Cell Pathology 2

• Loss of ability to divide • Loss of normal synthetic functions • Biochemical changes, followed by structural changes

-membrane blebbing -blebs fuse and become larger -cell membrane ruptures and releases the cells content

-smell blebs form -nucleus begins yo break apart and dna breaks into small pieces(organelles are also located in the blebs) -the cell breaks into several apoptopic bodies;the organelles are still functioning

Pyknosis(nuclear shrinkage) Karyolysis(nuclear fading|) Karyorrhexis(nuclear fragmentation)

• Necrosis is caused by factors external to the cell or tissue e.g. infections, toxins or trauma • It results in unregulated digestion of the cell components • Loss of cell membrane integrity and uncontrolled release of products of cell death brought about by autolysis • Inflammatory response in the surrounding tissue

-Haemorrhage -Resolution • Site, type and extent of injury • If cannot resolve, body attempts to repair -Repair • Removal of dead tissue • Action of neutrophils and macrophages • Granulation tissue

• Coagulative necrosis • Liquefaction (colliquative necrosis) • Caseating necrosis • Fat necrosis • Gangrenous necrosis

• Most common • Affects solid organs • Artery occlusion → ischaemia is most common cause(lack of blood flow) • Firm and pale • Cellular outline and tissue architecture maintained • Lack of lysosomes/ injury destroys lysosomal enzymes

• Semi-liquid • Degradation of cellular and extracellular components by hydrolytic enzymes • Cystic cavities containing fluid and cell debris • Main causes include cerebral infarction or bacterial infection • Loss of neurones • Many macrophages clearing cell debris

Soft and white – resembling cream cheese • Unstructured protein mass • Associated by tuberculosis

• Hard yellow material seen in dead adipose tissue • Pancreatitis → release of proteolytic & lypolytic enzymes • Breast trauma → release of fatty acids → inflammatory response

Dystrophic calcification ➢Large amounts of calcium enter the cell ➢Combine with phosphate to form crystals ➢Extracellular calcification can also occur

• Not a distinctive type of necrosis • Describes black dead tissue • Most common in lower limb of patients with severe atherosclerosis • Irreversible ischaemic damage

• Dry gangrene →Coagulative pattern of necrosis • Wet gangrene → Gram-negative bacteria converts it to liquefactive necrosis • Gas gangrene →Follows infection with gram-positive organism Clostridium welchii (found in the soil) →Releases toxins which produce gas

• Coagulative necrosis from ischaemic injury • Commonly caused by poor circulation or obstruction • Slow, gradual process • Usually seen in smokers, diabetics, atherosclerosis

• Largely affects moist tissues and organs • Characterized by liquefactive necrosis • Untreated wound infections. • Swelling and inflammation • Blockage of blood supply • oedematous, decayed, reddish to dark brown • Promotes further bacterial growth necrosis and gangrene

• Clostridia are the main etiologic agent • Invade wounds and injuries with diminished blood supply • Release gas-producing toxins. • Affected skin may appear greyish to purplish red • Bubbly skin which makes a crackling sound whenever pressed

• Programmed cell death • Normal process • Energy-dependent • Orderly packaging in membrane bound vesicles • Vesicles phagocytosed – no inflammatory response

-controlling cell number -tissue remodelling -removing damaged cells

Group of cells affected • Caused by injurious agent • Changes due to energy deprivation • Cells swell • Ruptured lysosome & cell leakage • Inflammatory response

• Single/few cells affected • Programmed cell death • Energy-driven • Cells shrink • Organelles & nuclear fragments packaged in vesicles • No inflammatory response