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Pulm Therapeutics > Exam 4 baby! > Flashcards

Exam 4 baby! Flashcards

1
Q

what things is gout linked to?

A

-co-morbid conditions
-diet
-medication use
-renal urate transporter genotypes (SLC2A9, ABCG2, SLCI7A3, SLC22A12)

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2
Q

Hyperuricemia and gout

A

-Uric acid is soluble at concentrations < 6.7 mg/dL, once solubility is saturated, UA precipitates into monosodium urate crystals.
-crystals deposit in the joints –> phagocytosed triggering an immune response
-excess serum uric acid is caused by: overproduction of urate, under-excretion of urate

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3
Q

which of the following disease states promote hyperuricemia in gout pts

A

-insulin resistance (DM)
-hyperlipidemia
-obesity
-renal insufficiency/chronic kidney disease
-hypertension
-organ transplantation
-CHF

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4
Q

What foods are hyperuricemic?

A

-meats (organs)
-seafood
-beer and liquor
-soft drinks
-fructose

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5
Q

what foods are uricosuric?

A

(increase the bodys abiliy to secrete uric acid in the urine)
-coffee
-dairy
-vitamin C

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6
Q

what medications are hyperuricemic?

A

*thiazide diuretics
*loop diuretics
*nicotinic acid
*aspirin (< 1 g/day)
-cyclosporine
-tacrolimus
-pyrazinamide
-levadopa
-ethambutol

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7
Q

what drugs are uricosuric?

A

(increase bodys ability to secrete UA into the urine)
*losartan
*fenofibrate

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8
Q

what is a gout presentation?

A

Gout flare/attack: rapid onset (within 24 hrs) of severe pain, erythema and swelling in a single or multiple joint
–> podagra: first metatarsophalangeal (big toe) joint involvement is most common
-also may affest ankles, fingers, wrists and elbows

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9
Q

what can a gout flare be precipitated by?

A

-alcohol ingestion
-high purine ingestion
-stress
-medications (including UA lowering agents)

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10
Q

Classic acute gout (“podagra”) clinical presentation

A

-monoarticular arthiritis
-frequently attacks the first big toe joint, although other joints of the lower extremities are also involved
-affected joint is swollen, erythematous and tender

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11
Q

Interval gout

A

-asymptomatic period between attacks

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12
Q

Tophaceous gout clinical presentation

A

-deposits of monosodium urate crystals in soft tissues
-complications include soft tissue damage, deformity, joint destruction, and nerve compression syndromes such as carpal tunnel syndrome
–> Tophi: mass of urate deposits in bone, cartilage, joints or tissues

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13
Q

Atypical gout clinical presentation

A

-polyarthritis affecting any joint, upper or lower
-may be confused with rheumatoid arthritis or osteoarthritis

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14
Q

Gouty nephropathy clinical presentation

A

-nephrolithiasis (kidney stones)
-acute and chronic kidney disease

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15
Q

Chronic gout complications include:

A

-pain
-joint, nerve and soft tissue damage
-physical deformity

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16
Q

How is gout diagnosed?

A

-diagnosed by synovial fluid aspiration and identification of monosodium urate crystals (not common)
-associated with a serum uric acid > 6.8 mg/dL (not always present)
**flare/attack presentation generally confirms diagnosis

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17
Q

Acute Gout therapy

A

-goals: reduce pain and duration of attacks
-use anti-inflammatory agents like: NSAIDs, colchicine, corticosteroids (oral or intrarticular)

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18
Q

NSAID use in gout tx

A

-cox inhibition
-Indomethacin, naproxen and sulindac are FDA labeled but any NSAID is fine to use
-timing of admin (< 24 hrs!!) is more important to treatment success than choice of agent (may require tx beyond 7 days)
-resolution of symptoms usually within 5-8 days of intiation

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19
Q

when do you want to avoid NSAIDs in gout tx?*

A

-renal insufficiency/failure (fluid retention)
-bleeding disorders/anti-coagulated patients
-peptic ulcer disease (increase the risk of GI ulcers)
-CHF (pts w/ hx of CAD or HF)
-older adults (> 75)

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20
Q

Colchicine in acute gout (and dosing)

A

MOA: inhibition of B-tubulin polymerization into microtubules, also prevents activation, degranulation, and migration of neutrophils
DOSE: 1.2 mg ( 2 tabs) po x 1 then 0.6 mg 1 hr later
(may have to continue beyond this dosage with colchicine or additional flare therapy)

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21
Q

Colchicine adverse effects

A

-often causes GI symptoms (diarrhea)
-hematologic abnormalities
-rhabdomyolysis
–> renal dysfunction and elderly pts are at increased risk, concomitant use of 3A4 inhibitors, P-gp inhibitors, fibrates and statin may increase the risk of myopathy
-dose adjust in CrCL < 30 and hepatic impairment

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22
Q

Colchicine clinical pearls: concomitant CYP3A4 and P-gp inhibitor users

A

-dose adjustments necessary (for prophylactic users too)
-do not use colchicine for flare therapy if using for prophylaxis
-concurrent use of colchicine and P-gp or strong CYP3A4 inhibitors is CONTRAINDICATED in renal impairment & hepatic impairment

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23
Q

Colchicine DDI: strong CYP3A4 inhibitors *

A

-clarithromycin
-Darunavir/ritonavir
-Itraconazole
-Ketoconazole

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24
Q

Colchicine DDI: moderate CYP3A4 inhibitors

A

-diltiazem
-erythromycin
-fluconazole
-verapamil

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25
Q

Colchicine DDI with P-glycoprotein inhibitors

A

-cyclosporine
-amiodarone
-ranolazine

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26
Q

corticosteroid use in acute gout tx

A

MOA: reduced polymorphonuclear leukocyte migration, suppresses the lymph system (immune suppression and anti-inflammatory effects)
–> Prednisolone 30-35 mg po qd x 5 days
–> prednisone 30-60 mg po qd for 2 days with taper over 10 days

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27
Q

Intra-articular triamcinolone use in acute gout tx

A

-if only one or 2 joints are involved, either intra-articular or oral cortiscosterioids are recommended
–> if an attack is polyarticular, systemic therapy is necessary!

