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
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
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
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
4
Q
what measure indicates fracture risk
A
bone mineral density
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
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
7
Q
what imaging is done for spinal osteoporosis
A
x-ray spine
DEXA, MRI, isotope bone scan
do DEXA if FRAX score intermediate
8
Q
when is DEXA not done
A
pt had vertebral fracture
9
Q
when is FRAX not done
A
pt over 50yr with fragility fracture
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)
11
Q
when are bisphosphonates contraindicated
A
renal impairment if eGFR <30l/min
12
Q
what are SE of bisphosphonate
A
GORD, oesophageal erosion
atypical fracture
osteonecrosis of jaw + external auditory canal
13
Q
how are bisphosphonate taken
A
orally
on empty stomach with water
pt sit upright for 30min before moving/eating
14
Q
what is denosumab
A
monoclonal Ab that targets RANK-ligand
reducing formation/function of osteoclasts
suitable in renal impairment
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
16
Q
what type of disease is gout
A
crystal arthropathy - associated with chronically high urate levels
inflammatory rheumatic disease
mono-arthritis
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)
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
19
Q
where are gouty tophi
A
hands, elbows, ears
due to subcutaneous uric acid deposits
20
Q
what characterises gout
A
painful mono-arthritis
with recurrent flares of joint inflammation
21
Q
what are RF for gout
A
obese, men
alcohol
high purine diet - meat, coffee
FH
PMH - CVD, kidney disease
DH - diuretic
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
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
24
what does joint aspiration of gout show
needle shaped, monosodium urate crystals
with negative befringement (in polarised light)
no bacteria
25
what would gout x-ray show
no loss of joint space
lytic bone lesions
punched out erosions - sclerotic borders and overhanging edges
26
what is acute gouty arthritis + how is it treated
acute monoarticular pain (mostly at night)
with heat + erythema at affected joint
treat with NSAID
27
how is uric acid eliminated from body
most filtered by glomeruli
from filtered urate, most absorbed along nephron (mainly at proximal tubule)
only 10% is excreted in urine
28
how is gout acutely managed
1) NSAID with PPI (for gastroprotection)
2) colchicine
3) oral steroid (prednisolone)
29
how is gout managed long-term
lifestyle changes:
exercise, reduce weight
better diet (no coffee, less meat)
reduce alcohol
xanthine oxidase inhibitors + uricosuric agents to reduce urate levels
30
what is allopurinol
xanthine oxidase inhibitor
to lower uric acid levels
another XO inhibitor = feboxustat
metabolised in liver, so can be used for renal impairment
31
when is colchicine used for acute gout
pt renal impaired, significant heart disease
32
how does gout + pseudo gout (chonedrocalcinosis/CPPD) differ
both crystal arthropathies causing mono-arthritis
gout = monosodium urate crystals, needle shaped, negative befrignement
pseudo gout = calcium pyrophosphate crystals, rod shaped, positive befringement
33
how does CPPD (calcium pyrophosphate deposition disease) present
mostly asymptomatic - picked up incidentally on x-ray
typical Q on psuedogout:
65yr+ with rapid onset hot, swollen, stiff, painful knee
34
what is CPPD associated with
pseudo gout associated with:
haemochromatosis
hyperPTH, familial hypocalciuric hyperCa, hypophosphatasia
hypoMg
35
how is pseudo gout investigated
first exclude septic arthritis, so do joint aspiration + ABx
36
what x-ray changes are seen with CPPD
similar to osteoarthritis:
loss of joint space
osteophytes
subchondral sclerosis + cysts
37
how is pseudo gout managed
if asymptomatic + incidental finding on X-ray = don't treat
if symptomatic:
1) NSAID + PPI
2) colchicine
3) intra-articular steroids
38
what are 2 types of allergic reaction
type 1 allergic/hypersensitivity (IgE) = immediate, 1-2 days after
type 4 hypersensitivity (T-cell) = 7-14 days after
39
how is skin type classified
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
40
how do wood light + dermascope differ
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
41
when is wood light + dermatoscope used
wood light = vitiligo, maelessezia yeast
vitiligo - depigmented areas enhanced
malessezia yeast - yellow/orange fluorescence
dermatoscope = lesions
42
what is flat area of colour change
if <5mm, macule
if 5+ mm, patch
43
what is solid elevated lesion
if <5mm, papule
if 5+ mm, nodule or plaque (if scaly)
44
what is circumscribed elevated lesion containing fluid
