Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

My Phase 3a > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Describe foetal circulation

A

Placenta –> umbilical vein –> IVC –> RV –> foramen ovale –> LA –> aorta –> umbilical arteries –> placenta
OR:… RV –> pulmonary artery –> ductus arteriosus –> aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 shunts foetal circulation has?

A
  1. Ductus venosus
  2. Foramen oval
  3. Ductus arteriosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of the Forman oval and ductus arterioles in the foetal circulation?

A

Used to bypass the non-functioning lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give 4 ways congenital heart disease may be identified/present?

A
  1. Antenatal US screening
  2. Detection of a heart murmur
  3. Cyanosis
  4. Heart failure
  5. Shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the hallmarks of an innocent ejection murmur?

A 
All have S in 
- aSymptomatic patient 
- Soft blowing murmur 
- Systolic murmur only, not diastolic 
- left Sternal edge 
AND normal HS with no added sounds, no parasternal thrill and no radiation 
30% children = innocent murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 3 possible causes of cyanosis in newborn with respiratory distress (RR >60bpm)

A
  1. Cardiac disorders –> transposition of great arteries, teratology of Fallot
  2. Respiratory disorders –> surfactant deficient, meconium aspiration, pulmonary hypoplasia
  3. Persistent pulmonary HTN of the newborn = filature of pulmonary vascular resistance to fall after birth
  4. Infection –> septicaemia from group B strep
  5. Metabolic disease –> metabolic acidosis and shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give 2 possible causes of heart failure in neonates

A

Often obstructed (duct dependent) systemic circulation problems

  1. Hypoplastic left heart syndrome
  2. Critical aortic valve stenosis
  3. Severe coarctation of the aorta
  4. Interruption of the aortic arch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give 2 possible causes of heart failure in infants

A

Due to High pulmonary blood flow

  1. Ventricular septal defect
  2. Atrioventricular septal defect
  3. Large persistent ductus arteriosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give 2 possible causes of heart failure in older children and adolescents

A

Often right or left heart failure

  1. Eisenmengers syndrome (right heart failure only)
  2. Rheumatic heart disease
  3. Cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give 2 possible causes of heart failure due to circulation failure

A
  1. Reduced oxygen carrying capacity –> anaemia
  2. Increased tissue demands –> sepsis
  3. Iatrogenic –> too much fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 3 symptoms of heart failure

A
  1. Breathlessness –> especially on feeding and exertion
  2. Sweating
  3. Poor feeding
  4. Recurrent chest infections
  5. Tachycardia and tachypnoea
  6. Heart murmur, gallop rhythm
  7. Cardiomegaly and hepatomegaly
  8. Sever acidosis, collapse, death –> if severe obstructive lesion causing duct dependent systemic circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 4 congenital heart problems that can cause a left to right shunt

A
  1. VSD
  2. ASD
  3. AVSD
  4. PDA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a VSD?

A

Defect in septum between right and left ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 5 signs of a VSD

A
  1. Poor feeding and failure to thrive
  2. tachypnoea
  3. Thrill
  4. Pansystolic murmur (LLSE)
  5. Sweating
  6. Gallop rhythm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Would you expect to see on a CXR of a patient with a VSD?

A
  1. Cardiomegaly
  2. Pulmonary oedema
  3. Enlarged pulmonary arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for a VSD?

A

Monitor
Large and HF present = diuretics, captopril, calories
Symptomatic after a year = surgery –> cardiac catheterisation or open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name the classifications of ASD

A
  1. Ostium secundum = middle of atrial septum with margins on both sides (standard = 80%) involving foreman ovale
    • Blood from left to right atrium
  2. Ostium primum = bottom of atrial septum, close to the mitral and aortic valves
    - Often associated with AVSD
  3. Sinus venosus = at the top of atrial septum, anatomically and echocardiographically hard to pick up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why are ASD’s often asymptomatic?

A

Because blood flow in the atria is low pressure and so breathlessness etc is uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give 3 signs of ASD

A
  1. Fixed and widely split S2 sound
  2. Ejection systolic murmur in pulmonary region (LUSE)
  3. Palpitations
  4. Recurrent chest infections
  5. Difficulty breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AVSD is a common defect in people with what chromosomal abnormality?

A

Trisomy 21 (Downs syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for an AVSD?

A

Surgery to repair at 2-5 years of age (to avoid long term complications)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a PDA?

A

Vessel connecting aorta and pulmonary artery is still patent
- Blood from aorta –> pulmonary artery due to pressure gradient so increased high pressure blood going into lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 3 signs of a PDA

A
  1. Poor feeding, failure to thrive
  2. Tachypnoea
  3. Active pericardium
  4. Thrill
  5. Continuous machinery murmur in pulmonary area
  6. Hepatomegaly
  7. Oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the management of congenital health defects that cause a L to R shunt

A
  1. Stabilise patient
  2. Increase calorie intake
  3. NG tube
  4. Dietetics and ACEi to prevent HF Symptoms
  5. Surgical repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Would a patient with a L –> R shunt or a R –> L shunt appear cyanotic?

A

A patient with a R –> L shunt = cyanotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name 2 congenital heart problems that can cause a R –> L shunt

A
  1. Teratology of fallout

2. Transposition of the great arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 4 components that make up Teratology of Fallot?

A
  1. Pulmonary stenosis
  2. VSD
  3. Overriding aorta
  4. Right ventricular hypertrophy (RVH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Give 3 signs of Teratology of Fallot

A
  1. Cyanosis
  2. Acidosis
  3. Collapse
  4. Harsh ejection systolic murmur (LSS)
  5. Hypercyanotic spells = irritability, inconsolable crying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the management of Teratology of Fallot?

A
  • Manage hyper cyanotic spells if >15 mins = sedation, pain relief, IV propranolol, bicarb
  • Very cyanosed = Black Taussig shunt
  • Surgical repair = at 6-9 months of age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the Transposition of the Great Arteries?

A

Great arteries come of f the wrong ventricle

  • Dexoygenated blood goes into aorta = central cyanosis
  • Oxygenated blood from lung goes into pulmonary artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What would you see on a CXR of a patient with Transposition of the Great Arteries?

A
  • Narrow upper mediastinum with an ‘egg on side’ appearance

- Increased pulmonary vascular markings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do you manage Transposition of the Great Arteries?

A
  1. Atrial septostomy at birth = make foramen oval bigger to increase mixing of blood
  2. Prostaglandin induction = maintain patent ductus arteriosus
  3. Surgical repair within 1 week = arterial switch operation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is coarctation of the aorta?

A

= Narrowing of aorta
Arterial duct tissue encircles the aorta at the point of insertion fo the duct
When the duct closes, the aorta constricts, causing severe obstruction to LV outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Give 3 signs of coarctation of the aorta

A
  1. Radio-femoral delay
  2. Weak femoral pulses
  3. Difference in pre and post ductal saturations
  4. 4 Limb BP = discrepancy between upper limb (higher and bounding pulses) and lower limb BP
  5. if PDA closed/closing babies = acidotic, collapse, HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give 3 signs of aortic stenosis

A

Can be asymptomatic

  1. Palpable thrill (in supersternal region and carotid area)
  2. Ejection systolic murmur (Aortic area = RUSE)
  3. Delayed and soft aortic 2nd sound
  4. LVH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is aortic stenosis managed?

A
  • Regular clinics and ECHOs
  • Symptoms on exercise or high resting pressure gradient (>64mmHg) across aortic valve = Balloon valvotomy
    - Aortic valve replacement eventually
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Give 3 signs of Pulmonary stenosis

A
  1. Ejection systolic murmur (LUSE) - often radiates to back
  2. Ejection click
  3. RV heave (if severe)
  4. RVH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is pulmonary stenosis managed?

A

Transcatheter balloon dilation –> when pressure gradient across pulmonary valve >64 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a possible consequence of persistent pulmonary hypertension, like that seen in CHD associated with a L –> R shunt?

A

Eisenmenger Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the pathophysiology beging Eisenmenger Syndrome

A

L to R shunt –> persistent plenary HTN –> high pressure pulmonary blood flow –> damage blood vessels –> pulmonary HTN –> back up blood into right heart, RV pressure increase –> shunt direction reverses (R –> L) –> cyanotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Name 3 congenital heart problems that are often associated with Down’s syndrome

A
  1. AVSD
  2. Teratology of Fallot
  3. VSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name 3 congenital heart problems that are often associated with Turner syndrome

A
  1. Coarctation of the aorta
  2. Aortic stenosis
  3. Aortic dissection
  4. Biscuspid aortic valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Name 3 URTI

A
  1. Rhinitis
  2. Otitis media
  3. Pharyngitis
  4. Tonsillitis
  5. Laryngitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name 3 LRTI

A
  1. Bronchitis
  2. Croup
  3. Epiglottitis (bacterial)
  4. Trachetitis
  5. Bronchiolitis
  6. Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Name 3 viruses that can cause childhood respiratory infections

A

80-90% of childhood resp infections = viral

  1. Respiratory syncytial virus (RSV)
  2. Rhinoviruses
  3. Parainfluenza
  4. Metapneumonovirus
  5. Adneoviruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name 3 important bacterial pathogens that can cause childhood respiratory infections

A
  1. Strep pneumoniae (pneumococcus)
  2. Haemophilus influenzae
  3. Moraxella catarrhalis
  4. Bordetella pertussis (= Whooping cough)
  5. Mycoplasma pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Give 3 risk factors for respiratory infections

A
  1. Parental smoking
  2. Poor socioeconomic status –> large family size, overcrowded, damp housing
  3. Poor nutrition
  4. Underlying lung disease –> bronchopulmonary dysplasia (preterm), CF, asthma
  5. Immunodeficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name 4 LRTI that could be caused by RSV

What investigation is done if RSV is suspected?

A
  1. Acute bronchiolitis
  2. Wheezy bronchitis
  3. Asthma exacerbation
  4. Pneumonia
  5. Croup
    Nasopharyngeal aspirate rapid testing –> PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Why are infants more susceptible to descending infection?

A

Poor innate immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is stridor and give 3 causes of stridor

A

High pitched audible wheezing/whistling sounds when a person inhales, exhales or both due to narrowed or partially blocked upper airway (monophonic) disrupting the airflow

  1. Croup
  2. Epiglottis
  3. Bacterial tracheitis
  4. Anaphylaxis
  5. Foreign body
  6. Laryngomalacia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is croup?

A

Acute larygnotracheobronchitis –> trachea, bronchi and larynx are all affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Who most commonly gets croup, and at what time of year?

A

6 months to 6 years old –> peak incidence = 2nd year of life
Autumn = most common time fo year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What virus commonly causes croup?

A

Parainfluenza virus

= Metapneumovirus, RSV, Influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Give 3 signs of croup

A
  1. Barking seal like cough –> often worse at night
  2. Preceded by low grade fever and coryza
  3. Stridor
  4. Hoarseness
  5. Recession
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do you treat croup?

A
  • Do NOT examine throat, force to lie down or agitate child
  • Can be self limiting
  • Steroids –> oral dexamethasone, oral prednisone, nebuliser steroids (budesonide)
  • Severe upper airway obstruction = nebulised epinephrine (adrenaline) with O2 by facemark
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Name a bacteria that causes epiglottitis?

A

H. influenza B (HiB)
Acute epiglottis = severe life threatening acute illness
Presents at 1-6 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Give 4 signs of acute epiglottitis

A
  1. Pyrexial (>39)
  2. Septic
  3. Stridor - soft inspiratory
  4. Drooling
  5. Huge inflamed epiglottis that blocks oesophagus –> muffled voice/don’t speak, sit forward, neck extended with open mouth, minimal/absent cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the management of acute epiglottitis?

A
  • Intubation (for 24 hours)
  • Blood cultures and IV Abx (cefuroxime) –> 2-5 days
  • Prophylaxis with rifampicin for close contacts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Give 2 possible causes of bronchitis

A

= bacterial

  1. Pneumococcus
  2. Haemophilus influenza
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Give 2 signs of bronchitis in children

A
  1. Chronic cough –> worse at night
  2. Sore throat
  3. Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Would you expect a patient with bronchitis or with bronchiolitis to be hypoxic and tachypnoeic?
Explain why

A

Bronchiolitis –> affects the respiratory portion of the airway, where gas exchange takes place therefore you may see hypoxia and tachypnoea

Bronchitis affects the conducting portion of the airway and so is unlikely to have these effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

When would a child usually present with bronchiolitis?

A

1-9 months old

- Rare after 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Give 3 risk factors of bronchiolitis

A
  1. Prematurity
  2. Chronic lung disease
  3. CF
  4. Immunocompromised
  5. Parental smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Give 2 possible causes of bronchiolitis

A
  1. RSV = 80%
  2. Rhinovirus
  3. Influenza
  4. Adenovirus
  5. Parainfluenza
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Give 3 signs of bronchiolitis

A

3-5 days of symptoms, coryza symptoms too

  1. Recurrent cough = sharp, dry
  2. Widespread wheeze
  3. Fine end inspiratory crackles
  4. Increasing breathlessness –> feeding difficulties
  5. Subcostal and intercostal recession
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is bronchiolitis managed?

A
  • Conservative
  • Oxygen or ventilation
  • NG feeds –> frequent but small
  • Ribavirin = antiviral
  • CF patients = broad spec Abx for 2-3 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is bronchiolitis prevented and who is offered prevention?

A

Monthly IM injection over winter of Palivizumab (monoclonal Abs)
High risk = Chronic lung disease, congenital heart disease, SCID, CF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is pneumonia?

A

Inflammation of the lung parenchyma with congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Give 3 possible viral causes of pneumonia

A

More common in young children

  1. RSV
  2. Influenza A and B
  3. Parainfluenza
  4. Adenovirus
  5. Metapneumovirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Give 3 possible bacterial causes of pneumonia

A

More common in older children

  1. Strep pneumococcus
  2. HiB
  3. Staph aureus
  4. Klebsiella
  5. Mycobacteria penumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Give 5 signs of pneumonia in children

A
  1. Fever
  2. Miserable
  3. Tachypnoea
  4. Cough
  5. Poor feeding
  6. Lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe the diagnostic criteria for pneumonia in children

A

History of cough and/or difficulty breathing (<14 days duration) with increased respiratory rate
- <2 months = >60/min
- 2 to 11 months = >50/min
- >11 months = >40/min
Bacterial pneumonia in children <3 y/o with fever, chest recession and RR >50/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What investigations might you do in a child who you suspect has pneumonia?

A
  • CXR –> look for consolidation
  • Blood cultures
    It is often difficult to get a sputum sample
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How do you treat pneumonia?

A
  • Oxygen, analgesia, IV fluids
  • Abx –> based on age, severity and CXR
    • Newborn = broad spec
    • Older infants = oral amoxicillin
    • > 5 y/o = amoxicillin or oral macrolide (erythromycin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What antibiotics might you use in a child with pneumonia caused by mycoplasma pneumoniae?

A

Mycoplasma pneumoniae is intracellular and so amoxicillin won’t work therefore give macrolides e.g. clindamycin, erythromyocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Give 2 possible complications of pneumonia

A
  1. Pleural effusions
  2. Empyema –> drain
  3. Fibrin strands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is a unilateral pleural effusion suggestive of?

A

Infection –> parapneumonia or empyema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is a bilateral pleural effusion suggestive od?

A

Fluid overload –> HF, nephrotic syndorme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is whooping cough caused by?

A

Bordetella pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How does whooping cough present?

A
  • Week of coryza (Catarrhal phase)
  • Paroxysmal cough followed by inspiratory whoop and vomiting (paroxysmal phase)
  • Symptoms gradually decrease over 3-6 weeks (convalescent phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How do you treat whooping cough?

A

Erythromycin –> decreases symptoms only if started during catarrhal phase
Close contacts = erythromycin prophylaxis, unvaccinated should be vaccinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the difference between wheeze and stridor?

A 
Wheeze = Expiratory polyphonic noise which indicates narrowing in the medium to small sized airways 
Stridor = Monophonic high pitched noise heard on inspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the aetiology of recurrent wheeze

A
  1. Persistent infantile wheeze
  2. Viral episodic wheeze
  3. Asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is persistent infantile wheeze normally associated with/exacerbated by?

A

Affects small airways

Associated with parental smoking or post viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Are inhalers likely to help a child with persistent infantile wheeze?

A

No - unlikely to help, symptoms improve as child gets older, usually resolved by 3 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is viral episodic wheee normally associated with/exacerbated by?

A

Normally follow URTI/viral infection

RFs = maternal smoking during and/or after pregnancy, prematurity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

How does viral episodic wheeze differ from asthma?

A
  • NO interval symptoms
  • NO excess of atopy
  • NO benefit from regular inhaled steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Are inhalers likely to help a child with viral episodic wheeze?

A

Bronchodilators may help in acute episodes
No benefit from inhaled steroids
Symptoms usually improve with age, resolve by 5 y/o mostly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is asthma?

A

Recurrent episode of SOB, wheeze and cough caused by reversible airway obstruction
- Most common chronic respiratory disorder in childhood, 15-20% of children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the 3 main pathophysiological characteristics of asthma?

A
  1. Ariflow limitation
  2. Airway hyper-responsiveness
  3. Bronchial inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Give 3 risk factors for asthma

A
  1. Eczema
  2. Hayfever
  3. Family history of atopic conditions
  4. Low birth weight
  5. Bottle fed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Name 3 possible precipitants of asthma

A
  1. Cold weather
  2. Exercise
  3. Strong emotions
  4. Allergens (dust/pollen)
  5. Pets
  6. Drugs –> NSAIDs, BB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Give 3 signs of asthma

A
  1. Wheeze
  2. Episodic cough
  3. SOB
  4. Diurnal variation –> worse at night and in early morning
  5. Interval symptoms
  6. Tachypnoea
  7. Barrel chest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the features of moderate acute asthma?

A
  • Oxygen saturation >92%
  • Peak flow >50% predicted
  • No clinical features of severe asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the features of Severe acute asthma?

A
  • Too breathless to talk or feed
  • Use of accessory neck muscle
  • Oxygen saturation <92%
  • RR > 50 bpm in children 2-5, >30 in children >5
  • Pulse >130/bpm in children aged 2-5, >120 bpm in children >5
  • Peak flow <50% predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the features of Life threatening acute asthma?

A
  • Oxygen saturation <92%
  • Poor respiratory effort
  • Cyanosis
  • Fatigue
  • Drowsiness/altered consciousness
  • Silent chest
  • Peak flow <33% predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What investigations might you do for someone with suspected asthma?

A
  • Spirometry
    - PEFR <80% predicted
    - FEV1:FVC <80%
    - Bronchodilator response to B agonist therapy  15% increase in FEV1 or PEFR
  • Skin prick testing for common allergens
  • CXR –> hyperinflation, flattened hemi-diaphragms, peribronchial cuffing, atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How would you manage an acute exacerbation of asthma in a child?

A
  • O2
  • Beta agonist nebulised
  • Prednisolone 1mg/kg
    If still not improving
  • Nebulised ipratropium or salbutamol
  • Aminophylline/MgSO4/salbutamol infusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Name 2 preventer inhalers

A

ICS act as preventers

  • Beclomethasone
  • Budesonide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Name 2 relievers inhalers

A

Beta agonists –> salbutamol

Muscarinic antagonist –> Ipratropium bromide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Describe the step-wise approach to asthma management

A

SABA -> SABA + ICS -> LABA + ICS -> LABA + increased dose of ICS -> LABA + daily PO steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give 3 long term risk of systemic steroids

A
  1. Adrenal suppression
  2. Growth suppression
  3. Osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Why might asthma treatment fail in children?

