Sample Pages

Contents iii

APPENDIX
for PGMEE

Volume 1

First Edition

Dr Vaibhav Bharat

Sample Pages MBBS, DNB General Surgery

Director, MedE@sy

Dr Aditi Bharat
MBBS, MD Anaesthesiology (TATA Memorial Hospital, Mumbai)

Dr Ishad Aggarwal
MBBS, MD Dermatology (IPGIMER, Kolkata)

Edited by
Dr Harshvardhan Bharadwaj
MBBS, M.Med, DA

KALAM BOOKS
 Contents v

Preface

First of all it is our pleasure and duty to thank all our readers, who have time and again shown faith in our en-
deavours. It is always encouraging if your work is appreciated and we are grateful to all our readers. We started
our Journey in 2011 with DNB CET Review which was an instant success and is our legendary creation till date.
The collections of tables in the form of APPENDIX, at the end of the book were much appreciated and is in high
demand even today. Hence we decided to recreate the magic of APPENDIX again, this time on a juggernautic
scale and precision.
With changing pattern of PGMEE we have included colour pictures in our APPENDIX and made it a totally co-
loured book in three easy to carry volumes. We have done our level best to come up with up-to-date material,
but to err is human, and we are humans too. However we constantly keep in touch with our readers through our
website www.medeasyindia.com, and our Facebook fan page https://www.facebook.com/MedEasyindia/ to
keep them updated with any correction, change or improvement in our book.
We heartily invite any suggestions, corrections or discussions of PG Medical entrance material and MCQs on our
mail id info@medeasyindia.com

Thanks
Authors/ Editors
APPENDIX FOR PGMEE
By Team MedE@sy

Sample Pages
 Contents vii

Contents

  Appendix  Anatomy 44. Dermatomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

1. Gametogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 45. Myotomes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
2. Male Gametogenesis (Spermatogenesis). . . . . . . . . . . . . . . . 1 46. Vertebral Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
3. Female Gametogenesis (Oogenesis). . . . . . . . . . . . . . . . . . . . 2 47. Vertebral Levels of organs. . . . . . . . . . . . . . . . . . . . . . . . . . . 48
4. Germ Layer Derivatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 48. Openings of Diaphragm (Mnemonic: Voice of America). . . 48
5. Mesogastrium. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 49. Vertebral Column. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
6. Adult Derivatives and Vestigial Remains of Embryonic 50. Foramina of the Skull. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
Urogenital Structures/ Structural Homologues in Males 51. Layers of Scalp (Mnemonic form) . . . . . . . . . . . . . . . . . . . . . 52
and Females . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
52. Muscles of Mastication
7. Development of Urinary Bladder . . . . . . . . . . . . . . . . . . . . . . 8 (Acting on Temporomandibular Joint) . . . . . . . . . . . . . . . . . 52
8. Development of Vagina. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 53. Movements Around TMJ. . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
9. General Time Course of Gonadal Development. . . . . . . . . . . 9
54. Extrinsic Muscles of tongue. . . . . . . . . . . . . . . . . . . . . . . . . . 53
10. Development of External Genitalia. . . . . . . . . . . . . . . . . . . . . 9
55. Anatomy of tongue. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
11. Development of Kidney Systems. . . . . . . . . . . . . . . . . . . . . . 10
56. Muscles of Soft Palate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
12. Development of CNS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
57. Muscles of Pharynx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
13. Branchial Arches. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
58. Cartilages of Larynx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
14. Development of the Arterial System . . . . . . . . . . . . . . . . . . 15
59. Joints and Ligaments of the Shoulder Region . . . . . . . . . . . 60
15. Anomalies of Aortic Arches. . . . . . . . . . . . . . . . . . . . . . . . . . 16
60. Anterior Axioappendicular Muscles . . . . . . . . . . . . . . . . . . . 62
16. Development of the Venous System . . . . . . . . . . . . . . . . . . 17
61. Posterior Axioappendicular Muscles. . . . . . . . . . . . . . . . . . . 62

Sample Pages
17. Abnormal Venous Drainage. . . . . . . . . . . . . . . . . . . . . . . . . . 18
18. Development of Diaphragm. . . . . . . . . . . . . . . . . . . . . . . . . 19
19. Development of GUT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
20. Limb Development. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
21. Some Important Epithelium Linings (Classification Wise). . 20
22. Some Important Epithelium Linings (System Wise) . . . . . . 21
23. Connective Tissues. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
24. Types of Fibres in Connective Tissue. . . . . . . . . . . . . . . . . . . 24
25. Types of Collagen and Associated Diseases. . . . . . . . . . . . . 25
26. Constituents of Connective Tissues in Various Tissues. . . . 25
27. Types of Cartilages. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
28. Types of Epiphysis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
29. Muscle Cells Types. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
30. Structural Classifications of Exocrine Glands. . . . . . . . . . . . 28
31. Classification of Exocrine Glands on the Basis of
Mechanism of Secretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
32. Lymphatic organs: Distinctive Morphological Features. . . . 30
33. Muscles Classification According Shape
and orientation of Fibres. . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
34. Cranial Nerve Nuclei. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
35. Cranial Nerve Components . . . . . . . . . . . . . . . . . . . . . . . . . . 32
36. Cranial Nerves FAQ. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
37. Lymphatic Drainage of Perineal & Abdominal Structures. . 33
38. Brachial Plexus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
39. Brachial Plexus Nerve Lesions. . . . . . . . . . . . . . . . . . . . . . . . 36
40. Brachial Plexus Upper & Lower Root Lesions. . . . . . . . . . . . 39
41. Lumbar Plexus (T12-L4) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
42. Sacral Plexus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
43. Nerve Compression or Entrapment Syndromes. . . . . . . . . . 41
62. Scapulohumeral (intrinsic Shoulder) Muscles . . . . . . . . . . . 63
63. Muscles of Arm. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
64. Muscles of Anterior Compartment of forearm . . . . . . . . . . 64
65. Muscles of Posterior Compartment of forearm. . . . . . . . . . 65
66. Intrinsic Muscles of Hand (Comprehensive) . . . . . . . . . . . . 66
67. Muscles of Hand (Simplified). . . . . . . . . . . . . . . . . . . . . . . . . 67
68. Muscles of Anterior Abdominal Wall . . . . . . . . . . . . . . . . . . 68
69. Muscles of Posterior Abdominal Wall. . . . . . . . . . . . . . . . . . 68
70. Corresponding Layers of Anterior Abdominal Wall,
Spermatic Cord, and Scrotum. . . . . . . . . . . . . . . . . . . . . . . . 69
71. Eponymous Fascia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
72. Muscles of Gluteal Region. . . . . . . . . . . . . . . . . . . . . . . . . . . 70
73. Muscles of the Anterior/Extensor Fascial
Compartment of the Leg. . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
74. Muscles of the Lateral Fascial Compartment of the Leg. . . 71
75. Ligaments of Ankle Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
76. Muscles & Tendons of Sole of Foot. . . . . . . . . . . . . . . . . . . . 72
77. Muscles of Sole of Foot (Comprehensive) . . . . . . . . . . . . . . 72
78. Components of Arches of Foot. . . . . . . . . . . . . . . . . . . . . . . 73
79. Engineering of Arches of Foot. . . . . . . . . . . . . . . . . . . . . . . . 74
80. Muscles of Pelvic Walls and Floor. . . . . . . . . . . . . . . . . . . . . 74
81. Perineal Pouches . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
82. Supports of Uterus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
83. Structures Passing Through Greater and Lesser Sciatic
foramina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
84. Anal Canal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
85. Anal Sphincters. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
86. Inguinal Canal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
viii Contents
  Appendix    Physiology
1. Body Compartments Overview. . . . . . . . . . . . . . . . . . . . . . . 83
2. Body Fluid Compartments Volume Measurements
Centre Alignment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
3. Ion Concentrations of Body Fluids . . . . . . . . . . . . . . . . . . . . 84
4. Constituents of Extracellular Fluid . . . . . . . . . . . . . . . . . . . . 85
5. Membrane Potential . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
6. Intracellular & Extracellular Concentrations and Nernst
Equilibrium Potential Values of Ions . . . . . . . . . . . . . . . . . . 87
7. Compartment Wise Buffer Systems . . . . . . . . . . . . . . . . . . . 87
8. Composition of Gastrointestinal Secretions. . . . . . . . . . . . . 87
9. Normal Transport of Substances by the intestine
and Location of Maximum Absorption or Secretion. . . . . . 88
10. Daily Water Turnover (ml) in the Gastrointestinal Tract . . . 88
11. Composition & Characteristic of Bile . . . . . . . . . . . . . . . . . . 89
12. Replacement Guidelines for Sweat and Gastrointestinal
Fluid Losses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
13. Osmolarity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
14. Glucose Transporter. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
15. Ionic Basis of Nerve Action Potential . . . . . . . . . . . . . . . . . . 91
16. Rate of Firing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
17. Refractory Periods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
18. Receptor Potential . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
Sample Pages
19. Myocardial Action Potential (Non Pacemaker) . . . . . . . . . . 93
20. Pacemaker Action Potential. . . . . . . . . . . . . . . . . . . . . . . . . . 95
21. Muscle Sensory Receptor. . . . . . . . . . . . . . . . . . . . . . . . . . . . 96
22. Stretch Reflex Vs inverse Stretch Reflex . . . . . . . . . . . . . . . . 97
23. Strength Duration Curve . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
24. Muscle Cells Types. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100
25. Isometric Versus Isotonic Exercise . . . . . . . . . . . . . . . . . . . 100
26. Contractile Apparatus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100
27. Sliding Filament theory of Muscle Contraction . . . . . . . . . 102
28. Classification of Fiber Types in Skeletal Muscles. . . . . . . . 105
29. Types of Nerve Fibres. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
30. Clotting Factors & Coagulation Cascade . . . . . . . . . . . . . . 106
31. Anticoagulant Mechanisms. . . . . . . . . . . . . . . . . . . . . . . . . 108
32. Deficiency of Clotting Factors . . . . . . . . . . . . . . . . . . . . . . . 109
33. Reticulocyte Count. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
34. Blood indices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
35. Neutrophil Count . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
36. Fluid Filtration Across Capillaries. . . . . . . . . . . . . . . . . . . . . 111
37. Gas Content of Blood. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
38. Resting Blood Flow and O2 Consumption
of Various organs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
39. Cardiac Cycle Phases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
40. Volume-Pressure Diagram During the Cardiac Cycle. . . . . 113
41. JVP Waveform. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
42. Heart Sounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
43. Central Vs Peripheral Chemoreceptor . . . . . . . . . . . . . . . . 116
44. Baroreceptors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
45. Fetal Erythrogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118
46. Fetal Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
47. Functional Classification of Vessels. . . . . . . . . . . . . . . . . . . 120
48. Respiratory Centres . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
49. Types of Hypoxia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
50. Pulmonary Volumes and Capacities . . . . . . . . . . . . . . . . . . 123
51. Dead Space. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
52. Rapidly Acting/ Small Molecule Neurotransmitters. . . . . 126
53. Slowly Acting/Large Molecule Neurotransmitters;
the Neuropeptides. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
54. Neurotransmitters and Hormones That influence Feeding
and Satiety Centers in the Hypothalamus . . . . . . . . . . . . . 128
55. Autonomic Nervous System. . . . . . . . . . . . . . . . . . . . . . . . . 129
56. Autonomic Effects on Various organs of the Body. . . . . . . 130
57. Physiology of Cerebellum . . . . . . . . . . . . . . . . . . . . . . . . . . 131
58. Hypothalamic Nuclei . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
59. Ascending (Sensory) Tracts of Spinal Cord. . . . . . . . . . . . . 133
60. Descending (Motor) Tracts of Spinal Cord . . . . . . . . . . . . . 136
61. Parasympathetic Ganglions in Head and Neck. . . . . . . . . . 138
62. Physiology of CSF . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
63. Important Values Regarding Excretory System. . . . . . . . . . 141
64. Renal Physiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
65. Determinants of GFR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
66. Autoreguation of GFR and Renal Blood Flow. . . . . . . . . . . 144
67. Effect of Afferent and Efferent Arteriole on Gfr and Renal
Blood Flow. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
68. Renal Clearance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
69. Free Water Clearance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
70. Acidification of the Urine & Bicarbonate Excretion. . . . . . 149
71. Prostaglandins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
72. General Features of Hormone Classes . . . . . . . . . . . . . . . . 150
73. Classification of Hormones by Mechanism of Action . . . . 150
74. Endocrine Glands, Hormones, and their Functions
and Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
75. Anterior Pituitary Hormone Expression and Regulation. . 153
76. Adrenal Gland . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154
77. Factors Affecting Growth Hormone . . . . . . . . . . . . . . . . . . 155
78. Gastrointestinal Hormone . . . . . . . . . . . . . . . . . . . . . . . . . . 156
79. Effects of Estrogen and Progesterone
on Different organs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
80. Uterine Cycle or Menstrual Cycle . . . . . . . . . . . . . . . . . . . . 157
81. Phases of Gastric Acid Secretion. . . . . . . . . . . . . . . . . . . . . 158
82. Stages of Deglutition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158
83. Urinary Bladder innervation . . . . . . . . . . . . . . . . . . . . . . . . 159
84. Micturition Reflex. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160
85. Urinary Bladder Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . 161
86. Decompression Sickness . . . . . . . . . . . . . . . . . . . . . . . . . . . 162
87. Stages of Sleep Awake Cycle and Its Disorders . . . . . . . . . 162
88. Sleep Waves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164
89. Sleep Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166
90. Methods of Heat Loss. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166
91. Mechanoreceptors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
92. Pain Pathway. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168
93. Terms Used in Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
 Contents ix

