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Rheumatoid Arthritis Flashcards

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1
Q

what is an autoimmune disease

A

disregulation of the immune system with loss of self-tolerance

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2
Q

what is myalgia

A

muscular pain

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3
Q

what are some common features of autoimmune diseases

A

malaise, fatigue, weight loss, myalgia, arthritis, anaemia

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4
Q

how is RA diagnosed

A

presence of synovitis in at least one joint, absence of alternative diagnosis and achievement of 6/10 on RA scale

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5
Q

what are the points on the RA scale

A 
2 to 10 large joints = 1pt
1 to 3 small joints = 2pts
4 to 10 small joints = 3pts
>10 joints = 5pts
upper limit of ULN = 2pts
greater than 3x ULN = 3pts
elevated acute phase response = 1pt
symptoms lasting >6wks = 1pt
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6
Q

what is the synovial layer

A

between ligaments

can become inflamed

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7
Q

what does a high ESR indicate

A

more inflammation

stands for erythrocyte sedimentation rate

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8
Q

who is more likely to get RA

A

women

increases with age then decreases after age 75

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9
Q

what is the cell level response to RA

A

macrophage forms major histocompatibility complex which attaches to a T-cell receptor and activates the T-cell
this releases activated B=cells that can activate macrohages
this causes inflammation

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10
Q

what antibodies are specific to rheumatoid arthritis

A

ACPA
anti-citrullinated protein antibodies
Anti-BiP, anti-SA

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11
Q

what antibodies are associated with RA

A

Anti-RA33, anti-calpastatin, ANCA and ANA, anti-collagen type II, anti-fibronectin, anti-GPI

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12
Q

what occurs during synovial inflammation and joint erosion

A

the synovial membrane becomes inflamed and cartilage begins to swell, synovial fluid is released and the joint capsule swells
eventually the bone erodes and the tendons become inflamed

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13
Q

what are the symptoms of arthritis

A

pain, stiffness in joints, symmetrical swelling in joints, fatigue, flu-like symptoms, morning stiffness

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14
Q

what affect does RA have on the skin

A

rheumatoid nodules, ulcers, vasculitis

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15
Q

what effect does RA have on the CNS and PNS

A

cerebrovascular disease, mononeuritis multiplex (vasculitis), carpal tunnel syndrome

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16
Q

what effect does RA have on the eyes

A

scleritis, episcleritis, sicca syndrome

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17
Q

what effect does RA have on the smaller arteries and veins

A

leucocytoclastic vasculitis

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18
Q

what effect does RA have on the heart

A

pericardial effusion, ischaemic heart disease, pericarditis

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19
Q

what effect does RA have on the blood

A

anaemia f chronic disease, neutropenia, haemolytic anaemia

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20
Q

what effect does RA have on the kidneys

A

amyloid disease

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21
Q

what effect does RA have on the lungs

A

pleural disease, pulmonary nodules, diffuse intersistal fibrosis, obliterative bronchitis

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22
Q

what are the radiology assessment tools for RA

A

sharp score, LArsen index

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23
Q

what are the disease activity indicators for RA

A

ACR response criteria
EULAR response criteria
disease activity score

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24
Q

what is the radiological evidence of early RA

A

soft tissue swelling, periarticular osteopenia, narrowing of joint space, loss of cartilage, cystic erosions

