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Year 5 😊✌🏼 > Paeds 2 > Flashcards

Paeds 2 Flashcards

1
Q

when would you refer someone with impetigo to secondary care?

A
  • if complications (e.g. sepsis, glomerulonephritis or deeper soft tissue infection) are suspected
  • if the patient is immunocompromised
  • in more widespread disease
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2
Q

Causative organism in whooping cough

A

bordatella pertussis

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3
Q

presentation of whooping cough

A
  • week of coryzal sx
  • followed by development of paroxysmal outs of coughing
  • typically worse at night
  • may be so severe that the cough causes vomiting
  • gasping for air between coughs may give rise to ‘whoop’
  • vigorous coughing can lead to nosebleeds or subconjunctival haemorrhages
  • pts may experience bouts of coughing for up to 3 months
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4
Q

When might patients with whooping cough benefit from medication?

A
  • if presenting within first 21 days of onset
  • macrolide abx (e.g. azithromycin)
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5
Q

Antibiotic for whooping cough

A

macrolide

  • clarithromycin if under 1 month of age
  • azithromycin if >1month of age

(can prescribe cotrimoxazole if macrolide are not tolerated; not under 6 weeks of age)

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6
Q

how long should children with whooping cough isolate for?

A
  • 48h of antibioticsc have been completed

or

21 days following the onset of symptoms

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7
Q

What abx for pregnant women with whooping cough?

A

erythromycin

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8
Q

most common cause of nephrotic syndrome in children?

A

minimal change disease

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9
Q

nephrotic syndrome triad

A

proteinuria
hypoalbuminaemia
oedema

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10
Q

main complications of minimal change disease

A
  • thrombosis (loss of antithrombin III in the urine; additionally steroids used to treat MCD can lead to thrombocytosis; there is an increased risk of both venous and arterial thrombosis in MCD)
  • increased risk of infection (due to loss of immunoglobulins in the urine)
  • hypercholesterolaemia (loss of albumin in urine leads to drop in oncotic pressure which triggers increased hepatic cholesterol synthesis; this increases cardiovascular risk)
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11
Q

Why is it important to vaccinate children with minimal change disease?

A
  • in minimal change disease there is increased urinary loss of protein
  • this includes immunoglobulins
  • loss of IGs leads to an increased risk of infection (especially from encapsulated bacteria such as strep pneumoniae)
  • make sure you vaccinate these children appropriately!
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12
Q

What is seen on glomeruli in minimal change disease?

A
  • on light microscopy nothing is seen (hence minimal change)
  • electron microscopy shows effacement of podocytes
  • no immune complexes on staining
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13
Q

underlying pathology in minimal change disease

A
  • cytokines cause effacement of podocytes
  • podocytes are usually negatively charged and thereby reject albumin and other negatively charged molecules
  • therefore if the podocyes are damaged, more proteins pass into the urine because the charge barrier has been disrupted
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14
Q

How do you manage minimal change disease?

A

steroids

90% children respond well

there is a risk of relapse

prednisolone doses as per BNFC:
- 60 mg/m2 once daily for 4–6 weeks until proteinuria ceases
- then reduced to 40 mg/m2 once daily on alternate days for 4–6 weeks
- then withdraw by reducing dose gradually
- maximum 80 mg per day.

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15
Q

Inflation breaths vs rescue breaths

A
  • inflation breaths are used in neonatal resuscitation
  • they are slower and more prolonged than rescue breaths
  • the aim is to inflate and clear fluid from the lungs of a neonate
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16
Q

Neonatal Resus

A
  1. 5 inflation breaths

reassess

  1. repeat inflation breaths (consider 2-person airway control)
  2. if chest moving but HR <60 bpm -> ventilate for 30s

reassess

  1. if HR <60 bpm strart chest compressions with ventilation breaths (3:1)

reassess every 30s

  1. if HR remains <60 bpm => consider venous access and drugs (e.g. atropine)
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17
Q

Resus: what is the main cause of bradycardia?

A

hypoxia

therefore neonatal Resus focuses on resp as opposed to cardio resus

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18
Q

Chonrdomalacia patellae

A

anterior knee pain caused by degeneration of the articular cartilage on the posterior surface of the patella

particularly common in children as a result of overuse in physical activities

may be exacerbated by running, climbing stairs and getting up from a chair

passive movements are generally painless

pts should receive physiotherapy to strengthen the quadriceps

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19
Q

How do growing pains present?

A

episodes of generalised aching in the legs that is symmetrical, worse at night, and never present at the start of the day

there is no limitation of physical activities and no abnormalities on examination

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20
Q

Features of TORCH infections

A

prematurity
jaundice
microcephaly
hepatosplenomegaly
thrombocytopenia
anaemia
seizures

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20
Q

Features of TORCH infections

A

prematurity
jaundice
microcephaly
hepatosplenomegaly
thrombocytopenia
anaemia
seizures

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21
Q

TORCH pathogens

A

toxoplasmosis
other (e.g. syphylis)
Rubella
cytomegalovirus
herpes simplex virus

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22
Q

What is formed from the neural tube?

