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phase 2a > Rheumatology & MSK > Flashcards

Rheumatology & MSK Flashcards

1
Q

what is the most common arthritis?

A

osteoarthritis

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2
Q

who gets osteoarthritis?

A 
older
females
overweight 
excessive joint use 
trauma/malalignment etc
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3
Q

how do you end up with bony changes in osteoarthritis?

A

mechanical forces –> cartilege lost
cartilege loss = cytokines - TNFa, IL-1, NO
cytokines = cartilege cannot repair properly
loss of cartilege = bone rubbing on bone
reactive changes in bone, it is not designed to rub on bone

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4
Q

reactive changes you see in the bone in osteoarthritis?

A 
loss of joint space 
osteophytes 
sclerosis
subchondral cysts  
synovial hypertrophy
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5
Q

what is sclerosis in relation to arthritis?

A

thickening and widening of the bone at the joint

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6
Q

what is an osteophyte?

A

an area of bone which has been reactively laid down in the wrong place

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7
Q

what joints might be affected in osteoarthritis? (give 5)

A 
those that are used a lot! 
knees
hips
sacro ileac
cervical spine 
wrist
carpmetacarpal - base of thumb 
DIP
PIP
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8
Q

how is the pain different in osteooarthritis vs inflammatory arthritis?

A

osteo - morning stiffness only lasting up to 15 mins, generally worsens throughout day
RA - - stiff for 30+ mins, better with use

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9
Q

apart from pain, give 3 other clinical presentations of osteoarthritis?

A 
effusion 
crepitus 
pt reports the joint 'gives way'
tender to palpation 
deformity 
herbedens/bouchards nodes
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10
Q

what are herbedens and bouchards nodes?

A 
soft tissue swellings on the fingers 
seen in the early stages of osteoarthritis
herbedens = DIP 
bouchards = PIP 
(HD AND BP)
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11
Q

when would arthroscopy be indicated?

A

knee ‘locking’ indicates a loose body which can be removed (arthroscopy)

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12
Q

4 x ray changes typical of osteoarthritis?

A 
LOSS 
L - loss of joint space 
O - osteophytes 
S - subchondral sclerosis 
S - subchondral cysts
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13
Q

some management options of osteoarthritis?

A 
physio
weight loss 
occupational therapy eg footwear, walking aid 
nsaid
opioid 
amytriptiline 
topical capsaicin 
steroid injection
hydroxychloroquine
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14
Q

what produces synovial fluid?

A

the synovial membrane

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15
Q

typical patient with RA?

A

post menpausal woman
smoker
past infection

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16
Q

what is the pathophysiology of RA?

A

a reaction to self antigens eg type II collagen, vimentin
= inflammation at the synovial membrane
= damage to soft tissue and cartilege
= damage to bone

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17
Q

what joints are affected in RA?

A

small joints
symmetrical
hands, wrists & feet
not DIP or spine

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18
Q

if you were examining the hands of someone with RA give 5 things you might expect to see?

A 
DIP not affected 
hurts to squeeze the joints
joints are warm 
ulnar deviation 
cannot make a fist 
z thumb
swan neck deformity
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19
Q

are there any systemic features of RA?

A 
myalgia, malaise and low grade fever, if the cytokines go around the body
Rheumatoid nodules - skin 
eye inflammation eg scleritis 
ihd/pericarditis 
lung inflam
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20
Q

3 blood tests you could do if you suspect RA?

A

ESR/CRP
rheumatoid factor - low sensitivity and specificity
anti-CCP (anti- cyclic citrillunated peptide) - good specificity, sensitive enough to highlight the most severe disease

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21
Q

some bony changes you might see on x ray in RA?

A

you dont see bony changes on x ray immediately!
soft tissue swelling
periarticular ostoepenia (low bone density)
loss of joint space
subluxation
erosion

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22
Q

3 drugs you could give in RA?

A 
Methotrexate 
sulphasalazine 
hydroxychloroquine 
infliximab 
short term NSAID
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23
Q

who gets gout?

A 
men over 40 - esp diabetes, overweight, hypertension 
purine rich diet 
renal impairment 
IHD
diuretics
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24
Q

what enzyme converts hypoxanthine to xanthine and xanthine to uric acid?

A

xanthine oxidase

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25
Q

what happens when urate crystals are deposited in the joint?

