2.5 about 24 minDeep Learning viewL2 p.32–39

Patterns and outcomes of acute inflammation

What the exudate looks like depends on how much leaks, whether fibrinogen gets out, whether neutrophils pile up and whether a surface is lost. How the episode ends depends on how much tissue was destroyed and whether the cause is gone.

Morphologic patterns: what the exudate looks like

L2 p.32–38

The lecture names five patterns. Each one tells you something about the cause: the size of the vascular leak, whether large proteins escape, which organism is involved and which surface is hit.

Five patterns and what produces themL2 p.32–38

  • Serous

    What forms
    Thin, watery fluid with too little fibrinogen to make fibrin
    Classic examples
    Blister of a second-degree burn; viral pleuritis; effusions
    Clue
    Clear fluid, few cells

  • Fibrinous

    What forms
    A larger leak lets fibrinogen out; it polymerizes on the surface
    Classic examples
    Pericarditis, pleuritis, peritonitis
    Clue
    Friction rub; shaggy “bread-and-butter” surface

  • Purulent (suppurative)

    What forms
    Pus: neutrophils, necrotic cells, edema fluid
    Classic examples
    S. aureus abscess, appendicitis
    Clue
    Localized, fluctuant collection

  • Pseudomembranous

    What forms
    Toxin kills mucosa; fibrin, necrotic epithelium and neutrophils form a membrane
    Classic examples
    Clostridioides (Clostridium) difficile colitis; diphtheria (pharynx, trachea)
    Clue
    Yellow plaques; diphtheria membrane bleeds when lifted

  • Ulcerative

    What forms
    Local loss of epithelium, extending into deeper tissue, with an inflamed base
    Classic examples
    Peptic ulcer, ulcerative colitis, herpes ulcers
    Clue
    Defect in a surface

Lecture image

Wrist with a tense blister filled with clear yellow fluid
Serous inflammation: a blister filled with clear, protein-poor fluid.L2 p.36

Lecture image

Heart with a shaggy yellow fibrin coat over the pericardial surface
Fibrinous pericarditis: a shaggy yellow coat of fibrin. The roughened layers rub during each heartbeat, heard as a friction rub.L2 p.35

Lecture image

Sheets of neutrophils and debris filling tissue (purulent exudate)
Purulent exudate: sheets of neutrophils and debris; their enzymes liquefy the tissue.L2 p.33

Lecture image

Colonoscopy view with many raised yellow plaques on the mucosa (arrows)
Pseudomembranous colitis: yellow plaques (arrows) of fibrin, mucus, neutrophils and necrotic epithelium after C. difficile toxin injury.L2 p.37

Abscess versus cellulitis

L2 p.32–34Ch. II cases p.12

The organism decides whether purulent inflammation stays put. Staphylococcus aureus carries coagulase, which converts fibrinogen to fibrin: the fibrin mesh traps bacteria and neutrophils and keeps the infection localized. Inside, neutrophil lysosomal enzymes liquefy everything into pus (2.3). Over days a wall of granulation tissue and later fibrous tissue forms around it: an abscess. Antibiotics penetrate the cavity poorly, so abscesses usually need drainage.

Group A Streptococcus makes hyaluronidase (and streptokinase), which dissolve the ground substance and fibrin, so infection spreads through subcutaneous tissue planes: cellulitis. The lecture's signs are an expanding area of redness, warmth, tenderness and swelling, fever, painful regional lymph nodes and red streaks running toward them, which are inflamed lymphatics (lymphangitis).

Localized versus spreading

Abscess

  • S. aureus: coagulase → fibrin wall
  • Localized pus; fluctuant
  • Liquefactive necrosis by neutrophil enzymes
  • Treat by drainage (± antibiotics)

Cellulitis

  • Group A strep: hyaluronidase, streptokinase
  • Diffuse, expanding redness; no collection
  • Red streaks (lymphangitis), tender nodes, fever
  • Treat with antibiotics
L2 p.32, 34

Four ways acute inflammation can end

L2 p.39

Teaching schematic

Acute inflammation

  • Complete resolution

    Little destruction; cells regenerate; exudate cleared

  • Scar (fibrosis)

    Framework destroyed, permanent cells, or fibrin not cleared

  • Abscess

    Pyogenic bacteria; pus walled off

  • Fistula

    Tract between two epithelial surfaces

  • Chronic inflammation

    Agent persists; macrophages and lymphocytes take over

An abscess can drain through a fistula or a sinus; any outcome with destroyed framework ends in some scar.

