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RESPIRATORY Flashcards

1
Q

what are the clinical features of ARDS?

A
  • Unexplained tachypnoea.
  • Increased hypoxaemia.
  • Central cyanosis.
  • Dyspnoea.
  • Fine crackles throughout both lung fields.
  • Fever, cough, and pleuritic chest pain if the underlying cause is pneumonia.
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2
Q

What is seen on chest x-ray in ARDS?

A

-Bilateral diffuse shadowing.

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3
Q

What is seen on ABG in ARDS?

A

-Low PaO2 / FiO2 ratio of < 300 on PEEP.

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4
Q

how is ARDS managed?

A
  • endotracheal intubation
  • prone position
  • supportive measures
  • Consider rescue therapy (extracorporeal membrane oxygenation) for patients with refractory hypoxaemia despite an FiO2 of 1.0 and high levels of positive end-expiratory failure.
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5
Q

what are the clinical features of allergic bronchopulmonary aspergillosis?

A
  • Cough.
  • Fever.
  • Wheeze.
  • Firm sputum plugs.
  • Pleuritic chest pain
  • commonly in teenagers with CF and young adults with asthma.
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6
Q

how is allergic bronchopulmonary aspergillosis diagnosed?

A
  • skin test for Aspergillosis fumigatus is positive
  • raised eosinophils
  • elevated IgE and IgG
  • central bronchiectasis on chest x-ray
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7
Q

how is allergic bronchopulmonary aspergillosis managed?

A
  • oral prednisone

- azole antifungal (itraconozole) as a second line therapy

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8
Q

what are the risk factors for simple pneumoconiosis?

A
  • Occupational exposure to silica (manufacture of toilet bowlers sinks, and ceramics).
  • Occupational exposure to coal (coal miners).
  • Occupational exposure to beryllium (manufacture of master alloy).
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9
Q

what are the symptoms of simple pneumoconiosis?

A
  • Dyspnoea on exertion.
  • Dry, non-productive cough.
  • Features of TB in silicosis (fever, haemoptysis, malaise).
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10
Q

what are the signs of simple pneumoconiosis?

A
  • Wheeze.
  • Crackles on auscultation.
  • Cyanosis (uncommon).
  • Clubbing (uncommon).
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11
Q

what is seen on chest x-ray in simple pneumoconiosis?

A
  • Rounded opacities in the upper lobes

- Calcification around hilar lymph nodes.

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12
Q

what is seen on CT scan in simple pneumoconiosis?

A

-upper zone interstitial fibrosis

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13
Q

what is seen on spirometry in simple pneumoconiosis?

A
  • Restrictive changes;

- Mixed pattern in progressive massive fibrosis

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14
Q

how is simple pneumoconiosis managed?

A
  • smoking cessation and removal of occupational exposure
  • advice regarding compensation via the Industrial Injuries Act.
  • corticosteroid therapy (prednisolone 40 mg) for patients with acute or chronic berylliosis.
  • Perform whole lung lavage for acute silicosis.
  • pulmonary rehabilitation to all patients with exertional dyspnoea.
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15
Q

what are the clinical features of asbestosis?

A
  • A history of occupational asbestos exposure such as shipyard and construction work, vehicle brake mechanic.
  • Progressive dyspnoea.
  • Cough.
  • Bilateral basal end-inspiratory crackles.
  • Chest pain.
  • Clubbing.
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16
Q

what is seen on chest x-ray in asbestosis?

A
  • Lower zone linear fibrosis

- Pleural thickening

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17
Q

what is seen on spirometry in asbestosis?

A
  • Restrictive changes (normal FEV1/FVC ratio)

- Reduced total lung capacity

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18
Q

what is seen on CT scan in asbestosis?

A
  • Lower zone linear interstitial fibrosis
  • Progressively involves the entire lung
  • Pleural thickening.
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19
Q

how is asbestosis managed?

A
  • Encourage smoking cessation.
  • Offer supportive therapy such as antibiotics and oxygen therapy where appropriate.
  • Consider pleural decortication if patients develop diffuse pleural thickening.
  • Consider lung transplant for end-stage respiratory failure (PaO2 < 60 mmHg despite oxygen therapy).
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20
Q

what are the risk factors for aspiration pneumonia?

A
  • Altered mental status secondary to alcohol, drugs, or anaesthesia.
  • Gastrointestinal disease such as GORD, hiatal hernia, achalasia.
  • Intubation or tracheostomy tube (ventilator associated pneumonia).
  • Nasogastric and percutaneous feeding.
  • Increasing age.
  • Poor oral hygiene.
  • Anaesthesia during pregnancy (Mendelson’s syndrome)
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21
Q

what are the clinical features of aspiration pneumonia?

A
  • Cough.
  • Dyspnoea.
  • Fever.
  • Pleuritic chest pain.
  • Tachypnoea.
  • Foul-smelling breath.
  • Crepitations.
  • Frothy or purulent sputum.
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22
Q

what are the clinical features of CAP?

A
  • productive cough
  • dyspnoea
  • pleuritic chest pain
  • fever
  • rigors and night sweats
  • confusion
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23
Q

how does mycoplasma pneumonia present?

A
  • Sore throat
  • erythema multiforme
  • encephalitis
  • uveitis
  • myocarditis
  • cold haemolytic anaemia
  • Raynaud’s
  • bullous myringitis (blisters on tympanic membrane
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24
Q

how does legionella present?

A
  • Confusion
  • headache
  • diarrhoea
  • myalgia
  • raised CK
  • interstitial nephritis
  • hyponatraemia
  • hypoalbuminaemia
  • high liver aminotransferases
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25
Q

which organisms can be detected on urinary antigen testing in pneumonia?

A
  • Legionella pneumophilia

- Streptococcus pneumoniae.

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26
Q

what is the immediate management of CAP?

A
  • oxygen
  • IV fluids if hypotensive
  • vasopressor if needed
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27
Q

what is the initial drug management of CAP?

A
  • amoxicillin or doxycycline for low severity
  • amoxicillin plus clarithromycin for moderate severity
  • co-amoxiclav or levofloxacin with clarithromycin for high severity or aspiration pneumonia
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28
Q

how is empyema managed?

A
  • Administer intravenous cefuroxime and metronidazole.
  • Perform urgent chest tube drainage.
  • Provide supportive care: Antipyretics for swinging fever and analgesia for pleuritic pain.
  • Provide fluid resuscitation if they are septic.
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29
Q

what are the risk factors for HAP?

A
  • Intubation and mechanical ventilation.
  • Co-morbidity, such as severe lung disease or immunosuppression.
  • Acid-suppression drugs.
  • Aspiration, which can complicate anaesthesia (Mendelson’s syndrome)
  • Depressed consciousness.
  • Chest or upper abdominal surgery.
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30
Q

what are the clinical features of HAP?

A
  • Cough with increasing sputum production.
  • Dyspnoea.
  • Fever.
  • Pleuritic chest pain.
  • Tachycardia.
  • Malaise and anorexia.
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31
Q

how is HAP treated?

A
  • oxygen, IV fluids and vasopressors if needed
  • oral co-amoxiclav for non-severe symptoms or signs and not at higher risk of resistance.
  • Consider doxycycline if patient has a penicillin allergy
  • piperacillin with tazobactam if severe symptoms or signs or at higher risk of resistance.
  • intravenous vancomycin or teicoplanin if suspected or confirmed MRSA.
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32
Q

what are the clinical features of pneumocystis jirovecii?

