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Paediatrics > Rheumatology and endocrinology > Flashcards

Rheumatology and endocrinology Flashcards

1
Q

What are the main treatments for inflammation?

A

Steroids - lots of S/E
Methotrexate
Biologics
- TNF inhibitors - etanercept, infliximab, adalimumab
Other biologic agents - rituximab, tocilizumab

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2
Q

What is juvenile idiopathic arthritis?

A

Onset before 16th birthday
No identifiable underlying cause - actively rule out other conditions
Persistent joint swelling (or painful restriction of movement) lasting at least 6 weeks

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3
Q

How is JIA diagnosed?

A

Blood
XR
History
Examination

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4
Q

What is the aim with JIA diagnosis?

A

Catch it early to prevent bony erosions of joint - these are irreversible and only treatment at this stage is joint replacement

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5
Q

What are the different types of JIA?

A 
Oligoarticular - persistent/extended
Polyarticular - RhF negative/positive
Enthesitis
Psoriatic arthrits
Systemic arthritis
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6
Q

How does JIA present?

A 
Persistent swelling
Joint stiffness in morning
Loss of ROM
Pain
Joint deformity
Warmth
Colour change
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7
Q

What is oligoarticular JIA?

A

= 4 joint
Often affects joints in lower limb
Examine from side and back as well as front
Persistent and extended

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8
Q

What is polyarticular JIA?

A

> 4 joints
Typically small joints
Occurs much more rapidly than oligoarticular

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9
Q

Why might children with JIA have growth abnormalities such as being taller on one side than the other?

A

Increased blood flow to areas of inflammation taking more GH to those areas - causes increased growth to areas of inflammation

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10
Q

What is a common complication of JIA?

A

Chronic anterior uveitis

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11
Q

What is chronic anterior uveitis?

A

Inflammation of uvea
Often a silent condition in children - no redness/pain
National screening programme every 3 months in those with JIA diagnosis with ophthalmologist

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12
Q

What is the problem with chronic anterior uveitis?

A

Can cause blindness

Can develop before arthritis and asymptomatic

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13
Q

What is psoriatic arthritis?

A

Psoriasis and arthritis together
Can appear at different points
Often runs in families

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14
Q

How is psoriatic arthritis diagnosed?

A

2 of

  • First degree relative with psoriatic arthritis
  • Pitting nails
  • Dactylitis (single inflamed digit)
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15
Q

What is enthesitis related arthritis?

A

Like ankylosing spondylitis
Inflammation of enthesitis
Presents with plantar fasciitis and inflammation of sacroiliac joints

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16
Q

What are the symptoms of systemic arthritis?

A

Spiking daily fever
Rash - typically appears with fever
Lymphadenopathy
Hepatosplenomegaly
Serousitis - pericardial effusions, pleural effusions, ascites
Related to IL-6
Associated mortality to biologics first-line treatment

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17
Q

What is pGALS?

A

MSK screening examination for school age children - must be able to follow commands

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18
Q

What are the sections of pGALS?

A

Gait
Arms
Legs
Spine

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19
Q

What do you ask the patient to do in the gait section of pGALS?

A

Observe walking normally
On tiptoe
On heels

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20
Q

What do you ask the patient to do in the arms section of pGALS?

A

Spread fingers wide - highlights swelling
Finger tuck - assesses ROM
Thumb to little finger
Squeeze metatarsal heads
Prayer sign 90, painful if synovitis
Hands to ceiling and look up - neck extension first to go in JIA
Hands behind head

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21
Q

What do you ask the patient to do in the legs section of pGALS?

A

Patella tap, cross-fluctuance better
Heel should touch bum - bend knee
Flex hip to 90 without fully flexing knee
Internal rotation of hip v painful in groin if hip disease present

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22
Q

What do you ask the patient to do in the spine section of pGALS?

A 
Tilt head to side
Reach for sky (already done)
Observe for scoliosis
Confirm scoliosis on forward flexion
Observe degree of lumbar flexion
3-finger jaw opening
Jaw affected in up to 60% of all JIA patients at diagnosis
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23
Q

What is the normal range for fasting plasma glucose?

A

3.5-5.6 mmol/l

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24
Q

What is the normal range for post-prandial plasma glucose?

A

< 7.8 mmol/l

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25
Q

What test might you do for diabetes?

A

Oral glucose tolerance test

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26
Q

What fasting glucose is the definition of diabetes?

A

> 7.0 mmol/l

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27
Q

What post OGTT glucose level is the definition of diabetes?

A

> 11.1 mmol/l

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28
Q

What HbA1c is the definition of diabetes?

A

> 6.5%

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29
Q

What fasting glucose suggests impaired glucose tolerance/pre-diabetes?

A

< 7.0 mmol/l

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30
Q

What post-OGTT glucose level suggests impaired glucose tolerance/pre-diabetes?

