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Year 4 Medicine > PAEDS > Flashcards

PAEDS Flashcards

1
Q

what is the sign for duodenal obstruction on abdo X-ray?

A

think double bubble

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2
Q

what is the investigation for appendicitis in children?

A

ultrasound

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3
Q

what is intususception?

A

invagination of proximal bowel into distal bowel (lead point in children)

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4
Q

what is the investigation and treatment of intususcpetion?

A

ultrasound
air enema reduction

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5
Q

where will foreign bodies get stuck with foreign body aspiration?

A

lodges in the bronchus

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6
Q

what is the sign of foreign body aspiration on CXR?

A

asymmetric lung volumes, hyperinflation

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7
Q

what is the inheritance of cystic fibrosis?

A

recessive

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8
Q

what is Perthes disease?

A

idiopathic avascular necrosis/infarction of the hip

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9
Q

what is a slipped capital femoral epiphysis?

A

idiopathic fracture through the proximal femoral growth plate

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10
Q

what is the difference between meningitis and meningococcal septicaemia?

A

meningitis is an infection of the meninges that can be caused by various organisms
meningococcal septicaemia is a systemic infection caused by Neisseria Meningitidis

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11
Q

what is the difference in presentation between meningitis and meningococcal septicaemia?

A

meningitis is unlikely to have a rash and will have neck stiffness and photophobia
meningococcal septicaemia will have a rapidly spreading purpuric rash

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12
Q

what are the causative organisms for meningitis in neonates and children?

A

neonate: E.coli, group B strep, listeria
children: viral, meningococcal, pneumococcal, haemophilus

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13
Q

When is delayed puberty in girls and boys?

A

girls: no sign of puberty by age 13 and no menarche after 15 years
boys: no sign of puberty by age 14

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14
Q

What is the diagnosis and investigation?
a few months old, recurrent vomiting after feeds, non-bilious, crying and difficulties sleeping

A

diagnosis is gastro-oesophageal reflux
investigation is pH study

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15
Q

What is the diagnosis and investigation and treatment?
2-8 weeks of age, vomiting after feeds, weight loss and metabolic alkalosis

A

diagnosis is pyloric stenosis
investigation is ultrasound (which shows thickened pylorus)
treatment is pyloromyotomy

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16
Q

What is the diagnosis and investigation and treatment?
young child, green bilious vomiting, abnormal fixation of small bowel mesentery making it prone to twisting

A

diagnosis is malrotation with volvulus
investigation is upper GI study
treatment is surgery since it is a surgical emergency ad has a risk of bowel infarction

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17
Q

What is the diagnosis and investigation?
infants or congenital, bilious vomiting, abdominal distension

A

diagnosis is bowel obstruction
investigation is AXR to evaluate the level of obstruction to proceed to contrast study

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18
Q

what is the sign to look for with duodenal obstruction on AXR?

A

double bubble

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19
Q

What is the diagnosis and investigation and treatment?
typical 3 months-1 year old, seasonal after viral illness, invagination of proximal bowel into distal (lead-point in older children)

A

diagnosis is intussusception
investigation is US
treatment is air enema reduction

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20
Q

What is the diagnosis and investigation?
periumbilical pain migrating to RIF, nausea, vomiting, fever

A

diagnosis is appendicitis
investigation is AXR (to see appendicloth) and US (to see a non-compressible blind-ending structure >6mm)

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21
Q

What is the diagnosis and investigation?
lower abdominal, RIF pain, in girls

A

diagnosis is ovarian cyst
investigation is US
avoid unnecessary operation
repeat US after 6 weeks to ensure resolution of cyst

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22
Q

what is the general clinical signs, investigation and treatment of chest infections?

A

clinically unwell, fever and sputum
CXR first investigation (airspace consolidation, air bronchograms, silhouette sign)
treatment: Abx, clinically

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23
Q

What is the diagnosis and investigation?
lodges in bronchus and causes obstruction, mostly infants

A

diagnosis is foreign body aspiration
investigation is CXR (asymmetric lung volumes, hyperinflation), and static lung volumes throughout the respiratory cycle (inspiration/expiration or lat decubitus film in infants or fluoroscopy)

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24
Q

What is the diagnosis and investigation?
reversible airway narrowing

A

diagnosis is asthma
investigation is CXR: overinflation, bronchial wall thickening, infection, collapse due to mucous plugging, pneumomediastinum or pneumothorax

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25
Q

What is the diagnosis and investigation?
genetic disorder (recessively inherited), mucous built up in airways leads to recurrent infections (pneumocystis, atypical Mycobacteria), poor growth, infertility, meconium ileus, diabetes

A

diagnosis is cystic fibrosis
investigation is CXR: mainly upper lobe bronchiectasis, bronchial thickening, infection, central lines

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26
Q

What is the diagnosis and investigation?
retrograde flow of urine from bladder towards kidney, associated with pyelonephritis, scarring

A

diagnosis is vesicoureteric reflux
investigation is a cystogram (contrast outlines ureters and renal collecting), and DMSA scan (scarring)

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27
Q

What is the diagnosis and investigation and treatment?
chronic obstruction due to folds in urethra, only in males, usually young child

A

diagnosis is posterior urethral valves
investigation is US (hydronephrosis, key hole appearance of bladder), and cystogram (dilated posterior urethra, normal anterior urethra)

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28
Q

What is the diagnosis?
clinically: UTI, abdo pain and vomiting
imaging: US dilated renal pelvis but not ureter
renogram: poor drainage

A

uteropelvic junction obstruction

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29
Q

In a child who is limping, what are the conditions to look for at the different ages?

A

if starting to walk: worry about developmental hip dysplasia
if 2-5 years old: look for hip effusion
if 5-8 years old: look for Perthes disease
if teenager: look for slipped capital femoral epiphysis

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30
Q

What is the diagnosis and investigation and complications?
abnormal position of the femoral head relative to the acetabulum, incidence 1:2000 births

A

diagnosis is developmental hip dysplasia
investigation is US at 6 weeks for early detection (eg subuluxed hip)
complications are, if untreated limping, leg shortening, degeneration and AVN

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31
Q

What is the diagnosis and what are the two differentiations?
cause is transient synovitis or infection causing a limp.

A

diagnosis is hip effusion
1. transient synovitis is common in children after viral infection, child systemically well
2. septic arthritis has fever, systemic symptoms and pain
this differentiation can be difficult on US

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32
Q

What is the diagnosis and investigation?
idiopathic avascular necrosis/ infarction of the hip, 13 % bilateral, age 5-8 years

A

diagnosis is Perthes disease
investigation is pelvic X-ray to show fragmented flattened femoral head

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33
Q

What is the diagnosis?
idiopathic fracture through the proximal femoral growth plate, bilateral in 1/3, clinically: hip pain but can be referred to knee, age 12-15 years, often obese children

A

slipped capital femoral epiphysis

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34
Q

What makes you think an injury is non-accidental in children?

A

discordance between stated history and history on imaging (minimal or no trauma)
typical fractures: multiple rib fractures, metaphyseal fractures, spiral long bone fractures, spinal fractures, complex skull fractures
healing fractures of different ages

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35
Q

What is the diagnosis?
corner fractures: triangular piece of bone
bucket handle fracture: crescentic piece of bone
most specific for child abuse

A

metaphyseal fractures

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36
Q

What is jaundice?

