Pathology Image Bank Edition 2 0 Updated Upto NEET PG 2021

Pathology
Image Bank
Index
Sl.No. Chapter Pg.No.
I General Pathology
Cell Injury, Cellular Adaptations and Cellular Ageing 09
Immunopathology Including Amyloidosis 25
Derangements of Homeostasis and Haemodynamics 46
Inflammation and Healing
50
Infectious and Parasitic Diseases 62
Neoplasia 66
Genetic and Paediatric Diseases
77
II Haematology and lymphoreticular tissue

Haematopoietic System and Disorders of Erythroid Series
85
Bleeding Disorders and Basic Transfusion Medicine 95
Disorders of Leucocytes and Lymphoreticular Tissues 111
III Systemic pathology

Blood Vessels and Lymphatics 119
Cardiovascular system
122
Respiratory System 127
Oral Cavity and Salivary Glands 140
Gastrointestinal Tract 141
Liver, Biliary Tract and Exocrine Pancreas 148
Kidney and Lower Urinary Tract 151
The Breast 158
Endocrine System 161
The Nervous System 165
Musculoskeletal System 166
IV Cytology 178
9
General Pathology
Cell Injury, Cellular Adaptations and Cellular Ageing
Cell Injury
CELL DEATHS
Programmed Non programmed
Apoptosis
Necroptosis Necrosis
Pyroptosis
Entosis
Ferroptosis
Netosis
AIIMS 18 & 19
Q. Apoptosis Vs Necrosis?
Robbin & Cotran Pathological basis of diseases (pg 33); Text book of Pathology , Harsh Mohan (pg9)
10
11
Apoptosis
Apoptotic cells are round to oval shrunken

masses of intensely eosinophilic cytoplasm
containing shrunken or almost normal
organelles
apoptotic bodies
Formation of membrane bound near
spherical bodies containing condensed
organelles around the cell.
Apoptotic bodies
Intrinsic pathway
Extrinsic pathway
mitochondrial pathway
Death receptor pathway
Cell injury
Mechanism of cell killing by • Growth factor withdrawal
cytotoxic T lymphocytes; • DNA damage (by radiation, toxins,
Initiated by engagement of death free radicals)
receptors (members of the TNF • Protein misfolding (ER stress)
receptor family)
Leads to leakage of pro-apoptotic proteins from

Binding of Fas and FasL activates Fas- mitochondrial membrane into cytoplasm and
associated death domain (FADD) in the subsequent caspase activation;
cytoplasm of the cell that activates Can be inhibited by anti-apoptotic members of
caspases. the BCL2 family,
Initiator caspase: Caspase 8,10 Initiator caspase: Caspase 9
Executioner caspase : Caspase 3,6,7

AIIMS 2020
Q. Which caspase binds to
cytochrome C and APAF?
Apoptosis
Robbin & Cotran Pathological basis of diseases (pg 33); Text book of Pathology , Harsh Mohan (pg 17)
12
Apoptosis
Extrinsic pathway Intrinsic pathway
TRALI Fas ligand

Cytochrome C release Release of SMAC
Binds to Binds to from mitochondria to (second mitochondrial
DR4 and DR5 CD 95(Fas) cytoplasm activator of caspases)
from mitochondria
Bind to APAF-1 Binds and neutralise IAP’s

Association of FADD and pro (apoptosis activating (Inhibitor of
caspase 8 to death domain factor -1) Apoptosis Proteins)
Wheel like hexamer(apoptosome)

Activation of caspase 8 and caspase 10 Activation of caspase 9
^
Activation of effector caspases(caspase 3 and 7)
AIIMS 2019
Substrate cleavage
Both intrinsic and extrinsic
pathways are seen in apoptosis
Morphological features of apoptosis
(90%) ( 10%3
13
REgULATION Of APOPTOSIS
Primarily by bcl-2 family of genes Located on chromosome 18
Pro-apoptotic
anti-apoptotic
(MEET're)
BAX and BAK
Bcl-2, Bcl-xL,Mcl -1 BAD, BIM, BID, Puma, and Noxa
IAP Cytochrome C
(Inhibitor of
Apoptosis Proteins)
Stimulates
Inhibits
APOPTOSIS
ExAmPLES Of APOPTOSIS
Physiological conditions Pathological conditions
1. Endometrial cells (Menstruation) 1. Councilman bodies: Viral hepatitis

2. Cell removal during embryogenesis 2. Gland atrophy following duct
3. Virus infected cells and Neoplastic obliteration as in cystic fibrosis
cells by cytotoxic T cells 3. Graft versus host disease (GVHD)
Pyroptosis
Emperipolesis
Apoptosis associated with fever
NOD like receptors activation
Activates inflammasome
Activates Caspase 1 and 11 Neet 2019

Q. IL- 1 is
activated by
Apoptosis which caspase?
Also activates IL -1 fever
AIIMS 2018
- Cells in living and intact state found Ferroptosis
Pyroptosis is involved
in cytoplasm of host cell Iron-dependent pathway of in recognition and

clearance of nectrotic
- ROSAI DORFMANN disease -
cell death induced by lipid cells
massive lymphadenopathy peroxidation.

Q. Identify emperipolesis?
14
Necrosis
Localised area of death of tissue followed later by degradation of
tissue by hydrolytic enzymes liberated from dead cells
Characterized by
Denaturation of cellular proteins,
Leakage of cellular contents through damaged membranes,
Local inflammation,
Enzymatic digestion of the lethally injured cell
Nuclear changes appear in one of three patterns,

karyolysis
Basophilia of the chromatin may fade,
Loss of DNA because of enzymatic degradation by endonucleases.
pyknosis
Characterized by nuclear shrinkage and increased basophilia.
Chromatin condenses into a dense, shrunken basophilic mass.
karyorrhexis
Pyknotic nucleus undergoes fragmentation.
With the passage of time (1 or 2 days), the nucleus in the necrotic cell totally disappears.
AIIMS 2019
Q.Light microscopic features
of irreversible cell injury?
15
Coagulative necrosis
ischaemic necrosis
– Most common type of necrosis
– Loss of nucleus with the cellular outline being preserved
– Associated with ischemia
– Seen in organs (heart, liver, kidney etc.) except BRAIN.
Normal kidney (N)
Necrotic cells in the infarct (I) showing
preserved cellular outlines with loss of
nuclei and an inflammatory infiltrate
Hallmark of coagulative
necrosis is the tomb stone
appearance
Liquefactive necrosis
COLLIQUATIVE NECROSIS
– Enzymatic destruction of cells
– Abscess formation
– Pancreatitis
– Seen in brain infarct and abscess cavity
Liquefactive
necrosis
gliosis
granulation
tissue
16
Caseous necrosis
– Combnination of coagulative and liquefactive necrosis

– Characteristic of TB
– Cheese like appearance of the necrotic material.
(because of the presence of high lipid content in
the cell wall of organism)
Viable lymphoid Granulomatous

inflammation Caseous necrosis
tissue
Fat necrosis
-
Focal areas of fat destruction, typically resulting from
release of activated pancreatic lipases into the
substance of the pancreas and the peritoneal cavity.
eg:- Traumatic fat necrosis of the breast and
mesenteric fat necrosis due to acute pancreatitis.
Cloudy appearance
Mixed inflammatory cells
17
Fibrinoid necrosis
– Complexes of antigens and antibodies
are deposited in vessel wall with leakage
of fibrinogen out of vessels
- Seen in PAN, Aschoff bodies (in rheumatic
[NEET't9)
heart disease) and malignant hypertension.

- The wall of the artery shows a
circumferential bright pink area of necrosis
with inflammation (neutrophils with dark
Fibrinoid necrosis in an artery. nuclei).
Gangrenous necrosis
Necrosis of tissue with superadded putrefaction

Dry gangrene coagulative necrosis
Wet gangrene liquefactive necrosis
Dry gangrene of the foot
The gangrenous area is dry, shrunken and dark and is
separated from the viable tissue by clear line of
separation.
18
Pathologic calcification
Abnormal tissue deposition of calcium salts, together with smaller amounts of
iron, magnesium, and other mineral salts.
FEATURE DYSTROPHIC CALCIFICATION METASTATIC CALCIFICATION
Definition Deposits of calcium salts in Deposits of calcium salts in

dead and degenerated tissues normal tissues
Calcium
metabolism Normal Deranged
Serum calcium
level Normal Hypercalcaemia
Reversibility Generally irreversible Reversible upon correction

of metabolic disorder
Hyperparathyroidism (due to
Necrosis (caseous, liquefactive, fat),
adenoma, hyperplasia, CRF), bony
infarcts, thrombi, haematomas,
destructive lesions (e.g. myeloma,
dead parasites, old scars,
Causes metastatic carcinoma), prolonged
atheromas, Monckeberg’s sclerosis,
immobilisation, hypervitaminosis D,
certain tumours, cysts, calcinosis
milk-alkali syndrome,
cutis
hypercalcaemia of infancy
Increased binding of phosphates with Increased precipitates of calcium

Pathogenesis necrotic and degenerative tissue, which phosphate due to hypercalcaemia
in turn binds to calcium forming at certain sites e.g. in lungs,
calcium phosphate precipitates stomach, blood vessels and cornea
Dystrophic calcification in degenerated

tunica media of muscular artery of uterine
myometrium in Monckeberg’s arteriosclerosis.
Adventitia
Lumen
Intima (uninvolved)
Media (calcification)
AIIMS 2019
Q. Calcification seen in Atheromatous plaque
19
Metastatic calcification in tubular

basement membrane in nephrocalcinosis due
to hypercalcaemia.
Calcification
Basement membrane
Tubules
Commonly Used Stains

Glycogen Carmine (best), PAS with diastase sensitivity
Lipids Sudan black, Oil Red ‘O’
Amyloid Congo Red, Thioflavin T (for JG apparatus

of kidney) and S
Calcium Von Kossa, Alzarine Red

Hemosiderin Perl’s stain
Trichrome Collagen appears blue

Smooth muscle appears red.
Basement membrane/ collagen Periodic acid-Schiff (PAS), Reticulin

Van Gieson, Masson’s trichrome
Glycogen PAS with diastase loss
Glycoproteins, glycolipids, PAS with diastase persistence
glycomucins (epithelial origin)
Acid mucin (mesenchymal origin) Alcian blue [AIIMS 2018 ]
Mucin (in general) Combined Alcian blue-PAS

Argyrophilic/ argentaffin granules Silver stains
Cross striations PTAH stain
Enzymes Myeloperoxidase, Acid phosphatase,
Alkaline phosphatase
Nucleolar organiser regions (NORs) Colloidal silver stain
AIIMS 2018
Q. Stain used for Acid mucin
20
PIGMENTS
Coloured substances present in most living beings including humans.
ENDOGENOUS PIGMENTS EXOGENOUS PIGMENTS
Normal constituents of cells or 1. Inhaledpigments
accumulate under special circumstances 2. Ingestedpigments
1. Melanin 3. Injectedpigments(Tattooing)
2. Melanin-likepigment
a. Alkaptonuria
b. Dubin-Johnsonsyndrome
3. Haemoprotein-derivedpigments
a. Haemosiderin
b. Acid haematin (Haemozoin)
c. Bilirubin
d. Porphyrins
4. Lipofuscin (Wear and tear pigment)
Lipofuscin granules in cardiac myocytes Compound naevus showing

granular, brown-black melanin pigment.
Anthracosis lung
Presence of abundant coarse black carbon
pigment in the septal walls and around the
bronchiole.
21
Cellular Adaptations
reversible changes in the size, number, phenotype, metabolic activity, or
functions of cells in response to changes in their environment.
Hypertrophy
③ Er
Increase in size and function of cells
•Results due to increase in growth factors or trophic stimuli.
•Includes puberty, lactating breasts and skeletal muscle fibres
(in body builders).
Atrophy Hyperplasia
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④
.
Reduced size of an organ or tissue B÷n÷ • Increase in number of cells.
resulting from a decrease in cell ⑤ • Results due to increase in growth factors,
size and number. increased expression of growth promoting
NORMAL CELL
Caused by ischemia,ageing, genes and increased DNA synthesis.
malnutrition etc. • Persists so long as the stimulus is present.
•May result due to chronic absence • e.g. breast development at puberty, endo-
of stimulus (disuse atrophy). metrial hyperplasia, benign hyperplasia of
METAPLASIA prostate, hyperplasia of liver cells after
partial hepatectomy.
Dysplasia
Reversible change of one type of epithelial or

mesenchymal adult cells to another type of
④
Abnormal multiplication of cells characterized by
adult epithelial or mesenchymal cells, usually in change in size, shape & loss of cellular organization
response to abnormal stimuli, and often reverts • The basement membrane is intactQ
back to normal on removal of stimulus. • Can progress to cancer
22
Physiologic hypertrophy of the uterus during pregnancy.
(A) Gross appearance of a normal uterus (right) and a gravid uterus (removed for postpartum bleeding).
(B) Small spindle-shaped uterine smooth muscle cells from a normal uterus
(C) large plump cells from the gravid uterus, at the same magnification.
Nodular hyperplasia of the prostate.
Hyperplasia of both fibromuscular elements

and epithelium seen as areas of intraacinar
papillary infoldings (convolutions) lined by
two layers of epithelium with basal polarity
of nuclei.
Metaplasia
Neet PG 2020
Q. Identify the change
seen in chronic smokers?
Metaplasia of columnar epithelium (left) to squamous epithelium (right) in a bronchus
23
Squamous metaplasia of the

uterine cervix.
Part of the endocervical mucosa is lined by

normal columnar epithelium while foci of
metaplastic squamous epithelium are seen
at other places.
Columnar metaplasia oesophagus

(Barrett’s oesophagus).
Part of the oesophagus which is normally lined

by squamous epithelium undergoes metaplastic
change to columnar epithelium of intestinal
type.
dysplasia
Uterine cervical dysplasia,
high grade lesion.
Shows increased number of layers of

squamous epithelium having marked
cytologic atypia including mitoses.
21yr old female with PAP Smear with hyperchromatic
nuclei,pleomorphism with low maturation index
involving almost all thickness.What is this called ?
A. Metaplasia
B. Dysplasia
C. Hyperplasia
D. Carcinoma [NEET 2021]
24
Cellular aging -
Result of a progressive decline in cellular function and viability caused by genetic

abnormalities and the accumulation of cellular and molecular damage due to the effects of
exposure to exogenous influences
Werner’s syndrome
Rare autosomal recessive disease,
Characterised by similar features of premature ageing, atherosclerosis and risk for development
of various cancers.
Defective gene product is a DNA helicase, a protein involved in DNA replication and repair and other
functions requiring DNA unwinding.
A defect in this enzyme causes rapid accumulation of chromosomal damage that may mimic some
aspects of the injury that normally accumulates during cellular aging.
Neet 2020
Q. Premature ageing in Werner’s syndrome is due to?
25
Immunopathology Including Amyloidosis

The Immune System
Immunity
Natural or innate immunity
non-specific Specific or adaptive immunity
antigenic specificity
First line of defense without
antigenic specificity Stimulated by exposure to microbes and
other foreign substances.
a) Humoral: comprised by complement.
b) Cellular: consists of neutrophils, a) Humoral: consisting of antibodies
macrophages, and natural formed by B cells.
killer (NK) cells. b) Cellular: mediated by T cells.
AIIMS 2020
ADCC is seen with NK cells,
Eosinophils and Neutrophils.
26
Neutrophils Lymphocytes
- Multi-lobed nuclei typically consisting of 3 to - Small lymphocytes have spherical

5 segments (polymorphonuclear neutrophils). heterochromatic nuclei, and scant cytoplasm.
- Contain specific granules that give the - Larger lymphocytes have indented nuclei with
cytoplasm a pale pink color. more cytoplasm containing azurophilic granules.
Monocytes
Eosinophils
- Monocytes are 12 to 15 µm in diameter

- Bi-lobed nucleus - Large nuclei indented or C- shaped
- Large cytoplasmic specific granules - Abundant cytoplasm
that are eosinophilic. - Lysosomal granules on light microscope
give the cytoplasm bluish-gray color.
Basophils
- Basophils are bi-lobed or S-shaped nuclei

