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Paediatrics > Respiratory > Flashcards

Respiratory Flashcards

1
Q

croup

A
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2
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asthma

A
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3
Q

bronchiectasis

A
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4
Q

COVID 19

A
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5
Q

whooping cough notifiable

A

yes

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6
Q

epidemiology whooping cough

A

cases in older children and adults tend to be much milder, whilst infants remain most at risk of hospitalisation and death due to pertussis (5). The incidence of pertussis tends to peak every 3-4 years for reasons that are poorly understoo

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7
Q

vaccines whooping cough

A

pertussis vaccines - 2, 3 and 4 mths of age, booster at 3 yrs and 4 mths

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8
Q

bacteria whooping cough

A

bordatella pertussis
gram negative bacillus
spreads by aerosolised droplets
bacteria attaches to respiratory epithelium and produce toxins which paralyse cilia and promote inflammation, impairing clearance of secretions

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9
Q

risk factors whooping cough

A

non vaccination
exposure to an infected individual

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10
Q

clinical features whooping cough

A
  1. catarrhal phase - 1-2 weeks
    Rhinitis
    Conjunctivitis
    Irritability
    Sore throat
    Low-grade fever
    Dry cough
  2. paroxysmal phase - 2-8 weeks
    severe paroxysms of coughing followed by inspiratory gasp, can result in vomiting
    if <3mths apnoea more common
  3. convalescent phase - 3 mths
    decreases in frequency and severity
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11
Q

ddx whooping cough

A

bronchiolitis
mycoplasma pneumonia
bacterial pneumonia

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12
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A
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13
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14
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15
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16
Q

management whooping cough

A

duration of cough <21 days= macrolide
Clarithromycin for those under 1 month, azithromycin or clarithromycin for those over 1 month
Co-trimoxazole is the 2nd line antibiotic where macrolides are contra-indicated or poorly tolerated
Further management is supportive, including paracetamol and / or ibuprofen for symptomatic relief and adequate fluid intake to prevent dehydration
can take up to 3 mths to reolve

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16
Q

hospital admission whooping cough indications

A

Who are under 6 months of age and acutely unwell
With significant breathing difficulties, e.g. apnoeic episodes, cyanosis, respiratory distress or severe paroxysms of coughing
Feeding difficulties
With significant complications, e.g. pneumonia or seizures

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16
Q

whooping cough avoiding school ?

A

The child should avoid nursery or school until they have had the cough for 21 days or have had antibiotics for 5 days

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16
Q

investigations whooping cough

A

<2 weeks - culture of nasopharngeal aspirate or swab…PCR testing
>2 weeks - anti pertussis toxin IgG serology, oral fluid testing for anti pertussis toxin
FBC - lymphocytosis

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17
Q

whooping cough complications

A

Secondary bacterial pneumonia (up to 20% of infants)
Seizures
Encephalopathy (rare)
otitis medis

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18
Q

bronchiolitis definition

A

viral infection of the bronchioles
most commonly caused by RSV

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19
Q

RSV

A

respiratory syncytial virus

20
Q

bronchiolitis epidemiology

A

children <2 yrs
1/3 will develop in first year of life
occurs during winter and spring months

21
Q

pathophysiology bronchiolitis

A

Proliferation of goblet cells causing excess mucus production
IgE-mediated type 1 allergic reaction causing inflammation
Bronchiolar constriction
Infiltration of lymphocytes causing submucosal oedema
Infiltration of cytokines and chemokines

22
Q

risk factors bronchiolitis

A

Being breast fed for less than 2 months
Smoke exposure (eg. parents’ smoke)
Having siblings who attend nursery or school (increased risk of exposure to viruses)
Chronic lung disease due to prematurit

23
Q

clinical features bronchiolitis

A

Low-grade fever
Nasal congestion
Rhinorrhoea
Cough
Feeding difficulty

24
Q

examination bronchiolitis

A

Tachypnoea
Grunting
Nasal flaring
Intercostal, subcostal or supraclavicular recessions
Inspiratory crackles
Expiratory wheeze
Hyperinflated chest
Cyanosis or pallo

25
Q

ddx bronchiolitis

A

pneumonia
HF
croup
CF

26
Q

investigations bronchiolitis

A

nasopharyngeal aspirae or throat swab
blood and urine culture
FBC
ABG
CXR - Hyperinflation
Focal atelectasis
Air trapping
Flattened diaphragm
Peribronchial cuffing

27
Q

urgent referral bronchiolitis

A

Apnoea
Child looks seriously unwell
Severe respiratory distress eg. grunting, marked recessions, respiratory rate >70
Central cyanosis
Oxygen sats < 92%
Hospital referral should be considered if any of the following are seen (4):

Respiratory rate > 60
Inadequate fluid intake (50-75% of usual volume)
Clinical dehydration

28
Q

bronchiolitis hospital management

A

Give oxygen if sats < 92% in room air
Give fluids via nasogastric or orogastric tube if inadequate oral intake
Consider CPAP if there is impending respiratory failure
Perform upper airway suctioning if there are upper airway secretions or apnoea

29
Q

discharge bronchiolitis

A

Clinically stable
Taking adequate oral fluids
Maintaining sats > 92% for more than 4 hours

30
Q

complications bronchiolitis

A

Hypoxia
Dehydration
Fatigue
Respiratory failure
Persistent cough or wheeze (very common and parents should be counselled that their child may cough for several weeks)
Bronchiolitis obliterans – Airways become permanently damaged due to inflammation and fibrosis

31
Q

prognosis bronchiolitis

A

lasts for 7-10 days
cough can last for 6 weeks

32
Q

CF definition

A

an autosomal recessive disease caused by a mutation in the CF transmembrane conductance regulator gene (CFTR) resulting in multisystem dysfunction. In 2000 the life expectancy of a child born in 2000 was 50 years

33
Q

epidemiology CF

A

approximately 1 in 25 Caucasian Europeans are carriers of a CF gene with approximately 1 in 2500 live births having CF. p.Phe508del (ΔF508) is the commonest mutation in the UK with this accounting for at least one mutation in 90% of people with CF in the UK, with 50% of those with CF in the UK are homozygous for this mutation

34
Q

CF respiratory tract

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.

The altered lung environment provides a niche for bacterial growth with the biofilm mode of growth providing ideal conditions to protect bacteria from the host immune system and the actions of antibiotics. The pro-inflammatory cascade contributes to tissue damage.

35
Q

CF pancreas

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’. Pancreatic insufficiency is closely related to genotype. Over time, endocrine pancreas is affected with 28% of those older than 10 years requiring treatment for CF-related diabetes mellitus.

36
Q

CF gi tract

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)

37
Q

CF repro tract

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

38
Q

risk factors

A

aut recessive
lots of mutations to teh CFTR gene
Different organs have different sensitivity to loss of CFTR protein function, with the vas deferens particularly sensitive in contrast to the lungs, which are less sensitive. Instead the lungs are more susceptible to other factors, like stochastic, environmental, and genetic modifiers-genes that modify the expression of CFTR protein

39
Q

clinical features CF

A

Neonates
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
Infancy
Failure to thrive
Recurrent chest infections
Pancreatic insufficiency: steatorrhoea
Childhood
Rectal prolapse
Nasal polyps (N.B. strongly suspect CF in children presenting with nasal polyps)
Sinusitis
Adolescence
Pancreatic insufficiency: diabetes mellitus
Chronic lung disease
DIOS, gallstones, liver cirrhosis

40
Q

examination 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)

41
Q

diagnosis of 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

42
Q

investigations 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

43
Q

chloride sweat test

A

This test measures the electrolyte concentration in sweat
Sweat sample is collected by pilocarpine iontophoresis. Careful technique must be employed to ensure and adequate sample is collected to avoid inaccurate results. A common reason for failure of the test is an insufficient sample in a small baby (limit 3kg).
A sweat chloride >60mmol/L is suggestive of CF. A sweat chloride of 40-60mmol/L is borderline and should be repeated
A single sweat test is not sufficient to diagnose CF, a second test or identification of genetic mutation
Faecal elastase to assess pancreatic function
Chest CT (high resolution) to assess for bronchiectasis (where bronchial diameter would exceed that of accompanying pulmonary vessels)
Genetic analysis

44
Q

management CF

A

patient and family education
twice daily physio
mycolytics - DNase, hypertonic saline
exercise
creon
fat soluble vitamins - A, D, E, K
monitor growth
nutrition as higher metabolic demands - build up milkshakes
sputum cultures - monitor for infections, with 2 weeks of abx
if pseudomonas - eradication
regular azithromycin
active segregation
minimise complications
annual review

45
Q

organisms CF

A

Staphyloccocus aureus, Haemophilus influenzae and Pseudomonas aeruginosa

46
Q

complications CF resp

A

allergic bronchopulmonary aspergillosis
bronchiectasis
haemoptysis
pulmonary HTN
pneumothorax
resp failure
nasal polyps

47
Q

complications GI CF

A

rectal prolapse
distal intestinal obstruction syndrome
CF releated liver disease

48
Q

complications endocrine CF

A

CF related diabetes - associated with rapid decline in lung function and disease progression - Clinical presentation can differ to typical type 1 DM and comprises weight loss, anorexia and fall in lung function
delayed puberty - avg of 2 yrs, reduced bone minteral density

49
Q

other complications CF

A

arthritis
reduced bone mineral density
sub or infetility

50
Q
A

Paediatrics (17 decks)

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