Acute Inflammation Flashcards
Clinical features of acute inflammation (Latin)
Rubor - redness Tumor - swelling Calor - heat Dolor - pain And loss of function
Where is histamine released from and in response to what?
Mast cells, basophils, platelets.
Physical damage, immunologic reactions, C3a, C5a, IL-1, factors from neutrophils and platelets
What does histamine cause?
Vascular dilation
Transient increase in vascular permeability
Pain
What is fluid loss from vessels a result of?
Increased hydrostatic(blood) and oncotic(interstitium) pressure.
Protein content in transudate and exudate
Exudate - high protein
Transudate - low protein
Mechanisms of vascular leakage
Endothelial contraction Cytoskeletal reorganisation Direct injury Leukocyte dependent injury Increased transcytosis - channels across endothelial cytoplasm
Infiltration of neutrophils
Margination - stasis causes neutrophils to line up at the edge of
blood vessels along the endothelium
Rolling - roll along endothelium
Adhesion - stick more avidly
Emigration - through blood vessel wall
How do neutrophils escape from vessels?
Relaxation of inter-endothelial cell junctions.
Digestion of vascular basement membrane.
O2 dependent killing mechanism
Produces superoxide and hydrogen peroxide.
H2O2-Myeloperoxidase-halide system - produces HOCl.
O2 independent killing mechanism
Lysozyme & hydrolases
Bactericidal Permeability Increasing Protein (BPI)
Cationic proteins (‘Defensins’)
Function of neutrophils
Phagocytise microorganisms
Results in purple to necrosis
Chemical mediators
Protease - kinins, complement system, coagulation/fibrinolytic system
Prostaglandins/Leukotrienes
Cytokines/Chemokines - interleukins, TNF
Increased blood flow chemical mediators
Histamine and prostaglandins
Vascular permeability chemical mediators
Histamine and leukotrienes
Neutrophils chemotaxis chemical mediators
C5a, LTB4, bacterial peptides
Phagocytosis chemical mediators
C3b
How does exudation of fluid combat injury?
Delivers plasma proteins to area of injury - immunoglobulins, inflammatory mediators, fibrinogen
Dilutes toxins
Increases lymphatic drainage - delivers microorganisms to phagocytes and antigens to immune system
What are the mechanisms that help combat injury?
Exudation of fluid
Infiltration of cells - removes pathogenic bacteria and necrotic debris
Vasodilation - increases delivery and temperature
Pain and loss of function - enforces rest, reduces chance of further traumatic damage
Local complications of acute inflammation
Swelling - blockage of tubes
Exudate - compression e.g. cardiac temponade
Loss of fluid
Pain and loss of function
Systemic effects of acute inflammation
Fever - IL-1 and TNFalpha
Leukocytosis - increase in wbc
Acute phase response - decreased appetite, raised pulse rate, altered sleep pattern
Acute phase proteins - CRP, alpha1 antitrypsin, heptoglobin, fibrinogen, serum amyloid A protein
Lobar pneumonia: causative organism, clinical course
Streptococcus pneumoniae.
Worsening fever, prostration, hypoxaemia, dry cough and breathlessness.
If treated can resolve completely.
Skin blister: causes, predominant features
Heat, sunlight, chemical.
Pain and profuse exudate, few inflammatory cells therefore exudate clear unless bacterial infection develops, resolution or scarring.
Abscess
Solid tissue. Inflammatory exudate forces tissue apart. Liquefactive necrosis in centre. High pressure therefore pain. Tissue damage and squash adjacent structures.
Acute inflammation in serous cavity
Ascites, pleural or pericardial effusion. Localised fibrin deposition.
