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Rheumatology Phase 2 > Rheumatology Lectures > Flashcards

Rheumatology Lectures Flashcards

1
Q

What joints are more effected in OA?

A

DIPJ, and CMCJ (i.e. base of thumb)

Also: spine, hips, knees

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2
Q

What joints are more effected in RA and how many?

A

MCPJ, PIPJ
Also: wrists, shoulder, elbow, knees, ankles toes
spine unaffected except the cervical vertebrae.

may not present with it at first, but eventually is polyarticular (5+ joints involved)

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3
Q

What is Rheumatology and what conditions do they look after?

A

medical management of MSK disease, esp joint and connective tissue disease.

inflammatory diseases of joints: crystal, infection, autoimmune (RA, Alkalosing Spondylitis, )

Non inflammatory disease: degenerative (OA), non degenerative (fibromyalgia)

(also vasculitis)

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4
Q

what differences will you seen between inflammatory vs degenerative history?

A 
Morning Stiffness
inflammatory:  > 1 hour, degen < 30mins
Pain
inflammatory: eases w/use, degen: worse w/use 
Inflammation 
inflammatory: red, hot, swollen, degen: not really, may be bony swelling if nodal OA (heberden's)
Response to NSAIDS
inflammatory: yes, degen: not as much 
Symmetricity:
inflam RA= sym, degen OA= less sym 
Epidemiology
inflammatory: the younger, psoriatic, family hist, 
degen: the older, previous sport played
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5
Q

If there is pain at rest AND at night this is more suggestive of?

A

tumour
infection
fracture

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6
Q

if the pain is neuralgic what might you expect to see and what does this suggest?

A

pain and paraesthesia (tickling sensation) in the dermatomal distribution
nerve compression

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7
Q

If there is pain in a part of the body which is not effected by local movement- this is suggestive of?

A

the pain is referred pain

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8
Q

what 4 key signs are suggestive or OA on an XR?

A 
LOSS
loss of joint space 
osteophyte formation 
sclerosis (subarticular)
subchondral cysts
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9
Q

What are Heberden’s and Bouchard’s nodes and where would you find them?

A

bony swellings occurring in OA
heberden’s= at DIPJ
bouchard’s = at PIPJ (less commonly affected in OA though)

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10
Q

A patient presents with a history similar to RA but its not RA. What might this be and what might you see on XR,

A

Psoriatic arthritis
10-40% of those with psoriasis are effected.
Arthritis may present before psoriasis though.
XR would see erosion (like in RA) but may be ‘pencil - in - cup’ type erosion.

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11
Q

What is ESR and why does it rise in infection or inflammation?

A

erythrocyte sedimentation rate
RATE the RBC settle to the bottom of test tube after centrifuge

infection and inflammation means there is increased fibrinogen produced, which sticks RBC together
so RBC are heavier, and fall to bottom of tube quicker
so fall faster- rate of settle is higher so raised ESR

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12
Q

What is CRP and why does it increase in inflammation or infection?

A

C- reactive protein

Macrophages (activated from the inflammation/infection) release IL-6 (pro-inflammatory cytokine).
IL-6 causes Liver to release CRP.
CRP binds to damaged cells and activates complement to produce more phagocytosis.

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13
Q

Why is CRP not massively important though in diagnosis?

A

IL-6 is also produced by adipocytes, therefore through the same mechanism obese people have raised CRP, in the absence of disease.

also rises and falls quickly- therefore if measure too late may be back to normal. Peaks at 48 hours.

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14
Q

What are autoantibodies and which ones are often positive in RA patients?

A

autoantibodies are immunoglobulins produced by the patients own immune system which binds to their own body’s cells causing inflammation/damage

ACCP- Anti-cyclic citrullinated peptide
RF- Rheumatoid Factor
both often positive in RA patients (seropositive)

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15
Q

What is SLE?

A

a multi system, auto immune disease where the body produces autoantibodies like anti nuclear antibody (ANA) which bind to ones own cells and causes tissue damage through a number of mechanisms. Effects almost any organ in the body, brain, heart, lungs, skin, joints, kidneys. Chronic disease which remits and relapses.

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16
Q

What are the signs/symptoms of SLE?

A

Raynaud’s, mouth ulcers, rash (esp butterfly rash on face), lupus nephritis, painful, swollen joints, fatigue, hair loss, fever, weight loss, lymphadenopathy

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17
Q

what antibodies are found in SLE? and what other conditions might it be associated with?

A

ANA (anti nuclear antibody) +
anti dsDNA +
rheumatoid factor +

associated with sjorgen’s and autoimmune thyroid disease

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18
Q

How to treat (maintain) SLE?

A

NSAIDs, hydroxychloroquine, methotrexate

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19
Q

What is the epidemiology of SLE?

A

9x more common in women than men.
more common in african/carribean/asian populations.
can be triggered by EBV

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20
Q

What is spondyloarthritis/spondyloarthropathy (SpA)?

A

Group of overlapping conditions which are all associated with the HLA B27 tissue type. These include: ankylosing spondylitis, psoriatic arthritis, reactive arthritis, enteric arthropathy. Each come with their own more specific set of symptoms but they have some main ones in common.

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21
Q

List the features of SpA that all the 4 different types may have in common:

A

SPINEACHES
Sausage Digit (Dactylitis- due to oedema and tenosynovitis, whole finger red and swollen)
Psoriasis (esp in psoriatic)
Inflammatory back pain (esp in ankylosing Sp)
NSAID good response
Enthesitis (inflammation at site of insertion tendon/ligament)
Axial Arthritis
Chron’s/Colitis (esp in enteric)
HLA B27
Extra- Articular manifestations/Eye (uveitis, rashs, ulcers)
Seronegativity (RF -ve)

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22
Q

Apart from overlapping features, what’s the main feature of ankylosing spondylitis and what can it lead to?

A

arthritis of vertebrae! (spondylo=vertebra)
and sacroilliac joints (radiates to buttocks- alternating buttock pain!)
have inflammatory back pain

inflammation around bone-> damage->new bone formation-> fusion
when it becomes fused, can cause patient to not be able to stand straight/look up properly

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23
Q

Name one of the three theories which explains the pathogenesis of SpA?

A

Molecular mimicry- (previous infection with antigen close to HLA B27, forms antibodies against infection but also HLA B27)
Misfolding theory (HLA B27 proteins unfold, accumulates in ER, pro-inflammatory cytokines released (IL 17) and causes inflammation)
Heavy Chain Homodimer Hypothesis (similar to above but is the heavy chains on HLA B27 which dimerise and accumulate)

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24
Q

what does inflammatory back pain look like?

A

age < 40
insidious onset
pain goes away with exercise- not with rest
worse as night time

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25
Q

What normally triggers reactive arthritis?

A

a few weeks after:
GI infection - campylobacter, shigella, salmonella
GU infection - chlamydia, ureaplasma

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26
Q

Reiter’s Triad (of reactive arthritis) includes what signs?

A

Arthritis
Urethritis
Conjuctivititis

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27
Q

What differential diagnosis should you include in a hot swollen joint and what should you do to exclude?

A

septic arthritis !!!!!!!!
gout

aspirate the joint!!!

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28
Q

What is JIA?

A

Junvenile Idiopathic Arthritis
Occurs when child under 16 has swollen/stiff/painful/limited joints for >6 weeks when all other causes (infection, trauma, reactive, malignancy, connective tissue disease has been ruled out.

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29
Q

In those who have been diagnosed with JIA, what should you always do?

A

Screen for uveitis - as can lead to blindness if untreated!

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30
Q

Treatment for JIA

A

non-medical: inform, educate, lease with school, physio, occupational health and psychology

Medical: NSAIDs, topical steroids, steroid injections, methotrexate, biologic drugs (i.e. anti TNF)

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31
Q

what is transitional medicine?

A

active process which attends to the medical, psychological and educational needs of adolescents as they move from paediatric to adult centred care
(bridging the gap between paediatric medicine (0-16) and adult medicine 16+

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32
Q

what happens in the adolescent brain which has an effect on their behaviour?

A

prefrontal and frontal cortex rapid development
by synaptic pruning
when we learn how we evaluate and respond to risk , and make decisions

during this time therefore they take experimental/risky behaviour

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33
Q

adolescents under taking experimental and risky behaviour is natural due to brain development during this time. but what implication does this have on transitional medicine?

A
  • chronically ill patients are more likely to try/take up these risky behavoiurs
  • associated with non-adherence to medical therapy
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34
Q

When talking to a young person, what must you always ask about?

A

HEADSS

home, education, activity, drugs/alcohol, sexual health, spirituality/suicide/sleep etc

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35
Q

What is the difference between nociceptive and neuropathic/central pain?

A

noiciceptive- associated with actual damage/inflammation of peripheral nerves/tissues
vs
neuropathic- previous damage to the nerves or malfunction in the pain processing systems (central) which causes more chronic pain that doesn’t respond to medication as well.

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36
Q

give some examples or nociceptive and some examples of neuropathic pain

A

nociceptive: cut, burns, fractures, cancer pain, RA,
neuropathic: fibromyalgia, IBS, migrane headache

or can have mixed!- i.e. like OA as some with normal x ray have lots of pain, then some with severe x-ray changing OA have no pain.

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37
Q

what is Pain Management Programme?

A

PMP- started by assessment with clinical nurse specialist, identifying the physical and psychological problems in life.
if they are deemed capable of completing the programme, enrolled where they might get:

individual psychology sessions
TENS machine trial
coping strategies (stretching, mindfulness etc)
sleep management

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38
Q

substances which increase the amount of pain felt:

A

substance P, glutamate, serotonin- 2a,3a, neurotensin, nerve growth factor

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39
Q

substance decreasing the amount of pain felt

A

noradrenaline, serotonin 1a,b, opioids, GABA, cannabanoids, adenosine

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40
Q

what causes difference in pain sensitivities within humans?

A

polymorphism in COMT gene

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41
Q

what is fibromyalgia?

A

a chronic syndrome (>3 months)
where pain is felt widespread (both sides of body, above and below waist)
when all other diseases have been excluded (no inflammation)
11+ out of 18 hyperalgesic locations will be painful on digital palpation.
Closely correlated with chronic fatigue syndrome

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42
Q

what other conditions are often associated with fibromyalgia?

A

Depression
IBS
chronic headaches
chronic fatigue syndrome

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43
Q

risk factors for fibromyalgia?

A

female, middle age, divorced, low income house hold, low educational status

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44
Q

Features of FM?

A

Pain:
widespread pain felt- often at tender points -
often aggravated by cold, stress, activity
morning stiffness

Fatigue:
due to non-restorative sleep
sleep disturbance- waking in night, waking unrefreshed 
(often severe)
low mood/irritable/weepy
poor concentration
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45
Q

differential diagnosis of FM- what will the investigations show if FM?

