Study Guide Biochemistry Department First year MBBS...CVS Histology Circulatory System Immune system General Anatomy Lymphatic system Circulatory system Cardiovascular Physiology Chemistry

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Study Guide

Biochemistry

Department

First year MBBS

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Study Guide

Department of Biochemistry

(2018-19)

1. Departmental introduction

Biochemistry department since the inception of the college has made a study and

note-worthy progress. The department is headed by Prof Dr Naheed Z Razwi ably

supported by a team of seasoned and experienced teachers. This department is well

known for providing not only world class training to the undergraduates but also in

breeding curiosity to know the unknown. The faculty members of this department who

are highly qualified and dedicated are the source of inspiration for all their students to

seek guidance for their academic and professional excellence. They along with the

Head of Department have established an up-to-date laboratory as well as student lab

that is an integrated life science teaching solution that include hardware, software and

curriculum materials that students and faculty used to record data from their own

bodies, animals or tissue preparations. A post graduate session has been established

where, under permission from the NUMS University we hope to start our M.Phil

(Biochemistry) classes in the very near future.

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Index 1. Vision/Mission

2. Guidelines

3. Learning Objectives

4. Table of specification

5. Faculty list

6. Departmental Library

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Vision statement: The vision of National University of Medical Sciences is to improve the quality of life

through education, research, innovation, and healthcare, thereby, contributing to endeavours to

make Pakistan and this world better place to live in.

Mission statement: To provide an excellent learning and teaching environment, inculcating ethical values

and social responsibilities in under-graduate and post-graduate medical and dental students

and nursing and allied health sciences students to enhance the level of comprehensive health

care in the Army/Country.

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Guidelines: 1st Year MBBS Curriculum Preamble.

This curriculum meets the standards of Pakistan Medical and Dental Council, Higher

Education Commission of Pakistan, and World Federation of Medical Education, so that our

students, on completion of program have required competencies as defined worldwide in a

graduate doctor. The curriculum for 1st year MBBS has been reviewed by faculty of

constituent/affiliated colleges in collaboration with Academic Directorate of NUMS.

Model.

NUMS curriculum, revised 2017, is based on SPICES model of educational strategies. It is

student centered, problem based, integrated, community oriented and systematic. Our

curriculum is evolved taking into consideration traditional, experiential, behavioral, and

constructivist perspectives of curricula.

Organization.

The curriculum of 1styear MBBS is modular. It is organized and the content taught is

integrated concurrently in themed modules. The themes form the building blocks of this

curriculum. There can be vertical thread of content across more than one module for the

content that does not fit into central theme of a module. In each module the sequencing of the

content is subject based.

Modules.

The key detail is as follows

1. There shall be three modules in an academic year.

2. Each module shall have a title. The name shall represent the content taught and

learned the majority of time in that module.

3. The duration of three modules shall be 8 – 10 weeks each.

4. The syllabus shall be integrated horizontally around systems of the body.

5. Additional chunks of content may be added in a module that exactly does not fit in the

central theme of the module.

6. There can be vertical thread of a content across more than one module for the content

that does not fit into central theme of a module

7. There shall by vertical integration to the extent decided by the medical college. 8. Total

Contact Hours of each subject as per PM&DC is under: -

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Subject Contact Hours

Anatomy 250

Physiology 250

Biochemistry 160

Pathology 15

Community Medicine 15

Medicine & Allied 15

Surgery & Allied 15

Radiology 05

Behavioural Sciences 10

*Subject is not assessed in FIRST Professional examination

Educational strategies:

The educational strategies overarching the curriculum shall be:

Student centered

Integration

Problem based

Structured

With component of community based and electives

Teaching and Learning methods (MIT)

Multiple learning strategies are used. Interactive lectures are used to provide students

entrance to topic needing much effort by the student to understand subject matter. We have

used Problem based learning to integrate basic and clinical sciences, and give a learning

experience that is contextual, realistic, and relevant. Small group discussions encourage

students to social learning bring their concepts and learning to be discussed and schemas

corrected and refined.

Working in labs provides experiential, hand on learning.

Time table / Structured Training Program

The colleges shall make their own structured training program, taking care of recommended

teaching hours in a subject as described by PM&DC.

Internal Assessment.

During the module the students shall be continually formatively assessed. The weightage of

internal assessment shall be 10 % in 1st professional MBBS Examination. There shall be three

modular and one pre -annual examination. The scores of tests at the end of each modular

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assessment and pre-annual examination shall be used for calculation of the internal

assessment.

Module and Pre-Annual Examination

There will be three module examinations, one at the end of each module.

There will be only one Pre-annual examination.

The structure of the paper of all the module examinations and pre-annual will be same as that

for annual examination though syllabus will be different.

The syllabus for modular examination will be announced by the department at least 02 weeks

prior to examination.

Pre-annual examination will be from whole syllabus.

The date sheet for Module and pre-annual examinations will be published by Examination

branch of college while the examinations will be conducted by respective department. The

result will be submitted to NUMS examination branch for incorporation in internal assessment

before annual examination Annual Professional Examination.

The University shall take the 1st professional Examination as per PM&DC guidelines at the

end of the academic year. Each subject section has table of specification of Module, Pre-

annual and Annual examination. Annual Theory & Practical Examination shall be of 200

marks each in; Anatomy, Physiology and Biochemistry. The pass score shall be 50% in theory

and practical separately. The detail marked distribution of 1styear is as under

S/N Subject MCQs PBQs/ SAQs/ SEQS

Int Assess

Sub

Total Oral & Practical

Int Assess

Sub

Total Grand Total

1 Anatomy 25 65 10 100 90 10 100 200

2. Physiology 25 65 10 100 90 10 100 200

3. Biochemistry 25 65 10 100 90 10 100 200

600

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STRUCTURED SUMMARY OF MODULES-1st YEAR

MODULES BLOCKS

THEMES ANATOMY PHYSIOLOGY BIOCHEMISTRY

Y1M1

1. Introduction 2.Cells and genetics 3. Blood 4. Loco motor (Upper limb)

Gross anatomy Upper limb General Anatomy General anatomical terms Bone Joints Muscular system Nervous system-I (Introduction) Embryology Mitosis and meiosis, Gametogenesis Ovulation &Implantation 1st week of development 2nd week of development 3rd week of development Histology Cell (Introduction, staining, cytoskeleton, cell junctions) Surface and glandular epithelium Connective tissue(General) Bone Cartilage Muscle

Cell, transport and general physiology + Genetics Nerve and membrane potential Muscle physiology Blood Immunity

Chemistry of Protein Nucleotides and Nucleic Acid Porphyrins & Hemoglobin Biochemistry of Cell & Biological membrane

