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Year 4 > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Name 5 categories of child abuse

A 
(PENS-F)
Physical
Emotional/psychological
Neglect
Sexual
Fabricated/induced illness
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2
Q

When should solid foods be introduced into an infants diet?

A

6 months

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3
Q

Until what age should breast feeding continue?

A

2 years

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4
Q

What is the normal cut off for weight loss that should occur during the first week of a child’s life?

A

They should not lose more than 10% of their birth weight in the first week, and this weight should be regained again by day 14

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5
Q

Describe the breast feeding hormone reflex

A

AP produces prolactin
PP produces oxytocin

suckling stimulates the AP and PP

Prolactin causes alveolar cells to make milk, and oxytocin lets the milk ‘down’
Baby then suckles and the breast is emptied

FIP (feedback inhibitor polypeptide) is released when the baby is not suckling which inhibits the alveolar cells from making milk

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6
Q

List 4 benefits of breast feeding to the baby

A

A-D

  • less allergies
  • close BOND with mother
  • Complete nutritional source
  • Developmental (high IQ)
Reduced infections (ear, gut, resp)
Reduced autoimmune conditions
Reduced SIDS risk
Reduced cardiovascular disease
Increases cognitive ability
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7
Q

List 4 benefits of breast feeding to the mother

A

E-H

  • economic (free)
  • fit (helps with weight loss)
  • guards (reduces breast, ovarian and uterine cancer risks)
  • reduced risk of Haemorrhage post partum
Reduced breast cancer risk
Reduced ovarian cancer risk
Reduced diabetes risk
Helps with weight loss
Builds bond with baby
Reduces post-natal depression
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8
Q

How is CF inherited, and describe the mutation?

A

Autosomal recessive
affects 1/2500 births
F508 mutation on chromosome 7 in the CFTR protein

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9
Q

Describe the pathophysiology of CF

A

Normal CFTR protein = allows chloride ions to leave mucosal cells and enter the lumen of organs
Defective CFTR = chloride ions cannot leave mucosal cells which leads to thickened, sticky secretions which cannot be cleared

Affects many organ systems:

  • lungs
  • pancreas (exocrine deficiency)
  • liver (fibrosis and thick bile)
  • reproductive system (non-functioning vans deferens and thickened cervical mucous)
  • poor growth and delayed puberty
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10
Q

What ENT complications can CF patient suffer from

A

Nasal polyps

Sinusitis

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11
Q

What common types of chest infections do CF patients get?

A

Pseudomonas aeriginosa
Mycobacterium abcessus
Burkholderia cepacia

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12
Q

Describe CF screening

A

Look for raised IRT (immunoreactive trypsin levels) on neonatal blood spot -> as the pancreatic duct shrivels up antenatally this means that enzymes get backed up into the blood

Genetic testing -> for CFTR mutation e.g. F508

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13
Q

Describe how CF may present

A

Meconium ileus
Recurrent infections
Failure to thrive

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14
Q

Describe the diagnostic tests for CF

A

Sweat testing (positive is Cl in sweat is >60mmol/L)

Stool testing (look for reduced faecal elastase)

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15
Q

Describe the treatments of CF

A 
MDT involvement
Chest physiotherapy
Dieticians ?gastrostomy
Prophylactic antibiotics
Fat soluble vitamins and enzyme replacement
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16
Q

What is the incidence of down syndrome and the 3 mechanisms of trisomy?

