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Pediatrics > Pediatric Pulmonary Disorders > Flashcards

Pediatric Pulmonary Disorders Flashcards

1
Q

What is the leading cause of infant hospitalization in US?

A

Bronchiolitis

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2
Q

What is bronchiolitis?

A
  • Common, acute lower respiratory tract infection that primarily affects small airways
  • Clinical syndrome of respiratory distress in children under 2 years of age
  • Frequent cause of hospitalization in infants/young children
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3
Q

What are characteristics of bronchiolitis?

A
  • Upper respiratory symptoms followed by
  • Acute onset of wheezing
  • Crackles
  • Hyperinflation
  • Tachypnea
  • Results in acute inflammation of airways
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4
Q

What is wheezing/lower airway infection under 2 until proven otherwise?

A

Bronchiolitis

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5
Q

Pathophysiology of bronchiolitis

A
  • Virus attacks and causes inflammation in small bronchioles
  • Edema, excessive mucus, and sloughed epithelial cells
  • Leads to obstruction of small airways and atelectasis making it difficult to breath
  • RSV cause in majority of cases, followed by enterovirus, rhinovirus, parainfluenza
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6
Q

Epidemiology of bronchiolitis

A
  • Yearly outbreaks during winter, spring, and small extent fall
  • Primarily in first 2 years of life
  • Most during 1st year of life
  • Peak ages 1-10 months
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7
Q

Risk factors for bronchiolitis

A
  • Prematurity
  • Age <12 weeks
  • Cardiopulmonary disorders
  • Anatomic defects of airways
  • Immunodeficiency
  • Neurologic disease
  • Lack of breastfeeding
  • Environmental causes
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8
Q

What is history in bronchiolitis

A
  • Onset in spring or winter
  • Age
  • Prior history of wheezing
  • Recent history of signs compatible with common cold
  • Decreased appetite
  • Decreased sleep
  • Increased fussiness
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9
Q

Physical exam in bronchiolitis

A
  • Increased respiratory rate
  • Irritable
  • Lethargic
  • Retractions
  • Expiratory grunting
  • Prolonged expiration
  • Cough
  • Expiratory wheeze
  • Otitis media
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10
Q

Diagnosis of bronchiolitis

A
  • Clinical
  • O2 sat
  • NP swab (do not need unless suspecting flu or for quarantine reasons)
  • Imaging usually not necessary
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11
Q

Treatment of bronchiolitis

A
  • Nonsevere managed outpatient
  • Supportive care and anticipatory guidance mainstays
  • Adequate hydration
  • Relief of nasal congestion (nasal suction)
  • Monitoring for disease progression
  • Education on clinical course and when to seek medical treatment for worsening symptoms

No steroids or abx! Can get worse around day 2-3 but should get better by week, cough/wheezing can be present for several months

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12
Q

When should bronchiolitis be hospitalized?

A
  • Persistently increased respiratory effort
  • Hypoxemia O2<92%
  • Apnea
  • Acute respiratory failure
  • Toxic appearance
  • Poor feeding
  • Lethargy
  • Dehydration
  • Parents unable to care for child at home
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13
Q

Inpatient management of bronchiolitis

A
  • Supportive care and anticipatory guidance
  • Adequate hydration
  • Respiratory care in stepwise approach: nasal suctioning, supplemental oxygen to maintain between 90 and 92%, infants at risk of respiratory failure receive trial of CPAP, ET intubation
  • Monitor for disease progression
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14
Q

When would ribavirin be used in bronchiolitis?

A
  • Significantly immunocompromised patients
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15
Q

Discharge criteria for bronchiolitis

A
  • Respiratory rate <60 breaths per minute for age <6 months
  • Patient stable using ambient air
  • Caretaker knows how to clear infant’s airway using bulb suctioning
  • Patient has adequate oral intake
  • Caretakers confident can provide care at home
  • Resources at home adequate to support
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16
Q

What should be avoided in bronchiolitis?

