Learning outcomes Flashcards
(140 cards)
1
Q
Compare pulmonary and systemic blood flow
A
Pulmonary blood flow refers to the flow of deoxygenated blood from the right side of the heart to the lungs, and the oxygenated blood from the lungs being pumped into the left side of the heart and is pumped around the body. Systemic blood flow refers to oxygen being deposited into the tissue and carbon dioxide being transported back to the lungs, the opposite of pulmonary circulation.
2
Q
Describe the main anatomical features of the airways and gross anatomical features of the lung
A
air can enter through the nose or the mouth, then through the nasopharynx through the larynx which is where the vocal cords are located and marks the end of the upper respiratory system. Here the channel splits into the trachea which consists of stiff cartilage, guarded by a flap called the epiglottis, and the oesophagus. Through the trachea the airways split between the two lungs into the bronchus which further divide into secondary bronchus, which then divide into bronchioles which finally end as alveoli. Surrounding the lungs is the pleural cavity, diaphragm a dome shaped muscle, ribs and muscles.
3
Q
Identify the different classes of airways and pneumocytes
A
Type 1 alveoli cells – thin for diffusion
type 2 alveoli cells surfactant – secrete surfactant, easing tension making breathing easier
macrophages
For the airways we have: Lymphocytes glands blood vessels epithelium mucus
as we progress from nose to lungs we lose cilia, mucous is lost and the epithelium become more squamous.
4
Q
State the mechanical factors that affect respiratory minute volume.
A
pressure (boyle’s law) temperature volume solubility resistance and the radii of airways the stretch of the lungs trans pulmonary pressure
5
Q
Explain why intrapleural pressure is always less than alveolar pressure.
A
intrapleural space is always being pulled at by the elastic pull of either the lungs or the ribs, however due to the tension of the fluid between the two membranes doesn’t separate. The alveolar pressure is always higher because it’s adhered to the ribs the pleural cavity allowing it to expand and compress.
6
Q
Be able to describe the anatomy of the pleural cavity
A
it consists of a visceral membrane binding it to the lungs, and a parietal membrane binding it to the ribs, with about 3ml of fluid in between the two membranes which encompass the lungs.
7
Q
Understand the relationship between the parietal and visceral pleura and why this is important for inflation of the lung
A
the small amount of fluid enables gliding but doesn’t allow for separation of the two membranes. They keep the lung adhered to the ribs through the membranes.
8
Q
Be able to describe how the muscles of respiration act to increase and decrease thoracic volume
A
the muscles such as the diaphragm contracts, and the external intercostal muscles, scalene muscles, sternocleidomastoid muscles pull on the ribs increasing thoracic space allowing for the lungs to increase in volume for inspiration, where as if the diaphragm relaxes, and the internal intercostal muscles contract pulling on the ribs and the abdominal muscles contract, the thoracic space decreases, decreasing lung volume increasing pressure triggering expiration.
9
Q
Relate Boyle’s law to the mechanics of breathing, inspiration and expiration
A
Boyle’s law dictates that as volume decreases, the pressure increases meaning there is an inverse relationship between the two. As someone inspires, the volume of the lungs increases and pressure decreases, so air can move from a place of high pressure to low pressure. As they expire, the volume decreases, and pressure increases so the gases move from an area of high pressure to low pressure.
10
Q
Define the various lung volumes and capacities and, provide approximate normal values for them.
A
tidal volume – volume of either a inspiration or expiration – 500ml
total lung volume – 6000ml
expiratory reserve volume – 1100ml
residual volume – 1200ml
inspiratory reserve volume – 3000ml
air from dead space – 150ml
vital capacity – tidal volume + expiratory reserve volume + inspiratory reserve volume – 4600ml
functional residual capacity – expiratory reserve volume + residual volume – 2300ml
inspiratory capacity – tidal capacity + inspiratory reserve volume – 3500ml
11
Q
State the role of pulmonary surfactant and the Law of Laplace
A
The role of pulmonary surfactant is to ease the fluid tension required for the absorption of oxygen to prevent the collapse of the alveoli. The law of Laplace (P=2T/r) is that increasing the volume of fluid within the alveoli increases the pressure, especially within smaller alveoli which is problematic as we need smaller alveoli instead of larger ones for increased surface area. Surfactant overcomes this as in a smaller space the concentration is increased and obstructs the affinity water molecules have for one another. This makes breathing easier, reduces recoil and increases lung compliance.
12
Q
Summarise the basic characteristics of obstructive and restrictive lung disease.
A
obstructive lung disease has a massive effect of air exhaled and slightly reduces the vital capacity. An example of this is COPD as its major effect is on the airways, this reduces the ratio between FEV1/FVC (forced expiratory volume 1 second/forced vital capacity).
restrictive lung disease reduces the amount of air exhaled and the vital capacity dramatically, such as pulmonary fibrosis as this limit the lung expansion. This doesn’t reduce the ratio and often requires a comparison of forced expiratory flow (average of a forced expiration) to recognise.
13
Q
Describe the tests used to identify abnormal lung function.
A
spirometry, it can be dynamic where the time taken to exhale a certain volume is measured or it can be static where only the volume is considered. It can measure tidal volume, expiratory reserve volume, inspiratory reserve volume, vital capacity and inspiratory capacity.
14
Q
Know the normal values for alveolar and arterial gas partial pressures
A
Pa oxygen - 100 mm hg
Pa carbon dioxide – 40 mm hg
PA oxygen – 40 mm hg
PA carbon dioxide – 46 mm hg
15
Q
Describe the difference between pulmonary and alveolar ventilation
A
pulmonary ventilation involves the tidal volume of each breath, then the number of breath per minute this tells us the total air getting into and out of the lungs. The alveolar ventilation refers to the fresh air for exchange reaching the alveolar, taking into account the dead air.
16
Q
Describe the factors that affect the oxyhaemoglobin dissociation curve.
A
Factors that affect the oxyhaemoglobin dissociation curve are temperature, and increase in temperature will shift the curve to the right, resulting less affinity between haemoglobin and oxygen, and a decrease will shift it to the left meaning during severe hypothermia oxygen isn’t being diffused to the tissues. Increasing pH will also shift the curve to the right, as well as increasing the partial pressure of carbon dioxide and 2,3-DPG which is a chemical released during hypoxia to encourage oxygen diffusion.
