Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RCPCH TAS/ AKP > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is the treatment for hip congenital hip dysplasia and what is the risk?

A

Pavlik harness - keeps hip flexed and abducted
Risk = avascular necrosis to head of femur

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

What is Perthes Disease?

A

Avascular necrosis of the femoral head –> revascularisation over 18-36m
More common boys 4-8y

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

What is Osgood-Schlatter?

A

Avascular necrosis of the tibial tuberosity

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

What is slipped upper epiphysis?

A

Displacement of the epiphysis of femoral head postero-inferiorly
More in obese teenage boys

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

Features of transient synovitis

A

2-12y
Often associated with recent / intercurrent viral illness
Sudden onset hip / knee (referred) pain
Otherwise well

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

Genetics and presentation of osteogenesis imperfecta

A
  • Dominant / recessive
  • Mutation COL1A1 or 2 –> abnormalities in production in alpha chain of Type 1 collagen –> bone fragility and low bone mass
  • Presentation: bowing frequent fractures, hypermobility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of Rickets

A

Vitamin D Deficiency (1,25-dihydrocholecalciferol deficiency)
Phosphate deficiency (low calcium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Presentation of Rickets

A

Bowed limbs
Metaphyseal swelling
Bone pain / miserable
Gross motor delay, delayed growth
Hypotonia, weakness
Bossed forehead
Delayed dentition
X-ray: cupping, splaying, fraying. General osteopenia

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

Rickets Biochemistry

A
  • Low Vit D
  • High PTH
  • High Alk Phos
  • Calcium / Phosphate normal or low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is osteopetrosis and how does it present?

A

Failure of bone resorption –> brittle
Faltering growth
Recurrent infection
Hypocalcaemia
Anaemia, thrombocytopenia

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

Common organisms for septic arthritis

A
  1. Staph. aureus
  2. Group A strep
  3. Gram negative bacilli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Common infections preceding reactive arthritis

A

Salmonella
Shigella
Campylobacter
STIs
Strep
Mycoplasma
Lyme’s

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

Extra-articular features of JIA

A

Anterior uveitis
Leg length discrepency
Rheumatoid nodues in RF +ve
Low grade fever - polyarthritis

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

Define oligoarticular JIA

A

4 or fewer joints in the 1st 6 months of disease. Commonly larger joints eg knees, ankles, elbows. Usually presents 2-4y.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Difference between extended oligoarthritis and polyarthritis

A

Extended oligoarthritis = Asymmetrical large and small
Polyarthritis = Symmetrical large and small (often fingers)

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

Features of systemic arthritis (Still’s disease)

A

Oligo / poly
Acute illness
Malaise, anorexia, weight loss
Daily fever >2w
Salmon pink rash (worse with fevers)
Hepatosplenomegaly
Serositis
Raised inflammatory markers, low Hb
More in young girls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of systemic onset JIA

A

IV Methylprednisolone

18
Q

Features of psoriatic arthritis

A

Asymmetric large and small
Dactylysis
Nail pitting
Psoriasis
+/- ant. uveitis
FHx

19
Q

Features of enthositis related arthritis

A

HLA B27 +ve
Lower limb large joints
Milder spine
Tendon / ligament inflammation

20
Q

What is macrophage activation syndrome and how does it present?

A

10% children with systemic JIA
Life threatening
Excessive activation and expansion of T cells and macrophages
- Presents: Continuous fever, low leukocytes / platelets –> multiple organ failure

21
Q

Presentation of juvenile onset SLE

A

Usually teens. Need 4 of:
Rash - malar, discoid
Photosensitivity
Mouth ulcers
Arthritis
Serositis - pleural, pericarditis
Renal disease - proteinuria, casts
Neuro-psych disorders - psychosis, seizures
Low Hb / Plt / WCC
Positive for: Anti-DNA, anti-Smith, antiphospholipid Ab, ANA

22
Q

Antibodies that may be present in SLE

A

Anti-Ro
Anti-La
Anti-dsDNA (most specific!)
Anti-Sm
Anti-RNP
ANA

23
Q

Treatment for SLE

A

Supportive, avoid sun
Analgesia
ACEi for HTN / proteinuria
Steroids
DMARDs - hydroxychloraquin, cylophosphamide (AI suppression)

24
Q

Why might children with SLE require life-long prophylactic ABx?

