study guide biochemistry department first year mbbs...cvs histology circulatory system immune system...
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Study Guide
Biochemistry
Department
First year MBBS
2
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
2. Introduction to use of Laboratory Equipment
Incubator
Water Bath
Hot Oven
3. Introduction to use of Laboratory Equipment
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.
LEARNING OBJECTIVES:
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:
1. Lippincott’s textbook of Biochemistry
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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LEARNING OBJECTIVES:
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.
3. Lippincott’s textbook of Biochemistry
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.
LEARNING OBJECTIVES:
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.
LEARNING OBJECTIVES:
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.
LEARNING OBJECTIVES:
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.
LEARNING OBJECTIVES:
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
Broad Themes of Module
(Theme: a subject that is being
integrated a majority of time of
module)
1.Thorax
2.Cardiovascular system
Subject Themes
Chemistry of carbohydrates
Chemistry of Lipids
Enzymes
Body Fluids
Minerals & Trace Elements
Prerequisite Module Y1M1
Mode of Information Transfer:
MIT
Lectures
Tutorials (PTT)
CBL
Practicals
Class tests
Biochemistry learning outcomes:
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
25
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.
LEARNING OBJECTIVES:
1. Chemistry and functions of GAGs
2. Heparin and its role in body
3. Proteoglycans chemistry and functions
REFERENCE BOOKS:
1. Harper’s text book of Biochemistry.
2. Davidson’s Practice of Medicine.
3. Lippincott’s textbook of Biochemistry
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:
Test Name Result Normal Values
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
LEARNING OBJECTIVES:
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.
LEARNING OBJECTIVES:
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:
Test Name Result Normal Values
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
LEARNING OBJECTIVES:
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
Learning Objectives:
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.
29
LAB INVESTIGATIONS:
Test Name Result Normal Values
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
LEARNING OBJECTIVES:
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
Broad Themes of Module
(Theme: a subject that is being
integrated a majority of time of
module)
Lower Limb
Respiratory System
Subject Themes
Nutrition
Water soluble vitamins
Fat Soluble vitamins
Prerequisite Module Y1M1&Y1M2
Mode of Information Transfer:
MIT
Lectures
Tutorials (PTT)
CBL
Practicals
Class tests
Biochemistry learning outcomes:
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.
Learning Objectives:
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
Davidson’s Practice of Medicine
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).
Learning Objectives:
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
Learning Objectives:
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
Davidson’s Practice of Medicine
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.
Learning Objectives:
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:
1. Harper’s text book of Biochemistry.
2. Davidson’s Practice of Medicine.
3. Lippincott’s textbook of Biochemistry
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
MBBS [email protected]
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
MBBS [email protected]
m
03334707
218
41
Dr, Anam
Zia
54400-
153046
3-4
12696-
D
30431/126
96-D/D
Demonstra
tor
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