Clinical Flashcards
embryonic stage of lung development
3rd to 7th week
at 28 days R and L mainstem bronchi are present
44th day PA from 6th aortic arch
initial branching into 5 lobes
failure to complete separation from esophagus
TE fistula
pseudoglandular stage
glandular appearance
weeks 5-17
rapid branching of pulmonary tree
mucus glands develop by 14th week
canalicular stage
16th to 24th week
capillary bed expands and endothelium thins
becomes thin enough to allow gas exchange
acceleration of tissue thinning and surfactant production
glucocorticoids
failure of capillary beds to form
alveolar capillary dysplasia
saccular stage
decrease in mesenchymal tissue
increase in type II maturation and surfactant
factor that decreases surfactant production
maternal diabetes
alveolar stage
36 weeks to 2-3 years
increased epithelial cells (most are type 2 pneumocytes but type 1 covers most of the alveolar structure)
changes in pulmonary vasculature
failure to change pulmonary vasculature
PPHN
VEGF
promotes angiogenesis
when blocked increase in alveolar size similar to emphysema
involved in development of BPD and ROP
retinoic acid
increase alveolarization
may decrease BPD
estrogen and testosterone
estrogen required fr adequate levels of surfactant
testosterone slows lung development
surfactant components
dipalmitoylphosphatidylcholine
phospholipids
proteins
cholesterol
surfactant protein A
most abundant
recycled by type II pneumocyte
opsonin-important in phagocytosis
deficiency still compatible with life
surfactant protein B
small but fusogenic-enhances spread and stability of surfactant mono layer
required for extra-uterine life
surfactant protein C
most hydrophobic
must be activated by surfactant protein B
functions to recruit phospholipids to lipid layer
AD deficiency-develop interstitial pneumonitis/emphysema
surfactant protein D
largest surfactant protein
not involved in stabilizing or recycling surfactant
found in other organs
main function in innate immunity (e. coli, salmonella, pseudomonas, RSV, adeno, flu A)
increases secretion of surfactant
glucocorticoids
estrogen
thyroid hormone
decreased secretion of surfactant
insulin
sources of surfactant inactivation
aspiration-BM, formula, sterile water
meconium
swallowed blood
pneumonia
betamethasone
increases surfactant production
decreases division and bronchial length
worsens body and lung growth if given to the mother
improves lung maturation if given to fetus
signs of respiratory distress
tachypnea grunting nasal flaring retractions cyanosis
transient tachypnea of newborn
failure for lung fluid to be reabsorbed
hormonal changes from labor cause reversal of Na channels
risks for transient tachypnea of newborn
males c section perinatal asphyxia umbilical cord prolapse depressed newborn (sedation)
presentation of transient tachypnea of newborn
CXR for diagnosis
develop minutes after delivery and resolve by 12-48 hrs
treatment-supportive (oxygen and nasal cPAP)
respiratory distress syndrome
surfactant deficiency (begins at 24 but 35 for adequate) leads to membrane formation (hyaline) impaired gas exchange
risk factors respiratory distress syndrome
prematurity caucasian and male previous baby with RDS perinatal asphyxia/cold stress perinatal infection multiple gestation infant of diabetic mother patent ductus arteriosus
presentation of respiratory distress syndrome
develop distress hours after delivery
worsen for first 3 days
adequate surfactant by 7 days of life
treatment of RDS
natural surfactant from porcine or bovine
artifical lack functional proteins
nasal cPAP/mechanical ventilation
congenital pneumonia
symptoms in first 24 hours of life
isolated to pulmonary system
only 10% have positive blood culture
sources of congenital pneumonia
infectious-e. coli, GBS, u. urealyticum
non-infectious-aspiration of blood or meconium
risk factors for congenital pneumonia
prolonged rupture of membranes (<12 hours)
maternal fever
uterine tenderness
foul smelling amniotic fluid
treatment for congenital pneumonia
antibiotics (amp and gent)
oxygen
nasal cPAP/mechanical ventilation
spontaneous pneumothorax
related to alveoli with defective formation during development
risk factors for spontaneous pneumothorax
difficult deliveries/birth trauma
large for gestational age-infants of diabetic mothers
positive pressure ventilation during resuscitation
connective tissue diseases
treatment for pneumothorax
avoid positive pressure
needle the chest
half require placement of chest tube
usually resolves in 3-4 days
congential diaphragmatic hernia
related to abnormal diaphragm formation during development
treatment for congenital diaphragmatic hernia
mechanical ventilation, replogle to LIS
surgery is potentially curative
chest x-rays in asthma
flattened diaphgram
hyperexpansion of lungs due to air trapping
Curschmann spirals
twisted mucous plugs mixed with sloughed epithelium
seen in asthma
Charcot-Leyden crystals
hexagonal bipyramidal crystals of eosinophil membrane proteins
seen in asthma
symptoms of acute sinusitis
URI facial pain, pressure or fullness purulent rhinorrhea maxillary toothache nasal obstruction
etiology of acute sinusitis
viral-rhino, adeno, influenza, parainfluenza
bacterial-strep pneumo, H flu, staph, moraxella
indications for antibiotics in acute sinusitis
dont resolve within 7 days or worsen moderate to severe pain temp of 101 periorbital swelling erythema and facial pain immunocompromised patients
signs of acute bronchitis
cough
nasal congestion
rhinorrhea
can persist for 3 weeks regardless of antibiotics
most common etiology of acute bronchitis
viral
treatment of acute bronchitis
antibiotics should not be given
symptom management with antitussive medications
procalcitonin level
marker of bacterial infection when deciding on antibiotic in acute bronchitis
signs of strep pharyngitis
sore throat fever tonsillar exudates cervical lymphadenopathy absence of cough
diagnostic tests for strep pharyngitis
rapid antigen detection test
throat culture (gold standard)
antibody titres should not be used routinely
suppurative complications of strep pyo
bacteremia cervical lymphadenitis endocarditis mastoiditis meningitis otitis media peri-tonsillar abscess pneumonia
non-supprative complications of strep pyo
post strep pharyngitis
rheumatic fever
DOC strep pyo
penicillin
erythro in allergy
air bronchogram
fluid fills alveoli-bronchus becomes visible
sign of airspace disease
solid spheres on CT
homogeneous from one side to another
blood vessels and masses
can be met nodules, AVM
hollow tubes on CT
lower density in center
bronchi and cavities
can be CF, bronchiectasis, TB