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Phase 3a ILA > Paeds > Flashcards

Paeds Flashcards

1
Q

27 week gestation baby, struggling to breath, reliant on 02

likely cause and treatment

A

Respiratory distress syndrome

Give surfactant therapy via tracheal tube
If anticipated give GCS antenatally
Clear airway, give high dose 02, CPAP, mechanical vent
Monitor SATs and vital signs, glucose and BG
Central venous line for parenteral nutrition

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2
Q

What Abx do you prescribe for resp distress syndome

A

Benpen 25mg/kg every 12 hours

+gentamicin 5mg/kg for ? infection

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3
Q

Why does hypoglycaemia occur in premature babies and how is it treated

A

Poor glycogen stores

  • prevented by early and frequent milk feeding
  • IV glucose to maintain levels about 2.6

IV dextrose conc can be increased

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4
Q

What is the risk of quick fluid increase in babies

A

GORD

aspiration

necrotising enterocolitis

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5
Q

How do you clinically assess jaundice level

A

bilirubin = 80umol/L

blanching skin starting on head and face -> trunk and limbs

Ix: transcutaneous bilirubin meter or blood sample

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6
Q

How do you manage neonatal jaundice

A

phototherapy - blue UV light converts unconjugated bili -> water soluble pigment excreted in urine

severe: blood transfusion

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7
Q

Is infantile jaundice serious?

A

over 50% newborns become visibly jaudiced - most physiological

jaundice from 2 days - 2 weeks is physiological

jaundice <24 hours likely haemolysis (rhesus haemolytic disease, ABO incompatability)

jaundice > 2 weeks ?biliary atresia

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8
Q

Differentials of newborn jaundice

A

rhesus

ABO incompatability

G6PD deficiency

congenital infection

physiological

breast milk jaundice

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9
Q

4 fields of development

A
  1. gross motor
  2. fine motor
  3. hearing speech and language
  4. social, emotional, behavioural
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10
Q

what is moro reflex

what would you be worried about if it persisted past 6 months?

A

sudden extension of head -> symmetrical extension then flex of arms

-cerebral disorder

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11
Q

what is cerebral palsy

A

Movement disorder resulting from a non-progressive lesion of motor pathways

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12
Q

Later appearing symptoms of cerebral palsy

A

depend on where lesion is, symptoms appear gradually as child does not develop as expected

  • learning difficulties
  • epilepsy
  • squint
  • visual/hearing/speech and language impairment
    *
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13
Q

Cerebral palsy causes

A

80% antenatal - gene deletions, infection, vascular occlusion

10% hypoxic ischaemic birth injury

10% post natal - trauma, meningitis, encephalitis

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14
Q

Early signs of cerebral palsy

A
  • floppy baby
  • feeding difficulties
  • delayed motor milestones
  • persistence of primitive symptoms
  • asym hand movement (preference of hand <12m)
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15
Q

Patterns of sypmtoms in Cerebral palsy

A
  1. spastic - 70% - lesion in pyramidal or corticospinal tract
  2. dystonic - 10% - lesion in basal ganglia
  3. ataxic - 10% cerebellum
  4. mixed - 10%
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16
Q

Presentation of spastic cerebral palsy

A

UMN signs

  • hemiplegic - unilat asymmetrical arm> leg
  • quadriplegic - all limbs arm>leg
  • diplegic - all limbs legs>arms
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17
Q

Cerebral palsy management

A

No cure

physiotherapy

splinting of affected contracted joints

botox injections - relax muscle in hyperonia, particularily for gait

SALT

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18
Q

EEG results from absence seizures

A

3Hz spike and wave

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19
Q

Absence seizure 1st line and side effects

A

Sodium Valproate

SE= weight gain, hair loss

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20
Q

How would you manage a squint in a child?

A

Refer to paediatric eye service

corrective glasses (refractive error)

occulsion with patch or penalisation with atropine drops (amblyopia - lazy eye)

surgery

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21
Q

Causes of faltering growth

A

inadequate intake

  • neglect, availability of food
  • impaired suck/swallow (cerebral palsy, cleft palate)

Inadequate retension: vomiting, GORD

malabsorpion: coeliac, CMPI

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22
Q

Urinalysis results suggesting UTI

A

Large amounts of leucocytes and nitrates

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23
Q

2 possible causative agents of UTI in children

A

e.coli

klebsiella

proteus

pseudomonas

strep faecalis

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24
Q

Medical mangement of UTI in chidren

A

IV cefotaxime

PO co-amox or trimethoprim

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25
Q

What imaging would you consider doing in child with UTI symptoms

A

USS

MCUG (micturating cystourethrogram) catheter passes contrast into bladder that shows up on XRay

