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3a > Paeds > Flashcards

Paeds Flashcards

1
Q

List the coryzal symptoms

A
  • Runny/snotty nose
  • Watery eyes
  • Sneezing
  • Mucus in throat
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2
Q

List the signs of respiratory distress

A
  • Raised resp rate
  • Use of accessory muscles - scalene, sternocleidomastoid, pectoralis major, trapezius, external intercostals
  • Head bobbing
  • Nasal flaring
  • Recessions/indrawing of chest - intercostal and abdo muscles so ribs are visible
  • Supraclavicular retractions
  • Tracheal tugging
  • Cyanosis
  • Abnormal airway noises
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3
Q

List the abnormal airway noises

A

Wheeze - narrowing of airways leading to whistle on expiration
Grunt -
Stridor - obstruction of upper airway leading to high pitch sound on inspiration

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4
Q

What is bronchiolitis and what causes it?

A

Inflammation or infection of bronchioles usually caused by Respiratory Syncytial Virus
Swollen bronchioles and mucus
Obstruction to airflow

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5
Q

How does bronchiolitis present and typical patient?

A

Under 1 year but usually 6 months
Can be up to 2 years if premature

Poor feed
Resp distress
Tachypnoea
Mild fever (39 degrees)
Apnoea

More likely to develop viral induced wheeze later on

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6
Q

How does the chest sound in bronchiolitis?

A

Harsh breath sounds
Wheeze
Crackles

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7
Q

Manage bronchiolitis?

A

Supportive
Ensure adequate intake
Avoid full stomach as this restricts breathing
Nasal drops/clearing
Supplementary O2
Ventilation if severe

Admission if under 3 months, pre existing condition, less than normal intake of milk, dehydrated, decreased resp rate or O2 sats low

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8
Q

How does virally induced wheeze present and typical patient?

A

fever, coryzal, cough 1-2 days proceeding SOB, resp distress

Under 3
hereditary element so may have a family history
increased risk of asthma in children prone to it

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9
Q

What is virally induced wheeze and what causes it?

A

Inflammation and oedema caused by RSV or rhinovirus
This triggers smooth muscle to constrict which leads to restricted airflow
= wheeze and resp distress

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10
Q

Virally induced wheeze vs asthma?

A

asthma - history of atopy, triggers eg. cold weather, pets, dust, emotions, exercise
VIW - presents before 3, symptoms only during viral infections

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11
Q

How does the chest sound in Virally induced wheeze?

A

expiratory wheeze throughout chest

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12
Q

Listening to chest: Harsh breath sounds, Wheeze, Crackles means?

A

Bronchiolitis

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13
Q

Listening to chest: focal wheeze means?

A

Obstruction such as inhalation of an object or a tumour

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14
Q

Listening to the chest: Expiratory wheeze throughout chest means?

A

Asthma
Virally induced wheeze

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15
Q

What is acute asthma and how does it present?

A

A rapid deterioration in symptoms

  • progressive worsening SOB
  • resp distress
  • tachypnoea
  • exp wheeze throughout chest
  • chest may sound tight
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16
Q

How might the chest sound in acute asthma?

A
  • expiratory wheeze throughout chest
  • tight
  • silent chest (urgent)
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17
Q

List the asthma treatment ladder?

A

???

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18
Q

How would a Moderate asthma status be categorised?

A

Moderate – PEFR more than 50–75% best or predicted and normal speech

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19
Q

How would a Severe asthma status be categorised?

A

Severe - PEFR 33–50% best or predicted OR RR of 30/min in 5 - 12 years, and 40/min in 2 - 5 OR pulse rate of 125/min in 5 - 12 years, and 140/min in 2 - 5
OR inability to complete sentences in one breath, accessory muscle use, or inability to feed (infants), with oxygen saturation of at least 92%

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20
Q

How would a Life threatening asthma status be categorised?

