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Rheum, derm Flashcards

1
Q

why does osteoporosis increase risk of fracture

A

low bone mass + low bone density
reduced bone density means bones are more fragile, so more likely to fracture

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1
Q

how is osteoporosis diagnosed

A

T score (bone mineral density compared to average young adult) less than -2.5

if T score -1 to -2.5 => osteopenia

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2
Q

how is bone mineral density measured

A

DEXA scan
T score is comparing to young healthy adult
Z score is comparing to someone of same: age, gender, ethnicity

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3
Q

why are old women prone to osteoporosis

A

menopause means less oestrogen, so more RANK-ligand

RANDK-ligand increases bone resorption, causing osteoporosis

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4
Q

what measure indicates fracture risk

A

bone mineral density

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5
Q

what are osteoporosis RF

A

old age, post-menopausal women
BMI <19
smoker, alcohol, immobile

PMH/FH of fragile fractures
RA, chronic conditions - CKD/thyroid/diabetes

DH long-term steroid use

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6
Q

how does spinal osteoporosis present

A

no early warning symptoms

height loss as dorsal kyphosis (stooping)

restrictive lung disease causing SOB
protuberant belly causing bloating/nausea

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7
Q

what imaging is done for spinal osteoporosis

A

x-ray spine
DEXA, MRI, isotope bone scan

do DEXA if FRAX score intermediate

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8
Q

when is DEXA not done

A

pt had vertebral fracture

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9
Q

when is FRAX not done

A

pt over 50yr with fragility fracture

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10
Q

how is osteoporosis treated

A

1) lifestyle - more exercise, better diet, stop smoking
2) check VitD + Ca to see if deficient

pharmacological:
1) bisphosphonate
2) another bisphosphonate

3) denosumab/romosumab (monoclonal Ab)
HRT (if pre-menopause)
raloxifene (selective E2 receptor modulator)
teraparitide (acts as PTH)
strontium (like Ca, stimulating osteoblast + inhibiting osteoclast)

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11
Q

when are bisphosphonates contraindicated

A

renal impairment if eGFR <30l/min

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12
Q

what are SE of bisphosphonate

A

GORD, oesophageal erosion
atypical fracture
osteonecrosis of jaw + external auditory canal

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13
Q

how are bisphosphonate taken

A

orally
on empty stomach with water
pt sit upright for 30min before moving/eating

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14
Q

what is denosumab

A

monoclonal Ab that targets RANK-ligand
reducing formation/function of osteoclasts

suitable in renal impairment

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15
Q

when to reassess bisphosphonate treatment

A

after 5yr (3-5yr)
repeat DEXA

continue bisphosphonate if:
T score less than -2.5 (as pt still high risk)
previous hip/vertebral fracture
on steroids

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16
Q

what type of disease is gout

A

crystal arthropathy - associated with chronically high urate levels

inflammatory rheumatic disease

mono-arthritis

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17
Q

what causes high total body uric acid conc

A

mainly from reduced clearance
(also from over-production of uric acid - as that is end product of purine degradation)

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18
Q

what is pathophysiology of gout

A

uric acid crystallises
forming needle-shaped crystals within/around joints
these build up under skin forming gouty tophi

blood identifies crystals as foreign so immune system attacks
causes pain + inflammation

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19
Q

where are gouty tophi

A

hands, elbows, ears

due to subcutaneous uric acid deposits

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20
Q

what characterises gout

A

painful mono-arthritis
with recurrent flares of joint inflammation

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21
Q

what are RF for gout

A

obese, men
alcohol
high purine diet - meat, coffee

FH
PMH - CVD, kidney disease
DH - diuretic

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22
Q

which joints are usually affected in gout

A

gout is mono-arthritis

MTP (base of big toe)
wrist, CMC (base of thumb), ankle, knee

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23
Q

how is gout investigated

A

as gout presents as hot, red, swollen joint - need to rule out septic arthritis first
so joint aspiration + ABx

then confirm gout by:
high serum urate
needle shaped, monosodium urate crystals with negative befringement (in polarised light)
no bacteria

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24
Q

what does joint aspiration of gout show

A

needle shaped, monosodium urate crystals
with negative befringement (in polarised light)
no bacteria

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25
Q

what would gout x-ray show

A

no loss of joint space

lytic bone lesions
punched out erosions - sclerotic borders and overhanging edges

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26
Q

what is acute gouty arthritis + how is it treated

A

acute monoarticular pain (mostly at night)
with heat + erythema at affected joint

treat with NSAID

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27
Q

how is uric acid eliminated from body

A

most filtered by glomeruli
from filtered urate, most absorbed along nephron (mainly at proximal tubule)
only 10% is excreted in urine

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28
Q

how is gout acutely managed

A

1) NSAID with PPI (for gastroprotection)
2) colchicine
3) oral steroid (prednisolone)

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29
Q

how is gout managed long-term

A

lifestyle changes:
exercise, reduce weight
better diet (no coffee, less meat)
reduce alcohol

xanthine oxidase inhibitors + uricosuric agents to reduce urate levels

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30
Q

what is allopurinol

A

xanthine oxidase inhibitor
to lower uric acid levels

another XO inhibitor = feboxustat
metabolised in liver, so can be used for renal impairment