A 
1/1000 births
Trisomy 21 caused by:
- non-disjunction (90%)
- translocation (5%)
- mosaicism (1%)
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17
Q

List physical appearance features of a DS child

A 
Prominent epicanthal folds
Upward slanting palpebral fissures
Small mouth and protruding tongue
Round face
Low set ears
Single palmar crease
Poor growth and short stature
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18
Q

List neuro complications of DS

A

Learning difficulties
Cataracts
Strabismus
Epilepsy

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19
Q

List cardiac complications of DS

A

Congenital heart disease in 50% children (get ECHO screened after birth)
AV septal defect is common, also VSD and tetralogy of fallot (= POR-V: pulmonary stenosis, overriding aorta, RV hypertrophy, VSD)

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20
Q

List GI complications of DS

A

Risk of duodenal atresia -> bilious vomiting and double bubble sign on AXR

Imperforate anus
Hirschprung’s disease
GORD
Coeliac disease

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21
Q

Describe screening for DS (invasive and non-invasive)

A

Non-invasive

  • first trimester bloods e.g. B-HCG and PAPP-A + maternal age = risk calculation
  • nuchal translucency on USS

Invasive:
- CVS/amniocentesis

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22
Q

What formula is used to calculate fluid requirements for children (not neonates)

A

4-2-1 rule
First 10kg = 4ml/kg/hr
Second 10kg = 2ml/kg/hr
Remaining kg = 1ml/kg/hr

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23
Q

What are the electrolyte requirements for paeds

A 
Na = 2-4mmol/kg/hr 
Cl = 2-4mmol/kg/hr 
K = 1-2mmol/kg/hr

(0.45% NaCl is usually best)

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24
Q

What is the formula used to calculate the desired volume of blood for a child for transfusion?

A

Transfusion volume = Hb (g) (desired - actual) x Weight (kg) x 4

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25
Q

Describe fluid boluses given to children in resus:

A

Always give 20ml/kg of 0.9% NaCl and then reassess in resus

Except give 10ml/kg in DKA, cardiogenic shock or haemorrhagic shock

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26
Q

Describe the presentation of pyloric stenosis

A

(hypertrophy of pyloric muscle causing gastric outlet obstruction)
Projectile vomiting soon after feeding (no bile)
A hungry baby with weight loss -> they become dehydrated and eventually not interested in feeding
Common 2-6 weeks
5M : 1F
Maternal family history

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27
Q

How is pyloric stenosis diagnosed?

A

Low Na and K are found -> metabolic alkalosis

Carry out a test feed and an USS will show peristalsis and a thickened pylorus

O/Ex: a pyloric mass which feels like an olive is palpable in the RUQ

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28
Q

How is pyloric stenosis treated?

A

Fluid resuscitate and correct electrolytes (0.45% saline, 5% dextrose, potassium supplementation)

Definitive mgx: pyloromyotomy

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29
Q

What is malrotation?

A

When the normal rotation and fixation of the bowel that should happen during 4-12wks gestation does not. The caecum lies close to the duodenal-jejunal flexure. There is a narrow midgut mesentery which is liable to volvulus.

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30
Q

How is malrotation diagnosed and treated?

A

Diagnosis -> barium contrast studies

Tx: resus, laparotomy and ladds procedure

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31
Q

What is NEC and how does it present?

A

Necrotising enterocolitis = an acute inflammatory disease which occurs in premature infants where there is bacterial invasion and necrosis of the bowel.

Presentation: Obstruction with bilious vomiting is the normal presentation in the first few days of life but can present later -> distended abdomen, blood in stool, bilious vomiting, pyrexia and feeding intolerance

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32
Q

How is NEC treated?

A

Conservative: fluids and abx
Surgical: bowel resection and stoma formation

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33
Q

What is atresia of the intestine?

A

A congenital narrowing or absent section of the intestine

Can occur anywhere in GI tract, but most commonly jejunum/ileum

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34
Q

What genetic condition is duodenal atresia linked with?

A

30% of infants with duodenal atresia have Down’s syndrome

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35
Q

What is Hirschprung’s disease?

A

An aganglionic piece of bowel (i.e. which lacks special nerve cells) is present. This means the muscle in this area cannot perform peristalsis and poo gets stuck in the bowels.

Commonly occurs at the anus and progresses upwards
Causes bowel obstruction and enlargement of the colon

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36
Q

How does Hirschprung’s disease present

A

90% present with delayed passage of meconium

Later presentations = abdominal distension, constipation, failure to thrive

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37
Q

What is intussusception and at what age does it present

A

Full thickness invagination of proximal bowel into distal bowel segment (commonly at ileo-caecal area)

Peak age = 2 months - 3 yrs

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38
Q

What are the symptoms of intussusception

A

TRIAD:

  1. abdominal pain
  2. redcurrant jelly stools (due to blood stained mucous)
  3. vomiting (maybe bilious depending on intuss site)
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39
Q

How is intussusception diagnosed and treated?

A

Dx: USS -> will show a target lesion/doughnut sign

Tx:
Resus if needed
Rectal air insufflation (air enema) is both diagnostic and therapeutic -> ONLY if no peritonitis
Surgery if peritonitis is present

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40
Q

What is meconium ileus/plug?

A

When the meconium which is sticky can form a plug or become blocked in the bowel
90% of cases, the child has cystic fibrosis

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41
Q

What are the presenting features of meconium ileus?

A

Delayed meconium passage (ie. not within the first 24hrs of delivery)
Feeding reluctantly
Bilious vomiting

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42
Q

How is meconium ileus diagnosed?

A

AXR

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43
Q

How is meconium ileus treated?

A

NGT -> to drain bile from stomach
Stop feeds
IV fluids +/- Abx
May need an enema/stoma/surgery

Later -> CF testing

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44
Q

What is biliary atresia and how does it present?

A

Progressive and idiopathic necrotising inflammation of part/all of the biliary tree

S/Sx: jaundice, pale stools and hepatomegaly

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45
Q

How is biliary atresia treated?

A

Tx: urgent hepato-porto-enterostomy (to allow bile to flow out of the duct system into the gut)

70% children need liver transplant

Long term Mgx: optimising growth and nutrition

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46
Q

What is the formula to estimate a child’s weight based on their age?

A

(Age + 4) x 2 (in kg)

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47
Q

List the paediatric indications for a CT head

A 
Witnessed LOC for >5 mins
Amnesia >5 mins
3 or more episodes of discrete vomiting
Signs of fractured base of skull
A post traumatic seizure with no history of epilepsy
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48
Q

List 5 causes of bilious vomiting

A 
Intussusception
Meconium plug
Hirschprung's disease
Necrotising enterocolitis
Gastroenteritis
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49
Q

Describe the differences between foetal and adult circulations AND what happens when the baby is born

A
  1. Ductus venosus - carries nutrient rich, oxygenated blood straight from the mother’s placenta to the foetal inferior IVC and into the RA of the heart (bypassing the liver)
  2. Foramen ovale - allows blood to pass RA -> LA (bypassing the lungs which are not yet functioning)
  3. Ductus arteriosus (becomes ligamentum arteriosum) - allows any blood which does pass into the RV and pulmonary artery to move straight from PA -> aorta (avoiding the lungs)

When baby takes first breath, this reduces pulmonary vascular resistance, there is an increase in LA filling as blood is returning from the now functioning lungs and the foramen ovale closes.

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50
Q

What is transient tachypnoea

A

Normally during labour the infant’s chest is squeezed as it passes through the birth canal and this helps to clear fluid from the lungs, however often infants can suffer from transient tachypnoea following a C-section when their lungs have not been squeezed as it can take several hours for the lung fluid to be resorbed, resulting in laboured & rapid breathing.

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51
Q

Describe respiratory distress syndrome

A

Deficiency of surfactant, often in premature babies, lowers surface tension leading to widespread alveolar collapse and inadequate gas exchange
Common in infants born < 28 weeks as type 2 pneumocytes have not secreted enough surfactant, rare at term but may occur in infants of DIABETIC mothers
Clinical signs = >60 breaths/min, laboured breathing
Tx: antenatal steroids (before birth)

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52
Q

Describe how choanal atresia may present?

