Lec 2 - Cell Damage & Necrosis

Cellular damage and necrosis

Atrophy

decrease of size due to shrinkage of cells

cellular adaptations

atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, anaplasia

causes of atrophy

lack of use, insufficient nutrition, aging

hypertrophy

increase in size due to increase in size of cells

causes of hypertrophy

increased workload (e.g. skeletal muscle growth, compensatory hypertrophy in unilateral kidney, increase of size of heart muscle to compensate for high BP)

hyperplasia

increase in size due to increase in number of cells (can only happen in cells capable of mitosis) (CAN LEAD TO INCREASED RISK OF CANCER)

metaplasia

substition of adult cell type, reversible (usually in response to chronic irritation) (e.g. substitution of simple columnar to stratified cuboidal epithelium in trachea of a smoker)

dysplasia

tissue where cells vary in size and shape, presence of abnormal cells — PAP smears test for this

anaplasia

poor cell differentiation

hypoxia

decrease of oxygen in tissue

causes of hypoxia

ischemia (decreased blood supply), altitude (decrease of atmospheric O2), respiratory disease, anemia, cardiac disease/decreased pumping action of heart)

middle meningeal artery tear

if this is severed, it can lead to an aneurysm or fistulas

physical causes of cell injury

hypoxia, mechanical forces, temperature extremes, electrical injury, radiation injury, chemical toxins, nutritional imbalances

frostnip

reversible

frostbite

permanent

effects of low intensity heat

heat stroke, burns → disrupts blood flow + cell membrane

effects of high intensity heat

severe burn → coagulation of blood vessels/tissue protein

effects of extreme cold

increase in blood viscosity, induce vasoconstriction, frostbite

endogenous chemical toxins

come from inside the body due to metabolic disorder (not getting rid of toxins)

exogenous chemical toxins

from outside the body

types of chemical toxins

exogenous, endogenous, drugs

steps of cell breakdown

nucleus disintegrates → lysis → cells release lysosomal/lytic enzymes → enzymes cause damage to nearby cells → enzymes diffuse into blood

infarction

area of cell death resulting from lack of oxygen

ischemia

decreased bloodflow to a certain organ/tissue

necrosis

death of cells/tissue within a living body

coagulative necrosis

due to denaturation of proteins. gray firm mass, cells maintain shape. e.g. myocardial or kidney infarction

caseous necrosis

cells transform into soft cheese-like centre and can bind with calcium, e.g. TB lesion

liquefication necrosis

cells break down and liquify due to the action of enzymes. this leads to the formation of a cystic fluid-filled cavity

gangrene

death of TISSUE (instead of cells which is necrosis) due to interrupted blood supply

dry gangrene

slow occlusion → loss of blood supply → tissue becomes dry, shrinks, turns brown then black. can have lineof demarcation or spontaneous amputation

wet gangrene

found in body part containing fluid and exposed to bacteria ie colon

gas gangrene

gas produced by metabolization process of bacteria (clostridium). e.g. agricultural accidents, IV drug use, war