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Infection & Immunity > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

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
Q

what lab tests are used to evaluate RA

A

ESR, CRP, RF (rheumatoid fctor), full blood count, electrolyte levels, creatinine levels, hepatic enzyme levels, urinalysis, synovial fluid analysis, ACPA

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26
Q

what is a DAS score

A

a rating of how painful, swollen or tender joints in the body are
joints included are DAS28

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27
Q

what DAS score gives high disease activity

A

5.1+

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28
Q

what DAS score indicates remission

A

2.6 to 3.2

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29
Q

what is the HAQDI scoring system

A 
patients rate task difficulty:
0 = no difficulty
1 = some difficulty
2 = much difficulty
3 = unable to do so
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30
Q

what are the comorbidity risks with RA

A

circulatory system, infections, respiratory system, digestive system, malignant neoplasm, genito-urinary system

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31
Q

what genotype is associated with severe RA

A

HLA-DRB1

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32
Q

what are the main categories of drug used to treat RA

A

analgesics, NSAIDS, glutocorticoids, csDMARDS (methotrexate), bMARDS

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33
Q

what are some examples of csDMARDS

A

methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, gold

34
Q

what is an example of triple therapy

A

methotrexate, hydroxychloroquine, sulfasalazine

35
Q

what are some examples of double therapy

A

methotrexate and leflunomide/sulfasalazine/hydroxychloroquine/gold
uulfasalazine and plaquenil (hydroxychloroquine)

36
Q

how does methotrexate work

A

substitutes as folic acid, interferes with the denovo synthesis of purines, affects rapid cell turnover

37
Q

what is the dose of methotrexate given

A

7.5 to 25mg weekly

takes 6-8wks for action

38
Q

what are the common side effects of methotrexate

A

malaise, nausea, rise in liver enzymes

oral ulcers, alopecia, lover and bone marrow toxicity can all be dose sensitive

39
Q

how does hydroxychloroquine work

A

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
Q

what is the recommended dose of hydroxychloroquine

A

200-400mg od

take 6-12wks for action

41
Q

what are the common side effects for hydroxychloroquine

A

rash, nausea, diarrhoea, difficulty reading

42
Q

how does sulfasalazine work

A

salicylic acid anti-inflammatory combined with sulfapyridine abx

43
Q

what is the recommended dose of sulfasalazine

A

bd dose
dose starts od and increases slowly to qds
takes 6-8wks to work

44
Q

what are some common side effects of sulphasalazine

A

malaise, nausea, rash, headaches, dizziness, abdominal pain

45
Q

how does leflunomide work

A

coverted to A177-1726 in the GI tract and liver which inhibits dihydro-orotate dehydrogenase in the synthesis of pyrimidines

46
Q

what is the recommended dose for leflunomide

A

10-20mg od

takes 6-8wks to work

47
Q

what are some common side effects of leflunomide

A

diarrhoea, nausea, malaise, hypertension, alopecia, rash

48
Q

how do TNF inhibitors work

A

inhibit TNF released by macrophages

49
Q

what are some risks of using TNF inhibitors

A

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
Q

what is rituximab

A

b-cell depleting monoclonal anti-CD20 anti-body
Fc receptor gamma-mediated antibody-dependent cytotoxicity
causes b-cell apoptosis

51
Q

how does abatacept work

A

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
Q

what are some RA surgeries

A

arthroplasty

tendon repair

53
Q

what are steroids derived from

A

hormones derived from mevalonic acid

54
Q

what enzyme produces mevalonic acid (used for steroids)

A

HMG-CoA reductase

the target for statins

55
Q

what steroid is converted to cholesterol

A

lanosterol

56
Q

what is the role of glutocortecoids

A

to promote glucogenesis and glycogen formation and reduce inflammation

57
Q

what are the three steps of cholesterol synthesis

A

cholesterol -> pregnenolone -> progestagens -> glucocorticosteroids/androgens/mineralcorticoids

58
Q

what structure gives anti-inflammatory action

A

hydroxy or ketone group at carbon 11 on steroids

59
Q

what basic structure do all steroids share

A

four ring structure (6,6,6,5)

60
Q

what do cortisol and cortisone do

A

stress hormones that promote gluconeogenesis

61
Q

how is prednisolone produced

A

from prednisone (keto derivative) by drug metabolism

62
Q

what disease results with excessive steroid use

A

Cushing’s syndrome

sudden withdrawal can result in adrenal insufficiency

63
Q

what is Cushing’s syndrome

A

the body reduces the amount of hormones it produces

tapering of steroids reduces this risk

64
Q

how do NSAIDS work

A

reduce the production of leukotrienes and thromboxanes (lipids)
they inhibit cyclooxygenase 1 and 2 (COX1 and 2)

65
Q

what is the function of cyclooxygenase

A

control synthesis of leukotrienes and thromboxanes
COX1 is constituative (produced in low levels in all tissues)
COX2 is inducible (in response to injury)

66
Q

what is aspirin

A

irriversible, selective COX1 inhibitor

effect is potenated by caffeine

67
Q

what is Reye’s syndrome

A

inflammation of the brain

risk of aspirin in <16s

68
Q

what is ibuprofen

A

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
Q

what is diclofenac

A

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
Q

what are selective COX2 inhibitors

A

selectively inhibit COX2
increased risk of cardiovascular complications, efficacy is similar to other NSAIDS
naproxen has lower cardiovascular risk but not widely used

71
Q

what does DMARD stand for

A

disease modifying anti-rheumatic drugs

72
Q

how does sulfasalazine work

A

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
Q

how does methotrexate work

A

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
Q

what does methotrexate effectiveness rely on

A

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
Q

how does leflunomide work

A

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
Q

how does terifunomide work

A

undergoes E/Z interconversion
inactivates dihydroororate dehydrogenase results on decreased availability of SNA precursors and hence proliferation of WBCs

77
Q

how does paracetamol work

A

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
Q

what is tofacitinib

A

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
Q

what are chloroquine and hydroxychloroquine

A

sulfate salts that promote oral bioavailability of treatments
chloroquine can cause renal toxicity

80
Q

what is azathiprine

A

purine analogue that inhibits proliferation of white blood cells
side effects include bone marrow suppression

81
Q

what is cyclophosphamide

A

‘mustard gas’
alkylates guanine residues in DNA
used in RA and vascilitis

82
Q

what is vascilitis

A

inflammation and destruction of blood vessels

Infection & Immunity (22 decks)

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