the diagnosis? Write about the biochemical basis and clinical features.

Analysis: 2.5 years old child, weaning period, poor protein intake leads to hypoalbuminemia. It
causes edema, distended abdomen due to fluid collection in the peritoneal cavity (Ascites) and
hepatomegaly (fatty liver), skin and hair changes due to poor nutrition
Hemoglobin reduced ( 11- 14 g/dl) - anemia
Total protein- reduced ( 6-8 g/dl) less , serum albumin – (3.5 – 5 g/dl) reduced
Nutritional disorder due to insufficient protein intake

Answer :
Diagnosis- Kwashiorkor
Weaning period- stopping breast feeding and switching over to solid food.
During the weaning period, the complications such as infections( Diarrhoea), nutritional
deficiency ( hair and skin changes), protein insufficiency, anemia can occur.
Hepatomegaly - Fatty liver changes due to insufficient lipoprotein synthesis for the transport of
lipids from liver to other tissues.
Hypoalbuminemia – decreased oncotic pressure – edema and ascites
Treatment - Introducing one new food once in three to four days to assess for any food allergy
3- 4gm/ day protein intake ,
Iron rich foods , egg, red meat can be given.

6. Hybridoma technology
Definition: Hybridoma technology is a technique for producing monoclonal
antibodies (one type -single clone) by fusing antibody-producing B lymphocytes
with immortal myeloma (cancer) cells.
Resulting hybridoma cells are:
1.Immortal (divide indefinitely)
2.Specific (produce one type of antibody)
Steps in Hybridoma Technology
1. Immunization: Mouse is injected with specific antigen to produce antibodies
which polyclonal. Each clone produces a single type of antibody.
2. Isolation of Spleen Cells: Mouse is sacrificed and spleen removed. From splenic
cells containing many clones of cells , single clone cells are isolated .
3.Fusion with Myeloma Cells:
Fusion of B cells with myeloma cells is done using Polyethylene Glycol (PEG).
For cell multiplication, DNA synthesis depends on nucleotides which are either
synthesized or obtained by salvage pathway. Salvage pathway requires HGPRTase
enzyme. Myeloma cells lack HGPRT enzyme (HGPRTase).
4. Selection in HAT Medium: The cells are then cultured in HAT medium. ( HAT
= Hypoxanthine + Aminopterin + Thymidine). Aminopterin inhibits dihydrofolate
reductase enzyme and inhibits de novo synthesis.
Unfused B cells die naturally.
Since B cells have HGPRTase and myeloma cells don’t have HGPRTase , only
fused cells can survive. Thus only hybridomas survive.
5. Screening:
By using ELISA technique, hybridomas can be identified for producing desired
antibody.
6. Cloning & Expansion:
Selected hybridoma cells produced in large number either by growing in culture
or in mouse peritoneal cavity.
7. Monoclonal Antibody Production:
Harvested from culture media or ascitic fluid.
Importance / Applications of Hybridoma Technology
Medical Diagnosis: ELISA, RIA, Detection of HIV, HBsAg, Pregnancy hormone
(hCG)
Therapeutics: Monoclonal antibodies for: Cancer (e.g., Trastuzumab, Rituximab)
Autoimmune diseases (e.g., Infliximab)
Research Use: Cell surface marker studies, Immunohistochemistry, Flow
cytometry
Other Uses: Vaccine development
Drug targeting
 7. Lipoprotein

Definition:
Lipoproteins are macromolecular complexes of lipids and proteins
(apolipoproteins) that transport lipids (cholesterol, triglycerides, phospholipids)
through blood.
Classification of Lipoproteins
Based on density, size, and electrophoretic mobility.

Type Density (g/ml) Major Lipid Function Apo Protein

Chylomicrons < 0.95 Triglycerides Transport dietary Apo AI , Apo B-48, Apo C-II,
TG from intestine Apo E

VLDL 0.95 – 1.006 Triglycerides Transport endogenous Apo B-100, Apo C-II, Apo E
TG from liver

IDL 1.006 – 1.019 TG + Cholesterol Intermediate in VLDL to Apo B-100, Apo E

LDL

LDL 1.019 – 1.063 Cholesteryl ester Transport cholesterol Apo B-100

from liver to tissues

HDL 1.063 – 1.21 Phospholipids + Reverse cholesterol Apo A-I, Apo C, Apo E
CE transport- Transport
cholesterol from tissues
to liver for excretion