A

they activate phagocytes –> inflammation –> joint pain (gout)

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26
Q

give 2 causes of too much uric acid production, other than diet?

A

increased cell turnover, as in:

  • myeloproliferative disorders
  • psoriasis
  • tumour lysis syndrome
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27
Q

what drugs can impair uric acid excretion?

A

tacrolimus
aspirin
thiazides

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28
Q

which joint is most commonly affected in gout?

A

1st MTPJ (metatarsalphalyngeal joint) - big toe

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29
Q

how does gout present?

A 
usually monoarticular - big toe/foot/ankle/knee
sudden onset 
1-3 weeks
intense pain esp at night
heat, swelling, redness 
stiffness
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30
Q

what do you see in the joint aspirate in gout?

A

needle shaped crystals

negatively birefringent

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31
Q

what do you see on an x ray in gout, how can you differentiate it from other arthritis?

A

joint effusion
punched out lesions

no loss of joint space
no periarticular osteopenia

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32
Q

how do you manage acute gout?

A

nsaids, colchicine
intrarticular steroid inj
rest and elevate
dont start allopurinol until the acute stage has finished

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33
Q

what drug is first line for maintaining remission of gout?
what is the mechanism of action?
2 side effects?

A

allopurinol
xanthine oxidase inhibitor, stops the conversion of purines to uric acid
rash, headache, hypersensitivity

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34
Q

what is the second line treatment for gout, when should it not be used?

A

febuxostat

not for renal or hepatic impairment

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35
Q

what foods have high purines?

A 
meat
seafood
alcohol
beans/lentils
mushrooms 
carbonated drinks / fructose
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36
Q

3 risk factors for pseudogout?

A 
osteoarthritis
age
haemachromotosis 
high PTH
low phosphate
low magnesium 
hypothyroidism
acromegaly
illness
surgery
trauma
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37
Q

pseudogout is caused by crystals of ?

A

calcium pyrophosphate

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38
Q

what joints does pseudogout affect?

A

larger - knee/wrist/elbow/shoulder

symmetrical, if chronic

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39
Q

what kind of crystals do you see in the joint aspirate in pseudogout?

A

rhomboid shaped

positively birefringent

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40
Q

what might you see on the x ray of pseudogout?

A

chondrocalcinosis
calcification of cartilege
(neither is specific)

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41
Q

what is the management for pseudogout?

A

aspiration to relieve pain
NSAID/colchicine/prednisolone to relieve pain
hydroxychloroquine/methotrexate may help

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42
Q

some infections that commonly trigger reactive arthritis?

A 
salmonella
shigella
yersinia enterocolitica 
chlamydia 
n. gonorrhoea (but more commonly causes gonococcal arthritis which is different)
(STI or GI)
e. coli (GI symptoms)
EBV - rarely
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43
Q

what is the presentation of reactive arthritis?

A

‘can’t see, pee or climb a tree’
conjunctivitis
sterile urethritis
arthritis

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44
Q

what is the arthritis like in reactive arthritis?

A

acute
asymmetrical
lower leg

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45
Q

some other things (apart from conjunctivitis, urethritis and arthritis) associated with reactive arthritis?

A 
iritis
keratoderma blenorrhagica - red pustules and brown scaly feet
circinate balanitis 
enthesitis
mouth ulcers
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46
Q

4 investigations you would do for ?reactive arthritis?

A

joint aspiration - to exclude septic arthritis and gout
serology/stool culture/STI swab - to find infectious cause
X ray - enthesitis, periosteal reaction
CRP

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47
Q

Typical exam presentation for ankylosing spondylitis?

A

young male

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48
Q

what HLA is ankylosing spondylitis associated with?

A

hla b 27

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49
Q

explain the pathophysiology of ankylosing spondylitis?

A

inflammation in the anterior corners of the spine
fat is laid down
fat is replaced with bone (syndesmophites)
joint fusion
=stiffness

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50
Q

what joints does ankylosing spondylitis affect?

A

spine
sacroiliac
1-3 joints
asymetrical

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51
Q

what is the time course of ankylosing spondylitis?

A

at least 3 months

with flares/remitting

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52
Q

is there morning stiffness in ankylosing spondylitis?

