Brainscape's Knowledge GenomeTM

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


See full index

Pediatrics exam 2 > Pediatric Pulmonology > Flashcards

Pediatric Pulmonology Flashcards

1
Q

Infant respiratory distress syndrome

A

Formerly known as Hyaline
Membrane Disease
○ Most common cause of respiratory
distress in the preterm infant
○ More likely if born before 37 weeks
gestation

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

Cause of IRDS:

A
  1. Prematurity of the lungs
  2. Deficiency in pulmonary
    surfactant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Surfactant

A
  • Mixture of phospholipids & proteins synthesized & excreted
    by Alveolar type II cells of the alveolus.
  • Decreases surface tension of the alveolar sac.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What cells make surfactant?

A

Alveolar type II

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

Surfactant deficiency =

A

high surface tension, alveolar collapse (atelectasis)
= ↑ pulmonary dead space
* Inflammation, pulmonary edema, hypoxia, poor oxygenation,
↑ respiratory effort, & eventually respiratory failure

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

Lung Development

A
  • Surfactant production begins ~20 weeks
  • ~24 weeks alveolar sacs are present (survival possible)
  • Overall survival rate ~50%
  • ~30% survive without severe morbidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Best prevention of IRDS

A

Prevention of preterm birth

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

Alveoli collapse causes:

A
  1. Decreased gas exchange
  2. Decreased lung compliance &
    functional residual capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Decreased gas exchange leads to:

A

○ Acidosis (Respiratory & metabolic)
○ Pulmonary vasoconstriction
○ Endothelial & epithelial breakdown
○ Leads to protein rich exudate
○ Hyaline membranes (accumulation of dead
cells and proteins that line the alveoli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Decreased lung compliance &
functional residual capacity

A

○ ↑ dead space
○ V/Q (ventilation/perfusion)
mismatch & Hypoventilation
○ Right-to-left Cardiac shunt
○ Hypoxemia & hypercarbia
○ Respiratory acidosis

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

Clinical Presentation of IRDS

A

○ Respiratory distress (min.
to hours after birth)
○ Dyspnea
○ Retractions
○ Hypoxia
○ Grunting
○ Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diagnosis of IRDS

A

○ Chest X-ray
■ Diffuse signs of both interstitial
& alveolar congestion
■ Air bronchograms
■ Interstitial reticular pattern
■ “ground glass appearance”
○ ABG
o Blood cultures

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

Treatment of IRDS

A

○ Intratracheal surfactant administration
○ Supplementary oxygen as needed
○ Mechanical ventilation as needed

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

Intratracheal surfactant administration

A

○ Requires intubation
○ Best if followed by rapid extubation and switch to CPAP
○ Good evidence for CPAP immediately after delivery of premature
infant (keeps the alveoli open at the end of expiration)
○ Or MIST (minimally invasive surfactant therapy) just uses thin
catheter into the trachea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What would glucocorticoids do in preventing IRDS?

A

○ Glucocorticoids administered to mother
○ Betamethasone or dexamethasone given to
mother if delivery necessary between 24-34
weeks
○ Stimulates maturation of the baby’s lung tissue & surfactant release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Exogenous Surfactant

A

○ Exogenous aerosol via endotracheal
tube
○ Used if pt unresponsive to CPAP or
HFNC
○ Natural & Synthetic Surfactant options
○ Natural may be superior
○ Poractant Alfa
○ Calfactant
○ Beractant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Complications of IRDS

A

● Respiratory Acidosis
● Metabolic Acidosis
● Pulmonary Edema
● Infection
● Air Leak - Pneumothorax,
Pneumomediastinum
● Necrotizing Enterocolitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bronchopulmonary Dysplasia

A

Formerly called Chronic Lung Disease of Infancy
● Chronic pulmonary condition
● Sequelae of neonatal acute respiratory
distress, regardless of cause
● Typically caused by prolonged
mechanical ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bronchopulmonary Dysplasia pathophysiology

A

○ Poorly understood
○ Supplemental O2 w/ premature
lungs
○ Barotrauma, Oxidative Stress
○ Premature lungs more
susceptible to inflammation
caused by mechanical
ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

“Considered present when there is prolonged need for
supplemental oxygen in premature infants after 28 days of
age… and who do not have other conditions requiring oxygen”

A

Bronchopulmonary dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical Presentation of Bronchopulmonary Dysplasia