A
  1. Adherence (compliance)
  2. Wrong diagnosis
  3. Environmental factors –> pets, smokers
  4. Choice of drug/device
  5. bad disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Give 5 differentials for a painful joint

A 
Life threatening differentials 
1. Leukaemia 
2. Septic arthritis 
3. NAI 
Pain and Swelling 
4. Trauma 
5. Infection 
6. Reactive swelling 
7. JIA
Pain and no swelling 
8. Hypermobile joint syndrome 
9. Perthe's disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the 3 main differentials for a limping child?

A
  1. Infection –> sepsis/osteomyelitis
  2. Trauma –> NAI, fracture
  3. Tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the likely cause of a limp in a child aged 0-3?

A
  1. Truama –> NAI, fracture
  2. Osteomyelitis/septic arthritis
  3. Developmental dysplasia of the hip (DDH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the likely cause of a limp in a child aged 3-10?

A
  1. Trauma
  2. Transient synovitis/irritable hip
  3. Osteomyelitis or septic arthritis
  4. Perthe’s disease
  5. JIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the likely cause of a limp in a child aged 10-15?

A
  1. Trauma
  2. Osteomyelitis/septic arthritis
  3. Slipped upper femoral epiphysis (SUFE)
  4. JIA
  5. Perthes disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What must you remember to consider as a differential in a limping child?

A

Intra-abdominal pathology –> hernia, testicular torsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Why might you want to ask about socioeconomic class and smoking status in child presenting with a limp?

A

Social deprivation and passive smoking are RFs for Perthe’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What investigations might you want to do on a child presenting with a limp?

A
  1. General observations –> HR, BP, temp, RR, O2 sats
  2. FBC, BM, ESR, CRP
  3. XR –> AP and lateral views of the joint and joints above and below
  4. USS –> effusion in joints
  5. CT/MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is a Toddlers Fracture?

A

Subtle displaced spiral fracture of the tibia

  • History of small fall or twisting injury
  • Immobilise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is Transient synovitis?

A

Acute onset joint inflammation following illness (often respiratory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How does transient synovitis present?

A
  • Sudden onset limp –> usually unilateral
  • Hip and/or knee pain
  • Limited ROM –> particularly internal rotation
  • Afebrile or mild fever, doesn’t appear ill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How do you manage transient synovitis?

A

Self limiting usually within 2 weeks

Rest, physio, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the most common organism that causes septic arthritis?

A

Staph aureus

- Most commonly in children <2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Give 3 signs of septic arthritis

A
  1. Systemically very unwell = acute febrile illness
  2. Pain at rest
  3. Hip kept flexed, abducted and externally rotated
  4. Raised WCC and CRP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Describe Kocher’s criteria

A 
Diagnosis of septic joint = 3/4 
- Temp >38.5 
- Cannot weight bare 
- ESR >40 
- WCC >12
(CRP >20 is independent RF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

How is septic arthritis managed?

A 
IV ABx (after aspirate) for up to 3 weeks 
- Surgical emergency and need joint washout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is Perthe’s disease?

A

A self limiting idiopathic disease characterised by vascular necrosis of the femoral head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Who is most commonly affected by Perthes disease?

A

Boys (80%) aged 5-10 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Give 3 risk factors for Perthe’s disease

A
  1. Low birth weight
  2. Low socioeconomic status
  3. Short stature
  4. Passive smoking
  5. FHx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Give 3 signs of Perthe’s disease

A
  1. Pain in hip or knee causing limp
  2. Trendelenburg sign
  3. Proximal thigh atrophy
  4. Decreased ROM –> especially abduction and internal rotation)
  5. Effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What investigations might you do for someone with suspected Perthes disease?

A
  • Roll test –> should invoke guarding or spasm
  • Assess ROM
  • AP and lateral XR
  • MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Describe the management of Perthe’s disease

A

Contain the hip, either on their own or with the aid of plasters, brace, physio or surgery
- >8y/o = surgical –> femoral/pelvic osteotomies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is SUFE?

A

Slipped upper femoral epiphysis = displacement of the upper femoral epiphysis on the metaphysis through the hypertrophic zone of the growth plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Who is most likely to be affected by SUFE?

A

A pre pubescent obese male (12-15 years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What can SUFE be associated with?

A
  • Hypothyroidism
  • Downs
  • Radio/chemotherapy
  • Obese, hypogonadal
  • Tall, thin, often boys, post growth spurt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

How does SUFE present?

A
  • Several week history of vague groin or thigh discomfort –> 40% bilateral
  • Antalgic/waddling gait
  • Decreased ROM
  • May be leg shortening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is the treatment of SUFE?

A

Analgesia

Surgical pinning of hip with or without reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is DDH?

A

Developmental dysplasia of the hip

- Abnormal development resulting in instability, dysplasia, subluxation and possible dislocation of the hip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Give 3 risk factors of DDH

A
  1. Female
  2. First born
  3. Breech birth
  4. Family history
  5. C section
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What tests can be done on clinical examination in the neonatal period to pick up DDH?

A
  1. Barlow test = whether hip is dislocatable –> adduct and depress
  2. Ortolani test = if hip is dislocated –> anterior and abduct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Give 3 symptoms of DDH

A
  1. Painless limp
  2. Delayed walking
  3. Prone to falls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Give 3 signs fo DDH

A
  1. Asymmetrical skin creases in thigh or buttock
  2. Unequal leg length
  3. Galeazzi sign (flex knees with feet together) –> if +ve affected femur appears short due to dislocated hip joint (-ve if bilateral DDH)
  4. Older children = limp, +ve trendelenburg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What investigations are done on someone who has suspected DDH?

A

USS = at 6-8 weeks

AP posterior XR = examination of choice after 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe the management of DDH

A
  1. Pavlik harness –> <6 months

2. Surgical reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are the 2 main risks associated with the surgical management of DDH?

A
  1. Avascular necrosis

2. Re-dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is chondrosarcoma?

A

A malignancy neoplasm of cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis (JIA)?

A

Persistent joint swelling/stiffness >6 weeks in children <16 and no other cause is identified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What investigations are done for someone with suspected JIA?

A

Diagnosis of exclusion

  • FBC, ESR, CRP
  • Infection –> throat swab, urinalysis, viral serology, cultures
  • RF, ANA
  • XR, US, MRI
  • Synovial fluid aspirate
  • Ophthalmology review
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What symptoms are associated with JIA?

A
  1. Swelling –> persistent
  2. Joint stiffness –> morning
  3. Loss of ROM
  4. Limp
  5. Pain
  6. Uveitis
  7. Fever
  8. Salmon pink rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What extra articular features might you see in someone with JIA?

A
  1. Psoriasis
  2. Dactylitis
  3. Nail pitting
  4. Rash
  5. Fluctuating fever
  6. Uveitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Name 5 types fo JIA

A
  1. Oligoarticular (commonest)
  2. Polyarticular
  3. Psoriatic
  4. Enthesitis related
  5. Systemic onset JIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Define oligoarticular JIA

A

<4 joint involved, often asymmetrical
Normal ANA+ and associated with a high risk of developing uveitis
Most commonly affects knee –> ankle –> wrist –> elbow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Define polyarticular JIA

A

> 4 joint involved, often symmetrical and more destructive
Commonly affects the small joints of hands/feet
Can be RF negative or RF positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How is RF negative polyarticular JIA diagnosed?

A

Diagnosis of exclusion = IgM RF negative 3 months apart

- Systemic features, asymmetrical joints, chronic hyperaemia, tenosynovitis, bursitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

How is RF positive polyarticular JIA diagnosed?

A 
Chronic symmetrical inflammatory polyarthritis with positive RF on 2 occasions at least 3 months apart (worst prognosis)
4 or more criteria for at least 6 weeks 
- Morning stiffness >1hr 
- Arthritis in at least 3 joints 
- Hand arthritis 
- Systemic arthritis 
- Rheumatoid nodules 
- Rheumatoid factor +ve
- Erosions on XR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

How is psoriatic arthritis diagnosed?

A

Inflammatory arthritis in the presents of psoriasis
OR
Inflammatory arthritis with dactylics OR psoriatic nail changes + first degree relative with psoriasis

  • Arthritis = asymmetrical large joint (knee, ankles) or small joint polyarthritis (MCP, PIP, DIP)
  • Dactylics, tendonitis, uveitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How is enthesitis related arthritis diagnosed

A

Arthritis with enthesitis (inflammation of tendons, ligamentous or muscular insertion on to bones)
OR
Arthritis alone or enthesitis alone with 2 of:
- Sacroiliac joint tenderness
- Inflammatory spinal pain
- HLAB27 +ve
- First degree relative FHx of uveitis
- Age of onset >6 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

How might enthesitis related arthritis present?

A
  • Oligo or polyarthritis in lower limbs
  • Enthesitis
  • Spinal pain
  • Systemic features
  • Acute anterior uveitis
  • Plantar fascitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What might you see on an X-ray of someone with enthesitis related arthritis?

A

Romanus lesions = small erosions of corners of vertebral bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What signs might you see in someone with systemic onset JIA?

A
  • Spiking daily fever
  • Salmon pink rash –> macular, urticarial
  • Lymphadenopathy
  • Hepatosplenomeagly
  • Polyserositis –> pericarditis, pleurites, sterile peritonitis
  • Arthritis –> after 6 months, oligo or polyarthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Describe the non medical treatment for JIA

A
  1. Information
  2. Education
  3. SUpport
  4. Liaison with school
  5. Exercise and physiotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Describe the medical treatment for JIA

A
  1. NSAIDs –> ibuprofen, naproxen, diclofenac
  2. Inraarticular steroid injection
  3. Methotrexate
  4. Anti TNF –> etanercept
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What must you screen for in a patient with JIA?

A

Uveitis –> every 3 months

- Often asymptomatic in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Give 5 potential consequences that can occur if you fail to treat JIA

A
  1. Damage
  2. Deformity
  3. Disability
  4. Pain
  5. Bony overgrowth
  6. Uveitis
  7. Ligament laxity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Name a severe, potentially life threatening complicated of systemic onset JIA

A

Macrophage activation syndrome (MAS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What signs might you see in someone with macrophage activation syndrome (MAS)?

A
  • High fever
  • Hepatosplenomegly
  • CNS dysfunction
  • Purpuric rash
  • Cytopaenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is the treatment for macrophage activation syndrome (MAS)?

A

Supportive treatment

Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Define osteoporosis in children

A

> 1 vertebral crush fracture
OR
Bone density <2.0 and either 2 or more long bone fractures by 10y/o or >3 fracture by 19 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Describe the aetiology of osteoporosis in children

A
  1. Inherited/congenital –> osteogenesis imperfecta, inborn errors, idiopathic
  2. Acquired –> drug induce, malabsorption, immobilisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What investigation might you do to determine fi a child has osteoporosis?

A

DEXA scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

How do you manage oestoporosis?

A
  • Calcium and vitamin D supplements
  • Regular weight bearing exercise
  • Minimise oral corticosteroids
  • Sometimes bisphosphonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is osteogenesis imperfecta?

A

AD inherited osteoporotic condition that leads to bone weakness in children
Due to defect in type 1 collagen genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Describe the inheritance of osteogenesis imperfecta

A

AD inheritance in 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Give 5 signs of osteogenesis imperfecta

A
  1. Bone fragility
  2. Fractures
  3. Deformity
  4. Impaired motility –> ligamentous laxity, sarcopenia
  5. Poor growth
  6. Deafness
  7. Blue sclera
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What classifications is used in osteogenesis imperfecta?

A 
Sillence classification 
    I = Mild 
    II = Lethal 
    III = Progressively deforming, severe
    IV = Moderate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Describe the treatment for osteogenesis imperfecta

A
  • MDT approach –> PT, OT, specialists, surgeons
  • Bisphosphonates –> pamidronate
  • Surgery if needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are bisphosphonates mode of action?

A

Inhibit osteoclasts
- In osteogenesis imperfecta they Increase LS and TB bone mass, reduce fracture frequency, increase vertebral height, suppress bone markers, reduce pain, increase overall mobility and have no adverse effect on growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What is rickets?

A

A disorder of bone mineralisation –> under mineralisation leading to bone weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is the main cause of rickets?

A

Vitamin D deficiency

  • Lack on sunlight
  • Poor nutrition = including prolonged unsupplemented breast feeding
  • Intestinal malabsorption = CF, coeliac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What does vitamin D do?

A
  1. Increase calcium absorption from the gut
  2. Increased calcium release from the bone
  3. Increases calcium reabsorption at the kidneys
  4. Maternal vitamin D influences bone size and mass in childhood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Give 3 sources of Vitamin D

A
  1. Sunlight
  2. Cereals
  3. Egg yolk
  4. Oily fish
  5. Spreads
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Give 4 signs of Rickets

A
  1. Metaphyseal swelling
  2. Bony deformities –> bowing legs
  3. Motor delay
  4. Hypotonia
  5. Fractures
  6. Craniotabes –> ping pong sensation of the skull
  7. Splayed and frayed metaphyses
  8. Harrison sulcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What investigations might you do to determine if a child has Rickets?

A
  1. Serum biochemistry –> low PO4, Raised AlkP
  2. Bone profile
  3. Measure Vitamin D levels –> low with raised PTH
  4. XR –> cupping and fraying of metaphyses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What vitamin D level suggests skeletal ill health?

A

<10 nmol/L
>25 nmol/L = possible adverse effects
>50 nmol/L = no obvious adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Describe the treatment of Rickets

A
  • Treat underlying problem

- If vitamin D deficiency, give Adcal D3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Secretion fo which hormone will increase in response to low calcium?

A

PTH

- Increase PTH = bone resorption, Ca reabsorption at kidneys and Ca absorption at gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Name an organism that commonly causes osteomyelitis in children

A

Staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Give 3 signs of osteomyelitis in children

A
  1. Joint pain
  2. Lethargy
  3. Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What investigations might you do on child who you suspect has an infected joint?

A
  • XR
  • MRI
  • Blood cultures
  • JOint aspirate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

How would you treat a child with osteomyelitis?

A

IV cefuroxime or IV flucloxicillin

6 weeks of treatment, can switch to PO when improving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Define UTI

A

Growth of bacteria within the urinary tract (10^5 organism/ml grown on culture of appropriate sample)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What is the importance of diagnosing UTI’s in children?

A
  • Can cause significant acute illness
  • 50% rate of reoccurrence
  • 50% have structural abnormality
  • Long term complications –> kidney scarring, HTN, CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is the most common causative organism of UTI in children?

A

E. coli

Can also have Klebsiella, proteus (B>G), pseudomonas (can indicate structural abnormality)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Give 3 signs of UTI in infants

A
  1. Fever
  2. Lethargy
  3. Irritability
  4. Poor feeding or failure to thrive
  5. Vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Give 3 signs of UTI in children

A
  1. Dysuria
  2. Frequency
  3. Abdominal pain or loin tenderness
  4. Fever with or without rigors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What investigations might you do on a child who you suspect has a UTI?

A
  1. Urine dip –> nitrates,
  2. MCS on clean catch urine
    Further investigations (if indicated)
  3. USS KUB —> obstruction, scarring, structural abnormalities
  4. DMSA –> renal scarring
  5. MCUG –> function of bladder and reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

When would you do a USS KUB on a child with a UTI?

A
  • <6 months old m
  • Recurrent UTIs
  • Atypical UTI = seriously ill/septic, poor urine flow, abdominal or bladder mass, raised creatinine, failure to respond to Abx within 48 hrs, infection with non E.coli organism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

What is the treatment for UTI in children?

A

IV cefuroxime

Switch to PO Trimethoprim if stable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

How would you treat a UTI that has been caused by ESBL E.coli?

A

Give Meropenem

- ESBL bacteria are resistant to all penicillin and cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What is oedema?

A

Increase in interstitial fluid

Clinically = swelling, pitting oedema, facial puffiness, ascites, pleural effusions, pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Give 3 causes of oedema

A
  1. Impaired lymph drainage –> lynmphoedema
  2. Impaired venous drainage –> venous obstruction
  3. Lower oncotic pressure (low albumin/protein) –> malnutrition, liver failure, nephrotic syndrome
  4. Salt and water retention –> impaired GFR, HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Give 3 causes of proteinuria in children

A
  1. Orthostatic proteinuria
  2. Glomerular abnormalities –> nephrotic or nephritic syndrome
  3. Increased glomerular filtration pressure
  4. Reduced renal renal mass
  5. HTN
  6. Tubular proteinuria
  7. Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Why does nephrotic syndrome occur?

A

Podocyte processes leak protein into urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What is nephrotic syndrome characterised by?

A
  1. Heavy proteinuria = frothy urine
  2. Hypoalbuminaemia (<35g/L)
  3. Oedema –> pitting, gravitational, facial swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Give 3 causes of nephrotic syndrome

A
  1. Minimal change disease (85%)
  2. Focal segmental glomerulosclerosis
  3. Membranoproliferative glomerulonephritis
  4. Membranous glomerulonephritis
  5. Congenital
  6. Secondary to –> HSP, SLE, malaria, allergens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What investigations would you do in someone with suspected nephrotic syndrome?

A
  • Urine dipstick –> protein
  • FBC, ESR, U+Es, creatinine, albumin (hypo), alb:Cr >250mg/mmol
  • Complement levels –> C3 and C4
  • Antistreptolysin O or anti-DNAase B titres and throat swab, cANCA, ANA
  • Urine MS&C –> haematuria/casts
  • Urinary electrolytes –> sodium concentration
  • Hep B and C screen
  • Malaria screen (if travel abroad)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Name the 3 types of nephrotic syndrome

A
  1. Steroid sensitive nephrotic syndrome = 85-90%
  2. Steroid resistant nephrotic syndrome
  3. Congenital nephrotic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Give 3 signs suggestive of steroid sensitive nephrotic syndrome

A
  • 1 to 10 years old (peak = 2-5y/o)
  • Norma BP
  • NO macroscopic haematuria
  • Normal renal function
  • Normal complement levels
  • NO features to suggest nephritis
  • Respond to steroids
  • Histology = “minimal change” usually
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

What is steroid sensitive nephrotic syndrome often precipitated by?

A

Respiratory infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

How do you treat steroid sensitive nephrotic syndrome?

A
  • Standard course of prednisolone for 1st episode = 60mg/m2 OD for 4 weeks then 40mg/m2 on alternate days for 4 weeks
  • Consider salt and water restriction, diuretics, Pen V, measles/varicella/pnuemonoccoal immunisations
  • Renal biopsy if unresponsive or atypical features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What is the prognosis of steroid sensitive nephrotic syndrome?

A 
1/3 = resolve directly 
1/3 = infrequent relapses 
1/3 = frequent relapses = steroid dependent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

Give 3 features suggestive of steroid resistant nephrotic syndrome

A
  1. Elevated BP
  2. Haematuria
  3. May have impaired renal function
  4. Features may suggest nephritis
  5. Failure to respond to steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

Give 3 causes of steroid resistant nephrotic syndrome

A
  1. Focal segmentaal glomerulosclerosis
  2. Membranoproliferative glomerulonephritis
  3. Membranous nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

Give 2 features of congenital nephrotic syndrome

A
  • Presents in 1st 3 months of life
  • Mostly recessively inherited
  • More commonly in consanguineous families
  • Associated with high mortality –> complications of hypoalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

Give 3 non glomerular causes of haematuria

A
  1. Infection
  2. Trauma to genitalia, urinary tract or kidneys
  3. Stone
  4. Tumours
  5. Sickle cell disease
  6. Bleeding disorders
  7. Renal vein thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

Give 3 glomerular causes of haematuria

A
  1. Actue GN
  2. Chronic GN
  3. IgA nephropathy
  4. Familial nephritis –> Alport syndrome
  5. Thin basement membrane syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

What is nephritis?

