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Phase 2a Sheffield Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Where are Anti-inflammatory steroids produced?

A

Adrenal Cortex

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2
Q

What is an example of a mineralcorticoid and where are they produced?

A

Aldosterone

Zona Glomerulosa

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3
Q

What is an example of a glucocorticoid and where are they produced?

A

Hydrocortisone

Zona fasiculata

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4
Q

How do glucocorticoids work?

A

interfere with gene transcription (They have zinc fingers)

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5
Q

How do mineralcorticoids work?

A

Metabolic changes and anti-inflammatory effect.

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6
Q

What is a consequence of prolonged hydrocortisone usage?

A

Muscle wasting
osteoporosis
Increased risk of infection

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7
Q

What is pulmonary vasculitis?

A

Inflammation of the pulmonary arterial wall

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8
Q

What is the treatment for pulmonary vasculitis?

A

Immunosuppressants as it is AI mediated.

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9
Q

What is whooping cough caused by?

A

Bordetella pertussis (Gram neg bacilli)

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10
Q

What is bordetella pertussis cultured on?

A

Bordet gengou agar

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11
Q

What are the symptoms of whooping cough?

A
  1. Chronic cough

2. Inspiratory whoop, posttusive vomiting

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12
Q

What is the treatment of whooping cough?

A

Clarithromyocin

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13
Q

What is the vaccination schedule for whooping cough?

A

8,12,16 weeks and at 3years 4 months with dTaP

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14
Q

What is coup?

A

Acute larygnotracheobronchitis affecting the trachea, bronchi and larynx.

Most common in children

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15
Q

What is the cause of coup?

A

Parainfluenza virus.

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16
Q

Who is at risk of CMV?

A

Immunocompromised patients.

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17
Q

Why is treatment of CMV difficult?

A

Long duration and potential toxicity

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18
Q

What is the difference between palliative and radical radiotherapy?

A

Radical – Daily treatment for 4-6 weeks.

Palliative – patient attends the minimum number of visits to control symptoms

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19
Q

What are some side effects of radiotherapy

A

Fatigue, anorexia, cough, oesophagitis and systemic symptoms.

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20
Q

What is a positive and negative of adding chemotherapy to radiotherapy?

A
  • Positive –> Survival advantage

- Negative –> increased risk of toxicity

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21
Q

What are the side effects of chemotherapy?

A

Alopecia, nausea/vomiting, peripheral neuropathy and constipation/diarrhoea.

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22
Q

What are the aims of palliative chemotherapy?

A
  1. Relieve symptoms
  2. Improve QOL
  3. Shrink tumours
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23
Q

What does pleural fluid contain?

A

Albumin and globulin

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24
Q

What produces pleural fluid and how much is found in a healthy cavity?

A

Produced –> Parietal pleura

15ml

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25
Q

What is the function of pleura?

A

Allows movement of the lung and lung expansion against the chest wall.

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26
Q

What diseases are associated with the pleura.

A
  1. Pleural effusions
  2. Pleural plaques
  3. Pneumothorax
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27
Q

What are the viral and bacterial causes of pharyngitis?

A
  • Viral usually e.g. rhinovirus and adenovirus

- Bacteria e.g. Streptococcus pyogenes

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28
Q

What is the centor criteria?

A

Determines the likelihood that a sore throat is bacterial

  1. Tonsillar exudate
  2. Fever >38
  3. Tender/enlarged anterior cervical lymph nodes
  4. Absence of cough
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29
Q

What is neutropenia?

A

A disease characterised by having an abnormally low concentration of neutrophils in the blood.

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30
Q

What is the cause of neutropenia?

A

Iatrogenic e.g. Chemo

Examples of iatrogenic suppression

  1. Corticosteroid use
  2. Chemo
  3. Immune suppression post organ transplant
  4. Rituximab
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31
Q

Give 4 examples of non-specific supression

A
  1. Malnutrition
  2. Alcohol
  3. Sepsis
  4. Trauma
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32
Q

How can illness be prevented in the immunocompromised?

A
  1. Hand hygiene
  2. Education
  3. Isolation
  4. Screen for TB before anti TNF therapy
  5. PCP prophylaxis of
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33
Q

What is the usual presentation of pulmonary infection in the immunocompromised?

A
  1. Pyrexia
  2. Lethargy
  3. Cough
  4. Breathlessness
  5. Hypxoic
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34
Q

What is empyema?

A

Pockets of pus that have collected in the body cavity.

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35
Q

What are the signs and symptoms of Empyema?

A
  • WBC/CRP doesn’t settle with Abx
  • Pain on deep inspiration
  • Pleural collection.
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36
Q

What is the management of empyema?

A

Drainage

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37
Q

What is Wegener’s Granulomatosis?

A

Vasculitis of an unknown aetiology, commonly involves the upper airway and endobronchi

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38
Q

What are the symptoms of Wegener’s Granulomatosis?

A
  1. Rhionorrhea
  2. Nasal mucosa ulceration
  3. Cough
  4. Haemoptysis
  5. Pleuritic chest pain
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39
Q

What serum investigations would you order in Wegener’s granulomatosis?

A
  • C-ANCA and anti-PR3 positive
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40
Q

What is the treatment of Wegener’s granulomatosis?

A
  1. If severe – high dose steroids

2. If non-end organ threatening – moderate steroids

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41
Q

What should the PaO2 be to be suitable for home O2?

A

PaO2 <7.3kPa when breathing room air.

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42
Q

Describe the assessment process of home O2?

A
  1. Blood gas measurements taken 3 weeks apart in a stable pt receiving bronchodilator therapy
  2. Pt should stop smoking
  3. Pt should have a PaO2<7.3kPa
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43
Q

What is Horners syndrome?

A

Results from apical lung cancer affecting the T1 nerve root.

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44
Q

What are the signs of Horner’s syndrome?

A
  1. Anhydrosis
  2. Miosis –> pupil contraction
  3. Ptosis
  4. Loss of cilospinal reflex
  5. Enophthalmos – backwards displace of the eyeball.
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45
Q

What is sarcoidosis?

A

Granulomatous disease that affects the organ system but typically lungs/lymph nodes.

Restrictive disease

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46
Q

What are the symptoms of Sarcoidosis?

A
  • Cough
  • SOB
  • Wheeze
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47
Q

What is the effect on the following in sarcoidosis?

metabolic 
neurological
bone
eyes
skin
A

Metabolic effect of sarcoidosis –> hypercalcaemia
Neurological effect –> inflammation of the meninges and seizures
Effect on bone –> arthralgia (pain in joints)
Effect on eyes –> Uveitis
Effect on skin –> erythema nodosum (red tender lumps)

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48
Q

What is the differential diagnosis of sarcoidosis?

A

Pulmonary TB and lymphoma

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49
Q

What is the treatment for sarcoidosis?

A

Steroids

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50
Q

What is a pneumothorax?

A

Air in the pleural space which leads to partial lung collapse.

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51
Q

What are the main types of pneumothorax?

A
  1. Traumatic e.g. stab wound
  2. Spontaneous –> can be primary (PSP) or secondary (SSP)
  3. Iatrogenic
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52
Q

What is the treatment for traumatic pneumothorax?

