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Rheumatology > Pharm > Flashcards

Pharm Flashcards

1
Q

Describe the anti-inflammatory effects of steroids?

A
  • bind and block promoter sites of proinflammatory genes IL-1 alpha and IL-2 beta, interacts directly w/ specific DNA sequences and other transcription factors
  • decreased production of tumor necrosis factor alpha
  • multiple cell specific effects
  • inhibition of proinflammatory mediators:
    phospholipase A2
    cyclooxygenase 2
    nitric oxide synthetase
    prostaglandins
    leukotrienes
    thromboxanes
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2
Q

Glucocorticoid effect on leukocytes?

A
  • decreased adherence to vascular endothelium: cant exit circulation as readily, entry to sites of infection and tissue injury impaired
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3
Q

Glucocorticoid effect on other cells (neutrophils, eosinophils, monocytes, lymphocytes)?

A
  • increase in neutrophils results in increased WBC: impaired transport, increased production from bone marrow, decreased apoptosis
  • decrease eosinophils: increased apoptosis, trapped in tissues
  • decrease in monocytes: decreased tissue accumulation, decreased migration from vasculature
  • decrease in lymphocytes - inhibition of T lymphocytes
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4
Q

glucocorticoid effects of acquired immunity?

A
  • decreased ag presenting cells: macrophages, dendritic cells - really decrease T cells and also B cells
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5
Q

If on chronic glucocorticoid therapy - what vaccines are CI?

A
  • live virus vaccines:

MMR, varicella, small pox

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6
Q

What are you at increased risk for if on glucocorticoids? How does duration of therapy change this?

A
  • short term high dose therapy: immediate reduction of phagocytic responses
  • long term therapy: main infections:
    herpes zoster
    staph
    candida
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7
Q

Major SEs assoc w/ glucocorticoid therapy?

A

generally time and dose dependent:

  • derm and soft tissue: skin thinning and appearance, alopecia, acne, hirsutism, straie, hypertrichosis
  • eye: cataract, IOP, glaucoma, exophthalmos
  • CV: arrhythmias, HTN, disturbance of lipoproteins, premature atherosclerotic disease
  • GI: gastritis, PUD, pancreatitis, steatohepatitis, visceral perforation
  • Renal: hypokalemia, fluid volume shifts
  • GU and repro: amenorrhea, infertility, intrauterine growth retardation
  • bone: osteoporosis, avascular necrosis
  • muscle: myopathy
  • neuropsych: euphoria, dysphoria/depression, insomnia, mania/psychosis, pseudotumor cerebri
  • endocrine: DM, hypothalamic-pituitary adrenal insufficiency
  • infectious disease: heightened risk of typical infetions, opp. infections, herpes zoster
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8
Q

Glucocorticoid actions on the bones?

A
  • bone resorption leading to decreased bone integrity

- decreased osteoblastic activity - decreased bone formation

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9
Q

What should you monitor regularly for pts on chronic steroids?

A
  • BP
  • serum glucose
  • lipid profile
  • eye exam
  • bone density
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10
Q

Pros of steroids?

A
  • no dose adjustment needed in renal impairment

- generally give good sx relief for pain secondary to inflammation

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11
Q

What should be used for short term sx management in RA?

A
  • NSAIDs or glucocorticoids can be used

- withdrawal once DMARDs have taken effect

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12
Q

Fxn of NSAIDs in RA?

A
  • may alleviate sxs

- don’t prevent irreversible jt damage

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13
Q

Fxn of glucocorticoids in RA?

A
  • good for quick sx relief
  • generally avoid long term admin due to toxicities
  • don’t have a very profound effect on decreasing jt destruction
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14
Q

Use of DMARDs and success in RA?

A
  • variable response among pts
  • d/c rate high due to toxicity or lack of efficacy
  • in general are continued indefinitely unless sig toxicity occurs
  • categorized as biological and nonbiological
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15
Q

Nonbiological DMARDs?

