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Paeds endo, musc, neuro, misc Flashcards

1
Q

What is the most common cause of CAH?

A

21-hydroxylase deficiency

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2
Q

Recall the signs and symptoms of CAH

A

Virilisation of external genitalia
Salt-losing crisis
Tall stature

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3
Q

What is the best initial investigation to do when there are ambiguous genitalia?

A

USS

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4
Q

What is the confirmatory investigation used to diagnose CAH?

A

Raised plasma 17-alpha-hydroxyprogesterone - cannot do in a newborn

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5
Q

What sodium and potassium levels are seen in a salt losing crisis?

A

Hyponatraemia, hyperkalaemia

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6
Q

What is the surgical management option for CAH?

A

For girls there is corrective surgery at early puberty to make the genitalia look more female

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7
Q

What is the medical management for CAH?

A

Lifelong hydrocortisone and fludrocortisone

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8
Q

How should a salt-losing crisis be managed?

A

IV hydrocortisone, IV saline, IV dextrose

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9
Q

What is the ‘classical triad’ of symptoms in DM?

A

Polydipsia, polyuria, weight loss

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10
Q

Recall the diagnostic criteria for DM

A
  1. Symptoms + fasting >7 OR random >11.1
  2. No symptoms + fatsing >7 AND random >11.1
  3. No symptoms + OGTT >11.1
  4. HbA1c > 6.5%
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11
Q

What OGTT result is considered ‘impaired’ glucose tolerance?

A

7.8-11.1

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12
Q

What fasting glucose result is considered ‘impaired’ glucose tolerance?

A

6.1-7.0

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13
Q

Recall the 1st and 2nd line options for insulin therapy

A

1st line = multiple daily injection basal-bolus: injections of short-acting insulin before meals, with 1 or more separate daily injections of intermediate acting insulin or long acting insulin analogue

2nd line = continuous SC insulin infusion (pump)

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14
Q

Recall the names of 2 types of long acting insulin

A

Glargine, determir

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15
Q

Recall the names of 3 types of short acting insulin

A

Lispro, apart, glulisine

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16
Q

Why should site of SC insulin injection be regularly rotated in T1DM?

A

Avoidance of lipohypertrophy

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17
Q

What should cap glucose be when fasting and after meals?

A

Fasting: 4-7

After meals: 5-9

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18
Q

When does annual monitoring for retinopathy/ nephropathy/ neuropathy begin?

A

12 years

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19
Q

How is DKA managed?

A
  1. Replace fluids: deficit + maintenance requirement
    Deficit volume = weight in kg x 10 x 5% for mild-mod DKA, or 10% for severe DKA
    Maintenance volume = LOWER for DKA, due to risk of cerebral oedema
    <10kg = 2mls/kg/hr
    10-40kg = 1ml/kg/hr
    40+kg = 40mls/hr
  2. After 1-2 hours, start insulin therapy - infuse at 0.05-0.1 units/kg/hour
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20
Q

What are the symptoms of HHS?

A

Weakness, leg cramps, visual disturbances
N+V
MASSIVE DEHYDRATION
Focal neurology

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21
Q

What is the best option for oral monotherapy in T2DM?

A

Metformin (biguanide)

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22
Q

What medications can be added for tx-resistant T2DM?

A

Sulphonylureas (eg glibenclamide)
Alpha-glucosidase inhibitors (eg acarbose)

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23
Q

Recall the 2 possible biochemical definitions of DKA

A
  1. Acidosis + bicarb <15
  2. pH <7.3 + ketones >3
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24
Q

How is DKA biochemically classified as mild/ mod/ severe?

A

Mild = pH <7.3, mod = <7.2. sev = <7.1

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25
Q

Recall the volume of fluid resus needed in a DKA emergency?

A

If shocked: 20mls/kg bolus over 15 mins

If not shocked: 10mls/kg bolus over 60 mins

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26
Q

How should fluids be replaced following the initial emergency in DKA?

A

Fluid deficit = 5% if mild-mod DKA, 10% if severe DKA
Deficit volume = weight x 10 x deficit%

Fluid maintenance in DKA specifically:
<10kg: 2mls/kg/hour
10-40kg: 1ml/kg/hour
40+kg: 40mls/kg/hour

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27
Q

What is the maintenance requirement of fluids in non-DKA situations?

A

First 10kg = 100mls/kg/day (4mls/kg/hour)

Next 10kg = +50mls/kg/day (2mls/kg/hour)

Every kg above 20kg = +20mls/kg/day (1ml/kg/hour)

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28
Q

Recall the % fluid deficit that correlates to each severity of DKA

A

Mild = 5%
Mod = 7%
Sev = 10%

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29
Q

Calculate the fluid requirement of a 20kg boy in DKA, with pH 7.15, who has already received a 10ml/kg bolus (200ml) over 60 mins

A

Calculation: (deficit x weight x 10) - initial, “shocked” bolus over 48 hours

Deficit if pH = 7.15 = 5% (7 x 20 x 10) = 1000
Initial bolus - 200: 1400-200 = 1200 over 48 hours
1200/48 = 25mls/ hour
Maintenance = (10 x 100) + (10 x 50) = 1500mls over 24 hours

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30
Q

When should insulin therapy be started in DKA?

A

After 1-2 hours of IV fluid replacement

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31
Q

How should insulin dose be calculated?

A

0.05-0.1 units/ kg/ hour

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32
Q

When should dextrose therapy be started in DKA?

A

When glucose is <14mmol/L

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33
Q

Recall 2 important possible complications of DKA with their symptoms

A

Cerebral odoema: Cushing’s triad of raised ICP (bradycarida, HTN, irregular breathing)

Hypokalaemia (typically asymptomatic)

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34
Q

What is the most common cause of delayed puberty in boys?

A

CDGP (constitutional delay of growth and puberty)

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35
Q

Recall the parameters for referral in growth restriction

A

If >75th centile, only refer once it drops by >=3 centiles

If 25th-75th centile, only refer once it drops by >=2 centiles

If <25th centile, refer once centile drops by >=1 centiles

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36
Q

What is the definition of delayed puberty in males and females?

A

Males: no testicular development (<4mL) by age of 14 years

Females: no breast development by age 13 years or no period by age 15

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37
Q

Recall 3 causes of Constitutional Delay of Growth and Puberty

A

Chronic disease
Malnutrition
Psychiatric (eg depression/ AN)

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38
Q

Recall some causes of hypogonadotrophic hypogonadism

A

Hypothalamopituitary disorders: panhypopituitarism, intercranial tumours
Kallman’s syndrome, PWS
Hypothyroidism (acquired)

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39
Q

Recall some causes of hypergonadotrophic hypogonadism (high LH ad FSH)

A

Congenital: cryptochidism (absence of 1 or both testes from scrotum), Kleinfelter’s, Turner’s

Acquired: testicular torsion, chemotherapy, infection, trauma, AI

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40
Q

How can delayed puberty be staged in boys vs girls?

A

Boys: Prader’s orchidometer
Girls: Tanner’s staging

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41
Q

What non-gonadotrophin hormones are important to measure as part of initial investigation of delayed puberty?

A

TSH
Prolactin

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42
Q

Recall 2 important imaging tests that may be done in investigation of delayed puberty?

A

Bone age (from wrist x ray)
MRI brain

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43
Q

How should CDGP be managed?

A

1st line: reassure and offer observation - they have a fantastic prognosis

2nd line: short course of sex hormone therapy
Boys: IM testosterone (every 6 weeks for 6 months)
Girls: transdermal oestrogen (6 months) and cyclical progesterone once established

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44
Q

How should primary testicular/ ovarian failure be treated?

A

Boys: regular testosterone injections
Girls: oestrogen replacement gradually

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45
Q

What are the age parameters for ‘early normal’ vs precocious puberty?

A

Early normal: girls = 8-10, boys = 9-12

Precocious: girls = <8, boys = <9

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46
Q

What are the different causes of gonadotrophin-dependent vs gonadotrophin-independent precocious puberty?

A

Gonadtrophin-DEPENDENT: often idiopathic, but may be due to CNS tumours

Gonadotrophin-INDEPENDENT: gonadal activation independent of HPG- may be due to ovarian (folllicular cyst, granuloma cell tumour, Leydig cell tuour, gonadoblastoma), or testicular pathology

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47
Q

What is premature thelarce?

A

Isolated breast development before 8 years

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48
Q

What does BL enlargement of the testicles indicate before puberty?

A

Gonadotrophin-dependent precocious puberty (intercranial lesion, ie optic glioma in NF1)

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49
Q

What does UL enlargement of a testicle indicate pre-puberty?

A

Gonadal tumour

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50
Q

What does small testes and precocious puberty indicate?

A

Tumour of CAH (adrenal cause)

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51
Q

What is the gold standard investigation for precocious puberty?

A

GnRH stimulation test

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52
Q

If CAH is suspected, what test should be done?

A

Urinary 17-OH progesterone

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53
Q

What is the medical treatment for precocious puberty?

A

GnRH agonist + GH therapy if gonadotrophin-dependent

If gonadotrophin-independent: -
Testotoxicosis: ketoconazole/ cyproterone
CAH: hydrocortisone + GnRH agonist

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54
Q

What are the 2 most common causes of dwarfism?

A

Achondroplasia

Hypochondroplasia

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55
Q

What is the phenotype of achondroplasia?

A

Arms and legs short, normal length thorax

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56
Q

What is the phenotype of hypochondroplasia

A

Small stature, micromelia (small extremities), large head

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57
Q

What gene mutation is associated with achondroplasia and hypochondroplasia?

A

FGFR3 - autosomal dominant mutation

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58
Q

Recall some signs and symptoms of osteogenesis imperfecta

A

Blue sclera, short stature, loose joints, hearing loss, breathing problems

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59
Q

Other than short stature, what are the symptoms of achondroplasia?

A

Hydrocephalus, depression of nasal bridge, marked lumbar lordosis, trident hands

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60
Q

What X ray findings may be present in achondroplasia?

A

Chevron deformity: metaphyseal irregularity

Flaring in long bones

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61
Q

Recall 4 possible causes of cogenital hypothyroidism, and whether they are inherited or not

A

Thyroid gland defects (eg missing, ectopic) - not inherited

Disorder of thyroid hormone metabolism - inherited

Hypothalamopituitary dysfunction (eg tumours, ischaemic damage) - not inherited

Transient hypothyroidism (eg due to maternal carbimazole or Hashimotos, not inherited)

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62
Q

Recall some signs and symptoms of congenital hypothyroidism including 3 unique symptoms

A

Unique: coarse features, macroglossia, umbilical hernia

Others: large fontanelles, low temp, jaundice, hypotonia, pleural effusion, short stature, oedema, etc

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63
Q

How should congenital hypothyroidism be investigated and treated in an infant?

A

Pretty much the same as an adult

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64
Q

What is the most common cause of acquired primary hypothyroidism?

A

Hashimoto’s autoimmune thyroiditis

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65
Q

Recall 2 genetic risk factors for hashimoto’s thyroiditis?

A

Down’s, Turner’s

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66
Q

What is the prognosis of growth for children with primary hypothyroidism?

A

Dw they can catch up :-)

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67
Q

What are the signs and symptoms of hyperthyroidism in the foetus?

A

High CTG trace and foetal goitre on USS

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68
Q

What are the signs and symptoms of hyperthyroidism in the neonate?

A

Same as adult

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69
Q

What is the medical management of hyperthyroidism?

A

Carbimazole/ propothiouracil for 2 years

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70
Q

What non-medical management options are there for hyperthyroidism in children?

A

Radioiodine treatment
Surgery

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71
Q

How is severe obesity, obesity and overweightness defined in children?

A

Severely obese: 99th centile
Obese: >95th centile
Overweight: 85th-94th centile

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72
Q

What causes impaired skeletal growth in rickets?

A

Inadequate mineralisation of bone laid down at the epiphyseal growth plates

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73
Q

Recall 3 deficiencies that can cause rickets?

A

Calcium
Vit D
Phosphate

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74
Q

What will an x ray show in Rickets?

A

Thickened and widened epiphysis
Cupping metaphysis
Bowing diaphysis

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75
Q

What will be the biochemical picture in rickets?

A

Reduced calcium and phosphate
Raised

Diagnostic = calcium x phosphate <2.4

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76
Q

How can rickets be treated?

A

Calcium supplements
Oral vitamin D2

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77
Q

What are the most common causes of fracture in a neonate?

A

Clavicle - from shoulder dystocia
Humerus/ femur - from breech delivery

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78
Q

What is the prognosis for neonatal fracture?

A

Great

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79
Q

How old does a child have to be prescribed codeine and morphine?

A

16

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80
Q

How should paediatric fractures be managed?

A

Pain management
Manipulation and reduction

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81
Q

How old does a child need to be to get a intramedullary nail?

A

4

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82
Q

What is the Ottawa ankle rule?

A

X ray only indicated if:

  • Pain in the malleolar zone AND bone tenderness at the posterior edge/ tip of the lateral malleolus OR
  • Pain in the malleolar zone AND bone tenderness at the posterior edge/ tip of the MEDIAL malleolus OR
  • An inability to bear weight both immediately and in the emergency department for four steps
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83
Q

What is the Ottawa knee rule?

A

X ray only indicated if: age 55+ OR isolated patellar tenderness OR cannot flex to 90 degrees OR an inability to bear weight both immediately and in the ED for 4 steps

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84
Q

What is Perthe’s disease?

A

Avascular necrosis of the femoral epiphysis from an interruption of blood supply, followed by revascularisation and reossification over 18-36 months

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85
Q

In which age group/ gender is Perthe’s most common?

A

4-8 y/o boys

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86
Q

Recall the signs and symptoms of Perthe’s

A

Insidious presentation: limp, knee pain, hip pain –> limb shortening

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87
Q

What investigations should be done for Perthes?

A

X ray +/- MRI

Roll test

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88
Q

What would an x ray show in Perthe’s disease?

A

Increased density of femoral head

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89
Q

What is the roll test?

A

Patient supine, roll affected hip internally and externally –> guarding or spasm in Perthe’s

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90
Q

How is Perthe’s managed?

A

Simple analgesia for pain management<6 years: observation - non-surgical containment using splints>6 years –> surgery

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91
Q

What is Osgood Shlatter Disease?

A

Osteochondritis (inflammation of the cartilage/ bone) of the patellar tendon insertion at the knee

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92
Q

Recall the most at-risk group for OSD?

A

10-15y who are physically active

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93
Q

Recall the signs and symptoms of OSD?

A

Gradual onset knee pain after exercise that is relieved by rest

Localised tenderness and swelling over tibial tuberosity

Hamstring tightness

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94
Q

What might be seen on X ray in OSD?

A

Fragmentation of the tibial tubercle and overlying soft tissue swelling

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95
Q

How should OSD be managed?

A

Simple analgesic packs (intermittent)

Protective knee pads

Stretching

Reassure - this will resolve over time, but may persist until end of growth spurt

Advise stopping/ reducing all sporting activity

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96
Q

What is chondromalacia patellae?

A

Anterior knee pain from degeneration of articular cartilage on posterior surface of patella

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97
Q

What is the general cause of chondromalacia patellae?

A

Overuse in physical activity

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98
Q

Recall the signs and symptoms of chondromalacia patellae

A

Anterior knee pain - exacerbated by movement –> painless passive movement but pain and grating sensation on repeated extension

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99
Q

How should chondromalacia patellae be managed?

A

Physio

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100
Q

What is osteochondritis dissecans?

A

Reduced blood flow causing cracks to form in the articular cartilage and subchondral bone –> avascular necrosis –> fragmentation of bone and cartilage with free movement of fragments –> activity related joint pain

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101
Q

Recall the signs and symptoms of osteochondritis dissecans?

A

Pain after exercise - catching, locking and giving way

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102
Q

What is osteomyelitis?

A

Infection of metaphysis of long bones, commonly the distal femur and proximal tibia

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103
Q

What is the most common pathogen implicated in osteomyelitis?

A

Staph aureus

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104
Q

What is the most common age group affected by osteomyelitis?

A

<5 years

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105
Q

How does the presentation of osteomyelitis compare to the presentation of septic arthritis?

A

Usually chronic in onset and less severe than septic arthritis (over a week rather than a day)

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106
Q

Recall the signs and symptoms of osteomyelitis?

A

Fever
Acute onset limb pain, immobile limb, skin swollen, tender and erythematous

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107
Q

What investigations should be done for suspected osteomyelitis?

A

Septic screen
BCs and FBC
Joint aspiration and MC+S
XR –> MRI of joint (shows soft tissue)

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108
Q

How should acute osteomyelitis be managed?

A

High dose IV empirical –> narrow spec Abx
1st line is flucloxacillin
Take BCs before staring IV Abx
Change to oral Abx as soon as CRP is back to normal
Surgical debridement may be necessary

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109
Q

What is septic arthritis?

A

Infectious arthritis of the synovial joint (vs osteomyelitis of bone)

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110
Q

Which joint is affected in 75% of cases of septic arthritis?

A

Hip

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111
Q

What is the usual pathogen implicated in septic arthritis?

A

S aureus

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112
Q

Recall the signs and symptoms of septic arthritis

A

Single joint warm, erythematous, tender, reduced range of movement, infants will hold the limb still

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113
Q

What investigations should be done for septic arthritis?

A

SAME AS OSTEOMYELITIS
Septic screen
BCs and FBC
Joint aspiration and MC+S
XR –> MRI of joint (shows soft tissue)

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114
Q

How should septic arthritis be managed?

A

Similar to osteomyelitis but not the same

IV flucloxacillin –> oral

Joint wash out and aspirated to dryness PRN

115
Q

What is Still’s disease?

A

Persistent joint swelling presenting before 16 years, in the absence of infection/ other defined cause

116
Q

What are the signs and symptoms of Still’s?

A

May be any number of joints
Gelling (stiffness after periods of rest)
Intermittent limp
Morning joint stiffness/ pain
Limited movement

117
Q

Recall some late signs of Still’s

A

Inflammation and bone expansion –> ‘knock knees’
Salmon-coloured rash (pathogenomic of systemic Still’s)

118
Q

What investigations should be done in suspected Still’s?

A

Clinical diagnosis mainly
Bloods + imaging to prove classification and prognostic info
ANA, FBC, RhF, CRP/ESR, anti-CCP
USS/ MRI

119
Q

How should Still’s be managed?

A

MDT rheuatology
NSAIDs
Corticosteroids (high to low dose)
DMARDs - if disease fails to respond to conventional treatments - methotrexate or sulfalazine
TNF alpha inhibitors if needed

120
Q

What is the prognosis for Still’s disease?

A

Most children can expect good disease control and quality of life
If poor disease control –> anterior uveitis and fractures

121
Q

What is the former name of reactive arthritis?

A

Reiter’s syndrome

122
Q

What are the most likely causative organisms in reactive arthritis?

A

Enteric bacteria - salmonella, shigella, campylobacter, yersinia

123
Q

Recall the signs and symptoms of reactive arthritis

A

Transient joint swelling (<6 weeks) following an extra-articular infection
Low grade fever

124
Q

Which joints are most typically affected by reactive arthritis?

A

Ankles/ knees

125
Q

What investigations should be done in suspected reactive arthritis?

A

A diagnosis of exclusion as no positive findings
Bloods (CRP normal or mildly elevated)
Normal XR

126
Q

How should reactive arthritis be managed?

A

Self-limting, NSAIDs will do for analgesia

127
Q

What is SUFE?

A

Displacement of epiphysis of femoral head posteroinferiorly

128
Q

Why does SUFE need prompt treatment?

A

To prevent avascular necrosis

129
Q

What age group is usually affected by SUFE?

A

10-15 years

130
Q

What is the biggest RF for SUFE?

A

Obesity

131
Q

What are the signs and symptoms of SUFE?

A

Limp/ hip pain +/- referred to the knee
Insidious or acute onset
“Loss of internal rotation of a flexed hip”
Trendelenburg gait positive

132
Q

What investigations should be done in suspected SUFE?

A

Hip XR in AP and frog-lateral view (both hips)

133
Q

How should SUFE be managed?

A

Analgesia, bed-bound
Surgical internal fixation at growth plate

134
Q

What is transient synovitis?

A

Irritable hip - 3-10 years

135
Q

What age group is affected by transient synovitis?

A

3-10 years

136
Q

What is a red flag for urgent hospital assesment in transient synovitis?

A

Age <3 with an acute limp

137
Q

What is the cause of transient synovitis?

A

Viral infection (so causes a low grade fever)

138
Q

How should transient synovitis be investigated and managed

A

Clinically - it is self-limiting

139
Q

What is DDH?

A

A spectrum of conditions affecting proximal femur and acetabulum - ranging from subluxation to frank dislocation

140
Q

What is true DDH?

A

Femoral head has a persistently abnormal relationship with the acetabulum–> abnormal bony development, premature arthritis and significant disability

141
Q

What are the 2 manoevres that are key to early detection of DDH?

A

Barlow - dislocate posteriorly out of the hip

Ortolani - relocate back into acetabulum on hip abduction

142
Q

What is the biggest RF for DDH?

A

Female

143
Q

Recall the signs and symptoms of DDH

A

Limp/ abnormal

Delayed crawling/ walking - toe-walking

Asymmetrical skin folds

Limb length discrepancy

144
Q

What age group are the Barlow and Ortolani manoevres appropriate for?

A

<6 months

145
Q

What other investigation can be done alongside B and O manoevres in suspected DDH?

A

USS

146
Q

What investigation should be done in children too old for B and O manoevres?

A

X ray

147
Q

What are the indications for USS neonatally regardless of presentation, and when is this USS done?

A

Born breech OR FHx pos of DDH
Done at 6 weeks

148
Q

How should DDH be managed in the newborn?

A

Pavlik harness (most will resolve spontaneously by 3-6w of age)
This keeps hips flexed and abducted

149
Q

How should DDH be managed in those >6 months old?

A

Surgery if conservative measures fail or there is no progress with harness

150
Q

What is a reflex anoxic seizure?

A

Episodes of tonic clonic fitting due to cardiac asystole secondary to vagal inhibition

151
Q

What are the causes of reflex anoxic seizure?

A

Can be triggered by pain, head trauma, cold food (ice cream), fright, fever

152
Q

What is a febrile convulsion?

A

A seizure and fever in the absence of intracranial infection

153
Q

What is the age group that can be affected by febrile convulsions?

A

6m to 3y

154
Q

What are the signs and symptoms of febrile convulsions?

A

Generalised tonic clonic seizure on background of fever

155
Q

What is the difference between a simple and complex febrile seizure?

A

Simple: do not cause brain damage and no increased risk of epilepsy

Complex: focal, <15 mins, repeated in same illness, increased risk of subsequent epilepsy

156
Q

What investigations should be done following a febrile seizure?

A

Identify and manage the cause of fever

No other main investigations (don’t do an EEG)

May potentially want to screen for meningitis/ encephalitis, do a urine MC+S and blood glucose

157
Q

How should febrile convulsion be managed during the seizure?

A

Protect from injury and do not restrain

If seizure lasts <5 minutes do nothing

If seizure lasts >5 mins and no drugs are available, call an ambulance

If drugs are available: after 5 mins administer PR diazepam OR buccal midazolam

158
Q

When should an ambulance be called for febrile convulsion?

A

1st seizure - of any duration or cause
Seizure lasts >5 mins with no drugs
Breathing difficuties

159
Q

Which children should be admitted to hospital following a febrile convulsion?

A

First febrile seizure<18 months old

Diagnostic uncertainty about the cause

Complex febrile seizure

Currently on Abx

160
Q

What system is used to classify seizures?

A

International League Against Epilepsy 2017

161
Q

What is the correct name for an absence seizure these days?

A

Generalised non-motor seizure

162
Q

What is the difference in symptoms between tonic-clonic and myoclonic?

A

Tonic clonic is the big one with violent muscle contractions, eyes rollingback, tongue biting, incontinence and both aura and post-ictal phenomena

Myoclonic = brief arrhythmic muscular jerking movement

163
Q

What is the most common form of childhood epilepsy?

A

Benign Rolandic Epilepsy - myoclonic seizures in a 3-12 year old

164
Q

What are the 3 different types of myoclonic epilepsy

A

Benign rolandic (3-12y)
Juvenile myoclonic epilepsy (12-18y)
Progressive myoclonic epilepsy

165
Q

What is the other name for benign rolandic seizures?

A

Sylvian seizures

166
Q

What are the signs and symptoms of benign rolandic epilepsy?

A

Myoclonic seizures during sleep involving face and UL with hypersalivation

167
Q

What are the signs and symptoms of juvenile myoclonic epilepsy?

A

Myoclonic seizures involving upper body just after waking up and beginning after puberty

168
Q

What is progressive myoclonic epilepsy?

A

Rare syndromes of combination of myoclonc and tonic-clonic seizures, with patient deteriorating over time

169
Q

For what type of epilepsy is treatment not usually given?

A

Benign Rolandic Epilepsy

170
Q

What type of antiepileptic actually exacerbates myoclonic seizures?

A

Lamotrigine

171
Q

What type of antiepileptic actually exacerbates absence seizures?

A

Carbamazapine

172
Q

What is the 1st line for rescue therapy for prolonged epileptic seizures?

A

Buccal midazolam

173
Q

Which antiepleptic drug requires monitoring?

A

Carbamazapine

174
Q

After how long seizure-free can antiepileptic therapy be stopped?

A

2 years

175
Q

Recall 2 Side effects of valporate

A

Weight gain, hair loss

176
Q

How is status epilepticus defined?

A

1 seizure lasting >5 mins OR
>2 seizures within a 5 min period without the person returning to normal between them 1 febrile seizures lasting >30 mins

177
Q

What is the age range of peak incidence for infantile spasm?

A

3-8 months

178
Q

What is an infantile spasm?

A

Sudden, rapid, tonic contraction of trunk and limb muscles with gradual relaxation over 0.5-2 seconds

179
Q

What is a ‘Salaam’ attack?

A

Head goes down and arms go up in the air

180
Q

How should West Syndrome be investigated?

A

EEG - shows hypoarrhythmias

181
Q

What is the prognosis for West syndrome?

A

Poor

182
Q

How should West syndrome be managed?

A

Vigabatrin or corticosteroids

183
Q

What investigations should be done for vasovagal syncope?

A

Lying and standing BP with ECG if indicated

FBC (to query anaemia/ bleeding)

184
Q

What are the indications for CT head in children?

A

Head injury + at least 1 of:
- suspected NAI
- post-traumatic seizure
- GCS <14
- Suspected skull fracture
- Focal neurology
OR
2 other risk factors
(LOC >5 mins, abnormal drowsiness, >3 episodes of vomiting, high-impact injury, amnesia > 5 mins)

185
Q

Give 2 signs of tear of the MMA

A

Battle sign
Racoon eyes

186
Q

What are the signs and symptoms of extradural haemorrhage?

A

Lucid interval followed by deterioration
Potential focal neurology

187
Q

How should extradural haemorrhage be managed?

A

Fluid resuscitation to correct hypovolaemia
Evacuation of haematoma and arrest bleeding

188
Q

What is the cause of subdural haemorrhage?

A

Tear in vein as it crosses subdural space

189
Q

What is the main symptom of subdural?

A

Gradually decreasing GCS

190
Q

What is often the cause of subdural in infants?

A

NAI

191
Q

Which infants are most at risk of intraventricular haemorrhage?

A

Premature babies due to VLBW

192
Q

What are the 2 main causes of intraventricular haemorrhage in infants?

A

ECMO in preterm babies with ARDS
Congenital CMV infection

ECMO = extracorporeal membrane oxygenation

193
Q

Recall the signs and symptoms of intraventricular haemorrhage

A

Sleepiness and lethargy, apnoea, reduced
Moro reflex, low tone, tense fontanelle

194
Q

Which investigation is used to diagnose intraventricular haemorrhage in a baby?

A

Trans-fontanelle USS

195
Q

How should intraventricular haemorrhage be treated in a baby?

A

Fluids
Anticonvulsant
Acetazolamide (to reduce CSF) and LP
Ventriculo-peritoneal shunt if hydrocephalus

196
Q

What is the difference between communicating and non-communicating hydrocephalus?

A

Communicatig: CSF flow obstructed after it enters the ventricles
Non-communicating: flow of CSF is obstructed WITHIN the ventricles

197
Q

What are the 2 causes of communicating hydrocephalus?

A

Meningitis
SAH

198
Q

What are the possible causes of non-communicating hydrocephalus?

A

Aqueduct stenosis:
Congenital causes: Dandy-Walker malformation or Chiari malformation

Acquired: IVH/ tumour

199
Q

What is the sunset sign?

A

Eyes appear to be driven down bilaterally - sign of raised ICP

200
Q

What are the 2 key investigations for hydrocephalus?

A

Cranial USS
Measurement of head circumference

201
Q

What is the first line management for hydrocephalus?

A

Ventriculoperitoneal shunt

202
Q

What is the second line management for hydrocephalus?

A

Furosemide - to inhibit CSF production

203
Q

What % of migraines have aura?

A

10%

204
Q

Is migraine likely to be UL or BL?

A

Could be either

205
Q

What are the symptoms of cluster headaches?

A

UL (eyes/ side of face) sharp throbbing pain, causing swelling/ watering inclusters

206
Q

What are some signs that migraine is secondary to something more sinister?

A

Visual field defects, gait or cranial nerve abnormalities, growth failure, papilloedema, early morning headache

207
Q

If simple analgesia doesn’t work, what is the 2nd line pain med in migraines?

A

Nasal sumatriptan

208
Q

Recall 2 prophylactic medications for migraine

A

Topiramate
Propranolol

209
Q

What is Tourette’s?

A

Chronic and multiple tics - starting before 18y old and persisting >1 year

210
Q

What are the 3 types of tic?

A

Motor, vocal or phonic

211
Q

Recall 2 therapies that are useful in tics

A
  1. Habit reversal therapy (learn movements to ‘compete’ with tics)
  2. Exposure with response prevention - help the child get used to the unpleasant feeling before a tic so that they can stop the tic occuring
212
Q

What is the first line medication for tic disorder?

A

Antipsychotics - eg risperidone

213
Q

What is the inheritance pattern of Duchenne muscular dystrophy?

A

x-linked recessive

214
Q

At what age does duchenne muscular dystrophy present, and at what age can it be diagnosed?

A

1-3y presentation
Can be diagnosed at 5y

215
Q

Which gene is deleted in Duchenne muscular dystrophy?

A

Dystrophin

216
Q

Describe the pathophysiology of duchenne muscular dystrophy?

A

Dystophin gene connects cytoskeleton to muscle fibres to ECM through membrane

Where deficient –> influx of Ca –> calmodulin breakdown –> excess free radicals –> myofibre necrosis

217
Q

What type of gait is seen in Duchenne muscular dystrophy?

A

Waddling

218
Q

Other than gait, what else is affected in early DMD?

A

Language delay

219
Q

What is Gower’s sign?

A

The need to turn prone to rise - seen in DMD

220
Q

How is the heart affected by Duchenne muscular dystrophy?

A

Primary dilated cardiomyopathy

221
Q

What is elevated in the plasma in Duchenne muscular dystrophy?

A

CKP (creatine phosphokinase) due to myofibre necrosis

222
Q

How should Duchenne muscular dystrophy be managed?

A

No cure - often management is to alleviate the symptoms
Physiotherapy to clear lungs and exercise to help prevent contractures
Medical:
- CPAP (due to weakness of intercostals)
- Glucocorticoids (to delay need for wheelchair)
- Cardioprotective drugs

223
Q

What is the difference between Beck’s MD and DMD?

A

Same signs and symptoms but often less severe and progresses at a slower rate

224
Q

What is the genetic cause of myotonic muscular dystrophy?

A

Autosomal dominant trinucleotide repeat disorder

225
Q

When does myotonic muscular dystrophy present?

A

20s to 30s

226
Q

In what way is myotonic muscular dystrophy the reverse of duchenne muscular dystrophy?

A

It affects small muscles more than large muscles

227
Q

Which form of MEN is NF1 associated with?

A

MEN2

228
Q

Recall some signs and symptoms of NF1

A

Café au lait spots
Neurofibroma
Axillary freckles
Lisch nodule

229
Q

What is tuberous sclerosis?

A

Rare genetic condition that causes mainly benign tumours to develop in different parts of the body

230
Q

Recall 3 cutaneous features of tuberous sclerosis

A

“Ash leaf” patch
Shagreen patches (rough skin on lumbar spine)
Angiofibromata (butterfly facial distribution)

231
Q

Recall some neurological features of tuberous sclerosis

A

Infantile spasms
Focal epilepsy
Intellectual disability (often with ASD)

232
Q

Why is there a risk of hydrocephalus in tuberous sclerosis?

A

Development of subependymal giant cell astrocytoma

233
Q

Which investigations are useful for diagnosing tuberous sclerosis?

A

CT/ MRI

234
Q

What is the layman’s term for the haemangioma in Sturge Weber syndrome?

A

Port wine stain

235
Q

Where does the haemangiomatous facial lesion present in Sturge Weber Syndrome?

A

Trigeminal nerve distribution

236
Q

Recall some signs and symptoms of Sturge Weber Syndrome

A

Epilepsy
Contralateral hemiplegia
Phaeochromocytoma
Intellectual disability
Glaucoma

237
Q

How should Sturge Weber Syndrome diagnosis be confirmed?

A

MRI

238
Q

What are the 3 symptoms that may present via somatisation?

A

Abdo pain
Reucrrent headaches
Limb pain

239
Q

What is Apley’s rule?

A

The further the pain is from the umbilicus, the more likely the pain is of an organic nature

240
Q

What is the 1st line management for somatisation?

A

Promote communication between family and children
Pain-coping skills ie relaxation techniques for headaches

241
Q

What should be done if 1st line treatments for somatisation fail?

A

Referral to CAMHS

242
Q

Which type of developmental delay has the best prognosis?

A

Isolated delay (global has association with syndromes that have poorer prognosis)

243
Q

How does the aetiology of conjunctivitis differ between children and adults?

A

In adults is usually viral or allergic, in children is more likely to be bacterial

244
Q

What is the most likely cause of sticky eyes in a <48 hours neonate?

A

Gonorrhoea

245
Q

What is the most likely cause of sticky eyes in a neonate in first 1-2w?

A

Chlamydia - often co-presents with pneumonia

246
Q

How should neonatal gonorrhoeal infection be investigated and treated?

A

Gram stain and culture
3rd gen cephalosporin (eg ceftriaxone)

247
Q

How should neonatal chlamydia infection be investigated and treated?

A

Immunofluorescent staining
Oral erythromycin

248
Q

Which is more common in children out of hypermetropia and myopia?

A

Hypermetropia

249
Q

What is the cause of Retinopathy of Prematurity?

A

Vascular proliferation leads to retinal detachment –> fibrosis and blindness

250
Q

What is the main RF for retinopathy of prematurity?

A

Uncontrolled use of high concentrations of oxygen

251
Q

What are the 2 key signs of retinopathy of prematurity?

A

Unusual eye movements
White pupils

252
Q

What is the first line treatment of retinopathy of prematurity?

A

Laser photocoagulation

253
Q

What is strabismus?

A

Abnormal alignment of eyes

254
Q

At what age is strabismus diagnosed?

A

1-4 years

255
Q

What are the 2 types of strabismus?

A

Non-paralytic (refractive error in one or more eyes)
Paralytic (squinting eye could be caused by motor nerve paralysis or SOL - 3rd nerve palsy)

256
Q

How should strabismus be managed?

A

1st line = glasses
2nd line = eye patching
3rd line = eye drops
4th line = eye muscle surgery

257
Q

Which burn pattern is typical of NAI?

A

Glove and stocking

258
Q

Which type of long bone fracture is indicative of NAI?

A

Spiral fractures

259
Q

What is the classic triad of features in shaken-baby syndrome?

A
  1. Retinal haemorrhages
  2. CT showing brain swelling/ encephalopathy
  3. CT showing subdural haematoma
260
Q

What needs to be ruled out in suspected NAI?

A

Leukaemia, ITP and haemophilia

261
Q

What is the definition of SIDS?

A

Deaths which remain unexplained after a post-mortem

262
Q

What is the peak age for SIDS?

A

2-4 months

263
Q

Recall some important risk factors for SIDS

A

Front-sleeping baby
Prematurity, LBW, male, maternal smoking, microenvironment (pillow, heat)

264
Q

For how long should parents share a room with baby?

A

6 months

265
Q

Which organisation provides support for SIDS?

A

Lullaby Trust

266
Q

For how long should a child be excluded from school if they have scarlet fever?

A

24 hours after antibiotics

267
Q

For how long should a child be excluded from school if they have whooping cough?

A

48 hours after Abx

268
Q

For how long should a child be excluded from school if they have measles?

A

4 days from onset of rash

269
Q

For how long should a child be excluded from school if they have rubella?

A

4 days from onset of rash

270
Q

For how long should a child be excluded from school if they have chickenpox?

A

Until all lesions crusted over

271
Q

For how long should a child be excluded from school if they have impetigo?

A

Until all lesions crusted over

272
Q

For how long should a child be excluded from school if they have mumps?

A

5 days from onset of swollen glands

273
Q

For how long should a child be excluded from school if they have influenza?

A

Until recovered

274
Q

When do fontanelle close by?

A

1 year usually, can be as late as 2

275
Q

What should be given before buccal midazolam in a fitting child?

A

Oxygen

276
Q

What infections are children with DiGeorge syndrome particularly at risk of and why?

A

Candidiasis
No thymus –> no T cells

277
Q

Give 2 causes of evanescent salmon pink rash

A

Listeriosis (neonate)
Juvenile idiopathic arthritis

278
Q

Why shouldn’t metoclopramide be given to children?

A

Can give oculogyric crises

279
Q

Recall 3 conditions that cause rigors in children?

A

Pyelonephritis
Influenza
Malaria

280
Q

How should burns be managed medically?

A

Cover for potential toxic shock syndrome with ceftriaxone and clindamycin

281
Q

How can the % of Total Burn Surface Area be measured OE?

A

Hand is 1% as a rough guide

282
Q

Recall the 5 points of the Fraser guidelines

A
  1. YP understands professional’s advice
  2. YP cannot be persuaded to inform parents
  3. YP is likely to begin/ continue having sex regardless of contraception
  4. Physical/ mental wellbeing likely to suffer from lack of contraception
  5. YP’s BI require them
283
Q

What % of children who have a febrile convulsion will have one again?

A

33-50%

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