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Pharmacology > Autocoids > Flashcards

Autocoids Flashcards

1
Q

Histamine storage sites

A

mast cells, basophils, enterochromaffin-like cells, neurons

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2
Q

H1 receptor location

A

peripheral nerve endings, CNS, smooth muscle of blood vessels, bronchi, and intestine

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3
Q

H1 receptor type

A

Gq coupled

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4
Q

H1 receptor activation- effects

A

vasodilation of small vessels; increased vessel permeability; bronchoconstriction; bronchospasm; urticaria; intestinal smooth muscle contraction

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5
Q

H2 receptor locations

A

gastric mucosa, heart, mast cells, CNS

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6
Q

H2 receptor type

A

Gs

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7
Q

H2 receptor activation- effects

A

Vasodilation of small blood vessels; Increased heart rate: reflex tachycardia and direct stimulation; Gastric acid secretion

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8
Q

H3 receptor locations

A

autoreceptors on histaminergic neurons in CNS and PNS; Gi-coupled

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9
Q

H3 receptor type

A

Gi

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10
Q

H4 receptor locations

A

Eosinophils, neutrophils, CD4 T-cells

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11
Q

H4 receptor type

A

Gi

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12
Q

Diphenhydramine

A

First generation H1 inverse agonist

  • tx for allergic rhinitis, itching, urticaria, motion sickness, insomnia
  • MOA: has antimuscarinic activity–> relieve of motion sickness; sedation via antagonism of CNS receptors; relief of allergy
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13
Q

Cetirizine

A

second generation H1 inverse agonist

  • minimal antimuscarinic activity
  • low CNS accumulation because pumped out by P-glycoprotein pump
  • 50% metabolized in liver as CYP3A4
  • fewer adverse reactions, CNS effects only at high doses
  • if CrCL<31 mL/min, do not exceed 5mg dose
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14
Q

Fexofenadine

A

second generation H1 inverse agonist

  • no antimuscarinic activity
  • low metabolism, 80% excreted in feces
  • low CNS accumulation because pumped out by P-glycoprotein pump
  • few adverse reactions
  • lower dose for patients with decreased renal function, do not take with fruit juice
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15
Q

Loratadine

A

second generation H1 inverse agonist

  • can be formulated with pseudophedrine
  • low CNS accumulation b/c effluxed from CNS by P-glycoprotein pump
  • extensive CYP3A4 metabolism–> many drug interactions
  • precautions: hepatic disease; if CrCL <30mL/min use loser dose
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16
Q

Cimetidine

A

H2 antagonist

  • H2 inverse agonist, reduces constitutive activity of H2 receptors on parietal cells, decreases acid secretion by 60%
  • PO or IV, usually 100-400 mg BID-QID or 800mg HS
  • non-selective inhibitor of CYP enzymes–> many drug interactions
  • 48% excreted in urine
  • adverse effects: headaches, blood dyscrasias
  • precautions: hepatic disease, renal insufficiency
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17
Q

Ergotamine

A

partial agonist or antagonist of 5-HT, DA, and a- adrenergic receptors

  • vasoconstriction of arteries and veins
  • decreased blood flow to extremities
  • oxytotic (uterine contractions, decreased postpartum bleeding)
  • adverse effects: ergotism
  • contraindications: CV disease, hepatic disease, renal failure, pregnancy- risk category X
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18
Q

Sumatriptan

A
  • Agonist at presynaptic 5-HT1D autoreceptors and 5-HT1B receptors
  • SC mode more effective than PO
  • metabolism by MAO-A in liver, excretion in feces and urine
  • adverse effects: fatal CV events, GI issues, injection site reaction
  • Precautions: hepatic disease, renal insufficiency
  • contraindications: CV disease, ischemic bowel disease
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19
Q

Serotonin syndrome

A

caused by excessive serotonin concentration at receptors, may be precipitated by concomitant use of drugs that increase serotonin secretion

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20
Q

management of serotonin syndrome

A
  1. remove precipitating drug and supportive care
  2. control agitation- benzodiazepines
  3. antagonize 5-HT actions: cyproheptadine (H1, 5-HT2, D3, M1-5 blocker)
  4. control hypertension and tachycardia: sodium nitroprusside, esmolol
  5. control hyperthermia: vecuronium, no role for antipyretics
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21
Q

Lipoxin receptor (ALX)

A

GI smooth muscle: relaxation; bronchial smooht muscle: relaxation; vascular smooth muscle: vasodilation; immune: inhibition

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22
Q

Prostaglandin E2 receptor (EP)

A

GI smooth muscle: increased motility; GI secretion: decreased acid/increased bicarb; penis: relaxation, erection; bronchial smooth muscle: relaxation, bronchodilation; uterus: tone, contractions; vascular smooth muscle: vasodilation, hypotension; immune: activation; platelets: decreased aggregation; kidney: increased renin release, vasodilation, increased GFR; nervous: increased body temp., hyperalgesia

23
Q

Prostacyclin receptor (IP)

A

bronchial smooht muscle: relaxation, bronchodilation; vascular smooth muscle: vasodilation, hypotension; platelets: decreased aggreation; kidney: increased renin release, vasodilation, increased GFR

24
Q

Thromboxane receptor (TXA2)

A

bronchial smooth muscle: contraction, bronchoconstriction; vascular smooth muscle: vasoconstriction, hypertension; platelets: increased aggreagation

25
Q

Prostaglandin D2 receptor (DP)

A

kidney: increased renin release, vasodilation, increased GFR. Smooth muscle contraction, inhibit platelet aggregation

26
Q

Prostaglandin F receptor (FP)

A

GI smooth muscle: increased motility; bronchial smooth muscle: contraction, bronchoconstriction; uterus: uterine tone, contractions; vascular smooth muscle: vasoconstriction, hypertension

27
Q

Leukotriene B4 receptor (BLT)

A

Immune: activation

28
Q

Leukotriene receptor CysLT

A

Bronchial smooth muscle: contraction, bronchoconstriction; vascular smooth muscle: vasoconstriction, hypertension; immune: activation; kidney: vasoconstriction, decreased GFR

29
Q

Hydrocortisone

A

Steroidal anti-inflammatory drug

  • anti-inflammatory, represses COX-2, decrased cytokine production, decreased endogenous inflammatory mediators, apoptosis of eosinophils
  • contraindications: abrupt discontinuation, Cushings
30
Q

Prednisone

A

Steroidal anti-inflammatory drug

  • similar mechanism as hydrocortisone
  • prodrug of prednisolone
  • TX for autoimmune, transplant, asthma, IBS, RA
  • half life 18-36 hours
31
Q

fluticasone

A

Medium potency steroid

  • TX for dermatoses, prophylaxis for asthma
  • similar mechanisms as hydrocortisone
  • metabolism by CYP3A4
  • inhaled form can cause oropharyngeal candidiasis
32
Q

Betamethasone

A

Steroid with anti-inflammatory potency 25-40; no mineralcorticoid potency; long duration

33
Q

Dexamethasone

A

Steroid with anti-inflammatory potency 30; no mineralcorticoid potency; long duration

34
Q

Fluprednisolone

A

Steroid with anti-inflammatory potency 15; no mineralcorticoid potency; intermediate duration

35
Q

Triamcinolone

A

Steroid with anti-inflammatory potency 5; no mineralcorticoid potency; intermediate duration

36
Q

Methylprednisolone

A

Steroid with anti-inflammatory potency 4; minimal mineralcorticoid potency; short-intermediate duration

37
Q

Fludricortisone

A

Steroid with anti-inflammatory potency 10 but used mostly for mineralcorticoid replacement (potency 250); intermediate duration

38
Q

General properties of NSAIDs

A

anti-inflammatory, antipyretic, analgesic (Not for neurologic pain); used for joint pain, muscle aches, rheumatoid arthritis, osteoarthritis, fever, dysmenorrhea, gout, prophylaxis of polyps and colon cancer

39
Q

NSAID mechanisms of action

A
  • inhibition of cyclooxygenase resulting in decreased prostaglandin synthesis
  • all have risk of CV and GI adverse effects
  • all are roughly equally efficacious
40
Q

Aspirin

A
  • Irreversible/ covalent COX inhibitor with 5x selectivity for COX1 over COX2
  • thrombosis prevention- antiplatelet activity is long lasting because platelets cannot regenerate inactivated COX
  • metabolized in liver to salicylic acid and excreted in urine
  • aspirin triad
  • can lead to Reye’s in children
41
Q

Ketorolac

A
  • NSAID: Competitive inhibitor of COX enzymes with 100x preference for COX-1 over COX-2
  • used for short term postsurgical pain that requires major analgesia
  • Parenteral dose followed by 10mg PO QID. 90% excreted in urine with 40% metabolized in liver
  • contraindications: salicylate sensitivity; aspirin triad; CrCL< 30 ml/min
42
Q

Indomethacin

A
  • NSAID: Competitive inhibitor of COX enzymes with 5x preference fo COX-1 over COX-2
  • used in premature infants to accelerate closure of patent ductus arteriosus
  • usually 3 doses given 12 hours apart for PDA; metabolized in liver and undergoes enterohepatic recirculation; 60% recovered in urine and 30% recovered in feces
  • precaution: seizure, psychiatric disease, Parkinsons, Pregnancy category D or B depending on trimester
  • contraindications: salicylate sensitivity; aspirin triad
43
Q

Naproxen

A
  • Competitive inhibitor of COX enzymes with 5x preference fo COX-1 over COX-2
  • Used mostly for analgesic and antipyretic properties than anti-inflammatory
  • largely bioavailabe; extensive hepatic metabolism and conjucation; 95% excreted in urine
  • adverse events: GI and derm
  • contraindications: salicylate sensitivity; aspirin triad
44
Q

Ibuprofen

A
  • Competitive inhibitor of COX enzymes with 2x preference for COX-1 vs COX-2
  • excreted in urine, 50-60% as metabolites
  • CNS, GI, rash, tinnitis, blurred vision
45
Q

Meloxicam

A
  • Competitive inhibitor of COX enzymes with 10x preference for COX-2 over COX-1
  • indicated for rheumatoid arthritis, osteoarthritis. Highly potent. COX-2 selective
  • Dose 7.5-10mg QD; highly bound to serum albumin, 70% metabolized by CYP2C9 and CYP3A4; excretion through urine and feces
46
Q

Celecoxib (Celebrex)

A
  • Competitive inhibitor of COX enzymes, 10-20-fold selective for COX-2 vs. COX-1
  • First FDA-approved selective COX-2 inhibitor; 97% metabolized in liver by CYP2C9
47
Q

Diclofenac

A
  • Competitive inhibitor of COX enzymes, 10-20-fold selective for COX-2 vs. COX-1
  • Metabolized in liver by CYP2C9 followed by glucuronidation or sulfation; excretion is 65% renal/ 35% biliary
  • adverse events: GI, eleveated liver function tests, renal- decreased blood flow, decreased GFR
48
Q

Acetaminophen

A
  • NOT an NSAID
  • Competitive inhibitor of COX enzymes in the CNS but not in periphery; binds to cannabanoids in spinal cord
  • In the liver, 85-90% is metabolized but 10-15% is converted via CYP2E1, 1A2, or 3A4 to a hepatotoxic metabolite, 85% renally excreted
  • adverse effect: Rash, pruritis, urticaria, GI at high doses, heptatoxicity treated with N-acetyl cysteine; renal tubule necrosis at high doses
  • precautions: alcoholism, hepatic disease, renal disease, tobacco smoking, salicylate sensitivity
49
Q

Alprostadil

A
  • prostanoid, agonist at EP receptors, increases cAMP and causes vasodilation
  • In men: used for erectile dysfunction in men who cannot tolerate nitro- compunds. In neonates: used to maintain patency of ductus arteriosus until surgery
  • Very potent, in men comes in powder form and reconstituted for injection; 81% albumin bound; metabolized by one pass through lungs, duration of action is 12-70 min
50
Q

Latanaprost

A
  • prostanoid used to treat glaucoma
  • Selective FP receptor agonist that reduces intraocular pressure by increasing the outflow of aqueous humor, decrease by 6-9 mmHg
  • Dosed by drops in eye, reduction in IOP begins within 3-4 hours and maximum effect in 8-12 hours; hydrolyzed by esterases in the cornea to biologically active acid
  • adverse effects: blurred vision, burning, itching, increased iris pigmentation, eyelash changes
  • do not use if active intraocular inflammation
51
Q

Misoprostol

A
  • Synthetic prostaglandin analog; agonist at EP receptors on parietal cells and uterine cells. GI: deceased cAMP, decreased acid secretion. Uterine: increased contractions, cervical dilation
  • used to prevent gastric ulcers (less effective than H2 antagonists); used to induce labor or abortion
  • In medical abortions given 48 hours following mifepristone, rapidly absorbed with peak levels after 9-15 minutes. Half life 20-40 minutes.
52
Q

Zileuton

A
  • Leukotriene inhibitor, specific 5-LOX inhibitor–> decreased leukotriene formation.
  • Causes inhibition of neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, decreased capillary permeability, leukotriene-induced smooth muscle contraction
  • 600 mg QID, rapidly absorbed with half life of 2.5 hours, apparent Vd of 1.2 L/kg, 93% bound to plasma proteins, substrate for CYP1A2, CYP2C9, CYP3A4
  • check LFTs before beginning treatment, do not use in active liver disease
53
Q

Zafirlukast

A
  • Peptide leukotriene receptor antagonist at G coupled CysLT receptors in muscles, mast cells, neutrophils.
  • used in prophylactic treatment of chronic asthma by inhibiting bronchoconstriction, edema, mucus secretion
  • 20 mg BID, rapidly absorbed with peak plasma concentration in 3 hours, food increases bioavailability, 99% bound to plasma protein with 8 hour plasma half life, metabolized by CYP3A4 and CYP3C9, most excreted in feces
54
Q

Montelukast

A
  • Antagonist at G coupled CysLT receptors in airway muscle, mast cells, neutrophils
  • used in prophylactic treatment of chronic asthma by inhibiting bronchoconstriction, edema, mucus secretion and for allergic rhinitis
  • given PO, 10 mg QD, rapidly absorbed, 99% bound to plasma protein, extensive hepatic metabolism with CYP3A4 and CYP2C9, excreted almost exclusively in bile
  • very similar to Zafirlukast but lower dose only once daily so more convenient for patients

Pharmacology (7 decks)

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