Sample Pages - Kalam BooksSample Pages Contents iii APPENDIX for PGMEE Volume 1 First Edition Dr...
42
Transcript of Sample Pages - Kalam BooksSample Pages Contents iii APPENDIX for PGMEE Volume 1 First Edition Dr...
Sample Pages
Sample Pages
Contents iii
APPENDIXfor PGMEE
Volume 1
First Edition
Dr Vaibhav Bharat 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
Sample Pages
Contents v
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 [email protected]
Thanks Authors/ EditorsAPPENDIX FOR PGMEEBy Team MedE@sy
Preface
Sample Pages
Contents vii
Appendix Anatomy 1. Gametogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
2. Male Gametogenesis (Spermatogenesis) . . . . . . . . . . . . . . . 1
3. Female Gametogenesis (Oogenesis) . . . . . . . . . . . . . . . . . . . 2
4. Germ Layer Derivatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
5. Mesogastrium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
6. Adult Derivatives and Vestigial Remains of Embryonic Urogenital Structures/ Structural Homologues in Males and Females . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
7. Development of Urinary Bladder . . . . . . . . . . . . . . . . . . . . . 8
8. Development of Vagina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
9. General Time Course of Gonadal Development . . . . . . . . . . 9
10. Development of External Genitalia . . . . . . . . . . . . . . . . . . . . 9
11. Development of Kidney Systems . . . . . . . . . . . . . . . . . . . . . 10
12. Development of CNS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
13. Branchial Arches . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
14. Development of the Arterial System . . . . . . . . . . . . . . . . . 15
15. Anomalies of Aortic Arches . . . . . . . . . . . . . . . . . . . . . . . . . 16
16. Development of the Venous System . . . . . . . . . . . . . . . . . 17
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
44. Dermatomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
45. Myotomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
46. Vertebral Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
47. Vertebral Levels of organs . . . . . . . . . . . . . . . . . . . . . . . . . . 48
48. Openings of Diaphragm (Mnemonic: Voice of America) . . 48
49. Vertebral Column . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
50. Foramina of the Skull . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
51. Layers of Scalp (Mnemonic form) . . . . . . . . . . . . . . . . . . . . 52
52. Muscles of Mastication (Acting on Temporomandibular Joint) . . . . . . . . . . . . . . . . 52
53. Movements Around TMJ . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
54. Extrinsic Muscles of tongue . . . . . . . . . . . . . . . . . . . . . . . . . 53
55. Anatomy of tongue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
56. Muscles of Soft Palate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
57. Muscles of Pharynx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
58. Cartilages of Larynx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
59. Joints and Ligaments of the Shoulder Region . . . . . . . . . . 60
60. Anterior Axioappendicular Muscles . . . . . . . . . . . . . . . . . . 62
61. Posterior Axioappendicular Muscles . . . . . . . . . . . . . . . . . . 62
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
Contents
Sample Pages
Contentsviii
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
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 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11846. Fetal Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
Sample Pages
Contents ix
94. Fast Vs. Slow Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
95. Visual Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
96. Auditory Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
97. Olfaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
98. Primary Sensations of Taste . . . . . . . . . . . . . . . . . . . . . . . . 176
Appendix Biochemistry
1. Enzyme inhibition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
2. Michaelis-Menten Equation. . . . . . . . . . . . . . . . . . . . . . . . 181
3. Difference Between Functional and Non-Functional Enzymes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
4. Lactate Dehydrogenase . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
5. Cofactors of Different Enzymes . . . . . . . . . . . . . . . . . . . . 183
6. Major Properties of the Glycosaminoglycans . . . . . . . . . . 183
7. Vitamins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
8. Subtypes of Vitamin K . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
9. Deficiencies and toxicities of Metals . . . . . . . . . . . . . . . . . 186
10. Principal Proteins of RBC Membrane . . . . . . . . . . . . . . . . 187
11. Oxygen Binding Mechanism of Hemoglobin . . . . . . . . . . 188
12. Shift of Oxygen Dissociation Curve . . . . . . . . . . . . . . . . . . 190
13. Steps of Heme/Porphyrin Ring Synthesis . . . . . . . . . . . . . 191
14. Lead toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
15. Purine Biosynthesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
16. Lesch Nyhan Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
17. The Principal Methods and Preparations Used in Biochemical Laboratories . . . . . . . . . . . . . . . . . . . . . . . . 196
18. Metabolic Pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
19. Substrates of Different organs . . . . . . . . . . . . . . . . . . . . . . 198
20. Carbohydrate Metabolism Overview . . . . . . . . . . . . . . . . 199
21. Tricarboxylic Acid Cycle (Tca Cycle/ Krebs Cycle/ Citric Acid Cycle) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
22. Glycolysis and Gluconeogenesis . . . . . . . . . . . . . . . . . . . . 200
23. ATP formation in the Catabolism of Glucose . . . . . . . . . . 203
24. Fate of Pyruvate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
25. Anaerobic Glycolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
26. Tests Based Upon Reducing Property of Sugars . . . . . . . . 206
27. Calories of Food Components . . . . . . . . . . . . . . . . . . . . . . 206
28. Plasma Concentrations of Metabolic Fuels (Mmol/L) in the Fed and Fasting States . . . . . . . . . . . . . . . . . . . . . . . 207
29. Summary of Few Important Aspects of the Complexes of ETC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
30. Respiratory Poisons, inhibitors & Uncouplers . . . . . . . . . 208
31. Glucose Transporter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
32. Factors Affecting Phosphorylase . . . . . . . . . . . . . . . . . . . . 210
33. Glycogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
34. Glycogenolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
35. Actions of insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
36. Effects of insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
37. ATP Production in Substrate Level Versus Oxidative Phosphorylation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
38. Free Energy of Hydrolysis of Some organophosphates of
Biochemical Importance . . . . . . . . . . . . . . . . . . . . . . . . . . 213
39. Respiratory Quotient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
40. Amino Acid Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214
41. Amino Acid Polarity and Charge . . . . . . . . . . . . . . . . . . . . 215
42. Essential and Non Essential Amino Acids . . . . . . . . . . . . . 215
43. Typical Range of Pka Values of Side Groups of Amino Acids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
44. Amino Acid Titration Curve . . . . . . . . . . . . . . . . . . . . . . . . 216
45. Transamination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
46. Ketogenic and Glucogenic Amino Acids . . . . . . . . . . . . . . 221
47. Biologically Important Compounds From Amino Acids . . 221
48. Reverse Codon Table of Amino Acids . . . . . . . . . . . . . . . . 222
49. Selenocysteine the 21st Amino Acid . . . . . . . . . . . . . . . . . 222
50. Amino Acids FAQ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222
51. Sites of Pathways of Protein Synthesis . . . . . . . . . . . . . . . 223
52. Disorders of Phenyl Alanine Metabolism . . . . . . . . . . . . . 223
53. Tyrosine Metabolism Disorders . . . . . . . . . . . . . . . . . . . . . 223
54. Metabolism of Sulphur Containing Amino Acids . . . . . . . 224
55. Protein Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
56. Current Concepts in Protein Folding . . . . . . . . . . . . . . . . . 225
57. Chaperones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226
58. Urea Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
