2 Cell Injury

8/11/2019 2 Cell Injury

1/22

ell injury

#Cells are constantly change their structure & function according to various

demands & stress.

# The Cells react to injury by :

1 -Adaptation= altered state that preserve ! vitality of ! Cs in response to stress

physiologic or pathological.

# Types of cell adaptation are :

a -Hypertrophy..increase in organ size d.t increase insizeof its Cs .

b -Atrophy... decrease in organ size of an organ d.t decrease in size of its Cs.c - Hyperplasia.increase in size of an organ d.t increase in numberof Cs

2 -Degeneration = reversible injury of Cs.

3 -Cell death=Irreversible injury.

# There are 2 patterns for cell death:

-Apoptosis. (single cell death).

- Necrosis.(Death of group of Cs)

Degeneration

Def:Reversible injury of living Cs leading to metabolic, functional & morphological changes.

Classification: Typical

1)Cloudy swelling & hydropic degeneration: d.t increaseintracellular water.

2)Fatty change: d.t increaseintracellularfat.

Atypical.(Intracellular accumulation & extracellular depositions)

1)Mucoid degeneration & myxomatous degeneration: disturbance of mucopolysaccharides.

2)Hyaline degeneration (or change).

3)Fibrinoid degeneration.

4)Amyloid degeneration.


2/22

2

2

CLOUDY SWELLING.(Albuminous degeneration)

Etiologyof degeneration

o

Physical:e.g. cold, heat, electrical, & irradiation.

o

Chemical:e.g. poisons, drugs, acids & alkalis

o

Infectious:e.g. bacteria, virus, & fungi

o Immunological:Ag-Ab reaction

o

Hypoxia:e.g. in anemia & loss of O2 carrying capacity.

Myocardial infarction and necrotic tissue

Pathogenesis:

o

Mitochondrial theory: mitochondrial damage --ATP production failure of Na/K pumpaccumulation of Na & H20 in ! cell.

o

Increase intracellular osmotic pressured.t: accumulation of metabolites.

o Bothintracellular accumulation of water.

Organs affected:parenchymatous organs (e.g. liver,kidney, heart & pancreas)

are mainly affected because Cs of these organs are highly active

containing ++ number of mitochondria.

N/E: -Organ is ++in size e tense capsule & smooth surface.

-Soft in consistency, e rounded borders & bulging cut surface

M/E -Cs are swollen e granular cytoplasm. Nucleus is normal (N)

-in Kidney tubules show ( Star shaped appearance)

Hydropic degeneration (Ballooning = Vacuolar(

Def: severe form of degeneration, severer than cloudy swelling.

N/E&M/E: Same as cloudy swelling except cytoplasm is vascularnot granular

Examples are: Accumulation of ++fluid in epidermal Cs as in burns or herpes simplex.


3/22

3

3

Fatty change (Degeneration OR Infiltration)

Def: Increase accumulation of intracellular neutral fat (Triglycerides) in

parenchymatous cells transforming into fat like cells

Sites: parenchymatous organs, most commonly in liver.

Cause: Same aetiology as degeneration But :

-Irritant is severe e short duration of action OR

-Irritant is mild e long duration of action + Etiology of fatty liver (discussed after)

Pathogenesis

A -Fatty degeneration= Mitochondrial theory:! injurious agent

injury to mitochondria release of mitoch. lipid in ! cytoplasm.

B - Fatty infiltration : Special mechanisms in ! liver:

1-

++ entry of free fatty acids into liver. e.g. ++intake or mobilization of fat from depots

.

2-

++ fatty acid synthesis in ! liver from glucose(DM) & amino acids

3-

++ rateof conversion of fatty acids to triglycerides (esterification).

4- --- fatty acid oxidation.

5- --- conjugation of fatty acids e apo-protein.

6- --- lipoprotein secretion from ! liver.

The above causes can act by 1 or more mechanisms, e.g. chronic alcoholism acts through 1,2,3 .

M/E: of fatty change in any organ:

Fat is dissolved during preparation:

1-In Hx/E: cells containing fat are enlarged

cytoplasm contain empty vacuoles W enlarge/coalesce/push nucleus

to oneside of cell giving (Signet ring appearance)

2- In Frozen section:

the fat appear in cytoplasm as droplet

W enlarge/coalesce/push nucleus to one side of cell giving

(Signet ring appearance)

can be stained by:- * Osmic acid black * Scarlet redRed

* Sudan III Orange


4/22

4

4

Pathological features:

N/E: Size : enlarged

2S

Shape :preserved

- Border : rounded

Colour :pale yellow

2C Consistency : soft C/S : bulges out, greasy to touch,diffuse or focal

M/E:Same as before +

Distribution:

- Focal: as in viral hepatitis.

