GENERAL PATHOLOGY- hemodynamic disorders- cellular adaptations- cell injury and cell death- inflammation- healing, repair and regeneration- neoplasia

 

MORPHOLOGICAL REACTIONS TO

ACUTE AND PERSISTENTSTRESS

CELLULAR ADAPTATIONSCELL INJURYCELL DEATH

 

Elements capable of causing cell injury

Chemical

Physical

Elements capable of causing cell injury

Biological

Cellular reaction varies

depending on the type

duration

and severity of injury

eg

Adaptation

atrophy

hypertrophy

hyperplasia

metaplasia

dysplasia

Limits of adaptation

Subcellular alterations

Reversible cell injury

“point of no return”

Irreversible cell injury

cell injury

Subcellular responses to cell injury

Lysosomal catabolism

 

Subcellular responses to cell injury

Induction of smooth endoplasmic reticulum

 Mitochondrial alterations

Cytosceleton abnormalities

Reversible cell injury

e.g.

cellular swelling

fatty change

Cellular swelling

 MACRO

 MICRO

Intracellular and extracellular accumulation (storage)

Normal cellular constituent accumulated in excess

e.g.

 Abnormal substances

Pigments

LIPIDS

Steatosis (fatty change)

Liposis (obesity)

 

Cholesterol and cholesterol esters

PROTEINS

GLYCOGEN

PIGMENTS

-exogenous

 -endogenous

CALCIFICATION

 physiologic

pathologic

Dystrophic calcification

Metastatic calcification

HYALIN CHANGEHYALIN CHANGE

-iintracellularntracellular

HYALIN CHANGEHYALIN CHANGE

-- extracellularextracellular

STAINING METHODS

metachromatic staining

One dye has the ability to produce different colors in various histological or cytological structures.

ATROPHY

 Shrinkage in the size of the cells by loss of cell substance

Cell death

necrosis

apoptosis

Necrosis-

„Death by injury”

cell death after exogenous stimuli

Apoptosis-

„Death by suicide”

cell death through activation of an internally controlled suicide program

Necrosis

morphologic changes following cell death in living tissue largely resulting from the action of enzymes on the lethally injured cell (live cells placed in fixative are dead but not necrotic)

Morphology:

Two concurrent processes:

enzymic digestion

denaturation of proteins

Denaturation predominanceCOAGULATIVE NECROSIS Enzyme digestion predominanceLIQUEFACTIVE NECROSIS

Ulcer (ulceration)Ulcer (ulceration)

ErosionErosion

Caseous necrosis

 

Fat necrosis (Balser necrosis)

APOPTOSIS“falling off”

- during development- as a homeostatic mechanism- as a defense mechanism- as a result of disease of noxious agents action- in aging

Programmed cell death is as needed for proper development as mitosis is

Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism

MORPHOLOGY:

Mechanisms

1. Signaling pathways

  

2. Control and integration stage

3. The execution phase

Apoptosis and cancersome viruses associated with cancers act to prevent apoptosis of the cells they have transformed

CELLULAR AGING

Cellular responses to injuryReversible injuryIrreversible cell injury

Cellular adaptationsatrophyhypertrophyhyperplasiametaplasiadysplasia

Intra- and extracellular storage

Cell deathapoptosisnecrosis

Cell aging

SUMMARY