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Therapeutics > Exam 4 lecture 4 > Flashcards

Exam 4 lecture 4 Flashcards

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
Q

non pharm treatment of RA

A

Education
Emotional support
Rest
Physical therapy
Heat
Splints/prosthetics
Surgery
Weight reduction

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26
Q

pharmacologic treatment of RA

A

NSAIDs
Corticosteroids
DMARDs
Biologic anti-TNFs
Biologic non-TNFs
Monoclonal antibody
Targeted synthetic DMARDs

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27
Q

can we reverse damae thats been done?

A

no, we only preserve function. Prevent damage early.

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28
Q

Which two drugs are never used alone for RA

A

NSAIDs and corticosteroids

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29
Q

Do NSAIDs alter disease progression? what is it effective for? What to combine it with? What doses should we use?

A

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))

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30
Q

Celecoxib should not be used for what patients

A

Patients with sulfa allergy

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31
Q

When are corticosteroids used? What is it combined with? Can it be used as monotherapy?

A

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

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32
Q

What drugs have steroid sparing effects

A

NSAIDs and DMArDs

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33
Q

What are low doses of corticosteroids? High doses? duration?

A

low dose- <10 prednisone
high > 10-60

short term < 3 month of therapy (longer duration= poor prognosis)

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34
Q

Duration for intraarticular injections of corticosteroid? Dose?

A

do NOT use > every 2-3 months
Use 10-25 mg/inj of HC per joint

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35
Q

short term adverse effects of corticosteroids

A

Hyperglycemia
mood changes
Elevated BP
Gastritis

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36
Q

Long term adverse effects of corticosteroids

A

Asceptic necrosis
Cataracts
Obesity
Growth failure
Osteoporosis

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37
Q

monitoring parameters for corticosteroids

A

BP every 3-6 months
BG every 3-6 months

38
Q

What are the 3 different types of DMARDs

A

Traditional DMARDs (conventional synthetic DMARDs)
Biologic response modifiers (biologic DMARDs)
Targeted synthetic DMARDs

39
Q

What does DMARDs stand for? What does it do? Onset?

A

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
Q

What are some conventional DMARDs drugs

A

Methotrexate (MTX)
Sulfasalazine (SSZ)
Hydroxychloroquine (HCQ)
Leflunomide

41
Q

what is the gold standard of RA treatment

A

Methotrexate
(ost predicatble benefit, best long term outcome)

42
Q

MOA of methotrexate

A

inhibits dihydrofolic acid reductase (inhibits neutrophil adhesion and chemotaxis)

43
Q

dosing of methotrexate (exam)? onset?

A

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
Q

Methotrexate adverse effects

A

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
Q

MTX contraindications

A

pre existing liver dysfunction (etOH abuse or chronic disease)
pregnancy
pre existing blood dyscrasias
pleural/peritoneal effusions
Crcl<40
immunodeficiency
leukopenia/thrombocytopenia

46
Q

MTX monitoring

A

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
Q

What type of drug is leflunomide? half life?

A

It is a prodrug that requires loading dose

14-16 days

48
Q

leflunomide adverse effects

A

Teratogenicity
Alopecia
Increased LFTs
Rash
Diarrhea

49
Q

LEF (leflunomide) monitoring

A

CBC, SCr, LFT

<3 mo: 2-4 wks
3-6 mo : 8-12 wks
>6 mo: 12 wks

50
Q

Sulfasalazine (SSZ) adverse effects? Is it a prodrug? Allergies?

A

gastrointestinal
- N/V/D, anorexia

Dermatologic
- rash/urticaria/photosensitivity

Hematologic
-leukopenia, thrombocytopenia

yes it is a prodrug

Not for pts with sulfa allergy

51
Q

monitoring for SSZ

A

Same as Lef and MTX

52
Q

what are advantages of hydroxychloroquin? unique Advrse effects of HCQ? monitoring HCQ?

A

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
Q

What are some biologic response modifiers (biologic DMARDs)

A

TNF neutralizers
IL1
IL6
Cosal stimulators

54
Q

Whatare some TNF neutralizers? MOA?

