GENERAL

PATHOLOGY
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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

CONTENTS
GENERAL FEATURES OF PATHOLOGY ........................................................................................................................... 4
FEATURES OF CELL INJURY ........................................................................................................................................ 4
HYPOXIA .................................................................................................................................................................... 4
AGEING ..................................................................................................................................................................... 4
NECROSIS .................................................................................................................................................................. 5
GENERAL FEATURES OF APOPTOSIS ......................................................................................................................... 5
APOPTOTIC AND ANTI APOPTOTIC PROTEIN ............................................................................................................ 6
CALCIFICATION .......................................................................................................................................................... 6
ATROPHY AND HYPERTROPHY .................................................................................................................................. 7
HYPERPLASIA AND METAPLASIA ............................................................................................................................... 7
STEM CELLS ............................................................................................................................................................... 7
FIXATIVES AND STAINS .............................................................................................................................................. 8
PIGMENT ................................................................................................................................................................... 9
BACTERICIDAL SYSTEM ............................................................................................................................................. 9
HYDROGEN PEROXIDASE .......................................................................................................................................... 9
OXIDATIVE STRESS .................................................................................................................................................... 9
FREE RADICAL............................................................................................................................................................ 9
NADPH OXIDASE ..................................................................................................................................................... 10
BASEMENT MEMBRANE.......................................................................................................................................... 10
INFLAMMATION .......................................................................................................................................................... 10
INFLAMMATORY MEDIATORS ................................................................................................................................. 10
HYDROSTATIC AND OSMOTIC PRESSURE ................................................................................................................ 13
GENERAL FEATURES OF INFLAMMATION ............................................................................................................... 13
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME ............................................................................................... 14
AUTOANTIGEN AND ASSOCIATED DISEASES ........................................................................................................... 14
ACUTE INFLAMMATION .......................................................................................................................................... 14
CHRONIC INFLAMMATION ...................................................................................................................................... 15
CHRONIC GRANULOMATOUS DISEASE ................................................................................................................... 15
GRANULOMA .......................................................................................................................................................... 15
COMPLEMENT SYSTEM ........................................................................................................................................... 16
OPSONIZATION ....................................................................................................................................................... 17
PHAGOCYTOSIS ....................................................................................................................................................... 17

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

CHEDIAK HIGASHI SYNDROME ................................................................................................................................ 17

CHEMOTAXIS ........................................................................................................................................................... 17
NEOPLASIA .................................................................................................................................................................. 18
CELL CYCLE .............................................................................................................................................................. 18
CAUSES OF NEOPLASIA ........................................................................................................................................... 18
FEATURES OF NEOPLASIA ....................................................................................................................................... 19
PROTOONCOGENES AND TUMOR SUPPRESSOR GENES ......................................................................................... 20
MANAGEMENT OF NEOPLASIA ............................................................................................................................... 21
GENERAL FEATURES OF TUMOR MARKERS ............................................................................................................ 22
CA-125 ..................................................................................................................................................................... 22
CEA .......................................................................................................................................................................... 22
AFP .......................................................................................................................................................................... 23
FEATURES OF TUMORS ........................................................................................................................................... 24

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

KEY TO THIS DOCUMENT

Text in normal font Must read point.
Asked in any previous medical entrance
examinations
Text in bold font Point from Harrisons
text book of internal medicine 18th
edition
Text in italic font Can be read if
you are thorough with above two

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

GENERAL FEATURES OF PATHOLOGY

FEATURES OF CELL INJURY
MC cause of Cell injury
Feature of reversible cell injury
Earliest tissue change following cell injury
Micropuncture of cell membrane with a needle. Repair
occurs by
Reperfusion injury is caused by
Reperfusion injury is associated with
elevation of
NOT a natural response to injury
Earliest change in reversible cell injury
Electron microscopic finding of reversible cell injury
Reversible cell injury

Irreversible cell injury is seen in

Irreversible cell injury is associated with
Most pathognomic sign of irreversible cell injury
Oncocytes are modified form of
Hemorrhagic infarct
Red infarct
Hemorrhagic infarction is seen in
White infarcts are NOT seen in

Hypoxia
Myelin figures
Neutrophilia
Linear movement of proteins
Superoxide ion
Creatine kinase
Anabolism
Hydropic change
Flocculent densities in mitochondria
Diminished generation of ATP, formation of blebs in
plasma membrane, detachment of ribosomes from
granular endoplasmic reticulum
Apoptosis
Accumulation of calcium in mitochondria
Amorphous densities in mitochondria
Mitochondria
Lung
Ovary, lung, small bowel
Venous thrombosis, Thrombosis, Embolism
Lung, Liver

HYPOXIA
Earliest indication of Hypoxia
First cellular change in hypoxia

Change in heart rate

Decreased oxidative phosphorylation in mitochondria

AGEING
Earliest change of ageing in cartilage
Cell aging is associated with
Theory behind ageing process
Ageing is due to
Elderly occurrence of cancer is due to
Hormone increases as ageing occurs
Liver spot is associated with
Replicative senescence is also known as
Progeria is due to mutation in
Werner syndrome

inability to regenerate articular cartilage

Decreased number of mitochondria, glycosylation of
DNA, glycosylation of RNA, shortened telomere
Free radical theory
Free radical injury
Increased telomerase activity
Cortisol
Ageing
Hay flick limit
Lamin A
Progeria of adult

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY
Hutchinson Gilford syndrome
Barthel index for
NOT associated with increased ageing
NOT compatible with ageing

Progeria of children
Assessment of ageing
Increased superoxide dismutase
Decreased cross linkage

NECROSIS
NOT a morphologic feature of necrosis
NOT a feature of necrosis
Type of Necrosis in hypoxic brain
Liquefactive Necrosis
Pyogenic infection and brain infarction are associated
with
MC Type of Necrosis
Coagulative necrosis is seen in
Coagulative Necrosis NOT seen in
Casseous necrosis
Casseous necrosis NOT seen in
Fat necrosis
Fibrinoid necrosis may be observed in
Fibrinoid necrosis

Fibrinoid necrosis is NOT seen in

Necrotic keratinocytes
Calcification in necrotic tissue
Chemotherapeutic drug can cause

Hyperchromasia
Cell shrinkage
Liquefactive necrosis
Brain
Liquefactive necrosis
Coagulative Necrosis
Myocardial infarction, thermal injury, tuberculosis
Brain
Tuberculosis , histoplasmosis
Leprosy, CMV, Wegener granulomatosis
Breast, Omentum, Retroperitoneal fat
Malignant hypertension, polyarteritis nodosa, Aschoff
nodule
Henoch Schonlein purpura, immune
vasculitis, preeclampsia, hyperacute
transplant rejection
Diabetic glomerulosclerosis
Graft versus host reaction, erythema multiforme, lichen
planus
Dystrophic calcification
Both necrosis and apoptosis

GENERAL FEATURES OF APOPTOSIS

Apoptosis is defined as
Apoptosis in isolated cell
Examples of apoptosis
Programmed cell death
Toll like receptors recognize bacterial products and
stimulates immune response by
Apoptotic bodies
Organelle involved in apoptosis
Cell death is due to
Apoptosis can occur by changes in
hormone levels in ovarian cycle. When
there is no fertilization of the ovum, the
endometrial cells die because
Capsase involved in extrinsic pathway

Programmed cell death

Death
Menstrual cycle, Tumor necrosis, GVHD, Pathological
atrophy
Apoptosis
FADD ligand apoptosis
Cell membrane found within organelles
Mitochondria
Deposition of extracellular amyloid
Involution of corpus luteum causes
estradiol and progesterone levels to fall
dramatically
Capsase 10

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY
NOT a feature of apoptosis
NOT a feature of apoptosis
NOT true about apoptosis
NOT true about apoptosis
Internucleosomal cleavage of DNA
Features of apoptosis
Light microscopic feature of apoptosis
Apoptosis initiation
Councilman bodies associated with
Ladder pattern of DNA electrophoresis in apoptosis is
caused by action of
In situ DNA nick end labeling can quantitate
Characteristic feature of apoptosis on light microscopy

Increase in cell size

Cellular swelling
Inflammation
Passive process
Apoptosis
Cytoplasmic blebs, Nuclear fragmentation
Intact membrane
Death receptors induce apoptosis when it is engaged by
fas ligand system
Apoptosis
Endonuclease
Fraction of cells in apoptotic pathway
Nuclear compaction

APOPTOTIC AND ANTI APOPTOTIC PROTEIN

CD 95 major role in
Capsases are involved in
Most important Executionary Capsase
Capsases associated with
Increased p53 levels induce
Cytosolic cytochrome c plays an important role in
Leads to apoptosis
Annexin V is a marker of
Apaf is activated by
Which inhibits apoptosis in Memory B cells
Memory cell in immune system are long lived and
escape apoptosis because
Anti apoptotic protein
Gene inhibiting apoptosis

Extrinsic apoptosis
Apoptosis
Capsase 3
Organogenesis/embryogenesis
Apoptosis
Apoptosis
Glucocorticoid
Apoptosis
Cytochrome c
Nerve growth factor
Nerve growth factor
Bcl 2, Bcl x
Bcl2

CALCIFICATION
Calcification begins in Mitochondria in all organs
EXCEPT KIDNEY
Calcification of soft tissues without disturbance of
calcium metabolism
Dystrophic calcification
Dystrophic calcification is seen in
Psammoma bodies
MC Site of Metastatic Calcification
Metastatic calcification
Metastatic calcification occur when calcium is in
Metastatic calcification starts in
Metastatic calcification is commonly seen in
Metastatic calcification

Basement Membrane
Dystrophic calcification
Calcification in dead tissue
Atheromatous plaque
Dystrophic calcification, Papillary Ca Thyroid, Serous
Cystadenocarcinoma Ovary, Meningioma
Lung
Kidney
Alkaline pH
Mitochondria
Renal tubules
Mitochondria involves earliest

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY
Common sites of metastatic calcification
NOT a common site of metastatic calcification
NOT a site of metastatic calcification
Heterotopic calcification

Lung, kidney, gastric mucosa

Parathyroid
Pancreas
Ankylosing spondylitis, Forrestiers disease (diffuse
idiopathic skeletal hyperostosis)

ATROPHY AND HYPERTROPHY

Histological feature of disuse atrophy
Increase in size of cells
Example for hypertrophy
Both hyperplasia and hypertrophy found in

Type II fibres are involved, associated

with angular atrophy
Hypertrophy
Right ventricular hypertrophy due to
systemic hypertension
Pregnant uterus

HYPERPLASIA AND METAPLASIA

Cellular response that results from reprogramming of
stem cells
Metaplasia is

Replacement of one epithelium by other

Metaplasia from
NOT a feature of metaplasia
NOT true about hyperplasia

Metaplasia
Reversible change, Slow growth, Reverse back to
normal with appropriate treatment, If persistent may
induce cancer transformation
Metaplasia
Stem cells
Loss of polarity
Increase in size of cell

STEM CELLS
Stem cells
Example for multipotent stem cell
Helps in self renewal in hematopoietic stem cells
Oligopotent stem cells
Unipotent stem cells
Totipotency
NOT true about stem cell
NOT a labile cell
Permanent cell
Options of multiplicity of stem cell
differentiation
When stem cell transforms to other tissues,
the process is known as

Found in yolk sac, Used in gene therapy, Found in

peripheral circulation, Proliferation and self renewal,
Differentiation, Dormant phase of cell cycle
Hematopoietic stem cells
Bmi1
Neural stem cells
Spermatological stem cells
Ability to form whole organism
Developmental elasticity
Hepatocyte
Neuron
Developmental plasticity
Trans differentiation

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

FIXATIVES AND STAINS

MC Fixative in Histological specimens
Commonly used fixative in diagnostic pathology
MC Fixative for Light Microscopy
MC Fixative for Electron Microscopy
Negative staining in electron microscope
Best fixative for cytological studies
Zenkers fixative
Bouin fixative
Carnoy fixative
Lipid in tissue detected by
Splenic macrophages in Gauchers disease differ from
those in ceroid histiocytosis by staining positive for
PAS does NOT stain
PAS does NOT stain
Colour of carcinoma is due to
Light brown perinuclear pigment seen of staining of
cardiac muscle fibre in grossly normal appearing heart
of 83 old man at autopsy
Non Endogenous pigment
Brown atrophy is due to
Hemosiderin is stained by
25 year renal transplant recipient died of meningitis. On
autopsy, gelatinous exudates with cystic masses round
encapsulated organism, stain
Reticulocytes are stained with
Acridine orange is a fluorescent dye used to bind
Frozen section biopsy NOT used for
Tissue block specimen preserved for
Sebaceous gland ca-stain used
Stain used for fungus
Silver methenamine stain is
Halls stain for
Reticulin stain for
Verhoeff , Van gieson stain
Luxol fast blue stain
Ulex europaeus
Mucicarmine
Von Kossa stain
Method of Identification of Sentinel node during Breast
Surgery
Basement membrane in renal biopsy is stained by
Collagen in renal biopsy is stained by
Diastase removes
Glycogen is associated with

Formaldehyde
Formaldehyde
10% Neutral Buffer Formalin
Glutaraldehyde
Osmium compounds
95% ethanol
Mercury
Picric acid
Lymph nodes in radical resection
Oil red O, Sudan III, Sudan black
Lipid
Lipid
Basement membrane of bacteria
Lipochrome
Lipochrome

Anthracotic Pigment
Lipofuscin
Prussian blue
Prussian blue

Brilliant cresyl blue

DNA and RNA
Amyloid
10 years
Oil red
Silver methenamine
Green
Bilirubin
Type III collagen
Elastic fibres
Myelin
Endothelium
Epithelial mucin
Calcium
Isosulfan Blue Dye
Jones-methenamine
Massons trichrome
Glycogen
FAS reaction

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GENERAL FEATURES OF PATHOLOGY

GENERAL PATHOLOGY

PIGMENT
Pigment in liver is caused by

Lipofuscin, Pseudomelanin, Wilsons disease, Malarial

pigment, Bile pigment
Lipochrome
Carbon
Lipofuscin

Wear and tear pigment in body refers to

MC exogenous pigment is
Brown atrophy is associated with

BACTERICIDAL SYSTEM
Most effective bactericidal system within phagocytes
Most important in bactericidal activity

Reactive oxygen metabolite mediated

H2O2 MPO halide system

HYDROGEN PEROXIDASE
Enzyme associated with formation of H2O2
Enzymes associated with breakdown of H2O2

Oxidase
Catalase, Peroxidase

OXIDATIVE STRESS
Enzymes reducing oxidative stress

Superoxide dismutase, Catalase, Glutathione

peroxidase, Ceruloplasmin
Vitamin C, Selenium, Glutathione peroxidase, Vitamin E
Vitamin A
Xanthine oxidase

Antioxidants
Does NOT handle oxidative damage in lens
Does NOT reduce oxidative stress

FREE RADICAL
Free radicals involved in cell injury
Enzyme contributing in generation of free oxygen
radicals with in neutrophils for killing intracellular
bacteria
Peroxisomal free radical scavenger
Pigment involved in free radical injury
Free radical scavengers
Absorption of radiant energy can result in
cell injury by causing hydrolysis of water.
This type of injury is protected by
Enzyme that protects brain from free radical injury
Fenton reaction leads to free radical generation when
In genetic deficiency of MPO, increased susceptibility
to infection is due to

Superoxide anion, hydrogen peroxide,

hydroxyl radical, peroxynitrite
Fentons reaction, NADPH oxidase

Superoxide dismutase, Glutathione peroxidase,

Catalase
Lipofuscin
Vitamin A,C,E, Glutathione
Glutathione peroxidase

Superoxide dismutase
Ferrous ions are converted into ferric ions
Inability to produce hydroxyl-halide radicals

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