Academics

Karachi Institute of Medical Sciences

Academics section

KIMS has an integrated modular system consisting of three modules in one year. Each module is of 10 weeks. Following are the subjects to be covered:

Foundation Year-1

(Revised 2016)
Module – 1

MODULAR, INTEGRATED, STUDENT CENTERED, AND PROBLEM BASED
National University of Medical Sciences Pakistan

Acknowledgement

This is Academic Year – 1 MBBS Curriculum of Army Medical College. NUMS and Army Medical College gives right to medical colleges affiliated with NUMS to adapt, or adopt this curriculum to the degree of need of affiliated medical colleges of NUMS


CURRICULUM PREPARED BY:

(Curriculum Committee)

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Prof. Brig Irfan Shukr, SI(M). MBBS, FCPS, FRCSEd, FFSTEd, MMEdn, DCPS-HPE.
Assoc. Dean (Academics & Med Edn)
Army Medical College

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Prof. Brig Shahid Jamal. MBBS, FCPS, FRCPath
President Curriculum Committee
Army Medical College

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Prof. Brig Shadab Ahmad But, SI(M). MBBS, MPhil, PhD(Anatomy)
Head of Anatomy Department
Army Medical College

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Prof. Col Khadija. MBBS, MPhil, FCPS (Anatomy), MCPS-HPE
Department of Anatomy
Army Medical College

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Assoc Prof. Lt Col. Umbreen Ahmad. MBBS, PhD (Physiology)
Head of Physiology Department
Army Medical College

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Prof. Lt Col Muhammad Alamgir. MBBS, FCPS (Physiology)
Department of Physiology
Army Medical College

Prof. Lt Col Amir Rasheed MBBS, PhD (Biochemistry)
Head of Department of Biochemistry& Molecular biology
Army Medical College

 


CURRICULUM APPROVED BY:

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Prof. Maj Gen Jawad Ansari. MBBS, FCPS, MRCP, FRCP, FCCP
Principal & Dean
Army Medical College

Overview

  • Model: AM College curriculum, revised 2015, 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 constructive perspectives of curricula.
  • Preface: The 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 world wide in a graduate doctor.
  • Organization: The curriculum is organized and integrated along important vertical and horizontal dimensions. The content taught is integrated concurrently in themed horizontal organization, and vertically across the years of medical education. The themes form the building blocks of this curriculum. These blocks unite to form three modules in the first year. In each block the sequencing of the content is logical, integrated and not subject based. Initial sequencing is on principles on which students knowledge, skill and attitudes will be founded, according to body systems. The aim is to minimize artificial separation of basic and clinical sciences.
  • Learning Strategies: Multiple learning strategies are used. Interactive lectures are used to provide students entrance to topic needing much effort by the student to understand, general review of theme or subject matter, update research and best evidence medical information, provoke thought, and understanding. 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. Workings in labs provides experiential, hand on learning.
  • Assessment: During the module the students are continually formatively assessed. At the end of module examination is formative with a summative component added to it. At the end of year is summative assessment according to the standards of PM&DC.

Module Structure

The duration of each of the three modules is 10 weeks, as follows:

Weeks Activity
a. Week – 1, to Week – 8: Teaching and Learning
b. Week – 9& 10: Self directed learning / end of module examination.

STRUCTURED SUMMARY

Code Y1-M1
Name Module One
Duration of module 10 Weeks
No of integrated blocks in the module 04
Blocks Themes 1. Introduction

2. Cells and genetics

3. Blood

4. Loco motor

Vertically integrated module themes across the blocks in vertical thread: 1.Gross anatomy Upper limb

Introduction to basic diseases relevant to 2.Relevant clinical sciences knowledge

3.Laboratory equipment use & experiments on carbohydrates and proteins

Prerequisite Module None
Subject MIT Per week In 08 weeks
Physiology Lectures 5 40
Biochemistry Lectures 3 24
Anatomy Lectures Histology 1 8
Lectures Embryology 1 8
Lectures Gen Anatomy 1 8
Dissection 3 24
BMS PBL for each subject 1 for each subject 8 for each subject
BMS Practical 1 8
Applied Clinical sciences Lectures 1 8
Pak studies Lectures 1 8

ASSESSMENT (TABLE OF SPECIFICATION)

Introduction:

It is formative, with summative element. Marks scored will add towards internal assessment marks, a component of summative examination.

There will be one theory paper and practical for anatomy, physiology and biochemistry. For practical the class will be divided into three batches A, B & C. each batch will have practical of anatomy, physiology and biochemistry separately on separate days

Schedule of exams:

Week 09 of the module
Mon Tue Wed Thurs Fri Sa Su
Self directed learning of Anatomy Theory paper

Anatomy

Self directed learning of physiology  Theory paper

Physiology

Self directed learning of biochemistry
Week 10 of the module
Mon Tue Wed Thurs Fri Sa Su
Theory paper

Biochemistry

Rest day before practical Practical of Anatomy, physiology and biochemistry Holiday

Practical exams schedule:

Mon Tues Wed Thurs Fri Sat Sun
Anatomy Last Theory paper day Rest day before practical Batch A Batch B Batch C Holiday
Physiology Batch C Batch A Batch B
Biochemistry Batch B Batch C Batch A

TABLE OF SPECIFICATION – EXAMINATION

Year: FirstModule: One
Code of Module: Y1M1

  1. SUBJECT: ANATOMY

TOS Theory examination: Total marks = 70

S. No Topic MCQ

20 x MCQs of 1 mark each

PBQ

1 X PBQ of 6 marks

2 X PBQ of 7 marks each

SAQ/SEQ

6 X SAQ/SEQ of 5 mark each

1. Embryology  04 (4marks) 01 (6marks)
2 Histology 05 (5marks) 01 ((5 marks)
3 General anatomy 02 (2marks) 01 (5 marks)
4 Upper limb 09 (9marks) 02 (7marks) 04 ((5 marks)
Total. 20 (20 marks) 3 (20 marks) 6 (30 marks)
Grand total 70
  1. TOS Practical examination: Total marks = 70.
Viva (theory) Practical
Examiner 1 Examiner 2 OSPE Observed station Manuals (Gross embryology & histology)
Gross embryology, embryology & X – rays Histology Long slides Surface marking
15 marks 15 marks 20 marks 10 marks 05 marks 02 marks 03 marks
  1. Theory Paper

Total numbers: 70

Time: 03 hours

Instrument of examination Topic Marks
Paper – A
Q – 1 MCQ X 20 20
Embryology 4
Histology 5
General anatomy 2
Upper limb 9
Q – 2 PBQ Embryology 6
Q – 3 PBQ Upper limb 7
Q – 4 PBQ Upper limb 7
Paper – B
Q – 5 SEQ/SAQ Histology 5
Q – 6 SEQ/SAQ General anatomy 5
Q – 7-10 SEQ/SAQ Upper limb 5
  1. SUBJECT: PHYSIOLOGY
  1. TOS Theory examination: Total marks = 70
S. No Topic No of MCQ
1 mark each
PBQ 2 X PBQ of 7 marks each.
1 X PBQ of 6 marks.
SAQ/SEQ

