Ch. 12 ARDS, Alveolar Diseases and COPD Flashcards Preview

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Flashcards in Ch. 12 ARDS, Alveolar Diseases and COPD Deck (20)
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What are DAD and ARDS?

DAD: diffused alveolar damage; pattern of reaction of alveolar cells to insults

ARDS: clinical description of DAD, when normal lungs progress rapidly to respiratory failure, commonly requiring ventilation, with "white-out" opacities in both lungs.


Describe the basic pathophys behind the exudative phase of DAD

1) Injury to endothelial cells
2) Leakage of protein-rich fluid from capillaries into interstitial space
3) Loss of Type I pneumocytes
4) Fluid enters alveolar spaces, depositing protein
5) Formation of hyaline membranes on injured alveolar walls
6) Type II pneumocytes replace the normal endothelial lining
7) Inflammatory cells accumulate due to cell injury


Describe the organizing phase of DAD

1) Fibroblast proliferation within alveoli. 2) Macrophages digest the hyaline membranes formed in the exudative phases.
3) Fibrosis thickens alveolar septa
4) Remodeling of lung produces cyst-like spaces in lung (honeycomb lung)


You bought yourself some Landsberg and did a CC fellowship to follow in his footsteps. There you learn that many of your ARDS patients will present like this:

You know some classic conditions that lead to ARDS are:

Dyspnea, tachypnea, hypoxemia, cyanosis, require mechanical ventilation, "white-out" CXR.

Oxygen toxicity, shock, gram-neg sepsis, aspiration of gastric contents, drugs like bleomycin, radiation, herbicides, DIC


What condition results from immaturity of the surfactant system in premature births?

Neonatal respiratory distress syndrome


Ms. Jones is a 50 y/o who comes in complaining of fever, productive cough, and SOB. After you exhaust all the usual suspects for a diagnosis, you get a biopsy.

The biopsy shows granular, eosinophilic material in the alveoli, and stains for surfactant, with little inflammation.

What does she have? If she got this genetically, what's the pathogenesis?

Alveolar proteinosis

Defective surfactant clearance by macrophages due to deficient GM-CSF (granulocyte-macrophage-colony-stimulating-factor)


What disease is described by the triad of diffuse alveolar hemorrhage, glomerulonephritis, and auto-antibodies to the basement membrane?

Goodpasture Syndrome

(hemoptysis, glomerulonephritis)


The patient presents with night sweats, dyspnea, weight loss, and a productive cough.

The CXR shows the complete opposite image of pulmonary edema, with peripheral alveolar infiltrates but no hilar pathology. You treat with corticosteroids and get quick resolution.

What does this patient have, and therefore what are you likely to find in their sputum?

Idiopathic Eosinophilic Pneumonia (eosinophils in sputum)

Can also get secondary eosinophilic pneumonia due to parasitic infection or Churg-Strauss


What is the Reid index and what is used to diagnosis?

Index measures the size of the mucous glands in proportion to the entire bronchial wall. If the index is >.5, the patient has chronic bronchitis


Describe the symptoms and development of chronic bronchitis. Are these patients blue-bloaters or pink-puffers?

Usually seen in smokers, increased bronchial mucus cells as a result of hyperplasia and hypertrophy

Causes a chronic productive cough producing copious amounts of sputum. Sputum obstructs airways, causing cyanosis, and cor pulmonale can occur, leading to edema; thus blue-bloaters.


This chronic lung disease is due to enlarged airspaces with destructed walls, but DOES NOT show fibrosis.



You meet a patient at Golisano that has emphysema. What is the most likely cause of emphysema in young adults?

What pattern of emphysema are they most likely to have? What other organ will be affected?

Alpha-1-antitrypsin deficiency (PiZ allele)

This enzyme normally inhibits elastase, which injures the lung elastic tissue. Without it, you can get emphysema as a non-smoker.

Panacinar emphysema with loss of alveolar septa

Liver cirrhosis due to accumulation of misfolded anti-trypsin.


Joe Camel, a 65 y/o lifelong smoker comes into your office. He tells you he's had dyspnea for the past 20 years, without much of a cough. He's working extra hard to breathe, pursing his lips, and is really skinny, except that his chest seems constantly over-expanded. His skin has a nice, pink, tinge.

What does he have? How did the smoking cause this? What part of the acini has he damaged?

Centrilobular emphysema: destruction of terminal bronchioles near end of tree (proximal) in the central part of the lobule.

The smoke induces an inflammatory reaction, and ploys release elastase, which destroys elastic tissue and impairs recoil, trapping air in the lungs.

Pink-puffers because increased respiratory rate allows oxygen levels to be maintained.


Which respiratory disorder has the following pathogenesis:

Allergens interact with IgE, causing mast cell degranulation and inflammation. The inflammation causes mucus hyper secretion and bronchoconstriction


Inflammatory mediators cause smooth muscle contraction, mucous secretion, increased vascular permeability, and edema.


Which proteins, released from eosinphils, aggravate bronchoconstriction and mucociliary function in asthma?

Leukotriene B4 and major basic protein


"The bronchial hyperresponsiveness in asthma is attributed to inflammatory reactions to diverse stimuli"

Name some inciting asthmatic stimuli

Viral respiratory infections (esp RSV)
Exercise, especially in the cold
Drug-induced (aspirin intolerant w/ nasal polyps)
Air pollution
Occupational asthma


Which disease would show lungs distended with air, with mucous plugs, many eosinophils, and hyperplasia of bronchial smooth muscle on biopsy?

Asthma, especially if the patient died in status asthmaticus (severe acute asthma unresponsive to therapy)


What are Curschmann spirals, Creola bodies and Charcot-Leyden crystals and what disease do they appear in?

Curschmann spirals: mucoid casts of airways that get coughed up

Creola bodies: compact clusters of epithelial cells expelled with coughing

Charcot-Leyden crystals: phospholipids of eosinophil cell-membrane, expelled with coughing



What would a PFT of a patient with an obstructive lung disease like chronic bronchitis, emphysema, or asthma show?

Decreased FVC (volume of air forcefully expired)
Decreased FEV1 (volume of air expired in first second)
Decreased FEV1:FVC ratio
Increased TLC (total lung capacity)

^All due to air trapping in lung


COPD can be thought of as a combination of which two obstructive lung diseases?

Chronic bronchitis and emphysema