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

MORPHOLOGICAL REACTIONS TO ACUTE AND PERSISTENT STRESS CELLULAR ADAPTATIONS CELL INJURY CELL 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

cell injury Subcellular alterations Reversible cell injury “point of no return” Irreversible 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 CHANGE intracellular

HYALIN CHANGE - extracellular

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 predominance COAGULATIVE NECROSIS   Enzyme digestion predominance LIQUEFACTIVE NECROSIS

Ulcer (ulceration) Erosion

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 cancer some viruses associated with cancers act to prevent apoptosis of the cells they have transformed

CELLULAR AGING

SUMMARY Cellular responses to injury Reversible injury Irreversible cell injury Cellular adaptations atrophy hypertrophy hyperplasia metaplasia dysplasia Intra- and extracellular storage Cell death apoptosis necrosis Cell aging