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
Osteoarthritis: When is there stiffness?
Morning stiffness lasting less than 1 hour
26
Osteoarthritis: Inactivity gelling definition
Stiff after resting for a period of time
27
Osteoarthritis: Symptom in the hand
Poor grip in the thumb
28
Osteoarthritis: Signs - Impact on the knee joint line
Tenderness
29
Osteoarthritis: Signs - Hip osteoarthritis presents with what specific sign?
Groin pain
30
Osteoarthritis: Signs - Signs in the joint (4)
Joint effusion Bony swellings Deformity Crepitus - Popping, Crackling or Clicking
31
Osteoarthritis: Signs - Genu varus in the knees
Bow legged - feet are touching and knees are not
32
Osteoarthritis: Signs - Genu valgus
The knees are touching whilst the feet do not
33
Osteoarthritis: Signs - What may present on the back of the knees in Knee Osteoarthritis?
Baker's Cysts
34
Osteoarthritis: Signs - For Cervical Spine Osteoarthritis
Pain and restriction of movement with occipital headaches
35
Osteoarthritis: Signs - Impacts of Osteophytes in Cervical Spine
May impinge on nerve roots to cause pins and needles or numbness
36
Osteoarthritis: Signs - Impact of osteophytes on the lumbar spine
Spinal stensosis
37
Osteoarthritis: Signs on X-Ray (4)
Marginal osteophytes Joint space narrowing Subchondral Sclerosis Subchondral Cysts
38
Osteoarthritis: Disadvantage of X-Rays
Insensitive in early disease
39
Osteoarthritis: Pharmacological management (2)
Analgesia - Paracetamol or NSAIDs Local Intra-articular Steroid Injections for flare ups
40
Osteoarthritis: Surgical Management Options (2)
Joint replacements Arthroscopic surgery
41
Osteoarthritis: Two types of Hip Replacement
Cemented Hybrid
42
Osteoarthritis: What material is used for cemented Total Hip Replacements?
PMMA - Polymethylmethacrylate
43
Osteoarthritis: How does a cemented THR work?
Via interdigitation into the bone surface
44
Osteoarthritis: Hybrid THR structure
Uncemented Cup with Cemented Stem
45
Osteoarthritis: What patients receive a hybrid THR?
Young patients
46
Osteoarthritis: Structure of Hyaline Cartilage (4)
Water Collagen Proteoglycans Chondrocytes
47
Osteoarthritis: Function of Chondrocytes in Hyaline Cartilage
Produce and regulate the ECM
48
Osteoarthritis: Function of Proteoglycans in Hyaline Cartilage
Provide compressive strength
49
Osteoarthritis: Pathophysiology - Why is medial osteoarthritis more common than lateral cases?
Twisting and pivoting on the medial knee and Genu Varum are more common
50
Osteoarthritis: Concern of steroid injections
Can accelerate Osteoarthritis
51
Rheumatoid Arthritis
Symmetrical chronic inflammatory disorder driven by an autoimmune mechanism of the synovial lining of the joints, tendon sheaths and bursa
51
Rheumatoid Arthritis:
52
Rheumatoid Arthritis: Peak age
20-40 years old
53
Rheumatoid Arthritis: Sex Epidemiology
More common in women
54
Rheumatoid Arthritis: What is this called in children under 16
Juvenile Idiopathic Arthritis
55
Rheumatoid Arthritis: What genes are involved? (3)
HLA-DRB1 HLA-DPB1 ATIC
56
Rheumatoid Arthritis: What type of immune reaction is this?
Type IV Hypersensitivity and Type III secondary hypersensitivity reactions
57
Rheumatoid Arthritis: What cytokines are activated?
IFN-Gamma IL-17 TNF IL-1 RANKL
58
Rheumatoid Arthritis: Function of IFN-Gamma
Activates macrophages and synovial cells
59
Rheumatoid Arthritis: Function of IL-17
Recruits neutrophils and monocytes
60
Rheumatoid Arthritis: Function of TNF and IL-1
Stimulates the production of proteases from the synovium
61
Rheumatoid Arthritis: Function of RANKL
Activated on T cells to stimulate bone resorption
62
Rheumatoid Arthritis: Mediated by what HLA gene?
HLA-DR4
63
Rheumatoid Arthritis: Process
1. Unknown antigen presented to naive T cells activates them 2. Initiates inflammatory cascade - activate B cells and macrophages
64
Rheumatoid Arthritis: B cells produce what?
IgG Rheumatoid Factor and IL-6
65
Rheumatoid Arthritis: What do macrophages produce?
Pro-inflammatory cytokines - TNF-alpha, IL-1 and IL-6
66
Osteomyelitis
Inflammation of the bone and the medullary cavity
67
Osteomyelitis: Typical location
Long bones
68
Osteomyelitis: 2 main patient groups at risk to inoculation
Post-trauma patients Surgical patients
69
Osteomyelitis: 2 main patient groups at risk of haematogenous spread
Children Immunosuppressed
70
Osteomyelitis: Open Fractures - What classification is used?
Gustilo Classification System
71
Osteomyelitis: Open Fractures - Causative Organisms of infection (2)
Staphylococcus aureus Aerobic gram negative bacteria
72
Osteomyelitis: Open Fractures - Management of infection of open fracture
Early aggressive debridement, fixation and soft tissue cover
73
Osteomyelitis: Open Fractures - Increasing classification of Gustilo Classification indicates what?
Increasing risk of anaerobic and gram negative infection
74
Osteomyelitis: Open Fractures - Type I Gustilo Classification
Puncture wound less than or equal to 1cm with minimal soft tissue injury - minimal wound contamination or muscle crushing
75
Osteomyelitis: Open Fractures - Type II Gustilo Classification
Wound is greater than 1cm in length with moderate soft tissue injury and coverage of the bone is adequate
76
Osteomyelitis: Open Fractures - Type 3a Gustilo Classification
Extensive soft tissue damage that is massively contaminated/severely comminuted/segmental fractures with adequate bone soft tissue coverage
77
Osteomyelitis: Open Fractures - Type 3b Gustilo Classification
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
78
Osteomyelitis: Open Fractures - Type 3c Gustilo Classification
Assoicated with an arterial injury requiring repair for li,hb salvage
79
Osteomyelitis: Diabetic or Venous Insufficiency - Risk Factors (4)
Previous foot ulceration Neuropathy Foot deformity Vascular disease
79
Osteomyelitis: Diabetic or Venous Insufficiency - Risk Factors (4)
Previous foot ulceration Neuropathy Foot deformity Vascular disease
80
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Has ... and ... dysfunction
Microvascular Vasomotor
81
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Why is there altered capillary exchange?
Capillary basement membrane thickening
82
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - What happens to the matrix proteins?
Glycation
83
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - Loss of function of what structures? (2)
Apocrine glands Eccrine Glands
84
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - In feet
Toes curled in claw position
85
Osteomyelitis: Diabetic or Venous Insufficiency - Clinical Presentation - What is the Cavus Deformity?
Increased pressure under the metatarsal heads
86
Osteomyelitis: Diabetic or Venous Insufficiency - Diagnosis Options (3)
Probe bones Radiograph MRI
87
Osteomyelitis: Diabetic or Venous Insufficiency - Management - Main Concept
Debridement and Antibiotics
88
Osteomyelitis: Diabetic or Venous Insufficiency - Management - Staphylococcus and Streptococcus management
Flucloxacillin IV Penicillin Allergic - Vancomycin Nil by Mouth - Doxycycline and Cotrimoxazole
89
Osteomyelitis: Diabetic or Venous Insufficiency - Management - Gram Negative Severe Case
IV Gentamicin or Aztreonam
90
Osteomyelitis: Diabetic or Venous Insufficiency - Management - Oral Cases
Cotrimoxazole or Doxycycline
91
Osteomyelitis: Diabetic or Venous Insufficiency - Management - Anaerobes
Metronidazole or Clindamycin
92
Osteomyelitis: Haeamatogenous Osteomyelitis
Bacteria from the blood results in an acute presentation
93
Osteomyelitis: Haeamatogenous Osteomyelitis - At risk groups (5)
Pre-pubertal children PWID Central Line or Dialysis patients Elderly Sickle Cell Disease Patients
94
Osteomyelitis: Haeamatogenous Osteomyelitis - PWID patient locations (4)
Sternoclavicular Joint Sternocostal Joint Sacroiliac Joint Pubic Symphysis
95
Osteomyelitis: Haeamatogenous Osteomyelitis - Organisms common in PWID patients (2)
Staphylococcus Streptococcus
96
Osteomyelitis: Haeamatogenous Osteomyelitis - Organisms unusual in PWID patients (4)
Pseudomonas Candida Eikenella corrodens Mycobacterium tuberculosis
97
Osteomyelitis: Haeamatogenous Osteomyelitis - Dialysis Patient common pathogens (2)
Staphylcoccus aureus Salmonella species
98
Osteomyelitis: Sickle Cell Osteomyelitis - Causative Organisms (2)
Staphyloccus aureus Salmonella species
99
Osteomyelitis: Sickle Cell Osteomyelitis - Clinical Presentation
Acute long bone osteomyelitis
100
Osteomyelitis: Sickle Cell Osteomyelitis - Pathogenesis
Infarct converts to bacteraemia then osteomyelitis
101
Osteomyelitis: Gaucher Disease
Autosomal recessive lysosomal storage disease resulting in the deposition of glucocerebrosides in the brain and other tissues
102
Osteomyelitis: Gaucher Disease - Often affects what bone?
Tibia
103
Osteomyelitis: Gaucher Disease - Main causative organism
Staphylococcus aureus
104
Osteomyelitis: Synovitis Acne Pustulosis Hyperostosis Osteitis presents in what patient groups?
Adults
105
Osteomyelitis: Gaucher Disease - Chronic Recurrent Multifocal Osteomyelitis presents in what patient groups?