A

> 7.8 but < 11.0 mmol/l

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31
Q

What HbA1c indicated impaired glucose tolerance/pre-diabetes?

A

5.7-6.4%

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32
Q

What HbA1c is normal?

A

4-5.6%

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33
Q

How common is diabetes in children?

A 
Prevalence 1/700-1000
22,000 under 17
97% T1DM
1.5% T2DM
1.5% rarer type
Very underdiagnosed
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34
Q

How is T1DM inherited?

A 
If mother has it 2% risk
If father has it 8% risk
Both parents 30% risk
Sibling 10% risk
DZ twin 15% risk
MZ twin 40% risk
Fathers transmit T1 to offspring 2-3x more than mothers
Mothers who develop diabetes before 8 transmit at same rate as diabetic fathers
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35
Q

What genes are involved in T1DM?

A

Around 20 identified
HLADR3
HLADR4

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36
Q

How is T2DM inherited?

A

Higher risk of transmission than T1
If either parent has T2 then 15% increase in risk
If both - 75% increase in risk
If non-identical twin has diabetes 10% increased risk
If identical twin has T2 then 90% increased risk

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37
Q

How does diabetic ketoacidosis occur?

A

Insulin deficiency and glucagon excess
Increase in blood ketones and blood glucose
Increase in blood ketones leads to vomiting and acidosis and increase in blood ketones and glucose leads to osmotic diuresis
Osmotic diuresis and vomiting lead to fluid and electrolyte depletion
Acidosis leads to cellular dysfunction
Acidosis and fluid and electrolyte depletion leads to cerebral oedema
Fluid and electrolyte depletion will lead to shock

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38
Q

How is DKA managed?

A 
Fluids
Insulin
Monitor glucose hourly
Monitor electrolytes especially K+ and ketones 2 hourly
Very strict fluid balance hourly
Hourly neuro obs
New diagnosis bloods
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39
Q

What are the different categories of symptoms of hypoglycaemia?

A

Autonomic

Neuroglycopenia

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40
Q

What autonomic symptoms of hypoglycaemia might you get?

A 
Irritable
Hungry
Nauseous
Shakey
Anxious
Sweaty
Palpitations
Pallor
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41
Q

What neuroglycopenia symptoms of hypoglycaemia might you get?

A 
Dizzy
Headache
Confused
Drowsy
Visual problems
Hearing loss
Problems concentrating
Slurred speech
Odd behaviour
LOC
Convulsions
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42
Q

How do you manage mild hypoglycaemia?

A

Check blood glucose
3-5 glucose tablets
100-200ml fizzy drink (not diet) or juice
60-100mls lucozade
Wait 10 mins - if no improvement repeat
Follow up with longer acting carb (bread/biscuit)
Check BG in 15 mins

43
Q

How do you manage moderate hypoglycaemia?

A 
As for mild if possible
Too unwell 0.5-1 tube glucogel
Wait 10 mins if no improvement repeat
Follow up with longer acting carb (bread/biscuit)
Check BG in 15 mins
44
Q

How do you treat severe hypoglycaemia?

A 
NBM
Glucagon s/c or IM injection
- If < 5 = 0.5mg
- If > 5 = 1mg
Wait 10 mins, when conscious give sugar
45
Q

What is important to remember when treated hypoglycaemia?

A 
Individual symptomatology
Avoid fat
Think of cause
Does insulin need adjusting
Hypo phenomena
- Unawareness
- Rebound
46
Q

What is it important to educate families on with diabetes treated?

A 
Injections
Choice of device
BG monitoring
Altering insulin
Hypoglycaemia
Sick day rules
Dietary guidance
Carbohydrate counting
Advice on exercise
Frequent early contact - 24 hr
- Novice to expert
- Honeymoon period
47
Q

What is important in diabetes management?

A 
Support
Education
MDT input
Liaison with school
Contact details of PDSNs
Frequent OPA
Diabetes UK/local groups
48
Q

Who is it important to provide education to in management of diabetes?

A 
Child
Family
Carers
School
At education clinics
Child to adult - taking control of their diabetes
49
Q

What are the aims of diabetes management?

A

Normal growth and development
As normal a childhood as possible
Transition with optimal HbA1c to help prevent complications
Avoidance of XS or severe hypos

50
Q

What medical issues for paeds are prevalent in diabetes management?

A

Growth
Puberty
Transition of autonomy

51
Q

What is the morbidity and mortality of diabetes like?

A

Life expectancy reduced by 23 years
2-3x increase likelihood of early death - dead in bed syndrome
DKA 10x bigger killer than hypos
30-40% develop microalbuminuria
25% require laser treatment for retinopathy
Complications worse for paediatric T2

52
Q

How is paediatric diabetes monitored?

A

HbA1c - 3 month profile
BG log book
AI screen
Glucose monitoring aim 4-7

53
Q

What is it important to educate on other than insulin use?

A

Alcohol
Contraception
Knowledge - exercise, sick day rules

54
Q

What do you need to examine in a diabetic check up?

A 
Eyes
Urine
Feet
BP
Injection sites
55
Q

What fluids should you give in DKA?

A 
Normal maintenance fluids + correct deficit
Correct over 48 hours
Assume 5% deficit if pH 7.2-7.29
Assume 7% deficit if pH 7.1-7.19
Assume 10% deficit if pH < 7.1
56
Q

What are the complications of DKA?

A 
Cerebral oedema
Shock
Hypokalaemia
Aspiration - vomiting
Thrombus
57
Q

Which symptoms come first in hypoglycaemia?

A

Autonomic

58
Q

What is the long term management of diabetes?

A

Basal bolus insulin
Diet - carbohydrate counting
- Insulin to carbohydrate ratio 1 unit for every 15g
- Correction factor 1 unit to bring blood glucose down by 8 for BG of 6
Daily education from nurses and dieticians

59
Q

What might indicate fragile bones in children?

A

Repeated fractures

60
Q

What might cause bent bones in children?

A

Previous fracture

Under-mineralised

61
Q

What might cause short bones in children?

A

Fractures
Under-mineralised
Dysplasia

62
Q

What bone diseases do we see in children?

A

Fragile bones
Bent bones
Short bones
Dense bones

63
Q

When are fractures more common?

A

Boys most likely to have fractures
Peak in boys 14-15
Peak in girls 11-12
Peaks correspond with peak growth velocity
In first year of life, equally likely to have fractures - look out for NAI

64
Q

Why might boys be more likely to have fractures?

A

Boys bone weak and fragile?
Boys clumsy?
Take more risks
Higher growth rates predispose to fracture
Bone architecture puts them at increased risk of fracture

65
Q

What is the definition of osteoporosis?

A

Disease characterised by low bone mass and michroarchitectural deterioration of bone tissue, leading to enhanced bone fragility and consequent increase in fracture risk

66
Q

What is the definition of osteoporosis in children?

A

1 or more vertebral crush fracture
OR
Size-adjusted bone density < -2.0 SDS plus either
- 2 or more long bone fractures by age 10
- 2 or more long bone fractures by age 19

67
Q

What are the inherited/congenital causes of osteoporosis in children?

A

Osteogenesis imperfecta
Inborn errors eg galactosemia
Haematological problems
Idiopathic

68
Q

What are the acquired causes of osteoporosis in children?

A 
Drug induced - especially steroids
Major endocrinopathies
Malabsorption
Immobilisation
Inflammation
69
Q

How common is osteogenesis imperfecta?

A

Prevalence 1 in 16,000

70
Q

How is osteogenesis imperfecta inherited?

A

Autosomal dominant in 85-90%

Mostly caused by defects in T1 collagen genes

71
Q

What are the S&S of osteogenesis imperfecta?

A 
Bone fragility
Fractures
Deformity
Brittle bones
Bone pain
Impaired mobility - ligamentous laxity, sarcopenia
Poor growth
Deafness
Hernias
Valvular prolapse
When very severe may be death in early life or pre-birth
72
Q

How is osteogenesis imperfecta classified?

A

Sillence classification

73
Q

What are the different types of osteogenesis imperfecta?

A

I - mild
II - lethal
III - progressively deforming, severe
IV - moderate

74
Q

How is osteogenesis imperfecta managed?

A

MDT

  • Physician - bone targeted drugs (bisphosphonates, complications), pain, associated medical problems
  • Surgeon - long bones, spine, skull base, hearing, teeth
  • Therapists, nurses - muscle strength/mobility, social, education
75
Q

What do bisphosphonates seem to do for osteogenesis imperfecta?

A 
Increased bone mass
Reduction in fracture frequency
Increased vertebral height
Reduced pain
Suppressed bone markers
Increased overall mobility
No adverse effect on growth
76
Q

What is osteogenesis imperfecta?

A

Group of rare diseases affecting bone tissue and characterised by extremely fragile bones that break or fracture easily often without apparent cause

77
Q

What causes rickets?

A

Vitamin D deficiency

Lack of sunlight and poor nutrition

78
Q

What does vitamin D do?

A

Makes calcium available - increases calcium absorption from gut and release from bone
Maternal vitamin D influences bone size and mass in childhood
Roles in immune function/tolerance

79
Q

What happens if you have maternal vitamin D deficiency and exclusive breast feeding?

A

Low vitamin D stores in newborn
Severe life-threatening cardiomyopathy, hypocalcaemia convulsions
Severe clinically apparent rickets eg metaphyseal swelling, bony deformity
Moderate radiological or biochemical changes

80
Q

What can cause rickets?