Y1M2 1.Thorax 2.Cardiovascu lar system

Gross anatomy Thorax Embryology Embryonic period, Fetal period Placenta and fetal

membranes Twining CVS Histology Circulatory System Immune system General Anatomy Lymphatic system Circulatory system

Cardiovascular

Physiology Chemistry of carbohydrates Chemistry of Lipids Enzymes Body Fluids Minerals & Trace Elements

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Y1M3 Lower Limb Respiratory System

Gross anatomy Lower Limb General Anatomy Skin Fascia Vertebral column Nervous system-II Embryology Birth defects Body cavities Respiratory system Muscular System Skeletal system except head and neck Development of limbs Histology Respiratory system

Physiology of respiration Deep sea physiology Aviation/space physiology High altitude physiology Exercise physiology

Nutrition Water soluble vitamins Fat Soluble vitamins

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MODULE-I

Biochemistry

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Summary:

Code Y1M1

Name Biochemistry

Duration 10 weeks

Broad Themes of Module

(Theme: a subject that is being

integrated a majority of time of

module)

1. Introduction

2. Cells and genetics

3. Blood

4. Loco motor (Upper limb)

Subject Themes

Chemistry of Protein

Nucleotides and Nucleic Acid

Porphyrins & Hemoglobin

Biochemistry of Cell & Biological

membrane

Prerequisite Module None

Mode of Information Transfer:

MIT

Lectures

Tutorials (PTT)

CBL

Practicals

Class tests

Biochemistry learning outcomes:

57 Biochemistry of

Cell & Biological

membrane

At the end of the learning of this set, the learners will be

able to

Illustrate and categorize different types of cytological

techniques.

Demonstrate basic techniques to study cell, separation

of materials through centrifugation, chromatography and

microscopy.

Differentiate cell organelles, their structure and

biochemical functions (Mitochondria, Ribosomes, Golgi

Apparatus, Endoplasmic Reticulum, Lysosomes,

Peroxisomes) and associated disorders.

Describe detailed chemical composition of Cell

Membrane and its biochemical significance.

Explain chemistry of receptors and signal transduction

along with the Biochemistry of membrane transport

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mechanism, active transport, passive transport, simple

and facilitated diffusion.

Chemistry

structure

nucleosides and

nucleotides:

and

of

On completion of this set the learners will be able to

Appreciate the detailed Chemistry and structure of

nucleosides and nucleotides with their biochemical

role, their derivatives along with their significance.

Describe the Synthetic derivative of purine and

pyrimidines, and their role in health and diseases.

Understand types of Nucleic acids, their structure and

functions.

58 Proteins:

By the time the learners finish the course they will be

able to

Explain the structure, functions and classification of

amino acids along with their buffering role in human

body in pH maintenance.

Describe Definitions, Biochemical importance and

classification of proteins based on, Physiochemical

properties, Functional, Nutritional, and structural basis.

Understand the details of Structure of proteins and their

significance.

Contrast the techniques for separation of proteins e.g.

salting out, Electrophoresis, Chromatography, and

Centrifugation.

Explain Immunoglobulins and their

biochemical significance.

Describe chemistry and functions of Plasma proteins &

their clinical significance.

59 Prophyrins and

hemoglobin:

At the end of this set, the learners will be able to

Explain Chemistry and biosynthesis of porphyrins and

their disorders (Porphyrias).

Describe Structures, functions and types of

haemoglobin, Oxygen binding capacity of haemoglobin,

factors affecting and regulating the oxygen binding

capacity of haemoglobin.

Detail the concepts of Degradation of heme, formation

of bile pigments, its types, transport and excretion,

Hyperbilirubinimea, their biochemical causes and

differentiation.

Discuss jaundice and its types, and kernictrus.

understand Haemoglobinopathies (Hb-S, thalassaemia

etc) and their biochemical causes.

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List of Practical:

S. No Practical Topics

1. Introduction to use of Laboratory Equipment

Glassware

Spectronic 20

Microlab


Incubator

Water Bath

Hot Oven


Centrifuge Machine

Electronic Balance pH

Meter

4. Types of Solutions, their preparation and clinical significance

5. Experiments on Proteins Qualitative Analysis - I

Biuret Test

Millon’s Test

6. Experiments on Proteins Qualitative Analysis - II

Ninhydrin Test

Aldehyde Test

7. Experiments on Proteins Qualitative Analysis - III

Sulphur Test

Xanthoproteic Test

List of Case Based Learning (CBL):

Topic: Cell (Leber Hereditary Optic Neuropathy LHON):

A 27-year-old boy presented to ophthalmic OPD with rapid deterioration of vision in

both eyes. He felt blurring of central in right eye eight weeks back which gradually

increased and now developed similar symptoms in other eye. His visual acuity is

6/36 in right and 6/12 in left eye. On fundus examination optic disc showed

edematous retinal nerve fiber layer and telangectatic vessels. A CT scan brain did

not reveal any inflammatory or space occupying lesion before or after optic chiasma.

These findings led the ophthalmologist to suspect LHON.

The buccal mucosa sample was sent to human molecular biology laboratory for

identification of genetic mutation (if any) leading to the condition and confirmation of

provisional diagnosis. The scientists in the lab separated mitochondria from the cells

by disrupting the cells and centrifugation at 700g once and at 12000 g twice for 15

and 5 minutes. Sequencing of MT-ND1, MT-ND4, MT-ND4L and MT-ND6 genes was

carried out and MT-ND1 was found to have point mutation. The diagnosis of LHON

was confirmed. MT-ND1 is the gene spanning 3,307 to 4,262 of mtDNA and encodes

for NADH dehydrogenase of ETC.

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RELATED INVESTIGATIONS:

Test Name Result

Visual field testing Central vision deterioration

CT Scan Brain Normal study

Mitochondria are one of the most important cell organelles and work mainly as

powerhouse of the cell. Many of the enzymes of mitochondrial function are encoded

by its own DNA called mtDNA which is inherited purely from mothers. Mutations and

their transfer to next generation is found not only in nuclear DNA but also in mtDNA.

Several diseases have been found to be caused by mitochondrial dysfunction which

is due to mutations in mtDNA and examples include lactic acidosis, mitochondrial

encephalopathy, stroke-like-episodes, LHON and Leigh syndrome.