Children
106
Osteomyelitis: Gaucher Disease - SAPHO
Synovitis Acne Pustulosis Hyperostosis Osteitis
107
Osteomyelitis: Gaucher Disease - CRMO
Chronic Recurrent Multifocal Osteomyelitis
108
Osteomyelitis: Gaucher Disease - SAPHO and CRMO Clinical Presentation (3)
Fever Weight Loss Generalised Malaise
109
Osteomyelitis: Gaucher Disease - SAPHO and CRMO sites involved (4)
Chest wall Pelvis Spine Lower Limb
110
Osteomyelitis: Vertebral Osteomyelitis - Risk Factors (5)
PWID IV site infections GU infections Post-operation Primary bacteraemia in the elderly
111
Osteomyelitis: Vertebral Osteomyelitis - Associated with what abscesses? (2)
Epidural abscess Psoas abscess
112
Osteomyelitis: Vertebral Osteomyelitis - Clinical Presentation (3)
Fever Insidious Pain Tenderness
113
Osteomyelitis: Vertebral Osteomyelitis - Diagnostic Results and Scans (3)
Increased WCC MRI or Ga-67 Scan Raised inflammatory markers
114
Osteomyelitis: Vertebral Osteomyelitis - Management
Drainaage of the large paravertebral or epidural abscesses with 6 weeks minimum of antibiotics
115
Osteomyelitis: Vertebral Osteomyelitis - MRI repeated if what occurs (3)
Unexplained increase in inflammatory markers Increasing pain New anatomically related sign or symptom
116
Osteomyelitis: Causative Organisms - Newborns (<4 months) - 4 examples
Staphylococcus aureus Enterobacter species Group A Streptococcus Group B Streptococcus
117
Osteomyelitis: Causative Organisms - Children (4 months-4 years) - 4 examples
Staphylococcus aureus Group A Streptococcus Haemophilus influenzae Enterobacter species
118
Osteomyelitis: Causative Organisms - Children and Adolescents (4-18 years) - 4 examples
Staphylococcus aureus Group A Streptococcus Haemophilus influenzae Enterobacter species
119
Osteomyelitis: Causative Organisms - Adults (3 examples)
Staphylococcus aureua Enterobacter Streptococcus species
120
Osteomyelitis: Causative Organisms - Sickle Cell Anaemia Patients (2 examples)
Staphylococcus aureus Salmonella species
121
Osteomyelitis: Two routes of infection
Haematogenous Exogenous
122
Osteomyelitis: Haematogenous Spread
Infection carried within the blood from another infected site
123
Osteomyelitis: Haematogenous Spread - Examples of sources (4)
Cellulitis PWIDs Central lines Dialysis
124
Osteomyelitis: Haematogenous Spread - Common location for children
Long bone metaphysis
125
Osteomyelitis: Haematogenous Spread - Most common location for adults
Vertebral involvement
126
Osteomyelitis: Exogenous Spread
Infection spread due to trauma or contiguous spread
127
Osteomyelitis: Exogenous Spread - Contiguous spread
Spread of infection from adjacent tissues
128
Osteomyelitis: Exogenous Spread - Examples of Contiguous Spread (2)
Secondary to infected foot ulcer in diabetic patients Secondary to pressure sores in elderly patients
129
Osteomyelitis: Pathophysiology - Impact due to leucocytes?
Enzymes from the leucocytes causes local osteolysis and pus formation that impairs local blood flow
130
Osteomyelitis: Pathophysiology - Sequestrum
Dead fragment of bone
131
Osteomyelitis: Pathophysiology - Once a ... is present, antibiotics will not cure the infection?
Sequestrum
132
Osteomyelitis: Pathophysiology - Involucrum
New bone formation around the area of necrosis
133
Osteomyelitis: Acute Pathophysiology - Why is this common in children?
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
134
Osteomyelitis: Acute Pathophysiology - How does co-existent septic arthritis occur in neonates and infants?
Metaphyses are intra-articular causing infection to spread into the joint
135
Osteomyelitis: Acute Pathophysiology - Why can abscesses extend along the subperiosteal space in infants?
Loosely applied periosteum
136
Osteomyelitis: Acute Pathophysiology - Children can develop a subacute osteomyelitis with an insidious onset how?
Bone reacts by walling of the abscess with a thin rim of sclerotic bone
137
Osteomyelitis: Acute Pathophysiology - Brodie's Abscess
Bone reacts by walling of the abscess with a thin rim of sclerotic bone
138
Osteomyelitis: Chronic Pathophysiology - Develops from what?
An untreated acute osteomyelitis
139
Osteomyelitis: Chronic Pathophysiology - In adults the infection tends to be in what part of the skeleton?
Axial skeleton
140
Osteomyelitis: Chronic Pathophysiology - Infections of the axial skeleton tend to originate from where?
Pulmonary, Intervertebral Disc or urinary infections that have spread via the blood
141
Osteomyelitis: Chronic Pathophysiology - Tuberculosis can cause chronic Osteomyelitis in what site?
The spine
142
Osteomyelitis: Clinical Presentation - Acute Presentation (4)
Abrupt onset of intense pain with point tenderness Erythema Heat Swelling
143
Osteomyelitis: Clinical Presentation - Acute presentation systemic findings (3)
Malaise Fever Chills
144
Osteomyelitis: Clinical Presentation - Chronic Presentation (3)
Loss of function Discharge Recurrent pain Swelling Erythema
145
Osteomyelitis: Clinical Presentation - Chronic Osteomyelitis of the Spine
Insidious onset of back pain which is constant and unremitting
146
Osteomyelitis: Chronic Osteomyelitis - Presentation on imaging (2)
Sequestra - pieces of necrotic bone that separate from the viable bone
147
Osteomyelitis: Chronic Osteomyelitis - How do sequestra form?
Bone ischaemia and necrosis due to elevated medullary pressure of bone marrow infiltration
148
Osteomyelitis: Two rare sites
Osteitis Pubis Clavicular osteomyelitis
149
Osteomyelitis: Osteitis Pubis - Risk factor for this
Urogynae procedures
150
Osteomyelitis: Clavicle Osteomyelitis - Risk factor for this
Neck surgery Subclavian Vein Catheterisation
151
Osteomyelitis: Gold Standard
Bone biopsy
152
Osteomyelitis: Management - Acute Osteomyelitis - If an abscess is present?
Drainage
153
Osteomyelitis: Management - Acute Osteomyelitis - Main treatment
IV antibiotics
154
Osteomyelitis: Management - Acute Osteomyelitis - If an infection fails to resolve what is there treatment pathway
Second line antibiotics Surgery to take a sample of the culture and remove infected bone or tissue
155
Osteomyelitis: Management - Chronic Osteomyelitis - What is not an option?
Antibiotics alone - cannot cure or erradicate infection
156
Osteomyelitis: Management - Chronic Osteomyelitis - What is surgery recommended for?
Gain deep bone tissue cultures to remove any sequestrum and to excise any infected or non-viable bone
157
Osteomyelitis: Management - Chronic Osteomyelitis - If debridement of the bone results in instability what is recommended?
Internal or external fixation
158
Prosthetic Joint Infection
Peri-prosthetic infection involving the joint prosthesis and adjacent tissue
159
Prosthetic Joint Infection: Risk Factors - Presence of what co-morbidities? (6)
Immunosuppression Rheumatoid Arthritis Diabetes Mellitus Malignancy Chronic Kidney Disease Lymphoedema
160
Prosthetic Joint Infection: Risk Factors - Use of what drugs? (3)
Corticosteroids TNF inhibitors Biologic modifying anti-rheumatic drugs
161
Prosthetic Joint Infection: Risk Factors - A history of what post-surgery? (2)
Prior arthroplasty Infection
162
Prosthetic Joint Infection: Risk Factors - Anaesthesiologist score of what?
>3
163
Prosthetic Joint Infection: Risk Factors - Post-operative complications (2)
Haematoma Wound infection
164
Prosthetic Joint Infection: Risk Factors - What type of infection?
Staphylococcus aureus bacteraemia
165
Prosthetic Joint Infection: Causative Organisms - Prosthetic Shoulder Arthroplasty Infection (2)
Coagulase negative Staphylococci Propionbacterium acnes
166
Prosthetic Joint Infection: Causative Organisms - Prosthetic Hip and Knee Arthroplasty infection (3)
Anaerobes Gram positive cocci - Coagulase negative staphylcocci or Staph aureus Aerobic Gram Negative bacilli - E. coli, Proteus mirabilis and Pseudomonas aeruginosa
167
Prosthetic Joint Infection: Causative Organisms - Gram Positive Bacteria (3)
Staphylococcus aureus Staphylococcus epidermidis Cutiibacterium acnes (common on upper limb prostheses)
168
Prosthetic Joint Infection: Causative Organisms - Gram Negative Bacterium (2)
E. coli Pseudomonas aeruginosa
169
Prosthetic Joint Infection: Mechanisms (3)
Direct inoculation at time of surgery Manipulation of the joint at the time of surgery Seeing of a joint due to haematogenous spread
170
Prosthetic Joint Infection: Pathophysiology - Early is due to what organisms? (2)
Staphylococcus aureus Coagulase negative staphylococci
171
Prosthetic Joint Infection: Pathophysiology - Chronic is due to what organisms? (3)
Staphylococcus aureus Coagulase negative staphylococci Corynebacterium
172
Prosthetic Joint Infection: Pathophysiology - Haematological due to what organisms? (2)
Staphyloccus aureus Gram negative bacilli
173
Prosthetic Joint Infection: Pathophysiology - Biofilm
Microbe-derived sessile community characterised by cell that attached to a substratum, interface or eachother
174
Prosthetic Joint Infection: Pathophysiology - Biofilms are embedded in what?
A matrix of extracellular polymeric substance
175
Prosthetic Joint Infection: Pathophysiology - Planktonic Bacteria
Free living bacteria - responsible for most symptoms
176
Prosthetic Joint Infection: Pathophysiology - Sessile Bacteria
Bacteria derived from Planktonic Bacteria due to phenotypic transformation that form a biofilm within an extracellular matrix
177
Prosthetic Joint Infection: Clinical Presentation (3)
Fever Joint pain Minimal swelling
178
Prosthetic Joint Infection: 4 diagnostic approaches
Culture - taken from peri-operative tissue Blood culture CRP Radiology
179
Prosthetic Joint Infection: Management
DAIR - Debridement + Antibiotics and Implant Retention IV therapy for 4-6 weeks with potential addition of Rifampicin
180
Prosthetic Joint Infection: Management - When should Rifampicin be added?
