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FM 1 > Autacoid pharmacology > Flashcards

Autacoid pharmacology Flashcards

1
Q

autacoid

A
  • endogenous substance that mediates inflammation

- seldom used therapeutically themselves, but antagonists and some agonists have uses

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2
Q

histamine

A
  • biosynthesized from histidine

- stored in mast cells, basophils, enterochromaffin cells, neurons

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3
Q

H1 histamine receptors

A 
peripheral nerve endings
CNS
smooth muscle of blood vessels
bronchi
intestine
Gq coupled
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4
Q

H2 histamine receptors

A 
gastric mucosa
heart 
mast cells
CNS
Gs coupled
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5
Q

histamine biosynthesis

A

made from histidine via histidine decarboxylase

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6
Q

Histamine metabolism

A

diamine oxidase

Histamine N-methyl transferase

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7
Q

histamine and immune response

A
  • mast cells and basophils release histamine when exposed to antigen
  • IgG or IgM mediated complement cascade activation triggers histamine release
  • inflammatory cells attracted to release histamine by chemotaxis
  • certain drugs (bezylisoquinoline NMJ blockers, opiods, succinylcholine) can displace histamine from storage cells
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8
Q

Ways to antagonize histamine

A
  • physiologic-drug that produces opposite effect-eg epinephrine-reverse anaphylaxis
  • inhibit release
  • receptor antagonists
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9
Q

Effects of peripheral histamine H1 receptor activation

A
  • vasodilation of small blood vessels (most impt effect)-flushing, decrease BP and total peripheral resistance (TPR)
  • increase vascular permeability-edema, urticaria
  • bronchoconstriction and bronchospasm
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10
Q

H1 antagonists

A

-allergic conditions, urticaria, insomnia, motion sickness, parkinsonian syndromes

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11
Q

diphenhydramine mechanism of action

A
  • H1 receptor inverse agonist, stabilizes inactive form of H1 receptors, blocks effects of histamine on H1 in GI tract, large blood vessels, bronchial muscle, uterus, and suppress edema, flare, pruritis
  • produce sedation via antagonism of CNS H1 receptors
  • has significant anti-muscarinic activity-effective in relief of nausea, vomiting, and vertigo from motion sickness; anti-parkinsonian agent
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12
Q

diphenhydramine adverse reactions

A
  • CNS-dizziness, confusion, sedation
  • antimuscarinic effects- mydriasis, xerostomia, reduced bronchial secretions, tachycardia, constipation, urinary retention
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13
Q

diphenhydramine precautions

A

-asthma, heart disease, hepatic disease, glaucoma, bladder obstruction, urinary retention, infants (sleep apnea and SIDS)

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14
Q

diphenhydramine description

A
  • benadryl, sominex
  • 1st gen antihistamine
  • allergic rhinitis, sneezing, itching, urticaria, motion sickness, insomnia
  • CYP2D6
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15
Q

cetirizine description

A
  • zyrtec
  • 2nd gen antihistamine, active metabolite of 1st gen hydroxyzine
  • for allergic conditions (rhinitis, sneezing, itching, urticaria)
  • less sedating than older H1 antagonists
  • formulated q/ pseudoephedrine as Zyrtec-D
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16
Q

Cetirizine mechanism of action

A
  • H1 receptor inverse agonist; stabilizes inactive form of H1 receptor, blocks effects in GI tract, uterus, large BV, bronchial muscle and suppresses edema, flare, pruritis
  • minimal antimuscarinic activity
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17
Q

cetirizine adverse rxns and precautions

A
  • few
  • CNS (high doses): sedation, fatigue
  • xerostomia
  • if CrCL
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18
Q

Fexofenadine description

A
  • allegra
  • 2nd gen antihistamine, active metabolite terfenadine
  • for allergic conditions (rhinitis, sneezing, itching, urticaria)
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19
Q

Fexofenadine mechanism of action

A
  • H1 receptor inverse agonist; stabilizes inactive form of H1 receptor, blocks effects in GI tract, uterus, large BV, bronchial muscle, and suppresses edema, flare, pruritis
  • virtually no antimuscarinic activity at therapeutic dose
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20
Q

Fexofenadine adverse rxns

A

few
GI-nausea, dyspepsia
CNS-drowsiness, sedation

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21
Q

fexofenadine precautions

A
  • decrease dose in pts with decreased renal function

- avoid taking w/ fruit juice -> decreased absorption

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22
Q

Loratadine description

A
  • Claritin Tavist ND
  • 2nd gen antihistamine
  • allergic reactions
  • formulated w/ pseudophedrine-Claritin D
  • desloratadine (Clarinex)-active metabolite
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23
Q