DMSA - injecting isotope pics taken with gamma camera

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26
Q

Diarrhoea differentials

A

chronic constipation with overflow

intussusception

meckel diverticulum

IBS, IBD

GE

coeliac, CMPI

toddler diarrhoea

hyperthyroid

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27
Q

Management of overflow dirrhoea

A

1- disimpaction, evacuate overloaded rectum completely -osmotic lax e.g. movicol or stimulant lax e.g. senna may be required

2-maintenance movicol to ensure ongoing pain free defecation, gradually reducing dose

*sufficient fluid and balanced diet, enouraged to sit on toilet after meals, star charts

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28
Q

Causes of proteinuria in children

A

orthostatic proteinuria (found only when child upright)

Glomerular abnormalities (minimal change disease, glomerulonephritis, abnormal glomerule basement membrane)

Nephrotic syndrome

increased glomerule filtration pressure

reduced renal mass

HTN

DM

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29
Q

Nephrotic syndrome symptoms and investigations

A
  • 1st =periorbital oedema (particularly on waking)
  • scrotal/vulval, leg and ankle oedema
  • ascites
  • breathlessness (bc pleural effusions and abdo distension)

Ix: heavy proteinuria and low plasma albumin

30
Q

Features of steriod sensitive nephrotic syndrome

A
  • 1-10 years
  • no macroscopic haematuria
  • normal BP
  • normal complement levels
  • normal renal function
  • responds well to steriods
31
Q

Management of steriod-sensitive nephrotic syndrome

A

oral pred 60mg 4 weeks

then 40mg on alt days 4 weeks

urine protein free approx 11 days

No response to above treatment - renal biopsy ?minimal change disease

32
Q

Complications of nephrotic syndrome

A
  • hypovolaemia
  • thrombosis
  • infection
  • hypercholesterolaemia
33
Q

Prognosis for steroid sensitive nephrotic syndrome

A

1/3 resolve directly

1/3 infrequent relapse

1/3 frequent relapse (steriod dependent)

34
Q

Stridor diff diagnosis

A

croup

epiglottitis

foreign body

acute anaphylaxis

35
Q

Symptoms of croup

A

prodome - coryzal and fever

barking cough

harsh stridor

36
Q

Croup cause and epi

A

parainfluenza virsus, RSV, influenza

6m-6y commonest in autumn

37
Q

croup management

A

mild - home

severe - hospital, oral dexamethasone, oral pred and neb steroids (budnesonide)

38
Q

What to watch for a child after giving nebulised epinephrine?

A

rebound symptoms after its worn off

39
Q

Bronchiolitis symptoms

A

coryzal

dry cough and breathlessness, feeding difficulty

40
Q

Bronchiolitis possible causative organsism

A

RSV

parainfluenza, rhinovirus, adenovirus

41
Q

What factors increase risk of bronchioltitis?

A

Preterm infants who develop bronchopulmonary dysplasia or underlying lung disease (CF) or have congential heart disease

42
Q

ix for bronchiolitis

A

Normally clinical

PCR analysis of nasopharyngeal secretions

CXR shows hyperinflation of lungs due to small airway obstruction, air trapping and focal atelectasis

43
Q

Bronchiolitis treatment

A

supportive

humidified oxygen via nasal canulae

monitor for apnoea

fluids NG or IV

44
Q

How can bronchiolitis be prevented

A

Vaccine

monoclonal antibody to RSV (palivizumab) given to

  • <2 yo with chronic lung disease who have required at least 28 days of 02 from birth or who are receving home 02
  • <6m with L->R shunt, pulmonary hypertension
  • <2 with severe congential immunodeficiency
45
Q

How is CF confirmed

A

Guthrie test - heel prick blood showing raised immunoreactive trypsinogen (IRT)

screening for common CF mutation and infants with 2 mutations have sweat test to confirm

46
Q

Which conditions are picked up on newborn screening test?

A

MCADD/MSUD

Glutaric Acidemia

Isovaleric acidemia

Congential hypothryoidism / CF

Homocystinuria

PKU

SC

47
Q

CF inheritance pattern

A

autosomal recessive

defection CFTR gene on chromosome 7

48
Q

CF pathophysiology

A

abnormal ion transport across epithelial cells

airway: reduction in airway surface liquid layer, impaired cillary function, retention of mucopurulent secretions
intestine: thick viscid meconium produced -> meconium ileus
pancreas: blocked ducts, pancreatic enzyme deficiency and malabsorption

sweat glands: abnormal function -> XS sodium and chloride in sweat

49
Q

How does CF present at diff ages

A

Antenatal: amniocentesis/CVS

Perinatal: Screening, bowel atresia, jaundice

Infancy: recurrent resp infections, diarrhoea, FTT, pancreatitis, nasal polyps

Adolescence: recurrent resp infections, bronchiectasis, atypical asthma, male infert

