EXAM 1 - Chapter 9

Acute inflammation

Rapid onset + rapid termination; controlled by chemical mediators

• involves vascular phase and cellular phase

Vascular phase

1. initial brief vasoconstriction

2. histamine and bradykinin mediators arrive which dilate vessels and makes them more permeable (redness and warmth)

3. fluid extravasation (fluid leaking out of vessel into tissue) resulting in edema

4. dilated vessels allow WBCs to travel to site of injury and phagocytize debris

5. formation of purulent exudate AKA pus

   1. abscess: localize collection of purulent exudate

   2. effusion: accumulation of fluid in body cavity (pleural effusion, pericardial effusion)

Cellular phase

1. chemical signals attract WBCs and platelets (chemotaxis)

2. WBCs line up along endothelium around site of injury (margination) and release inflammatory mediators

Systemic response to acute inflammation

Most signs due to chemical mediators: prostaglandins, TNF-alpha, interleukins (NSAIDS target these signals)

• fever

• tachycardia

• lymphadenopathy

• anorexia

• sleepiness

• lethargy

• anemia

• weight loss

Classic signs of inflammation

1. dolor (pain)

2. calor (heat)

3. rubor (redness)

4. tumor (swelling)

5. loss of function (function laesa)

WBC response in acute inflammation

FIRST

• 6 - 24 hours

• Neutrophils are first responders

  • mature neutrophils are segmented nuclei (“segs”)

  • immature neutrophils are “bands”

  • acute infection results in a shift to the left as more bands are produced than segs

  • neutrophils are capable of some phagocytosis and once engulfed, respiratory burst released free radicals that destroy microbes

• neutrophils gradually replaced by monocytes

SECOND

• 24 - 48 hours

• monocytes to macrophages which now predominate in persistent inflammation

• macrophages carry out phagocytosis

Viral infections

• lymphocytes dominate

Chronic inflammation

inflammation for weeks and months with no resolution/healing

EXAMPLES

• persistent infection: TB, syphilis, viruses

• hypersensitivity disorders: RA, lupus

• exposure to toxic agents: coal dust AKA anthracosis

• atherosclerosis: chronic inflammatory disease

CHRONIC differs from ACUTE inflammation in these ways

• predominance of monocytes, lymphocytes, macrophages

  • neutrophils are first on site so if macrophages are theres, you know it’s chronic

• continual secretion of cytokines which damage healthy tissues and stimulate more inflammation

• granuloma formation where macrophages aggregate and are transformed into epithelial-like cells

• T and B lymphocytes which amplify and perpetuate inflammatory signals (common in autoimmune disorders)

tissue is repeatedly damaged, healing is delayed, connective tissue replaces injured cells

tissue damage causes cell death and necrotic tissues ALSO stimulates inflammatory reaction, so tissues undergoing chronic inflammation can have regions of acute inflammation as well

potential complications of wound healing

• wound ruptures

  • high tension: abdominal wall and coughing

  • wound dehiscence: previously closed wound edges open and rupture

  • wound evisceration: internal tissues and organs protrude from open wound

  • REQUIRES PROTECTION with sterile, saline-moistened dressings and surgical evaluation

• keloid formation: hyperplastic epithelialization and excess collagen accumulation leading to hypertrophic scar

• contractures: inflexible shrinkage of wound which can limit mobility when it occurs across join surfaces (burns)

• stricture: narrowing of open area caused by scar tissue formation (EX: esophageal stricture following injury to esophagus)

• fistula: abnormal connection between two structures (EX: tracheoesophageal fistula)

• adhesion: abnormal bands of internal scar tissue that can limit mobility; often after invasive surgical procedures (EX: C-section)