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Musculoskeletal System > Disease Profiles 2 > Flashcards

Disease Profiles 2 Flashcards

1
Q

Systemic Lupus Erythematous: Management - Mild-Moderate Disease presents how?

A

Skin disease with arthralgia

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2
Q

Systemic Lupus Erythematous: Management - Mild-Moderate Disease

A

Hydroxychloroquine
Short course of NSAIDs for symptom control
Steroids - IA for arthritis and topical for cutaneous manifestations

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3
Q

Systemic Lupus Erythematous: Management - Moderate-Severe Disease presents how?

A

Inflammatory arthritis with organ involvement

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4
Q

Systemic Lupus Erythematous: Management - Moderate-Severe Disease

A

Hydroxychloroquine
Microphenylate
Treat organ complications appropriately

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5
Q

Systemic Lupus Erythematous: Management - Moderate-Severe Disease acute flare up

A

Immunosuppressants - Methotrexate or Azathioprine
Oral steroids for short periods - tries to induce remission

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6
Q

Systemic Lupus Erythematous: Management - Severe Organ Disease e.g. Lupus Nephritis or CNS lupus

A

IV steroids and Cyclophosphamide

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7
Q

Systemic Lupus Erythematous: Management - What may be considered for unresponsive cases? (2)

A

IV immunoglobulin
Rituximab

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8
Q

Systemic Lupus Erythematous: Potential complication

A

Increased risk of PE - consider if X-Ray is normal

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9
Q

Systemic Lupus Erythematous: Subcutaneous Cutaneous Lupus presentation

A

Small erythematous lesions on the neck, shoulders and forearms that spares the face

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10
Q

Systemic Lupus Erythematous: Discoid Lupus Erythematous presentation

A

Non-cancerous chronic skin condition that has erythematous raised scaled plaques with active inflammation that is triggered by UV light exposure

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11
Q

Systemic Lupus Erythematous: Discoid Lupus Erythematous affects what areas? (3)

A

Face
Neck
Head

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12
Q

Systemic Lupus Erythematous: Urine Dipstick Test will show what?

A

Anti DNA antibodies - these are toxic to the kidney so must test if SLE is suspected

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13
Q

Systemic Lupus Erythematous: If the urine dipstick test is positive for AdsDNAA then what must be conducted?

A

Biopsy to confirm nephritis

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14
Q

Sjogren’s Syndrome

A

Autoimmune condition that affects the exocrine glands characterised by lymphocytic infiltrates

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15
Q

Sjogren’s Syndrome: Epidemiology of sexes

A

Higher prevalence in females

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16
Q

Sjogren’s Syndrome: Most common patient group

A

Middle aged women

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17
Q

Sjogren’s Syndrome: Can be secondary to what conditions? (2)

A

Rheumatoid Arthritis
SLE

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18
Q

Sjogren’s Syndrome: Pathophysiology

A

Immune system attacks the lacrimal and salivary glands

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19
Q

Sjogren’s Syndrome: 6 main symptoms

A

Dry eyes - feel gritty
Dry mouth - may lead to a fissured tongue
Dry throat
Vaginal dryness
Joint pains
Fatigue

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20
Q

Sjogren’s Syndrome: Signs - impact on the parathyroid gland

A

Parotid gland enlargement

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21
Q

Sjogren’s Syndrome: Oral signs

A

Increased dental caries

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22
Q

Sjogren’s Syndrome: Schirmers Test

A

Used to determine whether the eye produces enough tears to keep it moist - this will present with ocular dryness

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23
Q

Sjogren’s Syndrome: What would be present within the blood? (4)

A

Positive for Anti-Ro and Anti-La antibodies
Raised IgG
Raised plasma viscosity/ESR

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24
Q

Sjogren’s Syndrome: What is present on lip gland biopsy?

A

Lymphocytic infiltrates

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25
Q

Sjogren’s Syndrome: Management - Management for symptom control (3)

A

Tear replacement
Salivary replacement
Analgesia - for pain

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26
Q

Sjogren’s Syndrome: Management - Main pharamaceutical used

A

Hydroxychloroquine - for arthralgia and fatigue

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27
Q

Sjogren’s Syndrome: Complications (3)

A

Increased risk of lymphoma
Peripheral neuropathy
Interstitial lung disease

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28
Q

Systemic Sclerosis or Scleroderma

A

Systemic connective tissue autoimmune disease characterised by vasculopathy, autoimmunity and fibrosis

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29
Q

Systemic Sclerosis or Scleroderma: Two types

A

Diffuse
Limited

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30
Q

Systemic Sclerosis or Scleroderma: Epidemiology of sexes

A

More common in women

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31
Q

Systemic Sclerosis or Scleroderma: Peak incidence

A

30-50 years old

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32
Q

Systemic Sclerosis or Scleroderma: Pathophysiology - Initiating Event

A

Etiologic agent combined with genetic predisposition

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33
Q

Systemic Sclerosis or Scleroderma: Pathophysiology - The initiating event induces activation of what? What does this activation cause?

A

Endothelial cells - causes leukocyte attraction and adhesion with tissue hypoxia

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34
Q

Systemic Sclerosis or Scleroderma: Pathophysiology - Myofibroblast formation occurs due to what?

A

Fibroblast, Fibrocyte and Endothelial cell activation

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35
Q

Systemic Sclerosis or Scleroderma: Diffuse SSc - Skin involvement occurs where?