Apo Protein Function

Apo A-I Activates LCAT (HDL metabolism)
Apo B-100 LDL receptor binding
Apo B-48 Chylomicron remnants uptake by liver
Apo C-II Activates lipoprotein lipase
Apo E Receptor-mediated uptake of remnants
Chylomicrons contains Apo AI, B48, CII, E
Function : Mediate exogenous fat transport pathway.
▪ Nascent chylomicrons - synthesized in the small intestine mucosal cells – Contains
dietary triacylglycerol, cholesteryl ester, phospholipids and Apo B48 and Apo A. They
enter lymphatics and reach circulation.
▪ In circulation, nascent chylomicrons get Apo C and E from HDL to form mature
chylomicrons.
▪ Apo CII activates Lipoprotein lipase (LPL) on luminal surface of endothelial cells
(mainly in the skeletal muscle, adipose tissue and heart tissues) and Triglycerides are
hydrolysed to fatty acids and glycerol. Glycerol reaches liver and forms glucose. Fatty
acids are mainly used by heart, skeletal muscle and adipose tissue.
▪ After removal of triglycerides and transfer of Apo AI and CII to HDL, chylomicron
remnants are formed containing Apo E and Apo B48 which are taken up by Liver
chylomicron remnant receptor or LDL receptor like protein 1.
▪ Insulin activates Lipoprotein lipase (LPL).

Very low density lipoprotein (VLDL) - mediates endogenous fat transport pathway.
Nascent VLDL with Apo B100 is synthesized by the liver and secreted into the blood.
In the circulation, nascent VLDL obtains Apo E and Apo CII from HDL to form
mature VLDL containing Apo B100, Apo CII and Apo E.
▪ LPL acts on triacylglycerol in VLDL.
▪ VLDL size is decreased and forms smaller particle. Apo CII is transferred to HDL.
Now, IDL with Apo B100 and Apo E is formed.
 ▪ IDL has two fates. 1. Taken up by the liver via APO B100 , E receptor
2. Some IDL after transfer of Apo E to HDL, cholesterol rich LDL with Apo 100 is
formed.
▪ LDL is taken up by receptor mediated endocytosis. LDL receptors are located in special
regions called Clathrin- coated pits. The Apo 100 binds to Apo B100 receptor in the
hepatic and extra hepatic tissues.

HDL mediates reverse cholesterol transport pathway.

▪ HDL transports cholesterol from peripheral tissues to liver for excretion.
▪ It acts as a reservoir of Apo C and Apo E in blood and exchanges them with n
▪ Chylomicrons and VLDL.
Synthesis : HDL is synthesized in liver and small intestine containing Apo AI and
phospholipids. It appears as a disc shaped particle made up of phospholipids with Apo
AI, CII and E .
▪ The Apo A1 of HDL activates plasma lecithin-cholesterol acyl transferase (LCAT)
Cholesterol + Lecithin Cholesteryl ester +Lysolecithin
LCAT
▪ The cholesterol from cell is transferred to HDL by ATP binding cassette transporter
protein A1. (ABCA1)
▪ Plasma Lecithin Cholesterol Acyl transferase enzyme converts Cholesterol from cells
into Cholesteryl ester which is non-polar moves to the core of HDL and makes it
spherical mature HDL (HDL 3).
▪ From HDL, Cholesteryl ester is transferred to VLDL, IDL and LDL by cholesteryl
 ester transfer protein (CETP) in exchange for triacylglycerol.
▪ In liver, the hepatic scavenger receptor B1(SR-B1) is involved in uptake of HDL.
▪ In liver, cholesterol is used for the synthesis of bile acids or excreted in to bile.
This completes the reverse cholesterol transport pathway mediated by HDL.