A

the condition of abnormally high levels of bilirubin in the blood.

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37
Q

Do RBCs contain conjugated or unconjugated bilurbin?

A

unconjugated bilirubin

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38
Q

Where is bilirubin conjugated?

A

the liver

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39
Q

What are the 2 ways that conjugated bilirubin is excreted?

A

via the biliary system into the GI tract or via the urine

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40
Q

When does physiologcal jaundice present in neonates?

A

Usually on the second or third day of life

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41
Q

Why are neonates more prone to jaundice?

A
  1. shorter lifespan of neonatal RBCs
  2. immature liver function at birth
  3. a relatively high concentration of β-glucuronidase in the small intestine
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42
Q

which babies are more prone to jaundice?

A
  1. preterm babies (tend to have higher bilirubin levels and more prolonged jaundice)
  2. breastfed babies (known as breast milk jaundice)
  3. babies with significant bruising or cephalohaematoma which can occur in difficult deliveries (breakdown of RBCs with cephalohaematoma causes higher bilirubin levels)
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43
Q

what is prolonged jaundice? what causes it?

A

when jaundice lasts longer than would be expected in physiological jaundice. >14 days for full term and >21 days for preterm.
Can be caused by biliary atresia, hypothyroidism and G6PD deficiency

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44
Q

what are the causes of neonatal jaundice?
1. increased production of bilirubin
2. decreased clearance of bilirubin

A
  1. haemolytic disease of the newborn, haemorrhage, hereditary spherocytosis, cephalohaematoma, G6PD deficiency, polycythaemia, sepsis and DIC
  2. prematurity, breast milk jaundice, neonatal cholestasis, Gilbert’s syndrome, congenital hypothyroidism, extrahepatic biliary atresia
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45
Q

What are the RFs of neonatal jaundice?

A

gestational age <38 weeks, previous sibling with neonatal jaundice, breastfeeding exclusively, visible jaundice in first 24 hours

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46
Q

What signs are seen on clinical exam for neonatal jaundice?

A

jaundice of the sclerae and gums, skin can be lightly pressed which may reveal jaundice on the blanched skin, signs of infection or bilirubin encephalopathy, nappy: pale chalky stools and dark urine (conjugated jaundice)

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47
Q

What are the 2 features that suggest pathological neonatal jaundice?

A

jaundice in first 24 hours of life and conjugated jaundice

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48
Q

What is hereditary spherocytosis?

A

an inherited disease where defects in RBC skeletal proteins cause RBCs to assume a spherical shape with a reduced lifespan > jaundice

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49
Q

What are the investigations of neonatal jaundice?

A

FBC and blood film (polycythaemia or anaemia), coonjugated bilirubin, blood type testing of mother and baby (ABO or rhesus incompatibility), direct Coombs test (haemolysis), thyroid function (hypothyroidism), blood and urine cultures (neonatal sepsis), G6PD levels (deficiency), liver USS (biliary atresia), genetic testing (Gilbert’s)

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50
Q

What is the management of neonatal jaundice?

A

either phototherapy or exchange transfusion (extreme cases)

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51
Q

What is the main complication of neonatal jaundice? What can it lead to?

A

kernicterus (bilirubin encephalopathy)
if prolonged, can lead to cerebral palsy, sensorineural hearing loss or cognitive impairment

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52
Q

What are the signs of kernicterus in a neonate?

A

presents with lethargy, hypotonia, and poor suck reflex
ie a less responsive, floppy, drowsy baby with poor feeding

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53
Q

what is brain asphyxia and HIE?

A

brain asphyxia: lack of oxygen and blood flow to the brain at birth. It is a consequence of intrapartum foetal hypoxia. Most infants will recover quickly with rapid resuscitation.
HIE (hypoxic ischaemic encephalopathy): prolonged or severe hypoxia leading to ischaemic brain damage. This is a neurological syndrome

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54
Q

what are the causes of HIE?

A

maternal shock, intra/antepartum haemorrhage eg placental abruption, placenta praevia, and uterine rupture, prolapsed cord, nuchal cord, difficult extraction eg shoulder sytocia, breech, and forceps converted to C-section

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55
Q

what are the 3 categories of HIE? what staging is used?

A

mild: - poor feeding, general irritability and hyper-alert
- resolves within 24 hours
- normal prognosis
moderate: - poor feeding, lethargy, hypotonia and seizures
- needs NG feeding
- can take weeks to resolve
- 40% develop cerebral palsy
severe: - reduced consciousness (coma), apnoeas, flaccid / severe hypotonia with absent reflexes, prolonged seizures
- up to 50% mortality
- up to 90% develop cerebral palsy

use Sarnat staging

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56
Q

what staging is used for HIE?

A

Apgars staging

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57
Q

What is the management of HIE?

A

rapid resus at birth
therapeutic hypothermia
maintain homeostasis eg U&E, Ca, Mg, blood glucose, Hb, blood gases, coag, support BP
Mild fluid restriction initially (e.g. 40mL/kg/day 10% dextrose) as there may be oliguria. Omit milk feeds for 1-2 days if HIE severe and then feed slowly. This is to avoid cerebral oedema
treat seizures

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58
Q

what are salmon patches and what do they look like? any treatment needed?

A

also known as stork marks or nevus simplex
small pink or red flat patches on an infant’s forehead, eyelids or nape of neck
usually disappear during infancy - no treatment required

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59
Q

what are port wine marks and how do they present? any treatment needed?

A

also known as naevus flammeus
vascular present at birth whcih occurs due to mature, dilated, dermal capillaries
macular, sharply circumscribed lesions that are pink, red or purple on any part of skin esp face and upper trunk
persist into adult life
treatment: pulse dye laser, anaesthetic cream, cosmetic camouflage

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60
Q

what is an important condition to consider with a port wine mark located in the trigeminal area?

A

consider Sturge-Weber syndrome
this is an underlying meningeal haemangioma and intracranial calcification leading to seizures
or if located on the eye leading to glaucoma, and learning disorders

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61
Q

what is strawberry naevus and how does it present? any treatment required?

A

also known as infantile haemangiomas
appear after birth before 1 month
benign overgrowth of endothelial cells of blood vessel
bright red, protuberant, compressible, shaprly demarcated lesions occurring esp on head and neck
typically get bigger over first 6-12 months and then disappear by age of 7
treatment ONLY if impacting function eg vision, ulceration or disfigurement: beta blockers (propanolol) first line, steroids or pulse dye laser treatment

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62
Q

what is slate-grey naevus and how does it present? any treatment required?

A

also known as mangolian spots or dermal melanocytosis
- Flat, blue or slate-grey lesions in lumbar-sacral area – usually 2-8cm wide
- melanocytes in deep dermis
- benign
- 80% of black and Asian babies
- Fade during first few years - no Rx required

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63
Q

what is erythema toxicum and how does it present? any treatment required?

A
  • widespread small pustules on a red base
  • in 1st 72 hours
  • tends to get worse then resolve
  • looks dramatic
  • common and benign
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64
Q

what are milia and how do they present? any treatment required?

A
  • keratin-filled tiny cysts = milk spots
  • very common
  • just under epidermis
  • benign
  • disappear within 2-4 hours
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65
Q

what is transient neonatal pustular melanosis and how does it present?

A
  • vesicles or superficial pustules
  • uncommon possible variant of erythema toxicum neonatorum
  • pigmented macules
  • present from BIRTH
  • benign or idiopathic
  • self-resolving
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66
Q

what is cephalohaematoma? what causes it? where is it?

A

a collection of blood between the skull and periosteum (subperiosteal bleed). caused by damage to blood vessels during a traumatic, prolonged or instrumental delivery.
usually in the parietal region, and sometimes the occipital

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67
Q

What are the main features of cephalohaematomas?

A

Does not cross suture lines, forms a swelling (soft bulge) on back of skull and feels soft, does not cross midline

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68
Q

What is the management of cephalohaematoma?

A

majority resolves spontaneously over a few months, but there is sometimes residual calcification. Rarely may require surgical removal

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69
Q

what are the complications of cephalohaematoma?

A

anaemia or hypotension - due to blood loss
hyperbilirubinaemia with/without jaundice - due to breakdown of Hb as blood is reabsorbed
infection (rare)
underlying skull fracture

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70
Q

what is rhesus haemolytic disease?

A

haemorrhage of foetal blood of differing rhesus group into the maternal circulation. This leads to maternal anti-D IgG production (usually foetus RhD +ve, mother RhD –ve).

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71
Q

what is the problem with rhesus incompatibility for future pregnancies?

A

The condition is usually asymptomatic or only mild in the 1st affected pregnancy, with severity increasing in subsequent pregnancies:
1. In 1st pregnancy, Rh –ve mother makes anti-D IgG antibodies at point of delivery
2. In 2nd pregnancy, these antibodies cross the placenta and react with antigen of foetal RBCs > foetal RBC haemolysis

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72
Q

which test picks up haemolytic disease of the newborn? when is it done?

A

indirect Coomb’s test
it is done at the 1st antenatal visit

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73
Q

what are some presentations of haemolytic disease of the newborn?

A

antenatal: foetal anaemia, hydrops foetalis, polyhydramnios
postnatal - may appear normal but can have hydrops foetalis, early jaundice, kernicterus, cutaneous haemopoietic lesions, hepatosplenomegaly, coagulopathy, thrombocytopenia, leucopenia
late - anaemia (pallor), inspissated bile syndrome

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74
Q

what is the prevention of haemolytic disease of the newborn? when is this done?

A

anti-D injections are given routinely on 2 occassions:
1. 28 weeks gestation
2. birth (if the baby’s blood group is found to be rhesus-positive)

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75
Q

give some examples of when anti-d injections should be given for sensitising events

A

antepartum haemorrhage, amniocentesis procedures, abdominal trauma

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76
Q

how do anti-d injections work?

A

anti-d meds attach to the rhesus d antigens on the fetal RBCs in the mother’s circulation, causing them to be destroyed. This prevents the mother’s immune system recognising the antigen and creating its own antibodies to the antigen. It act as a prevention for the mother becoming sensitised to the rhesus-d antigen.

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77
Q

what is the kleinhauer test? when is it performed? how does it work?

A

after 20 weeks gestation, this test is performed to see how much fetal blood has passed into the mother’s blood to determine whether further doses of anti-d are required
the test involves adding acid to a sample of the mother’s blood. fetal Hb is naturally more resistant to acid, while the mother’s Hb is destroyed. The number of cells still containing Hb (the remaining fetal cells) can then be calculated.

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78
Q

what should be checked postnatal for haemolytic disease of the newborn?

A

check cord serum bilirubin and Hb

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79
Q

what is the prognosis of haemolytic disease of the newborn?

A

Overall survival is 84-90%; mortality <20% even if hydropic
If hydrops persists then survival drops
Development normal for >90%
50% of babies have normal haemoglobin and bilirubin levels after birth. 25% have moderate disease and may require transfusion

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80
Q

what is prematurity classed as? what are the categories defined by WHO?

A

prematurity is birth before 37 complete weeks gestation
under 28 weeks: extreme preterm
28-32 weeks: very preterm
32-37 weeks: moderate to late preterm

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81
Q

what is the range for birth at limit of viability?

A

birth between 22-25 completed weeks gestation (typically 500g-1000g). ie infants born at <22 weeks gestation have a high likelihood of not surviving, compared with those born >25 weeks gestation which have a high likelihood of survival.

82
Q

what are the causes of prematurity?

A
  1. 25% deliveries are planned due to life threatening conditions eg pre-eclampsia, renal disease, severe growth restriction
  2. 30-40% due to premature or pre-labour rupture of membranes
  3. 25% due to an emergency event eg placental abruption, eclampsia or severe infection
  4. 40% have no identifiable cause
83
Q

what are some RFs for prematurity?

A

previous preterm delivery
multiple pregnancy
smoking and drug use in pregnancy
under or overweight in pregnancy
early pregnancy (within 6 months of previous pregnancy)
maternal illness eg chorioamnionitis, polyhydramnios, pre-eclampsia, diabetes, antiphospholipid syndrome, infection (genital tract, malaria, HIV, mycoplasma)
PROM
uterine malformation or cervical incompetence
placental disease eg dysfunction and antepartum haemorrhage
poor mental health or low socioeconomic status
physical injury or trauma

84
Q

what are some investigations for a premature baby?

A

labs: blood gas, FBC, U&E, blood culture, CRP, blood group and direct Coombs test / direct antiglobulin test
imaging / invasive: CXR, abdo XR, crUSS

85
Q

what is the management of premature babies antenatal, perinatal and postnatal?

A

antenatal: organise delivery plan in a hospital with tertiary level neonatal unit, consider foetal fibronectin screening and tocolytics to delay birth for transfer, give mother IM corticosteroids eg dexamethasone if <34 weeks gestation, give magnesium sulphate
perinatal: delivery can be vaginal if cephalic or C section if breech <32 weeks; foetal HR monitor during labour
postnatal: senior paediatrician present at birth if <28 weeks, delay cord clamping for 1 min, resp support, monitor O2 levels, measure weight and temp, maintain blood glucose with enteral feeds, TPN or 10% glucose, start Abx if infection (benzylpenicillin / gentamicin), start surfactant for RDS

86
Q

what are some complications of prematurity?

A
  1. Respiratory – surfactant deficiency causing respiratory distress syndrome (RDS), apnoea of prematurity, chronic lung disease/bronchopulmonary dysplasia (CLD/BPD)
  2. CNS – intraventricular haemorrhage, periventricular leucomalacia, retinopathy of prematurity
  3. GI – necrotising enterocolitis, inability to suck, poor milk tolerance
  4. Hypothermia
  5. Immunocompromise resulting in ↑risk and severity of infection
  6. Impaired fluid/electrolyte homeostasis – ↑transepidermal skin water loss, poor renal function
  7. Patent ductus arteriosus
  8. Anaemia of prematurity
  9. Jaundice – liver enzyme prematurity
  10. Birth trauma
  11. Perinatal hypoxia
  12. Later – ↑risk of adverse neurodevelopmental outcome, behavioural problems, sudden infant death syndrome (SIDS), non-accidental injury (NAI), and/or parental marriage break-up (due to impaired infant-maternal bonding, stress of long-term complications, etc)
87
Q

what is respiratory distress syndrome?

A

also known as hyaline membrane disease
histologically recognisable lung disease caused by surfactant deficiency. commonly occurs below 32 weeks

88
Q

what is the cause of respiratory distress syndrome? what are the RFs?

A

Surfactant is phospholipid produced by type II alveolar cells to reduce alveolar surface tension.
Inadequate surfactantleads tohigh surface tension withinalveoli. This leads to atelectasis, as it is more difficult for the alveoli and the lungs to expand. This leads toinadequate gaseous exchange, resulting in hypoxia, hypercapnia and respiratory distress (ie IWOB).
RF: prematurity, male infants, c-section, maternal DM, FH, hypothermia, perinatal asphyxia/hypoxia, congenital pneumonia, meconium aspiration

89
Q

what are the symptoms and signs of respiratory distress syndrome?

A

tachypnoea
intercostal, subcostal and sternal recession
nasal flaring
cyanosis
expiratory grunting

90
Q

what are the investigations of respiratory distress syndrome?

A

ABG (resp acidosis), oxygen sats, CXR: airway bronchograms, bilateral diffuse ground glass appearance, bell-shaped thorax

91
Q

what is the prevention of respiratory distress syndrome?

A

antenatal corticosteroids if labour <34 weeks with betamethasone or dexamethasone, 2 doses 12 hourly given to mother 1-7 days before birth; treat co-existing morbidities

92
Q

what is the management of respiratory distress syndrome?

A

self-limiting: stress of premature birth and developing RDS causes corticosteroid release from the adrenals - stimulates endogenous surfactant production, which will resolve the condition <7 days.
titration of inspired O2 against sats, nasal CPAP, mechanical ventilation (IPPV), exogenous surfactant via endotracheal tube, Abx until pneumonia has been excluded, nutrition

93
Q

what are the complications of respiratory distress syndrome?

A

short term: pneumothorax, infection, apnoea, intraventricular haemorrhage, pulmonary haemorrhage, necrotising enterocolitis
long term: chronic lung disease of prematurity, retinopathy of prematurity, neurological, hearing and visual impairment

94
Q

what is the difference between SGA and IUGR?

A

SGA is any foetus with a foetal abdominal circumference or estimated foetal weight < 10th centile for its gestational age. This can be constitutionally small without being at increased risk of complications
IUGR is a pathological in-utero growth restriction with an increased risk of foetal compromise.
IUGR can result in SGA due to a pathology reducing the amount of nutrients and oxygen being delivered to the foetus through the placenta

95
Q

what is the epidemiology of SGA and IUGR?

A

60% of SGA are constitutionally small
IUGR affects 3-10% of pregnancies and 20% of stillborns are thought to have evidence of IUGR

96
Q

what are the 2 categories of SGA?

A
  1. constitutionally small
  2. foetal growth restriction
97
Q

what are the 2 categories of foetal growth restriction?

A
  1. non-placental mediated: chromosomal or structural abnormalities, foetal infection, inborn errors of metabolism
  2. placental mediated: placental dysfunction, pre-eclampsia, autoimmune disease, hypertension, maternal eg low pre-pregnancy weight, malnutrition, severe anaemia, smoking
98
Q

what is the difference between asymmetrical and symmetrical IUGR?

A

asymmetrical: refers to disproportionate growth restriction with a greater decrease in foetal body and limbs compared to head circumference; caused by extrinsic factors eg placental insufficiency; oxygen and nutrients directed to brain and heart; affects foetus in later gestation
symmetrical: refers to proportionate growth restriction in all parts of foetus; caused by intrinsic factors eg genetic abnormalities and intrauterine infections; affects foetus early in gestation

99
Q

what are the major and minor RFs of SGA?

A

major: previous stillbirth, previous SGA foetus, cocaine use, maternal age > 40, maternal disease eg chronic hypertension, diabetes, threatened miscarriage, low PAPP-A, pre-eclampsia, cigarette smoking
minor: nulliparity, IVF singleton, maternal BMI <20 or >25, previous pre-eclampsia

100
Q

what are the histories for SGA/IUGR?

A

can be asymptomatic
for pre-eclampsia: severe headache, visual disturbances, epigastric pain and sudden onset oedema of hands, feet and face.
can present with abdo pain due to placental abruption

101
Q

what are the findings of clinical exam for SGA/IUGR?

A

SGA found during routine obstetric assessment
SGA findings: symphysis-fundal height < 10th centile; low EFW - serial measurements suggesting slow or static growth
IUGR findings: symphysis fundal height is decreased compared to gestational age (at least 3 cm); foetus is small for gestational age; foetal movements are reduced or absent

102
Q

what are the investigations for SGA/IUGR?

A

bedside: maternal vital signs, urine dipstick, CTG
labs: eg OGTT for gestational diabetes and serological screening for congenital intrauterine infections. for severe SGA can also do karyotyping for foetuses with structural abnormalities (amniocentesis antenatally)
imaging: serial USS, umbilical artery doppler, biophysical profile

103
Q

when are serial USS and umbilical artery dopplers done for SGA/IUGR? what are the findings?

A

serial USS: performed from 26-28 weeks gestation; decreased foetal growth with foetal weight < 10th centile, small placenta and oligohydramnios
umbilical artery doppler: performed every 3-4 weeks until delivery; can be normal with end-diastolic flow, can be absent end-diastolic flow, can be reverse end-diastolic flow

104
Q

what is the management of SGA?

A

Conservative: smoking cessation and drug counselling

Medical: women with co-morbidities eg hypertension and renal disease, should be medically optimised before and during pregnancy. In women at high risk of pre-eclampsia, antiplatelet agents eg aspiring 150mg daily, should be commenced at 12 weeks gestation until birth.

Delivery: expedited must be considered for foetal compromise. Can be induced vaginally or C-section.
Women with a SGA foetus between 24+0 and 35+6 weeks of gestation, where delivery is being contemplated, should also receive a single course of antenatal corticosteroids.

105
Q

what is the management of IUGR?

A

Conservative: optimise modifiable RFs eg smoking cessation, drug counselling, and healthy diet and exercise

Medical: treat underlying maternal condition eg gestational diabetes or pre-eclampsia, and medically optimise any co-morbidities. Maternal vital signs should be closely monitored alongside foetal status.

Surgical management / delivery:

  • delivery should be performed if there are signs indicating non-reassuring foetal status or maternal compromise
  • the goal is to delay delivery and prolong intrauterine life to gain foetal maturity, improve survival and reduce risks of morbidity and mortality
  • IOL offered to ALL patients
  • C-section strongly recommended when there are signs of foetal compromise eg absent and reduced end-diastolic flow in the umbilical artery
  • magnesium sulphate should be administered in gestation < 33+6 weeks for foetal neural protection, where delivery is contemplated
  • prenatal corticosteroids should be administered for IUGR foetus between 24+0 - 33+6 weeks gestation, up until 38+0 weeks where delivery is planned by C-section
  • when EFW < 10th centile and UA doppler is normal, delivery can be delayed until at least 37 weeks
106
Q

what is the prevention of SGA/IUGR?

A
  • reviewing and managing the underlying causes eg maternal co-morbidities
  • lifestyle advice eg smoking cessation and dietary advice
  • consider admin of low dose aspirin prior to 16 weeks of gestation
107
Q

what is the prognosis of SGA/IUGR?

A
  • Symmetric SGA infants often stay small
  • In placental cases of IUGR, ‘catch-up’ growth occurs after birth in majority of infants in first 1-2yrs of life > infants regain genetically determined weight and height centiles
    • However, in approx. 15-20% of IUGFR, catch-up growth does not occur > short stature
    • If there was slow head growth before 26 weeks they may show significant developmental delays at 4 years of age and impaired cognitive function
  • Perinatal mortality rates are 4-8x higher for growth-retarded infants, and morbidity is present in 50% of surviving infants
  • Birth weight below 2.5 kg have a 3x risk of death due to IHD
108
Q

what are some of the complications of SGA/IUGR?

A
  • Iatrogenic prematurity
  • Antenatal or intrapartum asphyxia
  • Preterm labour and operative delivery
  • Perinatal asphyxia
  • Perinatal death including stillbirth
  • Neonatal hypoglycaemia and hypocalcaemia
  • Necrotising enterocolitis
  • Adult-onset diseases (e.g. diabetes mellitus, obesity, coronary artery disease, hypertension)
  • Long-term disability eg cerebral palsy
109
Q

what is talipes, when does it occur and what are the 2 types?

A

talipes is a fixed abnormal ankle position that presents at birth, and is also known as clubfoot.
It can occur spontaneously or be associated with other syndromes. It is usually identified at birth or during the newborn exam.
either positional (normal foot that has been held in a deformed position in utero), or congenital (fixed structural alteration in morphology of foot)

110
Q

what does talipes equinovarus and talipes calcaneovalgus?

A

talipes equinovarus = plantar flexion and supination
talipes calcaenovalgus = dorsiflexion and pronation

111
Q

what is the epidemiology of talipes?

A

common at birth - 1/1000 congenital and positional is x5 more common
boys x2 more likely
in 50% it is bilateral

112
Q

what is the aetiology of talipes?

A

positional: the muscles are slightly tight around the ankle but the bones are unaffected. Abnormal foot position in utero. The foot can still be moved into the normal position.
congenital: neuromuscular and anatomical causes >
Muscle fibre abnormalities
Tilting and rotation of talus
Hypoplasia of anterior tibial artery
Polygenic multifactorial genetics
Arrested foetal development

113
Q

what are some conditions that are associated with talipes?

A

cerebral palsy, spina bifida, distal arthrogryposis, congenital myotonic dystrophy, trisomy 18, chromosome 22q11 deletion syndrome

114
Q

what are the RFs for positional talipes?

A

oligohydramnios
malpresentation ie breech
uterine abnormalities
multiple pregnancy

115
Q

what are the signs and symptoms of talipes?

A

Varies from mild to extremely rigid foot resistant to manipulation

In congenital talipes equinovarus:
- Hindfoot in rigid equinovarus (foot turned inwards and downwards) and forefoot adducted + supinated. Sole of foot points medially
Heel is high, with fibula prominent, and calf muscle and foot smaller than normal

In adulthood – may be residual adduction of foot, shortening of Achilles tendon and small foot

116
Q

what score is used to grade talipes which determines treatment?

A

Pirani score - 0-6
higher the score > higher number of casts required

117
Q

what is the management of talipes?

A

the Ponseti technique:
- This involves stretching and manipulation of the joint before setting in plaster cast – foot is repositioned and re-cast weekly for several months
- Achilles tenotomy (under LA) is performed at end of process to lengthen tendon and release tension
- Maintenance involves routine stretching – child will wear special boots full-time for 3months, then nightly for 3yrs, to prevent recurrence - referred to as ‘boots and bars’
- very successful treatment

orthopaedic surgery if this is unsuccessful
- Wedge excision of calcaneo-cuboid joint
- Fusion of midtarsal and subtalar joints
- Calcaneal osteotomy and talectomy
Positional talipes will resolve with time, and only required referral to a physiotherapist.

118
Q

which vaccines are inactivated (ie killed versions of pathogens)?

A

polio, flu, hepatitis A, rabies

119
Q

which vaccines are subunit & conjugate?

A

pneumococcus, meningococcus, hepatitis B, pertussis (whooping cough), haemophilus influenza type B, HPV, shingles (herpes-zoster virus)

120
Q

which vaccines are live attenuated?

A

measles, mumps and rubella, BCG, chickenpox, nasal influenza vaccine, rotavirus

121
Q

which vaccines are given at 2 months?

A

DTaP(diptheria, tetanus, pertussis)/IPV (polio)/Hib/HepB = 6 in 1
Pneumococcal conjugate vaccine (PCV)
Rotavirus
Meningitis B

122
Q

which vaccines are given at 3 months old?

A

6 in 1 (2nd dose), pneumococcal vaccine (PCV), rotavirus vaccine (2nd dose)

123
Q

which vaccines are given at 4 months old?

A

6 in 1 (3rd dose), meningitis B vaccine (2nd dose)

124
Q

which vaccines are given at 1 year old?

A

Hib/meningitis C booster
MMR (1st dose)
pneumococcal vaccine (2nd dose)
meningitis B vaccine (3rd dose)

125
Q

which vaccines are given at 2-10 years old?

A

nasal flu spray every year

126
Q

which vaccines are given at 3 years & 4 months old?

A

DTaP/ IPV(4-in-1 pre-school booster), MMR (2nd dose)

127
Q

which vaccines are given at 12/13 years old?

A

HPV vaccine - 2 jabs given 6-24 months apart

128
Q

which vaccines are given at 14 years old?

A

3 in 1 teenage booster: tetanus, diphtheria and polio
meningitis ACWY vaccine

129
Q

what is meningitis? what is the most common type?

A

it is caused by inflammation of the meninges (the outer membranes that cover the brain and spinal cord). Viral is more common than bacterial and all cases should be treated as bacterial until proven otherwise, as bacterial has a high mortality.

130
Q

what is meningococcal meningitis?

A

when the bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord

131
Q

what is the epidemiology of meningitis?

A

75% of cases of meningitis in <15 years old

132
Q

what can cause meningitis? what are the RFs?

A

Meningitis can be caused by bacteria, viruses, fungi, or be non-infective (secondary to some cancers including leukaemia and lymphoma, autoimmune diseases or drugs).
Young age is the most significant risk factor. Other risk factors include winter season, asplenia, immunocompromise, organ dysfunction, smoking and overcrowding.

133
Q

what is the bacterial aetiology of meningitis? what are the organisms for the different age groups?

A

It is most common in infants, with a second incidence peak in teenagers and young adults
transmitted via droplet spread and usually requires frequent or prolonged close contact
neonates: Group B strep, E. coli, strep pneumoniae, and Listeria monocytogenes
infants and young children: pneumoniae, n. meningitisis, H. influenzae type b
older children: pneumoniae, h. influenzae type b, n. meningitidis, gram negative bacilli, staphylococci, streptococci and L. monocytogenes
adolescents and adults: meningitidis, s. pneumoniae
hospital acauired: pneumoniae, e.coli, p. aeruginosa, s. aureus
immunocompromised: syphilis and TB

134
Q

what is the aetiology of aseptic meningitis?

