Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics Y2 Sem 2 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is the consequence with respect to inflammation? (4)

A

Loss of cartilage
Formation of scar tissue
Ligament laxity
Tendon contractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the prevelance of RA?

A

1-2% of adult population with women being more affected then men (3:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the symptoms of RA?

A

Symmetrical joint pain and stiffness >6 weeks,

Muscle pain

Fatique

RA nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does RA usually do as it progresses throughout the day?

A

Generally feels better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the key pathophysiology of Ra comparred to Osteo?

A

Symmetrical joints affected, greater than 1 hour in duration and presence of systemic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the stages of RA?

A

Early, intermediate and Late

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the most prominent skin symptom of RA?

A

Rheumatoid nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is diagnosis made with RA?

A

Joint involvement

Lab test findings (60-70%)
Elevated ESR and CRP
anti-CCp

Duration of symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the goal of RA treatment?

A

Prevent and control join damage
Prevent loss of funciton
Maintain QoL
Decrease Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A patient assessment of global disease assessment of what score is what we aim for?

A

<=2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is important with respect to RA diagnosis and recognition?

A

Significant damage occurs in first two years of disease, hence start within 3m of diagnosis dpeending on severity we treat aggresviely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the concept of “Tight Control:”

A

Remission or low disease activity
Quickly treat exacerbations
Add DMARDs or wearly switch
NSAID/Steroid
Reassessment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is considered responsible NSAID and glucocorticoid use?

A

Reduce/discontinue as disease enters remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the main classes of drugs used for maintenance of RA?

A

tDMARDs
Biologic DMARDs
Synthetic DMARDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the main classes of drugs used for RA flares?

A

Corticosteroids
NSAIDs/Analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is general overview of tDMARDs?

A

Slow onset of action
Controls symptoms
May delay or stop progression of disease
Requires monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are how tDMARDs

A

Hydroxychloriquine
Sulfasalazine
Methotrexate
Leflunomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is our main tDMARD?

A

methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the MOA of hydroxychloroquine?

A

Inhibits neutrophils and chemotaxis: IMpairs complement system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the MOA of sulfasalazine?

A

Prodrug metabolized into 5-ASA and sulfapyridine
Modulates mediators of inflammatory response; may inhibit TNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the MOA of methotrexate?

A

Anti-folate, less dna synthesis, repair, cellular rpelication and immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the MOA of leflunomide?

A

INhibits pyrimidine syntheisis, leading to anti-inflammatory effects

Modulates many signaling pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which Dmard has the slowest onset?

A

Hydroxychloroquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the target dosing of methotrexate?

A

7.5mg to 25mg po weekly, we aim for 15-25 though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the renal dosing targets of methotrexate?

A

50% of the target dosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the titration patter of methotrexate?

A

2.5 –>5mg per week. on a montly basis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which DMARD has the highest rate of nausea/diarrhea?

A

Leflunomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the renal range that we can dose methotrexate?

A

10-50ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the serious side effects of hydroxychloroquine?

A

Ocular toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the common side effects of methotrexate?

A

N/V/F

Stomatitis
Photosensitivity
Hair loss
Skin itch/burning/rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the typical dose of folic acid required?

A

1-5mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can be added to help with MTX tolerability?

A

PPI for 3 days around the MTX dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does folic acid help with specificaly?

A

Nausea/Vomiting
Fatique
Stomatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Hydroxychloroquine CI in?

A

Individuals with pre-existing retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Sulfasalazine Contraindicated in?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the contraindications of methotrexate?

A

Hematologic abnormalities
Pregnancy/breastfeeding
Severe hepatic impairment
Caution in lung dysfunction***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is leflunomide CI in?

A

Moderate-severe renal/hepatic impairement
Hematologic abnormalities or serious infection
Pregnancy/breastfeeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Drug interactions with methotrexate?

A

NSAIDs (But only at cancer therapy levels)

Trimethoprim (CI)
PPis (Only if MTX is >500mg/week)
Loop diuretics decrease clearance of MTX
Live Vaccines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is generally monitored with methotrexate therapy?

A

Disease activity
Radiographs every 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What should be monitored while on Methotrexate?

A

CBC and LFTs, creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What should be monitored when on sulfasalazine or leflunomide?

A

CBCs, LFTs, creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What has the best efficacy data for DMARDs?

A

Methotrexate/Leflunomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Which tDAMRD may be useful for early mild RA?

A

Hydroxychloroquine, which is best tolerated of the DMARDs.

***Usually combined with other DMARDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is generally next tDMARD for early mild RA?

