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15895.1590680943notepaedia Patho Sample
15895.1590680943notepaedia Patho Sample
3 Genetic Disorders 35
5 Immunology 63
6 Neoplasia 87
7 Anemia 103
8 Leukemia and Lymphoma 125
9 Blood vessels and CVS 152
10 Lungs 171
11 Kidney and Urinary Bladder 189
12 Central Nervous System 213
13 Gastrointestinal Tract 234
14 Liver 253
15 Breast 269
16 Male Genitals 278
17 Female Genitals 288
18 Endocrinology 300
1
1
CELLULAR
unrumm
RESPONSE
muumuus
stimuli
1 Altered Physiologicstimuli
OR CELLUR ADAPTATION
Non Lethalstimuli Eg DAtrophy
ii hypertrophy
iii yperplasia
Iv Metaplasia
2 LethalStimuli Transient Reversible cellinjury
Lethalstimuli Persistent Irreversible injury
1
Celldeath
1 NECROSIS
MORPHOLOGICAL CHANGES APOPTOSIS
NECROPTOSIS
PYROPTOSIS
3 Chronic InjuryStimuli Intracellularaccumulation
Eg FatsGlycogen Proteins
calcification
4 Sublethal Stimuli Persistent Induce cellularageing
CELLULAR
mmmm
ADAPTATIONS
mmmm
PregnanetUterus Barrett'sEsophagus
HYPERTROPHY
unnummmm
definition Sizeofcell 4 but NumberofcellSanne
Mechanism T in synthesis ofcellularprotein
Isalsoboth Physiological
mummmm Pathological
unmmunn
Eg Pregnantuterus Eg CardiacEnlargement
bothhypertrophy dit Valvulardefect
hyperplasia
2
HYPERPLASIA
muumuu
Liverregeneration
afterLiverResection
ATROPHY
muumuu
c
felf Hating
INTRACELLULAR PROTEIN
DEGRADATION PATHWAY
Ubiquitin Ligase activation
Ubiquitin
1
Targetprotein
v Thesearetakeninto
y t y
Activateproteasome Doublemembrane bound
organelle Autophagosome
Hi Contain ubitar.pro
degradationof Iv
Ubiquitin Tarprotein combinewithLysosome
14 HI
ATROPHY Degradationof
Protein
3
Both Pmhysmighongie Pathologicatmm
X y
duringfetal development Denervationatrophy
a Muscle
lossof notochord
Thyroglossalduct Ngeyrypey
3J fophy
Trauma
EndometrialAdenocarcinoma alw BOTH HUYEEEEKEELAtATROPHYm.ba
w talw
Type 1Endometrial Type 2Endo
Adenocarcinoma Adenocarcinoma
k k
GoodPrognosis Poorprognosis
I
i Bothareprecancerouslesion
METAPLASIA
unmurrumm
CELL
nvm
INJURY
ummm
ResponsibleforBrainprotection
i
from FRdamage
Mutation inSODgene AmyotrophicLateralSclerosis
Motorneurondisease
HYPOXIA
NEURONSSurvival
time
Most susceptible 3 4min
CARDIAC 2040Min
n30Min
FIBROBLAST hrstodays
n un of
Types cellw un
n un injury
Transientstimuli Persistentstimuli
Reversibleinjury irreversibleInjury
REVERSIBLE
unmurrunn
INJURY
mmmm
Ischaemia Hoz
v
t oxidative phosphorylationin mitochondria
t ATPproduction
Iv 5 lot ofNormal
N Injury
Nats 1 Firstsign cellswelling
ATP
in Nat
H2O exceptfor Apoptosis
KT 7 Kt
unmrumm
Firstsign Cellshrinkage
2 Vacuolar Degeneration
HydropicDegeneration
6 ditintracellularwateraccumulation
AKA CLOUDYSWELLING
Eg AcuteTubularnecrosisofkidney