LEARNING OBJECTIVES:

1. Structure and function of different organelles of the cell.

2. Structure, function and inheritance of mitochondria

3. Techniques for isolation and study of cell components and their importance in

clinical medicine

REFERENCE BOOKS:

1. Lippincott’s textbook of Biochemistry

2. Harper’s text book of Biochemistry

3. Davidson’s Practice of Medicine

Topic: Cell (I- Cell Disease- lysosomal targeting problems)

A female infant with a normal delivery after 38 weeks and normal intrauterine life

showed the physical findings characteristic of I-cell disease. She manifested

gargoyle face, progressive psychomotor retardation, and increased serum levels of

lysosomal enzymes with decreased activities in peripheral blood lymphocytes. The

diagnosis was made by the analyses of lysosomal enzymes. The child died at the

age of 2 years and 3 months due to respiratory insufficiency. By electron

microscopy, various-shaped membrane-bound vacuoles were observed in the

cytoplasm of various cells such as hepatocytes, myocardial muscle cells, epithelial

cells of the renal glomeruli, proximal renal tubular cells, fibroblasts, and

chondrocytes. By histochemical analyses we found that these intracytoplasmic

storage vacuoles contained glycosaminoglycan and proteoglycan.

In general, peripheral blood smears are performed to obtain information with regard

to various morphological features as an aid in the diagnosis of infection or

malignancy. This report presents a patient with I cell disease (inclusion cell disease),

a fatal lysosomal storage disorder caused by a defect in an enzyme responsible for

the transfer of mannose-6-phosphate ligands to precursor lysosomal enzymes. As a

consequence, most lysosomal enzymes are transported outside the cell instead of

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being correctly targeted into the lysosomes, resulting in the storage of

macromolecules in lysosomes. I cell disease, with its heterogeneous clinical

presentation, can be diagnosed by the presence of intracellular vacuole-like

inclusions in lymphocytes and fibroblasts, high serum lysosomal enzyme activities,

and a defect of N-acetylglucosamine-1-phosphotransferase. This report describes

the morphological aspects of peripheral lymphocytes in a blood smear of a patient,

the first clue to the final diagnosis of I cell disease. The observed vacuole-like

inclusions in lymphocytes of this patient were negative for periodic acid Schiff (PAS)

and Sudan black B staining, in contrast to earlier reports.


1. Structure and function of different organelles of the cell.

2. Structure, function and pathology of lysosomes

3. Enzyme processing and targeting to organelles

REFERENCE BOOKS:


2. Harper’s text book of Biochemistry

3. Davidson’s Practice of Medicine

Topic: Nucleic acids (Acute Gout):

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A moderately obese 54-year-old male appeared at the emergency department

complaining of severe pain of 10 hours’ duration in his left big toe. He stated that he

was a regular consumer of meat and soda (alcohol and sea food consumption are

also risk factors). He had no other significant medical history. On examination, his

left big toe was found to be red and markedly swollen around the

metacarpophalangeal joint, and exquisitely sensitive. There was no evidence of

arthritis elsewhere. Because of the history and location of the affected joint, the

attending physician suspected that the patient was having an attack of acute gout.

She ordered a number of lab tests, including a white cell count, determination of

serum uric acid, and x-ray examination of the affected joint. The x-ray findings were

non-specific; no indication of chronic arthritis was evident. Findings of other tests are

tabulated below. Under local anesthesia, arthrocentesis was performed on the

affected joint and a small amount of synovial fluid withdrawn and sent to the

laboratory for detection of cells and crystals. Typical needle-shaped crystals of MSU

showing negative birefringence were detected in the synovial fluid.

LAB INVESTIGATIONS:

Test Name Result Normal Values

Serum Uric acid 680 µmol/L Children 120-330

µmol/L

Adult Male 210-430

µmol/L

Adult Female 150-360

µmol/L

ESR 60 mm 1 – 10 mm in 1st hour

WBC Count 11.0 x 10 9 /

L

4.0 x 11.0 x 10 9 / L

RA Factor Negative Negative

Gout is a disease caused by hyperuricemia mostly due to genetic factors while diet

and lifestyle play a minor role in its causation. Uric acid is an end product of purine

metabolism and as it is already near its saturation limit in plasma, minor increase due

to mostly under-excretion from kidney or overproduction leads to its deposition in

crystal form mostly where the solvent is stagnant like synovial fluid of relatively

immobile joints. This crystallization appears first at the most immobile and coldest

fluid body, typically big toe joint space and typically at night because temperature is

further lower at night time and due to sleep and mobility is also further decreased.

Crystals in a smooth lubricated environment play havoc and cause acute

inflammatory response leading to severe pain, redness, warmth and loss of function

locally. Moreover, uric acid deposition in other soft tissues leads to formation of

tophi.

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1. Structure and chemistry of nucleosides and nucleotides.

2. Functions of nucleotides.

3. The biochemical basis of various clinical features

REFERENCE BOOKS:

1. Harper’s text book of Biochemistry.

2. Davidson’s Practice of Medicine.


Topic: Nucleic Acids (ADA Deficiency)

A little girl aged 11 months was brought by her parents to a children's hospital. She

had had a number of attacks of pneumonia and thrush (oral infection usually due to a

fungus Candida albicans) since birth. The major findings of a thorough workup were

very low levels of circulating lymphocytes (i.e. severe lymphopenia) and low levels of

circulating immunoglobulins. The attending pediatrician suspected SCID. Analysis of

a sample of red blood Cells revealed a low activity of ADA and very high level (about

50 times normal) of dATP. This confirmed the diagnosis of SCID due to deficiency of

ADA, the enzyme that converts adenosine to inosine.

The deficiency of ADA is inherited as autosomal recessive and accounts for almost

15% cases of SCID. T lymphocytes express high activity of enzyme normally. Lack

of ADA activity leads to accumulation of adenosine and dATP which is toxic to T

cells. Secondarily B lymphocytes are also affected and lead to impaired humoral

immunity.

Defective immune system allows different opportunistic infection to occur and recur.

An example of acquired immunodeficiency is AIDS. Such conditions can be treated

by, antibiotics, fortifying immune system by immunoglobulins and treating the root

cause.


Synthesis, ingestion and fate of nucleotides in human body

Role of Nucleotides in DNA synthesis and outcome of ADA deficiency The

biochemical basis of various clinical features

REFERENCE BOOKS:

Harper’s text book of Biochemistry. (Page 616) Davidson’s

Practice of Medicine.

Lippincott’s textbook of Biochemistry

Topic: Protein Chemistry (Creutzfeldt Jakob Disease)

A 70 years old man reported for the third time in last 3 weeks in medical OPD with

progressive difficulty in walking. He had muscle stiffness, twitching and involuntary

jerks in both legs. This patient was being treated by psychiatrists for depression,

agitation, mood swings, memory loss and thought problems for 2 weeks immediately

preceding the onset of current symptoms. Taking into account the rapid progression

and pattern of symptoms he was provisionally diagnosed as a case of Creutzfeldt

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Jakob Disease. The findings of MRI, EEG and spinal tap were consistent with the

diagnosis. Patient was put on supportive symptomatic treatment and relatives were

counseled.