A
  • spinal cord
  • brain
  • meninges
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23
Q

What is spina bifida?

A
  • it is a neural tube defect
  • occurs when the neural tube fails to close properly. particularly in the lower back
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24
Q

What are the different types of spina bifida?

A
  • spina bifida occulta
  • meningocele
  • myelomeningocele
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25
Q

Myelomenongocoele

A
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26
Q

Meningocle

A

= meningeal cyst
- least common form of spina bifida
- only meninges (not the spinal nerves) slip through the gaps between the deformed vertebrae
- usually no severe Sx

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27
Q

Spina bifida occulta

A
  • most common and least severe form of spina bifida
  • spinal tissue and spinal cord DO NOT protrude
  • no tissue is forced into spaces between vertebrae
  • no Sx
  • can be incidental finding on imaging
  • can have an overlying skin lesion (e.g. tuft of hair, lipoma, birth mark or dermal sinus)
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28
Q

What causes spina bifida?

A
  • cause unknown
  • RF: folate (B9) deficiency in pregnancy -> prenatal vitamins
  • spina bifida development occurs at around 4w of gestational age so a woman might not know that she is pregnant then yet, therefore food (e.g. bread, cereal) is often supplemented with folate.
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29
Q

RFs for spina bifida

A
  • folate deficiency
  • obesity
  • poorly controlled diabetes
  • taking meds that interfere with folate metabolism (e.g. anti-seizure meds)
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30
Q

Diagnosis of spina bifida:

A
  • myelomeningocoele: often diagnosed prenatally. Measure AFP in the blood, would be elevated. Also measure b-HCG, inhibin A, estriol and do an US. amniocentesis can also be performed.
  • spina bifida occulta: often accidental finding
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31
Q

Management of Myelomeningocoele

A

pre-natal surgery:
- can be dangerous to foetus and mother
- to close myelomeningocele

post-natal surgery
- done in the first few days of life to minimise the risk of infection (meningitis)

Even with the surgery additional measures have to be taken (e.g. urinary catheterisation, wheelchair/crutches) because of the damage to the underdeveloped spinal nerves cannot be repaired

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32
Q

DEFINE BRONCHIECTASIS

A

permanent dilatation of the bronchi resulting in chronic SOB productive of copious volumes of purulent sputum

typically results from chronic lung inflammation leading to fibrosis and permanent dilatation of the bronchi

it may be generalised or restricted to a lobe

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33
Q

causes of bronchiectasis

A

generalised:
- cystic fibrosis
- post-infectious (e.g. whooping cough)
- primary ciliary dyskinesia
- immunodeficiency
- chronic aspiration

focal:
- severe previous pneumonia
- congenital lung abnormality
- foreign body obstruction

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34
Q

What are muscular dystrophies?

A

A group of X-linked recessive disorders caused by the deletion of the dystrophin gene.

a deficiency in dystrophin leads to myocyte necrosis and a consequent release of CK.

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35
Q

Why do children with muscular dystrophy have bulky calves?

A

this is ‘pseudohypertrophy’

atrophied muscle has been replaced by fat and fibrous tissue

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36
Q

Becker muscular dystrophy life expectancy

A

normal

(whereas DMD is 20-30 yo)

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37
Q

Is bacterial or viral meningitis more common?

A

viral

(also called aseptic meningitis because of the inability to demonstrate presence of bacteria)

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38
Q

which viruses cause meningitis?

A

often enteroviruses e.g. coxsackie and echovirus)

herpes simplex can also cause meningitis (and encephalitis)

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39
Q

What are commoner causes of bacterial meningitis and

A

Neisseria meningitides
Streptococus pneumoniae

(Haemophilus influenzae îs a rare cause because of vaccine)

40
Q

How does ToF present?

A
  • presents in the first few months of life
  • hypercyanotic ‘get’ spells (child has episodes of central cyanosis while crying or feeding
  • O/E ejection systolic murmur (due to pulmonary stenosis)
41
Q

Inheritance pattern of Marfan syndrome

A

autosomal dominant

42
Q

How does DDH present later in life if missed at neonatal screening?

A
  • waddling or toe-walking gait
  • limited hip abduction
  • length discrepancy
  • asymmetrical skin folds
43
Q

RDS on CXR

A
  • bilateral and symmetrical ground glass shadowing
  • air bronchogram
44
Q

What types of laxatives are movicol and Senna?

