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TXP: Pulm/ Tox. And Rheumatology > Week 7: Gout, Osteoarthritis, Rheumatoid Arthritis, SLE > Flashcards

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

1
Q

Gout

A

most common form of inflammatory arthritis

“disease of kings

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2
Q

Gout epidemiology

A

increased age=increased risk

3-4:1 male: female

(female risk increases w. age w. estrogen loss

linked to:
comorbid conditions
diet
medication use
renal erate transporter gentotype (SLC2A9, ABCG2, SLC17A3, SLC22A12)

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3
Q

Patho of gout

A

purines (diet, tissue breakdown)-> uric acid (metabolized by uricase in most mammals, not humans)->metabolized to allantoin and excreted from body

UA soluble at conc <6.7 mg/dL

saturation causes crystallization into joints

phagocytosed triggering an immune respone

excess serum uric acis caused by
*overperoduction of urate
or underexcretion of urate

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4
Q

gout and disease states

A

DM
HLD
obseity
renal insufficiency/CKD
HTN
organ transplantation
CHF

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5
Q

FOOD AND GOUT

A

hyperuricemic
*meat
seafood
beer and liquor
soft drinks
fructose

Uricosuric (increase uric acid excretion in urine)
*coffee
dair
vitamin C

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6
Q

meds and gout

A

hyperuricemic meds
*THIAZIDES
LOOP DIURETICS
NICOTONIC ACID
ASPIRIN (<1G/DAY)
others..
cyclosporine
tacrolimus
pyrazinamide
levadopa
ethambutol

uricosuric meds
LOSARTAN
FENOFIBRATE

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7
Q

classic GOUT PRESENTATION

overall characteristic of flares:
common areas affected:
can be precipitated by:

A

presentation waxes and wanes . periods of asymptomatic until pt experiences acute gout attack

gout flare: (attack): onset within 24 of severe pain, erythema and swelling in a single or multiple joints

Podagro: first metacarsopholangeal joint (big toe) joint involvement most common

may calso effect ankles, fingers, wrists and elbows

can be precipitated by

alcohol ingestion
high purine ingestine
stress
meds (including UA lowering agents

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8
Q

other clinical presentations of gout

A

classic gout: monarticular arthritis, frquently attacks first metatarsalpholangeal join, although other joints of lower extremeitie are also frquently involved. affected joint i swollen, erythamatous, and tender

interval gout: asymptomatic period inbetween attacks

tophaceous gout: deposit of urate crystalls in soft tissues, . complications include soft tissue damage, deformity, joiint destruction, and nerve compression syndromes such as carpal tunnel syndrome

atypical gout: polyarthritis affecting any join upper or lower extremity. may be confused with rheumatoid or osteoarthritis

gout nephropathy: nephrolithiasis . acut and CKD

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9
Q

what is a tophi

A

mass of urate deposits in bone, cartilage, joints or tissues

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10
Q

gout dx

A

dx by synovial fluid aspiration and identification of monosodium urate crystals
* not routinely performed

!!Flare/ attack presentation along w. serum acid>6.8 mg/dL indicated treatment for gout!!

**note. elevated serum uric acid levels alone w. no presentation of gout symptoms does not warrant gout treatment

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11
Q

Goals of therapy for acute gout

A

reduce pain and duration of attacks

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12
Q

geenral anti-inflammatory agents for acute gout treatment

A

NSAIDS
colchcine
corticosteroids (oral or intrarticular)

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13
Q

General Acute Gout pharmacotherapy

NSAIDS

moa:

examples:

dosage:

A

General Acute Gout pharmacotherapy

moa:cox INHIBITION

examples: Indomethacin, naproxen, and sulindac have fda approved indications for gout (but any nsaid will do for the most part)

dosage: –

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14
Q

nsaid considerations for use in acute gout

timing:
when to avoid use:

A

timing of admin (<24 hrs) more important to treatment success than choice of agent

resolution of symptoms usually within 5-8 days
(may require treatment beyond 7 days)

AVOIDE USE IN:
*renal insufficiency/ failure
*bleeding disorder/anticoagulated pts
*peptic ulcer disease
*CHF
*older adult (>75)

