Resp - 13 - Obstructive Lung Disease

Front 1

obstructive lung disease includes which diseases

Back 1

COPD - emphysema, chronic bronchitis

Bronchial asthma

Bronchiectasis

Front 2

emphysema vs chronic bronchitis

Back 2

emphysema is an airspace disease - permanent enlargements of airspaces distal to terminal bronchiole and wall damage


chronic bronchitis is an airway disease

you can have both at the same time

Front 3

overinflation vs emphysema

Back 3

overinflation is enlargement of airspaces without destruction of the wal

like in coal workers pneumocosis or compensatory overinflation

Front 4

compensatory overinflation

Back 4

if remove one lung the other lung will show signs of overinflation

Front 5

acinus

Back 5

gas-exchanging structure of the lung, distal to terminal bronchiole

Front 6

centriacinar emphysema

Back 6

see in the upperzones more due to higher stress and distortion

see with tobacoo smoke because it impacts at bifurcations (thus centriacinar)

Front 7

panacinar emphysema

Back 7

see in lower zones - alpha1 antitripson deficiency - lack antiprotease throughout the acinus

lower zones because more blood flow = more neutrophils

Front 8

paraseptal (distal acinar) emphysema

Back 8

see with sponataneous pneuomothroax due to rupture of distended acini

young, tall/thin, adult males often

Front 9

smoking effect on emphysema

Back 9

increased reactive O2 species

inactivation of alpha1 antitrypsin

nicotine is chemotactic for neutrophils and macrophages which secrete elastase

Front 10

how does obstruction occur in emphsema?

Back 10

alveolar wall destruction reduces elastic recoil and support of wall (less teathering)

lack of elastic recoil means harder to push out air - reduced outflow pressure -> airway collapse

Front 11

bullous emphysema

Back 11

due to excessive weakness in wall structure - form large cavities > 1cm intraparencymal

Front 12

blebs

Back 12

> 1 cm subpleural pockets of trapped air due to weak wall structure

can rupture -> spontaneous pneumothorax

Front 13

how does emphysema cause pulmonary hypertension?

Back 13

destruction of pulmonary parenchyma includes vasculature

enlarged airpsaces can compress vasculature

tobacco smoke damages vascular walls

all decrease cross sectional area of pulmnary vascular bed -> increased resistance -
> pulmonary hypertension

Front 14

barrel chest

Back 14

increased AP diameter

see with emphysema

increased compliance of lung allows chest to expand

Front 15

chronic bronchtis

Back 15

due to chronic irritation of bronchiole lining -> nutrophilic inflam -> hyperplasia of mucous glands -> hypersecretion of mucus

metaplasia of goblet cells in small airways

squamous metaplasia - can -> squamous cell carcinoma

smoking etiology

increased suseptability to infection

Front 16

chronic bronchitis starts in which part of the respiratory tree?

Back 16

small airways

see clustering of pigmented alveolar macrophages (smokers macrophages) + goblet cell hyperplasia + lots of mucus plugging

Front 17

pink puffer

Back 17

emphysema

pink because they over ventilate the air spaces

Front 18

blue bloater

Back 18

chronic bronchitis

blue - cyanotic because greater airway resistance makes it harder to get air to alveoli

Front 19

COPD causes of death

Back 19

includes emphysema and chronic bronchitis

causes of death

respiratory acidosis -> coma

cor pulmonale due to pulm hypertension

pneumothorax (emphysema)

infection (chronic bronchitis)

Front 20

T/F emphysema and chronic bronchitis is reversible

Back 20

FALSE

Front 21

Asthma

Back 21

increased airway responsiveness - airway smooth muscle hyperreactive (type 1 hypersensitivity - IgE mediated)

reversible

genetic predisposition to allergen or nonallergin - easy to get release of inflammatory mediators

airway construction, inc vascular permeability, mucus secretion, epithelial damage, proliferation of smooth muscle cells

Front 22

asthma early phase and late phase

Back 22

early phase:
mast cell degranulation -> airway constriction, increased mucus secretion, edema, leukocyte recruitment

late phase:
eotaxin -> eosinophil activation/attraction

major basic protein -> epithelial damage, constriction

*leukotrienes -> prolonged constriction

Front 23

atopic vs nonatopic asthma

Back 23

atopic = allergic

nonatopic = nonallergic - due to a respiratory infection that cause increased sensitivity of vagal receptors

Front 24

drug induced asthma

Back 24

NSAIDS - inhibit COX -> decreased prostaglandins and RELATIVE increased leukotrienes

Front 25

asthma morphology

Back 25

airway remodling

sub-basement membrane fibrosis

inflammation

edema

hyperplasia of submucosal glands

hypertrophy and hyperplasia of smooth muscle

Front 26

what do you find in sputum of asthma patient

Back 26

eosinophils

charcot-leyden crystals - enlongated diamond shape - eosinophil protein

curschmann sprials - mucous strands in mucus plugs

*none of these are specific for asthma

Front 27

complications of asthma

Back 27

airway obstruction

aspergillosis infection

status asthmaticus - severe prolonged asthmatic reaction -> death

Front 28

bronchiectasis

Back 28

permanent dilation of bronchi and bronchioles due to chronic necrotizing inflammation (often due to infection)

see dilated bronchi with thick walls - walls are weak and collapsible

see with Cystic fibrosis, immotile cilia syndromes, lung rejection, rheumatoid lung, tumors, etc

impaired airway clearance -> pooling of secretions -> obstruction + airway dilation + infection

severe persistent cough with foul smelling sputum