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Cell Adaptations: Reversible changes (neither normal/injured)
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on removal of stress
Normal - without loss of physiology
Types-
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
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- Atrophy: Both size & number of cells ?
- associated with autophagy (performed by Lysosomes)
- Risk of TB infection - macrophage associated gene deletion
ATG5-5.
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Q. endometrial adenoca associated with - atrophy or hypoplasia
Hyperplasia - Type I endometrial adenoca.
Atrophy - Type II (Type II poor prognosis).
- Hyperplasia: Number of cells ?; Size same
- Hypertrophy: Size of cells?; number same.
- Metaplasia: Adult cell replaced ? another type of adult cell
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Stem all reprogramming mechanism
FirstRanker.com Squamous
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Respiratory tract columnar ? Squamous
associated with which vitamin deficiency Vitamin - A deficiency
Barett's esophagus. Squamous ? columnar.
- Intestinal metaplasia - Hallmark of Barett's esophagus
- Risk for cesophageal or brastaic Adenoca
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mucin in barett's: acidic - PH - 2.5
Stain used - Alcian blue.
Both Hyperplasia & Hypertrophy:
Pregnant uterus: major. Hypertrophy
Pregnant / pubertal Breast: Both hypertrophy + Hyperplasia.
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Lactating Breast - only Hypertrophy
CELL INJURY:
m/c Cause of cell injury - Ischemia/Hypoxia.
Neurons ? 3-4 mins.
Cardiac Tissue ? 20-40mins.
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most Resistant - Fibroblasts
FirstRanker.com I take four tasta
?oxidative Phosphorylation.
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?ATP (5-10% ? - cell injury)
Failure of Na+-K+ pump
I. Cell Swelling - 1st sign of all injury.
eg- Ballooning, degeneration of Hepatocytes
Except - Apoptosis. shrinkage 1st Sign
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water/Na+ appear as vacuole due to snadubility
-Hydropic degeneration / cytoplasmic vacuoles/
cloudy Swelling (ATN)
II. Ribosomal Degeneration - detachment due to swelling
up of endoplasmic Reticulum:
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* Todl. Reversible & Irreversible Injury Cell membrane damage
IV. Small amorphous densities in mitochondria - Reversible
Flacculent large densities ? Irreversible?
ultrastructural findings.
V. Nuclear change
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granular nuclear chromatin
? Change to...
Disaggregation of granular nuclear
chromatin
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most important
mild Marttain Severe?
Reversible injury Irreversible injury
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? phospholipase
Damage to cell membrane of
organelle alla po
Concentric lamellated figure (phospholipase+-Ca)
mielinoid bodies / myelin figures water
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? Present in both Reversible, Irreversible
Irreversible Reversible.
Irreversible Injury
Ca level ?-activates 3 enzymes
1) Phosphalifass. myelin figures?-maximum
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Mitochondria-large amorphous flocculent
densities
2) Protease - damage cytoskeletal protein damage.
Loss of cell architecture.
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nucleus-eosinophilic cytoplasm
nucleus-basophilic.
Damage of DNA / Nucleus.
Pyknosis clumping of chromatin
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Karyorhexis - fragmentation.
Karyolysis - chromatin lysis ? chromatin removed
? Basophilia of cell (chromatin dissolution)
Events
after cell death
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Necrosis
Cell Death
Apoptosis Necroptosis Pyroptosis
Necrosis:
Denaturation
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enzymatic
of protein
actions
?
Hydralytic action
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Tissue architecture
Tissue architecture-lost
Normal / intact
Coagulative N
Liquefactive N.
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m/c type
Bacterial / Basin infections
?m/c cause-Hypoxia.
m/c affecting - Heart (solid organs), Liver, kidney, spleen etc
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? Solid organs Heart - solid organs
Brain donot have- Fibrous stroma-collagen
Hypoxia - all organs: Coagulative necrosis
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Brain-liquefactive
- No collagen
- Rich is liquefactive enzymes
m/c. Cause in Brain ? Infections.
? Thermal Burns. Coagulative reagulojuret
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Coagulative Necrosis.
TB
* Gangrene. Srove
1st Coagulative necrosis
m/c site - lava limb.
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?
Dry default.
Liquefactive necrosis.
Tissue N. coagulative N
Architecture preserved.
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Cheesy material-Casseous N
due to myclic acid.
Wet Liquefactive.
Necrosis.
?variant of coagulative N.
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Coag. TB < day gangrene; TB > Wet gangrene
Necrosis
Zenker's-degeneration Necrosis. Prototype of Coagulative.
Zenker's > Gangrene > TB>Wet gangrene
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Lysosomal Permeability
?
Inflammation ?enzymes.
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? Apoptosis * cell membrane damage
No cell membrane
Damage.
?
Leakage of content
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No inflammation
?
* Inflammation
Physiological's/pathological Only pathological
Q.
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Programmed Cell Death
without Caspase activation
?
Necroapoptosis.
Caspase
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Hypaid - Necrosis + Apoptosis
Pyoptosis
-Neither apoptosis, no
E cell membrane damage
necrosis.
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inflammation
Pyrogen Induced Apoptosis
?Variant of necrosis.
Inflammation
?Both Physiological & pathological.
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cell membrane damage.
Physiological-eg-mammalian
growth plate formation.
Pathological
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Apoptosis - cell
(Active Process) - due to usage of ATP
from mitochondria.
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Active process > Programmed call Death
? Apoptosis enduad by loss of adhesion molecule
?
ANOIKIS
Q.
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Physiological Pathological
Organogenesis
Testfolding of proteins.
Cell deletion
?
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Cell deletion of auto
Apoptosis
reactive cells!
eg. Familial Hyperchlosterolemia
protective against
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Parkinson's, Alzheimers
autoimmunity.
Huntingtons GVHD
Cystic fibrosis. Salivary
Tumor all death.
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?Chemotherapy+ Radiotherapy-Necrosis / Apoptosis
Q
eg. (Severe stimuli) mild stimuli - only apoptosis
to cell
Glucocorticoid induce apoptosis.
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Apoptotic Body
-Viral Hepatitis
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Morphology-
earliest change all shrinkage
2) M/characteristic: Chromatin condensation > cell membrane intact
?No inflammation
4) Cytoplasm-eosinophilic.
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5) Phosphatidyl Serine Facepitous. (Lipid Receptors facing
Inwards.
? Apoptosis.
Hip outside
Amexin Dye - detector the flip: marker of Apoptosis.
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- stain used for Lipid
Liped Stain - Oil Red stain.
Glycogen ? PAS.
Sudan Black.
Osmium Tetraoxide
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Cell membrane bleb
Detach
Apoptotic Bodies
? cell membrane bound structure with cagandle,
may/maynt have nuclear remnants
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Phagocytosis
Receptor mediated ( no inflammation)
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Biochemistry of Apoptosis:
Pro Caspase
Hallmark of Apoptosis has themed sitantechn
DNA damage
Caspase ?endonuclease chromatin
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DNA damage Rutxided fragment.
Condensation
multiples of x200 Base Pairs
Internucleosomal DNA damage
Agarose Giel Pattern.
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due to Aep Ladder
Smeared
endonuclease. Pattern.
Pattern
?Seen in apoptosis necrosis, Pautcharecdeistiof Necrosis.
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Smearing Pattern- Necrosis
(11). Initiation Caspases
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a) Intrinsic - major pathway - Caspase-q
b) Extrinsic Caspase-8 Caspase 10
execution.caspases.
?
Caspase-3,6,7 Cas-3 m/I.
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Lendonuclease
Protoncogenes
Apoptotic Anti-apoptotic
Bcl-X6(stimulate) elenas Bcl-2
- BAX, BAK
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BH3 Proteins
BCL-XL (Lowering)
NTCL-1 2.
(m/c mutated en drug resistance)
Drug Resistance.
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P53>MCL-1 MCL-1 Drug Resistance protoniogene
P53-Tumor suppresor.
BH3 Proteins. Stress Sensors.
Bim
PUNTA
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Bad
NOXA
Bid.
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a) Intrinsic Pathway
Pathway
Stress
+ve 1
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BH3
BAX
Bcla
BAX.
Fimbibited BAx expressed
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on outer membrane.
Apoptosome
mitochondrial permeability...
Cyt-C-mitochondria - ETC
channels
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cytosolic Cyt-ca
? permeability / leakage of
Proteins
SMAC-
Cyt-c into cytosol
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DIABLO pastein
Apotesome
Inhibit
inhibitor of anti apoptosis
Initiate Caspase-9
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FirstRanker.com Death Receptor mediated
TNF-R-1 FAS-CD-95
Trimerization
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Death Receptor +
DLigaments.
Adaptar-protein
Flip.
Brocaspases 8, 10.
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Lip protein- Inhibitor of extrinsic pathway
Final pathway
C-9 C-8,10.
C,3,6,7
endonuclease chromatin Condensati
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Intrinsic textrinsic pathway.can accu
(Independly).
?Hallmark of Neuronal apoptosis - Apoptosis
inducing factor
(No caspases)
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tree - Radicals
? Produced normally
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unpaired election in outer cabit x
oxidation mechanism of damage
cell membrane damage
+
Cytoplasmic protein
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nuclear membrane dama
?
DNA damage (Somatic damage)
most potent / mest Reactive - OH
Free Radaly Lipofuschin Bovcum pigment
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cm dam
age
1) Ageing
?) malnutrition
iii) Cancer cachexia.
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Telltale sigh of ageing / Free Radical injury
? Brown atrophy of myocardium.
Carcinoid Specimen brown - Lipofuschin.
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Lipofuschin Hem
(m/c)
Sudan Black
Peal's prussian blue stain
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Jenous fenocyanide
07e2+ fenicfence
Osmium Tetraoxide
Annexin-V
On Oil Red-Ostain-best for oil- Frozen Section.
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FrozenSection - Intraoperative Biopsy
? Never confam diagnosis Immediately (confiam-2 days)
Temp: -15 to -30°C
14-15 - 20 minutes - ?) D-Bering/malignant.
Tentative iii) can tell metastasis to sentinel lymph node
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10) Resection margin involvement
1) Theory of Free Radical Damage for Ageing-mlaccepted
theory
1) Increased crasslinking of collagen, Theory for ageing
Anti-oxidant vitamins - Vitamin A, C,E.
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Bokins - Transferrin, Ceruloplasmin
?lenzymes - Catalase, glutathione peroxidase? Peroxisomal
Superoxide Dismutase.
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present
Glutathione peroxidase - most potent anti-oxidant
in body
Peracional enzymes - H20s paiduction & degradation
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Lysosomes H202 production only
?Brain protected from Freidadical Pryny SOD-1
Cu-Zinc SOD-1.
ANTL (motar rewon Lon disease)
Calcification
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Abnormal
Tissue
noimall
Tissue
Death/degenerated Re
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Cat
Rystrophic Calefication
metastatic Calcification
TB
Hyperparathyroidism
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IHOT (m/ccoduse)
?RHD.
prammoma bodies
m/c Parathyroid adenoma
Aneurysm
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Hypercalcemic Cousis.
monckebergs mediat
CaBreast > Calung.
Sclerosis.
Squashow
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Small coll
deductive Vitamin-A/D?
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lysis - Hypercalcemia
activate
Parathyroid-not-affected (calcified)/revelyaffeded
m/c affected alvedi (lung)
Calcification starts in mitochondrial except kidney-Basement
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Special Stain - 1) Von-Kossa [m/c, Best]
membrain
for Calcium 2) Alizarin-Red (most specific) for calcium
3) Calcein !!
4) Tetracycline Labelling stain (Best for bone mineral
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Melaunin-Fontana-Tasson.
Collagen o Contiective Tissue - Tasson Trichrome Collagen
Fungal Hyphae - Silver methenamine
Alzheimer's disease - Nanofibrillary tangles-Bielochousky stain
Ageing
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Telomeres-tronconding areas at the end of chromosomes
Progressive size & on fuither Replication
No Telomerus.
Et furons/degradation
Cellular ageing
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? Normal calls are capable of division of 60-70 times
Hayflick limit
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Telomeu ?lengthening - Carcinogencies
Telomerase RINA - defended DNA polymerase
Eresponsible for lengthening) (Reverse Transcriptas
present in Grem calls > Stemcells
Nosmal Somatic cell-rotelomerase
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most effective way of padenging lifespan Calaise
(smallamt) Red Wine Seautins ir pulke
Apoptosisey) Raduce faue Radical damage
1 glucose metabolism ) 1 snsulin sentivity
Werner Syndrome- NTEN
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Werner Syndrome - Prunatue aging.
defect in DNA Helicase.
(Repair)
Selver methamine Stain Fungus - Black/Brown
Background greenn
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Branching-aspergillus
Septate Branching
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Immungluarecence.
merexpeg-Dichaveicmivas (allows only alight)
Background-Black
Acanthamoeba - optically greenish white - cell wall
Calcofluor white stain
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INFLAMMATION
-Aaule inflammation-
I) Vascular events Ist Transient vasoconstriction
Vasodilatation
Vascular Parmeability) acute anlamind
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Stasis (Sathat reutrophil can
deviate to perphery)
Vascular Parmeability)
1) lordothelial gap - (m/c-mechanism)
at the level of venules. exakt lungs - capillaris.
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- Immediate / Transient response.
2) Drauct endothelial Injury - Immediate prolonged
mild endottieliaftinjury - suntur/paadiation,
daloyedspadongeleaper than star
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This download link is referred from the post: Medical PG Handwritten Notes 1st Year, 2nd Year, 3rd Year and 4th Year (Study Material)
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