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OS4-MS/Derm/Rheum > Pharm > Flashcards

Pharm Flashcards

1
Q

Which two DMARDs are contraindicated in pregnancy?

A

MTX and Leflunomide

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2
Q

Use of which DMARD would require a pt to have regular ophthalmologic exams?

A

Hydroxychloroquine

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3
Q

A reduced capacity to form MHC-peptide protein complexes with subsequent immune down regulation is the mechanism of action of this DMARD:

A

Hydroxychloroquine- raises pH of intracellular vacuoles where these MHC-peptide complexes occur. The rise in pH is not conducive to MHC-peptide bonding.

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4
Q 
Unexplained coughing or shortness of breath is a side effect most likely to be reported by pts taking:
MTX
Hydroxychloroquine
Leflunomide
Sulfasalazine
A

MTX - listen for “cellophane-like crackles posteriorly at the bases of the lungs on inspiration/expiration. MTX can also cause inflammation & fibrosis, but so can RA.

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5
Q

Which monoclonal antibodies (and one fusion protein) block the actions of TNF-a?

A 
Adalimumab
Certolizumab
Golimumab
Infliximab
Etanercept
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6
Q

Which Mab blocks CTLA-4 - B7 interaction?

A

Abatacept

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7
Q

Which Mab inhibits the action of IL-6?

And IL-1?

A

Tocilizumab (IL-6)

Anakinra (IL-1)

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8
Q

Which Mab inhibits action of CD20?

A

Rituximab

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9
Q

What biologic DMARD inhibits PDE4?

A

Apremilast

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10
Q

A pt receiving biological tx for RA who experiences a rapid decline in B cell numbers would most likely be taking:

A

Rituximab

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11
Q

A physician treating a pt for RA with a biological agent should be vigilant for signs of:

A

Blood dyscrasias & malignancy

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12
Q

During tx with a biological agent for RA, a pt should be advised to avoid:

A

Vaccines - their immune system is not strong enough to elicit the appropriate Ab response.
Also stop smoking because it decreases the efficacy of the DMARDs. Also, smoking is gross.

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13
Q 
When used during pregnancy, which of the following would most likely produce fetal adversity?
Anakinra
Etanercept
Rituximab
Tocilizumab
A

Rituximab- crosses placenta and can diminish fetal B cell population

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14
Q

Which Mab is contraindicated in pts with existing CV issues?

A

infliximab

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15
Q

Celecoxib was developed as a COX 2 inhibitor to replace indomethacin (COX neutral), which was shown to have this adverse effect: (Celecoxib does NOT do this)

A

increases bleeding time, increased CV risk

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16
Q

What is special about the NSAID Piroxicam when used in combination for tx of RA?

A

long half-life, convenient dosing schedule

17
Q

Reduction in the risk of GI erosion and bleeds is afforded by combining a traditional NSAID with:

A

proton pump inhibitor
Prostacyclin analog
H2 receptor blocker

18
Q

Ringing in the ears is a clear sign of ______ toxicity.

A

Salicylate

19
Q

Describe lethal salicylate toxicity.

A

High enough concentrations can cross the BBB, stimulate the respiratory center, resulting in respiratory alkalosis. But toxic buildup of salicylic acid within cells, disrupting intermediary metabolism, will cause metabolic acidosis. Then you get cerebral edema resulting in multi-organ failure.

20
Q

Which NSAID is most likely to cause hepatotoxicity at normal clinical doses?

A

Sulindac- 5-fold greater risk

21
Q

Describe how NSAID therapy could negatively impact the kidneys.

A

They block the production of prostacyclin, which is involved in microregulation of kidney perfusion in times of stress.

22
Q 
Appropriate lab tests for pts on NSAID therapy for RA include all of the following except:
LFTs
CBCs
Serum BUN/Cr
Vision
A

Vision

23
Q 
Pts should be screened for which of the following prior to initiating tx with glucocorticoids?
Ankle edema
Elevated BUN
Arrythmias
Anemia
A

Osteoporosis
Ankle edema
Glaucoma risk
pre-tx fasting blood (Glu?) levels

24
Q

How does colchicine treat/prevent acute gouty flare-ups?

Describe the negative side effects.

A

With its anti-microtubule function, colchicine inhibits neutrophil motility and thus prevents/attenuates the inflammatory response to the buildup of gout crystals.
colchicine only useful in gouty arthritis
Side FX:
GI disturbances (acute)
Blood dyscrasias (chronic)
Proximal weakness and elevated serum CPK (neuropathic)

25
Q

How does indomethacine work?

Describe the negative side effects.

A

It is a COX inhibitor, thus inhibiting production of prostaglandins that cause joint damage. (analgesic/antipyretic) Good for use in acute attacks.
Also inhibits leukocyte motility.
Side FX:
GI- ulcers, n/v.
CNS- severe frontal headache
Hematopoietic disorders
Antagonizes actions of furosemide & HCTZ

26
Q

How does allopurinol work?

Describe the adverse side effects.

A

Competetive inhibitor of xanthine oxidase. So, it prevents conversion of hypoxanthine —> xanthine, as well as xanthine —> uric acid.

SFX:
increases incidence of acute gout (due to mobilization of urate from joints & tissues)
hypersensitivity rxns
interacts with 6-mercaptopurine and penicillins.
Effects on liver function

27
Q

Which drug has better affinity for xanthine oxidase in both its oxidized and reduced forms and has less shitty side effects compared to allopurinol?

A

Febuxostat (Uloric)

mild SFX. elevated liver enzmes (x3) in 2-3% of pts

28
Q

How does the uricosuric agent Probenecid work?

Which drug reduces the efficacy of Probenecid?

A

Inhibits reabsorption of urate in the PCT of the kidney nephron.
Salicylates (aspirin) reduce probenecid efficacy.

29
Q

What the heck is pegloticase?
Why does it suck sometimes?
How do doctors make it suck less?

A

Pegloticase is a pegylated form of a pig urate oxidase. Urate oxidase acts to convert urate (uric acid) to allantoin. Unfortunately for humans (mortals), they do not have this magical enzyme. So, people in lab coats extract this agent from the anal pores of swine and then inject it into the veins of mortals. Mortals pay over $30,000 a year for this porcine anal extract.
Pegloticase has some untoward side effects such as flare ups of gout (omg the irony). This is attributable to the fact that pegloticase causes UA tophi to dissolve, which pisses off neutrophils which release angry cytokines resulting in inflammation. We can mitigate these effects by administering colchicine, NSAIDs, or steroids concurrently to prevent the flare ups.

30
Q

What is the MOA of infliximab?

A

binds to and neutralizes both soluble and TM TNF

31
Q

Describe the principal organ toxicities with chronic NSAID use, and ways to mitigate such effects.

A

GI tox = gastric ulcers, bleeding, iron deficiency; to mitigate - use enteric coating, PPI/H2 antagonist, or COX-2 selective agent
Hepatotox = hepatitis, mixed damage, cholestasis, ductopenia; incidence is low
Renal tox = renal ischemia/failure for messing with the PGI2/E2 synthesis needed for autoregulation of microvasculature; to mitigate -

32
Q

How does combined NSAID and low dose ASA treatment increase CV risk?

A

there is the potential for NSAIDs to inhibit the ability of ASA to reach its binding site in the platelet and irreversibly inhibit. Since most NSAIDs are reversible, you could lose antiplatelet activity and gain inc. CV risk.
SO you think you’re permanently inhibiting the platelets with your ASA, but maybe the NSAID got there first and falls off, then platelets are not inhibited anymore.

33
Q

Indicate the risk factors for GI AEs when a patient is taking NSAIDs.

A

age, male, hx of GI disorder, use of the following: ASA, warfarin, CSs, SSRIs, venlafaxine, or duloxetine; comorbidities of CVD, HTN, DM, liver/renal impairment; prolonged NSAIDs, H. pylori infxn, excess EtOH, heavy smoking

34
Q

Describe the MOA of Sulfasalazine.

A

a DMARD that is metabolized to sulfapyridine and mesalamine (by colonic bacteria) which have anti-inflammatory properties; beware the hypersensitivity reaction of sulfa drugs, and renal dysfunction

35
Q

Describe the MOA and AEs of Leflunomide.

A
  • its metabolite inhibits dihydroorotate dehydrogenase, a mitochondrial enzyme that catalyzes a step in de novo pyrimidine synthesis, and cell cycle arrest in B and T cells
  • elevated LFTs with chronic use, category X drug
36
Q

In what conditions is Hydroxychloroquine used?

A

malaria, RA, and SLE

37
Q

How do corticosteroids contribute to osteoporosis?

What can mitigate the risk of fractures?

A
  • CSs are a DMARD that act to increase the transcription of RANKL and GM-CSF, which activates osteoclasts and increases bone resorption
  • begin anti-osteoporotic therapy asap and maintain good nutrition (Ca, protein, Vit D)
38
Q

What is Apremilast used for, and what is its metabolism/elimination route?

A
  • used in the tx of plaque psoriasis and psoriatic arthritis

- hepatic metabolism, elimination in both urine and stool

OS4-MS/Derm/Rheum (10 decks)

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