Brainscape's Knowledge GenomeTM

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


See full index

Paediatrics > Respiratory development > Flashcards

Respiratory development Flashcards

1
Q

Lung development

A
  • Begins in the 4th week of gestation.
  • Extrauterine survival only becomes possible when terminal air sacs and the surrounding capillary network form at 26th week.
  • Alveolar formation begins by the 36th postconceptual week, but most alveoli form postnatally.
  • Type II pneumocytes begin producing surfactant at 24th week. Production of this mixture of phospholipids and surfactant proteins is critical for reducing surface tension and facilitating the inflation of alveoli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Chest wall and respiratory muscles development

A
  • The ribs extend horizontally in infants compared to a caudal angle in adults. So, the accessory muscles of respiration ineffective in infants. The rib cage also tends to move inward during inspiration due to the high cartilage content in the ribs of neonates and infants. The diaphragm increases its work to maintain tidal volume, which can lead to fatigue.
  • Adult diaphragm has low amounts of type I (slow twitch) muscle fibres. Prior to 37 weeks postconceptual age, less than 10% of the diaphragmatic fibers are type I. Term infant has 25% type I fibers, and an adult has approximately 50%. This means that the diaphragm is more likely to become fatigued in premature and term infants, leading to earlier respiratory failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Respiratory rate neonate

A

50 ± 10

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

Respiratory rate 6 months

A

30 ± 5

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

Respiratory rate 12 months

A

24 ± 6 also some for 3yrs and 5yrs roughly

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

Respiratory rate 9yrs

A

20 ± 5

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

Respiratory rate adults

A

12 ± 3

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

Factors affecting respiration

A
  • In both infants and adults, Pa o 2 , Pa co 2 , and pH control ventilation.
  • Increase in Pa co 2 leads to an increase in minute ventilation by increasing respiratory rate and tidal volume.
  • High inspired oxygen concentrations depress newborn respiratory drive, and low inspired oxygen concentrations stimulate it. However, continued hypoxia will eventually lead to respiratory depression. Hypoglycemia, anemia, and hypothermia also decrease respiratory drive.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Breathing patterns

A
  • Normal newborn breathing is periodic. There are pauses of less than 10 seconds and periods of increased respiratory activity. Periodic breathing is different from apnea, a ventilatory pause associated with desaturation and bradycardia.
  • Apnea is associated with prematurity and is treated with respiratory stimulants and with tactile stimulation such as stroking or rocking. Postoperative apnea in former premature infants is an important consideration in the planning of outpatient surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chest wall compliance increase or decrease ?

A

Chest wall compliance decreases throughout childhood due to the ossification of the ribs and development of thoracic muscle mass. The elastic recoil pressure of the lung increases throughout this time due to an increase in pulmonary elastic fibers.

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

Primary ciliary dyskinesia (PCD)

A
  • An inherited disorder characterized by impaired ciliary function leading to diverse clinical manifestations, including chronic sinopulmonary disease, persistent middle ear effusions, laterality defects, and infertility.
  • Although the estimated frequency of PCD is 1 in 12,000 to 1 in 20,000 live births, its prevalence in children with repeated respiratory infections has been estimated to be as high as 5%.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Normal Ciliary Ultrastructure and Function (brief)

A

Three types of cilia exist in the humans: motile cilia; primary (sensory) cilia; and nodal cilia.

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

Motile cilia

A

Hair-like organelles that move fluids, mucous, and inhaled particulates vectorially from conducting airways, paranasal sinuses, and eustachian tubes. The upper and lower respiratory tracts are continuously exposed to inhaled pathogens, and local defenses have evolved to protect the airway.

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

Motile cilia location

A
  • The respiratory epithelium in the nasopharynx, middle ear, paranasal sinuses, and larger airways are lined by a ciliated, pseudostratified columnar epithelium that is essential for mucociliary clearance.
  • A mature ciliated epithelial cell has approximately 200 uniform motile cilia that are anatomically and functionally oriented in the same direction, moving with intracellular and intercellular synchrony.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Primary (sensory) cilia

A
  • Are present during interphase on most cell types. These cilia lack a central microtubule doublet and dynein arms, thus creating a “9+0” arrangement and leaving them immotile.
  • For years, these structures were considered nonfunctional vestigial remnants, but primary cilia are important signalling organelles that sense the extracellular environment.
  • They are mechanoreceptors, chemosensors, osmosensors, and, in specialized cases, defect changes in light, temperature, and gravity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nodal cilia (The third distinct classification of cilia exists only during a brief period of embryonic development.)

A
  • “9+0” microtubule arrangement similar to that of primary cilia, but they exhibit a whirling, rotational movement, resulting in leftward flow of extracellular fluid that establishes body sidedness.
  • Nodal cilia defects result in body orientation abnormalities, such as situs inversus totalis , situs ambiguus , and heterotaxy associated with congenital heart disease, asplenia, and polysplenia.
17
Q

Genetics of Primary Ciliary Dyskinesia

A
  • PCD is typically has AR patterns of inheritance, although rare cases of AD and X-linked inheritance have been reported.
  • PCD is a genetically heterogeneous disorder involving multiple genes; mutations in any protein that is involved in ciliary assembly, structure, or function could theoretically cause disease.
  • 18 different genes have been linked to PCD
18
Q

Clinical manifestations lung

A
  • Neonatal respiratory distress
  • Chronic cough
  • Recurrent pneumonia
  • Bronchiectasis
19
Q

Clinical manifestations middle ear

A
  • Chronic otitis media

- Conductive hearing loss

20
Q

Clinical manifestations paranasal sinuses

A
  • Neonatal rhinitis
  • Chronic mucopurulent rhinitis
  • Chronic pansinusitis
  • Nasal polyposis
21
Q

Clinical manifestations GU

A

Male and female infertility

22
Q

LEFT-RIGHT ORIENTATION DEFECTS

A

Situs inversus
Heterotaxy
Congenital heart disease

23
Q

CENTRAL NERVOUS SYSTEM

A

Hydrocephalus

Retinitis pigmentosa

24
Q

Most patients with PCD present with …

A
  • Neonatal respiratory distress , manifested as tachypnea, hypoxemia, or even respiratory failure requiring mechanical ventilation. The upper respiratory tract is almost universally involved in PCD.
  • Persistent rhinosinusitis is common during infancy. Inadequate innate mucus clearance leads to chronic sinusitis and nasal polyposis.
  • Middle ear disease occurs in nearly all children with PCD, with varying degrees of chronic otitis media leading to conductive hearing loss and myringotomy tube placement, which is often complicated by intractable otorrhea.
25
Q

Later on patients with PCD present with …

A

Impaired mucociliary clearance of the lower respiratory tract leads to daily productive cough, often in young children, secondary to chronic bronchitis. Bacterial cultures of sputum or lavage fluid frequently yield nontypeable Haemophilus influenzae, Staph. aureus, Streptococcus pneumoniae, and Pseudomonas aeruginosa. Persistent airway infection and inflammation lead to bronchiectasis, even in preschool children. Clubbing is a sign of long-standing pulmonary involvement.

26
Q

Diagnosis of PCD

A
  • The diagnosis of PCD should be suspected in children with chronic or recurring upper and lower respiratory tract symptoms that begin in early infancy.
  • Currently based on the presence of characteristic clinical phenotype and ultrastructural defects of cilia, though this approach will miss affected individuals.
27
Q

The average age at PCD diagnosis…

A

is approximately 4 yr; a high index of suspicion is necessary.
- The diagnosis is delayed, even in children who have classic clinical features, such as chronic rhinosinusitis in infancy, persistent otitis media, or even situs inversus totalis .

28
Q

PCD imaging Dx

A

Imaging studies show extensive involvement of the paranasal sinuses.

  • Chest radiographs frequently demonstrate bilateral lung overinflation, peribronchial infiltrates, and lobar atelectasis.
  • Computerized x-ray tomography of the chest often reveals bronchiectasis, often involving the anatomic right middle lobe or lingual, even in young children.
  • Situs inversus totalis in a child who has chronic respiratory tract symptoms is highly suggestive of PCD, but this configuration occurs in only half of patients with PCD. Pulmonary function testing typically shows progressive intrathoracic airway obstruction.
29
Q

PCD gold standard

A
  • Transmission electron microscopy is the current gold standard to assess structural defects within the cilium.
  • Curettage from the nasal epithelium or endobronchial brushing provides a specimen for review.
  • Consistent defect in any aspect of the ciliary structure with concurrent phenotypic features is sufficient to make the diagnosis.
30
Q

Treatment PCD

A
  • No therapies correct ciliary dysfunction in PCD.
  • Tx is suppurative lung care regimen used in cystic fibrosis, but none have been adequately studied to demonstrate their efficacy in PCD.
31
Q

PCD develop increasing respiratory symptoms consistent with infection…

A

antimicrobial therapy should be instituted on the basis of respiratory culture results and bacterial sensitivities.

  • Early eradication strategies to clear bacteria from the PCD lung have not been studied.
  • Maintenance therapy with inhaled or oral antibiotics can be used cautiously in patients with PCD who have bronchiectasis or frequent exacerbations, not much evidence.
  • Immunizations against pertussis, influenza, and pneumococci are cornerstones of care.
  • Additional preventive measures include avoidance of cigarette smoke and other airway irritants.
32
Q

The use of β-adrenergic agonists in PCD…

A

increase ciliary beat frequency in normal epithelial cells, data is lacking that shows these agents improve function of dyskinetic cilia. Moreover, they do not necessarily provide bronchodilation in patients with PCD and obstructive airway disease.

33
Q

Surgical resection of bronchiectatic lung has been performed on patients with PCD, typically …

A

in cases of localized disease with severe hemoptysis or recurrent febrile illnesses. It is unclear whether surgical interventions provide reduction in symptoms or survival benefit.

34
Q

Follow ups

A

It is believed that progression and extent of lung disease can be slowed with early diagnosis and therapy. Thus, routine surveillance include (1) regular spirometry to monitor pulmonary function, (2) chest imaging, and (3) sputum or oropharyngeal cultures to assess lung respiratory flora.

35
Q

Prognosis

A

Patients with PCD typically have slower decline in pulmonary function than those with cystic fibrosis. Its prognosis and long-term survival are better. Many patients with PCD have a normal or near-normal life span, although some do experience progressive bronchiectasis and respiratory deterioration earlier in life.

36
Q

What is a stridor?

A
  • An abnormal, high-pitched sound produced by turbulent airflow through a partially obstructed airway at the level of the supraglottis, glottis, subglottis, or trachea.
  • Its tonal characteristics are extremely variable (ie, harsh, musical, or breathy); however, when combined with the phase, volume, duration, rate of onset, and associated symptoms, the tonal characteristics of the sound may provide additional diagnostic clues.
37
Q

Inspiratory stridor suggests…

A

a laryngeal obstruction

38
Q

Expiratory stridor implies…

A

tracheobronchial obstruction

39
Q

Biphasic stridor implies…

A

a subglottic or glottic anomaly

Paediatrics (5 decks)

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