A

Sulfasalazine, use if other options are not tolerated well, combined with other DMARDs generally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where does methotrexate have a place in therapy?

A

Generally all RA states, and can improve efficacy of biologics when combines.

Standard therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When is leflunomide used?

A

Replacement for MTX if not tolerated, may be added in low doses to MTX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the main classes of biologics for treatment of RA?

A

TNFa inhibitors
Interleukin 1 or 6 inhibitors
T-Cell co-stimulation inhibitors
B cell depletors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the common side effects of biologics?

A

N/D/Headache

Malaise (Which tends to occur the first couple of days in DAMRD therapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is concerns for all biologics with respect to route of administration

A

SC minor redness itching and swelling. IV may cause headache and nausea

Hypersensitivity

50
Q

What do we usually do prior to giving DMARD therapy?

A

Pretreat with acetaminophen, antihistamine, steroid to help decrease/mitigate risk of adverse reactions

51
Q

Is infection increased or decreased when on biologic therapy?

A

Increased, risk is generally highest at the beginning of therapy but decreases

52
Q

How can me mitigate the infection risk of bDMARDs

A
53
Q

What is an important cell to monitor during Bdmards therapy?

A

Neutropenia, where 20% will expeirence a decrease and this will lead to severity of infection

THIS IS NOT A REASON TO STOP THERAPY

54
Q

What do RA patients have a higher risk of developing”

A

Cancer (Skin, lymphomas)

55
Q

If someone has a previous lymphoma which biologic should be chosen/

A

Rituximab

56
Q

Which drugs to not contribute to antibody development?

A

IL-6 inhibitors

57
Q

Which bDMARDs may have a higher association of antibody development?

A

T cell inhibitors, B cell depletors (Not as much as TNF-inhibitors though)

58
Q

What may help in fighting against antibody development?

A

Methotrexate addition in therapy

59
Q

What are the 5 TNFa agents?

A

Adalimumab
Certolizumab
Etanercept
Golimumab
Infliximab

60
Q

Why doe we use TNF a inhibitors in RA?

A

Generally this is high in patients which leads to bone erosion

61
Q

What is the onset of TNF-a agents?

A

Within weeks

62
Q

Which DMARDs are indicated in combination with MTX?

A

Infliximab and Golimumab

63
Q

What is the dosing of adalimumab?

A
64
Q

What is the dosing of Certolizumab?

A
65
Q

What is the dosing of etanercept?

A
66
Q

What is the dosing of golilumab?

A
67
Q

What is the dosing of Infliximab?

A
68
Q

What are the contraindications of TNF-a DMARDs?

A

Active severe infection

HF in general (Moderate to severe in general)

69
Q

What are the drug interactions of TNFa?

A

Live vaccines
Additive immunosuppression with other drugs

70
Q

What are the AE of TNFa inhibitors?

A

Liver enzyme elevations which means we require monitoring

71
Q

What are some of the adverse effects of of TNFa inhibitors?

A

Cellulitis
Autoimmune skin diseases
Skin Malignancy

(These AE would be prudent to choose another class)

72
Q

What are some Autoimmune disease related adverse effects from TNFa?

A

Lupus
Vasculitis
Sarcoidosis
Psoriaisis

These seem to be reversed though and is more of a pseudoautoimmune disease

73
Q

Should we use TNFa for those who have a seizure risk?

A

No

74
Q

What are the monitoring parameters of TNF-a inhibitors/

A
75
Q

If TNFA has lost effect over time what should be done?

A

Check antibodies and we should consider switching or adding MTX therapy

76
Q

What are more effective IL-1 or IL-6 therapies for RA?

A

IL-6

77
Q

What is our IL-1 therapy?

A

Anakinra

78
Q

What is our IL-6 therapy

A

Tocilizumab, sarilumab

79
Q

What is the contraindications of Anakrina and Sarilumab?

A

Nothing

80
Q

What is the contraindications of Tocilizumab?

A

Active infections

81
Q

What is a benefit to the using Il-1 and IL-6 inhibitors?

A

They have renal evidence for as low as 30ml/min

82
Q

What are the adverse effects of anakinra?

A

Injection site reaction, headache, nausea
Adverse serious side effects the same as placebo.

83
Q

What are the potential AE of IL-6 inhibitors?

A

GI perforation (CI in patients who have gastric issues)
Dyslipidemia
Hypertension

84
Q

Do IL-6 inhibitors have antibody development against them?

A

no, makes them unique

85
Q

What are the drug interactions of all IL-1 or 6 inhibitors?