A

Increased glomerular cellularity restricts glomerular blood flow and therefore filtration is decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

What are the main features of nephritis?

A
  1. Macroscopic haematuria
  2. Salt and water retention –> HTN, oedema
  3. Proteinuria
  4. Impaired GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

Give 3 causes of acute nephritis

A
  1. Post infectious
  2. Vasculitis –> HSP, SLE, Wegner granulomatosis
  3. Anti-glomerular basement membrane disease (good pasture syndrome) = rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

How do you treat nephritis?

A

Treat water and electrolyte balance

Diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

Name a complication of nephritis

A

Rapidly progressive glomerulonephritis may occur = irreversible renal failure if left intreated
- renal biopsy, immunosuppression, plasma exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

What is acute post streptococcal glomerulonephritis?

A
  • Cause of nephritis
  • 1-2 weeks after nasopharyngeal or skin infection
  • Caused by group A beta haemolytic streptococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What are the features of acute post streptococcal glomerulonephritis?

A
  • Clinical nephritis 10 days post infection
  • Haematuria
  • Oedema
  • Decreased urine output
  • HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

What investigations would you do for someone with suspected acute post streptococcal glomerulonephritis?

A
  • FBC –> mild normochromic, normocytic anaemia
  • U&Es –> increased urea and creatinine, (hyperkalaemia, acidosis)
  • Immunology –> raised ASOT/antiDNAse B titre, low C3, C4
  • Throat/other swabs
  • Urinalysis –> haematuria, proteinuria, microscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

Describe the treatment of acute post streptococcal glomerulonephritis

A
  • Fluid balance –> salt and fluid restriction, diuretics
  • Correction fo other imbalances –> K+, acidosis
  • Dialysis
  • Penicillin –> treatment of strep infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

What is Henoch-Schoenlein Purpura?

A

A systemic vasculitis where there is deposition of IgA complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

What is HSP characterised by?

A
  • Purpuric, raised, palpable red rash, normally in extensors –> butt, back of legs/arms
  • Arthralgia
  • Periarticular oedema
  • Abdominal pain
  • Glomerulonephritis
  • HSP nephritis –> IgA deposition, haematuria, proteinuria, nephrotic syndrome, acute nephritis, renal impairment, HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Who is most likely to get HSP?

A
  • Occurs between 3-10 years old
  • More common in boys
  • More common in winter
  • Often preceded by URTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Give examples of children who are at increased risk of cancer

A
  1. Down’s syndrome children –> risk of leukaemia
  2. Immunocompromised children –> risk of lymphoma
  3. Neurofibromatosis 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

Name 3 embryonal tumours

A
  1. Wilm’s tumour
  2. Neuroblastoma
  3. Rhabdomyosarcoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

Give 3 possible presentations of paediatric malignant disease

A
  1. Localised mass –> lymphadenopthy, organomegaly, soft tissue/bony mass
  2. Problems with disseminated disease –> bone marrow infiltration
  3. Problems from localised mass –> airway obstruction, raised ICP, focal neurology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

An abnormal red reflex in a child may be a sign of what paediatric malignancy?

A

Retinoblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

What type of leukaemia is most common in children?

A

Acute Lymphoblastic Leukaemia (ALL)

- Peak incidence = 2-5 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

What is ALL?

A

Malignant proliferation of ‘pre-B’ or T cell lymphoid precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

Give 4 signs of ALL

A
  1. Anaemia
  2. Bleeding
  3. Bruising
  4. Bone/limb pain
  5. Fever
  6. Infections
  7. Fatigue
  8. Lymphadenopathy
  9. Hepatosplenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

What investigations might you do in a child to determine whether they have ALL?

A
  1. Blood film –> blastocytes
  2. Serum chemistry –> anaemia, low WCC, low platelets
  3. CXR
  4. BM aspirate
  5. Lumbar puncture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

Describe the treatment of ALL

A
  • Correct anaemia, low platelets, WBC
  • Allopurinol –> protect against cell lysis
  • 5 phase combination chemotherapy (2 years for girls, 3 years for boys)
  • A stem cell transplant = high risk or relapsed patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What are the 5 phases of chemotherapy in the treatment of ALL?

A
  1. Induction
  2. Consolidation
  3. Interim maintenance
  4. Intensification
  5. Maintenance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

What is AML?

A

Malignant proliferation of myeloid cell precursors

  • Presentation = pancytopaenia, lymphadenopathy
  • Treatment = All-trans retinoic acid followed by 4 courses of intensive myeloablative chemo, BMT in 1st remission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

Give 5 signs fo CNS malignancy in children?

A
  1. Headache –> early morning, worse on lying down
  2. Vomiting –> early morning
  3. Papilloedema
  4. Visual disturbances
  5. Squint
  6. Nystagmus
  7. Ataxia
  8. Behavioural/personality changes
  9. Infants = separation of sutures/tense fontanelle, increase HC, developmental delay/regression
    DEPENDS ON SITE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

Give 2 signs of a supratentorial tumour

A

= cortex

  1. Seizures
  2. Hemiplegia
  3. Focal neuro signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

Give 2 signs of a midline tumour

A
  1. Bitemporal hemianopia

2. Pituitary failure –> growth failure, DI, weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

Give 2 signs of a cerebellar/IVth ventricle tumour

A
  1. Truncal axtia
  2. Coordination difficulties
  3. Nystagmus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

Give 2 signs of a brainstem tumour

A
  1. CN defects
  2. Pyramidal signs
  3. Cerebellar signs
  4. Often NO raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

Give the 5 types of CNS tumour

A
  1. Pilocytic astrocytoma (40%) –> benign to highly malignant GBM, surgical removal
  2. Medulloblastoma (20%)
  3. Ependyoma (8%)
  4. Pontine glioma (6%) –> survival = 6-12 months
  5. Craniopharyngioma (4%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

Describe the general treatment for CNS malignancies

A
  1. Surgical resection + VP shunt (reduces risk of coning)
  2. Chemotherapy
  3. Radiotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

Give 5 signs that lymphadenopathy may be due to malignancy rather than a benign e.g. infection, AI

A
  1. Enlarging node without infective cause
  2. Persistently enlarged
  3. Unusual site –> e.g. supra-clavicular
  4. B symptoms –> e.g. fever, weight loss
  5. Abnormal CXR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

What is seen on a lymph node biopsy of someone with Hodgkins lymphoma?

A

Reed Sternberg cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

What staging is used in lymphoma?

A

Ann Arbor

  • 1 = single site
  • 2 = more than one site on one side
  • 3 = on both sides of the diaphragm
  • 4 = disseminated disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

What is the treatment for lymphoma?

A
  • Combination chemotherapy +/- radiation

- High dose therapy and BMT for those who have relapsed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Give 5 differentials for abdominal mass in children

A
  1. Hepatoblastoma
  2. Wilm’s tumour
  3. Neuroblastoma
  4. Lymphoma/leukaemia
  5. Constipation/bowel obstruction
  6. Enlarged kidneys –> polycystic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

What investigations might you do on a child with an abdominal mass?

A
  • USS
  • CT/MRI
  • Biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

What is a neuroblastoma?

A

Tumours arising from neural crest tissue in the adrenal medulla and sympathetic nervous system
- Most common <5 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

Give 2 signs of a neuroblastoma tumour

A
  1. Abdominal mass –> often cross the midline and envelops major vessels and lymph nodes
  2. Pallor
  3. Symptoms of metastases –> bone pain, weight loss, limp, hepatomegaly
  4. Lymphadenopathy
  5. Pancytopenia –> anaemia, infections, bruising
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

What investigations would you do in someone suspected to have a neuroblastoma?

A
  • Urinary catecholamine levels –> raised
  • Biopsy
  • Bone marrow biopsy
  • MIBG scan –> maps metastatic growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

Describe the treatment for a neuroblastoma

A
  • Surgery –> localised primary tumour often resectable
  • Chemotherapy –> before and/or after
  • Radiotherapy for high risk groups/relapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

What is a Wilm’s tumour?

A

Nephroblastoma = malignancy arising from embryonal renal tissue
- 80% before 5 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

Give 3 signs of a Wilm’s tumour

A
  1. Abdominal mass –> not likely to cross midline
  2. Abdominal pain
  3. Anorexia
  4. Haematuria
  5. Anaemia
  6. HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

Describe the treatment for a Wilm’s tumour

A
  • Chemotherapy –> before or after surgery
  • Surgery –> nephrectomy to partial nephrectomy
  • Radiotherapy –> for residual abdominal or pulmonary disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

Describe the aetiology of retinoblastoma

A
  1. Mutations in RB1 (tumour suppressor gene) located on chromosome 13
  2. Familial (bilateral disease)
  3. Sporadic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

Give 3 signs of a retinoblastoma

A
  1. Loss of red reflex (white reflex noted)
  2. Pain around the eye
  3. Poor vision
  4. Squint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

Describe the treatment for retinoblastoma

A

Laser therapy
Chemotherapy and radiotherapy
Surgery –> repair or removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
256
Q

How may a malignant bone tumour present?

A
  1. Persistent localised bone pain
  2. swelling
  3. Pathological fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
257
Q

Name 2 types of malignant bone tumour

A
  1. Ewings = more common in younger children

2. Osteogenic sarcoma = more common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
258
Q

Describe the treatment of a malignant bone tumour

A
  • Combination chemo
  • Resection
  • Radiotherapy –> in Ewings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
259
Q

Give 3 short term side effects of chemotherapy

A
  1. N+V
  2. Alopecia
  3. Immunosuppression –> infection
  4. Bone marrow suppression –> anaemia, brushing, infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
260
Q

Give 3 long term effects of chemotherapy

A
  1. Endocrine related –> growth and development
  2. Intellectual
  3. Fertility problems
  4. Psychological issues
  5. Cardiac and renal toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
261
Q

Where are red blood cells made?

A

In the bone marrow

- Stimulated by erythropoietin (produced by kidneys)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
262
Q

What are the normal levels of haemoglobin in

a) Neonates
b) 1-12 months
c) 1-12 years?

A

a) Neonates = <14g/dl
b) 1-12 months = <10g/dl
c) 1-12 years = <11g/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
263
Q

Give 3 causes of anaemia due to decreased production of RBC

A

a) Ineffective erythropoiesis
1. Iron/folic acid deficiency
2. Chronic inflammation –> JIA
3. Chronic renal failure
b) Red cell aplasia
4. Parvovirus B19 infection
5. Congenital
6. Fanconi anaemia
7. Aplastic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
264
Q

Give 3 causes of anaemia due to increased consumption of RBC

A

= Haemolysis

  1. Red cell membrane disorders –> hereditary spherocytosis
  2. Red cell enzyme disorders –> G6PD deficiency
  3. Haemoglobinopathies –> thalassaemia, sickle cell
  4. Immune –> haemolytic disease of the newborn, AI haemolytic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
265
Q

Give 3 causes of anaemia due to increased loss of RBC

A
  1. Bleeding
  2. Burns
  3. Splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
266
Q

Give 3 causes of microcytic anaemia

A
  1. Iron deficiency
  2. Thalassaemia
  3. Sideroblastic anaemia –> congenital or heavy metal poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
267
Q

Give 3 causes of normocytic anaemia

A
  1. Chronic inflammation = anaemia of chronic disease
  2. Acute bleed
  3. Renal failure
  4. Transient erhtyroblastocytopenia of childhood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
268
Q

Give 3 causes of macrocytic anaemia

A
  1. B12 deficiency
  2. Folate deficiency
  3. Hypothyroidism
  4. Bone marrow failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

What investigations would you do for someone with suspected anaemia?

A
  1. FBC and blood film
  2. Reticulocytes
  3. TSH
  4. B12, folate, ferritin
  5. LFTs –> bilirubin
  6. U&Es
  7. Hb electrophoresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
270
Q

What is the most common cause of anaemia in children?

A

Iron deficiency = microcytic, hypochromic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
271
Q

Give 3 causes of iron deficiency anaemia

A
  1. Poor intake –> particularly those who are breast fed, or high intake of cows milk, picky toddlers
  2. Malabsorption
  3. Blood loss
  4. Increased requirement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
272
Q

Give 3 signs of anaemia in children

A
  1. Pallor –> conjunctival, tongue, palmar creases
  2. Irritability
  3. Lethargy
  4. Tachycardia
  5. SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
273
Q

What is the treatment of iron deficiency anaemia?

A
  • Oral ferrous sulphate

- Increase iron in diet –> red meat, liver, kidney, oily fish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
274
Q

Describe the inheritance patten of hereditary spherocytosis

A

Autosomal dominant

- Mutations in genes for protein of red cell membrane (spectrum, ankyrin, band 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
275
Q

Give 3 possible symptoms of hereditary spherocytosis

A
  1. Jaundice
  2. Anaemia
  3. Splenomegaly
  4. Aplastic crisis
  5. Gallstones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
276
Q

How can hereditary spherocytosis be treated?

A
  • Oral Folic acid

- Splenectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
277
Q

Describe the inheritance pattern of G6PD deficiency

A

X linked recessive red cell enzymopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
278
Q

How can G6PD deficiency present?

A
  • Neonatal jaundice
  • Chronic non spherocytic haemolytic anaemia
  • Intermittent episodes fo intravascular haemolytic
  • Sporadic/acute haemolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
279
Q

How can acute haemolysis in G6PD deficiency be triggered?

A
  • Drugs –> antimalarials, quinolones, aspirin
  • Broad (fava) beans
  • Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
280
Q

What might you see on a blood film of someone with G6PD deficiency?

A

Bite cells and hemighosts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
281
Q

How is G6PD deficiency managed?

A
  • Education about acute haemolysis and precipitants to avoid
  • Transfusions and renal support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
282
Q

Describe the inheritance pattern of thalassaemia

A

Autosomal recessive

- Affects those from Indian subcontinent, Mediterranean and middle east most commonly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
283
Q

Give 3 signs of beta thalassaemia major

A
  1. Severe anaemia
  2. Jaundice
  3. Splenomegaly, hepatomegaly
  4. Failure to thrive/growth failure
  5. Bossing of skull, maxillary overgrowth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
284
Q

Describe the management of beta thalassaemia major

A
  1. Genetic counselling
  2. Regular blood transfusions
  3. Bone marrow transplant = cure
  4. Endocrine supplementation, fertility help, bone health
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
285
Q

What is a complications beta thalassaemia major?

A

Iron overload –> cardiac filature, cirrhosis, DM, infertility, growth failure
- Treatment = iron chelation = S/C deferoxamine or oral deferasirox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
286
Q

What is sickle cell disease?

A

Variant Hb chain = HbS

- Point mutation on codon 6 of the B globin gene causing glutamine to change to valine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
287
Q

Describe the inheritance pattern seen in sickle cell disease

A

Autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
288
Q

What RBC abnormalities occur in sickle cell?

A
  • Fragility
  • Prone to haemolysis
  • Occlusion of small vessels
  • Sickle shaped
  • Reduced lifespan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
289
Q

Name 3 consequences of sick cell disease

A
  1. Anaemia
  2. Infection
  3. Painful crises
  4. Stroke
  5. Acute chest syndrome –> pain, hypoxia, fever, +/- CXR signs
  6. Splenic sequestration = pooling of blood in spleen
  7. Aplastic crisis –> can be precipitated by parvovirus B19
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
290
Q

What is the affect of sickle cell disease on Hb and reticulocyte count?

A
  • Low Hb

- Raised reticulocyte count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
291
Q

Describe the treatment for sick cell disease

A
  • Avoid exposure to cold, dehydration, excessive exercise, stress, hypoxia
  • Prevention of crises and infection –> daily oral penicillin
  • Oral folic acid
  • Hydroxycarbamide (hydroxyurea) –> increased HbF
  • Transfusions
  • Stem cell transplant = cure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
292
Q

What is aplastic anaemia?

A

= bone marrow failure

Characterised by reduction or absence of all 3 main lineages in bone marrow leading to peripheral blood pancytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
293
Q

How does aplastic anaemia present?

A
  1. Anaemia = low RBC
  2. Infection = low WBC (especially neutrophils)
  3. Bruising and bleeding = thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
294
Q

Give 3 causes of bone marrow failure syndrome

A
  1. Congenital –> Fanconi’s anaemia
  2. Acquired aplasia anaemia
  3. Bone marrow infiltration –> leukaemia, lymphoma, neuroblastoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
295
Q

What are the 5 main components for homeostasis to work?

A
  1. Platelet –> number and function
  2. Coagulation factors
  3. Coagulation inhibitors
  4. Fibrinolysis
  5. Vascular integrity –> initiate and limit coagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
296
Q

What are the liver dependent clotting factors?

A

2, 7, 9 and 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
297
Q

Give 3 causes of thrombocytopenia due to decreased production of platelets

A
  1. Congenital thrombocytopenia
  2. Infiltration of bone marrow –> leukaemia, metastases, lymphoma
  3. Reduced platelet production by bone marrow –> low B12/folate, reduced TPO, medication (methotrexate, chemo), alcohol, infection, AI
  4. Dysfunctional production of platelets in BM –> myelodysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
298
Q

Give 3 causes of thrombocytopenia due to increased destruction of platelets

A
  1. Autoimmune –> ITP, SLE, primary/secondary
  2. Hypersplenism –> portal HTN, splenomegaly
  3. Drug related immune destruction –> heparin induced
  4. Consumption of platelets –> DIC, TTP, haemolytic uraemic syndrome, congenital heart disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
299
Q

What diagnosis would you suspect in a child with a single figure platelet count but is otherwise well?

A 
Immune Thrombocytopenia (ITP) 
- Normal blood film and clotting but very low platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
300
Q

Why does ITP occur?

A

Usually due to destruction of circulating platelets by anti platelet IgG autoantibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
301
Q

What can trigger acute ITP?

A

Viral infection –> occurs 1-2 weeks after

- Secondary ITP = malignancies (CLL), infection (HIV, hep C)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
302
Q

How do you manage ITP?

A

Majority are self limiting within 6-8 weeks

- Oral prednisolone, IV anti-d or IV IgG occasionally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
303
Q

What is disseminated intravascular coagulation (DIC)?

A

Coagulation pathway activation leading to diffuse fibrin deposition in the microvasculature and consumption of coagulation factors and platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
304
Q

Give 3 possible causes of DIC

A
  1. Severe sepsis or shock
  2. Extensive tissue damage –> trauma/burns
  3. Malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
305
Q

What would you see in the investigations of someone with DIC?

A
  • Prolonged prothrombin time and APTT
  • Low platelets
  • Low fibrinogen
  • High D dimers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
306
Q

How do you treat DIC?

A
  • Treat underlying condition
  • Platelet transfusion
  • Fresh frozen plasma –> contains clotting factors
  • Cryoprecipitate –> contains fibrinogen and some clotting factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
307
Q

Name 2 coagulopathies

A
  1. Haemophilia

2. Von Willebrand disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
308
Q

Describe the inheritance pattern seen in haemophilia

A

X linked recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
309
Q

Haemophilia A is due to a deficiency in which clotting factor?

A

Factor VIII (8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
310
Q

Haemophilia B is due to a deficiency in which clotting factor?

