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15021998-MSK > week 2 > Flashcards

week 2 Flashcards

1
Q

what is affected in RA?

A

synovium

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2
Q

what mediates RA?

A

HLA-DR4

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3
Q

describe RA

A

inflammatory arthritis, symmetirial, F>M. any age, 1% prevalence.
smoking and genetics lead to worse outcome.
presence of auto-antibodies gives worse prognosis.

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4
Q

commonly affected sites in RA

A

c1/C2, hand joints, wrist, elbow, shoulders, TMJ, knees, hips, ankle, feet. (synovium lined)

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5
Q

what is the hallmark of RA

A

synovitis. (spongey on examination)

Get inflammatory “pannus” with inflammatory cascade (osteoclasts erode, B cells give Rheumatoid factor, mast cells cause inflammation, and neutrophils….)

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6
Q

early RA and therapeutic window

A

<2 years, first 3 months best therapeutic window.

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7
Q

PC of RA

A
  • early morning stiffness greater than 30min
  • more than one area
  • hand joint
  • symmetrical
  • positive ‘squeeze’ test of MCP/MTP
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8
Q

diagnosis of RA

A

Hx, Examination,
bloods: FBC (check for anaemia of chronic disease, inc platelets ) CRP + ESR/PV [inflammatory markers]
radiology [for staging ]
autoantibodies [may be negative]

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9
Q

what is tenosynovitis

A

caused by RA. tendon sheath inflammation. causes carpal tunnel PIP, MCP, MTP joint inflammation.

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10
Q

autoantibodies to check for in RA

A

rheumatoid factor and anti-CPP (better)

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11
Q

imaging for RA

A

x-ray hand/feet. US. MRI (gold standard.)

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12
Q

how do you assess RA

A

DAS-28. <2.6= disease remission and >5.1 is high activity.

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13
Q

management of RA

A

rheumatologist, drugs, target good DAS28 score, steroid/NSAID’s, patient education.

High high with NSAID + steroids (not tot long as side effects - use as bridging therapy until DMARD’s kick in) initially then drop down once in remission (gain control the reduced drugs)

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14
Q

DMARDs in RA

A

Methotrexate
sulphasalazine
hydroxycholoroquine
(biologic therapy ).

also gold therapy, penicillamine, azothiaprine.

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15
Q

what do you need to check if giving biological therapy (anti-TNF)

A

bacterial and TB reactivation

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16
Q

how can steroids be administered in RA

A

oral, IM, IA.

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17
Q

how is MTX administered and what needs co-prescribed with Methotexate.

A

weekly injection.

folic acid.

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18
Q

risks of methotrexate

A

pneumonitis, LFT’s, teratogenic, reduced FBC.

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19
Q

what needs considered when prescribing biological therapy for RA patients

A

DAS28 score, TB/HIV/Hep B status, methotrexate co-prescibed. no live-attenuate vaccine (EG: yellow fever)

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20
Q

what are the signs of advanced RA

A

joint damage and deformity. atlanto-axial sublaxation

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21
Q

things to consider in paint with RA on medication

A

pregnancy, accelerate CVS risk, immunisations, stop smoking, keep DAS28 score good

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22
Q

what is the commonest arthritis

A

OA (osteoarthritis)

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23
Q

What happens in OA

A

progressive degenerative disease, thinning of cartilage with loss of joint space and bony spurs formation

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24
Q

pathogenesis of OA

A

loss of matrix of cartilage, cytokine release (Il-1, TNF, mixed metalloproteinases and prostaglandins).

fibrillated cartilage surface, bone formed not cartilage.

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25
Q

Pc of OA

A

gradual onset, mechanical pain, crepitius, stiffness, deformity/swellings of joints. reduced function and mobility. effusions and soft tissue swelling present.

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26
Q

common sites of OA

A

hip, knee, neck, big toes, thumb/fingers. (weight bearing/mechanical overuse/stress joints)

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27
Q

what are hebardons nodes

A

occur in OA, DIP bony enlagements

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28
Q

what are bouchards nodes

A

occur in OA, PIP bony enlargements.

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29
Q

what is a Baker’s cyst

A

synovial bursa in popliteal fossa.