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15
Q

General Acute Gout pharmacotherapy

Colchicine

moa:

examples:

dosage:

A

General Acute Gout pharmacotherapy

moa: inhibitoin og b-tubulin polymerization into microtubules, causing downregulation of inflammatory patways (also prevents activayion, degranulation and migration of neutrophils

examples:–

dosage:
1.2 mg (2 tabs) po x 1 then 0.6 mg 1 hr later
*may have to continue beyond this dosage w. colchicine or additional therapy

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16
Q

Considerations/pearls for colchicine

A

often causes GI symptoms

can cause:
*hematologic abnormalities
*rhabdomylisys
a) renal dysfunction and elderly patients are at increased risk
b)concaminant use of 3a4 inhibitors, pgp inhibitors, fibrates, and statin may increase risk of myopathy

Dose adjustment for..
*Crcl< 30mL/min
*severe hepatic impairment (no recommendations. if being used, reduce dose)

DDI: concaminant cyp3a4 and pgp inhibitor users
*dose adjustments necessary (for prophylactic users too)
do not dose colchicine for flare therapy if using prophylaxis
*concurrent use of colchicine and pgp or strong cyp3a4 inhibitors is CI in renal or hepatic impairment (fatal toxicities reported)

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17
Q

Colchicine DDI

DDI mechanism: Strong CYP3A4 inhibitors

examples:

dose adjustments:
*acute gout flare:
*ppx gout flare:

A

Colchicine DDI

DDI mechanism: Strong CYP3A4 inhibitors

examples: CLARITHROMYCIN, ITROCONAZOLE, KETOCONAZOLE, DARUNAVIR/RITONAVIR, atazanavir, nefazodone, lopinavir/ritonavir

dose adjustments:
*acute gout flare: single 0.6 mg dose followed by 0.3 mg 1 hr later dose to be repeated no earlier than 3 days
*ppx gout flare: 0.3 mg once qod to 0.3 mg once daily

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18
Q

Colchicine DDI

DDI mechanism: Moderate CYP3A4 inhibitors

examples:

dose adjustments:
*acute gout flare:
*ppx gout flare:

A

Colchicine DDI

DDI mechanism: Moderate CYP3A4 inhibitors

examples: VERAPAMIL, DILTIAZEM, ERYTHROMYCIN, FLUCONAZOLE, aprepitant, amprenavir

dose adjustments:
*acute gout flare: 1.2 mg dose; dose to be repeated no earlier than 3 days
*ppx gout flare: 0.3-0.6 mg daily (0.6 mg dose may be given as 0.3 mg twice daily)

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19
Q

Colchicine DDI

DDI mechanism: PGP inhibitors

examples:

dose adjustments:
*acute gout flare:
*ppx gout flare:

A

Colchicine DDI

DDI mechanism: PGP inhibitors

examples: CYCLOSPORINE, AMIODARONE, RANAZOLINE

dose adjustments:
*acute gout flare: single 0.6 mg dose; dose to be repeated no earlier than 3 days
*ppx gout flare: 0.3 mg once qod to 0.3 mg once daily

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20
Q

General Acute Gout pharmacotherapy

Coticosteroids

moa:

examples:

dosage:

A

General Acute Gout pharmacotherapy

Coticosteroids

moa: reduces polymorphnuclear leukocyte migration, supress the lymph system
*immune supression and anti-inflammatory effects

examples:prednisolone, prednisone, methylprednisolone, intra-articular triamcinolone

dosage:
*prednisolone 30-35 mg po x5days
*prednisone 30-60 mg po qd for 2 days with taper over 10 days
*intrarticualar triamcinolone:
a) large joint (knee):40 mg as a single dose
b)medium joint (eg wrist, ankle, elbow): 30 mg as a single dose
c) small joint (eg toe, finger): 10 mg as a single dose

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21
Q

corticosteroids considerations for acute gout flare

A

*if only one or two joints are involved, either IA or oral are recommended

if ana attack i polyarticular, systemic therapy is indicated

consider alternaive if dm, chf OR SEVERE gerd OR pud

Safe for use in renal impairment

AE (with short term use): leukocytosis, increases appetite, modd changes, elevated BG

