pathoma - chronic obstructive pulm disease

Question 1

what is the defining characteristic for all COPDs?

Answer 1

an obstruction to air getting OUT of the lung

Question 2

airway obstruction

Answer 2

FVC (5L = normal) and FEV1 (4L = normal) decreases but FEV1 decreases more

FEV1:FVC ratio decreases - this basically defines the disease

TLC is increasd (air trapping)

Question 3

chronic bronchitis

Answer 3

chornic productive cough lasting at leaset 3 months over a minimum of 2 years

highly associated with smoking

involves large airways (like the bronchus)

some of the mucous gets coughed up, but some goes down and plugs the airways obstructing the flow of air

Clincical features: productive cough, cyanosis (increase in PaCO2 and decrease in PaO2), increased risk of infection or cor pulmonale

Question 4

what are the two types of glands in the large airways?

Answer 4

serous glands - secrete watery material that humidifies the air

mucous glands - mucous traps particals (normally these glands make up 40% of epitlilia thickness) smokers get hypertrophy of these glands -

Question 5

what is the reid index

Answer 5

the reid index measures the thickness of these glands in relation to the thickness of epi (if its over 50% then they have bronchitis)

Question 6

why does an increase in PACO2 decrease the PAO2 in the alveoli in chronic bronchitis and other obstructive diseases

Answer 6

the alveoli can only handle a certian amount of pressure before it breaks, the more that pressure is taken up by CO2 the less O2 can fit in the alveoli

Question 7

what is cor pulmonale

Answer 7

when the vessels of the lung sense that there is not alot of O2 in that region they squeeze down to shunt blood to another part of the lung. if there is disease where all the areas of the lungs become low on O2 every vessel clamps down (increase the resistance of the pulm system) - because of this the right heart has to work harder = right vent hypertrophy and eventually it will fail (cor pulmonale is this failure)

Question 8

emphysema

Answer 8

destruction of alveolar air sacs

loss of elastic recoil and collapse of small airways leading to air trapping

• due to imbalance of proteases and antiproteases
  
  • alpha 1 anti trypsin is produced in the alveoli (antiprotease) to counter proteases produced during macrophage phagocytosis (inflamation)
  • either an increase in proteases or a decrease in antiproteases cuases the disease
    
    • smoking cuases massive inflamation in the lung = lots of proteases - most common cuase of smoking
      
      • results in centriacinar emphysema - more in upper lobes (upper lobes because smoke goes up)
    • alpha 1 anti trypsin defficiency - no good antiproteases - less common
      
      • results in panacinar emphysema more in lower lobes
      • liver cirrhosis may also be present - the body does produce A1AT but it is misfolded so it stays in hepatocytes in the liver = pile up in ER = cirrhosis
        
        • can see as purple blobs in hepatocytes that are PAS positive

Question 9

centriacinar emphysema

Answer 9

more common in smokers - smoke reaches the centriacinar part first and in higher concentrations so it gets inflamed the most

Question 10

panacinar emphysema

Answer 10

affects the entire acinus - because they dont have antiproteases anywhere so they get inflamation everywhere

Question 11

clinical features of emphysema

Answer 11

• dyspnea and coucgh with minimal sputum
• prolonged expiration with pursed lips (pink puffer)
• weight loss
• increased AP diameter of the chest (barrel chest)
• late complications
  
  • hypoxemia
  • cor pulmonale

Question 12

asthma

Answer 12

• reversible airway bronchoconstriction
• most often due to allergic stimuli (type 1 hypersensitive reaction)
• presents in childhood - often associated with allergic rhinitis, eczema, and family history of atopy
• IgE mediated activation of mast cells (early phase)
• inflamation perpetuates bronchoconstriction (late phase)
• clinical features (episodic)
  
  • dyspnea and wheezing
  • productive cough; curschmann spirals (in the product) admixed with carcot-leyden crystals (crystaline aggregates of eosinophils major basic protein)
  • severe, unrelenting attack can result in status asthmaticus and death

Question 13

non allergic cuases of asthma

Answer 13

exercise

viral infection

• asprin (aspirin intolerant asthma)
  
  • bronchospasms
  • nasal polyps

occupational exposures

Question 14

bronchiectasis

Answer 14

• permanent dilation of bronchioles and bronchi
  
  • dilated bronchiles result in turbulent flow which is an energy sink = makes it harder to blow out = less air out
• loss of airway tone results in air trapping
• kartageners syndrome - dyen arm messed up = not working cilia

Question 15

what cuases bronhiectasis

Answer 15

• due to necrotizing inflammation wiht damage to airway walls
  
  • cystic fibrosis
  • kartagener syndrome - defect in dyen arm of the cilia - cilia cant move
    
    • situs inversis
    • sterility
    • problems with the lungs
  • tumor or foreign body
  • necrotizing infection
  • allergic bronchopulmonary aspergillosis - seen in asthmatics and CF pateints

Question 16

what are the clinical features of bronchiectasis

Answer 16

• cough, dyspnea, and foul smelling sputum
• complications include: hypoxemia with cor pulmonale and secondary amyloidosis
  
  • amyloidosis
    
    • deposition of a misfolded protein
    • can be localized (in one organ) or systemic (in multiple organs)