How to study Pathology

'
Areas to focus
her patmet put

- ±-♂

IBQ’s - Thumb Rule

→ IMAGE
→ options
⇒ H10

⇒ DNA, RNA
Blue
⇒ REST
pink
FAT
clear ⇒
\ I
Silly mistakes to avoid!!
40' guns
⇒ ?

Areas not to focus !!

- MIC
- one lines
most spec,
→ most seem

Cellular Adaptation and Injury

cell
STRESS
 U
Reversib
k types

← STR Ersis tent

cell injury

Hyperplasia:

⑦↑ cell number
Definition:
(cells → which can divide)

of stem cells
meds : stimulation

Physiological: Menstrual

Endometrium - Proliferative

Estrogen"

c Persistent
Pathological: estrogen

Etiology

1) An Ovulatory cycle
(Puberty)
Hyper - 2) PLOD
- estrogenism 3) Granulosa cell tumor

4) Obesity

MT gland division - menorrhagia

Symp

⟂
Mx ⇒ ↑↑ number
of glands
 stress not removed
obesity

↑↑ risk → Endometrial
adeno carcinoma

Neoplasia Risk ?? --- YES

endometri
N

Ends "hyperplasia

① AT Gland: Strome
ratio

Hypertrophy
n cell size
Definition:
I TT MRNA → 7Th
mech protein

Physiological:
Skeletal muscle Hypertrophy
⇒
⇒ Body builder

meteor"
 Pathological:
CARDIAC
MUSCLE

(MT work DONE)

After load

Pre load Left

ventricle) TPR
⟂
Blood pressh
EDU
'pressure'
Volume"
systemic HT
Aortic regurgitation

✗ ① y
s
APICAL
concentric
Eccentric cardiac
cardiac Hypertrophy
↓ ↓ ↘"
Hypertro ph

NO RISK
Neoplasia Risk -

Hypertrophy
Both
along ⇒
& Hyperplasia
Pregnancy

→ Pregnancy, Puberty
Breast
 ① ② to pink

Metaplasia
mature epithelium
Definition: Adult

adult mature epithelium

stem call
Mechanism: Reprogram

GERD
Barret’s Esophagus:

AN acid 'esophagus'
⑧ - squamous
⟂
Need to neutralize acid

MUCIN secretion
changes to
Name
columnar epithelia
⇒ Intestinal metaplasia ×
⇒ COLUMNAR LINED OESOPHAGUS (LO)

⇒ Goblet cell metaplasia

Glandular metaplasia
⇒

Gross (stratified)
⇒ Pale
N

Red → (single layer)

Colum ⇒

Red velvet like mucosa

BE ⇒

⇒ screamo- multiple layer

Mt
column ⇒ Glands

Neoplasia risk -

① -sque

2 Colum

I → scream

Gland
Z

Spl stain mucin- clear

↓
 mucin
Alcian Blue acidic

Respiratory mucosa:

N - ciliated
I smoke destroy
cilia

changes- to squamous
Mlc -metaplasia 1 SMOKER persistin

Squamous cell carcinoma

other: - Vita A → Bitot spob

- myositis ossificans → mesenchyme

Atrophy - A- trophy → Gross term

-

Definition: ↓ cell number a size.

Causes:
→ Ischaemia

⇒ muscle atrophy
→ PEM

⇒ ulnar nerve
⇒ Denervation
palsy ⇒ Flat
Hypo Kenar

Post # ⇒ POP cart

→ Disuse ⇒
limb-becomes
small

Post menopausal ⇒ Endometrial

⇒
atrophy
(Irreversible)
 compresses @as
↓
symptoms

BOTH
Reversible or not ?
CAN ⇒ esp. endometrial
Neoplasia risk ? atrophy

Mechanism: AUTOPHAGY

Need to reduce
+ ↓ ATP
Golgi
2

10 golgi Lysosome

Removes excess
organelles

Retain the cellular

Lipofeesahib
debris
⇒ wear & Tear
• BROWN
⇒ cell aging /injury
- Para-nuclear
 µW D

*
v8

Cell Injury: Mlc- Ischaemia

↓ ☑ ATP

↓↓ Nat kt ATPase

•
Na accumulation

HL0 retained

l 1ˢᵗ Light MX
⇒ cellular swelling
② Fatty change
spongiform, vacuolar
+↓ th, esp Liver
Ballooning. Cloudy
swelling

Electron Mx:

l swollen ER

2 Detach Ribosomes
④ myelin figure
☁
→ Damaged PL

Amorphous density of mitochondria

5

reversible 2 irreversible.
Both

↑↑ intracellular Caat
Irreversible process !
(Point of no
return)

activates enzymes

Destroys membrane.
⇒
Phospholipase

Release intracellular content out

n
⇒ ☐ es. Troponin in mi
 almost always
Pathological.

