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IPFC 5 > Rheumatoid Arthritis Pathophysiology + Therapeutics > Flashcards

Rheumatoid Arthritis Pathophysiology + Therapeutics Flashcards

1
Q

What impact does gender have on RA

A

3x more women suffer from RA than men
- under 10 years and over 60 years the number is equal in genders

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2
Q

Men with RA are more likely than women to have (3)

A

More severe disease (decreased life expectancy)
Extra-articular manifestations
Join degradation

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3
Q

In females with RA.. Do hormones play a role? (3)

A

High exposure to estrogen, progestin, and corticoids seems to reduce risk of RA

  • RA gets better during pregnancy (high estrogen period)
  • RA flares are common postpartum (low estrogen period), though can be improved if breastfeeding
  • RA incidence increases after menopause
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4
Q

What impact on morbidity does RA have (2)
Independant risk factor for?

A
  • Increased rates of infection (TB, Herpes Zoster)
  • Increased rates of Cancer (including Lymphoma)

INDEPENDANT risk factor for Osteoporosis and CVD

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5
Q

T/F RA is symmetrical

A

True

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6
Q

Which gene for RA is the strongest implicated. Which MHC class is this in?

A

HLA-DRB1 gene
- MHC class 2 region

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7
Q

What is the shared Epitope theory

A

Many RA patients share this “citrullinated protein” that the body thinks is foreign.

  • The body then develops ACPAs against this protein
  • ACPAs are therefore an important diagnostic marker
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8
Q

What is citrullination?

A

During inflammation, (PAD enzymes) begin to “citrullinate” proteins
- Replacing arginine with citrulline (a non-standard amino acid)

Buildup of abnormal (citrullinated) proteins are seen as FOREIGN and attacked by antibodies (ACPAs) -> resulting in joint-destroying inflammation

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9
Q

What are powerful biomakers of RA disease (2)
How long can they be found before clinical presentation

A

Rheumatoid Factor
Anti-citrullinated protein Antibodies (ACPAs)

Can be found 15 years before clinical diagnosis

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10
Q

What is PANNUS?

A

The “pannus” is that synovial membrane which has become inflamed, and proliferating. The result:
- Joint swelling, stiffness, nodules, ulnar drifts, contractures, etc.

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11
Q

What are the Major central cytokines in the pathogenesis of RA (3)

A

TNFa
IL-6
IL-1

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12
Q

Differentiate between TNF-A and IL-6
Similarities?
Differences

A

TNFa
- activates cytokines
- suppresses REGULATORY T-cells (that help control immune process)
- promotes, pain, heat in joints

IL-6
- Promotes leukocyte and AUTOantibody production
- contributes to anemia, cognitive issues, lipid metabolism issues

BOTH TNF-a and IL-6 amplify osteoclast activation (BONE LOSS)

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13
Q

T/F there is a link of gut/mouth/infection to RA trigger

A

True

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14
Q

What is the relationship between RA and smoking (3)

A
  • EVER having smoked = HUGE increase in risk ACPA positive RA
  • LENGTH of time smoking (not # of cigs/day) increases risk
  • Smoking also reduces efficacy of RA medications (MTX, Hydroxychloroquine, TNF inhibitors)
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15
Q

What is the classic clinical presentation of RA

A
  • Fatigue, weakness, malaise, low-grade fever, loss of appetite
  • Joint pain (BILATERAL and SYMMETRIC), Joint tenderness/swelling, warm/red joints

In the MORNING: Loss of strength + stiffness (lasting >30-60 mins) - usually improves with activity

Non-joint Sx: dry eyes, nodules

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16
Q

What does the disease progression look like in RA

A

Begins in the SMALL PERIPHERAL joints -> develops in larger joints (elbows, shoulders, knees, cervical vertebrae, jaw)
○ PIP: Proximal interphalangeal joints
○ MCP: Metacarpophalangeal joints
HANDS/WRISTS are most affected by RA (…then elbows)

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17
Q

Differentiate between OA and RA

A

OA:
- loss of cartilage in joints -> increased bone production -> bone on bone inflammation -> HARD/BONY appearance
- Affects DISTAL and middle (metacarpal) phalanges

