Respiratory COPY

Question 1

what is FEV1? what is it like in healthy people?

Answer 1

• forced expiratory volume in 1 second
• in which a person takes a maximal inspiration and then exhales maximally as fast as possible. the important value is the fraction of the total “forced” vital capacity expired in 1 second
• healthy individuals can expire approximately 80% of the vital capacity in one second

Question 2

what is the procedure for measuring FEV1?

Answer 2

1. breath in to total lung capacity (TVC)
2. exhale as fast as possible until lungs emptied
3. total volume produced is the forced vital capacity (FVC)

Question 3

how does flow change with expiration?

Answer 3

flow is greatest at the start of expiration, it declines linearly with volume. FEF25 = flow at point when 25% of total volume to be exhaled has been exhaled

Question 4

what does FEV1 show AND
what are normal and abnormal values for FEV1?

Answer 4

• it’s a good overall assessment of lung health
• The result is compared with the predicted values,
  • if the FEV1 is 80% or greater than the predicted value = normal
  • if the FEV1 is less than 80% of the predicted value = low i.e abnormal

Question 5

what are the normal and abnormal values for FVC?
AND
What does a low FVC indicate

Answer 5

• less reproducible than FEV1
• the result is compared with the predicted values,
  
  • if the FVC is 80% or greater than the predicted value = normal
  • FVC is less than 80% of the predicted value = low i.e abnormal
• a low FVC = airway restriction

Question 6

what are features of type 1 respiratory failure? what is a common cause?

Answer 6

• pO2 (partial O2 pressure) is low
• pCO2 (partial CO2 pressure) is low or normal
• with type 1 = 1 change = low pO2 then normal/low CO2
• pulmonary embolism (form of ventilation-perfusion mismatch) most commonly causes Type 1
• also pulmonary oedema, pneumothorax + pneumonia

Question 7

what are features of type 2 respiratory failure? what is a common cause?

Answer 7

• pO2 is low
• pCO2 is high
• with type 2 = 2 changes = low pO2 + high pCO2
• alveolar hypoventilation causes Type 2
• e.g. COPD, asthma, motor neurone disease

Question 8

what are causes of respiratory failure?

Answer 8

• impaired ventilation (neural and mechanical problems)
• impaired perfusion, if extensive (cardiac failure or multiple PE)
• impaired gas exchange defects, if severe (emphysema or diffuse pulmonary fibrosis)
• hypoventilation (COPD, neuromuscular weakness, obesity, chest wall deformity, reduced drive)
• obstruction (asthma, COPD, OSA, pneumonia)
• diffusion (IPF, other ILDs, emphysema)
• perfusion (PE, cardiac failure, shunt, pulmonary hypertension)

Question 9

what are neural and mechanical problems which can lead to impaired ventilation which can cause respiratory failure?

Answer 9

• neural: narcotics, encephalitis, a cerebral space-occupying lesion, motor neurone disease (resulting in neuromuscular weakness)
• mechanical: airway obstruction, trauma, muscle disease and pleural effusion

Question 10

what are signs of hypercapnoea?

Answer 10

• bounding pulse
• flapping tremor
• confusion
• drowsiness
• reduced consciousness

Question 11

what is the FEV1/FVC and FEV1 and FVC like in obstructive respiratory disease?

Answer 11

• FEV1/FVC below 0.7

* FEV1 lower than FVC

Question 12

what are examples of obstructive respiratory disease? what are features of them?

Answer 12

• asthma: variable airflow obstruction and reversible
• COPD: relatively fixed airflow obstruction and may be a mixture of restrictive and obstructive disease
• bronchiectasis

Question 13

what is the FEV1/FVC and FEV1 and FVC like in restrictive respiratory disease?

Answer 13

• FEV1/FVC above 0.7
• FVC and FEV1 below 80% predicted value
• due to restriction, lung volumes are small and most of breath is out in first second

Question 14

what are examples of restrictive respiratory disease?

Answer 14

• sarcoidosis
• interstitial lung diseases
• obesity (OHS)
• scoliosis
• muscular dystrophy/ALS

Question 15

what is the transfer coefficient? how is it calculated?

Answer 15

• measure of ability of oxygen to diffuse across the alveolar membrane
• can calculate by inspiring a small amount of carbon monoxide, then hold breath for 10 seconds at total lung capacity, then the gas transferred is measured

Question 16

in what diseases is the transfer coefficient low?

Answer 16

• severe emphysema
• fibrosing alveolitis
• anaemia
• pulmonary hypertension
• idiopathic pulmonary fibrosis
• COPD

Question 17

in what diseases is the transfer coefficient high?

Answer 17

pulmonary haemorrhage

Question 18

what is COPD?

Answer 18

chronic obstructive pulmonary disease
• a disease state characterised by airflow limitation that is not fully reversible
• the airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

Question 19

what is COPD associated with the development of?

Answer 19

• chronic bronchitis: cough with sputum for 3 months for 2 or more years
• emphysema: histologically enlarged airspaces distal to terminal bronchioles, with destruction of alveolar walls

Question 20

what is the epidemiology of COPD?

Answer 20

• cigarette smoking is the major cause of COPD and is related to the daily average of cigarettes smoked and years spent smoking
• chronic exposure to substances
• alpha-1 antitrypsin deficiency
• patients are rarely symptomatic before middle-age

Question 21

chronic exposure to what things can lead to COPD?

Answer 21

• cigarette smoke
• occupational pollution
• outdoor air pollution
• inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas

Question 22

what is alpha-1 antitrypsin deficiency? what respiratory disease can it cause?

Answer 22

• causes early onset COPD (due to proteolytic lung damage)
• a rare cause of cirrhosis (due to accumulation of the abnormal protein in the liver)
• mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to reduced hepatic production of alpha-1 antitrypsin which normally inhibits the proteolytic enzyme, neutrophil elastase

Question 23

what is the pathophysiology of COPD?

Answer 23

• there are increased mucus-secreting goblet cells within the bronchial mucosa, especially in the larger bronchi
• in more advanced cases the bronchi become inflamed and pus is seen in the lumen
• chronic bronchitis
• emphysema

Question 24

what are features of chronic bronchitis in COPD?

Answer 24

• Chronic cough with sputum production
• Inflammation -> ciliary dysfunction, airway thickening and ↑ goblet cell size and number.
• ↑ goblet cell count -> mucous plugs -> narrowing of airways
• Must be present for most days for at least 3 months in 2 consecutive years.

Question 25

what are microscopic features of chronic bronchitis in COPD?

Answer 25

* microscopically there is infiltration of the bronchi and bronchioles with acute and chronic inflammatory cells * the epithelial becomes ulcerated and the squamous epithelium replaces the columnar cells (squamous metaplasia) when the ulcer heals

Question 26

what are features of inflammation in chronic bronchitis in COPD? what happens in early/late stages?

Answer 26

* the inflammation is followed by scarring and thickening of walls, narrowing the small airways * the small airways are affected early on, initially without breathlessness * the initial inflammation is reversible and accounts for the improvement if smoking is stopped early * in the later stages, the inflammation continues, even if smoking is stopped

Question 27

what are features of emphysema in COPD? what does it lead to?

Answer 27

* dilatation and destruction of the lung tissue distal to the terminal bronchioles * results in loss of elastic recoil, which normally keeps the airways open in expiration * leads to expiratory airflow limitation and air trapping * premature closure of airways limits expiratory flow while loss of alveoli decreases capacity for gas transfer

Question 28

what are features of centriacinar emphysema?

Answer 28

* distension and damage is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend are well preserved * extremely common

Question 29

what are features of panacinar emphysema?

Answer 29

* less common * distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae * associated with alpha-1 antitrypsin deficiency

Question 30

what are features of irregular emphysema?

Answer 30

scarring and damage that affects the lung parenchyma | patchily, independent of acinar structure

Question 31

what is V/Q (ventilation perfusion) and PaCO2 like in COPD?

Answer 31

- partly due to damage and mucus plugging of smaller airways from the chronic inflammation and rapid closure of smaller airways in expiration leading to loss of elastic support; this leads to a fall in PaO2 and increased work or respiration - CO2 excretion is less affected by V/Q mismatch and many patients have low-normal PaCO2 values due to increasing alveolar ventilation in an attempt to correct their hypoxia - other patients fail to maintain their respiratory effort and then their PaCO2 levels increase - in the short term, this rise in CO2 leads to stimulation of respiration, but in the longer term, these patients become insensitive to CO2 and come to depend on the hypoxaemia to drive ventilation

Question 32

what is the pathogenesis of cigarette smoke causing COPD?

Answer 32

- causes mucus gland hypertrophy in the larger airways and increased neutrophils, macrophages and lymphocytes in the airways, bronchi and bronchioles - inflammatory mediators (elastases, proteases, IL-1,-8 and TNF-alpha) are released and attract inflammatory cells, induce structural changes and break down connective tissue (protease-antiprotease imbalance) in the lung resulting in emphysema - inactivates alpha-1 antitrypsin

Question 33

what are symptoms of COPD?

Answer 33

- characteristic symptoms are productive cough with white or clear sputum, wheeze and breathlessness, usually following many years of a smokers cough - colds seem to settle on the chest and frequent infective exacerbations occur, with purulent sputum - symptoms can be worsened by cold or damp weather and atmospheric pollution

Question 34

what are systemic effects of COPD?

Answer 34

* hypertension * osteoporosis * depression * weight loss * reduced muscle mass with general weakness

Question 35

what is the seen on examination of COPD?

Answer 35

- breathless at rest, prolonged expiration, poor chest expansion, hyperinflated lungs (barrel chest) - pursed lips on expiration help to prevent alveolar and airway collapse

Question 36

what are complications of COPD?

Answer 36

- later stages are characterised by the development of respiratory failure: • PaO2 less than 8kPa (60mmHg) or • PaCO2 greater than 7kPa (53mmHg) - those with advanced disease may develop pulmonary hypertension (fluid retention, peripheral oedema, central cyanosis, breathlessness)

Question 37

what are differential diagnoses of COPD?

Answer 37

asthma, congestive heart failure, bronchiectasis, allergic fibrosing alveolitis, pneumoconiosis and asbestosis

Question 38

what is used to diagnose COPD?

Answer 38

- based on a history of breathlessness and sputum production in a chronic smoker - in the absence of a history of cigarette smoking then asthma is a more likely explanation, unless there is a family history suggesting alpha-1 antitrypsin deficiency - lung function test - CXR - high resolution CT scans used to show emphysematous bullae - haemoglobin and packed cell volume may be high due to persistent hypoxaemia and secondary polycythaemia - arterial blood gases may be normal or show hypoxia with/without hypercapnia in advanced cases - ECG is often normal - alpha-1 antitrypsin levels and genotypes

Question 39

what does a lung function test show in COPD? what is the FEV1/FVC and FEV like?

Answer 39

* shows progressive airflow limitation with increasing severity and breathlessness * FEV less than 80% predicted value * FEV1/FVC less than 0.7 - airway obstruction * multiple peak flow measurements may be necessary to exclude asthma

Question 40

what is stage 1 COPD?

Answer 40

FEV1 less than 80% of predicted value

Question 41

what is stage 2 COPD?

Answer 41

FEV1 50-79%

Question 42

what is stage 3 COPD?

Answer 42

FEV1 30-49%

Question 43

what is stage 4 COPD?

Answer 43

FEV1 less than 30% of predicted value

Question 44

what can be seen on a CXR in COPD?

Answer 44

* may be normal or show evidence of hyper-inflated lungs indicated by low, flattened diaphragms and a long narrow heart shadow * there may be reduced peripheral lung markings and bullae (complete destruction of lung tissue producing an airspace greater than 1cm)

Question 45

what is treatment of COPD?

Answer 45

- smoking cessation - bronchodilators - corticosteroids - prevention of infection (pneumococcal vaccination, influenza vaccine, antibiotics for exacerbations) - oxygen therapy - antimucolytic agents reduce sputum viscosity - diuretics to treat oedema - pulmonary rehabilitation - good diet to reduce weight - alpha-1 antitrypsin replacement

Question 46

how are bronchodilators used to treat COPD?

Answer 46

* inhaled (with spacer device if necessary) tiotropium bromide (a LAMA) used as an initial therapy with a rescue SABA e.g. salbutamol or terbutaline to prevent/reduce acute symptoms * a LABA e.g. formoterol or salmeterol is added in patients with persistent dyspnoea (difficulty breathing)

Question 47

how are corticosteroids used to treat COPD?

Answer 47

* prednisolone daily for two weeks should be given with measurements of lung function before and after the treatment * if there is an increase in FEV by more than 15% then discontinue prednisolone and move to inhaled corticosteroid e.g. beclometasone twice daily

Question 48

how is oxygen therapy used to treat COPD? how much is given?

Answer 48

* long term domiciliary oxygen therapy has survival benefits * prescribed to patients who no longer smoke * oxygen is given 19 hours per day every day via nasal prongs to increase arterial oxygen saturations to more than 90%

Question 49

what is the epidemiology of asthma?

Answer 49

- commonly starts in childhood between the ages 3-5 years and may either worsen or improve during adolescence - peak prevalence between 5-15 years - more common in developed countries

Question 50

what are the three characteristics of asthma?

Answer 50

* airflow limitation; usually reversible spontaneously or with treatment * airway hyper-responsivenes * bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage

Question 51

what are the two main types of asthma? what are causes of them?

