Week 7: Gout, Osteoarthritis, Rheumatoid Arthritis, SLE Flashcards

Question

General Chronic Gout pharmacotherapy Febuxistat (Urolic) moa: dosage: AE: CI: DDI: Considerations:

Answer 1

General Chronic Gout pharmacotherapy moa: chemically engineered selective xanthine oxidase inhibitor dosage: starting: 40 mg once daily; may increase to 80 mg qd in pts who do not achieve serum uric acid level <6 mg/dL after 2 weeks AE: headahce, arthtalgias, abd. pain, NV, abnormal lft, FLUSHING AND DIZZINESS CI: 6-MP, azathiopurine, theophylline DDI: 6-MP, azathiopurine, theophylline (febuxistat inc levels of these) Considerations: BBW: inc. cv death in pts with cv disease *theoretically can be used in ppl with allopurinol hypersensitivity, not sturcturally related. *no dose adjustments required for mild-mod renal or hepatic impairment. use caution in severe hepatic impairment or crcl<30 *concam nsaid or colchicine ppx may take up to 6 mo. to help prevent gout flares per package insert *if gout flare occurs, febuxistat doesnt need ot be d/c

Answer 2

General Chronic Gout pharmacotherapy Probenacid moa: inhibits reabsoprtion of uric acid at proximal conviluted tubule, increasing excretion dosage: 250 mg bid for 1 wek, may incr to 500 mg bid if needed, may increase to a mac od 2g/day (increase in 500 mf increments q4w) AE:-- CI: *Crcl<50 mL/min, *hx of nephrolithiasis * use of pcn, methotrexate, carbapenems (doripenem, meropenem) (inc conc due to decreased renal secretion *salicylates, decreased efficacy of probenecid DDI:use of pcn, methotrexate, carbapenems (doripenem, meropenem) (inc conc due to decreased renal secretion *salicylates, decreased efficacy of probenecid Considerations:--

Answer 3

General Chronic Gout pharmacotherapy Pegloticase moa: pegilated recombinant uricae: converts uric acid to allantolin so it can be excreeted dosage: *IV: 8mg q2w over atleast 2 hrs AE:infusion rections, anaphylaxis CI:-- DDI:-- Considerations: BBW: can cause anaphylaxis and infusion reactions *occurs within 2 hrs *premed w. antihistamines or corticosteroids *ppx w. low dose colchicine or nsaid x 6 mo

Answer 4

acute gouty arthritis attaks should be treates w. pharm therapy pharm treatment should be initiated ithin 24hrs of acute gout attack onset ongoing pharm urate lowering therapy (ULT) should not be interrupted during an acute gout attack

Answer 5

1. assess severity A) if pt has mild(0-4)-mod(5-6) pain, and an attack effecting 1 or few small joints, or 1-2 Large joints->can consider monotherapy B) if pt has severe (7+) pain, and polyarticular attack or an attack affecting multiple large joints-> can consider initial combo therapy (will discuss in another card) 2) Selecting Monotherapy a)NSAID b)Systemic corticosteroid c) colchicine ***supplementation w. topical Ice for any gout attack 3) Assess treatment outcome A) if inadequate response-> *consider switching to alternate monotherapy *consider combo therapy B) if successful outcome *pt education: including diet and lifestyle, role of uric acid excess in gout and as key treatment target; prompt self trt of subsequent acute gout attacks *consider indications for ULT or adjustment of ongoing ult

Answer 6

If pt has not been on ppx colchicine or not treated w. colchicine for an acute attack in the last 14 days.. can use oral colchicine: *1.2 mg, then 0.6 mg 1 hr later * then gout attack ppx can be started(0.6 mg po qd or bid), beginning 12 hrs or later, and continued until the acute gout resolves if pt is on ppx colchicine or has recieved colchicine for an acute attack w.in the past 14 days.. *choose alternative therapy (NSAID or coricosteroid)

Answer 7

full fda or ema approved dose of nsaid or a cox2 inhibitor... *continue intitial trt at full dose until gout attack has completely resolved

Answer 8

1) assess extent of joint involvement A) if 1-2 large joints: can consider IA CCS B) all cases of gout: ORAL: a)prednisone 0.5 mg/kg/day *duration: 5-10 dys then stop OR 2-5 days at full dose then taper for 7-10 days then stop b) methylprednisolone dose pack (6 day course) IA: dose dpeends on joint size (w. or w.o oral trt) IM: traiamcinolone acetonide 60 mg, then oral prednison as above (WONT BE TESTED ON THIS)

Answer 9

consider if *severe attack (polyarticular) *pts not responding to initial monotherapy recommended combos *nsaid +colchicine *PO CCS+ colchicine *IA CCS+ NSAID+/- colchicine *IA CCS+ PO CCS_/- colchicine NOTE: DO NOT USE PO NSAID AND PO CCS AS COMBO THERAPY

Answer 10

not all pts require chronic therapy lifestyle modification recommended for all pts, regardless of disease activity chronic therapy=UA lowering therapy +Flare prophylaxis *UA lowering therapy can illicit flares because remodeling of crystal deposits can dislodge? and trvael illiciting a flare elsewhere *ppx flare therapy should be given concaminanly w. Uric acid lowering therapy (ULT) chornic therapy shuold not be stopped during flare