A

yes

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53
Q

some presentations of ankylosing spondylitis? (4)

A 
lower back or buttock pain 
vertebral fractures 
enthesitis
dactylitis 
chest pain - costovertebral/costosternal joints 
eye inflammation 
kyphotic posture
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54
Q

what changes would you see on x ray in ankylosing spondylitis? (5)

A 
bamboo spine 
fusion of facet joints 
squaring of vertebral bodies 
ossification 
syndesmophites
subchondral sclerosis 
erosion
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55
Q

3 extra articular features of ankylosing spondylitis?

A 
anterior uveitis 
weight loss
fatigue 
anaemia 
pulmonary fibrosis 
aortitis
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56
Q

treatment for ankylosing spondylitis?

A

infliximab
Nsaids
steroids

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57
Q

osteomyelitis is?

A

infection of the bone

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58
Q

3 risk factors for osteomyelitis?

A 
inflammatory arthritis 
sickle cell
IVDU
immunocomp 
diabetes
prosthesis 
trauma
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59
Q

4 bacteria that commonly cause osteomyelitis?

A

staph aureus
pseudomonas aeruginosa
salmonella
TB

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60
Q

what bacteria is particularly associated with osteomyelitis in sickle cell?

A

salmonella

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61
Q

how might contigious spread come about?

A

from infectious soft tissue, eg an ulcer

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62
Q

what are some features of chronic osteomyelitis, why do they happen?

A

sequestrum
involcrums
because there is necrosis and the osteoblasts try to remodel

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63
Q

what types of bones are normally affected by haematogenous osteomyelitis?

A

long bones in children

vertebrae in adults

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64
Q

what is the clinical presentation of osteomyelitis?

A

rigor, sweats, malaise and fever
vertebral fractures
lesions/fractures take ages to heal
joint exudate - when infection has broken through the cortex

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65
Q

what is the gold standard investigation for osteomyelitis?

A

open bone biopsy - for culture and histology

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66
Q

what x ray changes would you see in osteomyelitis?

A 
cortical erosion
periosteal reaction
lucency
sclerosis 
sequestrae, involcrums
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67
Q

what can you see on mri and ct? - relating to rheumatology?

A

bone marrow inflammation

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68
Q

management for osteomyelitis? (3)

A

debridement
abx
analgaesia

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69
Q

2 differential diagnoses for osteomyelitis?

A 
cellulitis 
charcot 
avascular necrosis 
gout
fracture 
malignancy
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70
Q

what is septic arthritis?

A

infection of the joint

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71
Q

what bacteria commonly cause septic arthritis? (give 4)

A 
staph aureus
staph epidermis
strep A/B/pneumoniae 
n. gonoorhoea
pseudomonas 
e coli
TB
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72
Q

what is the most common bacteria in septic arthritis?

A

staph aureus

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73
Q

what bacteria is often associated with prosthetics in septic arthritis?

A

staph epidermis

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74
Q

pseudomonas septic arthritis is usually seen in who?

A

elderly
immunocomp
IVDU

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75
Q

what joints are most commonly affected by septic arthritis?

A

knee
hip
shoulder

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76
Q

presentation of septic arthritis?

A

hot, tender, red, swollen
very painful
limited range of movement
fever

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77
Q

3 investigations for septic arthritis?

A

arthrocentesis (joint aspiration) –> mc&s
blood culture
plain x ray

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78
Q

what investigation d you do if you suspect TB septic arthritis?

A

synovial biopsy

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79
Q

3 typical antibiotics for septic arthritis?

A

flucloxacillin
clindamycin
ciprofloxacin
vancomycin

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80
Q

how does gonococcal arthritis present?

A

fever, arthritis, tendonitis
multiple joints
maculopapular pustular rash on palms + soles

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81
Q

how would an infected prosthetic joint present?

A 
chronic low grade 
pain ever since it was done 
staph aureus/enterococci 
low esr, crp, normal wcc
diagnosis - joint aspirate 
arthropathy (remove and replace)
82
Q

the epidemiology of psoriatic arthritis?

A

10% pts with psoriasis
within 10yrs of getting psoriasis
typically middle aged

83
Q

3 main patterns of psoriatic arthritis?

A

symmetrical polyarthritis - hands, wrists, ankles, DIP - women
asymmetrical oligoarthritis - hands + feet
spondyloarthritis - spine - men

84
Q

is there morning stiffness in psoriatic arthritis?

A

yes

85
Q

extra articular features of psoriatic arthritis?

