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Musculoskeletal/Rheum > RHEUM Pharmacology > Flashcards

RHEUM Pharmacology Flashcards

1
Q

MOA: binds CD80 and CD86 and prevents T-cell co-stimulatory signal engaging with CD28.

A

Abatacept

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2
Q

MOA: Binds TNF-alpha; blocks its interaction with p55 and p75 surface receptors

A

Adalimumab

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3
Q

MOA: Competitively inhibits IL-1 alpha and IL-1beta binding to IL-1R1.

A

Certolizumab pegol

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4
Q

MOA: neutralizes membrane associated and solubule human TNF-alpha

A

Etancerept

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5
Q

MOA: Endogenous p75 acts as TNF antagonist but does NOT affect TNF alpha production or serum levels (just binds it up)

A

Etancercept

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6
Q

MOA: binds to and neutralizes both soluble and membrane TNF-alpha

A

Golimumab

Infliximab

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7
Q

MOA: Fab domain binds CD20 and Fc domain and recruits immune effector function to mediate B-cell lysis

A

Rituximab

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8
Q

MOA: binds both soluble (serum and synovial fluid) and membrane bound IL-6 receptors and inhibits signaling

A

Tocilizumab

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9
Q

MOA: Inhibition of AICAR transformylase →AICA riboside accumulation (inhibits adenosine deaminase)→ increase in adenosine concentration→ inhibition of lymphocyte proliferation; suppression of IL-1, TNF, INF-gamma, histamine release from basophils, chemotaxis of neutrophils; increases IL-4

A

Methotrexate

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10
Q

MOA: Active form (mesalamine) is anti-inflammatory (inhibits prostaglandin and leukotriene prodution.

A

Sulfasalazine

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11
Q

MOA: A77 1726 inhibits dihydroorotate dehydrogenaase (DHODH) which is located in cell mitochondria and catalyzes key step in de novo pyrimidine synthesis. T-and B-lymphocytes cell cycle progression is arrested and their interactions are interrupted; Ig production is suppressed; CYTOSTATIC

A

Leflunomide

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12
Q

MOA: Increases intracellular vacuole pH and alters processes like digestion of antigenic proteins (so no peptide-MHC protein complexes can be formed to stimulate CD4+ T cells—immune response is down-regulated.)

A

Hydroxychloroquine

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13
Q

Side effect:

  • Immunosuppression
  • Pulmonary Toxicity
  • Cat. X Teratogen
  • NO Breastfeeding
  • Avoid w/vaccination
  • Malig. lymphoma
  • GI toxicity
  • Dermatologic RXN
A

Methotrexate

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14
Q

Side effect:

  • Hematotoxic
  • NOT for people with hypersensitivity to sulfa drugs
  • Increased drug levels in slow acetylators
A

Sulfasalazine

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15
Q

Side effect:

  • Immunosuppression (not for patients with immunodeficiency, bone marrow dysplasia, or uncontrolled infection).
  • Cat. X Teratogen
A

Leflunomide

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16
Q

Side effect:

  • Corneal opacities, kerato/retinopathy
  • Hepatotoxicity
  • Blood dyscrasias
  • CNS toxicity (ex. ototoxicity, seizure)
A

Hydroxychloroquine

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17
Q

Monitoring tests for Methotrexate.

A

1) CBC with diff.
2) LFTs
3) Serum Creat/ BUN
4) Serum uric acid

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18
Q

Monitoring tests for sulfasalazine.

A

1) CBC with diff.
2) LFTs
3) Serum Creat/ BUN
4) Urinalysis

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19
Q

Monitoring tests for Leflunomide.

A

1) CBC with diff.
2) LFTs
3) Pregnancy test
4) Serum electrolytes (drug increases uric acid in urine/ lowers blood levels)

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20
Q

Monitoring tests for Hydroxychloroqine

A

1) CBCs

2) Opthalmalogic exam.

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21
Q

Major adverse effects for “biological drugs” used to treat RA.

A
  • Immunosuppression (especially with upper respiratory infections, watch out)
  • Malignancy
  • CHF or hypotension
  • Blood dyscrasias
  • Lupus-like syndrome
  • SJS/TEN
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22
Q

Which biological drug for RA requires that you use reliable contraception while you take the therapy and for 4-6 months after?

A

Rituximab

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23
Q

Which biological IV solution contains maltose (may complicate blood glucose tests)?

A

Abatecept IV

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24
Q

What NSAID is available formulated with misoprostol (PGE1 inhibitor) to reduce the risk of duodenal ulcers.

A

Diclofenac

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25
Q

Which NSAID also has a rectal preparation available?

A

Indomethacin

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26
Q

Whaich NSAID also has a parenteral preparation available?

A

Ketorolac

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27
Q

Which NSAID is COX-2 selective?

A

Celecoxib

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28
Q

Depolarizing agents.

A

Curiums and Curoniums (steroids) and D-Tubocurarine

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29
Q

Non-depolarizing agent.

A

Succinylcholine

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30
Q

Reversal agents.