A
  • high fever
  • breathlessness
  • dry cough
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33
Q

how is pneumocystis jirovecii treated?

A

-co-trimoxazole

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34
Q

what are the risk factors for developing asthma?

A
  • Personal or family history of atopic disease (asthma, eczema, allergic rhinitis).
  • Respiratory infections in infancy.
  • Exposure to tobacco smoke.
  • Premature birth and low birth weight.
  • Obesity.
  • Social deprivation.
  • Workplace exposures include flour dust and isocyanates from paint.
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35
Q

what are the clinical features of asthma?

A
  • Expiratory polyphonic wheeze.
  • Dry cough.
  • Shortness of breath.
  • Symptoms are episodic, diurnal (worse at night or in the early morning) and are triggered by exercise, exposure to cold air, allergens, NSAIDs, beta-blockers, and viral infections.
  • Occupational asthma is suggested when symptoms improve when not at work.
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36
Q

what is seen on spirometry in asthma?

A
  • FEV1/FVC is less than 70%.

- FEV1 is less than 80%.

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37
Q

What percentage FEV1 reversibility on bronchodilator testing is required for asthma diagnosis?

A

-12% or more.

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38
Q

what is the stepwise management of asthma in adults?

A
  • SABA
  • ICS
  • LTRA
  • LABA
  • ICS+LABA
  • Anti-muscarinic
  • theophylline
  • Oral steroids
  • sodium cromoglycate or nedocromil
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39
Q

which asthmatic patients should be given ICS?

A
  • Use an inhaler SABA three times a week or more.
  • Have asthma symptoms three times a week or more.
  • Are woken up at night by asthma symptoms once weekly.
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40
Q

what is the stepwise management of asthma in children?

A
  • SABA
  • ICS or LTRA <5 years
  • LABA with ICS
  • refer to respiratory physician
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41
Q

what are the clinical features of an acute asthma attack?

A
  • Inability to complete a sentence in one breath.
  • raised respiratory rate
  • tachycardia
  • use of accessory muscles
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42
Q

what are the features of a life threatening asthma attack?

A
  • A silent chest.
  • Normal PaCO2.
  • Cyanosis.
  • Bradycardia or hypotension.
  • Exhaustion.
  • Confusion
  • Coma.
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43
Q

what are the ABG features in acute asthma?

A
  • PaO2 < 6 kPa in a life threatening attack
  • A raised PaCO2 indicates near fatal asthma
  • A normal PaCO2 indicates exhaustion and life threatening asthma
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44
Q

how is an acute asthma attack managed in adults?

A
  • inhaled salbutamol every 20 minutes for 3 doses.
  • oxygen
  • salbutamol nebuliser
  • ipratropium bromide nebuliser
  • IV hydrocortisone or oral prednisone for 5 days
  • IV magnesium sulphate
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45
Q

how is an acute asthma attack managed in children?

A
  • salbutamol 10 puffs or nebuliser
  • ipratropium bromide nebuliser
  • oxygen
  • oral prednisone
  • IV aminophylline or salbutamol
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46
Q

what are the causes of bronchiectasis?

A
  • post-infective
  • Cystic fibrosis.
  • Bronchial obstruction due to lung cancer or foreign body aspiration.
  • Allergic bronchopulmonary aspergillosis.
  • Primary ciliary dyskinesia including Kartagener’s syndrome
  • Rheumatoid arthritis.
  • Ulcerative colitis.
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47
Q

what are the clinical features of bronchiectasis?

A
  • Persistent productive cough.
  • Large volumes of purulent sputum then becomes thick, foul-smelling and khaki coloured.
  • Breathlessness.
  • Haemoptysis, either frank or massive.
  • Halitosis.
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48
Q

what is seen on high resolution CT in bronchiectasis?

A
  • Thickened, dilated bronchi
  • Cysts
  • Characteristically the airways are larger than their associated blood vessels, giving a signet ring appearance.
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49
Q

how is bronchiectasis managed?

A
  • airway clearance therapy
  • prophylactic azithromycin with 3 or more exacerbations a year
  • surgery for localised disease
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50
Q

what are the features of an exacerbation of bronchiectasis?

A
  • Cyanosis.
  • Confusion.
  • Respiratory rate of more than 25 breaths per minute.
  • Marked breathlessness or laboured breathing
  • Peripheral oedema.
  • Temperature of 38 degrees of celsius or more.
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51
Q

what are the risk factors for developing COPD?

A
  • smoking
  • coal, grains and silica
  • air pollution
  • genetics
  • asthma
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52
Q

what are the symptoms of COPD?

A
  • Breathlessness that is persistent, progressive, and worse on exertion.
  • Chronic cough.
  • Regular sputum production.
  • Frequent lower respiratory tract infections.
  • Wheeze.
  • Weight loss.
  • Anorexia.
  • Fatigue.
  • Ankle swelling.
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53
Q

what are the signs of COPD?

A
  • Cyanosis.
  • Raised JVP.
  • Cachexia.
  • Hyperinflation of the chest.
  • Use of accessory muscles.
  • Pursed lip breathing.
  • Crackles on auscultation.
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54
Q

what are the post-bronchodilator spirometry features of COPD?

A
  • FEV1:FVC less than 70%

- FEV1 less than 80%.

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55
Q

define mild COPD according to GOLD stages

A

FEV1 80% of predicted value

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56
Q

define moderate COPD according to GOLD stages

A

FEV1 50 - 79% of predicted value.

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57
Q

define severe COPD according to GOLD stages

A

FEV1 30 - 49% of predicted value.

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58
Q

define very severe COPD according to GOLD stages

A
  • FEV1 30% of predicted value

- 50% of predicted value and respiratory failure.

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59
Q

which COPD patients should be given long term oxygen therapy?

A
  • With a PaO2 of less than 7.3 kPa.
  • With peripheral oedema, secondary polycythaemia, pulmonary hypertension, or nocturnal hypoxaemia.
  • SpO2 < 92% or less breathing air.
  • FEV1 < 30% predicted value.
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60
Q

how is COPD managed?

A
  • SABA or SAMA
  • LABA + ICS with asthmatic features (previous asthma, eosinophilia, diurnal variation)
  • LABA + LAMA with no asthmatic features
  • LABA + LAMA + ICS
  • Mucolytic
  • Prophylactic azithromycin with more than 3 exacerbations requiring steroids and one needing hospital admission in the last year
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61
Q

what are the clinical features of an acute exacerbation of COPD?

A
  • Increased breathlessness.
  • Increased cough.
  • Increased sputum production and change in sputum colour.
  • Increased wheeze and chest tightness.
  • Upper respiratory tract infections (cold or sore throat).
  • Ankle swelling.
  • Increased fatigue.
  • Acute confusion.
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62
Q

how are acute exacerbations treated in COPD?

A
  • nebulised salbutamol
  • predisolone
  • oxygen
  • BiPAP for respiratory acidosis
  • oral antibiotics (amoxicillin or doxocycline)
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63
Q

what are the respiratory features of CF?

A
  • recurrent respiratory infections
  • persistent, loose cough
  • purulent sputum
  • clubbing
  • sinusitis and nasal polyps
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64
Q

what are the GI features of CF?

A
  • steatorrhoea
  • failure to thrive
  • meconium ileus
  • cholesterol gallstones
  • cirrhosis
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65
Q

how is CF diagnosed?

