Pathology DK

ORR PART 2
GENERAL PATHOLOGY
CEREBELLUM ORR PATHOLOGY

CELL INJURY

• ATROPHY
• HYPERTROPHY
• HYPERPLASIA
• METAPLASIA

NECROSIS

COAGULATIVE NECROSIS

LIQUEFACTIVE NECROSIS FAT NECROSIS

CASEOUS NECROSIS

IDENTIFY the subtype of NECROSIS !

ONE Liners!
• Physiological / pathological
• Inflammation is absent / present
• Rapid phagocytosis of apoptotic cells due to

C1q and phosphatidylserine is called
…………………………………………………
• Annexin………is a marker for apoptosis.

ANOIKIS Caspase independent cell death/ programmed
necrosis
NECROPTOSIS Cell cannibalism with LC -3 as a marker
PYROPOPTOSIS Cell death due to loss of adhesion between cells
AUTOPHAGY Iron dependent free radial injury having loss of

mitochondrial cristae and damage of outer
mitochondrial membrane
FERROPTOSIS Formation of inflammasome and caspase 1/11
activation leading to fever
PIGMENTATION

Commonest pigment………

• A chronic alcoholic patient presented with
increasing abdominal girth and decreased liver
span. Liver biopsy featuring hepatocytes with
reddish inclusions?
Cryostat

• Sweet reticulin (collagen III) stain

Glycogen, fungal cell wall, mucin and basement membrane
PAS PAS-D

Categories of chemical fixatives
• Coagulant fixative (dehydrants): ethanol, methanol, and

acetone
• Cross linking fixative: formaldehyde, glutaraldehyde &

osmium tetroxide.
• Compound fixative: alcoholic formalin

INICET SPECIAL! (Review of Pathology)
• Efferocytosis: The capture and deletion of dying cells by

efferocytosis, is present to prevent the build-up of cellular debris.
• Emperipolesis: it is the movement of live cells following
internalization (“inside-round-about wandering”). Seen in
autoimmune hepatitis and Roasai Dorfman disease.
• Entosis: is the invasion of a living cell into another cell's
cytoplasm. There is active involvement of invading cells, which
does not happen in other forms of cell engulfment. It selectively
targets living cells, excluding dead cells or non-living material
such as cell debris. After internalization, engulfed cells are killed
by the host cell.
• Enclysis: a term used to indicate live CD4+ T cells being captured
by hepatocytes.
INFLAMMATION

Vascular changes

Endothelial cell Immediate transient Thorn prick
contraction response
Direct endothelial cell Immediate sustained Severe burns,
injury response septicemia
Endothelial cell Delayed transient Cytokine

retraction Response mediated injury,
hypoxia,
Bacterial
infections
Endothelial cell Delayed prolonged Late developing

damage response sunburn &
radiation
Sequence of cellular events

• Septicemia leads to Platelet
activation
• Activation of
……………………………….
(which converts arginine into
citrulline)
• Release of neutrophils
contents outside
• Bacteria being trapped
• High risk of …………………….
• Mitochondrial DNA not

involved
Chemical mediators
• Preformed mediators
• Freshly formed mediators

Cytokines
• IL 1
• IL 2
• IL 3
• IL 4
• IL 5
• IL 6
• IL 7
• IL 8
• IL 9
• IL 10
• IL 11
• IL 12 CEREBELLUM ORR PATHOLOGY
KININ SYSTEM

Quick One Liner Recap!
• The tissue factor that is released during
endothelial injury combines with factor
…………………to initiate the coagulation cascade.
• In pregnancy, coagulation factor/s ……………
decreased.
• A patient admitted in ICU on warfarin treatment
would have decreased gamma carboxyglutamate
residues of factors…………………………………………..
• Deficiency of clotting factor ………..does not
affect clotting in-vivo.
Chronic inflammation

Wound healing
• Myofibroblasts
• Granulation tissue
• Strength of wound healing

IMMUNITY

• T cell: B cell ratio in peripheral blood……………..
• CD markers for T cell………………………………..
• CD markers for B cell…………………………………
• CD markers for NK cell…………………………….
• CD 41/61……………….
• CD 45RO…………………

Professional APCs
Non professional APCs

• Fibroblasts of Skin
• Glial Cells in brain
• Pancreatic Beta Cells.
• Thymic Epithelial Cells
• Thyroid Epithelial Cells
• Vascular Endothelial cells
MHC molecules & T cell interaction