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30
Q

risk factors for OA

A

age, female, FHx, occupation, obesity, previous joint injury/abnormalities. underlying RA, gout, acromegaly

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31
Q

diagnosis of OA

A

Hx + Examination.
bloods - inflammatory markers raised usually.
X-rays (joint space narrowing, bony cyst, osteophytes, subchondrial sclerosis)

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32
Q

treatment of OA

A

non-pharam = educate, physio, weight loss, walking aid, footwear

pharma= analgesia, NSAID’s, pain modulators (gabapectin, amitriptyline), IA steroid (only short-term relief )

surgery = arthroscope washout, soft tissue trimming, joint replacement.

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33
Q

what does IA stand for

A

intraarticular

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34
Q

crystal arthropathies; name the two and their causing crystals

A

gout (monosodium urate) and psuedogout (calcium pyrophosphate dihydride/CPPD)

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35
Q

what is Gout

A

inflammartoy arthritis associated with monosodium urate crystal deposition. occurs in older men mostly. (1% population)

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36
Q

Gout pathogeneisis

A

PURINES from diet and DNA/ RNA sources (due to cell breakdown = cancer, weight loss, sepsis, psoriasis exacerbate) → hypoxanthine → xanthine → plasma Urate→ urine uric acid (water soluble but if dehydrated causes Gout)

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37
Q

what is hyperuracaemia

A

high uric acid in blood (>7mg/dL). present in 18% population. inc risk of Gout with higher uric acid levels in blood.

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38
Q

diagnosis of Gout

A

based on radiological finding, not hyperuracemia alone; [acute changes in uric acid levels often lead to Gout.]

however, 25% in acute attack have normal uric acid levels , optimum is 2 weeks after attack.

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39
Q

clinical presentation of Gout

A

rapid onset, big toe, sever pain, red/hot joint, up to 2 weeks.

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40
Q

DD of Gout

A

Gout, trauma, septic arthritis, seronegative arthritis (EG:psoriatic)

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41
Q

chronic polyarticular gout

A

chronic joint inflammation, inc uric acid, recurrent acute attacks, >10years.

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42
Q

investigation for gout

A

high CRP, ESR/PV. sometimes high WCC.

Xray normal actually, chronic shows erosions, joint destruction, overhanging osteophytes.

Aspirate joint = gold standard (differentiate between septic arthritis)

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43
Q

management of gout

A

acute= Nsaid’s or colchicine or corticostreroids (oral, IM, IA); analgesia (opiates and paracetamol).

chronic= lifesytle change (reduce red meat, seafood, beans and alcohol.). lose weight, inc fluids (non fructose - no fizzy drinks).
GIVE ALLOPURINOL/FEBUXOSTAT after acute attack stops and at low dose then step up checking uric acid levels. long term → reduce acute attacks.

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44
Q

what is pseudogout

A

occurs in elderly, calcium deposition in cartilage. related to OA. Alcohol and diet has no relevance

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45
Q

where does pseudogout commonly affect

A

knees, wrists, ankles.

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46
Q

diagnosis of pseudogout

A

joint aspirate shows rhomboid shaped crystals with weak +ive birefringence.

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47
Q

what is pseudogout associated with?

A

hyperparathryoidism, haemochromatosis, haemosidenosis, trauma, amyloidosis, gout, hypothryroidism.

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48
Q

treatment of pseudogout

A

nsaid’s, colchicine, steroid, rehydrate.
control other conditions. (gout therapy doesn’t work for psuedogout).

stop diuretics

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49
Q

name a rare for of psuedogout caused by hydroxyapatite crystals.

A

milwalkee shoulder - aggressive acute and rapid deteroration, occurs in females 50-60 years old.
alizain stain shows red clumps. (not seen in tayside)

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50
Q

CTD overview

A

often autoimmune disease (AID).

includes SLE, sjogre’s, polymyositis, APS, systemic sclerosis, mixed CTD.

CTD is caused by spontaneous overactivity of IS, systemic, autoimmune, every part of the body → inflammation/tissue damage.

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51
Q

SLE - systemic lupus erythematosus. risk factors

A

ethnicity (chinese/afro-americans/carribeans), female

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52
Q

what factors cause SLE to develop

A

hormones (oestrogen/HRT), envorinmental (viruses/UV light), genetics, immunology → SLE

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53
Q

pathogenies of SLE

A

antigen presenting cells → CD4 helper Tcell → Bcells (→ antibodies) + CD8 cytotoxic T cell. → cell death.

dead cells are left in the body too long in lupus and are then seen as antigen/threat triggering autoimmune attack

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54
Q

lupus characteristic disease pathway

A

inc turnover + longer to clear dead cells → immune complexes formation drives disease (inflammation of blood vessels occurs also) - type III hypersensitivity.

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55
Q

how does SLE causes renal disease? how is it diagnosed?

A

immune complexes deposited in mesangium; symptomatic and severe → necrosis and scarring (inc blood or protein in urine, seen on urinalysis.)

shows glomerular nephritis, renal biopsy if unsure.

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56
Q

cutanoues signs of SLE

A

mouth ulcers, hair thinning, butterfly/malar rash (post-UV light), discoid lupus → may scar.

chronic and acute.

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57
Q

Signs of SLE

A

renal disease, cutaneous, arthritis, serositis (pleural inflammation), neurological, haemolytic anaemia, thrombocytopenia, leukopenia

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58
Q

neurological signs of SLE

A

depression, psychosis, peripheral neuropathy.

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59
Q

classification of SLE

A

mild - joint and skin affected
moderate
severe- life-threatening = renal, ham, neuro affected

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60
Q

immunology of lupus

A

ana, ANTI-DNA. - best two

anti-Sm, Anti-Ro, Anti-RNP (lupus and others.)

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61
Q

symptoms of SLE

A

fever, fatigue, weight loss, myalgia, headache, anglarged lymph nodes, joint pain/swelling

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62
Q

what condition often occurs with SLE

A

APS - anti-phospholipid syndrome.

clots in artery/vein, causes recurrent miscarriage + PE/DVT [high D-dimer]

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63
Q

why are lupus patients more susceptible to infection?

A

low complement levels.
defective phagocytosis,
steroid/immunosuppressant drugs

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64
Q

investigations for lupus (Bloods only not screening )

A

ANA (+ive in hep C, HIV, RA, other AID’s)

Anti-double standed DNA (most associated and gives level of disease and associated with kidney disease - BEST)

anti-Ro. presence in pregnant SLE patients predicts neonatal problems (heart block)

anti-phospholipid → 3 blood tests. higher value then inc clot likelihood.

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65
Q

screening of lupus

A

multi-organ screening.

urinalysis always plus others if symptomatic (e.g.: CXR for lung problems).

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66
Q

flare-up of lupus causes what blood results

A

inc anti-DNA and reduced C4 level.

also inc PV/ESR but not CRP (never raised in SLE, in other AID’s can be raised )

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67
Q

what does CRP indicate

A
  • infection

- AID’s (apart from SLE)

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68
Q

treatment of SLE (generally)

A

GENERAL: educate, regular monitoring, avoid UV light, pregnancy issues.

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69
Q

treatment of SLE (mild)

A

NSAID’s and analgesia, (anti-malaria) hydroxycholoroquine/HCQ, helps with organ protection, joint pain and skin (therefore - everyone with SLE on HCQ)

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70
Q

treatment of SLE (moderate)

A

steroid is severe (low dose if joints, high dose if kidney)

+ immunosuppressants (1st line is cyclophosphamide, methotrexate, azathioprine ). → leads to reduced IS, bone marrow suppression, potentially teratogenic.

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71
Q

treatment of severe SLE

A

immunospuressant + steroid (IV and inc dose).

+Biological therapy = anti-CD20 + anti-Blys.
may acutely need Warfarin is haematology’s bad.

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72
Q

what are the symptoms of CTD

A

arthralgia, fatigue, myalgia, reynaud’s, alopecia, mucosal ulcers, unprovoked thrombosis/ pregancy losses, sicca (dryness) symptoms.