17
Q
State the factors that affect gas exchange
A
the partial pressure gradient
gas solubility
surface area
thickness of membrane
18
Q
state the differences between partial pressure and gas content.
A
partial pressure determines the pressure of which the gaseous form is pushing the gas into solution, it doesn’t equal gas content which refers purely to the gas in solution, which is partly determined by solubility and partial pressure.
19
Q
Compare oxyhaemoglobin dissociation for adult haemoglobin with that of foetal haemoglobin and myoglobin in relation to their physiological roles
A
myoglobin has the highest affinity for oxygen as it’s located in the muscles, then foetal haemoglobin as they both require the taking the oxygen from oxyhaemoglobin in order to meet energy demand.
20
Q
Identify the forms in which CO2 is carried in the blood.
A
7% of CO2 dissolves directly into the plasma, 23% can bind to haemoglobin to form deoxyhaemoglobin and 70% forms HC03- bicarbonate ions in solution.
21
Q
Identify the factors which favour CO2 unloading to the alveoli at the lungs.
A
the increase partial pressure of oxygen favours oxygen loading at the haemoglobin. On top of that carbon dioxide is being constantly removed at the lungs from plasma, meaning that the forms of CO2 transport are converted back into CO2 to try and from equilibrium, as well as the difference in partial pressure meaning that carbon dioxide will follow the gradient into the alveoli. Other factors like pH also favour oxygen loading which subsequently means carbon dioxide unloading.
22
Q
Explain the relationship between ventilation and perfusion and its significance in health.
A
ventilation and perfusion should ideally match each other in rate of flow per L/min. conditions like emphysema, fibrotic lung disease, pulmonary oedema and asthma can all reduce the amount of oxygen being absorbed this results in deoxygenated blood being reabsorbed and mixed with oxygenated blood causing hypoxia.
23
Q
Describe the term ‘shunt’.
A
shunt refers to the flow of blood through poorly ventilated areas, it when the rate of ventilation is less than perfusion, which is the opposite of alveolar dead space. Results in diverted blood flow as the systemic vessel around the effected alveoli is constricted and the bronchiole dilates.
24
Q
Describe the role of haemoglobin in the transport of O2 in the blood.
A
only 3ml of oxygen can dissolve into plasma which isn’t enough to meet demands. As a result, haemoglobin can take absorb much more oxygen (1g of Hg can absorb 1.34g of oxygen), maintaining the partial pressure gradient of oxygen from the alveoli to the blood. Its cooperative binding works in that the more oxygen it has the easier it is for oxygen to bind, and as it begins to unload it’s easier to lose its oxygen. It’s ideal for the factors that affect dissociation are the ones found in the tissues where oxygen is needed most, whist these factors aren’t found in the lungs meaning it can readily pick up oxygen.
25
Explain why the shape of the oxyhaemoglobin dissociation curve is important to O2 loading in the lungs and unloading in the tissues.
the sigmoid shape of the oxyhaemoglobin curve means that a large decrease in oxygen partial pressure translates only to a small decrease in oxygen saturation of oxyhaemoglobin. Even at partial pressure of 40mmHg, oxygen saturation is still at 75% leaving a large reserve.
26
Explain the action of carbonic anhydrase in CO2 transport
carbonic anhydrase (H20) helps convert the carbon dioxide into carbonic acid which then dissociates into bicarbonate and hydrogen ions, the excess hydrogen ions bind to deoxyhaemoglobin whilst the bicarbonate is pumped out the erythrocyte through a chloride channel into plasma.
27
Know the difference between anatomical, alveolar and physiologic dead space
alveolar dead space shouldn’t really be present in a healthy human, it occurs once a alveolar is no longer participating in gas exchange. Anatomical dead space is the air present in the airways that is unable to participate in gas exchange, it equates to roughly 150ml and is regularly replaced with fresh air or stale air from the alveoli. Physiological dead space is calculated by adding together the anatomical and alveolar dead space.
28
State the factors that determine arterial PO2
```
oxygen bound to haemoglobin
saturation of haemoglobin (temp, pH, PCO2, DPG)
total number of binding sites
oxygen dissolved in plasma
alveolar ventilation
perfusion of alveolar
composition of air
diffusion of oxygen
```
29
explain how respiratory motor movements are affected by the central nervous system
the diaphragm is innervated by the phrenic nerve, since the diaphragm is responsible for 70% of the work required for breathing it highlights how heavily influential the central nervous system is for control of breathing, if there is damage to the vertebrae C3,4,5 breathing ceases and results in death, this demonstrates that it is entirely dependent on the brain and it is not autonomous. The intercostal muscles that aid in breathing also are innervated and thus controlled by the intercostal nerves that stem from the spinal cord which their impulses originate from the brain stem.
30
List the factors involved in changing ‘respiratory drive’, rate and depth of breathing.
respiratory drive is controlled involuntary by the medulla and the pons, specifically the dorsal respiratory group (DRG) which controls the inspiratory muscles and the ventral respiratory group (vRG) which influences the expiratory and inspiratory muscles such as the pharynx, larynx and tongue. These centres are influenced by primarily chemoreceptors; however, they can also be influenced by chemoreceptors in the peripheral carotid and aorta. The further can be influenced by the limbic system through emotions, mechanoreceptors in the chest wall, or voluntarily by the higher centres of the brain but these can override by the brainstem.
31
Explain how, by monitoring the pH of CSF, the central chemoreceptors serve to regulate the arterial Pco2.
carbon dioxide and other gases can diffuse across the blood brain barrier whilst hydrogen ions cannot. These can then bind to carbon dioxide to form bicarbonate ions, these then bind to the central chemoreceptors, specifically the bound hydrogen ions then stimulate the DRG and VRG to increase the rate of ventilation, and if the concentration drops, the rate of ventilation reduces. This is known as hypercapnia as it is driven by the arterial partial pressure of carbon dioxide.
