Brainscape's Knowledge GenomeTM

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


See full index

Year 4: Child Health > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is croup also known as?

A

Acute Laryngotracheobronchitis.

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

How does croup present?

A

A harsh barking cough, stridor, hoarseness of voice, fever.

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

What is the peak incidence of croup?

A

2 years

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

What is the most common causative organism of croup?

A

Parainfluenza virus

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

Describe the history of a child with croup.

A

Typically 1-4 day history of non-specific cough, rhinorrhoea, fever progressing to a barking cough.

Symptoms worse at night, fever.

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

Describe the treatment for croup.

A

Single dose of oral dexamthasone 0.15mg/kg

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

What is the main causative organism of whooping cough?

A

Bordetella Pertussis bacterium

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

At what ages are the vaccines against pertussis given?

A

2, 3, an 4 months of age with a boost at 3 years and 4 months

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

Describe the gram staining of bordetella pertussis.

A

Gram-negative bacillus

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

Describe the 3 phases of whooping cough.

A
  1. Catarrhal (last 1-2 weeks)
  2. Paroxysmal phase (lasts 2-8 weeks)
  3. Convalescent phase (up to 3 months)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 2 investigations indicated in suspected whooping cough?

A
  1. Nasopharyngeal aspirate

2. Anti-pertussis toxin IgG serology

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

What immune cells drive classical allergic asthma?

A

TH2 type T-cells

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

Name some investigations you would call out in suspected childhood asthma.

A

Spirometry: FEV1:FVC < 70%
Peak expiratory flow rate
Skin prick testing

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

Describe the management of asthma.

A
  1. Short acting bra-2 agonist
  2. Inhaled corticosteroids
  3. Add on therapy i.e. long acting beta-2 agonist (LABA)
  4. Increase dose of inhaled corticosteroids
  5. Regular oral steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the clinical features of mild asthma.

A

SaO2 >92% in air, vocalising without difficulty, mild chest wall recession and moderate tachypnoea.

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

Describe the clinical features of moderate asthma.

A

SaO2 <92%, breathless, moderate chest wall recession.

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

Describe the clinical features of severe asthma.

A

SaO2 <92%, PEFR 33-50% best or predicted, cannot complete sentences in one breath or too breathless to talk/feed, heart rate >125 (over 5 years old) or >140 (2-5 years old), respiratory rate >30 (over 5 years) or >40 (2-5 years).

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

Describe the clinical features of life-threatening asthma.

A

SaO2 <92%, PEFR <33% predicted, silent chest, poor respiratory effort, cyanosis, hypotension, exhaustion, confusion

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

Describe the immediate management of an asthma exacerbation.

A 
Oxygen: SaO2 <94% should receive high flow oxygen to maintain saturations between 94-98%.
Bronchodilators: Inhaled SABA (salbutamol) – via nebuliser if severe. Inhaler and spacer device is as effective as nebuliser in children with mild/moderate asthma attack.
Ipatropium bromide (anti-muscuranic) added in if no or poor response to inhaled SABA
Corticosteroids: A short course (3 days) or steroids should be commenced. Oral prednisolone is first-line however if the child vomits or is too unwell to take oral medication intravenous hydrocortisone should be used.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the second line management of an asthma exacerbation.

A

Intravenous salbautamol can be considered with specialist input if there is no response to inhaled bronchodilators. It is essential to monitor for salbutamol toxicity.
Magnesium sulphate can be considered, as it has an effect as a bronchodilator.

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

Describe the safe discharge criteria of an asthma exacerbation.

A

Bronchodilators are taken as inhaler device with spacer at intervals of 4-hourly or more (e.g. 6 puffs salbutamol via spacer every 4 hours)
SaO2 >94% in air
Inhaler technique assessed/taught
Written asthma management plan given and explained to parents
GP should review the child 2 days after discharge

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

Why should aspirin not be prescribed to a child with asthma?

A

It is an NSAID which can trigger an inflammatory response

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

What is bronchiolitis?

A

A viral infection of the bronchioles.

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

What is the most common causative virus of bronchiolitis?

A

Respiratory syncytial virus (RSV)

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

What time of year does bronchiolitis commonly occur?

A

winter and spring

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

Name some risk factors of developing bronchiolitis.