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22
Q

Chronic therapy of gout goal

A

prevent future attacks and hyperuricemic sequelae by maintainging SUA <6.0
*prevent arthropathy, tophus frmation, nephrolithiasis, joint damage

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23
Q

General Chronic Gout pharmacotherapy classes and examples

A

Xanthine Oxidase Inhibitors
*Allopurnol
*Febuxistat

Uricosurics
*probenacid

Pegloticase

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24
Q

General Chronic Gout pharmacotherapy

Allopurinol

moa:

dosage:

AE:

DDI:

Considerations:

A

General Chronic Gout pharmacotherapy

moa: Xanthine oxidase inhibitor. blocks conversion of hypoxanthine to xanthine to uric acide

dosage:
starting: 50-100 mg qday
*100 mg po qd starting for normal renal function
*50 mg po qd in CKD stage 4 or worse
*increase q2-5 weeks to target <6 mg/dL
*may have to increase up to 800 mg to achieve target SUA
*can go above 300 mg po qday even in renal impairment depsite renal dosage adjustment PI recommendations

ae:
*rash:~2%. increased with coad w. amoxacillin, ampicillin, thiazides, ace-i. Prob best to d/c drug. mild rash can progress to SJS
*DRESS
*occurs in 0.1 pts
IMMEDIATELY d/c

DDI:
*warfarin (increases risk of bleeding)
*6-MP, azathioprine, theophylline (allopurinol can icnrease levels of these
*amaxaillin, ampicillin, thiazides, ace-i increase risk of rash

considerations:
*1st line therapy
*can be used overproducers or underexcreters of uric acid

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25
Q

General Chronic Gout pharmacotherapy

Febuxistat (Urolic)

moa:

dosage:

AE:

CI:

DDI:

Considerations:

A

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

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26
Q

General Chronic Gout pharmacotherapy

Probenacid

moa:

dosage:

AE:–

CI:

DDI:

Considerations:–

A

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:–

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27
Q

General Chronic Gout pharmacotherapy

Pegloticase

moa:

dosage:

AE:

CI:–

DDI:–

Considerations:

A

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

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28
Q

Mgt of acute gout attack
General principles

A

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

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29
Q

guidelines for acute gout attack

A
  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

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30
Q

Guideline acute flare dosing for colchicine therapy

A

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)

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31
Q

guideline flare dosing for nsaid or selective cox2

A

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

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32
Q

guideline fare dosing

corticosteroids

A

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)

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33
Q

combo therapy for acute gout attack

when to consider:
recommendations:

A

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

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34
Q

Gout chronic therapy gprinciples

A

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

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35
Q

Nonpharm recommendations for gout treatment

A

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

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36
Q

indications for chronic ULT for gout

A

> 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

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37
Q

chronic Therapy of gout goals

goal ua level:
what is 1st line trt:
when to montor ua levels:
if therapy not appropriate, what to do ?
how long is therapy and at what dose?

A

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

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38
Q

indication for swtch to pegloticase as chronic ULT

A

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

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39
Q

Flare ppx

A

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

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40
Q

serum UA lowering therapy PPX

when to initiate:

algorithm (including choices and doses)

A

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 (</10mg/day)+PPI if indicated
*only used if colchicine and NSAIDS both not tolerated, CI, or ineffective

monitor and evaluate gout symptoms while on ULT
*if no signs and symptoms
a) continue ppx for atleast 6 mo!! OR
3mo after achieving target serum urate appropriate for pt (no tophi on physical examination)
*6 mo after acgieving target serum urate appropriate for pt (one or more tophi detected on physical examination)
NOTE: TREAT FOR WHICHEVER DURATION IS GREATER

*if SS of gout (flare in last 3 mo palpable tophi present)
a)continue ppx therapy

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41
Q

epidemiology of Osteoarthritis (OA)

A

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

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42
Q

risk factors for OA

A

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

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43
Q

what is the #1 modifiable risk factor for OA

A

obesity

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44
Q

OA patho

A

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

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45
Q

OA classifications

A

Idiopathic (primary): no known cause

Secondary (classified by cause)

