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
alveolar disease characteristics
air bronchogram fluffy and indistinct confluent and homogeneous may have segmental or lobar distribution seen in pneumonia and pulmonary edema
interstitial lung disease characteristics
discrete
inhomogeneous
no air bronchogram
made up of lines (reticular), dots (nodular), both (reticulo-nodular)
atelectasis
opacified hemi-thorax from volume loss
shift of heart and mediastinal toward opacified hemi-thorax
pleural effusion
opacified hemi-thorax from large fluid
shift of heart and mediastinal structures away from side of opacified hemi-thorax
congestive heart failure
kerley B lines
pleural effusions
fluid in fissure
peri-bronchial cuffing
pneumothorax
visceral pleural white lines
absence of lung markings peripherally
tension-shift away from pneumothroax
carcinoma characteristics on CXR
thick wall
nodular
TB characteristics on CXR
thin wall
smooth margin
abscess on CXR
thick wall
smooth margin
air fluid level
most common cause of CAP
strep pneumo
viral pneumonia on CXR
bilateral infiltrates
CXR findings for pulmonary embolism
Hampton’s hump (hemidiaphragm elevated)
Westermark sign from enlargement of PA
causes of transudate effusions
CHF
nephrosis
liver cirrhosis
hypoalbuminemia
causes of exudative effusions
infections
malignancy
inflammatory disorders
benign asbestos related pleural effusions
develop after 15 years
pleural plaques from asbestos
circumscribed areas of pleural lining along ribs and diaphgram
benign in etiology
asbestosis as interstitial lung disease
progressive pulmonary fibrosis caused by inhalation of fibers
mesothelioma
from surface of pleural cavity
rare neoplasm
silicosis
crystalline silica from mining
10 years of exposure before x-ray changes
progressive nature
progressive fibrosis on CXR
systems approach to CXR
airway bones and soft tissue cardiac and mediastinum diaphgragm and gastric bubble effusions fields
pathophysiology of pneumothroax
gas within the pleural space
gases follow pressure gradient and flow into pleural space
tension pneumothorax is a medical emergency
possible treatment of pneumothorax
watchful waiting with or without supplemental oxygen
simple aspiration
tube drainage with or without pleurodesis
measurements from British Thoracic Society and US for pneumothorax
from outer edge at level of hilum >2cm large
US from apex >3cm large
characteristics of strep pneumo
extensive infiltrate usually abutting pleural space
prominent air bronchograms (ddx from staph)
predilection for lower lobes
characteristics of staph pneumo
patchy bronchopneumonia of segmental distribution, frequently bilateral
may be associated with atelectasis since airways are filled
pleural effusion in 50%
characteristics of mycoplasma pneumo
commonest cause of nonbacterial pneumonia
mild course; lasts 2-3 weeks
peak in autumn and winter
acute interstitial infiltrate in lower lobes, alveolar infiltrates usually unilateral
characteristics of aspiration pneumo
depends on position of patient when aspiration occurred
RLL most common
while standing will have bilateral LL
lying in left lateral decubitus-left sided
RUL from alcoholics who aspirate in prone position
pathophysiology of pleural effusion
imbalance between fluid production and fluid removal in pleural space
exudate
local factors
protein and LDH rich
transudate
systemic factors
low protein and low LDH
solitary pulmonary nodule
single, well defined lesion, usually rounded or slightly ovoid, surrounded by normal lung tissue
diameter must be 3cm or less (greater is malignant mass)
nodular mimics
nipple shadows
skin moles
prominent costochondral junction
guidelines for low risk
less than 4mm no investigation
4-6mm at 12 months
6-8mm at 6-12 and 18-24 months
greater than 8mm scan at 3,9, and 24
guidelines for high risk
less than 4mm at 12 months
4-6mm at 6-12 and 18-24 months
6-8mm at 3-6, 9-12, and 24 months
greater than 8mm scan at 3,9 and 24
CXR for TB
hilar and/or mediastinal lymphadenopathy
primary-upper lung filed infiltrate with or without cavitation
reactivation-large unilateral pleural effusion, pericardial effusion, or miliary pattern
bronchiectasis
dilation of medium sized airways
triad of bronchiectasis
chronic cough
excess sputum production
repeated infection
pathophysiology of asbestosis
fibers deposited at alveolar duct bifurcations and cause alveolar macrophage alveolitis
activated macrophages release cytokines (TNF, interleukin 1 beta and oxidant species) leads to fibrosis
mechanical irritation and inflammation initiates pleural scarring
diffuse pleural thickening from confluence of smaller parietal pleural plaques or extension of subpleural interstitial fibrosis
mechanism of clearance of asbestos fibers
lymphatic drainage and pleural cavities
silicosis pathophysiology
silica ingested by alveolar macrophages
breakdown of macrophage releases enzymes which produce fibrogenic response
requires 10-20 years of exposure
progressive despite cessation of dust exposure
imaging of silicosis
multiple small round opacities 1-10mm in size
usually in upper lobes
mostly in apical and posterior regions of upper lobes and apical portion of lower lobes
guidelines for AAA
repair in symptomatic AAA and in large asymptomatic
monitor infra/juxtarenal measuring 4.0-5.4cm with ultrasound every 6-12 months
AA <4cm ever 2-3 years
stage 1 CHF
redistribution
redistribution
cardiomegaly
broad vascular pedicle
13-18mmHg
stage 2 CHF
interstitial edema
Kerley lines peribronchial cuffing hazy contour of vessels thickened interlobar fissure 18-25mmHg
stage 3 CHF
alveolar edema
consolidation air bronchogram cottonwool appearance pleural effusion >25mmHg
most common cause of cough
post infectious
upper respiratory infection
viral
nonpulmonary causes for dyspnea
cardiac problems
anemia
neuromuscular disorders
most common cause of hemoptysis
bronchitis
other causes of hemoptysis
lung cancer
pulmonary vascular disorders (Goodpasture, Wegener)
coagulopathy or thrombocytopenia (still need source of bleeding)
sudden chest pain
pneumothorax
do not cause chest pain
chronic lung diseases
other causes of chest pain
pneumonia
abscess
pulmonary embolism
neoplasm
cause of rhonchi
airway obstruction
usually mucus secretions
cause of wheeze
airway obstruction
crackles
fluid in parenchyma
fine dry crackles
scarring and interstitial
common spontaneous pneumothorax
tall thin patients
COPD
pneumonia with hyperresonance
pleural effusion
pulmonary nodules
common
can be associated with connective tissue diseases
can be sign of lung malignancy
mets to lungs
testicular
thyroid
kidney
sound of edema
rales
sound of interstitial disease
fine crackles
sound of secretion in airway
rhonchi
sound of airway swelling
wheezing
COPD as umbrella term
includes emphysema, chronic bronchitis, adult asthma
definition of chronic bronchitis
chronic productive cough for at least 3 months in 2 successive years
most are smokers
more mucous production
emphysema
abnormal enlargement of air sacs of terminal bronchioles, accompanied by destruction of air space
results in air trapping and hyperinflation
COPD mixture
chronic bronchtiis
asthma
emphysema
asthma
chronic obstructive lung disorder with reversible and intermittent airway obstruction
interstitial disease
involves inflammation and secondary fibrosis of pulmonary interstitium
frequently coexists with obstructive disease
characteristics of chronic bronchitis
mucus gland hypertrophy
increased neutrophilic infiltrates
increased airway reactivity
increased sputum production
physical exam chronic bronchitis
wheezing
rhonchi
prolongation of expiratory phase
provocation of asthma attacks
cold
allergens
irritants
respiratory illness
inflammatory profiles COPD
PMNs CD8
inflammatory profiles asthma
IL4
IL5
CD4
severe asthma
may have bronchiolitis rather than pure asthma
requires treatment with corticosteroids
physical exam interstitial disease
fine dry crackles
no wheezing
digital clubbing may be present
cough and dyspnea
acute respiratory failure
drop in pH suggests decompensation
increased pCO2 in asthmatic
v bad
dd of COPD exacerbations
CHF
pneumonia
pulmonary embolism
treatment for COPD and asthma
bronchodilators inhaled steroids oral steroids anti-leukotriene agents theophylline
risk from chronic steroid use
osteoporosis
vaccinations for obstructive lung disease patients
influenza
pneumococcal vaccinations
causes blebbing
coalescing air sacs
emphysema
emphysema and cirrhosis
A1AT deficiency
most consistent exacerbation of asthma
viral infection
