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Pharmacology > Analgesics > Flashcards

Analgesics Flashcards

1
Q

Anti-migraine medications (4)

A
  • Perfenazine
  • Rizatriptan
  • Natalizumab
  • Zolmitripan
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2
Q

Triptan (riza or zolmi) mechanism of action

A

Selective serotonin agonists —> 5-HT1b/1d
- Vasoconstriction
- Inhibit trigeminal nerve nociception
- Inhibit vasoactive peptide secretion

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3
Q

Triptan side effects

A
  • Paresthesia, cold sensation
  • Serotonin sx
  • Hypertension
  • Vasospasm = ischemia
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4
Q

When should triptans NOT be given?

A

Within 24 hrs of ergot derivate, another 5HT agonist or SSRIs —> coronary spasm of serotonin sx

History of coronary artery disease or hypertension

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5
Q

Triptan ADME

A

A: oral, SC, nasal
D: low bound to proteins, cross placenta
M: riza = MAO; zolmi = CYP1A2 and MAO
E: urine

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6
Q

Perphenazine mechanism of action

A

D2 antagonist
—> antipsychotic 1st gen
—> extrapyramidal effects, strong antiemetic

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7
Q

Perphenazine main uses (3)

A
  • Schizophrenia
  • Acute anxiety
  • Severe nausea and vomiting
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8
Q

Perphenazine side effects (6)

A
  • Extrapyramidal
  • Neuroleptic malignant sx = more reflex, rigidity
  • Hyperprolactinemia
  • Hypotensino
  • Weight gain
  • CNS depression, seizures
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9
Q

Perphenazine ADME

A

A: oral
D: protein bound, widely distributes, crosses placenta
M: CYP2D6
E: urine and feces

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10
Q

Natalizumab mechanism of action

A

Target: a4 integrin
—> affects WBC adhesion and migration

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11
Q

Natalizumab uses

A
  • MS
  • Crohn
  • Migraine? (Según clasificación del Dr)
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12
Q

Natalizumab main possible side effect

A

Reactivation of latent JC virus —> PML

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13
Q

NSAID mechanism of action

A

Inhibition of COX1 and COX2 = less PGs
(Only irreversible is acetylsalicylic acid)

COX1: constitutively
COX2: mostly CNS

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14
Q

COX2 selective inhibitor

A

Celecoxib

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15
Q

NSAID ADME

A

A: rapid oral absorption
D: 95-99% protein bound, wide distribution
M: hepatic biotransformation
E: urine

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16
Q

NSAID uses (5)

A
  • Anti-inflammatory (RA)
  • Analgesic
  • Antipyretic
  • Antiplatelet
  • Uricosuric (gout)

Other: PDA closure, mastocytosis, niacin tolerance

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17
Q

NSAID side effects

A
  • GI: ulcers, reflux, pain, diarrhea
  • Hepatotoxicity
  • CV: COX2 inhibition = thrombosis risk
  • Renal: hypotension, nephropathy
  • Pregnancy: NOT in 3rd trimester
  • NOT 1-3 days before surgery
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18
Q

Paracetamol main side effect

A

Hepatotoxicity id >4g/day
—> give N-acetylcysteine

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19
Q

Paracetamol ADME

A

A: oral, IV
D: all tissues except fat
M: CYP2E1 —> NAPQI (toxic metabolite inactivated by glutathione)
E: urine

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20
Q

Which NSAIDS have a higher potency?

A

Keterolac
Diclofenac - can cause elevated transaminases

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21
Q

Sulindaco relevance as an NSAID

A

Increased anti-inflammatory activity

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22
Q

Diclofenac ADME

A

A: oral
D: SYNOVIAL FLUID, 99% protein bound
M: CYP2C
E: urine and feces

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23
Q

Naproxen relevance as an NSAID

A

Increased half life (9-25 hours)
More potency
Safer for people with CV history

24
Q

Ketoprofen relevance as an NSAID

A

Small half life (1-3 hours)
—> Quicker effect
Stronger than ibuprofen and diclofenac

25
Q

Piroxicam and meloxicam type of medication and uses

A

Enolic acid
- RA
- Osteoarthritis
- Acute pain and inflammation

26
Q

Medications with some selectivity for COX2

A
  • Celecoxib
  • Diclofenac
  • Meloxicam
27
Q

Enolic acid vs NSAID main difference

A

Enolic acids have a very high half life:
—> piroxicam = 50 hours
—> meloxicam = 15-20 hours

28
Q

Medication to use in patients with GI risk and why

A

Celecoxib, there are mostly COX1 receptors in the gastric mucosa

29
Q

Do NOT give celecoxib to patients with:

A

High cardiovascular risk

Sulfa allergy

30
Q

Colchicine mechanism of action

A

Binds to tubulin subunit —> inhibit microtubule polymerization —> inhibit phagocytosis of urate crystals, neutrophil activation, migration, and degranulation

= ANTI-GOUT AGENT

31
Q

Colchicine main side effects (5)

A
  • Narrow therapeutic window
  • GI symptoms
  • Myelosuppression
  • Rhabdomyolysis
  • Toxicity: renal, cardiac, CNS
32
Q

Allopurinol mechanism of action

A

XANTHINE OXIDASE INHIBITION —> xanthine is not degraded into uric acid

= less uric acid

33
Q

What is the first line agent for reducing uric acid in plasma?

A

Allopurinol

(Give colchicine before in gout treatment)

34
Q

When allopurinol is combined with ______, it causes bone marrow toxicity.

A

Azathioprine

35
Q

Allopurinol ADME

A

A: oral, IV
D: no protein binding, water distribution
M
E: urine

36
Q

Methocarbamol mechanism of action

A

CNS depressant
- Sedative
- Skeletal muscle relaxation

ACUTE relief

37
Q

Methocarbamol ADME

A

A: oral, IV, IM
D: 50% protein bound
M: hepatic
E: urine

38
Q

What type of medication is acemetacin?

A

NSAID
Used for osteoarthritis, RA, back pain, post-op pain

39
Q

Allopurinol

A

Uric acid decrease

40
Q

Colchicine

A

Prevent gout attacks

41
Q

Diclofenac

A

NSAID
Stronger than others

42
Q

Ketoprofen

A

NSAID
Moderate-severe pain

43
Q

Meloxicam

A

NSAID
Very strong, high risk of clots
RA, low GI and renal side effects

44
Q

Methocarbamol

A

Muscle relaxant

45
Q

Naproxen

A

NSAID
Long duration, safe when heart risk

46
Q

Piroxicam

A

NSAID
Better at reducing swollen joints

47
Q

Sulindac

A

NSAID

48
Q

Acemetacin

A

NSAID
AR and muscular

49
Q

Celecoxib

A

NSAID
Lower GI risk

50
Q

Paracetamol

A

Analgesic and anti-pyretic

51
Q

Perphenazine

A

Anti-psychotic
Scizophrenia
Severe nausea and vomiting

52
Q

Rizatriptan

A

5-HT receptor agonist
Migraine

53
Q

Natalizumab

A

Mab vs a4 integrin
No leukocyte adhesion
(MS and Crohn)

54
Q

Zolmitriptan

A

5-HT receptor agonist 1B and 1D
Acute migraine

55
Q

Rizatriptan vs zolmitriptan

A

R: first choice of treatment
Z: first choice for short-term

Pharmacology (13 decks)

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