A

Factor IX (9)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
311
Q

Give 3 signs of haemophilia

A
  1. Easy bruise
  2. Haematomas
  3. Mouth bleeding
  4. Joint bleeds –> prophylaxis needs to be given to prevent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
312
Q

Give 2 possible complications fo treatment for haemophilia

A
  1. Inhibitors –> antibodies to factor 8 or 9 so reduce treatment effect
  2. Vascular access becomes more difficult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
313
Q

Briefly describe the pathophysiology behind Von Willebrand disease

A

Bleeding disorder due to an abnormality of vWF
vWF acts as an adhesive bridge between platelets and the damaged sub-endothelium
Without it takes longer for bleeding to stop –> defective platelet plug formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
314
Q

Describe the inheritance pattern seen in vWD

A

Autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
315
Q

Describe the treatment for vWD

A

No cure

  • Mild = DDAVO –> causes secretion of factor VIII and vWF into plasma
  • Severe = plasma derived factor VIII concentrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
316
Q

Give 3 signs of thrombocytopenia

A
  1. Petechial rash
  2. Bruising
  3. Bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
317
Q

What does a low reticulocyte count indicate?

A

A production problem –> infection, renal disease, drugs, marrow failure/infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
318
Q

What does a high reticulocyte count indicate?

A

A degradation problem –> bleeding, haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
319
Q

Give 5 determinants of growth

A
  1. Parental phenotype and genotype
  2. Pregnancy factors
  3. Nutrition
  4. Psychosocial deprivation
  5. Hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
320
Q

When is growth velocity fastest?

A

IN utero and in infancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
321
Q

When does growth end?

A

When the epiphyses fuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
322
Q

What is hypochondroplasia?

A

A developmental disorder resulting in short limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
323
Q

What is the main factor driving infant growth?

A

Nutrition

324
Q

Give 5 differentials for short stature

A
  1. Constitutional delay
  2. Slow maturation
  3. Delayed puberty
  4. Idiopathic
  5. Environmental –> psychosocial
  6. Nutrition
  7. Skeletal disease
  8. Physical disease –> coeliac, IBD, CHD
  9. Turner syndrome
  10. Endocrine pathology
325
Q

What can cause an increased final height?

A
  1. Androgen/oestrogen excess
  2. GH excess
  3. Marfan’s
  4. Kleinfelters
326
Q

Name the scale that is used to describe physical development based on external sex characteristics

A

Tanner scale

327
Q

Define thelarche

A

Breast development

328
Q

Define adrenarche

A

Maturation of the adrenal gland –> androgen production –> body odour and mild acne

329
Q

Define pubarche

A

Growth of pubic hair

330
Q

What is the first sign of puberty in boys?

A

First ejaculation and testicular size >3ml

331
Q

Define delayed puberty

A

The absence of secondary sexual characteristics by 14 in females or 16 in males
= Hypogonadism

332
Q

What is the most likely cause fo delayed puberty in boys?

A

Constitutional delay –> runs in the family

333
Q

What must you rule out as a cause of delayed puberty in girls?

A

Turner syndrome (45XO)

334
Q

What is primary gonadal failure?

A

Hypergonadotrophic hypogonadism

335
Q

What is the affect of hypergonadotrophic hypogonadism on

a) FSH/LH
b) Oestrogen/Testosterone?

A

= High basal and stimulated gonadotrophin levels

a) High LH, FSH and GnRH
b) Low testosterone/oestrogen

336
Q

Give 4 causes of primary gonadal failure

A
  1. Chromosomal disorders –> turners, Klinefelter’s
  2. Gonadal dysgenesis
  3. Disorders of steroid biosynthesis –> CSH
  4. Chemotherapy or gonadal radiotherapy
  5. Gonadal infection –> mumps orchitis
  6. Gonadal trauma/torsion
337
Q

What is secondary and tertiary hypogonadism?

A

Hypogonadotrophic hypogonadism

338
Q

What is the affect of hypogonadotrophic hypogonadism on

a) FSH/LH
b) Oestrogen/Testosterone?

A

= Low/undetectable basal and stimulated gonadotrophin levels

a) low GnRH, LH and FSH
b) high testosterone/oestrogen

339
Q

Give 3 causes of secondary/tertiary hypogonadism

A
  1. Kallman’s syndrome
  2. Congenital hypopituitarism
  3. Syndromic associations –> Prader-WIlli
  4. Intracranial tumours
  5. Cranial irradiation
  6. TBI
  7. Anorexia, excessive exercise
340
Q

How might you investigate delayed puberty?

A
  • FBC
  • U&Es
  • TFTs
  • LH/FSH
  • Karyotyping
341
Q

How do you manage delayed puberty?

A
  • Constitutional delay = short course of sex steroid therapy
  • Permanent gonadotrophin deficiency or gonadal failure = long term sex steroids gradually increasing over 2-3 years –> IM testosterone (boys), oral ethinylestradiol + progesterone (girls)
342
Q

Give 3 potential consequences of delayed puberty

A
  1. Psychological problems
  2. Reproduction defects
  3. Reduced bone mass
343
Q

What is Turners syndrome?

A

45 XO

= Hypergonadotrophic hypogonadism

344
Q

Give 5 signs of Turner Syndrome

A
  1. Delayed puberty
  2. Short stature
  3. Recurrent otits media
  4. Webbed neck
  5. CV and renal malformations
  6. Low posterior hairline
  7. Widely spaced nipples
  8. Ovarian dysgenesis resulting in infertility
345
Q

How do you treat Turner Syndrome?

A
  • Growth hormone therapy
  • Oestrogen replacement for development of secondary sexual characteristics at the time of puberty (infertility will persist)
346
Q

What is Klinefelter’s Syndrome?

A 
47 XXY 
Primary hypogonadism (hypergonadotrophic hypogonadism)
347
Q

Give 3 signs of Klinefelter Syndrome

A
  1. Azoospermia = infertility, no sperm
  2. Gynaecomastia
  3. Testicular size <5ml
  4. Reduces pubic hai
  5. Tall stature
348
Q

What is Kallman syndrome?

A

There is a congenital deficiency of GnRH meaning the pituitary isn’t stimulated to release FSH and LH this leads to secondary gonadal failure

349
Q

What inheritance pattern is seen in Kallman Syndrome?

A

X linked recessive or dominant

350
Q

75% of people with which syndrome may have anosmia?

A

Kallman Syndrome

351
Q

Define precocious puberty

A

The onset of secondary sexual characteristics before 8 (in girls) or 9 (in boys)

352
Q

What must you rule out as a cause of precocious puberty in boys?

A

Brain tumour

353
Q

What is True precious puberty?

A

Central precocious puberty = gonadotrophin dependent

- Increase in GnRH

354
Q

Give 3 causes of true precocious puberty

A
  1. Idiopathic (most often girls)
  2. Intracranial tumours –> astrocyroma, craniopharyngioma
  3. Other CNS lesions –> hydrocephalus, arachnoid cyst, TBI
  4. Secondary central PP = early maturation of HPG axis –> CAH
355
Q

What is precocious pseudopuberty?

A

Peripheral precocious puberty = gonadotrophin independent

- Secondary sexual characteristics but no central activation of gonads

356
Q

Give 2 causes of precocious pseudopuberty

A
  1. Gonadal –> McCune-Albright syndrome, Ovarian tumour, testicular tumour
  2. Adrenal –> CAH, tumour
  3. HCG secreting tumour
  4. Itraogenic –> exogenous sex steroid administration
357
Q

What investigations might you do in someone who present with precocious puberty?

A
  • Examination –> Tanner scale, height/weight, growth records, parents heights, abdominal/testicular/neuro exam
  • Plasma LH and FSH
  • Plasma sex hormones –> oestrogen, testosterone
  • Other serum androgens –> 17-OH progesterone, DHEAS, androstenedione
  • Urine steroid profile
  • GnRH test
  • Imaging = Bone age XR, pelvic US, abdo US, MRI brain
358
Q

How would you treat precocious puberty?

A

GnRH analogues to suppress pulsatility of GnRH secretion –> SC or IM every 3 months

359
Q

What is Androgen Insensitivity Syndrome?

A

46XY

  • Occurs due to defects in the androgen receptor and results in a spectrum of under virilisied phenotypes
  • Complete = deletion of gene –> completely female phenotype
  • Partial = wide spectrum of phenotypic expression
360
Q

Name the test that can pick up congenital hypothyroidism

A

Guthrie test (heel prick, newborn screening blood spot)

361
Q

What is the most common cause of hypothyroidism

a) Worldwide
b) In the UK
c) In a consanguineous pedigree?

A

a) Worldwide = Iodine deficiency
b) In the UK = Thyroid dysgenesis (maldescent of thyroid, athyrosis)
c) In a consanguineous pedigree = Dyshormonogenesis (inborn error of thyroid hormone synthesis)

362
Q

Give 4 signs of congenital hypothyroidism

A
  1. Feeding probelms and failure to thrive
  2. Prolonged jaundice
  3. Cold and mottled skin
  4. Hoarse cry
  5. Hypotonia
  6. Constipation
  7. Low temperature
  8. Large fontanelle, broadened and flattened nose
  9. Goitre
363
Q

What is the treatment for a baby with congenital hypothyroidism?

A

Levothyroxine starting at 2-3 weeks of age

- Neonatal dose = 10-15 mag/kg OD

364
Q

What is a complication of untreated congenital hypothyroidism?

A

Congenital iodine deficiency syndrome/cretinism = severely stunted physical and mental growth
- Delayed mental development, learning difficulties, poor coordination

365
Q

A 10-day-old baby presents with collapse and shock. They have low sodium, high potassium and are found to be in metabolic acidosis, what is the most likely diagnosis?

A

Congenital adrenal hyperplasia

- The baby is having a salt-losing adrenal crisis

366
Q

What is Congenital Adrenal Hyperplasia (CAH)?

A

An autosomal recessive disease that is more common cause of insufficient cortisol and mineralocorticoid secretion
- Most often due to absence of enzyme 21-hydroxylase

367
Q

How may CAH presetn?

A
  1. Mineralocorticoid deficiency = renal salt wasting –> severe dehydration
  2. Glucocorticoid deficiency = adrenal crisis with hypoglycaemia and hypotension in setting of an intercurrent illness or physiological stress
  3. Females = ambiguous genitalia –> clitomegaly, degree of labia fusion, position of urethra/urogenital sinus
  4. Males = salt loss (80%) or tall stature and precocious puberty (20%)
368
Q

How can CAH be diagnosed biochemically?

A
  • Raised levels of 17-alpha-hydroxy-progesterone
  • Low serum Na
  • High serum K+
  • Metabolic acidosis
  • Hypoglycaemia
369
Q

Why might someone with CAH have low sodium and high potassium?

A

They are unable to produce aldosterone

370
Q

Describe the treatment for CAH

A
  • Immediate = Fluid, IV/IM hydrocortisone, glucose
  • Lifelong hydrocortisone and fludrocortisone
  • Monitor growth, skeletal maturity, plasma androgens and 17a hydroxyprogesterone
371
Q

What is a complication of CAH?

A

Adrenal crisis = urgent treatment with IV saline, glucose and hydrocortisone

372
Q

What would you expect the fasting plasma glucose level to be in the following

a) Diabetes
b) Impaired glucose tolerance
c) Euglycaemia?

A

a) Diabetes = >7 mmol/l
b) Impaired glucose tolerance = 5.7-7 mmol/l
c) Euglycaemia = 3.5-5.6 mmol/l

373
Q

What would you expect the post OGTT plasma glucose level to be in the following

a) Diabetes
b) Impaired glucose tolerance?

A

a) Diabetes = >11.1 mmol/l

b) Impaired glucose tolerance = 7.8-11 mmol/l

374
Q

What would you expect the HbA1c (%) to be in the following

a) Diabetes
b) Impaired glucose tolerance
c) Euglycaemia?

A

a) Diabetes = >6.5%
b) Impaired glucose tolerance = 5.7-6.4%
c) Euglycaemia = 4-5.6%

375
Q

Name 2 genes that have been identified inc asking T1DM

A
  1. HLADR3

2. HLADR4

376
Q

Briefly describe the pathophysiology of T1DM

A

AI destruction of pancreatic B cells so absence of insulin –> Insulin deficiency –> glycogenolysis, gluconeogenesis, ketogenesis –> increased ketone and glucose production –> vomiting, osmotic diuresis, acidosis –> fluid and electrolyte depletion –> cellular dysfunction, cerebral oedema, shock

377
Q

Give 3 symptoms fo T1DM

A
  1. Wight loss
  2. Polydipsia
  3. Polyuria
  4. Lethargic
  5. Skin infections
378
Q

How do you treat T1DM?

A

Insulin therapy
Carb counting
Lifestyle advice –> sex, drugs, alcohol, contraception, driving
Diet –> reduced refined carbs, no more than 30% fat
Education –> exercise, sick day rules, blood glucose monitoring, hypoglycaemia recognition

379
Q

What do you need to monitor in DM?

A
  1. Hba1c
  2. Retinopathy –> eye test every year
  3. Neuropathy –> foot checks
  4. Nephrophathy –> bloods, urine
  5. BP checks
  6. Annual bloods
380
Q

Briefly describe the pathophysiology behind DKA

A

No insulin –> lipolysis –> FFA’s –> oxidised in liver -> ketone bodies –> ketoacidosis
Glucose is not metabolised or stored so the body goes into a ‘starvation state’

381
Q

What is DKA characterised by?

A
  1. Acidosis, pH <7.3
  2. Raised ketones >3
  3. Hyperglycaemia >11.1 random
382
Q

Give 3 symptoms of DKA

A
  1. Unwell
  2. Lethargic
  3. Nausea
  4. Vomiting
  5. Abdominal pain
  6. Dehydration
383
Q

Give 3 signs of DKA

A
  1. Kassmaul breathing
  2. Subcostal and intercostal recessions
  3. tachycardia
  4. Hypotension
  5. Dry mucous membranes
  6. Ketotic breath
384
Q

Describe the management of DKA

A
  1. Fluid resuscitation = 0.9% NACl –> corrected gradually over 48 hours
  2. Insulin infusion
  3. Potassium replacement and cardiac monitoring
385
Q

Why is important to correct fluid balance slowing over 48 hours in someone with DKA?

A

Rapid fluid resuscitation can lead to cerebral oedema

386
Q

Give 3 possible complications of DKA

A
  1. Cerebral oedema
  2. Shock
  3. Hypokalaemia –> arrhythmias
  4. Aspiration
  5. Thrombus
387
Q

Define hypoglycaemia

A

Someone with blood glucose <4 mmol/L in diabetes

388
Q

Give 5 hypoglycaemic symptoms

A 
Autonomic symptoms 
1. Irritable
2. Hungry 
3. Nauseous 
4. Shakey 
5. Anxious 
6. Sweaty 
7. Pallor  
Neuroglycopenic symptoms
8. Dizzy
9. Headache
10. Confused
11. Slurred speech 
12. Hearing or visual problems
389
Q

Define a Tic

A

Sudden twitches, movements or sounds that people do repeatedly, they are involuntary

390
Q

Define a stereotypies

A

Repetitive rhythmic movements or sounds –> body rocking, head nodding, finger tapping, arm/hand flapping, waving, pacing

391
Q

Give 3 red flag symptoms of a headache being a SOL

A
  1. Worse lying down, with cough or straining
  2. Wakes up child
  3. Associated confusion and/or morning or persistent N+V
  4. Change in personality., behaviour or educational performance
392
Q

Give 3 red flag physical signs that may suggest a SOL

A
  1. Growth failure
  2. Visual field defects
  3. Squint
  4. Cranial nerve abnormality
  5. Torticollis
  6. Abnormal coordination or gait
  7. Papilloedema
  8. Bradycardia
  9. Cranial bruits
393
Q

Give 2 examples of primary headaches

A
  1. Migraine
  2. Tension
  3. Cluster
  4. Other –> cough, extertional headache
394
Q

Give 2 examples of a secondary headaches

A
  1. Raised ICP
  2. Space occupying lesion
  3. Trauma
  4. Infection
395
Q

Briefly describe tension headaches

A

Symmetrical, gradual onset, tightness/band/pressure

396
Q

Briefly describe migraine without aura

A

1-72 hours, bilateral, pulsatile over temporal or frontal area, GI disturbances, photophobia or phonophobia

397
Q

Briefly describe migraine with aura

A

Migraine preceded by visual, sensory or motor aura

398
Q

What is cerebral palsy?

A

An umbrella term covering a group of motor impairments syndrome secondary to non-progressive lesions or anomalies in the brain arising in the early stages of development
- Chronic disorder of movement and/or posture that present early (before 2y/o) and continues throughout life

399
Q

Give 3 causes of cerebral palsy

A
  1. 80% antenatal –> hypoxia, congenital infection, haemorrhage, ischaemia, genetic syndrome/structural maldevelopment
  2. 10% peri-natal –> hypoxia, infection, haemorrhage
  3. 10% postnatal –> hypoxia, infection (meningitis, encephalitis), haemorrhage, encephalopathy, trauma, hydrocephalus, hyperbilirubinaemia
400
Q

How does cerebral palsy often present?

A
  • Abnormal limb/trunk posture and tone in infancy with delayed motor milestone
  • Feeding difficulties
  • Abnormal gait once walking is achieved
  • Asymmetric hand function before 12 months
  • Primitive reflexes may persist
401
Q

Cerebral palsy is characterised according to neurological features, what are the categories?

A
  1. Spastic –> hemiplegic, quadriplegic, diplegia
  2. Dyskinetic
  3. Ataxic
402
Q

Briefly describe spastic cerebral palsy

A

Damage to UMN pathway –> increased spasticity with associated brisk tendon reflexes and extensor plantar responses

  • Clasp knife phenomenon
  • Ankle plantar flexion
  • Limited adduction and internal rotation of hip flexion
  • Wrist flexed and pronated
  • Shoulder adducted
  • Bulbar muscle may be spastic (dysphagia, dribbling)
403
Q

Briefly describe the 3 types of spastic cerebral palsy

A
  1. Hemiplegic –> Unilateral involvement of arm and leg, arm more affected than leg with face spared (causes = neonatal stroke)
  2. Quadriplegic –> all 4 limbs affected, trunk involved, poor head control, low central tone, seizures, microcephaly, intellectual impairment (causes = hypoxic-ischaemic encephalopathy)
  3. Diplegia –> all 4 limbs, legs affected more than arms (cause = periventricular brain damage with preterm birth)
404
Q

Briefly describe dyskinetic cerebral palsy

A
  • Muscle tone variable and primitive motor reflex patterns predominate, chorea, athetosis, dystonia
  • Intellect may be relatively unimpaired
  • Present with floppiness, poor trunk control and delayed motor development in infancy
  • Causes = hypoxic-ischaemic encephalopathy, hyperbilirubinaemia (due to rhesus disease of newborn)
405
Q

Briefly describe ataxic cerebral palsy

A
  • Early trunk and limb hypotonia, poor balance, delayed motor development
  • Incoordinate movement, intention tremor and taxis gait = later signs
  • Causes = genetic, acquired brain injury
406
Q

Why might the clinical signs of cerebral plays change over time?

A

As brain matures but the underlying aetiology is not progressive

407
Q

How might you investigate a child who is presenting with signs of cerebral palsy?

A
  1. US scan and MRI brain
  2. Genetic testing
  3. TORCH screen
  4. Metabolic tests
  5. Neurophysiological tests
  6. Histopathology
408
Q

What drug can be used to treat hypertonia in children with cerebral palsy?

