Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
21 Cards in this Set
- Front
- Back
|
Do bronchiolos possess cartilage or submucosal glands?
|
NO
|
|
|
3 to 5 terminal bronchioles =
|
Pulmonary Lobule
|
|
|
Also called terminal respiratory unit
Contains respiratory bronchioles |
Acinus
|
|
|
almost entire respiratory tree lined by ?
|
ciliated pseudostratified tall columnar epithelium
|
|
|
(1 of 10 neonatal autopsies)
3 major factors: -ABNORMALITIES CAUSING LUNG COMPRESSION diaphragmatic hernia (more often left sided) chest wall abnormalities ascites OLIGOHYDRAMNIOS via renal anomalies, PROM DECREASED RESPIRATION(anencephaly) |
agenesis or hypoplasia
|
|
|
known as bronchogenic cysts
from detached fragment of primitive foregut in lung tissue usually in children and young adults usually 1 to 4 cm with ciliated pseudostratified columnar lining treatment: surgery |
Foregut Cysts
|
|
|
portion of lung tissue without a connection to the normal airways
blood supply from aortic branches |
bronchopulmonary sequestration
|
|
|
located outside of the lung
mostly in infants with 50% cases diagnosed in first month of life “mass” with separate pleura 90% on the left side |
extralobar sequestration:
|
|
|
isolated ‘mass’ within the lung parenchyma
most cases thought to be acquired through recurrent episodes of pneumonia lower lobe in 98% of cases |
intralobar sequestration:
|
|
|
incomplete expansion of lung or collapse of previously inflated lung
airless parenchyma reduces oxygenation and predisposes to infection |
Atelectasis
|
|
|
due to complete obstruction of airway by excessive secretions (plugs) or exudates
see resorption of O2 in distal alveoli mediastinum may shift TOWARD affected lung found in asthma, chronic bronchitis, bronchiectasis and aspiration reversible |
Obstruction or resorption type Atelectasis
|
|
|
pleural cavity partially or completely filled by fluid, tumor, blood or air
seen in cardiac failure, neoplasms and tension pneumothorax mediastinum shifts AWAY FROM affected lung reversible |
Compression type Atelectasis
|
|
|
due to fibrosis within the lung or pleura
prevents lung expansion NOT reversible |
Contraction type Atelectasis
|
|
|
triggered by increased hydrostatic pressure (left sided heart failure)
gross: heavy ‘wet’ lungs, initially seen in lung bases microscopic: intra-alveolar precipitate, hemosiderin-laden macrophages (“heart failure” cells) and fibrosis with alveolar wall thickening (chronic cases) |
Hemodynamic or Cardiogenic Edema
|
|
|
alveolar septal injury by infections, drugs, shock
NO increase in hydrostatic pressure damage to vascular endothelium or to alveolar epithelial cells leakage of fluid and proteins into interstitial space and alveoli if diffuse, may lead to ARDS |
Edema by microvascular (capillary) injury
|
|
|
diffuse alveolar damage, shock lung and acute alveolar injury
see a rapid onset of severe respiratory insufficiency, cyanosis and arterial hypoxemia possibly refractory to O2 therapy may lead to multisystem organ failure |
ARDS
|
|
|
sepsis
diffuse pulmonary infection (viral, Mycoplasma, Pneumocystis, TB) gastric aspiration mechanical trauma (head injuries) |
Common causes of ARDS
|
|
|
Acute or Exudative Phase of ARDS
|
during the first week following lung injury
lungs are firm, red and edematous |
|
|
see hyaline membranes
fibrin-rich edema fluid cytoplasmic and lipid remnants of degenerated type I pneumocytes & endothelial cells |
Exudative phase of ARDS
|
|
|
Organizing phase of ARDS
|
begins about one week after injury
proliferation of type II pneumocytes fibroblastic proliferation in the interstitium and alveolar spaces marked thickening of alveolar septae hyaline membranes no longer formed |
|
|
secondary to capillary endothelial or alveolar epithelial injury
final common pathway- diffuse damage to alveolar capillary walls |
Pathogenesis of ARDS
|