- Zonal: toxemia & anemia.

- Diffuse: Nutritional cases

N.B: (Nut-meg liver) It is morphological term describe Focal Fatty change of liver

in case of chronic venous congestion of liver (will be discussed in circulatory disorder)

Heart

Two types:

1) Diffuse: occurs in severe injury

- Early: Heart becomes flabby, soft, ++ rupture AHF.

- Late: Myocardial fibers are replaced by fibrosis decrease in heart size.

2)

Patchy (Tabby cat) or tigroid appearance or frush breast. occurs in moderate injury

N/E: yellow streaks(fat) alternating e brown (intact ms fibers) areas mottledappearance.M/E: Same as before except (No signet ring appearance)

N.B:

1- Obesity fat deposition in fat deposits.

2- fatty change fat deposition in parenchymatous cells.

3- adeposity fat deposition in tissue of parenchymatous organ.

Kidney fatty change

N/E : ! same as liver+ Cut surface shows yellow streaks in ! cortex.

M/E : same as before+ Fat vacuoles appear in cytoplasm of proximal convoluted tubular Cs.

Fatty

liver


5/22

5

5

Disturbance of mucopolysaccharides

Def:++accumulation of mucopolysaccharides in epithelial Cs (mucoid degeneration) or

CT (myxomatous degeneration)

Mucoid degeneration Myxomatous degeneration

Def

EX

Occur

M/E

affect epithelial cell

1 - catarrhal inflammation

2 - mucoid adenocarcinoma

intracelluar

( signet ring appearance)

Swollen cells filled E` mucin

Pushing nucleus to one side

Of the cell

affect C.T

1 - Myxedema

2 - Myxoma (tumour)

Extracellular

( Wharton's Jelly)

Branching cells E` pale blue cytoplasm

Hyaline degeneration (hyalinosis)

Def : Structural changes of dead tissue into homogenous,pink,refractile,structurless material

Cause : Still Unknown

Types : 1 -Extracellular 2 -cellular

1) Extracellular (C.T hyalinosis)

A - Vascular:

-arteries 1- Atherosclerosis

-arterioles 1 - benign hypertension

2splenomegaly (central arteriole of spleen)

-capillaries 1-D.M

2 - Benign hypertension

3 - glomerulonephritis

B - Extravascular: 1- leiomyoma

2 - old thrombus or infarction


6/22

6

6

2) cellular

#Russel bodies in Rhinoscleroma:def of russel bodies hyaline degeneration of plasma cells

# Councilman bodies in viral hepatitis in liver: def of councilman bodies

hyaline degeneration of hepatocytes (it is proved to be apoptosis than degeneration)

# Corpora amylacia in benign prostatic hyperplasia

# Islets of langerhans of pancreas in D.M

zenker's hyaline degeneration (Necrosis)

= Hyalinosis in ! voluntary muscles occurs in severe infections & fevers, especially typhoid.

Sites :- Rectus abdominus,Diaphragm,Intercostal muscles.

Complication : Rupture of muscles & hemorrhage

Fibrinoid degeneration

Def :homogenous or granular, eosinophilic material e staining properties

like fibrin (destroyed collagen).

Examples:

Collagen diseases: e.g. Rh fever, polyarteritis nodosa, systemic lupus erythematosis (SLE).

Malignant hypertension: in ! walls of arterioles.

Amyloidosis

Def :disease complex (not a single disease) characterized by abn protein

deposited ( ) Cs in many tissues & organs of ! body variable clinical pictures

It has a uniform morphological appearance but different chemical composition.


7/22

7

7

Chemical nature of amyloid protein :

- 90% of amyloid structure is formed from protein called fibrillary protein w` is 2 types:

a) Major component :-

-AL:amyloid derived from light chain Ig.

-AA:amyloid derived from SAA(serum associated amyloid).

It is deposited in case of chronic inflamatory disease.

-AF:amyloid of familian medetrian fever(F.M.F).

-AE:amyloid of endocrine glands.

-AS:amyloid of senility.

B) Major component :-

-amyloid endocrine thyroid:- in medullary carcinoma of thyroid.

-pre-albumin.

-B2 microglobulin.

-B2 amyloid protein in alzehemir disease.

Clinical types of amyloidosis:

A Localized : occur in vocal cord

Thyroid gland

Heart

B Systemic : 3types -primary amyloidosis

-Secondary amyloidosis

-Familial (F.M.F)


8/22

8

8

Secondary amyloidosisprimary amyloidosis

Occur in any age

+ Syphilis Common

1 - Infective granuloma as T.B , Leprosy.2 - allergic granuloma as arthritis

3 - chronic suppurative granuloma as:

-chronis lung abscess

-chronic osteomylitis

-hodgkin's lymphoma

- bronchiectasis

AA(amyloid associated)

exceptSolid organ than Hollow organ

heart

Occur due to renal or hepatic failure.

Occur in old age

Rare

Of unknown cause associated E`dse c`h by production of Ig as:

multiple myeloma/non Hodgkin's

lymphoma (malignant tumour of B-

lymphocyte)

AL(light chain)

Hollow organ than Solid organ:

-hollow organ as heart,GIT,muscle.

-solid organ as

Liver,spleen,kidney

Occur due to heart failure.

Age

Incidence

Cause

Type = nature of

protein

Organ affected

Death

:of any amyloid organN/E:

Size : enlarged

2S

Shape :preserved

Capsule : tense

Colour : brown or gray

2C

Cosistency :firm,rubbery or waxy

Border : sharp.

Cut surface : flat.


9/22

9

9

of any amyloid organ::M/E

1 - Site of deposition : differ according to the organ.

2 - Shape of amyloid material :

Spread forward ,backward,laterally enclosing original

Cells ischemia , atrophy , degeneration and necrosis.

3 - Stains(method of demonstration of amyloid material):

)write it E` N/E: (gross staining*

A - Lugols iodine : stain amyloid : dark brown.

stain rest of tissue : dark brown.

B - iodine e` 1% sulphuric acid: stain amyloid : blue.

)write it E` M/E(microscopic staining:*

A - HX/E :amyloid appear homogenous refractilepale pinkmaterial.

B - Congo red stain : amyloid appear orange red.

C - Metachromatic stain : stain amyloid rose red.

stain rest of tissue violet.

D Immunohistological : momclonal Ab is directed against various chemical

form of amyloid.


10/22

1

1

Pathological features of amyloidosis in some organs

1) Liver

N.B: cause : secondary amyloidosis more thanprimaryamyloidosis. () .

N/E:As before + gross staining (write them) .

M/E:1 - site of deposition of amyloid material :- Space of disse-arterioles-venules.

- It begins in intermediate zone then spread in both direction.

2 - shape of amyloid material

3 - microscopic staining:

Clinical effects: - don't affect liver function except very late

- liver failure is rare..

2) Kidney : !most common & seriousN.B: cause :secondary amyloidosis more thanprimaryamyloidosis. ) )

N/E: -As before + gross staining (write them) +except only that (SIZE)

Early no change in size, later kidney is ++in size. In prolonged course it may become

small d.t ischemic changes (2 ry contracted kidney).

M/E :

1 - Shape of amyloid material:

2 - Microscopic staining:

3 - Site of deposition of amyloid material: diffuse deposition of amyloid material in:

a-

Afferent arterioles

thickening of the wall & narrowing of the lumen.

b-

Glomerular capillaries:

Amyloid deposit in ! basement membrane

c-

Collecting tubules :

Amyloid deposit in ! basement membrane.

Hyaline casts in ! tubular lumen.

Clinical effects: a - depsoition in afferent arteriole (Nephrotic syndrome) occur.

b - deposition in glomerular capillary (Diabetic insipidus) occur.

c - deposition in afferent arteriole (Renal failure) occur Later.

N.B: Nephrotic syndrome = generalized edema.

Q- patient e` chronic lung abscess ,Suddenly develop heavy proteinuriaand generalized edema

What is M/E of kidney? Write M/E of (Amyloid kidney)


11/22

3) Spleen :one of 2 patterns develop :

N.B: cause : secondary amyloidosis more thanprimaryamyloidosis. ) ( .

- there are 2 pattern of amyloid spleen :

a- Sago spleen = Focal type.

B- Diffuse amyloid spleen.

c- may be mixed type.

N/E:As before+gross staining (write them) except only one differenceaccordind to pattern:

C/S: -If focal type Brown dots on backround.

-If diffuse type Brown streaks on background.

M/E:: 1- Shape of amyloid material:

2- Microscopic staining:

3- Site of deposition : differ according to pattern :

If focal type amyloid is present in central arteriole then replace lymphoid

follicle So called Focal type.

If diffuse type amyloid is present in basement membrane of splenic sinusoids and

blood vessel Then compress lymphoid follicle So called diffuse type.

Clinical effects: Cause splenomegally.

Sago Spleen. Diffuse amyloid spleen.

Incidence

Size

Lymph follicle

C/S

M/E

Common

Moderately enlarged.

Atrophied by pressure.

Plenty brown dots.

Amyloid in central

Arteriole.

Rare

Marked enlarged.

Not atrophy.

Diffuse brown streaks.

Amyloid in blood vessel

and blood sinusoids.


12/22

2

2

4) Heart

Amyloid is deposited ( ) cardiac muscle fibers & walls of blood vessels. Subendocardium is mainly

affected especially seen in ! atria. Heart is ++in size. It may lead to heart failure or conduction defect.

5) Alimentary tract (stomach & intestine)

The mucosa is thickened by deposition of amyloid in basement membrane of capillaries. This lead to:

Atrophy of epithelium causing malabsorption.

Altered permeability causing diarrhea & electrolyte disturbance.

6)Tongue : this may cause macroglossia (++ tongue)

-Gingiva:Thickened gingiva.

-Peripheral nerve : Thickened, associated e neuropathy & axonal degeneration

Pathological calcification

Def : Deposition of Ca++ salts (phosphate & carbonate) in tissues other than bone & teeth.

N/E:Calcified area resembles chalk. It is dull opaque, white, e finely granular surface

& hard in consistency.

M/E: It is dark bluish, granular, e hematoxylin.

Types: 1 -Dystrophic calcification. It is ! commonest type.2 -Metastatic calcification.

3 -Stone formation.


13/22

3

3

1 ,2-Dystrophic calcification. It is ! commonest type

Dystrophic calcification Metastatic calcification

Def

Cause

Ex

Deposition of Ca in dead or

degenerated tissue e` normal Ca level.

1 - Local alkalinity of necrotic tissue.

2 - increase activity of

alkaline phosphatase.

a - in degenerated tissue:

- old scar.

- leiomyoma

- wall of chronic abscess.

b - in dead=necrotic tissue:

- infarction.

- fat necrosis.

- pus of chronic abscess.

c - calcinosis of unknown cause:

- Localized (calcinosiscircumscripta)

in skin-S.C tissue.

- generalized (calcinosisuniversalis)

in muscle and tendon.

Deposition of Ca in normal tissue e`

elevated Ca level.

1-increase blood Ca by:

- increase intake from diet.

- increase mobilization from bone.

- Sarcoidosis.

1 - gastric mucosa.

2 - renal tubules.

3 - lung alveoli.

4 - arteries.


14/22

4

4

3) Stone formation

increase Ca salt deposition in biliary tract, urinary tract & rarely in other ductal systems,

pigmentationDef : Pigments are colored substances that stain ! tissue. These ??

accumulate intracellularly. Pathological pigmentation includes two major fs:

I) Exogenous:

a-Anthracosis : Black pigmentation of ! lung d.t inhalation of carbon, which is engulfed by

macrophages. It is d.t air pollution. In ++ exposure lead to pulmonary fibrosis or emphysema.

b-Tattooing : Injection of colored pigments into ! skin, taken by dermal macrophages

II) Endogenous:

Melanin

- Formed by melanocytes from tyrosine by ! action of tyrosinase.

- Responsible for ! (N) color of skin, hair, eyes meninges & basal ganglia.

# Causes of melanin hyperpigmentatlon:

1 - Exposure to sun.

2-Addisons disease.

3- Chloasma of pregnancy : Pigmentation around nipple,face & genitalia.

4-Tumors of melanocytic origin :

a - benign : pigmented nevus .

b - malignant : malignant melanoma

5- Cafe au lait skin patches: in multiple neurofibromatosis

# Causes of melanin hypopigmentation:

1- Albinism: This is a generalized hypopigmentation d.t congenital tyrosinase deficiency.

Melanin pigment is absent from skin, hair & eyes.

2-Leukoderma: congenital or acquired (as in leprosy ).


15/22

5

5

Lipochrome pigment (Lipofuscin)

Def :yellowish brown pigment w present (N) in ! heart, testis,seminal vesicles, & adrenal cortex.

Example: brown atrophy of ! heart :

Cause: Senile atrophy.N/E:

1 - Heart small in size.

2 - wall of heart thin

3 - pericardial Fat disappear

And replaced by ( edematous jelly like tissue).

4 - Myocardium brown in colour

5 - Orifices of heart still large

6 - coronary artery Is tortuous

M/E:

1 - muscle fiber of heartare thin,atrophy.

2 - nuclei are pyknotic (small,eccentric,dark stained).

3 - yellowish brown lipochrome pigment on both sides of nucleus (peri-nuclear distal)

4 - Interstitial tissue show area of fibrosis.

5 - The section is stained e` HX/E only or Fat stain.

M/E: affected cell undergo

necrosis and fibrosis.

Effect:

- Liver pigmentary cirrhosis. hepatoma in 20% of cases.

- Pancreas diabetes mellitus.

- Heart heart failure.

- SkinHas a bronzed color d.t ++ melanin & Hemosiderin deposition.


16/22

6

6

Hemoglobin - derived pigments

1) Bilirubin : ++in jaundice.

ve e`Prussian blue test.

2) hemozoin (hematin) : brownish iron containing pigment associated e bilharziasis & malaria.

The pigment is produced by ! worm released into blood, then

engulfed by macrophages in liver & spleen (Parasitic pigmentation). -ve e` Prussian blue test, .

3) Hemosiderin:

- A brownish iron containing pigmen.+ve Prussian blue test.

# Types :

a -Localized hemosiderosis:

- In areas of hemorrhage

- blood leave bl.vessel to tissue fibrosis

- hemosiderin is phagocytosed by macrophage

b -Generalized hemosiderosis (Primary &2ry types)

1) 2ry hemosiderosis:

Causes:Iron overload d.t:

- Repeated blood transfusions.

- Hemolytic animas.

- Bone marrow hypofunction (Impaired utilization of iron).

Pathology :

a- normally,iron is stored in cells binding e` apoferrtin to form haemosidrine.

b- Excess haemosiderine appear in mononuclear phagocytic cells and in

advanced cases affect parenchymal cells.

2) 1ry hemosiderosis = Bronzed diabetes:

Causes :inborn error ch`by defect in apoferrtin-ferrtin system excess absorption of iron.

Pathogenesis:

Excess absorption of iron saturation of macrophage system deposition of iron in phagocytes and

in parenchymatous organ (more severe) injury and manifestation. Incidence:

male above 40 years

Female is protected by Menstruation.

N/E: affected organ is ( 3R ) enlarged-hard- Brown.


17/22

7

7

Cell death include

a - Necrosis b - Apoptosis

NECROSISDef :Death of a group of Cs e in a living body.

Causes :

Sameetiology of degeneration ( discussed before ) except only 2 difference:-

1-Irritant has Severe intensity

Prolonged duration

2-Chemical agents are proteolytic enzyme of amoebaPoisons-drugs

Pancreatic secretion

Pathogenesis:

1 - Severe mitochondrial damage and marked reduction of ATP production

Increase anaerobic glycolysis decrease of most enzymes except lysosomal enzymes.

2- destruction of cell membrane enzymes become free.

3- increase intracellular Ca increase of following enzymes :-

a - protease breakdown of cytoskeleton protein.

b - phospholipids destruction f membrane phospholipids.

c - Endonucleases breakdown of DNA chromatin fragmentation

pyknosis-karyorrhexis-karyolysis.

4- 2 processes underlie the basic morphological change:-

a-Denaturation of protein.

b-Enzymatic digestion of organelles and other cytosolic component by:-

*cellular lysosome autolysis.

*polymorphs lysosome.

#When denaturation predominates the cells retain their outline e` loss of cellular details

and the area is firm,pale,swollen.

#When enzymatic digestion predominates there is loss of architectural and structural detail

And the area is soft and filled e` turbid fluid.


18/22

8

8

Pathological changes:

N/E:the necrotic area is dfined

dull,opaque

firm

swollen

surrounded by zone of hyperemia(acute inflamation)

M/E =post necrotic change:-

1- Cellular

a - Nuclear :* pyknosis: small-dark stained nucleus.

* karyorrhexis: fragmentation of nucleus in cytoplasm.

* karyolysis : nucleus disappear due to chromatin hydrolysis.

B - cytoplasm :

* Cytomegaly : swollen of the cell.

* become more eosinophilic.

C-cell membrane :

* It disappear and enzymes become free.

2- Architecture

a - denaturation occur OR

b - lysis: autolysis:release proteolytic enzyme from tissue.

Heterolysis: release proteolytic enzyme from macrophage.

Fate of necrotic tissue :-

If small part :

*Liquifaction occur.

*Absorped by macrophage

Then undergo :

- Regeneration OR

- Fibrosis.

If large part :

*Encapsulation occur = Surrounded by fibrouscapsule.

Then undergo: Liquifaction OR

Calcification OR

Putrifaction occur gangreneOR

Bacterial infection occur pus abscess occur.


19/22

9

9

Types of necrosis:

1 - Coagulative necrosis 2 - liquefactive necrosis

Etiology

EX. and

pathogenesis

N/E

M/E

a - Cut of blood supply (ischemia)

- allinfarction exceptbraininfarction.

a - blockage ofaction of most

enzymes due to denaturation

of cellular protein by irritant.

b - As hydrolytic enzymes

are blocked

Preserved ararchitecture of

dead tissue it appear paler than

normal tissue like boiled meat.

Same as before

1 - Post necrotic change:

Nuclear,cytoplasmic,denaturation,

But Nolysis.2 - Lossof cellular details e`

Preservedarchitecture.

3 - blood vesselpersist for long time:-

(more resistant)

a - Cut of blood supply (ischemia).

b - Proteolytic enzymew` liquify

necrotictissue.

1 - Brain infarction:due to high lipidcontent

and lack of lymphatics.

2 - pyogenic abscess:due to proteolytic

enzymes frompus cells.

3 - amoebic abscess:due to liquifactive

enzymesproduced byparasite.

Liquified tissue and it is soft.

1 - Post necrotic change:

Nuclear,cytoplasmic,lysis,

But Nodenaturation.

2 - Complete loss of cellular details and

Lossof architecture.


20/22

21

21

3) Caseation necrosis

Etiology :allergy followed by liquefaction

EX : T.B and Syphilis ($).

N/E :the necrotic area is * yellow,dry.

* friable.

* Notsurrounded by hyperaemia.

M/E :1 - Post necrotic change.

2 -homogenous structurless pink eosinophilicarea.

T.B Syphilis($)

*Extent of Necrosis

*cellular details.

*occurrence

*giant cells

Wide

Complete loss

Rapid.

++

Limited.

Partial loss.

Take longer time

+ (less)


21/22

2

2

4) Fat necrosis: Necrosis of fat

Types :

a -Traumatic fat necrosis:

trauma to ! adipose tissue of subcutaneous fat & breast rupture of fat Cs

release of lipase self digestion of fat Cs.

N /E :Hard mass in ! breast + retraction of nipple. ?? mistaken for carcinoma.

M/E :Necrotic fat Cs appear cloudy e infiltration by neutrophils, macrophages

& foreign body giant Cs. Granulation tissue is formed around ! lesion,

& matureto form a fibrous tissue. ?? calcified.

b - Enzymaticfatnecrosis:

Occurs in acute hemorrhagic pancreatitis. Escape of lipases

& protease enzymes from ! ruptured pancreatic ducts

digestion of ! surrounding peritoneal fat Cs. ! liberated fatty acids

have a high affinity to combine e Ca++ forming Ca++ soaps.

5)Zenkers degeneration or necrosis: (described before)

6)Fibrinoid degeneration or necrosis: (described before)

Apoptosis

Def : * Single cell death OR

*Programmed cell death OR

*Cell suicide

It occur e`out inflammatory reaction in surrounding tissue.

E/M :- Chromatin condensation + Fragmentation of DNA by endonuclease

- Formation of membrane blebs.

- Apoptotic bodies consist of nuclear fragment surrounded by part of ! cell, which separate

engulfed by phagocytic Cs. In H&Eappear as small rounded eosinophilic bodies.


22/22

22

Examples

Physiologic pathologic

1 - Embryogenesis : atresia of

some structures

2 - Endometrium during menstruation

3 -physiologicatrophy of lactating

breast after weaning

1 - death of tumor cells

(competition for nutrition)

2 - death by cytotoxic T cells

Inrejection

3 - viral (councilman bodies

in viral hepatits)

4 - pathologic atrophy after

duct obstruction and

after decrease hormone production

Differences between necrosis and apoptosis:-

Necrosis Apoptosis

Cause

Mechanism

Tissue

reaction

Morphology

N/E

M/E

Pathological e.g Hypoxia,toxins

1-Membrane injury.

2-ATP depletion.

Inflammation.

-pale, dry , well defined.

-cellular swelling.

-coagulation of protein.

-destruction of organelles

Physiological or pathological.

1-Endonuclease activation.

No inflammation but phagocytosis

of apoptotic bodies by adjacent

cells.

-No changes & area appear normal.

-cell shrinkage.

-chromatin condensation.

-Apoptotic body.

Documents

2 Cell Injury