59. Denaturation and Precipitation of Proteins . . . . . . . . . . . 228
60. Cori Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
61. Aptamers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
62. De Novo Synthesis of Fatty Acids (Lipogenesis) . . . . . . . . 231
63. Fatty Acid Oxidation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
64. Beta Oxidation of Fatty Acids . . . . . . . . . . . . . . . . . . . . . . . 233
65. Cholesterol Biosynthesis . . . . . . . . . . . . . . . . . . . . . . . . . . 235
66. Steroid Hormone Synthesis . . . . . . . . . . . . . . . . . . . . . . . . 237
67. Vitamin-D: Synthesis and Metabolism . . . . . . . . . . . . . . . 238
68. Major Lipoprotein Classes . . . . . . . . . . . . . . . . . . . . . . . . . 238
69. Major Apolipoproteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
70. Chylomicrons. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
71. Lysosomal Storage Disorders . . . . . . . . . . . . . . . . . . . . . . . 240
72. Frederickson Classification of Hyperlipoproteinemias . . 242
73. Summary of the Major Drugs Used for the Treatment of Hyperlipidemia . . . . . . . . . . . . . . . . . . . . . . . 243
74. Newer Drugs for Dyslipidemia . . . . . . . . . . . . . . . . . . . . . . 244
75. Bile Acid and Salts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
76. Ketogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246
77. Types of Lipases in the Human Body . . . . . . . . . . . . . . . . . 248
78. DNA Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
79. Structural forms of DNA . . . . . . . . . . . . . . . . . . . . . . . . . . 250
80. DNA Sequences With Unusual Structures . . . . . . . . . . . . 251
81. Mitochondrial DNA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
82. Classes of Proteins involved in Replication . . . . . . . . . . . . 252
83. Mechanism of DNA Repair . . . . . . . . . . . . . . . . . . . . . . . . . 252
84. Human Diseases of DNA Damage Repair . . . . . . . . . . . . . 253
85. Epigenetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
86. Techniques of Molicular Biology . . . . . . . . . . . . . . . . . . . . 254
87. Some of the Enzymes Used in Recombinant DNA Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254
Sample Pages
Contentsx
88. Polymerase Chain Reaction . . . . . . . . . . . . . . . . . . . . . . . . 255 89. Milestones in Human Genome Sequencing . . . . . . . . . . . 256
Appendix Pharmacology
1. Kinetics of Elimination . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257
2. Dose Response Curve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
3. Types of Conjugation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260
4. P450s (CYPS), Drugs Metabolized (Substrates), inducers, and inhibitors . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
5. List of Prodrugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
6. Drugs and Cosmetic Rules of 1945 . . . . . . . . . . . . . . . . . . 262
7. Orphan Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
8. Clinical Trial and Preclinical Testing . . . . . . . . . . . . . . . . . 264
9. Pre-Clinical Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265
10. Drug Storage instructions. . . . . . . . . . . . . . . . . . . . . . . . . . 266
11. Cholinergic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
12. Muscarinic Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
13. Classification of Atropine Substitutes . . . . . . . . . . . . . . . . 267
14. Receptor Actions of Sympathomimetic and Dopaminergic Agents . . . . . . . . . . . . . . . . . . . . . . . . . 268
15. Endogenous Catecholamines . . . . . . . . . . . . . . . . . . . . . . . 268
16. Adrenergic Agonist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269
17. Therapeutic Classification of Adrenergic Drugs . . . . . . . . 270
18. Effects of Adrenaline on Blood Pressure . . . . . . . . . . . . . . 270
19. Vasomotor Re-Reversal . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
20. Classification of Alpha Adrenergic Blocking Agents . . . . . 271
21. Classification of Beta Blockers . . . . . . . . . . . . . . . . . . . . . . 272
22. Actions Ascribed to Different Types of Opioid Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
23. Opioid Drugs and their Actions on Opioid Receptors . . . 273
24. Methadone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
25. Serotonin Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274
26. 2Nd Generation Anti Histamine . . . . . . . . . . . . . . . . . . . . . . 275
27. Classification of Antibiotics . . . . . . . . . . . . . . . . . . . . . . . . 275
28. Post Antibiotic Effect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
29. Cephalosporins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277
30. Antibiotic Treatment of Pseudomonas Aeruginosa . . . . 278
31. Penicillin G . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
32. Classification of ESBL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
33. Antituberculous Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
34. Antituberculosis Drugs Dosage . . . . . . . . . . . . . . . . . . . . . 280
35. Antiviral Chemotherapy and Chemoprophylaxis . . . . . . . 281
36. Targets and Mechanism of Antiretroviral Drugs . . . . . . . . 285
37. Antiretroviral Drugs Used in the Treatment of HIV infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
38. Ocular Side Effects of HAART . . . . . . . . . . . . . . . . . . . . . . 289
39. Therapy for Chronic Hepatitis B . . . . . . . . . . . . . . . . . . . . . 289
40. Latest Guidelines for Treatment of Hepatitis C . . . . . . . . 290
41. Classification of Cancer Chemotherapy Agents . . . . . . . . 291
42. Anticancer Drug Toxicities . . . . . . . . . . . . . . . . . . . . . . . . . 296
43. Anticancer Drugs toxic Amelioration . . . . . . . . . . . . . . . . . 296
44. Classification of the Acute Emetogenic Potential of Antineoplastic Medication . . . . . . . . . . . . . . . . . . . . . . . . . 297
45. Calcineurin inhibitors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298 46. FDA Approved Monoclonal Antibodies &
Targeted therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 300 47. Monoclonal Antibodies Used in the Treatment
of Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 48. Features of Gpiib/Iiia Antagonists . . . . . . . . . . . . . . . . . . . 302 49. Rituximab . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303 50. Side Effects of Common Anti Epileptics . . . . . . . . . . . . . . 303 51. Classification of Anti Arrhythmic Drugs . . . . . . . . . . . . . . 305 52. Drugs Used in Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . 305 53. Commonly Used Antiarrhythmic Agents: Chronic oral
Dosing/Primary indications . . . . . . . . . . . . . . . . . . . . . . . . 306 54. Glucose-Lowering therapies for Type 2 Diabetes . . . . . . . 306 55. Insulins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308 56. Quick-Relief Medications for Asthma . . . . . . . . . . . . . . . . 309 57. Long-Term Control Medications for Asthma . . . . . . . . . . 310 58. Management of Childhood Asthma . . . . . . . . . . . . . . . . . 312 59. Use of Metered Dose inhaler . . . . . . . . . . . . . . . . . . . . . . . 313 60. Anti Hypertensive Medications . . . . . . . . . . . . . . . . . . . . . 314 61. Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315 62. Drug therapy of Gout . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 316 63. Commercially Available Steroid Hormones . . . . . . . . . . . 317 64. Drugs Used in Psoriasis . . . . . . . . . . . . . . . . . . . . . . . . . . . 318 65. Side Effect Profile of Antiparkinson Drugs . . . . . . . . . . . . 319 66. Drugs or Drug Groups Under investigation for
Use in Angina. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320 67. Plasma Expanders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320 68. Anticoagulants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321 69. Advantage and Consequences of Those Advantages
with LMWH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322 70. Drugs Affecting Platlet Function and Mechanism
of Action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322 71. Drugs Used in Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . 322 72. Tamoxifen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324 73. Bisphosphonates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324 74. Classification of Adverse Drug Reactions . . . . . . . . . . . . . 326 75. Gell and Coombs Classification of Immunologic Drug
Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326 76. Drugs Associated With Edema formation . . . . . . . . . . . . . 327 77. Drug induced SLE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327 78. Drug-induced Respiratory Reactions . . . . . . . . . . . . . . . . . 327 79. Drugs and Endocrine Disease . . . . . . . . . . . . . . . . . . . . . . 328 80. Effects of Drugs on Thyroid Hormones . . . . . . . . . . . . . . 329 81. Drugs Causing Megaloblastic Anemia . . . . . . . . . . . . . . . 330 82. Ototoxic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 330
Appendix Microbiology
1. Scientists and Titles in Microbiology . . . . . . . . . . . . . . . . . 331 2. Microbial Staining . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331 3. Gram and Acid-Fast Staining Methods . . . . . . . . . . . . . . . 332 4. Ziehl-Neelsen Acid-Fast Stain. . . . . . . . . . . . . . . . . . . . . . . 332
Sample Pages
Contents xi
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
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
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 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
Sample Pages
Contentsxii
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) . . . . . . . . . 405
2. Genotypes & Phenotypes in ABO System . . . . . . . . . . . . . 406
3. Reactions of ABO Groups . . . . . . . . . . . . . . . . . . . . . . . . . . 406
4. Selection of Blood and Plasma by ABO Type . . . . . . . . . . 406
5. Blood Components and indications for Use . . . . . . . . . . . 406
6. Shelf Life of Blood Components . . . . . . . . . . . . . . . . . . . . 407
7. Blood Component Separation . . . . . . . . . . . . . . . . . . . . . . 408
8. Complications of Massive Blood Transfusion . . . . . . . . . . 409
9. Hematopoietic Stem Cells . . . . . . . . . . . . . . . . . . . . . . . . . 410
10. Cells of Peripheral Smear . . . . . . . . . . . . . . . . . . . . . . . . . 412
11. Pathologic Red Cells in Blood Smears . . . . . . . . . . . . . . . . 413
12. Erythrocyte and Reticulocyte inclusions . . . . . . . . . . . . . . 415
13. Urinary Crystals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415
14. Urinary Cast . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416
15. Cellular Responses to injury . . . . . . . . . . . . . . . . . . . . . . . . 418
16. Reversible Cell injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418
17. Properties of the Principal Free Radicals involved in Cell injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419
18. Fixatives Used in Pathology . . . . . . . . . . . . . . . . . . . . . . . . 420
19. Histology/Pathology/Microbiology Stains . . . . . . . . . . . . 421
20. Hypertrophy, Hyperplasia and Atrophy. . . . . . . . . . . . . . . 423
21. Metaplasia, Dysplasia and Neoplasia . . . . . . . . . . . . . . . . 423
22. Necrosis Vs Apoptosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424
23. Mechanism of Apoptosis . . . . . . . . . . . . . . . . . . . . . . . . . . 426
24. Proteins in BCL 2 Superfamily . . . . . . . . . . . . . . . . . . . . . . 428
25. Types of Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 428
26. Types of Calcification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 429
27. Classification and Diagnosis of Amyloidosis . . . . . . . . . . . 429
28. Acute inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431
29. Principal Mediators of inflammation . . . . . . . . . . . . . . . . 432
30. Chemokines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433
31. Connective Tissue/ Wound Repair . . . . . . . . . . . . . . . . . . 434
32. Growth Factors and Cytokines Affecting Various Steps in Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . 436
33. Activators of Angiogenesis . . . . . . . . . . . . . . . . . . . . . . . . . 436
34. Inhibitors of Angiogenesis . . . . . . . . . . . . . . . . . . . . . . . . . 436
35. Growth Factors and Cytokines involved in Regeneration and Wound Healing . . . . . . . . . . . . . . . . 437
36. Pedigree & inheritance . . . . . . . . . . . . . . . . . . . . . . . . . . . . 438
37. Inheritance Patterns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 439
38. Terms Used in Genetics & inheritance . . . . . . . . . . . . . . . 440
39. Examples of Different inheritance Patterns . . . . . . . . . . . 441
40. Some Commonly Identified Microdeletion and Microduplication Syndromes FISH Analysis . . . . . . . 442
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
47. Oncogenes and Proto-oncogene . . . . . . . . . . . . . . . . . . . . 449
48. Tumor Suppressor Genes . . . . . . . . . . . . . . . . . . . . . . . . . 450
49. DNA Repair & Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451
50. Techniques Commonly Used for Mutation Detection . . . 451
51. HLA Markers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452
52. Paraneoplastic Syndromes Associated With Common Cancers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453
53. Tumor Markers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 454
54. Immunohistochemical Markers (IHC) . . . . . . . . . . . . . . . . 455
55. Immunohistochemical Marker Profiles of Soft Tissue Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 458
56. Carcinogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 458
57. Oncogenic Viruses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459
58. Cluster Differentiation Markers of Lymphoid Cell Maturation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460
59. Cluster Differentiation Markers of Myeloid Cell Maturation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 461
60. Cluster Differentiation Markers of Different Cells . . . . . . 461
61. Cluster Differentiation Markers of B Cell Lymphomas . . 462
62. Cluster Differentiation Markers of T Cell Lymphomas . . 462
63. CD Markers Flow Chart of Lymphoma and Leukemias . . 463
64. Hodgkins Vs Non Hodgkins . . . . . . . . . . . . . . . . . . . . . . . . 464
65. Clinical Staging of Hodgkin and Non-Hodgkin Lymphomas (Ann Arbor Classification) . . . . . . . . . . . . . . . . . . . . . . . . . 464
66. Grades of NHL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464
67. Frequency of involvement of Nodal Sites in Hodgkin Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465
68. Subtypes of Hodgkin’s Lymphoma . . . . . . . . . . . . . . . . . . 465
69. Treatment of Hodgkin’s Lymphoma . . . . . . . . . . . . . . . . . 466
70. Major Subtypes of Aml in the WHO Classification . . . . . . 466
71. Types of Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467
72. Thyroid Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
73. Prognosis of Thyroid Carcinoma . . . . . . . . . . . . . . . . . . . . 471
74. Malignant Epithelial Lung Tumors . . . . . . . . . . . . . . . . . . . 471
75. Types of Collagen and Associated Diseases . . . . . . . . . . . 473
76. Constituents of Connective Tissues in Various Tissues . . 474
77. Diseases With Granulomatous inflammation . . . . . . . . . . 474
78. Classification and Characteristics of Selected Immune-Mediated Vasculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
79. Antineutrophil Cytoplasmic Antibodies . . . . . . . . . . . . . . 476
80. Frequency of Arteriographic Abnormalities and Potential Clinical Manifestations of Arterial involvement in Takayasu’s Arteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
81. Most Common in Arteritis and Aneurysm . . . . . . . . . . . . 477
82. Vascular Pathology of Hypertension . . . . . . . . . . . . . . . . . 477
Sample Pages
Contents xiii
83. Major Primary Glomerulonephritis . . . . . . . . . . . . . . . . . . 478
84. Causes of Nephritic Syndrome . . . . . . . . . . . . . . . . . . . . . 480
85. Types of Deposits in Different Types of GN . . . . . . . . . . . 481
86. Lupus Nephritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481
87. Genetic Causes of Non-Syndromal SRNS/FSGS . . . . . . . . 482
88. Summary of Renal Cystic Diseases . . . . . . . . . . . . . . . . . . 482
89. Types of Cirrhosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
90. Patterns of injury in Drug- and toxin-induced Hepatic injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483
91. Scheuer Classification for Grading and Staging of Chronic Hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484
92. Stages of Chronic Hepatitis B infection . . . . . . . . . . . . . . . 484
93. Antinuclear Antibody (ANA) Patterns and Clinical Associations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 484
94. Autoimmune Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . 485
95. Types of Grafts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 487
96. Graft-Versus-Host Disease (GVHD) . . . . . . . . . . . . . . . . . . 488