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31
Q

when is colchicine used for acute gout

A

pt renal impaired, significant heart disease

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32
Q

how does gout + pseudo gout (chonedrocalcinosis/CPPD) differ

A

both crystal arthropathies causing mono-arthritis

gout = monosodium urate crystals, needle shaped, negative befrignement

pseudo gout = calcium pyrophosphate crystals, rod shaped, positive befringement

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33
Q

how does CPPD (calcium pyrophosphate deposition disease) present

A

mostly asymptomatic - picked up incidentally on x-ray

typical Q on psuedogout:
65yr+ with rapid onset hot, swollen, stiff, painful knee

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34
Q

what is CPPD associated with

A

pseudo gout associated with:
haemochromatosis
hyperPTH, familial hypocalciuric hyperCa, hypophosphatasia
hypoMg

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35
Q

how is pseudo gout investigated

A

first exclude septic arthritis, so do joint aspiration + ABx

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36
Q

what x-ray changes are seen with CPPD

A

similar to osteoarthritis:
loss of joint space
osteophytes
subchondral sclerosis + cysts

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37
Q

how is pseudo gout managed

A

if asymptomatic + incidental finding on X-ray = don’t treat

if symptomatic:
1) NSAID + PPI
2) colchicine
3) intra-articular steroids

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38
Q

what are 2 types of allergic reaction

A

type 1 allergic/hypersensitivity (IgE) = immediate, 1-2 days after

type 4 hypersensitivity (T-cell) = 7-14 days after

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39
Q

how is skin type classified

A

Fitzpatrick (6 types)

eumelanin human skin colour score (5 types) - more modern
based on melanin index indicating amount of eumelanin (more = darker)

melanin index = how pt’s skin reflects lights of certain wavelengths, measured using skin reflectance instrument

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40
Q

how do wood light + dermascope differ

A

wood light - hand held UV light source, used for vitiligo and malessezia yeast
vitiligo = depigmented areas enhanced
malessezia yeast = yellow/orange fluorescence
(visible rays not seen due to nickel oxide filter)

dermatoscope - see subsurface skin structures in epidermis, derma-epidermal junction, upper dermis
used for lesions

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41
Q

when is wood light + dermatoscope used

A

wood light = vitiligo, maelessezia yeast
vitiligo - depigmented areas enhanced
malessezia yeast - yellow/orange fluorescence

dermatoscope = lesions

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42
Q

what is flat area of colour change

A

if <5mm, macule
if 5+ mm, patch

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43
Q

what is solid elevated lesion

A

if <5mm, papule
if 5+ mm, nodule or plaque (if scaly)

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44
Q

what is circumscribed elevated lesion containing fluid

A

if <5mm, vesicle
if 5+ mm, bulla

if it contains pus, pustule

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45
Q

how do erosion + ulcer differ

A

erosion = shallow, affecting epidermis only

ulcer = loss of epidermis + part of dermis, leaving depressed moist lesion

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46
Q

what is cyst

A

sac in dermis
contains semisolid/liquid material

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47
Q

how do scaly + lichenificated surfaces differ

A

scaly = heaping of stratum corneum or keratin

lichenificated = from scratching/rubbing, epidermis thickens

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48
Q

what is BCC

A

basal cell carcinoma - most common skin cancer
affects stratum basal of epidermis

slow growing
locally invasive - unlikely to metastasise

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49
Q

what is main RF for BCC

A

longterm UV radiation
(can develop into a scar)

UV exposure mutates DNA - esp p53 tumour suppressor gene9q22

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50
Q

how does BCC present

A

on sun-exposed areas - head, neck

small slow-growing lesions
raised pearly edges
telangiectasia

if symptomatic - pain, bleeding, ulcer

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51
Q

what are BCC subtypes

A

nodular (most common)
superficial
morphoeic - uncommon, prone to recurrence
basosquamous - mixed BCC and SCC with infiltrative growth pattern, so more aggressive

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52
Q

how is BCC diagnosed

A

clinical diagnosis

confirm with excision biopsy

only do imaging if evidence of invasion

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53
Q

what is high-risk BCC

A

young pt <25yr, immunocompromised
recurrent lesions

lesion on nose, lip, ear, around eyes

poorly defined margin

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54
Q

how is BCC managed

A

gold standard - excision (surgical)
5mm margin if high risk

if high risk, moh micrographic surgery

destructive:
surgical - curette/cautery (superficial BCC), cryotherapy (conservative)
topical/non-surgical (superficial BCC) - topical immunotherapy (aldara/imiquimond), photodynamic therapy, radiation therapy

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55
Q

when is topical/non-surgical management done for BCC

A

topical management is destructive technique
used for superficial BCC

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56
Q

what is gorlin-goltz syndrome

A

autosomal dominant condition (PTCH1/2, SUFU)
basal cell nevus syndrome - cause multiple early onset BCC

treat with vismodegib (pathway inhibitor - systemic)
as surgery/radiotherapy not suitable

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57
Q

what is SCC

A

squamous cell carcinoma - 2nd most common cancer
affects keratinocytes in supra-basal epidermal layer

can metastasise

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58
Q

what are premalignant lesions for SCC

A

bowen disease (SCC in situ - confined to epidermis only)

actinic keratoses, keratin horns

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59
Q

what is peak incidence for SCC

A

> 40yr, male

common in fair skin
commonest skin cancer for black/asian

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60
Q

what are RF for SCC

A

prolonged UV exposure (excessive sunbed use)

smoking
immunosuppressed - leukemia/lymphoma, renal transplant

environmental carcinogen - arsenic, aromatic hydrocarbon, insecticide, herbicide

HPV, genodermatoses (xeroderma pigmentosum), HIV

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61
Q

how does SCC present

A

on scalp, face, hands (sun-exposed sites)

fast growth rate
friable/ulcerated nodule, surface crusting

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62
Q

how does SCC look in dermascope

A

white circles/structureless areas
looped blood vessels
central keratin plug

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63
Q

how is SCC diagnosed

A

clinical diagnosis + confirm with biopsy

excision biopsy if small + well-demarcated
incisional biopsy if large + peripheral margins

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64
Q

what are features of high-risk SCC

A

2+cm diameter, 4+mm depth
head/neck affected - ear as high recurrence, lip as likely metastasis

poorly differentiated
perineurial + lymphovascular invasion

immunosuppressed

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65
Q

how is SCC managed

A

1st line = surgical

excision biopsy - peripheral margins depend on how high risk SCC is
low risk 4+ mm (can curette/cautage instead of excision)
high risk 6+ mm
v.high 10+ mm

primary + post-op radiotherapy

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66
Q

what is Bowen disease

A

SCC malignant cells confined with full thickness of epidermis

non-tender, non-indurated
hyperkeratotic papule or plaque
on sun-exposed sites - ears, face, hands, lower legs

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67
Q

how is Bowen disease managed

A

cryotherapy
curette, cautage

surgical excision

topical 5-FU imiquinod
radiotherapy

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68
Q

what is melanoma

A

malignant tumour of melanocytes (pigment producing cells)
from stratum basale of epidermis

metastasises early

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69
Q

what are RF of melanoma

A

UV light - sunburns, sun beds
living by equator + higher evaluation

FH - FAMM syndrome

fair skin (Fitzpatrick type 1/2) - having too many moles, or dysplastic moles

PMH melanoma, premalignant lesions

immunosuppressed

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70
Q

where are melanomas

A

male - trunk
female - lower limb

most melanomas develop de novo on normal skin

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71
Q

how does melanoma present

A

early on asymptomatic
changes in existing mole - if locally advanced, bleeds/ulcers

ABCDE
asymmetry
border irregular
colour changes/uneven
diameter 6+ mm
evolving lesion

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72
Q

how is melanoma diagnosed

A

excision biopsy - needs 2mm peripheral margin with subcutaneous fat at deep margin

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73
Q

what are major + minor signs of melanoma

A

for diagnosis, needs 1+ major and 3+ minor signs for referral:

major - change size, irregular shape, irregular colour

minor - 7mm diameter, inflammation, oozing, changed sensation

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74
Q

what are 5 melanoma subtypes

A

superficial spreading
nodular
lentigo maligna melanoma
amelantonic melanoma
acral lentiguous

superficial spreading - most common, 30-50yr
malignant cells within epidermis (in-situ)

nodular - affects M more, 50+yr
grows vertically, arises de novo
not that affected by sun exposure

lentigo maligna melanoma - on head/neck
macular intraepidermal neoplasm
sunlight is most important pathogenic factor

amelantonic melanoma

acral lentiguous - on palms, soles, under nails

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75
Q

what prevention advice for melanoma

A

stay in shade 11am-3pm
wear SPF 30+ and protective clothing (hat, sunglasses)
avoid sunbed

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76
Q

what stage of melanoma does cancer spread to other organs

A

stages 1/2 are localised to skin
stage 3 spread to lymph nodes
stage 4 spread to other organs

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77
Q

how is melanoma managed

A

WLE wide local excision - improves loco regional control by removing micro metastases

systemic treatment:
targeted therapy if BRAF mutation
immunotherapy (single or combined - nivolumab, ipillumab)

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78
Q

what determines peripheral margin for WLE in melanoma

A

breslow thickness of melanoma - thicker it is, larger peripheral margin + deep margin down to deep fascia

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79
Q

when to do sentinel lymph node biopsy for melanoma

A

if breslow thickness 0.8+ mm

if SLNB confirms lymph node metastasis, treat with completion lymphadenectomy

80
Q

when is targeted therapy done for melanoma

A

if BRAF mutation

81
Q

what causes solar lentigines

A

solar lentiggine = harmless patch of darkened skin
very common in <40yr

UV radiation causes local proliferation of melanocytes
so melanin accumulates within keratinocytes

82
Q

what lesion has waxy, stuck on appearance

A

seborrheic keratosis
(can look pigmented, may have horn cyst)

benign lesion - sign of skin ageing

83
Q

what is leser-trelat sign

A

rapid onset of multiple seborrheic keratoses - rapid increase in number + size

if young pt, indicates paraneoplastic process so investigate for cancer

84
Q

what cancers are associated with leser treat sign

A

leser-trelat = rapid onset of many seborrheic keratoses

adenocarcinoma of colon/stomach
SCC
lymphoma, leukaemia

85
Q

why should multiple dysplastic naevi be monitored

A

indicate pt’s predisposition to melanoma - esp if FH

but melanomas usually develop de novo

86
Q

what is actinic keratosis

A

sun-induced scaly lesions that can become malignant

risk of transforming to SCC increases if:
with time + more lesions

87
Q

how is actinic keratosis managed

A

cryotherapy
topicals - 5-FU, imiquimod
photodynamic therapy, laser

88
Q

how do punch, incisional, excision biopsy differ

A

punch = small cylindrical tissue removed
for larger tumour

incisional = only a portion of tissue removed
for larger tumour

excision = whole tissue removed with a margin of normal tissue
for easily accessible area - not if cosmetically sensitive or near vital anatomical structure

89
Q

what is vasculitis

A

inflammation of blood vessels
large = aorta, medium, small = arterioles/capillaries

inflammation leads to tissue ischaemia (from stenosis) or aneurysms

vasculitis can cause organ dysfunction

90
Q

what are eg of different types of primary vasculitis

A

large (affects aorta) = GCA, takayasu

medium = kawasaki, polyarteritis nodosa

small (affects arteriole/capillary):
ANCA associated - Wegner (granulomatosis with polyangiitis) chrug-strauss (same but eosinophilic), microscopic polyangiiitis
immune mediated - IgA vasculitis (hence-schein purpura), anti-GBM, cyroglobulinaemia vasculitis

91
Q

when are purpura/petechiae seen in vasculitis

A

small/medium cell arteritis - since they are more superficial

92
Q

what is polymyalgia rheumatica

A

inflammatory condition causing pain + morning stiffness
in shoulders, pelvic girdle, neck

strongly associated with GCA

moderate acute phase response (raised ESR/CRP)
dramatic early response to steroids

more common in women 50yr+ (north Europe)

93
Q

how does PMR (poly myalgia rheumatic) present

A

pain in shoulders, pelvic girdle, neck
morning stiffness 45min+ (worse after rest, disturbed sleep)

systemic symptoms
peripheral arthritis/oedema of wrist/knee

50yr+ women, north Europe

94
Q

what is diagnostic criteria for PMR

A

age 50yr+
duration 2wk+

bilateral shoulder/pelvic girdle ache
morning stiffness 45min+

acute phase response - raised ESR/CRP
confirm +ve response to prednisolone

95
Q

is muscle strength impaired in PMR

A

NO

but muscle pain makes testing difficult + disuse atrophy can occur

96
Q

what are important differentials to exclude for PMR diagnosis

A

GCA - very high ESR/CRP, needs a higher dose of steroids

active infection/cancer - steroid treatment could mask symptoms, delaying diagnosis

97
Q

before starting steroid treatment, what tests need to be done

A

FBC
CRP/ESR - raised
serum protein electrophoresis (for myeloma) - no paraprotein
RF, anti-CCP (for RA) - negative
ANA (for SLE) - negative

UE, LFT, TSH, CK - normal
CXR - normal

98
Q

how is PMR managed

A

low dose oral prednisolone 15mg/day
follow-up in 1wk
continue steroid dose for 3wk, then taper slowly

if steroid resistant, consider methotrexate

for PMR, should have dramatic response
inflammatory markers return to normal within 1 month (CRP more reliable marker than ESR)

taper steroid dose slowly - avoid addisonian crisis
bisphosphonates (+ Ca, VitD) - prevent osteoporosis
PPI - gastroprotection

99
Q

how do CRP + ESR differ

A

CRP = acute inflammation
ESR = long-term

100
Q

what precautions are taken for steroid therapy

A

taper steroid dose slowly - avoid addisonian crisis
sick day rules - increase steroids if pt unwell

bisphosphonates (+ Ca, VitD) - prevent osteoporosis
PPI - gastroprotection

101
Q

what is PMR prognosis like

A

good
rapid/dramatic initial response to steroid - symptoms resolve in 1-3 days

treatment needed for 1-2yr
as relapse is common

102
Q

what is GCA (giant cell arteritis)

A

also temporal arteritis
affects superficial temporal artery (branch of external carotid)

systemic vasculitis of large (+ medium) arteries
needs early recognition/treatment - otherwise, blindness + jaw claudication can occur

strongly associated with PMR

103
Q

how does GCA present

A

unilateral severe headache (in temporal region)
temporal artery is pulseless, red/thick/tender

blurred/double vision
scalp tenderness
jaw/tongue claudication (as facial/lingual artery affected)

50yr+ women, north Europe

104
Q

what vision disturbances occur in GCA

A

usually monocular

transient vision loss - amourosis fugax
partial field defect

105
Q

how is GCA diagnosed

A

clinical presentation
raised inflammatory markers - very high ESR/CRP

either 1 or both:
temporal artery biopsy (1cm length) - multinucleate giant cells
duplex US - hypo echoic ‘halo’ sign, stenosis of temporal/axillary artery

(additional - PET scan, shows increased FDG uptake in temporalis region as active large cell arterirtis)

106
Q

why does temporal artery biopsy need to be 1cm length or more

A

GCA involves skip lesions, so patchy inflammation occurs

biopsy shows immune cell infiltration into smooth muscle cell layer - as GCA is pan-arteritis