A

Drainage ASAP

Chest drainage site –> bound by pect major, latissimus dorsi and the nipple in men or the 5th ICS in women.

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53
Q

What is a tension pneumothorax?

A

Pleural tear creates 1 way valve through which air passes in inspiration

Increased intra-pleural pressure –> Resp distress, cardiac arrest and shock.

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54
Q

What is the treatment for a tension pneumothorax?

A

Needle decompression.

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55
Q

What is pneumoconiosis?

A

A group of lung disorders that that reflects inhaled dust/toxins

e.g. Coal workers pneumoconiosis, silicosis, asbestos exposure and extrinsic allergic alveolitis

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56
Q

What is silicosis and what does those affected have a higher risk of?

A

reflects silica structure and may occur in grinding related occupations and mining practices

TB and cancer

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57
Q

What are the consequences of asbestos exposure?

A
  1. Lung cancer
  2. Persistent Pleural effusion
  3. Diffuse pleural fibrosis
  4. Diffuse interstitial lung fibrosis
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58
Q

What is the histological pattern in those in RA with lung disease.

A

Paralleling usual interstitial pneumonia (UIP)

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59
Q

How does Anti IgE therapy work in asthma?

A
  • Works as Ab binds to and neutralises free IgE, preventing IgE binding
  • results in decreased mast cell sensitisation –> allergens can’t activate mast cells.
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60
Q

Why are inhaled medicines better in asthma?

A

They are more likely to reach the target sites.

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61
Q

What is an epidemic?

A

More cases in a region/country

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62
Q

What is a pandemic?

A

Epidemics that span international boundaries.

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63
Q

What are the consequences of pandemics?

A
  1. High morbidity
  2. Excess mortality
  3. Social disruption
  4. Economic disruption
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64
Q

What factors suggest a pandemic will be likely?

A
  • More travel
  • Increasing world population
  • Rise in intensive farming
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65
Q

What factors suggest pandemics will not be likely?

A
  1. Healthier populations due to medical advances
  2. Better healthcare
  3. Vaccination
  4. Antivirals
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66
Q

What is interstitial lung disease?

A

Diseases of the alveolar/capillary interaction. Increased scarring around the alveoli so an increased diffusion pathway for gaseous exchange

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67
Q

What are the 5 major categories of Interstitial Lung diseases?

A
  1. Associated with systemic disease e.g. rheumatological
  2. Environmental aetiology
  3. Granulomatous disease e.g. sarcoidosis
  4. Idiopathic e.g. IPF
  5. Other
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68
Q

What are the signs and symptoms of interstitial lung disease?

A
  1. Cough
  2. Breathlessness
  3. Finger clubbing
  4. Evidence of systemic disease
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69
Q

What investigation would you order in interstitial lung disease?

A
  • CXR
  • Blood tests
  • Pulmonary function tests
  • Bronchoscopy with biopsy
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70
Q

Is interstitial lung disease restrictive or obstructive?

A

Restrictive

Fibrosis causes decreased gas transfer and decreased PaO2

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71
Q

What is the treatment for interstitial lung disease?

A
  • Remove the exposure

- Steroids

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72
Q

What are 3 examples of chronic interstitial lung disease?

A

Interstitial pneumonia
Sarcoidosis
Rheumatoid arthritis

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73
Q

What is the pathology of chronic interstitial lung disease?

A

Increasing fibrous tissue within lung parenchyma resulting in increased stiffness and decreased expansion

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74
Q

What is the effect of chronic interstitial lung disease on lung volumes?

A
  1. Reduced TCO, VC and FEV1

2. FEV1/FVC ratio and PEFR normal.

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75
Q

What is the treatment for chronic interstitial lung disease?

A

Steroids and immunosupressive agents.

Lung transplant

Drugs can cause issues as they can generate free radicals.

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76
Q

What are the signs and symptoms of Idiopathic pulmonary fibrosis?

A
  1. Dyspnoea on exertion
  2. Dry cough
  3. Elderly effected

Progressive fibrosis in the alveoli that limits a patients ability to respire

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77
Q

What is IPF?

A

A disease characterised by chronic inflammation and permanent scarring in the alveoli. Respiratory ability is affected, chest infection + hypoxic damage likely.

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78
Q

What investigations would you order in IPF?

A
  1. Pulmonary function tests
  2. CXR
  3. Bloods –> Neutrophil count up
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79
Q

What risk factors is associated with IPF?

A
  • Dust inhalation
  • Smoking
  • Exposure to infectious agents
  • Long term antidepressant use
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80
Q

What is the treatment for IPF?

A

Lung transplant and supportive care –> only treatment to increase survival

Broad spectrum Abx if patient has acute exacerbation

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81
Q

What 3 things would you look for on pulmonary tests for IPF?

A
  • Reduced TLCO
  • Restrictive spirometry, Low FEV1 and FVC but normal ratio
  • Low/normal PaO2
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82
Q

Eicosanoid pathway - What does phospholipase A2 do?

A

Converts phospholipid to arachidonic acid

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83
Q

Eicosanoid pathway - 5 Lipoxygenase do?

A

Converts arachidonic acid to leukotrienes

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84
Q

Eicosanoid pathway - What does COX do?

A

Converts archidonic acid to prostaglandins

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85
Q

What inhibits phospholipase A2 and why is this good in asthma treatment?

A

Archidonic acid not converted so less inflammation and reduced TXA2.

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86
Q

Describe the eicosanoid pathway briefly.

A

Phospholipid is converted into arachidonic acid, it can then be converted to prostaglandins by COX or leukotrienes by 5 lipoxygenase.

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87
Q

What is bronchiolitis and who is it common in?

A

airway obstruction caused by inflammation of the bronchioles and increased mucus secretion

Children.

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88
Q

What is the cause of bronchiolitis?

A

RSV infection.

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89
Q

What is the difference between bronchiolitis and bronchitis?

A

Bronchitis = inflammation of bronchi epithelium due to irritants or chemicals

Bronchiolitis = Inflammation of bronchioles and increased mucus secretion due to RSV infection

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90
Q

What investigations would you use to diagnose bronchiolitis?

A
  1. CXR

2. Viral and bacterial swabs

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91
Q

What is the management of bronchiolitis?

A
  • Supplemental O2
  • Fluids, nutrition
  • Airway support
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92
Q

What is the pathophysiology of chronic bronchitis?

A

Exposure to irritants and chemicals e.g. smoke –> as and hyperplasia of mucus secreting glands –> increased mucus –> airway obstruction. Neutrophil + macrophage involvement –> bronchi inflamed.

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93
Q

What is the usual cause of infective bronchitis?

A

Viral, acute bronchitis caused by adenovirus

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94
Q

What is the investigations in infective bronchitis?

A

CXR

Viral and bacterial swabs

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95
Q

What is the cause of chronic bronchitis?

A

Often tobacco smoking induced and can be aggravated by pollution and infections.

reversible!

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96
Q

How do you diagnose chronic bronchitis?

A

a persistent cough and sputum for >3months in 2 consecutive years.

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97
Q

What is the effect of chronic bronchitis on lung function?

