TO DO MSK & RHEUM Flashcards

1
Q

RHEUM PHYSIOLOGY
Explain why ESR levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased fibrinogen –> RBC’s clump together –> RBC’s fall faster = increased ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

RHEUM PHYSIOLOGY
Explain why CRP levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased IL-6 levels –> CRP produced in response to IL-6 –> CRP raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SPONDYLARTHRITIS
Give 6 signs of spondyloarthritis

A

SPINE ACHE

  1. Sausage digits = dactylics
  2. Psoriasis
  3. Inflammatory back pain
  4. NSAID responsive
  5. Enthesitis
  6. Arthritis
  7. Crohn’s/UC
  8. HLAB27
  9. Eye - uveitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ANKYLOSING SPONDYLITIS
what is the clinical presentation of ankylosing spondylitis

A

pain + stiffness → worse with rest/at night + improves with movement

SYMPTOMS
- back pain
- reduced spinal movement
- dyspnoea
- peripheral arthritis + dactylitis
- painful red eye

SIGNS
- pain in buttock or along axial spine
- reduced lumbar flexion (when patient tries to touch toes)
- loss of lumbar lordosis
- reduced chest expansion
- asymmetrical peripheral joint pain (oligoarthritis)
- anterior uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ANKYLOSING SPONDYLITIS
What investigations might you do in someone who you suspect to have ankylosing spondylitis?

A

CRP + ESR - raised
HLA B27 genetic test
X-ray of spine + sacrum
MRI spine - bone marrow oedema in early disease before x-ray changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ANKYLOSING SPONDYLITIS
what are the signs on x-ray?

A
  • Bamboo spine
  • Squaring of vertebral bodies
  • dagger sign
  • Subchondral sclerosis + erosions
  • Syndesmophytes
  • Ossification of ligaments, discs + joints
  • Fusion of facet, SI + costovertebral joint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ANKYLOSING SPONDYLITIS
What is the diagnostic criteria for ankylosing spondylitis?

A
  1. > 3 months back pain
  2. Aged <45 at onset
  3. Plus one of the SPINE ACHE symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ANKYLOSING SPONDYLITIS
What is the treatment for ankylosing spondylitis?

A

1st line
- regular exercise regimes
- NSAIDs
- corticosteroid injections
- DMARD (if NSAIDs not tolerated/ineffective) = ADALINUMAB, ETANERCEPT or INFLIXIMAB

2nd line
- surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PSORIATIC ARTHRITIS
what are the clinical features of psoriatic arthritis

A
  • Asymmetrical oligoarthritis (60%) - affects DIP joints
  • Large joint arthritis (15%)
  • Enthesitis - inflammation of entheses
  • Dactylitis - inflammation of full finger
  • Nail changes (pitting, onycholysis)
  • inflammatory joint pain
  • plaques of psoriasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PSORIATIC ARTHRITIS
What investigations might you do in someone you suspect to have psoriatic arthritis?

A

X-ray

- Erosion in DIPJ + periarticular new-bone formation  - Osteolysis  - Pencil-in-cup deformity 

Bloods

  • ESR + CRP - normal or raised
  • Rheumatoid factor -ve
  • anti-CCP - negative

Joint aspiration - no bacteria or crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PSORIATIC ARTHRITIS
How do you treat psoriatic arthritis?

A

MILD DISEASE
- NSAIDS + physiotherapy
- intra-articular steroids

PROGRESSIVE DISEASE
- DMARDs (1st line = methotrexate, sulfasalazine is alternative)
- biologic agents (etanercept or infliximab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

REACTIVE ARTHRITIS
What investigations might you do in someone you suspect to have reactive arthritis?

A

swab from infected site - urethral, cervical or rectal
stool sample
joint aspiration (to rule out septic arthritis)

full screening for STIs
HLA-B27 serology
x-rays of affected joints
ophthalmological evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

REACTIVE ARTHRITIS
How is reactive arthritis treated?

A

1st line
- NSAIDs
- intra-articular corticosteroids
- antibiotics if active STI

2nd line
- oral corticosteroids
- DMARD (methotrexate or sulfalazine)
- infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

OESTEOPOROSIS
Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone micro-architecture
  5. Mineralisation
  6. Geometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

OESTEOPOROSIS
Why can RA cause osteoporosis?

A

RA is an inflammatory disease

High levels of IL-6 and TNF –> increase bone resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

OESTEOPOROSIS
Give 5 risk factors for osteoporosis

A
  • old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian

‘SHATTERED’

  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol + tobacco use
  • Thin (BMI < 18.5)
  • Testosterone (low)
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease (e.g. myeloma or RA)
  • Dietary low calcium /malabsorption or Diabetes type 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

OESTEOPOROSIS
which endocrine diseases can be responsible for causing osteoporosis?

A
  1. Hyperthyroidism and primary hyperparathyroidism - TH and PTH increase bone turnover
  2. Cushing’s syndrome - cortisol leads to increase bone resorption and osteoblast apoptosis
  3. Early menopause, male hypogonadism - less oestrogen/testosterone to control bone turnover
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

OESTEOPOROSIS
which medications can cause osteoporosis?

A
  • glucocorticoids (steroids
  • phenytoin
  • heparin
  • ciclosporin
  • PPIs
  • pioglitazone
  • SSRIs
  • Aromatase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

OESTEOPOROSIS
What is a T score?

A

Is a standard deviation that is compared to a gender-matched young adult mean

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

OESTEOPOROSIS
what is the treatment for osteoporosis?

A

CONSERVATIVE
- weight-bearing exercise
- vitamin D + calcium intake
- smoking cessation
- reduce alcohol consumption

MEDICAL (DEXA <-2.5)
- 1st line = bisphosphonates (alendronic acid or zoledronic acid) + calcium and vit D supplement (adcal D3)
- 2nd line = denosumab or raloxifene (post-menopausal women) or PTH receptor agonist (teriparatide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

OESTEOPOROSIS
Give 3 disadvantages of HRT

A
  1. Increased risk of breast cancer
  2. Increased risk of stroke and CV disease
  3. Increased risk of thrombo-embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

OESTEOPOROSIS
How do bisphosphonates work?

