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39 Cards in this Set

  • Front
  • Back

A febrile

W/o fever

B-cells

Secrete anti-bodies to neutralize infectious agents via opsonization

T-cells

Respond to Cell mediated chronic inflammatory process

Macrophage

Clean up debris via phagocytosis



- secrete cytokines promoting angiogenesis & fibrosis (PDGF, FGF, IL-1, and TNF)

Toll-like Receptors (TLRs)

Recognize nonhuman microbes:


1) ds RNA of viruses


2) bacterial DNA


3) bacterial endotoxin

Caspase-1

Activated by inflammation proteins responding to bacteria to produce interleukin-1 (IL-1)

Lectin

Bind fungal polysaccharides --> trigger cellular defense

What cause the contraction of epithelial walls during inflammation?

Histamine and leukotrienes

Leukocyte rolling

P-selectin & E-Selectin (endothelial cells) interact w/ L-selectin (neutrophils)

Leukocyte rolling

P-selectin & E-Selectin (endothelial cells) interact w/ L-selectin (neutrophils)

Integrins

Forms firm adhesion between neutrophil and endothelial cells.

Leukocyte rolling

P-selectin & E-Selectin (endothelial cells) interact w/ L-selectin & sialylated ligands (neutrophils)

Integrins

Forms firm adhesion between neutrophil and endothelial cells (vascular cell adhesion molecule-1 VCAM-1)



- Genetic Lack of integrin Beta chain = prevention of firm adhesion



- interact w/ fibronectin (ecm protein i.e. Actin) = focal adhesions --> intracellular signaling--> cell growth, differentiation, & migration

Complement C3b

Opsonin to facilitate phagocytosis

Bradykinin

Causes pain and increased vascular permeability

Complement C3a

Causes increased vascular permeability by releasing histamine from MAST CELLS

Complement C3a

Causes increased vascular permeability by releasing histamine from MAST CELLS

Myeloperoxidase

Present in neutrophil granules and converts H2O2 to HOCL- (anti microbial agent)

Interferon-y (IFN-y)

From CD4 and CD8 lymphocytes (T-cells) and stimulate macrophage production of Nitric Oxide Synthase (NOS)



- also transform macrophages into epithelium cells in granulomatous inflammation

Leukotriene B4

- Potent neutrophil chemotaxic factor



- vasoconstrictor & bronchoconstrictor

NO

Endothelial = Vasodilation & inhibit platelet activation



Macrophage = microbial killing

TNF

Produced by activated macrophages--> fever (along w/ IL-1), metabolic wasting, hypotension



- also induce lymphocyte activation and fibroblasts proliferation (converting fibrinogen to fibrin)

Prostaglandins

Promote vasodilation & pain

Leukotriene E4

Vasoconstrictor

Complement C5a

Neutrophil chemoattractant

Complement C5a

Neutrophil chemoattractant

Complement C5-9

Membrane Attack Complex

Protein C

Stops conversion of prothrombin to thrombin

Abscess

Localized collection of neutrophils

Chronic Inflammation

Preponderance of mononuclear cells (lymphocytes, macrophages, and plasma cells)

Liquefactive Necrosis

Appears after staph infection

Interleukin-1 (IL-1)

Secreted by macrophages to produce:


1) Fever


2) Leukocyte adherence


3) Fibroblast proliferation


4) Cytokine secretion

Prostaglandins

Produced by stimulation from pyrogens in the hypothalamus which "reset the thermostat"

Vitamin C Deficiecy

Scurvy



- reduces Lysol oxidase activity which helps to cross-link fibrillation collagen (provide tensile strength)

Interleukin-2 (IL-2)

Activated lymphocytes



- mutation = T-cell neoplasm

Throboxane A2

Vasoconstriction & platelet aggregation

Repair

Day 1: fibrin & inflammatory cells


Day 2-3: macrophages & granulation tissue


Days 4-5: neovascularization


Week 2: collagen is prominent (fewer vessels & inflammatory cells)

Creatinine Kinase

If elevated = myocardial necrosis --> replaced by fibrous scar

Cardinal signs of Acute Inflammation

1) pain (pain)


2) redness (rubor)


3) warm (calor)


4) swelling (tumor)


5) loss of movement (functio laesa)