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phase 2a mine > msk top tier > Flashcards

msk top tier Flashcards

1
Q

in what condition is it typical to see DIPJ joint, knee and 1stCMC(carpometocarpal = thumb base) arthritis distribution

A

OA

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2
Q

is OA more common in men or women

A

women

- + rises post menopause

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3
Q

race association with OA

A

less common in black, A-C, asian, malaysian

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4
Q

name 5 conditions that increase one’s risk of OA

A

obesity - pro inflam (TNF, IL1, adipokines)
– esp knee/hip

local trauma - accelerates damage

inflammatory arthritis

hypermobile joints/ congential hip dysplasia (wear/tear starts earlier)

diabetic neuropathy

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5
Q

where would you expect to see OA in
1 farmers
2 labourers
3 footballers

A

1 hips
2 small joints/hands
3 knees

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6
Q

OA pathophysiology

A

progressive degeneration in response to insult/injury (Wear/tear)

loss of articular cartilage

exposed bone–> sclerosis (thickened) + cyst formation (less thick)

disorder bone repair - cartilagenous growths –> calcification –> osteophytes

inflammation present (even though this s degenerative, not inflammatory arthritis)

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7
Q

what is inflammatory OA

  • AKA
  • features
  • treatment
A

= “erosive OA”

more inflammation than typical OA

no psoriasis (rule out PSA)
big knuckle spaces (MCPjoint)
joint 'locks' - bone/cartilage fragment (Arthroscopy)

DMARD therapy

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8
Q

name 5 potential signs of OA

A 
gait alteration 
joint swelling
deformity
tenderness
limited range of movement
crepitations 
joint locking
no systemic signs!
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9
Q

name 3 symptoms of OA

A

painful, tender
swelling
deformity
functional impairement

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10
Q

describe OA joint distribution

A 
often unilateral 
often one set of joints (but multijoint)
often begins at base of thumb -1st CMCj (trouble opening jars/taps)
DIP
knees spine hip
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11
Q

heberdens node

A

DIP

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12
Q

bouchards node

A

PIP

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13
Q

OA of hip pain feels like?

A

groin pain (rather than lateral hip pain)

if patient complaints of hip pain- usually=back

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14
Q

OA investigations

A 
x ray (LOSS)
Loss of joint space
Osteophyte
Subchondral sclerosis
subchondral cysts
\+ gull wing appearance (like flat m) on articular joint surface

MRI can see earlier changes but most dont need this

bloods
- normal esr, normal/slightly raised crp

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15
Q

OA management

  • non medical
  • pharmacological
  • surgical
A

non medical (weight loss, education, physiotherpay, walking aids etc)

pharmacological
- analgesisa (NSAIDS, opioids, steroid injectuions etc)

surgical
- athroscopy (if loose bodies of cartilage/bone - knee locking)
osteotomy (bone cut/shaped/realigned)
athroplasty (replaced)
fusion (ankle/foot – but decreased movement)

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16
Q

what is arthroplasty

  • when is it done
  • s/e
A

joint replacement

for uncontolled pain, esp at night

comes with slight decrease in function

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17
Q

what is arthrocopy

A

Only indication for arthroscopy= for loose bodies- cartilage/bone!
Associated with knee locking

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18
Q

what is osteotomy

A

bone is cut/ realigned/ shortened

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19
Q

are men or women more affected by RA

A

women

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20
Q

most common RA age group?

A

40-60

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21
Q

genetic factors associated with RA

A

HLA DR4
HLA DRB1

+ associated with other autoimmune conditions

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22
Q

triggers of RA

A

stress

trauma

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23
Q

RA pathophysiology

A

inflammation of synovium (synovitis) and joint capsule

B,T cells, neutophils, cytokines

capillaries form within synovium- angiogenesis

synovial villli form - proliferate –> pannus (tumour-like mass). this grows over articular cartilage and destroys it and the subchondral bone! by erosion!