97. Clinical Grading of Acute GVHD . . . . . . . . . . . . . . . . . . . . . 489
98. Clinical Staging of Acute GVHD . . . . . . . . . . . . . . . . . . . . . 489
99. Bleeding and Clotting Disorders . . . . . . . . . . . . . . . . . . . . 489
100. Approach to A Patient With Bleeding Disorder . . . . . . . . 490
101. Different Tests of Bleeding/ Clotting Disorders . . . . . . . . 492
102. Reference Values of Common Tests of Hemostasis and Blood Coagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492
103. Causes of Hemoglobinuria . . . . . . . . . . . . . . . . . . . . . . . . . 493
104. Diseases With Granulomatous inflammation . . . . . . . . . . 493
105. The Prion Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
106. Neurodegenerative Diseases Associated With Aggregated Proteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 494
107. Inherited Diseases of the Red Cell Membrane-Cytoskeleton . . . . . . . . . . . . . . . . . . . . . . . . . . 494
108. Types of Hereditary Spherocytosis . . . . . . . . . . . . . . . . . . 495
109. Diseases With Predominantly intravascular Hemolysis . . 495
110. Types of Microcytic Anemia . . . . . . . . . . . . . . . . . . . . . . . . 496
111. Causes of Macrocytic Anemia . . . . . . . . . . . . . . . . . . . . . . 497
112. Approach to Anemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 498
113. Biochemical Tests for the Diagnosis and Differentiation of Cobalamin and Folate Deficiencies . . . . . . . . . . . . . . . . . . 499
114. Causes of Pure Red Cell Aplasia . . . . . . . . . . . . . . . . . . . . . 500
115. WHO Classification of Chronic Myeloproliferative Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500
116. Myocardial infarction Time of onset of Key Events in Ischemic Cardiac Myocytes . . . . . . . . . . . . . . . . . . . . . . . . 500
117. Evolution of Morphologic Changes in Myocardial infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501
118. Enzymes Elevated in Myocardial infarction . . . . . . . . . . . 501
119. Transudate Vs. Exudate . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
120. Conditions Associated With Abnormal Alkaline Phosphatase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
121. Few Important Bodies in Medical Science . . . . . . . . . . . . 503
122. Types of Rosettes in Histopathology . . . . . . . . . . . . . . . . . 505
123. Intestinal Polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505
Appendix Forensic Medicine
1. Important Definitions of FMT . . . . . . . . . . . . . . . . . . . . . . 509
2. Titles Related to FMT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
3. Various Declarations Adopted by WMA in Chronological Order . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
4. Types of Offence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
5. Inquest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
6. Summons or Subpoena . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
7. Cross Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 511
8. Indian Evidence Act (IEA) . . . . . . . . . . . . . . . . . . . . . . . . . 511
9. Criminal Procedure Code 1973 . . . . . . . . . . . . . . . . . . . . . 512
10. Indian Penal Code, 1860 (Act No. 45 of Year 1860) . . . . . 512
11. Prosessional Negligence Vs Misconduct . . . . . . . . . . . . . . 519
12. Types of Negligence (Malpraxis) . . . . . . . . . . . . . . . . . . . . 519
13. Defence/ Doctrine in Favour and Against A Doctor . . . . . 520
14. Professional Secrets and Previleged Communication . . . 520
15. Identification of Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
16. Identification of Race . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 523
17. Identification of Sex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 524
18. DNA Fingerprinting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 525
19. Tests Used for Detection of Blood . . . . . . . . . . . . . . . . . . . 526
20. Dactylography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527
21. Poroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
22. Autopsy Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
23. Signs of Death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
24. Post Mortem Caloricity . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
25. Post Mortem Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . 530
26. Adipocere Vs Mummification . . . . . . . . . . . . . . . . . . . . . . 531
27. Incised Wound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
28. Types of Abrasions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
29. Contusion/Bruise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
30. Laceration and Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
31. Difference Between incised, Lacerated and Stab Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 534
32. Antemortem Vs Postmortem injury . . . . . . . . . . . . . . . . . 535
33. Suicidal Vs Homicidal Wound . . . . . . . . . . . . . . . . . . . . . . 535
34. Types of Stab Wound on the Basis of Weapon Used . . . . 535
35. Types of Burn injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535
36. Corrosive injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 536
37. Pedestrian injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 536
38. injuries Sustained by Vehicle Occupants . . . . . . . . . . . . . 537
39. Types of Blast injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 538
40. Bullet Kinetics and injury . . . . . . . . . . . . . . . . . . . . . . . . . . 539
41. Ballistic Phenomenon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 540
42. Types of Bullets in forensic Medicine . . . . . . . . . . . . . . . . 541
43. Types of Gun Powder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542
44. Gun Shot Residue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 542
45. Classification of Firearms . . . . . . . . . . . . . . . . . . . . . . . . . . 543
46. Components of Gunshot and Its Effects . . . . . . . . . . . . . . 544
47. Bullet Wound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 544
48. Shotgun Firearm injuries . . . . . . . . . . . . . . . . . . . . . . . . . . 545
Sample Pages
Contentsxiv
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
Sample Pages
Appendix for PGMEE (Volume 1)8
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 distinguished1. 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 .
APPENDIX 8: DEVELOPMENT OF VAGINA
Ε Endoderm → primitive gut → cloaca → urogenital sinus and anorectal canal. Ε The sinovaginal bulb originates from urogenital sinus. Ε 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.
Ε The first and second portions of Mullerian duct forms the fimbriae and the fallopian tubes while distal segment forms the uterus and upper vagina.
Ε Distal most portion of sinovaginal bulb forms the Hymen.
Sample Pages
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 disappearsThe anastomotic network around the duodenum develops into a single vessel, the portal vein
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 sinusoidsLigamentum terescommunication between the left umbilical vein and the right hepatocardiac channel, the ductus venosus obliterates to form ligamentum venosum
Cardinal Veins
Common cardinal (Duct of Cuvier)
Right SVC
Left Oblique vein of left atrium& coronary sinus
Anterior cardinal Right SVC, internal jugular veins
Left Vanishes
Lt-Rt Anastomosis
Left brachiocephalic vein
Sample Pages
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 man becomes fused to another bone
Coracoid process of scapula, posterior tubercle of 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 located
Single nuclei, Centrally located Single nuclei, Centrally located
Banding Actin and myosin form distinctive bands
Actin and myosin form distinctive bands
Actin and myosin; No distinctive bands
Z-disks Present Present Absent, cytoplasmic dense bodies are present
T tubules T tubules at A-I junction; triads present
T tubules at Z disk; diads present No T tubules; no triads
Cellular junctions No junctional complexes Intercalated disks Gap junctions
Neuromuscular junctions
Present Not present; contraction is intrinsic Not present; contraction is intrinsic, neural, or hormonal
Ca+ binding Troponin Troponin Calmodulin
Regeneration Limited; satellite cells None High
Sample Pages
Appendix for PGMEE (Volume 1)54
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
Palatoglossal arch
Midline groove of tongue
Palatine tonsil
Foliate papillae
Fungiform papilla
Palatopharyngeal arch
Termial sulcus
Dorsum of tongue
Lingual tonsil
Circumvallate papilla
Filiform papilla
Root 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.