A
  1. Reduced FEV1/FVC ratio
  2. Reduced PEFR
  3. Increased TLCO
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98
Q

What are the signs of chronic bronchitis?

A
  • Chronic productive cough
  • Wheeze and crackles
  • Hypoxic + hypercapnic
  • Cyanosis
  • Vasoconstriction –> pulmonary hypertension  cor pulmonale
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99
Q

How can chronic bronchitis cause cor pulmonale?

A
  • Pulmonary vasoconstriction in lungs in an attempt to shunt blood to better ventilated alveoli
  • Pulmonary hypertension –> RHF –> Cor Pulmonale
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100
Q

What is airway obstruction as defined by spirometry?

A
  1. FEV1 <80% predicted

2. FEV1/FVC <0.7

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101
Q

What is the pathophysiology of emphysema?

A

Irritants and chemicals trigger inflammatory mediators to release matrix destructive enzyme –> elastin destruction and enlargement of alveolar air spaces –> air trapping

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102
Q

What is the cause of emphysema?

A
  • Tobacco smoke induced
  • Associated with alpha-1-antitrypsin deficiency (protease inhibitor) – tobacco smoke inhibits
  • Coal dust exposure
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103
Q

What are the signs of emphysema?

A
  1. Pursed lip breathing
  2. SOB
  3. Barrel chest
  4. Weight loss
  5. CO2 retention
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104
Q

What happens in chronic emphysema?

A
  • Patient may be hypercapnic, hypoxic and have progressive R side HF (Cor pulmonae).
  • This is due to pulmonary vasoconstriction –> fibrosis and tissue destruction
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105
Q

What is a pleural fibroma?

A

Fibrous tumour of the pleura

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106
Q

What is a consequence of a pleural fibroma?

A

can grow to massive size and compress on lung tissue. Occasionally they secrete insulin related factors so produce hypoglycaemic symptoms

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107
Q

What is bronchiecstasis?

A

Irreversible and abnormal dilation of the bronchi with chronic inflammatory and fibrotic changes. Leads to a build-up of excess mucus and predisposes the person to chest infections.

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108
Q

What is the pathophysiology of bronchiecstasis?

A
  1. Failed mucocillary clearance and impaired immune function –> prone to infection
  2. Leads to inflammation and therefore progressive lung damage

Bronchitis –> bronchiectasis –> fibrosis

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109
Q

What is the cause of bronchiecstasis?

A
  • Often post-infective e.g. previous pneumonia
  • Congenital causes e.g. primary ciliary dyskinesia.
  • 50% idiopathic
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110
Q

What bacteria cause bronchiecstasis?

A
  • Haemophilus influenzae
  • Pseudomonas aeruginosa
  • Staph aureus
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111
Q

What are the symptoms of bronchiecstasis?

A
  1. Chronic productive cough
  2. Recurrent chest infection
  3. Dyspnoea and wheeze
  4. Recurrent exacerbations
  5. Chest pain
  6. Haemoptysis
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112
Q

What are the investigations necessary in bronchiecstasis?

A
  1. CT
  2. Spirometry –> obstructive
  3. Sputum culture
  4. CXR
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113
Q

What is the treatment for bronchiecstasis?

A
  1. Education
  2. Smoking cessation
  3. Annual influenzas + pneumococcal vaccinations
  4. Anti-inflammatories
  5. Bronchodilators
  6. Improved mucus Clearance
  7. Abx
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114
Q

What is inspiratory reserve volume?

A

Additional vol of air that can be forcible inhaled after a tidal volume inspiration.

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115
Q

What is expiratory reserve volume?

A

additional vol of air that can be forcibly exhaled after a tidal volume expiration

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116
Q

What is forced vital capacity?

A

The max volume of air that can be forcibly exhaled after maximal inhalation

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117
Q

What is total lung capacity?

A

the vital capacity + residual volume. Maximum amount the lungs can hold

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118
Q

What is residual volume?

A

Volume of air remaining in the lungs after a maximal inhalation

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119
Q

What is functional residual capacity?

A

Volume of air remaining in the lungs after a tidal volume exhalation

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120
Q

What is the definition of tidal volume?

A

volume of air moved in and out of the lungs during a normal breath

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121
Q

What is FEV1?

A

Volume of air that can be forcibly exhaled in 1 sec

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122
Q

What is peak expiratory flow?

A

greatest rate of airflow that can be obtained during forced expiration. Age sex and height can all affect PEF.

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123
Q

What is TLCO?

A

The extent to which O2 passes from the alveoli into the blood.

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124
Q

What two equations can work out TLC?

A
  1. TLC = VC+RV

2. TLC = TV + FRC + IRV

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125
Q

What is the normal tidal volume?

A

500ml

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126
Q

What is an equation for FRC?

A

ERV+RV

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127
Q

What is the transfer coefficient?

A

Ability of O2 To difuse across the alveolar membrane

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128
Q

How can you test the transfer coefficient?

A

Low dose CO is inspired, pt asked to hold breath for 10sec and the amount of gas transfer is measured

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129
Q

What diseases can cause a low transfer coefficient?

A
  1. Emphysema
  2. Anaemia
  3. Fibrosing alveolitis
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130
Q

What disease can cause a high transfer coefficient?

A

Pulmonary haemorrhage

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131
Q

How can you test respiratory function?

A

A 6 minute walk

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132
Q

What is a consolidation on a CXR?

A

Regions of the lung filled w/ liquid e.g. pulmonary oedema –> Areas appear white and dense.

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133
Q

What are 2 causes of breathlessness?

A

Heart disease, anaemia

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134
Q

What are 3 signs of an infection?

A
  1. Temperature
  2. Increased neutrophils
  3. Increased CRP
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135
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibody (AI disorder)

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136
Q

What is the mechanism for ANCA?

A
  1. Activates neutrophils and monocytes, neutrophils adhere to endothelial cells
  2. Degranulation and free radicals are released
  3. Free radicals damage the endothelium, further neutrophil recruitment =+ve feedback
  4. This can cause vasculitis as it inflames the vessel wall.

ANCA associated vasculitis is caused by it.

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137
Q

What are the common effects of RA on the lung?

A
  • Pleural effusion
  • Fibrosing alveolitis
  • Airway disorders e.g. bronchiolitis and bronchiectasis
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138
Q

What is Guillian Barre syndrome?

A

Demyelinating polyneuropathy - can present 6 weeks post flu/cmv

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139
Q

What 3 factors can affect TLCO?

A
  • Alveoli/capillary interaction
  • Hb concentration
  • Cardiac output
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140
Q

What are occupational lung disorders?

A

Lung disorders due to a response or inhaling something at work e.g. dust, gas fumes, aerosol

141
Q

What is the damage mechanisms of occupational lung disorders?

A
  1. Direct injury
  2. Infection
  3. Allergy e.g. EAA
  4. Chronic inflammation
  5. Destruction of lung tissue
  6. Lung fibrosis
  7. Carcinogenesis
142
Q

How can you prevent occupational lung disorders?

A
  1. Risk assessment
  2. Legal requirement under COSHH
  3. Prevent and mimise exposure to harmful substances
  4. Monitor workers health so problems are identified early
143
Q

What is an example of occupational asthma?

A

Bakers asthma –> caused by flour.

144
Q

How can you diagnose occupational asthma?

A
  1. PEFR at their place of work and a history to see if it worsens at work
  2. Serum immunology –> IgE to specific workplace allergen.
145
Q

What are consequences of occupational lung disease?

A
  • Loss of income

- Increased morbidity and mortality

146
Q

What is a complication of bronchoscopy?

A

Pneumothorax and pneumonia

147
Q

What is the cause of sinusitis?

A

Viral

148
Q

What is the function of the medulla?

A

Detects h+ conc of the CSF

149
Q

What is the function of the carotid and aortic bodies?

A

Chemoreceptors respond to an increased CO2 and decreased O2

150
Q

What are the radiological indications for bronchoscopy?

A
  1. Lobar collapse
  2. Presence of a mass
  3. Persistent consolidation
151
Q

What are the non-radiological indications for bronchoscopy?

A
  1. Hemoptysis
  2. Cough
  3. Wheeze
  4. Stridor
152
Q

What is atopy?

A

A tendency to develop IgE mediated responses to common aeroallergens.

153
Q

What is the function of inositol triphosphate?

A
  1. IP3 increases free cystolic Ca2+ by releasing it from IC components
  2. Ca2+ activates MLC kinase = bronchial smooth muscle contraction
154
Q

What is asbestosis?

A

Phagocytes are frustrated –> chronic inflammation and permanent scarring –> asbestosis.

155
Q

What is a common cause of acute airway obstruction?

A

Can be caused by a tumour or foreign bodies with distal collapse of the lung

156
Q

What does the activation of M3 receptor cause?

A
  • Bronchoconstriction
  • Vasodilation
  • Glandular secretions
157
Q

Where do pulmonary emboli arise from?

A

dislodged DVT –> usually iliofemoral veins.

158
Q

What are the symptoms of small peripheral PE’s?

A
  1. Breathlessness
  2. Pleuritic Chest pain

Consequence –> Infarction, ventilation but no perfusion – dead space.

159
Q

What are the symptoms of large central PEs?

A
  1. Severe central chest pain
  2. Pale and sweaty

Consequence of a large central PE –> Ischaemia, resistance to flow that can result in RHF

160
Q

What are the investigations in Pulmonary embolism?

A
  • CXR, ECG, D-Dimer
  • V/Q lung scan –> shows ventilated areas w/ perfusion defects.
  • CTPA –> Detects emboli
161
Q

What is a D-dimer?

A

protein fragment found when a blood clot has been degraded by fibrinolysis.

162
Q

What is the well’s scoring system?

A
  1. Clinical signs and symptoms of DVT
  2. Tachycardic
  3. Recent immobilisation
  4. Previous DVT
  5. Haemoptysis
  6. Malignancy

If score is above 4 it is likely.

163
Q

What is the treatment for PE?

A
  1. Thrombolysis for large PE
  2. LMWH and oral warfarin
  3. NOAC
  4. Analgesia
164
Q

What is the differential diagnosis of PE?

A

asthma, COPD, Pneumonia, MI

165
Q

What are the signs of large PE?

A
  1. Shocked
  2. Central cyanosis
  3. Raised JVP
  4. Accentuation of second heart sound
166
Q

What are the risk factors for PE?

A

Obesity, Recent surgery, Malignancy, Immobility and OCP/HRT

167
Q

How is pulmonary hypertension defined?

A

mPAP <25mmHg and Secondary RV failure

168
Q

What are the causes of pulmonary hypertension?

A
  1. Heredity
  2. Idiopathic
  3. Drug use
  4. HIV
  5. Secondary to left heart disease (valvular systolic/diastolic dysfunction)

Increase caused by –> Increased resistance to flow and increased flow rate.

169
Q

What are the symptoms of Pulmonary hypertension?

A
  1. Dyspnoea on exertion
  2. Lethargy/fatigue
  3. Syncope

Symptoms as RV failure develops –> pulmonary oedema, abdo pain

170
Q

What are the signs of pulmonary hypertension?

A
  1. RV hypertrophy
  2. Loud pulmonary second sound
  3. Right parasternal heave
  4. Enlarged proximal pulmonary arteries
  5. In advanced there is signs of RHF –> Elevated JVP, Hepatomegaly and pleural effusion
171
Q

What investigations would you order in pulmonary hypertension?

A
  1. ECG –> RV hypertrophy
  2. Spirometry
  3. CXR –> Enlarged proximal pulmonary arteries
  4. Echocardiography
172
Q

What is the treatment of Pulmonary hypertension?

A
  1. Initial treatment is O2
  2. Warfarin –> risk of thrombosis
  3. Diuretics for oedema
  4. Ca2+ blockers as pulmonary vasodilators
173
Q

How does pulmonary hypertension cause peripheral oedema?

A

Blood accumulates in PA, RV experiences greater afterload and works harder to get it out of the ventricle into the artery.

This is due to RV hypertrophy + right heart failure = peripheral oedema.

174
Q

What are the potential causes of Pleural effusion?

A
  1. Heart/renal failure (transudate)
  2. Hypoalbuminaemia (transudate)
  3. Malignancy (exudate)
  4. Infection (exudate)
  5. Inflammation (exudate)
175
Q

How can you diagnose pleural effusion?

A
  1. Taking a good history
  2. Imaging
  3. Thoracentesis –> can tell you transudates vs exudates
176
Q

What are the investigations of pleural effusion?

A
  1. CXR

2. Ultrasound

177
Q

What is the treatment of pleural effusion?

A

Treatment of pleural effusion with transudate cause e.g. H/RF –> Treat underlying cause

Treatment of pleural effusion with exudate cause e.g. inflammation –> Drainage

178
Q

What are the features of restrictive lung disease?

A
  • FVC reduced
  • FEV1/FVC ratio normal
  • TLC is also reduced
179
Q

What is a giveaway for restrictive lung disease?

A

If a patient doesn’t have chronic wheeze it is likely to be restrictive lung disease.

180
Q

What are the features of obstructive lung disease?

A
  • FEV is <80% predicted
  • FVC is normal
  • FEV1/FVC ratio <0.7
  • TLC is increased
181
Q

What is an example of reversible obstructive lung disease?

A

Asthma

182
Q

What is the giveaway for obstructive lung disease?

A

If a patient has a chronic wheeze it is likely to be obstructive lung disease.

183
Q

Describe respiratory innate immunity

A
  1. Mucous, mucouscillary escalator, macrophages and neutrophils are all involved.
  2. Cough reflex and epiglottis closing off trachea on swallowing.
184
Q

Describe respiratory adaptive immunity

A
  1. B cells produce mainly IgG and IgA antibodies
  2. T cells – CD4, CD8 and regulatory.

Neutrophils can destroy bacteria –> ROS, proteases and NETs

185
Q

What is the cough reflex affected by?

A
  • Pain
  • Sedation
  • Opiates
186
Q

What is cillia function affected by?

A
  • Infection

- Primary dyskinesia

187
Q

What are the 3 types of Immunosuppression?

A
  1. Granulocyte defect – associated with chemo
  2. B cell defect – associated with rituximab and haematological malignancy.
  3. T cell defect – associated with immunosuppression/HIV
188
Q

Describe the IgE binding and activating mast cell process.

