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Final Year > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What is the ductus venosus?

A

Connects umbilical vein and IVC
Allows blood to bypass liver

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2
Q

What is the role of foramen ovale?

A

Connects RA to LA
Allows blood to bypass RV and pulmonary circulation

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3
Q

What is the role of the ductus arteriosus?

A

Connects pulmonary artery with aorta
Allows blood to bypass pulmonary circulation

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4
Q

When does the foramen ovale close and what does it become?

A

Fossa ovalis
Closes at first breath- Breath expands alveoli, decreases pulmonary vascular resistance, causes fall in pressure in RA, LA pressure greater than RA = Squashes atrial septum and closes foramen ovale

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5
Q

What can be given to keep the ductus arteriosus open?

A

Prostaglandin E

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6
Q

Which shunt is affected by prostaglandin E?

A

Keeps ductus arteriosus open

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7
Q

When does the ductus arteriosus close and what does it become?

A

Closes after 2-3d
Becomes ligamentum arteriosum
Increased blood oxygenation causes drop in circulating prostaglandins

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8
Q

When does the ductus venosus close and what does it become?

A

Stops functioning after umbilical cord clamped
Structurally closes after 2-3wks
Becomes ligamentum venosum

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9
Q

What are the features of innocent murmurs?

A

Soft
Short
Systolic
Symptomless
Situation dependent- Quieter on standing/only appears when unwell

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10
Q

What features of a murmur would prompt further investigation?

A

Murmur louder than 2/6
Diastolic
Louder on standing
Failure to thrive/feeding difficulty/cyanosis/SOB

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11
Q

What are the investigations done for murmurs?

A

ECG
Chest xray
ECHO

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12
Q

Which murmurs are pansystolic?

A

Mitral regurgitation (mitral area)
Tricuspid regurgitation (tricuspid area)
Ventricular septal defect (left lower sternal border)

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13
Q

List the ejection systolic murmurs

A

Aortic stenosis (aortic area)
Pulmonary stenosis (pulmonary area)
HCOM (4th ICS on L sternal border)

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14
Q

What causes splitting of the 2nd heart sound?

A

Pulmonary valve closing slightly later than aortic valve
During inspiration chest wall and diaphragm pull lungs and heart open- Negative intrathoracic pressure- Causes R side of heart to fill faster as pulls blood in from venous system- Increased volume in RV means takes longer to empty causing delay in pulmonary valve closing

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15
Q

Describe the examination findings of an atrial septal defect

A

Mid-systolic, crescendo-decrescendo loudest at upper left sternal border
Fixed split 2nd heart sound (blood flows from LA-RA increasing volume of blood in RV to empty before pulmonary valve can close)

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16
Q

Describe examination findings of patent ductus arteriosus

A

Continuous crescendo-decrescendo machinery murmur that may continue during 2nd heart sound (makes 2nd heart sound difficult to hear)

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17
Q

Which part of ToF dictates the severity of the condition?

A

The degree of pulmonary stenosis

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18
Q

What does the murmur in ToF arise from?

A

Pulmonary stenosis- Ejection systolic murmur loudest in pulmonary area

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19
Q

Which heart defects can causes cyanosis and why?

A

VSD
ASD
PDA
Transposition of great arteries
Cyanotic as cause R-L shunt

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20
Q

What causes cyanosis in cyanotic heart disease?

A

Deoxygenated blood enters systemic circulation
Blood bypasses pulmonary circulation and lungs
Occurs across R-L shunt

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21
Q

Which cyanotic heart defects are not always cyanotic and why?

A

VSD, ASD and PDA
Pressure in L heart>R heart, blood flows from high to low, prevents R-L shunt
If pulmonary pressure increases beyond systemic pressure = Starts R-L shunt and cyanosis = Eisenmenger syndrome

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22
Q

Which cyanotic heart defect always causes cyanosis?

A

Transposition of Great Arteries
Right side of heart pumps directly into aorta and systemic circulation

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23
Q

What is patent ductus arteriosus?

A

Fails to close (normally stops functioning within 1-3d and closes within 2-3wks)
Flow of blood from aorta to pulmonary artery

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24
Q

What are the risk factors for developing a PDA?

A

Genetics
Maternal rubella infection
Prematurity

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25
Q

Outline presentation of PDA

A

Can be asymptomatic and close spontaneously
Can be asymptomatic throughout childhood and present in adulthood with signs of HF
SOB
Difficulty feeding
Poor weight gain
LRTIs
Continuous crescendo-decrescendo machinery murmur continues during 2nd heart sound

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26
Q

Outline pathophysiology of PDA

A

L-R shunt from aorta-pulmonary artery
Causes increase in pressure in pulmonary vessels= Pulmonary HTN, R heart strain, R ventricular hypertrophy
Increased blood through pulmonary vessels and returning to L side of heart = Left ventricular hypertrophy

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27
Q

Outline diagnosis of PDA

A

ECHO
Doppler flow studies

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28
Q

Outline management of PDA

A

Monitor until 1y with ECHO
Trans-catheter/surgical closure after 1y or sooner if symptomatic

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29
Q

Outline atrial septal defect

A

Hole in septum between 2 atria
L-R shunt
Can then lead to Eisenmenger syndrome

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30
Q

What is the difference between an atrial septal defect and foramen ovale?

A

Foramen ovale is normal until becomes patent after birth
Every atrial septal defect is abnormal

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31
Q

What are the complications of ASD?

A

*Stroke (VTE)- DVT travels to R side then crosses to left and can travel to brain
AF or atrial flutter
Pulmonary HTN and R sided HF
Eisenmenger syndrome

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32
Q

Outline presentation of ASD

A

Mid-systolic, crescendo-decrescendo murmur in upper L sternal border
Fixed split 2nd HS
SOB
Difficulty feeding
Poor weight gain
LRTIs
Adult- Dyspnoea, HF, stroke
Link between PFO and migraine with aura

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33
Q

Outline management of ASD

A

If small and asymptomatic- Watch and wait
Transvenous catheter closure or open heart surgery
Anticoagulants in adults- Aspirin/warfarin/NOACs

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34
Q

What is a VSD?

A

Congenital hole in septum between ventricles

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35
Q

Which genetic conditions are associated with VSD?

A

Downs syndrome
Turners syndrome

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36
Q

What is the direction of blood flow in VSD?

A

Increased pressure in LV means L to R meaning its acyanotic
Leads to right sided overload and right sided HF
Eventually switches to R to left shunt and Eisenmenger syndrome

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37
Q

Outline presentation of VSD

A

Initially asymptomatic and can present in adulthood
Poor feeding, dyspnoea, tachypnoea, failure to thrive
Pan systolic murmur in L lower sternal border in 3rd/4th ICS
Systolic thrill on palpation

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38
Q

What are the causes of a pansystolic murmur?

A

VSD
Mitral regurgitation
Tricuspid regurgitation

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39
Q

What is the management of VSD?

A

Small with no evidence pulmonary HTN or HF- Watch, can close spontaneously
Transvenous catheter closure via femoral vein or open heart surgery

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40
Q

What is there an increased risk of in VSD?

A

Infective endocarditis

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41
Q

What are the 3 underlying lesions that can result in Eisenmenger syndrome?

A

ASD
VSD
PDA

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42
Q

What is Eisenmenger Syndrome?

A

Blood flows from R to L across structural heart lesion, bypassing lungs

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43
Q

Which lesions can result in Eisenmenger syndrome?

A

ASD
VSD
PDA

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44
Q

What is the timeline for a lesion leading to Eisenmenger syndrome?

A

Develops after 1-2y in large shunts
Adulthood in small shunts
Develops quicker during pregnancy- If history of ‘hole in heart’ offer ECHO and close monitoring

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45
Q

List some findings related to R-L shunt and chronic hypoxia

A

Cyanosis
Clubbing
Dyspnoea
Plethora complexion (red complexion related to polycythaemia)

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46
Q

What is the cause of polupycythaemia?

A

Cyanosis
- Bone marrow responds to low oxygen sats and produces more RBCs and Hb to increase O2 carrying capacity of blood
Polycythaemia= Plethoric complexion due to high conc. Hb

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47
Q

What is a risk following polycythaemia?

A

Blood is more viscous due to higher conc. RBCs and O2= Increased risk thrombus formation

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48
Q

List examination findings of Eisenmenger syndrome

A

Right ventricular heave
Loud P2
Raised JVP
Peripheral oedema
ASD- Mid systolic, crescendo decrescendo murmur loudest at upper left sternal border
VSD- Pan systolic murmur loudest at lower left sternal border
PDA- Continuous crescendo decrescendo machinery murmur

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49
Q

What is the prognosis of Eisenmenger syndrome?

A

Can reduce life expectancy by approx. 20y
Causes of death- HF, VTE, infection, haemorrhage
Mortality can be up to 50% in pregnancy

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50
Q

What is the definitive management of Eisenmenger syndrome?

A

Correct underlying defect to prevent development of Eisenmenger syndrome
Once pulmonary pressure high enough and syndrome develops not reversible- Only treatment is heart-lung transplant

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51
Q

Outline medical management of Eisenmenger syndrome

A

Oxygen for symptom management
Sildenafil for pulmonary HTN
Treat arrhythmias
Venesection for polycythaemia
Anticoagulation for prevention thrombosis
Prophylactic ABs to prevent infective endocarditis

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52
Q

What is coarctation of the aorta?

