1) Transient vasoconstriction

2) Vasodilation

3) Exudation

4) Stasis

5) Adhesion and rolling

6) Margination (pavementing)

Serous - water blister, bullous dermatitis

Fibrinous - uremic pericarditis

Suppurative/Purulent - pyogenic infections

Mixed - fibroniopurulen

Hemorrhagic - proteus pneumonia

1) Tumor - exudation

2) Rubor - hyperemia

3) Calor - dilated vessels

4) Dolor - irritation of nerves

5) Loss of function

- Factor XII

1) Inflammation

Vascular Endothelium:

- Increased expression of adhesion molecules

- Produce more IL-1

- Increased clotting

Leukocyte

- Activation

- Cytokine production

2) Repair

Fibroblasts

- Proliferate

- Increased collagen synth

Systemic manifestations of inflammation

- fever

- leukocytosis

- increased acute phase

- decreased appetite

- increased sleep

Blood vessels:

- relaxes smooth muscle

- decrease adhesion of WBCs and platelets

Macrophages:

- increase phagocytosis

Hageman factor (Factor XII)

--> clotting fibronolytic system

      --> fibrin split products

--> Kallikrein-kinin system

      --> Kinins (bradykinin)

Complement system activation

--> C3a, C5a

End Result: Increased cascular permeability --> Edema

Mast cells/basophil degeneration --> Histamine

Platelets --> Serotonin

Inflammatory cells

--> Platelet-activating factor; Prostaglandins, Leukotrienes

Within Tissues:

- Abscesses: focal areas of suppuration

- Phlegmons (cellulitis): spreading abscess

On surfaces:

- Ulcers: focal necrosis and inflammation

- Pseudomembranes: diffuse ulceration, spreading ulcers

IL-1, IL-6, TNFalpha, PGE, NO

End result: fever

Caused by: constriction of outer blood vessels

IL-1, TNF, CSF, GSF

Differential Dx: Immature Band Cells = leukocytosis (inflammation)

1) Resolution

2) Chronic inflammation

3) Organization (scar/fibrosis, loss of function)

Acute: Neutrophils

Chronic: replaced by Macrophages

1) Debridement and removal of injured tissue and debris

- phagocytosis

- collagenase, elastase

2) Antimicrobial activity

- NO, ROS

3) Chemotaxis and proliferation of fibroblasts and keratinocytes

- PDGF

- TGF-beta

- TNF

- IL-1

- KGF-7

4) Angiogenesis

- VEGF

- FGF-2

- PDGF

5) Deposition and remodeling of ECM

- TGF-beta

- PDGF

- TNF

- OPN

- IL-1

- collagenase

- MMPs

1) Non-necrotizing

- Sarcoid

- Foreign Bodies

2) Necrotizing

- TB (caseating)

- Rheumatoid arthritis

3) Suppurative

- chalazion

- cat-scratch dz

1) Foreign body type

2) Langhans type - seen in TB and sarcoid

Multinucleated giant cells have enhanced phagocytic activity, but a short lifespan :(.

1) Nodular scarring

2) Calcification (if necrosis)

3) Cavity formation

1) Priming - TNF, IL-6

2) Proliferation

- Growth factors: HGF, TGF-alpha

- Adjuvants: Norepi, Insulin, TH, GH

3) Growth inhibition

- Growth inhibitors: Activin, TGF-beta

VEGF (Vasecular Endothelial GF)

angiopoeitins

PDGF (platelet-derived GF)

TGF-beta

Initial: clot/scab

1-3 days: acute inflammation (PMNs)

3-5: macrophages replace neutrophils

1 week: granulation tissue, fibroblasts

1-4 weeks: more scar, less granulation tissue

2-3 months: remodeling of scar

1) Endothelial precursor cell (EPC) migration

EPC migrate from bone marrow to site of injury --> stimulate wound to grow towards intact vessels

2) Pre-existing blood vessel growth

Intact blood vessels are stimulated by growth factors (e.g. VEGF) to grow towards wound

Major way: pre-existing BV growth

False.

Sweat glands, hair follicles, melanocytes do no regenerate --> Scars lack pigment

Day 4.

At the beginning fibrous clot provides some tensile strength.  At day 4, macs and neutrophils are busy phagocytosing and eats some of the fibrin clot.

MMP produced to inhibit IL-1.

MMP breaks down collagen.

TGF-beta inhibits MMP

Too much:

- Strictures

- keloid (tumor-like)

- Exuberant granulation tissue

Too little:

- Fistulas

- Sinus tracts

- Dehiscence (wound pulls apart, 4 days after MI)