The protein misfolding which is contagious from abnormal to normal protein leads to

prion diseases. Prion diseases, such as Creutzfeldt-Jakob disease, occur when prion

protein, which is found throughout the body but whose normal function isn't yet

known, begins folding into an abnormal three-dimensional shape. This shape change

gradually triggers prion protein in the brain to fold into the same abnormal shape.

Through a process scientists don't yet understand, misfolded prion protein destroys

brain cells. Resulting damage leads to rapid decline in thinking and reasoning as well

as involuntary muscle movements, confusion, difficulty walking and mood changes.


Chemistry of amino acids

Levels of protein folding and how it is carried out

Abnormalities in protein structure/folding

REFERENCE BOOKS:

Lippincott’s illustrated reviews of Biochemistry

Harper’s text book of Biochemistry.

Davidson’s Practice of Medicine.

Topic: Protein Chemistry (Emphysema- α 1 antitrypsin deficiency)

A 68-year-old Caucasian man with a 25 pack-year smoking history presented with

new-onset dyspnea on exertion in the setting of workplace dust exposure. During his

evaluation, he was found to have α1-antitrypsin deficiency with evidence of

development of pulmonary emphysema. Workplace spirometric monitoring over 10

years of surveillance for an on-the-job respirator fit program demonstrated a sharp

downward slope in forced expiratory volume in one second, or FEV1, during his

periods of most significant dust exposure, which was attenuated after discontinuation

of his workplace exposure.

Blood and other body fluids contain a protein, α1-antitrypsin (α1-AT, A1AT, currently

also called α1-antiproteinase), that inhibits a number of proteolytic enzymes (also

called proteases or proteinases) that hydrolyze and destroy proteins. α1-AT

comprises more than 90% of the α1-globulin fraction of normal plasma. α1-AT has

the important physiologic role of inhibiting neutrophil elastase ––a powerful protease

that is released into the extracellular space, and degrades elastin of alveolar walls,

as well as other structural proteins in a variety of tissues. Most of the α1-AT found in

plasma is synthesized and secreted by the liver. In the normal lung, the alveoli are

chronically exposed to low levels of neutrophil elastase released from activated and

degenerating neutrophils. This proteolytic activity can destroy the elastin in alveolar

walls if unopposed by the action of α1-AT, the most important inhibitor of neutrophil

elastase. Because lung tissue cannot regenerate, emphysema results from the

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destruction of the connective tissue of alveolar walls. Smoking causes the oxidation

and subsequent inactivation of that methionine residue, thereby rendering the

inhibitor powerless to neutralize elastase. Smokers with α1-AT deficiency, therefore,

have a considerably elevated rate of lung destruction and a poorer survival rate than

nonsmokers with the deficiency.


Fibrous proteins

Normal structure and synthesis of collagen and elastin

Abnormalities of fibrous proteins

REFERENCE BOOKS:

Lippincott’s textbook of Biochemistry Harper’s

text book of Biochemistry. (Page 616)

Davidson’s Practice of Medicine.

Topic: Porphyrins and Hemoglobin (Hepatitis A)

A 31 years old man presented with jaundice, nausea, anorexia, restlessness,

lethargy, fatigue and dark color urine for three days. Color of his stools was normal

and there was no itching on the skin. He was not having pyrexia and intensity of

jaundice was not of fluctuating type. There was no history of significant weight loss.

There was mild pain in the right hypochondrium. He did not have any known

hemoglobinopathy. He was non-alcoholic and there was no history of use of any

drug recently.

Ultrasonography showed no fatty infiltration of liver.

Lab Investigations:

S/N Test Result Reference values

1 Serum Total bilirubin 42 µmol/L Adult 2-17µmol/L

2 Conjugated Bil (direct) 10 µmol/L 0-4 µmol/L

3 Unconjugated Bil (indirect) 32 µmol/L 0-13 µmol/L

4 Urine bilirubin Present Absent

5 Urinary urobilinogen Increased 0-4 mg/ 24 hrs

6 Serum ALT 2800 U/L Male Upto 42 U/L

Female upto 32

7 ALP 54 U/L 132-365 U/L adults

Levels higher in children

8 AST 40 U/L Upto 37 U/L

9 GGT 32 U/L Upto 30 U/L

10 Plasma haptoglobin normal -

11 Serum albumin 33 g/dL 35-50g/L

12 Hep B surface antigen (HBsAg) in

serum

Negative Negative

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13 Anti HCV antibody (anti HCV Ab) in

serum

Negative Negative

14 Anti Hep A antibody (IgM) Positive Negative

Hepatitis A is a viral infection and resultant inflammation of the liver caused by Hep

A virus. Unlike Hep B and C this virus does not cause chronic disease and causes

acute severe and self-limiting hepatitis making the patient immune against this virus

for rest of his life. Unlike Hep B and C which are transmitted through blood or sex,

hep A virus is transmitted through orofecal route. Senescent RBCs are broken in

spleen and heme and globin separated and globin degraded into amino acids in

fixed leukocytes of spleen. Heme is oxidized to biliverdin and bilirubin which leaves

reticuloendothelial system and travel in plasma in protein bound form. Hepatocytes

uptake and conjugate bilirubin for excretion from body in biliary route. Viral infection

of liver affects not only conjugation but also other functions of the liver like albumin

synthesis. This results in jaundice hypoalbuminemia and edema (later in chronic

cases only), though liver has got the capability to handle 300 times more bilirubin in

normal state and a capacity of hepatocyte regeneration. Chronic cellular damage,

fibrosis and regeneration leads to liver failure and a condition called cirrhosis of liver

which is leading cause of death due to hep B and C infections.


Synthesis and degradation of heme

Metabolism of bilirubin in body

Role of hepatocyte in bilirubin handling and its diseases (inherited and acquired)

REFERENCE BOOKS:

Lippincott’s textbook of Biochemistry

Harper’s text book of Biochemistry

Davidson’s Practice of Medicine

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MODULE-II

Biochemistry

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Summary:

Code Y1M2

Name Biochemistry

Duration 10 weeks




module)

1.Thorax

2.Cardiovascular system

Subject Themes

Chemistry of carbohydrates

Chemistry of Lipids

Enzymes

Body Fluids

Minerals & Trace Elements

Prerequisite Module Y1M1


MIT

Lectures

Tutorials (PTT)

CBL

Practicals

Class tests


Carbohydrate

Chemistry

Upon successful completion of this course, students will

be able to:

Define and classify carbohydrates with the

understanding of biochemical nature, significance of

important member of each group.

Explain structure of carbohydrates, isomerism and

properties of monosaccharide.

Enist different dietary sources and understand common

disorders related tochemistry of CHO.

Describe important homo and hetero Polysaccharides,

their important examples and biochemical role,

Understand the biomedical importance of carbohydrates

and their derivatives in health and disease conditions

Lipid Chemistry By the time the students finish the course, they will be

able to:

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Define and classify lipids on different basis along with

appropriate examples.

