Inflammation Flashcards
Cellular Injury
Anything that causes damage to cells
The trigger for the inflammatory process
The first five steps of the inflammatory process
Mast cell degranulation
Activation of the coagulation cascade
Activation of the kinin cascade
Release of chemotactic factors
Activation of the complement cascade
Complement system
Functions include bacterial lysis, vasodilation and increased vascular permeability, triggers mast cell degranulation, chemotaxis and opsonization (immune system process that uses opsonins to tag foreign pathogens for elimination by phagocytes)
Kinin
Turn into bradykinin which is responsible for pain, chemotaxis, and increased vascular permeability and vasodilation
Coagulation cascade
Role in activating the kinin system, factor XII hangman factor (intrinsic coagulation cascade) also activates kinin
—> goal to form a fibrin mesh to stop bleeding and to trap microorganisms
Chemotactic factors
Attract neutrophils, eosinophils and monocytes all which begin phagocytosis
Neutrophils first to respond in 6-8 hr
Monocytes respond in 1-7 days
Neutrophils and monocytes —> eventually die and release intracellular contents
—> triggers acute phase reactants
Mast cell degranulation
Major step of inflammatory cascade
Results in the activation of acute cell reactants
Degranulation —> releases histamine, cytokines, leukotrienes, platelet-activating factor and prostaglandins
Histamine
Histamine is responsible for causing vasodilation, increases vascular permeability and increases blood flow to the site of injury
—> erythema and swelling
H1
Receptors promote inflammation
Present in smooth muscle especially bronchi
When stimulated —> bronchoconstriction
Basis for asthma attack or reactive airway disease
H2
Receptors having anti-inflammatory properties
Found in gastric mucosa
Stimulation of H2 receptors induces secretion of gastric acid
Drugs such as ranitidine, Tagamet and famotidine inhibit H2 receptors
Cytokines
Can react quickly or may be more delayed
IL4 is released early in the inflammatory response
- responsible for B cell proliferation & antibody production
IL13 is released later in the inflammatory response
- chemotaxis, B cell proliferation & antibody production
TNF (tumor necrosis factor) is releases in early and late inflammatory response
-leukocyte emigration
-increased vascular permeability
Leukotrienes
Known as slow reaction substances of anaphylaxis (SRS-A)
Tend to prolong the inflammatory response
Cause vasodilation and attract neutrophils, monocytes and eosinophils
Target of inhibition for the drug singular
Prostaglandins
Produced by the arachidonic pathway
Function to cause vasodilation, platelet aggregation at the site of injury, pain and fever
Platelet-activating factor (PAF)
Derived from fatty acids in the plasma membrane
Can be made by neutrophils, monocytes, endothelial cells and platelets
Works in a similar fashion as leukotrienes and causes endothelial cell retraction, increased vascular permeability, activates platelets and enhances leukocyte adhesion to endothelial cells
Monocytes (additional fx’s)
Monocytes become macrophages when they enter the tissue
Responsible for presenting antigens to the CD4 cells which trigger T cell immunity
Monocytes release cytokines
-IL1 :Fever, activates phagocytes and lymphocytes —> also increases the release of IL6
-IL6 :Stimulates the production of acute phase reactants and promotes the growth and stimulation of RBCs
-TNF :fever, increases secretion of pro inflammatory proteins by the liver, muscle wasting and induces thrombosis
-Growth Factor :promote the production and maturation of neutrophils
Inflammation diseases
Pathophysiologic process of asthma, autoimmune diseases, lupus, RA, gout, atherosclerosis m cerebral edema, cirrhosis, and hepatitis
Inflammation can be acute or chronic
Chronic inflammation —> pathological process —> permanent organ damage/tissue scaring
Polyunsaturated fats
Essential fatty acids which can only be derived from diet
Omega- 3 and Omega- 6