Respiratory

Question 1

What does the respiratory system consist of and what are their functions?

Answer 1

Upper and lower airway.
Upper airway: filters, warm and moisten the air
Lower airway: ventilates and exchanges gas

Question 2

Describe the lungs and its functions.

Answer 2

It is a soft spongy organ with the upper part being the apex and lower part the base.
Functions include: gas exchange, inactivate vasoactive substances, convert angiotensin I to angiotensin II, reservoir for blood storage and heparin producing cells located in the capillaries.

Question 3

Where does gas exchange and how?

Answer 3

Gas exchange occurs in the respiratory lobules/Alveoli. Oxygen moves from the alveoli to pulmonary capillaries as dissolved gas.
This is able to occur due to a concentration gradient.
carbon dioxide also travels as along the concentration gradient.

Question 4

Describe the dual blood supply to the lungs?

Answer 4

1. Pulmonary circulation: brings DEOXYGENATED blood from the RIGHT side of the heart via the pulmonary artery. Oxygenated blood returns via the pulmonary veins into the LEFT.
2. Bronchial circulation:
   Distributes blood to the conducting airways and supporting structures.
   Warms and humidifies air in the conducting airways. Bronchial blood vessels are the only ones to undergo angiogenesis when vessels in the pulmonary circulation are obstructed.

Question 5

What is lung compliance?

Answer 5

How much the lungs can inflate. It is a measure of the change in lung volume that occurs with the change in intrapulmonary pressure.
Normal compliance in the average adult is 200ml.
It is determined by elastin, collagen fibres, water content, surface tension

Question 6

List the common tests used to determine the presence of a respiratory disorder.

Answer 6

- Visual examination (cyanosis etc.)
– Peak flow meters
– Spirometry
– Pulse oximeter
– Auscultation (Breath sounds)
– X-ray
– Blood gases

Question 7

Describe what normal breathing sounds like.

Answer 7

Normal breath sounds vary over different anatomical sites.
– Bronchial: loud, high pitched
– Bronchovesicular: medium pitched
– Vesicular: soft, low pitched, gentle, rustling sounds

Question 8

Describe what abnormal breathing may sound like.

Answer 8

Abnormal/adventitious breath sounds may:
– Be absent
– Sound wet = pulmonary oedema
– Be noisy: air passing past sputum = pneumonia
– Be a wheeze: narrow airways = asthma

Question 9

Define the term COPD

Answer 9

Chronic obstructive pulmonary disease
– In COPD, less air moves in and out
of the lungs because:
– Air sacs have lost their
elasticity
– walls between air sacs are
destroyed
– airways are thick and inflamed
– excessive mucus production
clogs airways

Question 10

Compare and contrast the clinical manifestations observed in a patient with bronchitis and with a patient with emphysema.

Answer 10

Chronic bronchitis
– Have a sputum producing cough
– Blue bloater: poorly oxygenated lung causing cyanosis
– Right sided heart failure due to pulmonary hypertension (Cor pulmonale)
resulting from constriction of pulmonary blood vessels
– Peripheral oedema due to right sided heart failure
– Acidosis resulting from CO2 retention

Emphysema
– Pink Puffer: oxygenated but strains to breath due to collapse of the airways
during expiration.
– Not cyanotic, therefore not blue in colour (except in extreme cases)
– Pursed lip breathing with rapid respiratory rate
– Barrel chest

Question 11

Name the three common pathophysiological changes that occur in chronic bronchitis?

Answer 11

Chronic Bronchitis is the result of
inflammation for more than 3
months in the bronchi and
bronchioles.
– Muscle spasm
– Mucus production
– Inflammation

Question 12

Describe the complications associated with chronic bronchitis

Answer 12

• persistent inflammation with swelling and increased fibrosis/scarring
  of the lining of the respiratory tract;
  – increased number (hyperplasia) and size (hypertrophy) of both mucus- secreting glands and goblet cells—both of which contribute to the production of large volumes of thick mucus;
  – variable degrees of bronchial smooth muscle hyperplasia; and
  – increased bronchial wall thickness
  – may lead to acidosis due to CO2 retention
  – right sided heart failure due to pulmonary hypertension resulting
  from constriction of pulmonary blood vessels
  – peripheral oedema due to right sided heart failure

Question 13

State two pathophysiological changes that occur in emphysema.

Answer 13

• Abnormal dilation of the
  alveoli.
  – Loss of lung elasticity.

Emphysema: is characterised by the loss of elastin and other major structural proteins in the lower airways, resulting in the
widespread destruction of alveoli.
-– The major pathophysiologic change that leads to this widespread destruction is the excessive release of proteolytic enzymes from neutrophils and alveolar macrophages.

Question 14

Define ARDS and describe what it is.

Answer 14

• Acute respiratory disease
  -prevents gas exchange
• mostly associated with septicaemia
  -Caused by a major lung injury e.g. inhaling chemicals, pneumonia,
  septic shock, trauma.
  – Creates oedema in the air sacs preventing gas exchange.
  – Condition that gives rise to type 1 respiratory failure

Question 15

symptoms fo ARDS

Answer 15

Difficulty breathing
– Low blood pressure and other organ failure
– Rapid breathing
– Shortness of breath
– Symptoms usually develop within 24 to 48 hours of the injury
or illness.
– Often, people with ARDS are so sick they cannot complain of symptoms.

Question 16

Define pulmonary oedema and discuss how it develops.

Answer 16

Fluid accumulation in the tissue
and air spaces
– Leads to impaired gas
exchange
– Causes:
– Cardiogenic (LVF/CHF
leads to fluid backing up
onto the lungs)
– Non-cardiogenic
(hypertensive crisis, upper
airway constriction, neurogenic causes)

Question 17

Define bronchiolitis. Explain who is susceptible to bronchiolitis and how are they treated.

Answer 17

Inflammation of the bronchioles (smallest air
passage)
– Triggered by various viruses (eg Respiratory
Syncytial Virus)
– Most common <2 years of age
– Treatment includes:
– rest
– antibiotics are NOT given as it is usually
caused by a virus
– frequent fluid
– oxygen (severe cases)
– IV fluid (severe cases)

Question 18

Define pertussis and how it is treated. Who is at risk?

Answer 18

Also known as whooping cough
– Potentially fatal bacterial disease caused by
Bordetella pertussis
– Treatment is of little benefit to infected person, however, some antibiotics may be used e.g. erythromycin
– Vaccination best strategy
– Unvaccinated individuals and the immunocompromised
person are most at risk

Question 19

Describe the pathophysiology of Pneumothorax.

Answer 19

Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura (which surrounds the lungs) or the parietal pleura and chest wall. As air separates the visceral and parietal pleurae, it destroys the negative pressure of the pleural space and disrupts the equilibrium between the elastic recoil forces of the lung and chest wall. The lung then tends to recoil by collapsing towards the hilum .

Question 20

Describe the Signs and symptoms of Pneumothorax

Answer 20

Clinical manifestations of spontaneous or secondary pneumothorax begin with sudden pleural pain, tachypnoea and dyspnoea (rapid breathing and difficulty breathing, respectively).

Question 21

Describe the pathophysiology of Emphysema

Answer 21

(The major pathophysiologic change is the widespread destruction is the excessive release of proteolytic enzymes from neutrophils and alveolar macrophages.)
Emphysema begins with destruction of alveolar septa, which eliminates portions of the pulmonary capillary bed and increases the volume of air in the alveoli.Alveolar destruction produces large air spaces within the lung tissue and air spaces adjacent to pleurae. These areas are not effective in gas exchange. The loss of alveolar tissue means a loss of the respiratory membrane where gases cross between air and the blood, resulting in a significant ventilation–perfusion mismatching and hypoxaemia

Question 22

Describe signs and symptoms of emphysema

Answer 22

• Pink Puffer: oxygenated but strains to breath due to collapse of the airways
  during expiration.
  – Not cyanotic, therefore not blue in colour (except in extreme cases)
  – Pursed lip breathing with rapid respiratory rate
  – Barrel chest
  -tightness of chest
  -shortness of breath
  -whistling breathing sounds
  -cough with mucous

Question 23

Describe complications of Emphysema:

Answer 23

Complications can include: 
Airway obstruction
Air trapping 
Loss of surface area for gas exchange 
Frequent exacerbations 
Infections, bronchospasms. 
Resulting in hypoventilation and hypercapnia, reduction in SA in alveoli for gas exchange and infections can occur and pneumonia and pneumothorax.

Question 24

Describe the pathophysiology of Chronic Bronchitis

Answer 24

Chronic bronchitisis defined as hyper-secretion of mucus and chronic productive cough for at least 3 months of the year (usually the winter months) for at least 2 consecutive year.
Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages and lymphocytes into the bronchial wall. Continual bronchial inflammation causes bronchial oedema and increases the size and number of mucous glands and goblet cells in the airway epithelium. Thick, tenacious mucus is produced and cannot be cleared because of impaired ciliary function. The defence mechanisms of the pulmonary system are compromised, increasing susceptibility to pulmonary infection and injury.

Question 25

Describe the signs and symptoms of Chronic bronchitis

Answer 25

- Persistent cough which produces sputum and mucous for at least 3 months per year in two consecutive years - Prominent vessels also present in chest x ray - fatigue - Chest discomfort - wheezing – Blue bloater: poorly oxygenated lung causing cyanosis – Right sided heart failure due to pulmonary hypertension (Cor pulmonale) resulting from constriction of pulmonary blood vessels – Peripheral oedema due to right sided heart failure – Acidosis resulting from CO2 retention

Question 26

Describe the homeostasis process seen in chronic bronchitis

Answer 26

- the patient will be taking deeper bigger breaths to try gain oxygenation for the body -

Question 27

Describe the homeostasis process seen in chronic bronchitis

Answer 27

- the patient will be taking deeper bigger breaths to try gain oxygenation for the body (this is why the chest diameter expands) and to get rid of the carbon dioxide trapped - the cough present is the body function of trying to get rid of the mucous - the kidneys will also try to cope with the respiratory acidosis (seen in the increase of HCo3), which attempts to create a metabolic alkalosis - hypertension due to body trying to pump blood around body with oxygen

Question 28

Explain the pathophysiology behind pulmonary embolism

Answer 28

(occurs due to DVT) Pulmonary embolism is occlusion of a portion of the pulmonary vascular bed by an embolus (see Fig. 25.32 ), which can be a thrombus (blood clot), tissue fragment, lipids (fats), foreign body or an air bubble (air embolism). Poor perfusion may be caused by blood clot (pulmonary embolism)

Question 29

list the signs and symptoms of pulmonary embolism.

Answer 29

- tachypnoea - dyspnoea - chest pain - increased dead space - ventilation/perfusion imbalance - decreased PaO2 - pulmonary infarction - pulmonary hypertension - decreased cardiac output - systemic hypotension - shock

Question 30

What are the complications that arise from pulmonary embolism? - not sure need to maybe edit/research

Answer 30

hypoxic vasoconstriction decreased surfactant release of neurohumoral and inflammatory substances pulmonary oedema atelectasis can lead to heart failure, cardiac arrest and pulmonary hypertension

Question 31

Describe the homeostasis process against pulmonary embolism. - (edit add more)

Answer 31

The pulmonary circulation has a high capacitance and therefore can occlude around 50% of the vessels in the lung before your heart starts over working. (but a massive pulmonary embolism is life threatening).

Question 32

Describe the pathophysiology of asthma.

Answer 32

Asthma is likely to result from a complex interaction of genetic and environmental components. It can be defined as: "… a heterogeneous disease [meaning that it varies considerably for different people], usually characterised by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation" The principal characteristics of asthma are airway inflammation, airway hyper-responsiveness and mucus hyper-secretion resulting in airflow obstruction, leading to symptoms of dyspnoea, cough, chest tightness and wheeze. 12 The airflow limitation resulting from these physiological changes is episodic and usually reversible.

Question 33

List some signs and symptoms of asthma.

Answer 33

When asthma is well controlled individuals should experience few if any symptoms. However, some may be :expiratory wheezing, dyspnoea, cough, prolonged expiration, tachycardia and tachypnoea (increased ventilatory rate). Severe episodes involve the accessory muscles of ventilation and wheezing is heard during both inspiration and expiration. Pulsus paradoxus (an exaggerated decrease in systolic blood pressure during inspiration) may be noted. Lung function measured by spirometry is reduced. Because the severity of blood gas alterations is difficult to evaluate by clinical signs alone, arterial blood gas levels should be measured if oxygen saturation falls below 90%. The usual findings are hypoxaemia with an associated respiratory alkalosis.

Question 34

Describe complications of asthma.

Answer 34

airway resistance increases and flow rates decrease. Impaired exhalation = air trapping and hyperinflation and increases work of breathing alveolar gas pressure rises and causes decreased alveoli perfusion leading to uneven ventilation/perfusion = hypoxaemia hyperventilation is also triggered by lung receptors which causes a decrease in PaCo2 and increases pH. these complications can worsen as obstruction worsens, leading to hypoventilation, carbon dioxide retention and respiratory acidosis. and can be life threatening

Question 35

Describe the physiology of Acute respiratory distress syndrome.

Answer 35

Acute respiratory distress syndrome results from an acute diffuse injury to the alveolar–capillary membrane and decreased surfactant production. the hallmark of acute respiratory distress syndrome is lung inflammation. There is activation of the inflammatory response, including complement, cytokines, arachidonic acid metabolites and platelet-activating factor Injury to the pulmonary capillary endothelium stimulates platelet aggregation (platelets sticking together) and intravascular thrombus formation. Endothelial damage also initiates the complement cascade, stimulating neutrophil and macrophage activity and the inflammatory response.Activated neutrophils release a battery of inflammatory mediators, these mediators extensively damage the alveolar–capillary membrane and greatly increase capillary membrane permeability.

Question 36

List symptoms of ARDS

Answer 36

- Difficulty breathing – Low blood pressure and other organ failure – Rapid breathing – Shortness of breath – Symptoms usually develop within 24 to 48 hours of the injury or illness. – Often, people with ARDS are so sick they cannot complain of symptoms.

Question 37

Explain some complications of ARDS

Answer 37

Leads to inflammation of the lungs leading to impaired gas exchange. – This leads to a release of inflammatory mediators, hypoxaemia - the alveolar capillary damage of acute respiratory distress syndrome often cause widespread inflammation, endothelial damage and capillary permeability throughout the body, resulting in the systemic inflammatory response syndrome, which lead to = multiple organ dysfunction syndrome – Is often fatal and requires admission to intensive care. - can be susceptible to infection = pneumonia - The lungs become less compliant, ventilation of alveoli decreases and pulmonary blood flow is shunted right to left. The work of breathing increases. The end result is acute respiratory failure.

Question 38

Describe what is meant by the term lung compliance

Answer 38

- Refers to the ease with which the lungs can be inflated. – Think about blowing up a balloon (first it is difficult, gets easier once it has been stretched). – Is a measure of the change in lung volume that occurs with the change in intrapulmonary pressure. - Normal compliance in both lungs in the average adult is 200mL/cm H2O e.g. every time the intrapulmonary pressure increases by 1cm/H20, the lung volume expands by 200mL. – Determined by elastin and collagen fibers, water content, surface tension and the compliance of the thoracic cage

Question 39

which conditions can | decrease/increase lung compliance?

Answer 39

decreases lung compliance: - acute respiratory distress syndrome due to the pulmonary oedema - restrictive lung diseases such as fibrosis - obesity - scoliosis - pneumothorax Increase: - obstructive lung disorders/disease such as asthma, emphysema, chronic bronchitis due to the loss of elastic tissue (elastic recoil is decreased) - ageing

Question 40

Discuss the changes in physiology that occur in obstructive and restrictive lung disease.

Answer 40

Obstructive airway diseases are characterised by airflow obstruction or limitation that causes more difficulty during expiration. More force — that is, the use of the accessory muscles of expiration — is required to expire a given volume of air or emptying of the lungs is slowed, or both. Obstructive: - lungs become more inflated= blockage to airway exchange - exhalation is impaired - total lung capacity normal - forced vital capacity normal - decreased expiratory flow rate Restrictive: - the lung cannot fully expand= not as much air into lung - accompanied by decreased total lung capacity - forced vital capacity decreased - normal or decreased expiratory flow rate

Question 41

Discuss the effect hypoxaemia would have on the pulmonary vessels.

Answer 41

- blood vessels in pulmonary circulation undergo extreme vasoconstriction when exposed to hypoxia - enabling blood to be redirected from areas with poor ventilation to good ventilation - if alveolar oxygen falls below 60mmHg, vasoconstriction will occur and blood flow eventually will cease.