A

Congenital condition
Narrowing of aortic arch, usually around ductus arteriosus
Reduces pressure of blood flowing to arteries distal to narrowing and increases pressure proximal to narrowing

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53
Q

Which genetic condition is associated with coarctation of aorta?

A

Turners syndrome

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54
Q

Outline presentation of coarctation of the aorta

A

Weak femoral pulses
Higher BP in limbs before narrowing and lower in limbs after narrowing
May have systolic murmur below left clavicle and left scapula
Tachypnoea and increased work of breathing
Underdeveloped left arm where reduced flow to left subclavian artery
Underdevelopment of legs

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55
Q

Outline management of coarctation of the aorta

A

Prostaglandin E to keep ductus arteriosus open whilst awaiting surgery

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56
Q

What is aortic valve stenosis?

A

Narrowing of aortic valve
Restricts blood flow from LV into aorta

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57
Q

Outline presentation of aortic valve stenosis

A

Can be asymptomatic
Fatigue
SOB
Dizziness
Fainting
Symptoms worse on exertion
Severe AS- Presents with HF within mths of birth
Ejection systolic murmur loudest in aortic area, crescendo-decrescendo radiating to carotids
Ejection click just before murmur, palpable thrill during systole, slow rising pulse and narrow pulse pressure

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58
Q

List complications of aortic stenosis

A

LV outflow tract obstruction
HF
Ventricular arrhythmias
Bacterial endocarditis
Sudden death, often on exertion

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59
Q

Outline diagnosis of aortic valve stenosis

A

ECHO
ECG
Exercise testing

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60
Q

Outline management of aortic stenosis

A

Percutaneous balloon aortic valvoplasty
Surgical aortic valvotomy
Valve replacement

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61
Q

What is comgenital pulmonary valve stenosis?

A

3 leaflets that can develop abnormally, becoming thickened or fused
Results in narrow opening between RV and pulmonary artery

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62
Q

List associations of pulmonary stenosis

A

ToF
William syndrome
Noonan syndrome
Congenital rubella syndrome

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63
Q

Outline presentation of pulmonary stenosis

A

Often asymptomatic
Fatigue on exertion
SOB
Dizziness
Fainting
Ejection systolic murmur loudest in pulmonary area
Palpable thrill in pulmonary area
RV heave due to RV hypertrophy
Raised JVP with giant a waves

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64
Q

Outline investigations of pulmonary stenosis

A

ECHO

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65
Q

Outline management of pulmonary stenosis

A

Balloon valvuloplasty via venous catheter
If valvuloplasty not appropriate- Open heart surgery

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66
Q

What are the 4 co-existing pathologies of Tetralogy of Fallot?

A

VSD
Overriding aorta
Pulmonary valve stenosis
Right ventricular hypertrophy

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66
Q

Which pathology in Tetralogy of Fallot determines severity?

A

Degree of pulmonary stenosis- Thickened valve means more deoxygenated blood encouraged to travel across VSD to travel into the aorta

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67
Q

What is an overriding aorta?

A

Entrance to aorta is further right than normal- When RV contracts and sends blood up, higher proportion of deoxygenated blood enters aorta

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68
Q

List risk factors for Tetralogy of Fallot

A

Rubella infection
Increased maternal age
Alcohol consumption in pregnancy
Diabetic mother

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69
Q

How is Tetralogy of Fallot investigated?

A

ECHO with doppler flow studies
Chest xray- Boot shaped heart due to RV hypertrophy

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70
Q

Outline presentation of Tetralogy of Fallot

A

Ejection systolic murmur caused by pulmonary stenosis
Severe- HF before 1y

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71
Q

List signs and symptoms of Tetralogy of Fallot

A

Cyanosis
Clubbing
Poor feeding
Poor weight gain
Ejection systolic murmur
Tet spells

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72
Q

What are Tet spells?

A

Intermittent symptomatic periods where R-L shunt becomes temporarily worsened precipitating a cyanotic episode
PVR increases or systemic resistance decreases
Precipitated by walking, physical exertion or crying

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73
Q

Outline non-pharmacological management of Tet spells

A

Older- Squat
Younger- Knees to chest
Both increases systemic vascular resistance, encouraging blood to enter pulmonary vessels
Supplementary oxygen

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74
Q

Outline pharmacological management of Tet spells

A

Beta blockers- Relaxes RV and improves flow to pulmonary vessels
IV fluids- Increases pre-load and volume of blood flowing to pulmonary vessels
Morphine- Can decrease respiratory drive= More effective breathing
Phenylephrine infusion- Increases SVR

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75
Q

Outline management of ToF

A

Prostaglandin infusion- Maintains ductus arteriosus
Total surgical repair- Open heart surgery

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76
Q

What is the prognosis of ToF?

A

Depends on severity
Poor without treatment
Corrective surgery= 90% patients live to adulthood

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77
Q

What is Ebstein’s anomaly?

A

Tricuspid valve set low in right side of heart (towards apex)
Causes bigger RA and smaller RV
Leads to poor flow to pulmonary vessels
Often associated with R-L shunt across atria via ASD
Cyanosis

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78
Q

Which syndrome is Ebtein’s anomaly associated with?

A

Wolff-Parkinson-White Syndrome

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79
Q

Outline presentation of Ebstein’s anomaly

A

HF- Oedema
Gallop rhythm with 3rd and 4th HS
Cyanosis
SOB and tachycardia
Poor feeding
Collapse or cardiac arrest

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80
Q

When does Ebstein’s anomaly present?

A

A few days after birth when ductus arteriosus closes

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81
Q

How is Ebstein’s anomaly diagnosed?

A

ECHO

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82
Q

Outline management of Ebstein’s anomaly

A

Treat arrhythmias and HF
Prophylactic ABs to prevent infective endocarditis
Surgical correction

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83
Q
A
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84
Q
A
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85
Q
A
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86
Q

Which conditions are associated with Transposition of the GReat arteries?

A

VSD
Coarctation of the aorta
Pulmonary stenosis

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86
Q

What is the pathophysiology of Transposition of the Great Arteries?

A

Aorta and pulmonary trunk swapped
RV pumps blood into aorta and LV pumps blood into pulmonary vessels
Immediately life threatening
CYANOSED

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86
Q

Outline presentation of Transposition of Great Arteries

A

Cyanosis at or within a few days of birth
Patent ductus arteriosus can initially compensate
Respiratory distress
tachycardia
Poor feeding
Poor weight gain
Sweating

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87
Q

Outline management of Transposition of Great Arteries

A

VSD allows for mixing of blood to provide time for definitive treatment
Prostaglandin infusion- Maintains ductus arteriosus
Balloon septostomy- Insert catheter in foramen ovale via umbilicus- Inflate balloon to create large ASD
Open heart surgery definitive- Cardiopulmonary bypass

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88
Q

What is bronchiolitis?

A

Inflammation and infection in bronchioles
Common in winter
Children <1y, most common <6mths

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89
Q

What is the causative organism of bronchiolitis?

A

Respiratory syncytial virus (RSV)

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90
Q

Outline presentation of bronchiolitis

A

Coryzal- Snotty, sneezy, mucus in throat, watery eyes
Signs of resp. distress
Dyspnoea
Tachypnoea
Poor feeding
Mild fever (<39 degrees C)
Apnoeas
Wheeze and crackles on auscultation

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91
Q

What are the signs of respiratory distress?

A

Raised RR
Use of accessory muscles
Intercostal and subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis
Abnormal airway noises

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92
Q

What is the function of grunting?

A

Caused by exhaling with glottis partially closed- Increases PEEP

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93
Q

What is stridor?

A

High pitched inspiratory noise caused by obstruction of upper airway

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94
Q

What is the typical course of RSV?

A

Bronchiolitis:
Starts as URTI with coryzal symptoms
Chest symptoms over 1st 2 days following onset coryzal symptoms
Symptoms generally worst on day 3-4
Symptoms last 7-10d
Most fully recover within 2-3wks
Increases incidence of viral induced wheeze later in childhood

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95
Q

When shoudl you consider admission in children with bronchiolitis?

A

<3mths or any pre-existing conditions (prematurity, Down syndrome, CF)
<75% normal milk intake
Clinical dehydration
RR >70
O2 sats <92%
Respiratory distress
Apnoeas
Parents not confident in managing condition at home

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96
Q

Outline management of bronchiolitis

A

Supportive management:
Ensure adequate intake
Saline nasal drops and suctioning
Supplementary oxygen

Ventilatory support:
High-flow humidified oxygen
CPAP
Intubation and ventilation

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97
Q

What are the most helpful signs of poor ventilation on ABG?

A

Rising pCO2- Shows airways collapsed, can’t clear waste CO2
Falling pH- CO2 is building up
Respiratory acidosis
If also hypoxic- Type 2 respiratory failure

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98
Q

What is the role of Palivizumab in bronchiolitis?

A

Targets RSV
Give as prophylaxis mthly
Given to high risk- Ex-premature or CHD
Provides passive protection

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99
Q

What is a viral induced wheeze?

A

Acute wheezy illness caused by viral infection
Small children have small airways- Small inflammation restricts small airways more and constricts SM

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100
Q

Which law is associated with viral induced wheeze?

A

Poiseuille’s law
Flow rate is proportional to radius of tube to power of 4
Eg: Halving diameter of tube decreases flow rate by 16 fold

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101
Q

Outline management of viral induced wheeze

A

Same pathway as acute asthma in children

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102
Q

Outline presentation of viral induced wheeze

A

Evidence of viral illness for 1-2d preceding onset of:
SOB
Signs of respiratory distress
Expiratory wheeze throughout chest

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103
Q

What are the causes of a focal wheeze?

A

Focal airway obstruction:
Inhaled foreign body
Tumour

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104
Q

What are the features of viral induced wheeze compared to asthma?

A

Presents before 3y age
No atopic history
Only occurs during viral infections

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105
Q

What are the potential triggers of asthma?

A

Infection
Exercise
Cold weather
Animals
Dust
Smoke
Doof allergens

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106
Q

Outline presentation of asthma

A

Progressively worsening SOB
Signs of resp. distress
Tachypnoea
Expiratory wheeze throughout chest
Chest can sound ‘tight’ on auscultation, with reduced air entry
Silent chest- Life-threatening

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107
Q

Outline moderate severity of acute asthma

A

Peak flow >50% predicted
Normal speech

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108
Q

Outline severe presentation of acute asthma

A

Peak flow <50% predicted
Sats <92%
Unable to complete sentences in one breath
Signs of resp. distress
Resp rate: >40 1-5y, >30 >5y
HR: >140 1-5y, >125 >5y

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109
Q

Outline life-threatening presentation in acute asthma

A

Peak flow <33% predicted
Sats <92%
Exhaustion and poor resp effort
Hypotension
Silent chest
Cyanosis
Altered consciousness/confusion

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110
Q

Outline management of severe acute asthma

A

Supplemetary O2
Inhaled/nebulised salbutamol
Inhaled/nebulised ipratropium bromide
IV magnesium sulphate
IV aminophylline

Also give oral prednisolone (for 3d) or IV hydrocortisone

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111
Q

Outline management of mild acute asthma

A

Outpatient regular salbutamol inhaler via spacer (eg: 4-6 puffs every 4h)

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112
Q

Outline step down of acute asthma management

A

Work back down ladder
Must have been off nebuliser at least 24h before discharged
Typical stepdown regime: Inhaled salbutamol 10 puffs 2hrly, 10 puffs 4hrly, 6 puffs 4hrly, 4 puffs 6hrly

Monitor potassium

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113
Q

What are the SEs of salbutamol?

A

Tachycardia
Tremor
Hyperkalaemia

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114
Q

When can a patient be discharged following an acute asthma attack?

A

Considered well- 6 puffs 4hrly salbutamol
Prescribe reducing regime for at home
Finish course of steroids

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115
Q

What is asthma?

A

Chronic inflammatory airway disease
Smooth muscle of airway hypersensitive, responds to stimuli by constricting and causing airflow obstruction
Bronchoconstriction reversible with bronchodilators (salbutamol)

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116
Q

What are the atopic conditions?

A

Asthma
Eczema
Hay fever
Food allergies

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117
Q

Outline presentation suggesting diagnosis of asthma

A

Episodic symptoms with intermittent exacerbations
Diurnal variability (worse at night and early morning)
Dry cough with wheeze and SOB
Typical triggers
Atopic conditions
FHx Asthma or atopy
Bilateral widespread ‘polyphonic wheeze’
Symptoms improve with bronchodilators

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118
Q

Outline diagnosis of asthma

A

Spirometry with reversibility testing
Direct bronchial challenge test (with histamine or methacholine)
FeNO
Peak flow variability (diary)

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119
Q

Outline long term management of asthma in <5y

A
  1. SABA inhaler (salbutamol)
  2. Low dose ICS or LTRA (montelukast)
  3. Add other option from step 2
  4. Refer
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120
Q

Outline medical long term management of asthma in 5-12y

A
  1. SABA
  2. Low dose ICS
  3. LABA (salmeterol)- Only continue if good response
  4. Medium dose ICS- COnsider adding LTRA (montelukast) or oral theophylline
  5. High dose ICS
  6. Refer
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121
Q

Outline long term asthma management >12y

A
  1. SABA
  2. Low dose ICS
  3. LABA (salmeterol)- Only continue if good response)
  4. Medium dose ICS- Consider LTRA or oral theophylline or LAMA (tiotropium)
  5. High dose ICS and combine step 4 with option of oral salbutamol and refer
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122
Q

Outline ICS use in children

A

Can slightly reduce growth velocity and cause small reduction in final height if used >12mths
Less of a problem with low doses
Effect of poorly controlled asthma is worse

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123
Q

Outline presentation of pneumonia

A

Cough (wet and productive)
High fever
Tachypnoea
Tachycardia
Increased WOB
Lethargy
Delirium
Hypoxia
Hypotension

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124
Q

What are the characteristic chest signs of pneumonia?

A

Bronchial breath sounds- Harsh breath sounds, equally loud on inspiration and expiration, caused by consolidation of lung tissue around airway
Focal coarse crackles- Air passing through sputum
Dullness to percussion- Lung collapse and/or consolidation

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125
Q

What is the most common cause of pneumonia?

A

Strep pneumonia

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126
Q

When is Group B strep pneumonia common?

A

Pre-vaccinated infants
Often contracted at birth as colonises vagina

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127
Q

What are typical findings of staph aureus pneumonia?

A

CXR- Pneumatocoeles (round air filled cavities) and consolidation in multiple lobes

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128
Q

When is haemophilus influenza a common cause of pneumonia?

A

Pre-vaccinated/unvaccinated

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129
Q

When is mycoplasma pneumonia considered as the cause of the pneumonia?

A

Atypical bacteria with extra-pulmonary manifestations (eg: Erythema multiforme)

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130
Q

What is the most common cause of viral pneumonia?

A

RSV

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131
Q

Outline investigations of pneumonia

A

CXR
Sputum cultures and throat swabs for bacterial cultures and viral PCR
Blood cultures
Capillary blood gas

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132
Q

Outline management of pneumonia

A

1st line- Amoxicillin
Add macrolide (erythromycin/clarithromycin/azithromycin) to cover atypical
IV if sepsis or problem with intestinal absorption
Oxygen as required

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133
Q

Outline management of recurrent LRTIs

A

FBC
CXR
Serum Igs
Test IgG to previous vaccines- Immunoglobulin class-switch recombination deficiency (unable to convert IgM to IgG)
Sweat test- CF
HIV test

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134
Q

What is croup?

A

Acute infective respiratory disease
6mth-2y
URTI causing oedema in larynx
Caused by parainfluenza virus

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135
Q

What is the most common causative organism of croup?

A

Parainfluenza virus

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136
Q

Why is diphtheria vaccinated against?

A

Causes croup
Croup caused by diphtheria leads to epiglottitis and has high mortality

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137
Q

Outline presentation of croup

A

Increased WOB
Barking cough
Hoarse voice
Stridor
Low grade fever

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138
Q

Outline management of croup

A

Oral dexamethasone- Very effective

Severe:
1. Oral dex
2. Oxygen
3. Nebulised budesonide
4. Nebulised adrenalin
5. Intubation and ventilation

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139
Q

What is the most common cause of epiglottitis?

A

Haemophilus influenza type B (HiB)- Rare now vaccinated against

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140
Q

Outline presentation suggesting 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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141
Q

Outline investigations of epiglottitis

A

DO NOT EXAMINE
Lateral xray of neck- Thumbprint sign (shouldn’t really xray)

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142
Q

Outline management of epiglottis

A

DO NOT EXAMINE PATIENT
Alert most senior paediatrician and anaesthetist
Prepare for an intubation (may not be required but need to be ready at all times)

Once airway secure:
IV antibiotics- Ceftriaxone
Dexamethasone

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143
Q

Outline prognosis of epiglottis

A

Most recover w/o requiring intubation
If intubated, most extubated after a few days and make full recovery

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144
Q

What is a common complication of epiglottitis?

A

Epiglottic abscess- Collection of pus around epiglottitis
LIFE THREATENING EMERGENCY

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145
Q

What is laryngomalacia?

A

Part of larynx above vocal cords causes partial airway obstruction
Leads to chronic stridor on inhalation when larynx flops across airway
Usually resolves as larynx matures

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146
Q

What is the classic shape of the epiglottis in laryngomalacia?

A

Omega shape

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147
Q

Outline presentation of laryngomalacia

A

Infants, peaks at 6mths
Inspiratory stridor- Intermittent and more prominent when feeding/upset/lying on back
No associated respiratory distress
Can cause difficulty feeding

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148
Q

Outline whooping cough

A

URTI
Pertussis (bacteria)
Coughing fits so severe, unable to take in air between coughs- Whoop to forcefully suck air in
Vaccinated
NOTIFIABLE

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149
Q

Outline presentation of whooping cough

A

Start: Mild coryzal symptoms, low grade fever and mild dry cough
More severe coughing after a week- Sudden and recurring attacks of coughing with cough free periods between- Paroxysmal
Large inspiratory whoop
Can cough so hard they give themselves a pneumothorax

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150
Q

Outline diagnosis of whooping cough

A

Nasopharyngeal/nasal swab with PCR testing or bacterial culture- Can confirm diagnosis within 2-3wks onset of symptoms
If cough present >2wks- Can test for anti-pertussis toxin IgG

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151
Q

Outline management of pertussis

A

Supportive care
Within 21d- Macrolides (azithromycin, erythromycin, clarithromycin)
Co-trimoxazole alternative
Close contacts require prophylactic antibiotics if in vulnerable group

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152
Q

What is a key complication of whooping cough?

