lec 4+5 Obstructive pulmonary disease

Question 1

Cause and results of Obstructive pulmonary disease:

Answer 1

Anatomic obstruction: Asthma
Loss of elastic recoil: emphysema

result:
-Normal or increased Total lung capacity (because of loss of elastic recoil)
- slightly Decreased **Forced vital capacity (max air you can breathe out)
-Forced expiratory volume (FEV1)** is decreased significantly

Question 2

Emphysema is:

Answer 2

-permanent enlargment of air spaces distal to the terminal bronchioles in the acinus.
-Acinus : bronchiole, alveolar duct, alveolus

basically, destruction of acni wall but without fibrosis

Question 3

Types of emphysema and their pathogenisis :

(simple)

Answer 3

Centriacinar
Panacinar
pathogenisis:
1) protease- Antiprotease imbalance
2) Oxidant- Antioxidant imbalance

Question 4

what is Protease-antiprotease imbalance:

Answer 4

-Protease, elastase and oxidase from inflam cells damage elastic tissue and collagen

-a decrease in antiproteases can produce acini wall damage—-emphysema

can be genetic deficiency or smoking

Question 5

1) Centriacinar emphysema

Answer 5

-involves proximal acinus
-more severe in upper lobes
-more in male smokers and chronic bronchitis patients.
-presence of bulla is common

Question 6

2)panacinar emphysema:

Answer 6

-Involves entire acinus
-more severe in lower zones and bases
-more genetic: so a1 antitrypsin deficiency

Question 7

3)Distal emphysema:

paraseptal

Answer 7

-involves pleural surface and connective tissue of septa
-more in upper lobe and subpleural
-adjacent to fibrosed area
-prescence of multiple bulla

very similar to centriacinar

Question 8

4)Irregular emphysema

Answer 8

-common but asymptomatic.
-acinus is unlikely involved.
-associated with scarring of healed inflammation.

Question 9

Conditions related to emphysema:

Answer 9

-enlargment of air spaces w/o destruction of walls

-bullous emphysema : any type with formation of subpleural air filled cysts

Question 10

Morphology of emphysema:

Answer 10

Destruction of alveolar walls
collapse of adjacent spaces
diminished blood vessles in septa
later—- pulmonary hypertension

Question 11

Clinical course of emphysema:

Answer 11

-decreased FEV1/FVC ration
-dyspnea is first symptom
-insidious then progressive dyspnea
-tachypnea and hyperventilation (pink puffer)
-Blue bloater (in chronic bronchitis)
-Decreased O2 level and increased CO2 level— cyanosis

Question 12

Signs of chronic bronchitis:

on level of bronchi

Answer 12

-Productive cough for 3 months, for 2 years consistently
-simple chronic bronchitis—- mucoid sputum , but is not enough to obstruct airflow in early stage

Question 13

Hypersecretion of mucus is a result of:

Answer 13

1) hypertrophy and hyperplasia of mucus glands
2) increase in goblet cells by metaplasia
3) recurrent infections

Question 14

Reid index:

Answer 14

-measure of degree of chronic bronchitis
-Thickness of submucosal mucus secreting glands vs thickness between epithelium and cartialage.

<0.4 normally

Question 15

Morphology of chronic bronchitis:

Answer 15

-Edematous congested mucus
-luminal thick mucus

Microscopic:
-non eosinophillic cell infiltrate
-squamous metaplasia and dysplasia
-inc in mucus glands, and goblet cells

Question 16

PURE emphysema vs PURE bronchitis:

Answer 16

Bronchitis:
-inflammation and mucus hypersecretion in large airways
-airway obstruction in small airways

Emphysema: Acini wall damage and loss of elastic recoil

Question 17

Blue bloater vs pink puffer:

Answer 17

Blue bloater (COPD):
* chronic cough
* purulent sputum
* hemoptysis
* cyanosis
* obesity
* secondary polycythemia vera
* hypercapnia

Pink puffer (emphysema):
* minimal cough
* hyperventilation and tachypnea
* cachexia

Question 18

Bronchiectasis is:

Answer 18

chronic necrotizing inflammation of bronchi AND bronchioles with destruction of the muscle and elastic tissue in the wall.

