INTERNATIONAL MEDICAL SCHOOL

BACHELOR’S IN MEDICAL SCIENCE

SUBJECT/CODE: PATHOPHYSIOLOGY OF RESPIRATORY
SYSTEM/QPT20302P
Lab 4 : COPD AND ASTHMA
LECTURER NAME: DR.MOHANAD RAHMAN

NAME: ILHAASHINI KRISHNAN

IC NUMBER: 010301-05-0546
ID NUMBER: 012021090323
INTRODUCTION
Bronchiectasis is a complication of COPD, and it’s a chronic condition. Bronchiectasis is an

abnormal and permanent dilation of bronchi.Smoking is the primary cause of bronchiectasis.

Moreover, prolonged exposures to harmful particles and gases from industrial smoke,

chemical gases, vapours, mists and fumes. (King P,2009)

Basically the nicotin cannot digested and excreted in our body.The nicotin will deposits in the

bronchus and bronchioles.The deposition of nikotin will stimulate the two type of cells which

is epithelial cells and dendritic cells.This cells will stimulate other type of WBC such as T cell

and macrophage.The stimulated cells will release cytokines such as interleukins.This

substance stimulare the mucous cells of the gland to secrete mucous.Mucous secreted called

hypermucus secretion.The muscle of the bronchus thickens and narrow.The vessel also

vasodilate and increase the permeability of vessel wall.The exudate will cover the mucous

membrane and damage the cilia.Some cells will die called necrosis. These changes in airway

structure further contribute to pooling of thick mucus, and the self-perpetuating cycle of

infection and inflammation, which promotes progressive airway damage and recurrent

infections.

Although the majority of individuals with bronchiectasis have impaired mucociliary clearance

and excess sputum production, not all patients are persistently colonised with bacteria.

Bacterial colonisation and markers of inflammation in sputum are intermittent in most people.

Patients often remain colonised with the same micro-organism during acute exacerbations as

well as a stable clinical state. (King P,2009)

 DISCUSSION
Chronic bronchitis

Thick wall of
Damaged cilia bronchus

Inflammatory cells

Mucus

There will be narrowing of the bronchus.There is also hypertrophy of the wall of the

bronchus.There is the presence of mucus.We can also see the damaged cilia.There is also

presence of inflammatory cells.Mucous glands also increase in number and size.

Emphysema

Bleeding
Inflammatory cells

Nicotine
The wall of the alveoli damaged
deposited

There will be destruction of wall of alveoli.The capillary wall also destructed due to nicotine.We

can find also the accumulation of blood and inflammatory cells.We can also can observe

mucous and presence of nicotine deposited.

Bronchiectasis

The nicotine will deposits.This will cause the mucous glands to enlarged.There will

hypertrophy of glands.Futhermore,increase secretion of mucous.The tissue will die called

necrosis.The death cell will be replaced by fibrous tissue.We can also can observe

inflammatory cells.

Atelectasis

Usually,the alveoli in barrow shape.But in this case there will be elongated alveoli due to

pressure.The rupture of capillaries due compression cause by tuberculosis and

pneumonia.Bleeding also occurs where the accumulation of blood in the alveoli.We can also

observe numerous of inflammatory cells.

Lung abscess

We can observe the pus which is semisolid.The composition of pus is death cells

blood,wbc,toxins,mucous.The pus will damaged the tissue called necrosis.Death tissue

replaced by fibrous tissue.We can also can observe the inflammatory cells.

CONCLUSION
The trigger and pathogenesis of asthma, explain the role of IGE in condition.

The Asthma triggers are allergens,cold air,frangrances,food and drinks,pollutants,cigarette

smoke,strong emotions,exercise,respiratory tract infections,and bad weather such as

humidity,breathing in cold and dry air.Pathogenesis of Asthma divided into two phase which

are acute response which occur within minutes and a late phase occur after 4-8 hours.In the

airway,the initial sensitization to antigen will stimulate the dendritic cells.The dendritic cells will

stimulate the T cells and production of cytokines such as IL-4,IL-5 and IL-13.The interleukin

will stimulate the B cell.The B cell then stimulate the IgE.IgE then stimulate Eosinophil,Mast

cell and Basophil.Eosinophil produce mediators such as histamine induce bronchospasm and
increase vascular permeability.Mast cell produce mediators such as prostaglandins which

induce bronchospasm and vasodilation.Basophil produce leukotrienes to induce

bronchospasm ,vascular permeability and mucous production.Platelet-activating factor also

release which cause aggregation of platelets and release of histamine.Mast cell also produce

tryptase which inactivate normal bronchodilator.The late phase reaction:The arrival of

leukocytes at the site of mast cell degranulation lead to eosinophil and neutrophil to release

IL-4 and IL-5 which will produce platelet-activating factor and tumor necrosis

factor.Eosinophils produce major basic protein, eosinophilic cationic protein and eosinophil

peroxidase ( toxic to epithelial cells).Release of more mediators to activate more mast cells

cause epithelial cell damage.At the end the bronchoconstriction occurs with mucus production

and also inflammation making it difficult for air to move in.

The findings of the chest examination in case of asthma and COPD patients

Wheezing sound can be heard.There will be hyperinflation,increased work of

breathing.Crackles sound also can be heard due to presence of mucous in the airway.

REFERENCES

• King P. The pathophysiology of bronchiectasis. Int J Chron Obstruct Pulmon Dis.

2009;4:411-419 https://doi.org/10.2147/COPD.S6133

• National Asthma Education and Prevention Program, Third Expert Panel on the

Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the

Diagnosis and Management of Asthma. Bethesda (MD): National Heart, Lung, and

Blood Institute (US); 2007 Aug. Section 2, Definition, Pathophysiology and

Pathogenesis of Asthma, and Natural History of Asthma. Available from:

https://www.ncbi.nlm.nih.gov/books/NBK7223/

• https://bronchiectasis.com.au/bronchiectasis/bronchiectasis/pathophysiology