Pathophysiology Emphysema

Steroids Expectorants Primary: inherited alpha-1

Emphysema antitrypsin deficiency leads to Inhaled irritants from the environment
Bronchodilators abnormal release of proteolytic causes inflammation in the airways
enzymes, or secondary:
Pharmacological Antibiotics enzymatic environmental irritants lead to
⦁ Physical therapy digestion of abnormal release of proteolytic
bronchiolar Inflammation leads to increased mucus
⦁ Oxygen therapy septa, elastic
enzymes production, hyperatrophy and
receiving 3 LPM TREATMENT Adequate hyperplasia of the mucos glands
tissue, and Large air spaces develop
via face mask hydration capillary beds (bullae); hyperinflation of
alveoli; and development
of air spaces close to mucus produced is thick and sticky,
Position patient in Expiration becomes difficult pleura. V/Q mismatching promoting infiltration of pathogens,
high fowlers while due to loss of elastic recoil and hypoxemia and decreases ciliary action resulting
in bed in reduced mucus clearance from the
Exposure to airways
55-year-old, male with Increased residual air volume and
dust and cold decreased caliber of the bronchioles
COPD
Causative Factors Inflamed endothelial cells, mucus builds
Air trapping during each up narrows the airways, decreased
inspiration leads to coughing. ventilation/perfusion ratios and
Allergies Hyper expansion of the chest and
Signs and oxygenation
increased workload of respiratory
Genetic Symptoms Complete Diagnostic muscles
predisposition blood count Tests airways eventually become
Cigarette which deals with Pulmonary Leads to obstructed and close, especially
Smoking the a-antitrypsin Function hypoventilation upon expiration. Airtarpping
⦁ Worsening cough ABG Studies and hypercapnia occurs.
recessive gene High Hgb
⦁ Tightness of chest
Respiratory tract High Hct
⦁ Profuse
infection is a high expectoration of Low PaO2 Hypoventilation occurs leading to
risk due to CXR High PaCO2 hypoxemia and hypercapnia
mucoid sputum
increased mucus ⦁ DOB Low Ph level
and poor O2 ⦁ Emaciated Low O2 sat
⦁ Central Cyanosis ⦁ Platelet count
⦁ Prolonged expiration ⦁ FBS- high
Enlarged heart
⦁ Plenty of rhonchi ⦁ BUN Low FVE
with a flattened
⦁ Crea High RV
diaphragm.
⦁ NA
Consolidation in
⦁Cl the lung fields is
⦁ Ca observable
NARRATIVE EXPLANATION

The presenting case is all about Mr. C.A, 55 years old truck driver who admitted to MVH
due to worsening cough associated with chest tightness, sputum expectoration and difficulty of
breathing. He is exposed to fumes, smokes, dust particles and admit the he is a long-time
smoker who consume 30 sticks per day for 35 years. Due to its habit which is smoking, it comes
from inhalation of toxins that increase oxidative level and will have devastative effect. Because
of that, the immune response and inflammatory response initiates and the macrophages in the
lungs clear the air spaces for infection, toxic and allergic particles. Exposure to these inhaled
toxins will cause alveolar macrophages to secrete many inflammatory mediators and cytokines
and they will enhance imunnoresponse recruiting neutrophils to the exposed area. Increased
neutrophils will now cause increase in protease mainly elastase which destroys elastic fibers.
Furthermore, macrophages also excrete harmful chemicals particularly metalloproteases
causing damage to the tissue. Damaged to the lungs specifically the alveoli will now degrade its
elastin that cause enlarge air spaces that will lead to impaired gas exchange and ineffective
airway clearance. If it happens, the receptors detect decrease in oxygen level/hypoxemia and
the body must comply by increasing its respiratory rate and heart rate to meet the body’s
needs that is reflected by his x-ray results which enlarged heart with flattened diaphragm. In
addition, decrease in elastin also removes the ability of the lungs to recoil, therefore that
patient experiencing forceful breathing and air trapping that is evident in his lab results – low
vital capacity, low force expiratory volume and high residual volume as well as presenting signs
and symptoms.