Autacoids

Front 1

What are the functions of autacoids? (6)

Back 1

inflammation
blood pressure
smooth muscle contraction
GI function
body temperature
platelet aggregation

Front 2

What is the difference between "classical" hormones and autocoids?

Back 2

classical hormones act (via the blood stream) on distant organs

autacoids act on neighboring cells

Front 3

How does the inflammatory response effect host defense?

Back 3

makes tissue accessible to immune cells (makes blood vessels leaky so fluids and cells can enter aka edema)

Front 4

What are the phases of inflammation? (2)

Back 4

Acute phase- increased capillary permeability

Delayed phase- cellular infiltration which helps with resulition (tissue healing) and chronic prolifferation (tissue degeneration and fibrosis)

Front 5

Histamine biosynthesis.
What is histamine made from?

Back 5

Histamine is formed from L-histidine by histidine decarboxylase

Front 6

Where is histamine stored?

Back 6

Histamine is stored in granules within mast cells (and basophils)

mast cells can be located in the skin, intestinal mucosa, lung mucosa

basophils are located in the blood

Front 7

When is histamine released?

Back 7

histamine is released upon synthesis from epidermal cells GASTRIC Mucosal cells, CNS neurons, and rapidly growing tissue

Front 8

How does histamine effect the cardiovascular system?
(what receptors and effect caused by each receptor)

Back 8

vasoconstriction (dec. BP)
Histamine binds to H1 receptors of endothelium--> release of NO and PGI2 cause vasodilation by relaxation of smooth muscle
(effect is rapid and short lasting)

Histamine binds to H2 receptors on vascular smooth muscle-->cAMP causes relaxation of smooth muscle
(effect is slow and sustained)

Histamine bindig to H1 receptors--> contraction of endothelial cells causes increased capillary permeability

Front 9

How does histamine interact with neurons and what effect does this cause?

Back 9

H1 receptors--> stimulation of sensory nerve endings and release of substance p -->itching, pain, and uticaria

H3 receptors in CNS--> regulation of arousal and wakefulness

Front 10

What is the triple response of lewis?

Back 10

release of histamine that causes flush, flare, and wheal

Front 11

How does histamine effect extravascular smooth muscle?

Back 11

H1 receptors--> constriction of extravascular smooth muscle

-bronchoconstriction
-gastrointestinal diarrhea

Front 12

How does Histamine effect gastric acid secretion?

Back 12

H2 receptors--> increases gastric acid secretion

Front 13

What are the theraputic uses of H1 antagonists? (5)

Back 13

Antiallergy--> depends on the contribution of histamine relative to other autacoids
- used to decrease allergic rhinitis, conjunctivitis, edema and uticaria
- has little efect on anaphylaxis (pt needs epi pen)

Sedation--> H1 receptors in CNS
-drug must pass BBB (1st generation only)
- use as sleep aids

Anticholinergic effects--> nonallergic rhinorrhea, motion sicknness, antiparkinson,

Antidopaminergic--> antiparkinsons

Voltage Na channels--> local anesthetic

Front 14

What are the side effects of H1 antagonists? (6)

Back 14

Sedation

Anticholinergic effects--> dry mouth, urinary retention, blurred vision

CNS excitation (toxic od)--> hallucination, ataxia, convulsions

tolerance--> increased P450 expression

gastrointestinal--> N/V, constipation, loss of appetite(reduced if given with meal)

Torsades de Pointes--> cardiac toxicity, lengthened QT interval

Front 15

H1 antagonists and Torsades de Pointes

Back 15

occures with astemizole and terfenadine (no longer on the market) combined with ketaconazole and erythromycin

prolonged QT interval by reducing K efflux and keeping membrane depolarized longer

Front 16

What are the theraputic uses of H2 antagonists?

Back 16

acid reflux, ulcers, Zollinger-Ellison syndrome (gastrin secreting tumor)

Front 17

What are the side effects of H2 antagonists?

Back 17

headach, nausea, diziness, gynecomastia (men), galactorrhea (women), loss of libido (cimetidine, bc it functions as an androgen receptor antagonist after long term treatment)

few CNS effects bc drugs don't pass BBB (except in elderly bc of breakdown of BBB--> delirium, confusion, and slurred speech)

Cimetidine causes inhibition of P450 (slows metabolism of warfarin, phenytoin, slufonylureas, and calcium channel blockers)

Front 18

What are the H2 antagonists?

Back 18

cimetidine
ranitidine
famotidine
nizatidine

Front 19

What are the H1 antagonists?

Back 19

1st classsiphenhydramine, dimenhydrinate, doxylamine, chlopheniramine, and promethazine

2nd generation- terfenadine, astemizole, loratidine, desloratidine, fexofenadine, cetrizine

Front 20

How and where is Platelet Activatig Factor (PAF) synthesized?

Back 20

- synthesized de novo in response to a stimulus such as antigen antibody reactions, thrombin, collagen and other autocoids

-PAF is synthesized in platlets, neutrophils, monocytes, mast cytes, eosinophils, and vascular endothelium

Front 21

What does PAF do?

Back 21

Cardiovascular effects (vasodilator and increased vascular permeability)

potent stimulator of platelet aggregation

chemotaxis annd activation of eosinophils, neutrophils and monocytes

contracts gastrointestinal, uterine PGE mediated, and airway smooth muscle lt and tx mediated peripheral airways

ulcerogenic

involved in ovulation, implantation, and labor

Front 22

Wat are the therapeutic uses for PAF?

Back 22

-uses to determine what embryos should be used for successful implantatoin

-PAF is used to supplement human embryo growth media (50% increase in success rate)

Front 23

What are the theraputic uses of PAF antagonists?

Back 23

-under development for treatment of ischemic heart disease (bc PFC vasoconstriction of coronary vessels)