A

Maternal vitamin D deficiency
Lack of exposure to sunlight
Lack of vitamin D in diet
Prolonged unsupplemented breast feeding

81
Q

What children are most likely to get rickets?

A

Refugee children from muslim backgrounds - maternal vitamin D deficiency, poor diet
African families

82
Q

How is rickets diagnosed?

A

Hx and examination

Tests - biochemistry, XRs

83
Q

How does rickets present?

A 
Metaphyseal swelling
Bowing deformities
Slowing of linear growth
Motor milestones delay due to bone weakness
Hypotonia
Fractures
Respiratory distress
84
Q

Should mothers take vitamin D during pregnancy?

A

Yes

85
Q

What is rickets?

A

Failure to mineralise new bone

Very weak bones

86
Q

What biological disturbances might you get in rickets?

A

Low PO4 (fasting)
Serum Ca variable
Raised serum alkaline phosphatase
Raised PTH, low 25OH-D

87
Q

How is rickets treated?

A

Treat underlying problem
Vit D deficiency cause hypocalcaemia - vit D and calcium (possibly give IV)
Vit D deficiency causing rickets - vit D (+/- calcium) - increasing dose with age/size

88
Q

What does a high TSH in the heel prick test suggest?

A

Congenital hypothyroidism

89
Q

What are the symptoms of congenital hypothyroidism?

A 
Prolonged jaundice
Sleeping longer/more often than usual
Off feeds
Large fontanel
Constipation
Large, swollen tongue
Low muscle tine
Swelling around eyes
Poor/slow growth
Cool, pale skin
Large belly with navel sticking out
Often asymptomatic when presents
90
Q

What is pGALS useful for?

A 
Fever
Limp
Motor milestone delay
Clumsy
Chronic disease with joint problems - IBD/HSP
91
Q

What are the 3 questions you ask before pGALS?

A

Do you have any pains in any muscles of joints?
Do you have any problems getting dressed in the morning?
Do you have any trouble getting up or down the stairs?

92
Q

What common conditions might you pick up in pGALS?

A 
JIA
Hypermobility
Marfans/connective tissue disorder
Scoliosis
Henoch scholen purpura
Psoriatic arthritis
Isolated joint infection/septic arthrits
93
Q

What positive findings might you see in a pGALS?

A 
Dactylitis
Tendon inflammation
Scoliosis
Knock-knees
Leg length discrepancy
94
Q

What are the implications for a child with JIA?

A 
Daily medical treatment
Special education
Social services
Limitations in daily activities
Development
Feeding
Speech
Surgery needs
Separation/hospitalisation
95
Q

What are the implications for parents and family with a child with JIA?

A

Mourning - despair, denial, guilt, anger/blame, acceptance
Shame
Rejection and anger at child
Whole set of extra tasks
Responsibilities and worries
Demands can take over family life
Impact of financial security and interfamily relationships

96
Q

Who is part of the paediatric rheumatology team?

A 
Nurse specialists
Psychology
Parents and family
Daycare team
Physiotherapy
OT
School
Pharmacy
GP
Family support groups
Social worker
Adolescent and adult rheumatology consultant
Transition team
Paediatric and adolescent rheumatology consultant
Other specialities
Ophthalmology consultant
97
Q

What are the aims of JIA treatment?

A

Induce remission - intraarticular steroids
Maintain remission - methotrexate
Escalation therapy - era of biologics

98
Q

What health risk behaviours might you get in adolescents with chronic illness?

A

Experimental behaviour - hallmark of adolescence, necessary in cognitive development
Ill young people more likely to engage in risks
Related to non-adherence

99
Q

What biological effect might chronic illness have on a child?

A

Delayed growth/puberty

100
Q

What psychological effect might chronic illness have on a child?

A

Sick role
Regression
Mental health especially girls
Body image

101
Q

What social effect might chronic illness have on a child?

A

Decreased independence
Failure of peer relationships
Poor school attendance
Family dynamics

102
Q

What happens during adolescence that might affect their treatment of chronic illness?

A

Move from dependent child to independent adult
Biological and sexual maturation
Risk-taking behaviour
Development of abstract thinking and adult reasoning
Develop personal identity
Education and vocation
Brain development - starting the engine without training the driver
Transfer from paediatric to adult care

103
Q

What are the key elements of transitional care?

A 
Early start
Key worker
Written policy
Written healthcare transition plan - personalised
Flexible policy on timing
Medical summary
Training programme for professionals
Education programme
Development of patient's skills
104
Q

How do you communicate with adolescents?

A

HEADDSS

  • Home
  • Education
  • Activities
  • Drugs and alcohol
  • Depression and suicide
  • Sexual health
  • Spirituality/sleep/something else

Paediatrics (21 decks)

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