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Musculoskeletal System > Disease Profiles > Flashcards

Disease Profiles Flashcards

1
Q

Osteoarthritis

A

Degenerative joint disease that occurs due to changes in the articular cartilage causing structural changes and functional impairment

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2
Q

Osteoarthritis: Primary Osteoarthritis presents when?

A

From 50 years old

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3
Q

Osteoarthritis: 5 main causes

A

Ageing
Biomechanical stress
Degeneration
Malalignment
Genetic impacts

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4
Q

Osteoarthritis: Examples of Biomechanical Stress? (3)

A

Obesity
Injury
Occupational use

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5
Q

Osteoarthritis: Example of degenerative causes

A

Meniscal tear

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6
Q

Genu varum

A

Load through the medial compartment of the hinge of the knee joint - predisposes patients to medial osteoarthritis

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7
Q

Genu valgus

A

Load through the lateral compartment of the hinge of the knee joint - predisposes patients to lateral compartment osteoarthritis

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8
Q

Osteoarthritis: Causes of primary osteoarthritis (2)

A

No avert cause
Age-related

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9
Q

Osteoarthritis: Causes of secondary osteoarthritis (5)

A

Predisposing conditions
Excess or inappropriate weight bearing
Deformity
Injury
Systemic conditions

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10
Q

Osteoarthritis: Overview of the pathophysiology of Osteoarthritis

A

Degeneration of the cartilage with failed repair attempts due to inflammatory drivers

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11
Q

Osteoarthritis: Stages of Pathophysiology (4)

A
  1. Injury to chondrocytes due to biochemical and genetic factors
  2. Chondrocyte proliferation with release of inflammatory mediators
  3. Inflammatory changes in the synovium and subchondral bone
  4. Repetitive injury and chronic inflammation
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12
Q

Osteoarthritis: 4 hallmarks of Osteoporosis Pathophysiology

A

Loss of chondrocytes - causes loss of cartilage
Loss of sub-chondral bone with attempted remodelling
Disruption to and loss of cartilage matrix
Changes in the subchondral bone and synovium

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13
Q

Osteoarthritis: Early Features (4)

A

Combined damage and remodelling to the hyaline cartilage
Chondrocyte clusters
Small fissures within the cartilage
Fibrillation

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14
Q

Osteoarthritis: Late Features - Impact on cartilage

A

Completely worn away - enables bone to bone interactions and loss of joint space

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15
Q

Osteoarthritis: Late Features - Impact on the synovium

A

Accumulation of synovial fluid deep to the joint space

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16
Q

Osteoarthritis: Late Features - Accumulation of synovial fluid causes the formation of what?

A

Subchondral cysts

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17
Q

Osteoarthritis: Late Features - Eburnation

A

The generation of a polished surface enables subchondral sclerosis

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18
Q

Osteoarthritis: Late Features - Remodelling enables the formation of what and where?

A

Osteophytes at joint margins

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19
Q

Osteoarthritis: Late Features - Impact on the synovial capsule?

A

Thickened

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20
Q

Osteoarthritis: Localised Osteoarthritis

A

Osteoarthritis affecting the hips, knees, finger interpharyngeal joints and the facet joints of the lower cervical and lumbar spines

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21
Q

Osteoarthritis: Generalised Osteoarthritis

A

Osteoarthritis at either the spinal or hand joints with at least 2 other joint regions

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22
Q

Osteoarthritis: What is the clinical sign of Generalised Osteoarthritis?

A

Heberdens Nodes on the DIPs

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23
Q

Osteoarthritis: Locations (4)

A

Hips
Knees
Lower lumbar and cervical vertebrae
PIP and DIP joints of the fingers

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24
Q

Osteoarthritis: Onset

A

Insidious

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25
Q

Osteoarthritis: When is there stiffness?

A

Morning stiffness lasting less than 1 hour

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26
Q

Osteoarthritis: Inactivity gelling definition

A

Stiff after resting for a period of time

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27
Q

Osteoarthritis: Symptom in the hand

A

Poor grip in the thumb

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28
Q

Osteoarthritis: Signs - Impact on the knee joint line

A

Tenderness

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29
Q

Osteoarthritis: Signs - Hip osteoarthritis presents with what specific sign?

A

Groin pain

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30
Q

Osteoarthritis: Signs - Signs in the joint (4)

A

Joint effusion
Bony swellings
Deformity
Crepitus - Popping, Crackling or Clicking

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31
Q

Osteoarthritis: Signs - Genu varus in the knees

A

Bow legged - feet are touching and knees are not

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32
Q

Osteoarthritis: Signs - Genu valgus

A

The knees are touching whilst the feet do not

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33
Q

Osteoarthritis: Signs - What may present on the back of the knees in Knee Osteoarthritis?

A

Baker’s Cysts

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34
Q

Osteoarthritis: Signs - For Cervical Spine Osteoarthritis

A

Pain and restriction of movement with occipital headaches

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35
Q

Osteoarthritis: Signs - Impacts of Osteophytes in Cervical Spine

A

May impinge on nerve roots to cause pins and needles or numbness

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36
Q

Osteoarthritis: Signs - Impact of osteophytes on the lumbar spine

A

Spinal stensosis

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37
Q

Osteoarthritis: Signs on X-Ray (4)

A

Marginal osteophytes
Joint space narrowing
Subchondral Sclerosis
Subchondral Cysts

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38
Q

Osteoarthritis: Disadvantage of X-Rays

A

Insensitive in early disease

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39
Q

Osteoarthritis: Pharmacological management (2)

A

Analgesia - Paracetamol or NSAIDs
Local Intra-articular Steroid Injections for flare ups

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40
Q

Osteoarthritis: Surgical Management Options (2)

A

Joint replacements
Arthroscopic surgery

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41
Q

Osteoarthritis: Two types of Hip Replacement

A

Cemented
Hybrid

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42
Q

Osteoarthritis: What material is used for cemented Total Hip Replacements?

A

PMMA - Polymethylmethacrylate

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43
Q

Osteoarthritis: How does a cemented THR work?

A

Via interdigitation into the bone surface

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44
Q

Osteoarthritis: Hybrid THR structure

A

Uncemented Cup with Cemented Stem

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45
Q

Osteoarthritis: What patients receive a hybrid THR?

A

Young patients

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46
Q

Osteoarthritis: Structure of Hyaline Cartilage (4)

A

Water
Collagen
Proteoglycans
Chondrocytes

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47
Q

Osteoarthritis: Function of Chondrocytes in Hyaline Cartilage

A

Produce and regulate the ECM

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48
Q

Osteoarthritis: Function of Proteoglycans in Hyaline Cartilage

A

Provide compressive strength

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49
Q

Osteoarthritis: Pathophysiology - Why is medial osteoarthritis more common than lateral cases?

A

Twisting and pivoting on the medial knee and Genu Varum are more common

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50
Q

Osteoarthritis: Concern of steroid injections

A

Can accelerate Osteoarthritis

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51
Q

Rheumatoid Arthritis

A

Symmetrical chronic inflammatory disorder driven by an autoimmune mechanism of the synovial lining of the joints, tendon sheaths and bursa

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51
Q

Rheumatoid Arthritis:

A
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52
Q

Rheumatoid Arthritis: Peak age

A

20-40 years old

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53
Q

Rheumatoid Arthritis: Sex Epidemiology

A

More common in women

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54
Q

Rheumatoid Arthritis: What is this called in children under 16

A

Juvenile Idiopathic Arthritis

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55
Q

Rheumatoid Arthritis: What genes are involved? (3)

A

HLA-DRB1
HLA-DPB1
ATIC

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56
Q

Rheumatoid Arthritis: What type of immune reaction is this?

A

Type IV Hypersensitivity and Type III secondary hypersensitivity reactions

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57
Q

Rheumatoid Arthritis: What cytokines are activated?

A

IFN-Gamma
IL-17
TNF
IL-1
RANKL

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58
Q

Rheumatoid Arthritis: Function of IFN-Gamma

A

Activates macrophages and synovial cells

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59
Q

Rheumatoid Arthritis: Function of IL-17

A

Recruits neutrophils and monocytes

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60
Q

Rheumatoid Arthritis: Function of TNF and IL-1

A

Stimulates the production of proteases from the synovium

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61
Q

Rheumatoid Arthritis: Function of RANKL

A

Activated on T cells to stimulate bone resorption

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62
Q

Rheumatoid Arthritis: Mediated by what HLA gene?

A

HLA-DR4

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63
Q

Rheumatoid Arthritis: Process

A
  1. Unknown antigen presented to naive T cells activates them
  2. Initiates inflammatory cascade - activate B cells and macrophages
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64
Q

Rheumatoid Arthritis: B cells produce what?

A

IgG Rheumatoid Factor and IL-6

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65
Q

Rheumatoid Arthritis: What do macrophages produce?

A

Pro-inflammatory cytokines - TNF-alpha, IL-1 and IL-6

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66
Q

Osteomyelitis

A

Inflammation of the bone and the medullary cavity

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67
Q

Osteomyelitis: Typical location

A

Long bones

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68
Q

Osteomyelitis: 2 main patient groups at risk to inoculation

A

Post-trauma patients
Surgical patients

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69
Q

Osteomyelitis: 2 main patient groups at risk of haematogenous spread

A

Children
Immunosuppressed

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70
Q

Osteomyelitis: Open Fractures - What classification is used?

A

Gustilo Classification System

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71
Q

Osteomyelitis: Open Fractures - Causative Organisms of infection (2)

A

Staphylococcus aureus
Aerobic gram negative bacteria

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72
Q

Osteomyelitis: Open Fractures - Management of infection of open fracture

A

Early aggressive debridement, fixation and soft tissue cover

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73
Q

Osteomyelitis: Open Fractures - Increasing classification of Gustilo Classification indicates what?

A

Increasing risk of anaerobic and gram negative infection

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74
Q

Osteomyelitis: Open Fractures - Type I Gustilo Classification

A

Puncture wound less than or equal to 1cm with minimal soft tissue injury - minimal wound contamination or muscle crushing

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75
Q

Osteomyelitis: Open Fractures - Type II Gustilo Classification

A

Wound is greater than 1cm in length with moderate soft tissue injury and coverage of the bone is adequate

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76
Q

Osteomyelitis: Open Fractures - Type 3a Gustilo Classification

A

Extensive soft tissue damage that is massively contaminated/severely comminuted/segmental fractures with adequate bone soft tissue coverage

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77
Q

Osteomyelitis: Open Fractures - Type 3b Gustilo Classification

A

Extensive soft tissue damage with periosteal stripping and bone exposure that is usually contaminated and comminuted but flap coverage is required to provide soft tissue coverage

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78
Q

Osteomyelitis: Open Fractures - Type 3c Gustilo Classification

A

Assoicated with an arterial injury requiring repair for li,hb salvage

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79
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Risk Factors (4)

A

Previous foot ulceration
Neuropathy
Foot deformity
Vascular disease

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79
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Risk Factors (4)

A

Previous foot ulceration
Neuropathy
Foot deformity
Vascular disease

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80
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Has … and … dysfunction

A

Microvascular
Vasomotor

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81
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Why is there altered capillary exchange?

A

Capillary basement membrane thickening

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82
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - What happens to the matrix proteins?

A

Glycation

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83
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Loss of function of what structures? (2)

A

Apocrine glands
Eccrine Glands

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84
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - In feet

A

Toes curled in claw position

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85
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - What is the Cavus Deformity?