A

Extremities - Above or below the elbows and knees + Face + Trunk

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36
Q

Systemic Sclerosis or Scleroderma: Diffuse SSc - Raynauds Presentation occurs when?

A

Coinciding with or following the onset of symptoms

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37
Q

Systemic Sclerosis or Scleroderma: Diffuse SSc - When does significant organ involvement occur?

A

Early

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38
Q

Systemic Sclerosis or Scleroderma: Diffuse SSc - What antibodies are associated with this? (2)

A

Anti-SCL-50 antibody
Anti-RNA polymerase III

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39
Q

Systemic Sclerosis or Scleroderma: Limited SSc - Skin involvement occurs where?

A

Confined to the face, hands, forearms and feet

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40
Q

Systemic Sclerosis or Scleroderma: Limited SSc - When does Raynaud presentation occur?

A

Precedes the onset of other symptoms

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41
Q

Systemic Sclerosis or Scleroderma: Limited SSc - When does significant organ involvement occur?

A

Occurs later

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42
Q

Systemic Sclerosis or Scleroderma: Limited SSc - What antibody is associated?

A

Anti-centromere antibody

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43
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Impacts on the face (4)

A

Small mouth with puckering
Beaked nose
Thickened and tight skin - lack of wrinkles
Telangiectasia

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44
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - What is the triphasic phenomenon of Raynauds Disease? (3)

A

Blanching
Acrocyanosis - purple or blue
Reactive hyperaemia - redness

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45
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Impact on the skin

A

Thickening

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46
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Impact on the GIT (7)

A

Dysphagia - due to disruption of the vasculature around the oesophagus
GORD
Gastric Antravascular Ectasia (GAVE)
Malabsorption
Fluctuating bowel habit - constipation and diarrhoea
Faecal incontinence

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47
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Cardiopulmonary Impacts (3)

A

Interstitial lung disease
Pulmonary arterial hypertension
Myocardial Disease

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48
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Renal impacts

A

Scleroderma renal crisis
Non-specific progressive renal dysfunction

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49
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Presentation of Scleroderma renal crisis

A

Uncontrolled hypertension with proteinuria and worsening renal function

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50
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Scleroderma Renal Crisis associated with what? (2)

A

Associated with Anti-RNA Polymerase III Antibody
High steroid dose

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51
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation - Impact on the hands

A

Sclerodactyly - hardening of the skin of the hands to cause a claw like shape

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52
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation of Diffuse SSc (5)

A

Joint contractures
Skeletal myopathy
Interstitial lung disease
Myocardial involvement
Renal crisis

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53
Q

Systemic Sclerosis or Scleroderma: Clinical Presentation of Limited SSc (40

A

Raynauds Disease - digital ischaemia
Oesophageal disease
Pulmonary hypertension
Malabsorption

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54
Q

Systemic Sclerosis or Scleroderma: Red Flags of Clinical Presentation (5)

A

Onset of Raynaud’s in mid-adulthood - with SOB and Telangiectasia
Digital ulcers
Ischaemia
Skin tightness
Loss of dexterity in the hands

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55
Q

Systemic Sclerosis or Scleroderma: What antibody is present in both types?

A

Anti-RNA Polymerase

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56
Q

Systemic Sclerosis or Scleroderma: What antibody is present in limited SSc?

A

Anti-centromere

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57
Q

Systemic Sclerosis or Scleroderma: What antibody is present in diffuse SSc?

A

Anti-topoisomerase (Anti-Scl-70)

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58
Q

Systemic Sclerosis or Scleroderma: Management steps of Raynaud’s Disease (4)

A
  1. Calcium Channel Blockers - Nifedipine first
  2. PDE-5 Inhibitor - Sildenafil
  3. Prostacyclin Infusion - Iloprost
  4. Endothelin Receptor Antagonist - Bosentan
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59
Q

Systemic Sclerosis or Scleroderma: Pulmonary Hypertension Management - If not treated what will this lead to?

A

Right Heart Failure

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60
Q

Systemic Sclerosis or Scleroderma: Pulmonary Hypertension Management (4)

A

PDE-5 Inhibitor
Endothelin Receptor Antagonists
Eproprostenol infusions
Oxygen

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61
Q

Systemic Sclerosis or Scleroderma: Pulmonary Hypertension Management - Examples of PDE-5 Inhibitors (30

A

Sildenafil
Tadalafil
Vardenafil

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62
Q

Systemic Sclerosis or Scleroderma: Pulmonary Hypertension Management - Examples of Endothelin Receptor Antagonists (3)

A

Bosentan
Ambrisentan
Macitentan

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63
Q

Systemic Sclerosis or Scleroderma: Stages of Pulmonary Fibrosis Management (4)

A
  1. Mycophenolate mofetil - anti-inflammatory
  2. Rituximab
  3. Nintedanib - this is an anti-fibrotic
  4. Cyclophosphamide - for aggressive disease
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64
Q

Systemic Sclerosis or Scleroderma: Renal Crisis Management (2)

A

ACE Inhibitors
Dialysis for serious cases

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65
Q

Systemic Sclerosis or Scleroderma: Skin Fibrosis Management (2)

A

Methotrexate
Mycophenolate

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66
Q

Spondyloarthrides: Epidemiology - Geographically more common when?

A

Northern hemisphere
Scandinavian countries

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67
Q

Spondyloarthrides: Reactive Arthritis

A

Infection-induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultured

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68
Q

Spondyloarthrides: Reactive Arthritis - Most common preceding infections (2)

A

Urogenital
Enterogenic

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69
Q

Spondyloarthrides: Reactive Arthritis - What genetic predisposition is present?