Tip 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 circumvallate papillae
They are large in size 1-2 mm in diameter and are 8-12 in number. They are situated immediately in front of the sulcus terminalis.
Fungiform papillae
The fungiform papillae are numerous near the tip and margins of the tongue, but some of them are also 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.
Sample Pages
Appendix for PGMEE (Volume 1)108
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 plasminogen inhibitor
It is a polypeptide produced by endothelial cells. It acts as a natural inhibitor of the extrinsic pathway by inhibiting TF-VIIa complex. Protein S enhances the interaction of factor Xa in the presence of calcium and phospholipids.
Protein C pathway The propagation phase of the coagulation is inhibited by the Protein C pathway that primarily consist of four key elements:
Ε 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)
Ε Thrombomodulin - A transmembrane receptor on the endothelial cells, it prevents the formation of the clot in the undamaged endothelium by binding to the thrombin
Ε Endothelial protein C receptor is another transmembrane receptor that helps in the activation of Protein C
Ε 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 dependent protease inhibitor/protein Z (PZI)
It is a recently described component of the anticoagulant system that is produced in the liver. It inhibits Factor Xa in reaction requiring PZ and calcium.
Sample Pages
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 SYSTEMThe 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 divisionsThe 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 visceral effectors.
Autonomic nervous system
Parasympathetic nervous system
Smpathetic nervous 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
Sample Pages
PHYSIOLOGY 133
APPENDIX 58: HYPOTHALAMIC NUCLEIRegion Area Nucleus Function
Anterior Medial Preoptic nucleus Thermoregulation/ Heat loss centre
Supraoptic nucleus (SO) Vasopressin (ADH) release
Paraventricular nucleus (PV) CRH release Oxytocin and to a lesser extent antidiuretic hormone
Anterior hypothalamic nucleus (AH)
Thermoregulation/ Heat loss centre (set point comparison) Heat loss if core temp > set point
Suprachiasmatic nucleus Circadian rhythms
Part of supraoptic nucleus (SO) Vasopressin release
Tuberal Medial Dorsomedial hypothalamic nucleus (DM)
Blood Pressure, Heart Rate, GI stimulation
Ventromedial nucleus (VM) satiety centre(controls eating)lesion causes voracious appetite
Arcuate nucleus (AR)/ Infundibular nucleus/ Periventricular nucleus
Endocrine function (releasing hormones)- controls Adenohypophysis
Lateral Lateral hypothalamic area Feeding centre (thirst and hunger)-lesion causes anorexia
Posterior Medial Mammillary nuclei (part of mammillary bodies) (MB)
Memory, Feeding reflex
Posterior nucleus (PN) 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 column
(Anterior white funiculus)
Anterior spinothalamic tract (With lateral spinothalamic tract, forms spinal lemnisus)
Axon of 1st order neuron dorsal root ganglia and terminate in medial part of dorsal horn (1st relay stn)
Axon Begins in Nucleus propriusTerminates on 3rd order neurons in Ventral Posterior Nucleus of thalamus (VPN)
3rd order neuron from posterior limb of internal capsule to post central gyrus (sensory)
Some fibres Ascend several segments before crossing overMostly crossed, some uncrossed
Crude touch sensation
Sample Pages
PHYSIOLOGY 173
APPENDIX 96: AUDITORY PATHWAYFigure 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-MA1. Eighth nerve2. Cochlear nucleus3. Superior olivary complex4. Lateral lemniscus5. Inferior colliculus6. Medial geniculate body7. Auditory Cortex (Brodmann’s area 41)
APPENDIX 97: OLFACTIONOlfactory Mucous Membrane
The olfactory receptor cells are located in a specialized portion of the nasal mucosa, the yellowish pigmented olfactory mucous membrane. The olfactory membrane lies in the superior part of each nostril. 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)
Sample Pages
Appendix for PGMEE (Volume 1)188
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.”
Ε A low PO2 in peripheral tissues promotes the synthesis in erythrocytes of 2,3-bisphosphoglycerate (BPG) from the glycolytic intermediate 1,3-bisphosphoglycerate.
Ε The hemoglobin tetramer binds one molecule of BPG in the central cavity formed by its four subunits. Ε 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.
Ε BPG forms salt bridges with the terminal amino groups of both chains via Val NA1 and with Lys EF6 and His H21. Ε BPG therefore stabilizes deoxygenated (T state) hemoglobin by forming additional salt bridges that must be broken prior to conversion to the R state.
Ε 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.
Ε Deoxyhemoglobin binds one proton for every two O2 molecules released, contributing significantly to the buffering capacity of blood.
Ε The somewhat lower pH of peripheral tissues, aided by carbamation, stabilizes the T state and thus enhances the delivery of O2.
“Heme iron forms a covalent bond with the imidazole nitrogen of the “proximal” histidine at F8.” Ε 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.
Ε The mechanism for this property can be explained in part by the interactions in the heme pocket. Ε 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)
Sample Pages
Appendix for PGMEE (Volume 1)190
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
Ε 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.
Ε 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.
Ε As a consequence, one pair of alpha/beta subunits rotates 15 degrees with respect to the other, compacting the tetramer. Ε 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.
Ε These changes significantly increase the affinity of the remaining unoxygenated hemes for O2, as subsequent binding events require the rupture of fewer salt bridges.
Ε The terms T and R also are used to refer to the low-affinity and high-affinity conformations of allosteric enzymes, respectively.