Loratadine mechanism of action

A

-H1 receptor inverse agonist; stabilizes inactive form of H1 receptor, blocks effects in GI tract, uterus, large BV, bronchial muscle, and suppresses edema, flare, pruritis

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24
Q

Loratadine pharmacokinetics, adverse reactions, and precautions

A
  • CYP3A4
  • few; CNS-HA, sedation, xerostomia
  • hepatic ds; if CrCL
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25
Q

H1 receptor antagonists

A

diphenhydramine
cetirizine
fexofenadine
loratadine

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26
Q

Effects of peripheral H2 receptor activation

A
  • vasodilation of small blood vessels
  • increase HR-reflex tachycardia and direct stimulation
  • gastric acid secretion
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27
Q

H2 antagonists and gastric acid secretion

A
  • treat peptic ulcer ds
  • not as effective as PPI but cheap, very safe, and OTC (60-70% decrease in 24hr acid secretion)
  • especially effective at inhibiting nocturnal acid secretion, less effective on meal stimulated acid secretion
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28
Q

Cimetidine description

A
  • Tagamet
  • 1st commercially available drug for peptic ulcer ds
  • indicated for GERD, peptic ulcer ds, intermittent dyspepsia
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29
Q

cimetidine mechanism of action

A
  • inverse agonist; reduces constitutive activation of H2 receptors on parietal cells
  • decreases acid secretion by 60-70%
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30
Q

cimetidine adverse rxns

A
  • moderate to severe HA

- rare blood dsycrasias: neutropenia, agranulocytosis, leukopenia, thrombocytopenia, pancytopenia

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31
Q

cimetidine precautions

A

-hepatic disease (CYP metabolized), renal insufficiency

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32
Q

serotonin

A
  • 5-HT
  • biosynthesized from tryptophan
  • stored mostly in enterochromaffin cells, some in platelets and synaptic vesicles
  • mostly G-protein coupled receptors; one ligand gated ion channel (5-HT3)
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33
Q

Serotonin biosynthesis and metabolism

A

tryptophan -tryphtophan hydroxylase -> 5-hydroxy tryptophan - aromatic AA decarboxylase -> serotonin

-MAO->aldehyde dehydrogenase or AANAT->ASMT -> melatonin

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34
Q

effects of 5-HT

A
  • CNS: affect mood, appetite, sexual activity, thermoregulation, sensory perception, sleep, memory, cognition; mediates vomiting
  • GI: suppress (5-HT3) or promote (5-HT4) GI motility
  • CV-clotting, vasoconstriction ->BP, migraine
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35
Q

Migraine

A
  • debilitating headache characterized by unilateral throbbing pain w/ nausea/vomiting, sensitivity to light and sound, visual disturbances, and duration of 4-72 hours
  • w/ (classic) or w/o (common) aura
  • neurogenic origin followed by vasodilation
  • 5-HT key mediator of pathogenesis
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36
Q

Ergotamine description

A
  • Ergomar

- ergot alkaloid used to relieve migraines; ~70% effective in controlling acute attacks

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37
Q

ergotamine mechanism of action

A
  • complex; some of the pharmacologic actions are unrelated to each other and some actions are even mutually antagonistic
  • partial agonist of antagonist activity @ 5-HT, dopamine, and a-adrenergic receptors; causes vasoconstriction of arteries and veins and decreased blood flow to peripheries
  • oxytocic agent-increase force and frequency of uterine contractions, decrease postpartum bleeding by constricting the placental vascular bed
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38
Q

ergotamine adverse reactions

A
  • GI: NVD, xerostomia
  • ergotism: angina, asthenia, coronary vasopasm, cramps, myalgia, paresthesias, change in HR, vasoconstriction-> hyperthermia, necrosis
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39
Q

ergotamine precautions

A
  • all absolute
  • CV-angina, arteriosclerosis, CAD, HTN, peripheral vascular ds, Raynaud’s, thrombophlebitis, MI, stroke
  • hepatic ds, biliary tract ds, cholestasis
  • renal failure or impairment
  • FDA pregnancy category X
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40
Q

sumatriptan description

A
  • Imitrex
  • approved for tx of acute migraine w/ or w/o aura; give asap after onset
  • not for long term migraine prophylaxis
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41
Q

sumatriptan mechanism of action

A

-agonist at presynaptic 5HT1D autoreceptors (shut down serotonin release) and at vascular 5-HT1B receptors -> vasoconstriction

