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
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
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
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
5
Q
T/F RA is symmetrical
A
True
6
Q
Which gene for RA is the strongest implicated. Which MHC class is this in?
A
HLA-DRB1 gene
- MHC class 2 region
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
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
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
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.
11
Q
What are the Major central cytokines in the pathogenesis of RA (3)
A
TNFa
IL-6
IL-1
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)
13
Q
T/F there is a link of gut/mouth/infection to RA trigger
A
True
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)
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
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)
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
18
Q
What are extra-articular manifestation of RA (8)
A
- Rheumatoid Nodules
- found on many joints/pressure points. Usually small, PAINLESS, don’t interfere with function
More common in men than women - Vasculitis
- Inflammatory cells invade blood vessel walls -> vessel infarction
Can cause skin breakdown -> permanent skin ULCERation - Eyes:
- Keratoconjunctivitis sicca (dry eye syndrome). Can be from Sjogren Syndrome (which is common in RA) + Itchy eyes - BONES:
- RA is an INDEPENDENT risk factor for Osteoporosis - Blood:
- anemia, splenomegaly, leukopenia, neutropenia - Felty’s syndrome:
- splenomegaly + neutropenia (may also get thrombocytopenia) - Lungs:
- pleuritis, pleural effusion, interstitial fibrosis, pneumonitis, lung nodules - 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
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
20
Q
T/F Radiographic findings and lab markers early in the disease can detect RA
A
False
21
Q
What are the 4 categories of the 2010 ACR/EULAR classification
What score = definite RA
A
- # and joint size
- RF and ACPA
- Symptoms under 6 weeks or 6+weeks
- CRP and ESR
Score of 6 or more = definite RA
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+
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
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
25
T/F Lab markers are more helpful with diagnosis than prognosis
False
26
What are rheumatoid factors?
What does a positive RF indicate?
Is the test sensitive or specific?
Good for chronic monitoring?
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
27
Anti-Cyclic Citrullinated Peptide (ACCP) Test:
Sensitivty and specificity?
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
28
Which Acute phase reactants is useful for monitoring disease activity?
What are the other markers used for tissue injury/inflammation?
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
29
What hematology are used to diagnose RA (3)
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
30
When do you do X-rays in RA diagnosis
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
31
What are the 3 broad patterns of clinical progression of RA
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
32
What is the MOA of glucocorticoid
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
33
Why is prednisone the glucocorticoid choice in RA? (3)
What dose of prednisone is equivalent to the amount of cortisol the body makes
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
34
Why is prednisone dosing usually in the morning (3)
- 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
35
What is the best route of administration of steroid in active polyarthritis
How many can you give per year
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)
36
What is the fastest route of administration of steroid in? Examples
Contraindications?
Intraarticular injection
Triamcinolone (kenalog)
Methylprednisone Depo-medrol
CI
- active polyarthritis too many joints
37
When would you use oral prednisone in? Duration?
HIGH dose/short term
LOW dose/short-term
LOW dose/long term
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)
38
What are the following onsets in terms of pain and inflammation for the following treatments
Analgesics
Glucocorticoid
NSAIDS
DMARDS
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
39
What are the risks of chronic glucocorticoid use (7)
* 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
40
Glucocorticoids in pregnancy
What class?
When to not use
When to use?
What to watch out for?
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
41
Why do we taper glucocorticoids (3)
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
42
What are withdrawal symptoms of glucocorticoid if you stop abruptly or taper too quick (4 organs)
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
43
Which factors are dependant on the rate at which prednisone can be tapered? (4)
- Dose of prednisone being used
- Duration
- Indication
- Medical conditions and patient specific factors (age, frailty, comorbodities)
44
When do we taper prednisone and when do we not need to
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.
45
Which DMARD is first line choice in RA
Methotrexate
46
Why is methotrexate in combo with biologic effective?