A

Increased pressure under the metatarsal heads

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86
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Diagnosis Options (3)

A

Probe bones
Radiograph
MRI

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87
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Management - Main Concept

A

Debridement and Antibiotics

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88
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Management - Staphylococcus and Streptococcus management

A

Flucloxacillin IV
Penicillin Allergic - Vancomycin
Nil by Mouth - Doxycycline and Cotrimoxazole

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89
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Management - Gram Negative Severe Case

A

IV Gentamicin or Aztreonam

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90
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Management - Oral Cases

A

Cotrimoxazole or Doxycycline

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91
Q

Osteomyelitis: Diabetic or Venous Insufficiency - Management - Anaerobes

A

Metronidazole or Clindamycin

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92
Q

Osteomyelitis: Haeamatogenous Osteomyelitis

A

Bacteria from the blood results in an acute presentation

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93
Q

Osteomyelitis: Haeamatogenous Osteomyelitis - At risk groups (5)

A

Pre-pubertal children
PWID
Central Line or Dialysis patients
Elderly
Sickle Cell Disease Patients

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94
Q

Osteomyelitis: Haeamatogenous Osteomyelitis - PWID patient locations (4)

A

Sternoclavicular Joint
Sternocostal Joint
Sacroiliac Joint
Pubic Symphysis

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95
Q

Osteomyelitis: Haeamatogenous Osteomyelitis - Organisms common in PWID patients (2)

A

Staphylococcus
Streptococcus

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96
Q

Osteomyelitis: Haeamatogenous Osteomyelitis - Organisms unusual in PWID patients (4)

A

Pseudomonas
Candida
Eikenella corrodens
Mycobacterium tuberculosis

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97
Q

Osteomyelitis: Haeamatogenous Osteomyelitis - Dialysis Patient common pathogens (2)

A

Staphylcoccus aureus
Salmonella species

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98
Q

Osteomyelitis: Sickle Cell Osteomyelitis - Causative Organisms (2)

A

Staphyloccus aureus
Salmonella species

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99
Q

Osteomyelitis: Sickle Cell Osteomyelitis - Clinical Presentation

A

Acute long bone osteomyelitis

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100
Q

Osteomyelitis: Sickle Cell Osteomyelitis - Pathogenesis

A

Infarct converts to bacteraemia then osteomyelitis

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101
Q

Osteomyelitis: Gaucher Disease

A

Autosomal recessive lysosomal storage disease resulting in the deposition of glucocerebrosides in the brain and other tissues

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102
Q

Osteomyelitis: Gaucher Disease - Often affects what bone?

A

Tibia

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103
Q

Osteomyelitis: Gaucher Disease - Main causative organism

A

Staphylococcus aureus

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104
Q

Osteomyelitis: Synovitis Acne Pustulosis Hyperostosis Osteitis presents in what patient groups?

A

Adults

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105
Q

Osteomyelitis: Gaucher Disease - Chronic Recurrent Multifocal Osteomyelitis presents in what patient groups?

A

Children

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106
Q

Osteomyelitis: Gaucher Disease - SAPHO

A

Synovitis Acne Pustulosis Hyperostosis Osteitis

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107
Q

Osteomyelitis: Gaucher Disease - CRMO

A

Chronic Recurrent Multifocal Osteomyelitis

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108
Q

Osteomyelitis: Gaucher Disease - SAPHO and CRMO Clinical Presentation (3)

A

Fever
Weight Loss
Generalised Malaise

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109
Q

Osteomyelitis: Gaucher Disease - SAPHO and CRMO sites involved (4)

A

Chest wall
Pelvis
Spine
Lower Limb

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110
Q

Osteomyelitis: Vertebral Osteomyelitis - Risk Factors (5)

A

PWID
IV site infections
GU infections
Post-operation
Primary bacteraemia in the elderly

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111
Q

Osteomyelitis: Vertebral Osteomyelitis - Associated with what abscesses? (2)

A

Epidural abscess
Psoas abscess

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112
Q

Osteomyelitis: Vertebral Osteomyelitis - Clinical Presentation (3)

A

Fever
Insidious Pain
Tenderness

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113
Q

Osteomyelitis: Vertebral Osteomyelitis - Diagnostic Results and Scans (3)

A

Increased WCC
MRI or Ga-67 Scan
Raised inflammatory markers

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114
Q

Osteomyelitis: Vertebral Osteomyelitis - Management

A

Drainaage of the large paravertebral or epidural abscesses with 6 weeks minimum of antibiotics

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115
Q

Osteomyelitis: Vertebral Osteomyelitis - MRI repeated if what occurs (3)

A

Unexplained increase in inflammatory markers
Increasing pain
New anatomically related sign or symptom

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116
Q

Osteomyelitis: Causative Organisms - Newborns (<4 months) - 4 examples

A

Staphylococcus aureus
Enterobacter species
Group A Streptococcus
Group B Streptococcus

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117
Q

Osteomyelitis: Causative Organisms - Children (4 months-4 years) - 4 examples

A

Staphylococcus aureus
Group A Streptococcus
Haemophilus influenzae
Enterobacter species

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118
Q

Osteomyelitis: Causative Organisms - Children and Adolescents (4-18 years) - 4 examples

A

Staphylococcus aureus
Group A Streptococcus
Haemophilus influenzae
Enterobacter species

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119
Q

Osteomyelitis: Causative Organisms - Adults (3 examples)

A

Staphylococcus aureua
Enterobacter
Streptococcus species

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120
Q

Osteomyelitis: Causative Organisms - Sickle Cell Anaemia Patients (2 examples)

A

Staphylococcus aureus
Salmonella species

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121
Q

Osteomyelitis: Two routes of infection

A

Haematogenous
Exogenous

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122
Q

Osteomyelitis: Haematogenous Spread

A

Infection carried within the blood from another infected site

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123
Q

Osteomyelitis: Haematogenous Spread - Examples of sources (4)

A

Cellulitis
PWIDs
Central lines
Dialysis

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124
Q

Osteomyelitis: Haematogenous Spread - Common location for children

A

Long bone metaphysis

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125
Q

Osteomyelitis: Haematogenous Spread - Most common location for adults

A

Vertebral involvement

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126
Q

Osteomyelitis: Exogenous Spread

A

Infection spread due to trauma or contiguous spread

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127
Q

Osteomyelitis: Exogenous Spread - Contiguous spread

A

Spread of infection from adjacent tissues

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128
Q

Osteomyelitis: Exogenous Spread - Examples of Contiguous Spread (2)

A

Secondary to infected foot ulcer in diabetic patients
Secondary to pressure sores in elderly patients

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129
Q

Osteomyelitis: Pathophysiology - Impact due to leucocytes?

A

Enzymes from the leucocytes causes local osteolysis and pus formation that impairs local blood flow

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130
Q

Osteomyelitis: Pathophysiology - Sequestrum

A

Dead fragment of bone

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131
Q

Osteomyelitis: Pathophysiology - Once a … is present, antibiotics will not cure the infection?

A

Sequestrum

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132
Q

Osteomyelitis: Pathophysiology - Involucrum

A

New bone formation around the area of necrosis

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133
Q

Osteomyelitis: Acute Pathophysiology - Why is this common in children?

A

The metaphyses of children’s long bones contain abundant tortuous vessels with poor flow that causes an accumulation of bacteria and infection towards the epiphysis

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134
Q

Osteomyelitis: Acute Pathophysiology - How does co-existent septic arthritis occur in neonates and infants?

A

Metaphyses are intra-articular causing infection to spread into the joint

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135
Q

Osteomyelitis: Acute Pathophysiology - Why can abscesses extend along the subperiosteal space in infants?

A

Loosely applied periosteum

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136
Q

Osteomyelitis: Acute Pathophysiology - Children can develop a subacute osteomyelitis with an insidious onset how?

A

Bone reacts by walling of the abscess with a thin rim of sclerotic bone

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137
Q

Osteomyelitis: Acute Pathophysiology - Brodie’s Abscess

A

Bone reacts by walling of the abscess with a thin rim of sclerotic bone

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138
Q

Osteomyelitis: Chronic Pathophysiology - Develops from what?

A

An untreated acute osteomyelitis

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139
Q

Osteomyelitis: Chronic Pathophysiology - In adults the infection tends to be in what part of the skeleton?

A

Axial skeleton

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140
Q

Osteomyelitis: Chronic Pathophysiology - Infections of the axial skeleton tend to originate from where?

A

Pulmonary, Intervertebral Disc or urinary infections that have spread via the blood

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141
Q

Osteomyelitis: Chronic Pathophysiology - Tuberculosis can cause chronic Osteomyelitis in what site?

A

The spine

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142
Q

Osteomyelitis: Clinical Presentation - Acute Presentation (4)

A

Abrupt onset of intense pain with point tenderness
Erythema
Heat
Swelling

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143
Q

Osteomyelitis: Clinical Presentation - Acute presentation systemic findings (3)

A

Malaise
Fever
Chills

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144
Q

Osteomyelitis: Clinical Presentation - Chronic Presentation (3)

A

Loss of function
Discharge
Recurrent pain
Swelling
Erythema

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145
Q

Osteomyelitis: Clinical Presentation - Chronic Osteomyelitis of the Spine

A

Insidious onset of back pain which is constant and unremitting

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146
Q

Osteomyelitis: Chronic Osteomyelitis - Presentation on imaging (2)

A

Sequestra - pieces of necrotic bone that separate from the viable bone

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147
Q

Osteomyelitis: Chronic Osteomyelitis - How do sequestra form?

A

Bone ischaemia and necrosis due to elevated medullary pressure of bone marrow infiltration

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148
Q

Osteomyelitis: Two rare sites

A

Osteitis Pubis
Clavicular osteomyelitis

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149
Q

Osteomyelitis: Osteitis Pubis - Risk factor for this

A

Urogynae procedures

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150
Q

Osteomyelitis: Clavicle Osteomyelitis - Risk factor for this

A

Neck surgery
Subclavian Vein Catheterisation

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151
Q

Osteomyelitis: Gold Standard

A

Bone biopsy

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152
Q

Osteomyelitis: Management - Acute Osteomyelitis - If an abscess is present?

A

Drainage

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153
Q

Osteomyelitis: Management - Acute Osteomyelitis - Main treatment

A

IV antibiotics

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154
Q

Osteomyelitis: Management - Acute Osteomyelitis - If an infection fails to resolve what is there treatment pathway

A

Second line antibiotics
Surgery to take a sample of the culture and remove infected bone or tissue

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155
Q

Osteomyelitis: Management - Chronic Osteomyelitis - What is not an option?

A

Antibiotics alone - cannot cure or erradicate infection

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156
Q

Osteomyelitis: Management - Chronic Osteomyelitis - What is surgery recommended for?

A

Gain deep bone tissue cultures to remove any sequestrum and to excise any infected or non-viable bone

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157
Q

Osteomyelitis: Management - Chronic Osteomyelitis - If debridement of the bone results in instability what is recommended?

A

Internal or external fixation

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158
Q

Prosthetic Joint Infection

A

Peri-prosthetic infection involving the joint prosthesis and adjacent tissue

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159
Q

Prosthetic Joint Infection: Risk Factors - Presence of what co-morbidities? (6)

A

Immunosuppression
Rheumatoid Arthritis
Diabetes Mellitus
Malignancy
Chronic Kidney Disease
Lymphoedema

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160
Q

Prosthetic Joint Infection: Risk Factors - Use of what drugs? (3)

A

Corticosteroids
TNF inhibitors
Biologic modifying anti-rheumatic drugs

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161
Q

Prosthetic Joint Infection: Risk Factors - A history of what post-surgery? (2)

A

Prior arthroplasty
Infection

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162
Q

Prosthetic Joint Infection: Risk Factors - Anaesthesiologist score of what?

A

> 3

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163
Q

Prosthetic Joint Infection: Risk Factors - Post-operative complications (2)

A

Haematoma
Wound infection

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164
Q

Prosthetic Joint Infection: Risk Factors - What type of infection?

A

Staphylococcus aureus bacteraemia

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165
Q

Prosthetic Joint Infection: Causative Organisms - Prosthetic Shoulder Arthroplasty Infection (2)

A

Coagulase negative Staphylococci
Propionbacterium acnes

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166
Q

Prosthetic Joint Infection: Causative Organisms - Prosthetic Hip and Knee Arthroplasty infection (3)

A

Anaerobes
Gram positive cocci - Coagulase negative staphylcocci or Staph aureus
Aerobic Gram Negative bacilli - E. coli, Proteus mirabilis and Pseudomonas aeruginosa

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167
Q

Prosthetic Joint Infection: Causative Organisms - Gram Positive Bacteria (3)

A

Staphylococcus aureus
Staphylococcus epidermidis
Cutiibacterium acnes (common on upper limb prostheses)

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168
Q

Prosthetic Joint Infection: Causative Organisms - Gram Negative Bacterium (2)

A

E. coli
Pseudomonas aeruginosa

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169
Q

Prosthetic Joint Infection: Mechanisms (3)

A

Direct inoculation at time of surgery
Manipulation of the joint at the time of surgery
Seeing of a joint due to haematogenous spread

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170
Q

Prosthetic Joint Infection: Pathophysiology - Early is due to what organisms? (2)

A

Staphylococcus aureus
Coagulase negative staphylococci

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171
Q

Prosthetic Joint Infection: Pathophysiology - Chronic is due to what organisms? (3)

A

Staphylococcus aureus
Coagulase negative staphylococci
Corynebacterium

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172
Q

Prosthetic Joint Infection: Pathophysiology - Haematological due to what organisms? (2)

A

Staphyloccus aureus
Gram negative bacilli

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173
Q

Prosthetic Joint Infection: Pathophysiology - Biofilm

A

Microbe-derived sessile community characterised by cell that attached to a substratum, interface or eachother

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174
Q

Prosthetic Joint Infection: Pathophysiology - Biofilms are embedded in what?

