Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

33 Cards in this Set

  • Front
  • Back
What are the main types of COPD
Chronic bronchitis
Define chronic bronchitis
Production of excessive mucus in the bronchial tree on most days for at least 3 months a year for 2 successive years
Describe the changes in chronic bronchitis
1. increased size of mucus glands
2. Increased Reid index (ratio of thickness of mucus glands to thickness of bronchial wall)
3. some inflammation
Features of chronic bronchitis
-mostly older men
-cigarette smokers or dusty occupations
-frequently associated with centrilobular emphysema
Define emphysema
3Ds: dilation and destruction distal to the terminal bronchiole
4 types of emphysema
1. centriloular- blue bloaters
2. panlobular- pink puffers
3. paraseptal- very focal, near scar. not associated with general symptoms
4. irregular- diffuse plate-like scars in lungs
-No fibrosis; alveolar wall is large and dilated.
-When the alveolar wall is knocked out, the alveolar capillaries and the ability to do diffusion are knocked out
-small airways are supported by alveolar walls. When the alveoli are knocked out, small airways collapse prematurely- proximal damage
-looks like "popcorn
-destruction is confied to the terminal and respiratory bronchioles
-prefers apex of lungs
-terminal bronchioles, respiratory bronchioles, and alveoli are dilated and destroyed
-no regional preference in lungs
Hallmarks of emphysema
-normal septae but loss of uniform architecture
-no fibrosis
-when the dilated and destroyed areas coalesce they form bullae which are dead spaces and no gas exchange takes place there
How do you diagnose emphysema
x-ray studies and pulmonary function studies
What is bronchiectasis
permanent state of abnormal airway dilation resulting from chronic necrotizing infection.
-You lose the natural taper-off = "tram lines"
Causes of bronchiectasis
1.bronchial obstruction- tumor, foreign body, mucus impaction
2. hereditary or congenital conditions- CF
3. Some sort of necrotizing pneumonia with tissue destruction (TB)
Two factors that must happen to get bronchiectasis
1. obstruction
2. recurrent infection
What are the anatomic types of bronchiectasis
Cylindroid and Saccular
Define asthma
Reversible airway narrowing which over time can produce specific morphological changes. Increased irritation of the tracheobronchial tree leads to paroxysmal narrowing of bronchial airways, may reverse with treatment
Morphological changes associated with asthma
1. Curshmann Spirals- mucus casts of small airways
2. Eosinophils
3. Charcot-Leydon Crystals- casts of eosinophil membranes
4. bronchial structural alterations- thickening of bronchial epithelial basement membrane, edema, infiltration of bronchial walls by eosinophils, hypertrophy of submucosal glands, and hyperplasia of bronchial smooth muscle.
5. Mucus plugging may be common
Someone dies and the have hyperinflated lungs. why did they die?
Could be status asthmaticus. they would be hyperinflated from mucus plugging. people die due to the work of breathing
Types of asthma
1. Immune and non-immune are the most common
2. Aspirin sensitive
3. Industrial
4. Asperigillosis
Interplay of cellular infiltrate and mesenchymal reaction that works at the small airway. Neutrophilic. Bronchiole swelling can occur upstream. Can get fibrous plugs in bronchiolitis.
Spectrum of bronchiolitis
Asthmatic type changes. Chronic bronchitis/emphysema-associated bronchiolar changes. Cellular bronchitis. Bronchiolitis obliterans.
End stage restrictive interstitial fibrosis
-Honeycomb appearance
-When lung is injured it responds with granulation tissue (fibroblasts and new capillaries). When alveoli are injured, they respond with fibrosis
Restrictive Lung Disease
Principal morphological change is thickening of the alveolar wall or interstitial space either by cellular infiltrate or by fibrosis
-Move air in and out quickly since airways are held open.
-Maximum ventilatory capacity is very high
-With fibrosis, new vascular beds can't be recruited so a drop in PaO2 with exertion occurs
Current idea on cause of idiopathic interstitial fibrosis
An imbalance between cell-mediated factors that improve tissue restoration and those antibody-mediated factors that lead to fibroblast activity and matrix deposition in the interstitium.
How do you diagnose restrictive lung disease
Open lung biopsy
What is the temporal profile with restrictive lung disease
There is an acute type with diffuse alveolar damage and a chronic type
Cell mediated versus antibody mediated response in lung
Cell-mediated involves TH1 and leads to tissue restoration while antibody-mediated involves TH2 and leads to fibrosis via fibroblast activity. IFN gamma is TH1
Define pneumoconiosis
Pulmonary diseases caused by inhalation of inorganic dusts. Silica, Asbestos, and coal dust
Pathophys of pneumoconiosis
When dust is first inahled, alveolar macrophages dictate the response. there will be a reaction that increases fibrosis of alveolar wall and alveolus. This can lead to restrictive lung disease
How do you diagnose pneumoconiosis
tissue or xray
Hypersensitivity pneumonitis
an immune response in the lungs to inhaled antigens. example is bird antigens causing granulomatous rxn in lungs
Define pulmonary edema (cardiac)
extrusion of edema fluid, initially in the interstitium, and then in the alveolar filling phase, produced by cardiac failure. causes an increase in V/Q mismatch. You diagnose it by history, physical exam and xray. may be in a few minutes or chronic.
Pulmonary edema (noncardiac)
the destruction of the alveolar epithelium or endothelium resulting in interstitial edema and alveolar filling edema in the setting of normal cardiac function. Caused by injury to alveolar endothelium or epithelium. There is an exudative phase (first week), then a proliferative phase (weeks one to three), then a fibrotic phase (week three on)
How do you distinguish cardiac and noncardiac pulmonary edema
Compare the pressures. In non-cardiac edema, the heart pressures are fine while they are not fine in cardiac edema.