Respiratory PBL ILO’s

Question 1

Structure and function of the chest wall:

Answer 1

The chest wall is compromised of skin, fat, muscle and the thoracic Skelton. It provides protection to vital organs (eg heart and major vessels, lungs and liver).

Question 2

Structure and function of the pleural cavity:

Answer 2

The pleural cavity is a space between the visceral and parietal pleura. The space contains a tiny amount of serous fluid, which has two key functions:
The serous lucid continuously lubricates the pleural surface and makes it easy for them to slide over each other during lung inflation and deflation.
The serous fluid also generates surface tension which ills the visceral and parietal pleura adjacent to each other allowing the thoracic cavity to expand during inspiration.

Question 3

Name the respiratory muscles of inspiration:

Answer 3

Sternocleidomastoid
Scalenes
Pectoralis major and minor
Sarratus anterior
External intercostals
Diaphragm

Question 4

Nam the expiratory muscles of respiration:

Answer 4

Internal intercostals
Obliques
Transverse Abdominis
Recuts Abdominis

Question 5

Structure and function of the sternum:

Answer 5

Maubrium
Body
Xiphisternum

Protection. Your sternum, along with your ribs, works to protect the organs of your torso, such as your heart, lungs, and chest blood vessels.
Support. Your sternum also provides a connection point for other parts of your skeletal system, including your collarbone and most of your ribs.

Question 6

Function of the ribs:

Answer 6

The ribs are the bony framework of the thoracic cavity. The ribs form the main structure of the thoracic cage protecting the thoracic organs, however their main function is to aid respiration. There are twelve pairs of ribs. Each rib articulates posteriorly with two thoracic vertebrae by the costovertebral joint.

Question 7

Function of thoracic vertebrae:

Answer 7

Your thoracic spine consists of 12 vertebrae, labeled T1 through T12. Vertebrae are the 33 individual, interlocking bones that form your spinal column. These bones help protect your spinal cord from injury while allowing you to twist and turn. Your thoracic spine and ribcage also protect your heart and lungs. The joints in your thoracic spine are tight enough to protect these vital organs but loose enough to allow for the movements of breathing — inhaling and exhaling.

Question 8

Structure and function of the thoracic inlet/ outlet

Answer 8

The thoracic inlet/ outlet (clinically) is defined as the space in the lower neck between the thorax and axilla through which the subclavian vein, subclavian artery, and brachial plexus travel from their central origins to their peripheral termini.

Question 9

Intercostal spaces

Answer 9

The intercostal spaces are the spaces between the ribs, there are 11 on each side and are numbered according to the rib which is the upper border of the space. They contain three layers of muscle, the external, internal and innermost layers, with the neurovascular bundle found between the internal and innermost layers.

Question 10

Describe and explain the 3 types of Intercostal muscles:

Answer 10

The external intercostal muscles
• Outermost muscle, has fibres which run in a downwards, forwards and medial direction from the inferior border of the superior rib to insert on the outer lip of the inferior rib.

The internal intercostal muscle 
	• The middle layer of the intercostal space. This muscle has fibres which run in a downwards, backwards and lateral direction from the inferior border of the superior rib to insert on the superior border of the inferior rib, 
 
The innermost intercostals
	• 3 muscles which are collectively known as the transverse thoracic group.

Question 11

What is the neurovascular bundle and where would it be found?

Answer 11

The neurovascular bundle consist of a nerve, artery and a vein between the internal and innermost muscles.

Question 12

Where does posterior intercostal artery arise from?

Answer 12

Thoracic aorta

Question 13

Where o the anterior intercostal arteries arise from?

Answer 13

Internal thoracic musculophrenic

Question 14

Where do posterior intercostal veins drain to?

Answer 14

Azygos system

Question 15

Where do anterior intercostal veins drain in to?

Answer 15

Internal thoracic or musclophrenic

Question 16

What do the intercostal nerves supply?

Answer 16

• The intercostal nerves supply the intercostal muscles, the parietal pleura and overlying skin and supply somatic innervation.

Question 17

Diaphragm:

Answer 17

Diaphragm
• Dome shaped skeletal muscle with a central tendon, it has a left and right dome.
• The origin of the diaphragm consists of three parts, the sternal which rises at the posterior surface of the xiphisternum, the costal which rises at the lower 6 ribs and their costal margins and the vertebral which rises from the right crus (from bodies L1-3), and left crus (from L1-2), medial & lateral arcuate ligaments.
• T5 of the thoracic vertebrae during expiration
• Openings for the inferior vena cava (T8) oesophagus (T10) and aorta (T12)
• Fibrous pericardium fused to the central tendon.
The costophrenic recess is the area between the chest wall and the dome

Question 18

Functional anatomy of ventilation - inspiration/ inhalation:

Answer 18

• Inhalation is initiated by the contraction of the diaphragm.
• Contents of the abdomen are moved downward and the ribcage to expands
• Chest cavity expands so the lungs can also expand into it.
• Larger thoracic volume and a negative pressure (with respect to atmospheric pressure) inside the chest.
• The external intercostal muscles also contract to pull the ribcage both upward and outward when you inhale to further help enlarge the chest cavity, decreasing the pressure and causing air to flow in via the pressure gradient.

Question 19

Functional anatomy of ventilation - expiration/ exhalation:

Answer 19

• Exhalation is generally a passive process since the lungs have a natural elasticity
• They recoil from the stretch of inhalation and air flows back out until the pressures in the chest and the atmosphere reach equilibrium therefore air travels out.

Question 20

Inspiratory accessory muscles:

Answer 20

• There are accessory muscles of inspiration which are recruited during exercise or patients with breathing difficulties.
• The pectoralis major and pectoralis minor, the serratus anterior, the sternocleidomastoid is and scalene all assist in elevating the rib cage during inhalation.

Question 21

Costochondral joint:

Answer 21

1. Costochondral joint
   • The costochondral joint is the connection between a rib and its costal cartilage.
   • The joint is formed by two articular surfaces: the roughened cup-shaped anterior end of the rib and the rounded lateral end of the costal cartilage.
   • They costochondral articulations themselves are immobile, they do not permit movement.
   • But the costal cartilages provide a flexible attachment for the anterior ends of the ribs to the sternum and may undergo slight bending and twisting movements that facilitate widening of the thoracic diameters during breathing.

Question 22

Costovertebral joint:

Answer 22

2. Costovertebral joint
   • The costovertebral joints are the joints that connect the ribs to the vertebral column.
   • The movements of these joints are called ‘pump handle’ or ‘bucket-handle’, the long axes of the necks of the rib move in this motion, resulting in raising and lowering the sternal ends.
   • During inspiration, the transverse diameter of the thorax is increased by the ribs swinging outward.

Question 23

Sternocostal joint:

Answer 23

3. Sternocostal joints
   • The sternocostal joints lie between the costal cartilages of the first to the seventh ribs and the sternum.
   • The joint between the first rib and the sternum is cartilaginous, but all others are synovial.
   • Each is surrounded by a capsule and supported by radiate movements. The main function of the sternocostal joint is to facilitate the mechanical ventilation by allowing the costal cartilage to glide with the ribs during inspiration and expiration.

Question 24

Three stage stress response:

Answer 24

The stress response is considered to include three stages—alarm, resistance, and exhaustion:
Alarm stage: activation of the hypothalamus, sympathetic nervous system and adrenal glands
Resistance stage: hormone levels raised, essential body systems are at peak performance
Exhaustion stage: body is unable to respond further/is damaged by the increased demands of the stress

Question 25

Physiological features of stress response:

Answer 25

Physiological features of stress response: Significant effects of the stress response include the following: • Increased cardiac output (Elevated blood pressure and increased heart rate) • Bronchodilation and increased ventilation • Increased blood glucose levels (resulting from glycogenolysis and gluconeogenesis in the liver and protein catabolism in muscle, as well as lipolysis ) • Arousal of the central nervous system • Decreased inflammatory and immune responses (cortisol reduces the early and later stages)

Question 26

What is lidocaine and how does it work?

Answer 26

Local anaesthetic involves numbing an area of the body without causing someone to lose consciousness This is usually for smaller operations or procedures Can recover from them quicker than the use of general anaesthetic How do they work: • Stop the nerves in a part of your body sending signals to your brain • Won't feel any pain but can feel pressure / movement • Takes a few minutes to lose feeling • Medication usually wears off after a couple of hours Forms of local anaesthetic: • Injections • Creams • Gels • Sprays • Ointments

Question 27

Uses of local anaesthetics:

Answer 27

Uses of local anaesthetics: • Treating pain ○ e.g. sprays and gels can help with mouth ulcers and sore throats ○ e.g. long term joint pain can be treating by combination of local anaesthetic and steroid injection • Preventing pain during + after surgery ○ Usually in minor procedures such as wisdom tooth removal, minor skin operations on lesions, some eye surgeries, biopsies, performing a lumbar puncture, inserting a central line, hand surgery, sutures ○ Can be used in major surgery if the patient needs to be away e.g. certain brain surgeries • Epidurals and spinal anaesthetics ○ Local anaesthetic injected into the epidural space or spine ○ Numb large areas of the body by stopping pain signals travelling along nerves in the spine ○ Child birth, hip replacements • Peripheral nerve block ○ Inject local anaesthetic to numb nerves supplying a particular part of the body e.g arm ○ Ultrasound scan is used to pinpoint the nerve when injecting ○ Takes 30mins to become effective

Question 28

Risks and side effects of lidocaine:

Answer 28

Risks and side effects • Some discomfort when injection is given • Tingling sensation as medication wears off • Minor bruising, bleeding or soreness at site of injection • Can sometimes get temporary side effects: ○ Dizziness ○ Headaches ○ Blurred vision ○ Twitching muscles/shivering ○ Continuing numbness, weakness or pins and needles ○ Find it hard to urinate/leaking after epidural • Very rarely can have an allergic reaction. Can lead to fits (seizures) or cardiac arrest

Question 29

Demonstrate knowledge of the changes in pleural pressure during respiration:

Answer 29

· The alveolar and atmospheric pressures are greater than the intrapleural pressure. Therefore, connections between the alveoli and pleural space, or surrounding atmosphere and pleural space, will lead to air moving down a pressure gradient into the pleural space. · This increases the intrapleural pressure, potentially compressing the lungs. Air will continue to move into the pleural space until the pressure gradient equilibrates or the connection into the pleural space seals off.

Question 30

What happens in a tension pneumothorax?

Answer 30

· In a tension pneumothorax, air enters the pleural space through a one-way valve and is therefore unable to leave the pleural space. The intrapleural pressure exceeds the atmospheric pressure, leading to collapse of the ipsilateral lung and a shift of the mediastinum away from the pneumothorax. · In severe cases, the increased intrapleural pressure can compress the heart and surrounding vasculature, reducing cardiac output and venous return. If untreated, this may lead to cardiac arrest.

Question 31

Pleural pressure during inspiration:

Answer 31

Inspiration: · Diaphragm and inspiratory intercostal muscles actively contract  expansion of thorax. Interpleural pressure drops (usually ~-4mmHg at rest) becomes more subatmospheric/more negative · Intrapleural pressure drops · Lower alveolar pressure compared to atmospheric pressure allows air to flow 1. Diaphragm contracts which causes thorax to expand 2. This pulls the outer pleural membrane (the one facing the thoracic cavity) causing a drop in intrapleural pressure 3. The inner pleural membrane then pulls on the lungs, causing the lungs to expand, this causes the pressure gradient, allowing air to flow into the lungs *opposite in expiration

Question 32

Pleural pressure during expiration:

Answer 32

Expiration · Relaxation of the diaphragm and elastic recoil of tissue decreases thoracic volume  increasing intraalveolar pressure and intrapleural pressure · Higher alveolar pressure compared to atmospheric pressure allows air to flow out of lungs, alveoli shrink due to elastic recoil *If intrapleural pressure becomes positive e.g. lungs become punctured/damaged) – causes lungs to collapse

Question 33

First and second step of taking a chest x ray:

Answer 33

First step: confirm details • Patient details: name, date of birth and unique identification number. • Date and time the film was taken • Previous imaging: useful for comparison. Second step: check the quality of the chest radiograph (RIPE) Rotation The medial aspect of each clavicle should be equal distance from the spine. The spinous processes should also be in vertically orientated against the vertebral bodies. Inspiration The 5-6 anterior ribs, lung apices, both costophrenic angles and the lateral rib edges should be visible. Good inspiration by the patient during the X-ray will stretch the thoracic cavity outwards and separate the pulmonary vessels, allowing for greater visualisation. Projection Note if the film is front to back (anterior to posterior - AP) or back to front (posterior to anterior - PA) If there is no label, then assume it’s a PA film (if the scapulae are not projected within the chest, it’s PA). Exposure The left hemidiaphragm should be visible to the spine and the vertebrae should be visible behind the heart.

Question 34

ABCDE interpretation to a chest x ray:

Answer 34

Third step: structured interpretation of a chest X-ray • Airway: trachea, carina, bronchi and hilar structures. • Breathing: lungs and pleura. • Cardiac: heart size and borders. • Diaphragm: including assessment of costophrenic angles. • Everything else: mediastinal contours, bones, soft tissues, tubes, valves, pacemakers and review areas.