Culture is positive for Rifampicin-sensitive staphylococci
181
Septic Arthritis
Inflammation of the joint space due to infection
182
Septic Arthritis: Causative Organisms - Most common causes in adults (2)
Staphylococcus aureus Streptococci
183
Septic Arthritis: Causative Organisms - Most common cause in children
Haemophilus influenzae
184
Septic Arthritis: Causative Organisms - Most common cause in young adults
Neisseria gonorrhoea
185
Septic Arthritis: Causative Organisms - Most common cause in the elderly, PWID and acutely ill
Escherichia coli
186
Septic Arthritis: Causative Organisms - Potential viral causes (3)
Parovirus Rubella Dengue virus
187
Septic Arthritis: Mechanisms of spread (4)
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
188
Septic Arthritis: Symptoms (5)
Rubor Calor Dolor Tumor Function laesa
189
Septic Arthritis: Signs (2)
Systemic fever Reduced ROM
190
Septic Arthritis: Impact on blood results (2)
Increased WCC Increased inflammatory markers
191
Septic Arthritis: 4 Diagnostic Tests (4)
Aspiration Fluid - for microscopy and culture Bloods X-ray or MRI Exclude crystals
192
Septic Arthritis: Management - Empirical treatment for Staphylococcus aureus
Flucloxacillin
193
Septic Arthritis: Management - If less than 5 years old
Flucloxacillin (for S. aureus) + Ceftriaxone (for H. influenzae cover)
194
Septic Arthritis: Management - Length of IV antibiotics
1-2 weeks
195
Septic Arthritis: Management - Length of oral antibiotics
4-6 weeks
196
Bursitis
Inflammation of the synvoium-lined sacs that protect bony prominences and joints
197
Bursa
Small fluid filled sac lined by synovium around a joint to prevent friction between tendons, bones, muscle and skin
198
Bursitis: The six types of knee bursa
Semi-membranous bursa Subcutaneous pre-patellar bursa Subcutaneous infra-patellar bursa Deep infra-patellar bursa Subsatorial bursa Supra-patellar bursa
199
Bursitis: Mechanism of Injury
Repeated pressure or trauma
200
Bursitis: What can develop due to secondary infection?
Abscess
201
Bursitis: Main causative organism
Staphylococcus aureus
202
Bursitis: Management
IV Flucloxacillin once a day for 2 weeks + Oral therapy for 2-4 weeks
203
Bursitis: Management if penicillin allergy
Clindamycin
204
Pyomyositis
Acute intramuscular infection secondary to haeamtogenous spread of the microorganism into the body of a skeletal muscle
205
Pyomyositis: Most common in what areas? (3)
Tropical Regions - Asia, Africa and Caribbean
206
Pyomyositis: Most common in what population ages?
Children Young adults
207
Pyomyositis: What population groups are at risk to this? (3)
PWID Diabetes mellitus Immunosuppressed
208
Pyomyositis: Most common causative organism
Staphylococcus aureus
209
Pyomyositis: Risk factors in Tropical countries (2)
MSSA Immune competent Children
210
Pyomyositis: Risk factor in Temperate Countries
Immunosuppressed
211
Pyomyositis: Caustive organisms within the perineum
Gram Negative Bacteria
212
Pyomyositis: Causative organisms in immunosuppressed individuals (3)
Pseudomonas Beta haemolytic streptococcus Enterococcus
213
Pyomyositis: Causative organisms in tropical climates
MSSA infection
214
Pyomyositis: Causative organism for contaminated wounds
Clostridium species
215
Pyomyositis: Clinical Presentation - local
Localised muscular swelling, tenderness and fluctuance in progress
216
Pyomyositis: Skin Clinical Presentation
Skin erythema and warmth
217
Pyomyositis: Systemic Symptoms (3)
Fever Haemodynamic instability Sepsis
218
Pyomyositis: Investigation choices (4)
Pus culture US CT MRI
219
Pyomyositis: Management
Debridement and Antibiotics
220
Pyomyositis: Complications
Compartment Syndrome within the anterior tibial compartment
221
Myonecrosis
Life-threatening necrotising soft tissue infection
222
Myonecrosis: Most common causative organism
Clostridium perfringens
223
Myonecrosis: Alternate name for Gas Gangrene
Clostridial Myonecrosis
224
Myonecrosis: Clostridial Myonecrosis cause what alteration to the skin?
Bronze discolourisation to the skin
225
Myonecrosis: Examples of causative organism (4)
Clostridium perfringes Clostridium septicum Clostridium novvi Clostridium histolyticum
226
Myonecrosis: Traumatic causative organism
Clostridium perfringes
227
Myonecrosis: Causative organism of Clostridial myonecrosis
Clostridium septicum
228
Myonecrosis: Risk Factors (4)
Deep penetration injuries Bowel or biliary tract surgery IM Adrenaline injection Retained placenta
229
Myonecrosis: Symptoms (3)
Swelling Erythema Pain
230
Myonecrosis: Signs (4)
Tachycardia Hypotension Elevated CRP and Creatinine Kinase LRINEC Score >4
231
Myonecrosis: 2 diagnostic tests
Radiography Culture and Gram Stain
232
Myonecrosis: What would radiography show?
Gas present in the tissue
233
Myonecrosis: What would culture show?
Gram Positive Bacilli
234
Myonecrosis: Progress in changes in colour
1. Bronze 2. Red or Purple 3. Black and overlying bullae
235
Myonecrosis: What would MRI show?
Characteristic feathering pattern of soft tissue
236
Myonecrosis: Management
Emergency debridement and antibiotics
237
Myonecrosis: What antibiotics are used?
Clindamycin and Penicillin
238
Viral Myositis
Muscle inflammation due to a viral infection
239
Viral Myositis: Clinical presentation (3)
Muscle weakening Fatigue Pain
240
Viral Myositis: What may precede muscular weakness and pain?
Fever
241
Viral Myositis: Typical causative viruses (5)
HIV Human T-Lymphocytic Virus CMV Rabies Dengue
242
Viral Myositis: Typical causative parasites (4)
Schistosoma Taenia Trichinella Echinococcus
243
Viral Myositis: What do bloods show?
Elevated Creatinine Kinase
244
Tetanus
Acute infection affecting the nervous system due to the neurotoxins of a Clostridium tetani infection
245
Tetanus: Description of Clostridium tetani
Gram positive anaerobic bacilli
246
Tetanus: Mechanism of action
C. tetani spores within the soil enter the body via broken skin
247
Tetanus: Incubation period
4 days. toseveral weeks
248
Tetanus: Pathophysiology Stages
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
249
Tetanus: C. tetani binds to inhibitory neurones to have what effect?
The release of neurotransmitters
250
Tetanus: The neurotoxin induces what?
Spastic paralysis
251
Tetanus: Clinical Presentation (3)
Trismus - lock jaw Risus sardonicus - Muscle spasms Dysphagia
252
Tetanus: Diagnostic investigation
Culture
253
Tetanus: Result of culture
Anaerobic gram positive with a terminal spore
254
Tetanus: Management (3)
Surgical debridement Anti-toxin Antibiotics - 7-10 days
255
Tetanus: Prevention
Toxoid vaccination at 2, 3 and 4 months
256
Spondyloarthropathies
Family of inflammatory arthritides characterised by the involvement of both the spine and joints
257
Spondyloarthropathies: Associated with what gene?
HLA-B27
258
What diseases are associated with the HLA-B27 gene? (PAIR Pneumonic)
Psoriatic arthritis Ankylosing spondylitis IBS + Enteropathic arthritis Reactive arthritis
259
Spondyloarthropathies: Higher prevalence in what regions?
Northern hemisphere - especially the scandinavian countries
260
Spondyloarthropathies: Reactive arthritis
Autoimmune reaction to infection e.g. Chlamydia, Shigella, Salmonella and Campylobacter
261
Spondyloarthropathies: Enteritis associated Arthritis
Organisms with high lipopolysaccharide content in the cell wall that triggers an immune reaction
262
Spondyloarthropathies: Shared features - Involve what regions (2)
Sacroiliac joints Spine
263
Spondyloarthropathies: Inflammatory Arthritis features (3)
Oligoarticular (<5 joints) Asymmetrical Lower limb predominantly
264
Synovitis
Inflammation of the joint and tendon sheath linings
265
Spondyloarthropathies: Enthesitis
Inflammation at sites where ligaments and tendons attach to bones
266
Spondyloarthropathies: Dactylitis
Inflammation of the entire digit
267
Spondyloarthropathies: Extra-articular features - Eyes
Ocular inflammation
268
Spondyloarthropathies: Extra-articular features - Mucous membranes
Mucocutaneous lesions
269
Spondyloarthropathies: Extra-articular features - Heart (2)
Aortic incompetence Heart block
270
Ankylosing Spondylitis: Peak age of diagnosis
20-30 year olds
271
Ankylosing Spondylitis
Chronic inflammatory disease of the axial skeleton that leads to partial or even complete fusion and rigidity of the spine
272
Ankylosing Spondylitis: More common in what sex?
Males
273
Ankylosing Spondylitis: Genetic predisposition
HLA-B27
274
Ankylosing Spondylitis: 3 stages of development
1. Inflammation of the ligaments and joints 2. Formation of syndesmophytes 3. Fusion of the discs
275
Ankylosing Spondylitis: Main symptom
Dull pain in the Spine and neck
276
Ankylosing Spondylitis: Onset of symptoms
Gradual that progresses slowly
277
Ankylosing Spondylitis: Is there stiffness present? If so when and for how long?
Yes - Morning for 30 minutes
278
Ankylosing Spondylitis: What makes morning stiffness better?
Activity
279
Ankylosing Spondylitis: Late Ankylosing Spondylitis presents with what?
Question mark posture - Loss of lumbar kyphosis with pronounced cervical lordosis
280
What is the Schobers Test?