A
  • Being breast fed for less than 2 months
  • Smoke exposure
  • Having siblings who attend nursery or school
  • Chronic lung disease due to prematurity
27
Q

Name some laboratory tests that should be carried out if you suspect bronchiolitis.

A

Nasopharyngeal aspirate or throat swab – RSV rapid testing and viral cultures
Blood and urine culture if child is pyrexic
FBC
Blood gas (ABG) if severely unwell – this may detect respiratory failure and the need for respiratory support, but should not be done routinely

28
Q

What is bronchiectasis?

A

Abnormal dilatation of the airways with associated destruction of bronchial tissue.

29
Q

Describe the inheritance pattern of Primary Ciliary Dyskinesia.

A

Autosomal recessive

30
Q

Name 2 congenital syndrome associated with bronchiectasis.

A
  1. Youngs syndrome

2. Yellow-nail syndrome

31
Q

Describe the key clinical feature of bronchiectasis.

A

Chronic productive cough

32
Q

Describe what you would see on examination of bronchiectasis.

A
  • Flinger clubbing
  • Inspiratory crackles
  • Wheezing
33
Q

What is the gold standard investigation to diagnose bronchiectasis?

A

High resolution CT

34
Q

Wha are the features see on a high resolution CT that are indicative of a diagnosis of bronchiectasis?

A
  • Bronchial wall thickening
  • Diameter of the bronchus larger than that of the accompanying bronchial artery (signet ring sign)
  • Visible peripheral bronchi
35
Q

What type of bronchiectasis is common in CF?

A

Bilateral upper lobe

36
Q

What type of bronchiectasis is common in post-TB infection?

A

unilateral upper lobe

37
Q

What type of bronchiectasis is common in foreign body inhalation?

A

focal lower lobe

38
Q

Describe the spirometry pattern of a patient with bronchiectasis.

A

Spirometry may be completely normal in mild disease. In advanced disease there can either be an obstructive pattern or a mixed obstructive and restrictive pattern, as severe scarring begins to compromise lung compliance.

39
Q

Describe the management of bronchiectasis.

A
  • Chest Physiotherapy
  • Bronchodilators if a wheeze is present
  • Antibiotics against isolated organisms
40
Q

Name 3 of the most common causative organisms in bronchiectasis.

A

non-encapsulated Haemophilus influenzae, Streptococcus penumoniae and Moraxella catarrhalis

41
Q

Describe the associated changes to the bronchi in bronchiectasis.

A

Structural damage and destruction of the cilia

42
Q

Describe the genetic disease pattern of CF.

A

Autosomal recessive

43
Q

What mutation causes CF?

A

CFTR (Transmembrane conductance regulator gene)

44
Q

Describe the pathophysiology of the reparatory tract in CF.

A

The CTFR gene encodes the CFTR protein – a chloride channel that is present in numerous epithelial tissues. Chloride is driven against its concentration gradient using ATP.

In the airway, CFTR is present on airway epithelial cells and submucosal glands and when defective results in disruption to chloride ion movement and also affects sodium reabsorption (by disturbing the function of ENaC) which reduces the amount of water in secretions. This results in reduced airway surface liquid.

The airway surface liquid is an important component of the mucociliary escalator and also has key immunological functions. The effects of reduced airway surface liquid serve to impede mucus clearance.

45
Q

Describe the pathophysiology of the pancreas in CF.

A

In the pancreas the pancreatic duct is usually occluded in-utero causing permanent damage to the exocrine pancreas rendering patients with CF ‘pancreatic insufficient’.

46
Q

Describe the pathophysiology of the GI tract in CF.

A

In the gastrointestinal tract, the small intestine secretes viscous mucus which can cause bowel obstruction in-utero which can cause meconium ileus. In the biliary tree in-utero, CF can cause cholestasis which can result in neonatal jaundice. Later in life the same pathology can result in distal intestinal obstruction syndrome (DIOS) and CF-related liver disease (14% of patients).

47
Q

Describe the pathophysiology of the reproductive tract in CF.

A

98% of men with CF are infertile due to a congenital absence of the vas deferens. In women nutrition is likely to be an important predictor of successful pregnancy. It is suggested that the timing of pregnancy be carefully planned, as pregnancy is often associated with a deterioration in lung health.

