Professional Documents
Culture Documents
1. Cell injury
1. Cell injury
DR PREETI SHARMA
MBBS, MD
GOLD MEDALLIST
One Liners
● 102
Most common cause of cell injury HYPOXIA
● Most common cause of hypoxia ISCHEMIA Bloodsupply x
● Cell most sensitive to hypoxia BRAIN NEURONS 3 5 mins
● Cell most resistant to hypoxia FIBROBLAST
Injury
a
Adaptation
Cell death
Reversible Cell Injury
Hypoxia to 2
IN
Eigg
CHANGE
e
t
iF_yy
wre
Nat Kt ATPase
pump
8
4201 HYDRO pic
I NEW X
g CHANGE
8 CELLULAR
E SWELLING
I FIRST
2MY MORPHOLOGICAL
CHANGE
EYEres
Myelin figure
start IT REV C I
IP in IRREV C I
Composition
PHOSPHOLIPID y Cat
MCQ
A. Cytoplasm
B. Nucleus
C. Cell membrane
D. Ribosomes
WAIT
A RER
H
Head
Ip
I
Nuclear in
damaging
2 points
Irreversible Cell Injury Membrane
defining damage
Mito
damage
XX Wm x x x
MI
F
phospholipase
nuclease
protease
n Mudiessarolution
condensation fragmentation
gggggi
CELLDEATI
Necrosis
Pathological celldeath
D Inflammation
1. Coagulative Necrosis
O
a
ARCHITECTURE PRESERVED
E YEE
dead
g É
APPEARANCE
kidney
I
COLLIQUATIVE
Necrosis
MALAKAR
Ketosis
BRAIN
3. Caseous Necrosis Him g
Fungal infection
CCHistoplasma
High
tent.i
tepid
in
TUBERCULATE
cell wall
Cat Ey
O
Alipase
CHALKY Blatfat
WHITE go
Cart faatid
Carta
5. Fibrinoid Necrosis
PAN
Malignant H TN
SCE
6. Gangrene
G Coag Necrosis
G Lig necrosis
O
7. Zenker’s Degeneration
iÉaÉ
0Coag.Necrosi
IypyoidfeverCS.Typhi Rectus Abdominis
SKELETAL Muscle Necrosis
Diaphragmatic
muscle
Fix
10 Neutral
Buffered
formalin
MCQ
A 61 YEAR OLD female patient presents with left sided chest
pain, radiating to the left arm and jaw. patient explains that the
pain has increased severely over the past 40minutes. She is
immediately rushed to the hospital. Cardiac enzymes are
elevated. The patient is admitted and started on thrombolytic
therapy. However on the fifth day of observation she suddenly
collapses and dies. Which of the following necrosis are you
most likely to find in the heart of this patient?
A. Liquefactive necrosis
B. Coagulative necrosis
C. Fat necrosis
D. Fibrinoid necrosis
Apoptosis
cell
●
●
Definition
Caspase Dependent Programmed
Inflammation? death
jaggy
enzyme
Es
g
ÉXageaving
organogenesisembryogenesis if defective
fused fingers
● Physiological COUNCILMAN BODY Hc syndactyly
●
OF
Pathological
CIVATTE BODY lichen Planus
Mechanism Of Apoptosis M I
caspas s5 5
Apoptosis
Initiation
a
Execution
Extrinsic
caspases
g
Pathway
Intrinsic
Pathway
CASPASE 9
ExtrinsicPathwad 8
Extrinsic
FCDIgligand TRIMER'sAton
satiric cell
OF Fas CD95
Procaspase 8,10
Caspase 8,10
Initiation- Intrinsic Pathway INTRINSIC
e
If Ux
Stressors
cell
BIP BAX
BIM NOXA PUMA
APOPTosome
I
A PAR I activate