if <5mm, vesicle
if 5+ mm, bulla
if it contains pus, pustule
45
how do erosion + ulcer differ
erosion = shallow, affecting epidermis only
ulcer = loss of epidermis + part of dermis, leaving depressed moist lesion
46
what is cyst
sac in dermis
contains semisolid/liquid material
47
how do scaly + lichenificated surfaces differ
scaly = heaping of stratum corneum or keratin
lichenificated = from scratching/rubbing, epidermis thickens
48
what is BCC
basal cell carcinoma - most common skin cancer
affects stratum basal of epidermis
slow growing
locally invasive - unlikely to metastasise
49
what is main RF for BCC
longterm UV radiation
(can develop into a scar)
UV exposure mutates DNA - esp p53 tumour suppressor gene9q22
50
how does BCC present
on sun-exposed areas - head, neck
small slow-growing lesions
raised pearly edges
telangiectasia
if symptomatic - pain, bleeding, ulcer
51
what are BCC subtypes
nodular (most common)
superficial
morphoeic - uncommon, prone to recurrence
basosquamous - mixed BCC and SCC with infiltrative growth pattern, so more aggressive
52
how is BCC diagnosed
clinical diagnosis
confirm with excision biopsy
only do imaging if evidence of invasion
53
what is high-risk BCC
young pt <25yr, immunocompromised
recurrent lesions
lesion on nose, lip, ear, around eyes
poorly defined margin
54
how is BCC managed
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
55
when is topical/non-surgical management done for BCC
topical management is destructive technique
used for superficial BCC
56
what is gorlin-goltz syndrome
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
57
what is SCC
squamous cell carcinoma - 2nd most common cancer
affects keratinocytes in supra-basal epidermal layer
can metastasise
58
what are premalignant lesions for SCC
bowen disease (SCC in situ - confined to epidermis only)
actinic keratoses, keratin horns
59
what is peak incidence for SCC
>40yr, male
common in fair skin
commonest skin cancer for black/asian
60
what are RF for SCC
prolonged UV exposure (excessive sunbed use)
smoking
immunosuppressed - leukemia/lymphoma, renal transplant
environmental carcinogen - arsenic, aromatic hydrocarbon, insecticide, herbicide
HPV, genodermatoses (xeroderma pigmentosum), HIV
61
how does SCC present
on scalp, face, hands (sun-exposed sites)
fast growth rate
friable/ulcerated nodule, surface crusting
62
how does SCC look in dermascope
white circles/structureless areas
looped blood vessels
central keratin plug
63
how is SCC diagnosed
clinical diagnosis + confirm with biopsy
excision biopsy if small + well-demarcated
incisional biopsy if large + peripheral margins
64
what are features of high-risk SCC
2+cm diameter, 4+mm depth
head/neck affected - ear as high recurrence, lip as likely metastasis
poorly differentiated
perineurial + lymphovascular invasion
immunosuppressed
65
how is SCC managed
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
66
what is Bowen disease
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
67
how is Bowen disease managed
cryotherapy
curette, cautage
surgical excision
topical 5-FU imiquinod
radiotherapy
68
what is melanoma
malignant tumour of melanocytes (pigment producing cells)
from stratum basale of epidermis
metastasises early
69
what are RF of melanoma
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
70
where are melanomas
male - trunk
female - lower limb
most melanomas develop de novo on normal skin
71
how does melanoma present
early on asymptomatic
changes in existing mole - if locally advanced, bleeds/ulcers
ABCDE
asymmetry
border irregular
colour changes/uneven
diameter 6+ mm
evolving lesion
72
how is melanoma diagnosed
excision biopsy - needs 2mm peripheral margin with subcutaneous fat at deep margin
73
what are major + minor signs of melanoma
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
74
what are 5 melanoma subtypes
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
75
what prevention advice for melanoma
stay in shade 11am-3pm
wear SPF 30+ and protective clothing (hat, sunglasses)
avoid sunbed
76
what stage of melanoma does cancer spread to other organs
stages 1/2 are localised to skin
stage 3 spread to lymph nodes
stage 4 spread to other organs
77
how is melanoma managed
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)
78
what determines peripheral margin for WLE in melanoma
breslow thickness of melanoma - thicker it is, larger peripheral margin + deep margin down to deep fascia
79
when to do sentinel lymph node biopsy for melanoma
if breslow thickness 0.8+ mm
if SLNB confirms lymph node metastasis, treat with completion lymphadenectomy
80
when is targeted therapy done for melanoma
if BRAF mutation
81
what causes solar lentigines
solar lentiggine = harmless patch of darkened skin
very common in <40yr