- Contain cytoplasmic specific granules that stain
blue to purple
- Basophilia of the granules is due to the presence
of heparin and sulfated glycosaminoglycans.
Inicet 2020
Q. Identify the WBC’s?
27
agranulocytosis
marked reduction in neutrophils
caused by
(1) inadequate or ineffective granulopoiesis or
(2) increased destruction or sequestration of
neutrophils in the periphery
Inadequate or ineffective granulopoiesis
• Suppression of HSCs,
- In aplastic anemia and infiltrative marrow disorders (tumors, granulomatous disease);
- Granulocytopenia is accompanied by anemia and thrombocytopenia.
• Suppression of committed granulocytic precursors by exposure to certain drugs.
• Disease states associated with ineffective hematopoiesis,
- Megaloblastic anemia and myelodysplastic syndrome,
in which defective precursors die in the marrow.
• Rare congenital conditions (Kostmann syndrome),
- Inherited defects in specific genes impair granulocytic differentiation.
Accelerated destruction or sequestration of neutrophils

• Immunologically mediated injury to neutrophils,
- Idiopathic,
- Associated with a well-defined immunologic disorder (systemic lupus erythematosus),
- By exposure to drugs.
• Splenomegaly,
- Leads to sequestration and destruction of neutrophils in the spleen and modest neutropenia,
- Associated with anemia and thrombocytopenia.
• Increased peripheral utilization,
- Can occur in overwhelming bacterial, fungal, or rickettsial infections.
The most common cause of

NEET 2018
agranulocytosis is drug toxicity.
Q. Most common cause of agranulocytosis?
28
Pan B cell Pan T cell markers

markers NK cell markers
CD 19, 20, 21, 23 CD3, CD7 and CD2 CD2, CD16 and CD56
CYTOKINES
Immunomodulating agents composed of soluble proteins, peptides and glycoproteins secreted
by haematopoietic and non-haematoopoietic cells in response to various stimuli.
[MEET 2019]
29
Chemokines
Family of small (8 to 10 kDa) proteins that act primarily as chemoattractants
for specific types of leukocytes.
Types of chemokine
• • A Fractalkine
CXC C-C C C x3 c
(C- cysteine; X- amino acid) (No amino acid)
Neutrophil RECRUITS ALL WBC RECRUITS ONLY Chemotactic

recruiting EXCEPT NEUTROPHIL LYMPHOYTES for monocytes
and t cells
EOTAXIN
IL - 8 MCP - 1 LYMPHOTActin -
RANTES
Pyrogens
Induce fever [NEET't94 i 8) Q. Substances that induce fever are?
Exogenous pyrogens Lipopolysaccharides (LPS) of barterial walls

Endogenous pyrogens IL- 1, TNF and prostaglandins (PGE2)
30
HLA SYSTEM AND MAJOR HISTOCOMPATIBILITY COMPLEX

Human Leucocyte Antigens
Gene complexes of proteins on the surface of all nucleated cells of the body and platelets.
Immense importance in matching donor and recipient for organ transplant
Located on short arm (p) of chromosome 6
Identified by CD8+
(T suppressor) lymphocytes
Identified by B cells and

CD4+ (T helper) cells.
TRANSPLANT REJECTION
Autografts donor and recipient is the

same individual.
Isografts donor and recipient of the
same genotype.
Allografts donor is of the same species
but of a different genotype.
Xenografts donor is of a different species

from that of the recipient.
Neet 2020
Q. Graft from Identical twin is?
31
DISEASES OF IMMUNITY
PRIMARY IMMUNODEFICIENCY DISEASES
Diseases are caused by genetic (inherited) defects that affect the
- Defense mechanisms of innate immunity (phagocytes, NK cells, or complement) or
- Humoral and/or cellular arms of adaptive immunity (mediated by B and T lymphocytes)
1. Severe combined immunodeficiency diseases
(Combined deficiency of T cells, B cells and lgs)
(i) Reticulardysgenesis Failure to develop primitive marrow reticular cells
(ii) Thymic alymphoplasia No lymphoid stem cells
(iii) Agammaglobulinaemia (Swiss type) No lymphoid stem cells
(iv) Wiscott-Aldrich syndrome Cell membrane defect of haematopoietic stem cells;
associated features are thrombocytopenia and eczema
(v) Ataxia telangiectasia Defective T cell maturation
2. T cell defect
DiGeorge’s syndrome Epithelial component of thymus fails to develop
(thymic hypoplasia)
3. B cell defects
(Antibody deficiency diseases)
(i) Bruton’s X-linked agammaglobulinaemia Defective differentiation from pre-B to B cells
(ii) Autosomal recessive agammaglobulinaemia Defective differentiation from pre-B to B cells
(iii) IgA deficiency Defective maturation of IgA synthesising B cells
(iv) Selective deficiency of other lg types Defective differentiation from B cells to
specific Ig-synthesising plasma cells
(v) Immune deficiency with thymoma Defective pre-B cell maturation
4. Common variable immunodeficiencies

(characterised by decreased lgs and serum antibodies and variable CMI)
(i) With predominant B cell defect Defective differentiation of pre-B to mature B cells
(ii) With predominant T cell defect
(a) Deficient T helper cells Defective differentiation of thymocytes to T helper cells
(b) Presence of activated T cell disorder of unknown origin
T suppressor cells
(iii) With auto antibodies to B and T cells Unknown differentiation defect
32
SECONDARY IMMUNODEFICIENCY DISEASES

1. Infections AIDS (HIV virus); other viral, bacterial and protozoal infections
2. Cancer Chemotherapy by antimetabolites; irradiation
3. Lymphoid neoplasms Deficient T and B cell functions
(lymphomas, lymphoid leukaemias)
4. Malnutrition Protein deficiency
5. Sarcoidosis Impaired T cell function
6. Autoimmune diseases Administration of high dose of steroids toxic to lymphocytes
7. Transplantcases Immunosuppressive therapy
Severe combined immunodeficiency (SCID)

Constellation of genetically distinct syndromes, all having common defects in
both humoral and cell-mediated immune responses
X-linked
most common form
=50% to 60% of cases
-
more common in boys than in girls
The genetic defect in the X-linked form is a mutation in the common γ-chain (γc)
subunit of cytokine receptors
• The remaining cases of SCID are inherited as autosomal recessive.
The most common cause of autosomal recessive SCID is a deficiency of the
enzyme adenosine deaminase (ADA).
AIIMS 2019
Genes involved are JAK-3, RAG-1, IL-7R
Q. Genes involved in SCID?
Hyper-IgM Syndrome
Group of genetic disorders in which the B-cells cannot switch to other kind of antibodies,
resulting in the overproduction of IgM and underproduction of IgA, IgG, and IgE.
Clinical manifestations include recurrent sinopulmonary infections, Pneumocystis carinii
pneumonia, and Cryptosporidium parvum infection, with very low levels of IgG, IgA, and
normal/high levels of IgM.
Flow cytometry analysis shows peripheral blood B-lymphocytes that lack expression of
surface CD40.
33
Expression of CD40 on B cells. Panel a and c: B-cell gating on side scatter and
CD19 in normal and patient, respectively. Panel b: Normal expression of CD40
on B-cells. Panel d: B-cells with absence of CD40 expression in patient
[11-111452019] Q. Diagnosis of Hyper IgM syndrome from the image ?
HYPERSENSITIVITY REACTIONS
Exaggerated or inappropriate state of normal immune response with onset of
adverse effects on the body.
Form of antigen- antibody reaction
1. Immediate type in which on administration of antigen, the reaction occurs immediately
(within seconds to minutes).
Immune response is mediated largely by humoral antibodies (B cell mediated).
Include type I, II and III.
2. Delayed type in which the reaction is slower in onset and develops within 24-48 hours and
the effect is prolonged. Q. Type 1 reaction is mediated by ?
It is mediated by cellular response (T cell mediated)
Includes Type IV reaction.
Cell/mediator responsible for Delayed hypersentivity reaction ?
A.Cytotoxic T cells C.Dendritic cells
B.Macrophages D.IgG 4 [NEET 2021]
34
FEATURE TYPE I TYPE II (ANTIBODY-MEDIATED,

(ANAPHYLACTIC, ATOPIC) CYTOTOXIC)
Definition Rapidly developing Reaction of humoral

immune response in a antibodies that attack
previously sensitised cell surface antigens and
person cause cell lysis
Peak action time 15-30 minutes 15-30 minutes
Mediated by IgE antibodies IgG or IgM antibodies
Etiology Genetic basis, pollutants, HLA-linked, exposure to
viral infections foreign tissues/cells
Examples i. Systemic anaphylaxis i. Cytotoxicantibodiestoblood cells
(administration of antisera and (autoimmune haemolytic anaemia, transfusion
drugs, stings) reactions, erythroblastosis foetalis, ITP,
ii. Local anaphylaxis (hay fever, leucopenia, drug-induced)
bronchial asthma, food allergy, ii. Cytotoxicantibodiestotissue components
cutaneous, angioedema) (Graves’ disease, myasthenia gravis, male
sterility, type I DM, hyperacute reaction
against organ transplant)
FEATURE TYPE III (IMMUNE-COMPLEX, TYPE IV (DELAYED,

ARTHUS REACTION) T CELL-MEDIATED)
Definition Results from deposition of antigen- Cell-mediated slow and

antibody complexes on tissues prolonged response
Peak action
time
Within 6 hours After 24 hours
Mediated by IgG, IgM antibodies Cell-mediated
Etiology Persistence of low grade infection, CD8+ T cells, cutaneous
environmental antigens, autoimmune process antigens
Examples i. Immunecomplex glomerulonephritis i. Reactionagainst mycrobacterial
ii. Goodpasture’s syndrome, antigen (tuberculin reaction,
iii. Collagendiseases(SLE, rheumatoid arthritis) tuberculosis, tuberculoid leprosy)
iv. PAN ii. Reactionagainst virus-infected cells
v. Drug-inducedvasculitis iii. Reactionagainst tumour cells
35
36
AUTOIMMUNE DISEASES
Body’s immune system fails to distinguish between ‘self’ and ‘non-self’ and reacts by
formation of autoantibodies against one’s own tissue antigens.
Pathogenesis of
autoimmunity
37
Systemic Lupus Erythematosus (SLE)

Autoimmune disease involving multiple organs, characterized by a vast array of
autoantibodies, particularly antinuclear antibodies (ANAs).
Injury is caused mainly by deposition of immune complexes and binding of antibodies to
various cells and tissues.
The hallmark of SLE is the production of autoantibodies.
antinuclear antibodies (ANA)

The auto-antibodies formed against DNA, histones, non histone proteins bound to
RNA and nucleolar antigens.
i) Antinuclear antibodies (ANA)
- Antibodies against common nuclear antigen that includes DNA as well as RNA.
- Demonstrable in about 98% cases and are used as screening test.
ii) Antibodies to double-stranded (anti-dsDNA)
- Most specific for SLE, especially in high titres,
- Present in 70% cases.
III) Anti-Smith antibodies (anti-Sm)
- Antibodies appear against Smith antigen which is part of ribonucleoproteins.
- Also specific for SLE but is seen in about 25% cases.
iv) Other non-specific antibodies (lack specificity for SLE)
a) Anti-ribonucleoproteins (anti-RNP)
- Seen in 40% cases of SLE but seen more often in Sjögren’s syndrome.
b) Anti-histone antibody,
- Antibody against histone associated with DNA in chromatin,
- Seen in drug-induced lupus than in SLE.
c) Antiphospholipid antibodies (APLA) or lupus anticoagulant
- Tests for thrombotic complications in cases of SLE.
d) Anti-ribosomal P antibody
- Antibody against protein in ribosomes and is seen in CNS lupus.
Autoantibodies against nuclear and cytoplasmic components of the
cells are demonstrable in plasma by immunofluorescence tests
38
Immunofluorescence patterns
39
Staining patterns of antinuclear antibodies
Homogeneous PATTERN Speckled pattern
- Diffuse staining of nuclei - Seen with antibodies against

- Typical of antibodies reactive with various nuclear antigens, including
dsDNA, nucleosomes, and histones, Sm and RNPs.
- Common in systemic lupus
erythematosus.
centromeric pattern Nucleolar pattern
- The pattern of staining of anti-

- Typical of antibodies against
centromere antibodies is seen in some
cases of systemic sclerosis, Sjögren nucleolar proteins.
syndrome, and other diseases.
40
ORGAN INVOLVEMENT
Kidney Lupus nephritis

Heart Libman-Sacks endocarditis having vegetations on both the sides of
the valvular surface. There is also presence of pericarditis.
Mouth Oral ulcers are usually painless
Joints Non-erosive arthritis involving 2 or more peripheral joints
with tenderness and effusion
Skin Erythematous rash present over malar region is also called
‘butterfly rash’. Exposure to sunlight accentuates the erythema.
Blood Presence of autoimmune cytopenia (anemia, neutropenia or
thrombocytopenia). The presence of LE cell or hematoxylin body is also seen.
LE CELL PHENOMENON
Q. Conditions showing
ANAs cannot penetrate the intact cells and thus cell nuclei positive LE test ?
should be exposed to bind them with the ANAs.
The binding of exposed nucleus with ANAs results in

LE body or haematoxylin body
homogeneous mass of nuclear chromatin material
Phagocytic leucocyte, commonly polymorphonuclear
LE cell
neutrophil, and sometimes a monocyte, which engulfs the
homogeneous nuclear material of the injured cell.
Mass is engulfed by a neutrophil, displacing the nucleus of neutrophil to the rim of

the cell, it is called LE cell
Mass, more often an intact lymphocyte, is phagocytosed by a monocyte, it is
called Tart cell.
Other conditions showing positive LE test
- Rheumatoid arthritis, lupoid hepatitis, penicillin sensitivity
41
Damaged cell + ana
Le body
Fr
Engulfment of le body by neutrophil
\
I
Engulfed
le body
Le cell
Typical LE cell
There are two LE cells having

rounded masses of amorphous
nuclear material (LE body) which
has displaced the lobes of
neutrophil to the rim of the cell.
Libman-Sacks endocarditis
Libman-Sacks endocarditis of the mitral

valve in lupus erythematosus.The
vegetations attached to the margin of
the thickened valve leaflet are
indicated by arrows.
42
lupus nephritis
Q. Wireloop lesions are seen

in which class of SLE?
Focal proliferative
glomerulonephritis,
with two focal necrotizing lesions
at the 11 o’clock and 2 o’clock
positions (H&E stain).
Diffuse proliferative
glomerulonephritis.
Marked increase in cellularity
throughout the glomerulus
(H&E stain).
43
“wire loop” lesions
Lupus nephritis showing a glomerulus with

several “wire loop” lesions representing
extensive subendothelial deposits of
immune complexes (periodic acid-Schiff
stain).
- Seen in SLE type IV and MPG
Electron micrograph of a renal

glomerular capillary loop
Subendothelial dense deposits
(arrowheads) correspond to “wire
loops” seen by light microscopy.
B- basement membrane.
Deposition of IgG antibody in a

granular pattern, detected by
immunofluorescence.
[AIIMS 2018]
Q. Diagnosis of Lupus
nephritis from SLE.
44
Scleroderma (Systemic Sclerosis)