A

it is diagnosed when CSF has WBCs on microscopy but the gram-stain is negative and no bacteria are cultured on standard media
partly treated bacterial meningitis
viral meningitis accounts for over half of all cases of meningitis: enterovirus, mumps, hsv, herpes zoster, hiv, measles and influenza
fungal: cryptococcus
atypical bacterial: TB, syphilis and Lyme disease
kawasaki disease
parasites

135
Q

what are non-infective causes of meningitis?

A

malignant cells: leukaemia, lymphoma
chemical meningitis: intrathecal drugs, contaminants
drugs: NSAIDs, trimethoprim
sarcoidosis
SLE
Behcet’s disease

136
Q

what is the pathogenesis sequence of meningitis?

A
  • Colonisation and invasion of nasopharyngeal epithelium
  • Invasion of the bloodstream
  • Attachment to and invasion of the meninges
  • Induction of inflammation with leak of proteins leading to cerebral oedema
  • Alteration in cerebral blood flow and metabolism
  • Cerebral vasculitis
137
Q

what is the triad in meningitis signs?

A

fever, neck stiffness and altered mental state

138
Q

what are the early symptoms and signs of meningitis?

A
  • vague and non-specific: fever, headache, N/V lethargy, irritability, muscle or joint pains, refusing food or fluids, respiratory symptoms, appearing unwell. Can be easily confused with flu-like illnesses.
  • less common: chills, shivering, diarrhoea, abdominal pain, sore throat and coryzal symptoms
139
Q

what are the later more specific symptoms and signs of meningitis?

A
  • bulging fontanelle in infants
  • neck stiffness in children over one, or back rigidity
  • Kernig’s sign (knees and hips flex on bending the head forward)
  • Brudzinski’s sign (knees and hips flex on bending the head forward)
  • non-blanching rash (meningococcal disease) - petechiae or purpura
  • photophobia
  • leg pain
  • mottled skin or unusual skin colour, cold hands and feet
  • altered mental state
  • prolonged cap refill time
  • shock (tachycardia, hypotension, resp distress, poor urine output)
  • neurological symptoms
    • seizures
    • paresis, focal neurological deficits (cranial nerve involvement, abnormal pupils)
140
Q

why is there an extremely low threshold for doing a LP as part of the septic screen in infants with unexplained fevers or serizures?

A

infants do not get classical symptoms of meningism with meningitis

141
Q

what are the investigations for meningitis?

A

bedside: vitals (for shock), blood sugar (mental state)
labs: U&Es, FBC, clotting, blood culture, glucose, blood gases and meningococcal PCR
imaging: CT is sometimes performed if there are focal neurological deficits or if specific underlying cause ie mastoiditis is suspected
lumbar puncture

142
Q

what are the results of LP for normal, viral, bacterial and TB meningitis?

A

normal (healthy): clear, 0-4 WBC, lymphocytes, 0.2-0.4 protein, 3-6 glucose
viral: clear/hazy, 20-1000 WBC, lymphocytes, >1 protein, normal glucose
bacterial: cloudy/turbid purulent, 500-5000 WBC, neutrophils,&raquo_space; 1 protein, <glucose
TB: fibrin web, 100-500 WBC, lymphocytes, 0.1-0.5 protein, <glucosex

143
Q

what is the management of meningitis?

A

ABC initial priority, immediately begin Abx empirically
suspected cases of meningococcal meningitis in community - IV benzylpenicillin
suspected cases in hospital: if > 3months IV ceftriaxone; if >3 months IV cefotaxime + amoxicillin/ampicillin
supportive therapy for viruses, or acyclovir for herpes
steroids
monitor hourly vitals, pupil reaction, fluid balance, gcs
inform public health!!!!

144
Q

what is purpura? what is the problem concerning?

A

reddish/purplish, non-blanching discolouration of the skin due to small superficial vessel bleeding - can also occur in mucous membranes
it is not a disease but an indication of underlying cause of bleeding
implies problem with platelets rather than clotting factors

145
Q

what are petechiae and ecchymoses?

A

petechiae = small purpuric lesions less than 2mm in diameter
ecchymoses = larger purpura more than 2mm across (commonly referred to as a bruise)

146
Q

what are the non-thrombocytopenic causes of purpura?

A

congenital: hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), connective tissue disease (Ehlers-Danlos syndrome and pseudoxanthoma elasticum), congenital CMV and rubella
acquired: septicaemia, viral infections
allergic/vasculitis: Henoch-Schonlein purpura, SLE, RA
drug-induced: steroids and sulfonamides
senile purpura, trauma, scurvy, dependent purpura with venous hypertension and factitial purpura, vasomotor straining (strenuous coughing or isometric exercise)

147
Q

what are the thrombocytopenic causes of purpura?

A

impaired platelet production:
- generalised bone marrow failure eg leukaemia, aplastic anaemi, myeloma, marrow infiltration by solid tumours
- selective reduction in megakkaryocytes eg drugs like co-trimoxazole, chemicals, viral infections
excessive platelet destruction:
- immune problems eg immune thrombocytopenia, secondary immune thrombocytopenia (SLE, viral infections, drugs), post-transfusion purpura
- coagulation problems eg DIC, immune thrombocytopenia, haemolytic uraemic syndrome
sequestration of platelets (in splenomegaly)
dilutional loss (following massive transfusion of stored blood)

148
Q

what is seen on clinical exam of purpura?

A

characteristic rash that does not blanch on pressure - perform glass test
note nature of lesiosn: size, confluence, blisters, infection, changing, location (localised > ?trauma, lower leg distribution > ?venous hypertension)
if <2cm = petechiae
if >2cm = bruising or ecchymoses
if tender suggests inflammatory process
always check mucous membranes
check for hepatomegaly, splenomegaly or neurological signs

149
Q

what usually precedes Henoch-Schonlein purpura?

A

URTI due to beta-haemolytic strep infection

150
Q

where does long-term strong steroid use usually present as a rash?

A

on the extensor surfaces of the hands, arms and thighs

151
Q

what is factitial purpura? what do they indicate?

A

this may be considered where there are episodes of inexplicable bleeding/bruising
they may represent severe emotional or psychiatric disturbance, may also be a sign of abuse

152
Q

what are some of the investigations for purpura?

A

FBC (leukaemia), ESR (inflammation), platelets, LFTs (liver disease)
coag screen (clotting factor deficiencies)
blood film and plasma electrophoresis
autoantibody screen for connective tissue disorders
INR if on warfarin
check BP, urinalysis, blood U&E and ASOT (if HSP likely)
clinical condition may indicate further investigations eg blood cultures and lumbar puncture

153
Q

what is the management of purpura?

A

make a diagnosis and manage appropriately
if sepsis possible admit and start IV Abx
if platelet count <20 urgent transfusion
stop any drug likely to be causative
keep in mind non-accidental injury and check anogenital injury
never give IM injection > haematoma will develop
consider a skin biopsy if diagnosis remains unclear

154
Q

what is sepsis?

A

a dysregulated response to infection which may result in organ damage and death

155
Q

what is the most common cause of septicaemia in children? what are the other pathogens that cause septicaemia?

A

most common = neisseria meningitidis serogroup B
staph aureus, strep pneumoniae, group a&b strep, e.coli

156
Q

what are the risk factors for neonatal sepsis?

