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Final > Orthopaedics and Rheumatology > Flashcards

Orthopaedics and Rheumatology Flashcards

1
Q

Describing fractures

  • complexity
  • comminution (types of break)
  • location
  • displacement
A
  • Simple = closed, comminuted = open
  • impaction, greenstick, transvers, oblique, spiral, compounded
  • distal/proximal/mid shaft
  • degree of translation/angulation/shortening
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2
Q

What score used for 10 year fracture risk

A

FRAX (3 person, 3 frac, 3 put in, 2 conditions)

  • Age Sex BMI
  • Previous fracture, parent hip fracture, low BMD on femoral neck
  • RA, secondary osteoporosis (T1DM, osteogenesis imperfects, hyperthyroid etc)
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3
Q

5 commonest fractures

A

Clavicle, Arm, Wrist, Hip, Ankle

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4
Q

Fractures at risk for avascular necrosis

A 
Scaphoid
Femoral Head (intracapsular)
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5
Q

Bones of the wrist

A

Scared lovers try positions that they can’t handle

  • Scaphoid
  • Lunate
  • Triquentrum
  • Pisiform
  • Trapezium
  • Trapezoid
  • Capitate
  • Hamate
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6
Q

Types of Wrist fracture

A

Colles (dorsal displacement)
Smiths (Volar displacement)
Scaphoid

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7
Q

Wrist fracture Tx

A

Manipulation under anaesthetic (Biers) if indicated

Immobilisation

May need K-wires or ORIF

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8
Q

Scaphoid

  • Mechanism
  • Sign
  • XR efficiency
  • Tx
A

FOOSH

Tenderness in anatomical snuffbox

Difficult to view (missed in 20%) esp initially

Cast immobilisation, repeat exam and XR iat 10-14 days.

May need surgical management

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9
Q

Which nerve in anatomical snuffbox

A

Radial nerve (sensory branch)

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10
Q

Complication of scaphoid fracture

A

avascular necrosis

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11
Q

Colles

  • who at risk
  • mech
  • complication
  • Tx
A

fall with osteoporosis

FOOSH with dorsiflexed wrist

Median nerve damage (also ulnar)

Reduction (±internal fixation) and immobilisation

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12
Q

Smith

  • mech
  • complication
  • Tx
A

Fall backwards

Median nerve damage

Reduction and surgical fixation then immobilisation

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13
Q

Fractures NOF

  • definition
  • types (3)
A

up to 5cm below lesser trochanter

  • intracapsular (may disrupt blood supply to femoral head - avasc necrosis)
  • extra capsular trochanteric (distal to capsule, involving or between trochanters)
  • extra capsular subtrochanteric (below lesser trochanter up to 5cm distal)
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14
Q

NOF

  • Typical cas..
  • RF
  • Presentation
A
  • Post minor trauma in elderly
  • Falls (instability, lack of core strength, gait disturbance), FRAX, Osteoporosis, Malignancy
  • Pain in outer upper thigh or groin, radiates to knee, not weight bearing, Leg adducted and externally rotated
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15
Q

NOF investigations

A

AP/Lateral XR

MRI if not obvious on XR

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16
Q

Grading #NOF

A

Gardens classification

1-4

1 = incomplete fracture
4 = complete fracture, displaced in over 50%
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17
Q

NOF Initial Tx

A

Analgesia (not NSAIDs bleed risk)

Surgery within 1 day

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18
Q

Intracapsular #NOF surgery

A

Undisplaced/young = internal fixation with cannulated screws

Displced = hemiarthroplasty to replace femoral head

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19
Q

Extracapsular #NOF surgery

A

internal fixation with screws

If more distal and femoral support needed, DHS

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20
Q 
#NOF mortality
1 month, 3 month
A

10%

33%

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21
Q

NOF surgery complications

A

infection, haemorrhage, avascular necrosis, DVT (dalteparin), pneumonia

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22
Q

When get femoral shaft fracture

A

high velocity, high energy e.g. RTA.

High energy mean often assoc with soft tissue damage

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23
Q

Which bones commonly broken in ankle fracture

A

Tid, Fib, Talus

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24
Q

Two joints of ankle

A

Ankle (where tis and fib meet talus) & Syndesmosis (between tis and fib)

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25
Q

When to consider ankle break

A

Obvious deformity, inability to weight bear, bony tenderness

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26
Q

When to XR ankle

A

Ottawa ankle rules

  • over 55
  • can’t wt bear 4 steps
  • Bone tenderness over posterior edge or tip of lateral/medial malleolus

AP/Lateral/Oblique (15 degrees)

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27
Q

Ankle # Tx

A

If NV comp or dislocation then reduce under sedation

surgical reduction and fixation
4-6 weeks in moulded cast
Analgesia
Elevation
Re-assess NV status

XR of reduction (48 hr, 7 day, 2 weeks

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28
Q

Main worrying complication of fracture

A

Compartment syndrome

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29
Q

When to suspect compartment syndrome and Tx

A
  • pain out of proportion, 6 Ps (pain, parasthesia, Pallor, Paralysis, Perishingly cold) –> Prompt Fasciotomy
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30
Q

Compartment syndrome pathology

A
  • Increase pressure due to blood and intracompartmental swelling
  • leads to muscle and nerve ischaemia –> necrosis –> vicious cycle
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31
Q

Diagnosis of compartment syndrome

A

Compartment pressure over 20 = suggestive, over 40 = diagnostic

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32
Q

2 main complications of compartment syndrome

&Prevention

A

Neuromuscular necrosis (fasciotomy)

Myogloinuria –> renal failure (Aggressive IV fluids)

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33
Q

Stages of fracture healing

A

1) Haematoma (hrs): Macrophages and leukocytes move to area and secret inflammatory agents
2) Fibrocartilaginous soft callus (days): inflammation leads to angiogenesis and inc chondrocytes to secrete collagen and proteoglycans (soft callus)
3) Bony Callus (weeks): Endocondral ossification and direct bone formation. Woven bone replaces soft callus
4) Bone remodelling (months): woven bone replied by organised cortical bone (osteoclast/blast activity) continuous remodelling = no scarring

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34
Q

Fracture healing time

A

3-12 weeks

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35
Q

Frozen shoulder

  • Joint affected
  • Mechanism
  • Pres
  • Age
  • Assoc
  • Classic sign
  • Tx
A

Glenohumeral

Thickening and contraction of glenohumeral joint capsule ± formation of adhesions. spontaneous or post injury

