Study BIOL 472 Topic 5 Flash Cards

 
Pile Management Card
BIOL 472 Topic 5

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PGI2 and TxA2
PGI2 and TXA2 work as antagonists
thromboxanes
promote clotting
prostaglandins
most of which are pro-inflammatory
calmodulin
-4 binding areas for Ca+2
changes shapes of proteins
-activates/inhibits
-calmodulin-dependent kinases
Ca as 2nd messenger
-increased by:

-G protein activating ion gates
-IP3 releasing Ca+2 from ER
-active transport of Ca+2 out of cell blocked
-opening voltage-gated channels
IP3, DAG
-effector= phospholipase C
-causes IPI2 to be converted to IP3, DAG
-DAG activates protein kinases

-IP3 makes ER leaky to Ca+2, increase cytosol Ca+2
-mediates cell responses
-Ca+2= 3rd messenger?
cAMP
-elicits glycogenlysis in liver
-2nd messenger
-adenylyl cyclase is effector protein
-cAMP activates cAMP-dependednt protein kinases
-phosphorylates proteins (inhibits or activates)

to stop:
-phosphodiesterasedegrades cAMP
if blocked, cAMP runs wild

-cGMP analog
2nd messenger system
-activate G proteins in PM
-can be cAMP, IP3, DAG, Ca+2
-1st messenger binds
-receptor activates G protein
-activates effector proteins in PM
-effector protein generates 2nd messenger
-G protein "couples" receptor and effector
receptor couples w/ protein kinase
-messenger binds to receptor
-receptor activates tyrosin kinase
-P's protein (ATP)
-mediates cell response (esp. growth and devel)
-insulin
receptor w/ ion channel
-messenger binds to receptor
-receptor activates channel
-ex: neurotransmitter action postsynaptically
lipid insoluble messages
-use PM receptors
-receptor w/ ion channel
-receptor w/ protein kinase
lipid soluble message
-steroid hormones pass right through PM and nucleus
-intracellular receptors
-regulate gene transcription
anti-asthmatic/allergy
-singulair
-block leukotriene pathways
acetaminophens
-tylenol
-good analgesix and antipyretic
-poorly understood
-nont really anti-inflammatory
-Cox3?
indomethacin
-more powerful, esp. for arthritus
naproxens
-aleve
-similar to ibuprofens
ibuprofens
-motrin, advil
-inhibit inflammatory rxns in pathway, esp. PGI2
aspirins
-esp. anti-clotting pathways, can lead to ulcers
aspirins/NSAIDs
-inhibit cyclooxygenase, which converts AA to endoperoxides
-several classes: aspirins, IBprofen, napoxens, indomethacin
-all inhibit COX1 or 2 to some degree
COX
-enzyme that is responsible for formation of endoperoxides
-inhibition of COX can provide relief from the symptoms of inflammation and pain
-method of action of non-steroidal anti-inflammatory drugs (aspirin and ibuprofen)
SRA-A
-slow reacting substance anaphylaxis
-mixture of the leukotrienes
-secreted by mast cells during allergic reaction
-stimulates T cells, interleuken, interferon production
-bronchoconstriction
-increase vascular permeability
leukotrienes
-produced by lipoxygenase on AA
-secreted by certain wbc's
TxA2
-is a thromboxane
-generated from prostaglandin H2 by thromboxane-A synthase
-major component of blood clots
-very short half life
-vasoconstrictor, bronchoconstrictor
-increases blood aggregation
PGI2
-prostocyclin
-vasodilator, bronchodilator
-decreases platelet aggregation
COX 2
-pain and inflammatory pathway
-COX2 inhibitors
COX1
-platelet aggregation, protects stomach
NSAID
non steroidal anti infammatory drugs
cyclooxygenase
-converts AA to entoperoxides
-inhibited by aspirin, NSAIDS
-COX 1 and 2
phospholipase A
-converts phospholipid to Arachindonic acid
-inhibited by glucorticoids (steroids)
3 classes of eicosinoids
-protoglandins
-thromboxanes
-leukotrienes
eicosanoids
-lipid-derived paracrine signals
-derived from arachidonic acid
-present in PM phosopholipids
autocrine agents
-action on same cell that secreted them
-responses mediated by receptors in membrane, cytoplasm, nucleus
paracrine agents
-rapidly degraded
-only affect local tissue
-does not enter blood stream
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