50
Q

6w infant with 3w hx wheeze, poor feeding - SOB on feeding, poor weight gain dx

A

Heart failure

51
Q

VSD examination findings

A

thrill, harsh pansystolic murmur loudest at left sternal edge

tachypnoea, intercostal and sternal recession

fine creps both lungs

hepatomegaly

52
Q

heart failure secondary to VSD invesitgations

A

CXR (cardiomegaly, enlarged pul arteries, increased pul vasular markings, pul oedema)

ECG (biventricular hypertrophy by 2m)

Echo (anatomy of defect

53
Q

Management for HR secondary to VSD

A

diuretics + captopril

additional calorie input

surgery at 3-6m to prevent Eisenmenger syndrome

54
Q

Management of dehydrated child after rehydration fluids and maintenance fluids have been prescribed

A

insulin - started after 1 hour, monitor BG regularly to aim for gradual reduction (2mmol/h)

potassium - will fall with insulin treatment so give K replacement as soon as urine is passed, give until K stable

Acidosis - normally self corrects

55
Q

Most likely cause of congential hypothyroidism in UK, worldwide and consanguineous pedigree

A

UK- maldescent of thyroid and athyrosis

world - iodine deficiency

CP- dyshormonogenesis - error of thyroid hormone synthesis

56
Q

Clinical features of congential hypothyroidism

A
  • aysmptomatic picked up on screening
  • FTT, feeding problems
  • prolonged jaundice
  • constipation
  • pale dry skin
  • delayed development
57
Q

management of congential hypothryoidism

A

thyroxine started 2-3 weeks of age

*early treatment essential to prevent LD*

lifelong oral thyroxine titrating dose to maintain normal growth, TSH and T4 levels

start on 10-15mcg/kg OD increase by 5mcg/kg every 2 weeks

58
Q

Diff diagnosis for unwell neonate

A

Trauma, tumour, thermal

Heart disease, hypovolaemia, hypoxia

Endocrine

Metabolic disturbances

Inborn errors of metabolism

Seizures, CNS abnormality

Forumula error

Intestinal catastrophe

Toxins

Sepsis

59
Q

Adrenal corticol insufficiency presentation

A

salt losing crisis, hypotension and/or hypoglyaemia

GE like illness -> dehydration -> recovery until next episode

60
Q

adrenal corticol insufficiency diagnosis

A

hyponatraemia and hyperkalaemia, often associated with metabolic acidosis and hypoglycaemia

low plasma cortisol and plasma ACTH conc high

synacthen test plasma cortisol conc remain low

61
Q

Adrenal cortical insufficiency management

A

adrenal crisis = urgent treatment with IV saline, gluocose and hydrocortisone (parents taught how to inject IM hydrocortisone during emergency)

long term = glucocorticoid and mineralocorticoid replacement

GCC dose X3 when ill or for an operation

62
Q

Causes of adrenal cortical insufficiency

A

cortiocosteriod therapy

congential adrenal hyperplasia

addisons (rare in children)

63
Q

Adrenal layers and produts

A

Glomerulosa - mineralocorticoids (aldosterone)

Fasciculata - glucocorticoids (cortisol)

Reticularis - sex (DHEA)

64
Q

What is involved in a septic screen

A

BC (sepicaemia)

Urine (UTI)

CXR (LRTI, pneuomia)

LP (meningitis)

FBC/U+E/CRP

65
Q

CSF results for meningococcal septicaemia with meningitis

A

WCC raised

neutrophils

glucose low

portein raised

gram -ve diplococci

66
Q

Management for meningococcal septicaemia with meningitis

A

ABCDE

<3m IV cefotaxime 50mg/kg

>3m ceftriaxone OD

benpen in community -> hospital

+amoxicillin to cover listeria

67
Q

What is purpura and what causes it?

A

red/purple discolourations on skin non blanching

caused by bleeding under the skin

Neisseria meningitides lyses -> releases endotoxin -> clotting factor XII activated -> DIC

68
Q

How is meningitis passed on and how can you prevent this?

A

exchange of resp secretions during close contact

Ciprofloxain (rifampicin if allergic)

Vaccinations

69
Q

Rifampicin SE and CI

A

SE: fever, chills, aching, flu

CI: liver disease, pregnancy/breast feeding, warfarin

70
Q

Kawasaki diagnosis criteria

A

fever for 5 days + 4/5 below

bilateral conjutival infection

MM changes (dry lips, strawberry tongue)

rash

swollen red hands/feet (later)

cervical lymphadenopathy

71
Q

Kawasaki management

A

IVIG

aspirin

echo for CAA

Phase 3a ILA (4 decks)

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