A

Inhibit cholesterol formation –> osteoclast apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

VASCULITIS
Describe the pathophysiology of of vasculitis

A

Vessel wall destruction –> perforation and haemorrhage

Endothelial injury –> thrombosis and infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

GIANT CELL ARTERITIS
what are is the clinical presentation of giant cell arteritis?

A
  1. Headache, typically unilateral over temporal area
  2. Temporal artery/scalp tenderness
  3. Jaw claudication
  4. Visual symptoms - vision loss (painless)
  5. Systemic symptoms - fever, malaise, lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

GIANT CELL ARTERITIS
What are the investigations for giant cell arteritis?

A
  • ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
  • Halo sign on US of temporal and axillary artery
  • Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GIANT CELL ARTERITIS
What is the diagnostic criteria for giant cell arteritis?

A
  1. Age >50
  2. New headache
  3. Temporal artery tenderness
  4. Abnormal artery biopsies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

GIANT CELL ARTERITIS
Describe the treatment for giant cell arteritis

A
  1. High dose corticosteroids - prednisolone ASAP
  2. DMARDs - methotrexate (sometimes)
  3. Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

GRANULOMATOSIS WITH POLYANGIITIS
What is the pathophysiology of granulomatosis with polyangiitis?

A

Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GRANULOMATOSIS WITH POLYANGIITIS
where in the body can be affected?

A

ears
sinuses
lungs
kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

GRANULOMATOSIS WITH POLYANGIITIS
What are the clinical features?

A

SYMPTOMS
- epistaxis
- sinus congestion
- cough +/- haemoptysis
- haematuria
- joint pain
- paraesthesia and numbness

SIGNS
- nasal crusting or bleeding
- nasal or oral inflammation
- saddle nose deformity
- crackles or wheeze
- tender, swollen joints
- signs of peripheral neuropathy
- vasculitic rash (purpura)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

GRANULOMATOSIS WITH POLYANGIITIS
What investigations might you do in someone you suspect to have granulomatosis with polyangiitis?

A

ANCA testing - c-ANCA
CRP/ESR = raised
renal function tests
urine dipstick + microscopy
CXR/CT chest
renal biopsy (gold standard) = necrotising glomerulonephritis
FBC - high eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

GRANULOMATOSIS WITH POLYANGIITIS
What is the treatment for granulomatosis with polyangiitis?

A

1st line
- corticosteroids (prednisolone)
- cyclophosphamide
- maintenance therapy (azathioprine or methotrexate)

2nd line
- rituximab (may be used instead of cyclophosphamide)
- plasma exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

OSTEOARTHRITIS
Describe the pathophysiology of osteoarthritis

A

Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

OSTEOARTHRITIS
Name the 2 main pathological features of osteoarthritis

A
  1. Cartilage loss

2. Disordered bone repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

OSTEOARTHRITIS
What are the symptoms of OA?

A

SYMPTOMS
- Joint pain worsened by movement and relieved by rest
- Stiffness after rest – gelling
- Only transient (<30 minute) morning stiffness
- joint locking

SIGNS
- heberdens nodes (nodes at DIP joint)
- bouchards nodes (nodes at PIP joint)
- thenar muscle wasting
- first carpometacarpal joint most affected
- crepitus in knees
- joint tenderness
- antalgic gait
- restricted internal rotation when hip flexed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

OSTEOARTHRITIS
Give 5 radiological features associated with OA

A

LOSS

  1. Loss of joint space - articular cartilage destruction
  2. Osteophyte formation - calcified cartilaginous destruction
  3. Subchondral sclerosis - exposed
  4. Subchondral cysts
  5. Abnormalities of bone contour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

OSTEOARTHRITIS
Describe the pharmacological management of OA

A

1st line
- simple analgesia (paracetamol)
- topical NSAIDs

2nd line
- oral NSAIDs with PPI
- weak opioids (codeine)
- topical capsaicin
- intra-articular corticosteroid injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

OSTEOARTHRITIS
Nodal osteoarthritis can affect the DIP and PIP joints. What are the 2 terms sued for nodes on these joints?

A
  1. PIP = Bouchard’s nodes

2. DIP = Heberden’s nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Give an example of an autoimmune connective tissue disease

A
  1. SLE
  2. Systemic sclerosis (scleroderma)
  3. Sjogren’s syndrome
  4. Dermatomyositis/Polymyositis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

SLE
Describe the pathogenesis of SLE

A

Type 3 hypersensitivity reaction = immune complex mediated

Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

SLE
what are the clinical features of SLE?

A

GENERAL
- fatigue
- fever
- lymphadenopathy

DERMATOLOGICAL
- malar ‘butterfly’ rash
- photosensitivity
- discoid rash
- livedo reticularis
- non-scarring alopecia
- raynauds phenomenon

MSK
- arthralgia
- non-erosive arthritis

PULMONARY
- pleurisy
- interstitial lung disease
- PE

CARDIOVASCULAR
- pericarditis/myocarditis

GI
- lupus peritonitis
- mesenteric artery occlusion

RENAL
- lupus nephritis (diffuse proliferative glomerulonephritis)

OPHTHAMOLOGICAL
- keratoconjunctivitis
- sjogrens syndrome

HAEMATOLOGICAL
- warm autoimmune haemolytic anaemia
- thrombocytopaenia
- antiphospholipid syndrome

OTHER
- mouth + nose ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

SLE
What investigations might you do in someone who you suspect has SLE?

A
  • FBC = anaemia, neutropenia, thrombocytopenia,
  • CRP/ESR = RAISED ESR and NORMAL CRP
  • U&Es - renal function
  • clotting screen = prolonged APTT in antiphospholipid syndrome
  • complement (C3+4) = low in active disease
  • Serum autoantibodies = ANA, anti-dsDNA

to consider
- urinalysis = proteinuria + haematuria in lupus nephritis
- joint x-rays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

SLE
Describe the pharmacological treatment for SLE

A

ACUTE FLARE
- mild = prednisolone + hydroxychloroquine + NSAIDs
- moderate/severe = prednisolone + hydroxychloroquine + immunosuppressant (azathioprine or ciclosporin)
- refractory cases = biologics (rituximab)

MAINTENANCE
- hydroxychloroquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

SYSTEMIC SCLEROSIS
Describe the pathophysiology of scleroderma

A

Various factors cause endothelial lesion and vasculopathy
Excessive collagen deposition –> inflammation and auto-antibody production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

SYSTEMIC SCLEROSIS
what are the features of limited scleroderma?

