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MRCPCH Clinicals > MSK And Other > Flashcards

MSK And Other Flashcards

1
Q

How does ulnar nerve palsy present?

A

Sensory - medial 1 1/2 fingers

Motor - claw hand, sparing of the air eminence

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2
Q

How does median nerve palsy present?

A

Sensory - thumb and lateral fingers

Motor - unable to bring thumb and lateral fingers in

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3
Q

How does radial nerve palsy present?

A

Sensory - anatomical snuffbox

Motor - wrist drop

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4
Q

How does Erbs palsy present?

A

C5/6 nerve injury

90% completely recover within a year

Asymmetrical Moro
Elbow extension, forearm pronation, wrist flexion

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5
Q

What is Klumpke’s paralysis?

A

C8/T1 injury

Claw hand
can be associated with Horner syndrome

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6
Q

How does hyper mobility present?

A

Arthralgia - strengthen muscles around joint, footwear and posture

Delayed walking and clumsiness

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7
Q

How does Ehlers-Danlos present?

A

Paper like scars
Skin hyper-elasticity
Joint hyper-elasticity

Classical - severe, associated with PPROM and preterm delivery
Vascular - fragile blood vessels

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8
Q

How does polyarticular JIA present?

A

> 5 joints within 6 months

RF -ve

  • 25% ANA positive
  • if you get, worse outcome

RF +ve

  • 75% ANA positive
  • symmetrical, typically hands and feet
  • 50% destructive
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9
Q

How does oligoarticular JIA present?

A

Most common
Typically large joints, swollen +/- pain

ANA positivity correlates with chronic uveitis

Good improvement with methotrexate and infliximab
Most resolve within 6 months, some have a relapse within first year or become polyarticular

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10
Q

How does systemic onset JIA present?

A

Fever >6 weeks
Macular, salmon pink non pruritic rash - worse with heat

Polyarticular loss, anorexia
Lymphadenopathy, hepatosplenomegaly
Pericarditis, pleural effusions
Anaemia, leukocytosis, thrombocytosis

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11
Q

How is JIA managed?

A

Pharmacological

  • NSAIDS + omeprazole
  • intra-articular steroids
  • systemic steroids
  • DMARDs - methotrexate
  • monoclonal antibodies

Non pharmacological

  • PT/OT
  • hydrotherapy, splints
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12
Q

How is psoriatic arthritis diagnosed?

A

Chronic inflammatory arthritis <16yrs followed by psoriasis within 15yrs

Dactyl it is
Nail pitting
Rash
FH

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13
Q

How does dermatomyositis present?

A

Muscle weakness - proximal shoulder and limb girdle

Lethargy

Rash - purple over eyes lids and cheeks, also extensors

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14
Q

What are signs of rickets?

A 
Delayed dentition, dental caries
Delayed closure of anterior fontanelle
Bow legs
Swelling of epiphyses of wrists and ankles
Long bone curving
Pathological #
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15
Q

What foot deformities can be seen?

A

Toe walking - normal until 3. CP, DMD, leg length discrepancy, ASD

Flat feet - resolves around 6

Intoeing

Foot drop

Talipes - parental PT, casting

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16
Q

How is HSP managed?

A

Urine dip - haematuria +/- proteinuria
Blood pressure
FBC/U&E/clotting

NSAID only if normal renal function
Severe abdo pain, arthritis - consider PO pred

If HTN, macroscopic haematuria or proteinuria - weight, height, BP, PCR, throat swab, bloods

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17
Q

How is HSP monitored?

A

Initial weekly urine dip
Review at 3 months and 6 months with BP

Discuss with nephrologist if:

  • hypertension
  • abnormal renal function
  • nephritic syndrome: haematuria, proteinuria, oedema, HTN, renal impairment, oliguria
  • nephrotic syndrome: urine PCR raised, low plasma urine
  • macroscopic haematuria for >5 days
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18
Q

How does HSP present?

A

Skin

  • erythematous, macular —> purpuric rash over extensors and buttocks
  • can be associated with oedema

GI

  • abdo pain
  • D+V, bloody stools, upper GI haemorrhage
  • can be associated with intussusception

Articular
- arthralgia, no effusions

Renal

  • haematuria, proteinuria
  • nephrotic syndrome
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19
Q

How does ITP present?

A

Autoimmune - triggered by viral illness

Petechia and purpura with falling platelet count

Usually self limiting and benign - might need IVIG if severe disease. Can be associated with ICH

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20
Q

What are clinical features of anaemia?

A

Jaundiced

Koilonychia

Pallor of nail beds and mucus membranes

Flow murmur

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21
Q

What causes anaemia?

A

Defective production/maturation

  • iron deficiency
  • chronic disease, decreased erythropoietin production
  • prematurity
  • vitamin B12/folate deficiency
  • marrow failure: aplastic anaemia, infiltration, drugs

Loss of red cells

  • menstruation
  • NSAIDs
  • IBD
  • CMPA

Excessive destruction
- haemolytic anaemia

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22
Q

How does hereditary spherocytosis present?

A

Northern European
Pallor
Jaundice
Splenomegaly or splenectomy/cholecystectomy scar

Pigmented gallstones

FBC shows raised reticulocytes and spherocytes

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23
Q

How is hereditary spherocytosis managed?

A

Folic acid

May require splenectomy - then pneumococcal, meningococcal and HiB vaccinations

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24
Q

What clinical findings are seen in thalassaemia?

A

Mild jaundice and pallor
Palpable spleen
Can have hypopigmented papules on abdomen from SC desferrioxamine

Extramedullary haemopoiesis

  • frontal bossing
  • malar hyperplasia
  • hepatosplenomegaly
  • long bone #
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25
Q

How is thalassaemia managed?

A

Transfuse >100
Chelation therapy to remove iron - given as 8-12hr SC infusion
Folic acid
Bone marrow transplant

Can have problems with growth and puberty, liver cirrhosis and cardiac problems

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26
Q

What clinical findings are seen with sickle cell disease?

A

Mild jaundice and pallor
?cholecystectomy scar
Infant splenomegaly, none palpable in older children

Acutely

  • infection
  • dehydration
  • chest sequestration
  • abdominal enlarged spleen
  • joints dactylitis
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27
Q

How is sickle cell managed?

A

Asymptomatic until 5-6 months - HbF to HbA

Chronic anaemia - only transfused if chronic pain
May require hydroxyurea

Jaundice - raised unconjugated bilirubin

Aplastic crisis - typically secondary to parvovirus

Acute painful crises - dactylitis, abdo pain, bone pain
Tx: warmth, hydration, oxygen, analgesia

Splenic sequestration - rapid enlargement, blood pools in spleen and causes circulatory collapse
Tx: blood transfusion

Functional asplenia - secondary to autosplenectomy (multiple infarcts), at risk of infection from encapsulated organisms
Tx: full immunisation and Pen V

Acute chest syndrome: acute resp illness with new chest x-ray findings, drop in Hb, pain
Tx: abx, oxygen, transfusion

Stroke: exchange transfusion, annual screening of transcranial Doppler

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28
Q

What is haemophilia A?

A

Reduced factor VIII

Raised APTT, otherwise normal clotting

May have severe bruising at birth/post imms
Otherwise when crawling - typically bleeding into joints (haemarthroses)
Joint swollen and warm - may cause degenerative changes or fixed joint

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29
Q

How is haemophilia managed?

A

Mild - vasopressin (releases endogenous factor VIII)
Tranexamic acid
Avoid NSAIDs

Recombinant factor VIII - can develop inhibitors

PT

30
Q

What is haemophilia B?

A

Low factor IX

31
Q

What is Von Willebrand disease?

A

Carrier protein to protect factor VII from enzymes and mediate platelet adhesions

nosebleed and easy bruising
Tx: vasopressin and tranexamic acid

32
Q

How is eczema treated?

