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Medicine > Rhemuatology > Flashcards

Rhemuatology Flashcards

1
Q

whats SLE

A

inflammatroy autoimmune connective tissue disease. autoantibodies against proteins in the nucleus of cells = antinuclear antibodies - ANA

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2
Q

symtpoms of SLE

A

systemic
malar rash- photosentivity
fatigue
weight loss
fever
arthraglia
myalgia
non erosive arthritis
sob
pleuritic pain
hair loss
reynauds phenomoen
mmouth ulcers
splenomegaly/ lymphendopathy

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3
Q

whats the common person to present with sle

A

women
asian
middle age- young §

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4
Q

what invvestigations do you do for sle

A

blood test for ANA - healthy people can be psotive so do if they have symptoms

anti-ds DNA postive
anti-smith

FBC- normocytic anemia of chronic disease
low c3 and c4
high crp and esr
urine protein:creatinine ratio to find renal fucntion and renal biopsy to see if lupus neprhtitis

high immunoglobulins

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5
Q

whats the complications of sle

A

cv disease - v high cause death =. inflam of bv causes hypertension and coronary artery disease

lupus nethiritis

pleurisy
interstial lung disease leading to pulmonary fibrosis

pericardiditis
anemiea - normocytic. can also have thrombocytopenia, leucocytopenia, neutropenia

infection

anti phospholipid syndrome- VTE

neuropsyciatric sle => optic neuritis, pscyhosis, transverse myelitis (inflam spine)

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6
Q

what treatment sle

A

immunosupressants if not reacting to treatment or severe sle

first line =
NSAIDs
prednisolone
hydroxychloroquine - first line mild sle
suncream and sun avoidance

methotrexate
ciclosporin
azathioprine
tacrolimus
lefunomide
mycophenolate mofetil

rituximab = targets CD20 on b cells
belimumab = targets b cell activating factor

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7
Q

whats systemic sclerosis

A

autoimmune inflammatory ad fibrotic conective tissue disease

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8
Q

whats the features of limited cutaneous systemic scleorsis

A

CREST
calcinosis
raynauds
oesophageal dysmotility
sclerodactyl
telangiectasia

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9
Q

whats the features of diffuse cutaneous systemic sclerosis

A

CREST
and affects interna; organs:

cv= ht and coronary artery disease

lungs= pulmonary ht and pulmonary fibrosis

kinde= glomerulonepthritis and scleroderma renal crisis= acute server ht and renal failure

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10
Q

whats scleroderma

A

hardening of skin
shiny and tight without normal folds
hands and face esp

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11
Q

whats scelrodactyl

A

skin tightens around joints so decrease range of movement and fucntion
skin cxan break and ulcerate

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12
Q

whats telangiectasia

A

dilated small bv in skin

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13
Q

on x ray what see on hands of pateint with systemic sclerosis

A

white dots= calcinoisis

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14
Q

what happens in oesophageal dysmotility in systemic scleoriss

A

connective tissues dysdunction in oesopahgus
swallowing difficulties
acid reflux
oesophagitis

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15
Q

patient has gradual onset of dry cough and sob and got raynauds and hardening of skin on hands
what is this

A

pulmonary fibrosis

diffuse cutaneous systemic sclerosis

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16
Q

what autoantibodies do most patients have in systemic sclerosis

A

Antinuclear antibodies= ANA = not specific to systemic sclerosiis

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17
Q

what antibodies suggest pt has limited cutaneous systemic scleorisis

A

anti-centromere antibodies

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18
Q

what antibodies suggest diffuse cutaneous systemic sclerosis

A

anti-Scl-70 antibodies

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19
Q

how do you distinguish between pt with raynauds and if they have got systemic sclerosis

A

nailfold capillaroscopy

if its abnormal
avascualr areas
micro haemoorages then indicates systemic scleorsis

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20
Q

how to diagnose systemic sclerosis

A

nailfold capillaroscopy
features
antibodies

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21
Q

management of systemic scleroisis

A

steroids and immunosupressants for diffuse disease and treat complications eg. pulmonary fibrosis

non med=
no smoking
skin stretching to maintain range of motion
regular emolients
avoid cold = raynauds
hysoi
occupational therpay

meds=
nifedipine= raynauds
ppi and pr motility meds for gi
analgesia= joint pain
antibiotics for skin infection
anti hypertensive meds
treat pulmoanry ht
supportive for pulmonary fibrosis

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22
Q

patient got a bad headache on left side of forehead
hurts to brush their hair and when they eat they get pain in their jaw after a bit like cramp

what is this

A

giant cell arteritis/ temporal arteritis

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23
Q

whats giant cell arteritis

A

systemic vasculaties of emdium and larger arteries
typically affects temporal arteries

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24
Q

s and s of giant cell arteritis

A

headache key feature
servere unilateral
forehead and around temple
may hurt to bursh hair- scalp tender
jaw claudication
blurred/double vision
irreversibe painless complete sight loss can occur rapudly

fever
weight loss and loss apetite
fatigue
musce aches
peripheral oedema

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25
Q

whats inital management for giant cell arteritis

A

steroids imediately before confirming diagnosis
40-60mg prednisolone once daily
review in 48 hrs - should get response to treamtent

aspirin 75mg od to decrease vision loss and stroke
ppi to protect against steroids
referal to vascualr durgeon for temporal artery biopsy
to rheumatology
to ophthalmology same day if get vision symtooms