48
Q

Describe the clinical presentation of neonates with CF.

A

Meconium ileus – 10% of children present with abdominal distension, delayed passage of meconium and bilious vomiting in the first days of life.
Since the introduction of screening for CF in neonates (part of the Guthrie test) the majority of cases of CF are identified here (however it is important to note that it is a screening test and still needs diagnostic testing)4
Failure to thrive
Prolonged neonatal jaundice

49
Q

Describe the clinical presentation of infants with CF.

A

Failure to thrive
Recurrent chest infections
Pancreatic insufficiency: steatorrhoea

50
Q

Describe the clinical presentation of children with CF.

A

Rectal prolapse
Nasal polyps (N.B. strongly suspect CF in children presenting with nasal polyps)
Sinusitis

51
Q

Describe the clinical presentation of adolenents with CF.

A

Pancreatic insufficiency: diabetes mellitus
Chronic lung disease
DIOS, gallstones, liver cirrhosis

52
Q

Describe the examination of a child with CF.

A

Hands: finger clubbing
Face: nasal polyps
Chest: hyperinflated, crepitiations, portacath (indwelling vascular access device)
Abdomen: faecal mass (if constipated/DIOS), may have a scar from ileostomy (meconium ileus)

53
Q

How do you diagnose CF?

A

A diagnosis of CF can be made if there is a fitting clinical history and a positive chloride sweat test which may be supported by the identification of two identified mutations.

54
Q

Name 7 investigative tests required in a patient with suspected CF.

A

Chest radiograph: to assess for hyperinflation, there may be evidence of bronchial thickening (undertaken annually as part of annual assessment) Some units undertake CT scanning.
Chloride sweat test (at diagnosis and annually if in receipt of CFTR potentiator/corrector therapy)
Microbiological assessment e.g. cough swab/sputum sample (at every clinical encounter)
Glucose tolerance test (at annual assessment at teenage and beyond)
Liver function test and coagulation (at annual assessment)
Bone profile (at annual assessment)
Lung function testing – spirometry / lung clearance index

55
Q

During the chloride sweat test, over what level is suggestive of CF?

A

> 60mmol/L (Note a single sweat test is not sufficient to diagnose CF)

56
Q

Describe the management of CF.

A
  • Patient and family education
  • Twice-daily airway physiotherapy
  • Pancreatic enzyme supplement (Creon) with meals that contain fat
  • Fat soluble vits
  • Monitor growth
  • Infections should be treated with 2 week long antibiotics
  • Annual review
57
Q

Name some respiratory complications of CF.

A
  • Allergic bronchopulmonary aspergillosis
  • Bronchiectasis
  • Pulmonary hypertension and left heart strain
  • Pneumothorax
  • Nasal polyps
58
Q

Name soem GI complicaitons of CF.

A
  • Rectal prolapse
  • Distal intestinal obstructive syndrome (DIOS)
  • Liver disease i.e. cholestasis, gallstones, liver cirrhosis
59
Q

Name some endocrine complications of CF.

A
  • CF related diabetes (CFRD)

- Delayed puberty

60
Q

What vitamin doesn’t necessarily need to be replaced in patients with CF?

A

B as it is not fat soluble (A, D, E and K should be replaced)

61
Q

The CFTR protein is what kind of protein.

A

A Cl- channel

62
Q

Absence of which male reproductive structure in CF patients leads to an infertility rate of 98% in male sufferers?

A

Vas deferens

63
Q

Describe the spectrum of severity of COVID-19 in paediatric patients.

A
  • Mild: No pneumonia or mild pneumonia
  • Severe: Dyspnoea, oxygen sats <93%, >50% lung infiltrates within 24-48 hours
  • Critical: Respiratory failure, septic shock, and/or multiple organ dysfunction/failure
64
Q

Describe the investigations you would carry out in a child with COVID-19.

A
  • Chest X-ray (Bilateral infiltrates on. Radiopaedia have a good selection of CXR’s and CT scans here)
  • Inflammatory markers (CRP and ESR elevated)
  • Full blood count (lymphonpenia, neutrophilia)
  • Liver enzymes (elevated)
  • Lactate dehydrogenase (elevated)
  • D-dimer (raised)

Year 4: Child Health (16 decks)

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