A

Can get vasculitis –> splenic infarction –> immunodeficiency

25
Q

Presentation of jeuvenile dermatomyositis

A

Teens - AI
Erythematous rash + 2 of:
-Symmetrical weakness of prox muscles
- Periorbital swelling / discolouration
- Grotton’s papules - scaly rash of PIP/ MIPs
- Increased muscle enzyme: CK, AST, LDH
- EMG changes
- Biopsy - necrosis + inflammation
- MRI changes - diffuse white

Also may get lung disease, oligoarthritis

26
Q

Presentation of Duchenne Muscular Dystrophy

A

More commonly boys. Progressive muscle degeneration.
Around 5y
Waddling gait
Gower’s sign (weak limb girdle)
Enlarged calves
Language delay
Slower, climbs stairs 1 by 1
Raised CK
Beyond ant. horn, no fasiculations

27
Q

Inheritance pattern of Duchenne Muscular dystrophy

A

X-linked recessive deletion of dystrophin gene (Xp21)

28
Q

Inheritance of myotonic dystrophy

A

Autosomal Dominant
Expanding CTG trinucleotide repeats on Ch 19 –> anticipation

29
Q

Presentation of myotonic dystrophy

A

Congenital - severe. Hypotonia, feeding difficulty, resp. distress

Later onset - hypotonia, myopathic face, GDD.

Later complications - DM, cataracts, cardiac involvement

30
Q

Common sites for osteomyelitis and most common organism

A

Distal femur
Proximal tibia
Organism: Staph. Aureus

31
Q

Presentation of HSP (small vessel vasculitis)

A
  1. Abdominal pain
  2. Arthritis
  3. Non-thrombotic palpable purpura occur over buttocks and legs.
    May follow URTI.
    +/- intussusception
    = IgA immune complex deposition in smaller vessels
32
Q

Diagnostic criteria of Kawasaki (medium vasculitis)

A

Fever >38 for 5 days or more, + 4 of:
- Erythema / cacking lips and oral mucosa
- Bilateral non-purulent conjunctivitis
- Rash (diffuse, maculopapular, erythematous
- Erythema and oedema of hands / feet –> desquamation and peeling
- Cervical LN >1.5cm

33
Q

Major complication of Kawasaki

A

MI and coronary artery aneurysm

34
Q

Treatment for Kawasaki

A

IV Ig
High dose aspirin
Antiplatelet
Some may need steroid / immunosuppression

35
Q

Describe Erb’s palsy

A
  • Injury C5 and C6 roots.
  • Motor: shoulder abduction and forearm flexion “waiter’s tip” deficit
  • Sensory deficits – reduced sensation over posterior lateral aspect of arm, thumb, index finger (digital branches of medial nerve).
36
Q

Describe presentation C7/8 injury

A

‘Ulnar claw’ – difficultly extending at elbow and wrist. Sensory – posterior and medial aspects of the arm.

37
Q

Which antibody is most associated with Polyarticular JIA?

A

Rheumatoid factor

38
Q

Which antibody is most associated with Oligoarticular JIA?

A

ANA

39
Q

Antibody associated with Sjogren’s syndrome

A

Anti-Ro

40
Q

What is present in the urine in Rhabdomyolisis?

A

Myoglobin

41
Q

Which fracture is most associated with NAI?

A

Metaphyseal fracture
Caused by shearing forces
“corner” or bucket handle” fractures

RCPCH TAS/ AKP (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions