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Pharmacology > Autocoids > Flashcards

Autocoids Flashcards

1
Q

define autacoids

A

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

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2
Q

autacoid types

A

eicosanoids, histamine, seratonin, kinins

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3
Q

Types of eicosanoids

A

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

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4
Q

leukotrienes (LTB, LTC, LTD, etc) effects

A

Increase leukocyte chemotaxis and bronchoconstriction

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5
Q

prostaglandins (PGE 1&2) effects

A
  1. vasodilation 2. Increase uterine contractions 3. Decrease gastric acid secretion & Increase gastric mucus production (protective)
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6
Q

prostaglandins (PGF2a) effects

A
  1. Increase uterine contractions 2. Increase aqueous humor flow
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7
Q

medicinal prostaglandins

A

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

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8
Q

Mifepristone (RU 486)

A

synthetic steroid with antiprogestational effects

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9
Q

Mifepristone (RU 486) uses

A

abortions, followed 48 hrs later by misoprostol

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10
Q

Alprostadil (MUSE)

A

naturally occuring form of PGE1

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11
Q

Alprostadil (MUSE) uses

A

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

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12
Q

Misoprostol (Cytotec)

A

synthetic analog of PGE1

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13
Q

Misoprostol (Cytotec) uses

A

protective effects on gastric mucosa (prevention of ulcers)

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14
Q

Latanoprost (Xalatan)

A

PGF2α-derivative eye drops

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15
Q

Latanoprost (Xalatan) uses

A

opththalmic tx for glaucoma

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16
Q

Prostaglandin antagonists (NSAIDs)

A

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

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17
Q

Prostaglandin antagonists (corticosteroids)

A

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

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18
Q

histamine actions

A
  1. involved in allergic & inflammatory rxns (Increase vascular permeability, bronchoconstriction); 2. involved in pain & itching; 3. Increase gastric acid secretion
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19
Q

histamine location

A

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

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20
Q

histamine receptors

A

H1, H2

21
Q

H1 receptors

A

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

22
Q

H2 receptors

A

in stomach (stimulation of gastric acid secretion)

23
Q

H1 Receptor Blockers

A

classic antihistamines that block mediated response in target tissues

24
Q

Division of H1 Receptor Blockers

A

1st Generation & 2nd Generation

25
Q

Use of 1st Gen H1 Receptor Blockers

A

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

26
Q

Use of 2nd Gen H1 Receptor Blockers

A

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

27
Q

antihistamine uses

A
  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)
28
Q

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

A

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

29
Q

H1 blockers t 1/2’s

A

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

30
Q

H1 blockers (1st gen) AE

A

low specificity (sedation, dry mouth, blurred vision)

31
Q

H1 blockers (2nd gen) AE

A

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

32
Q

H2 blockers uses

A

GERD & ulcers

33
Q

H2 blockers MoA

A

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

34
Q

5HT Receptors

A

Serotonin receptors

35
Q

serotonin (5-Hydroxytryptamine) receptors

A

5HT1, 5HT2, 5HT3, 5HT4

36
Q

5HT1 actions

A

vasoconstrictor

37
Q

5HT1 uses

A

tx of migraine HA

38
Q

Headache diagnosis

A

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

39
Q

Potential cause of migraine pain

A

Possibly due to extracranial and intracranial arterial dilation

40
Q

General forms of Migraine HA tx

A

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

41
Q

migraine specific tx

A

5HT 1D receptor agonists (triptans & dihydroergotamine)

42
Q

5HT 1D receptor agonists MoA

A

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

43
Q

5HT 1D receptor agonists types

A

triptans, dihydroergotamine

44
Q

triptan tx

A

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

45
Q

triptan AE

A

may cause ↑Increase BP & cardiac events

46
Q

triptan contraindications

A

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

47
Q

serotonin syndrome

A

serious drug interaction associated with MAO-inhbitor

48
Q

dihydroergotamine

A

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

49
Q

Prophylaxis for Migraines

A

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

Pharmacology (12 decks)

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