A 
hypothyroidism
SLE
PMR (polymyalgia rheumatica)
inflammatory myopathy 
inflammatory arthritis (ie RA)
myeloma- high calcium(CRAB)

in FM investigations will be all normal

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46
Q

To rule out the ddx for FM what tests would you do?

A 
U+E - calcium (myeloma)
FBC- anaemia (myeloma+ others) 
Creatinine- kidney function (myeloma) 
Autoantibodies: ANA, dsDNA, (SLE) 
ESR/CRP (infection/inflammation)

Avoid unnecessary investigations- as this encourages illness behaviour

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47
Q

How do you manage FM?

A

EDUCATE- patient and family

SLEEP
non- REM sleep V important for normal muscle function
Improve by:
increase exercise, remove stressors, low dose amitriptyline

EXERCISE
Graded aerobic exercise programme

Behavioural therapy- ie CBT can help with coping strategies

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48
Q

What is hypermobility?

A

‘ability to move joints beyond their expected range’

normal in children, decreases with age, often asymptomatic, but can cause widespread pain
may get recurrent sprain/dislocations

BUT could be a marker of serious genetic condition Marfan’s/ Ehlers Danlos

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49
Q

What is Marfan’s, and what is the most concerning complication?

A

autosomal dominant condition (75% inherited, 25% new mutation)
connective tissue disease caused by abnormal fibrilin so there is poor elasticity

aortic dissection

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50
Q

What is Ehler’s Danlos, + worst complication?

A

autosomal (most dominant, few recessive) connective tissue disease due to faulty collagen. Leaves tissue MORE elastic. (stretchy skin)

worries about aortic dissection

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51
Q

what is hypermobiltity diagnosed by?

A

brighton criteria

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52
Q

In what situations might an X-ray be normal in the initial disease process?

A
  • Fracture may take longer to show up (scaphoid- 10 days)
  • Fracture might not be seen on X-ray (neck of femur 5% can’t be seen)
  • Bone destruction only apparent when 60% + of bone density has been lost - won’t detect early lytic tumours
  • Early arthritis may be normal, changes only seen later
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53
Q

Benefits of X-ray.

A

cheaper
more readily available
less radiation

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54
Q

What should you always request when ordering an x-ray and why?

A

2 views!
might only be able to see fracture in a certain view

dislocation/fracture needs assessment in 2 planes

foreign bodies more easily located

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55
Q

why are x-rays not as good sometimes?

A

in early arthritis, cannot detect early changes - MRI, bone scan, ultrasound can

lytic tumours will not be detected until 60% density is lost

does not show extension of tumour beyond cortex or accurate size

bad for assessing soft tissue

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56
Q

What is CT?

A

computerised tomography

tube of X-rays, images continuous slices in a number of planes.

can be manipulated into 3D imaging of bone- good for bone detail!

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57
Q

When might a CT be contraindicated?

A

pregnant women- foetus/children v sensitive to these X-rays,

only do if life threatening

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58
Q

What are the disadvantages of CT?

A

High dose of radiation (esp head/spine) - but weigh up between this and risk of missing pathology

Not great at soft tissue imaging- MRI much better

not as readily available/cheap as x -ray

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59
Q

What are CTs used for?

A

assess acute injuries where an X-ray is inadequate (esp spinal)

gives great bone detail:
so more info about fracture assessment/healing

look for lose bone fragments in joint

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60
Q

what is ultrasound?

A

high frequency sound waves pass through soft tissue and are reflected at interfaces - refections are measured by probe

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61
Q

Why are ultrasounds very safe?

A

no radiation, no powerful magnetic field, sound waves not harmful.

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62
Q

What are ultrasounds good for?

A

soft tissue, tendon, ligament injuries

assess joints, effusions, synovial abnormalities

can guide biopsy/fluid drainage

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63
Q

What is not great about ultrasounds?

A

limited to superficial tissue,
no deep joint structures
artefacts (anisotropy) common

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64
Q

what is MRI?

A

magnetic resonance imagine
patient subjected to v v powerful magnetic field

different tissues releases energy at different rates

early released in 2 stages:
T1 (spinning proton in lattice) and
T2 (adjacent spinning protons) relaxations

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65
Q

what pathology can you seen on MRI?

A

soft tissue damage around bones and joints (esp in early disease when X-ray comes back normal - i.e. in OA)

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66
Q

what is bad about MRI?

A 
long scan time (25 mins) - time consuming
narrow container- px claustrophobic 
can get artefacts
expensive 
number of contraindications
fine anatomical detail not as good
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67
Q

What is good about MRI?

A

no harm on tissues from magnetic field

good for soft tissue + bone pathology

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68
Q

What contraindications are there to MRI?

A

those with:
electronic implants (ie pacemaker)
metallic heart valve s
neurosurgical clip

CANT have anything around metal as may be a lethal projectile

avoid in pregnancy as unsure of effects

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69
Q

explain what a bone scan is

A

nuclear medicine- radioactive tracer attached to biologically active substance is injected IV and is taken up by tissues during that chemical.

gamme rays produced are picked up by gamma camera

can pick up abnormal bone with increased bone growth

triphasic (blood flow, blood pooling, osteoblastic)

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70
Q

What is good about a nuclear bone scan?

A

gamma rays- so high energy pass through tissue without damage (non-ionising)

gets PHYSIOLOGICAL info about bone and joint

good to detect mets

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71
Q

what is not as good about a bone scan?

A

non speciifc- can’t tell difference between infection and inflammation

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72
Q

What is vertebroplasty and when would you do it?

A

injected cement into vertebral body

relieves pain from vertebral compression fractures (i.e. in OA, mets, trauma

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73
Q

What is vasculitis?

A

inflammation of the blood vessel walls, causing destruction (aneurysm, rupture) or stenosis (impairment of blood flow)

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74
Q

why is the presentation of vasculitis so varied? what are the generic/systemic symptoms?

A

Depending on which blood vessels are inflamed will effect different organs. Therefore symptoms will be based on which organs are effected. (can effect all system- brain, eye, heart, lungs, kidney, skin)

systemic: very very fatigued, raised ESR/CRP
(malaise, fever, weight loss, arthralgia, myalgia)

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75
Q

What are the causes of vasculitis?

A

Primary:
Giant cell arteritis (large)
ANCA associated: Wegener’s Granulomatosis AKA Granulomatosis with Polyangitis- GPA

Secondary: 
to infection (ie HIV, hep B, C) 
to malignancy 
to RA 
to SLE
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76
Q

what is giant cell arteritis?

A

also called cranial/temporal arteritis

inflammation of the extra cranial branches of the carotid arteries- esp the temporal and ophthalmic arteries

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77
Q

symptoms/signs of giant cell arthritis include:

A

headache (may be one sided)

tenderness around temporal artery (i.e. esp when brushing hair)

palpable temporal artery with decreased pulse

jaw claudication (pain in jaw after chewing)

acute vision loss- may present to ophthalmology, typically monocular, without pain, can be transient

unequal/weak pulses

78
Q

If you suspect GCA, what do you do?

A

start steroids immediately (prednisolone) -to prevent irreversible vision loss

diagnosis gold standard: temporal artery biopsy (within 7 days of treatment started)

use falling ESR/CRP to guide treatment

79
Q

What is ANCA and is it positive in giant cell arteritis?

A

ANCA- anti neutrophil cytoplasmic antibody (autoantibody)

it is negative in GCA.

80
Q

What is the management post initial treatment of GCA?

A

steroid for 2 years, gradually decreasing amount (due to morbidity from long term steroid use)

Give PPI and osteoporosis prophylaxis due to steroids

81
Q

what is wagener’s granulomatosis?

A

AKA gramulomatosis with polyangitis _ GPA
granulomatous inflammation and necrosis of the small and medium vessels (arterioles, capillaries, venules)

can lead to multi organ damage

but has a predilection for resp tract and kidneys

82
Q

What are the signs and symptoms in wagerer’s granulomatosis?

A

resp: sinusitis, epistaxis, cartilage damage- saddle nose deformity, breathing problems, white rings (cavity) on CXR
kidney: proteinuria, hematuria

Also can effect skin so: rashes, ulcers

(also other systems can get affected and have symptoms but these are the most likely)

83
Q

treatment of GPA?

A

if getting severe organ damage: high dose steroids, supportive care in ITU

if non organ threatening: moderate dose steroids, and methotrexate

follow ANCA - if disappears, indication treatment is working

may require treatment for many years

84
Q

What is RA?

A

chronic, autoimmune, inflammatory disease characterised by symmetrical, deforming, peripheral polyarthritis.

85
Q

in general what joints does RA effect?

A

synovial

86
Q

explain what happens to the joints in the onset of RA?

A
  1. inflammation and proliferation (formation of pannus)

a ‘stress’ (unknown) occurs and immune cells i.e. neutrophils etc come into the joint space and attack the synovial membrane

here they release pro inflammatory cytokines

this causes angiogenesis (blood vessels form)
and synovium proliferate and therefore thicken

as it thickens it will cover the cartilage and articular surfaces, - this is pannus

87
Q

how does pannus cause the signs and symptoms of RA?

A

secretes more synovial fluid- which contributes to the swelling and pain

pannus released matrix metalloproteinases which degrade the cartilage

and bone destruction also occurs (osteoclasts?)

which over time is painful and can lead to loss of joint mobility and even permanent deformity

88
Q

what antibodies are involved in RA?

A

rheumatoid factor and ACCP (anti cyclic cittrulinated peptide)

89
Q

apart from the joint what other parts of the body can be affected by RA and how?

A

eyes- dry, painful, red (episcleritis)

neurological- entrapments- ie carpal tunnel, elbow(ulnar), tarsal tunnel, spinal cord compression

heart- pericarditis, pericardial effusions

blood- anaemia (normocytic of chronic disease), enlarged spleen, palpable lymph nodes

lungs- caplans syndrome (with coal duct exposure), rheumatoid nodules, pleural effusions

kidneys-amyloid deposits in the kidney (advanced)

90
Q

a patient comes in with swollen joints and you investigate for RA- what results might you get?

A

raised ESR and CRP
sero positive- RF and ACCP
maybe anaemia

91
Q

what is rheumatoid factor

A

autoantibody which may be positive in RA patients.

antibody against the Fc portion of IgG (antibody against and antibody)

92
Q

risk factors for OA?

A

Age

Female (esp after menopause)

genetic- more common in
Caucasian, low in black

Obese (weight baring)

Job- manual labour/using small joints a lot, farming, football
Local Trauma to the joint (i.e. remember dad will get OA in knee!)

93
Q

pathogenesis of OA

A

predominantly thought to be wear and tear disease
but there is some inflammation due to pro inflammatory cytokines being released

combination of both leads to a loss of cartilage (due to lack of homeostasis between synthesis and degradation of the ECM) and disordered remodelling of bone

94
Q

what is the crystal responsible in gout?

and when do they form?