A

A matrix of extracellular polymeric substance

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175
Q

Prosthetic Joint Infection: Pathophysiology - Planktonic Bacteria

A

Free living bacteria - responsible for most symptoms

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176
Q

Prosthetic Joint Infection: Pathophysiology - Sessile Bacteria

A

Bacteria derived from Planktonic Bacteria due to phenotypic transformation that form a biofilm within an extracellular matrix

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177
Q

Prosthetic Joint Infection: Clinical Presentation (3)

A

Fever
Joint pain
Minimal swelling

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178
Q

Prosthetic Joint Infection: 4 diagnostic approaches

A

Culture - taken from peri-operative tissue
Blood culture
CRP
Radiology

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179
Q

Prosthetic Joint Infection: Management

A

DAIR - Debridement + Antibiotics and Implant Retention
IV therapy for 4-6 weeks with potential addition of Rifampicin

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180
Q

Prosthetic Joint Infection: Management - When should Rifampicin be added?

A

Culture is positive for Rifampicin-sensitive staphylococci

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181
Q

Septic Arthritis

A

Inflammation of the joint space due to infection

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182
Q

Septic Arthritis: Causative Organisms - Most common causes in adults (2)

A

Staphylococcus aureus
Streptococci

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183
Q

Septic Arthritis: Causative Organisms - Most common cause in children

A

Haemophilus influenzae

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184
Q

Septic Arthritis: Causative Organisms - Most common cause in young adults

A

Neisseria gonorrhoea

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185
Q

Septic Arthritis: Causative Organisms - Most common cause in the elderly, PWID and acutely ill

A

Escherichia coli

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186
Q

Septic Arthritis: Causative Organisms - Potential viral causes (3)

A

Parovirus
Rubella
Dengue virus

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187
Q

Septic Arthritis: Mechanisms of spread (4)

A

Haematogenous spread
Direct invasion via a penetrating wound
Spread of the infectious focus into adjacent tissue
Spread from a focus of osteomyelitis in adjacent bone

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188
Q

Septic Arthritis: Symptoms (5)

A

Rubor
Calor
Dolor
Tumor
Function laesa

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189
Q

Septic Arthritis: Signs (2)

A

Systemic fever
Reduced ROM

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190
Q

Septic Arthritis: Impact on blood results (2)

A

Increased WCC
Increased inflammatory markers

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191
Q

Septic Arthritis: 4 Diagnostic Tests (4)

A

Aspiration Fluid - for microscopy and culture
Bloods
X-ray or MRI
Exclude crystals

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192
Q

Septic Arthritis: Management - Empirical treatment for Staphylococcus aureus

A

Flucloxacillin

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193
Q

Septic Arthritis: Management - If less than 5 years old

A

Flucloxacillin (for S. aureus) + Ceftriaxone (for H. influenzae cover)

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194
Q

Septic Arthritis: Management - Length of IV antibiotics

A

1-2 weeks

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195
Q

Septic Arthritis: Management - Length of oral antibiotics

A

4-6 weeks

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196
Q

Bursitis

A

Inflammation of the synvoium-lined sacs that protect bony prominences and joints

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197
Q

Bursa

A

Small fluid filled sac lined by synovium around a joint to prevent friction between tendons, bones, muscle and skin

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198
Q

Bursitis: The six types of knee bursa

A

Semi-membranous bursa
Subcutaneous pre-patellar bursa
Subcutaneous infra-patellar bursa
Deep infra-patellar bursa
Subsatorial bursa
Supra-patellar bursa

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199
Q

Bursitis: Mechanism of Injury

A

Repeated pressure or trauma

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200
Q

Bursitis: What can develop due to secondary infection?

A

Abscess

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201
Q

Bursitis: Main causative organism

A

Staphylococcus aureus

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202
Q

Bursitis: Management

A

IV Flucloxacillin once a day for 2 weeks + Oral therapy for 2-4 weeks

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203
Q

Bursitis: Management if penicillin allergy

A

Clindamycin

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204
Q

Pyomyositis

A

Acute intramuscular infection secondary to haeamtogenous spread of the microorganism into the body of a skeletal muscle

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205
Q

Pyomyositis: Most common in what areas? (3)

A

Tropical Regions - Asia, Africa and Caribbean

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206
Q

Pyomyositis: Most common in what population ages?

A

Children
Young adults

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207
Q

Pyomyositis: What population groups are at risk to this? (3)

A

PWID
Diabetes mellitus
Immunosuppressed

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208
Q

Pyomyositis: Most common causative organism

A

Staphylococcus aureus

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209
Q

Pyomyositis: Risk factors in Tropical countries (2)

A

MSSA Immune competent
Children

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210
Q

Pyomyositis: Risk factor in Temperate Countries

A

Immunosuppressed

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211
Q

Pyomyositis: Caustive organisms within the perineum

A

Gram Negative Bacteria

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212
Q

Pyomyositis: Causative organisms in immunosuppressed individuals (3)

A

Pseudomonas
Beta haemolytic streptococcus
Enterococcus

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213
Q

Pyomyositis: Causative organisms in tropical climates

A

MSSA infection

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214
Q

Pyomyositis: Causative organism for contaminated wounds

A

Clostridium species

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215
Q

Pyomyositis: Clinical Presentation - local

A

Localised muscular swelling, tenderness and fluctuance in progress

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216
Q

Pyomyositis: Skin Clinical Presentation

A

Skin erythema and warmth

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217
Q

Pyomyositis: Systemic Symptoms (3)

A

Fever
Haemodynamic instability
Sepsis

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218
Q

Pyomyositis: Investigation choices (4)

A

Pus culture
US
CT
MRI

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219
Q

Pyomyositis: Management

A

Debridement and Antibiotics

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220
Q

Pyomyositis: Complications

A

Compartment Syndrome within the anterior tibial compartment

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221
Q

Myonecrosis

A

Life-threatening necrotising soft tissue infection

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222
Q

Myonecrosis: Most common causative organism

A

Clostridium perfringens

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223
Q

Myonecrosis: Alternate name for Gas Gangrene

A

Clostridial Myonecrosis

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224
Q

Myonecrosis: Clostridial Myonecrosis cause what alteration to the skin?

A

Bronze discolourisation to the skin

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225
Q

Myonecrosis: Examples of causative organism (4)

A

Clostridium perfringes
Clostridium septicum
Clostridium novvi
Clostridium histolyticum

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226
Q

Myonecrosis: Traumatic causative organism

A

Clostridium perfringes

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227
Q

Myonecrosis: Causative organism of Clostridial myonecrosis

A

Clostridium septicum

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228
Q

Myonecrosis: Risk Factors (4)

A

Deep penetration injuries
Bowel or biliary tract surgery
IM Adrenaline injection
Retained placenta

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229
Q

Myonecrosis: Symptoms (3)

A

Swelling
Erythema
Pain

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230
Q

Myonecrosis: Signs (4)

A

Tachycardia
Hypotension
Elevated CRP and Creatinine Kinase
LRINEC Score >4

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231
Q

Myonecrosis: 2 diagnostic tests

A

Radiography
Culture and Gram Stain

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232
Q

Myonecrosis: What would radiography show?

A

Gas present in the tissue

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233
Q

Myonecrosis: What would culture show?

A

Gram Positive Bacilli

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234
Q

Myonecrosis: Progress in changes in colour

A
  1. Bronze
  2. Red or Purple
  3. Black and overlying bullae
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235
Q

Myonecrosis: What would MRI show?

A

Characteristic feathering pattern of soft tissue

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236
Q

Myonecrosis: Management

A

Emergency debridement and antibiotics

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237
Q

Myonecrosis: What antibiotics are used?

A

Clindamycin and Penicillin

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238
Q

Viral Myositis

A

Muscle inflammation due to a viral infection

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239
Q

Viral Myositis: Clinical presentation (3)

A

Muscle weakening
Fatigue
Pain

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240
Q

Viral Myositis: What may precede muscular weakness and pain?

A

Fever

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241
Q

Viral Myositis: Typical causative viruses (5)

A

HIV
Human T-Lymphocytic Virus
CMV
Rabies
Dengue

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242
Q

Viral Myositis: Typical causative parasites (4)

A

Schistosoma
Taenia
Trichinella
Echinococcus

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243
Q

Viral Myositis: What do bloods show?

A

Elevated Creatinine Kinase

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244
Q

Tetanus

A

Acute infection affecting the nervous system due to the neurotoxins of a Clostridium tetani infection

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245
Q

Tetanus: Description of Clostridium tetani

A

Gram positive anaerobic bacilli

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246
Q

Tetanus: Mechanism of action

A

C. tetani spores within the soil enter the body via broken skin

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247
Q

Tetanus: Incubation period

A

4 days. toseveral weeks

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248
Q

Tetanus: Pathophysiology Stages

A
  1. C. tetani enters the wound
  2. Toxin is produced locally and passes via the bloodstream along nerves to the CNS
  3. Motor neurones at the anterior horn and brainstem become hyperactive as the toxin attacks the Renshaw Cells
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249
Q

Tetanus: C. tetani binds to inhibitory neurones to have what effect?

A

The release of neurotransmitters

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250
Q

Tetanus: The neurotoxin induces what?

A

Spastic paralysis

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251
Q

Tetanus: Clinical Presentation (3)

A

Trismus - lock jaw
Risus sardonicus - Muscle spasms
Dysphagia

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252
Q

Tetanus: Diagnostic investigation

A

Culture

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253
Q

Tetanus: Result of culture

A

Anaerobic gram positive with a terminal spore

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254
Q

Tetanus: Management (3)

A

Surgical debridement
Anti-toxin
Antibiotics - 7-10 days

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255
Q

Tetanus: Prevention

A

Toxoid vaccination at 2, 3 and 4 months

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256
Q

Spondyloarthropathies

A

Family of inflammatory arthritides characterised by the involvement of both the spine and joints

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257
Q

Spondyloarthropathies: Associated with what gene?

A

HLA-B27

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258
Q

What diseases are associated with the HLA-B27 gene? (PAIR Pneumonic)

A

Psoriatic arthritis
Ankylosing spondylitis
IBS + Enteropathic arthritis
Reactive arthritis

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259
Q

Spondyloarthropathies: Higher prevalence in what regions?

A

Northern hemisphere - especially the scandinavian countries

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260
Q

Spondyloarthropathies: Reactive arthritis

A

Autoimmune reaction to infection e.g. Chlamydia, Shigella, Salmonella and Campylobacter

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261
Q

Spondyloarthropathies: Enteritis associated Arthritis

A

Organisms with high lipopolysaccharide content in the cell wall that triggers an immune reaction

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262
Q

Spondyloarthropathies: Shared features - Involve what regions (2)

A

Sacroiliac joints
Spine

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263
Q

Spondyloarthropathies: Inflammatory Arthritis features (3)

A

Oligoarticular (<5 joints)
Asymmetrical
Lower limb predominantly

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264
Q

Synovitis

A

Inflammation of the joint and tendon sheath linings

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265
Q

Spondyloarthropathies: Enthesitis

A

Inflammation at sites where ligaments and tendons attach to bones

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266
Q

Spondyloarthropathies: Dactylitis

A

Inflammation of the entire digit

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267
Q

Spondyloarthropathies: Extra-articular features - Eyes

A

Ocular inflammation

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268
Q

Spondyloarthropathies: Extra-articular features - Mucous membranes

A

Mucocutaneous lesions

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269
Q

Spondyloarthropathies: Extra-articular features - Heart (2)

A

Aortic incompetence
Heart block

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270
Q

Ankylosing Spondylitis: Peak age of diagnosis

A

20-30 year olds

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271
Q

Ankylosing Spondylitis

A

Chronic inflammatory disease of the axial skeleton that leads to partial or even complete fusion and rigidity of the spine

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272
Q

Ankylosing Spondylitis: More common in what sex?

A

Males

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273
Q

Ankylosing Spondylitis: Genetic predisposition

A

HLA-B27

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274
Q

Ankylosing Spondylitis: 3 stages of development

A
  1. Inflammation of the ligaments and joints
  2. Formation of syndesmophytes
  3. Fusion of the discs
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275
Q

Ankylosing Spondylitis: Main symptom

A

Dull pain in the Spine and neck

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276
Q

Ankylosing Spondylitis: Onset of symptoms

A

Gradual that progresses slowly

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277
Q

Ankylosing Spondylitis: Is there stiffness present? If so when and for how long?

A

Yes - Morning for 30 minutes

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278
Q

Ankylosing Spondylitis: What makes morning stiffness better?

A

Activity

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279
Q

Ankylosing Spondylitis: Late Ankylosing Spondylitis presents with what?

A

Question mark posture - Loss of lumbar kyphosis with pronounced cervical lordosis

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280
Q

What is the Schobers Test?

A

Used to measure lumbar spine flexion

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281
Q

Ankylosing Spondylitis: Schobers Test Result

A

<20 cm

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282
Q

Schober Test Result

A

Measure 5cm below the posterior iliac crest and 10cm above
Whilst the patient is upright
Ask them to bend forwards and remeasure the distance between the two
Normal is >20cm

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283
Q

Ankylosing Spondylitis: Impact on chest

A

Reduced chest expansion

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284
Q

Ankylosing Spondylitis: Extra-articular features - Eyes

A

Anterior uveitis

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285
Q

Ankylosing Spondylitis: Extra-articular features - Heart

A

Aortic regurgitation

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286
Q

Ankylosing Spondylitis: Extra-articular features - Pulmonary involvement

A

Upper lobe fibrosis

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287
Q

Ankylosing Spondylitis: Extra-articular features - Neurological involvement

A

Atlantoaxial Subluxation - misalignment of the 1st and 2nd cervical vertebrae

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288
Q

Ankylosing Spondylitis: Blood results

A

Raised inflammatoy markers
HLA-B27 present

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289
Q

Ankylosing Spondylitis: X-Ray - Bone density

A

Reduced in later disease

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290
Q

Ankylosing Spondylitis: X-Ray - Syndesmophyte appearance

A

Bony spurs from the vertebral bodies bridge the intervertebral disc causing fusion leading to bamboo spine

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291
Q

Ankylosing Spondylitis: MRI presentations (3)

A

Sacroiliitis - active inflammation
Bone marrow oedema
Enthesitis of the spinal ligaments

292
Q

Ankylosing Spondylitis: What classification is used for axial spondylarthritis

A

ASAS classification criteria

293
Q

Ankylosing Spondylitis: What is the criteria? (2)

A

Patients with >3 months of back pain + age of onset >45
Sacrolitis on imaging + >1 SpA feature OR HLA-B27 positive + <2 other SpA features

SpA features - inflAmmatory back pain, arthritis, Enthesitis, Dactylitis or raised CRP

294
Q

Ankylosing Spondylitis: Management - Non-pharmacological treatment options (4)

A

Physiotherapy
Occupational therapy
Orthotics
Chiropodist

295
Q

Ankylosing Spondylitis: Management - First line pharmacological treatment

A

NSAIDs

296
Q

Ankylosing Spondylitis: Management - Options for symptomatic cases (3)

A

Corticosteroids
Topical steroids
Eyedrops

297
Q

Ankylosing Spondylitis: Management - If unresponsive to NSAIDs and Methotrexate what pharmaceutical should be used?

A

Anti-TNF

298
Q

Ankylosing Spondylitis: Management - Last line pharmacological intervention

A

Secukinumab - Anti-IL-17

299
Q

Psoriatic Arthritis

A

Inflammatory arthritis associated with psoriasis (10-15% do not have psoriasis)

300
Q

Psoriatic Arthritis: Aetiology

A

Occurs in up to 30% of people affected by skin psoriasis

301
Q

Psoriatic Arthritis: Clinical Presentation - Predominantly affects what joints?

A

In the hands and feet

302
Q

Psoriatic Arthritis: Clinical Presentation - Usual pattern

A

Asymmetrical oligoarthritis

303
Q

Psoriatic Arthritis: Clinical Presentation - Some patients have a predisposition to what joints being affected?

A

DIP joints of the fingers or toes

304
Q

Psoriatic Arthritis: Clinical Presentation - Extra-articular impacts (3)

A

Eye disease
Nail pitting
Nail onycholysis

305
Q

Psoriatic Arthritis: Arthritis Mutilans

A

Aggressive and destructive form of the condition that occurs in the hands -involves reabsorption of bone and collapsed soft tissue

306
Q

Psoriatic Arthritis: Diagnosis - Blood results

A

Increased inflammatory markers

307
Q

Psoriatic Arthritis: Diagnosis - X-ray has what features? (3)

A

Marginal erosions and whiskering
Osteolysis
Enthesitis

308
Q

Psoriatic Arthritis: Management - Non-pharmacological options (4)

A

Physiotherapy
Occupational therapy
Orthotics
Chiropodist

309
Q

Psoriatic Arthritis: Management - First line pharmacological management

A

NSAIDs

310
Q

Psoriatic Arthritis: Management - Pharmacological management for symptomatic cases (3)

A

Corticosteroids
Topical steroids
Eyedrops

311
Q

Psoriatic Arthritis: Management - Pharmacological management if unresponsive to NSAIDs and Methotrexate

A

Anti-TNF

312
Q

Psoriatic Arthritis: Management - Pharmacological last line

A

Secukinumab - Anti-IL-17

313
Q

Infectious Arthritis: Causative organism in adults

A

Staphyloccus aureus

314
Q

Infectious Arthritis: Causative organism in young children

A

Haemophilus influenzae

315
Q

Infectious Arthritis: Causative organism in young adults

A

Gonococcal infection

316
Q

Infectious Arthritis: Sickle Cell Anaemia patients are predisposed to what?

A

Salmonella arthritis

317
Q

Infectious Arthritis: What joint is most common?

A

Knee

318
Q

Crystal Arthropathy

A

Disorders characterised by deposition of minerals in the joints and soft tissues leading to inflammation

319
Q

Crystal Arthropathy: Three examples

A

Gout
Pseudogout
Hydroxyapatite Deposits

320
Q

Gout

A

Arthritic presentations as a result of monosodium urate crystal deposition due to defective urate metabolism

321
Q

Gout: Peak incidence age

A

20-80 years old

322
Q

Gout: More common in what sex?

A

Men

323
Q

Gout: When and why does the risk increase in women?

A

After the menopause - oestrogen promotes the excretion of uric acid

324
Q

Gout: Risk Factors (5)

A

Genetic predisposition
Alcohol
Obesity
Drugs
Purine rich food

325
Q

Gout: 4 Stages of Pathophysiology

A
  1. Hyperuricaemia - excess uric acid in the blood
  2. Deposition of monosodium urate crystals within the joint
  3. Complement activation and monocytes attempt phagocytosis of the crystals to lyse neutrophils
  4. Lysosomal enzymes (IL-1 + TNF-Alpha + IL-6) are released to cause tissue injury and inflammation
326
Q

Gout: Two mechanisms of development

A

Increased production of urate
Reduced excretion of urate

327
Q

Gout: Increased urate production - Can occur due to deficiency of what?

A

HGPRT

328
Q

Function of HGPRT in urate metablism

A

Impairs the purine nucleotide salvage pathway leading to degradation of urate

329
Q

Gout: Increased urate production - Examples of diseases that cause increased cell turnover (3)

A

Psoriasis
Cancer
Tumour lysis following chemotherapy

330
Q

Gout: Increased urate production - Can be due to intake of what? (2)

A

Alcohol - high in purines
High dietary purine diet

331
Q

Gout: Reduced urate excretion - Causes (5)

A

Chronic renal disease
Thiazide Diuretics
Volume depletion e.g. HF
Hypothyroidism
Cytotoxics

332
Q

Gout: Reduced urate excretion - Example of a cytotoxic that causes this?

A

Cyclosporin

333
Q

Gout: Mechanism of Urate Synthesis

A

Purines > Hypoxanthine > Xanthines to form plasma urate

334
Q

Gout: How is urate excreted?

A

Renal filtration of urate - reabsorbed in the PCT and limited excretion from the DCT

335
Q

Gout: Uric acid is the final product of what?

A

Breakdown of Adenosine and Guanine in DNA metabolism

336
Q

Gout: Why do crystals precipitate?

A

Due to reduced solubility

337
Q

Gout: Crystallisation occurs in joints when?

A

At lower temperatures

338
Q

Gout: What increases the production of pro-inflammatory cytokines?

A

Phagocytosis of crystals by macrophages

339
Q

Gout: Chronic gouty arthritis and tophaceous gout are a result of what?

A

Chronic Granulomatous Inflammatory Response to deposited crystals

340
Q

Gout: Histology of Gouty Tophus

A

Amorphous eosinophilic debris and inflammation

341
Q

Gout: Acute Gout - Classic site of disease

A

MTP joint of the foot
Can also impact the ankle or knee joint

342
Q

Gout: Acute Gout - Onset

A

Abrupt overnight

343
Q

Gout: Acute Gout - Clinical presentation

A

Severely painful hot swollen joint that may mimic septic arthritis

344
Q

Gout: Acute Gout - Lasts how long?

A

10 days without treatment
3 days with treatment

345
Q

Gout: Chronic Tophaceous Gout - Presentation

A

Painless white accumulations of uric acid that can occur in soft tissue and occasionally erupt through the skin

346
Q

Gout: Chronic Tophaceous Gout - Often associated with what drug?

A

Thiazide diuretics

347
Q

Gout: Chronic Tophaceous Gout - Blood factors

A

High serum uric acid

348
Q

Gout: Chronic Tophaceous Gout - Can result in what?

A

Destructive erosive arthritis

349
Q

Gout: Diagnosis in Bloods (30

A

Serum uric acid is increased
Raised inflammatory markers
Renal impairment - detected via U&Es and GFR

350
Q

Gout: Diagnosis via Cytology

A

Joint fluid is examined under cross-polarized light to detect needle shaped crystals

351
Q

Gout: Histological appearance (3)

A

No crystals present
Amorphous eosinophilic debris and inflammation
Giant cells

352
Q

Gout: Acute Gout - Management - First line

A

NSAIDs

353
Q

Gout: Acute Gout - Management - Second Line

A

Colchicine if NSAIDs not suitable

354
Q

Gout: Acute Gout - Management - What patient groups are NSAIDs unacceptable for?

A

Patients with heart failure
Patients with Chronic Kidney Failure

355
Q

Gout: Acute Gout - Management - Side effects of Colchicine

A

Diarrhoea

356
Q

Gout: Acute Gout - Management - Third Line

A

Oral/IM/Intra-articular Steroids

357
Q

Gout: Prophylactic Management - Should be started when?

A

1 week after an acute attack

358
Q

Gout: Prophylactic Management - Requires cover with what?

A

NSAIDs or Colchicine

359
Q

Gout: Prophylactic Management - First line

A

Xanthine Oxidase Inhibitors

360
Q

Gout: Prophylactic Management - Examples of Xanthine Oxidase Inhibitors

A

Allopurinol
Febuxostat

361
Q

Gout: Prophylactic Management - Second line

A

Uricosuric Drugs

362
Q

Gout: Prophylactic Management - Examples of Uricosuric Drugs

A

Sulfinpyrazone
Probenecid
Benzbromarone

363
Q

Gout: Prophylactic Management - Third Line

A

IL-1 Inhibitors

364
Q

Gout: Prophylactic Management - Example of IL-1 inhibitor

A

Canakinumab

365
Q

Gout: Prophylactic Management - Uric Acid Target

A

300-360 micromol/L

366
Q

Gout: Prophylactic Management - Indications (6)

A

One or more attacks of gout in a year despite lifestyle changes
Presence of gouty tophi or chronic gouty arthritis
Uric acid calculi (kidney stones)
Chronic renal impairment
Heart failure - when unable to stop diuretics
Chemotherapy patients that develop gout

367
Q

Gout: What drug must be avoided?