Difference between oil, fat, waxes and vegetable ghee

as well as the process of hydrogenation and iodination,

saponification, acid number polansky,s number and

other physical attributes.

Describe saturated, unsaturated, poly unsaturated,

essential, non essential, Trans and cis type of fatty acids

and their significance in health and disease.

Distinguish structure of Glycero and sphingophospholids

as well as other different complex lipids and appreciate

their biochemical significance.

Describe Eicosanoids, their functions in health and

disease and the inhibitory action of NSAIDS and steroids

on them.

Recognize the sterol structure and different important

steroids especially the cholesterol, its functions and

significance with regards to IHD.

Summarize classification of lipoproteins, chemical

composition, functions and disorders

Understand the rancidity, its types and lipid per oxidation

and its clinical implications.

Enzymes At the end of the course, students are expected to be

able to:

Define different terms e.g, Coenzymes, co-factors,

holozymes, prosthetic group, ribozymes, zymogens

isozymes etc.

Classify enzymes and describe mechanism of enzyme

actions.

Explain different properties of enzymes and factors

affecting enzymes activity.

Illustrate enzyme kinetics in relation to Michaelis-Menten

Equation and Lineweaver- Burke plot.

Describe enzyme regulations, activation, inhibition and

biomedical importance of synthetic inhibitors.

Understand role of enzymes in clinical diagnosis and

therapeutics.

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Body Fluids By the time the students finish the course, they will be

able to:

Define pH, buffers and briefly explain their mechanism of

action.

Explain Henderson- Hasselbalch Equation and develop

problem-solving skills based on this equation.

Describe Types of particles, solutions and colligative

properties

Understand the phenomenon of osmosis and osmotic

pressure and its implications regarding clinical situations.

Explain Surface tension, viscosity & their importance

related to body fluids.

Minerals and

Trace elements

By the end of the course, the students will be able to:

Classify minerals (macro minerals e.g Na, K, Ca, Cl, PO4

and micro minerals e.g Fe, Zn, Mg, Se, I, Cu, Cr, Cd,

Mn). Describe absorption/resorption and body regulation

of minerals, nutritional sources, RDAs, toxicity and

deficiency states of minerals.

Enlist the trace elements and briefly explain their

biochemical significance.

List of Practicals:

S. No CONTENTS

EXPERIMENT- 4. EXPERIMENTS ON

BENEDICT'S TEST

CARBOHYDRATES /

EXPERIMENT-5. MOLISCH TEST

EXPERIMENT -6. IODINE TEST

EXPERIMENT-7. FEHLINGS TEST

EXPERIMENT-8. SELIWANOFF'S TEST

EXPERIMENT -15. EXPERIMENT ON LIPIDS (RANCIDITY OF

FATS)

EXPERIMENT -16. MICROSCOPIC STUDY

CRYSTALS

OF CHOLESTEROL

EXPERIMENT- 17. COLOUR TESTS FOR

(SALKOWSKIS TEST)

CHOLESTEROL

EXPERIMENT -18. LIEBERMANN BURCHARD TEST

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List of Case Based Learning Scenerios:

Topic: CHO chemistry (Anticoagulation)

A 62-year-old female presented to clinic with pain, swelling and redness to her right

lower leg. She stated that she was experiencing right calf pain worse with walking.

She noted that she returned home from a vacation to Europe last week which

included a 15-hour flight. The patient's vital signs were stable and she was afebrile.

The patient had a past medical history including hypertension and type 2 diabetes

both of which were controlled with oral medications.

On examination, physician noticed that patient’s right leg to be slightly erythematous

and her calf is tender to touch. She had trace pedal edema in the affected leg and

limps slightly when walking. Her right calf was greater in size compared to her left.

Given this patient's medical history as well as her recent sedentary activity on her

long flight, physician suspected her to have DVT and ordered a venous ultrasound of

her right leg. Ultrasound results reveal a deep venous thrombus in her popliteal

vein. Based on this patient's ultrasound results, doctor prescribed her five days of

subcutaneous injectable heparin as well as coumarin. She was instructed her to

return to the clinic in five days to recheck her INR. She was issued strict instructions

to return should she develop chest pain or shortness of breath.


1. Chemistry and functions of GAGs

2. Heparin and its role in body

3. Proteoglycans chemistry and functions

REFERENCE BOOKS:




Topic: Enzymes (Diagnosis of biliary obstruction)

A 40 years old female presented with jaundice and pain in epigastrium for three

days. She also complained of nausea, vomiting, itching on skin, anorexia, pale color

stools and dark color urine. On examination her skin and sclerae were yellow. There

was no history of fever or weight loss over last few months. Ultrasonography

abdomen showed gall stones and no mass in the bile duct was seen. Other lab

investigations are as under

LAB INVESTIGATIONS:


Serum bilirubin Total 40µmol/L 2-17 µmol/L

26

Conjugated 22 µmol/L 0-4 µmol/L

Unconjugated 18 µmol/L 0-13 µmol/L

Serum ALT 46 U/L Upto 40 U/L

AST 49 U/L Upto 40 U/L

ALP 620 U/L 132-365 U/L

GGT 130 U/L Upto 30 U/L

Enzymes are mostly intracellular species or they are secreted into specific cavities

e.g, digestive enzymes. Normal cellular turnover causes some release into the

plasma and that constitute the basis for normal levels of plasma enzymes. If a

certain enzyme in increased more than normal in plasma, it means cellular rupture in

the tissue in which this particular enzyme or its specific isoform was abundant.

Isoforms or isozymes of one enzyme mean a single change in primary structure of

protein which does not affect the activity or stability of enzyme much but give

different bands on electrophoresis. Increase in plasma ALT means hepatocellular

damage


1. Classification of enzymes

2. Factors affecting enzyme activity

3. Mechanism of enzyme action

Topic: Enzyme

A 65 years old chronic alcoholic reported to surgical OPD CMH Rwp with complains

of weight loss, anorexia & abdominal pain radiating to the back. Physical

examination showed a palpably enlarged gall bladder. Lab investigation showed:

Lab Investigation:

Computed tomogharapgy showed a mass in the head of pancreas. The patient

was diagnosed as a case of obstructive jaundice due to the pancreatic

adenocarcinoma.

Patient Value

Serum conjugated bilirubin

level

Increased

Urine bilirubin Present

Urine urobilinogen Absent

Fecal urobilinogen Absent

Serum ALP Highly Increased

Serum ALT Marginally Increased

Serum AST Marginally Increased

Many diseases that cause tissue damage result in an increased release of

intracellular enzymes into the plasma. The level of specific enzyme activity in the

plasma frequently correlates with the extent of tissue damage. Alkaline

27

phosphatase (ALP) is elevated in certain bone and liver diseases. ALP is useful for

the diagnosis of rickets, hyperparathyroidism, carcinoma of bone, and

obstructive jaundice.