A

“stigmines”
Edrophonium
Sugammedex

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31
Q

Do depolarizing or non-depolarizing have longer half lives?

A

non-depolarizing have longer half lives

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32
Q

AE: Non-depolarizing drug that causes seizures by liver metabolism building up laudanosine.

A

Atracurium

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33
Q

AE: Neuromuscular Blocking Agents that block Cardiac M receptor.

A

pancuronium

rocuronium

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34
Q

AE: Neuromuscular Blocking agents that block cause histamine release.

A

Tubocurarine

Atracurium

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35
Q

AE: Neuromuscular blocking agents that block Nictotinic N ganglia.

A

Tubocurarine

36
Q

AE: malignant hyperthermia (high temp, muscle pain, brown urine), hyperkalemia, stimulation of Nicotinic N, histamine release, and stimulation of cardiac M receptors (decrease HR).

A

Succinylcholine

37
Q

Drug given to treat malignant hyperthermia.

A

Dantrolene

38
Q

MOA: Drugs that blocks acetylcholinesterase to reverse neuromuscular block.

A

Neostigmine, Edrophonium, Pyridostigmine

39
Q

What are AchE inhibitors given to reverse neuromuscular block given with?

A

Antimuscarinic agents (to prevent the negative effects of AchE inhibitors like bradycardia, bronchospasm, GI peristalsis, increased bladder tone)

40
Q

MOA: pore structure into which the steroidal NMB inserts, preventing the blocker from being capable of accessing the binding site on the Ach nicotinic receptor (reverse any depth of NM blockade)

A

Sugammadex

41
Q

MOA: inhibit the reuptake of serotonin and norepinephrine

fibromyalgia drug

A

Duloxetine and Milnacipran

42
Q

MOA: inhibit presynaptic alpha-2-delta subunits of L-type calcium channels→inbitis excitatory transmission by glutamate (alleviates neuropathic pain, anxiety and pain)

(fibromyalgia drug)

A

Pregabalin

43
Q

Off label drugs for fibromyalgia.

A

amitriptyline (tricyclic antidepressant)
fluoxetine (SSRI)
cyclobenzaprine (muscle relaxer)

44
Q

MOA: Central (CNS) action in reticular activating system and spinal cord leading to sedation and altered perception of pain. It is believed (but not proven) that generalized sedation is the basis for the muscle relaxation. NO DIRECT EFFECT on neuronal conduction, neuromuscular transmission or muscle excitability.

A

Carisoprodol

45
Q

MOA: tricyclic antidepressant-like drug for muscle spasm that has central action; possibly at the level of the brain stem.

A

cyclobenzaprine

46
Q

MOA: No direct effect on muscle or excitation-contraction coupling. Effects thought to be due to generalized sedative action. Pain relief due to altered pain perception.

A

Methocarbamol

47
Q

MOA: agonist on pre-synaptic α-2 receptor agonist leading to decreased activation of polysynaptic spinal cord motor neurons with concomitant reduction in muscle tone but NOT muscle strength. VERY WEAK anti-hypertensive.

A

Tizanidine

48
Q

MOA: acts as GABAB agonist at multiple levels in spinal cord, producing either inhibitory signals or hyperpolarizing and thereby reducing the excitatory (aspartate and glutamate) polysynaptic pathways. Pain relief in spinal cord from inhibition of substance P action.

A

Baclofen

49
Q

MOA: decreases muscle contraction by directly interfering (ryanodine receptor) with calcium ion release from the sarcoplasmic reticulum within skeletal muscle cells. Effectively it “uncouples” the excitation-contraction process

A

Dantrolene

50
Q

List the skeletal muscle relaxers.

A

Carisoprodol
Cyclobenzaprine
Methocarbamol
Tizanidine

51
Q

List the drugs to treat spasticity.

A

Botulinum Toxin
Tizanidine
Baclofen
Dantrolene

52
Q

AE: BBW for suicidal ideation; mild increases in HR/BP; hyponatremia secondary to SIADH

A

SSRIs: Duloxetine, Milnacipran

53
Q

Which SSRI does NOT have CYP metabolism.

A

Milnacipran

54
Q

AE: Rebound symptom worsening upon withdrawal; worsening depression and suicidal thoughts should be monitored; Dizziness, sedation, blurred vision and xerostomia

A

Pregabalin

55
Q

AE: Drowziness and dizziness are most common, together with other CNS manifestations like agitation, insomnia, vertigo, ataxia; systemic effects of sedation include asthenia, temporary vision loss, mydriasis, orthostatic hypotension. Additive sedation if combined with other sedative agents.

A

Carisoprodol

56
Q

AE: GI problems are major: paralytic ileus; Anticholinergic effects (drowsiness, dizziness, fatigue, N/V, constipation, etc.); additive depression with depressant drugs/alcohol; increase QT interval

A

Cyclobenzaprine

57
Q

AE: Increased depression with drugs/alcohol; drowsiness, dizziness, lightheadedness, blurred vision, N/V, HA and irritability.

