Respiratory 1

Question 1

Describe the anatomy of the respiratory tract.

Answer 1

Split into upper and lower respiratory tract.
Upper: organs outside the thorax: nose, pharynx & larynx
Lower: organs within the thorax - trachea, bronchi, alveolar duct, bronchioles & alveoli.

Question 2

How is the respiratory tract structured to increase SA for gas exchange?

Answer 2

The trachea leads from the larynx down into the lungs. It then splits into two at the carina (ridge of cartilage in the trachea between the division of the two main bronchi) to form the left and right bronchus.

Each bronchi branch into many bronchioles leading to alveoli where gas exchange takes place. This structuring allows for a large SA for gas exchange.

Question 3

What can be found on the surface of the epithelium of the alveoli?

Answer 3

Pseudostratified columnar epithelium
Type 1 & 2 alveolar cells

Question 4

What are type 1 alveolar cells ?

Answer 4

• Thin squamous epithelium covering alveoli
• Minimise the distance between the inhaled gasses and blood vessels that will then absorb the gases to carry around the body.

Question 5

What are type 2 alveolar cells ?

Answer 5

• Defenders of the alveoli
• Secrete a surfactant that reduces water tension in the lungs (keeps alveolar surface free from fluid).
• During injury, these cells spread to reform the alveolar epithelium - they are progenitor cells.

Question 6

Where is the pseudostratified columnar epithelium found?

Answer 6

Higher up the respiratory tree in the bronchioles and bronchi

Question 7

What structure is found within the pseudostratified columnar epithelium that acts as a barrier against infection?

Answer 7

The pseudostratified columnar epithelium have little cilia that carry mucus up towards the pharynx to allow for coughing to remove mucous or swallowing into the stomach.

Question 8

Describe the function of the lungs

Answer 8

• Site of gas exchange: O2 absorption, CO2 removal. Occurs by diffusion with gases moving from the area of lower conc (partial pressure).
• Acid- base balance: CO2 + H2O <–> H2CO3 <–> H+ + HCO3-

Question 9

What are the 3 mechanisms that maintain body acid-base balance?

Answer 9

• Lungs
• Kidneys
• Buffer system

Question 10

How does the brain and lungs maintain an acid-base balance in the blood?

Answer 10

Chemoreceptors in the aortic arch and the carotid artery detect a change in O2 / CO2 conc. Increase in Co2 and simultaneous decrease in O2 conc is detected = signal sent to respiratory centres in the brainstem to increase the rate and depth of breathing (ventilation)= causing you to inhale more O2 and exhale more CO2. These centres also receive input from pH receptors – CO2 makes blood more acidic by producing carbonic acid.

Normally, excess CO2 and therefore acid base balance is partially controlled by breathing –pH receptors detect a drop in pH (blood more acidic) to trigger increased ventilation in lungs to remove CO2 = restoring blood pH.

Question 11

How do the kidneys maintain an acid-base balance?

Answer 11

Cells of the kidney reabsorb bicarbonate (HCO3-) from the urine back to the blood and they then secrete H+ ions into the urine.

By adjusting the amounts reabsorbed and secreted, they balance the bloodstream’s pH.

Question 12

What is asthma?

Answer 12

Inflammatory disease affecting children and adults. 160 000 diagnoses per year.

Causes reversible inflammation of the bronchioles, causing the muscles around them to contract and bronchioles narrow. (activated mast cells release histamine)

The mucosa of the airways (lining) becomes oedematous – blocked up with fluid and there can be excess mucus production in an attempt to remove irritant.

Question 13

What is episodic bronchoconstriction?

Answer 13

Breathing normally between episodes of asthma attacks.

Episodes can be triggered. Often worse at night or early in the morning.

In severe asthma, there may be chronic inflammation that requires preventative medication – or less commonly lead to chronic lung impairment.

Question 14

List the triggers of asthma

Answer 14

Allergies, pollution particulates, inhaling smoke (smoking, passive smoking), cold weather, exercise, infections, some patients sensitive to NSAIDs such as ibuprofen.

Question 15

What does it mean if patients with asthma are atopic?

Answer 15

Asthmatic pts have a predisposition to an immune response when triggered by antigens / allergens. Excess IgE antibodies produced that are responsible for allergic reactions.

They may also have hay fever or eczema.

Question 16

The management of asthma using drugs is a stepwise approach. List the different types of asthma drugs.

Answer 16

Short-acting Beta-2 Agonist- e.g. Salbutamol

Inhaled corticosteroid

Leukotriene Receptor Antagonist - e.g. Montelukast

Long-acting Beta-2 Agonist - e.g. Salmeterol, Formoterol.

Maintenance and Reliever Therapy - MART (combination therapy): E.g. Fostair (beclomethasone, formoterol).

Long-acting Muscarinics- e.g. Ipratropium, Prednisolone

Other: Theophylline - long acting bronchodilator

Question 17

Describe the action of Salbutamol.

Answer 17

Salbutamol is used to manage an asthma attack in medical emergencies. It is a Beta-2 Agonist – dilates airways by relaxing smooth muscle. They’re not specific to airway receptors, so often act on other B receptors causing sensation of palpitations for example. B agonists act on sympathetic pathways and stimulate the heart to beat faster.

Question 18

What are the effects of asthma on OH?

Answer 18

Increased risk of caries, periodontal disease, ulcers and oral candidiasis:

1. Breathing through the mouth = dry mouth = reduced protection from saliva.
2. Preventative inhalers such as Salbutamol can thicken saliva = increasing the risk of dental caries.
3. Mild acid content in inhalers can cause erosion
4. Steroid inhalers (Budesonide) can lead to oral thrush

Question 19

If Salbutamol is insufficient, what other medication can the patient be on?

Answer 19

Pt may also be put on a daily preventer inhaler consisting of an inhaled corticosteroid to reduce airway inflammation. Meds often end in ‘azone’ or ‘anide’ e.g. Budesonide.

Question 20

What advice is given to patients who have steroid inhalers?

Answer 20

– advise pts to wash mouth out after using inhaler. Can also get a spacer (increase the likelihood of inhaler getting down into lungs rather than ending up in mouth & throat).

Question 21

If corticosteroids are insufficient to control asthma, pts are then placed on a Leukotriene Receptor Antagonist such as Montelukast. What is the action of this tablet?

Answer 21

– dilates the airways like the reliever, but also acts as an anti-inflammatory like the preventer.

Question 22

Why would a long-acting Beta-2 Agonist be required?
(e.g. Salmeterol, Formoterol).

Answer 22

• Used when a Leukotriene Receptor Antagonist is not enough to control asthma.
• Long-acting Beta-2 Agonist has the same mechanism as reliever inhaler but lasts longer. Started in addition to already being on reliever and preventer inhaler.

Question 23

What is MART? - Maintenance and reliever therapy

Answer 23

• Combination of inhalers used.
• Inhalers for managing poorly controlled asthma.
• Contains preventer and reliever drug. Taken regularly. E.g. Fostair (beclomethasone, formoterol).

Question 24

When would a long-acting Muscarinics (Ipratropium, theophylline, prednisolone) be required for asthma?

Answer 24

When all other tx is not enough to control pts asthma.
The drug e.g. Ipratropium (bronchodilator) - blocks the broncho-constriction.

Theophylline – act to dilate airways and are anti-inflammatory.

Prednisolone tablets – long term or a rescue medication if they have a bad flare such as being in hospital, or on a reducing course of prednisolone after leaving hospital.

Question 25

What questions should the pts be asked during MH that indicates their level of asthma control?

Answer 25

• Asthma mild, mod, or severe?
• Recent hospital admission within the last year?
• Type of inhalers used, inhaled corticosteroids?
• Triggers / allergies.
• If on 3 or more drugs = worse control of asthma. [Lower threshold for calling ambulance if they have an asthma attack = call sooner].

*How many drugs are in the inhalers gives an indication of how well managed the patient’s asthma is normally.

Question 26

In acute asthma exacerbation, what signs / symptoms do we need to look for in the AIRWAY?

Answer 26

Shortness of breath

Tight chested (bronchiole constriction impeding ventilation).

Coughing and wheeze (mucous in oedema of the mucosa can cause coughing and can hear constricted bronchioles as wheeze ‘expiratory lower pitched sound’).

Question 27

In acute asthma exacerbation, what signs / symptoms we need to look for in the BREATHING?

Answer 27

*High RR, Hypoxia, reduced PEF.

Pts often compensate for feeling short of breath by sitting upright. Their body will try to maintain adequate ventilation by increasing respiratory rate and depth to compensate narrowed airways.

May be using accessory muscles to breathe e.g. intercostal muscles but in a clothed pt what you will likely see is tensing of sternocleidomastoid as they breathe.

Question 28

In acute asthma exacerbation, what signs / symptoms we need to look for in the CIRCULATION?

Answer 28

• High HR, arrhythmia.

HR increases in an attempt to deliver the limited O2 supply around the body faster. But if compensatory mechanisms are insufficient, the pt may decompensate and become hypoxic – evident on pulse oximetry.

Question 29

What are the indications of moderate asthma severity?
[RR, HR, O2 sat, Peak Exp. flow, Other indications]

Answer 29

Respiratory rate: <25 bpm
Heart rate: <110 bpm
O2 saturations: >92%
Peak expiratory flow: Between 50-75% of best or predicted.
Other: increasing symptoms, speech normal.

Question 30

What are the indications of an acute severe asthma?
[RR, HR, O2 sat, Peak Exp. flow, Other indications]

Answer 30

Respiratory rate: 25 bpm or more
Heart rate: 110 bpm or more
O2 saturations: >92%
Peak expiratory flow: Between 33-50% of best or predicted.
Other: inability to complete full sentences
*Call ambulance

Question 31

What are the indications of a life threatening asthma?
[RR, HR, O2 sat, Peak Exp. flow, Other indications]

Answer 31

Respiratory rate: 25 bpm or more
Heart rate: arrhythmia
O2 saturations: <92%
Peak expiratory flow: <33% of best or predicted.
Other: altered consciousness, cyanosis & poor respiratory effort, drowsy *no longer compensating.
*Call ambulance

Question 32

Bronchial constriction causes reversible airway obstruction which is why exacerbations are episodic in nature. However, asthma can chronically cause a degree of permanent airway obstruction and repeated exacerbations can lead to ___________ and ____________.

Answer 32

fibrosis and inflammation within bronchioles.

Question 33

How can airway obstruction be measured for patients with asthma?

Answer 33

• Airway obstruction is measured using a peak expiratory flow meter; which measures the maximum rate at which a pt can exhale air.
• This is limited in an asthmatic pt by their bronchial constriction. So, they may have a lower baseline than a healthy pt or a normal baseline but in an attack, their peak expiratory flow drops.

Question 34

What makes the peak expiratory flow a KEY investigation to do as a part of ABCDE assessment during an acute asthma attack?

Answer 34

• Allows us to catergorise the severity of asthma attack and treat appropriately.
• Pts may not appear distressed if they are having an acute severe or life-threatening episode -> they have exhausted compensatory mechanisms such as the elevated respiratory rate. Use the severity to inform loading dose of salbutamol and deciding when to call ambulance.

Question 35

During MH, what questions should we ask the patient about their history of asthma?

Answer 35

Previous life-threatening attack?
Hospital in past year with asthma? - indicating severity
Recent frequent use of reliever inhaler? (struggling with asthma) – will tire sooner.
Which medications? - if on 3 or more asthma medications = poor control.
Dental anxiety? - may trigger asthma.

Question 36

What is chronic obstructive pulmonary disease?