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73
Q

AID’s general points

A 
female > male
often overlap,
primary or secondary
most is B cell mediated (gives antibodies)
inc CVS risk
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74
Q

what is APS (anti-phospholipid syndrome)

A

venous or arterial thrombosis+ adverse pregnancy. can be primary or secondary. [anti-cardiolipin antibody present]

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75
Q

what type of rash is associated with APS (and what causes it?)

A

Livedo reticulitis

(mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. caused by swelling of the venules owing to obstruction of capillaries by small blood clots. )

76
Q

what antibodies are associated with APS (3 of them)

A

IgM/IgG anti-cardiolipin.
IgM/IgG Beta2-glycoproteins,
lupus anticoagulants

77
Q

treatment for APS

A
  • life-long anticoagulation for thrombosis;
  • aspirin/herpain to reduced pregnancy complications;
  • HCQ.
78
Q

what is Sjogren’s

A

chrnoic autoimmune inflammatory disorder causing dry eyes/mouth (reduced gland function).

  • primary or secondary
  • female 50-60 years
79
Q

PC of sjogrens’

A

“gritty eyes”
dry mouth/eyes/vagina.
dental caries
joint pains, fatigue, bilateral parotid gland enlargement.

80
Q

antobodies in Sjogrens

A

anti-Ro, anti-LA,

inc IgG, inc ESR, inc Rheumatoid factors

81
Q

diagnosis of Sjogrens

A

salivary gland US + biopsy

82
Q

treatment for Sjogren’s

A

artificial tear supplements, cyclosporin eye drops, punctal plugs, saliva supplements, HCQ, immunosuppression (MTX)

83
Q

what is systemic sclerosis

A

fibrosis + vascular endothelial changes.

Skin involved distal to elbow and not torso.

84
Q

what diseases is associated with systemic sclerosis

A

raynaud’s.

85
Q

symptoms/signs of systemic sclerosis

A

pulmonary hypertension (common complication)
small intestinal bacterial overgrowth.
sclerodactyly, calcinosis, osephageal dysmobility, ILD.
scelroderma (thickening of skin) and telangiectasia (spider veins).

86
Q

what antibody is associated with systemic sclerosis

A

anti-centromere antibody

87
Q

summarise diffuse cutaneous Systemic sclerosis

what is affected

A

skin involvement proximal to elbows and torso involved. rapid skin change and early organ involvement.
ILD>pulmonary hypertension. renal crisis may occur.

88
Q

diffuse cutaneous Systemic sclerosis antibodies

A

anti-toposiomerarse/anti-SCL-70/anti-RNA III polymerase antibody

89
Q

treatment of systemic sclerosis

A

raynauds → CCB’s, phosphodiesterase inhibitors
digital ulcers → iloprost infusions
reflux → PPI/H2 antagonist.
lung disease → immunospuression
pulmoary hypertension → CCB, endothelin receptor antagonist, prostacyclin, O2 (at home).
control BP.
small intestinal bacterial overgrowth → antibiotics

90
Q

describe MTCD (mixed CTD)

A

features of SLE, SS, polymyositis.

Pulmonary hypertension is common complication.

91
Q

MTCD antibody

A

anti-RNP antibody

92
Q

MCTD treatment

A

depends of symptoms and major organ involvement.

93
Q

polymyositis antibody

A

anti-Jo1 (and others)

94
Q

generally how do you investigate and treat CTD’s

A

investigations = Examination +Hx, bloods, urinalysis and screening = pulmonary function tests/CXR/ECHO/ CT….

treatment = depends on severity. (NSAID’S, steroid short term, HCQ, treat symptoms.)
if joint involvement → DMARD’s/short steroids.
organ involvment → immunosupression and high dose steroid.

tailor treatment to symptoms (except HCQ in SLE for everyone)

95
Q

define spondylarthropathies

A

a family of conditions characterised by involvement of both spine and joints (in HLA-b27 predisposed individuals)

96
Q

what conditions does being HLA-b27 positive increase risk of?

A

ankylosing spondylitis, crohn’s, uvetitis, reactive, psoriatic, enteropathic arthritis (higher in northern european countries.)

people can be HLA-B27 positive without disease or any symptoms.

97
Q

back pain difference between mechanical and inflammatory

A

mechanical - worsened by activity, sore at end of day

inflammatory - helped by movement and worse in morning with stiffness.

98
Q

what do spondylarthropathies have in common symptoms-wise with rheumatoid disease

A

SI and spinal involvement, enthesitis, dactylitis, eye inflammation, (rare) heart block/aortic regurgitation

99
Q

what is ankylosing spondylitis

A

chronic systemic inflammatory involvement primarily affecting spine.
sarcoiliac common, large joint involvement uncommon

100
Q

who does AS usually affect and how

A

> male, adolescent to adulthood, enthesopathy occurs. get fusion of spine (syndemophytes)

101
Q

how to diagnose AS

A

Hx and Exam (Schober’s test, and occipital to wall test)
MRI → shows sacroilitis
blood → HLA-B27, ESR, CRP, PV.
X-rays → sacroilitis, syndemophytes, “bamboo spine”.

102
Q

treatment of AS

A

physio, OT, NSAID’s, DMD (sulphazine, MTX), anti-TNF and Anti-Il-17(biological)

103
Q

what is psoriatic arthritis

A

most patients have psoriasis in skin,

no rheumatoid nodules/rheumatoid factor (RF) negative.

104
Q

features of psoriatic arthritis

A

psoraisis, nail pitting, onycholysis, dactylitis, enthesitis, eye disease.

105
Q

what are the 5 types/subgroups? of psoriatic arthritis

A

hand/feet, spine, dactylitis, Arthritis mutilans (aggressive+erosive), Oligoarticular (few joints), Polyarticular (many )

106
Q

how to diagnose psoriatic arthritis

A

Hx, Exam, bloods (raised inflammatory but -ive RF),

x-rays= “pencil in cup, osteolysis, marginal erosions”

107
Q

treating psoriatic arthritis

A

NSAID, corticosteroid, immunosupressant (MTX, AZA). anti-TNF/anti-Il-17.
physio, OT, orthotics.

108
Q

what is reactive arthritis

A

infection induced systemic illness, primary inflammatory synovitis with no viable organisms (sterile)

109
Q

what causes reactive arthritis

A

post-infection (GU or enterogenic usually)
1-4 weeks delay.
90% settle in 6 months.

110
Q

characteristic of reactive arthritis (+ who does it affect)

A

20-40 year olds, M=F ratio, HLA-B27 +ive,

nail, eye, ulcers, fever, malaise common

111
Q

diagnosis of reactive arthritis

A

Hx, Exam, blood (raised inflammatory markers, FBC and U+E, HLA-b27. culture,)
aspirate joints and x-ray affected joints.

112
Q

treatment of reactive arthritis

A

self-limiting usually, recurrence/persistance rare usually good prognosis; Nsaids, steroids, (IA once sepsis ruled out/oral), antibiotics for underlying infection.

if chronic- DMARDs (sulphalazine as MTX is tetarogenic).
OT and physio

113
Q

what is enteropathic arthritis

A

associated with Crohns/UC, arthritis in several joints (esp knee, ankle, wrists, elbow).
flares worsen in IBD flares. [20% have Sacroiliac involvement.]

114
Q

symptoms of enteropathic arthritis

A

loose watery (mucous/bloody) stool, fever, weight loss, skin (pyroderma gangrenosum) and uveitis, enthesitis, aphalanous ulcers.

115
Q

investigations for enteropathic arthritis

A

upper/lower GI biopsy, joint aspirate (no organisms/crystals), high CRP/PV, Xray/MRI showing sacroilitis.
USS showing synovitis/tinosynovitis.

116
Q

treatment for enteropathic arthritis

A

treat IBD, NSAID not usually good as exacerbates IBD, mild analgesia.
steroid (IM/IA/oral), DMD (MTX, SSZ, AZA). Anti-TNF

(consult GI for advanced treatments)

117
Q

enthesitis means what?

A

inflammation where tendons insert into bone

118
Q

what is vasculitis

A

presence of leukocytes/immune complexes present in vessel walls

119
Q

Name some types of vasculitis and where they affect

A

Many (HSP, Wegeners[Granulomatosis with polyangiitis (GPA], chung-strauss [Eosinophilic granulomatosis with polyangiitis], microspoic polyangitis…)
can affect large medium and small vessels depending on type of vasculitis.
vasculitis can be primary or secondary (to SLE, RA…)

120
Q

what test can be done for vasculitis to classify

A

ANCA.