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26
Q

when do you give 60mg prednisolone to pt wth suspected fiant cell arteritis

A

if got jaw claudication or vision symtpoms give the higher dose of prednisolone

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27
Q

whats do you do for ongoing managemnt for giant cell arteirtis if diangosis been confirmend

A

continute steorids until sysmtos resolved then weak off slowly

dont stop= dont stop steroids abruptly as risk adrenal crisis

s= sick day rules= increase steroids if ill
t= treamtent card carry with
o= osteoprosis protection due to steroids- bisphosphonated vit d and ca
p= ppi for gastric protection

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28
Q

what risk factors are there for giant cell arteritis

A

strong link between giant cell arteritis and polymylagia rheumatica

female over 50 caucasian

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29
Q

what investigations do if suspect giant cell arteritis

A

rasied ESR= 50mm/hr or more
clinical presentation
temporal artery biopsy finsings
these three give diangosis of it

may also do
fbc= see normocytic anaemia/ thrombocytosis= raised platelets
rasied CRP
duplex ultrasound of temporal artery and see hypoechoic halo sign

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30
Q

what will you see on biopsy of temporal artery in giant cell arteritis

A

multinucleated giant cells

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31
Q

hypoechoic halo sign on temporal artery us suggest what

A

giant cell arteritis

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32
Q

whats polymyositis and dermatomyositis

A

autoimmune disorders = inflamm of teh musces

polymyositis = chronic inflammation of muscles

dermatomyositis= connective tissue disorder= chronic inflammation of skin and muscle

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33
Q

what csn casue polymyositis/dermatomyositis

A

cancer can casues t= paraneopplastic syndrome
breast
ovarian
gastric
lung

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34
Q

s and s of dermatomyositis and polymyostits

A

muscle pain, fatigue, weakness
bilaterally and affect proximal muscles most
shoulder and pelvic girdle mostly affected
develops over weeks

dermatomyositis also has skin :
gottron lesions - scaly red patches on knucles, elbows, knees
photosensitive erythematous rasy on back, shoulders, neck
purple rash on face and eyelids
periorbital oedema
subcutaneous calcinosis

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35
Q

whats the key investigation for diagnosing polymyositis and dermatomyositis

A

creatine kinase bloods
over 1000

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36
Q

when can creatine kinase be raised

A

dermatomyositis
polymyositis
rhabdomyolysis
AKI
MI
statins
strenuous exercise

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37
Q

what antibodies are seen in polymyositis

A

Anti-Jo-1 antibodies
also seen sometimes in dermatomyositis though

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38
Q

what antiboides seen in dermatomyositits

A

anti-mi-2 antibodies
anti nucelar antibodies
can see anti-jo-1 antibodies sometimes

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39
Q

what investigaions do for dermatomyositis and polymyositis

A

creatine kinase bloods
antibidies - anti-jo-1, anti-mi-2 antibodies- antinucelar antiboides
electromyography
muscle biopsy= gives definitive diagnosis

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40
Q

management of polymyositis and dermatomyositits

A

corticosteroids first line
physio/ot
asses for underlying cancer

if steroids not working
immunsupressants- aziathioprine
iv imunoglobulins
biological- etanercept / infliximab

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41
Q

whats cause of osteoarthritis

A

in synovial joints
not imflammatory
genetic, overuse, injury
worn down and chondrocytes repairing it

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42
Q

rf for OA

A

obesity
age
occupatipn
trauma
female
fam hist

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43
Q

signs and symtpoms of OA

A

joint pain
stiffness
worsedned by activity - worse in eveing
may have morning stiffness but doednt last more than 30 mins
deformity
insatbility
decreased fucntion of joiny
haberdens nodes in DIP in hand
bouchards nodes in PIP in hand
weak grip/ muscle wasting
decreased rang of motion
squaring at base of thumb at carpometacarpal joint

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44
Q

x ray findings of OA

A

LOSS
loss of joint space
osteophyte
subarticular sclerosis = white on edgess
subchondral cysts= dark holes in bone

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45
Q

joints commonly affected in OA

A

hip
knees
sacroiliac joint
DIP in hands
MCP thumb
wrist
cervical spine

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46
Q

examine hip for OA finding

A

groin pain often first symtok
internal and external rotation to be reduced first

check not trochanteric bursitis by pressing on hip

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47
Q

how to diagnose OA

A

no investigations if over 45, typical activity related pain, no morning stiffness or doesnt last more than 30 mins

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48
Q

management for OA

A

physio
occupational therpay
psycho
weight loss
orthotics
step wise analgeisa:
oral paracetamol, topical nsaids/ topical capsaicin= dec substance p
2= add oral nsaids and ppi
3= opaites=codeine and morophine. morphine se are withdrawal and dependence so not good for chronic pain

intraarticular injection
joint replacement

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49
Q

whats rheumatoid arthritis

A

symeetrical polyarthritis
inflammatroy arthritis
autoimmune= chronic inflammation of synovial lining of joints, tendons, bursa sheaths

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50
Q

risk factors of RA

A

female
any age
fam hist
genetic associations= HLA DR1
HLA DR4

antibodies:
rheumatoid factor - 70% of patients
anti CCP antibodies - can have before develop RA

