Einy.

Not e
Notesim the
Concepts

70% Notes

1. Cell Injury
19

#
· -

I - -

throm -
-

3.0% Ma milmD X E
Ithi
-

By Dr Devesh Mishra c YR-NEEDS

Orient
*

MBBS, MD , AIIMS I
'Micet
[2015-16)
options
-

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add

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maration.
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-

Y
↓
X
 Stimuli
↓ ↓ Y
X
2)
Physiological ↳ Persistent
21 19

2) Lethal 3) Chronic injurious

Y Y sublethal
X 9c-accumulations.
/or
cellular isch X

Pigments.
in
substances.

adaptatiovnerside eing ↓
· Bil. ⑪
far prcain
e · Melanin
↓ glycogen
Iron-ping MC

(steatosis]

male3
"

Stimuli MC form
ene
more
I can
#
-I

remove T4
 Cellular -
Adaptation
↓ A *
A
I
2
2)
Atrophy 2]
Hypertrophy 3
Hyperplasia Metaplasia.

Size: ↓
· S ↑ · S same.
->
:
- N
2 Adult EMature) Cell

Number. ↓ · No
->same . No. A ↓
>
replaced by
:- 9c-pr. 2.
↓

argent
-

degrad Both
I
another
type of
Mature cell.

Hypertrophy -

cysosome 2 proteasomes -Hyperplasia.

2
a)
:
Y

Autophagyin
- "Lactating"
*
- Breast-tissue

eating. Only Hypertrophy

* a Endomet. Ad.ca.
9 2.

Atwordy Hyperplasia.
Type i Type
I
·

S good
 Metaplasia

e.g.

Resp. Ep 11
mechanism
11 a

cell-reprogramming
Stem
I Es

11
Smoking
I
88
⑦

(Adult
Columnarepith) Ault
Squamous cell.

I
I
22.
Squamous &
Stem-cell- Metaplasia
->
reprogramming
 Metaplasia
↓
types
Formative
x X
⑦
Spileial (me)
I Mesenchymal
⑪
eg
Matype X

1
↓
Squamous Metaplasia Myosis" ossificans.
↓
As
-n.
"[Resp. 6", 2x.) (BC)
Bee
wedes inflame
↓ ->
· ano
Vitamint ↓ I

·Al
&
A4
Eat
Hydroxyapatites
 Barrett's Esophagus =Frisk-> Es. Adenoca

ma
GERD

08-1
Alcian
Vacuoles -> MUGM- Blue

O &
↓ ->
en
↓
-
Stain

"Goblet"
Nu cells.

"Squamous cell."
Columnar cells. X

(Esoph)
↳ Intestinal
reprogramm
H

Columnar -> Metaplasia

Stamcen.
Metuplasia
 30 yrs male; MNC-worker, GERDG
Al
Barrelt's(commn)
Es.bx
ish?Es.
=>

=> Ad.ca.

↳ ⑧
>

Vacuoles.
↓
MUCIM
X

Squamous cell
I
Columnar-cell ⑬
 Or Alcian Blue Stain

00.0
H-
"I 11

&
> MVCIM Gobletcell
-

↓
2 u I

2.
sacidic 7.sAlkaline)
->
-

R Y N
Barrelt's
Esopli Intestinal
lesion.
 Lethal stimuli
-cell-injury. celling
-
I
19 11 is(02
M Mitocho

↓ isch/02 -em
- cen
Transient Persistent
-
damage. ·- Forg
I ↓

Rev. Irrer,
inj
My-memb
in
L ~
Chr. damage
N (DNA)
"Celtdeath"
↓
Morph changes
Al
1) Mecrosis.
Apoptosis.
Dis Pyroptosis.
Y ferroptosis.
Mecroptosis.
1) Reversible
Injury
mesischlozboxia. Phosphory
[Mitoch] X

:atreate
deg of Hepat- Acte
e.g. Ballooning Hepatitis.
&.
the
cell-swelling
a
except
de

Apoptosis. 2.

