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Phase 3a Jemima > Paediatrics - Cardio, resp and gastro > Flashcards

Paediatrics - Cardio, resp and gastro Flashcards

1
Q

what are the three fetal shunts

A

ductus venosus
foramen ovale
ductus arteriosus

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2
Q

what is the ductus venosus

A

it is a shunt that connects the umbilical vein to the inferior vena cava and allows blood to bypass the liver

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3
Q

what is the foramen ovale

A

it is a shunt that connects the right atrium with the left atrium and allows blood to bypass the right ventricle and pulmonary circulation

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4
Q

what is the ductus arteriosus

A

it is a shunt that connects the pulmonary artery with the aorta and allows the blood to bypass the pulmonary circulation

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5
Q

what in the body helps to maintain the ductus arteriosus

A

prostaglandins

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6
Q

what are the three causes of pan-systolic murmur

A

mitral regurgitation
tricuspid regurgitation
ventricular septal defect

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7
Q

what are the three causes of an ejection systolic murmur

A

aortic stenosis
pulmonary stenosis
hypertrophic obstructive cardiomyopathy

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8
Q

what causes splitting of the second heart sound

A

during inspiration there is a negative intra-thoracic pressure. This causes the right side of the heart to fill faster. the increased volume in the right ventricle causes it to take longer for the right ventricle to empty during systole causing a delay in the pulmonary valve closing. As it closes slightly later than the aortic valve it causes the second heart sound to be split

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9
Q

what murmur does an atrial septal defect cause

A

a mid systolic crescendo decrescendo murmur
- loudest at the upper left sternal boarder
- with a fixed split second heart sound

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10
Q

what murmur is heart with a patent ductus arteriosus (normally severe one)

A

continuous crescendo -decrescendo machinery murmur which may continue into the second heart sound

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11
Q

what murmur is heart with a tetralogy of fallot

A

an ejection systolic murmur due to the pulmonary stenosis

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12
Q

what conditions can/do cause cyanotic heart disease

A
  • ventricular septal defect
  • atrial septal defect
  • patent ductus arteriosus
  • transposition of the great arteries
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13
Q

how does a patient ductus arteriosus usually present

A

shortness of breath
difficulty feeding
poor weight gain
lower respiratory tract infections

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14
Q

how is patient ductus arteriosus diagnosed

A

echocardiogram
- use of doppler flow studies

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15
Q

how is a patient ductus arteriosus managed

A

monitored up until 1 year of age using echo
then after 1 its highly unlikely for the PDA to spontaneously close and trans-catheter or surgical closure will be performed

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16
Q

what are the different types of atrial septal defect

A
  1. ostium secundum, where the septum secundum fails to fully close leaving a hole
  2. patient foramen ovale
  3. ostium primum, where the septum primum fails to fully close leaving a hole
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17
Q

what are complications of atrial septal defect

A

stroke (VTE)
atrial fibrillation or atrial flutter
pulmonary hypertension and right sided heart failure
eisenmenger syndrome

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18
Q

how does atrial septal defect present

A

mid systolic crescendo decrescendo murmur
fixed splitting of the second heart sound
shortness of breath
difficulty feeding
poor weight gain
lower respiratory tract infections

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19
Q

how does atrial septal defect present in adults

A

dyspnoea
heart failure
stroke

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20
Q

how is atrial septal defect managed

A

small and asymptomatic - watch and wait
large/symptomatic - transvenous catheter closure and anticoagulants

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21
Q

what conditions is ventricular septal defect often associated with

A

downs syndrome
turners syndrome

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22
Q

how does ventricular septal defect present

A

poor feeding
dyspnoea
tachpnoea
failure to thrive

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23
Q

how is a ventricular septal defect treated

A

small/asymptomatic - watch and wait
larger/symptomatic - transvenous catheter closure, open heart surgery and antibiotic prophylaxis due to increased IE risk

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24
Q

what is Eisenmenger syndrome

A

it occurs when blood flows from the right side of the heart to the left across a structural lesion bypassing the lungs

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25
Q

what three underlying lesions can lead to Eisenmenger syndrome

A

atrial septal defect
ventricular septal defect
patient ductus arteriosus

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26
Q

what is the pathophysiology of Eisenmongers syndrome

A

ASD or VSD allows a left to right shunt causing pulmonary hypertension. When pulmonary pressure becomes greater than systemic pressure then the shunt reverses and becomes right to left. This means that blood bypasses the lungs and causes cyanosis

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27
Q

what types of examination finding would you have in Eisenmengers syndrome

A

ones relating to the pulmonary hypertension
- right ventricular heave, loud P2, raised JVP, peripheral oedema
ones relating to the underlying septal defect
ones relating to the right to left shunt and chronic hypoxia
- cyanosis, clubbing, dyspnoea, plethoric complexion

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28
Q

what is the prognosis for someone with Eisenmenger syndrome

A

reduced life expectancy by around 20 years
- main causes of death are heart failure, thromboembolism, infection and haemorrhage

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29
Q

what is the management for Eisenmenger syndrome

A

once pulmonary pressure is high enough to cause the syndrome it is irreversible so you have to control the symptoms
- oxygen
- treatment of pulmonary htn with sildenafil
- treat arrhythmias
- treat poylcythaemia with venesection
- prevent and treat thrombosis with anticoags
- prevent IE with prophylactic abx
only definitive treatment is a heart -lung transplant

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30
Q

what is coarctation of the aorta

A

when there is a narrowing of the aortic arch, usually around the ductus arteriosus

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31
Q

what genetic condition is coarctation of the aorta associated with

A

Turners syndrome

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32
Q

how does coarctation of the aorta present

A
  • week femoral pulses
  • tachypnoea
  • poor feeding
  • grey floppy baby
  • left ventricular heave
  • underdeveloped left arm
  • underdeveloped legs
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33
Q

how is coarctation of the aorta managed

A

in severe cases babies will require input very soon after birth
- prostaglandin E is given to keep the ductus arteriosus open while awaiting surgery
- surgery will be performed to correct the coarctation and ligate the ductus arteriosus

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34
Q

how does aortic stenosis present

A

fatigue
shortness of breath
dizziness
fainting
symptoms are typically worse on exertion

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35
Q

what are signs of aortic valve stenosis

A

ejection systolic murmur - crescendo decrescendo and radiates to carotids
- ejection click
- palpable thrill
- slow rising pulse and narrow pulse pressure

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36
Q

how is aortic valve stenosis managed

A

regular echo, ECG and exercise testing to monitor the progression of the disease
- percutaneous balloon aortic valvoplasty
- surgical aortic valvotomy
- valve replacement

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37
Q

what are complications of aortic valve stenosis

A

left ventricular outflow tract obstruction
heart failure
ventricular arrhythmias
bacterial endocarditis
sudden death, often on exertion

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38
Q

what other conditions is pulmonary valve stenosis associated with

A

tetralogy of fallot
william syndrome
noonan syndrome
congenital rubella syndrome

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39
Q

how does pulmonary valve stenosis present

A

normally discovered during routine baby checks
fatigue on exertion
shortness of breath
dizziness
fainting

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40
Q

what are the signs associated with pulmonary valve stenosis

A

ejection systolic murmur
palpable thrill
right ventricular heave
raised JVP - giant A waves

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41
Q

how is pulmonary valve stenosis managed

A

mild - follow up with watch and waiting
severe - balloon valvuloplasty via venous catheter or open heart surgery

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42
Q

what is tetralogy of fallot

A

a condition where there are four coexisting pathologies
1. ventricular septal defect
2. overriding aorta
3. pulmonary valve stenosis
4. right ventricular hypertrophy

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43
Q

what are risk factors for tetralogy of fallot

A

rubella infection
increased age of the mother (over 40)
alcohol consumption in pregnancy
diabetic mother

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44
Q

what investigations are done with tetralogy of fallot

A

Echo and doppler flow studies
- boot shaped heart due to right ventricular thickening

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45
Q

how does tetralogy of fallot present

A

mostly picked up on antenatal scans before the child is born
- cyanosis
- clubbing
- poor feeding
- poor weight gain
- ejection systolic murmur
- tet spells

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46
Q

what is a tet spell

A

this is intermittent symptomatic periods where the right to left shunt becomes temporarily worsened - if a child is walking, physically exerting themselves or crying.
the child will become irritable, cyanotic and short of breath

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47
Q

how do you treat a tet spell

A

older children - squat
younger children - pull their knees to their chest
- supplementary oxygen
- beta blockers to relax the ventricle
- IV fluids to increase pre load
- morphine
- sodium bicarb to buffer metabolic acidosis
- phenylephrine infusion to increase SVR

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48
Q

how is tetralogy of fallot managed

A

in neonates prostaglandin infusion is given to maintain the ductus arteriosus
total surgical repair by open heart surgery is the definitive treatment

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49
Q

what is Ebsteins anomaly

A

it is a congenital heart condition where the tricuspid valve is set lower in the right side of the heart than normal causing a bigger right atrium and a smaller right ventricle

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50
Q

what other heart conditions is Ebsteins abnormality associated with

A

atrial septal defect
Wolff-parkinson-white syndrome

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51
Q

how does Ebsteins anomaly present

A

evidence of heart failure
gallop rhythm heard on auscultation
addition of a third and fourth heart sound
cyanosis
shortness of breath
tachypnoea
poor feeding
collapse
cardiac arrest