Ε The overall conformational changes to hemoglobin appear to be the greatest after three molecules of O 2 have been added. Ε 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
Right shift ( - CADET turns to Right), Decrease affinity, increase P50,
Left shift, increase affinity, Decrease P50
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- Exercise5. T- Increase in body temperature
1. Decrease CO2
2. Alkalosis (High pH)3. Decreased 2,3 DGP4. Decreased body temperature5. High Fetal hemoglobin6. Carboxyhemoglobin7. Methemoglobinemia
Sample Pages
BIOCHEMISTRY 191
APPENDIX 13: STEPS OF HEME/PORPHYRIN RING SYNTHESIS
Enzyme Location Substrate Product Porphyria Clinical Lab test
ALA synthase (Rate limiting)
Mitochon-drion
Glycine, succi-nyl CoA
D-Amino-levulinic acid
X linked Sidero-blastic anemia
Anemia ↓RBC count, ↓Hb
ALA dehydratase (Zinc containing, Sensitive to lead poisoning)
Cytosol D-Amino-levulinic acid
Porphobilino-gen
ALA-Dehydratase deficiency
Abdominal pain, neuropsychiatric symptoms
↑Urinary ALA and copropor-phyrin III
PBG deaminase/ HMB synthase/ Uroporphy-rinogen I synthase
Cytosol Porphobilino-gen
Hydroxymethyl bilane
Acute intermit-tent porphyria
Abdominal pain, neuropsychiatric symptoms
↑Urinary ALA and PBG
Uroporphyrinogen III synthase
Cytosol Hydroxymeth-ylbilane
Uroporphy-rinogen III
Congenital erythropoietic porphyria
No photosensi-tivity
↑Urinary, fecal & RBC uropor-phyrin I
Uroporphyrinogen III decarboxylase
Cytosol Uroporphyrin-ogen III
Coproporphy-rinogen III
Porphyria cuta-nea tarda
Photosensitivity ↑Urinary uro-porphyrin I
Coproporphyrinogen III oxidase
Mitochon-drion
Coproporphy-rinogen III
Protoporphy-rinogen IX
Coproporphyria Photosensitivity, abdominal pain, neuropsychiatric symptoms
↑Urinary ALA, PBG, & copro-porphyrin III & fecal copropor-phyrin III
Protoporphyrinogen oxidase
Mitochon-drion
Protoporphy-rinogen IX
Protoporphy-rin IX
Variegate por-phyria
Photosensitivity, abdominal pain, neuropsychiatric symptoms
↑Urinary ALA, PBG, & copro-porphyrin III & fecal protopor-phyrin IX
Ferrochelatase (Sen-sitive to Lead poison-ing)
Mitochon-drion
Protoporphy-rin IX
Heme Erythropoietic protoporphyria
Photosensitivity ↑Fecal & RBC protoporphyrin IX
Sample Pages
BIOCHEMISTRY 197
APPENDIX 18: METABOLIC PATHWAYS
Anabolic pathways Are those involved in the synthesis of larger and more complex compounds from smaller precursors—Anabolic pathways are endothermic. Anabolic reactions require an input of energy, generally in the form of the phosphoryl group transfer potential of ATP and the reducing power of NADH, NADPH, and FADH2
Synthesis of protein from amino acids and the synthesis of reserves of triacylglycerol and glycogen.
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 between the anabolic and catabolic pathwaysIn aerobic organisms, the citric acid cycle is an amphibolic pathway, one that serves in both catabolic and anabolic processes.
eg, the citric acid (TCA) cycle.
Sample Pages
Appendix for PGMEE (Volume 1)258
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)
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
Sample Pages
Appendix for PGMEE (Volume 1)298
APPENDIX 45: CALCINEURIN INHIBITORS
Mechanism of action
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.
Classification Systemic Topical
Cyclosporine Tacrolimus
TacrolimusPimecrolimus
Cyclosporine Ε Produced by the fungus species Beauveria nivea Ε 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 :
Ε 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.
Ε Clinical indications for cyclosporine are kidney, liver, heart, and other organ transplantation; rheumatoid arthritis.
Side effects Ε The principal adverse reactions to cyclosporine therapy are renal dysfunction, tremor, hirsutism, hypertension, hyperlipidemia, and gum hyperplasia
Ε Hyperuricemia may lead to worsening of gout, increased P-glycoprotein activity, and hypercholesterolemia. Ε Nephrotoxicity occurs in the majority of patients treated and is the major indication for cessation or modification of therapy.
Sample Pages
Appendix for PGMEE (Volume 1)300
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 (VEGF)
Metastatic colorectal cancer, nonsmall cell lung cancer, metastatic breast bancer
Cetuximab chimeric Epidermal growth factor receptor (EGFR)
Colorectal cancer, Head and neck cancer
Certolizumab pegol
humanized Inhibition of TNF-α signalling Crohn’s disease, rheumatoid arthritis
Daclizumab humanized IL-2Rα receptor (CD25) Transplant rejection
Dasatinib Targeted bcr-abl, src family, c-kit, EPHA2, PDGFR-β
CML, Ph+ ALL
Erlotinib Targeted EGFR Non–small cell lung cancer
Eculizumab humanized Complement system protein C5 Paroxysmal nocturnal hemoglobinuria
Efalizumab humanized CD11a Psoriasis
Gemtuzumab humanized CD33 Acute myelogenous leukaemia (with calicheamicin)
Golimumab humanized TNFα Rheumatoid & psoriatic arthritis, active ankylosing spondylitis
Imatinib Targeted c-kit, bcr-abl, PDGFR CML, GIST
Ibritumomab tiuxetan
Murine CD20 Non-Hodgkin lymphoma (with yttrium-90 or indium-111)
Infliximab chimeric Inhibition of TNF-α signalling Several autoimmune disorders like Crohn’s disease
Lapatinib Targeted EGFR and HER2 Breast cancer
Muromonab-CD3
Murine T cell CD3 Receptor Transplant rejection
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 A (VEGF-A)
Macular degeneration
Rituximab chimeric CD20 Non-Hodgkin lymphoma
Sunitinib Targeted second-generation receptor tyrosine kinase inhibitors
RCC, Imatinib resistant GIST, Progressive GIST, progressive 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 (Herceptin)
humanized ErbB2/HER2 Breast cancer
Sample Pages
Appendix for PGMEE (Volume 1)308
Footnote: Anti diabetic Drugs to be given in subcutaneous route:
Ε Insulin
Ε GLP-1 analogue: Exenadide, Liraglutide
Ε Amylin analogue: Pramlintide
Used both in Type 1 & Type 2 diabetes Ε Insulin
Ε Amylin analogue: Pramlintide
Ε α–Glucosidase inhibitors: Acarbose
APPENDIX 55: INSULINS
Highly purified mono-component insulin
Porcine Actrapid- Regular Short acting
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 Insulin aspart Insulin glulisine
Ultra short acting
Insulin glargine Long acting
70% large particle, insoluble, long
acting crystalline (Ultralente)
30% small particle, short acting, amorphous, (Semi-
lente)
Intermediate acting Lente insulin
Sample Pages
MICROBIOLOGY 349
APPENDIX 27: PHASES OF THE MICROBIAL GROWTH CURVEThe 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 Rate
Comments
Lag Zero Ε 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.
Ε Enzymes and intermediates are formed and accumulate until they are present in concentrations that permit growth to resume.
Ε If the cells are taken from an entirely different medium, it often happens that they are 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 Ε The cells are in a steady state. Ε 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.
Ε 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.
Ε For aerobic organisms, the nutrient that becomes limiting is usually oxygen. Ε 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 stationary
Zero Ε Eventually, the exhaustion of nutrients or the accumulation of toxic products causes growth to cease completely.
Ε In most cases, however, cell turnover takes place in the stationary phase. Ε 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 (death)
Ε After a period of time in the stationary phase, which varies with the organism and with the culture conditions, the death rate increases until it reaches a steady level.
Ε In most cases the rate of cell death is much slower than that of exponential growth. Ε 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.