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51
Q

s and s RA

A

stiffness worse in morning/ improves with activity
pain
swelling
multiple joints
often symmetircal
hands, feet, ankles, wrist, MCP, PIP in hands
onset can be rapid/months years

dip in hands vvvv rarely affected in RA so if are probs oa

systemic symtoms =
fatigue
weight loss
flu like
muscle aches, weakenss

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52
Q

whats palindromic RA

A

short episodes of inflammatroy arthritis with pian and stiff and swelling but 1-2 days then resolves

if got rf and anti ccp may progress to full RA

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53
Q

whats atlantoaxial subluxation

A

cervical spine
axis and peg shift with atlas due to synovitis damage to ligaments and bursa

need take care with gerneal anesthetic and intubatio n

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54
Q

signs of RA in hands

A

swan neck deformity = hyperextended PIP with flexed DIP
Boutonnieres deformity (hyperextended DIP with flexed PIP
z shaped deformity in thumb
ulnar deviation at mcp joint= fingers pushed towards little finger

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55
Q

signs in eyes of ra

A

scleritis
episcleritis
keratitis
keratoconjunctive
cataracts secondary to steroids
retinopathy secondary to chloroquine

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56
Q

extra articular mannifestrations of RA

A

Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
Bronchiolitis obliterans (inflammation causing small airway destruction)
Felty’s syndrome (RA, neutropenia and splenomegaly)
Secondary Sjogren’s Syndrome (AKA sicca syndrome)
anameia
cardiovascular disease
rheumatoid nodules
lymphadenopathy
carpal tunnel syndrome
amyloidosis

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57
Q

xray features of RA

A

joint destruction and deformity
soft tissue swelling
periarticular osteopenia
bony erosisions

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58
Q

investigations for RA

A

diangosis mainly clinical
rheumatoid factor
if rf negative check for anti CCP antibodies
inflammatory markers- crp, esr
x ray of hands and feet
ultra sound of joints to see if synotivitis

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59
Q

whtas diangositc criteria for RA

A

Referral
NICE recommend referral for any adult with persistent synovitis, even if they have negative rheumatoid factor, anti-CCP antibodies and inflammatory markers. The referral should be urgent if it involves the small joints of the hands or feet, multiple joints or symptoms have been present for more than 3 months.

Diagnosis
Diagnostic criteria come from the American College of Rheumatology (ACR) / European League Against Rheumatism (ELAR) from 2010:

Patients are scored based on:

The joints that are involved (more and smaller joints score higher)
Serology (rheumatoid factor and anti-CCP)
Inflammatory markers (ESR and CRP)
Duration of symptoms (more or less than 6 weeks)
Scores are added up and a score greater than or equal to 6 indicates a diagnosis of rheumatoid arthritis.

DAS28 Score
The DAS28 is the Disease Activity Score. It is based on the assessment for 28 joints and points are given for:

Swollen joints
Tender joints
ESR/CRP result
It is useful in monitoring disease activity and response to treatment.

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60
Q

what drugs are used to manage RA

A

short term glucocorticoids used at start maybe to allow time for mards to work

DMARDS= disease modifying anti rheumatic drugs
methotrexate
leflunomide
sulfasalazine
anti tnf drugs
rituxiab
hydroxychloroquine

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61
Q

how does methotraxate work and main SE

A

interfer with metabolism of folate - making of nucelic acid and supress immune system

injection/tablet once a week
folic acid 5mg once a week taken a diff day to methotraxate

se=
mouth ulers and mucositis
liver toxicity
pulmonary fibrosis
bone marrow suppresion and leukopenia
teratogenic

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62
Q

how does sulfasalzine work and main se

A

immunosupressant and anti inflam
potentially effect on folate metabolism
safe in pregnancy

se=
temporary male infertility as dec sperm count
bone marrow suppression

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63
Q

leflunomide work and main se

A

immunosuppresant
interfernwith production of pyramidine

se= mouthulcers and mucosisits
increased bp
rashe
peripheral neuropahty
liver toxicity
bone marrow supresion and leukopenia
teratogenic

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64
Q

how does hydroxycholoquine work and main se

A

anti malarial
immunosupressant - interact with toll like receptors
distrupt antigen [resentation and increas ph in lysosomes
safe in pregnancy

se=
nightmares
decreased visual acuity= macular toxicity
liver toxicity
skin pigementation

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65
Q

how does rituximab work and se

A

monoolonal antibody
targers cd20 protein on b cells
destriction of b cells
used in cancer of b ells too

se=
night sweats
thrombocytopenia
peripheral neuropathy
liver and lung toxicity
vulnerabtilty to infection/sepsis

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66
Q

what anti tnf drugs are there and the main se

A

TNF is a cytokine that stimulates inflammation

monocolonal antibodies to TNF:
adalimumab
infiximab
golimumab
certouzumab pegol

etancercept= Etanercept is a protein that binds TNF to the Fc portion of IgG and thereby reduces its activity.

se= vulnerability to infection/sepsis
reactivation of TB/hep B

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67
Q

main / diff se of the DMARDS

A

Methotrexate: Bone marrow suppression and leukopenia and highly teratogenic

Leflunomide: Hypertension and peripheral neuropathy and teratogenic

Sulfasalazine: Male infertility (reduces sperm count)

Hydroxychloroquine: Nightmares and reduced visual acuity

Anti-TNF medications: Reactivation of TB or hepatitis B

Rituximab: Night sweats and thrombocytopenia

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68
Q

whats psoriatic artrhitis

A

inflammatory arthritis asscoaited with psoraisis
vary in severity
stuff and sore but can get destroyed joint= arthritismutilans