Answer 11

Stay hydrated Exercise Encourage smoking cessation Healthy overall diet *Limit alcohol intake *limit purine intake (sweetbreads, liver, kidney, sardine, shellfish) *limit high fructose corn syrup *encourage lowfat or non fat dair products, vegetables weightloss program if overweight or obese

Answer 12

>1 sq tophi, radiographic evidence of dmaage attributable to gout OR frequent flares (>/2 /years) may consider trt if... hx of >1 attack, but <2 attacks per year those w. first gout flare w. following characteristics AND any of these CKD stage 3 UA> 9 mg/dL urolithiasis (kidney stones) if decision is made tht pt needs ult duraing a flare, it shouldbe initiated during a flare

Answer 13

goal serum urate level: <6 mg/dL allopurinol is 1st line gaent UA levels should be monitored q 2-5 weeks w. increases in ULT intensity until goal is reached *increase dose of XOI, add probenecid if appropriate therapy required to reach goal of <6mg/dL shoul dbe continued indefinately

Answer 14

XOI trt, uricosurics, and other interventions failed to achieve goal UA levels, and pt continues to have >/2 flare/yr OR non reslovng tophi

Answer 15

pps w. antiinflammatory meds should be intiated when ULT is intiated same agents as for flare trt at diff dose shold be continued for 3-6 mo. based on resolution of symptoms and absence of tophi

Answer 16

when to initiate: *w. or just prior to initiating ULT CHOICES: a)first line *low dose colchicine 0.6 mg qd or bid OR *low dose nsaids (ex naproxen 250mg) b) second line *low dose prednisone or prednisolone (

Answer 17

disease of elderly as ppulations age common: 1/5 ppl have OA by 2040, 25.9% will have OA expected reletavily expensive condition $9233 per person

Answer 18

obesity sex: men at oyungr, female at older occupations (jobs that ave regular mechanical stress) participation in certain sportss joint injury or surgery genetic predisposition

Answer 19

Under normal conditions, cartilage matrix is subjected to a dynamic remodeling process in which low levels of degradative and synthetic enzyme activities are balanced, such that the volume of cartilage is maintained. In OA cartilage, however, matrix degrading enzymes are overexpressed, shifting this balance in favor of net degradation, with resultant loss of collagen and proteoglycans from the matrix

Answer 20

Idiopathic (primary): no known cause Secondary (classified by cause) *note: can also be classified by joint involvement

Answer 21

traumatic (accidents) gongenital/genetic: metabolic: pagets disease, wilsons disease, nutritional defficiencies neuropathic: Charcot arthropathy HEmatologic: Hemophilia, sicklecell disease Other: Gout, RA

Answer 22

hand pain, aching or stifness and 3 or 4 of following treatments 1)hard tissue enlargement of 2 or more of 10 selected joints 2)hard tissue enlargement of 2 or more DIP joints 3)fewer han 3 swollen MCP points 4)deformity of atleast 1 of 10 selected joints

Answer 23

signs bony enlargement of affected joints of affected joints *heberdens nodes (develop slowly, non painful, lateral and medial aspects of the joint) *bouchards nodes: same as heberdens nodes, at diff locations limitation of range of motion crepitus w. motion pain w. motion malalignment and/or joint deformity

Answer 24

most common cause of arthritis and chronic disability among older ppl in US radiographic abnormalities present in >30% persons>65 y.o symptomatic kknee OA occurs in ~10% of ppl >65 yo leading indication for >250k total knee arthroplasties in US / year

Answer 25

JOINT PAIN MORNING STIFFNESS JOINT INSTABILITY LOSS OF FUNCTION OCCASIONAL SYNOVITIS bowleggednes (vargus) knock knees (valgus)

Answer 26

clinical classification knee pain and atleast 3 of following 6 criteria 1. >50 yo 2.stiffness lasting <30 min 3. crepitus (grating sound produced by friction of bone 4.bony tenderness 5.bony enlargement 6. no warmth to touch *not most sensitive, least

Answer 27

clinical and lab classification knee pain and atleast 5 of following 9 criteria 1. >50 yo 2.stiffness lasting <30 min 3. crepitus (grating sound produced by friction of bone 4.bony tenderness 5.bony enlargement 6. no warmth to touch 7. esr <40 MM/HR 8. rf<1:40 9. Synnovial fluid: clear, viscous, or wbc <2000/mm^3

Answer 28

atleast 1 of following of 3 *age>50 y,o *stiffness <30 min *crepitus AND osteophytes (detected by radiography) least sensitivity, most specific (negatives are true negatives)

Answer 29

HIP PAINand atleast 2 of folowing 3 features *esr<20 mm/hr *radiographic femoral or acetabular osteophytes *radiographic joint space narrowing (superior, axial and/or medial) 89% sensitivity and 91 percent specitivity