32
Explain how the peripheral chemoreceptors become important during hypoxia and acid-base imbalance.
during hypoxia the peripheral chemoreceptors in the carotid and aorta are sensitive to a singnifcant fall in arterial partial pressure changes for oxygen or acid base Imbalance, this is due to long term exposure of carbon dioxide to the central chemoreceptor rending it insensitive to changes. This makes what would normally be a secondary receptor essential for altering ventilation.
33
Outline the role of the respiratory system in acid-base disturbances
when the peripheral chemoreceptors detect a change in blood pH, where the concentration of hydrogen ions increase and the pH decreases known as acidosis, this can trigger an increase in ventilation known as hypoventilation to reduce the concentration of carbon dioxide. However, if the concentration of hydrogen ions decreases it can induce a decrease in the rate of ventilation known as hyperventilation in order to produce more hydrogen ions and can also trigger vomiting and retention of carbon dioxide.
34
Explain the basis of rhythm in respiration
we don’t consciously think about breathing, instead it’s a form of homeostatic control the rhythm of breathing trying to maintain respiratory acid base balance, partial pressure of carbon dioxide and oxygen. This is achieved through the brain stem and chemoreceptors which involuntarily regulate our breathing in response to stimuli. Co-ordinated by the firing of smooth and repetitive bursts of action potentials in the DRG to inspiratory muscles.
35
Identify the sites of chemoreceptors and identify the stimuli which activate them
chemoreceptors are located in the peripheral carotid and aorta, and the central medulla. They can be stimulated by changes in pH, carbon dioxide partial pressure and oxygen partial pressure.
36
strategies for management of COPD.
smoking cessation is key, but for management of COPD is a multi disciplinary team is required. Inhalers for relief, vaccines and pulmonary rehabilitation, long term oxygen therapy and lung volume reduction. This as well as psychological support, physiotherapy and nutritional assessment.
37
Describe the classes of drugs and modes of delivery available in the management of obstructive lung diseases, both asthma and COPD.
inhalers or nebulizers are the forms of delivery available
short acting bronchodilators
SABA – salbutamol
SAMA – ipratropium
long acting bronchodilators
LAMA – long acting anti-muscarinic agents
LABA long acting beta 2 agonist
high dose corticosteroids
however antibiotics or Long Term oxygen may be necessary
38
Define the role of patient education in the management of asthma and COPD.
patient education in the management of asthma and COPD is essential because asthma unlike COPD is reversible to an extent whilst COPD is progressive, persistent and productive. Whilst asthma can occur at any age but for COPD is more likely to occur after the age of 35. With COPD things like nocturnal hypoxia and family history is uncommon, with a possible allergy reaction. Whereas asthma is more familial, with nocturnal hypoxia being common and commonly linked to allergies. This biggest important aspect Is that smoking is often the biggest cause behind to COPD where as smoking can exacerbate asthma but is not responsible.
39
Describe the clinical management of acute, exacerbated COPD
the clinical management acute exacerbated asthma requires antibiotics if necessary for the bacterial infection, corticosteroids, oxygen at 70-80% saturation, nebulizer bronchodilators and perhaps hospital admission with investigations such as X-rays, ECG and blood cultures to rule out other possibilities.
40
Describe the defining features and epidemiology of asthma, its proven and putative aetiological factors.
asthma’s defining features is chronic but variable wheezing, shortness of breath and cough with response to asthma treatment. With one million UK being afflicted with it there are many causes resulting in the multiple hits aetiology with factors like genes, lung function, atopy and later exposures to stimulants like rhinovirus, exercise or smoking.
41
Differentiate the main causes of wheezing illness.
wheezing illnesses are causes by bronchoconstriction with airway wall thickening and increased luminal secretions making the airways smaller increasing the chance of a wheezing sound. This could mean it’s asthma but however this doesn’t rule out other conditions such as a foreign body presence, cystic fibrosis, immune deficiency, trachea-bronchomalacia or ciliary dyskinesia.
42
Discuss possible reasons for the changing prevalence and severity of respiratory disease with child’s age and possible links with respiratory disease in adult life.
more awareness now about the harmful effects of smoking, and youthful exposure to potential allergens such as mould and dust and their influence on children.
43
Describe the symptoms and clinical patterns of asthma.
asthma can have various severities, and different ages of onset and heterogeneity in response with different triggers. It fluctuates and is variable. Making it difficult to diagnose.
44
Define the specific features to be included in the clinical history of asthma.
wheezing, shortness of breath at rest, parental asthma and response to treatment. Recent viral infections that induce a wheeze and ideally over the age of 5 but not essential. More than one trigger is ideal as well. Cough variant asthma doesn’t exist, cough predominant asthma however is not uncommon.
45
Define the investigations used to diagnose asthma.
examination and spirometry not effective forms of diagnosis. The key part of the investigation is taking a proper history and waiting to see the response to treatment to either salbutomal or ICS.
46
Be aware of the term remodelling.
remodelling refers to the structural changes the lung can undergo when exposed to infection of insult at an early age that triggers structural changes such as excessive luminal secretions, and tissue overgrowth or chronic inflammation that results in restricted airways. Such conditions include asthma
47
Understand the relationship between respiratory illness in childhood and adulthood.
respiratory illness developed early on in childhood impedes the development of the lungs and thus determines the severity of future respiratory illnesses through-out adulthood and also sets the peak for the inevitable respiratory decline.
48
Understand the “tracking” of pulmonary function from early life into adulthood and factors which influence tracking
tracking of pulmonary function from early life into adulthood enables us to make predictions regarding the anticipated decline of respiratory function. This enables us to make the necessary precautions or give advice regarding whether or not they are in the risk zone of serious respiratory diseases such as COPD. Factors that influence tracking is whether the child was born prematurely, smoking, nutrition, ETS (alpha1 AT deficiency), low birth weight, maternal infection, chemical exposure pre-natal and post-natal, serious lung infections. As this can drastically alter the time of deuteriation and can potentially put the individual into the danger zone for developing serious lung diseases and thus reduce their quality of life and expectancy.