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69
Q

whats the number of patients with psoraisis who will get psoriaatic arthritis

A

10-20% in first 10 years of skin cahnges

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70
Q

signs and symptoms of psoriatic arthritis

A

inflammatroy pain or joint swelling
a few patterns:

spondyltic pattern=
common in med
back stiff, sacroilits, atlanto-axial involement

symmetrical polyarthritis= simmilar to RA
more commen in women
hands, wrists, ankles, DIP (not really n MCP o fthumb unlike RA)

asymmetrical pauciarthritis
= mainly digits and feet
only a few joints affectd

other areas:
achiles tendon
plantar fascia
spine

skin:
get plauques of psoriasis !
pitting of nails
oncholysis= nail come off from nail bed
dactylitis= inflam of full finger
enthesits= inflam of tendon where inserts to bone

eye disease= conjunctivits and anterior uveitis
aortitis
amyloidosis

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71
Q

whats arthritis mutilans

A

severe form of psoriatic arthritis
in phalanxes
osteolysis of boned around oint so shortens digits = skin folds over and gives telescopic finger apperance

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72
Q

investigations for psoritatic arthritis

A

pest tool then refer to rheumatologist
xray
bloods = negative rf

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73
Q

what investifgations for psoritatic arthritis

A

xray
bloods- negative rf
pest screening tool

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74
Q

what x ray cahnges seen in psoriatic arthritis

A

periostitis= cauing thick and irregular outline of bone
ankylosis= bones fuse
osteolysis= destruction of ohone
dactylitis= show soft tissue swelling
pencil in cup appearance

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75
Q

managemnt of psoratic arthritis

A

nsaids for pain
dmards = methotraxate, lefluomide, sulfasalozine

anti tnf= etanercept, infliximab, adalimumab

ustekinumab= last line after tnf
monocolonal abx
targets interleukin 12 and 23

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76
Q

whats reactive arthritis

A

infection elsewhere in the body causes immune system to go wrng and so get inflam in other parts of body that the infection isnt in
= synovitis occurs in the joint as a reaction to recent infective trigger
infalm of joint
= no infection in the joint !!

77
Q

whats a differential for reactive arthritis

A

septic artrhitis

78
Q

what gene is linked to reactive arthritis

A

HLA B27 gene= seronegatove spondylarthropy group

79
Q

what casues reactive arthritis

A

infection
usually
STI = comonly chlamydia
gastroenteritis

(gonorrhea casues gonococcal septic artrhitis so differential)

80
Q

what sti is common to casue reactive arthritis

A

chlamydia

81
Q

what s and s fro reactive arthritis

A

single joint
develops within 4 weeks of infection
acute monoarthritis affecting single joint commonly the knee

warm
swollen
painful

assocaitations=
anterior uveitis
circunate balonitis = dermatis of head of penis
bilaterla conjunctivitis (non infective)

cant see, pee, or climb a tree

82
Q

management of reative arthritis and investigations

A

hot, swollen painful joint singular! = hot joint policy= assume seotic arthritis until excluded so give antibiotics until septic arthrits has been excluded

also aspirate the knee = sample for gram staining, culutre and sensitivity to exclude septic arthritis
sample for crystal examination to lookvfor hout/ pseudogout

once excluded septic arthritis then: nsaids
steroid injection into joint
systemic steroids if multiple joints affected
most reoslves within 6 months and dont recur. if do may need dmards

83
Q

whats septic arthritis

A

infection in the joint, in the synovial fluid and tissues
not rhematological

84
Q

s and s of septic arthritis

A

fever
hot joint- swollen, painful

85
Q

casues of septic athritis

A

injury to joint- trauma/dog bite / bad cut
hameatogenous spread - infection from elsewhere
joint surgery complication

86
Q

risk factors for septic arthrits

A

gonorrhea!
inkect drugs
artifical joint
recent joint surgery
RA
weak immune system

87
Q

whats ankylosing spondylitis

A

Ankylosing spondylitis (AS) is an inflammatory condition mainly affecting the spine that causes progressive stiffness and pain
can progress to fusion of spine and sacroiliac joints

part of the seronegative spondyloarthropathy group= most paintets with AS have HLA B27 gene

88
Q

what joints are mostly affected in ankolysing spondylitis

A

vertebral column joints
sacroiliac joints

89
Q

whats a main complication of ankylosing spondylitis

A

vertbreal fractires

90
Q

s and of ankolyising spondylitis

A

young male adult in late teens / 20s
symtpoms gradual over 3 motnhs
lower back pain and stiffness
sacroiliac pain in buttock region
worse with rest= worse at night in sleep/in mornings
improves with movement
takes at least 30 min for stiffness to go in the mornings
flucuating symtoms

can affect other organ systems too :
restrictive lung disease due to restricted chest wall movment as can get inflammed costosternal joints
chest pain due to inflamed costovertebral and costosternal joints
weight loss and fatigue
enthesitis = plantar fascitis and achilles tendotitis
dactylitis
anaemia
anterior uveitits
aoritits
heart block due to heart fibrors
pulmonary fiboris of upper lobes
IBD

91
Q

investigations for ankolyising spondylitis

A

schobers test= bend less than 20cm
inflam markers- crp, esr
HLA B27
xray soine and sacrum
mir = bone marrow oedema = shows early on before x ray changes