A

Allopurinol

368
Q

Pseudogout

A

Arthritic presentations due to depositions of calcium pyrophosphate crystals within the fibrocartilage of a joint

369
Q

Pseudogout: How do the crystals appear on imaging?

A

Dense deposits on X-Ray

370
Q

Pseudogout: Most common patient group

A

Elderly

371
Q

Pseudogout: Chrondrocalcinosis

A

Calcium pyrophosphate deposition within the cartilage and soft tissue in the absence of acute inflammation

372
Q

Pseudogout: Affects what areas?

A

Fibrocartilage of the knees, wrists and ankles

373
Q

Pseudogout: Risk Factors (6)

A

Hypercalcaemia
Hyperparathyroidism
Haemachromatosis
Hypomagnesaemia
Ochronosis
Hypothyriodism

374
Q

Pseudogout: Mechanism of pathophysiology

A

Crystals formation within the cartilage, menisci and discs of joints expand and rupture into the joint to cause joint damage

375
Q

Pseudogout: Blood results

A

Increased inflammatory markers

376
Q

Pseudogout: Histology results

A

Rhomboid shaped crystals with weak positive birefringence

377
Q

Pseudogout: Management options (4)

A

NSAIDs
Colchicine
Steroids
Rehydration

378
Q

Hydroxyapatite Deposition Disease

A

Deposition of basic calcium phosphate into the joints and soft tissue to cause inflammation

379
Q

Hydroxyapatite Deposition Disease: Most commonly affected site

A

Shoulder - Milwaukee shoulder

380
Q

Hydroxyapatite Deposition Disease: Most common in what sex?

A

Females

381
Q

Hydroxyapatite Deposition Disease: Highest incidence age group

A

50-60 years

382
Q

Hydroxyapatite Deposition Disease: Associated with the release of what chemical mediators? (3)

A

Collagenases
Serine proteases
IL-1

383
Q

Hydroxyapatite Deposition Disease: Presentation

A

Acute onset of joint pain

384
Q

Hydroxyapatite Deposition Disease: Diagnostic technique

A

X-Ray

385
Q

Hydroxyapatite Deposition Disease: Management - First Line

A

NSAIDs
Intra-articular steroid
Local anaesthetic

386
Q

Hydroxyapatite Deposition Disease: Management - Second Line

A

Surgical removal of calcifications for cases refractory to attempt at conservative treatment

387
Q

Hydroxyapatite Deposition Disease: Management - Last line treatment

A

Partial or Total Arthroplasty

388
Q

Mysathenia Gravis

A

Severe autoimmune neuromuscular disorder characterised by severe muscular weakness and progressive fatigue

389
Q

Mysathenia Gravis: Associated with what other diseases? (3)

A

SLE
Rheumatoid arthritis
Thyrotoxicosis

390
Q

Mysathenia Gravis: Most common age

A

60-70 years old

391
Q

Mysathenia Gravis: Most common age in women

A

<40 years old

392
Q

Mysathenia Gravis: Most common age in males

A

> 60 years old

393
Q

Mysathenia Gravis: 10% are associated with what?

A

Thymic tumours

394
Q

Mysathenia Gravis: Basic pathophysiology

A

Auto-reactive antibodies (auto-IgG) bind to post-synaptic ACh receptors on muscle cells

395
Q

Mysathenia Gravis: What type of immune reaction is this?

A

Type II hypersensitivity

396
Q

Mysathenia Gravis: What two moleculaes are inolved in activating auto-reactive B cells?

A

CD4+ TH cells
AChR self-antigens

397
Q

Mysathenia Gravis: Pathophysiology Pathway - Initiating event

A

CD4+ TH cells are activated by unfolded AChR subunits on thymic epithelial cells

398
Q

Mysathenia Gravis: Pathophysiology Pathway - Activated CD4+ TH Cells hae what action?

A

Stimulate auto-reactice B cells to produce anti-AChR IgG autoantibodies

399
Q

Mysathenia Gravis: Pathophysiology Pathway - Anti-AChR autoantibodies have what function?

A

Attack thymic myoid cells expressing intact AChR

400
Q

Mysathenia Gravis: Pathophysiology Pathway - The formation of AChR immune complexes causes what to occur?

A

Activation of APCs causing the auto-antibody response to recognise intact AChRs of normal muscle cells

401
Q

Mysathenia Gravis: Pathophysiology Pathway - The binding of auto-antibodies to AChR on normal muscle cells has what impact?

A

Blocks the binding of endogenous ACh ligands to their receptors

402
Q

Mysathenia Gravis: Pathophysiology Pathway - How are AChRs eventually destroyed? (2)

A

Antibody-bound receptors are internalised and degraded
AChR antibodies bound to complement lead to the destruction of the muscle endplate

403
Q

Mysathenia Gravis: Pathophysiology Pathway - Destruction of AChR endplates have what overall impact?

A

Reduced amplitude of endplate potentials to cause impaired signal conduction at the neuromuscular junction

404
Q

Mysathenia Gravis: Presentation - Eyes (2)

A

Double vision - due to extra-ocular muscle weakness
Drooping of the eyelids

405
Q

Mysathenia Gravis: Presentation - Face (2)

A

Weakness of the facial movements
Fatigue in the jaw when chewing

406
Q

Mysathenia Gravis: Presentation - ENT (20

A

Difficulty in swallowing
Slurred speech

407
Q

Mysathenia Gravis: Diagnosis - Autoantibodies (3)

A

Anti-AChR
Anti-MuSK
Anti-LRP4

408
Q

Mysathenia Gravis: Diagnosis - 3 alternate tests to autoantibodies (3)

A

Scan of the thymus - may detect a thymoma
Repetitive nerve stimulation
Edrophonium or Neostigmine Testing - blocks the breakdown on ACh

409
Q

Mysathenia Gravis: Management - First Line

A

Pyridostigmine - increases neurotransmission by a reversible anti-cholinesterase agent

410
Q

Mysathenia Gravis: Management - Second Line Options (4)

A

Corticosteroids e.g. Prednisolone
Azathiprine
Mycophenolate
Rituximab

411
Q

Mysathenia Gravis: Management - Last Line or First line if thymic tumour is present

A

Thymectomy

412
Q

Mysathenia Gravis: Management for Crisis - If respiration is impaired

A

O2 and Ventilator

413
Q

Mysathenia Gravis: Management for Crisis - How to prevent autoimmune reactions?

A

IV Immunoglobulin

414
Q

Mysathenia Gravis: Management for Crisis - How to remove auto-reactive Antibodies from the serum?

A

Plasmapheresis

415
Q

Osteoporosis

A

Quantitative defect of the bone characterised by reduced bone mineral density and increased porosity

416
Q

Osteoporosis: Loss of bone mineral density starts at what age normally?

A

30 years

417
Q

Osteoporosis: 3 risk factors for Primary Osteoporosis

A

Post-menopausal women
Senile patients
Genetics - genes regulating the osteoclastic activity and Vitamin D Receptors

418
Q

Osteoporosis: Primary Osteoporosis - What race are at an increased risk?

A

White caucasians

419
Q

Osteoporosis: Primary Osteoporosis - Environmental risk factors (4)

A

Smoking
Alcohol abuse
Lack of exercise
Poor diet

420
Q

Osteoporosis: Primary Osteoporosis - These patients are at risk to what musculoskeletal problems?

A

Colles fracture
Vertebral insufficiency

421
Q

Osteoporosis: Primary Osteoporosis - Type I

A

Osteoporosis due to exacerbated loss of bone in the post-menopausal period

422
Q

Osteoporosis: Primary Osteoporosis - Type II

A

Osteoporosis of old age individuals with a rapid decline in bone mineral density

423
Q

Osteoporosis: Primary Osteoporosis - 3 environmental risk factors for Type II

A

Chronic disease
Inactivity
Reduced sunlight exposure - reduced Vitamin D

424
Q

Osteoporosis: Primary Osteoporosis - What fractures predominate in Type II Osteoporosis?

A

Femoral neck fractures
Vertebral fractures

425
Q

Osteoporosis: Secondary Osteoporosis - Risk factors (4)

A

Endocrine disorders
Gastrointestinal Disorders
Drugs - Alcohol or Corticosteroids
Immobilisation

426
Q

Osteoporosis: Secondary Osteoporosis - Examples of Endocrine disorders thayt increase risk (3)

A

Cushing’s Syndrome
Hyperparathyroidism
Hyperthyroidism

427
Q

Osteoporosis: Secondary Osteoporosis - Examples of Gastrointestinal Disorders that increase risk (4)

A

Hepatic insufficiency
Malabsorption
Malnutrition
Vitamin C or D deficiency

428
Q

Osteoporosis: Peak bone mass occurs when?

A

Young adulthood

429
Q

Osteoporosis: Environmental factors determining peak bone mass (4)

A

Physical activity
Muscle strength
Diet
Hormonal stasis

430
Q

Osteoporosis: Normal degeneration of the bone per year

A

0.7%

431
Q

Osteoporosis: Age related changes in bones (2)

A

Reduced proliferative and biosynthetic capacity of osteoblasts
Response to growth factors is attenuated

432
Q

Osteoporosis: Alterations in blood components (3)

A

Reduced calcium
Elevated PTH
Vitamin D deficiency

433
Q

Osteoporosis: Impact of the menopause

A

Post-menopause there is low oestrogen causing osteoclasis to exceed osteoblastic activity

434
Q

Osteoporosis: Indirect effects of Corticosteroids on bone

A

Inhibition of gonadal and adrenal steroid production

435
Q

Osteoporosis: Direct effects of corticosteroids on bone (3)

A

Reduced osteoblast activity and lifespan
Suppression of replication of osteoblast precursors
Reduction in calcium absorption

436
Q

Osteoporosis: Common osteoporotic fracture sites (4)

A

Proximal femur
Sacrum and pubic rami
Thoracolumbar vertebral bodies
Distal radius

437
Q

Osteoporosis: Fracture of the vertebral body can results in what two things? (2)

A

Thoracic kyphosis
Loss of heght

438
Q

Osteoporosis: How is the risk assessed?

A

10 year osteoporotic fracture risk calculator

439
Q

Osteoporosis: Osteopenia

A

1-2.5 Standard deviations below mean peak bone mass

440
Q

Osteoporosis: Diagnostic definition

A

> 2.5 deviations below mean peak bone mass

441
Q

Osteoporosis: Secondary causes of fractures (30

A

Steroids
Early menopause
Anorexia

442
Q

Osteoporosis: When is a DEXA scan referred? (2)

A

Anyone with a 10 year risk assessment for any OP fracture of at least 10%
Any patient above 50 years with a low trauma fracture

443
Q

Osteoporosis: What does a DEXA scan determine?

A

Bone mineral density

444
Q

Osteoporosis: Severe Osteoporosis definition

A

> 2.5 standard deviations below the mean peak bone masswith a fragility fracture

445
Q

Osteoporosis: How is Multiple Myeloma ruled out?

A

Protein electrophoresis
Bence Jones proteins analysed

446
Q

Osteoporosis: Lifestyle Advice (5)

A

Increase calcium intake
High intensity strength training
Low-impact weight bearing exercise
Avoidance of excess alcohol
Avoidance of smoking

447
Q

Osteoporosis: Calcium intake aim for general population

A

700mg

448
Q

Osteoporosis: Calcium intake aim for post-menopausal women

A

1000mg

449
Q

Osteoporosis: Management - What is given if there is dietary deficiency or limited sunlight exposure?

A

Calcium or Vitamin D supplements

450
Q

Osteoporosis: Management - When must calcium supplements not be given?

A

Within 2 hours of oral bisphosphonates

451
Q

Osteoporosis: Management - First line for a majority of patients?

A

Oral Bisphosphonates

452
Q

Osteoporosis: Management - Function of Oral Bisphosphonates

A

Reduce osteoclastic resorption

453
Q

Osteoporosis: Management - Examples of Oral Bisphosphonates (3)

A

Alendronic acid
Risedronate
Etidronate

454
Q

Osteoporosis: Management - When should Oral Bisphosphonates be considered?

A

When a T score </= to 2.5 is present

455
Q

Osteoporosis: Management - Second line management for a majority of patients

A

Zoledronic Acid

456
Q

Osteoporosis: Management - Dose And Administration route of Zoledronic Acid

A

Once yearly intravenous bisphosphonate

457
Q

Osteoporosis: Management - MOA of Desunomab

A

Monoclonal antibody that reduces osteoclast activity

458
Q

Osteoporosis: Management - MOA of Treiparatide

A

Recombinant parathyroid hormone that stimulates bone growth rather than reduces bone loss

459
Q

Osteoporosis: Management - MOA of Treiparatide

A

Recombinant parathyroid hormone that stimulates bone growth rather than reduces bone loss

460
Q

Osteoporosis: Management - Teriparatide is used when?

A

To reduce the risk of vertebral and non-vertebral fractures in post-menopausal women with severe osteoporosis

461
Q

Osteoporosis: Management - When is Teriparatide recommended over oral Bisphosphonates?

A

In post menopausal women with at least 2 moderate or 1 severe low trauma vertebral fracture to prevent vertebral fracture

462
Q

Osteoporosis: Management - MOA of Romosozumab

A

Monoclonal antibody that binds to and inhibits sclerostin to increase bone formation and reduce bone resorption

463
Q

Osteoporosis: Management - When is Romosozumab recommended?

A

For post menopausal women with severe ostroporosis who have had a fragility fracture and are at imminent risk of further fracture

464
Q

Osteomalacia

A

Qualitative defect of the bone with abnormal softening of the bone due to deficient mineralisation of osteoid secondary to inadequate amounts of calcium and phosphorous

465
Q

Rickets

A

Qualitative defect of the bone with abnormal softening of the bone due to deficient mineralisation of osteoid secondary to inadequate amounts of calcium and phosphorous in children

466
Q

Osteomalacia and Rickets: Two main causes

A

Insufficient calcium absorption
Phosphate deficiency - due to increased renal loss

467
Q

Osteomalacia and Rickets: Aetiologies (4)

A

Vitamin D deficiency
Hypophosphataemia
Long term Anti-convulsant use
Chronic Kidney Disease

468
Q

Osteomalacia and Rickets: Cuases of Vitamin D deficiency (3)

A

Malnutrition
Malabsorption
Lack of sunlight exposure

469
Q

Osteomalacia and Rickets: Causes of Hypophosphatemia (4)

A

Re-feeding Syndrome
Alcohol abuse
Malabsoprtion
Renal Tubular Acidosis

470
Q

Osteomalacia and Rickets: How is this triggered by Chronic Kidney Disease?

A

Reduced phosphate resorption and failure of activation of Vitamin D resulting in Secondary Hyperparathyroidism

471
Q

Osteomalacia and Rickets: What is the function of Vitamin D?

A

Stimulates the absorption of calcium from the GI tract, Kidney and bone
Induces osteoblasts to release Osteocalcin

472
Q

Osteomalacia and Rickets: Initial impacts of Vitamin D deficiency? (2)

A

Hypocalcaemia
Elevated PTH

473
Q

Osteomalacia and Rickets: The hypocalcaemia and elevated PTH due to Vitamin D deficiency have what secondary effects? (3)

A

Increases calcium absorption
Increased Osteoclastic activity
Release of Calcium from the bone

474
Q

Osteomalacia and Rickets: Reduced Vitamin D has what affect on the kidneys?

A

Increased renal excretion of phosphate

475
Q

Osteomalacia and Rickets: Increased renal excretion of phosphate due to Vitamin D deficiency has what effect on the bone?

A

Impairs bone mineralisation

476
Q

Osteomalacia and Rickets: Impaired bone mineralisation of the matrix has what overall impact?

A

Bone remodelling

477
Q

Osteomalacia and Rickets: Bone remodelling is idfferent in these conditions, why?

A

Newly formed osteoid is not fully mineralised causing thick osteoid seams and causes the bone to become weak

478
Q

Osteomalacia and Rickets: Presentation - Bone pain where?

A

Pelvis
Spine
Femora

479
Q

Osteomalacia and Rickets: Presentation - Symptoms of Hypocalcaemia (6)

A

Paraesthesiae - burning sensation in the limbs
Muscle cramps
Irritability
Fatigue
Seizures
Brittle nails

480
Q

Osteomalacia and Rickets: Presentation - Signs in the bones of ricket patients

A

Deformation due to soft bones

481
Q

Osteomalacia and Rickets: Presentation - Presents with proximal …

A

Myopathy

482
Q

Osteomalacia and Rickets: Presentation - Oral symptoms

A

Dental defects

483
Q

Osteomalacia and Rickets: Diagnostic test

A

X-Ray

484
Q

Osteomalacia and Rickets: X-Ray - 2 features

A

Poor corticomedullary differentiation
Pseudofractures - Pubic rami, Proximal femora, Ulna and Ribs

485
Q

Osteomalacia and Rickets: Blood results (3)

A

Decreased calcium
Decreased serum phosphate
Increased serum ALP

486
Q

Osteomalacia and Rickets: Management

A

Vitamin D Therapy + Calcium and Phosphate Supplementation

487
Q

Osteomalacia and Rickets: Management - Vitamin D therapy dose and duration

A

400-800 IU per day after loading IU per day for 12 weeks

488
Q

Osteomalacia and Rickets: What must be considered for Chronic Renal Disease?

A

Patients may have a high 25-OG-Vitamin D so treatment must be titrated to PTH levels

489
Q

Avascular Necrosis

A

Necrosis of the bone marrow due to loss of an effective vascular supply

490
Q

Avascular Necrosis: More common in what sex?

A

Males

491
Q

Avascular Necrosis: Typical Age

A

35-50 years

492
Q

Avascular Necrosis: Risk Factors - What coagulation disorders? (4)

A

Those with increased coaguability:
- Thrombophilia
- Sickle Cell disease
- Antiphospholipid deficiency in SLE
- Pregnancy

493
Q

Avascular Necrosis: Risk Factors - Biochemical causes

A

Hyperlipidaemia - increased fat in circulation

494
Q

Avascular Necrosis: Risk Factors - Why can risk be increased by alcohol or steroid use and abuse? (3)

A

Altered fat metabolism - results in mobilisation of fat in the circulation
Sludges up the capillary system to promote coagulation in prone areas of the bone
Increased fat content in the marrow causes compression on the outflow from the bone to cause stasis and ischaemia

495
Q

Avascular Necrosis: Risk Factors - Dysbaric disorders increase risk, what are they?

A

Nitrogen gas bubbles forming in the circulation after a rapid depressurisation after deep sea diving

496
Q

Avascular Necrosis: Risk Factors - What mechaical problems increase risk?

A

Fractures of the scaphoid or femoral head

497
Q

Avascular Necrosis: Commonly affected sites (6)

A

Femoral head
Femoral condyles
Head of the humerus
The capitellum
The proximal pole of the scaphoid
The proximal part of the talus

498
Q

Avascular Necrosis: What vessels are damaged in scaphoid fracture?

A

Retrograde blood supply

499
Q

Avascular Necrosis: What vessels are damaged in femoral fractures?

A

Circumflex arteries

500
Q

Avascular Necrosis: How does thrombophilia cause AVN?

A

Causes blood clots

501
Q

Avascular Necrosis: How does alcoholism cause AVN?

A

Causes fat microemboli

502
Q

Avascular Necrosis: How does Sickle cell disease?

A

Causes sickle cell crisis

503
Q

Avascular Necrosis: Pathophysiology - The hypoxic death of bone and haemopoietic cells causes what 3 effects? (3)

A

Stimulates periosteal nociceptors
Reabsorption of dead bone tissue
Demineralisation of the bone

504
Q

Avascular Necrosis: Pathophysiology - Osteochondritis dissecans

A

Reabsorption of deab bone tissue causes separation of the articular surface from the dead subchondral bone

505
Q

Avascular Necrosis: Pathophysiology - Idiopathic AVN pathophysiology initiating event

A

Coagulation of the intraosseous microcirculation causes a venous thrombosis to induce retrograde arterial occlusion

506
Q

Avascular Necrosis: Pathophysiology - Retrograde arterial occlusion encourages what to arise?

A

Intraosseous hypertension

507
Q

Avascular Necrosis: Pathophysiology - Intraosseous hypertension causes what two things to occur?

A

Decreased blood flow which results in necrosis of the bone segment

508
Q

Avascular Necrosis: Pathophysiology - What initially occurs following necrosis of bone segments?

A

Patchy sclerosis - this precedes subchrondral collapse
Irregularity of the articular surface

509
Q

Avascular Necrosis: Pathophysiology - Resultant bone and joint damage can lead to what?

A

Secondary Osteoarthritis

510
Q

Avascular Necrosis: Clinical Presentation

A

Can be assymptomatic - joint pain presents when progression to collapse or osteoarthritis has occured

511
Q

Avascular Necrosis: Clinical Presentation of a Femoral Head/Hip AVN

A

Insidious onset of groin pain that is exacerbated by movement

512
Q

Avascular Necrosis: Diagnosis - Features on X-Ray (3)

A

Sclerosis surrounding the necrotic region
Collapsed bone segments
Sub-chondral locking or catching

513
Q

Avascular Necrosis: Diagnosis - X-ray sign for femral head AVN

A

Hanging rope sign - Patchy sclerosis of the weight bearing area of the femoral head with a lytic zone underneath formed by granulation tissue from the attempted repair

514
Q

Avascular Necrosis: Management - Treatment is dependent on what classification system?

A

Steinburg Classification

515
Q

Avascular Necrosis: Management - Stage 0 Steinburg Classification

A

Normal Radiograph + Normal MRI and Bone scan

516
Q

Avascular Necrosis: Management - Stage I Steinburg Classification

A

Normal Radiograph + Abnormal MRI and/or bone Scan

517
Q

Avascular Necrosis: Management - Stage II Steinburg Classification

A

Cystic or Sclerotic Radiograph + Abnormal MRI and /or bone scan

518
Q

Avascular Necrosis: Management - Stage III Steinburg Classification

A

Crescent sign (Subchondral collapse) + Abnormal MRI or bone scan

519
Q

Avascular Necrosis: Management - Stage IV Steinburg Classification

A

Flattening of the femoral head + Abnormal MRI and/or Bone scan

520
Q

Avascular Necrosis: Management - Stage V Steinburg Classification

A

Narrowing of the joint + Abnormal MRI and/or Bone Scan

521
Q

Avascular Necrosis: Management - Stage VI Steinburg Calssification

A

Advanced degenerative changes + Abnormal MRI and/or Bone scan

522
Q

Avascular Necrosis: Management - What classifications are reversible?

A

Steinburg Classifications 0-II

523
Q

Avascular Necrosis: Management - What classifications are irreverisble?

A

Steinburg classifications III-VI

524
Q

Avascular Necrosis: Management - Options for reversible cases (4)

A

Bisphosphanates
Core decompression - drilling is performed to decompress the bone to prevent further necrosis
Currettage and bone grafting
Vascularised fibular bone graft

525
Q

Avascular Necrosis: Management - Options for irreversible cases (2)

A

Total joint replacement
Rotational osteotomy - if <15% of the femoral head is damaged

526
Q

Hyperparathyroidism: Function of PTH - Role in Osteoclast activity

A

Activates Osteoclasts to increase bone resorption and release calcium

527
Q

Hyperparathyroidism: Function of PTH - Role in Calcium regulation

A

Increases resorption of calcium by renal tubules

528
Q

Hyperparathyroidism: Function of PTH - Role in Phosphate Activity

A

Increases urinary excretion of phosphate

529
Q

Hyperparathyroidism: Function of PTH - Role in Vitmin D activity

A

Increased synthesis of Active forms of Vitamin D

530
Q

Hyperparathyroidism: Clinical Presentation - Presentations as a result of increased Osteoclasis (2)

A

Decreased bone mass
Prone to fractures deformity and degenerative joint diseases

531
Q

Hyperparathyroidism: Clinical Presentation - Osteoporosis occurs where?

A

Phalanges
Vertebrae
Femur

532
Q

Hyperparathyroidism: Clinical Presentation - Osteoporosis has prominent changes in what section of the bone?

A

Cortical bone and medullary cancellous bone

533
Q

Hyperparathyroidism: Clinical Presentation - What is present within marrow spaces?

A

Fibrovascular tissue

534
Q

Hyperparathyroidism: Clinical Presentation - What tumours may appear?

A

Brown Tumours

535
Q

Hyperparathyroidism: Clinical Presentation - What cells are present in brown tumours?

A

Giant cells

536
Q

Hyperparathyroidism: Clinical Presentation - Haemorrhage associated with brown tumours has what two effects?

A

Macrophage reactions
Increased processes of organisation and repair

537
Q

Paget’s Disease of Bone

A

Chronic condition involving cellular remodelling and deformity of one or more bones

538
Q

Paget’s Disease of Bone: Incidence in age

A

Most are >50 years

539
Q

Paget’s Disease of Bone: More common in what sex?

A

Males

540
Q

Paget’s Disease of Bone: Genes involved? (2)

A

SQSTM1/P62 gene or RANKL - both increase the activity f NF-KB

541
Q

Paget’s Disease of Bone: Other name

A

Osteitis Deformans

542
Q

Paget’s Disease of Bone: Viruses involved? (3)

A

Paramyxovirus
Measles
RSV

543
Q

Paget’s Disease of Bone: Viruses involved? (3)

A

Paramyxovirus
Measles
RSVRole of Measles iPaget’s Disease of Bone: n Paget’s?

544
Q

Paget’s Disease of Bone: Viruses involved? (3)

A

Paramyxovirus
Measles
RSV

545
Q

Paget’s Disease of Bone: Role of Measles in Paget’s?

A

MVNP nucleocaspid is present and activates osteoclast activity

546
Q

Paget’s Disease of Bone: Pathophysiology - First stage

A

Osteolytic - resorption pits are present with large osteoclasts

547
Q

Paget’s Disease of Bone: Pathophysiology - Second stage

A

Mixed stage of osteoclastic activity and osteoblastic activity

548
Q

Paget’s Disease of Bone: Pathophysiology - Final stage

A

Osteosclerotic stage - causes enlarged bone of increased density and with a coarse trabecular pattern

549
Q

Paget’s Disease of Bone: Pathophysiology - Net result

A

Thick excess bone with abnormal reversal lines that provide a mosaic pattern - the bone is soft and porous

550
Q

Paget’s Disease of Bone: Pathophysiology - Commonly affected bones (4)

A

Long bones
Pelvis
Lumbar spine
Skull

551
Q

Paget’s Disease of Bone: Clinical presentation - Pain occurs due to what? (2)

A

Micro-fractures
Compression neuropathies

552
Q

Paget’s Disease of Bone: Clinical presentation - Leontiasis ossea

A

Overgorowth of the facial and cranial bones

553
Q

Paget’s Disease of Bone: Clinical presentation - Platybasia

A

Skull base abnormality that is flat

554
Q

Paget’s Disease of Bone: Clinical presentation - Sabre tibia

A

Malformation of the tibia in which there is anterior bowing

555
Q

Paget’s Disease of Bone: Clinical presentation - Increased metabolism rate presents how? (2)

A

Warm skin
High output heart failure

556
Q

Paget’s Disease of Bone: Clinical presentation - Potential Secondary Malignancies (2)

A

Osteosarcoma
Fibrosarcoma

557
Q

Paget’s Disease of Bone: Clinical presentation - What symptom may present if the skull is affected?

A

Deafness

558
Q

Paget’s Disease of Bone: Diagnosis - 3 key tests

A

X-Ray
Isotope bone scan
Alkaline Phosphatase

559
Q

Paget’s Disease of Bone: Diagnosis - Early presentation on X-ray

A

Lytic phase presents with well defined lucency

560
Q

Paget’s Disease of Bone: Diagnosis - Late presentation on X-ray

A

Sclerotic phase with enlarged bone, increased density and coarse trabecular pattern

561
Q

Paget’s Disease of Bone: Diagnosis - Purpose of the isotope bone scan?

A

Shows distribution of disease

562
Q

Paget’s Disease of Bone: Diagnosis - Alkaline Phosphatase results

A

Elevated with normal LFTs

563
Q

Paget’s Disease of Bone: Management

A

Treat with Bisphosphanates if analgesia does not manage pain

564
Q

Soft Tissue Tumours: Examples (6)

A

Ganglion Cyst
Nodular fasciitis
Myositis ossificans
Superficial fibromatoses
Deep fibromatosis
Tenosynovitis

565
Q

Ganglion Cyst

A

Outpouching of the synovium lining of joints and filled with synovial fluid

566
Q

Ganglion Cyst: Two aetiologies (2)

A

Developmental e.g. Juvenile Bakers Cyst
Underlying joint damage or arthritis causes build up of pressure within the joint

567
Q

Ganglion Cyst: Why is this not a true cyst?

A

No epithelial lining

568
Q

Ganglion Cyst: What is present histologically?

A

Degenerative changes within the connective tissue
Space present with myxoid material

569
Q

Ganglion Cyst: Clinical presentation - Occur where?

A

Around a synovial joint or a synovical tendon sheath

570
Q

Ganglion Cyst: Clinical presentation - Common locations

A

Wrist
Feet
Knees

571
Q

Ganglion Cyst: Clinical presentation - Size

A

Up to 1cm

572
Q

Ganglion Cyst: Management

A

Normally self-resolving - if localised discomfort or cosmesis can be excised

573
Q

Nodular Fasciitis

A

Benign proliferation of fibroblastic and myofibroblastic cells

574
Q

Nodular Fasciitis: What patient group does this affect?

A

Young adults

575
Q

Nodular Fasciitis: Aetiology

A

25% of cases are associated with prior trauma

576
Q

Nodular Fasciitis: Histology = Mature where?

A

At the periphery

577
Q

Nodular Fasciitis: Histological appearance (3)

A

Highly cellular
Mitoses present
Plump cells - these are stellate and spindle cells

578
Q

Nodular Fasciitis: Clinical presentation

A

Superficial or deep lesion of less than 5cm that is usually well circumscribed

579
Q

Nodular Fasciitis: Management

A

Self-resolving

580
Q

Myositis Ossificans

A

Abnormal calcification of a muscle haematoma following trauma

581
Q

Myositis Ossificans: Aetiology

A

Associated with preceding trauma

582
Q

Myositis Ossificans: Histological appearance

A

Cellular proliferation with evidence of bone formation and zonation

583
Q

Myositis Ossificans: Clinical presentation

A

Initial soft swelling followed by hardness

584
Q

Myositis Ossificans: Diagnostic criteria

A

Peripheral mineralisation around bone on X-Ray or MRI

585
Q

Myositis Ossificans: Management and the criteria

A

Intervene only if symptoms are problematic
Must wait until maturity of ossification as there is a risk of recurrence at 6-12 months

586
Q

Superficial Fibromatoses

A

Non-metastatising fibroproliferative lesions that form within connective tissue

587
Q

Superficial Fibromatoses: Risk factors (3)

A

Alcohol
Diabetes Mellitus
Anticonvulsants

588
Q

Superficial Fibromatoses: Epidemiology of sexes

A

More common in men

589
Q

Superficial Fibromatoses: Average Age

A

60 years old

590
Q

Superficial Fibromatoses: Clinical Presentation - Dupuytren’s

A

Contracture of the hand that is a deformity due to knots of tissue forming under the skin of the palm

591
Q

Superficial Fibromatoses: Clinical Presentation - Peyronie’s

A

Non-cancerous condition due to fibrous scar tissue developing on the penis to cause curved and painful erections

592
Q

Superficial Fibromatoses: Histology of Dupuytren’s (4)

A

Firm white-grey tissue
Nodules and fascicles present
Bland fibroblasts
Dense collagen

593
Q

Deep Fibromatosis: Peak age

A

Teenagers to 30 years old

594
Q

Deep Fibromatosis: Associated mutations (2)

A

APC
Beta-catenin

595
Q

Deep Fibromatosis: What condition is a predisposing factor for this?

A

Gardner’s Syndrome

596
Q

Deep Fibromatosis: Associated with what physiological period?

A

Pregnancy

597
Q

Deep Fibromatosis: Sites (3)

A

Mesenteric tissue
Musculo-aponeurotic tissue of the abdominal wall
Limb girdles

598
Q

De Quervain’s Tenosynovitis

A

Inflammation of the tendon sheaths within the first compartment

599
Q

De Quervain’s Tenosynovitis: Locations (2)

A

Abductor pollicis longus
Extensor pollicis brevis

600
Q

De Quervain’s Tenosynovitis: Epidemiology - most common age

A

30-50 years

601
Q

De Quervain’s Tenosynovitis: Associated with what condition?

A

Rheumatoid Arthritis

602
Q

De Quervain’s Tenosynovitis: Associated with what physiological time?

A

Pregnancy

603
Q

De Quervain’s Tenosynovitis: Typical presentation

A

Repetitive strain injury with pain over the radial styloid process at the wrist

604
Q

De Quervain’s Tenosynovitis: What test can be used to test this?

A

Finklestein’s Test - patient makes a fist over the thumb and the hand is in ulnar deviation to reproduce pain

605
Q

De Quervain’s Tenosynovitis: What investigations may be conducted?

A

USS or X-ray to rule out Carpometacarpal joint osteoarthritis

606
Q

De Quervain’s Tenosynovitis: Conservative management

A

Splint and rest with analgesics

607
Q

De Quervain’s Tenosynovitis: Surgical management

A

Surgical decompression

608
Q

Benign Tumours: What benign tumour is due to t(X:18)?

A

Synovial Sarcoma

609
Q

Benign Tumours: What benign tumour is due to t(2:13)?

A

Alveolar Rhabdomyosarcoma

610
Q

Benign Tumours: What benign tumour is due to t(11:22)?

A

Ewing’s Sarcoma

611
Q

Liposarcoma

A

Malignant tumour of the fat

612
Q

Liposarcoma: Peak age of incidence

A

50-60 years old

613
Q

Liposarcoma: What two genetic abnormalities are associated with this?

A

t(12:16)
Amplification 12q13-q15

614
Q

Liposarcoma: Locations

A

Deep soft tissue of the extremities or retroperitoneum

615
Q

Liposarcoma: Histology

A

Well-differentiated pelomorphic myxoid character

616
Q

Lipoma

A

Benign neoplastic proliferation of subcutaneous fat

617
Q

Lipoma: Usually occurs where?

A

Subcutaneous fat

618
Q

Lipoma: Clinical features (4)

A

Large - can be several cm
Less well defined
Slow growing
Painless

619
Q

Lipoma: Has no changes in what structure?

A

Skin

620
Q

Lipoma: Management

A

Surgical excision if symptomatic

621
Q

Leiomyoma: Presents most commonly where?

A

Uterus

622
Q

Leiomyoma: Less common areas

A

Errector pilae
Deep soft tissue
Muscularis of the gastrointestinal tract

623
Q

Leiomyoma: Histology Characteristics (2)

A

1-2cm
Fascicles of spindle cells - cigar shaped nuclei with minimal atypia and few mitoses

624
Q

Leiomyosarcoma: Epidemiology of sexes

A

More common in femlaes

625
Q

Leiomyosarcoma: What structures are impacted by this?

A

Deep soft tissues of the extremities
Retroperitoneum e.g. from the great vessels

626
Q

Leiomyosarcoma: Management

A

Must be excised - if not complete it can recur and can be lethal due to local metastasis and invasion

627
Q

Rhabdomyoma

A

Benign lesion of the cardiac muscle

628
Q

Rhabdomyoma: What patient group is affected?

A

Paediatric age groups

629
Q

Rhabdomyoma: What impact does this have on the heart? (2)

A

Valvular obstruction or occupies the cardiac chamber

630
Q

Rhabdomyoma: 50% associated with what conditions?

A

Tuberous sclerosis and mutations of TSC1 and 2

631
Q

Rhabdomyosarcoma

A

Malignant soft tissue sarcoma that develops from muscle or fibrous tissue

632
Q

Rhabdomyosarcoma:What are the 3 types?

A

Embryonal Rhabdomyosarcoma
Alveolar Rhabdomyosarcoma
Pleomorphic Rhabdomyosarcoma

633
Q

Rhabdomyosarcoma: What is the most common type?

A

Embryonal Rhabdomyosarcoma

634
Q

Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - Presents when?

A

In childhood

635
Q

Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - Sites (4)

A

Botyroides - Genital tract
Genitourinal Tract
Periorobital - Head and Neck
Common bile duct

636
Q

Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - What genetics are involved?

A

Deletion of Xp11.15

637
Q

Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - Presents when?

A

In young adults or older age groups

638
Q

Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - Sites

A

Arise in the wall of hollow structures - head or neck

639
Q

Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - What genetics are involved?

A

FOXO1 PAX 3 or 7 Translocation
t(2:13) translocation
t(1:13) translocation

640
Q

Rhabdomyosarcoma: Pleomorphic Rhabdomyosarcoma - Presents in what age groups?

A

Older age groups

641
Q

Rhabdomyosarcoma: Pleomorphic Rhabdomyosarcoma - Immunohistochemistry shows what?

A

MYOD1 and Myogenin

642
Q

Benign Cartilaginous Tumours: Two examples

A

Enchondroma
Osteocondroma

643
Q

Benign Cartilaginous Tumours: Enchondroma - Occurs where?

A

In the digits

644
Q

Benign Cartilaginous Tumours: Enchondroma - Can be part of what syndrome?

A

Ollier’s and Maffuci

645
Q

Benign Cartilaginous Tumours: Osteochondroma - Occurs where?

A

At the metaphysis of long bones - especially around the knee

646
Q

Chondrosarcoma

A

Malignant tumour that produces cartilage

647
Q

Chondrosarcoma: More common in what age group?

A

> 40

648
Q

Chondrosarcoma: What types are more common in younger patients?

A

Mesenchymal and Clear Cell Tumours

649
Q

Chondrosarcoma: Histological presentation

A

Nodules of grey or white cartilaginous tissue with gelatinous matrix

650
Q

Chondrosarcoma: Invasion pattern

A

Locally invasive into the bone and muscle and fat - to surround the pre-existing bone trabecula

651
Q

Chondrosarcoma: 6 types

A

Conventional
Intramedullary
Juxtacortical
Clear Cell
Mesenchymal
De-differentiated

652
Q

Chondrosarcoma: Locatuion of intramedullary types

A

Central to the bone

653
Q

Chondrosarcoma: Location of the Juxtacortical types

A

Peripheral to the bone

654
Q

Chondrosarcoma: Clear Cell Chondrosarcoma

A

Malignant chondrocytes that have an abundant cytoplasm

655
Q

Chondrosarcoma: Clear Cell Chondrosarcoma is associated with what?

A

Osteoclastic cells
Reactive bones

656
Q

Chondrosarcoma: Mesenchymal Chondrosarcoma appearance

A

Sheets of well-differentiated hyaline-appearing cartilage with surrounding small cells

657
Q

Chondrosarcoma: De-differentiated type

A

Low grade chondrosarcoma with a separate high grade component that does not produce cartilage

658
Q

Chondrosarcoma: Locations

A

Pelvis
Shoulder
Ribs

659
Q

Chondrosarcoma: Location of Clear Cell types

A

Epiphyses of long tubular bones

660
Q

Chondrosarcoma: Grade III commonly metastasise where?

A

To the lung via the blood

661
Q

Simple Osteoma: Occurs in what bones?

A

Cranial bones

662
Q

Simple Osteoma: Multiple osteoma lesions occur in what syndrome?

A

Garner’s Syndrome

663
Q

Osteoid Osteoma: Size

A

<2cm

664
Q

Osteoid Osteoma: Occurs most commonly in what patient groups?

A

Young men

665
Q

Osteoid Osteoma: Occurs in what skeleton and what bones of this?

A

Appendicular skeleton - mainly the femur and tibia

666
Q

Osteoid Osteoma: Occurs mainly in what section of the bone?

A

The cortex

667
Q

Osteoid Osteoma: The osteoma is surrounded by what?

A

Reactive bone

668
Q

Osteoid Osteoma: Clinical presentation

A

Severe nocturnal pain

669
Q

Osteoid Osteoma: Management

A

Aspirin or NSAIDs to relieve pain

670
Q

Osteoblastoma: Impacts what structures?

A

Posterior vertebrae

671
Q

Osteoblastoma: Problem with management?

A

Pain is not relieved by aspirin

672
Q

Osteoblastoma: What is not present histologically?

A

Reactive bone

673
Q

Ewing’s Sarcoma

A

Malignant primary bone tumour of the endothelial cells in the bone marrow

674
Q

Ewing’s Sarcoma: Presents in what age groups?

A

10-20 years - Children and Adolescents

675
Q

Ewing’s Sarcoma: What genetics are inolved?

A

t(11:22)

676
Q

Ewing’s Sarcoma: Presents where?

A

In any soft tissue and bony location - often in the long bones of adolescents

677
Q

Ewing’s Sarcoma: What is the concern with this?

A

Highly malignant - destructive and rapidly growing

678
Q

Ewing’s Sarcoma: Waht are the potential cells of origin? (2)

A

Primitive mesenchymal cell
Neuroectodermal cell

679
Q

Ewing’s Sarcoma: Presentation

A

Hot swollen tender joint or limb

680
Q

Ewing’s Sarcoma: Presentation on bloods

A

Raised inflammatory markers - mimics infection

681
Q

Ewing’s Sarcoma: Why is surgical excision not recommended?

A

As the tumour is of the bone marrow, function can be reduced post-surgery

682
Q

Ewing’s Sarcoma: Management of choice

A

Radiotherapy or Chemotherapy

683
Q

Soft Tissue Rheumatism

A

Pain that is caused by inflammation or damage to the ligaments near a joint rather than the bone or cartilage

684
Q

Soft Tissue Rheumatism: What is the most common area for pain?

A

Shoulder

685
Q

Soft Tissue Rheumatism: Causes of this in the shoulder (5)

A

Adhesive capsulitis
Rotator cuff tendinosis
Calcific tendonitis
Impingement
Partial or Full rotator cuff tears

686
Q

Soft Tissue Rheumatism: Less common sites (4)

A

Elbow - Medial and lateral epicondylitis
Wrist - De-Quervains Tenosynovitis
Pelvis
Foot - Plantar fascitis

687
Q

Soft Tissue Rheumatism: Diagnosistic examinations

A

X-ray

688
Q

Soft Tissue Rheumatism: Diagnosistic examinations

A

X-ray

689
Q

Soft Tissue Rheumatism: What is shown on X-Ray?

A

Calcific tendonitis

690
Q

Soft Tissue Rheumatism: Management

A

Rice and Physiotherapy
Surgery - if pain is not removed

691
Q

Joint hypermobility Syndrome

A

Patient with hypermobile joints that develops chronic pain lasting 3 months or longer

692
Q

Joint hypermobility Syndrome: Epidemiology of sexes

A

More common in females

693
Q

Joint hypermobility Syndrome: Presents when?

A

Childhood or the 3rd decade

694
Q

Joint hypermobility Syndrome: Associated with what genetic abnormalities? (2)

A

Marfans Syndrome
Ehlers Danlos Syndrome

695
Q

Joint hypermobility Syndrome: Clinical Presentation (3)

A

Joint pain and stiffness
Frequent sprains and dislocations
Thin stretchy skin

696
Q

Joint hypermobility Syndrome: Criteria of the Modified Beighton Score (4)

A

A >10 degree hyperextension of the elbow
Passive extension of the fingers or a >90 degree extension of the fifth finger
Hyperextension of the knee >10 degrees
Touch the floor with the palms of their hands when reaching down without bending knees

697
Q

Joint hypermobility Syndrome: What is used for diagnosis?

A

Modified Beighton Score

698
Q

Joint hypermobility Syndrome: Diagnosis of Modified Beighton Score

A

Hypermobile if >4/9

699
Q

Joint hypermobility Syndrome: Management

A

Patient education with physiotherapy
Analgesia if pain

700
Q

Connective Tissue Disorders

A

Conditions associated with spontaneous overactivity of the immune system and act via specific autoantibodies

701
Q

Connective Tissue Disorders: Examples (6)

A

Systemic Lupus Erythematous
Sjogrens Syndrome
Systemic sclerosis or Scleroderma
Dermatomyositis
Polymyositis
Anti-Phospholipid Syndrome

702
Q

Systemic Lupus Erythematous

A

Systemic autoimmune condition in which the immune system attacks cells and tissue to cause inflammation and tissue damage

703
Q

Systemic Lupus Erythematous: More common in what population group?

A

Women of child-bearing age

704
Q

Systemic Lupus Erythematous: More common in what countries/races? (4)

A

Afro-carribean
Hispanic american
Asia
China

705
Q

Systemic Lupus Erythematous: What are two risk factors?

A

Infection
Smoking

706
Q

Systemic Lupus Erythematous: Pathophysiology - Initiating Event

A

Loss of immune regulation - leads to increased and defective apoptosis

707
Q

Systemic Lupus Erythematous: Pathophysiology - Impact on necrotic cells

A

Release nuclear material

708
Q

Systemic Lupus Erythematous: Pathophysiology - The release of nuclear material from necrotic cells has what impact?

A

Nuclear material acts as auto-antigens to induce autoimmunity

709
Q

Systemic Lupus Erythematous: Pathophysiology - The release of auto-antibodies causes what to happen?

A

Antigen-Auto-antibody complexes form and are deposited on the basement membrane

710
Q

Systemic Lupus Erythematous: Deposition of Ag-Ab complexes on the basement membrane has what impact?

A

Activates complement to attract the leukocytes to release cytokines

711
Q

Systemic Lupus Erythematous: The release of cytokines from leukocytes has what impact?

A

Causes enzyme release from neutrophils to cause damage to the endothelial cells of the basement membrane

712
Q

Systemic Lupus Erythematous: Cutaneous Features (5)

A

Subcutaneous or discoid lupus
Acute cutaneous lupus
Non-scarring alopecia
Oral ulceration
Photosensitive rash

713
Q

Systemic Lupus Erythematous: Alternate clinical presentation - Musculoskeletal features

A

Arthritis - synovitis or tenderness of at lesast 2 joints with >30 minutes of early morning stiffness

714
Q

Systemic Lupus Erythematous: Alternate clinical presentation - Neurological (5)

A

Delirium
Psychosis
Seizures
Headaches
Cranial Nerve Disorder

715
Q

Systemic Lupus Erythematous: Alternate clinical presentation - What inflammatory presentation occurs?

A

Serositis - causes pleural effusion, pericardial effusion or acute pericarditis

716
Q

Systemic Lupus Erythematous: Alternate clinical presentation - Haematological (4)

A

Leukopenia
Thrombocytopenia
Haemolytic anaemia
Lymphadenopathy

717
Q

Systemic Lupus Erythematous: Alternate Clinical Presentation - Renal (3)

A

Proteinuria - >0.5g in 24 hours
Nephritis
Red cell casts

718
Q

Systemic Lupus Erythematous: Diagnosis - What classification system is used?

A

EULAR/ACR SLE Classification Criteria - Score >10 required

719
Q

Systemic Lupus Erythematous: Diagnosis -What complement factors are high within the blood?

A

C3 and C4

720
Q

Systemic Lupus Erythematous: Diagnosis - What antibody must be positive?

A

Anti-nuclear Antibody (ANA)

721
Q

Systemic Lupus Erythematous: Diagnosis - What antibody is positive in 60% of patients?

A

Anti-double stranded DNA antibodies (AdsDNAA)

722
Q

Systemic Lupus Erythematous: Diagnosis - AdsDNAA corelates with what?

A

Disease activity

723
Q

Systemic Lupus Erythematous: Diagnosis - AdsDNAA is associated with what?

A

Lupus nephritis

724
Q

Systemic Lupus Erythematous: Diagnosis - Anti-phospholipid ANtobodies are asosociated with what? (2)

A

Venous and Arterial thrombosis
Recurrent miscarriage

725
Q

Systemic Lupus Erythematous: Diagnosis - APLA presents with what?

A

Livedo reticularis - mottled discolourisation of the skin

726
Q

Systemic Lupus Erythematous: Diagnosis - APLA antoibodies (3)

A

Lupus anticoagulant
Anti-cardiolipin antibodies
Anti-beta 2 glycoprotein antibodies

727
Q

Systemic Lupus Erythematous: Diagnosis - Anti-Ro antibodies are associated with what?

A

Associated with neonatal lupus and congenital heart block

728
Q

Systemic Lupus Erythematous: Diagnosis - Anti-Sm antibodies are associated with what?

A

Highly specific for lupus

Musculoskeletal System (9 decks)

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