121
Q

name for chung-strauss and wegener’s

A

CS -[Eosinophilic granulomatosis with polyangiitis]

W - [Granulomatosis with polyangiitis (GPA],

122
Q

investigating vasculitis

A

ELISA, IIF, pairing of results (PR3 + MPO)
→ biopsy affected system(s).

can use BVAS (Birmingham vasculitis assesment score)

123
Q

treatment of vasculitis

A

localised → steroid and MTX/AZA.

generalised → cyclophosphamide +steroid or rituximab + steroid (or alternatives). potentially plasma exchanger.

refractory → not working on cycle/steroid → IV immunoglobulins + ritiximab + plasma exchanger.

124
Q

prognosis of vasculitis

A

90% 5 year survival rate, 0% if untreated.

125
Q

polymyositis/dermatomyositis PC

A

F>M, idiopathic inflammatory myopathies, 40-50 years old, inc malignancy incidence (paraneoplastic syndrome).
WEAKNESS is PC

126
Q

dermatomyositis signs

A

dermato = skin involvement [shawl and gottron’s signs and heliotope rash]

127
Q

histology of polymyosits/dermatomyosisis

A

fibre necrosis, degredation, regeneration, inflammatory cell inflitrate.

128
Q

muscle weakness worsening over months, usually symmetrical proximal muscles

A

polymyosits/dermatomyosisis

129
Q

other features of polymyosits/dermatomyosisis

A

lung - ILD +muscle weakness. dysphagia, myocarditis, fever, weight loss, raynaud’s, non-erosive polyarthritis

130
Q

what age group is malignancy risk particularly associated with in patients with polymyosits/dermatomyosisis

A

> 45 males.

131
Q

what to check for in Hx of polymyosits/dermatomyosisis

A

D.mellitis, thyroid, statins, steroids, FHx, alcohol/ilict drugs

132
Q

what tests to do in examination for polymyosits/dermatomyosisis

A

inspect/observe.

confrtonational testing or isotonic testing

133
Q

how do you diagnoses polymyosits/dermatomyosisis

A 
muscle enzymes (CK), inflammatory markers raised. electrolytes, Ca2+, PTH, TSH, autoantiboideis (ANA+anti-Jo1). 
EMG (electromyography). Biopsy, MRI
134
Q

treatment of polymyosits/dermatomyosisis

A

glucocorticoids, AZA, MTX, ciclosporin, IV immunoglobulin, ritixumab.

135
Q

what is inclusion body myositis

A

> 50years, M>F, more insideous onset (slow but harmful), digital muscle weakness.
weakness often asymmetrical and in wrist and finger flexors and quads/tibial muscles leg.

occasionally misdiagnosed as polymyosits

136
Q

investigations for inclusion body myositis

A

lower CK levels than polymyositis (PM)
biopsy shows “inclusion bodies”.
poor response to therapy.

137
Q

how does polymyalgia rheumatica present

A

STIFFNESS AND PAIN

> 50years, 1% prevelence, ache in shulder/hip girdle, morning stiffness, symmetrical, fatigue, fever, weight loss, reduced movement of shoulders, neck and hips. Muscle strength is normal

138
Q

what is PMR associated with

A

giant cell arteritis/temporal arteritis.

139
Q

giant cell arteritis/temporal arteritis symptoms

A

symptoms - which is granulation arteritis of large vessels in cranium causing jaw claudication, headache, scalp tenderness and visual loss. (sue to temporal artery supplying optic nerve.) - get tender artery with no pulse

140
Q

giant cell arteritis/temporal arteritis treatment

A

15mg prednisolone as test and clears up instantly

141
Q

diagnosing PMR

A

exclude other diagnoses, ESR/PV/CRP raised, temporal artery biopsy.

142
Q

treatment for PMR

A

rapid and dramatic response to low dose steroid (prednisolone). 40mg if no visual involvement and 60mg if visual disturbances. reduce dose slowly over 2 years.