A
  • methotrexate
  • sulfasalazine
  • hydroxychoroquine
  • leflunomide
  • D-Penicillamine
  • gold salt
  • azithroprine
  • cyclosporine
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16
Q

Biological DMARDs?

A
  • etanercept
  • adilimumab
  • infliximab
  • aakinra
  • abatacept
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17
Q

What should you do if there is failure to achieve remission in 3 months on DMARD therapy?

A
  • change DMARD

- or go to combo therapy

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18
Q

How long does it take DMARD to be maximally effective?

A
  • 3-6 months - assess efficacy: if undesirable results add on therapy or switch to another agent
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19
Q

Drug choice is dependent on what factors in RA (DMARDs)?

A
  • disease severity
  • prognostic factors
  • pt preference
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20
Q

DMARD of choice for initial tx of RA?

A
  • methotrexate (rheumatrex)
  • benefit seen in 2-6 wks
  • generally well tolerated
  • starting dose 7.5 mg once weekly
  • also MC used drug for RA
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21
Q

MOA of methotrexate? What needs to be supplemented?

A
  • stimulates adenosine release from fibroblasts and endothelial cells
  • reduces neutrophil adhesion
  • suppression of cell mediated immunity
  • antiproliferative effect on synovial fibroblasts and endothelial cells
  • inhibition of IL-1, IL-6, and IL-8
  • inhibits synovial collegenase gene suppression
  • structual analog of folic acid, inhibits binding of dihydrofolic acid to dihydrofolate reductase inhibiting purine synthesis
  • all pts need supplemental folic acid of 1 mg daily
  • minimal drug interactions, renal excretion, 50% protein bound
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22
Q

CIs and dosing of methotrexate?

A
  • PO, IM, SQ
  • CIs:
    women who are contemplating pregnancy
    preg
    liver disease or excessive ETOH intake
    GFR less than 30 ml/min
  • wk dosing: don’t spread the dose out over the week, otherwise liver toxicity
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23
Q

SEs of methotrexate?

A
  • hepatotoxicity
  • pulm toxicity
  • myelosuppression
  • nephrotoxicity
  • fatigue
  • decreased ability to concentrate
  • alopecia
  • nausea
  • upset stomach
  • loose stools
  • soreness of mouth
  • rash on extremities
  • HA
  • fever
  • at about 2-5 yrs up to 35% of pts have d/c drug due to SEs
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24
Q

Toxicity of methotrexate? What monitoring is done?

A
  • myelosuppression: worse if concomitant use of NSAIDs
  • hepatotoxicity including cirrhosis
  • pulm toxicity

monitoring: q 1-2 months
- CBC
- LFTs
- albumin
- Cr
- pre tx CXR

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25
Q

Use of sulfasalazine (azulfdine) for RA? MOA?

A 
- 2nd line drug for RA
 MOA:
-inhibition of PMN cell -migration
-reduced lymphocyte responses
- inhibits angiogenesis
- decreases inflammatory cytokines and IgM rheumatoid factor production
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26
Q

Metabolism and excretion of sulfasalazine?

A

30% absorbed in small bowel then excreted into feces in the bile = about 90% of drug remains in feces by time it reaches large bowel
- need coliform bacteria to break it down into sulfapyridine and 5-aminosalicylic acid

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27
Q

CI to sulfasalazine?

A
  • sulfa allergy
  • preg cat D (at full term)
  • GI or GU tract obstruction
  • porphyria
  • platelet ct less than 50k
  • LFTs greater than 3x ULN
  • hepatitis
  • men that want to conceive
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28
Q

SEs of sulfasalazine?

A

dose dependent

  • nausea and diarrhea
  • intestinal or urinary obstruction
  • oral ulcers
  • orange yellow pigmentation of skin
  • HA
  • depression
  • neutropenia
  • thrombocytopenia (this and neutropenia occurs in up to 25% of pts)
  • agranulocytosis
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29
Q

Monitoring for toxicity of sulfasalaxine?

A
  • toxicity: myelosuppression
  • monitoring:
    CBC monthly x 3
    then CBC q 3 months
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30
Q

Use of leflunomide (Avara) in RA?