A

Life threatening - PEFR less than 33% best or predicted, or oxygen saturation of less than 92%, or altered consciousness, or exhaustion, or cardiac arrhythmia, or hypotension, or cyanosis, or poor respiratory effort, or silent chest, or confusion

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21
Q

What type of inheritance is cystic fibrosis?

A

autosomal recessive

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22
Q

Explain the pathophysiology of cystic fibrosis

A

It is caused by a genetic mutation of the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7. This gene codes for transmembrane cAMP-activated chloride channels.
The defect leads to defective ion transport, airway surface liquid depletion and defective mucocilliary clearance.
The build up of mucus causes obstruction, infection and inflammation.

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23
Q

Which gene is mutated in cystic fibrosis and what does it code for? What is the most common variant of this mutation?

A

the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7
it codes transmembrane cAMP-activated chloride channel
most common variant is the delta-F508

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24
Q

3 key consequences of cystic fibrosis?

A

Thick pancreatic and biliary secretions
Low volume thick airway secretions
Congenital bilateral absence of the vas deferens in males

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25
Q

How does CF affect the pancreas, intestines and liver?

A

CF causes thick pancreatic and biliary secretions.
The secretions cause blockage of the ducts, resulting in a lack of digestive enzymes (such as pancreatic lipase) in the digestive tract.
This leads to poor nutrient absorption in the intestines.

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26
Q

How does CF affect the lungs?

A

CF causes low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation, widened airways and susceptibility to airway infections

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27
Q

Why are men with CF usually infertile?

A

There is usually congenital bilateral absence of the vas deferens in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility

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28
Q

how is CF screened? what other condition at birth may point towards CF? how does it present?

A

screened for at birth using the newborn bloodspot test

babies may have meconium ileus:
20% of babies with CF have thick and sticky meconium
it gets stuck and obstructs the bowel
it presents as not passing meconium within 24 hours, abdominal distention and vomiting.

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29
Q

What condition may be suggested by the following: recurrent lower respiratory tract infections, failure to thrive or pancreatitis? Name other symptoms.

A

cystic fibrosis

other symptoms:
Chronic cough
Thick sputum production
Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
Abdominal pain and bloating
Parents may report the child tastes particularly salty when they kiss them, due to the concentrated salt in the sweat
Poor weight and height gain (failure to thrive)

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30
Q

examination findings on a child with suspected CF?

A

Low weight or height on growth charts
Nasal polyps (due to the chronic congestion and infection that CF can cause)
Finger clubbing (caused by chronically low blood levels of oxygen)
Crackles and wheezes on auscultation
Abdominal distention

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31
Q

what causes clubbing in children?

A

Hereditary clubbing
Cyanotic heart disease
Infective endocarditis
Cystic fibrosis
Tuberculosis
Inflammatory bowel disease
Liver cirrhosis

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32
Q

3 methods of diagnosis for CF?

A

Newborn blood spot testing is performed on all children shortly after birth and picks up most cases
The sweat test is the gold standard for diagnosis
Genetic testing for CFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling, or as a blood test after birth

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33
Q

how is the sweat test performed for CF? what is the diagnostic chloride concentration for cystic fibrosis?

A

patch of skin is chosen for the test, Pilocarpine is applied to the skin. Electrodes are placed either side of the patch and a small current is passed between the electrodes. This causes the skin to sweat. The sweat is absorbed with lab issued gauze or filter paper and sent to the lab for testing for the chloride concentration. The diagnostic chloride concentration for cystic fibrosis is more than 60mmol/l.

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34
Q

What are the 2 key bacteria that CF patients are at risk of? What is taken to prevent one of these? What is used to treat the other?

A

Staph aureus - patients take prophylactic flucloxacillin to prevent infection

Pseudomonas aeruginosa - hard to treat and worsens prognosis, can often become resistant to antibiotics hence CF children should avoid each other to minimise transmission. can be treated with long term nebulised antibiotics such as tobramycin. Oral ciprofloxacin is also used.

