Respiratory system

What is Asthma

Chronic ==**inflammatory disorder of lungs**==

Where does asthma affect

==**Bronchi and bronchioles**== are inflamed and constricted

==**Airflow obstructed**==

Who does asthma affect

INCIDENCE – 4.3% of the population worldwide. Average annual asthma prevalence is higher in children (9.5%) than adults (7.7%

Extrinsic causes of asthma

==**Common in children**==

Definite external cause ➢ underlying allergic disorder ➢ Atopic ➢ Produce allergic antibodies to everyday substances (antigens) e.g. pollen, dust mites, foodstuffs

what are the intrinsic factor of asthma

==Common in adults==

linked to hyper-responsive reactions e.g. infection, cold exercise, stress , cigarette smoke

How intrinsic asthma are developed

Chemical biological substance in workplace – sensitivity

Unnecessary contact with antibiotics – sensitisation

Atopy genetic component + environment

Abnormal antibody production – childhood exposure to antigens and tobacco smoke

what are the various wheeze phenotypes and classification

**Transient early wheezing**

**Non-atopic wheezing**

**IgE-mediated (atopic) wheezing**

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what is the transient early wheezing

==First 3–5 years of life==; no family history of asthma, no allergic sensitization.

what is non- apotic wheezing

Wheezing up to adolescence, no atopy or no allergic sensitization, associated with a viral respiratory infection \[respiratory syncytial virus (RSV)\] experienced in the first 3 years of life.

IWhat is gE-mediated (atopic) wheezing

“Classic asthma phenotype” characterized by persistent wheezing (atopic), early allergic sensitization, significant loss of lung function in the first years of life, and airway hyperresponsiveness

Asthma – Pathophysiology

smooth muscle ➢ lined with ciliated cells ➢ mucus secreting glands

decrease air flow

blood through pulmonary circulation not fully oxygenated

hypoxaemia /hypercapnia

Pathological Characteristics of Asthma

**Inflammation of the airways**

**Bronchial hyper-reactivity**

**Reversible airways obstruction**

How is asthma an inflammatory disorder?

__Mast cells__ close to airway’s blood supply

__Mast cell secretes cytokines__ – histamine \[bronchoconstriction, narrows the airways

Smooth muscle contraction, mucus production increases, capillary permeability goes down

Asthma effects

Bronchoconstriction + swelling + increased secretions reduce lumen.

This restricts air entering / leaving the alveoli blood through pulmonary circulation not fully oxygenated.

Causes hypoxaemia /hypercapnia

What does asthma airway looks like

Narrowed Airways (limited airflow)

Tightened muscle, contracts airway

Inflamed thickened airways wall

Vicious Mucus in airways

Inflammation in asthma leads to swelling, secretions, constriction and reduced lumen

Asthma – pathophysiology

Asthma attack features

__Bronchoconstriction/ Airflow limitation__ – few minutes after trigger – early reaction ➢ Resolved if trigger withdrawn ➢

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__Prolonged attack__ – late phase reaction ➢ After 4-8 hours and may last for a day or more. May be fatal, respiratory arrest

Care – management of Asthma

**1000-1200 people die.**

==**90% preventable**==; more than 10% teenagers

➢ Continuous monitoring – until stabilised ➢ Maintain oxygen saturation >92% ➢ Bronchodilators and steroids

Sputum collection – **yellow/ green** – infection

➢ Advice - Smoking and weight reduction

Drugs for Asthma

__Preventers - controllers__

➢ Corticosteroids or sodium cromogilate

➢ Reduce inflammation that leads to pathological conditions

__Relievers__ ➢ Salbutamol or terbutaline ➢ Produce bronchodilation

Acute severe asthma

➢25 breaths /minute

➢Tachycardia – 110 beats / minute ➢Expiratory flow < 50%

➢Inadequate response to nebulised bronchodilators - intravenous bronchodilators /hydrocortisone

➢ High oxygen concentration given ➢Mechanical ventilation

Chronic asthma

Lung structure altered – long-term inflammation Features similar to Chronic obstructive pulmonary disease (COPD) ➢ SMOKING ➢ SMOKY, COLD CONDITIONS, CLIMATE, DAMPNESS, HIGH AIR POLLUTION ➢ DAMAGE TO LUNG TISSUE AND AIRFLOW OBSTRUCTION (inflamed and thickened bronchial walls)

* Chronic asthma and bronchiectasis (chronic dilation of bronchioles)
* Emphysema
* Chronic bronchitis

What is EMPHYSEMA

➢ Loss of ==**alveolar elasticity**==

➢ ==**Permanent enlargement of air spaces**==

(less surface area for gas exchange)

➢ Destruction of alveolar walls

Pathophysiology of emphysema?

➢ Smoke irritants reach alveoli ➢ Stimulate migration of WBCs into the area Neutrophils, macrophages increases

**Emphysema secrete** Neutrophils/macrophages secrete elastase

➢ **Elastase – digests elastin (gives alveoli elastic properties) destroy alveolar wall**

➢ Other **protease enzymes digest proteins in the wall of the alveoli** – progressive elasticity destruction

Destruction of alveolar wall

Smoke particles in alveoli

Neutrophils phagocytosing smoke particles

Macrophages

Area of the cell membrane digested by proteases

Elastic tissue being digested

Features - emphysema?

➢ Elastic recoil

Pressure of exhaled air in small bronchioles not maintained ➢ Collapse of bronchioles

➢ Air does not efficiently leave the alveoli – hyperinflated ➢ Bronchial collapse – airway obstruction

Chronic bronchitis - pathophysiology

long-term inflammation of the bronchi, mostly by in Inhaled smoke

– affects the tissue lining the airways- normal ciliated non-ciliated squamous