94. Fast Vs. Slow Pain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171 39. Respiratory Quotient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
95. Visual Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171 40. Amino Acid Structure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
96. Auditory Pathway. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 41. Amino Acid Polarity and Charge . . . . . . . . . . . . . . . . . . . . . 215
97. Olfaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 42. Essential and Non Essential Amino Acids. . . . . . . . . . . . . . 215
98. Primary Sensations of Taste. . . . . . . . . . . . . . . . . . . . . . . . . 176 43. Typical Range of Pka Values of Side Groups
of Amino Acids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
  Appendix   Biochemistry 44. Amino Acid Titration Curve. . . . . . . . . . . . . . . . . . . . . . . . . 216
45. Transamination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
1. Enzyme inhibition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
46. Ketogenic and Glucogenic Amino Acids. . . . . . . . . . . . . . . 221
2. Michaelis-Menten Equation. . . . . . . . . . . . . . . . . . . . . . . . 181
47. Biologically Important Compounds From Amino Acids. . . 221
3. Difference Between Functional and Non-Functional
48. Reverse Codon Table of Amino Acids . . . . . . . . . . . . . . . . . 222
Enzymes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
49. Selenocysteine the 21st Amino Acid . . . . . . . . . . . . . . . . . . 222
4. Lactate Dehydrogenase . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
50. Amino Acids FAQ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222
5. Cofactors of Different Enzymes . . . . . . . . . . . . . . . . . . . . . 183
51. Sites of Pathways of Protein Synthesis. . . . . . . . . . . . . . . . 223
6. Major Properties of the Glycosaminoglycans. . . . . . . . . . . 183
52. Disorders of Phenyl Alanine Metabolism. . . . . . . . . . . . . . 223
7. Vitamins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
53. Tyrosine Metabolism Disorders. . . . . . . . . . . . . . . . . . . . . . 223
8. Subtypes of Vitamin K . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
54. Metabolism of Sulphur Containing Amino Acids. . . . . . . . 224
9. Deficiencies and toxicities of Metals. . . . . . . . . . . . . . . . . . 186
55. Protein Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
10. Principal Proteins of RBC Membrane. . . . . . . . . . . . . . . . . 187
56. Current Concepts in Protein Folding. . . . . . . . . . . . . . . . . . 225
11. Oxygen Binding Mechanism of Hemoglobin . . . . . . . . . . . 188
57. Chaperones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226
12. Shift of Oxygen Dissociation Curve. . . . . . . . . . . . . . . . . . . 190
58. Urea Cycle. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
13. Steps of Heme/Porphyrin Ring Synthesis. . . . . . . . . . . . . . 191
59. Denaturation and Precipitation of Proteins. . . . . . . . . . . . 228
14. Lead toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
60. Cori Cycle. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
15. Purine Biosynthesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192

Sample Pages
61. Aptamers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
16. Lesch Nyhan Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
62. De Novo Synthesis of Fatty Acids (Lipogenesis). . . . . . . . . 231
17. The Principal Methods and Preparations Used
in Biochemical Laboratories. . . . . . . . . . . . . . . . . . . . . . . . . 196 63. Fatty Acid Oxidation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
18. Metabolic Pathways. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197 64. Beta Oxidation of Fatty Acids. . . . . . . . . . . . . . . . . . . . . . . . 233
19. Substrates of Different organs. . . . . . . . . . . . . . . . . . . . . . . 198 65. Cholesterol Biosynthesis . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
20. Carbohydrate Metabolism Overview . . . . . . . . . . . . . . . . . 199 66. Steroid Hormone Synthesis. . . . . . . . . . . . . . . . . . . . . . . . . 237
21. Tricarboxylic Acid Cycle (Tca Cycle/ Krebs Cycle/ 67. Vitamin-D: Synthesis and Metabolism . . . . . . . . . . . . . . . . 238
Citric Acid Cycle) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199 68. Major Lipoprotein Classes. . . . . . . . . . . . . . . . . . . . . . . . . . 238
22. Glycolysis and Gluconeogenesis . . . . . . . . . . . . . . . . . . . . . 200 69. Major Apolipoproteins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
23. ATP formation in the Catabolism of Glucose . . . . . . . . . . . 203 70. Chylomicrons. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
24. Fate of Pyruvate. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204 71. Lysosomal Storage Disorders. . . . . . . . . . . . . . . . . . . . . . . . 240
25. Anaerobic Glycolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205 72. Frederickson Classification of Hyperlipoproteinemias . . . 242
26. Tests Based Upon Reducing Property of Sugars. . . . . . . . . 206 73. Summary of the Major Drugs Used for the
27. Calories of Food Components. . . . . . . . . . . . . . . . . . . . . . . 206 Treatment of Hyperlipidemia. . . . . . . . . . . . . . . . . . . . . . . . 243
28. Plasma Concentrations of Metabolic Fuels (Mmol/L) 74. Newer Drugs for Dyslipidemia. . . . . . . . . . . . . . . . . . . . . . . 244
in the Fed and Fasting States. . . . . . . . . . . . . . . . . . . . . . . . 207 75. Bile Acid and Salts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
29. Summary of Few Important Aspects of the Complexes 76. Ketogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246
of ETC. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207 77. Types of Lipases in the Human Body. . . . . . . . . . . . . . . . . . 248
30. Respiratory Poisons, inhibitors & Uncouplers . . . . . . . . . . 208 78. DNA Structure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
31. Glucose Transporter. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210 79. Structural forms of DNA . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
32. Factors Affecting Phosphorylase. . . . . . . . . . . . . . . . . . . . . 210 80. DNA Sequences With Unusual Structures . . . . . . . . . . . . . 251
33. Glycogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 81. Mitochondrial DNA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
34. Glycogenolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 82. Classes of Proteins involved in Replication. . . . . . . . . . . . . 252
35. Actions of insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212 83. Mechanism of DNA Repair. . . . . . . . . . . . . . . . . . . . . . . . . . 252
36. Effects of insulin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212 84. Human Diseases of DNA Damage Repair. . . . . . . . . . . . . . 253
37. ATP Production in Substrate Level Versus Oxidative 85. Epigenetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
Phosphorylation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213 86. Techniques of Molicular Biology. . . . . . . . . . . . . . . . . . . . . 254
38. Free Energy of Hydrolysis of Some organophosphates of 87. Some of the Enzymes Used in Recombinant
Biochemical Importance . . . . . . . . . . . . . . . . . . . . . . . . . . . 213 DNA Research. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254
x Contents

88. Polymerase Chain Reaction. . . . . . . . . . . . . . . . . . . . . . . . . 255 44. Classification of the Acute Emetogenic Potential of
89. Milestones in Human Genome Sequencing. . . . . . . . . . . . 256 Antineoplastic Medication. . . . . . . . . . . . . . . . . . . . . . . . . . 297
45. Calcineurin inhibitors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298
  Appendix   Pharmacology 46. FDA Approved Monoclonal Antibodies &
Targeted therapies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 300
1. Kinetics of Elimination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 47. Monoclonal Antibodies Used in the Treatment
2. Dose Response Curve. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258 of Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
3. Types of Conjugation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260 48. Features of Gpiib/Iiia Antagonists. . . . . . . . . . . . . . . . . . . . 302
4. P450s (CYPS), Drugs Metabolized (Substrates), 49. Rituximab . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
inducers, and inhibitors. . . . . . . . . . . . . . . . . . . . . . . . . . . . 261 50. Side Effects of Common Anti Epileptics . . . . . . . . . . . . . . . 303
5. List of Prodrugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261 51. Classification of Anti Arrhythmic Drugs . . . . . . . . . . . . . . . 305
6. Drugs and Cosmetic Rules of 1945. . . . . . . . . . . . . . . . . . . 262 52. Drugs Used in Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . 305
7. Orphan Drugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263 53. Commonly Used Antiarrhythmic Agents: Chronic oral
8. Clinical Trial and Preclinical Testing . . . . . . . . . . . . . . . . . . 264 Dosing/Primary indications. . . . . . . . . . . . . . . . . . . . . . . . . 306
9. Pre-Clinical Phase. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265 54. Glucose-Lowering therapies for Type 2 Diabetes. . . . . . . . 306
55. Insulins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308
10. Drug Storage instructions. . . . . . . . . . . . . . . . . . . . . . . . . . 266
56. Quick-Relief Medications for Asthma. . . . . . . . . . . . . . . . . 309
11. Cholinergic Drugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
57. Long-Term Control Medications for Asthma . . . . . . . . . . . 310
12. Muscarinic Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
58. Management of Childhood Asthma . . . . . . . . . . . . . . . . . . 312
13. Classification of Atropine Substitutes. . . . . . . . . . . . . . . . . 267
59. Use of Metered Dose inhaler. . . . . . . . . . . . . . . . . . . . . . . . 313
14. Receptor Actions of Sympathomimetic
60. Anti Hypertensive Medications. . . . . . . . . . . . . . . . . . . . . . 314
and Dopaminergic Agents. . . . . . . . . . . . . . . . . . . . . . . . . . 268
61. Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315
15. Endogenous Catecholamines. . . . . . . . . . . . . . . . . . . . . . . . 268
62. Drug therapy of Gout. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 316
16. Adrenergic Agonist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269
63. Commercially Available Steroid Hormones . . . . . . . . . . . . 317

Sample Pages
17. Therapeutic Classification of Adrenergic Drugs. . . . . . . . . 270
64. Drugs Used in Psoriasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 318
18. Effects of Adrenaline on Blood Pressure. . . . . . . . . . . . . . . 270
65. Side Effect Profile of Antiparkinson Drugs . . . . . . . . . . . . . 319
19. Vasomotor Re-Reversal . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
66. Drugs or Drug Groups Under investigation for
20. Classification of Alpha Adrenergic Blocking Agents. . . . . . 271 Use in Angina.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
21. Classification of Beta Blockers. . . . . . . . . . . . . . . . . . . . . . . 272 67. Plasma Expanders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
22. Actions Ascribed to Different Types of 68. Anticoagulants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321
Opioid Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273 69. Advantage and Consequences of Those Advantages
23. Opioid Drugs and their Actions on Opioid Receptors . . . . 273 with LMWH. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322
24. Methadone. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273 70. Drugs Affecting Platlet Function and Mechanism
25. Serotonin Receptors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274 of Action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322
26. 2Nd Generation Anti Histamine. . . . . . . . . . . . . . . . . . . . . . . 275 71. Drugs Used in Osteoporosis. . . . . . . . . . . . . . . . . . . . . . . . . 322
27. Classification of Antibiotics . . . . . . . . . . . . . . . . . . . . . . . . . 275 72. Tamoxifen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324
28. Post Antibiotic Effect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276 73. Bisphosphonates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324
29. Cephalosporins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 74. Classification of Adverse Drug Reactions. . . . . . . . . . . . . . 326
30. Antibiotic Treatment of Pseudomonas Aeruginosa . . . . . 278 75. Gell and Coombs Classification of Immunologic Drug
Reactions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
31. Penicillin G. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
76. Drugs Associated With Edema formation. . . . . . . . . . . . . . 327
32. Classification of ESBL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
77. Drug induced SLE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327
33. Antituberculous Drugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
78. Drug-induced Respiratory Reactions. . . . . . . . . . . . . . . . . . 327
34. Antituberculosis Drugs Dosage . . . . . . . . . . . . . . . . . . . . . . 280
79. Drugs and Endocrine Disease . . . . . . . . . . . . . . . . . . . . . . . 328
35. Antiviral Chemotherapy and Chemoprophylaxis. . . . . . . . 281
80. Effects of Drugs on Thyroid Hormones . . . . . . . . . . . . . . . 329
36. Targets and Mechanism of Antiretroviral Drugs. . . . . . . . . 285
81. Drugs Causing Megaloblastic Anemia . . . . . . . . . . . . . . . . 330
37. Antiretroviral Drugs Used in the Treatment of
82. Ototoxic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 330
HIV infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
38. Ocular Side Effects of HAART . . . . . . . . . . . . . . . . . . . . . . . 289
  Appendix   Microbiology
39. Therapy for Chronic Hepatitis B. . . . . . . . . . . . . . . . . . . . . . 289
40. Latest Guidelines for Treatment of Hepatitis C . . . . . . . . . 290 1. Scientists and Titles in Microbiology. . . . . . . . . . . . . . . . . . 331
41. Classification of Cancer Chemotherapy Agents. . . . . . . . . 291 2. Microbial Staining. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331
42. Anticancer Drug Toxicities. . . . . . . . . . . . . . . . . . . . . . . . . . 296 3. Gram and Acid-Fast Staining Methods. . . . . . . . . . . . . . . . 332
43. Anticancer Drugs toxic Amelioration. . . . . . . . . . . . . . . . . . 296 4. Ziehl-Neelsen Acid-Fast Stain. . . . . . . . . . . . . . . . . . . . . . . 332
 Contents xi