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35
Q

How is CF managed? how often are they monitored?

A

Chest physiotherapy - clears mucus
exercise - improve resp function
high calorie diet - for malabsorption
CREON tablets - contain digestive enzymes
prophylactic flucloxacillin - to reduce staph aureus infections
treating chest infections as they occur
bronchodilators eg. salbutamol
nebulised DNase - breaks down dna material in resp secretions to make them less thick
vaccinations up to date
lung and liver transplant in end stage
Fertility treatment involving testicular sperm extraction for infertile males
Genetic counselling

followed up every 6 mponths

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36
Q

conditions CF patients are at risk of?

A

90% of patients with CF develop pancreatic insufficiency
50% of adults with CF develop cystic fibrosis-related diabetes and require treatment with insulin
30% of adults with CF develop liver disease
Most males are infertile due to absent vas deferens

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37
Q

What is epiglottitis? Caused by which pathogen? How serious is it and why?

A

Inflammation and swelling of the epiglottis caused by infection, typically with haemophilus influenza type B.

The epiglottis can swell to the point of completely obscuring the airway within hours of symptoms developing. Therefore, epiglottitis is a life threatening emergency.

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38
Q

Epiglottitis vs croup?

A

Both upper airway infections

epiglottitis = unwell looking, abrupt onset, high fever, usually more severe stridor, minimal/absent cough, unable to swallow/speak

croup = well looking, viral prodrome and slower onset, moderate fever, mild stridor, barking cough, able to swallow

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39
Q

you see an unvaccinated child presenting with a fever, sore throat and difficulty swallowing. They are sitting forward and drooling. What is this? Why is being unvaccinated relevant?

A

Epiglottitis

Epiglottitis is now rare due to the routine vaccination program, which vaccinates all children against haemophilus.

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40
Q

Typical epiglottitis presentation?

A

Patient presenting with a sore throat and stridor
Drooling
Tripod position, sat forward with a hand on each knee
High fever
Difficulty or painful swallowing
Muffled voice
Scared and quiet child
Septic and unwell appearance

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41
Q

Describe an xray of a child with epiglottitis? What causes this? What can the xray exclude?

A

Performing a lateral xray of the neck shows a characteristic “thumb sign” or “thumbprint sign”. This is a soft tissue shadow that looks like a thumb pressed into the trachea.

This is caused by the oedematous and swollen epiglottis.

Neck xrays are also useful for excluding a foreign body.

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42
Q

You see a quiet child presenting with a high fever, stridor and pain when swallowing. What should you NOT do? What is your first step to manage them?

A

Epiglottitis

Do not distress the patient as this could prompt closure of the airway. Do not perform any investigations as this could leave them upset - leave them in their comfort zone.

The most important thing is to alert the most senior paediatrician and anaesthetist available.

43
Q

What is the main management of epiglottitis?

A

Secure the airway!

Most patients don’t need intubation, but there is an ongoing risk of sudden upper airway closure, so preparations to perform intubation (tracheostomy) should be made.

44
Q

Which additional treatments are used in Epiglottitis after the airway is secured?

A

Additional treatment once the airway is secure:
IV antibiotics (e.g. ceftriaxone)
Steroids (i.e. dexamethasone)

45
Q

Name the common complication of epiglottitis. What is it lol?

A

A common complication to be aware of is the development of an epiglottic abscess, which is a collection of pus around the epiglottis. This also threatens the airway, making it a life threatening emergency. Treatment is similar to epiglottitis.

46
Q

What condition presents similarly to CF? What type of inheritance? What does it lead to?

A

Primary ciliary dyskinesia (PCD) or Kartagner’s syndrome

An autosomal recessive condition which causes dysfunction of the motile cilia around the body, most notably in the respiratory tract. This leads to a buildup of mucus in the lungs, providing a great site for infection that is not easily cleared. This leads to a similar respiratory presentation to cystic fibrosis, with frequent and chronic chest infections, poor growth and bronchiectasis.