Answer 30

hip pain: gradual onset, increases with joint use, relieved (incompletely) with reset as the disease becomes more severe: *morning stiffness and pain (up to 30 min) *pain at rest or at night are common STRONFEST clinical indicator is pain exacerbated by intern or external rotation of the hip while the knee is in full extension

Answer 31

can use more than one modality consider pt comfort exercise, braces, etc. *un

Answer 32

storngly recommended *exercise *self efficacy and self management programs *first carpometacarpal (CMC) orthosis conditionally recommended: *heat or tpx cooling *cbt *acupuncture *kinesiotaping *hand orthosis other than CMC *paraffin

Answer 33

storngly recommended exercise self efficacy and self management programs weight loss(if overweight) Tai-Chi Cane Tibiofemoral (TF) brace for TF OA conditionally ecommended *heat, tpx cooling cbt acupuncture kinseotaping balancetraining yoga patellofemoral (PF) knee brace for PF OA radiofrequency ablation

Answer 34

strongly recommended exercise self efficacy and self management programs weightloss (if overweight) tai chi cane conditonaly recommended heat tpx cooling cbt acupuncutre balance training yoga

Answer 35

duration, intensity, frequency *unknown *driven by what pt is comfortable with pt preference patient access possible options *walking *stationary bike *isokinetic(dynamic contraction, speed control), isometric (static tension, maintains strength) *rsistance training w. or w.o props *aquatic exercise

Answer 36

multi disciplinary group based on skill building and education skill building *goal setting *problem solving *positiv thinking education *fitness goals *joint protection *medication

Answer 37

Hand orthosis: goes over cmc joint: supporting joint kinesiotaping: functions similarly to a brace but more flexible in terms of movement. tape supports hand and muscle of hands or knees parrafin: wax that heats up braces: tibiofemoral (TF) *patellofemoral (PF)

Answer 38

knee OA: TTENS(transcutaneous electrical nerve stimulation (TENS) conditionally recommened against: manual therapy (w. or w.o exercise) massage therapy modified shoes wedged shoes pulsed virbation therapy hand OA conditionally recommended against *iontophoresis hip OA: strong recommended against TENS conditionally recommended against manual therapy (w. or w.o exercise) massage therapy modified shoes wedged insoles

Answer 39

no disease modifying agents for OA meds are for pain relief

Answer 40

(strongly recommended therapy)SRT: oral NSAIDS lowest possible dose thats effective for shortest duration as possible conditionally recommended therapy (CRT) topical NSAIDS IA CCS APAP TRamadol duloxetine chondroitin

Answer 41

A)proprionic derived nsaids *ibuprofen naproxen ketoprofen fenoprofen oxaprozin b)acetic acid derived nsaid indomethacin diclofenac ketorolac etodolac sulindac tolmetin c)fenmates derivatives *meclofenamate mefenamic acid enolic acid derivatives peroxicam meloxicam alkanone derivatives *nabumetone

Answer 42

SRT: oral NSAIDS topical NSAIDs IA CCS CRT: APAP tramadol duloxetine topical capsaicin

Answer 43

srt: oral NSAIDS IA CCS (guided by imaging) crt: APAP tramadol duloxetine

Answer 44

sra: biphosphonates glucosamine hydrochloROQUINE methotrexate tnf inhibitors il-1 receptor antagonists cra: IA hyaluranoic acid colchicine non-tramadol opioids fish oil vit d topical capsaicin

Answer 45

sra: biphosphonates glucosamine hydrochloROQUINE methotrexate tnf inhibitors il-1 receptor antagonists platelet rich plasma stem cell injection chondroitin cra: IA hyaluranoic acid IA botulinum toxin prolotherapy: injection of hypertoinc dextrose colchicine non-tramadol opioids fish oil vit d topical capsaicin

Answer 46

sra: biphosphonates glucosamine hydrochloROQUINE methotrexate tnf inhibitors il-1 receptor antagonists platelet rich plasma stem cell injection chondroitin IA Hyaluronic acid cra: IA botulinum toxin prolotherapy: injection of hypertoinc dextrose colchicine non-tramadol opioids fish oil vit d topical capsaicin

Answer 47

consider pt factors *what has worked in the past? *what is the pt comfortable doing *what other conditions does the pt have? ex: HTN, cv disease, HF, CKD, GI bleeding risk etc.

Answer 48

symptoms present for >6 weeks warmth and swelling over affected joints with or w.o pain prolonged morning stiffness>30 min fatigue weakness, decreasedmood, low-grade fever positive rheumatoid nodules joint deformity in late disease

Answer 49

MOST COMMONLY EFFECTS small joints (hands wrist, ankles and feet bilaterally larger weight beighring joint sless commonly effected

Answer 50

ANTI-CITRULLINATED PROTEIN ANTIBODIED (acpa): 96% in ra rheumatoid factor (RF):70-80% in ra antinuclear antibodies (ANA): ~20% in ra also... elevated nonspecific inflammatory markers such as ESR, CRP synovial fluid analysis wbc1500-25000m//^3

Answer 51

CHALENEGES: no single tet or physical finding *early detection is difficult acr/eular criteria: *serology/acute phase reactants *duration of SS *joint involvement