A 
EDUCATION (application of emollients/recognition of infection)
Avoid allergens and exacerbating factors
Nail care - keep short
Emollients (E45, cetraben)
Topical steroids (hydrocortisone, eumovate, betnovate, dermovate)
Tacrolimus
Occlusive bandaging
PTx
Antibiotics/antivirals
33
Q

How does psoriasis present?

A

Well demarcated, red plaques over extensor surfaces

34
Q

How do infantile haemangiomas present?

A

Appear at 1-2 months
Rapid expansion in first year, then stationary for another year and then slowly involute.
50% gone at 5yrs, 90% gone at 9yrs

Complications: ulceration, infection, haemorrhage
May interfere with vision, urination or airway
Can involve liver and be fatal in untreated

Tx: propranolol, corticosteroids, laser therapy

Kasabach Merrit syndrome - enlarging haemangioma causing platelet, clotting factor and red cell consumption

35
Q

How does generalised lipodystrophy present?

A

Tall, advanced skeletal maturation, prominent muscles, cliteromegaly/penilemegaly
Acanthosis nigricans, hirsutism, hepatomegaly, insulin resistant diabetes

Can cause systemic symptoms: renal, cardiac, neuro, seizures, developmental delay, hyperinsulinaemia/hypertriglyceridaemia

36
Q

What causes molluscum contagiosum?

A

Poxvirus

Most resolve within 18 months

37
Q

How does ichthyosis present?

A

Dry, thickened skin
Can present at birth as a collodion baby

Complications: corneal dystrophy, infection, faltering growth

Treat with emollients, PO retinoids, abx

38
Q

How does ectodermal dysplasia present?

A

Usually X-linked

Unable to sweat - can lead to hyperthermia

Nails: thick, fragile, dysmorphic
Skin: dry, atrophic, wrinkled
Hair: sparse
Facies: thick lips, saddle nose, frontal bossing, maxillary hypoplasia, cleft lip/palate
Eye: dry, corneal ulcers
Teeth: early use of prosthesis
Mucosa: dry mouth, thick nasal secretions

Can lead to recurrent chest infections, otitis media and dysphagia

Faltering growth

39
Q

How does epidermolysis bullosa present?

A

Development of vesicles, bullae or erosions in response to trauma

Varies in severity
Can cause oesophageal strictures, anaemia, secondary infection, joint contractions, skin cancer

40
Q

What causes erythema multiforme?

A

Infection: herpes simplex, mycoplasma, EBV

Infiltration: leukaemia, lymphoma

Inflammation: SLE

Iatrogenic: penicillin, NSAIDS

Can have mucosal involvement

41
Q

What is Stevens-Johnson syndrome?

A

Prodromal illness

Severe erosion of >2 mucosal surfaces

Can lead to high fluid loss

If >30% involvement is TEN

42
Q

How are preterm babies plotted on growth charts?

A

If 32-36+6 plot on preterm bit

Then plot with cGA until 1yr if >32 or 2yrs if <32

43
Q

How do you calculate mid parental height?

A

(Dad’s height + mum’s height) / 2
+/- 7cm

Should be within 8.5cm

44
Q

What is the normal pattern of growth of children?

A

Infancy - nutrition
Childhood - GH + IGF-1
Puberty - sex steroids

Catch-up growth - infants born IUGR/SGA who catch up centiles, usually happens by 4yrs

Catch-down growth - infants born LGA who fall through the centiles and then follow a lower centile

45
Q

What is constitutional delay in growth/puberty and what needs to be ruled out?

A

Slowed height velocity just before puberty therefore crosses down centiles

Check when parents went through puberty
Ix may show low LH/FSH and young bone age

Check no chronic disease/endocrine condition
Rule out Turners

46
Q

What is precocious puberty?

A

Breast development <8yrs
Testicular volume 4ml <9yrs

May be tall for familial height

47
Q

What causes delayed bone age?

A 
High cortisol
Emotional deprivation
Delayed puberty (low androgens/oestrogen)
Poor nutrition
GH deficiency
Chronic disease
Turner syndrome
Constitutional delay
48
Q

What causes advanced bone age?

A

Increased androgens/oestrogen (precocious puberty)
Hyperthyroidism
Sotos syndrome (cerebral gigantism)
Weaver syndrome

49
Q

What are causes of tall stature?

A

Familial
Obesity

Syndromes:
Marfan
Homocystinuria
Sotos
Kleinfelters
Beckwith-Wiedemann

Endocrine:
Hyperthyroidism
Precocious puberty - brain tumour, CAH, adrenal tumour
GH excess

50
Q

What examination findings are seen in Marfan?

A

Tall for family size (but one parent may have it)

Hands - arachnodactyly (ask to encircle little finger and thumb around wrist), thumb adducts across palm

Head - long, thin face, high arched palate, dental crowding
- lens dislocation, up and in

Chest - pectus excavatum/carinatum

  • aortic root dilation (diastolic murmur)
  • mitral valve prolapse (late systolic murmur at apex)

Back - scoliosis/kyphosis

Hands to floor
Pes planus

51
Q

How is Marfans managed?

A

Yearly echo to assess aortic root dimensions
Opthalmology
Regular BP

52
Q

How does homocystinuria present?

A 
Similar to Marfan but 
Joint contracture
Ruddy complexion
IQ affected
Osteoporosis
No cardiac involvement
Thromboembolic risk
53
Q

How does Klinefelter present?

A 
Male XXY
Tall
Small testes
Delayed puberty
Poor facial/pubic hair growth
Low IQ
Breast cancer risk
54
Q

How does XYY present?

A

Tall
Normal IQ
Behavioural problems

55
Q

How does Sotos present?

A

Born LGA with macrocephaly

Face - hypertelorism, prominent forehead and chin
Large hands/feet/ears/nose/genitalia

Hypotonia +/- dyspraxia

Normal final adult height

56
Q

What are causes of short stature?

A

Familial short stature
Constitutional delay of growth and puberty

IUGR –> chronic disease process

Endocrine

  • GH deficiency
  • hypothyroidism
  • Cushing syndrome

Syndrome

  • Turner
  • Noonan
  • Russell-Silver
  • Prader-Willi
  • Cornelia de Lange

Skeletal dysplasia

  • achondroplasia
  • hypochondroplasia

Emotional deprivation/neglect

57
Q

How is GH deficiency diagnosed?

A

Midfacial hypoplasia
Excess subcutaneous fat

Check IGF-1 level

Insulin tolerance test - give a dose of insulin and then measure GH levels every 15 mins

58
Q

What are indications for GH treatment?

A

GH deficiency

Turner

SHOX deficiency

Prader-Willi

Chronic renal insufficiency

SGA without catchup at 4yrs

59
Q

What are side effects of GH treatment?

A

SC injection
Given every day

Lipoatrophy/hypertrophy
Transient headache
Oedema
Hypothyroidism
Scoliosis - in patients who were always going to develop it
Arthralgia
SUFE
Insulin resistance - if diabetic
60
Q

How does Turners present?

A

Short stature - plot growth on specific chart

ARMS

  • oedema of hands
  • hypoplastic nails
  • short 4th/5th metacarpal
  • wide carrying angle

HEAD/NECK

  • recurrent otitis media
  • webbed neck
  • high arched palate

CHEST

  • wide spaced nipples
  • Coarc, bicuspid aortic valve, aortic dissection
  • ?breast development

ABDOMEN

  • primary amenorrhoea, delayed puberty, streak ovaries
  • hyperlipidaemia
  • T2DM
  • HTN
61
Q

What screening is done in Turner syndrome?

A 
Cardiac screen
GH replacement
Oestrogen/progesterone replacement
Educational needs
Audiology
HTN
Coeliac
62
Q

How does Noonan present?

A

Short stature

HANDS
- cubitus valgus

FACE

  • hypertelorism
  • epicathic folds
  • ptosis
  • micrognathia
  • low set eaars
  • deep philtrum

ABDO

  • hernia
  • crypto-orchidm
63
Q

How does Russell-Silver present?

A

Short stature
Normal head circumference - but looks big

ARMS

  • hemi-hypertrophy
  • clinodactyly
  • camptodactyly (fixed flexion)

HEAD

  • small, triangular face with micrognathia
  • blue sclerae
  • prominent nasal bridge and downturned mouth

ABDO

  • hypospadius/undescended testes
  • feeding difficulties
64
Q

How does mucopolysaccharidoses present?

A

Short stature

ARMS
- carpal tunnel

HEAD

  • coarse facial features (thick lips, frontal bossing, broad nose)
  • cornea ?clouding
  • cherry red spot
  • nasal discharge and upper airway obstruction

CHEST
- congestive heart failure

ABDO

  • umbilical hernia
  • hepatosplenomegaly

OTHER

  • joint stiffness
  • kyphosis/scoliosis
  • developmental examination
65
Q

What are types of MPS?

A

Hunters - no corneal clouding, GDD
Hurlers - corneal clouding, GDD
Morquio - corneal clouding, normal intelligence
Sanfillipo - less physical but severe GDD

66
Q

How does achondroplasia present?

A

Short stature - has specific growth chart

LIMBS

  • short, broad hands with trident appearance
  • ligamental laxity
  • rhizomelic limb shortening
  • tibial bowing
  • evidence of spinal cord compression

FACE

  • frontal bossing
  • flat nasal bridge
  • large head
  • chronic otitis media
  • dental malocclusion

CHEST

  • pulmonary hypertension secondary to recurrent sleep apnoea
  • spirometry - reduced lung capacity
67
Q

What causes cushingoid appearance?

A

ACTH dependent

  • Cushing’s disease (pituitary tumour causing ACTH release)
  • ectopic ACTH releasing tumour

ACTH independent

  • excess steroids
  • adrenal tumour
  • McCune Albright syndrome
68
Q

How is a cushingoid child examined?

A

Small stature - plot on height/weight chart
Features - moon face, thin skin with striae, hump back
?Cause of steroid requirement

HANDS

  • check BP - may be raised
  • proximal myopathy
  • axillary hair

FACE

  • facial features
  • acne

ABDO
- scars from abdominal surgery

TO COMPLETE

  • pubertal stages
  • fundoscopy: pituitary tumour causing papilloedema
  • full examine of system causing disease
69
Q

How to examine thyroid?

A

GENERAL
- cachexic/overweight

HANDS

  • tremor (hyper)
  • cool/warm peripheries
  • pulse rate and rhythm
  • clubbing
  • measure BP
  • proximal myopathy
  • REFLEXES (slow in hypo)

HEAD

  • exophthalmos/ptosis
  • ophthalmoplegia
  • lid oedema/lag
NECK
Inspection
- goitre
- if scar ?hoarse voicce
- take a drink, thyroid moves up
stick tongue out - thyroglossal cyst moves up
- examine tongue for thyroglossal cyst

Palpation

  • stand behind, size, shape, consistency
  • drink
  • lymphadenopathy

Percussion
- sternum for retrosternal extension

Auscultation
- mass for bruit

TO COMPLETE

  • plot growth
  • stage puberty
  • euthyroid/hyper/hypo
  • other signs of autoimmunity
70
Q

What are thyroid symptoms?

A 
Energy levels
School performance
Heat/cold intolerance
Sweatiness
Constipation/diarrhoea
Appetite, weight loss/gain
Muscle weakness
71
Q

Causes of goitre?

A

Autoimmune thyroiditis - Hashimoto
Graves
Simple - normal function
Hyperplasia - iodine deficiency

Diffuse nodular - thyroiditis, carcinoma, Langerhan’s cell histiocytosis

If euthyroid - don’t treat, check antibodies

72
Q

What causes neck lumps?

A

Infection

  • reactive after oral infection can last months
  • TB/EBV/CMV/Bartonella/toxoplasmosis

Infiltration

  • thyroid malignancy
  • sternomastoid tumour
  • goitre

Idiopathic

  • thyroglossal cyst
  • haemangioma
  • branchial cyst

MRCPCH Clinicals (5 decks)

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