UV radiation causes local proliferation of melanocytes
so melanin accumulates within keratinocytes
82
what lesion has waxy, stuck on appearance
seborrheic keratosis
(can look pigmented, may have horn cyst)
benign lesion - sign of skin ageing
83
what is leser-trelat sign
rapid onset of multiple seborrheic keratoses - rapid increase in number + size
if young pt, indicates paraneoplastic process so investigate for cancer
84
what cancers are associated with leser treat sign
leser-trelat = rapid onset of many seborrheic keratoses
adenocarcinoma of colon/stomach
SCC
lymphoma, leukaemia
85
why should multiple dysplastic naevi be monitored
indicate pt's predisposition to melanoma - esp if FH
but melanomas usually develop de novo
86
what is actinic keratosis
sun-induced scaly lesions that can become malignant
risk of transforming to SCC increases if:
with time + more lesions
87
how is actinic keratosis managed
cryotherapy
topicals - 5-FU, imiquimod
photodynamic therapy, laser
88
how do punch, incisional, excision biopsy differ
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
what is vasculitis
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
what are eg of different types of primary vasculitis
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
when are purpura/petechiae seen in vasculitis
small/medium cell arteritis - since they are more superficial
92
what is polymyalgia rheumatica
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
how does PMR (poly myalgia rheumatic) present
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
what is diagnostic criteria for PMR
age 50yr+
duration 2wk+
bilateral shoulder/pelvic girdle ache
morning stiffness 45min+
acute phase response - raised ESR/CRP
confirm +ve response to prednisolone
95
is muscle strength impaired in PMR
NO
but muscle pain makes testing difficult + disuse atrophy can occur
96
what are important differentials to exclude for PMR diagnosis
GCA - very high ESR/CRP, needs a higher dose of steroids
active infection/cancer - steroid treatment could mask symptoms, delaying diagnosis
97
before starting steroid treatment, what tests need to be done
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
how is PMR managed
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
how do CRP + ESR differ
CRP = acute inflammation
ESR = long-term
100
what precautions are taken for steroid therapy
taper steroid dose slowly - avoid addisonian crisis
sick day rules - increase steroids if pt unwell
bisphosphonates (+ Ca, VitD) - prevent osteoporosis
PPI - gastroprotection
101
what is PMR prognosis like
good
rapid/dramatic initial response to steroid - symptoms resolve in 1-3 days
treatment needed for 1-2yr
as relapse is common
102
what is GCA (giant cell arteritis)
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
how does GCA present
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
what vision disturbances occur in GCA
usually monocular
transient vision loss - amourosis fugax
partial field defect
105
how is GCA diagnosed
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
why does temporal artery biopsy need to be 1cm length or more
GCA involves skip lesions, so patchy inflammation occurs
biopsy shows immune cell infiltration into smooth muscle cell layer - as GCA is pan-arteritis
107
how is GCA managed
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
how is GCA treatment monitored
checking ESR/CRP
109
if pt at risk of glucocorticoid toxicity or have relapsed, what treatment is given for their GCA
steroid-sparing agent = methotrexate, tocilizumab (monoclonal Ab to IL-6)
110
what is takayasu arteritis
also called pulseless disease
granulomatous arteritis inflaming aorta + primary branches
affects young women (10-40yr), asian
111
how does takayasu arteritis present
initially constitutional then vascular damage symptoms
systemic symptoms (FLAW)
carotidynia (tender carotid artery)
reduced/absent/weak peripheral pulse
limb claudication
angina, abdo pain
112
what is ACR diagnostic criteria for takayasu arteritis
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
what investigations are done for takayasu arteritis
incidental finding on CT chest
then do MRI angio to see which arteries are stenosed/occluded
raised ESR/CRP
114
how is takayasu arteritis managed
high dose steroids
(with bisphosphonate/Ca + PPI)
if steroid-resistant = methotrexate
angioplasty can be done for symptomatic relief
115
what organ dysfunction can occur from vasculitis
systemic symptoms - FLAW
skin - rash
NS - mono/poly-neuropathy
kidney - glomerulonephritis
muscle - myalgia
joint - arthritis
lung - infiltrate, nodule
bowel - ischemia/infarction
116
what is polyarteritis nodosa
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
are ANCA antibodies present in polyarteritis nodosa
NO
118
