obstructive lung diseases

Question 1

what is emphysema

Answer 1

the irreversible enlargement of the airspaces distal to the terminal bronchiole, often accompanied by destruction of the alveolar walls.

Question 2

what are the two forms of emphysema for us and whats more common

Answer 2

centriacinar is the more common form. in this form the destruction of the walls occurs in the respiratory bronchioles while the alveoli remain normal
in panacinar emphysema there is uniform dilation of the acinus from the respiratory bronchiole to the alveoli

Question 3

which form of emphysema is more associated with alpha 1 antitrypsin

Answer 3

panacinar is. this is because it is more total destruction of the acinus associated with smoking and AA1 deficinecy. makes sense as having a pre-disposition would result in more widespread destruction

Question 4

what are the three factors of pathogenesis of emphysema

Answer 4

protease-antiprotease imbalance, release of inflammatory mediators, oxidative stress.
these things resulting in destruction of elastic tissue within the alveoli and bronchiole walls

Question 5

what do we see on the X ray of the emphysema

Answer 5

flattened diaphragm, inflation of apex above the clavicle, horizontal orientation of the ribs, Decreased bronchovascular lung markings (the
thread shadow of bronchial and vascular trees
in normal lung)

Question 6

what do we see clinically in emphysema patients

Answer 6

there is obstruction of expiration due to loss of elastic recoil. there is thus airway collapse during expiration so patients purse their lips to prevent this - they are thus pink puffers.
barrell chested as chests are hyperinflated.

Question 7

what is cor pulmonale

Answer 7

In advanced cases, increase in pulmonary capillary pressure
(pulmonary hypertension) could lead to right side heart
failure – called ‘cor pulmonale’ (cor = heart disease caused by
pulmonary disease).

Question 8

what is chronic bronchitis

Answer 8

persistent cough with sputum production as there is mucus hypersecretionm inflammation, recurrent infection and fibrosis.

Question 9

why are the bronchitis patients the blue bloaters

Question 10

pathogenesis of bronchitis

Answer 10

smoking triggers chronic inflammation. in response to the inflammation the bronchial wall undergoes metaplasia of surface endothelium, and there is hypertrophy and hyperplasia of mucus secreting glands in the submucosa.
obstruction from mucus secretion predisposes infection - perpetuating infection

Question 11

Th2 cell pathogenesis of asthma

Answer 11

allergen is presented to the Th2 cells activating them. these cells cause B cells to class switch to IgE.
when re-exposed to antigen we get a type 4 hypersensitivity as the Th2 cells release IL4 stimulating IgE production in B cells. IL5 recruiting and activating local eosinophils. IL13 stimulating mucus production. with these attracted leukocytes we get the late phase response

Question 12

tell me about the late phase response of asthma

Answer 12

With these leukocytes, especially the eosinophils we get the late phase response of asthma as there is recruitment of eosinophils, neutrophils and lymphocytes causing inflammation. The main one is the eosinophils releasing proteins and other cytokines to cause damage to the airways.
Over time the late phase response results in: basement membrane thickening, hyperplasia of the bronchial smooth muscle, hypertrophy of mucosal glands, and hyperplasia of goblet cells and damage to the epithelium. This can lead to the chronic severe asthma when less poorly managed resulting in more severe attacks.

Question 13

tell me about the immediate phase response of asthma

Answer 13

gE which is released and bound to mast cells activating them. On repeat exposure to the antigen the IgE on the mast cells is cross linked and we get a type one hypersensitivity as cytokines are released causing inflammation.
These cytokines cause the immediate asthma response whereby we see bronchoconstriction as the cytokines cause vagal stimulation and PNS activating the muscarinic receptors. Also get increased vascular permeability, mucus production and airway blockage and increased recruitment of the leukocytes.
This is done through things like leukotriennes and things.

Question 14

what is bronchiectasis

Answer 14

permanent dilation of the bronchi and bronchioles due to destruction of their walls

Question 15

pathogenesis of bronchiectasis

Answer 15

it is the result of repeated cycles of infection with subsequent destruction of the bronchial smooth muscle and elastic tissue, resulting in healing by fibrosis.