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
What are some symptoms of emphysema and when do they begin?
- Dyspnea, coughing, wheezing, weight loss, barrel-chested, hunched over, breathing through pursed lips
- clinical manifestations begin when at least 1/3 of pulmonary parenchyma is damaged
Where does para septal emphysema occur? Does it produce COPD? What is there an increase risk of?
- distal acini
- no COPD
- increased risk of spontaneous pneumothorax with rupture of us pleural blebs
IRREGULAR EMPHYSEMA:
- associated with?
- COPD?
- associated with scar tissue
- no COPD
CHRONIC BRONCHITIS definition?
Productive cough for at least 3 months for 2 years
Pathophysiology of chronic bronchitis
Irritation –> hypersecretion of mucous–> alterations in small airways of the lung, fibrosis
Histology of chronic bronchitis
Mucous gland hyperplasia in trachea + bronchi, Reid index of wall thickness to mucous gland layer (normal 0.4), goblet cell metaplasia
Long term Chronic bronchitis can lead to: (3)
- COPD
- Cor pulmonale and heart failure
- Atypical metaplasia/dysplasia (pre-cancerous)
Pink puffers
Emphysema
Blue bloaters
Chronic bronchitis
Symptoms of chronic bronchitis
Other than chronic sputum, dyspnea on exertion
Most common respiratory disease in kids
Asthma
Asthma with IgE mediated hypersensitivity, what will be a positive test
Atopic asthma, allergen sensitization, skin reaction positive
Asthma with no allergen sensitization and negative skin test result. What is its common trigger
Non-atopic asthma, viral respiratory infection
Pathophysiology of atopic asthma:
Initial sensitization –> IL-4 (switch to IgE) and IL-5 ( eosinophil chemotaxis) –> release mediators–> bronchoconstriction, mucous, leukocytes –> late phase 4-8 hours –> eotaxin (for eosinophils) –> eosinophils release mbp and damage epithelial cells and constrict airway
Status astmaticus
Unremitting attacks that result in fatality
Histology of asthma: (4)
Mucous plugs (curschmann spirals), eosinophils, Charcot Leyden crystals, airway remodeling
What is bronchiectasis? What does it destroy
Permanent dilatation of bronchi and bronchioles, destruction of cartilage and elastic tissue
What causes bronchiectasis? (4)
Cystic fibrosis, infections (TB is most common), bronchial obstruction (like a carcinoma), primary ciliary dyskinesia, aspergillosis
What is primary ciliary dyskinesia?
Absent dynein (ATPase for movement) arm in cilia, often have kartagener syndrome with it
What part of lungs does bronchiectasis affect
Lower lobes
Histology of bronchiectasis
Very dilated airways
Symptoms of bronchiectasis:
So much foul smelling sputum!, hemoptysis, dyspnea, orthopnea
Complication of bronchiectasis
Cor pulmonale
Causes of restrictive lung disorders (2)
Chest wall disorders, interstitial and infiltration diseases
Clinical and pulmonary symptoms of restrictive disease (5)
Dyspnea, tachypnea, end inspiratory crackles, b/l infiltrative lesions (nodules, irregular lines, ground-glass shadows), honeycomb lung (fibrosis in advanced stage)
What age group has interstitial pulmonary fibrosis?
40-70
Pathogensis of idiopathic pulmonary fibrosis
Unknown agent –> repeated cycles of epithelial injury/activation –> cytokine release –> alveolar interstitial fibrosis –> proximal dilation of small airways
Histology and gross morphology of lung in idiopathic pulmonary fibrosis
Usual interstitial pneumonia (patchy interstitial fibrosis), honeycomb fibrosis , grossly cobblestoned lung
What part of lung is affected in idiopathic pulmonary fibrosis
Lower lobes
what are heart failure cells?
Hemosiderin laden macrophages
Symptoms of idiopathic pulmonary fibrosis (3)
Dyspnea on exertion, dry cough, cyanosis/clubbing (late)
What are Masson bodies and in what disease can you find them?
Polyploid plugs of loose connective tissue in cryptogemic organizing pneumonia
Connective tissue diseases with pulmonary involvement (3)
- Rheumatoid arthritis
- Systemic sclerosis
- Lupus erythematosus
Characteristics of the lung in rheumatoid arthritis
Interstitial fibrosis with or without rheumatoid nodules, chronic pleuritic with or without effusion
4 main causes of pneumoconiosis
- Coal dust
- Silica
- Asbestos
- Beryllium
Most dangerous particle size in pneumonconiosis
1-5 micrometers –> reach terminal airways and sacs. If they are smaller than this they can reach the alveoli and be phagocytosis by the macrophages
Which is the mildest form of coal workers pneumoconiosis
Anthracosis
What size buildup in simple coal workers pneumoconiosis and what part of lung does it affect
1-2mm coal macules and larger coal nodules in upper lobes and upper portions of lower lobes
What can simple coal workers pneumoconiosis lead to
Centriacinar emphysema if coal deposits adjacent to respiratory bronchioles
Size of coal deposits in complicated coal workers pneumoconiosis, and what may happen in the middle of these deposits
Blackened scars greater than 2 cm, usually have a necrotic center
What can complicated coal workers pneumoconiosis lead to: (2)
Pulmonary HTN and cor pulmonale
What is the most common occupational disease in the world
Silicosis
What deposits in silicosis and where in lung
Crystalline silicone dioxide (Quartz), upper lung
Pathophysiology of silicosis
Macrophages eat the quartz and it causes them to release cytokines which stimulate fibrosis
What 2 things do you see on radiography in advanced silicosis
Nodular opacities that progress to hard collagenous scars and eggshell calcifications in hilar nodes
What disease is associated with silicosis
Increased susceptibility to tuberculosis