General pathology Robbins ch2

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)

Most often microbial origin

- 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

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)

Arteriolat dilation
Icreased vascular permeability
Endothelial action

In platelets dense bodies granules, released during platelet aggregation

Arteriolat dilation
Icreased vascular permeability

Prostaglandins
Leukotriens
Lipoxins

Leukocytes
Mast cells
Endothelial cells
Platelets

1. Cyclooxygenase stimulate synthesis of prostaglandins and thromboxane
2. Lipoxygenase is responsible fro production of leukotriens and lipoxins

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

A. Alterative infl (parenchymatous)
B. Exudative
1. serous
2. catharral
3. purulent
4. fibrinous
5. gangrenous
C. Proliferative

1. Resolution of tissue structure and function
2. Tissue destruction and persistent acute infl (abscess, ulcer, fistula or scar)
3. Conversion to chronic infl

Necrotic change predominate. Almost no exudate.
Eg: viral hepatitis, lyssa, diphteric endocarditis and myocarditis

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

Overproducion of mucin superimposed on low grade infl reaction. On mucous membranes.
Eg: rhinitis, nasopharyngitis, bronchitiss, catharral bronchopneumonia

(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

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.

Inflammation is secondary changed due to ischemia or bacteria

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.

Pain
Fever
Clotting

Chemotaxis
Vasoconstriction
Increased Permeability

INHIBIT chemotaxis
Vasodilatation
Counteract actions of leukotrienes

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)

Potent vasodilator
Produced from the action of nitric oxide synthetase from arginine

PRIMARY
(Also called AZUROPHILIC, or NON-specific)
- Myeloperoxidase
- Lysozyme (Bact.)
- Acid Hydrolases
SECONDARY
(Also called SPECIFIC)
- Lactoferrin
- Lysozyme
- Alkaline Phosphatase
- Collagenase

Produced in CNS (neurons)
SUBSTANCE P
NEUROKININ A

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

1) PERSISTENCE of Infection
2) PROLONGED EXPOSURE to insult
3) AUTO-IMMUNITY

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

- 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