- ⑳

NOW-20
NEX.
=> Notes.
- 22
-

1. Cell Injury 5yrsPYRIMICET

->

*
I
Topics +
NEET

By Dr Devesh Mishra # Revision

-
*****

every day:I-etors. Attes

MBBS, MD , AIIMS A 11
1

Motes
-

Analyt TinyMotes.

4-5hug n.
4/7/19
t

i
X

Refer Textbook
-
--

Extra
I

ad
Telegram channel Instagram
 Stimuli
X
Physiological
↓ Y
"
11

2) 2) Lethal" 3) Chronic injurious ↳ Persistent

Y Y sublethal
&
X "Change
Intracellular
cell-adapt
↓ -
Physiol I

celling accumul
X

Mitoch
1 proteinPigm.
I

remove
-

Bioch mee
de
Stimuli -
Morkt. ↓
↓
isch (02 incomp
⑭ State
-
-
fatglycogen [O]
Compl.
R- Mc ↳
Combl. Reversible.
FR
L 222.

Aging
 Cellular -
Adaptation
↓ A R
X A
2)
Atrophy 2]
Hypertrophy 3) Hyperplasia 4 Metaplasia.
Sa S= :
Size:
· ·

↓
-
1 cell (Mature/Adull).
Number. ↓ · No= · No.4 replaced
>

ach:9C-pre anmersype.
degrad
↓
of Mature cell.

①
Protesome (Prdeyrad)
⑪
lysosome. Autogy
gieatina
g ne
I Both

Hypersply
[PPrey-Breast
reg-nterns
->
=>

Hyperplasia
=>

tiss

attating
I Breasttissue I

# Endomet Ad-ca
Only Hypertrophy
-

222

air
X
↓ X
⑪ a "twopm 2

Atrophy
-

⑰
⑪
Hyperplasia
-

IP
-Bad g2q
=
 22
Metaplasia
↓
Mechanism
I 21 a

mess
Stem-cell-reprogramming
of p <
Smoking
Aly
"

⑧
&

Squamous
commonalthe
cell.

re-programming
as
>
->
 Metaplasia
↓

x
types X

①elial (me ⑪
Mesenchymal/connective
Metype a
N
Myosifis ossificans
eg Smoker column
"Squamo. trauma-muscle bone

Squamous iny- form.

metaplasia.
I
↓
inflamm H 11

(Resp. truel
↓
-
apatite
222. salts
oft
aw. Vit
Ab/4
 Barrett's "Esophagus
%

"
↓ I

Ma

rude
GERD

⑧ == -
am

Goblet
19

Squamous cell cells.

Es
↳ Stem cell
umnaspag=antera
reprogramm
 Joyrs male; MMC-worker, GERDG
Al Barrelt'sE
Es.bX &x? =

-Risk ? Adica.
->

Esolh

-
dgg

X
I
S
quamous Column.
cell. cell
 Alcian he stain= MrcM

0 0. 0 > Much
H-
↓
2.
sacidic 7.sAlkaline)
Barrelt's-
N

Intestinal
muciu
 Lethal
stimuli-celling I
ische4, 2
↓
I
↓oxid-phosph
MCC (mitoch)
↓
-R damage.
↓ isch (402)- *
- em
-pr
Transient Persist. -
Me-Mel

My A ↳ NA=
Rev.
iny.
Irreu, mut.