A
  • antiinflammatory
  • antiproliferative
  • decreases progression of jt erosions and jt space narrowing
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31
Q

MOA of leflunomide (Avara)?

A
  • competitive inhibitor dihydrofolate reductase
  • this decreases the production of pyrimidines: decreased B and T cell proliferation
  • similar to methotrexate
  • MTX inhibits purine synthesis
  • leflunomide inhibits pyrimidine synthesis
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32
Q

Half life of Leflunomide? What should women that want to conceive do?

A
  • half life of active metabolite: 15-18 days
    washout perior for women who want to conceive is 2 yrs.
    Activated charcoal and cholestyramine can be used to reduce the half life to 1 day
  • time to response: 1-3 months
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33
Q

CI to Leflunomide?

A
  • pregnancy
  • preexisting liver disease
  • alcoholism
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34
Q

SEs of Leflunomide?

A
  • MC: diarrhea, rash, reversible alopecia, hepatoxicity
  • wt loss
  • HTN
  • bone marrow suppression
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35
Q

Toxicity and monitoring of Leflunomide?

A 
- toxicity: 
hepatotoxicity
bone marrow suppression
- monitoring:
monthly x 6 mo, then q 2 months
CBC
liver enzymes
Creatinine
36
Q

Leflunomide (avara) interactions?

A
  • weak inhibitor of CYP2C9
  • may increase warfarin levels
  • Rifampin may increase levels of leflunomide
  • bile acid sequesterants decrease effectiveness of leflunomide
  • really only use this if pt isn’t tolerating methotrexate
37
Q

What is hydroxychloroquine? When is it used?

A
  • antimalarial
  • doesn’t limit progression of RA - used as a single agent only with mild RA and no evidence of jt destruction on X-ray, and no inflammatory markers or autoimmune markers on labs - otherwise usually is add on to methotrexate
  • time to response:
    2-6 months
38
Q

MOA of hydroxychloroquine? Toxicity and monitoring?

A

MOA:
interferes w/ normal ag processing, inhibits lysosomal enzymes and IL-1 release, inhibition of PMNs and lymphocyte responses
- toxicty:
macular damage
- monitoring:
fundoscopic and visual field exams q 6-12 months

39
Q

SEs and drug interaction of hydroxychloroquine?

A 
- SEs:
nausea
diarrhea
abdominal discomfort
photosensitivity
skin pigmentation changes
rash
macular damage
- drug interactions:
decreased metabolism of BBs (except for atenolol and nadolol), may increase cyclosporine and digoxin levels
40
Q

What do you use in tx of severe RA?

A
  • use of combo DMARD therapy
  • switch to another TNF inhibitor w/ different MOA
  • may need ongoing glucocorticoid therapy
  • may need ongoing NSAIDs
  • no role for narcotic analgesics unless end stage disease
41
Q

What TNF inhibitors are used in tx of RA?

A
  • Etanercept (enbrel)
    SQ injection 1-2 times weekly, self admin
  • Infliximab (remicade): IV infusion q 6 wks
  • Adalimumab (Humira): SQ injection q 2 wks
42
Q

MOA of TNF blockers?

A
  • bind to TNF-alpha making it inactive:
    interferes w/ inflammatory activity - decreased production of IL-6 and CRP, ultimately decreasing jt damage
  • bind to surface TNF alpha, cell lysis occurs
  • time to effect: 2-3 doses
43
Q

SEs of TNF inhibitors?

A
  • injection site infections
  • infusion rxn infliximab (remicade)
  • serious infections leading to sepsis
  • don’t admin live vaccines while on meds
  • response to other vaccines may be diminishes
  • stop med until infections clear
44
Q

CIs of TNF inhibitors?

A
  • latent TB infection: BBW: need TB test b/f starting meds

- high risk for opportunistic infections

45
Q

When can remicade not be used (Interaction)?

A
  • not to be used in conjunction w/ abatacept (orencia) or anakinra (Kineret) due to increased risk of infection
46
Q

Why is infliximab used in conjunction w/ methotrexate?

A
  • b/c decreases development of infliximab abs
47
Q

Cost of TNF inhibitors?

A
  • all spendy

- etanercept - usual dose is 25 mg sq wkly or 50mg sq once wkly - $758/wk or $39, 416/yr

48
Q

Toxicity and monitoring of TNF inhibitors?

A 
- toxicity:
 injection site rxn
increased risk of local or systemic infection
- monitoring:
PPD prior to therapy
periodic CBC
49
Q

What is Anakinra (Kineret)? MOA?

A
  • immune modulator - recombinant IL-1 receptor antagonist
  • daily SQ injection
  • MOA: blocks IL-1 receptor to decrease degree of jt destruction and inflammation
  • dose response: w/in 12 wks
50
Q

Cautions w/ Anakinra use?

A
  • decrease dose in w/ GFR less than 30ml/min
  • no known pharmacokinetic drug interactions
  • don’t give in combo w/ TNF inhibitors due to increased risk of infection
51
Q

CIs of Anakinra use?

A
  • sensitivity to E coli derived proteins
  • preexisting infection or high risk for infection
  • not to be used in combo w/ TNF inhibitors
52
Q

SEs of Anakinra?

A
  • skin irritation at injection site (50% of pts): erythema, inflammation, pain
  • infection
  • possibility of angioedema and anaphylaxis
  • decrease in WBCs:
    monitoring - CBC monthly x3 then q 4 months x 1 yr
53
Q

What are the nonpreferred DMARDs?

A
  • D-penicillamine (depen, cuprimine)
  • azithroprine (Imuran)
  • cyclosporine A (sandimmune, Neoral)
  • gold compounds
54
Q

What is D-penicillamine (Depen, Cuprimine)? Role in RA?

A
  • chelating agent used for tx of: wilson’s disease, arsenic poisoning, copper, lead and mercury poisoning
  • unknown mechanism in RA other than depresses T cell activity
  • preg D
55
Q

What is Azithroprine (Imuran)? Preg? adjust dose for what? Downside?

A
  • prodrug for mercaptopurine
  • inhibitrs enzymatic actiivity reqd for DNA sythesis: decreased production of T and B cells
  • adjust dose for decreased renal clearance
  • preg D
  • major toxicity is bone marrow suppression
  • carcinogenic:
    lymphoma in post transplant pts, hepatosplenic T cell lymphoma in IBD pts
56
Q

What is the MOA of cyclosporine A (Sandimmune, Neoral)? Major toxicity? BBW?

A
  • blocks activation of T cells and IL-2
  • follow blood levels
  • many drug interaction that increase its concentration
  • sandimmune and neoral are not bioequivalent
  • major toxicity is renal failure
  • BBW: only physicians experienced in immunosuppressive therapy should rx this - SO STAY AWAY from this!
57
Q

Use of Gold compounds in tx of RA? MOA?

A
  • parenteral gold (injection) has similar efficacy but greater toxicity compared w/ other traditional (DMARDs) used in RA
  • oral gold has less efficacy than most other agents
  • starting dose for oral therapy is $1345/month
  • MOA: unknown, decreases prostaglandin production
  • mostly used as an add on
58
Q

What meds should a lupus pt avoid that may provoke exacerbations?

A
  • sulfa containing abx: sulfadiazine, trimethoprim/sulfamethoxazole
  • minocycline
  • oral contraceptives
59
Q

What meds are notorious for causing drug induced lupus?

A
  • procainamide
  • hydralazine
  • griseofulvin
  • these meds don’t seem to cause exacerbations of idiopathic lupus but may cause drug induced lupus
60
Q

Meds in lupus targeted for specific organ/system involvement?

A
  • antimalarials work for both cutaneous and MSK involvement: hydroxycholorquine, may prevent renal and CNS damage, may decrease disease flares
  • cutaneous: topical therapies whenever possible
  • MSK: NSAIDs
61
Q

What is used in lupus pt if there is sig organ involvement?