Used to measure lumbar spine flexion
281
Ankylosing Spondylitis: Schobers Test Result
<20 cm
282
Schober Test Result
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
283
Ankylosing Spondylitis: Impact on chest
Reduced chest expansion
284
Ankylosing Spondylitis: Extra-articular features - Eyes
Anterior uveitis
285
Ankylosing Spondylitis: Extra-articular features - Heart
Aortic regurgitation
286
Ankylosing Spondylitis: Extra-articular features - Pulmonary involvement
Upper lobe fibrosis
287
Ankylosing Spondylitis: Extra-articular features - Neurological involvement
Atlantoaxial Subluxation - misalignment of the 1st and 2nd cervical vertebrae
288
Ankylosing Spondylitis: Blood results
Raised inflammatoy markers HLA-B27 present
289
Ankylosing Spondylitis: X-Ray - Bone density
Reduced in later disease
290
Ankylosing Spondylitis: X-Ray - Syndesmophyte appearance
Bony spurs from the vertebral bodies bridge the intervertebral disc causing fusion leading to bamboo spine
291
Ankylosing Spondylitis: MRI presentations (3)
Sacroiliitis - active inflammation Bone marrow oedema Enthesitis of the spinal ligaments
292
Ankylosing Spondylitis: What classification is used for axial spondylarthritis
ASAS classification criteria
293
Ankylosing Spondylitis: What is the criteria? (2)
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
Ankylosing Spondylitis: Management - Non-pharmacological treatment options (4)
Physiotherapy Occupational therapy Orthotics Chiropodist
295
Ankylosing Spondylitis: Management - First line pharmacological treatment
NSAIDs
296
Ankylosing Spondylitis: Management - Options for symptomatic cases (3)
Corticosteroids Topical steroids Eyedrops
297
Ankylosing Spondylitis: Management - If unresponsive to NSAIDs and Methotrexate what pharmaceutical should be used?
Anti-TNF
298
Ankylosing Spondylitis: Management - Last line pharmacological intervention
Secukinumab - Anti-IL-17
299
Psoriatic Arthritis
Inflammatory arthritis associated with psoriasis (10-15% do not have psoriasis)
300
Psoriatic Arthritis: Aetiology
Occurs in up to 30% of people affected by skin psoriasis
301
Psoriatic Arthritis: Clinical Presentation - Predominantly affects what joints?
In the hands and feet
302
Psoriatic Arthritis: Clinical Presentation - Usual pattern
Asymmetrical oligoarthritis
303
Psoriatic Arthritis: Clinical Presentation - Some patients have a predisposition to what joints being affected?
DIP joints of the fingers or toes
304
Psoriatic Arthritis: Clinical Presentation - Extra-articular impacts (3)
Eye disease Nail pitting Nail onycholysis
305
Psoriatic Arthritis: Arthritis Mutilans
Aggressive and destructive form of the condition that occurs in the hands -involves reabsorption of bone and collapsed soft tissue
306
Psoriatic Arthritis: Diagnosis - Blood results
Increased inflammatory markers
307
Psoriatic Arthritis: Diagnosis - X-ray has what features? (3)
Marginal erosions and whiskering Osteolysis Enthesitis
308
Psoriatic Arthritis: Management - Non-pharmacological options (4)
Physiotherapy Occupational therapy Orthotics Chiropodist
309
Psoriatic Arthritis: Management - First line pharmacological management
NSAIDs
310
Psoriatic Arthritis: Management - Pharmacological management for symptomatic cases (3)
Corticosteroids Topical steroids Eyedrops
311
Psoriatic Arthritis: Management - Pharmacological management if unresponsive to NSAIDs and Methotrexate
Anti-TNF
312
Psoriatic Arthritis: Management - Pharmacological last line
Secukinumab - Anti-IL-17
313
Infectious Arthritis: Causative organism in adults
Staphyloccus aureus
314
Infectious Arthritis: Causative organism in young children
Haemophilus influenzae
315
Infectious Arthritis: Causative organism in young adults
Gonococcal infection
316
Infectious Arthritis: Sickle Cell Anaemia patients are predisposed to what?
Salmonella arthritis
317
Infectious Arthritis: What joint is most common?
Knee
318
Crystal Arthropathy
Disorders characterised by deposition of minerals in the joints and soft tissues leading to inflammation
319
Crystal Arthropathy: Three examples
Gout Pseudogout Hydroxyapatite Deposits
320
Gout
Arthritic presentations as a result of monosodium urate crystal deposition due to defective urate metabolism
321
Gout: Peak incidence age
20-80 years old
322
Gout: More common in what sex?
Men
323
Gout: When and why does the risk increase in women?
After the menopause - oestrogen promotes the excretion of uric acid
324
Gout: Risk Factors (5)
Genetic predisposition Alcohol Obesity Drugs Purine rich food
325
Gout: 4 Stages of Pathophysiology
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
Gout: Two mechanisms of development
Increased production of urate Reduced excretion of urate
327
Gout: Increased urate production - Can occur due to deficiency of what?
HGPRT
328
Function of HGPRT in urate metablism
Impairs the purine nucleotide salvage pathway leading to degradation of urate
329
Gout: Increased urate production - Examples of diseases that cause increased cell turnover (3)
Psoriasis Cancer Tumour lysis following chemotherapy
330
Gout: Increased urate production - Can be due to intake of what? (2)
Alcohol - high in purines High dietary purine diet
331
Gout: Reduced urate excretion - Causes (5)
Chronic renal disease Thiazide Diuretics Volume depletion e.g. HF Hypothyroidism Cytotoxics
332
Gout: Reduced urate excretion - Example of a cytotoxic that causes this?
Cyclosporin
333
Gout: Mechanism of Urate Synthesis
Purines > Hypoxanthine > Xanthines to form plasma urate
334
Gout: How is urate excreted?
Renal filtration of urate - reabsorbed in the PCT and limited excretion from the DCT
335
Gout: Uric acid is the final product of what?
Breakdown of Adenosine and Guanine in DNA metabolism
336
Gout: Why do crystals precipitate?
Due to reduced solubility
337
Gout: Crystallisation occurs in joints when?
At lower temperatures
338
Gout: What increases the production of pro-inflammatory cytokines?
Phagocytosis of crystals by macrophages
339
Gout: Chronic gouty arthritis and tophaceous gout are a result of what?
Chronic Granulomatous Inflammatory Response to deposited crystals
340
Gout: Histology of Gouty Tophus
Amorphous eosinophilic debris and inflammation
341
Gout: Acute Gout - Classic site of disease
MTP joint of the foot Can also impact the ankle or knee joint
342
Gout: Acute Gout - Onset
Abrupt overnight
343
Gout: Acute Gout - Clinical presentation
Severely painful hot swollen joint that may mimic septic arthritis
344
Gout: Acute Gout - Lasts how long?
10 days without treatment 3 days with treatment
345
Gout: Chronic Tophaceous Gout - Presentation
Painless white accumulations of uric acid that can occur in soft tissue and occasionally erupt through the skin
346
Gout: Chronic Tophaceous Gout - Often associated with what drug?
Thiazide diuretics
347
Gout: Chronic Tophaceous Gout - Blood factors
High serum uric acid
348
Gout: Chronic Tophaceous Gout - Can result in what?
Destructive erosive arthritis
349
Gout: Diagnosis in Bloods (30
Serum uric acid is increased Raised inflammatory markers Renal impairment - detected via U&Es and GFR
350
Gout: Diagnosis via Cytology
Joint fluid is examined under cross-polarized light to detect needle shaped crystals
351
Gout: Histological appearance (3)
No crystals present Amorphous eosinophilic debris and inflammation Giant cells
352
Gout: Acute Gout - Management - First line
NSAIDs
353
Gout: Acute Gout - Management - Second Line
Colchicine if NSAIDs not suitable
354
Gout: Acute Gout - Management - What patient groups are NSAIDs unacceptable for?
Patients with heart failure Patients with Chronic Kidney Failure
355
Gout: Acute Gout - Management - Side effects of Colchicine
Diarrhoea
356
Gout: Acute Gout - Management - Third Line
Oral/IM/Intra-articular Steroids
357
Gout: Prophylactic Management - Should be started when?
1 week after an acute attack
358
Gout: Prophylactic Management - Requires cover with what?
NSAIDs or Colchicine
359
Gout: Prophylactic Management - First line
Xanthine Oxidase Inhibitors
360
Gout: Prophylactic Management - Examples of Xanthine Oxidase Inhibitors
Allopurinol Febuxostat
361
Gout: Prophylactic Management - Second line
Uricosuric Drugs
362
Gout: Prophylactic Management - Examples of Uricosuric Drugs
Sulfinpyrazone Probenecid Benzbromarone
363
Gout: Prophylactic Management - Third Line
IL-1 Inhibitors
364
Gout: Prophylactic Management - Example of IL-1 inhibitor
Canakinumab
365
Gout: Prophylactic Management - Uric Acid Target
300-360 micromol/L
366
Gout: Prophylactic Management - Indications (6)
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
Gout: What drug must be avoided?
Allopurinol
368
Pseudogout
Arthritic presentations due to depositions of calcium pyrophosphate crystals within the fibrocartilage of a joint
369
Pseudogout: How do the crystals appear on imaging?
Dense deposits on X-Ray
370
Pseudogout: Most common patient group
Elderly
371
Pseudogout: Chrondrocalcinosis
Calcium pyrophosphate deposition within the cartilage and soft tissue in the absence of acute inflammation
372
Pseudogout: Affects what areas?
Fibrocartilage of the knees, wrists and ankles
373
Pseudogout: Risk Factors (6)
Hypercalcaemia Hyperparathyroidism Haemachromatosis Hypomagnesaemia Ochronosis Hypothyriodism
374
Pseudogout: Mechanism of pathophysiology
Crystals formation within the cartilage, menisci and discs of joints expand and rupture into the joint to cause joint damage
375
Pseudogout: Blood results
Increased inflammatory markers
376
Pseudogout: Histology results
Rhomboid shaped crystals with weak positive birefringence
377
Pseudogout: Management options (4)
NSAIDs Colchicine Steroids Rehydration
378
Hydroxyapatite Deposition Disease
Deposition of basic calcium phosphate into the joints and soft tissue to cause inflammation
379
Hydroxyapatite Deposition Disease: Most commonly affected site
Shoulder - Milwaukee shoulder
380
Hydroxyapatite Deposition Disease: Most common in what sex?
Females
381
Hydroxyapatite Deposition Disease: Highest incidence age group
50-60 years
382
Hydroxyapatite Deposition Disease: Associated with the release of what chemical mediators? (3)
Collagenases Serine proteases IL-1
383
Hydroxyapatite Deposition Disease: Presentation
Acute onset of joint pain
384
Hydroxyapatite Deposition Disease: Diagnostic technique
X-Ray
385
Hydroxyapatite Deposition Disease: Management - First Line
NSAIDs Intra-articular steroid Local anaesthetic
386
Hydroxyapatite Deposition Disease: Management - Second Line
Surgical removal of calcifications for cases refractory to attempt at conservative treatment
387
Hydroxyapatite Deposition Disease: Management - Last line treatment
Partial or Total Arthroplasty
388
Mysathenia Gravis
Severe autoimmune neuromuscular disorder characterised by severe muscular weakness and progressive fatigue
389
Mysathenia Gravis: Associated with what other diseases? (3)
SLE Rheumatoid arthritis Thyrotoxicosis
390
Mysathenia Gravis: Most common age
60-70 years old
391
Mysathenia Gravis: Most common age in women
<40 years old
392
Mysathenia Gravis: Most common age in males
>60 years old
393
Mysathenia Gravis: 10% are associated with what?
Thymic tumours
394
Mysathenia Gravis: Basic pathophysiology
Auto-reactive antibodies (auto-IgG) bind to post-synaptic ACh receptors on muscle cells
395
Mysathenia Gravis: What type of immune reaction is this?
Type II hypersensitivity
396
Mysathenia Gravis: What two moleculaes are inolved in activating auto-reactive B cells?
CD4+ TH cells AChR self-antigens
397
Mysathenia Gravis: Pathophysiology Pathway - Initiating event
CD4+ TH cells are activated by unfolded AChR subunits on thymic epithelial cells
398
Mysathenia Gravis: Pathophysiology Pathway - Activated CD4+ TH Cells hae what action?
Stimulate auto-reactice B cells to produce anti-AChR IgG autoantibodies
399
Mysathenia Gravis: Pathophysiology Pathway - Anti-AChR autoantibodies have what function?
Attack thymic myoid cells expressing intact AChR
400
Mysathenia Gravis: Pathophysiology Pathway - The formation of AChR immune complexes causes what to occur?
Activation of APCs causing the auto-antibody response to recognise intact AChRs of normal muscle cells
401
Mysathenia Gravis: Pathophysiology Pathway - The binding of auto-antibodies to AChR on normal muscle cells has what impact?
Blocks the binding of endogenous ACh ligands to their receptors
402
Mysathenia Gravis: Pathophysiology Pathway - How are AChRs eventually destroyed? (2)
Antibody-bound receptors are internalised and degraded AChR antibodies bound to complement lead to the destruction of the muscle endplate
403
Mysathenia Gravis: Pathophysiology Pathway - Destruction of AChR endplates have what overall impact?
Reduced amplitude of endplate potentials to cause impaired signal conduction at the neuromuscular junction
404
Mysathenia Gravis: Presentation - Eyes (2)
Double vision - due to extra-ocular muscle weakness Drooping of the eyelids
405
Mysathenia Gravis: Presentation - Face (2)
Weakness of the facial movements Fatigue in the jaw when chewing
406
Mysathenia Gravis: Presentation - ENT (20
Difficulty in swallowing Slurred speech
407
Mysathenia Gravis: Diagnosis - Autoantibodies (3)
Anti-AChR Anti-MuSK Anti-LRP4
408
Mysathenia Gravis: Diagnosis - 3 alternate tests to autoantibodies (3)
Scan of the thymus - may detect a thymoma Repetitive nerve stimulation Edrophonium or Neostigmine Testing - blocks the breakdown on ACh
409
Mysathenia Gravis: Management - First Line
Pyridostigmine - increases neurotransmission by a reversible anti-cholinesterase agent
410
Mysathenia Gravis: Management - Second Line Options (4)
Corticosteroids e.g. Prednisolone Azathiprine Mycophenolate Rituximab
411
Mysathenia Gravis: Management - Last Line or First line if thymic tumour is present
Thymectomy
412
Mysathenia Gravis: Management for Crisis - If respiration is impaired
O2 and Ventilator
413
Mysathenia Gravis: Management for Crisis - How to prevent autoimmune reactions?
IV Immunoglobulin
414
Mysathenia Gravis: Management for Crisis - How to remove auto-reactive Antibodies from the serum?
Plasmapheresis
415
Osteoporosis
Quantitative defect of the bone characterised by reduced bone mineral density and increased porosity
416
Osteoporosis: Loss of bone mineral density starts at what age normally?
30 years
417
Osteoporosis: 3 risk factors for Primary Osteoporosis
Post-menopausal women Senile patients Genetics - genes regulating the osteoclastic activity and Vitamin D Receptors
418
Osteoporosis: Primary Osteoporosis - What race are at an increased risk?
White caucasians
419
Osteoporosis: Primary Osteoporosis - Environmental risk factors (4)
Smoking Alcohol abuse Lack of exercise Poor diet
420
Osteoporosis: Primary Osteoporosis - These patients are at risk to what musculoskeletal problems?
Colles fracture Vertebral insufficiency
421
Osteoporosis: Primary Osteoporosis - Type I
Osteoporosis due to exacerbated loss of bone in the post-menopausal period
422
Osteoporosis: Primary Osteoporosis - Type II
Osteoporosis of old age individuals with a rapid decline in bone mineral density
423
Osteoporosis: Primary Osteoporosis - 3 environmental risk factors for Type II
Chronic disease Inactivity Reduced sunlight exposure - reduced Vitamin D
424
Osteoporosis: Primary Osteoporosis - What fractures predominate in Type II Osteoporosis?
Femoral neck fractures Vertebral fractures
425
Osteoporosis: Secondary Osteoporosis - Risk factors (4)
Endocrine disorders Gastrointestinal Disorders Drugs - Alcohol or Corticosteroids Immobilisation
426
Osteoporosis: Secondary Osteoporosis - Examples of Endocrine disorders thayt increase risk (3)
Cushing's Syndrome Hyperparathyroidism Hyperthyroidism
427
Osteoporosis: Secondary Osteoporosis - Examples of Gastrointestinal Disorders that increase risk (4)
Hepatic insufficiency Malabsorption Malnutrition Vitamin C or D deficiency
428
Osteoporosis: Peak bone mass occurs when?
Young adulthood
429
Osteoporosis: Environmental factors determining peak bone mass (4)
Physical activity Muscle strength Diet Hormonal stasis
430
Osteoporosis: Normal degeneration of the bone per year
0.7%
431
Osteoporosis: Age related changes in bones (2)
Reduced proliferative and biosynthetic capacity of osteoblasts Response to growth factors is attenuated
432
Osteoporosis: Alterations in blood components (3)
Reduced calcium Elevated PTH Vitamin D deficiency
433
Osteoporosis: Impact of the menopause
Post-menopause there is low oestrogen causing osteoclasis to exceed osteoblastic activity
434
Osteoporosis: Indirect effects of Corticosteroids on bone
Inhibition of gonadal and adrenal steroid production
435
Osteoporosis: Direct effects of corticosteroids on bone (3)
Reduced osteoblast activity and lifespan Suppression of replication of osteoblast precursors Reduction in calcium absorption
436
Osteoporosis: Common osteoporotic fracture sites (4)
Proximal femur Sacrum and pubic rami Thoracolumbar vertebral bodies Distal radius
437
Osteoporosis: Fracture of the vertebral body can results in what two things? (2)
Thoracic kyphosis Loss of heght
438
Osteoporosis: How is the risk assessed?
10 year osteoporotic fracture risk calculator
439
Osteoporosis: Osteopenia
1-2.5 Standard deviations below mean peak bone mass
440
Osteoporosis: Diagnostic definition
>2.5 deviations below mean peak bone mass
441
Osteoporosis: Secondary causes of fractures (30
Steroids Early menopause Anorexia
442
Osteoporosis: When is a DEXA scan referred? (2)
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
Osteoporosis: What does a DEXA scan determine?
Bone mineral density
444
Osteoporosis: Severe Osteoporosis definition
>2.5 standard deviations below the mean peak bone masswith a fragility fracture
445
Osteoporosis: How is Multiple Myeloma ruled out?
Protein electrophoresis Bence Jones proteins analysed
446
Osteoporosis: Lifestyle Advice (5)
Increase calcium intake High intensity strength training Low-impact weight bearing exercise Avoidance of excess alcohol Avoidance of smoking
447
Osteoporosis: Calcium intake aim for general population
700mg
448
Osteoporosis: Calcium intake aim for post-menopausal women
1000mg
449
Osteoporosis: Management - What is given if there is dietary deficiency or limited sunlight exposure?
Calcium or Vitamin D supplements
450
Osteoporosis: Management - When must calcium supplements not be given?
Within 2 hours of oral bisphosphonates
451
Osteoporosis: Management - First line for a majority of patients?
Oral Bisphosphonates
452
Osteoporosis: Management - Function of Oral Bisphosphonates
Reduce osteoclastic resorption
453
Osteoporosis: Management - Examples of Oral Bisphosphonates (3)
Alendronic acid Risedronate Etidronate
454
Osteoporosis: Management - When should Oral Bisphosphonates be considered?
When a T score
455
Osteoporosis: Management - Second line management for a majority of patients
Zoledronic Acid
456
Osteoporosis: Management - Dose And Administration route of Zoledronic Acid
Once yearly intravenous bisphosphonate
457
Osteoporosis: Management - MOA of Desunomab
Monoclonal antibody that reduces osteoclast activity
458
Osteoporosis: Management - MOA of Treiparatide
Recombinant parathyroid hormone that stimulates bone growth rather than reduces bone loss
459
Osteoporosis: Management - MOA of Treiparatide
Recombinant parathyroid hormone that stimulates bone growth rather than reduces bone loss
460
Osteoporosis: Management - Teriparatide is used when?
To reduce the risk of vertebral and non-vertebral fractures in post-menopausal women with severe osteoporosis
461
Osteoporosis: Management - When is Teriparatide recommended over oral Bisphosphonates?
In post menopausal women with at least 2 moderate or 1 severe low trauma vertebral fracture to prevent vertebral fracture
462
Osteoporosis: Management - MOA of Romosozumab
Monoclonal antibody that binds to and inhibits sclerostin to increase bone formation and reduce bone resorption
463
Osteoporosis: Management - When is Romosozumab recommended?
For post menopausal women with severe ostroporosis who have had a fragility fracture and are at imminent risk of further fracture
464
Osteomalacia
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
Rickets
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
Osteomalacia and Rickets: Two main causes
Insufficient calcium absorption Phosphate deficiency - due to increased renal loss
467
Osteomalacia and Rickets: Aetiologies (4)
Vitamin D deficiency Hypophosphataemia Long term Anti-convulsant use Chronic Kidney Disease
468
Osteomalacia and Rickets: Cuases of Vitamin D deficiency (3)
Malnutrition Malabsorption Lack of sunlight exposure
469
Osteomalacia and Rickets: Causes of Hypophosphatemia (4)
Re-feeding Syndrome Alcohol abuse Malabsoprtion Renal Tubular Acidosis
470
Osteomalacia and Rickets: How is this triggered by Chronic Kidney Disease?
Reduced phosphate resorption and failure of activation of Vitamin D resulting in Secondary Hyperparathyroidism
471
Osteomalacia and Rickets: What is the function of Vitamin D?
Stimulates the absorption of calcium from the GI tract, Kidney and bone Induces osteoblasts to release Osteocalcin
472
Osteomalacia and Rickets: Initial impacts of Vitamin D deficiency? (2)
Hypocalcaemia Elevated PTH
473
Osteomalacia and Rickets: The hypocalcaemia and elevated PTH due to Vitamin D deficiency have what secondary effects? (3)
Increases calcium absorption Increased Osteoclastic activity Release of Calcium from the bone
474
Osteomalacia and Rickets: Reduced Vitamin D has what affect on the kidneys?
Increased renal excretion of phosphate
475
Osteomalacia and Rickets: Increased renal excretion of phosphate due to Vitamin D deficiency has what effect on the bone?
Impairs bone mineralisation
476
Osteomalacia and Rickets: Impaired bone mineralisation of the matrix has what overall impact?
Bone remodelling
477
Osteomalacia and Rickets: Bone remodelling is idfferent in these conditions, why?
Newly formed osteoid is not fully mineralised causing thick osteoid seams and causes the bone to become weak
478
Osteomalacia and Rickets: Presentation - Bone pain where?
Pelvis Spine Femora
479
Osteomalacia and Rickets: Presentation - Symptoms of Hypocalcaemia (6)
Paraesthesiae - burning sensation in the limbs Muscle cramps Irritability Fatigue Seizures Brittle nails
480
Osteomalacia and Rickets: Presentation - Signs in the bones of ricket patients
Deformation due to soft bones
481
Osteomalacia and Rickets: Presentation - Presents with proximal ...
Myopathy
482
Osteomalacia and Rickets: Presentation - Oral symptoms
Dental defects
483
Osteomalacia and Rickets: Diagnostic test
X-Ray
484
Osteomalacia and Rickets: X-Ray - 2 features
Poor corticomedullary differentiation Pseudofractures - Pubic rami, Proximal femora, Ulna and Ribs
485
Osteomalacia and Rickets: Blood results (3)
Decreased calcium Decreased serum phosphate Increased serum ALP
486
Osteomalacia and Rickets: Management
Vitamin D Therapy + Calcium and Phosphate Supplementation
487
Osteomalacia and Rickets: Management - Vitamin D therapy dose and duration
400-800 IU per day after loading IU per day for 12 weeks
488
Osteomalacia and Rickets: What must be considered for Chronic Renal Disease?
Patients may have a high 25-OG-Vitamin D so treatment must be titrated to PTH levels
489
Avascular Necrosis
Necrosis of the bone marrow due to loss of an effective vascular supply
490
Avascular Necrosis: More common in what sex?
Males
491
Avascular Necrosis: Typical Age
35-50 years
492
Avascular Necrosis: Risk Factors - What coagulation disorders? (4)
Those with increased coaguability: - Thrombophilia - Sickle Cell disease - Antiphospholipid deficiency in SLE - Pregnancy
493
Avascular Necrosis: Risk Factors - Biochemical causes
Hyperlipidaemia - increased fat in circulation
494
Avascular Necrosis: Risk Factors - Why can risk be increased by alcohol or steroid use and abuse? (3)
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
Avascular Necrosis: Risk Factors - Dysbaric disorders increase risk, what are they?
Nitrogen gas bubbles forming in the circulation after a rapid depressurisation after deep sea diving
496
Avascular Necrosis: Risk Factors - What mechaical problems increase risk?
Fractures of the scaphoid or femoral head
497
Avascular Necrosis: Commonly affected sites (6)
Femoral head Femoral condyles Head of the humerus The capitellum The proximal pole of the scaphoid The proximal part of the talus
498
Avascular Necrosis: What vessels are damaged in scaphoid fracture?
Retrograde blood supply
499
Avascular Necrosis: What vessels are damaged in femoral fractures?
Circumflex arteries
500
Avascular Necrosis: How does thrombophilia cause AVN?
Causes blood clots
501
Avascular Necrosis: How does alcoholism cause AVN?
Causes fat microemboli
502
Avascular Necrosis: How does Sickle cell disease?
Causes sickle cell crisis
503
Avascular Necrosis: Pathophysiology - The hypoxic death of bone and haemopoietic cells causes what 3 effects? (3)
Stimulates periosteal nociceptors Reabsorption of dead bone tissue Demineralisation of the bone
504
Avascular Necrosis: Pathophysiology - Osteochondritis dissecans
Reabsorption of deab bone tissue causes separation of the articular surface from the dead subchondral bone
505
Avascular Necrosis: Pathophysiology - Idiopathic AVN pathophysiology initiating event
Coagulation of the intraosseous microcirculation causes a venous thrombosis to induce retrograde arterial occlusion
506
Avascular Necrosis: Pathophysiology - Retrograde arterial occlusion encourages what to arise?
Intraosseous hypertension
507
Avascular Necrosis: Pathophysiology - Intraosseous hypertension causes what two things to occur?
Decreased blood flow which results in necrosis of the bone segment
508
Avascular Necrosis: Pathophysiology - What initially occurs following necrosis of bone segments?
Patchy sclerosis - this precedes subchrondral collapse Irregularity of the articular surface
509
Avascular Necrosis: Pathophysiology - Resultant bone and joint damage can lead to what?
Secondary Osteoarthritis
510
Avascular Necrosis: Clinical Presentation
Can be assymptomatic - joint pain presents when progression to collapse or osteoarthritis has occured
511
Avascular Necrosis: Clinical Presentation of a Femoral Head/Hip AVN
Insidious onset of groin pain that is exacerbated by movement
512
Avascular Necrosis: Diagnosis - Features on X-Ray (3)
Sclerosis surrounding the necrotic region Collapsed bone segments Sub-chondral locking or catching
513
Avascular Necrosis: Diagnosis - X-ray sign for femral head AVN
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
Avascular Necrosis: Management - Treatment is dependent on what classification system?
Steinburg Classification
515
Avascular Necrosis: Management - Stage 0 Steinburg Classification
Normal Radiograph + Normal MRI and Bone scan
516
Avascular Necrosis: Management - Stage I Steinburg Classification
Normal Radiograph + Abnormal MRI and/or bone Scan
517
Avascular Necrosis: Management - Stage II Steinburg Classification
Cystic or Sclerotic Radiograph + Abnormal MRI and /or bone scan
518
Avascular Necrosis: Management - Stage III Steinburg Classification
Crescent sign (Subchondral collapse) + Abnormal MRI or bone scan
519
Avascular Necrosis: Management - Stage IV Steinburg Classification
Flattening of the femoral head + Abnormal MRI and/or Bone scan
520
Avascular Necrosis: Management - Stage V Steinburg Classification
Narrowing of the joint + Abnormal MRI and/or Bone Scan
521
Avascular Necrosis: Management - Stage VI Steinburg Calssification
Advanced degenerative changes + Abnormal MRI and/or Bone scan
522
Avascular Necrosis: Management - What classifications are reversible?
Steinburg Classifications 0-II
523
Avascular Necrosis: Management - What classifications are irreverisble?
Steinburg classifications III-VI
524
Avascular Necrosis: Management - Options for reversible cases (4)
Bisphosphanates Core decompression - drilling is performed to decompress the bone to prevent further necrosis Currettage and bone grafting Vascularised fibular bone graft
525
Avascular Necrosis: Management - Options for irreversible cases (2)
Total joint replacement Rotational osteotomy - if <15% of the femoral head is damaged
526
Hyperparathyroidism: Function of PTH - Role in Osteoclast activity
Activates Osteoclasts to increase bone resorption and release calcium
527
Hyperparathyroidism: Function of PTH - Role in Calcium regulation
Increases resorption of calcium by renal tubules
528
Hyperparathyroidism: Function of PTH - Role in Phosphate Activity
Increases urinary excretion of phosphate
529
Hyperparathyroidism: Function of PTH - Role in Vitmin D activity
Increased synthesis of Active forms of Vitamin D
530
Hyperparathyroidism: Clinical Presentation - Presentations as a result of increased Osteoclasis (2)
Decreased bone mass Prone to fractures deformity and degenerative joint diseases
531
Hyperparathyroidism: Clinical Presentation - Osteoporosis occurs where?
Phalanges Vertebrae Femur
532
Hyperparathyroidism: Clinical Presentation - Osteoporosis has prominent changes in what section of the bone?
Cortical bone and medullary cancellous bone
533
Hyperparathyroidism: Clinical Presentation - What is present within marrow spaces?
Fibrovascular tissue
534
Hyperparathyroidism: Clinical Presentation - What tumours may appear?
Brown Tumours
535
Hyperparathyroidism: Clinical Presentation - What cells are present in brown tumours?
Giant cells
536
Hyperparathyroidism: Clinical Presentation - Haemorrhage associated with brown tumours has what two effects?
Macrophage reactions Increased processes of organisation and repair
537
Paget's Disease of Bone
Chronic condition involving cellular remodelling and deformity of one or more bones
538
Paget's Disease of Bone: Incidence in age
Most are >50 years
539
Paget's Disease of Bone: More common in what sex?
Males
540
Paget's Disease of Bone: Genes involved? (2)
SQSTM1/P62 gene or RANKL - both increase the activity f NF-KB
541
Paget's Disease of Bone: Other name
Osteitis Deformans
542
Paget's Disease of Bone: Viruses involved? (3)
Paramyxovirus Measles RSV
543
Paget's Disease of Bone: Viruses involved? (3)
Paramyxovirus Measles RSVRole of Measles iPaget's Disease of Bone: n Paget's?
544
Paget's Disease of Bone: Viruses involved? (3)
Paramyxovirus Measles RSV
545
Paget's Disease of Bone: Role of Measles in Paget's?
MVNP nucleocaspid is present and activates osteoclast activity
546
Paget's Disease of Bone: Pathophysiology - First stage
Osteolytic - resorption pits are present with large osteoclasts
547
Paget's Disease of Bone: Pathophysiology - Second stage
Mixed stage of osteoclastic activity and osteoblastic activity
548
Paget's Disease of Bone: Pathophysiology - Final stage
Osteosclerotic stage - causes enlarged bone of increased density and with a coarse trabecular pattern
549
Paget's Disease of Bone: Pathophysiology - Net result
Thick excess bone with abnormal reversal lines that provide a mosaic pattern - the bone is soft and porous
550
Paget's Disease of Bone: Pathophysiology - Commonly affected bones (4)
Long bones Pelvis Lumbar spine Skull
551
Paget's Disease of Bone: Clinical presentation - Pain occurs due to what? (2)
Micro-fractures Compression neuropathies
552
Paget's Disease of Bone: Clinical presentation - Leontiasis ossea
Overgorowth of the facial and cranial bones
553
Paget's Disease of Bone: Clinical presentation - Platybasia
Skull base abnormality that is flat
554
Paget's Disease of Bone: Clinical presentation - Sabre tibia
Malformation of the tibia in which there is anterior bowing
555
Paget's Disease of Bone: Clinical presentation - Increased metabolism rate presents how? (2)
Warm skin High output heart failure
556
Paget's Disease of Bone: Clinical presentation - Potential Secondary Malignancies (2)
Osteosarcoma Fibrosarcoma
557
Paget's Disease of Bone: Clinical presentation - What symptom may present if the skull is affected?
Deafness
558
Paget's Disease of Bone: Diagnosis - 3 key tests
X-Ray Isotope bone scan Alkaline Phosphatase
559
Paget's Disease of Bone: Diagnosis - Early presentation on X-ray
Lytic phase presents with well defined lucency
560
Paget's Disease of Bone: Diagnosis - Late presentation on X-ray
Sclerotic phase with enlarged bone, increased density and coarse trabecular pattern
561
Paget's Disease of Bone: Diagnosis - Purpose of the isotope bone scan?
Shows distribution of disease
562
Paget's Disease of Bone: Diagnosis - Alkaline Phosphatase results
Elevated with normal LFTs
563
Paget's Disease of Bone: Management
Treat with Bisphosphanates if analgesia does not manage pain
564
Soft Tissue Tumours: Examples (6)
Ganglion Cyst Nodular fasciitis Myositis ossificans Superficial fibromatoses Deep fibromatosis Tenosynovitis
565
Ganglion Cyst
Outpouching of the synovium lining of joints and filled with synovial fluid
566
Ganglion Cyst: Two aetiologies (2)
Developmental e.g. Juvenile Bakers Cyst Underlying joint damage or arthritis causes build up of pressure within the joint
567
Ganglion Cyst: Why is this not a true cyst?
No epithelial lining
568
Ganglion Cyst: What is present histologically?
Degenerative changes within the connective tissue Space present with myxoid material
569
Ganglion Cyst: Clinical presentation - Occur where?
Around a synovial joint or a synovical tendon sheath
570
Ganglion Cyst: Clinical presentation - Common locations
Wrist Feet Knees
571
Ganglion Cyst: Clinical presentation - Size
Up to 1cm
572
Ganglion Cyst: Management
Normally self-resolving - if localised discomfort or cosmesis can be excised
573
Nodular Fasciitis
Benign proliferation of fibroblastic and myofibroblastic cells
574
Nodular Fasciitis: What patient group does this affect?
Young adults
575
Nodular Fasciitis: Aetiology
25% of cases are associated with prior trauma
576
Nodular Fasciitis: Histology = Mature where?
At the periphery
577
Nodular Fasciitis: Histological appearance (3)
Highly cellular Mitoses present Plump cells - these are stellate and spindle cells
578
Nodular Fasciitis: Clinical presentation
Superficial or deep lesion of less than 5cm that is usually well circumscribed
579
Nodular Fasciitis: Management
Self-resolving
580
Myositis Ossificans
Abnormal calcification of a muscle haematoma following trauma
581
Myositis Ossificans: Aetiology
Associated with preceding trauma
582
Myositis Ossificans: Histological appearance
Cellular proliferation with evidence of bone formation and zonation
583
Myositis Ossificans: Clinical presentation
Initial soft swelling followed by hardness
584
Myositis Ossificans: Diagnostic criteria
Peripheral mineralisation around bone on X-Ray or MRI
585
Myositis Ossificans: Management and the criteria
Intervene only if symptoms are problematic Must wait until maturity of ossification as there is a risk of recurrence at 6-12 months
586
Superficial Fibromatoses
Non-metastatising fibroproliferative lesions that form within connective tissue
587
Superficial Fibromatoses: Risk factors (3)
Alcohol Diabetes Mellitus Anticonvulsants
588
Superficial Fibromatoses: Epidemiology of sexes
More common in men
589
Superficial Fibromatoses: Average Age
60 years old
590
Superficial Fibromatoses: Clinical Presentation - Dupuytren's
Contracture of the hand that is a deformity due to knots of tissue forming under the skin of the palm
591
Superficial Fibromatoses: Clinical Presentation - Peyronie's
Non-cancerous condition due to fibrous scar tissue developing on the penis to cause curved and painful erections
592
Superficial Fibromatoses: Histology of Dupuytren's (4)
Firm white-grey tissue Nodules and fascicles present Bland fibroblasts Dense collagen
593
Deep Fibromatosis: Peak age
Teenagers to 30 years old
594
Deep Fibromatosis: Associated mutations (2)
APC Beta-catenin
595
Deep Fibromatosis: What condition is a predisposing factor for this?
Gardner's Syndrome
596
Deep Fibromatosis: Associated with what physiological period?
Pregnancy
597
Deep Fibromatosis: Sites (3)
Mesenteric tissue Musculo-aponeurotic tissue of the abdominal wall Limb girdles
598
De Quervain's Tenosynovitis
Inflammation of the tendon sheaths within the first compartment
599
De Quervain's Tenosynovitis: Locations (2)
Abductor pollicis longus Extensor pollicis brevis
600
De Quervain's Tenosynovitis: Epidemiology - most common age
30-50 years
601
De Quervain's Tenosynovitis: Associated with what condition?
Rheumatoid Arthritis
602
De Quervain's Tenosynovitis: Associated with what physiological time?
Pregnancy
603
De Quervain's Tenosynovitis: Typical presentation
Repetitive strain injury with pain over the radial styloid process at the wrist
604
De Quervain's Tenosynovitis: What test can be used to test this?
Finklestein's Test - patient makes a fist over the thumb and the hand is in ulnar deviation to reproduce pain
605
De Quervain's Tenosynovitis: What investigations may be conducted?
USS or X-ray to rule out Carpometacarpal joint osteoarthritis
606
De Quervain's Tenosynovitis: Conservative management
Splint and rest with analgesics
607
De Quervain's Tenosynovitis: Surgical management
Surgical decompression
608
Benign Tumours: What benign tumour is due to t(X:18)?
Synovial Sarcoma
609
Benign Tumours: What benign tumour is due to t(2:13)?
Alveolar Rhabdomyosarcoma
610
Benign Tumours: What benign tumour is due to t(11:22)?
Ewing's Sarcoma
611
Liposarcoma
Malignant tumour of the fat
612
Liposarcoma: Peak age of incidence
50-60 years old
613
Liposarcoma: What two genetic abnormalities are associated with this?
t(12:16) Amplification 12q13-q15
614
Liposarcoma: Locations
Deep soft tissue of the extremities or retroperitoneum
615
Liposarcoma: Histology
Well-differentiated pelomorphic myxoid character
616
Lipoma
Benign neoplastic proliferation of subcutaneous fat
617
Lipoma: Usually occurs where?
Subcutaneous fat
618
Lipoma: Clinical features (4)
Large - can be several cm Less well defined Slow growing Painless
619
Lipoma: Has no changes in what structure?
Skin
620
Lipoma: Management
Surgical excision if symptomatic
621
Leiomyoma: Presents most commonly where?
Uterus
622
Leiomyoma: Less common areas
Errector pilae Deep soft tissue Muscularis of the gastrointestinal tract
623
Leiomyoma: Histology Characteristics (2)
1-2cm Fascicles of spindle cells - cigar shaped nuclei with minimal atypia and few mitoses
624
Leiomyosarcoma: Epidemiology of sexes
More common in femlaes
625
Leiomyosarcoma: What structures are impacted by this?
Deep soft tissues of the extremities Retroperitoneum e.g. from the great vessels
626
Leiomyosarcoma: Management
Must be excised - if not complete it can recur and can be lethal due to local metastasis and invasion
627
Rhabdomyoma
Benign lesion of the cardiac muscle
628
Rhabdomyoma: What patient group is affected?
Paediatric age groups
629
Rhabdomyoma: What impact does this have on the heart? (2)
Valvular obstruction or occupies the cardiac chamber
630
Rhabdomyoma: 50% associated with what conditions?
Tuberous sclerosis and mutations of TSC1 and 2
631
Rhabdomyosarcoma
Malignant soft tissue sarcoma that develops from muscle or fibrous tissue
632
Rhabdomyosarcoma:What are the 3 types?
Embryonal Rhabdomyosarcoma Alveolar Rhabdomyosarcoma Pleomorphic Rhabdomyosarcoma
633
Rhabdomyosarcoma: What is the most common type?
Embryonal Rhabdomyosarcoma
634
Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - Presents when?
In childhood
635
Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - Sites (4)
Botyroides - Genital tract Genitourinal Tract Periorobital - Head and Neck Common bile duct
636
Rhabdomyosarcoma: Embryonal Rhabdomyosarcoma - What genetics are involved?
Deletion of Xp11.15
637
Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - Presents when?
In young adults or older age groups
638
Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - Sites
Arise in the wall of hollow structures - head or neck
639
Rhabdomyosarcoma: Alveolar Rhabdomyosarcoma - What genetics are involved?
FOXO1 PAX 3 or 7 Translocation t(2:13) translocation t(1:13) translocation
640
Rhabdomyosarcoma: Pleomorphic Rhabdomyosarcoma - Presents in what age groups?
Older age groups
641
Rhabdomyosarcoma: Pleomorphic Rhabdomyosarcoma - Immunohistochemistry shows what?
MYOD1 and Myogenin
642
Benign Cartilaginous Tumours: Two examples
Enchondroma Osteocondroma
643
Benign Cartilaginous Tumours: Enchondroma - Occurs where?
In the digits
644
Benign Cartilaginous Tumours: Enchondroma - Can be part of what syndrome?
Ollier's and Maffuci
645
Benign Cartilaginous Tumours: Osteochondroma - Occurs where?
At the metaphysis of long bones - especially around the knee
646
Chondrosarcoma
Malignant tumour that produces cartilage
647
Chondrosarcoma: More common in what age group?
>40
648
Chondrosarcoma: What types are more common in younger patients?
Mesenchymal and Clear Cell Tumours
649
Chondrosarcoma: Histological presentation
Nodules of grey or white cartilaginous tissue with gelatinous matrix
650
Chondrosarcoma: Invasion pattern
Locally invasive into the bone and muscle and fat - to surround the pre-existing bone trabecula
651
Chondrosarcoma: 6 types
Conventional Intramedullary Juxtacortical Clear Cell Mesenchymal De-differentiated
652
Chondrosarcoma: Locatuion of intramedullary types
Central to the bone
653
Chondrosarcoma: Location of the Juxtacortical types
Peripheral to the bone
654
Chondrosarcoma: Clear Cell Chondrosarcoma
Malignant chondrocytes that have an abundant cytoplasm
655
Chondrosarcoma: Clear Cell Chondrosarcoma is associated with what?
Osteoclastic cells Reactive bones
656
Chondrosarcoma: Mesenchymal Chondrosarcoma appearance
Sheets of well-differentiated hyaline-appearing cartilage with surrounding small cells
657
Chondrosarcoma: De-differentiated type
Low grade chondrosarcoma with a separate high grade component that does not produce cartilage
658
Chondrosarcoma: Locations
Pelvis Shoulder Ribs
659
Chondrosarcoma: Location of Clear Cell types
Epiphyses of long tubular bones
660
Chondrosarcoma: Grade III commonly metastasise where?
To the lung via the blood
661
Simple Osteoma: Occurs in what bones?
Cranial bones
662
Simple Osteoma: Multiple osteoma lesions occur in what syndrome?
Garner's Syndrome
663
Osteoid Osteoma: Size
<2cm
664
Osteoid Osteoma: Occurs most commonly in what patient groups?
Young men
665
Osteoid Osteoma: Occurs in what skeleton and what bones of this?
Appendicular skeleton - mainly the femur and tibia
666
Osteoid Osteoma: Occurs mainly in what section of the bone?
The cortex
667
Osteoid Osteoma: The osteoma is surrounded by what?
Reactive bone
668
Osteoid Osteoma: Clinical presentation
Severe nocturnal pain
669
Osteoid Osteoma: Management
Aspirin or NSAIDs to relieve pain
670
Osteoblastoma: Impacts what structures?
Posterior vertebrae
671
Osteoblastoma: Problem with management?
Pain is not relieved by aspirin
672
Osteoblastoma: What is not present histologically?
Reactive bone
673
Ewing's Sarcoma
Malignant primary bone tumour of the endothelial cells in the bone marrow
674
Ewing's Sarcoma: Presents in what age groups?
10-20 years - Children and Adolescents
675
Ewing's Sarcoma: What genetics are inolved?
t(11:22)
676
Ewing's Sarcoma: Presents where?
In any soft tissue and bony location - often in the long bones of adolescents
677
Ewing's Sarcoma: What is the concern with this?
Highly malignant - destructive and rapidly growing
678
Ewing's Sarcoma: Waht are the potential cells of origin? (2)
Primitive mesenchymal cell Neuroectodermal cell
679
Ewing's Sarcoma: Presentation
Hot swollen tender joint or limb
680
Ewing's Sarcoma: Presentation on bloods
Raised inflammatory markers - mimics infection
681
Ewing's Sarcoma: Why is surgical excision not recommended?
As the tumour is of the bone marrow, function can be reduced post-surgery
682
Ewing's Sarcoma: Management of choice
Radiotherapy or Chemotherapy
683
Soft Tissue Rheumatism
Pain that is caused by inflammation or damage to the ligaments near a joint rather than the bone or cartilage
684
Soft Tissue Rheumatism: What is the most common area for pain?
Shoulder
685
Soft Tissue Rheumatism: Causes of this in the shoulder (5)
Adhesive capsulitis Rotator cuff tendinosis Calcific tendonitis Impingement Partial or Full rotator cuff tears
686
Soft Tissue Rheumatism: Less common sites (4)
Elbow - Medial and lateral epicondylitis Wrist - De-Quervains Tenosynovitis Pelvis Foot - Plantar fascitis
687
Soft Tissue Rheumatism: Diagnosistic examinations
X-ray
688
Soft Tissue Rheumatism: Diagnosistic examinations
X-ray
689
Soft Tissue Rheumatism: What is shown on X-Ray?
Calcific tendonitis
690
Soft Tissue Rheumatism: Management
Rice and Physiotherapy Surgery - if pain is not removed
691
Joint hypermobility Syndrome
Patient with hypermobile joints that develops chronic pain lasting 3 months or longer
692
Joint hypermobility Syndrome: Epidemiology of sexes
More common in females
693
Joint hypermobility Syndrome: Presents when?
Childhood or the 3rd decade
694
Joint hypermobility Syndrome: Associated with what genetic abnormalities? (2)
Marfans Syndrome Ehlers Danlos Syndrome
695
Joint hypermobility Syndrome: Clinical Presentation (3)
Joint pain and stiffness Frequent sprains and dislocations Thin stretchy skin
696
Joint hypermobility Syndrome: Criteria of the Modified Beighton Score (4)
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
Joint hypermobility Syndrome: What is used for diagnosis?
Modified Beighton Score
698
Joint hypermobility Syndrome: Diagnosis of Modified Beighton Score
Hypermobile if >4/9
699
Joint hypermobility Syndrome: Management
Patient education with physiotherapy Analgesia if pain
700
Connective Tissue Disorders
Conditions associated with spontaneous overactivity of the immune system and act via specific autoantibodies
701
Connective Tissue Disorders: Examples (6)
Systemic Lupus Erythematous Sjogrens Syndrome Systemic sclerosis or Scleroderma Dermatomyositis Polymyositis Anti-Phospholipid Syndrome
702
Systemic Lupus Erythematous
Systemic autoimmune condition in which the immune system attacks cells and tissue to cause inflammation and tissue damage
703
Systemic Lupus Erythematous: More common in what population group?
Women of child-bearing age
704
Systemic Lupus Erythematous: More common in what countries/races? (4)
Afro-carribean Hispanic american Asia China
705
Systemic Lupus Erythematous: What are two risk factors?
Infection Smoking
706
Systemic Lupus Erythematous: Pathophysiology - Initiating Event
Loss of immune regulation - leads to increased and defective apoptosis
707
Systemic Lupus Erythematous: Pathophysiology - Impact on necrotic cells
Release nuclear material
708
Systemic Lupus Erythematous: Pathophysiology - The release of nuclear material from necrotic cells has what impact?
Nuclear material acts as auto-antigens to induce autoimmunity
709
Systemic Lupus Erythematous: Pathophysiology - The release of auto-antibodies causes what to happen?
Antigen-Auto-antibody complexes form and are deposited on the basement membrane
710
Systemic Lupus Erythematous: Deposition of Ag-Ab complexes on the basement membrane has what impact?
Activates complement to attract the leukocytes to release cytokines
711
Systemic Lupus Erythematous: The release of cytokines from leukocytes has what impact?
Causes enzyme release from neutrophils to cause damage to the endothelial cells of the basement membrane
712
Systemic Lupus Erythematous: Cutaneous Features (5)
Subcutaneous or discoid lupus Acute cutaneous lupus Non-scarring alopecia Oral ulceration Photosensitive rash
713
Systemic Lupus Erythematous: Alternate clinical presentation - Musculoskeletal features
Arthritis - synovitis or tenderness of at lesast 2 joints with >30 minutes of early morning stiffness
714
Systemic Lupus Erythematous: Alternate clinical presentation - Neurological (5)
Delirium Psychosis Seizures Headaches Cranial Nerve Disorder
715
Systemic Lupus Erythematous: Alternate clinical presentation - What inflammatory presentation occurs?
Serositis - causes pleural effusion, pericardial effusion or acute pericarditis
716
Systemic Lupus Erythematous: Alternate clinical presentation - Haematological (4)
Leukopenia Thrombocytopenia Haemolytic anaemia Lymphadenopathy
717
Systemic Lupus Erythematous: Alternate Clinical Presentation - Renal (3)
Proteinuria - >0.5g in 24 hours Nephritis Red cell casts
718
Systemic Lupus Erythematous: Diagnosis - What classification system is used?
EULAR/ACR SLE Classification Criteria - Score >10 required
719
Systemic Lupus Erythematous: Diagnosis -What complement factors are high within the blood?
C3 and C4
720
Systemic Lupus Erythematous: Diagnosis - What antibody must be positive?
Anti-nuclear Antibody (ANA)
721
Systemic Lupus Erythematous: Diagnosis - What antibody is positive in 60% of patients?
Anti-double stranded DNA antibodies (AdsDNAA)
722
Systemic Lupus Erythematous: Diagnosis - AdsDNAA corelates with what?
Disease activity
723
Systemic Lupus Erythematous: Diagnosis - AdsDNAA is associated with what?
Lupus nephritis
724
Systemic Lupus Erythematous: Diagnosis - Anti-phospholipid ANtobodies are asosociated with what? (2)
Venous and Arterial thrombosis Recurrent miscarriage
725
Systemic Lupus Erythematous: Diagnosis - APLA presents with what?
Livedo reticularis - mottled discolourisation of the skin
726
Systemic Lupus Erythematous: Diagnosis - APLA antoibodies (3)
Lupus anticoagulant Anti-cardiolipin antibodies Anti-beta 2 glycoprotein antibodies
727
Systemic Lupus Erythematous: Diagnosis - Anti-Ro antibodies are associated with what?
Associated with neonatal lupus and congenital heart block
728
Systemic Lupus Erythematous: Diagnosis - Anti-Sm antibodies are associated with what?
Highly specific for lupus