Mechanism of action of enzymes

Factors affecting enzyme activity

Role of enzymes in clinical diagnosi

Topic: Body Fluids

A 45-year-old male previously known to have duodenal ulcer presents with

complaints of persistent vomiting for past 36 hrs. He has no history of abdominal

pain. He complains of being dizzy when he stands up.

On examination his pulse is 95 beats/min, blood pressure is 90/50mmHg with

sunken eyes and dry oral cavity.

LAB INVESTIGATIONS:


Plasma Na+ 130mEq/L 135 – 145mEq/L

pH 8 7.35 -7.45

Urea 50mg/dl 10-40mg/dl

Cl- 80mEq/L 90-106mEq/L


1. Body fluid compartments.

2. Regulation of water balance

3. Weak acids and bases

4. Henderson Hassel Balch equation

CBL Session

A middle aged man was brought to emergency department with a history of

persistent vomiting and profuse watery diarrhea for the last 10 hours. Pt had a rapid

feeble pulse, sunken eyes and coated tongue. His blood pressure was 80/40 mm of

Hg. He was diagnosed as a case of acute gastroenteritis. Related lab

investigations:

Result Normal value

Serum Na + 130 meq/L 135-145 meq/L

“ K + 2.8 meq/L 3.5-5 meq/L

“ Urea 50 mg/dl upto 40 mg/dl

“ Creatinine 1.2 meq/L 0.6-1.2 mg/dl

“ Cl - 76 meq/L 96-106 meq/L

Learning Objectives:

Movement of materials across cell membranes Simple

diffusion

28

Carrier mediated diffusion and active transport

Osmosis and surface tension

Topic: Minerals (Copper Storage Disease, WD disease)

An 8-years boy was brought to PAEDS OPD in the hospital. He was presenting mild

cognitivedeterioration and clumsiness and common parkinsonian features.

Parents informed that the child had delayed slurred speech. It was also informed by

the parents that on opening arms child present wing-beating tremors. On details

family history parents informed that three years girls died two years earlier because

of same symptoms. Physician observed Kayser–Fleischer rings (KF rings) using

slit lamp and skin turgor&Spasticity was poor. Persistent elevatedlevels of serum

alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were

observed. The attending pediatrician suspected Wilson Disease. Liver nodular

growths were observed in abdominal USG. To confirm diagnosis Liver FNAC was

performed which showed very high level of copper accumulation. High level of

copper was also observed in 24-hour urine exam. Furthermore, reduced Serum

ceruloplasmin levels was observed. In order to confirm the Wilson disease whole

blood samples was sent to molecular laboratory for genetic analysis in ATP7B gene.

S.No Tests Patients Refence

1 ALT 134U/L Upto 42 U/L

2. Urine Cu 65mmol/L >1mmol/l

3. Serum Cu 75mmol 11-24mmol/L

4. Serum ceruloplasmin 8 mg/L 15-20mg/L

5. USG abdomin Nodular liver Negative


Copper metabolism in Human and its absorption

Functions of Copper

Dietary sources of Copper

Copper containing Enzymes

Topic: Iron Deficiency Anemia:

A multiparous female presented in medical OPD with the complaints of generalized

weakness, occasional dizziness, easy fatigability and shortness of breath. She

belonged to a low socio-economic status. Her past medical history reveals

postpartum hemorrhage.

On examination she was pale, her pulse was 90 beats/min, blood pressure was

100/70mmHg.

https://en.wikipedia.org/wiki/Kayser%E2%80%93Fleischer_ring




29

LAB INVESTIGATIONS:


Hb 8.5g/dl 12-14g/dl

MCV 70fl 80-100fl

MCH 20pg 27- 31pg

MCHC 28g/dl 32- 36g/dl

S.Fe 34 g/dl 50- 170 g/dl

TIBC 400µg/dl 250- 370µg/dl

S. Ferritin 10µg/L 15- 150µg/L

Peripheral

Smear

Blood Hypochromia

Microcytosis


1. Classify minerals

2. Sources, Absorption and Transport of Iron

3 Disorders of iron metabolism

30

MODULE-III

Biochemistry

31

Summary:

Code Y1M3

Name Biochemistry

Duration 10 weeks




module)

Lower Limb

Respiratory System

Subject Themes

Nutrition

Water soluble vitamins

Fat Soluble vitamins

Prerequisite Module Y1M1&Y1M2


MIT

Lectures

Tutorials (PTT)

CBL

Practicals

Class tests


Nutrition At the end of this set students will be able to

Describe the concept of food, nutrition, Diet and Balanced

Diet.

Define different parameters regarding food and nutrition

like RDA, etc.

Concepts of BMR, Caloric requirements of the body,

Energy Balance.

Appreciate carbohydrates, fats and proteins as major

food source and their nutritional requirements.

Understand the nutritional quality of a protein, essential

amino acids their nutritional importance and nitrogen

balance.

Elaborate the sources of carbohydrates, their glycemic

index.

Recall the nutritional importance of fats and fatty acids,

essential fatty acids, saturated, unsaturated and poly

unsaturated fatty acids.

32

Understand and estimate caloric requirements of the

body.

Describe the concept of Balanced Diet.

Explain nutritional requirements in: - Pregnancy -

Lactation - New born and in nutritional disorders.

Explain Protein Energy Malnutrition.

Differentiate between Marasmus and Kwashiorkor.

Water soluble vitamins

After completion of this unit students will be able to

Classify water soluble vitamins.

Describe the chemistry of water soluble vitamins.

Explain the Biochemical Functions of water soluble

vitamins.

Differentiate the deficiency manifestations of water

soluble vitamins, Hypervitaminosis and its clinical fall

outs Enlist the daily allowances and sources of water

soluble vitamins.

Describe the hypervitaminosis of water soluble vitamins.

Fat Soluble vitamins

After completion of this unit students will be able to

Explain general features of fat soluble vitamins.

Explain the chemistry of fat soluble vitamins.

Describe the biochemical Functions of fat soluble

vitamins.

Explain the deficiency manifestations of fat soluble

vitamins.

Enlist the daily allowances and sources of fat soluble

vitamins.

Describe causes and manifestations of Hypervitaminosis

and toxicity.

List of Practicals:

EXPERIMENT -19. TESTS FOR URINE ABNORMALITIES-I

EXPERIMENT -20. TESTS FOR URINE ABNORMALITIES-II

EXPERIMENT -21. PREPARATION OF URINE REPORT BY ANALYZING

GIVEN SAMPLE OF URINE 73

At the end of the year the learner will be able to

Operate the centrifuge machine

33

Identify the presence of specific amino acids (aromatic amino acids, sulpher

containing amino acids)

Differentiate fibrous and globular proteins

Detect proteins in urine Perform

Molisch’s test for general detection of Carbohydrate. Iodine

test for polysaccharides (starch &glycogen).

