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3a > Paeds MSK/Rhem > Flashcards

Paeds MSK/Rhem Flashcards

1
Q

Define DDH

A

Structural abnormality in the hips leading to instability and potential for subluxation or dislocation

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2
Q

What are the 6 RF for DDH

A
  • First degree Fx
  • Female
  • Breech presentation
  • High birth weight
  • Oligohydramnios
  • Prematurity
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3
Q

When is DDH screened for ?

A

-Neonatal examination at birth and at 6-8 weeks

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4
Q

What findings on a NIPE may suggest DDH?

A
  • Different leg lengths
  • Restricted hip abduction on one side
  • Significant bilateral restriction in abduction
  • Difference in the knee level when hips are flexed
  • Clunking of the hips on special tests
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5
Q

What are the 2 special tests to look for DDH?

A
  • Ortolani test

- Barlow test

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6
Q

What is the ortolani test ?

A
  • Looks for DDH
  • With the hips and knees flexed, gentle pressure is used to abduct the hips and apply pressure behind the legs to see if the hips will dislocate anteriorly
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7
Q

What is the barlow test ?

A
  • Looks for DDH
  • Gentle downward pressure is placed on the knees through the femur to see if the femoral head with dislocate posteriorly.
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8
Q

What is the diagnostic test for DDH?

A

-USS

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9
Q

How is DDH managed if presents at <6 mnths ?

A
  • Pavlik harness
  • Keeps the baby’s hips flexed and abducted.
  • Usually on for 6-8 weeks.
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10
Q

How is DDH managed if presents >6 mnths or if harness fails?

A
  • Surgery

- After surgery an hip spica cast is used to immobilise the hips

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11
Q

Define osteogenesis imperfecta

A

-Genetic condition resulting in brittle bones that are prone to fracture

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12
Q

What causes osteogensis imperfecta ?

A
  • Genetic mutations that affect the formation of collagen

- 8 different genetic abnormalities with varying severities

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13
Q

How does osteogenesis imperfecta present ?

A
  • Recurrent and inappropriate fractures
  • Hyper-mobility
  • Blue/grey sclera
  • Triangular face
  • Short stature
  • Deafness from early childhood
  • Dental problems
  • Bone deformities : esp bowed legs and scoliosis
  • Joint and bone pain
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14
Q

How is osteogenesis imperfecta diagnosed ?

A
  • Usually clinical

- X-ray used in fractures and for bone deformitis

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15
Q

How is osteogenesis imperfecta managed ?

A
  • Bisphosphonates to increased bone density (e.g. alendronate)
  • Vit D supplementation to prevent deficiency
  • Physio and occupational therapy
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16
Q

Define rickets

A

-Defective bone mineralisation causing ‘soft’ and deformed bones

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17
Q

What 2 vitamin deficiencies cause rickets ?

A
  • Vitamin D

- Calcium

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18
Q

What are the sources of vitamin D?

A
  • Sunlight

- Eggs, oily fish or forified cereals

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19
Q

What are the sources of calcium ?

A
  • Dairy productes

- Green vegetables

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20
Q

What is a rare form of rickets?

A
  • Hereditary hypophosphataemic rickets
  • Genetic defect causing low phosphate
  • Most common : X-linked dominant
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21
Q

What are the potential symptoms of rickets ?

A
  • Lethargy
  • Bone pain
  • Swollen wrists ! widening of joint space
  • Bone deformity
  • Poor growth
  • Dental problems ! no teeth development
  • Muscle weakness
  • Pathological or abnormal fractures
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22
Q

What 5 bone deformities can occur in rickets?

A
  • Bowing of the legs
  • Knock knees
  • Rachitic rosary : ribs expand at the costochondral junctions causing lumps along the chest
  • Craniotabes : soft skull with delayed closure of sutures and frontal bossing
  • Delayed teeth
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23
Q

What are the RF for rickets ?

A

Anything that increases the risk of vit d deficiency

  • Darker skin
  • Low exposure to sunlight
  • Live in colder climates
  • Spend majority of their time indoors
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24
Q

What are the 5 common blood results in rickets ?

A
  • Serum 25-hydroxyvitamin D of less than 25 nmol/L
  • Calcium : low
  • Phosphate : low
  • Alkaline phosphatase : high
  • Parathyroid hormone : high
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25
Q

What investigation is required to diagnose rickets ?

A
  • X ray

- May show joint widening and osteopenia (more radiolucent bones)

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26
Q

How is rickets prevented ?