Autoimmune disorder characterised by fibroblast stimulation and collagen
deposition in the skin and internal organs.
Diffuse Scleroderma
- Presence of anti-DNA topoisomerase antibodies (Scl-70).
- Widespread skin involvement at onset, with rapid progression and early visceral involvement.
- Symptoms include dysphagia, malabsorption, arrhythmia (due to cardiac fibrosis), exertional
dyspnea and renal insufficiency.
Limited scleroderma
- Presence of anti-centromere antibodies.
- Skin involvement is often confined to fingers, forearms, and face.
- Visceral involvement occurs late, clinical course is relatively benign.
- Some patients develop CREST syndrome
(Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.)
CLINICAL FEATURES
i) claw-like flexion deformity of hands;
ii) Raynaud’s phenomenon;
iii) oesophageal fibrosis
iv) malabsorptionsyndrome;
v) respiratory distress;
vi) malignanthypertension;
vii) pulmonary hypertension; and
viii) biliarycirrhosis.
Extensive deposition of dense collagen in the

dermis with virtual absence of appendages (hair
follicles) and foci of inflammation (arrow)
Q. Antibodies present in diffuse and

limited scleroderma?
45
Raynaud’s phenomenon
- Vasoconstriction of peripheral blood vessels in response to cold or stress exposure
Predisposing Factors Precipitating Factors
1. 15 and 40 years old. 1. Smoking
2. More in Women 2. Working with vibrating Cold exposure
3. Climate- winter machinery
3. Emotional distress Stress
4. Exposure to the cold
Digital artery
contraction spasm
Occlusion of
arteries
Tissue ischemia
vasoconstriction - white
Sharply demarcated pallor of the Cyanosis of the fingertips. cyanosis - blue
distal fingers resulting from the rapid blood reflow- red
closure of digital arteries.
SjOgren Syndrome
Chronic disease characterized by Q. Antibodies present in Sjogren
- Dry eyes (keratoconjunctivitis sicca) and syndrome?
- Dry mouth (xerostomia)
Due to immunologically mediated destruction of the lacrimal and salivary glands.
primary form sicca syndrome
Presence of anti-ribonucleoprotein antibodies like SS-A (Ro) and SS-B (La).
Intense lymphocytic and plasma cell infiltration with

ductal epithelial hyperplasia in a salivary gland. Enlargement of the salivary gland
46
Derangements of Homeostasis and Haemodynamics

Thrombosis
IIEET 207
'
[MEET 2020]
Q. Thrombosis
is initiated by?
Virchow triad in thrombosis
FEATURE ARTERIAL THROMBI VENOUS THROMBI

Blood flow Formed in rapidly flowing Formed in slow moving
blood of arteries and heart blood in veins
Sites Common in aorta, coronary, Common in superficial varicose
cerebral, iliac, femoral, renal and veins, deep leg veins, popliteal,
mesenteric arteries femoral and iliac veins
Thrombogenesis Formed following endothelial cell Formed following venous stasis e.g. in
injury e.g. in atherosclerosis abdominal operations, child birth
Development Usually mural, not occluding the Usually occlusive, take the cast of
lumen completely, may propagate the vessel in which formed, may
propagate in both directions
Macroscopy Greywhite, friable with lines Redblue with fibrin strands and
of Zahn on surface lines of Zahn
Microscopy
Distinct lines of Zahn composed Lines of Zahn with more
of platelets, fibrin with abundant red cells
entangled RBC & WBC
Effects Ischaemia leading to infarcts Thromboembolism, oedema, skin
e.g. in the heart, brain etc ulcers, poor wound healing
47
Thrombus in an artery
Thrombus is adherent to the arterial wall and is seen occluding most of the lumen. It shows
lines of Zahn composed of granularlooking platelets and fibrin meshwork with entangled red
cells and leucocytes.
HYPERCOAGULABLE STATES (THROMBOPHILIA)
INHERITED (PRIMARY) FACTORS
i) Deficiency of antithrombin III
ii) Deficiency of protein C
iii) Deficiency of protein S [MEET 2018]
iv) Mutation in factor V Leiden
Q. Identify the
v) Defects in fibrinolysis (dysfibrinogenaemia, plasminogen disorders) causes of
vi) Increased levels of coagulations factors (II and VIII) hypercoagulable
states?
ACQUIRED (SECONDARY) FACTORS
Risk factors Predisposing clinical conditions
i) Advancing age, i) Heart diseases (myocardial infarction, CHF, rheumatic mitral
ii) prolonged bedrest, stenosis, cardiomyopathy)
iii) prolonged immobilisation ii) Vascular diseases (atherosclerosis, aneurysms of the aorta and
iv) cigarette smoking, other vessels, varicosities of leg veins)
v) obesity iii) Hypercoagulable conditions (polycythaemia, myeloproliferative
disorders, dehydration, nephrotic syndrome, disseminated cancers)
Antiphospholipid antibody
iv) Shock
(APLA) syndrome:
v) Tissue damage e.g. trauma, fractures, burns, major surgery on
i) Lupus anticoagulant antibody bones, abdomen or brain.
ii) Anticardiolipin antibody vi) Late pregnancy and puerperium
vii) Certain drugs (anaesthetic agents, oral contraceptives, HRT).
48
Coagulation in vivo and in laboratory
'
(AIIMS 20 )
[All Ms LOT
Q. Deficiency of
which coagulation
factor does not
affect clotting in
vivo
49
intrinsic and Extrinsic pathway in vivo
Following an endothelial injury a tissue factor is released,this combines with another factor marked as ‘A’in the given
image.The factor marked as ‘A’ aids in the following conversion.What is the factor marked as ‘A’ ?
IX IXA X XA
A.Factor VII
B.Factor VIII A A Tissue Factor
C.VonWillibrand Factor
D.Factor XII
ooo ooo
Endothelium
Thromboelastography
i. Method used for testing the efficacy of blood coagulation
ii. TEG is mostly used in surgery, anaesthesiology, emergency departments, ICU’s, and Labour &
Delivery departments.
iii. Assess the platelet function, clot strength, and fibrinolysis.
[AIIMS 2019 ] [1-11111952020]
Prothrombin time
evaluates extrinsic
Q. Test to identify the entire
pathway. coagulation pathway?
50
Inflammation and Healing

Phagocytosis
Process by which bacteria are killed/eaten up by the white blood cells.
Lysosomes are important organelles required for phagocytosis.
Phagocytosis involves sequential steps
• Recognition and attachment of particle to be ingested by leukocyte;
• Engulfment, with subsequent formation of a phagocytic vacuole;
• Killing of the microbe and degradation of the ingested material.
Opsonisation
Coating of the bacteria so that they are easily phagocytosed by the WBC
opsonins → Chemicals causing opsonisation
i) IgG opsonin
- Fc fragment of immunoglobulin G;
- Naturally-occurring antibody in the serum that coats the bacteria
- PMNs possess receptors for the same.
ii) C3b opsonin
- Fragment generated by activation of complement pathway.
- Strongly chemotactic for attracting PMNs to bacteria. [MEET ] 2018
iii) Lectins
Q. Identify the
- Carbohydrate-binding proteins in the plasma Opsonin ?
- Bind to bacterial cell wall.
Incorporation Phagolysosome
Opsonisation Pseudopod within the cell formation after
of the engulfing the (phagocytic fusion of
opsonised lysosome of the
particle. particle vacuole) and
degranulation cell.
51
Principal Mediators of Inflammation
Mediator Source Action
Histamine Mast cells, Vasodilation, increased vascular [ AIIMS 2019]

basophils,
platelets permeability, endothelial activation
Mast cells,
Prostaglandins leukocytes Vasodilation, pain, fever
Mast cells,
Increased vascular permeability,
Leukotrienes
leukocytes chemotaxis, leukocyte adhesion
and activation
Local: endothelial activation

Cytokines Macrophages,
(expression of adhesion molecules)
(TNF, IL-1, IL-6) endothelial cells,
Systemic: fever, metabolic
mast cells
abnormalities, hypotension (shock)
Chemokines
Leukocytes,
activated
Chemotaxis, leukocyte activation
macrophages
Vasodilation, increased vascular

Platelet- Leukocytes, permeability, leukocyte
activating mast cells
factor adhesion, chemotaxis,
degranulation, oxidative burst
Leukocyte chemotaxis and activation,

Plasma direct target killing (membrane
Complement (produced in liver) attack complex), vasodilation (mast
cell stimulation)
Plasma
Increased vascular permeability,
Kinins (produced in liver) smooth muscle contraction,
vasodilation, pain
Robbin & Cotran Pathological basis of diseases (pg 85)

52
Leukocyte Recruitment to Sites of Inflammation
The journey of leukocytes from the vessel lumen to the tissue is a multistep process that is
:mediated and controlled by adhesion molecules and cytokines called chemokines.
This process can be divided into sequential phases :
1. In the lumen: margination, rolling, and adhesion to endothelium.
- Vascular endothelium in its normal state does not bind circulating cells or allow
their passage.
- In inflammation the endothelium is activated and can bind leukocytes as a prelude
to their exit from blood vessels.
2. Migration across the endothelium and vessel wall.
3. Migration in the tissues toward a chemotactic stimulus.
The multistep process of leukocyte migration through blood vessels, shown here for neutrophils.
The leukocytes first roll, then become activated and adhere to endothelium, then transmigrate across the endothelium,
pierce the basement membrane, and migrate toward chemoattractants emanating from the source of injury. Different
molecules play predominant roles in different steps of this process: selectins, in rolling; chemokines (usually displayed
bound to proteoglycans), in activating the neutrophils to increase avidity of integrins; integrins, in firm adhesion; and
CD31 (PECAM-1), in transmigration. ICAM-1, Intercellular adhesion molecule 1; IL-1, interleukin-1; PECAM-1, platelet
endothelial cell adhesion molecule (also known as CD31); TNF, tumor necrosis factor.
Arrange the cellular events of inflammation in the correct order :

i. Rolling A.iv - i - iii- ii
ii.Stable adhesion B.ii - iii - iv - i
iii.Cytokine mediated integrin activation C.iv - ii - iii - i
iv.Endothelial margination D.iii - iv - ii - i
Reference :
Robbins and Cotran Pathologic Basics of Diseases 10Ed. Pg : 77
53
granulomatous InFlammatIon
Chronic inflammation characterized by formation of granuloma
Granuloma
Aggregation of macrophages surrounded by a collar of mononuclear cells principally lymphocytes
Macrophages may get activated to form epithelioid cells (epithelium like cells)
Fuse together to form a bigger cell giant cell
Giant cells in inflammation

Foreign body giant cells
- Contain numerous nuclei (up to 100) which are uniform in size and shape
and resemble the nuclei of macrophages.
- Nuclei are scattered throughout the cytoplasm.
- Seen in chronic infective granulomas, leprosy and tuberculosis.
Langhans’ giant cells
- Seen in tuberculosis and sarcoidosis.
- Nuclei are like the nuclei of macrophages and epithelioid cells.
- Nuclei are arranged either around the periphery in the form of horseshoe or ring, or are
clustered at the two poles of the giant cell.
Touton giant cells
- Multinucleated cells have vacuolated cytoplasm due to lipid content
- Seen in xanthoma.
Aschoff giant cells
- Multinucleate giant cells are derived from cardiac histiocytes
- Seen in rheumatic nodule
Q. Giant cell seen in

TB and Sacrcoidosis?
Text book of Pathology , Harsh Mohan (pg131)

54
Giant cells in tumours

Anaplastic cancer giant cells
- larger, have numerous nuclei which are hyperchromatic and vary in size and shape.
- Derived from dividing nuclei of the neoplastic cells
e.g. carcinoma of the liver, various soft tissue sarcomas.
Reed-Sternberg cells
- Malignant tumour giant cells which are generally binucleate
- Seen in various histologic types of Hodgkin’s lymphomas.
Osteoclastic giant cells of bone tumour
- Giant cell tumour of the bones or osteoclastoma has uniform
distribution of osteoclastic giant cells spread in the stroma.

55
Touton giant cells Osteoclastic giant cells
FLORET LIKE GIANT CELL GLASSY TYPE GIANT CELL
Common conditions resulting in granuloma formation

• Tuberculosis
• Sarcoidosis (Non caseating granuloma)
• Brucellosis
• Cat scratch disease (Stellate shaped or round granuloma) •
Syphilis (Gumma)
• Lymphogranuloma inguinale
• Leprosy
• Inflammatory bowel disease (IBD)
[NEET 2018J
Q. Stellate shaped giant cell

is seen in which disease?

56
TUBERCULOSIS
Koch’s disease
Chronic pulmonary and systemic disease caused most often by M. tuberculosis,
Leading infectious cause of death worldwide.
Tissue response in tuberculosis represents classical example of chronic
granulomatous inflammation in humans.

57
Weeks Years
TIME AFTER INFECTION
Primary infection
Primary pulmonary tuberculosis, Ghon complex
I Exposed to mycobacteria
Formation of Ghon’s focus:

2
Subpleural fibrocaseous lesion
of lung parenchyma.
Ghon’s complex:
:
Ghon’s focus and involved
hilar lymphnodes
The gray-white parenchymal focus is under the pleura in

Heals by itself the lower part of the upper lobe (red arrow). Hilar lymph
nodes with caseation are seen on the left (blue arrow).
5% progress and spreads to other parts of body -> Miliary TB

95% latent- reactivated in immunocompromised stage -> Secondary TB
58
Ranke complex
The Ghon’s complex undergoes

progressive fibrosis and calcification.
EVOLUTION OF TUBERCLE
10-14 days
59
tubercle at low
magnification
Shows central granular

caseation surrounded by
epithelioid and multinucleate
giant cells.
[MEET 2020]
Q. Identify Caseating granuloma ?
tubercle at high
magnification
Caseating epithelioid cell

granulomas with a few
Langhans’ giant cells in the
cortex of lymph node.
acid-fast stain
Macrophages showing presence of
acid-fast bacilli in Ziehl-Neelsen
staining.
60
Secondary pulmonary
tuberculosis
The upper parts of both

lungs are riddled with gray-
white areas of caseation
and multiple areas of
softening and cavitation.
Miliary
tuberculosis of
the spleen
The cut surface shows

numerous gray-white
tubercles.
[NEET 2018]
Q. Identify the condition

from the image?
STEM CELL
[NEET 2020]
Have the dual property of being able to self renew
Stem cells do not divide without
and to give rise to differentiated cells and tissues. any regulatory stimulus
totipotent cells Multipotent cells

Can form an entire organism autonomously. Can form multiple cell lineages but cannot
Only zygote (fertilized egg) has this feature. form all of the body’s cell lineages.
Hematopoietic stem cells
oligopotent cells uni/Mono potent cells
Can form more than one cell lineage but Can form a single differentiated
are more restricted than multipotent cells. cell lineage.
Neuron stem cells Spermatogonial stem cells
61
Stem cells are located in special sites called niches.
Stem cells location function
Oval cells Canals of Herring of the liver Forming hepatocytes

and biliary cells
Satellite cells Basal lamina of myotubules Differentiate into
myocytes after injury
Limbus cells Canals of Schlemm Stem cells for the cornea
Ito cells Subendothelial space of Disse Store vitamin A
Paneth cells Bottom of crypts Host defense against

microorganisms
Liver stem cells (oval cells) are located in

the canals of Hering (thick arrow),
structures that connect bile ductules
(thin arrow) to parenchymal
hepatocytes.
Q. Location of
Liver stem cells?
62
Infectious and Parasitic Diseases

VIRAL INFECTIONS
Measles
Warthin-Finkeldey cells
lymphoid organs typically have marked
follicular hyperplasia, large germinal
centers, and randomly distributed
multinucleate giant cells, called Warthin-
Finkeldey cells, which have eosinophilic
nuclear and cytoplasmic inclusion bodies
Q. Diagnose the disease
[NEET 2018J from the image?
herpesvirus
HSV-infected cells contain large, pink

to purple intranuclear inclusions
(Cowdry type A) that consist of viral
replication proteins and virions at
various stages of assembly that push
the host cell chromatin out to the
edges of the nucleus
Cytomegalovirus (CMV)
Prominent intranuclear basophilic

inclusions spanning one-half of the
nuclear diameter are usually set off
from the nuclear membrane by a
clear halo.
63
Epstein-Barr virus
Causes:
Stewart granuloma
NK/T lymphoma
Lethal midline Granuloma
EBV
Enters the cell through CD 21

(Complement receptor 2)
Enters B lymphocytes
T cells identify them(CD8 cells)
Change shape into DOWNEY cell

Ballerina skirt appearance
Atypical lymphocytes in infectious mononucleosis.
CD8 increase
B lymphocytes decrease Infectious mononucleosis like condition
Acquire mutation -
t (8,14) cmyc - > Burkitt’s lymphoma
t (2,8)
t (8,22) Most common cancer :
GASTRIC CANCER
REL gene -> Hodgkin’s lymphoma
NK/T lymphoma
BCL6- > diffuse large B cell lymphoma
Also causes : Leiomyosarcoma/ Duncan’s disease

