Brainscape's Knowledge GenomeTM

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


See full index

Year 5 > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Murmur from patent ductus arteriosus

A

Continous Decresendo “machinery” murmur

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

Murmur in tetralogy of Fallot

A

Pulmonary stenosis

Ejection systolic murmur (loudest at pulmonary area)

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

Types of right to left shunt heart defects in children

A 
Ventricular septal defect (VSD)
Atrial septal defect (ASD)
Patent ductus arteriosis 
Transposition of the great arteries 
Tetralogy of Fallot (includes VSD, overriding aorta, pulmonary valve stenosis and right ventricular hypertrophy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which of the childhood heart diseases, actually causes cyanosis in children and why?

A

Transposition of the great arteries - because the right side of the heart pumps blood directly into the aorta and systemic circulation

Tetralogy of Fallot - as has right to left shunt (so blood doesn’t get oxygenated

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

Risk factors for patent ductus arteriosus (PDA)

A

Rubella infection

Prematurity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of patent ductus arteriosus

A

Shortness of breath
Difficulty feeding
Poor weight gain
Respiratory tract infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why does the patent ductus usually close in the first few days of life

A

Increased pulmonary flow which enhances prostaglandin clearance

Lack of prostaglandin results in closure of duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of patent ductus arteriosus

A

Indomethacin / Ibuprofen

These inhibit prostaglandin synthesis and help to close the connection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which genetic conditions are ventricular septal defects associated with?

A

Down’s syndrome

Turners syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Murmur heard in ventricular septal defect

A

Pan systolic murmur - prominently heard at left lower Sternal border in 3rd/4th intercostal space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Eisenmenger Syndrome

A

Where you get a right to left shunt - causing cyanosis

It occurs secondary to either arterial/ventricular septal defect or patent ductus arteriosus (note these are usually non cyanotic heart defects). After 1-2 years of life these left to right shunts become right to left shunts due to the increases pressure in the pulmonary vessels and pulmonary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the only definitive management of Eisenmenger syndrome

A

Heart-lung transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which genetic condition is coarction of the aorta associated with?

A

Turner’s syndrome

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

Presentation of coarction of the aorta in neonates

A 
Weak femoral pulses 
Systolic murmur - heard below the left clavicle 
Tachypnoea 
Poor feeding 
Grey and floppy baby
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is severe coarctation managed in neonates

A

Prostaglandin - to keep open ductus arteriosus (so blood can get to systemic system distal to coarctation)

Emergency surgery - to correct the coarctation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is ebstein’s anomaly

A

Congenital heart condition associated with lithium in pregnancy

Abnormally shaped tricuspid valve - leads to larger right atrium and smaller right ventricle
Causes right to left shunt between right and left atria (ASD) causing cyanosis

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

Cause of bronchiolitis

A

Respiratory syncytial virus (RSV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Common age of presentation for bronchiolitis

A

Children <1 year

Usually occurs in winter

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

Pathophysiology of bronchiolitis

A

Inflammation and infection in the bronchioles (the small airways of the lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Presentation of bronchiolitis

A 
Coryzal symptoms (snotty nose, sneezing, mucus, watery eyes)
Signs of respiratory distress 
Dyspnoea
Tachypnoea 
Poor feeding 
Mild fever (under 39)
Wheeze and crackles on auscultation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the signs of respiratory distress in children

A 
Raised RR
Use of accessory muscles of breathing - e.g, sternocleidomastoid, abdominal, intercostal 
Intercostal and subcostal recessions 
Nasal flaring 
Head bobbing 
Tracheal tugging 
Cyanosis (due to low oxygen sats)
Abnormal airway noises - e.g, wheezing, grunting, stridor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Reasons for admission to hospital in infants with bronchiolitis

A

Under 3 months
Pre existing condition - prematurity, Down’s syndrome, cystic fibrosis
Clinical dehydration
RR >70
Sats <92%
Moderate to severe respiratory distress signs
Apnoeas
Parents struggling/not confident managing at home

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

Management of bronchiolitis in hospital

A

Supportive management
Adequate fluids - orally, NG or IV depending on severity
Supplementary oxygen - if sats <92%
Ventilatory support if required

NOTE: little evidence for nebulised bronchodilators, steroids or abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the monoclonal antibody given for prophylaxis against bronchiolitis

Which babies are given it?