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24
Q

what type of immune reaction is RA

A

autoimmune

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25
Q

is RA mainly chronic, subacute or acute

A

chronic

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26
Q

what is the joint distribution typical of RA

A

symmetrical -bilateral
polyarthritic
mainly smaller joints- hands and feet
DIP sparing!!!

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27
Q

name 3 defromities associated with RA

A

1 mobile nodules (elbows, back of hands, lungs)
2 ulnar drift (fingers displaced towards ulnar(little finger))
3 swan neck (tendons- DIP arched)
4 z thumb deformity (thumb z shape)
5 boutonniere (DIP thumb opposite of arched)

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28
Q

pallindromic RA=

A

(A type)

episodic RA. never persistent

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29
Q

does RA have systemic sign/symptoms?

A

yes- fatigue/malasise

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30
Q

does OA have systemic sign/symptoms?

A

no

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31
Q

what does antiCCP indicate?

what does it stand for

A

RA

anti-cyclic citrullinated peptide

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32
Q

RA investigations (7)

A

bloods

  • Anaemia
  • High ESR/CRP
  • Thrombocytosis (high)

+ rheumatoid factor (antibody against IgG heavy chain)- not specific – also in othe autoimmune

+ anti CCP – highly specific

antinuclear antibody

synovial fluid biopsy – high neutrophil count but sterile (rule out infection)

XRAY - LESS
Loss of articualr space
Erosion of articular cartilage and bone
Soft tissue swelling
Soft bones- osteopenia
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33
Q

RA treatment

A

non-pharm

  • smoking cessation
  • depression
  • occupational therapy/rehab

pharm

  • DMARDS (methotrexate)
  • bioological DMARDs
  • corticosteroids
  • NSAIDs
  • analgesia
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34
Q

pro and con of corticosteroids for RA

A

suppress disease, helps pain and swelling

but risks long term toxicity

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35
Q

pro and con of NSAIDs for RA

A

reduces pain and stiffness

but no effect on disease progression

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36
Q

RA complication- name 5

A

lung involvement - rheumatoid nodules

heart - pericardial rub/infection/effusion

scleritis/episcleritis

spinal cord compression

anaemia

(plus GI, vasculitis, kidney amyloidosis, muscle wasting, bursitis, sjorgens)

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37
Q

what is the most likely MSK cause of intersitial lung disease

A

RA

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38
Q

gout age and gender

A

men

middle aged

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39
Q

pseudogout age and gender

A

elderly

women

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40
Q

gout race risk factors

A

chinese
polynesian (pacific islands- somoa, figi, tonga, tom said mauri people)
fillipino
with westernised diet

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41
Q

gout diet

A

alcohol esp beer
red meat, liver
shellfish
sugar - fructose drinks

all these things are high purines

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42
Q

is hyperuricaemia more commonly due to underexcretion or overproduction

A

underexcretion

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43
Q

name 5 causes of underexcretion of uric acid (hyperuricaemia)

A 
aspirin
renal impairment 
dehydration
diabetes
diuretics

hypertension
hypothyroid
hyperparathyroid
obesity

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44
Q

name 3 causes of uric acid overproduction (hyperuricaemia)

A 
high purine intake (diet)
increased cell turnover
-psoriasis
-leukemia
-lymphoma
hyperlipidemia
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45
Q

triggers for gout attack

A

alcohol/shellfish binges
sepsis
MI
trauma (can be as minor as toe stubbing, surgery)
dehydration
sudden start/stop or hypouricaemic therapy

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46
Q

triggers for pseudogout attak

A 
trauma
illness 
surgery -esp parathyroid removeal 
hypothyroid
hyperparathyroid
T4 replacement
blood transfusion -- excess iron
most spontaneous
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47
Q

how do crystal arthropathies cause arthritis

A

urate crystals activate phagocytes – inflamamtion

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48
Q

gout crystal=

A

monosodium urate

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49
Q

pseudogout crystal substance=

A

calcium pyrophosphate

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50
Q

purine conversion to uric acid

then uric acid –> ?

