Acute and chronic inflammation

Get Started. It's Free
or sign up with your email address
Inflammation by Mind Map: Inflammation

1. Acute

1.1. Cardinal Signs

1.1.1. Redness (rubor) and warmth (calor) Vasodilation histamine prostaglandins bradykinin

1.1.2. Swelling (tumor) exudate (postcapillary venules) histamine tissue damage

1.1.3. Pain (dolor) bradykinin PGE2

1.1.4. Fever pyrogens ex. LPS from bacteria macrophages release IL-1, TNF

1.2. Mediators

1.2.1. Toll-like receptors (TLRs) present on cells of the innate and adaptive system activated by PAMPS/DAMPS CD14 on macrophages recognizes LPS on gram-negative activetes results in upregulation of NF-kB

1.2.2. Arachidonic acid (AA) metabolites released from the phospholipid cell membrane by phospholipase cyclooxygenase (COX) 5-lipooxygenase

1.2.3. Mast cells distributed throughout connective tissue activated tissue trauma C3a and C5a cross-linking of cell-surface IgE by antigen response

1.2.4. Complement activation classical alternative mannose-binding lectin (MBL) Function C5a C3b MAC

1.2.5. Hageman factor (Factor XII) Activated upon exposure to subendothelial or tissue collagen coagulation and fibrinolytic systems complement kinin system

1.3. Characterized

1.3.1. Edema

1.3.2. innate cells neutrophil function arrival macrophages arrival 2-3 days after infl. begins phagocytosis manage the next step of the inflammatory process

2. Chronic

2.1. characterized

2.1.1. lymphocytes activation binding antigen/MHC complex 2nd signal T TCR complex recognizes antigen presented on MHC B activation

2.1.2. plasma cell in tissue

2.2. delayed response

2.2.1. adaptive immunity

2.3. stimuli include

2.3.1. persistent infection viruse mycobacteria parasites fungi

2.3.2. autoimmune disease

2.3.3. foreign material

2.3.4. some cancers

2.4. Granulomatous Inflammation

2.4.1. subtype of chronic

2.4.2. characterized granuloma collection of epithelioid histiocytes surrounded by giant celles a rim of lymphocytes

2.4.3. formation macrophages secrete IL-12 CD4+ differentiate into Th1

2.4.4. noncaseating lake central necrosis common etiologies foreign material sarcoidosis beryllium exposure Crohn disease cat scratch disease

2.4.5. caseating cental necrosis common etiologies tuberculosis fulgal infections