107
Q

how is GCA managed

A

start steroid treatment immediately - before confirming diagnosis
to reduce risk of vision loss

oral prednisolone 40-60mg /day
(if visual symptoms or jaw claudication, increase to IV methylprednisolone 500-1000mg daily for 3 days)

when condition controlled, wean steroids over 1-2yr
give PPI + Ca/VitD with steroids
aspirin 75mg to reduce vision loss and strokes

108
Q

how is GCA treatment monitored

A

checking ESR/CRP

109
Q

if pt at risk of glucocorticoid toxicity or have relapsed, what treatment is given for their GCA

A

steroid-sparing agent = methotrexate, tocilizumab (monoclonal Ab to IL-6)

110
Q

what is takayasu arteritis

A

also called pulseless disease
granulomatous arteritis inflaming aorta + primary branches

affects young women (10-40yr), asian

111
Q

how does takayasu arteritis present

A

initially constitutional then vascular damage symptoms

systemic symptoms (FLAW)

carotidynia (tender carotid artery)
reduced/absent/weak peripheral pulse
limb claudication
angina, abdo pain

112
Q

what is ACR diagnostic criteria for takayasu arteritis

A

at least 3 of:

<40yr

limb claudication

reduced brachial pulse of 1/both arms
10mmHg difference in BP between both arms

bruit over subclavian artery or abdominal aorta

arteriographic evidence of narrowing/occlusion of:
entire aorta, primary branches, or large arteries in UL/LL

113
Q

what investigations are done for takayasu arteritis

A

incidental finding on CT chest
then do MRI angio to see which arteries are stenosed/occluded

raised ESR/CRP

114
Q

how is takayasu arteritis managed

A

high dose steroids
(with bisphosphonate/Ca + PPI)

if steroid-resistant = methotrexate
angioplasty can be done for symptomatic relief

115
Q

what organ dysfunction can occur from vasculitis

A

systemic symptoms - FLAW

skin - rash
NS - mono/poly-neuropathy
kidney - glomerulonephritis
muscle - myalgia
joint - arthritis
lung - infiltrate, nodule
bowel - ischemia/infarction

116
Q

what is polyarteritis nodosa

A

systemic necrotising vasculitis of medium/small arteries (bifurcating arteries and their branches)

associated with HepB virus, mono neuritis multiplex, renal infarcts
40-60yr male or female

117
Q

are ANCA antibodies present in polyarteritis nodosa

A

NO

118
Q

how does polyarteritis nodosa present

A

constitutional symptoms - fever, myalgia, appetite/weight loss
rash

strong involvement of:
kidneys - renal infarction, HTN due to RAAS
nerves - peripheral neuropathy, mononeuritis multiplex
GI - abdo pain, GI bleeds

119
Q

what are 2 types of ANCA antibodies + how do they differ

A

cANCA - stains cytoplasms, directed against PR3 antigen

pANCA - stains perinuclear region, directed against MPO antigen

120
Q

what are eg of ANCA-associated vasculitis

A

inflammation of small vessels

causes pulmonary haemorrhage, glomerulonephritis

microscopic polyangiitis
Wegner - granulomatosis with polyangiitis
churg-strauss - eosinophilic granulomatosis with polyangiitis

121
Q

what is microscopic polyangiitis

A

necrotising vasculitis of small/medium arteries

p-ANCA +ve, affects MPO antigen

122
Q
A
123
Q

what is Werner (granulomatosis with polyangiitis)

A

necrotising vasculitis of small arteries

presents with saddle-shaped nose as orbital/nasal bridge collapse
sinusitis, epistaxis

cANCA +ve, affects PR3 antigen

124
Q

how does wegner present

A

granulomatosis with polyangiitis
saddle-shaped nose from nasal bridge collapse

skin rash
lung nodules, pulmonary haemorrhage
glomerulonephritis (active urinary sediment shows RBC casts, microscopic haematuria)
GI bleed

sinusitis, epistaxis
tracheal stenosis
eye proptosis
orbital + nasal bridge collapse
conductive hearing loss

125
Q

how to diagnose Wegner

A

blood test - cANCA +ve (PR3)
tissue histology

126
Q

what is churg-strauss

A

eosinophilic/allergic granulomatosis with polyangiitis

associated with allergy, asthma

pANCA +ve (MPO antigen)

127
Q

how does churg-strauss present

A

allergy, late-onset asthma

mono/poly-neuropathy
pulmonary infiltrates
sinusitis, nasal polyposis
skin rash

128
Q

how are ANCA-associated vasculitis managed

A

if non-threatening = glucocorticoid + methotrexate or myclophenoate

if organ/life threatening = glucocorticoid + rituximab or cyclophosphamide

[if rapidly progressive renal failure or pulmonary haemorrhage = plasma exchange]