A

Botox for muscle spasticity

409
Q

Describe the support that is offered to someone with cerebral palsy

A
  1. Physiotherapists –> mobility and hand function
  2. SALT –> communication
  3. Feeding support
  4. Sleeping support
    Holistic, child focussed and with an MDT approach
410
Q

Define seizure

A

Sudden disturbance of neurological function caused be an abnormal or excessive neuronal discharge
- Epileptic or non-epileptic

411
Q

Define epileptic seizure

A

Excessive, unsynchronised neuronal discharges in the brain cause paroxysmal changes in behaviour, sensation or cognitive processes

412
Q

Give 3 possible causes of epileptic seizures

A
  1. Idiopathic (70-80%)
  2. Secondary –> cerebral dysgeneis/malformation, vascular occlusion, damage (congenital infection, hypoxic-ischaemic encephalopathy, haemorrhage)
  3. Cerebral tumour
  4. Neurodegenerative disorder
  5. Neurocutaneous syndrome
  6. Congenital –> NF, TORCH, tuberous sclerosis
413
Q

Give 3 possible causes of non epileptic seizures

A
  1. Febrile seizures
  2. Metabolic –> hypoglycaemia, hypocalcaemia, hypomagnzsia, hypo/hypernatraemia
  3. Head trauma
  4. Meningitis/encephalitis
  5. Poisons/toxins
414
Q

What are febrile seizures?

A

An epileptic seizures accompanied by a fever in the absence of intracranial infection due to bacterial meningitis or viral encephalitis
= Brief generalised tonic-clonic seizure

415
Q

What is the prognosis if febrile seizures?

A
  • 30-40% further febrile seizures
  • Simple = no effect on intellectual performance or risk of developing epilepsy
  • Complex (focal, prolonged, repeated in same illness) = 4-12% risk of subsequent epilepsy
416
Q

What is a neonatal seizure?

A

Typically repetitive, rhythmic (clonic) movements of the limbs which persist despite restraint and are often accompanied by eye movements and changes in respiration

417
Q

Name 3 possible causes of neonatal seizures

A
  1. Hypoxic-ischaemic encephalopathy
  2. Cerebral infarction
  3. Septicaemia/meningitis
  4. Metabolic –> hypoglycaemia, hypo/hypernatraemia
  5. Intracranial haemorrhage
  6. Cerebral malformations
  7. Drug withdrawal
  8. Congenitaal infection
  9. Kernicterus
418
Q

How long do epileptic seizures tend to last for?

A

30-120 seconds

419
Q

Give 3 signs of epileptic seizures

A
  1. Movement
  2. Tongue biting
  3. Head turning
  4. Muscle pain
420
Q

What is a generalised seizure?

A

Discharge arises from both hemispheres

LOC, no warning, symmetrical, bilateral seizure discharge on EEG or varying asymmetry

421
Q

Give 3 examples of generalised seizures

A
  1. Absence
  2. Myoclonic
  3. Tonic
  4. Generalised tonic clonic
  5. Atonic
422
Q

What are absence seizures?

A

Seizures where there is a transient loss of consciousness with an abrupt onset and termination
Momentary unresponsiveness with motor arrest
Last <30s, usually <10s
Developmentally normal but can interfere with school

423
Q

What can absence seizures evolve into?

A

Juvenile myoclonic epilepsy (JME)

424
Q

How might you investigates suspected absence seizures?

A

EEG = 3Hz spike and wave

Observe episode = hyperventilation, ask child to blow on windmill

425
Q

What medications can be given to treat absence seizures?

A

Ethosuxamide or Sodium Valporate –> Lamotrigine

426
Q

What would you expect to see in a myoclonic seizure?

A

Isolated muscle jerking

- Brief, often repetitive, jerking movements of the limbs, neck or trunk

427
Q

What would you expect to see in a tonic seizure?

A

Generalised increase in tone

428
Q

What would you expect to see in a atonic seizure?

A

Transient sudden loss of muscle tone

429
Q

What would you expect to see in a generalised tonic-clonic seizure?

A

Sudden onset rigid phase followed by a convulsion in which the muscle jerk rhythmically
- Other symptoms = LOC, tongue biting, urine incontinence

430
Q

What AED is offered to those suffering from generalised seizures?

A

Sodium valproate –> lamotrigine –> carbamazepine

431
Q

What is a focal seizure?

A

Seizure that arises from one part of 1 hemisphere +/- LOC +/- aura

432
Q

What might you see in a frontal focal seizure?

A

Involves motor and premotor cortex

  • Clonic movements –> Jacksonian March, Todds palsy
  • Asymmetrical tonic seizures
  • Atonic seizures
433
Q

What might you see in a temporal focal seizure?

A

= most common

  • Aura/warning signs = smell, taste abnormalities, distortions of shape/sounds
  • Automatism = lip smacking, chewing, fumbling
  • Deja vu, jamais vu
  • Emotional disturbance –> terror, panic, anger, elation
434
Q

What might you see in a occipital focal seizure?

A

Visual phenomena –> spot, line, flashes

435
Q

What might you see in a parietal focal seizure?

A

Sensory disturbances –> tingling, numbness

436
Q

What AED is offered to those suffering from focal seizures?

A

Carbamazepine –> lamotrigine –> sodium valproate

437
Q

What are the signs of juvenile myoclonic epilepsy?

A

Clumsiness (myoclonic seizures) and GTCS that occur shortly after waking and are often provoked by sleep deprivation
- Onset in 2nd decade

438
Q

What is West syndrome?

A

Infantile spasms

  • 4 to 6 months
  • Violent flexor spasm of head, trunk and limbs by extension of the arms
  • Lasts 1-2 s, often multiple bursts of 20-30s, often on waking
  • EEG = hypsarrhythmia
  • Treatment = vigabatrin or corticosteroids
  • Prognosis = most lose skills, develop learning disability or epilepsy
439
Q

What investigations might you do in someone presenting with seizures?

A
  1. Eye witness accounts/viedo
  2. ECG
  3. EEG
  4. MRI or CT –> identify possible causes
  5. Functional –> PET, SPECT
440
Q

Why must you do an ECG in those suffering from seizures?

A

To check for arrhythmia as the causes –> long QT syndrome

441
Q

What surgery can be done to treat epilepsy?

A
  • Vagal nerve stimulation
  • Resection fo affected area
  • Hemispherectomy
442
Q

Give 2 possible side effects of Ethosuximide

A
  • Drowsiness
  • N+V
  • Rash
  • Headaches
443
Q

Give 2 possible side effects of Sodium Valproate

A
  1. Appetite increases –> increase in weight
  2. Liver failure –> monitor LFTs over 1st 6months
  3. Pancreatitis
  4. Reversible hair loss
  5. Oedema
  6. Ataxia
  7. Teratogenicity, Tremor, Thrombocytopaenia
  8. Encephalopathy –> due to increased ammonia
444
Q

Give 2 possible side effects of Lamotrigine

A
  1. Skin rash
  2. Diplopia, blurred vision
  3. Levels affected by enzyme inhibitors/inducers
445
Q

Give 2 possible side effects of Carbamazepine

A
  1. Rash
  2. Neutropenia
  3. Hyponatraemia
  4. Ataxia
  5. Liver enzyme induction
446
Q

What is status epilepticus?

A

Seizure lasting 5 minutes or repeated seizures for 30 minutes without recovery of consciousness

447
Q

Describe the treatment for status epilepticus

A
  • ABCDE
  • 5 mins: Benzodiazepine e.g. IV lorazepam
  • 10mins later: Further benzodiazepine
  • Prepare PR paraldehyde
  • Prepare phenytoin
  • Call for senior support
  • 10mins later: IV phenytoin
448
Q

How long do non-epileptic seizures tend to last for?

A

1-20 minutes

- Very pale –> falls to floor –> hypoxia may induce brief generalised tonic-clonic seizure –> rapid recovery

449
Q

Give 3 signs of non-epileptic seizures

A
  1. Eyes closed
  2. Talking/crying
  3. Pelvic thrusting
450
Q

Name 3 conditions that are commonly diagnosed as being epilepsy?

A
  1. Sandifer syndrome
  2. Bengin neonatal slöe myoclonus
  3. Syncope
451
Q

What is syncope?

A

Insufficient blood or O2 supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes
- Clonic movements can occur

452
Q

What non neurological disease is Sandifer Syndrome associated with?

A

GORD

- Patients present with GORD and a characteristic neck movement disorder

453
Q

Name 3 possible causes of Paroxysmal disorders

A
  1. Breath holding attack = Cries –> holds breath –> goes blue –> goes limp –> sometimes LOC –> rapid spontaneous recovery
  2. reflex anoxic (non-epileptic) seizures
  3. Syncope
  4. Migraine
  5. Benign paroxysmal vertigo
  6. Cardiac arrhythmia
  7. Pseudoseizures
  8. Tics
454
Q

What are the 2 main types of Strabismus?

A
  1. Manifest = esotropia, exotropia, hypertropia, hypotropia

2. Latent = esophoria, exophoria, hyperphoria, hypophoria

455
Q

Name and briefly describe the types of manifest strabismus?

A
  1. Esotropia/convergent = one eye straight ahead, one eye turned inwards towards nose
  2. Exotropia/divergent = one eye straight ahead, one eye turning outwards
  3. Hypertropia = deviating eye is pointing upwards
  4. Hypotropia = deviating eye is pointing downwards
456
Q

Name and briefly describe the types of latent strabismus?

A

When eyes are straight when both eyes are open, but a deviation of the visual axes can be elicited when each eye is covered

  1. Esophoria = tendency for eye to turn inwards under the cover
  2. Exophoria = tendency for eye to turn outwards under the cover
  3. Hyperphoria = tendency for eye to deviate upwards under the cover
  4. Hypophoria = tendency for eye to deviate downwards under the cover
457
Q

Describe the aetiology of strabismus

A
  1. Multifactorial –> hereditary and refractive error (need glasses)
  2. Unknown cause
  3. Secondary to loss o vision
  4. Cerebral palsy
  5. Febrile illness can trigger it
  6. Primary neurological aetiology (SOL) = rare –> brain tumour, stroke
458
Q

What is more concerning a paralytic squint or a non paralytic squint?

A

Paralytic squints = SOL so never correct

  • Non paralytic = malalignment usually, can be corrected
459
Q

Name 2 ways in which strabismus can be investigates?

A
  1. Cover test = will determine presence and direction –> Eye that is covered is the one that turns and then when cover removed eyes swap
  2. Corneal reflections –> Shinning pen torch into eye to see corneal reflections = reflections in different positions in the 2 eyes
    - It is important to assess visual acuity too
460
Q

What type of squint may require neurological-imaging?

A

Paralytic squints –> as may be due to SOL (Brain tumour)

461
Q

What does the management of strabismus aim to achieve?

A
  1. To restore comfortable binocular single vision
  2. To achieve/restore good alignment of the 2 eyes
  3. To eliminate diplopia
462
Q

Give 3 conservative management techniques for strabismus

A
  1. Glasses
  2. Prism for diplopia
  3. Orthoptic exercises
  4. Eye patch –> over the good eye
463
Q

Give 2 other management techniques for strabismus

A
  1. Surgery

2. Botox

464
Q

Define ambylopia

A

Defective visual acuity which persists after correction of the refractive error and removal of any pathology

465
Q

Describe the treatment for ambylopia

A
  1. Refractive adaptation = wear appropriate glasses for 16 weeks
  2. Occlusion of better seeing eye
  3. Atropine drops in better eye
466
Q

Describe the epidemiology of ADHD

A

5% school aged children

M:F = 4:1 (1:1 into adulthood)

467
Q

Describe the aetiology of ADHD

A
  • Genetic and environmental
  • Neuroanatomical and neurochemical factors too
  • CNS insults –> Fetal alcohol syndrome, premature, NF, LBW
468
Q

What are the 3 core behaviours of ADHD?

A
  1. Hyperactivity
  2. Inattention
  3. Impulsivity
469
Q

Give 3 signs of hyperactivity in ADHD

A
  1. Squirms and fidgets
  2. Cannot remain seated
  3. Talks excessively
  4. Noisy
  5. Girls = often small things –> giggling, hair twisting, talk too much, overreacting
470
Q

Give 3 signs of inattention in ADHD

A
  1. Easily distracted
  2. Not listening
  3. Mind wandering
  4. Struggling at school
  5. Forgetful
  6. Organisational problems
  7. Difficulty sustaining attention
  8. Loses important items
  9. Makes careless mistakes
471
Q

Give 3 signs of impulsivity in ADHD

A
  1. Blurts out answers
  2. Difficulty waiting turns
  3. Interrupts
  4. When older = alcohol, drugs, car accidents, pregnancy
472
Q

What is the diagnostic criteria for ADHD?

A

6/9 inattentive symptoms and 6/9 hyperactivity/impulsivity symptoms

  • Present before 12 years and occur in >1 place and in a primary setting
  • Clear evidence that symptoms interfere with social/academic function
473
Q

How does ADHD typically present in primary school age children (6-12 y/o)?

A
  • Hyperactivity most often seen
  • Distractibility
  • Motor restlessness
  • Impulsive and disruptive behaviour
  • Associated = learning disorders, low self-esteem, repetition of classes
474
Q

How does ADHD typically present in adolescent age children (13-17 y/o)?

A
  • Difficulty in planning and organisation
  • Persistent inattention
  • Reduction of motor restlessness
  • Associated = aggressive, antisocial behaviour, alcohol/drug problems, emotional problems, accidents
475
Q

What tools can be used in order to diagnose ADHD?

A
  1. Clinical interview = any RFs –> pregnancy, birth, development, social Hx
  2. ADHD nurse classroom observation
  3. Questionnaires (SNAP)
  4. Quantitative behavioural analysis
476
Q

Describe the treatment for ADHD

A
  1. Education
  2. Parenting programmes and school support
  3. Medications –> stimulant medications and non-stimulant medications or combined
477
Q

Give an examples of a stimulant medications

A

Increase amounts of dopamine released in the brain
Methylpenidate
- Short acting = Ritalin
- Long acting = Delmosart
SE = HTN, loss of appetite, psychiatric symptoms

478
Q

Give an examples of a non-stimulant medications

A

Reduce breakdown of norepinephrine in the brain
Atomoxetine (SNRI)
Guanfacine

479
Q

Describe the epidemiology of ASD

A

1% prevalence

Boys > girls

480
Q

Give 4 signs of ASD

A
  1. Communication problems
  2. Social interaction difficulties
  3. Social imagination difficulties
  4. Sensory issues
481
Q

What communication problems might a child with ASD show?

A
  • Lack of desire to communicate at all
  • Communicating needs only
  • Disordered or delayed language
  • Repeats speech/echolalia
  • No understanding of jokes, very literal
  • Poor non verbal communication –> gesture, body language
482
Q

What social interaction problems might a child with ASD show?

A
  • Struggles to understand social roles
  • Often no desire to interact with others
  • Touches inappropriately, plays alone, poor eye contact, finds it hard to take turns
  • No understanding of unspoken social rules
483
Q

What social imagination problems might a child with ASD show?

A
  • Struggles with change
  • Obsessions/rituals
  • Repetitive with play
  • Unable to play or write imaginatively
484
Q

Describe the treatment for ASD

A
  • Education and games to encourage social communication
  • Visual aids and timetables
  • Parenting workshops and school liaison
    No medications available
485
Q

When can strawberry marks/haemangiomas be dangerous?

A

Usually self limiting but beware over eye, in airway

  • Limit ability of eye to develop
  • Can use BB to treat them –> only when justified not for cosmetic reasons
486
Q

What condition are cafe au last patches associated with?

A

Neurofibromatosis

487
Q

What is chicken pox caused by?

A

Varicella zoster virus

488
Q

How does chicken pox present?

A

High contagious rash and fever

  • 200–500 lesions start on head and trunk, progress to peripheries
  • Appear as crops of papules, vesicles with surrounding erythema and pustules at different times for up to 1 week
489
Q

What is the treatment for chicken pox?

A

Usually self limiting
Treatment = symptomatic
Severe or immunocompromised = IV acyclovir

490
Q

Give 2 possible complications of chicken pox

A
  1. Secondary bacterial infection with staph or group A strep –> TTS, necrotising fasciitis
  2. Encephalitis
  3. Purpura fulminans
491
Q

What happens if chicken pox is reactivated?

A

Shingles (herpes zoster) = widespread itchy apolar rash in dermatomal distribution

492
Q

How does measles present?

A

Prodromal CCCK = cough, coryza, conjunctivitis, Koplik spots
- Fever, coryza and non itchy maculopapular rash

493
Q

What is Slapped Cheek Syndrome?

A

= fifth disease, parvovirus B19

  • Viral infection common in children 6-10
  • Self limiting 1-3 weeks
  • Usually asymptomatic or erythema infectiosum (viraemic phase followed by distinctive bright red rash to develop on both cheeks), once rash appears infection no longer contagious
494
Q

What is hand, foot and mouth caused by?

A

Coxsackie or enterovirus 71

495
Q

How does mumps present?

A
  • Incubation period is 15-24 days and infectivity up to 7 days after onset of parotid swelling
  • Onset = fever, malaise, parotitis
  • Only one side swollen initially –> bilateral over a few days
    Usually self limiting
496
Q

Give 2 possible complications of mumps

A
  1. Boys become infertile

2. Hearing loss

497
Q

Describe Molluscum contagiosum?

A

= Common pox viral infection

  • Pink umbilicate papules, presenting as clusters of small round papules
  • Exacerbated by active eczema or topical steroids
  • Common in children –> warm, overcrowded environment
  • Self limiting within a year
498
Q

Describe Impetigo

A

Causes by staph aureus or strep, localised and very contagious

  • Superficial rapidly spreading initially clear blisters that develop into straw-coloured dirty looking lesions with yellow crusting
  • Topical treatment (mupirocin), oral Abx if severe
499
Q

What is scaled skin/red man syndrome

A

Exotoxin mediated epidermolysis secondary to Staph aureus infection (reaction to staph toxin)

  • Extensive tender erythema with flaccid superficial blisters/bullae
  • Erosions and +ve Nikolsky sign
  • Crusting around eyes, mouth and fever
  • Treatment = IV anti-staph Abx
500
Q

What is scarlet fever?

A

Reaction to strep toxin

- Highly contagious bacterial infection affecting children between 2-8 years

501
Q

How does scarlet fever present?

A

Prodrome = fever, committing, abdominal pain
Exanthematous phase = fine red rash (feels like sandpaper) in neck and chest spreading to flexors, strawberry tongue, anterior cervical lymphadenopathy

502
Q

How is scarlet fever treated?

A

Penicillin V for 10 days

503
Q

3-year-old, 7-day history of high fevers. Now developed red eyes, a rash, sore mouth and throat. Miserable and unwell with a diffuse maculopapular rash on his torso. He has bilateral injected conjunctiva, red cracked lips and a strawberry tongue. 3x2cm cervical swelling and swollen reddened palms.
Give 3 differentials

A
  1. Kawasaki disease
  2. Scarlet fever
  3. Shingles/chickenpox
  4. Measles - ask about immunisation history
504
Q

What is Kawasaki disease?

A

Multi-system disease characterised by systemic vasculitis

505
Q

What is the diagnostic criteria for Kawasaki disease?

A 
Fever for >5 days
AND not explained by another disease 
AND 4/5 of the following: 
- Conjunctivitis (bilateral)
- Cracked lips/strawberry tongue
- Cervical lymphadenopathy
- Rash
- Swollen and red extremities
506
Q

What mighty see on the blood results in a patient with Kawasaki disease?

