Inflammation & Wound Healing

Vocabulary flashcards covering key concepts from the inflammation and wound healing lecture notes.

Inflammation

Nonspecific tissue response to injury that evolves through phases and can last from minutes to months; has a protective role

May be caused by chemicals, physical forces, microbes, etc

Acute Inflammation

sudden onset and short duration

marked by the presence of neutrophils

example is lobar pneumonia

Chronic Inflammation

lasts a long time

marked by the presence of macrophages, lymphocytes, monocytes

example is chronic ulcerative colitis

Inflammation as a Vital Reaction

inflammation is only in living tissue, not necrotic or dead tissue

if present after death, means they had a pre-death infection

Signs of Inflammation

calor, rubor, tumor, dolor, functio laesa

Calor

Heat; one of the five cardinal signs of inflammation; increased tissue temperature due to hyperemia.

Rubor

Redness; one of the five cardinal signs of inflammation; redness from increased blood flow (vasodilation) to the area.

Tumor

Swelling; one of the five cardinal signs of inflammation; edema from plasma leakage into interstitial spaces.

Dolor

Pain; one of the five cardinal signs of inflammation; pain from tissue distortion and chemical mediators.

Functio laesa

Loss of Function; one of the five cardinal signs of inflammation; impaired function due to tissue injury and swelling.

Hyperemia

Increased blood flow to an area, contributing to redness and warmth.

Vasodilatation

Relaxation of pre-capillary sphincters increasing arterial inflow into capillaries; leads to redness, swelling, and tissue warmth

Precapillary Sphincters

Smooth muscle rings regulating the entry of blood into capillaries (vasoconstriction); stimulus causes nervous signal transits signal to smooth muscles

Edema

Fluid leakage from capillaries into interstitial tissue causing swelling.

Hemoconcentration

increase in the percentage of formed elements compared to plasma in the blood; occurs when plasma leaves vessel walls

Rouleaux

Stacks of hemoconcentrated red blood cells that slow flow during inflammation.

Pavementing

Adhesion of neutrophils to the endothelium; one of the most important triggers to release mediators of inflammation

Develop elongated protrusions and become sticky, which allows them to adhere to the endothelial

Occurs after margination

Margination

Movement of leukocytes to the periphery of blood flow toward endothelium.

Occurs before pavementing

Inflammation Circulatory Changes

1- vasoconstriction

2- vasodilation

3- capillary network filled with arterial blood (tissue becomes red, swollen, warm)

4- dilation of capillaries and venules

5- plasma filtration through vessel wall (causes edema, leaves only formed )

6- RBCs form Rouleaux

7- Margination & Pavementing

8- WBC emigration

9- chemotaxis

10- phagocytosis

Diapedesis (Emigration)

Occurs when PMNs become less prominent and are replaced by macrophages, lymphocytes, and plasma cells

adhesion of PMNs to endothelium, insertion of cytoplasmic pseudopods between endothelial junctions, passage through basement membrane, ameboid movement away from vessel towards cause of inflammation

Emigration Steps

1- adhesion of PMNs to endothelium

2- insertion of cytoplasmic pseudopods between endothelial junctions

3- passage through basement membrane

4- ameboid movement away from vessel towards cause of inflammation

Interleukins (IL-1)

Cytokines that activate surface components of leukocytes and endothelium; highly concentrated at site of inflammation

Chemotaxis

Active movement of leukocytes toward a chemotactic gradient from bacteria or damaged tissue.

Opsonins

Molecules that coat pathogens to enhance phagocytosis.

Phagocytosis

Engulfment and destruction of pathogens by neutrophils and macrophages after PMN cell membrane attached to bacterial cell wall

Phagocytic Vacuole

Vacuole within a phagocyte containing an engulfed particle, where it is then killed

Pus

Viscous yellow exudate of dead neutrophils and debris; purulent inflammation.

Purulent (Suppurative) Inflammation

Inflammation dominated by pus and neutrophils

Example: abscess

Abscess

localized collection of pus within an organ to tissue; surrounded by a capsule of granulated tissue

best example: lung abscess

Most Common Pyrogen Prostaglandins

IL-2

TNF

Serous Inflammation

Mildest form of inflammation with serous, clear fluid exudate; early stage of inflammation

Examples: 2nd degree burns, herpes virus vesicles, blisters

Fibrinous Inflammation

Exudate rich in fibrin; seen on serosal surfaces (e.g., pericarditis; 'bread and butter' pericarditis).

Best Example: fibrinous pericarditis

Fistula

channels between 2 cavities or hollow organs and the surface of the body

occur in Chrons Disease and Ulcerative Colitis

Ulcerative Inflammation

inflammation of body surfaces or mucosa of hollow organs; can cause ulcers or loss of epithelial lining

Examples: gastric ulcer, intestinal ulcer

Ulcers

defects in epithelium that may extend to deeper tissues

Pseudomembranous Inflammation

Type of ulcerative inflammation combined with fibrinopurulent exudate

Pseudomembrane contains fibrin, pus, cell debris, and mucous

Leads to C. difficile

Granulomatous Inflammation

Chronic inflammation NOT preceded by acute PMN inflammation

Example: TB and certain fungal diseases

Caseating Granuloma

Granuloma with central necrosis typical of tuberculosis.

Miliary Spread

spread of TB to oxygen-rich organs

Wound Healing

Repair of tissue after injury; may progress to chronic inflammation if tissue destruction is extensive

myofibroblasts, angioblasts, then fibroblasts

Labile Cells

Continuously dividing cells (stem cells); divide at a regular rate and give rise to differentiated cells throughout the lifespan; easily repair skin wounds or mucosal ulcers

Example: RBCs, intestinal crypt cells

Stable Cells

Quiescent cells; do not regularly divide but can be stimulated to re-enter division; form parenchymal organs (liver or kidneys)

Example: liver can regenerate after a partial hepatectomy

Permanent Cells

Nondividing cells that do not proliferate

Example: neurons, myocardial cells

Fibrous Scarring

how a loss of myocardial cells repair, does not form functional cardiac cells

Gliosis

how a loss of brain cells repair, stimulated by astrocytes

Cells of Wound Healing

neutralization by leukocytes, macrophages, connective tissue cells, and epithelial cells

myofibroblasts, angioblasts, fibroblasts

Myofibroblasts

Hybrid cell with characteristics of smooth muscle and fibroblasts; contracts wound edges to bring margins together during first few days of healing; lays down collagen

Angioblasts

Form new blood vessels in healing tissue; proliferate at margins of wounds 2-3 days after incision; wound is covered by the 5th-6th day; allows for increased blood flow and oxygen supply required for collagen

Fibroblasts

Cells that produce extracellular matrix, including fibronectin and collagen; recruited by macrophages

Fibronectin

provides tensile strength to connective tissue matrix and has the ability to glue substances and cells together

Collagen Type III

Initial immature collagen laid down by fibroblasts in wound healing.

Collagen Type I

Mature collagen that provides tensile strength; replaces Type III over time.

Granulation Tissue

Immature collagen tissue of initial healing

Vascularized connective tissue with macrophages, myofibroblasts, angioblasts, and fibroblasts

Scab

Coagulated blood over a wound early in healing; later replaced by granulation tissue.

First Intention Healing

Clean incision site with a scab is invaded by neutrophils; then macrophages secrete substances leading to the growith of myofibroblasts, angioblasts, and fibroblasts; epithelium will eventually reform

Example: sterile surgical wounds

Second Intention Healing

Healing of wounds with large separations or infections; wound contraction cannot be done by myofibroblasts, so granulation tissue remains exposed; epithelium will not reform

Prolonged healing with chance of not healing completely

Delayed Wound Healing Factors

Site of wound, infection, mechanical factors, age, circulatory status, nutritional and metabolic factors

Deficient Scar Formation

granulation tissue forms very slowly; may result from ischemia, metabolic disturbances, or inadequate collagen production

Excess Scar Formation

leads to formation of hypertrophic scars (keloids) formed by Type III collagen; results from defective remodeling of scar tissue

Wound Healing Complications

deficient scar formation, excess scar formation

Dehiscence

Separation of wound margins due to weak scar or infection.

Keloid

Hypertrophic scar with excess Type III collagen and poor remodeling.

Scar

Collagen-rich tissue that forms after wound healing; ideally formed 3-6 weeks after injury

Age Healing Delay

wounds heal faster in children compared to adults or elderly

Circulatory Status Healing Delay

ischemic tissue heals poorly

Nutritional & Metabolic Factor Healing Delay

proteins and certain vitamins (C) are essential for wound healing

Mechanical Factors Healing Delay

faster healing if margins can be neatly juxtaposed and field kept immobile

Infection Healing Delay

sterile wounds heal faster than infected wounds

Wound Site Healing Delay

skin wounds heal well, brain wounds do not heal at all

Ischemia

Reduced blood supply; impairs healing (diabetes is chronic ischemia).