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85 Cards in this Set

  • Front
  • Back
Histamine
Key chemical in acute inflammation

Mast cell

Arteriole vasodilation

Increased venular permeability
Rubor acute inflammation
Redness

Arteriole vasodilation (histamine)
Calor acute inflammation
Heat

Arteriole vasodilation (histamine)
Tumor actue inflammation
Swelling

Increased vessel permeability (histamine)
Dolor acute inflammation
Pain

Bradykinin, PGE
Acute inflammation
Neutrophil dominant

Increased IgM
Initial vessel events
Transient vasoconstriction ----> arteriolar vasodilation---> Increased venular permeability
Neutrophil rolling acute inflammation
Due to selectins
Integrins
Neutrophil adhesion molecules

C5a and leukotriene B4 activate

Neutrophil margination
CD11/ CD18
Markers for integrins
Endothelial cell adhesion molecules
Activated by IL-1 and TNF
ICAM
Intercellular adhesion molecule
VCAM
Vascular cell adhesion molecule
Leukocyte adhesion molecule defect
Failure of umbilical cord to separate

Poor wound healing
Decreased Activation neutrophil adhesion molecules
Neutrophilic leukocytosis

Corticosteroids
Increased activation neutrophil adhesion molecules
Neutropenia

Endotoxins
Chemotaxis
Directed movement

C5a and LTB4
Opsonizing agents
IgG

C3b

Enhance phagocytosis
Neutrophils, Monocytes, Macrophages
Receptors for IgG, C3b
O2- dependent MPO system
Most potent microbicidal system

Neutrophils, monocytes
Production of superoxide form O2
NADPH oxidase with NADPH cofactor

Produces respiratory burst
Nitroblue tetrazolium (NBT)
Test for respiratory burst
Superoxide dismutase
Converts superoxide to peroxide
Myeloperoxidase
Lysosomal enzyme that combine peroxide + Cl to form bleach (HOCl)
MIcrobicidial defects
Chronic granulomatous disease childhood (XR)

Myeloperoxidase deficiency (AR)
Chronic graulomatous disease
Absent NADPH oxidase---> no respiratory burst

Staphylococcus aureus not killed (catalse positive)

Streptococcus killed (catalase negative)
Myeloperoxidase deficiency
AR

Respiratory burst present

No bleach produced
Opsonization defect
Bruton's agammaglobulinemia

XR

Decreased IgG
Phagocytosis defect
Chediak- Higashi (see cell injury)

Also has defect in microtubule polymerization
COX inhibitors
Non- steroidals (non-selective)

Selective COX-2 inhibitors
PGE2
Vasodilation

Fever
PGI2
Vasodilator

Prevent platelet aggregation
Nitric oxide
Vasodilator

FR gas from conversion arginine to citrulline
IL-1 and TNF
Fever

Synthesis acute phase reactants in liver, leukocytosis
IL-6
Stimulated by IL-1

Stimulates synthesis of acute phase reactants
Acute phase reactants
Fibrinogen

Ferritin

C- reactive protein
Bradykinin
Kinin produced in conversion of factor XII to factor XI

Pain

Vasodilator

Increased vessel permeability

Cough/ angioedema ACE inhibitors
Anaphylatoxins
C3a and C5a

Directly stimulate mast cell release of histamine
Prostaglandin I2
Synthesized by endothelial cells

Vasodilator

Inhibits platelet aggregation
Lipoxygenase
Hydroxylation of arachidonic acid
Zileuton
Inhibits lipoxygenase
Zafirlukast, Montelukast
Block lipoxygenase receptor
LTC4, -D4, -E4
Bronchoconstrictors
TXA2
Synthesized by platelets

Platelet aggregation, vasoconstriction, bronchoconstriction
Dipyridamole
Inhibits thromboxane synthase
Corticosteroids
Inhibits phospholipase A2

Activation neutrophil adhesion molecules

Neutrophilic leukocytosis

Lymphopenia

Eosinopenia
Fever
Right shift OBC

Hostile to bacterial/ viral replication
Chronic inflammation
Monocyte/ macrophage

Increased IgG

Repair by fibrosis
Granuloma
Cellular immunity

Macrophages interact with Th1 class cells (memory cells)
Positive PPD
Langerhan's cells process PPD and interact with Th1 class cells
Suppurative inflammation
Abscess

Staphylococcus aureus (coagulase)
Cellulitis
Subcutaneous inflammation

Streptococcus pyogenes (hyaluronidase)
Pseudomembranous inflammation
Toxins from Corynebacterium diphtheriae, Clostridium diffcile
Cell cycle
Key checkpoint G1 to S phase
TP53 and Rb suppressor genes
Arrests cell in G1 phase for DNA repair or apoptosis
BAX gene
Stimulates apoptosis

Activated by TP53 suppressor gene if too much DNA damage
Extracellular matrix
Basement membrane

Interstitial matrix
Complete restoration
Cell must be capable of duplication, no damage to basement membrane
Scar tissue
End- product of repair by connective tissue
Collagen
Triple helix of cross-linked alpha chains

Cross- links at points of hydroxylation (lysyl oxidase) increase tensile strength
Type I collagen
Bones

Tendons
Type III collagen
Early wound repair
Type IV collagen
Basement membrane
Type X collagen
Epiphyseal plate
Laminin
Key basement membrane glycoprotein
Fibronectin
Key interstitial matrix glycoprotein
Angiogenesis in repair
Basic fibroblast growth factor

Vascular endothelial growth factor
Key event in wound repair
Granulation tissue formation

Fibronectin responsible
Granulation tissue
Becomes scar tissue
Collagenases
Zinc cofactor (metalloproteine)

Type III collagen replaced by Type I collagen
Tensile strength of healed wound
80% original strength
Inhibition wound healing
Infection (MCC; S. aureus)

Zinc deficiency

DM
Ehlers- Danlos syndrome
Defects in collagen synthesis and structure

Hyperelasticity
Scurvy
Decreased collagen tensile strength by decreasing cross-links at points of hydroxylation
Keloid
Excessive type III collagen

Common in blacks
Pyogenic granuloma
Exuberant granulation tissue

Bleeds when touched
Healing primary intention
Clean wound

Appose wound margins with suture
Healing secondary intention
Infected wound

Leave wound open

Myofibroblasts important
Liver injury
Regenerative nodules

Abnormal cytoarchitecture
Lung injury
Type II pneumocyte repair cell
CNS injury
Astrocyte and microglial cell repair cells

Gliosis
WBC alterations acute inflammation
Neutrophilic leukocytosis, left shift, toxic granulation
Erythrocyte sedimentation rate
Increased fibrinogen enhances rouleau
C- reactive protein
Indicator acute inflammation and inflammatory atheromatous plaque
Polyclonal gammopathy
Diffuse elevation y-globulins

Increased IgG

Chronic inflammation