H
ing
cell-death.
↓
Morph Mec=

Ap
Pyroptosis
Mecroptosis
 1) Reversible
Injury
isch (4,02]
Ballooning deg. Hep
↑
↓oxid phospl. (mitch-dam) e.g. [Acute Hepatitis
I] Earliest
↓
↓ATP cell-in I
- >

cell-swelling
11

except"
u
Als

hydropie/counseling
22
22.
Cell
Apoptosis, shrink.
ATP

↳ 2.
4
+

effmx
-J
(ATM)
Kidney 22

condly swelling
-
Tubular
Ep. cell.

ingt
-- large

an
 &
⑪ Reving anele EM=ultrastruct
-

x org -

·
⑪ ⑪ Mitoch

⑨
sucking
I swelling
a
222.
2
b
small
Ribosomal b
amorphous
detachment densities. -

22
amorphous densities
all

Rev. [ Irrew.
Small) <large)
Ning
ein.
# m.imp in in

ca+ (cytosolic)
+

↓ I
- -

id * Severe. *4
I
A
Irrer
Rewin
↓, t 22

Phospholipase. -memb.damoguite.
PL + catt

H
conc. lamin. Strud-
Aly
& 22

Myelin figures. Em
 ~Structurin figures

Y
-

> Cone, laminated

Whorl-like-
⑩ Nu-Damage.
⑭
granular
- a

8
⑧ o
fibrillas - Mu-chromatin
oo

⑳ > h loss of gel fibril)

⑧ cumbing
cig
 injury
Irreversible

Peristisch (402)
↓
444 Catt(cytosolia)
↓ ↓
I I
① ⑪ proteases.
phospholipase "Endonucleases.
A ↓ ↓

Myelin figures. (MC)

-

cytoskel. Nu-chromatin
pr dest (DNA)
-Mitoch => amorph
large A
damage.
loss
densities. of
call-architect
 Endonvelease
↓
-
↓ Mu-damage ↓
to
Pykno
22
⑪ >
Karyolysis.
Sis
⑪
A yorhexis" .I ->
s of chromation
dissolution.
Nu -

fragmentation. ↓

get numbintghe I
⑳O
->:

->:
.
--
↓ Basophilia.
↑
Eosinophilia
"Mu-dust"
-
-
 "Mecrosis.
↳
~

2-palterns
Y ↓
Coagulative Liquefactive
: Denaturation of protein
↓ e.g.
ischaemic. Ensymatic
=>

damage.
↓

tiss"ect I peeredin Hydrolytic action

Tissue
=>

I lost.
eg. isch-infarction
arch

solid-organscollagen
-

Rig
~
Heart-
①7
Brain-infarction
-
No-collagen
Kidney
-

- lives -
rich in lig. Ens
-
spleen
11 E Infections
Toxin/Ensymes
tissue
architect-
↳
s
act" Issue
↑
- architect
-

lost

I
- infections?
Kidney
 special types, Mecros is
A ↓ A A Fibrin
122. +IC
I
Gangrene 2 Caseous 3 Fat 4 Fibrinoid
me site- LL. ↓ ↓
X
-
· TB. FrameEnzyme al PAN
->

Dry
MC Wet.
·

Coagtlig. e Acute

malig-
Pancreatitis. HTM.
-
-

↓ ↓ 22.

Cheesy Cross Grss

·
#
tissue infection 22

Ashoff-bodies.
U

Chalky-white
·

↓ alt
Arch EN12
22.

Acid.
H A Mycolic FFA+ catt

Coag. Nee Lig. M. ·

mir.
Caseating Saponification.
Gramloma DM
↓
No-fibrinoid - Mec.
 omental

tissue,
-
Acute
↑

pancreatitis 22
7
22

a ally-white
H

11
carA
-

tissue Fat.Nec.
Lung Caseas M.
-

Cheesy
--
-
T.B.
 4BF
Fibrinoid necrosis
-

-IC.
Ic-med.
E-damage
=>

MNC (Est-BE ↳
- Infection/inflamm
-
piocogulants.
1,
0 Coag. Path
fibrin
->
-
I -BRIM -Pink I

Amorphous

00 ⑭ RBC Is
↳* T
↑

-
·
B= fibrinoid Mec.

O O &
8
->

T
⑳

>
< - ⑳
I ⑧
⑧
↑

L
Vasculitis, E-cell -
 Necrosis
=
=
Apoptosis
=
-

Mech A Permeab. ↑ Mitoch-permeab

lysosomal
↓
I

↑Ens-leall.