47
Q

Other than the lungs, where else can Primary ciliary dyskinesia affect the cilia? What does this lead to?

A

he cilia in the fallopian tubes of women and the tails (flagella) of the sperm in men, leading to reduced or absent fertility.

48
Q

In which population is Primary ciliary dyskinesia most common and why?

A

It is more common in populations where there is consanguinity, meaning the parents are related to each-other. Consanguinity increases the risk of a child having two copies of the same recessive genetic mutation.

49
Q

What is Kartagner’s Triad?

A

Paranasal sinusitis
Bronchiectasis
Situs Inversus

50
Q

What is Situs Inversus? What about Dextrocardia? Prognosis?

A

a condition where all the internal (visceral) organs are mirrored inside the body. Therefore the heart is on the right, the stomach is on the right and the liver is on the left.

Dextrocardia is when only the heart is reversed.

Situs inversus on its own does not cause any problems, and patients can expect to live a normal life. A small number have associated congenital heart disease, such as transposition of the great arteries.

51
Q

How are situs inversus and primary ciliary dyskinesia related to eachother in terms of stats?

A

25% of patients with situs inversus will have primary ciliary dyskinesia. 50% of patients with primary ciliary dyskinesia have situs inversus.

52
Q

What is the key investigation to diagnose primary ciliary dyskinesia?

A

take a sample of the ciliated epithelium of the upper airway and examine the action of the cilia
A sample can be obtained through nasal brushing or bronchoscopy. Often several samples are required.

53
Q

How to manage primary ciliary dyskinesia?

A

Management is similar to cystic fibrosis and bronchiectasis with daily physiotherapy, a high calorie diet and antibiotics.

54
Q

A premature baby presents with low oxygen sats, poor feeding, and crackles and wheezes on chest auscultation. What could this be? How is it diagnosed and what will this child require?

A

Chronic lung disease of prematurity (CLDP), also known as bronchopulmonary dysplasia

Diagnosis is made based on chest xray changes. These babies suffer with respiratory distress syndrome and require oxygen therapy or intubation and ventilation at birth.

55
Q

How can Chronic Lung Disease of Prematurity be prevented?

A

Giving corticosteroids (e.g. betamethasone) to mothers that show signs of premature labour at less than 36 weeks gestation can help speed up the development of the fetal lungs before birth and reduce the risk of CLDP.

Once the neonate is born:
Using Continuous positive airway pressure (CPAP) rather than intubation and ventilation when possible
Using caffeine to stimulate the respiratory effort
Not over-oxygenating with supplementary oxygen

56
Q

How to manage a baby with Chronic Lung Disease of Prematurity?

A

Babies may be discharged from the neonatal unit on a low dose of oxygen to continue at home, for example 0.01 litres per minute via nasal cannula. They are followed up to wean the oxygen level over the first year of life.

require protection against respiratory syncytial virus (RSV) to reduce the risk and severity of bronchiolitis. This involves monthly injections of a monoclonal antibody against the virus called palivizumab.

57
Q

What is croup? Typical age?

A

an acute infective upper respiratory tract infection causing oedema in the larynx. It typically affects children aged 6 months to 2 years

58
Q

What is the classic cause of croup? What other viruses are common causes?

A

parainfluenza virus

also:
Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

59
Q

Why did croup previously have a high mortality?

A

Croup used to be caused by diphtheria. Croup caused by diphtheria leads to epiglottitis and has a high mortality. Vaccination mean that this is very rare in developed countries.

60
Q

How does croup present?

A

Increased work of breathing
“Barking” cough, occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever

61
Q

How is croup managed?

A

Most cases can be managed at home with simple supportive treatment (fluids and rest).
hand washing and staying off school
Oral dexamethasone is very effective. This is usually a single dose of 150 mcg/kg, which can be repeated if required after 12 hours. Prednisolone is sometimes used as an alternative where dexamethasone in not available (e.g. by GPs).