A

CREST
1. Calcinosis - skin calcium deposits
2. Raynauds
3. Esophageal reflux/stricture
4. Sclerodactyly - thick tight skin on fingers/toes
5. Telangiectasia - dilated facial spider veins
Pulmonary arterial hypertension

  • skin thickening distal to elbows + knees
  • ## raynauds phenomenon often precedes skin changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

SYSTEMIC SCLEROSIS
what are the features of diffuse scleroderma?

A

Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST

  1. Proximal scleroderma
  2. interstitial lung disease
  3. Bowel involvement
  4. hypertension
  5. Renal crisis
  • skin thickening extends proximally, affecting trunk + proximal limbs predominantly
  • raymauds phenomenon occurs before or after skin changes
  • early visceral involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

SYSTEMIC SCLEROSIS
what are the investigations?

A

BLOODS
- FBC = anaemia (microcytic)
- U&Es = may demonstrate renal failure
- CRP + ESR = elevated

ANTIBODIES
- ANA = positive
- anti-centromere = limited systemic sclerosis
- anti-Scl 70 = diffuse systemic sclerosis

to consider
- ECG + echo
- CXR
- pulmonary function tests
- -barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

SYSTEMIC SCLEROSIS
Describe the management of scleroderma

A

SKIN
- emollient
- methotrexate (for skin thickening)
- prednisolone (for pruritus)

RAYNAUDS
- avoid cold + wear gloves
- nifedipine
- topical nitrate (if poor response)
- sildenafil (if ulcers present)

PULMONARY ARTERY HTN
- bosentan

INTERSTITIAL LUNG DISEASE
- cyclophosphamide

RENAL CRISIS
- ACE inhibitor
- dialysis (if required)

GI
- PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

SJOGRENS
What is the pathophysiology of sjögren’s syndrome?

A

T-lymphocyte mediated type 4 hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

SJOGRENS
What investigations might you do in someone who you suspect to have sjögren’s syndrome?

A
  • lip biopsy
  • schirmers test (measure tears produced)
  • antibodies = anti-Ro and anti-La
  • ESR/CRP = elevated

to consider
- occular surface staining
- unstimulated salivary flow rate
- total protein
- MRI
- joint x-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

SJOGRENS
What is the treatment for sjögren’s syndrome?

A
  • Artificial tears, artificial saliva, vaginal lubricants
  • Hydroxychloroquine
  • NSAID
  • M3 agonist - pilocarpine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

DERMATOMYOSITIS
what are the clinical features of dermatomyositis?

A

SYMPTOMS
- symmetrical muscle weakness
- difficulty walking, lifting arms + standing up
- myalgia
- joint pains
- dysphagia
- feeling depressed

SIGNS
- muscle tenderness (around pelvic + pectoral girdle)
- shawl sign (red rash over shoulders, arms + upper back in v-shape)
- heliotrope rash (dusky red rash on hands or face)
- Gottrons papules (red/purple hardened or eroding areas of skin on upper surface of finger joints/knees and elbows)
- periungual telangiectasia (dilated capillaries at skin folds around nail bed
- photosensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

DERMATOMYOSITIS
What investigations might you do in someone who you suspect has dermatomyositis?

A
  • CRP/ESR = raised
  • LFTs = ALT/AST raise
  • TFTs
  • CK, LDH + ANA = raised
  • myositis-specific auto-antibodies = anti-jo 1 and anti-Mi 2
  • electromyogram

to consider
- muscle biopsy
- skin biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

DERMATOMYOSITIS
What is the treatment for dermatomyositis?

A

1st line
- exercise + physio
- sun protective measures

2nd line
- immunosuppressants (methotrexate, azathioprine or cyclophosphamide)
- immunoglobulin therapy
- biologic (rituximab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

SEPTIC ARTHRITIS
what are the causes of septic arthritis?

A
  • staph.aureus = most common in all age groups
  • staph.epidermidis = prosthetic joints
  • strep.pyogenes = children <5yrs
  • n.gonorrhoea = young sexually active
  • pseudomonas aeruginosa = immunosuppressed, elderly + IVDU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

SEPTIC ARTHRITIS
Describe the treatment for septic arthritis

A

ANTIBIOTICS
- IV for 2 weeks followed by oral for 4 weeks
- empirical = flucloxacillin (clindamycin in penicillin allergy)
- suspected MRSA = vancomycin
- gonococcal = cefotaxime or ceftriaxone

SURGERY
- arhtroscopic washout
- srugical debridement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

OSTEOMYELITIS
What organisms can cause osteomyelitis?

A
  1. Staph. aureus = most common
  2. Coagulase negative staph (s. epidermidis)
  3. Aerobic gram negate bacilli (salmonella)
  4. haemophilus influenza
  5. Mycobacterium TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

OSTEOMYELITIS
What bones are likely to be affected by hematogenous seeding in adults?

A

Vertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

OSTEOMYELITIS
What bones are likely to be affected by hematogenous seeding in children?

A

Long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

OSTEOMYELITIS
Why do vertebrae tend to be affected by hematogenous seeding in adults?

A

With age, the vertebrae become more vascular meaning bacterial seeding is more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

OSTEOMYELITIS
Why do long bones tend to be affected by hematogenous seeding in children?

A

In children the metaphysis of long bones has a high but slow blood flow and basement membrane are absent meaning bacteria can move from the blood to bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

OSTEOMYELITIS
what changes to bone might you see histologically in acute osteomyelitis?

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

OSTEOMYELITIS
what changes to bone might you see histologically in chronic osteomyelitis?

A
  1. Necrotic bone - ‘squestra’
  2. New bone formation ‘involucrum’
  3. Neutrophil exudates
  4. Lymphocytes and histiocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

OSTEOMYELITIS
Why does chronic osteomyelitis lead to sequestra and new bone formation?