Pain and loss of function

40-65

Diabetes (esp if bilateral), thyroid

Loss of external rotation

Analgesia (Para, NSAID), Physio, activity

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36
Q

Bone remodelling process

A

Osteocytes send signal to osteoclasts/blasts

Osteoclasts resorb bone matrix (resorption pit) and inc serum calcium

Osteoclasts undergo apoptosis and signal osteoblasts

Osteoblast synthesise new bone matrix which then undergoes mineralisation by Ca/phosphate

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37
Q

Osteoprotegrin function

A

Osteoprotegrin secreted by Osteoblasts inhibits activation of RANK by RANKL - this is lost following menopause and inc osteoclastic activity

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38
Q

RANK and RANKL

A

RANK = osteoclast receptor

RANKL = ligand released by osteoblasts which activate RANK (reduced activate by Osteoprotegrin)

RANKL activates RANK

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39
Q

Osteoporosis

- Definition

A

Skeletal disease with low bone mass leading to fragility and fracture (at mechanical which wouldn’t usually #)

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40
Q

T-score & interpretation

Z-score

A

Using DEXA for BMD
- Gives number for S.D below healthy adult mean

Score -2.5 T -1 = Osteopenia
Score less than -2.5 = Osteoporosis

Z = compared to age matched mean

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41
Q

Common Osteoporotic #

A

Spine (vertebral crush)
Wrist (distal radius)
Hip (proximal femur)

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42
Q

Osteoporosis pathophys

A

Decreased bone formation - Osteoblasts
Increase bone breakdown - Osteoclasts

BMD decreases with age (primary) and other (secondary e.g. steroids).. depends on peak attained BMD in life

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43
Q

Osteoporosis symptoms

A

None until Fracture

Loss of height, Kyphosis

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44
Q

RF/secondary osteoporosis

A

SHATTERED (Use FRAX to look at 10 year risk of #)

S steroids + Cushings
H hyperTH/PTH
A alcohol&tobacco
T thin
T Testosterone dec
E early menopause
R Renal/Liver dysfunc
E Erosive/inflam dis (RA, myeloma, mets)
D dietary Ca/T1DM (malabsorption of calcium/Vit D)
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45
Q

Drug causes osteoporosis

A

Steroids

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46
Q

What is used for Bone mineral density

A

DEXA scan

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47
Q

Investigations in osteoporosis

A

DEXA
Blood: FBC, U&E (Ca), LFT, TFT,
Serum: Ig, paraproteins, Bence Jones
Bony profile: Ca, PO4, ALP, PTH all normal

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48
Q

Osteoporosis Tx

A

Lifestyle: smoking, alcohol, wt bearing exercise, balance (reduce fall risk), Calcium and Vit D rich diet

Med: Bisphosphonates (Alendronic acid) + Ca/Vit D

Raloxifen is selective oestrogen receptor modulator and can be used in women

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49
Q

Bisphosphonates

  • E.G
  • Mech
  • SE
A

Alendronic acid, Risedronate

inhibit osteoclastic bone resorption

Take before food (rubbish absorption) and large tablet

GI SE: difficulty swallowing, Oesophagitis, Gastric ulcers, osteonecrosis of the jaw

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50
Q

Osteoporosis - Ca PO4 ALP PTH

A

All normal

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51
Q

Osteomalacia (rickets) - Ca PO4 ALP PTH

A

Ca & PO4 decreased
ALP & PTH increased

  • Vit D deficiency and other try to compensate
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52
Q

Hyper PTH (primary) - Ca PO4 ALP PTH

A

Ca, ALP and PTH increased
PO4 decreased

  • high PTH
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53
Q

CKD - Ca PO4 ALP PTH

A

Ca decreased

All other increased (to compensate for renal loss)

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54
Q

Pagets - Ca PO4 ALP PTH

A

All normal apart from ALP increase

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55
Q

What is Osteomalacia

A

Disorder of bone mineralisation

Low Vit D leading to low Ca and PO4

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56
Q

PTH functions

A

Inc Osteoclast function (inc Ca mobilisation)

GI: inc absorption of PO4 and Ca

Kidney: inc activation Vit D (1,24vD3 via 1-alphahydroxylase: CALCITRIOL) decreases Ca excretion + Increases PO4 excretion

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57
Q

Who is at risk Vit D deficiency

A

Dark skin, Old/Young, Obese, Alcohol, vegetarian, low socioeconomic

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58
Q

Causes of Vit D deficiency

A

Lack of sun, inadequate diet

Renal disease: defective 1,25 form = osteodystrophy

Drugs: anticonvulsants, rifampicin (Liver - stop 25-hydroxycholecalciferol)

Genetic: Vit D dependant Rickets Type I & type II

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59
Q

Rickets

  • What
  • Pres
A

This is osteomalacia in children (soft bone formation due to low VitD/Ca

Leg bowing, knock knees, softening skull (craniotabes), Dental abnormalities (enamel)
Symptoms of hypocalcaemia (Confulsions, arrhythmia/arrest, Tetany, Spasms)

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60
Q

Osteomalacia

  • Symptoms
  • Signs
A

Widespread bone tenderness (low back pain and hips)
Proximal muscle weakness, Fatigue

Costochondral swelling, spinal curvature, hypocalcaemia (CATS)

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61
Q

Osteomalacia/Rickets investigations

A

Serum 25-Hydroxyvitamin D (low)

U&E/Renal/LFT/PTH

Ca & PO4 low

PTH high, ALP very high

DEXA low BMD, Iliac crest biopsy (failed mineralisation)

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62
Q

Management of Vit D deficiency

A

Ca and Vit D

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63
Q

Pagets

  • What is happening
  • Phases
  • Which bones
A

Increased bone turnover

Lytic phase: increase osteoclastic resorption

Sclerotic phase: Rapid bone formation by osteoblasts (disorganised and mechanically weaker)

Axial skeleton: lumbosacral spine, pelvis, skull, femur, tibia

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64
Q

Pagets Presentation

A

Bone pain and Deformity
Pain at night

70% asymptomatic

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65
Q

What is raised in Paget’s

A

Alk Phos

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66
Q

Bone deformities seen in Paget’s

A

Sabre tibia (Large and bowing)
Kyphosis
Skull bossing
Enlarged jaw

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67
Q

Paget’s complications

A

Pathological fractures (heavy bleeding - v vascular)
Deafness/tinnitus (CN8 compression by ossicles
Osteosarcoma
Inc bone vascularity may lead to high output cardiac failure

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68
Q

Paget’s investigations

A

ALP high
CA, PO4, PTH normal

XR: Lytic and sclerotic bone lesions, cotton wool pattern of multifocal skull sclerosis

Isotope bone scans (radioisotope scan shows increased boney metabolism)

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69
Q

Paget’s Tx

A

Pain - NSAID & Paracetamol

Reduce progression - Bisphosphonates (Zoledronate single IV dose)

Monitor - ALP

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70
Q

Inflammatory Vs Degenerative arthopathy

A

Inflam: Worse morn, ease on use, red/hot/swollen (synovial and boney), responds to NSAIDs

Degen: Worse with use, mainly evening, prior, not inflamed, little swelling (may have boney)

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71
Q

Which joints in hands affected:

RA
OA

A

RA: MCP, MTP, PIP

OA: DIP, base of thumb

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72
Q

What stimulates acute phase proteins

A

IL1, IL6, TNF
–> inc fibrinogen (ESR) & CRP

Inflammation and infection processes

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73
Q

What is ESR

What affects it

A

RBCs cross linked due to higher fibrinogen production by Liver as response to IL6. they sediment quicker.