A

Bronchiectasis

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153
Q

What is CLDP?

A

Chronic lung disease of prematurity- Bronchopulmonary dysplasia
Those born <28wks gestation- Suffer with RDS and require oxygen therapy/intubation and ventilation at birth

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154
Q

How is CLDP diagnosed?

A

Based on CXR changes and when infant requires O2 therapy after reach 36wks

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155
Q

Outline feature of CLDP

A

Low O2 sats
Increased WOB
Poor feeding and weight gain
Crackles and wheeze
Increased susceptibility to infection

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156
Q

Outline prevention methods of CLDP before infants birth

A

Betamethasone (corticosteroids) to mother’s showing signs of premature labour at <36wks gestation- Speeds up development of fetal lungs before birth

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157
Q

Outline prevention methods of CLDP in newborn

A

CPAP rather than intubation and ventilation when possible
Use caffeine to stimulate respiratory effort
Do not over oxygenate

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158
Q

Outline management of CLDP

A

Protect against RSV- Reduce risk and severity of bronchiolitis
Give mthly injections palivizumab

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159
Q

Outline CF

A

Autosomal recessive
Affects mucus glands
Mutation of CFTCR gene on Chr7

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160
Q

What are the key consequences of the cystic fibrosis mutation?

A

Thick pancreatic and biliary secretions- Block ducts- Lack of digestive enzymes
Low volume thick airway secretions- Reduce airway clearance- Bacterial colonisation and infection susceptibility
Congenital bilateral absence of vas deferens

161
Q

Outline presentation of CF

A

Newborn spot test

Meconium ileus- First sign of CF- Meconium thick and sticky- Gets stuck and obstructs bowel- Not passing meconium within 24h birth, abdo distension and vomiting

162
Q

How can CF present later in childhood?

A

Recurrent LRTIs
Pancreatitis
Failure to thrive

163
Q

List symptoms of CF

A

Chronic cough
Thick sputum production
Recurrent RTIs
Loose, greasy stools (steatorrhoea)- Lack of fat digesting lipase enzymes
Abdo pain and bloating
Salty sweat
Failure to thrive

164
Q

List signs of CF

A

Low weight or height on growth charts
Nasal polyps
Finger clubbing
Crackles and wheezes on auscultation
Abdo distension

165
Q

List causes of clubbing in children

A

Hereditary clubbing
Cyanotic HD
Infective endocarditis
CF
TB
IBD
Liver cirrhosis

166
Q

Outline diagnosis of CF

A

Newborn blood spot testing
Sweat test- Gold standard
Genetic testing- CFTR (amniocentesis or CVS)

167
Q

Outline the sweat test

A

Used to diagnose CF
Pilocarpine applied to skin on patch
Electrodes placed either side causing skin to sweat
Chloride conc.- CF >60mmol/l

168
Q

What are the key colonisers in CF?

A

Staph aureus
Pseudomonas aeruginosa

169
Q

Outline CF and Pseudomonas

A

Once colonised with pseudomonas- Very difficult to get rid of
Treatment- Long term nebulised ABs (tobramycin) and oral ciprofloxacin

170
Q

Outline management of CF

A

Chest physiotherapy- Clear mucus, reduce risk of infection
Exercise
High calorie diet
CREON tablets- Digest fats in pancreatic insufficiency
Prophylactic flucloxacillin
Salbutamol as required
Nebulised DNase- Breaks down DNA material in respiratory secretions
Nebulised hypertonic saline
Vaccines- Pneumococcal, influenza, varicella

171
Q

Outline monitoring requirements in CF

A

Clinic every 6mths
Monitor sputum for colonisation
Screening- Diabetes, osteoporosis, Vit D deficiency, liver failure

172
Q

Outline prognosis of CF

A

Life expectancy approx. 47y
90% develop pancreatic insufficiency
50% develop CF-related diabetes and require insulin
30% develop liver disease

173
Q

What is primary ciliary dyskinesia?

A

Kartagner’s syndrome
Autosomal recessive
Affects cilia of various cells in the body
More common in consanguineous communities (parents related)
Build up of mucus in lungs- Similar presentation to CF
Affects cilia in fallopian tubes and flagella of sperm- Reduced fertility

174
Q

Which condition is primary ciliary dyskinesia associated with?

A

Situs inversus

175
Q

What is Kartagner’s triad?

A

Paranasal sinusitis
Bronchiectasis
Situs inversus

176
Q

Outline diagnosis of primary ciliary dyskinesia

A

FHx and history of consanguinity in parents
CXR- Situs inversus
Semen analysis
Sample of ciliated epithelium- Nasal brushing or bronchoscopy

177
Q

Outline management of PCD

A

Similar management to CF and bronchiectasis

178
Q

What are the complications of appendicitis?

A

Gangrene and rupture leading to peritonitis

179
Q

When is the peak incidence of appendicitis?

A

10-20y

180
Q

What are the signs and symptoms of appendicitis?

A

Abdo pain- Central moving to RIF
Tenderness in McBurney’s point
Loss of appetite
Nausea and vomiting
Rovsing’s sign- Palpate LIF causes pain in RIF
Abo guarding and rebound and percussion tenderness- Suggests peritonitis

181
Q

What are the signs of peritonitis in appendicitis?

A

Rebound tenderness and percussion tenderness caused by ruptured appendix

182
Q

Outline diagnosis of appendicitis

A

Clinical presentation and raised inflammatory markers
CT scan
US- Rule out gynae causes
Diagnostic laparoscopy- Diagnose and perform appendicectomy in same procedure

183
Q

Outline management of appendicitis

A

Laparoscopic surgery- Appendicectomy

184
Q

What is Meckel’s diverticulum?

A

Malformation of distal ileum
Usually asymptomatic
Can bleed/inflame/rupture causing volvulus or intussusception

185
Q

What is mesenteric adenitis?

A

Inflamed abdominal lymph nodes
Abdo pain
Usually in younger children
Associated with tonsillitis or URTI
No treatment required

186
Q

What is intussusception?

A

Bowel telescopes into itself
Thickens size of bowel and narrows lumen
Palpable mass and obstruction to passage of faeces
More common in 6mth-2y boys

187
Q

Which conditions are associated with intussusception?

A

Concurrent viral illness
Henoch-Schonlein purpura (HSP)
CF
Intestinal polyps
Meckel diverticulum

188
Q

Outline presentation of intussusception

A

Redcurrent jelly stool
Colicky abdomen
PAle, lethargic, unwell
RUQ sausage-shaped mass
Vomiting
Intestinal obstruction

189
Q

Outline management of intussusception

A

US or contrast enema
Therapeutic enema- Air/water/contrast pumped into colon to try to force bowel into normal position
Surgical reduction
If gangrenous/perforated- Surgical resection

190
Q

What are the complications of intussusception?

A

Obstruction
Gangrenous bowel
Perforation
Death

191
Q

What is Hirschsprung’s disease?

A

Congenital
Nerve cells of myenteric plexus absent in distal bowel and rectum
Bowel loses motility

192
Q

What is total colonic aganglionosis?

A

Hirschsprung’s disease
Aganglionic section of colon doesn’t relax, causing it to become constricted- Loss of movement of faeces and obstruction

193
Q

What are the associations with Hirschsprung’s disease?

A

Downs syndrome
NF
Waardenburg syndrome
Multiple endocrine neoplasia type II

194
Q

Outline presentation of Hirschsprung’s disease

A

Delay in passing meconium >24h
Chronic constipation since birth
Abdo pain and distension
Vomiting
Poor weight gain and failure to thrive

195
Q

What is Hirschsprung-associated enterocolitis?

A

Inflammation and obstruction of intestine
Presents within 2-4wks of birth
Fever, abdo distension, diarrhoea, features of sepsis
LIFE THREATENING

196
Q

What are the complications of Hirschsprung-associated enterocolitis?

A

Toxic megacolon and perforation of bowel
Requires urgent ABs, fluid resus, decompression of obstructed bowel

197
Q

Outline management of Hirschsprung’s disease

A

Abdo xray
Rectal biopsy- Absence of ganglionic cells
If enterocolitis- Initial fluid resus and management of intestinal obstruction- IV ABs
Surgical removal of aganglionic section of bowel

198
Q

List causes of intestinal obstruction

A

Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Intussusception
Imperforate anus
Malrotation of intestines with volvulus
Strangulated hernia

199
Q

Outline presentation of intestinal obstruction

A

Persistent vomiting- May be bilious
Abdo pain and distension
Failure to pass stools/wind
Abnormal bowel sounds- High pitched and tinkling early, absent later

200
Q

Outline diagnosis of intestinal obstruction

A

Abdo xray- Dilated loops of bowel proximal, collapsed loops distal
Absence of air in rectum

201
Q

Outline management of intestinal obstruction

A

Nil by mouth
Nasogastric tube to drain stomach and stop vomiting
IV fluids to correct dehydration
Paediatric surgical referral

202
Q

What is biliary atresia?

A

Congenital
Section of bile duct narrowed or absent
Cholestasis- Bile cannot be transported from liver to bowel- Conjugated bile not excreted

203
Q

Outline presentation of biliary atresia

A

Presents shortly after birth- Sig. persistent jaundice due to high conjugated bilirubin levels (Lasts >14d)

204
Q

How is biliary atresia diagnosed?

