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Acute and Chronic Inflammation

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Title: Acute and Chronic Inflammation


1
Acute and Chronic Inflammation
  • March 4, 2009
  • Dr. Eileen McKay

2
Objectives
  • List the five cardinal signs of inflammation.
  • Describe the events that occur during acute
    inflammation.
  • List chemical mediators that are involved in
    inflammation.
  • List possible outcomes of acute inflammation.
  • Describe the morphology of chronic inflammation.
  • Describe the morphology of granulomatous
    inflammation.
  • List causes of granulomatous inflammation.
  • Define and differentiate pus, abscess, and ulcer.
  • Describe the morphology of an ulcer.
  • List the systemic effects of inflammation.

3
Inflammation
  • Host response to cellular injury.
  • Protective function.
  • Harmful effects of unchecked inflammation and
    excess tissue damage.
  • Pharmaceuticals aimed at controlling the host
    response.

4
  • Acne
  • Acute appendicitis
  • Otitis media
  • Conjuctivitis
  • Brain Abscess
  • Wound infections
  • Chorioamnionitis

5
5 Cardinal Signs of Inflammation
  • Dolor pain
  • Tumor swelling
  • Rubor redness/erythema
  • Calor heat
  • Functio laesa loss of function

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Stage of Acute Inflammation
  • Combined VASCULAR response and CELLULAR response
  • 1. alterations in vascular caliber that lead to
    an increase in blood flow
  • 2. structural changes in the microvasculature
    that permit plasma proteins and leukocytes to
    leave the circulation
  • 3. emigration, accumulation and activation of
    leukocytes to eliminate offending agent

8
ACUTE INFLAMMATION
  • VASCULAR REACTION
  • Vasodilation
  • Increased permeability
  • Stasis
  • Leukocyte accumulation
  • CELLULAR REACTION
  • Leukocyte extravasation
  • Margination
  • Diapedesis
  • migration
  • Leukocyte activation
  • Phagocytosis
  • Termination of inflammatory response clean up

9
Mechanisms for Increased Vascular Permeability
  • Gaps due to endothelial contraction
  • Direct injury
  • Leukocyte-dependent injury
  • Increased transcytosis
  • New blood vessel formation

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NEUTROPHILS
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13
Chemical Mediators
14
Systemic Effects of Acute Inflammation
15
Evaluating a Patient for Acute Inflammation
  • Superficial inflammation
  • Pain, swelling, erythema
  • Loss of function
  • Generalized fatigue
  • Loss of appetite
  • Systemic signs
  • Vital signs
  • Fever
  • Increased pulse and heart rate
  • Laboratory investigations
  • Elevated white blood cell count and left shift
  • Acute-phase reactants

16
Neutrophil left shift or bandemia
17
Outcomes of Acute Inflammation
  • Complete resolution
  • Abscess formation
  • Chronic inflammation
  • Scar formation

18
Morphologic Patterns of Acute Inflammation
  • Serous inflammation
  • Fibrinous inflammation
  • Suppurative/purulent inflammation
  • Ulcerative inflammation

19
Serous Inflammation example blister
20
Edema and Fluid Collections
  • Exudate
  • Associated with acute inflammation
  • Increased vascular permeability
  • Specific gravity gt 1.020
  • Protein and cellular debris present due to
    increased vascular permeability
  • Transudate
  • No change in vascular permeability
  • Specific gravity lt 1.012
  • No increase in protein concentration
  • Occurs with osmotic or hydrostatic imbalance in
    vascular compartment (ie. nephrotic syndrome)

21
Fibrinous Inflammation example fibrinous
pericarditis
22
Suppurative/purulent inflammation example
acute appendicitis
23
Another example Bacterial pneumonia
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26
Ulcerative inflammation example gastric ulcer
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28
Acute vs Chronic Inflammation
  • Acute inflammation is a more rapid event with
    shorter duration.
  • Cannot be ignored
  • Chronic inflammation is delayed and prolonged.
  • May follow acute inflammation or arise de novo as
    a low grade process
  • May be asymptomatic
  • Associated with tissue destruction/ architectural
    changes with angiogenesis and possibly fibrosis.

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30
Morphology of Chronic Inflammation
  • Characterized by mononuclear infiltrate with
    macrophages, lymphocytes, and plasma cells.

31
Acute vs Chronic Inflammation
32
Granulomatous Inflammation
  • Granulomas can be necrotizing or non-necrotizing.
  • Consist of aggregates of histiocytes/activated
    macrophages with eventual formation of external
    collar of lymphocytes.
  • Multinucleated giant cells may be present.
  • Response to injurious agents that cannot be
    successfully eradicated by humoral and cellular
    immune reactions.

33
Causes of Granulomatous Inflammation
  • Organisms
  • Mycobacteria
  • Cat- scratch disease
  • Leprosy
  • Brucellosis
  • Syphilis
  • Mycotic infections
  • Lymphogranuloma inguinale
  • Foreign Bodies
  • Irritant lipids
  • Berylliosis
  • Autoimmune disorders
  • Crohns disease
  • Sarcoidosis

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