Answer 51

``` • allergic/eosinophilic asthma (70%): - allergens and atopy - childhood asthma often accompanied by eczema • non-allergic/non-eosinophilic (30%): - exercise, cold air and stress - smoking and non-smoking associated - obesity associated - starts in middle-age ```

Question 52

what are genetic factors that may lead to asthma?

Answer 52

* genes controlling the production of cytokines IL-3,-4,-5,-9,-13 * ADAM33 is associated with airway hyper-responsiveness and tissue remodelling

Question 53

what are environmental factors that may lead to asthma?

Answer 53

* early childhood exposure to allergens and maternal smoking * growing up in a ‘clean’ environment may predispose towards an IgE response to allergens whereas growing up in a ‘dirtier’ environment may allow the immune system to avoid developing allergic responses

Question 54

what are risk factors for asthma?

Answer 54

- personal history of atopy - family history of asthma or atopy - obesity - inner-city environment - premature birth - socio-economic deprivation

Question 55

what are precipitating factors for asthma?

Answer 55

* occupational sensitisers such as wood dust, bleaches and dyes, isocyanates (industrial coating and spray painting) and latex * cold air and exercise * atmospheric pollution and irritant dusts * diet; more fruit and veg is protective * emotion * drugs such as NSAIDs can trigger attacks, also beta-blockers result in bronchoconstriction, leading to airflow limitation and potential attack * allergen-induced asthma

Question 56

what is the primary abnormality in asthma?

Answer 56

primary abnormality in asthma is narrowing of the airway which is due to smooth muscle contraction, thickening of the airway wall by cellular infiltration and inflammation and the presence of secretions within the airway lumen

Question 57

what do mast cells release in asthma?

Answer 57

• histamine results in bronchoconstriction (via H1 receptor) and inflammation • tryptase • prostaglandin2 • cysteine leukotrienes result in bronchoconstriction and inflammation • TNF-alpha, IL-3 (increases number of mast cells), -4 (causes IgE synthesis) and -5; result in inflammation and airway remodelling • all act on smooth muscle, small blood vessels, mucus-secreting cells and sensory nerves cause the immediate asthmatic reaction

Question 58

what do eosinophils do in asthma?

Answer 58

- found in large numbers in the bronchial wall and secretions - attracted to the airway by IL-3 and IL-5, they also prime eosinophils for enhance mediator secretion - when activated, eosinophils release LTC4 and major basic protein, eosinophilic cationic protein and eosinophilic peroxidase these are toxic to epithelial cells - both the number and activation of eosinophils are rapidly decreased by corticosteroids

Question 59

what do dendritic cells and lymphocytes do in asthma?

Answer 59

- abundant in mucous membranes of the airways and the alveoli - dendritic cells play a role in the initial uptake and presentation of allergens to lymphocytes - T helper lymphocytes activate and release cytokines

Question 60

what are the changes in the lung 30 minutes after allergen challenge in asthma?

Answer 60

there is bronchoconstriction

Question 61

what are the changes in the lung 3 hours after allergen challenge in asthma?

Answer 61

the initial bronchoconstriction decreases, then inflammation occurs due to the vasodilation which decreases blood flow and leads to a build up of white blood cells, increased vascular permeability and unregulated adhesion molecules

Question 62

what are the changes in the lung 6 hours after allergen challenge in asthma?

Answer 62

there is worsening inflammation resulting in eosinophils (attracted to site by IL-5) releasing their mediators that result in a second wave of bronchoconstriction

Question 63

what is the pathophysiology of remodelling in asthma?

Answer 63

* airway smooth muscle undergoes hypertrophy and hyperplasia leading to a larger fraction of the wall being occupied by smooth muscle tissue * the airway wall is thickened by the deposition of repair collagens and matrix proteins below the basement membrane * deposition of matrix proteins, swelling and cellular infiltration expand the submucosa beneath the epithelium so that, for a given degree of smooth muscle shortening there is excess airway narrowing * swelling outside the smooth muscle layer reduces the retractile forces exerted by the surrounding alveoli so the airways close more easily * the epithelium is stressed and damaged with loss of ciliated columnar cells * increase in number of mucus-secreting goblet cells * damage to the epithelium makes it more vulnerable to infection by common respiratory viruses and pollution

Question 64

what is the clinical presentation of asthma?

Answer 64

- intermittent dysponea - wheeze - cough (especially nocturnal); frequent symptom in children - sputum - symptoms worse at night - episodic shortness of breath - provoking factors: allergens, infections, menstrual cycle, exercise, cold air

Question 65

what is the clinical presentation of asthma during an attack?

Answer 65

* there is reduced chest expansion * prolonged expiratory time * bilateral expiratory polyphonic wheezes * tachypnoea

Question 66

what is the clinical presentation of uncontrolled asthma?

Answer 66

* PEFR less than 50% * respiratory rate less than 25 * pulse less than 110 * normal speech

Question 67

what is the clinical presentation of a severe asthma attack?

Answer 67

* inability to complete sentences * pulse greater than 110bpm * respiratory rate greater than 25/min

Question 68

what is the clinical presentation of a life threatening asthma attack?

Answer 68

* silent chest * confusion and exhaustion * cyanosis (PaO2 less than 8kPa) * bradycardia * PEFR less than 33%

Question 69

what is the immediate treatment of an asthma attack?

Answer 69

* oxygen therapy to maintain O2 sat (94%-98%) * nebulised 5mg salbutamol (+ ipratropium if life threatening) * prednisolone (with/without hydrocortisone IV) * take ABGs and repeat within 2 hours if severe attack or patient deteriorating * CXR if no response to treatment * check PEFR within 15-30 mins/regularly * oximetry to ensure SaO2 is greater than 92%

Question 70

what are differential diagnoses of asthma?

Answer 70

pulmonary oedema, COPD (may co-exist), large airway obstruction caused by foreign body/tumour, pneumothorax, bronchiectasis

Question 71

what is used to diagnose asthma?

Answer 71

- RCP3 questions (nocturnal waking, usual symptoms, interference with ADLs) - asthma control test - lung function tests (PEFR, spirometry, CO test) - exercise tests - trial of corticosteroids - exhaled nitric oxide (measures eosinophilic inflammation and corticosteroid response) - blood and sputum tests (eosinophilia) - skin prick tests to help identify allergic trigger factors - history

Question 72

how is asthma control test used to diagnose asthma? what are the results?

Answer 72

* 25: well controlled * 20-24: on target * less than 20: off target

Question 73

how is peak expiratory flow rate used to diagnose asthma?

Answer 73

measurement on waking, prior to taking a bronchodilator and before bed, after a bronchodilator - asthma is diagnosed by demonstrating a greater than 15% improvement in FEV1 or PEFR following the inhalation of a bronchodilator

Question 74

how is asthma distinguished from COPD?

Answer 74

* COPD is a later disease more dominantly of smokers * more of a relentless progressive dyspnoea with wheeze * less day-day variation * winter symptoms and sputum production in COPD * overlap can occur

Question 75

what are the aims of treatment of asthma?

Answer 75

* abolish symptoms * restore normal or best possible lung function * reduce risk of severe attacks * enable normal growth to occur in children * minimise absence from school or employment * avoidance of identified causes if possible * use of lowest effective doses of medication to minimise side effects

Question 76

what is used to treat asthma?

Answer 76

- control of extrinsic factors when specific allergen triggers are identified - bronchodilators - anti-inflammatory steroids - other agents with bronchodilator activity - steroid-sparing agents

Question 77

what are some types of bronchodilators used to treat asthma?

Answer 77

- beta2-agonists - muscarinic antagonists - methylxanthines

Question 78

what are features of beta2-agonists used to treat asthma?

Answer 78

- are beta-2 selective i.e. work only in lungs, however in high doses the B2-agonists are not selective and will act on other receptors - lead to bronchodilation - beta-agonists also inhibit mast cell activity thereby reducing inflammatory response - at high concentrations e.g. in badly controlled asthmatics a tolerance may develop due to B2-receptor desensitisation

Question 79

what short acting beta agonists are used to treat asthma? how long do they act for?

Answer 79

- salbutamol (partial agonist) - terbutaline - 4 hours - prescribed as two puffs as required

Question 80

what long acting beta agonists are used to treat asthma? how long do they act for?

Answer 80

- salmeterol - formoterol (full agonist) - 12 hours - longer acting since there are more lipophilic so they remain in the tissue for longer

Question 81

what short and long acting muscarinic antagonists are used to treat asthma?

Answer 81

- short-acting e.g. ipratropium | - long acting e.g. tiotropium - has high affinity and disassociates slowly from muscarinic receptors

Question 82

what is the mechanism of action of muscarinic antagonists? how are they used to treat asthma?

Answer 82

- act on airway M3 receptors - normally ACh (parasympathetic) binds to M3 receptor bound to Gq protein resulting in phospholipase C converting phosphate to DAG resulting in protein kinase C production resulting in smooth muscle contraction - muscarinic antagonists prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action

Question 83

what is the mechanism of action of methylxanthines? how are they used to treat asthma?

Answer 83

these are phosphodiesterase inhibitors; prevent the conversion of cyclic-AMP to 5’-AMP resulting in a build up of cyclic-AMP and thus increased smooth muscle relaxation

Question 84

what are examples of methylxanthines used to treat asthma?

Answer 84

theophylline (non-selective so has wide range of side effects e.g. CVS, CNS and GI tract) and aminophylline

Question 85

what are features of inhaled corticosteroids used to treat asthma? what are the different types of corticosteroids?

Answer 85

- all patients who have regular persistent symptoms need regular treatment with inhaled corticosteroids - there are two types of corticosteroids; mineralocorticoids and glucocorticoids - hydrocortisone has anti-inflammatory properties but also has significant mineralocorticoid action so is not suitable as a treatment - instead, semi-synthetic glucocorticoids that have reduced or no mineralocorticoid action and improved anti-inflammatory effects are used

Question 86

what are examples of inhaled corticosteroids used in asthma?

Answer 86

* prednisolone * beclomatasone * budesonide

Question 87

what is the effect of glucocorticoids on genes?

Answer 87

- glucocorticoids interfere with gene transcription - glucocorticoid receptor is found on the promoter region of DNA and has zinc fingers that anchor receptor to DNA and recognise discrete sequences - there is either a + glucocorticoid response element which increases transcription or -GRE response, which decreases transcription

Question 88

what is a +GRE response?

Answer 88

+GRE results in increased lipocortin which inhibits PLA2 meaning there is a decrease in arachidonic acid and thus a decrease in prostaglandins and leukotrienes resulting in reduced inflammation and thus reducing symptoms

Question 89

what is a -GRE response?

Answer 89

-GRE results in the suppression of cytokines e.g. TNF, IL-5 and IL-3 thereby reducing inflammation and thus reducing symptoms

Question 90

what are side effects of inhaled corticosteroids in asthma?

Answer 90

* susceptibility to infection due to cytokine suppression | * metabolic such as osteoporosis and muscle wasting

Question 91

what are other agents with bronchodilator activity that are used to treat asthma? what are some examples?

Answer 91

* leukotriene receptor antagonist e.g. montelukast | * oral corticosteroids needed for those not controlled on inhaled corticosteroids

Question 92

what are examples of steroid-sparing agents that are used to treat asthma?

Answer 92

* methotrexate * ciclosporin * IV immunoglobulin * anti-IgE monoclonal antibody (omalizumab)

Question 93

what is the guideline medication regime for asthma?

Answer 93

* SABA * SABA + ICS * SABA + LABA + ICS * SABA + LABA + ICS + 4th drug e.g. anti-IgE monoclonal etc. (severe)

Question 94

what is the PEFR and treatment of step 1 (occasional symptoms, less frequent than daily) asthma?

Answer 94

- 100% predicted - as-required SABAs - if used more than once daily, move to step 2

Question 95

what is the PEFR and treatment of step 2 (daily symptoms) asthma?

Answer 95

- <80% predicted regular inhaled preventer therapy: - anti-inflammatory drugs; inhaled low-dose corticosteroids up to 800ug daily - leukotriene receptor antagonists, theophylline and sodium cromoglycate are less effective - if not controlled, move to step 3

Question 96

what is the PEFR and treatment of step 3 (severe symptoms) asthma?

Answer 96

- 50-80% predicted inhaled corticosteroids and long-acting inhaled beta-2 agonist: - continue inhaled corticosteroid - add regular inhaled LABA - if still not controlled, add either LTBA, modified release oral theophylline or beta-2 agonist - if not controlled, move to step 4

Question 97

what is the PEFR and treatment of step 4 (severe symptoms uncontrolled with high-dose inhaled corticosteroids)?

Answer 97

- 50-80% predicted high dose inhaled corticosteroids and regular bronchodilators: - increase high-dose inhaled corticosteroids up to 2000ug daily - plus regular LABAs - plus either LTRA or modified release theophylline or beta2-agonist

Question 98

what is the PEFR and treatment of step 5 (severe symptoms deteriorating) asthma?

Answer 98

<50% predicted regular oral corticosteroids - add prednisolone 40mg daily to step 4

Question 99

what is the PEFR and treatment of step 6 (severe symptoms deteriorating in spite of prednisolone) asthma?

Answer 99

<30% predicted hospital admission

Question 100

what is hypersensitivity pneumonitis/extrinsic allergic alveolitis?

Answer 100

* previously called extrinsic allergic alveolitis * type of ILD; distinct cellular infiltrates and extracellular matrix deposition in lung distal to the terminal bronchiole i.e. diseases of the alveolar/capillary interface

Question 101

what are interstitial lung diseases?

Answer 101

ILDs are a group of lung diseases affecting the lung interstitium (the tissue and space around the air sacs of the lungs)

Question 102

what is the epidemiology of hypersensitivity pneumonitis?

Answer 102

- usually a disease of adults - caused by an allergic reaction affecting the small airways and alveoli in response to an inhaled antigen or the ingestion of a causative drug - there is diffuse, granulomatous inflammation of the lung parenchyma and airways in people who have been sensitised by repeated inhalation of organic antigens in dust - there are acute, subacute and chronic forms - acute and subacute forms cause a recurrent pneumonitis - chronic disease can cause fibrosis, emphysema and permanent lung damage - one of the most common causes worldwide is farmer’s lung - associated with many jobs and hobbies

Question 103

what jobs and hobbies is hypersensitivity pneumonia associated with?

Answer 103

* farmers lung; due to exposure to mouldy hay, Micropolyspora faeni and Aspergillus umbrosus * bird/pigeon fanciers lung; due to exposure to avian proteins in droppings * cheese-workers lung; due to exposure to mouldy cheese, Penicillium casei * malt-workers lung; due to exposure to mould malt, Aspergillus clavatus * humidifier fever; due to contaminated humidifying systems in air conditioners or humidifier in factories (especially in printing works), variety of bacteria

Question 104

what are risk factors for hypersensitivity pneumonitis?

Answer 104

- pre-existing lung disease - specific occupations including farmers, cattle workers, ventilation system workers, vets and those jobs that involve working with chemicals - bird keeping - regular use of hot tubs

Question 105

what is the pathophysiology of hypersensitivity pneumonitis?

Answer 105

- the allergic response to the inhaled antigen involves both cellular immunity and the deposition of immune complexes (type 3 hypersensitivity reaction) resulting in inflammation through the activation of complement via the classical pathway - some of the inhaled antigen may lead to inflammation by directly activating the alternate complement pathway - these mechanisms attract and activate alveolar and interstitial macrophages so that continued exposure results in pulmonary fibrosis

Question 106

what happens in the acute phase of hypersensitivity pneumonitis?

Answer 106

the alveoli are infiltrated with acute inflammatory cells

Question 107

what happens in the chronic phase of hypersensitivity pneumonitis?

Answer 107

granuloma formation and obliterative bronchiolitis

Question 108

what is the pathophsyiology of farmers lung in hypersensitivity pneumonitis?

Answer 108

• fungus in mouldy hay is inhaled • if individual is already sensitised to the organism, a type III immune complex hypersensitivity reaction follows • clinically there is acute dyspnoea and cough a few hours after inhalation of the antigen • one of the earliest features is bronchiolitis • later, chronic inflammatory cells are seen in the interstitium together with non-caseating granulomas • may resolve on antigen withdrawal but if there is chronic exposure then pulmonary fibrosis develops

Question 109

what is the clinical presentation of acute (4-6hours post exposure) hypersensitivity pneumonitis?

Answer 109

* fever * rigors * myalgia * dry cough * dyspnoea * crackles (no wheeze) * chest-tightness * patients may be mistakenly diagnosed with a chest infection * symptoms related to level of exposure

Question 110

what is the clinical presentation of subacute hypersensitivity pneumonitis?

Answer 110

* occurs with intermittent or lower-level exposure * history or repeated acute attacks * signs same as acute, symptoms less severe and more gradual onset * can be present as recurrent pneumonia * improvement is seen in weeks to months following removal from exposure

Question 111

what is the clinical presentation of chronic hypersensitivity pneumonitis?

Answer 111