143
Q

what is Fibromyalgia

A

PAIN and SLEEP DISORDER

common, not associated with inflammation, unknown cause (psychological as may begin after emotion/physical trauma) 20-50year old women, 2-5% prevelence.

144
Q

PC of fibromyalgia

A

pain in shoulder, lower back, chest wall.
diffuse and chronic and varies in intensity, symptoms worsen on exacerbation, stress or fatigue.
get unrefreshing sleep, IBS, poor concentration, headache.
excessive tenderness on palaption (18 points) no other MSK abnormalities

145
Q

how to diagnose fibromyalgia

A

no diagnositc test, inflammatro markers normal, absence of explanation of symptoms

146
Q

treatment of fibromyalgia

A

educate, graded excretes response, CBT, complementary medicine, analgesia, low grade ant-depressants, gabapentin/pregabalin

147
Q

side effects of steroids

A 
osteoporisis so give Ca2+/Vit D supplements
weight gain  [long term]. (inc appetite and water retention)
cataracts/glaucoma
easy bruising/skin thinning
infection
worsening of diabetes
hypertension
inc body hair growth
148
Q

summarise autoimmune diseases

A

self-reaction, high titres of auto-antiboidies or auto-reactive T cells.
rarely monogenic usually polygenic

149
Q

examples of autoimmune diseases

A

graves, MG, sacroid, RA, vitiligo, type 1 diabetes, MS, pernicous anaemia, SLe, sjorgen’s…. F>M

150
Q

give example for monogenic AID

A

IPEx, x-linked, FOXP3 gene (essential for Tc ell regulation).
early childhood with overwhelming autoimmunity causing diahoirrea, eczema, infection, diabetes.

151
Q

how do you treat IPEX

A

imunosupression, total perental care, bone marrow transplant, insulin

152
Q

what does the FOXP3 gene do

A

regulates Tcells, il-10 and TGF-beta deactivate self-reactions.

153
Q

where are the MHC/HLA class molecules on genome

A

chromosome 6 short arm

154
Q

strep M5 protein causes what ?

A

rheumatic fever (post-strep throat infection) may leads to mitral stenosis as heart proteins same as M5 on strep.

155
Q

what are the mechanisms of AID

A

molecular memory,
super-antigens,
antigen sequestration,
unrelated bystander activation

156
Q

SLE is what type AID

A

hypersensitivty type 3.

insoluble immune complexes are deposited and cause AID (activate compliment and phagocytes). Uv light, infection, wound cause cell death and inc SLE.

157
Q

mutation in what genes affect cell clearance therefore causing lupus?

A

C1q or Mac-1

158
Q

how is any inflammatory arthritis treated

A

DMARD (MTX, SAS, HCQ, biologicals) and symptoms relief (NSAID, paracetamol, opiates, atypical analgesia)

159
Q

paracetamol in inflammatory arthritis

A

pure analgesic [little anti-inflammatory action]

component of many anlgesic e.g. co-codamol/codydramol. safe unless overdose

160
Q

analgesic prescription

A

non-opiod,mild opiod, strong opiod (until pain is controlled).
options include co-codamol, dihydrocodene, tramadol, amitriptyline, gabapentin

161
Q

NSAIDS in arthritis

A

used in inflammatory arthritis, mechanical pain, pleuitic pain and other painful conditions [e.g. gout.]

162
Q

adverse affects of NSAID’s

A

dyspepsia, oseophagitis, gastritis, PEPTIC ULCER, small/large bowl ulceration, RENAL impairment, ASTHMA exacerbation, inc CVS risk

163
Q

types of NSAIDs

A

aspirin, ibuprofen, Celecoxib…

Cox2 inhibitors.

164
Q

what are DMARD’s.

A

disease modifying anti-rheumatic drugs; MTX usually 1st line, HCQ (milder).
use aggressively then wear off (as adverse steroid/NSAIDS effects.)
slow acting (weeks-months), so give steroid until effect kicks in. There are pure anti-inflm=ammatories and lower CRP, ESR, and reduce rate of joint damage.

