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finals > paeds part 2 > Flashcards

paeds part 2 Flashcards

1
Q

diagnosis of nephrotic syndrome in children?

A

proteinuria (> 1 g/m^2 per 24 hours)
hypoalbuminaemia (< 25 g/l)
oedema

also hyperlipidaemia
hypercoagulable state (due to loss of anti-thrombin III)
predisposition to infection (due to loss of immunoglobulins)

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2
Q

causes of nephrotic syndrome in children?

A

minimal change disease (most common)
focal-segmental glomerulosclerosis
post-streptococcal nephritis

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3
Q

histological hallmark of minimal change disease?

A

fused podocytes

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4
Q

ix of nephrotic syndrome in children?

A

urine dipstick
FBC, ESR, C3, C4, U&Es
antistreptolysin O or Anti-DNAse
urine MC&S

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5
Q

tx of nephrotic syndrome in children?

A

if steroid-sensitive (85-90%)- prednisolone 60mg/m2/day until proteinuria ceases

if steroid resistant- diuretics, salt restrictrion, ACEi, NSAIDs
cyclophosphamide +/- ciclosporin

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6
Q

prognosis of nephrotic syndrome in children?

A

1/3 resolve, 1/3 infrequent relapses, 1/3 frequent relapses

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7
Q

causes of faltering growth?

A

1) Inadequate intake- impaired suck-swallow, inadequate availability of food
2) Inadequate retention- GORD, vomiting
3) Malabsorption- coeliac, CF, CMPI
4) Failure to utilise nutrients- syndromes
5) Increased requirements- thyrotoxicosis, CF, malignancy, chronic infection

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8
Q

is UTI more common in boys or girls?

A

boys until 3 months

after that higher in girls

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9
Q

cause of UTI?

A

E.coli

after that klebsiella, proteus, pseudomonas

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10
Q

presentation of UTI in infants, younger children and older children?

A

Infants- poor feeding, vomiting, irritability
Younger children- abdo pain, fever, dysuria
Older children- dysuria, frequency, haematuria

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11
Q

mx of UTI in children?

A

referral to a paediatrician in <3 months
>3 months with upper UTI- consider for admission. If not, cephalosporin or co-amoxiclav for 7-10 days
>3 months with lower UTI- trimethoprim or nitrofurantoin for 3 days

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12
Q

Ix of atypical UTI?

A

USS of kidneys and urinary tract
MAG 3 or MCUG (micturating cysturethrogram) to detect obstruction and vesicoureteric reflux- backflow of urine into ureter and kidney
DMSA to look for renal scarring

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13
Q

what is haemolytic uraemic syndrome?

A

caused by an abnormal destruction of red blood cells.
followed prodrome of bloody diarrhoea e.g. E.coli
clog the filtering system of the kidney leading to->
acute renal failure
thrombocytopenia
microangiopathic haemolytic anaemia

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14
Q

S&S of HUS?

A

Abdominal pain
decreased urine output
normocytic anaemia

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15
Q

Ix of HUS?

A

Fragmented blood film
stool culture
FBC

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16
Q

tx of HUS?

A

Supportive

plasma exchange if severe

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17
Q

what is Henoch-schonlein purpura?

A

vasculitis involving small vessels of the skin
IgA mediated
follows URTI-strep pyogenes

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18
Q

features of HSP?

A

Purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
feature of IgA nephropathy- haematuria, renal failure

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19
Q

tx of HSP?

A

supportive
analgesia for arthralgia
prednisolone if severe
self-limiting

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20
Q

tx of nocturnal enuresis?

A

enuresis alarm
desmopressin
advise of fluid intake and toileting behaviour

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21
Q

what is cystic fibrosis?

A

AR disorder causing increased viscosity of secretions

due to a defect in CFTR gene which codes for cAMP sodium chloride channel- F508 defect on chr 7

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22
Q

presentation of CF?

A

Neonatal period- (20%) meconium ileus, prolonged jaundice
Recurrent chest infections (40%)
Malabsorption (30%)- steatorrhoea, failure to thrive
Other features (10%)- liver disease

late features- short stature, DM, delayed puberty, rectal prolapse, nasal polyps, male infertility, female subfertility

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23
Q

diagnosis of CF?

A

Guthrie heel prick- 6-9 days of life
Sweat test- high chloride ions
Faecal elastase (low)
gene abnormalities in CFTR gene

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24
Q

mx of CF?