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52
Q

how is Ebsteins abnormality treated

A
  • treating the arrhythmias and heart failure
  • prophylactic antibiotics
  • surgical correction
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53
Q

what is transposition of the great arteries

A

this is where the right ventricle pumps blood into the aorta and the left ventricle pumps blood into the pulmonary circulation creating two separate circulations that dont mix

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54
Q

what other heart conditions is transposition of the great arteries associated with

A

ventricular septal defect
coarctation of the aorta
pulmonary stenosis

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55
Q

what does immediate survival of a baby with transposition of the great arteries depend on

A

depends on having a shunt
- patient ductus arteriosus
- atrial septal defect
- ventricular septal defect

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56
Q

how does transposition of the great arteries present

A

often diagnosed during antenatal screening
presents with cyanosis at/within a few days of birth
respiratory distress
tachycardia
poor feeding
poor weight gain
sweating

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57
Q

how is transposition of great arteries managed

A

prostaglandin infusion to maintain ductus arteriosus
balloon septostomy to create a large atrial septal defect to allow blood to flow to the lungs
open heart surgery is the definitive management - arterial switch procedure

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58
Q

what is bronchiolitis

A

it is when there is inflammation and infection in the bronchioles. it is normally caused by a virus

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59
Q

what is the most common cause of bronchiolitis

A

respiratory syncytial virus (RSV)

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60
Q

how does bronchiolitis present in children

A

coryzal symptoms - runny nose, sneezing, mucus in throat and watery eyes
signs of respiratory distress
dyspnoea
tachypnoea
poor feeding
mild fever (under 39)
apnoeas (episode where child stops breathing)
wheeze and crackles on auscultation

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61
Q
A

raised resp rate
use of accessory muscles
intercostal and subcostal recessions
nasal flaring
head bobbing
tracheal tugging
cyanosis
abnormal airway sounds

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62
Q

what are abnormal airway sounds

A

wheezing - whistling heard on expiration
grunting
stridor - high pitched inspiratory noise caused by obstruction of upper airway

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63
Q

what is the typical course of an RSV infection

A
  • usually starts as an upper resp tract infection with coryzal symptoms
  • from this point half get better spontaneously
  • the other half will develop chest symptoms over the first 1-2 days following onset of coryzal sx
  • symptoms generally are worse on day 3-4
  • symptoms will usually last 7-10 days total
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64
Q

when might a child need admission for bronchiolitis

A

aged under 3 months
pre existing conditions - prematurity, downs syndrome, cystic fibrosis
50-75% or less of their normal milk intake
clinical dehydration
resp rate over 70
oxygen sats under 92
moderate to severe resp distress
apnoeas
parents not confident in ability to manage at home

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65
Q

how is bronchiolitis managed

A

supportive management
- ensuring adequate intake: orally, NG or IV
- saline nasal drops and nasal suctioning
- supplementary oxygen
- ventilator support if needed

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66
Q

what ventilator support may be required in children with bronchiolitis

A
  1. high flow humidified oxygen via tight nasal cannula (has positive end expiratory pressure)
  2. continuous positive airway pressure, using a sealed nasal cannula
  3. intubation and ventilation
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67
Q

what signs indicate a poor ventilation

A

rising pCO2
falling pH

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68
Q

what is Palivizumab

A

it is a monoclonal antibody that targets RSV
- monthly injection is given as a prevention against bronchiolitis
- given to high risk babies
- not a true vaccine, only provides passive protection

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69
Q

what is viral induced wheeze

A

describes an acute wheezy illness caused by a viral infection

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70
Q

how to tell if its viral induced wheeze or asthma

A

typically viral induced wheeze
- presents before 3
- no atopic history
- only occurs during viral infections

where as asthma can be triggered by many things, has many signs and symptoms associated with it and shows variable and reversible airflow obstruction

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71
Q

how does viral induced wheeze present itself

A

evidence of a viral illness for 1-2 weeks preceding the onset of:
- shortness of breath
- signs of respiratory distress
- expiratory wheeze throughout the chest

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72
Q

How is viral induced wheeze managed in children

A

it is managed the same way as acute asthma in children

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73
Q

what is acute asthma

A

it is an acute exacerbation of asthma characterised by rapid deterioration in the symptoms of asthma

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74
Q

how does acute asthma present

A

progressively worsening shortness of breath
signs of respiratory distress
fast respiratory rate (tachypnoea)
expiratory wheeze
chest can sound tight on auscultation

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75
Q

what is the criteria for a moderate acute asthma attack

A

peak flow > 50% predicted
normal speech
saturations normal

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76
Q

what is the criteria for a severe asthma attack

A

peak flow <50 % predicted
saturations <92%
unable to complete sentences in one breath
signs of respiratory distress
resp rate >40 in 1-5yrs and >30 in over 5yrs
heart rate >140 in 1-5 yrs and >125 in over 5yrs

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77
Q

what is the criteria for life threatening asthma attack

A

peak flow <33% predicted
saturations <92%
exhaustion and poor resp effort
hypotension
silent chest
cyanosis
altered consciousness/confusion

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78
Q

how is acute asthma managed

A
  1. supplementary oxygen
  2. bronchodilators (salbutamol, ipratropium, magnesium sulphate)
  3. steroids to reduce airway inflammation
  4. antibiotics
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79
Q

how are bronchodilators stepped up in acute asthma attack

A
  1. inhaled or nebulised salbutamol
    2, inhaled or nebulised ipratropium bromide
  2. IV magnesium sulphate
  3. IV aminophylline
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80
Q

in moderate to severe acute asthma what is the stepwise approach taken to control the attack

A
  1. salbutamol inhalers via a spacer (10 puffs every 2 hours)
  2. nebulisers with salbutamol/ipratropium bromide
  3. oral prednisolone
  4. IV hydrocortisone
  5. IV magnesium sulphate
  6. IV salbutamol
  7. IV aminophylline
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81
Q

what ion should be monitored when on high doses of salbutamol

A

potassium - can cause a hypokalaemia

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82
Q

when a child is leaving hospital after acute asthma attack what should they be discharged home with

A

can be discharged when the child is well on 6 puffs 4 hourly of salbutamol
- prescribed a reducing regime of salbutamol to continue at home
- finish steroids if those were started
- provide safety net information
- provide individualized asthma action plan

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83
Q

what are the atopic conditions

A

asthma
eczema
hay fever
food allergies

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84
Q

what presentation might suggest a diagnosis of asthma

A

episodic symptoms with intermittent exacerbations
diurnal variability, typically worse at night and early mornings
dry cough with wheeze
shortness of breath
typical triggers
history of other atopic conditions such as eczema/hay fever
family history
bilateral widespread polyphonic wheeze
symptoms improve with bronchodilators

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85
Q

what are typical triggers for asthma

A

dust
animals
cold air
exercise
smoke
food allergies

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86
Q

how is asthma diagnosed

A

history and examination
- spirometry with reversibility testing
- direct bronchial challenge test with histamine or methacholine
- fractional exhaled nitric oxide
- peak flow variability

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87
Q

how do you treat asthma in children under the age of 5

A
  1. start with a short acting beta 2 agonist inhaler (salbutamol)
  2. add low dose corticosteroid inhaler or leukotriene antagonist
  3. add the other option from step 2
  4. refer to specialist
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88
Q

how do you treat asthma in children aged 5-12

A
  1. salbutamol
  2. add a regular low dose corticosteroid
  3. add salmeterol (LABA)
  4. titrate up the corticosteroid
  5. consider adding oral leukotriene receptor antagonist or oral theophylline
  6. increase the dose of corticosteroid
  7. refer to specialist
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89
Q

how do you treat asthma in children over the age of 12

A

the same as in adults
1. salbutamol
2. low dose corticosteroid inhaler
3. LABA i.e salmeterol
4. titrate up the corticosteroid to medium dose
5. consider oral leukotriene receptor antagonist or oral theophylline or LAMA
6. titrate up the corticosteroid to high dose
combine additional treatments from step 5
7. add oral steroids and refer to specialist

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90
Q

how does pneumonia present

A

cough - wet, productive
high fever - >38.5
tachypnoea
tachycardia
increased work of breathing
lethargy
delirium

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91
Q

what are signs that indicate pneumonia

A

tachypnoea
tachycardia
hypoxia
hypotension
fever
confusion

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92
Q

what are the characteristic chest signs of pneumonia

A

bronchial breath sounds - harsh, loud on inspiration and expiration
focal coarse crackles - air passing through sputum
dullness to percussion - lung tissue collapse/consolidation

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93
Q

what are causes of pneumonia

A

strep. pneuminia
group A strep
group B strep
staph aureus
haem. influenzae
mycoplasma pneumonia
respiratory syncytial virus
parainfluenza virus
influenza virus

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94
Q

how is pneumonia investigated

A

chest X ray
sputum cultures/throat swabs
viral PCR
blood cultures
capillary blood gas
blood lactate

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95
Q

how is pneumonia managed

A

amoxicillin (plus adding a macrolide such as clarithromycin/azithromycin will cover atypical)
- macrolides used as monotherapy in patients with penicillin allergy

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96
Q

what is croup

A

croup is an acute infective respiratory disease affecting children 6 months to 2 years (normally)
it affects the upper respiratory tract