Reduces the antidrug antibody formation to the biologic
47
What is the MOA of methotrexate
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
What is the methotrexate initial and target dosing
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
What is the next step if a patient is intolerant to oral MTX
Switch to SC injections
50
What is the renal dosing for MTX
CrCL 30-60mL/min: lower initial doses, gradual dose increase
CrCl <30mL/min: CONTRAINDICATED
51
Time to Initial response and full effect of the following csDMARD
MTX
LEF
SSQ
HCQ
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
Methotrexate
Common side effects (6)
Serious ADRs (3)
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
Folic acid dosing in methotrexate
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
What OTC product can help the foggy thinking and fatigue from methotrexate
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
Methotrexate in Pregnancy
washout period
Breastfeeding
Men and women must d/c 3 months prior to conception
- use birth control
No breastfeeding on MTX
56
Baseline monitoring for MTX (9)
- pregnancy test
- hepatitis
- HIV
- CBC, SCr, LFTs, chest X-ray, TB skin test
- Albumin
57
Ongoing monitoring for MTX (4)
When specifically to do blood work?
How often in the first year?
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
What is considered abnormal LFT's while on MTX?
if AST, ALT levels >2x ULN on 2+ occasions - STOP MTX
Consider resuming once levels are <2x ULN
59
T/F NSAIDs cannot be used with MTX in RA patients
False
- ok at low doses of 25-30mg
- only a concern in oncology doses
60
Methotrexate Contrainidications
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
What is the 2nd-line csDMARD in RA
Leflunomide
62
Out of the 4 csDMARDs, which of them are shown to reduce radiographically confirmed progession of RA
MTX
Leflunomide
63
MOA of Leflunomide (2)
prodrug -> converted into Teriflunomide
* Competitively inhibits dihydro-orotate dehydrogenase -> inhibits pyrimidine synthesis
* Reduces IL-8, TNFa and increases IL-10 (which is good)
64
Dosing of leflunomide
Renal dosing
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
Common side effects of Leflunomide (8)
Serious side effects (5)
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
Leflunomide in pregnancy
Washout period?
2 year washout period.
Go on effective birth control if of child bearing age
67
What is the antidote if unexpected pregnancy on leflunomide
Cholestyramine 8g TID for 11 days
68
What are the drug interactions with leflunomide (2)
Warfarin
Rifampin
69
Leflunomide Baseline monitoring
Ongoing monitoring
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
T/F Sulfasalazine is not as effective as MTX
True
71
MOA of sulfasalazine
Which cytokines does it affect (4)
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
Sulfasalazine dosing
Staring dose 500mg, target dose 3g/day (important due to GI S/Es)
Take with food, preferable enteric-coated tablets
73
Who should not use sulfasalazine? (2)
Sulfa allergies
Glucose-6-phosphate deficiency
74
Sulfasalazine common side effects (4)
Rare side effects (1)
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
Sulfasalazine drug interactions (3)
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
Sulfasalazine in pregnancy
Safe and compatible
77
Which csDMARD is the best tolerated and least toxic?
Which is least effective?
All Hydroxycholorquine
- NO effect on joint damage
78
What are other benefits of hydroxychloroquine beyond inflammation (3)
- Improves glucose/lipid profiles
- lowers fasting insulin levels and resistance
- lowers A1C
79
Hydroxychloroquine MOA
Inhibits B/T cells, antigen processing, IL-1,6 release
80
Hydroxychloroquine dosing
200-400mg daily
(MAX dose 5mg/kg/day) for retinal toxicity
Take with food or milk
81
Hydroxychloroquine common side effects (3)
Rare side effects (6)
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
What tests to get at baseline (2)
No routine blood work required
Ocular exam + ECG (qtc prolongation)
83
Hydroxychloroquine in pregnancy, breastfeeding
Safe
84
Hydroxychloroquine drug interactions (3)
* Amiodarone: risk of peripheral neuropathy
* Digoxin: increased digoxin levels
Hypoglycemic meds: risk of hypoglycemia increased
85
What are contraindications to TNA-a inhibitors (3)
1. Susceptibility to or presence of infection
2. Active malignancy or history of malignancy
3. CHF NYA III
86
What monitoring do you need for TNF-a and ALL BIOLOGICS (7)
- hepatitis
- HIV
- CBC, SCr, LFTs, chest X-ray, TB skin test (LTBI)
87
What is the safety profile of TNF-a (3)
Injection site rxn
Infections
Increase in skin cancers
Infusion rxn for infliximab
88
Rituxan Class
Contraindications (2)
Rare safety (1)
Class: B-cell depleters
CI
1. Susceptibility to or presence of infection
2. Type 1 hypersensitivity rxn (allergy)
Rare safety
- Progressive multifocal leukoencephalopathy
89
Abatacept (Orencia) IV
Drug class
CI
Rare safety
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
Anakinra (kineret)
Class
CI
Class: IL-1 inhibitor
CI
- known allergy to E. coli derived proteins
91
Tocilizumab Actemra
Class
Safety
IL-6 inhibitor
Safety same as TNF-a
-GI perforations
92
Sarilumab (KEVZARA)
Class
Safety
IL-6 antagonist
Safety same as TNF-a
93
What is first line biologic in RA
Anti-TNF a
94
What is 2nd line therapy if they fail an Anti-TNFa
Different Anti-TNFa
OR
Abatacept (orencia) T-cell
Rituximab (rituxan) B-cell
Tocilizumab (actemra) IL-6
95
Which biologic is best for:
Active malignancy
History of malignancy
Active
- all DMARD therapy delayed
History
- Consider HCQ, SSZ, or Rituximab
- Avoid TNFa-treatment
96
Which biologic is best for Hepatitis
Pre-vaccinate with Hep vaccines
Then give Anti-TNF or abatacept or rituximab
97
Difference between biologic and JAK inhibitor
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
MOA of JAK inhibitor
Blocking JAK enzymes results in blocked cytokine signalling -> reduce further inflammation
Specifically involves the JAK-STAT pathway -> affecting DNA transcription/Cytokine signalling
99
Dose of Tofacitinib
Renal/hepatic
Drug interaction CYP 3A4 (ketoconazole)
5mg PO daily instead of BID
100
Monitoring for JAK inhibitors
Vaccinations
Chest x ray, TB, hepatitis
Pregnancy test
Signs of infection
CVS risk + risk of thrombosis
Ongoing:
LFTs, CBC, lipids + renal function
101
JAK inhibitors safety (4)
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
When are ideal administrations of vaccines in RA patients
2-4 weeks prior to starting treatment
103
Glucocorticoids
Flu vaccine
Other non-live vaccines
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
What is the only RA therapy where you have to make changes when getting the Flu shot
Methotrexate
- hold for 2 weeks after vaccination
105
What is the only RA therapy where you have to make changes when getting a non-live vaccine
Rituximab
- hold for at least 2 weeks after vaccination
106
For DMARDS and glucocorticoids, how long do you have to hold before and after giving a live vaccine
4 weeks before
4 weeks after
107
For biologics and rituximab, how long do you have to hold before and after giving a live vaccine
1 dosing interval before (rituximab is 6 months before)
4 weeks after
108
For JAK inhibitors, how long do you have to hold before and after giving a live vaccine
1 week before
4 weeks after
109
How long do you stop before surgery
Biologics
JAKi
MTX, LEF, SSZ, HDXY
Biologics
- 2 half-lives (28 days usually)
JAKi
- 1 week before
MTX, LEF, SSZ, HDXY
- No need to stop
110
How to treat patient is positive for LTBI pre-DMARD
* Start TB treatment with isoniazid
* Hold Biologic or JAK during treatment - restart after 1-2 months of TB treatment
111
When do you stop biologic treatment during sickness
Moderate or severe infections on antibiotics
No need to stop for Mild infection (eg. sore throat, common cold)
112
Compare between treatments
Triple therapy MTX + HCQ + SSZ
Biologics
Not inferior and much cheaper
- just big pill burden
113
Compare between treatments
non-MTX dmard + biologic
Biologic
Adding non-MTX csDMARD to TNFa is superior to TNFa alone
114
What only drug can you add to JAK inhibitors
MTX
115
T/F there is evidence of benefit of combo therapy of csDMARD without MTX
False