A

monosodium urate crystals (negatively birefringent needles)

sudden change in concentration (i.e. after taking in lots of purines, or the kidneys can’t excrete, or given too much allopurinol at a time)

  • when the concentration of uric acid rises above a certain level (400)

or when the precipitation point is lowered by COLD temp (i.e. sticking your foot out under the duvet at night)

95
Q

how is uric acid made and excreted by the body?

A

made: from purine breakdown
excreted: by the kidneys (most is reabsorbed after filtration then secreted back into the urine)

96
Q

what steps in purine breakdown form uric acid?

and what enzyme does this?

A

purine -> hypoxanthine -> xanthine -> uric acid

xanthine oxidase

97
Q

under what circumstances would there be an increased in uric acid in the blood? (and therefore possibly gout)

A 
when there is too much purine in the body (so more uric acid is produced) 
ie from: 
increase in diet, 
increase cell turnover (psoriasis) 
increased cell death (chemo)
inborn error of metabolism

when there is not enough excretion of uric acid (kidneys)
- this is more likely
(high insulin levels, genetics in transporters)

98
Q

how many people with hyperuricaemia will get gout?

A

1 in 5 hyperurcaemics get gout

99
Q

what diseases does gout increase you risk of?

A

CVS disease (hypertension stroke, MI)
diabetes
renal disease
OA damage to joint

100
Q

typical presentation of gout?

A

hot, swollen, red, joint
(often one which has been injured before)
most commonly big toe!
v painful

101
Q

what dietary advise might you give to someone with gout/high uric acid

A

lower purine intake

decrease: 
red meat 
seafood
alcohol (esp beer, wine is the least bad) 
fructose (esp smoothies) 
high sugar foods/drinks

increase: diary- protective for gout

102
Q

why does a low carb diet help in gout prevention?

A

less carbs - less hyperglycaemic episodes
less insulin produced
(high insulin levels prevent the excretion of uric acid from the kidneys)
so less insulin= more excreted

103
Q

why might you be genetically predisposed to getting gout?

A

polymorphism in the uric acid transporters in the kidney tubules

104
Q

what pharmacological treatment is firstly line to treat ACUTE gout episodes?

A

Colchicine (anti inflammatory for gout specifically, but get diarrhoea)

105
Q

if you can’t give them Colchicine what else might you use to treat gout?

A

NSAIDs

steroid injection into the joint

106
Q

what else might help reduce the pain/inflammation in an acute gout attack?

A

ice pack to joint

vit C and cherries

107
Q

What pharmacological treatment can be given to someone at high risk of gout?/ prevent gout reoccuring?

A

allopurinol

```
stop diuretics
or change to diuretic- losartan which gets rid of uric acid
~~~

108
Q

What is the aim with allopurinol and how do you achieve it?

A

100mg a day start
aim to get levels to:
BELOW 300
keep increasing dose of allopurinol so long as they can tolerate it to achieve this
be careful to precipitate acute gout attacks though by sudden reduction in conc of uric acid

109
Q

what are the side effects of allopurinol?

A

rashes, headache, myalgia

rare, hypersensitivity

110
Q

what is an alternative drug to allopurinol?

A

febuxostat

111
Q

if there is severe and recurrent gout: what two medications can be used instead?

A

rasburicase
pegloticase

these are uricases
can be given IV in pre chemo treatment

112
Q

why do you not want to get the uric acid level lower than 200?

A

low uric acid levels associated with Alzheimer’s disease

gout= protective of alzheimer’s?

113
Q

what is a tophi and why do you want to get rid of it?

A

painless deposits of monosodium urate crystals (gout) under the surface of the skin/joints/catilage

get rid because they release proteolytic enzymes which cause erosion and can cause long term pain/damage after it’s gone

114
Q

How is pseudo-gout different from normal gout?

A

looks and feels like gout, but is caused by a different crystal:

calcium pyrophosphate- positively birefringent

115
Q

how can you prevent pseudo-gout?

A

no long term medication like allopurinol

look for underlying causes- i.e. in calcium metabolism (thyroid, parathyroid disease etc)

116
Q

When someone presents with a hot swollen joint, what will be in the differential and how do you rule it out?

A

septic joint!!! must rule out

ASPIRATE (and test before abx)

117
Q

What drugs are used in RA which aren’t disease modifying?

A

NSAIDs- anti inflammatory by inhibiting COX enzyme
(aim to inhibit COX2 but often non selective and will act on COX1 also- might get peptic ulcer so give with PPI if long term)
ie ibuprofen,
diplofenac and naproxen(older, less selective)

Corticosteroids- also anti- inflammatory, reduce the action and number of white blood cells
can be injected into joint

118
Q

What disease modifying drugs can be used in RA?

A

METHOTREXATE- gold standard! (give folate supplements with it)
Sulphasalazine,
Leflunomide
‘gold injections’
Azothiaprine- must test the patient first to see they don’t have an enzyme which can convert it into a substance which causes bone marrow toxicity
Biologics

119
Q

Which cytokines are important in RA and therefore which biologics are also used as DMARDs?

A

TNFa - which then produces IL 1, IL6
these are all pro inflammatory cytokines

Anti-TNF drugs
Monoclonals: infliximab, adalimumab
Decoy Receptors : etanercept

IL6 monoclonals: tociluzimab

Also B cell knock outs- Rituximab, binds to CD20 only found on B cells, preventing their proliferation so less antibodies.

T cell knock outs- Abatacept
normally requires 2 signals to activate T cells- CD28 receptor and MHC on APC.
This prevents the CD28 receptor being bound to, so they are not activated

120
Q

Problems with biologic drugs?

A

EXPENSIVE

over time might see the production of antibodies against the drugs, so reduced efficacy

increased risk of bacterial, viral and fungal infection

121
Q

problems with DMARDs like methotrexate? so what should you do when they are on them?

A 
all carry risk of toxicity 
all work on immune system- can cause bone marrow suppression 
can upset the liver 
can cause nausea/diarrhoea
can cause hair loss 
all teratogenic to the foetus

monitor them- regular blood tests, every 3 months, (more at the beginning)
FBC, UE, LFTs

122
Q

what parts of the hand are supplied by the median nerve?

sensory and motor

A

sensory- palmar side,
thumb to middle of ring finger

motor- LLOAF B 
2 lateral lumbricals 
OAF B= thenar eminence
opposens pollicis, 
abductor pollicis brevis,  
flexor pollicis brevis
123
Q

what is carpal tunnel syndrome

A

where the median nerve gets compressed/entraped as it travels through the carpal tunnel (made by the flexor retinaculum (transverse carpal ligament) and the wrist bones)

124
Q

what symptoms might you get from carpal tunnel syndrome?

A

numbness, tingling, pain in the median nerve distribution (thumb to half of ring finger)

wasting or weakness of the thenar eminence muscles (OAF)

125
Q

what treatments can be used to carpal tunnel syndrome?

A

Keep it in a fixed position - wrist brace
NSAIDs (reduce inflammation)
Corticosteroid injection (reduce inflammation)
Surgical- cut the transverse carpal ligament, opens and relieves the pressure

126
Q

what risk factors increase chances of carpel tunnel syndrome?

A

repetitive stress injury- typing
or meat cutters- abattoir, painters/decorators

obesity
RA
pregnancy
diabetes

127
Q

what tests can you go to check for carpal tunnel syndrome?

A

tinel’s test - tapping on the transverse carpal ligament- will reproduce the symptoms
phalen’s test- flex wrist for 1-2 mins, will feel the tingling

128
Q

what can you get from continuously using chain saw or drills etc?

A

vibration white finger/ raynauds phenomenon with industrial origin

129
Q

what is lateral epicondylitis and what is it also known as?

A

aka tennis elbow

inflammation and swelling of the tendons of the wrist extensors due to repetitive wrist extension (RSI)

130
Q

what test would you do if you suspected lateral epicondylitis and how would you treat it?

A

cozen’s test- hold the wrist in extended position, try to push down against it- this should cause pain in the outside of elbow

treated with rest and NSAIDs
or steroid injection
surgery (but v rare)

131
Q

in an acute trauma situation, what are the first things you should address and how?

A

Airway- chin lift, suction

Breathing - and ventilation, look, listen, feel, resp rate, sats

Circulation- BP and IV access. transfuse if hypotensive and tachycardic - with universal O negative or massive transfusion packs 1:1:1 RBC:platelets:plasma

Disabilities- GCS scale, neuro injury

Extremities- legs and arm injury etc

132
Q

what is the ‘lethal triad’ which damage control orthopaedics aims to prevent?

A

acidosis (from hypoperfusion)
coagulopathy (from loss of blood)
hypothermia (from exposure)

133
Q

what does damage control orthopaedics refer to?

A

limiting initial early surgery, in order to stabilise MSK injuries and stop bleeding, to allow the patients physiology to recover before operating on them.

This prevents a second hit of trauma from the surgery itself

134
Q

what is the difference between an adult and a child bone?

A

both have diaphysis (shaft) and metaphysis (periarticular part)

but children have the epiphysis (growth plate) separating the two- so remodelling can occur and will grow back to normal location, whilst adult bone will heal where its set

child: periosteum is thicker, which contains the blood supply, so more blood = faster healing
child: more collagen = more bendy and more likely to fracture

135
Q

what must you do in X rays of fractures?

A

always get 2 views

always take one before AND after manipulation of the bone

136
Q

what are the key steps in fracture management? (RIR)

A

reduce- process of restoring bone ends/fracture fragments to their correct anatomical position

immobilise- essential to allow healing in the correct position (once its reduced). can be done by internal or external fixation

rehabilitate- regaining strength and normal function to the area

137
Q

what are the ways of immobilising a fracture?

A

non operatively:
split,
cast,
traction (only in children, will recover quickly and spend a lot of time in bed anyway)

operatively:
internal fixation: intermedullary nails, K wires, plate and screw

external fixation: ex-fix (cage)
Taylor spatial frame (open fractures

138
Q

what must you be very careful of in operating on children bones?

A

beware of the growth plate
damage may lead to growth arrest
cause stunting or angular/length deformities

139
Q

what is a greenstick fracture?

A

fracture seen in children but not in adults
the bone is softer therefore bends and breaks (only through half the bone)

unicortical fracture- the periosteum is so thick, only breaks on one side and remains hinged on the other side

140
Q

what do the Salter Harris Fractures refer to?

A

fractures involving the epiphyseal growth plate
there are I-V
guides prognosis and management
the higher the number the worse the prognosis

141
Q

describe the 5 Salter Harris fractures?

A

I- S- straight across
II- A- above the growth plate and away (through and up)
III- L- lower than the growth plate (through and down)
IV- TE- through everything
V- R- rammed (crush injury to the growth plate)

142
Q

what is an NAI and when would you suspect?

A

non-accidental injury
suspect if:
multiple fractures at different healing stages
multiple bruises
posterior rib fractures
long bone fractures in a non-ambulant (non walking) child
spiral fractures (in humerus/femur from twisting)

143
Q

what to do if you suspect a NAI?