-
E
222- ↓ em-intact
=
X ↓
em-rupture?
No-inflammation?
·

Y
=

) x ↓
Patrol. Viral
29
⑭
Mar
·

inflammation I
Physiol.
-
I
Hepatitis
Le
Ey ①
organogensis.
#
Councilman 22.

72
my Pathological
Bodies
Killing of Inflamm
⑪. -

me aiw HCV
-
cells - after for
-
over
--
-

⑭ - we removed b
1
Killing of cells
(Prevent Art)
-
falling,
ORF
Apoptosis. I
am - Mitoch

1 ATP.

Programmed
cell-death
"Aries(Energy-depent
f A -

e.g.
gene-programm
-> Ap
->
Pyroptosis.
Mecroptosis.
=>

Autophagy.
 Apoptosis (MEMIEL(Gross.
Morphology of
①
Earliest-> cell-shrink.
⑪ M. charac-->Ch.
clumping.EAP).
⑪ CME intact
I No-inflamm
⑭ ⑭ -hosphatidylserine
e
Abe
·
A+Anneander
-Psafeig"I
 Bes-Jobfotic
~

bodiesin
e.g. Councilman

forganelle.
bodies.

⑪ End-outcome?
A prevent
En-remnant -

Efferocytosis. Al
-
-
efferocy Phagout
variant
of thag ·
No-cM-mp1=
- CM-rupt-
f
Ep.cell no-inflame inflamm
P effrocytes [Muc ⑰

⑰od.
Ap
-
Mec
Istromal
cell.

M Savager
efferocytosis
 Mechanism 22.
·

of Apoptosis

pro-Caspase
(inactive.
⑦
Caspase(e) -> Endonuclease.
2
flatratinof Ay X
Ap.
ch-clumping
=

M-DNA damage.
↓
*"of 180-200 BP.
"Specific" -

, 20
Internucleosomal
=>

DNet-damage.
 Agarose gel electrophoresis: "Endonuclease"
I
⑭ # 222
S
BR 222
-
->S

I
- 80D ->
" # meaning
be
Mec
-
-> 600
--
- -

-> 400

200
=

①
Step-ladder.
"Irin"in
1 Ap" [Charactnot
dx]
1) Mec.
 Programmed cell-death

genes
↓
Proto-onco
genes. I
-

↓
Pro-Ap Anti-Al.
i
·

BCL-Xs(4) 2. Behre

BeL-XL(X)
I
·

· Bax
Ball "Stress sensors"
e
·
·

Blts-family.T(cell-surface) CarPancreas
A -

Bim
- -

PUMA
:Bad -
NOXA
2 Bid.
 Mechanism
of Ap
↓ events ↓
R
-
Initiation 2 executiona
&I

Caspase", 8,9,10 Caspases

I
=
(3,6,7
--- ↳pathway
9.
122
-

Intrinsic
X

b) Extrinsic ⑬
H ↓
Edum.
-C-10
C- (Human)
q 28 -

animal
I intrinsic path (tch) Stress-Radilhem/HI,
↑Mitoch -

permeab) ⑰
·
mitos
Cy e ETC/eth
yos. Cytex Ap
·

X
I ""BHz pro"" -

smnesian
x Bcl-2
B

airicyte, e
->

X
>
Apoptosome
IAP"
-

pro-G-9 >C-9
 "Extrinsic path" (Death
Rmen)
11 -
Initiat
ID Ex
↓
9-9 C-2/10.
DR.
①
TMF-P-1 x+
⑪ FAS:CD95? Exec