*note: can also be classified by joint involvement

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46
Q

secondary causes of OA

A

traumatic (accidents)

gongenital/genetic:

metabolic: pagets disease, wilsons disease, nutritional defficiencies

neuropathic: Charcot arthropathy

HEmatologic: Hemophilia, sicklecell disease

Other: Gout, RA

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47
Q

ACR criteria for Hand OA

A

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

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48
Q

clinical features of hand OA

Signs

A

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

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49
Q

Knee OA epidemiology

A

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

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50
Q

clnicnal features of knee OA

A

JOINT PAIN

MORNING STIFFNESS

JOINT INSTABILITY

LOSS OF FUNCTION

OCCASIONAL SYNOVITIS

bowleggednes (vargus)
knock knees (valgus)

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51
Q

ACR criteria for knee OA

A

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

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52
Q

clinical and lab classification if knee OA

A

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

  1. esr <40 MM/HR
  2. rf<1:40
  3. Synnovial fluid: clear, viscous, or wbc <2000/mm^3
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53
Q

acr radiographic criteria fro knee OA

A

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)

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54
Q

ACR criteria: HIP OA

A

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

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55
Q

clinical featurs of hip OA

A

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

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56
Q

non pharm treatment of OA considerations

A

can use more than one modality

consider pt comfort

exercise, braces, etc.
*un

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57
Q

non pharm management of hand OA

A

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

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58
Q

non phar knee OA

A

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

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59
Q

non pharm treatment for hip OA

A

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

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60
Q

exercise considerations for OA

A

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

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61
Q

Self efficacy and self management programs for OA

A

multi disciplinary group based on skill building and education

skill building
*goal setting
*problem solving
*positiv thinking

education
*fitness goals
*joint protection
*medication

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62
Q

other therapies for non pharmt trt of OA

A

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)

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63
Q

conditionally and strongly recommended against non pharm treatments for OA

A

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

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64
Q

pharm therapy for OA considerations

A

no disease modifying agents for OA

meds are for pain relief

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65
Q

pharm treatment for hand OA

A

(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

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66
Q

types of non selective nsaids

A

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

67
Q

pharm trt for knee OA

A

SRT:
oral NSAIDS
topical NSAIDs
IA CCS

CRT:
APAP
tramadol
duloxetine
topical capsaicin

68
Q

pharm trt for hip OA

A

srt:
oral NSAIDS
IA CCS (guided by imaging)

crt:
APAP
tramadol
duloxetine

69
Q

pharm mgt recommended AGAINSt for hand OA

A

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

70
Q

pharm mgt recommended AGAINSt for knee OA

A

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

71
Q

pham mgt recommended against forhip OA

A

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

72
Q

overall considerations for trt of OA

A

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.

73
Q

clinical prsentation of RA

A

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

74
Q

joint involvement in RA

A

MOST COMMONLY EFFECTS small joints (hands wrist, ankles and feet bilaterally

larger weight beighring joint sless commonly effected

75
Q

lab findings for pts with RA

A

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

76
Q

dx of ra

A

CHALENEGES:
no single tet or physical finding
*early detection is difficult

acr/eular criteria:
*serology/acute phase reactants
*duration of SS
*joint involvement

77
Q

disease severity evaluation in RA

A

Disease activity Score

scale 0 to 9.4

high disease activity :>5.1

mod diseasy activity: >/3.2 to </5.1

low disease actiity : >/2.6 to <3.2

remission: <2.6

78
Q

RA vs OA

age:
onset:
development:
SS:
joint involvement:
joint stiffness duration:
joint pain:
symmetry:
auto antibodies:

A

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

79
Q

GOALS OF therapy of RA

A

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

80
Q

Non pharm therapy for RA

A

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

81
Q

non disease modifying therapy for RA

A

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

82
Q

disease modifying therapy for RA

categories

A

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

83
Q

treatment prinicples for RA

A

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

84
Q

dmard THERAPY algorithm for RA

A

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

85
Q

poor prognostic factors for RA

A

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

86
Q

csDMARDS
MTX

indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

87
Q

csDMARDS
HCQ

indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

88
Q

csDMARDS
sulfasalazine (SSZ)

indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

89
Q

csDMARDS
Leflunomide (LEF)

indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

90
Q

monitoring for csdmards

A

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

91
Q

general bdmard considerations for use in RA

A

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

92
Q

TNF-inhibitor subq options

A

etanercept (Enbrel)

adalimumab (humira)

golimmumab (simponi)

Certolizumab (Cimzia)

93
Q

TNF-a biologics-sub q options

drug: etanercept (enbrel)

dosing:

use w. mtx:

common ADR:

A

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

94
Q

TNF-a biologics-sub q options

drug: adalimmumab

dosing:

use w. mtx:

common ADR:

A

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

95
Q

TNF-a biologics-sub q options

drug: golimumab (simponi)

dosing:

use w. mtx:

common ADR:

A

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

96
Q

TNF-a biologics-sub q options

drug: certolizumab

dosing:

use w. mtx:

common ADR:

A

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

97
Q

TNF-inhibitor iv options

A

Inflixumab (Remicade)

Golimumab (Simponi Aria)

98
Q

TNF-a biologics- IV options

drug: INFLIXIMAB (Remicade)

dosing:

use w. mtx:

common ADR:

A

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

99
Q

TNF-a biologics- IV options

drug: golimumab (Simponi Aria)

dosing:

use w. mtx:

common ADR:

A

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

100
Q

TNF-I Safety concerns

A

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

101
Q

non TNF-I biologics- list of subq options

A

abatacpt (orencia)

sarilumab (kevzara)

toclizumab (Actemra)

Anakinra (Kinret)

102
Q

non -TNF-a biologics- sq options

drug: abatacept (Orencia)

dosing:

cell target:

common ADR:

A

non -TNF-a biologics- sq options

drug:

dosing: 125 mg once weekly

cell target: t cells

common ADR: URTI, headache, nasopharyngitis, nausea

103
Q

non -TNF-a biologics- sq options

drug: sarilumab

dosing:

cell target:

common ADR:

A

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

104
Q

non -TNF-a biologics- sq options

drug: toclizumab

dosing:

cell target:

common ADR:

A

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

105
Q

non -TNF-a biologics- sq options

drug: ANAKinra (kineret)

dosing:

cell target:

common ADR:

note:

A

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

106
Q

considertionf for non tnf-i

A

all used as monotherapy or w. non biologic dmard

107
Q

non -TNF-a biologics- IV options

drug: abatacept (oriencia)

dosing:

cell target:

common ADR:

note:–

A

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:–

108
Q

non -TNF-a biologics- IV options

drug: rituximab

dosing:

cell target:

common ADR:

note:

A

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

109
Q

Monitoring for bDMARDS

A

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

110
Q

JAK inhibitors

indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

111
Q

JAK inhibitor examples

A

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

112
Q

treatment considerations foR RA

what is 1st line?
when to add when mono therapy not working?

A

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

113
Q

reaching trt target for RA

A

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

114
Q

comorbities to ocnsider in RA

A

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

115
Q

vaccinations in pts w. RA

A

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

116
Q

two forms of Lupus

A

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

117
Q

SLE epidemiology

A

women 9x more likely during child bearing years

most common age child bearing age: 16-55 y.o

black and hispanic 4x mor likely

118
Q

etiology of sle

A

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

119
Q

phases of sle

Preclinical Phase

A

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

120
Q

SLE patho

clinical phase aka SLE specific phase

A

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

121
Q

basic picture of patho sle

A

suceptibility(geentics, complement levels, hormone levels) +environmental insult causes..

autoimmune proliferation

leads to…autoantibody production

122
Q

SLE timeline

A

extremely variable

123
Q

SLE presentation

A

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

124
Q

acr DX CRITERIA FOR sle

A

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

SOAP
BRAIN
MD

125
Q

SOAP :SLE

A

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

126
Q

BRAIN: SLE

A

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

127
Q

MD sle

A

malar rash
discoid rash

128
Q

serological testing for sle dx

A

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

129
Q

antiphospholipid syndrome and sle (APS)