A 
standard x ray 
skeletal survey to find other healing ones 
always admit the child 
refer to safe guarding services 
treat as normal
144
Q

what is osteoporosis

A

a metabolic bone disease characterised by low bone mass and mineral density with micro architectural deterioration of bone tissue

145
Q

what does your bone mass do throughout aging?

A

increases throughout puberty
peaks at 25 yo
decreases gradually throughout life
when get to menopause (in women) massive drop in bone mass

146
Q

what is the pathophysiology in osteoporosis after menopause?

A

drop in oestrogen means lose the normal balance of bone resorption and bone formation.
osteoclasts continue to resorb bone, and osteoblasts lay down new bone but not at the same rate.
so for each turnover you lose some bone.
trabeculi decrease in thickness and eventually perforate
RANKL overrides the protection of OPG

147
Q

what are the risk factors for osteoporosis?

A

SHATTERED
Steroids
Hyper-thyroidism, parathyroidism, calciuria
Alcohol and tobacco use
Thin (low BMI)
Testosterone decrease
Early menopause
Renal or liver failure
Erosive inflammatory bone disease (RA or myeloma)
Dietary (calcium low, or malabsorption of calcium due to low vitamin D, diabetes mellitus

148
Q

what is the test for finding osteoporosis? and what will it tell you

A

DEXA- bone densitometry on hip and lumbar spine
tells you the bone mineral density in (g/cm2)

T score- how many standard deviations the BMD is from the mean BMD of young adult.
Z score- how many standard deviations the BMD is from the mean BMD of average adult of the same age

(NB: so if you scanned someone very old, may have a very poor T score, but the Z score might be ok)

149
Q

What T scores suggest pathology?

A

of T score
above -1 = normal
-1 to -2.5 = osteopenia
less than -2.5 = osteoporosis

150
Q

what lifestyle advice would you give to someone with osteopenia or osteoporosis?

A

quit smoking,
reduce alcohol consumption
increase weight bearing exercise
calcium and vitamin D rich diet- or through supplements

reduce risk of falls to prevent fracture:
balance exercises (Tai Chi)
home adaptations

151
Q

what is your first line treatment for osteoporosis?

A

bisphosphonates (like alendronic acid)

calcium and vitamin D supplements

152
Q

what other anti-resorptive drugs other than bisphosphonates may be used in osteoporotic patients?

A

HRT- hormone replacement therapy (oestrogen) given to post menopausal women - but this is used to prevent not treat osteoporosis

denosumab- monoclonal antibody against the RANK ligand, which normally activates osteoclasts. therefore osteoclasts stop working

153
Q

what is the only anabolic treatment for osteoporosis? how does it work and why can’t it be used forever in a patient?

A

teriparatide- despite being a recombinant of parathyroid hormone (which normally when released causes bone resorption) intermittent exposure to it activates osteoblasts more than osteoclasts, therefore increases bone density and trabecular structure.

but risk of osteosarcoma increases therefore max 2 years of use.

154
Q

what other assessment would you do with someone who is suspected to be osteoporotic?

A

FRAX- estimation of risk of having an osteoporotic fracture in the next 10 years based on a number of risk factors- such as age, height and weight, family history, smoking, steroid use, previous fractures etc

must be over 40 yo for it to be reliable

155
Q

what is osteomyelitis and who does it normally affect?

A

inflammation of the bone secondary to infection in the bone

bimodal age distribution- young and elderly

156
Q

How does the bone become infected in osteomyelitis?

A

directly- bacteria goes into bone, which may be made easier by an open fracture - trauma

from adjacent tissues- if there is an infection in the soft tissue, it can spread into the bone- esp in diabetic patients

indirectly- via the blood (haemtogenous seeding) patient has bacteriaemia-
in children will spread to long bone (thick periosteum, high rate of blood flow)
in adults: to vertebra.

157
Q

who is at risk of osteomyelitis?

A

diabetic patients

anyone likely to get a bacteraemia: IVDU, has a line, sickle cell, catheter and UTI

158
Q

Most likely cause of osteomyelitis?

A

Staph Aureus

or coagulase negative staphlococcus- ie epidermidis

159
Q

what is the pathophysiology in acute osteomyelitis?

A

inflammatory cells
swelling
oedema
vascular congestion and small vessel thrombosis

160
Q

what is the pathophysiology of chronic osteomyelitis?

A

inflammatory exudate in the marrow leads to increased intramedullary pressure.
exudate may rupture through the periosteum
so periosteal blood supply is disrupted
lack of blood leads to necrosis
pieces of separated dead bone (sequestra) are formed
new bone is formed around the sequestrum (involucrum)

161
Q

what are the symptoms of OM?

A

dull pain at site over a few days, might be aggravated by movement

(if in hip, vertebra, pelvis may not has as many symptoms)

162
Q

what are the signs of OM?

A

systemic: fever, rigors, malaise, sweats
local: tender, red, swelling, warmth
chronic: deep ulcers which aren’t resolves after treatment, non healing fractures, draining sinus tract

163
Q

what tests would you do if you suspected OM and what would you expect to see if it was correct?

A

Bloods- might have high WBC, raised ESR and CRP
+culture

Plain X ray- but may not see changes if less than 2 weeks

MRI/CT

bone biopsy

164
Q

key test to do in OM?

A

find the causative organism
blood culture or bone biopsy
if too systemically ill before can be cultured, give empirical abx (but make sure to take bloods first)
treat with abx based on organism found

165
Q

what differential diagnosis would you have in OM?

A 
cellulitis 
charcot joint 
gout 
avascular necrosis 
fracture
166
Q

how do you treat OM? and how do you know its working?

A 
surgery (resection of infected bone) 
antimicrobial therapy (tailored based on culture sensitivities, need high prenetrance, may need IV to start)

guided by ESR/CRP - if doesn’t decrease, reimage

167
Q

If there is osteomyelitis and the blood culture is negative, what might you suspect and what should you do?

A

TB CAN CAUSE OM
will have much slower onset

must do bone biopsy instead (will find caveating granulomas)

168
Q

what are the signs and symptoms of a septic joint?

A

red, hot, swollen, painful joint (normally monoarticular but don’t rule out if not)
may also be systemically unwell i.e. with fever, malaise, rigours, sweats

169
Q

What two things must you do if you suspect a septic joint?

A

ASPIRATE THE JOINT!!!!!

blood cultures

170
Q

what might you expect the joint aspirate to look like if it is septic?

A

yellow, thick, creamy, pusy, sticky- probably infection

otherwise should be clear, runny, and thin

171
Q

why might ESR be low on admission even though the joint is septic? (leukocytes and CRP still high though)

A

ESR can be slow to rise (and slow to fall) so may not have risen yet

172
Q

what is the most common causative organism for native joint infection? list some others it might be?

A

STAPH AUREUS MOST COMMON

streptococci, neisseria gonorrhoea, …..

173
Q

how would you treat a septic joint?

A

Joint wash out- SURGERY or can do with repeated aspiration but not as effective

antibiotics- guided by the cultures, one with high penetrance

stop any immunosuppressive therapy (i.e. like in RA patient, take off methotrexate and biologics) until it flares up again bad enough to risk the immunosuppression

174
Q

If someone is on steroids chronically but are found to have a bad infection what should you do and why?

A

they will not produce their natural cortisol

so need to do it for them by doubling their normal dose to give them the stress response

175
Q

why and how would we rather prevent prosthetic joint infection than treat it?

A

why- most cost effective, money on prevention will go further than money on septic revision

how- lamina flow theatre, constant clean airflow, more curtains/sheets for separating, disposable gowns, gowns have hoods and masks

176
Q

what methods can be used to treat an infected prothesis? and what has the best outcome?

A

suppress with abx only (if unfit for surgery/multiple joints)

debridement and retention of prothesis (only in early post operative infection)

excision arthroplasty: could just take it out and not put it back in but significant disability so normally EXCHANGE arthroplasty

2 different ways:
one stage exchange arthroplasty (take it out, remove all infection, put new one back in)

2 stage exchange arthroplasty- best outcome!!
take it out, wait until all infection is gone, and then reconstruct

177
Q

what substances can you use in arthroplasty to prevent recurrent infection/sepsis of the joint?

A

bone cement that has antibiotics in

local antibiotic spacer- if doing 2 stage exchange arthroplasty, leave spacer in there after removal and before replacement

178
Q

what is the common radiological feature in RA?

A

peri articular erosions

179
Q

how would you treat mechanical back pain?

A 
encourage them to keep moving 
simple analgesics (paracetamol, ibuprofen) 
can take short time off work
180
Q

what percent of bone density can be lost before it is seen on an x-ray?

A

60%

181
Q

what is ehlors danlos?

A

an inherited condition causing defective collagen, which normally helps tissues to resist deformation

182
Q

name 3 autoimmune connective tissue disorders?

A

SLE
primary sjogren’s syndrome
systemic sclerosis

183
Q

what type of drugs might you use to treat SLE skin and joint manifestations?

A

anti malarials

184
Q

what is a typical SLE presentation?

A

mouth ulcers
fever
pleuritic chest pain
painful white fingers (raynauds)

185
Q

what is associated with SLE?

A

deforming arthritis, photosensitive rash, seizures, PE

186
Q

what presentation might be suggestive of GCA?

A

giant cell arteritis

acute sight loss (occlusion of optics) 
right sided/one sided headache (temporal arteritis)
jaw claudication (pain on chewing) 
early morning stiffness 
general malaise
187
Q

what tests might indicate GCA?

A 
inflammatory markers (ESR and CRP) will be up 
ANCA NEGATIVE (will be positive in small cell arteritis)
188
Q

how do you treat GCA?

A

corticosteroids (IV maybe)

189
Q

systemic onset JIA might present with?

A 
thrombocytosis (too many platelets- high platelet count) 
high ferritinaemia 
daily fever 
evanescent rash
(obvs joint pain?)
190
Q

first line treatment for FM?

A

graded exercise therapy

and correct sleep disturbances to reduce fatigue

191
Q

what is CREST syndrome?

A

limited cutaneous form of systemic sclerosis/limited scleroderma, is an acronym for its main features which are:

Calcinosis- deposition of calcific nodules, esp in the hands

Raynaud’s phenomenom- white, cold fingers due to mass vasoconstriction of the small blood vessels to the digits

Esophageal dysmotility - atrophy of the smooth muscle wall, presents with dysphagia

Sclerodactyly - thickening and then tightness of the skin around the fingers

Telangiectasias - small dilated blood vessels in the skin esp on face and mucous membranes

192
Q

what is systemic sclerosis/diffuse scleroderma ?

A

an autoimmune multi system connective tissue disorder, where the body continues to deposit collagen as though its responding to injury

which has all the symptoms of CREST but affects skin all over the body and also affects the internal organs like the heart, lung and kidneys. can get hypertension, pulmonary hypertension and SOB

Rheumatology Phase 2 (1 decks)

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