A
  • Breastfeeding women should taken vitamin D supplements (10 micrograms per day)
  • Formula fed babies are at lower risk as it is fortified with vitamin D
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27
Q

How is rickets managed ?

A
  • Vitamin D (ergocalciferol) : 6mnths to 12 yrs is 6,000 IU per day for 8-12 wks
  • Calcium supplementation
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28
Q

Explain the pathophysiology behind rickets

A
  • Low vitamin D
  • This leads to malabsorption of calcium and phosphate
  • Low calcium and phosphate leads to defective bone mineralisation
  • Low calcium leads to secondary hyperparathyroidism
  • Increased parathyroid hormone leads to increased calcium reabsorption from bone and further issues with bone mineralisation
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29
Q

What is transient synovitis ?

A

-Temporary irritation and inflammation in the synovial membrane of the joint

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30
Q

What age group is transient synovitis most common in ?

A

3-10 years

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31
Q

How does transient synovitis present ?

A
  • Usually occurs within a few weeks of a viral illness
  • Limp
  • Refusal to weight bear
  • Groin or hip pain
  • Mild low grade temperature
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32
Q

What is a serious differential in a child with joint pain and fever ?

A

-Septic arthritis

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33
Q

How is transient synovitis managed ?

A
  • Simple analgesia

- Safety net to attend A&E if symptoms worsen or they develop a fever !

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34
Q

Define septic arthritis

A

-Infection inside a joint

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35
Q

when is septic arthritis most common ?

A

<4 yrs of age

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36
Q

How does septic arthritis usually present ?

A
  • Single joint
  • Rapid onset : hot red swollen painful joint
  • Refusing to weight bear
  • Stiffness and reduced range of motion
  • Systemic Sx : fever, lethargy, sepsis
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37
Q

What is the most common bacterial cause of septic arthritis ?

A

-Staph aureus

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38
Q

What 4 other bacteria can cause septic arthritis ?

A
  • Neisseria gonorrhoea (sexually active teenagers)
  • Group A strep
  • Haemophilus influenza
  • E.coli
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39
Q

Give 4 other differential diagnosis for septic arthritis

A
  • Transient synovitis
  • Perthes
  • Slipped upper femoral epiphysis
  • JIA
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40
Q

How is septic arthritis managed ?

A
  • Joint aspiration for gram staining, crystal microscopy, culture and Abx sensitivities.
  • Empirical IV abx
  • Sugical drainage and washout where necessary
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41
Q

What is perthes disease?

A
  • Idiopathic, avascular necrosis of the femoral head due to disruption of blood flow
  • Affecting the epiphysis of the femur
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42
Q

At what age does perthes most commonly occur?

A
  • Boys aged 5-8

- Can occur between 4-12 yrs

43
Q

How does perthes disease present?

A

-Slow onset of : pain in the hip or groin, limp, restricted hip movements and possible referred pain to knee

44
Q

How is perthes diagnosed ?

A
  • X ray
  • Technetium bone scan or MRI if sx persist
45
Q

How is perthes managed ?

A
  • <6 = conservative
  • Older : surgical management
46
Q

What is the main complication of perthes?

A
  • Soft and deformed femoral head leading to early hip osteoarthritis
  • this is due to the revascularisation and neovascularisation that occurs over time
47
Q

What is a slipped upper femoral epiphysis (SUFE) ?

A

-Where the head of the femur is displaced along the growth plate

48
Q

Who is SUFE more likely to occur in ?

A
  • Boys (8-15 with an average age of 12)

- Obese children

49
Q

What is the typical exam q for SUFE?

A
  • Usually in an adolescent obese male going through a growth spurt
  • Hx of mild trauma causing symptom onset -> pain is usually disproportionate to the trauma
50
Q

How does SUFE present ?

A
  • Hip, groin, thigh or knee pain
  • Restricted range of hip movement
  • Painful limp
  • Restricted movement in the hip : particularly restricted internal rotation
51
Q

On examination, what movement will be restricted in SUFE?

A
  • > Internal rotation

- > They will prefer external rotation

52
Q

How is SUFE diagnosed ?

A

X-ray !
Plain X-ray of BOTH hips (AP and frog-leg views)
Both hips as its bilateral in 20% of cases

53
Q

How is SUFE managed ?

A

-Surgery

54
Q

What is osteomyelitis ?

A

-Infection in the bone and bone marrow, typically in the metaphysis of long bone

55
Q

What bacteria is the most common cause of osteomyelitis ?

A

-Staph aureus

56
Q

Give 5 risk factors for osteomyelitis

A
  • Male
  • <10 yrs
  • Open bone fracture
  • Orthopaedic surgery

-Sickle cell anaemia : salmonella

57
Q

What is chronic osteomyelitis ?

A

-Deep seated, slow growing infection with more subtle features

58
Q

How with acute osteomyelitis present ?

A
  • Fever
  • Refusing to use the limb or weight bear
  • Pain
  • Swelling
  • Tenderness
59
Q

How is osteomyelitis investigated ?

A

-MRI
-Blood culture
- Bone marrow aspiration or bone biopsy if necessary

60
Q

How is osteomyelitis managed ?

A
  • Antibiotics

- May require drainage and debridement

61
Q

What is an osteosarcoma and where does it most commonly affect ?

A
  • Bone cancer
  • Femur = most common
  • Tibia and humerus also commonly affected
62
Q

What age group are usually affected with osteosarcomas ?

A

10-20 yrs

63
Q

How does an osteosarcoma present ?

A
  • Persistent bone pain
  • Bone pain worse at night and may wake from sleep
  • Bone swelling
  • Palpable mass
  • Restricted joint movement
64
Q

How is an osteosarcoma diagnosed ?

A

-Urgent direct access xray within 48 hrs

65
Q

What would an xray show in an osteosarcoma ?

A
  • Poorly defined lesion in the bone with destruction of the normal bone and a ‘fluffy’ appearance
  • Periosteal reaction = ‘sun-burst’ appearance due to irritation of the lining of the bone.
66
Q

What may be raised in blood tests in an osteosarcoma ?

A

-Raised alkaline phosphatase (ALP)

67
Q

What is the main complication of an osteosarcoma ?

A
  • Pathological bone fractures and metastasis

- Surgical resection also often leads to limb amputation

68
Q

What is Talipes ?

A
  • Clubfoot : fixed abnormal ankle position

- Fixed abnormal ankle position presenting at birth

69
Q

What is talipes equinovarus ?

A

-Ankle in plantar flexion and supination

70
Q

What is talipes calcaneovalgus ?

A

-Ankle in dorsifelxion and pronation

71
Q

How is clubfoot managed ?

A

-Ponseti method

72
Q

What is the ponseti method ?

A
  • Used to treat club foot
  • The foot is manipulated towards a normal position and a cast used to hold it in position. This is repeated until the foot is in the correct position
  • A brace is then used to hold the feet in the correct position when not walking until around 4 yrs of age
73
Q

What is positional talipes ?

A
  • The ankle is in a plantar flexion and supination position but is not fixed
  • The muscles around the ankle are tight but the boney structure is not affected
  • Managed using physio
74
Q

What is achondroplasia ?

A
  • Most common common cause of disproportionate short stature (dwarfism)
  • It is a type of skeletal dysplasia
75
Q

What is the cause of achondroplasia?

A

-Genetic mutations in the FGFR3 gene (fibroblast growth factor receptor 3) on chromosome 4 leading to abnormal function of the epiphyseal plates.

76
Q

What kind of genetic inheritance leads to achondroplasia ?

A
  • Autosommal dominant -> heterozygous

- > Homozygous gene mutations are fatal in the neonatal period

77
Q

What are the main features of achondroplasia ?

A
  • Average height of 4 feet
  • Short digits
  • Bow legs
  • Disproportionate skull
  • Foramen magnum stenosis
  • Frontal bossing
78
Q

Give 6 associations with achondroplasia

A
  • Recurrent otitis media
  • Kyphoscoliosis
  • Spinal stenosis
  • Obstructive sleep apnoea
  • Obesity
  • Cervical cord compression and hydrocephalus as a result of foramen magnum stenosis
79
Q

What is osgood-schlatters disease?

A

Inflammation at the tibial tuberosity where the patella ligament inserts leading to anterior knee pain in adolescents

80
Q

When does osgood-schlatters typically occur?

A
  • 10 to 15 yrs old

- More common in males

81
Q

How does osgood-schlatters present ?

A

Gradual onset :

  • Pain at the anterior aspect of the knee
  • Pain exacerbated by physical activity, kneeling and extension of the knee
  • Visible or palpable heard and tender lump at the tibial tuberosity
82
Q

How is Osgood-Schlatters managed ?

A
  • Reduction in physical activity
  • Ice
  • NSAIDs
  • Once symptoms have settled : stretching and physio
83
Q

What is a rare complication of Osgood-Schlatters?