Type I Type II Type III Type IV
Name
Antibody
involved
Examples

• Hyperacute
• Acute
• Chronic

GVH Disease
• Acute GVHD
• Chronic GVHD

Disease Antibody
SLE with neonatal lupus Anti histidyl aminoacyl-tRNA

synthetase
SLE with APLA syndrome Anti Ro antibody
Rheumatoid arthritis Anti RNA polymerase
Dermatomyositis Anti beta 2 glycoprotein antibody
Systemic sclerosis Anti U1-RNP
Mixed Conn Tissue disorder Anti citrullinated antibody

Disease Features
Bruton’s disease Anaphylaxis on bld transfusion
Common Variable Small sized platelets with skin
Immunodeficiency Disease rash
Ig A deficiency Eczema and coarse facies with
retained primary teeth
Hyper IgM syndrome IL-2R, JAK3 and ZAP 70 mutation
Job syndrome Reduced Ig in both M/F with
normal B cells in blood
Wiskott Aldrich syndrome CD 40-CD40L defective
interaction
SCID BTK defect
Amyloidosis

NEOPLASIA

Characteristics
• Metastasis
• Rate of growth
• Invasion
• Anaplasia

Role of genetic mutations
• Proto-oncogenes
• Tumor suppressor genes
• Dysregulation of apoptosis
• Defect in gene repair

Q Protooncogene to oncogene transformation
occurs by:
• Amplification
• Promoter
• Enhancer insertion
• Point mutation.

Special points!
• Warburg effect: glucose hunger
• Oncometabolite formation

Reason for Warburg effect!

Carcinogens

Microbial carcinogenesis..20th book

• CML/ALL/Alv RMS/Myxoid liposarcoma
t(9;22)……………………….
t(12;16)……………….t(2;13)…………………
CEREBELLUM
STANDARD MARKERS ORR
GIVENPATHOLOGY
IN THE 20TH BOOK
IMMUNE CHECKPOINT INHIBITORS

• Tisagenlecleucel for B-cell ALL
• Side effect: Cytokine release syndrome
CEREBELLUM PATHOLOGY ORR

HEAMATOLOGY

Match the following!
AGE SITE
 Adult and children  ASIS
 Obese adult  TIBIA
 Infants  PSIS

• Variation of the individual shape of the RBCs is
………………………….
• Anisocytosis is calculated with the help of
…………………………………………..

• Identify the cell and name the best stain for
the same………………………..

IMPORTANT FACTS AT A GLANCE!

NORMAL SMEAR

Very important !

Microcytic Hypochromic Cells with clinical history

Iron profiles in different conditions
IDA AOCD THAL. TRAIT SIDEROBLASTIC
ANEMIA
SERUM
FERRITIN
SERUM IRON
%TRANSFERRIN
SATURATION
TIBC
SPECIAL TESTS
MENTZER INDEX
GENETIC
TESTING
S TFr Ratio
Log Ferritin
INICET ONLY!

QUICK RECAP!
B12 DEFICIENCY FOLATE DEFICIENCY
Neurological
symptoms
Serum MMCoA
Methylmalonyluria
Serum Homocysteine
Special points

Thalassemia

Beta thalassemia : gene
5 most common genetic mutations in India are
IVS 1-5 (G>C), 619bp deletion, IVS 1-1 (G>T),
Codon 41/42 and codon 8/9
Alpha thalassemia : gene deletion

3.7 deletion >>> 4.2 deletion

• MENTZER INDEX

HbH inclusions

Q A 25-year-old pregnant woman presents with
fatigue and abdominal pain in the emergency
room. She reports feeling unwell for the past
few days. Every morning, she notices that her
urine is tea-colored, which slowly resolves
throughout the day. She has a low-grade fever.
On physical exam, her skin is jaundiced, her
liver edge is palpable, and she has abdominal
tenderness to palpation. Her physicians are
suspicious of Budd-Chiari syndrome.
MAHA

WHITE BLOOD CELLS

Differentiation!

L

L

POPCORN CELL

ANAPLASTIC T -CELL LYMPHOMA

Alibert-Bazin disease

Diagnostic criteria for plasma cell myeloma
Clonal bone marrow plasma cell percentage ≥10% or biopsy-proven
plasmacytoma and ≥1 of the following myeloma-defining events:

Harrison 21st

LCH

HEMATOLOGY 3

20TH BOOK

TEG

TEG PATTERNS

SYSTEMIC PATHOLOGY

RENAL SYSTEM

Glomerulopathies
Nephritic syndrome
Nephrotic syndrome

PSGN

SUBEPITHELIAL HUMP

RPGN

• 40 year old female with arthralgia, painless
oral ulcer, oliguria, hematuria and urine RBC
casts is likely to be suffering from ………………..

BERGER DISEASE

ALPORT SYNDROME

Goodpasture syndrome

MINIMAL CHANGE DISEASE

Special silver staining!

MPGN I MPGN II
Classical and alternate pathway Alternate pathway activation
activation
Absent C3NeF present
Subendothelial immune Intramembranous immune
complexes complexes
(C1/C3/C4,IgG) (only C3 deposition)
Tram track/Double contour Dense deposit disease
appearance

MPGN
• Idiopathic
• Secondary
 Infections (HIV, HBV, HCV, Malaria, Toxoplasma)
 CLL
 Antitrypsin deficiency

MPGN I

MPGN II

FSGS

Idiopathic FSGS
Secondary FSGS
• HIV-associated nephropathy
• Heroin nephropathy
• Sickle cell disease
• Morbid obesity
• IgA nephropathy
• Unilateral renal agenesis or renal dysplasia
• Reflux nephropathy,
• Hypertensive nephropathy
Diabetic Nephropathy

• MC

• Papillary structure and Psammoma bodies present
• Multifocal, B/L and maximal angioinvasion
• Associated with trisomy 7 (Sporadic and familial) and
loss of chromosome Y in sporadic Variant.
• Long term Dialysis associated RCC variant
• Overall Best prognosis
• Associated with Birt Hogg Dube syndrome
• Shows extreme hypodiploidy
• Microscopic appearance: Nest like appearance of
cells with peri-nuclear halo
ONCOCYTOMA

Nephrolithiasis

MALAKOPLAKIA

GASTROINTESTINAL TRACT

Meckel’s diverticulum

HIRSCHPRUNG DISEASE
• Failure of migration ………………………………….. in

intestine (MC ……..) is the embryological basis.
• Male child with failure to pass meconium and
also has abd. distension. Suction biopsy is done!
BARRET ESOPHAGUS

Barret’s progressing to cancer

CMV esophagitis

Achalasia cardia
• Due to the selective loss of

………………………………………………….at the lower
end of the esophagus
Esophageal cancer

Esophageal Adenocarcinoma

Warthin silver stain for ?

Gastric cancer
Diffuse type Intestinal type

GIST

TB Typhoid

Pseudomembrane colitis

Whipple disease

Celiac sprue
 Infant who was recently weaned from breast

milk presented with malabsorptive diarrhea and
failure to thrive.
 Biopsy from ……………….revealed villous atrophy,
crypt hyperplasia and CD8+ cell infiltrates in
lamina propria.
Giardiasis

Crohn disease: skip lesions

Cobblestone mucosa

Creeping fat

Crohn’s histology

String sign of Kantor

Ulcerative colitis

Pseudopolyps

Ulcerative colitis

Crypt abscess

“Lead pipe” appearance

Hyperplastic polyp: benign polyp (L colon)

Juvenile polyp
• ………….with ………………….
• Polyp has cystically dilated glands which are
filled with mucin, inflammatory cells in lamina
propria
Peutz Jegher polyp
• GI polyps in ……………..
• Can initiate
intussusception
• M/E: smooth muscle is
seen extending into the
lamina propria epithelial
layer in
………………………………...
• Multiple GI hamartomatous
polyps
• Increased risk of multiple
cancer
• Mutation affects…………….
Cronkhite Canada syndrome
• GI hamartomatous
polyposis
• Alopecia
• Onychodystrophy,
• Hyperpigmentation
• Diarrhea

Adenoma

• HNPCC synd
Defective DNA repair
……………………………
• FAP synd
…………………………..

Colon carcinoma
May present as CUP

• ………….......................... (breakdown product
of serotonin) appears in urine in carcinoid
tumor.

RESPIRATORY SYSTEM

• MC lung injury in a patient with COVID 19 is
……………………………………………………………
• A middle aged female who was on ventilator

died due to COVID-19. The expected
histological finding on her post mortem is
………………………(thick fibrin lining alveoli)

 Endothelium (B) shows swelling and vacuolization in
COVID-19 infection.

