Autocoids

Question 1

define autacoids

Answer 1

short-lived physiologically active endogenous substances that act locally then undergo rapid inactivation

Question 2

autacoid types

Answer 2

eicosanoids, histamine, seratonin, kinins

Question 3

Types of eicosanoids

Answer 3

derived from fatty acids in the body: 1. prostaglandins 2. prostacyclin 3. thromboxanes 4. leukotrienes

Question 4

leukotrienes (LTB, LTC, LTD, etc) effects

Answer 4

Increase leukocyte chemotaxis and bronchoconstriction

Question 5

prostaglandins (PGE 1&2) effects

Answer 5

1. vasodilation 2. Increase uterine contractions 3. Decrease gastric acid secretion & Increase gastric mucus production (protective)

Question 6

prostaglandins (PGF2a) effects

Answer 6

1. Increase uterine contractions 2. Increase aqueous humor flow

Question 7

medicinal prostaglandins

Answer 7

Mifepristone (RU 486), Alprostadil (MUSE), Misoprostol (Cytotec), Latanoprost (Xalatan)

Question 8

Mifepristone (RU 486)

Answer 8

synthetic steroid with antiprogestational effects

Question 9

Mifepristone (RU 486) uses

Answer 9

abortions, followed 48 hrs later by misoprostol

Question 10

Alprostadil (MUSE)

Answer 10

naturally occuring form of PGE1

Question 11

Alprostadil (MUSE) uses

Answer 11

transuretrhal suppository or injection for ED; keep ductus arteriosus open (congenital cardiac abnormalities until the infant can undergo corrective cardiac sx)

Question 12

Misoprostol (Cytotec)

Answer 12

synthetic analog of PGE1

Question 13

Misoprostol (Cytotec) uses

Answer 13

protective effects on gastric mucosa (prevention of ulcers)

Question 14

Latanoprost (Xalatan)

Answer 14

PGF2α-derivative eye drops

Question 15

Latanoprost (Xalatan) uses

Answer 15

opththalmic tx for glaucoma

Question 16

Prostaglandin antagonists (NSAIDs)

Answer 16

PGs involved in inflammatory process; NSAIDs prevent synthesis of PGs at inflammation sites

Question 17

Prostaglandin antagonists (corticosteroids)

Answer 17

Inhibit phospholipase (preventing formation of arachidonic acid & Pgs)and inhibiting inflammation

Question 18

histamine actions

Answer 18

1. involved in allergic & inflammatory rxns (Increase vascular permeability, bronchoconstriction); 2. involved in pain & itching; 3. Increase gastric acid secretion

Question 19

histamine location

Answer 19

virtually everywhere in body: 1. Increase concentration in respiratory tract, GI tract, skin; 2. high concentrations in mast cells and basophils (stored in granules in mast cells); 3. component of some venoms and insect sting secretions

Question 20

histamine receptors

Answer 20

H1, H2

Question 21

H1 receptors

Answer 21

exocrine excretion, bronchial smooth muscle & mucosa, intestinal smooth muscle, sensory n. endings (cause itching & pain)

Question 22

H2 receptors

Answer 22

in stomach (stimulation of gastric acid secretion)

Question 23

H1 Receptor Blockers

Answer 23

classic antihistamines that block mediated response in target tissues

Question 24

Division of H1 Receptor Blockers

Answer 24

1st Generation & 2nd Generation

Question 25

Use of 1st Gen H1 Receptor Blockers

Answer 25

1st: still widely used due to low cost and effectiveness

Question 26

Use of 2nd Gen H1 Receptor Blockers

Answer 26

2nd: more specific to H1 receptors and less CNS penetration (less AE)

Question 27

antihistamine uses

Answer 27

1. Tx of allergic rhinitis & urticaria (most effective when used prophylactically) 2. Tx/prevention of motion sickness 3. Treatment of insomnia (not preferred to to Aes)

Question 28

Why are 1st gen antihistamines used for motion sickness and insomnia?

Answer 28

1) Motion Sickness – Prevent/diminish N/V mediated by chemoreceptor & vestibular pathways, due to blockade of central H1 and muscarinic receptors 2)Insomnia - more sedation with first generation

Question 29

H1 blockers t 1/2's

Answer 29

1st gen shorter than 2nd gen; 2nd gen has increase compliance due to fewer pills

Question 30

H1 blockers (1st gen) AE

Answer 30

low specificity (sedation, dry mouth, blurred vision)

Question 31

H1 blockers (2nd gen) AE

Answer 31

high specificity for H1 receptors (fewer AE - reduced drowsiness/sedation due to lack of CNS penetration)

Question 32

H2 blockers uses

Answer 32

GERD & ulcers

Question 33

H2 blockers MoA

Answer 33

inhibition of H2 receptors in GI tract (inhibit gastric acid secretion)

Question 34

5HT Receptors

Answer 34

Serotonin receptors

Question 35

serotonin (5-Hydroxytryptamine) receptors

Answer 35

5HT1, 5HT2, 5HT3, 5HT4

Question 36

5HT1 actions

Answer 36

vasoconstrictor

Question 37

5HT1 uses

Answer 37

tx of migraine HA

Question 38

Headache diagnosis

Answer 38

Migraine without aura (classical, ~75%) or with aura (common)

Question 39

Potential cause of migraine pain

Answer 39

Possibly due to extracranial and intracranial arterial dilation

Question 40

General forms of Migraine HA tx

Answer 40

symptomatic, migraine specific (addressing the source of HA), and prophylaxis

Question 41

migraine specific tx

Answer 41

5HT 1D receptor agonists (triptans & dihydroergotamine)

Question 42

5HT 1D receptor agonists MoA

Answer 42

believed to cause vasoconstriction or inhibit release of proinflammatory neuropeptides on trigeminal n. innervating cranial blood vessels

Question 43

5HT 1D receptor agonists types

Answer 43

triptans, dihydroergotamine

Question 44

triptan tx

Answer 44

individual response varies, may need to try more than one drug

Question 45

triptan AE

Answer 45

may cause ↑Increase BP & cardiac events

Question 46

triptan contraindications

Answer 46

cardiac eval needed prior to use if pt has risk factors for CAD

Question 47

serotonin syndrome

Answer 47

serious drug interaction associated with MAO-inhbitor

Question 48

dihydroergotamine

Answer 48

given IV, major SE is nausea, most pts prefer triptans

Question 49

Prophylaxis for Migraines

Answer 49

beta -blockers (propanolol, nadolol), amitriptyline, divalproex, verapamil