6 X SAQ/SEQ of 5 mark each

1. Cell, transport and general physiology 5 (5 marks) 1 ((5 marks)
2 Nerve and membrane potential 3 (3 marks) 1 (7 marks) 1 ((5 marks)
3 Muscle physiology 3 (3 marks) 1 (7 marks) 1 (5 marks)
4 Blood 4 (4 marks) 1 (6 marks) 1 ((5 marks)
5 Immunity 5 (5 marks) 2 (10 marks)
Total. 20 (20 marks) 3 (20 marks) 6 (30 marks)
Grand total 70
  1. TOS Practical examination: Total marks = 70.
Viva (theory) Practical
Examiner 1 Examiner 2 OSPE
Observed Unobserved Viva + Performance Procedure Copy
15 15 10 8 14 5 3
  1. Theory Paper

Total numbers: 70

Time: 03 hours

Instrument of examination Topic Marks
Paper – A
Q – 1 MCQ X 20 Topic 20
5 X Cell, transport and general physiology
3 X Nerve and membrane potential
3 X Muscle physiology
4 X Blood
5 X Immunity
Q – 2 PBQ Nerve and membrane potential 7
Q – 3 PBQ Muscle physiology 7
Q – 4 PBQ Blood 6
Paper – B
Q – 5 Cell, transport and general physiology Cell, transport and general physiology 5
Q – 6 Nerve and membrane potential Nerve and membrane potential 5
Q – 7 Muscle physiology Muscle physiology 5
Q – 8 Blood Blood 5
Q – 9 Immunity Immunity 5
Q – 10 Immunity Immunity 5

Important Note: If PBQ from immunity is given in place of blood then 2 SAQs/SEQs will be from blood and one SAQ/SEQ from immunity

  1. SUBJECT: BIOCHEMISTRY
  1. TOS Theory examination: Total marks = 70
S. No Topic No of MCQ

1 mark each

PBQ

2 X PBQ of 7 marks each.

1 X PBQ of 6 marks.

SAQ/SEQ

6 X SAQ/SEQ of 5 mark each

1. Chemistry of Protein 5 (5 marks) 1 (7 marks) 2 (10 marks)
2 Nucleotides and Nucleic Acid 5 (5 marks) 1 ((5 marks)
3 Porphyrins & Hemoglobin 5 (5 marks) 2 (7 & 6 marks) 2 (10 marks)
4 Biochemistry of Cell & Body Fluids+ Biological membrane 5 (5 marks) 1 (5 marks)
Total. 20 (20 marks) 3 (20 marks) 6 (30 marks)
Grand total 70
  1. TOS Practical examination: Total marks = 70.
Viva (theory) Practical
Examiner 1 Examiner 2 OSPE
Observed Unobserved Viva + Performance Procedure Copy
15 15 10 8 14 5 3
  1. Theory Paper.

Total numbers: 70

Time: 3 hours

Instrument of examination Topic Marks
Paper – A
Q – 1 MCQ X 20 Topics 20
Chemistry of Protein
Nucleotides and Nucleic Acid
Porphyrins & Hemoglobin
Biochemistry of Cell & Body Fluids+ Biological membrane
Q – 2 PBQ Chemistry of Protein 7
Q – 3 PBQ Porphyrins & Hemoglobin 7
Q – 4 PBQ Porphyrins & Hemoglobin 6
Paper – B
Q – 5 SEQ/SAQ Chemistry of Protein 5
Q – 6 SEQ/SAQ Chemistry of Protein 5
Q – 7 SEQ/SAQ Nucleotides and Nucleic Acid 5
Q – 8 SEQ/SAQ Porphyrins & Hemoglobin 5
Q – 9 SEQ/SAQ Porphyrins & Hemoglobin 5
Q – 10 SEQ/SAQ Biochemistry of Cell & Body Fluids+ Biological membrane 5

TOPICS (With MIT & Name of Instructor)

Topics Discipline Mode of Information Transfer Name of Instructor
INTRODUCTION
Homeostasis – I Physiology Interactive Lecture
Homeostasis – II Physiology Interactive Lecture
Introduction to Anatomical Terms Anatomy Interactive Lecture
Anatomical Position and directional terms Anatomy Interactive Lecture
Biomolecules Biochemistry Interactive Lecture
CELL AND GENETICS
Cytology- Techniques for study of cell Biochemistry Interactive Lecture
Cell membrane Physiology

Biochemistry

Interactive Lectures
Cell Organelle – I Physiology

Biochemistry

Interactive Lectures
Role of Cell Organelles in Metabolism Physiology

Biochemistry

Interactive Lectures
Cell Membrane Physiology

Biochemistry

Interactive Lectures
Genetic control of cell function

Chemistry of signals and receptors

Physiology

Biochemistry

Interactive Lectures
Cell Biochemistry SGD
Active transport, passive transport and facilitated diffusion Physiology Interactive Lecture
Nucleotide-I Biochemistry Interactive Lecture
Cytoskeleton / Cell locomotion Physiology Interactive Lecture
Transport across cell membrane – I Physiology Interactive Lecture
Transport across cell membrane – II Physiology Interactive Lecture
Cell structure Anatomy Interactive Lecture
Cell junctions Anatomy Interactive Lecture
Epithelium- I Histology Interactive Lecture + Lab
Epithelium- II Histology Histology Lab
Connective tissue – I Histology Histology