A

glucocorticoids

  • cardiopulmonary
  • hepatic
  • renal
  • hemolytic anemia
  • immune thrombocytopenia
  • other immune modulators used for severe disease and when steroid resistant: methotrexate, cyclophosphamide, azathiprine, mycophenolate, rituximab
62
Q

What should be the tx for lupus pt if antiphospholipid ab positive?

A
  • lifelong anticoag: warfarin to achieve INR of 2-3
63
Q

Tx of acute attacks of gout?

A

1 - NSAIDs
naproxen, indomethacin
2 - colchine
3 - steroids

64
Q

How can gout be prevented?

A
  • avoidance of meds that increase uric acid
  • decrease serum uric acid:
    xanthine oxidase inhibitors: allopurinol (zyloprim), febuxostat
    uricosuric drugs: probenecid
65
Q

What are the general principles of gout tx?

A
  • start meds as soon as pt perceives an attack coming on
  • ok to stop tx 2-3 days after sx resolution unless steroids then need a slower taper to prevent rebound attack
  • don’t initiate urate-lowering therapies in acute gout
66
Q

Tx in acute gout?

A
  • NSAIDs: if no CI exist (ulcers, renal failure, GI bleeding, allergy)
  • colchicine: use if CI to NSAIDs
  • corticosteroids: use if CI to NSAIDs and colchicine or if other therapies fail to resolve sxs
67
Q

MOA of NSAIDs in gout? CIs?

A
  • in general inhibit cyclooxygenase and ultimately production of mediators of inflammation: prostaglandins, prostacyclin, thromboxane
  • CIs:
    CrCl less than 60ml/min, active duodenal or gastric ulcers, heart failure, uncontrolled HTN, allergy, chronic anticoag
68
Q

NSAIDs lead to an increased risk of what? For pts on ASA what should they do?

A
  • lead to increased risk of stroke, MI, CHF, afib, CV death
  • naproxen at high doses doesn’t seem to increase CV risks but at lower doses is similar to other NSAIDs
  • risks seem to increase for long term use (over 1 month)
  • for pts on aspirin: take 1 ASA 2 hrs prior to NSAID therapy
69
Q

Duration of NSAIDs in acute gout tx? What NSAIDs are used?

A
  • key to sx relief is beginning tx at onset of sxs
  • 5-7 days of therapy is usual
  • can reduce dose if needed after good sx response
  • continue for about 2 days after complete resolution of sxs
  • Indomethacin: 50 mg TID
  • Naproxen: 500 mg BID
  • Celecoxib (celebrex) - cox2 inhibitor - less GI bleeding: 800 mg initial dose then decrease to 400 mg BID, avoid if hx of sulfa allergy
70
Q

When is colchicine (colcrys) used in gout tx?

A
  • for acute attacks
  • use if NSAID intolerance or CI
  • most likely to be effective if tx started w/in 24 hrs of sx onset
  • not beneficial for attacks ongoing for more than 72 hrs
  • if loading dose w/in last 2 wks - don’t repeat it
  • loading dose is 1.2 mg
  • followed by a dose of 0.6 mg 1 hr later then 12 hrs later move to dosing for prophylaxis 0.6 mg QD or BID
  • if already on chronic colchine and have acute attack - give a loading dose and then continue on to BID dosing
71
Q

MOA of colchicine? Metabolism, preg?

A
  • MOA: prevents activation degranulation and migration of neutrophils assoc w/ mediating some gout sxs
  • onset of action to pain relief: 18-24 hrs
  • metabolism: hepatic via CYP3A4
  • half life: 27-31 hrs
  • time to peak serum concentration: 30 min to 3 hrs
  • preg cat: C
72
Q

SEs of colchicine?

A
  • diarrhea up to 77%
  • nausea
  • vomiting
  • reversible peripheral neuropathy
  • bone marrow suppression
  • myopathy: at risk if renal dysfxn, elderly or concomitant use of:
    cyclosporine, diltiazem, verapamil, fibrates, statins
73
Q

When should you make dose adjustments of colchicine?