how does polyarteritis nodosa present
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
what are 2 types of ANCA antibodies + how do they differ
cANCA - stains cytoplasms, directed against PR3 antigen
pANCA - stains perinuclear region, directed against MPO antigen
120
what are eg of ANCA-associated vasculitis
inflammation of small vessels
causes pulmonary haemorrhage, glomerulonephritis
microscopic polyangiitis
Wegner - granulomatosis with polyangiitis
churg-strauss - eosinophilic granulomatosis with polyangiitis
121
what is microscopic polyangiitis
necrotising vasculitis of small/medium arteries
p-ANCA +ve, affects MPO antigen
122
123
what is Werner (granulomatosis with polyangiitis)
necrotising vasculitis of small arteries
presents with saddle-shaped nose as orbital/nasal bridge collapse
sinusitis, epistaxis
cANCA +ve, affects PR3 antigen
124
how does wegner present
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
how to diagnose Wegner
blood test - cANCA +ve (PR3)
tissue histology
126
what is churg-strauss
eosinophilic/allergic granulomatosis with polyangiitis
associated with allergy, asthma
pANCA +ve (MPO antigen)
127
how does churg-strauss present
allergy, late-onset asthma
mono/poly-neuropathy
pulmonary infiltrates
sinusitis, nasal polyposis
skin rash
128
how are ANCA-associated vasculitis managed
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
what is anti-GBM (good pasture) disease
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
what is bechet disease
systemic vasculitis affecting arteries + veins
presents with recurrent oral/genital ulcers
associated with HLA-B51 antigen
common in Japan, turkey, North Africa, Iran
131
how does behcet disease present
recurrent oral/genital ulcers (3x a year)
painful erosions, leaving 'red halo'
erythema nodosum, aceniform
uveitis (eyes), retinal thrombosis
arthritis
132
how is behcet disease diagnosed
pathergy test:
sterile needle pricks forearm, wait 24-48hr to see if non-hypersensitivity changes (erythema, induration/thickening)
associated with HLA-B51 antigen
133
what is RA - rheumatoid arthritis
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
how does RA present
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
which joints are affected in RA
symmetrical distal polyarthritis
MCP
PIP, wrist, MTP
136
what is palindromic rheumatism
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
what are extra-articular manifestations of RA
systemic symptoms - FLAW, myalgia
felty syndrome - RA, neutropenia, splenomegaly
sjorgen syndrome - dry mouth/eye
eye: scleritis, episcleritis, keratitis
138
what are rheumatoid nodules
firm, painless lumps under the skin
seen on elbows, fingers
139
how is RA diagnosed
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
what 2 antibodies are checked in RA
RF - autoantibody (IgM) that targets Fc region of IgG immunoglobulins, triggering systemic inflammation
anti-CCP - more sensitive/specific than RF
141
what x-ray changes are seen in RA
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
what scoring systems are used for RA
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
how is RA managed
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
how is palindromic rheumatism managed
hydroxychloroquine
145
how is RA treatment monitored
check CRP + DAS28 score
146
which DMARD are teratogenic
methotrexate, leflunomide
(hydroxychloroquine + sulfasalazine are safe in pregnancy)
147
how is RA affected in pregnancy
pregnancy can improve RA symptoms
but if flare-up give: hydroxychloroquine or sulfasalazine
148
what is methotrexate __
MOA
typical dose
SE
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
what is sulfasalazine __
MOA
typical dose
SE
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
what is leflunomide __
MOA
typical dose
SE
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
what biologics are used for RA
anti-TNF = adalimumab, infliximab, etanercept
anti-CD20 = rituximab
anti-IL6 = tocilizumab
JAK inhibitor = tofacitinib, baricitinib
T-cell co-stimulation inhibitor = abatecept
152
what diseases are associated with tocilizumab + rituximab
both are biologics used for RA
tocilizumab (anti-IL6) - transient dyslipidemia
rituximab (anti-CD20) - PML (progressive multifocal leukoencephalopathy)
153
what are SE of tyrosine-kinase inhibitors
TKI are specific binding but have wide-reaching effects
SE: dyslipidaemia, thromboembolic disease, increased infection (esp herpes zoster)
[nausea, skin reactions]
154
what screening has to be done before using tyrosine-kinase inhibitors
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
how do RA + ankylosing spondylitis differ
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
what are the types of seronegative arthritis
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