A

HLA-B27

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70
Q

Spondyloarthrides: Reactive Arthritis - Most common age group

A

20-40 years old

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71
Q

Spondyloarthrides: Reactive Arthritis - Causative organisms secondary to urogenital infection (2)

A

Chlamydia
Neisseria

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72
Q

Spondyloarthrides: Reactive Arthritis - Causative organisms secondary to Enterogenic infection (3)

A

Salmonella
Shigella
Yersinia

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73
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation - 1-4 weeks after infection - General symptoms (3)

A

Fever
Fatigue
Malaise

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74
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation - 1-4 weeks after infection - Musculoskeletal presentations (2)

A

Asymmetrical monoarthritis or oligoarthritis
Enthesitis

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75
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation - 1-4 weeks after infection - Presentation of mucocutaneous lesions (4)

A

Keratodema Blenorrhagica
Cicinate balanitis
Painless oral ulcers
Hyperkeratotic nails

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76
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation - 1-4 weeks after infection - Ocular presentation (2)

A

Iritis
Conjunctivitis

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77
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation - 1-4 weeks after infection - Visceral manifestations (2)

A

Mild renal disease
Carditis

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78
Q

Spondyloarthrides: Reactive Arthritis - Clinical Presentation of Reiters Syndrome (3)

A

Urethritis
Conjunctivitis/Uveitis/Iritis
Arthritis

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79
Q

Spondyloarthrides: Reactive Arthritis - Diagnosis - Blood results

A

Increased inflammatory markers

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80
Q

Spondyloarthrides: Reactive Arthritis - Diagnosis - What cultures are taken? (3)

A

Blood
Urine
Stool

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81
Q

Spondyloarthrides: Reactive Arthritis - Diagnosis - How is infection ruled out?

A

Joint fluid analysis

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82
Q

Spondyloarthrides: Reactive Arthritis - Management for most cases

A

90% of cases resolve spontaneously

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83
Q

Spondyloarthrides: Reactive Arthritis - Management for chronic progressive erosive disease

A

Immunosuppression

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84
Q

Spondyloarthrides: Enteropathic Arthritis

A

Inflammatory arthritis involving the peripheral joints and sometimes the spine in association with those with inflammatory bowel disease

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85
Q

Spondyloarthrides: Enteropathic Arthritis - Aetiology

A

Worsening of symptoms during flare ups of IBD

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86
Q

Spondyloarthrides: Enteropathic Arthritis - Pathophysiology

A

Organisms with high lipopolysaccharide in the cell wall trigger an immune reaction

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87
Q

Spondyloarthrides: Enteropathic Arthritis - Musculoskeletal presentation (2)

A

Arthritis in several joints
Enthesitis

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88
Q

Spondyloarthrides: Enteropathic Arthritis - Most common joints affected (4)

A

Knees
Ankles
Elbows
Wrists

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89
Q

Spondyloarthrides: Enteropathic Arthritis - Gastrointestinal symptoms (3)

A

Loose watery stools - with mucous and blood
Weight loss
Apthous oral ulcers

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90
Q

Spondyloarthrides: Enteropathic Arthritis - Impact on the eyes

A

Uveitis

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91
Q

Spondyloarthrides: Enteropathic Arthritis - Diagnosis - Blood results

A

Raises inflammatory markers - CRP and Plasma viscosity

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92
Q

Spondyloarthrides: Enteropathic Arthritis - Diagnosis - What is show on X-ray or MRI?

A

Sacroilitis

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93
Q

Spondyloarthrides: Enteropathic Arthritis - Diagnosis - What is shown on Ultrasound? (2)

A

Synovitis
Tenosynovitis

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94
Q

Spondyloarthrides: Clinical Presentation - Two types of back pain

A

Mechanical
Inflammatory

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95
Q

Spondyloarthrides: Characteristics of mechanical back pain

A

Worsened by activity
Worse at the end of the day that recovers with rest

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96
Q

Spondyloarthrides: Characteristics of inflammatory back pain

A

Worsened by rest - early morning stiffness >30 minutes
Improved with activity

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97
Q

Muscular Disease: 3 Types

A

Inflammatory Myopathies
Polymyalgia Rheumatica
Fibromyalgia

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98
Q

Muscular Disease: Inflammatory Myopathies is characterised by what?

A

Weakness

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99
Q

Muscular Disease: 3 Types of Inflammatory Myopathies

A

Polymyositis
Dermatomyositis
Immune Mediated Necrotising Myopathy (IMNM)

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100
Q

Muscular Disease: Polymyalgia Rheumatica characterised by what?

A

Pain and Stiffness

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101
Q

Muscular Disease: Fibromyalgia characterised by what?

A

Pain and Fatigue

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102
Q

Myopathy

A

Disease of the muscle in which muscle fibres do not function properly resulting in muscular weakness

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103
Q

Polymyositis: Epidemiology of the sexes

A

More common in females - twice as common

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104
Q

Polymyositis: Peak incidence

A

40-50 years

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105
Q

Polymyositis: Increased incidence in what condition?

A

Malignancy

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106
Q

Polymyositis: General presentation

A

Symmetrical muscle weakness in the proximal muscles

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107
Q

Polymyositis: Onset of inflammatory myopathies

A

Insidious onset that worsens with time

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108
Q

Polymyositis: Clinical Presentation - Lungs (2)

A

Inflammatory lung disease
Respiratory muscle weakness

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109
Q

Polymyositis: Clinical Presentation -Oesophageal symptom

A

Dysphagia

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110
Q

Polymyositis: Clinical Presentation -Cardiac symptom

A

Myocarditis

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111
Q

Polymyositis: Clinical Presentation -General Systemic Symptoms (4)

A

Fever
Weight loss
Raynauds Disease
Inflammatory arthritis

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112
Q

Polymyositis: Clinical Presentation - Presentation in the hands

A

Dryness

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113
Q

Polymyositis: Dermatomyositis

A

Inflammatory disorder of the skin and underlying tissue

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114
Q

Polymyositis: Dermatomyositis - Gottron’s Papules

A

Pink or purple eruptions on the face, scalp, neck, shoulders and knuckles followed by swelling

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115
Q

Polymyositis: Dermatomyositis - Heliotrope Rash

A

Red or purple rash of the eyelids

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116
Q

Polymyositis: Dermatomyositis - 3 signs

A

Gottron’s Papules
Heliotrope Rash
Shawl Sign

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117
Q

Polymyositis: Dermatomyositis - Shawl Sign

A

Widespread flat red area on the upper back, shoulders and back of the neck

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118
Q

Polymyositis: Clinical Examination - Two types of clinical examinations

A

Confrontational Testing
Isotonic Testing

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119
Q

Polymyositis: Clinical Examination -Confrontational testing

A

Direct testing of power by pushing and pulling of muscles

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120
Q

Polymyositis: Clinical Examination -Isotonic testing

A

30 second sit to stand test that is repeated

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121
Q

Polymyositis: Main diagnostic test

A

Muscle Biopsy

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122
Q

Polymyositis: What does a muscle biopsy show?

A

Perivascular inflammation with muscular necrosis

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123
Q

Polymyositis: What is shown on electromyopathy? (3)

A

Increased fibrillations
Abnormal motor potentials
Complex repetitive discharges

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124
Q

Polymyositis: MRI may show what 4 characteristics?

A

Muscle inflammation
Oedema
Fibrosis
Calcification

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125
Q

Polymyositis: Management options (3)

A

Corticosteroids
Immunosuppression
Biologics - IV Ig or Rituximab

126
Q

Polymyositis: Complication

A

Increased risk of malignancy - Ovarian, Breast, Stomach, Lung, Bladder or Colon Cancer

127
Q

Polymyositis: Risk of malignancy is greatest in what sex?

A

Men

128
Q

Polymyositis

A

Idiopathic inflammatory myopathy causing symmetrical proximal muscle weakness

129
Q

Polymyositis: Pathophysiology

A

CD8+ T cell mediated process against non-necrotic muscle fibres in response to nuclear and cytoplasmic autoantigens

130
Q

Polymyositis: Those with interstitial lung disease may test positive for what antibody?

A

Anti-Jo-1 antibody

131
Q

Polymyositis: Non-specific auto-antibodies

A

ANA
Anti-RNP

132
Q

Polymyositis: Myositis specific auto-antibodies

A

Anti-Jo-1
Anti-SRP

133
Q

Polymyalgia Rheumatica

A

Inflammatory condition of unknown aetiology that affects elderly individuals

134
Q

Polymyalgia Rheumatica: Epidemiology of age

A

Patients over 50 years

135
Q

Polymyalgia Rheumatica: Geographical epidemiology

A

Higher incidence in northern regions

136
Q

Polymyalgia Rheumatica: Associated with what condition?

A

Giant Cell Arteritis

137
Q

Polymyalgia Rheumatica: Systemic Symptoms (4)

A

Fatigue
Anorexia
Weight loss
Fever

138
Q

Polymyalgia Rheumatica: Main symptom

A

Proximal myalgia of the hip and shoulder girdles

139
Q

Polymyalgia Rheumatica: Onset of shoulder or hip pain

A

Morning stiffness - lasts for at least 45 minutes

140
Q

Polymyalgia Rheumatica: Is pain improved or worsened with movement?

A

Worsened

141
Q

Polymyalgia Rheumatica: Is muscle strength impacted?

A

No

142
Q

Polymyalgia Rheumatica: Impact on the nerves

A

Carpal tunnel syndrome

143
Q

Polymyalgia Rheumatica: Diagnosis relies on what?

A

Clinical diagnosis

144
Q

Polymyalgia Rheumatica: Blood results

A

Increased inflammatory markers - increased ESR, Plasma viscosity and CRP

145
Q

Polymyalgia Rheumatica: Temporal or Giant Cell Arteritis

A

Granulomatous arteritis of large vessels e.g. in the temporal arteries

146
Q

Polymyalgia Rheumatica: Temporal or Giant Cell Arteritis - Symptoms (4)

A

Headache
Scalp tenderness
Jaw claudication
Amaurosis fugax - visual loss
Tender enlarged non-pulsatile temporal arteries

147
Q

Polymyalgia Rheumatica: Main principle

A

There is a rapid response to low dose steroids - the dose should then be gradually reduced over 18-24 months

148
Q

Polymyalgia Rheumatica: Management - Polymyalgia Rheumatitis

A

Start prednisolone at 15mg daily

149
Q

Polymyalgia Rheumatica: Management - Giant Cell Arteritis

A

Start prednisolone at 40-60mg daily

150
Q

Fibromyalgia

A

Neurosensory disorder characterised by chronic musculoskeletal pain

151
Q

Fibromyalgia: Epidemiology of sexes

A

Increased prevalence in women

152
Q

Fibromyalgia: What lifestyle factors may initiate this? (2)

A

Emotional or physical trauma

153
Q

Fibromyalgia: May occur secondary to what? (2)

A

Rheumatoid Arthritis
SLE

154
Q

Fibromyalgia: Has what impacts on the nervous pathways? (3)

A

Increased cutaneous nociception
Increased sympathetic outflow
Increased muscle nociception

155
Q

Fibromyalgia: Patients tend to have a reduction in what?

