Lung Path Flashcards
which bronchi is straight
right
what size particles are most dangerous
.5-5um
lobule
cluster of terminal bronchioles w/attached acini
acinus
respiratory bronchiole and all attached alveolar ducts and sacs
pulmonary hypoplasia
common 10% neonatal autopsy
seen w/fetal compression and other anomalies
congenital foregut cysts
detached section of maldeveloped foregut presents as mass or incidental finding, possibly in adulthood mediastinal and hilar locations not connected to airway usually bronchogenic w/respiratory epi some esophageal, some enteric
cystic adenomatoid malformation
CPAM
Hamartomatous lesions w/abnormal bronchiolar tissue
types of CPAM
type I- large cysts good prognosis
type II- medium cysts, poorer prognosis since associated w/other congenital malformations
bronchopulmonary sequestrations
areas of lungs w/o normal connections to airways
blood supply is from systemic aa
extralobar bronchopulmonary sequesterations
external to lung
may have other congenital anomalies
intralobar bronchopulmonary sequestrations
w/in lung
associated w/recurrent local infection and/or bronchiectasis
most likely an acquired lesion
respiratory distress in newborn
excessive maternal sedations fetal head injury blood or amniomtic fluid aspiration intraunterine hypoxia from cord hyaline membrane disese
hyaline membrane diease stats
most common
1000 deaths in 2002, but 25000/year in 60s
hyaline membrane disease
can occur in term infants, but usually preterm
rate inversely proportional to gestational age
associated w/males, materal DM, multiple gestations, and c-section before onset of labor
immature lungs
deficiency of surfactant
alveoli development
20wks- glandular
30wks- saccular
term- alveolar
bronchopulmonary dysplasia
> 28 days of O2 therapy in infant >36weeks post mentrual age
alveolar hypoplasia and thickened walls
dysmorphic capillaries and decreasesed VEGF
cytokines (TNF, IL8, etc)
increased and may have role
cystic fibrosis
widespread disorder in epi transport affecting fluid secretion in exocrine glands and epi of resp, GI, and repro tracts
viscid secretions
autosomal recessive
CFTR gene chrom 7
most common lethal genetic condition in Caucasians
Dx criteria for CF
one or more characteristic phenotypic features or a Hx or CF in sibling or positive newborn screening test
AND
an increased sweat chloride on 2+occasions or 2CFTR mutations or demonstration of abnomral epi nasal ion transport
Tx of CF- pancreas
oral pancrelipase
may progress to DM
Tx of CF- vit deficiency
oral fat soluble vitamins
parenteral nutrition
Tx of CF- pulomonary
postural drainage and chest percussion bronchcodilators mucolytic agents Antibiotics hypertonic saline high dose ibuprofen slows lung disease progression
apparent life threatening event (ALTE)
if survive at risk for future respiratory death
prolonged apnea, diminished responses to hypercarbia or hypoxia
often premature or have mechanical disorders leading to compromise
no longer considered true SIDs
atelectatsis
incomplete expansion- neonatal
acquired collapse- adults can be due to: resorption/obstruction, compression, or contraction
ALL AT RISK FOR INFECTION
resorption/obstruction atelectasis
airway obstruction, mucus, foreign body, tumor
mediastinal shift toward involved lung
compression atelectasis
external pressure including elecated diaphragm
mediastinal shift away from involved lung
contraction atelectasis
secondary to fibrosis
irreversible
types of pulmonary edema
hemodynamic
microvascular
hemodynamic pulmonary edema
most common
increased hydrostatic pressure due to left sided heart failure
basal lower lobes
heart failure cells
secondary infections
if chronic leads to alveolar fibrosis (brown lung)
microvascular (alveolar) injury pulmonary edema
increased permeability
caused by infection, toxic injry,
if diffuse leads to ARDS
non-cardiogenic pulmonary edema criteria
acute onset of dyspnea
hypoxemia
b/l infiltrates
absence of primary left heart failure
non-cardiogenic pulmonary edema etiology
wide spread disorers injuries may be related to mediators such as cytokine, oxidants, TNF, ILs, TGF beta, susceptibility may be heritable may progress to ARDS OR AIP
Adult ARDS
shock rapid onset, life threatening occurs in patients w/severe disease diffuse damage to alveolar capillary walls -> neutrophilic migration secondary loss of surfactant prothrombotic milieu
infectious conditions associated w/adult ARDS
Sepsis
diffuse pulmonary infections
gastric aspiration
physical injury ARDS
mechanical trauma, including head injuries pulmonary contusions near-drowning fractures w/fat emboli burns ionizing radiation
inhaled irritants ARDS
O2 toxicity
smoke
irritant gases and chemicals (paraquat)
other causes of ARDS
cardiac reperfusion injury
ARDS clinical
patients are already ill when ARDS superimposed rapid onset profound dyspnea and tachypnea cyanosis and respiratory failure diffuse b/l inflitrates up to 60% fatal permanent damage
acute interstitial pneumonia (AIP)
symptoms similar to ARDS no associative causative disorder 59 yrs, M=F acute respiratory failure following illness 33-74% mortality rate w/in 2 months
obstructive lung disease
limit rate of flow
FEV1/FVC reduces
due to resistance at any level
obstructive lung disease examples
COPD, chronic bronchitis, asthma
restrictive lung disease
limit total lung capacity and residual volume
near normal flow rates
restrictive lung disease examples
chest wall disorders, obesity, ARDS, interstitial fibrosis, penumoconioses
COPD classifications
centriacinar/cantrilobular
panacinar/panlobular
distal acinar/paraseptal
irregular/paracicatrical
centriacinar/centrilobular
smoking, smoking, smoking
predominately upper lobes/apices
panacinar/panlobular
alpha-1 antitrpsin deficiency, smoking
predominately ant/lower lobes
distal acinat/paraseptal
- subpleural and adjacent to septate
- may be bullous and cause spontaneous penumothrorax in young adults
- associated w/previous damaged lung
irregular/paracicatrical
common, but focal and usually asymptomatic associated w/scarring
proteolytic digrestion of alveolar walls in COPD
via neutrophil-secreted elastase
normally inhibited by alpha 1 antitrypsin
COPD clinical
symptoms after 1/3 of lung damaged barrel chest low FEV1, high TLC, and RV pink puffer bullous emphysema repsiratory acidosis cor pulmonale
COPD Tx
quit smoking bronchodilators steroids bullectomy transplant
other conditions w/increased air
compensatory hyperinflation
obstructive overinflation
interstitial emphysema
compensatory hyperinflation
due to loss of adjacent tissue
obstructive overinflation
trapped air
-ball valve obstruction by object
collaterals feeding around obstruction, life threatenting,
alveolar pores of kohn, bronchiloloalveolar canals of lambert
-congenital lobar overinflation from lack of bronchial cartilage
interstitial emphysema
any air in inetersitium
chronic bronchitis
clinically defined as 3 mo productive cough/year for 2 consecutive years smoking, smoking, smoking hypersecretion of mucus increased reid index brochiolitis obliterans in small airways superimposed infection dyspnea and cor pulmonale blue bloaters
reid index
normal <.4
thickness of gland/thickness of walls
hypertrophy of bronchial submucosal glands