Lab

Mitosis and meiosis Embryology Interactive Lecture
Gametogenesis-I Embryology Interactive Lecture
Gametogenesis-II Embryology Interactive Lecture
Gametogenesis-III Embryology Interactive Lecture
Fertilization Embryology Interactive Lecture
First week of development Embryology Interactive Lecture
Second week of development – I Embryology Interactive Lecture
Second week of development – II Embryology Interactive Lecture
Third week of development-I Embryology Interactive Lecture
Third week of development-II Embryology Interactive Lecture
Upper limb Anatomy SGD
General anatomy of bone General Anatomy Interactive Lecture
General anatomy of blood General Anatomy Interactive Lecture
Nucleotide-II Biochemistry Interactive Lecture
Nucleotides-III Biochemistry Interactive Lecture
Protein chemistry-I Biochemistry Interactive Lecture
BLOOD
Composition & Functions of blood, plasma proteins Physiology Interactive Lecture + Lab
Bone Marrow Physiology Interactive Lecture + Lab
RBC Physiology Interactive Lecture + Lab
Regulation of Erythropoiesis Physiology Interactive Lecture
Haemoglobin/ Fate of RBC Physiology Interactive Lecture + lab
Anaemia Physiology Interactive Lecture + SGD
Polycythemia Physiology Interactive Lecture + SGD
WBC-I Physiology Interactive Lecture +Lab
WBC-II Physiology Interactive Lecture Lab
Inflammation Physiology Interactive Lecture + SGD
Immunity-I Physiology Interactive Lecture + SGD
Immunity-II Physiology Interactive Lecture + SGD
Allergy / Hypersensitivity Physiology Interactive Lecture + SGD
Hemostasis-I Physiology Interactive Lecture + Lab
Hemostasis-II Physiology Interactive Lecture + Lab
Anti Clotting Mechanisms Physiology Interactive Lecture
Bleeding disorders Physiology L Interactive Lecture
Blood Groups-I Physiology Interactive Lecture +Lab
Blood Groups-II Physiology Interactive Lecture + Lab
Transfusion reactions Physiology Interactive Lecture + SGD
Structure of RBCs + WBC’s Histology Interactive Lecture + Lab
Lymph node and tonsils Histology Interactive Lecture + Lab
Thymus and spleen I Histology Interactive Lecture + Lab
Upper limb Anatomy SGD
Protein chemistry-II Biochemistry Interactive Lecture
Chemistry of Protein Biochemistry Interactive Lecture
immunoglobulin’s Biochemistry Interactive Lecture
Chemistry of Protein-IV Biochemistry Interactive Lecture
Chemistry of Proteins Biochemistry Tutorial
Haemoglobin Biochemistry Interactive Lecture
Oxygen binding capacity of haemoglobin, factors affecting and regulating the oxygen binding capacity of haemoglobin Physiology Interactive Lecture +SGD
Chemistry and Biosynthesis of Porphyrins and its disorders (Porphyrias)-II Biochemistry Interactive Lecture
Prophyrins Biochemistry Tutorial
Degradation of heme- III Biochemistry Interactive Lecture
Haemoglobinopathies Biochemistry Interactive Lecture
Prophyrins and Hemoglobin Biochemistry Tutorial
Techniques for study of cell Biochemistry Tutorial
LOCOMOTOR
RMP Physiology Interactive Lecture + SGD
Action Potential-I Physiology Interactive Lecture + SGD
Action Potential-II Physiology Interactive Lecture + SGD
Conduction of N. Impulse Physiology Interactive Lecture + SGD
Sk. Muscle-I Physiology Interactive Lecture
Sk. Muscle-II Physiology Interactive Lecture
NMJ-I Physiology Interactive Lecture
NMJ-II Physiology Interactive Lecture
Smooth Muscle-I Physiology Interactive Lecture
Smooth Muscle-II Physiology Interactive Lecture
Applied Aspects of Nerve & Muscle Physiology Physiology
Upper limb Gross Anatomy SGD
Histology of nervous tissue Histology Interactive Lecture
Neuron Histology Interactive Lecture + Lab
Nerve and ganglia Histology Interactive Lecture + Lab
Histology of skeletal muscle Histology Interactive Lecture + Lab
Histology of smooth muscle Histology Interactive Lecture + Lab
General anatomy of nervous system General Anatomy Interactive Lecture
General anatomy of lymphatic system General Anatomy Interactive Lecture
General anatomy of muscular system General Anatomy Interactive Lecture

LEARNING OUTCOMES

1. CELL STRUCTURE Anatomy · Define animal cell and give main differentiating points between animal and plant cells

· Enumerate various components of a typical animal cell

· Describe the role of each component in cell function

2. ANATOMICAL

POSITION AND DIRECTIONAL TERMS

Anatomy •Describe the anatomical planes with the help of diagrams.

Ø Coronal

Ø Sagittal

Ø Horizontal

Ø Parasagittal

•Describe the terms of movements and demonstrate each on subject.

Ø Flexion

Ø Extension

Ø Adduction

Ø Abduction

Ø Supination

Ø Pronation

3. EPITHELIUM- I Anatomy · Classify the body tissues into four main categories

· Explain the histological structure of each category with examples

Ø Simple

Ø Stratified

4. EPITHELIUM- I Anatomy · Identify types of epithelial tissue under microscope:

Ø Simple

Ø Stratified

· Enlist two points of identification for each type

· Draw labelled diagram of each type of epithelium on sketch copy

5. EPITHELIUM-II Anatomy · Classify epithelium with examples according to

shape and number of cells

· Describe histological structure of each type of epithelium

· Enumerate cell junctions and describe their histological structure

· Explain the transformation of one epithelial type into the other by giving
examples

· Explain the role of epithelium in the development of tumors and regeneration
of cells

6. CONNECTIVE TISSUE – I Anatomy · Explain the components of connective tissue

· Classify the connective tissue with examples

· Describe each connective tissue type by giving examples

· Explain the role of fibroblasts in wound contraction

· Describe the role of collagen in keloid and hypertrophic scar

· Explain the role of macrophages in removing cellular debris during physiological
involutional processes.

7. CONNECTIVE TISSUE -II Anatomy · Identify different types of connective tissue under microscope

· write two points of identification for each slide

· Draw labelled diagram of each type of connective tissue on sketch copy

8. MITOSIS AND MEIOSIS Anatomy · Discuss the events of mitosis and meiosis with the help of models.

· Enlist the differences between mitosis and meiosis.

· Describe the structural abnormalities in chromosomes like

Ø Euploid

Ø Aneuploid

Ø Trisomy

Ø Nondisjunction

Ø Translocation

· Co-relate the structural abnormalities with clinical conditions like Downs’ Syndrome, Klinefelters’ Syndrome, Turner syndrome

9 FERTILIZATION Anatomy · Explain the processes of:

Ø Passage of spermatozoa through the corona radiata barrier

Ø penetration of spermatozoa through the zonapellucida

Ø penetration of the spermatozoa through the oocyte membrane

· Explain the a crosome reaction and capacitation reaction

· Explain the restoration of the diploid number of chromosomes, determination of the sex and initiation of cleavage as a result of fertilization.

· Explain the terms like IVF and assisted IVF.

10 GAMETOGENESIS-I Anatomy · Describe the events of spermatogenesis

· Describe the events of spermiogenesis

· Describe the morphological changes during maturation of the gametes

· Enlist the differences between spermiogenesis and spermatogenesis

· Describe the relationship of sub-fertility with production of abnormal sperms

· Define terms like azospermia, oligospermia

11 GAMETOGENESIS-II Anatomy · Describe the maturation of oocytes before birth

· Describe the maturation of oocytes at puberty

· Describe the relation of ovarian cycle with maturation of follicles.

12 GAMETOGENESIS-III Anatomy · Describe the stages of follicular maturation

Ø Primary

Ø Preantral

Ø Secondary

Ø Preovulatory.

· Describe the structure and formation of corpus luteum and corpus albicans

· Describe the mechanism of ovulation

· Describe the middle pain (mittelshimerz) associated with ovulation

13 FIRST WEEK OF DEVELOPMENT Anatomy · Describe the sequential phases of human development during first week.

· Describe the changes in uterus at time of implantation.

· Explain the process of cleavage

· Explain the formation of morula and blastula

· Describe the formation of inner and outer cell mass within the blastocyst cavity

· Describe the mechanism of abnormal implantation WITH CLINICAL SIGNIFICANCE

14 SECOND WEEK OF DEVELOPMENT – I Anatomy · Describe the sequential phases of human development during second week

· Explain why the second week is known as “week of two’s”

· Explain the formation of syncytio and cytotrophoblast.