5. Sterilization, Antisepsis & Disinfection. . . . . . . . . . . . . . . . 333
6. Disinfectants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333
7. Physical Methods of Sterilization . . . . . . . . . . . . . . . . . . . . 334
8. Chemical Methods of Sterlization. . . . . . . . . . . . . . . . . . . . 334
9. Efficacy of Chemical Disinfection. . . . . . . . . . . . . . . . . . . . . 336
10. Working Temperature and Time for Different Techniques
of Heat Sterilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
11. Sterilization of Some Important Materials. . . . . . . . . . . . . 337
12. Efficacy of Sterilisation Methods. . . . . . . . . . . . . . . . . . . . . 338
13. Sterilization of Prions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 338
14. Types of Immunity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
15. Antigen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
16. Antibody . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
17. Antigen- Antibody Reaction Curve . . . . . . . . . . . . . . . . . . . 340
18. Immunoglobulins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 340
19. Hypersensitivity Reactions. . . . . . . . . . . . . . . . . . . . . . . . . . 341
20. Cytokines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342
21. Complements System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344
22. Human MHC Gene Products. . . . . . . . . . . . . . . . . . . . . . . . 345
23. Serological Test. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346
24. Chemokines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346
25. Immunodeficiency Diseases . . . . . . . . . . . . . . . . . . . . . . . . 346
26. Classes of Human Pathogens and their Lifestyles . . . . . . . 348
56. Basis of Typing / Sub-Classification of Bacteria . . . . . . . . . 364
57. Virulence Factors of Bacteria. . . . . . . . . . . . . . . . . . . . . . . . 364
58. Clinical Implications of Important Bacteria. . . . . . . . . . . . 364
59. Characteristics of Medically Important Streptococci. . . . . 365
60. Important infections Caused by Staph Aureus. . . . . . . . . . 366
61. Acute infectious Diarrhea . . . . . . . . . . . . . . . . . . . . . . . . . . 367
62. Viral Causes of Gastroenteritis Among Humans . . . . . . . . 367
63. Characteristics of Gastroenteritis Caused by Viral and
Bacterial Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 368
64. Mechanism of Diarrhoea. . . . . . . . . . . . . . . . . . . . . . . . . . . 368
65. Types of E Coli. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 368
66. Important Clinical Features of Neisseriae. . . . . . . . . . . . . . 369
67. Neisseria & Chlamydia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369
68. Treponema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 370
69. Actinomycosis Vs Nocardia . . . . . . . . . . . . . . . . . . . . . . . . . 370
70. Mycobacteria that Infect Humans. . . . . . . . . . . . . . . . . . . . 371
71. Runyon Classification of Mycobacteria. . . . . . . . . . . . . . . . 372
72. Atypical Mycobacteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 372
73. Virus Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
74. FAQ Virus Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
75. Shape of Viruses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375
76. Viroids. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375
77. Prions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376

Sample Pages
27. Phases of the Microbial Growth Curve. . . . . . . . . . . . . . . . 349
28. Prokaryotes Vs Eukaryotes. . . . . . . . . . . . . . . . . . . . . . . . . . 350
29. Bacterial Genetics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350
30. Mechanisms of Antigenic Variation. . . . . . . . . . . . . . . . . . . 351
31. Vertical Transmission of Some Important Pathogens . . . . 352
32. Classification of Bacteria . . . . . . . . . . . . . . . . . . . . . . . . . . . 352
33. Shape & Arrangement of Bacteria. . . . . . . . . . . . . . . . . . . . 353
34. Motility of organism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353
35. Bacterial Oxygen Requirement . . . . . . . . . . . . . . . . . . . . . . 353
36. Bacterial Capsule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 354
37. Bacterial Flagella Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . 354
38. Spore forming Bacteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355
39. Bacterial interference With Phagocytes. . . . . . . . . . . . . . . 355
40. Nosocomial infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356
41. Drugs of Choice for infectious Disease Prophylaxis. . . . . . 356
42. Exotoxin Vs Endotoxin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357
43. Characteristic of Different toxins. . . . . . . . . . . . . . . . . . . . . 357
44. Growth Factors of Micro organisms . . . . . . . . . . . . . . . . . . 358
45. Alternative/ Common Names of Bacteria . . . . . . . . . . . . . 358
46. Numerically Named Diseases . . . . . . . . . . . . . . . . . . . . . . 359
47. Important Tests/Skin Tests. . . . . . . . . . . . . . . . . . . . . . . . . . 359
48. Important Fevers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
49. Organisms Causing UTI. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360
50. Commensals in Human Body. . . . . . . . . . . . . . . . . . . . . . . . 360
51. Categories of Culture Media . . . . . . . . . . . . . . . . . . . . . . . . 361
52. Different Classes of Specific Culture Media. . . . . . . . . . . . 362
53. Specific Culture Media Uses . . . . . . . . . . . . . . . . . . . . . . . . 362
54. Colony Appearance on Culture. . . . . . . . . . . . . . . . . . . . . . 363
55. Bacterial Identification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
78. Viral inclusion Bodies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376
79. Common Routes of Viral infection in Humans. . . . . . . . . . 377
80. influenza Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377
81. Sites of Predilection for Human Herpes Virus (HHV). . . . . 378
82. Clinical and Epidemiologic Features of Viral Hepatitis. . . . 379
83. Serologic Patterns of Hepatitis B infection. . . . . . . . . . . . . 380
84. Human Papilloma Virus. . . . . . . . . . . . . . . . . . . . . . . . . . . . 381
85. HPV Vaccine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382
86. Viral Hemorrhagic Fevers. . . . . . . . . . . . . . . . . . . . . . . . . . . 383
87. Virus Associated With Human Malignancy. . . . . . . . . . . . . 383
88. infectious Agents Associated With Lymphoid
Malignancy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384
89. Chandipura Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384
90. Antiviral Chemotherapy and Chemoprophylaxis. . . . . . . . 385
91. Fungi Vs Bacteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389
92. Classification of Fungi & Mycosis . . . . . . . . . . . . . . . . . . . . 389
93. KOH Mount. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
94. Forms of Fungus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392
95. Some Important Fungal infections . . . . . . . . . . . . . . . . . . . 393
96. Diagnostic Features of Some Important Fungus . . . . . . . . 393
97. Protozoan Parasites . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393
98. Characteristic Features of the Malaria Parasite
(Romanowsky-Stained Preparations) . . . . . . . . . . . . . . . . . 394
99. Diseases Due to Helminths . . . . . . . . . . . . . . . . . . . . . . . . . 395
100. Parasitic Nematode . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397
101. FAQ Lists of Parasitology . . . . . . . . . . . . . . . . . . . . . . . . . . . 398
102. Mode of infection of Parasites. . . . . . . . . . . . . . . . . . . . . . . 400
103. Parasite infecting Different Tissues. . . . . . . . . . . . . . . . . . . 400
104. Parasites Present in Muscles. . . . . . . . . . . . . . . . . . . . . . . . 400
xii Contents
105. Some Recently Recognized infectious Agents and
Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401
106. Influenza A Virus including Subtype H1N1. . . . . . . . . . . . . 401
107. Guidelines on Categorization of Seasonal
influenza A H1N1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 404
  Appendix   Pathology
1. Blood Collection System (Vacutainer System) . . . . . . . . . .
2. Genotypes & Phenotypes in ABO System. . . . . . . . . . . . . .
3. Reactions of ABO Groups. . . . . . . . . . . . . . . . . . . . . . . . . . .
4. Selection of Blood and Plasma by ABO Type. . . . . . . . . . .
5. Blood Components and indications for Use. . . . . . . . . . . .
6. Shelf Life of Blood Components . . . . . . . . . . . . . . . . . . . . .
7. Blood Component Separation. . . . . . . . . . . . . . . . . . . . . . .
8. Complications of Massive Blood Transfusion. . . . . . . . . . .
9. Hematopoietic Stem Cells. . . . . . . . . . . . . . . . . . . . . . . . . .
10. Cells of Peripheral Smear . . . . . . . . . . . . . . . . . . . . . . . . . .
11. Pathologic Red Cells in Blood Smears. . . . . . . . . . . . . . . . .
12. Erythrocyte and Reticulocyte inclusions. . . . . . . . . . . . . . .
13. Urinary Crystals. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
14. Urinary Cast. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
15. Cellular Responses to injury. . . . . . . . . . . . . . . . . . . . . . . . .
Sample Pages
16. Reversible Cell injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
17. Properties of the Principal Free Radicals involved
in Cell injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
18. Fixatives Used in Pathology . . . . . . . . . . . . . . . . . . . . . . . . .
19. Histology/Pathology/Microbiology Stains . . . . . . . . . . . . .
20. Hypertrophy, Hyperplasia and Atrophy. . . . . . . . . . . . . . .
21. Metaplasia, Dysplasia and Neoplasia. . . . . . . . . . . . . . . . .
22. Necrosis Vs Apoptosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
23. Mechanism of Apoptosis. . . . . . . . . . . . . . . . . . . . . . . . . . .
24. Proteins in BCL 2 Superfamily . . . . . . . . . . . . . . . . . . . . . . .
25. Types of Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
26. Types of Calcification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
27. Classification and Diagnosis of Amyloidosis. . . . . . . . . . . .
28. Acute inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
29. Principal Mediators of inflammation . . . . . . . . . . . . . . . . .
30. Chemokines. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
31. Connective Tissue/ Wound Repair . . . . . . . . . . . . . . . . . . .
32. Growth Factors and Cytokines Affecting Various
Steps in Wound Healing. . . . . . . . . . . . . . . . . . . . . . . . . . . .
33. Activators of Angiogenesis. . . . . . . . . . . . . . . . . . . . . . . . . .
34. Inhibitors of Angiogenesis. . . . . . . . . . . . . . . . . . . . . . . . . .
35. Growth Factors and Cytokines involved
in Regeneration and Wound Healing . . . . . . . . . . . . . . . . .
36. Pedigree & inheritance. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
37. Inheritance Patterns. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
38. Terms Used in Genetics & inheritance . . . . . . . . . . . . . . . .
39. Examples of Different inheritance Patterns . . . . . . . . . . . .
40. Some Commonly Identified Microdeletion
and Microduplication Syndromes FISH Analysis . . . . . . . .
41. Genetic Risk Assessment in X- Linked Recessive
inheritance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 443
42. Genetic Risk Assessment in Autosomal Recessive
inheritance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444
43. Translocation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444
44. Genes Associated With Hereditary Cancer. . . . . . . . . . . . . 445
45. Cell Cycle. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447
46. Cancer Genesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 448
405 47. Oncogenes and Proto-oncogene. . . . . . . . . . . . . . . . . . . . . 449
406 48. Tumor Suppressor Genes . . . . . . . . . . . . . . . . . . . . . . . . . . 450
406 49. DNA Repair & Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451
406 50. Techniques Commonly Used for Mutation Detection. . . . 451
406 51. HLA Markers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452
407 52. Paraneoplastic Syndromes Associated With Common
408 Cancers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453
409 53. Tumor Markers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 454
410 54. Immunohistochemical Markers (IHC). . . . . . . . . . . . . . . . . 455
412 55. Immunohistochemical Marker Profiles of
413 Soft Tissue Tumors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 458
415 56. Carcinogens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 458
415 57. Oncogenic Viruses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459
416 58. Cluster Differentiation Markers of Lymphoid
418 Cell Maturation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460
59. Cluster Differentiation Markers of Myeloid
418
Cell Maturation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 461
60. Cluster Differentiation Markers of Different Cells . . . . . . . 461
419
61. Cluster Differentiation Markers of B Cell Lymphomas . . . 462
420
62. Cluster Differentiation Markers of T Cell Lymphomas . . . 462
421
63. CD Markers Flow Chart of Lymphoma and Leukemias . . . 463
423
64. Hodgkins Vs Non Hodgkins . . . . . . . . . . . . . . . . . . . . . . . . . 464
423
65. Clinical Staging of Hodgkin and Non-Hodgkin Lymphomas
424
(Ann Arbor Classification) . . . . . . . . . . . . . . . . . . . . . . . . . . 464
426
66. Grades of NHL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464
428
67. Frequency of involvement of Nodal Sites in Hodgkin
428 Lymphoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465
429 68. Subtypes of Hodgkin’s Lymphoma . . . . . . . . . . . . . . . . . . . 465
429 69. Treatment of Hodgkin’s Lymphoma . . . . . . . . . . . . . . . . . . 466
431 70. Major Subtypes of Aml in the WHO Classification. . . . . . . 466
432 71. Types of Endocarditis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467
433 72. Thyroid Carcinoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
434 73. Prognosis of Thyroid Carcinoma. . . . . . . . . . . . . . . . . . . . . 471
74. Malignant Epithelial Lung Tumors. . . . . . . . . . . . . . . . . . . . 471
436 75. Types of Collagen and Associated Diseases. . . . . . . . . . . . 473
436 76. Constituents of Connective Tissues in Various Tissues. . . 474
436 77. Diseases With Granulomatous inflammation. . . . . . . . . . . 474
78. Classification and Characteristics of Selected Immune-
437 Mediated Vasculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
438 79. Antineutrophil Cytoplasmic Antibodies . . . . . . . . . . . . . . . 476
439 80. Frequency of Arteriographic Abnormalities and Potential
440 Clinical Manifestations of Arterial involvement
441 in Takayasu’s Arteritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
81. Most Common in Arteritis and Aneurysm. . . . . . . . . . . . . 477
442 82. Vascular Pathology of Hypertension. . . . . . . . . . . . . . . . . . 477
 Contents xiii

