Clinical skills - Monoarticular joint pain Flashcards

1
Q

Major joints

A
Hip 
Knee 
Shoulder 
Elbow 
Ankle
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2
Q

Symptoms of OA

A
Pain esp at night 
Swelling 
Deformity 
Reduced mobility 
Daily activities compromised
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3
Q

Management of OA

A
Lose weight if overweight 
Painkillers 
Ease off on aggravating activity 
Exercise 
Walking stick 
Shoe wear
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4
Q

Clinical management of OA

A
NSAIDs 
Physiotherapy 
Intra-articular injections 
Joint replacement 
Excision femoral head 
Osteotomy 
Athrodesis
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5
Q

Osteotomy

A

Cutting and realignment of bone

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6
Q

Pros of joint replacement

A

Almost instant cure of arthritic pain
Return of mobility
‘Normal life’ - get life back
Majority of joints are long lasting, only few need revisions

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7
Q

Cons of joint replacement

A

Operation
Major complications e.g death
Revision surgeries
Need to be careful

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8
Q

Options of surgeries

A

Fixation method
Bearing surface
Bone preserving/ sacrificing
Hemiarthroplasty/ total

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9
Q

Cemented joint replacement

A

Coated in hydroxypapatite

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10
Q

Principles of joint replacement operations

A

Bearing surface

Fixation to bone

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11
Q

Problems w/ joint replacement surgery

A

Infections
Aseptic looseinng
Metal on metal

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12
Q

Knee replacement surgeries

A

Total knee replacement - ACL always sacrificed
Unicompartmental total knee replacement
Patellar femoral joint replacement

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13
Q

Total knee replacement

A

PCL preserving

PCL sacrificing

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14
Q

Unicompartmental tkr

A

Fixed bearing

Mobile bearing

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15
Q

Complications of surgery

A
Infection 
Dislocation 
Thromboembolic disease 
Leg length discrepancy 
Nerve palsy 
Fracture 
Ongoing pain
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16
Q

How long do hip and knee replacements last

A

10-15 yrs

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17
Q

What properties should joint replacement material have

A
Strength 
Elastic modulus 
Biocompatible 
Bearing surface 
Attachment to bone
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18
Q

Crystals in crystal arthritis

A
Monosodium urate (uric acid) - gout 
Calcium pyrophosphate - Pseudogout
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19
Q

Characteristic of synovial fluid in crystal synovitis

A
>3.5 ml
Low viscosity 
Straw/ opaque colour vs clear
>10,000 WBC/ mm3 vs 200
>50% PMN vs <25
Crystals present
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20
Q

Pathognesis of crystal arthritis

A

Over production of uric acid (exogenous or endogenous)
Underexcretion of uric acid (abnormal renal handling of urate)
A combination of both

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21
Q

Causes of hyperuricemia

A

Overproduction

Under excretion

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22
Q

Causes of hyperuricemia -overproduction

A

Excess dietary purines
Alcohol abuse
Myleoproliferative disorder
Lymphoproliferative disorder

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23
Q

Causes of hyperuricemia - under excretion

A

Renal disease

Polycystic kidney disease

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24
Q

Drugs causing hyperuricemia

A

CANT LEAP

Cyclosporine
Alcohol 
Nicotinic acid 
Thiazides 
Lasix (feusemide)
Ethambutol 
Aspirin (low dose)
Pyrazinamide
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25
Q

Stages of crystal arthritis

A

Asymptomatic hyperuricemia
A/c gouty attack
Intercritical gout
Advanced tophaceous gout

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26
Q

Predisposing factors of crystal arthritis

A

Immediate post op period after major surgery
Stroke
Fasting
Alcohol abuse
Large intake of food w/ high purine content
Local infection

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27
Q

Lab tests for crystal arthritis

A
Joint fluid analysis 
Culture to rule out infection 
Renal function 
Urine dipstick - haemoturia (gout and kidney stone)
S. uric acid and WCC < 15,000/mm3
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28
Q

Differential diagnosis of crystal arthritis

A

Degree of infl - diff to RhA
Matched only by other crystal disease (pseudogout) or infection
Podagra (1st MTP joint pain) characteristic of gout

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29
Q

Core aspects of management of crystal arthritis

A

Patient education
Diet - low purine
Reduce alcohol - increases serum urate production and reduces renal clearance
Weight reduction

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30
Q

Food high in purines

A

Red meat
Animal organs
Fish e.g mackerel, herring, sardines

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31
Q

Treatment of acute attacks of gout

A
Joint rest and local ice 
NSAIDs or COX inhibitors 
Oral steroids
Local steroid injection 
Oral colchicine
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32
Q

Intercritical gout

A

2 or more attacks in a year

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33
Q

Treatment of intercritical gout

A

Diet
Alcohol
Colchicine prophylaxis - 1st 3-6 months to reduce freq. of attacks
Urate lowering drugs

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34
Q

Side effects of colchicine prophylaxis

A

Rash
Hepatoxicity
Severe hypersensitivity

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35
Q

Urate lowering drugs

A

Allopurinol
Uricosuric drugs
Presence of kidney stone or tophi - allopurinol drug of choice
Not started for 2-3 weeks after an a/c attack

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36
Q

Uricosuric agents

A

Increase excretion of uric acid in urine, reducing uric acid in blood plasma
Probenoid, Sulfinpyrazone & benzobromarone
Small risk of uric acid stone formation

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37
Q

Allopurinol

A

Most commonly used drug in lowering uric acid
Xanthine oxidase inhibitor: xanthine –> uric acid
Lowers serum and urinary uric acid excretion
Only started after lifestyle changes

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38
Q

Alternative to allopurinol

A

Febuxostat

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39
Q

Pseudogout

A

Deposition of CPPD in joint cartilage
Chondrocalcinosis
Presence of CPPD crystals associated w/ aggressive, destructive OA
A/c and c/c forms

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40
Q

Chondrocalcinosis

A

Calcified cartilage on a x-rays

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41
Q

Conditions predisposing Pseudogout

A
Ageing 
Hyperparathyroidism 
Haemochromatosis 
Hypomagnesia 
Hypophosphatasia 
Acromegaly 
Trauma 
Infection 
OA
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42
Q

Clinical manifestations of pseudogout

A
Asymptomatic chondrocalcinosis
Radiographic evidence w/out joint symptoms 
Common in 8th decade 
No attacks occur 
CPPD deposition in joints 
Cartilage damage 
Acceleration of OA
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43
Q

Acute Pseudogout

A
a/c mono arthritic - 25%
Occurs more in elderly women than men 
Knee most involved - symmetrical 
Attacks are self limiting 
Parathryoidectomy and severe medical illness can ppt attack
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44
Q

Chronic pseudogout

A

Can mimic OA or RhA - pseudo OA more common

CPPD crystals associated w/ more severe OA and found in 60% of knee joints at time of replacement

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45
Q

Diganosing pseudogout

A

History
Clinical examination
Joint fluid analysis
X-ray

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46
Q

Lab tests for pseudogout

A

Ca, s. uric acid, Mg, Ferritin, PTH
Synovial fluid analysis
-ve Gram stain and -ve cultures
CPPD crystals - rhomboid shaped and weakly +ve birefringent

47
Q

Radiographic appearance of pseudogout

A

Calcium deposition at triangular fibrocartilage
Subchondral sclerosis
Joint space narrowing
Subchondral cysts formation

Most common at radiocarpal articulation and 2nd and 3rd MCP

48
Q

Differential diagnosis of pseudogout

A

Degree of infl matched by gout and active infection
Gout - 1st MTP
Rapid acceleration of infl - Pseudogout
RhA and Pseudogout can coexist

49
Q

Evaluation of patient w/ Pseudogout

A
Hx - family hx of hereditary chondrocalcinosis or haemochromatosis
Metabolic association 
Hyperparathyroidism 
Hypomagnesia 
Hypophosphotasia 
Ca, PO4, LFT, Mg, uric acid
50
Q

Treatment of acute pseudogout

A

Joint aspiration
Steroid injection
Anti-infl

51
Q

Treatment of chronic pseudogout

A

Anti-infl
Periodic intra-articular steroid injection
Associated disease managed

52
Q

Crystal composition in gout

A

Needle like

53
Q

Birefringent of gout crystals

A

-vely

54
Q

Most common joints affected in gout vs pseudogout

A

1st MTP vs Knee

55
Q

Radiography of gout vs peusodgout

A

Rat bite vs white lines of chrondocalcinosis

56
Q

OA is a disease of the entire joint incl

A

Cartilage, synovium, ligaments and bone

Breakdown –> pain and stiffness

57
Q

Causes of 2’ OA

A
Trauma 
Infection - septic arthritis 
Infl -RhA 
Perthe's disease 
Slipped upper femoral epiphysis
58
Q

OA in hips

A

Head of femur loses shiny articular surface

Superior aspect is collapsed

59
Q

OA in knees

A

Genau varus

Loss of space in articular cartilage causes twisting into midline

60
Q

OA in hands

A

Heberden’s nodes

61
Q

Heberden’s nodes

A

Tender, bony swellings on DIPJs

62
Q

Orthopaedic surgery

A

Arthrodesis

Arthroplasty

63
Q

Arthrodesis

A

Fusion - leads to loss of movement
Sacrifice movement
Pain relief
Durable

64
Q

Arthroplasty

A

Replacement
Total joint arthroplasty (head and socket), pain relief, keep movement, may not be durable
Hemi -arthroplasty - half
Excision arthroplasty - removing joint

65
Q

Immediate arthroplasty complications

A

Technical e.g. periopertaive fracture

66
Q

Early arthroplasty complications

A

Infection

Dislocation - constrained or unconstrained (not as aseptic)

67
Q

Late arthroplasty complications

A
Aseptic loosening (bone implant interface)
Wear
68
Q

Which pinches can a thumb do

A

Key pinch
Tip pinch
Tripod pinch

69
Q

Elbow OA

A
Infl - RA 
Pain flexion/ extension 
Pain pronation/ supination 
Ulna-humeral
Radiocapitellar - loss of joint space
70
Q

Shoulder arthroplasty is an example of ..

A

Rotator cuff arthroplasty - but can be sublaxed, acromion degeneration. ‘Cuff’ stabilised and initiates movements of shoulder

71
Q

Radiographic appearance of OA

A

LOSS

Loss of joint space
Osteophytes
Subchondal cysts
Subchondral sclerosis

72
Q

Articular pain

A

From joint capsule, synovial, cartilage
Diffuse, deep pain
Pain on active and passive movement
Swelling common and may have crepitus, instability, deformity

73
Q

Examples of articular pain

A

Arthritis

Synovitis

74
Q

Where does non-articular pain come from

A

Soft tissues - tendons, ligaments, bursa, muscles

75
Q

Features of non-articular pain

A

Localised focal tenderness removed from joint capsules
Painful active but NOT passive movement
Swelling uncommon

76
Q

Examples of non-articular pain

A

Bursitis
Tendonitis
Myostitis

77
Q

Causes of acute infl mono arthritis

A

Infection
Crystal induced
Rheumatic disease

78
Q

Infection as a cause of acute infl mono arthritis

A

Bacterial - septic arthritis
Viral - ReA (rapid course)
Fungal
Mycobacteria

79
Q

Rheumatic disease as a cause of acute infl mono arthritis

A

RhA
SLE
Sarcoid

Usually polyarticular

80
Q

Causes of acute non-infl monoarthrtitis

A

Tumour
Degenerative
Internal derangement
Haemiarthrosis

81
Q

Tumour as a cause of acute non-infl monoarthrtitis

A

Osteosarcoma

Metastatic disease

82
Q

Degenerative causes of acute non-infl monoarthrtitis

A

Infl flare of OA

Erosive OA

83
Q

Internal derangement as a cause of acute non-infl monoarthrtitis

A

Meniscal tear
Fracture
Ligament tear

84
Q

Hemiarthrosis as a cause of acute non-infl monoarthrtitis

A

Trauma
Over anti-coagulation
Clotting disorder

85
Q

Prevalence of RhA

A

0.5 -1%

86
Q

M to F ratio of RhA

A

2.5 to 1

87
Q

Diurnal variation of RhA

A

Worse in AM

Can also be periodic

88
Q

Systemic symptoms of RhA

A

Fatigue
Wt loss
Swelling in salivary glands

89
Q

Investigations in RhA

A
Systemic review 
FBC 
CRP/ ESR 
Raised platelets 
Anti - CCP
ANA
Joint erosions seen on X-rays
90
Q

Why is PsA difficult to diagnose

A

Bone is affected before the skin

91
Q

M to F ratio of PsA

A

1:1

92
Q

Typical onset of PsA

A

During middle age

93
Q

Prevalence of PsA

A

0.1 -1.0%

94
Q

X-rays in PsA

A

Joint erosions

Whittling at end of phalanges - bone in cup

95
Q

Treatment of PsA

A

Using anti-infl and corticosteroids

96
Q

Who is mostly affected by ReA

A

Young people

97
Q

M to F predominance of ReA

A

20:1

98
Q

Which joints does ReA usually affect

A

Large joints e.g. knees and ankles

99
Q

What proportion of patients w/ ReA will develop AS

A

1/3

100
Q

How does ReA react to steroids

A

Responds well

101
Q

Examples of intra-articular corticosteroids

A

Methylprednisolone

Triacinolone

102
Q

Hydroxychloroquine

A

Useful for mild disease, lupus w/ skin and joint involvement
200mg daily taken w/ food

103
Q

Side effects of hydrochloroquine

A

GI disturbance
Headaches
Skin reactions
Retinal toxicity

104
Q

Where is tophi deposited

A

Tophi can be formed and deposited in ANY joint or bone

105
Q

Viscosity of synovial fluid in joint infl

A

Decreased

106
Q

Non-uniform blood staining in synovial fluid

A

Indicative of trauma

107
Q

Histology of OA

A

Wear and tear effect on articular cartilage —> fissures & eburnation
Causes degeneration and loss of ground substance (glycosaminoglycans)
Results in loss of elasticity and erosion of cartilage
Bones then rub together
Attempt at repair causes osteophytes

108
Q

Sclerosis vs chondrocalcinosis

A

Subchondral sclerosis is in the bone

Chondrocalcinosis is in the soft tissue

109
Q

Why do we usually not see swelling in hip osteoarthritis

A

Hip is a very deep joint

110
Q

What aspect of the knee does OA usually affect

A

Medial weight-bearing surface

111
Q

Se of allopurinol

A

Fever, rash and a decreased white cell count

112
Q

Risk factors for tophaceous gout

A

Hyperextension
Heart failure
Renal impairment

113
Q

What can cause bilateral prepatellar bursitis

A

Gout