A
  • Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
  • this causes interruption of periosteum blood supply which results in necrosis and sequestra
  • therefore new bone forms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

OSTEOMYELITIS
Describe the usual treatment for osteomyelitis

A

ACUTE PERIPHERAL OM/ACUTE OM IN PATIENT WITH DIABETIC FOOT
- 1st line = IV flucloxacillin
- if MRSA suspected = vancomycin
- if pseudomonas = piperacillin/tazobactam
- supportive = analgesia, hydration
- 2nd line = surgical debridement

VERTEBRAL OM
- referral to infectious diseases
- if neuro involvement = surgery
- no neuro involvement = vancomycin + ceftriaxone
- supportive = analgesia + hydration

CHRONIC OM
- MDT referral
- consideration for surgery
- optimise contributing co-morbidities
- treat acute flares with IV antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

RHEUMATOID ARTHRITIS
Name 3 risk factors of RA

A
  1. Smoking
  2. Women
  3. family history
  4. Other AI conditions
  5. genetic factors - HLA-DR4 and HLA-DRB1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

RHEUMATOID ARTHRITIS
Describe the pathophysiology of RA

A
  1. Chronic inflammation - B/T cells and neutrophils infiltrate
  2. Proliferation –> pannus formation (synovium grows out and over cartilage)
  3. Pro-inflammatory cytokines –> proteinases –> cartilage destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

RHEUMATOID ARTHRITIS
what are the signs of RA?

A
  1. Symmetrical polyarthorpathy (typically small joints of hands and feet (MCP, PIP, MTP) + progresses to larger joints)
  2. boutonniere deformity (PIP flexion + DIP hyperextension)
  3. swan-neck deformity (PIP hyperextension + DIP flexion)
  4. Z-thumb deformity (hyperextension of thumb IP joint with flexion of MCP joint)
  5. ulnar deviation
  6. rheumatoid nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

RHEUMATOID ARTHRITIS
RA extra-articular involvement: describe the haematological effects

A

Felty’s syndrome (RA + splenomegaly + neutropenia) Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

RHEUMATOID ARTHRITIS
RA extra-articular involvement: describe the effects on the kidney

A

Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

RHEUMATOID ARTHRITIS
What is seen on an X-ray of someone with RA?

A

LESS:

  • Loss of joint space (due to cartilage loss)
  • Erosion
  • Soft tissue swelling
  • Soft bones = osteopenia
  • subluxation
  • periarticular osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

RHEUMATOID ARTHRITIS
Describe the treatment for rheumatoid arthritis

A

PRIMARY CARE
- NSAIDs
- refer to specialist
- physiotherapy + occupational therapy

SECONDARY CARE
- DMARD (methotrexate, sulfasalazine or hydroxychloroquine)
- steroids can be given whilst DMARDs take effect
- biologics (abatacept, rituximab)

MANAGING FLARES
- NSAIDs
- intra-articular steroid injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

GOUT
Give 3 causes of gout

A

= Hyperuricaemia

  1. Impaired excretion - CKD, diuretics, hypertension
  2. Increased production - hyperlipidaemia
  3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

GOUT
Name 3 common precipitants of a gout attack

A
  1. Aggressive introduction of hypouricaemic therapy
  2. Alcohol or shellfish binges
  3. Sepsis, MI, acute severe illness
  4. Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

GOUT
Name 4 diseases that someone with gout might have an increased risk of developing

A
  1. Hypertension
  2. CV disease - e.g. stroke
  3. Renal disease
  4. Type 2 diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

GOUT
How would you treat acute gout?

A

ACUTE FLARE
- 1st line = NSAIDs or colchicine with PPI
- 2nd line = intra-articular steroids

PREVENTION
- 1st line = allopurinol
- 2nd line = febuxostat
- may require colchicine to help cover first couple of weeks as allopurinol + febuxostat can cause gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

PSEUDOGOUT
What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

PSEUDOGOUT
Describe the treatment for pseudogout

A
  • anti-inflammatory = NSAIDs or colchicine
  • corticosteroid = intra-articular steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

PSEUDOGOUT
How can you distinguish OA from pseudogout?

A

Pattern of involvement –> Pseudo = wrists, shoulders, ankle, elbows
Marked inflammatory component –> Elevated CRP and ESR Superimposition of acute attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

PSEUDOGOUT
What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

GOUT
What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

FIBROMYALGIA
Give 3 disease that might be included in the differential diagnosis for fibromyalgia

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

SARCOMA
Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

BONE CANCER
What are secondary bone tumours?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

BONE CANCER
What investigations might you do in someone you suspect has bone cancer?

A

1st line → x-ray
Gold standard → biopsy
Bloods → FBC, ESR, ALP, lactate dehydrogenase, Ca, U+E
CT chest/abdo/pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

BONE CANCER
What might you seen on an X-ray of someone with bone cancer?

A

Onion skin/sunburst appearance = Ewings

Colman’s triangle = osteosarcoma, Ewings, GCT, Osteomyelitis, metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

BONE CANCER
What staging is used for bone cancers?

A

Enneking grading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

BONE CANCER
How are bone cancers treated?

A
MDT management 
Benign 
- NSAIDS
- Bisphosphonates (alendronate) 
- symptomatic help 

Malignancy = surgical excision –> limb sparing/amputation
radio/chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

SARCOMA
Where does Ewings sarcoma arise from?

A

mesenchymal stem cells

90
Q

SARCOMA
Name 3 soft tissue sarcomas

A
  1. Liposarcoma = malignant neoplasm of adipose tissue
  2. Leiomyosarcoma = malignant neoplasm of smooth muscle
  3. Rhabdomyosarcoma = malignant neoplasm of skeletal muscle
91
Q

PHARMACOLOGY
Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
92
Q

PHARMACOLOGY
Give 5 potential side effects of steroids

A
  1. Diabetes
  2. Muscle wasting
  3. Osteoporosis
  4. Fat redistribution
  5. Skin atrophy
  6. Hypertension
  7. Acne
  8. Infection risk
93
Q

PHARMACOLOGY
Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
94
Q

PHARMACOLOGY
Name a TNF blocker

A

InfliximabAdalimumab

95
Q

PHARMACOLOGY
Name a monoclonal antibody that binds to CD20 on B cells

A

Rituximab - binds to CD 20 –> B cell depletion

96
Q

PHARMACOLOGY
Describe the mechanism of action of infliximab

A

Inhibits T cell activation

97
Q

PHARMACOLOGY
Name 2 drugs that act on the HMGcoA pathway

A
  1. Bisphosphonates - alendronate

2. Statins - simvistatin

98
Q

OSTEOARTHRITIS
what are the signs of osteoarthritis?