* usually no history of preceding acute symptoms * if the source of antigen is removed only partial improvement of symptoms * cyanosis and clubbing may develop * weight loss * increasing dyspnoea * type 1 respiratory failure

Question 112

what are differential diagnoses of hypersensitivity pneumonitis?

Answer 112

infection, connective tissue disorders causing ILDs, pulmonary fibrosis, asthma, drug-induced ILD

Question 113

what is used to diagnose hypersensitivity pneumonitis?

Answer 113

- CXR - FBC (raised WCC, increased ESR) - lung function test (reversible restrictive defect, reduced gas transfer during acute attacks) - bronchoalveolar lavage (analysis of lymphocyte cound and CD4/CD8 ratio)

Question 114

what is seen on CXR in hypersensitivity pneumonitis?

Answer 114

* fibrotic shadow in upper zone of lung (upper zone mottling/consolidation) * diffuse small nodules and increased reticular shadowing may be present but not specific

Question 115

what is the treatment of acute hypersensitivity pneumonitis?

Answer 115

* remove allergen * give O2 (35-60%) * oral prednisolone followed by reducing dose

Question 116

what is the treatment of chronic hypersensitivity pneumonitis?

Answer 116

* avoid exposure to allergen * long term steroids can achieve chest x-ray and physiological improvement * corticosteroids

Question 117

what are types of occupational lung disorders? what can they each be caused by?

Answer 117

- acute bronchitis and oedema from irritants such as sulphur dioxide, chlorine, ammonia or nitrogen oxides - pulmonary fibrosis from inhalation of inorganic dust e.g. coal, silica, asbestos, iron and tin - occupational asthma - hypersensitivity pneumonitis - bronchial carcinoma due to asbestos, polycyclic hydrocarbons and radon in mines

Question 118

what is pneumoconiosis?

Answer 118

pneumoconiosis means the accumulation of dust in the lungs and the reaction of the tissue to its presence

Question 119

what is the epidemiology of coal-workers pneumoconiosis? what is the pathophysiology?

Answer 119

- common dust disease in countries that have or have had coal-mines - caused by the inhalation of coal dust particles over 15-20yrs - these particles are ingested by alveolar macrophages in the small airways and alveoli which then die, releasing enzymes and causing fibrosis

Question 120

what is the diagnosis of simple pneumoconiosis?

Answer 120

- produces fine micro nodular shadowing in the chest x-ray | - graded on CXR

Question 121

what can simple pneumoconiosis progress to?

Answer 121

- can progress to the development of progressive massive fibrosis - this almost never occurs in mild pneumoconiosis but risk increases with more severe simple pneumoconiosis

Question 122

what is the pathophysiology of progressive massive fibrosis?

Answer 122

- patients develop round fibrotic masses mostly situated in the upper lobes sometimes with necrotic central cavities - rheumatoid factor and anti-nuclear antibodies are both often present in the serum of patients with PMF and also in those suffering from asbestosis or silicosis - there is apical destruction and disruption of the lung resulting in emphysema and airway damage

Question 123

what is the clinical presentation of progressive massive fibrosis?

Answer 123

- due to progression of coal workers pneumoconiosis - sufferers have considerable effort dyspnoea and fibrosis - sputum may be black

Question 124

what is the diagnosis of progressive massive fibrosis?

Answer 124

- seen on CXR with upper-zone fibrotic masses - rheumatoid factor and anti-nuclear antibodies are both often present in the serum of patients with PMF and also in those suffering from asbestosis or silicosis - lung function tests show a mixed restrictive and obstructive ventilatory defect with loss of lung volume, irreversible airflow limitation and reduced gas transfer

Question 125

what is the treatment/progression of progressive massive fibrosis?

Answer 125

- manage by avoiding coal dust exposure and claim compensation - disease can progress or develop even after coal exposure has ceased and may lead to respiratory failure

Question 126

where is silicosis seen? what is it caused by? what is its pathogenesis?

Answer 126

- uncommon but seen in stonemasons, sand-blasters, pottery and ceramic workers and foundry workers involved in fettling - caused by the inhalation of silica dioxide which is very fibrogenic - silica is particularly toxic to alveolar macrophages and readily initiates fibrogenesis

Question 127

what is seen on CXR and spirometry in silicosis?

Answer 127

- CXR appearance show diffuse nodular pattern in upper and mid-zone and thin streaks of calcification (egg-shell calcification) of the hilar nodes - spirometry shows a restrictive ventilatory defect

Question 128

what is the clinical presentation of silicosis?

Answer 128

patients have progressive dyspnoea and an increased incidence of TB

Question 129

what is the treatment of silicosis?

Answer 129

manage by avoiding exposure to silica and claim compensation

Question 130

where has asbestos been used? why?

Answer 130

has widely been used in roofing, insulation and fireproofing due to its resistance to heat, acid and alkali

Question 131

what are types of asbestos?

Answer 131

- chrysolite (white asbestos, 90%; least fibrogenic) - crocidolite (blue asbestos, 6%; most fibrogenic and most likely to cause asbestosis and mesothelioma) - amosite (brown asbestos, 4%; least common, intermediate fibrogenicity)

Question 132

is crocidolite (white asbestos) easily inhaled or not? why/why not? what are features of it?

Answer 132

crocidolite is easily inhaled due to its thin long shape but also easily trapped in the lungs, its also resistant to macrophage and neutrophil enzymatic destruction

Question 133

what is asbestosis? what is its pathophysiology?

Answer 133

- type of ILD; distinct cellular infiltrates and extracellular matrix deposition in lung distal to the terminal bronchiole - fibrosis of the lungs caused by asbestos dust, which may or may not be associated with fibrosis of the parietal or visceral layers of the pleura - significant time lag between exposure and development of disease, particularly mesothelioma (20-40 years)

Question 134

what is the clinical presentation of asbestosis?

Answer 134

* progressive disease characterised by breathlessness and progressive dyspnoea and accompanied by finger clubbing and bilateral basal end-inspiratory crackles * also causes pleural plaques and increases risk of mesothelioma and bronchial adenocarcinoma

Question 135

what is the treatment of asbestosis?

Answer 135

only symptomatic management is known e.g. corticosteroids

Question 136

what is byssinosis?

Answer 136

- an occupational lung disease caused by exposure to cotton dust in inadequately ventilated working environments - commonly occurs in workers who are employed in yarn and fabric manufacture industries - occurs worldwide but is declining particularly in areas where the number of people employed in cotton mills is falling

Question 137

what is the clinical presentation of byssinosis?

Answer 137

* symptoms occur on the first day back at work after a break with improvement as the week progresses * chest tightness, cough and breathlessness occur within the first hour in dusty areas of the cotton mill * those with asthma are affected badly by the cotton dust

Question 138

what is the diagnosis of byssinosis?

Answer 138

there are no changes on CXR and aetiology/nature of disease is unknown

Question 139

what is berylliosis?

Answer 139

chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds; a form of beryllium poisoning

Question 140

what is beryllium? where is it used?

Answer 140

* beryllium is a copper alloy with high tensile strengths and resistance to high temperature and corrosion * widely used in the aerospace industry, atomic reactors and many electrical devices

Question 141

what is the clinical presentation of berylliosis?

Answer 141

* when beryllium is inhaled it can cause a systemic illness with a clinical picture similar to sarcoidosis * progressive dyspnoea with pulmonary fibrosis * rare

Question 142

what is bronchiectasis? what does it result from?

Answer 142

• chronic infection of the bronchi and bronchioles leading to permanent dilatation of these airways • results from pulmonary inflammation and scarring due to infection, bronchial obstruction or lung fibrosis - the resulting scarring causes airway distortion and dilatation with further inflammation in the wall of the damaged airway due to secondary infection

Question 143

what is the epidemiology of bronchiectasis? what triggers it?

Answer 143

- more common in women than men - may develop after lung infections - it is the pathological end point of many diseases - present at any age but increases with age

Question 144

what lung insults can cause bronchiectasis?

Answer 144

- post infection (most common) - congenital - mechanical bronchial wall obstruction (foreign body, post-TB stenosis, lymphnodes/tumour) - allergic bronchopulmonary aspergillosis - HIV - ulcerative colitis - hypogammaglobulinaemia - rheumatoid arthritis

Question 145

what can cause post infection bronchiectasis?

Answer 145

- previous pneumonia - granulomatous disease e.g. TB - measles, whooping cough - allergic bronchopulmonary aspergillosis - pertussis - bronchiolitis

Question 146

what can cause congenital bronchiectasis?

Answer 146

- cystic fibrosis - deficiency of bronchial was elements - primary ciliary dyskinesia (Kartagener’s syndrome)

Question 147

what is the pathophysiology of bronchiectasis?

Answer 147

- failure of mucociliary clearance and impaired immune function contribute to continued insult to bronchial wall, through the recruitment of inflammatory cells and uncontrolled neutrophilic inflammation; bronchitis → bronchiectasis → fibrosis - airways dilate due to pulmonary inflammation and scarring, as fibrosis contracts - secondary inflammation changes lead to further destruction of airways

Question 148

what is the clinical presentation of bronchiectasis?

Answer 148

- usually the lower lobes are affected - chronic cough with production of copious amounts of foul smelling purulent sputum (khaki coloured) with intermittent haemoptysis - dyspnoea - finger clubbing especially in cystic fibrosis - wheeze - infection usually characterised by increased sputum volume and increased purulence - chest pain - recurrent exacerbations with long recovery time

Question 149

what are differential diagnoses of bronchiectasis?

Answer 149

COPD, asthma, TB, chronic sinusitis, cough due to acid reflux, pneumonia, pulmonary fibrosis, cancer, inhalation of foreign body

Question 150

what is used to diagnose bronchiectasis?

Answer 150

- CXR - sputum culture (bacterial colonisation) - high resolution CT - spirometry (obstructive pattern) - sinus X-rays (may have rhinosinusitis) - sweat test for all patients under 40, if cystic fibrosis suspected (will see high chloride concentration if CF) - bronchoscopy to locate site of haemoptysis, exclude obstruction and obtain culture samples - immunology e.g. total IgE to exclude bronchopulmonary aspergillosis

Question 151

what is seen on CXR in bronchiectasis?

Answer 151

* dilated bronchi with thickened walls (tramline and ring shadows) * multiple cysts containing fluid showing up as cystic shadows

Question 152

what major pathogens are seen in bronchiectasis?

Answer 152

- Haemophilus influenza - Streptococcus pneumoniae - Staphylococcus aureus - Pseudomonas aeruginosa

Question 153

what is seen on high resolution CT in bronchiectasis?

Answer 153

* thickened, dilated bronchi with cysts at the end of bronchioles * airways larger than associated blood vessels

Question 154

what is used to treat bronchiectasis?

Answer 154

- improved mucus clearance (postural drainage, chest physio, mucolytics) - antibiotics - bronchodilators such as nebulised salbutamol is useful for asthma or COPD sufferers - anti-inflammatory agents e.g. long term azithromycin can reduce exacerbation frequency - surgery in localised disease or to control severe haemoptysis

Question 155

what antibiotics are used to treat bronchiectasis?

Answer 155

* treatment of exacerbations usually lasts 2 weeks * if pseudomonas aeruginosa then high dose oral ciprofloxacin twice daily * Haemophilus influenzae responds to oral amoxicillin, co-amoxiclav or doxycycline; some multi-resistant species need IV cephalosporin * if Staphylococcus aureus then give flucloxacillin

Question 156

what is cystic fibrosis?

Answer 156

- genetic disorder affecting mostly the lungs, pancreas, liver, kidneys and intestines - inherited in autosomal recessive manner - caused by mutations in both copies of the gene for the CFTR protein - one of the most common lethal autosomal recessive conditions in caucasians - 25% condition and 50% carrier risk

Question 157

what is the epidemiology of cystic fibrosis?

Answer 157

- much less common in Afro-Caribbean and Asian people - multi-system disease although respiratory problems are usually the most prominent - most people with CF also have pancreatic insufficiency

Question 158

what are risk factors for cystic fibrosis?

Answer 158

- family history | - caucasians

Question 159

where is the CF gene located? what protein does it code for?

Answer 159

CF gene is located on the long arm of chromosome 7 coding for the cystic fibrosis transmembrane regulator (CFTR) protein • transport protein on membrane of epithelial cells that acts as a chloride channel • transports chloride ions • normally it actively exports negative ions especially Cl-, and Na+ passively follows causing an osmotic gradient and movement of water out of the cell and into the mucus

Question 160

what is the commonest mutation that causes cystic fibrosis?

Answer 160

commonest mutation is the F508 deletion mutation and accounts for 70% of cases

Question 161

what is the pathophysiology of cystic fibrosis in the lung?

Answer 161

- in the lungs, CFTR dysfunction leads to dehydrated airway surface liquid, mucus stasis, airway inflammation and recurrent infection - the changes in the composition of airway surface liquid predispose the lung to chronic pulmonary infections - this process originates in the small airways, leading to progressive airway obstruction and bronchiectasis

Question 162

what is the clinical presentation of cystic fibrosis in neonates?

Answer 162

* failure to thrive * meconium ileus - bowel obstruction due to thick meconium (earliest stool) * rectal prolapse * whilst the lungs of babies born with CF are structurally normal at birth, frequent respiratory infections soon develop and are the presenting feature

Question 163

what is the clinical presentation of cystic fibrosis in the upper and lower respiratory tract?

Answer 163

* cough * thick mucus * wheeze * recurrent infections * bronchiectasis and airflow limitation * sinusitis * nasal polyps * spontaneous pneumothorax * haemoptysis and breathlessness (late) * the resultant inflammatory response damages the airways and results in progressive bronchiectasis, airflow limitation and eventually respiratory failure

Question 164

what is the clinical presentation of cystic fibrosis in the alimentary system?

Answer 164

* thick secretions * reduced pancreatic enzymes (due to mucus blocking pancreatic duct) * pancreatic insufficiency diabetes and steatorrhoea * distal intestinal obstruction syndrome * reduced bicarbonate * maldigestion and malabsorption thus poor nutrition (associated with pulmonary sepsis) * cholesterol gallstones and cirrhosis * increased incidence of peptic ulcers and malignancy

Question 165

what are other clinical presentations of cystic fibrosis?

Answer 165

* males infertile due to atrophy of vas deferens and epididymis * females able to conceive but often develop secondary amenorrhea as disease progresses * salty sweat * clubbing * osteoporosis

Question 166

what is used to diagnose cystic fibrosis?

Answer 166

- clinical history - family history of disease - one or more of these: • sweat test: will show high sodium and chloride concentrations greater than 60mmol/L (Cl- will be higher) • absent vas deferens and epididymis • GI and nutritional disorders - genetic screening for CF mutations - faecal elastase test; good at excluding exocrine pancreas disease (protease is produced by pancreas and found in faeces) - in CF patient there will be low or no levels of elastase due to mucus blocking release - microbiology

Question 167

what microbiological species are looked for in cystic fibrosis diagnosis?

Answer 167

* Pseudomonas aeruginosa * Mycobacterium abscessus * Enterobacter spp. * Klebsiella * Prevotella spp. (anaerobe)

Question 168

what is the treatment of cystic fibrosis?

Answer 168

- lung function (FEV1) and BMI should be recorded at every appointment - education to improve QoL and good nutrition and prompt treatment of exacerbations - stop smoking - prophylactic antibiotics (flucloxacillin for S. aureus and amoxicillin for H. influenzae) - pseudomonal and flu vaccine - if MRSA present then treat with rifampicin and fucidin - if Pseudomonas aeruginosa present then treat with ciprofloxacillin and nebulised colomycin - regular chest physiotherapy (postural drainage, forced expiratory techniques) - B2 agonists and inhaled corticosteroids for symptomatic relief - mucolytics such as dornase alfa (nebulised) or inhaled DNAse to clear airways of mucus - pancreatic enzyme replacement - fat soluble vitamin supplements (ADEK) - screening and treatment for osteoporosis - amiloride inhibits Na+ transport thus less thick mucus - bilateral lung transplant

Question 169

how is bilateral lung transplant used to treat cystic fibrosis?

Answer 169

* patient needs to be on maximal therapy and fully compliant, psychologically well * needs to be sick but not too sick * HLA compatibility * reasonable bone health * if M abscessus bacteria present then cannot receive transplant since it can be associated with a rapid decline and active infection may preclude transplantation * post transplant; major immunosuppressants

Question 170

what is sarcoidosis? what does it affect? what does it typically present with?

Answer 170

* type of ILD * a multi-system granulomatous disorder of unknown cause * affects any organ system, but commonly involves the mediastinal lymph nodes and lung * typically presents with bilateral hilar lymphadenopathy, pulmonary infiltration and skin or eye lesions

Question 171

what is the epidemiology of sarcoidosis?

Answer 171

- usually affects adults aged 20-40 years - more common in women - prevalence highest in Northern Europe - African-Caribbeans are affected more frequently and more severely than Caucasians, particularly by extra-thoracic disease - often detected on routine X-ray - first degree relatives have an increased risk of developing sarcoidosis (particularly in Caucasians)

Question 172

what is the pathophysiology of sarcoidosis?

Answer 172

- typical sarcoid granulomas consist of focal accumulations of epithelioid cells, macrophages and lymphocytes (mainly T cells) - generally unknown

Question 173

what is the clinical presentation of sarcoidosis? what does acute sarcoidosis commonly present with?

Answer 173

- in 20-40% the disease is discovered incidentally, after a routine CXR and is thus asymptomatic - sarcoidosis can affect any organ but has a predilection to the lung - acute sarcoidosis commonly presents with erythema nodusum (red lumps form on the shins and less commonly thighs and forearms) with/without polyarthralgia; it usually resolves spontaneously - constitutional symptoms (fever, weight loss, fatigue) - respiratory symptoms - other symptoms

Question 174

what are respiratory symptoms of sarcoidosis?

Answer 174

* 90% have abnormal CXRs with bilateral lymphadenopathy with/without pulmonary infiltrates/fibrosis * dry cough * progressive dyspnoea * reduced exercise tolerance * chest pain

Question 175

what are other symptoms of sarcoidosis?

Answer 175

* lymphadenopathy * hepatomegaly * deranged LFTs * splenomegaly * conjunctivitis * glaucoma * anterior uveitis * hypercalciuria * enlargement of lacrimal and parotid glands * Bell’s palsy; lesion of facial nerve (CN7) * facial numbness, dysphagia and visual field defects * lupus pernio - blueish-red/purple nodules and plaques over nose, cheek and ears * renal stones * cardiac arrhthmias * heart block

Question 176

what are differential diagnoses of sarcoidosis?

Answer 176

rheumatoid arthritis, lymphoma, metastatic malignancy, TB, lung cancer, SLE, idiopathic pulmonary fibrosis and multiple myeloma

Question 177

what is used to diagnose sarcoidosis?

Answer 177

- CXR (used for staging) - blood tests - bronchoscopy - ECG (arrythmias/BBB) - lung function tests (normal/reduced lung volumes, impaired gas transfer and restrictive ventilatory defect) - tissue biopsy (diagnostic; non-caseating granuloma) - broncheolar lavage (increased lymphocytes and neutrophils)

Question 178

what is stage 0 sarcoidosis?

Answer 178

normal

Question 179

what is stage 1 sarcoidosis?

Answer 179

bilateral hilar lymphadenopathy

Question 180

what is stage 2 sarcoidosis?

Answer 180

pulmonary infiltrates with BHL

Question 181

what is stage 3 sarcoidosis?

Answer 181

pulmonary infiltrates without BHL

Question 182

what is stage 4 sarcoidosis?

Answer 182

progressive pulmonary fibrosis, bulla formation | (honeycombing - confluence of two or more elements of the bronchial tree) and bronchiectasis

Question 183

what blood tests are done in diagnosis of sarcoidosis?

Answer 183

* raised ESR * lymphopenia * raised LFT * raised Ca2+ * raised immunoglobulins * serum ACE * 24 hour urinary calcium if blood serum normal

Question 184

what is the treatment of sarcoidosis?

Answer 184

- worse outcomes in patients with Afro-Caribbean and Asian descent those with extrathoracic disease - patients with bilateral hilar lymphadenopathy don't need treatment since most will recover spontaneously - do not treat symptomatic patients at Stage 1 - do not treat asymptomatic patients at Stage 2 or 3 - corticosteroids - transplantation in severe cases - treat extra-organ complications - acute: bed rest and NSAIDs

Question 185

how are corticosteroids used to treat sarcoidosis?

Answer 185

* prednisolone orally then gradually reduce dose * in severe illness give IV methylprednisolone * if steroid-resistant then methotrexate, but close monitoring required

Question 186

what is idiopathic pulmonary fibrosis?

Answer 186

* type of chronic scarring ILD characterised by a progressive and irreversible decline in lung function; distinct cellular infiltrates and extracellular matrix deposition in lung distal to the terminal bronchiole i.e. diseases of the alveolar/capillary interface * there is patchy fibrosis or the interstitium and minimal or absent inflammation, acute fibroblastic proliferation and collagen deposition * also known as cryptogenic organising pneumonia

Question 187

what is the epidemiology of idiopathic pulmonary pneumonia?

Answer 187

- a progressive chronic pulmonary fibrosis of unknown aetiology although 20% of patient give history of occupational exposure to metals and wood dusts - mean onset is in the sixties and presentation is very uncommon under the age of 50 - males are twice as likely to be affected

Question 188

what is the pathophysiology of idiopathic pulmonary pneumonia?

Answer 188

- the pathogenesis of IPF is unknown - repetitive injury to the alveolar epithelium, caused by currently unidentified environmental stimuli leads to repair of the damaged tissue - in IPF, the wound healing mechanisms become uncontrolled, leading to the over-production of fibroblasts and deposition of increased extracellular matrix in the interstitium with little inflammation - structural integrity of the lung parenchyma is disrupted; there is loss of elasticity and impaired gas exchange, leading to progressive respiratory failure

Question 189

what are risk factors that are implicated in triggering the aberrant wound healing in idiopathic pulmonary fibrosis?

Answer 189

* cigarette smoking * infectious agents (CMV, Hep C, EBV) * occupational dust exposure (metals, woods) * drugs; methotrexate, imipramine * chronic GORD * genetic predisposition

Question 190

what is the pattern of lung disease of idiopathic pulmonary fibrosis?

Answer 190

- most patients with IPF show a pattern of lung disease described as usual interstitial pneumonitis - this pattern of disease is characteristically patchy with the sub-pleural regions of the lower lobes predominantly affected - there is variable interstitial inflammatory infiltrate in the affected areas of the lung with collapse of the lung architecture and the development of mystically dilated spaces within the fibrotic areas of the lung (honeycombing) - a characteristic feature is the presence of areas of immature fibrous tissue or ‘fibroblastic foci’ in the less severely affected areas

Question 191

what is clinical presentation of idiopathic pulmonary fibrosis?

Answer 191

- dry cough with/without sputum - exertional dyspnoea - malaise - weight loss - arthralgia - cyanosis - finger clubbing - fine bi-basal end-inspiratory crackles

Question 192

when can deterioration and acute exacerbations occur in idiopathic pulmonary fibrosis?

Answer 192

- step-wise deterioration can occur due to pneumothorax, pulmonary embolism or intercurrent infection - but acute exacerbations with no identifiable cause are well recognised and are associated with increased mortality

Question 193

what are the differential diagnoses of idiopathic pulmonary fibrosis?

Answer 193

COPD, asthma, bronchiectasis, congestive heart failure, atypical pneumonia, lung cancer, asbestosis and hypersensitivity pneumonitis

Question 194

what is used to diagnose idiopathic pulmonary fibrosis?

Answer 194

- blood tests - CXR - high resolution CT (more sensitive than CXR) - spirometry/respiratory function test - lung biopsy

Question 195

what blood tests are used to diagnose idiopathic pulmonary fibrosis?

Answer 195

* arterial blood gas - low PaO2, and if severe then high PaCO2 too * raised CRP * raised immunoglobulins * check antinuclear antibodies and rheumatoid factor to exclude autoimmune rheumatic disease * spirometry/RFT (shows restrictive pattern)

Question 196

what is seen on CXR in idiopathic pulmonary fibrosis?

Answer 196

* small volume lungs with increased reticular shadowing (complex network of curvilinear opacities similar to a net) at the bases * may be normal in early disease

Question 197

what is seen on high resolution CT in idiopathic pulmonary fibrosis?

Answer 197

- abnormalities are more pronounced at the bases - reticulation is most evident in the lung peripheries/subpleura - traction bronchiectasis: the fibrotic process distorts the normal lung architecture, pulling the airways open and causing bronchiectasis - honeycombing: there are basal layers of small, cystic airspaces with irregularly thickened walls composed of fibrous tissue

Question 198

what is the treatment of idiopathic pulmonary fibrosis?

Answer 198

- median survival time is 2-5 years - serial lung function testing is used to monitor disease progression - best supportive care (oxygen, rehabilitation, palliative care) - treat GORD since it contributes to repetitive alveolar epithelial damage - treat cough - pirfenidone (an antifibrotic agent that can slow the rate of FVC decline (need to check eligibility)) - lung transplant - do not give high-dose steroids unless diagnosis of IPF is in doubt

Question 199

what is the pressure like in the lung?

Answer 199

* the lung circulation offers a low resistance to flow compared to the systemic circulation (about 90mmHg) * normal mean pulmonary artery pressure (mPAP) is 14 +/- 3 mmHg with an upper limit of normal of 20mmHg

Question 200

what are the causes of pulmonary hypertension?

Answer 200

- pulmonary vascular disorders (PE, primary pulmonary hypertension, veno-occlusive disease) - diseases of the lung and the parenchyma (COPD, chronic lung disorders) - MSK (kyphoscoliosis, poliomyelitis, myasthenia gravis) - disturbance of respiratory drive (OSA, morbid obestiy, CVD) - cardiac (mitral stenosis, left ventricle failure, left atrial myxoma, congenital heart disease) - increase in pulmonary vascular resistance or increase in pulmonary blood flow - appetite suppression drugs - type 1 glycogen storage diseases e.g. von Gierke disease - lipid storage disease - rheumatic autoimmune disease - hepatic mass - sickle cell disease - familial - can be idiopathic

Question 201

what is the pathophysiology of pulmonary hypertension?

Answer 201

- hypoxic vasoconstriction, inflammation, cell proliferation resulting in narrower vessels and increased right ventricular pressure caused pulmonary hypertension - leads to the damage of the pulmonary endothelium resulting in the release of vasoconstrictors e.g. endothelin which increases pulmonary vascular resistance, meaning the right ventricle must pump harder, causing right ventricular hypertrophy - increased platelet and leukocyte adhesion, elevated serotonin and other factors cause further vasoconstriction and remodelling, further increasing PVR - patients develop right ventricular hypertrophy, dilatation and eventually failure resulting in death

Question 202

what is the clinical presentation of pulmonary hypertension?

Answer 202

- exertional dyspnoea, lethargy and fatigue are the initial features due to an inability to increase cardiac output with exercise - ankle swelling - chest pain - syncope - as right ventricular failure develops there will be oedema and abdominal pain from hepatic congestion - loud pulmonary second sound - right parasternal heave caused by right ventricular hypertrophy - in advanced disease there are features of right heart failure (cor pulmonale)

Question 203

what are features of cor pulmonale in pulmonary hypertension?

Answer 203

* elevated jugular venous pressure * prominent V wave if tricuspid regurgitation present * hepatomegaly * pulsatile liver * peripheral oedema * ascites * pleural effusion

Question 204

what are differential diagnoses of pulmonary hypertension?

Answer 204

cor pulmonale, cardiomyopathies, primary right | ventricular heart failure, CHF, portal hypertension

Question 205

what is used to diagnose pulmonary hypertension?

Answer 205

- CXR - ECG (right ventricular hypertrophy and P pulmonale) - echocardiogram - LFTs to detect portal hypertension - autoimmune screening

Question 206

what is seen on CXR in pulmonary hypertension?

Answer 206

* enlarged proximal pulmonary arteries which taper distally * enlarged heart * may also reveal cause of pulmonary hypertension e.g. emphysema or calcified mitral valve

Question 207

what is seen on ECG in pulmonary hypertension?

Answer 207

right ventricular hypertrophy and P pulmonale (tall and peaked P wave)

Question 208

what is seen on an echocardiogram in pulmonary hypertension?

Answer 208

* right ventricular dilatation and/or hypertrophy | * can show cause of pulmonary hypertension e.g. intra-cardiac shunt

Question 209

what is the treatment of pulmonary hypertension?

Answer 209

- treat underlying cause - oxygen - warfarin for intrapulmonary thrombosis - diuretics for oedema - CCBs - oral endothelin receptor antagonist e.g. bosenten - phosphodiesterase-5 inhibitors - prostanoid (mediators of vasoconstriction) analogues e.g. inhaled iloprost - consider heart-lung transplant in young patients

Question 210

what are the lung pleura? what are their functions?

Answer 210

* lungs are covered by a thin serous layer known as the visceral pleura * this is reflected on the chest wall and pericardium as the parietal pleura * the lung hila connect the visceral and parietal pleura * allow movement of the lung against the chest wall * coupling system between lungs and chest wall * clearing fluid from the pulmonary interstitium

Question 211

what is the function of the fluid in the pleural space?

Answer 211

there is normally a small amount of fluid in the pleural space, between the parietal and visceral pleura, which lubricates movement between them

Question 212

what does the pleural fluid contain?

Answer 212

- proteins: mainly albumin, globulin and fibrinogen | - many mesothelial cells, monocytes and lymphocytes

Question 213

what is the production and reabsorption of the pleural fluid?

Answer 213

* pleural fluid is produced and reabsorbed by the parietal pleura (lymphatic stoma) * reabsorption occurs mainly at the dependent areas of parietal pleura i.e. posteriorly and inferiorly - in these areas more lymphatic stoma are found * drainage of fluid is achieved by the lymphatic pump; contractions of smooth muscles of lymphatic walls

Question 214

what is a pleural effusion? when may pain be felt?

Answer 214

* a pleural effusion is the excessive accumulation of fluid in the pleural space * parietal pleura is highly sensitive to pain

Question 215

what is the epidemiology of pleural effusion?

Answer 215

- seen in adults and less commonly in children - recurrent pleural effusions are seen malignant mesothelioma - pleural effusions are either transudates or exudates

Question 216

what are risk factors for pleural effusion?

Answer 216

- previous lung damage | - asbestos exposure

Question 217

what are features of transudates in pleural effusion?

Answer 217

* pleural fluid protein is less than 30g/L since vessels are normal so only fluid is able to leak out and not protein * occurs when the balance of hydrostatic forces in the chest favour the accumulation of pleural fluid i.e. increased pressure due to the backing up of blood in left sided congestive heart failure

Question 218

what are causes of transudation in pleural effusion?

Answer 218

- high venous pressure (heart failure, constrictive pericarditis, fluid overload) - hypoproteinaemia (cirrhosis, hypoalbuminaemia, nephrotic syndrome) - peritoneal dialysis - hypothyroidism

Question 219

what causes exudation in pleural effusion?

Answer 219

* pleural fluid protein is more than 30g/L since endothelial cells of vessels are further apart meaning fluid and protein is able to leak out * occurs due to the increased permeability and thus leakiness of pleural space/capillaries usually due to inflammation, infection or malignancy * pneumonia * malignancy * TB * pulmonary infarction * lymphoma * mesothelioma * asbestos exposure * myocardial infarction

Question 220

what can pleural effusions consist of?

Answer 220

- transudates - exudates - blood (haemothorax) - pus (empyema) - lymph fluid (chylothorax) caused by leakage of lymph from the thoracic duct as a result of trauma or infiltration by carcinoma

Question 221

what is the clinical presentation of pleural effusion?

Answer 221

- can be asymptomatic - dysponea (the build up of fluid results in increased pressure on the lungs resulting in breathing difficulties) - pleuritic chest pain - cough - loss of weight (malignancy) - chest expansion reduced on side of effusion - in large effusion the trachea may be deviated away from effusion - if there is associated lung collapse the trachea will deviate towards the lesion - stony dull percussion note on affected side - diminished breath sounds on affected side - decreased tactile vocal fremitus - loss of vocal resonance

Question 222

what is used to diagnose pleural effusion?

Answer 222

- CXR - ultrasound (identifies presence of pleural fluid, guides diagnostic/therapeutic aspiration) - diagnostic aspiration - if aspiration is inconclusive then consider parietal pleural biopsy

Question 223

what is seen on CXR in pleural effusion? when is it detected?

Answer 223

* detected when 300ml or more fluid is present * small effusions reduce the costophrenic angles * larger ones are seen as water-dense shadows with concave upper borders * a completely flat horizontal upper border implies that there is also a pneumothorax

Question 224

how is diagnostic aspiration used to diagnose pleural effusion? what is it investigated for?

Answer 224

* known as thoracentesis or pleural tap * needle inserted under anaesthesia * appearance of the pleural fluid is noted * sample is sent for pH (acidic indicates infection), cytology (differential white cell count and malignant cells) and microbiology (gram stain and culture) if infection suspected

Question 225

what is the appearance of fluid in in different types of pleural effusion?

Answer 225

- purulent in empyema (pus effusion) - turbid (cloudy/opaque) in infected effusion - milky in chylothorax (lymph fluid effusion)

Question 226

what is the treatment of pleural effusion?

Answer 226

- depends on the underlying cause - exudates are usually drained if symptomatic - transudates are managed by treatment of underlying cause - malignant effusions usually reaccumulate after drainage - pleurodesis (an injection that causes the adhesion of the visceral and parietal pleura to prevent reaccumulation of the effusion e.g. tetracycline) - surgery if persistent collections and increasing pleural thickness on ultrasound

Question 227

what is parapneumonic effusion?

Answer 227

pneumonia with associated pleural effusion

Question 228

what is pneumothorax? what does it lead to?

Answer 228

* abnormal collection air in the pleural space (between lung and chest wall) * leads to partial or complete collapse of the lung

Question 229

what is the epidemiology of pneumothorax?

Answer 229

- occurs spontaneously or secondary to chest trauma - spontaneous pneumothorax is most common in young males - pneumothorax is much more common in males - often patients are tall and thin

Question 230

what causes pneumothorax?

Answer 230

- caused by the rupture of a pleural bleb/sub-pleural bulla (serous filled blister), usually apical, thought to be due to congenital defects in the connective tissue of the alveolar walls - both lungs are affected with equal frequency i.e. can occur in any lung right or left equally - in patients over 40 years of age the usual cause is underlying COPD

Question 231

what are rarer causes of pneumothorax?

Answer 231

* bronchial asthma * carcinoma * breakdown of a lung abscess leading to bronchopleural fistula * severe pulmonary fibrosis with cyst formation * TB * pneumonia * cystic fibrosis * trauma (penetrating or rib fracture) * iatrogenic e.g. pacemakers or central lines

Question 232

what are risk factors for pneumothorax?

Answer 232

- being male - smoking increases risk - age; pneumothorax due to pleural bleb rupture is most likely to occur between 20-40yrs old, especially if person is very tall and underweight - on mechanical ventilation

Question 233

what is the pathophysiology of pneumothorax?

Answer 233

- normally, the pressure in the pleural space is negative but this is lost once there is communication with atmospheric pressure, the elastic recoil of the lung then causes it to deflate partially - if the communication between the airways and the pleural space remains open then a bronchopleural fistula results - once the communication between the lung and the pleural space is closed, air will be reabsorbed slowly for example a 50% collapse of the lung will take around 40 days to reabsorb completely once the air leak is closed

Question 234

when can recurrence occur in a pneumothorax?

Answer 234

about a third of patients will have a recurrence, for these patients chemical pleurodesis with talc is used for patients when surgery is contraindicated

Question 235

what is tension pneumothorax?

Answer 235

pneumothorax occuring under pressure, compressing lungs and decreasing venous return; tends to occur in ventilation, resuscitation, trauma or in patients with lung disease

Question 236

what are common findings in tension pneumothorax?

Answer 236

tachycardia, tachypnoea, low O2, low BP and trachea deviated away from the affected side

Question 237

what is the clinical presentation of pneumothorax?

Answer 237

- there may be no symptoms, especially in patients who are fit and young with a small pneumothorax - may be a sudden onset of dyspnoea and/or unilateral pleuritic chest pain - as the pneumothorax enlarges the patients becomes more breathless and may develop pallor and tachycardia - patients with asthma or COPD may present with a sudden deterioration - mechanically ventilated patients may present with hypoxia or an increase in ventilation pressures - there will be reduced expansion, hyper-resonance to percussion and diminished breath sounds of the affected lung - in tension pneumothorax the trachea is deviated away from the affected side

Question 238

what are differential diagnoses of pneumothorax?

Answer 238

pleural effusion, chest pain, pulmonary embolism

Question 239

what is used to diagnose pneumothorax?

Answer 239

- CXR | - ABG (check for hypoxia)

Question 240

how is CXR used to diagnose pneumothorax?

Answer 240

* do not request in tension pneumothorax as it wastes time * look for area devoid of lung markings, peripheral to the edge of the collapsed lung * trachea deviated away from affected side in tension pneumothorax * edge of collapsed lung can be seen

Question 241

what is the treatment of pneumothorax?

Answer 241

- pneumothorax due to trauma, haemothorax or mechanical ventilation requires a chest drain - for tension pneumothorax do needle aspiration then chest drain, needle aspiration first - needle aspiration to remove excess air - observation - oxygen for hypoxia - surgery for persistent pneumothorax - smoking cessation reduces recurrence of pneumothorax

Question 242

what is the epidemiology of bronchial carcinoma?

Answer 242

- most common malignant tumour worldwide with around 1.4 million deaths annually - the third most common cause of death in the UK after ischaemic heart disease and cerebrovascular disease - slightly more common in men than women but incidence in women is increasing due to women smoking more

Question 243

what are risk factors for bronchial carcinoma?

Answer 243

- cigarette smoking (including passive smoking); accounts for more than 90% of lung cancer - occupational (asbestos, coal, tar, chromium, arsenic, nickel, petroleum, iron oxide) - environmental (radon exposure, ionising radiation) - host factors (lung disease, HIV, genetic factors)

Question 244

what are types of bronchial carcinoma?

Answer 244

- small cell lung carcinoma - squamous carcinoma - adenocarcinoma - large cell and differentiated carcinoma - carcinoid tumours

Question 245

what is the epidemiology of small cell lung carcinoma?

Answer 245

* strongly associated with cigarette smoking | * has often spread by the time of presentation

Question 246

what is the pathophysiology of small cell lung carcinoma?

Answer 246

* often arises in a central bronchus * arises from endocrine cells * secretes polypeptide hormones * has early development of widespread metastases

Question 247

what is the treatment and the prognosis of small cell lung carcinoma?

Answer 247

* chemotherapy is the primary treatment | * poor prognosis

Question 248

what is the epidemiology of non-small cell lung carcinoma?

Answer 248

* cigarette smoking association | * may have metastasised by the time of diagnosis

Question 249

what is the treatment of non-small cell lung carcinoma?

Answer 249

* often treated best by surgical oblation with lymph node sampling * chemotherapy may be used and radiotherapy can be used as a follow up for contamination margin * more susceptible to new therapy such as tyrosine kinase therapy

Question 250

what is the pathophysiology of squamous cell carcinoma?

Answer 250

- tumours are usually central in location and frequently cavitate with central necrosis - arise from epithelial cells, associated with keratin production - cause obstructive lesions of bronchus with post-obstructive infection - local spread common - metastasise relatively late

Question 251

what is the pathophysiology of adenocarcinoma in the lungs?

Answer 251

- may be central or peripheral - usually single lesions but they can arise in a multifocal pattern, sometimes bilaterally - originate from mucus-secreting glandular cells - metastases common especially to; pleura, lymph nodes, brain, bones, adrenal glands

Question 252

what is the epidemiology/diagnosis of adenocarcinoma in the lungs?

Answer 252

- most common cell type in non-smokers | - commonly associated with asbestos

Question 253

what are features of carcinoid tumours in the lung?

Answer 253

- usually associated with presentation at an earlier age (middle age) and have characteristic neuroendocrine secreting cells and relatively low rates of invasion and growth - however they are still malignant

Question 254

what are features of lymphomas in the lung?

Answer 254

involve the lung primarily but are usually a component of disseminated disease

Question 255

what is the main lung lymphoma?

Answer 255

the main lung lymphoma is known as baltoma (Bronchus Associated Tissue Lymphoma) - it is a B cell lymphoma, and responds to standard chemotherapy regimes

Question 256

what are features of hamartomas in the lungs?

Answer 256

benign; irregular proliferations of benign/normal tissues that are not normally found in this pattern within lung tissue - the commonest in the lung is that of the chondroid hamartoma which incorporates cartilage, glandular tissue, fat, fibrous tissue and blood vessels

Question 257

what are the sites of metastatic spread from the lung? how can they present?

Answer 257

- liver (anorexia, nausea, weight loss and right upper quadrant pain radiating across the abdomen) - bone (bony pain and pathological fractures occur as a result of tumour spread) - adrenal glands (usually asymptomatic) - brain (presents as space-occupying lesions with signs of raised ICP) - tumours can also spread within the chest and may directly involve the pleura and ribs resulting in pain and bone fractures

Question 258

what are examples of cancers that metastasise to the lungs? which one most commonly does this?

Answer 258

- breast cancer - bowel cancer - renal cell carcinoma - bladder cancer

Question 259

what are symptoms of non-metastatic bronchial carcinoma?

Answer 259

* cough; most commonly encountered symptom, having a 3-week cough merits a CXR * breathlessness; central tumours can occlude large airways resulting in lung collapse and breathlessness on exertion * haemoptysis; fresh/old blood coughed up due to the tumour bleeding in the airway * chest pain * wheeze * recurrent infections e.g. pneumonia * clubbing

Question 260

what are symptoms of metastatic disease in bronchial carcinoma?

Answer 260

* bone pain * headache * seizures * neurological deficit * hepatic pain * abdominal pain

Question 261

what are some paraneoplastic changes in bronhcial carcinoma?

Answer 261

- secretion of parathyroid hormone - syndrome of inappropriate ADH secretion - secretion of adrenocorticotropic hormone; stimulates the secretion of glucocorticoid steroid hormones from the adrenal cortex - hypertrophic pulmonary osteo-arthropathy - finger clubbing - non-infective endocarditis - DIC

Question 262

what is used to diagnose bronchial carcinoma?

Answer 262

- TNM classification - CXR - CT (used to stage) - bronchoscopy (to give histology and assess operability) - cytology (sputum and pleural fluid) - bloods

Question 263

what is T1, T2, T3 and T4 in the TNM classification for bronchial carcinoma?

Answer 263

- T1 - < 3cm - T2 - > 3cm - T3 - invades chest wall, chest wall, diaphragm and pericardium - T4 - invades mediastinum, heart, great vessels, trachea, oesophagus, vertebra, carina, malignant effusion, metastases in same lobe

Question 264

what is N0, N1, N2 and N3 in the TNM classification for bronchial carcinoma?

Answer 264

- N0 - no nodes - N1 - hilar nodes - N2 - same side mediastinal nodes or subcarinal - N3 - contralateral mediastinum or supraclavicular

Question 265

what is m1a and m1b in the TNM classification for bronchial carcinoma?

Answer 265

- m1a - tumour on same side | - m1b - tumour is elsewhere

Question 266

what is seen on CXR in bronchial carcinoma?

Answer 266

* appears as round shadow * the edge has a fluffy spiked appearance * hilar enlargement * consolidation * lung collapse * pleural effusion

Question 267

what is the treatment of non-small cell lung cancer? (80% of lung cancers)

Answer 267

* surgical excision for peripheral tumours with no metastatic spread * curative radiotherapy is an alternative if respiratory reserve is poor; complications include radiation pneumonitis and fibrosis * chemotherapy and/or radiotherapy for more advanced disease e.g. with monoclonal antibodies targeting the epidermal growth factor receptor e.g. cetuximab

Question 268

what is the treatment of limited small cell lung tumours?

Answer 268

combined chemotherapy and radiotherapy

Question 269

what is the treatment of extensive small cell lung tumours?

Answer 269

chemotherapy | - may respond to this but usually relapse

Question 270

what is the treatment of SVC obstruction in small cell lung tumours?

Answer 270

superior vena cava stent, radiotherapy, dexamethasone

Question 271

what is endobronchial therapy? how is it used to treat small cell lung tumours?

Answer 271

used to treat symptoms of airway narrowing: - tracheal stenting - cryotherapy - brachytherapy (a radioactive source is placed close to the tumour)

Question 272

what drugs are used to treat small cell lung tumours?

Answer 272

- analgesia - steroids - antiemetics - codeine - bronchodilators - antidepressants

Question 273

what is mesothelioma? what is it strongly associated with?

Answer 273

- tumour of the mesiothelium (thin layer of tissue that covers many of the internal organs) - strongly associated with asbestos exposure - can occur in lung pleura, mesothelial cells of the peritoneum, pericardium and testes

Question 274

what is the epidemiology of mesothelioma?

Answer 274

- malignant mesothelioma is more common in men than women - most often presents between 40-70 years - exposure to asbestos is a well-established cause, but relationship is complex; only 20% of patients have pulmonary asbestosis - there is a latent period between exposure and development of the tumour may be up to 45 years

Question 275

what is the pathophysiology of mesothelioma? how does it spread?

Answer 275

- it is a high grade malignancy of the pleura, that spreads around the pleura surfaces, but can also start in the pericardial space, peritoneal space and in the paratesticular space - tumour begins as nodules in the pleura which extend as a confluent sheet to surround the lung and extend into fissures - the chest wall is often invaded, with infiltration of intercostal nerves, giving severe intractable pain - lymphatics may be invaded, giving hilar node metastases

Question 276

what is the clinical presentation of mesothelioma?

Answer 276

- chest pain - dyspnoea - weight loss - finger clubbing - recurrent pleural effusions - breathlessness

Question 277

what are signs of metastases in mesothelioma?

Answer 277

lymphadenopathy, hepatomegaly, bone pain/ | tenderness, abdominal pain/obstruction

Question 278

what is used to diagnose mesothelioma?

Answer 278

- CXR and CT - bloody/straw coloured pleural fluid - pleural biopsy

Question 279

what is seen on CXR and CT in mesothelioma?

Answer 279

- unilateral pleural effusion | - pleural thickening

Question 280

what is the treatment of mesothelioma?

Answer 280

- surgery for extremely localised mesothelioma - generally it is resistant to surgery, chemotherapy and radiotherapy - average time from diagnosis to death is around 8 months - refer all mesothelioma deaths to HM coroner - poor prognosis (8 months until death)

Question 281

what is Goodpasture's syndrome?

Answer 281

the co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage and the presence of circulating antibodies directed against an intrinsic antigen of the basement membrane of the kidney and lung

Question 282

what is the epidemiology of Goodpasture's syndrome?

Answer 282

- rare in children - usually occurs in individuals over 16 years old - in adults its more common in men

Question 283

what is the pathophysiology of Goodpasture's syndrome?

Answer 283

- specific autoimmune disease caused by a type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often AKI and CKD) - there are circulating antiglomerular basement membrane antibodies

Question 284

what is the clinical presentation of Goodpasture's syndrome?

Answer 284

- typically starts with symptoms of upper respiratory tract infection e.g. sneezing, nasal discharge, nasal congestion, runny nose and fever - cough - intermittent haemoptyis - tiredness - anaemia which may result from persistent intrapulmonary bleeding - acute glomerulonephritis

Question 285

what are differential diagnoses of Goodpasture's syndrome?

Answer 285

- idiopathic pulmonary haemosiderosis - SLE - rheumatoid arthritis

Question 286

what is idiopathic pulmonary haemosiderosis?

Answer 286

clinically similar to Goodpasture’s but no anti-basement membrane antibodies and kidneys less involved. seen in children under 7 and associated with cow’s milk. cough, anaemia and pulmonary haemorrhage

Question 287

what is used to diagnose Goodpasture's syndrome?

Answer 287

- presence of anti-basement membrane antibodies in the blood - CXR - kidney biopsy (crescentic glomerulonephritis)

Question 288

what is seen on CXR in Goodpasture's syndrome?

Answer 288

transient patchy shadows/pulmonary infiltrates due to pulmonary haemorrhage often in lower zones

Question 289

what is the treatment of Goodpasture's syndrome?

Answer 289

- some patients may spontaneously improve - others proceed on to renal failure - treat shock - vigorous immunosuppressive treatment • corticosteroids • plasmapheresis

Question 290

what is Wegener's granulomatosis?

Answer 290

* granulomatous disease of unknown aetiology * type of ANCA-associated vasculitis * renamed granulomatosis with polyangitis (GPA) * multisystem disorder of unknown origin characterised by necrotising granulomatous inflammation and vasculitis of small and medium vessels

Question 291

what is the pathophysiology of Wegener's granulomatosis?

Answer 291

- ANCA - inflammation of blood vessels with granulomas - autoantibodies are made to neutrophil proteins - as neutrophil rolls along blood vessels before it migrates into tissues, autoantibodies bind to it and activate neutrophils inappropriately (before they have entered tissues where there are no pathogens) - this results in the recruitment of more neutrophils and more activated neutrophils when there is no infection - this results in the production of reactive oxygen species and neutrophil degranulation, leading to the generation of microabscesses, recruitment of monocytes, macrophages and lymphocytes to make granulomas - results in devastating inflammation affecting many organs including lung and kidney

Question 292

what is the clinical presentation of Wegener's granulomatosis?

Answer 292

- lesions involve upper respiratory tract, lungs and kidneys - starts with severe rhinorrhea and subsequent nasal mucosal ulceration (characteristic ‘saddle-nose’ deformity) - cough - pleuritic pain - haemoptysis - renal disease causes rapidly progressive glomerulonephritis with crescent formation, proteinuria or haematuria - may be skin purpura or nodules, peripheral neuropathy, arthritis/arthralgia

Question 293

what are differential diagnoses of Wegener's granulomatosis?

Answer 293

Churg-Strauss syndrome - also affects small arteries, males in 40s, triad of rhinitis (inflammation of inside of nose) and asthma, eosinophilia and systemic vasculitis. high eosinophil count. ANCA positive

Question 294

what is used to diagnose Wegener's granulomatosis?

Answer 294

- bloods - CXR - CT (diffuse alveolar haemorrhage) - urinalysis to check for proteinuria and haematuria; if present then consider renal biopsy

Question 295

what is seen in bloods in Wegener's granulomatosis?

Answer 295

* c-ANCA is positive * elevated PR3 antibodies * raised ESR and CRP

Question 296

what is seen on CXR in Wegener's granulomatosis?

Answer 296

nodular masses or pneumonic infiltrates with cavitation; clear migratory pattern

Question 297

what is the treatment of Wegener's granulomatosis?

Answer 297

- depends on extent of disease - severe disease (biopsy-proven renal disease) should be treated with corticosteroids and cyclophosphamide or rituximab to induce remission - azathioprine and methotrexate are usually used as maintenance

Question 298

where do most clots that cause pulmonary thromboembolus and infarct come from?

Answer 298

most clots that cause clinically relevant pulmonary emboli actually come from the pelvic and abdominal veins, but femoral DVT, and even occasionally axillary thrombosis can be the origin of the clot

Question 299

what are rarer causes of pulmonary thromboembolus and infarcts?

Answer 299

* right ventricular thrombus (post-MI) * septic emboli (right-sided endocarditis - bacterial vegetation) * fat embolism (due to long bone fracture) * air embolism * amniotic fluid embolism * neoplastic cells * parasites * foreign material during IV drug misuse

Question 300

what are the risk factors for pulmonary thromboembolus and infarcts?

Answer 300

- Virchow's triad - immobility post-op or paralysis - obesity - pregnancy - dehydration - malignancy - high oestrogen - combined oral contraceptive pill - polcythaemia - nephrotic syndrome - inherited - Protein C or S deficiency or Factor V Leiden (thrombophilia) - smoking - hypertension - recent surgery especially abdominal/pelvic or hip/knee replacement - leg fracture - age greater than 60 years old

Question 301

what are the three main factors that predispose you to a clot?

Answer 301

1. circulatory stasis 2. endothelial injury 3. hypercoagulable state

Question 302

what is the pathophysiology which leads to a pulmonary embolism?

Answer 302

- thrombi arise from a venous thrombosis in the pelvis or legs, clots break off and pass through the veins, through the IVC then through the right side of the heart into the pulmonary circulation where it becomes lodged in the small capillaries supplying the alveoli, resulting in a pulmonary embolism - after PE, lung tissue is ventilated but not perfused, resulting in intrapulmonary dead space and resulting in impaired gas exchange - after some hours, the non-perfused lung no longer produces surfactant resulting in alveolar collapse which in turn exaggerates hypoxaemia - the primary haemodynamic consequence of PE is a reduction in the cross-sectional area of the pulmonary atrial bed which causes an elevation of pulmonary arterial pressure due to the increased resistance and a reduction in cardiac output

Question 303

what is the clinical presentation of pulmonary embolism? what is the most common symptom? which symptoms are present only when an infarction has occurred?

Answer 303

- sudden onset unexplained dyspnoea is most common and often only symptom - pleuritic chest pain and haemoptysis are present only when infarction has occured - dizziness - ask about risk factors - past history or family history of thromboembolism - pyrexia - cyanosis - tachypnoea - tachycardia - hypotension - raised jugular venous pressure - pleural rub - pleural effusion

Question 304

what is used to diagnose pulmonary thromboembolism and infarction?

Answer 304

- CXR - ECG - blood gases (normal or hypoxaemia or respiratory failure) - plasma D-dimer - ultrasound - CT pulmonary angiography is the gold standard test

Question 305

what is seen on CXR in pulmonary thromboembolism and infarction?

Answer 305

* often normal * decreased vascular markings * blunting of costophrenic angle (due to small effusion) * wedge-shaped areas of infarction * pulmonary oligaemia (local reduction in blood perfusion) in massive embolism * make sure its not an MI or pneumothorax

Question 306

what is seen on ECG in pulmonary thromboembolism and infarction?

Answer 306

* may be normal * may show sinus tachycardia * right atrial dilation with tall peaked P waves in lead II * right bundle branch block * right ventricular strain (inverted T wave in V1 to V4)

Question 307

what is seen on plasma D-dimer in pulmonary thromboembolism and infarction?

Answer 307

type of fibrinogen degradation product that is released into the circulation when a clot begins to dissolve; is elevated in PE • D-dimers are elevated in other conditions e.g. cancer, pregnancy and post-operatively and a positive result is not diagnostic of PE and requires further imaging • a negative result in those who have a low or intermediate clinical probability of PE effectively rules out PE and no imaging is needed

Question 308

what does a negative result in plasma D-dimer indicate?

Answer 308

a negative result in those who have a low or intermediate clinical probability of PE effectively rules out PE and no imaging is needed

Question 309

what does a positive result in plasma D-dimer indicate?

Answer 309

a positive result means that PE may be present but is not a definitive diagnosis, it may not actually be present as there are many other conditions that have elevated D-dimers

Question 310

what is the gold standard test for PE?

Answer 310

CT pulmonary angiography

Question 311

what is the treatment of pulmonary embolism?

Answer 311

- high flow oxygen (60-100%); give to all patients unless they have significant chronic lung disease - anticoagulate with low molecular weight heparin e.g. enoxaparin or dalteparin - IV fluids and inotropic agents can be used in severe cases to improve the pumping of the right heart - thrombolysis for massive PE; can improve pulmonary perfusion quicker than anticoagulation e.g. alteplase; side effect is risk of bleeding in the brain/gut only use in severe disease - surgical embolectomy - vena cava filter in patients who still develop emboli despite adequate anticoagulation

Question 312

what is done to prevent further PE long term?

Answer 312

* placed on vitamin K antagonist such as warfarin * target INR is between 2-3 * patients mobilised * TED stockings

Question 313

what is the mechansim of action of warfarin? how is it remembered?

Answer 313

placed on vitamin K antagonist such as warfarin (acts by preventing vitamin K being used by liver to produce clotting factors 2,7,9 and 10 (1972)) - Warfarin affects the Extrinsic pathway by the Prothrombin Time (WEPT) for a period of 3-6 months

Question 314

what is the management of massive PE?

Answer 314

* oxygen if hypoxic * morphine with anti-emetic if patient is in pain or very distressed * surgical embolectomy * vena cava filter in patients who still develop emboli despite adequate anticoagulation * anticoagulate with LMWH e.g. enoxaparin or dalteparin * IV fluids and inotropic agents can be used in severe cases to improve the pumping of the right heart * consider immediate thrombolysis (alteplase) if critically ill * systolic BP less then 90mmHg; start rapid colloid infusion → if still low then give dobutamine → still low, give IV noradrenaline → still low after 30-60mins treatment then is definitely PE → begin thrombolysis * systolic BP more than 90mmHg; start warfarin → confirm diagnosis

Question 315

what is protection against pathogenic bacteria in the upper respiratory tract provided by?

Answer 315

- mucosal defences (cough reflex, mucus barrier and respiratory cilia, surface secretions) - innate immune defences (impaired by immunodeficiency) - adaptive immune defences

Question 316

how long do respiratory viruses usually last? what can they lead to?

Answer 316

- usually transient - may lead to bacterial super-infection - influenza A virus in particular causes systemic symptoms

Question 317

what are complications of respiratory viruses?

Answer 317

- pharyngitis - sinusitis - otitis media - bronchitis - rarely pneumonia

Question 318

what are viral illnesses that lead to respiratory infection?

Answer 318

- rhinovirus (common cold, bronchitis, sinusitis) - influenza A virus (flu) - coronaviruses - adenoviruses (upper respiratory tract infection, pharyngitis, bronchitis, pneumonia) - respiratory syncytial viruses (bronchiolitis, pneumonia)

Question 319

what are some emergency respiratory infections?

Answer 319

- severe acute respiratory syndrome (SARS) - middle east respiratory syndrome novel coronavirus (MERS-nCV) - avian influenza

Question 320

what is the epidemiology of pharyngitis/tonsillitis? what are bacterial and viral causes?

Answer 320

- the most common viruses to cause pharyngitis are adenoviruses of which there are about 32 serotypes - can also be caused by rhinovirus, Epstein Barr virus and acute HIV infection - bacterial causes include: Lancefield Group A Beta-haemolytic streptococci e.g. streptococci pyogenes

Question 321

what is the clinical presentation of pharyngitis/tonsillitis?

Answer 321

- sore throat - tender glands in the neck - high temperature - vital signs stable - large tonsils with exudate - tender anterior cervical lymph nodes - fever - oropharynx and soft palate are reddened - tonsils are inflamed and swollen - within 1-2 days the tonsils lymph nodes enlarge

Question 322

what is the treatment of pharyngitis/tonsillitis?

Answer 322

- self-limiting disease - symptomatic treatment - no antibiotics required - persistent and severe tonsillitis should be treated with phenoxlymethylpenicilin or cefaclor

Question 323

what is sinusitis?

Answer 323

infection of the paranasal sinuses that is bacterial or occasionally fungal

Question 324

what is the aetiology of sinusitis?

Answer 324

- bacterial: • Streptococcus pneumoniae (40%) • Haemophilus influenzae (30-35%) - most commonly associated with upper respiratory tract infection and occasionally asthma

Question 325

what is the clinical presentation of sinusitis?

Answer 325

- fever, facial pain and purulent nasal discharge - pain in left ear and into the teeth - cold and facial pain - past history of allergic rhinitis and uses steroid nasal spray

Question 326

what is used to diagnose sinusitis?

Answer 326

- frontal headache - purulent rhinorhoea (where nasal cavity filled with significant amount of mucus fluid) - bacterial sinusitis presents with unilateral pain and purulent discharge with or without fever for more than 10 days - facial pain with tenderness - fever

Question 327

what is the treatment of sinusitis?

Answer 327

- nasal decongestants such as xylometazoline | - broad spectrum antibiotics such as co-amoxiclav (H.influenzae can be resistant to amoxicillin)

Question 328

what are complications of treatment of sinusitis?

Answer 328

brain abscess, sinus vein thrombosis and orbital cellulitis

Question 329

what is the epidemiology of acute epiglottitis?

Answer 329

- formerly a life-threatening infection of the epiglottis, usually in children under 5 years of age - child becomes severely ill with a high fever and severe airflow obstruction may rapidly occur - adults can also have the disease - rare due to introduction of Hib vaccine

Question 330

what are features of acute epiglottitis in adults?

Answer 330

* most severen cases due to Haemophilus influenzae * also from causes of pharyngitis and other bacterial infections of airway * caused by additional pathogens in immunocompromised e.g. AIDS

Question 331

what is the clinical presentation of acute epiglottitis?

Answer 331

- sore throat - odynophagia - inspiratory stridor - unwell - fatigue, weight loss and diarrhoea with oral thrush - high fever - severe airflow obstruction - meningitis - septic arthritis - osteomyelitis

Question 332

what is the treatment of acute epiglottitis?

Answer 332

- can be a life-threatening emergency and requires urgent endotracheal intubation - IV antibiotics e.g. ceftazidime

Question 333

what is the epidemiology of whooping cough? what is it caused by?

Answer 333

- caused by Bordatella pertussis, a gram-negative coccobacillus (rod) - Bordatella parapertussis and Bordatella bronchiseptica produce milder infections - mainly a disease of childhood with 90% of cases occurring below 5 years of age - however, no age is exempt as the antibody levels fall over the years, although in adults, mild infection may not be recognised

Question 334

what is the pathophysiology of whooping cough?

Answer 334

- highly contagious and spread by droplet infection - in early stages it is indistinguishable from other upper respiratory tract infections - lymphoid hyperplasia and Th17 skewing of immune response contribute to chronic inflammation and cough

Question 335

what are the virulence factors of whooping cough? what do they each do?

Answer 335

Bordatella pertussis • filamentous haemagglutinin and fimbriae aid adherence • adenylate cyclase toxin (ACT) inhibits phagocyte chemotaxis and T-cell activation • pertussis toxin an A/B toxin that ADP ribosylates G proteins and inhibits alveolar macrophage host defence • tracheal cytotoxin (peptidoglycan derived) and dermonecrotic toxin cause epithelial necrosis

Question 336

what is the clinical presentation of whooping cough?

Answer 336

- chronic cough - febrile - sub-conjuntival haemorrhage - lungs clear to ausculation - vomiting

Question 337

what are the different phases of whooping cough?

Answer 337

- incubation period is 7-10 days - catarrhal phase (1-2 weeks) - paroxysmal phase (1-6 weeks) (pneumonia, encephalopathy, subconjunctival haemorrhage)

Question 338

what is the clinical presentation of the catarrhal phase in whooping cough?

Answer 338

1-2 weeks • patient highly infectious • cultures from respiratory cultures are positive in 90% of cases • malaise • anorexia • rhinorhoea (nasal cavity congested with significant amount of mucus) • conjunctivitis

Question 339

what is the clinical presentation of the paroxysmal phase in whooping cough?

Answer 339

1-6 weeks • begins 1 week later from catarrhal phase • coughing spasms • classic inspiratory whoop is only seen in younger individuals in whom the lumen of the respiratory tract is compromised by mucus secretion and mucosal oedema • these coughing spasms usually terminate in vomiting • cough for more than 14 days

Question 340

what is used to diagnose whooping cough? what are the criteria?

Answer 340

- chronic cough and one clinical feature indicated pertussis - chronic cough and history of contact or microbiological diagnosis is used to confirm pertussis - suggested clinically by the characteristic whoop and history of contact with an infected individual - PCR tests are rapid and highly sensitive - but culture of a nasopharyngeal swab remains necessary for definitive diagnosis

Question 341

what is the treatment of whooping cough?

Answer 341

- antimicrobials such as macrolides e.g. clarithromycin will eliminate carriage of bacteria and reduce symptoms in catarrhal stage and early paroxysmal stage - in the paroxysmal stage, antibiotics have little role to play in altering the course of the illness - vaccination; acellular pertussis as part of the dTap vaccine (diptheria, tetanus and acellular pertussis) at 2,3,4 months and 3-4 years

Question 342

what is the epidemiology of acute laryngitis?

Answer 342

- mainly due to parainfluenza viruses | - most severe in children under the age of 3 years

Question 343

what is the pathophysiology of acute laryngitis?

Answer 343

- inflammatory oedema extends to the vocal cords and the epiglottis, causing narrowing of the airway; there may be associated tracheobronchitis - progressive airway obstruction may occur, with recession of the soft tissue of the neck and abdomen during inspiration and in severe cases central cyanosis

Question 344

what is the clinical presentation of acute laryngitis?

Answer 344

- 3 year old presents to casualty with his mother - he has a prominent barking cough and is crying - on examination is febrile, has a respiratory rate of 40 and cyanosed with prominent intercostal recessions - has inspiratory stridor - voice become hoarse with a barking cough (croup)

Question 345

what is the treatment of acute laryngitis?

Answer 345

- Nebulised adrenaline gives short-term relief | - oral or intramuscular corticosteroids should be given with oxygen and adequate fluids

Question 346

what is pneumonia?

Answer 346

* defined as infection/inflammation of the substance of the lungs * an acute lower respiratory tract infection

Question 347

what are types of pneumonia?

Answer 347

- community-acquired pneumonia - hospital-acquired pneumonia - immunocompromised patients - aspiration pneumonia

Question 348

what is the epidemiology of community-acquired pneumonia?

Answer 348

* in a person with no underlying immunosuppression or malignancy * occurs across all ages but commoner in extremes of age * may be primary or secondary to underlying disease

Question 349

what are causes of community-acquired pneumonia?

Answer 349

* Streptococcus pneumoniae is the commonest cause * followed by Haemophilus influenzae and Mycoplasma pneumoniae * S. aureus, Legionella species, Moraxella catarrhalis and Chlamydia * harder to culture and identification relies on serology or antigen testing * these are not susceptible to beta lactams, but are susceptible to macrolides e.g. clarithromycin

Question 350

what are features of localised and diffuse community-acquired pneumonia?

Answer 350

- infection can be localised, when the whole of one or more lobes is affected - infection can be diffuse, when the lobules of the lung are mainly affected, often due to infection centred on the bronchi and bronchioles (bronchopneumonia)

Question 351

what is hospital-acquired pneumonia?

Answer 351

defined as new onset of cough with purulent sputum, along with a compatible X-ray demonstrating consolidation, in patients who are beyond 48hrs of their initial admission to hospital or who have been in a healthcare setting within the last 3 months (including nursing/residential homes)

Question 352

what is the second most common form of hospital-acquired infection?

Answer 352

HAP is the second most common form of hospital acquired infection after UTIs

Question 353

what are the causative organisms in hospital-acquired pneumonia?

Answer 353

aerobic Gram negative bacilli/rods are most commonly involved: - Pseudomonas aeruginosa - Escherichia coli (E.coli) - Klebsiella pneumoniae - S. aureus is increasingly recognised in HAP, particularly MRSA - HAP due to Staph. aureus is more common in patients with diabetes mellitus or head trauma and in those on intensive care units

Question 354

what causes immunocompromisation in patients? what are they at risk of?

Answer 354

* in patients who are immunosuppressed either due to a genetic defect, immunosuppressive medication or AIDS * they are at risk not only from all the usual organisms that can cause pneumonia but also from opportunistic pathogens that would not be expected to cause disease * these opportunistic pathogens can be commonly occurring microorganisms or bacteria, viruses and fungi e.g. Pneumocystis jiroveci

Question 355

what is aspiration pneumonia?

Answer 355

- type of lung infection that is due to a relatively large amount of material from the stomach or mouth entering the lungs - acute aspiration of gastric contents into the lungs can produce an extremely severe and sometimes fatal illness owing to the intense destructiveness of gastric acid - seen in those with stroke, myasthenia, bulbar palsies and lack of consciousness - it can complicate anaesthesia, particularly during pregnancy (Mendelson syndrome)

Question 356

what are the organisms indicated in CAP?

Answer 356

``` • Streptococcus pneumoniae (most common) • Haemophilus influenzae • atypical: - Mycoplasma pneumoniae - Chlamydophila pneumoniae • enteric Gram negative bacteria: - E.coli - Klebsiella pneumoniae ```

Question 357

what are organisms indicated in HAP?

Answer 357

``` • Gram negative bacteria: - Pseudomonas aeruginosa - E.coli - Klebsiella pneumoniae • Staphylococcus aureus including MRSA ```

Question 358

what are risk factors for pneumonia?

Answer 358

- under 16 - over 65 - co-morbidities (HIV, diabetes, CF, COPD, bronchiectasis) - smoking - excess alcohol - IV drug use - immunosuppressant therapy (prolonged corticosteroids)

Question 359

what is the onset of pneumonia?

Answer 359

- Pneumococcal pneumonia is typically acute in onset with prominent respiratory symptoms and fever - atypical pathogens that cause pneumonia tend to have a slower onset, with more prominent extra-pulmonary symptoms and complications

Question 360

what do the bacteria do in the body in pneumonia? what would usually happen to them?

Answer 360

- bacteria ‘translocate’ to the normally sterile distal airway - where they overwhelm resident host defence (particularly alveolar macrophages and neutrophils) - normally alveolar macrophages will ingest the bacteria and produce humoral factors - antibodies would be produced as well as microbial factors and the bacteria will be destroyed - however when the host defence is overwhelmed the alveolar macrophages change roles and coordinate response e.g. they instruct Th17 to stimulate neutrophils to fill the alveolar space and produce an inflammatory exudate - normally this is resolved and bacteria are cleared with the inflammatory cells being removed by apoptosis

Question 361

when does severe disease result in pneumonia?

Answer 361

* excessive inflammation * lung injury * failure to resolve without lung damage

Question 362

what is the clinical presentation of pneumonia?

Answer 362

- symptoms of; fever, night sweats, raised respiratory rate, productive cough and absence of upper respiratory tract symptoms makes pneumonia more likely - fever +/- raised respiratory rate and heart rate and low BP - rigors - malaise - anorexia - dyspnoea since alveoli become filled with pus and debris, thus imparting gas exchange. coarse crackles are often heard on auscultation, due to consolidation of the lung parenchyma - signs of consolidation on percussion and auscultation (dull to percussion, decreased air entry, bronchial breath sounds) - dry or productive cough (cough is non-productive in atypical causes such as Mycoplasma pneumoniae and Chlamydophila pneumoniae) - purulent sputum (rusty sputum is characteristic of Streptococcus pneumoniae in CAP) - pleuritic chest pain - cyanosis - confusion (might be the only sign in the elderly)

Question 363

what is used to diagnose pneumonia?

Answer 363

- CXR - blood tests (elevated WCC) - ESR and CRP significantly elevated - U+Es, LFTs, RFTs - pulse oximetry and arterial blood gas analysis (to define respiratory failure) is needed if O2 sat is below 94% - since pneumonia is a common initial presenting illness in patients with previously undiagnosed HIV infection, a HIV test should be offered to all patients with pneumonia - microbiological tests (sputum culture and antibiotic sensitivities, Gram stain, blood culture, serology) - CURB-65 used to assess severity of CAP

Question 364

what is seen on CXR in pneumonia?

Answer 364

* radiological abnormalities can lag behind clinical signs * a normal CXR on presentation should be repeated after 2-3 days if CAP is suspected clinically * look for ‘air bronchogram’ in consolidated area (black branch)

Question 365

what does a multilobar appearance on CXR suggest in pneumonia?

Answer 365

S. pneumoniae, S. aureus and Legionella spp.

Question 366

what do multiple abscesses on CXR suggest in pneumonia?

Answer 366

S. aureus

Question 367

what does upper lobe cavity on CXR suggest in pneumonia?

Answer 367

Klebsiella pneumoniae, but must exclude TB first

Question 368

how is CURB-65 used to diagnose pneumonia?

Answer 368

one point each for: - confusion - urea (greater than 7mmol/L) - respiratory rate greater than 30/min - BP less than 90mmHg systolic and/or 60mmHg diastolic - age greater than 65

Question 369

what are the scores in CURB-65 for CAP? how is each category treated?

Answer 369

- 0-1 = mild, only admit if social circumstance or single worrying feature - 2 = moderate, admit to hospital - 3-5 = severe, admit and monitor closely - 4-5 = consider admission to critical care unit

Question 370

how is oxygen used to treat pneumonia?

Answer 370

- maintain O2 sats between 94-98% (provided the patient is not at risk of CO2 retention, due to loss of hypoxic drive in COPD) - in patients with COPD, saturations should be maintained between 88-92%

Question 371

when should first-dose antibiotics be given in pneumonia?

Answer 371

first dose of antibiotics should be administered within 4 hours of presentation in hospital and treatment shouldn't be delayed whilst investigations are awaited

Question 372

what is antibiotic treatment of mild and severe pneumonia?

Answer 372

- narrow spectrum antimicrobials if mild = amoxicillin 5-7 days - IV antibiotics if severe = co-amoxiclav or clarithromycin 7-10 days

Question 373

what is the treatment of severe Legionella spp. pneumonia?

Answer 373

ensure fluoroquinolone is in regimen, either alone or with clarithromycin

Question 374

what is PVL?

Answer 374

Panton-Valentine leukocidin; a cytotoxin produced by some aggressive strains of S. aureus that causes a necrotising pneumonia

Question 375

what is the treatment of necrotising pneumonia or other features of Panton-Valentine leukocidin producing S. aureus infection?

Answer 375

- IV linezolid - IV clindamycin - IV rifampicin

Question 376

what is the treatment of pneumonia caused by Pseudomonas aeuginosa?

Answer 376

IV ceftazidime with gentamicin/tobramycin

Question 377

how is pneumonia prevented?

Answer 377

* polysaccharide pneumococcal vaccine (protects against 23 serotypes) * influenza vaccine to those who are older than 65 years, immunocompromised or with comorbidities * smoking cessation

Question 378

what are complications of pneumonia?

Answer 378

- respiratory failure - hypotension, due to a combination of dehydration and vasodilation due to sepsis - parapneumonic effusion and empyema • pleural effusions are common in pneumonia • the majority are simple exudative effusions • but empyema may develop, where there is pus/purulent fluid in the pleural space - lung abscess

Question 379

what is an empyema?

Answer 379

collection or gathering of pus within a naturally existing anatomical cavity; e.g. pleural empyema is empyema of the pleural cavity

Question 380

what are indications of empyema in pneumonia?

Answer 380

- ongoing fever - failure of fever or markers of inflammation (WBC/CRP) to settle on antibiotics - pain on deep inspiration - signs of pleural collection (stony dull percussion, reduced air entry)

Question 381

how is parapneumonic effusion and empyema diagnosed?

Answer 381

thoracocentesis - fluid would be yellow and turbid (cloudy/opaque) - pH less than 7.2 - low glucose CXR shows pleural effusion

Question 382

what is seen in thoracocentesis in parapneumonic effusion and empyema?

Answer 382

- fluid would be yellow and turbid (cloudy/opaque) - pH less than 7.2 - low glucose

Question 383

what is the treatment of parapneumonic effusion and empyema?

Answer 383

chest drain immediately and antimicrobials - co-amoxiclav - piperacillin-tazobactam - meropenam (for anaerobic coverage)

Question 384

what is a lung abscess?

Answer 384

- a type of liquefactive necrosis of the lung tissue and formation of cavities (more than 2cm) containing necrotic debris and fluid caused by microbial infection - severe localised suppuration within the lung associated with cavity formation visible on CXR

Question 385

what are causes of lung abscess?

Answer 385

- aspiration (alcoholics, oesophageal obstruction) - inadequately treated CAP - TB - foreign body inhalation - septic emboli (usually containing Staphylococci) - Streptcoccus milleri (viridans streptococci, alpha-haemolytic and optochin resistant) - anaerobics e.g. Klebsiella pneumonia - other Gram negative bacteria

Question 386

what is the treatment of lung abscess as a complication of pneumonia?

Answer 386

* prolonged antibiotics for up to 6 weeks | * surgical drainage may be required

Question 387

what is the epidemiology of tuberculosis?

Answer 387

- one third of worlds population is infected - 9 million cases per year with 2 million deaths - global incidence on the decline - majority of cases are seen in Africa and Asia (India and China) - cause of death for most people with HIV

Question 388

what 4 microbiological species cause tuberculosis?

Answer 388

* Mycobacterium tuberculosis (most common cause) * Mycobacterium bovis (where milk is unpasteurised) * Mycobacterium africanum * Mycobacterium microti

Question 389

what are features of the 4 microbiological species that cause tuberculosis?

Answer 389

* aerobic, non-motile, non-sporing, slightly curved rods/bacilli with a thick waxy capsule * acid-fast bacilli (resist decolorisation); go red/pink with Ziehl-neelsen stain * only stained weakly with Gram stain due to high lipid content in their cell wall * slow growing; generation time is 15-20 hours * resistant to phagolysosomal killing by macrophage, hence granulomatous * able to remain dormant * airborne infection spread via respiratory droplets * only a small number of bacteria need to be inhaled for infection to develop

Question 390

what are the risk factors for tuberculosis?

Answer 390

- origination from a high-incidence country e.g. Sub-saharan Africa - HIV + resulting in immunosuppression - immunosuppressant therapy (chemotherapy or monoclonal antibody therapy) - diabetes mellitus - IVDU - ageing - malnutrition - homeless i.e. poverty - prisons - smoking - alcohol

Question 391

what do the TB-causing microbiological species do in the body in primary tuberculosis?

Answer 391

• once inhaled into the lung, alveolar macrophages ingest the bacteria • the bacilli/rods then proliferate inside the macrophages and cause the release of neutrophil chemoattractants and cytokines, resulting in an inflammatory cell infiltrate reaching the lung and hilar lymph nodes • macrophages present the antigen to the T lymphocytes with the development of a cellular immune response • a delayed hypersensitivity-type reaction occurs, resulting in tissue necrosis and formation of a granuloma • granulomatous lesions consist of a central area of necrotic material caused caseation, surround by epithelioid cells and Langerhans giant cells with multiple nuclei • lymphocytes are present and there is a varying degree of fibrosis

Question 392

what is the primary Ghon focus in primary tuberculosis?

Answer 392

- the initial granuloma that forms is called the Primary Ghon Focus - found in the upper region of the lung in the sub pleural region - the Ghon focus is seen on CXR as a small calcified nodule often in the upper parts of the lower lobes or the lower parts of the upper lobes in the midzone, happens where bacilli settle

Question 393

where can primary and secondary lesions in TB occur?

Answer 393

- upper regions of lung in subpleural region - primary lesion can also occur in the GI tract, particularly in the ileocaecal region - bacilli can be taken to the lymph nodes (mediastinal, hilar, paratracheal and subclavicular) and secondary lesions can develop here

Question 394

what is the Ghon complex?

Answer 394

the primary Ghon focus and caseous lesions in the lymph nodes are called the Ghon complex, in primary TB

Question 395

what happens to the damaged areas in primary TB?

Answer 395

* the caveated areas heal completely and may become calcified * some of these calcified nodules contain bacteria, which are contained by the immune system and the hypoxic acidic environment created within the granuloma; these bacteria are capable of lying dormant for many years * if the bacteria cannot be contained and there is dissemination of the primary infection this can lead to miliary tuberculosis, whereby TB spreads to other organs

Question 396

what percentage of people get primary TB and develop disease?

Answer 396

* upon initial contact with infection, less than 5% of patients develop active disease * this percentage increases to 10% within the first year of exposure

Question 397

what is latent TB?

Answer 397

in the majority of people who are infected, the immune system contains the infection and the patient develops cell-mediated immunity memory to the bacteria

Question 398

what is reactivation tuberculosis?

Answer 398

* majority of TB cases are due to reactivation of latent infection (this is post-primary TB) usually occurs when there is depression of host immune system e.g when older or in severe infection * the initial contact usually occurred many years earlier * in patients with HIV infection, newly acquired TB is common

Question 399

what are other types of TB?

Answer 399

* GI TB * TB of bone and spine * miliary TB (widespread systemic TB) * CNS TB * pericardial TB * TB of the skin

Question 400

what is the clinical presentation of TB?

Answer 400

- any manifestation of TB can occur in primary or reactivation disease - extrapulmonary involvement is far less common in primary disease - systemic features (weight loss, fever, anorexia, night sweats, malaise) - pulmonary TB - lymph node TB (swelling, discharge) - bone TB (pain, swelling, Pott's disease) - abdominal TB (ascites, abdominal lymph node swelling, ileal malabsorption) - genitourinary TB (epididymitis, frequency, dysuria, haematuria) - CNS TB (bacilli, exudate, raised ICP, cranial palsies, meningitis, headache, vomiting, confusion, coma) - extrapulmonary TB

Question 401

what is the clinical presentation of pulmonary TB?

Answer 401

• can be asymptomatic • productive cough with occasional haemoptysis • cough for more than 3 weeks • can be pleuritic pain if pleural involvement • chest pain • breathlessness • can be hoarse voice if laryngeal involvement - consolidation - pleural effusion - pulmonary collapse caused by compression of a lobar bronchus by enlarged nodes

Question 402

what is used to diagnose TB?

Answer 402

- CXR - sputum - bronchoscopy if no sputum available - histology (presence of caseating granuloma) - culture - nucleic acid amplification (differentiates between tuberculous and non-tuberculous mycobacteria) - lumbar puncture and CSF examination - latent TB diagnosis (tuberculin skin test and interferon gamma release assays)

Question 403

what is seen on CXR in TB?

Answer 403

* patchy or nodular shadows in the upper zones with loss of volume, and fibrosis with/without cavitation * consolidation * with miliary TB the CXR may be normal or show miliary shadows

Question 404

what is seen on sputum in TB? what is it stained with?

Answer 404

* stained with an auramine-phenol fluorescent test (more sensitive but less specific), it highlights bacilli as yellow-orange on a green background * Ziehl-Neelsen (will appear red if TB) stain for acid- and alcohol-fast bacilli

Question 405

what is seen in the culture in TB? what culture is done?

Answer 405

* liquid/broth culture | * solid culture on Lowenstein-Jensen slopes or Middlebrook agar

Question 406

how is the tuberculin skin test used to diagnose TB? what are the results?

Answer 406

- TB antigen is injected intradermally - cell-mediated response at 48-72 hours is recorded - stimulates type 4 hypersensitivity reaction - if positive then indicates immunity and thus contact with TB - consider interferon gamma testing - immunosuppressed or miliary TB wont react (false negative) - only moderately specific (false positives) - won’t easily distinguish infection from disease

Question 407

how are interferon gamma release assays used to diagnose TB?

Answer 407

- use antigens specific to M. tuberculosis e.g. ESAT-60 and CFP10 to distinguish between this and BCG vaccine or environmental mycobacteria - IGRAs demonstrate exposure to M. tuberculosis but not active infection

Question 408

what is the treatment of fully sensitive TB? what drugs are used?

Answer 408

patients with fully sensitive TB require 6 months of treatment (in CNS TB they need 12 months): - rifampicin for 6 months - isoniazid for 6 months - pyrazinamide for 2 months - ethambutol for first 2 months - compliance is critical to reduce relapse and resistance - to aid compliance there are special clinics called direct observed therapy where they give medication under supervision

Question 409

what are features of rifampicin in TB treatment? what are some side effects?

Answer 409

- bactericidal, blocks protein synthesis; effective throughout treatment course - used for 6 months for fully sensitive TB - side effects; red urine, hepatitis and drug interactions

Question 410

what are features of isoniazid in TB treatment? what are some side effects?

Answer 410

- bactericidal for rapidly growing bacilli (blocks cell wall synthesis), most effective in initial stages - used for 6 months for fully sensitive TB - side effects; hepatitis and neuropathy

Question 411

what are features of pyrazinamide in TB treatment? what are some side effects?

Answer 411

- bactericidal initially, less effective later - used for first 2 months for fully sensitive TB - side effects; hepatitis, arthralgia/gout and rash

Question 412

what are features of ethambutol in TB treatment? what are some side effects?

Answer 412

- bacteriostatic, blocks cell wall synthesis - used for first 2 months for fully sensitive TB - side effects; optic neuritis

Question 413

how is TB prevented?

Answer 413

* active case finding to reduce infectivity i.e CXR of patients contacts etc. * detection and treatment of TB via community nursing team using Mantoux and IGRAs * vaccination

Question 414

how is the BCG vaccination used to prevent TB? what organism is it derived from?

Answer 414

* live attenuated vaccine derived from Mycobacterium bovis that has lost its virulence * variable efficacy but is still recommended in certain situations in developed countries i.e. neonates from high risk groups * no longer offered routinely due to lack of cost efficacy * shown to reduce risk of disseminated and CNS TB in babies and children

Question 415

what are normal ABG values?

Answer 415

- pH: 7.35-7.45 - PaCO2: 4-6 kPa - PaO2: 10-14 kPa - HCO3: 22-26 mmol/L - SaO2: more than 95%

Question 416

what form of oxygen are you measuring in ABGs?

Answer 416

when measuring PaO2 in blood you are not measuring the total O2 but instead only whats dissolved in serum and not what is bound to haemoglobin

Question 417

what are the steps for ABG interpretation?

Answer 417

1. is there respiratory failure? 2. what is the pH? Acidemia or Alkalemia? 3. what is the primary disorder present? 4. is there appropriate compensation? 5. is there an anion gap? 6. what is the differential for the clinical processes?

Question 418

what is respiratory failure? when does it occur?

Answer 418

- inability to deliver suitable oxygenation to maintain aerobic metabolism at a cellular level - occurs when there is hypoxaemia that is PaO2 less than 8.0kPa

Question 419

what is Hb saturation?

Answer 419

the more binding of O2 there is to haemoglobin (Hb), the more haemoglobin becomes less accepting of O2 - Hb sat of 50% is expected at venous blood return - Hb sat of 90% is expected at artery

Question 420

how does carbon monoxide bind to Hb? how can ABGs detect this?

Answer 420

carbon monoxide (CO) binds to haemoglobin 200x more avidly than O2: • if you only looked at the O2 sats then it will look normal since the CO binding will reflect good haemoglobin saturations • however if you looked at the ABGs you will see the real picture

Question 421

what is the alveolar-arterial difference?

Answer 421

- P(A-a)O2 is the alveolar-arterial difference in partial pressure of O2 - normal P(A-a)O2 ranges from 1-4kPa breathing room air (it increases with age)

Question 422

what does an elevated alveolar-arterial difference indicate?

Answer 422

- a higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries - with the exception of right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem with the lungs

Question 423

what is PaO2? can it tell us how much O2 is in the blood?

Answer 423

since PaO2 reflects only free O2 dissolved in plasma and not those bound to Hb, PaO2 cannot tell us “how much” O2 is in the blood

Question 424

what is SaO2? does it tell us how much O2 is in the blood?

Answer 424

* the percentage of all the available heme binding sites saturated with O2 is the haemoglobin oxygen saturation * note: SaO2 alone doesn't reveal how much O2 is in the blood; for that we also need to know the haemoglobin content

Question 425

what is the CaO2? what can it tell us?

Answer 425

* tissues need a requisite amount of O2 molecules for metabolism * neither PaO2 nor the SaO2 provide information on the number of O2 molecules i.e. how much O2 is in the blood * only CaO2 tells us how much O2 is in the blood; this is because CaO2 is the only value that incorporates the haemoglobin content

Question 426

what are causes of hypoxaemia?

Answer 426

- reduced PaO2 - usually from lung disease (most common physiologic mechanism: V/Q mismatch) - reduced SaO2 - most commonly from reduced PaO2, other causes include CO poisoning or a rightward shift of the O2 dissociation curve - reduced haemoglobin content - anaemia

Question 427

what can cause decreased tissue oxygen uptake?

Answer 427

- mitochondrial poisoning e.g. cyanide poisoning) | - left-shifted haemoglobin dissociation curve e.g. from acute alkalosis, excess CO or abnormal haemoglobin structure

Question 428

what are causes of tissue hypoxia?

Answer 428

- hypoxia (low PaO2 and/or low CaO2) - reduced oxygen delivery to the tissues - decreased tissue oxygen uptake

Question 429

what is acidosis? what are the different types and what causes them?

Answer 429

* a primary physiologic process that, occurring alone, tends to cause acidemia * metabolic acidosis from decreased perfusion (lactic acidosis) * respiratory acidosis from hypoventilation

Question 430

what is alkalosis? what are the different types and what causes them?

Answer 430

* a primary physiological process that, occurring alone, tends to cause alkalemia * metabolic alkalosis from excessive diuretic therapy * respiratory alkalosis from acute hyperventilation

Question 431

what is respiratory acidosis?

Answer 431

failure to get rid of CO2, resulting in a decrease in pH as CO2 builds up

Question 432

what are causes of respiratory acidosis?

Answer 432

* hyperventilation * COPD * any cause of respiratory failure (pulmonary embolism: type 1, hypoventilation: type 2)

Question 433

what is the compensation for respiratory acidosis? how long does this take?

Answer 433

• the kidneys will increase H+ secretion (in the form of ammonium) and will also release more HCO3- into the plasma which will increase pH as a result of the use of the ammonium buffer • the increase in pH will take days

Question 434

what is respiratory alkalosis?

Answer 434

too much CO2 lost, resulting in an increased pH as CO2 is lost

Question 435

what are causes of respiratory alkalosis?

Answer 435

* CO2 depletion due to hyperventilation * hypoxia * type 1 respiratory failure e.g. pulmonary embolism - decrease in O2 and a decrease/no change in CO2

Question 436

what is the compensation of respiratory alkalosis?

Answer 436

* the kidneys will decrease H+ secretion thereby retaining H+, and helping return pH to normal * the decreased H+ secretion will also result in a decrease in HCO3- reabsorption resulting in more HCO3- excretion and thus a fall in plasma HCO3- further helping to increase pH and return it back to normal

Question 437

what is metabolic acidosis?

Answer 437

excess acid production (intercalated cells release acid) resulting in a decrease in pH

Question 438

what are causes of metabolic acidosis?

Answer 438

* renal failure * GI HCO3- loss * dilution of blood - more H2O in blood the more acidic it gets * failure of H+ excretion i.e. hypoaldosternonism whereby insufficient aldosterone is released so less Na+ reabsorbed meaning less H+ secreted using Na+/H+ countertransporter * excess H+ e.g. ketoacidosis

Question 439

what is the compensation for metabolic acidosis?

Answer 439

the decrease in pH will stimulate chemoreceptors of the lung resulting in enhanced respiration resulting in a fall in CO2 resulting in an increase in pH

Question 440

what is metabolic alkalosis?

Answer 440

metabolic condition in which the pH of tissue is elevated beyond the normal range

Question 441

what are causes of metabolic alkalosis?

Answer 441

* increase in pH * vomiting (due to the loss of gastric secretions which are rich in HCL) * volume depletion * alkali ingestion * hyperaldosteronism * hyperkalaemia - resulting in increased aldosterone release

Question 442

what is the compensation of metabolic alkalosis?

Answer 442

the increase in pH inhibits the chemoreceptors of the lung thereby reducing respiration thereby increasing CO2, resulting in a decrease in pH

Question 443

what are values for respiratory acidosis?

Answer 443

- decreased pH - increased HCO3- - increased pCO2

Question 444

what are values for metabolic acidosis?

Answer 444

- decreased pH - decreased HCO3- - decreased pCO2

Question 445

what are values for respiratory alkalosis?

Answer 445

- increased pH - decreased HCO3- - decreased pCO2

Question 446

what are values for metabolic alkalosis?

Answer 446

- increased pH - increased HCO3 - increased pCO2

Question 447

an accumulation of air around the heart

Answer 447

pneumomediastinum

Question 448

a collection of air in the lung tissue

Answer 448

cyst or bulla

Question 449

a collection of infected fluid in the pleural cavity

Answer 449

empyema

Question 450

an area of collased lung

Answer 450

atelectasis

Question 451

pneumomediastinum =

Answer 451

an accumulation of air around the heart

Question 452

cyst or bulla in the lung =

Answer 452

a collection of air in the lung tissue

Question 453

empyema =

Answer 453

a collection of infected fluid in the pleural cavity

Question 454

atelectasis

Answer 454

an area of collased lung

Question 455

atelectasis =

Answer 455

an area of collapsed lung

Question 456

CTPA =

Answer 456

CT pulmonary angiogram

Question 457

what is respiratory failure

Answer 457

* Fundamentally, it is a failure of gas exchange and an inability to maintain normal blood gases.

Question 458

causes of acute resp. failure

Answer 458

opiate overdose trauma pulmonary embolism

Question 459

causes of chronic respiratory failure

Answer 459

COPD fibrosing lung disease

Question 460

what are the characteristics of type 1 resp. failure

Answer 460

* low blood [O2] = hypoxemia * low or normal [CO2] = hypocapnia/normal

Question 461

what are the characteristics of type 2 resp. failure?

Answer 461

* low blood [O2] = hypoxemia * high [CO2] = hypercapnia

Question 462

# think broadly causes of Type 1 resp. failure

Answer 462

1. airway disorders 2. congential 3. infection 4. vasculature problems 5. neoplasm

Question 463

Causes of type 2 resp. failure

Answer 463

1. **airway disorders** - COPD, asthma 2. **drugs** 3. **neurological** - loss of resp. drive 4. **metabolic**

Question 464

T1RF treatment

Answer 464

* Oxygen delivery – increasing the FiO2 * Treat the primary cause of hypoxia e.g. abx for pneumonia * Assess airway patency

Question 465

T2RF treatment

Answer 465

* Oxygen delivery – increasing the FiO2 * **must be careful delivering O2 as these pts rely on oxygen for resp. drive.** * **they switch from CO2 dependent resp. drive to hypoxic drive due to tolerance to chronic hypercapnia.** * **so too much oxygen will tell their brain they don't need to breath.** * Treat the primary cause of hypoxia e.g. abx for pneumonia * Assess airway patency * Assisted ventilation: non/invasive, used when: * Inadequate PaO₂ despite increasing FiO₂ * Increasing PaCO₂ * Patient tiring

Question 466

what are the types of hypoxia

Answer 466

* Hypoxic hypoxia – low arterial O2 tension in blood * Anaemic hypoxia – not enough Hb to carry O2 * Stagnant hypoxia – blood flow to the tissue us so slow * Histotoxic hypoxia – toxic agent prevents cell from using O2 e.g. CO

Question 467

clinical features of hypercapnia

Answer 467

* irritability * Headache * Warm skin * Bounding pulse * Confusion * Somnolence * Coma

Question 468

what is the mediastinum

Answer 468

The mediastinum is the **central compartment** of the thoracic cavity, located **between the two pleural sacs**. It contains most of the thoracic organs, and acts as a passageway for structures traversing the thorax on their way into the abdomen.

Question 469

what is respiratory failure

Answer 469

* Fundamentally, it is a failure of gas exchange and an inability to maintain normal blood gases.

Question 470

causes of acute resp. failure

Answer 470

opiate overdose trauma pulmonary embolism

Question 471

causes of chronic respiratory failure

Answer 471

COPD fibrosing lung disease

Question 472

what are the characteristics of type 1 resp. failure

Answer 472

* low blood [O2] = hypoxemia * low or normal [CO2] = hypocapnia/normal

Question 473

what are the characteristics of type 2 resp. failure?

Answer 473

* low blood [O2] = hypoxemia * high [CO2] = hypercapnia

Question 474

# think broadly causes of Type 1 resp. failure

Answer 474

1. airway disorders 2. congential 3. infection 4. vasculature problems 5. neoplasm

Question 475

Causes of type 2 resp. failure

Answer 475

1. **airway disorders** - COPD, asthma 2. **drugs** 3. **neurological** - loss of resp. drive 4. **metabolic**

Question 476

T1RF treatment

Answer 476

* Oxygen delivery – increasing the FiO2 * Treat the primary cause of hypoxia e.g. abx for pneumonia * Assess airway patency

Question 477

T2RF treatment

Answer 477

* Oxygen delivery – increasing the FiO2 * **must be careful delivering O2 as these pts rely on oxygen for resp. drive.** * **they switch from CO2 dependent resp. drive to hypoxic drive due to tolerance to chronic hypercapnia.** * **so too much oxygen will tell their brain they don't need to breath.** * Treat the primary cause of hypoxia e.g. abx for pneumonia * Assess airway patency * Assisted ventilation: non/invasive, used when: * Inadequate PaO₂ despite increasing FiO₂ * Increasing PaCO₂ * Patient tiring

Question 478

what are the types of hypoxia

Answer 478

* Hypoxic hypoxia – low arterial O2 tension in blood * Anaemic hypoxia – not enough Hb to carry O2 * Stagnant hypoxia – blood flow to the tissue us so slow * Histotoxic hypoxia – toxic agent prevents cell from using O2 e.g. CO

Question 479

clinical features of hypercapnia

Answer 479

* irritability * Headache * Warm skin * Bounding pulse * Confusion * Somnolence * Coma

Question 480

what is the mediastinum

Answer 480

The mediastinum is the **central compartment** of the thoracic cavity, located **between the two pleural sacs**. It contains most of the thoracic organs, and acts as a passageway for structures traversing the thorax on their way into the abdomen.

Question 481

describe the structure of the lower airways

Answer 481

trachea → left and right main bronchi → lobar bronchi → segmental bronchi → respiratory bronchioles → terminal bronchioles → acini - containing alveolar ducts and alveoli.

Question 482

what is the carina

Answer 482

**A ridge at the base of the trachea that separates the openings of the right and left main bronchi**

Question 483

what is the hilum and what does it contain

Answer 483

hilum = the passageway for the contents of the root of the lung * root of the lung consists of * a bronchus, * pulmonary artery, * two pulmonary veins, * bronchial vessels, * pulmonary plexus of nerves and lymphatic vessels.

Question 484

where is the dive to breath controlled and what triggers it

Answer 484

- in the medulla oblongata - triggered by CO2 in the form of H2CO3 - an acid