A
  • older than 70
  • CrCl less than 30 ml minute
  • avoid in dialysis pts

in these drugs:

  • strong CYP3A4 inhibitors: clarithromycin, itraconazole, ketoconazoel, nefazodone, HIV protease inhibitors
  • moderate CYP3A4 inhibitors: diltiazem, erythromycin, fluconazole, grape fruit juice, verapamil
  • P-glycoprotein inhibitors: cyclosporine, ranolazine, amiodarone
74
Q

CIs to colchicine?

A
  • renal impairment

- hepatic impairment

75
Q

If no relief of sxs of gout while on colchicine what should you od?

A
  • add on glucocortiocoid if no relief after 24 hrs

- or may be used cautiously in conjunction w/ an NSAID (if not CI)

76
Q

Types of glucocortiocoids used in gout?

A
  • intraarticular
  • oral: for those who can’t take NSAIDs, colchicine and not candidates for jt injection
  • prednisone 30-50 mg daily until resolution then taper off over a wk
  • IV or IM: if not a candidate for any other route or med
77
Q

What is used as management b/t gout attacks?

A
  • avoidance of meds that increase uric acid or inhibit renal excretion of uric acid:
    thiazide and loop diuretics
    niacin
    aspirin
  • meds to reduce serum uric acid are indicated if:
    2 or more episodes/yr
    tophi
    chronic kidney disease, stage 2 or greater
78
Q

How long should you wait after an acute attack of gout b/f initiating prevention therapy? What can this stimulate?

A
  • wait 2 wks
  • initiation of antihyperuricemic therapy can stimulate a gout attack
  • lowering the uric acid levels too quickly can stimulate a gout attack
  • prophylactic colchicine therapy is used when initiating urate lowering therapy to reduce attacks:
    colchicine 0.6 mg qday to BID
79
Q

When is allopurinol used? what is goal for serum urate level?

A
  • agent of choice for urate lowering
  • xanthine oxidase inhibitor
  • goal for serum urate level is less than 6 - check 2-4 wks after dose adjustment, recheck in 3 months to confirm, recheck q 6 months to yearly
80
Q

MOA of allopurinol?

A
  • inhibits xanthine oxidase needed for eventual conversion of hypoxanthine to uric acid
  • onset of action: 1-2 wks
  • half life: active metabolite: 18-30 hrs
  • adjust dose for renal impairment:
    100mg daily for CrCl over 60ml/min
    lower dose for less than 60ml/min
  • normal adult dosing:
    100 mg/day and increase weekly to 200-600mg/day depending on disease severity and urate levels
81
Q

SEs of Allopurinol?

A
  • skin rash: D/C drug
  • gout attack
  • diarrhea
  • nausea
  • elevated liver enzymes
  • hypersenitivity rxns (SJS):
    ACEI, amoxicillin/ampicillin, diuretics
  • bone marrow suppression:
    use w/ caution w/ other drugs that cause myelosuppression
  • hepatotoxicity
82
Q

When is probenecid used? MOA? CI?

A
  • 2nd line agent if unable to take allopurinol
  • uricosuric agent
  • blocks tubular reabsorption of filtered urate and increases uric acid excretion by the kidney
  • not effective if CrCl less than 50ml/min
  • CI: hx of nephrolithiasis (uric acid or Ca stones)
83
Q

Drug interactions w/ probenecid? Prevention of uric acid stones?

A
  • lots of drug interactions: causes an increase in concentration of other drugs - PCN
  • to prevent development of uric acid stones - pt education to increase fluid intake, may need an agent to alkalinize the urine - potassium citrate to maintain urine pH over 6
84
Q

What meds decrease uric acid levels?

A
  • losartan
  • fenofibrate
  • vitamin C 500mg daily
  • cherries
85
Q

NSAIDs and steroids cause what? and what can this cause? What should you monitor?

A
  • they cause fluid retention
  • cause HTN
  • may cause sig CHF exacerbations
  • many hosp admissions for CHF have been caused by admin of these meds
  • need to monitor closely for edema in pts at high risk for fluid retention and may need to adjust usual diuretic doses during tx

Rheumatology (8 decks)

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