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Musculoskeletal > Pharm > Flashcards

Pharm Flashcards

0
Q

What are the DMARDs for treating RA?

A

Methotrexate, hydroxychloroquine, leflunomide, sulfasalazine

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1
Q

What are DMARDs?

A

Drugs from many classes with no common properties other than the ability to improve inflammatory symptoms and slow the progression of joint erosions.

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2
Q

Methotrexate MOA in immunosupression

A

Inhibition of AICAR transformylase, which catalyzes the last step in biosynthesis of inosine monophosphate. Inhibition leads to AICA riboside accumulation so you end up with more adenosine around and that inhibits lymphocyte proliferations and suppresses secretion of IL1, inf-gamma, and tnf, and all sorts of other good stuff

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3
Q

Methotrexate metabolism

A

When it enters cell methotrexate undergoes polyglutamation which serves to retain drug intercellularly. Hepatic metabolism and enterohepatic recirculation

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4
Q

Methotrexate elimination

A

Primarily via the kidney, competition with weak acids and prebenecid

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5
Q

Contraindications to methotrexate

A

Pregnancy, HIV

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6
Q

Adverse effects of methotrexate

A

Bone marrow suppression, pulmonary toxicity, malignant lymphomas, dermatological rxns, GI toxicity (in pts with PUD or ulcerative colitis, with NSAIDs).
Don’t vaccinate while on methotrexate

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7
Q

Monitoring parameters for methotrexate

A

CBC with differential, LFTs, serum creatinine/BUN, serum uric acid

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8
Q

What is sulfasalazine?

A

Oral drug used in pts who respond inadequately to salicylates or other NSAIDs. Metabolized to active components sulfapyridine and masalamine by bacteria in colon

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9
Q

Sulfasalazine MOA

A

Anti-inflammatory action results from mesalamine inhibiting prostaglandin and leukotriene production

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10
Q

Sulfasalazine elimination

A

Renal- caution in pts with renal dysfunction

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11
Q

Sulfasalazine contraindications

A

Hypersensitivity to 5-aminosalicylate, salicylate, or sulfonamide drugs

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12
Q

Sulfasalazine toxicities

A

Potentially fatal blood dyscrasias

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13
Q

Monitoring parameters for sulfasalazine

A

CBC w/diff, LFTs, serum creatinine/BUN, urinalysis

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14
Q

Leflunomide MOA

A

Activity via metabolite A77 1726, inhibiting dihydroorotate dehydrogenase in mitochondria. T and B lymphocyte cell cycle progression arrested and collaborative interaction interrupted. Immunoglobulin production also suppressed.

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15
Q

Leflunomide elimination

A

A77 1726 exhibits uricosuric effect. Elimination in feces and other conjugated.

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16
Q

Leflunomide toxicities

A

Hepatic toxicity with chronic use (caution in alcoholics)

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17
Q

Contraindications of leflunomide

A

Severe immunodeficiency, bone marrow dyscrasia, or uncontrollably infection
Pregnancy
Heavy alcohol use

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18
Q

Monitoring of leflunomide

A

CBC w/diff, LFTs, pregnancy testing, serum electrolytes

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19
Q

Hydroxychloroquine MOA

A

Increases intracellular vacuole pH so MHC II proteins can’t be assembled. So the drug diminishes formation of peptide-MHC protein complexes required to stimulate CD4 t cells

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20
Q

Hydroxychloroquine elimination

A

Extensive and slow renal elimination after partial hepatic metabolism

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21
Q

Contraindications of hydroxychloroquine

A

Ocular disease, alcoholism

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22
Q

Toxicity of hydrochloroquine

A

Blood dyscrasia, CNS (polyneuritis, ototoxicity, seizures, and neuromyopathy)

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23
Q

Abatacept administration

A

IV/SC

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24
Q

Abatacept structure

A

Fusion protein: human CTLA4/IgG1 Fc fragment

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25
Q

Abatacept MOA

A

Binds CD80 and CD86, prevents T-cell co-stimulatory signal engaging with CD28

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26
Q

Adalimumab administration

A

SC

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27
Q

Adalimumab structure

A

TNF- alpha monoclonal antibody

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28
Q

Adalimumab MOA

A

Binds TNF-alpha, blocks it’s interaction with the p55 and p75 cell surface receptors

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29
Q

Anakinra administration

A

SC

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30
Q

Ankinra structure

A

Recombinant human interleukin-1 receptor antagonist (IL-1Ra)

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31
Q

Anakinra MOA

A

Competitively inhibits IL-1 alpha and IL-1 beta binding to interleukin-1 type 1 receptor (IL-1R1)

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32
Q

Certolizumab pegol administration

A

SC

33
Q

Certolizumab pegol structure

A

Fab fragment of humanzed TNF-alpha antibody

34
Q

Certolizumab pegol MOA

A

Neutralizes membrane-associated and soluble human TNF-alpha

35
Q

Etanercept administration

A

SC

36
Q

Etanercept structure

A

Extracellular ligand-binding portion of human p75 TNF receptor linked to part of human IgG Fc (2:1 ration p75/Fc)

37
Q

Etanercept MOA

A

Endogenous p75 acts as a TNF antagonist. As a recombinant TNFR p75 bound to the Fc fragment of the human IgG1, etanercept binds to and inactivated TNF but doesn’t affect TNF production or serum levels

38
Q

Golimumab administration

A

SC

39
Q

Golimumab structure

A

Human-derived TNF-alpha antibody (variable and constant regions)

40
Q

Golimumab MOA

A

Binds to and neutralizes both soluble and transmembrane TNF-alpha

41
Q

Infliximab administration

A

IV

42
Q

Infliximab structure

A

Chimerical IgG1k monoclonal antibody against TNF-alpha

43
Q

Infliximab MOA

A

Binds to and neutralizes both soluble and transmembrane TNF-alpha

44
Q

Rituximab administration

A

IV

45
Q

Rituximab structure

A

Chimeric IgG1k monoclonal antibody against B-lymphocyte CD20 receptor

46
Q

Rituximab MOA

A

Fab domain binds CD20 and Fc domain recruits immune effector functions to mediate B-cell lysis (complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and induction of apoptosis are possible mechanisms). Sensitizes drug-resistant human B-cell lymphoma cell lines to cytotoxic chemotherapy

47
Q

Tocilizumab administration

A

IV

48
Q

Tocilizumab structure

A

Humanzed IL-6 receptor-inhibiting monoclonal antibody

49
Q

Tocilizumab MOA

A

Binds to soluble (serums and synovial fluid) and membrane-bound IL-6 receptors & inhibits signaling

50
Q

Biological agents adverse effects

A

Immunosupression, increased risk of malignancy, cardiovascular effects, blood dyscrasia, and other for Some specific drugs

51
Q

Which biological agents have increased likelihood of malignancy?

A

Adalimumab, certolizumab pegol, Etanercept, golimumab, and Infliximab

52
Q

Biological agents implicated in CHF or hypotension/angina/dysrhythmia

A

Adalimumab, golimumab, Infliximab, and Rituximab

53
Q

Contraindication in use of Infliximab?

A

Moderate-severe heart failure

54
Q

Blood dyscrasias reported in which biological agents?

A

Anakinra, certolizumab, Rituximab and tocilimumab

55
Q

A lupus-like syndrome is most likely with which biologicals?

A

Adalimumab, certolizumab, Etanercept, Infliximab

56
Q

Stevens-Johnson syndrome reported with what biological?

A

Rituximab

57
Q

Which biological may complicate blood glucose tests and why?

A

Abatacept IV solution contains maltose

58
Q

Patients with what SC drugs require special counseling? What is that counseling?

A

Abatacept, Adalimumab, anakinra, certolizumab, Etanercept, golimumab all need patient education about appropriate injection sites and the need for injection site rotation

59
Q

Liver function tests recommended when using what biologicals?

A

Golimumab, Infliximab, and tocilimumab

60
Q

What special counseling is needed for women taking Rituximab?

A

They must use reliable contraception while taking the drug and avoid pregnancy for 4-6 months after therapy.

61
Q

So corticosteroids and RA…. Is that a good thing?

A

Basically yes, low-medium dose glucocorticoids are beneficial in treating RA and the risks are not as big a deal as people make them out to be.

62
Q

How do glucocorticoids work?

A

The majority of the anti-inflammatory effects occur via cytosolic GC receptors that get activated and up regulate or downregulate protein synthesis by binding specific DNA binding sites. Also negatively interfere with the function of transcription factors like NF-kB, AP-1, and NF-AT. Get reduced synthesis of proinflammatory cytokines and reduced production of receptor activator of nuclear factor kappa B ligand

63
Q

Which steroids mentioned are injectable?

A

Hydrocortisone, triamcinolone, betamethasone, and dexamethasone

64
Q

Cox 2 selective NSAID?

A

Celecoxib

65
Q

Does taking NSAIDs with food help with GI disturbances?

A

There is no evidence this helps. It may actually be worse to do this bc the drug absorption is changed and people are all like, “omg I’m still in pain I’ll take more ibuprofen” and then they have a bigger dose and get worse side effects

66
Q

What NSAID inhibits aspirin’s activity?

A

Ibuprofen

67
Q

Only NSAID associated with significant adverse effects in normal clinical doses?

A

Sulindac

68
Q

NSAID with highest liver safety profile?

A

Ibuprofen

69
Q

What receptor is being targeted in NM blocking drugs?

A

Nicotinic M receptor - neuromuscular end plate

70
Q

What are the non-depolarizing agents in neuromuscular blocking drugs?

A

Atracurium, cisatracurium, D-tubocurarine, pancuronium, rocuronium, vecuronium

71
Q

Metabolic info for non-depolarizing drugs?

A

Rapid distribution, slow elimination.

Hepatically eliminated < duration than renal

72
Q

Adverse effect of atracurium?

A

Seizures from metabolic product laudanosine

73
Q

Why is cisatracurium better than atracurium?

A

Has less dependence on hepatic inactivation, produced less laudanosine so less concern about seizures

All the advantages of atracurium with fewer side effects

74
Q

Succinylcholine —what’s its deal

A

Extremely short duration of action. Rapidly hydrolyzed by pseudoxholinesterase. Very good for short procedures like intubation

75
Q

Adverse effects of succinylcholine

A

All sorts of bad stuff: hemodynamics changes, Hyperkalemia (can be lethal), prolonged blockade, increased iop and icp, muscle pain, myoglobinemia, malignant hypothermia, anaphylaxis

76
Q

Treatment of malignant hypothermia?

A

Dantrolene

77
Q

Name some Reversal agents

A

Pyridostigmine, neostigmine, edrophonium, and sugammedex

78
Q

What does sugammedex do?

A

It rapidly encapsulates steroids and reverses any depth of blockade of neuromuscular blockade. Doesn’t work against non-steroidal neuromuscular blocking agent

79
Q

Important to remember about NM blockers!

A

They don’t relieve pain or anxiety! Just paralyze.

Musculoskeletal (3 decks)

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