Answer 52

Disease activity Score scale 0 to 9.4 high disease activity :>5.1 mod diseasy activity: >/3.2 to /2.6 to <3.2 remission: <2.6

Answer 53

age: *RA: varibale *OA:>50 y.o onset: *RA:VRIABLE *OA:gradual development: *RA: autoimmune *OA: wear and tear SS; *RA: constitutional and joint *OA: localized to joint Joint involvement: *RA:small joints of hands, wrists and feet *OA: large weight bearing joints joint stiffness: *RA:>30 min *OA:<30 min joint pain: *RA:w. use and at rest *OA:w. use symmetry *RA: bilateral *OA:unilateral auto antibodies *RA: present *OA:none

Answer 54

treat to target approach w. low disease activity as an acceptabletarget improve SS of joint pain and stiffness by reducing inflammation slow disease progressionand prevent joint damage

Answer 55

REST weight loss physical and occupational therapy *assistive devices *exercise *physiotheraoy patient education *surgery-severe ra *tendon repair, arhtroplasty, tenosynovecotomy

Answer 56

NSAIDS *decrease joint pain and inflammation *acute ysmptom relief *adjunct to disease modifying agents CCS: *decrease joint pain and inflammation bridge to disease modifier *short term high doses or flares *long term low doses for refractory diseasse **prefer to ass or switch disease modifier

Answer 57

Conventional synthetic csDMARDS: *mathotrexate, hydroxychloroquine, sulfasalzine, leflunomide *others: gold salts, minocycline, CsA, cyclophosphamide, D-penicillamine biologic dmard *TNF inhibitors (etanercept, infliximan, adalimumab, golimumab, certolizumab *non tnf inhibitors (abatacept, rituximab, tocilizumab, anakinra, sarilumab) targeted synthetic (tsDMARD; JAK inhibitors) *tofacitinib, baricitinib, upadacitinib

Answer 58

INITIATE CSdmards within 3 mo of onset of persistent symptoms short term CCS for bridging to dmard onset *guidelines recommendavoind CCS theraoy if possible, however many pts require a short course for symptm relief step up strategy *additional dmards when disease burden not adequately controlled treat to target approach *remission may not be achievable in all pts

Answer 59

1)assess disease activity if pt is dmard naive: a) low disease activity: *csdmard monotherapy: HYDROXYCHLOROQUINE (HCQ) *alternative (selfasalazine>mtx>leflunomide b)mod-high disease activity *csmard monotherapy: MTX 2) is pt at target of low disease activity or remission? YES: continue regimen *must be at traget for atleast 6mo before dose reduction/dmard d/c continue >/1 dmard due to risk of disease progression *if d/c, d/c gradually *if symptoms return, reinitiate dmard NO: *if non mtx csdmard monotherapy.. switch to mtx *if oral mtx not at target-> switch ot sq mtx over addition to another dmard *if absence of poor prognostic factors-> add csdmard *if poor prognostic factors-> add bdmard or tsdmard 3) is pt at low disease acivity or remission YES: continue regimen NO: *optimize above therapy, then: add/switch to bdmard or tsdmard or a diff class asssess DMARD use for efficacy q3 mo

Answer 60

persistent mod-high disease activity score despite csdmard high acute phase reactant levels high swollen joint count presence of rf and/or ACPA, especially at high levels presence of early erosion failure of 2 or more csdmards

Answer 61

csDMARDS MTX indication: 1st line csdmard of choice except in dmard naive pt w. mod-severe disease activity moa: folate antagonist dosing: 7.5 mg PO qw titrated to >/15 mg weekly w.in 4-6 weeks *if unable to tolerate weekly oral dose, split oral doseover 24 hr orswitch to sq AE: *NV *stomatitis *dizziness/faituge/headache *pneumonitis/pulmonary fibrosis *myelosupression *immunosupression *hepatotoxicity/inc. lfts *alopecia *rash CI: pregnancy and breastfeeding, liver or renal impairment, immunodeficiency, myelosupression onset of effect: 1-2 months considerations: *folatesupplementation decreases ADR w.o reducing efficacy

Answer 62

csDMARDS HCQ indication: usually used in combo w. other dmards or as monotherapy for low disease activity moa: unkown, but inhibits cytokine production dosing: *initial: 400-600 mg po daily *maintenance: 200-400 mg po daily or divided doses AE:NVD, qtc prolongation, irreversible retinal damage, photosensitivity CI: ocular disease-dose dependent retinopathy liver disease onset of effect:2-4 months considerations: *may be used in pregancy 8preferable risk profie compared to other dmards

Answer 63

csDMARDS sulfasalazine (SSZ) indication: monotherapy or in combo w.other dmards moa:unkown: acive metabolites (sulfapyridine and 5-asa) responsible for anti inflammatory properties dosing: 500-1000 mg po daily (up to 3g has been used) AE: nv abdominalpain, anorexia headache reversible oligospermia rash, puritis, urticaria, blood dyscrasias CI: sulfa allergy, intestinal or urinary obstruction, renal and caution in hepatic impairment onset of effect: 1-3 mo considerations: *preffered dmard in pregnancy

