Path 3: Inflammation Flashcards
Steps of inflamation
1) Recognition of of noxious agent
2) Recruitment of leukocytes and plasma proteins
3) Removal of stimulus (mainly by phagocytes)
4) Regulation (terminates reaction)
5) Repair of tissue
Mediator of vascular changes in inflamation
Histamine
Three components of acute inflammation:
1) Small vessel dilation (increase blood flow)
2) Increased microvasculature permeability (enables leukocytes to leave circulation)
3) Emigration of leukocytes from microcirculation to the offending site
Exudate
Extravascular fluid with high protein containing cellular debris
Transudate
Fluid with low protein content
Increased vascular permeability accomplished by
Contraction of endothelial cells
Contraction of endothelial cells in inflammation is induced by
Histamine, bradykinin and other chemical mediators
Edema is drained via
Lymphatics
Lymphagitis vs lymphadenitis
Lymphagitis: lymphatic system inflammation
Lymphadenitis: inflmmation of draining lymph nodes
Reactive lymphadenitis
Hyperplasia of lymphoid follicles and increased lymphocytes causes lymph node enlargement
Often seen with red streaks near wound
Chemokines
adhesion molecules and cytokines that mediate leukocyte migration from vessel lumen to tissue
Diapedesis
AKA transmigration
Procress in which leukocytes migrate through intact endothelium
Chemotaxis
Locomotion along chemical gradient. Leukocytes move toward attractants such as bacterial products, cytokines and complement products
_____ initially predominate in inflamatory infiltrate
Neutrophils (6-24 hours)
______ replace neutrophils in inflammatory infiltrate
Monocytes (24-48 hours)
Steps of phagocytosis
Recognition and attachment of particle to be ingested
Engulfment
Killing of microbe
Phagocytosis is dependent on polymerization of ______
Actin filaments
Killing of microbes in lysosomes is accomplished with
Reactive oxygen species (ROS)
Enzymes
Respiratory burst
Oxidative reaction that accompanies phagocytosis
Neutrophil Extracellular traps (NETs)
Extracellular fibrillar networks that concentrate antimicrobial substances at sites of infection and trap microbes, helping to prevent their spread
Neutrophil half lives
Are short. They commit seppuku a few hours after leaving blood
Histamine is secreted by
granule exocytosis
Prostaglandins, leukotrines and cytokines are produced _____ during inflamation
De novo
Plasma derived mediators
e.g. Complement proteins. produced in liver and circulate in inactive form. Activated by proteolytic cleavages
Two major vasoactive amines
Histamine and serotonin
Prostaglandin production
Arachandonic acid converted by COX1 and COX2
Thromboxane A2
Prostaglandin that causes vasoconstriction, promotes platelet aggregation
Prostacylin PGI2
Causes vasodilation, inihibits platelet aggregation
PGD 2 and PGE 2
Vasodilation
Increased vasular permeability
Leukocyte chemotaxis
Leukotrienes C4 D4 E4 cause
Bronchospasm
TNF and IL-1 function
Leukocyte recruitment and adhesion
TNF pathological effects
Decreased CO
Insulin resistance
Vascular permeability
What triggers classical complement pathway
C1 binding to IgM or IgG
How is the alternative pathway activated
Bacterial surface molecule in the absence of antibody
How is the lectin pathway activated
C1 is activated by plasma mannose binding lectin
Serous inflammation
Marked by exudation of cell poor fluid into spaes created by cell injury
(burn blister)
Fibrinous inflammation
occurs with large vascular leaks or procoagulant stimulus
Purulent abscess
Made of pus, an exudate of neutrophils, liquified necrotic cell debris, and edema
Ulcer
Excavation caused by sloughing of inflammed necrotic tissue
Chronic inflammation caused by
Persistent infections
Hypersensitivity reactions
Prolonged toxic agent exposure
Chronic inflamation characterized by
Mononuclear cell infiltration
Tissue destruction
Attempts at healing by connective tissue replacement
Kupffer cells
Macrophages in liver
Macrophages are derived from
Bone marrow in post natal life
Yolk sac and liver during development
Alternatively activated macrophages (M2)
Stimulate tissue repair and anti-inflammatory effects
Major basic protein
Secreted from eosinophil granule to injure wormz
Granulomatous inflammation
Characterized by collections of activated macrophages, often T cells and associated with necrosis
Foreign granuloma
Granuloma that forms around foreign body that does not have antigenic properties (sutures, talc)
Immune granulomma common cause
Tuberculosis :)
Features of acute phase response (systemic inflammation)
Fever
Leukocytosis
Elevated acute phase proteins (C-reactive protein, fibrinogen)
Infections associated with leukopenia
Rickettsiea, typhoid, protozoa
What stimulates angiogenesis
VEGF
Vascular endothelial growth factor
TGF-B
Tissue growth factor B. Activated by M2 cells. Important for connective tissue deposition during repair
