Cellular Injury2

8/2/2019 Cellular Injury2

1/28

CELLULAR INJURY

1. ADAPTIVE GROWTHRESPONSES

Dr. Taghrid Gamal Eldin


2/28

1. Adaptive growthresponses If there is increased demands but the

cells cant divide; Hypertrophyproduces enlarged cells with increased

functional capacity.Example : skeletal muscles

When there is decreased demands;atrophy; reduced cell size but the cellnumber is retained ( to provide forfurther demands)


3/28

In hyperplasia : there is particular growthstimulus that causes new cell production

( mitosis) but in limited numbers. Examples ;

-Callus: epidermal hyperplasia.

-Endometrial hyperplasia normal menstrualcycle.

-Enlarged lymph nodes in response tochronic infection

- On surgical removal of the kidney ; somecells of the other kidney undergohypertrophy & other cells becomehyperplasic.


4/28

Metaplasia andDysplasia Metaplasia: the conversion of one cell

type to another .

It is due to chronic exposure to

unfavorable conditions. It is reversible process.

Example : the replacement of respiratory

epithelial cell by thicker and toughercells with normal appearance { able towithstand the inhaled irritants,, cigarettesmoking , industrial irritants,, }


5/28

Dysplasia; is seen in epithelium whenthere is more severe and prolonged

irritation.The architecture is distorted & the cells

show pleomorphism.

Pleomorphic cells: cells that arevariable in size and shape, larger moredarkly stained nuclei and increased rates

of mitosis.- Reversible condition but < metaplasia. In

smokers

- Associated with chronic bronchitis in


6/28

Neoplasia

Neoplasia means formation of tumormass. It is irreversible alteration in thecell growth pattern.

Developmental and geneticabnormalities can produce:

Aplasia: Lack of organ development.

Hypoplasia : inadequate developmentso the resulting tissue is immature andfunctionally deficient.


7/28

N.B. adaptive responses to changingdemands atrophy, hypertrophy,hyperplasia and regeneration arereversible.

In neoplasia the transformation isirreversible.

It is the imbalance between growthstimulus and growth inhibition thatproduces inappropriate tissueovergrowth,, newly formed cells grow

without control,,


8/28

Thank You

C ll I j d D th


9/28

Cell Injury and Death2- Reversible and irreversible

Cell Injury When normal conditions are restored or

when only moderate injury has occurredthe cell may return to normal function

(reversible injury)Reversible changes:Functional

Injury is often reversible because thecells adaptive responses enable it tocope with injury or adverse conditions

Examples:


10/28

1- AlternativeMechanisms Hypoxia

Glycolysis : a cell can rely on glycolysisinstead of oxidative phosphorylation .

2-Altered SizeHypertrophy

Hyperplasia

Atrophy: -disuse atrophy e.g. poliomyelitis

-pressure atrophy e.g. tumor masscan cause atrophy of the nearby tissue


11/28

3-Apoptosis

Reduction of the cell number by aprocess of self destruction

Called programmed cell death because it

is a genetically regulated process Examples:

-Apoptosis of overproduced cells during

embryonic life.-Cytotoxic T cells destroy other cells by

inducing apoptosis.


12/28

4- Cell Stress Proteins

On exposure to anoxia , toxins, increasedtemperature and trauma .. The cell respondby producing cell stress proteins .. Heatshock or heat stress proteins.

* They bind to damaged proteins .. Makeit easier for the enzymes to destroy suchproteins before they make clumps inside thecells.

*They stabilize the proteins long enoughto enable them to refold and becomefunctional once again

*The stabilizing stress proteins and thedenatured proteins easily pass through


13/28

5-Organelle Changes

Increase mitochondrial production inresponse to the increase in energydemand.

Increase agranular endoplasmicreticulum (AER) production by the livercells in response to increased number oftoxic substances required to bedetoxified by the liver cells


14/28

Cell and TissueAccumulation Much injury disrupts the cells

metabolism or its protein synthesiscapabilities.

As a result .. Various substancesaccumulates within the cells.