(cell-shrinkage)
Discrete
(ATM)
-
Kidney
X

a
Reving 11

change
Hydropic
Y
2

Cloudy swelling
-
 a

eving ↓ organelle.
EM
=
Eultrastructurally)
2
I
I chondria

as ofswelling.
detachment
esweing
i 3)
a

Smallamorphous
deposit
Revinj - imp"ion" in
celiy
m.

↓
↑ Ca+
[Cytosolic]
A H
mild Severe 4
↓
① "Rev
·
i

⑪ -
er. j.I
in
Es.
Phospholipase
-

↑mila-catt s
↓ V 2

Pidamage. (membracei damap

cone whole-like

⑨
Struct
↓ R
PL* catt
N

Myelin figures.
Rev. K Errer,
iny
 SM= Myelin
Cultrastructural)
figures

or
PL+Catt
 (Rev. inj),
⑭damage.
- a
⑪ . .

gyfibrillar chromatin.
a
·
2 co
-
Basophilia
&per a
tiny,
crumbing chromatiec ne
of
 Irreversible injury
E

Persist isch1402
A
↑ Severe Cat
I

de
Icytosolic ↓
x
·Plipase
↓
I
Proteases.
⑪ Endonuclease
↓

Myelinfig. (max)
↓ -
Mu-damage (sequential)
R
cytoskeletal
pr-damage ↓
↓

Mitoch=>ae "Tryo"xis. Karyolysis

by ↓, 20
I
I
Pyknosis. -

amorphous ↓

of
loss cell A

densities.
↓
Mu.-fragment. cur
lysts
architect
. chr
clumps. -!
· i-shrink. -
0
22
↓ Basoph
02
of cell
·
42: of cell
 Mecrosis.
D
↳ ↳
~

Dar 2-palterns
Y Mc 2 ↓
Coagulative Liquefactive.
isch-infarction. Edenaturation) dam.
he
protein
->
·

Enzymatic
22
als
of ~

tissue
Arch
preserved
=>
2 Eydrolytic damage
tissue
-> lost.
its Arch
gen
e.g. solid
organs Brain
I
No-collagen
infarction
Heart-
-

↳ rich
·

in
lig. Ens.
Kinder A
Lig. Nec.

Infections. Toxins/Ens.
=
↓

Lig. Mec.
 Kidney
tissue Kidney
architect-
↳
·
000 &
Kidney.
pres. Issue
- architect
Kidney
- -
-

> lost

- <

-
isch-inf I

Infective
-

-
 special types, Mecros is
A ↓ A A

wayinaminorics
I
Gangrene 2 Caseous 3 Fat 4 Fibrinoid

i
range n
-
-

Twet"
a
↓
Breast Pancreatitis.

"Cry"
"T. B."

Long Lig.M.
+

Irose coag-path
bactlorg Gross
·
:
Cheesy" chalky-white
A

att
Cag.
Mec.
2.
Toxin/Ens Cat FFA
Mycolic
IDiorpious
Y Acid &

Lig. Mee
·
:
·
Mc sile->LL
&
Caseating No
fibrinoid
Mea
Granuloma.
 R omental

tissue,
-
2 Acute
↑

pancreatitis

Lung tissue

·
0
Gaseous
TB
Mec.
[neesy) ->
Myh
Lining
↓
Fat.
white

ok
Mec.
 Fibrinoid

S
necrosis Fibrin IC
+
-

culitis? I

cr
BU
xx
⑧&

①
4
Tt Etining.
E 8 9-8
↳ ⑳

· mrc-cytomegamase.
⑧
⑧

wal
nepalbrin
-
 Necrosis Apoptosis.
b

Rysosomal "permeas
· 4 Mitoch-permeab. Charact

I
Cm intact.
Enzymes
⑧
->

↓
Y
X
iscm-rupture. No-inflammation
↳ & Apoptosis.
>Pathol.
inflammation
I
y
Physiol.
x
↓
organogenesis (Emy
RolRagioR
X
x eg.D &

Only pathological.
·

"Killing, inflam
·
cells.

