Pharm Block 2- Intro

Front 1

hallmarks of acute inflamm

Back 1

-vasodilation
-increased vascular permeability
-recruitment of neutrophils

Front 2

hallmarks of chronic inflamm

Back 2

-prolonged duration
-participation by lymphocytes, plasma cells, macs, fibroblasts, angioblasts

Front 3

potentially harmful effects of inflammation

Back 3

-inflamm cells may release lysosomal enzymes (collagenase and proteases)
-inflamm swelling may obstruct airway or be within cranial cavity causing death

Front 4

histamine (type, cell source, phys response, mech)

Back 4

-biogenic amine
-from mast cells and basophils (and other sources like neurons in stomach)
-causes vasodilation, increased vasc permeability, and pain
-works by activation of GPCRs

Front 5

bradykinin (type, cell source, phys response, mech)

Back 5

-peptide
-from endothelial cells
-causes vasodilation, increased microvessel permeability, pain
-works by activation of GPCRs

Front 6

complement (type, cell source, phys response, mech)

Back 6

-plasma proteins
-synthesized by liver, circulate in blood
-cause chemotaxis (recruit inflamm cells), release of mediators from neutrophils, can cause tissue damage
-specific receptors on cell surface cause osmotic lysis and activation of GPCRs

Front 7

C-reactive protein (type, cell source, phys response, mech)

Back 7

-plasma protein
-from liver in response to cytokines; from adipocytes
-causes acute phase reactions; activates complement cascade; mediates phagocytosis
-marker of inflamm (CRP)
-binds to phospholipids in bact and damaged cells (may be specific receptors in macs)

Front 8

what can an elevated CRP level be associated with?

Back 8

-increased risk of diabetes, hypertension, and CV disease

Front 9

cytokines (type, cell source, phys response, mech)

Back 9

-secreted proteins like IL1 and TNF-a
-from nearly all inflamm cells
-acute phase rxn/fever (both), sepsis (TNFa), fibroblast and lymphocyte prolif (IL1)
-work by binding specific receptor proteins to induce gene expression of number of proteins via NFkB and AP1

Front 10

TNF-a

Back 10

-acute phase rxn
-fever
-sepsis

Front 11

IL-1

Back 11

-acute phase rxn
-fibroblast and lymphocyte proliferation
-fever

Front 12

mech of cytokines

Back 12

-bind specific receptors--> activates NFkB and AP1--> increase:
-COX (fever) and lipoxygenases
-adhesion molecule expression
-induce collagenase (fibrosis)

Front 13

adenosine (type, cell source, phys response, mech)

Back 13

-purine nucleotide from breakdown of ATP
-from all cells
-is increased extracellularly during injury to act as an ANTI-inflamm
-inhibits cytokine action
-via activation of GPCRs

Front 14

cell adhesion molecules (type, cell source, phys response, mech)

Back 14

-family of proteins
-from endothelial cells, platelets, leukocytes
-causes leukocyte adhesion to endothelium and recruit activated platelets
-Ca2+-dep mech via "contact molecules"

Front 15

oxygen-derived free radicals (type, cell source, phys response, mech)

Back 15

-superoxide, hydroxy radical
-from all cells
-used for intracell killing of bact by neutrophils
-via protein oxidation, lipid peroxidation, and DNA mutations

Front 16

what are considered lipid mediators of inflammation?

Back 16

-eiconsanoids (arach acid derivatives)
-steroids

Front 17

prostaglandins (type, cell source, phys response, mech)

Back 17

-arach acid deriv
-from virtually all cells
-cause vasodilation/constriction, pain, fever, platelet aggregation (via thromboxane)
-use specific GPCRs
-responsive to NSAIDs

Front 18

leukotrienes (type, cell source, phys response, mech)

Back 18

-arach acid deriv
-from macs and neutrophils
-increase vascular permeability and cause bronchoconstriction
-use GPCRs

Front 19

glucocorticoids (type, cell source, phys response, mech)

Back 19

-steroids
-from adrenal cortex
-inhibit cytokines, inhibit phospholipase A2 (dec PGs and LTs), inhibit COX-2, inhibit cell adhesion molecules
-via activation of NUCLEAR receptors

Front 20

steroids as anti-inflamm drugs

Back 20

-bind to cytoplasmic receptors --> localizes to nucleus --> txn of certain target genes
-often used for chronic inflamm

Front 21

leukotriene antagonist drug

Back 21

-zafirlukast: competitive antagonist of leukotriene receptors
-zileuton: inhibits LT synthesis