83. Major Primary Glomerulonephritis. . . . . . . . . . . . . . . . . . . 478   Appendix   Forensic Medicine

84. Causes of Nephritic Syndrome . . . . . . . . . . . . . . . . . . . . . . 480
85. Types of Deposits in Different Types of GN . . . . . . . . . . . . 481 1. Important Definitions of FMT . . . . . . . . . . . . . . . . . . . . . . . 509
2. Titles Related to FMT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
86. Lupus Nephritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481
3. Various Declarations Adopted by WMA in
87. Genetic Causes of Non-Syndromal SRNS/FSGS . . . . . . . . . 482
Chronological Order . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
88. Summary of Renal Cystic Diseases . . . . . . . . . . . . . . . . . . . 482
4. Types of Offence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
89. Types of Cirrhosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
5. Inquest. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
90. Patterns of injury in Drug- and toxin-induced
6. Summons or Subpoena . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
Hepatic injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
7. Cross Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 511
91. Scheuer Classification for Grading and Staging of Chronic
8. Indian Evidence Act (IEA) . . . . . . . . . . . . . . . . . . . . . . . . . . 511
Hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484
9. Criminal Procedure Code 1973. . . . . . . . . . . . . . . . . . . . . . 512
92. Stages of Chronic Hepatitis B infection. . . . . . . . . . . . . . . . 484
10. Indian Penal Code, 1860 (Act No. 45 of Year 1860). . . . . . 512
93. Antinuclear Antibody (ANA) Patterns and Clinical
Associations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484 11. Prosessional Negligence Vs Misconduct. . . . . . . . . . . . . . . 519
94. Autoimmune Diseases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 485 12. Types of Negligence (Malpraxis). . . . . . . . . . . . . . . . . . . . . 519
95. Types of Grafts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 487 13. Defence/ Doctrine in Favour and Against A Doctor. . . . . . 520
96. Graft-Versus-Host Disease (GVHD) . . . . . . . . . . . . . . . . . . . 488 14. Professional Secrets and Previleged Communication. . . . 520
15. Identification of Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
97. Clinical Grading of Acute GVHD. . . . . . . . . . . . . . . . . . . . . . 489
16. Identification of Race . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 523
98. Clinical Staging of Acute GVHD. . . . . . . . . . . . . . . . . . . . . . 489
17. Identification of Sex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 524
99. Bleeding and Clotting Disorders . . . . . . . . . . . . . . . . . . . . . 489
18. DNA Fingerprinting. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 525
100. Approach to A Patient With Bleeding Disorder. . . . . . . . . 490
19. Tests Used for Detection of Blood. . . . . . . . . . . . . . . . . . . . 526
101. Different Tests of Bleeding/ Clotting Disorders . . . . . . . . . 492
20. Dactylography. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527
102. Reference Values of Common Tests of Hemostasis and

Sample Pages
Blood Coagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492 21. Poroscopy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
103. Causes of Hemoglobinuria. . . . . . . . . . . . . . . . . . . . . . . . . . 493 22. Autopsy Techniques. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
23. Signs of Death. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
104. Diseases With Granulomatous inflammation. . . . . . . . . . . 493
24. Post Mortem Caloricity . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
105. The Prion Diseases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
25. Post Mortem Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 530
106. Neurodegenerative Diseases Associated With Aggregated
Proteins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 494 26. Adipocere Vs Mummification . . . . . . . . . . . . . . . . . . . . . . . 531
107. Inherited Diseases of the Red Cell 27. Incised Wound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
Membrane-Cytoskeleton. . . . . . . . . . . . . . . . . . . . . . . . . . . 494 28. Types of Abrasions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
108. Types of Hereditary Spherocytosis . . . . . . . . . . . . . . . . . . . 495 29. Contusion/Bruise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
109. Diseases With Predominantly intravascular Hemolysis. . . 495 30. Laceration and Types. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
110. Types of Microcytic Anemia. . . . . . . . . . . . . . . . . . . . . . . . . 496 31. Difference Between incised, Lacerated and Stab
Wounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 534
111. Causes of Macrocytic Anemia. . . . . . . . . . . . . . . . . . . . . . . 497
32. Antemortem Vs Postmortem injury . . . . . . . . . . . . . . . . . . 535
112. Approach to Anemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 498
33. Suicidal Vs Homicidal Wound . . . . . . . . . . . . . . . . . . . . . . . 535
113. Biochemical Tests for the Diagnosis and Differentiation of
Cobalamin and Folate Deficiencies. . . . . . . . . . . . . . . . . . . 499 34. Types of Stab Wound on the Basis of Weapon Used. . . . . 535
114. Causes of Pure Red Cell Aplasia. . . . . . . . . . . . . . . . . . . . . . 500 35. Types of Burn injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535
36. Corrosive injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 536
115. WHO Classification of Chronic Myeloproliferative
Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500 37. Pedestrian injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 536
116. Myocardial infarction Time of onset of Key Events in 38. injuries Sustained by Vehicle Occupants . . . . . . . . . . . . . . 537
Ischemic Cardiac Myocytes. . . . . . . . . . . . . . . . . . . . . . . . . 500 39. Types of Blast injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 538
117. Evolution of Morphologic Changes in Myocardial 40. Bullet Kinetics and injury. . . . . . . . . . . . . . . . . . . . . . . . . . . 539
infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501 41. Ballistic Phenomenon. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 540
118. Enzymes Elevated in Myocardial infarction . . . . . . . . . . . . 501 42. Types of Bullets in forensic Medicine. . . . . . . . . . . . . . . . . 541
119. Transudate Vs. Exudate . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502 43. Types of Gun Powder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542
120. Conditions Associated With Abnormal Alkaline 44. Gun Shot Residue. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542
Phosphatase. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502 45. Classification of Firearms. . . . . . . . . . . . . . . . . . . . . . . . . . . 543
121. Few Important Bodies in Medical Science. . . . . . . . . . . . . 503 46. Components of Gunshot and Its Effects. . . . . . . . . . . . . . . 544
122. Types of Rosettes in Histopathology. . . . . . . . . . . . . . . . . . 505 47. Bullet Wound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 544
123. Intestinal Polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505 48. Shotgun Firearm injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . 545
xiv Contents

49. Shotgun Contact & Short Range (Comprehensive) . . . . . . 546
50. Rifled Firearm. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 547
51. Clinical Effects of Hyperthermia on Body. . . . . . . . . . . . . . 548
52. Physical Methods of torture/Corporal Punishment. . . . . . 548
53. Diatom Test. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
54. Important Fractures in forensic. . . . . . . . . . . . . . . . . . . . . . 549
55. Hanging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 550
56. Signs/Tests for Live Birth . . . . . . . . . . . . . . . . . . . . . . . . . . . 551
57. Natural Vs Criminal Abortion. . . . . . . . . . . . . . . . . . . . . . . . 552
58. Toxicology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 553
59. Specific Antidotes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 561
60. Poison Specific Coloured Findings. . . . . . . . . . . . . . . . . . . . 562
61. Post Mortem Staining. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 563
62. Specific Odour of Poisons . . . . . . . . . . . . . . . . . . . . . . . . . . 563
63. Gastric Lavage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 564
64. Resemblence of Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . 564
65. Treatment and Prophylaxis of Opium & Alcohol
Dependence Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . 565
66. Preservatives Used in Poisoning. . . . . . . . . . . . . . . . . . . . . 565
67. Special organ Preservation in Poisoning. . . . . . . . . . . . . . . 565
68. Toxicological Examination . . . . . . . . . . . . . . . . . . . . . . . . . . 566
69. Abortifacient Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
70. Activated Charcoal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
71. Toxicology FAQ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
72. Muehrcke’s Line Vs Mee’s Line . . . . . . . . . . . . . . . . . . . . . . 567
73. Pesticides Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . 567
74. Narcotic and Psychotropic Drugs. . . . . . . . . . . . . . . . . . . . 568
75. Date Rape Drugs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569
76. Classification of Snakes . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569
77. Fatal Dose of Venoms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569
78. Poisonous Vs Non Poisonous Snakes . . . . . . . . . . . . . . . . . 570
79. First Aid Myths of Snake Bite. . . . . . . . . . . . . . . . . . . . . . . . 570
80. First Aid “Do It Right” Protocol . . . . . . . . . . . . . . . . . . . . . . 570
81. National Snake Bite Treatment Protocol (india). . . . . . . . . 571
82. Classification of Sexual offences. . . . . . . . . . . . . . . . . . . . . 573
83. Paraphilias. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 573
84. Indian Medical Council Act, 1956 (102 of 1956) 30th
December, 1956. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574
85. MTP Act . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574
86. Transplantation of Human organ Act 1994. . . . . . . . . . . . . 575
87. Street Names of Common Psychotropic Drugs . . . . . . . . . 576

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8 Appendix for PGMEE (Volume 1)

APPENDIX 7:  DEVELOPMENT OF URINARY BLADDER

Embryologically, the trigone of the bladder is derived from the caudal end of mesonephric ducts, which is
of mesodermal origin (the rest of the bladder is endodermal). In the female the mesonephric ducts regresses, causing the
trigone to be less prominent, but still present. Since both the mesonephric ducts and ureters originate in the mesoderm, the
mucosa of the bladder formed by incorporation of the ducts (the trigone of the bladder) is also mesodermal. With time, the
mesodermal lining of the trigone is replaced by endodermal epithelium, so that finally the inside of the bladder is completely
lined with endodermal epithelium.
During the fourth to seventh weeks of development, the Cloaca divides into the urogenital sinus anteriorly and the anal canal
posteriorly. Three portions of the urogenital sinus can be distinguished
1. The upper and largest part is the urinary bladder.Initially, the bladder is continuous with the allantois, but when the lumen of
the allantois is obliterated, a thick fibrous cord, the Urachus, remains and connects the apex of the bladder with the umbilicus.
In the adult, it is known as the median umbilical ligament.
2. The next part is a rather narrow canal, the pelvic part of the urogenital sinus, which in the male gives rise to the prostatic and
membranous parts of the urethra.
3. The last part is the phallic part of the urogenital sinus. It is flattened from side to side, and as the genital tubercle grows, this
part of the sinus will be pulled ventrally .

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APPENDIX 8:  DEVELOPMENT OF VAGINA
ΕΕ Endoderm → primitive gut → cloaca → urogenital sinus and anorectal canal.
ΕΕ The sinovaginal bulb originates from urogenital sinus.
ΕΕ Distally sinovaginal bulb and proximally overgrowth of Mullerian duct at Mullerian tubercle results in formation of vaginal
plate which on canalization forms upper and lower vagina respectively.
ΕΕ The first and second portions of Mullerian duct forms the fimbriae and the fallopian tubes while distal segment forms the
uterus and upper vagina.
ΕΕ Distal most portion of sinovaginal bulb forms the Hymen.
 ANATOMY 17

APPENDIX 16:  DEVELOPMENT OF THE VENOUS SYSTEM

Vitelline Veins
(The proximal part of the left vitelline vein and distal part of right vitelline vein disappears)
Right vitelline Vein Hepatocardiac/Superior/terminal portion of the IVC, Superior mesenteric vein
Left vitelline Vein Proximal part disappears
The anastomotic network around the duodenum develops into a single vessel, the portal vein

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UMBILICAL VEINS: (The right umbilical vein and the part of the left between the liver and the sinus venosus degenerate)
Right umbilical vein Hepatic sinusoids (degenerates early in fetal life)
Left umbilical vein Hepatic sinusoids
Ligamentum teres
communication between the left umbilical vein and the right hepatocardiac channel, the ductus
venosus obliterates to form ligamentum venosum
Cardinal Veins
Common cardinal (Duct of Right SVC
Cuvier) Left Oblique vein of left atrium& coronary sinus
Anterior cardinal Right SVC, internal jugular veins
Left Vanishes
Lt-Rt Left brachiocephalic vein
Anastomosis
 ANATOMY 27

APPENDIX 28:  TYPES OF EPIPHYSIS

Epiphysis Definition/Function Example
Pressure epiphyses Takes part in transmission of weight Head of femur, condyles of tibia, lower end of
radius
Traction epiphyses Provide attachment to more than 1 tendon Trochanter of femur, tubercles of humerus,
mastoid process.
Atavistic epiphyses Phylogenetically an independent bone which in Coracoid process of scapula, posterior tubercle of
man becomes fused to another bone talus, ostrigonum.
Aberrant epiphyses Not always present Head of metacarpal, base of other metacarpal

APPENDIX 29:  MUSCLE CELLS TYPES

Skeletal Cardiac Smooth
Nuclei Multinucleated, peripherally Single nuclei, Centrally located Single nuclei, Centrally located
located
Banding Actin and myosin Actin and myosin form distinctive Actin and myosin; No distinctive
form distinctive bands bands bands
Z-disks Present Present Absent, cytoplasmic dense
bodies are present
T tubules T tubules at A-I junction; T tubules at Z disk;  diads present No T tubules; no triads
triads present

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Cellular junctions
Neuromuscular
junctions
Ca+ binding
Regeneration
 No junctional complexes
 Present 

 Troponin 
Limited; satellite cells 
Intercalated disks 
Not present; contraction is intrinsic

 Troponin 
None
Gap junctions 
Not present; contraction is
intrinsic, neural, or  hormonal
Calmodulin
High
54 Appendix for PGMEE (Volume 1)

APPENDIX 55:  ANATOMY OF TONGUE

Parts Root, Tip, and Body, which has (a) a curved upper surface or dorsum, and (b) an inferior surface.
Dorsum The dorsum is divided into oral and pharyngeal parts. The inferior surface is confined to the oral part only.
The dorsum of the tongue is convex in all directions. It is divided into:
(a) An oral part or anterior two-thirds
(b) A pharyngeal part or posterior one-third, by a faint V-shaped groove, the sulcus terminalis. The two limbs of
the ‘V meet at a median pit, named the foramen caecum. They run laterally and forwards up to the palatoglossal
arches. The foramen caecum represents the site from which the thyroid diverticulum grows down in the embryo.
Epiglottis
Palatopharyngeal arch