A

Conjugated and unconjugated bilirubin
High conjugated bilirubin- Liver processing bilirubin for excretion but not able to flow through biliary duct into bowel

205
Q

Outline management of biliary atresia

A

Kasai portoenterostomy
Often require full liver transplant

206
Q

What are the features of Crohn’s?

A

N- No blood or mucus
E- Entire GI tract
S- Skip lesions on endoscopy
T- Terminal ileum most affected and Transmural (full thickness) inflammation
S- Smoking RF

Associated with weight loss/strictures/fistulas
Diarrhoea, abdo pain, bleeding, weight loss, anaemia

207
Q

What are the features of Ulcerative Colitis?

A

C- Continuous inflammation
L- Limited to colon and rectum
O- Only superficial mucosa affected
S- Smoking protective
E- Excrete blood and mucus
U- Use aminosalicylates
P- Primary sclerosing cholangitis

Diarrhoea, abdo pain, bleeding, weight loss, anaemia

208
Q

What are the extra-intestinal manifestations of IBD?

A

Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
Episcleritis and iritis
Inflammatory arthritis
Primary sclerosing cholangitis (UC)

209
Q

How is IBD diagnosed?

A

Faecal calprotectin
Endoscopy- Gold standard
Imaging- US, CT, MRI- Look for complications (fistulas, abscesses, strictures)
Bloods- Infection, anaemia, thyroid, kidney, liver function

210
Q

Outline inducing remission in Crohn’s

A

1st line- Steroids (eg: Oral prednisolone or IV hydrocortisone)
2nd line- Immunosuppression- Azathioprine/mercaptopurine/methotrexate/infliximab/adalimumab

211
Q

Outline maintaining remission in Crohn’s

A

1st line- Azathioprine, mercaptopurine
2nd line- Methotrexate, infliximab, adalimumab

212
Q

Outline inducing remission in UC

A

Mild to moderate:
1st line- Aminosalicylate (eg: Mesalaxine)
2nd line- Corticosteroids (eg: Prednisolone)

Severe:
1st line- IV corticosteroids (eg: Hydrocortisone)
2nd line- IV ciclosporin

Can surgery- Remove colon and rectum to form J pouch

213
Q

Outline maintaining remission in UC

A

Aminosalicylate (eg: Mesalazine)
Azathioprine
Mercaptopurine

214
Q

Which antibodies are associated with coeliac disease?

A

Anti-TTG
Anti-EMA

215
Q

What is coeliac disease?

A

AI
Exposure to gluten causes immune reaction- Creates inflammation in small intestines
Particularly jejunum
Causes atrophy of intestinal villi

216
Q

Outline presentation of coeliac disease

A

Failure to thrive
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis

Rarely neuro- Peripheral neuropathy, cerebellar ataxia, epilepsy

217
Q

Which condition is dermatitis herpetiformis associated with?

A

Coeliac disease

218
Q

What is the most common gene association of coeliac disease?

A

HLA-DQ2

219
Q

What condition is always tested for in patients newly diagnosed with T1D?

A

Coeliac disease

220
Q

What is the link between IgA deficiency and coeliac disease?

A

Anti-TTG and anti-EMA are IgA
When testing for these antibodies-Test total IgA levels- If total IgA is low- Coeliac test will be negative even if have condition

221
Q

Outline diagnosis of coeliac disease

A

Must be on diet containing gluten to test
Check Total IgA levels to exclude IgA deficiency
Antibodies- Anti-TTG (1st choice) and Anti-EMA
Endoscopy and intestinal biopsy- Crypt hypertrophy, villous atrophy

222
Q

What is seen on an endoscopy and intestinal biopsy in coeliac disease?

A

Crypt hypertrophy
Villous atrophy

223
Q

List associations with coeliac disease

A

T1D
Thyroid disease
AI hepatitis
PBC
PSC
Down syndrome

224
Q

What are the complications of untreated coeliac disease?

A

Vit deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of intestine
NHL
Small bowel adenocarcinoma

225
Q

Outline management of coeliac disease

A

Lifelong gluten free diet

226
Q

What us acute gastritis?

A

Inflammation of stomach- Presents with nausea and vomiting

227
Q

What is enteritis?

A

Inflammation of intestines
Presents with diarrhoea

228
Q

Outline management of gastroenteritis?

A

Isolate patient
Treat dehydration
ABs generally not recommended

229
Q

What are the most common causes of viral gastroenteritis?

A

Rotavirus
Norovirus
Adenovirus (less common- More subacute diarrhoea)

230
Q

Outline E.coli gastroenteritis

A

Only certain strains cause gastroenteritis
Spread contact with faeces/unwashed salad/contaminated water
Produces shiga toxin- Leads to HUS- Use of ABs increases risk
Abdo cramps, bloody diarrhoea, vomiting

231
Q

Outline Campylobacter Jejuni as a cause of gastroenteritis

A

Traveller’s diarrhoea
Gram negative spiral bacteria
Spread- Raw poultry, untreated water, unpasteurised milk
Incubation 2-5d, symptoms resolve after 3-6d
Abdo cramps, diarrhoea with blood, vomiting, fever
Azithromycin or ciprofloxacin- If severe

232
Q

Outline Shigella as a cause of gastroenteritis

A

Spread- Faeces contaminating drinking water/swimming pools/food
Incubation 1-2d, resolve within 1wk
Bloody diarrhoea, abdo cramps, fever
Can produce shiga toxin and cause HUS
Treat severe cases- Azithromycin or ciprofloxacin

233
Q

Outline salmonella as a cause of gastroenteritis

A

Spread- Raw eggs/poultry, food contaminated with infected faeces of small animals
Incubation 12h-3d, symptoms resolve within 1wk
Watery diarrhoea with mucus/blood, abdo pain, vomiting
Antibiotics only if severe- Guided by stool culture and sensitivities

234
Q

Outline Bacillus Cereus as a cause of gastroenteritis

A

Gram positive rod
Rice left at room temperature
Growing on food- Produces cereulide toxin- Causes abdo pain, cramping, vomiting within 5h- In intestine produces different toxins that cause watery diarrhoea within 8h- Resolves within 24h

235
Q

Outline Yersinia Enterocolitica as a cause of gastroenteritis

A

Gram negative bacillus
Eating raw/undercooked pork, spread through contamination with urine/faeces of rats and rabbits
Children, water/bloody diarrhoea. abdo pain, fever and lymphadenopathy
Can last >3wks

Older children- Mesenteric lymphadenitis causing R sided abdo pain

236
Q

Outline Staph aureus toxin as a cause of gastroenteritis

A

Can grow on eggs/dairy/meat
Diarrhoea, perfuse vomiting, abdo cramps, fever
Start within hrs of digestion and settle within 12-24h

237
Q

Outline Giardiasis as a cause of gastroenteritis

A

Parasite
Spread via pets, farmyard animals and humans
Faecal oral transmission
May cause diarrhoea or no symptoms
Diagnose- Stool microscopy
Treat- Metronidazole

238
Q

Outline principles of gastroenteritis management

A

Infection control
Stay off school until 48h after symptoms completely resolved
Stool MC&S
Attempt fluid challenge
Rehydration solution- Dioralyte
Antidiarrhoeal meds not recommended

239
Q

Outline post-gastroenteritis complications

A

Lactose intolerance
IBS
Reactive arthritis
Guillain-Barre syndrome

240
Q

Outline pyloric stenosis

A

Hypertrophy of pyloric sphincter
Increasingly powerful peristalsis in stomach results in projectile vomiting

241
Q

Outline features of pyloric stenosis

A

Presents within 1st few wks of life
Hungry baby, thin, failure to thrive
Projectile vomiting
Olive shaped mass in upper abdomen
Blood gas- Hypochloric metabolic alkalosis

242
Q

What would a blood gas show in pyloric stenosis?

A

Hypochloric metabolic alkalosis

243
Q

Outline management of pyloric stenosis

A

Diagnose- Abdo US
Treat- Laparoscopic pyloromyotomy (Ramstedt’s operation)
Prognosis- Excellent

244
Q

What is Gastro-oesophageal reflux?

A

Contents of stomach reflux through lower oesophageal sphincter
In babies- Immaturity of LOS- Usually resolves by 1y

245
Q

Outline presentation of GOR

A

Chronic cough
Hoarse cry
Distress, crying, unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain

> 1y- Heartburn, acid regurg, retrosternal/epigastric pain, bloating, nocturnal cough

246
Q

Outline management of GOR

A

Small, frequent meals
Burping regularly
Not over-feeding
Keep baby upright after feeding (i.e. not lying flat)

More problematic cases:
Gaviscon mixed with feeds
Thickened milk/formula
PPIs (omeprazole)

Rarely may require barium meal and endoscopy
Surgical fundoplication if very severe- Rare

247
Q

What is Sandifer’s syndrome?

A

Rare condition
Brief episodes of abnormal movement associated with GOR
Usually neurologically normal

Torticollis- Forceful contraction of neck muscles causing twisting of neck
Dystonia- Abnormal contractions causing twisting movements, arching back/unusual postures

Resolves as reflux improves

REFER as differential diagnoses- Infantile spasms and seizures

248
Q

Outline presentation of constipation

A

<3 stools/wk
Hard stools, difficult to pass
Rabbit dropping stools
Straining/painful passage of stool
Abdo pain
Retentive posturing
Rectal bleeding associated with hard stools
Faecal impaction causing overflow soiling
Hard stools may be palpable in abdo
Loss of sensation of need to open bowels

249
Q

What is encopresis?

A

Faecal incontinence
Not pathological until 4y
Usually sign of chronic constipation- Rectum stretched and loses sensation

250
Q

What is desensitisation of the rectum?

A

Patients develop habit of not opening bowels when need to- Ignore sensation of full rectum
Lose sensation over time and open bowels less frequently
Leads to faecal impaction
Makes more difficult to treat constipation

251
Q

What are the secondary causes of constipation?

A

Hirschsprung’s disease
CF
Hypothyroidism
SC lesions
Sexual abuse
Intestinal obstruction
Anal stenosis
Cows milk intolerance

252
Q

What are the complications of constipation?

A

Pain
Reduced sensation
Anal fissures
Haemorrhoids
Overflow soiling
Psychosocial morbidity

253
Q

Outline management of chronic constipation

A

High fibre diet, good hydration
Movicol 1st line laxative
Disimpaction regime if faecal impaction
Encourage and praise visiting toilet

254
Q

Outline abdominal migraines

A

May occur before develop traditional migraines when older
Episodes of central abdo pain lasting >1h

255
Q

What are the features of abdominal migraine?

A

Central abdo pain lasting >1h
Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura

256
Q

Outline acute management of abdominal migraine

A

Low stimulus environment (quiet, dark room)
Paracetamol
Ibuprofen
Sumatriptan

257
Q

Outline preventative management of abdominal migraine

A

Pizotifen

258
Q

What are the withdrawal SEs of pizotifen?

A

Depression
Anxiety
Poor sleep
Tremor

259
Q

What is T1d?

A

Pancreas can’t produce insulin
Glucose can’t get into cells- Cells think no glucose in body- Hyperglycaemia

260
Q

What is the ideal blood glucose conc.?

A

4.4-6.1mmol/l

261
Q

Outline production and role of insulin

A

Produced by pancreas by beta cells in Islets of Langerhans
Reduces blood sugar levels
Causes cells to absorb glucose
Causes muscle and liver cells to absorb glucose and store as glycogen

262
Q

Outline production and use of glucagon

A

Increases blood sugar levels
Produced by alpha cells in Islets of Langerhans in pancreas
Stimulates liver to breakdown glycogen into glucose (glycogenolysis) and convert proteins and fats into glucose (gluconeogenesis)

263
Q

Outline ketogenesis

A

Occurs when insufficient supply of glucose and glycogen stores depleted
Liver converts fatty acids into ketones
Water soluble fatty acids- Can cross BBB and be used by the brain
Acetone smell if in ketosis

264
Q

Outline presentation of T1D

A

Often present in DKA
or
Hyperglycaemia:
Polyuria
Polydipsia
Weight loss

Secondary enuresis and recurrent infections

265
Q

How is T1D diagnosed?

A

Bloods- FBC, renal profile, formal lab glucose
Blood cultures if suspected infection
HbA1c- Blood sugar over previous 3mths
TFTs and TPO (AI thyroid disease)
anti-TTG- Coeliac disease
Insulin antibodies, anti-GAD antibodies and islet cell antibodies

266
Q

Outline basics of long term management of T1D

A

SC insulin regimes
Monitor dietary carbs
Monitor blood sugar levels waking/each meal/before bed
Monitor for and manage complications

267
Q

Outline basal bolus regimes of insulin in T1D

A

Basal- Injection of long acting insulin (lantus) in evening- Constant background insulin throughout day
Bolus- Injection short acting insulin (actrapid)- 3x/d before meals

268
Q

Outline tethered pumps

A

Replaceable infusion sets and insulin
Attached at belt with tube that connects from pump to insertion site
Controls for infusion on pump itself

269
Q

Outline patch pumps

A

Sit directly on skin
When run out of insulin- Replace entire patch pump and new pump attached
Controlled by separate remote

270
Q

Outline hypoglycaemia in T1D

A

Caused by too much insulin, not enough carbs or issues with absorption (diarrhoea, vomiting, sepsis)

271
Q

What are the symptoms of hypoglycaemia?

A

Hunger
Tremor
Sweating
Irritability
Dizziness
Pallor
Reduced consciousness
Coma
Death

272
Q

Outline management of hypoglycaemia

A

Rapid acting glucose (lucozade) and slower acting carbs (bread)

Severe:
IV glucose or IM glucose

273
Q

What are the causes of hypoglycaemia?

A

T1D
Hypothyroidism
Glycogen storage disorders
GH deficiency
Liver cirrhosis
Alcohol and fatty acid oxidation defects (MCADD)

274
Q

What is the management of hyperglycaemia in T1D?

A

If not in DKA:
Increase insulin dose
Can take several hrs

275
Q

What are the long term macrovascular complications of T1D?

A

Coronary artery disease
Peripheral ischaemia- Poor wound healing, ulcers, diabetic foot
Stroke
HTN

276
Q

What are the microvascular complications of T1D?

A

Peripheral neuropathy
Retinopathy
Glomerulosclerosis

277
Q

What are the infection related complications of T1D?

A

UTIs
Pneumonia
Skin and soft tissue infections- Particularly feet
Oral and vaginal candidiasis

278
Q

Outline monitoring of T1D

A

HbA1c every 3-6mths
Cap blood glucose
Yrly ophthalmology appointment
Flash glucose monitoring- 5min lag behind BM

279
Q

Outline pathophysiology of DKA

A

Extreme hyperglycaemic ketosis
Not producing insulin/not injecting adequate replacement
Results in:
Ketoacidosis
Dehydration
Potassium imbalance

280
Q

Outline ketoacidosis in DKA

A

Cells in body have no fuel- Initiate ketogenesis
Glucose and ketone levels increase
Initially kidneys produce bicarbonate to buffer ketone acids which use up bicarbonate- Blood becomes acidotic

281
Q

Outline dehydration in DKA

A

Hyperglycaemia overwhelms kidneys and glucose filtered into urine drawing water out with it
Polyuria and polydipsia

282
Q

Outline potassium imbalance in DKA

A

Insulin normally drives potassium into cells
No insulin- Serum potassium high/normal
Kidneys balance blood potassium- Excrete excess in urine
Total body potassium- Low
When treatment with insulin started- Severe hypokalaemia- Arrhythmias

283
Q

What are patients with T1D in DKA at risk of developing?

A

Cerebral oedema
Dehydration and hyperglycaemia- Water moves out of brain cells
Rapid correction of this causes rapid shift of fluid into brain cells- Oedema

284
Q

How is the risk of cerebral oedema in DKA management managed?

A

Monitor GCS during fluid resus
Slow IV fluids
IV mannitol and IV hypertonic saline

285
Q

Outline presentation of DKA

A

Polyuria
Polydipsia
N+V
Weight loss
Acetone breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of underlying trigger, eg: Sepsis

286
Q

Outline diagnosis of DKA

A

Hyperglycaemia >11mmol/l
Ketosis >3mmol/l
Acidosis <7.3

287
Q

Outline management of DKA

A
  1. Correct dehydration over 48h
  2. Give fixed rate insulin infusion
    Prevent hypoglycaemia- IV glucose when blood glucose <14mmol/l
    Add potassium to IV fluids- Monitor K+ closely
288
Q

What is adrenal insufficiency?

A

Adrenal glands don’t produce enough steroid hormones- Cortisol and aldosterone

289
Q

Outline primary adrenal insufficiency

A

Addison’s disease
Adrenal glands damaged
Reduced secretion cortisol and aldosterone
AI

290
Q

Outline secondary adrenal insufficiency

A

Inadequate ACTH stimulating adrenal glands
Low levels of cortisol released
Result of loss/damage pituitary gland
Can be due to congenital hypoplasia of pituitary/surgery/infection/loss of blood flow/radiotherapy

291
Q

Outline tertiary adrenal insufficiency

A

Inadequate CRH release by hypothalamus
Usually result of being on long term steroid causing suppression of hypothalamus

292
Q

What are the features of adrenal insufficiency in babies?

A

Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive

293
Q

What are the features of adrenal insufficiency in older children?

A

Nausea and vomiting
Poor weight gain or weight loss
Anorexia
Abdo pain
Muscle weakness/cramps
Developmental delay or poor academic performance
Bronze hyperpigmentation- Addison’s- High ACTH levels stimulating melanocytes

294
Q

Outline investigations of adrenal insufficiency

A

U&Es- Hyponatremia and hyperkalaemia
Blood glucose- Hypoglycaemia
Test cortisol, ACTH, aldosterone and renin levels before giving steroids

295
Q

Outline hormone results in Addisons disease

A

Low cortisol
High ACTH
Low aldosterone
High renin

296
Q

Outline hormone results in secondary adrenal insufficiecy

A

Low cortisol
Low ACTH
Normal aldosterone
Normal renin

297
Q

Outline the short synacthen test

A

ACTH stimulation test
Confirms adrenal insufficiency
Give synacthen (synthetic ACTH)- Blood cortisol measured at baseline, 30mins and 60mins
ACTH stimulates healthy adrenal glands to produce cortisol- Should double
<Double indicates primary adrenal insufficiency

298
Q

Outline management of adrenal insufficiency

A

Hydrocortisone- Glucocorticoid- Replaces cortisol
Fludrocortisone- Mineralocorticoid- Replaces aldosterone

Steroid card and emergency ID tag
Increase dose during acute illness

299
Q

Outline monitoring in adrenal insufficiency

A

Growth and development
BP
U&Es
Glucose
Bone profile
Vit D

300
Q

Outline sick day rules

A

Dose of steroid needs increasing and given more regularly until illness resolved
Blood glucose monitored closely- Risk of hypoglycaemia
If D+V- IM injection steroid and likely admission for IV

301
Q

What is an Addisonian Crisis?

A

Adrenal crisis
Acute presentation of severe Addisons

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatremia, hyperkalaemia

302
Q

Outline management of Addisonian crisis

A

Intensive monitoring
IV hydrocortisone
IV fluid resuscitation
Correct hypoglycaemia

303
Q

What is congenital adrenal hyperplasia?

A

Caused by congenital deficiency of 21-hydroxylase enzyme
Underproduction of cortisol and aldosterone and overproduction of androgens
Autosomal recessive

304
Q

What is the function of testosterone?

A

Androgen hormone
High levels in men, low levels in women
Promotes male sexual characteristics

305
Q

Outline glucocorticoid hormones

A

Help body deal with stress
Raises blood glucose
Reduces inflammation
Suppresses immune system
CORTISOL
Released in response to ACTH from anterior pituitary

306
Q

Outline mineralocorticoid hormones

A

Act on kidneys to balance salt and water in blood
ALDOSTERONE
Released by adrenal gland in response to renin
Acts on kidneys to increase sodium reabsorption into blood and increase potassium secretion into urine
Increases sodium and decreases potassium

307
Q

Outline pathophysiology of congenital adrenal hyperplasia

A

Deficiency in 21-hydroxylase enzyme
Progesterone not converted to aldosterone or cortisol- Gets converted to testosterone instead

Low aldosterone and cortisol
High testosterone

308
Q

Outline presentation of severe cases of CAH

A

Female- Virilised genitalia and enlarged clitoris

Shortly after birth- Hyponatremia, hyperkalaemia, hypoglycaemia

Poor feeding
Vomiting
Dehydration
Arrhythmias

309
Q

Outline presentation of female patients with mild CAH

A

Tall for age
Facial hair
Absent periods
Deep voice
Early puberty

Skin hyperpigmentation- Increased ACTH due to low cortisol

310
Q

Outline presentation of male patients with mild CAH

A

Tall for age
Deep voice
Large penis
Small testicles
Early puberty

Skin hyperpigmentation- Increased ACTH due to low cortisol

311
Q

Outline management of CAH

A

Cortisol replacement- Hydrocortisone
Aldosterone replacement- Fludrocortisone
Corrective surgery offered if virilised genitalia

312
Q

Outline the role of GH

A

Produced by anterior pituitary
Stimulates cell reproduction and growth of organs, muscles, bones, height
Stimulates release of IGF-1 by liver- Promotes growth in children

313
Q

Outline pathophysiology of GH deficiency

A

Congenital:
Disruption to GH axis at hypothalamus or pituitary gland
Can be due to genetic mutation in GH1 or GHRHR genes or empty sella syndrome

Acquired:
Secondary to infection/trauma/surgery

314
Q

Outline presentation of GH deficiency

A

Micropenis
Hypoglycaemia
Severe jaundice
Poor growth
Short stature
Slow development of movement and strength
Delayed puberty

315
Q

Outline investigations of GH deficiency

A

GH stimulation test- Test response to meds that normally stimulate release of GH- Eg: Insulin, glucagon, arginine, clonidine- GH deficiency= Poor response

Test for thyroid and adrenal deficiency
MRI brain
Genetic testing- Turner syndrome and Prader-Willi syndrome
Xray or DEXA scan- Assess bone age

316
Q

Outline treatment of GH deficiency

A

Daily SC injections somatropin (GH)
Close monitoring height and development

317
Q

Outline congenital hypothyroidism

A

Child born with underactive thyroid
Screened for on newborn blood spot

318
Q

How can congenital hypothyroidism present?

A

Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development

319
Q

What are the causes of acquired hypothyroidism?

A

AI thyroiditis (Hashimoto’s)

320
Q

Outline Hashimoto’s thyroiditis

A

AI inflammation of thyroid gland and subsequent underactivity
Anti-TPO antibodies and antithyroglobulin antibodies

321
Q

Which conditions are associated with Hashimoto’s thyroiditis?

A

T1D
Coeliac disease

322
Q

Which antibodies are associated with Hashimoto’s thyroiditis?

A

Anti-TPO
Antithyroglobulin

323
Q

What are the symptoms of Hashimoto’s thyroiditis?

A

Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss

324
Q

Outline management of hypothyroidism

A

Investigate TFTs, thyroid US and thyroid antibodies
Levothyroxine OD

325
Q

What is a hydrocele?

A

Collection of fluid within tunica vaginalis surrounding testes

326
Q

What is a simple hydrocele?

A

Common
Fluid trapped in tunica vaginalis
Fluid reabsorbed over time, hydrocele disappears

327
Q

What is a communicating hydrocele?

A

Tunica vaginalis connected with peritoneal cavity
Hydrocele fluctuates in size

328
Q

Outline examination of hydrocele

A

Soft, non-tender swelling around one testes
Transilluminate with light

329
Q

Outline management of hydrocele

A

US confirms diagnosis
Simple- Resolve in 2y
Communicating- Surgery to remove/ligate processus vaginalis

330
Q

What is hypospadias?

A

Urethral meatus displace to underside of penis towards scrotum
Can be associated with chordee- Head of penis bends down
Congenital condition

331
Q

Outline management of hypospadias

A

Do not circumcise until urologist confirms ok
Surgery after 3-4mths age

332
Q

What are the complications of hypospadias?

A

Difficulty urinating
Cosmetic and psychological concerns
Sexual dysfunction

333
Q

What is cryptorchidism?

A

Testes that have not descended out of abdomen
May be palpable in inguinal canal

334
Q

What risks are associated with undescended testes?

A

Testicular torsion
Infertility
Testicular cancer

335
Q

What are the risk factors for undescended testes?

A

FHx
Low birth weight
SGA
Prematurity
Maternal smoking during pregnancy

336
Q

Outline management of undescended testes

A

Watch and wait- Normally descend in 1st 3-6mths
Orchidopexy between 6-12mths

337
Q

What are retractile testicles?

A

Normal in boys not yet reached puberty for testes to move out of scrotum into inguinal canal when cold/cremasteric reflex activated
If fail to to descend following puberty- Orchidopexy

338
Q

What is a posterior urethral valve?

A

Tissue at proximal end of urethra causes obstruction of urine output
Newborn boys
Causes back pressure in bladder, ureters and kidneys- Hydronephresis
Prevents full emptying

339
Q

Outline presentation of posterior urethral valve

A

Difficulty urinating
Weak urine stream
Chronic urinary retention
Palpable bladder
Recurrent UTIs
Impaired kidney function

Severe- Bilateral hydronephresis and oligohydramnios
Oligohydramnios leads to underdeveloped fetal lungs and respiratory failure shortly after birth

340
Q

Outline investigations of posterior urethral valve

A
341
Q

Outline management of posterior urethral valve

A

Mild- Observe and monitor
Temporary urinary catheter to bypass valve
Definitive- Ablation/removal of extra urethral tissue (cystoscopy)

342
Q

What is a Wilms’ tumour?

A

Specific tumour affecting kidney in children <5y

343
Q

Outline presentation of Wilms’ tumour

A

<5y
Mass in abdomen
Abdo pain
Haematuria
Lethargy
Fever
HTN
Weight loss

344
Q

Outline diagnosis of Wilms’ tumour

A

US of abdomen
CT or MRI- Staging
Biopsy- Definitive

345
Q

Outline management of Wilms’ tumour

A

Surgical excision of tumour and affected kidney (nephrectomy)
Adjuvant chemo/radiotherapy

346
Q

What is a multicystic dysplastic kidney?

A

One of baby’s kidneys made up of multiple cysts, other normal- Good prognosis
Rarely bilateral- Causes death in infancy
Cystic kidney may atrophy and disappear <5y old

347
Q

What is the risk of having a single kidney in later life?

A

UTIs
HTN
CKD

348
Q

Outline diagnosis of multicystic kidney

A

Antenatal US scan

349
Q

Outline management of multicystic dysplastic kidney

A

No treatment required

350
Q

Outline autosomal recessive polycystic kidney disease (ARPKD)

A

Most common in children
Diagnosed on antenatal US

351
Q

What are the causes of ARPKD?

A

Cystic enlargement of renal collecting ducts
Oligohydramnios, pulmonary hypoplasia, Potter syndrome
Congenital liver fibrosis

352
Q

How does ARPKD present?

A

Antenatal- Oligohydramnios, polycystic kidneys
Lack of amniotic fluid leads to Potter syndrome and pulmonary hypoplasia
May require dialysis within 1st few days of life
Most develop end-stage renal failure before adulthood

353
Q

List ongoing problems a patient with PKD may have throughout their life

A

Liver fibrosis and failure
Portal HTN- Oesophageal varices
Progressive renal failure
HTN due to renal failure
CLD

354
Q

What is the prognosis of PKD?

A

Poor
Around 1/3rd survive to adulthood

355
Q

What is enuresis?

A

Involuntary urination
Nocturnal- Bed wetting
Diurnal- Day wetting

Daytime control- 2y
Nighttime urination- 3-4y

356
Q

Outline primary nocturnal enuresis

A

Never been consistently dry at night

357
Q

What are the causes of primary nocturnal enuresis?

A

Overactive bladder- Frequent small volume urination prevents development of bladder capacity
Fluid intake prior to bedtime
Failure to wake during sleep
Psychological distress
Secondary causes- Chronic constipation, UTI, LD, cerebral palsy

358
Q

Outline management of primary nocturnal enuresis

A

2wk diary
Reassure if <5y- Likely to resolve
Lifestyle changes
Encouragement and positive reinforcement
Treat underlying causes
Enuresis alarms
Pharmacological treatment

359
Q

Outline secondary nocturnal enuresis

A

Previously been dry >6mths

360
Q

List causes of secondary nocturnal enuresis

A

UTI
Constipation
T1D
New psychosocial problems
Maltreatment

361
Q

Outline diurnal enuresis

A

Daytime incontinence
Dry at night but still episodes of urinary incontinence during day

362
Q

List causes of diurnal enuresis

A

Urge- Overactive bladder
Stress- Leakage during stressors
Recurrent UTIs
Psychosocial problems
Constipation

363
Q

Outline pharmacological management of enuresis

A

Desmopressin- Reduces volume urine produced by kidneys- Take at bedtime to reduce nocturnal enuresis
Oxybutynin- Reduces contractility of bladder in urge incontinence
Imipramine- TCA

364
Q

Outline haemolytic uraemic syndrome (HUS)

A

Small thrombosis in small blood vessels throughout body
Triggered by Shiga toxins
Most commonly affects children following episode of gastroenteritis
ABs and anti-motility (eg: Loperamide) increase risk

365
Q

Which bacteria can produce shiga toxin?

A

Shigella
E. coli

366
Q

What is the classic triad of HUS?

A

Microangiopathic haemolytic anaemia
AKI
Thrombocytopenia (low platelets)

367
Q

Outline presentation of HUS

A

1st symptoms- Diarrhoea- Bloody within 3d
1 wk later:
Fever
Abdo pain
Lethargy
Pallor
Reduced urine output (oliguria)
HAematuria
HTN
Bruising
Jaundice (due to haemolysis)
Confusion

368
Q

Outline management of HUS

A

MEDICAL EMERGENCY
Stool culture

Supportive management:
Hypovolaemia- IV fluids
HTN
Severe anaemia- Blood transfusions
Severe renal failure- Haemodialysis

Self-limiting- Most patients fully recover with good care

369
Q

Outline nephritis

A

Inflammation within nephrons of kidney

Reduction in kidney function
Haematuria
Proteinuria- Less than in nephrotic syndrome

370
Q

What are the most common causes of nephritis?

A

Post-streptococcal glomerulonephritis
IgA nephropathy

371
Q

Outline post-streptococcal glomerulonephritis

A

Occurs 1-3wks after beta-haemolytic strep infection (eg: Tonsillitis)
Causes AKI
Management- Supportive- Antihypertensives and diuretics

372
Q

Outline IgA nephropathy

A

Related to HUS- IgA vasculitis
Teenagers or young adults

373
Q

What is seen on a renal biopsy in IgA nephropathy?

A

IgA deposits
Glomerular mesangial proliferation

374
Q

Outline management of IgA nephropathy

A

Supportive management of renal failure
Immunosuppressants- Steroids and cyclophosphamide- Slow progression of disease

375
Q

Outline nephrotic syndrome

A

Basement membrane in glomerulus becomes highly permeable to protein- Leaks from blood into urine
Most common between 2-5y

376
Q

Outline presentation of nephrotic syndrome

A

Frothy urine
Generalised oedema
Pallor

Deranged lipid profile- High cholesterol, triglycerides, low density lipoproteins
High BP
Hyper-coagulability- Increased tendency to form blood clots

377
Q

Outline classic triad of nephrotic syndrome

A

Proteinuria (++)
Oedema
Low serum albumin

378
Q

Outline causes of nephrotic syndrome

A

Most common- Minimal change disease

Secondary to intrinsic kidney disease:
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

Secondary to underlying systemic illness:
HSP
Diabetes
Infection (HIV, hepatitis, malaria)

379
Q

Outline minimal change disease

A

Most common cause of nephrotic syndrome in children
Can occur in healthy children w/o risk factors
Urinalysis- Small molecular weight proteins and hyaline casts

380
Q

Which condition shows small molecular weight proteins and hyaline casts on urinalysis?

A

Minimal change disease- Nephrotic syndrome

381
Q

Outline management of minimal change disease

A

Corticosteroids (prednisolone)
Prognosis good but may reoccur)

382
Q

Outline management of nephrotic syndrome

A

High dose steroids (eg: Prednisolone)- 4wks then wean off over 8wks
Low salt diet
Diuretics- Treat oedema
Albumin infusions if severe hypoalbuminaemia
AB prophylaxis if severe
If steroid resistant- ACE-is and immunosuppressants

383
Q

Outline complications of nephrotic syndrome

A

Hypovolaemia
Thrombosis- Clotting proteins lost in kidneys
Infection- Kidneys leak Igs
Acute/chronic renal failure
Relapse

384
Q

What is vulvovaginitis?

A

Inflammation and irritation of vulva and vagina
Common in girls 3-10y
Less common after puberty due to oestrogen

385
Q

Outline presentation of vulvovaginitis

A

Soreness
Itching
Erythema around labia
Vaginal discharge
Dysuria
Constipation

Urine dip- Leukocytes but no nitrites (often confused for UTI)

386
Q

Outline management of vulvovaginitis

A

Avoid washing with soap and chemicals
Avoid perfumed or antiseptic products
Good toilet hygiene- Wipe front to back
Keep area dry
Emoolients- Sudacrem to soothe
Loose cotton clothing
Treat constipation and worms

387
Q

What is acute pyelonephritis?

A

Infection UTI infection affects tissue of kidney
Can lead to scarring and reduced kidney function

388
Q

What is cystitis?

A

Inflammation of bladder
Result of bladder infection

389
Q

What are the symptoms of UTI?

A

Fever- May be only symptoms
Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency
Suprapubic pain
Dysuria
Incontinence

390
Q

Outline diagnosis of acute pyelonephritis

A

> 38 degrees
Loin pain or tenderness

391
Q

Outline diagnosis of UTI

A

Urine dip
If nitrites and leukocytes- Send MSU to lab

392
Q

Outline management of UTIs

A

All children <3mths with fever- Immediate IV ceftriaxone, full septic screen and LP considered

> 3mths- Oral ABs if otherwise well

Features of sepsis or pyelonephritis- Inpatient IV ABs

Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin

393
Q

Outline investigations of recurrent UTIs

A

<6mths 1st UTI- Abdo US within 6wks or during if recurrent UTIs/atypical bacteria
Recurrent UTIs- Abdo US within 6wks
Atypical UTIs- Abdo US during illness

DMSA 4-6mths after illness- Assess for damage from recurrent/atypical UTIs

MCUG- Investigate atypical/recurrent UTIs <6mths old or VUR

394
Q

What is vesico-ureteric reflux?

A

Urine has tendency to flow from bladder back to ureters
Predisposes patients to upper UTIs and subsequent renal scarring
Diagnosed by MCUG

395
Q

Outline management of VUR

A

Avoid constipation
Avoid excessively full bladder
Prophylactic ABs

396
Q

Outline surfactant

A

Surface tension- Attraction of molecules in liquid to each other, keeps alveoli closed
Surfactant- Produced by type II alveolar cells- Reduces surface tension- Increases lung compliance- Promotes equal expansion all alveoli during inspiration
Produced between 24-34wks gestation

397
Q

Outline cardiorespiratory changes at birth

A

During birth- Thorax squeezed clearing fluid from lungs
Birth, temperature change, sound and physical touch stimulate baby’s 1st breath
Adrenaline and cortisol released in response to stress of labour- Stimulate respiratory effort
1st breath- Expands alveoli, decreases PVR- Fall in pressure RA- LA greater pressure= Closure of foramen ovale (fossa ovalis)
Increased blood oxygenation- Drop in circulating prostaglandins= Closure of ductus arteriosus (ligamentum arteriosum)
Immediately after birth- Ductus venosus stops functioning as umbilical cord clamped- Structurally closes a few days later (ligamentum venosum)

398
Q

What is hypoxic-ischaemic encephalopathy?

A

Extended hypoxia to brain in neonate
Potentially life-long consequences- Cerebral palsy

399
Q

Outline principles of neonatal resuscitation

A

Warm baby
Calculate APGAR at 1, 5, 10mins

Stimulate breathing- Dry vigorously, neutral head position, check for obstruction

Inflation breaths:
2 cycles 5 inflation breaths
No response- 30 secs ventilation breaths
No response- Chest compressions

3:1

IV drugs and intubation considered
Possible HIE- Therapeutic hypothermia with active cooling

400
Q

Outline APGAR

A

Appearance:
0- Blue/pale centrally
1- Blue extremities
2- Pink

Pulse:
0- Absent
1- <100
2- >100

Grimace:
0- No response
1- Little response
2- Good response

Activity:
0- Floppy
1- Flexed arms and legs
2- Active

Respiration:
0- Absent
1- Slow/irregular
2- Strong/crying

401
Q

Outline delayed umbilical cord clamping

A

Placental transfusion
Improves Hb, iron stores and BP
Reduces risk of intraventricular haemorrhage and necrotising enterocolitis
Increases risk of neonatal jaundice

1min delayed cord clamping in uncompromised neonates

402
Q
A

Final Year (14 decks)

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