A

Threshold to sensations - pain/heat/noise/strong odours

156
Q

Fibromyalgia: Length of time

A

> 3 months of widespread pain

157
Q

Fibromyalgia: Where is pain felt?

A

Symmetrically above and below the waist and at the axial spine

158
Q

Fibromyalgia: Central symptoms (5)

A

Chronic headaches
Dizziness
Sleep disorders
Cognitive impairment
Anxiety/Depression

159
Q

Fibromyalgia: Msucular symptoms (3)

A

Myofascial pain
Fatigue
Twitches

160
Q

Fibromyalgia: Systemic symptoms (3)

A

Pain
Weight gain
Cold symptoms

161
Q

Fibromyalgia: Symptom of the urinary tract

A

Problems urinating

162
Q

Fibromyalgia: Symptom. ofthe reproductive tract

A

Dysmenorrhoea

163
Q

Fibromyalgia: Diagnosis criteria (4)

A

Patient experiences widespread pain with unrefreshed sleep, cognitive symptoms and fatigue that have been present at the same level for >3 months

164
Q

Fibromyalgia: Management - Examples of analgesia (2)

A

Gabapentin
Pregabalin

165
Q

Fibromyalgia: Management - Options (3)

A

Graded exercise programme
Cognitive behavioural therapy
Anti-depressants

166
Q

Vasculitis

A

Inflammation of blood vessels

167
Q

Vasculitis: Primary vasculitis

A

The result of an inflammatory response that targets the vessel wall with no known cause

168
Q

Vasculitis: Secondary vasculitis

A

Vasculitis that occurs as a result of infection, drugs, toxin, cancer or as part of another inflammatory disorder

169
Q

Vasculitis: Can lead to what 3 pathological states?

A

Inflammation - can block the blood vessel
Ischaemia
Necrosis of tissue

170
Q

Vasculitis: Classifications - Large vessel vasculitis (2)

A

Takayasu arteritis
Giant cell arteritis

171
Q

Vasculitis: Classifications - Medium vessel vasculitis (2)

A

Polyarteritis nodosa
Kawasaki disease

172
Q

Vasculitis: Classifications - ANCA-associated small vessel vasculitis (3)

A

Microscopic polyangiitis
Granulomatosis with polyangitis (Wegner Syndrome)
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)

173
Q

Vasculitis: Classifications - Immune complex mediated small vessel vasculitis (3)

A

Cryoglobulinaemic vasculitis
IgA Vasculitis (Henoch-Schonlein Syndrome)
Hypocomplementeric Urticarial Vasculitis

174
Q

Vasculitis: Systemic symptoms (4)

A

Fever
Malaise
Weight Loss
Fatigue

175
Q

Large Vessel Vasculitis

A

Primary vasculitis that causes chronic granulomatous inflammation - mainly of the aorta and its major branches

176
Q

Large Vessel Vasculitis: Two main types

A

Temporal giant cell arteritis
Takayasu Arteritis

177
Q

Large Vessel Vasculitis: Takayasu Arteritis - Main age of incidence

A

<40 years old

178
Q

Large Vessel Vasculitis: Takayasu Arteritis - Epidemiology of sexes

A

More common in females

179
Q

Large Vessel Vasculitis: Takayasu Arteritis - More prevalent in what population?

A

Asian

180
Q

Large Vessel Vasculitis: Takayasu Arteritis - Early features (6)

A

Low grade fever
Malaise
Night sweats
Weight loss
Arthralgia
Fatigue

181
Q

Large Vessel Vasculitis: Takayasu Arteritis - What is the main feature of this?

A

Claudication in the upper and lower limbs

182
Q

Large Vessel Vasculitis: Takayasu Arteritis - If untreated what can occur? (2)

A

Vascular stenosis
Aneurysms

183
Q

Large Vessel Vasculitis: Takayasu Arteritis - Bruit is most common where?

A

In the carotid arteries

184
Q

Large Vessel Vasculitis: Takayasu Arteritis - Blood results

A

Increased inflammatory markers

185
Q

Large Vessel Vasculitis: Takayasu Arteritis - What imaging is used?

A

MR Angiogram - detects thickened vessel walls and stenosis

186
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Most common age

A

50-60 years old

187
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Strong association with what?

A

Polymyalgia rheumatica

188
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Central symptom

A

Unilateral acute temporal headache with focal tenderness on direct palpation

189
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Symptoms in the head (3)

A

Jaw claudication - due to ischaemia of the maxillary artery
Visual disturbances
Visual loss - amaurosis fugax

190
Q

Large Vessel Vasculitis: Giant Cell Arteritis - When should this diagnosis be considered?

A

Differential diagnosis of a new-onset headache in 50 year old patients or older with an elevated ESR, CRP or plasma viscosity

191
Q

Large Vessel Vasculitis: Giant Cell Arteritis - First line test

A

Temporal Artery US

192
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Gold standard test

A

Temporal artery biopsy

193
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Why may a temporal artery biopsy be negative?