A

○ IRDS patients are at greatest
risk of developing BPD
○ Persistent respiratory
symptoms
○ Airway hyperreactivity
○ Requirement for continued
supplemental oxygen beyond
28 days old

22
Q

Diagnostic Evaluation of Bronchopulmonary Dysplasia

A

Clinical diagnosis
○ Hx of prolonged ventilation
○ Need for continued O2
Assessing the patient several weeks
after birth helps determine severity
CXR will demonstrate non-specific findings
○ pulmonary edema, cystic spaces, atelectasis

23
Q

Bronchopulmonary Dysplasia prevention

A

○ Therapeutic, but minimalistic approach to
mechanical ventilation preferred
○ Recognition of RDS & surfactant use
○ ↑ time on“vent” & ↑ O2 being delivered → ↑ risk of developing BPD

24
Q

Bronchopulmonary Dysplasia treatment

A
  • Nutrition supplementation (Many BPD
    patients have oral hypersensitivity with
    an aversion to eating)
  • Fluid restriction, diuretics
  • O2 supplementation as needed
  • Wean from mechanical ventilation and
    O2 as quickly as possible
  • Exacerbations may require hospitalization
25
Q

Prognosis of Bronchopulmonary Dysplasia

A

○ Ranges
● Lung function may be altered for life
○ Hyperinflation & damage to small
airways occasionally leads to COPD &
Pulmonary Hypertension later in life
○ Increased risk of developing asthma

26
Q

Pediatric Pneumothorax

A

● Pneumothorax in children is uncommon,
but significant & life-threatening
● Highest risk = intubated, premature
neonates

27
Q

Several causes of pediatric pneumothorax

A

○ Iatrogenic
○ Traumatic
○ Primary Spontaneous- without known lung disease
○ Secondary Spontaneous- with known lung disease

28
Q

Pathophysiology of Pediatric Pneumothorax

A

○ Disruption of the pleural membrane (visceral or parietal)
→ loss of intrapleural negative pressure & lung collapse
● Hypoxia and dyspnea caused by
○ Decreased vital capacity
○ Decreased alveolar partial pressure
of O2

29
Q

Pediatric pneumothorax Common signs & symptoms

A

■ Dyspnea
■ Cyanosis
■ Hypoxemia
■ Chest pain
○ Physical exam reveals ↓ breath sounds & hyperresonant percussion on the affected side

30
Q

Diagnostic Evaluation of Pediatric Pneumothorax

A

○ Pneumothorax is generally a clinical diagnosis that can usually be confirmed with an upright Chest X-ray
○ A tension pneumothorax should be diagnosed based on clinical signs Death can occur before CXR is performed!

31
Q

Pediatric Pneumothorax management and prognosis

A

○ If diagnosed in outpatient clinic setting, emergent transfer to the ER via EMS is advised.
■ Needle decompression immediately if tension pneumo
○ If large & symptomatic, chest tubes are placed to evacuate pleural space air & encourage lung re-expansion.
○ If the pneumothorax was an isolated event & treatment occurred quickly → good prognosis
○ If associated with trauma → prognosis is variable.
○ Risk of recurrence is high in Cystic Fibrosis patients.

32
Q

Oxygen Therapy for Infants

A

● For a patient who is breathing spontaneously but is hypoxic, several
oxygen delivery methods are available.
● Different methods of delivery are
available, most common include the
Blow-by, Head hood, Nasal cannula, Face
mask, nCPAP, High Flow Nasal Cannula
(HFNC), Intubation
● Although the hood is efficient for young
infants, the nasal cannula is more often used
(more mobility).
● In contrast, head hoods & nonrebreather masks are able to
deliver concentrations as high as 90-100%.
● While providing oxygen therapy, pulse oximetry should be
monitored closely.

33
Q

Even at high flow rates, O2 delivered by
nasal cannula rarely reaches inspired O2
concentrations over _____.

A

40-45%

34
Q

T/F Too much oxygen therapy can be bad to the infant

A

T

35
Q

Hyperoxia

A

may cause oxygen toxicity,
BPD, retinopathy of prematurity (ROP) (damage caused by oxygen free radicals)

36
Q

Pediatric Sleep Apnea

A

● A condition characterized by partial or complete episodic airway
obstruction that occurs during sleep. (Snoring)
○ Usually accompanied by hypoxemia, hypercapnia, &/or sleep
disruption.

