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62 Cards in this Set

  • Front
  • Back
Cardinal signs of inflammation
Calor - Heat
Rubor - Redness
Tumor - Swelling
Dolor - Pain
Functio laesa - Loss of function
Outcomes of acute inflammation
Elimination of noxious stimuli
Repair
Persistent chronic inflammation
Exudation: definition and content
Increased passage of protein-rich fluid into interstitial tissue.
-globulins
-fibrin deposition
-factors promoting healing
Cell adhesion molecules
Selectins - recognize carbohydrate group on neutrophils
Integrins - ICAM-1, VCAM-1 bind integrins on neutrophils
Histamine
-Mast cells
Increased vascular permeability
Vasodilation
(Bronchial constriction)
Serotonin
-Platelets
Vasodilation
Arachidonic acid derivatives
Prostaglandins-->Vasodilation, edema(PGE2, PGI2)
Leukotrienes--> Vasoconstriction;Increased permeability
Cytokines
-Inflammatory cells, endothelium
IL-2,IL-4: Stimulate lymphocyte proliferation
IL-10, TGF-beta: Suppress lymphocyte proliferation
IFN-gamma, TNF-alpha: Macrophage activation
Phagocytosis
-opsonins
IgG
C3b(complement protein)
collectins
Serous inflammation
Outpouring of watery, protein-poor fluid from serum or secretions from mesothelial cells lining peritoneal, pleural and pericardial cavities
ex. skin blister
Fibrinous inflammation
High vascular permeability due to more severe injuries. Fibrinogen pass endothelial barrier.
-fibrinoous exudate - lining of body cavities, meninges, pericardium and pleura.
Suppurative(purulent) inflammation
Large amount of pus(neutrophils)-->purulent exudate
Pyogenic organisms more likely to form local suppuration.
Abscess-focal collection of pus
- seeding of pyogenic organisms into tissue or secondary infection of necrotic foci
Histamine
-Mast cells
Increased vascular permeability
Vasodilation
(Bronchial constriction)
Ulcer
Local defect-> shedding of necrotic tissue
Ulceration.>only in tissue necrosis on or near a surface
-mucosa of mouth
-stomach
-intestine
-genitourinary tract
Serotonin
-Platelets
Vasodilation
Primary disorder of phagocytosis:
Chronic granulomatous disease
Deficiency in phagcyte oxidase generating ROS. Activated macrophages accumulate and form ´granulomas``
Mutation on X-chromosome, 2/3 are males.
Arachidonic acid derivatives
Prostaglandins-->Vasodilation, edema(PGE2, PGI2)
Leukotrienes--> Vasoconstriction;Increased permeability
Cytokines
-Inflammatory cells, endothelium
IL-2,IL-4: Stimulate lymphocyte proliferation
IL-10, TGF-beta: Suppress lymphocyte proliferation
IFN-gamma, TNF-alpha: Macrophage activation
Phagocytosis
-opsonins
IgG
C3b(complement protein)
collectins
Histamine
-Mast cells
Increased vascular permeability
Vasodilation
(Bronchial constriction)
Serous inflammation
Outpouring of watery, protein-poor fluid from serum or secretions from mesothelial cells lining peritoneal, pleural and pericardial cavities
ex. skin blister
Serotonin
-Platelets
Vasodilation
Fibrinous inflammation
High vascular permeability due to more severe injuries. Fibrinogen pass endothelial barrier.
-fibrinoous exudate - lining of body cavities, meninges, pericardium and pleura.
Arachidonic acid derivatives
Prostaglandins-->Vasodilation, edema(PGE2, PGI2)
Leukotrienes--> Vasoconstriction;Increased permeability
Suppurative(purulent) inflammation
Large amount of pus(neutrophils)-->purulent exudate
Pyogenic organisms more likely to form local suppuration.
Abscess-focal collection of pus
- seeding of pyogenic organisms into tissue or secondary infection of necrotic foci
Cytokines
-Inflammatory cells, endothelium
IL-2,IL-4: Stimulate lymphocyte proliferation
IL-10, TGF-beta: Suppress lymphocyte proliferation
IFN-gamma, TNF-alpha: Macrophage activation
Ulcer
Local defect-> shedding of necrotic tissue
Ulceration.>only in tissue necrosis on or near a surface
-mucosa of mouth
-stomach
-intestine
-genitourinary tract
Phagocytosis
-opsonins
IgG
C3b(complement protein)
collectins
Primary disorder of phagocytosis:
Chronic granulomatous disease
Deficiency in phagcyte oxidase generating ROS. Activated macrophages accumulate and form ´granulomas``
Mutation on X-chromosome, 2/3 are males.
Serous inflammation
Outpouring of watery, protein-poor fluid from serum or secretions from mesothelial cells lining peritoneal, pleural and pericardial cavities
ex. skin blister
Histamine
-Mast cells
Increased vascular permeability
Vasodilation
(Bronchial constriction)
Fibrinous inflammation
High vascular permeability due to more severe injuries. Fibrinogen pass endothelial barrier.
-fibrinoous exudate - lining of body cavities, meninges, pericardium and pleura.
Serotonin
-Platelets
Vasodilation
Suppurative(purulent) inflammation
Large amount of pus(neutrophils)-->purulent exudate
Pyogenic organisms more likely to form local suppuration.
Abscess-focal collection of pus
- seeding of pyogenic organisms into tissue or secondary infection of necrotic foci
Arachidonic acid derivatives
Prostaglandins-->Vasodilation, edema(PGE2, PGI2)
Leukotrienes--> Vasoconstriction;Increased permeability
Ulcer
Local defect-> shedding of necrotic tissue
Ulceration.>only in tissue necrosis on or near a surface
-mucosa of mouth
-stomach
-intestine
-genitourinary tract
Histamine
-Mast cells
Increased vascular permeability
Vasodilation
(Bronchial constriction)
Cytokines
-Inflammatory cells, endothelium
IL-2,IL-4: Stimulate lymphocyte proliferation
IL-10, TGF-beta: Suppress lymphocyte proliferation
IFN-gamma, TNF-alpha: Macrophage activation
Serotonin
-Platelets
Vasodilation
Primary disorder of phagocytosis:
Chronic granulomatous disease
Deficiency in phagcyte oxidase generating ROS. Activated macrophages accumulate and form ´granulomas``
Mutation on X-chromosome, 2/3 are males.
Phagocytosis
-opsonins
IgG
C3b(complement protein)
collectins
Arachidonic acid derivatives
Prostaglandins-->Vasodilation, edema(PGE2, PGI2)
Leukotrienes--> Vasoconstriction;Increased permeability
Serous inflammation
Outpouring of watery, protein-poor fluid from serum or secretions from mesothelial cells lining peritoneal, pleural and pericardial cavities
ex. skin blister
Cytokines
-Inflammatory cells, endothelium
IL-2,IL-4: Stimulate lymphocyte proliferation
IL-10, TGF-beta: Suppress lymphocyte proliferation
IFN-gamma, TNF-alpha: Macrophage activation
Fibrinous inflammation
High vascular permeability due to more severe injuries. Fibrinogen pass endothelial barrier.
-fibrinoous exudate - lining of body cavities, meninges, pericardium and pleura.
Phagocytosis
-opsonins
IgG
C3b(complement protein)
collectins
Suppurative(purulent) inflammation
Large amount of pus(neutrophils)-->purulent exudate
Pyogenic organisms more likely to form local suppuration.
Abscess-focal collection of pus
- seeding of pyogenic organisms into tissue or secondary infection of necrotic foci
Serous inflammation
Outpouring of watery, protein-poor fluid from serum or secretions from mesothelial cells lining peritoneal, pleural and pericardial cavities
ex. skin blister
Ulcer
Local defect-> shedding of necrotic tissue
Ulceration.>only in tissue necrosis on or near a surface
-mucosa of mouth
-stomach
-intestine
-genitourinary tract
Fibrinous inflammation
High vascular permeability due to more severe injuries. Fibrinogen pass endothelial barrier.
-fibrinoous exudate - lining of body cavities, meninges, pericardium and pleura.
Primary disorder of phagocytosis:
Chronic granulomatous disease
Deficiency in phagcyte oxidase generating ROS. Activated macrophages accumulate and form ´granulomas``
Mutation on X-chromosome, 2/3 are males.
Suppurative(purulent) inflammation
Large amount of pus(neutrophils)-->purulent exudate
Pyogenic organisms more likely to form local suppuration.
Abscess-focal collection of pus
- seeding of pyogenic organisms into tissue or secondary infection of necrotic foci
Ulcer
Local defect-> shedding of necrotic tissue
Ulceration.>only in tissue necrosis on or near a surface
-mucosa of mouth
-stomach
-intestine
-genitourinary tract
Primary disorder of phagocytosis:
Chronic granulomatous disease
Deficiency in phagcyte oxidase generating ROS. Activated macrophages accumulate and form ´granulomas``
Mutation on X-chromosome, 2/3 are males.
Arachidonic acid
-two major pathways
Cyclooxygenase
-Prostaglandins
-Thromboxanes
Lipooxygenase
-Leukotrienes
-Lipoxins(inhibitors of inflammation)
Aspirin
-mechanism
Block function of cyclooxygenase- inhibit prod of prostaglandins.
- fever-inhibit production of PG by perivascular cells of hypothalamus
-inhibit production of thromboxane-`blood thinner´
Platelet-activating factor
Derived from phospholipid-membranes of neutrophils, monocytes, basophils, endothelial cells
-vasoconstriction
-bronchoconstriction
-vasodilation
-increased vascular permeability
Aggregate platelets
TNF and IL-1
-prod.
-secretion
Secretion stimulated by:
-endotoxin
-immune complexes
Produced by:
-activated macrophages, mast cells, endothelial cells ++
TNF and IL-1
-functions
Endothelial activation
TNF:increase thrombogenicity of endothelium, aggregation and activation of neutrophils.
IL-1:activate tissue fibroblasts
Granulomas
Persistent T-cell response to certain microbes
-M. Tuberculosis
-T. Pallidum
-fungi
Pyrogens
-exogenous
-endogenous
LPS
TNF and IL-1
Acute-phase proteins
CRP - C-reactive protein
Fibrinogen (binds to erythrocytes, basis for ESR)
SAA - Serum amyloid A