A

Palivizumab

Ex-Premature babies and those with congenital heart defects

Given once monthly - as levels of circulating antibodies decrease over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Differentiating between viral induced wheeze and asthma in children?

A

Viral induced wheeze:

  • Presents before 3 years of age
  • no atopic Hx
  • only occurs during viral infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Age of presentation of Croup

A

6 months - 2 years

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

Causes of croup

A

Parainfluenza virus (most common)
Influenza
RSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Presentation of Croup

A 
Increased work of breathing 
“Barking” cough 
Hoarse voice 
Stridor 
Low grade fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Management of croup

A

Mild - managed at home

Moderate-severe - oral Dexamethasone (prednisolone if dex is not available)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When to admit to hospital with Croup

A

Moderate/severe e.g, easily audible stridor at rest
Children <6 months
Patients with underlying conditions e.g, Down’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Cause of epiglottitis

Why is epiglottitis not seen regularly anymore

A

Haemophilus influenza type B

Due to HiB vaccine given to children

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

Presentation of epiglottitis

A 
Sore throat 
Stridor 
Drooling 
High fever 
Septic and unwell child 
Scared and quiet child
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

X-ray of neck finding in epiglottitis

A

Thumb sign - looks like thumb pressed into the trachea (causes by oedematous and swelled epiglottitis)

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

Management of epiglottitis

A

Senior paediatrician and anaesthetics

Secure the airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is laryngomalacia?

A

Where the supraglottic larynx is structured in a way that allows it to cause partial airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Common age of presentation of laryngomalacia

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Management of laryngomalacia

A

The problem usually resolves as the larynx matures and grows and is better able to support itself from flopping over the airway

Rarely tracheostomy or surgery may be needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Cause of whooping cough

A

Bordetella pertussis

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

Presentation of whooping cough

A

Sudden and recurring attacks of coughing with free periods in between (paroxysmal coughing)
Loud inspiratory whoop when coughing ends
Apnoeas
Patients may cough so much they faint or vomit

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

Management of whooping cough

A

Notify public health
Supportive care
Macrolide abx e.g, erythromycin can be beneficial in early stages

Symptoms typically resolve within 8 weeks

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

What is chronic lung disease of prematurity (CLDP)?

A

Respiratory distress syndrome occurring in premature babies (those born before 28 weeks gestation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What measure is taken to prevent chronic lung disease of prematurity (CLDP)

A

Giving corticosteroids (betamethasone) to mothers that show signs of premature labour (<36 weeks)

This can help speed up the development of the fetal lungs before birth and reduce the risk of CLDP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the number of people that are carriers of the cystic fibrosis gene in the UK

A

1 in 25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is an early sign of cystic fibrosis in newborns

A

Meconium ileus - where meconium is not passed within the first 24 hours

This can present with abdominal distension and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is cystic fibrosis usually diagnosed at birth?

What are the other ways of diagnosing it?

A

Using the newborn blood spot test

Sweat test (gold standard) - pilocarpine is applied to patch of skin and electrodes are passed through causing skin to sweat, this is then tested in the lab for chloride concentration 
Genetic testing - can be performed in pregnancy by amniocentesis or chorionic villous sampling, or as a blood test after birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Symptoms of cystic fibrosis

A 
Chronic cough 
Thick sputum production 
Recurrent respiratory tract infections 
Loose, greasy stools 
Abdominal pain and bloating 
Salty skin
Failure to thrive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Management of cystic fibrosis

A

Chest Physiotherapy
High calorie diet
CREON tablets - to help with pancreatic insufficiency
Prophylaxtic abx - flucloxacillin to prevent staph aureus
Bronchodilators
Nebulised DNase (dornase Alfa) - can help with secretions
Vaccinations - including pneumococcal, influenza and varicella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the two most common infections in cystic fibrosis to remember?

A

Staph aureus - patients take prophylactic flucloxacillin for this
Pseudomonas - once this is colonised it is particularly hard to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Life expectancy of a patient with cystic fibrosis

A

47 years

50
Q

Differentials for vomiting in children

A 
Gastro-oesophageal reflux  
Pyloric stenosis 
Gastroenteritis 
Appendicitis 
Intussusception 
Meningitis
51
Q

Management of gastro oesophgeal reflux in infants

A

Encourage small meals, avoid over feeding
Burning regularly to help milk settle
Keep baby upright after feeds
Can use gaviscon rich feeds or ranitidine liquid formula

52
Q

Common causes of gastroenteritis in children

A

Rotavirus
Norovirus
E.coli (consider e.coli 0157 in bloody diarrhoea and HUS)
Campylobacter (travellers diarrhoea)

53
Q

School isolation in gastroenteritis

A

Children need to stay off school until 48 hours after symptoms have completely resolved

54
Q

Pathophysiology of coeliac disease

A

Autoantibodies produced in response to exposure to gluten
Autoantibodies then attack the epithelial cells of intestine and lead to inflammation in small bowel
Causes atrophy of the intestinal villi
Leads to problems with absorption

55
Q

Symptoms of coeliac disease in children

A 
Failure to thrive 
Diarrhoea 
Fatigue 
Weight loss 
Mouth ulcers
56
Q

What is the rash associated with coeliac disease called?

A

Dermatitis herpetiformis - blistering skin rash typically occurring on abdomen

57
Q

Which endocrine condition is closely linked with coeliac disease

A

Type 1 diabetes

58
Q

What are the auto antibodies produced in coeliac disease

A 
Tissue trans glutaminase (anti-TTG)
Endomysial antibodies (EMAs)

These are both types of IgA antibodies and so you must test levels of IgA antibodies first - as if these are low you may get a false negative

59
Q

What is biliary atresia?

A

Congenital condition
Where section of bile duct is either narrowed or absent resulting in cholestatis
This results in accumulation of conjugated bilirubin

60
Q

What is Hirschsprung disease?

A

Congenital condition

Results in absence of nerve cells in the myenteric plexus in the distal bowel and rectum

61
Q

How does Hirschsprung disease present?

A 
Delayed passage of meconium after birth (>48 hours)
Abdominal distention 
Vomiting 
Chronic constipation 
Failure to thrive/poor weight gain
62
Q

How is Hirschsprung disease diagnosed?

A

Rectal biopsy - will show absence of ganglion cells

63
Q

Management of Hirschsprung disease

A

Surgical removed of a ganglionic section of bowel

64
Q

What is intussusception?

A

Where there is telescoping of the bowel - the bowel folds in on itself

65
Q

What age does intussusception usually present?

A

Age 6 months - 2 years

66
Q

Presentation of intussusception

A 
Severe colicky pain 
Pale, lethargic and unwell child 
Red currant jelly stool 
Sausage shaped mass in RUQ
Vomiting 
Intestinal obstruction
67
Q

Diagnosis of intussusception

A

USS - will show target sign

68
Q

Management of intussusception

A

Theraputic enemas - can be used to try to reduce the intussusception

Surgical reduction may be necessary

69
Q

Pathophysiology of pyloric stenosis

A

Hypertrophy (thickening) of the pylorus in the stomach
Prevents food from traveling into the duodenum
Infants usually present with projectile vomiting

70
Q

Blood gas seen in pyloric stenosis

A

Hypochlorite metabolic alkalosis - as the baby is vomiting up HCL from the stomach

71
Q

Management of pyloric stenosis

A

Laparoscopic pyloromyotomy (Ramstedt’s operation)

72
Q

When would you investigate further in UTIs in children?

A

All children under 6 months with first UTI - USS within 6 weeks
Children with recurrent UTIs - USS within 6 weeks
Children with atypical UTI - USS during illness

DMSA scans should be used 4-6 months after the illness to assess for damage from recurrent or atypical UTIs

73
Q

What is a DMSA Scan

A

Dimercaptocuccinic acid scan - involves injecting radioactive material (DMSA) and using a gamma camera to assess how well the material is taken up by the kidneys

Where there are patches of the kidney that have not taken up the material - this indicates scarring that may be as a result of a previous UTI

74
Q

What is vesico-ureteric reflux (VUR)?

A

Where there is a backflow or urine from the bladder into the ureters

This predisposes children to developing UTIs and subsequent renal scarring

75
Q

How is vesico-ureteric reflux diagnosed?

A

Using a micturating cystourethrogram (MCUG)
- contrast injected into bladder and taking a series of X-ray films to determine whether the contrast is refluxing back into the ureters

76
Q

How is vesico-ureteric reflux managed?

A

Avoiding constipation
Avoiding excessively full bladder
Prophylactic abx
Surgical input from paediatric urology

77
Q

Difference between primary and secondary nocturnal enuresis

A

Primary - where the child has never managed to be consistently dry at night

Secondary - where the child has previously been dry for at least 6 months

78
Q

Causes of nocturnal enuresis

A 
Overactive bladder 
Psychological distress
Constipation 
UTIs 
Type 1 diabetes
79
Q

Management of nocturnal enuresis

A

Lifestyle changes - reduced fluid in evenings, encouragement and positive reinforcement
Treat underlying factors - e.g, constipation
Enuresis alarms
Pharmacological treatment - e.g Desmopression

80
Q

What are the different causes of neonatal jaundice?

A 
Physiological Jaundice - e.g, in prematurity 
Breast milk jaundice 
Biliary atresia 
Haemolytic disease of the newborn 
Sepsis 
G6PD deficiency
81
Q

When would you be worried in neonatal jaundice?

A

If jaundice presents in first 24 hours following birth

If jaundice persists >2 weeks following birth (>3 weeks for premature babies)

82
Q

What is the pathophysiology of breast mild jaundice?

A

Components of breast milk inhibit the ability of liver to process bilirubin

Breast milk may lead to slowing of peristalsis in bowels - increasing reabsorption of bilirubin

83
Q

Why is jaundice in newborns usually a normal physiological process ?

When would this be expected to end

A

Because fetus and neonate have less developed lever function
So there is a normal rise in bilirubin shortly after birth

Usually resolves by 10 days

84
Q

Management of jaundice in newborns

A

Monitor unconjugated bilirubin levels
May require phototherapy
Extremely high levels may require exchange transfusion - removing the blood from the neonate and replacing it with donor blood

85
Q

How does phototherapy work

A

Converts unconjugated bilirubin into isomers that can be excreted in bile and urine without requiring conjugation in the liver

86
Q

What is the risk of excessive bilirubin levels in neonates

A

Kernicterus - type of brain damage caused by excessive bilirubin levels

87
Q

Red flags in development milestones

A

Not able to hold object at 5 months
Not sitting unsupported at 12 months (should be 6 months)
Not standing independently at 18 months
Not walking independently at 2 years (should be walking by 15 months)
No words at 18 months (should be saying words by 1 year)

88
Q

What is the age in which febrile convulsions present?

A

6 months - 5 years

89
Q

What is the difference between cyanotic breath holding spells and reflex anoxic seizures

A

Cyanotic breath holding spell - LOC and seizure after child is really upset and crying so forget to breath

Reflex anoxic seizures - LOC and seizure after the child is startled

90
Q

What is cerebral palsy?

A

Permanent neurological problems resulting from damage to the brain at around the time of birth

91
Q

Causes of cerebral palsy

A 
Maternal infections 
Trauma during pregnancy 
Birth asphyxia 
Pre term birth 
Meningitis in neonate 
Severe neonatal jaundice
92
Q

What are the different types of cerebral palsy?

A

Spastic - hypertonia due to damage to upper motor neurons
Dyskinetic - damage to basal ganglia
Ataxic - damage to cerebellum

93
Q

Signs and symptoms of cerebral palsy in children?