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25
what lab tests are used to evaluate RA
ESR, CRP, RF (rheumatoid fctor), full blood count, electrolyte levels, creatinine levels, hepatic enzyme levels, urinalysis, synovial fluid analysis, ACPA
26
what is a DAS score
a rating of how painful, swollen or tender joints in the body are joints included are DAS28
27
what DAS score gives high disease activity
5.1+
28
what DAS score indicates remission
2.6 to 3.2
29
what is the HAQDI scoring system
``` patients rate task difficulty: 0 = no difficulty 1 = some difficulty 2 = much difficulty 3 = unable to do so ```
30
what are the comorbidity risks with RA
circulatory system, infections, respiratory system, digestive system, malignant neoplasm, genito-urinary system
31
what genotype is associated with severe RA
HLA-DRB1
32
what are the main categories of drug used to treat RA
analgesics, NSAIDS, glutocorticoids, csDMARDS (methotrexate), bMARDS
33
what are some examples of csDMARDS
methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, gold
34
what is an example of triple therapy
methotrexate, hydroxychloroquine, sulfasalazine
35
what are some examples of double therapy
methotrexate and leflunomide/sulfasalazine/hydroxychloroquine/gold uulfasalazine and plaquenil (hydroxychloroquine)
36
how does methotrexate work
substitutes as folic acid, interferes with the denovo synthesis of purines, affects rapid cell turnover
37
what is the dose of methotrexate given
7.5 to 25mg weekly | takes 6-8wks for action
38
what are the common side effects of methotrexate
malaise, nausea, rise in liver enzymes | oral ulcers, alopecia, lover and bone marrow toxicity can all be dose sensitive
39
how does hydroxychloroquine work
anti-malarial medication used in inflammation, highly concentrated in cells and increases cellular pH - it interferes with the cell's ability to degrade and process proteins
40
what is the recommended dose of hydroxychloroquine
200-400mg od | take 6-12wks for action
41
what are the common side effects for hydroxychloroquine
rash, nausea, diarrhoea, difficulty reading
42
how does sulfasalazine work
salicylic acid anti-inflammatory combined with sulfapyridine abx
43
what is the recommended dose of sulfasalazine
bd dose dose starts od and increases slowly to qds takes 6-8wks to work
44
what are some common side effects of sulphasalazine
malaise, nausea, rash, headaches, dizziness, abdominal pain
45
how does leflunomide work
coverted to A177-1726 in the GI tract and liver which inhibits dihydro-orotate dehydrogenase in the synthesis of pyrimidines
46
what is the recommended dose for leflunomide
10-20mg od | takes 6-8wks to work
47
what are some common side effects of leflunomide
diarrhoea, nausea, malaise, hypertension, alopecia, rash
48
how do TNF inhibitors work
inhibit TNF released by macrophages
49
what are some risks of using TNF inhibitors
infusion reactions with infliximab, injection site reactions with adalimumab and enanercept risk of infection, malignancy, neurological complications, autoimmune disease and worsening of congestive heart failure
50
what is rituximab
b-cell depleting monoclonal anti-CD20 anti-body Fc receptor gamma-mediated antibody-dependent cytotoxicity causes b-cell apoptosis
51
how does abatacept work
t-cell co-stimulation soluble receptor composed of CTLA-4 and Fc fragment of IgG blocks reactions with CD28 on t-cells cause t-cell death
52
what are some RA surgeries
arthroplasty | tendon repair
53
what are steroids derived from
hormones derived from mevalonic acid
54
what enzyme produces mevalonic acid (used for steroids)
HMG-CoA reductase | the target for statins
55
what steroid is converted to cholesterol
lanosterol
56
what is the role of glutocortecoids
to promote glucogenesis and glycogen formation and reduce inflammation
57
what are the three steps of cholesterol synthesis
cholesterol -> pregnenolone -> progestagens -> glucocorticosteroids/androgens/mineralcorticoids
58
what structure gives anti-inflammatory action
hydroxy or ketone group at carbon 11 on steroids
59
what basic structure do all steroids share
four ring structure (6,6,6,5)
60
what do cortisol and cortisone do
stress hormones that promote gluconeogenesis
61
how is prednisolone produced
from prednisone (keto derivative) by drug metabolism
62
what disease results with excessive steroid use
Cushing's syndrome | sudden withdrawal can result in adrenal insufficiency
63
what is Cushing's syndrome
the body reduces the amount of hormones it produces | tapering of steroids reduces this risk
64
how do NSAIDS work
reduce the production of leukotrienes and thromboxanes (lipids) they inhibit cyclooxygenase 1 and 2 (COX1 and 2)
65
what is the function of cyclooxygenase
control synthesis of leukotrienes and thromboxanes COX1 is constituative (produced in low levels in all tissues) COX2 is inducible (in response to injury)
66
what is aspirin
irriversible, selective COX1 inhibitor | effect is potenated by caffeine
67
what is Reye's syndrome
inflammation of the brain | risk of aspirin in <16s
68
what is ibuprofen
reversible COX 1 and 2 inhibitor analgesic, anti-inflammatory and antipyretic activity largely due to COX2 inhibition only S-enantiomer is active (naproxen is S-enantiomer but rest are racemic) risk of ulcers due to COX1 inhibition
69
what is diclofenac
strong COX2 inhibitor, weak COX1 inhibitor increases risk of cardiovascular complications but reduced risk of ulcers duration of action is 6-8hours due to accumulation is synovial fluid
70
what are selective COX2 inhibitors
selectively inhibit COX2 increased risk of cardiovascular complications, efficacy is similar to other NSAIDS naproxen has lower cardiovascular risk but not widely used
71
what does DMARD stand for
disease modifying anti-rheumatic drugs
72
how does sulfasalazine work
scavenges toxic reactive oxygen species produced by neutrophils (white blood cells) by inhibiting NFK-beta in the gut, the azo group is reduced to aminosalicylic acid which is the radical scavenger
73
how does methotrexate work
slow-binding inhibitor of mammlian and bacterial dihydrofolaye reductase (DHFR) DHFR uses NADPH to perform the reaction slow-binding changes the enzyme and increases binding affinity methotrexate binds to bacterial enzyme and to NADPH complex
74
what does methotrexate effectiveness rely on
substrate concentration and incubation time build up of NADPH levels increases drug potency aim is to reduce dose do not all WBCs are affected
75
how does leflunomide work
inhibits dihydroorodate reductase, an FMN-dependent (FMN= flaromononucleotide) oxidoreductase involved in uracil and thymine biosynthesis pro-drug hydrolysed to form terifunomide in plasma and intestinal mucosa
76
how does terifunomide work
undergoes E/Z interconversion inactivates dihydroororate dehydrogenase results on decreased availability of SNA precursors and hence proliferation of WBCs
77
how does paracetamol work
inhibitos cycloocygenase enzymes by quenching the oxidising species produced by the enzyme more potent inhibitor of COX2 than COX1 so may have cardivascular side effects does not increase inflammatory mediators used in treatment for osteoarthritis
78
what is tofacitinib
non-tyrosine kinase (janus kinase-JAK) invilved in cytokine signalling highly expressed in RA patients tofacitinib inhibits JAKs and if a reversible ATP inhibitor long lasting treatment
79
what are chloroquine and hydroxychloroquine
sulfate salts that promote oral bioavailability of treatments chloroquine can cause renal toxicity
80
what is azathiprine
purine analogue that inhibits proliferation of white blood cells side effects include bone marrow suppression
81
what is cyclophosphamide
'mustard gas' alkylates guanine residues in DNA used in RA and vascilitis
82
what is vascilitis
inflammation and destruction of blood vessels

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