A

prematurity
low birth weight
maternal infections
PROM (>18 hours)
invasive procedures eg IV access or intubation
immunocompromised

157
Q

what are the clinical features of septicaemia? why is it difficult to identify in children?

A

history of fever, lethargy, nausea and vomiting, headache, abdo pain
signs of shock: hypotension, tachycardia, cool peripheries, confusion
children often compensate well and develop hypotension as a late sign

158
Q

what is meningococcal septicaemia? what are the early signs? what are the clinical features?

A

it is a complication of meningitis which occurs when the infection moves beyond the CNS into the blood
early signs: leg pain, cold peripheries, mottling, dyspnoea
shock: fever, headache, malaise, thirst, poor urine output, pain, altered mental state, CRT >2s, tachycardia, hypotension, resp symptoms or difficulty breathing
rash: non-blanching (>12 hours) - initially maculopapular, then petechial or purpuric
CNS - altered conscious level, increased ICP, paresis or focal neurological deficits, seizures
Kernig’s sign and Brudzinki’s sign

159
Q

what are the investigations for septicaemia?

A

glass test - for a typical non-blanching purpuric or petechial rash
Bloods: FBC (WCC), CRP, U&E, renal function tests, LFTs, clotting screen (INR), blood gas (lactate and acidosis); DIC has PT and aPTT elevated with a low platelet count and fibrinogen level
blood cultures
meningococcal PCR
pharyngeal swab
urine dipstick
lumbar puncture
aspirate from other sterile sites suspected of being infected
CXR
abdo and pelvic USS

160
Q

what is the management of septicaemia?

A

Sepsis 6:

  1. Blood cultures
  2. Urine output monitoring (with catheterisation if necessary)
  3. Fluids (IV or IO)
  4. Abx (IV or IO)
    • Intravenous cefotaxime and amoxicillin in patients under 3 months.
    • Intravenous ceftriaxone in patients over 3 months old.
  5. Lactate (check)
  6. Oxygen - high flow

Children are particularlyprone to hypoglycaemia when unwell and this should be promptly corrected with a2ml/kg bolus of 10% dextrose if blood sugar is<3mmol/L

In addition,corticosteroids e.g: intravenous dexamethasone, is given in those over 3 months old to reduce neurological complications.

If in the community setting, give benzylpenicillin IM or IV prior to urgent transfer to hospital as long as it does not delay transfer

161
Q

what are the complications of septicaemia?

A

early: seizures, increased ICP, hydrocephalus, cerebral venous thrombosis, adrenal haemorrhage, DIC
late: hydrocephalus, deafness, scarring of skin, developmental delay, limb amputations

162
Q

what is Hirschprung’s disease?

A

Also known as congenital aganglionic megacolon disease, which is a congenital disease where ganglionic cells fail to develop in the large intestine. Absence of parasympathetic ganglion cells (myenteric plexus) in the bowel wall > leads to functional bowel obstruction
as cells can’t relax. This commonly presents as delayed or failed passage of meconium around birth.

163
Q

what is the epidemiology of Hirschprung’s disease? what are the 3 types?

A

International incidence = 1 case per 1500-1700
Around 90% of these present in neonatal period, with the median age of presentation at 2 days.
Males have a higher incidence (4:1)
Associated with chromosomal abnormalities eg 10-15% Downs
Types:
1. short segment - most common (85% of cases)
aganglionosis is restricted to the rectosigmoid portion of the colon
2. long segment - less common (10% of cases)
aganglionosis extends past the rectosigmoid portion of the colon to the splenic flexure
3. total colonic aganglionosis - very rare
entire colon is affected, associated with a high mortality and morbidity

164
Q

what is the aetiology and pathophysiology of Hirschprung’s disease?

A

The ganglionic cells of the myenteric and submucosal plexuses in the bowel aren’t present proximally from the anus to a variable length along the large intestine.
most common aetiology of the disease is due to the arrest of the neuroblast, derived from the neural crest migration in foetal development between week 8 to 12. (failure to migrate to the hindgut)
aganglionic segment remains in a tonic state leading to failure in peristalsis and bowel movements. Faeces in the rectum fail to trigger relaxation of the internal anal sphincter due to aganglionosis

165
Q

what are the clinical features of Hirschprung’s disease?

A

The classic triad:abdominal distension andbilious vomiting withfailure to pass meconium
Classically it presents as failure to pass meconium within 48 hours of birth.
Failure to pass faeces leads to dilation of the proximal bowel. The faecal mass can be palpated in the left lower abdomen. The abdomen is sometimes tympanic due to intestinal distension.
Rectal Exam commonly reveals an empty rectal vault and can result in the forceful discharge of gas and faecal material.
If short segment disease – may present later with chronic constipation and FTT. Also overflow incontinence

166
Q

what are the investigations for Hirschprung’s disease?

A

initial: plain AXR (dilated loops of bowel with airless rectum)
FBC (infection for necrotising enterocolitis)
contrast enema (short transition zone between the proximal end of the colon and the narrow distal end of colon; a rectal diameter similar or equal to the sigmoid colon is highly suggestive of Hirschprung’s disease)
gold standard: rectal suction biopsy (aganglionosis in the submucosa)

167
Q

what is the management of Hirschprung’s disease?

A

initial: Iv Abx, nasogastric tube insertion, bowel decompression
definitive: surgery 1. Swenson 2. Soave 3. Duhamel
All involve resecting the aganglionic section of bowel and connecting the unaffected bowel to the dentate (pectinate) line (or just above the dentate line in the pull-through)

168
Q

what are the complications of Hirschprung’s disease?

A

Hirschsprung associated enterocolitis (HAEC) is the main cause of mortality of patients with Hirschsprung’s disease
- stasis of faeces leads to bacterial overgrowth (esp C. diff, staoh aureus and anaerobes) within the colon
- often presents as fever, vomiting, diarrhoea, abdo tenderness, and eventually sepsis if not recognised enough
- emergency treatment = fluid resuscitation, bowel decompression and broad spectrum IV Abx

Enterocolitis is an uncommon but serious complication of surgery.
- long segment and total colonic aganglionosis are at a higher risk of developing enterocolitis

169
Q

what are the features of Kawasaki disease?

A

CRASH and burn
Conjunctivitis (bilateral)
Rash (non-vesicular)
Adenopathy (cervical)
Swollen, strawberry tongue
Hand swelling (or feet)
Burn - fever lasts >5days and is very high

170
Q

what triad of symptoms is in keeping with a shaken baby?