RA:
- Proliferation of soft tissue + fluid accumulation in the joints -> SPONGY joints (fluid-filled)
- Affects PROXIMAL and middle (metacarpal) phalanges

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18
Q

What are extra-articular manifestation of RA (8)

A
  1. Rheumatoid Nodules
    - found on many joints/pressure points. Usually small, PAINLESS, don’t interfere with function
    More common in men than women
  2. Vasculitis
    - Inflammatory cells invade blood vessel walls -> vessel infarction
    Can cause skin breakdown -> permanent skin ULCERation
  3. Eyes:
    - Keratoconjunctivitis sicca (dry eye syndrome). Can be from Sjogren Syndrome (which is common in RA) + Itchy eyes
  4. BONES:
    - RA is an INDEPENDENT risk factor for Osteoporosis
  5. Blood:
    - anemia, splenomegaly, leukopenia, neutropenia
  6. Felty’s syndrome:
    - splenomegaly + neutropenia (may also get thrombocytopenia)
  7. Lungs:
    - pleuritis, pleural effusion, interstitial fibrosis, pneumonitis, lung nodules
  8. Heart:
    - Pericarditis, Myocarditis, CAD
    • RA is INDEPENDENT risk factor for MI
    • Lipid paradox: CVD mortality in RA is associated with LOWER TC and LDL levels (and also higher ESR). This is the opposite of non-RA patients.
      ○ Therefore, TC:HDL ratio is the better indicator of CVD risk in RA

Other: Lymphadenopathy, Renal issues

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19
Q

What is used to diagnose RA

A

No single test or physical finds can be used

History and physical exam is the majority

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20
Q

T/F Radiographic findings and lab markers early in the disease can detect RA

A

False

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21
Q

What are the 4 categories of the 2010 ACR/EULAR classification

What score = definite RA

A
  1. # and joint size
  2. RF and ACPA
  3. Symptoms under 6 weeks or 6+weeks
  4. CRP and ESR

Score of 6 or more = definite RA

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22
Q

What is the Disease Activity score 28 (DAS28)
What is the remission, low, moderate, high disease score

A
  • Looks at 28 joints + lab markers (ESR or CRP)
  • Good to evaluate patient’s response to treatment (good in office)

Remission: <1.6
Low disease activity <2.4
Moderate disease activity <3.7
High disease activity 3.7+

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23
Q

What is the health assessment questionnaire
What does it evaluate? (5)
Benefit?

A

Evaluates
- disability
- Pain
- Medication effects
- Costs of care
- Mortality

Benefit: Short, commonly used in MD office

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24
Q

What is the global assessment of disease activity

A

rated by patient (PGA) and evaluator/clinician (EGA)
- Patient usually scores themselves higher than the Clinician

Still useful for pt to get better perspective of their disease

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25
Q

T/F Lab markers are more helpful with diagnosis than prognosis

A

False

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26
Q

What are rheumatoid factors?
What does a positive RF indicate?
Is the test sensitive or specific?
Good for chronic monitoring?

A

Proteins produced by your immune system that can attack healthy tissue in your body
- Healthy people DON’T produce RF.

* Presence of RF indicates GENERAL Autoimmune disease (Lupus, Sjogren's), Malaria, Rubella, Hep C, after vaccination (in healthy pt)
	○ But Positive RF + Arthritis symptoms is relatively specific for RA diagnosis

* RF+ occurs in most RA patients. Indicates more aggressive disease + extra-articular manifestations

RF levels rarely change with disease activity -> RF levels NOT good for chronic monitoring

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27
Q

Anti-Cyclic Citrullinated Peptide (ACCP) Test:
Sensitivty and specificity?

A

Similar sensitivity to RF test,
Higher SPECIFICITY than RF test (positive result almost always means RA positive)

Can be positive in other diseases: TB, SLE, Sjogren’s, Scleroderma

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28
Q

Which Acute phase reactants is useful for monitoring disease activity?
What are the other markers used for tissue injury/inflammation?

A

ESR (Erythrocyte sedimentation rate):
* High ESR + CRP is a stronger indication of future radiographic progression than CRP alone
* Not REQUIRED for RA diagnosis

CRP (C-Reactive Protein): general indication of inflammation, produced by liver
* Useful for monitoring disease activity

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29
Q

What hematology are used to diagnose RA (3)

A

Hemoglobin: will be low in Anemia of chronic disease. Will also NOT respond to iron
- Less than normal, but still >90g/L in RA

Serum Albumin: Often low. Correlated directly with disease severity
- Albumin: Will fall with disease severity

Platelet Count (thrombocytosis):
- Rise during severe RA and fall in correlation with disease activity

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30
Q

When do you do X-rays in RA diagnosis

A

Even though X-rays are not 100% indicative of RA
Once pt is diagnosed with RA
- X-ray at baseline then follow X-rays Q6-12 months, and we want to see NO CHANGE

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31
Q

What are the 3 broad patterns of clinical progression of RA

A

Long Clinical remissions (10%) of patients): prolonged remission that may result in RF test being negative (with the occasional flare)

Intermittent disease (15-30% of patients): partial-complete remissions lasting up to 1 year.
* Flares/relapses often involve NEW joints

Progressive disease (MOST of patients): destruction of joints over time -> disability
Treatment is CRITICAL

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32
Q

What is the MOA of glucocorticoid

A

Enter the nucleus of the cell to alter mRNA synthesis

  • Result: up-regulation of anti-inflammatory genes + down-regulation inflammatory genes
  • Also inhibits Phospholipase A2 -> reduced arachidonic acid release -> reduced prostaglandin synthesis
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33
Q

Why is prednisone the glucocorticoid choice in RA? (3)
What dose of prednisone is equivalent to the amount of cortisol the body makes

A

Prednisone
- Moderate glucocorticoid potency
- Intermediate duration of action
- Low mineralocorticoid potency

5-7.5mg of prednisone mimics the amount of cortisol the body makes daily
- body stops making steroid when you supplement with prednisone

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34
Q

Why is prednisone dosing usually in the morning (3)

A
  • Giving GCs in the morning best mimics the body’s natural release of cortisol (circadian rhythm)
  • Giving GCs in the morning may have less HPA axis suppression (natural cortisol suppression) than PM dosing
  • Giving GCs at night may cause insomnia
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35
Q

What is the best route of administration of steroid in active polyarthritis
How many can you give per year

A

IM
- useful while waiting for the benefits of DMARDs to kick in

LIMIT of 3-4 IM corticosteroid shots per year (ADRs are common if given more)

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36
Q

What is the fastest route of administration of steroid in? Examples
Contraindications?

A

Intraarticular injection
Triamcinolone (kenalog)
Methylprednisone Depo-medrol

CI
- active polyarthritis too many joints

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37
Q

When would you use oral prednisone in? Duration?

HIGH dose/short term
LOW dose/short-term
LOW dose/long term

A

HIGH dose/short term
- 30-60mg daily for 5-10 days

LOW dose/short-term
- 5-10mg daily for <3 months

LOW dose/long term
- 5-10mg daily for 3+ months
- if using 7.5mg+ daily for 3+ months consider osteoporosis prophylaxis (calcium, Vit D, bisphosphonate PRN)

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38
Q

What are the following onsets in terms of pain and inflammation for the following treatments

Analgesics
Glucocorticoid
NSAIDS
DMARDS

A

Analgesics (Tylenol, NSAIDs, COX2, IR opioids)
- Pain relief - <1h
- Inflammation relief - 2-4 weeks

Glucocorticoids
- Pain AND inflammation relief - 1-4 days

DMARDs
- Inflammation relief - 2-6 months

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39
Q

What are the risks of chronic glucocorticoid use (7)

A
  • Osteoporosis/fractures, GI bleed
    • Risk of DM, MI/stroke, HTN, dyslipidemia
    • Fluid retention
    • Infection, reactivation of latent TB (LTBI)
    • Cataracts, increased IOP
    • Cushingoid features (obesity, moon face)
    • Worsening psychiatric symptoms (depression, insomnia, psychosis)

Impairment of HPA Axis response and the adrenal cortex production - Why we taper

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40
Q

Glucocorticoids in pregnancy
What class?
When to not use
When to use?
What to watch out for?

