rosh- obstructive ld

7/31/2019 Rosh- Obstructive LD

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OBSTRUCTIVE

LUNG DISEASESROSHNI SANKARA

SUBRAMANIAN


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OBSTRUCTIVE DISEASES

Obstructive lung disease is a category ofrespiratory disease characterized byairwayobstruction

inflamed and easily collapsible airways

obstruction to airflow

problems exhaling
http://en.wikipedia.org/wiki/Respiratory_diseasehttp://en.wikipedia.org/wiki/Airway_obstructionhttp://en.wikipedia.org/wiki/Airway_obstructionhttp://en.wikipedia.org/wiki/Airway_obstructionhttp://en.wikipedia.org/wiki/Airway_obstructionhttp://en.wikipedia.org/wiki/Respiratory_disease


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OBSTRUCTIVE DISEASES

In these diseases:

TLC and FVC are normal or slightly increased

Marked by decreased expiratory flow (FEV1) Ratio of FEV1 to FVC is decreased


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OBSTRUCTIVE CONDITIONS

Asthma

Emphysema

Chronic bronchitis Bronchiectasis

Bronchiolitis

COPD


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ASTHMA

Characterized by episodic, reversible

bronchospasm resulting from broncho

constriction in response to various stimuli


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ASTHMA

Triggers

Allergens

Exercise

Respiratory infections

Drugs and food additives

Nose and sinus problems

GERD

Emotional stress


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Inflammation causes obstruction of airways

by:

Acute bronchoconstriction

Swelling of bronchial wall

Chronic production of mucous

Remodeling of airways walls


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Two main processes are seen in thepathophysiology of asthma in the airways.

1. Inflammatory reaction

2. Remodeling


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Cells involved in chronic allergic

inflammation

1. Eosinophils

2. Mast cells

3. T-lymphocytes

4. Neutrophils 5. Basophils


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ASTHAMA- pathology

Early phase response: 30 60 minutes

Allergen or irritant activates mast cells

Inflammatory mediators are released

histamine, bradykinin, leukotrienes, prostaglandins, platelet-activating-factor, chemotactic factors, cytokines

Intense inflammation occurs

Bronchial smooth muscle constricts

Increased vasodilation and permeability Epithelial damage

Bronchospasm

Increased mucus secretion

Edema


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ASTHAMA- pathology

Late phase response: 5 6 hours

Characterized by inflammation

Eosinophils and neutrophils infiltrate

Mediators are released mast cells releasehistamine and additional mediators

Self-perpetuating cycle

Lymphocytes and monocytes invade as well

Future attacks may be worse because of increasedairway reactivity that results from late phase response Individual becomes hyperresponsive to specific allergens and

non-specific irritants such as cold air and dust

Specific triggers can be difficult to identify and less

stimulation is required to produce a reaction


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Airway remodeling

thickening of basement membrane

edema

size of submucosal glands

muscular hypertrophy

inflammatory infiltrate in bronchial walls


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Asthma: Early Clinical

Manifestations

Expiratory & inspiratory wheezing

Dry or moist non-productive cough

Chest tightness Dyspnea

Anxious &Agitated

Prolonged expiratory phase Increased respiratory & heart rate

Decreased PEFR


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Asthma: Early Clinical

Manifestations

Wheezing

Chest tightness

Dyspnea Cough

Prolonged expiratory phase [1:3 or 1:4]


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Asthma: Severe Clinical

Manifestations Hypoxia

Confusion

Increased heart rate & blood pressure

Respiratory rate up to 40/minute & pursed lipbreathing

Use of accessory muscles

Diaphoresis(excessive sweating) & pallor

Cyanotic nail beds

Flaring nostrils


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COPD


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Chronic Obstructive Pulmonary

Disease: COPD

Disease of airflow obstruction that is

not totally reversible

Chronic Bronchitis

Emphysema

Ch i B hi i


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Chronic Bronchitis Common in smokers (> 90%), passive

inhalation of smoke and smog-ridden cities

Definition: Based on clinical grounds.persistent productive cough for at least 3consecutive months and at least 2 consecutive

years Occurrence: (Increased mucus production)

a) simple chronic bronchitis

i) raises mucoid sputumii) airflow not obstructedb) chronic mucopurulent bronchitis

i) mucus and pusii from secondar infection

) h i th ti b hiti


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c) chronic asthmatic bronchitisi) bronchitis with intermittent

hypersensitivity and asthmatic

constriction (difficult to diagnosefrom atopic asthma)

d) chronic obstructive bronchitis

i) difficult outflow as measured bypulmonary function test

P th i


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Pathogenesis Hypersecretion of mucus

a) beginning in large airways

b) smoking single most important causativefactor

Increased transcription of mucin gene

(MUC5AC) by cigarette smokea) enlargement of mucus secreting glands

(major consequence)

b) hyperplasia and hypertrophy of mucussecreting cells and increase proportion ofmucus to serous secretions.

i) Reid index size of mucus glands

C h ith t l t i d fi it l


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Cough with sputum may last indefinitelywithout respiratory obstruction

usually accompanies emphysema

Some patients develop COPD withoutflow obstruction

a) hypercapnia

b) hypoxemiac) exertional dyspnead) cyanosisblue-bloaters

Progression of diseasea) pulmonary hypertension (Cor Pulmonale)b) cardiac failure

Metaplasia of bronchial epithelium


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2 E h


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2. Emphysema Permanent enlargement of airspaces

distal to terminal bronchioles and is

accompanied by destruction of theirwalls


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T f h


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Types of emphysemaa) Panacinar (panlobular) emphysema

i) uniformly enlarged acini

ii) lower lung zonesiii)1-antitrypsin definciency

b) Centrilacinar emphysemai) dilation upstream with normal distal

portions

ii) more common than panacinar (~95% of cases)iii) seen in heavy smokers, often in

association with chronic bronchitis


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c) Distal Acinar (paraseptal) emphysema

i) proximal acini normal and distal

part most involvedii) upper half of lungs/near pleura

d) irregular

i) acini irregularly involvedii) airspace enlargement with fibrosisiii) most are asymptomatic and not

clinically significant

Centriacinar and panacinar are the onesthat cause clinical airflow obstruction

Incidence


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IncidenceCentrilobular most common and severe in

men

Clear association with cigarette smoking2 Theories

i) protease-antiprotease imbalance

ii) oxidant-antioxidant imbalance

Protease antiprotease Hypothesis


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Protease-antiprotease Hypothesisa) patients with deficiency of antiprotease,1-antitrypsin (AAT) have increased

tendency to develop emphysemab) about 1% of all patients have this defectc)1-antitrypsin major inhibitor of

proteases, particularly elastased) homozygous patients with genetic AAT

deficiency develop emphysema

Sequence:


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Sequence:a) neutrophils (primary source of proteases)

sequestered in pulmonary capillaries

(lower zones primarily)i) smoking neutrophils &

macrophages

ii) CD8+ T cells cause directdamage and/or recruit macrophages

b) few gain access to alveolar space

c) release of proteolytic enzymes + ROS(reactive oxygen species)d) low levels of1-antitrypsin damage to

elastin (via elastase)e em h sema ensues


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Oxidant-antioxidant hypothesisLung has antioxidants

a) superoxide dismutaseb) glutathione

Smoke has many oxidant species which

deplete these normal scavengersa) activated neutrophils also has ROS Oxidative injury depletes or destroys

native antiproteasesa)Functional1- antitrypsin definciency

even though blood enzyme is notdeficient


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Signs:a)Barrelchested and dyspneicb) Hyperventilation

c) Normal blood gases (-pink puffers) Some patients have other pulmonary disease

a) do not hyperventilate and becomecyanotici)blue-bloaters (chronic bronchitis)

b) death from Right CHF, coma, acidosis,pulmonary fatigue


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Bronchiectasis


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Bronchiectasis Permanent dilation of bronchi and

bronchioles caused by destruction of the

muscle and elastic supporting tissueresulting or associated withchronic necrotizing infection.

Is not primary disease but secondary topersisting infection or obstruction causedby variety of conditions.

Cough and purulent sputum Irreversible Bronchial dilation

Most often caused by:


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Most often caused by:a) bronchial obstruction

i) tumors

ii) foreign bodiesiii) localized to obstructed lung

segment

b) congenital or hereditary conditioni) cystic fibrosisii) immunodeficiency states (IgE

deficiency) repeated infectionsiii) Kartagener syndrome (Structuralabnormalities of cilia (decreasedmucocilliary clearance)

- Sterilit in males/females


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c) necrotizing pneumonia (S. aureus, K.pneumoniae)

i) post tubercular bronchiectasissignificant cause of morbidity

B hi li i


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Bronchiolitis

Bronchiolitis is an acute inflammatory injury ofthe bronchioles that is usually caused by a viralinfection.

severe symptoms are usually only evident in

young infants

Bronchiolitis usually affects children youngerthan 2 years, with a peak in infants aged 3-6

months

Bronchioles are small airways, less than 2 mm indiameter, and lack cartilage and submucosal

glands


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Bronchiolitis is very contagious. The virus thatcauses it is spread from person to person bydirect contact with nasal secretions, airborne

droplets, and fomites.The effects of bronchiolar injury include the

following:

Increased mucus secretion Bronchial obstruction and constriction

Alveolar cell death, mucus debris, viral invasion

Bronchiolitis - Pathophysiology


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Air trapping

Atelectasis

Reduced ventilation that leads toventilation/perfusion mismatch

Labored breathing

Ninety percent of cases are caused by respiratorysyncytial virus (RSV)

Bronchiolitis - Pathophysiology


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Cough

Dyspnea

Wheezing Poor feeding

Hypothermia or hyperthermia

Wheezing Hypoxia

Nasal flaring

Bronchiolitis- signs & symptoms


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