Lethal midline Granuloma Q. Mutation in Burkitt’s
(Perforation of nasal septum) lymphoma?
64
DISEASES CAUSED BY PARASITES

MALARIA
FILARIASIS
Wuchereria bancrofti and Brugia

malayi are responsible for causing
Bancroftian and Malayan filariasis.
The lymphatic vessels inhabit the
adult worm, especially in the lymph
nodes, testis and epididymis.
Microfilariae seen in the circulation
are produced by the female worm
65
AMOEBIASIS
flaskshaped ulcers
Amoebic infection begins as a small
area of necrosis of mucosa which may
ulcerate. These ulcerative lesions may
enlarge, develop undermining of margins
of the ulcer due to lytic action of the
trophozoite and have necrotic bed.
Q. Flask shaped ulcers
[NEET 2019] are caused due to ?
DISEASES CAUSED BY FUNGI

Cutaneous candidiasis
cutaneous lesions caused

by Candida albicans
Change in the shape of nail plate (paronychia)

Colonisation in the intertriginous areas of the
skin, axilla, groin, infra and intermammary,
intergluteal folds and interdigital spaces.
MYCETOMA
Madura foot.
Chronic suppurative infection involving a limb,
shoulder or other tissues and is characterised by
draining sinuses.
Lesions extend deeply into the subcutaneous
tissues, along the fascia and eventually invade the
bones. They drain through sinus tracts which
discharge purulent material and black grains. The
surrounding tissue shows granulomatous reaction
Brown granule lying in necrotic tissue in the
discharging sinus.
66
Neoplasia
CYTOMORPHOLOGY OF NEOPLASTIC CELLS
Anaplasia
Lack of differentiation [NEET2018]
Q. Anaplasia refers to?
Hallmark of malignant transformation.
1. Pleomorphism – It is the variation in the size and shape of the cells.
2. Hyperchromasia – Increased nuclear material or DNA is responsible for dark staining of the cells
In normal cells, the nuclear cytoplasmic (or N: C) ratio is 1:4 , 1: 1 in anaplastic cells.
3. Increased mitosis gives rise to atypical bizarre mitotic figures.
4. Loss of polarity due to disturbed orientation of anaplastic cells.
5. Presence of tumor giant cells having big hyperchromatic nuclei.
Microscopic appearance of loss

of nuclear polarity (B)
contrasted with normal basal
polarity in columnar epithelium
(A). The basement membrane is
intact in both.
67
mitotic figures
Nuclear features of
malignant cells in
malignant melanoma:—
Pleomorphism, anisonucleosis,
increased N/C: ratio, nuclear
hyperchromatism and
prominent nucleoli.
68
A multinucleate tumour giant

cell in osteosarcoma.
Multinucleate tumour giant cells

or giant cells containing a single
large and bizarre nucleus,
possessing nuclear characters of
the adjacent tumour cells,
Metastasis
Spread of a tumor to sites that are physically discontinuous with the

primary tumor.
Pathways of spread
Direct seeding of Lymphatic spread Hematogenous spread
body cavities and
surfaces
•Involvement of peritoneal Usual for carcinomas Usual for sarcomas

cavity (in ovarian cancer). Pattern of lymph node Thinner walls of veins
involvement follows natural causes preferential venous
•Surface of abdominal route of lymphatic drainage. invasion in comparison to
viscera (mucus secreting arterises.
appendicle cancer causing Sentinel lymph node is the
pseudomyxoma peritonei). first lymph node to receive Liver and lungs are the most
lymph flow from a primary commonly affected organs.
tumor.
Q. Organs most affected • Invasion of veins is particularly
in hematogenous spread? Seen in melanoma, breast and prominent in hepatocellular
colon cancer. cancer and renal cell cancer.
69
Metastatic carcinoma in lymph nodes
A, Matted mass of lymph nodes surrounded by increased fat. Sectioned surface shows merging capsules
of lymph nodes and replacement of grey brown tissue of nodes by large grey white areas of tumour.
B, Masses of malignant cells are seen in the subcapsular sinus and extending into the underlying nodal
tissue.
Metastatic sarcoma lung
A- Sectioned surface of the lung shows replacement of slaty-grey spongy parenchyma with
multiple, firm, grey-white nodular masses, some having areas of haemorrhages and necrosis.
B- Microscopic appearance of pulmonary metastatic deposits from sarcoma.
70
MOLECULAR BASIS OF CANCER
Normal cell cycle and its regulators

The cell cycle is driven by kinases which act when bound to proteins called cyclins, hence
known as cyclin-dependent kinases (CDKs).
Q. Which is the
phase of DNA
synthesis?
G1 Pre-synthetic phase
S Synthetic phase (DNA synthesis)
G2 Post-synthetic pre-mitotic phase
M Mitotic phase: Cells divide and produce new cells, which either
directly re-enter next cycle or pass into non- proliferative G0 phase
G0 Quiescent state: Cells in this state remain quiescent for variable

periods, but can be recruited in cell cycle if stimulated later.
71
CELL CYCLE REGULATORS
CIP KIP FAMILY INK/ARF FAMILY
p21 p14 p16

p27 p57
(Produced
by p53)
Inhibits CDK-4 Prevents feedback

Inhibits cyclin D-CDK4 inhibition of p53
Proto-oncogenes - Normal genes required for cell proliferation and differentiation

Oncogenes - Genes promoting autonomous cell growth in cancer cells
Oncoproteins - Proteins lacking regulatory control and responsible for promoting cell growth
CARCINOGENESIS
Multi-step process which requires accumulation of multiple genetic changes either as
germline or somatic mutations. mutations
inhibition of Affecting genes Defect in DNA

activation of
protooncogenes tumour- regulating apoptosis repair genes
suppressor gene
Hallmarks of cancer
72
Oncogenes
Review of Pathology and Genetics,Sparsh Gupta

73
tumour-suppressor gene
Review of Pathology and Genetics,Sparsh Gupta

74
RB gene
Located on long arm (q) of chromosome 13
Q. Location of RB gene?
Codes for a nuclear transcription protein called pRB
oncogenic viruses
non- multiplying cells
RB
RB Phosphorylation inactivation
active or Activation of the

hypophosphorylated
state transcription factor E2F
cell multiplication
role of p53 in maintaining the integrity of the genome

[AIIMS 2019]
‘molecular policeman’ and ‘guardian of the genome’ Q. If DNA is damaged, which

Present on chromosome 17p gene causes cell cycle arrest?
75
Activation of normal p53 by DNA- Activation of cells with loss

damaging agents or by hypoxia or mutations of the p53 gene
Cell cycle arrest in G1 and induction of DNA repair by

DNA damage does not induce cell
transcriptional upregulation of the cyclin-dependent
cycle arrest or DNA repair,
kinase inhibitor CDKN1A (encoding the cyclin-
dependent kinase inhibitor p21) and GADD45 genes.
Genetically damaged
cells proliferate
Successful repair of
DNA allows cells to If DNA repair fails, p53
proceed with the cell triggers either apoptosis or malignant neoplasms
cycle; senescence.
Human Diseases of DNA Damage Repair
Defective Nonhomologous End-Joining Repair (NHEJ)

1. Severe combined immunodeficiency disease (SCID)
2. Radiation-sensitive severe combined immunodeficiency disease
(RS-SCID)
Defective Homologous Repair (HR)
1. AT-like disorder 4. Werner syndrome (WS) [NEET 2020]
(ATLD) 5. Rothmund-Thomson syndrome (RTS) Q. Werner
2. Nijmegen breakage 6. Breast cancer susceptibility 1 syndrome is
syndrome (NBS) due to?
and 2 (BRCA1, BRCA2)
3. Bloom syndrome (BS)
Defective DNA Nucleotide Excision Repair (NER)

1. Xeroderma pigmentosum (XP)
2. Cockayne syndrome (CS) Mismatch repair defect is seen in :
3. Trichothiodystrophy (TTD) A. Xeroderma Pigmentosa
Defective DNA Base Excision Repair (BER) B. HNPCC
C. Familial adenomatous polyposis
1. MUTYH-associated polyposis (MAP) D. Ataxia Telengectasia [NEET 2021]
Defective DNA Mismatch Repair (MMR)

1. Hereditary nonpolyposis colorectal cancer (HNPCC)
76
blue cell tumours
malignant small round cell tumours
Presence of lymphocyte-like round nuclear size

and dense blue chromatin
a) Rhabdomyosarcoma (embryonal and alveolar types)
b) Primitive neuroectodermal tumour (PNET)
c) Ewing’s sarcoma
d) Neuroblastoma
e) Malignant lymphomas.
[AIIMS ]
2019
Q. Diseases with
Small blue round cells of small round cell?
Ewing Sarcoma
Cytology of cervical smears
(A) Normal cervicovaginal smear shows

large, flattened squamous cells and
groups of metaplastic cells;
interspersed are neutrophils. There are
no malignant cells.
(B) Abnormal cervicovaginal smear shows

numerous malignant cells that have
pleomorphic, hyperchromatic nuclei;
interspersed are normal
polymorphonuclear leukocytes.
77
Genetic and Paediatric Diseases

Inheritance pattern
Autosomal recessive inheritance
Autosomal dominant inheritance
[MEET2020]
Q. Identify the
inheritance from
the pedigree chart?
X-linked recessive inheritance
78
Autosomal dominant inheritance
Autosomal recessive inheritance
79
X linked recessive diseases
X Linked dominant diseases

- Vitamin D resistant rickets (hypophosphatemic rickets )
Q. Inheritance in
Fragile -X syndrome?
80
TRIPLE REPEAT MUTATIONS
Mutation is characterized by a long repeating sequence of three nucleotides.

Dynamic in nature Degree of amplification of a sequence of three
nucleotides increases during gametogenesis.
Expansions in non-coding regions Expansions in coding regions
“Loss of function” type mutation “Gain of function” type mutation

Mutant proteins aggregate as Mutant proteins interfere
intranuclear inclusions with other proteins
Fragile X syndrome Huntington’s disease

•Friedrich’s ataxia Spinobulbar muscular atrophy(Kennedy’s disease)
Myotonic dystrophy • Spinocerebellar ataxia types 1, 2, 3, 6, 7
The trinucleotide repeat expansions in the non-coding regions involve different repeats as
Fragile X syndrome (CGGQ), Friedrich’s ataxia (GAAQ) and Myotonic dystrophy (CTGQ).
TRIPLE REPEAT MUTATIONS
Fragile X syndrome Huntington’s disease Friedrich’s ataxia
X linked recessive Autosomal dominant Autosomal recessive
CGG repeats CAG repeats GAA repeates

coding for frataxin
[NIEET 2019 ]
[NEET 2020]
Q. Mutation in Fragile X Q. Mutation seen in
syndrome? Huntington’s chorea.
81
CHROMOSOMAL DISORDERS
④EET 19]
'
Alzheimer’s
disease is
commonly
associated with
Down’s
syndrome.
82
[AUNIS 2018]
Webbing of neck is
associated with higher risk
of cardiac anomalies
MITOCHONDRIAL INHERITANCE
Mutation in the mitochondrial DNA has the characteristic feature of maternal inheritance
because the ovum contains the mitochondria with their abundant cytoplasm whereas sperms
contains minimal number of mitochondria.
Mothers transmit their mtDNA to both their sons and daughters, only the daughters are able to
transmit the inherited mtDNA to future generations.
Leber hereditary optic neuropathy is a prototype of this type of disorder
[AIIMS 2019]
Q. Identify
Mitochondrial
inheritance?
83
inborn-errors of metabolism
[AIIMS 2020] Q. Fabry’s disease is due to?
84
Niemann-Pick disease (in liver)
The hepatocytes and Kupffer

cells have a foamy, vacuolated
appearance due to deposition of
lipids.
Gaucher disease (involving the bone marrow)
Wright stain hematoxylin and eosin.

Gaucher cells are plump macrophages that characteristically have the appearance
in the cytoplasm of crumpled tissue paper due to accumulation of glucocerebroside.
Pompe disease (Glycogen storage disease type II)
(A) Normal myocardium with abundant (B) Patient with Pompe disease showing myocardial
eosinophilic cytoplasm. fibers full of glycogen seen as clear spaces.
85
Haematology and lymphoreticular tissue

Haematopoietic System and Disorders of Erythroid Series
BONE MARROW EXAMINATION
bone marrow needle

Salah and Klima’s Needle for aspiration- Reusable
Jamshidi needle for biopsy
Salah needle has screw Klima’s needle
[AIIMS 2019 ]
Q. Identify the
needles?
Jamshidi needle for biopsy
[AIIMS 2020]
Q. Diseases with Dry Tap on aspiration?

86
PATHOLOGICAL rbc forms
87
88
89
Anemia
Reduction of the total circulating red cell mass below normal limits
Characterized by the clinical features of pallor of skin and nails, dizziness,
palpitations, lethargy and fatigue.
[Auras 2019]
Q. Micro cystic
anemia is seen
in?
Sideroblastic anaemia
Bone marrow aspirate smear in Perls’

stain shows marked excess of
reticular iron and a ringed
sideroblast (arrow) showing Prusian
blue granules in the cytoplasm.
90
Iron deficiency anaemia
PBF showing microcytic hypochromic anaemia Bone marrow aspirate showing

with moderate microcytosis and hypochromia. micronormoblastic erythropoiesis
Megaloblastic anaemia
PBF showing prominent macrocytosis of Examination of bone marrow aspirate showing

red cells and hypersegmented neutrophils. megaloblastic erythropoiesis.
[ AIIMS 2020]
Q. Identify megaloblastic anemia ?
91
hemolytic anemia
Marrow aspirate smear

There is an increased number of
maturing erythroid progenitors
(normoblasts).
Hereditary spherocytosis
Peripheral smear shows anisocytosis

and several dark-appearing
spherocytes with no central pallor.
Howell-Jolly bodies (small, dark
nuclear remnants) are seen in some
of the red cells of this asplenic
patient.
Q. Howell-Jolly
bodies are seen in ?
Osmotic fragility test in hereditary

spherocytosis showing increased fragility
92
Glucose-6-phosphate dehydrogenase deficiency
Peripheral blood smear
Red cells with precipitates of denatured
globin (Heinz bodies) revealed by supravital
staining.
As the splenic macrophages pluck out
these inclusions,“bite cells” like the one in
this smear are produced.
[AIIMS 2020]
Q. Cells seen in G6PD deficiency?
Regarding Glucose-6-Phosphate Dehydrogenase Deficiency which among the following is/are true ?
i. Decrease in NADPH A.All are true
ii.Decrease in reduced glutathione B.i and ii
iii.Decrease in lipid peroxidation C.i,ii and iv
iv.Decreased RBC membrane damage D.i,ii,iii
Sickle cell anaemia

PBF shows crescent shaped
elongated red blood cells, a
few target cells and a few
erythroblasts.
β-Thalassemia major
93
X-ray film of the skull showing new

bone formation on the outer table,
producing perpendicular radiations
resembling a crewcut.
Q. Osmotic fragility
test in B
Thalassemia?
Osmotic fragility testing B-thalassaemia major showing decreased fragility

Aplastic anemia
Low power. High power.

Bone marrow biopsy- Markedly hypocellular marrow contains mainly fat cells.
94
Clinical
manifestations of
Vit B 12 Deficiency
Clinical 20yr old boy presents with gum bleeding and easy bruisibility.Fever for
Manifestations of
Aplastic anaemia one month Hb 3,TLC 15,000,Platelet count 15000.On examination Pallor
present,Petechial rash present all over the body.Peripheral smear
shows :macrocytes,hypocellular bone marrow,absent megakaryocyte,no
immature cells.What is most probable diagnosis ?
A. Disseminated TB involving bone ematirx
B. Idiopathic Acquired Aplastic anemia
C. Paroxysmal Nocturnal Hemoglobinuria
D. Myelodysplastic syndrome [NEET 2021]
Clinical
Manifestations
of IDA
Other features in advanced stage:

Cheilosis (fissures at corners of mouth)
Koilonychia (spooning of fingers)
Clinical
manifestation
for
Hypoalbuminemia
95
Bleeding Disorders and Basic Transfusion Medicine
BLEEDING DISORDERS (HAEMORRHAGIC DIATHESIS)
Thrombocytopenia
Reduction in the peripheral blood platelet count below the lower limit of normal i.e. below 150,000/μl.
Q. Causes of
thrombocytopenia?
Immune Thrombocytopenic Purpura (ITP)

Characteristically
increased number of
megakaryocytes with
single nonlobulated nuclei
and reduced cytoplasmic
granularity.
96
Blood group systems
Major Blood ABO blood group system

Grouping System Rh blood group system
Minor Blood MNS blood group system

Grouping System p blood group system
Familial Blood Kell, Daffy, Lutheran, Lewis, Deigo etc..