A

● Deformity and bony enlargement of the joints
● Limited joint movement
● Muscle wasting of surrounding muscle groups
● Crepitus (grafting) due to disruption of normally smooth articulating surfaces of joints
● May be joint effusion
● Heberden’s nodes are bony swellings at DIPJs
● Bouchard’s nodes occur at proximal interphalangeal joints

99
Q

REACTIVE ARTHRITIS
what treatment should be used if reactive arthritis relapses?

A

methotrexate or sulfasalazine

100
Q

SJOGRENS
what are the complications of Sjogren’s syndrome?

A
  • eye infections- oral problems (dental cavities, candida infections)
  • vaginal problems (candidiasis, sexual dysfunction)

RARE

  • pneumonia and bronchiectasis
  • non-hodgkin’s
  • vasculitis
  • renal impairment
  • peripheral neuropathy
101
Q

GIANT CELL ARTERITIS
which arteries are particularly affected by giant cell arteritis?

A
  • aorta and vertebral arteries
  • Cerebral arteries affected in particular e.g. temporal artery
  • Opthalmic artery can also be affected potentially resulting in permanent ortemporary vision loss
102
Q

ANTIPHOSPHOLIPID SYNDROME
what are the risk factors for antiphospholipid syndrome?

A
  • diabetes
  • hypertension
  • obesity
  • female
  • underlying autoimmune condition
  • smoking
  • oestrogen therapy
103
Q

ANTIPHOSPHOLIPID SYNDROME
what is the clinical presentation of antiphospholipid syndrome?

A
  • thrombosis
  • miscarriage
  • livedo reticularis - purple lace rash
  • ischaemic stroke, TIA, MI
  • DVT, budd-chiari syndrome
  • thrombocytopenia
  • valvular heart disease, migraines, epilepsy
104
Q

ANTIPHOSPHOLIPID SYNDROME
what is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding tophospholipid on the surface of cells such as endothelial cells, platelets andmonocytes
  • Once bound, this change alters the functioning of those cells leading tothrombosis and/or miscarriage
  • Antiphospholipid antibodies (aPL) cause CLOTs:
    • Coagulation defect
    • Livedo reticularis - lace-like purplish discolouration of skin
    • Obstetric issues i.e. miscarriage
    • Thrombocytopenia (low platelets)
105
Q

ANTIPHOSPHOLIPID SYNDROME
what is the treatment for antiphospholipid syndrome?

A

PRIMARY PROPHYLAXIS
- low dose aspirin

AFTER VTE EPISODE
- lifelong warfarin
- 1st episode INR = 2-3
- if experience further VTE whilst on warfarin, INR = 3-4

106
Q

GRANULOMATOSIS WITH POLYANGIITIS
what are the complications of granulomatosis with polyangiitis?

A

Glomerulonephritis

107
Q

SARCOMA
what condition is osteosarcoma associated with?

A

Paget’s disease

108
Q

SARCOMA
what is the appearance of osteosarcoma on x-rays?

A

bone destruction and formation,

soft tissue calcification produces a sunburst appearance

109
Q

SARCOMA
what is the clinical presentation of ewing’s sarcoma?

A

● Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

● Painful swelling, redness in surrounding area, malaise, anorexia, weight loss, fever, paralysis and/or incontinence if affecting the spine, numbness in affected limb

110
Q

SARCOMA
which is the most common sarcoma in adults?

A

chondrosarcoma

111
Q

BONE CANCER
which types of malignancy cause bone pain?

A
  • multiple myeloma
  • lymphoma
  • primary bone tumours
  • metastases - secondary bone tumour
112
Q

ANTIPHOSPHOLIPID SYNDROME
what is the prophylactic treatment for antiphospholipid syndrome?

A

aspirin or clopidogrel for people with aPL

113
Q

SYSTEMIC SCLEROSIS
what are the risk factors for scleroderma?

A
  • exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
  • bleomycin
  • genetic
114
Q

POLYMYOSITIS
what is polymyositis?

A

a rare muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres

115
Q

what is the clinical presentation of polymyositis?

A
  • symmetrical progressive muscle weakness and wasting - affects proximal muscles of shoulder and pelvic girdle
  • difficulty squatting, going upstairs, rising from chair and raising hands above head
  • involvement of pharyngeal, laryngeal and respiratory muscles = dysphagia, dysphonia and respiratory failure
  • pain and tenderness = uncommon
116
Q

what is the clinical presentation of dermatomyositis?

A
  • heliotrope (purple) discolouration of eyelids
  • scaly erythematous plaques over knuckles (Gotton’s papules)
  • arthralgia, dysphagia and raynauds
117
Q

what are the investigations for polymyositis/dermatomyositis?

A

Muscle Biopsy

Bloods
- serum creatine kinase, aminotransferases, lactate dehydrogenase (LDH) and aldolase all raised

Immunology
ANA, Anti jo1, anti mi2

118
Q

what is the treatment for polymyositis/dermatomyositis?

A
  • bed rest + exercise plan
  • oral prednisolone
  • steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
  • hydroxychloroquine for skin disease
119
Q

OSTEOPOROSIS
what factors are used in the FRAX score calculation?

A
  • age
  • sex
  • height and weight
  • previous fractures
  • smoking
  • parent fractured hip (FHx)
  • steroid (glucocorticoid use)
  • RA
  • secondary osteoporosis
  • alcohol consumption (>3 units)
  • femoral neck bone mineral density
120
Q

RHEUMATOID ARTHRITIS
what is the diagnostic criteria for RA?

A

RF RISES - >6 weeks and >4 of following:

  • RF positive
  • Finger/hand/wrist involvement
  • Rheumatoid nodules present
  • Involvement of >3 joints
  • Stiffness in morning >1 hr
  • Erosions on x-ray
  • Symmetrical involvement
121
Q

RAYNAUDS
what is the treatment for raynauds phenomenon?

A

Lifestyle - protect the hands, stop smoking

Medications - CCB

122
Q

SYSTEMIC SCLEROSIS
what is limited scleroderma?

A
  • skin involvement limited to hands, face, feet and forearms
  • characteristic ‘beak’-like nose and small mouth
  • Microstomia - small mouth
123
Q

SYSTEMIC SCLEROSIS
what is diffuse scleroderma?

A

skin changes develop more rapidly and are more widespread
Raynaud’s phenomenon coincident with skin involvement
GI, Renal, Lung involvement

124
Q

PAGETS DISEASE
what is paget’s disease?

A

localized disorder of bone remodelling
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

125
Q

PAGETS DISEASE
what are the clinical features of paget’s disease?