Ε 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
Sample Pages
MICROBIOLOGY 357
APPENDIX 42: EXOTOXIN VS ENDOTOXINExotoxin Endotoxin
Secreted by
-Secreted by bacteria.-Are present in gram-positive & some gram negative bacteria (ie. Shiga’s dysentery, Bacillus, ETEC, Vibrio, Pertussis & Pseudomonas)
-Endotoxin is a component of the cell wall-Are present only in gram-negative bacteria
Chemistry Polypeptide LipopolysaccharideLocation of genes Plasmid or bacteriophage Bacterial chromosomeToxicity High Low Clinical effects Various effects Fever, shockMode of action Various modes Includes TNF and interleukin-1Antigenicity Induces high-titer antibodies called antitoxins Poorly antigenicVaccines Toxoids used as vaccines No toxoids formed and no vaccine availableHeat stability Destroyed rapidly at 60°C (except staphylococcal enterotoxin) Stable at 100°C for 1 hourTypical diseases Tetanus, botulism, diphtheria Meningococcemia, sepsis by gram-negative
rods
APPENDIX 43: CHARACTERISTIC OF DIFFERENT TOXINSToxins Mechanism of Action
Strychnine Ε Post-synaptic inhibition of Neurotransmitter Glycine in Spinal cord. Ε Acts on Antr.horn cell of spinal cord & inhibit post synaptic potential leading to release excitation.
Botulinum Ε During the growth of C botulinum and during autolysis of the bacteria, toxin is liberated into the environment.
Ε Seven antigenic varieties of toxin (A to G) are known. Ε 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.
Ε 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.
Ε 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.
Ε 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.
Ε 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 Ε Tetanospasmin toxin inhibit presynaptic release of Neurotransmitter Glycin & GABA in CNS. Ε Toxins acts on Moter end plate, Spinal cord, Brain & Sympathetic nervous system.
Sample Pages
Appendix for PGMEE (Volume 1)376
APPENDIX 77: PRIONS Ε 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.
Ε Prions may have incubation periods of years before clinical manifestations of the infections become evident Ε 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.
Ε 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.
Ε 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.
Ε 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 VirusesFeature Prions Conventional Viruses
Particle contains nucleic acid No YesParticle contains protein Yes, encoded by cellular genes Yes, encoded by viral genesInactivated rapidly by UV light or heat No YesAppearance in electron microscope Filamentous rods (amyloid-like) Icosahedral or helical symmetryInfection induces antibody No YesInfection induces inflammation No Yes
APPENDIX 78: VIRAL INCLUSION BODIESIntra cytoplasmic Acidophilic Negri bodies Rabies
Guarnieri bodies Variola (small pox), vacciniaBollinger bodies FowlpoxHenderson Peterson bodies Molluscum contagiosumPaschen Small pox
Basophilic Halber staedtler prowazek (HD Body)
Chlamydia trachomatis
Levinthal cole lillie (LCL body) Chlamydia psittaci Intra nuclear Acidophilic Cowdry type A Herpes, chicken pox, yellow fever
Torres bodies Yellow feverCowdry type B Polio virus
Basophilic Cowdry type B AdenovirusCowdry 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
Sample Pages
MICROBIOLOGY 379
HHV-2/ HSV-2 Sacral ganglia Mostly below waist lesions Ε Genital herpes Ε Aseptic meningitis Ε Neonatal infections
HHV-3/ Varicella Zoster Virus Sensory ganglia Chicken pox, ZosterHHV-4 / Ebstein Barr Virus Lymphoid tissue Infectious Mononucleosis, Burkitt’s lymphomaHHV-5/ Cyto Megalo Virus Salivary glands,
KidneyPetechiae, Hepatosplenomegaly & jaundice (m.c), CMV 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 virus
Lymphoid tissue Roseola infantum/ 6th disease/ Exanthema subitum, Focal Encephalitis
HHV-7/ R K virus Lymphoid tissueHHV- 8 Lymphoid tissue Kaposi’s sarcoma
APPENDIX 82: CLINICAL AND EPIDEMIOLOGIC FEATURES OF VIRAL HEPATITISFeature HAV HBV HCV HDV HEV
Family Picornaviridae Hepadnaviridae Flaviviridae Unclassified UnclassifiedGenus Hepatovirus Orthohepadnavirus Hepacivirus Deltavirus Hepevirus Virion 27 nm,
icosahedral42 nm, spherical 60 nm, spherical 35 nm, spherical 30–32 nm,
icosahedralEnvelope No Yes (HBsAg) Yes Yes (HBsAg) No Genome ssRNA dsDNA ssRNA ssRNA ssRNAStability Heat & acid
stableAcid-sensitive Ether-sensitive,
acid-sensitiveAcid-sensitive Heat-stable
Prevalence High High Moderate Low, regional RegionalIncubation (days) 15–45, mean 30 30–180, mean 60–90 15–160, mean 50 30–180, mean 60–90 14–60, mean 40Onset Acute Insidious or acute Insidious Insidious or acute AcuteAge preference Children, young
adults Young adults (sexual and percutaneous), babies, toddlers
Any age, but more common in adults
Any age (similar to HBV)
Young adults (20–40 years)
TransmissionFecal-oral +++ – – – +++Percutaneous Unusual +++ (MC mode of
transmission)+++ +++ –
Perinatal – +++ ± + –Sexual ± ++ ± ++ –ClinicalSeverity Mild Occasionally severe Moderate Occasionally severe MildFulminant 0.1% 0.1–1% (most common,
>50% of all cases of viral fulminant hepatitis)
0.1% 5–20% (highest chances of progression to fulminant hepatitis)
1–2%
Progression to chronicity
None (HAV remains self limited & does not progress to chronic liver disease.
Occasional (1–10%) (90% of neonates)
Common (>50% to upto 85%)
Common (<5% coinfection, 80% upon super infection)
None
Sample Pages
MICROBIOLOGY 385
APPENDIX 90: ANTIVIRAL CHEMOTHERAPY AND CHEMOPROPHYLAXISInfection Drug Route Dosage Comment
Influenza A and B: Treatment
Oseltamivir Oral Adults: 75 mg bid x 5 d Children 1–12 years: 30–75 mg bid, depending on weight,a x 5 d
Oseltamivir’s side effects of nausea and vomiting can be reduced in frequency by drug administration with food. Zanamivir may exacerbate bronchospasm in patients with asthma. Amantadine and rimantadine are not recommended for routine use unless antiviral susceptibilities are known because of widespread resistance in A/H3N2 viruses since 2005–2006 and in pandemic A/H1N1 viruses in 2009–2010.
Zanamivir Inhaled orally
Adults and children >7 years: 10 mg bid x 5 d
Amantadine
Oral Adults: 100 mg qd or bid x 5–7 d Children 1–9 years: 5 mg/kg per day (max, 150 mg/d) x 5–7 d
Rimantadine
Oral 100 mg qd or bid x 5–7 d in adults
Influenza A and B: Prophylaxis
Oseltamivir Oral Adults: 75 mg/d Children >1 year: 30–75 mg/d, depending on weight
Prophylaxis must be continued for the duration of exposure and can be administered simultaneously with inactivated vaccine. Unless the sensitivity of isolates is known, neither amantadine nor rimantadine is currently recommended for prophylaxis or therapy.
Zanamivir Inhaled orally
Adults and children >5 years: 10 mg/d
Amantadine or rimantadine
Oral Adults: 200 mg/d Children 1–9 years: 5 mg/kg per day (maximum, 150 mg/d)
RSV infection Ribavirin Small-particle aerosol
Administered 12–18 h/d from reservoir containing 20 mg/mL x 3–6 d
Use of ribavirin is to be “considered” for treatment of infants and young children hospitalized with RSV pneumonia and bronchiolitis, according to the American Academy of Pediatrics.
