Respiratory

Question 1

What is the Pathophysiology of Asthma

Answer 1

Hyper-responsive / hypersensitive airways
Asthma is a chronic, reversible disease that involves inflammation of the lower airways. The gross pathology of asthmatic airways is hyperinflation,
1) bronchoconstriction/spasm, 2)
mucosal oedema & 3) plugging, mucous gland hyper-secretion and cilia cell disruption.

1. Antigen Enters body or irritant/ Exposure.
2. Antigen attaches to IgE antibodies on the mast cells lining the respiratory tract causing a local reaction.
3. Mast cells degranulate releasing histamine and other inflammatory substances.
4. This causes
   
   • Brochcospasm,
   • Mucosal hypersecretion & impaired mucocillary function and - - Increases vascular
5. This causes small airway obstruction, mus
   permeability
6. Air continues to enter but unable to be expired leading to gas trapping
7. Stretch receptors note the hyperinflation and patient begins to hyperventilate
   7) Ventilation/ Perfusion (V/Q) is interrupted due to intraplural and alveolar gas pressure increase.
   8) Co2 Retained leading to respiratory acidosis.
   9) Decreased Venous return, patient becomes hypoxic
   10) Decreased Cardiac output (CO)
   11) Decreased Cerebral Perfusion
   12) COMA/ PEA arrest/ Death.

Question 2

What is the Pathophysiology of COPD.

Answer 2

Obstructive pulmonary disease is characterized by difficult expiration ( lung disease characterized by chronic obstruction of
lung airflow that interferes with normal breathing and is not fully reversible) There are 3 diseases under this umbrella term

1) Asthma - Reversible
2) Chronic Bronchitis - Non-reversible
3) Emphysema - Non-reversible

Chronic Bronchitis (blue bloater)

• Inflammation of the bronchi caused by irritants or infection: This causes mucous production.
• Thickening of Bronchial wall.
• Increase in number and size of mucous glands causes an increase in susceptibility to infections.
• Continuous injury and/ or infections create a vicious cycle, thickening of walls (narrowing of lumen) continues, impaired capillary function.
• Gas trapping.

Emphysema (Pink puffer)

• Lung tissue changes rather than mucous production and inflammation
• This occurs from Elastase being released. (breaks down elastic tissue).
• Abnormal permanent enlargement of gas exchange airways & Alveolar (Without obvious fibrosis).
• Hyperinflation of Alveolar
• Loss of elastic recoil (Increase in compliance with gas trapping).
• Loss of elastic tissue, can cause airway collapse
• Formation of bullaw & blebs

Question 3

What is the Pathophysiology Pneumonia

Answer 3

An infection of the lower respiratory tract and more specifically, the lung parenchyma. This leads to inflammation, alveolar exudates and consolidation.

• Can be hospital acquired, community acquired or aspiration.
• Can be viral bacterial or mycoplasm,

Question 4

What is the Pathophysiology of Pulmonary Embolism (P.E)

What are some signs

Answer 4

Occlusion of the pulmonary vasculature by: thrombus, tissue fragment, fat or air. The
impact depends on the extent of pulmonary blood flow obstruction.

P.E's can be hard to recognize. 
History is your biggest indicator of suspicion. 
-  Stasis in bed
- Recent surgery
- DVT
- Pregnancy
-  Previous red, swollen, sore calf
• Hypotension
• Increased respiratory rate with obvious distress
• Pain
• Increased heart rate
• Clear, equal breath sounds
• Cyanosis
• Altered conscious state