Organelle changes EM Examination
0
omg
O OJO y L 1h20
i i
i
Ribosomes
ERswelling
a Ribosomaldetachment
Basta 6
Iii Mitochondria
AbsenceofCristal
Cristal Mitochondrial
Puca Swelling
cellinj Yoo o smallamorphous
densities
N
IV Important Factorforcellinjury Cat
cytosolic
ID
PLtcazt
Na41420
Ca c cast WHORLLIKE
v MYELINFIGURES
Mild9 AM ummm mmmm
I irreversible madeuptoPLtCa2t
Reversible seeninbothreversible irreversible
H injuryCMD
cytosolic CaucmildM e
I t
Phospholipase
Iv
DLConcellmembrane
Nucleus damage
Eosinophilic CPinklred
Bas.co
ohificgraygyoanrfaffbnrillarY
In Reversible
injury
i Disaggregationofgranulartfibrillary Nu chromatin
REVERSIBLE INJURY
Bunnummmm ummm
because of Persistentlethalstimuli
I
14CytosolicCadet
Activates
y
v v v
Phospholipase Proteases Endonuclease
Hi Hi Hi
Cellmembranedamage damageofcytoskeleton Nu damage
t protein k
i N'Myelinfiguresimax H DNAchromatin
ii EM Large flocculent amorphous Lossofcellarchitecture 1 Pyknosis
densitiesin mitochondria sE9YEAh
qarryyoj.fryhe.fi DAMAGE
7
it PYKNOSIS O
i Clumpingcondensation
ofchromatid
V 1
Shrinkage ofNucleus
iilkaryo rrhexis Nuclearfragmentation
Fragmentednuclei
E
iii karyolysis chromatin Lysis dissolution
decreasedbasophilia
Thrownout
Irreversibleinjury celldeath
Morphologicalchanges
NECROSIS
murmur
2patternsof Necrosis
i COAGULATIVENECROSIS ii LIQUEFACTIVE NECROSIS
MCpatternofnecrosis
Denaturation ofProtein DATLysosomalpermeability
1 k
Tissuearchitecture Preserved Enzymesleakout
Ischaemic infarction ofsolid to
Eg Enzymaticdamage ofcell
organsEg Heart Mc
Kidney HYDROLYTIC DAMAGE
Liver Tissuearchitecture Lost
EXCEPT INBRAIN Eg i Ischaemicinfarction of
Ischaemicinfarction Brain
thereisnostromalsupport
ofabsence ofcollagen
alsobrainisrichin
Liquefactive enzymes
ii Infections
SPECIAL
mmmm
TYPES
mm
1 GANGRENE
MCsite LOWERLIMB
a Dry gangrene b Wetgangrene
tissuearchitectureispresevered Bacterialcontamination
i EgofCoagulativenecrosis ToxinEnzymerelease
TypeofLiquefactivenecrosis
8
2 CASEOUS NECROSIS
i
It'scalledlikethis ofcheesy
mum appearance
Gross
YellowishWhitedebris
Seen in TB cheesy dit presence of MYCOLICACID
Onmicroscopic examination Coagulative LiquefactiveNecrosis
Amorphous GranularPinkstructure
considered as Variantofcoagulative Necrosis
3 FATNECROSIS
Itmay bedue to
a Enzymes bTrauma
Acutepancreatitis EgBreastinj
4
Lipase released
to
act onLipids
t
Release FA
combinewithCaa
calledsaponification
i GROSS Chalkywhite
appearance
MIE 2EccentricNu
Normal
I 08
Anucleated GHOSTCELL
Fat
cell Fat
cell
PinkCytop
Ba Ba M
Amorphous
Basophilicdeposits
510Calciumdeposits
80
d
5 FIBRINOLDNECROSIS
Presence of Fibrin 1 Immune
Complex AgtAb
Pathology Vesselwalldamage
k
Coagulationpathway Fibrinformation