CMV disease Ganciclovir IV 5 mg/kg bid x 14–21 d; then 5 mg/kg per day as maintenance dose
Ganciclovir, valganciclovir, foscarnet, and cidofovir are approved for treatment of CMV 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 mg/d as maintenance dose
Valganciclovir has largely supplanted oral ganciclovir and is frequently used in place of IV ganciclovir.
Foscarnet IV 60 mg/kg q8h x 14–21 d; then 90–120 mg/kg per day as maintenance dose
Foscarnet is not myelosuppressive and is active against acyclovir- and ganciclovir-resistant herpesviruses.
Cidofovir IV 5 mg/kg once weekly x 2 weeks, then once every other week; given with probenecid and hydration
Fomivirsen Intravitreal
330 mg on days 1 and 15 followed by 330 mg monthly as maintenance
Fomivirsen has reduced the rate of progression of CMV retinitis in patients in whom other regimens have failed or have not been well tolerated. The major form of toxicity is ocular inflammation.
Varicella: Immuno competent host
Acyclovir Oral 20 mg/kg (maximum, 800 mg) 4 or 5 times daily x 5 d
Treatment confers modest clinical benefit when administered within 24 h of rash onset.
Valacyclovir Oral Children 2–18 years:20 mg/kg tid, not to exceed1 g tid, x5 d
Sample Pages
PATHOLOGY 413
APPENDIX 11: PATHOLOGIC RED CELLS IN BLOOD SMEARSRed Cell Type Description Underlying Change Disease State Associations
Acanthocyte (spur cell)
Irregularly spiculated red cells with projections of varying length and dense center
Altered cell membrane lipids
Abetalipoproteinemia, parenchymal liver disease, postsplenectomy
Basophilic stippling
Punctuate basophilic inclusions
Precipitated ribosomes (RNA)
Coarse stippling: Lead intoxication, thalassemia Fine stippling: A variety of anemias
Bite cell (degmacyte)
Smooth semicircle taken from one edge
Heinz body pitting by spleen
Glucose-6-phosphate dehydrogenase deficiency, drug-induced oxidant hemolysis
Burr cell (echinocyte) or crenated red cell
Red cells with short, evenly spaced spicules and preserved central pallor
May be associated with altered membrane lipids
Usually artifactual; seen in uremia, bleeding ulcers, gastric carcinoma
Cabot rings
Circular, blue, threadlike inclusion with dots
Nuclear remnant Postsplenectomy, hemolytic anemia, megaloblastic anemia
Ovalocyte (elliptocyte)
Elliptically shaped cell
Abnormal cytoskeletal proteins
Hereditary elliptocytosis
Howell-Jolly bodies
Small, discrete, basophilic, dense inclusions; usually single
Nuclear remnant (DNA) Postsplenectomy, hemolytic anemia, megaloblastic anemia
Hypochromic red cell
Prominent central pallor Diminished hemoglobin synthesis
Iron deficiency anemia, thalassemia, sideroblastic anemia
Macrocyte Red cells larger than normal (>8.5 μm), well filled with hemoglobin
Young red cells, abnormal red cell maturation
Increased erythropoiesis; oval macrocytes in megaloblastic anemia; round macrocytes in liver disease
Microcyte Red cells smaller than normal (<7.0 μm)
— Hypochromic red cell
Sample Pages
PATHOLOGY 447
APPENDIX 45: CELL CYCLE
Sample Pages
Appendix for PGMEE (Volume 1)460
Hepadna virusHepatitis B virus (HBV)
Hepatitis B (infectious hepatitis)
Liver cancer
Adenoviridae Acute respiratory disease; Common cold
Adenocarcinomas (cancer of glandular epithelial tissues)
Poxviridae Smallpox; cowpox Miscellaneous
Oncogenic RNA Viruses of The Family Retroviridae
Virus Cancer
Human T-cell leukemia virus (HTLV-1; HTLV-2)
Adult T-cell leukemia, Lymphoma
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 MATURATIONIMMUOPHENOTYPING: LYMPHOID
CELL MATURATION
Sample Pages
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
Sample Pages
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 DISEASESAutoantigen 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
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
Sample Pages
Appendix for PGMEE (Volume 1)512
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)
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 ISection 1-5
Introduction
Chapter IISECTION 6-52
General Explanations
Sample Pages
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) (Pisiform- last bone in the wrist- 12-17)
18-19 (Lower end of radius-16-17, lower end 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.
Identification of age by Sternum
Appearance Fusion
Manubrium 5-6 months intra uterine 60 years with body
Sample Pages
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 tests
Thin layer chromatography
Electrophoresis
Species specific tests
Immunological tests (Precipitin test, Heamagglutination inhibition test, Latex test)Enzymological tests (LDH Electrophoresis)
To differentiate human blood with animal blood
Blood group detection tests
Immunological tests: Absorption-Elution test (a.k.a Acid dilution test, Acid elution test) Mixed agglutination test Absorption inhibition test Enzymological tests: Vertical disc, vertical or horizontal slab, isoelectric focusing, cellulose acetate membrane
Absolute diagnosis of blood group is not possible. Can detect blood groups in old and dry stains
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. 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 mobiles2. Capacitive or CMOS readers use capacitors and thus electrical current to form an image of the fingerprint3. Ultrasound fingerprint readers costly 4. ThermalNote:The little fingers are never recorded because they are not particularly well suited for fingerprint comparisonMost 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
ΕΕ Fingerprints are formed during Intrauterine life. ΕΕ Fingerprints are 100% accurate method of identification ΕΕ 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 ΕΕ No two person can have same Finger prints, not even identical twins ΕΕ Chances of two person having identical fingerprints is 1 in 64000 millions ΕΕ Faint and invisible finger prints (Latent Fingerprints)can be made visible by special techniques like Aluminium hydroxide. ΕΕ Finger prints can be taken from dead bodies and even putrified bodies. ΕΕ The first Fingerprint Bureau in world was established at Kolkata on 12th June 1897 at Writer’s building.
Sample Pages
FORENSIC MEDICINE 545
Skull bone Beveled inner table Beveled outer table
Singeing, Blackening, Burning, Tattooing, Grease/dirt collar
Present Absent
APPENDIX 48: SHOTGUN FIREARM INJURIES
Contact/ Point Blank range
Close range Short range Intermediate range Long/ Distant shot
Distance Contact Upto 1 meter 1-2 meters 2-4 meters > 4 meters
Size Large lacerated with cavitation due to gases.
Bullet size entry wound Single circular aperture 4-5 cm in diameter.
Central hole with small peripheral Satellite holes
Central hole absent . Small individual
Shape Shotgun entry wound is round, elliptical, cruciate, triangular, and single upto 30 cm. Edges are normally inverted (may be everted due to bone underneath or gases coming out)
Between 30 cm to 1 m, the rim of the wound is irregular and often called a ‘Rat-hole’ in the USA because of the nibbled edges, the same appearance is called ‘scalloping’ in the UK. There may be annular abrasion and bruising/”rat nibbling”
Irregular margins of central entry wound without any satellite wounds
Irregular margins of a central entry wound with few satellite independent entry wounds are seen from 2 mtr and above
all pellets show independent entry wound from 4 meters onwards.
Abrasion ring/ Grease collar
Present Present Absent Absent Absent
Burning & Singeing of hair
Present Present Absent Absent Absent
Soot Blackening / Smudging
Present Present Present Absent Absent
Sample Pages