A

Episodic cyanosis which is worse when the baby feeds and improves when they cry (due to occlusion of bone/soft tissue at the back of the nostril)

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53
Q

Why are pre-term infants at increased risk of infection?

A

As IgG is transferred across the placenta in the final trimester

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54
Q

Describe the common pathogens that can cause early and late onset infections in newborn infants

A
  1. Early onset sepsis (within 48hrs of birth)
    Usually due to bacteria which ascended the birth canal and entered the amniotic fluid. Caused by E.COLI and mother may have fever during labour. Presents with resp distress, apnoea and temperature instability
  2. Late onset sepsis (>48hrs from birth)
    Nosocomial or environmental infections
    STAPH EPIDERMIS is the most common pathogen in NICU from indwelling catheters
  3. GROUP B STREP can cause LATE AND EARLY infection
    20% of women have vaginal carriage of this bug
    Colonised mothers can be given prophylactic Abx
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55
Q

Describe the neonatal resus flow chart

A
  1. As soon as baby is born, it will sit on mother for 1 minute and start the timer on the resuscitaire (delayed cord clamping occurs
  2. Baby is then brought over to resuscitaire and stimulate with towel for a few seconds
  3. Assess tone, breathing and HR
  4. If not breathing/gasping -> give 5 inflation breaths (3 seconds long) and LOOK FOR CHEST MOVEMENT
  5. If still not good chest movement, consider 2 person technique and repeat the 5 inflation breaths
  6. Once chest is moving, assess HR (if <60 then provide ventilation breaths, if >60 then ask senior!) -> may needs sats probe and tailored O2 etc.
56
Q

Describe the components of the APGAR score

A

Appearance (blue/pink with blue extremities/pink)
Pulse (absent/<100/>100)
Grimace (floppy/minimal response to stimulation/maximal response to stimulation)
Activity = ‘muscle tone’ (absent/flexed arms and legs/active)
Respiration (absent/slow and irregular/vigorous cry)

57
Q

Define the cut off for neonatal jaundice and list 3 reasons why newborns can become visibly jaundiced:

A

Serum bilirubin >85umol/L

  1. Shorter RBC lifespan (70 days not 120) therefore more breakdown and Hb production
  2. Newborns have a lot of RBC’s!
  3. Hepatic bilirubin metabolism (converting UC -> C) is less effective in the first few days of life
58
Q

Define ‘prolonged jaundice’ and what can cause it

A

Prolonged = >14 days in a term infant and >21 days in a preterm infant

The commonest cause of prolonged jaundice is breast feeding (mechanism unclear, but thought to be due to increased enterohepatic circulation of BR)

59
Q

List causes of 1) unconjugated, 2) conjugated hyperbilirubinaemia

A

1) Unconjugated = most common type, caused by:
- haemolytic disease (ABO incompat, Rh factor)
- physiological
- breast feeding
- hypothyroidism
- infection (sepsis/UTI)

2) Conjugated = rarer, but most common cause to rule out is BILIARY ATRESIA

60
Q

What complication can occur with unconjugated hyperbilirubinaemia?

A

Unconjugated BR can be deposited in the brain causing kernicterus (encephalopathy, as bilirubin is neurotoxic and can present with lethargy and poor feeding, occurs when serum BR levels >400umol/L)

61
Q

How is neonatal jaundice treated?

A

1) Phototherapy using 450nm wavelength of light (converts the UCBR into soluble pigment which can be excreted)
2) Exchange transfusion

62
Q

List the top 5 causes of respiratory distress in the neonate

A
  1. Transient tachypnoea of the newborn (delayed resorption of lung fluid)
  2. Respiratory distress syndrome (surfactant deficiency)
  3. Meconium aspiration
  4. Pneumothorax
  5. Infection
63
Q

List the top 5 causes of cyanosis in the neonate

A
  1. Any cause of respiratory distress
  2. Persistent pulmonary hypertension
  3. Congenital (cyanotic) heart disease
  4. Tracheo-oesophageal fistula
  5. Diaphragmatic hernia
64
Q

List signs of dehydration in a child:

A 
Tearless, sunken eyes
Sunken fontanelles
Reduced tone
Drowsy
Reduced skin turgor
Cold peripheries
Increased CRT
Reduced urine output
65
Q

What does an abnormal Galleazi test suggest?