A
  • IgE binds to high affinity receptors on the mast cell surface.
  • There is cross-linking and biochemical cascades
  • The mast cells are sensitised and there is degranulation
189
Q

What does mast cell degranulation release?

A
  1. Pre-formed histamine
  2. Newly synthesised eicosanoids e.g. cysteinyl leukotrienes (cys LTs) and prostaglandin D2
  3. Cytokines e.g. IL-3,4,5
190
Q

What is the function of

IL-3
IL-4
IL-5

A

IL-3 is responsible for increasing the number of mast cells

IL-4 is responsible for IgE synthesis

IL-5 is responsible for pro-inflammatory and eosinophil survival

191
Q

Mast cell mediators - What are Cys-LT, histamine and cytokines responsible for?

A

Inflammation

192
Q

Mast cell mediators - What are Cys-LT, Cytokines and enzymes responsible for?

A

Responsible for airway remodelling

193
Q

Mast cell mediators - What are Cys-LT and histamines responsible for?

A

Lung mast cell mediators responsible for bronchoconstriction.

194
Q

What is the mechanism behind chronic infection?

A
  • Infection wont clear, chronic neutrophil recruitment and persistent cellular activation
  • Pro-inflam mediators are released = tissue damage
195
Q

What are the 5 types of tissue mediated damage?

A
  1. Tissue damage in chronic infection
  2. Excessive immune response
  3. Failure to control the immune response
  4. On target immune response
  5. Off target immune response e.g. AAV and goodpastures syndrome
196
Q

What it the cause of excessive immune response in ARDS and COPD?

A

Tissue damage due to chronic infection.

197
Q

What are 2 common URT infections and their cause?

A
  1. Common cold –> Rhinovirus

2. Sore throat –> adenoviruses. EBV

198
Q

What virus can cause pneumonia?

A
  • Adenoviruses, Influenza A+B, Measles, VZV
199
Q

What are the main antigens on Influenza A?

A
  1. Hemagglutinin (H) –> Grappling hook, grabs onto cells

2. Neuraminidase (N) –> cuts newly formed virus loose from infected cells

200
Q

What type of influenza is commonly behind severe and extensive outbreaks?

A

A - due to lots of mutations and it replicates alot.

201
Q

What is antigenic drift?

A

When there are small mutations and minor antigenic variation –> seasonal epidemics

202
Q

What is antigenic shift?

A

When there are large mutations and major antigenic variation –> pandemics

203
Q

How do mast cell mediators affect airways and blood vessels?

A

results in bronchoconstriction + vasodilation

204
Q

Describe allergen challenge

A

30 mins after –> bronchoconstriction and reduced FEV1

3 hours after –> Vasodilation = increased Vasc permeability = inflammation and reduced bronchoconstriction and upregulated adhesion molecules

6 hours after –> worsening inflammation, eosinophil involvement and 2nd wave bronchoconstriction

205
Q

What is the treatment for influenza?

A

Supportive care.

Antivirals can be given to reduce the risk of transmission.

206
Q

What is reproduction number?

A

avg number of secondary cases generated from a primary case.

Measles has a high productive number.

207
Q

How is the flu transmitted?

A
  • Aerosol – coughing and sneezing –> inhale particles

- Droplet – hand to hand

208
Q

What is cystic fibrosis?

A

AR disease resulting in abnormal exocrine gland function. (1 in 25 are carriers)

209
Q

What is the pathogenesis of Cystic fibrosis?

A

Defect in chromosome 7 coding CFTR protein. Cl- transport is affected and there is a production of thickened mucus secretions.

210
Q

What are the signs of Cystic fibrosis?

A
  • SOB/Wheeze
  • Poor growth and weight
  • Persistent coughing, sometimes with phlegm –> frequent lung infections inc pneumonia.
  • Frequent bulky, greasy stools and difficulty with BM.
211
Q

What are the complications of cystic fibrosis?

A
  • Malnutrition due to malabsorption, delayed puberty, weight loss + growth retardation
  • Nasal polyps
  • Resp failure + cor pulmonale
  • DM
  • Breathlessness
  • Finger clubbing, frequent resp infections.
212
Q

What is the management of Cystic fibrosis?

A
  1. Prevention of lung disease e.g. Vaccination
  2. Supporting therapies –> good diet
  3. Surveliance –> monitor FEV1
  4. Antibiotic therapy
  5. Hypertonic saline –> mucus thinner and Ivacaftor –> reduces mucus
  6. Bronchodilators
  7. Steroids
213
Q

What does CF do to the mucus and how?

A

CF increases the viscosity and tenacity of bronchial mucus

  • Failure to excrete Cl- leads to Na+ retention
  • This then leads to H2O retention
214
Q

What codes for the CFTR and what ions does it transport?

A

Chloride, thiocyanate.

215
Q

What cells are responsible for inflammation in asthma?

A

Mast cells and eosinophils are responsible for inflammation in asthma

216
Q

Give 3 reasons why the airways are hyperreactive in asthmatics

A
  1. Inflammatory ifiltrate
  2. Eosinophils
  3. Epithelium destruction gives easier access to bronchoconstriction
217
Q

What is the mechanism behind hypersensitivity (neurogenic inflammation)

A

Sensory nerve activation initiates impulses that stimulate CGRP

This is pro inflame and activates mast + goblet cells.

218
Q

What are the main functions of CGRP?

A
  1. Pro inflammatory
  2. Mast cell activation –> mediator release
  3. Innervation of goblet cells –> mucus release
219
Q

What makes LABA long acting?

A

Increased lipophilicity

220
Q

Where would you find B1, B2,B3 adrenergic receptors?

A

Beta 1 adrenergic receptors are found in the heart

Beta 2 adrenergic receptors are found in the lungs

Beta 3 adrenergic receptors are found in the adipose tissue

221
Q

How is PKA synthesised from beta 2 receptor activation?

A
  1. Beta 2 interacts with Gs activating adenylate cyclase

2. Adenylate cyclase converts ATP to cAMP this leads to PKA synthesis = bronchodilation

222
Q

What are the functions of cAMP?

A
  1. Stabilisation of mast cells, inhibits mast cell mediator release
  2. Relaxes airway smooth muscle
223
Q

What happens after M3 receptor activation?

A
  • M3 interacts with Gq. Phospholipase C activated

- Leads to DAG and IP3 production which further leads to Ca2+ and PKC production

224
Q

How do muscarinic antagonists work?

A

Muscarinic antagonists work by preventing M3 Receptor activation so reduction in Ca2+ activation

  • Means less MLC kinase is produced, and you have less muscle contraction.
225
Q

How do Methylxanthines work?

A
  • Increase cAMP and therefore PKA production

- PKA Inhibits MLC kinase so you have less muscle contraction.

226
Q

What does MLC kinase do?

A

Phosphorylation MLC which causes muscle contraction

227
Q

What inhibits and activates MLC kinase?

A
  • Inhibited by PKA (which is produced by cAMP)

- Activated by Calmodium (produced from Ca2+)

228
Q

How do beta agonists and methylxanthines reduce symptoms?

A
  • Result in increased cAMP and therefore PKA. MLC kinase is inhibited so less contraction
  • Results in bronchodilation
229
Q

How do muscarinic receptors alleviate symptoms?

A
  • Block M3 Receptor activation so less Ca2+ production

- Less MLC is activated so less contraction –> bronchodilation

230
Q

What is the cause and epidemiology of Pneumocystitis pneumonia?

A

Caused by Pneumocystis jirovecii. Seen in people with a weak immune system.

231
Q

What are the signs and symptoms of pneumocystitis pneumonia?

A
  • Hypoxia
  • Progressive breathlessness and dry cough
  • Lymphopenia typical (CD4<200)
232
Q

What investigations would you order in suspected pneumocystitis pneumonia?

A
  • CXR
  • Biopsy
  • Sputum Sample
233
Q

What is the treatment for pneumocystitis pneumonia?

A
  • High dose co-trimoxazole

- Consider secondary prophylaxis

234
Q

What is hypersensitivity pneumonitis?

A

Lung inflammation due to hypersensitivity reaction to an allergen.

235
Q

What is the pathophysiology of hypersensitivity pneumonitis?

A

Inhalation of organic dusts that lead to a T3 hypersensitivity reaction –> inflammatory response in alveoli and small airways.

236
Q

What is the cause of hypersensitivity pneumonitis?

A
  • Bird fanciers lung –> proteins presence in birds faeces

- Farmers lung –> Due to mouldy hay and aspergillus spores

237
Q

What are the typical symptoms of hypersensitivity pneumonitis?

A

If farmers lung is persistent, fibrosis can occur, may be signs of dyspnoea, weight loss and a cough

238
Q

What are the symptoms of hypersensitivity pneumonitis?

A
  1. Fever
  2. Malaise
  3. Cough
239
Q

What investigations would you order in hypersensitivity pneumonitis?

A
  • CXR
  • Nonspecific CRP/ESR
  • Neutrophilia – WBC/FBC
  • History
240
Q

What is the treatment for hypersensitivity pneumonitis?

A
  • Remove the cause!

- Prednisone

241
Q

What is mesothelioma?

A

A high grade malignancy of the pleura that spreads around the pleural spaces. Lung becomes encased by tumour. It’s strongly associated with asbestos exposure.

242
Q

What is the cause of mesothelioma?

A

occupational – asbestos exposure

243
Q

What are the signs of mesothelioma?

A
  1. Breathlessness
  2. Chest pain
  3. Weight loss
  4. Sweating
  5. Abdo pain
244
Q

What are the consequences of asbestos exposure?

A

plaques, effusion, asbestosis, mesothelioma and bronchial carcinoma.

245
Q

What investigations would you order in mesothelioma?

A
  1. CXR
  2. CT scan
  3. Pleural biopsy
246
Q

What is the treatment for mesothelioma?

A
  1. Symptom control
  2. Palliative chemo or radiotherapy
  3. Radical surgery (removal of tumour blood supply)

Local – surgery and radiotherapy
Systemic – chemotherapy

247
Q

Why is the treatment for mesothelioma difficult?

A

Treatment is difficult as it is incurable and resistant to surgery, chemo and radiotherapy. The average time from diagnosis to death is about 8 months.

248
Q

Who is at risk of pneumonia?

A

Elderly, children, people with COPD, Immunocompromised people and nursing home
residents.

249
Q

Describe the pathogenesis of pneumonia

A
  1. Bacteria translocate to normally sterile distal airway
  2. Resident host defence is overwhelmed
  3. Macrophages, chemokines and neutrophils produce an inflammatory response

Pneumonia can be severe as –> excessive inflammation, lung injury and resolution failure.

250
Q

How is pneumonia resolved?

A
  • Bacteria are cleared and inflammatory cells are removed by apoptosis
251
Q

What intrinsic factors cause pneumonia?

A

cold temperatures, infection, stress, exercise and various pollutants

252
Q

What are 3 protective features of the resp tract?

A
  • Teeth
  • Commensal bacteria
  • Swallowing reflex
  • Epiglottis closes resp tract
  • Mucocillary escalator
  • Coughing and sneezing
253
Q

What are the symptoms of pneumonia?

A
  1. Productive cough
  2. Sweats and fever
  3. Breathlessness
  4. Pleuritic chest pain
  5. Myalgia, headache, arthralgia suggests atypical pneumonia.
254
Q

What are the signs of pneumonia?

A
  1. Fever
  2. Lung consolidation –> bronchial breath sounds and dull to percuss.
  3. Pleural effusion
  4. Crackles and wheeze
  5. Abnormal vital signs
255
Q

What investigations could you order in pneumonia?

A
  1. CXR –> air bronchogram in consolidated area
  2. FBC –> WBC
  3. U+E
  4. LFT
  5. CRP
  6. Microbiology –> sputum culture, blood culture and serology
256
Q

How can you prevent pneumonia?

A
  1. Children are given PCV
  2. Smoking cessation is encouraged
  3. Influenza vaccines are given to the children or elderly.
257
Q

What is CURB65?

A

CURB65 – way of assessing the severity of community acquired pneumona –> effects mortality.

  • Confusion
  • Urea >7mmol
  • RR>30/min
  • BP reduced 90/60
  • > 65.
258
Q

Give two common bacteria that cause pneumonia

A
  • Streptococcus pneumoniae - gram positive cocci stain, alpha haemolytic and optochin sensitive.
  • Haemophilus influenzae –> treat with co-amoxiclav or doxycycline (GRAM NEG)
259
Q

Groups of people who are at risk of developing klebisella pneumonia (gram neg bacilli)

A
  • Homeless people
  • Alcoholics
  • People in hospital
260
Q

What people are at risk of hospital acquired pneumonia?

A
  1. Elderly
  2. Ventilator associated
  3. Post-operative patients
261
Q

What are some less typical pathogens that can cause pneumonia?

A
  1. Mycoplasma pneumoniae
  2. Chlamydia Psittaci/pneumoniae
  3. Coxiella burnetti
  4. Legionella pneumophila

Hard to grow so serology and antigen tests are used.

Antibiotics used –> macrolides like clarithromycin as they are often resistant to beta lactams.

262
Q

Describe the treatment for mild pneumonia (CURB65 0-1)

A

PO amoxicillin in the community

263
Q

Describe the treatment for moderate pneumonia (CURB65 2)

A

PO Amoxicillin and clarithromycin in hospital

264
Q

Describe the treatment for severe pneumonia (CURB65 3)

A

IV co-amoxiclav and clarithromycin in hospital

265
Q

Describe the treatment for severe pneumonia (CURB65 of 4)

A

Treat in hospital, consider admission to critical care.

266
Q

What is COPD subdivided into?

A
  1. Chronic bronchitis

2. Emphysema

267
Q

What is likely to exacerbate COPD?

A

Viral infection e.g. RSV, influenza, rhino and coronavirus

268
Q

What is the effect of COPD on RV/TLC?

A

Both raised

269
Q

What are the main causes of COPD?

A

Smoking, genetics, socio-economic factors, occupation and the environment all contribute to COPD.

270
Q

What cells are involved in COPD?

A

CD8+ is involved and Neutrophils and macrophages

271
Q

What are the symptoms of COPD?

A
  1. Breathlessness
  2. Wheeze
  3. Chronic cough
  4. Sputum
272
Q

How can you diagnose COPD?

A
  1. Progressive airflow obstruction
  2. FEV1/FVC ratio <0.7
  3. Lack of reversibility
273
Q

What is the treatment for COPD?

A
  1. Smoking Cessation
  2. Pulmonary rehabilitation
  3. SABA/LABA for symptom relief
  4. ICS
  5. Lung volume reduction surgery
274
Q

Give an advantage and disadvantage of Inhaled corticosteroids (ICS)

A

Advantage –> Improve QOL, improve Lung function and reduce the likelihood of exacerbations

Disadvantages –> increased risk of pneumonia

275
Q

What are the consequences of COPD exacerbation?

A
  1. Worsened symptoms
  2. Decreased lung function
  3. Negative impact on QOL
  4. Increased mortality
  5. Huge economic costs
276
Q

How can you treat COPD exacerbations?

A
  1. Oxygen
  2. Bronchodilators
  3. Systemic steroids
  4. Abx if breathlessness or sputum production
277
Q

How can you prevent future exacerbations?

A
  1. Smoking cessation
  2. Vaccination
  3. LABA/LAMA/ICS
278
Q

How is T1 respiratory failure defined as?

A
  • Hypoxia –> decreased PaO2

- PaCO2 is normal or slightly low due to hyperventilation

279
Q

What is the cause of T1 respiratory failure?

A
  • Airway obstruction
  • Failure of O2 to diffuse into the blood
  • V/Q mismatch
  • Alveolar hypoventilation
280
Q

How is T2 Respiratory failure defined as?

A
  • Hypoxia and hypercapnia –> Decreased PaO2 and increased PaCO2
  • Alveolar hypoventilation
281
Q

What is the cause of T2 respiratory failure?

A

Alveolar hypoventilation

282
Q

What are the signs of Hypercapnia?

A
  1. Bounding pulse
  2. Flapping tremor
  3. Confusion
283
Q

What diseases can obstruct the airway and cause T1 resp failure?

A
  • COPD
  • Obstructive sleep apnoea
  • Asthma
284
Q

What 5 conditions can lead to alveolar hypoventilation and cause T1+T2 resp failure?

A
  • Opiates
  • Emphysema
  • Obesity
  • Neuromuscular weakness
  • Chest wall deformity
285
Q

What can cause a failure of O2 to diffuse properly causing T1 resp failure?

A
  • Emphysema

- ILD e.g. IPF, sarcoidosis

286
Q

What are examples of diseases that can cause v/q mismatch and cause T1 resp failure?

A
  • Cardiac failure
  • PE (dead, V/Q mismatch)
  • Shunt (V/Q =0)
  • Pulmonary hypertension
287
Q

What are the treatments for V/Q mismatch?

A

Ventilation support - CPAP and BIPAP

288
Q

What is CPAP?

A

Ventilation support often given to people with Obstructive Sleep apnoea. It improves gaseous exchange by providing a continuous positive airway pressure.

289
Q

What is BIPAP?

A
  • Ventilation support given for people with acute exacerbations of COPD

Causes pressure to decrease when you breathe out and increase when you breathe in –> improving ventilation to perfused alveoli

290
Q

What are some differential diagnoses of Dyspnoea?

A
  • Heart failure
  • PE
  • Pneumonia
  • Lung cancer
291
Q

What is the MRC dyspnoea scale to assess breathlessness?

A

5 statements that describe the entire range of resp disability from none to almost compete incapacity

292
Q

Shortness of breath can lead to excercise limitation, what is 3 consequences of this?

A
  1. Muscle wasting
  2. Depression and anxiety
  3. Disability
293
Q

SSC are derived from neuroendocrine cells, why is this significant?

A

can secrete peptide hormones such as ACTH, PTHrP, ADH and HCG.

294
Q

What is the 5 year survival rate of lung cancer?

A

8-10%

295
Q

How does a PET scan work?

A
  • FDG is taken up rapidly by dividing cells, tumours appear hot on the scan
  • PET scans are functional rather than anatomical.
296
Q

Describe the TNM classification

A
  1. Tumour (T1-T4)
  2. N – Nodal involvement (N0-3)
  3. M – Metastases (M0-1)

Increased staging = decreased survival.

297
Q

Where are 5 places that lung cancer commonly metastasies too?

A

Bone, brain, liver, lymph nodes and adrenal glands.

298
Q

What is a paraneoplastic syndrome and what is an example?

A

Paraneoplastic syndromes  disorders triggered by immune response to a neoplasm

Examples of paraneoplastic syndromes –> Finger clubbing, anorexia, weight loss, hypercalcaemia and hypernatremia

299
Q

What hormone changes would you expect to result in paraneoplastic changes?

A

PTH and increased ADH in SIADH.

300
Q

What tests would you do on someone with lung cancer to see if they’re fit for operation?

A
  1. ECG
  2. Lung function tests
  3. Determine performance status
301
Q

What cancers may spread to the lung?

A

Breast, prostate, Kidney, melanoma and lymphoma

302
Q

What is the likely presentation of someone with a carcinoid tumour?

A
  1. Younger age
  2. Characteristic neuroendocrine secreting cells
  3. Low rates of invasion and growth

Early symptoms – Change in cough, wheeze and hemoptysis
Late symptoms – weight loss and lethargy

303
Q

What is the difference between a carcinoid tumour and a small cell cancer?

A

Small Cell cancers often metastasise and so prognosis is poor

Carcinoid tumours are malignant but have low rates of invasion and growth.

304
Q

What are 3 causes of lung cancer?

A
  1. Smoking
  2. Asbestos exposure –> occupational
  3. Radon exposure
  4. Coal tar exposure
  5. Chromium exposure
305
Q

What are 6 symptoms of local lung cancer?

A
  1. Chest pain
  2. Wheeze
  3. Breathlessness
  4. Cough
  5. Haemoptysis
  6. Recurrent chest infections
306
Q

What are 6 symptoms of metastised lung cancer?

A
  1. Bone pain –> waking up in the night from pain
  2. Headache
  3. Seizures
  4. Neurological deficit
  5. Hepatic and or abdo pain
  6. Weight loss
307
Q

What investigations would you order in suspected lung cancer?

A
  • CXR
  • CT scan
  • Bronchoscopy
  • Surgical and percutaneous biopsy
  • Bloods
308
Q

What are 3 main cell types that make up NSCLC?

A
  • Squamous cell (20%) –> Most common in smokers
  • Adenocarcinoma (40%)
  • Large cell
309
Q

How can malignant bronchial tumours be divided?

A

Malignant bronchial tumours are divided into Non-small cell and small cell cancer.

  • Non-small cell fits into TNM staging
  • Small cell cancer has a worse prognosis
310
Q

What are 3 features of Asthma?

A
  • Causes a reduction in TLCO
  • 10% due to occupation
  • PEF is variable
311
Q

What are 3 characteristics of Asthma?

A
  1. Airflow obstruction
  2. Hyperresponsiveness to a range of stimuli
  3. Bronchial inflammation
312
Q

Describe the airway remodelling seen in Asthma

A
  1. Hypertrophy and hyperplasia of smooth muscle cells that narrow the airway lumen
  2. Deposition of collagen below the BM thickens the airway wall.
  3. Eosinophils also play a role in remodelling.

The airways are hyper-reactive which leads to inflammation

313
Q

What happens when IgE binds to mast cells?

A

release of vasoactive substances causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.

314
Q

What occupations are linked to asthma?

A

paint sprayers, animal breeders, bakers, laundry workers

315
Q

How can reversibility be tested in asthma?

A

When given a beta agonist –> 400ml increase in FEV1 or 20% increase in PEFR

316
Q

How can the RCP3 be used to assess the severity of asthma?

A
  1. Recurrent nocturnal waking
  2. Usual asthma symptoms during the day
  3. Interefence with ADL’s?
317
Q

What is the first line treatment in asthma?

A
  • Nebulised salbutamol with oxygen

- IV corticosteroids and abx if evidence of infection.

318
Q

How can aspirin induce asthma?

A
  • Aspirin inhibits COX –> Increase in arachidonic acid

- This is shunted to increased leukotriene production = inflammation.

319
Q

What is Asthma?

A

An inflammatory disease characterised by hyper responsive airways. Airway obstruction is reversible, inappropriate smooth muscle contraction.

320
Q

What factors exacerbate asthma?

A

Allergens, Stress, Viral infections, Drugs e.g. aspirin, Cold weather, Exertion, Fumes, Often worse at night

321
Q

What are the signs of asthma?

A
  1. Secretions
  2. Obstructive spirometry
  3. Variable PEFR
  4. Reversibility when given a B2 antagonist FEV1 >20%
  5. Diurnal variation.
322
Q

What are the symptoms of asthma?

A
  1. Breathlessness
  2. Diurnal variation – often worse in the morning
  3. Cough
  4. Episodic wheeze
  5. Chest tightness
323
Q

What investigations would you order in asthma?

A
  1. PEFR
  2. Spirometry should be in an obstructive pattern  FEV1<80%, FEV1/FVC <0.7, PEFR is variable
  3. Test for atopy – RAST, skin prick test
  4. CXR
  5. Eosinophil count
  6. O2 saturation
324
Q

What are the histopathological changes seen in Asthma?

A
  1. BM thickening
  2. Epithelium metaplasia, increase no. of goblet cells that leads to mucus hypersecretion.
  3. Increase in inflammatory gene expression on many cell types.
325
Q

How can you diagnose acute severe asthma?

A
  • RR over 25
  • Tachycardic – 110
  • PEFR –> 35-50% predicted
  • Unable to complete a sentence in one breath.
326
Q

Describe the management of Asthma

A
  1. Improve control and avoid triggers
  2. Smoking cessation
  3. Beta agonists provide symptomatic relief
  4. ICS are anti-inflammatory
  5. Sometimes a short course of systemic steroids
327
Q

What are side effects of systemic steroids?

A

skin thinning, oral candida, hypertension, osteoporosis, DM

328
Q

What are the principles of asthma treatment?

A
  1. Alleviate symptoms – bronchodilators (beta agonists, muscarinic antagonists, methylxanthines)
  2. Target inflammation – steroids
329
Q

Describe allergic asthma.

A

When an innocuous allergen triggers an IgE mediated response. The immune recognition processes are faulty so there is increased IgE, IL3,4 and 5 production.

330
Q

Describe non allergic asthma

A

Airway obstruction induced by exercise, cold air and stress.

331
Q

What is 3 features of Mycobacterium TB?

A
  1. Acid fast bacilli
  2. Waxy cuticle
  3. Grows slowly  hard to culture
  4. Phagolysosomal killing resulting in granulomatous disease
332
Q

What is the cause of

Primary TB
Abdo TB

A

Primary tb –> caused by a Ghon complex (lesion)

Abdo TB –> Mycobacterium Bovis (can be found in unpasteurised milk)

333
Q

What are some risk factors for TB?

A

Live in a high prevalence area, IVDU, Homelessness, alcoholism, HIV+

334
Q

How is TB transmitted?

A

Aerosol transmission –> inhaled and enter the lung

335
Q

Describe the pulmonary infection in TB

A
  • Bacilli settle in lung apex.

- Macrophages and lymphocytes mount an effective immune response that encapsulates and contains the organism forever.

336
Q

Describe the pathogenesis of Pulmonary TB

A
  1. Bacili and macrophages form primary focus
  2. Mediastinal lymph nodes enlarge
  3. Primary focus and enlarged lymph nodes = primary complex
  4. Granuloma develops into a cavity
  5. The cavity fills with TB bacilli –> expelled when the patient coughs

Granuloma cavity more likely to develop in the apex of the lung as there is more air and less blood supply/immune cells.

337
Q

Where can TB spread too?

A
  1. Bone and joints –> pain and swelling
  2. Lymph nodes –> swelling and discharge
  3. CNS – TB meningitis
  4. Military TB –> Disseminated
  5. Abdo TB –> Ascites, malabsorption
  6. GU TB –> Sterile, pyuria, WBC in GU tract.
338
Q

How can you diagnose Latent TB?

A

diagnosed with Mantoux test –> T4 hypersensitivity

339
Q

What are the side effects of

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

A

Side effects of rifampicin = red urine, hepatitis, drug interactions (enzyme inducer)

Side effects of isoniazid = hepatitis, neuropathy

Side effects of pyrazinamide = Hep, Gout, Rash

Side effects of ethambutol = Optic Neuritis

340
Q

What factors increase the risk of TB drug resistance?

A
  1. If patient has had previous treatment
  2. If they live in a high risk area
  3. Contact with a resistant TB
  4. Poor response to therapy
341
Q

What are issues associated with TB drug resistance?

A
  • TB difficult to treat
  • Medication course >20 months
  • Increased risk of side effects
  • Increased relapse rate
342
Q

How can you prevent TB?

A
  1. Active case finding
  2. Detect and treat latent tb
  3. Vaccination – BCG
343
Q

How can TB cause hypercalcaemia?

A
  • Granulomatous disease –> Increased vit D production so increased bone resorption
  • Increased absorption from the gut and increased reabsorption from the kidney
  • Also seen in sarcoidosis
344
Q

What is the special culture used to grow TB and how does it work?

A

Lowenstein Jensen slope –> Special culture medium to grow TB

  1. Contains growth factors that promote mycobacterial growth
  2. Contains small amounts of penicillin that prevents pyogenic bacteria growth.
345
Q

How does TB typically present?

A
  1. Weight loss
  2. Night sweats
  3. Anorexia
  4. Malaise
346
Q

How does pulmonary TB present?

A
  1. Cough
  2. Chest pain
  3. Breathlessness
  4. Haemoptysis
347
Q

What would you expect to see in a CXR of a patient with TB?

A
  • Consolidation
  • Collapse
  • Pleural effusion
348
Q

What is the treatment of TB?

A
  1. Rifampicin (6 months)
  2. Isoniazid (6 months)
  3. Pyrazinamide (2 months)
  4. Ethambutol (2 months)

Phase 2a Sheffield Medicine (10 decks)

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