Grouping System
Abo blood group system

Abo blood group: CARBOHYDRATE
Seen in all cells, secretions, tissues except CSF
ABO Blood groups has naturally occurring antibodies, primarily IgM (does not cross placenta)
Antibodies developed around 3 months of life.
A,B or O gene is located on chromosome 9

H gene are located on chromosome 19
H gene products are fucosyl (glucosyl) transferases and gives fucose

H gene forms “H“ substance
Fucose Glycoproteins/Glycolipid H SUBSTANCE
A H substance + N- acetylgalactosamine (NAG)
B H substance + GALACTOSE
Ab H substance + N- acetylgalactosamine (NAG) + galactose
O H substance + no A AND B TRANSFERASE
BOMBAY BLOOD GROUP : h SUBSTANCE NOT PRESENT
O blood group: Greatest amount of H substance

A1b group: Least amount of H substance
97
Rh Blood group
c
C Chromosome 1 codes for Rh antigen
Antigens D - most immunogenic
E Natural antibodies are not present against Rh antigen.
e Antibodies are produces only on sensitisation,
Proteins which are always IgG (cross placenta)
Present only in RBC
Haemolytic disease of newborn
Developed at birth
Kell system
2nd most immunogenic antigen after Rh antigen
Causes haemolytic disease of newborn
Absence of Kell Acanthocytes (irregular spicules)
Causes of acanthocytes: (Excess outer lipid membrane increase)

- Liver diseases causes increase in cholesterol
- A B lipoproteinemia
- Absence of kell blood group- Mc Leod phenotype
DUFFY BLOOD GROUP
Seen in RBC & tissues ;Causes haemolytic disease of newborn
P. Vivax and P. Knowlesi uses Duffy blood group to enter the cell
(P. Knowlesi found in Malaysia , spread from chimpanzees)
IL- 8 uses this blood group
- Neutrophilic recruiting cytokine
- x Chemokine
LEWIS BLOOD GROUP

Not made by RBC
Absorbed from plasma
Antigen for H pylori
98
Autoimmune haemolytic anemia
AIHA
WARM COLD
Presence of IgG and C3d
Presence of Anti-Rh autoantibodies
Presence of extra vascular hemolysis
COLD AGGLUTININ PAROXYSMAL COLD
DISEASE HEMOGLOBINURIA
Presence of IgM and C3d Presence of IgG
Against RBCs having I/i antigen Against RBCs having P antigen
Presence of intravascular hemolysis Presence of intravascular hemolysis
No spherocytes, Haemophagocyclosis & spherocytes
Red cell agglutination seen present
Special IgG antibody against P antigen
Donate Landsteiner Ab
RBC RBC
- Biphasic antibody
Zeta potential
IgG Antibody coats the RBC ( Opsonisation/ sensitisation )
IgG - incomplete antibody
Can coat RBC but cannot bridge
Space in between - zeta potential enters Spleen
Cannot cause lysis
Extravascular hemolysis
IgM - complete antibody
Cause hemolysis
RBC comes out as spherocytes Anemia
Overcomes zeta potential
(membranes removed)
Coomb’s test
Test done to identify sensitised cells.
Coomb’s Sera contains Anti IgG. Bridge the zeta potential. Agglutination
Direct Coomb’s test - Coomb’s antisera directly on the cells
Indirect coomb’s test - Compatibility testing

- Done in plasma
In Hemolytic disease of newborn Indirect Coombs test is done in Mother

Direct Coomb’s test is done in foetus.
99
Rouleaux formation: Aggregations of red blood cells (RBCs)

Increased serum proteins
Seen in Multiple myeloma
Increased protein also causes the blue background.
Blue background is also seen when sample is collected in heparin
BLOOD GROUPING
Blood grouping
Testing of red cells Testing of plasma
(antigens) (antibody)
Reverse testing
Forward testing
When plasma is given without testing in emergency ; AB is given.

When red cells is given without testing in emergency, O is given.
Bombay blood group

Forward testing Reverse testing
No ABH antigen Anti-A, Anti-B, Anti-H
Does not react with Reacts with

Anti-A, Anti-B, Anti-C A ceLls, B cells, O cells
100
Gel card technology

Column agglutination
Preloaded card used in blood banks
A +ve
Types of donors
Voluntary Weight > 45kg - 350 ml Blood
Replacement Weight > 55kg - 450 ml Blood
Directed AGE- 18 to 65 yrs
Paid- not allowed in India Hb > 12.5g/dl
Autologous- Bombay blood group Temp: afebrile
Storing own blood for future purpose SBP: 100- 140mmHg
DBP: <90mmHg
101
PRE DONATION bAG
Diverts 10-30ml of initial blood

Enables diversion and collection of first amount of blood
which usually contains skin particles and bacteria.
Risk of bacterial sepsis is minimised.
Bio mixer
Prevents micro-clot formation

Blood mixes with anticoagulant
Homogenous mixing of blood and
anticoagulant
Steps in Phlebotomy
Step1: Identify donor and label blood collection bag and test tubes
Step 2: Select the vein
Step 3: Disinfect the skin
Step 4: Perform venepuncture
Step 5: Monitor the donor and the donated unit
Step 6: Remove the needle and collect samples
Bio sealer
Seals the blood bag
Used for sterile disconnection,
Permanent and consistent leak free seals on
thermoplastic tubing
102
Anticoagulants and actions
Acid citrate 21 days

dextrose Not used
Citrate phosphate
dextrose
28 days
Citrate phosphate 35 days
dextrose adenine Commonly used
Saline adenine
42 days Mannitol preserves pressure in RBC
glucose mannitol
Citrate- Anticoagulant by chelating calcium

Sodium di- Phosphate - Prevents fall in pH
Dextrose- Supports the ATP generation by glycolytic pathways
Adenine- Synthesises ATP, extends shelf life of RBC
COMPONENTS
After centrifugation, the following components are formed
Plasma
BUFFY COAT- PLATELETS AND WBCs
RBC
Fresh frozen plasma

Plasma contains all coagulation factors
It is freezes immediately and stored at -18C,
Valid for 1 year
Platelet
Platelet is separated from buffy coat
Stored at 20 C-24 C
Valid for 5days
From 350ml of bag- 50ml platelets are formed- random donor platelets
1 bag will increase platelet by 10%
Approximately 4 bags of platelet are issued to a person
103
platelet refractiveness
Antibodies are formed against Antigen of 4 different people,
Does not respond to platelet transfusion
Single donor platelets
Prepared by platelet aphaeresis machine
200ml of platelets are taken from a person
The other components are send back to the person
No platelet refractiveness
Stored at room temp
Life - 5 days
Packed RBCs
2 C- 6 C in blood bank refrigerator
Life depends upon the anticoagulant
Most common contaminant of stored blood

Yersinia enterocolitica
Platelets have only ABO antigen , No Rh antigen.

Still Rh typing is done for platelets to rule out red cell contamination during
segregation from buffy coat
Red cell Platelets

contaminated
platelets
Single donor platelets

Jumbo bag Random donor
(200ml) platelets
(50ml)
104
Aphaeresis machine
Used to separate out one particular component from donor’s blood while returning the reminder
back to circulation.
Also used in Stem cell separation.
The minimum platelet count required to donate spheres is platelets is 150,000/uL
AABB standards limits spheres is platelet donation to no more than twice in a 7 day period
and no more than 24 times per year.
Low incidence of allergic reaction.
1 apheresis platelet unit is equivalent of 6 to 10 Random donor platelets
The interval between two blood donations should be at least 12 weeks
At least 48hrs must elapse after plasma heresies or cytapheresis before whole blood is
collected from a donor
Aphersis should be done only after 90 days of whole blood collection or in an event when red
cells are not returned at the end of heresies.
Most common complication -Hypocalcemia
Citrated blood is returned back
Citrate chelates calcium
Hypocalcemia
Tetany
Temperature Protocol
Whole blood/ RBC:
Whole blood 2C-6C
RBC PRBC - Start transfusion in 30mins
- End in 4 hrs
PLATELETS 20 C - 24 C 5 days Platelets/ FFP:
Fresh - Start within 20mins
frozen -18 C 1 year Needle Size: 18G
plasma
Filter: 170 - 260µ
105
TYPES OF BLOOD BAGS
Double Blood Bag
Single Blood Bag
For whole blood collection. For whole blood collection
Contains CPDA solution. Separation of red blood cells and plasma,
Capacity of 350ml and 450ml obtained through the process of
centrifugation and extraction.
Triple Blood Bag
Triple Blood Bag with SAGM, for whole blood collection
Separation of red blood cells, plasma and platelets.
Primary bag contains CPD and one satellite bag
contains SAGM.
Quadruple Blood bag
It comes with SAGM for whole blood collection
Separation of red blood cells, plasma and platelets through the buffy coat method.
Primary bag - CPD solution and has 3 satellite bags.
One satellite bag - 100 ml capacity to prepare platelets through the buffy coat method.
Valid for 5 days of platelet storage.
Single Blood Bag Double Blood Bag
Triple Blood Bag Quadruple Blood bag

106
FRESH FROZEN PLASMA
Stored at -18 C
If required immediately, FFP is thawed in water bath .
Validity reduces to 24 hours.
If FFP is thawed at 4 C , then cryoprecipitate is formed
Cryoprecipitate
Composition Given for Fibronectin
Factor 8 - Von willebrand deficiency Fibrin glue
Factor 13 - Thalassemia Used in open Cardiovascular
Fibrinogen - Hemophilia A surgeries for immediate clotting
Fibronectin
Von Willebrand factor Cryoprecipitate is not given in Hemophilia B (Factor 9 deficiency)
Cryo poor plasma

The left over product after removing Cryoprecipitate from FFP
Indication: Thrombotic thrombocytopenic purpura
Deficiency of ADAMTS Thrombus full of platelets
VWF bind with gp1b of platelets and form clots

ADAMTS causes cutting of VMF thereby preventing clots
VMF cannot be given to patients with TTP hence Cryopoor plasma is given
Special components
Washed RBC’s Graft Vs Host disease
For patients with allergic reaction Transplant patients are immunosuppressed
RBC is washed in distilled water Attack of donor lymphocytes - GVHD
Stored at 1 C - 6 C Target organs-
Validity - 24hrs Skin - Rash
Frozen RBC’s
Liver - Jaundice
-120 C GIT- Diarrhoea
Used in Bombay blood group Acute GVHD- <100 days
Validity - 10yrs Chronic GVHD- >100 days- Systemic Sclerosis
Glycerol is used
Radiated RBC’s
For transplantation Radiated RBC- Viable for 28 days
Done to prevent GraftVs Host disease. Radiated Platelets - Viable for 4hrs
107
Filters
1st generation 2nd generation
Commonly used Micro aggregate filters
Clot filters For filtering WBC, Platelets, fibrin threads
170 - 250µ 20 - 40M
3rd generation
Leucocyte filters
Used in repeated blood transfusions like Thalassemia patients
Common adverse reaction like fever and chills is due to
leukocytes, leucocyte filter prevents this adverse reaction
Leucocytes reduced platelets is < 5 x 10 leucocytes
Lowers incidence post transfusion fever and Cytomegalovirus. (CMV)
All newborns are given blood through this filter
These filters prevent the risk of HLA alloimmunization.
Does not prevent Transfusion associated- GVHD
Autologous blood transfusion

Acute normovolemic
PRE - OPerative hemodilution
7 days before surgery Before surgery and after anesthesia
Never <72hrs before surgery Supplement the taken volume in form of colloid/crystolloid
Hb: >11g/dL Transfuse the blood during/ after surgery
Post operative
Intraoperative blood salvage
blood salvage Can be given within 6 hrs
Collect the shed blood during operation Can cause cytokine response
Store at 1 C - 6 C Allergies can occur
Transfuse within 24hrs
108
Testing done before blood transfusion
TTI testing Cross match

Hepatitis B Plasma
Hepatitis C (more important as antibodies present
HIV in plasma and destroy red cells)
Malaria Red cells
Syphilis
Minor cross matching Major cross matching
Checking the patients Checking the plasma of

red cell against donor’s the patient against the
plasma donor red cell
Transfusion reactions
Acute < 24hrs Delayed >24hrs

Immune Immune
Acute hemolytic transfusion reaction DHTR
PTP
Febrile non-hemolytic transfusion reactions GVHD
Allergic
TRALI Nonimmune
Nonimmune
Repeated transfusion
Sepsis Disease Thalasemia
- Acute
- Delayed Hemosiderosis
Transfusion associated circulatory overload
109
Acute hemolytic transfusion reaction

Cause: Mismatch, Bombay blood group
Present with hematuria
Febrile Non hemolytic transfusion reaction
> 1 C rise from baseline
Due to cytokine from donor lymphocytes
Allergic
Due to transfer of lymphocytes from donor
TRALI
Transfusion associated lung injury
Usually occur due to plasma products
Antibodies are present in the donor plasma against

HLA/ Human neutrophil antigen
Neutrophil activation
Recruit IL-8
Damage endothelium of alveoli
Hyaline membranes
Acute lung injury
Transfusion associated circulatory overload

BP
Tachycardia
Delayed hemolytic transfusion reaction
Cause: Duffy mismatch
Post transfusion purpura

Antibodies against HpA
After 7 days
110
Complication after transfusion

Hypocalcemia
Citrate chelates calcium and causes Hypocalcemia
Hypomagnesaemia
Because of large volume of magnesium poor fluid and citrate overload
Hyperkalemia
Because of haemolysis of RBC from storage, irradiation or both
Hypokalemia
Because of re-entry into transfused RBC’s,
Release of stress hormones or metabolic alkalosis
Massive transfusion
Replacement of >1 time the total blood volume within 24hrs or
Replacement of more than 50% of the blood volume in 3 hrs in an adult
Complications
Metabolic alkalosis> acidosis
Hyperkalemia. Ventricular arrhythmia/ cardiac arrest
Hypocalcemia/ citrate toxicity
Depletion of coagulation factors. Increased risk of DIC
Dilutional thrombocytopenia
Hypothermia
blood transfusion reaction protocol

111
Disorders of Leucocytes and Lymphoreticular Tissues

LYMPHOHAEMATOPOIETIC MALIGNANCIES
chronic myeloid leukaemia (CML)
Peripheral blood smear shows

many mature neutrophils, some
metamyelocytes, and a myelocyte
The blood reveals a leukocytosis, often
exceeding 100,000 cells/mm3, which
consists predominantly of neutrophils,
band forms, metamyelocytes,
myelocytes, eosinophils, and basophils.
112
acute myeloblastic leukaemia (AML)

The diagnosis of AML is based on the presence of at least 20% myeloid blasts in the
bone marrow.
Acute myeloid leukemia without

maturation
Myeloblasts have delicate nuclear chromatin,
two to four nucleoli, and more voluminous
cytoplasm than lymphoblasts
Acute promyelocytic leukemia with the t(15;17)

(FAB M3 subtype).
Bone marrow aspirate shows neoplastic
promyelocytes with abnormally coarse and
numerous azurophilic granules. Presence of
several cells with bilobed nuclei and a cell in the
center of the field that contains multiple
needle-like Auer rods.
[AUNTS 2019T
Multiple Auer rods clustered

together- FAGGOT CELL.
Acute myeloid leukemia with monocytic

differentiation (FAB M5b subtype).
Peripheral smear shows one monoblast
and five promonocytes with folded
nuclear membranes.
113
Hodgkin Lymphoma
Arises in a single node or chain of nodes and spreads first to anatomically contiguous lymphoid
tissues. Morphologi- cally, the distinctive feature of Hodgkin lymphoma is the presence of
neoplastic giant cells called Reed-Sternberg cells.
Reed-Sternberg cells and variants

