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82 Cards in this Set
- Front
- Back
Histamine
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Key chemical in acute inflammation
Mast cell Arteriole vasodilation Increased venular permeability |
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Rubor acute inflammation
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Redness
Arteriole vasodilation (histamine) |
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Calor acute inflammation
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Heat
Arteriole vasodilation (histamine) |
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Dolor acute inflammation
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Pain
Bradykinin, PGE |
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Acute inflammation
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Neutrophil dominant
Increased IgM |
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Initial vessel events
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Transient vasoconstriction---> arteriolar vasodilation ---> Increased venular permeability
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Neutrophil rolling acute inflammation
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Due to selectins
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Integrins
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Neutrophil adhesion molecules
C5a and leukotriene B4 activate Neutrophil margination |
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CD11/ CD18
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Markers for integrins
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Endothelial cell adhesion molecules
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Activated by IL-1 and TNF
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ICAM
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Intercellular adhesion molecule
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VCAM
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Vascular cell adhesion molecule
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Leukocyte adhesion molecule defect
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Failure of umbilical cord to separate
Poor wound healing |
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Decreased activation neutrophil adhesion molecules
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Neutrophilic leukocytosis
Corticosteroids |
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Increased activation neutrophil adhesion molecules
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Neutropenia
Endotoxins |
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Chemotaxis
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Directed movement
C5a and LTB4 |
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Opsonizing agents
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IgG, C3b
Enhance phagocytosis |
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Neutrophils, monocytes, macrophages
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Receptors for IgG, C3b
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O2-dependent MPO system
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most potent microbial system
neutrophils monocytes |
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Production of superoxide from O2
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NADPH oxidase with NADPH cofactor
Produces respiratory burst |
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Nitroblue tetrazolium (NBT)
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Test for respiratory burst
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Superoxide dismutase
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Converts superoxide to peroxide
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Myeloperoxidase
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Lysosomal enzyme that combines peroxide + Cl to form bleach (HOCl)
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Microbicidal defects
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Chronic granulomatous disease childhood (XR)
Myeloperoxidase deficiency (AR) |
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Chronic granulomatous disease
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Absent NADPH oxidase---> no respiratory burst
Staphylococcus aureus not killed (catalse positive) Streptococcus killed (catalase negative) |
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Myeloperoxidase deficiency
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AR
Respiratory burst present No bleach produced |
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Opsonization defect
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Bruton's agammaglobulinemia--- XR, Decreased IgG
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Phagocytosis defect
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Chediak- Higashi (defect in microtubule polymerization)
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COX inhibitors
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Non-steroidals (non- selective)
Selective COX-2 inhibitors |
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PGE2
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Vasodilation
Fever |
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PGI2
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Vasodilator
Prevent platelet aggregation |
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Nitric oxide
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Vasodilator
FR gas from conversion arginine to citrulline |
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IL-1 and TNF
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Fever
Synthesis acute phase reactants in liver, leukocytosis |
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IL-6
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Stimulated by IL-1
Stimulates synthesis of acute phase reactants |
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Acute phase reactants
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Fibrinogen
Ferritin C-reactive protein |
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Bradykinin
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Kinin produced in conversion of factor XII to factor XI
Pain, vasodilator, increased vessel permeability Cough/ angioedema ACE inhibitors |
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Anaphylatoxins
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C3a and C5a
Directly stimulate mast cell release histamine |
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Prostaglandin I2
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Synthesized by endothelial cells
Vasodilator Inhibits platelet aggregation |
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Lipoxygenase
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Hydroxylation of arachidonic acid
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Zileuton
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Inhibits lipoxygenase
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Zafirlukast, Montelukast
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Block lipoxygenase receptor
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LTC4, -D4, -E4
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Bronchoconstrictors
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TXA2
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Synthesized by platelets
Platelet aggregation Vasoconstriction Bronchoconstriction |
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Dipyridamole
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Inhibits thromboxane synthase
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Corticosteroids
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Neutrophilic leukocytosis
Lymphopenia Eosinopenia |
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Fever
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Right shift OBC
Hostile to bacterial/ viral replication |
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Chronic inflammation
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monocyte/ macrophage
Increased IgG Repair by fibrosis |
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Granuloma
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Cellular immunity
Macrophage interact with Th1 class cells (memory cells) |
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Positive PPD
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Langerhans cells process PPD and interact with Th1 class cells
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Suppurative inflammation
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Abscess
Staphylococcus aureus (coagulase) |
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Cellulitis
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Subcutaneous inflammation
Streptococcus pyogenes (hyaluronidase) |
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Pseudomembranous inflammation
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Toxins from Corynebacterium diphtheriae
Clostridium difficile |
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Cell cycle
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Key checkpoint G1 to S phase
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TP53 and RB suppressor genes
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Arrests cell in G1 phase for DNA repair or apoptosis
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BAX gene
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Stimulates apoptosis
Activated by TP53 suppressor gene if too much DNA damage |
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Extracellular matrix
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Basement membrane
Interstitial matrix |
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Complete restoration
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Cell must be capable of duplication
No damage to basement membrane |
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Scar tissue
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End- product of repair by connective tissue
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Collagen
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Triple helix of cross- linked alpha chains
Cross- links at points of hydroxylation (lysyl oxidase) increase tensile strength |
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Type I collagen
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Bones
Tendons |
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Type III collagen
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Early wound repair
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Type X collagen
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Epiphyseal plate
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Laminin
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Key basement membrane glycoprotein
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Fibronectin
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Key interstitial matrix glycoprotein
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Angiogenesis in repair
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Basic fibroblast growth factor
Vascular endothelial growth factor |
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Key event in wound repair
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Granulation tissue formation
Fibronectin responsible |
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Granulation tissue
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Becomes scar tissue
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Collagenases
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Zinc cofactor (metalloprotease)
Type III collagen replaced by Type I collagen |
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Tensile strength of healed wound
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80% original strength
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Inhibition wound healing
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Infection (MCC; S. aureus)
Zinc deficiency Diabetes M |
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Ehlers- Danlos syndrome
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Defects in collagen synthesis and structure
Hyperelasticity |
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Scurvy
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Decreased collagen tensile strength by decreasing cross-links at points of hydroxylation
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Keloid
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Excessive type III collagen
Common in blacks |
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Pyogenic granuloma
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Exuberant granulation tissue
Bleeds when touched |
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Healing primary intention
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Clean wound
Leave wound open Myofibroblasts important |
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Liver injury
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Regenerative nodules
Abnormal cytoarchitecture |
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Lung injury
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Type II pneumocyte repair cell
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CNS injury
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Astrocyte and microglial cell repair cells
Gliosis |
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WBC alterations acute inflammation
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Neutrophilic leukocytosis
Left shift Toxic granulation |
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Erythrocyte sedimentation rate
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Increased fibrinogen enhances rouleau
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C - reactive protein
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Indicator acute inflammation and inflammatory atheromatous plaque
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Polyclonal gammopathy
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Diffuse elevation y-globulins
Increased IgG Chronic inflammation |