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30 Cards in this Set

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Cellular response of leukocytes
1. Emigration (moves between endothelial cells)
2. Chemotaxis (attracted to site of injury)
3. Phagocytosis (neutrophils and monoc-macroph)
4. IC microbial killing (free radicals (ROS, NO) and lysosomal enzymes)
Exogenous mediators of acute inflammation
Most often microbial origin
Endogenous mediators of acute inflammation
- Vasoactive amines: histamine, serotonis
- Arachidonic acid metabolites: 1. the cyclooxygenase pw; platelet TxA2 (vasoconstrictor), endothelial PGI2 (vasodilator). 2. the lipoxygenase pw; HPETE
- cytokines; IL-1 nad TNF induce acute phase responses
- kinin system
- complement system
- NO
Relase of preformed histamin from mast cell, in response to:
1. physical injury such as trauma or heat
2. immune reactions involving binding IgE Ab to Fc receptors on mast cells
3.Ca3 and Ca5 of complement and anaphylatoxins
4. leukocyte-derived histamine-releasing proteins
5. neuropeptides (eg substance P)
6. certain cytokines (eg IL-1, IL-8)
Action of histamine
Arteriolat dilation
Icreased vascular permeability
Endothelial action
Serotonin
In platelets dense bodies granules, released during platelet aggregation

Arteriolat dilation
Icreased vascular permeability
Arachidonic Acid (AA) metabolites
Prostaglandins
Leukotriens
Lipoxins
Major sourses for arachidonc acid metabolites (eicosanoids) in inflammation
Leukocytes
Mast cells
Endothelial cells
Platelets
Two major enzymatic pathways for metabolism of arachidoic acid metabolites
1. Cyclooxygenase stimulate synthesis of prostaglandins and thromboxane
2. Lipoxygenase is responsible fro production of leukotriens and lipoxins
Activated Hageman factor (XIIa) initiates four systems involved in the inflammatory response:
1. the kinin system, producing vasoactive kinins
2. the clotting system, inducing the activation of thrombin, fibrinopeptides, and factor X, all with infl properties
3. the fibrinolytic system, producing plasmin and inactivating thrombin
4. the complement system, producing the anaphylatoxins C3a and C5a
Dr. Vernerova's classification of morphologic changes in acute inflammation
A. Alterative infl (parenchymatous)
B. Exudative
1. serous
2. catharral
3. purulent
4. fibrinous
5. gangrenous
C. Proliferative
Outcome of acute inflammation
1. Resolution of tissue structure and function
2. Tissue destruction and persistent acute infl (abscess, ulcer, fistula or scar)
3. Conversion to chronic infl
Alterative (parenchymal) inflammation
Necrotic change predominate. Almost no exudate.
Eg: viral hepatitis, lyssa, diphteric endocarditis and myocarditis
Exudative: serous inflammation
Mild infl. Watery, low protein content, few cells, derived from blood or serous lining cells.
Eg: skin blisters, effusion (=accumulation of fluid) (pleural, peritonela, pericardial), 2nd degree burn, viral meningitis, joint effusion
Exudative: catharral inflammation
Overproducion of mucin superimposed on low grade infl reaction. On mucous membranes.
Eg: rhinitis, nasopharyngitis, bronchitiss, catharral bronchopneumonia
Exudative: purulent inflammation
(suppurative, pyogenic)
Large amounts of both necrotic and viable neutrophils and liquefied necrotic tissue. Produces mainly by staphylococci.
1. on serous membr: empyema thoracis, leptomeningitis, peritonitis purulenta
2. on mucous mebmr: pyosalpingitis, bronchitis, folliculitis
3. interstitial (involvement of stroma): abscess or phlegmone
Exudative: fibrinous inflammation
More severe injury. Typical in lining of body cavities (meninges, pericardium, pleura-->serous membr).
Mucous membr: crupous / pseudomembranous / necrotizing / ulcerative.
Interstitial type (acute phase of reumatic fever)
Outcome: resolution or organisation. Histo: eosinophilic meshwork.
Exudative: gangrenous inflammation
Inflammation is secondary changed due to ischemia or bacteria
Proliferative inflammation
Characteristic feature is formation of CT due to granulation tissue or due to hyperplasia. Many fibroblasts.
Eg: productive polyserositis, palmar faciitis.
Increased healing compered to other types of infl.
Prostaglandins
(thromboxanes included)
Pain
Fever
Clotting
Leukotrienes
Chemotaxis
Vasoconstriction
Increased Permeability
Lipoxins
INHIBIT chemotaxis
Vasodilatation
Counteract actions of leukotrienes
CYTOKINES/CHEMOKINES
CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation.
TNFα, IL-1, by macrophages
CHEMOKINES are small proteins which are attractants for PMNs (>40)
NITRIC OXIDE
Potent vasodilator
Produced from the action of nitric oxide synthetase from arginine
LYSOSOMAL CONSTITUENTS
PRIMARY
(Also called AZUROPHILIC, or NON-specific)
- Myeloperoxidase
- Lysozyme (Bact.)
- Acid Hydrolases
SECONDARY
(Also called SPECIFIC)
- Lactoferrin
- Lysozyme
- Alkaline Phosphatase
- Collagenase
NEUROPEPTIDES
Produced in CNS (neurons)
SUBSTANCE P
NEUROKININ A
SEQUENCE OF EVENTS (acute infl)
NORMAL HISTOLOGY
VASODILATATION
INCREASED VASCULAR PERMEABILITY
LEAKAGE OF EXUDATE
MARGINATION, ROLLING, ADHESION
TRANSMIGRATION (DIAPEDESIS)
CHEMOTAXIS
PMN ACTIVATION
PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion)
TERMINATION
100% RESOLUTION, SCAR, or CHRONIC inflammation
CAUSES of
CHRONIC INFLAMMATION
1) PERSISTENCE of Infection
2) PROLONGED EXPOSURE to insult
3) AUTO-IMMUNITY
SYSTEMIC MANIFESTATIONS
(NON-SPECIFIC) (of chronic infl)
FEVER, CHILLS
C-Reactive Protein (CRP)
“Acute Phase” Reactants
Erythrocyte Sedimentation Rate (ESR) increases
Leukocytosis
Pulse, Blood Pressure
Cytokine Effects, e.g., TNF(α), IL-1
Diseases with granulomatous inflammation
- Tuberculosis
- Leprosy
- Syphilis
- Cat-scratch disease
- Sarcoidosis
- Crohn's disease
- Schistosomiases
- Histoplasmosis
- Cryprococcosis

Granulomas may be found in:
- Granuloma annulare (skin, unknown cause)
- Aspiration pneumonia
- Reumatoid arthritis (reumatoid nodules)
- Pneumocycstic pneumonia