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97
Q

what are causes of croup

A

parainfluenza
influenza
adenovirus
RSV
diphtheria (rare)

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98
Q

how does croup present

A

increased work of breathing
barking cough (clusters)
hoarse voice
stridor
low grade fever

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99
Q

how is croup managed

A

can be managed at home with supportive treatment
during an attack sit the child up to help them breath
oral dexamethasone is very effective (150mcg/kg)

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100
Q

what stepwise options are there is severe croup to get control of symptoms

A

oral dexamethasone
oxygen
nebulised budesonide
nebulised adrenalin
intubation and ventilation

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101
Q

what is epiglottitis

A

inflammation and swelling of the epiglottis caused by infection

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102
Q

what is the typical cause of epiglottitis

A

haem. influenza type B

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103
Q

what are presentations that suggest a possible epiglottitis

A

sore throat and stridor
drooling
tripod position
high fever
difficulty or painful swallowing
muffled voice
scared and quiet child
septic and unwell appearance

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104
Q

what investigations are done for suspected epiglottitis

A

if the patient is acutely unwell and epiglottitis is suspected then investigations should not be performed
- can do lateral x ray of the neck (thumb sign)

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105
Q

how is epiglottitis managed

A

Emergency !
key think is to not distress the child as it can make the airway close
alert senior paediatrician and anaesthetits
- secure the airway via intubation
- potentially do a tracheostomy
- once the airway is secure give IV antibiotics (ceftriaxone) and steroids (dexamethasone)

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106
Q

what is a common complication of epiglottitis

A

epiglottic abscess - collection of pus around the epiglottis

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107
Q

what is laryngomalacia

A

it is a condition affecting infants where the part of the larynx above the vocal cords is structured in a way that allows it to cause partial airway obstruction

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108
Q

what are the structural changes in laryngomalacia

A

the aryepiglottic folds are shortened which pulls on the epiglottis and changes its shape to a characteristic omega shape
the tissue surrounding the supraglottic larynx is softer and has less tone than normal, meaning it can flow across the airway, which happens particularly in inspiration

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109
Q

how does laryngomalacia present

A

inspiratory stridor - becomes more prominent when feeding, upset, lying on their back, in upper respiratory tract infections

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110
Q

what is the management of laryngomalacia

A

the problem resolves as the larynx matures and grows, usually no interventions are required
- rarely a tracheostomy is necessary
- surgery can improve symptoms

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111
Q

what is whooping cough

A

it is an upper respiratory tract infection caused by bordetella pertussis

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112
Q

how does whooping cough present

A

starts with mild coryzal symptoms
low grade fever
more severe cough after about a week - paroxysmal cough

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113
Q

how is whooping cough diagnosed

A

nasopharyngeal or nasal swab with PCR testing or bacterial culture
where the cough has been present for more than 2 weeks patients can be tested for the anti-pertussis toxin immunoglobulin G

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114
Q

how is whooping cough managed

A
  1. its a notifiable disease - tell public health
  2. supportive care
  3. macrolide antibiotics: azithromycin, erythromycin, clarithromycin (co-trimoxazole as alternative)
  4. close contacts given prophylactic antibiotics
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115
Q

what is a key complication of whooping cough

A

bronchiectasis

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116
Q

what is chronic lung disease of prematurity

A

typically occurs in babies under 28 weeks. They suffer respiratory distress syndrome, due to their lungs not being mature

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117
Q

what are features of chronic lung disease of prematurity

A

low oxygen saturations
increased work of breathing
poor feeding and weight gain
crackles and wheezes on chest auscultation
increased susceptibility to infection

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118
Q

how can you prevent chronic lung disease of prematurity

A

pre birth
- giving corticosteroids to mothers that show premature signs of labor (less than 36 weeks)

once the neonate is born
- use CPAP rather than intubation and ventilation where possible
- using caffeine to stimulate resp effort
- not over oxygenating with supplementary oxygen

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119
Q

how is chronic lung disease of prematurity managed

A

sleep study to assess oxygen saturations during sleep
babies may be discharged from the neonatal unit with low dose oxygen to use at home
monthly injections of palivizumab to protect them against RSC and reduce the risk of bronchiolitis

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120
Q

what genetic mutation causes cystic fibrosis

A

mutation of the cystic fibrosis transmembrane conductance regulatory gene (CFTR) on chromosome 7
- most common is the delta - F508

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121
Q

what channels are affected in cystic fibrosis

A

chloride channels

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122
Q

what are the key consequences of the cystic fibrosis mutation

A
  1. thick pancreatic and biliary secretions causing blocked ducts and lack of digestive enzymes
  2. Low volume thick airway secretions
  3. congenital bilateral absence of the vas deferens
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123
Q

how does cystic fibrosis present

A

meconium ileus is often the first sign
recurrent lower respiratory tract infections
failure to thrive
pancreatitis

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124
Q

how is cystic fibrosis screened for

A

it is screened for at birth with the newborn bloodspot test

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125
Q

what is primary ciliary dyskinesia

A

it is an autosomal recessive condition which affects the cilia of various cells in the body

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126
Q

what does primary ciliary dyskinesia cause dysfunction in

A

in motile cilia around the body, most notably in the respiratory tract leading to a build up of mucus in the lungs
also affects cilia in fallopian tubes in women

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127
Q

what is the Kartagner’s triad

A

it describes the three key features of primary cilia dyskinesia
- paranasal sinusitis
-bronchiectasis
-sinus inversus

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128
Q

what is sinus inversus

A

it is a condition where all the internal organs are mirrored in the body
- 25% of patients with sinus inversus have primary ciliary dyskinesia
- 50% of patients with primary ciliary dyskinesia have sinus inversus

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129
Q

how is primary ciliary dyskinesia diagnosed

A
  • patients typically present with recurrent respiratory tract infections
  • examination
  • chest x ray
  • semen analysis can diagnose male infertility
    Sample of ciliated epithelium = gives diagnosis
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130
Q

how can a sample of ciliated epithelium be obtained

A

nasal brushing or bronchoscopy

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131
Q

how is primary ciliary dyskinesia managed

A

daily physiotherapy
high calorie diet
antibiotics - prophylaxis

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132
Q

what are medical causes of abdominal pain

A

constipation
urinary tract infection
coeliac disease
IBD
IBS
mesenteric adenitis
abdominal migraine
pyelonephritis
henloch-schnlein purpura
tonsilitis
diabetic ketoacidosis
infantile colic
dysmenorrhoea
Mittelschmerz
ectopic pregnancy
PID
ovarian torsion
pregnancy

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133
Q

what are surgical causes of abdominal pain

A

appendicitis
intussusception
bowel obstruction
testicular torsion

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134
Q

what are red flags for serious abdominal pain

A

persistent or bilious vomiting
severe chronic diarrhoea
fever
rectal bleeding
weight loss or faltering growth
dysphagia
nighttime pain
abdominal tenderness

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135
Q

what investigations can be done which may indicate the abdominal pathology

A
  • anaemia can indicate IBD/coeliac
  • raised inflammatory markers can indicate IBD
  • raised anti-TTG/EMA indicated coeliac
  • raised faecal calprotectin indicated IBD
  • positive urine dipstick indicated UTI
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136
Q

what is recurrent abdominal pain

A

a diagnosis of recurrent abdominal pain is made when a child presents with repeated episodes of abdominal pain without an identifiable underlying cause

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137
Q

what other diagnosis does recurrent abdominal pain overlap with

A

abdominal migraine
irritable bowel syndrome
functional abdominal pain

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138
Q

what does recurrent abdominal pain often correspond with

A

stressful life events
- increased sensitivity and inappropriate pain signals from visceral nerves in the gut

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139
Q

what is the management for recurrent abdominal pain

A

distracting the child from the pain
encourage parents to not ask about the pain
advice about sleep, eating, diet, exercise, stress
probiotic supplements
avoid NSIADS
address psychological trigger and exacerbating factors
support from school

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140
Q

what is abdominal migraine

A

it is episodes of central abdominal pain which lasts more than 1 hour which may be associated with
- nausea and vomiting
- anorexia
- pallor
- headache
- photophobia
- aura

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141
Q

how are acute attacks of abdominal migraine managed

A

low stimulus environment
paracetamol
ibuprofen
sumatriptan

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142
Q

what are prevention medications used for abdominal migraine

A

pizotifen - serotonin agonist
propranolol
cyproheptadine - antihistamine
flunarazine

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143
Q

what are causes of constipation in children

A

idiopathic
functional constipation
Hirschsprungs
cystic fibrosis
hypothyroidism
spinal cord lesions
sexual abuse
intestinal obstruction
anal stenosis
cows milk intolerance

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144
Q

how does constipation present in children

A

less than 3 stools a week
hard stools that are difficult to pass
rabbit dropping stool
straining and painful passages of stool
abdominal pain
holding abnormal postures
rectal bleeding
faecal impaction causing overflow diarrhoea
hard stool may be palpable
loss of sensation of need to open bowels

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145
Q

what is encopresis

A

it is the term for faecal incontinence and is usually a sign of chronic constipation where the rectum becomes stretched and looses sensation