Answer 64

csDMARDS LEF indication: mono or ocmbo w. other dmards moa:inhibits pyrimidine synthesis->decrease lymphocyte proliferation dosing: loading dose: 100 mg PO once daily for 3 days maintenance dose: 10-20 mg po daily AE: NVD reversible alopecia rash peripheral neuroathy htn CI: pregnancy and breastfeedings (teratogenicity across genders)-> levels may take months to decrease *liver disease onset of effect:1-3 months considerations: long t1/2, may be detectable for up to 2 years *cholestyramine rmoves drugs and its active metabolites

Answer 65

monitor cbc lfts and scr based on duration of therapy MTX, LEF, SSZ <3mo: q2-4w 3-6 mo:q8-12w >6 mo:q12w HCQ: none after baseline additoinal specific drug monitoring: MTX: r/o pregnancy, chest xray at baseline HCQ: opthalmologic exam at baseline and q3mo SSZ: r/o G6PD deficiency at baseline LEF: r/o pregnancy at baseline

Answer 66

geenrally well tolerated but costly target pro inflammatory cytokines *TNF-a, IL-1, IL-6, B cells, T cells when to use based on algorithm: mod-high disease activity despite dmard monotherapy unable to tolerate / ci TO CSDMARD adequate trial :tnfI biologics: 3 mo non tnfI biologics: 6 mo

Answer 67

etanercept (Enbrel) adalimumab (humira) golimmumab (simponi) Certolizumab (Cimzia)

Answer 68

TNF-a biologics-sub q options drug: etanercept (enbrel) dosing: 50 mg weekly OR 25 mg twice weekly use w. mtx: w. or w.o common ADR:pancytpenia, injection site rxn, diarrhea, rash

Answer 69

TNF-a biologics-sub q options drug: dosing:40 mg q2w. if no mtx, 40mg weekly use w. mtx: w. or w.o common ADR: sinusitis, urti, antiboy formation, injection site reaction, hadache, rash

Answer 70

TNF-a biologics-sub q options drug: dosing: 50 mg once monthly use w. mtx: must be w. methotrexate common ADR: URTIE, nasopharyhgitis, antibody formation, injection site reaction

Answer 71

TNF-a biologics-sub q options drug: dosing: 400 mg at 0,2,4 weeks then 200 mg q 2 weeks use w. mtx: with or without common ADR: URTI, UTI, antibody formation, dizziness, htn, rash

Answer 72

Inflixumab (Remicade) Golimumab (Simponi Aria)

Answer 73

TNF-a biologics- IV options drug: dosing: 3mg/kg over /> 2 hrs at 0, 2, and 6 weeks then 3-10 mg/kg q4-8weeks use w. mtx: must be used with methotrexate common ADR: URTI, infusion related reactions (premedicate w. antihistamine, APAP, CCS), headache, abdominal pain, antibod formation

Answer 74

TNF-a biologics- IV options drug: dosing: 2mg/kg over 30 min at weeks 0, 4, then 2 mg/kg q8weeks use w. mtx: preffered w. methotrexate common ADR: URTI, ALT/AST elevation, HTN, rash, neutropenia, antibody formation

Answer 75

BBW *risk of malignancy-> lymphoma and other malignancies *serious infections leading to hospitaliztion or death-> opportunistic fungal viral, and bacterial functions May lead to exacerbations of *MS/MS like symptoms *SLE/ SLE like symptoms *HF-> avoic in NYHA class III or IV of LVEF<50% Latent TB and HepB infections-> screen all pts for tb and hepatitis b before intiaition

Answer 76

abatacpt (orencia) sarilumab (kevzara) toclizumab (Actemra) Anakinra (Kinret)

Answer 77

non -TNF-a biologics- sq options drug: dosing: 125 mg once weekly cell target: t cells common ADR: URTI, headache, nasopharyngitis, nausea

Answer 78

non -TNF-a biologics- sq options drug: sarilumab dosing: 200 mg q2w cell target: IL-6 inhibitor common ADR: URTI, UTI, injection site erythema, neutropenia, increased LFTs, antibody formation

Answer 79

non -TNF-a biologics- sq options drug: dosing: <100 kg: 162 mg qow (increase to weekly as tolerated) >/100 kg: 162 mg cell target: IL-6 common ADR: URTI, nasopharyngitis, headache, HTN, increased LFTs, increased lipids

Answer 80

non -TNF-a biologics- sq options drug: dosing: 100 mg once daily cell target: IL-1 common ADR: URTI, rash, pyrexia, influenza like illness, gastroenteritis, vomiting, antibody formation note: limited use given reduced efficacy compared to other bdmardS

Answer 81

all used as monotherapy or w. non biologic dmard

Answer 82

non -TNF-a biologics- IV options drug: dosing: wieight based dosing at 0,2, and 4 weeks, then q4 weeks cell target: t cells common ADR: URTI, nasopharyngitis, nausea, htn, infusion reaction note:--