A

retinal haemorrhages, subdural haematoma and encephalopathy

171
Q

Which of the following can be associated with developmental delay?
congenital infection
neglect
prematurity
sensory impairment
all of the above

A

all of the above

172
Q

Children with autistic spectrum disorder have problems in which two domains?
fine motor
gross motor
language
social

A

language
social

173
Q

At what age would you be concerned that a child wasn’t walking?
12 months
15 months
18 months
2 years

A

18 months

174
Q

which investigation should be performed in any child with speech delay?
audiology
blood lead
karyotype
thyroid function test

A

audiology

175
Q

which 2 of these conditions are associated with developmental delay?
CHARGE syndrome
cystic fibrosis
sickle cell disease
trisomy 21

A

CHARGE syndrome
trisomy 21

176
Q

in a 2 y.o. boy who is not yet walking and has large calves, the most likely diagnosis is?
cerebral palsy
duchenne muscular dystorphy
normal late walker
spina bifida

A

duchenne muscular dystrophy

177
Q

which 2 of these following features would prompt urgent referral?
hand preference at 6 months
loss of previously acquired skills
not babbling at 3 months
not walking at 15 months

A

loss of previously acquired skills
hand preference at 6 months (bad to get this early, should have hand preference at 18 months)

178
Q

which of the following features increases the likelihood of an underlying genetic cause for a developmental delay?
cardiac abnormalities
parental consanguinity
dysmorphic features
seizures

A

all of the above

179
Q

which of the following conditions is more common in children with consanguineous parents?
trisomy 21
autism spectrum disorder
Tay-Sachs disease
tuberous sclerosis

A

Tay-Sachs disease
(tuberous sclerosis is usually dominant and spontaneous)

180
Q

int utero exposure to which of the following can be associated with developmental delay?
alcohol
carbamazepine
sodium valproate

A

all of the above
anti-epileptics drugs are associated with developmental delay

181
Q

an unvaccinated 2 y.o. boy presents with a high fever. on exam he is miserable with red eyes, a cough and runny nose. he has a confluent, erythematous rash. what virus is most likely to be responsible for his symptoms?
influenza A
measles
rubella
varicella zoster

A

measles - cough, coryza, conjunctivitis

182
Q

what are the 3 C’s of measles?

A

cough, coryza, conjunctivitis

183
Q

a 12 month old girl presents with a febrile convulsion. she has just received her routine immunisations. which immunisation is most likely to have cause her febrile convulsion?
DTaP/IPV/Hib/HepB
MenB
MMR
Pneumococcal

A

MenB - strong association with febrile convulsion!

184
Q

a 6 y.o. refugee from Cameroon has not received any immunisations. he has just been diagnosed with HIV and has a very low CD4 count. which vaccine should he not receive?
DTaP/IPV/Hib/HepB
MenB
MMR
pneumococcal

A

MMR - this is a live vaccination

185
Q

what are the 2 ‘live’ vaccines?

A

MMR and BCG - avoid in young people who are immunocompromised eg steroids, chemo, HIV with low CD4 count

186
Q

a baby girl is born at 28 weeks gestation. when should she receive her first set of immunisations?
at 8 weeks chronological age
at 8 weeks corrected gestational age
on discharge from the neonatal unit
when she no longer requires respiratory support

A

at 8 weeks chronological age - even though they are underdeveloped, their antibodies that they inherited passively from their mum still disappear at the same time

187
Q

a baby born is born to an unvaccinated mother who had a mild febrile illness associated with rash during early pregnancy. he has a microcephaly, bilateral cataracts and fails his newborn hearing screen. which infection is his mother most likely to have?
measles
mumps
rubella
varicella

A

rubella - congenital rubella syndrome specifically associated with dual sensory impairment ie eye and ear problems
CMV (usually asymptomatic) also causes lots of problems - intracranial calcifications
varicella more likely to cause scarring rather than serious problems

188
Q

which virus in the mother is associated with the baby having intracranial calcifications?

A

CMV - mother usually asymptomatic

189
Q

an 8 week old baby boy presents with projectile vomiting around 30 minutes after every feed. he is hungry and keen to take feeds. on exam he appears underweight. what is the most likely cause for his symptoms?
gastro-oesophageal reflux
infectious gastroenteritis
intestinal atresia
pyloric stenosis

A

pyloric stenosis

190
Q

a 2 y.o. girl presents with a several week history of diarrhoea, often containing undigested food she is otherwise thriving. what is the most likely cause for her symptoms?
coeliac disease
crohn’s disease
infectious gastroenteritis
toddler’s diarrhoea

A

toddler’s diarrhoea

191
Q

a 5 y.o. boy presents with watery diarrhoea and new onset soiling, having previously not opened his bowels for a week. he complains of abdominal pain. his abdomen is distended. what is the most likely cause for his symptoms?
constipation with overflow
crohn’s disease
infectious gastroenteritis
lactose intolerance

A

constipation with overflow

192
Q

a 5 week old baby presents with effortless vomiting after feeds. she is unsettled and starting to refuse bottles. what is the most likely cause for her symptoms?
gastro-oesophageal reflux
infectious gastroenteritis
intestinal atresia
pyloric stenosis

A

gastro-oesophageal reflux

193
Q

what is effortless vomiting most likely to be?

A

gastro-oesophageal reflux

194
Q

a 2 day of baby presents with bilious vomiting. on examination, her abdomen is distended. what is the most likely cause for her symptoms?
gastro-oesophageal reflux
infectious gastroenteritis
intestinal atresia
pyloric stenosis

A

intestinal atresia

195
Q

a 2 y.o. girl presents with longstanding diarrhoea which is difficult to flush. she is underweight, although her abdomen is distended. what is the most likely cause for her symptoms?
coeliac disease
crohn’s disease
infectious gastroenteritis
toddler’s diarrhoea

A

coeliac disease - skinny person with abdominal distension and diarrhoea

196
Q

what is ‘difficult to flush’ diarrhoea and which condition is associated with it?

A

steatorrhoea
coeliac (and cystic fibrosis)

197
Q

a 5 y.o. boy presents with profuse watery diarrhoea after a recent trip to Pakistan. his abdomen is generally tender and he appears dehydrated. what is the most likely cause for his symptoms?
constipation with overflow
crohn’s disease
infectious gastroenteritis
lactose intolerance

A

infectious gastroenteritis

198
Q

a 3 y.o. girl presents with extensive bruising. examination is unremarkable aside from multiple bruises, more pronounced over bony prominences. FBC: Hb 123 WBC: 8.4 platelets: 4
what is the most likely diagnosis?
acute lymphoblastic leukaemia
immune thrombocytopenic purpura
metastatic neuroblastoma
non-accidental injury

A

immune thrombocytopenic purpura

199
Q

a 3 y.o. girl presents with extensive bruising. on examination, she is pale with multiple bruises and significant hepatosplenomegaly. FBC: Hb 64 WBC 28.4 platelets 4
what is the most likely diagnosis?
acute lymphoblastic leukaemia
immune thrombocytopenic purpura
metastatic neuroblastoma
non-accidental injury

A

acute lymphoblastic leukaemia

200
Q

a 13 y.o. boy presents with a short history of headaches. these are associated with nausea and vomiting. they are worse when he is tired and improve after he has rested in a dark room. what is the most likely diagnosis?
brain tumour
meningitis
migraine
sinusitis

A

migraine

201
Q

a 3 month old girl presents with extensive bruising. examination is unremarkable aside from multiple bruises. FBC: Hb 124 WBC: 7.4 platelets 234
what is the most likely diagnosis?
acute lymphoblastic leukaemia
immune thrombocytopenic purpura
metastatic neuroblastoma
non-accidental injury

A

non-accidental injury

202
Q

a 13 y.o. with a short history of headaches associated with nausea and vomiting. worse first thing in the morning and sometimes wake him from sleep. what is the most likely diagnosis?
brain tumour
meningitis
migraine
sinusitis

A

brain tumour

Year 4 Medicine (7 decks)

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