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FRACP Paediatrics > Respiratory > Flashcards

Flashcards in Respiratory Deck (28)
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1
Q

What are the volumes and capacities of the lungs?

A
  • 4 volumes and 4 capacities.
  • Volumes do not overlap, capacities do.
  • Capacities are made up of different combinations of lung volumes.
  • Volumes:
  • -> tidal volume: amount of air moved in and out of lung during each breath.
  • -> expiratory reserve volume: amount exhaled with maximal effort after tidal expiration.
  • -> inspiratory reserve volume: amount inhaled with maximal effort following tidal inspiration.
  • -> residual volume: volume of gas remaining in the lungs after maximum expiration.
  • Capacities:
  • -> inspiratory capacity: amount inspired by maximum effort following tidal expiration (tidal volume + inspiratory reserve volume).
  • -> functional residual capacity: amount of gas in lungs following tidal expiration (expiratory reserve volume + residual volume).
  • -> Vital capacity: amount of gas moved with max inspiratory and expiratory effort (inspiratory reserve volume + tidal volume + expiratory reserve volume).
  • ->Total lung capacity: volume of gas occupying lungs after max inspiration (inspiratory reserve volume + tidal volume + expiratory reserve volume + residual volume).
2
Q

What percentage of the alveolar epithelial surface is made up by Type I pneumocytes?

A
  • 95%

- 5% Type II but they make up 60% of the cells in the alveoli.

3
Q

What is the purpose of Type II pneumocytes?

A
  • Lamella bodies are formed containing phospholipids.
  • Lamella bodies secreted to the alveolar lumen by exocytosis.
  • Myelin tubules form and create a phospholipid film.
  • Hydrophobic tails face the alveolar lumen.
4
Q

Where do pulmonary alveolar macrophages originate?

A
  • The bone marrow.
5
Q

What is the function of pulmonary alveolar macrophages?

A
  • Ingest small particles that evade the mucocillary elevator.
  • Process inhaled allergens for immunologic attack.
  • Secrete substances that stimulate granulocyte and monocyte formation in the bone marrow.
6
Q

At what level of the spinal cord do the phrenic nerves originate and what are the implications of this?

A
  • C3-C5.
  • Transection of the spinal cord above C3 is fatal without mechanical ventilation.
  • Transection of the cord below C5 is not as the phrenic nerve remains intact and thus the diaphragm is functional.
7
Q

What percentage of tracheoesophageal fistulas are related to a syndrome?

A
  • 50%
8
Q

What is the most common form of TOF?

A
  • C type (87%).
  • Upper oesophagus terminates in a blind pouch.
    TOF originates from distal oesophagus.
9
Q

What is the most common oesophageal anomaly in children?

A
  • Oesophageal atresia (1.7/10,000)

- 90% associated with TOF.

10
Q

What syndrome is most frequently associated with TOF?

A
  • VATER/VACTERL (vertebral, anorectal, cardiac, tracheal, oesophageal, renal, limb).
11
Q

In what percentage of children with syndrome associated TOF are cardiac and vertebral anomalies seen?

A
  • 32% and 24% respectively.
12
Q

What are the most common complications following TOF repair?

A
  • Usually in first 5y post-repair.

- Anastomotic stricture, refistulisation, anastomotic leak.

13
Q

What features of TOF repair contribute to increased complication rate?

A
  • GORD is common and increases frequency of anastomotic stricture.
  • Also worsens reactive airways disease seen in GORD.
14
Q

What intrathoracic malignancy most often causes chylothorax?

A
  • Lymphoma.
15
Q

In newborns what causes chylothorax?

A
  • Rapid increase in venous pressure during delivery leads to rupture of the thoracic duct.
16
Q

What laboratory findings confirm chylothorax?

A
  • Fluid TG level >1.24mmol/L, pleural fluid: serum TG level >1.0 with cholesterol < 5.18mmol/L.
  • Chylomicrons are present on analysis.
  • Elevated fluid T-lymphocytes.
17
Q

What are complications of chylothorax?

A
  • Malnutrition (calories, protein and electrolyte loss).
  • Hypogammaglobulinaemia and impaired cell mediated immunity.
  • Loss of T lymphocytes can cause infection in neonates.
  • Avoid live virus vaccines.
18
Q

What are the predominant fats found in chyle?

A
  • Triglycerides in chylomicron form.

- Esterified long chain fatty acids.

19
Q

What is the treatment of chylothorax?

A
  • Enteral feeds with high protein with low fat or medium chain triglycerides.
  • PRN thoracentesis.
  • TPN if no improvement 1-2/52.
  • If ongoing consider: pleuroperitoneal shunt, thoracic duct ligation, fibrin glue.
  • Neonates with output >50ml/kg/d on maximal therapy 3/7 - consider surgery.
20
Q

What is the alveolar air equation?

A
  • PAO2 = (baro P - PH2O) X FiO2 - (PCO2 x 1/R)
21
Q

How is surfactant homeostasis maintained in the alveoli?

A
  • Balanced production of surfactant by type II alveolar cells clearance by uptake and catabolism in alveolar macrophages.
22
Q

What is PU.1 transcription factor?

A
  • Nuclear transcription factor involved in the regulation of alveolar macrophage maturation.
  • Reduction in PU.1 leads to impaired alveolar macrophage function.
23
Q

What is pulmonary alveolar proteinosis?

A
  • Rare.
  • Progressive accumulation of surfactant due to insufficient clearance.
  • Believed to be due to accumulation of surfactant that is produced normally but is unable to be catabolised and cleared by macrophages.
  • Deficiency in PU.1 as well as neutralising antibodies or mutations or deficiency of GM-CSF.
24
Q

What are the 5 phases of lung development?

A
  • Embryonic (26d-6w).
  • Pseudoglandular (6-16w)
  • Canalicular (16-28w).
  • Saccular (28-36w).
  • Alveolar (36w- infancy).
25
Q

What is the triad seen in Kartagener syndrome?

A
  • Bronchiectasis, chronic sinusitis, situs inversus.
26
Q

What is the treatment for Aspergillus found on BAL?

A
  • 1m itraconazole.
27
Q

What is the treatment for allergic bronchopulmonary aspergillosis?

A
  • Oral steroids for 2 weeks and then wean slowly.

- Oral itraconazole - stop 1m after finishing steroids.

28
Q

What are the typical blood findings of undiagnosed CF?

A
  • Hyponatraemic, hypochloraemic alkalosis.