129
Q

what is anti-GBM (good pasture) disease

A

autoantibodies attack glomerular basement membrane
on kidneys (glomerulonephritis) + lungs (diffuse alveolar - pulmonary haemorrhage)

peak incidence 20-30yr F + 60-70yr M

has temporal + spatial clusters

130
Q

what is bechet disease

A

systemic vasculitis affecting arteries + veins

presents with recurrent oral/genital ulcers
associated with HLA-B51 antigen

common in Japan, turkey, North Africa, Iran

131
Q

how does behcet disease present

A

recurrent oral/genital ulcers (3x a year)
painful erosions, leaving ‘red halo’

erythema nodosum, aceniform
uveitis (eyes), retinal thrombosis
arthritis

132
Q

how is behcet disease diagnosed

A

pathergy test:
sterile needle pricks forearm, wait 24-48hr to see if non-hypersensitivity changes (erythema, induration/thickening)

associated with HLA-B51 antigen

133
Q

what is RA - rheumatoid arthritis

A

symmetrical poly arthritis (5+ joints) of small joints in hands/feet

autoimmune condition, causing chronic inflammation of synovial lining

usually women, aged 30-50yr
(RF - smoking, obesity)
associated with HLA-DR4

134
Q

how does RA present

A

joint: pain, stiffness, swelling
morning stiffness 45+ min
pain worse at rest (esp at night), better with activity

palpation feels ‘boggy’ from joint tenderness and synovial thickening

systemic symptoms - FLAW, myalgia

Atlanta-axial sublaxation causing spinal cord compression (emergency)

hand signs only in severe RA:
boutonniere (flex PIP, extend DIP)
swan-neck (extend PIP, flex DIP)
z-shaped thumb
ulnar deviation

135
Q

which joints are affected in RA

A

symmetrical distal polyarthritis

MCP
PIP, wrist, MTP

136
Q

what is palindromic rheumatism

A

self-limiting episodes of inflammatory arthritis

episodes of joint pain/swelling/stiffness lasting few days, then completely resolving

if antibodies (RF, anti-CCP) present, then likely progresses to RA

137
Q

what are extra-articular manifestations of RA

A

systemic symptoms - FLAW, myalgia

felty syndrome - RA, neutropenia, splenomegaly
sjorgen syndrome - dry mouth/eye
eye: scleritis, episcleritis, keratitis

138
Q

what are rheumatoid nodules

A

firm, painless lumps under the skin
seen on elbows, fingers

139
Q

how is RA diagnosed

A

if persistent synovitis, urgent referral to rheumatology

check if antibodies present - RF, anti-CCP (more sensitive/specific)

raised inflammatory markers - ESR, CRP
x-ray changes (US/MRI to look for synovitis)

140
Q

what 2 antibodies are checked in RA

A

RF - autoantibody (IgM) that targets Fc region of IgG immunoglobulins, triggering systemic inflammation

anti-CCP - more sensitive/specific than RF

141
Q

what x-ray changes are seen in RA

A

loss of joint space
bony erosions - bare areas where synovial in direct contact with bone (as no cartilage)
subchondral sclerosis
subchondral cysts

periarticular osteopenia - loss of bone density around joints
soft tissue swelling (synovitis)

142
Q

what scoring systems are used for RA

A

HAQ for functional ability - check immediately at diagnosis, then compare when on treatment

DAS28 for monitoring disease activity - assess joint swelling/tenderness, ESR/CRP result

143
Q

how is RA managed

A

short-term steroids used to induce remission by settling flares
NSAID given for pain relief

maintain remission:
1) mono therapy with DMARD - methotrexate, leflunomide, sulfasalazine
2) combine DMARD
3) biologic + methotrexate

144
Q

how is palindromic rheumatism managed

A

hydroxychloroquine

145
Q

how is RA treatment monitored

A

check CRP + DAS28 score

146
Q

which DMARD are teratogenic

A

methotrexate, leflunomide

(hydroxychloroquine + sulfasalazine are safe in pregnancy)

147
Q

how is RA affected in pregnancy

A

pregnancy can improve RA symptoms

but if flare-up give: hydroxychloroquine or sulfasalazine

148
Q

what is methotrexate __
MOA
typical dose
SE

A

MOA - dihydrofolate reductase inhibitor
interferes with folate metabolism to prevent DNA replication

typical dose - 10-25mg weekly (with 5mg folate the day after)

SE - teratogenic, anaemia, thrombocytopenia, leukopenia
[GI disturbance - N+V, mouth ulcer, mucositis]

149
Q

what is sulfasalazine __
MOA
typical dose
SE

A

MOA - prodrug, gut bacteria breaks it down to sulfapyridine (active component) + 5-ASA

typical dose - 2-3g daily

SE - orange urine, reduced male fertility
skin reaction, anaphylaxis
thrombocytopenia, leukopenia
headache
GI disturbance - N+V, diarrhoea

150
Q

what is leflunomide __
MOA
typical dose
SE

A

MOA - interferes with pyrimidine production, preventing DNA/RNA formation

typical dose - 10-20mg daily

SE - teratogenic, HTN, peripheral neuropathy, paraesthesia
[skin reactions
anaemia, thrombocytopenia
headache
GI disturbance - N+V, diarrhoea, anorexia, mouth ulcer, mucositis]

151
Q

what biologics are used for RA

A

anti-TNF = adalimumab, infliximab, etanercept

anti-CD20 = rituximab

anti-IL6 = tocilizumab

JAK inhibitor = tofacitinib, baricitinib

T-cell co-stimulation inhibitor = abatecept

152
Q

what diseases are associated with tocilizumab + rituximab

A

both are biologics used for RA

tocilizumab (anti-IL6) - transient dyslipidemia

rituximab (anti-CD20) - PML (progressive multifocal leukoencephalopathy)