42
Q

sumatriptan adverse rxns

A
  • potentially fatal CV events: coronary artery vasospasm, arrhythmias, MI, cardiac arrest
  • GI: NVD, vasospastic effects leading to bowel ischemia, abdominal pain, bloody diarrhea, and cramping
  • injection site rxn (50%): pain, burning
43
Q

sumatriptan description

A
  • Imitrex
  • approved for tx of acute migraine w/ or w/o aura; give asap after onset
  • not for long term migraine prophylaxis
44
Q

sumatriptan mechanism of action

A

-agonist at presynaptic 5HT1D autoreceptors (shut down serotonin release) and at vascular 5-HT1B receptors -> vasoconstriction

45
Q

sumatriptan adverse rxns

A
  • potentially fatal CV events: coronary artery vasospasm, arrhythmias, MI, cardiac arrest
  • GI: NVD, vasospastic effects leading to bowel ischemia, abdominal pain, bloody diarrhea, and cramping
  • injection site rxn (50%): pain, burning
46
Q

sumatriptan precautions

A
  • *CV-angina, arteriosclerosis, arrhythmia, CAD, HTN, peripheral vascular ds, Raynauds, thrombophlebitis, MI, stroke
  • *Ischemic bowel disease
  • hepatic ds
  • renal insufficiency
47
Q

serotonin syndrome

A
  • caused by excessive serotonin concentration at its receptors
  • can be precipitated by the concomitant use of drugs that enhance synaptic serotonin [ ]s, usually developoing in less than 12 hrs (SSRI) (ecstasy)
  • Sx-anitation, hyperthermia, flushing, GI disturbances, myoclonus, rhabdomyolysis, tremor, seizures
48
Q

Hydrocortisone description

A
  • cortizone-10
  • natural steroid hormone secreted by adrenal cortex
  • main uses are antiinflammatory: anaphylaxis, asthma, COPD, IBS, rheumatic disorders, dermatoses
  • drug of choice for glucocorticoid replacement therapy in patients w/ adrenal insufficiency
  • low potency topical corticosteroids are safest for chronic use, may be used in infants and young children
49
Q

Eicosanoids

A
  • from 20-C essential FA-arachidonic acid most abundant precursor
  • biosynthesis is limited by the availability of free arachidonic acid-released from membrane phospholipids by PLA2
50
Q

hydrocortisone/cortisol

A
  • main glucocorticoid in humans
  • stimulate GNG, increase glood glucose and insulin secretion
  • promote lipolysis and lipogenesis, increase fat deposition
  • stimulate protein and bone catabolism
  • CNS: improve mood, increase motor activity, decrease sleep, decrease memory
  • immunosuppressive, antiinflammatory effects (IL-1, 2, 6 and TNF-a all stimulate CRH and activate HPA axis)
51
Q

Hydrocortisone description

A

-cortizone-10

52
Q

hydrocortisone mechanism

A
  • acts via nuclear receptors to modulate gene expression
  • anti-inflammatory-represses COX-2 expression; decrease cytokine production, increase formation and release of endogenous inflammatory mediators, apoptosis of eosinophils
53
Q

prednisone mechanism

A
  • prodrug of prenisolone, must be metabolized in vivo prednisolone
  • acts via nuclear receptors to modulate gene expression
  • anti-inflammatory-represses COX-2 expression; decrease cytokine production, increase formation and release of endogenous inflammatory mediators; apoptosis of eosinophils
54
Q

hydrocortisone precautions

A
  • *abrupt discontinuation of prolonged systemic therapy
  • *cushings syndrome
  • preexisting bacterial, viral, and fungal infections
  • patients receiving corticosteroids chronically should be assessed periodically for cataracts
55
Q

prednisone description

A
  • sterapred, generic
  • immunosuppressive oral corticosteroid; most prescribed
  • tx for autoimmune disorders, allograft rejection, asthma, IBS, rheumatoid arthritis, etc
56
Q

prednisone mechanism

A
  • prodrug of prenisolone, must be metabolized in vivo prednisolone
  • acts via nuclear receptors to modulate gene expression
  • anti-inflammatory-represses COX-2 expression; decrease cytokine production, increase formation and release of endogenous inflammatory mediators; apoptosis of eosinophils
57
Q

prednisone adverse rxns

A
  • (more common with high doses or prolonged therapy)
  • CNS: HA, insomnia, vertigo, depression, anxiety, euphoria, personality changes, psychosis
  • GI-NVD, anorexia, gastritis
  • cataracts
  • opportunistic infections
58
Q

prednisone precautions

A
  • *cushings ds
  • *high doses and long term therapy can suppress HPA axis-avoid abrupt DC of prolonged therapy
  • preexisting bacterial, viral, fungal infections
  • patients receiving corticosteroids chronically should be assessed periodically for cataracts
59
Q