A

Methocarbamol

58
Q

AE: hepatocellular toxicity; rebound hypertonicity, tachycardia and hypertension (need to taper down, especially after high drug doses); additive depression with CNS depressents; additive hypotension; asthenia, xerostomia, dizziness, sedation, hypotension.

A

Tizanidine

59
Q

AE: BBW for “rebound” neural activity (seizures, confusion, hallucinations, psychiatric disturbances (especially in those with preexisting CNS conditions!)) and increased spasticity (perhaps advancing to rhabdomyolysis, multisystem failure and death); additive CNS depression; additive hypotension with MAOIs and antihypertensives; increase blood glucose; drowsiness, etc.

A

Baclofen

60
Q

AE: floppy baby syndrome; muscle weakness leading to drooling, dysarthria, enuresis, myalgias and backache; additive CNS depression; if combined with CCB→ Vfib and CV collapse

A

Dantrolene

61
Q

Fibromyalgia drug that must be monitored for serum creatinine.

A

Pregabalin

62
Q

Muscle relaxer that has to be monitored for serum creatinine/BUN.

A

Carisoprodol

63
Q

Spasticity drugs that must be monitored for LFTs.

A

Tizanidine

Dantrolene

64
Q

MOA: Irreversible acetylation of COX-1 in platelets.

A

Aspirin

65
Q

MOA: Produces analgesia and anti-pyretic actions in the CNS by inhibiting COX1 and COX2

A

Acetaminophen

66
Q

AE:

  • Greater GI toxicity than NSAID
  • Hepatotoxicity
  • Renal toxicity (rare)
  • Salicylate poisoning (respiratory alkalosis from hyperventilation)→ CV collapse
A

Aspirin

67
Q

AE:

-Acute hepatic failure (metabolic production of highly reactive adducts)

A

Acetaminophen

68
Q 
Drug that you need to monitor:
LFTs
Serum creatinine/BUN
Serum Salicylate concentration
Stool Guaiac
A

Aspirin

69
Q

MOA: reversible, alosteric competitive inhibitor of xanthine oxidase (converts xanthine to hypoxanthine which is converted to uric acid) AND also metabolized (oxidation by XO) to oxypurinol which is a non-competitive inhibitor of XO (when molecule is formed, it binds irreversibly to enzyme and kills it).

A

Allopurinol

70
Q

MOA: direct inhibitor of both the oxidized and reduced forms of xanthine oxidase and the enzyme-inhibitor complex is highly stable

A

Febuxostat

71
Q

MOA: small molecule that is secreted into the tubular fluid by an organic acid transporter; uric acid is secreted into the tubular fluid by a uric acid transporter (NOT affected by drug)—drug competes with uric acid for reabsorption at the brush border transporter (decreasing the amount of uric acid that is reabsorbed/increases uric acid excretion in the urine).

A

Probenecid

72
Q

MOA: This drug works by depolimerizaiton of microtubules of migrating cells so that the cells (PMN/WBC) coming toward the gout cannot move—this prevents the release of pro-inflammatory cytokines and STOPS the gout attack and can be used to prevent recurrence of gouty arthritis.

A

Colchicine

73
Q

MOA: COX inhibitor that inhibits leukocyte motility (blocks ability of immune response to attack uric acid crystals→ reduces pain associated with inflammatory response)

A

Indomethacin

74
Q

MOA: rapidly lowers serum levels of uric acid and reduces urinary excretion of uric acid; increases serum levels of allantoin and urinary excretion of allantoin (5 times more soluble than uric acid)

A

Pegloticase

75
Q

AE: increase incidence of active gout (crystals may dissolve and cause flare-ups—so give NSAID); hypersensitivity reactions (dermatitis, exfoliative dermatitis); effects on liver function (need LFTs every 6 weeks at start)

A

Allopurinol

76
Q

AE: transaminase elevations >3 times the upper limit

A

Febuxostat

77
Q

AE: patient needs to drink a lot of water to prevent kidney stones as the uric acid crystals in joints break down

A

Probenecid

78
Q

AE: GI disturbances (acute—sign you have given too much) and blood dyscrasias (chronic)

A

Colchicine

79
Q

AE: occur in 50% of patients: GI (N/V, ulcers); CNS (severe frontal HA); Hematopoietic disorders

A

Indomethacin

80
Q

AE: VERY EXPENSIVE; patients need to be prophylactically (with colcicine) protected because crystals can break down in joints and cause gout flares; not for patients with antibodies against the PEG moitey

A

Pegloticase

81
Q

Gout drug with longest half life.

A

Pegloticase

82
Q

Gout drug that will antagonize furosemide and HCTZ (diuretics).

A

Indomethacin

83
Q

Gout drug that’s action is inhibited by Salicylates/NSAIDs→ switch to tylenol

A

Probenecid

84
Q

Drug with DDIs with: 6-mercaptopurine used for blood cancers (reduce dose to 25%); ampicillin/related antibiotics are contraindicated (because will lead to skin problems)!

A

Allopurinol

85
Q

What drug do you use in patients who cannot tolerate allopurinol or have renal dysfunciton?

A

Febuxostat

Musculoskeletal/Rheum (12 decks)

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