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Paediatrics Flashcards

1
Q

Define cow’s milk protein allergy

A

This can be an Ig-E or non-IgE-mediated response to proteins in cow’s milk.

An IgE-mediated allergy gives an immediate urticarial reaction with facial swelling and pruritis.

A non-IgE-mediated allergy causes GI symptoms including colic, GORD, blood/mucus in the stool and faltering growth. Onset in hours.

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2
Q

How would you investigate a differential of cow’s milk protein allergy further?

A
  • Examine the child
  • Investigate for other causes of allergic reaction/FTT
  • Skin prick testing
  • IgE blood test
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3
Q

How would you manage cow’s milk protein allergy?

A
  • If any hint of anaphylaxis, ABC approach.
  • Eliminate cow’s milk protein from mother’s diet if breastfed.
  • Change to hypoallergenic extensively hydrolysed/amino acid formula if bottle-fed.
  • Reassure parents that allergies to cow’s milk often resolve in early childhood.
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4
Q

Define acute appendicitis

A

Acute appendicitis is inflammation of the appendix, classically causing fever, abdominal pain (central then moving to RIF), nausea, anorexia and vomiting. It is the most common cause of a surgical abdomen in childhood.

It is rarely seen in children <5 yrs, but it is important not to miss, as around 90% perforate.

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5
Q

How would you investigate a differential of acute appendicitis further?

A
  • Clinical picture should guide treatment. Appendicitis is a progressive condition, so regular clinical reviews are important.

Other tests may be useful:

  • FBC, CRP, ESR (N.B. neutrophilia not always present)
  • Urine dip (N.B. WCC organisms are not uncommon given the proximity to the bladder)
  • Ultrasound scan to confirm diagnosis and look for complications (e.g. abscess, perforation)
  • Faecoliths may be seen on plain abdominal X-ray
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6
Q

How would you manage acute appendicitis?

A
  • Appendicectomy is the definitive treatment

- If the patient is unstable prior to laparotomy, fluid resuscitation and IV antibiotics may be needed.

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7
Q

Define asthma

A

Asthma is the most common chronic respiratory condition of childhood. It is a reversible condition characterised by the triad of bronchial inflammation, smooth muscle contraction and excessive mucus secretion. It classically presents with a polyphonic expiratory wheeze, cough, SOB and chest tightness, with symptoms being worse early in the morning and late at night. Asthma is often associated with other atopic conditions such as eczema and food allergy.

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8
Q

How would you investigate a differential of asthma further?

A
  • Examine the child
  • Diagnosis frequently clinical with younger children
  • Test response to bronchodilators +/- skin prick testing to identify triggers.
  • Continue to monitor with PEFR (looking for diurnal variation) and FEV1 (improvement of >12% after bronchodilator is characteristic of asthma)
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9
Q

How would you control asthma?

How would you manage asthma in an acute exacerbation?

A

The management of asthma is carried out in a step-wise fashion.

1) SABA (+ low dose ICS if uncontrolled with SABA alone)
2) Add LTR antagonist
3) Swap LTRA for LABA
4) Swap to MART (LABA + ICS)
5) Increase ICS dose and refer to specialist

In an acute exacerbation, management is as follows:

Moderate attack: keep patient calm, SABA 2-4 puffs (increase to 10 over 10 min if needed), PO prednisolone 1-2mg/kg

Severe attack: High flow oxygen, SABA via spacer (10 puffs) or nebulised salbutamol (2.5mg if <8yrs, 5mg if >8yrs), PO prednisolone, consider inhaled ipratropium/IV beta-2 agonist.

Life-threatening: High-flow oxygen, nebulised SABA (doses above), assess continuously and repeat PRN.
PO prednisolone, nebulised ipratropium. Consider IV beta-2 agonist, discuss with PICU in case of need for ventilation and other IV therapy.

If responding, continue treatment and discharge when stable on 4hrs of treatment. Continue oral prednisolone foe 3-7 days. Review inhaler technique and organise personalised follow-up.

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10
Q

Define impetigo

A

Localised, highly contagious Staph. or Strep. skin infection most commonly occurring in infants and young children. Lesions are usually on the face, neck and hands, and begin as erythematous macules. They then form vesicles that rupture, giving characteristic confluent honey-coloured crusted lesions.

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11
Q

How would you investigate a differential of impetigo further?

A

Clinical picture

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12
Q

How would you manage impetigo?

A
  • Topical antibiotics for mild cases e.g. mupirocin
  • PO antibiotics needed for more severe cases e.g. flucloxacillin
  • Children should not go to school until lesions are dry
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13
Q

Define rheumatic fever

A

It is a short-lived, multisystem autoimmune response to a preceding (2-6 weeks) infection with group A beta-haemolytic streptococcus (e.g. Strep. pyogenes - often skin or pharyngeal). The disease mainly affects children aged 5-15 years, and chronic rheumatic heart disease follows in 80%.

