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Pediatrics > Lung Diseases > Flashcards

Lung Diseases Flashcards

1
Q

3 Main Pediatric Lung Diseases

A

Respiratory Distress Syndrome (RDS)
Sudden Infant Death Syndrome (SIDS)
Cystic Fibrosis (CF)

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2
Q

What is another name for RDS?

A

Hyaline membrane disease

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3
Q

Define RDS

A

Lung disease in a preterm infant resulting from insufficient surfactant

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4
Q

What is the major cause of morbidity & mortality in infants born prior to 30 weeks gestation?

A

RDS

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5
Q

What product has changed clinical course & decreased morbidity & mortality rates in RDS?

A

Exogenous surfactant

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6
Q

Epidemiology of RDS

A

Incidence decreases over 35 weeks
More severe in male infants
More severe & common in white infants

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7
Q

Increased Incidence Risk Factors of RDS

A 
Low gestation
Male sex
White race
Maternal DM (decreased lung development & surfactant production)
C-section pre-onset of labor
Perinatal asphyxia
Maternal HTN
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8
Q

Decreased Incidence Risk Factors of RDS

A

Prolonged rupture of membranes
Chronic congenital infections
Maternal substance abuse
Antenatal corticosteroid exposure

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9
Q

2 Major Issues in RDS

A

Immature lungs

Lack of surfactant

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10
Q

Reasons for Immature Lungs

A

Born before lung development

Born before surfactant production

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11
Q

At what stage can true gas exchange occur?

A

Saccular stage

Alveolar ducts present

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12
Q

Reasons for Lack of Surfactant

A

Production begins at 23-24 weeks

Adequate amounts not produced until 35 weeks

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13
Q

What does surfactant do?

A

Reduces surface tension in alveoli
Facilitates lung expansion
Prevents alveolar collapse

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14
Q

Other Issues in RDS

A

Excessively compliant chest walls
Weakness of respiratory muscles
Alveolar collapse

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15
Q

Pathophysiology of RDS

A 
Alveolar collapse alters V/Q
Pulmonary shunting
Arterial hypoxemia
Metabolic acidosis
Vasoconstriction
Pulmonary HTN
May have R to L shunting
Increased pulmonary blood flow
Pulmonary edema
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16
Q

How do the lungs appear in hyaline membrane disease?

A

Solid & congested with diffuse atelectasis

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17
Q

What are hyaline membranes made from?

A

Plasma proteins leaked from damaged capillaries

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18
Q

PE findings in RDS

A 
Progressive tachypnea
Retractions
Grunting
Cyanosis
Decreased breath sounds
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19
Q

Diagnostics of RDS

A

CXR

ABGs

20
Q

Findings with CXR in RDS

A

Increased density of lung fields
Reticulogranular infiltrates
Air bronchograms
Elevation of diaphragm

21
Q

ABG Findings in RDS

A

Hypoxemia
Hypercarbia
Metabolic acidosis

22
Q

How does exogenous surfactant drastically change the course of RDS?

A

Decreased need for oxygen
Decreased mechanical ventilation
Reduce incidence of gas leaks

23
Q

What needs to be done for babies with RDS?

A

Stabilization
Cardiopulmonary function monitoring
Adequate respiratory support
Proper thermal, metabolic, & nutritional support

24
Q

Prevention of RDS

A

Prevention of premature delivery

Antenatal corticosteroids

25
Q

What do antenatal corticosteroids do?

A

Improve lung compliance
Increase lung volume
Decrease capillary protein leak

26
Q

Complications of RDS

A 
Hemorrhagic pulmonary edema
Capillary rupture & interstitial fluid
May be seen with exogenous surfactant
First 5-7 days of life
Rapidly fatal
27
Q

Define SIDS

A

Sudden unexpected death of an infant less than 1 year of age, with onset of the fatal episode apparently occurring during sleep, that remains unexplained after a thorough investigation, including a complete autopsy & review of the circumstances of death & clinical history

28
Q

Age and time of death in SIDS

A

Sparing in 1st month
Increases in 2nd month
Peak incidence at 3 months
Occurs during the night

29
Q

Possible Maternal Risk Factors for SIDS

A 
Young age
Multiparity
Smoking & drug abuse during pregnancy
Previous fetal deaths
Anemia during pregnancy
Placenta previa
Premature rupture of membranes
Low social class
Low family income
Short inter-pregnancy interval
Unmarried mother
Partner unemployed
Late attendance of antenatal clinic
Postnatal depression
Attendance to psychiatrist
UTI in pregnancy
30
Q

Possible Infantile Risk Factors in SIDS

A 
Male
Low birth weight
Premature
Blood type B
Low APGAR scores
Low hematocrit @ 48 hours
Not using a pacifier
Prone/side sleeper
Bed-sharing
Overheating
Formula fed
Siblings in family
Sleeping in own room
Previous SIDS in family
Previous cyanotic episode
31
Q

What is the most important preventable risk factor for SIDS?

A

Maternal smoking

32
Q

Risks to child from maternal smoking include

A

Fetal hypoxemia
Inhibition of airway growth and development
Decreased ability to arouse to noxious stimuli
Increased susceptibility to respiratory tract infections

33
Q

How do pacifiers help to prevent SIDS?

A

Reduce arousal threshold

No evidence to discourage pacifier use

34
Q

Why is a prone position a risk to develop hypercapnia?

A

Rebreathing of expired air
Hypoxemia
Upper airway closure
Arousal deficit

35
Q

Pathology of SIDS

A

Intrathoracic petechial hemorrhages
Frothy secretions around mouth & nose
Evidence of URI
Hypoxic tissue markers
Abnormalities in brain stem serotoninergic system

36
Q

Monitored events of SIDS have shown

A

Apnea, bradycardia, unlikely primary mechanism
No arousal reaction
Gasping occurs in majority of victems

37
Q

Prevention of SIDS

A 
Supine sleeping
Firm sleep surface
Soft objects out of crib
Don't sleep with infant
Smoke-free environment
Pacifier at nap & bedtime
Avoid overheating
38
Q

Define Cystic Fibrosis

A

Syndrome of chronic sinopulmonary infections, malabsorption & nutritional abnormalities

39
Q

Organ Dysfunction in CF

A 
Sinuses: sinusitis, nasal polyps
Lungs: endobronchitis, bronchiectasis
Pancreas: exocrine insufficiency, CF DM
Intestine: meconium ileus, constipation
Liver: focal sclerosis
Vas Deferans: failure to develop
Sweat gland: salt-losing dehydration
40
Q

CF Related Complications

A 
Stunting, wasting
Micronutrient deficiencies
Steatorrhea
Intestinal obstruction
Intussusception
Hypoelectrolytemia
Airway infection
Progressive obstructive lung disease
Bronchiectasis
DM
Rectal prolapse
Sinusitis
Vasculitis
Non-alcoholic steatohepatitis
Male infertility
41
Q

Genetics of CF

A

Large gene on chromosome 7
Carrier rate high
Autosomal recessive

42
Q

Diagnostics of CF

A

One or more symptoms
Positive “newborn screen”
CFTR dysfunction- sweat chloride
Emphasis on the process

43
Q

“End Stage” Lung Disease in CF

A

Bronchiectasis
Infection
Inflammation
Mucous plugging

44
Q

Physiologic Abnormalities in CF

A

Severe airflow obstruction

Increased RV, FRC

45
Q

Treatment for CF

A 
Airway clearance therapy
Antibiotics
Inhaled mucolytics
Bronchodilators
Enzyme replacement
Fat soluble vitamins
Azithromycin
Ibuprofen

Pediatrics (23 decks)

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