Benedict’s test for reducing carbohydrates.

Barfoed’s test to differentiate reducing mono and disaccharides.

Selivenoff’s test for detection of keto sugars. Test

on rancidity of fats.

Examination of cholesterol crystals.

Salkowski’s tes for presence of cholesterol.

Liebermann Burchard test for the determination of cholesterol in blood

List of Case Based Learning Scenerios:

Topic: Vitamin A Deficiency:

A 54-year-old male reported to medical OPD with a complaint of slow onset,

progressive difficulty in seeing the objects at night. The problem had increased over

the past six months. He had stopped driving because he could not see the road,

properly. All forms of artificial light seemed dim; however, daytime vision was normal.

He never had any other past ocular problems. There was no difficulty in

distinguishing colors.

Investigations:

Name of test Patient Value Reference

Range

vitamin A level 0.12 mg/L

0.30-1.20 mg/L

The patient was diagnosed as a case of Nyctalopia (night blindness) due to vitamin A

deficiency. He was started on oral vitamin A 10,000 international units (IU), twice a

day. After one month of treatment, the patient reported improvement in his vision.

Vitamin A is a fat soluble vitamin, necessary for a variety of functions such as vision,

proper growth and differentiation reproduction and maintenance of epithelial cell.

Night blindness (nyctalopia) is one of the earliest symptoms of vitamin A deficiency.

Vitamin A deficiency can occur as a result of malnutrition, malabsorption, or poor

vitamin metabolism due to liver disease.


Sources & biochemical function of Vitamin A.

34

Wald's visual cycle

Deficiency of vitamin A

Hypervitaminosis A

References Books:

1 Harper’s Text book of Biochemistry

2 Lippincott’s text book of Biochemistry


Internet and other reference sites

Topics: Folic Acid and Pregnancy

A 37 Years female, with 21st week of gestation, belonging to a rural area, reported in

obstetric OPD for a routine examination. She looked pale and malnourished.

On abdominal examination her fundal height was not in accordance to her LMP. She

was advised for anomaly scan and other base lines.

Investigations:

PARAMETERS PATEINT NORMAL

RANGES

REFERENCE

Hb 9g/dl 12- 15g/dl

MCV 103fl 80-100fl

MCH 32pg 27-31pg

S.Folic acid 0.5ng/ml 2-20 ng/ml

Anomaly Scan Anencephalic fetus

On the basis of clinical history, examination and investigations she was

diagnosed as case of NTD (neural tube defect).


Sources of folic acid

Absorption and metabolism of folic acid

Deficiency effects of vitamin B9

Reference Books:

Lippincott’s Biochemistry (Latest Edition)

Harper’s Textbook of Biochemistry

35

Davidson’s principles of Medicine

Internet & other related journals

Topic: Scurvy

A 9 Year child presented on family OPD, with complaints of spongy bleeding gums

with loose teeth. Her mother gives the H/O his delayed healing in wounds. She tells

that he has sometimes red dots on legs and bleed from the nose.

On investigation, X-Ray shows bone thinning; CBP shows low level of Hb, raised

TLC. RBCs show howell jolly bodies. He was diagnosed as scorbutic.

Learning Objects:

What is the differential diagnosis?

What is etiology

Give the biochemical basis if this.

Enlist the functions of the missing biomolecule Cause

diagnosis & management of scurvy.

Reference Books:

Lippincott’s Biochemistry (Latest Edition)

Harper’s Textbook of Biochemistry

Davidson’s principles of Medicine Internet

& other related journals

Topic: Bleeding disorder due to vit. K deficiency

A postpartum woman from a rural Baluchistan community gave birth to a baby girl

with the aid of a midwife at home. She brought the baby to the hospital because of

continued bleeding and oozing from the umbilical stump. It is likely that this bleeding

diathesis is secondary to a deficiency of vitamin K.

Lab Investigations:

Test Name Level Normal Values

Prothrombin Time

Prothrombin Time 16 Sec 13Sec

P.T.T.K

36

Patient 38 Sec 34Sec

Bleeding Time

Bleeding Time 09 Min 2-8 min

Coagulation Time

Coagulation Time 12 Min 6-11.5 min

Fibrin – D – Dimer

Result 260 ng /ml < 250 ng / ml

Plasma Fibrinogen

Plasma Fibrinogen 450 mg / dl 200 – 400 mg / dl


1. Classification of Vitamin

2. Fat soluble vitamins

3. Vitamin K sources, function

4. Vitamin K deficiency

References Books:

Harper’s Text book of Biochemistry

Lippincott’s text book of Biochemistry


Internet and other reference site

Topic: Vitamin B12 (Pernicious Anemia)

A 35 years old female presented to the physician with the complaints of severe

weakness, weight loss, loss of appetite, depression and memory loss. She had an

excision of a gastric ulcer 4 years ago. On examination, she has tingling and

numbness in hands and feet, pale yellow skin, red and thick, decreased positional

and vibrational sense. On advice of physician, following lab investigations were

carried out

Lab Investigations:

Parameters Normal Value Patient value

Haemoglobin 12-14g/dl 8.9g/dl

RBC count 4-5.5X1012/L 3.0x1012 /L

MCV 76-96fL >100fL

Serum Vit B12 150-600pmol/L <70mg/dl

Urinary methymalonic

acid

Upto 0.5umol/L Raised

Schilling’s Test Normal Low

37

Vitamin B12 deficiency is more common in patients who fail to absorb the vitamin

from the intestine. A severe malabsorption of vitamin B12 leads to pernicious

anemia. It is an autoimmune disorder results in destruction of the gastric parietal

cells that are responsible for the synthesis of a glycoprotein called intrinsic factor.

Vitamin B12 obtained from the diet binds to intrinsic factor in the intestine and

subsequently transported into the general circulation. Lack of intrinsic factor prevents

the absorption of vitamin B12, resulting in pernicious anemia. Patients with

cobalamin deficiency are usually anemic, but later on neuropsychiatric symptoms

can be developed. Vitamin B12 deficiency can cause weakened bones and may lead

to hip fractures. An enlarged liver is another symptom.


