Assessment Questions

Test and refresh your knowledge with these assessment questions:

1.Identify and briefly explain the different types of hypoxia.

Answer:

There are four types of hypoxia:

i.lood supply to the tissues is inadequate

ii.lood is unable to carry enough oxygen to the tissues

iii.nadequate amounts of oxygen entering the lungs

iv.are unable to use the oxygen reaching them

2. Identify and briefly explain the defence mechanisms of the respiratory tract.

Answer:

The upper respiratory tract has:

·    Mucociliary escalator – the mucous membrane of the trachea is composed of pseudostratified ciliated columnar epithelium with numerous goblet cells (mucus producing cells) and function as a mucociliary escalator. The mucus traps inhaled debris or foreign particles, the cilia propel the mucus towards the pharynx, where it is swallowed.

·    Coughing

The lower respiratory tract has:

·    Alveolar macrophages – large particles (>10 µm in diameter) are usually trapped by the nasal hair or in the mucus of the upper respiratory tract. Smaller particles (2–10 µm in diameter) are usually trapped in the mucus of the bronchi and bronchioles and then removed by the mucociliary escalator. However, particles smaller than 2 µm can enter the alveoli, where they are phagocytosed by the macrophages.

3.Briefly discuss the pathophysiology of pneumonia, indicating the different types.

Answer:

Pneumonia refers to infection of the pulmonary parenchyma, i.e. bronchioles and alveoli. It may develop as an acute primary infection or may occur as a secondary infection due to another respiratory or systemic condition. It occurs when the normal defence mechanisms are bypassed and a pathogen gains access to the lower respiratory tract causing an extensive inflammatory response.

Pathogen

Typical – bacterial

Atypical – variety of organisms including: Mycoplasma pneumoniae, viruses and fungi

Area of infection

Lobar pneumonia – confluent consolidation involving one or more lung lobe. Most often due to Streptococcus pneumoniae (pneumococcus)

Bronchopneumonia – widespread small patches usually affecting both lungs especially lower lobes. Causative organisms more varied, including: Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms

Setting

Community-acquired – describes infection caused by organisms (bacterial or viral) found in the community; begins outside the hospital or develops within 48 hours after admission to hospital

Healthcare-associated – occurs in someone who has had a recent hospitalisation or resides in a care home, receiving chronic dialysis or home infusion therapy

Hospital-acquired – nosocomial infection, LRTI not present on admission or develops 48 hours or more following admission

Ventilator-associated – nosocomial infection that occurs in a person requiring mechanical ventilation 48 hours or more following intubation. May occur in 9–27% of ventilated patients (Kalanuria et al., 2014)

4.Identify the risk groups and factors for developing tuberculosis.

Answer:

·    Young adults – male > female

·    People living in developing countries

·    Level of poverty

·    Healthcare workers who are exposed to disease on frequent basis

·    Those with compromised/weakened immune systems

·    Cancer

·    Human immunodeficiency virus (HIV) infection

·    Smoking

·    Host deficiency in IL-2 promoting T-helper 1 response (de Martino et al., 2014)

·    Foreign-born individuals living in impoverished areas

·    Undernutrition

5.What are the signs and symptoms of tuberculosis?

Answer:

Signs and symptoms are not always initially apparent but may include: mild fever, cough with purulent sputum, fatigue and night sweats. As the disease progresses dyspnoea, wheezing haemoptysis, chest pain, weight loss and anorexia may become apparent.

6.Briefly explain what a pleural effusion is and identify the different types.

Answer:

A pleural effusion is an abnormal collection of fluid in the pleural cavity. They can be categorised as: hydrothorax (serous fluid, transudative or exudative), empyema (pus), chylothorax (chyle) and haemothorax (blood).

7. What are the different types of atelectasis?

Answer:

There are three different types of atelectasis: compression atelectasis, absorption atelectasis and surfactant impairment.

8. Explain the inflammatory response in atopic asthma.

Answer:

The early phase response follows antigen exposure. The dendritic cells activate T-helper 2 cells to produce interleukins (ILs) IL-5, IL-4, IL-13. Eosinophils are recruited to the lung mucosa. IgE antibodies attach to mast cell surface causing them to degranulate their contents. The inflammatory mediators, such as histamine, cause vasodilation and altered capillary permeability resulting in mucosal oedema, smooth muscle contraction resulting in bronchospasm and mucous secretion. This narrows the airways and obstructs airflow. Eosinophil products cause damage to the lung epithelial tissue.

9.Describe the physiological mechanism of ‘air trapping’.

Answer:

Smooth muscle in the walls of the airways constrict and the lumen narrows increasing resistance to airflow, particularly on expiration. High airway resistance causes the airways to collapse just before expiration, trapping air in the alveoli and causing hyperinflation and non-uniform ventilation.

10.Explain the inflammatory mechanisms responsible for mucous overproduction in chronic bronchitis.

Answer:

The inflammatory mechanisms responsible for mucous overproduction is attributed to Th1cells and specifically the subset Th17 cells. Interleukin 6 (IL-6) and interleukin 17 (IL-17) induce the production of proteins called mucins by lung epithelial cells which contribute to thick mucus production and the formation of mucous plugs which block the airway lumen. This is consolidated by impaired mucociliary clearance due to dysfunction and loss of cilia.

11.Describe the types of emphysema.

Answer:

Centriacinar emphysema refers to the central or proximal parts of the acini and is associated with smokers and is often seen in COPD. Panacinar emphysema involves the acini at the terminal alveoli and is associated with α-antitrypsin deficiency, an autosomal recessive inherited disorder where there is a deficiency of the enzyme α1-antitrypsin.

12.Explain the physiological mechanisms that lead to thick mucus secretions in cystic fibrosis.

Answer:

The defective cystic fibrosis transmembrane conductance regulator (CFTCR) protein leads to impaired chloride transport which leads to increased absorption of sodium and water into the circulation. This results in the secretion of thick tenacious mucus and dehydration of the mucociliary layer which reduces ciliary mobility and leads to ineffective clearing of mucus. Airway obstruction from mucous plugs and chronic inflammation and infection result in respiratory signs and symptoms.

13.Identify the sources that can cause pulmonary embolism.

Answer:

PE can originate from numerous sources including deep vein thrombus (DVT) (commonly in lower extremities), tumours, fat, amniotic fluid, foreign bodies, air and sepsis.

14.Differentiate between Type I and Type II respiratory failure.

Answer:

·    Type I (hypoxaemic): Low O2 and normal or low PCO2. Often from dysfunction of gaseous exchange.

·    Type II (hypercapnic): Low O2 with high PCO2. Often from dysfunction of alveolar ventilation.