Inflammation - Pathology - Medbullets Step 1

Overview
- Cardinal signs of inflammation
  - rubor (redness)
    
    result of vasodilation specifically the arteriolar smooth muscle
    
    mediated by prostaglandins, bradykinin, and histamine
  - dolor (pain)
    
    result of sensitization of pain nerve endings
    
    mediated by bradykinin and PGE₂
  - calor (heat)
    
    result of vasodilation (increased blood flow)
    
    mediated by prostaglandins, bradykinin, and histamine
  - tumor (swelling)
    
    result of increased permeability of post capillary venules leading to an exudate
  - functio laesa (loss of function)

Stages of Inflammation
- Fluid exudation
  - endothelial injury
  - ↑ post-capillary venule permeability
  - vasodilation
- Leukocyte activation
  - emigration
  - chemotaxis (bacterial products, complement, chemokines)
  - phagocytosis
  - killing
- Potential outcomes
  - restoration of normal structure
  - granulation tissue
    
    highly vascularized and fibrotic
  - abscess
    
    fibrosis surrounding pus
  - fistula
    
    abnormal communication
  - fibrosis/scarring
    
    collagen deposition resulting in altered structure and function

Acute vs. Chronic
- Acute
  - chemical mediators
    
    activation of Toll-like receptors (TLRs) by pathogen-associated molecular patterns (PAMPs)
    
    arachidonic acid metabolites
    
    prostaglandins and leukotrienes
    
    complement system
    
    hageman factor (Factor XII)
  - defined by the effector cells
    
    neutrophils
    
    eosinophils
    
    antibodies
  - rapid onset (seconds to minutes)
  - may have long lasting "acute" inflammation
- Chronic
  - defined by effector cells
    
    monocytes
    
    plasma cells
  - characterized by persistent destruction and repair
  - associated with
    
    blood vessel proliferation
    
    fibrosis
  - granulomas are a subtype of chronic inflammation
    
    the body attemps to contain a substance that it perceives as foreign but is unable to eliminate
    
    formation is mediated by interferon-γ release from Th1 cells which activate macrophages
    
    macrophages release IL-12 which activates Th1 cells
    
    granuloma formation is maintained by IL-12 and TNF-alpha
    
    defining feature is the presence of epithelioid histiocytes
    
    presence of multinucleated giant cells is not required for a granuloma
    
    two types
    
    caseating
    
    presence of central necrotic zone
    
    e.g. TB, fungal infections
    
    noncaseating
    
    lack of central necrotic zone
    
    e.g. sarcoidosis, beryllium, Crohn disease, cat scratch disease (Bartonella), and Wegener's granulomatosis

Action	Numeric Key	Letter Key	Function Key
Show Bullets		S	Enter (frontside only)
20%	1	N
40%	2	H
60%	3	F	Enter (backside only)
80%	4	E
100%	5	M
Toss	0	T