Palatine tonsil
Lingual tonsil
Palatoglossal arch

Termial sulcus
Foliate papillae
Circumvallate papilla

Midline groove of tongue

Dorsum of tongue
Fungiform papilla
Filiform papilla

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Root

Tip
The root is attached to the mandible and soft palate above, and to the hyoid bone below. Because of these
attachments we are not able to swallow the tongue itself. In between the two bones, it is related to the
geniohyoid and mylohyoid muscles.
The tip of the tongue forms the anterior free end which, at rest, lies behind the upper incisor teeth.
Papillae of the tongue
These are projections of mucous membrane or corium which give the anterior two-thirds of the tongue its characteristic
roughness. These are of the following three types
Vallate or They are large in size 1-2 mm in diameter and are 8-12 in number. They are situated immediately in front of
circumvallate the sulcus terminalis.
papillae
Fungiform The fungiform papillae are numerous near the tip and margins of the tongue, but some of them are also
papillae scattered over the dorsum
Filiform papillae The filiform papillae or conical papillae cover the presulcal area of the dorsum of the tongue, and give it a
characteristic velvety appearance. They are the smallest and most numerous of the lingual papillae. Each is
pointed and covered with keratin; the apex is often split into filamentous processes
Artery, Vein and Lymphatics of Tongue
Arterial supply It is chiefly derived from the lingual artery, a branch of the external carotid artery. The root of the tongue is
also supplied by the tonsillar and ascending pharyngeal arteries
Venous drainage The arrangement of the vena comitantes veins of the tongue is variable. Two venae comitantes accompany
the lingual artery, and one vena comitantes accompanies the hypoglossal nerve. The deep lingual vein is the
largest and principal vein of the tongue. It is visible on the inferior surface of the tongue. It runs backwards
and crosses the genioglossus and the hyoglossus below the hypoglossal nerve. These veins unite at the
posterior border of the hyoglossus to form the lingual vein which ends either in the common facial vein or
in the internal jugular vein.
108 Appendix for PGMEE (Volume 1)

APPENDIX 31:  ANTICOAGULANT MECHANISMS

Physiological anticoagulation mechanisms act to reduce thrombin production or reduce the effects of thrombin
Antithrombin Antithrombin (AT), previously known as AT III is the main inhibitor of thrombin. It is a serine protease
inhibitor, which binds and inactivates thrombin, factor IXa, Xa, XIa and XIIa. The enzymatic activity of AT
is enhanced in the presence of heparin. However, the plasma concentration of heparin is low and does
not contribute significantly to the in vivo activation of AT. AT is activated by binding of heparin sulphate
present on endothelial cell surface. Other thrombin inhibitors are heparin cofactor II, α2 macroglobulin
and α1-antitrypsin.
Tissue factor It is a polypeptide produced by endothelial cells. It acts as a natural inhibitor of the extrinsic pathway by
plasminogen inhibiting TF-VIIa complex.  Protein S enhances the interaction of factor Xa in the presence of calcium and

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inhibitor phospholipids. 
Protein C pathway The propagation phase of the coagulation is inhibited by the Protein C pathway that primarily consist of
four key elements:
ΕΕ Protein C is a serine protease with potent anticoagulant, profibrinolytic and anti-inflammatory
properties. It is activated by thrombin to form activated protein C (APC) and acts by inhibiting
activated factors V and VIII (with Protein S and phospholipids acting as cofactors)
ΕΕ Thrombomodulin - A transmembrane receptor on the endothelial cells, it prevents the formation of
the clot in the undamaged endothelium by binding to the thrombin
ΕΕ Endothelial protein C receptor is another transmembrane receptor that helps in the activation of
Protein C
ΕΕ Protein S is a vitamin K-dependent glycoprotein, synthesised by endothelial cells and hepatocytes.
It exists in plasma as both free (40%) and bound (60%) forms (bound to C4b-binding protein). The
anticoagulant activity is by virtue of free form while the bound form acts as an inhibitor of the
complement system and is up regulated in the inflammatory states, which reduce the Protein S levels
thus resulting in procoagulant state. It functions as a cofactor to APC in the inactivation of FVa and
FVIIIa. It also causes direct reversible inhibition of the prothrombinase (FVa-FXa) complex
Protein Z It is a recently described component of the anticoagulant system that is produced in the liver. It inhibits
dependent protease Factor Xa in reaction requiring PZ and calcium. 
inhibitor/protein Z
(PZI)
 PHYSIOLOGY 129

Insulin Galanin (GAL)

Cholecystokinin (CCK) Amino acids (glutamate and γ-aminobutyric acid)
Glucagon-like peptide (GLP) Cortisol
Cocaine- and amphetamine-regulated transcript (CART) Ghrelin
Peptide YY (PYY) Endocannabinoids

APPENDIX 55:  AUTONOMIC NERVOUS SYSTEM

The autonomic nervous system (ANS) is the part of the nervous system that is responsible for homeostasis. Except for skeletal
muscle, which gets its innervation from the somatomotor nervous system, innervation to all other organs is supplied by the
ANS. Nerve terminals are located in smooth muscle (eg, blood vessels, gut wall, urinary bladder), cardiac muscle, and glands
(eg, sweat glands, salivary glands). Although survival is possible without an ANS, the ability to adapt to environmental stressors
and other challenges is severely compromised. Controls vegetative functions, hence also called as vegetative nervous system:
Temperature, Digestion, Heart rate, Respiration, blood pressure, metabolism
The classic definition of the ANS is the preganglionic and postganglionic neurons within the sympathetic and parasympathetic
divisions
The peripheral motor portions of the ANS are made up of two neurons:
1. Preganglionic : The cell bodies of the preganglionic neurons are located in the intermediolateral column (IML) of the spinal
cord and in motor nuclei of some cranial nerves. In contrast to the large diameter and rapidly conducting ALPHA motor
neurons, preganglionic axons are small-diameter, myelinated, relatively slowly conducting Beta fibers. A preganglionic axon
diverges to an average of eight or nine postganglionic neurons
2. Postganglionic neurons : The axons of the postganglionic neurons are mostly unmyelinated C fibers and terminate on the

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visceral effectors.
Autonomic nervous system

Parasympathetic Smpathetic nervous

nervous system system

The ANS has two major divisions: the sympathetic and parasympathetic nervous systems. In addition, the ANS includes the
enteric nervous system within the gastrointestinal tract
 PHYSIOLOGY 133

APPENDIX 58:  HYPOTHALAMIC NUCLEI

Region Area Nucleus
Anterior Medial Preoptic nucleus
Supraoptic nucleus (SO)
Paraventricular nucleus (PV)
Anterior hypothalamic nucleus
(AH)
Suprachiasmatic nucleus
Part of supraoptic nucleus (SO)
Tuberal Medial Dorsomedial hypothalamic
nucleus (DM)
Ventromedial nucleus (VM)
Arcuate nucleus (AR)/
Infundibular nucleus/
Periventricular nucleus
Function
Thermoregulation/ Heat loss
centre
Vasopressin (ADH) release
CRH release
Oxytocin and to a lesser extent
antidiuretic hormone
Thermoregulation/ Heat loss
centre (set point comparison)
Heat loss if core temp > set po
int
Circadian rhythms
Vasopressin release
Blood Pressure, Heart Rate, GI
stimulation
satiety centre(controls eating)
lesion causes voracious
appetite
Endocrine function (releasing
hormones)- controls
Adenohypophysis

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Posterior
Lateral

Medial
Lateral hypothalamic area

Mammillary nuclei (part of

mammillary bodies) (MB)
Posterior nucleus (PN)
Feeding centre (thirst and
hunger)-lesion causes anorexia

Memory, Feeding reflex

Increase blood pressure

Pupillary dilation
Thermoregulation (generates
shivering, if core temp <set
point)

Note: Paraventricular nucleus is not to be confused with periventricular nucleus.

APPENDIX 59:  ASCENDING (SENSORY) TRACTS OF SPINAL CORD

Situation Tract From 2nd order neuron To Crossing over Function
Anterior Anterior Axon of 1 st
Axon Begins in 3 order neuron
rd
Some fibres Crude touch
column spinothalamic order neuron Nucleus proprius from posterior Ascend several sensation
tract (With lateral dorsal root Terminates on 3rd limb of internal segments before
(Anterior spinothalamic ganglia and order neurons in capsule to post crossing over
white tract, forms terminate in Ventral Posterior central gyrus Mostly crossed,
funiculus) spinal lemnisus) medial part of Nucleus of (sensory) some uncrossed
dorsal horn (1st thalamus (VPN)
relay stn)
 PHYSIOLOGY 173

APPENDIX 96:  AUDITORY PATHWAY

Figure shows the major auditory pathways. It shows that nerve fibers from the spiral ganglion of corti enter the dorsal and
ventral cochlear nuclei located in the upper part of the medulla. At this point, all the fibers synapse, and second-order neurons
pass mainly to the opposite side of the brain stem to terminate in the superior olivary nucleus. A few second order fibers also
pass to the superior olivary nucleus on the same side. From the superior olivary nucleus,the auditory pathway passes upward
through the lateral lemniscus. Some of the fibers terminate in the nucleus of the lateral lemniscus, but many bypass this nucleus
and travel on to the inferior colliculus, where all or almost all the auditory fibers synapse. From there, the pathway passes to the
medial geniculate nucleus, where all the fibers do synapse. Finally, the pathway proceeds by way of the auditory radiation to the
auditory cortex, located mainly in the superior gyrus of the temporal lobe.
Auditory pathway Mnemonic: E-COLI-MA
1. Eighth nerve
2. Cochlear nucleus
3. Superior olivary complex
4. Lateral lemniscus
5. Inferior colliculus
6. Medial geniculate body
7. Auditory Cortex (Brodmann’s area 41)

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APPENDIX 97:  OLFACTION
Olfactory The olfactory receptor cells are located in a specialized portion of the nasal mucosa, the yellowish
Mucous pigmented olfactory mucous membrane. The olfactory membrane lies in the superior part of each nostril.
Membrane Medially, the olfactory membrane folds downward along the surface of the superior septum; laterally, it
folds over the superior turbinate and even over a small portion of the upper surface of the middle turbinate.
Olfactory mucous membrane is said to be the place in the body where the nervous system is closest to the
external world
1. Macrosmatic animals: In dogs and other animals in which the sense of smell is highly developed, the
area covered by olfactory membrane is large
2. Microsmatic animals: In humans area covered by olfactory membrane is small hence sense of
smell is less developed. In humans, it covers an area of 5 cm2 in the roof of the nasal cavity near the
septum (2.4 cm2 in each nostril)
188 Appendix for PGMEE (Volume 1)

APPENDIX 11:  OXYGEN BINDING MECHANISM OF HEMOGLOBIN

The tetrameric structure of hemoglobin permits cooperative interactions that are central to its function. For example,
2,3-bisphosphoglycerate (BPG) promotes the efficient release of O2 by stabilizing the quaternary structure of
deoxyhemoglobin.”
ΕΕ A low PO2 in peripheral tissues promotes the synthesis in erythrocytes of 2,3-bisphosphoglycerate (BPG) from the glycolytic
intermediate 1,3-bisphosphoglycerate.
ΕΕ The hemoglobin tetramer binds one molecule of BPG in the central cavity formed by its four subunits.
ΕΕ However, the space between the H helices of the chains lining the cavity is sufficiently wide to accommodate BPG only when
hemoglobin is in the T state.
ΕΕ BPG forms salt bridges with the terminal amino groups of both chains via Val NA1 and with Lys EF6 and His H21.
ΕΕ BPG therefore stabilizes deoxygenated (T state) hemoglobin by forming additional salt bridges that must be broken prior
to conversion to the R state.
ΕΕ Residue H21 of the g subunit of fetal hemoglobin (HbF) is Ser rather than His. Since Ser cannot form a salt bridge, BPG binds
more weakly to HbF than to HbA. The lower stabilization afforded to the T state by BPG accounts for HbF having a higher
affinity for O2 than HbA.
ΕΕ Deoxyhemoglobin binds one proton for every two O2 molecules released, contributing significantly to the buffering capacity
of blood.
ΕΕ The somewhat lower pH of peripheral tissues, aided by carbamation, stabilizes the T state and thus enhances the delivery of
O2.

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“Heme iron forms a covalent bond with the imidazole nitrogen of the “proximal” histidine at F8.”
ΕΕ The binding of oxygen to the iron molecule causes the hemoglobin molecule to undergo conformational changes that affect
the binding of oxygen to other heme sites.
ΕΕ The mechanism for this property can be explained in part by the interactions in the heme pocket.
ΕΕ The two histidines of globin (E7, F8) are located immediately above and below iron, which is in the plane of the pyrrole
ring in oxyhemoglobin. (see figure below)
190 Appendix for PGMEE (Volume 1)

Figure (B) The iron atom moves into the plane of the heme on oxygenation. Histidine F8 and its associated residues are pulled
along with the iron atom
ΕΕ The binding of the first O2 molecule to deoxy Hb shifts the heme iron toward the plane of the heme ring from a position
about 0.6 nm beyond it.
ΕΕ This motion is transmitted to the proximal (F8) histidine and to the residues attached thereto, which in turn causes the
rupture of salt bridges between the carboxyl terminal residues of all four subunits.
ΕΕ As a consequence, one pair of alpha/beta subunits rotates 15 degrees with respect to the other, compacting the tetramer.
ΕΕ Profound changes in secondary, tertiary, and quaternary structure accompany the high-affinity O2-induced transition of
hemoglobin from the low-affinity T (taut) state to the high-affinity R (relaxed) state.
ΕΕ These changes significantly increase the affinity of the remaining unoxygenated hemes for O2, as subsequent binding events
require the rupture of fewer salt bridges.
ΕΕ The terms T and R also are used to refer to the low-affinity and high-affinity conformations of allosteric enzymes,
respectively.
ΕΕ The overall conformational changes to hemoglobin appear to be the greatest after three molecules of O 2 have been added.
ΕΕ In general, proteins that undergo an allosteric change from the tense to a relaxed state are better able to interact with
substrate in the relaxed state

APPENDIX 12:  SHIFT OF OXYGEN DISSOCIATION CURVE

Left shift, increase affinity, Decrease P50

Right shift ( - CADET turns to Right), Decrease affinity, increase P50,

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1. C- Increase CO2
2. A- Acid (Low pH), Chronic anemia (due to increased 2,3 BPG)
3. D- Increased 2,3-Diphosphoglycerate (2,3 DPG, AKA 2,3-Bisphosphoglycerate, 2,3
BPG)
4. E- Exercise
5. T- Increase in body temperature
1.
2.
3.
4.
5.
6.
7.
Decrease CO2
Alkalosis (High pH)
Decreased 2,3 DGP
Decreased body temperature
High Fetal hemoglobin
Carboxyhemoglobin
Methemoglobinemia
 BIOCHEMISTRY 191

APPENDIX 13:  STEPS OF HEME/PORPHYRIN RING SYNTHESIS

Enzyme Location Substrate Product Porphyria Clinical Lab test
ALA synthase (Rate Mitochon- Glycine, succi- D-Amino- X linked Sidero- Anemia ↓RBC count,
limiting) drion nyl CoA levulinic acid blastic anemia ↓Hb
ALA dehydratase (Zinc Cytosol D-Amino- Porphobilino- ALA-Dehydratase Abdominal pain, ↑Urinary ALA
containing, Sensitive levulinic acid gen deficiency neuropsychiatric and copropor-
to lead poisoning) symptoms phyrin III
PBG deaminase/ HMB Cytosol Porphobilino- Hydroxy Acute intermit- Abdominal pain, ↑Urinary ALA
synthase/ Uroporphy- gen methyl bilane tent porphyria neuropsychiatric and PBG
rinogen I synthase symptoms
Uroporphyrinogen III Cytosol Hydroxymeth- Uroporphy- Congenital No photosensi- ↑Urinary, fecal
synthase ylbilane rinogen III erythropoietic tivity & RBC uropor-
porphyria phyrin I
Uroporphyrinogen III Cytosol Uroporphyrin- Coproporphy- Porphyria cuta- Photosensitivity ↑Urinary uro-
decarboxylase ogen III rinogen III nea tarda porphyrin I
Coproporphyrinogen Mitochon- Coproporphy- Protoporphy- Coproporphyria Photosensitivity, ↑Urinary ALA,
III oxidase drion rinogen III rinogen IX abdominal pain, PBG, & copro-
neuropsychiatric porphyrin III &
symptoms fecal copropor-
phyrin III
Protoporphyrinogen Mitochon- Protoporphy- Protoporphy- Variegate por- Photosensitivity, ↑Urinary ALA,
oxidase drion rinogen IX rin IX phyria abdominal pain, PBG, & copro-
neuropsychiatric porphyrin III &

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Ferrochelatase (Sen-
sitive to Lead poison-
ing)
Mitochon-
drion
Protoporphy-
rin IX
Heme Erythropoietic
protoporphyria
symptoms

Photosensitivity
fecal protopor-
phyrin IX
↑Fecal & RBC
protoporphyrin
IX
 BIOCHEMISTRY 197

APPENDIX 18:  METABOLIC PATHWAYS

Anabolic pathways Are those involved in the synthesis of larger and more complex Synthesis of protein from
compounds from smaller precursors—Anabolic pathways are amino acids and the
endothermic. synthesis of reserves of
Anabolic reactions require an input of energy, generally in the form triacylglycerol and glycogen.
of the phosphoryl group transfer potential of ATP and the reducing
power of NADH, NADPH, and FADH2
Catabolic pathways Are involved in the breakdown of larger molecules, commonly
involving oxidative reactions; they are exothermic, producing
reducing equivalents, and, mainly via the respiratory chain, ATP.
Amphibolic pathways which occur at the “crossroads” of metabolism, acting as links eg, the citric acid (TCA) cycle.
between the anabolic and catabolic pathways
In aerobic organisms, the citric acid cycle is an amphibolic pathway,
one that serves in both catabolic and anabolic processes.

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258 Appendix for PGMEE (Volume 1)

APPENDIX 2:  DOSE RESPONSE CURVE

Simple dose response curve hyperbolic in shape while log DRC is sigmoid in shape. There are three important parameters-
potency, efficacy and slope
Potency It is the measure of the amount of drug needed to produce the response. Drug producing same response at
lower dose is more potent (in DRC more the dose response curve towards left, greater is the potency i.e. A > B
> C > D)

Efficacy It is the maximum effect produced by a drug. It is clinically more important than potency. (On DRC- More is
the peak of curve greater is its efficacy i.e. A>B>C>D)

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Slope Steeper is the slope more are the chances of getting the response drastically with increase in dose. I.e. steep
DRC means narrow therapeutic index
298 Appendix for PGMEE (Volume 1)

APPENDIX 45:  CALCINEURIN INHIBITORS

Mechanism of
action

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Classification
These drugs bind to an immunophilin (cyclophilin for cyclosporine or FKBP-12 for tacrolimus), resulting in
subsequent interaction with calcineurin to block its phosphatase activity. Calcineurin is required for movement
of a component of the nuclear factor of activated T lymphocytes (NFAT) into the nucleus NFAT, in turn, is
required to induce a number of cytokine genes, including that for interleukin-2 (IL-2), a prototypic T-cell growth
and differentiation factor.

Cyclosporine
Systemic
Tacrolimus
Topical

Tacrolimus Pimecrolimus
Cyclosporine ΕΕ Produced by the fungus species Beauveria nivea
ΕΕ Can be administered intravenously or orally
Pharmacokinetics: Cyclosporine is extensively metabolized in the liver by CYP3A and to a lesser degree by the
gastrointestinal (GI) tract and kidneys. Cyclosporine and its metabolites are excreted principally through the
bile into the feces. Cyclosporine also is excreted in human milk. In the presence of hepatic dysfunction, dosage
adjustments are required. No adjustments generally are necessary for dialysis or renal failure patients.
Indications :
ΕΕ Cyclosporine is FDA-approved for the treatment of psoriasis. Other cutaneous disorders that typically respond
well to cyclosporine are atopic dermatitis, alopecia areata, epidermolysis bullosa acquisita, pemphigus
vulgaris, bullous pemphigoid, lichen planus, and pyoderma gangrenosum.
ΕΕ Clinical indications for cyclosporine are kidney, liver, heart, and other organ transplantation; rheumatoid
arthritis.
Side effects
ΕΕ The principal adverse reactions to cyclosporine therapy are renal dysfunction, tremor, hirsutism,
hypertension, hyperlipidemia, and gum hyperplasia
ΕΕ Hyperuricemia may lead to worsening of gout, increased P-glycoprotein activity, and hypercholesterolemia.
ΕΕ Nephrotoxicity occurs in the majority of patients treated and is the major indication for cessation or
modification of therapy.
300 Appendix for PGMEE (Volume 1)

APPENDIX 46:  FDA APPROVED MONOCLONAL ANTIBODIES & TARGETED THERAPIES

Antibody Type Target Indication
(What it’s approved to treat)
Abciximab chimeric Inhibition of glycoprotein IIb/IIIa High risk angioplasty
Adalimumab Human Inhibition of TNF-α signalling Inflammatory diseases –mostly autoimmune disorders like
rheumatoid arthritis, psoriatic arthritis, Crohn’s disease

Alemtuzumab humanized CD52 Chronic lymphocytic leukaemia, Tcell lymphoma

Basiliximab chimeric IL-2Rα receptor (CD25) Transplant rejection
Bevacizumab humanized Vascular endothelial growth factor Metastatic colorectal cancer, nonsmall cell lung cancer,
(VEGF) metastatic breast bancer
Cetuximab chimeric Epidermal growth factor receptor Colorectal cancer, Head and neck cancer
(EGFR)
Certolizumab humanized Inhibition of TNF-α signalling Crohn’s disease, rheumatoid
pegol arthritis
Daclizumab humanized IL-2Rα receptor (CD25) Transplant rejection
Dasatinib Targeted bcr-abl, src family, c-kit, EPHA2, CML, Ph+ ALL
PDGFR-β
Erlotinib Targeted EGFR Non–small cell lung cancer
Eculizumab humanized Complement system protein C5 Paroxysmal nocturnal hemoglobinuria
Efalizumab humanized CD11a Psoriasis

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Gemtuzumab
Golimumab

Imatinib
Ibritumomab
tiuxetan
Infliximab
humanized
humanized

Targeted
Murine

chimeric
CD33
TNFα

c-kit, bcr-abl, PDGFR

CD20

Inhibition of TNF-α signalling

Acute myelogenous leukaemia (with calicheamicin)
Rheumatoid & psoriatic arthritis, active ankylosing
spondylitis
CML, GIST
Non-Hodgkin lymphoma (with yttrium-90 or indium-111)

Several autoimmune disorders like Crohn’s disease

Lapatinib Targeted EGFR and HER2 Breast cancer
Muromonab- Murine T cell CD3 Receptor Transplant rejection
CD3
Natalizumab humanized Alpha-4 (α4) integrin, Multiple sclerosis and Crohn’s disease
Omalizumab humanized Immunoglobulin E (IgE) Mainly allergy-related asthma
Palivizumab humanized An epitope of the RSV F protein Respiratory Syncytial Virus
Panitumumab Human Epidermal growth factor receptor Metastatic colorectal carcinoma
Ranibizumab humanized Vascular endothelial growth factor Macular degeneration
A (VEGF-A)
Rituximab chimeric CD20 Non-Hodgkin lymphoma
Sunitinib Targeted second-generation receptor RCC, Imatinib resistant GIST, Progressive GIST, progressive
tyrosine kinase inhibitors well-differentiated pancreatic neuroendocrine tumors
(pNET)
Sorafenib Targeted Raf, PDGF, VEGFR, c-kit RCC
Temsirolimus Targeted mTOR RCC
Tositumomab Murine CD20 Non-Hodgkin lymphoma
Trastuzumab humanized ErbB2/HER2 Breast cancer
(Herceptin)
308 Appendix for PGMEE (Volume 1)

Footnote:
Anti diabetic Drugs to be given in subcutaneous route:
ΕΕ Insulin
ΕΕ GLP-1 analogue: Exenadide, Liraglutide
ΕΕ Amylin analogue: Pramlintide
Used both in Type 1 & Type 2 diabetes
ΕΕ Insulin
ΕΕ Amylin analogue: Pramlintide
ΕΕ α–Glucosidase inhibitors: Acarbose

APPENDIX 55:  INSULINS

Highly purified mono- Porcine Actrapid- Regular Short acting
component insulin Porcine Monotard- Lente Intermediate acting
Porcine Insulatard- NPH
Porcine Mixtard 30% regular, 70% Isophane
Human insulin Human Actrapid- Regular Short acting
Human Monotard- Lente Intermediate acting
Human Insulatard- NPH
Human Mixtard 30% regular, 70% Isophane
Insulin analogues Insulin Lispro Ultra short acting
Insulin aspart

Sample Pages Insulin glulisine

Insulin glargine
70% large particle,
insoluble, long
acting crystalline
(Ultralente)
30% small particle, short
acting, amorphous, (Semi-
lente)
Long acting

Intermediate acting
Lente insulin
 MICROBIOLOGY 349

APPENDIX 27:  PHASES OF THE MICROBIAL GROWTH CURVE

The phases of the bacterial growth curve shown in Figure are reflections of the events in a population of cells, not in individual
cells (batch culture).