A

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

130
Q

Lupus nephritis

epidemiology
patho
dx
SS

A

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

131
Q

considerations for MEDS USED TO TREAT sle

TOPICALS

A

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)

132
Q

MEDS USED TO TREAT sle

NSAIDS

A

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

133
Q

considerations for topical steroi duse for rashes in sle

A

location of rash

sseverity of rash

potency os steroid

CYCLIC application

medium (cream vs lotion v gel)

134
Q

pharm treatment forSLE

HCQ
indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

135
Q

HCQ monitoring

A

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

136
Q

Systemic Glucocorticoids in sle treatment

A

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 </7.5 mg/d or equiv
c)ideally, taper off ocpletely

AE: hpa supression, osteoporosis, hyperlipidemia, moon faces, amenorrhea, immosupression, obesity, echymosis etc.

137
Q

belimumab (benlysta)
indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

138
Q

Anifrolumab (Saphnelo)
indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

139
Q

immunosupressants indications in sle trt

A

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

140
Q

immunosupressants use in sle trt

mTX

A

indication: CONCAMINANT ra or main problem of arthritis

more effective than AZA

ae: bone marrow supession, gi toxicity, hepatotoxicity, nephortoxicity

141
Q

immunosupressants use in sle trt

azathioprine (AZA)

A

indication: second line after steroids for a more moderate disease course

safest for pregnancy

ae: bone marrow supression, n/v

142
Q

immunosupressants use in sle trt

micophenolate mofetil/sodium (mmf)

A

indication: proliferative LN, second line for membranous ln

also usful in non renal disease

ae: gi side effects
risks of hematological, cv, teraogenicity

143
Q

immunosupressants use in sle trt

cyclophosphamide

A

was LN gold standard

incrediby toxic

ex: organ threatening dardiopulmonary, renal, or neuro disease

can cause permament infertility

144
Q

immunosupressants use in sle trt

cyclosporine

A

useful in membranous LN.

can cause HTN

145
Q

immunosupressants use in sle trt

rituximab

A

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

146
Q

immunosupressants use in sle trt

calcineurin inhibitors

A

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

147
Q

Voclosporin
HCQ
indication:
moa:
dosing:
AE:
CI:
onset of effect:
considerations:

A

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

148
Q

pharm treatment for sle condierations

A

treat to target

shared decision making btw pt and md

149
Q

non pharm management for sle

A

trigger avoidance
*sunscreens(broad spectrum)
*avoid photosensitizing agents

prevent/eradicate infection
*treat agressively
*immunizations/vaccines

150
Q

EULAR sle pharm algorithm

A

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

151
Q

eular target goals for sle

A

low disease activity

SLEDA<=4; HCQ-PREDNISONE <=7.5 MG/D

immunosupressives (in stable doses-well tolerated)

152
Q

adjunct therapy to sle harm treatment

A

sun protection
vaccinations
exercise
no smoking
body weight
blood presure
lipids
glucose

anti platelets
anticoags (in aPL+ pts)

153
Q

guideline recommendations fo rskin disease in sle

A
154
Q

refactory/severe sle agents

A

methotrexate

mycophenolate

AZA
*pregnant pts

Cyclophosphamide
*rserve for organ threatening
*rescue therapy in non responds

155
Q

adjunctive therapy

belimumamb

A

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

156
Q

basic lupus nephritis care

A

induction: immunosupressant (MMF or CYC) PLUS steroid

remissoin: taper doses and switch immunosupressants if needed

157
Q

Class III-IV LN trt

A

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

158
Q

class V lupus nephritis treatment

A

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

159
Q

other LN care points

A

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

160
Q

Pregnancy and sle

A

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

161
Q

LN in pregnancy trt

A

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

162
Q

trt of APS (+) or APS

A

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

163
Q

monitoring for sle and followup

A

SS: q3-6 mo at office visits
adverse drug events

q6mo or less often
UA
BMP
CBC
lipid panel
serologic disease markers

TXP: Pulm/ Tox. And Rheumatology (7 decks)

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