Cell Injury, Inflammation & repair

Inflammation

first response to tissue damage (a noxious stimulus)

alerts immune system

attempts to limit tissue damage

repairs the tissues

can be acute or chronic inflammation = definition is gone/missing bony landmarks

acute inflammation

immediate and rapid

short time frame (within the 1st couple days)

innate immune system

triggered by noxious stimuli

noxious stimuli

body reacting to something invading tissue area

ex. bacteria, pathogens, chemicals, trauma, radiation

Chronic Inflammation

persistent agent, persistent imnmune reactions and slow

repeated acute inflammation

longtime frame (weeks-months-years)

cell mediated immunity

response to monocytes (in blood), macrophages (in tissue from monocyte), and lymphocytes (plasma B’ cells)

may have fibrosis

fibrosis

formation of CT/collagen being laid down

5 cardinal signs of inflammation

calor/heat

rubor/redness

tumor/swelling

dolor/pain

loss of function

Rubor

Redness

caused by the dilation of arterioles

increased blood flow

Calor

increased chemical activity and increased blood flow to skin surface area

tumor

swelling

caused by accumulation of blood and damaged tissue cells

dolor

pain

direct injury of nerve fibers, pressure of hematoma on nerve endings

chemical irritants - badykinin, histamine, prostaglandin (brain perceives as pain)

loss of function

increased pain/swelling

to get pt. moving to get swelling and inflammation down

contain the inflammation/swelling

cascade of events of inflammatory response

vasoconstriction followed by vasodilation - clot then get nutrients

cells become more permeable

protein fluid/exudate leaks out

edema of tissue occurs - bc the protein leaks out

neutrophils begin phagocytosis and attach to the endothelium and diapedesis occurs

chemotaxis occurs

increase in WBCs and Liver is stimulated to produce c-reactive proteins to get rid of the microbes

chemical mediators (prostaglandins) trigger pain response

diapedsis

migration of cells/transportation

chemotaxis

attraction of neutrophils to toward the infected cell

Chemicals of inflammation

cytokines

complements

kinins

histamines

leukotrienes & prostaglandins

cytokines

cause a response of anotehr system

histamines

release mast cels/cytokines

leukotrienes & prostaglandins

proinflammatory

leukotrienes - stimulates other cells

prostaglandins - gastric muscosa

Reversible cell injury

cell injury with loss of cell function and structural changes occur

the cell can revert to normal if the stress/injury/noxious stimulus is removed

irreversible cell injury

cell passes “point of no return”

it cannot recover if pathologic stimulus were removed

usually needs a persistant noxious stimuli to get here

physiologic tissue adaption

healthy tissue → stress → cell injury → reversible or positive tissue adaptation

pathological tissue adaption

healthy tissue → stress → persistent → maladaptation → may lead to death

Types of Tissue adaptations

Hyperplasia

hypertrophy

metaplasia

dysplaisa

hyperplasia

increase in the number of cells

hypertrophy

increase in the volume/size of cells

metaplasia

reversible change of one mature cell type into another

often a response to chronic irritation, may result in risk for malignant trasnformation

can see a change in DNA

dysplasia

excess cell growth, loss of normal cell structure

can revert to normal or become malignant

the happens before malignant state usually

Necrosis

pathological tissue death - has negative consequences to organ/tissue

due to external factors

membrane gets damaged

cells swell

nucleus shrinks, leaks out, ruptures, and gets absorbed into system - cell cannot live without a nucleus

4 types: coagulative/blood clotting, liquefactive/brain, gangrenous/lack of blood supply, caseous/traumatic tissue injury

apoptosis

physioligcal or pathological tissue death

targeted pre programmed cell death

DNA damaged

no inflammation

2 pathways: ligand binding and mitochondrial pathways → promot apoptosis

Factors that Injure Cells

Hypoxia

infection - can take over/septic (whole body; outline/draw line to keep track of ow fast it spreads)

chemicals and toxins - often from working with them

mechanical forces

trauma

radiation - kills rapidly dividing cells

immune system - if overactive/not functioning normally

genetics - effects protein synthesis

nutritional deficits - cells need proper nutrition

Hypoxia explained

cell injury ischemia: hypoxia = low O₂ amount, anoxia = no O₂

reduced or complete lack of O₂ due to obstruction of airflow

• inadequate transport of O₂ in lung or blood

• inability of cell to use O₂

organs can sustain hypoxia for minutes (2-4 on average/brain) to hours (heart/kidneys) before cell death

Phases of Healing - after cell injury

initially hemostasis - vasoconstriction then vasodilation

inflammation

proliferation and migration

remodeling and maturation

how fast/slow process is depends on low vs high grade damage

Hemostais

seconds to hours

vasoconstriction

platelet aggregation

leucocyte migration

inflammatory phase

hours to days

early - neutrophil

chemoattractant release

late macrophages

phagocytosis and removal of foreign body/bacteria

proliferative phase

days to weeks

fibroblast prolifersation

collagen synthesis

ECM reorganization

angiogenesis (new blood flow)

granulation tissue formation

epithelialization

remodeling

weeks to months

remodeling

epithelialization

ECM remodeling

increase in tensile strength of wound

after this stage = healed tissue