Pediatric lung diseases Flashcards

1
Q

Causes of hypoxia

A

VQ mismatch, hypoventilation, shunt, diffusion, altitude, hemoglobinopathies

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2
Q

Define compliance and minute ventilation

A

compliance= ∆V/ ∆P. Minute ventilation= respiratory rate x tidal volume

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3
Q

Compare pulmonary anatomy in children vs adults

A

In Children (esp infants) The larynx is higher and more anterior and the epiglottis is floppy, the narrowest part of the airway is below the vocal cords Intercostal muscles are weaker, Diaphragm is relatively flat and ribs are horizontal

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4
Q

Pediatric signs of respiratory distress

A

Lethargy, Poor feeding, Grunting (closing the glottis before the end of exhalation), Children with chronic respiratory disease may have trouble gaining weight due to increased energy expenditure with increased work of breathing and poor feeding

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5
Q

Signs of upper airway obstruction in kids

A

Stridor (inspiratory, expiratory or biphasic). Signs of severe obstruction include drooling, dysphagia, and dyspnea/distress

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6
Q

Increased lung volume later in life is mainly due to what?

A

alveolar expansion- Conducting airways are mostly formed by 17 weeks in utero

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7
Q

Developmental pulmonary problems in first 6 weeks

A

Pulmonary agenesis, Tracheoesophageal fistula, laryngomalacia and Vascular malformation leading to airway compression
Pulmonary agenesis, Tracheoesophageal fistula, laryngomalacia and Vascular malformation leading to airway compression
Pulmonary agenesis, Tracheoesophageal fistula, laryngomalacia and Vascular malformation leading to airway compression

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8
Q

Laryngomalacia- age of onset, definition, symptoms, duration

A

Congenital disorder of the upper airway that presents at birth/early in life. The cartilaginous support for the supraglottic structures is underdeveloped. Most common cause of stridor in infants. Stridor is worse with eating, crying, laying down, activity. Often outgrown by 1-2 yrs

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9
Q

Developmental pulmonary problems in weeks 6-16

A

Airway/cartilage abnormalities such as tracheobronchomalacia

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10
Q

Symptoms of tracheobronchomalacia

A

recurrent wheeze, a hoarse cough, and recurrent illnesses

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11
Q

Croup syndrome definition

A

Acute inflammatory diseases of the larynx, including viral croup (laryngotracheobronchitis), epiglottitis (supraglottitis), and bacterial tracheitis. Patients can present with acute or subacute symptoms, including stridor

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12
Q

Viral croup- cause, physiology and symptoms

A

Caused by parainfluenza virus serotypes. Edema in the subglottic space causes most of the upper airway obstruction. Symtpoms include barking cough and stridor, fever is absent or low grade, and if severe can have retractions, air hunger and cyanosis

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13
Q

Viral croup- imaging and treatment

A

Neck radiograph shows subglottic narrowing (steeple sign). Mild croup (cough and no stridor at rest) is treated supportively. More severe croup (stridor at rest) is treated with nebulized epinephrine and glucocorticoids.

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14
Q

Epiglottitis- cause, physiology and symptoms

A

Medical emergency! Caused by H. influenza type B usually. Inflammation and swelling of the supraglottic structures (epiglottis and arytenoids) can develop rapidly and lead to life-threatening upper airway obstruction. Sudden onset of high fever, dysphagia, drooling, muffled voice, inspiratory retractions, cyanosis, and soft stridor

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15
Q

Epiglottitis treatment and prognosis

A

Endotracheal intubation immediately, antibiotics. Prompt treatment has good results and recurrence is unusual

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16
Q

Bacterial tracheitis- cause, physiology and symptoms

A

Usually caused by staph aureus. Severe form of laryngotracheobronchitis that results in inflammatory edema, purulent secretions and pseudomembranes. Signs of viral croup that develop into high fever, toxicity, and progressive or intermittent severe upper airway obstruction that is unresponsive to standard croup therapy.

17
Q

Bacterial tracheitis- diagnosis and treatment

A

Diagnose with Bronchoscopy showing a normal epiglottis and the presence of copious purulent tracheal secretions and membranes. Treatment with endotracheal intubation, antibiotics, debridement of tracheal secretions.

18
Q

Symptoms of lower airway problems

A

hypoxemia (from VQ mismatch), wheeze (monophonic if large airway, polyphonic wheeze if smaller airways), and crackles in the alveoli

19
Q

Potential pulmonary problems drom developmental weeks 16-26

A

diaphragmatic hernia, oligohydramnios or any disruption of growth. Potters syndrome causes renal agensis so there is no fetal urine, thus there is too little amniotic fluid and the fetus does not inhale/swallow the urine and lungs are underdeveloped

20
Q

Bronchiolitis - cause and symptoms/exam

A

Acute respiratory illness from respiratory syncytial virus (RSV) usually, but can be from adenovirus, mycoplasma, etc. Characterized by acute onset tachypnea, labored breathing, and/or hypoxia, Irritability, poor feeding, expiratory Wheezing and crackles on chest auscultation.
Acute respiratory illness from respiratory syncytial virus (RSV) usually, but can be from adenovirus, mycoplasma, etc. Characterized by acute onset tachypnea, labored breathing, and/or hypoxia, Irritability, poor feeding, expiratory Wheezing and crackles on chest auscultation.