92
Q

what x ray changes in ankolysing spondylitia

A

bamboo spine = later stage
squaring vertebral bodies
subchondral scleorisis and erosiions
syndesmophytes
ossification of ligaments, discs, joints
fusion of facet, sacroilian and costovertebral joints
loose curveture of spine so pushes head forward

93
Q

management fir ankylosing spondylitis

A

nsaids - after 2-4 weeks no improvement swap nsaids
steroids for flare ups
anti tnf = etancercept, infliximab, adalimumab, certolimumab pegol
secukinumab = monocolonal ab against IL17
physio
exercise and mobilisation
avoid smoking
bisphosphonates to treat osteoporosis
treat complciations
surgery if deformities

94
Q

what is in the seronegative spondyloarthropathy group

A

reactive arthritis
ankolysing spondylitis
psoratic arthritis

have HLA B27 gene
negative rheumatoid factor
get rashes, back pain, GI symptoms - IBD, uveitis

95
Q

how to diagnose sle

A

presence of ANA antibodies (most have it so good to exclude it) and clinical features
anti ds DNA more if have it then have lupus

96
Q

what antibody is very specific to sle

A

anti-double stranded DNA
unlikely to have this and not ahve sle

70% pt with sle have them

97
Q

whats discoid lupus erthematous

A

non cancerous chronic skin condition

98
Q

rf for discoid lupus erthamtous

A

women
20-40
dark skinned
smokers
sle ay ahve dle
fa hist

99
Q

s ands of discoid lupus erthematous

A

coin shaped lesions
on face,ears,scalp
lesions photosenetive= worsened by sun
scarrig alopecia= hair loss in affected area and wont grow back
hyoer/hypopigmentated scars = lesion goes and leaves discoloured scar

lesions are:
dry
erythamatous
patchy
crusty and scaling
inflammed
not itchy or painful

100
Q

mnagment of discoid lupus erythamatous

A

skin biopsy to confirm
sun protection
topical steroiuds
intralesioanl steroid injections
hydroxychloroquine

101
Q

whats polymylagia rheumatica

A

inflammatory condition
pain and stiffness to shoulders, pelvic girdle and neck

102
Q

risk factors for polymyalgia rhemmatica

A

women
over 50s
norhtern european

103
Q

whats polymylagia rhemuatica strongly associated with

A

giant cell arteritis

104
Q

bilateral shoulder pain
wakes up at night in pain
in moeings takes an hour to get going cus stiff
what is this

A

polymyalgia rhemuatica

105
Q

s and s of polymylagia rhematica

A

presents at least 2 weeks
bilateral shoulder pain
bilateral pelvic girdle pain
worse with movement
interfers with sleep
morning stiffness lasting more than 45mins
weight loss
fatigue
low mood
low grade fever
upper arm tenderness
carpal tunnel syndrome
pitting oedema

106
Q

whats an impotant question to ask if suspect polymyalgia rhemautica

A

ask re vision
strong link with giant cell arteritis

if got vision issues steroids of bigger dose cus at risk of temporal aarteritis = blind

107
Q

what differntial diagnosis are there for polymyalgia rhemuatica

A

osteoarthritis
fibromyalgia
osteomalacia
rhemautoid arthritis
SLE
myositis = rom polymyositis or statins
cervical spondylosis
adhesive capsulitis of both shoulders
hypo/hyperhtroidism

108
Q

what medication can casue myositis

A

statins

109
Q

how do you diangose polymyalgia rheumatica

A

exclusion
clinical presentation
repsonse to steroids

110
Q

what investigfations do you do for polymyalgia rheumatica

A

ESR, CRP, plasma viscosity raised= however normal doest rule out pmr
FBC
u and e
lft
see if rhematoid facotr= RA
urine dipstick
calcium= raised the hyperparathroidism / cancer
low ca then osteomalacia
serum protien electrophoresis= myeloma/protein disorders
tsh= thryoid function
creatine kinase= myositits

consider doing=
ANA= sle
anti-ccp= RA
urine bence jones protien= myeloma
CXR= lung and mediastinal abnormalities

111
Q

once excluded all other casues how do you manage polymyalgia rheumatica

A

steorids

Initially patients are started on 15mg of prednisolone per day.

Assess 1 week after starting steroids. If there is a poor response in symptoms it is probably not PMR and an alternative diagnosis needs to be considered. Stop the steroids.

Assess 3-4 weeks after starting steroids. You would expect a 70% improvement in symptoms and inflammatory markers to return to normal to make a working diagnosis of PMR.

If 3-4 weeks of steroids has given a good response then start a reducing regime with the aim of getting the patient off steroids:

15mg until symptoms are fully controlled then
12.5mg for 3 weeks then
10mg for 4-6 weeks then
Reduce by 1mg every 4-8 weeks
If symptoms reoccur whilst on the reducing regime then they may need to increase the dose or stay on the dose longer before reducing again. It can take 1-2 years to fully wean off. If there is doubt about the diagnosis, difficulty controlling symptoms, difficult weaning steroids or steroids are required for more than 2 years refer to a rheumatologist.