Typical

Plexiform lesions in PAH

SILICOSIS

ANTHRACOSIS

PLEURAL PLAQUES

ASBESTOS BODY

LUNG CANCER: SQUAMOUS CELL
KERATIN
PEARLS
P63 +

ADENOCARCINOMA OF LUNG
TTF POSITIVE
IMMUNOSTAINING IN
INSET
GLAND FORMING TUMOR

CELLS

SMALL CELL LUNG CANCER
SMALL DEEPLY
BASOPHILIC CELLS
HAVING NEITHER GLAND
FORMATION NOR
SQUAMOUS PATTERN
BASOPHILIC STAINING OF
VASCULAR WALLS FROM
NECROTIC TUMOR CELLS:
AZZOPARDI EFFECT
HIGH EXPRESSION OF BCL-2; NEUROSECRETORY GRANULES IN TUMOR CELLS

LARGE CELL CANCER
LARGE PELOMORPHIC
CELLS: DIAGNOSIS OF
EXCLUSION

ADENOCARCINOMA IN SITU

Seborrheic keratosis

Adenocarcinoma Malignant mesothelioma

Pulmonary Hamartoma

SYSTEMIC PATHOLOGY-2
ENDOCRINOLOGY
• A middle aged female presents with painless thyroid swelling. Her
TSH levels were elevated. Biopsy revealed lymphocytic infiltrates and
Hurthle cells. What is the likely diagnosis?
• A middle aged female presents with painless thyroid swelling. Her
TSH levels were reduced. Biopsy revealed papillae formation and
scalloping of the colloid. What is the likely diagnosis?
Thyroid cancers
Q A 20-year-old female with thyroid mass whose histology revealed
orphan annie eyed nuclei. The diagnosis is………………………….
Nuclear features >>> papillae formation
• Thyroid cancer with increased serum calcitonin………………..
• Thyroid cancer arising from parafollicular cells……………………
• Thyroid cancer with RET gene mutation and so, advised prophylactic
thyroidectomy……………………….
MTC
Pheochromocytoma
CVS
MYOCARDIAL INFARCTION: Coagulative
necrosis
MI: Macrophage and Granulation Tissue
REPERFUSION INJURY
Special staining: TTC
RHEUMATIC HEART DISEASE
CARDIAC VEGETATIONS
CARDIAC VEGETATIONS
LIBMAN SACK ENDOCARDITIS RHEUMATIC HEART DISEASE
CARDIAC VEGETATIONS
INFECTIVE ENDOCARDITIS MARANTIC ENDOCARDITIS
HOCM……
DILATED CARDIOMYOPATHY
DCM
• NINJA STAR hyperchromatic

nuclei
• Associated with…………………
mutation”
CARDIAC TUMORS
RHABDOMYOMA
TEMPORAL ARTERITIS
TAKAYASU ARTERITIS
KAWASAKI DISEASE
BUERGER DISEASE
ANCA
MPO-ANCA PR3 ANCA
WEGENER’S GRANULOMATOSIS
MONCKEBERG SCLEROSIS
ANEURYSM
Raynaud Phenomenon
CNS Tumors
SCHWANNOMA
Verocay body
Glioblastoma multiformae
Oligodendroglioma
• Frontal lobe tumor with calcification
• “Fried egg appearance” of tumor cells
• Perineural satellitosis +
• Chicken fence capillaries also seen
Meningioma
• MC primary benign brain tumor in adults is meningioma.
• F>>>M, has PR +
Pilocytic astrocytoma
• Most common primary benign tumor in children
• Arises as a cystic mass in cerebellum
• Microscopically,
a. Projections arising from bipolar cells.
b. Rosenthal Fibres: Presence of hair like, cork-screw shape
eosinophilic fibers
Medulloblastoma
Homer wright pseudorosettes
Primary CNS lymphoma
• Primary CNS lymphoma develops in immunosuppressed patients
• Usually it is a Diffuse large B cell Lymphoma
• Hooping is present

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ORR PART 2

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

• Rapid phagocytosis of apoptotic cells due to

CEREBELLUM ORR PATHOLOGY

PYROPOPTOSIS Cell death due to loss of adhesion between cells

AUTOPHAGY Iron dependent free radial injury having loss of

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

• Coagulant fixative (dehydrants): ethanol, methanol, and

• Cross linking fixative: formaldehyde, glutaraldehyde &

• Compound fixative: alcoholic formalin

CEREBELLUM ORR PATHOLOGY

• Efferocytosis: The capture and deletion of dying cells by

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

Endothelial cell Delayed transient Cytokine

Endothelial cell Delayed prolonged Late developing

CEREBELLUM ORR PATHOLOGY

• Bacteria being trapped

• High risk of …………………….

• Mitochondrial DNA not

• Freshly formed mediators

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

• Strength of wound healing

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

Non professional APCs

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

SLE with neonatal lupus Anti histidyl aminoacyl-tRNA

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

CEREBELLUM ORR PATHOLOGY

 Adult and children  ASIS