49
state the common upper respiratory tract infections
```
common cold (coryza)
sore throat syndrome
croup
laryngitis
sinusitis
acute epiglottitis – caused by group A beta haemolytic streptococci
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50
Describe the clinical features of a lung abscess
lung abscesses are the result of necrotic tissue being encapsulated to prevent further spread. It can be caused by tumours, aspiration, certain organisms such as staph aureus, pneumococci and klebsiella, or a metastatic in pyaemia (bacterial blood infection of the lung)
51
Describe the pathogenesis of bronchopneumonia and lobar pneumonia and the complications and consequences of lower respiratory tract infection
bronchopneumonia is often bilateral resulting in a patchy opacification. This is the result of inflammation of the bronchioles leading to the consolidation of pus within the alveoli. This is due to the failure of the macrophage mucociliary escalator system, perhaps being previously ulcerated or damaged by a virus such as influenza. Lobar pneumonia whilst having the same aetiology is different in that it is confined to one lobe of the lung. This is due to the nature of the bacteria causing the secondary infection being for more potent in stimulating the immune system to over act, causing consolidation of fluid. As a whole section of the lung is inflicted it spreading to the pleural membrane is far more likely. Failure of organisation of the inflammation may result in pleurisy, fibrosis of the lung known as an emphysema, necrosis of lung tissue leading to an abscess or even death.
52
Be aware of causes of recurrent pneumonia.
recurrent lung infections are often a warning sign of an organic cause to the problem. It may be a local bronchial obstruction such as a tumour, or local pulmonary damage as with bronchiectasis, generalised lung disease with COPD and cystic fibrosis or a non-respiratory disease such as aspiration or they may be immunocompromised.
53
Be aware of the different spectrum of hospital acquired (nosocomial) pneumonia compared with community acquired pneumonia
the different spectrum of pneumonia is classified in regards to understanding the aetiology of the infection. As community acquired Pneumonia will likely be a different strain in comparison to a hospital acquired pneumonia, with the hospital one being more likely to be antibiotic resistant. There is also pneumonia in the immunocompromised, atypical pneumonia, aspiration pneumonia and recurrent pneumonia.
54
Contrast the management of asthma with strategies for management of COPD.
bronchial asthma is considered to be reversible condition whether it be spontaneously or as a result of medical intervention, the smooth muscle contraction and inflammation can be modified by drugs.
COPD was considered non-reversible but this is changing. By pharmacologically targeting the smooth muscle tone and inflammation of the small airways the condition can be improved. With emphysema the loss of alveolar attachments is the most important aspect.
55
Describe the major pathological features of the common obstructive lung disease emphysema and their complications
chronic bronchitis and emphysema results from smoking, pollution, age and genetic susceptibly, or rarely an alpha 1 antiprotease deficiency.
emphysema is the increasing size of airspaces distal to the terminal bronchiole arising from dilation or the destruction of their walls without fibrosis. It can be centriacinar, in which the it’s isolated mainly to bronchiolar dilation and then alveolar tissue is lost and is counted by number. Pan-acinar, are is more uniform and is measured by area, it’s associated with a alpha 1 antitrypsin deficiency. Peri-acinar/scar bullous emphysema, a bulla is an emphysematous space greater than 1cm, if just underneath the pleura it’s referred to as a bleb. It results from an abundance of elastase protease enzymes this is triggered by the presence of a foreign body stimulating neutrophils and macrophages such as smoking, which also inhibits elastin synthesis and leads to uncontrolled tissue mdestruction.
56
Describe the defining features and epidemiology of COPD.
COPD is a progressive chronic disease, with airflow obstruction that doesn’t have a significant change over the timeframe of months, lung impairment is fixed with some minor reversibility.
In the U.K 1.2 million people are diagnosed with COPD meaning likely prevalence is 2 million. Globally it’s more than 300 million people with COPD with it being more common in men with basic education in a low income household
57
Describe the symptoms and clinical patterns of COPD.
for symptoms, other possible diagnoses are to be excluded such as asthma or heart failure. Worsening over the years being key. Gradual onset of breathlessness with little variation from things like stairs, housework, dressing and at rest. Cough and sputum, smoker’s cough, sputum production, particularly in winter or all year. Wheeze typically upon exertion, weight loss if severe and peripheral oedema as indication of how severe.
cyanosis, with a carbon dioxide flap, barrel chest, paradoxical movements of ribs, abdomen. Prolonged expiration with a wheeze and palpable liver.
58
Define the specific features to be included in the clinical history of COPD.
clinical history is very important as to rule out asthma, other respiratory diseases or ischaemic heart disease. To consider other drugs such as inhalers, or steroids. Then the personal and social history such as their occupation, potential exposures and smoking history.
59
Explain how to assess the severity of acute COPD.
if the FEV1 is less than 30-49% from a spirometry test is indicative of COPD. Other signs such as weight loss and the existence of peripheral oedema are also indicative of severe COPD. Increasing breathlessness, wheezing, unable to sleep, sputum with pus, confusion and drowsiness. The results of a chest radiograph, blood gases, full blood count and sputum culture.
60
Define the investigations used to diagnose COPD.
spirometry, with FEV1 <80% with FEV1/FVC ratio of <70%.
full pulmonary function testing, measuring lung volumes with gas trapping as there will be an increased residual volume and increased total lung capacity (RV/TLC >30%). As well as carbon monoxide gas transfer being decreased. Their response to minimal bronchodilator reversibility and minimal response to oral corticosteroids, response to steroids suggest asthmatic component, COPD will often have an insignificant response.
other investigations include chest radiograph and looking for flattened diaphragm, bullae, hyperinflated lung fields. Other tests include a blood gas test (type 1/type 2). Full blood count to see if there is evidence of secondary polycythaemia. ECG to determine right axis deviation as common with right cor pulmonale or a sputum analysis
61
Describe similarities and differences between asthma and COPD
primarily smoking cessation, as it continues to degrade or if it’s exacerbated then COPD management requires nebulized bronchodilators, beta 2 and anti-muscarinic medication, oxygen, oral/iv corticosteroid, antibiotics, diuretic iv aminophylline, respiratory stimulant.
62
Describe the common clinical presentations of lung tumours, including local and extrathoracic symptoms and signs.
grows clinically silent for years, often presents late in natural history. Often there is a bronchial obstruction, either collapse, endogenous lipid pneumonia, infections and bronchiectasis. There is pleural inflammation and direct invasion of the chest wall with the phrenic nerves, left recurrent laryngeal nerve, brachial plexus and cervical sympathetic. Then there is lymph node metastases going to the liver, adrenals, bone, brain and skin. There is a range of skeletal, endocrine, neurological, cutaneous, hematologic, cardiovascular and renal non-metastatic paraneoplastic syndromes.
63
Describe the causes of a localised opacity (coin lesion) on the chest xray.
xray.
solitary pulmonary nodule is a mass or lesion under 3cm in size, often incidentally found. Often it can be caused by a granuloma, pneumonia, or an abscess. However if cancerous it may likely be a metastasis from another primary tumour which common, otherwise it could also be a bronchial gland tumour, lymphoma or a sarcoma.
64
Define the types of lung carcinoma.
there are two main pathways of lung carcinogenesis, in the lung periphery as adenocarcinoma as a result of the bronchioalveolar epithelial stem cells transforming. Then in the central lung airways there is squamous cell carcinoma, as a result of bronchial epithelial stem cells transforming. Then there is small cell carcinoma(endocrine effects of ACTH, siADH) and large cell carcinoma (endocrine PTH) .
65
Describe how lung cancer spreads both within and outwith the thorax.
A primary lung cancer can form metastasis which can then lead to it spreading to other organs like the liver, adrenals, bone, brain and skin. Locally it can directly invade the mediastinum or the nerve supply
66
Define the common organisms causing upper respiratory infection
the organisms that cause upper respiratory infections is bacteria such as haemolytic streptococcus beta, H influenza, M catarrhalis, mycoplasma, S. Aureus, and streptococci. Viruses such as adenovirus, rhinovirus influenza A, B, Para’flu 1, 3, RSV.
67
Describe the major pathological features of the common obstructive lung diseases,chronic bronchitis
chronic bronchitis and emphysema results from smoking, pollution, age and genetic susceptibly, or rarely an alpha 1 antiprotease deficiency. Chronic bronchitis causes the large airway glands and goblet cell hyperplasia (over proliferation) with inflammation and fibrosis being common. Where- as in small airways goblet cells appear and long-term inflammation and fibrosis can occur.
68
Define the principles of management of pulmonary vascular diseases.
the principles of management take into consideration the age, sex, comorbidity, physiological parameters and genetics when dealing with pulmonary vascular disease. Often the best course of treatment is a general one initially, or by targeting the underlying causes of the disease, hence why medication is opted for rather than invasive surgery.
69
Describe the pathogenesis of deep vein thrombosis, pulmonary embolism, and pulmonary infarction.
embolisms, or blood clots are likely to form within in the deep veins of the legs, this is because it’s a low pressure low flow system. If stimulated by surgery, cancer, major trauma, pregnancy, significant cardiopulmonary disease or by a genetically inherited thrombophilia. It then travels to the pulmonary arteries, and has three possible outcomes, it could lodge itself into a peripheral artery and cause pulmonary infraction resulting in that section of the lung dying. However, it could break up into several pieces travelling through pulmonary arteries. Finally, it could be a massive embolism, causing cardiac arrest if it lodges itself in the main pulmonary artery due to the reduced cardiac output.
70
Define pulmonary hypertension and outline the major causes
pulmonary hypertension is when the arterial systolic pressure measures greater then 25mm Hg. It can be primary (rare) or secondary (older people, common). This can be caused by a range of conditions such as heart failure, emphysema, COPD or thromboembolic hypertension, or simply be idiopathic. There are some miscellaneous causes such as portal hypertension (liver), HIV, collagen vascular disease, congenital heart disease (L to R shunt from high pressure to low pressure).
71
Describe the diagnostic investigative procedures used in pulmonary vascular disease.
Diagnostic techniques such as ECG, blood gas test, full blood counts are commonly used. So are radiography tests such as X-rays and CT scans for underlying cancer causes (abdomen or mammography) as well as a lung function test. Less commonly a right heart catheter can be inserted to directly measure blood pressure of the pulmonary artery but can calculate wedge pressure and cardiac output, echocardiography is also an excellent method for detecting issues.
specifically form an embolism thrombophilia testing may be employed, a ventilation/perfusion (V/Q) scan, CT pulmonary angiogram, and a D-dimer test.
72
Describe the investigation of restrictive lung disease and the approach to management of the common diseases (sarcoidosis, occupational lung disease, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis).
The investigation of the restrictive lung disease normally involves spirometry test, a chest x ray and a average rate of FEV test. If sarcoidosis treatment involves the use of corticosteroids to reduce inflammation, however it can be self limiting. Further tests include calcium and ACE levels in the serum and a biopsy.
73
Describe the clinical symptoms associated with restrictive lung disease.
the symptoms associated with restrictive lung disease revolve around breathlessness, normal or high FEV1/FVC, tired, fatigue, with a cough. Joint pains and shin rashes if sarcoidosis.
if hypersensitivity pneumonitis there can be a fever, crackles, wheeze, tachypnoea, antibodies, malaise and myalgia. However if it is UIP, then there is cyanosis and clubbing as well.
74
dentify the lung interstitium and describe the functional effects of interstitial lung disease.
interstitial disease results in proliferation of the interstitium the connective tissue between the basement membranes and the alveolar walls, with fibroblasts laying down excess collagen, and elastin reducing the stretch ability of the lungs and increasing the thickness of the alveolar membrane reducing the rate of diffusion in the lungs. This is as a result of inflammation of the lungs, either acute that leads to, or only chronic. This is partially due to the destruction of the cell walls by neutrophils in response to a pathogen or by some other non-organic substance.
75
Describe the aetiology and pathogenesis of diffuse alveolar damage syndrome,
diffuse alveolar damage syndrome is caused by major trauma, chemical injury, drugs or idiopathic in that the cause is unknown, and that the neutrophils of the host begin destroying the cell walls in an inflammatory response, resulting in an oedema and inflammation then eventually fibrosis.
76
Recall the causes and effects of endstage lung fibrosis/ honeycomb lung.
the causes of lung fibrosis is long term chronic inflammation as that in a granulomatous response, or UIP. The endstage is severely reduced lung capacity, putting severe strain on the heart causing heart failure, type 1 respiratory failure and hypoxia. This is due to diffusion impairment because of the increasing membrane thickness.
77
Describe the genetics and presenting features of cystic fibrosis.
