breathing diseases

Question 1

asthma - early development

Answer 1

allergen stimulates TH2 cells which stimulate B cells to produce IgE and eosinophils.
IgE binds to mast cell surfaces to prepare for next exposure
type 1 hypersensitivity

Question 2

asthma main issue

Answer 2

obstruction from bronchoconstriction and mucous hypersecretion

Question 3

asthma response - immediate phase + mediator

Answer 3

mast cell degranulation from re exposure = vasodilation, increased permeability, edema, eosinophil activation makes them more aggressive.
bronchospasm (vagal nerve stimulated)
mediated by histamine

Question 4

asthma response - late phase

Answer 4

eosinophils think we are under attack and end up damaging self tissue.
IL5 release from mast cells + TH2 cells = eosinophil infiltration in tissue where they release factors that damage it - esp epithelium
repeated triggers and damage = remodelling of tissue

Question 5

asthma remodelling

Answer 5

increased goblet cells and glandular tissue = excessive mucous production = plug formation
fibrosis of BM
hyperplasia + trophy of smooth muscle cells = bronchoconstriction

Question 6

asthma histology

Answer 6

eosinophilic infiltration
SMC hypertrophy
goblet cell hyperplasia
thick fibrous BM

Question 7

chornic bronchitis memory image

Answer 7

blu bloater - obese, younger, cynosis, inflammtion

Question 8

chronic bronchiti main issue

Answer 8

triggers cause chronic inflammation of bronchial epithelium
all effects result in mucous trapping + bronchoconstriction = obstruction
can lead to infections and emphysema from chronic damage to bronchus from inflammation

Question 9

chronic bronchitis - fts

Answer 9

loss of ciliated epithelia + replaced by goblet cells
increased mucous cells + decrease serous cells = hyper-secretion of thick mucous
hypertrophy + plasia of SMC = bronchoconstriction

Question 10

chronic bronchitis - presentation

Answer 10

persistent productive cough for over 3 months for 2 years

Question 11

emphysema memory image

Answer 11

pink puffer - old thing, hyper-infalted, quiet chest, enlarged destroyed airways

Question 12

emphysema main issue

Answer 12

net imbalance of protective vs destructive factors = destruction of alveolar walls. so need to use accessory muscles to breath out from loss of recoil and collapse of airways = obstruction.
can be induced by inflammatory cells, oxidative stress, pollutants..
repeated infection can = chronic bronchitis

Question 13

emphysema fts

Answer 13

alveolar wall destroyed
panacinar OR centriacinar
hyperinflation apex above clavicles, horizontal ribs, decreased lung markings, diminution of heart shadow, flattened diaphragm.

Question 14

Bullous emphysema

Answer 14

bubble looking aspect of lungs(alveoli level) in advanced emphysema
air pocketss from air trapping and consolidation of tissue
in both pan or centri