A

Infliximab
Golimumab
certolizumab
adalimumab
Etanercept

Inhibit TNF, all in different ways. We can switch therapies within class

55
Q

TNF neutralizers warnings/precautions? Blackbox?

A

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
Q

TNF neutralizer adverse effects

A

Headache/ rash
Risk of infection (upper respiratory common)
inj site rxn
CHF exacerbation
Malignancy
Demyelinating disease

57
Q

ROA of etanercept? ROA of

A

sq

58
Q

Is infliximab a monotherapy forRA?

A

No, indicated in combo with MTX

59
Q

What is adalimumab indicated in? Monotgherapy of combo?

A

Patients with inadequate response to one or more DMARDs

Both monotherapy and combo

60
Q

ROA of adalimumab

A

Sc

61
Q

golimumab indication? monotherapy or combo?

A

Used in moderate to severe RA

Used in combo with MTX

62
Q

monitoring parameters for golimumab

A

CBC and PLT
LFTs

63
Q

Certolizumab indication? Monotherapy or combo? ROA

A

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
Q

What are some additional BRM BDMARDS

A

Anakinra- IL-1 inhibitor

65
Q

Anakinra indication? Alone or n combination? MOA? ROA?

A

Moderate to severe RA in pts who have failed one or more DMARDS

Alone or in combination

IL-1 inhibitor

SQ

66
Q

adverse effects of Anakinra? Monitoring?

A

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
Q

Name a selective T cell costimulation moduylator

A

Abatacept

68
Q

Abatacept indication? monotherapy or combination?

A

moderate to severe RA use if inadequate response to on or more DMARDs

Monotheraoy or combination with DMARD

69
Q

Can we combine Abatacept with TNF inhibitors or IL-1 antagonists

A

No

70
Q

do we use biologic response modifiers in combination?

A

No
TNF, IL-1 co t cell stimulators. When we say combination we are thinking of mtx and all those.

71
Q

ROA of abatacept

A

IV

72
Q

Name IL-6 inhibitors? Indication? Alone or in combo? ROA?

A

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
Q

Blackbox warning of IL-6? CI?

A

serious infection

contraindicated in pts with liver toxicity, thrombocytopenia and neutropenia

74
Q

Adverse effects of IL-6 inhibitors (Unique abnormalities)

A

Lipid abnormalities (unique)

serious infection
Liver
Blood dysgratias
Thrombocytopenia
Intestinal perforations/infusion rxn (tocilizumab)

75
Q

Monitoring IL-6 inhibitors

A

Neutrophil count, platelet count, LFTs, Lipid profiler

76
Q

Name an Anti-CD 20 antibody

A

Rituximab

77
Q

Indication of rotuximab? monotherapy or combination? ROA? What is unique about giving rituximab?

A

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
Q

Adverse effects rituximab. Monitoring?

A

Every adverse affect

Monitoring
CBC, SCr, vitals during infusions

79
Q

Name targeted synthetic DMARDs *

A

Janus kinase inhibitors

80
Q

Indication for Janus kinase inhibitors? ALon eor combo? ROA?

A

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
Q

Name the JAK inhibitors

A

Tofactinib
Barictinib
Upadactinib

82
Q

Drug i/a of JAK inhibitors

A

Cytochrome P 450 i/a

83
Q

Adverse effects of JAK inhibitors

A

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
Q

Which labs make use ignore JAK inhibitors as an option

A

Hemoglobin- <9
ANC<1000
ALC<500

85
Q

Monitoring parameters of JAK inhibitors

A

lymphocyte count
Neutrophil count
Hemoglobin
Liver enzymes
Lipid profile (Unique along with Il-6)

86
Q

Which two classes have lipid profile monitoring

A

JAK inhibitors and IL-6 inhibitors

87
Q

if we have a clinical diagnosis of RA, what do we do 1st

A

Phase I- Start methotrexate (Leflunomide or sulfasalazine if contraindicated to methotrexate)

combine with short term glucocorticoids

88
Q

What do we do if we do not see improval after 3 months or aulure to achieve target at 6 months

A

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
Q

What if still no response to phase II

A

Change to bDMARD or a JAK inhibitor

90
Q
A

Therapeutics (38 decks)

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