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28
Q

Corticosteriod use in acute gout: AEs

A

-consider alt if DM, CHF or severe GERD or PUD
-safe for use in renal impairment
-AEs: (w/ short term use): leukocytosis, increased appetite, mood changes, elevated blood glucose

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29
Q

Chronic therapy for gout

A

-goals: prevent future attacks and hyperuricemic sequelae by maintaining SUA < 6.0
want to prevent complications like: arthropathy, tophus formation, nephrolithiasis, joint damage

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30
Q

Allopurinol

A

-xanthine oxidase inhibitor
-can be used if pt has hyperuricemia and gout = 1st line agent

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31
Q

Allopurinol ADRs

A

-RASH: potentially INCREASED by co-admin with: amoxicillin, ampicillin, thiazides and ACE-I
–> probs best to d/c drug
-ALLOPURINOL HYPERSENSITIVITY: DRESS: rash + fever + eosinophils + hepatitis - immediately STOP the drug

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32
Q

Allopurinol drug interactions

A

-warfarin
-6-MP
-azathioprine
-theophylline
-amoxicillin
-ampicillin
-thiazides
-ACE-I

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33
Q

Allopurinol dosing

A

-starting dose 50-100 mg qs
–> 100 mg po qd (normal renal function)
–> 50 mg po qd in CKD stage 4 or worse
-increase q 2-5 weeks to target < 6 mg/dL
(may have to increase up to 800 mg to achieve target SUA

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34
Q

Febuxostat (Uloric) for chronic gout

A

-chemically engineered, selective xanthine oxidase inhibitor

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35
Q

Febuxostat (Uloric) for chronic gout: dosing

A

-40 mg once daily, may increase to 80 mg once daily in pts who do not achieve a serum uric acid level < 6 mg/dL after 2 weeks
*concomitant NSAID or colchicine prophylaxis up to 6 months to help prevent gout flares per package insert
-if gout flare occurs, febuxostat does not need to be discontinued

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36
Q

Febuxistat adverse reactions

A

-headache, arthralgias, abdominal pain, nausea, abnormal LFTs, flushing and dizziness
-pts should be monitored for cardiovascular events
BBW: cardiovascular death - pts with established CV disease had a higher rate of CV death
CI with: 6-MP, azathioprine, and theophylline

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37
Q

Probenicid

A

MOA: competitively inhibits the reabsorption of uric acid at proximal convoluted tubule by promoting its excretion and reducing serum uric acid levels
Dosing: 250 mg BID for 1 week, may increase to 500 mg BID id needed (MDD 2 grams)
*avoid use in CrCl < 50 ml/min & avoid with hx of nephrolithiasis

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38
Q

Probenicid DDIs

A

-avoid concomitant use with:
- penicillin
-methotrexate
-carbapenems
-salicylates

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39
Q

Pegloticase for chronic gout tx

A

-approved for chronic gout refractory
IV 8 mg every 2 weeks over at least 2 hrs
BBW: anaphylaxis and infusion reactions
–> pre-med with antihistamines and corticosteroids
-prophylaxis with low dose colchicine or NSAID x 6 months

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40
Q

combination therapy options for gout

A

use when:
–> severe attack
–> polyarticular
–> pts not responding to initial monotherapy
do NOT combine oral corticosteroids and oral NSAIDs

-NSAIDs + colchicine
-PO corticosteroid + colchicine
- intra-articular steroid + NSAID +/- colchicine
-intra-articular steroid + PO steroid +/- colchicine

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41
Q

what life style modifications are recommended for all pts with gout?

A

-limiting alcohol
-limiting purine intake
-limit high-fructose corn syrup
-using a weight loss program
-smoking cessation
-stay well hydrated

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42
Q

how to do chronic therapy in gout?

A

-chronic therapy = UA lowering therapy + flare prophylaxis
-UA lowering therapy initiation can illicit flares
-prophylactic flare therapy should be given concomitantly with UA lowering therapy
*chroni therapy should NOT be stoped during flare

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43
Q

what is the indications for pharmacologic treatment for chronic gout therapy?

A

> /= 1 subcutaneous tophi, radiographic evidence of damage attributable to gout OR frequent flares ( > 2 per year)

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44
Q

what may you consider treatment for chronic therapy of gout?

A

-hx of > 1 attack, but < 2 attacks per year
-those with first gout flare with the following: CKD stage > 3, [UA] > 9, urolithiasis
(if decision is made that patient requires ULT during a flare, it should be initiated during the flare

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45
Q

1st line agent in gout chronic therapy?

A

-Allopurinol
(goal serum urate level < 6 mg/dL
-UA levels should be monitored every 2-5 weeks with increases in ULT intensity until goal is reached (increase dose of XOI, add probenecid if appropriate)
-therapy required to reach goal of < 6 mg/dL should be continues indefinitely

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46
Q

when do you switch to pegloticase in chronic gout therapy?

A

(3rd line option)
-XOI treatment, uricosurics, and other interventions have failed to achieve goal UA level, and patients continue to have >/= 2 flares per year OR non-resolving tophi

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47
Q

What is flare priphylaxis in gout tx?

A

-prophylaxis with anti-inflammatory medications should be initiated when ULT is initiated
-same agent as for flare tx, at different dose
-should be continued for 3-6 months, based on resolution of symptoms and absence of tophi

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48
Q

2 first line therapies for prophylaxis initiation for gout

A
  • low dose colchicine: 0.6 mg once or twice daily
    -low dose NSAIDs (with PPI if indicated) ; Naproxen 250 mg BID
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49
Q

second line option for gout prophylaxis

A

-low dose prednisone or prednisolone (< 10 mg/day)
**if colchicine and NSAIDs are BOTH not tolerated, contra-indicated or ineffective

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50
Q

what is the duration of gout prophylaxis treatment?

A

-at least 6 months OR
-3 months after achieving target serum urate appropriate for the patient (no tophi detected on physical exam)
-6 months after achieving target serum urate appropriate for the patient (one of more tophi detected on physical exam)

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51
Q

Gout prophylaxis tx conclusions

A

-gout is a disease with periods of remission and flares
-flares are managed with therapies targeted to reduce pain and inflammation
-chronic therapy is aimed at reducing serum uric acid levels to reduce future flares

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52
Q

Risk factors for OA

A

-obesity (~1 modifiable risk factor)
-sex (males develop from a younger age while females at an older age)
-occupation (lots of kneeling standing, repeated mechanical stress)
-participation in certain sports
-joint injury or surgery
-genetic predisposition

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53
Q

Conditions present in osteoarthritis (at a joint for example)

A

-bone cyst
-thickened capsule
-synovial inflammation/hypertrophy
-cartilage fibrillation
-meniscal degeneration
-osteophyte formation
-subchondral bone thickening
-bone marrow lesion

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54
Q

how does cartilage gain nutrients?