A

-Full avulsion fracture where the tibial tuberosity is separated from the rest of the tibia

84
Q

Explain the pathophysiology behind Osgood-Schlatters

A
  • Stress from running, jumping etc + growth in the epiphyseal plate results in inflammation on the tibial epiphyseal plate
  • Multiple small avulsion fractures occur, where the patella ligament pulls away tiny pieces of bone
  • This leads to growth of the tibial tuberosity = visible lump
  • This lump is tender due to inflammation but as the bone heals it becomes hard and non-tender
85
Q

What is kawasaki disease ?

A

Systemic medium-sized vessel vasculitis

86
Q

Who does kawasaki disease typically affect?

A
  • Children <5 yrs
  • Asian children (japanese or korean)
  • Boys
87
Q

What is a key complication of kawasaki disease ?

A

-Coronary artery aneurysm

88
Q

What are the key features of kawasaki disease ?

A

CRASH AND BURN

  • C : conjunctivitis (bilateral)
  • R : rash (widespread erythematous maculopapular)
  • A : adenopathy (cervical & usually unilateral)
  • S : strawberry tongue and cracked lips
  • H : hands (desquamation)

-BURN : high fever >5 days

89
Q

Give 3 investigation results usually seen in kawasaki disease

A
  • FBC : anaemia, leukocytosis and thrombocytosis
  • LFTS : hypoalbuminaemia and elevated liver enzymes
  • Raised ESR
90
Q

How is kawasaki disease managed ?

A
  • High dose aspirin
  • IV immunoglobulins
  • Echo
91
Q

What is a risk of using aspirin in children ?

A

-Reye’s syndrome

92
Q

What is rheumatic fever ?

A
  • Autoimmune condition caused by group A beta-haemolytic streptococcal (typically streptococcus pyogenes causing tonsilitis).
  • The antibodies to target the bacteria also target antigens on the cells of the person’s body (e.g. myocardium of the heart)
  • Leads to type 2 hypersensitivity reaction where the immune system begins attacking cells through the body.
93
Q

What is the diagnostic criteria for rheumatic fever

A
  • Evidence of strep infection + two major criteria or 1 major and 2 minor
  • Major :
    • J : Joint arthritis
    • O : Organ inflammation (e.g. carditis)
    • N : Nodules
    • E : Erythema marginatum rash
    • S : Sydenham chorea
  • Minor :
    • F : Fever
    • E : ECG changes(prolonged PR interval) without carditis
    • A : Arthralgia without arthritis
    • R : Raised inflammatory markers
94
Q

What should be given for tonsilitis caused by streptococcus to prevent rheumatic fever ?

A

-Phenoxymethylpenicillin (penicillin V) for 10 days

95
Q

What is Ehlers-Danlos syndrome ?

A
  • Autosommal dominant

- Defect in collagen, resulting in hyper-mobility causing joint pain and soft and stretchy skin

96
Q

What score is used to assess hypermobility on EDS

A

-Beighton score : palms flat on floor, elbows, knees, thumb and little finger hyperextend

97
Q

What is a common cardiac involvement of EDS?

A
  • Aortic regurgitation

- Postural Orthostartic tachycardia Syndrome

98
Q

What is Henoch-Schonlein Purpura ?

A

-IgA vasculitis affecting the skin, kidneys and GI tract

99
Q

What can tigger Henoch-Schonlein purpura and what are the 4 common features ?

A
  • URTI or gastroenteritis
  • Common in <10 yrs
  • Purpura
  • Joint pain
  • Abdo pain : can lead to GI haemorrhage, intussusception and bowel infarction
  • IgA nephritis : haematuria and proteinuria !
100
Q

What would be a common exam presentation in henoch-scholein purpura

A

-8 yr old, recent gastroenteritis. Purpura starting on legs and speading to buttock. Arthralgia in knees and ankles. Abdo pain. Haematuria and proteinuria on dipstick.

101
Q

What would be a common exam presentation in henoch-scholein purpura

A

-8 yr old, recent gastroenteritis. Purpura starting on legs and speading to buttock. Arthralgia in knees and ankles. Abdo pain. Haematuria and proteinuria on dipstick.

102
Q

Give 4 non infective causes of a fever lasting >5 days in a child

A
  • Stills Disease
  • Leukaemia
  • Rheumatic fever
  • Kawasaki
103
Q

How does systemic JIA present ?

A
  • Subtle salmon-pink rash
  • Joint pain
  • High swinging fevers
104
Q

What medications can be used to treat JIA?

A
  • NSAIDs
  • Steorid injections
  • DMARDS (e.g methotraxate, sulfasalazine)
  • Biologics : adalimumab, infliximab

3a (45 decks)

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