Protease activation

s Destroys protein ⇒ Intense

eosinophilia"

Nuclease

much Nuclease Karya-there's

Nuclear
- pyknosis
⑤
Karyolysis

→ PINK
NECROTIC TISSUE
Types of necrosis
Coagulative Liquefactive
- MIC → BRAIN infarct

- All solid organ → Acute pancreatitis

infarct
Abscess cavity,
→
wet gangrene.
Meek - Protein
meds - Lysosomal
degradation
activation

⇒ Architecture
⇒ Architecture
lost
maintained

(less force)

Ghost cells ⊖
GHOST cells ⊕
 Necrotic → architecture
maintain

- Gross term
Caseous Necrosis

↳ cheese like.

- Granular variant'
Mx ⇒
lipid content of TB'

Etiology ⇒ TB

His to plasma,
⇒
cocci didio my costs
 Granular

O id = Like.
Fibrinoid Necrosis
necrosis
vessel wall
⇒

vasculitis
Causes:
: Type II HS - SLE

: malignant HT

vessel

fibrinoid

✓ 11-15
Fat Necrosis

Traumatic
Enzymatic

any tissue
Acute Pancreatitis
rich in fat
Liquefactive)
⟂
necrosis
Lipase released

⟂ Any necrosis
FAT ⟂
- Peri pancreatic fat
necrosis can cause
- Omentum calcification

Breast → Trauma 7
Group of cell
MACRO
CALCIFICATION
 APO- PTOSIS
Apoptosis

Physiological Pathological

⇒ Embrological → VIRUS
⇒ webbed fingers
⇒ webs destroyed → DNA mutation

⇒ Thymus → self reacting

lymphocytes → Intracellular protein
accumulation
⇒ Endometrium atrophy

OVERVIEW OF APOPTOSIS

Execution
Initiator

cell membrane.
(Extrinsic pathway)
CASPASE )
caspase 8,10 3,6

mitochondrial mediated

(Intrinsic pathway)

[ CASPASE 9 ]
 infection
Extrinsic Pathway Of Apoptosis viral

FAS
F- ADD Associated
cell
virus FAS receptor Death
CD95)
Domain
n FAS ligand
CP8
Pro-caspase
Active 8110
8,10

Intrinsic Pathway of Apoptosis

Basic Gene Groups
Anti Pro Sensors of cell
I'- Long life. stress
BAX, BAK BID, BAD, BIM
B CL2
Puma
Mcl - l
Note
BCL ✗ s
BCC XL
Normal cell ↓⟂ Cytoplasmic
☒ CL2
exit of
☑ cytochrome C
•

• I cytochrome C

(mic pathway
DNA mutation
After Stress intrinsic'

TT sensors of cell
stress
(BIM)

⟂
Destroys B CL2
Activate
BAD 2 BAK
F

exit of + A PAR-I
Promote
to cytoplasm (Apoptosis Activating
aft-c
factor)

Apoptosome

caspase 9
Pro caspan
9
 Intrins
Extrin

Cysteine containin
CASPASE
protean

⟂
Cleaves after

aspartate

Execution Phase
Destroy

- CASPASE 3.6 ⟂⇐ protein

cells shrink

- Endonuclease.
DNA fragmentation

Chromatin
condensation
for apoptosis
↳ Hallmark

- Small cell
- •
111
- Dark pink Cyto

- condensed dark
nuclei

APOPTOTIC BODY
 will be removed
EAT ME
by macrophages SIGNALS

→ complement

Eats without ⇒ Phosphatidyl serin

releasing R0S
⇒ Thrombospondin
EFFEROCYTOSIS

Methods to Identify
→ cytochrome C
① Biochemical
in cytoplasm

② H2E

binds to phosphatidy)
③ 'Annexin' serine.

TOWEL assay
④

⑤ DNA gel electrophoresis

 APOPTOSIS

①
SMEARING PATTERN

DNA
5ᵗʰ NECROSIS
frog.
1 <
STEP LADDER

Pattern

Necroptosis FLIP ase

CMV

FAS -FAS-l
studied
⟂ STOPPED
in CMV
FADD
8, 10
RIP complex

Mike → phosphorylation
 ⇒ 550

NEURO' PORES in cell membrane

Programmed of NECROSIS
necrosis

- caspase independent
Physio ⇒ mammalian
apoptosis
growth plate

Paths : -Cmv, viral induced

Hepatitis

- stoats hepatitis

- Reperfusion injury

⇒ Neurodegenerative

IBD
Pyroptosis

Intra cellular organism

O
C0TTcholesterol
TT Urate crystals ✓
Triggers

Inflammasome

It β converting enzyme)
pro-caspase 1
Caspase -1

Activates IL-1 Caspar 415

DEATH
Inflamme, fever

Ferro ptosis

↑↑ Intracellular
Free Fe
 consumes antioxidant
TD ROS
(⟂ Glutathione
I
peroxide)
prone tionjury'

Intracellular accumulation – Why ?

of cell injury
→ Evidences

Fatty Change MX- CLEAR

⇒ Liver , Heart
Mlc
Alcohol
→ Etiology or
Fatty liver
NAFLD (M/C)

S Enlarged, yellow colour

Gross

⇒ Tissue processing
MX
'Alcohol'
↳ Remove fat

Mx ⇒ clear
- empty space

- STAIN ⇒ oil red 0

Sudan Black B

FROZEN SECTION

⇒ Demonstrate fat
 Mx- pink
Protein/Glycogen

Liver
-
Glycogen
Protein
PAS
t
+
✓ , Digested
Diastase
unchanged
Sacchandese
- ve

+ Ve Repeat PAS

PAS ⊕ Diastan

PAS + Diastase sensitive

resistant Glycogen

Protein Von Gierke

α, -anti trypsin

+ colour
PAS
 Pigments

BLACK
Exogenous
Endogenous

⇒ Coal
BROWN

⇒ Tattoo
- Lipofers chin

⇒ Para nuclear

melanin ⇒ skin

↳ Masson Fontane

⇒ copper
Iron

- Hemosiderin -Patholog. ⇒ o rain stain

- Perls Prussian Blue Rhodamine/ Rhodanine

will not stain ferritin

Perls ⊕

Hemosiden

river
 - Mx- BLUE
Calcification

calcification
Meta-state

in Honer stasis
change

⟂
Hypercalcemia

TT PTH P → Adenoma
Elio ⇒
at → CKD

resorption > myeloma

⇒ Bone
→ metastasis

→ Deficicienny

organs
LUNGS ⇒ MIC
capillary →
> Rich
→ Renal

GIT → TT Ca Ca}
>
Ca salts
⇒

Neurotransmitter - psychiatric
-
→ Ca disturban

BLUE STAIN
Mt ⇒

von- Kossa stairs 1m/c)

Alizarin
red-specific
 CALCIFICATION:
D4S-TROPIC

Degenerating
valvular calcification
⇒ cardiac
sclerosis
medial
⇒ monkeberg

→ PSA MOMMA BODY

DEAD
↳⟂ blood) → ischaemia -
Tip necrosis
→
Tumour
① Papillae in name Psamomme
R ② serous in name
Finger a central
vessel → meningiome, Leiomoyome
necros

centre (↓ ↓ Blood) Is Ch

whorled

Psamomme bodies
n
 response to anything
Inflammation → Body's
external

Inflammatory cells

Neutrophil ☁.

cant see - chromatin

thread, cell member.
granules

BENT NUCLEI •

- /
Eosinophils
- ✓
Pink granules

Lymphocye
t

small round
blue cell

→ viral
⇒ Auto immune disorder
 ma rop

⇒ FOAM CELLS
0
clear cytoplasm

⇒ cell of chronic
inflammation

Plasma cell
perinuclear
Had /

- Eccentric
nuclei
- Clock face chromatin
- Pink cytoplasm

Inflammation types

Acute Chronic
Hour- Days Days, months, years
2pm
cell. Neutrophil Macrophage

Hallmark ✓
✓
Tissue destruction
⇒ Tse vascular
permeability 2 Healing by fibrosis
Acute inflammation - Phases s Bacteria

→ STREPTO

vaso constriction
Vascular Phase I
(transient)

Immediate and Transient vasodilation

MILD STIMULI
Coffee spill)
> cells →
0 006
Histamine margination
10-15 min
Ends. GAP FORMATION - vascular
- selection helps

Immediate and prolonged

stimuli
moderate
↓
ends injury
Reversible
- upto 2ⁿᵈ L

Heals → inflammation
STOPS
 Delayed and prolonged RADIOTHERAPY
UV rays
⇒ Post radiation
mutation ⇒ side effects
12-24 hrs
✓ 5- 7 days
minimum
Ends damage
⇒ minimum gap
⟂
LAST DNA repair Inf- stops two radiation,
2h-48hr5 - 2 weeks

Leukocyte Mediated damage

12.17
Cellular Phase

Process -

Rolling
Adhesion

Diapedesis
Chemotaxis

Endogenous:

Exogenous:

Phagocytosis and Killing

Respiratory Burst
Diseases involving inflammation

Disease Defect
LAD 1

LAD 2

Chediak Higashi
syndrome

Chronic
Granulomatous
disease
MPO deficiency

NET
 Mediators of inflammation

Cellular Cellular Plasma

(preformed) (Synthesized)

Preformed Cellular Mediators

Histamine




Serotonin




Lysosomal Enzyme
 Newly Synthesized Cellular Mediators

Arachidonic Acid metabolites


Cytokines – Systemic Effects
























Chronic inflammation

































Types of granuloma

Necrotising (Caseating) Non-Necrotising


















Giant cells
Wound Healing
Delay in wound healing
Keloid Hypertrophic Scar
Genetics

Basics definitions

Gene

Allele

Homozygous

Heterozygous

Exon

Intron

Splicing

Mutation

Pedigree Analysis

Symbols
Rules of Pedigree analysis

1)
2)
3)
4)

Solve Pedigree ??
Relative Risk Calculation

AD –
Features of AD Diseases

Thumb rule to remember diseases ?

 Neurofibromatosis
Nervous
Tuberous sclerosis
Urinary Polycystic kidney disease
Gastrointestinal Familial polyposis coli
Hereditary spherocytosis
Hematopoietic
von Willebrand disease
Marfan syndrome
Ehlers-Danlos syndrome
Skeletal
Osteogenesis imperfecta
Achondroplasia

AR Inheritance
Features of AR

Thumb rule to remember diseases ?

 System Disorder
Cystic fibrosis
Phenylketonuria
Galactosemia
Homocystinuria
Metabolic
Lysosomal storage diseases
α1-Antitrypsin deficiency
Wilson disease Hemochromatosis
Glycogen storage diseases
Hematopoietic Sickle cell anemia Thalassemias
Endocrine Congenital adrenal hyperplasia
Skeletal Alkaptonuria

X-linked disease
Non-Mendelian Inheritance-
Trinucleotide repeat disease
Fragile X syndrome Huntington Chorea
Imprinting Disorder

Imprinting ?
Angelman Prader willi
Mitochondrial Diseases
Mosaics
Somatic Mosaic

Germline Mosaic
Immunology

Graft Rejection

Types of graft

Allo
Auto
Iso
Xeno

Transplant requirements

Solid organ HSCT

Graft rejection

Hyper Acute rejection

Acute Rejection

Cellular Humoral
Humoral
Chronic rejection
Amyloidosis
Types

AL

AA

AB2m
AB

ATTR

ACal

Organs and findings

Kidney

Liver
Spleen

Heart

Tongue
Diagnosis
NEOPLASIA

Two features – Never forget

Basic Terminologies

Terms P
-oma
-carcinoma

-sarcoma

Benign tumour of melanocytes

Malignant Tumour
CNS tumour
Blood ?!

Hamartoma
Choristoma

Microscopy

Pleomorphism

High NC ratio

Mitosis

Loss of polarity
Story of Molecular Hallmarks !
Self-sufficiency of Growth factors

Genes Diseases
RAS

BRAF

EGFR
Her2Neu

JAK 2

ABL

RET
Insensitive to growth inhibitory factors

Basics features
RB Gene
P53 gene
CDH1 gene
VHL gene
APC Gene
Evasion of Apoptosis
Warburg effect
Evasion of immune response
Limitless replicative potential
Angiogenesis
Metastasis

Routes of Mets
Carcinoma

Sarcoma

Body cavities

Drop

Intra - vessel

Ovary
Steps of Metastasis
Carcinogens

Chemical Carcinogens

Direct Indirect
Radiation carcinogenesis

Microbial carcinogens
Organism Gene/Patho Cancer

HTLV

HPV

EBV

HHV8

HBV/HCV

H Pylori
Schistosoma

Clinical diagnosis
Patterns of Neoplasia

General Patterns
Mesenchymal = Spindle = Elongated nuclei
UNIQUE PATTERNS