A

-via the loading and unloading of the joints providing nutrients to the condocytes + movement is important for sustaining joint health

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55
Q

Secondary OA causes

A

-traumatic: accidents –> damage to articular cartilage, muscles, alignment
-congenital/genetic
-metabolic: paget’s disease, wildons disease, nutritional deficiencies
-neuropathic: charcot arthropathy ( pts cant feel pain even if they are doing damamge)
-hematologic: hemophilia, sickle cell disease
-other: gout, RA

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56
Q

ACR criteria of hand OA

A

*hand pain, aching or stiffness with 3 or 4 of the following:
-hard tissue enlargement of 2 or more of 10 selected joints
-hard tissue enlargement of 2 or more DIP joints
-fewer than 3 swollen MCP joints
-deformity of at least 1 of 10 selected joints

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57
Q

Clinical features of hand OA

A

-bony enlargement of affected joints (heberden’s nodes, bouchard’s nodes)
-limitation of range of motion
*crepitus with motions (grinding/friction)
*pain with motion
*malalignment and/or joint deformity

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58
Q

Hand involvement in hand OA (3 features)

A

-fusiform appearance
-Bouchard’s nodes (PIP): same as Heberden’s nodes, at a different location, less common
-Heberden’s nodes (DIP): develop slowly, non-painful, lateral and medial aspects of the joint

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59
Q

Knee OA facts

A

-most common cause of arthritis and of chronic disability among older persons in the US
-radiographic abnormalities present in > 30% of persons over 65 y/o
-symptomatic knee osteoarthritis occurs in ~ 10% of persons > 65 y/o
-leading indication for >250,000 total knee arthroplasties in US per year

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60
Q

Clinical features of knee OA

A

-joint pain
-morning stiffness
-joint instability or buckling
-loss of function
-occasional synovitis

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61
Q

ACR criteria for knee OA

A

knee pain AND at least 3 of the following:
-age > 50 y/o
-stiffness lasting < 30 mins
-crepitus
-bony tenderness
-bony enlargement
-no warmth to touch!
(most sensitive, least specific)

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62
Q

ACR criteria for knee OA: lab findings

A

-ESR < 40 mm/hr
-RF <1:40
-synovial fluid: clear, viscous, or WBC < 2,000/mm^3

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63
Q

ACR clinical and radiographic criteria for knee OA

A

at least 1 of the following:
-age > 50
-stiffness < 30 mins
-crepitus
AND osteophytes and knee pain
(least sensitive, most specific)

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64
Q

ACR criteria: Hip OA

A

Hip pain and at least 2 of the following:
-ESR < 20mm/hr
-radiographic femoral or acetabular osteophytes
-radiographic joint space narrowing (superior, axial, and/or medial)

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65
Q

Clinical features of Hip OA

A

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

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66
Q

Hand OA: strongly rec non-pharm

A

-exercise
-self-efficacy and self management programs
-first caropmetacarpal (CMC) orthosis

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67
Q

Hand OA: conditionally rec non-pharm

A

-heat, therapeutic cooling
-cognitive behavioral therapy
-acupunture
-kinesiotaping
-hand orthoses other than CMC
-paraffin

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68
Q

Knee OA: strongly rec non-pharm

A

-exercise
-self-efficacy and self-managment programs
-weight-loss (if overweight)
-Tai-chi
-cane
-tibiofemoral (TF) brace for TF OA

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69
Q

Knee OA: conditionally rec non-pharm

A

-heat, therapeutic cooling
-cognitive behavioral therapy
-acupuncture
-kinesiotaping
-balance training
-yoga
-patellofemoral (PF) knee brace for PF OA
-radiofrequency ablation

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70
Q

Hip OA: strongly rec non-pharm

A

-exercise
-self-efficacy and self-management programs
-weight-loss
-tai-chi
-cane

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71
Q

Hip OA: conditionally rec non-pharm

A

-heat, therapeutic cooling
-cognitive behavioral therapy
-acupuncture
-balance training
-yoga

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72
Q

the role of exercise in OA

A

-duration, intensity and frequency = unknown
-patient preference
-pt access
-possible options: walking, stationary bike, isokinetic and isometric,
-resistance training with and without props
-aquatic exercise

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73
Q

other random therapies that are non-pharm for OA

A

-hand orthosis
-kinesiotaping (tapping of the knee)
-paraffin (dipping hand in warm wax and allowing it to cool)
-braces (TF, PF)

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74
Q

Knee OA: non-pharm strongly rec against

A

TENS

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75
Q

knee OA: non-pharm conditionally rec against

A

-manual therapy
-massage therapy
-modified shoes
-wedged insoles
-pulsed vibration therapy

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76
Q

Hand OA: non pharm conditionally rec against

A

-iontophoresis (putting hands in fluid that sends electrical charge thru them

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77
Q

Hip OA: non-pharm strongly recommend against

A

TENS (transcutaneous electrical nerve stimulation)

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78
Q

Hip OA: non-pharm conditionally recommend against

A

-manual therapy
-massage therapy
-modified shoes
-wedged insoles

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79
Q

Goals of pharmacotherapy for OA

A

*there are no disease modyfying agents
#1: pain relief
-maintenance/ improvement of joint mobility
-limit functional impairment
overall = improve quality of life

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80
Q

Hand OA pharm therapy: strong rec

A

Oral NSAIDs (should use lowest dose for the shortest amount of time)

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81
Q

Non-selective oral NSAID options for OA tx

A

-Indomethacin, sulindac, tolmetin, diclofenec, ketorolac, etodolac
-ibuprofen, naproxen, flurbiprofen, ketoprofen, fenoprofen, oxaprozin
-mclofenamate, mefenamic acid
-nabumetone
-peroxicam, meloxicam

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82
Q

Hand OA: pharm that is conditionally recommended

A

-topical NSAIDs
-intra-articular steroids
-acetaminophen
-tramadol
-duloxetine
-chondroitin

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83
Q

Knee OA: pharm that is strongly recommended

A

-oral NSAIDs
-topical NSAIDs
-intra-articular steroids

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84
Q

Knee OA pharm that is conditionally recommended

A

-acetaminophen
-tramadol
-duloxetine
-topical capsaicin

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85
Q

Hip OA pharm that is strongly recommended

A

-oral NSAIDs
-intra-articular steroids (guided by imaging)

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86
Q

Hip OA pharm that is conditionally recommended

A

-acetaminophen
-tramadol
-duloxetine

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87
Q

Hand OA pharm strongly rec AGAINST

A

-bisphosphonates
-glucosamine
-hydroxychloroquine
-methotrexate
-TNF inhibitors
-IL-1 receptor antagonists

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88
Q

Hand OA pharm conditionally rec AGAINST

A

-inta-articular hyaluronic acid
-topical capsacin
-colchicine
-non-tramadol opioids
-fish oil
-vitamin D

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89
Q

Knee OA pharm strongly rec AGAINST

A

-bisphosphonates
-glucosamine
-hydroxychloroquine
-methotrexate
-TNF inhibitors
-IL-1 receptor antagonists
-platelet rich plasma
-stem cell injection
-chondroitin

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90
Q

Knew OA: pharm conditionally rec AGAINST

A

-intra-articular hyaluronic acid
-intra-articular botulinum toxin
-prolotherapy
-colchicine
-non-tramadol opioids
-fish oil
-vitmain D

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91
Q

Hip OA pharm strongly rec AGAINST

A

-bishosphonates
-glucosamine
-hydroxychloroquine
-methotrexates
-TNF inhibitors
-IL-1 receptor antagonists
-platelet rich plasma
-stem cell injection
-chondroitin
-intra-articular hyaluronic acid

92
Q

Hip OA pharm conditionally rec AGAINST

A

-intra-articular botulinum toxin
-prolotherapy
-colchicine
-non-tramadol opioids
-fish oil
-vitamin D

93
Q

Signs and symptoms of RA

A

*symptoms present for > 6 weeks:
-warmth and swelling over affected joints with or without pain
-prolonged morning stiffness > 30 min
-fatigue, weakness, decreased mood, low-grade fever
-positive rheumatoid nodules (rare)
-joint deformity in late disease

94
Q

what joints are most commonly involved in RA?

A

most common is the small joints:
-hands
-ankles
-feet
–> metacarpophalangeal joints, proximal interphalangeal joints, wrist bones

95
Q

what types of joint deformities are seen in RA?

A

-rheumatoid nodules
-boutonniere deformity of thumb
-ulnar deviation of metacarpophalangeal joints
-swan-neck deformity of fingers
-hallux valgus
-hammer toe & rheumatoid nodule

96
Q

Lab findings that are present in RA:

A

-anti-citrullinated protein antibodies (ACPA)
-rheumatoid factor (RF)
-antinuclear antibodies (ANA)
-elevation of nonspecific markers of inflammation: ESR and C-reactive protein
-synovial fluid analysis WBC count 1,500-25,000

97
Q

Disease activity score in RA

A

high: > 5.1
Moderate: 3.2- < 5.1
Low: 2.6- < 3.2
remission: < 2.6

98
Q

Features of Rheumatoid arthritis

A

-variable age
-variable onset
-auto immune development
-constitutional and joint symptoms
-small joint of hands, wrists and feet involved
-joint stiffness lasts > 30 mins
-joint pain present with use and at rest
-see bilateral effects
-antibodies are present

99
Q

Goals of care in RA

A

-treat to target approach with low disease activity as an acceptable target
-improve symptoms of joint pain and stiffness by reducing inflammation
-slow disease progression and prevent joint damage

100
Q

Non-pharm therapy for RA

A

-rest
-weight loss
-physical & occupational therapy: assistive devices, exercise, physiotherapy
-pt education
-surgery: for severe RA (tendon repair, arthroplasty, tenosynovectomy)

101
Q

Non-disease modifying therapies for RA: NSAIDs

A

-decrease joint pain and inflammation
-acute symptom relief
-adjunct to disease modifying agents

102
Q

Non-disease modifying therapies for RA: Steroids

A

-decrease joint pain and inflammation
-bridge to disease modifier onset of action
-short term high doses for flares
-long term low doses for refractory disease (prefer to add of switch disease modifier)

103
Q

Treatment Principles of RA

A

-initiate csDMARDs within 3 months of onset of persistent symptoms
-short term glucocotorticoids for bridging to DMARD onset
-step up therapy: additional DMARDs when disease burden not adequately controlled
-treat to target approach = targeting low disease activity or remission

104
Q

Methotrexate in RA

A

-considered 1st line for med-high disease activity
MOA: folate antagonist
-folate supplementation decreases ADRs without reducing efficacy –> administer the day after MTX dose is given
-onset of effect: 1-2 months

105
Q

Methotrexate RA dosing

A

7.5 mg PO once weekly titrated to > 15 mg weekly within 4-6 weeks
-if unable to tolerate weekly oral dose: split oral dose over 24 hrs or switch to SubQ

106
Q

Methotrexate ADRs

A

-N/V/D
-stomatitis
-dizziness/fatigue/headache
-pneumonitis/pulmonary fibrosis
-myelosuppression
-immunosuppression/increased infection risk
-hepatoxicity/increase LFTs
-alopecia
-rash

107
Q

When do you want to AVOID Methotrexate us in RA?

A

-pregnancy and breastfeeding
-liver or renal disease
-immunodeficiency
-myelosuppression

108
Q

Hydroxychloroquine use in RA

A

-used as mono-therapy for low disease activity
-inhibits cytokine production
-onset of action is up to 2-4 months
-may be used in pregnancy

109
Q

Hydroxychloroquine dosing in RA

A

initial: 400-600 mg PO daily
Maintenance: 200-400 mg PO daily or divided doses

110
Q

Hydroxychloroquine ADRs (in RA)

A

-N/V/D
-QTc prolongation
-Irreversible retinal damage
-photosensitivity and hyperpigmentation of the skin (blue/black)
-preferable risk profile compared to other DMARDs

111
Q

What population do you want to AVOID hydroxychloroquine in? (RA)

A

-ocular disease: dose dependent retinopathy
-caution in liver disease

112
Q

Sulfasalazine use in RA

A

-can be used as monotherapy or in combination with other DMARDs
preferred DMARD in pregnancy
-active metabolites are responsible for anti-inflammatory properties
-onset of effect: 1-3 months

113
Q

Sulfasalazine dosing in RA

A

500 to 1000 mg PO daily (up to 3 g has been used)

114
Q

Sulfasalazine ADRs (on RA)

A

-N/V/abdominal pain, anorexia
-headache
-reversible oligospermia
-rash, prutitus, urticaria
-blood dyscarias

115
Q

when to avoid Sulfasalazine in RA?

A

-sulfa allergy
-intestinal or urinary obstruction
-porphyria
-renal impairment, caution hepatic impairment

116
Q

Leflunomide in RA therapy

A

-can be used as monotherapy or in combination with other DMARDs
-inhibits pyrimidine synthesis (decreases lymphocyte proliferation)
-onset of effect: 1-3 months
(long 1/2 life –> may be detectable up to 2 yrs )
-cholestyramine removes the drug and its active metabolites

117
Q

Leflunomide dosing in RA therapy

A

Loading dose: 100 mg PO once daily x 3 days
Maintenance dose: 10-20 mg PO daily

118
Q

Leflunomide ADRs

A

-N/V/D
-reversible alopecia
-rash
-peripheral neuropathy
-hypertension

119
Q

Who do you want to AVOID use of Leflunomide in RA tx?

A

-pregnancy and breastfeeding –> teratogenicity across both genders, levels may take months to decrease
-liver disease

120
Q

Over all monitoring for cDMARDs

A

-monitor CBC, LFTs, and SCr based on duration of therapy

121
Q

Monitoring for methotrexate

A

-rule out pregnancy at baseline, chest x-ray at base line

122
Q

monitoring for hydroxychloroquine

A

ophthalmologic exam at baseline and every 3 months

123
Q

monitoring for sulfasalazine

A

rule out G6PD deficiency at baseline

124
Q

monitoring for Leflunomide

A

rule out pregnancy at baseline

125
Q

Biologic therapy principles

A

-generally well tolerated, but COSTLY
-target pro-inflammatory cytokines ( TNF-a, IL-1, IL-6, B cells, T cells)
-use when moderate - high disease activity despite DMARD mono therapy
-unable to tolerate/contraindication to csDMARD
–> TNFi: 3 months
–> non-TNFi: 6 months

126
Q

TNFi Biologics SubQ option: Etanercept (Enbrel)

A

-use with or w/o MTX
ADRs: pancytopenia, injection site rxn, diarrhea, rash

127
Q

TNFi Biologics SubQ option: Adalimumab (Humira)

A

-use with or without MTX
ADRs: sinusitis, URITI, antibody formation, injection site reaction, headache, rash

128
Q

TNFi Biologics SubQ option: Golimumab (Simponi)

A

*must be with MTX
ARDs: URTI, nasopharyngitis, antibody formation, injection site reaction

129
Q

TNFi Biologics SubQ option: Certolizumab

A

-with or without MTX
ADRs: URTI, UTI, antibody formation, dizziness, HTN, rash

130
Q

TNFi Biologics IV option: Infliximab (Remicade)

A

*MUST be with MTX
ADRs: URTI, infusion related reaction (pre-med with antihistamine, APAP, corticosteroids), headache, abdominal pain, antibody formation

131
Q

TNFi Biologics IV option: Golimumab (Simponi Aria)

A

-preferred with MTX
ARDs: URTI, ALT/AST elevation, HTN, rash, neutropenia, antibody formation

132
Q

BBW associated with TNF inhibitors

A

-malignancy –> lymphoma and other malignancies
-serious infections leading to hospitalization or death –> opportunistic fungal, viral and bacterial infections

133
Q

What can TNFi’s lead to the exacerbation of?

A

-multiple sclerosis/multiple sclerosis-like symptoms
-systemic lupus erythematosus/lupus like syndrome
-heart failure –> AVOID in class 3 and 4 or LVEF < 50%
-latent TB and Heb B infections –> SCREEN all pts for TB and hep B before initiation

134
Q

Non- TNFi biologics SubQ: Abatacept (Orencia)

A

-T cells
ADRs: URTI, headache, nasopharyngitis, nausea

135
Q

Non- TNFi biologics SubQ: Sarilumab (Kevzara)

A

-IL-6 inhibitor
ADRs: URTI, UTI, injection site erythema, neutropenia, increased LFTs, antibody formation

136
Q

Non- TNFi biologics SubQ: Tocilizumab (Actemra)

A

IL-6 inhibitor
ADRs: URTI, nasopharyngitis, headache, HTN, increased LFTs, increased lipids

137
Q

Non- TNFi biologics SubQ: Anakira (kineret)

A

IL-1 inhibitor (sucks tho)
ARDs: URTI, rash, pyrexia, influenza like illness, gastroenteritis, vomiting, antibody formation

138
Q

Non- TNFi biologics IV options: Abataceept (orencia)

A

T cells
ARDs: URTI, nasopharyngitis, headache, nausea, HTN, infusion reaction

139
Q

Non- TNFi biologics IV options: Rituximab (Rituxan)

A

Anti-CD20 antibody
ADRs: URTI, UTI, nasopharyngitis, PML, infusion reactions (pre med with antihistamin, APAP, corticosteroids)
**reserved for those who fail other bDMARD or with hx of lymphoprofliferative disorder

140
Q

Non- TNFi biologics IV options: Tocilizumab (Actemra)

A

-IL-6 inhibitor
ARDs: URTI, nasopharyngitis, headache, HTN, increased LFTs, increased lipids, injection site reaction

141
Q

JAK inhibitor therapy principles

A

MOA: inhibits Janus Kinase enzymes which blocks transcriotion of inflammatory genes
daily oral adminstration
-when to use:
–> moderate-high disease activity despite DMARD monotherapy
–> unable to tolerate/contraindication to csDMARD
–> used alone or in combo with MTX or other nonbiologic DMARDs

142
Q

BBWs of JAK inhibitors

A

-risk of opportunistic infections –> SCREEN for latent TB and hepatitis B before initiation
-lymphoma and other malignancies
-thrombosis, including DVT, PE, arterial thrombosis

143
Q

JAK Inhibitor: Tofacitinib (Xeljanz)

A

-ADRs: increases HDL & LDL, headache, URTI, UTI, GI perforation, anemia, neutropenia, skin cancer, PE, infections

144
Q

JAK inhibitor: Baricitinib (Olumiant)

A

ARDs: inc AST/ALT, nausea, herpes zoster & other infections, GI perforation, thrombosis, infections

145
Q

JAK inhibitor: Upadacitinib (Rinvoq)

A

ARDs: inc HDL, LDL, TC, and AST/ALT, nausea, URTI, skin cancer, GI perforation, thrombosis, anemia, neutropenia, infections

146
Q

When treating RA, what are our first line choices for therapy?

A

1: MTX monotherapy for DMARD-naive patients with moderate-severe disease activirt
1: low disease activity - hydroxychloroquine
-addition of csDMARD, bDMARD, ot tsDMARD is preferred over triple therapy
-switching to a bDMARD or tsDMARD of a different class is recommended over switching to an agent in the same class

147
Q

What are the timelines for reaching treatment target in RA?

A

-continue regimen for > 6 months before dose reduction or DMARD discontinuation
-continue > 1 therapeutic dose DMARD lifelong due to risk of flares and disease progression
-if discontinuing a DMARD, taper gradually to avoid a flare-up
-if symptoms return, re-initiate DMARD

148
Q

Comorbidities to consider: active TB

A

avoid biologics and JAK until treatment is complete

149
Q

Comorbidities to consider: latent TB

A

may use biologics after 1 month of starting TB treatment

150
Q

Comorbidities to consider: Hepatitis B

A

use caution with biologics and JAKs, screen first

151
Q

Comorbidities to consider: pregnancy

A

avoid MTX and LEF

152
Q

Comorbidities to consider: heart failure

A

-avoid TNFi in class 3 or 4
-non-TNFi are preferred

153
Q

Comorbidities to consider: liver disease

A

avoid MTX or LEF
-use caution with HCQ and SSZ

154
Q

Comorbidities to consider: lymphoproliferative disorder

A

prefer Rituximab

155
Q

Vaccines to give before DMARD initiation

A

(give at least 2 weeks before initiation)
-pneumococcal
-influenza (inactive)
-hepatitis B
-recombinant HPV & live herpes zoster (do not give last 2 with TNFi biologics!)

156
Q

Major points of lupus:

A

-categorized into 2 forms: SLE and DLE
-of unknown origin
-an inflammatory autoimmune disorder
-chronic, with relapses and remissions
-difficult to diagnose

157
Q

SLE: systemic

A

-can affect all organ systems
–> presents with a malar rash: more diffuse and often occurs across malar (cheekbones) and sometimes eyebrows

158
Q

DLE: discoid

A

-primarily affects skin (lesions can be found on face or scalp)
–> presents with discoid rash: can lead to permanent scarring and alopecia, can also occur inside mouth (lesions are usually round, red with scaling or crusting visible)
-DLE can progress to SLE over time, the rate of progression thot to be very low

159
Q

Key factors that influence development of SLE

A

-genetics and epigenetic
-environment
-hormones

160
Q

Environment connections to SLE

A

-ultraviolet light (sun is #1 environmental SLE trigger!)
-stress, smoking
-medications (hydralazine, procainamide) –> often reversible upon d/c but it takes ~1 year for all symptoms to go away
-viruses or virus like elements (EBV)

161
Q

Hormone connection to SLE

A

ESTROGEN
-higher SLE risk on oral contraceptive users than in never-users
-inc risk in postmenopausal women administered estrogen
PROLACTIN
-some associations with disease severity in non-pregnant pts and clinical activity in pregnant pts
-decreased SLE risk associated with breastfeeding

162
Q

Pathogenesis of SLE: preclinical phase

A

biomarkers are present but not tests for
-dysregulation of cellular apoptosis: (cells become apoptotic in higher rates than normal)
–> increases in apoptosis
–> clearance deficiencies
-nuclear autoantigens present to:
–> dendritic cells: “INF-a factories” (furthers the inflammatory response)
–> B cells: autoantibodies serologic hallmarks of SLE
-may take years to manifest as SLE

163
Q

Pathogenesis of SLE: impaired tolerance

A

(immune system being unresponsive to foreign materials that has the potential to cause an immune response)
-precipitant factors/insult result
-activated dendritic cells present auto-Ag to CD4+ T cells; T cells communicate with B cells = auto-Ab productions

164
Q

Pathogenesis of SLE: SLE-specific phase

A

-Ab bind to soluble auto-Ag (immune complexes) –> auto-Ag are elements of cell, such as nucleic acids, lymphocytes and erythrocytes and platelets
-these immune complexes deposit in vasculature and susceptible tissues (skin, kidney)
type 3 hypersensitivity reaction
–> neutrophils/complement activate to destroy Ab-Ag complex
–> INF-a, TNF, immune reaction leads to tissue damage
–> inability to clear complexes efficiently
= INFLAMMATION

165
Q

SLE timeline: pre-clinical phase

A

-autoantibodies: general –> specific
(brought on by genetics, epigenetic, environment hormones)

166
Q

SLE timeline: clinical phase

A

1- inflammation, initial organ involvement
2- flares, additional organ involvement, & damage of tissue
3- co-morbidities malignancies & infections are often caused by SLE

167
Q

Presentation of SLE

A

-immune complexes can affect ANY organ system
–> variable manifestations
–> ACR diagnostic criteria
–> most common initial presentation includes fever, arthralgias, and rash in a women of childbearing age

168
Q

ACR diagnostic criteria * SOAP BRAIN MD*

A

need 4/11 to diagnose
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders
Renal involvement
Antinuclear Ab
Immunology
Neurologic disorder
Malar rash
Discoid rash

169
Q

ACR diagnostic criteria: Serositis

A

-inflammation of mucus membrane somewhere in the body
–> pericarditis or pleuritis: pain, rub, effusion
-pain upon inspiration, parodic or effusion is viewed on a radiographic examination or an audible rub upon auscultation

170
Q

ACR diagnostic criteria: oral ulcerations

A

-typically painless
-rough to touch and may appear scaly

171
Q

ACR diagnostic criteria: arthritis

A

-non-erosive, 2+ peripheral joints, characterized by tenderness, swelling, or effusion & redness/fluid in the joint
-most common bc the immune complexes readily deposit into the joints

172
Q

ACR diagnostic criteria: photosensitivity

A

-skin rash as a result of sun exposure (can be anywhere on the body)

173
Q

ACR diagnostic criteria: blood disorders

A

-hemolytic anemia w/ reticulocytosis OR
-leukopenia on > 2 occasions OR
-lymphopenia on > 2 occasions OR
-thrombocytopenia in absence of offending drugs

174
Q

ACR diagnostic criteria: renal involvement

A

-persistent proteinuria
-cellular casts (RBCs or granular cell casts)

175
Q

ACR diagnostic criteria: antinuclear antibodies

A

ANA
-once of the hallmarks of serologic signs of SLE

176
Q

ACR diagnostic criteria: immunologic disorder

A

-anti-DNA Ab
-anti-smith nuclear antibodies (Sm)
-antiphospholipid antibodies: anticardiolipin & lupus anticoagulant

177
Q

ACR diagnostic criteria: neurologic disorder

A

-seizure in absence of offending drug or known metabolic problem
-psychosis in absence of offending drug or known metabolic problem

178
Q

Other presentations of lupus

A

-fatigue
-fever
-weight loss
-myalgia
-avascular necrosis
-pulmonary HTN
-chest pain
-raynaud’s phenomenon
-headache
-intersititual ling disease
-myocarditis
-nausea
-dyspepsia
-abdominal pain
-acute renal disease
-dry eyes
-alopecia
-retinal changes

179
Q

Serologic testing: antinuclear antibodies

A

-low positive predictive value
-very high negative predictive value (~>3% chance of having lupus if negative)
-good for EXCLUDING lupus, but not a 100% guarantee if clinical features of lupus exist
*immunofluorescence studies: RIM = most indicative of SLE)

180
Q

Serologic testing: anti-dsDAN Ab

A

-target genetic material in nucleus, causing organ damage
-perform after ANA titer to confirm
-part of extractable nuclear antigen (ENA) panel

181
Q

Serologic testing: anti-Sm Ab

A

-smoth proteins help RNA keep its 3D structure
-part of ENA panel

182
Q

Antiphospholipid Syndrome (APS) in lupus

A

-hypercoaguable state, autoimmunity
–> anticardiolipin and lupus anticoagulant (result in a hypercoaguable state, increasing risk of thrombotic event)
~50% of SLE patients are aPL(+)
–> APL(+) + thrombotic event = APS (50-70% of aPL(+) SLE pts will have an event = secondary APS
phospholipid syndrome is not official until a pt has a thrombotic event

183
Q

Why is APS so important?

A

-significant morbidity and mortality risks
-> 10% of pts with SLE will have a clot that can be life-threatening
-associated with DVTs, stroke and neurologic manifestations
-associated with unexplained pregnancy loss, premature brith due to preeclampsia, spontaneous abortion

184
Q

Lupus Nephritis

A

-was once the most common cause of death in SLE pts (now it is infection)
-evident in ~ 38% of adults at time of diagnosis; 50-60% will develop nephritis within 10 yrs of diagnosis
kidney inflammation due to either:
a. intravascular deposition of immune complexes in glomeruli
b. formation of immune complexes on self-antigens on glomerular basement membrane

185
Q

Lupus nephritis: diagnostic criteria

A

-persistent proteinuria and/or cellular casts
-renal biopsy and histology to confirm

186
Q

4 top highest group potency of topical steroids to be used in SLE

A

1- clobetasol, fluocinonide high-dose, halobetasol
2- desoximetasone, fluocinonide, med dose
3- betamethathasone valerate ointment, fluticasone ointment
4- mometasone cream, triamcinolone med dose ointment

187
Q

3 of the lowest steroid potency topical in SLE tx

A

1- fluticasone cream, most triamcinolone products
2- most desonide products, low dose triamcinolone cream
lowest: hydrocortisone products

188
Q

NSAID use in SLE

A

-for pain and inflammation caused by various SLE symptoms
-acute or chronic
concerns: GI, cardiac, renal and hepatic
-monitor via CBC
–> aspirin before NSAID; consul pts to take aspirin an hour before NSAID and a few hours after NSAID

189
Q

Hydroxychloroquine in SLE tx

A

-DMARD
-for long term managment of SLE and DLE
most useful drug!
-will have little to no immediate effect, usually takes 2-4 months to work –> use NSAIDs to control symptoms in meantime
-adequate trail period of 6 months: then you can switch to another DMARD or immunosuppressant

190
Q

Hydroxychloroquine SEs in SLE

A

-monotor for response to tx & adverse effects (flu-like symptoms or ocular toxicity) –> major risj factors include dose, length of therapy, CKD, previous retinol or macular disease (exam at baseline, 5 yrs out and every year thereafter
-allergic skin eruptions
-skin & hair pigmentation changes
-hematologic changes: agranulocytosis, neutropenia, aplastic anemia, thrombocytopenia, pancytopenia
-GI upset, myopathies/palsies/CNS (d/c drug & these will go away)
-cardiomyopathy & hearing loss = rare

191
Q

Glucocorticosteroids in SLE treatment

A

-rapid symptom relief: can even use pulse IV steroids for fast relief
adjunctive treatment, reserved for:
1- moderate- severe initial presentation
2- organ threatening or life-threatening SLE
3- inadequate response to HCQ/NSAID
4- poor QOL without
Goal: use the smallest dose for the shortest time, taper off completely (if possible)

192
Q

Glucocorticoid AEs from long term use in SLE

A

-osteoporosis
-hyperlipidemia
-fat redistribution
-moon facies
-growth failure
-amenorrhea
-immunosuppression
-HPA suppression
-cataracts
-obesity
-seizures
-ecchymosis
-muscle weakness
-acne

193
Q

Belimumab (Benlysta) use in SLE

A

-B lymphocyte stimulator antagonist
-routes of admin: IV infusion q month (ages 5+) & SC self-injection (approved for adults only)
adjunctive med:
- non-active CNS, autoantibody-positive SLE!!
-musculoskeletal or cutaneous disease unresponsive to HCQ/NSAID/steroid
-lupus nephritis
–> takes 2-4 months to work

194
Q

Belimimab AEs

A

most common: N/D, allergic reaction, infusion reactions
-depression/suicidality/CNS effects: ~ double the risk of serous psychiatric side effects
-progressive multifocal leukoencephalopathy (PML!)
-avoid life vaccines and other biologics, –> serious infection
-not tested in pregnant or breastfeeding women

195
Q

Anifrolumab (saphnelo) use in SLE tx

A

-adjunct to standard therapy in SLE
-interferon antagonist: reduce immune cell recruitment, symptomatic improvements
-symptomatic benefits, stabilizes organ disease
-IV infusion 1 4 weels
-NOT indicated in active LN or CNS disease

196
Q

when do you want to use immunosuppressants in SLE?