A
  • Inhaled bronchodilators: albuterol –> may have modest short-term effect but doesn’t affect outcome and may have adverse events, can be tried if patient is severe
  • Systemic glycocorticoids: little effect
  • Inhaled saline: some studies show efficacy, some don’t
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17
Q

Patient education in bronchiolitis

A
  • Return to office or ED if symptoms worsen
  • Explain course of illness
  • 18% symptomatic after 3 weeks
  • 9% after 4 weeks, especially in young ingants
  • Link to recurrent wheezing within 2 years of initial episode
  • Some can have lung abnormalities beyond 10 years, but rare
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18
Q

What is the course of bronchiolitis?

A
  • Most improve w/in several days
  • Cough/congestion resolve within 1-2 weeks
  • Hospitalized patients discharged within 3-7 days
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19
Q

What is Palivizumab?

A
  • Humanized monoclonal antibody against RSV F glycoprotein
  • Immunoprophylaxis with this may prevent hospitalization in certain infants
  • First dose given before RSV season, followed by dose every 28-30 days throughout RSV season
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20
Q

Recommendations for palivizumab

A
  • Infants born at < or = 28 weeks, 6 days gestational age and <12 months at start of RSV season
  • Infants <12 months of age with chronic lung disease of prematurity
  • Infants <12 months of age with hemodynamically significant CHD
  • Infants and children <24 months of age with congenital lung disease of prematurity necessitating medical therapy (supplemental O2, bronchodilator, diuretic, or chronic steroid therapy) within 6 months prior to beginning of RSV season
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21
Q

What is nirsevimab?

A
  • Long-acting monoclonal antibody for use in newborns and infants to protect against RSV
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22
Q

When is nirsevimab recommended?

A
  • All infant younger than 8 months born during or entering their first RSV season, including those recommended by the American Academy of Pediatrics to receive palizumab
  • Infants and children aged 8 through 19 months who are at increased risk of severe RSV disease and entering their second RSV season, including those recommended by AAP to receive palivizumab
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23
Q

Considerations for 2023-2024 RSV season in regard to plaivizumab vs nirsevimab admin

A
  1. If Nirsevimab administered, palivizumab should not be administered later that season
  2. If Palivizumab initially administered for season and <5 doses administered, infant should receive 1 dose of nirsevimab. No further palivizumab should be administered
  3. If palivizumab administered in season 1 and child eligible for RSV prophylaxis in season 2, child should receive nirsevimab in season 2 if available. If nirsevimab is not available, palivizumab should be administered as previously recommended
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23
Q

Timing of nirsevimab

A
  • First week of life for infants born shortly before and during RSV season based on geography
  • Nirsevimab should be administered shortly before start of RSV season for infants younger than 8
  • Administer shortly before start of RSV season for infants and children 8-19 months of age who are at increased risk of severe RSV
  • May be given to age-eligible infants and children who have no yet received a dose at any time during the season
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23
Q

Which children are recommended to receive nirsevimab in their second RSV season?

A
  • Children with chronic lung disease of prematurity who required medical support any time during the 6-month period before the start of 2nd RSV season
  • Severely immunocompromised
  • Cystic fibrosis with manifestations of severe lung disease or weight-for-length that is <10th percentile
  • American Indian and Alaska Native children
24
Q

Is coadministration of nirsevimab with vaccines recommended?

A

Yes

25
Q

What is cystic fibrosis?

A
  • Autosomal recessive disease involving multiple organs, especially pancreas and lung
  • Most common lethal genetic disease in US
  • Usually develop obstructive disease, that leads to progressive respiratory failure and death
  • MC in caucasians
26
Q

Pathophysiology of cystic fibrosis

A
  • Mucociliary clearance problem
  • Defect in CF gene on chromosome 7 that encodes CFTR (epithelial chloride channel)
  • Problems with salt and water movement across cell membranes –> abnormally thick secretions
  • CFTR located in lungs, upper respiratory tract, sweat glands, pancreas, intestines, liver, reproductive tract
27
Q

Diagnosis of CF

A
  • Newborn screening (heel prick in hospital)
  • One of following symptoms:
  • Meconium ileus: delay pass of meconium –> abd distension
  • Respiratory symptoms: recurrent pna, wheezing
  • Failure to thrive: fall off growth curve in 1st few years

in 19th century diagnosed with salty sweat

28
Q

What is meconium ileus in CF

A
  • Obstruction of bowel by meconium in terminal ileum
  • Diagnostic of CF and should be presumed as having CF until a sweat test or genotyping obtained
29
Q