· Explain the characteristics of growth of syncytiotrophoblast

15 SECOND WEEK OF DEVELOPMENT – II Anatomy · Explain the establishment of uteroplacental circulation

· Describe the mechanism of transformation of connecting stalk into umbilical cord

· Explain the formation of amniotic cavity

· Explain the formation of chorion, secondary yolk sac and chorionic plate.

· Explain the clinical relevance of production of βhcg by the syncytiotrophoblast and pregnanacy test.

16 THIRD WEEK OF DEVELOPMENT-I Anatomy · Describe the sequential phases of human development during 3rd to 8th weeks

· Describe the formation of neural tube and gastrulation.

· Enumerate the derivatives of ectoderm, mesoderm and endoderm

17 THIRD WEEK OF DEVELOPMENT-II Anatomy · Describe the formation of notochord from prechordal plate

· Describe the formation of paraxial,lateralplate and intermediate mesoderm

· Describe the involvement of germ disc layers in teratogenesis associated with gastrulation like situsinversus and caudal dysgenesis

18 GENERAL ANATOMY OF MUSCLES Anatomy · Classify muscles with examples according to Shape Histology

· Describe the general features of skeletal muscle

· Describe the blood supply and nerve supply of muscle

· Explain the actions of

Ø A prime mover or agonist

Ø Fixators

Ø A synergist

Ø An antagonist with examples.

19 HISTOLOGY OF MUSCLES Anatomy
  • Describe the histological features of muscle.
  • Describe the histological differences of different types of muscles
  •  Identify the type of muscle on given slides under microscope.
  • Draw labelled diagram of the identified structures with the help of eosin and hematoxylin pencils on the histology notebooks
  • List two points of identification
20 SCAPULA Anatomy
  • Identify important bony land marks of scapula
  • Identify the attachment of clinically important muscles
  • Identify the attachment of clinically important ligaments
  • Identify the common sites of fracture of scapula on radiographs correlating its predisposition to fracture
21 MUSCLES OF SCAPULARR REGION Anatomy
  • Perform dissection to identify main muscles of scapular region along with their nerve supply
22 CLAVICLE Anatomy
  • Identify important bony land marks of clavicle
  • Identify the attachment of clinically important muscles
  • Identify the attachment of clinically important ligaments
  • Identify common sites of fracture of clavicle with the help of radiographs
  • Identify the common sites of fracture of scapula on radiographs correlating its predisposition to fracture
23 HUMERUS Anatomy
  • Identify important bony land marks of humerus
  • Identify the attachment of clinically important muscles
  • Identify the attachment of clinically important ligaments
  • Identify common sites of fracture of humerus with the help of radiographs
  • Identify the common sites of fracture of scapula on radiographs correlating its predisposition to fracture
24 MUSCLES OF SHOULDER REGION Anatomy · Describe the movements of

Ø Deltoid

Ø pectoralis major

Ø Serratus anterior

Ø Trapezius

· Describe features of Paralysis of

Ø Serratus Anterior

Ø Deltoid

Ø rotator cuff muscles

25 RADIUS Anatomy
  • Identify important bony land marks of radius
  • Identify the attachment of clinically important muscles
  • Identify the attachment of clinically important ligaments
  • Identify the common sites of fracture of scapula on radiographs correlating its predisposition to fracture
26 MUSCLES OF ARM Anatomy
  • Perform dissection to identify main muscles of arm along with their nerve supply
27 ULNA Anatomy
  • Identify important bony land marks of ulna
  • Identify the attachment of clinically important muscles
  • Identify the attachment of clinically important ligaments
  • Identify the common sites of fracture of scapula on radiographs correlating its predisposition to fracture
28 MUSCLES OF FOREARM Anatomy
  • Perform dissection to Identify main muscles of forearm along with their nerve supply
29 AXILLA Anatomy
  • Describe boundaries of axilla
  • Describe contents of axilla
  • Describe Injury to the Axillary Vein and artery
  • Describe enlargement of Axillary Lymph Nodes in context of CA breast
30 CUBITAL FOSSA Anatomy
  • Perform dissection to Identify muscles forming boundaries of cubital fossa
  • Perform dissection to Identify contents of cubital fossa
31 MUSCLES OF HAND Anatomy
  • bones of hand
  • Describe functions of muscles in

thenar compartment hypothenar compartment adductor compartment central compartment interosseous compartments

  • Describe the fibrous of sheaths of the digits of the hand
  • Discuss the anatomical structures involved in Tenosynovitis
32 FACIAL SPACES OF PALM Anatomy
  • Palmar aponeurosis
  • Enumerate Fascial spaces of palm
  • Describe boundaries of spaces of palm
  • Describe contents of spaces
  • Describe clinical importance of spaces of palm
33 BRACHIAL PLEXUS Anatomy · Describe formation of brachial plexus

· Enumerate nerves originating from

Ø Cords

Ø Roots

Ø Trunks

· Describe Injuries to inferior parts of the brachial plexus (Klumpke paralysis)

· Describe Injuries to superior parts of the brachial plexus (Erb-Duchenne palsy)

34 NERVES OF ARM Anatomy
  • Describe formation of axillary and musculocutanous nerve
  • Describe distribution of nerve
  • Describe clinically important relations
  • Describe the anatomical sites of lesion of nerve correlating them to sensory and motor loss within area of distribution.
35 ARCHES OF HAND Anatomy · Describe formation of nerve

· Describe distribution of nerve

· Describe clinically important relations

· Discuss the effects of lesion of nerve at forearm and wrist

· Discuss anatomical structures involved in carpal tunnel syndrome

36 VEINS OF UPPER LIMB

CUTANEOUS NERVE SUPPLY

Anatomy · Describe formation of nerve

· Describe distribution of nerve

· Describe clinically important relations

· Discuss the sensory and motor loss associated with leison of nerve

37 NERVES Anatomy · Describe formation of nerve

· Describe distribution of nerve

· Describe clinically important relations

· Discuss sensory and motor loss associated with wrist-drop

38 SHOULDER JOINT Anatomy
  • Describe the course of clinically important nerves in hand
  • Enumerate branches of each nerve
  • Discuss the anatomical sites of lesion of nerve correlating them to sensory and motor loss within area of distribution
39 AXILLARY ARTERY Anatomy
  • Describe the extent of axillary artery ,ulnar and radial arteries
  • Describe branches of above arteries
  • Describe the anatomical sites of leison of artery correlating them to ischemia within area of distribution.
40 ARCHES OF HAND Anatomy
  • Describe the formation of superficial and deep palmar arches in hand
  • Compare the contribution of ulnar and radial arteries for formation of arches
  • Describe the structures involved in Laceration of Palmar Arches
41 VEINS OF UPPER LIMB

CUTANEOUS NERVE SUPPLY

DERMATOMES

Anatomy
  • describe the formation of basilic vein
  • describe the formation of cephalic vein
  • describe the location of median cubital vein
  • describe the areas of drainage of above veins
  • discuss the importance of median cubital vein for venipuncture
42 ·
43 SHOULDER JOINT Anatomy · Describe movements of joint