A

What class?
- Pregnancy class C

When to not use?
- Do not use 1st trimester (can cause oral cleft formation)

When to use?
- 2nd/3rd trimester + breastfeeding
- consider LOCAL steroid injections

What to watch out for?
- In diabetic patients who are pregnant, watch for elevated glucose

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41
Q

Why do we taper glucocorticoids (3)

A

Not tapering can lead to ADRENAL CRISIS: if the body is put through STRESS (surgery, trauma, etc) with very low cortisol stores, it won’t be able to handle the situation -> could be fatal

Cortisol usually controls sodium levels:
- Without it: more sodium is lost from kidneys + potassium is reabsorbed

Cortisol usually helps blood vessels constrict:
- Without it: blood vessels relax too much = decreased intravascular tone, vascular tone, cardiac output, renal perfusion

Cortisol usually helps control BP:
- Without it: postural hypotension, compensatory tachycardia + eventual vascular collapse

= elevated nitrogen + creatinine

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42
Q

What are withdrawal symptoms of glucocorticoid if you stop abruptly or taper too quick (4 organs)

A

GI: NV
Pain: Arthralgia, myalgia, fever, lower chest & abdominal ain
CNS: dizziness, fainting, weakness, fatigue, confusion, delirious, lethargic
Heart: hypotension
Other: weight loss, electrolyte imbalances, shock/death

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43
Q

Which factors are dependant on the rate at which prednisone can be tapered? (4)

A
  • Dose of prednisone being used
  • Duration
  • Indication
  • Medical conditions and patient specific factors (age, frailty, comorbodities)
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44
Q

When do we taper prednisone and when do we not need to

A

Who should taper (and not just stop):
- Pt on >7.5mg/day for >3 weeks (When HPA Axis suppression is seen)
○ Though we can do it for patients on less for shorter time (seen HPA axis suppression in just 2 weeks

If prednisone course is <7-10 days (at ANY dose), you can just STOP (no taper needed)

What if patient in hospital MUST stop abruptly: since they are being closely monitored, this is okay.

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45
Q

Which DMARD is first line choice in RA

A

Methotrexate

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46
Q

Why is methotrexate in combo with biologic effective?

A

Reduces the antidrug antibody formation to the biologic

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47
Q

What is the MOA of methotrexate

A

MOA: Folate agonist with immunosuppressive/anti-proliferative effects

  • Inhibits DHFR (which reduces folate, needed for nucleic acid synthesis) (dihydrofolate reductase)
  • Increases release of adenosine -> anti-inflammatory effects
  • Reduces cytokine production, TNFa concentrations, and leukotrienes
48
Q

What is the methotrexate initial and target dosing

A

Start at 10mg PO/SCC and titrate to target of 25mg
- increase by 2.5-5mg every 1-2 weeks
- Max dose is 30mg

At doses over 15mg switch to SC for more bioavailability

49
Q

What is the next step if a patient is intolerant to oral MTX

A

Switch to SC injections

50
Q

What is the renal dosing for MTX

A

CrCL 30-60mL/min: lower initial doses, gradual dose increase

CrCl <30mL/min: CONTRAINDICATED

51
Q

Time to Initial response and full effect of the following csDMARD
MTX
LEF
SSQ
HCQ

A

MTX
- initial: 6-12 weeks
- full: 12 weeks

LEF
- initial: 2-4 weeks
- full: 12 weeks

SSQ
- initial: 8 weeks
- full: 12 weeks

HCQ
- initial: 12-16 weeks
- full: 24 weeks

52
Q

Methotrexate
Common side effects (6)
Serious ADRs (3)

A

Common side effects
- Post-MTX “sick day”: N/V, fatigue, flu-like symptoms
- Headache
- Hair loss (reversible),
- diarrhea
- sun sensitivity
- oral ulcers

Serious ADRs
- Bone marrow suppression (dose related)
- Hepatitis (upper quadrant pain)
- Infections (subacute pneumonitis) (sudden dry cough) –> D/C THERAPY

