Chapter 15 - The Lung Flashcards
Type of pneumocyte that makes surfactant
Type II
Causes of pulmonary hypoplasia
- Compression
- impede normal expansion
1. oligohydramnios-not enough fluid to go in lungs and expand
2. diaphragmatic hernia
Pneumocyte covering 95% of alveolar surface
Type I
Epithelium for most of respiratory tree & where is it not this?
Pseudostratified, tall, columnar, ciliated epithelial cells except for vocal cords (stratified squamous)
- RESORPTION ATELECTASIS caused by? <– And what can cause this?
- Reversible/irreversible?
- Which way will mediastinum shift?
- Why do alveoli collapse?
- Complete obstruction of airway by mucous plugs post op, aspiration, neoplasms
- shift towards affected lung
- alveoli collapse because a lack of distal air and resorption of pre-existing trapped O2
- COMPRESSION ATELECTASIS caused by?
- why do alveoli collapse?
- which way does the mediastinum shift?
- reversible/irreversible?
- pleural cavity is partially or completely filled by exudate, tumor, blood, air
- pressure collapses small airways under the pleura
- shifts away from affected lung
- reversible
- CONTRACTION ATELECTASIS caused by?
- reversible/ irreversible?
- fibrotic changes cause prevent expansion
- irreversible :(
What are the 2 types of pulmonary edema?
- Hemodynamic pulmonary edema
2. Micro vascular injury
Hemodynamic pulmonary edema caused by and an example
Increased hydrostatic pressure, like left sided CHF
- What do the lungs look like in hemodynamic edema grossly?
- histology?
- heavy wet lungs
- heart failure cells
- alveolar capillaries engorged
- intra-alveolar pink precipitate
- eventually brown induration
Pathophysiology behind edema caused by microvascular injury
Primary injury to vascular endothelium/epithelial cells –> leakage of fluids and fluids into interstitial space –> leaks to alveoli –> can cause acute respiratory distress syndrome
Examples of edema caused by micro vascular injury
Infections (pneumonia, sepsis), aspiration, drugs
What is acute lung injury & and what’s it’s most severe form
- Abrupt onset of hypoxemia and pulmonary lung infiltrates w/o cardiac failure
- acute respiratory distress syndrome (ARDS)
Histology of ARDS
Diffuse alveolar damage, waxy hyaline membranes on alveoli
Pathophysiology of ARDS
Injury to endothelial/epithelial cells –> shift to pro-inflammatory state –> cytokine release –> neutrophil chemotaxis –> neutrophils damage alveolar epithelium –> dysregulation of coag system
Resolution and late findings in ARDS
Type II pneumocytes make surfactant and make more type I pneumocytes
Predisposing conditions to ARDS (10)
*Gram negative sepsis, *gastric aspiration, *trauma with shock, *pulmonary infections like SARS, heroin, smoke inhalation, acute pancreatitis, cardiopulmonary bypass, DIC, fat embolism
Physical findings for ARDS
Dyspnea, tachypnea, inspiratory infiltrates b/l, respiratory acidosis, unresponsive to O2, V/Q mismatch
Obstructive Lung Diseases (4) can’t get air in/out?
Can’t get air out:
- Bronchitis
- Bronchi ecstasies
- Asthma
- Emphysema
Types of emphysema (4)
- Centriacinar
- Panacinar
- Paraseptal
- Irregular
CENTIACINAR
- What part does this affect
- associated with what
- what lobe
- central/proximal acini
- associated with smokers
- upper lobes
PANACINAR
- what part of alveoli?
- associated with?
- what part of lung
- whole acinus from bronchioles to terminal alveoli
- associated with alpha 1-anti trypsin deficiency
- lower lung
Pathophysiology of emphysema
Cigarette smoke –> chemotactic for neutrophils and creates free radicals –> inactivates antiproteases (functional alpha1 antitrypsin deficiency) –> increase in neutrophil elastase <– congenital alpha1 antitrypsin deficiency
Genes involved in alpha1 antitrypsin deficiency!?!
Normal M allele and homozygous ZZ allele which has an 80% chance of getting Panacinar emphysema