Other GI tract issues in CF

A
  • Volvulus, intestinal atresia, or meconoium peritonitis d/t meconium ileus
  • Poor hydration of intestinal contents, decreased pancreatic secretions, and fecal statis can cause distal intestinal obstruction syndrome
  • Rectal prolapse d/t excessive straining or difficulty passing stool with defecation, or coughing d/t increased intraabdominal pressure
30
Q

Symptoms in respiratory/sinus tract of CF

A
  • Chronic sinusitis
  • Nasal polyps
  • Persistent cough
  • Lower respiratory tract: infections with S. aureus, HIB, and pseudomonas –> persistent production cough, cycle of infection and inflammation, destruction of airways –> bronchiectasis
  • Complications such as pneumothorax, death from cor pulmonale, respiratory failure caused by recurrent pulmonary infections
31
Q

Pancreas conditions in CF

A
  • Abnormal electrolyte secretion –> dehydration of ductal secretions –> blockage of ducts
  • Destruction of pancreatic acini –> decreased pancreatic enzymes –> pancreatic insufficiency
  • Diabetes, secondary to destruction of pancreatic islet cells
  • Recurrent pancreatitis
  • Pancreatic insufficiency –> malabsorption of fats, proteins, carbohydrates, and fat-soluble vitamins such as A,D,E, and K
  • Children have a hard time growing/gaining weight, which results in failure to thrive
32
Q

Liver conditions in CF

A

Biliary cirrhosis with portal hypertension

33
Q

Impact of CF on MSK

A

Osteopenia and osteoporosis

34
Q

Impact of CF on electrolyte imbalance

A
  • Increased electrolytes in sweat –> loss of body electrolytes –> metabolic alkalosis
35
Q

Impact of CF on GU

A
  • Male infertility
  • Reduced testicular size and testosterone levels
  • Bilateral absence of vas deferens
  • Delayed pubertal development d/t poor nutritional status and decrease in glucose tolerance
  • Abnormal menstrual cycles
  • Female infertility due to thick, sticky vaginal mucosa
36
Q

Gold standard CF diagnostic

A

Sweat chloride testing

37
Q

Sweat chloride testing indications

A
  • Two weeks old and weight >2 kg
  • Positive screening of newborn
  • Meconium ileus
  • Older children and adults with suggestive symptoms
  • Siblings of patients with confirmed CF
38
Q

How is sweat chloride testing performed?

A

Collection of sweat with pilocarpine iontophoresis

39
Q

What is normal sweat chloride? Borderline? POsitive?

A
  • Normal <30 mmol/L
  • Borderline: 40-60 mmol/L
  • Positive >60 mmol/L
40
Q

When would genotyping of CF be performed?

A
  • After positive sweat chloride test
  • Carrier status patients or those with borderline sweat chloride testing
41
Q

What is the purpose of fecal elastase testing?

A
  • Screens those with CF for pancreatic insufficiency
  • Checks for pancreatic elastase-1, absent in over 80% with CF
42
Q

General Treatment of CF

A
  • Followed by CF foundation accredited care center
  • Evaluation by pediatrician, pediatric pulmonologist, respiratory therapist, nurse, dietician, social worker
  • Should be seen quarterly to check adequacy of therapies, as well as growth, nutrition, and pulmonary function
43
Q

Respiratory treatment of CF

A
  • Airway clearance and aggressive antibiotic use
  • Pulmozyne: mucolytic decreases viscosity of purulent CF sputum
  • Hypertonic saline
  • Inhaled bronchodilators
  • Chest physiotherapy
  • Antibiotics for chronic pseudomonas infections, screen sputum every 3 months, IV and inhaled tobramycin
  • CFTR modulator drugs: Kalydeco, Orkambi, Trikafta
  • Vaccinations
44
Q

GI treatment of CF

A
  • Pancreatic enzyme supplementation combined with high calorie, high protein, high fat diet
  • Daily vitamins
  • Caloric supplements
  • G-tube placement and supplemental feedings in FTT
45
Q