Answer 83

non -TNF-a biologics- IV options drug: dosing: 1g at 0, 2, weeks (one cycle); may repeat cycle q16-24 weeks based on response cell target: anti-cd20 antibody common ADR: URTI, UTI, nasopharyngitis, PML, infusion reactions (premedicatew. antihistamine, apap, ccs) note: *served for those who fail other bdmard or w. hx of lymphoproliferative disorder *should be used w. mtx, other options may be monotherapy or be used w. other NONBIOLOGIC dmards

Answer 84

All patients should be screened for latent tb AND hep B prior to initiation Baseline: *TNF-I: CBC, LFTs(infliximab) *Abatacept: CBC and done periodically thorughout treatment *Rituximamb: CBC and done w. each dose *IL-1 I: CBC *il-6: CBC, ANC, LFTs, flp after 4-8 weeks *TNF-I: LFTs(infliximab) *Abatacept: -- *Rituximamb-- *IL-1 I-- *il-6: cbc, lftS, flp Q3mo *TNF-I: -- *Abatacept: -- *Rituximamb: CBC *IL-1 I: CBC *il-6: cbc, lftS, *TNF-I: -- *Abatacept: -- *Rituximamb-- *IL-1 I-- *il-6: flp

Answer 85

indication: *mod-high disease asctivity depsired dmard monotherapy *unable to tolerate/ ci TO CS DMARDS moa: inhibit janus kinase (jak( ENZYMES WHICH BLOCKS TRANcription of inflammatory genes dosing: AE: CI: onset of effect: considerations: *BBW: risk of opportunistic infections, lymphoma and malignancies, thrombosis, including dvt, PE, arterial thrombosis *daily oral administration *used alone or in combo w. mtx or NONbiologic therapY

Answer 86

Tofacitinib (Xeljanz) dose: IR: 5 mg BID, XR 11 mg daily ADR: increased hdl and ldl, headahce, UTI, URTI, GI perforation, anemia, neutropenia, skin cancer, PE, infections Baricitinib (olumiant) dose: 2mg daily ADR: inc ast/alt, nausea, herpes zoster and othr infections, gi perforation, thormbosis, infections upadacitinib (Rinvoq) dose: 15mg daily ADR: inc hdl/ldl, tc, and a/alt, nausea, urti, skin cancer, gi perforation, thormbosis, anemia, neutropenia, infections

Answer 87

1ST LINE: MTX MONOTHERAPY DMARD-NAIVE PT W. MOD-SEVERE DISEASE ACTIVITY *recommended over lef, bdmard, tsdmard, or trippletherapy for dmard naive pts addition of csdmard, bdmard, or ts dmard is preffered over tripple therapy swithcing to a bdamrd or tsdmard of a diff class if recommneded over switching to an agent in same class

Answer 88

continue treatment for >/6 mo before dose reduction or dmard d/c continue atleast 1 dmard at therepeutic dose lifeling to prevent relapse or disease progression if d/c dmard, taper slowly to avoid a flareup if symptoms return, re-initiate dmard

Answer 89

active tb: aboiv biologics or jaki latent tb: may use biologics after one month of starting tb trt hep b: use caution w. biologics and jaki, screen first pregnancy: avoid mtx and lef HF: avoid tnfi in nyha III-Iv *non tnf-i are preffered liver disease: avoid mtx or lef *use cuaition w. hcq and ssz kymphoproliferative disordr: prefer rituxumab

Answer 90

2 weeks Before dmard therapy, pneumococcal, influenza (inactive) hep b, hpv, and live herpez zoster virus for biologic agents, live vaccines (such as live herpes zoster) should not be given

Answer 91

SLE: systemic: can affect all organ systems *malar rash (butterfly rash) Discoid: primarily effects skin *discoid rash: can lead to permamanent scarring and alopecia , can also occur inside he mouth

Answer 92

women 9x more likely during child bearing years most common age child bearing age: 16-55 y.o black and hispanic 4x mor likely

Answer 93

unkown genetics: risks for offspring w. mothers having sle environment: UV light #1 environmental factor, stess, smoking, medications like hydralazine and procainamide Viruses: e.g EBV Hormones: high levels of estrogen (higher sle risk in oral contraceptive users , and inc in post menopausal women given estrogen Prolactin: decreased sle risk associated w. breastfeeding

Answer 94

preclinical: *asymptomatic dysregulation of cellular apoptosis increass in apaoptosis clearance deficiencies due to macrophages: a *nuclea autoantigens presnt to: *dendritic cells: IFN a factories *b cells autoantibodies *something triggers this to causing impaired tolerance: *precipitting facrots/initial insult *activated dendritic cells present auto antibodies to communicate w. b cells

Answer 95

ab self bind to form antibody immune complexes these immune complexes deposit in vasculatrue and suceptible tissues (skin, kidney etc. it is a type III hypersensitivity reaction 8neutrophils complement activta rto destroy immune complexes, IFN, TNF , immune reaction leads to tissue damage, inability to clear complexes efficiently, causing ... INFLAMMATION

Answer 96

suceptibility(geentics, complement levels, hormone levels) +environmental insult causes.. autoimmune proliferation leads to...autoantibody production