153
Q

what are SE of tyrosine-kinase inhibitors

A

TKI are specific binding but have wide-reaching effects

SE: dyslipidaemia, thromboembolic disease, increased infection (esp herpes zoster)
[nausea, skin reactions]

154
Q

what screening has to be done before using tyrosine-kinase inhibitors

A

T-SPOT to screen for TB (as biologics - esp TKI can reactivate latent TB)

CXR within last 6 months

FBC, UE, LFT
HIV, HepB, HepC, varicella

155
Q

how do RA + ankylosing spondylitis differ

A

RA = symmetrical distal poly arthritis, affects small joints of hands/feet

AS = axial disease, affects spine
(sometimes causes peripheral, asymmetric oligioarthritis of large joints)

156
Q

what are the types of seronegative arthritis

A

seronegative RA = RA characteristics, but -ve for RF/anti-CCP

PEAR - psoriatic arthritis, enteropathic arthritis, ankylosing spondylitis, reactive arthritis

psoriatic - psoriasis, nail changes
enteropathic - associated with IBD
AS - axial disease so affects sacroiliac + vertebral column joints (strongly associated with HLA-B27 gene)
reactive - acute mono arthritis, 1-4wk after gastroenteritis (infective diarrhoea) or STI (chlaymdia)

if none of the above, likely seronegative arthritis - unspecified

157
Q

how do RA + seronegative arthises differ

A

RA = associated with HLA-DR4
usually 30-50yr
more common in female

PEAR = associated with HLA-B27 (esp AS)
young onset
AS more common in male, others M=F

158
Q

what extra-articular features are associated with ___
psoriatic arthritis
enteropathic arthritis
ankylosing spondylitis
reactive arthritis

A

psoriatic arthritis - psoriasis

enteropathic arthritis - gut inflammation

ankylosing spondylitis - osteoporosis
4As:
aortic regurgitation murmur, aortic aneurysm, AV heart block,
apical lung fibrosis - reduced chest expansion
amyloidosis
Achilles tendonitis (entesopathy)
(anaemia of chronic disease)

reactive arthritis - conjunctivitis, genital inflammation

159
Q

which bacteria causes reactive arthritis

A

chlaymdia

gonorrhoea would cause septic arthritis instead

160
Q

what is reiter’s triad for reactive arthritis

A

arthritis, urethritis, conjunctivitis

161
Q

what investigations are done for reactive arthritis

A

aspirate/culture synovial fluid
urinalysis
stool culture, STD screen

check HLA-B27, CRP/ESR

consider blood cultures - if gonoccocal, can cause disseminated septic arthritis

162
Q

how is reactive arthritis managed

A

treat underlying cause
most resolve rapidly after treatment

NSAID
intr-articular or oral steroids

if HLA-B27 +ve, worse prognosis

163
Q

what investigations are done if suspecting AS

A

schober test - shows restricted lumbar movement

also do x-ray to check spine/sacrum
MRI to check for bone marrow oedema

164
Q

what x-ray changes are seen in AS

A

squaring of vertebral bodies
subchondral sclerosis/erosions
joint fusion - facet, sacroiliac, costovertebral
ossification, syndesmophytes (bone growth where ligaments insert onto bone)

if advanced - bamboo spine

165
Q

what features indicate inflammatory arthritis

A

insidious onset
chronic 3+ months
morning stiffness 45+ min, disturbed sleep (esp 2nd half of night)
pain improves with exercise

166
Q

what is diagnostic criteria for AS

A

limited lumbar motion
low back pain for 3+ months, improves with exercise and worse with rest
reduced chest expansion
bilateral sacroilitis grade 2-4, or unilateral sacroilitis grade 3-4 on x-ray

167
Q

how is AS managed

A

physiotherapy, smoking cessation

1) NSAID
2) try another NSAID
3) biologic - anti-TNF (adalimumab)

168
Q

after NSAID are trialled, what medication is used for AS

A

first trial 2 different NSAID
then try biologic (anti-TNF)

DMARD not used as they are for peripheral disease - not axial

169
Q

what are 5 patterns of psoriatic arthritis

A

asymmetrical oligoarthritis
asymmetrical poly arthritis

symmetrical poly arthritis
spondyloarthropathy (sacroilitis predominant)

arthritis mutilans (most severe) - rapidly progressive, deforming (causes telescopic digits - as osteolysis of bones around fingers)

170
Q

how is psoriatic arthritis managed

A

PT/OT, derm liason
NSAID, analgesic

DMARD - but not hydroxychloroquine as it worsens skin disease
methotrexate preferred

biologic - anti-TNF (adalimumab)
[anti-IL17, apremilast PO]

171
Q

what is eczema

A

chronic atopic condition
has relapsing-remitting course (comes as flares)

presents in first few years of life

due to defects in skin barrier (so it no longer has normal continuity)
causes inflammation in skin

172
Q

how does eczema present

A

scaly, itchy, dry, erythematous patches
on flexor surfaces (inside of elbows/knees)

itchiness can lead to scratching, causing lichenification (thickening of skin)

173
Q

what is diagnostic criteria for eczema

A

itchy skin condition in last 12 months

+ at least 3 of:

dermatitis in flexor surfaces (inside of elbows/knees)
PMH of flexural dermatitis
PMH of dry skin
PMH/FH of atopy
onset before 2yr

174
Q

what is use of CDQLI score on eczema

A

determine impact eczema is having on child’s QOL

175
Q

what is atopy

A

abnormally exaggerated IgE response to allergen exposure

pt at risk of: atopic eczema, allergic rhinitis, asthma

176
Q

what triggers eczema

A

defects in skin barrier allow entry for irritants, microbes and allergens

177
Q

how do irritant + allergen differ

A

irritant = causes non-specific skin response to direct chemical skin change
temp, sun, clothes, stress, intercurrent infection

allergen = causes delayed hypersensitivity reaction (type 4), involving immune response (T cell, cytokines)
food, animal fur/wool, dust

178
Q

what during pregnancy + breast-feeding can prevent eczema

A

pregnancy - nothing (diet restriction doesn’t work)

breast-feeding - continue for at least 4 (ideally 6) months
prevents atopic eczema, cow milk allergen, wheezing in early childhood

179
Q

what to do if infant has cow-milk allergy

A

contact dietitian
dairy-free diet + milk substitute

180
Q

how is eczema managed

A

treat all atopic problems - eczema, allergic rhinitis, asthma
patient education - identify triggers (food diary)

aim to manage flares
1) emollients (or bath oils)
2) topical immunomodulators - steroids, calcinuerin inibitori
3) antihistamines

if severe eczema:
4) photodynamic therapy
5) systemic immunomodulators

181
Q

what are emollients

A

first line treatment of eczema - aim for as thick/greasy as tolerated

thin = cream, thick = ointment
50:50 LP (liquid paraffin) - v.greasy
(also flammable so pt shouldn’t smoke)

educate pt to use in large amounts often - use everyday even when eczema not present

emollients are soap substitute
(also used instead of shampoo for children <1yr)

182
Q

what is 2nd line management for eczema

A

1st line = emollient

2nd line = topical immunomodulator - steroids, calcineurin inhibitors

aim to use weak steroid for short time
hydrocortisone (mild) -> mordasone -> eumovate -> betnovate -> dermovate (v.potent)

topical hydrocortisone 1-2.5%
applied OD/BD
use sparingly on active areas or areas that were active in past 48hr

continue for 48hr after symptoms subsidise

if steroids ineffective, then use calcineurin inhibitors

183
Q

what is the strongest steroid used for eczema on face

A

mordasone
(only hydrocortisone 1-2.5% or mordasone used for face eczema)

184
Q

what are eczema complications

A

eczema herpeticum

opportunistic bacterial skin infection - usually staph aureus (causes impetigo)

185
Q

what is eczema herpeticum

A

dermatological emergency
due to vesicular eruption of HSV (or VZV)

treat by stopping steroids
start aciclovir

(if periorbital involvement - needs ophthalmology, incase dendritic ulcers)

186
Q

how do atopic + seborrheic eczema differ

A

atopic = looks dry/inflammed
affects flexor surfaces (inner elbows/knees)
involves pruritic, irritability, sleepless

seborrheic = looks greasy/flaky
affects oily areas (scalp, face, chest, skin folds)
earlier onset - wks after birth
milder (not itchy) - so treat with emollients + mild steroid

187
Q

what is impetigo

A

superficial bacterial skin infection
mainly from staph aureus (also strep pyogenes)

presents with ‘golden crust’
weeping, pustules, fever, malaise

188
Q

how is impetigo diagnosed + managed

A

impetigo diagnosis with swab
treat with antibiotics - flucloxacillin

(steroids + antiseptics for infected eczema)

189
Q

where is infant seborrheic dermatitis on body

A

scalp - cradle cap
flexures, nappy area

190
Q

what is urticaria/hives/wheals

A

small itchy/pruritic lumps on skin with patchy erythematous rash

associated angioedema + skin flushing

191
Q

what causes acute + chronic urticaria

A

acute (<6wk duration) - due to allergic reaction
drugs (penicillin, salicylate), infection (Hep A/B/C, HSV, EBV, strep)
contrast, latex, food

chronic (recurrent for 6+ wk) - due to autoimmune reaction
autoimmune, idiopathic/spontaneous, pressure, cold, sun

192
Q

what is pathophysiology of urticaria

A

due to histamine + pro-inflammatory cytokines release
from mast cells and basophils in upper dermis

causes vasodilation -> localised swelling (angioedema) and marked itching (pruritus)

193
Q

what is angioedema

A

fluid moving into peripheral tissue
in deep dermis and subcutaneous layer

194
Q

is bradykinin involved in urticaria

A

NO

bradykinin related angioedema is not associated with urticaria or pruritus

195
Q

what type of urticaria does not involve itching

A

hereditary angioedema = swelling but no itch
low C4 as c1-esterase deficiency

196
Q

what are involved in urticarial vasculitis

A

ANA
C3, C4
cryoglobulins

197
Q

how is urticaria managed

A

antihistamines (esp fexofenadine for chronic urticaria)

if severe flare, short-term oral steroids

if v.severe, consider: montelukast, omalizumab (monoclonal Ab against IgE), cyclosporin

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