112
Q

whats importnant to think about when on long term steroids - 3 weeks or more

A

dont stop
= dont suddenly stop the steroids=adrenal crisis

s= sick day rules= if ill take more
t= treatment card to alert people
o=osteoposotsis= take bisphosphonates, ca and vit d to prevent osteoporosis caused by steroids
p= ppi= gastric protection

113
Q

urine bence jones protein means what

A

myeloma

114
Q

what are antinucelar antibodies

A

If you send a test for antibodies to extractable nuclear antigens (anti-ENA antibodies) the lab will check for antibodies to specific proteins in the cell nucleus.

theres lots of types of them

115
Q

anti-smith

A

highly specific to sle
not sensitive

116
Q

anti centromere antibodies

A

most linked to limited cutaneous systemic scleorisis

117
Q

anti -Ro

A

sjorgens syndrome

118
Q

anti-La

A

sjorgens syndrome

119
Q

anti-scl-70

A

systemic scleorsis

120
Q

anti-Jo-1

A

dermatomyositis

121
Q

antiphospholipd antibodies can occur secondary to what condition

A

SLE - can occur in up to 40% of patients
can get antiphospholipid syndrome => increase risk of VTE

122
Q

whats antiphospholipid syndrome

A

autoimmune
disorder associated with anti phospholipid antibodies => hypercoaguable state

123
Q

whats the three antiphospholipid antibodies

A

lupus anticoagulant
anticardiolipin antibodies = aCL
anti-beta-2-glycoprotein 1

antibodies interfere with coagulation and create a hypercoagulable state

124
Q

what assocaitions / signs get with antiphospholipid syndrome

A

thrombosis
complications in pregancy esp recurrent miscarriage

VTE= PE and DVT

arterial thrombosis
= stroke, MI, renal thrombosis

pregnanyc complications =
recurrent miscarriages, still birth, preeclampsia

thrmbocytopenia = low platelts as the antobodies bind to and activate the platelets which then get consumed in process

livedo reticularis = purple lace like rash

libmann-sacks endocarditis= non bacterial endocardits- vegetations to valves esp mitral valve
libmann-sacks endocaritis is associated with sle and antiphospholipid syndrome

125
Q

differntials of antiphospholid syndrome

A

other procoagulation - pill, nephrotic syndrome
other casues miscarriage
reccurent small stroke= multiple scleorisis

126
Q

investigation antiphospholid syndrome

A

young adults under 50 and woen with reccurent3 or more miscarriage before 10 weeks gestation investigate

look at levels of the antiphospholipid antibodies= on two occasions at least 12 weeks apart
FBC = haemolytic anaemia, thrombocytopenia
clotting screen
mri brain, ches, abdo - pe clotting etc
doppler us of legs look for dvt
echo- look at heart valves

127
Q

how to diagnose antiphospholid syndrome

A

history of thrombosis and persitant antibodies

128
Q

causes of antiphospholid syndrome

A

can occur on own
can be secondary to other autoimmune conditions esp sle
can occur due to infection

129
Q

management for antiphsopholid syndrome

A

long term warfarin - inr 2-3 to prevent thrombosis
pregant women give low molecular weight heparin eg. enoxaparin and aspirin to prevent comoplcations = warfarin contraindicated in pregnancy

lifestule= stop smoking
health diet
exercise
reduce alchol
cv, diabetes, hypertension,hyperlipidaemia management

130
Q

whats sjorgrens syndrome

A

autoimmune condition that affects exocrine glands

131
Q

patient has dry mouth and they have sore painful eyes and bad dental hygeine

what is this

A

sjorgrens syndrome

132
Q

s and of sjorgrens syndrome

A

dry mucous membranes =

dry mouth
dry eyes
dry vagina

complications:
eye problems= conjunctivits, corneal ulcers

oral problems=candia infections, dental cavities

vaginal problems = candidiasis, sexual dysfucntion

can rarely affects other organs:
pneumonia and bronchiectasis
non-hidgkins lymphoma
peripheral neuropathy
vasculitis
renal impairment

133
Q

patient has schirmer test less than 10mm

what test is this for and mean

A

sjorgrens syndrome

less than 10mm so sigificant

134
Q

what investigations do you do for sjorgrens syndrome

A

schirmer test
= filter paper on lower eyelid
leave 5 mins
if tears travel less than 10mm significant

15mm is for a normal healthy person

135
Q

what is secondary sjorgrens syndrome

A

sjorgrens syndrome occurs related to rheumatoid arthritis / SLE

136
Q

what primary sjorgrens syndrome

A

condition occurs in isolation

137
Q

anti - Ro antibodies are associated with what illness

A

sjorgrens syndrome

138
Q

what antibodies are assciated with sjorgrens syndrome

A

anti-Ro
anti-La

139
Q

whats gout

A

type of crystal arthropathy
have chronically high uric acic blood levels = get urate crystals depositied in the joint = causes inflammation and destruction of joint

can have high uric acid levles and not get gout

140
Q

whtas gouty tophi

A

tophi are subcutaenous depsits of urinc acid that typically affect the small joints and conecctive tissue of the hands, elbows and ears= on x ray see sof tissue swelling amybe

affects DIP in hands most

firm lumps under the skin get aroud 10 years after first attack if not amanged

141
Q

hot
swollen
painful joint
came on quicly

what could it be

A

gout
septic arthritis!
reactive arthritis
psudeogout

142
Q

s and s of gout

A

acute onset
sigle joint
hot swollen painful
base of big toe mtp mainy affected first
wrists
base of thumb= carpometacarpal jount
can affect bigger joints - knee, ankle

143
Q

risk factors for gout

A

male
obesity
high purine diet- meat and seafood
alcohol
diuretics
cv / renal disease
fam history