Type I Hyperlipoproteinemia
Defect- LPL deficiency or Apo CII deficiency. -
Mode of inheritance- Autosomal Recessive
Clinical features- Abdominal pain due to pancreatitis, lipemia retinalis, eruptive
skin xanthomas, hepato-spleenomegaly.
Diagnosis: Serum TAG is increased. Serum cholesterol is normal.
A creamy layer appears on the top of plasma kept for 24 Hours which is due to
chylomicrons.
▪ Treatment : Restriction of fat intake and inclusion of MCT oils such as palm kernel
oil, coconut oil and SCT fats such as butter, cream.
Type II a Hyperlipoproteinemia
Defect- LDL receptor, Autosomal dominant disorder
Clinical features: Xanthelasma, arcus senilis (the graying of the eye), tendon
xanthomas.
▪ Atherosclerosis and coronary heart disease are common.
▪ Diagnosis: Serum cholesterol is 2-3 times increased. Serum TAG is normal. LDL and
Apo B in serum is elevated. Serum is clear.
 Management : Cholesterol intake - less than 300 mg per day. Animal fats should be
avoided. Intake of fiber rich diet and exercise.
Statin drugs - HMG-CoA reductase inhibitors reduce serum cholesterol
Cholestyramine, a bile acid binding resin by increasing the excretion of bile acids
Niacin reduces both TGL and Cholesterol.
Type IIb Hyperlipoproteinemia (Familial combined hyperlipidemia)
▪ It is a rare, autosomal recessive disorder characterized by elevated blood LDL and
VLDL level. It is due to overproduction of Apo B100 and LDL receptor deficiency.
▪ Clinical features Xanthelasma, arcus senilis, tendon xanthomas.
▪ Diagnosis Both Serum TAG and cholesterol are increased. Serum is slightly turbid due
to elevated TGL. Both LDL and VLDL are increased. Apo B100 is increased.
▪ Treatment Drugs Statins, fibrate and niacin are useful. Niacin reduces both LDL
cholesterol, VLDL triacylglycerol. So, niacin has antiatherosclerotic property.

Type III Hyperlipoproteinemia (Familial dysbetalipoproteinemia or Broad beta disease)

▪ It is autosomal recessive disorder characterized by elevated blood IDL level. It is due

to defect in Apo E synthesis. So IDL (VLDL remnants) are not taken up by liver.
▪ Clinical features: Tuberoeruptive xanthomas and palmar xanthomas. Coronary disease
is common.
▪ Diagnosis: Due to cholesterol rich IDL, Serum cholesterol is much increased. Serum
TAG is slightly elevated. Serum is turbid. In electrophoresis of lipoproteins, there will
be broad beta band.

Type IV Hyperlipoproteinemia (Familial hypertriglyceridemia)

▪ It is autosomal recessive disorder characterized by elevated blood VLDL due to its

increased synthesis and decreased elimination.
▪ Clinical features: Pancreatitis can occur at very high TAG levels. The most common
symptoms of pancreatitis are severe abdominal pain. Eruptive xanthomas may also be
present.
▪ Diagnosis: Due to TAG rich VLDL, serum triglycerides is much increased. Serum
cholesterol is slightly elevated and serum is turbid.

Type V Hyperlipoproteinemia
▪ It is autosomal recessive disorder characterized by elevated blood chylomicron and
VLDL levels. It is due to increased VLDL synthesis and decreased LPL activity.
▪ Clinical features Eruptive xanthomas and pancreatitis may occur.
Applications / Clinical Importance:
1. Cardiovascular Risk: LDL promotes atherosclerosis
2. HDL has protective role against atherosclerosis and heart disease.
Diagnostic Lipid Profile:
Total cholesterol – 140-200 mg/dl
HDLc – 40-60 mg/dl in male and 50 -70 mg/dl in female
LDLc- less than 100mg/dl
VLDLc - less than 30 mg/dl
Triglycerides- 50-15- mg/dl.
Drug Targets:
Statins → inhibit HMG-CoA reductase → ↓ LDL
Fibrates → ↑ HDL, ↓ TG
Niacin → ↓ VLDL, LDL
5. Laboratory Tests:
Electrophoresis and Ultracentrifugation are used for lipoproteins separation.
8.Tumor markers and the diagnostic importance
Tumor marker is a biological substance which indicates the presence of cancer.

It is synthesized and released by cancer cells or it can be produced by the normal surrounding cells in
response to cancer.

They can be hormones, proteins and other molecules and they are found in an increased amount in
the blood, other body fluids or tissues which suggests the presence of a type of cancer.

Tumour markers can be used for screening, diagnostic , monitoring for recurrence, and prognostic
purpose.

Tumor markers Associated cancer or tumor

Oncofetal antigens
• α-Fetoprotein (AFP) • Hepatocellular, germ cell cancers
• Carcinoembryonic antigens (CEA) • Colorectal, gastrointestinal, pancreatic,
lung
Hormones
• Calcitonin • Thyroid
• Growth hormone • Pituitary adenoma, renal, lung
• Parathyroid hormone • Liver, renal, breast, lung
• Prolactin • Pituitary adenoma, renal, lung
• Human chorionic gonadotropin (HCG) • Teratoma of testes, choriocarcinoma

Glycoproteins
• CA 125 • Ovarian, endometrial
• CA 549 • Breast, ovarian
Proteins
• β-microglobulin • Multiple myeloma, B-Cell lymphoma
• C-peptide • Insulinoma
• Ferritin • Liver, lung, breast, leukemia
• Immunoglobulin (Bence Jones • Multiple myeloma
protein)
• Prostatic specific antigen (PSA) • Prostate

Enzymes
• Amylase • Pancreatic
• Alkaline phosphatase • Bone, liver, leukemia, sarcoma
• Prostatic acid phosphatase • Prostate
• Lactate dehydrogenase • Liver, lymphomas, leukemia
9. Prostaglandins

Def: Prostaglandins (PGs) are bioactive lipids derived from arachidonic acid (a 20-
carbon polyunsaturated fatty acid) and belong to a group called eicosanoids.

Importance: They act as local hormones (autocrine/paracrine) involved in

inflammation, pain, fever, vascular tone, and smooth muscle activity.

Synthesis of Prostaglandins:
1. Arachidonic acid release
Released from membrane phospholipids by phospholipase A₂
2. Cyclooxygenase (COX) Pathway
Cyclooxygenase enzymes (COX-1 and COX-2) convert arachidonic acid →
Prostaglandin G₂ (PGG₂)
3. By peroxidase , PGG2 is converted to prostaglandin H₂ (PGH₂)
3. PGH₂ is a common precursor for various prostaglandins:
PGE₂, PGF₂α, PGI₂ (prostacyclin), TXA₂ (thromboxane A₂)
 Drugs that Inhibit Prostaglandin Synthesis:

Drug/Class Action
NSAIDs (e.g. Aspirin, Ibuprofen) Inhibit COX-1 and COX-2 → ↓ PG synthesis
Aspirin Irreversible COX inhibitor, anti-
inflammatory, anti-platelet
Paracetamol Weak COX inhibitor in peripheral tissues
Glucocorticoids Inhibit Phospholipase A₂ → block AA
release → ↓ PGs
Celecoxib Selective COX-2 inhibitor – anti-
inflammatory with fewer gastric side effects

Clinical applications:
Fever, pain, inflammation → mediated by PGE₂
Gastric ulcers risk increases if COX-1 is inhibited.
Menstrual cramps → linked to PGF₂α
Thrombotic risk → due to imbalance between TXA₂ and PGI₂
Functions of Eicosanoids
Eicosanoids Functions Clinical aspects
Prostaglandins Thromboxane TXA2 In platelets- TXA2 inhibitors are
Vaso and broncho being developed for
constriction cancer treatment
Promotes platelet
aggregation
PGI2 In endothelium- Used for the
Vasodilation management of
Inhibits platelet pulmonary arterial
aggregation hypertension (PAH)
PGE2 In tissues- Used in Bronchial
Bronchodilator asthma, labour and
Smooth muscle abortion
contraction
Response to fever
Uterine contraction
PGF2α In tissues- Labour, abortion,
Inflammation, Glaucoma
reproduction,
smooth
muscle ,contraction
Uterine contraction

Leukotrienes LTA4, LTB4 Inflammation, Monteukast-

Chemoattractant, leukotriene receptor
 LTC4,LTD4, LTE4 Slow reacting antagonists – used
substance of in allergic rhinitis,
Analhylaxis Asthma

• 10.Describe the secondary structure of proteins.

➢ Folding of primary structure forms secondary structure by interaction between amino acid
residues which are about 3–4 apart in linear sequence.
➢ The folding of short (3- to 30-residue), contiguous segments of polypeptide into
geometrically ordered units.

Bonds involved in the secondary structure are primarily noncovalent bonds like:

• Hydrogen Bond (Most important bond)Hydrophobic Bond

• Electrostatic Bond (Ionic Bond, Salt Bridges)
• van der Waals forces.

Secondary Structures of Proteins include:

• Alpha Helix
• Triple helix
• Beta Pleated Sheet
• Loops
• Bends
• Turns

Alpha helix:

➢ Alpha helix is the most common and stable secondary structure.

➢ Proline due to its cyclic structure and rigidity, cannot form alpha helix and introduce kinks or
bends.
➢ Right-handed Spiral Structure.
➢ Structure stabilized primarily by intrachain hydrogen bonds.
➢ Each turn formed by 3.6 Amino Acid residues.
➢ Distance between each turn of alpha helix (called Pitch) is 0.54 nm.
➢ Examples of Proteins whose major secondary structure is Alpha Helix: Hemoglobin.
Beta pleated sheets:

➢ The second most common (hence‚ ‘beta’) recognizable regular secondary structure in
proteins.
➢ Polypeptide chain is almost fully extended.
➢ In contrast to intrachain hydrogen bond in alpha helix, here it is interchain hydrogen bonds
between two adjacent chains.
➢ Adjacent strands in a sheet can run in the same direction (parallel beta pleated sheets) or
opposite direction (antiparallel beta pleated sheets).
➢ Turns and bends: Short segments of amino acid that join two units of secondary
structures. Example: beta turn & beta bends.
➢ Glycine is the smallest amino acid without side chain and highly flexible. So it is involved
in turns and bends

Super secondary structures: Secondary structural elements join to form super secondary
Structures. Examples:
• Helix-Turn-Helix motif
• Leucine zipper motif
• Zinc finger motif

11.Dietary fiber and its importance

Dietary fibers:
➢ Complex Carbohydrates not digested by human digestive enzyme.
➢ Otherwise called Non-starch Polysaccharide.
➢ Classified as: 1) soluble dietary fibers: Pectin, mucilage, gums
2) insoluble dietary fibers: cellulose, hemicellulose, lignin
➢ Recommended daily allowance for dietary fibers: 40g per day.
Importance of dietary fibers:
➢ Slow gastric emptying and reduce the stool transit time.
➢ Increase bulk of the stool and eliminate bacterial toxins.
➢ Prevent constipation and hemorrhoids (Anal piles)
➢ Improve glucose tolerance by decreasing rate of absorption of glucose.
➢ Decrease absorption of dietary cholesterol and reduce plasma cholesterol levels.
➢ Binds to bile salt and decrease its enterohepatic circulation thereby increase the excretion
of cholesterol.
➢ Decrease the risk of GI cancers - colon and rectum, cardiovascular disease and diabetes
mellitus.

12.AETCOM

13. Why carnitine is supplemented in pre-term babies ?

Pre-term babies have been shown to be at risk for carnitine deficiency due to limited stores and
reduced ability to synthesize carnitine. Especially, in case total parenteral nutrition (TPN), they
mainly depend upon fatty acids which require carnitine. Hence, carnitine must be supplemented in
pre-term babies.
14. Why haem is given for porphyria treatment ?

Heme inhibits the synthesis of ALA synthase by acting as a co-repressor. Hence it inhibits the
formation of porphyrin intermediates, thus alleviating symptoms of porphyria

15. Why there is hyperkalemia in severe diabetes mellitus ?

In severe diabetes mellitus, potassium levels are increased due to insulin deficiency and acidosis.

1. Insulin deficiency can cause inefficient functioning of Na+-K+-ATPase pump, thus resulting in
impaired intracellular shift of potassium.

2. In acidosis, plasma hydrogen ions enter in to the cells to get buffered by cellular proteins
and drives out the potassium to maintain ionic equilibrium.

3. In kidney, sodium reabsorption occurs in exchange for H+ and K+ ions. In acidosis, H+ ions
are secreted more in stead of potassium for sodium reabsorption. This results in retention of
more potassium causing hyperkalemia.

16. Why peripheral cell membrane proteins and extracellular domains of integral proteins are
glycosylated ?

Sugar molecules attached to glycosylated proteins due to their hydrophilic nature, helps in the
interaction of peripheral cell membrane proteins with other compounds in aqueous medium.

So, glycosylation of extracellular domains of integral proteins enhance the protein stability, folding,
and help many functions such as cell-cell interactions, immune response and signalling.

17. Why serum potassium should be analysed immediately after sample collection ?

Delay in analysing serum potassium after sample collection may result in leakage of potassium from
the cells into blood, resulting in falsely raised potassium levels / pseudohyperkalemia – a pre-
analytical error. Hence, to avoid this, potassium levels must be analysed immediately after sample
collection.