Intro to obstrutive and restrictive lung diseases--Semester 1 Mini 3

Chronic Obstructive pumonary Disease

Diffculty with expiration due to anatomic narrowing airways that reduced elastic recoil

Difficulity with inspiration

due to reduced total lung capacity

can be caused by Fibrosis

The most iar that can be inhaled or exhaled in a single breath

it is decreased in retrictive lung disease

it the air that you expelled in one sec

decreased in COPD

Tell you what type of disorder you have>

low ratio you probally have COPD, same ratio you have a restrictive Pumonary disease

it is the distal part of the lung to the terminal bronchile and contains respiratory bronchiole, alveolar duct and alveolar sacs.

3-5 terminal repiratory units

this is used to define emphysema

Type II

Emphysema and Chronic bronchitis

Dull sound--> indication of fluid in the lung. should should hollow

Fluind in the lung---> edema

Type of Emphysema that has uniform enlargment of acinus (terminal respiratory unit)

Irreversible overinflation of air spaces distal to the terminal bronchiloes with destruction of their wall

can lead to formation of bullus

Enlargment of central parts of the acinus Respiratory bronchi or aveloar duct, sparing the peripheral alveoli

not very clinically significant

Smoking mostly

Enzymatic distrution of alveolar wall, due to definincy and alpha anti trypsin def.

Pathogenic cause of emphysema. destruction of alveolar walls due to an imbalance between protease and protease inhibitors

pt with herditory alpha 1 antitrypsin deficicy develop emphysema--panacinar at young age

recruits PNLs and macrophages--release protease like elastase and at the same time. smoke and macrophages inactivate alpha 1 anti trypsin

common

releated to smoking

Dyspnea with prolonged expiration, cough, expectoration associated iwth bronchitis

Barrel shaped chest with slowing of forced espiration.

death in severve cases due to respiratory failure and CHF (cor pulmonale)

rupture of bullae

Tension pneumothroax

Emphysema

COPD

cough with sputum for at least 3 months to 2 years

chronicifrritation and inflammation of the bronchial mucosa

hypersecretion ofmucus

hypertrophy of mucus glands

bronchi and bronchioles are obstruced by mucs pugs and show hypermina and edema and cellular infilration

epithelium may sow squamus metaplasia and dysplasia

Chronic Broncitis

chronic inflamation of alveolar wall progressing to interstitial pumonary fibrosis and ending in a honeycob lungs

Initial event- injyr to alveolar epith/endotheilum (ARDs)

Eary acute event- aleolitis, with inflammatory changes

Late even- diffuse interstial fibrosis--> honey comb lungs

Begins with alveolar wall and gets thicker with fibrosisi

Occupational and enviorment cause--coal workers pneumoconisis

• Anthroacoisis--harmless
• Simple CWP-- aggregates of coal dust with macrophage--no significat dysfunciton

Progressive massive fibrosis- or compliacted disbling respiratory insufficncy

Upper zones more effected the lower zones

inhalation of sillica particles causes dense nodular fibrosis

silica lead to macrophages activation and release fobrogenc fcators

heavey exposure to to asbestos particles---> lead to fibrous silicates

asbestos induces pleural effusion and adhesion. fibrocalcific plaques and is associated with increase risk of bronchogenic carcinoma na d pleural mesothelioma

Asbestos ferruginous body

Asbestos body

can also see huge plurea or can attach to iron coataintin