A

Chest physiotherapy several times a day is essential to clear mucus and reduce the risk of infection and colonisation
Exercise improves respiratory function and reserve, and helps clear sputum
High calorie diet is required for malabsorption, increased respiratory effort, coughing, infections and physiotherapy
CREON tablets to digest fats in patients with pancreatic insufficiency (these replace the missing lipase enzymes)
Prophylactic flucloxacillin tablets to reduce the risk of bacterial infections (particularly staph aureus)
Treat chest infections when they occur
Bronchodilators such as salbutamol inhalers can help treat bronchoconstriction
Nebulised DNase (dornase alfa) is an enzyme that can break down DNA material in respiratory secretions, making secretions less viscous and easier to clear
Nebulised hypertonic saline
Vaccinations including pneumococcal, influenza and varicella

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25
Q

CF patients are prone to infections caused by?

A

staph aureus
pseudomonas aeruginosa
aspergillus

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26
Q

cause of croup?

A

parainfluenza virus

6 months- 3 years

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27
Q

features of croup?

A

stridor
barking cough (worse at night)
fever
coryzal symptoms

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28
Q

mx of croup?

A

dexamethasone 150mg/kg ONCE then reassess
High flow O2
Nebulised adrenaline

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29
Q

cause of bronchiolitis?

A

RSV
respiratory syncytial virus
most common cause of LRTI in <1 years old

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30
Q

features of bronchiolitis?

A 
coryzal symptoms
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles
feeding difficulties
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31
Q

Ix of bronchiolitis?

A

nasopharyngeal aspiration- immunofluorescence may show RSV

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32
Q

mx of bronchiolitis

A

supportive- humidified O2, NG feeds, fluids

Palivizumab- monoclonal Ab, IM once a month through autumn and winder for immunocompromised, CHD, CF, down’s

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33
Q

Ix for a child failing to thrive?

A

Bloods- FBC, U&E, LFT, TFT, Ig, IgA TTG
Urine- MC&S
Stool- MC&S
CXR and sweat test

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34
Q

what is transient tachypnoea of the newborn?

A

commonest cause of resp distress in the newborn period
caused by delayed resorption of fluids in the lungs
most common after C-sections
CXR- hyperinflation of lungs and fluid in the horizontal fissure

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35
Q

what causes acute epiglottitis?

A

Haemophilus influenza type B

incidence decreased since vaccination

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36
Q

features of acute epiglottitis?

A

rapid onset
high temp, generally unwell
stridor
drooling of saliva

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37
Q

mx of acute epiglottitis?

A

do NOT examine throat- can cause airway obstruction
call anaesthetist to intubate
IV cefuroxime

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38
Q

cause of whooping cough?

A

Bordetella pertussis (gram negative bacteria)

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39
Q

features of whooping cough?

A

should be suspected in a person who has an acute cough >14 days without apparent cause, and has one or more of the following features:

  • paroxysmal cough- worse at night and after feeding
  • inspiratory whoop
  • post-tussive vomiting
  • undiagnostic apnoeic attacks in young infants
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40
Q

diagnosis of whooping cough?

A

per nasal swab culture
PCR and serology
admit if under 6 months

41
Q

mx of whooping cough?

A

oral macrolide e.g. clarithromycin if the cough is within prev 21 days
household contacts offered Abx prophylaxis
School exclusion- 48 hours after commencing Abx
NOTIFIABLE DISEASE

42
Q

When are congenital heart diseases usually picked up?

A

antenatal 20 weeks gestation- foetal echo

43
Q

left to right shunts?

A

breathlessness, asymptomatic
VSD
ASD
PDA

44
Q

right to left shunts?

A 
cyanotic
TOF
TPGA
Coarctation of aorta
Hypoplastic left heart syndrome
45
Q

causes of CHDs?

A

maternal rubella,SLE, Diabetes
warfarin
foetal alcohol syndrome
downs, pataus, turners, Edwards syndromes

46
Q

what happens to the foetal circulation pre and post delivery?

A

foramen ovale between atria and ductus arteriosus between pulmonary artery and aorta (to bypass lungs)
blood flows R -> L

at birth, first breath increases pulmonary blood flow and LA pressure, no placenta decreases RA pressure so causes foramen ovale to close

first hour/days of life- ductus arteriosus closes

47
Q

what are the innocent murmurs?

A 
Venous hums and Still's murmur
1. aSymptomatic murmur
2. Soft blowing murmur- venous hum
3. Systolic murmur only
4. Left sternal edge- Still's murmur
changes with position
48
Q

what causes a venous hum?

A

turbulent blood flow returning to the heart

heard as a continuous blowing noise just below the clavicles

49
Q

what is a still’s murmur heard?

A

low-pitched sounds heard best at left sternal edge

50
Q

features of a PDA?

A

Associated with prematurity
continuous machinery murmur beneath the clavicles
mx- Indomethacin (NSAID) closes the correction in the majority of cases
prostaglandin is useful to keep the duct open until after surgical repair

51
Q

4 features of tetralogy of fallot?

A
  1. VSD
  2. RVH
  3. Pulmonary stenosis
  4. Overriding aorta
    CXR- boot-shaped heart, ECG shows RVH
    Mx- surgical repair
52
Q

when does transposition of the great arteries classically present?

A

on day 2 when ductus arteriosus opens

53
Q

presentation of heart failure in infants?

A

SOB worse on exertion e.g. feeding, sweating, poor feeding and recurrent chest infections

54
Q

what is respiratory distress syndrome?

A

causes by a deficiency in surfactant (produced by type 2 pneumocytes in the alveolar epithelium) which lowers surface tension and leads to widespread alveolar collapse and inadequate gas exchange

55
Q

RF for RDS?

A

Prematurity
male sex
diabetic mothers

56
Q

features of RDS?

A 
Tachypnoea
laboured breathing
chest wall recession, chest hyperinflation
nasal flaring
expiratory grunt
tracheal tug
decreased feeds
57
Q

CXR of RDS?

A

ground glass appearance

58
Q

mx of RDS?

A

maternal steroids during pregnancy for prevention
O2
assisted ventilation
exogenous surfactant given via ET tube

59
Q

referral points in terms of child development for smiling, babbling, 1-2 words, sitting unsupported and walking?

A 
no smiling at 10 weeks
no sitting unsupported at 12 months
no walking at 18 months
no babbling at 8 months
no words after 2 years
60
Q

causes of developmental delay?

A
  1. genetics
  2. pregnancy- congenital infections, drugs and alcohol exposure
  3. birth- prematurity, birth asphyxia
  4. childhood- meningitis, neglect/abuse, hearing/visual impairment, NAI
61
Q

what is Prader-Willi syndrome?

A

gene deleted from Chr 15
if father- Prada willi
if mother- Angelman
causes hypotonia during infancy, short stature, hypogonadism, childhood obesity, learning difficulties

62
Q

signs of down’s syndrome?

A

Trisomy 21
Umbilical hernia, macroglossia, hypotonia, short stature, congenital heart disease, epicanthic folds, bradycephaly, single palmar crease, flattened nose

63
Q

mx of Down’s syndrome?

A

ECHO at birth
regular hearing, visual, dental follow up
coeliac screening

64
Q

later complications of down’s syndrome?

A 
subfertility
learning difficulties
short stature
resp infections
ALL
hypothyroidism
Alzheimers
65
Q

what is cerebral palsy?

A

a permanent disorder of movement and posture to a non-progressive lesion of motor pathways in the developing brain

66
Q

causes of CP?

A

80% is antenatal- CV haemorrhage or ischaemia, congenital infection, structural maldevelopment
10% is hypoxic-ischaemic- injury
10% is post-natal- periventricular leukomalacia, meningitis/encephalitis etc

67
Q

types of CP?

A

Spastic (80%)- UMN lesion, hypertonia, rigidity, hyperreflexia (quadriplegic, hemiplegic etc)
Athetoid- affects basal ganglia
Ataxic- poor concentration, cerebellar lesions, ataxic gait, intention tremor
Mixed

68
Q

mx of spasticity of CP?

A

oral diazepam
oral and intrathecal baclofen
botox
orthopaedic surgery

69
Q

types of seizures in childhood?

A

JME
Infantile spasms (west syndrome)
Absence seizures
Febrile Convulsions

70
Q

features of JME?

A

classic history is throwing drinks or cereal about in the morning

71
Q

mx of JME?

A

sodium valproate or lamotrigine

72
Q

SEs of sodium valproate?

A

Teratogenic, so patients need careful advice about contraception
Liver damage and hepatitis
Hair loss
Tremor

73
Q

what is west syndrome?

A

brief spasms beginning in first few months of life
1. flexion of head, trunk, limbs -> extension of arms
lasts 1-2 secs
2. progressive mental handicap
3. EEG
poor prognosis

74
Q

tx of absence seizures?

A

sodium valproate

75
Q

mx of seizures in a child?