A

Due to skip lesions

194
Q

Large Vessel Vasculitis: Giant Cell Arteritis - Presentation on biopsy (3)

A

Transmural inflammation of all 3 layers
Patchy infiltration by lymphocytes, macrophages and multinucleated giant cells
Vessel wall thickening causing distal ischaemia

195
Q

Large Vessel Vasculitis: Management - First step

A

Prednisolone 40-60 mg

196
Q

Large Vessel Vasculitis: Management - Long term for Takayasu Arteritis

A

Steroid sparing agents - Leflunamide or Methotrexate

197
Q

Large Vessel Vasculitis: Management - Long term for Giant Cell Arteritis

A

Gradual reduction in steroid dose over 18-24 months

198
Q

Large Vessel Vasculitis: Management - For resistant or relapsing GCA

A

Toclizumab

199
Q

ANCA-associated small vessel vasculitis: Aetiology - Causes (3)

A

S. aureus
E. coli
Klebsiella pneumoniae

200
Q

ANCA-associated small vessel vasculitis: Aetiology - Environmental factors

A

Silica

201
Q

ANCA-associated small vessel vasculitis: Aetiology - Drugs (4)

A

Propylthiouracil
Hydralazine
D-penicillamine
Minocycline

202
Q

ANCA-associated small vessel vasculitis: 3 types

A

EGPA - Eosinophilic Granulomatosis with Polyangiitis
GPA - Granulomatosis with Polyangiitis
MPA - Microscopic Polyangiitis

203
Q

ANCA-associated small vessel vasculitis: EGPA triad

A

Late onset asthma
Eosinophilia
Granuloma

204
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis

A

Granulomatous inflammation affecting the small and medium sized vessels in the upper and lower respiratory tract, eyes or kidneys

205
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - More common in what countries?

A

Northern Europe

206
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Epidemiology of sexes

A

More common in males

207
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Typical age on diagnosis

A

35-55 years

208
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - ENT features (6)

A

Sinusitis
Saddle nose -due to cartilage damage from ischaemia
Nose bleeds
Oral ulcers
Deafness
Sub-glottic inflammation

209
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Respiratory Symptoms (4)

A

Haemoptysis
Pulmonary infiltrates
Diffuse alveolar haemorrhage
Cavitating nodules on CXR

210
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Ocular features (6)

A

Conjunctivitis
Episcleritis
Uveitis
Optic nerve vasculitis
Retinal artery occlusion
Proptosis - bulging of one or both eyes

211
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Cutaneous features (2)

A

Palpable purpura
Cutaneous ulcers

212
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Renal feature

A

Necrotising glomerulonephritis

213
Q

ANCA-associated small vessel vasculitis: Granulomatosis with Polyangiitis - Nervous features (3)

A

Mononeuritis multiplex
Sensorimotor polyneuropathy
Cranial nerve plexus

214
Q

ANCA-associated small vessel vasculitis: Blood results (3)

A

C3 and C4 initially increased - they then fall due to destruction in active disease
ESR/PV/CRP increased
Anaemia is common

215
Q

ANCA-associated small vessel vasculitis: Eosinophilic Granulomatosis with Polyangiitis - Affects what blood vessels?

A

Small and medium sized vessels

216
Q

ANCA-associated small vessel vasculitis: Eosinophilic Granulomatosis with Polyangiitis - Affects what systems of the body?

A

Respiratory Tract
Skin

217
Q

ANCA-associated small vessel vasculitis: Microscopic Polyangiitis

A

Necrotising vasculitis of the small vessels with few immune deposits

218
Q

ANCA-associated small vessel vasculitis: Microscopic Polyangiitis - Typical location (3)

A

Pulmonary system
Renal system
Skin

219
Q

ANCA-associated small vessel vasculitis: Microscopic Polyangiitis - What is a common clinical presentation?

A

Necrotising glomerulonephritis

220
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - ANCAs

A

Anti-neutrophil cytoplasmic antibodies

221
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - What do ANCAs do?

A

Auto-antibodies against antigens in the cytoplasm of neutrophil granulocytes

222
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - What ANCA is present in GPA?

A

cANCA

223
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - What ANCA is present in EGPA?

A

pANCA

224
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - What ANCA is present in MPA?

A

pANCA

225
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - PR3 present most commonly in what type?

A

GPA

226
Q

ANCA-associated small vessel vasculitis: Diagnosis - Autoantibodies - MPO most common in what types?

A

EGPA
MPA

227
Q

ANCA-associated small vessel vasculitis: Management - Localised disease definition

A

Upper and/or lower respiratory tract disease without any other systemic involvement or constitutional symptoms

228
Q

ANCA-associated small vessel vasculitis: Management - Early systemic definition

A

Any systemic involvement without any organ or life threatening circumstances

229
Q

ANCA-associated small vessel vasculitis: Management - Generalised definition

A

Renal (Creatinine <500) or other organ threat

230
Q

ANCA-associated small vessel vasculitis: Management - Systemic definition

A

Renal (Creatinine >500) or other vital organ failiure

231
Q

ANCA-associated small vessel vasculitis: Management - Refractory disease definition

A

Progressive disease that is unresponsive to steroids and cyclophosphamide

232
Q

ANCA-associated small vessel vasculitis: Management - Localised or Early systemic disease