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14
Q

How would you investigate a differential of rheumatic fever further?

A

Examine - pericardial rub, significant murmur, migratory arthritis, erythema marginatum (pink macules on trunk and limbs, centre then fades giving a pink outline), Sydenham chorea.
Bloods - ESR, CRP, raised leukocytes

Echo - pericardial effusion, tamponade

ECG - prolonged P-R interval

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15
Q

How would you manage rheumatic fever?

A
  • Bed rest
  • High dose aspirin (monitor serum levels)
  • Corticosteroids if inflammation does not subside
  • Treat symptomatic heart failure with diuretics and ACEi
  • Pericardiocentesis if needed
  • Monthly IM benzathine penicillin/PO daily penicillin prophylaxis or erythromycin if allergic for prophylaxis (continued for 10 years after acute episode or the age of 21, whichever is longer)
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16
Q

Define scarlet fever

A

A group A Streptococcal infection precedes the symptoms of scarlet fever by a few days. The symptoms include headache, tonsillitis, rough maculopapular rash with perioral sparing and a white coated tongue, which may be sore and swollen

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17
Q

How would you investigate a differential of scarlet fever further?

A
  • Examine the child, as diagnosis may be clinical

- Throat swabs can be taken

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18
Q

How would you manage scarlet fever?

A

Penicillin V or erythromycin if allergic to prevent complications such as acute glomerulonephritis and rheumatic fever.

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19
Q

Define Staphylococcal scaled skin syndrome

A

An exfoliative staphylococcal toxin can cause separation of the epidermis through the granular cell layers. The skin can be separated on gentle pressure (Nikolsky’s sign), leaving areas of denuded skin, which generally heal without scarring. Children may also develop coryza, accompanied by a local purulent infection around the eyes, nose and mouth.

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20
Q

How would you investigate a differential of Staphylococcal scalded skin syndrome?

A

Make sure to rule out NAI

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21
Q

How would you manage Staphylococcal scalded skin syndrome?

A

IV flucloxacillin, analgesia and monitor fluid balance

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22
Q

Define bronchiolitis

A

Bronchiolitis is the most common serious respiratory infection of infancy. RSV is the pathogen in 80%, the remainder are accounted for by parainfluenza virus, rhinovirus, adenovirus, influenza virus, and human metapneumovirus. Inflammation of the small airways lead to a dry cough, dyspnoea (usually leading to a reduction in feeding) and coryza.

23
Q

How would you investigate a differential of bronchiolitis further?

A
  • Clinical picture on examination (fine end-expiratory crackles, expiratory wheeze, signs of increased work of breathing).
  • Pulse oximetry is the only investigation needed unless there is suspicion of respiratory failure, in which case CXR and blood gases are indicated.
24
Q

How would you manage bronchiolitis?

A

The management is essentially supportive. Most recover within 2 weeks

Criteria for admission:

apnoea (observed or reported)
persistent oxygen saturation of < 90% when breathing air
inadequate oral fluid intake (50–75% of usual volume)
severe respiratory distress – grunting, marked chest recession, or a respiratory rate over 70 breaths/minute.

  • Humidified oxygen delivered by head box or nasal cannulae (concentration guided by pulse oximetry)
  • Monitor for apnoea
  • Fluids may be needed IV or via NG tube
  • CPAP or mechanical ventilation required in a small proportion of admitted patients.
  • RSV is highly contagious, so good infection control measures are important
25
Q

Define bacterial meningitis

A

This is meningeal inflammation due to a bacterial infection. It remains a serious infection, with 10% mortality and considerable morbidity. Bacterial meningitis usually follows on from bacteraemia, and most of the damage is due to the host response rather than the microorganisms themselves. The inflammatory response below the meninges can cause a vasculopathy, which can lead to infarction and hydrocephalus.

The most common organisms are as follows:

<6 months: Group B Strep., E. coli, L. monocytogenes
6 months to 6 years: N. meningitides, H. influenza, S. pneumoniae
>6 years: N. meningitides, S. pneumoniae

26
Q

How would you investigate a differential of bacterial meningitis?

A
  • Firstly make sure that the child does not require immediate resuscitation.
  • FBC (inflammatory markers)
  • Glucose and blood gas (acidosis)
  • Coagulation screen (LP contraindicated in coagulopathy)
  • Blood cultures
  • Rapid antigen testing for causative organisms
  • Viral PCR
  • LP for CSF unless contraindicated
  • Consider TB, CT/MRI & EEG
27
Q

How would you manage bacterial meningitis?

A
  • IM Benzylpenicillin should be given before reaching hospital
  • IV cefotaxime (investigations SHOULD NOT delay this)
  • Supportive
  • Dexamethasone may help reduce complications (controversial)
28
Q

Define viral meningitis

A

Viral inflammation of the meninges is the most common form of meningitis. Most cases are self-limiting, and the most common causative organisms are enterovirus, EBV and adenovirus

29
Q

How would you investigate a differential of viral meningitis?

A
  • Firstly make sure that the child does not require immediate resuscitation.
  • FBC (inflammatory markers)
  • Glucose and blood gas (acidosis)
  • Coagulation screen (LP contraindicated in coagulopathy)
  • Blood cultures
  • Rapid antigen testing for causative organisms
  • Viral PCR
  • LP for CSF unless contraindicated
  • Consider TB, CT/MRI & EEG
30
Q

How would you manage viral meningitis?

A

Treatment is supportive, and most children make a full recovery.

31
Q

Define encephalitis

A

Encephalitis is inflammation of the brain parenchyma, and may be caused by direct invasion (HSV), postinfectious immunological response (after chicken pox) or a slow viral infection (HIV or SSPE)

32
Q

How would you investigate a differential of encephalitis?

A
  • Commonly clinically similar to meningitis, so investigations are similar
  • Firstly make sure that the child does not require immediate resuscitation.
  • FBC (inflammatory markers)
  • Glucose and blood gas (acidosis)
  • Coagulation screen (LP contraindicated in coagulopathy)
  • Blood cultures
  • Rapid antigen testing for causative organisms
  • Viral PCR
  • LP for CSF unless contraindicated
  • Consider TB, CT/MRI & EEG
33
Q

How would you manage encephalitis?

A

Treat encephalitis as HSV until it can be ruled out definitively. This is with high dose IV acyclovir

34
Q

Define cerebral palsy

A

CP is an umbrella term for a permanent disorder of movement and/or posture and of motor function due to a non-progressive abnormality in the developing brain. 80% of such injuries are antenatal, and only 10% are perinatal.

The motor disorders of CP are often accompanied by disturbances of cognition, communication, vision, perception, sensation, behaviour, seizure disorder and secondary musculoskeletal problems. Although the causative lesion is non-progressive and damage to the brain is static, clinical manifestations emerge over time, reflecting the balance between normal and abnormal cerebral maturation. Motor dysfunction is usually evident early, often from birth. If the brain injury occurs after the age of 2 years, it is diagnosed as acquired brain injury.

35
Q

How would you investigate a differential of cerebral palsy?

A

The diagnosis is made on clinical assessment, with high-risk patients being identified in the neonatal period.

The different sub types are:
Spastic (bilateral/unilateral)
Dyskinetic
Ataxic
Other
36
Q

How would you manage cerebral palsy?

A
  • Educate the parents as soon as possible
  • MDT approach involving: paeds, physio, OT, SALT, psychologist, specialist health visitor, dietician, social worker, school liason.
  • Botulinum toxin injections, anticonvulsants, cochlear implants and intrathecal baclofen may also help symptomatic management.
37
Q

Define congenital adrenal hyperplasia

A

Cortisol is inadequately produced due to enzyme defects, leading to a rise in ACTH, adrenal hyperplasia and an overproduction of androgenic cortisol precursors. This causes virilisation of female foetuses along with salt loss due to reduced aldosterone production. Salt loss may be the only feature in male foetuses, as excess virilisation does not occur until later in life.

38
Q

How would you investigate a differential of congenital adrenal hyperplasia?

A
  • Clinical examination of the neonate
  • U&E (hyponatraemia, hyperkalaemia)
  • Measurement of cortisol precursors in the blood
39
Q

How would you manage congenital adrenal hyperplasia?

A
  • Conservative: educate parents
  • Medical: glucocorticoid replacement in all, mineralocorticoid replacement if salt loser
  • Surgical: clitoral reduction and vaginoplasty
40
Q

Define atrial septal defect

A

There are two main types of ASD:

Secundum ASD (80% of ASDs)
Partial atrioventricular septal defect (AVSD or primum ASD).

Both present with similar symptoms and signs, but their anatomy is quite different. The secundum ASD is a defect in the centre of the atrial septum involving the foramen ovale.

Partial AVSD is a defect of the atrioventricular septum and is characterized by:
An interatrial communication between the bottom end of the atrial septum and the atrioventricular valves (primum ASD)
Abnormal atrioventricular valves, with a left atrioventricular valve which has three leaflets and tends to leak (regurgitant valve).

41
Q

How would you investigate a differential of atrial septal defect?

A
  • Clinical examination
  • CXR: cardiomegaly, enlarged pulmonary vessels
  • ECG: Secundum - RBBB, RAD. Primum - ‘superior’ QRS axis
  • Echocardiogram to define anatomy
42
Q

How would you manage atrial septal defect?

A

Children with significant ASD (large enough to cause right ventricle dilation) will require treatment. For secundum ASDs, this is by cardiac catheterization with insertion of an occlusion device, but for partial AVSD surgical correction is required. Treatment is usually undertaken at about 3 years to 5 years of age in order to prevent right heart failure and arrhythmias in later life.

43
Q

Define ventricular septal defect

A

VSDs are common, accounting for 30% of all cases of congenital heart disease. There is a defect anywhere in the ventricular septum, perimembranous (adjacent to the tricuspid valve) or muscular (completely surrounded by muscle). They can most conveniently be considered according to the size of the lesion.

44
Q

How would you investigate a differential of VSD?

A
  • Clinical examination
  • CXR
  • ECG
  • Echocardiogram
45
Q

How would you manage VSD?

A

Small VSD (<3mm) will close spontaneously.

Large VSD (>3mm): Drug therapy for heart failure is with diuretics, often combined with captopril. Additional calorie input is required. There is always pulmonary hypertension in children with large VSD and left-to-right shunt. This will ultimately lead to irreversible damage of the pulmonary capillary vascular bed. To prevent this, surgery is usually performed at 3 months to 6 months of age in order to:

  • Manage heart failure and faltering growth
  • Prevent permanent lung damage from pulmonary hypertension and high blood flow.
46
Q

Define persistent ductus arteriosus

A

The ductus arteriosus connects the pulmonary artery to the descending aorta. In term infants, it normally closes shortly after birth. In PDA it has failed to close by 1 month after the expected date of delivery due to a defect in the constrictor mechanism of the duct. The flow of blood across a PDA is then from the aorta to the pulmonary artery (i.e. left to right), following the fall in pulmonary vascular resistance after birth.

47
Q

How would you investigate a differential of PDA?

A
  • Clinical examination
  • No CXR or ECG changes unless PDA is large. If so, findings are similar to VSD
  • Echocardiogram
48
Q

How would you manage PDA?

A

Closure is recommended to abolish the lifelong risk of bacterial endocarditis and of pulmonary vascular disease. Closure is with a coil or occlusion device introduced via a cardiac catheter at about 1 year of age. Occasionally, surgical ligation is required

49
Q

Define tetralogy of Fallot

A

In tetralogy of Fallot, there are four cardinal anatomical features:

A large VSD
Overriding of the aorta with respect to the ventricular septum
Subpulmonary stenosis causing right ventricular outflow tract obstruction
Right ventricular hypertrophy as a result.

It is the most common cause of congenital cyanotic heart disease

50
Q

How would you investigate a differential of tetralogy of Fallot?

A
  • Clinical examination (differentials: transposition of the great arteries)
  • CXR: small, boot-shaped heart, concavity on the left heart border.
  • ECG: normal at birth, hypertrophy when older
  • Echocardiogram to define anatomy
51
Q

How would you manage tetrallogy of Fallot?

A

Initial management is medical, with definitive surgery at around 6 months of age. It involves closing the VSD and relieving right ventricular outflow tract obstruction, sometimes with an artificial patch which extends across the pulmonary valve.

Infants who are very cyanosed in the neonatal period require a shunt to increase pulmonary blood flow. This is usually done by surgical placement of an artificial tube between the subclavian artery and the pulmonary artery (a modified Blalock–Taussig shunt), or sometimes by balloon dilatation of the right ventricular outflow tract.

Hypercyanotic spells are usually self-limiting and followed by a period of sleep. If prolonged (beyond about 15 min), they should be given prompt treatment, according to need, with:
Sedation and pain relief (morphine is excellent)
Intravenous propranolol (or an α adrenoceptor agonist), which probably works both as a peripheral vasoconstrictor and by relieving the subpulmonary muscular obstruction that is the cause of reduced pulmonary blood flow
Intravenous volume administration
Bicarbonate to correct acidosis
Muscle paralysis and artificial ventilation in order to reduce metabolic oxygen demand.

52
Q

Define biliary atresia

A

There is progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree. Without intervention, chronic liver failure develops and death occurs within 2 years. The exact aetiology is unknown. Clinical presentation is with mild jaundice and pale stools (the colour may fluctuate but becomes increasingly pale as the disease progresses). They have normal birthweight followed by faltering growth. Hepatomegaly is often present initially, and splenomegaly develops due to portal hypertension.

53
Q

How would you investigate a differential of biliary atresia?

A
  • Raised conjugated bilirubin
  • Abnormal LFTs
  • Fasting abdominal ultrasound may demonstrate an absent or contracted gallbladder, although it may be normal.
  • Endoscopic retrograde cholangiopancreatography (ERCP) shows abnormal biliary tree
54
Q

How would you manage biliary atresia?

A
  • Surgical correction
  • Nutritional support and fat-soluble vitamin supplementation
  • May need liver transplant

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