A

The shorter femur = DDH on that side!

66
Q

List RFx for DDH (developmental dysplasia of the hip):

A

Female gender
Breech delivery
Positive family history of DDH

67
Q

What investigative method is used to diagnose DDH?

A

USS

68
Q

What bone complications can arise from DDH?

A

Avascular necrosis
Osteoarthritis
Re-dislocation

69
Q

How is DDH treated?

A

Babies wear Pavlik harness

Surgical reduction if this fails/discovered later in life

70
Q

List indications for urinalysis in children

A 
Infection (all infants <1yr with unexplained temp)
Haematuria
?Sexual abuse
Failure to thrive
Abdominal pain
Hypertension
Neonatal prolonged jaundice
71
Q

List methods of collecting urine from children

A 
Cotton wool in nappy
Clean catch
Bag
Suprapubic aspiration
Indwelling catheter
72
Q

How do you collect an MSSU (mid stream specimen of urine)?

A

Should be a MID stream specimen of urine
Ask parents to clean the perineum of the infant or child (from front to back)
Should be a “clean catch” into a foil dish- no touching the inside of the dish
Then decanted into a urine pot

73
Q

Why might nitrites not be present in the urine sample of infants <1yr?

A

As the urine must have been in the bladder for at least 4 hours for nitrates to form

74
Q

What does a low specific gravity suggest?

A

Dilute urine

75
Q

List indications for using a peak flow meter

A

Diagnostic
Monitor response to treatments
Marker of severity in exacerbations

76
Q

Counsel how to use a peak flow meter

A

Set the counter back to zero before starting
Hold so that your fingers don’t obstruct the dial (from beneath/both hands)
Sit up straight/perform standing
Take a breath in to completely fill your lungs
Make a good seal on the mouthpiece, make sure teeth/tongue aren’t in the way
Blow out into the peak flow as hard and as fast as you can
Look at the counter after you perform the test (make a note)
You usually Take the best of 3 goes.

You should ensure that their technique is good enough that the repeatability of the best 2 are within 10%.

77
Q

Counsel how to use an inhaler + spacer

A

Shake well before use
Remove cap
Check expiry date on the inhaler
Prime before first use/if not used for weeks (with one puff)
Keep chin up and create tight seal
Breathe out before using
Breathe in over 2-4 seconds starting as you deliver the puff
Give enough time for inhaler to reset (at least 30 seconds!) before next puff (5-10 breaths in a spacer). Breaths MUST be slow to ensure the drug doesn’t hit the back of the throat and you get optimum delivery to the lungs.

If using a steroid inhaler can advise using just before brushing teeth in morning/evening

We would never advocate using a MDI (metered dose inhaler) without a spacer. Only if there wasn’t one available, but we would always encourage them to have one with their Salbutamol. (Use spacers up to ~5yrs old)

78
Q

What are the ‘paeds’ sepsis 6?

A
  1. IV access and bloods
  2. Antibiotics
  3. Fluid resus
  4. Involve senior/specialist early
  5. Oxygen
  6. Consider inotropic support early
79
Q

What proportion of 3 month olds experience GORD

A

50%

80
Q

What complications can arise if GORD is not treated in infants?

A

Failure to thrive
Oesophagitis
Aspiration pneumonia

81
Q

When does paediatric coeliac disease commonly present?

A

During weaning at 6-9 months when gluten-containing foods are introduced into the diet

82
Q

How does paeds coeliac present?

A 
Failure to thrive
Malabsorptive symptoms
Fatty pale stools
Muscle wasting
Distended abdomen
83
Q

How is coeliac disease diagnosed (describe specific features to look for!)

A 
anti-TTG antibody
Duodenal mucosal biopsy, looking for:
1) Villous atrophy
2) Crypt hyperplasia
3) Increased intra-epithelial lymphocytes
84
Q

List 5 causes of paediatric diarrhoea

A
  1. Starvation (green, watery mucous)
  2. Response to infection elsewhere e.g. pneumonia
  3. Infection of GI system e.g. E.coli, salmonella
  4. Surgical - intussusception
  5. Surgical - Hirschprung’s disease
85
Q

What is the most common causative agent of gastroenteritis in children?

A

Rotovirus

86
Q

Describe Meckel’s diverticulum

A

A type of TRUE (contains all 4 layers of the bowel wall) diverticulum, occurs congenitally

  • 2inches long
  • 2 feet from the ileocaecal valve
  • affects 2% of the population
  • presents ~2yrs of age
87
Q

What are the most common organisms that cause septic arthritis in children?

A

Staph aureus

Strep pneumoniae

88
Q

List 6 causes of hepatomegaly in paeds

A
  1. Infection/inflammation e.g. hepatitis/autoimmune conditions
  2. Congestive cardiac failure/Budd-Chiairi
  3. Infiltration (e.g. by tumours such as neuroblastoma)
  4. Obstruction of the biliary system -> biliary atresia, gallstones
  5. Storage disorder (of glycogen, lipids, metals, CF)
  6. Idiopathic
89
Q

List 5 causes of splenomegaly in paeds

A
  1. Infection (EBV/CMV)
  2. Haematological (hereditary spherocytosis/sickle cell)
  3. Inflammatory disorders e.g. sarcoidosis, RA
  4. Cirrhosis and liver disease e.g. portal HTN, portal vein thrombosis
  5. Neoplastic
90
Q

What are the top 6 causes of rectal bleeding in paeds?

A
  1. Local e.g. anal fissure
  2. Blood swallowed from epistaxis
  3. Gastroenteritis
  4. Intussusception
  5. IBD
  6. Acid ulceration
91
Q

List RFx for paeds IBD

A
  1. Bottle feeding
  2. FHx of IBD / FHx of AI conditions e.g. RA, thyroid disease
  3. Parental smoking
  4. Peri-anal signs (50% of paeds crohn’s will have diagnostic signs on inspection)
92
Q

Name 4 bacteria which can cause bloody gastroenteritis

A
  1. E.coli
  2. Yersinia
  3. Salmonella
  4. Campylobacter
  5. Shigella
  6. C.Diff
93
Q

What is the most common gene mutation in achondroplasia?

A

FGFR3

94
Q

List the 5 most common intrauterine infections

A

TORCH

  • toxoplasmosis
  • other (syphilis)
  • rubella
  • cytomegalovirus
  • HSV (herpes simplex virus)
95
Q

Name the teratogenic effects of the following drugs if taken in pregnancy:

  1. Phenytoin
  2. Carbemazipine/sodium valproate
  3. Lithium
  4. Warfarin
  5. Tetracycline
A
  1. Phenytoin - cleft palate, cardiac defects…
  2. Carbemazipine/sodium valproate - neural tube defects
  3. Lithium - Ebstein’s anomaly (= TRAD: tricuspid incompetence, RV enlargement, ASD, dysrhythmias)
  4. Warfarin - frontal bossing, cardiac defects
  5. Tetracycline - teeth discolouration
96
Q

List the three phases of growth

A

Infantile -> from conception to 2 years (GH and thyroxine dependent)

Childhood (2 yrs to adolescence)

Pubertal phase - from adolescence until final height reached (controlled by sex steroids and ends when epiphyseal fusion occurs)

97
Q

What is the formula used to correct for plotting the growth of premature babies?

A

Baby’s current age (weeks) - (40 - gestation in weeks at birth)

98
Q

What complication can occur in paeds DKA if resuscitation fluids are given too soon

A

Cerebal oedema

99
Q

What infective agent causes acute epiglottitis?

A

Haemophilus influenza B

100
Q

At what age does epiglottis commonly present and how?

A

2-6yrs
Stridor & drooling
Sudden onset
Pyrexia >38

101
Q

List the viruses which can cause acute croup

A

PAIR viruses

  • parainfluenza
  • adenovirus
  • influenza A/B
  • RSV
102
Q

At what age does croup commonly present and how?

A

6 months - 3 years

Inspiratory stridor and barking cough

103
Q

How is croup treated?

A

Oxygen
Steroids (oral dex)
Nebulised adrenaline if worsens

104
Q

What is the causative agent of acute bronchiolitis?

A

RSV (respiratory syncytial virus) commonly

Sometimes bacterial

105
Q

At what age does bronchiolitis commonly present and how?

A

6 weeks - 6 months

Coryzal symptoms and a progressive wheeze

106
Q

What is the causative agent of pertussis?

A

An UTRI caused by bordetella pertussis bacteria (childhood vaccine is advised)

107
Q

How does pertussis normally present, and how is it treated?

A

Common <6 months
Inspiratory whoop / whooping cough

Treat with Abx

108
Q

Describe the salter harris classification of growth plate injuries:

A

SALTER

  1. A # Straight across the growth plate
  2. A # Above the growth plate (metaphysis!!!)
  3. A # below (Low) the growth plate (epiphysis!!!)
  4. A # Through the growth plate
  5. A # Entire growth plate is Rammed together
109
Q

Describe a greenstick vs a buckle fracture

A

Greenstick = bend in a bone and the cortex is broken on one side

Torus = slight bulge of the radial cortex (but cortex is still in tact)

110
Q

What is Perthe’s disease?

A

Avascular necrosis of the femoral head in children
Idiopathic and cause unknown
Presents 4-10 years
Presents with groin/hip/knee pain and limp
Reduced hip abduction + internal rotation
Treatment = rest+/- surgery

111
Q

Describe SUFE, the age it normally presents at and how?

A 
Slipped upper femoral epiphysis
10-16yrs
Presents with pain and limping
Obesity is the main risk factor
Can be bilateral
Is a type 1 salter harris #
112
Q

What type of fracture in children is pathognomic of non-accidental injury/

A

Metaphyseal (bucket handle) fracture

113
Q

What are the NICE guidelines for the investigation of UTI’s in children 6 months-3yrs for

a) atypical infection?
b) recurrent infection?

A

a) Atypical infection -> USS at the time, and DMSA scan 4 months later
b) Recurrent infection -> USS 6 weeks after the scan and DMSA 4 months later

114
Q

How can you differentiate a cephalohaematoma from caput succadaneum?

A

Cephalohaematoma is sub-periosteal, therefore does not cross the suture lines

Caput can cross the midline and extend over suture lines

115
Q

Describe the AMPLE mnemonic used to take a side history in A&E

A 
A - allergies
M - medications
P - PMHx
L - last meal/drink
E - environment, more about the event
116
Q

What is the underlying worry with a ‘boggy’ skull?

A

That there is an underlying skull fracture

117
Q

Describe categories of pathology that could cause a ‘limping’ child

A

Tiny TIM!

Tumour
Trauma
Infection
Inflammation
Mechanical
MSK
118
Q

Describe neuroblastoma

A

Tumour of neural crest cells, commonly in adrenals but can present anywhere in sympathetic NS
Common presentation of a limping child as bone is a common met site
Usually <5yrs

119
Q

Describe Ewing’s sarcoma and osteosarcoma and how they are differentiated

A

Ewing’s sarcoma = primary bone tumour (malignant), presents in teens
Osteosarcoma = primary bone tumour (malignant), presents in teams and second peak in elderly

Ewing’s -> moth-eaten, lucent lesions
Osteo -> blastic white lesions with periosteal reactions (Codman’s triangle) - google pics!

120
Q

What is the most common infective agent in osteomyelitis in children?

A

Staph aureus

121
Q

Describe Reiter’s syndrome

A

M>F

  • urethritis
  • arthritis (reactive - no infection in joint!)
  • conjunctivitis
  • +/- plantar fasciitis
122
Q

Describe transient synovitis of the hip

A

Hip held flexed and externally rotated
Proceeded by coryzal illness
Also called irritable hip
3-10yrs
Pain may be referred to the knee
Bloods may show slight inflammation and USS may show effusion
Just conservative rest and analgesia until can weight bear again

123
Q

Describe the pathophysiology behind DMD and BMD

A 
DMD = duchenne muscular dystrophy (x-linked recessive - only M affected!- show's Knight's move inheritance where a carrier mother with an affected father passes the disease onto her son)
BMD = Becker's muscular dystrophy

DMD = out of frame mutation in the DMD gene which means abnormal ‘dystrophin’ protein is made, which usually acts as an intracellular linking protein for fibrin molecules -> this means that muscles cannot contract properly

BMD = less severe as it is an ‘in-frame’ mutation, so muscle weakness is not as severe

124
Q

Why should aspirin not be given to children?

A

Can cause Reye’s syndrome

vomiting, rapid breathing, can cause brain and liver damage

125
Q

Define cerebral palsy

A

A group of permanent (usually non-progressive) disorders affecting motor and postural functioning, usually attributable to a disturbance that occurred to the developing fetal brain

126
Q

List differentials for proteinuria in the child

A
  • minimal change disease
  • FSGS
  • membranous glomerulonephritis (antiphospholipase A receptor)
127
Q

List differentials for haematuria in the child

A
  • IgA nephropathy
  • Post-infectious glomerulonephritis
  • Goodpasture’s syndrome (antibodies against T4 collagen on basement membranes of lungs and kidneys causing haematuria and haemoptysis)
  • vasculitic causes (MPA and GwP)
128
Q

List the diagnostic features of ADHD

A

Attention deficit hyperactivity disorder

  • inattention
  • hyperactivity
  • impulsitivy
129
Q

List the diagnostic features of ASD

A

Autistic spectrum disorder

  • repetitive, stereotyped behaviour
  • difficulty with social interactions
  • impaired communication
130
Q

What is included in an adolescent HEADS screen

A 
Home life
Education
Activities and hobbies
Drugs/drinking
Sex/smoking/suicide
131
Q

What are the features of Kawasaki disease

A

CRASH & burn (fever)

  • conjunctivitis
  • strawberry RED tongue
  • lymphAdenopathy (cervical)
  • skin on hands and feet dry
  • rash on hands
  • persistent fever for >5 days
132
Q

Describe the causative agent and the features of paediatric hand, foot & mouth disease

What is it’s treatment?

A

Caused by coxsackie A virus

Pink/grey blisters on hands/feet and in mouth, which peel off after a week and leave no scarring

Treatment = supportive + analgesia

133
Q

Describe the flow chart for the management of childhood asthma

A
  1. SABA (salbutamol)
  2. Low dose ICS

Still uncontrolled,
<5yrs = LTRA (T for tiny)
>5yrs = LABA (A for adult)

134
Q

List 3 cyanotic paediatric cardiac disorders

A

3T’s

  • Tetralogy of fallot
  • Transposition of great arteries
  • Tricuspid atresia
135
Q

Describe the features in tetralogy of fallot

A

CYANOTIC = PORV

  1. Pulmonary stenosis (R outflow obstruction)
  2. Over-riding aorta
  3. RV hypertrophy
  4. VSD
136
Q

Describe the features of Ebstein anomaly

A

TRAD

  1. Tricuspid incompetence
  2. RV enlargement
  3. ASD
  4. Dysrhythmias

Year 4 (28 decks)

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