A

Decrease IL1 or 6 activity (Increased Cyp activity)

86
Q

What is a DI of tocilizumab?

A

Simvastatin increase by 4-10x

87
Q

What should be monitored while on IL-1 therapy

A

Anakinra, Baseline CBC, LFTs, Creatinine

88
Q

What should be monitored while on IL-6 therapy?

A

Tocilizumab and Sarilumab

CBC LFT Creatinine
Lipid panel
Blood pressure
Latent/active infection

89
Q

What are T-cell co-stimulation inhibitors?

A

INhibits T-Cell activate and is used in inadequate response to TNF ainhibitros

Generally used either in monotherapy or combined hterapy

90
Q

What is the downside to T-Cell co-stimulation inhibitors?

A

MD; 125mg SQ once weekly

91
Q

What are the AE lof T-Cell co-stimulation inhibitors?

A

COPD exacerbation influence (May even a CI in some circumstance

Very similar to TNF, lower infections though

Hypertension

Blood glucose increased (pushing over to being diabetic)

Unknown if antibodies impact efficacy/safety

92
Q

What are the positives of T-Cell co-stimulation inhibitors?

A

No impact on liver function

93
Q

What need to be monitored when on T-Cell co-stimulation inhibitors??

A

Infection
TB/Hep
CBCs. creatinine
Blood pressure
Blood glucose

94
Q

What are the B-Cell depletors function/

A

Causes lysis of B-Cells

95
Q

What is the B-Cell depletors drug?

A

rituximab

96
Q

What is the T-cell co-stimulation inhibitor drug?

A

Abatacept

97
Q

Where have B-Cell depletors been studied?

A

Combination with MTX and failure on a TNF inhbitor

98
Q

What is the onset of B-Cell depletors?

A

up to 6 months sometimes

99
Q

WHat is the efficacy data of B-Cell depletors?

A

Does not work well in RF-negative patients and does not hault radigraphic progression

100
Q

What is the dosing nieche with B-Cell depletors?

A

Must pretreat with methylprednisolone, acetaminophen and diphenhydramine

101
Q

How is B-Cell depletors doesed?

A

2 cose course 1g IV given two weeks apart and retreat when needed ~6 months

102
Q

What needs to be withholded prior to recieving Rituximab?

A

Hypertension medication

103
Q

What are the AE of B-Cell depletors?

A

Hypertension
GI perforation
Blood glucose increase
Mucocutaneous reactions (SJS, TEN)

Less likely lead to ABx development

104
Q

What needs to be monitored when on B-Cell depletors?

A

CBC, LFTs, creatinine, TB, Hep B/C screening

105
Q

Take some time to look at the table

A
106
Q

What is a Janus Kinase inhibitor?

A

Newer drug, and it 4th of 5th line

Tyrosine kinase inhibitor

Must be taken in combination with MTX

107
Q

What are the Janus Kinase Inhibitors?

A

Tofacitinib, Baricitinib, Upadacitinib

108
Q

What are the warnings of Janus Kinase Inhibitors??

A

CV risk
Malignancy

109
Q

What are the DI of Janus Kinase Inhibitors?

A

Tofactinib/upadacitinib are are major 3A4 substrates

110
Q

What needs to be monitored while on Janus Kinase Inhibitors?

A

Tb testing
lipids
CBCs
LFTs

111
Q

What are the uses for CS in RA therapy?

A

Help to improve QUALY

112
Q

What are the typical doses of prednisone?

A

10-15mg equivalents per day, taper and d/c as symptoms improve though.

113
Q

What are the three treatment modalities used on chronic treatment with CS?

A

Dose of 5-10mg prednisone equivalent per day
Long term steroid safety issues become apparent
Increase need for monitoring

114
Q

What is pulse therapy?

A

Where we administer high doses of steroid (MP 1000mg IV for 3 days), for 6-8 months and it would be done in the hospital

115
Q

What are the safety issues with Pulse therapy?

A

Cardiovascular collapse, hypoK+, MI, infection

116
Q

What should be monitored when on steroids?

A

Cataracts, lipids, glucose, osteoporosis, weight gain

117
Q

WHat is intra-articular injections?

A

Temporary resolvement of the affected joint. Not really great since we are dealing with a chronic condition

118
Q

WHat are the potential issues with intra-articular injections?

A

Tendon rupture
Septic arthritis

119
Q

What is the max dose per day that we aim for with CS therapy?

A

10mg/d,

120
Q

Should CS be used as monotherapy?

A

No

121
Q
A

Therapeutics Y2 Sem 2 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions