Modifiable Factors: 1.

Environment- presence of allergen such as pollens, furs of animals, dust, smoke particles from cigarettes such nitrosamine, acrolein, and benzopyrene. 2. Exposure to Sulfur Dioxide 3. Exercise and hyperventilation 4. Occupational allergens such as magnesium ribbon, silicon particles etc. 5. Allergy to Iodine, and Iodine containing materials. rhinorrhea (excess nasal secretion), itching, and nasal congestion and obstruction with nasal flaring.

VII. PATHOPHYSIOLOGY Theoretical Based

Non-modifiable Factors: 1. Genetics. 2. Sudden change in environmental temperature 3. Exacerbation of a previous asthma 4. Family History 5. Age

Entrance of allergen from the nostrils with subsequent inflammatory response. Inflammatory response prevents the entrapment of the allergen. The allergen enters the bronchus. The body compensates by activating these 2 mechanisms:

The parasympathetic nervous system is activated. Postganglionic parasympathetic fibers release acetylcholine next to the Reissessen muscle.

Reissessen muscle has an M3 type muscarinic receptor on their membrane. The activation of this receptor by acetylcholine will activate an intracellular Gq protein. In turn will activate the PLC pathway.

Antigen presenting cells ingest the allergens, presenting pieces of the allergen to other immune system cells. Th2 cells are formed and consequently, activates the humoral immune system. The humoral immune system produces antibodies to fight against the allergen.

This causes an influx of calcium ion in the cell, causing contraction of the smooth muscle. The muscle contraction causes the diameter of the bronchus to decrease.

Inflammatory response which includes the production of prostaglandin that causes vasodilation. Histamine also is produced by mast cells causing further vasodilation and increase in capillary permeability. Leukocyte secretes leukotriene which increases the attraction of WBC to the inflamed site.

Bronchospasm

Narrowed bronchus and increased airflow velocity produce a lung sound called wheezing. Also, the partial obstruction of the airway caused by secretion of mucus and bronchospasm produces a sound called ronchi

VII. PATHOPHYSIOLOGY Goblet Theoretical Based cells are irritated by the presence of allergens in the bronchus. In response, they increase the production of mucus in order to trap the allergen. Also, the inflammation increases the mucusproducing capacity of the goblet cells.

Increased mucus production with subsequent clogging of the bronchus.

Because of the decrease in O2 level in the blood,the lungs tries to compensate by using the accessory muscles if inspiration such as the sternocleidomastoid, scalene,serratus anterior to name a few.

Decrease in O2 level in the blood with subsequent decrease in the V/Q ratio.

The lungs try to expectorate the mucus as well as the allergen present in the bronchus.

Cyanosis

Alveolar collapse caused by fluid accumulation Cough Popping open of collapsed airway and alveoli The change in thoracic pressure caused by prolonged coughing causes backflow of gastric content to the esophagus

Use of accessory muscles during inspiration.

Chemoreceptors sense the increase in CO2 level in the blood. The medulla oblongata sends impulses to the intercostals muscles and the diagphragm via the intercostal and phrenic nerve. Consequently, this increases the respiratory rate.

Crackles

Subcostal retraction

Tachypnea with shortness of breath.

Gastroesophageal reflux disease.

Tiredness in ADL that is usually can be completed easily.