`

Signs and symptoms of acute CF exacerbation

A
  • New/increased cough
  • New/increased sputum production or chest congestion
  • Decreased exercise tolerance or DOE
  • increased fatigue
  • Decreased appetite
  • Dyspnea at rest/increased RR
  • Change in sputum appearance
  • +/- fever
  • Increased nasal congestion
46
Q

Treatment of acute CF exacerbation

A
  • Systemic abx treatment always
  • Identify from sputum cultures
  • At least one antibiotic to cover each pathogenic bacteria that is cultured from respiratory secretions and two for P. aeruginosa infections
47
Q

Prognosis of CF

A
  • Lung transplant: 5-year post survival 50-60%, risky, anti-rejection drugs
  • Median survival 47 years, rate of lung disease progression determines survival rate
48
Q

What is Infant Respiratory Distress syndrome primarily a disease of?

A
  • preterm infants
  • especially of diabetic mothers
49
Q

Pathophysiology of Infant respiratory distress syndrome

A
  • Surfactant expressed in lung in third trimester reduces alveolar surface tension allowing expansion of lungs
  • Deficiency of pulmonary surfactant in immature lung = primary cause
  • Noncompliant, stiff lungs that are structurally immature with insufficient surfactant –> amount of pressure needed to open alveoli increased leading to atelectasis at end expiration
  • –> ventilation/perfusion mismatch, hypoxemia, hypercarbia, persistent HTN
50
Q

Clinical features of IRDS

A
  • Almost always premature
  • Presentation min to hours after birth
  • Intercostal/subxiphoid retractions
  • Tachypnea
  • Nasal flaring
  • Diminished breath sounds
  • Cyanosis
  • Expiratory grunting
51
Q

Diagnosis of IRDS

A
  • Premature infant with onset of progressively worsening respiratory failure shortly after birth
  • CXR shows low lung volume and a classic diffuse ground-glass appearance
  • Pulse ox
  • ABG

`

52
Q

Treatment of IRDS

A
  • Basic principles of neonatal care: thermoregulation, cardio support, nutritional support, early infection care
  • Nasal CPAP initial preferred intervention
  • Surfactant replacement
53
Q

Prevention of IRDS

A
  • Prevention of prematurity, asphyxia, avoidance of maternal fluid overload
  • Prenatal administration of single course of steroids to women in preterm labor or at risk of delivery within next 7 days between 24-34 weeks gestation
  • Dexamethasone
  • If PROM give steroids and wait 1 week
54
Q

What is thyroglossal duct cyst?

A
  • Cyst of epithelial remnants of thyroglossal tract
  • Most common form of congenital neck mass
  • Presents as midline neck mass at level of thyrohyoid membrane, closely associated with hyoid bone
  • Arises as cystic expansion of remnant of thyroglossal duct tract
  • Theory that lymphoid tissue associated with tract hypertrophies at time of regional infection, occluding tract with resultant cyst formation
55
Q

Clinical features of thyroglossal duct cyst

A
  • Midline upper neck mass that is cystic
  • No symptoms, may be slightly tender
  • Often preceding upper respiratory infection: cyst from base of tongue to level of suprasternal notch, moves superiorly when swallowing
  • Can become infected and have some degree of inflammation at presentation
56
Q

Diagnosis of thyroglossal duct cyst

A
  • CT of neck with contrast: confirms diagnosis and gives info on size, extent, and location
  • Fine-needle aspiration to diagnose or exclude other diagnoses
  • MRI
  • US –> would start with US to see texture but CT/ FNA definitive
57
Q

Treatment of TDS

A
  • Surgery with sistrunk procedure
  • Do not perform surgery during acute inflammation or infection
58
Q

What is sistrunk procedure?

A

Resection of cyst and mid-portion of hyoid bone in continuity and resection of a core of tissue from hyoid upwards towards foramen cecum

59
Q

What would you do if acute inflammation or infection of TDS?

A
  • Treat with broad spectrum antibiotics
  • Augmenting (amoxicillin-clavulanate)
  • Clindamycin
  • Cephalexin
  • Surgical excision after inflammation/infection controlled

Pediatrics (12 decks)

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