53
Q

Folic acid dosing in methotrexate

A

since MTX depletes the folate stores (supplementing can help with some ADRs)
* 5mg/week or 2.5mg twice weekly or 1mg daily x5days/week - ALL EFFECTVE
Important: do not take folate on the same say as MTX (≥24 hours separate)

54
Q

What OTC product can help the foggy thinking and fatigue from methotrexate

A

DM syrup

May help with fatigue, foggy thinking (DM is a NMDA blocker)
Dosing: 2 tsps. BID on the 3 days surrounding MTX dose (day before, of, after)

55
Q

Methotrexate in Pregnancy
washout period
Breastfeeding

A

Men and women must d/c 3 months prior to conception
- use birth control

No breastfeeding on MTX

56
Q

Baseline monitoring for MTX (9)

A
  • pregnancy test
  • hepatitis
  • HIV
  • CBC, SCr, LFTs, chest X-ray, TB skin test
  • Albumin
57
Q

Ongoing monitoring for MTX (4)
When specifically to do blood work?
How often in the first year?

A

CBC, LFTs, SCr, albumin
(monthly for first 3 months, then more/less frequently depending on results q4-12 weeks)

Always do Blood work the day BEFORE weekly MTX dose (LFTs may be high following dose)

58
Q

What is considered abnormal LFT’s while on MTX?

A

if AST, ALT levels >2x ULN on 2+ occasions - STOP MTX
Consider resuming once levels are <2x ULN

59
Q

T/F NSAIDs cannot be used with MTX in RA patients

A

False
- ok at low doses of 25-30mg
- only a concern in oncology doses

60
Q

Methotrexate Contrainidications

A
  1. Alcohol: discouraged due to risk of hepatotoxicity with MTX
    - Restrict (1-2 drinks/week) or ABSTAIN (better)
  2. Smoking:
    - may decrease efficacy of MTX and etanercept (Swedish study)
  3. Trimethoprim-containing antibiotics:
    - AVOID with MTX (blocks excretion + increases folate deficiency)
    - SEPTRA, Bactrim, Proloprim (single agent Trimethoprim)
61
Q

What is the 2nd-line csDMARD in RA

A

Leflunomide

62
Q

Out of the 4 csDMARDs, which of them are shown to reduce radiographically confirmed progession of RA

A

MTX
Leflunomide

63
Q

MOA of Leflunomide (2)

A

prodrug -> converted into Teriflunomide
* Competitively inhibits dihydro-orotate dehydrogenase -> inhibits pyrimidine synthesis
* Reduces IL-8, TNFa and increases IL-10 (which is good)

64
Q

Dosing of leflunomide
Renal dosing

A

Dosing: STARTING dose 10mg -> titrate up to 20mg
* Take with food
Renal dosing: caution in MILD renal disease, CONTRAINDICATED in mod-severe renal impairment

65
Q

Common side effects of Leflunomide (8)
Serious side effects (5)

A

Common
- GI (diarrhea, N/V, stomach pain), weight loss,
- elevated LFTs
- hair loss (reversible)
- Minor URTIs
- headaches
- HTN
- Rash

Rare
- BM supression
- Hepatitis
- infections
- profound weight loss
- INTERSTITIAL LUNG disease (penumonitis, fibrosis)

66
Q

Leflunomide in pregnancy
Washout period?

A

2 year washout period.
Go on effective birth control if of child bearing age

67
Q

What is the antidote if unexpected pregnancy on leflunomide

A

Cholestyramine 8g TID for 11 days

68
Q

What are the drug interactions with leflunomide (2)

A

Warfarin
Rifampin

69
Q

Leflunomide Baseline monitoring
Ongoing monitoring

A

Baseline (same as MTX)
- pregnancy test
- hepatitis
- HIV
- CBC, SCr, LFTs, chest X-ray, TB skin test
***BP, no albumin

Ongoing
CBC, LFTs, SCr
(monthly for first 3 months, then more/less frequently depending on results q4-12 weeks)

70
Q

T/F Sulfasalazine is not as effective as MTX

A

True

71
Q

MOA of sulfasalazine

Which cytokines does it affect (4)

A

prodrug, converted by colonic bacteria into Sulfapyridine + 5-ASA
- Thus, using antibiotics reduces efficacy (need gut bacteria to convert this drug)

5-ASA suppresses pro-inflammatory cytokines (IL-1,6,12, TNFa)

POOR EFFECT ON JOINT DAMAGE (little radiographic efficacy)

72
Q

Sulfasalazine dosing

A

Staring dose 500mg, target dose 3g/day (important due to GI S/Es)
Take with food, preferable enteric-coated tablets

73
Q

Who should not use sulfasalazine? (2)

A

Sulfa allergies
Glucose-6-phosphate deficiency

74
Q

Sulfasalazine common side effects (4)
Rare side effects (1)

A

Common
- N/V/D, anorexia, abdominal pain (mostly GI).
- Urine/sweat discolouration (yellow/orange)
- Photosensitivity
- Skin rash

RARE: skin reactions - SJS, DRESS, etc… (due to sulfa component)

75
Q

Sulfasalazine drug interactions (3)

A
  1. Warfarin: SSZ has anticoagulant effects
  2. Digoxin: SSZ inhibits Digoxin absorption (at higher doses)
  3. Methotrexate: increased levels of SSZ and MTX (not a relevant interaction)
76
Q

Sulfasalazine in pregnancy

A

Safe and compatible

77
Q

Which csDMARD is the best tolerated and least toxic?
Which is least effective?

A

All Hydroxycholorquine
- NO effect on joint damage

78
Q

What are other benefits of hydroxychloroquine beyond inflammation (3)

A
  • Improves glucose/lipid profiles
  • lowers fasting insulin levels and resistance
  • lowers A1C
79
Q

Hydroxychloroquine MOA

A

Inhibits B/T cells, antigen processing, IL-1,6 release

80
Q

Hydroxychloroquine dosing

A

200-400mg daily
(MAX dose 5mg/kg/day) for retinal toxicity
Take with food or milk

81
Q

Hydroxychloroquine common side effects (3)
Rare side effects (6)

A

Common
- Nausea (from bitter taste, rare vomiting), diarrhea, gas, stomach pain, anorexia
- Bluish-black hyperpigmentation
- skin rash (due to sunlight)

Rare
- corneal and retinal deposition
- blindness
- myopathy, cardiomyopathy
- sun sensitivity
- ringing in the ears
- Headache, dizziness

82
Q

What tests to get at baseline (2)

A

No routine blood work required

Ocular exam + ECG (qtc prolongation)

83
Q

Hydroxychloroquine in pregnancy, breastfeeding

A

Safe

84
Q

Hydroxychloroquine drug interactions (3)

A
  • Amiodarone: risk of peripheral neuropathy
    • Digoxin: increased digoxin levels
      Hypoglycemic meds: risk of hypoglycemia increased
85
Q

What are contraindications to TNA-a inhibitors (3)

A
  1. Susceptibility to or presence of infection
  2. Active malignancy or history of malignancy
  3. CHF NYA III
86
Q

What monitoring do you need for TNF-a and ALL BIOLOGICS (7)

A
  • hepatitis
  • HIV
  • CBC, SCr, LFTs, chest X-ray, TB skin test (LTBI)
87
Q

What is the safety profile of TNF-a (3)

A

Injection site rxn
Infections
Increase in skin cancers

Infusion rxn for infliximab

88
Q

Rituxan Class
Contraindications (2)
Rare safety (1)

A

Class: B-cell depleters

CI
1. Susceptibility to or presence of infection
2. Type 1 hypersensitivity rxn (allergy)

Rare safety
- Progressive multifocal leukoencephalopathy

89
Q

Abatacept (Orencia) IV
Drug class
CI
Rare safety

A

Class: T-Cell Co-stimulation inhibitor

CI
1. Susceptibility to or presence of infection
2. Type 1 hypersensitivity rxn (allergy)

Rare safety
- minor infusion rxn

90
Q

Anakinra (kineret)
Class
CI

A

Class: IL-1 inhibitor

CI
- known allergy to E. coli derived proteins

91
Q

Tocilizumab Actemra
Class
Safety

A

IL-6 inhibitor

Safety same as TNF-a
-GI perforations

92
Q

Sarilumab (KEVZARA)
Class
Safety

A

IL-6 antagonist

Safety same as TNF-a

93
Q

What is first line biologic in RA

A

Anti-TNF a

94
Q

What is 2nd line therapy if they fail an Anti-TNFa

A

Different Anti-TNFa
OR
Abatacept (orencia) T-cell
Rituximab (rituxan) B-cell
Tocilizumab (actemra) IL-6

95
Q

Which biologic is best for:
Active malignancy
History of malignancy

A

Active
- all DMARD therapy delayed

History
- Consider HCQ, SSZ, or Rituximab
- Avoid TNFa-treatment

96
Q

Which biologic is best for Hepatitis

A

Pre-vaccinate with Hep vaccines
Then give Anti-TNF or abatacept or rituximab

97
Q

Difference between biologic and JAK inhibitor

A

JAK inhibitors are SMALL molecules that work INSIDE the cells (biologics work outside the cell)
JAK inhibitors are given ORALLY (small molecules), Biologics must be injected

98
Q

MOA of JAK inhibitor

A

Blocking JAK enzymes results in blocked cytokine signalling -> reduce further inflammation
Specifically involves the JAK-STAT pathway -> affecting DNA transcription/Cytokine signalling

99
Q

Dose of Tofacitinib
Renal/hepatic
Drug interaction CYP 3A4 (ketoconazole)

A

5mg PO daily instead of BID

100
Q

Monitoring for JAK inhibitors

A

Vaccinations
Chest x ray, TB, hepatitis
Pregnancy test
Signs of infection
CVS risk + risk of thrombosis

Ongoing:
LFTs, CBC, lipids + renal function

101
Q

JAK inhibitors safety (4)

A

Same as biologic
- risk of TB, infections, lymphoma, increased LFTs and hepatitis

Can increase cholesterol LDL and HDL
increased risk of CVS, cancer, and thrombosis
Avoid live vaccines

102
Q

When are ideal administrations of vaccines in RA patients

A

2-4 weeks prior to starting treatment

103
Q

Glucocorticoids
Flu vaccine
Other non-live vaccines

A

Flu
- give at all doses

Other non-live vaccines
- OKAY unless ≥20mg prednisone daily (then defer - flu shot okay at ALL doses of prednisone)

104
Q

What is the only RA therapy where you have to make changes when getting the Flu shot

A

Methotrexate
- hold for 2 weeks after vaccination

105
Q

What is the only RA therapy where you have to make changes when getting a non-live vaccine

A

Rituximab
- hold for at least 2 weeks after vaccination

106
Q

For DMARDS and glucocorticoids, how long do you have to hold before and after giving a live vaccine

A

4 weeks before
4 weeks after

107
Q

For biologics and rituximab, how long do you have to hold before and after giving a live vaccine

A

1 dosing interval before (rituximab is 6 months before)
4 weeks after

108
Q

For JAK inhibitors, how long do you have to hold before and after giving a live vaccine

A

1 week before
4 weeks after

109
Q

How long do you stop before surgery
Biologics
JAKi
MTX, LEF, SSZ, HDXY

A

Biologics
- 2 half-lives (28 days usually)

JAKi
- 1 week before

MTX, LEF, SSZ, HDXY
- No need to stop

110
Q

How to treat patient is positive for LTBI pre-DMARD

A
  • Start TB treatment with isoniazid
    • Hold Biologic or JAK during treatment - restart after 1-2 months of TB treatment
111
Q

When do you stop biologic treatment during sickness

A

Moderate or severe infections on antibiotics

No need to stop for Mild infection (eg. sore throat, common cold)

112
Q

Compare between treatments
Triple therapy MTX + HCQ + SSZ
Biologics

A

Not inferior and much cheaper
- just big pill burden

113
Q

Compare between treatments
non-MTX dmard + biologic
Biologic

A

Adding non-MTX csDMARD to TNFa is superior to TNFa alone

114
Q

What only drug can you add to JAK inhibitors

A

MTX

115
Q

T/F there is evidence of benefit of combo therapy of csDMARD without MTX

A

False

IPFC 5 (10 decks)

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