23,6,7
+ Dligand tist

Cm
I

" ⑪E Et
↓
Ar
#
Ch. clump
X ↓
crE AP
proC-8 -> 2-8
To To
 PCB -

Mitoch
·withfr-e-activation ⑪ E-Caspase
X
⑪
N

R damage
- & 3F
-

As ACHV
Ferroptosis.
=

Necroptosis. ↓ 22.
Pyroptosis. Fest
--

⑯
-

H I
↓
↓ induce
Nect Ab
C-3,6,7 2-1, 4, 5, Il
Lo
Ferroptosis.
2,9,10
rantof liter
->

A A &M. infect
em-intal- ProILE It1. No-inflam
CM-rupture No-inflam grogen 1

No-M
A Cm-rupt
Mu-damage. ch
clump
Inflamm Ifraum Mech to
Ra

Ry-ca
variant
of
 Free Radicals akas-
oxidants ROS.
=

: Chemical sp.-"unpaired e-"outer-orbit

-

damage-r
I

↑
Stress produced
-> MOA- oxid,
Muerte
↑
-

>44 = FR-dam - Aging

~
447 FR -

Anti-Aging
"Oxidants" Antioxidants
I

**. wit Proteins.

&

Enzymes
2

·
823
2

A, , Ea
y
Ceruloplasmin
=

i
Catalase
H202 Transferrin."
·

Glutathione
=>

HOd8 peroxidase.
·
OH'- Moster. I
↳A
SOD (superoxide).
dismutase
Potent I
mut
Prevent ER-damage
Als ↓

Brin
Amyotrophic
lateral S4.MN+2mN
 FR
A
damage

↳emCPL) ->
"Brow-pig
"

I
⑳.

⑤
⑧
Lipofuschin) Iron
(Ma)
8.
⑧

al
↓
I oil-Red-Ost * Perl's
leriy Prussian blue
Sudan Black B
-

Stain
-
 H2- .

be
0
stain
↑
- Perl'sPrussian
Eine stain
oil-Red-0. Stain
Fran
-

1
↓
11

Brownpigment"
Y
⑧
↓
pign.
↓
O
Lipof:
↳ Aging
-

es
Irm.

000 6 Severe malnutrition

Ca-each exia.
"Wear a tear big
"

Li or

tell-tale Sign of Ahing"

"
 Black
Sudah B-stain

-- tipid
-
-
 Aging
↓
7 m.
imp hypothesis."ERdamage theory"
↑ Stress Aging. Y

①-cross-linking. "Aging4"
↓ # 11

4->
RFR-dam
4
Aging Hypothesis
# Molecular. Aging.
an

TelomeresSnowDanstrate
* #
e
shortening -> Aging.
#e --
b 4

299.

wbornetdir. (40-60 times)

[
⑪ Cell-div. I
↓
Clifetime)
2
N
Ishorter
limit
over Hayflick
-

A
-

↓ all

infusion/degrad
Cell-Aging
Aging
 Most-effective method 22
↓

i
Werten
Prolong-life span.
-WernerSand
-

re

ama
Carrie
① -
restriction
approprial

!
a
⑪ "I stress"
22.

RED Wine" -> SIRTUIM

(small) ·
IFR-damage
-

Dr.
·

Misfolding
·
I Metabolism. Coverall
↑ Glucose metabolism.
↑
[ => 4 Insulin
sensitivity]
 calcification >Starts > Mitochond
except
types
2 of Renal
X ↓
X
·

dead Tissue I Normal BM

Tissue - Abn- ·

damage
· ·

· Catt -> *4
·
Ca I Normal
↓
G
Metastatic cate.
↓
Dystrophic catt
MCC

LM-damage
⑪ Atheroscensis.
- TB
I metastasis -[:Fyperparathyroidism
-

mec P. Adenoma.

⑪ Pammoma-bodies.
Vit.! A
record
-

in
↓
Osteodast.
 HE9
amomnous] at CH i

122
Bestfonc ⑪
Alizarin. Red
--

VON-KOSSA
-

>Ca++
(Black) y catt
catt
I special
Stain >
0

00
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