A 
psoriatic skin plaques 
pitting / onikolysis 
enthysitis 
conjuntivitis/uveitis 
aortitis
86
Q

3 x ray features of psoriatic arthritis?

A

pencil in cup - due to central erosion of bone
osteolysis
fusion

soft tissue swelling
periostitis

87
Q

what is ustekumab?

A

il-12, il-23 inhibitor biologic - used for inflam arthritis

88
Q

what is the epidemiology of lupus?

A

women
15-30
african-carribean or asian

89
Q

what genetic associations is there in lupus?

A

HLA DR2
HLA DR 3
complement C4 allele

90
Q

what are the antibodies against in lupus?

A

ANA - anti nuclear antibody
anti ds-DNA

also sometimes phospholipids etc

91
Q

what kind of hypersensitivity reaction is lupus? how is it mediated?

A

type 3 hypersensitivity

T, B, cells, ytokines and complement

92
Q

some clinical presentations (5) of lupus?

A

malar erythromatous rash - ‘butterfly’
muscle & joint pain - arthritis is symmetrical and affects the tendons and ligaments more than the bone
fatigue
fever
discoid/photosensitivity rash/lupus profundus
alopecia
raynauds
nephritis
pericarditis
headache – seizure – mononeuropathy – psychosis
autoimmune haemolytic anaemia

93
Q

what tests would you do for lupus?

A

ANA - non specific but negatively predictive
anti DS DNA - more specific
urinalysis for asymptomatic proteinuria
complement (low)
ESR high, CRP normal - in managed lupus. In a flare, CRP is also high

94
Q

treatment of lupus? (5)

A 
hydroxychloroquine 
methotrexate 
rituximab 
NSAIDs/steroids for short term 
warfarin - because antiphospholipid syndrome = greater risk of clotting 
manage triggers eg sunlight
95
Q

what is osteoporosis?

A

low bone density

+ architectural deficits in bone

96
Q

5 risk factors for osteoporosis?

A 
inflam arthritis / connective tissue dis
IBD 
high PTH 
cushings 
low oestrogen/testosterone (low bodyweight/athlete/post menopausal)
reduced skeletal loading 
fractures 
family history 
smoking/alcohol
renal/liver failure
97
Q

what is bone strength determined by?

A

bone mineral density (at its peak and the rate of loss)
size
quality - architecture/turnover/mineralisation

98
Q

how does menopause affect osteoporosis?

A

oestrogen is supposed to restrict bone turnover
with oestrogen gone there is more bone turnover
cancellous bone is particularly affected

99
Q

why do bones weaken with age? (what part of the bone is affected?)

A

there is a reduction in trabecular thickness and the number of trabeculae decrease

100
Q

what system is used to predict the risk off osteoporotic fracture? what things does it consider?

A

FRAX

bmi, age, smoking, drugs, medical history

101
Q

what is a DEXA scan?

A

dual energy x ray absorptiometry
measures bone mineral density
at most common fracture sites - hip, lumbar spine, distal radius
t score - how different to a young healthy adult it is

102
Q

what is osteopenia?

A

weakening of the bone, but not as much as osteoporosis

103
Q

how does alendronate work?

A

-onate = bisphosphonate
inhibit farnesyl phosphatase
– > osteoclast apoptosis

104
Q

some treatments for osteoporosis? (4)

A

bisphosphonate eg alendronate
HRT
denosumab - RANK-L antibody - prevents osteoclast activation
teriparatide - PTH analogue, decreases bone resorption
raloxifene - stimulates oestrogen receptors on bone

105
Q

primary bone tumours originate from the _____ tissue

A

mesenchymal

106
Q

what is osteochondroma? 3 things to say

A

forms cartilege
benign
long bones of men under 25

107
Q

what is osteosarcoma? 4

A

bone forming (produce osteoid)
malignant
in the young
ALP will be raised, as osteoblast hyperactivity

108
Q

what is a giant cell bone tumour?

A

malignant or benign
osteoclasts
after trauma

109
Q

what is an osteoid osteoma?

A 
benign 
bone forming 
osteoblasts 
disorganised blood vessels and trabeculae
pain worse at night
110
Q

what is a ewing sarcoma?

A 
malignant 
bone marrow 
mesenchymal stem cells/neuroectodermal cells
very young 
lamellated bone
can compress nerves
lytic bone lesions, onion skinning
111
Q

chondrosarcoma?

A

forms cartilege
old people
chondrocytes

112
Q

osteoblastoma?

A

benign
bone forming
axial skeleton
can compress nerves

113
Q

what kind of anaemia in myeloma?

A

microcytic

114
Q

some presentations of a bone tumour? - 5

A

constant, non mechanical bone pain
swelling
fracture
b symptoms - fever, night sweats, malaise
avascular necrosis
symptoms of nerve compression - numbness/weakness

115
Q

serum ____ is high in secondary bone tumours

A

calcium

116
Q

____ level is a marker of osteoBLAST activity?

A

ALP

117
Q

do sclerotic or lytic lesions mean benign/malignant?

A 
sclerotic = healed or benign 
lytic = malignant
118
Q

what does the zone of transition tell you?

A

wide zone of transition - means there is poor definition of healthy | not healthy - so more likely to be malignant
narrow zone of transmission does not always mean benign, beware of myeloma esp in old people

119
Q

stages of the periosteal reaction and what they tell you about the tumour?

A
  1. callus - slow growing
  2. lamellated / onion skinning - slow growing but deffo a tumour - ewings
  3. sunburst spicules, codmans triangle – an aggressive tumour eg osteosarcoma
120
Q

how to tell on an x ray if something if a tumour of bone or cartilege?

A

cartilege: popcorn stippling / rings and arcs eg chondrosarcoma
bone: fluffy/trabecular

121
Q

what other conditions is fibromyalgia associated with?

A

functional eg IBS, chronic fatigue

inflammatory eg RA, SLE

122
Q

why may the pain signals be amplified in fibromyalgia?

A

high substance p

low 5ht

123
Q

allodynia is ___

A

pain in response to a non painful stimulus

124
Q

what is the pain like in fibromyalgia, what pattern of joints are affected?

A

widespread
symmetrical
above and below the waist
morning stiffness

125
Q

what do you need to remember to exclude in fibromyalgia?

A

osteoarthritis - probably not the same presentation
hypothyroidism
anything inflam - esr/crp
lupus
hypercalcaemia - would cause the same parasthesia

126
Q

management of fibromyalgia?

A

amitriptyline
duloxetine
lifestyle

127
Q

what is sjogrens syndrome?

A

secondary to RA
anti-Ro and anti-La antibodies (anti-La is more specific)
dry mucus membranes - eyes/mouth/vagina

128
Q

what is osteomalacia?

A

‘soft bone’ due to defective mineralisation - eg low calcium

129
Q

why is osteomalacia less common in the UK than it once was

A

used to be common because we have little sunlight in the UK

no foods are fortified with vit D

130
Q

3 risk factors for osteomalacia?

A 
lack of exposure to sunlight eg indoors, lots of clothing
dark skin
malabsorption eg IBD 
low dietary vit D, eg vegan 
kidney disease (they activate vit D)
131
Q

in the skin, ________ (made from ________) is metabolised to vit D3, in the presence of _______

A

previt D3
cholesterol
UVB

132
Q

vit D is important for bones because ________

A

it is needed for the absorption of calcium and phosphate from the GI tract

133
Q

in the ________, vit D3 is metabolised to _________

A

liver

calcidiol/25-hydroxyvitamin D

134
Q

in the _______, _________ is metabolised to __________ (calcitriol)

A

kidney
25 hydroxyvitamin D
1,25-dihydroxyvitamin D

135
Q

how does the body respond to low vit D?

A

there will be low calcium and phosphate (because vit D is needed to absorb them)
so PTH is released
PTH mobilises calcium from bones
= bone weakness –> osteomalacia

136
Q

what is ricketts?

A

osteomalacia in children, before the growth plates have fused

137
Q

4 presentations of osteomalacia?

A 
bone pain - esp hip/rib/pelvis/thigh/foot
fractures
muscle weakness/pain 
muscle spasm due to hypocalcaemia 
fatigue 
waddling gait - late sign
138
Q

first line investigation for osteomalacia?

A

serum 25-hydroxyvit D

139
Q

gold standard test for osteomalacia?

A

iliac bone biopsy with double tetracycline labelling

140
Q

in osteomalacia ALP will be ..

A

high

141
Q

what is the supplementary vitamin D (that you would give for osteomalacia) called?

A

cholecalciferol

142
Q

what is spondylolithesis & lumbar spondylosis?

A

spondylolithesis = vertebrae slips out of place

lumbar spondylosis = damage to the intervertebral disk

143
Q

what is facet joint syndrome?
how does it develop?
what position relieves it?

A

secondary to lumbar spondylosis
joints become misaligned – secondary osteoarthritis
worse when bending backwards

144
Q

what is fibrositic nodulosis?

A

tender nodules in the buttock

145
Q

when does the pain happen if it is caused by mechanical lower back pain?

A

sudden onset
worse in evening or on exercise
no morning stiffness

146
Q

when there is a visible muscle spasm in the lower back, the pain is generally better when..

A

sitting or lying

147
Q

when would you do a spinal x ray in lower back pain?

A 
when there is red flags eg 
nocturnal pain
leg pain
sphincter disturbance 
violent trauma
148
Q

a differential for lower back pain with no obvious cause or red flags?

A

polymyalgia rheumatica – muscle ache affecting the shoulders, arms, hips, neck
will have a raised ESR

149
Q

epidemiology of vasculitis?

A

50 +
associated with polymyalgia & RA
in general rare, GCA is the most common type

150
Q

aetiology of vasculitis? 3

A 
idiopathic 
autoimmune 
secondary to infection 
secondary to RA 
drugs
151
Q

in GCA which layers of the artery are affected? what is the net effect of this?

A

tunica media + interna

inflammation = narrowing of lumen

152
Q

what arteries are commonly affected in GCA?

A

common temporal (splits into frontal + temporal)
linguinal / facial
cilliary (to retina)

153
Q

4 presentations of cranial GCA?

A

abrupt temporal unilateral headache
changes to vision - amaurosis faux/diplopia/flashing lights
scalp tenderness
jaw claudication
visible dilation of temporal artery on side of face

154
Q

presentation of non temporal GCA? 3

A

polymyalgia
chronic low grade fever/malaise
limb claudication

155
Q

what is the gold standard investigation for cranial GCA?

what other imaging could you use?

A

temporal artery biopsy
(you see giant multinucleated cells)

duplex temporal artery ultrasound - halo sign + inflammation

156
Q

how could you image for systemic / non cranial vasculitis?

A

PET-CT using a glucose tracer

157
Q

what blood tests results would you see in vasculitis?

A

raised ESR
normocytic anaemia
thrombocytosis
raised ALP

158
Q

treatment for GCA

A

initially - iv prednisolone
wean off steroids after 1-2 yrs
methotrexate or tocilizumab if steroids not tolerated

159
Q

what size vessels does ANCA vasculitis affect?

A

small

160
Q

what are the two ANCA associated vasculitides?

A

p-ANCA: microscopic polyangiitis, eosinophillic, UC, primary schlerosing cholangitis
c-ANCA: granulomatosis with polyangiitis (aka wegeners)

161
Q

some general features of all vasculitis? 4

A 
pain 
purpura 
HTN 
neuropathy 
fever 
weight loss
162
Q

what is an intervertebral disk made up of?

A

outer fibrous : annulus fibrosis

inner gel like : nucleus propulsus. becomes dehydrated over time

163
Q

what part of the spine is usually affected by vertebral disk degeneration?

A

lumbar

164
Q

how does vertebral disk degeneration present?

A 
shooting pain 
sudden onset 
radiates to arms/legs 
muscle spasm 
tingling / parasthesia / numbnesss
165
Q

two types of surgery for prolapsed vertebral disks?

A

corpectomy

discectomy

166
Q

what is pagets disease of the bone?

A

excessive activity of osteoblasts and osteoclasts

167
Q

what is the epidemiology of pagets?

A

over 40
triggered by infection
genetic link

168
Q

3 phases of pagets disease?

A
  1. lytic: osteoclasts – low density bone
  2. lytic + blastic – patchy lysis and sclerosis
  3. blastic (latent) - osteoblasts lay down weak new bone
169
Q

clinical presentation of pagets?

A

generalised bone pain
fracture
deformity
hearing loss

170
Q

what do you see on x ray in pagets? 3

A

cotton wool skull
lysis (osteolysis circumscripta) + sclerosis
big bones
v shaped defects in long bones

171
Q

treatment for pagets?

A

bisphosphonate eg allendronate

172
Q

what do you need to give alongside bisphosphonates? how do they need to be taken?

A

calcium/vit D supplement
once a week
sitting upright
empty stomach

173
Q

3 drugs that can cause drug induced lupus?

A

isoniazid
procainamide
hydralazine

174
Q

what antibiotics interact with methotrexate to cause pancytopenia?

A

trimethoprim
because they are both anti folate drugs
(they both have meth in)
they also compete for renal excretion

175
Q

some presentations of granulomatosis with polyangiitis?

A 
upper and lower resp tract 
- granulomas in lungs 
- haemoptysis 
- saddle nose 
glomerulonephritis 
weight loss/night sweats 
coagulopathy
PE
mitral stenosis 
pulm hypertension
conjunctivitis
176
Q

what colour are the fingers in raynauds?

A

white – blue – red

177
Q

what are some causes of secondary raynauds?

what features distinguish secondary raynauds from primary?

A

lupus, drugs, trauma

red marks on the nail bed, asymmetrical - suggestive of secondary

178
Q

what fbc results would you expect in lupus?

A

low WCC
low platelet
(antiphospholipid syndrome = increased clotting but not because of platelets)

179
Q

what blood test results would you see in pagets?

A

raised ALP

normal calcium, phosphate, PTH, etc

179
Q

what blood test results would you see in pagets?

A

raised ALP

normal calcium, phosphate, PTH, etc

180
Q

symptoms of L4 (L3-L4) lesion?

A

thigh to calf pain

loss of knee jerk

181
Q

symptoms of L5 (L4-L5) lesion?

A

weak dorsiflexion

buttock to foot pain

182
Q

symptoms of L1 lesion?

A

sciatic pain
buttock to ankle pain
loss of ankle jerk

183
Q

what is a normal/osteopenic/osteoporotic T score?

A 
osteosclerosis = 2.5 or more 
normal = 1 - -1
osteopenia = -1 or less 
osteoporosis = -2.5 
severe osteoporosis = -2.5 or less + silly fracture
184
Q

what does schoberg’s test measure, what diagnosis is a positive result associated with?

A

spine mobility

ankylosing spondylitis

185
Q

presentation of antiphospholipid syndrome?

A 
CLOT 
C - coagulopathy - raised APTT normal PT 
L - livedo reticularis - red/blue skin 
O  - obstretic problems eg miscarriage 
T - thrombocytopenia 
can be primary, or secondar, eg to lupus
(also non infective endocarditis)
186
Q

risk factors for osteoporosis?

A 
S  - steroid
H - hyperthyroid, hyperparathyroid
A - alcohol, smoking 
T - thin
T - testosterone decrease
E - early menopause 
R - renal/liver failure (less vit D activation)
E - erosive bone dis
D - diet/diabetes
187
Q

‘hidden’ places where you may find psoriasis?

A

scalp
behind ears
genitals

188
Q

which primary cancers are most likely to metastasise to bone?

A

breast/prostate
lung
kidney (renal cell carcinoma)
thyroid

189
Q

what blood test is used to monitor lupus?

A

ESR

190
Q

what antibodies are there in anti phospholipid syndrome?

A

anti cardiolipin - also in syphilis
lupus anticoagulant
anti beta 2 Glyco Protein 1
= hypercoagulable state

191
Q

microscopic polyangiitis affects only the

A

kidney and lung

192
Q

eosinophilic granulomatosis presents similarly to

A

allergy

asthma

193
Q

Henoch-Schoenlein purpura

A

rash
abdo pain
glomerulonephritis
arthritis/arthralgia

194
Q

what is a swan neck deformity?

A

hyperextension of PIP

hyperflexion of DIP

195
Q

what is burronaires deformity?

A

feature of RA
hyperflexion of PIP
hyperextension of DIP

196
Q

explain how to do Schober’s test?

A 
have the patient stand 
locate L5 vertebrae 
mark a point 10cm above and 5cm below 
as pt to bend over as far s they can 
measure the new distance
less than 20cm is positive for AS
197
Q

how are asthma attacks categorised according to severity? (for people aged 12+)

A

moderate = peak flow below 75%

acute severe = peak flow below 50%, resp 25+, pulse 110, accessory muscle use, or unable to complete sentence

life threatening: peak flow below 33%, sats less than 92%, confused, or silent chest

198
Q

what is acute severe asthma in a child 5-12?

A

resp rate 30

pulse 125

199
Q

what is acute severe asthma in child 2-5 yrs?

A

resp rate 40

pulse 140

phase 2a (10 decks)

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