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Exam 4 lecture 4 Flashcards

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1
Q

Define rheumatoid artheritis

A

Chronic disease, involves symmetrical joint involvement, most common systemic inflammatory disease

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2
Q

epidemiology of RA

A

Occurs at any age. Usually between 30-50 yo.

shortens lifespan by 3-18 years

affects females more than males

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3
Q

How does RA happen

A

The disease involves the joint being invaded by inflammatory cells (macrophages, T cells and plasma cells). They release cytokines and leading to cell proliferation and death.

Pannus develops. Pannus is the development of inflammed synovium. It invades the bone and cartilage, leading to destruction of joint.

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4
Q

What are some prodromal effects patients with RA report

A

Fatigue, weakness
loss of appetite

Joint pain
Low grade fever
Stiffness + Muscle ache, Joint swelling

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5
Q

Diagnostic criteria for RA

A

joint involvement, Serology, duration of symptoms, acute phase reactants. Diagnosed with RA if there is a score of 6 or more.

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6
Q

Most common joints involved in RA

A

Wrists, hands and feet

May involve- elbow, knees, hip ankles

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7
Q

What are the most common joints in the hand with RA

A

Metacarpal and proximal interphalangeal joints are most common

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8
Q

What are some extraarticular manifestations of RA

A

Rheumatoid nodules
Vasculitis
Pulmonary
Ocular
Cardiac
Feltys

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9
Q

Where are rheumatoid nodules common?

A

Hands, elbow, forearms (pressure points)
usually asymptomatic

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10
Q

Define vascultits

A

Inflammation of small, superficial blood vessels

can lead to necrosis

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11
Q

Pulmonary effects of RA

A

Pleural effusions
Pulmonary fibrosis
Nodules
Interstitial pneumonitis

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12
Q

Ocular manifestations of RA

A

Keratoconjuctivitis Sicca

  • itchy dry eyes + inflammation
    Sjorgens syndrome (combo of inflammation in eye and itchy and dry eyes)

inflammation in sclera, episclera, cornea

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13
Q

cardiac manifestations of RA

A

Increased CV risk
Pericarditis
Conduction abnormalities

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14
Q

What is feltys syndrome

A

Splenomegaly and neutropenia in RA

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15
Q

What are some other manifestations of RA

A

Lymphadenopathy
Renal disease (associated with tx)
Thrombocytosis
Anemia

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16
Q

Lab indicators for patients with RA

A

Anemia
thrombocytosis (platelet counts may increase or decrease)
ESR (erythrocyte sedimentation rate )
CRP
RF (hall mark for RA)
Anti-CCP
ANA
Joint aspirations
Radiographic findings

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17
Q

What type of indicator is ESR (erythrocyte sedimentation rate)? What is normal? WHat is elevated/

A

Non-specific indicator
Normal- 0-20
Elevated>20

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18
Q

What is CRP level that may indicate RA? What value indicates bacterial infection?

A

> 0.5

> 10 may indicate bacterial infection

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19
Q

What is RF (rheumatoid factor)

A

Antibody specific for IgM.
Not all pts with RA are RF+ (60-70%)

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20
Q

What type of test is Anti-CCP

A

High specificity autoantibody presence test. Present in earlier disease and can be predictive for erosive disease. It is also a marker of poor prognosis

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21
Q

What are ANA in diagnosis of RA

A

Elevated titers suggest autoimmune disease. More indicative of SLE.

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22
Q

What does the joint aspiration of an RA patient look like

A

The fluid recovered from the joint is turbid (less viscous)
Turbidity due to WBC count.

Glucose normal to low compared to serum

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23
Q

What is the hallmark way to diagnose RA

A

radiographic changes (joint space narrowing and erosions of bone)

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24
Q

Tx goals of RA

A

improve/increase quality of life
Reduce morbidity and mortality

Alleviate signs and symptoms of disease
Preserve function
Prevents structural damage and deformity
control/avoid extra articular manifestations

