Inflammation and Wound Healing

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

Objectives

.

Inflammation

Nonspecific, predictable tissue response to injury with vascular and cellular changes; dynamic process.

• caused by many things

• has several phases

• protective role - uncontrollable = harmful (ie Pulmonary TB eroding pulmonary vessels)

Calor (Heat)

Inflammation cardinal sign; increased tissue temperature due to hyperemia.

Rubor (Redness)

Inflammation cardinal sign; redness from increased blood flow.

Tumor (Swelling)

Cardinal sign; edema from plasma leakage and capillary dilation.

Dolor (Pain)

Cardinal sign; pain from mediators irritating nerves during inflammation.

Functio laesa

Cardinal sign; loss of function of the inflamed tissue.

Acute inflammation

Sudden onset, short duration; protective but can have harmful effects like fever.

Chronic inflammation

Long-standing inflammation often with macrophages, lymphocytes and tissue destruction.

Signs of Inflammation

By Celsius

• Calor, Rubor, Tumor, Dolor, Functio laesa

Circulatory Changes of Inflammation

1. Change in blood flow

2. Mech. stimulus stimulates the nerves to signal smooth muscle cells of pre-capillary arterioles = regulate inflow of blood into capillaries

   • Relaxation of smooth muscles = blood in capillaries → redness, swelling, warmth

First response of arterioles to injury = vasoconstriction (seconds) then vasodilation and relaxation

Hyperemia

Increased blood flow to inflamed tissue causing warmth and redness.

Vasodilatation

Relaxation of arteriolar smooth muscle; increased inflow of blood.

Precapillary sphincter

Sphincter regulating blood entrance to capillaries; its dilation promotes hyperemia.

Edema

Extravascular accumulation of fluid due to increased capillary permeability and filtration.

Rouleaux

Stacks of erythrocytes that slow capillary flow during inflammation.

Margination and Pavementing

Margination and adhesion of leukocytes to endothelium at sites of injury. WBC

Margination and Pavementing

Leukocytes develop sticky protrusions on their cytoplasm and adhere to endothelial cells lining the capillaries

Diapedesis / Emigration

Leukocytes crossing the endothelium to reach tissue.

Leukocyte Adhesion Molecules

In leukocytes and endothelial cells

Interleukins

Cytokines driving inflammation; highest concentration at the site of injury.

• Mediators of inflammation

• Greatest concentration at site of inflammation

Emigration of Leukocytes

1. Adhesion of PMNs to endothelium

2. Insertion of cytoplasmic pseudopods btw junctions of endothelial cells

3. Passage through basement membrane

4. Ameboid movement away from vessel toward cause of inflammation

TNF (Tumor Necrosis Factor)

Pro-inflammatory cytokine; mediates fever and inflammatory responses.

Opsonins

Molecules (e.g., Ig, C3b) that tag pathogens to enhance phagocytosis.

C3b (Complement)

Complement component; acts as an opsonin to enhance phagocytosis.

Phagocytosis

Engulfment and destruction of microbes by phagocytes.

Pus

Viscous yellow fluid of dead/dying PMNs and debris.

Inflammation Clinicopathologic Correlation

• Usually produce fever or Leukocytosis

  • fever caused by acute inflammation from endogenous pyrogen

  • leukocytosis = number exceed 12-15,000 (normal is less than 10k) nonspecific symptoms

Serous inflammation

Mild exudate consisting of clear, watery fluid.

• typical of viral infections and automimmune disorders like SLE

Fibrinous inflammation

Exudate rich in fibrin; can form shaggy layers on surfaces.

• seen in many bacterial infections (Strept throat)

• Also in Fibrinis pericarditis

Purulent Inflammation

• Typically caused by pus forming bactera ie Strep and Staph

• Localized collection of pus with an organ or tissue = abscess

  • An abscess has a central portion of purulent material surrounded by a wall capsule of fibrotic tissue

  • Ruptures abscess = sinus cavity or can form fistula (channels btw 2 preexisting cavities or organs and the surface of the body)

Pseudomembranous inflammation

• Form of ulcerative inflammation

Inflammation with pseudomembrane formed by fibrinopurulent exudate (e.g., C. difficile colitis).

Ulcerative inflammation

Ulcer formation: defect of epithelium with possible deeper involvement.

Granulomatous inflammation

Special form of chronic inflammation with granuloma formation; TB is a prototype.

• not preceded by an acute, PMN mediated inflammation

• may be caused by antigens that evoke a cell mediated hypersensitivity rxn

• TB is the prototype granulomatous disease

Caseating granuloma

Granuloma with central caseous necrosis seen in TB.

Wound healing

Repair of tissue after injury; can be by primary or secondary intention.

• Classified into 3 groups based on capacity to proliferate

• Most important cells are leukocytes, macrophages, connective tissue cells, epithelial cells

Labile cells

Continuously dividing cells (stem cell–like); e.g., intestinal crypt cells.

Stable (quiescent) cells

• Do not divide regularly, but can

Injury-responsive cells that divide infrequently but can re-enter the cell cycle (e.g., hepatocytes).

Permanent cells

Nondividing cells (neurons, myocardium) that repair by scarring.

• heart repair = fibrous scarring

• Brain repair by Gliosis

Myofibroblasts

Contractile fibroblasts that pull wound margins together during healing.

• Enables proliferating epithelial cells to cover surface defect

• First few days, properties of smooth muscle cells and fibroblasts

Angioblasts

Precursors of blood vessels

Vascular progenitor cells that form new blood vessels in healing tissue.

• 2-3 days after incision

Fibroblasts

Cells that produce MOST extracellular matrix; synthesize collagen and fibronectin.

• Fibronectin - provides tensile strength and glues other substances and cells together

• Collagen - first has immature type III collagen laid down by fibroblasts

Type I collagen

Mature, strongest collagen type; predominates in healed tissue.

Granulation tissue

Vascularized connective tissue with macrophages, myofibroblasts, angioblasts; temporary matrix.

Re-epithelialization

Epithelial cells proliferate and cover the wound surface from margins.

First intention (primary union)

Healing with apposed wound edges; scab formation and organized repair.

• healing of sterile wounds

Secondary intention

Healing of large defects with separated edges; slower, more scar formation.

• nonsterile, infected wounds

Delayed wound healing

Healing delayed by site, infection, mechanical factors, age, circulatory status, nutrition.

• most important determinants of healing are; site, and infection

• Mech. factors - minimal movement, juxtaposed edges, age, circulatory status (ie diabetes), nutritional and metabolic factors

Wound dehiscence

Separation of wound margins due to impaired healing or weakness.

Keloids

Hypertrophic scars with excessive Type III collagen; defective remodeling.

Scar

Final remodeled connective tissue with collagen, restoring strength.

Vitamin C (ascorbic acid)

Nutritional factor essential for collagen synthesis and wound healing.

Complications of Wound Healing

• Deficient Scar Formation - sluggish formation of granulation tissue in diabetic PTs due to ischemia and metabolic disturbances

  • inadequate collagen production in PTs with corticosteroid