1.

Cell Injury -

By Dr Devesh Mishra
MBBS, MD , AIIMS
Hyspor
Marathon
-
Telegram channel
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ort.

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-

s-
*

⑧
 Cell-iry (Adapt
Cell-Adapt
#

Physiol stimuli
--ell-versible"
changes.
Physiol
I
-

realbiomea
- Morke

↓
te ~PM
-

change(B
 It
2
cellular. Adapti n
Abhy
2)
Hypertrophy
2) 3) Metaplasia.
R
-
Hyperplasia
-

↓
S4

[
=S: same.
a) Size I
=

:
N M 4 1 Mature cell
b) NO
=

same.
- =
=

↓ EAdult cell)
-99
Mech
tin A replaced
↓ by
#Pregnhs
↓

[
2

⑰- lysosomes
both
b
Dr.
Dr.
Hypertrophy
I
another

Hyperplasia like of
Preg. Breast
2.

Autophagy
e mature
#
cell,
an

Lactating Breast-My Hypetoply

 Metaplasia
↓
"Mech"
Smoke

8Nl* au
ows"cenEsquamous
tract. Column. Ep.
a metaplasia
I
⑰
22
Y
rest. tract

Stem reprogramming
&R

E
Mech
I Vitamin Ad,
a
a

Wit A 4
 Metaplasia
tissue -
⑦ ⑪ Contine Mesenchymae
me ↓ 2
sq. metap. ⑫
ossificans
=>

(Resp.r/cx)
2. myochs- ↓
Barrelt's
Esophagus.
->

->
m, muscle.
Bones.
!
-> R
I inflam

st
GERD Alian Blue

Frisk - of), Afivacuoles - Mount

↓
↓
Goblet
cells.
& Sq-cell
Column, cells
Ad.ca.
Esophagus ↓

colte 3
Intestinal
=

Metaplasia.
 I
"Rings"
0O * Observ

cmparism
00 *
 301m, MC, GERD, Esby? ax?
rish
-
-

↳ -

! Colincel
sq.cells. BE
 Blue stain. (PI. Stain)
n
ooium" Acidic pit
⑧
-
ets-pi
 R.
Pathol. Stimuli
Hi
↳ isch
1,
↓ oxid.
Phosphoryl
celling <Mitochond)

cetiring R
I

McC
em
↓
dyt
↓
ischaemia (402) - -
My-mens

⑪ Transient ③
Persistent
-
Nu-DNA

Al ↓
Reversible
- Irrer. I cell-death
injury. ing n
Morkh.Ch.

Nic
-
Ap.

-Pyroptosis.
Mecroptosis.
-
is Rev inj is (402)
↓ oxid phosph. (Mitoch)
↓
Rev.
↓ ATP inj

mateman
Earliesin
2] celular,
- swelling finding
in

Erinya cell-injury
BalHepatocytes
looning 1 ↓
Except "

Apoptosis.
(cell-shrink)
2.
Acute
Hepatitis.
 Em =ultrastruct.

Reving to
⑧
organce -
# Mitochondria

fin
·

⑧ ing"wening
"Small
⑨

[
f
E swelling
⑨ -

amorphous.
⑬- Ribosomal detachment. densities.

I amorphous
All
densities. -
Mitoch

Rer. * Irner.
smalls. (larges
 ATM
(kidney)
=>

⑳
⑭ 7

wenee
,
 m.imp
on

cell-ing
++
↓ Cytosolie) -

I
mild Severe 444

tring
↓
irrer
A
inj
mild cattyphospholipase.
PL-dest. (memb]
pass; ↓
PLICate
2.

c++ cotc.
&
=> whorlline
I

laminated app.
R
-
0

myelin figures.
Ein

myelin"
-

figure. Ren (ie

[Pee
# #-Damage.Reving

·
·
..-cyt
a -> I
fibrillar
MU-Basophilic (Blue) granular
Normal

-
FR
K
chromatin
2.
Rew
icy.
clumbing
 grew, iny.
↓
*** Cat+ (cytosol).
4-
*
① Plipase " proteases. ⑪ Endocase
↓
↓ ↓
⑪=> MK-DNA
Mycin Fig (max) digest damage.
cyteetal pr - R
R
⑯I Sequence.
Mitoch-
large cell-archit."
↓ ↳
amorphous Loss
of
Pyunosi
ryo s
hexisonysis
①
--

densities. -

in

itscamping
Chromatin

E lysis (dissol
age outside
CM

-..

to Basophilia.
 Mecrosis.
i - 22.
I
⑪ Liquefactive.
agulative. (M

ch
Denatur of proteins Enzym, damage
->

↓
~Hydrolytic
11
tissue a -

Arch=> preserved ↓
tissue
arch. I lost
-
eg. isch-infarction 222
A
- isch-infarct-in
solid-organs
-

No-collagen

Enterarere
-

rich in
-
lig. Ens.
Bact, infections.
=>

-
-agree o
fiss. Arch
↓
lost
Al
Lig-Mee
 spl.
tybe
Mec.
↑-

fibrinoid.
↓ ↓
① ⑪ TB ⑭
Gangrene
↓
⑪ fat-Mec. ↓

-Bag
both
mc, LL Trauma-Enzym. = Seen-in.
HTM

--
-i. Goss
-BreastPancreatitis. Malignant
Vasculitis [PAM]
a 5] wet -shoulder.
ipase
tycme> cheesy-app" hi Aschoff bodies (RID).

tissue
Suffering (Toxin
M

Caseous Mee. Gross.

=>
&22.
↓ re DM + No
fibrinoid
cally-white
fiss. lost Ne
arch-pres. As Nec

↓ I
in Acid.
Lig. my acid.4 Cat R

fatty
Mee
coag.
Mee.
~"Immune"
#Mech

suponification. complex
 A cut
Pancreatis'
↓

omental
tiss

Chally
white
-

4
FAT.

I
MEC. -

11

Cheesy"ITB
-
-
Fibrinoid -
Mec.

d
7 Immune-complexes.
all

Ent
↑

Inflame
wall > Endoth-damage"
- ⑰
picoagulants
↓
⑦N

stone fast-blood Coagul path

0
-

M -
80::448 Floor
Erin
⑪ PinMorphous
hylman
↓
Ec
↓ -

Cytokine.
"
FIBRIM
a -

MeC.

Pink. amorphous
H
FIBRIM
 ↑
2
Mec. Ap.
↑ -4
lysosomal
↓
11
permeab
a
Mitoch-permeab.

e ner
↑
Enzymes
↓

emcontacted
=>

[Inflammation
a
CM- rupture &

a
* Physios + Pathological.
#Always pathological?
 "Falling
Apoptosis. - off"
↓
# mimp
organelle - Arch. 22.

PCD < Energy

Active process:

Programmed-ca
depend pr
i
Death

"

gires" IAD"
Mecroptosis
i Pyroptosis.
 ① Earliest-
um
⑪ Acharact
cell-shrinkage.
222
&.
chromatin-
clumping.
->

⑪ CM-intact
not-inflamm
8:Apoptoti
⑭
rlebs
.

fasterre
a

⑪ Endoutcome?
-
22

efferocytosis. (Spt Klaviant

of Pragocyt]
att
ferous Phagory.
↓
-
cm-rupt
X-No-inflamm -

inflame.
p H

Mec
-Ap.
#
pro-aspase - activation
⑰
Y
" ↑

Indonuclease."
Endounclease
# ↓ I
DNA-damage
↓
Chromatin -

Clumping EAb]
Specif Base Pairs.
(ix" of 200 BP]
Internucleosomal DNA-damage22.
 - Agarose gel electrophoresis: allEndonuclease.
- L

atauhere
800
*
600

400

2. In 200 -

Step-ladder-pattern.
 I
genes.
↳
222

↓ Proto-oncogenes.-I
I
Fo- Ap ⑪ Anti-Ap
N
I BCLE
=

BAX
=

= BAY
=>
BxL-XL,
CM
BcL
XS(4) 22.
= -

#MCL-1

-familyStressres
-

=Batte
=
MOXA
 Mech-Al.
↓ -
I
initiation C-activ (C-8,9,10
#
Execution 2-active

"I-t
" I
3, 6,7
2
Intrinsic path Extrinsic path.
-
zu +
2-10
↓
I
29
"
Cig" (Human) S

animals. n
Clump.
 em)
·- cyt.c -> ETC
⑦ "Intrinsic path.
EM "Is ⑰ fos.
->
(mitoch) (oxid-bl)
Cytc -. Ap.

Stress-sensors.

BH-3
--

⑦1

Em TDera e
11

BAs" E

.
H

"E". mA * Apoptosome
"
Far

*t S

pro-C-9 -> 0.9

⑪ e-path. ED-R-med)
2 a

DTMF-PIFdefined
Digan, "FASECD95]
--
⑯
Exec
My DB
/
quit
D
M gnt Ext
↓ d
2,3,6,7-

Activation. ↳
H

~roCs c8/1
&

Pump. (AP)
 PCD
I
-
cont caspase" 5,
activ
⑪
&aspase activ Al
I ↓ Pro-IL1->I719
Pyroptosis
I
Necroptosis. I-
↓ I

Enflamm Pyrogen-induced
CM - rupture
to

(4)

[infiam.
9 em-rupt
variantof
=>
Mec.
I
 FR ana =

oxidants. = produced
def.. "Chemical sp -
↓
incomple
e-counter-orbita [ Mitoch
unfaired
Ein

M
ART cont damage
damage "Y,"oxidation"
FRoxidants
->

Anti-oxidants.
↓
"Aging"
& - Reactive/Potent. Vitamin
M.
↓ ↓
Proteins.(Festl
⑳

O is
Catalase Transferrin
& ACE
022 "i Glutathione / Ceruloplasmin.
·
[42)
Hod: Peroxidase
MY SOD:Superoxide
dismutase.
⑫
Y

Aging
↓

...
0
or
O
Brown-big
&

Lipofuschin
1)
-Aging
malnutrition
"
-
Severe

-
Ca-Cachexia.
 .

#
-Brown

pi
I
-
Lipfuschin Iron. -

Oil-Red pers' Prussian

A
· Oil-Red-0 stain
Sudan Black Blue-stain.
O stain.
Al

↑ lipid
·

B. I

o re
 de
id
⑧

O --

0
 Aging imp
hypothesis. - ERing
-> m-

Mol.
=>
level.
↓

shortening-aw"Aging
"

Telomere

ch
# #-> T short DNA-seq. end
=

0
t

[froibeent
O

I I fusi o n
I d eas
-
Normal-cell an
↓
celtdiv
--
=

shorter
-
> -

=I
Telomere-shorten
T-ended
2

n-fusion/degrad. _Cell-Aging.
lifetime? to-Gotimes (HAYFlick-limit]
X

40 div.
# M. effective
method 222
As =

4 life span Werner

Werner
=

E
A
Calorie
striction ·Y
Premade
⑦ e
⑰
SIRTUIM FR-ing
- ↓ pr.misfolding !
Red ↓ Grall)Metabolism
↑
alt-> DNA
icase ent
wine
(small
Insulin
↑
↓ sensitivity. * I
Glucose metabolism.
Repair's defect.
↓
Prem.
Aging.
 &
Catt,
cfication
Starts -> Mitoch. except I
Kidney
Basement Memb
A
X Dead ↓
Tissue -
Tissue hae
-

-Cate
=
94 22

Dystrophic-
R Metastatic cat
t
(N/Tis
inHyperdarathyroidism.We
MCC
i) Metstatic
- -
LM I

in Atherosclerosis.

mi Psammoma bodies.
in) RID valvulardamage
- -
-

7 entire
oritto
Osteoclast.
(mod. Mas
BONE
 Se Morphous
-deep-Blue
dep -> 2a++

↑
???
Catt
222.
5 SpI. stain
->
0

Asa
S-VOM
-ROSSA to
⑩ck-cat
catt.
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