Diagnostic Reed-Sternberg cell Reed-Sternberg cell, mononuclear variant.
Two nuclear lobes, large inclusion-like nucleoli, and

Q. Identify Reed-Sternberg cell?
abundant cytoplasm, surrounded by lymphocytes,
macrophages, and an eosinophil. Reed-Sternberg cell,
lymphohistiocytic variant
Reed-Sternberg cell, lacunar variant
Folded or multilobated nucleus
114
Subtypes of Hodgkin Lymphoma [NEET 'i8] Q. Identify the types of Hodgkin lymphoma?
Has excellent prognosis [All MS 2020J
nodular sclerosis type lymphocyte predominance type
popcorn cells
Well-defined bands of pink, acellular collagen that Numerous mature-looking lymphocytes surround
subdivide the tumor into nodules scattered, large, pale-staining lymphohistiocytic
variants (popcorn cells)
mixed-cellularity type
Binucleate Reed-Sternberg cell is surrounded

by reactive cells including eosinophils (bright
red cytoplasm), lymphocytes, and
macrophages.
Q. Popcorn cells are seen
in which type of HL?
115
Non-Hodgkin Lymphomas
[AIIMS 2020
Hairy cell leukemia
• Morphologically distinct, very indolent tumor of mature B cells that involves spleen and marrow.
• Highly associated with mutations in the BRAF serine/threonine kinase.
Immunophenotype
Express the pan-B-cell markers CD19 and CD20; surface Ig (usually IgG);
and certain relatively distinctive markers, such as CD11c, CD25, CD103, and annexin A1.
Phase-contrast microscopy shows tumor In stained smears, these cells have round or
cells with fine hairlike cytoplasmic folded nuclei and modest amounts of pale blue,
projections. agranular cytoplasm.
116
Acute lymphoblastic leukemia
Lymphoblasts with condensed nuclear

chromatin, small nucleoli, and scant
agranular cytoplasm
The tumor cells have scant basophilic
cytoplasm and nuclei somewhat larger than
those of small lymphocytes
Chronic lymphocytic leukemia
Peripheral blood smear is flooded with

small lymphocytes with condensed
chromatin and scant cytoplasm.A
characteristic finding is the presence of
disrupted tumor cells (smudge cells)
A coexistent autoimmune hemolytic anemia
explains the presence of spherocytes
(hyperchromatic, round erythrocytes).
Diffuse large B-cell lymphoma.
Tumor cells have large nuclei,

open chromatin, and prominent
nucleoli.
Q. Chromosomal
rearrangements of Diffuse
large B-cell lymphoma.
117
Follicular lymphoma (lymph node)

(A) Nodular aggregates of
lymphoma cells are present
throughout lymph node.
1. Patient with generalised fatigue,tiredness.Primary clinical
examination is uneventful.Normal TLC and DLC.No
immature cells seen.Superficial discrete lymph nodes
enlarged.On biopsy showed effaced architecture,indented
nucleus,prominent nucleolus containing atypical cells.CD
10 and BCL 2 Positive.
A. Follicular lymphoma
B. Burkitts lymphoma
C. Non Hodgkin’s lymphoma
D. Mycoses fungoides [NEET 2021]
(B) At high magnification, small

lymphoid cells with condensed
chromatin and irregular or
cleaved nuclear outlines
(centrocytes) are mixed with a
population of larger cells with
nucleoli (centroblasts).
Burkitt lymphoma
(A) At low power, numerous pale tingible body (B) At high power, tumor cells have multiple
macrophages are evident, producing a “starry sky” small nucleoli and high mitotic index.The lack
appearance. of significant variation in nuclear shape and
size lends a monotonous appearance.
118
Mantle cell lymphoma
(A) At low power, neoplastic

lymphoid cells surround a small,
atrophic germinal center, producing
a mantle zone pattern of growth.
[Auras 2020]
Q. Overexpression of
cyclin D is seen in ?
(B) High-power view shows a

homogeneous population of small
lymphoid cells with somewhat irregular
nuclear outlines, condensed chromatin,
and scant cytoplasm. Large cells
resembling prolymphocytes (seen in
chronic lymphocytic leukemia) and
centroblasts (seen in follicular
lymphoma) are absent.
Multiple Myeloma
Plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia, renal failure,
and acquired immune abnormalities.
Normal marrow cells are largely
replaced by plasma cells including
forms with multiple nuclei, prominent
nucleoli, and cytoplasmic droplets
containing immunoglobulin.
CRAB criteria
HyperCalcemia,
Renal dysfunction,
Anemia,
Bone lesions
119
Systemic pathology
Blood Vessels and Lymphatics
Abdominal aortic aneurysm
(A) External view, gross photograph of a

large aortic aneurysm that ruptured
(rupture site is indicated by the arrow).
(B) Opened view, with the location

of the rupture tract indicated by a
probe.The wall of the aneurysm is
exceedingly thin, and the lumen is
filled by a large quantity of layered
but largely unorganized thrombus.
Giant cell (temporal) arteritis.
Hematoxylin-and-eosin stain of Elastic tissue stain demonstrating focal

Temporal artery of a patient with classic
section of temporal artery showing destruction of internal elastic
giant cell arteritis shows a thickened,
giant cells at the degenerated membrane (arrow) and intimal
nodular, and tender segment of a
internal elastic membrane in active thickening (IT) characteristic of long-
vessel on the surface of head
arteritis (arrow). standing or healed arteritis.
120
Takayasu arteritis.
(A) Aortic arch angiogram showing

narrowing of brachiocephalic,
carotid, and subclavian arteries
(arrows).
(B) Gross photograph of two cross-

sections of the right carotid artery
shown in (A) demonstrating marked
intimal thickening and adventitial
fibrosis with minimal residual lumen.
(C) Destruction and fibrosis of the

arterial media associated with
mononuclear infiltrates and
inflammatory giant cells (arrows).
Polyarteritis nodosa.
There is segmental fibrinoid necrosis and
thrombotic occlusion of the lumen of this
small artery. part of the vessel wall at the
upper right (arrow) is uninvolved.
Kawasaki disease vasculitis
resembles that seen in PAN
[NEET 2020]
Kawasaki disease is due to arteritis

of medium - large blood vessels.
121
Thromboangiitis obliterans (Buerger disease).
The lumen is occluded by a

thrombus containing abscesses
(arrow), and the vessel wall is
infiltrated with leukocytes.
Kaposi sarcoma.
(A) Gross photograph

illustrating coalescent red-
purple macules and plaques
of the skin.
(B) Histologic appearance of

the nodular stage of Kaposi
sarcoma, demonstrating sheets
of plump, proliferating spindle
cells.
Q. Identify Kaposi sarcoma?
122
Cardiovascular system
ISCHAEMIC HEART DISEASE
One-day-old infarct showing coagulative

necrosis and wavy fibers (elongated and
narrow, as compared with adjacent normal
fibers at right). Widened spaces between
the dead fibers contain edema fluid and
scattered neutrophils.
Dense polymorphonuclear leukocytic

infiltrate in an acute myocardial
infarction that is 3 to 4 days old.
Removal of necrotic myocytes

by phagocytosis (approximately
7 to 10 days).
123
Granulation tissue
characterized by loose
collagen and abundant
capillaries
Healed myocardial infarct in which

the necrotic tissue has been
replaced by a dense collagenous
scar. The residual cardiac muscle
cells show evidence of compensatory
hypertrophy.
124
'
[NEET 19] Identify the complication of MI?

Complications of myocardial infarction
Anterior myocardial rupture in

Rupture of the ventricular septum (arrow)
an acute infarct (arrow)
Fibrinous pericarditis, showing a dark, roughened

Complete rupture of a necrotic
epicardial surface overlying an acute infarct.
papillary muscle
Early expansion of anteroapical infarct with

wall thinning (arrow) and mural thrombus. Large apical left ventricular aneurysm (arrow).
125
Rheumatic Heart Disease
Acute rheumatic mitral valvulitis superimposed
on chronic rheumatic heart disease. Small
vegetations (verrucae) are visible along the
line of closure of the mitral valve leaflet
(arrows). Previous episodes of rheumatic
valvulitis have caused fibrous thickening and
fusion of the chordae tendineae.
A 34yr old woman presented with fever,migratory arthritis of lower large

joints,tachycardia.Murmur is Pancystolic.On Echo Mitral regurgitation is
present.The biopsy shows the following ?
A. Aschoff body C. Granulomatous vasculitis
B. Granuloma anulare D. Epitheloid granuloma [NEET 21]
Microscopic appearance of an Aschoff

body.The myocardium exhibits a
circumscribed nodule of mixed mononuclear
inflammatory cells with associated necrosis;
within the inflammation, large activated
macrophages show prominent nucleoli, as
well as chromatin condensed into long, wavy
ribbons (caterpillar cells; arrows).
Mitral stenosis with diffuse fibrous thickening and

distortion of the valve leaflets and commissural
fusion and thickening of the chordae tendineae
[NEET 2019]
Button hole/ fish mouth appearance
126
Infective (bacterial) endocarditis.
Endocarditis of mitral valve (subacute,

caused by Streptococcus viridans)
Acute endocarditis of congenitally

bicuspid aortic valve (caused by
Staphylococcus aureus) with extensive
cuspal destruction and ring abscess
(arrow). [NEET 2020T
Large,friable,irregular
vegetations are seen in
infective endocarditis
Dilated cardiomyopathy
Histologic section demonstrating variable

myocyte hypertrophy and interstitial fibrosis
(collagen is highlighted as blue in this Masson
trichrome stain).
[NEET 2019 ]
Strongly associated with

Alcohol abuse.
127
Respiratory System
pneumonia
Typical Pneumonia
Congestion with consolidation
Lobar pneumonia
1. Congestion: (1 to 2 days)
Due to vascular engorgement and alveolar transudates
2. Red hepatization: (3 to 4 days)
Massive neutrophil exhumation with haemorrhage, resembling liver
3. Grey hepatization : (5 to 7 days)
Red cell disintegration , persistence of fibrin purulent exudates
4. Resolution: (8 to 10 days)
Bronchopneumobia
Patchy exudate eyes consolidation of lung parenchyma
Acute neutrophilic suppurative exudation
Atypical pneumonia
Walking pneumonia
Congestion without consolidation due to lack of alveolar exudates
Most common cause: Mycoplasma pneumoniae
Infection and inflammation of lung parenchyma

Neutrophil filled alveoli
128
Stages of bacterial pneumonia
Acute pneumonia.
The congested septal capillaries
and numerous intra-alveolar
neutrophils are characteristic of
early red hepatization. Fibrin nets
have not yet formed.
Early organization
of intra-alveolar exudate, seen
focally to be streaming through the
pores of Kohn (arrow).
Advanced organizing pneumonia.
The exudates have been converted

to fibromyxoid masses rich in
macrophages and fibroblasts.
129
Bronchopneumonia Lobar pneumonia
Section of lung showing patches Gray hepatization.

of consolidation (arrows). The lower lobe is uniformly consolidated.
Aspiration pneumonia
Giant cells around foreign body
Keratin like material in alveoli -> foreign body
Foreign body is better appreciated in polarising microscopy Q. What is Golden
pneumonia?
Lipoid pneumonia- Aspiration of liquid like kerosene
Lipid laden macrophages- Golden pneumonia
Giant cells Homogenous material Lipid laden macrophages

Meconium aspiration pneumonia
Rugby balls - Meconium
Aspirated membranes present.
Rugby balls
Membranes
130
Pulmonary alveolar proteinosis

Alveoli filled with protein material
IN NEONATES Q.Electron
microscopy finding in
Due to improper development of lamellar body Pulmonary Alveolar
Mutation in ATP-binding cassette protein member 3 (ABCA3) proteinosis in infants.
In electron microscopy: Onion skin appearance
IN ADUTS
Due to loss of GM-CSF signalling
Blocks the terminal differentiation of alveolar macrophages
impairing ability to catabolise surfactant
The alveoli are filled with a dense,

amorphous, protein-lipid granular
precipitate, while the alveolar walls are
normal.
Pulmonary alveolar proteinosis

associated with mutation of the
ABCA3 gene.An electron micrograph
shows type 2 pneumocytes containing
small surfactant lamellae with
electron dense cores, an appearance
that is characteristic of cases
associated with ABCA3 mutations.
131
EMPHYSEMA
Irreversible enlargement of the airspaces distal to the terminal bronchiole, accompanied by
destruction of their walls.
132
Panacinar (Panlobular) emphysema showing involvement of the entire lobules and whole of acinus.
Bullous emphysema
large subpleural bullae (upper left).
A) Centriacinar emphysema. Central areas show (B) Panacinar emphysema involving

marked emphysematous damage (E) the entire pulmonary lobule.
133
INTERSTITIAL LUNG DISEASE

[AIIMS 2020]
PNEUMOCONIOSIS Q. Match the disease and agent causing the disease?
COAL WORKERS PNEUMOCONIOSIS- Carbon

Macrophages in alveoli eat up the carbon
Release cytokines -> fibrosis
Proximal part of acinus gets distended -> centriacinar emphysema
Complete distension -> Panacinar
Distal part distended -> Periacinar
Centriacinar is the most common type seen in smoker sand coal workers
Histologic appearance of the lung in coal-workers’ pneumoconiosis. Coal macules composed

of aggregates of dust- laden macrophages and collagens are seen surrounding respiratory
bronchioles. The alveoli and respiratory bronchioles surrounding the coal macule are
distended.
134
Silicosis- Silica
Extensive fibrosis - fibrotic nodules
Typically affects upper part of lung
More toxic (not digested by macrophages)
Can involve hilar lymphnodes -> egg shell calcification
CT Lung -Crazy pavement pattern (Seen also in COVID)
Ground glass opacities in lung
Appearance of ground glass opacities with superimposed

Silicosis interlobar and intralobular septal thickening
Microscopic picture of the lung in silicosis.

The silicotic nodule consists of hyaline centre surrounded by concentric layers of collagen which
are further enclosed by fibroblasts and dust-laden macrophages. Polarising microscopy in
photomicrograph on right shows bright fibres of silica.
135
Asbestosis
Partially digested by macrophages
Asbestos bodies inside macrophages.
Macrophages also eat up RBC ,
Asbestos bodies coated by iron -> Ferruginous bodies -> pearls Prussian blue positive
Release of cytokines by macrophages cause interstitial fibrosis
Develops Mesothelioma in later stages (latent period: 25 - 40yrs)
More severe in the lower zone of lung
Q. Identify asbestos bodies?
High-power detail of an asbestos An asbestos body is an asbestos fibre coated with

body, revealing the typical beading glycoprotein and haemosiderin giving it beaded or
and knobbed ends (arrow) dumbbell-shaped appearance with bulbous ends.
Ferruginous bodies Asbestos bodies
136
TUMORS
LUNG CANCER
EPITHELIAL NEUROENDOCRINE
Squamous cell Benign/ BODERLINE Malignant

carcinoma Adenocarcinoma
TYPICAL Carcinoid
ATYPICAL CARCINOID Small cell
carcinoma
Squamous cell carcinoma
Islands of invading malignant squamous cells are seen. A few well-developed cell nests with
keratinisation are evident.
Central in location
Precursor:- Squamous metaplasia/ dysplasia of bronchial epithelium
Cavitation +
Associated with pan coast tumor and golden pneumonia Q. Paraneoplastic
manifestation of Squamous
Paraneoplastic manifestaions - Hypercalcemia cell carcinoma?
On electron microscopy: intercellular bridging -> desmosomes

On light microscopy: Keratinization- Keratin/ epithelial/ squamous pearls
Markers Subtypes
Most common cancer in smokers
p40 Keratinising
p63 Non- keratininzing Most common cancer
Basaloid squamous cell carcinoma associated with hypercalcemia
Breast cancer
137
•
Is a highly malignant tumor with a strong relationship to cigarette smoking; only about 1% occurs in
nonsmokers.
•
May arise in major bronchi or in the periphery of the lung.
•
No known pre-invasive phase.
•
Most aggressive of lung tumors, metastasizing widely and fatal.
•
Comprised of relatively small cells with scant cytoplasm, ill-defined cell borders, finely granular
nuclear chromatin (salt and pepper pattern), and absent or inconspicuous nucleoli.
•
The cells are round, oval, or spindle- shaped, and nuclear molding is prominent.
•
There is no absolute size for the tumor cells, but in general they are smaller than three times the
diameter of a small resting lymphocyte (a size of about 25 μm).
•
The mitotic count is high.
•
Necrosis is common and often extensive.
•
Basophilic staining of vascular walls due to encrustation by DNA from necrotic tumor cells
(Azzopardi effect) is frequently present.
•
On Electron microscopy :
- Shows dense-core neurosecretory granules
- Expression of neuroendocrine markers such as chromogranin, synaptophysin, and CD56; and
the ability of some of these tumors to secrete hormones
•
Here is anthracotic pigment in macrophages in a hilar
lymph node.
Anthracosis is nothing more than accumulation of
÷ carbon pigment from breathing dirty air.