After
completing
their f

/ Partichemotaxis.

"Killingof ARmYppis.
prevent
A.I.
Apoptosis ↑
= M.
Mitoch
imp.organelle -> (ATP) (Energy
Active

"Faining
-

pr.
off"
2R.
R

"Programmed Active
11

t
cell-death.
Pcp
Process. Energy due
Ap*
" Pyroptosis.
Mecroptosis.

My Perroptosis,
 E
Apoptosis
Morphology of
↓ 22.
I Earliest-> Cell-shrink
2) M. characte-> Cho
Clumbing"(AP)
No-inflaum
3) CM-intact ->

⑭
I
,
PR (phosphatidylserine)

PortAnnexin
Ap - ·

QApe
I marker
of Apa
e
Bi
a
councilman a

Bodies.
 Apoptosis
Morphology of
End-outcome ofEfferocytosis at A

6) efferocytosis Phagocytosis.
00_Eb.
Bodies. I
-em-intactCM-rupture(
-

PR Sertes.
Inflamm
+
-

o-inflamm
-

-prevent -
Al ·
PromoteA.I.
Mechanism Apoptosis
of
*
pro-Caspase. 8? C-activ. >Endonuclease.
N I
Hallmarkof W
Chrom-
Ap-activ MM-DNA
clump
damage. -AP)
↓

"
Specific frag
"X"of
"I

400 BP
&

↳ Internudessome
 Agarose gel electrophoresis:
#M-DNA-damage
I S

800

↑
-

S
-
↑
/
smening
600-
A
400 -
I

-
-
↳ A
Mec.
2.

↑ I
200 I
-
2 11 t A B
Stepladder"
↓ pattern->
Andonuclease
Seen in
2
↓

1) Ap charactnotdy

l Nec.
 Programmed cell-death

genes > Th-supp, genes p53 -

↓

↓ Proto-oncogenes. -

I
A
Iro-Ap. Anti-AP
-

I 22.
I ① BCL-2
BCL-Xs(4)
⑪ BC X
L(X)
-

11] Bax =

"MCL-12.
hi Ban ((a-Pancreus)
family proteins cell-surface."
22
·

Il il

i) "BH,
.

2 ↓ "Stress 11

Bim. PUMA sensors

·
Bad
-
·
NoxA

Bid
·
 Mechanism
of Ap
↓ ↓
11
-
Initiation 2 execution
11

11
&aspase >
Caspase > 3,6,7

---

X
↳pathway Y

Ema]
↓
9. Intrinsic b) Extrinsic
L

eg C8-

lower
Go"
N
Human
animals."
-
 path ( Mitchi
11 I1
I Intrinsic Stress
R
2
MINITC.
Cyt.C-
-
·

⑰
cytos. Cytes Ap.
2.
·

X
t
-

BH-3

j
SMALDIAT198
Mit.
Is
-

!
-

Ce
- Beth

↳
Ap. activ. Fact-1
22.

cytosol. Cyt.c. PF-1

+

↓
"Ap". IAP
OX Apoltosome 2

↓ 22

pro-C-9- C-9
 ( Death-R-mediatedS
11 Extrinsic path Ap. mech
↓ -
defined)
a) TNF-R-1 (best Initiat
A
Exec
↓
by FAS=CD95 2.
9.p. Ep.
2-3,6,7.
↓
-

↓
C-9
2 I

↓
Drit"Digands. Endonuclease

"
↓
Ch. Clump
emI ↓ CAPD
-> Adapter pr
⑰
X

Cytop.- bro-C- >- V

 Programmed
PCB
-
-
cell-death.
Rx
of
Y
11 N
X Cancer
p1 37
7
withoute-activation
↑

I
E-Caspase ·> qq cell.
As ACHV

-Erroptosis.
2
↓
Necroptosis. "

*
A Pyroptosis P
C-3,6,7
PCD
A
CM-rupture. C-1,4,5,111 8,9,10

Nocm-rupt
No-inflame
-

Pyrogen (I2
~ ·

N
1cm-intact
·

~ 2.
No-inflamm
Inflamm
·

9-1,4,5,11 M. charact
↓
· Muders -
Normal
of
Variant Nec.

Pro-tt.**SEE1
- clump - Mitoch damage
camin.

·emp,e
- -

Variant
of
 Free Radicals: ala oxidants.
Mitoch
x ↓
↳
Normally
produced
chemicalsp.->
unpaired e-conter-orbit).
Ar 11 ↓ FRA MOA=
em
oxid. damage cut
Aging"
pr

S
Stress 4 Ma-mcht
-
MY-DNA

Anti-Aging. -> I, stress I

**4
↑
oxidants FR 11

Anti-oxidants
1

↓
0
&

-
Proteins
-

2
Vitauius? En3.
02a
atalase
↑

stsTransferrin
-

·
2

H202 A,?, E. a
-

isSIutathione -
M. potent
-

HOC1-(Pr.cell) Peroxidase. ⑪ Git- Ceruloplasmin

22[DH M.
M.
potent
Reactive.
1) SOD
)prevents
↓
Brain in from ER.
mut

Amyoteblelatein
UmM + LMN
5
Games.
↑
FR
A
&e-damage

Brwn-bigPerinuclearY
X

↓memb.(PL) =>
I * 2.

Lipofuschin
⑳.

I
> Hemosiderin
& H Y X
⑧
Aging-pig.
·

G
⑧
8.
·
Ca-cachexia.

· Severe Malnutrition.

Spl
stain
 H2- .

-
~Lipofuschin 2

X
Perl'sPrussian
E

Feta
14199 (1
Blue stain
⑪ oil-Red 0. Stain ⑰
=
#

i
a

0
4

Brownpigment
11

↓ ↓ 0
Lipofuschin Flemosidents.
--
-

088
 Black
Sudah
-
B-stain
H
⑧ Lipid
-
-
Aging,
damage manga.
11

imp hypothesis
sating
8
m.

a
I
&

->cross-linking of collagen
⑧

Telomere:
shortening
2.

~
alwAging
22.
**Fort DNA
2-

Hayflick-limit.
*

stretches. end ofch. P

I Newborn

#
*

prevent ↓

fusion/degrad cell
↓
ch destined
- for
every-ell-div A
22.
50times

Ishort" Telomere"finished."
-
2 I

40-60 times
I

fusion/d. - -

cell-division
A
I
Cell-Aging. Rar
-
life time
 U 11
Most-effective method
11 ↓ 11 Werner WerMEr

Prolong-life span
Premature
=
TEM-I
N I
-

Erfugehere
-
"Calorie restriction"
-

⑰
"Red" *,""Sitnin
11

1.

wine
My
↳mult ↓
I
⑰
Putindefective
-
·
F A
Insulin
sensitivity.
·

·
IMetabolism ↓
4 Glucose metabolism.↑
Coverally
~
 calcification >Starts "Mitocho" except
X
7 -
-

Kidney
(Basmut).
memb
2types
X
X

med
[
Y 11

Tissue - Aby -a
·
· Tissue -> Normal -
I
-
11
degen. *4
-
· Catt ->
·
Catt - Normal -

↓
-=

2 = Y

G e

Catt
Metastatic cate

e.g. Dystrophic ↓
McC
I TB. LM It A

Hyperparathyroidism
1
Atherosclerosis"
i)
my Metastatic (n
MCC

Retinoic :*,Esterdasts.
19

1) Psammoma
Adenoma
2
bodies.
P. ↓
-

Bone

Pa eating
As
↑Catt
My Vitamin -

toxicity. 5 Uit.A I

Vit D
·

(metast

-
 HE9 -
Blue.
>
deeply
-
--

amorphous
-
H
S10-catt.
22
I
U 4
VON-KOSSA Alizarin Red-

↳
aruppu"
-

Y
Y
catt
--

⑧
special
Stain >
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