· Describe clinically important ligaments of joint

· Enumerate nerve supply and blood supply of joint

· Describe the anatomical significance of carrying angle

· Descibe anatomical structures involved in dislocation of shoulder joint

44 ELBOW JOINT Anatomy
  • Describe movements of joint
  • Describe clinically important ligaments of joint
  • Enumerate nerve supply and blood supply of joint
  • Describe the anatomical significance of carrying angle
  • Discuss anatomical structures involved in dislocation of Elbow Joint
  • Discuss anatomical structures involved in Subluxation and Dislocation of the Radial Head
45 WRIST JOINT Anatomy
  • Describe movements of joint
  • Describe clinically important ligaments of joint
  • Enumerate nerve supply and blood supply of joint
  • Discuss the anatomical structures involved in Wrist fractures
46 IMAGING OF UPPER LIMB Anatomy
  • Identify the bones and bony articulations of upper limb on AP and Lateral view Radiographs
47 HISTOLOGY OF LYMPHOID TISSUE Anatomy · Describe the histological features of

Ø Lymph node

Ø Thymus

Ø Spleen

· Tonsil with the help of drawings on board in the skill lab

· Identify the type of lymphoid tissue on given slides under microscope.

· Draw a labelled diagram of the identified structures with the help of eosin and hematoxylin pencils on the histology notebooks

· List two points of identification

48 STEM CELL Anatomy · Describe development of blood cell from stem cell
49 RED BLOOD CELL (RBC) · Explain the structure of RBC

· Relate the functions of the RBC with its structure

50 WHITE BLOOD CELL · Explain the structure of WBC
General Anatomy Of Muscles Classify muscles with examples according to Shape Histology Describe the general features of skeletal muscle Describe the blood supply and nerve supply of muscle Explain the actions of A prime mover or agonist Fixators A synergist An antagonist with examples.
51 Histology Of Muscles Describe the histological features of muscle. Describe the histological differences of different types of muscles Identify the type of muscle on given slides under microscope. Draw labelled diagram of the identified structures with the help of eosin and hematoxylin pencils on the histology notebooks List two points of identification
52 USE OF MICROSCOPE Anatomy Identify parts of microscope

Explain the working of microscope at different magnifications

Describe the method of focusing of slide at different magnifications

PHYSIOLOGY
53 General Physiology Physiology Know the functional organization of human body.

Know the parameters needed for the control of the ‘internal environment’.

Understand the principles of the mechanics of homeostasis

Able to differentiate between positive and negative feedback as the control systems of the body

Relate positive and negative feedback system with common examples

Differentiate between composition of intracellular and extra cellular fluid

Know the functional organization of human body.

Know the parameters needed for the control of the ‘internal environment’.

54 Cell Physiology Physiology Comprehend organization of the physical structure of the cell (cell Membrane, cytoplasmic organelles, nuclear membrane, nuclear organelles)

Understand the functional systems of the cells (ingestion, digestion, synthesis, extraction of energy from nutrients)

Overview movements of cells (amoeboid, ciliary etc)

Know the genes in the cell nucleus

Explain the process of transcription and translation (synthesis) in the cells

Understand the gene functions performed in the cells

Comprehend the genetic control of cells functions and cells-reproduction

Classify various modes of transport of substances across the cell-membrane

Compare and contrast amongst the processes of osmosis, diffusion, facilitated diffusion, primary active transport, secondary active transport

Relate the modes of transport with common examples in human body

Appreciate the physiological significance of the transport of substances through the cell membrane

55 BLOOD AND RELATED DISORDERS Physiology Appreciate the composition of blood and general functions of blood.

Know different types of plasma protein.

Comprehend composition of plasma protein and their functions and importance for the human body.

Overview sites of hemopoiesis in the body during different stages of life along with composition and functions of bone marrow.

Understand different types of blood cells, their physiological characteristics with functional differences.

Know the formation, types and functions of hemoglobin along with its association with different kinds of anemia.

Classify anemia its types and causes.

Identify the factors regulating erythropoiesis and maturation of RBC.

Comprehend basis of immune system of the body and tissues related with immunity.

Know the types of immunity, mechanism of their development and characteristics of different immune mechanisms and significance of vaccination.

Describe the role and functions of white blood cells in providing protection to the body against injury.

Appreciate the physical and functional characteristics of different WBCs and physiological significance of leucopenia, leukocytosis and leukemia.

Comprehend the composition and functions of reticulo- endothelial system.

Know the principles of blood grouping and physiological significance.

Identify the various blood groups and hazards of matched and mismatched blood transfusion with especial reference to Erythroblastosis fetalis.

Know various processes involved in hemostasis.

Appreciate the characteristics of platelets and their importance in hemostasis.

Comprehend the physiology of clotting factors and mechanism of blood clotting.

Know the effect of deficiency of platelets and clotting factors in hemostasis with clinical significance of hemophilia.

56 LOCOMOTION Physiology Ø Explain different mechanisms of transportation for maintenance of cellular homeostasis

Ø Understand the basis of development of membrane potential across excitable membrane.

Ø Know Nernst potential and its importance in generation of membrane potential.

Ø Comprehend different mechanisms responsible for the genesis of membrane potential (role of channels, carrier proteins).

Ø Understand the mechanisms by which different factors (stimuli) produce changes in membrane potential.

Ø Draw different phases of action potential and explain ionic changes occurring during each phase of action potential.

Ø Comprehend the response to the application of two successive stimuli are given during different phases of action potential (refractory period, its types and importance).

Ø Classify different types of nerve fibers.

Ø Know generation of nerve impulse and its transmission in different types of nerve fibers (myelinated and non myelinated nerve fibers) with their characteristics.

Ø Know structural and functional changes taking place in nerve fibers in case those are damaged.

Ø Illustrate functional and histological differences in different types of muscles.

Ø Draw and label neuromuscular junction, the sequence of events taking place during neuromuscular transmission and factors affecting thereof.

Ø Explain the motor unit and its physiological importance.

Ø Appreciate the mechanism of transmission of signals from the nerve fiber to different muscles. Know the structure and different characteristics of three types of muscle.

Ø Appreciate the ionic and chemical basis of muscle contraction.

Ø Explain the energy expenditure during muscle contraction.

Ø Understand different phases of muscle contraction and effect of multiple stimuli on different phases of muscle contraction.

Ø Comprehend clinical importance of neuromuscular transmission in patients of myasthenia gravis.

Ø Appreciate the characteristics and differences between isometric and isotonic contraction, tetanization, contracture remainder, rigor mortis etc.

Ø Appreciate characteristics of smooth muscle contraction with their physiological significance.

BIOCHEMISTRY & MOLECULAR BIOLOGY
57 CELL Biochemistry · Cytology- Techniques for Study of cell

· Cell Organelles I- Nucleus, Genetic control of cell function

· Role of cell Organelles in metabolism- Mitochondria, Ribosomes, Golgi Apparatus, Endoplasmic Reticulum, , Lysosomes, Peroxisomes

· Cell membrane- Chemical Composition and significance

· Chemistry of signals and receptors- Biochemistry of membrane transport mechanism, active transport, passive transport, simple and facilitated diffusion

Chemistry and structure of nucleosides and nucleotides: Biochemistry · Chemistry and structure of nucleosides and their biochemical role-Nucleotides, structure, their derivatives and their biochemical role-I

· Synthetic derivative of purine and pyrimidines, their role in health and disease-Nucleic acids, their types, their types, structure and functions-II

58 Proteins: Biochemistry · Protein chemistry: Definitions, Biochemical importance and classification of proteins based on , Physiochemical properties, Functional, Nutritional, Structural-Amino acids, their structure, properties & functions-Classification and nutritional significance of amino acids- Dissociation, titration and importance of amino acid in pH maintenance-I

· Structure of proteins and their significance-Separation of proteins e.g. salting out, Electrophoresis, Chromatography, Centrifugation-II

· Immunoglobulins and its biochemical significance -III

· Plasma proteins & their clinical significance-IV

59 Prophyrins and hemoglobin: Biochemistry · Structures, functions and types of haemoglobin-Oxygen binding capacity of haemoglobin, factors affecting and regulating the oxygen binding capacity of haemoglobin-I

· Chemistry and biosynthesis of porphyrins and its disorders (Porphyrias)-II

· Degradation of heme, formation of bile pigments, its types, transport and excetion- Hyperbilirubinimea, their biochemical causes and differentiation, jaundice and its types-III

· Haemoglobinopathies (Hb-S, thalassaemia etc) and their biochemical causes. IV

Case Base Learning Scenarios

  1. Anatomy

CBL Case-1

Mrs. Ahmed, a 31-year-old woman, had an uneventful first pregnancy. At 16 weeks’ gestation, a triple screen blood test was normal, indicating a 1/275 risk of Down syndrome; based on this test result, prenatal diagnosis was not considered. An ultrasound examination performed at 18 weeks’ gestation revealed no abnormalities. Mrs. Ahmed’s family history is significant for a 12-yearold maternal first cousin with Down syndrome. At birth, Mr. and Mrs. Ahmed’s infant daughter was noted to have hypotonia, a heart murmur, and facial features suggestive of Down syndrome. Blood was obtained then for chromosomal studies; one week later, trisomy 21 (47, XX, +21) was confirmed.

Learning objectives:

  • List the major medical complications in newborns with Down

syndrome.

  • Explain how the karyotype of an affected child influences risk assessment for the parents’ future pregnancies.
  • To be able to recognize the clinical manifestations of trisomy 21.
  • To be able to analyze inheritance mechanisms of HLA genes and explain ramifications for tissue transplantation.

Learning Resources

Langman’s medical embryology

The developing human, Keith L. Moore

CBL Case-2

A 58-year-old woman presents to her physician complaining of rib and back pain following a trip-and-fall accident. She was concerned that she may have broken something. On physical exam, the physician notes some rib tenderness, but also finds a palpable mass in her right breast. The woman says she does not perform monthly self-exams on her breasts and has not had a breast exam since her last checkup several years ago. A mammogram, rib films, and spine films are ordered by the physician. The mammogram shows a large mass consistent with cancer in her right breast, and the bone films show multiple osseous lesions consistent with metastatic disease.

Learning objectives:

  • Where is breast tissue in a healthy individual least likely to be found?
  • Learn the anatomy of the axilla.
  • Learn the anatomy of the breast and relationship to the axilla
  • Clinical importance of axilla in relation to breast diseases
  • Describe the general gross features of the breast and its blood supply.
  • Describe the lymphatic drainage of the breast.
  • Breast cancer screening recommendations and controversies
  • Incidence and mortality from breast cancer
  • Identify the High risk groups
  • Management of abnormal clinical breast exam

Learning Resources

Clinical Anatomy by Snells,

Clinically Oriented Anatomy by Keith. L. Moore

CBL Case-3

The goalkeeper in a soccer match fell on his outstretched left arm. He felt an immediate pain in the shoulder region and was unable to move his arm. At the hospital the arm was abducted and the deltoid muscle looked flat or hollow. The injured arm looked “too long”, and there was intense pain on attempting to move the arm. A plain radiograph of the region showed that the humeral head was lying below the glenoid labrum and that there was no fracture of the humerus. The diagnosis was an anterior dislocation of the shoulder, and the orthopedic surgeon recommended Kocher’s maneuver for management.

Learning objectives:

  • Why did the deltoid appear flat and hollow?
  • What neurovascular structures are liable to be injured in such a condition? How do you examine the patient to rule that out?
  • Discuss the causes of shoulder instability
  • Identify the risk factors contributing to shoulder instability
  • What constitutes the rotator cuff and how it facilitates ROM in shoulder joint?
  • What factors/structures provide stability to shoulder joint?
  • What is the relationship between stability and range of movement (ROM) at any synovial joint?
  • Demonstrate range of movement of shoulder joint and correlate with muscles responsible for the said movements.
  • Describe the blood and nerve supply of shoulder joint with emphasis on the special features that help to maintain the stability and movements.
  • Which imaging modalities are frequently used for Shoulder joint investigations?
  • What is arthroscopy? Does it have any role in traumatic shoulder

Learning Resources

Clinical Anatomy by Snells,

Clinically Oriented Anatomy by Keith. L. Moore

CBL Case-4

One evening while playing in the yard, a father picked up his four-year-old daughter by her hand and started swinging her around in a circle. At first the girl giggled, but all of a sudden, she cried out in pain. When her father put her down, he noticed that she was holding her elbow. Her arm was partially flexed and pronated, and she was unable to supinate her hand without considerable pain, so her parents took her to the emergency room. When the physician palpated her elbow, she found that the joint was tender, especially on the lateral side, but all of the bony landmarks were in their normal locations, leading the physician to suspect that the head of the radius had slipped out of the annular ligament. Radiographs proved inconclusive. Fairly certain of the diagnosis, however, the physician attempted to reposition the head of the radius by supinating the forearm fully and then flexing the elbow. She felt a small pop on the lateral side of the cubital fossa as the head of the radius slipped back into position and within a few moments the girl’s elbow was as good as new.

Learning objectives

  • What is the annular ligament and where is it located?
  • What are the bony landmarks that are readily palpable at the elbow?
  • What are the other common injuries to the elbow include?
  • Why might the radiographs have been unhelpful in this situation?
  • What nervous structure is particularly vulnerable in elbow injuries and where is it located?
  • Identify the normal structures related to elbow joint
  • Relate the changes that may occur due to fracture in this area

Learning Resources

Clinical Anatomy by Snells,

Clinically Oriented Anatomy by Keith. L. Moore

CBL Case-5

A couple, both in their late 30s, is having difficulty conceiving a child. Early in their marriage about, 10 years ago, they used birth control methods, but they stopped using all forms of birth control more than 2 years ago. Despite this, a pregnancy has not resulted. On routine physical examination, both the man and woman seem to be in excellent health. Because no obvious cause of their fertility problem is noted, the couple is referred to a local fertility clinic for specialized treatment. The tests conducted there suggested a sperm-cervical mucus incompatibility. After considering adoption, gestational surrogacy, and remaining childless, the couple returns three months later and requests IVF (in vitro fertilization). On the second of two regimented attempts, the couple is delighted to learn that a pregnancy has resulted.

Learning objectives:

  • Illustrate the steps, mechanism and outcomes of fertilization &

implantation.

  • Explain capacitation and its importance in fertilization
  • Summarize the events that occur as a sperm fertilizes an oocyte
  • Describe embryological basis and manifestations of normal and

aberrant implantation.

  • Describe IVF (in vitro fertilization).

Learning Resources

Langman’s medical embryology

The developing human, Keith L. Moore

CBL Case-6

A 28-year-old dentist consults her physician, complaining that she feels tingling and slight pain in her right hand. The symptoms are localized to her thumb, index, middle and lateral side of her ring finger. The sensations are more intense at night or if she overworks. Recently, she has experienced some weakness in her grasp and finds it more difficult to hold her instruments. Also, movements of her right thumb are not as strong as before. On examination there was loss of power on certain movements of the thumb. She has impaired appreciation of light touch and pin pricks to the thumb, index, middle and lateral side of her ring finger, but sensation to her palm was not affected. Pressure and tapping over the flexor retinaculum causes tingling sensations.

Learning objectives

  • What is the carpal tunnel? What is contained in it?
  • Two muscles that are affected by carpal tunnel syndrome are the abductor pollicis brevis and the opponens pollicis. How would you test their function?
  • If this was the case, what roots or trunks would have to be involved and why is this unlikely to be the cause of the problem?
  • What causes the symptoms of carpal tunnel syndrome?
  • What structures might be endangered by surgery and need to be avoided?

Learning Resources

Clinical Anatomy by Snells,

Clinically Oriented Anatomy by Keith. L. Moore

CBL Case-7

A healthy 21 year old man reported to hospital with chief complaints of long standing swellings (more than ten years duration) of left forearm which were progressively increasing in size and number for few months. Occasionally they were associated with pain and discomfort. Patient did not give history of antecedent trauma or weight lifting. On examination there were multiple soft, cystic, compressible swellings 2 x 2 cm on the lateral aspect of left forearm along cephalic vein distribution), which reappeared on relieving the pressure. Bilateral pulses were normal. There was no history suggestive of lower limb varicosities or family history of varicose veins. Ascending phlebography was obtained which recorded cephalic vein varicosities with saccular enlargements. The patient underwent successful treatment of varicose veins by excision of cephalic vein from elbow to wrist under general anesthesia. Post-operative recovery was uneventful. Follow up at 2 months showed no residual or recurrent varicosities.

Learning objectives:

  • Identify and demonstrate the areas of distribution and features of the superficial veins of the upper limb.
  • Identify and demonstrate the major superficial veins of the upper limb
  • Difference between superficial and deep veins.
  • Identify the vessels in relation to the veins of the upper limb.
  • Applied anatomy of superficial veins of upper limb.
  • Applied anatomy of varicose veins

Learning Resources

Clinical Anatomy by Snells,

Clinically Oriented Anatomy by Keith. L. Moore

  1. Biochemistry

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.

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 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)

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.

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:

  1. Synthesis, ingestion and fate of nucleotides in human body
  2. Role of Nucleotides in DNA synthesis and outcome of ADA deficiency
  3. The biochemical basis of various clinical features

REFERENCE BOOKS:

  1. Harper’s text book of Biochemistry. (Page 616)
  2. Davidson’s Practice of Medicine.
  3. 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 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:

  1. Chemistry of amino acids
  2. Levels of protein folding and how it is carried out
  3. Abnormalities in protein structure/folding

REFERENCE BOOKS:

  1. Lippincott’s illustrated reviews of Biochemistry
  2. Harper’s text book of Biochemistry.
  3. 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 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:

  1. Fibrous proteins
  2. Normal structure and synthesis of collagen and elastin
  3. Abnormalities of fibrous proteins

REFERENCE BOOKS:

  1. Lippincott’s textbook of Biochemistry
  2. Harper’s text book of Biochemistry. (Page 616)
  3. Davidson’s Practice of Medicine.

Topic: Porphyrins and Hemoglobin (Hepatitis A)

A 31 year 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
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:

  1. Synthesis and degradation of heme
  2. Metabolism of bilirubin in body
  3. Role of hepatocyte in bilirubin handling and its diseases (inherited and acquired)

REFERENCE BOOKS:

  1. Lippincott’s textbook of Biochemistry
  2. Harper’s text book of Biochemistry
  3. Davidson’s Practice of Medicine
  1. Physiology

PBL 1

Mr. Zeeshan, a 43 years old mess waiter, reported in medical OPD with complaints of difficulty in standing for long duration while serving the meals, for last six months. His general physical examination revealed normal pulse, blood pressure and temperature. However, the doctor observed drooping of his eye lids. His symptoms ameliorated for several hours by administering a test dose of neostigmine. Laboratory investigations confirmed the presence of antibodies to nicotinic acetylcholine receptors in the blood and end plate potentials recorded on electromyography were weak. CT scan chest was normal. The physician managed the case conservatively by anticholinesterase drugs and patient responded to the treatment very well.

Learning objectives:

To learn the physiological basis of:

  1. Skeletal muscle contraction especially for sustained contractions while standing.
  2. Transmission of motor signals to skeletal muscle in nerve fibers.
  3. Neuromuscular transmission at NMJ.
  4. Factors/drugs that effect transmission at NMJ.
  5. Pathophysiology and treatment options of myasthenia gravis.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 2

A 6-year-old boy is brought to the family physician after his parents noticed that he had difficulty moving his arms and legs after a soccer game. About 10 minutes after leaving the field, the boy became so weak that he could not stand for about 30 minutes. Questioning revealed that he had complained of weakness after eating bananas, had frequent muscle spasms, and occasionally had myotonia, which was expressed as difficulty in releasing his grip or difficulty opening his eyes after squinting into the sun. After a thorough physical examination, the boy was diagnosed with hyperkalemic periodic paralysis. The family was advised to feed the boy carbohydrate-rich, low-potassium foods, give him glucose-containing drinks during attacks, and have him avoid strenuous exercise and fasting.

Learning objectives:

  1. To understand Frank-Starling’s law as applied to skeletal muscle mechanics.
  2. To correlate electrolyte influences on skeletal muscle contraction.
  3. To know details of contractile elements of skeletal muscles.
  4. To gain insight into skeletal muscle fuel metabolism.
  5. To understand force velocity relationship of skeletal muscles.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 3

A 32-year-old woman presents to her primary care physician’s office with difficulty chewing food. She states that when she eats certain foods that require significant amount of chewing (e.g., meat), her jaw muscles become weak and “tired.” After a period of rest, her jaw muscles regain their strength until she eats again. The patient is diagnosed with myasthenia gravis and is started on neostigmine, an acetylcholinesterase (AChE) inhibitor.

Learning objectives:

  1. To define concepts of chronaxie and rheobase.
  2. To differentiate between fast and slow muscle fibers characteristics.
  3. To compare skeletal, smooth and cardiac muscle fiber properties.
  4. To compare neuromuscular transmission of skeletal and smooth muscles.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 4

A 21-year-old man presents to a rural emergency center with a 1-day history of progressive stiffness of the neck and jaw, difficulty swallowing, stiff shoulders and back, and a rigid abdomen. Upon further questioning, the patient reports that the stiff jaw was the first symptom, followed by the stiff neck and dysphagia. On examination he is noted to have stiffness in the neck, shoulder, and arm muscles. He has a grimace on his face that he cannot stop voluntarily and an arched back from contracted back muscles. The physician concludes that the patient has “tetanic” skeletal muscle contractions. A 3-cm laceration is noted on his left foot. The patient reports sustaining the laceration about 7 days ago while he was plowing the fields on his farm. He has not had a tetanus booster. He is diagnosed with a tetanus infection, and an injection of the tetanus antitoxin is given.

Learning objectives:

  1. To understand pathophysiology of tetanic muscle contractions.
  2. To differentiate between concepts of tetany, tetanus and tetanization.
  3. To understand mechanisms underlying muscle fatigue.
  4. To gain insight into latch mechanism of smooth muscle contraction.
  5. To identify factors relating to efficient smooth muscle contraction.
  6. To elaborate hormonal factors governing smooth muscle contraction.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, SusanM. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 5

A 14-year-old girl complained of fatigue and loss of stamina. Her appetite was marginal, as she was very conscious of maintaining her body weight at 96 pounds. Her monthly menstrual flow was always heavy and long, from its onset at twelve years of age. Relevant laboratory findings included the following:

Hematocrit (Hct) 28%
Hemoglobin (Hgb) 9 g/dL
Iron 16 µg/dL
Bone marrow iron Absent
Erythrocytes Small and pale

Suggested treatment for this patient of iron deficiency anemia included ferrous sulfate or ferrous gluconate for six months orally between meals, since food may reduce absorption. A well-balanced diet was also suggested, as well as a gynecological examination.

Learning objectives:

  1. To identify various stages of erythropoiesis along with role of various growth and differentiation inducers.
  2. To develop conceptual understanding of erythropoiesis regulation.
  3. To develop a mind map of iron metabolism in human body.
  4. To critically reflect on working definition of anemia.
  5. To interpret clinical manifestations of anemia.
  6. To identify hematologic picture in various types of anemia.
  7. To elaborate pathophysiology of various types of anemias.
  8. To develop a working knowledge of polycythemia.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 6

A 36 years lady consulted her physician with complaints of generalized weakness, easy fatigability for the last one year and recent development of sore throat and fever for 3 days. Her physical examination revealed pulse 98/min, temperature 101 F, respiratory rate 18/min and blood pressure 120/80 mm Hg. Her throat was red and congested. Her personal history revealed birth of five children in last 8 years. Her lab investigation reveal Hb 8.2 gm/dl with hypochromic microcytic RBCs (MCV=62 fl, MCH 21 pg, MCHC 27%), TLC was 16,200/ul with 82% neutrophils, 12% lymphocytes, 4% monocytes, 1% basophils and 1% eosinophils. She was advised oral antibiotics for one week and antianemics for 03 months.

Learning objectives:

  1. To learn the physiological basis of manifestations of illness and body’s immune response.
  2. To learn the role of various leucocytes in acute bacterial infections.
  3. To correlate fever and increased pulse rate with body’s immune response.
  4. To know the physiological basis of :
  • Inflammation
  • Pallor and tachycardia
  • Weakness & fatigability
  1. To understand the causes of anemia, leucocytosis and deranged DLC.
  2. To learn the mechanism of development of leucocytosis.

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

PBL 7

A 10 year old boy came to OPD with high grade fever, sore throat and dysphagia to solids for past 04 days. History revealed that he had multiple similar episodes over past 02 yrs.

On examination, tonsils were swollen and enlarged. Lab. investigations were as under:

Count Showed Normal Values
Neutrophils 80% (60-65%)
Eosinophils 1-5% (1-5%)
Basophils 0-1% (0-1%)
Lymphocytes 30% (20-40%)
Monocytes 1-6% (1-6%)

Lab report shows “neutrophilia”. He was diagnosed as a case of “streptococcal tonsillitis”.

Learning objectives:

To develop answers to following queries:

  1. Which type of immunity was generated in this patient?
  2. Why neutrophil count is increased in this patient? What is their role in this infection?
  3. What are the classical signs of inflammation in above patient?
  4. What is the role of helper T- Lymphocytes in streptococcal tonsillitis?
  5. How complement system is activated in above scenario?
  6. What are types based on morphology of W.B.C’s?
  7. Describe briefly the functions of different types of W.B.C.s.
  8. What is the role of macrophage/antigen presenting cells in immunity?
  9. What are different immune deficiency diseases?
  10. What are autoimmune diseases?
  11. Discuss briefly Immunization?

Resources:

  1. Guyton and Hall Textbook of Medical Physiology, 13th Edition by John E. Hall.
  2. Human Physiology: From Cells to Systems, 8th Edition by Lauralee Sherwood.
  3. Ganong’s Review of Medical Physiology, 24th Edition (LANGE Basic Science) by Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen Brooks.
  4. Electronic modes

List of Practical work

 

List of Histology Practical’s- 1st Year MBBS Class first module
Topic
Histology and Its Methods of Study
Epithelial Tissue- I
Epithelial Tissue- II
Connective Tissue-I
Connective Tissue-II
Nervous tissue-I
Muscle tissue-I
Lymphoid Organs-I
Lymphoid Organs-II

List of Practical 1st Year MBBS

Physiology

 

  1. Lab work protocol & safety guidelines – Physiology Lab
  2. Study of the compound (binocular) microscope
  3. Determination of specific gravity of blood
  4. Determination Osmotic fragility of RBCs
  5. Estimation of Hemoglobin (Hb) Concentration
  6. Determination of Haematocrit (Hct).
  7. Determination of Erythrocyte Sedimentation Rate (ESR)
  8. Hemocytometer, Automated Blood Cell Counting and Determination of Red Blood Cell (RBC) Count.
  9. Determination of Absolute Red Cell Values (Blood Indices).
  10. Determination of Total Leukocyte (TLC).
  11. Determination of Deferential Leukocyte Count (DLC).
  12. Determination of Platelet count
  13. Determination of Coagulation Profile
  14. Determination of ABO & Rh blood group
  15. Phenomenon of Muscle Fatigue in Human Index Finger and Effect of Circulatory Occlusion.
  16. Demonstration of Triple Response

BIOCHEMISTRY PRACTICAL

1st YEAR MBBS CLASS

40th MBBS COURSE

1st Module

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

STRUCTURED TRAINAING PROGRAM

08 weeks time table is attached as ANNEX – A.

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