A

Methotrexate + Steroids

233
Q

ANCA-associated small vessel vasculitis: Management - Second line amanagement for localised or early systemic disease

A

Azathioprine + steroids

234
Q

ANCA-associated small vessel vasculitis: Management - First line management for generalised disease

A

Cyclophosphoamide + Steroids followed by azathioprine for maintenance

235
Q

ANCA-associated small vessel vasculitis: Management - Second line management for generalised disease

A

Rituximab + Steroids

236
Q

ANCA-associated small vessel vasculitis: Management - First line management for systemic disease

A

Cyclophosphamide + Steroids followed by azathioprine for maintenance

237
Q

ANCA-associated small vessel vasculitis: Management - Second line management for Systemic disease

A

Rituximab + Steroids

238
Q

ANCA-associated small vessel vasculitis: Management - Management for systemic disease with creatinine > 500

A

Plasma exchange

239
Q

ANCA-associated small vessel vasculitis: Management - Refractory Disease

A

IV immunoglobulins
Rituximab

240
Q

Non-ANCA-associated small vessel vasculitis: Two types

A

Henoch-Schlein Purpura
Cryoglobulinaemia

241
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura

A

Acute immunoglobulin A mediated disorder with generalised vasculitis involving the small vessels of the skin, GIT, Kidneys, Joints and CNS

242
Q

Non-ANCA-associated small vessel vasculitis: Cryoglobulinaemia

A

Increased serum cryoglobulin with no dominant IgA deposits

243
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - Peak age of incidence

A

2-11 years

244
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - Most patients have what prior to disease? (3)

A

Preceding illness 1-3 weeks before - URTI, Pharyngeal infection or GI infection

245
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - Most common associated organism

A

Group A streptococcus

246
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - GI presentation (2)

A

Colicky abdominal pain
Blood diarrhoea

247
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - Skin manifestation

A

Purpuric rash over the gluteal region and lower limbs

248
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - In 50% of cases what system is involved?

A

Renal

249
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - Management

A

Self-limiting - resolves in 8 weeks

250
Q

Non-ANCA-associated small vessel vasculitis: Henoch-Schlein Purpura - What must be screened?

A

Urinalysis to screen for renal involvement

251
Q

Paediatric Orthopaedic Disorders

A

A persisting qualitative motor disorder appearing before the age of three years due to non-progressive damage to the encephalon occuring before growth of the CNS is complete

252
Q

Paediatric Orthopaedic Disorders: Pathophysiology of Muscle weakness

A
  1. Pathology leads to loss of connections to the lower motor neurones
  2. Negative features of upper motor neurone syndrome
253
Q

Paediatric Orthopaedic Disorders: Symptoms. ofmuscle weakness pathologies (4)

A

Weakness
Fatifuability
Poor balance
Sensory deficits

254
Q

Paediatric Orthopaedic Disorders: Mechanical mechanism of Muscle weakness

A
  1. Induces muscle shortening
  2. Causes bony torsion and joint instability
  3. Degenerative arthritis
255
Q

Paediatric Orthopaedic Disorders: Pathophysiology of muscle spasticity

A
  1. CNS pathology leads to loss of inhibition of lower motor neurones
  2. Positive features of upper motor syndrome
256
Q

Paediatric Orthopaedic Disorders: Symptoms of muscle spasticity (4)

A

Spasticity
Hyperreflexia
Clonus - involuntary muscle contractions
Co-contraction

257
Q

Paediatric Orthopaedic Disorders: Neural mechanism of muscle spasticity

A
  1. Induces muscle shortening
  2. Induces bony torsion and joint instability
  3. Degenerative arthritis
258
Q

Ambulation

A

The ability to walk without the need for any kind of assistance

259
Q

Congenital Talipes Equinovarus

A

Developmental disorder of the lower limb defined as fixation of the foot in adduction, suppination. andvarus position

260
Q

Genu Varum

A

Bow legged structure - the legs curve outward at the knees whilst the feet and ankles touch

261
Q

Genu Varum: When is this normal?

A

Those under the age of 2

262
Q

Genu Varum: May be considered abnormal if what is present? (4)

A

Unilateral
Severe
Short stature
Painful

263
Q

Genu Varum: 5 associated pathophysiologies

A

Skeletal dysplasia
Rickets
Enchondroma
Blounts Disease
Trauma - may cause physeal injury

264
Q

Genu Varum: Blounts Disease

A

Growth arrest of the medial tibial physis of unknown aetiology

265
Q

Genu Valgum

A

Legs touch at the knees whilst their feet and ankles are spread apart

266
Q

Genu Valgum: When is this normal?

A

Peak age at 3.5 years

267
Q

Genu Valgum: 3 causative pathologies

A

Tumours - Enchondroma or Osteochondroma
Rickets
Neurofibromatosis

268
Q

Genu Valgum: Refer if (4)

A

Asymmetric
Painful
Severe - greater than 2 Standard deviations over normal
>8cm intermalleolar distance at age 11

269
Q

In-toeing

A

Refers to a child who, when walking and standing, will have feet that point towards the midline

270
Q

In-toeing: May be releated to what 3 pathophysiologies?

A

Femoral neck anteversion
Internal tibial torsion
Metatarsus adductus

271
Q

In-toeing: Often exaggerated by what?