The outcome depends on how much tissue was destroyed, whether the tissue can regenerate, and whether the cause persists.L2 p.39

The lecture's five outcomesL2 p.39

  • Complete resolution

    When it happens
    Injury limited and short-lived; little tissue destroyed; cells can regenerate
    Example
    Lobar pneumonia: alveolar walls survive, exudate is cleared

  • Scar (fibrosis)

    When it happens
    Substantial destruction, especially of the supporting framework; permanent cells; a large fibrin exudate that cannot be cleared
    Example
    Healed abscess cavity; organized pleural fibrin; myocardial infarct

  • Abscess

    When it happens
    Pyogenic organisms; pus walled off
    Example
    Diverticular or lung abscess

  • Fistula

    When it happens
    Inflammation erodes through two epithelium-lined surfaces and connects them (a sinus is a tract that ends blindly)
    Example
    Diverticulitis → colovesical fistula (air in the urine); Crohn disease

  • Progression to chronic inflammation

    When it happens
    The agent persists or the response keeps re-igniting
    Example
    Chronic osteomyelitis; peptic ulcer that will not heal

How the response switches off

L2 p.39

Inflammation is too destructive to run until it burns out; ending it is an active program. The lecture's termination slide gives the main elements: mediators with a short half-life, and lipoxins that inhibit neutrophil transmigration and chemotaxis and signal macrophages to eat apoptotic bodies.

  • Mediators decay: histamine, kinins, prostaglandins and cytokines are made in bursts and broken down within minutes to hours. Once the stimulus is cleared, production stops.
  • Neutrophils die: they live only hours to a day or two in tissue and then undergo apoptosis.
  • A lipid-mediator switch: early prostaglandins induce 15-lipoxygenase in neutrophils, so arachidonic acid is turned into lipoxins instead of LTB₄. Resolvins and protectins, made from omega-3 fatty acids, act the same way. Aspirin acetylates COX-2 so that it makes “aspirin-triggered” lipoxins.
  • Macrophages clear the debris (efferocytosis): they recognize phosphatidylserine on apoptotic neutrophils and engulf them without alarm. Eating apoptotic cells switches macrophages to make TGF-β and IL-10, which dampen inflammation and start repair.
  • Other brakes: IL-1 receptor antagonist, IL-10, lymphatic drainage of fluid and debris, and a vagal anti-inflammatory reflex that restrains TNF release.
L2 p.39Ref. · Robbins, termination of the acute inflammatory response

From inflammation to repair

  1. Cause removed
  2. Mediators decay; no new ones made
  3. Neutrophils undergo apoptosis
  4. Lipoxins and resolvins stop further recruitment
  5. Macrophages engulf apoptotic cells
  6. Macrophages release TGF-β and IL-10
  7. Vessels reseal; lymphatics drain; repair begins (2.7)

Core activity · The Missing Arrow

The Missing Arrow

Complete the causal chain. Place the missing step by dragging a card onto a gap, or tap a card and then tap the gap. Some gaps need an event; others need the mechanism that links one event to the next.

An abscess has been drained and the bacteria are gone. Complete the chain that ends the response and starts repair.

  1. Bacteria cleared from the tissue
  2. no new stimulus; short-lived mediators decay

Cards

Tap or drag a card. Placing a used card moves it.

Knowledge check · 2.5

Answer, read why, and try again whenever you like. Answers are kept in both study modes.

0 of 5 correct
  1. Q1Abscess: lysosomal enzymesL2 p.32–33Ch. II cases p.12

    A 63-year-old man with constipation has four days of lower abdominal pain, fever (39.1 °C) and left lower quadrant tenderness. White count is 19,000/mm³. CT shows a thickened descending colon with multiple diverticula and a 5.0-cm, low-attenuation pelvic lesion with air-fluid levels, which is drained.

    Release of which substance is most likely responsible for forming the drained lesion?

  2. Q2Fibrinous inflammation: image recognitionL2 p.35

    A 66-year-old man dies 5 days after a large transmural myocardial infarction. In his last days a scratchy sound was heard with each heartbeat. The heart at autopsy is shown.

    Lecture image

    Heart with a shaggy yellow fibrin coat over the pericardial surface

    What produced the coating on the heart's surface?

  3. Q3Pseudomembranous inflammation: image recognitionL2 p.37

    A 72-year-old woman develops profuse watery diarrhea a week after starting clindamycin. Colonoscopy is shown.

    Lecture image

    Colonoscopy view with many raised yellow plaques on the mucosa (arrows)

    What are the yellow plaques made of?

  4. Q4Resolution: lipoxinsL2 p.26, 39

    Which arachidonic-acid products stop neutrophil transmigration and chemotaxis and signal macrophages to phagocytose apoptotic cells as inflammation ends?

  5. Q5Outcomes: fistulaL2 p.39

    A 67-year-old man treated for diverticulitis two months ago now notices bubbles of air when he urinates, and he has recurrent urinary tract infections with bowel organisms.

    Which outcome of acute inflammation explains this?

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