A 
ABC, O2, check BG, IV access, time
5 mins- IV lorazepam or buccal midazolam
15 mins- repeat lorazepam
20 mins- phenytoin over 20 mins (call for help)
40 mins- rapid sequence induction
76
Q

what is ADHD?

A

Inattention and/or hyperactivity/impulsivity that is persistent

77
Q

mx of ADHD?

A

10 week initial ‘watch and wait’ approach
1st line- methylphenidate (CNS stimulant)
SE- abdo pain, nausea, dyspepsia, cardio toxic
need baseline ECG

78
Q

what is osteogenesis imperfecta?

A

a group of disorders of collagen metabolism resulting in bone fragility and fractures
AD inheritance

79
Q

features of OI?

A

fractures following minor trauma
blue sclera
deafness secondary to otosclerosis
dental imperfections are common

80
Q

Ix of OI?

A 
bloods- FBC, U&amp;E, CRP, Vit D, Ca, PTH
XR
Skeletal survey
ECHO
MRI if suspect tumour
81
Q

causes of jaundice in the first 24 hours?

A 
ALWAYS PATHOLOGICAL
rhesus haemolytic disease
ABO haemolytic disease
hereditary spherocytosis
G6PD deficiency
neonatal sepsis
82
Q

what causes jaundice from 24 hours to 2 weeks?

A

due to increase RBC conc and decreased half life-physiological

83
Q

causes of prolonged jaundice?

A

biliary atresia (needs surgical intervention), hypothyroidism, UTI, breast milk jaundice, TORCH infection

84
Q

what is conjugated bilirubin?

A

Unconjugated bilirubin is conjugated in the liver. Conjugated bilirubin is excreted in two ways: via the biliary system into the gastrointestinal tract and via the urine.

85
Q

what causes jaundice in the premature neonate?

A

In premature babies, the process of physiological jaundice is exaggerated due to the immature liver.

86
Q

Ix of prolonged jaundice?

A

Full blood count and blood film for polycythaemia or anaemia
Conjugated bilirubin: elevated levels indicate a hepatobiliary cause
Blood type testing of mother and baby for ABO or rhesus incompatibility
Direct Coombs Test (direct antiglobulin test) for haemolysis
Thyroid function, particularly for hypothyroid
Blood and urine cultures if infection is suspected. Suspected sepsis needs treatment with antibiotics.
Glucose-6-phosphate-dehydrogenase (G6PD) levels for G6PD deficiency

87
Q

complications of jaundice?

A

kernicterus- encephalopathy resulting from deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei

88
Q

features of kernicterus?

A 
sleepiness
poor feeding
poor muscle tone
high-pitched cry
irritability
seizures
arched back
89
Q

mx of jaundice?

A

phototherapy- converts unconjugated bilirubin into harmless water-soluble metabolites-> excreted in bile and urine
exchange transfusion

90
Q

causes of congenital hypothyroidism?

A

seen in heel prick test

  • maldescent of the thyroid and athyrosis
  • dyshormogenesis
  • iodine deficiency
  • hypothyroidism due to TSH deficiency
91
Q

what is congenital adrenal hyperplasia?

A

21-hydroxylase deficiency- deficiency of steroids and aldosterone
high levels of ACTH due to low steroid level
high ACTH can produce adrenal androgens that may virilise a female patient

92
Q

presentation of CAH in males and females?

A

females- virilisation of external genitalia
males- salt loss (80%) or tall stature and precocious puberty

salt loss= metabolic acidosis, vomiting, dehydration, weight loss, floppiness

93
Q

what do glucocorticoid hormones do?

A

act to help the body deal with stress, raise blood glucose, reduce inflammation and suppress the immune system

94
Q

mx of salt losing crisis?

A

IV sodium chloride, hydrocortisone, fludrocortisone

95
Q

what is the definition of precocious puberty?

A

development of secondary sexual characteristics before 8 years in females and 9 years in males

96
Q

what is ‘true’ causes of precocious puberty?

A

premature activation of HPO axis

in males- CNS lesions, HCG secretion, hepatoblastoma, primary hypothyroidism

97
Q

what is androgen insensitivity syndrome?

A

an x-linked condition due to end-organ resistance to testosterone causing males to have a female phenotype

98
Q

causes of non-blanching purpuric rash?

A

meningococcal, HSP, enterovirus, thrombocytopenia

99
Q

key consequences of CF mutation?

A

Thick pancreatic and biliary secretions that cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract
Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections
Congenital bilateral absence of the vas deferens in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility

finals (14 decks)

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