Question 35

Trachea observations in a chest x ray:

Answer 35

Trachea Inspect the trachea for evidence of deviation: • The trachea is normally located centrally or deviating very slightly to the right. • If the trachea appears significantly deviated, inspect for anything that could be pushing or pulling the trachea. Make sure to inspect for any paratracheal masses and/or lymphadenopathy. True tracheal deviation: Pushing of the trachea: large pleural effusion or tension pneumothorax. Pulling of the trachea: consolidation with associated lobar collapse. Apparent tracheal deviation: Rotation of the patient can give the appearance of apparent tracheal deviation, so as mentioned above, inspect the clavicles to rule out the presence of rotation.

Question 36

Carina and bronchi observation on a chest X ray:

Answer 36

Carina and bronchi The carina is cartilage situated at the point at which the trachea divides into the left and right main bronchus. On appropriately exposed chest X-ray, this division should be clearly visible. The right main bronchus is generally wider, shorter and more vertical than the left main bronchus. As a result of this difference in size and orientation, it is more common for inhaled foreign objects to become lodged in the right main bronchus - aspiration pneumonia. Depending on the quality of the chest X-ray you may be able to see the main bronchi branching into further subdivisions of bronchi.

Question 37

Hilar structure observations on a chest X ray:

Answer 37

Hilar structures The hilar consist of the main pulmonary vasculature and the major bronchi. Each hilar also has a collection of lymph nodes which aren’t usually visible in healthy individuals. The hilar are usually the same size, so asymmetry should raise suspicion of pathology. Causes of hilar enlargement or abnormal position • Bilateral symmetrical enlargement is typically associated with sarcoidosis or TB. • Unilateral/asymmetrical enlargement may be due to underlying malignancy (cancer). • Abnormal hilar position can also be due to a range of different pathologies. You should inspect for evidence of the hilar being pushed (e.g. by an enlarging soft tissue mass) or pulled (e.g. lobar collapse).

Question 38

Lung observation on a chest x ray:

Answer 38

Lungs When interpreting a chest X-ray you should divide each of the lungs into zones. Compare each zone between lungs, noting any asymmetry (some asymmetry is normal and caused by the presence of various anatomical structures e.g. the heart). Some lung pathology causes symmetrical changes in the lung fields, which can make it more difficult to recognise, so it’s important to keep this in mind (e.g. pulmonary oedema). Increased airspace shadowing in a given area of a lung field may indicate pathology (e.g. consolidation/malignant lesion). The complete absence of lung markings should raise suspicion of a pneumothorax. Egs- lung cancer, pneumonia, pneumothorax,

Question 39

Pleura observations on a chest X ray:

Answer 39

Pleura The pleura are not usually visible in healthy individuals. If the pleura are visible it indicates the presence of pleural thickening which is typically associated with mesothelioma. Inspect the borders of each lung to ensure lung markings extend all the way to the edges of the lung fields (the absence of lung markings is suggestive of pneumothorax). Fluid (hydrothorax) or blood (haemothorax) can accumulate in the pleural space, resulting in an area of increased opacity on a chest X-ray. In some cases, a combination of air and fluid can accumulate in the pleural space (hydropneumothorax), resulting in a mixed pattern of both increased and decreased opacity within the pleural cavity. Tension pneumothorax A tension pneumothorax is a life-threatening condition which involves an increasing amount of air being trapped within the pleural cavity displacing (pushing away) mediastinal structures (e.g. the trachea) and impairing cardiac function. If a tension pneumothorax is suspected clinically (shortness of breath and tracheal deviation) then immediate intervention should be performed without waiting for imaging as this condition will result in death if left untreated.

Question 40

Cardiac observation on a chest X ray:

Answer 40

Cardiac In a healthy individual, the heart should occupy no more than 50% of the thoracic width. • This rule only applies to PA chest X-rays (as AP films exaggerate heart size), so you should not draw any conclusions about heart size from an AP film. Cardiomegaly is said to be present if the heart occupies more than 50% of the thoracic width on a PA chest X-ray. Assess the heart’s borders Inspect the borders of the heart which should be well defined in healthy individuals: • The right atrium makes up most of the right heart border. • The left ventricle makes up most of the left heart border. The heart borders may become difficult to distinguish from the lung fields as a result of pathology which increases the opacity of overlying lung tissue: Reduced definition of the right heart border is typically associated with right middle lobe consolidation. Reduced definition of the left heart border is typically associated with lingular consolidation.

Question 41

Diaphragm observation on a chest x ray:

Answer 41

Diaphragm The right hemidiaphragm is, in most cases, higher than the left in healthy individuals (due to the presence of the liver). The diaphragm should be indistinguishable from the underlying liver in healthy individuals on an erect chest X-ray, however, if free gas is present (often as a result of bowel perforation), air accumulates under the diaphragm causing it to lift and become visibly separate from the liver. There are some conditions which can result in the false impression of free gas under the diaphragm, known as pseudo-pneumoperitoneum, including Chilaiditi syndrome. Chilaiditi syndrome involves the abnormal position of the colon between the liver and the diaphragm resulting in the appearance of free gas under the diaphragm (because the bowel wall and diaphragm become indistinguishable due to their proximity).

Question 42

Costrophrenic angles observed by a chest x ray:

Answer 42

Costophrenic angles In a healthy individual, the costophrenic angles should be clearly visible on a normal chest X-ray as a well defined acute angle. Loss of this acute angle, sometimes referred to as costophrenic blunting, can indicate the presence of fluid or consolidation in the area. Costophrenic blunting can also develop secondary to lung hyperinflation as a result of diaphragmatic flattening and subsequent loss of the acute angle (e.g. chronic obstructive pulmonary disease).

Question 43

Name some types and what a pneumothorax is:

Answer 43

What is pneumothorax? Pneumothorax occurs when air gets into the pleural space separating the lung from the chest wall. It can occur spontaneously or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology. Types: Primary pneumothorax: occurs in a patient without a known respiratory disease. Secondary pneumothorax: occurs in a patient with pre-existing respiratory disease. Tension pneumothorax is caused by trauma to chest wall that creates a one-way valve that lets air in but not out of the pleural space.

Question 44

Causes of primary pneumothorax:

Answer 44

Causes of primary pneumothorax include: • Often unknown • May be due to rupture of a subpleural air bleb (found in the pleural space). • The bleb itself is caused by alveolar rupture, which lets air travel through the interlobular septum into the subpleural space.

Question 45

Causes of secondary pneumothorax:

Answer 45

Causes of secondary pneumothorax include: • COPD: (70% of secondary pneumothorax): rupture of air bulla (air-filled space in lungs, caused by emphysematous destruction of lung tissue). • Asthma: rupture of air bulla or subpleural air bleb, though the mechanism is still poorly understood. • Cystic fibrosis: endobronchial obstruction causing increased pressure in the alveoli, leading to alveolar rupture. • Marfan syndrome: abnormal lung connective tissue leads to increased formation of air bulla (which rupture), and tall body habitus increases mechanical stress on lung apices (exacerbating bulla rupture).

Question 46

Causes of a tension pneumothorax:

Answer 46

Causes of tension pneumothorax include: • Penetrating/blunt trauma • Mechanical ventilation or non-invasive ventilation (NIV) • Conversion of simple pneumothorax to tension pneumothorax

Question 47

How is normal physiological function affected by a pneumothorax?

Answer 47

How is normal physiological function affected by pneumothorax? • The one-way valve means that during inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space. • Therefore, more air keeps getting drawn into the pleural space with each breath and cannot escape = intrapleural pressure exceeds the atmospheric pressure, leading to collapse of the ipsilateral lung • This is dangerous as it creates pressure inside the thorax that will push the mediastinum across away from the pneumothorax. • The mediastinum kinks the big vessels in the mediastinum and cause cardiorespiratory arrest. In severe cases, the increased intrapleural pressure can compress the heart and surrounding vasculature, reducing cardiac output and venous return. If untreated, this may lead to cardiac arrest.

Question 48

Signs of tension pneumothorax:

Answer 48

Signs of Tension Pneumothorax • Tracheal deviation away from side of pneumothorax • Reduced air entry to affected side • Increased resonant to percussion on affected side • Tachycardia • Hypotension

Question 49

Clinical examination and usual findings for suspected pneumothorax:

Answer 49

Investigations: Clinical examination A full respiratory examination should be performed in suspected cases of pneumothorax. Typical clinical findings in pneumothorax include – on the same side as the pneumothorax. • Hyper-resonant lung percussion • Reduced breath sounds. • Reduced lung expansion. Typical clinical findings in tension pneumothorax include: • Tracheal deviation away from the pneumothorax • Severe tachycardia • Hypotension

Question 50

Peripheral chemoreceptors:

Answer 50

Peripheral chemoreceptors • Located in carotid body and aortic body • Detect large changes in partial pressure of oxygen (pO2) as arterial blood supply leaves the heart • When oxygen levels are low, afferent impulses trave via glossopharyngeal and vagus nerves to medulla oblongata and pons in the brainstem • A number of responses are then coordinated which aim to restore pO2: ○ Respiratory rate and tidal volume are increased to allow more oxygen to enter lungs and diffuse into blood ○ Blood flow directed towards kidneys and brain ○ Cardiac output is increased to maintain flow

Question 51

Central chemoreceptors:

Answer 51

Central chemoreceptors • Located in the medulla oblongata of the brainstem • Detect changes in arterial partial pressure of pCO2 • When changes are detected, the receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation to restore normal pCO2 ○ Detection of an increase pCO2 = increased ventilation ○ Detection of decrease pCO2 = decreased ventilation Mechanism behind how central chemoreceptors detect changes in arterial pCO2 is more complex, and is related to changes in pH of the cerebral spinal fluid • pH of CSF is established by ratio of pCO2 : HCO3- • The pH of the CSF is inversely proportional to the arterial pCO2 ○ A small decrease in pCO2 leads to an increase in pH of CSF which stimulates the respiratory centres to decrease ventilation ○ A small increase in pCO2 leads to a decrease in the pH of the CSF which stimulates the respiratory centres to increase ventilation

Question 52

What is hypoxia?

Answer 52

• Hypoxia is when the tissues of your body don’t have enough oxygen • Lung disease and heart disease both increase your risk of hypoxia

Question 53

Right lung

Answer 53

The right lung has three lobes and two fissures. Normally, the lobes are freely movable against each other because they are separated, almost to the hilum, by invaginations of visceral pleura. These invaginations form the fissures: ▪ The oblique fissure separates the inferior lobe ( lower lobe ) from the superior lobe and the middle lobe of the right lung . ▪ The horizontal fissure separates the superior lobe ( upper lobe ) from the middle lobe.

Question 54

What important structures are on the medial surface of the right lung?

Answer 54

The medial surface of the right lung lies adjacent to a number of important structures in the mediastinum and the root of the neck ( Fig. 3.45B ). These include the: ▪ heart, ▪ inferior vena cava, ▪ superior vena cava, ▪ azygos vein, and ▪ esophagus. The right subclavian artery and vein arch over and are related to the superior lobe of the right lung as they pass over the dome of the cervical pleura and into the axilla.

Question 55

Left lung

Answer 55

The left lung is smaller than the right lung and has two lobes separated by an oblique fissure. The oblique fissure of the left lung is slightly more oblique than the corresponding fissure of the right lung. The inferior portion of the medial surface of the left lung, unlike the right lung, is notched because of the heart's projection into the left pleural cavity from the middle mediastinum. From the anterior border of the lower part of the superior lobe a tongue-like extension (the lingula of the left lung ) projects over the heart bulge.

Question 56

The medial surface of the left lung lies adjacent to which important features?

Answer 56

The medial surface of the left lung lies adjacent to a number of important structures in the mediastinum and root of the neck. These include the: ▪ heart, ▪ aortic arch, ▪ thoracic aorta, and ▪ esophagus. The left subclavian artery and vein arch over and are related to the superior lobe of the left lung as they pass over the dome of the cervical pleura and into the axilla.

Question 57

Where is the trachea and where does it bifurcate?

Answer 57

The trachea is a flexible tube that extends from vertebral level CVI in the lower neck to vertebral level TIV/V in the mediastinum where it bifurcates into a right and a left main bronchus.

Question 58

Bronchial tree order

Answer 58

Each main bronchus enters the root of a lung and passes through the hilum into the lung itself. The right main bronchus is wider and takes a more vertical course through the root and hilum than the left main bronchus ( Fig. 3.47A ). Therefore, inhaled foreign bodies tend to lodge more frequently on the right side than on the left. Secondary bronchi (supplies a lobe) Tertiary bronchi (supply bronchopulmonary segments) Terminal bronchioles … conducting zone Respiratory zone…. Respiratory bronchioles Alveolar ducts Alveolar sacs

Question 59

What is a bronchopulmonary segment?

Answer 59

Bronchopulmonary segments A bronchopulmonary segment is the area of lung supplied by a segmental bronchus and its accompanying pulmonary artery branch. Tributaries of the pulmonary vein tend to pass intersegmentally between and around the margins of segments. Each bronchopulmonary segment is shaped like an irregular cone, with the apex at the origin of the segmental bronchus and the base projected peripherally onto the surface of the lung. A bronchopulmonary segment is the smallest functionally independent region of a lung and the smallest area of lung that can be isolated and removed without affecting adjacent regions. There are ten bronchopulmonary segments in each lung ( Fig. 3.48 ); some of them fuse in the left lung.

Question 60

Anatomical names of the lungs

Answer 60

Apex (top) Hilum: A pulmonary artery Two pulmonary veins A main bronchus Bronchial vessels Nerves Lymphatics Anterior border Posterior border Inferior border Costal surface (attaches to ribs) Mediastinal surface Diaphragmatic surface (base) • Each lung has: ○ Base on the diaphragm ○ Apex projecting above rib I and into the root of the neck ○ Two surfaces § Costal surface lies immediately adjacent to ribs and intercostal spaces of thoracic wall § Mediastinal surface lies against mediastinum anteriorly and vertebral column posteriorly □ Contains hilum which structures enter and leave through ○ Three borders § Inferior border → sharp and separates the base from costal surface § Anterior/posterior borders → separate costal surface from medial surface □ Anterior border is also sharp □ posterior border is smooth and rounded

Question 61

Why is the right lung slightly bigger than the left lung?

Answer 61

• Right lung is slightly larger than left. Middle mediastinum contains the heart and bulges more to the left than to right

Question 62

The conducting portion

Answer 62

The conducting portion • Conducting piece = nasal cavity, trachea, bronchi & bronchioles • Luminal surfaces of this entire portion → ciliated pseudostratified columnar epithelium & contain goblet cells ○ Role → excrete mucus that serves as first line of defense against incoming environmental pathogens ○ Cilia move mucus-bound particulate up and away for expulsion from the body • In most proximal airway, hyaline cartilage rings support the larger respiratory passages (trachea & bronchi) to facilitate passage of air ○ Three major cell types in this region 1. Ciliated □ Each lined with 200-300 cilia, account for more than half of all epithelial cells in conducting airway 2. Non-ciliated Secretory cells 3. Basal cells • As the degree of branching within the airway tree continues, the epithelium gradually changes from pseudostratified to simple cuboidal…the predominant cells become non-ciliated cells Functions: • Conducting portion (nose, pharynx, larynx, trachea, bronchi and bronchioles) → serve to humidify, warm and filter air ○ Humidification → requires serous and mucous secretions ○ Warming → relies on the extensive capillary network that lays within alveoli ○ Filtration → occurs by trapping mechanism of mucus secretions and ciliary beating § Goblet cells → columnar epithelial cells that secrete high molecular weight mucin glycoproteins into the lumen of the airway and provide moisture to epithelium while trapping incoming particulate and pathogens

Question 63

The gas exchange portion

Answer 63

The gas-exchange portion • Composed of millions of alveoli → lined by an extremely thin, simple squamous epithelium ○ This allows for the easy diffusion of oxygen and carbon dioxide • Additionally, cuboidal, surfactant-secreting cells, Type II pneumocytes are also found lining the walls of alveoli ○ Surfactant has a vital role in lowering the surface tension of water to allow for effective gas exchange • Type I pneumocytes → flattened cells that create a very thin diffusion barrier for gases ○ Tight junctions connect one cell to another ○ Principal functions are gas exchange and fluid transport • Type II pneumocyte → secrete surfactant, this decreases surface area between thin alveolar walls, and stops alveoli from collapsing uring exhalation ○ These cells connect to the epithelium and other constituent cells by tight junctions ○ Also play a vital role in acting as progenitor cells to replace injured or damaged Type I pneumocytes Functions: • Gas exchange → inhaled air diffuses through alveoli into the pulmonary capillaries. CO2 diffuses at same time from capillaries into the alveoli

Question 64

How is ventilation controlled in the brain?

Answer 64

Ventilation Control: The Brain • Involuntary ventilation occurs subconsciously • The organs involved in ventilation (diaphragm and intercostal muscles) are stimulated by the pons and the medulla (located in the brain) • Pons + medulla (respiratory centre of the brain) send impulses to the primary respiratory muscles, via the phrenic and intercostal nerves, which stimulates contraction.

Question 65

What are the groups of neurones called involved in breathing?

Answer 65

Groups of neurons involved in ventilation • Ventral: expiration • Dorsal: inspiration Pontine: rate and pattern of breathing

Question 66

Short acting beta 2 adrenergic receptor agonists

Answer 66

Short acting beta 2 adrenergic receptor agonists, for example salbutamol. These work quickly but the effect only lasts for an hour or two. Adrenalin acts on the smooth muscles of the airways to cause relaxation. This results in dilatation of the bronchioles and improves the bronchoconstriction present in asthma. They are used as “reliever” or “rescue” medication during acute exacerbations of asthma when the airways are constricting.

Question 67

Inhaled corticosteroids (ICS)

Answer 67

Inhaled corticosteroids (ICS), for example beclometasone. These reduce the inflammation and reactivity of the airways. These are used as “maintenance” or “preventer” medications and are taken regularly even when well.

Question 68

Long acting beta 2 agonists (LABA)

Answer 68

Long-acting beta 2 agonists (LABA), for example salmeterol. These work in the same way as short acting beta 2 agonists but have a much longer action.

Question 69

Long acting muscarinic antagonists (LAMA)

Answer 69

Long-acting muscarinic antagonists (LAMA), for example tiotropium. These block the acetylcholine receptors. Acetylecholine receptors are stimulated by the parasympathetic nervous system and cause contraction of the bronchial smooth muscles. Blocking these receptors leads to bronchodilation.

Question 70

Leukotriene receptor antagonists

Answer 70

Leukotriene receptor antagonists, for example montelukast. Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways. Leukotriene receptor antagonists work by blocking the effects of leukotrienes.

Question 71

Theophylline

Answer 71

Theophylline. This works by relaxing bronchial smooth muscle and reducing inflammation. Unfortunately it has a narrow therapeutic window and can be toxic in excess so monitoring plasma theophylline levels in the blood is required. This is done 5 days after starting treatment and 3 days after each dose changes.

Question 72

Maintenance and reliever therapy (MART)

Answer 72

Maintenance and Reliever Therapy (MART). This is a combination inhaler containing a low dose inhaled corticosteroid and a fast acting LABA. This replaces all other inhalers and the patient uses this single inhaler both regularly as a “preventer” and also as a “reliever” when they have symptoms.

Question 73

Adverse effects of anti inflammatory drugs used in asthma treatment:

Answer 73

Adverse effects of anti-inflammatory drugs · Dysphonia (effect of voice box, altered voice) · Oropharyngeal candidiasis · Adrenal suppression · Osteoporosis · hyperglycaemia

Question 74

What is the aim of step wise asthma treatment:

Answer 74

Aim of treatment: § No daytime symptoms § No night-time awakening due to asthma § No need for rescue medication § No asthma attacks § No limitations on activity including exercise § Normal lung function (FEV and/or PEF >80%) predicted or best § Minimal side effects from medication

Question 75

Step wise treatment for asthma therapy:

Answer 75

Intermittent reliever therapy (usually blue inhaler-short term, short acting β2 agonist) and regular preventer therapy (usually brown inhaler – corticosteroid) *see table below on doses Initial add-on therapy – long-acting β2 agonist, which should be considered before increasing dose of inhaled corticosteroid Combination inhalers recommended to: o Guarantee that long acting β2 agonist is not taken without inhaled corticosteroid o Improve inhaler adherence Additional controller therapies o If control remains poor on low-dose inhaled corticosteroids plus a long-acting β2 agonist, recheck diagnosis, assess adherence to existing medication and check inhaler technique before increasing therapy o Increase the dose of inhaled corticosteroids from low dose to medium dose, if not already on these doses o Consider adding a leukotriene receptor antagonist Referred to specialist care

Question 76

Grading acute asthma:

Answer 76

Moderate • PEFR 50 – 75% predicted • Speaking full sentences Severe • PEFR 33-50% predicted • Resp rate >25 • Heart rate >110 • Unable to complete sentences in one breath Life-threatening • PEFR <33% • Sats <92% • Becoming tired • Altered consciousness level • No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”. Near fatal asthma- raised PCO2 and/or requiring mechanical ventilation with raised inflation pressures

Question 77

Treatment of moderate acute asthma:

Answer 77

Treated at home or in primary care Admit people with a moderate asthma exacerbation with worsening symptoms despite initial bronchodilator treatment and/or who have had a previous near-fatal asthma attack. Medication: β2 agonist bronchodilators In most cases nebulised β2 agonists given in high doses act quickly to relieve bronchospasm with few side effects. Ipratropium bromide Combining nebulised ipratropium bromide with a nebulised β2 agonist produces significantly greater bronchodilation than β2 agonist alone, leading to faster recovery and shorter duration of admission. • Ipratropium bromide is a type of anticholinergic medication which opens up the medium and large airways in the lungs. Dose: Salbutamol 2.5 mg (to be repeated x2 over 60 min if required) Add nebulised ipratropium bromide (250–500 micrograms 3–4 times a day) to β2 agonist treatment

Question 78

Acute severe asthma treatment:

Answer 78

Acute severe asthma Admit patients with any feature of a severe asthma attack persisting after initial bronchodilator treatment. Medication: Oxygen Give controlled supplementary oxygen to all hypoxaemic patients with acute severe asthma via a face mask, Venturi mask or nasal cannula. Hypercapnia indicates the development of near-fatal asthma and the need for emergency specialist/anaesthetic intervention. Steroid therapy Steroids reduce mortality, relapses, subsequent hospital admission and requirement for β2 agonist therapy. The earlier they are given in the acute attack the better the outcome. Give steroids in adequate doses to all patients with an acute asthma attack. Intravenous aminophylline In an acute asthma attack, IV aminophylline is not likely to result in any additional bronchodilation compared with standard care with inhaled bronchodilators and steroids. Some patients with near-fatal asthma or life-threatening asthma with a poor response to initial therapy may gain additional benefit from IV aminophylline. Antibiotics If there is convincing evidence of bacterial infection! Dose Maintain saturation levels >88-92% Oral prednisolone (40–50 mg daily) until recovery (minimum 5 days) IV hydrocortisone (100 mg six hourly) continued for 5 days

Question 79

Life threatening asthma treatment

Answer 79

Life threatening asthma Admit patients to ICU if: Persistent or worsening hypoxia Hypercapnia Feeble respiration Reduced GCS Respiratory arrest Confusion Deteriorating PEF Exhaustion Acidosis V magnesium sulphate infusion • Should only be used following consultation with senior medical staff. • PEF < 50% best or predicted Intravenous salbutamol Intravenous hydrocortisone Admission to ICU/HDU Intubation in worst cases This decision should be made early because it is very difficult to intubate with severe bronchoconstriction Dose: 1.2–2 g IV infusion over 20 minutes in saline

Question 80

When should you arrange emergency admission for a person with breathlessness?

Answer 80

Arrange emergency admission for people with: • Rapid onset or worsening of symptoms of suspected heart failure. • Suspected sepsis. • Anaphylaxis. • ECG suggesting a cardiac arrhythmia or myocardial infarction. • Clinical features of: ○ Pulmonary embolism. For more information, see the CKS topic on Pulmonary embolism. ○ Pneumothorax. ○ Cardiac tamponade. ○ Pulmonary oedema. ○ Superior vena cava syndrome. • Any features of a severe or life-threatening asthma attack. ○ Altered level of consciousness or acute confusion. ○ Arrhythmia. ○ Cyanosis. ○ Elevated respiratory rate. ○ Exhaustion. ○ Hypotension. ○ Oxygen saturation less than 92%. ○ Peak expiratory flow rate less than 50% of predicted. ○ Poor respiratory effort. ○ Silent chest. • Any features of a severe or life-threatening chronic obstructive pulmonary disease (COPD) exacerbation. ○ Acute confusion or impaired consciousness. ○ Already receiving long-term oxygen therapy. ○ Cyanosis. ○ Oxygen saturation less than 90% on pulse oximetry. ○ Poor or deteriorating general condition including significant comorbidity (such as cardiac disease or insulin-dependent diabetes). ○ Rapid onset of symptoms. ○ Severe breathlessness. ○ Worsening peripheral oedema.

Question 81

Managing acute breathlessness whilst waiting for emergency admission

Answer 81

Managing acute breathlessness whilst waiting for emergency admission 1) Sit the person up. 2) If the person has an oxygen saturation of 94% or less, give oxygen and continuously monitor their oxygen saturation levels while waiting for transfer to hospital. • Use a 24% Venturi mask at 2-3 L/min for people with suspected chronic obstructive pulmonary disease (COPD), morbid obesity, a chest wall deformity, or a neuromuscular disorder. ○ This is because they are at risk of hypercapnic respiratory failure. 3) Aim for an oxygen saturation of 88-92%. • If the oxygen saturation remains below 88% following oxygen administration with a 28% Venturi mask, change to either a nasal cannula at 2-6 L/min or a simple face mask at 5 L/min and aim for an oxygen saturation of 88-92% — the A&E department should be alerted in advance that the person is a high priority. 4) Identify and treat people with clinical features of: • Acute exacerbation of chronic obstructive pulmonary disease (COPD) • Acute severe asthma (peak expiratory flow rate less than 50% of predicted) • Anaphylaxis • Pulmonary oedema • Silent myocardial infarction • Supraventricular tachycardia (SVT) • Tension pneumothorax

Question 82

Managing breathlessness when emergency admission is not required

Answer 82

Managing breathlessness when emergency admission is not required 1) For people who do not require emergency admission or urgent referral, manage the underlying cause of breathlessness. • Anxiety-related breathlessness • Asthma • Bronchiectasis • Chronic obstructive pulmonary disease (COPD) • Community-acquired pneumonia • Interstitial lung disease • Lung/lobar collapse • Pleural effusion Managing breathlessness that remains of uncertain cause Reassess for risk factors and clinical features that may indicate a serious underlying condition that requires emergency admission. If emergency admission is not required, arrange routine referral.

Question 83

Common cardiac causes of breathlessness

Answer 83

Common cardiac causes of breathlessness include: • Silent myocardial infarction. • Cardiac arrhythmia. • Acute pulmonary oedema. • Chronic heart failure.

Question 84

Common causes of pulmonary breathlessness

Answer 84

Common pulmonary causes of breathlessness include: • Asthma. • Chronic obstructive pulmonary disease (COPD). • Pneumonia. • Pulmonary embolism. • Lung cancer. • Pleural effusion.

Question 85

Epidemiology of asthma

Answer 85

• Asthma affects more than 300 million people worldwide including 11.6% of children aged 6 to 7 years. • In the UK, over 8 million people, or approximately 12% of the population, have been diagnosed with asthma. However, some may have grown out of the condition, and 5.4 million people are receiving asthma treatment. • Approximately 160,000 people in the UK are diagnosed with asthma each year, however, incidence rates went down by around 10% between 2008 and 2012. • The incidence of asthma is higher in children than in adults. • In early childhood, asthma is more common in boys than in girls, but by adulthood, the sex ratio is reversed. • Asthma accounts for 2-3% of primary care consultations, 60,000 hospital admissions, and 200,000 bed days per year in the UK. • Occupational asthma may account for 9–15% of adult-onset asthma. It is reported to be the most common industrial lung disease in the developed world. • Every 10 seconds someone is having a potentially life threatening asthma attack. And on average 3 people die from an asthma attack a day in the UK. • The cost of asthma to the NHS is around 1 billion per year.

Question 86

Aetiology of asthma

Answer 86

People with asthma have swollen (inflamed) and "sensitive" airways that become narrow and clogged with sticky mucus in response to certain triggers. Genetics, pollution and modern hygiene standards have been suggested as causes, but there's not currently enough evidence to know if any of these do cause asthma. Symptoms: Infection Night time or early morning Exercise Animals Cold/damp Dust Strong emotions Occupational exposure Pollutants

Question 87

Pathophysiology of asthma and what type of inhaler is used.

Answer 87

• Airway Muscle: the thin layer of muscle within the wall of an airway can contract to make it tighter and narrower. In people with asthma, this muscle is often “twitchy” and contracts more easily and more strongly than in people who do not have asthma. (Reliever inhaler) • Inflammation / Swelling: the inside walls of the airways are often swollen and inflamed, leaving less space inside. (Preventer) • Mucus: mucus production is normally a protective response, but in severe asthma, it is excessive and can block the inside of the airways. (Preventer) • Fibrosis or Scarring: ongoing inflammation in the airways can lead to development of scar tissue and “tissue remodelling”. This results in thickened airway walls and increased smooth muscle.

Question 88

What is atopy?

Answer 88

When you have atopy, your immune system is more sensitive to common allergic triggers that you breathe in or eat. So you have a stronger-than-normal reaction to these allergens, such as dust, pollen, peanuts, or shellfish. If you have allergies or asthma, there’s a chance atopy is behind it. Atopy is a problem with your immune system that makes you more likely to develop allergic diseases. Your genes cause this problem.

Question 89

What conditions are related to atopy?

Answer 89

Atopy makes you more likely to have allergic conditions like these: • Asthma • Eczema • Allergic rhinitis (hay fever) • Allergies to shell fish, eggs and nuts

Question 90

Bronchial hyperresponsiveness

Answer 90

• Bronchial hyperresponsiveness is defined as an increase in sensitivity to a wide variety of airway narrowing stimuli, which can be both chemical and physical. • The hyper-activity of the bronchial smooth muscle leading to bronchoconstriction, increasing air flow resistance and decreased air flow. • Those with bronchial hyperresponsiveness experience excessive responses to even small doses of stimuli. Although different stimuli may provoke different responses among different individuals. • Providing evidence that bronchial hyperresponsiveness is heterogenous.

Question 91

Hypersensitivity

Answer 91

• Th2 cells can promote the Type 1 hypersensitivity response. • This is an immediate reaction which involves the Th2 cells activating downstream B cells to produce immunoglobulin E (Ig-E), which mediates the release of antibodies against the soluble antigen. • This results in mast cell degranulation and release of histamine and other inflammatory mediators, including proteinoids, platelet activating factor and leukotrienes, creating a cycle of chronic inflammation. • The process causes bronchoconstriction and epithelial damage, leading to remodelling of the airway and bronchospasm.

Question 92

Bronchospasm

Answer 92

• Bronchospasm is when the muscles that line the bronchi start to contract and spasm, which causes airway narrowing. • This reduces the amount of oxygen that enters the blood and the amount of carbon dioxide that leaves the blood. • This can make it harder to breath as the lungs are trying to compensate and can cause wheezing (a high-pitched whistling sound). • Bronchospasm can also cause frequent coughing without wheezing and feeling short of breath.

Question 93

Wheezing

Answer 93

In asthma, because of bronchoconstriction the airflow through a narrowed airway becomes turbulent, causing vibration of the airway walls; this vibration produces the sound of wheezing.

Question 94

What is the difference between an agonist and antagonist drug?

Answer 94

An agonist is a drug that binds to the receptor producing a similar response to the intended chemical and receptor. Whereas an antagonist is a drug that binds to the receptor either on the primary site or on another site, which all together stops the receptor from producing a response.

Question 95

Example of an agonist drug.

Answer 95

For instance, let’s take opioid receptors in the brain. Endorphins are the natural agonists for opioid receptors. They bind to opioid receptors and produce the effect of pain relief. Therefore, endorphins are natural pain relievers. The pain medication morphine (and the illegal drug heroin) are artificial agonists of opioid receptors. They produce pain relief or a “high” by mimicking the action of the natural agonist. Another example is serotonin. Serotonin, a natural neurotransmitter or chemical messenger in the brain, is a natural agonist for the 5-HT2A receptors. The synthetic hallucinogenic drug LSD is an artificial agonist of the 5-HT2A receptors. Complete agonists (fast acting): Examples of direct agonists include morphine and nicotine. Methadone, which is used to treat opioid addiction, is a full opioid agonist. Partial/indirect agonist (slow acting) : An example is Buprenorphine, a medication used to treat drug addiction to opioids. Inverse agonists: For example, an antihistamine medication, an H1 receptor antagonist, has some inverse agonist activity.

Question 96

Example of an antagonist drug

Answer 96

An antagonist binds to a cell and makes it unable for the agonists to bind to the cell receptor appropriately. As a result, the agonists are rendered ineffective. Heroin is an agonist for the opioid receptor. If someone has taken a potentially fatal heroin overdose, naloxone (an opioid receptor antagonist) can reverse the effects. Naloxone (brand name Narcan) works by blocking or occupying all the opioid receptors, preventing morphine or heroin from binding and activating them. An overdose victim who is unconscious and near death can become fully conscious quite dramatically within seconds of receiving naloxone. Competitive antagonist Non competitive antagonist Irreversible antagonist

Question 97

Name some obstructive pulmonary diseases

Answer 97

Obstructive - • COPD • Chronic bronchitis and emphysema • Asthma • Bronchiectasis • Cystic fibrosis

Question 98

Name some restrictive pulmonary diseases

Answer 98

Restrictive • Interstitial lung disease i.e. pulmonary fibrosis • Chest wall pathology - Kyphosis or scoliosis • Obesity • Neuromuscular disease i.e. ALS, Muscular dystrophy

Question 99

What can PFT’s give an insight to?

Answer 99

PFTs can give insight into • Airways large and small • Parenchyma - (potions of lungs involved in gas exchange) • Pulmonary vasculature • Bellows/pump mechanism neural control

Question 100

Name some types of PFT’s

Answer 100

Types of PFTs • Spirometry - including flow volume loop • Lung volumes • Diffusing capacity of CO (DlCO) • Peak Flow (PEFR)

Question 101

What happens during a spirometry test?

Answer 101

What happens during test • Patient is seated and a clip is placed on the nose to prevent air escaping from that route. • Patient will inhale fully so lungs are filled with air to the max possible • Patient closes mouth around the mouthpiece with no gaps or room for escape. • Patient will exhale as quickly and as forcefully as they possibly can. • Test will be repeated at least 3 times • Test may be repeated 15 minutes after a dose of bronchodilator to see if relief is given by this

Question 102

What values are produced from a spirometry test?

Answer 102

Values produced from spirometry (these will be compared to predicted normal values for a person of the same sex, age and height. • A patient's forced expiratory volume (FEV1) - (the volume exhaled in the first second after deep inspiration and forced expiration) • A patient's forced vital capacity (FVC )- (the total volume of air a patient can exhale forcibly, in one breath) • A Patient's FEV1:FVC ratio • PEFR • Maximum Voluntary Ventilation (MVV) • Result will be given in the form of curves on a graph

Question 103

How is a Diffusing capacity of CO (DLCO) test carried out?

Answer 103

Diffusing capacity of CO (DLCO) - a test for gas exchange capacity. • Give the patient a measured amount of CO via face mask • Ask them to take a maximal inhale and hold for 10s • Patient then exhales maximally • Measure the amount of CO in the exhaled air. Carbon monoxide has a strong affinity for haemoglobin so a normal patient with a good level of gas exchange ability (i.e. healthy parenchyma) should be able to absorb all the inhaled CO to the bloodstream. If a patient does not do this, then their sites of gas exchange are impaired as CO cannot diffuse into the blood via sites of gas exchange.

Question 104

Red flags of lung cancer

Answer 104

Signs and Symptoms General • Shortness of breath • Cough Red Flag • Haemoptysis (coughing up blood) • Finger clubbing • Recurrent pneumonia • Weight loss • Lymphadenopathy – often supraclavicular nodes are the first to be found on examination

Question 105

Referral and recognition pathway for lung cancer

Answer 105

• Refer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for lung cancer if they: ○ Have chest X-ray findings that suggest lung cancer, or ○ Are aged 40 years and over with unexplained haemoptysis. • Offer an urgent chest X-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 years and over if they have two or more of the following unexplained symptoms, or if they have ever smoked and have one or more of the following unexplained symptoms: § Cough. § Fatigue. § Shortness of breath. § Chest pain. § Weight loss. § Appetite loss. • Consider an urgent chest X-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 years and over with any of the following: Persistent or recurrent chest infection. Finger clubbing. Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy. Chest signs consistent with lung cancer. Thrombocytosis. Use the same pathway for suspected mesotheliomas

Question 106

Aims and management of COPD

Answer 106

The goal of COPD management is to improve a patient's functional status and quality of life by preserving optimal lung function, improving symptoms, and preventing the recurrence of exacerbations. Long Term Management 1) It is essential for people to stop smoking. Continuing to smoke will progressively worsen their lung function and prognosis. They can be referred to smoking cessation services for support to stop. 2) Patients should have the pneumococcal and annual influenza vaccine. 3) If indicated, patients can be offered pulmonary rehabilitation

Question 107

Step 1 management for COPD patients

Answer 107

STEP 1: SABA or SAMA Short acting bronchodilators: beta-2 agonists (salbutamol or terbutaline) or short acting antimuscarinics (ipratropium bromide).

Question 108

Step 2 of COPD management

Answer 108

STEP 2: If they do not have asthmatic or steroid responsive features they should have a combined long acting beta agonist (LABA) plus a long acting muscarinic antagonist (LAMA). • “Anoro Ellipta”, “Ultibro Breezhaler” and “DuaKlir Genuair” are examples of combination inhalers. If they have asthmatic or steroid responsive features they should have a combined long acting beta agonist (LABA) plus an inhaled corticosteroid (ICS). • “Fostair“, “Symbicort” and “Seretide” are examples of combination inhalers. If these don’t work then they can step up to a combination of a LABA, LAMA and ICS. • “Trimbo” and “Trelegy Ellipta” are examples of LABA, LAMA and ICS combination inhalers.

Question 109

Management for more severe cases of COPD

Answer 109

• Nebulisers (salbutamol and/or ipratropium) • Oral theophylline • Oral mucolytic therapy to break down sputum (e.g. carbocisteine) • Long term prophylactic antibiotics (e.g. azithromycin) • Long term oxygen therapy at home • Long term oxygen therapy is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale). It can’t be used if they smoke as oxygen plus cigarettes is a significant fire hazard.

Question 110

At home typical treatment for a COPD exacerbation

Answer 110

Typical treatment if they are well enough to remain at home: • Prednisolone 30mg once daily for 7-14 days (steroid) • Regular inhalers or home nebulisers • Antibiotics if there is evidence of infection

Question 111

Treatment for exacerbation of COPD which requires hospitalisation

Answer 111

In hospital: • Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h) • Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone) • Antibiotics if evidence of infection • Physiotherapy can help clear sputum

Question 112

Options for COPD exacerbation in severe cases which aren’t responding to first line treatment:

Answer 112

• IV aminophylline • Non-invasive ventilation (NIV) • Intubation and ventilation with admission to intensive care • Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate

Question 113

SABA examples, indications and limitations

Answer 113

Salbutamol or Terbutaline SABA Bronchodilators Short acting bronchodilator Use for conditions associated with reversible airways obstruction during breathlessness and exercise limitations Find tremor Tachycardia (arrhythmias) Headache Palpitations Hypokalaemia

Question 114

SAMA examples, indications and limitations

Answer 114

Ipratropium bromide SAMA Bronchodilators Short acting antimuscarinics Used for reversible airways obstruction, particularly in chronic obstructive pulmonary disease Arrhythmias Constipation Cough Dizziness Dry mouth Headache Nausea Gastrointestinal motility disorder

Question 115

LABA examples, indications and limitations

Answer 115

Salmeterol or Formoterol LABA Bronchodilators Long acting beta agonist Used for reversible airways obstruction in patients requiring long-term regular bronchodilator therapy Muscle cramps Dizziness Nausea Tremor Tachycardia (arrhythmias) Headache Palpitations Hypokalaemia

Question 116

LAMA examples, limitations and indications

Answer 116

Tiotropium LAMA Bronchodilators Long acting muscarinic antagonist Maintenance treatment of chronic obstructive pulmonary disease Dry mouth Difficulties in passing urine in men Arrhythmias Constipation Cough Dizziness Headache Nausea

Question 117

ICS examples, indications and limitations

Answer 117

Prednisolone Orally Hydrocortisone IV Beclomethasone ICS Corticosteroids Inhaled corticosteroids Used in exacerbation of chronic obstructive pulmonary disease (if increased breathlessness interferes with daily activities) Oral candidiasis Dysphonia (hoarseness) Pneumonia

Question 118

How is a CT scan used in the diagnosis of COPD?

Answer 118

• Chest computed tomography (CT) scan: ○ Help support diagnosis of COPD ○ Can identify emphysema better and at an earlier stage than CXR § CT → can measure extent of emphysema within lungs ○ Also identify other changes of COPD → enlarged arteries in the lungs

Question 119

What is seen on a CT showing chronic bronchitis?

Answer 119

What is seen in a CT? • Chronic bronchitis ○ Bronchial wall thickening ○ Enlarged vessels ○ Repeated inflammation = scarring with bronchovascular irregularity and fibrosis

Question 120

What is shown on a CT diagnosing emphysema?

Answer 120

• Emphysema ○ Diagnosed by alveolar septal destruction and airspace enlargement ○ Centrilobular → predominantly in upper lobes ○ Panacinar → predominantly in lower lobes ○ Paraseptal → occurs near lung fissures and pleura ○ Formation of giant bullae = compression of mediastinal structures ○ Rupture of pleural blebs may produce spontaneous pneumothorax/pneumomediastinum

Question 121

Spirometry test for a COPD patient

Answer 121

Spirometry To perform spirometry, patient takes the biggest breath possible and blows it out as fast as they can During this procedure, the total volume of air that the patient can exhale in one breath is measured → FVC The amount of air that the patient can exhale in the first second is also measured → FEV1 • COPD patients often have narrowing or inflammation of the airways. This hinders how fast air can leave the lungs • This leads to a decrease in FEV1 • If the FEV1 is decreased disproportionately to the FVC, a diagnosis is made for COPD • To determine if the decrease is disproportionate, the FEV1/FVC ratio is calculate • An FEV1/FVC ratio <0.07 after bronchodilator is typically diagnostic of COPD

Question 122

What is cor pulmonale?

Answer 122

Cor pulmonale is right sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries. This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.

Question 123

Respiratory causes of cor pulmonale

Answer 123

Respiratory Causes • COPD is the most common cause • Pulmonary Embolism • Interstitial Lung Disease • Cystic Fibrosis Primary Pulmonary Hypertension

Question 124

Signs and symptoms of cor pulmonale

Answer 124

Presentation Often patients with early cor pulmonale are asymptomatic. The main presenting complaint is shortness of breath. Unfortunately shortness of breath is also caused by the the chronic lung diseases that lead to cor pulmonale. Patients may also present with peripheral oedema, increased breathlessness of exertion, syncope (dizziness and fainting) or chest pain. Examine the patient for the signs of cor pulmonale: • Hypoxia • Cyanosis • Raised JVP (due to a back-log of blood in the jugular veins) • Peripheral oedema • Third heart sound • Murmurs (e.g. pan-systolic in tricuspid regurgitation) • Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

Question 125

Management of cor pulmonale

Answer 125

Management Management involves treating the symptoms and the underlying cause. Long term oxygen therapy is often used to help the hypoxia induced vasoconstriction. The prognosis is poor unless there is a reversible underlying cause.

Question 126

What is interstitial lung disease?

Answer 126

ILD is an umbrella term used to describe over 200 conditions that cause inflammation and scarring of the lungs. A more technically correct term would be "Diffuse parenchymal lung disease" As disease often progresses to affect more than just the interstitial. The main pathophysiological process involves chronic inflammation of whatever cause, leading to fibrosis and further inflammation that spreads beyond the interstitial, and towards the parenchyma. Most ILDs share in common, the structural remodelling of the distal airspaces leading to impaired gas exchange. It was once thought that chronic inflammation itself was the cause of the structural changes seen in ILD, but now it is thought that tissue injury (either caused by inflammation or some other factor), and subsequent aberrant healing cause collagenous fibrosis to build up in the lung tissues. Many ILDS follow on from some kind of injury to the distal air spaces, like infection, radiation, or environmental exposure.

Question 127

Pathophysiology of interstitial lung disease

Answer 127

Pathophysiology of Interstitial lung disease • Acute inflammatory responses as a result of injury can disrupt epithelial and endothelial integrity. • This leads to inflammation, and as a result, recruitment of leukocytes and an increase in angiogenesis. • Resolution of inflammation via apoptotic and phagocytic pathways will usually restore tissue integrity, leaving minimal damage however problems occur when there is a persistent irritant (exogenous) or another endogenous cause of chronic inflammation. Exogenous irritants can include allergens, toxic chemicals, radiation or other persistent irritants. • Dysregulated healing response can eventually evolve into an interstitial lung disease as chronic inflammation and fibroblast overactivity leads to scarring and fibrosis that reaches the parenchyma. • Fibrotic tissue is unable to expand and becomes stiff. The alveoli become poorly ventilated and the gas exchange distance becomes wider and thus inefficient, leading to poor gas exchange and thus the clinical issues presented in ILD. `

Question 128

Causes of inflammation or tissue damage in interstitial lung disease

Answer 128

Causes of inflammation or tissue damage • Autoimmune disease i.e. lupus, rheumatoid arthritis, sarcoidosis, and scleroderma. • Lung inflammation due to foreign substance inhalation (dust, mould, fungal spores, allergens) • Medicines ( nitrofurantoin, bleomycin, amiodarone, methotrexate, gold infliximab. (x ray belo shows amiodarone induced fibrosis) • Radiation • Occupational exposure to asbestos, coal dust, cotton dust, silica dust. (these are occupational lung diseases). • Infection and partial recovery from diseases like TB, or COVID.

Question 129

What are the classifications of interstitial lung disease?

Answer 129

Known cause eg: Drug Induced Smoking Related Radiation Induced Chronic Aspiration (i.e. secondary to GORD) Pneumoconiosis (occupational exposure to inhaled dust or metal) Connective tissue disease i.e. (SLE Hypersensitivity Pneumonitis (asthma and atopy) Idiopathic eg: Idiopathic interstitial pneumonia • Idiopathic Pulmonary Fibrosis • Acute interstitial Pneumonia • Cryptogenic Organising Pneumonia Sarcoidosis Other

Question 130

What is pneumoconiosis?

Answer 130

Ocupationional lung disease - Pneumoconiosis - a group of chronic lung diseases caused by exposure to a mineral dust or a metal, the most common ones are asbestosis, silicosis, coal workers pneumoconiosis (black lung) and beryliosos (berylium disease)

Question 131

How does asbestos cause ILD?

Answer 131

Asbestosis • The main pathogenic cause of asbestosis is interstitial fibrosis caused by the inflammation that asbestos fibbers trigger. Following an inhalation of asbestos, fibres are distributed in the lungs, and macrophages are recruited to clear them, though asbestos is notoriously difficult to digest. The persistence of these fibres initiates immune responses that recruit fibroblasts that deposit collagen in the interstitial and surrounding tissues. • Macrophages also secrete reactive oxygen species in response to asbestos fibres which also contributes to tissue injury. Macrophages also digest the extracellular environment via secretion of plasminogen activator factor or PAF, which contributes to further damage. • The reactive oxygen species as well as asbestos fibres moving through the epithelium injure the type 1 alveolar cells. These injured cells will also produce fibroblast growth factors. This recruits and fibroblasts, lymphocytes, and that then proliferate heavily, right at the sites of gas exchange. • Asbestosis is a progressive disease, fibrosis increases over time, as the asbestos cannot be cleared naturally and contributes to a sustained immune response. • Severity of asbestosis is proportional to the dose received.

Question 132

Normal pH range

Answer 132

7.35-7.45

Question 133

Normal PaO2 range

Answer 133

10.7-13.3kPa

Question 134

Normal PaCO2 range

Answer 134

4.7-6.0 kPa

Question 135

Normal HCO3 range

Answer 135

22-28mmol/l

Question 136

Normal BE (base excess) range

Answer 136

-2 to +2

Question 137

Normal lactate range

Answer 137

0.5 - 1 mmol/L

Question 138

Type 1 vs type 2 respiratory failure

Answer 138

T1RF = hypoxaemia (PaO2 <8kPa) with normocapnia (PaCO2 <6.0kPa) Due to VQ mismatch - volume of air flowing in and out of lungs is not matched with flow of blood to the lung tissue Eg PE, bronchoconstriction, PE T2RF= hypoxaemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa) Due to alveolar hypoventillation- unable to adequate oxygenate and eliminate CO2 Eg COPD, pneumonia, rib fracture, obesity, MND, opiates

Question 139

Describe respiratory acidosis and give causes for this

Answer 139

Decreased pH Increased CO2 Normal HCO3- • Respiratory acidosis: inadequate alveolar ventilation leading to CO2 retention ○ Causes: respiratory depression e.g. opiates, asthma, COPD, Guillain-Barre, latrogenic

Question 140

Describe respiratory alkalosis and give causes of this

Answer 140

Increased pH Due to decreased CO2 HCO3- is normal · Respiratory alkalosis: excessive alveolar ventilation, more CO2 than normal exhaled ○ Causes: panic attack, pain, hypoxia, PE, pneumothorax, latrogenic

Question 141

Does respiratory acidosis with metabolic compensation increase or decrease bicarbonate?

Answer 141

Increase

Question 142

Does respiratory alkalosis with metabolic compensation increase or decrease bicarbonate?

Answer 142

Decrease

Question 143

Metabolic acidosis

Answer 143

Decrease pH Decrease HCO3- Normal CO2 • Metabolic acidosis: increased acid production/acid ingestion OR decreased acid excretion/increased rate of GI and renal HCO3- loss *Anion gap: artificial measure to determine presence of unmeasured anions e.g. albumin *Formula: Na+ - (Cl- + HCO3-), normal gap: 4-12mmol/L ○ Causes of high anion gap (due to increased production/ingestion or reduced excretion of H+ by the kidneys: diabetic ketoacidosis. Lactic acidosis, aspirin overdose, renal failure ○ Causes of normal anion gap (due to loss of HCO3-, which is replaced by Cl in plasma: GI loss of HCO3-, renal tubular disease, Addison’s disease

Question 144

Metabolic alkalosis

Answer 144

Increase HCO3- Increase pH Normal CO2 · Metabolic alkalosis: decreased H+ conc. leading to increased bicarbonate ○ Causes: GI loss of H+ ions e.g. vomiting, diarrhoea, renal loss of H+ ions e.g. loop and thiazide diuretics, heart failure, cirrhosis, latrogenic

Question 145

Metabolic acidosis with respiratory compensation

Answer 145

Decrease HCO3- Decrease pH Decrease CO2

Question 146

Metabolic alkalosis with respiratory compensation

Answer 146

Increase HCO3- Increase pH Increase CO2

Question 147

What is ABG results interpreted?

Answer 147

Interpreting results Step 1: pH - normal, acidaemia, alkalaemia? Step 2: Whichever of respiratory (CO2) or metabolic (BC) that is contributing to effect will be the cause, e.g. acidaemia from metabolic acidosis Step 3: Any compensation? Non-causative component acting in the opposite to normalise abnormality? Yes = incomplete compensation, e.g. acidaemia with metabolic acidosis with partial respiratory compensation

Question 148

Interpret this ABG pH 7.2 PCO2 4.1 kPa PO2 9.0 kPa BC 13

Answer 148

Metabolic acidosis with resp compensation

Question 149

Patient with ABG presenting: pH 7.51 PCO2 2.0kPa Bicarbonate 25mmol/l

Answer 149

Respiratory alkalosis

Question 150

A frail patient with cellulitis on the ward has an ABG pH 7.20 PCO2 4.1 kPa PO2 9.0 kPa BC 13 Lactate 6.5 What does the blood gas show? Is there compensation? Why do you think this is happening?

Answer 150

Metabolic acidosis No compensation due to frailty

Question 151

An ABG of an anxious patient pH 7.52 PCO2 1.8 kPa PO2 13.0 kPa BC 24 What does the blood gas show? Is there compensation? Why do you think this is happening?

Answer 151

Respiratory alkalosis No compensation Hyperventilation

Question 152

A patient with advanced COPD presents to ED with a cough pH 7.36 PCo2 9.6 kPa PO2 9.0 kPa BC 38

Answer 152

Metabolic alkalosis with respiratory compensation

Question 153

A patient with COPD presents an Acute Kidney Injury pH 7.12 Pco2 9.8 kPa Po2 9.3 kPa BC 25 What does the blood gas show? What might be the cause?

Answer 153

Respiratory acidosis Can’t compensate sue to acute kidney injury

Question 154

The night F1 put a COPD patient on 15litres non-rebreather as they had SaO2 of 87%, this is their ABG 10 hours later FiO2 80-100% SaO2 95% pH 7.23 PaO2 21 kPa PaCO2 12.6 BC 27 What is going on? What should you do?

Answer 154

O2 was too high - stops the hypoxia drive and can cause T2 resp failure COPD patient has chronic hypercapnia therefore should be aiming for 88-92% stats

Question 155

What changes does smoking cause to the respiratory system?

Answer 155

The main components of these changes are: • narrowing and remodelling of the airways • increased number of goblet cells • enlargement of mucus-secreting glands of the central airways, • alveolar loss • vascular bed changes leading to pulmonary hypertension.

Question 156

Role of the cilia and the affect smoking has on this

Answer 156

Cilia The bronchus in the lungs are lined with hair like projections called cilia that move microbes and debris out of the airways. Scattered throughout the cilia are goblet cells that secrete mucus which helps protect the lining of the bronchus and trap microorganisms. • Toxicants in tobacco smoke paralyse the cilia and eventually destroy them, removing an important protection in the respiratory system. • Ciliary dysfunction and increased goblet cell size and number causes the airways to become inflamed and leads to excessive mucus secretion. • Excessive mucus secretion impairs ventilation and also makes the lungs more susceptible to infection.

Question 157

Effect of smoking on the alveoli

Answer 157

Alveoli • Smoking also causes the walls of the alveoli to break down and join together, forming larger air spaces than normal. • Elastin breakdown and subsequent loss of alveolar integrity causes emphysema. The lungs ability to provide the blood with sufficient oxygen to supply the body is thus impaired.

Question 158

Effect of smoking on the airways

Answer 158

Airways • Smoking induces airway remodelling which thickens the epithelium, lamina propia, and smooth muscle, causing the airways to become more narrow. • In addition, reduced elastic recoil, fibrotic changes in lung parenchyma, and also luminal obstruction of airways by secretions, all contribute to increased airway resistance, reducing airflow and causing breathlessness.

Question 159

Describe COPD

Answer 159

Chronic Obstructive Pulmonary Disease (COPD) is a chronic respiratory condition characterised by airflow obstruction caused by damage to lung tissue. It is most commonly the result of a combination chronic bronchitis and emphysema as a result of smoking. · Unlike asthma, in COPD there is little or no reversibility of the obstruction. · The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of lung tissues to certain particles. · It does not change markedly over several months = it is slowly progressive. · In COPD the FEV1:FVC ratio is <70%. · COPD can also be diagnosed in patients with FEV1:FVC ratio is >70% on the basis of clinical signs and symptoms – such as shortness of breath, or cough. · Around 30% of cases of COPD will have normal spirometry at diagnosis.

Question 160

Pathophysiology of COPD

Answer 160

· Hypersecretion of mucus due to marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells= ↓ lumen size and ↑ gas diffusion distance. · Abnormal dilation of air spaces with destruction of alveolar walls · Inflammation and scarring = ↓ size of lumen of airways and ↓ lung elasticity · Initially small airways are affected and this initial inflammation is reversible, whereas in later stages larger airways become affected and the process is no longer reversible · Epithelial layer becomes ulcerated and squamous epithelium may be replaced by columnar cells= ↑ gas diffusion distance

Question 161

The three pain pathological affects in COPD

Answer 161

1. Loss of elasticity of the alveoli 2. Inflammation and scarring – reducing the size of the lumen, as well as reducing elasticity 3. Mucus hypersecretion – reducing the size of the lumen and increasing the distance gasses have to diffuse. · Emphysematous bullae will often form, which are essentially just large closed off air spaces with trapped air inside them.

Question 162

Chronic bronchitis

Answer 162

· An enlargement in mucus secreting glands (hypertrophy) · An increased number of goblet cells (hyperplasia) · The main cell involved in this reaction are neutrophils. · After events of inflammation, there will be scarring and fibrosis of the tissue. · This thickens the walls of the airway= reduces the size of the lumen thus decreasing FEV1 + increasing the distance that gasses must travel to diffuse properly. · The inflammatory process will also cause bronchoconstriction – thus in some cases of COPD where bronchoconstriction is a factor, bronchodilators, such as salbutamol may be of some use for symptom relief. · Initially, the small airways are affected by chronic bronchitis, and this initial inflammation is reversible if smoking is stopped soon enough. · Later, the larger airways become affected, and the process is no longer reversible. · In the later stages there will be fibrosis, and squamous cell metaplasia, further narrowing the bronchial lumen.

Question 163

Aetiology of COPD

Answer 163

Aetiology · Smoking - 10 – 20% of all smokers will develop COPD - Up to 50% of those with a >20 pack year smoking history will get COPD · Coal mining · Exposure to air pollution – particularly from indoor fires and cooking in the developing world · Genetic, i.e. α1 –antitrypsin deficiency causes emphysema · Low socioeconomic status and low birth weight are predisposing factors - Low birth weight is associated with reduce maximum lung capacity in adulthood · Asthma and COPD may also co-exist

Question 164

What is used to measure oxygen levels

Answer 164

Pulse oximeter Arterial blood gas

Question 165

Indications to when O2 needs prescribing

Answer 165

Indication • Hypoxaemia – oxygen does not treat the underlying cause of hypoxaemia, you must take a systematic approach to identify the cause! • Exacerbation of longstanding lung disease e.g. COPD, cystic fibrosis, fibrosis • Severe kyphosis • Respiratory muscle weakness • Overdoes of drugs causing respiratory depression (opiates, benzodiazepines)

Question 166

What is target oxygen saturation?

Answer 166

Monitoring Requirements Aim for oxygen saturations of 94-98% in those not at risk of type 2 respiratory failure/hypercapnic respiratory failure Aim for oxygen saturation of 88-92% in COPD patients/patient known to be at risk of hypercapnic respiratory failure

Question 167

Type: Nasal cannulae When is it used? %O2 How does it work/ What does it look like? Advantages? Issues/disadvantages

Answer 167

Nasal cannulae Mild hypoxaemia when the patient is not critically unwell Delivers 24-30% O2 The nasal cannulae tubing is placed around the patients face with the prongs at the nostrils. The tubing is secured behind the patients head/around their ears • Comfortable • Doesn't obstruct eating/drinking • Easy to wear • Do not use if patient breathes through their mouth • High flows (>4L/min) dry and irritate nasal passages • FiO2 not closely controlled

Question 168

Type: Simple face mask/ Hudson mask When is it used? %O2 How does it work/ What does it look like? Issues/disadvantages

Answer 168

Simple face mask/Hudson mask Mild to moderate hypoxia Delivers 30-40% O2 (flow rate 5-10L) The mask is positioned over the patients nose and mouth with an elastic strap behind their head • FiO2 not closely controlled • Risk of aspiration if patient vomits whilst wearing the mask

Question 169

Type: 15 Litre Non rebreathable mask When is it used? %O2 How does it work/ What does it look like? Advantages? Issues/disadvantages

Answer 169

Non-rebreather/reservoir mask Moderate to severe hypoxia Delivers about 85% O2 when used with a 15L/min flow rate A high FiO2 concentration is achieved by inhaling from both the reservoir bag and the direct oxygen source The mask is positioned over the patients nose and mouth with an elastic strap behind their head • The reservoir bag needs to be filled before the mask is fitted to the patient • Don't have a true seal so breathing in some room air is unavoidable and performance of the device can vary depending on the seal Ensure the reservoir bag fills by temporarily obstructing the valve before positioning the non-rebreather mask on the patient.

Question 170

Type: Venturi mask When is it used? %O2 How does it work/ What does it look like? Advantages? Issues/disadvantages

Answer 170

Venturi mask COPD patients Delivers a constant FiO2 – a fixed performance device Flow rate and percentage oxygen delivered are denoted by colours on the mask The mask is positioned over the patients nose and mouth with an elastic strap behind their head Blue: 2-4L/min, 24% FiO2 White: 4-6L/min, 28% FiO2 Orange: 31% FiO2 Yellow: 8-10L/min, 35% FiO2 Red: 10-12L/min, 40% FiO2 Green: 12-15L/min, 60% FiO2 • Controlled O2 therapy • If the flow rate of the oxygen is lower than the recommended amount for a specific Venturi mask, the mask won’t deliver the stated FiO2. • If you increase the oxygen flow rate beyond the rate recommended for the mask, it will not continue to increase FiO2

Question 171

Type: Humidified oxygen When is it used? %O2 How does it work/ What does it look like? Advantages? Issues/disadvantages

Answer 171

Humidified oxygen Oxygen is passed through a humidifying device producing a sterile vapour. Most effective when gas reaching the alveoli is body temperature with a relative humidity of 100% Reduced the drying effect of standard oxygen • Water can pool in the oxygen tubing and obstruct the flow of oxygen is not drained regularly

Question 172

Type: High flow O2 When is it used? %O2 How does it work/ What does it look like? Advantages? Issues/disadvantages

Answer 172

• Wide-bore nasal cannula • O2 driven through a humidified circuit • Delivers up to 100% O2 therapy • Improves work of breathing

Question 173

CPAP/ BIPAP Who is it used in and how is it used?

Answer 173

CPAP: • Neonates • Mild obstructive sleep apnoea (OSA) BIPAP: • Hypercapnic respiratory failure • Severe OSA • Tight fitting mask that supplies higher than atmospheric pressure to splint open airways and prevent them from collapsing • Can be used with/without oxygen CPAP: pressure constant BIPAP: pressure drops during expiration phase to encourage more movement of air in and out the lungs

Question 174

What is a fever?

Answer 174

What is fever? NICE defines a fever as 'an elevation of body temperature above the normal daily variation’. It recognizes that this is often hard to define, as normal temperature varies depending on the person, the body site where temperature is measured, and the time of day (body temperature is normally lowest in the early morning and highest in the early evening). · Usually, above 38°C or higher. A fever is your body's natural response to many common illnesses such as: · Flu · Tonsilitis · Kidney or UTIs Fever helps your body fight infections by stimulating your immune system (your body’s natural defence). By increasing your body’s temperature, a fever makes it harder for the bacteria and viruses that cause infections to survive.

Question 175

How is body temperature regulated?

Answer 175

Thermoregulation Temperature Regulation · The skin is the body’s main heat-dissipating surface. The amount of blood flow to the skin determines the degree of heat loss and, therefore, the core body temperature. · The sympathetic nervous system influences the blood flow through AVAs. · At rest, the sympathetic nervous system dominates and acts to constrict the AVAs. · The thermoregulatory centre in the hypothalamus detects changes in core temperature. · The thermoregulatory centre regulates the body’s temperature by altering the level of sympathetic outflow to the cutaneous vessels. In high core temperatures Sympathetic innervation is decreased, reducing the vasomotor tone in the AVAs. More blood flows through the AVAs and reaches the superficial venous plexus (near the skin’s surface). This increases heat loss and reduces core temperature. In low core temperatures Sympathetic innervation is increased, increasing the vasomotor tone in the AVAs. Less blood flows to the apical skin (of nose, lips, ears, hands and feet). This reduces heat loss and increases the core temperature.

Question 176

Paracetamol and it’s mechanisms in reducing fever

Answer 176

Drug Paracetamol Common indications · Paracetamol is a first-line analgesic for most forms of acute and chronic pain. · The World Health Organization (WHO) pain ladder (originally designed to guide the treatment of cancer pain) uses regular paracetamol as the basis of treatment, with weak/moderate then strong opioids added incrementally until pain is controlled. · Paracetamol is an antipyretic that can reduce fever and its associated symptoms (e.g. shivering). · Its safety makes it a popular choice as a first-line analgesic Mechanism of action • The mechanisms of action of paracetamol are poorly understood. • Paracetamol is a weak inhibitor of cyclo-oxygenase (COX), the enzyme involved in prostaglandin metabolism. • In the brain, COX inhibition appears to increase the pain threshold and reduce prostaglandin E2 (PGE2) concentrations in the thermoregulatory region of the hypothalamus, controlling fever. Important adverse effects · At treatment doses, paracetamol is very safe with few side effects. · Lack of COX-1 inhibition means that it does not cause peptic ulceration or renal impairment or increase the risk of cardiovascular events (unlike NSAIDs). · In overdose, paracetamol causes liver failure. Warnings · Paracetamol dose should be reduced in people at increased risk of liver toxicity, either because of increased NAPQI production (e.g. in chronic excessive alcohol use, inducing metabolising enzymes) or reduced glutathione stores (e.g. in malnutrition, low body weight (<50 kg) and severe hepatic impairment). · This is particularly important where paracetamol is given by IV infusion. Interactions There are few clinically significant interactions between paracetamol and other drugs.

Question 177

Ibroprofen and it’s mechanisms in reducing fever

Answer 177

Drug Ibuprofen, non-steroidal anti-inflammatory drugs Common indications · As needed’ treatment of mild-to-moderate pain (e.g. dysmenorrhoea, dental pain) as an alternative to or in addition to paracetamol. · Analgesia from a single dose of an NSAID is similar to that from paracetamol. · Paracetamol is therefore preferred, particularly in those at risk of adverse effects. · Regular treatment for pain related to inflammation, particularly of the musculoskeletal system, e.g. in rheumatoid arthritis, severe osteoarthritis and acute gout. Mechanism of action · NSAIDs inhibit prostaglandin synthesis from arachidonic acid by inhibiting cyclo-oxygenase (COX) – chemical pathway for pain · It reduces the ability of your body to make prostaglandins which are chemicals that promote pain, inflammation and fever. · With fewer prostaglandins in your body, fever eases, and pain and inflammation is reduced. Important adverse effects · Gastrointestinal (GI) toxicity, renal impairment and increased risk of cardiovascular events (e.g. myocardial infarction and stroke). · The likelihood of adverse effects differs between NSAIDs- ibuprofen is associated with the lowest risk of GI effects. · Low-dose ibuprofen is associated with the lowest risk of cardiovascular events. · High BP · Headaches and dizziness · Hypersensitivity reactions- bronchospasm and angioedema, and fluid retention, which can worsen hypertension and heart failure. Warnings Avoid NSAIDs in: ✗severe renal impairment, ✗heart failure, ✗liver failure and known ✗NSAID hypersensitivity. If NSAID use is unavoidable in patients at high risk of adverse effects (e.g. prior peptic ulcer disease or GI bleeding, CVD, renal impairment), use the safest NSAID at the lowest effective dose for the shortest possible time. Interactions · Many drugs increase the risk of NSAID-related adverse effects, including: · Peptic ulceration – low-dose aspirin, corticosteroids; · GI bleeding –anticoagulants (e.g. warfarin, direct-oral anticoagulants) · SSRIs- venlafaxine · Renal impairment – ACE inhibitors, diuretics. · NSAIDs also reduce the therapeutic effects of other antihypertensives. Administration Oral NSAIDs should be taken with food to minimise GI upset.

Question 178

Describe and list some Polymorphonuclear leukocytes white blood cells

Answer 178

• Types of white blood cell that include: ○ Neutrophils ○ Eosinophils ○ Basophils ○ Mast cells • They are a subtype of leukocytes, which protect body against infectious organisms • PMNs are also called granulocytes because they contain & release granules ○ Contents of granules vary by cell type ○ In case of neutrophils → granules contain proteins & substances that help fight infection ○ For mat cells & basophils → histamine is released when the cell degranulates. This breakdown triggers a defensive inflammatory response.

Question 179

Origin of polymorphonuclear leukocytes white blood cells (PMN’s’

Answer 179

Haematpoietic stem cells in the bone marrow Differentiate into myeloid stem cells Differentiate into myeloblast Differentiate into granulocytes: Eosinophil Neutrophil Basophil Origin of PMNs • Develop form haematopoietic stem cells in bone marrow ○ Just like other WBCs, RBCs & platelets • Haemapoietic stem cell precursors are those cells committed to forming a new kind of cell • From precursors, the blood-forming cells follow two pathways: ○ Lymphoid cell line → cells differentiate to become lymphocytes ○ Myeloid cell line → cells can become different types of PMNs and other blood cells • PMNs (except mast cells) are found primarily in blood ○ However, they often follow the immune systems chemical signals and move to different sites in the body where they are needed

Question 180

Innate vs acquired immune response

Answer 180

Innate vs acquired immune response • PMNs are part of the non-specific innate immune system • Innate → means the cells don’t need to learn to recognise the invaders, they attack anything that the body considers foreign ○ Innate response differs from the acquired ○ In the acquired → specialised immune cells learn to recognise specific invaders ○ Acquired immune response involves: § B cells § T cells § Antigen-presenting cells

Question 181

Neutrophil function

Answer 181

Function • Varies with each cell type Neutrophils • First-line defence against bacteria, viruses and fungal infections • Tissue injury → body release chemotactic factors to attract neutrophils

Question 182

Eosinophil function

Answer 182

Eosinophils • Involved in allergic reactions & also fight parasitic infections • High levels of eosinophils can result from other conditions → including drug reactions or immune system disorders like eosinophilic esophagitis

Question 183

Basophils function

Answer 183

Basophils • Involved in allergic reactions • Also secrete histamine and other compounds that cause inflammation • Basophils → the bloodborne equivalent of mast cells

Question 184

Mast cells function

Answer 184

Mast cells • Live in tissues and play an important role in respiratory and digestive conditions • Two major subtypes: ○ Connective tissue mast cells → trigger inflammation ○ Mucosal mast cells → keep the gut in balance • Histmaine and other substances within these PMNs (such as heparin) help regulate the immune response

Question 185

Lymphocyte function

Answer 185

Lymphocytes • Begin journey in the bone marrow • Once formed, they travel to and perform various functions within the lymphatic system • They travel throughout the system in a fluid called lymph • Lymph travels through lymph nodes → lymph nodes are responsible for filtering lymph so that bacteria, viruses, parasites, fungi and other invaders can be isolated and neutralised by lymphocytes • They are also found in lymphoid tissues and organs throughout the body

Question 186

B Cells

Answer 186

• B cells → involved in adaptive, antibody-driven immunity ○ They release antibodies that attach to the antigen of the invader ○ This inactivates or 'tags' the invader for destruction ○ Produced in bone marrow. § Mature in bone marrow and specialise. ○ Two main types of B cells: § Plasma cells → produce large volumes of antibodies that target and bind to foreign invaders § Memory B cells → help your immune system 'remember' foreign invaders so that it can launch a new attach if the invader returns

Question 187

T cells and the different types

Answer 187

• T cells → mainly involved in adaptive, cell-mediated immunity ○ Does not involve antibodies but instead directly target or kills foreign cells ○ Travel from bone marrow to a small gland located called the thymus → here they mature and specialise ○ Different types: § Cytotoxic → directly target and attack foreign invaders like bacteria, viruses and certain cancer cells § Helper t cells → recruit and coordinate other immune cells to help fight infection § Natural killer T cells → can kill certain tumour cells and also target infected cells for destruction. Function as part of innate immune response § Regulatory T cells → adjust the immune response to avoid overreaction that can cause the body harm § Memory T cells → 'remember' foreign invaders so that a new attack can be launched if the invader returns

Question 188

What are macrophages?

Answer 188

What are they? • Type of white blood cell • Carry out various functions: ○ Engulf and digest microorganisms ○ Clear out debris and dead cells ○ Stimulate other cells involved in immune function • Confer innate immunity • Also secrete anti-inflammatory cytokines • Form from monocytes, which derived from the bone marrow

Question 189

Types and function of macrophages

Answer 189

Types • M1 → aka classically-activate macrophages. Activate by pathogen invasion and play a large role in the immune response to foreign pathogens e.g. bacteria • M2 → aka alternatively-activated macrophages. Play a role in wound healing, tissue repair, and have an anti-inflammatory role Function • M1 → detect, engulf and destroy bacteria. They do this through phagocytosis. ○ Phagocytosis → process by which cells ingest or engulf other cells or particles ○ M1 macrophrages promote inflammation, extracellular matrix destruction, apoptosis of invading cells by releasing various cytokines and nitric oxide to aid in cellular destruction, as well as antigen presentation • M2 → needed for regeneration of connective tissue during wound healing. ○ Produce vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-Β1 which allows for vascular stability and wound repair ○ Also function to phagocytose bacteria and damaged tissue around the wound

Question 190

Characteristics of acute inflammation

Answer 190

Pain Heat Redness Swelling Loss of function

Question 191

During inflammation why do you feel: hot (calor) red (rubor) pain (dolor) Swelling (tumour) Loss of function (functio laesa)

Answer 191

Why you feel hot (calor) and red (rubor): 1. Immune system releases inflammatory mediators such as bradykinin and histamine. 2. Blood vessels in the injured tissue vasodilate. 3. More blood flow leads to the area becoming inflamed (swelling), red, and hot. Why you feel pain (dolor): 1. Increased blood flow to injured area results in inflammation 2. Release of both histamines and bradykinin triggers neurons to send pain signals to the brain 3. Injured area feels painful *** This is a protective function because if the site hurts, you are more likely to leave it alone and let it heal*** Why there is a swelling (tumour): 1. Immune system encourages more tissue fluid to diffuse into the inflamed tissue 2. This causes swelling. Why there is loss of function (functio laesa) 1. Local nerve endings are stimulated at the site of injury from mechanical and chemical mediators.

Question 192

In order for a tissue to undergo true regeneration what 2 criteria must be met?

Answer 192

1. The injured cells must be capable of proliferation (like in labile and quiescent tissues) 2. The underlying stroma must be intact.

Question 193

Why are lungs so vulnerable?

Answer 193

Why are lungs so vulnerable? • Lungs are highly vulnerable to damage due to their structure and function, they are exposed to a lot of non sterile air. • Lungs have a very low density of cells in relation to volume • Cells at the mucosal surface are the cells most vulnerable to damage, yet they are also the cells responsible for the functionality of the lung(elasticity and gas exchange) , any non regenerable damage will result in impairment of function as gay exchange requires a specific tissue organisation, which is lost after tissue replacement.

Question 194

How do lungs deal with damage?

Answer 194

How do lungs deal with damage • Rapid detection of tissue damage or infection in lung is done by pattern recognition receptors, which recognise pathogen associated molecular patterns and danger associated molecular patterns. • Inflammatory response is initiated upon detection, • Neutrophils move from the blood vessels, phagocytose pathogens and then die. • Macrophages then phagocytose dead and dying neutrophils and reduce the proinflammatory signalling. • Stromal cells within the lung release IL-6 this is a cytokine, the levels of which are critical driving fibrosis.

Question 195

What is the difference between tissue repair, tissue regeneration and tissue replacement (scarring), and give examples?

Answer 195

Tissue repair - restoration of tissue architecture and function after an injury. This is a process that involves both of the below two processes, and the predominance of one over the other depends on the site of injury, extent of damage, and the tissue that needs to be repaired. Tissue Regeneration - where new growth completely restores portions of damaged tissue to their normal state. replacing damaged cells functioning identical copies Tissue Replacement (scarring) - this refers to the replacement of severely damaged tissue, or non-regenerable tissue with new layers of connective tissue instead of regenerating the old cells with new ones Continuously Dividing Tissues (Labile Tissues) • HP Bone marrow cells • Skin and hair • GIT epithelium • Seminiferous Cells Quiescent Tissues (stable tissues) • Hepatocytes • Lymphocytes • Proximal convoluted tubule cells Permanent tissues • RBC • Cardiac Muscle • Skeletal Muscle • Neurones

Question 196

What step approach does inflammation lead too?

Answer 196

Localised effects on local tissues eg vasodilation, activation of endothelial cells to display adhesion molecules Activation of pro inflammatory systems eg clotting and kinin system activated Recruitment and activation of cells of the immune system macrophages and monocytes recruited, mast cells, esonophils eg release cytokines Leads to an acute phase response (neutrophils and macrophages respond to inflammation by releasing even more cytokines) eg interleukins start to act

Question 197

Role of interleukins in inflammatory response during the acute phase response

Answer 197

neutrophils and macrophages respond to inflammation by releasing even more cytokines: • IL-1 act on the central nervous system to cause fever, lethargy and anorexia • IL-6 simulates the liver to produce acute phase proteins (opsonins) • IL-8 recruits and activates neutrophils • IL-2 and IL-12 activate natural killer cells • Tumour necrosis factor alpha (TNF-α) has the same action of all of the interleukins above

Question 198

5 clinical signs of inflammation

Answer 198

Acute inflammation begins within seconds to minutes following injury to tissues and lasts for a few days. It is characterised by five cardinal features: • Redness (rubor) – secondary to vasodilatation and increased blood flow • Heat (calor) – localised increase in temperature, also due to increased blood flow • Swelling (tumour) – results from increased vessel permeability, allowing fluid loss into the interstitial space • Pain (dolor) – caused by stimulation of the local nerve endings, from mechanical and chemical mediators • Loss of function (functio laesa).

Question 199

What are the 5 groups bacteria are classified into?

Answer 199

Bacteria are classified into five groups according to their basic shapes: spherical (cocci), rod (bacilli), spiral (spirilla), comma (vibrios) or corkscrew (spirochaetes). They can exist as single cells, in pairs, chains or clusters. Bacteria can also be split into aerobes (need oxygen to live) and anaerobes (need absence of oxygen to live)

Question 200

What is gram positive and gram negative bacteria?

Answer 200

Gram staining can also be used to classify bacteria. Gram-positive bacteria and gram-negative bacteria respond differently to certain types of antibiotics, due to differences in the cell walls. Under a Gram stain Gram-positive bacteria look blue-purple; Gram-negative look red-pink. Gram-negative bacteria are surrounded by a thin peptidoglycan cell wall, which itself is surrounded by an outer membrane containing lipopolysaccharide. Gram-positive bacteria lack an outer membrane but are surrounded by layers of peptidoglycan many times thicker than is found in the Gram-negatives.

Question 201

What are the mechanisms of antibiotic action?

Answer 201

Antimicrobial agents can be divided into groups based on the mechanism of antimicrobial activity. The main groups are: agents that inhibit cell wall synthesis, depolarize the cell membrane, inhibit protein synthesis, inhibit nuclei acid synthesis, and inhibit metabolic pathways in bacteria.

Question 202

Broad spectrum antibiotics vs narrow spectrum antibiotics

Answer 202

Broad spectrum antibiotics: affect a wide range of bacteria e.g. amoxicillin, gentamicin, ampicillin, doxycycline, quinolones They can target both gram-positive and gram-negative bacteria. Narrow spectrum antibiotics: affect a few types of bacteria e.g. penicillin, fidaxomycin, sarecycline

Question 203

Describe pneumonia

Answer 203

Infection of the lung tissue (just a bad chest infection), can be seen as consolidation on a chest x ray.

Question 204

Classification of pneumonia

Answer 204

Classification: 1. Community acquired pneumonia – developed outside of hospital 2. Hospital acquired pneumonia – developed more than 48hr after hospital admission • Usually pseudomonas, klebsiella, S. aureus, MRSA 3. Aspiration pneumonia – developed due to aspiration, e.g. after inhaling foreign material such as food 4. Location- Lobar vs bronchopneumonia • Lobar: Within the whole of one or more lobes • Bronchopneumonia: Affects lobules of lungs with bronchi and bronchioles more diffuse consolidation 5. Ventilator acquired

Question 205

Clinical presentations of pneumonia

Answer 205

Clinical presentation: · Shortness of breath · Cough productive of sputum (rusty coloured) · Fever · Haemoptysis · Pleuritic chest pain (sharp chest pain worse on inspiration) · Delirium (acute confusion associated with infection) · Sepsis secondary to the pneumonia Inc tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion · Auscultation  Bronchial breath sounds – harsh breath sounds  Focal coarse crackles – air passing through sputum (similar to using a straw to blow into a drink)  Dullness to percussion – lung tissue collapse/consolidation

Question 206

Most common responsible organisms which cause pneumonia

Answer 206

Responsible organisms (common): · Streptococcus pneumoniae (50%) • Common in elderly, almost always a preceding viral infection · Haemophilus influenzae (20%) • Frequent causes of exacerbation of chronic bronchitis in COPD

Question 207

What is the most common bacteria to cause pneumonia?

Answer 207

Streptococcal pneumoniae which causes pneumococcal pneumonia Commonest bacterial pneumonia • Gram +ve diplococci • Commoner in elderly, alcoholics, post-splenectomy, immuno-suppressed • Almost always a preceding viral infection • Followed by fever, pleuritic chest pain, cough productive of rusty coloured sputum • CXR= Lobar consolidation • Urine send for pneumococcal antigen • Treatment: Penicillin based Abx or cephalosporins • Prevention: Pneumococcal vaccine, 5 yearly

Question 208

What type of pneumonia is likely to break out in boarding schools, unis and families?

Answer 208

Chlamydia pneumoniae – Outbreaks in institutions and families – Person-to-person spread (not via animal reservoir) – Causes pharyngitis, laryngitis, sinusitis, followed by pneumonia – CXR= Segmental infiltrates

Question 209

What type of pneumonia is likely if a patient has pet birds?

Answer 209

Chlamydia psittaci – Causes psittacosis – History of exposure to birds- especially parrots – Causes headache, fever, dry cough, lethergy, arthalgia, hepato-splenomegaly

Question 210

What pneumonia usually occurs in elderly, diabetics and alcoholics?

Answer 210

Klebsiella pneumoniae: – Rare – Typically occurs in elderly, diabetics, alcoholics – Usually causes severe pneumonia (typically bronchopneumonia, and affects upper lobes) – Can cause a cavitating pneumonia, lead to abscesses

Question 211

Staphylococcus aureus

Answer 211

Staphylococcus aureus – Uncommon bacterial cause of pneumonia – Usually preceded by influenza infection – Risk if elderly, IV drug users, patients with long-term IV catheters, immunosuppression – Typically gives bronchopneumonia with cavities which later can form abscesses and empyema can develop

Question 212

What type of pneumonia is likely to occur in a patient with an exacerbation of chronic bronchitis in COPD?

Answer 212

Haemophilus influenzae: – Frequent cause of exacerbation of chronic bronchitis in COPD and can lead to pneumonia if COPD.

Question 213

Viral pneumonia

Answer 213

• Very uncommon • Usually due to influenza A virus – Others: adenovirus, measles, CMV, varicella zoster • SARS (Severe Acute Respiratory Syndrome): – Due to coranovirus – High mortality rate – Outbreak in 2003

Question 214

What type of pneumonia is likely for someone who has just returned from holiday/cruise?

Answer 214

Legionella pneumophilia (atypical cause of pneumonia) • Colonizes water tanks up to 60 degreesC • Causes outbreaks in hotels (hotel air conditioning/hot water systems) • Flu-like symptoms precede chest symptoms (usually dry cough) • CXR: Bi-basal consolidation, lymphopenia • Complications: D+V, hepatitis, hyponatraemia, haematuria • Diagnosis: Plasma serology – Urine testing for legionella antigen • Treatment: Macrolide e.g. Clarithromycin, Erythromycin +/- Rifampicin • Mortality= 10%

Question 215

What does mycoplasma pneumonia commonly cause?

Answer 215

Erythema Multiforme -Typically target lesions, raised, round, can appear oedemartous - Severe cases involve oral mucosa causing Steven Johnson Syndrome (severe

Question 216

Mycoplasma pneumonia

Answer 216

Mycoplasma pneumonia • Epidemics usually occur every 4 years • Usually occurs in teens and those in 20s • Commoner in boarding institutions • Generalize malaise, headache, arthalgia before chest symptoms • CXR= Reticulo-nodular shadowing or patchy consoldiation • Investigations: Mycoplasma serology (ie. blood test for Mycoplasma IgM) – Cold agglutins- can cause haemolytic anaemia • Complications: Skin rash/erythema multiforme, myocarditis/pericarditis, haemolytic anaemia/low platelets, neurological abnormalities, GI symptoms • Treatment: Macrolides e.g. Clarithromycin, Erythromycin

Question 217

Atypical pneumonia

Answer 217

Atypical pneumonia · Caused by an organism that cannot be cultured or detected using gram stain · Don’t respond to penicillin – treat with macrolides (clarithromycin), fluoroquinolones (levofloxacin) or tetracyclines (doxycycline) Eg Legionella pneumophilia

Question 218

Innate immunity

Answer 218

Innate immunity • Immunity that is present at birth and lasts a person's entire life. • The host's first line of defence and is intended to prevent infection and attack of invading pathogens • Innate immunity is an antigen-independent (non-specific) mechanism which is fast (minutes to hours of encountering the antigen) • The adaptive response takes longer (days to weeks) • No immunologic memory - unable to recognize or “memorize” the same pathogen should the body be exposed to it in the future. • It consists of a cellular response by the innate immune system, a chemical response by cytokines and complement and the subsequent initiation of an acute inflammatory response

Question 219

Anatomical barriers which block the entry of microbes

Answer 219

• Skin • Epithelial and mucous membranes • Mucous • Tears • Stomach acid • Ear wax

Question 220

Physiological barriers which maranta in environments to inhibit pathogen growth

Answer 220

Maintenance of environments to inhibit pathogen growth • Temperature • Low pH • Chemical mediators (lysosomes and interferons)

Question 221

Common bacterial causes of pneumonia

Answer 221

Common causes • Streptococcus pneumoniae (50%) • Haemophilus influenzae (20%) Other Causes and Associations • Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease • Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis • Staphylococcus aureus in patients with cystic fibrosis

Question 222

Presentations and clinical signs of pneumonia

Answer 222

Presentation • Shortness of breath • Malaise • Cough productive of sputum • Fever • Haemoptysis (coughing up blood) • Pleuritic chest pain (sharp chest pain worse on inspiration) • Delirium (acute confusion associated with infection) • Sepsis Signs There may be a derangement in basic observations. These can indicate sepsis secondary to the pneumonia: • Tachypnoea (raised respiratory rate) • Tachycardia (raised heart rate) • Hypoxia (low oxygen) • Hypotension (shock) • Fever • Confusion • Cyanosis There are characteristic chest signs of pneumonia: • Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway. • Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink. • Dullness to percussion due to lung tissue collapse and/or consolidation.

Question 223

CURB 65 score

Answer 223

CURB65 Score NICE recommend using the scoring system CRB-65 out of hospital and CURB-65 in hospital. The only difference is that out of hospital you do not count urea. When you see someone out of hospital with a CRB-65 score of anything other than 0 NICE suggest considering referring to the hospital. • C – Confusion (new disorientation in person, place or time) • U – Urea > 7 • R – Respiratory rate ≥ 30 • B – Blood pressure < 90 systolic or ≤ 60 diastolic. • 65 – Age ≥ 65 The CURB 65 score predicts mortality (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%). The scoring system is there to help guide whether to admit the patient to hospital: • Score 0/1: Consider treatment at home • Score ≥ 2: Consider hospital admission • Score ≥ 3: Consider intensive care assessment

Question 224

Investigations of pneumonia

Answer 224

Patients in the community with CRB 0 or 1 pneumonia do not necessarily need investigations. NICE suggest considering a “point of care” test in primary care for CRP level to help guide management, however this is not widely available. If they arrive in hospital they will probably get a minimum of: • Chest xray • FBC (raised white cells) • U&Es (for urea) • CRP (raised in inflammation and infection) Patients with moderate or severe cases should also have: • Sputum cultures • Blood cultures • Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing) Inflammatory markers such as white blood cells and CRP are roughly raised in proportion to the severity of the infection. The trend can be helpful in monitoring the progress of the patient towards recovery. For example, repeating WBC and CRP after 3 days of antibiotics may show a downward trend suggesting the antibiotics are working. CRP commonly shows a delayed response so may be low on first presentation then spike very high a day or two later despite the patient improving on treatment. WBC typically responds faster than CRP and give a more “up to date” picture. Patients that are immunocompromised may not show an inflammatory response and may not have raised inflammatory markers.

Question 225

Hospital treatment for pneumonia

Answer 225

Antibiotics: IV/oral Fluids- IV fluids: patients may be dehydrated, correct any deficit and prescribe maintenance fluids as appropriate. O2 mask if required- Aim for saturation of 94-98% in patients without underlying lung disease. In patients at risk of type II respiratory failure (e.g. COPD) aim for saturations of 88-92%. Pain killers eg paracetamol, ibroprofen, aspirin

Question 226

Complications of pneumonia

Answer 226

Complications • Sepsis • Pleural effusion • Empyema • Lung abscess • Death

Question 227

Pneumonia vaccination

Answer 227

Pneumonia vaccination If you're at risk of getting seriously ill with pneumonia, it's recommended you get the pneumococcal vaccine, also known as the pneumonia vaccine. It protects against an infection that can cause pneumonia. People at high risk include: • babies • adults aged over 65 • people with heart, lung, liver, kidney or neurological conditions with a risk of aspiration • people with diabetes • people with a weakened immune system, for example, you have a condition that stops your immune system working properly, or you are having treatment to suppress your immune system

Question 228

Treatment for antibiotics

Answer 228

Antibiotics Always follow your local area guidelines. These are developed by looking at the bacteria in the local area for their antibiotic resistance so are specific to that population. Moderate or severe pneumonia or septic patients usually start with IV antibiotics. These are then changed to oral antibiotics guided by clinical improvement or improvement in their inflammatory markers. • Mild CAP: 5 day course of oral antibiotics (amoxicillin, cephalosporins or macrolide) • Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)