A 
Failure to meet milestones 
Increased or decreased tone in limbs 
Hand preference before 18 months old 
Problems with feeding/swallowing 
Problems with coordination, speech or walking
94
Q

Management of cerebral palsy

A

Multidisciplinary:
Physiotherapy
Occupational therapy - adaptions to everyday living
Speech and language therapy

Medications - e.g, baclofen for spastic muscles

95
Q

What is the most common type of muscular dystrophy?

A

Duchennes muscular dystrophy

96
Q

What is the common sign seen in children which indicates muscular dystrophy?

A

Gower’s sign

Children using hands and knees to get from sitting to standing - this is because the muscles around pelvis are not strong enough to get their body up without help of arms

97
Q

Genetic pattern of inheritance in duchennes muscular dystrophy

A

X-linked recessive

Defective gene for dystrophin - a protein which helps hold muscles together at the cellular level

98
Q

Usual age of presentation of duchennes muscular dystrophy

A

Age 3-5 years

99
Q

Life expectancy of patients with duchennes muscular dystrophy

A

25-35 years

100
Q

Pathophysiology of cow’s milk protein allergy

A

IgE mediated
Hypersensitivity to protein in cows milk
More common in formula fed babies

Non allergic

101
Q

Presentation of cows milk protein allergy

A

Presents before age of 1 - when switching from breast to formula milk (or through breastfed milk when mother is consuming dairy products)
GI symptoms - bloating, coming, diarrhoea
Allergic symptoms - hives, angioedema, cough, wheeze, sneezing, watery eyes, eczema

102
Q

Diagnosis of cows milk protein intolerance

A

Skin prick testing

103
Q

Management of cows milk protein intolerance

A

Breast feeding milk - avoid dairy
Replace formula with hydrolysed formulas - where proteins are already broken down so they don’t trigger immune response

Most children will outgrow cows milk protein intolerance by age 3 (often earlier) - so every 6 months infants can be trial on milk ladder e.g, malt milk biscuits and slowly build up towards diet containing milk

104
Q

Features of kawasakis disease

A 
Fever for more than 5 days 
Strawberry tongue 
Cracked lips 
Cervical lymphadenopathy 
Bilateral conjunctivitis
105
Q

Management of kawasakis disease

A

High dose aspirin - due to risk of thrombus

IV immunoglobulins - to reduce risk of coronary artery aneurysms

106
Q

Infectivity of chicken pox

A

4 days before rash

5 days after rash first appeared

107
Q

Presentation of chicken pox

A

Fever initially
Itchy rash starting on head/trunk and spreading
Systemic upset usually mild

108
Q

Management of chicken pox

A

Keep child cool
Calamine lotion
School exclusion - until lesions are dry and have crusted over (usually around 5 days after onset of rash)

109
Q

Why should you avoid taking NSAIDs in chicken pox

A

These can increase the risk of bacterial infection of the lesions

110
Q

Clinical features of measles

A

Conjunctivitis
Fever
Koplik spots - white spots on buccal mucosa
Rash - starts behind ears then spreads to whole body (maculopapular rash)

111
Q

Most common complication of measles

A

Otitis media

112
Q

Features of scarlet fever

A 
Fever - lasting 24/48 hours 
Headache 
Nausea/vomiting 
Sore throat 
Strawberry tongue
Rash - fine punctuate erythema (pinhead) generally on torso (described as having a sandpaper texture)
113
Q

Management of scarlet fever

A

Abx - oral penicillin V for 10 days

114
Q

Complications of scarlet fever

A

Otitis media
Rheumatic fever - 20 days post infection
Acute glomerulonephritis - 10 days post infection

115
Q

How does threadworms usually present

A

Perinatal itching (particularly at night)

116
Q

Management of threadworms

A

Hygiene measures for household

Mebendazole (medication to treat worms) - single dose given to all household members

117
Q

Virus causing roseola infantum

A

Human herpes virus 6 (HHV6)

118
Q

Typical age of presentation in roseola infantum

A

6 months - 2 years

119
Q

Presentation of roseola infuntum

A

High fever of rapid onset
Maculopapular rash starting on trunk and limbs
Febrile convulsions occur in 10-15%

120
Q

Virus causing hand foot and mouth disease

A

Coxsackie A16

Year 5 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions