W0 - Cell adaptations and inflammation

atrophy

decrease in cell size

hypertrophy

increase in cell size

hyperplasia

increase in cell number

metaplasia

change from one cell type to another

dysplasia

abnormal development of cells

causes of atrophy

ischaemia, pressure, disuse, malnutrition, lack of hormonal stimulation

types of hyperplasia

physiological, compensatory, pathological

difference between physiological and pathological

physiological occurs due to a "normal" process, pathological occurs due to a pathogen

what type of tissue usually undergoes metaplasia

epithelium to better respond to stressors

why is dysplasia dangerous?

strongly linked to cancer

what causes cell injury?

encountering an injurious stimuli or failing to maintain a steady state

hypoxia

not enough oxygen in tissues, usually due to ischaemia or hypoxaemia

chemical agents

chemicals that directly injure cells, leading to increased permeability of membranes

physical agents

physical damage resulting in cell damage, usually penetrating wounds or environmental stressors (e.g. sunburn)

infectious agents

virus or bacteria damaging cells

genetics

genetic abnormalities resulting in greater injury chance

immune reactions

immune cells (e.g. cytokines) releasing chemicals that harm normal cells as well as pathogens

nutritional imbalances

too much or too little nutrition

senescence

physical aging leading to decreased ability of cells to age

cell swelling process

lack of oxygen ==> anaerobic respiration ==> inability to pump out sodium ==> cell dilation / swelling

free radical damage

immune system activation ==> release of free radicals ==> damage to cell components and dna

calcium homeostasis

increased calcium ==> activation of enzymes ==> breakdown of cellular components

what are the reversible cell injuries?

cellular swelling and intracellular accumulations

what are the two types of cell death

apoptosis and necrosis

what's the difference between apoptosis and necrosis

apoptosis is an active process, that does not cause inflammation, necrosis is a passive process that does cause inflammation

apoptosis steps

initiation ==> cell shrinkage ==> release of membrane bound fragments ==> phagocytosis

coagulative necrosis

often due to hypoxic damage, leading to cell rupturing and surrounding tissues becoming more acidic and denaturing, leading to proteins becoming more grey or opaque

liquefactive necrosis

often due to ischaemia, enzymes break down debris and cell parts, liquefying the dead tissue

caseous necrosis

cheese-like appearance, not fully digested

where is coagulative necrosis regularly found

tissue high in protein or blood supply

where is liquefactive necrosis regularly found

areas with high concentration of digestive enzymes (e.g. brain)

where is caseous necrosis regularly found

lung tissue from tuberculosis

fat necrosis

lipase breaks down lipids forming free fatty acids (FFAs) and undergo saponification

where is fat necrosis regularly found

pancreas and surrounding abdominal structures

gangrene

large areas of necrotic tissue

three types of gangrene

dry, wet, gas

dry gangrene

dominated by coagulative necrosis, usually dry, shrinking, blackened

wet gangrene

dominated by liquefactive necrosis, cold swollen, black and usually due to an infection

gas gangrene

occurs from clostridium bacteria, that produces hydrogen sulfide gas that gets trapped in tissues and appears as bubbles

infarction

tissue death due to ischaemia

what triggers acute inflammation

necrosis

what mediator begins the acute inflammation process

mast cells

what is the vascular response to inflammation

vasodilation and increased permeability

what is the cellular response to inflammation

phagocytosis from neutrophils (early), and macrophages later

inflammation signs

heat, erythema, oedema, pain, loss of function

calor

heat

rubor

erythema

fibrinous inflammation

fibrin-rich exudate

serous inflammation

watery and protein poor fluid accumulation (e.g. blister)

ulcer

erosion of epithelial layer exposing underlying tissue

abscess

pus or purulent discharge containing dead leukocytes

chronic inflammation

inflammation lasting two weeks or longer

key characteristic of chronic inflammation

infiltration of macrophages and lymphocytes of the affected area

granulomatous inflammation

chronic inflammation with granulomas

wound healing steps

inflammation, proliferation, remodeling

labile tissue

constantly replicating

permanent tissue

cannot regenerate

stable tissue

can regenerate, but only due to injury

what determines whether primary or secondary intention healing?

amount of tissue loss, minimal => primary intention, large => secondary

what determines outcome of wound healing?

type of tissue, severity or location, and nutrient supply