144
Q

investigfations for gout

A

can be clinically diagnosed or can be aspirated

remeber need to initally exclude septic arthritis!
aspirate joint
x ray of joint

145
Q

if aspirated joint in gout what will the fluid show

A

no bacteria!
needle shaped crystals
negative birefringent of polarised light
monosodium urate cyrstals

146
Q

if did x ray of joint with gout what see

A

normally joint space is maintained
lytic lesions in bone
punched out erosiions
erosions can have sclerotic borders with overhanging edges

rem inflammation is occuring and destruction of joint so getting some bad remodelling and erosion

147
Q

management of person comes in with gout symtoms

A

acute flare=
NSAIDs= first line
colchicine = second line
steroids= third line

148
Q

se and when use of colchicine

A

iuse whe nsaids not appropriate eg. renal impairemnt r significant heart disease

se=
gastro upset
can get diarrhoea. dose dependant though

149
Q

management of gout overall

A

acute flare= nsaids first line
colchicine second line
steroids third line

was aciute attack settled they can then have prophylaxis:
start on allopurinol. if they get an acute attack again then they keep taking the prophylaxis meds but then also add the acute flare meds eg. nsaids firstly
also do lifestyle changes:
loose weight
hydrated
dec alcohol consumption
reduce purine based foods= meat and seafodd

150
Q

how does allopuriol work

A

decrease uric acid levels
xanthine oxidase inhibitor

151
Q

whats psudogout

A

crystal arthropathy
calcium pyrophosphate crystals depostied in joint

152
Q

how swollen stiff knee and shoulders

what could this be

A

pseudogout

153
Q

s and s of pseudogout

A

older adult
stiff, hot, swollen, painful joit
knee most common
can get in shpulder,s wrists and hips
chronic condition affecting multiple joints
often milder than gout and septic arthritis
can be acute
can be chronic like oa with inflam signs

154
Q

s and s of pseudogout

A

older adult
hot, swollen,stiff painful joubt
often knee
shoulders, writst and hip can be too
chronic condition and can affect multiple joints
often milder than septic arthrits and gout
can be acute
can be chronic like oa but with inflam signs too

155
Q

risk factors of pseudogout

A

dehydration
hyperparathryoidism
hypothryoidism
dialysis
surgery
long term use of steroids

156
Q

investigations for pseudogout

A

aspirate joint need exclude septic artrhtis
aspirate joint find: no bacterial growth
calcium pyrophosphate crystals
thomboid shaped crystals
postitive birefringent of polarised light
x ray = choncrocalcinosis= white line in middle of joint soace = definitive diagnsoi

similar to oa= loss
loss of joit space
osteophytes
subchondral cyst
subarticular sclerosis

157
Q

see chondrocalcinosis in x ray what this mean

A

psuedogout

158
Q

positive birefringent of polarised light and rhomboid shaped crystals and calcium pyrophospate crystals mean what in joint fluid

A

pseudogout

159
Q

management of pseudogout

A

if asymtomatic nothig
symptoms usually spontaenously resovle
nsaids
colchicine
joint aspiration
steroid injections oral steroids
arthrocentesis.

160
Q

whats behcets disease

A

complex inflam conditionrelapsing and remitting

161
Q

key feature of behcets disease

A

recurrent mouth and gential ulceres

162
Q

what gene is HLA B51 lined with

A

behcets disease

163
Q

differentials for muth ulcers

A

behcets diseaseibd-crohns simple apthous ulcers
squamous cell carcinoma
herpes simplex ulcers
coxsachie A virus inflam conditions- RA
folate deficiency

164
Q

features of behcets diseasae

A

mouth and gential ulcers]2-4 weeks heal
at least 3 recurrent epidosed in a year
red halo and painful

skin= easily inflammed
erythema nodosum
papules and pustules like acne
vasculitic type rashes

eye= refer to emergency review
anterior/psoterior uveitis
retinal vasculitis
retinal haemorrhage

msk=
morning stuffnes
arthralgia
oligoarthritis - often knee, ankle- swellig of joint but no bone destruction

gi= inflam and ulceration
ileum
caecum
ascending colon

cns= memoray impairemet
headahce and migraine
aspetic menigitis
menigioencephalitis

veins= thrombosis forms but dont embolsim as to cell wall
DVT
thrombus in pulmonary veins cerebal venous sinus thrombosis
budd chiari syndrome

lungs=
pulmoanry ayerusm if rupture fatal - haemptyisis

165
Q

investigation for behcets disease

A

clinical diagnosis
pathergy test- use sterile needle make subcut abrasion on arm. leave 24-48hrs then look. if weal 5mm or more shows non specific hypersentivity. see in behcets, sweets sydrome and pyoderma gangrenosum

166
Q

management of behcets disease

A

topical steroids for oral ulcers- soluble betamethasone tabletssystemic steroids- oral prednisolone
cochicine = as anti inflamtopical anesthestoc for gential ulcers- lidocaine ointment
immunosupressant s- azathioprine
biologics- infliximab

167
Q

whats pagets disease

A

disorder of bone turnover
excessive bone turnover due to excessive osteoclast and osteobalst activity and its not corodinated so get pathcy areas of lysis (low denstiy) and sclerosis(high denstiy)
get enlarged and misshapen bones and esp affect the axial skeleton

168
Q

s and s of pagets disease

A

older adults
bone pain
bone deformity
hearing loss if affects the bones of inner ear
fractures