Cystic fibrosis is an autosomal recessive gene with high prevalence in Caucasian Europeans, ranging to about 1/25 people. Typically, people with cystic fibrosis cough thick mucus, haemoptysis, shortness of breath, pale oily offensive stools, GI tract issues such as prolapse. Other issues include diabetes and re occurring chest infections, reduced growth and weight. There is as anaemia, oedema’s, liver disease, jaundice and vitamin deficiencies as less common signs.
78
Define the possible complications of cystic fibrosis.
Unusual bacteria such as pseudomonas aeruginosa can drastically reduce life expectancy as it can form a biofilm within the lung. As well as burkholderia cepacian can also reduce life expectancy, or form cepacian syndrome and rapidly deteriorate the patient. Included in this is m. abscessus which can cause very rapid degradation. Infections include in pneumonitis, bronchiectasis, scarring and abscesses. Other complications involve infertility, especially in males, diabetes, degrading lung function and shorter life expectancy, increased chance of developing crohn’s disease. A pneumothorax may occur and can be fatal, as well as haemoptysis due volume, if large enough may need an embolization.
79
Outline the management of pancreatic insufficiency and chest infection.
the management of pancreatic insufficiency involves taking enteric coated enzyme medication, non-steroidal anti-inflammatories, high energy diet, lipid soluble vitamins and antibiotics for chest infections. Sometimes proton pump inhibitors are considered for improving the enzyme pellets. The general management since it is a multi organ disease is for a mutlii-disciplinary team and surveillance for early treatment of infection.
80
Explain the options available for antenatal and post natal screening for cystic fibrosis
post natal there is the gurthie card, a blood spot test on day 5, the initial screen for immune-reactive trypsinogen, then a mutation analysis for the 4 most common type of cystic fibrosis, as well as monitoring weight. If older and missed the test, it can be picked up as the children grow up stunted, under weight and with recurrent chest infections. That and there is a sweat test.
81
Appreciate the differing issues associated with the management of adult and paediatric patients with Cystic Fibrosis.
for early year segregating the kids to prevent cross infection, airway clearance and mucolytic are important alongside prophylactic antibiotics and vaccinations.
Usually as adults get older they will suffer from a chronic infection, then management then changes to supressing the bacterial load, treating exacerbations and reducing inflammation. Since there is continual decline of function, at some point palliative or lung transplant has to be considered. Often trying to treat the other symptoms is important as well as there are gastrointestinal issues, liver disease, diabetes, fertility issues and osteoporosis.
82
Appreciate the social, educational and economic impact of cystic fibrosis on the child and the family.
the educational part is important for understanding the reality, and the realistic outcomes that it is a life reducing disease, the chances of their children having it. The social part of segregation is important in order to avoid other individuals with cystic fibrosis to prevent cross infection, however a strong sense of social support is really important for the individual inflicted with cystic fibrosis. The economic impact can be tremendous if it wasn’t for the NHS.
83
Understand the role of transplantation.
the role of transplanting is as a last resort, it’s not curative but simply prolongs life and doesn’t prevent other effects of cystic fibrosis. It’s a risky procedure with only a limited supply of lungs available, social, health and psychological aspects have to be considered.
84
describe the public health duties of doctors managing cases of Tuberculosis.
the public health duty of the doctor is to identify the organism, attempt to cure or prevent further infection, notify the relevant authorities and to search out the source and other potentially infected people by conducting a heaf/tuberculin exposure test of tuberculoprotein. If positive, or older than the age of 16 further tests include a sputum smear, culture, chest radiograph, biopsy, CT and bronchoscopy. Another duty is to vaccinate people under the age of 16 against tb.
85
Describe the global distribution of tuberculosis and its impact on tuberculosis in the UK.
the global distribution of tuberculosis is that 2 billion people are infected with it, this does not necessarily mean that everyone presents with the disease. The areas of high prevalence is globally in south Africa and south east Asia, specifically areas with high HIV prevalence also have high TB rate. The issue is prevalent in areas off poverty, overcrowding and poor nutrition. This is a problem in areas of high migration, poverty and overcrowding in the u.k.
86
Describe the pathogenesis of tuberculosis in its primary, post-primary and fibrocaseous forms in the lung.
primary infection results from no prior exposure to tuberculosis, it spreads through the lymphatics of the hilar. It can spread to the other organs of the body or it can heal with or without a scar, remain latent or progress to tuberculous bronchopneumonia which has a poor prognosis with widespread tb and lobar collapse and cavitation.
post-primary infection can occur months or years after initial infection either due to changes in immunity, health or re-exposure the infection. The response is altered due to exposure but it can cause pulmonary disease, and essentially effect any tissue particularly the skeletal, brain and lungs.
fibrocaseous forms from the activated macrophages damaging epithelioid cells in an attempt to phagocytose the mycobacterium, the accumulation of macrophages, epithelioid and langhan’s cells forms granuloma which may form a central caseating necrosis due to the large volumes of lipids associated.
87
Describe the histopathology of tuberculosis
Tuberculosis is a slow growing non-motile aerobic mycobacterium, with a thick outer lipid filled membrane. Conventional stains don’t work on it since it is an alcohol and acid fast bacilli, instead a zheel neelsen stain is required, it will stand out as a blue curved rod in a stain. It’s very resistant to destruction by neutrophils and macrophages
88
Describe the common clinical presentations of tuberculosis.
the clinical presentation of tuberculosis is often a productive chest cough, sneezing, pleural effusion, shortness of breath, symptoms that resemble pneumonia. Often primary infection will present with fever, erythema nodosum and malaise. For post infection there may be haemoptysis, pleuritic pain, systematically unwell and night sweats. People at risk are poor social backgrounds, immunosuppressed, diabetes, prior tb. There are little signs but crackles, bronchial breathing and rarely finger clubbing.
89
Define the major groups of antituberculous drugs, their pharmacological profiles and side effects, and their practical application in the management of tuberculosis.
a multi drug therapy is used to prevent resistance. Firstly rifampicin(orange tears, induced liver enzyme, contraception ineffective, hepatitis), isoniazid(hepatitis and peripheral neuropathy), ethambutol(optic neuropathy) and pyrazinamide (gout) is used for two months, then rifampicin and isoniazid for 4 months.
90
For chronic asthma symptoms: know when to start asthma treatment
ICS should be started in using their reliever 3 or more times a week, waking up at night, exacerbations or symptomatic more than 3 times a week
91
For chronic asthma symptoms: know which treatment to start
doses of drugs, minimal systemic exposures. Through mainly inhalers of anti-muscarinics, beta 2 agonists, steroids. Relievers such as salbutomal and terbutaline SABA. As well as ICS for preventer. Often this can be escalated more by a specialist to oral steroids, leukotrienes, immunity suppressive drugs.
92
For chronic asthma symptoms: know when to escalate treatment
if still regularly using reliever, symptoms more than 3 times a week, increasing symptoms, PEF >50-70% predicted.
93
For acute asthma: know when to start treatment
if heart rate is greater than 110
inability to complete a sentence
PEF 33%-50%
respiratory rate greater than 25 a min
94
For acute asthma: know which treatment to start
may be given intravenously or through nebulisers if inhaler cannot be used. Things like beta 2 agonists, steroids, anti-muscarinic, leukotriene, theophylline’s, monoclonal ab’s, oxygen, magnesium.
ventilation, or chest drains may be required and intensive care.
not beta blockers, NSAIDS, aspirin, sedatives, opiates.
95
For acute asthma: know when to escalate treatment
if altered consciousness, exhausted, arrhythmia, hypotension, cyanosis, silent chest, raised PaCO2.
96
Know how to monitor (both acute and chronic) asthma
```
spirometry
peak flow
bronchodilator reversibility
allergy tests
exhaled NO
CXR
```
97
Appreciate that there is great uncertainty regarding treatment escalation in children with chronic asthma
for children there is the uncertainty that it may not be asthma. That also the side effects of beta 2 stimulants such as tremor, cramp, headaches, flushing, palpitations and angina can effect quality of life, and steroid exposure can stunt growth.
98
Understand the role of non-pharmacological interventions in chronic asthma
```
asthma action plan
weight loss
vaccines
allergen avoidance
physiotherapy
smoking cessation
bronchial thermoplasty
```
99
Describe the principles of management of inoperable, non- small cell lung cancer with radiotherapy and/or chemotherapy, the side effects of these treatments and their likely outcomes.
non-small cell lung cancer doubles every 129 days. Treatment depends on type, and the patients wishes. Often success will be determined by the patients wellbeing and performance. Stage 1 and 2 may be operated on with adjuvant chemotherapy or radiotherapy both pre and post operatively. Stage three will be treated with chemotherapy and 55Gy radiotherapy. Use of immunotherapy increasing and second line treatments are increasing.
100
Describe the principles of management of small cell lung cancer
small cell lung cancer doubles every 29 days, presentation is similar to other forms but secretes SIADH and ACTH resulting in confusion. It occurs around in 15% of patients. Straight to chemotherapy, with cisplatin and etoposide, ideally with early thoracic radiotherapy and prophylactic cranial radiation. Survival with treatment is 16 months, secondary therapy isn’t as effective with only a 2 year survival rate but returning.
101
describe the other treatment strategies which are important in the palliation of lung cancer.
systemic therapy removes symptoms and increases length of survival. Often chemo, immune or targeted radiotherapy used. 4 cycles of therapy are used in the U.K, with palliative care quality of life is very important especially with bone pain
102
Describe the investigation of restrictive lung disease and the approach to management of the common diseases (sarcoidosis, occupational lung disease, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis).
spirometry, a forced vital capacity less than 80% of normal. Then to find the cause CXR, history, pulmonary function, blood tests, urinalysis, ECG, TB and eye exam. Furthermore a bronchoscopy and ultrasound, or video assisted thoracoscopy lung biopsy. If caused by sarcoidosis, NSAIDS, topical steroids or systemic steroids depending on severity. If it is idiopathic pulmonary fibrosis then palliative care, oral anti-fibrotic drugs pirfenidone and nintedanib, or surgical lung transplant. if hypersensitivity pneumonia then remove cause of sensitivity, then depending on severity of fibrosis treatment could involve steroids of anti-fibrotic drugs.
103
Describe individual and population strategies to reduce smoking.
increasing taxes reduced rate of smoking. Main is the protection of children, selling only to over 18 year olds, not being allowed to smoke in private vehicles with kids, not being allowed to do proxy purchases or vending machines and standardised packaging. As well as limits on tar, carbon monoxide, bans on flavours, terms of mild and ultrasmooth and well as picture warnings and minimum packet sizes, banning of smoking in public and workplaces and regulation of tobacco sale
104
Describe epidemology of smoking.
the people most likely to be smoking are those permanently sick or disabled, unemployed and seeking work, or looking after the family/home. Likely to be younger, single, unskilled and lower educated.
105
Describe economics and politics of smoking.
77% of packet price goes to the tax man, earning close to £10 billion. Only 5000 people are employed by the tobacco industry in the U.K.
106
CURB 65 stands for
```
Confusion
Blood urea >7
Respiratory rate >30
Diastolic Blood pressure <60
age >65
```
107
Describe the clinical management of lower respiratory infection,particularly with regard to pneumonia.
with pneumonia it depends on the CURB score (confusion, blood urea >7, respiratory rate >30, diastolic blood pressure <60 and age >65). Score of 1 treat with amoxycillin or clarithromycin, 2 amoxycillin and clarithromycin, 3-5 Co-amoxiclav and clarithromycin. With further oxygen, I.V. fluids, CPAP, intubation and ventilation.
108
Be aware of the general approach to management of the rarer lung infections empyema.
the management of an empyema will include a chest drain and a long 6 week antibiotic treatment with intrapleural t-PA/DNase. If this doesn’t work surgery may be required.
109
Describe the common organisms leading to lower respiratory infection
strep pneumonia, H.influenza, legionella, staph aureus, mycoplasma pneumoniae, chlamydia psittaci and RSC, parainfluenza, influenza A, B and adenovirus.
110
Neurological conditions associated with respiratory muscle weakness. Presenting symptoms and signs of r espiratory muscle weakness.
breathlessness, orthopnea, ankle swelling, morning headache, recurrent chest infections, disturbed sleep. Look for paradoxical chest wall motion. Sleep apnoea presentation. Conditions associated with sleep apnoea. Consequences of untreated sleep apnoea. Management options. Other conditions causing excessive daytime sleepiness.
muscle relaxation, narrow pharynx and obesity may lead to closure of the upper airway causing snoring and oxygen desaturation resulting in frequent microarousals. It’s often a sign of hypertension, risk of stroke and heart disease and results in an impaired quality of life. Other conditions include narcolepsy, a familial condition treated using medication, chronic ventilatory failure caused by COPD, chest wall abnormalities, respiratory muscle weakness and central hypoventilation.
111
tidal volume
500ml
112
total lung volume
600ml
113
expiratory reserve volume
1100ml
114
residual volume
1200ml
115
inspiratory reserve volume
3000ml
116
anatomical dead space
150ml
117
vital capacity
4600ml
118
inspiratory capacity
3500 ml
119
functional residual capacity
2300ml
120
describe the pathological features of asthma and complications
for Asthma the main pathological feature is type 1 hypersensitivity due as a result of specific inappropriate response for IgE antibodies on mast cells, their degranulation upon exposure to the stimuli result in chemotactic factors triggering microthrombins , prostaglandins, histamine and lysosomal enzymes in a exaggerated inflammatory response. Spasmogens such as histamine also trigger an immediate response, these result in smooth muscle contraction along with the hypersensitivity result in chronic inflammation with the formation of mucus and plasma exudate and epithelial shedding obstruct airways.
121
Explain why COPD causes hypoxia
hypoxaemia results from COPD as a result of the ventilation/perfusion imbalance as a result of the loss of surface area, airway obstruction and reduced respiratory drive. As a result pulmonary arteriolar vasoconstriction occurs as a response to the alveolar oxygen tension falling as a form of a protective mechanism. As a result, hypertrophy can occur of the right ventricle due to the loss of capillary bed and secondary polycythaemia (haemocrit elevation).
122
describe the aetiology and pathogenesis of sarcoidosis,
sarcoidosis is a granulomatosis hypersensitivity reaction resulting In a chronic inflammatory response whilst it’s idiopathic as to the reason for it is unknown it can result in fibrosis. It can occur in other systems too.
123
describe the aetiology and pathogenesis of idiopathic pulmonary fibrosis.
usual interstitial pneumonitis, or idiopathic pulmonary fibrosis can be seen with connective tissue diseases, drug reaction, post infection or after industrial exposure and is the most likely cause of fibrosis, it is unknown however. The main pathology of it is that there is spots of various stages of inflammation throughout the lung close to the pleural surface.
124
describe the aetiology and pathogenesis of hypersensitivity pneumonitis
hypersensitivity pneumonitis is an inflammatory response to long term exposure to antigens, it can arise from exposure to mouldy hay, or bird fevers. There are many examples of this. It’s an example of type 3 and 4 hypersensitivity reactions normally restricted to the upper airways.
125
Describe the clinical features of bronchiectasis
bronchiectasis is the pathological dilation of bronchi in response to severe recurring infections, obstruction or lung parenchymal destruction. They often start in childhood and result in abundant foul smelling sputum as well as haemoptysis. It’s an antagonistic cycle of damage, dilation, poor mucous escalator resulting in more damage, more dilation etc.
126
Describe the clinical features of pneumonia
pneumonia often presents with malaise, fever, chest pain, cough, purulent sputum, dyspnoea. With signs of pyrexia, tachpnoea, central cyanosis, dullness on percussion, bronchial breathsounds, inspiratory crepitations and increased vocal resonance.
127
Describe the clinical features of empyema.
Empyema often presents with a swinging fever, chest pain and absent cough.
128
Describe the clinical features of lung abscess
symptoms of a lung abscess are non-specific with lethargy, weight loss and high swinging fever.
129
Describe the clinical features of bronchiectasis
Bronchiectasis presents with chronic cough, daily sputum productions, and sometimes a wheeze, dyspnoea, tiredness, flitting chest pain and haemoptysis, with finger clubbing and course inspiratory crepitations.
130
Describe the clinical features of acute bronchitis,
Bronchitis often presents with loose rattly cough and sometimes vomiting if a child and should last roughly for 16 days.
131
Investigations of respiratory muscle weakness and sleep apnoea
Assessment of hypoventilation through overnight oximetry and lung function as well as fluoroscopic screening of diaphragms. Often the treatment is oxygen therapy, and non-invasive ventilation
132
management of respiratory muscle weakness and sleep apnoea
Management involves weight reduction, avoidance of alcohol, diagnose endocrine disorders, positive airway pressure and mandibular repositioning splint. Consequences are that they may not be able to drive until treatment and their condition is deemed satisfactory.
133
treatment for lung abcesses
Treatment of a lung abscess involves prolonged antibiotics, drainage via the bronchial tree or percutaneous.
134
treatment for bronchiectasis
treatment of bronchiectasis involves chest physiotherapy, appropriate antibiotics and inhaled beta 2 agonist and inhaled corticosteroids.
135
symptoms of croup, Cause, management and duration
Croup – common, stridor, hoarse voice, barking cough. Self limiting condition and caused by para’flu 1 then treated with oral dexamethasone. Often lasts for a few days (3)
136
describe treatment for tonsilitis
Tonsillitis/pharyngitis - viral or bacterial, throat swab to test. If bacterial give 10 days’ penicillin not amoxycillin
137
management of EB glandular fever and expected recovery time
EB glandular fever – sore throat normally lasts for about 4/5 days on average, longer than a week is a cause for concern.
138
what is otitis media?
management
expected duration
otitis media – swollen, red bulging ear drum with absence of light reflex. Common, self-limiting condition, use analgesia instead of antibiotics. Ear aches commonly last for about 8 days.
139
describe Rhinitis and expected duration
Rhinitis – very common, self limiting. Red itchy watery eyes, sneezing, congestion, itchy throat. A normal Runny nose on average runs for about two weeks
140
Epiglottis
cause
symptoms
treatment
epiglottis – very dangerous, rare with stridor and drooling. Require antibiotics and intubation. Caused by h. influenza type B. swollen epiglottis can result in suffocation.