Smokers have the most pronounced anthracosis.
The anthracotic pigment looks bad, but it causes no
major organ dysfunction.
Patient with Squamous cell carcinoma of lung. During pulmonectomy,

there was blackish hilar lymph node of 1 cm.Identify the cause of
pigmentation :
A. Asbestos C. Lipofuscin
B. Anthracotic pigment. D. Melanin [NEET 21]
138
Adenocarcinoma
Located in periphery Most common primary
Most common lung cancer associated with thrombophebiltis lung cancer in females
and non smokers
Paraneoplastic manifestations- Neurological
Earlier known as bronchoalveolar carcinoma, now known as Adenocarcinoma in-situ
Express thyroid transcription factor- 1 (TTF-1)
Electron microscopy shows short plump microvilli
MARKER
Hyperplasia of epithelium
TTF -1 is positive in adenocarcinoma lung, thyroid
Well defined glands cancer and small cell carcinoma also.
NAPSIN A is positive only in adenocarcinoma
Carcinoma
TYPES
Micro invasive:
< 3cm in size and < 5mm invasion
Associated with scarring
Mucinous:
spreads aerogenouslyforming satellite tumors
Lepidic cells- (Butterfly sitting on fence)

Alveolar wall lined by flattened epithelial cells
A, Photomicrograph shows lepidic growth pattern of tumour cells along the alveoli. B, It shows
alveolar walls lined by cuboidal to tall columnar mucin-secreting tumour cells having papillary
growth pattern.
139
Mesothelioma
Associated with Simian virus 40
Long microvilli and abundant tonofilaments but absent microvilli us
rootless and lamellar bodies.
BAP 1 gene is associated
Asbestos related mesothelioma - 25- 40yrs latent period
All lung cancers are CK 7 positive except mesothelioma

Mesothelioma is CK 5/6 positive
Other markers of mesothelioma : Calretinin
Thick, firm, white pleural tumor

tissue that ensheathes the
lung.
Histologic variants of malignant mesothelioma. (A) Epithelioid

type. (B) Mixed type, stained for calretinin
(immunoperoxidase method). The epithelial component is
strongly positive (dark brown), while the sarcomatoid
component is less so.
140
Oral Cavity and Salivary Glands

Pleomorphic adenoma
The epithelial element is comprised of ducts, acini, tubules, sheets and strands of
cuboidal and myoepithelial cells. These are seen randomly admixed with mesenchymal
elements composed of pseudocartilage which is the matrix of myxoid, chondroid and
mucoid material.
Warthin’s tumour
Warthin’s tumour, showing eosinophilic epithelium forming glandular and

papillary, cystic pattern with intervening stroma of lymphoid tissue.
141
Gastrointestinal Tract
Esophagus
Barrett esophagus.
(A) Normal gastroesophageal junction.

(B) Barrett esophagus. Note the
small islands of residual pale squamous
mucosa within the Barrett mucosa.
[NEET2019]
Increases risk of
adenocarcinoma
(C) Histologic appearance of the

gastroesophageal junction in
Barrett esophagus. Note the
transition between esophageal
squamous mucosa (left) and
Barrett metaplasia, with
abundant metaplastic goblet
cells (right).
Esophageal cancer.
Esophageal adenocarcinoma organized Squamous cell carcinoma composed of

into back-to-back glands. nests of malignant cells
142
Stomach
Helicobacter pylori gastritis
(A) Spiral-shaped H. pylori are (B) Intraepithelial and

highlighted in this Warthin- (C) Lymphoid aggregates with
lamina propria
Starry silver stain. Organisms germinal centers and abundant
neutrophils are
are abundant within surface subepithelial plasma cells within
prominent
mucus. the superficial lamina propria
gastric carcinomas
Adenocarcinoma is an
[NEET 2018] epithelial tumour of stomach.
143
144
SMALL INTESTINE
Celiac disease
[MEET 2020]
Duodenal biopsy
shows crypt
hyperplasia.
[AIIMS 2020J
Increased risk of
GI lymphoma.
(A) Advanced cases of celiac disease (B) Infiltration of the surface epithelium by
show complete loss of villi, or total T lymphocytes, which can be recognized by
villous atrophy. Dense plasma cell their small, densely stained nuclei relative to
infiltrates in the lamina propria. larger, pale-staining epithelial nuclei
Whipple disease
Dense accumulation of Macrophages contain periodic acid– Intact rod-shaped bacilli

distended, foamy Schiff (PAS)–positive, diastase- identified by electron
macrophages in the small resistant granules that represent microscopy
intestinal lamina propria. partially digested bacteria within
lysosomes
145
INFLAMMATORY BOWEL DISEASE (IBD)
Q. Skip lesions
are seen in?
146
Ulcerative colitis in active phase
The microscopic features seen are superficial ulcerations, with

mucosal infiltration by inflammatory cells and a ‘crypt abscess’.
Crohn’s disease of the ileum
The histological features present are: transmural chronic inflammatory cell

infiltration, deep fissures into the bowel wall, submucosal widening due to
oedema, some prominent lymphoid follicles and a few non-caseating epithelioid
cell granulomas in the bowel wall.
147
LARGE BOWEL
Familial adenomatous polyposis
Group of disorders with multiple polyposis of the colon with autosomal dominant inheritance pattern.
(A) Hundreds of small polyps are
present throughout this colon with a
dominant polyp .
[NEET 2020]
Q. Identify juvenile polyp?
(B) Three tubular adenomas

are present in this single
microscopic field.
Hamartomatous polyps: Peutz-Jeghers polyp.
Microscopically, tree- like branching of muscularis mucosae. The lining epithelium is by

normal-appearing epithelial cells. The glands may show hyperplasia and cystic change
"
[AIIMS 2020]
A 11yr oldchild comes with abdominal pain and h/o intussusception.Endoscopy

was done there was polyps present in the intestine.Biopsy was taken and
Histopathological image is shown below.What is type of polyp ?
A.Hamartomatous C.Adenomatous
B.Inflammatory D.Neoplastic [INICET 2021]
148
Liver, Biliary Tract and Exocrine Pancreas

Acute viral hepatitis
Variable degree of necrosis of hepatocytes; and mononuclear cellular infiltrate in

the lobule. Mild degree of liver cell necrosis is seen as ballooning degeneration while
acidophilic Councilman bodies (inbox) are indicative of more severe liver cell injury.
Alcoholic cirrhosis
in an active drinker after long-term abstinence
Thick bands of collagen separate Most scars are gone

rounded cirrhotic nodules.
149
Alcoholic cirrhosis
The characteristic diffuse nodularity of

the surface is induced by the underlying
fibrous scarring.The average nodule size
is 3 mm typical of the “micronodular”
cirrhosis of alcoholic liver disease.The
greenish tint is caused by cholestasis.
Microscopically, this cirrhosis is

marked by small nodules entrapped in
blue-staining fibrous tissue; fatty
accumulation is no longer seen in this
“burned-out” stage
Fatty liver (alcoholic steatosis)
Most of the hepatocytes are distended with large lipid vacuoles with peripherally displaced nuclei.
150
α1-Antitrypsin deficiency.
Autosomal recessive disorder of protein folding marked by very low levels of circulating
α1-antitrypsin (α1AT)
Most common clinically significant mutation is PiZ; homozygotes for the PiZZ protein have
circulating α1AT levels that are only 10% of normal
Characterized by the presence of round-to-oval cytoplasmic globular inclusions in
hepatocytes, which are strongly periodic acid–Schiff (PAS)-positive and diastase-
resistant
Q. Disorder seen in α1-
Antitrypsin deficiency.
(A) Periodic acid–Schiff stain after

diastase digestion of the liver,
highlighting the characteristic
magenta cytoplasmic granules.
(B) Electron micrograph showing

endoplasmic reticulum dilated by
aggregates of misfolded protein.

151
Kidney and Lower Urinary Tract

Kidney
Nephrotic Membranoproliferative Glomerulonephritis

syndrome glomerulonephritis
Ig A Nephropathy
Minimal change Most common cause in world
disease
(Child) Post streptococcal
glomerulonephritis
Most common cause in india
Focal segmented
glomerular sclerosis
(Adults) Rapidly progressive
glomerulonephritis
End stage- Aggressive
Membraneous
Nephropathy
(Elderly)
[AIIMS 2019]
Nephrotic Vs
Nephrotoc
syndrome?
152
Acute proliferative glomerulonephritis
Normal glomerulus. Glomerular hypercellularity is due to

intracapillary leukocytes and
proliferation of intrinsic glomerular cells.
Immunofluorescent stain demonstrates

Typical electron-dense subepithelial
discrete, coarsely granular deposits of
“hump” and a neutrophil in the lumen.
complement protein C3
Crescentic glomerulonephritis
Compressed glomerular tufts and

the crescent-shaped mass of
proliferating epithelial cells and
leukocytes within the Bowman
capsule.
153
Minimal change disease
Normal electron microscopy
Flattened podocytes
Focal segmental glomerulosclerosis
Due to Podocytes injury
Caused by
HIV
Obesity
Reflex Damaged podocytes Sclerosis
Renal ablation
Sickle cell anemia
(A) Segmental sclerosis involves the (B) High-power view showing hyaline
upper half of both glomeruli. insudation (arrow) and lipid (small vacuoles)
in sclerotic area.
154
Membranous nephropathy
Immune complex mediated Antibodies are formed against antigen
Antigen - Phospholipisd A2
Antigen antibody complex
Subepithelial deposition
B/w BM and podocytes
Proliferation of Basement membrane
Basement membrane thickening
On light microscopy
- Thickened BM
PAS/ Silver stain
-Spikes and dome pattern
On electron microscopy
Sub-epithelial immune complex
Immunofluorescence
- Fluoro isothicyanate ( green colour)
- Granular immunofluorescence
155
IgA nephropathy
Affects 25 - 40 yrs age group
Due to excess of Ig A or not able to metabolise Ig A
Occurs after upper respiratory or lower respiratory infection
Antigen - Glycosylated Ig A
Ig G Antibodies against antigen
Antigen- antibody complex Mesangioproliferative

glomerulonephritis
Deposits in the mesangium of kidney
Mesangial cell proliferation
(A) Light microscopy

showing mesangial
proliferation and
matrix increase.
(B) Characteristic
deposition of IgA,
principally in mesangial
regions, detected by
immunofluorescence.
156
Post streptococcal glomerulonephritis
Immune complex mediated
Caused by B haemolytic streptococci
Antigen- streptococcal progenitor exotoxin B - SPE B
Antigen combines with Antibody
Antigen - antibody complex
Deposited in the sub endothelium
Neutrophil flooding in capillary
Endocapillary proliferation
Ag- Ab jumbs from sub endothelium to subepithelium
large subepithelial hump
Within 6 weeks heals by itself

Complement deposition (C1, C3, C4)
Rapidly progressive glomerulonephritis

Hallmark: basement membrane damage
Basement membrane damage

Coagulation protein leaks into bowman’s capsule
Fibrinogen mainly
Parietal cells starts proliferating to eat up fibrogen
Crescent
Crescent
Crescent - Fibrinogen , inflammatory cells , parietal cells [MEET 2020J
Very big crescent can interact visceral epithelial cells Anti GBM antibodies testing
to be done for RPGN type 1.
157
Diabetic kidney
Basement membrane thickening
Hallmark - Kimmelstiel Wilson lesion
Excess glycogen deposits - smooth nodules

Nodular glomarulosclerosis
Basement membrane thickening is seen in

MPGS
Membraneous nephropathy
SLE
IgA
Insudative lesions
- leak out of proteins from capillaries
into bowman’s capsule (capsular drops )or
stick to capillaries(fibrin caps)
Lupus nephritis
- Seen in SLE
type IV and MPG
- Duplication of Basement membrane due to subendothelial deposists
158
Breast
Fibroadenoma
Most common benign tumor of the female breast.
Two-thirds of fibroadenomas harbor driver mutations in MED12.
Arises from intralobular stroma
Always benign, Limited to intralobular stroma
Proliferation of stroma
Compression of acini
Slit shaped channels acini
Tumors are well- circumscribed, rubbery, grayish white nodules that bulge above the
surrounding tissue and often contain slit-like spaces lined by epithelium
159
Ductal Carcinoma in Situ

Comedo DCIS
Linear and branching High-grade proliferation associated with

calcifications within the large central zones of necrosis and
ductal system. calcifications fills several ducts.
Cribriform DCIS Micropapillary DCIS
Rounded (cookie cutter–like) Produces complex bulbous protrusions without

spaces, often filled with fibrovascular cores
calcified secretory material
160
Lobular carcinoma in situ (LCIS)
(A) Monomorphic population of small, (B) Immunoperoxidase study shows E-cadherin–

rounded, loosely cohesive cells fills and positive normal luminal cells that have been
expands the acini of a lobule. The underlying undermined by E-cadherin–negative LCIS cells
lobular architecture can still be recognized. spreading along the basement membrane.
The cells extend into the adjacent duct by
pagetoid spread.
Phyllodes Tumor
Arises from intralobular stroma but pushes into interlobular stroma in a finger / plant like manner.
Malignancy depends on
Stromal cellularity
Mitotic activity
Nuclear atypia
Infiltration borders
Compared to a fibroadenoma,
there is increased stromal
cellularity and overgrowth, giving
rise to the typical leaf-like
architecture.
161
Endocrine System
Hashimoto’s thyroiditis.
Autoimmune disease that results in destruction of the [NEET 2020]
thyroid gland and gradual and progressive thyroid failure. Q. Hurthle cells are seen in ?
Histologic features include: lymphoid cell infiltration with formation of lymphoid follicles having
germinal centres; small, atrophic and colloid-deficient follicles; presence of Hurthle cells which
have granular oxyphil cytoplasm and large irregular nuclei; and slight fibrous thickening of
lobular septa.
Graves’ disease
Follicles are lined by tall, columnar epithelium.

