MSK Flashcards

1
Q

What is Osteoarthritis?

A

Loss of articular cartilage
Wear & tear of joints
MC type of arthritis

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2
Q

RF OA

A

Elderly
After 55 years, females (menopause increases risk)
Previous joint trauma
Genetics
Obesity
RA
Gout
Obesity - low-grade inflam state, not mechanical RF
Joint hypermobility
Occupation! - manual labour (small joints of hands), farming (hips), football (knees)

OSTEOPOROSIS = ↓OA RISK !

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3
Q

Signs / Symptoms OA

A

Typical Px : Elderly patient w/ hip or knee pain (weight-bearing joints) or carpometacarpal joint (base of thumb)

Asymmetrical!
LESS THAN 30 mins morning stiffness
↓Pain with rest
Pain at end of day
↑Pain with activity
Crepitus
Bony swellings - DIP (Heberden’s) and PIP (Bouchard’s)
Effusion
Synovitis
Functional impairment
Tenderness
Deformities

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4
Q

DDx OA

A

RA
Gout
Pseudogout

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5
Q

Causes OA

A

Most - 1º (idiopathic)

2º - caused by other diseases e.g. obesity, haemochromatosis,
??

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6
Q

Ix OA

A

XR - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

CRP might be elevated

Rheum factor + ANA = NEG

MRI - shows early articular cartilage injury and subchondral BM changes

Aspiration of synovial fluid - if painful effusion, shows viscous fluid w few leucocytes

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7
Q

Main pathological features of OA

A

Loss of cartilage
Disordered bone repair

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8
Q

Tx OA

A

Conservative :
Px ed
Exercise
↓weight
Physio
Footwear
Occupational therapy
Walking aid

Medical
> Topical - NSAIDs, Capsaicin
> Oral - NSAIDs (caution!) w/ PPI if long term, paracetamol

Opioids - if above hasnt worked

not rlly gonna offer unless rllyyy bad and nothing else works ->
Intra-articular steroid injections (only short term relief - 2-10 weeks) - hyaluronic acid

Surgery
Remove osetophytes
Joint replacement - if VERY severe
Arthroscopy - ONLY if loose bodies (lasts only 10-15 years)

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9
Q

What is a loose body?

A

When small pieces of articular cartilage break off and “floats” in synovial fluid
Causes joints to lock

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10
Q

What are some indications of a loose body?

A

Uncontrollable pain (esp at night)
Significant limitations

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11
Q

What is Rheumatoid Arthritis?

A

A chronic, autoimmune, inflammatory symmetrical polyarthritis

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12
Q

RF RA

A

Female BEFORE menopause (After menopause, incidence is equal between M and F)

Family history
Smoking!!
Autoimmune conditions
Stress
Infection

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13
Q

Signs / Symptoms RA

A

Joint pain worse in mornings/with cold
Morning stiffness > 30 mins
Loss of function
Fatigue + malaise
Pain decreases with use
Warm, red, tender joints

Joints : SYMMETRICAL!
Small = MCP + PIP (not DIP usually)
Large (as disease progresses) = wrists, elbows, shoulders, knees, ankles

HAND DEFORMITIES : usually at IP joints
1. Ulnar deviation
2. Swan neck (or Z thumb)
3. Boutonniere deformity

Rheumatoid nodules at pressure points - elbow
Carpal tunnel syndrome
Popliteal cyst

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14
Q

What happens in a swan neck deformity?

A

PIP hyperextension
DIP flexion

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15
Q

What happens in a Boutonniere deformity?

A

PIP flexion
DIP hyperextension

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16
Q

Extra-Articular symptoms RA

A

Soft tissue :
Nodules! - usually at pressure points
Bursitis
Tenosynovitis
Muscle wasting

Haematological
Palpable lymph nodes
Splenomegaly
Anaemia
Felty’s triad (rare)

Eyes
Sicca
Sjogren’s
Episcleritis
Scleritis

Neuro
Mild sensory neuropathy (peripheral - legs>arms)
Cord compression
Myelopathy

Skin
Vasculitis

Lungs
Pleural effusion
Rheum nodules
Diffuse fibrosing alveolitis

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17
Q

Diagnostic criteria RA

A

Needs 4/7 of following

  1. Morning stiffness > 30 mins
  2. Arthritis of 3 or more joints
  3. Arthritis of hand joints
  4. Symmetrical
  5. Rheumatoid nodules
  6. Rheumatoid factor pos
  7. Radiographic changes - LESS
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18
Q

DDx RA

A

SLE
Psoriatic arthritis
Symmetrical seronegative spondyloarthropathies

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19
Q

Ix RA

A

XR - LESS
Loss of joint space
Erosions (peri-articular)
Soft tissue swelling
Soft bones (osteopenia)

Bloods
> Rheum factor = POS in 70% patients (but not specific)
> Anti-CCP = POS, vvv specific but not routinely done (If pos = worse prognosis)
> FBC - ↑ platelets, ↑ ESR, ↑ CRP, normochromic normocytic anaemia

MRI/US - erosions at joint margins and bones

If effusion present, then aspiration of joint = CLoudy bc ↑↑WBC

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20
Q

Tx RA

A

Upon diagnosis : 1st Line :
DMARDs - Methotrexate, Leflunomide
+
5-asa - Sulfasalazine

2nd Line:
Biologic - TNF-inhibitor

Symptom control - NSAID

If acute exacerbations, steroids (IM methyprednisolone)

MDT management - Rheum, OT, physio, GP

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21
Q

What is Osteoporosis?

A

Low bone mass
∴ bone fragility + ↑ fracture risk

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22
Q

What is osteopenia?

A

Precursor to osteoporosis
T score between -1 and -2.5

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23
Q

What is Osteomalacia?

A

Poor bone mineralisation
bc lack of calcium (adult form of rickets)
∴ soft bones

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24
Q

Causes Osteoporosis

A

1º - post-menopause & age

2º - ↑bone turnover, SHATTERED
Steroid use (prednisolone)
Hyperthyroidism/Hyperparathyroidism
Alcohol/smoking
Thin (low BMI)
Testosterone low
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease e.g. RA, myeloma
Dietary calcium low

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25
Q

Why does early menopause/post-menopause cause Osteoporosis?

A

Oestrogen protects bones

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26
Q

RF Osteoporosis

A

Think : Patient, Disease, Medication
Also think : SHATTERED

Patient
Old age
Female
FHx
↓BMI
Alcohol & smoking
Diet - ↓Ca2+ (lactose intolerant)
Athletes

Disease
Joint disease (RA, SLE)
Hyperthyroidism, Hyperparathyroidism
↑Cortisol - Cushing’s
↓Oestrogen/Testosterone
Renal disease (↓Vit D)
Previous fractures
Anorexia

Medication
Corticosteroids
Hormonal

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27
Q

Pathophysiology Osteoporosis

A

Essentially : ↑Resorption by osteoclasts, ↓formation by osteoblasts

W/ age, trab architecture changes :
↓Trab thickness
↓Connections in horizontal trab
∴ ↓Trab strength and ↑ fracture risk

Oestrogen def causes remodelling imbalance

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28
Q

What is osteoporosis characterised by?

A
  1. ↑↑Bone turnover
  2. Mostly cancellous bone loss
  3. Microarchitectual disruption

∴ NET LOSS OF BONE

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29
Q

Why is horizontal trabeclae very important?

A

Eular-Buckling theory

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30
Q

What is Eular-Buckling theory?

A

Baso,
In a column, less likely to bend or snap if there are fixed points
don’t quote me on this but basically what it means i think

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31
Q

Signs / Symptoms Osteoporosis

A

ASYMPTOMATIC UNTIL FRACTURE

Hip - neck of femur (if elderly falls on side/back)

Wrist - Distal radius, Colle’s/Smith’s fracture (fall on outstretched arm)

Verterbra - shorter/stooping, sudden onset on pain in spine - often radiates to front

Fragility fractures

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32
Q

Ix Osteoporosis

A

DEXA BMD (Dual energy XR & absorptiometry bone mineral density) - T-score
< - 2.5 + fracture = severe OP
< -2.5 = OP
between -1 and -2.5 = osteopenia
> -1 = Normal

XR

FRAX - fracture risk assessment (age, sex BMI, prev. fractures, steroids)

FBC - normal Calcium phosphate and alklaine phosphate

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33
Q

Tx Osteoporosis

A

1st line - ORAL BISPHOSPHONATES
1- alendronate daily
2 - diff oral bis e.g. risendronate
3 - If CI to bis, then strontium ranelate (↓ fracture rate)

Denosumab - monoclonal Ab, inhibits RANK which would otherwise activate osteoclasts

HRT - in menopausal women
Raloxifene - SERM (selective oestrogen receptor modulator), similar to HRT

Testosterone for men

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34
Q

How should you tell patients to take bisphophonates?

A

w LOTS of water and sitting upright for > 30 mins
Wait at least 30 mins before eating

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35
Q

Mechanism of Bisphosphonates for Osteoporosis

A

Inhibits bone resorption by inhibiting enzyme Farnesyl Pyrophosphate synthase by removing ruffled border
∴ ↓osteoclast activity

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36
Q

Prevention Osteoporosis

A

Adcal D3 - VitD & Ca2+
Ca2+ rich diet
HRT - for postmenopausal women
Corticosteroids - consider prophylactic bis
Regular weight bearing exercise
Stop smoking and alcohol
DEXA scans

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37
Q

S/E Bisphosphonates

A

Osteonecrosis of jaw
GI distress
↓ Ca2+
Renal toxicity
Oesophageal ulcers

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38
Q

What is Systemic Lupis Erythematosus?

A

Inflammatory, multisystem, autoimmune condition

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39
Q

What is SLE assoc w?

A

Raynaud’s
Anti-Phospholipid syndrome

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40
Q

Typical Patient of SLE

A

Female
20 - 40 years old
More common in Afro-Caribbean and Asian population

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41
Q

RF SLE

A

Pre-menopausal women
Afro-Caribbean/Asian
Genetics - HLA: DR2, DR3, C4, A, Null Allele
Drugs - Hydralazine, Isoniazide, procainamide, penillamine !
UV light
Smoking
EBV

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42
Q

What type of hypersensitivity reaction is SLE?

A

TYPE 3

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43
Q

Pathophysiology of SLE

A

Autoantibodies are produced by B cells
These target autoantigens
∴ form IMMUNE COMPLEXES (T3) at a variety of sites

∴ complement system activated
∴ neutrophil influx
∴ INFLAMMATION

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44
Q

Signs / Symptoms SLE

A

Remitting and relapsing

V non-specific symptoms : Malaise, fatigue, myalgia, rash, weight loss, skin problems, fever

Correctable ulnar deviation

Haematologically :
Anaemia
Thrombocytopenia
Neutropenia
Lymphopenia
Raynaud’s

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45
Q

Ix SLE

A

MUST HAVE 4/11 OF FOLLOWING FOR DIAGNOSIS !!!!!!!!

MD SOAP BRAIN
Malar rush - butterfly rash on face
Discoid rash

Serositis - pleuritis, pericarditis
Oral ulcers
Arthritis (non-erosive - similar to RA)
Photosensitivity - rashes on sun exposed areas

Blood disorder - ALL LOW
Renal disease - proteinuria
Anti-nuclear antibody POSITIVE
Immunological disorder - anti ds-DNA
Neuro disorder - seizures, myasthenia gravis etc

∴ INVESTIGATIONS WILL INCLUDE :
> Anti-nuclear antibody test (sens but not spec)
> Double stranded DNA antibody (spec but not sens)
> Other Abs - RF, anti-cardiolipin, Anti-RO, Lupus antibodies

↑ ESR (CRP might be normal)
↓C3 + C4
MRI/CT brain

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46
Q

POP QUIZ!
Patient comes in with multi-systemic disorder, ↑ ESR but normal CRP
What do you think of?

A

SYSTEMIC LUPUS ERYTHEMATOSUS

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47
Q

Tx SLE

A

Avoid triggers - UV protections
Lifestyle - stop smoking, weight loss
Topical - suncream etc


If ACUTE - IV Cyclophosphamide + high dose prednisolone

If NOT severe - Anti-malarial e.g. hydroxychloroquine and/or steroids e.g. prednisolone

IF severe - Immunouppressives e.g. Cyclophosphamide, methotrexate, ciclosporin, azathioprine

NSAIDs
Anti-coagulants
Plasmapheresis

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48
Q

Monitoring SLE

A

Kidney function should be monitored!

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49
Q

What is Gout?

A

Inflammatory arthritis assoc w/ hyperuricaemia

Negatively bifringent needle-shaped monosodium urate crystals

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50
Q

Typical patient of Gout

A

Men > 40 years !
Chinese, Polynesian, Filipino IF westernised diet (not in native county!)

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51
Q

Causes Gout

A

1. Under-excretion of Uric Acid
Hyperuricaemia
Alcohol
Obesity
DM (insulin resistance = ↑insulin)
HTN
Hypothyroidism, Hyperparathyroidism
Drugs - low dose aspirin, diuretics, lead poisoning, ethambutol, pyrazinamide, cyclosporine, tacrolimus
Renal - defect in URAT1 transported in kidney, seen in kidney disease

2. XS purines TOO MUCH RED MEAT, ORGAN MEAT, SHELLFISH, ANCHOVIES, ALCOHOL
Also : Metabolic syndrome - hyperlipidaemia
Lesch-Nyhan syndrome

3. ↑Production of uric acid
Chemo/Radiotherapy
Surgery - cell death
Carcinoma
Psoriasis
Myeloproliferative diseases - polycythaemia vera

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52
Q

Causes of Gouty attack

A

Anything that causes sudden alteration in uric acid conc

Aggressive intro/Sudden stop of hypo-uricaemic therapy
Alcohol/Shellfish binges
Sepsis, MI, acute severe illness
Trauma, surgery, dehydration

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53
Q

RF Gout

A

↑ Alcohol
Purine rich foods - shellfish, organ meat etc
High fructose intake - sugar
FHx
Age
Obesity
DM
IHD
HTN

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54
Q

Pathophysiology Gout

A

Purine from diet
Gets converted -> Hypoxanthine -> Xanthine

Then, Xanthine -> Uric acid
Catalysed by xanthine oxidase
Excreted in kidneys

If ↑↑Uric acid, XS is converted to monosodium urate crystals and deposited in tissues - TOPHI

Monosodium urate crystals can cause inflammation - ∴ more pain
Tends to form in peripheral joints (big toe) bc temperature is cooler and/or if previous trauma in joint

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55
Q

Signs / Symptoms Gout

A

Sudden onset of agonising pain, swelling and tenderness and redness - “toe on fire”

Pain precipitated by excess food, alcohol, dehydration, diuretic therapy
Recurrent episodes
Red, shiny, warm, PAINFUL joint w white deposits (tophi) on skin
Skin over joint has peeled off

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56
Q

DDx Gout

A

Septic Arthritis
Tophaceous gout

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57
Q

Ix Gout

A

JOINT ASPIRATION!! - to rule out septic arthritis, ALWAYS RULE OUT A RED, HOT JOINT

X-Ray ! - punched out erosions near joint

GS!! Polarised light microscopy - neg bifringent needle shaped monosodium crystals

Bloods - raised serum urate (can be normal)

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58
Q

POP QUIZ
A patient comes in with a hot, red joint. What do you do?

A

ASPIRATE ASPIRATE ASPIRATE!!!
ALWAYS RULE OUT A RED, HOT JOINT
to rule out septic arthritis

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59
Q

Tx Gout

A

Lifestyle - kcal restriction, modify diet, weight loss, ↓alcohol
DAIRY - protective! & cherries, vitamin C

1st line - NSAIDs e.g. ibuprofen

2nd line - Colchicine (If NSAIDs CI)

Prophylaxis - Xanthine oxidase inhibitors e.g. Allopurinol ! (rapidly reduces serum urate levels)

DO NOT use Allopurinol during acute attack!! Wait 3 weeks after attack to give
& ALSO give Colchicine for 6 months OR NSAID for 6 weeks otherwise will induce a gouty flare

Febuxostat if Allopurinol CI

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60
Q

What is Pseudogout?

A

Deposition of calcium pyrophosphate crystals in joints
Usually larger joints!
Knee > Wrist > Shoulder > Ankle > Elbow

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61
Q

Typical patient of Psuedogout

A

Female > 70 years

62
Q

RF Pseudogout

A

Old age
OA
Hyperparathyroidism
Haemochromatosis
Hypophosphataemia
DM

63
Q

Pathophysiology of Pseudogout

A

Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue
Chondrocalcinosis = radiological appearance

64
Q

What is chondrocalcinosis?

A

Linear calcification parallel to articular surfaces

65
Q

Causes of acute Pseudogout attack

A

Direct trauma to joint
Intercurrent illness
Surgery - esp parathyroidectomy
Blood transfusion, IV fluids
T4 replacement
Joint lavage

66
Q

Signs / Symptoms Pseudogout

A

Severe jont pain
Acute synovitis
Acute hot, swollen joint
Fever
Stiffness

67
Q

What are Tophi?

A

Onion-like aggregates of monosodium urate crystals with inflammatory cells

68
Q

What is Tophaceous Gout?

A

Appears in people w/ persistently high levels of uric acid
Tophi form in skin around joints - ear, fingers, Achilles tendon

Tophi release proteolytic enzymes ∴ erosions to bone

Assoc w/ renal impairment and/or long-term use of diuretics

69
Q

S/E Colchicine

A

Diarrhoea
Abdo pain

70
Q

S/E Allopurinol

A

Rash
Fever
Low WBC

71
Q

How to distinguish OA and Pseudogout

A
  1. Pattern on involvement - which joint?
  2. Marked inflam component
  3. Superimposition of acute attack
72
Q

What is Pseudogout also known as?

A

Pyrophosphate arthropathy

73
Q

Ix PseudoGout

A

XRAY - evidence of chondrocalcinosis

JOINT ASPIRATION - ALWAYS ASPIRATE A RED HOT JOINT

GS Polarised light microscopy - positively bifringent rhomboid shaped calcium pyrophosphate crystals

FBC - ↑ WBC

74
Q

Tx Pseudogout

A

1st line - NSAIDs
2nd line - Colchicine

Analgesia
Physio
Rest and icepacks

Long term Tx :
Try anti-rheum treatment e.g. methotrexate, hydroxychloroquine

Synovectomy if bad
Surgery

75
Q

Name the 5 most common tumours that spread to bone

A

LEAD KETTLE - PB KTL
Prostate
Breast

Kidney
Thyroid
Lung

76
Q

Typical patient of 1º Bone tumours

A

Rare
Usually only seen in YA and children

77
Q

RF 1º Bone tumours

A

Radiation - XR, CT
Padget’s disease

78
Q

MC : 1º or 2º bone tumours?

A

79
Q

Name the types of Benign 1º bone tumours

A
  1. Osteochondroma
  2. Giant cell tumour
  3. Osteoblastoma & osteoid osteomas
80
Q

Name the types of Benign 1º bone tumours
AND state who they affect and where on the body if you can

A

OGO

1. Osteochondroma
Males < 25 years old
Develop in metaphysis of long bones (distal femur, distal tibia, ilium, scapula)

2. Giant cell tumour
Develop in epiphysis of long bones (distal femur, proximal tibia)

3. Osteoblastoma & osteoid osteomas
From osteoblasts, forms nidus

81
Q

Name the types of Malignant 1º bone tumours

A

OEC

  1. Osteosarcomas
  2. Ewing’s sarcomas
  3. Chondrosarcoma
82
Q

What is Osteosarcoma strongly associated with?

A

Padget’s

83
Q

What age does Osteosarcoma usually affect?

A

15-19

84
Q

Where does Osteosarcoma usually affect?

A

Knees or proximal humerus
Destroys bones, spreads to tissues
RAPIDLY METASTASISES TO LUNGS

85
Q

Which 1º rapidly metastasises to the lungs?

A

Osteosarcoma!

86
Q

What age range does Ewing’s sarcoma usually affect?
Is it a common disease?

A

RARE
< 25 years old
15 years old = peak incidence

87
Q

What areas does Ewing’s sarcoma usually affect?

A

Hips + long bones

88
Q

How does Ewing’s sarcoma specifically tend to present?

A

Painful swelling/redness in long bones of arms, legs, chest, pelvis
Sometimes skull, flat bones of trunk

Can cause paralysis +/- incontinence if affects spine

89
Q

What region does chondrosarcoma usually affect?

A

Pelvis MC
Also : femur, humerus, scapula, ribs

90
Q

How does chondrosarcoma specifically tend to present?

A

Deep, dull pain
Affected area is swollen and tender

91
Q

How does an osteoid osteoma specifically tend to present?

A

Pain worsens at night

92
Q

Osteochondroma and Osteoblastoma can both press on ______

A

spinal cord
∴ numbness, limb weakness, avascular necrosis

93
Q

Chondrosarcoma forms from?

A

Chrondrocytes

94
Q

What is Enteric Arthritis?

A

Arthritis 2ºto IBD

95
Q

Cause Enteric Arthritis

A

Bacteria

96
Q

RF Enteric Arthritis

A

MALE&raquo_space; Female

97
Q

Signs / Symptoms Enteric Arthritis

A

Asymmetrical joints
Synovitis affecting PERIPHERAL JOINTS
Monoarticular OR polyarticular
Large joints - knees, ankles, feet
Sacroilitis

98
Q

Tx Enteric Arthritis

A

Will subside with remission of IBD

99
Q

What is Vasculitis?

A

Inflam of blood vessels

100
Q

Conditions assoc w Vasculitis

A

Infective - subacute IE
Non infective - SLE, Scleroderma, Polymyositis, Dermatomyositis, Goodpasture’s

101
Q

What does Giant Cell Arteritis affect?

A

Affects aorta +/- its major branches - carotid, vertebral arteries
TEMPORAL ARTERY

102
Q

RF Giant Cell Arteritis

A

> 50 !!
Atherosclerosis
Females&raquo_space;>
Smoking
Hx of polymalgia rhematica

103
Q

Signs / Symptoms Giant Cell Arteritis

A

HEADACHE - New onset, unilateral over temporal area
Scalp tenderness - hurts to brush hair
Jaw claudication
Visual disturbances - blurred vision, diplopia, amaurosis fugax, blindness

104
Q

Ix Giant Cell Arteritis

A

↑ESR +/- ↑CRP , (ESR > 50mm/hour)

GS!!!* TEMPORAL ARTERY BIOPSY
Giant cells, granulomatous inflam


On examination, temporal arteries might be tender + thickened on palpation
Pulse might be diminished
US - Halo sign of temporal and axillary artery

105
Q

Tx Giant Cell Arteritis

A

High dose glucocorticoid ASAP
Usually Prednisolone 40-60mg

106
Q

Comps Giant Cell Arteritis

A

Blindness
Irreversible neuropathy

107
Q

Big vessels - Vasculitis
What is it?

A

Giant cell arteritis

108
Q

Medium vessels - Vasculitis
What is it?

A

Polyarteritis Nodosa

109
Q

Small vessels - Vasculitis
What is it?

A

Granulomatosis w Polyangiitis

110
Q

Where does Polyarteritis Nodosa affect?

A

Mid-sized vessels in locations like :
Skin
GI tract
Kidneys
Heart

111
Q

RF Polyarteritis Nodosa

A

HEP B
Hep C
HIV
MC in developing countries

112
Q

Ix Polyarteritis Nodosa

A

↑ESR +/- CRP
HBsAg

BIOPSY - transmural fibrinoid necrosis

113
Q

Signs / Symptoms Polyarteritis Nodosa

A

Peripheral neuropathy - mononeuritis multiplex
Cutaneous/Subcutaneous nodules !!!
Unilateral orchitis!!!
Abdo pain
Livedo reticularis
HTN

114
Q

What is Livedo reticularis?

A

Mottled, purplish, lace-like rash

115
Q

Tx Polyarteritis Nodosa

A

If Hep B pos - antiviral agents, plasma exchange and corticosteroids

If Hep B neg - corticosteroids + cyclophosphamide

116
Q

Where does Granulomatosis w Polyangiitis affect?

A

Small vessels
Resp tract + Kidneys

117
Q

What age group does Granulomatosis w Polyangiitis affect?

A

Late teens
Early adulthood

118
Q

Signs / Symptoms Granulomatosis w Polyangiitis

A

CLASSIC SIGN = Saddle shaped nose!!
bc perforated nasal septum

Epistaxis
Crusty nasal/ear secretions - hearing loss
Sinusitis
Might be mistaken for pneumonia - cough, wheeze, haemoptysis

119
Q

Ix Granulomatosis w Polyangiitis

A

FBC - ↑Eosinophils
Histology - granulomas

c-ANCA !!!
NOT p-ANCA

120
Q

what does ANCA stand for?

A

Anti-Neutrophil Cytoplasmic Abs

121
Q

Tx Granulomatosis w Polyangiitis

A

Nasal corticosteroids
Cyclophosphamide

122
Q

When is Septic Arthritis MC?

A

< 4 years
or Older adults

123
Q

Pathophysiology Septic Arthritis

A

Infection of at least 1 joint by pathogenic inoculation by microbes
Either directly or haematogenously

124
Q

Causes Septic Arthritis

A

Staph. Aureus - MC!!
Group A Strep - Strep Pyogens
E. Coli
Neisseria gonorrhoea
Haem. Influenzae

Can be a comp of joint replacement

125
Q

RF

A

Pre-Existing joint disease (OA or RA)
Prosthetic joint
IVDU
Immunosuppression
Alcohol
DM
Intra-articular corticosteroid injection

126
Q

Signs / Symptoms Septic Arthritis

A

HOT RED SWOLLEN JOINT
Refusing to weight bear (kids usually), stiffness, reduced range of motion

Knee or hip usually! Usually only one knee
CONSIDER IN EVERY CHILD W A JOINT PROBLEM !!!!!!

Fever
Lethargy
Sepsis

127
Q

Onset of Septic Arthritis

A

< 2 weeks

128
Q

DDx Septic Arthritis

A

Transient sinovitis
Perthes disease
Slipper upper femoral epiphysis
Juvenile idiopathic arthritis

129
Q

Ix Septic Arthritis

A

ASPIRATE !!!! - gram stain, crystal microscopy, MC+S

Blood culture
WBC - might be raised
ESR/CRP ↑

130
Q

Tx Septic Arthritis

A

Aspirate + Surgical drainage + washout of joint to clear infection if severe !

Empirical Abx e.g. flucloxacillin
Spec Abx - after results (cont for 3-6 weeks)

Analgesia
Be esp cautious w immunosupp patients
Consult orthopedic team!

131
Q

What is Osteomyelitis?

A

Inflam of BONE

132
Q

Cause Osteomyelitis

A

Staph. Aureus - If haematogenous
Staph. Epidermidis - Exogenous/Local

133
Q

MC mode of infection Osteomyelitis

A

Haematogenous!
But also through surgery

134
Q

RF Osteomyelitis

A

Open fracture
Orthopaedic ops
DM - esp foot ulcers
Periph arterial disease
IVDU
Immunosuppresion
Children - URTI or varicella infection

135
Q

Signs / Symptoms Osteomyelitis

A

Limp/Reluctance to weight beat (children)
Non-Spec pain and tenderness at site of infection
Fever
Erythema
Swelling

136
Q

Ix Osteomyelitis

A

FBC - ↑WBC
↑ ESR/CRP

X-Ray - can see periosteal reaction
If neg, doesn’t discount!

GS MRI

Blood cultures, bone cultures

137
Q

Tx Osteomyelitis

A

Abs - 6 weeks flucloxacillin (+rifampicin for first 2 weeks)

Clindamycin if penicillin allergy!
Vancomycin - MRSA

Surgery - debridement of infected bone and tissue

138
Q

Advice for taking bisphophonates

A

First thing in morning
Empty stomach
Remain upright for 30 mins after taking

139
Q

What is a classic patient of Fibromyalgia?

A

20 - 50 year old woman with poor socioeconomic status

140
Q

Signs / Symptoms Fibromyalgia

A

↑Sensitivity to pain
Fatigue
Fibro-fob - problems with memory and conc
Morning stiffness
Headaches
IBS

141
Q

Ix Fibromyalgia

A

11 tender points in 9 pairs of sites, for at least 3 months
http://www.fibromyalgiaawareness.com/2012/04/fibromyalgia-tender-points-poster.html
^^^^^ NOT RECOMMENDED AS DIAGNOSIS NOW BUT KEEP IN MIND

Now - widespread pain in combo w fatigue, sleep difficulties, memory issues

142
Q

Tx Fibromyalgia

A

Education
Exercise + Relaxation
Analgesia
CBT

143
Q

What is Sjogren’s?

A

Autoimmune condition that affects exocrine glands
∴ Dry mucous membranes

144
Q

RF Sjogren’s

A

1º - just happens

FHx - 1st degree relative = 7x risk!!
Female
40+

145
Q

Signs / Symptoms Sjogren’s

A

Dry mouth
Dry eyes
Dry vagina

146
Q

Ix Sjogren’s

A

Anti-Ro and Anti-La antibodies

POS Schirmer test

147
Q

Describe the Schirmir test

A

Insert folded filter paper under lower eyelid with strip hanging out over eyelif
Tear travelling < 10mm is POS test!!

Healthy adults = tear travels > 15mm

148
Q

Tx Sjogren’s

A

Artificial tears, artificial saliva, vaginal lubricants

Hydroxychloroquine used to halt progression

149
Q

Comps Sjogren’s

A

Eye infection - conjugutivitis
Oral problems - dental cavity
Vaginal problems - candidiasis, sexual dysfunction

150
Q
A