Definition and classification of water soluble vitamins

Source, synthesis, absorption of Hematopoietic vitamins

Functions of Hematopoietic vitamins

Diseases and treatment of Hematopoietic vitamins

REFERENCE BOOKS:




At the end of the year the learner will be able to discuss the following topics with

detailed understanding of biochemistry along with their clinical correlations:

Cell organelles

Nucleotides

Plasma proteins

Jaundice

Thalaesemisias

Kernictrus

Pernicious anemia

Scurvy

Ricketts

Osteoporosis

Vitamin K deficiency

Kawashiorker and merasmus

Enzymes and clinical diagnosis

Therapeutic use of enzymes

Lactose intolerance

38

First Professional MBBS Examination

BIOCHEMISTRY

Table of Specifications for Annual First Professional Examination:

Theory

Time Allowed =03 hrs (Including MCQs)

Marks of theory paper =90

Internal assessment =10

Total marks =100

Pass Marks =50

25 x MCQs (on separate sheet) (25 Marks) Time =30 min

Q. No. 1,2,3,4,5,6,7,8,9

(7x SAQs/SEQs (C1 & C2) = 07 marks each

2 x SAQs/SEQs (C3) = 08 marks each) (65 Marks) Time = 2 hours 30

Topic

NUMBER OF MCQs

(25)

(C1=10 marks,

C2=10 marks, C3=5 marks)

1 mark each

NUMBER OF SAQs/SEQs (09)

7x SAQs/SEQs (C1 &

C2) = 07 marks each

2 x SAQs/SEQs

(C3) = 08 marks

each

Chemistry of Protein & Amino

Acids 03 01

Any 2 from whole courses

Enzymes 03 01

Vitamins 03 01

Porphyrins & Hemoglobin 03 01

Chemistry of CHO, Nutrition 04 01

Chemistry of lipids +

Minerals and Trace elements

04 01

Nucleotides and Nucleic Acid,

Biochemistry of cell & Body

Fluids

+ Biological membrane

05

01

Total 25 (25 Marks) 09 (65 Marks)

minutes

39

Theory: Internal Assessment (IA) Calculation

A B C D

Roll No.

Name

All Modules/

Pre annual

Exams or any other exam

Total Marks of internal

assessment

Out 0f 10

Total Marks Sum of Marks obtained x10/ sum of total marks in all

exams

Table of Specifications for Annual Professional Exam: Practical

Viva (Theory) 50

marks Practical 40

marks

Total

Internal

Examine

r

External Examine r

OSPE (20) Viva +

Performance

Journa

l Observed

(2 Station)

Unobserved

(10 Station)

25 25 10 10 15 5 90

Practical: Internal Assessment Calculation

A B C D

Roll No.

Name

OSPE /PTT/ Class tests throughout the year /Pre annual

Exams or any other exam

Total Marks of

internal assessment

Out 0f 10

Total Marks Sum of Marks obtained x10/ sum of total marks in all

exams

40

No____ Dated:

_______ 2019

Department of

Biochemistry

CMH LMC, Lahore

Subject : Updatd Nominal Roll -Faculty Members

Name CNIC

No

PMDC

Reg

No

PMDC

Faculty No

Designatio

n

Qualification Email Address Mobile No,

Resident

No &

Office

Phone No

Maj Gen

Dr. Abdul

Khaliq

37405-

489911

7-5

3944-P 0046/3944

-PM

Professor MBBS,M phill,

CHPE,FNAMS,F

CPS, Ph D,

FRCP

Dr.

Naheed Z

Razwi

35202-

217901

3-0

Non

medic

al

12970/Non

Medical

Professor MSc, MPhil,

PhD

[email protected] 03215733

307

Dr. Irum

Fayyaz

61101-

112201

2-4

16303-

P

6036/1630

3-P/M

Professor MBBS, MPhil iram_nadeem@yaho

o.com

03344239

089

Dr.

Aamenah

Malik

35201-

886104

2-8

45084-

P

15671/450

84-P/M

Associate

Professor

MBBS, MPhil [email protected] 03008443

469

Dr. Huma

Ashraf

37405-

031496

6-4

1712-

AJK

7789/1712

-AJK/M

Associate

Professor

MBBS, MPhil huma.monim.zat.ash

@ gmail.com

03218377

79

Dr. Sahar

Javed

35202-

750103

5-0

9830-

D

10623/983

0-D/D

Asst.

Professor

BDS.

MPhil

saaharjaved@

yahoo.com

03219436

069

04236500

257

Dr.Hira

Sohail

35201-

597938

4-8

62242-

P

11596/622

42-P/M

Asst.

Professor

M.Phil MBBS dr_hirasohail@

hotmail.com

03454232

459

04235893

382

Dr.M.

Omar

Akeel

35202-

705881

6-7

70114-

P

16985/701

14-P/M

Demonstra

tor

MBBS [email protected]

m

03334325

566

Dr.

Mustafa

Haider

35202-

614344

0-9

77793-

P

27659/777

93-P/M

Demonstra

tor


m

03214246

584

Dr.Khade

eja Anjum

34202-

269512

2-4

77841-

P

27366/778

41-P/M

Demonstra

tor

MBBS [email protected] 03215067

651

Dr, Anam

Malik

35202-

493284

2-8

65637-

P

17003/656

37-P/M

Demonstra

tor


m

03334707

218

mailto:[email protected]









41

Dr, Anam

Zia

54400-

153046

3-4

12696-

D

30431/126

96-D/D

Demonstra

tor

BDS [email protected]

m

03324684

045

Dr, Amna

Noor

35202-

098851

7-0

19389-

D

Demonstra

tor

BDS Amna-

noor1@hotmail,com

03314357

467

Dr.Taske

en Zahra

34603-

181465

2-0

85915

_P

Demonstra

tor

MBBS [email protected] 03334464

593

42

Recommended Books

Textbook of Medical Biochemistry (MN

Chatterjea)

Lippincott’s Biochemistry

Harper’s Illustrated Biochemistery

Hashmi’s complete Textbook of

Biochemistry

Essentials of Medical Biochemistry vol1

Essentials of Medical Biochemistry vol

2

43

Departmental library

Textbook of Medical Biochemistry (MN

Chatterjea)

8th Edition

Lippincott’s Biochemistry 7th Edition

Pre Test Biochemistry and Genetics 4th Edition

Instant Biochemistry (Faiq) 2nd Edition

Biochemistry A Case-Oriented

Approach

4th Edition

Textbook of Physiology and

Biochemistry

9th Edition

Harper’s Illustrated Biochemistery 29th Edition

Hashmi’s complete Textbook of

Biochemistry

5th Edition

BRS Biochemistry Molecular Biology &

Genetics

5th Edition

Kaplan Medical Biochemistry and

Genetics

Essentials of Medical Biochemistry vol1 7th Edition

Essentials of Medical Biochemistry vol

2

7th Edition

Clinical chemistry : Principles, Methods

and Interpretations

3rd Edition

Textbook of Biochemistry with clinical

correlations

6th Edition

Clinical chemistry (MARSHALL) 2nd Edition

Organic Chemistry ( Vollhardt)

Mathews Van Holde Biochemistry

Documents

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