Diffuse symmetric
The crowded, enlarged epithelial cells project
enlargement of the gland and
into the lumens of the follicles. These cells
a beefy deep red parenchyma.
actively resorb the colloid in the centers of
the follicles, resulting in the scalloped
appearance of the edges of the colloid.
162
goitre
Thyroid enlargement caused by compensatory hyperplasia and hypertrophy of the follicular
epithelium in response to thyroid hormone deficiency.
A. Diffuse goitre (simple nontoxic goitre or colloid goitre).
B. Nodular goitre (multinodular goitre or adenomatous goitre).
Simple goitre
Microscopy shows large follicles distended by colloid and lined by flattened follicular epithelium.
Nodular goitre.
The predominant histologic features are: nodularity, extensive scarring with foci of
calcification, areas of haemorrhages and variable-sized follicles lined by flat to high
epithelium and containing abundant colloid.
163
THYROID CANCER
Papillary carcinoma of the thyroid
The macroscopic appearance of a papillary well-formed papillae.

carcinoma with grossly discernible papillary
[MEET 2020]
structures.
Q. Orphan Annie eye nuclei are seen in ?
Cells obtained by fine-needle aspiration of a

High power shows cells with
papillary carcinoma. Characteristic
characteristic empty-appearing nuclei,
intranuclear inclusions are visible in some of
sometimes called “Orphan Annie eye”
the aspirated cells.
nuclei.
164
Follicular carcinoma.
(A) Cut surface of a follicular carcinoma with (B) A few of the glandular lumens
substantial replacement of the lobe of the contain recognizable colloid.
thyroid.The tumor has a light-tan appearance
and contains small foci of hemorrhage.
Medullary carcinoma of the thyroid
(A) These tumors typically show (B) Histology demonstrates abundant

a solid pattern of growth and do deposition of amyloid, visible here as
not have connective tissue homogeneous extracellular material,
capsules. derived from calcitonin secreted by the
neoplastic cells
165
Nervous system
Schwannoma (neurilemmoma)
Whorls of densely cellular (Antoni A) and loosely cellular (Antoni B) areas with
characteristic nuclear palisading (Verocay bodies).
[ MEET 2020] Q. Verocay bodies are seen in ?
Meningioma
Transitional type. The cells have features of both syncytial and fibroblastic type and
form whorled appearance. Some of the whorls contain psammoma bodies.
166
Musculoskeletal System
Osteosarcoma
The lower end of the femur shows a bulky expanded tumour in the region of metaphysis
sparing the epiphyseal cartilage. Sectioned surface of the tumour shows lifting of the
periosteum by the tumour and eroded cortical bone. The tumour is greywhite with areas
of haemorrhage and necrosis.
Hallmarks of microscopic picture of the usual osteosarcoma are the sarcoma cells
characterised by variation in size and shape of tumour cells, bizarre mitosis and multinucleate
tumour giant cells, and osteogenesis i.e. production of osteoid matrix and bone directly by the
tumour cells.

167
Osteochondroma
Osteocartilaginous exostosis, upper end humerus. The amputated head of the long bone
shows mushroomshaped elevated nodular areas. These nodules have cartilaginous caps
and inner osseous tissue.
The overlying cap shows

mature cartilage cells
covering the underlying
mature lamellar bone
containing marrow spaces.

168
Giant cell tumour (osteoclastoma).
The end of the long bone is expanded in the region of epiphysis. Sectioned surface shows
circumscribed, dark tan, haemorrhagic and necrotic tumour.

169
④EET 2020J Q. Identify Liposarcoma?

Liposarcoma
The tumour shows characteristic, univacuolated and multivacuolated lipoblasts with bizarre nuclei.
Inset in the right photomicrograph shows close-up view of a typical lipoblast having
multivacuolated cytoplasm indenting the atypical nucleus.
Ewing’s sarcoma
Characteristic microscopic features are irregular lobules of uniform small tumour cells with
indistinct cytoplasmic outlines which are separated by fibrous tissue septa having rich vascularity.
Areas of necrosis and inflammatory infiltrate. Inbox in the right photomicrograph shows PAS
positive tumour cells in perivascular location.
170
Hematology
Blood collection tube
EDTA- ethylenediamine tetra acetic acid

Used for routine blood test
- CBC-Hb, TLC
- PS
- ESR by wintrobes method
- Reticulocyte counts
It acts by chelating on calcium molecules
1.50- 2.2 mg/ml
Di potassium salt - Ideal
K2EDTA
Liquid
To easily differentiate hematology from blood bank specimens
Each has a specially designed cross match label for required American
Association of Blood bank (AABB) patient identification.
Pink colour vial for blood banking
[AIIMS 2018,2020T Q. Identify the tubes and

anticoagulant used?
Pearly white top
This tube contains EDTA and a special

polyester material
Used for the collection of plasma for
molecular (PCR) tests.
171
Dark green top tube (sodium heparin)

Lithium or sodium salt
0.2mg/mL of blood
Viability of 48 hrs
Used in:
- Best tube for Flow cytometry
- Osmotic fragility test
- Blood gas analysis
- Immunophenotyping
It gives blue background for wright, s stain smears
Grey top tube

(potassium oxalate/ sodium fluoride)
Quantity-2mg/ mL
Anticoagulant - Potassium oxalate
Used for blood sugar estimation since it inhibits enslave enzyme in glycolysis
Most specimens are preserved at 25 C for 24 hours and at 4 C for 48 hrs
After the tube has been filled with blood , immediately invert the tube 8-10 times to mix
and ensure adequate anticoagulation of the specimen
172
Red top tube

Plastic
Serum vial
Clot activator but no gel
5-6 inversions
Clot time- 60mins
Used for
- Chemistry,
- Serology,
- Immunohematology
Black top
Only for ESR by westergrens
Blood in 1:4 ratio
3.8% of sodium citrate
Action : removes calcium
Gold top tube

Serum separator tube
This tube contains a clot activator and a serum gel separator
Used in
- Biochemistry
- Vit B12 and folate assay
Blood clotting time : 30mins
173
Yellow top tube
Acid citrate dextrose
Used for the collection of whole blood for special tests
- HLA Phenotyping,
- DNA isolation
- Paternity testing
It also contains Sodium polyanethole sulfonate (SPS) - most
common anticoagulant used in commercial blood culture bottles
Draw of blood
Order of blood collection Heparin tube is avoided in genetic testing
Blood culture tube or vial
Citrated tube for coagulation
Serum tubes with or without clot activator,

with or without gel separator
Heparin tube
EDTA tube
Glycolytic inhibitor
174
ESR Determination
Longer tube is better for ESR
EDTA- wintrobe tube due to more sedimentation
Smaller tube
110m long with an internal bore diameter of 3 mm.
The tube is closed at one end.
Tube is graduated on both sides from 0-10
in ascending and descending order
ESR and PCV can be tested
Layers in the wintrobe’s tube after centrifugation
- Plasma layer
- Buffy coat (WBC& Platelets )
- Packed RBC’s (hematocrit)
CITRATE- Westergren’s tube

Open at both ends
Length is 30cm
Internal bore diameter - 2.5mm
Can hold about 1 ml of blood
Calibrated from top to bottom: 0- 200mm
Stages of RBC settle

Rouleux - 10mins
Normal Fall- 0-15mm/hr
Sedimentation - 40 mins
Packing - 10mins Fibrogen Rouleux formation ESR
ESR ESR Important diagnostic criteria- ESR level

- Afibrinogemia - Multiple myeloma Temporal arthritis prognosis
- Polycythemia - A/c phase reactants
- Sickle / Spherocytes - Fever
- Viscosity - Inflammation/ infection
175
PLATELET COUNTING
REES AND ECKER DILUTING FLUID
Composition
Trisodium citrate - 3.8gm
Brilliant crestless blue - 0.1gm (stain platelet)
[All NIS 2020]
40% formalin- 0.2 ml
Distilled water- 100ml Q. REES AND ECKER
DILUTING FLUID is used
for counting?
Final pH- at 25 C. - 6.8-7.0
WBC COUNTING
TURK FLUID
Composition
Glacial acetic acid- lyse RBC
Gentian violet (1%)- stain WBC
Distilled water
RBC COUNTING
No stain
DACIE fluid HAYEM FLUID
Composition Composition
Trisodium citrate- 3gm Sodium chloride - 0.5gm
Formalin - 1ml Sodium sulphate- 2.5gm
Distill water - 99ml Mercuric chloride- 0.25gm
Distilled water - 100ml
Commonly used
Thoma pippette
176
Thoma pippette
RBC Pippette
Red beaded tube
Marking will be till 101
Used for RBC and platelet counting
Larger counts
Size of bulb is larger
Size of lumen is smaller
WBC Pippette
White beaded tube
Marking will be at 11
Used for WBC counting
Smaller counts
Size of bulb is smaller
Size of lumen is larger
In leukaemia , due to large counts RBC count is used to count WBC
Neubauer chamber
Peripheral cells- WBC counting
Central smaller cells - platelets
Thick cover slip- depth of chamber should be 0.1mm
Includes:
- Neubauer’s slide
- cover slip
- RBC Pipette
- WBC pipette
177
RBC counting WBC Counting
N x 200 (DIL) x 50 (1/5 x 1/5 x 0.1) x 5 N x 20 (DIL) x 10/4

N x 10,000 N x 50
No. Of cells in neubeaur chamber=

N x dilution factor x Volume of chamber in which cells counted
Fixatives
Keeps morphology as in body
Heat- used earlier
Chemical
Coagulant
- coagulation of proteins
- Cytological fixated- Pap smear
- eg:- Alcohol, acetone
Cross linking
- eg:- Aldehydes, metal salts
Compound Examples of cross
- eg:- alcoholic formalin linking fixative ? [AIIMS 2020J
Best histological fixative

- 10% buffered neutral formalin
(pH - 7.2- 7.4)
Frozen section
Cryostat machine - releases liquid nitrogen - freezes specimen
Can be done on formalin fixed tissue
Formalin fixative
Very good penetration 1mm/hr
Irritant to nose and eyes
Subsequent use of most staining procedures can be done
Produces black pigment in tissue due to improper pH.
pH should be monitored
178
Saccomano fixative
- 50% ethanol + 2% carboxylase
- Used in cytology (fluids and specimens)
Carnoy fixative
- Used in hemorrhagic fluid to lyse RBC
- Used in karyoptyping
Ethanol : Chloroform: Glacial acetic acid
6:3:1
Bouins fixative
- yellow color
- Contains
}
Picric acid
Acetic acid Compound fixative
Formaldehyde
- Testicular biopsy are usually fixed in Bouins , very fragile
- Used in Cell block- converted cells into histopathology specimens
Cytology
Types of cytology samples
Aspiration cytology Body fluids Exfoliative cytology
- Needle aspiration - CSF, pleural fluid - Cells are shed naturally
Eg: FNAC Eg:-Bronchoalveolar Lavage, Pap smear
Aspiration cytology
FNAC
Fine needle aspiration cytology
FNNAC
Fine needle non aspiration cytology
Vascular lesion eg: thyroid
179
BODY Fluids
Saccomano fixative
Sputum
Mucus Bronchial aspirates 12 -24 hrs if refridgerated
Mucocle fluid
Pleural 24 - 48 hrs without

Protein Peritoneal refridgeration
Pericardial
Urine 1 - 2 hrs delay even if

Low mucus
or protein Csf refridgerated
Squash smear- used for CNS samples

Squash and then speard the cells
Exfoliative cytology
Pap smear
From squamocolumnar junction
Layers of CERVIX
Basal cells
- Never shed , does not come in Pap smear
Parabasal cells
- Rounded cell
- Never respond to hormones
- Usually seen in menopause
SQUAMOUS CELLS
Polygonal cells
-
Superficial squamous cells
- Top most polygonal cells
- Respond maximum to estrogen
- Pink in colour
-
Intermediate
- Polygonal cells between superficial cells and parabasal cells
- Respond maximum to progesterone (pregnant)
- Greenish - blue color
180
INTERMEDIATE CELL
SUPERFICIAL
SQUAMOUS CELL
PARABASAL CELLS
Seen in menopausal age group
Granuloma cell tumour of ovary
Estrogen secreting tumour
Metastasis to other ovary
Presence of superficial squamous
cells in menopausal age group
Columnar cells
- Arranged back to back
- Picket fence manner
Adequate Pap smear

5000 cells/10 HPF in
8000-12000 squamous cells for conventional PS/10 HPF
liquid based cytology
10 endocervical cells
Lactobacillus
181
Leptothrix
- Long version of lactobacillus

- May have tricomonas infection
Sickle like cells in

GI biopsy - Giardia
human papillomavirus
Koilocytes
Superficial cells with larger nuclei
And halo surrounding it
Raisinoid nuclei
Cytomegalovirus
Both nuclear and cytoplasmic inclusions

Nuclear inclusions surrounded by halo
182
Herpes simplex virus
Multinucleate intermediate squamous cell
Moulding of nuclei
Margination - big infusion in center , normal
chromatins pushed to periphery
Pink colour intranuclei Cowdry type viral inclusions
Bacterial vaginosis
Clue cells
Vaginal epithelial cells that
have bacteria adherent to
their surfaces
Absence of lactobacillus
Actinomyctes
Cotton wool appearance
Common in IUCD users
Tadpole cells
Orange color cell
Well differentiated squamous cell carcinoma
Candida
Small , uniform , round budding yeast
Liquid based cytology for identifying small candida
183
Liquid based cytology

Thin prep
Sure path
Techniques of Conventional Sure path

Thin prep
pap smear papanicolaou
Fixation Ethanol Methanol Ethanol
Collection device
Collection Sample rinsed in vial left n vial
Smear on slide
Ayer spatula Using Cervical
broom
Uniform
Cell sample
Random distribution Uniform distribution
distribution over
over 13mm of slide
20 mm of slide
184
Shush kebab effect
Spores and pseudohyphae appear as piercing each other
Candida in liquid base cytology
Staining of pap smear

Fixative: 95% ETHANOL
Q. Fixative used in Pap smear?
STAINS
Nuclear staining: Hematoxylin
Cytoplasm staining : Orange G
Eosin Azure( Eosin Y, Light green, Bismarck brown Y)
FIXATION USING ETHANOL
NUCLEAR STAINING USING HEMATOXYLIN
CYTOPLASMIC STAING USING OG AND ea
Dehydration by alcohol
Clearing by xylene
Mounting by DPX
Mirotome- produce slides
DONE IN HISTOPATHOLOGY
Impregnation by paraffin wax (Instead of moulding)
Embedding - block
185

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Pathology

II Haematology and lymphoreticular tissue

III Systemic pathology

Programmed Non programmed

Apoptotic cells are round to oval shrunken

Leads to leakage of pro-apoptotic proteins from

Initiator caspase: Caspase 8,10 Initiator caspase: Caspase 9

Executioner caspase : Caspase 3,6,7

TRALI Fas ligand

Bind to APAF-1 Binds and neutralise IAP’s

Wheel like hexamer(apoptosome)

Activation of effector caspases(caspase 3 and 7)

Morphological features of apoptosis

Primarily by bcl-2 family of genes Located on chromosome 18

1. Endometrial cells (Menstruation) 1. Councilman bodies: Viral hepatitis

Activates Caspase 1 and 11 Neet 2019

Also activates IL -1 fever

in cytoplasm of host cell Iron-dependent pathway of in recognition and

massive lymphadenopathy peroxidation.

Nuclear changes appear in one of three patterns,

– Combnination of coagulative and liquefactive necrosis

Viable lymphoid Granulomatous

Mixed inflammatory cells

heart disease) and malignant hypertension.

Necrosis of tissue with superadded putrefaction

Definition Deposits of calcium salts in Deposits of calcium salts in

Reversibility Generally irreversible Reversible upon correction

Increased binding of phosphates with Increased precipitates of calcium

Dystrophic calcification in degenerated

Metastatic calcification in tubular

Commonly Used Stains

Amyloid Congo Red, Thioflavin T (for JG apparatus

Calcium Von Kossa, Alzarine Red

Trichrome Collagen appears blue

Basement membrane/ collagen Periodic acid-Schiff (PAS), Reticulin

Mucin (in general) Combined Alcian blue-PAS

Lipofuscin granules in cardiac myocytes Compound naevus showing

Reversible change of one type of epithelial or

Physiologic hypertrophy of the uterus during pregnancy.

Hyperplasia of both fibromuscular elements

Metaplasia of columnar epithelium (left) to squamous epithelium (right) in a bronchus

Squamous metaplasia of the

Part of the endocervical mucosa is lined by

Columnar metaplasia oesophagus

Part of the oesophagus which is normally lined

Shows increased number of layers of

Result of a progressive decline in cellular function and viability caused by genetic

Immunopathology Including Amyloidosis

- Multi-lobed nuclei typically consisting of 3 to - Small lymphocytes have spherical

- Monocytes are 12 to 15 µm in diameter

- Basophils are bi-lobed or S-shaped nuclei

Inadequate or ineffective granulopoiesis

Accelerated destruction or sequestration of neutrophils

The most common cause of

Pan B cell Pan T cell markers

Neutrophil RECRUITS ALL WBC RECRUITS ONLY Chemotactic

Exogenous pyrogens Lipopolysaccharides (LPS) of barterial walls

HLA SYSTEM AND MAJOR HISTOCOMPATIBILITY COMPLEX

Identified by B cells and