A

can be asymptomatic

SYMPTOMS
- bone pain (femur/pelvis, skull)
- facial pain (if skull disease with CN V involvement)
- hearing loss (if skull disease with CN VIII involvement)

SIGNS
- bony deformities (skull bossing, bone bowing, prognathism)
- pathological fracture
- reduced visual acuity (if CN II involvement)
- local temperature rise (due to increased metabolic activity)

126
Q

PAGETS DISEASE
what are the investigations for paget’s disease?

A

plain film x-ray
radionucleotide bone scan
LFTs = raised ALP
bone profile = calcium normal
vitamin D level = normal

to consider
- urinalysis
- bone biopsy

127
Q

PAGETS DISEASE
what is the management for paget’s disease?

A

ASYMPTOMATIC
- observation

SYMPTOMATIC/HIGH RISK
- 1st line = bisphosphonates (alendronic acid or zolendronic acid)
- 2nd line = calcitonin
- supportive measures = education, analgesia, orthoses, walking aids

SEVERE DISEASE
- surgery

128
Q

OSTEOMALACIA
what are the causes of osteomalacia?

A

malnutrition (most common)
vitamin D deficiency
drug induced
defective 1-alpha hydroxylation
Liver disease

129
Q

OSTEOMALACIA
what is the clincial presentation of osteomalacia?

A

SYMPTOMS
- generalised bone pain (rib, hip, pelvis, thigh and foot pain)
- proximal muscle weakness
- difficulty walking upstairs
- fracture (secondary to mild trauma)

SIGNS
- waddling gait
- signs of hypocalcaemia e.g. Chvostek sign
- skeletal deformities

130
Q

OSTEOMALACIA
what are the investigations for Osteomalacia / rickets?

A
  • serum calcium + phosphate
  • serum 25-hydroxyvitamin D
  • PTH level
  • serum ALP
  • renal and liver function

to consider
- plain x-rays (pseudofractures, osteopenia, coarsened trabeculae)
- DEXA scan
- iliac bone biopsy with double tetracycline labelling

131
Q

OSTEOMALACIA
what is the management for osteomalacia/rickets?

A

depends on vitamin D levels

VITAMIN D DEFICIENCY
- loading regimen followed by maintenance dose of vitamin D
- increased oral calcium intake

VITAMIN D INSUFFICIENCY
- only treat if pt has concomitant risk factors
- same as above

ADEQUATE VITAMIN D
- vitamin D supplementation

132
Q

PSOROIATIC ARTHRITIS
what is the diagnostic criteria?

A

CASPAR criteria

  • history of psoriasis (+2)
  • psoriatic nail changes (+1)
  • RF negative (+1)
  • history of dactylitis (+1)
  • radiological evidence = juxta-articular peristitis (+1)

score >2 = positive diagnosis

133
Q

REACTIVE ARTHRITIS
what are the clinical features?

A

SYMPTOMS
- joint pain and swelling
- urethral discharge + dysuria
- painful red eyes
- rash
- rectal discharge

SIGNS
- asymmetrical oligoarthritis (painful joints, affecting <5 joints, most likely to affect knee)
- urethritis +/- epididymo-orchitis or mucopurulent cervicitis
- conjunctivitis
- cutaneous lesions on genitals + feet
- proctitis and/or anal discharge

134
Q

POLYMYALGIA RHEUMATICA
what are the clinical features?

A
  • bilateral shoulder +/- pelvic girdle pain for >2 weeks
  • stiffness lasting >45 mins after walking/resting
  • systemic symptoms (low-grade fever, weight loss, fatigue, depression)
  • bilateral pitting oedema
  • carpal tunnel syndrome
135
Q

BURSITIS
what is the management?

A

1st line
- conservative = rest, ice, compression
- analgesia = paracetamol, ibuprofen

2nd line
- corticosteroid injection

3rd line
- bursectomy

136
Q

COMPARTMENT SYNDROME
what are the clinical features?

A

6Ps of acute ischaemia
- pain
- pallor
- perishingly cold
- pulseless
- parasthesia
- paralysis

  • muscle swelling
137
Q

COMPARTMENT SYNDROME
what are the investigations?

A
  • intracompartmental pressure monitoring
  • serum CK + urinary myoglobin
  • U&Es
  • USS with doppler
138
Q

COMPARTMENT SYNDROME
what is the management of chronic compartment syndrome?

A
  • massage + stretching
  • physio
  • orthotics
  • anti-inflammatories (NSAIDS)
  • surgical fasciotomy
139
Q

PATHOLOGICAL FRACTURE
what are the causes?

A

GLOBAL
- osteoporosis
- CKD-metabolic bone disease
- hyperparathyroidism

FOCAL
- metastatic cancer
- infection
- primary bone tumours
- bone biopsies

140
Q

PATHOLOGICAL FRACTURE
what scoring system can be used?

A

Mirels scoring system - used to guide the need for prophylactic fixation

141
Q

PATHOLOGICAL FRACTURE
what are the clinical features?

A
  • pain without clear causes
  • pain disproportionate to injury
  • increased pain with weight bearing
  • localised tenderness
  • localised swelling
  • abnormal movement
  • bone deformity
142
Q

LOWER LIMB FRACTURES
what are the different types of femur fracture?

A
  • shaft
  • distal

are typically high energy injuries e.g. motorbike crash

143
Q

LOWER LIMB FRACTURES
what are the key features of a patella fracture?

A
  • inability to straight leg raise
  • tenderness of the kneecap
144
Q

LOWER LIMB FRACTURES
what are the most common mechanisms of injury for patella fractures?

A
  • direct blow to knee e.g. dashboard injury
  • rapid contraction of quadriceps against flexed knee
145
Q

LOWER LIMB FRACTURES
what are the different types of tibial fracture?

A
  • segond fracture
  • tibial plateau fracture
  • tibial shaft fracture
  • toddler’s fracture
  • tibial plafond fracture
146
Q

LOWER LIMB FRACTURES
what are the different types of fibula fractures?

A
  • maisonneuve fracture
  • lateral malleolar fracture
147
Q

LOWER LIMB FRACTURES
what is a segond fracture of the tibia?

A
  • small avulsion fracture of lateral tibial plateau
  • caused by internal rotation + varus stress
  • typically caused by sporting injuries
  • associated with ACL injury
148
Q

LOWER LIMB FRACTURE
what are common features of tibial shaft fractures?