62
Q

Stepwise options in severe croup to get control of symptoms?

A

Oral dexamethasone
Oxygen
Nebulised budesonide
Nebulised adrenalin
Intubation and ventilation

63
Q

Name common non-organic causes for abdo pain

A

Non-organic:
Constipation
urinary tract infection
coeliac disease
inflammatory bowel disease
IBS
tonsilitis

in adolescent girls:
dysmenorrhoea
ovulation pain
ectopic pregnancy
pelvic inflammatory disease
ovarian torsion
pregnancy

64
Q

Name common surgical causes for abdo pain

A

surgical causes:
appendicitis - central abdo pain spreads to right iliac fossa
intussusception - colicky non specific, red currant jelly stools
bowel obstruction - pain, distension, constipation, vomiting
testicular torsion - sudden onset unilateral testicular pain, abdo pain, nausea, vomiting

65
Q

Abdo red flag symptoms to look out for?

A

weight loss or faltering growth
persistent or bilious vomiting (bright green)
severe chronic diarrhoea
fever
rectal bleeding
dysphagia
night time pain
abdo tenderness

66
Q

what can abdo pain, anaemia and raised inflammatory markers indicate? what might a stool sample show?

A

IBD. Raised faecal calprotectin

67
Q

what can abdo pain with anaemia and raised anti-TTG indicate? what other antibodies could be raised?

A

coeliacs. anti-EMA

68
Q

A child presents with abdo pain, nausea, pallor and reduced appetite. The examination is normal. what else could this be? what other symptoms may they have? how should it be managed?

A

abdominal migraine
may also have:
Headache
Photophobia
Aura

treating acute attacks and preventative measures

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

prevent:
Pizotifen, a serotonin agonist (needs to be withdrawn slowly when stopping as it is associated with withdrawal symptoms such as depression, anxiety, poor sleep and tremor)
Propranolol, a non-selective beta blocker
Cyproheptadine, an antihistamine
Flunarazine, a calcium channel blocker

69
Q

why should preventative medication for abdominal migraines be withdrawn slowly?

A

Pizotifen is the main preventative medication - It needs to be withdrawn slowly when stopping as it is associated with withdrawal symptoms such as depression, anxiety, poor sleep and tremor.

70
Q

what is recurrent abdo pain?

A

when a child presents with repeated episodes of abdominal pain without an identifiable underlying cause. it often corresponds to stressful life events, such as loss of a relative or bullying

the leading theory for the cause is increased sensitivity and inappropriate pain signals from the visceral nerves (the nerves in the gut) in response to normal stimuli.

71
Q

how can recurrent abdo pain be managed?

A

Distracting the child from the pain with other activities or interests
Encourage parents not to ask about or focus on the pain
Advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise and reducing stress
Probiotic supplements may help symptoms of irritable bowel syndrome
Avoid NSAIDs such as ibuprofen
Address psychosocial triggers and exacerbating factors
Support from a school counsellor or child psychologist

72
Q

features in a history/exam that suggest constipation?

A

Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools
Abdominal pain
Holding an abnormal posture, referred to as retentive posturing
Rectal bleeding associated with hard stools
Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
Hard stools may be palpable in abdomen
Loss of the sensation of the need to open the bowels

73
Q

what is Encopresis?

A

faecal incontinence. This is not considered pathological until 4 years of age
usually a sign of chronic constipation where the rectum becomes stretched and looses sensation
Large hard stools remain in the rectum and only loose stools are able to bypass the blockage and leak out, causing soiling.

74
Q

rare causes of encopresis?

A

Spina bifida
Hirschprung’s disease
Cerebral palsy
Learning disability
Psychosocial stress
Abuse

75
Q

lifestyle factors which can contribute to/increase risk of constipation?