165
Q

dangers of MTX [methotrexate]

A

regular monitoring for drop in WBC,
LFTs for hepatotoxicity,
pulmonary function tests regularly as pneumonitis and
pulmonary fibrosis occur (rare)
kidney failure
rash and mouth ulcers (ulcerative stomatitis)
teratogenic.

co-prescribe folic acid. (mechanism unknown but evidence is good)

166
Q

when to use DMARDs

A

new onset RA, active inflammatory disease.

167
Q

why use leflunomide?

A

similar efficacy/side effects to MTX. also teratogenic. used if TMX not suitable

168
Q

why use MTX?

A

RA, CTD, psoriatic arthritis, vasculitis

169
Q

why use SAS?

A

often combined with MTX in early inflammatory arthritis.
causes naesea, SJS, rash/mouth ulcers, hepatitis, neutropenia, reversible oligozoospermon (reduced sperm count temporarily)

170
Q

HCQ used in?

A

no effect on joint damage, used in CTD (lupus, Ra, sjogren’s).
retinopathy rare and irreversible side effect

171
Q

Other DMARD’s [sodium acrothromalate (gold) and penicillamine oral ] used for what and their side effects include?

A

sodium acrothromalate (gold) and penicillamine oral (used in RA)

side effects - bone marrow suppression, glomerulitis, rash, mouth ulcers, → monitor FBC, and urine for protein

172
Q

anti-TNF is used for what?

A

RA, AS, psoartic arthritis, subcutanrous (DAS28 score of >5.1 with previous MTX and DMARD’s tried)

173
Q

Anti-TNF side effects/risks

A

inc risk of infection (esp TB; so screen for Hepatitis B/C and HIV and TB beforehand).

malignant uncertainty

contraindicated in P.fibrosis or H.Failure (safe in pregnancy )

174
Q

which biologics are used in RA?

A

RA = anti-TNF, rituximab (anti-CD20 B cells), Tocilzumab (Il-6) and abatecept (CTLA-4 Ig)

175
Q

which biologics are used in psoriatic arthritis?

A

anti-TNF, ustekinumab (il-12+23), secukinimab (il-17)

176
Q

which biologics are used in CTD?

A

rituximab

177
Q

which biologics are used in AS?

A

anti-TNF, secukinimab

178
Q

Gout acute treatment

A

NSAID/colchicine if unsiutable (side effect is diahorrea), prednisolne (oral, IA, IM).

179
Q

gout prophylaxis

A

allopurinol (wait until post-acute attack) or febuxostat

both uricosurics = lower rate in blood by inc in urine

180
Q

allopurinol mechanism of action and side effects.

A

-xanthine oxidase inhibitor, rapid reduction in uric acid levels may induce exacerbation of gout is prescribed acutely.

  • vasculitis/skin rash common (switch to febuxostat).
  • patients with pre-existing renal impairment need to lower dose and azathioprine interaction can cause irreversible bone marrow suppression.
181
Q

gout pathway

A

purine → xanthine → uric acid → crystal deposit and gout

182
Q

what can neither febuxostat or allopurinol be prescribed with and why

A
  • azathioprine (interaction)

- can cause irreversible bone marrow suppression

183
Q

febuxostat mechanism of action and side effects

A

also xanthine oxidase inhibitor, for those who cannot tolerate allopurinol.

safe in renal impariement.
used in caution with IHD (ischemic heart disease)

184
Q

what do uricosurics do?

A

inc uric acid in urine and therefore reduced in blood.

185
Q

indications for corticosteroids

A

CTD, vasculitis, RA, PMR, giant cell arteritis

given oral, IA, IM, IV, soft tissue injections - use short term

186
Q

adverse effects of steroids

A 
high BP,
 inc weight  (centripetal obesity due to inc appetite and fluid retention), 
muscle wasting, 
skin atrophy, 
diabetes, 
osteoporosis (give Ca2+/Vit D supplements), 
cushingoid appearance and buffalo hump at neck.
cataract, glaucoma, 
fluid renetion, 
adrenal suppression, 
immunosupression, 
AVN of femoral head(seen in lupus)

to reduce toxicity - short-term, lowest possible dose, wear off to other immunosupressants, watch CVS risk factor, osteoporosis prophylaxis

15021998-MSK (19 decks)

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