15/28

a) Hydropic Changes:

Hydropic changes

injuryDecrease

ATP

production

DecreaseNa pump

activityIncreaseosmotic

pressure in thecell

Influx ofwater

VacuolationProgression tohydropic changes


16/28

b) Fatty Changes

c) Residual bodies: are derived fromphagosomes whose contents are notexpelled , but are retained when

lysosome numbers are inadequate tocomplete digestion.

d) Hyaline changes ; deposition ofhyaline tissue between the cells ,,usuallyproteins,, found in damaged arterioles,damaged liver cells, neurons, renal

tubules.


17/28

Reversible Changes :Structural Blebs: cytoplasmic bulges that project from

the surface of the cell due to distorted andstretched cell membrane.

Myelin figures: focal coiling of the cell

membrane Damage of some membrane structures

e.g. microvilli Injury in organelles membranes allow

water to leak into organelles .. Organellesbecome enlarged and distorted (Golgicomplex, ER, Mitochondria)

Dispersed ribosomes in the cytoplasm ofinjured cells.

N.B. in reversible injury, the nuclear


18/28

Irreversible injury &necrosis Severely injured cells cant recover its

normal functions, show more structuralchanges.

Structural Changes: 1- Plasma membrane shows extreme

distortion associated with different degreesof increased permeability( allows increasedinflux of sodium, calcium, and water)

* gaps in the membrane .. Leads to escapeof vital constituents. *in extreme cases ,rupture of the cell

membranes take place.


19/28

Irreversible injury &necrosis 2- Mitochondria and ER membrane

undergo similar breakdown. 3-Lysosomes: the less stable lysosomal

membranes break releasing their destructivecontents.

4-Nucleus: the single most significantindicator of irreversible cell injury is analtered nucleus

*Karyolysis: DNA degradation, nucleusseems to fade and melt into the cytoplasm.

*Pyknosis: the nucleus may shrink andcondense.

*Kar orrhexis: Break u into densel


20/28

Mechanisms of Cell injury

Damage to Cell Membranes (affectpermeability)

Damage to Cytoskeleton


21/28

Cell Death

Changes in functional capacity inresponse to injury

Cellsovercome theeffect of injury

Cells recover butnot at its normal

levels

No recovery is

possible

recovery

Non reversibleeffects

Death


22/28

Necrosis

Definition: the condition of cell death. It is accompanied by changes in the cells

& tissues.

The contents of the cell are broken downby endogenous enzymes & by theenzymes of phagocytic cells.

The resulting debris is removed & tissue

healing follows. Lysosomes release their enzymes into

the cytoplasm & these initiate thechemical breakdown of cell constituents.


23/28

Types of necrosis

1. Coagulation Necrosis: Following tissue death , most tissues

become firm for a period of few weeks.

Cell proteins . Quickly denatured Lsosomal enzymes are also affected &

unable to digest the cell .. This willdelay the breakdown of damaged cells

until . The arrival of phagocytes ..Tissue retain its organization thedenatured proteins are responsible fortissue coagulation.


24/28

1. Coagulation Necrosis

a. Caseous necrosis:

Type of coagulation necrosis

Seen in tuberculosis

b. Gangrene or Gangerenous Necrosis:Type of coagulation necrosis

Characterized b putrefaction

Foul smelling gases are produced Caused by noxious products of anaerobic

bacteria that is able to multiply in theoxygen deprived necrotic tissue


25/28

2. Liquefaction Necrosis

The necrotic tissue breaks down quietpromptly and coagulation dont occur.

Examples;;

*typically follow brain necrosis due toischaemia.

*follow certain bacterial infections :

bacterial enzymes liquefy the necrotictissue.


26/28

Calcification

Calcium deposition often occurs at thesites of necrosis regardless of the type ofnecrosis

1. Dystrophic calcification: Calcium crystals are deposited and

progressive deposition produce larger

masses that lead to significant rigidity &brittleness in the affected tissue.


27/28

Calcification

2. Metastatic calcification Differ from dystrophic atrophy in 2 ways;

A. Occur in normal tissue as opposed to

necrotic tissue.

B. Deposition is a consequence toexcessive calcium level hypercalcaemia.


28/28

THANK YOU

Documents

Cellular Injury2