A

Running

272
Q

In-toeing: Femoral Neck Anteversion - Normal physiology of the femur

A

Normally points slightly anteriorly to increase the internal rotation of the hip

273
Q

In-toeing: Femoral Neck Anteversion - Normal angle of femur at birth

A

30-40 degrees

274
Q

In-toeing: Femoral Neck Anteversion - Normal angle of femur at maturity

A

10-15 degrees

275
Q

In-toeing: Internal Tibial Torsion is usually seen when?

A

1-3 years old - resolved by 6 years

276
Q

In-toeing: Metatarsus Adductus - management if not passively corrected

A

Serial casting between 6 to 12 months

277
Q

Curly Toes

A

Minor overlapping of the toes

278
Q

Curly Toes: Most common toes affected?

A

3rd or 4th toes

279
Q

DDH

A

Developmental Dysplasia

280
Q

Developmental Dysplasia

A

Dislocation or subluxation of the femoral head during the perinatal period that affects subsequent development of the hip joint

281
Q

Developmental Dysplasia: Epidemiology of sexes

A

More common in women

282
Q

Developmental Dysplasia: What hip. ismost commonly affected?

A

Left hip

283
Q

Developmental Dysplasia: High in what race?

A

Native americans

284
Q

Developmental Dysplasia: Low in what race?

A

African

285
Q

Developmental Dysplasia: What hormone increase the risk of this?

A

Relaxin - only acts on females so increased risk in women

286
Q

Developmental Dysplasia: Risk Factors (4)

A

Breech birth
Oligohydramnios - larger children
First born >4kg
Moulded baby - e.g. twins

287
Q

Developmental Dysplasia: What screening is conducted for this?

A

Neonatal baby checks
Selective US Screening - conducted on high risk births
6-8 week GP check

288
Q

Developmental Dysplasia: What patients are screened by US in Scotland?

A

Breech births
1st Degree family history
Moulded babies

289
Q

Developmental Dysplasia: Baby Hip Examination - what is inspected?

A

Asymmetry
Loss of knee height
Crease of asymmetry
Less abduction in flexion

290
Q

Developmental Dysplasia: Barlows Test - what is a positive test?

A

Adduct the hip whilst applying light pressure on the knee with your thumb to direct the force posteriorly
If the hip is unstable - palpable subluxation or dislocation

291
Q

Developmental Dysplasia: Ortolani’s Test - what is a positive test?

A

Flex the hips and knees of a supine patient to 90 degrees - with your index fingers place anterior pressure on the greater trochanter and gently abduct the infants legs
If there is a distinctive clunk heard. andfelt as the femoral head relocates anteriorly into the acetabulum - this is a positive test

292
Q

Developmental Dysplasia: Gold standard investigation

A

Ultrasound

293
Q

Developmental Dysplasia: When is US most helpful and why?

A

Under 3 months of age as the ossification nucleus begins to develop after 3 months

294
Q

Developmental Dysplasia: When are X-Rays useful and why?

A

Most useful after 4-6 months of age - as before this the femoral head epiphysis is unossified

295
Q

Developmental Dysplasia: Management for early DDH

A

Pavlik Harness 23-24 hours per day for up to 12 weeks until the Ultrasound is normal

296
Q

Developmental Dysplasia: Pavlik Harness description

A

Harness holding the hips in an abducted and flexed position

297
Q

Developmental Dysplasia: Management of Late DDH

A

Surgery -Closed Reduction spica or Open reduction spica

298
Q

Developmental Dysplasia: Option for children with persistent dislocation over 18 months old

A

Open reduction with an osteotomy

299
Q

SUFE

A

Slipped Upper Femoral Epiphysis

300
Q

Slipped Upper Femoral Epiphysis

A

Condition mainly affecting overweight pre-pubertal adolescent boys where the femoral head epiphysis slips inferiorly in relation to the femoral neck

301
Q

Slipped Upper Femoral Epiphysis: Peak incidence age

A

8-18 years old

302
Q

Slipped Upper Femoral Epiphysis: Risk Factors (4)

A

Pubertal growth
Endocrine or Metabolic dysfunction - e.g. Pituitary or Thyroid dysfunction
Renal osteodystrophy
Increased weight

303
Q

Slipped Upper Femoral Epiphysis: Pathophysiology Mechanism

A

The growth plate physis is not strong enough to support the body weight and the femoral epiphysis slips due to the strain

304
Q

Slipped Upper Femoral Epiphysis: What ay prevent onset?

A

Growth spurt

305
Q

Slipped Upper Femoral Epiphysis: Main symptom

A

Hip, groin, thigh or knee pain with a limp

306
Q

Slipped Upper Femoral Epiphysis: How can some patients present with just pain in the knee?

A

Due to the obturator nerve supplying the hip and knee joint

307
Q

Slipped Upper Femoral Epiphysis: 2 clinical signs

A

Antalgic gait
Loss of internal rotation of the hip

308
Q

Slipped Upper Femoral Epiphysis: Impact on the lower limb (3)

A

Short
Loss of internal rotation
Loss of deep flexion

309
Q

Slipped Upper Femoral Epiphysis: What diagnostic test is conducted?

A

X-Ray in lateral view to ensure mild degrees of slip are detected

310
Q

Slipped Upper Femoral Epiphysis: Management

A

Urgent surgery to pin the femoral head

311
Q

Slipped Upper Femoral Epiphysis: Risk of managing severe acute slip with gentle manipulation

A

Avascular necrosis

312
Q

Slipped Upper Femoral Epiphysis: Chronic severe slios may require what management?

A

Osteotomy

Musculoskeletal System (9 decks)

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