Answer 97

extremely variable

Answer 98

variable manifestations due to effects on any organ system ACR DX CRITERIA most common presentation, woman of child bearing rage presenting w. rash, fever, arthralgias

Answer 99

only need 4/11 *has 85% sensitivity *95% specificity SOAP BRAIN MD

Answer 100

S: SEROSITIS: *pericarditis or pleuritis (pain rub/effusion O: oral ulceration *typically painless Arthritis: non erosive, usually case 2+ peripheral joints Photosensitivity *malar rash but any rash

Answer 101

BLOOD DIsorders *meolytic anemia, or leukopenia, or lymphopenia, or thrombocytopenia Renal involement *proteinuria or cellular casts Antinuclar antibodies (ANA) *hallmark serological signs of sle immunologic disorder *anti smith nuclear antigen *anti phospholipids *anti-dna ab Neurologic disorder *seizure *psychosis

Answer 102

malar rash discoid rash

Answer 103

1.ANA testing low positive predictive value high neg predictive value (helpful for excluding lupus, but now 1000% especially if clniical featurs are present 2.rim immunofluroessence 3.anti-dsDNA ab 4.anti-sm ab

Answer 104

hypercoagulable sate , autoimmunity ~50% of sle pt are aPL+ aPl(+) PLUS thrombotic event=APS *anticardiolipin and lupus anticoagulant( blood thinning effects in vitro, coagulating effects in vivo) important because: greatly increases risk fo rclotting event, inc morbidity and mortality. must lower a risk ofevent, including dvt, stroke, and neurologic manifestations aps associated w. premature births, eclampsia, and stillbirths

Answer 105

was most common cause of death in sle pts (now its infection) in ~35% of ppl at time of dx formation of immune complexes and lodging into glomeruli or forming in flomeruli, causing inflammation *6 classes dx: persisent proteinuria and or cellular catss renal biopsy and histology to confirm SS: fomay urine *peripheral edema *concamiant htn *class III-VI are more severe and require immunosupression or preparation for transplant

Answer 106

dose more important than drug choose appropriate drugs for where rash i s located cousel an dproper use and handeling steroid ocncerns , use topical cni (TACROLIMUS)

Answer 107

for pain and inflammation caused by various sle symptoms acute or chronic GI, cardiac, renal, concerns monitor: kidney function, cbc aspirin may be used to prevent clots in sle pts. counsel pt aspirin must be taken atleast 1 hr before nsaid

Answer 108

location of rash sseverity of rash potency os steroid CYCLIC application medium (cream vs lotion v gel)

Answer 109

indication: long term management of SLE and DLE 8most utuilized in lupus moa: dosing: *supress: 400 mg QD-BID maintenance: 200-400 mg QD AE: flu like symptoms, ocular toxicity (inc risk include incr doses, length of therapy, ckd,) allergic skin reactions refractory to antihistamines, skin an dhair pigmintation changes, hematologic changed (agranulocytosis, aplastic anemia, thrombocytopenia, pancyotpenia), gi upset, myopathies/palsies/cns effects, rare: cardiomyopathy and hearing loss CI: onset of effect: 2-4 months to work. nsaids and steroids can be used to control ymptoms. adequate trial period 6 months considerations: *rudces skin rashes, major organ involvement, mortality over time, good in pregnant women *adequate trial atleast 6 months

Answer 110

CBC, liver function, kidney function at baseline and periodically throughout therapy Ocular toxicity mointoring: at baseline, then at 5 years, then annually therafter if pt a increased risk for qtc prolongation, do ekg at baseline and if clinically indicated

Answer 111

rapid symptom relief can even use pulse iv stroids for false relief adjunctive trt reserved for *mod-sev initial presentation *organ threatening or life threatening sle inadequate response to hcq/nsaid poor qol w.o it dose: A)supressive dose: prednisone 20-60 mg/d IV pulse: B)TAPER 10-20%Q5-7 DAYS until its minimized to a daily dose of

Answer 112

indication: * adjunctive therapyused in non-active cns, ANA+ SLE *first mAb fda approved for sle *adjuncive therapy for incomplete response to HCQ/NSAID/STEROID *fda approved as adjunctive therapy for lupus nephritis moa: b lymphocyte stimulator antagonist ( blymphocyte stimulator activates, stimulates and prevents normal apoptosis of b cells) dosing: AE: allergic rxn, infusion rxn, DEPRESSION/suicidality, PML(brain infection tht is rare) CI: psychosis or dementia, not tested for safety or efficacy in these ppl, onset of effect: 2-4 months considerations: given IV or SQ do not use live vaccines

Answer 113

indication: adjunct to standard therapies in SLE moa: interferon antagonist (reduce immune cell recruitment and allowsymptomatic improvements, stbializes organ disease dosing: IV infusionq4w AE: CI: onset of effect: considerations: not indicated in active LN or cns DISEASE

Answer 114

poor symptom control after hcq/steroids indicated for organ threataning sle, mainly lupus nephirtis (often used in combo w. steroids ex: azothioprine, cyclophosphamid, cyclosporine, methotrexate, mycophenolate

Answer 115

indication: CONCAMINANT ra or main problem of arthritis more effective than AZA ae: bone marrow supession, gi toxicity, hepatotoxicity, nephortoxicity

Answer 116

indication: second line after steroids for a more moderate disease course safest for pregnancy ae: bone marrow supression, n/v

Answer 117

indication: proliferative LN, second line for membranous ln also usful in non renal disease ae: gi side effects risks of hematological, cv, teraogenicity

Answer 118

was LN gold standard incrediby toxic ex: organ threatening dardiopulmonary, renal, or neuro disease can cause permament infertility

Answer 119

useful in membranous LN. can cause HTN

Answer 120

not formally indicated for sle, but can be used in pts who are refractory to everything else

Answer 121

most commonly tacrolimus, for proliferative LN alone or in combo w. MMF

Answer 122

indication: adjunct to immunosupressants to LN moa: po calcineurin inhibitor (decrease cytokine production, lymphocyte proliferation. dosing: PO AE: nephrotoxicity if eGFR<45 CI: do not use w. cyclophosphamide onset of effect: considerations: BBW for infections and malignancies 3a4 interactions, including grapefruit

Answer 123

treat to target shared decision making btw pt and md

Answer 124

trigger avoidance *sunscreens(broad spectrum) *avoid photosensitizing agents prevent/eradicate infection *treat agressively *immunizations/vaccines

Answer 125

mild sle 1s line: HCQ or GC PO/IM refractory: HCQ or/+ GC PO/IM/, MTX/AZA moderate 1st line: HCQ or GC PO/IM, MTX/AZA, CNI, MMF refracory: HCQ or GC PO/IM, Bel, CNI, MMF Severe: 1st line: HCQ or GC PO/IM, MMF, CYc REFRACORY: HCQ or GC PO/IM, cyc, rtx

Answer 126

low disease activity SLEDA<=4; HCQ-PREDNISONE <=7.5 MG/D immunosupressives (in stable doses-well tolerated)

Answer 127

sun protection vaccinations exercise no smoking body weight blood presure lipids glucose anti platelets anticoags (in aPL+ pts)

Answer 128

methotrexate mycophenolate AZA *pregnant pts Cyclophosphamide *rserve for organ threatening *rescue therapy in non responds

Answer 129

adjuntive to immunosupressants useful in adjunct to help lower steroid doses frequent relapses despite hcq/steroid in addition to steroind therapy (not inplace of it iv or sc available (sc adults only not indicated in active cns disease

Answer 130

induction: immunosupressant (MMF or CYC) PLUS steroid remissoin: taper doses and switch immunosupressants if needed

Answer 131

A)intial: GC+MMF or GC +lowdose IV CY or GC+MMF+TAC **severe: all above optoins and GC+high dose IV CY B) assess response in 3-12mo. (target goal is reductio in proteinureia <=25% of stable gfr at first 3 mo., <=50% reduc by 6 mo, and < 0.5-0.7 g/24hr of proteinuria at 12 mo. *Yes: add MMF or AZA w. no or low dose GS *if non responding disease or relapses: switch to alternative inductio therapy or add TAC to MMF or rituximab. consider repeat kidney biopsy

Answer 132

Upr<3 gr/24hr *RAAS blockade *consider GC+MMF Upr >3gr/24hr *RAAS blockade *GC+MMF B) assess response in 3-12mo. (target goal is reductio in proteinureia <=25% of stable gfr at first 3 mo., <=50% reduc by 6 mo, and < 0.5-0.7 g/24hr of proteinuria at 12 mo. Yes: continue same trt w. gradual tapering no: GC+MMF (alternative: IV CY or cni) RESPONCE AT 3-12 MONTHS? yes: continue no: CNI monotherapy or add MMF or high done iv cy or rituximab

Answer 133

use ace/arb in pt who have glomerular disease and *persistant proteinuria (>/ 0.5g/24hr and or *htn (target <130/80 mmg use statin therapy in ldl>100

Answer 134

pregnancy risk stratification should occur ealy after dx of sle *HCQ not associated w. congenital malformations. inc risk of flair if dc during pregnancy nsaids *unsafe in 3rd smeester shbut should avoid anyway *manage pain with apap topical steroids

Answer 135

mild: hcq/aza clinicaly active ln: non fluronated oral steorid can be used *aza *max dose 2mg/kg/day) if necesary to control ln PRETERM DELIVERY CONSIDERED (AFTER 28 WEEKS) IF LN highly active

Answer 136

aPL+ w. no event not pregnant: daily low dose aspirin(LDA) (81mg) *reserve for pt w. cv risk pregnant: *LDA +/- lmwh APS not pregnant a)arterial: warfarin INR 3-4 b)venous: warfarin INR 2-3

Answer 137

SS: q3-6 mo at office visits adverse drug events q6mo or less often UA BMP CBC lipid panel serologic disease markers

Week 7: Gout, Osteoarthritis, Rheumatoid Arthritis, SLE Flashcards

(163 cards)