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146
Q

at what age is encopresis considered pathological

A

4 and above

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147
Q

what are other causes of encopresis other than chronic constipation

A

spinal bifida
Hirschprungs disease
cerebral palsy
learning disability
psychological stress
abuse

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148
Q

what lifestyle factors can contribute to the development of constipation

A

habitually not opening the bowels
low fibre diet
poor fluid intake and dehydration
sedentary lifestyle
psychological issues

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149
Q

what is desensitisation of the rectum

A

this is when patients keep ignoring the sensation of a full rectum and not opening their bowels, leading to a loss of that sensation and they start to retain faeces. This leads to faecal impaction which further exacerbates the problem

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150
Q

what are red flags in regard to constipation

A

not passing meconium within 48hrs of birth
neurological signs or symptoms
vomiting
ribbon stool - anal stenosis
abnormal anus
abnormal lower back or buttocks
failure to thrive
acute severe abdominal pain and bloating

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151
Q

what are complications of constipation

A

pain
reduced sensation
anal fissures
haemorrhoids
overflow and soiling
psychosocial morbidity

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152
Q

how is constipation managed

A

correct any reversible contributing factors - high fibre diet and good hydration
start laxatives - movicol
faecal impaction may require a disimpaction regimen with a high dose of laxatives at first
encourage and praise visiting the toilet

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153
Q

what causes in GORD in children

A

in babies there is immaturity of the lower oesophageal sphincter which allows reflux easily

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154
Q

how does GORD in children present

A

signs of problematic reflux includes
0 chronic cough
- hoarse cry
- distress, crying or unsettled after feeding
- reluctance to feed
- pneumonia
- poor weight gain
children over 1 year - heartburn, acid regurgitation, retrosternal or epigastric pain, bloating and nocturnal cough

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155
Q

what are possible causes of vomiting in children

A

overfeeding
GORD
pyloric stenosis - projectile vomiting
gastritis or gastroenteritis
appendicitis
infections such as UTI, tonsillitis or meningitis
intestinal obstruction
bulimia

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156
Q

what are red flags of vomiting in children

A

not keeping any feed down
projectile or forceful vomiting
bile stained vomit
haematemesis or meleana
abdominal distension
reduced consciousness, bulging fontanelle or neurological signs
respiratory symptoms
blood in the stool
signs of infection
rash, angioedema and other signs of allergy
apnoea

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157
Q

how is GORD in children managed

A

conservative: small frequent meals, burping regularly, not over feeding, keep the baby upright after feeding
medical: Gaviscon mixed with food, thickened milk or formula, proton pump inhibitors
surgical: barium meal and endoscopy, surgical fundoplication

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158
Q

what is sandifers syndrome

A

it is a rare condition causing brief episodes of abnormal movements associated with gastroesophageal reflux in infants

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159
Q

what are the key features of sandifers syndrome in children

A

torticollis - forceful contraction of the neck muscles causing twisting of the neck
dystonia - abnormal muscle contractions causing twisting movements and arching of the back

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160
Q

what causes pyloric stenosis

A

hypertrophy and narrowing of the pylorus which prevents food traveling from the stomach into the duodenum

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161
Q

what age does pyloric stenosis present

A

the first few weeks of life

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162
Q

how does a child with pyloric stenosis typically present

A

thin
pale
failure to thrive
projectile vomiting

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163
Q

why do you get vomiting in pyloric stenosis

A

after feeding there is increasingly powerful peristalsis in the stomach as it tries to push food into the duodenum. This eventually becomes so powerful it ejects food into the oesophagus and out of the mouth

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164
Q

what might the stomach of a baby with pyloric stenosis feel like post feeding

A

firm round mass in the upper abdomen

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165
Q

what will a blood gas of a child with pyloric stenosis show

A

hypochloric (low chloride) metabolic alkalosis
- due to the vomiting of hydrochloric acid

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166
Q

how is pyloric stenosis diagnosed

A

abdominal ultrasound

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167
Q

how is pyloric stenosis treated

A

laparoscopic pyloromyotomy (Ramstedts operation)
- incision in the smooth muscle to widen it

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168
Q

what is acute gastritis

A

it is inflammation of the stomach

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169
Q

what is enteritis

A

it is inflammation of the intestines

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170
Q

what is gastroenteritis

A

it is inflammation all the way from the stomach to the intestines

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171
Q

how does gastroenteritis present

A

with nausea, vomiting and diarrhoea

172
Q

what is the most common cause of gastroenteritis in children

A

viral - rotavirus, norovirus, (and adenovirus)

173
Q

what is the main concern with gastroenteritis

A

dehydration

174
Q

what is steatorrhoea

A

greasy stools with excessive fat content

175
Q

what are differential diagnosis of diarrhoea

A

infection - gastroenteritis
inflammatory bowel disease
lactose intolerance
coeliac disease
cystic fibrosis
toddlers diarrhoea
IBS
medications - antibiotics

176
Q

what type of e.coli produces the shiga toxin

A

e.coli 0157

177
Q

how is E.coli gastroenteritis spread

A

contact with infected faeces, unwashed salads or contaminated water

178
Q

what are symptoms of E.coli 0157

A

abdominal cramps
bloody diarrhoea
vomiting

179
Q

what can Shiga toxin lead to

A

haemoytic uraemic syndrome

180
Q

do you use antibiotics to treat E.coli

A

NO - antibiotics increase the risk of haemolytic uraemic syndrome so antibiotics should be avoided if gastroenteritis is considered

181
Q

what is a common cause of travelers diarrhoea

A

campylobacter jejuni

182
Q

what is the most common bacterial cause of gastroenteritis worldwide

A

campylobacter jejuni

183
Q

what type of bacteria is campylobacter jejuni

A

it is a gram negative bacteria
it has a curved or spiral shape

184
Q

how is campylobacter jejuni spread

A

raw or improperly cooked poultry
Untreated water
Unpasteurised milk

185
Q

what are symptoms of campylobacter jejuni

A

abdominal cramps
diarrhoea - often with blood
vomiting
fever

186
Q

what is the disease course with campylobacter jejuni

A

incubation in normally 2-5 days
symptoms resolve after 3-6 days

187
Q

what are common treatments of campylobacter jejuni

A

azithromycin
ciprofloxacin

188
Q

how is shigella spread

A

by contaminated water, swimming pools and food

189
Q

what is the disease time course for shigella

A

incubation period is 1-2 days
symptoms resolve within 1 week without treatment

190
Q

what are symptoms of shigella infection

A

bloody diarrhoea
abdominal cramps
fever

191
Q

what toxin can shigella produce and what can it cause

A

shiga toxin which can cause haemolytic uraemic syndrome

192
Q

how is severe cases of shigella treated

A

azithromycin
ciprofloxacin

193
Q

how is salmonella spread

A

eating raw eggs or poultry
eating food contaminated with the infected faeces of small animals

194
Q

what are symptoms of salmonella

A

watery diarrhoea - can have mucus or blood
abdominal pain
vomiting

195
Q

what is the disease course of salmonella infection

A

incubation is 12 hours to 3 days
symptoms normally resolve within 1 week

196
Q

what type of bacteria is bacillus cereus

A

it is a gram positive rod which is spread through inadequately cooked food

197
Q

what food does bacillus cereus grow on

A

fried rice left out a room temperature

198
Q

what toxin does bacillus cereus produce which causes symptoms

A

cereulide

199
Q

what is the symptoms of bacillus cereus infection

A

abdominal cramping and cramping within 5 hours of ingestion
produce different toxins in intestines which causes watery diarrhoea

200
Q

how quick do the symptoms of bacillus cereus resolve

A

within 24 hours

201
Q

what is the typical course of bacillus cereus infection

A

vomiting within 5 hours
diarrhoea after 8 hours
resolution after 24 hours

202
Q

How is Yersinia Enterocolitica spread

A

eating raw or undercooked pork
contamination with urine or faeces of other mammal such as rats/rabbits

203
Q

who does Yersinia most frequently affect

A

children

204
Q

what are symptoms of Yersinia

A

watery and bloody diarrhoea
abdominal pain
fever
lymphadenopathy
older children and adults present with abdominal pain due to mesenteric lymphadenitis

205
Q

what is the infection course in Yesinia

A

incubation is 4-7 days
illness can last 3 weeks or more

206
Q

how can staphylococcus aureus cause gastroenteritis

A

through production of toxin which cause intestinal inflammation

207
Q

what are symptoms of Staphylococcus aureus toxin

A

diarrhoea
perfuse vomiting
abdominal cramps
fever

208
Q

how does staphylococcus aureus toxin cause gastroenteritis

A

it grows on food such as eggs, dairy and meat and when they are ingested it causes intestinal inflammation

209
Q

what is Giardia lamblia

A

it is parasite which lives in the intestines of mammals

210
Q

how does giardia lamblia cause gastroenteritis

A

they release cysts in stools of infected mammals which contaminate food or water
- foecal oral transmission

211
Q

how can Giardia lamblia present

A

chronic diarrhoea

212
Q

how is Giardia lamblia diagnosed

A

stool microscopy

213
Q

how is giardia lamblia treated

A

metronidazole

214
Q

what are principles of gastroenteritis management

A

good hygiene
barrier nursing
patient isolation
maintaining patient hydration
microscopy, culture and sensitivities