A

purines –> hypoxanthine –> xanthine (may use xanthine oxidase here- sources vary)

xanthine –> uric acid using xanthine oxidase

uric acid

  • excreted by kidnyes
  • excess –> monosodium urate –> deposited in joints
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51
Q

gout joint distribution

A

polyarticular
asymmetrical

toes - esp big toe (1st MTPJ)
ankles
feet

(also knees, wrist, finger)

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52
Q

pseudogout joint distrubtion

A

monoarticular
joint surface

knees = most common
wrist
shoulder
ankle
elbow

(MCP (big knuckle))

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53
Q

is gout/pseudogout acute or chronic condition

A

can be acute or chronic

chronic condition but is episodic with acute flare ups

pseudogout often resolves by self 1-3w but we speed it up :)

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54
Q

tophi =

A

onion like aggregates of urate crystals with inflammatory cells around the joint

seen in chronic gout. can take long time to resolve. can consider it a gout complication

soft tissue masses, replaced by crystals

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55
Q

crystal arthropathies investigation

A

joint aspiration –> polarised light microscopy

Xray

bloods

  • raised wbc
  • raised esr
  • serum uric acid
  • serum creatinine - check for renal impairment

Examination- check ears for deposits

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56
Q

what does gout look like under polarised light microscopy

A

negatively birefringent needles of monosodium crystals (N)

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57
Q

what does pseudogout look like under polarised light microscopy

A

(weakly) positive birefringent rhomboid shaped of calcium pyrophosphate crystals (P)

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58
Q

gout xray

A 
BEST
bony hooks (from erosions)
erosions (rat bite, punched out erosions)
space intact (no joint space lost)
tophi
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59
Q

pseudo gout xray

A

chrondocalcinosis = linear calcification parallel to articular surfaces, in joint gap

differentaites from OA (subcondral sclerosis)

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60
Q

pharmacological management of crystal arthropathies

A

anti-inflam

  • NSAIDs
  • colchine (if NSAIDs not tolerated)
  • steroids

xanthine oxidase inhibitors - PREVENTATIVE- prevent uric acid production
(gout only)
-allopurinol
(-febuxostat)

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61
Q

what is given for crystal arthropathies if NSAIDs cannot be tolerated

A

colchine

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62
Q

non pharmacological crystal arthropathies management

A

diet change
weight loss
physiotherapy

joint aspiration
- esp pseudogout

potential for surgery-
if long term
- synovectomy
- joint replacement

pseudogout = screen for associated conditions

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63
Q

when should you screen for associated conditions of pseudo gout

A

early onset - <55y
polyarticular (usually mono)
frequent/recurrent episodes

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64
Q

there is a long list of associated conditions for pseudogout. name 3

A

haemochromatosis (most common)
hyperPTH
hypothyroidism
acromegaly

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65
Q

what is bursitis

where

seen in what conditions

A

inflammation of fluid sacs that cushion joints

Commonly elbow swelling. Could also be knee, shoulder, ankle

seen in crystal arthropathies, RA

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66
Q

gout complications

A

kidney disease (uric acid deposits)

bursitis

ear deposits

tophi

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67
Q

is osteoperosis more common in men or women

A

women

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68
Q

osteoperosis risk factors to do with patient

A 
old age
menopause
thin/ low BMI
family history
diet-low ca
athlete
alcohol
smoking
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69
Q

osteroperosis risk facots to do with patient disease

A
  • joint - RA/SLE
  • hyperthyroidism /hyperparathyroidism
  • cushings (high cortisol)
  • low oes/test (hypogonadism, anorexia, menopause)
  • renal disease (lower vit d)
  • previous fractures
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70
Q

osteoperosis risk factors to do with drugs

A 
corticosteroids
hormonal 
-aromatase inhibitors
-GnRH analogues
-androgen deprivation
-depo provera (contraceptive)
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71
Q

primary osteoperosis causes

A

menopause (oes protects)

age (bone density naturally lost)

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72
Q

secondary osteoperosis causes

A

SHATTERED
Steroid use - (osteoclast activation)
Hyperthyroidism, hyperparathyroidism, hypercalciuria (inc turnover)
Alcohol + smoking
Thin (BMI<18.5)
Testosterone decrease (eg prostate cancer, hypogonadism)
Early menopause
Renal / liver failure
Erosive/ inflammatory bone disease (eg RA, myeloma)
Dietary decrease - low calcium, malabsorption, lactose intol, T1DM

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73
Q

osteomalacia vs osteoperosis

A

In ostoporosis, bone mineralisation is normal but there is reduced amount of bone
In osteomalacia bone mineralisation is reduced but there is normal amount of bone

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74
Q

bone mineral density=

how does it change with age

A

bone mass

quick rise in childhood/puberty and decline after menopause/old-ness

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75
Q

how do you measure bone density

A

bone densitometry aka DEXA

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76
Q

inflammatory disease effect on bone

A

bone turnover increase - increased bone resorption (osteoclast activity)

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77
Q

endocrine disease effect on bone

  • thyroid
  • parathyroid
  • cushings
  • oes
  • test
A

thyroid hormone and PTH –> increase in bone turn over

high cortisol (cushing’s syndrome) –> increased bone resorption, increased osteoblast apoptosis

oestrogen and testosterone restrains bone turnover

78
Q

how does skeletal loading affect bone

A

decreased skeletal loading increases resorption – strong bones not needed (immobility, low BMI)

79
Q

microarchitecture of osteoperosis

A

trabeculae broken away –> big holes –> less strong

trabeculae thickness decreases in thickness
- decrease more in horizontal than vertical (because vertical is used more than horizontal)

80
Q

alcohol effect on bone

A

bad for osteoblast

81
Q

smoking effect on bone

A

decreases vitD increases bone turnover

82
Q

dowagers hump

A

what i have! neck slumpy thing

osteoperosis

83
Q

symptoms of osetoperosis

A

asymptomatic until fracture

84
Q

where do you fall to break neck of femur

A

fall on side/back

85
Q

fall on outstretched arm

A

distal radius (thumb wrist )

86
Q

kyphosis

A

stooping

87
Q

DEXA

A

dual energy xray absorptiometry (aka bone densitometry)

low raditation dose

t score compares bone density to young adult mean - male /female

0 to -1 = normal

  • 1 to -2.5 = osteopenia
  • 2.5 beyond= osteoperosis
88
Q

is X ray useful for osteoperosis

A

it is insensitive

89
Q

what is FRAX assessment

- who can take it

A

predicts risk of fracture in next 10 y by looking at risk factors
only suitable if 40y+

90
Q

first line osteoperosis treatment

  • eg
  • how does it work
  • take it when?
A
  • bisphophonates (eg alendronic acid)
    (oral)

antiresorptive = decrease osteoclast activity , decrease bone turnover and causes osteoclast apoptosis

best taken in morning, empty stomach (no food/med), sat up (prevent reflux)

91
Q

non first line osteoperosis treatment (3)

A

(First line= bisphosphonates)]

monoclonal antibody to RANK ligand – denosumab

HRT , oes supplement

teriparatide = PTH analogue . increase osteoblast activity – not only stops decline but rebuilds and restores (v good but expensive)

92
Q

lifestyle osteoperosis treatment

A
  • stop alcohol/ smoking
  • do weight bearing excericese
  • calcium and vit d supplement / in diet
93
Q

what is the genetic component of spondyloartopathies

A

HLA B27

94
Q

when is onset for ankylosing spondylitis

A

teens/20s

95
Q

ankylosing spondylitis race association

A 
low = african, japanese
high = N america
96
Q

reactive arthritis : male or female

A

male

97
Q

ankylosing spondylitis: male or female

A

male

98
Q

what is HLA B27

A

human leukocyte antigen. On all cells except rbc , so they are APC (tissue type)

not = cause, makes more susceptible for ANKYLOSING SPONDYLITIS (different strength of link for each condition)

99
Q

molecular mimicry theory

A

HLA B27 looks similar to infectious agents’ peptides to cause a (auto)immune response – autoimmune agonist

100
Q

mis folding theory

A

HLA B27antigen trapped in ER. this causes an inflammatory response – IL23 released

101
Q

Heavy chain homodimer hypothesis

A

B27 heavy chains form stable dimers (two identical molecules connected) which accumulate in the endoplasmic reticulum and can bind to other factors and so produce pro-inflam mediators

102
Q

reactive arthritis triggers

A

usually genital vs GI

Common cause of reactive arthritis = STI –
Chlamydia, gonorrhea

Also GI associated ones
salmonella, shigella, yersinia, campylobacter

This infection may have resolved/ be asymptomatic but still can affect

UTIs, bowel infection

103
Q

ankylosing spondylitis pathophysiology

A
  • chronic inflammation of spine and sacroiliac joints (SIJ)- destroys them
  • erosive damage repaired (joints replaced with fibrin )–> less movement range

new bone formation – ossification makes it immobile. joint/bony fusion

104
Q

syndesmophytes

A

bony growth originating inside a ligament, often the spine

105
Q

when is psoriasis seen with psoriatic arthritis

A

before/after/never

106
Q

reactive arthritis pathophysiology

A

inflammation of synovial membrane, tendons, and fascia –autoimmune response

triggered by an infection at a distant site, normally 2-6w before (often STI)

107
Q

where does reactive arthriits commonly affect

A

lower limb

108
Q

what is enteropathic arthritis associated with

A

this is a type of spondyloarthropthy

it is associated with IBD

109
Q

where does enteropathic arthritis affect

A

lower limbs
asymmetrical
episodic

110
Q

general spondyloarthopathies feature

A

SPINE ACHE

Sausage digit -- dactylitis (tendon/joint inflam)
Psoriasis
Inflam back pain
NSAIDs -good response
Enthesitis

Arthritis
Crohns/colitis/CRP elevated
HLAB27+
Eye- uveitis/iritis

111
Q

psoriasis =

A

ON SKIN
red
itchy

ON NAIL
thickened, flakey, lifting

can hide – scalp, ears, nails, belly button, genital

112
Q

enthesitis

A

heel

inflammation of junction between ligament / tendon and bone

113
Q

uveitis/irits (seen in spondyloathropathies) presents as ?

A

blurred vision
painful
red eye

children= ASYMPTOMATIC - so screened if have juveniile arthritis

114
Q

what are juvenile arthrits children scanned for

A

uveitis/iritis

= asymptomatic in children!!

115
Q

what condition do you think of with alternating buttock pain

A

sponfyloarthropathies

116
Q

what condition do you think of with bamboo spine

what is happening

A

ankylosing spondylitis

new bone formation and fusion of vertebrae

117
Q

is ankylosing spondylitis a-/symmetrical?

A

asymetrical

118
Q

ankylosing spondylitis symptoms

A 
Weight loss
Fever, fatigue
buttock/thigh pain
neck/back stiffness (thoracic and cervical)
Can cause SOB

progressed :
need to turn body to turn head (neck movement poor)
cant see sun/mirrored glasses extreme kyphosis

119
Q

5 types of psoriatic arthritis

A
  • distal arthritis (DIP only)
  • RA-like (symmetrical, polyarth) – most common
  • axial (sacroilitis)
  • arthritis mutilans (severe hand/feet deformation)
  • large joint (asymmetrical oligoarthritis)
120
Q

reactive arthritis presentation

A

reiter’s triad

  • cant see (conjunctivitis/uveitis)
  • cant pee (urethritis)
  • cant climb a tree (Arthritis)

also

  • skin things: psoriasis/keratoderma
  • willy thing : circinate balantis
  • mouth/mucosal ulcers
121
Q

ankylosing spondylitis diagnosis criteria

A 
3+ months back pain
sacroilitis (xray/MRI)
SPINEACHE features
limited back movement
age under 45 y
122
Q

x ray/MRI features of spondyloarthropathies

A 
syndesmophytes
sacroilitis
sclerosis
erosions
joint fusion
123
Q

ankylosing spondylitis treatmnet

A

non-pharm

  • physiotherapy , occupational therapy
  • excercise

pharm

  • NSAIDs = first line
  • DMARDs - if peripheral arthritis)
  • antiTNF (biologics) if NSAIDs is insufficient
  • local steroid injections

surgery
- straighten spine
hip replacement

124
Q

psoriatic arthritis treatment

A
  • immunosuppressive DMARDs

- biological drugs is DMARDs insufficent – antiTNF/ IL blockers

125
Q

reactive arthritis treatment

A 
NSAIDs 
steroid injections
antibiotics if infection persists
DMARDs 
TNF blockers= last resort
126
Q

what is happening to incidence of osteomyelitis and why

A

increasing incidence

-PVD and dibaetes

127
Q

age - osteomyelitis

A

bimodal: children + old

128
Q

main cause (route ) of osteomyelitis in children, adults and elderly

A 
children= heamotgenous seeding
adults= direct inoculation
elderly = contiguous spread
129
Q

name 5 risk factors for osteomylitis

A

1 poor vascular supply
- diabetes (foot ulcer–> infection), sickle cell, arterial disease
2 immune deficiecny/suppression
3 high risk behaviour
- high risk of trauma, IVdrug use, alcohol in excess
4 bone/joint problems
- prosthetics/surgery, inflam arthrit
5 risk factors for haemotgenous osteomyelitis
-catheters, dialysis, central lines, UTIs

130
Q
  • most common bacterial cause of osteomyelitis
  • why is
  • others
A

staph aureus

  • good at adhering,
  • can live intracellularly
  • can live on skin and invade through skin breaches
also
MRSA
staph epidermis
salmonella
pseudomonas

also
steprococci
fungi
TB etc

not haemophilius influenzae (vaccine)

131
Q

direct innoculation (osteomyelitis)

  • causes
  • mono or poly microbial
  • what age group
A

exposed bone

  • trauma- open wound
  • surgery
  • mono/poly microbial

most common cause for adults

132
Q

contiguous spread (osteomyelitis)

  • causes
  • mono or poly microbial
  • what age group
A
  • adjacent soft tissue infection spreads to bone
  • cellulitis

mono/polymicrobial

most common cause in elderly

133
Q 
haematogenous seeding
(osteomyelitis)
-causes
-mono or poly microbial
- what age group
A

blood flow

  • in children long bones affected> vertabrae
  • in adults: vertabrae > long bones

monomicrobial

most common cause for children

134
Q

why are long bones affected by ostemylitis in children

A

blood flow is slower over the growth plate so bacteria settle well here
no basement membrane
high blood flow

135
Q

why are vertebrae affected by osteomylitis in adults

A

high blood supply to vertebrae

136
Q

osteomyelitis acute vs chronic

A 
acute = <2w
chronic= >6w + chronic, by definition, involves necrosis
137
Q

osteomyelitis pathophysiology

A
  • infection spread reaches bone (3 routes)
  • inflammatory response
  • vascular congestion
  • small vessel thrombosis
  • inflammatory exudate increases pressure so periosteum ruptures
  • periosteal blood supply interupted
  • necrosis , bone death. sequestra and involucrum
138
Q

sequestrum and involucrum formation

A 
sequestrum = dead pieces of bone
involucrum= new bone that forms outside of this

these are features of CHRONIC osteomyelitis

139
Q

features of chronic osteomyelitis

A

non-healing fractures
deep/large ulcers
draining sinus tract – a passage (sinus tract) forms from infection to skin from which pus drains

140
Q

do you see systemic signs/symptoms with osetomyelitis

A 
yes
fevers
rigors
sweats
malaise
fatigue
141
Q

onset of osteomyleitis

A

days

142
Q

classic symptoms of ostemyelitis

A

weakness
dull local pain
– aggrevated by movement

(+ cardinal inflam signs)

143
Q

what would blood investifations on osteomyelitis show

A

raised ESR/CRP
raised WBC
blood culture = positive

(chronic bloods may have normal ESR/CRP/WBC)

144
Q

osteomyeitis investigations

A

bloods
bone bopsu
x ray - do one, and again in 2w. if no changes –>mri (picks up sooner)

(PET is good but expesive)

145
Q

what are you looking for with xray osteomyelitis

A

erosion
periosteal reaction (=formation of new bone)
sclerosis
sequestra (like darker oval/shape– dead bone)
soft tissue swelling

146
Q

periosteal reaction=

A

formation of new bone

147
Q

when is bed rest advised for osteomyelitis

A

if site is spinal

148
Q

osteomyelitis pharmaco treatment

  • =what
  • probelems with this
A 
antibiotics
broad spectrum whilst pending culture. 
often: flucloxacillin (6w) or clindamycin if allergic to penicillin
triple therapy is used if cause is TB
monitor response with imaging/ ESR+CRP

bacteria virulence factors + penetration of drug to bone is variable, and is worsened by poor vascular supply so antibiotics ned to be taken for longer

149
Q

surgical treatment for osteomyeltisi

A
  • debridement (removal of dead / damaged/ foreign objects inc bone)
  • replacement (prosethis)
  • abscess drainage
150
Q

is septic arthritis more common in men or women

A

equal

151
Q

how common is septic arthritis

A

rare

152
Q

name 5 risk factors for septic arthritis

A 
1 damaged joint- RA/ prosethis/ surgery
2 immunosuppressed
3 low socio-econmic status
4 IV drug user
5 intra articular injection users
6 osteomyelitis
153
Q

most common bacterial cause of joint infection

A

staph aureus

154
Q

most common bacterial cause of prosthetic cause of joint infection

A

staph aureus

also staph epidermis

155
Q

gonococcal arthritis

  • commonness
  • mono/poly/ same/different to normal
  • test for it
A

this is the minority (majority = staph aureus, non-gonococcal)

polyarthritis (normal mono with infection)

synovial fluid = negative, so need to look at the blood culture

156
Q

most common septic arthritis distrubtuion

A 
knee
hip 
shoulder
but can be any 
normally just one
157
Q

do you get systemic features in septic arthritis

A

yes

fever, tachy, malaise

158
Q

what does septic arthritis look like in the immunosupressed/elderly

A

presentation may be muted

159
Q

septic arthritis triad

A

impaired range of movement
joint pain
fever

160
Q

bloods for septic arthritis

A

CRP rises quickly
ESR rises more slowly
high wbc- neutrophilia
blood culture

161
Q

septic arthritis investigations

A

joint aspirate

  • need to do OFF antibiotics
  • bad if cloudy +pale. should be yellow and transparent
  • polarised light microscopy (rules gout/ pseudpgout)

STI screen

x ray

162
Q

what are you looking for on xray with septic arthrititis

A

extra bone formation
periosteal changes (fluffy)
lytic areas
do again after 2w

163
Q

septic arthritis management

A

antibiotics (flucoxycilin from staph aureus . clindamycin/erythromycin if allergic to pencillin)

joint aspiration!- decompress the joint

analgesia

steroid sick day rules

off load joint (splinter)

stop RA medication

surgical:

  • prosethis
  • debridement
  • excision/exchange arthroplasty of prosthetic joint (depending on how much surgery patient can toleratE)
164
Q

SLE gender association

A

f&raquo_space;m

165
Q

age range for SLE

A

15-45

high incidence premenopausal

166
Q

race assocaition SLE

A

Black af
a-c
asians
hispanic

167
Q

Genetic associtation

A

HLAD DR2

168
Q

is smoking protective or a risk factor for SLE

A

risk factor

169
Q

SLE flare up triggers

A
  • sunlight overexposure (B>A UV light)
  • oestrogen - preg, contraceptives
  • infection
  • stress
  • sulfasalazine (DMARD
170
Q

What is important to rule out before treating SLE

A

Infection

because the treatment is immunosuppressive

171
Q

SLE pathophysiology

A

dysfunction of apoptosis
- intracellular material isnot disposed of correctly by pahgocytes –> apoptic remnant (Cells and fragments) transfer to lymphoid tissue.
This is taken up by APC, allowing autoantibody to nuclear material to develop (=antiDsDNA antibodies)

B cell hyperactivity (dysfunction) –> Ab –> immune response (autoimmune)

inflammation –> tissue damage (antiDsDNA antibodies (autoantibodies) attack nuclear matterial in tissues)

172
Q

why is their an increase in thrombosis with SLE

A

thrombosis mediated by phospholipid antibodies

173
Q

do you see systemic signs in SLE

A

yes

fever, fatigue, weight loss, headache

174
Q

jaccoud’s arthropathy =

A

non-deforming /erosive (correctable) arthritis

sometimes seen in SLE

175
Q

common presentation features of SLE

A

often non-specific and begins mild

fever
mouth ulcers
fatigue
phtosensitive rash
butterfly rash

flare-ups occur - relapsing and remitting

176
Q

SLE has many other presentations name 5

A
  • Hair loss, alopecia
  • Fever,
  • fatigue,
  • weight loss,
  • headache
  • Myalgia = muscle pain
  • Arthralgia
  • Myositis = muscle inflammation
  • joint pain/swelling (RA like)
  • Raynauds
  • Pleuritic chest pain
  • Deforming arthritis (Symmetrical, non-erosive, polyarticular)
  • Seizures
  • Many rash forms, some specific, some not
  • -Discoid rash = deep + sensitive
  • Pericarditis
  • hypertension
  • MI
  • Psychosis - many inc anxiety, depression
  • Proteinuria
  • Renal failure eventually
  • Vasculitis
177
Q

SLE investigations

+whether they are specific or not

A
  • ANA+ (antinuclear antibodies)
    • not specific, but sensitive
  • high ESP, normal CRP
    • specific
  • antiDsDNA antibodies (double stranded DNA)
    • specific but not as sensitive

antiRo/antiLA autoantibodies
–?

  • bloods
  • low platelets, rbc, nuetophils, lymphocytes
    • not specific
  • u/e s raised in advanced renal disease

skin/ renal biopsy – IgG and complement depositon

178
Q

pharmacological SLE management

A

antimalarials – (hydroxy)chloroquine

steroids (prednisolone) for rashes

NSAIDs/steroids for joints

immunosuppressants

glucocorticoids high dose for complications

179
Q

cyclophasphamide = what type of drug

A

immunosuppressant

180
Q

chloroquine = what type of drug

A

antimalarials

181
Q

non pharm SLE management

A 
UV protection
manage risk of 
-atherosclerosis
-screen for other organ involvement
-look for phospholipid antibodies (they mediate increase in thrombosis)
182
Q

does SLE complications include the lung?

where else?

A

no – this is more RA

thrombosis (gangrene, stroke, MI…)

renal failure

cv disease

cerebreal vasculitis

183
Q

sulfasalazine = what type of drug

A

DMARD

184
Q

methotrexate = what type of drug

A

DMARD

185
Q

teriparatide = what type of drug

A

PTH analogue

186
Q

denosumbad = what type of drug

A

monoclonal antibody to RANKligand

antiresorpative drug

187
Q

alendronic acid= what type of drug

A

bisphosphonate (antiresorpative)

188
Q

allopurinol= what type of drug

A

xanthine oxidase inhibitor

189
Q

what gel and coombs category does SLE fit into

A

type 3 sensitivity

Deposition of immune complexes in tissue
Complement activation
Neutrophil and cytokine influx
inflammation

190
Q

sle curable?

A

no. manageable

191
Q

age for juvenile arthritis

A

16 or younger

192
Q

RA first line

what is taken with this

A

DMARD- methotrexate

glucocorticoids whilst DMARD kicks in

phase 2a mine (38 decks)

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