how do RA + seronegative arthises differ
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
what extra-articular features are associated with ___
psoriatic arthritis
enteropathic arthritis
ankylosing spondylitis
reactive arthritis
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
which bacteria causes reactive arthritis
chlaymdia
gonorrhoea would cause septic arthritis instead
160
what is reiter's triad for reactive arthritis
arthritis, urethritis, conjunctivitis
161
what investigations are done for reactive arthritis
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
how is reactive arthritis managed
treat underlying cause
most resolve rapidly after treatment
NSAID
intr-articular or oral steroids
if HLA-B27 +ve, worse prognosis
163
what investigations are done if suspecting AS
schober test - shows restricted lumbar movement
also do x-ray to check spine/sacrum
MRI to check for bone marrow oedema
164
what x-ray changes are seen in AS
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
what features indicate inflammatory arthritis
insidious onset
chronic 3+ months
morning stiffness 45+ min, disturbed sleep (esp 2nd half of night)
pain improves with exercise
166
what is diagnostic criteria for AS
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
how is AS managed
physiotherapy, smoking cessation
1) NSAID
2) try another NSAID
3) biologic - anti-TNF (adalimumab)
168
after NSAID are trialled, what medication is used for AS
first trial 2 different NSAID
then try biologic (anti-TNF)
DMARD not used as they are for peripheral disease - not axial
169
what are 5 patterns of psoriatic arthritis
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
how is psoriatic arthritis managed
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
what is eczema
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
how does eczema present
scaly, itchy, dry, erythematous patches
on flexor surfaces (inside of elbows/knees)
itchiness can lead to scratching, causing lichenification (thickening of skin)
173
what is diagnostic criteria for eczema
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
what is use of CDQLI score on eczema
determine impact eczema is having on child's QOL
175
what is atopy
abnormally exaggerated IgE response to allergen exposure
pt at risk of: atopic eczema, allergic rhinitis, asthma
176
what triggers eczema
defects in skin barrier allow entry for irritants, microbes and allergens
177
how do irritant + allergen differ
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
what during pregnancy + breast-feeding can prevent eczema
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
what to do if infant has cow-milk allergy
contact dietitian
dairy-free diet + milk substitute
180
how is eczema managed
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
what are emollients
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
what is 2nd line management for eczema
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
what is the strongest steroid used for eczema on face
mordasone
(only hydrocortisone 1-2.5% or mordasone used for face eczema)
184
what are eczema complications
eczema herpeticum
opportunistic bacterial skin infection - usually staph aureus (causes impetigo)
185
what is eczema herpeticum
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
how do atopic + seborrheic eczema differ
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
what is impetigo
superficial bacterial skin infection
mainly from staph aureus (also strep pyogenes)
presents with 'golden crust'
weeping, pustules, fever, malaise
188
how is impetigo diagnosed + managed
impetigo diagnosis with swab
treat with antibiotics - flucloxacillin
(steroids + antiseptics for infected eczema)
189
where is infant seborrheic dermatitis on body
scalp - cradle cap
flexures, nappy area
190
what is urticaria/hives/wheals
small itchy/pruritic lumps on skin with patchy erythematous rash
associated angioedema + skin flushing
191
what causes acute + chronic urticaria
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
what is pathophysiology of urticaria
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
what is angioedema
fluid moving into peripheral tissue
in deep dermis and subcutaneous layer
194
is bradykinin involved in urticaria
NO
bradykinin related angioedema is not associated with urticaria or pruritus
195
what type of urticaria does not involve itching
hereditary angioedema = swelling but no itch
low C4 as c1-esterase deficiency
196
what are involved in urticarial vasculitis
ANA
C3, C4
cryoglobulins
197
how is urticaria managed
antihistamines (esp fexofenadine for chronic urticaria)
if severe flare, short-term oral steroids
if v.severe, consider: montelukast, omalizumab (monoclonal Ab against IgE), cyclosporin