A

Habitually not opening the bowels
Low fibre diet
Poor fluid intake and dehydration
Sedentary lifestyle
Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)

76
Q

describe the process of desensitisation of the rectum

A
  1. patients develop a habit of not opening their bowels and ignore the sensation of a full rectum
  2. Over time they loose the sensation of needing to open their bowels, and they open their bowels even less frequently.
  3. They start to retain faeces in their rectum.
  4. This leads to faecal impaction (large, hard stool blocks the rectum)
  5. Over time the rectum stretches as it fills with more and more faeces leading to further desensitisation

The longer this goes on, the more difficult it is to treat the constipation and reverse the problem.

77
Q

Secondary causes of desensitisation of the rectum

A

Hirschsprung’s disease
Cystic fibrosis (particularly meconium ileus)
Hypothyroidism
Spinal cord lesions
Sexual abuse
Intestinal obstruction
Anal stenosis (can be caused by overuse of laxatives)
Cows milk intolerance

78
Q

What is Hirschsprung’s disease

A

a birth defect in which some nerve cells are missing in the large intestine, so a child’s intestine can’t move stool and becomes blocked

79
Q

Red flags to look out for with a history of constipation and what could be causing them?

A

Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
Vomiting (intestinal obstruction or Hirschsprung’s disease)
Ribbon stool (anal stenosis)
Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
Acute severe abdominal pain and bloating (obstruction or intussusception)

80
Q

complications of desensitisation of the bowel?

A

Pain
Reduced sensation
Anal fissures
Haemorrhoids
Overflow and soiling
Psychosocial morbidity

81
Q

Define prematurity

A

birth before 37 weeks gestation
the more premature, the worse the outcomes

Under 28 weeks: extreme preterm
28 – 32 weeks: very preterm
32 – 37 weeks: moderate to late preterm

82
Q

associations with prematurity?

A

Social deprivation
Smoking
Alcohol
Drugs
Overweight or underweight mother
Maternal co-morbidities
Twins
Personal or family history of prematurity

83
Q

Why do newborn babies commonly get jaundice?

A

Jaundice is common in newborn babies because babies have a high number of red blood cells in their blood, which are broken down and replaced frequently. A newborn baby’s liver is not fully developed, so it’s less effective at processing the bilirubin and removing it from the blood.

84
Q

Name the three foetal shunts

A

Ductus arteriosus. protects lungs against circulatory overload. allows the right ventricle to strengthen. …

Ductus venosus. fetal blood vessel connecting the umbilical vein to the IVC. …

Foramen ovale. shunts highly oxygenated blood from right atrium to left atrium.

85
Q

What is an innocent/flow murmur?

A

caused by fast blood flow through various areas of the heart during systole

Soft
Short
Systolic
Symptomless
Situation dependent (murmur gets quieter or disappears with standing or only appears when the child is unwell or feverish)

86
Q

Which pansystolic murmurs can be heard where?

A

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

87
Q

Which ejection-systolic murmurs can be heard where?

A

Aortic stenosis heard at the aortic area (second intercostal space, right sternal border)
Pulmonary stenosis heard at the pulmonary area (second intercostal space, left sternal border)
Hypertrophic obstructive cardiomyopathy heard at the fourth intercostal space on the left sternal border

88
Q

what normally happens to the ductus arteriosus after birth?

A

ductus arteriosus normally stops functioning within 1-3 days of birth, and closes completely within the first 2-3 weeks of life

89
Q

RF for patent ductus arteriosus

A

Premature birth. Patent ductus arteriosus occurs more commonly in babies who are born too early than in babies who are born full term.
Family history and other genetic conditions.
Rubella in mum during pregnancy.
Being female

90
Q

explain the pathophys behind patent ductus arteriosus

A

The pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery. This creates a left to right shunt where blood from the left side of the heart crosses to the circulation from the right side. This increases the pressure in the pulmonary vessels causing pulmonary hypertension, leading to right sided heart strain as the right ventricle struggles to contract against the increased resistance. Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy. The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy.

91
Q

How could a PDA present?

A

A patent ductus arteriosus can be picked up during the newborn examination if a murmur is heard. It may also present with symptoms of:

Shortness of breath
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

92
Q

Describe the type of murmur you may here in PDA

A

A small patent ductus arteriosus may not have any abnormal heart sounds. More significant PDAs cause a normal first heart sound with a continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear.

93
Q

how to diagnose a PDA?

A

The diagnosis of PDA can be confirmed by echocardiogram. The use of doppler flow studies during the echo can assess the size and characteristics of the left to right shunt. An echo is also useful for assessing the effects of the PDA on the heart, for example demonstrating hypertrophy of the right ventricle, left ventricle or both.

94
Q

management of PDA?

A

Patients are typically monitored until 1 year of age using echocardiograms. After 1 year of age it is highly unlikely that the PDA will close spontaneously and trans-catheter or surgical closure can be performed. Symptomatic patient or those with evidence of heart failure as a result of PDA are treated earlier.

95
Q

what is an atrial septal defect?

A

An atrial septal defect is a defect (a hole) in the septum (the wall) between the two atria. This connects the right and left atria allowing blood to flow between them.

96
Q

pathophys of atrial septal defect

A

An atrial septal defect leads to a shunt, with blood moving between the two atria. Blood moves from the left atrium to the right atrium because the pressure in the left atrium is higher than the pressure in the right atrium. This means blood continues to flow to the pulmonary vessels and lungs to get oxygenated and the patient does not become cyanotic, however the increased flow to the right side of the heart leads to right sided overload and right heart strain. This right sided overload can lead to right heart failure and pulmonary hypertension.

97
Q

During development, how do walls form between the atria in the heart? What are the walls called?

A

During the development of the fetus the left and right atria are connected. Two walls grow downwards from the top of the heart, then fuse together with the endocardial cushion in the middle of the heart to separate the atria. These two walls are called the septum primum and septum secondum.
There is a small hole in the septum secondum called the foramen ovale. The foramen ovale normally closes at birth.

98
Q

types of atrial septal defects from most?

A

Ostium secondum, where the septum secondum fails to fully close, leaving a hole in the wall.
Patent foramen ovale, where the foramen ovale fails to close (although this not strictly classified as an ASD).
Ostium primum, where the septum primum fails to fully close, leaving a hole in the wall. This tends to lead to atrioventricular valve defects making it an atrioventricular septal defect.

99
Q

complications of atrial septal defect?

A

Stroke in the context of venous thromboembolism (see below)
Atrial fibrillation or atrial flutter
Pulmonary hypertension and right sided heart failure
Eisenmenger syndrome

100
Q

How can ASD lead to stroke?

A

Normally when patients have a DVT and this becomes an embolus, the clot travels to the right side of the heart, enters the lungs and becomes a pulmonary embolism. In patients with an ASD the clot is able to travel from the right atrium to the left atrium across the ASD. This means the clot can travel to the left ventricle, aorta and up to the brain, causing a large stroke.

101
Q

What might you auscultate in a patient with an ASD and why?

A

ASDs cause a mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound. Splitting of the second heart sound is where you hear the closure of the aortic and pulmonary valves at slightly different times. This can be normal with inspiration, however a “fixed split” second heart sound means the split does not change with inspiration or expiration.

This occurs in an atrial septal defect because blood is flowing from the left atrium into the right atrium across the atrial septal defect, increasing the volume of blood that the right ventricle has to empty before the pulmonary valve can close. This doesn’t vary with respiration.

102
Q

how might ASD present in an adult?

A

It may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure or stroke

103
Q

typical symptoms of ASD in childhood?

A

Shortness of breath
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

104
Q

management of ASD?

A

Patients with an ASD should be referred to a paediatric cardiologist for ongoing management. If the ASD is small and asymptomatic, watching and waiting can be appropriate. ASDs can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery.

Anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke in adults.

3a (8 decks)

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