Infection/inflammation, RBC shape/No, Drugs - steroids, obesity (fat makes IL6)

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74
Q

Which acute phase protein is faster on and off?

A

CRP (1 day peak) is faster coming on and going off after inflammation than ESR (7 day peak)

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75
Q

What is CRP

A

Acute phase protein which increases in inflammatory conditions, connective tissue disorder, neoplasia, infection (esp bacterial)

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76
Q

OA pathology & XR

A

degeneration of articular cartilage/failure to maintain cartilage matrix synthesis

Lost joint space, osteophytes at margins

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77
Q

Common joints in OA

A

Knees, hips, DIP, Base of thumb, spine

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78
Q

OA RF

A

Age, Female, Obese, Occupation, Genetics, Joint laxity/instability

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79
Q

Common OA presentation

A

Patient over 45
Activity related joint pain (relieved by rest)
No morning stiffness
Some stiffness after rest (gelling)

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80
Q

OA signs

A

Reduced ROM
Crepitus
Pain on movement (disuse atrophy and weakness poss)
Boney swelling/deformity: osteophytes, DIP (Heberden’s) & PIP (Bouchard’s)

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81
Q

OA XR 4 features

A

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

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82
Q

Investigations in OA

A

XR - 4 features
Bloods - normal
Joint aspirate - (Septic/Gout?) normal
RF, Anti-CCP + ANA negative

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83
Q

Ddx for hip and knee OA

A

Bursitis
Referred pain (hip to knee)
gout
Seropositive and seronegative arthritidies

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84
Q

Management of OA

A

Lifestyle
- weight loss, screen depression, exercise supporting muscles

Pain

  • Local capsaicin/topical NSAID (1st line)
  • +Paracetamol
    • NSAID ± PPI (gastro-protection)

Other
- intra-articular steroid injection (methylpred)

Surgery
- Arthoplasty for persistent disease affecting QoL

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85
Q

Pathophysiology underlying:

Joint space loss

Sclerosis

cysts

A
  • Cartilage loss
  • Micro fracture due to loss of cartilage
  • Seeping of synovial fluid
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86
Q

RA Xray

A

Periarticular erosions

Osteopenia

Soft tissue swelling (may be seen on XR)

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87
Q

RA definition

A

Chronic autoimmune disease with inflammation of synovial joints leading to joint/periarticular tissue destruction

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88
Q

RA & OA symmetry

A

RA = Symmetrical

OA = Asymmetrical

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89
Q

Joints affected in RA

A

Small joints of hands and feet

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90
Q

Pathology of RA

A

Inflammation of synovium.

increased angiogenesis, influx of inflammatory cells (T cells, Macrophages, Plasma cells), release of LI1/IL7/TNF

Joint destruction

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91
Q

Pannus

A

This is proliferation of reactive synovium - Locally invasive synovial tissue

Synovial hypertrophy over articular cartilage during active disease. causes destruction

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92
Q

Features seen in RA

A

RF +ve in 80%
Anti CCP in 70% ( most specific test)
HLA DR in 25%

Ulnar deviation, morning stiffness,
Swan neck, Boutonniere, Z-deformity

Cervical spine (Atlanto-axial instability)

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93
Q

Pattern of RA

A

Small joints, symmetrical, MCP, MTP, PIP swelling.

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94
Q

Extrarticular RA features

A

Nodules: extensor surface of tendon s and lungs

Serositis: Pleuritis/pericarditis (pleuritic chest pain

eye: Sjogrens (scleritis, episcleritis)

Resp: nodules, caplans syndrome, pulmonary fibrosis

Anaemia of chronic disease

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95
Q

RA lung disease

  • % of RA
  • symptoms
  • Types
A

seen in 30%

dyspnoea, cough, wheeze

Interstitial fibrosis
Nodules (may lead to effusion)
Caplans (when seen with coal workers pneumoconiosis - round peripheral lesions)

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96
Q

RA investigations

A 
RF (antibody to IgG) in 70% 
Anti-CCP in 70%
XR hands and Feet
- periarticular erosions and osteopenia
FBC - normocytic anaemia of chronic disease
ESR/CRP raised
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97
Q

Monitoring RA

A

DAS28 (Disease activity score) less than 3.2 = well controlled over 5.1 = active

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98
Q

RA Treatment

A

1st line: DMARD (Methotrexate plus sulfasalazine)

Corticosteroid bridging therapy and as an adjunct (Prednisolone)

NSAIDs in short term

2nd line: Biologics

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99
Q

EGs of DMARDs (Mm CASH)

A 
Methotrexate 
Sulfasalazine
Ciclosporin
Azathioprine
Hydroxychloroquine
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100
Q

How is Methotrexate given?

A

Weekly

Folic acid 5mg (24 hours after)

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101
Q

How doe MTX work & SE

A

Antimetabolite
Inhibits DNA synthesis

BM suppression, Mucosal damage, mouth ulcers, hepatic cirrhosis, pulmonary fibrosis

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102
Q

MTX contraindications

A

Other folate antagonists: Trimethoprim, phenytoin

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103
Q

MTX monitoring

A 
CXR
FBC
LFT
U&E
Monitoring: before starting, two weekly until established, 3 monthly
6 weekly after changing dose
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104
Q

Possible SE of all DMARDS

A

Myelosuppression (sore throat, fever), irreversible retinopathy, Teratogenicity

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105
Q

Biologics mechanism of action?

A

MABs
(etanercept is a receptor fusion protein)

Rituximab - Anti CD20
Tocilizumab - IL6 receptor therapy
Abatacept - Anti T-cell

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106
Q

RA pathology

A 
Autoimmune activation of T-cells against body tissues (inc synovium)
Cytokine release (IL1/6/TNF) activating other immune cells (neutrophils, macrophages)

B-cells products RF

Osteoclast activation and inflammatory destruction cause erosive damage

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107
Q

Causes of high Urate (in Gout)

A
  • Reduced renal excretion (90%)
  • Drugs (diuretics impart orate excretion)
  • High insulin/Sugars also impairs excretion
  • High intake (diet)
  • High cell turnover
  • High cell damage: surgery, trauma, infection
  • High cell death: chemo
108
Q

What is Gout

A

Monosodium Urate crystals in joint

109
Q

Features of hyperuricaemia

A

Gout

Uric acid stones

110
Q

Gout RF

A

Alcohol (beer), purine rich food (red meat, seafood), diuretics, DM, CKD, CHD, HTN

111
Q

Gout presentation

A

Acute monoarthropathy (commonly 1st MTP joint) can also be knee, mid tarsal, wrist, ankle

Severe joint inflammation, fever, malaise.

112
Q

Ddx Gout

A

Septic arthritis (mono arthritis)

113
Q

What are Tophi

A

Aggregates of crate crystals.

Common in joints/tendons

114
Q

Gout investigations

A

Serum urate - raies

Joint aspirate - Negatively birefringent needles shape (MSU)

XR: soft tissue swelling, punched out lesions, tophi, sclerosis

115
Q

Gout management:

  • Acute
  • Prophylaxis
A

NSAIDs e.g. Naproxen 10-14 days (high dose initially then reduce)

Lifestyle, manage RF (diuretics, DM)
Prophylactic drugs (start two weeks post attack): Allopurinol/febuxastat (Xanthine oxidase inhibitors
116
Q

How is Uric acid produced?

A

purines(nucleotides) –> Xanthine –(xanthine oxidase)–> uric acid

117
Q

Pseudogout crystals

A

Calcium Phospopyrate

Positively birefringent rhomboids

118
Q

Precipitants to pseudogout

A

Dehydration, illness, hyperparathyroid (inc calcium)m Wilsons, long term steroids

119
Q

Presentation of pseudogout

A

Acute joint pain/swelling/inflammation/hot

Monoarticular

if chronic - similar to OA but more severe: pain, stiff, swelling, crepitus

120
Q

Investigations pseudogout

A

Joint aspirate: positively birefringent Rhomboids, neutrophils
–> exclude septic arthritis

Joint XR: opacification of articular cartilage on joint surface

121
Q

Management of pseudogout

A

No specific, just symptomatic

Ice packs, elevation, aspiration, NSAID, Into-articular steroid injections

122
Q

Pathophysiology of connective tissue disorders

A

IgG antibody antigen form complex

complex deposition in tissue

Complexes attract complement

Complement reactions attract neutrophils causing inflammation

Enzymes/cytokines etc cause further inflammation

123
Q

What is SLE

A

Inflammatory multisystem autoimmune disorder with antinuclear antibodies

124
Q

HLA mutation in SLE

A

DR2/DR3 (Again: Think Dopamine Rash)

125
Q

SLE other possible presentations

A 
Raynauds (50%)
Other autoimmune (alopecia, thyroiditis, arterial/venous embolus - antiphospholipid syndrome)
126
Q

Criteria for SLE (needs to meet 4 of these)

A

DOPAMINE RASH

D discoid rash
O oral ulcers
P photosensitivity
A arthritis
M malar rash
I immunology (anti-Smith, anti-dsDNA, Antiphospholipid)
N neurological symptoms (seizures/psychosis)
E ESR raised (NOT CRP)
R renal disorder (proteinuria)
A ANA positive
S serositis (pleura/pericardia)
H haematological (pancytopenia)
127
Q

SLE investigations

A

ESR/CRP - ESR raised only

FBC: pancytopenia

AAB: ANA (95%), antidsDNA (60%), antiphospholipid antibodies (anticardiolipin

Complement levels; low C3/C4 in active disease (complement action against immune complexes in CTD)

Urinalysis: casts, haematuria, proteinuria

U&E: Renal disease (raised Urea and creatinine)

CXR: Pleural effusions
ECG: pericarditis (saddle)

128
Q

SLE management

A

Lifestyle: smoking, sun protection, exercise

Joints: NSAID ± hydroxychloroquine ± steroids

Nephritis: cyclophosphamide/tacrolimus/mycophenolate + prednisolone + hydroxychloroquine

129
Q

Antiphospholipid syndrome

A

Autoimmune condition against phospholipids (don’t confuse with good pastures - antiGBM)

130
Q

Antiphospholipid syndrome AAB

A

Anticardiolipin

lupus anticoagulant

131
Q

Antiphospholipid syndrome assoc diseases

A

SLE 30%
RA
Systemic sclerosis
Sjogrens

132
Q

Antiphospholipid syndrome Presentation

A

Vascular thrombosis
Adverse preg outcomes ( one after 10 weeks OR 3x before 10 weeks) - pregame’s loss, pre-eclampsia
Stroke

Thrombocytopenia

133
Q

Investigations and diagnosis of Antiphospholipid syndrome

A

Lupus anticoagulant/anti-cardiolipin present on two occasions 12 weeks apart

Low platelets and prolonged APTT (even though thrombosis tendency)

134
Q

Antiphospholipid syndrome treatment

A

Lifestyle: avoid smoking, avoid OCP, healthy diet, low alcohol.

Warfarin target INR 2-3

135
Q

Sjogren’s syndrome Def

A

Autoimmune condition with lymphocytic infiltration of exocrine glands

136
Q

What is Sicca syndrome

A

Assoc with Sjogren’s syndrome

Dry eyes (eye and conjunctiva), Dry mouth, Enlarged parotids

137
Q

Assoc diseases with Sjogren’s syndrome

A

SLE
RA
Systemic sclerosis
(CREST)

138
Q

Epidemiology of Sjogren’s syndrome

A

More in women

30-40 yr old

139
Q

Sjogren’s syndrome presentation

A

Dry/eyes/mouth/vaginal
(diminished lacrimal and salivary activity)

Enlarged Parotid

Other: Fatigue, myalgia, Raynaud’s (20%), vasculitis

140
Q

Areas affected by Sjogren’s (affects exocrine secretions)

A

Mouth: difficulty eating, altered taste, oral candidiasis

Bronchi: dry cough

Pharynx/Oesoph: dysphagia

Pancreas: malabsorption

141
Q

Sjogren’s syndrome investigations

A

Schirmer tear test (tear test): +ve if less than 5mm in 5 mins

AAb: anti-Ro, RF, ANA, anti-La

Sialography (salivary gland radiography)

Biopsy of gland: mononuclear infiltrate (B and T cells)

Rose-Bengal stringing eyes

142
Q

Sjogren’s syndrome Tx

A

Artificial tears, artificial saliva (drink plenty), Oral pilocarpine (Muscarine parasympathomimetic)

Joint pain: NSAID + hydroxychloroquine + Steroid (Prednisolone)

143
Q

CREST meaning and what is the disease?

A

Systemic sclerosis

Calcinosis - calcium deposits in the skin

Raynauds (vasospasm in response to cold/stress medial fingers)

Esophageal dysfunction - Acid reflux and decrease motility

Sclerodactyly - thick/tight skin on fingers/hands

Telangiectasia - dilatation of superficial capillaries giving red marking on skin surface

144
Q

Systemic sclerosis pathophys

A

Multisystem autoimmune

Inc fibrosis is central part of disease

increased fibroblastic activity = excessive collagen/Fibrosis

Immune system activation = vascular damage (Raynaud’s, renal, GI, heart, lungs)

145
Q

RF Systemic sclerosis

A

FH
Viral infection (EBV, CMV)
Chemical exposure (pesticides, plastics)
Drugs: Bleomycin, Vit K

146
Q

Systemic sclerosis Presentation

A

Skin hardening/tightening in hands/face
Oesophagela symptoms
Raynauds

Fatigue and weight loss

147
Q

Complications of Raynauds

A

Peripheral digital ischaemia due to recurrent spasm of digital arteries

(Raynauds occurs dur to SSc, SLE, Beta-block, Thrombocytosis

148
Q

Skin features of Systemic sclerosis

A

Raynauds, swelling, thick+hard=sclerodactyly, Calcinosis

149
Q

MSK features Systemic sclerosis

A

Joint pain, swelling, myalgia, ROM loss

150
Q

GI features Systemic sclerosis

A

Heartburn/reflux/oesophagitis, dysphagia, reduced oesophageal and GI motility (constipation)

151
Q

Pulmonary features Systemic sclerosis

A

Pulmonary fibrosis (interstitial disease) in 80% - dry cough etc

Pulmonary artery hypertension (leading cause of death)

152
Q

Important complications of Systemic sclerosis

A

GI bleed (acid)

Renal crisis (ANCA glomerulonephritis and vascular disease)

Pulmonary HTN (leading cause of death)

153
Q

Systemic sclerosis investigations

A

FBC (microcytic if GI bleed, haemolytic in renal crisis)

U&E (Ur&Cr high in renal crisis)

ESR/CRP (more commonly ESR raised)

Pulmonary function (Spirometry - FVC decreased. As is DLCO -diffusion capacity to CO)

Antibodies: ANA (90%)

154
Q

Systemic sclerosis Tx

A

Physio, avoid smoking, home exercise, prevent Raynauds (gloves, Nifedipine-CCB)

GI - PPI for life

Pulmonary - cyclophosphamide (fibrosis), sildenafil (PA HTN) + O2

arthritis/synovitis - Prednisalone

Skin - Topical emollient ± topical corticosteroid (itch) ± topical cyclophosphamide (for thickening)

Renal - ACEi for AKI/HTN

155
Q

Monitoring Systemic sclerosis

A

Yearly lung function (spirometry, lung volumes, DLCO)

Yearly Echo

156
Q

Polymyositis:

  • Definition
  • which muscles
  • Extra-muscular involvement
A

Autoimmune CTD with inflammation to striated muscles

Proximal

Skin, joints (arthralgia, Raynauds), oesophagus (dysphagia), heart (AV nodal), lungs (Interstitial lung disease)

157
Q

What Ddx to rule out in Polymyositis:

A

Neoplasms

  • Lung (CXR)
  • Breast
  • Ovary (Ca125)
  • Pancreas (Ca19-9)

This phenomenon is seen in paraneoplastic syndrome

158
Q

Polymyositis presentation

A

Non painful, progressive proximal muscle weakness (esp pelvic girdle - difficulty rising from chairs, stairs)

breathlessness (lung disease)

159
Q

Polymyositis investigations

A

Creatinine Kinase - Elevated

AAb - anti-Jo-1 (assoc with poor prog: lung disease)

Electromyography and muscle biopsy for confirming Dx (fibrillation potentials at rest)

160
Q

Tx for Polymyositis & Dermatomyositis

A

Early therapy!
1st line: Steroids (anti-Jo = long term)

If steroids fail immunosuppressive e.g. azathioprine

Lung disease: cyclophosphamide ± ciclosporin

161
Q

Polymyositis complications

A

Inc risk malignancy

GI ulceration - melaena, haematemesis

Interstitial lung disease

AV nodal disease

162
Q

What is Ehler Danlos

  • Skin/joint
  • CV
  • Occular
  • Hearing
A

Defective collagen structure/processing/production

increased elasticity/hypermobility (prone to dislocation)

Heart valve abnormal (mitral prolapse), Aortic root dilatation, aneurysm

Abnormal globe/cornea

Tinnitus (ossicle laxity)

163
Q

Ehler Danol management

A

Physiotherapy: regular gentle exercise

Genetic counselling

Echo: mitral valve, aortic root dilatation

164
Q

What is leading cause of Aortic root dilatation

A

Marfan’s

165
Q

Marfan’s Pres

  • describe person
  • skin
  • CV
  • lungs
  • eyes
  • joints
A

tall, skinny, white man. long arms and legs

striae

Aortic dilatation, dissection, mitral regurg, aneurysms

pleural rupture - pneumothorax

closed angle glaucoma

hyper mobility
(can touch thumb to wrist on sam hand)

166
Q

Investigations/ managing Marfan’s

A

Annual echo (aortic root)

CVMRI

MDT: geneticist, ophthalmologist, cardiologist, orthop

Avoid maximal exertion: scuba, weight lifting

Prophylactic beta block: reduce MAP and pulse rate

167
Q

What is meant by seronegative arthropathy

A

Group of rheumatic diseases where RF is negative.

involvement of axial skeleton, peripheral joints and enthesitis (tendons/ligament), Dactylitis

168
Q

What is Reiter’s syndrome?

A

Seronegative arthropathy with triad of:

1) Conjunctavitis
2) Urethritis
3) Arthritis
4) Dactylitis

Anterior uveitis is also sometimes seen.

169
Q

What is HLA and what HLA mutation seen in seroneg arthropathy

A

Major histocompatibility complex - contain genes for immune function

Involved in cell surface antigen presenting proteins (chr 6)

HLA B27

170
Q

Examples of Serotonegative Arth

A

Ankylosing Spondylitis

Reiter’s syndrome

Enteropathic arthritis (assoc with IBD)

Psoriatic arthritis

JIA

171
Q

Typical presentation and site of enthesitis

A

Pain, stiffness, tenderness

Achilles, Sacroilitis, plantar fascia.

172
Q

Ankylosing spondylitis:

  • Definition
  • Genetics
A

Seronegative spondyloarthropathy of axial skeleton. Sacroilitis and spondylitis (vertebral inflammation)

HLA B27, Autosomal dominant

173
Q

Diagnostic features of Ank Spond

A

Inflammatory back pain & enthisitis

Stiff and pain walking an in early morning

Gradual onset

Improvement with movement

Age at onset over 40

Tender sacroiliac region (felt in buttocks

Limited spinal movement

174
Q

Ank Spond presentation

A

Insidious, relapse and remit

Fever and WL in active disease

Inflammatory back pain

Peripheral enthesitis: Achilles, plantar fasciitis

peripheral arthritis: asymmetric, hips/shoulder/chest wall (chostochondritis)

175
Q

Ank Spond extrarticular features

A

Eyes: anterior uveitis (painful red eye and photophobia)

CV: aortic dissection and regurgitation (aortitis)

Lung: restrictive disease, limited chest expansion (costovertebral/sternal involvement), apical fibrosis

176
Q

Ank Spond examination findings

A

Reduced chest expansion

Schobers test: reduced forward flex

177
Q

Ank Spond investigation findings

A

Pelvis XR: sacroilitis

HLA B27 +ve

XR spine: bamboo spine (late), erosion, squaring, syndesmophwytes (vertebral fusions)

178
Q

The As of association with Ank Spond

A 
Apical fibrosis
Anterior uveitis
Aortic regurg
Achilles tendonitis
AV node block
Amyloidosis
179
Q

Management Ank Spond

A

No cure - control symptoms and complications

Physio/Rehab/Exercis

1st line: NSAIDs (±para analgesia)

If NSAIDs don’t help pain: TNF alpha inhibition

Enthesitis: corticosteroid injection

For peripheral arthritis: DMARD (sulfasalazine)

180
Q

What is Psoriatic arthritis

A

Seronegative inflammatory arthritis (axial, peripheral, enthesitis) in those with psoriasis

181
Q

Psoriatic arthritis pattern

A

DIP most common

Asymptomatic oligoarthritis

Arthritis mutilans: severe and destructive. Osteolysis/bone shortening gives pencil in cup

182
Q

DDX and how to rule out

A

Similar to RA

This will be antiCCP negative (RA will be more likely +ve)

183
Q

Extra-articular Psoriatic arthritis features

A

PSORIASIS

Nail pitting, dactylics, Enthesitis

184
Q

Psoriatic arthritis investigations

A

XR hands and feet

  • Erosion in DIP
  • Osteolysis
  • Pencil in cup deformity

ESR/CRP normal or elevated
AntiCCP -ve

185
Q

Psoriatic arthritis management

A

NSAID + Physio + Joint injection

If peripheral arthritis / high ESR/CRP: DMARD (methotrexate)

Spondylitis: NSAID + physio + TNF alpha

186
Q

Reactive arthritis

  • How long post exposure
  • Which microbes
  • What is reiters
  • Arthritic pattern
A

1-4 weeks

Campylobacter, salmonella, shigella, chlamydia

Cant see, Cant wee, can’t bend knee (triad)

Acute onset lower limb oligoarthritis

187
Q

Investigate reactive arthritis

A

Ask Hx
GI/GU sample and culture, serology chalmyd

Joint aspirate to rule out septic

188
Q

Reactive arthritis Vs gonococcal

A

Reactive is cross reaction and can be caused by chlamydia.

Gonococcal is septic arthritis

189
Q

What is enteropathic arthritis?

A

Arthritis with IBD (mainly UC)

40% of IBD

lower limb peripheral arthritis

Consider sulfasalazine but treating underlying bowel is best

190
Q

Vasculitis

  • Definition
  • Causes
A

Inflammation of BV

Primary (50%), Secondary (Infection-20%, Inflammation-20%, drugs etc)

191
Q

Vasculitis infections causes

A

URTI causes flare of Granulomatosis with Polangitis (weighers)

192
Q

Vasculitis inflammatory causes

A

SLE, RA, Crohn’s

193
Q

Vasculitis drug induced

A

Beta-lactams

Sulphonamides

194
Q

Vasculitis classification & examples

A

Large vessel

  • GCA
  • Takayasu’s
  • Polymyalgia rheumatica

Medium vessel

  • Kawasaki’s
  • Polyarteritis Nodosa

Small vessel

  • Wegners/GPA
  • Churg-strauss (
195
Q

GCA

  • Definition
  • Main complication
  • Who
  • Presentation
A

inflammatory granulomatous arteritis

  • aorta
  • large cerebral arteries

20% get anterior ischaemic optic neuritis (inflame in ophthalmic artery)
- Sudden visual loss = medical emergency

More in women and over 50

Recent temporal headache + Scalp tenderness + Jaw claudication + visual symptoms (transient diplopia, visual loss like curtain coming down)

196
Q

GCA

  • Investigation and findings
  • Treatment
A

Palpation of temporal artery: tender, absent pulse

ESR over 50

Temporal artery biopsy shows granulomatous inflammatory arteritis (multinucleate giant cells, intimal hypertrophy)

High dose Prednisolone (1mg/kg/day) 4 weeks
+ Aspirin

(osteoprotect for prednis - Ca+VitD+Bisphos)

If refractory: MTX

197
Q

Polymyalgia Rheumatica

  • Pres
  • Assoc with
  • Investigations and diagnosis
  • Tx
A

Morning pain/stuff shoulder/neck/pelvic girdle. Systemic feature (malaise, fever)

50% with GCA (spectrum)

Inc ESR/CRP
Check FBC, U&E, TFT, Bone profile for ddx
Morning stiff over 45 min for over 2 week in over 50s

Prednisolone start high (15mg for 3 weeks) and taper down. Tx for t yrs (add osteoprotect - VitD/Ca/Bisphos)

198
Q

Takyasu’s (Pulseless arteritis)

  • who
  • pathophys
  • features
  • complications
A

Women (esp Japan) 20-40

inflammatory occlusive disease of aorta and branches

fever, wt loss, arthralgia, limb claud/angina/headache/dizzy/abdo pain/haemoptysis/haematuria

stenosis/occlusion/dilatation/aneurysm of aorta and large branches off it

199
Q

Takyasu’s Examination findings

A

Difference in standing BP ovre 1ommHg

High BP (renal stenosis)

Impalpable peripheral pulse

Arterial bruite on all arteries

Aortic regurgitation (dilatation)

200
Q

Takyasu’s Investigations

A

High ESR (over 50)

Aortic angiography (CT/MRI) showing occlusion/stenosis/aneurysm/thickened wall of aorta and large branches & pulmonary arteries)

201
Q

Takyasu’s Treatment

A

Prednisolone + Aspirin + Bone protection

If persistent use TNF alpha blocker (Etanercept, infliximab)

202
Q

E.G of TNF alpha bloceker

A

Etanercept

Infliximab

203
Q

DMARD commonly used in SLE

A

Hydroxychloroquine (also useful in Sjögren & Malaria)

204
Q

Kawasaki’s

  • Who
  • Def
A

Children 6m-5yr

Idiopathic self limiting vasculitis

205
Q

Kawasaki’s

  • Tx
  • Management
A

Aspirin (normally not recommended due to Reye’s)

1st line IV immunoglobulin + high dose aspirin)

long term aspirin + cardiology follow up

206
Q

Kawasaki’s Classical features

A

CRASH & burn

C conjunctivitis (bilateral)
R rash (non-vesicular = no vesicles)
A adenopathy (Cervical&unilateral)
S strawberry tongue (+ inflamed lips/mouth)
H hand/feet - erythema/swelling/desquamation

Burn - fever over 5 days

207
Q

Kawasaki’s Complications

A

Coronary artery aneurysm.

208
Q

Subgroups of small vessel vasculitides

A

ANCA associated
(C-ANCA and P-ANCA)

Immune complex mediated (IgA vasculitis - Henoch-Schonlein, Anti-GBM disease

209
Q

ANCA assoc small vessel vasculitis

A

Granulomatosis with polyangitis (Wegners)

Chrug Strauss

210
Q

Granulomatosis with polangitis triad

A

ELK disease (think of an elk)

ENT - upper resp tract involve (saddle nose, nasal septum perforated)

Lungs - Lower respiratory tract involve (SOB, Haemoptysis, Chest pain)

Kidneys - Glomerulonephritis - nephritic (oedema, HTN, Haematuria)

211
Q

GPA histology

A

Granuloma, Vasculitis

212
Q

GPA investigations

A

Kidney: urinalysis (haematuria, proteinuria, RBC casts)

Lung: CT-chest (caveatting lung nodules)

Serology: C-ANCA

FBC (anaemia), ESR raised

213
Q

GPA management of flare

A

IV Methylprednisolone + Oral Prednisolone + Cyclophosphamide

Maintain with Oral Pred, MTX, Folic acid

214
Q

P-ANCA assoc vasculitis

A

Churg Strauss: small vessel vasculitis giving sinusitis, glomerulonephritis and Purpuric rash

CXR - pulmonary infiltrates, ground glass attenuation

Biopsy: necrotising granulomas

215
Q 
IgA vasculitis (Henoch-Scönlein purpura)
- Typical patient
A

Young man with previous URTI - GpA Strep (pyogenes)

216
Q

IgA vasculitis (Henoch-Scönlein purpura) Pathophys

A

IgA immune complexes in small vessels giving Arthralgia/abdo pain/rash (purpura on buttocks and extensor surfaces)

217
Q

IgA vasculitis (Henoch-Scönlein purpura) Vs IgA glomerulonephritis

A

Bergers & HSP have very similar Pathophysiology but HSP is more likely nephrotic and Bergers nephritic

218
Q

IgA vasculitis (Henoch-Scönlein purpura) Tx

A

Ibuprofen/Para for joint and abdominal pain

Steroids for Kidney function

219
Q

Goodpasture’s

  • Organs affected
  • AAb
  • Typical patient
A

Lungs and Kidneys (anti BM)

Glomerulonephritis (Renal failure), pulmonary haemorrhage (haemoptysis)

Male (20-30/60-70), reduced urine output, haemoptysis, oedema, SOB, cough etc

220
Q

Goodpasture’s

Investigations

A

Renal function: abnormal

Urinalysis: Nephritis (blood+protein)

Renal biopsy: DO THIS URGENTLY! Crescenteric glomerulonephritis
Anti GBM - positive

221
Q

Goodpasture’s

Tx

A

Oral Prednisolone + cyclophosphamide + Plasmapheresis

222
Q

When is renal biopsy contraindicated

A 
Sole native kidney
Neoplasm
Bleeding disease
Uncontrolled severe HTN
acute pyelonephritis
223
Q

Vasculitis screen

A

Haem: FBC, ESR, clotting

Biochem: U&E = Cr (renal function), LFT

CRP

Immunoglobulins: ANCA, RF, complement (C3/4 - SLE), anticardiolipin, cryoglobulins)

Micro: HBV, HCV, urine microscopy and culture

Radiology CXR

224
Q

Septic arthritis

  • When to consider
  • Why important
  • Most common site/organism
A

Acutely inflamed joint (monoarth) esp if immunocompromised/prosthetic

Ca destroy a joint in under 24 hours

Knee (in 50%)
Staph aureus

225
Q

Septic arthritis

Causes

A

Staph aureus +
Strep (GBS) = 90%

Gonococcal if sexual active (don’t confuse with Reiter’s - Chlamyd)

226
Q

Septic arthritis

presentation

A

Hot, Red, Swollen, Immobile

227
Q

Prosthetic Septic arthritis presentation

A

Prolonged low grade course, gradually inc pain, no swelling or fever

there is cellulitis

228
Q

Septic arthritis

RF

A

Prosthetic joint (X10), RA, OA, IVDU, Alcoholism, DM, Immunosuppression, overlying skin infection

229
Q

Septic arthritis

investigations

A

URGENT aspiration of synovial fluid - Gram stain and culture + polarised microscopy (exclude crystal arthropathy) CULTURE PRE ABx

Blood culture (X2) ± gonococcal (rectal, urethral, pharyngeal)

Acute phase proteins (ESR, CRP, WCC raise)

CT/MRI for periarticular abscess/osteomyelitis

230
Q

Septic arthritis

management

A

Surgical drainage and lavage (wash) + High dose IV abx (2/3 wk)

If suspect:

  • G+ Vancomycin,
  • G- 3rd gen cephalosporin

For Staph - fluclox
MRSA - Vancomycin/Teicoplanin
Gonococcal - 3rd gen cephalosporin

231
Q

Septic arthritis

complications

A

Osteomyelitis

Joint destruction

232
Q

Prosthetic Septic arthritis Management

A

Remove joint and put in antibiotic impregnated spacer

233
Q

Osteomyelitis

  • Best investigation
  • Definition
  • Types of sequestration
A

Plain film Xray

Infection of bone marrow (may spread to cortex/periosteum)

Haematogenous - bacterial seeding from far source(assoc with children with vascular metaphysis)

Direct - overlying infected tissue e.g. following trauma/surgery

234
Q

Osteomyelitis

- Organism

A

S Aureus mainly

In IVDU Pseudomonas

In Sickle Cell Salmonella

235
Q

Osteomyelitis RF

A

Trauma, Prosthetics, DM, PAD, Chronic joint disease, Alcohol/IVDU, immunosuppression

236
Q

Haematogenous Osteomyelitis in children Vs adults

A

Children - long bones

Adults - Vertebral bodies

237
Q

Osteomyelitis Pres

A

Acutely febrile, painful (immobile imp, back pain), swelling, tenderness, erythema

(in DM chronic disease may have absent signs of local infection and absent pain due to neuropathy

238
Q

What is Potts disease

A

This is vertebral Osteomyelitis secondary to TB

239
Q

Osteomyelitis investigations

A

FBC (WCC)
Blood cultures (+ve)
Acute phase markers (ESR, CRP)
Xray - appears dark, soft tissue swelling, patchy osteopenia

Cultures from derided bone

240
Q

Management Osteomyelitis

A

Bone and soft tissue debridement

Stabilise and immobilise bone

Local Abx + IV Abx (initial = vancomycin and then culture dependant)
Staph - Fluclox
MRSA- Vanco/Teico

Analgesia

Amputation may be needed in chronic cases e.g. diabetes

241
Q

Fibromyalgia

  • definition
  • who
  • diagnosis
  • management
A

Chronic widespread pain, peripheral hyper excitability and altered pain perception

More in women 20-50

Pain in all 4 quadrants (11.18 tender points) for Over 3 months

1st line: Amitryptaline + CBT

2nd line: Gabapentin/Pregabalin

242
Q

RED Flags back pain

A

TUNA FISH

Trauma
Unexplained WL (Ca, Myeloma)
Neurological (e.g. bowel/bladder dysfunction - cuada equina)
Night pain
Age (Over 50 or below 20)
Fever & night sweats (osteomyelitis, Ca, Psoas abscess)
IVDU/Immunosuppressed
Steroid use (Immunocomp, Osteoporosis)
History of Cancer (Prostate, Breast, Lung, Renal)

243
Q

Cervical back pain causes

A

Spondylosis

Disc degen & Oa

244
Q

Cervical OA complications

A

Spinal stenosis

245
Q

Thoracic back pain

  • Relevance
  • Worrying Ddx
  • Orthopaedic cause
A

More commonly due to serious pathology than cervicolumbar pain

Pancoast and other lung tumour, oesophagus, stomach, liver, gallbladder

Degenerative disc disease

246
Q

Lower back pain serious pathologies

A

Cauda equina - saddle anaesthesia, perianal sensory loss, bladder dysfunction

Ank Spond - Worse on waking

Spinal fracture - sudden onset pain, received by lying down, structural deformity/step

Cancer/infection - Pain remains on lying down, night pain, IVDU, recent infection (haematogenous osteomyelitis)

247
Q

When to refer Lower back pain

A

TUNA FISH

Over 6 weeks of pain

248
Q

Lower back pain DDX

15-30yrs
Over 50

A

Trauma, Fracture, Preg, Anky spond, Prolapsed disc

Degen, Osteoporotic collapse, myeloma, spinal stenosis, malignancy, Paget’s

249
Q

Back pain investigations

A

Plain Xray only if indicated by Red flags

MRI good for soft tissue + nerve impingement

ESR, CRP, Alk Phos, PSA, Ca markers

250
Q

Metastatic Lesion types

A

Prostate = Sclerotic

Lung, Renal = Lytic

Breast = Sclerotic or lytic

251
Q

Back pain/disc herniation/sciatica management

A

Keep active and analgesia 1st (NSAIDs)

Physio

Psychosocial management if sickness behaviour/depressiom

Opioids if NSAIDs ineffective or contraindicated

Lumbar discectomy (only if severe nerve compression)

252
Q

Bone tumours in Adults & Children epidemiology

A

In adults secondary tumours/mets more common

In children primary tumours more common

253
Q

Benign bone tumours

A

Osteoid osteoma, chondroma, osteochondroma

254
Q

Malignant bone tumours

A

Osteosarcoma
Myeloma
Ewing’s sarcoma

255
Q

Cancers that spread to bone

A 
Prostate
Breast
Lung
Kidney
Thyroid
Myeloma
256
Q

Bone tumour symptoms

A 
Bone pain unremitting worse at night
Swelling
Effusion
Deformity
Nodes
Pathological #
weight loss
257
Q

Osteoid osteoma

  • What is it
  • Tx
A

Benign bone tumour

Pain - NSAIDs
Local excision = curative

258
Q

Osteosarcoma

  • Who
  • Assoc disease
  • Where
  • Presentation
  • XR findings
A

Most common in children

Pagets

Epiphysis of long bones (75% knee)

Painless lump, rapidly forms mets to lung

Soft tissue calcification = Hair on end sign. Codman’s triangle = tumour raises periosteum from bone and creates new area of bone

259
Q

Ewings sarcoma

  • Who
  • Pres
  • XR
A

Typically boy around 15

Mass or swelling, long bones, chest, pelvis
Pain, Redness, malaise, Fever

Bone destruction with onion skin layers of periosteal bone formation, Codmans triangle

260
Q

Benign Vs Malignant tumours

A

Weel defiend, sharp zone of transition from tumour to normal = benign (Vice versa)

Uniform periosteum = benign

Multilayered/sun-ray periosteum = Aggressive

Soft tissue mass = malignant

261
Q

Bone tumour investigations

A

Isotope bone scans (PET - esp good for mets)

XR

Alk phos/Ca2+ (hypercalcaemia)
CT/MRI for staging
Biopsy (fine needle)

262
Q

Bone tumour Tx

A

Benign - analgesia and excision

Malignant - Complex MDT. refer to sarcoma clinic

263
Q

Danger of Pathological fractures

A

Potential for dissemination / local recurrence

264
Q

Initial Tx of RA

A

MTX + Another (e.g. Sulfasalazine) + Short course Prednisalone

265
Q

What is a sub capital fracture?

If displaced how tx?

A

Intracapsualr

Hemiarthroplasty (cannulated screws if not displaced)

Final (26 decks)

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