A

High CRP, WCC and ESR

High platelet count

507
Q

Why must you always do a Echo when a patient presents with Kawasaki disease?

A

Potential complication = coronary artery aneurysm

- Need ECHO at presentation, 2 weeks and 6 weeks

508
Q

Describe the treatment for Kawasaki disease

A

IV immunoglobulin

High dose Aspirin (1st 14 days) then low dose (until 6 week ECHO)

509
Q

Why do you give high dose aspirin to children with Kawasaki disease?

A

To prevent thrombosis

- These children have thrombocytosis so are at risk of thrombosis

510
Q

What is choanal atresia?

A

Failure of nose to canalise
Presentation = cyclical going blue –> crying pink, stop crying blue
Treatment - dilation +/- stent insertion

511
Q

Name 2 congenital problems with the throat

A
  1. Laryngeal atresia

2. Laryngomalcia

512
Q

How does laryngomalacia present?

A
  • Normal voice, stridor worse on feeing and exertion
  • Worse when supine
  • Failure to thrive
  • Increased work of breathing
513
Q

What are the criteria for considering a tonsillectomy?

A
  1. > 7 episodes of acute tonsillitis in a year

2. Obstructive sleep apnoea or sleep deprived breathing

514
Q

Give 3 potential consequences of hearing loss?

A
  1. Speech and language delay
  2. Social problems –> behaviour issues
  3. Academic underachievement
  4. Social isolation
515
Q

How does hearing loss in children often present?

A
  1. Parental concern
  2. Speech, behavioural or educational problems
  3. Incidentally on screening
516
Q

What are the 3 types of hearing loss?

A
  1. Conductive hearing loss
  2. Sensorineural hearing loss
  3. Mixed
517
Q

Where does conductive hearing loss stem from?

A

From abnormalities of the ear canal or the middle ear

518
Q

Give 3 causes of conductive hearing loss

A
  1. Otitis media
  2. Glue ear
  3. Ear wax
  4. Perforated ear drum
  5. Eustachian tube dysfunction –> Downs, cleft palate
519
Q

Describe the management of conductive hearing loss

A
  • Wait = most resolve on their own
  • Grommet insertion
  • Temporary hearing aid
  • Permanent conductive losses = bone anchored hearing aid can be fitted
520
Q

Where does sensorineural hearing loss stem from?

A

Caused by lesion in cochlea or auditory nerve (inner ear) and is usually present at birth

521
Q

Give 3 risk factors for sensorineural hearing loss

A
  1. Family history
  2. SCBU
  3. Consanguinity
522
Q

Give 3 possible causes of sensorineural hearing loss

A
  1. Genetic
  2. Antenatal and perinatal –> congenital infection, preterm
  3. Postnatal –> meningitis, encephalitis, head injury, drugs, neurodegenerative disorders
523
Q

Describe the management of sensorineural hearing loss

A
  • Usually hearing aids

- Cochlear implants

524
Q

How would you manage mixed hearing loss?

A
  • Address conductive problem first

- Hearing aids

525
Q

When is hearing tested in children?

A
  1. Newborn hearing screen
  2. School entry hearing rest
  3. Long term monitoring done in high risk groups –> CF, CMV, Downs, cleft, head trauma
526
Q

Is the newborn hearing screen an objective or subjective test?

A

Objective = response or no response

- If concerns –> follow up with evoked response audiometry

527
Q

What are the 3 aims of hearing testing in children?

A
  1. Measuring hearing threshold (dB)
  2. To be frequency specific (Hz)
  3. Obtain single ear information if possible
528
Q

Name 4 types of subjective hearing testing

A
  1. Behavioural observational audiometry
  2. Distraction testing
  3. Visual reinforcement audiometry
  4. Performance testing and play audiometry
529
Q

What is otitis media?

A

Infection of the inner ear

530
Q

Name 2 organisms that can cause acute otitis media

A
  1. Strep pneumoniae

2. H. influenzae

531
Q

Give 3 symptoms of acute otitis media

A
  1. Pain
  2. Fever
  3. Generally unwell
  4. Otorrhoea
532
Q

What would you see on examination of someone with otitis media?

A

Red, bulging tympanic membrane

Loss of normal high reflex

533
Q

Describe the treatment for acute otitis media

A
  • Watch and what
  • Analgesia
  • If recurrent = board spec Abx
  • Consider grommet
534
Q

Give 2 potential complications of acute otitis media

A
  1. Extracranial = mastoiditis, TM perforation

2. Intracranial = meningitis, abscess

535
Q

What is glue ear?

A

Otitis media + effusion

- Often asymptomatic except hearing loss

536
Q

What causes glue ear?

A

Infection

- 45% follow acute OM

537
Q

How do you manage glue ear?

A
  • Conservative
  • Grommets
  • Hearing aids –> alternative to surgical intervention
  • Surgical = if hearing loss 25-30 dB on 2 occasions 2/12 apart
538
Q

When might a grommet be indicated?

A
  1. Recurrent acute OM
  2. Chronic glue ear
  3. Eustachian tube dysfunction
539
Q

What is cholesteatoma?

A

Erosive condition affection middle ear and mastoid

  • Can lead to life threatening intracranial infection
  • Offensive discharge, conductive hearing loss, vertigo, facial nerve palsy (rare)
  • Treatment = Surgery and Abx
540
Q

Define vomiting

A

Physical act that results in a forceful expulsion of gastric contents (aided by a sustained contraction of the abdominal muscles and the diaphragm at a time when the cardia of the stomach is raised, and the pylorus is contracted)

541
Q

Define regurgitation

A

Effortless expulsion of gastric contents (healthy infants and older children who eat in excess)

542
Q

Define rumination

A

Frequent regurgitation of ingested food (largely behavioural)

543
Q

Define posseting

A

Small volume vomits during or between feeds in otherwise well child

544
Q

Give 5 differentials for vomiting

A
  1. GORD
  2. Infection –> gastroenteritis
  3. Food allergy/intolerance
  4. Intestinal obstruction
  5. Appendicitis
  6. Coeliac disease
  7. Over feeding –> common in bottle fed infants
  8. Necrotising enterocolitis
  9. Malrotation - biliary vomit
  10. DKA
545
Q

Give 3 causes of intestinal obstruction that can cause vomiting

A
  1. Pyloric stenosis
  2. Duodenal atresia
  3. Intussusception
  4. Hirschsprung’s
546
Q

Give 3 important neonatal causes of vomiting

A
  1. Malrotation
  2. Hirschsprung’s disease/meconium ileus/intestinal atresia
  3. Necrotising enterocolitis
  4. Infection
547
Q

How might malrotation in a neonate present?

A

Obstruction with bilious vomiting

Abdominal pain and tenderness

548
Q

When does malrotation normally present?

A

First 1-3 days of life

549
Q

Any presenting with dark green vomiting needs what urgent investigation?

A

An urgent upper GI contrast study to assess intestinal rotation

550
Q

Give a potential consequence of malrotation

A

SMA blood supply to small intestine can be compromised –> infarction

551
Q

What is pyloric stenosis?

A

A disease characterised by hypertrophy of the pyloric muscle causing gastric outlet obstruction

552
Q

When does pyloric stenosis normally present?

A

Between 2 and 7 weeks (around 4 weeks)

553
Q

Give 3 signs of pyloric stenosis

A
  1. Vomiting –> projectile, milky, straight after feeding
  2. Hunger after vomiting
  3. Weight loss
  4. Visible gastric peristalsis and palpable mass on test feed (often RUQ)
554
Q

What investigations mighty you do in a neonate you suspect to have pyloric stenosis?

A
  1. U+E
  2. Blood gas = hypokalaemia, hyponatraemia
  3. USS –> hypertrophy to pyloric sphincter
555
Q

What would a blood gas on a neonate with pyloric stenosis show?

A

Metabolic alkalosis = low K+ and Cl-

Baby has vomited up all HCl and kidneys go into overdrive –> increased K+ secretion

556
Q

How would you treat a neonate with pyloric stenosis?

A
  • IV fluids and correct electrolyte disturbances
  • Repeat gases to monitor alkalosis
  • Stop feeding to stop vomiting
  • Pyloromyotomy once stable
557
Q

What is intussusception?

A

Where proximal bowel telescopes into a distal segment –> obstruction, inflammation, bloody stools

558
Q

When does intussusception usually present?

A

6 months of age (3 months to 2 years)

559
Q

Give 3 signs of intussusception

A
  1. Colickly pain –> draws legs up
  2. Vomiting –> milky then green
  3. Abdominal mass = sausage shaped in RUQ
  4. Red currant jelly stool
560
Q

What investigations might you do on a child who you suspect has an intussusception?

A
  • USS = target sign

- Abdominal XR = distended small bowel

561
Q

Describe the treatment for intussusception

A
  1. Air enema (unless peritonitis is present)
  2. Analgesia
  3. IV fluids if shocked
  4. Surgery
562
Q

What is duodenal atresia?

A

A congenital absence or complete closure of the duodenum

Causes intestinal obstruction in neonates

563
Q

On an abdominal XR on a neonate duodenal atresia what would you expect to see?

A

A double bubble sign

564
Q

What syndrome is associated with duodenal atresia?

A

20-40% have Down’s syndrome

565
Q

Give 5 causes of bilious vomiting in children

A
  1. Volvulus
  2. Hirschsprung’s
  3. Necrotising enterocolitis
  4. Intussusception
  5. Bowel obstruction
  6. Strangulated hernia
  7. Adhesions
566
Q

Give 4 important causes of vomiting in infants

A
  1. GORD
  2. Food intolerance
  3. Pyloric stenosis
  4. Intussusception
  5. Strangulated hernia
  6. Raised ICP
  7. Infection
567
Q

Give 4 important causes of vomiting in older children

A
  1. Acute appendicitis
  2. Strangulated hernia
  3. Pancreatitis
  4. Cyclical vomiting syndrome
  5. DKA
  6. Medications, alcohol, illicit drugs
  7. Post operative
  8. Infection
568
Q

What is GORD (gastro-oesophageal reflux)

A

Involuntary passage of gastric contents into the oesophagus with or without regurgitation or vomiting
Disease = presence of troublesome Sx and/or complications of persistent GOR

569
Q

Give 3 warning signs of GORD

A
  1. Bilious vomiting
  2. Persistent forceful vomiting
  3. New onset vomiting >6 months
  4. Failure to thrive
  5. Diarrhoea/constipation
  6. Fever
  7. HSM
570
Q

Give 3 severe symptoms/signs of GORD

A
  1. Faltering growth
  2. Oesophagitis +/- strictures
  3. Apnoea
  4. Aspiration
  5. Iron deficiency anaemia
571
Q

What investigations might you do for someone with suspected GORD?

A
  1. pH –> 24 hours oesophageal monitoring
  2. Barium swallow and meal
  3. Endoscopy
572
Q

How do you treat GORD?

A
  • Position = 30 degrees head up prone position after feeds
  • Thicken feeds
  • Change feeds
  • Drugs –> antacid, H2 blocker (ranitidine), PPI (omeprazole)
  • Surgery –> Nissan fundoplication
573
Q

What is an allergy?

A

Immune mediated response with symptoms and signs that occur within 2 hours of infection of specific food and fully resolve within 24 hours in a sensitised individual

574
Q

What is an intolerance?

A

Abdominal non immune response to specific foods or additives, primarily characterised by GU symptoms (discomfort, pain, diarrhoea)

575
Q

Give 3 symptoms of cow’s milk allergy?

A
  1. Vomiting
  2. Abdominal pain
  3. Diarrhoea
  4. Malabsorption
  5. Intestinal bleeding
  6. Urticaria and lip swelling
576
Q

What is the treatment for cow’s milk allergy?

A

Specialised formula feeds –> hydrolysed or amino acid feeds

577
Q

A 6-month old breast fed infant developed widespread urticaria immediately after the first formula feed.

a) What investigation might you do?
b) What is the most likely diagnosis?

A

a) Skin-prick test for cow’s milk

b) IgE mediated cow’s milk allergy

578
Q

A 4-month-old infant, formula fed since birth, has loose stools and faltering growth. Skin prick test to cow’s milk is negative but elimination of cow’s milk results in resolution of symptoms which return on trial re-introduction. What is the most likely diagnosis?

A

Non-IgE mediated cow’s milk allergy

579
Q

Briefly describe the pathophysiology behind lactose intolerance

A

A deficiency of intestinal lactase prevents the hydrolysis of lactose
The osmotic load of the unabsorbed lactose causes secretion of fluid and electrolytes until osmotic equilibrium is reaches –> diarrhoea

580
Q

Give 3 causes of lactose intolerance

A
  1. Primary = deficiency in lactase
  2. secondary = small intestine injury from infection, coeliac, IBD
  3. Post infective lactose intolerance
581
Q

Give 2 symptoms of lactose intolerance

A
  1. Explosive watery stools
  2. ABdominal distension m
  3. Flactulance
  4. Audible bowel sounds
582
Q

What test can be done to check for lactose intolerance?

A

Hydrogen breath test

583
Q

What is constipation?

A

Infrequent passage of stool associated with pain and difficulty, or delay in defecation

584
Q

What is encopresis?

A

Involuntary faecal soiling or incontinence secondary to chronic constipation
= overflowing diarrhoea

585
Q

What is the criteria used to diagnose functional constipation?

A

ROME III criteria

  • 2 or fewer defecations per week
  • At least 1 episode of decal incontinence per week
  • Retentive posturing or stool retentive
  • Painful or hard bowel movements
  • Presence of a large faecal mass in the rectum
  • Large diameter stools that may obstruct the toilet
586
Q

Give 3 red flag symptoms of constipation

A
  1. Delayed passage of meconium (>24 hours) –> Hirschsprung’s
  2. Fever, vomiting, bloody diarrhoea
  3. Failure to thrive
  4. Tight, empty rectum with presence of palpable abdominal faecal mass
587
Q

How do you manage constipation?

A
  • Diet.fluids and exercise
  • Behavioural advice m
  • Medications –> softeners, bulking agents, stimulants, enema
  • Disimpaction regime for overflow diarrhoea
588
Q

Give 4 causes of diarrhoea

A
  1. Overflow diarrhoea due to constipation
  2. Chronic no-specific diarrhoea
  3. Malabsorption
  4. Enteric infection
  5. IBD
  6. Drug induced
  7. Non-intestinal –> hyperthyroid, neuroblastoma
589
Q

Give 2 infection causes of diarrhoea

A
  1. Virus –> adenovirus, rotavirus, norovirus
  2. Bacterial –> campylobacter jejuni, salmonella, E.coli
  3. Protozoa –> giardiasis
590
Q

How might diarrhoea present?

A
  1. Diarrhoea +/- bloody stool
  2. Fever +/- vomiting
  3. Dehydration –> sunken fontanelle, dry mucus membranes, abnormal skin turgor, decreased consciousness, no tears, prolonged CRT
591
Q

How do you manage diarrhoea?

A

Oral rehydration solution –> IV is in shock or deteriorating
Abx –> bacterial gastroenteritis complicated by septicaemia or systemic infections
NO antiemetics or anti-motility drugs

592
Q

With which HLA molecules is coeliac disease often associated with?

A

DQ2 and DQ8

593
Q

Briefly describe the pathophysiology behind Coeliac Disease

A

o T cell mediated AI disease of the small bowel
o Gliadin from gluten deaminated by tissue transglutaminase –> increases immunogenicity
o Gliadin recognised by HLA-DQ2 receptor on APC –> inflammatory response
o Plasma cells produce anti-gliadin and tissue transglutaminase –> T cells/cytokine activated
o Consequences = villous atrophy and compensatory crypt hyperplasia –> malabsorption

594
Q

Give 3 risk factors for developing Coeliac Disease

A 
1. Family history 
2, T1DM 
3. Down's syndrome 
4. IgA deficiency 
5. Often associated with other AI disease
595
Q

Give 3 symptoms of coeliac disease

A
  1. Bloating
  2. Abdominal pain
  3. Diarrhoea and steatorrhoea
  4. Dermatitis herpetiformis
  5. Dental enamel defects
  6. Neonatal failure to thrive, buttock wasting, irritability at 8-24 months
596
Q

Describe the diagnostic criteria for coeliac disease

A
  1. Characteristic histology after endoscopy and duodenal biopsy = villous atrophy, crypt hyperplasia, increased lymphocytes
  2. Positive serology, tTG and anti-gliadin antibodies
  3. Symptom resolution with gluten exclusion
  4. Resolution of antibodies
597
Q

Give 2 possible complications of coeliac disease

A
  1. Osteoporosis –> DEXA scans
  2. Anaemia
  3. Secondary lactose intolerance
598
Q

Give 2 examples of Inflammatory bowel disease (IBD)

A
  1. Crohn’s disease

2. Ulcerative Colitis

599
Q

Describe Crohn’s disease

A

A type of inflammatory bowel disease that affects anywhere from the mouth to the anus (mainly terminal ileum)
It is us characterised by patchy (skip lesions), non caseating granulomatous inflammation that can affect any layer of the bowel wall (transmural) causing cobblestone damage (deep ulcers and fissures)

600
Q

Give 3 symptoms of Crohn’s disease

A
  1. Ulcers
  2. General ill-health = severe, fatigue, malaise
  3. Growth failure/weight loss
  4. Abdominal pain
  5. Diarrhoea
601
Q

Give 3 extra-intestinal signs o f Crohn’s disease

A
  1. Oral ulcers
  2. Uveitis
  3. Arthralgia
  4. Erythema nodosum
  5. Clubbing
602
Q

How do you treat Crohn’s disease?

A
  • Smoking cessation
  • Corticosteroids = remission, nutrition optimisation, hydration
  • Immunomodulators
  • Biologics –> infliximab
  • Surgical resection
603
Q

Give 2 possible complications of Crohn’s disease

A
  1. Small bowel obstruction
  2. Abscess/fistulae formation
  3. Perforation
  4. Anal skin tag/fissure/fistula
  5. Malnutrition
604
Q

Describe Ulcerative Colitis

A

A type of IBD that starts at the rectum and spreads proximally but only affects the colon
Continuous inflammation that is confined to the mucosa
Pseudopolyps

605
Q

Give 3 symptoms of UC

A
  1. Episodic/chronic diarrhoea +/- blood/mucus
  2. PR bleeding
  3. Colicky pain
  4. Weight loss
  5. Growth failure
606
Q

Give 2 extraintestinal signs of UC

A
  1. Erythema nodosum
  2. Arthritis
  3. Iritis and episcleritis
  4. CLubbing and orał ulcers
607
Q

How do you treat UC?

A
  • Smoking protects
  • Induction = Aminosalicylates (mesalamine) –> corticosteroids
  • Remission = Aminosalicylates –> 6MP/Azathioprine
  • Surgical resection
608
Q

Give 2 possible complications of UC

A
  1. Toxic dilatation –> perforation risk
  2. Increased risk of colorectal cancer
  3. Ankylosing spondylitis
  4. Uveitis, episcleritis, iritis
  5. Primary sclerosing cholangitis (PSC)
609
Q

What investigations might you want to do on someone who you suspect has IBD?

A
  1. ESR and CRP
  2. Measure Hb –> often microcytic anaemia (IDA)
  3. Low serum albumin
  4. Endoscopy
  5. Biopsy
610
Q

What histological findings would you see on a biopsy taken from someone with IBD?