A
  • raised immunoreactive trypsinogen on blood spot

- increased concentration of chloride in sweat

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66
Q

how are the respiratory features of CF managed?

A
  • airway clearance
  • salbutoamol
  • an inhaled mucolytic such as dornase alfa, hypertonic saline or mannitol
  • prophylactic azithromycin
  • lung transplant
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67
Q

how is chronic pseudomonas infection managed in CF?

A
  • Colistimethate sodium nebuliser is first line

- If there is clinical deterioration, consider nebulised aztreonam or nebulised tobramycin

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68
Q

what are the clinical features of foreign body aspiration?

A
  • Choking.
  • Bilateral persistent monophonic wheeze.
  • Dyspnoea.
  • Intractable cough.
  • Fever.
  • Unilateral decreased breath sounds.
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69
Q

how should foreign body aspiration be managed if the patient it conscious?

A
  • Encourage the patient to cough.
  • Perform chest thrusts for infants if coughing is ineffective.
  • Perform abdominal thrusts for children and adults if coughing is ineffective.
  • Perform flexible bronchoscopy to remove the foreign body if the patient has cervicofacial trauma.
  • Perform rigid bronchoscopy to remove the foreign body if there is asphyxia, stridor, or radio- opaque object seen on chest radiograph.
  • Perform surgery if repeated bronchoscope attempts fail.
  • Perform thoracotomy with pulmonary resection for cases of destroyed segment, lobe, or lung.
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70
Q

what are the risk factors for developing hypersensitivity pneumonitis?

A
  • Exposure to mouldy hay or vegetable material (Farmer’s lung).
  • Handling pigeons or cleaning lofts (Bird fancier’s lung).
  • Turning germinating barley (Maltworker’s lung).
  • Exposure to contaminated humidifying systems in air conditioners or factories (Humidifier fever).
  • Turning mushroom compost (Mushroom workers).
  • Exposure to mouldy cheese (Cheese washer’s lung).
  • Exposure to mouldy grapes (Winemaker’s lung).
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71
Q

what are the symptoms of hypersensitivity pneumonitis?

A
  • Dyspnoea.
  • Cough.
  • Fever and chills.
  • Malaise.
  • Anorexia and weight loss.
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72
Q

what are the signs of hypersensitivity pneumonitis?

A
  • Tachypnoea.
  • Coarse end-inspiratory crackles.
  • Wheeze.
  • Cyanosis.
  • Clubbing.
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73
Q

what is seen on chest x-ray in hypersensitivity pneumonitis?

A
  • Fluffy nodular shadowing
  • Streaky shadows
  • Honeycomb lung.
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74
Q

what is seen on CT in hypersensitivity pneumonitis?

A
  • Reticular and nodular changes

- Ground glass opacity.

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75
Q

what is seen on lung function testing in hypersensitivity pneumonitis?

A
  • Restrictive changes (normal FEV1/FVC ratio)

- Reduced carbon monoxide gas transfer.

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76
Q

what is seen on bronchoalveolar lavage in hypersensitivity pneumonitis?

A
  • Positive antibody

- lymphocytosis

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77
Q

how is hypersensitivity pneumonitis treated?

A
  • avoid antigen

- oral prednisolone

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78
Q

what are the risk factors for developing pulmonary fibrosis?

A
  • Cigarette smoking.
  • Advancing age.
  • Male gender.
  • Exposure to wood and metal dusts.
  • Infections such as EBV.
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79
Q

what are the symptoms of pulmonary fibrosis?

A
  • Progressive dyspnoea.
  • Non-productive cough.
  • Cyanosis
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80
Q

what are the signs of pulmonary fibrosis?

A
  • Fine bilateral end expiratory crackles.

- Finger clubbing.

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81
Q

what is seen on chest x-ray in pulmonary fibrosis?

A

Basilar and subpleural reticular opacities

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82
Q

what is seen on CT in pulmonary fibrosis?

A
  • Basilar and subpleural reticular opacities

- (reticular) honeycombing.

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83
Q

how is pulmonary fibrosis managed?

A
  • smoking cessation
  • assess QoL
  • Supplemental oxygen if oxygen saturation <80%
  • anti-fibrotics e.g. pirfenidone or nintedanib
  • lung transplant
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84
Q

how is an acute exacerbation of pulmonary fibrosis managed?

A
  • Admit to hospital.
  • Offer high dose corticosteroids (prednisolone).
  • Consider azathioprine or cyclophosphamide if there is no response to corticosteroids.
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85
Q

what are the clinical features of langerhans’ cell granulomatosis?

A
  • Bone pain or swelling.
  • Skin rash that may be ulcerative or necrotic.
  • Cough.
  • Dyspnoea.
  • Hepatosplenomegaly.
  • Jaundice.
  • Ascites
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86
Q

what is seen on chest and bone x-ray in langerhans’ cell granulomatosis?

A
  • CXR: Multiple small cysts (honeycomb lung).

- bone XR: Punched out lytic lesions.

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87
Q

how is respiratory disease managed in langerhans’ cell granulomatosis?

A
  • Encourage smoking cessation.

- Give vinblastin and prednisolone for severe disease.

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88
Q

how is skin disease managed in langerhans’ cell granulomatosis?

A

Give topical betamethasone for an ulcerative or necrotic rash

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89
Q

how is bone disease managed in langerhans’ cell granulomatosis?

A
  • Perform surgery

- give methylprednisolone.

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90
Q

what are the risk factors for developing lung cancer?

A
  • Cigarette smoking.
  • Radon gas exposure.
  • Family history.
  • Older age.
  • Asbestos exposure.
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91
Q

what are the respiratory features of lung cancer?

A
  • Persistent cough.
  • Breathlessness which may be due to tumour obstruction or underlying lung disease.
  • Haemoptysis, typically blood-tinged sputum.
  • Wheeze.
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92
Q

what are the features of local invasion of lung cancer?

A
  • Sharp pleuritic chest pain
  • Small muscle wasting in the hand (Brachial plexus).
  • Horner’s syndrome (superior cervical ganglion).
  • Dysphagia.
  • Paralysis of the ipsilateral hemidiaphragm (phrenic nerve).
  • Hoarseness.
  • Facial swelling (SVC)
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93
Q

what are the features of metastatic spread of lung cancer?

A
  • Liver metastasis includes anorexia, nausea and weight loss.
  • Brain metastasis includes raised intracranial pressure, headache, confusion.
  • Weight gain with an ACTH-secreting tumour.
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94
Q

how is small cell carcinoma managed?

A
  • Offer surgical resection for early stage disease (T1-2a, N0, M0).
  • Offer platinum-based combination chemotherapy (carboplatin and etoposide) for extensive disease (T1-4, N0-3, M1a/b).
  • Offer anthracycline containing chemotherapy (topetocan) for relapsed disease in whom chemotherapy is suitable.
  • Offer radiotherapy for palliation.
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95
Q

how is non-small cell lung carcinoma treated?

A
  • Offer surgical resection for early stage disease.
  • Offer radical radiotherapy with SABR for patients with early stage disease who reject surgical resection
  • Consider chemoradiotherapy (cisplatin and vinnorelbine) for stage II or III disease that are not suitable for surgery.
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96
Q

what are the clinical features of laryngeal carcinoma?

A
  • hoarse voice
  • may be deep, harsh and breathy or weak
  • otalgia
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97
Q

what are the clinical features of mesothelioma?

A
  • Shortness of breath.
  • Diminished breath sounds.
  • Dullness to percussion.
  • Chest pain
  • Dry and non-productive cough.
  • Fatigue.
  • Fever.
  • Weight loss.
  • Sweats.
98
Q

what is seen on chest x-ray in mesothelioma?

A
  • Unilateral pleural effusion
  • Irregular pleural thickening
  • Reduced lung volume.
99
Q

what is seen on CT in mesothelioma?

A
  • Pleural thickening
  • Discrete pleural plaques
  • Enlarged hilar lymph nodes
  • Chest wall invasion.
100
Q

what is the definitive diagnostic investigation in mesothelioma?

A

thoracoscopic biopsy

101
Q

how is operable mesothelioma managed?

A
  • Perform extra-pleural pneumonectomy.
  • Give pre-operative chemotherapy (cisplatin + pemetrexed + cyanocobalamin + folic acid).
  • Give adjunct radiotherapy.
102
Q

how is inoperable mesothelioma managed?

A
  • Give chemotherapy (cisplatin + pemetrexed (cisplatin + pemetrexed + cyanocobalamin + folic acid).
  • Give radiotherapy.
103
Q

what are the risk factors in adults for obstructive sleep apnoea?

A
  • Male (2:1).
  • Obesity.
  • Neck circumference greater than 43 cm.
  • Family history.
  • Smoking.
  • Alcohol intake before bed.
  • Sleeping supine .
  • Hypothyroidism.
  • Craniofacial abnormalities.
104
Q

what are the risk factors in children for obstructive sleep apnoea?

A
  • Adenotonsilar hypertrophy.
  • Obesity.
  • Congenital conditions (Down’s syndrome).
  • Hypotonia
  • Muscle weakness
  • Achondroplasia
  • Cerebral palsy
  • Craniofacial abnormalities
105
Q

what are the clinical features of obstructive sleep apnoea in adults?

A
  • Excessive daytime sleepiness and snoring and impaired concentration.
  • Witnessed choking noises while sleeping.
  • Feeling unrefreshed on waking.
  • Mood swings, personality changes, depression.
  • Nocturia.
106
Q

what are the clinical features of obstructive sleep apnoea in children?

A
  • Snoring and pauses in breathing, which may be followed by a gasp or snort.
  • Restlessness and sudden arousals from sleep, laboured breathing, unusual sleep posture, bedwetting.
  • Daytime irritability, poor concentration, decreased performance at school, tiredness and sleepiness, failure to gain weight or growth, mouth breathing.
107
Q

how should suspected sleep apnoea be investigated?

A
  • Epworth sleepiness score

- polysomnography: At least five episodes of apnoea or hypopnoea per hour of sleep.

108
Q

how is obstructive sleep apnoea managed?

A
  • mandibular advancement device
  • CPAP
  • adjunct modafinil or armodafinil for somnolence
  • Consider upper airway surgery (tracheotomy, maxillomandibular advancement) in patients in whom CPAP or oral appliances are not accepted, tolerated, or have failed.
  • Refer to ENT specialist to consider adenotonsillectomy for children with evidence of adenotonsillar hypertrophy.
  • Encourage weight loss in obese patients as secondary prevention.
109
Q

what are the risk factors for developing pneumothorax?

A
  • Smoking.
  • Family history of pneumothorax.
  • Tall and slender body.
  • Male gender.
  • Young age.
  • Presence of underlying lung disease such as COPD, severe asthma, pulmonary TB, cystic fibrosis, and Pneumocystis jirovecii infection.
110
Q

what are the clinical features of a pneumothorax?

A
  • Sudden onset unilateral pleuritic pain.
  • Dyspnoea.
  • ipsilateral reduced breath sounds.
  • Ipsilateral hyperinflation of the hemi-thorax.
  • Ipsilateral hyper-resonance on percussion.
111
Q

what are the clinical features of tension pneumothorax?

A
  • Hypotension and tachycardia.
  • Tracheal deviation to the opposite side.
  • Shock.
  • Cyanosis.
  • Loss of consciousness.
112
Q

how is a small primary spontaneous pneumothorax treated?

A
  • Consider observation and discharge.
  • Review in 2 - 4 weeks as an outpatient.
  • Perform video-assisted thoracoscopic surgery (VATS) if recurs more than twice.
113
Q

how is a large primary spontaneous pneumothorax treated?

A
  • Perform percutaneous aspiration using a 16-18G cannula for a large primary spontaneous pneumothorax.
  • Insert a chest drain size 8-14F in the fifth intercostal space in the mid-axillary line if percutaneous aspiration is unsuccessful.
  • Give supplemental oxygen to maintain oxygen saturation of 94% to 98%, or 88% to 92% in patients are at risk of hypercapnic type 2 respiratory failure
  • Consider video-assisted thoracoscopic surgery (VATS) if chest drain aspiration is unsuccessful.
114
Q

how is a small secondary spontaneous pneumothorax treated?

A
  • Give high flow oxygen and target oxygen stations close to 100% unless patient is at risk of hypercapnic type 2 respiratory failure.
  • Admit and observe for at least 24 hours.
115
Q

how is a large secondary spontaneous pneumothorax treated?

A
  • Management is same as that of a large primary spontaneous pneumothorax.
  • Consider chemical pleurodesis in patients who are unable or unwilling to undergo VATS.
116
Q

how is a tension pneumothorax managed?

A
  • immediate decompression by inserting a large-bore cannula into the pleural space through the second intercostal space in the mid-clavicular line.
  • immediate decompression using open thortacosotmy if the tension pneumothorax is secondary to trauma. Use the fourth or fifth intercostal space in the mid-axillary line.
  • Give high flow oxygen and target oxygen saturations of close to 100% unless the patient is at risk of hypercapnic type 2 respiratory failure.
  • Insert a chest drain size 8-14F immediately after decompression.
  • Offer ibuprofen and or codeine phosphate for pain relief.
117
Q

define pulmonary hypertension

A

mean pulmonary artery pressure (mPAP) of greater than 25 mmHg at rest as measured on right heart catheterisation.

118
Q

what are the symptoms of pulmonary hypertension?

A
  • Dyspnoea.
  • Fatigue.
  • Weakness.
  • Angina.
  • Syncope.
  • Abdominal distension.
119
Q

what are the signs of pulmonary hypertension?

A
  • Left parasternal heave.
  • Loud pulmonary second heart sound.
  • Soft pan-systolic murmur with tricuspid regurgitation.
  • Early diastolic murmur with pulmonary regurgitation.
  • Raised JVP.
  • Ascites.
  • Peripheral oedema.
  • Hepatomegaly.
120
Q

how should patients with pulmonary hypertension with a positive response to vasodilator therapy be treated?

A
  • Offer a calcium channel blocker (nifedipine) as the first line management.
  • Offer atrial septostomy or lung transplantation for patients who progress despite optimal medical treatment.
121
Q

how should patients with pulmonary hypertension with a negative response to vasodilator therapy be treated?

A
  • Offer an endothelin receptor antagonist (ambrisentan / bosentan) or phosphodiesterase 5 inhibitor (sildenafil) as the first line management.
  • Offer an inhaled prostanoid (iloprost) for low risk patients who do not respond to first line management.
  • Offer parental prostanoids (epoprostenol) required if patients do not respond to inhaled therapy.
  • Offer atrial septostomy or lung transplantation for patients who progress despite optimal medical treatment.
122
Q

what are the causes of hypoxia?

A
  • Fluid filling of alveolar spaces (ARDS, alveolar haemorrhage (Goodpasture’s syndrome and granulomatosis with polyangitis).
  • Collapse of alveolar spaces (pneumothorax)
  • Redistribution of blood form from functional alveoli (shunting)
  • Loss of blood flow to alveolar tissue (pulmonary embolism)
  • Underlying loss of pulmonary tissue (emphysema, trauma, fibrosis).
  • Thickening or fluid build up at alveolar membranes (pneumonia).
123
Q

what are the causes of hypercapnia?

A
  • Poor ventilatory muscle function (Guillain-Barre, drug overdose).
  • Obstruction of airways and alveoli (asthma, COPD, pulmonary oedema).
  • Secretions in the small airways and alveoli (COPD, cystic fibrosis).
  • Chest wall abnormalities (traumatic flail chest, kyphoscoliosis).
124
Q

what are the clinical features of respiratory failure?

A
  • Dyspnoea.
  • Confusion.
  • Tachycardia.
  • Accessory breathing muscle use.
  • Stridor.
  • Inability to speak.
  • Retraction of intercostal spaces.
  • Cyanosis.
  • Anxiety.
  • Headache.
  • Hypoventilation
125
Q

what is seen on ABG in respiratory failure?

A
  • pH < 7.38
  • PaO2 < 8 kPa
  • PaCO2 > 7 kPa.
126
Q

how is respiratory failure managed?

A
  • Perform airway clearance (laryngoscopy, bronchoscopy) in patients with airway obstructions
  • Administer supplemental oxygen (nasal cannula, face mask) in stable patients immediately
  • Consider non-invasive ventilation (BiPAP or CPAP) in stable patients if supplemental oxygen delivered by a nasal cannula or face mask is unsuccessful.
  • Perform endotracheal intubation and mechanical ventilation in unstable patients with progressive hypoxia or hypercapnia, in order to protect the airway and reduce the risk of aspiration.
  • Treat the underlying cause.
127
Q

what are the complications associated with ventilation?

A
  • Dental injury and soft tissue trauma of the lips and mouth with intubation.
  • Skin necrosis with CPAP and BiPAP.
  • Pneumothorax with NIV and intubation.
  • Endotracheal tube misplacement or dislodgement.
  • Hospital acquired pneumonia (nosocomial infection) with NIV and intubation.
  • Nasal mucosa damage and superficial infection, raising the risk of colonisation with MRSA.
128
Q

what are the risk factors for developing sinusitis?

A
  • Asthma.
  • Allergic rhinitis.
  • Smoking.
  • Nasal polyps.
  • Deviated nasal septum.
  • Cystic fibrosis.
129
Q

what are the clinical features of viral sinusitis?

A
  • Fever.
  • Store throat.
  • Myalgia.
  • Clear nasal discharge.
130
Q

what are the clinical features of bacterial sinusitis?

A
  • Purulent nasal discharge.
  • Frontal facial pain that is worse when leaning forwards.
  • Nasal obstruction.
  • ‘Double sickening’ where symptoms worsen after an initial improvement.
131
Q

how is chronic sinusitis diagnosed?

A
  • Perform anterior rhinoscopy: Polyps; Purulence; Structural abnormalities.
  • Perform nasal endoscopy: Polyps; Purulence; Structural abnormalities.
132
Q

how is acute sinusitis managed?

A
  • paracetamol
  • intranasal steroid
  • phenoxymethylpenicillin for severe non-life-threatening acute bacterial sinusitis
  • Offer co-amoxiclav for severe life-threatening acute bacterial sinusitis where the patient is systemically very unwell
133
Q

how is chronic sinusitis managed?

A
  • nasal irrigation with saline solution

- intranasal steroid (mometasone) for chronic sinusitis.

134
Q

what are the risk factors for a PE?

A
  • Deep vein thrombosis.
  • Previous venous thromboembolism.
  • Active cancer.
  • Recent surgery.
  • Significant immobility such as hospitalisation or bed rest.
  • Lower limb trauma or fracture.
  • Pregnancy and 6 weeks postpartum.
  • Increasing age.
  • The use of combined oral contraception or hormone replacement therapy.
  • Obesity.
  • One or more significant medical comorbidities such as heart disease.
  • Varicose veins.
  • Thrombophilia.
135
Q

what are the symptoms of a PE?

A
  • Dyspnoea.
  • Tachypnoea.
  • Pleuritic chest pain.
  • Leg pain and swelling (usually unilateral).
  • Retrosternal chest pain due to right ventricular ischaemia.
  • Dizziness or syncope due to right ventricular failure.
136
Q

what are the signs of a PE?

A
  • Tachycardia.
  • Hypoxaemia (oxygen saturations less than 94%)
  • Pyrexia.
  • Raised JVP.
  • Gallop rhythm, a widely split second heart sound, tricuspid regurgitate murmur.
  • Pleural rub.
  • Hypotension (systolic blood pressure less than 90 mmHg).
137
Q

what factors are incorporated into the PE wells score?

A
  • painful leg swelling
  • alternative diagnosis is less likely than a PE
  • Tachycardia
  • immobilisation for more than 3 days or surgery in the previous 4 weeks
  • haemoptysis
  • malignancy
138
Q

what is seen on ECG in PE?

A
  • Sinus tachycardia
  • Right axis deviation
  • Right bundle branch block, S1Q3T3.
139
Q

what investigations should be conducted in a suspected PE with a wells score of more than 4?

A

-CTPA with interim therapeutic anticoagulation

140
Q

what investigations should be conducted in a suspected PE with a wells score of 4 or less?

A
  • D-dimer test
  • interim therapeutic anticoagulation if D-dimer results cannot be obtained within 4 hours.
  • Arrange admission to hospital for immediate CTPA if the D-dimer test is positive.
  • Stop interim therapeutic anticoagulation and consider an alternative diagnosis if the D-dimer test is negative.
141
Q

when should a V/Q scan be used in suspected PE?

A
  • Pregnant women.
  • Renal impairment.
  • Contrast allergy.
  • Younger patients.
142
Q

how are haemodynamically unstable PE patients managed?

A
  • Give intravenous fluids (0.9% NaCl or Hartmann’s solution) over 15 minutes and monitor for signs of right heart failure.
  • Start oxygen therapy to target saturations of 94 - 98%, or 88 - 92% in patients at risk of hypercapnic respiratory failure.
  • Start unfractioned heparin prior to thrombolysis. Stop UFH within 24 hours.
  • Commence thrombolytic therapy (streptokinase or alteplase).
  • Give an inotropic agent (noradrenaline or dobutamine) if systolic blood pressure remains < 90 mmHg after thrombolysis.
  • Consider pulmonary embolectomy if the above interventions have failed.
143
Q

how is a haemodynamically stable PE patient managed?

A
  • Haemodynamically stable patients (normotensive) should commence oral anticoagulation and either be admitted or discharged based on their PESI.
  • Offer a DOAC (apixaban for 7 days or rivaroxaban for 21 days) for patients with no co-morbidities, or who have active cancer. It should hone be continued for 3 months.
  • Offer unfractioned heparin and warfarin for at least 5 days, followed by warfarin alone for patients with renal impairment or established renal disease. It should then be continued for 3 months.
  • Offer LMWH and warfarin for at least 5 days, followed by warfarin alone for patients with triple positive antiphospholipid syndrome. It should then be continued for 3 months.
  • Consider stopping anticoagulation after 3 months in patients with a provoked DVT, or 6 months if the patient has cancer.
  • Consider continuing anticoagulation after 3 months in patients with an unprovoked DVT. Use the HAS-BLED score to assess risk of major bleeding.
144
Q

which PE patients should be considered for an IVC filter?

A
  • An absolute contraindication to oral anticoagulation (active bleeding, recent intracranial haemorrhage).
  • Recurrent PE despite adequate anticoagulant treatment, including adjustments in dose and use of alternative agents.
145
Q

what are the clinical features of TB?

A
  • Weight loss.
  • Fever.
  • Night sweats.
  • Anorexia.
  • Malaise.
  • Shortness of breath.
  • Haemoptysis.
146
Q

what are the symptoms and signs of extrapulmonary TB?

A
  • Lymphadenopathy suggest lymphatic TB.
  • Bone or joint pains, back pain, joint swelling suggest joint or spinal TB.
  • Abdominal pain and ascites suggests gastrointestinal TB.
  • Pyuria suggests renal TB.
  • Headache, vomiting, irritability, confusion, cranial nerve abnormalities suggests TB meningitis.
  • Skin lesions such as erythema nodosum suggests cutaneous TB.
  • Breathlessness, chest pain, ankle swelling may suggest TB pericarditis
147
Q

what is seen on chest x-ray in active TB?

A
  • Consolidation in upper lobes
  • Cavitation
  • Hilar lymphadenopathy
148
Q

how is active TB diagnosed?

A

-sputum AFB culture with Ziehl–Neelsen staining

149
Q

how is latent TB diagnosed?

A

-Mantoux test

150
Q

how is active TB managed?

A
  • Initial phase: Offer 2 months of isoniazid with pyridoxine, rifampicin, pyrazinamide and ethambutol.
  • Continuation phase: Offer 4 months (10 months if CNS involvement) of isoniazid with pyridoxine and rifampicin.
151
Q

how is latent TB managed?

A
  • Offer 3 months of isoniazid with pyridoxine and rifampicin for patients under 35 years and in whom hepatotoxicity is a concern.
  • Offer 6 months of isoniazid with pyridoxine if interactions with rifamycins are a concern (HIV and transplant).
152
Q

what are the side effects of isoniazid?

A

-polyneuropathy

153
Q

what are the side effects of rifampicin?

A
  • induces liver enzymes

- orange body secretions

154
Q

what are the side effects of ethambutol?

A

-optic neuritis with colour blindness

155
Q

what are the side effects of pyrazinamide?

A

-hyperuricaemia and gout

156
Q

what factors are incorporated into the feverPAIN score?

A
  • fever
  • absent cough
  • symptom onset <3 days ago
  • inflamed tonsils
  • tonsillar exudate
157
Q

how should a sore throat with feverPAIN score of 0/1 be treated?

A

no antibiotics

158
Q

how should a sore throat with feverPAIN score of 2/3 be treated?

A
  • No antibiotic

- back-up antibiotic given (to be given if no improvement in 3 to 5 days

159
Q

how should a sore throat with feverPAIN score of 4+ be treated?

A
  • Immediate antibiotic

- back up antibiotic prescription

160
Q

what is the first line treatment for pharyngitis?

A
  • phenoxymethylpenicillin,

- clarithromycin or erythromycin given if penicillin allergy

161
Q

what are the clinical features of acute otitis media?

A
  • pain in the ear
  • fever
  • tympanic membrane is seen to be bright red and bulging with loss of the normal light reflection
  • may be perforation
162
Q

how is otitis media managed?

A
  • analgesia
  • If the child is under 2 with bilateral infection, or there is otorrhoea give either and immediate or back-up antibiotic prescription to be collected after 3 days if symptoms worsen
  • If the child is systemically unwell, vomits, or is at high risk of complications, give an immediate antibiotic prescription and refer if severe.
  • First line: Amoxicillin, clarithromycin or erythromycin
  • Second line: co-amoxiclav
163
Q

how is otitis media with effusion managed?

A
  • Children with conductive hearing loss and developmental delay require referral to ENT
  • Other children can be actively observed for 6-12 weeks
  • The non-surgical management includes hearing aids and autoinflation
  • Surgical management includes grommet ventilation tubes insertion
  • If these problems recur after grommet extrusion, reinsertion of grommets with adjuvant adenoidectomy is usually advocated.
164
Q

what are the indications for tonsillectomy in children?

A
  • Recurrent severe tonsillitis (as opposed to recurrent URTIs)
  • A peritonsillar abscess (quinsy)
  • Obstructive sleep apnoea (the adenoids will also normally be removed).
165
Q

what are the indications for adenoidectomy in children?

A
  • Recurrent otitis media with effusion with hearing loss

- Obstructive sleep apnoea

166
Q

what is quinsy?

A

-a collection of pus outside the capsule of the tonsil usually located adjacent to its superior pole.

167
Q

what are the clinical features of quinsy?

A
  • trismus
  • the pus pushes the uvula across the midline to the opposite side.
  • The area is usually hyperaemic and smooth
168
Q

how is quinsy treated?

A
  • diathermy dissection
  • laser excision
  • coblation
169
Q

what are the clinical features of croup?

A
  • barking cough
  • harsh stridor
  • hoarseness
  • usually preceded by fever and coryza.
  • The symptoms often start, and are worse, at night.
  • There may be sternal recession, agitation and lethargy
170
Q

how is croup managed?

A
  • oral dexamethasone
  • nebulised adrenaline
  • tracheal intubation if respiratory failure
171
Q

what are the clinical features of bacterial tracheitis?

A
  • similar to severe viral croup
  • child has a high fever
  • appears toxic
  • rapidly progressive airways obstruction with copious thick airway secretions.
172
Q

how is bacterial tracheitis managed?

A

-IV cefotaxime or ceftriaxone

173
Q

what are the features of epiglottitis?

A

o High fever in an ill, toxic-looking child
-An intensely painful throat that prevents the child from speaking or swallowing

  • saliva drools down the chin
  • Soft inspiratory stridor and rapidly increasing respiratory difficulty over hours
  • The child sitting immobile, upright, with an open mouth to optimise the airway.
174
Q

how is epiglottitis managed?

A
  • endotracheal intubation or tracheostomy

- ceftriaxone or cefotaxime, followed by 3-5 days of oral co-amoxiclav

175
Q

what are the features of the catarrhal phase of whooping cough?

A
  • a week of coryza
176
Q

what are the features of the paroxysmal phase of whooping cough?

A
  • characteristic paroxysmal or spasmodic cough
  • followed by a characteristic inspiratory whoop
  • During a paroxysm, the child goes red or blue in the face, and mucus flows from the nose and mouth.
  • The whoop may be absent in infants, but apnoea is a feature at this age.
  • Epistaxis and subconjunctival haemorrhages can occur after vigorous coughing.
  • lasting 3-6 weeks
177
Q

how is whooping cough diagnosed?

A
  • culture of a per-nasal swab

- PCR testing of nasopharyngeal swab

178
Q

how is whooping cough managed?

A
  • Prescribe clarithromycin for infants less than one month of age if the onset of the cough is within 21 days.
  • Prescribe azithromycin for infants and children older than one month of age, as well as non-pregnant adults if the onset of the cough is within 21 days.
  • Offer co-trimoxazole in this group if a macrolide is contraindicated.
  • Prescribe erythromycin for pregnant woman if the onset of the cough is within 21 days.
179
Q

what are the clinical features of bronchiolitis?

A
  • Preceding coryzal prodrome with runny nose
  • Persistent cough
  • Tachypnoea
  • Wheeze
  • Fever
  • Poor feeding
180
Q

what are the examination findings in bronchiolitis?

A
  • Sharp, dry cough with tachypnoea
  • Subcostal and intercostal recession
  • Hyperinflation of the chest:
  • –Prominent sternum
  • –Liver displaced downwards
  • Fine end-inspiratory crackles
  • High-pitched wheezes – expiratory > inspiratory
  • Tachycardia
  • Cyanosis or pallor.
181
Q

how is bronchiolitis managed?

A
  • Humidified oxygen is delivered via nasal cannulae
  • Fluids
  • CPAP or full ventilation
182
Q

how is bronchiolitis prevented?

A
  • A monoclonal antibody to RSV

- palivizumab

183
Q

what are the clinical features of flu?

A
  • fever
  • shivering
  • generalized aching in the limbs.
  • This is associated with severe headache, soreness of the throat and a dry cough that can persist for several weeks.
  • Diarrhoea
184
Q

how is flu diagnosed?

A

-viral throat swab for haemaglutinin antibody

185
Q

how is flu treated?

A
  • bed rest and paracetamol
  • antibiotics to prevent secondary infection in those with chronic bronchitis, cardiac or renal disease.
  • neuraminidase inhibitors in high risk patients
186
Q

what are the clinical features of hyperventilation syndrome?

A
  • chest pain
  • Hyperpnoea
  • Tachypnoea
  • Dyspnoea
  • wheeze
  • Dizziness
  • Weakness
  • Confusion
  • Agitation
  • Depersonalization
  • visual hallucinations
  • syncope or seizure
  • paraesthesias (usually upper limbs and bilateral)
  • peri-oral numbness.
  • Bloating
  • Belching
  • Flatus
  • epigastric pressure (due to aerophagia)

dry mouth (due to mouth breathing and anxiety).

187
Q

how is acute hyperventilation syndrome managed?

A
  • Reassuring the patient.
  • Alleviating severe anxiety (e.g. use of Benzodiazepine).
  • Establishment of normal breathing pattern (instructing the patient to breathe more abdominally using the diaphragm; physically compressing the upper chest and instructing the patient to exhale maximally to reduce hyperinflation).
188
Q

what are the clinical features of pleurisy?

A
  • sharp localised pain

- worse on deep inspiration, coughing and occasionally on twisting and bending movements

189
Q

what are the clinical features of oropharyngeal carcinoma?

A
  • painless swelling or lump in the neck
  • a sore throat or tongue
  • earache
  • difficulty swallowing or moving mouth and jaw
  • changes in voice
  • bad breath
  • unexplained weight loss.
190
Q

what are the symptoms of nasopharyngeal carcinoma?

A
  • a lump in the neck
  • Hearing loss (usually only in 1 ear)
  • Tinnitus (hearing sounds that come from inside the body rather than from an outside source)
  • a blocked or stuffy nose
  • Nosebleeds
191
Q

what are the chest x-ray appearances of pleural effusion?

A
  • obliteration of the costophrenic angle

- dense homogenous shadows occupying part of or all of the hemithorax.

192
Q

what are the features and causes of a transudative pleural effusion?

A
  • <30g/L protein
  • <200 IU/L lactic dehydrogenase
  • heart failure
  • nephrotic syndrome
  • liver failure
  • malabsorption
  • hypothyroidism
  • constrictive pericarditis
  • meig’s syndrome
193
Q

what are the features and causes of a exudative pleural effusion?

A
  • > 30g/L protein
  • > 200 IU/L lactic dehydrogenase
  • pneumonia
  • empyema
  • malignancy
  • PE
  • pulmonary infarction
  • TB
  • SLE
  • RA
  • Dressler’s syndrome
194
Q

what are the causes of pulmonary oedema?

A
  • Cardiovascular, usually left ventricular failure (post-MI or ischaemic heart disease).
  • valvular heart disease
  • arrhythmias
  • malignant hypertension.
  • ARDS from any cause, eg trauma, malaria, drugs.
195
Q

what are the symptoms of pulmonary oedema?

A
  • Dyspnoea
  • orthopnoea (eg paroxysmal)
  • pink frothy sputum.
196
Q

what are the signs of pulmonary oedema?

A
  • Distressed, pale, sweaty.
  • Tachypnoea
  • pink frothy sputum
  • pulsus alternans
  • Raised JVP
  • fine lung crackles
  • triple/gallop rhythm
  • wheeze (cardiac asthma).
  • Usually sitting up and leaning forward.
197
Q

how is pulmonary oedema managed?

A
  • Daily weights, aim reduction of 0.5kg/day, check observations at least 4 times a day.
  • Change to oral furosemide or bumetanide.
  • If on large doses of loop diuretic, consider the addition of a thiazide (eg bendroflumethiazide or metolazone 2.5–5mg daily PO).
  • ACE-i if LVEF <40%.
  • If ACE-i contraindicated, consider hydralazine and nitrate
  • Also consider beta-blocker and spironolactone (if LVEF <35%).
  • Consider digoxin ± warfarin, especially if AF.
198
Q

what is anatomic dead space?

A
  • all of the air in the respiratory system other than the alveoli
  • it is unavailable for gas exchange.
  • It has a volume of 150 ml.
199
Q

what is physiologic dead space?

A
  • Physiologic dead space is the air in poorly perfused alveoli plus the anatomic dead space
  • it is unavailable for gas exchange.
  • It has a volume of 1.5L
200
Q

define tidal volume

A
  • volume of air inspired or expired with each normal breath

- 500 ml

201
Q

define inspiratory reserve volume

A
  • the extra volume of air that can be inspired over and above the normal tidal volume when the person inspires with full force
  • 3000 ml
202
Q

define expiratory reserve volume

A
  • the maximum volume of air that can be expired by forceful expiration after the end of a normal tidal expiration
  • 1100 ml
203
Q

define residual volume

A
  • the volume of air remaining in the lungs after the most forceful expiration
  • 1200 ml
204
Q

define inspiratory capacity

A
  • the tidal volume plus the inspiratory reserve volume.
  • It is the amount of air that a person can breathe in, beginning at the normal expiratory level and distending the lungs to the maximum amount
  • 3500 ml
205
Q

define functional residual capacity

A
  • the expiratory reserve volume plus the residual volume.
  • It is the amount of air that remains in the lungs at the end of normal expiration
  • 2300 ml
206
Q

define vital capacity

A
  • the inspiratory reserve volume plus the expiratory reserve volume plus the tidal volume
  • It is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent and then expiring to the maximum extent
  • 4600 ml
207
Q

define total lung capacity

A
  • equals the vital capacity plus the residual volume
  • It is the maximum volume to which the lungs can be expanded with the greatest possible effort
  • 5800 ml
208
Q

define forced vital capacity

A

-the volume of air that is expired when the person inspires maximally then exhales with maximum expiratory effort as rapidly and completely as possible.

209
Q

define forced expiratory volume

A

-the amount of air that is expired during the first second of the forced vital capacity manoeuvre.

210
Q

what are the adverse effects of SABAs?

A
  • Activation of β2-adrenoreceptors causes tachycardia, palpitations, anxiety and tremor
  • promotes glycogenolysis so causes increased blood glucose.
211
Q

which drugs interact with SABAs?

A
  • beta blockers reduce their effectiveness
  • concomitant use with theophylline
  • corticosteroids causes hypokalaemia.
212
Q

to which patients should SABAs be given cautiously?

A
  • cardiovascular disease
  • diabetes mellitus
  • hypothyroidism
213
Q

what are the adverse effects of ICS?

A
  • Oral candida
  • hoarse voice
  • pneumonia in COPD.
214
Q

What are the adverse effects of LABAs

A
  • muscle cramps
  • Activation of β2-adrenoreceptors causes tachycardia, palpitations, anxiety and tremor
  • promotes glycogenolysis so causes increased blood glucose.
215
Q

what are the adverse effects of anti-muscarinics?

A

-dry mouth

216
Q

in which patients should anti-muscarinics be used cautiously?

A
  • Caution in patients with glaucoma due to increased intra-ocular pressure.
  • Caution in patients with arrhythmias.
217
Q

what are the adverse effects of leukotriene receptor antagonists?

A
  • Abdominal pain and headache are common.
  • Churg-Strauss syndrome and hepatotoxicity are rare.
  • Zafirlukast may cause agranulocytosis.
218
Q

with which drugs do LTRA interact?

A

-reduces anti-coagulation effect of warfarin

219
Q

how should oxygen be administered?

A
  • Target SpO2 of 94-98% via a nasal cannula (44%) in most patients.
  • Target SpO2 of 88-92% via a Venturi mask (28%) in patients with type 2 respiratory failure.
  • Prescribe a reservoir mask (85%) for patients in critical illness and with SpO2 less than 85%.
220
Q

what are the adverse effects of phosphodiesterase type 5 inhibitors?

A
  • Common side effects include flushing, headache and nasal congestion
  • Serious side effects include hypotension, tachycardia, palpitations and vascular events.
221
Q

with which drugs do phosphodiesterase type 5 inhibitors interact?

A
  • Any drugs that increase nitric oxide, including nitrates and nicorandil
  • any other vasodilators such as alpha blockers, calcium channel blockers
  • cytochrome P450 inhibitors such as amiodarone, diltiazem, fluconazole.
222
Q

in which patients should phosphodiesterase type 5 inhibitors be used cautiously?

A
  • Avoid in patients who have recently had a vascular event

- Caution in patients with severe hepatic or renal impairment.

223
Q

what are the adverse effects of anti-histamines?

A
  • Chlorphenamine causes sedation while newer drugs do not
  • common side effects include antimuscarinic effects such as blurred vision and dry mouth
  • severe side effects include hypersensitivity reactions and extrapyramidal effects.
224
Q

what are the side effects of nasal decongestants such as pseudoephedrine?

A
  • Common effects include anxiety, insomnia, headaches, hypertension
  • serious effects include hallucinations, angle-closure glaucoma and urinary retention.
225
Q

in which patients should nasal decongestants such as pseudoephedrine be used cautiously?

A
  • diabetes
  • hypertension
  • hyperthyroidism
  • BPH
  • risk of angle-closure glaucoma.
226
Q

what are the adverse effects of cephalosporins?

A
  • Nausea and diarrhoea
  • less frequently antibiotic-associated colitis
  • Hypersensitivity
  • seizures.
227
Q

in which patients should cephalosporins be used cautiously?

A
  • Caution in patients at risk of C.difficile infection (elderly and hospital) and in patients with epilepsy and renal impairment.
  • Avoid in patients with known hypersensitivity reactions.
228
Q

with which drugs do cephalosporins interact?

A
  • Enhance anti-coagulant effect of warfarin by killing gut flora that synthesise vitamin K
  • increase nephrotoxicity of aminoglycosides
  • reduced efficacy of valproate.
229
Q

what are the adverse effects of metronidazole?

A
  • Nausea and vomiting
  • metallic taste
  • hypersensitivity
  • neuropathy, seizures and encephalopathy.
230
Q

with which drugs does metronidazole interact?

A
  • Increases anticoagulant effect of warfarin
  • increased risk of toxicity with phenytoin and lithium
  • decreased plasma concentration of phenytoin with impaired antimicrobial activity.
  • alcohol causes disulfiram like reaction with flushing, headache, nausea and vomiting
231
Q

what are the adverse effects of Piperacillin with tazobactam?

A
  • Nausea and diarrhoea and less frequently antibiotic-associated colitis
  • hypersensitivity reactions.
232
Q

in which patients should piperacillin-tazobactam be used cautiously?

A
  • Caution in patients at risk of C.difficile infection and those with moderate or several renal impairment
  • avoid with history of penicillin allergy.
233
Q

with which drugs do piperacillin tazobactam interact?

A
  • Reduced renal excretion of methotrexate, increasing risk of toxicity
  • Enhance anticoagulant effect of warfarin by killing gut flora that synthesise vitamin K.
234
Q

what are the adverse effects of fluoroquinolones?

A
  • Nausea and diarrhoea
  • hypersensitivity reactions
  • seizures and hallucinations
  • rupture of muscle tendons
  • prolong QT interval.
235
Q

in which patients should fluoroquinolones be used with caution?

A
  • Caution in patients with seizures
  • QT prolongation
  • G6PD deficiency
  • avoid in patients with tendon disorders.
236
Q

with which drugs do fluoroquinolones interact?

A
  • Increased risk of seizures with NSAIDs
  • increased risk of tendon rupture with prednisolone
  • prolonged QT interval with amiodarone, antipsychotics; macrolides and SSRIs
  • toxicity with theophylline increased anticoagulant affect with warfarin.
237
Q

what are the adverse effects of tetracyclines?

A
  • Nausea and vomiting
  • oesophageal irritation and ulceration
  • photosensitivity
  • discolouration of tooth enamel
  • intracranial hypertension.
238
Q

in which patients should tetracyclines be used with caution?

A
  • Avoid in pregnancy, breastfeeding or children under 12.

- Caution in patients with renal impairment.

239
Q

with which drugs do tetracyclines interact?

A
  • Divalent cations such as calcium (dairy products), antacids or iron
  • enhanced anticoagulant effect of warfarin by killing bacteria that synthesise vitamin K.
240
Q

what are the adverse effects of co-trimoxazole?

A
  • Nausea, vomiting and sore mouth
  • skin rash
  • severe anaphylaxis
  • haematological disorders such as anaemia, leucopenia and thrombocytopenia
  • hyperkalaemia and elevated plasma creatinine.
241
Q

in which patients should co-trimoxazole be used with caution?

A
  • Avoid in first trimester of pregnancy due to increased risk of foetal abnormalities
  • caution in folate deficiency, renal impairment, neonates and elderly.
242
Q

with which drugs do co-trimoxazole interact?

A
  • Hyperkalaemia with aldosterone antagonists, ACEIs and ARAs
  • Adverse haematological effects with folate antagonists (methotrexate) and drugs that increase folate metabolism (phenytoin)
  • enhanced anticoagulant effect of warfarin by killing bacteria that synthesise vitamin K

FINALS (18 decks)

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