Phase Growth Comments

Rate
Lag Zero ΕΕ Represents a period during which the cells, depleted of metabolites and enzymes as the result
of the unfavourable conditions that existed at the end of their previous culture history, adapt
to their new environment.
ΕΕ Enzymes and intermediates are formed and accumulate until they are present in
concentrations that permit growth to resume.
ΕΕ If the cells are taken from an entirely different medium, it often happens that they are

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genetically incapable of growth in the new medium. In such cases a long lag may occur,
representing the period necessary for a few mutants in the inoculums to multiply sufficiently
for a net increase in cell number to be apparent.
Exponential Constant ΕΕ The cells are in a steady state.
ΕΕ New cell material is being synthesized at a constant rate, but the new material is itself
catalytic, and the mass increases in an exponential manner.
ΕΕ This continues until one of two things happens: either one or more nutrients in the medium
become exhausted, or toxic metabolic products accumulate and inhibit growth.
ΕΕ For aerobic organisms, the nutrient that becomes limiting is usually oxygen.
ΕΕ When the cell concentration exceeds about 1 x 107/mL (in the case of bacteria), the growth
rate will decrease unless oxygen is forced into the medium by agitation or by bubbling in air.
When the bacterial concentration reaches 4–5 x 109/mL, the rate of oxygen diffusion cannot
meet the demand even in an aerated medium, and growth is progressively slowed
Maximum Zero ΕΕ Eventually, the exhaustion of nutrients or the accumulation of toxic products causes growth to
stationary cease completely.
ΕΕ In most cases, however, cell turnover takes place in the stationary phase.
ΕΕ There is a slow loss of cells through death, which is just balanced by the formation of new cells
through growth and division. When this occurs, the total cell count slowly increases although
the viable count stays constant.
Decline Negative ΕΕ After a period of time in the stationary phase, which varies with the organism and with the
(death) culture conditions, the death rate increases until it reaches a steady level.
ΕΕ In most cases the rate of cell death is much slower than that of exponential growth.
ΕΕ Frequently, after the majority of cells have died, the death rate decreases drastically, so that a
small number of survivors may persist for months or even years.
ΕΕ This persistence may in some cases reflect cell turnover, a few cells growing at the expense of
nutrients released from cells that die and lyse
 MICROBIOLOGY 357

APPENDIX 42:  EXOTOXIN VS ENDOTOXIN

Exotoxin Endotoxin
Secreted by -Secreted by bacteria. -Endotoxin is a component of the cell wall
-Are present in gram-positive & some gram negative bacteria -Are present only in gram-negative bacteria
(ie. Shiga’s dysentery, Bacillus, ETEC, Vibrio, Pertussis &
Pseudomonas)
Chemistry Polypeptide Lipopolysaccharide
Location of genes Plasmid or bacteriophage Bacterial chromosome
Toxicity High Low
Clinical effects Various effects Fever, shock
Mode of action Various modes Includes TNF and interleukin-1
Antigenicity Induces high-titer antibodies called antitoxins Poorly antigenic
Vaccines Toxoids used as vaccines No toxoids formed and no vaccine available
Heat stability Destroyed rapidly at 60°C (except staphylococcal enterotoxin) Stable at 100°C for 1 hour
Typical diseases Tetanus, botulism, diphtheria Meningococcemia, sepsis by gram-negative
rods

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Toxins
APPENDIX 43:  CHARACTERISTIC OF DIFFERENT TOXINS
Mechanism of Action
Strychnine ΕΕ Post-synaptic inhibition of Neurotransmitter Glycine in Spinal cord.
ΕΕ Acts on Antr.horn cell of spinal cord & inhibit post synaptic potential leading to release excitation.
Botulinum ΕΕ During the growth of C botulinum and during autolysis of the bacteria, toxin is liberated into the
environment.
ΕΕ Seven antigenic varieties of toxin (A to G) are known.
ΕΕ Types A, B, and E (and occasionally F) are the principal causes of human illness. Types A and B have
been associated with a variety of foods and type E predominantly with fish products. Type C produces
limberneck in birds; type D causes botulism in mammalsother than humans.
ΕΕ Botulinum toxin is absorbed from the gut and binds to receptors of presynaptic membranes of motor
neurons of the peripheral nervous system and cranial nerves.
ΕΕ Although all botulinum toxins have different molecular targets, they have same mechanism of action.
Proteolysis by the light chain of botulinum toxin of either synaptobrevin, syntaxin, or SNAP-25 in the
neurons inhibits the release of acetylcholine at the synapse of peripheral nerves, resulting in lack of
muscle contraction and paralysis.
ΕΕ The SNARE proteins are synaptobrevin, SNAP 25, and syntaxin. The toxins of C botulinum types A and E
cleave the 25,000-MW SNAP-25. Type B toxin cleaves synaptobrevin.
ΕΕ C botulinum toxins are among the most toxic substances known: The lethal dose for a human is probably
about 1-2 µg. The toxins are destroyed by heating for 20 minutes at 100°C.
Teatanus ΕΕ Tetanospasmin toxin inhibit presynaptic release of Neurotransmitter Glycin & GABA in CNS.
ΕΕ Toxins acts on Moter end plate, Spinal cord, Brain & Sympathetic nervous system.
376 Appendix for PGMEE (Volume 1)

APPENDIX 77:  PRIONS

ΕΕ Prions are infectious particles composed entirely of protein. They have no DNA or RNA. Prion’s are unusually resistant to
physical and chemical agents such as heat, irradiation and formalin. Therefore incineration is recommended.
ΕΕ Prions may have incubation periods of years before clinical manifestations of the infections become evident
ΕΕ They cause diseases such as Creutzfeldt-Jakob disease and kuru in humans and mad cow disease and scrapie in animals. These
diseases are called transmissible spongiform encephalopathies. The term spongiform refers to the sponge-like appearance of
the brain seen in these diseases. The holes of the sponge are vacuoles resulting from dead neurons.
ΕΕ Prion proteins are encoded by a cellular gene. When these proteins are in the normal, alpha-helix configuration, they are
nonpathogenic, but when their configuration changes to a beta-pleated sheet, they aggregate into filaments, which disrupts
neuronal function and results in the symptoms of disease.
ΕΕ Prions are unusually resistant to standard means of inactivation. They are resistant to treatment with formaldehyde (3.7%),
urea (8 M), dry heat, boiling, ethanol (50%), proteases, deoxycholate (5%), and ionizing radiation. However, they are sensitive
to phenol (90%), household bleach, ether, NaOH (2 N), strong detergents (10% sodium dodecyl sulfate), and autoclaving (1
hour, 121 °C). Guanidine thiocyanate is highly effective in decontaminating medical supplies and instruments.
ΕΕ Because they are normal human proteins, they do not elicit an inflammatory response or an antibody response/ Immune
response in humans
Comparison of Prions and Conventional Viruses
Feature Prions Conventional Viruses
Particle contains nucleic acid No Yes
Particle contains protein Yes, encoded by cellular genes Yes, encoded by viral genes
Inactivated rapidly by UV light or heat No Yes
Appearance in electron microscope Filamentous rods (amyloid-like) Icosahedral or helical symmetry
Infection induces antibody No Yes

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Infection induces inflammation No Yes

APPENDIX 78:  VIRAL INCLUSION BODIES

Intra cytoplasmic Acidophilic Negri bodies Rabies
Guarnieri bodies Variola (small pox), vaccinia
Bollinger bodies Fowlpox
Henderson Peterson bodies Molluscum contagiosum
Paschen Small pox
Basophilic Halber staedtler prowazek (HD Chlamydia trachomatis
Body)
Levinthal cole lillie (LCL body) Chlamydia psittaci
Intra nuclear Acidophilic Cowdry type A Herpes, chicken pox, yellow fever
Torres bodies Yellow fever
Cowdry type B Polio virus
Basophilic Cowdry type B Adenovirus
Cowdry type A/Owl’s eye CMV (Owl’s eye inclusion body with
surrounding halo and multiple indistinct
cytoplasmic, basophilic inclusions)
Both Intra cytoplasmic and Intra nuclear Warthin finkeldey Measles
 MICROBIOLOGY 379

HHV-2/ HSV-2 Sacral ganglia Mostly below waist lesions

ΕΕ Genital herpes
ΕΕ Aseptic meningitis
ΕΕ Neonatal infections
HHV-3/ Varicella Zoster Virus Sensory ganglia Chicken pox, Zoster
HHV-4 / Ebstein Barr Virus Lymphoid tissue Infectious Mononucleosis, Burkitt’s lymphoma
HHV-5/ Cyto Megalo Virus Salivary glands, Petechiae, Hepatosplenomegaly & jaundice (m.c), CMV
Kidney mononucleosis, Haemorrhagic retinitis in Immunocompromised pts,
intrauterine infection (m.c cause), complicates organ transplant
(m.c pathogen), pneumonia in transplant pts
HHV-6/ Human B cell Lymphotropic Lymphoid tissue Roseola infantum/ 6th disease/ Exanthema subitum, Focal
virus Encephalitis
HHV-7/ R K virus Lymphoid tissue
HHV- 8 Lymphoid tissue Kaposi’s sarcoma

APPENDIX 82:  CLINICAL AND EPIDEMIOLOGIC FEATURES OF VIRAL HEPATITIS

Feature HAV HBV HCV HDV HEV
Family Picornaviridae Hepadnaviridae Flaviviridae Unclassified Unclassified
Genus Hepatovirus  Orthohepadnavirus  Hepacivirus  Deltavirus  Hepevirus 
Virion 27 nm, 42 nm, spherical 60 nm, spherical 35 nm, spherical 30–32 nm,
icosahedral icosahedral

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Envelope No Yes (HBsAg) Yes Yes (HBsAg) No
Genome ssRNA dsDNA ssRNA ssRNA ssRNA
Stability Heat & acid Acid-sensitive Ether-sensitive, Acid-sensitive Heat-stable
stable acid-sensitive
Prevalence High High Moderate Low, regional Regional
Incubation (days) 15–45, mean 30 30–180, mean 60–90 15–160, mean 50 30–180, mean 60–90 14–60, mean 40
Onset Acute Insidious or acute Insidious Insidious or acute Acute
Age preference Children, young Young adults (sexual and Any age, but more Any age (similar to Young adults
adults percutaneous), babies, common in adults HBV) (20–40 years)
toddlers
Transmission
Fecal-oral +++ – – – +++
Percutaneous Unusual +++ (MC mode of +++ +++ –
transmission)
Perinatal – +++ ± + –
Sexual ± ++ ± ++ –
Clinical
Severity Mild Occasionally severe Moderate Occasionally severe Mild
Fulminant 0.1% 0.1–1% (most common, 0.1% 5–20% (highest 1–2%
>50% of all cases of viral chances of progression
fulminant hepatitis) to fulminant hepatitis)
Progression to None (HAV Occasional (1–10%) (90% Common (>50% to Common (<5% None
chronicity remains self of neonates) upto 85%) coinfection, 80% upon
limited & does super infection)
not progress
to chronic liver
disease.
 MICROBIOLOGY 385

APPENDIX 90:  ANTIVIRAL CHEMOTHERAPY AND CHEMOPROPHYLAXIS

Infection Drug Route Dosage Comment
Influenza A and Oseltamivir Oral Adults: 75 mg bid x 5 d Oseltamivir’s side effects of nausea and
B: Treatment  Children 1–12 years: 30–75 mg vomiting can be reduced in frequency by drug
bid, depending on weight,a x 5 d administration with food.
Zanamivir Inhaled Adults and children >7 years: 10 Zanamivir may exacerbate bronchospasm in
orally mg bid x 5 d patients with asthma.
Amantadine Oral Adults: 100 mg qd or bid x 5–7 d Amantadine and rimantadine are not
  Children 1–9 years: 5 mg/kg per recommended for routine use unless antiviral
day (max, 150 mg/d) x 5–7 d susceptibilities are known because of
widespread resistance in A/H3N2 viruses since
Rimantadine Oral 100 mg qd or bid x 5–7 d in
2005–2006 and in pandemic A/H1N1 viruses
  adults
in 2009–2010.
Influenza A and Oseltamivir Oral Adults: 75 mg/d Prophylaxis must be continued for the
B: Prophylaxis  Children >1 year: 30–75 mg/d, duration of exposure and can be administered
depending on weight simultaneously with inactivated vaccine.
Zanamivir Inhaled Adults and children >5 years: 10 Unless the sensitivity of isolates is known,
orally mg/d neither amantadine nor rimantadine is
currently recommended for prophylaxis or
Amantadine or Oral Adults: 200 mg/d therapy.
rimantadine Children 1–9 years: 5 mg/kg per
day (maximum, 150 mg/d)
RSV infection  Ribavirin Small- Administered 12–18 h/d from Use of ribavirin is to be “considered” for
particle reservoir containing 20 mg/mL treatment of infants and young children
aerosol x 3–6 d hospitalized with RSV pneumonia and

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bronchiolitis, according to the American
Academy of Pediatrics.
CMV disease  Ganciclovir IV 5 mg/kg bid x 14–21 d; then 5 Ganciclovir, valganciclovir, foscarnet, and
mg/kg per day as maintenance cidofovir are approved for treatment of CMV
dose retinitis in patients with AIDS. They are also
used for colitis, pneumonia, or “wasting”
syndrome associated with CMV and for
prevention of CMV disease in transplant
recipients.
Valganciclovir Oral 900 mg bid x 21 d; then 900 Valganciclovir has largely supplanted oral
mg/d as maintenance dose ganciclovir and is frequently used in place of
IV ganciclovir.