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25
non pharm treatment of RA
Education Emotional support Rest Physical therapy Heat Splints/prosthetics Surgery Weight reduction
26
pharmacologic treatment of RA
NSAIDs Corticosteroids DMARDs Biologic anti-TNFs Biologic non-TNFs Monoclonal antibody Targeted synthetic DMARDs
27
can we reverse damae thats been done?
no, we only preserve function. Prevent damage early.
28
Which two drugs are never used alone for RA
NSAIDs and corticosteroids
29
Do NSAIDs alter disease progression? what is it effective for? What to combine it with? What doses should we use?
DO NOT alter disease progression Use in combination with DMARDs. effective in reducing pain, swelling and stiffness Dose at anti inflammatory doses (remember doses for antiinflammation (they are higher))
30
Celecoxib should not be used for what patients
Patients with sulfa allergy
31
When are corticosteroids used? What is it combined with? Can it be used as monotherapy?
Used in patients with extra-articular manifestations and acute flares. Used for antiinflammatory and immunosuppressive properties Not used as monotherapy Used in combination with DMARDs
32
What drugs have steroid sparing effects
NSAIDs and DMArDs
33
What are low doses of corticosteroids? High doses? duration?
low dose- <10 prednisone high > 10-60 short term < 3 month of therapy (longer duration= poor prognosis)
34
Duration for intraarticular injections of corticosteroid? Dose?
do NOT use > every 2-3 months Use 10-25 mg/inj of HC per joint
35
short term adverse effects of corticosteroids
Hyperglycemia mood changes Elevated BP Gastritis
36
Long term adverse effects of corticosteroids
Asceptic necrosis Cataracts Obesity Growth failure Osteoporosis
37
monitoring parameters for corticosteroids
BP every 3-6 months BG every 3-6 months
38
What are the 3 different types of DMARDs
Traditional DMARDs (conventional synthetic DMARDs) Biologic response modifiers (biologic DMARDs) Targeted synthetic DMARDs
39
What does DMARDs stand for? What does it do? Onset?
Disease modifying anti rheumatic drugs Potential to decrease/prevent joint damage and preserve joint integrity Timing of initiation is critical Onset of action is delayed
40
What are some conventional DMARDs drugs
Methotrexate (MTX) Sulfasalazine (SSZ) Hydroxychloroquine (HCQ) Leflunomide
41
what is the gold standard of RA treatment
Methotrexate (ost predicatble benefit, best long term outcome)
42
MOA of methotrexate
inhibits dihydrofolic acid reductase (inhibits neutrophil adhesion and chemotaxis)
43
dosing of methotrexate (exam)? onset?
2.5 mg tablets start at 7.5 mg per week by mouth or IM at 4-6 weeks titrate to 15 mg per week, you can go as high as 20 mg per week Onset- 1-2 months
44
Methotrexate adverse effects
Gastrointestinal side effects (N/V/D) biggest issue with pts stomatitis/mucositis (NEED TO TAKE WITH 1 mg FOLIC ACID SUPPLEMENT DAILY) Hepatic -cirrhosis -hepatitis - fibrosis pulmonary -pneumonitis -fibrosis Dermatologic -rash Urticaria Alopecia Teratogenic - wait one cycle on BCP Wait 3 months before considering conceotion
45
MTX contraindications
pre existing liver dysfunction (etOH abuse or chronic disease) pregnancy pre existing blood dyscrasias pleural/peritoneal effusions Crcl<40 immunodeficiency leukopenia/thrombocytopenia
46
MTX monitoring
baseline CXR CBC SCr LFTs Albumin Maintenance (CBC, SCr, LFT) <3 months- 2-4 wks 3-6 months- 8-12 wks >6 months- 12 wks
47
What type of drug is leflunomide? half life?
It is a prodrug that requires loading dose 14-16 days
48
leflunomide adverse effects
Teratogenicity Alopecia Increased LFTs Rash Diarrhea
49
LEF (leflunomide) monitoring
CBC, SCr, LFT <3 mo: 2-4 wks 3-6 mo : 8-12 wks >6 mo: 12 wks
50
Sulfasalazine (SSZ) adverse effects? Is it a prodrug? Allergies?
gastrointestinal - N/V/D, anorexia Dermatologic - rash/urticaria/photosensitivity Hematologic -leukopenia, thrombocytopenia yes it is a prodrug Not for pts with sulfa allergy
51
monitoring for SSZ
Same as Lef and MTX
52
what are advantages of hydroxychloroquin? unique Advrse effects of HCQ? monitoring HCQ?
Advantage- no myelosuppression, only renal and hepatic Ocular toxicity is unique to HCQ (retinal toxicity) GI (N/V/D) Vision exam every 6-12 months Mildest effectiveness, mildest adverse effects,
53
What are some biologic response modifiers (biologic DMARDs)
TNF neutralizers IL1 IL6 Cosal stimulators
54
Whatare some TNF neutralizers? MOA?
Infliximab Golimumab certolizumab adalimumab Etanercept Inhibit TNF, all in different ways. We can switch therapies within class
55
TNF neutralizers warnings/precautions? Blackbox?
increase risk of infection DO NOT USE IN COMBO with IL-1 or t cell co stimulatory modulators or other biologics blackbox warning- Increase neurologic/demyelinating disorders Malignancies COngestive F Hepatitis B reactivation No concurrent live vaccine administration
56
TNF neutralizer adverse effects
Headache/ rash Risk of infection (upper respiratory common) inj site rxn CHF exacerbation Malignancy Demyelinating disease
57
ROA of etanercept? ROA of
sq
58
Is infliximab a monotherapy forRA?
No, indicated in combo with MTX
59
What is adalimumab indicated in? Monotgherapy of combo?
Patients with inadequate response to one or more DMARDs Both monotherapy and combo
60
ROA of adalimumab
Sc
61
golimumab indication? monotherapy or combo?
Used in moderate to severe RA Used in combo with MTX
62
monitoring parameters for golimumab
CBC and PLT LFTs
63
Certolizumab indication? Monotherapy or combo? ROA
RA patients with moderate to severe disease can bealone or in combo with non-BRM DMARDS ROA- Only IV is infliximab all others are SQ including this
64
What are some additional BRM BDMARDS
Anakinra- IL-1 inhibitor
65
Anakinra indication? Alone or n combination? MOA? ROA?
Moderate to severe RA in pts who have failed one or more DMARDS Alone or in combination IL-1 inhibitor SQ
66
adverse effects of Anakinra? Monitoring?
Inj site rxn H/a, N/v, flu like sc HS to e coli derive dproteins Decreasd neytrophils reduce dose for CrCl<30 Monitor- neutrophl count monthly for 3 months
67
Name a selective T cell costimulation moduylator
Abatacept
68
Abatacept indication? monotherapy or combination?
moderate to severe RA use if inadequate response to on or more DMARDs Monotheraoy or combination with DMARD
69
Can we combine Abatacept with TNF inhibitors or IL-1 antagonists
No
70
do we use biologic response modifiers in combination?
No TNF, IL-1 co t cell stimulators. When we say combination we are thinking of mtx and all those.
71
ROA of abatacept
IV
72
Name IL-6 inhibitors? Indication? Alone or in combo? ROA?
Tocilizumab and sarilumab Indication- moderate to severe RA after inadequate response to one or more MDARDs Alone OR in combination with MTX or another DMARD IV- tocilizumab SQ- sarilumab
73
Blackbox warning of IL-6? CI?
serious infection contraindicated in pts with liver toxicity, thrombocytopenia and neutropenia
74
Adverse effects of IL-6 inhibitors (Unique abnormalities)
Lipid abnormalities (unique) serious infection Liver Blood dysgratias Thrombocytopenia Intestinal perforations/infusion rxn (tocilizumab)
75
Monitoring IL-6 inhibitors
Neutrophil count, platelet count, LFTs, Lipid profiler
76
Name an Anti-CD 20 antibody
Rituximab
77
Indication of rotuximab? monotherapy or combination? ROA? What is unique about giving rituximab?
Moderate/severe RA Used in inadequate response to TNF antagonist Used in combo with MTX IV infusion (administer methylprednisone before infusion tor educe adverse effects) (Unique)
78
Adverse effects rituximab. Monitoring?
Every adverse affect Monitoring CBC, SCr, vitals during infusions
79
Name targeted synthetic DMARDs *
Janus kinase inhibitors
80
Indication for Janus kinase inhibitors? ALon eor combo? ROA?
Moderate to severe RA after inadequate response to TNF Alone or in combo with MTX or another DMARD (not with biologic response modifier) Oral (Unique)
81
Name the JAK inhibitors
Tofactinib Barictinib Upadactinib
82
Drug i/a of JAK inhibitors
Cytochrome P 450 i/a
83
Adverse effects of JAK inhibitors
DO not use in hepatic impairment Risk of infection Risk of malignancy Major adverse CV events Thrombosis GI perforations No live vaccines Upper respiratory H/A Nausea
84
Which labs make use ignore JAK inhibitors as an option
Hemoglobin- <9 ANC<1000 ALC<500
85
Monitoring parameters of JAK inhibitors
lymphocyte count Neutrophil count Hemoglobin Liver enzymes Lipid profile (Unique along with Il-6)
86
Which two classes have lipid profile monitoring
JAK inhibitors and IL-6 inhibitors
87
if we have a clinical diagnosis of RA, what do we do 1st
Phase I- Start methotrexate (Leflunomide or sulfasalazine if contraindicated to methotrexate) combine with short term glucocorticoids
88
What do we do if we do not see improval after 3 months or aulure to achieve target at 6 months
Phase II discontinue and try another therapy If poor prognosis factors present- Add a bDMARD or JAK inhibitor If poor prognosis factors absent change to or add a second conventional synthetic DMARD (leflunomide, sulfasalazine or csDMARD combination (plus glucocorticoid)
89
What if still no response to phase II
Change to bDMARD or a JAK inhibitor
90

Therapeutics (38 decks)

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