Fluticasone description

A
  • Cutivate, flovent
  • Medium potency steroid used topically to relieve sx of dermatoses and psoriasis and intranasally for allergic and nonallergic rhinitis; used in tx of asthma, but for prophylaxis only
60
Q

Fluticasone mechanism

A
  • acts via nuclear receptors to modulate gene expression
  • anti-inflammatory-represses COX-2 expression; decrease cytokine production, increase formation and release of endogenous inflammatory mediators; apoptosis of eosinophils
61
Q

Fluticasone adverse reactions

A
  • pruritis, burning, hypertrichosis-mild and self-limiting

- hoarseness, irritation, secondary infections eg oropharyngeal candidiasis w/ inhaled form

62
Q

NSAIDs mechanism of action

A
  • irreversible inhibition of cyclooxygenase (COX) enzymes involved in prostaglandin biosynthesis
  • COX-1-constitutively present in almost all tissues
  • COX-2-constitutively expressed only in brain, kidney, and bone; inducible in response to certain mediators of inflammation
63
Q

Steroid drugs

A
  • hydrocortisone
  • prednisone
  • fluticasone
64
Q

Aspririn description

A
  • ASA, Bayer, generic
  • first NSAID, synthesized in 1853 and marketed late 1890s
  • Salicylate chemical class
  • used for thrombosis prevention, prevents or reduces risk of MI in pts w/ a history of MI, coronary bypass, angioplasty, angina, stroke, transient ischemic attacks
  • 5x more COX 1 vs 2
65
Q

NSAIDs mechanism of action

A
  • inhibition of cyclooxygenase (COX) enzymes involved in prostaglandin biosynthesis
  • COX-1-constitutively present in almost all tissues
  • COX-2-constitutively expressed only in brain, kidney, and bone; inducible in response to certain mediators of inflammation
66
Q

NSAID black box warnings

A

-increased risk of cardiovascular and GI adverse effects

67
Q

Aspririn description

A
  • ASA, Bayer, generic
  • first NSAID, synthesized in 1853 and marketed late 1890s
  • Salicylate chemical class
  • used for thrombosis prevention, prevents or reduces risk of MI in pts w/ a history of MI, coronary bypass, angioplasty, angina, stroke, transient ischemic attacks
68
Q

Aspirin adverse rxns

A
  • GI disturbances: NVD, mucosal damage, bleeding pain
  • tinnitus or hearing loss w/ high doses
  • hypersensitivity and anaphylactic rxns-pts w/ chronic urticaria, asthma, chronic rhinitis
69
Q

ketorolac adverse rxns and extra precautions

A
  • CNS: HA, dizziness, drowsiness
  • GI-NVD, damage to mucosa, gastric bleeding, abdominal pain
  • *CrCL
70
Q

NSAID precautions

A
  • *Salicylate sensitivity
  • *aspirin triad
  • heart ds
  • renal ds
  • prior hx of GI bleeds or perforation
  • bleeding disorders: hemophilia, thrombocytopenia, vit k deficiency
71
Q

Ketorolac description

A
  • Toradol
  • promoted mainly as strong analgesic, not anti-inflm drug
  • used short term (
72
Q

Indomethacin adverse rxns and extra precautions

A
  • CNS: dizziness, HA, fatigue/malaise, depression, tremor, ataxia
  • GI disturbances: NVD, damage to mucosa, gastric bleeding, abd pain
  • Pregnancy category D risk in 3rd trimester
  • CNS-seizure disorder, parkinsons, major depression
73
Q

NSAID precautions

A
  • *Salicylate sensitivity
  • *aspirin triad
  • *CrCL
74
Q

Indomethacin description

A
  • Indocin
  • NSAID of indole and indene acetic acid class
  • in premies, used to accelerate closure of patent ductus arteriosus (need low prostaglandins)
  • 3-5x more COX 1 vs 2
75
Q

Indomethacin adverse rxns and extra precautions

A
  • CNS: dizziness, HA, fatigue/malaise, depression, tremor, ataxia
  • GI disturbances: NVD, damage to mucosa, gastric bleeding, abd pain
  • Pregnancy category D risk in 3rd trimester
76
Q

Naproxen description

A
  • Aleve, Anaprox
  • Naphthylpropionic acid class
  • marketed as S-enantiomer
  • Better for lower back pain?; rheumatoid arthritis
  • 3-5x more COX 1 vs 2
77
Q

Naproxen adverse rxns

A
  • GI: NVD, damage to mucosa, gastric bleeding, abdominal pain; risk of upper GI bleeding double that of OTC ibuprofen
  • Derm-rashes, urticaria, alopecia
78
Q

Ibuprofen description

A
  • Advil
  • phenylpropionic acid class
  • quite effective as analgesic-dental procedures use
  • 2x more COX 1 vs 2
79
Q

Ibuprofen adverse rxns

A
  • CNS: dizziness, HA, nervousness
  • GI: NVD, damage to mucosa, gastric bleeding, abdominal pain
  • Rash
  • Tinnitus
  • Blurred vision
80
Q

Meloxicam description

A
  • Mobic
  • potent enolcarboxamide NSAID
  • indicated for rheumatoid arthritis or osteoarthritis
  • 10x more COX 2 vs 1
81
Q

Meloxicam adverse rxns

A

GI: pain, dyspepsia, nausea

82
Q

Celecoxib description

A
  • Celebrex
  • first FDA approved selective COX 2 inhibitor
  • 10-20x more COX 2 vs 1
83
Q

Celecoxib adverse rxns

A
  • GI disturbances: dyspepsia, NVD, abdominal pain
  • dizziness
  • rash
84
Q

Diclofenac description

A
  • phenylacetic acid class

- 10-20x more COX 2 vs 1

85
Q

Diclofenac adverse rxns

A
  • GI: upset stomach, heartburn, bleeding, ulceration, perforation, elevated LFTs
  • Renal-decreased blood flow, decrease GFR
86
Q

Acetaminophen description

A
  • Tylenol
  • analgesic and antipyretic activity but no anti-inflammatory activity or platelet effects
  • preferred analgesic/antipyretic when aspirin contraindicated
87
Q

acetaminophen mechanism

A
  • competitive inhibitor of COX 1 and 2 w/in CNS but not periphery
  • binds to cannabinoid receptors in spinal cord
88
Q

acetaminophen adverse rxns

A
  • rash, pruritis, urticaria
  • GI (high doses)-NV, anorexia, and abdominal pain w/in 2-3 hrs after high dose
  • hepatoxicity- in acute overdose, 2-3 days pass before maximum liver damage becomes apparent, antidote is IV N-acetyl cysteine
  • renal tubule necrosis w/ high/chronic doses
89
Q

Acetaminophen precautions

A
  • alcoholism
  • hepatic ds
  • renal ds-if CrCL
90
Q

Acetaminophen pharmcokinetics

A

-in liver, 85-90% is harmlessly metabolized but 10-15% is converted via CYP 2E1, 1A2, 3A4 to a chemically reactive, potentially hepatotoxic molecule

91
Q

Alprostadil description

A

Synthetic PGE1 for erectile dysfunction, maintain patent ductus arteriosus

92
Q

Alprostadil mechanism

A

Agonist at EP receptor-> increase cAMP -> vasodilation

93
Q

Latanoprost description

A

Synthetic PGF2a analog prodrug

Used to reduce elevated intraocular pressure in pts with open angle glaucoma or ocular HTN

94
Q

Latanoprost mechanism of action

A

Selective FP receptor agonist, believed to reduce IOP by increasing outflow of aqueous humor

95
Q

Misoprostol description

A
  • potent synthetic prostaglandin analog for gastric ulcer prevention
  • pregnancy termination, induce labor
96
Q

Misoprostol mechanism

A
  • agonist @ EP receptors on parietal cells in stomach-> decrease cAMP-> decrease acid secretion, promote mucous and bicarbonate secretion
  • agonist @ EP receptor in uterus, stimulates and increases amplitude and frequency of uterine contractions, dilates cervix
97
Q

Zileuton description

A
  • leukotriene inhibitor
  • benzothiophene derivative of N-hydroxyurea
  • indicated for prophylaxis and chronic treatment of asthma
98
Q

Zileuton mechanism

A
  • Specific 5-LOX inhibitor- decrease leukotriene formation
  • clinical response is inhibition of neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, decreased capillary permeability, decreases leukotriene induced smooth muscle contractions
99
Q

Zafirlukast description

A

Synthetic, selective peptide leukotriene receptor antagonist indicated for prophylaxis and chronic tx of asthma in adults and children

100
Q

Zafirlukast mechanism

A
  • antagonist at g-protein coupled cysteinyl leukotriene receptors in airway smooth muscle, mast cells, and neutrophils
  • inhibits bronchoconstriction, edema, mucous secretion
101
Q

Montelukast description

A
  • asthma maintenance therapy
  • also tx of allergic rhinitis
  • singulair
102
Q

Montelukast mechanism

A

Antagonist at G protein coupled cysteinyl leukotriene receptors in airway smooth muscles, mast cells, neutrophils
-inhibit bronchoconstriction, edema, mucous secretion

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