A

movical - osmotic

Senna - stimulant laxative

45
Q

types of spastic CP

A
  • hemiplegic (involving arm and leg on one side)
  • quadriplegic (involving all four limbs)
  • diplegic (all 4 limbs but legs affected more than arms)
46
Q

Admission criteria for bronchiolitis?

A
  • apnoea
  • sats <92%
  • <50% fluid intake
  • persistent, severe respiratory distress
47
Q

HUS triad

A
  • microangiopathic haemolytic anaemia (pallor)
  • thrombocytopenia (bruising)
  • acute renal failure (e.g. reduced urine output)
48
Q

When does HUS occur?

A

5-10 days post diarrhoea disease with E coli O157 and Shigella dysenteriae infection

49
Q

When is puberty considered to be delayed?

A

absence of pubertal development by 14 in girls and 15 in boys

50
Q

commonest cause of infantile gastroenteritis

A

rotavirus

51
Q

Three commonest forms of congenital cyanotic heart disease

A
  • TGA
  • ToF
  • tricuspid atresia
52
Q

Does fragile X syndrome occur more commonly in males or females?

A

1:1

X-linked dominant

much milder phenotype in females

53
Q

Route of administration of lorazepam, midazolam and diazepam in paediatric status epileptics

A

IV/IO Lorazepam
buccal midazolam
rectal diazepam

54
Q

What is the commonest cause of chronic joint pain in children?

A

juvenile idiopathic aarthritis

55
Q

incidence of JIA

A

1 in 1000 children/adolescents are affected

56
Q

sx of JIA

A
  • initially presents with systemic signs followed by joint pain.

Systemic signs include:
- Fevers
- Malaise
- Salmon pink rash
- Joint involvement can be in or multiple joints

57
Q

Mx of JIA

A

MDT (incl PT, OT, paeds, ophthal, ortho)
Psychological support

Options for medical management include:
- NSAIDs (symptom control only)
- Steroids (intra-articular or oral)
- Steroid-sparing agents e.g., methotrexate or biologics such as TNF-a inhibitors

58
Q

Complications of JIA

A

Flexion contractures (requiring physio and splints)
Joint destruction (requiring prostheses at young ages)
Growth failure (from steroids and chronic disease)
Anterior uveitis (causing visual impairment)

59
Q

Definitive mx of malrotation

A

Ladd’s operation

This is performed, either open or laparoscopically, by untwisting the midgut volvulus, fixing the malrotated bowel in the correct location, removing Ladd’s bands (congenital adhesions) and performing an appendicectomy

(Ladd’s bands, sometimes called bands of Ladd, are fibrous stalks of peritoneal tissue that attach the cecum to the retroperitoneum in the RLQ).

60
Q

Into which space is the anaesthetic injected into in C-sections?

A

subarachnoid

61
Q

Sx of congenital rubella syndrome

A

Organ dysfunction (heart, ears, eyes e.g. loss of red reflexes, abnormal AOAEs)
Microcephaly
Micrognathia
Haematological abnormalities
Low birth weight
Later children may have developmental delay and learning disability
Neonates also may develop a characteristic petechial rash described as a “blueberry muffin” rash.

62
Q

What type of hypersensitivity reaction is HSP?

A

type 3

(due to deposition of immune complexes)

63
Q

Name 4 trinucleotide repeat disorders

A

Huntington’s disease (CAG repeats in HTT gene on Chr 4)
Friedrich’s Ataxia (CGAA repeat in FXN gene on Chr 9)
Myotonic dystrophy (CTG repeat in DMPK gene on Chr 19)
Fragile X Syndrome (CGG repeat in FMR1 gene on Chr 10 -> X=10)

64
Q

Which commonly used drugs can lower seizure threshold?

A

Antibiotics, antidepressants, antipsychotics

-> remember 3 A’s (Abx, ADs, APs)

65
Q

What is the underlying pathology in laryngomalacia?

A

the laryngeal cartilage is soft and floppy with an abnormal epiglottis and/or arytenoid cartilages.

it is a laryngeal birth defect

66
Q

What is the commonest cause of congenital stridor?

A

laryngomalacia

67
Q

investigations for laryngomalacia

A

flexible laryngoscopy

68
Q

Mx of laryngomalacia

A

should resolve on its own by 1 yr of age (as the larynx grows and the cartilaginous ring stiffen)

69
Q

what can exacerbate stridor due to laryngomalacia?

A

intercurrent respiratory infections

70
Q

stridor and wheeze - which is on inspiration and on expiration?

A

wheeze is expiratory (caused by narrowing of the lower airways)

stridor is inspiratory (due to narrowing of the upper airways)

71
Q

Management of croup (incl. dose)

A

oral dexamethasone (150mg/kg) 1 dose

give oxygen if sats are low

in some cases, if the sats have not improved to be =/>95%, another dose may be given 12-24h later.

if the child deteriorates, nebuliser adrenaline can be given (400 micrograms / kg, max dose 5 mg; dose to be repeated after 30 minutes if necessary)

72
Q

Commonest cause of acute stridor in children

A

croup
(laryngotracheobronhcitis)

73
Q

another term for croup

A

laryngotracheobronchitis

74
Q

Indications for hospital referral/admission in acute bronchiolits

A
  • Apnoeic episodes (commonest in babies <2 months and may be the presenting feature)
  • Intake <50 per cent of normal in preceding 24 hours
  • Cyanosis
  • Severe respiratory distress – grunting, nasal flaring, severe recession, respiratory
    rate >70/min
  • Congenital heart disease, pre-existing lung disease or immunodeficiency
  • Significant hypotonia, e.g. trisomy 21 – less likely to cope with respiratory
    compromise
  • Survivor of extreme prematurity
  • Social factors
75
Q

What sample to identify pathogen in bronchiolitis?

A

NPA (nasopharyngeal aspirate)

-> PCR, viral immunofluorescence, culture

does not really affect management, more for epidemiological purposes

76
Q

Management of Bronchiolitis

A

SUPPORTIVE

  • keep sats >92%
  • NG feed if cannot maintain >50% of normal
  • IV fluids reserved for severe cases and restricted to 2/3 of maintenance
  • nasal and oral suction can be helpful
  • capillary blood gas if the child is deteriorating
  • CPAP if needed (to avoid ventilation)

d/c when wet enough to recover from home; but many continue to wheeze for weeks. May have similar reactions with subsequent infections.

variable study results with regards to use of traditional asthma meds. leukotriene antagonists may have a role.

Avoid tobacco smoke.

77
Q

morphological features of erythema multiforme

A

diagnosis is made on finding the classic target-like papules with an erythematous outer border, an inner pale ring and a dusky purple to necrotic centre.

78
Q

What rash is associated with mycoplasma pneumoniae infection?

A

erythema multiforme

79
Q

Mx of erythema mutliforme

A

no mx required, resolves on its own

80
Q

What is typical of mycoplasma pneumoniae infection?

A
  • long period of post infectious ‘pertussis-like’ cough post infection
  • can present with erythema multiforme
  • acute hx
81
Q

tests to dx CF and what they show

A
  • sweat test shows elevated Na+ and Cl- conc
  • genetic testing for mutations in the CFTR gene
82
Q

commonest cause of finger clubbing in children

A

CF

83
Q

Conversion disorder

A

is the presence of neurological symptoms without any underlying neurological cause.

84
Q

How is threadworm managed?

A

100 mg Mebendazole

for affected person and household members

may have to be repeated in 2w

hygiene advice (e.g. and washing, washing towels, bedding, sleepwear, soft toys etc.)

85
Q

What are the sx of threadworm infection?

A
  • itching, especially around anus and vagina
  • worse at night
  • irritability, crying

white ‘threads’ in poo

86
Q

Dose of and RoA for mebendazole for threadworm infection

A

100 mg PO

same dose for children and adults

once only (may have to be repeated in weeks if necessary)

87
Q

What % individuals have a Meckel diverticulum?

A

2%

88
Q

What does a Meckel Diverticulum contain?

A

ectopic gastric mucosa or pancreatic tissue

89
Q

How does a Meckel Diverticulum form?

A

ill remnant of the Vitelli-intestinal duct

(used to be connected to the umbilicus, a little piece of ilium is left protruding in MD)

90
Q

How does Meckel’s diverticulum present?

A

often asymptomatic

severe rectal bleeding (often with Hb drop)

Or presents with:
- intussusception
- volvulus
- diverticulitis (can mimic appendicitis)

91
Q

Mx of Meckel’s diverticulum?

A

surgical resection

92
Q

What Ix for DDH?

A

<6m USS of hips

> 6m X-ray

93
Q

What Ix for DDH?

A

<6m USS of hips

> 6m X-ray

94
Q

What are the risk factors for DDH?

A

FH
breech at 36w (independent of presentation at birth)
breech at delivery
female (6x more likely)
first born child

95
Q

Surgical management of DDH

A
  • if conservative management failed or if dx after ?months
  • reduction under GA, can be open or closed; putting ball back in socket.
  • 6 weeks cast post op
96
Q

What position does the Pavlik harness hold the child hips in?

A

Abducted and flexed

97
Q

complications of DDH

A

pain
hip locking/clicking
asymmetrical buttock creases.

leg length discrepancy

98
Q

What is the inheritance pattern of myotonic, Becker and Duchenne Muscular dystrophy>

A

Myotonic - trinucleotide repeat disorder, autosomal dominant

Becker - X-linked recessive

Duchenne - X linked recessive

Year 5 😊✌🏼 (53 decks)

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