Foscarnet IV 60 mg/kg q8h x 14–21 d; then Foscarnet is not myelosuppressive and is

90–120 mg/kg per day as active against acyclovir- and ganciclovir-
maintenance dose resistant herpesviruses.
Cidofovir IV 5 mg/kg once weekly x 2 weeks,  
then once every other week;
given with probenecid and
hydration
Fomivirsen Intra 330 mg on days 1 and 15 Fomivirsen has reduced the rate of
vitreal followed by 330 mg monthly as progression of CMV retinitis in patients in
maintenance whom other regimens have failed or have
not been well tolerated. The major form of
toxicity is ocular inflammation.
Varicella: Acyclovir Oral 20 mg/kg (maximum, 800 mg) 4 Treatment confers modest clinical benefit
Immuno or 5 times daily x 5 d when administered within 24 h of rash onset.
competent host  Valacyclovir Oral Children 2–18 years:20 mg/kg
tid, not to exceed1 g tid, x5 d
 PATHOLOGY 413

APPENDIX 11:  PATHOLOGIC RED CELLS IN BLOOD SMEARS

Red Cell Type Description Underlying Change Disease State Associations
Acanthocyte Altered cell membrane Abetalipoproteinemia, parenchymal
(spur cell) lipids liver disease, postsplenectomy

Irregularly spiculated red cells with

projections of varying length and
dense center
Basophilic Precipitated ribosomes Coarse stippling: Lead intoxication,
stippling (RNA) thalassemia
Fine stippling: A variety of anemias

Punctuate basophilic inclusions

Bite cell Heinz body pitting by Glucose-6-phosphate dehydrogenase
(degmacyte) spleen deficiency, drug-induced oxidant
hemolysis
Smooth semicircle taken from one
edge
Burr cell May be associated with Usually artifactual; seen in uremia,
(echinocyte) or altered membrane lipids bleeding ulcers, gastric carcinoma
crenated red cell
Red cells with short, evenly spaced

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spicules and preserved central pallor
Cabot rings Nuclear remnant Postsplenectomy, hemolytic anemia,
megaloblastic anemia

Circular, blue, threadlike inclusion

with dots
Ovalocyte Abnormal cytoskeletal Hereditary elliptocytosis
(elliptocyte) proteins

Elliptically shaped cell

Howell-Jolly Nuclear remnant (DNA) Postsplenectomy, hemolytic anemia,
bodies megaloblastic anemia

Small, discrete, basophilic, dense

inclusions; usually single
Hypochromic red Prominent central pallor Diminished hemoglobin Iron deficiency anemia, thalassemia,
cell synthesis sideroblastic anemia
Macrocyte Red cells larger than normal (>8.5 Young red cells, abnormal Increased erythropoiesis; oval
μm), well filled with hemoglobin red cell maturation macrocytes in megaloblastic anemia;
round macrocytes in liver disease
Microcyte Red cells smaller than normal (<7.0 — Hypochromic red cell
μm)
 PATHOLOGY 447

APPENDIX 45:  CELL CYCLE

Sample Pages
460 Appendix for PGMEE (Volume 1)

Hepadna virus Hepatitis B (infectious Liver cancer

Hepatitis B virus (HBV) hepatitis)
Adenoviridae Acute respiratory disease; Adenocarcinomas (cancer of glandular epithelial tissues)
Common cold
Poxviridae Smallpox; cowpox Miscellaneous
Oncogenic RNA Viruses of The Family Retroviridae
Virus Cancer
Human T-cell leukemia virus (HTLV-1; Adult T-cell leukemia, Lymphoma
HTLV-2)
Sarcoma viruses of cats, chickens, rodents Sarcomas (cancer of connective tissues)
Mammary tumor virus of mice Mammary gland tumors
Feline leukemia virus (FeLV) Feline leukemia

APPENDIX 58:  CLUSTER DIFFERENTIATION MARKERS OF LYMPHOID CELL MATURATION

IMMUOPHENOTYPING: LYMPHOID
CELL MATURATION

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 PATHOLOGY 463

Enteropathy-associated T-cell lymphoma + + + -(+) +(-) +(-) -

Adult T-cell leukaemia/lymphoma + + - +(-) -(+) +(-) -
Footnote: + = >90% positive:  +(-) = >50% positive;  -(+) = <50% positive;  - = <10% positive.
ALCL-Anaplastic large cell lymphoma;  C=Cytoplasmic;  S-Surface.
 

APPENDIX 63:  CD MARKERS FLOW CHART OF LYMPHOMA AND LEUKEMIAS

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 PATHOLOGY 485

Note: SLE, systemic lupus erythematosus; MCTD, mixed connective tissue disease; SCLE, subacute cutaneous lupus
erythematosus; PSS, progressive systemic sclerosis; CREST, calcinosis, Raynaud phenomenon, esophageal involvement;
sclerodactyly; and telangiectasia

APPENDIX 94:  AUTOIMMUNE DISEASES

Autoantigen Autoimmune Diseases
CELL- OR ORGAN-SPECIFIC AUTOIMMUNITY 
Acetylcholine receptor Myasthenia gravis
Actin Chronic active hepatitis, primary bilary cirrhosis
Adenine nucleotide translator (ANT) Dilated cardiomyopathy, myocarditis
Adrenoreceptor Dilated cardiomyopathy
Aromatic L-amino acid decarboxylase  Autoimmune polyendocrine syndrome type 1 (APS-1)
Asialoglycoprotein receptor Autoimmune hepatitis
Bactericidal/permeability-increasing protein (Bpi) Cystic fibrosis vasculitides
Calcium-sensing receptor Acquired hypoparathyroidism
Cholesterol side-chain cleavage enzyme (CYPlla) Autoimmune polyglandular syndrome-1
Collagen type IV-3-chain Goodpasture syndrome
Cytochrome P450 2D6 (CYP2D6) Autoimmune hepatitis

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Desmin Crohn disease, coronary artery disease
Desmoglein 1 Pemphigus foliaceus
Desmoglein 3 Pemphigus vulgaris
F-actin Autoimmune hepatitis
GM gangliosides Guillain-Barré syndrome
Glutamate decarboxylase (GAD65) Type 1 diabetes, stiff man syndrome
Glutamate receptor (GLUR) Rasmussen encephalitis
H/K ATPase Autoimmune gastritis
17--Hydroxylase (CYP17) Autoimmune polyglandular syndrome-1
21-Hydroxylase (CYP21) Addison disease
IA-2 (ICA512) Type 1 diabetes
Insulin Type 1 diabetes, insulin hypoglycemic syndrome (Hirata disease)
Insulin receptor Type B insulin resistance, acanthosis, systemic lupus erythematosus
(SLE)
Intrinsic factor type 1 Pernicious anemia
Leukocyte function-associated antigen (LFA-1) Treatment-resistant Lyme arthritis
Myelin-associated glycoprotein (MAG) Polyneuropathy
Myelin-basic protein Multiple sclerosis, demyelinating diseases
Myelin oligodendrocyte glycoprotein (MOG) Multiple sclerosis
Myosin Rheumatic fever
p-80-Collin Atopic dermatitis
Pyruvate dehydrogenase complex-E2 (PDC-E2) Primary biliary cirrhosis
512 Appendix for PGMEE (Volume 1)

Section 114A IEA In a prosecution for rape, where the question is whether sexual intercourse was without the consent of the
woman, and she states in her evidence that she did not consent, the court shall presume that she did not
consent.
Section 126 IEA Professional communication
Section 151 IEA Indecent and scandalous questions
Section 152 IEA Court may forbid any question which appears insulting or offensive

APPENDIX 9:  CRIMINAL PROCEDURE CODE 1973

2 (c) CrPc Defines cognizable offences ie arrest without warrant ( rape , murder,dacoity)
26 CrPc Division of offences
39 CrPc Inform police about every illegal event (A government doctor is bound to report all cases of poisoning whether
suicidal or accidental or homicidal to police) (A private practitioner is bound to inform only homicidal poisoning)
Non compliance/not reporting  in above matters is punishable under section 176 IPC, Giving false information on
such matters is punishable under section 177 IPC
40 CrPc Inform police about every death (A government doctor is bound to inform all unnatual deaths to police)
53 CrPc Procedure of examination of accused (can be done w/o consent if on request of S.I.)
53 (a) CrPc Procedure of examination of  RAPE accused
54 CrPc Accused himself can ask court to get him medically examined to prove his innocence
61-69 CrPc Summons (See APPENDIX: SUMMONS OR SUBPOENA)

Sample Pages
160 CrPc Police I.O. has the power to summon any witness (exept female , male<15 yrs)
161 CrPc Police recording of statement in cases
164 (a) CrPc Procedure of examination of RAPE VICTIM
164 CrPc MAGISTRATE recording of statement in cases
174 CrPc Police inquest
174 (3) CrPc Procedure in dowry death
175 CrPC Power to summon persons (Medical  practitioner can be summoned by I.O.  and he is bound to attend)
176 CrPc Magistrate inquest (custodial death, dowry death, death in mental asylum)
291 CrPc This is accepted as evidence in a higher court when it has been recorded and attested by a magistrate in the
presence of the accused who had an opportunity of cross examining the witness
357 (c) CrPc Free treatment by all medical institution to RAPE/ ACID ATTACK victims
409 CrPc Withdrawl of cases  by session judge
410 CrPc Withdrawl of cases by judicial magistrate
411 CrPc Withdrawl of cases executive magistrate
412 CrPc Reasons to be recorded for withdrawl of cases
416 CrPc Postponement of execution of a pregnant woman (upto 6 months after delivery) or change it to life imprisonment
by high court

APPENDIX 10:  INDIAN PENAL CODE, 1860 (ACT NO. 45 OF YEAR 1860)
Sections Particulars
Chapter I Introduction
Section 1-5
Chapter II General Explanations
SECTION 6-52
 FORENSIC MEDICINE 521

APPENDIX 15:  IDENTIFICATION OF AGE

Identification of age by Galstaun chart (most accepted) age in years
Ossification centre Girls (years) Boys (years)
Elbow 13-15 (Head of radius-14, Olecranon -15) 15-17 (Head of radius-16, Olecranon -17)
Wrist 16-17 (Lower end of radius-16.5, lower end of ulna-17) 18-19 (Lower end of radius-16-17, lower end
(Pisiform- last bone in the wrist- 12-17) of ulna-18) (Pissiform- last bone in the wrist-
9-12)
Shoulder 17-18 19-20
Iliac crest 17-19 19-20
Ischial tuberosity 20 20
Inner end of clavicle 20 22
Lower end of femur 14-17 14-17
Lower end of tibia 14-15 15-17
Identification of intrauterine age
Hasse’s rule Upto 5 months, square root of length of foetus in cm is the age of foetus
After 5 months, age in lunar months multiplied by 5 is the length of the foetus , i.e. 1/5th of the length
of the fetus in cm gives the age in lunar months. Sometimes separately referred to as Morison’s rule
Identification of age by Carpal bones
There are 8 carpal bones and Pisiform is last to appear. Approximate age before appearance of Pisiform can be given from the
number of carpal bones. i.e. Total number of carpal bones= Age in years
At 9th year all 8 carpal bones are present.

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Identification of age by Sternum
Appearance Fusion
Manubrium 5-6 months intra uterine 60 years with body
 FORENSIC MEDICINE 527

Spectroscopic test Spectroscopy Confirmatory, Most specific, requires sizeable stain

(> 1 cm2). Can detect both recent as well as old blood
stains
Physiochemical Thin layer chromatography
tests Electrophoresis
Species specific Immunological tests (Precipitin test, To differentiate human blood with animal blood
tests Heamagglutination inhibition test, Latex test)
Enzymological tests (LDH Electrophoresis)
Blood group Immunological tests: Absolute diagnosis of blood group is not possible.
detection tests Absorption-Elution test (a.k.a Acid dilution test, Can detect blood groups in old and dry stains
Acid elution test)
Mixed agglutination test
Absorption inhibition test
Enzymological tests:
Vertical disc, vertical or horizontal slab, isoelectric
focusing, cellulose acetate membrane

APPENDIX 20:  DACTYLOGRAPHY

AKA: Dactuloscopy, Dermatographics, Galton systen, Fingerprint study
Sir Henry Galton (1892) depending on the arrangements of papillary ridges classified the finger prints into 4 major primary
types.

Sample Pages
1. Arch = 7% (Plain and Tented)
2. Loop = 65% (Most common, Ulnar loop and Radial loop)
3. Whorl = 25% (Circular, Spiral clockwise, Spiral Counterclockwise)
4. Composite: Mix of all three patterns above (2–3%)

Whorl pattern Loop pattern Arch pattern

There exist four types of fingerprint readers:

1. Optical readers take a visual image of the fingerprint using a digital camera. Cheap and used in mobiles
2. Capacitive or CMOS readers use capacitors and thus electrical current to form an image of the fingerprint
3. Ultrasound fingerprint readers costly
4. Thermal
Note:
The little fingers are never recorded because they are not particularly well suited for fingerprint comparison
Most suitable fingerprints in fingerprint scanners : Index finger > Thumb > Middle finger > Ring finger .
Most suitable for ink impression fingerprints on papers/ documents: Thumb > Index finger > Middle finger > Ring finger
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Fingerprints are formed during Intrauterine life.
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Fingerprints are 100% accurate method of identification
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In practice minimum 12 point matching is considered as proof of identity (In India), however traditionally 16 points matching
is considered by most foreign Authors. Question can be asked in two forms. Minimum matching and normally considered
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No two person can have same Finger prints, not even identical twins
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Chances of two person having identical fingerprints is 1 in 64000 millions
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Faint and invisible finger prints (Latent Fingerprints)can be made visible by special techniques like Aluminium hydroxide.
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Finger prints can be taken from dead bodies and even putrified bodies.
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The first Fingerprint Bureau in world was established at Kolkata on 12th June 1897 at Writer’s building.
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Skull bone Beveled inner table Beveled outer table

Singeing, Blackening, Present Absent
Burning, Tattooing,
Grease/dirt collar

APPENDIX 48:  SHOTGUN FIREARM INJURIES

Contact/ Point Close range Short range Intermediate range Long/ Distant shot

Sample Pages
Blank  range
Distance Contact Upto 1 meter 1-2 meters 2-4 meters > 4 meters
Size Large lacerated with Bullet size entry wound Single circular Central hole with Central hole absent
cavitation due to aperture 4-5 cm small peripheral . Small individual
gases. in diameter. Satellite holes
Shape Shotgun entry Between 30 cm to 1 m, Irregular Irregular margins all  pellets show
wound is round, the rim of the wound margins of of a central entry independent entry
elliptical, cruciate, is irregular and often central entry wound  with  few wound from 4
triangular,   and single called a ‘Rat-hole’ in wound without satellite independent meters onwards.
upto 30 cm. Edges the USA because of any satellite entry wounds are
are normally inverted the nibbled edges, the wounds seen from 2 mtr and
(may be everted due same appearance is above
to bone underneath called ‘scalloping’ in
or gases coming out) the UK. There may be
annular abrasion and
bruising/”rat nibbling”
Abrasion Present Present Absent Absent Absent
ring/ Grease
collar
Burning & Present Present Absent Absent Absent
Singeing of
hair
Soot Present Present Present Absent   Absent  
Blackening /
Smudging
Sample Pages