215
Q

what are post gastroenteritis complications

A

lactose intolerance
irritable bowel syndrome
reactive arthritis
guillian barre syndrome

216
Q

what is coeliac disease

A

it is an autoimmune condition where exposure to gluten causes an immune reaction which created inflammation in the small intestine

217
Q

what are the antibodies present in coeliac disease

A

anti tissue transglutaminase
anti endomysial
deaminated gliadin peptides antibodies

218
Q

what area of the bowel is particularly affected by coeliac disease

A

jejunum

219
Q

what is the effect coeliac disease has on the small intestine

A

causes atrophy of the intestinal villi as the antibodies target the epithelial cells of the intestine

220
Q

how does coeliac disease present

A

can be asymptomatic
failure to thrive
diarrhoea
fatigue
weight loss
mouth ulcers
anaemia secondary to iron, B12 or folate deficiency
dermatitis herpetiformis - itchy blistering rash
neurological symptoms - peripheral neuropathy, cerebellar ataxia, epilepsy

221
Q

what are the genetic associations with coeliac disease

A

HLA- DQ2 gene - 90%
HLA - DQ8

222
Q

how is coeliac disease diagnosed

A

must be on gluten while being diagnosed
- total immunoglobulin A levels to exclude IgA deficiency
- check anti TTG and EMA
- endoscopy and biopsy of the jejunum

223
Q

what will endoscopy and biopsy of the small intestine show in coeliac disease

A

crypt hypertrophy
villous atrophy

224
Q

what are complications of untreated coeliac disease

A

vitamin deficiency
anaemia
osteoporosis
ulcerative colitis
enteropathy associated T cell lymphoma of the intestine
non Hodgkin lymphoma
small bowel adenocarcinoma

225
Q

what is the treatment of coeliac disease

A

life long gluten free diet

226
Q

what are features of Crohns disease

A

No blood or mucus in stool (less common)
Entire GI tract
Skip lesions on endoscopy
terminal ileum is most affected
transmural thickness
smoking is a risk factor
weight loss
strictures
fistulas

227
Q

what are features of ulcerative colitis

A

continuous inflammation
limited to the colon and the rectum
only the superficial mucosa is affected
smoking is protective
excrete blood and mucus
associated with primary sclerosing cholangitis

228
Q

how does IBD present in children

A

suspect IBD in children/teenagers with:
perfuse diarrhoea
abdominal pain
bleeding
weight loss
anaemia
systemically unwell during flairs with fevers, malaise and dehydration

229
Q

what are the extra-intestinal manifestations of IBD

A

finger clubbing
erythema nodosum
pyoderma gangrenosum
episcleritis and iritis
inflammatory arthritis
primary sclerosing cholangitis - ulcerative colitis

230
Q

how is IBD diagnosed

A

bloods - anaemia, infection, thyroid, kidney and liver function
Faecal calprotectin - 90% sensitive and specific
endoscopy - OGD and colonoscopy with biopsy
imaging - ultrasound, CT and MRI to identify any fistulas/abscesses/strictures

231
Q

what things are important to monitor in children with IBD

A

growth and pubertal development
- particularly during exacerbations or being treated with steroids

232
Q

how is remission induced in crohns

A

Steroids - oral prednisolone or IV hydrocortisone
if steroids dont work consider adding an immunosuppressant - azathioprine, mercaptopurine, methotrexate, infliximab, adalimumab

233
Q

how is remission maintained in crohns

A

First line: Azathioprine or mercaptopurine
Alternatives: methotrexate, infliximab, adalimumab

234
Q

when is crohns treated surgically

A

then the disease only affects the distal ileum it is possible to resect this area
can be used to treat strictures and fistulas

235
Q

how is remission induced in ulcerative colitis

A

First line: aminosalicylate (mesalazine)
second line: corticosteroids
severe disease: first line IV corticosteroids and second line IV ciclosporin

236
Q

how do you maintain remission in ulcerative colitis

A

aminosalicylate
azathioprine
mercaptopurine

237
Q

how can ulcerative colitis be treated surgically

A

as it only affects the coon and rectum removal of both will remove the disease
- patient is left with a permanent ileostomy or an ileo-anal anastomosis (J pouch)

238
Q

what is biliary atresia

A

it is a congenital condition where a section of the bile duct is either narrowed or absent resulting in cholestasis

239
Q

how does biliary atresia present

A

presents shortly after birth with significant persistent jaundice

240
Q

what causes jaundice in babies with biliary atresia

A

high levels of conjugated bilirubin

241
Q

what are initial investigations done in babies with significant jaundice

A

conjugated and unconjugated bilirubin to determine where the cause of the jaundice is

242
Q

what is the management of biliary atresia

A

surgery - kasai portoenterostomy
involves attaching a section of the small intestine to the opening of the liver
often patients require a full liver transplant to resolve the condition

243
Q

what are causes of intestinal obstruction

A

meconium ileus
Hirschsprungs disease
oesophageal atresia
duodenal atresia
intussusception
imperforate anus
malrotation of the intestines with a volvulus
strangulated hernia

244
Q

how does intestinal obstruction present

A

persistent vomiting - may be bilious
abdominal pain and distension
failure to pass stool or wind
abnormal bowel sounds - high pitched, tinkling, absent

245
Q

how is intestinal obstruction diagnosed

A

abdominal X ray - loops of dilated bowel
absence of air in the rectum

246
Q

how is intestinal obstruction managed

A

referral to the paediatric surgical unit
nil by mouth
nasogastric tube
IV fluids
treat underlying cause

247
Q

what is Hirschsprungs disease

A

it is a congenital condition where nerve cells of the mesenteric plexus are absent in the distal bowel and rectum

248
Q

what is the mesenteric plexus

A

it forms the enteric nervous system, which runs all the way along the bowel in the bowel wall. It is responsible for stimulating peristalsis of the large bowel

249
Q

what is the key pathophysiology of Hirschsprungs disease

A

there is the absence of parasympathetic ganglion cells
- dont travel all the way down to the colon so section left without the cells

250
Q

what is total colonic aganglionosis

A

this is when the entire colon is affected - no nerve innervation in the entire colon

251
Q

in Hirschsprungs disease is the aganglionic bowel constricted or dilated

A

it is constricted as it cant relax leading to the loss of movement of faeces and subsequent obstruction

252
Q

what other syndromes is Hirschsprungs disease associated with

A

Downs syndrome
neurofibromatosis
Waardenberg syndrome
multiple endocrine neoplasia type II

253
Q

how does Hirschsprungs disease present

A

varies on the individual and the how much bowel is affected
- delay in passing meconium
- chronic constipation since birth
- abdominal pain and distension
- vomiting
- poor feeding and failure to thrive

254
Q

what is Hirschsprung associated enterocolitis

A

it is inflammation and obstruction of the intestine occurring in about 20% of neonates with Hirschsprungs disease

255
Q

how does Hirschsprung associated enterocolitis present

A

2-4 weeks after birth with fever, abdominal distension, diarrhoea (blood) and features of sepsis
- life threatening !!!!

256
Q

what can Hirschsprung associated enterocolitis lead to

A

toxic megacolon and perforation of the bowel

257
Q

how is Hirschsprung associated enterocolitis treated

A

antibiotics
fluid resuscitation
decompression of the obstructed bowel

258
Q

how is Hirschsprungs disease managed

A

definitive management is surgical removal of the aganglionic section of the bowel

259
Q

how is Hirschsprungs disease diagnosed

A

Abdominal ultrasound
rectal biopsy is used to confirm the diagnosis

260
Q

what is intussusception

A

it is a condition where the bowel invaginates or telescopes into itself

261
Q

what is intussusception associated with

A

concurrent viral illness
Henoch-schlonlein purpura
cystic fibrosis
intestinal polyps
Meckel diverticulum

262
Q

what occurs during intussusception

A

the bowel folds inwards in itself when thickens the overall size of the bowel and narrows the lumen in the folded area leading to palpable mass in the abdomen and obstruction to the passage of faeces

263
Q

who does intussusception typically occur in

A

infants 6 months to 2 years
more common in boys

264
Q

how does intussusception present

A

severe colicky abdominal pain
pale, lethargic and unwell child
redcurrant jelly stool
upper right quadrant mass on palpation - sausage shaped
vomiting
intestinal obstruction

265
Q

how is intussusception managed

A

therapeutic enemas
surgical reduction if enemas dont work

266
Q

how is intussusception diagnosed

A

ultrasound scan or contrast enema

267
Q

what are complications of enemas

A

obstruction
gangrenous bowel
perforation
death

268
Q

what is appendicitis

A

it is inflammation of the appendix due to infection trapped within the appendix by an obstruction

269
Q

what are signs of appendicitis

A

central abdominal pain which moves to the right iliac fossa over time and becomes localised there
loss of appetite
nausea and vomiting
Rosvings sign
guarding
rebound tenderness
percussion tenderness

270
Q

how is appendicitis diagnosed

A

clinical presentation and raised inflammatory markers
CT scan
ultrasound scan in women to exclude ectopic pregnancy and ovarian torsion

271
Q

what are differential diagnosis of appendicitis

A

ectopic pregnancy
ovarian cysts
Meckels diverticulum
mesenteric adenitis
appendix mass

272
Q

what is the management of appendicitis

A

appendicectomy - definitive management
laparoscopic surgery

273
Q

what are complications of an appendicectomy

A

bleeding
infection
pain
scars
damage to bladder, bowel and other organs
anaesthetic risks
removal of normal appendix
venous thromboembolism

274
Q

what should be checked routinely though out childhood to ensure a child is growing normally

A

height
weight

275
Q

when is the most rapid rate of growth in a childs life

A

in the first year of life

276
Q

when is it acceptable for a child to loose weight

A

in the first few days of life when feeding is being established it is acceptable for a child to lose up to 10% of their birth weight

277
Q

what are the thresholds of concern based on a childs growth chart

A
  • a fall across one or more weight centile spaces if the birthweight was below 9th centile
  • a fall across two or more centile spaces if if the birthweight was between 9-91st centile
  • a fall across three or more centile spaces if birthweight was above the 91st centile
  • when current weight is below the second centile for age, no matter the birthweight
278
Q

what is the most common cause of faltering growth in children

A

inadequate dietary intake

279
Q

which children may have their own/different growth charts to normal

A

those with certain genetic conditions
- downs syndrome
- achondroplasia
- DiGeorge syndrome
- turners syndrome

280
Q

what are causes of inadequate nutritional intake in children

A

inadequate food provided - social
problems with eating - fussiness, mechanical issues
lifestyle - unbalanced diet

281
Q

what are causes of inadequate nutrient absorption or increased losses in children

A

malabsorption - CF, crohns, coeliac
vomiting - GORD, pyloric stenosis
diarrhoea - chronic infection, ulcerative colitis

282
Q

what are causes of increased nutritional requirements or ineffective utilisation in children

A

congenital heart disease
malignancy
metabolic syndromes - T1DM, hyperthyroidism
chronic inflammation or recurrent infections
chronic systemic disease

283
Q

what are the three causes for faltering growth in children

A

inadequate nutrient intake
inadequate nutrient absorption or increased losses
increased nutrient requirements or ineffective utilisation

284
Q

what is mid parental height

A

it gives an estimate of the childs predicted final height - genetic potential

285
Q

how do you calculate mid parental height

A

Males: (mums height + dads height)/2 +7cm
Females: (mums height +dads height)/2 -7cm

286
Q

when might mid parental height indicate an issue

A

if the childs current height centile is more than two centiles below the mid parental height centile

287
Q

what investigations should be done when a child is exhibiting faltering growth

A

history and examination
FBC
blood film
iron studies
vitamin D levels
U+E
LFT
inflammatory markers
tTG

288
Q

what is the management for a child with faltering growth

A
  • dietary advice and advice about mealtimes and then plot again to reassess after time
  • dietician referral
  • investigate and treat any underlying cause
289
Q

what advice should be given around mealtimes for children

A

Mealtimes should be relaxed and enjoyable
Balanced, nutritional meals should be offered
Ideally children should eat with the family- parents and/or other children
Young children should be encouraged to feed themselves, even if this is messy
Mealtimes should not be too brief or too long
Reasonable boundaries should be set for mealtime behaviour (while avoiding punitive approaches)
Coercive feeding should be avoided
There should be regular eating schedules (for example three meals and two snacks in a day)

290
Q

what are complications of faltering growth

A

permanent short stature
immunodeficiency
damage to growing brain - behavioral issues, poorer developmental and cognitive outcomes

291
Q

what are the three common stages constipation presents in childhood

A

weaning in infants
toilet training in toddlers
starting school

292
Q

what is chronic constipation

A

when it has lasted more than 8 weeks

293
Q

what are risk factors for paediatric constipation

A

diet low in fibre
low fluid intake
intercurrent illness
post operative bed rest or analgesia
psychological difficulty with toilet training

294
Q

what is type 1 on the bristol stool chart

A

separate hard lumps, like nuts
hard to pass

295
Q

what is type 2 on the bristol stool chart

A

sausage shaped but lumpy

296
Q

what is type three on the bristol stool chart

A

like a sausage but with cracks on the surface

297
Q

what is type 4 on the bristol stool chart

A

like a sausage/snake
smooth and soft

298
Q

what is type 5 on the britol stool chart

A

soft blobs
clear cut edges
passed easily

299
Q

what is type 6 on the bristol stool chart

A

fluffy pieces with ragged edges
mushy stool

300
Q

what is type 7 on the bristol stool chart

A

watery
no solid pieces
entirely liquid

301
Q

what is necrotising enterocolitis

A

it is the most common surgical emergency in neonates
- acute inflammatory disease predominantly affecting preterm infants

302
Q

what causes necrotising enterocolitis

A

exact cause is unknown
damage to the intestinal mucosa can occur due to vascular insults, toxin exposure, infection and genetic factors
this damage allows pathogenic colonisation of normal commensal bacteria

303
Q

what are risk factors to developing necrotising enterocolitis

A

85% of cases in premature babies or low birth weight
abnormal dopplers
antibiotic treatment lasting longer than 10 days or multiple courses
enteral feeding
cows milk formula
congenital heart disease

304
Q

how does necrotising enterocolitis present

A

new feed intolerance
vomiting
increasing volume of NG aspirate
distended abdomen which is tender and tense
Haematochezia - fresh blood in the stool

305
Q

what clinical findings may be present in a child with necrotising enterocolitis

A

abdominal distension, tender to palpation and can feel tense or wooden
reduced bowel sounds
palpable abdominal mass
visible intestinal loops
signs of sepsis

306
Q

what are differential diagnosis to necrotising enterocolitis

A

sepsis
intussusception
volvulus
hirschsprungs disease

307
Q

what investigations should be done for suspected necrotising enterocolitis

A

bloods - FBC, CRP
blood cultures
blood gas - raised lactate or acidosis
imaging - abdominal ultrasound 1st, X-ray

308
Q

what is the management of necrotising enterocolitis

A

infant nil by mouth
NG tube
assess for sepsis
IV fluids
IV antibiotics
surgery - if there is evidence of perforation, laparotomy carried out to remove perforated and necrotic bowel

309
Q

what are complications of necrotising enterocolitis

A

bowel perforation
DIC
sepsis
adverse neurodevelopmental outcomes
short bowel syndrome
formation of strictures
enterocolic fistulae
abscess formation

310
Q

what is marasmus

A

it is severe undernutrition - a deficiency in all the macronutrients that the body required to function (carbohydrates, fats and protein)

311
Q

what happens to the body in marasmus

A

the body will use its own storage of adipose tissue and then muscle for energy
it begins to shut down functions to conserve energy - cardiac activity slows, low blood pressure, low body temperature
immune system compromised
digestive system may begin to atrophy due to lack of food

312
Q

what are causes of marasmus

A

poverty and food scarcity
wasting diseases such as AIDS
infections such as chronic diarrhoea
anorexia
inadequate breastfeeding or early weaning
child abuse or neglect

313
Q

what are the external signs of marasmus

A

visible wasting of fat and muscle
prominent skeleton
head appears large for the body
face may appear old
loose dry skin
dry brittle hair or hair loss
sunken fontanelles in infants
lethargy, apathy, weakness
weight loss of more than 40%
BMI below 16

314
Q

what other symptoms can marasmus cause

A

dehydration
electrolyte imbalance
low blood pressure
slow heart rate
low body temperature
gastrointestinal malabsorption
stunted growth
developmental delays
anaemia
osteomalacia or rickets

315
Q

how is marasmus diagnosed

A

physical examination
plot on growth chart
measure upper arm circumference and height to weight ratios
bloods - FBC and look for deficiencies

316
Q

how is marasmus treated

A

stage 1: rehydration and stabilisation (REhydration SOlution for MALnutrition- ReSoMal)
stage 2: nutritional rehabilitation - may last 2-6 weeks
stage 3: follow up and prevention

317
Q

what is Kwashiorkor

A

it is a type of malnutrition characterised by severe protein deficiency causing fluid retention and a swollen distended abdomen

318
Q

who does Kwashiorkor affect

A

found in developing countries with high rates of poverty and food scarcity
poor sanitary conditions and high prevalence of infectious diseases
most common in children (3-5)

319
Q

what are the symptoms of Kwashiorkor

A

oedema
bloated stomach with ascites
dry brittle hair and hair loss
dermatitis - dry peeling skin, scaly patches
enlarged liver
depleted muscle mass but retained subcutaneous fat
dehydration
loss of appetite
irritability and fatigue
stunted growth in children

320
Q

what other complications can Kwashiorkor cause

A

hypoglycaemia
hypothermia
hypovolaemia
electrolyte imbalances
immune system failure
cirrhosis of the liver and liver failure
atrophy of the pancreas
atrophy of the gastrointestinal mucosa
growth and developmental delays
starvation and death

321
Q

what causes Kwashiorkor

A

diet of mostly carbohydrates
weaning with inadequate food replacement
lack of essential vitamins and minerals
lack of dietary antioxidants
parasites, and infectious diseases
significant life stress

322
Q

how is Kwashiorkor diagnosed

A

physical examination
history
measure childs weight to height ratio
measure childs height to age ratio

323
Q

how is Kwashiorkor treated

A
  1. treat/prevent hypoglycaemia (can occur when calories are introduced)
  2. treat/prevent hypothermia
  3. treat/prevent dehydration - ReSoMal
  4. correct electrolyte imbalances
  5. treat/prevent infection - antibiotics
  6. correct any micronutrient deficiencies
  7. start cautious feeding
  8. achieve catch up growth - once child is stabilised calories can be increased to 140%
  9. provide sensory stimulation and emotional support
  10. prepare for follow up after recovery
324
Q

what can happen in Kwashiorkor and marasmus if feeding occurs to quickly

A

re-feeding syndrome
life threatening !!

325
Q

what is meckels diverticulum

A

it is a congenital disorder where there is a small outpouching of the inner wall of the intestine

326
Q

what are the rule of 2s of meckels diverticulum

A

Meckels diverticulum occurs in 2% of the population
only 2% of people with it develop complications or symptoms
symptoms usually appear in children under 2
symptoms occurs twice as often in those assigned male at birth
it is usually located about 2 feet from the lower end of the small intestine
it may have either two types of ectopic tissue in it - stomach or pancreatic

327
Q

what are symptoms of meckels diverticulum

A

there wont be any unless there are complications
- blood in the stool
- anaemia symptoms
- abnormal abdominal swelling
- tenderness of stomach
- cramping
- nausea and vomiting

328
Q

what complications may arise in meckels diverticulum

A
  1. Gastrointestinal bleeding due to ectopic tissue secreting digestive juices leading to ulcers
  2. diverticulitis due to bacterial infection
  3. intestinal obstruction either due to extra tissue obstructing the bowel or intussusception
329
Q

what causes Meckels diverticulum

A

it occurs early in fetal development when the yolk sac is replaced by the placenta
the duct which connected the yolk sac to the embryo (vitelline duct) detaches and the fetus absorbs it
sometimes it doesnt detach or resorb fully and a remnant is left which becomes meckels diverticulum

330
Q

what are risk factors for Meckels diverticulum

A

may be more likely to have it if you have other congenital disorders such as oesophageal atresia or anorectal malformation
male sex
age under 50

331
Q

how is Meckel’s diverticulum diagnosed

A

accidental finding due to other condition
when symptoms present - history and exam
Meckels scan - imaging that can detect ectopic stomach tissue in diverticulum
Mesenteric arteriography (angiogram)
endoscopy

332
Q

what is the treatment for Meckels diverticulum

A

if it causes complications the patient can have a small bowel resection, cutting out the small piece of bowel with the diverticulum in it
- laparoscopic

333
Q

what is colic

A

when a baby cries nonstop for more than three hours a day at least three days a week
- inconsolable

334
Q

when does colic start

A

colic typically starts within the first ew weeks after birth
it peaks between 4 and 6 weeks of age
it typically ends rather abruptly when the baby is 3-4 months

335
Q

how common is colic

A

affects about 20% of babies

336
Q

what are symptoms of colic

A

repeated periods of inconsolable crying - hours
clenches fists
legs curled up over their tummy
arched back
hard swollen abdomen
passing of gas
active grimacing or painful look on their face
face turning bright ref or deeper shade after long periods of crying

337
Q

what causes colic in babies

A

abdominal pain or discomfort from gas
reflex
food allergies
milk protein intolerance
under or overfeeding
overstimulation
early form of migraine headache
emotional reaction to frustration, fear or excitement
underdeveloped digestive system

338
Q

what are complications of colic

A

toll on parents - stress
postpartum depression
shaken baby syndrome

339
Q

how is colic diagnosed

A

history and exam
- check for physical illness

340
Q

how is colic treated

A

there is no cure
keep a record - breastfeeding
try different brands of formula
skin to skin contact
rocking
swaddling
singing/white noise
burping the baby
warm baths

341
Q

what is cows milk allergy

A

unlike lactose intolerance CMA is an allergic reaction to proteins in the milk

342
Q

what are the two types of cows milk allergy

A

IgE mediated food allergy - immediate
non IgE mediated food allergy - delayed

343
Q

what are symptoms of cows milk allergy

A

often start in the early weeks and months of life
skin reactions - hives, eczema, redness, itching
GI issues - vomiting, diarrhoea, abdo pain, discomfort
resp symptoms - sneezing, runny nose, coughing, wheezing, SOB
general discomfort can display fussiness, irritability and refusal to feed

344
Q

how is cows milk allergy diagnosed

A

history and exam
referral to childrens specialist allergy service
allergy focused history
trial elimination of all cows milk protein

345
Q

what alternatives can be used for cows milk

A

breastfeeding - mother to not eat dairy products
hypoallergenic formula
amino acid formula

346
Q

how is cows milk allergy managed

A

dietician referral
use hypoallergenic formula
avoid all cows milk

347
Q

what is a choledochal cyst

A

they are congenital cystic dilations of the biliary tree

348
Q

what are choledochal cysts associated with

A

biliary atresia
hepatic fibrosis

349
Q

how does choledochal cysts present

A

typical triad:
abdominal pain
jaundice
abdominal mass

350
Q

what are type 1 choledochal cysts

A

these are the most common
1a. dilation of extrahepatic bile duct (entire)
1b. dilation of extrahepatic bile duct (focal segment)
1c. dilation of the common bile duct portion of extrahepatic duct

351
Q

what are type 2 choledochal cysts

A

true diverticulum from extrahepatic bile duct

352
Q

what are type 3 choledochal cysts

A

dilation of extrahepatic bile duct within the duodenal wall

353
Q

what are type 4 choledochal cysts

A

4a. cysts involving both intra and extrahepatic ducts
4b. multiple dilations/cysts of extrahepatic ducts only

354
Q

what are type 5 choledochal cysts

A

multiple dilations or cysts of intrahepatic ducts only

355
Q

what are type 6 choledochal cysts

A

dilation of cystic ducts

356
Q

how are choledochal cysts diagnosed

A

imaging can be achieved with US, CT ERCP and PTC or MRI
history and examination

357
Q

how are choledochal cysts treated

A

people with type 1, 2 and 4 usually undergo surgical resection of the cyst due to risk of malignancy
- hepaticojejunostomy

358
Q

what are complications of choledochal cysts

A

stone formation
malignancy - cholangiocarcinoma
cyst may rupture leading to bile peritonitis
pancreatitis

359
Q

what is poor feeding in infants

A

term used to describe an infant that has little interest in feeding, or not feeding enough to receive the necessary nutrition required for adequate growth

360
Q

what are causes of poor feeding in infants

A

premature birth - havent developed sucking reflex
diarrhoea
ear infections
cough and colds
teething
congenital hypothyroidism
Downs syndrome
hypoplastic left heart/heart defects
moving to solid foods

361
Q

what is neonatal hepatitis

A

it is inflammation of the liver in newborns typically between 1-2 months after birth

362
Q

what viruses are known to cause neonatal hepatitis

A

rubella
CMV
Hepatitis A, B, C

363
Q

what are causes of neonatal hepatitis

A

Viral
Genetic disorders - cholestasis, alpha 1 anti-trypsin deficiency, whilsons
idiopathic

364
Q

what are symptoms of neonatal hepatitis

A

jaundice
dark urine
light stools
swelling of the abdomen
failure to grow and gain weight at expected rate

365
Q

how is neonatal hepatitis diagnosed

A

history and exam
bloods - infection
liver biopsy - distinguish biliary atresia from neonatal hepatitis

366
Q

how is neonatal hepatitis treated

A

no specific treatment - depends on underlying cause
vitamin supplements
phenobarbital - stimulates liver to secrete more bile
formular containing more easily digested fats are also given

367
Q

how long does neonatal hepatitis caused by hep A take to clear up

A

within about six months

368
Q

what is imperforate anus

A

it is a congenital anorectal malformation where a normal anal opening is absent at birth

369
Q

what are symptoms of imperforate anus

A

failure to pass first meconium within 24 hours
meconium in the urine
girls may have fourchette fistula
boys may have posterior urethral fistula

370
Q

how is imperforate anus treated

A

posterior sagittal anorectoplasty

371
Q

what is gastroschisis

A

it is a paraumbilical defect with evisceration of the abdominal contents

372
Q

what is omphalocele

A

it is a defect of the umbilical ring with herniation of the abdominal viscera. it is covered by the peritoneum and amniotic membrane

373
Q

what are the two types of liver failure

A

acute liver failure (fulminant hepatic failure)
chronic liver failure

374
Q

what are common causes of acute liver failure in children

A

toxin or virus exposure causing liver damage
- too much paracetamol

375
Q

what are common causes of chronic liver failure

A

long term liver disease
- biliary atresia
- metabolic liver disease (Wilson)
- hepatitis

376
Q

what are symptoms of liver failure

A

confusion and disorientation
pain or tenderness
weakness
fatigue
nausea
vomiting
dark urine
easy bleeding
itching
small, spider like vessels visible in the skin
chills

377
Q

what are complications of liver failure

A

liver encephalopathy
jaundice
coagulopathy
portal hypertension
ascites
hepatomegaly

378
Q

how is liver failure diagnosed

A

bloods - FBC, albumin, bilirubin, LFTs, PT
ultrasound
CT scan

379
Q

how is liver failure treated

A

treatment depends on stage of liver failure, and the underlying cause
- may require liver transplant

380
Q

at what age is toddlers diarrhoea most common

A

between the ages of 1-5

381
Q

what are the symptoms of toddlers diarrhoea

A

chronic nonspecific diarrhoea
- three or more loose watery stools per day (can be more than 10 per day)
- can sometimes see undigested food in stool
- mild abdominal pain
- child will seem generally well in themselves

382
Q

what causes toddlers diarrhoea

A

thought that the balance of fluid, fibre and undigested sugars/food in a childs large bowel prevents fluid being absorbed correctly leading to loose stools
- NOT due to malabsorption or food intolerance

383
Q

how can toddlers diarrhoea be treated

A

the four Fs
Fat - want a higher fat diet in children
Fluid - 6-8 cups per day and reducing sugary drinks
fruit juice/fruit squash and fruit - high amounts can irritate the gut
fibre - too low or too high fibre diet can contribute to the diarrhoea

384
Q

what are the commonest viruses/bacteria in small children

A

strep pneumonia
RSV
mycoplasma
Human metapneumovirus
pertussis
influenza/parainfluenza

385
Q

what are the mot common reasons a child presents to the hospital with breathlessness

A

asthma
bronchiolitis
pneumonia
croup

386
Q

what is Galactosemia

A

rare hereditary disorder of carbohydrate metabolism that affects the bodies ability to convert galactose to glucose

386
Q

what causes galactosemia

A

deficiency in the GALT enzyme which is vital for conversion of galactose into glucose

387
Q

what are symptoms of galactosemia

A

within a few days of birth baby loses appetite and will vomit excessively
jaundice
hepatomegaly
amino acids and protein in urine
growth failure
ascites
oedema
diarrhoea
irritability
lethargy
failure to thrive

388
Q

what can galactosemia lead to

A

liver failure
kidney dysfunction
brain damage - arrested mental development
cataracts
ovarian impairement

389
Q

what causes symptoms in galactosemia

A

due to loss of GALT enzyme there is an abnormal accumulation of galactose related chemicals in organs leading to SX

390
Q

what is the inheritance pattern of galactosemia

A

autosomal recessive

391
Q

how is galactosemia diagnosed

A

bloods - Galactose-1-phosphate elevated in RBC and GALT is reduced
genetic testing
newborn screening programs

392
Q

what is the treatment for galactosemia

A

lactose restricted diet - do NOT do lactose tolerance test
speech therapy
individual education plans/learning help
hormone replacement therapy
antibiotics
genetic counselling

393
Q

what is infective endocarditis

A

this is an infection of the endothelium (inner surface) of the heart, most commonly affecting the heart valves

394
Q

what are risk factors for developing infective endocarditis

A

IV drug use
structural heart pathology
chronic kidney disease (particularly on dialysis)
immunocompromised
history of infective endocarditis

395
Q

what structural abnormalities can increase the risk of endocarditis

A

Valvular heart disease
Congenital heart disease
Hypertrophic cardiomyopathy
Prosthetic heart valves
Implantable cardiac devices (e.g., pacemakers)

396
Q

what are causes of infective endocarditis

A

The most common cause is Staphylococcus aureus.
Other causes include:
Streptococcus (notably the viridans group of streptococci)
Enterococcus (e.g., Enterococcus faecalis)
Rarer causes include Pseudomonas, HACEK organisms and fungi

397
Q

what are presenting symptoms of infective endocarditis

A

Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)
failure to thrive

398
Q

what are key examination findings for infective endocarditis

A

New or “changing” heart murmur
Splinter haemorrhages (thin red-brown lines along the fingernails)
Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet)
Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes)
Roth spots (haemorrhages on the retina seen during fundoscopy)
Splenomegaly (in longstanding disease)
Finger clubbing (in longstanding disease)

399
Q

what investigations should be done for infective endocarditis

A

blood cultures BEFORE starting antibiotics
ECHO - transoesophageal echo is more sensitive and specific

400
Q

what is the modified dukes criteria

A

it is a criteria that can be used to diagnose infective endocarditis and requires either:
one major plus three minor
five minor criteria

401
Q

what are the major criteria in the modified dukes criteria

A

persistently positive blood cultures
specific imaging findings i.e vegetation seen

402
Q

what are minor criteria in the modified dukes criteria

A

predisposition
fever above 38 degrees
vascular phenomena (splenic infarction, intracranial haemorrhage, janeway lesions)
immunological phenomena (osler nodes, roth spots and glomerulonephritis)
microbiological phenomena

403
Q

how is infective endocarditis managed

A

IV broad spectrum antibiotics (amoxicillin and optional gentamicin) given for 4 weeks for patients with native heart valves and 6 weeks for those with prosthetic heart valves
surgery is required for heart failure relating to valve pathology, large vegetations or abscesses, infections not responding to antibiotics

404
Q

what are the key complications for infective endocarditis

A

Heart valve damage, causing regurgitation
Heart failure
Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
Glomerulonephritis, causing renal impairment

405
Q

what is an innocent murmur

A

it is a common murmur in children caused by fast blood flow through various areas of the heart during systole

406
Q

what are the typical features of a innocent murmur

A

Soft
Short
Systolic
Symptomless
Situation dependent, particularly if the murmur gets quieter with standing or only appears when the child is unwell or feverish

407
Q

what are the differential diagnosis for pan-systolic murmurs

A

Mitral regurgitation heard at the mitral area (fifth intercostal space, mid-clavicular line)
Tricuspid regurgitation heard at the tricuspid area (fifth intercostal space, left sternal border)
Ventricular septal defect heard at the left lower sternal border

408
Q

what is cyanotic hear disease

A

this occurs when deoxygenated blood enters the systemic circulation

409
Q

how does cyanotic heart disease occur

A

it occurs when blood is able to bypass the pulmonary circulation and the lungs. This occurs due to a right to left shunt

410
Q

what causes heart failure in children

A

heart muscle disease or enlargement of the heart muscle (cardiomyopathy)
decrease in the blood supply to the heart (rare in children)
heart valve disease
cardiac arrhythmias
anaemia
infections
medicine side effects

411
Q

what are the symptoms of heart failure in children

A

oedema of the feet, ankles, legs, stomach, liver and neck veins
respiratory distress, especially with activity
poor feeding and weight gain
fatigue
excessive sweating while feeding, playing or exercising
weight loss
syncope
chest pain

412
Q

how do you diagnose heart failure in a child

A

Blood and urine tests.
Chest X-ray. The X-ray may show heart and lung changes.
Electrocardiography (ECG). .
Echocardiography (echo).
Cardiac catheterization. The doctor puts a small, flexible tube (catheter) into a blood vessel and moves it to the heart. This measures pressure and oxygen levels inside the heart.

413
Q

what are the most common causes of heart failure in children

A

cardiomyopathies and congenital heart defects

414
Q

how is heart failure treated in children

A

control of symptoms - nutritional support, oxygen support
diuretics - furosemide, spironolactone
ACE inhibitors
Beta blockers
inotropes - digoxin
dopamine and dobutamine to increase CO and decrease systemic and pulmonary vascular resistance
devise therapy; implantable cardioverted defibrillator and cardiac resynchronization therapy
heart transplant

415
Q

what types of arrhythmias are there in infants and children

A

AV nodal reentrant tachycardia
atrial flutter
atrial fibrillation
premature atrial contractions
premature ventricular contractions
ventricular tachycardia
ventricular fibrillation
bradycardia
heart block
sick sinus syndrome

416
Q

what is AV nodal reentrant tachycardia

A

this is causes sudden episodes of an abnormally fast heart rate starting in the atria. THis is the most common cause of super-ventricular tachycardia in children

417
Q

what are causes of arrhythmia in children

A

chest pain
difficulty eating
dizziness, syncope
fatigue or weakness
heart palpitations
irritability
shortness of breath

418
Q

what are causes of arrhythmia in children

A

most children have no underlying structural issues
- cardiomyopathy
- inherited conditions like long QT syndrome or catecholaminergic polymorphic ventricular tachycardia
- certain medications
- congenital heart disease
- electrolyte imbalance
- fever, dehydration, stress, inflammation
- infection

419
Q

how is arrhythmia diagnosed in children

A

bloods
echo
ECG
holter monitor - measures electrical activity over 24 hours

420
Q

how is arrhythmia treated in children

A

some done need treatment
antiarrhythmic medications: beta blockers or calcium channel blockers
ablation
cardioversion - traditional or chemical
implantable device
maze surgery - cuts/burns in heart tissue to stop faulty electrical signals

421
Q

what is sick sinus syndrome

A

where the sinus node is affected/damaged meaning it is unable to generate normal heartbeats at a normal rate, which can result in heartbeats that are too slow or too fast

422
Q

what are symptoms of sick sinus syndrome

A

Fainting.
Lightheadedness or dizziness.
Heart palpitations.
Exhaustion.
Shortness of breath.
While exercising: Feel tired, Have trouble breathing.

423
Q

what causes sick sinus syndrome

A

injury or breakdown of current in heart or SA node directly
injury to SA node
medication
genetic causes
metabolic causes

424
Q

what are risk factors for sick sinus syndrome

A

heart surgery
medications such as beta blockers or calcium channel blockers
metabolic issues such as high potassium or low calcium
diseases such as rheumatic fever, sarcoidosis or diphtheria
genetic mutations

425
Q

how is sick sinus syndrome treated

A

permanent pacemaker
medication for a fast heart rate
catheter ablation

426
Q
A

Phase 3a Jemima (16 decks)

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