A

-for poor symptom control after HCQ/steroids
-indicated for organ-threatening SLE, mainly lupus nephritis
-often used in combination with steroids

197
Q

methotrexate in SLE

A

-concomitant RA or main problem of arthritis
-more effective than AZA
-AEs: bone marrow suppression, GI toxicity, heptaotoxicity, nephrotoxicity etc

198
Q

Azathioprine in SLE

A

-considered second-line after steroids for a more moderate disease course
safest in class during pregnancy (after HQC)
AEs: bone marrow suppression, N/V

199
Q

Mycophenolate mofetil (MMF) in SLE tx

A

-proliferative LN, second - line for membranous LN
-also useful in non-renal disease
-GI side effects, hemoatological, cardiovascular and teratogenicity

200
Q

Cyclophosphamide use in SLE tx

A

(was LN gold standard) BUT super toxic
use for organ threatening cardiopulmonary, renal or neuropsychiatric disease
SEs: hematologic, cardiac, neurologic toxicity & can cause permanent infertility!

201
Q

Cyclosporine in SLE tx

A

-conclusive evidence that is useful in membranous LN
SEs: hematologic, nephrotoxic, neurotoxic side effects, among others (HTN)

202
Q

rituximab in SLE tx

A

-off label in pts with severe renal, hematologic or neuropsychiatric SLE refractory to other agents (failure of MMF/CYC in LN or relapsing disease

203
Q

calcineurin inhibitor in SLE tx

A

-most commonly tarcolimus, for proliferative LN alone or in combination with MMF

204
Q

Vaclosporin (Lupkykins) use in SLE tx

A

-adjunct to immunosuppressants in active LN
-PO calcineurin inhibitor: dec cytokine production, lymphocyte proliferation
BBW: for infections and malignancies
-should NOT be used with CYC
-nephrotoxicity if eGFR < 45
-CYP3A4 interactions; including grapefruit

205
Q

what are the 4 overreaching principles in treat to targer in SLE?

A

1- shared decisions between pts and MD
2- porlong survival, minimizing organ damage, improve health-related QOL
3- understanding of SLE may require multidisciplinary management
4- monitoring, follow-up, adjustments to therapy

206
Q

treat to target in SLE: 11 recs

A

1- remission or reduced disease activity
2- flare prevention is realistic goal
3- not necessary to escalate treatment in asymptomatic pts with stable or increasing serological activity
4- prevent damage to accrual
5- pay attention to HRQOL
6-recognize and treat LN early
7-optimize LN outcomes with 3 years immunosuppressive therapy after induction
8-lowest possible dose of steroid
9- pat attention to APS
10-give serious consideration to using antimalarials
11- supportive txs should be used when needed

207
Q

Non-pharm/prevention things in SLE

A

-Trigger avoidance: sunscreen, avoid photosensitizing agents
-Prevent/eradicate infection: treat aggressively, immunizations/vaccines
-sun-protection, vaccines, exercise, no smoking, body weight, bp, lipids, glucose

208
Q

SLE pharmacotherapy: MILD

A

HCQ +/-
NSAID +/-
topical steroid +/-
PO/IM steroid

209
Q

SLE pharmacotherapy: moderate to severe

A

-everything for mild +
-immunosupp +/-
-belimumab or antifrolimub +/-
IV steroid

210
Q

what to use for SLE skin disease:

A

topicals (buffered by HCQ)
-#1: steroids (oral if skin disease is the main symptom)
-calcineurin inhibitors
-HCQ
-systemic steroids
(if still no improvement/control):
-methotrexate
-mycophenolate
-retnoids
-dapsone

211
Q

Systemic corticosteroids in SLE tx

A

-rapid symptom relief
-use suppressive dose (pred 20-60 mg)
-use IV pulse (dose by weight/severity)
–> transition to PO, may allow for lower initial PO dose
PO: taper 10-20% q 5-7 days
miminize daily dose < 7.5 mg/day pred equiv

212
Q

What are tx options for refractory/severe SLE?

A

-methotrexate
-mycophenolate
-azathioprine –> use for prego pts
-cyclophosphamide –> reserve for organ-threatening disease & rescue therapy in non-responders

213
Q

Basica Lupus nephtitis care

A

-immunosuppressant (MMF or CYC) PLUS steroid
remission: taper doses and switch immunosuppressants as needed

214
Q

treatment for class 3-4 lupus nephritis

A

-GC + low-dose IV CY or GC + MMF
-if response in 3-12. months: swtich to MMF or AZA
-if NO response in 3-12 months: switch to alt therapy or add TA or Rituximab

215
Q

Class 5 lupus nephritis tx

A

UPr < 3 grams/24hr –> RAAS
UPr > 3 grams/24 hr –> RAAS, GC + MMF

216
Q

Other LN care points

A

-use ACEi or ARB in SLE pts who have glomerular disease and:
-persistent proteinuria (> 0.5 g/24hr) and/or
-hypertension
-use statin therapy in LDL > 100 mg/dL: SLE and reduced GFR both independent risk factors for accelerated atherosclerosis

217
Q

RIsk categories in SLE and what to do for successful pregnancy?

A

Risk: pre-eclamsia, congenital heart block & miscarriages
For success: wait until remission, adhere to drugs & use low dose steroids if needed

218
Q

Pregnancy concerns with drugs in SLE

A

-HCQ: NOT associated with congenital malformations, benefir far outweights the risk & increased risk of flare if d/c during pregnancy
-NSAIDs: unsafe in 3rd trimester but should avoid anyway, manage pain with APAP
-topical steroids: use low dose

219
Q

LN care in pregnancy

A

-mild disease activity: HCQ/AZA
-clinically active LN:
–> non fluorinated oral glucocorticoid
–> aza (max dose 2 mg/kg/day) if necessary to control LN or reduce dose of steroid (MMF, CYC, MTX = teratogenic)
-pre-term delivery (after 28 weeks) considered if LN highly active

220
Q

TX of a pt who is aPL (+), no event & not pregnant

A

low dose aspirin (81 mg/d)

221
Q

TX of a patient who is aPL (+), no event and pregnant

A

-low dose aspirin +/- LMWH

222
Q

TX of a patient who has APS (has antibodies and an event) and pregnant

A

-low dose aspirin +/- LMWH

223
Q

TX of a patient who has APS (has antibodies and an event) not pregnant & ARTERIAL clot

A

-warfarin with INR 3-4

224
Q

TX of a patient who has APS (has antibodies and an event) not pregnant & venous clot

A

(pulm. embolism)
-warfarin with INR 2-3

225
Q

Monitoring and follow up for SLE

A

-signs/sx every 3-6 months at office visits –> adverse drug events
-every 6 months: UA, BMP, CBC, lipid panel & serological disease markers

Pulm Therapeutics (4 decks)

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