169
Q

investifations and findings for pagets disease

A

x ray

see bone enlargemnt and deformity
osteoporosis circumscripta= defined less dense lesions
cotton wool apperance of skull= poorly defined pathcy areas of scleoris and lysis

v shaped defects in long bones
bichem =raised alp and normal other lft
normal ca
normal phospahte

170
Q

rasied alp normal other lft
normal ca and nmormal phospahte
what could this be

A

pagets disease

171
Q

cotton wool appereance of skull means what

A

pagets diease

172
Q

management for pagets disease

A

bisphosphonaes- work well
vitd and ca= esp if on bisphosphonatesnsaids for bone pain
surgery if fractures
monitor ALP - should normalsiefollow up to do xray to ehcl osteosarcoma not there

173
Q

person has pagets disease put now got pins and needles in left arm

A

spiano stenosis

174
Q

what two main complications of pagets disease

A

osteosarcoma= increase risk with pagets disease = have increased focal bone pain, bone swelling, pathological fractures = plain xray to see

spinal stenosis- if get neuro s and s treat with bisphosphonates or surgery = do mri to see

175
Q

whats osteomalacia

A

soft bones
defective bone mineralsiation
in adults after growth plates fused
rickets is it in children before growth plates fused

176
Q

cause of osteomalacia

A

vit d deficinecy

due to low sun exposure and no vit d supplementation

malabsorbtion disorders=eg. ibd

kidney issues eg. ckd= not activating vitamin d

get low vit d and so low ca and phospahte cus needed for absotbtion of them in kindey and intestines. vit d helps refulate bone turnover and promotes bone reasborbtion to boost serum ca.

low calcium then means have secondary hyperparathroidssm to try increase serum ca so then have eevn more bone reabsobrtion and sp have more problesm wtih bone mineralisation

177
Q

s and s of osteomalacia

A

may not have any
weak bones
painful bones
muscle weakness
pathological fracturs
fatigue
in children get bowing of legs, can get knock knees though hypocalcaemic seizures if severe

178
Q

investigtions for osteomalacia

A

renal fucntion, lfts, pth level

low ca
low phosphate
high ALP
anameia if malabsorbtion issue

main diangostic is:
serum 25 hydroxyvitamin d
= less than 25nmmol/l is vit d deficincey
25-50 is vit d insufficency 75 is opitmal if 50-75 then healthyx ray= osteopenia= more radiolucent bone
dexa scan show low bone mineral densitiy

179
Q

treatment for osteomalacia

A

colecaliferol = vit d

50,000 IU once weekly for 6 weeks
or
20,000 IU once weekly for 7 weeks
or
4000 IU daily for 10 weeks

then have maintence dose for restof life of 800IU daily
if only vit d insufficency go stragiht for the manitenece dose

180
Q

risk factors for osteomalacia

A

low vit d in diet low exposure to sun

ddarker skin

live in colder climate
spend most time indoors

malabsirbtion disorders
infant purely breastfed esp after 6 motnhs old
begetarian/vegan
alcholism

181
Q

risk facotrs for osteoporois

A

female
older age
bmi under 18.5
decrease mobility and activity
ra
alcholol and smoking
long term corticosteorids
ssri, ppi, amntiepileptics, antioestrogens
psot menopausal women not on hrt = oestrogen is priotective but now have lower elvesl

182
Q

whats osteopotoiss

A

reduction in bone desntjty so less strong bone and more prone to fracures

183
Q

invetigations for osteoproros

A

first do FRAX acore - do on women over 65, men over 75 and people with risk facotrs - such as endocrine disorders and hist of falls= risk of fragility fractire in next 10 years

then do dexa scan if frax score says to

frax score may say kow risk if so reasure , intermediate risk then dexa scan and reasses, high risk start treatment

dexa scan = says either reasure and lifestyle adivce or reat

dexa scan = want t score at hip
if t score at hip less than -2.5 SD tjen osteoporosis -1 to -2.5 is osteopenia

184
Q

treatment for osteopotooss

A

first line bisphosphonates if dexa t at hip is less than -2.5 SD

vit d and ca if not got adequate ca intake = calcichew d3

vit d if got adequate ca levles but lack sun exposure
lifestle advice= acivity and exercise

stop smokinglow lcholl
maitian health ywegiht adeeuquate ca intale and vit d intake and avoid falls

other meds if cant have bisphosophnates =
denosumimab = stops osteoclast acivity strantium ranelate = increase osteoblast dec osteoclast
raloxifiene= seoncdary prevetion = selective oestrogen receptorhrt if ealry menopause

185
Q

se of bisphonates and the names of some

A

first line
decrease osteoclast acitivty
orally once a week= alendronate or riserdronate or iv yearly zolendronic acid se= relfiux and oesphageal erosisions so take sat upright before food and dont move for 30mins se= osteonecorisis of jaw
osteonecrisis of extrnal auditory cancal
atypical fractres

186
Q

whats the follow u time for tratment for osteoporiss

A

lifestyle adive then folow up in 5 years]on bisphosphaoates then frax and dexa scan in 3-5years
if goo then can have 18month-3 years break then reasses

187
Q

se of strantium ranelate

A

increase risk of dvt, pe and mi

188
Q

Crepitus with pain early sign of

A

OA

189
Q

osteogeneisis imperfecta bloods

A

normal Ca, PTH, PO4, ALP

Medicine (11 decks)

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