37
Q

Risk factors of pediatric sleep apnea

A

○ Adenotonsillar hypertrophy
○ Obesity
○ Facial or laryngeal abnormalities
○ CNS dysfunction or disease
○ Neuromuscular disease

38
Q

Pathophysiology of pediatric sleep apnea

A

○ One of the most common
causes in children is enlarged
tonsils & adenoids → upper
airway obstruction.
○ CNS disorders (like Cerebral Palsy or
brain stem compression) can cause a
central apnea.
○ Obesity of the face & neck can also
cause obstruction.

39
Q

Clinical Presentation of pediatric sleep apnea

A

○ Snoring with apneic events & gasps.
○ Daytime (and nighttime) mouth breathing
■ Possible clue to tonsillar/adenoid hypertrophy or decreased
muscle tone of lips, tongue, and throat
○ Daytime sleepiness is seen, but is less common in kids than adults
○ Behavior issues, ADHD, anxiety/depression

40
Q

Untreated Sleep Apnea

A

○ Associated with cardiovascular
complications
○ Impaired growth, & Failure to Thrive
○ Learning Problems
○ Behavioral Problems

41
Q

Diagnostic Evaluation pediatric sleep apnea

A

○ Screen for snoring during WCCs.
○ A soft tissue lateral face/neck film may
show hypertrophy - Related to airway
abnormalities. (Down Syndrome)
○ Polysomnography is diagnostic for
obstructive & central apnea.

42
Q

Pediatric Sleep Apnea management

A

○ Tonsillectomy & Adenoidectomy are mainstays of treatment.
○ Weight management in obese children
is often beneficial as well.
○ Continuous Positive Airway Pressure (CPAP)
is needed for patients who fail surgical
therapy, or those who are not surgical
candidates (known central apnea).

43
Q

Foreign Body Aspiration risk factors

A

● Most common culprits are small, round
foods, such as hot dogs, grapes, berries,
nuts, seeds, etc.
● If the obstruction is significant,
progressive cyanosis, loss of
consciousness, seizures, bradycardia, &
cardiopulmonary arrest can follow
without treatment.

44
Q

frequent cause of accidental pediatric death

A

Foreign Body Aspiration

45
Q

Some common areas of foreign body lodging include:

A

○ Supraglottic airway- Most common
■ May trigger laryngospasm
○ Esophagus
■ Can compress the airway
○ Trachea
■ If object makes it through larynx
○ Large Bronchi
- Distal right bronchus is the most
common bronchial location

46
Q

Most common area a foreign body will lodge if aspirated

A

Supraglottic airway

47
Q

Treating a complete obstruction of FBA

A

○ If the patient is awake but unable to speak, moves air poorly, or is cyanotic, they are considered unstable & intervention is required immediately.
○ If under 1 year old, child should be placed face down over arm or lap.
Give 5 rapid back blows between the scapula, turn infant over & give 5
rapid chest compressions.
○ If over 1 year old, abdominal thrusts from behind (Heimlich maneuver)
should be attempted.
○ After back, chest, or abdominal thrusts, open mouth with jaw thrust &
carefully remove object if visualized. No blind sweeps!

48
Q

Rigid Bronchoscopy is the gold standard for diagnosis for

A

Foreign Body Aspiration

49
Q

Treating a partial obstruction

A

○ If patient is stable (forcefully
coughing & well oxygenated),
they may be able to forcefully
cough the object out.
○ If blockage progresses or patient’s
efforts fail, foreign body must be
removed with bronchoscopy or
laryngoscopy.

50
Q

Treating a complete obstruction

A

○ If the child is unresponsive (or becomes unresponsive during back, chest, or abdominal thrusts), must start CPR, which may dislodge the object.
○ If complete airway blockage &
ventilation w/ bag-valve mask or
endotracheal tube fails, the skilled
clinician should consider a
Percutaneous Needle Cricothyrotomy.

51
Q

Percutaneous Needle Cricothyrotomy

A

Performed by extending the neck,
attaching a 3-5 mL syringe to a 14-18
gauge IV catheter, & inserting catheter
through the cricothyroid membrane.
● Aspirate air to confirm position.
● Remove the syringe & needle, attach to ET
tube adapter & ventilate.

Pediatrics exam 2 (6 decks)

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