A
  • open fractures and compartment syndrome
  • due to lack of fascial compartment + subcutaneous tissues of shin
149
Q

LOWER LIMB FRACTURE
what is a toddlers fracture?

A
  • spiral fracture without injury to fibula
  • stable fracture without displacement
  • requires no intervention other than monitoring
150
Q

LOWER LIMB FRACTURES
what is a maisonneuve fracture of the fibula?

A
  • spiral fracture of proximal fibula associated with ankle instability
  • caused by pronation-external rotation mechanism e.g. stepping off curb awkwardly
151
Q

LOWER LIMB FRACTURE
how are lateral malleolar fractures of the fibula typically sustained?

A

rolling the ankle

152
Q

LOWER LIMB FRACTURES
what are the different types of foot fractures?

A
  • jones fracture
  • lisfranc injury
  • calcaneal fracture
  • talar neck fracture
153
Q

LOWER LIMB FRACTURES
what is a jones fracture of the foot?

A
  • fracture of 5th metatarsal base
  • can be caused by repetitive strain in athletes
154
Q

LOWER LIMB FRACTURES
what is a lisfranc injury of the foot?

A

-tarsometatarsal fracture + dislocation where 1st + 2nd metatarsals articulate with tarsals
- caused by falling from height

155
Q

LOWER LIMB FRACTURE
what is the most commonly fractured tarsal in the foot?

156
Q

LOWER LIMB FRACTURES
what are the clinical features of a hip fracture?

A
  • inability to weight bear
  • shortened + externally rotated leg
157
Q

LOWER LIMB FRACTURES
what is a complication of hip fractures?

A
  • avascular necrosis (most commonly occurring with neck of femur fractures)
158
Q

LOWER LIMB SOFT TISSUE INJURIES
what is the clinical presentation of greater trochanteric pain syndrome?

A
  • gradual onset
  • lateral hip + buttock pain
  • worse with activity, prolonged standing or sitting
  • tenderness over greater trochanter
  • trendelenberg gait
159
Q

LOWER LIMB SOFT TISSUE INJURIES
what are the common investigations?

A
  • x-ray
  • USS
  • MRI
  • arthroscopy (gold standard for meniscal + cruciate ligament ruptures)
160
Q

LOWER LIMB SOFT TISSUE INJURIES
what is the management for lower limb soft tissue injuries?

A

1st line
- RICE (rest, ice, compression, elevation)
- analgesia (paracetamol, ibuprofen)
- physio

2nd line
- surgery

161
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the different types?

A
  • frozen shoulder
  • supraspinatus tendinopathy
  • rotator cuff tear
  • medial epicondylitis (golfers elbow)
  • lateral epicondylitis (tennis elbow)
  • de quervains tenosynovitis
  • dupuytrens contracture
162
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the clinical features of frozen shoulder?

A
  • painful phase followed by stiffness
  • stiffness on active + passive movement, particularly external rotation
  • subsequent thawing to resolution
  • total duration is 1-3 years
163
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the clinical features of supraspinatus tendinopathy?

A
  • positive empty can test
  • painful arc on shoulder abduction between 60-120 degrees
164
Q

UPPER LIMB SOFT TISSUE INJURIES
what muscles make up the rotator cuff?

A
  • supraspinatus
  • infraspinatus
  • teres minor
  • subscapularis
165
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the clinical features of rotator cuff tear?

A
  • shoulder pain + weakness
  • special tests = gerbers lift off, neers and hawkins
166
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the clinical features of medial epicondylitis?

A
  • pain at medial epicondyle
  • radiates down forearm
  • pain on wrist flexion + pronation
  • paraesthesia in ulnar nerve distribution
167
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the clinical presentation of lateral epicondylitis?

A

pain on resisted wrist extension

168
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for frozen shoulder?

A
  • primary
  • secondary to trauma, surgery or reduced mobilisation
169
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for supraspinatus tendinopathy?

A
  • overhead activities compounded by narrowing joint space
170
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for rotator cuff tears?

A
  • trauma
  • repetitive strain
  • associated with overhead activities
  • chronic degeneration
171
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for medial epicondylitis?

A

repetitive use - golfers elbow

172
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for lateral epicondylitis?

A

repetitive use - tennis elbow

173
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the clinical presentation of de quervains tenosynovitis?

A
  • radial wrist pain over radial styoid process
  • pain on resisted thumb abduction
  • finkelsteins test positive
174
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the mechanism of injury for de quervains tenosynovitis?

A

repetitive strain injury

175
Q

UPPER LIMB SOFT TISSUE INJURIES
what are the common investigations?

A
  • x-rays
  • USS
  • MRI
176
Q

UPPER LIMB SOFT TISSUE INJURIES
what is the management of upper limb soft tissue injuries?

A

1st line
- RICE (rest, ice, compression, elevation)
- analgesia (paracetamol, ibuprofen)
- physio

2nd line
- surgery

177
Q

LYME DISEASE
what is it caused by?

A

infection by borrelia burgdorferi from tick bites

178
Q

LYME DISEASE
what are the clinical features of early disease?

A

erythema migrans rash (bulls-eye)

179
Q

LYME DISEASE
what are the clinical features of early disseminated disease?

A
  • multiple bulls eye rashes
  • weakness of facial muscles (CN VII palsy)
180
Q

LYME DISEASE
what are the clinical features of late disease?

A
  • arthritis (oligoarthritis with synovitis)
  • unilateral discolouration of extensor surfaces (acrodermatitis chronica atrophicans)
181
Q

LYME DISEASE
what are the investigations?

A
  • clinical diagnosis if presenting with erythema migrans (bulls eye rash)

without rash
- ELISA antibodies to borrelia burgdorferi
- immunoblot test

182
Q

LYME DISEASE
what is the management?

A

1st line
- doxycycline BD for 21 days
- if unsuitable, use amoxicillin instead

2nd line
- if not managed by 1st antibiotics a second course of antibiotics is considered

183
Q

SYSTEMIC SCLEROSIS
what are the different types?

A
  • limited systemic sclerosis = anti-centromere antibodies
  • diffuse systemic sclerosis = anti-Scl 70 antibodies
184
Q

SYSTEMIC SCLEROSIS
what are the general clinical features?

A

DERMATOLOGICAL
- sclerodactyly (prayer sign)
- skin tightening + fibrosis
- digital ulcers
- calcinosis (lumpy calcium deposits)
- telangiectasia
- perioral furrowing (skin wrinkling around mouth)
- beaked nose
- microstomia (tightening skin around mouth)

CARDIOVASCULAR
- raynauds
- hypertension

RESPIRATORY
- interstitial lung disease
- pulmonary hypertension

GI
- oesophageal dysmotility

RENAL
- renal crisis (acute renal failure with hypertension)

185
Q

SJOGRENS
what are the risk factors?

A
  • age (40-60)
  • female sex
  • family history
  • concurrent autoimmune conditions (RA, SLE, scleroderma and primary biliary cholangitis)
186
Q

SEPTIC ARTHRITIS
what is the diagnostic criteria?

A

Kocher criteria
- non-weight bearing = 1
- temp >38.5 = 1
- ESR > 40mm/hr = 1
- WCC >12x10 9/L = 1

score of 2 = 40% probability
score of 3 = 93% probability

187
Q

OSTEOMALACIA
what are the risk factors?

A
  • limited exposure to sunlight
  • dark skin
  • dietary vitamin D deficiency (fish, cheese, eggs)
  • CKD
  • liver dysfunction
  • malabsorption (IBD)
  • anticonvulsant use (phenytoin, carbamazepine + phenobarbital use)
188
Q

UPPER LIMB FRACTURES
what are the features of a Colle’s fracture?

A
  • transverse fracture of radius
  • 1 inch proximal to radio-carpal joint
  • dorsal displacement + angulation
189
Q

UPPER LIMB FRACTURES
how is the deformity described in a Colle’s fracture?

A

dinner fork type deformity

190
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for a Smith’s fracture?

A

falling backwards onto the palm of outstretched hand or falling with wrists flexed (reverse Colle’s)

191
Q

UPPER LIMB FRACTURES
what are the features of Smith’s fracture?

A

volar angulation of distal radius fragment

192
Q

UPPER LIMB FRACTURES
how is the deformity described in Smith’s fracture?

A

garden spade deformity

193
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for Bennett’s fracture?

A
  • impact on flexed metacarpal, caused by fist fights
194
Q

UPPER LIMB FRACTURES
what are the features of Bennett’s fracture?

A
  • intra-articular fracture at the base of the thumb metacarpal
    (triangle fragment at the base of metacarpal)
195
Q

UPPER LIMB FRACTURES
how is the deformity described in Bennett’s fracture

A

triangular fragment at base of metacarpal on x-ray

196
Q

BACK PAIN
what is the management of mechanical back pain?

A

CONSERVATIVE
- reassurance + patient education
- regular exercise +/- physio

MEDICAL
- 1st line = NSAIDs (IBUPROFEN) +/- PPI
- 2nd line = codeine +/- paracetamol
- 3rd line = benzodiazepines (DIAZEPAM) if maximum 5 days for muscle spasm)

do not use opioids or antidepressants for low back pain

197
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for a Monteggia’s fracture?

A

fall onto outstretched hand with forced pronation

198
Q

UPPER LIMB FRACTURES
what are the features of a Monteggia’s fracture?

A
  • dislocation of proximal radioulnar joint in association with ulnar fracture
199
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for Galeazzi fractures?

A

fall onto the hand with rotational force superimposed

200
Q

UPPER LIMB FRACTURES
what are the features of a Galeazzi fracture?

A
  • radial shaft fracture with dislocation of distal radioulnar joint
  • bruising over lower forearm
201
Q

UPPER LIMB FRACTURES
what is a barton’s fracture?

A

distal radius fracture (Colles/Smiths) with associated radiocarpal dislocation

202
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for a Barton’s fracture?

A

fall onto extended and pronated wrist

203
Q

UPPER LIMB FRACTURES
what is the most common carpal fracture?

A

scaphoid fractures

204
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for a scaphoid fracture?

A

fall onto outstretched hand

205
Q

UPPER LIMB FRACTURES
what are the clinical features of a scaphoid fracture?

A

swelling + tenderness in anatomical snuffbox
pain on wrist movements + longitudinal compression of thumb

206
Q

UPPER LIMB FRACTURES
what imaging is required for a scaphoid fracture?

A

ulnar deviation AP x-ray

207
Q

UPPER LIMB FRACTURES
what is the mechanism of injury for a radial head fracture?

A

fall onto outstretched hand

208
Q

UPPER LIMB FRACTURES
what are the clinical features of a radial head fracture?

A
  • tenderness at head of radius
  • impaired movement at elbow
  • sharp pain at lateral side of elbow at extremes of rotation (supination + pronation)
209
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for Segond fracture of tibia?

A

internal rotation + varus stress (sporting injuries)

210
Q

LOWER LIMB FRACTURE
what are tibial plateau fractures?

A
  • periarticular injuries of proximal tibia
  • divided into 6 types based on Schatzker classification
211
Q

LOWER LIMB FRACTURES
what is the mechanism of injury for tibial plateau injuries?

A

varus or valgus injuries causing medial or lateral involvement respectively

212
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for tibial shaft fractures?

A

direct blows, falls or indirectly (through twisting motions)

213
Q

LOWER LIMB FRACTURE
what is a tibial plafond fracture?

A

fracture of distal tibia
often presents with severe ankle pain + inability to weight bear

214
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for a tibial plafond fracture?

A

high energy axial load (e.g. fall from height or car crash)
talus is driven into plafond causing #

215
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for a maisonneuve fracture?

A
  • caused by pronation-external rotation mechanism e.g. stepping off curb awkwardly
216
Q

LOWER LIMB FRACTURE
what is the classification system for lateral malleolar fractures?

A

Weber classification

type A = # distal to syndesmosis
type B = # at level of syndesmosis
type C = # proximal to syndesmosis

217
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for Jone’s fracture?

A
  • inversion injury to foot
  • repetitive stress or overuse (e.g. in athletes)
218
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for a Lisfranc injury?

A

axial load applied to hyperplantarflexed foot (e.g. falling from a height)

219
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for a calcaneal fracture?

A

traumatic axial loading (e.g. falling from a height)

to heel bone

220
Q

LOWER LIMB FRACTURE
what is the mechanism of injury for a talar neck fracture?

A

forced dorsiflexion with axial loading (carries high risk of avascular necrosis)