-leads to PERMANENT enlargment of bronchioles

Question 19

predisposing conditions of bronchiectasis:

Answer 19

1)Bronchial obstruction
-localized (F.B or tumor)
-generalized (asthma, bronchitis)
2)congenital
-cystic fibrosis
-Immunodeficiency
-kartagners syndrome
3)post necrotizing supparative inflammation

Question 19

important

Pathogenisis of bronchiectasis:

Answer 19

-Obstruction of bronchus wall+ infection
-continous dialation and exudate accumilation

Question 20

Asthma is :

Answer 20

A CHRONIC inflammatory process of wheezing (small airway obstruction during expiration)

chest tightness, cough early in the morning or at night

Question 21

important

Morphology of bronchiectasis:

Answer 21

-more in lower lobes and bilateral
-occurs in distal bronchial tree
-wall shows:
acute and chronic inflam cells
squamous metaplasia of lining
fibrosis

Question 22

Clinical picture of bronchiectasis:

VERYYYY SIMILAR TO CHRONIC BRONCHITIS

Answer 22

-chronic cough
-purulent sputum
-hemoptysis
-CLUBBING
-core pulmonale

Question 23

Summary of bronchiectasis:

Answer 23

-irreversibly dialated thick walled bronchi
-honeycombing, tram-line, cystic, signet ring sign can all be seen in imaging
-the vicious cycle and p.aeuroginosa contributes to severity of disease

Question 24

manifestations of asthma:

Answer 24

episodic attacks
widespread narrowing of airways

Question 25

Type 1 asthma: allergic asthma

Answer 25

Atopy: largest risk factor for developing asthma
-Rhinitis, eczema, urticaria
-inc IgE

develops early

Question 25

Clinical features of asthma occur because of:

Answer 25

-Repeated immediate hypersensitivity
-Late phase reactions in lung

these reactions give rise to:
1)intermittent and reversible airway obstruction
2)Chronic bronchial inflammation WITH eosinophils
3)Bronchial smooth muscle cell hypertrophy and hyperreactivity

chronic bronchitis is WITHOUT eosinophils

Question 26

Type 2-Non atopic asthma

develops later

Answer 26

Normal IgE levels
no allergy history
-suspect is virus or pollutants

Question 27

Pathogenisis in atopic asthma:

Answer 27

-type 1 hypersensitivity reaction
-linked to abnormalities of TH2 cytokines

-GENETIC PREDISPOSITION (ADAM33):
transmembrane protein implicated in bronchial hyperresponsiveness

mast cell and EOSINOPHIL activation

Question 28

1) early phase of asthma: 30-60 mins

Answer 28

allergen activates TH2 cells
IL’s turn on IgE, eosinophils—- activate mast cells
bronchoconstriction

Question 29

2)Protracted late phase: (4-8 hours later)

Answer 29

-antigen in submucosa: more mast cells and neutrophils
-mast cells— chemotactic factors for eosinophils and neutrophils (IL4,5,PAF,TNF)

Question 30

Prognosis of asthma:

Answer 30

maturation of immune response against asthmatic response, so mortality is low

Question 30

pathology of asthma:

Answer 30

1)edema, congestion— increase in eosinophils
2)mucus cell and smooth muscle hypertrophy any hyperplasia and goblet cells metaplasia
3)necrosis of surface epithelium
4)lumen of bronchi and bronchioles contain
a)charcot leyden crystals from eosinophil
b)curschmann’s spirals from epithelial necorsis

Question 31

ways to diagnose asthmatic patient:

Answer 31

-lung function test
-blood gasses
-chest x ray
-skin test