A
  1. Mucosal inflammation
  2. Crypt damage
  3. Ulceration
611
Q

Describe the treatment for IBD

A
  1. Steroids
    2, Dietary modifications
  2. Immunosuppressants –> methotrexate and infliximab
612
Q

Give 3 benefits of using immunosuppressants as opposed to steroids of the treatment of IBD

A
  1. Safe
  2. Effective
  3. Steroid sparing
  4. Prevent relapse
613
Q

What is guarding?

A

Contraction of abdominal wall musculature, classically in response to underlying peritoneal inflammation

614
Q

Describe the difference between voluntary and involuntary guarding

A

Voluntary = contraction of abdominal wall musculature in anticipation of a painful stimulus

Involuntary = ‘true’ guarding = conduced at the reflex arc level (most needs surgery)

615
Q

Give 3 GI causes of abdominal pain

A
  1. IBS
  2. Constipation
  3. Gastritis
  4. Peptic ulcer
  5. Malrotation
  6. Appendicitis
  7. IBD
  8. Abdominal migraine
616
Q

Give 3 gynaecological causes of abdominal pain

A
  1. Dysmenorrhoea
  2. PID
  3. Ectopic pregnancy
  4. Ovarian torsion
617
Q

Give 3 Hepatobiliary causes of abdominal pain

A
  1. Hepatitis
  2. Gallstones
  3. Pancreatitis
618
Q

Give 2 urinary causes of abdominal pain

A
  1. UTI

2. PUJ obstruction

619
Q

Give 3 surgical causes of acute abdominal pain

A
  1. Appendicitis
  2. Non specific abdominal pain
  3. Ovarian pathology
  4. Meckel’s diverticulum
  5. Pancreatitis
  6. Intussusception
620
Q

Give 3 signs of appendicitis

A
  1. Anorexia
  2. Pyrexia
  3. Abdominal pain –> initially central and colicky to RIF
  4. Vomiting
  5. RIF rebound tenderness
621
Q

Why is central trauma and bruising to the abdomen a concern?

A

Bruising and trauma to the abdomen is a concern because mid-line structures such as the pancreas, spleen, bowel and liver may be damaged

622
Q

If you suspect trauma and abdominal organ damage what investigation might you do?

A

CT

623
Q

Give 3 differentials for abdominal pain and rectal bleeding

A
  1. Anal fissures
  2. Haemorrhoids
  3. Polyps
  4. Infective causes
  5. Meckel diverticulum
    If melaena = gastritis or duodenal ulcer
624
Q

What is Meckel diverticulum a remnant of?

A

Vitelline duct (joins yolk sac to midgut lumen in foetus)

625
Q

Give 3 signs of Meckel diverticulum

A
  1. Severe rectal bleeding
  2. Intussusception
  3. Volvulus
626
Q

How would you treat Meckel diverticulum?

A

Surgical resection

627
Q

Give 3 differentials for abdominal mass

A
  1. Constipation
  2. Appendicitis
  3. Organomegaly
  4. Nephroblastoma/Wilm’s tumour
628
Q

Define faltering growth

A

Failure to gain adequate weight or achieve adequate growth during infancy and early childhood
NICE defines it as weight that has fallen down 2 centime lines

629
Q

Give 3 nonorganic causes of faltering growth?

A
  1. Feeding problems –> insufficient breast milk, poor techniques
  2. Lack of regular feeding times
  3. Difficulty feeding
  4. Low socioeconomic status
  5. Maternal depression
  6. Neglect or child cabuse
630
Q

Give 2 organic causes of faltering growth

A
  1. Impaired suck/swallow –> promoter dysfunction, cerebral palsy, cleft palate
  2. Crohn’s disease
  3. Cystic fibrosis
  4. Liver disease
  5. Chronic renal failure
  6. Malabsorption
631
Q

Give 2 causes of faltering growth due to increased requirements

A
  1. Chronic illness –> CHD, CKD, CF
  2. Thyrotoxicosis
  3. Malignancy
  4. Chronic infection –> HIV, immune deficiency, TB
632
Q

Why is prompt intervention important when managing a child with faltering growth?

A

Prompt intervention can avoid problems such as cognitive delay, feeding and behavioural problems and low maternal self-esteem

633
Q

You do a lumbar puncture and find, turbid, raised WCC (polymorphs) raised proteins and low glucose, is this likely to be due to a bacterial or a viral infection?

A

Bacterial

634
Q

You do a lumbar puncture and find clear, raised WCC (lymphocytes), normal proteins and normal glucose, is this likely to be due to a bacterial or a viral infection?

A

Viral

635
Q

Give 2 contraindications for a lumbar puncture

A
  1. Cardiorespiratory instability
  2. Focal neurological signs
  3. Signs of raised ICP
  4. Coagulopathy
  5. Thrombocytopenia
  6. Local infection at LP site
636
Q

Give 2 viral causes of meningitis

A
  1. Enterovirus
  2. Adenovirus
  3. Mumps
637
Q

What bacteria commonly causes meningitis in children?

A
  • Neonatal = GBS, E.coli, mysterious monocytogenes
  • 1 month - 6 years = Neisseria meningitidis, S. pneumonia, H. influenzae
  • > 6 years = Neisseria meningitidis
638
Q

How does a child with meningitis present?

A
  • Non specific in <18 months = fever, poor feeding, vomiting, irritability
  • Older child = neck stiffness
  • Bacterial meningitis = neck stiffness, bulging fontanelle, decreased consciousness, status epilepticus
  • Non blanching purpuric rash = meingincoccal sepsis
639
Q

Why does a child with meningococcal septicaemia develop a rash?

A

Due to bacterial endotoxins damaging blood vessels –> vasculitis –> bleeding into SC tissue –> thrombosis and DIC

640
Q

What investigations might you do on a child who you suspect has meningitis?

A
  • Thorough history and examination
  • Blood cultures
  • Lumbar puncture
641
Q

Describe the treatment for a child with meningitis

A
  • IV ceftriaxone (80mg/kg/od) or cefotaxime (50mg/kg/od)
  • Dexamethasone –> reduce risk of long term complications
  • Prophylaxis is needed to prevent further spread
642
Q

Name 2 drugs that can be given as meningitis prophylaxis

A
  1. Rifampicin

2. Ciprofloxacin

643
Q

Who must you notify when you diagnose a child with meningitis?

A

Public Health England

644
Q

Define sepsis

A

Dysregulated host response leading to end organ dysfunction

645
Q

What is a septic screen?

A

Checks for infection, in particular meningitis

  1. Urine sample
  2. Blood tests
  3. Lumbar puncture
646
Q

Give 2 causes of encephalitis

A
  1. Herpes simplex virus
  2. Enterovirus
  3. Post infectious encephalopathy –> following chickenpox
  4. Slow virus infection –> HIV
647
Q

Give 2 signs of encephalitis

A
  1. Fever
  2. Altered consciousness
  3. Behavioural changes
  4. Seizures
648
Q

How do you treat encephalitis?

A

Parenteral high dose acyclovir

649
Q

What is Toxic Shock Syndrome caused by?

A

Toxin producing Staph aureus and group A strep

650
Q

What is TSS characterised by?

A
  1. Fever >39 degree
  2. Hypotension
  3. Diffuse erythematous, macular rash
651
Q

Give 3 causes of immune deficiency

A
  1. Primary = intrinsic defect in immune system –> inherited X linked or AR disorders
  2. Incurrent bacterial or viral infection
  3. Malignancy
  4. Malnutrition
  5. HiB infection
  6. Immunosuppressive therapy
  7. Splenectomy
652
Q

Give 3 signs of immune deficiency

A
  1. Frequent infections
  2. Infection with unusual organisms
  3. Severe infections
  4. Failure to thrive
  5. Extensive candidiasis
653
Q

Who would you investigate for Severe immune deficiency?

A
  • Children who present with Severe, Prolonged, Unusual or Recurrent (SPUR) infections
  • Those with family history
654
Q

Name 5 vaccine preventable diseases

A
  1. Tetanus
  2. Diphtheria
  3. Whooping cough
  4. Polio
  5. Measles
  6. Mumps
  7. Rubella
655
Q

Give an example of a live, attenuated vaccine

A
  1. MMR
  2. BCG
  3. Rotavirus
656
Q

Give an example of an inactivated vaccine

A
  1. Influenza

2. Diphtheria

657
Q

How do infants get HIV?

A

Due to vertical transmission = intrauterine, intrapartum and postpartum (breastfeeding)

658
Q

How are children likely to be affected by HIV?

A
  • Infections
  • Asymptomatic
  • Lymphadenopathy
  • Parotitis
  • Candidiasis
659
Q

How is HIV diagnosed in children?

A
  • Children <18 months born to infected month = transplacental maternal IgG HIV antibodie –> +ve test confirms exposure NOT HIV infection
  • <18 months most affective test = HIV DNA PCR –> 2 -ve within first 3 months of life, at least 2 weeks after completion of postnatal antiretroviral therapy = NOT infected
  • Children >18 months = antibody detection
660
Q

How is HIV managed in children?

A
  • HIV infant medication starts at 4 weeks
  • Antiretroviral therapy = 2 nucleoside reverse transcriptase inhibitor (Abacavir, Didanosine)
    AND 1 non-nucleoside reverse transcriptase inhibitor (Efavirenz) OR 1 protease inhibitor (Atazanavir)
661
Q

Name the most common congenital infections

A

TORCH

  • Toxoplasma gondii
  • Other = Parvovirus, varicella zoster, syphillis
  • Rubella
  • CMV
  • Herpes simplex
662
Q

A baby makes many adaptations to ex-utero life, give 4 CV adaptations

A
  1. Closure of foetal shunts –> foramen oval, ductus arteriosus
  2. Perfusion of the lungs
  3. Fall in pulmonary artery pressure and increase in systemic BP
  4. Increase in cardiac output
663
Q

A baby makes many adaptations to ex-utero life, give 2 respiratory adaptations

A
  1. Foetal lung fluid removed, filled with air
  2. Surfactant released
  3. Gaseous exchange
664
Q

A baby makes many adaptations to ex-utero life, aside from CV and respiratory give 4 adaptations

A
  1. Control of own movements
  2. Independent hormonal responses
  3. Thermoregulation
  4. Feeding
  5. Immunocompetence
  6. Conversion to adult haemoglobin
665
Q

Give 5 medical problems that preterm infants may suffer from

A
  1. Respiratory distress syndrome
  2. Apnoea and bradycardia
  3. Patent ductus arteriosus
  4. Infection
  5. Jaundice
  6. Intraventricular haemorrhage
  7. Cystic periventricular leukomalacia
  8. Necrotising enterocolitis
  9. Retinopathy of prematurity
  10. Hypothermia
666
Q

What long term problems can a pre term baby develop?

A
  1. Retinopathy of prematurity
  2. Chronic lung disease
  3. Osteopenic bones
  4. Neurodevelopmental delays
667
Q

Give 3 functions of surfactant

A
  1. Reduces surface tension
  2. Prevents alveoli collapse
  3. Allows homogenous aeration
668
Q

When is surfactant produced?

A

From 34 weeks gestation

- Production increases rapidly 2 weeks before birth

669
Q

Where is surfactant produced?

A

By T2 pneumocytes

670
Q

What can mothers be given antenatally to prevent surfactant deficiency?

A

Steroids can be given to the mother to encourage foetal surfactant release

671
Q

Give 3 causes of surfactant deficiency

A
  1. Respiratory distress syndrome
  2. Chronic lung disease of prematurity
  3. Non compliant lungs
  4. Unequal aeration
  5. Reduced lung volume
672
Q

Give 3 signs of respiratory distress in a child

A
  1. Tachypnoea, RR = 40-60
  2. Subcostal and intercostal recession
  3. Stridor
  4. Tracheal tug
  5. Cyanosis
673
Q

How would you manage respiratory distress in a neonate?

A
  1. O2
  2. Intubate
  3. CO2 monitoring
  4. Surfactant therapy
  5. Nasal CPAP and mechanical ventilation
  6. Fluids if indicated
674
Q

Briefly describe the pathophysiology of chronic lung disease of prematurity

A

There is reduced lung volume and reduced alveolar SA –> diffusion defect
This often leads to recurrent hospital admissions and increased mortality

675
Q

What is apnoea of prematurity

A

When a preterm infant has no repository drive due to lack of myelination around the brain stem (not fully myelinated until 32/34 weeks) –> they forget to breathe
- Often associated with bradycardia

676
Q

Describe the treatment for apnoea of prematurity?

A
  1. Nasal CPAP

2. Stimulation = caffeine

677
Q

Give 2 benefits of breast feeding for the infant

A
  1. Reduces the risk infection
  2. Reduces the risk of allergic disease
  3. Reduces the risk of GORD
  4. Increased IQ and cognition
678
Q

Give 2 benefits of breast feeding for the mother

A
  1. Reduces the risk of some types of cancer –> breast, uterine, ovarian, endometrial
  2. Reduces the risk of PPH and postnatal depression
  3. Optimum child spacing
  4. Less food/medical expenses
679
Q

How would you feed a baby born at 27 weeks?

A

NG tube feeds

- At 35 weeks you can start breast/bottle feeding as this is when suckling reflex develops

680
Q

Give 5 signs of hepatic dysfunction in children

A
  1. Encephalopathy
  2. Jaundice
  3. Epistaxis
  4. Ascites
  5. Varices
  6. Spider naevi
  7. Bruising
  8. Palmar erythema
    9 Clubbing
  9. Malnutrition and faltering growth
681
Q

Give 3 reasons why newborns become jaundiced

A
  1. RBC lifespan is shorter –> increased bilirubin production
  2. Hepatic bilirubin metabolism is less efficient –> septic immaturity
  3. Absence of gut flora impedes elimination of bile pigment
682
Q

Give 3 causes of high levels of unconjugated bilirubin

A
  1. Haemolytic Disease
  2. Phsyiological
  3. Infection/sepsis
  4. Breast bilk jaundice
  5. CF
  6. Hypothyroidism
683
Q

Describe the treatment for high levels of unconjugated bilirubin

A
  1. Phototherapy

2. Exchange transfusion

684
Q

How does phototherapy work in treatment jaundice?

A

Light converts unconjugated bilirubin into a water soluble pigment

685
Q

When might exchange transfusion be used in the treatment of jaundice?

A

If bilirubin rises to very dangerous levels and phototherapy alone is not effective

686
Q

What area of the brain does high levels of unconjugated bilirubin affects?

A

The basal ganglia

687
Q

Why are high levels of unconjugated bilirubin concerning in a neonate?

A

Unconjudgated bilirubin is fat soluble and can diffuse into brain tissue
High levels can lead to kernicterus and then cerebral palsy

688
Q

What is kernicterus?

A

Brian damage due to high levels fo unconjugated bilirubin

689
Q

Give 3 signs of kernicterus

A
  1. Lethargy progressing to hypertonia then hypotonia
  2. Poor feeding
  3. Fever
  4. High-pitched cry
  5. Opisthotonos (spasm of the muscles causing backward arching of the head, neck, and spine)
  6. Seizures
  7. Coma
690
Q

Give 2 possible complications of kernicterus

A
  1. Deafness
  2. Gaze disturbance
  3. Cerebral palsy
  4. Death
691
Q

When is jaundice most likely to occurs

A

Physiological Janice is common

Appears after 24 hours, peaks around 3 or 4 days and usually resolves by 14 days

692
Q

What are the likely causes of jaundice in a neonate who is <24 hours old?

A
  1. Sepsis
  2. Haemolytic causes –> haemolytic disease of the newborn, rhesus haemolytic disease, hereditary spherocytosis, G6PD deficiency
  3. TORCH infections
693
Q

Why is it important to identify a neonate with haemolytic cause of their jaundice?

A

The bilirubin is unconjugated and if allowed to reach high levels could cause kernicterus

694
Q

Give 3 causes of jaundice at 24 hours to 2 weeks of age

A
  1. Physiological jaundice
  2. Breast milk jaundice
  3. Infection –> UTI
  4. Congenital hypothyroidism
  5. Haemolytic cause
695
Q

Give 2 causes of jaundice > 2 weeks of age due to unconjugated hyperbilirubinaemia

A
  1. Infection
  2. Physiological or Breast milk jaundice
  3. Hypothyroidism
  4. Haemolytic disease
696
Q

Give 2 causes of jaundice > 2 weeks of age due to conjugated hyperbilirubinaemia

A
  1. Biliary atresia

2. Neonatal hepatitis syndrome

697
Q

What is biliary atresia?

A

When there is progressive fibrosis and obliteration of the extra-hepatic and intra-hepatic biliary tree
Chronic liver failure and death can occur within 2 years

698
Q

Give 3 signs of biliary atresia

A
  1. Prolonged neonatal jaundice (develops after 2 days)
  2. Failure to thrive
  3. Pale white stools and dark urine = obstructive jaundice
  4. Hepatomegaly
699
Q

What investigations might you do to determine whether a child has biliary atresia?

A
  1. Measure transcutaneous bilirubin = conjugated bilirubin raised
  2. LFTs would be abnormal
  3. ERCP imaging
700
Q

What is the treatment for biliary atresia?

A
  • Surgery to bypass fibrotic ducts = hepatoportoenterostomy (Ksai procedure)
  • Nutrition and vitamin supplementation
  • If unsuccessful or late presentation = liver transplant
701
Q

Give 2 causes of neonatal hepatitis

A
  1. Idiopathic = 80%
  2. CMV
  3. Rubella
  4. Hepatitis A, B or C
702
Q

What investigations would you do on someone with suspected neonatal hepatitis?

A

Liver biopsy = multinucleated giant cells and rosette formation
LFTs = increase unconjugated and conjugated bilirubin

703
Q

Why are preterm babies at increased risk of infection?

A

Active IgG transfer happens in the last 3 months of pregnancy

704
Q

Shat Abx would you prescribe empirically to reduce the risk of neonatal infection in a preterm baby?

A
  • Benzylpenicillin (50mg/kg BD)

- Gentamicin (5mg/kg OD)

705
Q

What is necrotising enterocolitis?

A

Inflammation and necrosis of a portion of the GI tract

706
Q

What can increase the risk of necrotising enterocolitis?

A

IUGR

707
Q

What can decreased the risk of necrotising enterocolitis?

A

Breast feeding and probiotics

708
Q

Give 3 signs of necrotising enterocolitis

A
  1. Feed intolerance
  2. Vomiting
  3. Distended abdomen
  4. Stool contains fresh blood
  5. Shock
709
Q

How can you treat necrotising enterocolitis?

A

Stop oral feeding

Broad spectrum Abx

710
Q

Give the cause of retinopathy of prematurity

A

Hyperoxic insult

- Can lead to blindness

711
Q

How could you treat retinopathy of prematurity?

A

Laser therapy

712
Q

Give 2 reasons why preterm infants are particularly vulnerable to hypothermia

A
  1. Large SA relative to mass
  2. Thin and heat permeable skin
  3. Little fat for insulation
    - Temps are maintained using incubators
713
Q

Give 4 differentials for the acute scrotum

A
  1. Testicular torsion
  2. Epididymo-orchitis
  3. Trauma
  4. Acute hydrocele
  5. Idiopathic scrotal oedema
  6. Torsion of Hydatid/appendix of testicle (‘blue dot’)
714
Q

Give 5 signs and symptoms of testicular torsion

A
  1. Severe, constant pain
  2. Sudden onset pain
  3. Vomiting
  4. Tenderness
  5. Swelling
  6. Redness
715
Q

In what age groups is testicular torsion more common?

A

Neonates and peri-pubertal

716
Q

How is testicular torsion managed?

A

Surgery –> within 6 hours to save testicle

717
Q

What is hypospadias?

A

Displacement of urethral meatus (ventral), hooded foreskin and a bend in the shaft (chordee = ventral curve)

718
Q

Give 2 differentials for a groin swelling in children

A
  1. Hernia

2. Hydrocele

719
Q

Give 3 signs of an inguinal hernia

A

1, Can’t get above it
2. Reducible
3. Often indirect in children
Will need surgical repair

720
Q

Give 3 signs of a hydrocele

A
  1. Can get above it
  2. Confined to scrotum
  3. Non reducible
    Should resolve by 2 years old
721
Q

How are undescended testes classified?

A
  1. Retractile = Testis can be manipulated into the bottom of the scrotum without tension but subsequently retracts into inguinal region, pulled up the cremasteric muscle (corrects with age)
  2. Palpable = Palpable in the groin but cannot be manipulated into the scrotum
  3. Impalpable = NO testis felt on examination
722
Q

What investigations do you do for someone with undescended testes

A
  1. US

2. Hormonal tests = for bilateral impalpable testes

723
Q

How do you treat undescended testes?

A
  • Laparoscopy for impalpable

- Orchidopexy = surgical placement of testis in scrotum

724
Q

At what point will testes not descend spontaneously?

A

After 6 months of age

725
Q

Give 3 differentials for head and neck lumps in children

A
  1. Lymphadenopathy
  2. Thyroglossal cyst (moves when stick tongue out)
  3. Goitre
  4. Malignancy
  5. Branchial arch remnants
  6. Dermoid cysts
726
Q

What are the red flag signs for head/neck lumps in children?

A

> 2cm for >2 weeks and enlarging

727
Q

Define childhood disability

A

Someone who has a physical or mental impairment that results in a marked, pervasive limitation on activity
e.g. Downs, Cerebral plasy

728
Q

Give 3 factors that influence childhood disability

A
  1. Environment
  2. Social background
  3. Impairment
729
Q

What is cystic fibrosis?

A

Defect in CFTR gene (Chr 7) –> affecting pancreas, lungs, liver and gonads, thickens secretions

730
Q

Give 5 signs of cystic fibrosis

A
  1. Neonate = meconium ileus, fralure to thrive
  2. Cough = loose, productive or purulent sputum
  3. Wheeze
  4. Recurrent infections
  5. Haemoptysis
  6. Pancreatic insufficiency
  7. Male infertility (absent vas deferens)
  8. Maldigestion and malabsorption
  9. Clubbing
731
Q

How is cystic fibrosis diagnosed?

A
  • Newborn blood spot test = Guthrie test
  • Sweat test
  • Raised immunoreactive trypsin
  • Genetic testing
732
Q

How is cystic fibrosis managed?

A
  • Physio
  • Prophylactic oral Abx
  • Nebulised DNAase or hypertonic saline
  • BIlateral lung transplant
  • Pancreatic replacement therapy
  • High calorie diet
733
Q

Give 2 complications of cystic fibrosis

A
  1. DM

2. Liver disease

734
Q

What is Duchenne Muscular Dystrophy?

A

X linked recessive muscle degeneration disorder due to deletion at Xp21 causing no functional dystrophin
- Increase creatinine kinase

735
Q

How does DMD present?

A

Around 4 years old

  • Difficulty standing = Gowers sign (need to turn prone to rise)
  • Waddling gait
  • Language delay
  • Calf pseudohypertrophy
  • Respiratory failure
  • Scoliosis
  • Learning difficulties = 1/3
736
Q

How do you manage DMD?

A
  • Exercise
  • Passive stretching and night splints
  • Orthotics
  • Physio
  • Surgical repair of scoliosis
737
Q

What conditions does the newborn blood spot (Guthrie test) screen for?

A
  1. Cystic fibrosis
  2. Congenital hypothyroidism
  3. Sickle Cell Disease
    6 Metabolic diseases –> MCADD, phenylketonuria and maple syrup disease etc
738
Q

Name 3 diseases with AD inheritance

A
  1. ADPKD
  2. Huntington disease
  3. Marfan’s
739
Q

Give 3 characteristics of AD inheritance

A
  1. Vertical transmission
  2. Mutation transmitted from Male to male
  3. Every generation affected
  4. Both males and females affected
  5. 50% chance of inheritance
740
Q

Name 3 disease with AR inheritance

A
  1. Cystic Fibrosis
  2. Sickle Cell Disease
  3. Haemochromatosis
  4. Phenylketonuria
741
Q

Give 3 characteristics of AR inheritance

A
  1. Both patients must be carriers
  2. Often only one generation is affected
  3. 2/3 carrier risk for unaffected siblings
742
Q

Give an example of an X linked disease

A

Duchenne and Becker muscular dystrophy

743
Q

Give 3 characteristics of X linked inheritance

A
  1. Male > female affected
  2. NO male to male transmission
  3. 50% of daughters are carriers and 50% of sons are affected
744
Q

Give 4 example son non-mendelian inheritance

A
  1. Multifactoral –> neural tube defects
  2. Mitochondrial
  3. Genomic imprinting
  4. Gonadal mosaicism
745
Q

Give an example of a neural tube defect

A

Spina Bifida

- More likely to happen is there is folic acid deficiency or maternal deficiency

746
Q

Give 2 exmaples of genomic imprinting

A
  1. Prader Willi = Caused by a deletion in the paternally inherited chromosome 15 (15q11-13) or maternal uniparental disomy
  2. Angelmans Syndrome = Caused by a deletion in the Maternally inherited chromosome 15 or paternal uniparental disomy
747
Q

Give 2 symptoms of Prader Will syndrome

A
  1. Neonatal hypotonia
  2. Poor feeding
  3. Moderate developmental delay and learning difficulties
  4. Hyperphagia and obesity
748
Q

Give 2 symptoms of Angelmans Syndrome

A
  1. “Happy puppet” = unprovoked laughing.clapping
  2. Microcephaly
  3. Severe cognitive impairment
  4. Seizures
  5. Ataxia
  6. Broad based gait
749
Q

What is gonadal mosaicism?

A

Gonadal mosaicism is when there are two different populations of cells in the gonads
One population is normal and the other is mutated
All gametes from the mutated line are affected

750
Q

Why does Down’s syndrome occur?

A

Autosomal trisomy due to

  1. Meiotic non disconjunction (94%)
  2. Translocation (5%)
  3. Moasiacism (1%)
751
Q

Give 3 signs of Down’s syndrome

A
  1. Learning/developmental delay
  2. Hypotonia
  3. Short stature
  4. CHD
  5. Brushfield spots
  6. Single palmar crease
  7. Flat occiput
  8. Wide ‘sandal’ gap between big and 2nd toe
752
Q

What is Edwards syndrome and give 2 features?

A

Trisomy 18

  1. Low birthweight
  2. Prominent occiput
  3. Small mouth and chin
  4. Short sternum
  5. Flexed, overlapping fingers
  6. ‘Rocker-bottom’ feet
  7. Cardiac and renal malformations
753
Q

What is Patau Syndrome and give 2 features

A

Trisomy 13

  1. Structural defect of brain
  2. Scalp defects
  3. Small eyes (microphthalmia) and other eye defects
  4. Cleft lip and palate
  5. Polydactyly
  6. Cardiac and renal malformations
754
Q

Define child development

A

The biological, psychological and emotional changes that occur between birth and adolescence as the individual processes from dependency to crashing autonomy
It is a continuous process with a predictable sequence however each childs development is unique

755
Q

Give 5 influences on a child’s development

A
  1. Genetic factors
  2. Stimulating environment
  3. Pregnancy factors –> premature, mums health
  4. Healthy attachment
  5. Medical conditions
  6. Abuse/neglect/domestic violence
  7. Healthy peer relationships
  8. Education
  9. Nutrition
  10. Parenting style
756
Q

What are the 4 domains of child development?

A
  1. Gross Motor
  2. Fine motor and vision
  3. Speech, language and hearing
  4. Social interaction and self-care skills
757
Q

What are the developmental milestones for gross motor function?

A
  • 3m = lifts head on tummy
  • 6m = chest up with arm support, can sit unsupported
  • 8m = crawling
  • 9m = pulls to stand
  • 12m = walking
  • 2 years = walking up stairs
  • 3 years = jumping
  • 4 years = hopping
  • 5 years = rides a bike
758
Q

With regards to gross motor development, at what age would you expect a child to do the following

a) Walking
b) Jumping
c) Crawling
d) Walking up stairs?

A

a) Walking = 12 months
b) Jumping = 3 years
c) Crawling = 8 months
d) Walking up stairs = 2 years

759
Q

What are the developmental milestones for fine motor and visual function?

A
  • 4m = grabs an object using both hands
  • 8m = takes objects in each hand
  • 12m = scribbles with crayons e.g. circle, cross, square
  • 18m = builds a tower of 2 cubes
  • 3 years = builds a tower of 8 cubes
760
Q

With regards to fine motor and visual development, at what age would you expect a child to do the following

a) Drawing with crayons
b) Building a tower of 8 cubes
c) Takes an object in each hand
d) Builds a tower of 2 cubes

A

a) Drawing with crayons = 12m
b) Building a tower of 8 cubes = 3 years
c) Takes an object in each hand = 8m
d) Builds a tower of 2 cubes = 18m

761
Q

What are the developmental milestones for speech, language and hearing?

A
  • 3m = laughs and squeals
  • 9m = can make sounds such as ‘dada’ and ‘mama’
  • 12m = can say one word
  • 2 years = can form short sentences and name body parts
  • 3 years = speech is mainly understandable
  • 4 years = knows colours and can count
  • 5 years = knows the meaning of words
762
Q

With regards to speech, language and hearing, at what age would you expect a child to do the following

a) Form short sentences and name body parts
b) Knows colours and can count
c) Laughs and squeals
d) Has mainly understandable speech

A

a) Forms short sentences and name body parts = 2 years
b) Knows colours and can count = 4 years
c) Laughs and squeals = 3 months
d) Has mainly understandable speech = 3 years

763
Q

What are the developmental milestones for social interaction and self-care skills?

A
  • 6 weeks = smiles
  • 6 months = finger feeds
  • 9m = waves bye-bye
  • 12m = uses cutlery
  • 2 years = undresses, feeds toys
  • 3 years = plays with others, names a friend
  • 4 years = dresses with no help, plays a board game
764
Q

With regards to social interaction and self-care skills, at what age would you expect a child to do the following

a) Uses cutlery
b) Plays with others, names a friend
c) Smiles
d) Waves bye-bye

A

a) Uses cutlery = 12 months
b) Plays with others, names a friend = 3 years
c) Smiles = 6 weeks
d) Waves bye-bye = 9 months

765
Q

What does ‘The healthy child programme’ encourage?

A
  1. Encourages care to keep children healthy and safe
  2. Promotes healthy eating and activity
  3. Identifies problems in children’s development
  4. Identifies ‘at risk’ families for more support
  5. Ensures children are prepared for school
766
Q

When does universal surveillance of developmental occur?

A
  • Neonatal examination (NIPE) –> within 72 hours
  • Blood spot –> 5-9 days, midwife
  • Baby review (14 days old) –> health visitor
  • 6-8 week check –> GP
  • At 1 year (for development problems)
  • Between 2-2.5 years (for development problems)
767
Q

Give 2 examples of concerning child development with regards to gross motor function

A
  1. Not sitting by 12 months

2. Not walking by 18 months

768
Q

Give an example of concerning child development with regards to fine motor function

A

Hand preference before 18 moths –> neuro condition like cerebral palsy

769
Q

Give a speech and language examples that may suggest concerning child development

A

No clear words by 18 months –> hearing/learning disability? ASD?

770
Q

Give two examples of concerning child development with regards to social development

A
  1. No response to carers interaction by 8 weeks
  2. No smiling by 3 months –> vision impairment?
  3. No interest in playing by 3 years
771
Q

Give 3 red flags in development

A
  1. Regression of development
  2. Poor health/growth
  3. Significant family history
  4. Findings on examination –> microcephaly, dysmorphic features
  5. Safeguarding indicators
772
Q

Give 5 causes of developmental delay

A
  1. Genetics
  2. Pregnancy
  3. Factors around birth
  4. Factors in childhood
  5. Environmental
773
Q

Give 2 examples of genetic causes of developmental delay

A
  1. Chromosomal disorders –> Downs
  2. Single gene disorders –> Duchenne
  3. Polygenic –> ASD, DHD
  4. Micro-deletions or micro duplications
774
Q

Give 2 examples of pregnancy related causes of developmental delay

A
  1. Congenital infections –> CMV, HIV
  2. Exposure to drugs/alcohol –> FAS
  3. MCA infarct
775
Q

Give 2 examples of birth related causes of developmental delay

A
  1. Prematurity

2. Birth asphyxia (due to hypoxia)

776
Q

Give 2 examples of childhood medical causes of developmental delay

A
  1. Infections –> meningitis
  2. Chronic illness
  3. hearing or visual impairment
  4. Acquired brain injury
777
Q

Give 2 examples of environmental causes of developmental delay

A
  1. Abuse and neglect

2. Low stimulation

778
Q

How might you investigate someone’s child development if you suspected that there was something wrong?

A

Thorough history and examination
Tailor any investigations to the child e.g.
- Boys not walking by 18m check creatinine kinase for Duchenne
- Focal neurological signs -> MRI brain
- Genetic testing
- Unwell, failure to thrive -> metabolic investigations
There is no ‘developmental screen’, investigations need to be tailored towards to the child

779
Q

Name 3 primitive reflexes

A
  1. Moro
  2. Grasp
  3. Rooting
  4. Stepping response
  5. Asymmetrical tonic neck reflex
780
Q

What is the Moro reflex?

A

The startle reflex = primitive reflex
- Response due to a sudden loss of support, sudden extension of the head causes symmetrical extension then flexion of the arms

781
Q

Name 2 postural reflexes

A
  1. Labyrinthine righting
  2. Postural suport
  3. Lateral propping
  4. Parachute
782
Q

Why should primitive reflexes disappear?

A

Primitive reflexes should gradually disappear as postural reflexes develop
- Essential for good motor development

783
Q

Why is it concerning is primitive reflexes persist?

A

May be a sign of CNS dysfunction

784
Q

Define Self harm

A

Wide range of things that people do to hurt themselves in a deliberate and usually hidden way, which are damaging
- Act with intent to hurt self but no intention to kill self

785
Q

Give 3 predisposing factors for a child developing depression

A
  1. Family history
  2. Stress in pregnancy
  3. Poor attachment
  4. Poverty
  5. Isolation
786
Q

Give 3 precipitating factors for a child developing depression

A
  1. Trauma
  2. Drugs
  3. Infections
  4. Puberty
  5. Exam stress
  6. Sexual abuse
  7. Bullying
787
Q

Give 3 perpetuating factors for a child developing depression

A
  1. Chronic illness
  2. Malnutrition
  3. Ongoing neglect
  4. Ongoing poverty
788
Q

Give 4 symptoms of depression

A
  1. Persistent sadness or low mood
  2. Loss of interest or enjoyment
  3. Fatigue
  4. Poor or increased sleep
  5. Poor or increased appetite
  6. Low concentration
  7. Low self confidence
  8. Feelings for guilt and self blame
  9. Hopelessness
789
Q

Describe the non medical and medical treatment of depression

A

Non medical = Education, CBT, IPT, family therapy

Medical = fluoxetine, sertraline, citalopram

790
Q

What is the diagnostic criteria for anorexia?

A

Deliberately keeping weigh below 85% of expected

- Restricted dietary choice
- Excessive exercise 
- Induced vomiting, use of appetite suppressants and diuretics

Also have dread of fatness and can have endocrine effects (amennorhoea)

791
Q

Give 5 risk factors for developing anorexia

A
  1. Social pressure
  2. Perfectionist character traits
  3. Family attitudes towards food
  4. Low self esteem
  5. Occupation/interests
  6. Family history
  7. Past of present life evens –> abuse, illness, grief
792
Q

What screening tool can be used for investigation earring problems?

A

SCOFF
• Do you make yourself Sick because you’re uncomfortably full?
• Do you worry that you’ve lost Control over how much you eat?
• Have you recently lost more than 6kg (about One stone) in 3 months?
• Do you believe you’re Fat when others say you’re thin?
• Would you say that Food dominates your life?

793
Q

Describe the treatment for anorexia

A
  1. Family therapy
  2. IPT
  3. CBT
    Weight restoration at 0.5kg/week
    - Monitor for re-feeding syndrome
794
Q

Give 5 ways in which radiological imaging for a child differs to imaging an adult

A
  1. Size
  2. Growth plates
  3. Skull sutures
  4. Ossification
  5. Congenital problems –> dextrocardia, osteogensis imperfecta
795
Q

What night an abdominal XR be indicated on a child?

A
  1. Abdominal distension –> obstruction
  2. Abdominal pain of unknown cause
  3. Constipation
796
Q

What analgesia is appropriate for a paediatric fracture?

A

Paracetamol

Oromorph

797
Q

Give 5 causes of dehydration

A
  1. Dysphagia –> cerebral palsy, developmental delay
  2. VOmiting
  3. Behavioural/Psychiatric
  4. Neglect
  5. Burns/Sepsis
  6. Cystic fibrosis
  7. Kidney disease –> renal tubular disease, renal dysplasia
798
Q

Give 4 signs of dehydration

A
  1. thirst
  2. Dry mucous membranes
  3. Restlessness, irritability
  4. Sunken eyes/fontanelle
  5. Reduced skin turgor
  6. Decreased urine output
  7. Reduced consciousness
  8. Cold, mottled peripheries
  9. Anuria
799
Q

How much should you feed to a neonate?

A 
150ml/kg/day 
Day 1 = 60ml/kg/day 
Day 2 = 90ml/kg/day 
Day 3 = 120ml/kg/day 
Day 4 onwards = 150ml/kg/day
800
Q

What fluid should you give to a neonate?

A

10% dextrose

801
Q

What fluid should you give to children?

A

0.9% Sodium Chloride + 5% glucose +/- KCl

802
Q

How do you calculate the rate at which to give maintenance fluids to a child?

A

100ml/Kg/day for first 10Kg
50ml/Kg/day for the next 10Kg
20ml/Kg/day for every Kg after that

803
Q

When taking a history from a teenager, the HEADDS framework can be used, describe this framework

A 
Home
Education
Activity
Drugs/alcohol
Depression/suicide
Sexuality
804
Q

Give 4 risk factors for child abuse

A
  1. Lack of parental support, parental indifference or intolerance
  2. Parental mental health probelms
  3. Parental alcohol or drug abuse
  4. Domestic violence within the family
  5. Young parental age
  6. Failure of child to meet parental expectations/aspirations
  7. Poverty
805
Q

Name the 4 broad categories of child abuse

A
  1. Physical injury –> bruises, scratches, burns, fractures
  2. Sexual abuse –> behaviour change, physical symptoms e.g. bleeding, STI, pregnancy
  3. Emotional abuse –> relationships high in criticism and low in warmth
  4. Neglect –> care that does not meet the needs of a child
806
Q

How does child abuse present?

A
  • Disclosure
  • Injury observed –> at school
  • Incidental findings
807
Q

How would you manage a child whom you suspect is a victim of child abuse?

A
  • Thorough history –> ensure good documentation, are there any discrepancies?
  • Examination –> use body charts
  • FBC, clotting, swabs, bone profile, skeletal survey
  • Social services assessment +/- police input

My Phase 3a (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions