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Pharm > RA meds > Flashcards

RA meds Flashcards

1
Q

What is the cellular cause of RA? What type of hypersensitivity is this?

A

T cell activation

Also, immune factor stage

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2
Q

What are the three stages of RA?

A

Initiation stage
Amplification
Final stage (chronic inflammation)

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3
Q

What is the antibody that is elevated in RA? What is this?

A

Rheumatoid factor

IgM to the Fc of IgG

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4
Q

What are the chemokines that are released in RA? What do these cause?

A

TNF-a
IL1
IL6

Inflammation and fibrosis

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5
Q

What is the first line treatment for RA?

A

NSAIDs (ASA, acetaminophen, indomethacin, IBU etc)

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6
Q

What is the role of glucocorticoids in RA?

A

Reduce the inflammation and cause dramatic improvement in RA

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7
Q

What are the disease -modifying anti-rheumatic drugs (DMARDs)? MOA?

A

Drugs that reduce inflammation, improve symptoms, and slow bone damage

MOA unknown

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8
Q

Do NSAIDs affect the course of RA? What about DMARDs?

A

No for NSAIDs

Yes for DMARDs

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9
Q

What is the timeframe of onset for DMARDs?

A

slow (6 weeks to 6 months)

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10
Q

What are the two different DMARDs?

A

Synthetic and biologic

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11
Q

What is the MOA of methotrexate? What is the effect in RA treatment?

A

Inhibits AICAR transformylase to increase extracellular adenosine and inhibit T cell activation

First line treatment for RA

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12
Q

What is the MOA of cyclosporin?

A

Inhibits IL1 and IL2 receptor production

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13
Q

What is the MOA of cyclophosphamide?

A

Crosslinks DNA to prevent cell replication

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14
Q

What is the MOA of azathioprine?

A

Interferes with nucleic acid metabolism and synthesis, and inhibits cell proliferation

Suppressed B and T cell function

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15
Q

What is the MOA of Leflunomide? What is its role in RA treatment?

A

Inhibits ribonucleotide synthesis and causes cell cycle arrest

First agent for RA

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16
Q

What are the antimalarial agents that are used to treat RA? MOA?

A

Chloroquine and hydroxychloroquine

MOA unknown

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17
Q

What are the biological DMARDs?

A

Organic compounds made by living cells modify biologic responses

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18
Q

What are the two drugs that are anti-TNF-a antibodies?

A

Etanercept

Infliximab

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19
Q

What is the MOA of rituximab?

A

B cell depleting agent

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20
Q

What is the MOA of abatacept?

A

T-cell costimulation inhibitor

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21
Q

What is the MOA of Anakinra?

A

IL-1 cytokine inhibitor

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22
Q

What is the MOA of Etanercept?

A

anti-TNF-a antibodies

23
Q

What is the MOA of Infliximab?

A

anti-TNF-a antibodies

24
Q

What is the definition of a migraine?

A

HA from 4-72 hours
Is: unilateral, pulsating, moderate-severe pain
Associated with N/v

25
Q

What are the characteristics of migraine headaches (location, quality, severity, aggravating factors,)?

A

Unilateral
Pulsating quality
Aggregated by physical activity

26
Q

Which gender is more commonly affected with migraines?

A

Women

27
Q

What two parts of the head anatomy are affected with migraine HAs?

A

Dural vasculature

CN V dysfunction

28
Q

What happens to the blood vessels in migraine headaches?

A

Vasodilation in the brain, causes stimulation of the mechanoreceptors in the trigeminal nerve, causing ssx.

29
Q

What are the temporal progression of migraine headaches?

A
  1. Premonitory phase
  2. Aura
  3. HA
  4. Resolution
  5. Postdrome
30
Q

What are the ssx of the postdrome phase of migraine HAs?

A

Hangover, fatigue

31
Q

What happens to the cerebral blood flow with the progression of a migraine HA?

A

Lower in aura phase, then big increase in HA phase

32
Q

What are the three main specific migraine treatments?

A

Ergotamine
Dihydroergotamine
Triptans

33
Q

Who are the candidates for preventative therapy for migraines?

A

Unresponsive to acute attack meds

Frequent attacks

34
Q

What are the two beta blockers that are used in migraine headaches?

A

Propranolol (beta 1 and 2)

Metoprolol (beta 1)

35
Q

What is Amitriptyline?

A

TCA antidepressant

36
Q

What are the two anticonvulsants used to treat migraine HAs?

A

Valproic acid

Topiramate

37
Q

What is the MOA of valproic acid?

A

GABA-A receptor agonist

38
Q

What is the MOA of Topiramate?

A

GABA-A receptor agonist

39
Q

What is the MOA of Verapamil?

A

CCB

40
Q

What is the side effect of overuse of NSAIDs for the treatment of migraines?

A

Can transform migraine into a more severe, chronic disorder

41
Q

What type of drug is meperidine? What drug should this never be used with?

A

Opiate analgesic

42
Q

What type of drug is butorphanol?

A

Opiate analgesic

43
Q

What are the antiemetics that are used for migraine HAs?

A

Metoclopramide
Chlorpromazine
Prochlorperazine

44
Q

What is the MOA of Metoclopramide?

A

weak 5HT3 receptor antagonist

45
Q

What is the MOA of Chlorpromazine?

A

Centrally acting D2 receptor antagonist

46
Q

What is the MOA of Prochlorperazine?

A

Centrally acting D2 receptor antagonist

47
Q

What are the two ergot derivatives?

A

Ergotamine

Dihydroergotamine

48
Q

What is the MOA of ergot derivatives? What are these used for?

A

Vasoconstriction d/t stimulation of alpha adrenergic and 5HT 1D receptors

Used for Acute migraines

49
Q

What are the disadvantages of ergot derivatives?

A

Complex pharmacology and pharmacokinetics

Potent and sustained vasoconstrictive effect

50
Q

What is the MOA of sumatriptan (and other Triptans)? What does this cause? What are these used for?

A

Selective 5HT 1D and 1B receptor agonists used in the treatment of migraine HAs

Inhibit nociception of CN V, cause cranial vasoconstriction

51
Q

Why are the triptans better to treat migraine HAs over ergot derivatives?

A

More selective pharmacology

Safer

52
Q

What is the ultimate treatment for migraine headaches?

A

Sleep

53
Q

What is the major adverse effect of triptans?

A

Agina

MI (Rarely)

Pharm (73 decks)

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