caspase 9
Execution 3 6,7
caspase
apoptotic
0
f bodies
MY
o
I by
signal
to
FLIPPING OF
Phosphate
killing
Annexing Anagni
Identification Of Apoptosis HAIRY CELL
Apoptosis
Q ANNEXIN I LEUKEMIA
● Marker
O CD 95 Fas
o
●
●
D
Molecular marker
Microscopic examination
● Gel electrophoresis
D DHallmark O
1 smearing ofApop
I Apink
494Necro's's T A BLUE
NUCLEAR CHROMATIN
Apop CONDENSATION
MCQ
A. Necrosis
B. Apoptosis
C. Both
D. None
Bty
Necroptosis
CASPASE INDEPENDENT PROGRAMMED CELL DEATH
ÉF
ÉWftffsteatoepatihs
formation
Pancreatitis
I
Mechanism Of Necroptosis
TNF TNF RC
I
É
ML KL phosphorylation
NECROPTOSIS
MCQ
oi
g
MCQ
● Hypertrophy
● Hyperplasia
● Atrophy
● Metaplasia
● Dysplasia
D'D
or
O
O 7gooo t
g
stone
Intestine
UB
0 a
Estrogen
Éey a
hdinydrster.me
R
ÉEdTFodApg
FINASTERIE
Itg muscle atrophy seen in
y
Io
Nervesuppy X
I Estrogen Endometrial
atrophy
Endometrial
cancer
Endo Atrophy
Endo IP
t
t
Endo cancer
Endo cancer
OO
Poppy
FEEL
0
REFERSTATEMENITE
ofsteOPA
Reprogram
ÉmaEi
EGERlL
Columnar Bath
toff
Gobineau
metaplasia
ggg.gs YIdIcianB've
Barrett's
O O cancend
Eso
O
y
Item
TETE 2
E dit Trave
Lower limb trauma
egg
All are true about metaplasia
except?
1)Slow growth
3)irreversible
4)Can be precancerous
Accumulations and stains
MELANIN
SUBSTANTIANIGRATIFIETORE'T I HMB4
Fatin
Q
Tarot Tabbycat app
gtwÉIGÉj
É
X Tomas
D) First site of deposition of calcium is the endoplasmic reticulum
Q) Which Of The Following Stains Is Best Suited For The Diagnosis Of
Glycogen?
A. Oil red O
fat
Fe Hemosedean
B. Perl’s stain
C. PAS
D. Congo red
Amyloid
carbonate
It
Autophagy
1 Marker?
Inhabalism
If Eating
● 2016: Noble prize autophagy
LC3
s
Malnutrition Senile AB
eg
● Yoshinori ohsumi
diseasey
Gene?
Atg1
Cellular Ageing
il
FREE RADICAL INJURY
●
I
Why are we ageing?!!
Telomereshoratening
TELOMERE TTA 999
IT
q SHORTER I each
cell division
BIRTH Max telomeres
TELRASEE
shortingelomere
Itelomerased
d
Immortality
SIR Tu ins
● How to prolong lifespan??
calorie o
restriction
Role of sirtuins?
D
A B
C
d I 1 YR
Anti Re DM
Benefit cancers
ageing of
sirtuins
Premature ageing
Progeroid Syndrome
CHILDHOOD PROGERA
HUTCHINSON
GILFORD
Werner
Syndrome
ADULT SX
PROGERIA
I
dit DNA Helicase
defect
Werner syndrome is defect in?
t
1) DNA helicase
2) NER genes
3) MMR genes
4) All of the above
Note! PREMATURE EN I
AGEING
YI
N
Wer er M
Wer er
Syndrome Syndrome
Free Radical Injury- FORMATION??
FREE RADICAL INJURY
Y R O S Reactive
formation species
02 Fenton's Rn
Poisons MOST
chemicals
FerjeftiePotent
OH
sterox
Oz
ÉÉer 43 3
dismutase
Hydrogen Hydroxyl
Free Radical Injury- PROTECTION?
ANTIOXIDANTS Vit A C E
CuesCERULOPLASMIN
Enzymts
catalase
ÉÉ GlutathionePeroxidase
d