21
Q

Bronchiolitis - relevant anatomy and symptoms

A

Nasal obstruction plus decreased compliance of lungs (stiff) causes early retractions to increase tidal volume, tachypnea, and grunting (Infants close the vocal cords at end expiration to keep airways open-laryngeal breaking)

22
Q

Bronchiolitis pathophysiology

A

Decreased surface area for gas exchange leads to increased oxygen need. Permanently Thickened interstitium causes decreased compliance and increased respiratory distress

23
Q

Bronchiolitis -diagnosis and treatment

A

Diagnosis: clinical. CXR findings are non specific (hyperinflation, peribronchial cuffing, interstitial markings and atelectasis). Treatment: Most effective is prevention. Monoclonal antibodies (palivizumab or synagis) are effective. Hospitalization required in young infants, hypoxemia on room air, respiratory distress. Prognosis is good.

24
Q

Asthma- physiology and symptoms

A

Asthma is caused by airway inflammation leading to increased mucous production, bronchial hyperreactivity, and airway edema • Recurrent symptoms of airway obstruction (cough, shortness of breath, chest tightness) • At least partial reversal of bronchospasm and symptom relief with a bronchodilator (e.g. a beta agonist such as albuterol) • All other diagnoses ruled out

25
Q

At what age can PFTs be used for diagnosis

A

Over 6 years old

26
Q

Asthma -treatment, prevention and prognosis

A

Inhaled beta agonist acutely for bronchial hyperreactivity, but inhaled corticosteroids is the chronic treatment of choice. Most children who wheeze only with illness grow out of their symptoms by age 12. Allergic asthma will most likely continue after 12

27
Q

Common acquired cause of parenchymal lung disease

A

Viral or bacterial pneumonia

28
Q

What is a parenchymal disease

A

Disorders that affect the alveoli and associated structures and may also affect the airways

29
Q

Community acquired bacterial pneumonia - symptoms, physical exam and diagnosis

A

• Fever, cough, dyspnea and tachypnea. Also may have evidence of infection at other sites • Abnormal chest examination (crackles or decreased breath sounds). • Abnormal chest radiograph (infiltrates, hilar adenopathy, pleural effusion).

30
Q

Community acquired bacterial pneumonia -treatment and prognosis

A

Empiric antibiotic therapy - ampicillin and aminoglycoside (5 yrs old). All children younger than 3 months should be admitted for treatment. Prognosis is good

31
Q

Bronchopulmonary dysplasia description

A

Acute respiratory distress in the first week of life, Required oxygen therapy or mechanical ventilation, with persistent oxygen requirement at 36 weeks gestational age or 28 days of life.

32
Q

Bronchopulmonary dysplasia pathogenesis

A

The premature lung makes insufficient functional surfactant; antioxidant defense mechanisms are not mature to protect the lung from the toxic oxygen metabolites, and lungs show early inflammation and hypercellularity followed by healing with fibrosis. Progressive lung injury occurs from oxygen toxicity, barotrauma, and inflammation

33
Q

Describe compliance of infant chest walls

A

Chest walls are more compliance with less negative pressure outward/recoid. Small airways start to close at end exhalation (atelectasis at baseline)

34
Q

Bronchopulmonary dysplasia clinical course

A

Ranges from a mild increased oxygen requirement that gradually resolves over a few months to more severe disease requiring tracheostomy and chronic mechanical ventilation for the first 2 years of life.

35
Q

Bronchopulmonary dysplasia treatment and prognosis

A

Artificial surfactant, prenatal glucocorticoids, and protective ventilatory strategies. Lung function may be altered for life including hyperinflation and damage of small airways Kids have higher risk for persistent hypoxemia, airway hyperreactivity, pulm HTN, neurodevelopmental problems

36
Q

Cystic fibrosis cause

A

Autosomal recessive mutation of CF transmembrane conductance regulator (CFTR) protein. Most common is ∆F508. This results in thick secretions. It affects the airways and pulmonary parenchyma

37
Q

Cystic fibrosis symptoms, physical exam, diagnosis

A

• Greasy, bulky, malodorous stools; failure to thrive. • Recurrent respiratory infections. • Digital clubbing on examination. • Bronchiectasis on chest imaging. • Sweat chloride > 60 mmol/L. Newborn screening measures immunoreactive trypsin (pancreatic enzyme) which is elevated in CF

38
Q

Cystic fibrosis infections

A

Most common is Pseudomonas aeruginosa. Chronic infection leads to airflow obstruction and progressive airway and lung destruction resulting in bronchiectasis.

39
Q

Cystic fibrosis treatment

A

Pancreatic enzymes, high caloric diet, airway clearance therapy, antibiotics