Answer 36

Airways obstruction often caused by smoking.
- Smoking causes damage to bronchi and alveoli. The cells produce excess mucous to clear the smoke causing hypertrophy of mucus cells.
- Mucous and cells causes airway obstruction: Chronic bronchitis (long-term inflammation of bronchi)
- Damage to walls of alveoli – [thin membranes between each alveoli] causing merging and formation of large bullae or emphysema.

Question 37

Pts with COPD may have either or both chronic bronchitis & emphysema. What are the similarities and differences in symptoms they may have?
And which medications do they use similar / different to asthma?

Answer 37

Symptoms similar to asthma: breathlessness, wheeze, cough but CHRONIC – rather than episodic.
Bronchitis causes hypertrophy of mucous glands in airways = obstruction that is irreversible.
Some response to drugs used in asthma e.g. Salbutamol, Salmeterol, Tiotropium - dilation of airways.
Can use inhaled corticosteroids to reduce inflammatory response (risk of oral candida).
Carbocisteine – mucolytic. Thins excess mucous so easier clearance.
Pts with COPD are more prone to chest infections, so clearance of mucous is important. Pts may require more ABs.

Question 38

What are the symptoms of severe COPD?

Answer 38

Barrel-chested – expanded lungs at rest. Struggle to exhale gas from lungs.

Pursed-lip breathing – to increase pressure in thorax to help them exhale. Exhalation comes from a pressure gradient from lungs to outside.

Long-term oxygen therapy due to chronic hypoxia.

Right-sided heart failure in late stages of disease leading to oedema (increased resistance to blood flow through lungs due to tissue damage – putting a strain on RHS of heart)

Question 39

What are the two types of respiratory failure in COPD?

Answer 39

Type 1 – hypoxia (low oxygen saturations but normal CO2 levels in blood – due to impairment of gas exchange)

Type 2 – hypercapnia (high CO2 in blood. Due to difficulty ventilating and exhaling waste CO2 – seen in COPD)

Question 40

Patients with COPD are at risk of type 2 Respiratory Failure. Why is this?

Answer 40

Chronically, pts with COPD may get used to a lower O2 level. Chemoreceptors reset to new normal : O2 88-92% (so deliver O2 at saturation level appropriate to pt group)

[Healthy pt O2 saturation: 95-100%]

Question 41

Why do we need to be careful during a medical emergency when giving oxygen to a patient with COPD?

Answer 41

• If we give them too much O2 in an exacerbation, the respiratory rate and depth decrease = less CO2 is exhaled. The body is responding to excess O2 due to change in receptor tolerance. The body also increases blood supply to parts of lungs that are poorly ventilated (not good at expanding and collapsing) – but these areas are still poor at removing CO2 from lungs. Reduced ventilation means more carbon dioxide

*High O2 in blood displaces CO2 from where it is buffered by haemoglobin which disrupts the acid-base balance making blood more acidic. Pt appears flushed, has headache, flapping tremor (hands rhythmically flap), confusion, drowsy.

Question 42

Describe what happens during anxiety that leads to hyperventilation

Answer 42

Anxiety causes pt to increase rate and depth of respiration. – pt blowing off CO2 which can result in a respiratory alkalosis. Alkaline and raised pH in blood (low CO2 levels in blood). This is responsible for symptoms such as tingling sensations, lightheaded. Short of breath, fast heart rate.

Breathing techniques can manage symptoms: encourage slow breathing through pursed lips. Offer a drink - this naturally slows breathing.
Other breathing techniques: abdominal breathing, limited air flow nostril breathing, alternate nostril breathing.

Question 43

How can we manage different aspects of care in a patient with COPD?

Answer 43

• Smoking cessation - advise to stop smoking
• Consider access arrangements (difficulty with mobility due to breathlessness)
• Up to date MH – drug history.
• Positioning – lying flat causes shortness of breath.
• Dry mouth – mouth breathing with pursed lip breathing.
• Oral candida
• Consider drug interactions with BNF
• Be prepared for exacerbation particularly triggered by infections