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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is chronic obstructive pulmonary disease (COPD)?

A

Non-reversible long-term deterioration in air flow through the lungs, caused by damage to lung tissue

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2
Q

Describe the epidemiology of COPD

A

Symptoms usually present between 40-60

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3
Q

What is the main cause of COPD?

A

Smoking

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4
Q

What are 6 risk factors for COPD?

A
  1. Smoking
  2. Age
  3. Second-hand smoke exposure
  4. Occupational exposure (mining/dust/cottonwood)
  5. Pollution (heating fuel/outdoor pollutants)
  6. Genetics (A1AT deficiency)
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5
Q

Describe the pathophysiology of COPD

A
  • Obstructed airflow through the airways increases the difficulty ventilating the lungs
  • = short of breath and prone to infection
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6
Q

What are the 2 main types of COPD?

A
  1. Chronic bronchitis
  2. Emphysema
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7
Q

What is chronic bronchitis?

A

Hypertrophy and hyperplasia of mucus glands and infiltration of chronic inflammation cells into the bronchi

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8
Q

What is emphysema?

A

Destruction of elastin layer in ducts, alveoli and respiratory bronchioles

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9
Q

What is alpha-1-antitrypsin (A1AT) and what does it do?

A
  • Protease inhibitor made in the liver
  • Inhibits neutrophil elastase (enzyme that digests connective tissue)
  • Function to protect the lungs from damage caused by infection, inflammation and smoking
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10
Q

How does an A1AT deficiency affect the liver?

A
  • Mutant A1AT builds up
  • Causes tissue damage
    = cirrhosis and HCC (hepatocellular carcinoma)
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11
Q

How does an A1AT deficiency affect the lungs?

A
  • Lack of normal A1AT
  • = excess protease enzymes
  • Lung tissue attacked
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12
Q

What is IE COPD?

A

Infective exacerbations COPD - when patients experience exacerbations due to infection

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13
Q

Describe the pathophysiology of chronic bronchitis

A
  • Hypertrophy and hyperplasia of mucus glands
  • Infiltration of chronic inflammation cells (e.g. macrophages/lymphocytes) into the bronchi
  • Causes mucous secretion, ciliary dysfunction and a narrowed lumen
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14
Q

Describe the pathophysiology of emphysema

A
  • Destruction of elastin layer in ducts, alveoli and respiratory bronchioles
  • Air trapping distal to blockage, causing bullae
  • Centriacinar emphysema is the most common (affects respiratory bronchioles - due to smoking)
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15
Q

What are 7 typical presentations of COPD?

A
  1. Typically a long-term smoker
  2. Finger clubbing
  3. Shortness of breath
  4. Cough
  5. Sputum production
  6. Wheeze
  7. Recurrent respiratory infections
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16
Q

How does IE COPD present?

A

Acute worsening of symptoms

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17
Q

What are 8 clinical presentations of chronic bronchitis?

A
  1. Chronic productive cough with purulent sputum
  2. Dyspnoea
  3. Cyanosis (may develop pulmonary HTN)
  4. Peripheral oedema
  5. Obesity
  6. Haemoptysis
  7. Rhonchi (large airway sounds)
  8. Wheezing
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18
Q

What are 8 clinical presentations of emphysema?

A
  1. Dyspnoea/tachypnoea
  2. Minimal cough
  3. Pink skin, pursed-lip breathing
  4. Accessory muscle use
  5. Cachexia (weakness/wasting of body)
  6. Hyperinflation (barrel chest)
  7. Weight loss
  8. Quiet chest
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19
Q

What are 6 clinical presentations of an A1AT deficiency in the liver?

A
  1. Tiredness
  2. Loss of appetite
  3. Weight loss
  4. Oedema
  5. Jaundice
  6. Haematemesis/blood in stool
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20
Q

What are 5 clinical presentations of an A1AT deficiency in the lungs?

A
  1. SOB
  2. Excessive cough with sputum production
  3. Wheeze
  4. Decreased exercise capacity/persistent fatigue
  5. Chest pain (worse on inhalation)
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21
Q

Describe the MRC dyspnoea scale

A

Allows patients to describe the extent to which their breathlessness affects their mobility:
- Grade 1 = breathless on strenuous exercise
- Grade 2 = breathless on walking up hill
- Grade 3 = breathless that slows on flat
- Grade 4 = stop to catch breath after 100m walking on flat
- Grade 5 = unable to leave the house due to breathlessness

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22
Q

What are 7 investigations for patients with COPD?

A
  1. Spirometry = FEV1/FVC <0.7
  2. FEV1 (stage 1 >80%, stage 4 <30% predicted value)
  3. CXR (exclude lung cancer and other pathologies)
  4. FBC (chronic hypoxia –> polycythaemia)
  5. BMI (weight loss)
  6. ECG (if cardiac concerns)
  7. Serum A1AT levels
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23
Q

What are 4 investigations for patients with IE COPD?

A
  1. ABG:
    - CO2 retention –> acidosis
    - T1RF = normal pCO2 + low pO2
    - T2RF = high pCO2 + low pO2
  2. CXR
  3. FBC
  4. U&E
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24
Q

What are 4 investigations for patients with an A1AT deficiency?

A
  • Serum A1AT levels (low)
  • Liver biopsy (cirrhosis, mutant protein in hepatocytes)
  • Genetics (A1AT mutant gene)
  • CT thorax (bronchiectasis, emphysema)
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25
Q

What is an investigation for patients with chronic bronchitis?

A

FBC - elevated haemoglobin

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26
Q

What is an investigation for patients with emphysema?

A

CXR = hyperinflation with flattened diaphragms

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27
Q

What is the general treatment for COPD?

A
  • Smoking cessation
  • Pneumococcal vaccine
  • Annual flu vaccine
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28
Q

What is step 1 treatment for COPD?

A
  • SABA e.g. salbutamol, terbutaline
  • SAMA e.g. ipratropium bromide
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29
Q

What is step 2 treatment for COPD?

A

If no asthmatic/steroid response:
- LABA e.g. salmeterol
- LAMA e.g. tiotropium
If asthmatic/steroid response:
- LABA e.g. salmeterol
- ICS e.g. budesonide

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30
Q

What is an asthmatic/steroid response?

A

Responds well to salbutamol

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31
Q

What is step 3 treatment for COPD?

A

Long term oxygen therapy (LTOT)

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32
Q

What is the treatment for IE COPD?

A

Steroids (hydrocortisone/prednisolone) + nebulised bronchodilators (salbutamol/ipratropium bromide) + antibiotics

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33
Q

What is the treatment for severe IE COPD?

A
  • IV aminophylline (bronchodilator)
  • Non invasive ventilation (NIV):
  • Continuous positive airway pressure (CPAP)
  • Bilevel positive airway pressure (BIPAP)
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34
Q

What is the treatment for A1AT deficiency?

A
  • Smoking cessation
  • Symptomatic treatment (inhalers, O2 therapy)
  • Organ transplant for end stage liver/lung disease
  • Augmentation (replacement)
  • Monitor for HCC
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35
Q

What is a complication of emphysema?

A

Pneumothorax due to bullae

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36
Q

What is a complication of A1AT deficiency?

A

Liver cirrhosis/HCC

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37
Q

What is the difference between COPD and asthma?

A

COPD = actual damage to lungs
Asthma = bronchoconstriction (in response to something)

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38
Q

What is asthma?

A

Chronic inflammatory condition of the airways causing episodes of reversible airway obstruction due to bronchoconstriction and excessive secretion production

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39
Q

What are 6 triggers of asthma?

A
  1. Cold air
  2. Exercise
  3. Cigarette smoke
  4. Air pollution
  5. Allergens (pollen/cats/dogs/horses/mould)
  6. Time of day (early morning/night)
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40
Q

What are 4 risk factors for asthma?

A
  1. Atopy (genetic tendency/family/personal history to develop allergic diseases e.g. eczema, asthma, hayfever)
  2. Low birth weight
  3. Not breastfed
  4. Exposure to allergens (e.g. housedust/mites/pollen/smoke)
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41
Q

Describe the pathophysiology of asthma

A
  • Smooth muscles of bronchi contract (bronchoconstriction) causing reduction in the diameter of airways
  • Narrow airways cause an obstruction to airflow going in and out of the lungs
  • Reversible airway obstruction
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42
Q

What are the 2 types of asthma and what is the difference?

A

Allergic (70%):
- IgE mediated type 1 hypersensitivity reaction
- Due to environmental trigger
- Often early presentation
Non allergic (30%)
- Non IgE mediated
- Presents later
- Associated with smoking

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43
Q

How does asthma typically present?

A

Episodes of:
- Wheeze (widespread, polyphonic)
- Dyspnoea
- Chest tightness
- Dry cough
- Diurnal variability

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44
Q

What does a localised wheeze suggest?

A

Foreign bodies

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45
Q

What are 3 investigations for patients with asthma?

A
  1. Spirometry with reversibility testing
    - FEV1 reduced (<80% predicted value)
    - FVC normal
    - FEV1/FVC <0.7
  2. FeNO3 (exhaled nitric oxide):
    - Adult >40pbb
    - Children >35pbb
  3. Peak flow measurement
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46
Q

What is the stepwise treatment for long-term asthma?

A
  1. SABA e.g. salbutamol
  2. ICS e.g. budesonide
  3. LRTA (leukotriene receptor antagonist) e.g. montelukast
  4. LABA e.g. salmeterol
  5. Increase ICS dose
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47
Q

What is the stepwise treatment for acute asthma?

A
  1. Oxygen
  2. Salbutamol nebulisers (SABA)
  3. Ipratropium bromide nebulisers (SAMA)
  4. Hydrocortisone IV or oral prednisolone (steroids)
  5. IV magnesium sulphate
  6. Aminophylline/IV salbutamol
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48
Q

What is tuberculosis (TB)?

A

Infectious disease caused by the mycobacterium tuberculosis bacteria

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49
Q

Describe the epidemiology of TB

A
  • More common in non-UK born patients
  • More common in immunocompromised
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50
Q

Describe mycobacterium tuberculosis bacteria

A
  • Acid fast bacilli with waxy coating
  • Slow growing
  • Resistant to phagolysosomal killing and able to remain dormant
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51
Q

What does acid-fastness mean?

A

Resistant to acids in gram staining

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52
Q

What are 5 risk factors for TB?

A
  1. Known contact with active TB
  2. Immigrants from areas of high TB prevalence
  3. People with relatives or close contacts from countries with a high rate of TB
  4. Immunosuppression due to HIV, immunosuppressant medications etc.
  5. Homeless people/drug users/alcoholics
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53
Q

Describe the pathophysiology of TB

A
  • Alveolar macrophages ingest bacteria and rods proliferate inside
  • Drain into hilar lymph nodes –> present antigen to T lymphocytes –> cellular immune response
  • Delayed hypersensitivity reaction –> tissue necrosis and granuloma formation
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54
Q

How is TB spread?

A

Inhaling saliva droplets from infected people (airborne infection)

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55
Q

Where is the most common site for TB?

A

Lungs

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56
Q

What are 8 other sites for TB (extrapulmonary TB)?

A
  1. Lymph nodes
  2. Pleura
  3. CNS
  4. Pericardium
  5. GI system
  6. GU system
  7. Bones/joints
  8. Skin (cutaneous TB)
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57
Q

What is active TB?

A
  • Active infection
  • Majority of cases = immune system is able to kill and clear infection
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58
Q

What is latent TB?

A

Immune system encapsulates sites of infection and stops the progression of the disease

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59
Q

What is secondary/reactivated TB?

A

Latent TB reactivates

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60
Q

What is miliary TB?

A
  • Immune system is unable to control the disease
  • Causes a disseminated, severe disease
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61
Q

What are the 4 main clinical presentations of TB?

A
  1. Cough (with or without haemoptysis)
  2. Fever
  3. Night sweats
  4. Weight loss
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62
Q

What are 6 investigations for patients with TB?

A
  1. Ziehl-Neelsen stain
  2. Mantoux test
  3. Interferon-gamma release assay (IGRA)
  4. CXR
  5. Bacterial cultures
  6. Nucleic acid amplification test
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63
Q

How does TB appear on Ziehl-Neelsen stains?

A

Bright red/pink against blue background

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64
Q

What is a mantoux test?

A
  • Test for latent TB
  • Looks for previous immune response to TB
  • Inject tuberculin (collection of TB proteins) into intradermal space on forearm
  • Creates a bleb
  • Positive result = induration of >5mm
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65
Q

What is interferon-gamma release assay (IGRA)?

A
  • Used to confirm a diagnosis of latent TB
  • Sample of blood taken and mixed with antigens from TB bacteria
  • Patients with previous contact with TB will release interferon-gamma (from WBCs) as part of the immune response = positive result
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66
Q

What does a CXR look like in patients with primary TB?

A

Patchy consolidation, pleural effusions and hilar lymphadenopathy

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67
Q

What does a CXR look like in patients with reactivated/secondary TB?

A
  • Patchy/nodular consolidation
  • Cavitation (gas filled space in lungs) in upper cavity
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68
Q

What does a CXR look like in patients with disseminated/miliary TB?

A

Picture of ‘millet seeds’ uniformly distributed throughout lung fields

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69
Q

What do bacterial cultures and nucleic acid amplification tests test for in TB?

A

Cultures = tests for resistance to antibiotics
Nucleic acid = looks for TB DNA

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70
Q

What is the treatment for latent TB?

A

Only needed if risk of reactivation:
- Isoniazid and rifampicin for 3 months
- Isoniazid for 6 months

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71
Q

What is the treatment for acute pulmonary TB?

A

RIPE:
R - rifampicin for 6 months
I - isoniazid for 6 months
P - pyrazinamide for 2 months
E - ethambutol for 2 months

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72
Q

What is the BCG vaccine?

A
  • Given to patients that are at higher risk of contact with TB
  • Intradermal infection of live attenuated TB
  • Offers protection against severe and complicated TB
  • Less effective against pulmonary TB
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73
Q

What are 2 side effects of rifampicin?

A
  1. Red/orange discolouration of secretions e.g. urine, tears
  2. Induced of cytochrome P450 enzymes (reduces the effect of drugs metabolised by this system e.g. COC)
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74
Q

What is a side effect of isoniazid?

A
  • Can cause peripheral neuropathy
  • Pyridoxine (vitamin B6) usually co-prescribed prophylactically to reduce the risk of peripheral neuropathy
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75
Q

What is a side effect of pyrazinamide?

A

Can cause hyperuricaemia –> gout

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76
Q

What is a side effect of ethambutol?

A

Can cause colour blindness and reduced visual acuity

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77
Q

What are rifampicin, isoniazid and pyrazinamide all associated with?

A

Hepatotoxicity

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78
Q

What is pneumonia?

A

Infection of lung tissue (acute lower respiratory tract infection)

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79
Q

What are the 2 most common causes of pneumonia?

A
  1. Streptococcus pneumoniae (50%)
  2. Haemophilus influenza (20%)
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80
Q

What are 3 other types of pneumonia?

A
  1. Moraxella catarrhalis (in immunocompromised patients or those with chronic pulmonary disease)
  2. Pseudomonas aeruginosa (in patients with CF or bronchiectasis)
  3. Staphylococcus aureus (in patients with CF)
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81
Q

What is Legionella pneumophila (Legionnaire’s disease)?

A
  • Type of atypical pneumonia
  • Caused by infected water supplies or air conditioning units
  • Presents with hyponatraemia (as it causes SIADH)
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82
Q

What is Coxiella burnetii (a.k.a Q fever)?

A
  • Type of atypical pneumonia
  • Linked to exposure to animals and their bodily fluids (e.g. a farmer)
  • Causes flu-like symptoms
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83
Q

What is Chlamydia psittaci?

A
  • Type of atypical pneumonia
  • Typically contracted from contact with infected birds (e.g. parrots)
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84
Q

Describe the pathophysiology of pneumonia

A
  • Inflammation of lung tissue
  • Causes sputum to fill airways and alveoli
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85
Q

What are 5 types of pneumonia?

A
  1. Community acquired pneumonia (CAP)
  2. Hospital acquired pneumonia (HAP)
  3. Aspiration pneumonia
  4. Pneumocystis pneumonia
  5. Atypical pneumonia
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86
Q

What is the difference between community acquired pneumonia (CAP) and hospital acquired pneumonia (HAP)?

A

CAP = developed outside of hospital
HAP = developed more than 48 hours after hospital admission

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87
Q

What is aspiration pneumonia?

A

Developed as a result of aspiration (inhalation of foreign material e.g. food)

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88
Q

What is pneumocystis/fungal pneumonia (PCP)?

A
  • Pneumocystis jiroveci (PCP)
  • Occurs in immunocompromised patients e.g. HIV patients
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89
Q

What is atypical pneumonia?

A

Caused by an organism that cannot be cultured in the normal way or detected using a gram stain

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90
Q

What are 5 types of atypical pneumonia?

A
  1. Legionella pneumophila (Legionnaire’s disease)
  2. Mycoplasma pneumonia
  3. Chlamydophila pneumoniae
  4. Coxiella burnetii (a.k.a Q fever)
  5. Chlamydia psittaci
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91
Q

What are 7 clinical presentations of pneumonia?

A
  1. SOB
  2. Cough with sputum production
  3. Fever
  4. Haemoptysis
  5. Pleuritic chest pain (sharp chest pain worse on inspiration)
  6. Delirium (acute confusion associated with infection)
  7. Sepsis
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92
Q

What are 3 characteristic chest signs of pneumonia?

A
  1. Bronchial breath sounds (harsh breath sounds equally loud on inspiration and expiration)
  2. Focal coarse crackles (air passing through sputum in airways)
  3. Dullness to percussion
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93
Q

What causes the characteristic chest signs of pneumonia?

A
  • Bronchial breath sounds = consolidation of lung tissue around airway
  • Dullness to percussion = lung tissue collapse and/or consolidation
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94
Q

How does fungal/pneumocystis pneumonia (PCP) present?

A
  • Dry cough without sputum
  • SOBOE
  • Night sweats
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95
Q

What is mycoplasma pneumoniae?

A
  • Type of atypical pneumonia
  • Causes a milder pneumonia
  • Causes a rash = erythema multiforme (varying sized target lesions formed by pink rings with pale centres)
  • Can cause neurological symptoms
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96
Q

What is Chlamydophila pneumoniae?

A
  • Type of atypical pneumonia
  • Often in school aged children
  • Mild to moderate pneumonia and wheeze
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97
Q

What are 4 investigations for patients with pneumonia?

A
  1. CXR (shows consolidation)
  2. FBC (raised WCs)
  3. U&Es (for urea)
  4. CRP (raised - may not be raised in immunocompromised)
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98
Q

What are 3 extra investigations for patients with moderate to severe pneumonia?

A
  1. Sputum cultures
  2. Blood cultures
  3. Legionella and pneumococcal urinary antigens
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99
Q

What is the severity assessment for patients with pneumonia?

A

CRB-65 (outside of hospital)/CURB-65 (in hospital):
C - confusion
U - urea >7
R - respiratory rate >30
B - blood pressure <90 systolic or <60 diastolic
65 - age >65

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100
Q

What is the treatment for mild CAP?

A
  • 5 day course of oral antibiotics
  • Amoxicillin or macrolide (e.g. clarithromycin)
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101
Q

What is the treatment for moderate to severe CAP?

A
  • 7-10 day course of dual antibiotics
  • Amoxicillin + macrolide (e.g. clarithromycin)
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102
Q

What is the treatment for moderate to severe pneumonia or septic patients?

A
  • Dual antibiotics
  • Give IV antibiotics first then change to oral antibiotics after improvement
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103
Q

What is the treatment for fungal/pneumocystis pneumonia (PCP)?

A

Co-trimoxazole

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104
Q

What is the treatment for atypical pneumonia?

A
  • Don’t respond to penicillins
  • Macrolides (e.g. clarithromycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline)
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105
Q

What are 5 complications of pneumonia?

A
  1. Sepsis
  2. Pleural effusion
  3. Empyema
  4. Lung abscess
  5. Death
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106
Q

What is cystic fibrosis?

A

Autosomal recessive genetic condition affecting mucus glands

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107
Q

Describe the epidemiology of CF?

A
  • Around 1 in 25 people are carriers of the mutation
  • 1 in 2500 children have CF
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108
Q

What is the cause of CF?

A

Genetic mutation of the cystic fibrosis transmembrane conductance regulatory (CFTR) gene on chromosome 7 (most common variant is delta-F508 mutation)

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109
Q

Describe the pathophysiology of CF

A
  • The CFTR protein usually secretes Na+ and Cl- ions which makes mucus watery
  • A defect in this gene prevents water from entering the mucus causing it to be thick
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110
Q

What are the 3 main pathophysiological results of CF?

A
  1. Thick pancreatic and biliary secretions that cause blockage of the ducts, resulting in a lack of digestive enzymes
  2. Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisations and susceptibility to airway infections
  3. Congenital bilateral absence of vas deferens
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111
Q

Which 6 microbial colonisers are most common in patients with CF?

A
  1. Staphylococcus aureus
  2. Pseudomonas aeruginosa
  3. Haemophilus influenza
  4. Klebsiella pneumoniae
  5. Escherichia coli
  6. Burkhodheria cepacia
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112
Q

Which microbial coloniser is most dangerous to patients with CF?

A

Pseudomonas aeruginosa (often develops resistance to multiple antibiotics)

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113
Q

What are 11 clinical presentations of CF?

A
  1. Recurrent lower respiratory tract infections
  2. Failure to thrives (poor weight/height gain)
  3. Pancreatitis
  4. Chronic cough
  5. Thick sputum production
  6. Loose, greasy stools (steatorrhoea)
  7. Abdominal pain/bloating/distension
  8. Child tastes particularly salty when parents kiss them
  9. Nasal polyps
  10. Finger clubbing
  11. Crackles and wheeze on auscultation
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114
Q

What are 4 investigations for patients with CF?

A
  1. Newborn bloodspot test (heel prick test)
  2. Meconium ileus
  3. Sweat test (gold standard)
  4. Genetic testing for CFTR gene
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115
Q

What is meconium ileus

A
  • 20% of CF patients have a thick and sticky meconium which doesn’t usually pass within 24 hours (as it gets stuck and obstructs the bowel)
  • Along with abdominal distension and vomiting
  • Often first sign of CF
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116
Q

What is meconium?

A

First stool that a baby passes (usually black and within 24 hours of birth)

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117
Q

What is the sweat test?

A

Gold standard investigation for diagnosing CF
- Pilocarpine is applied to a patch of skin
- Electrodes are placed either side of the patch and a small current is passed between electrodes
- Causes the skin the sweat and sweat is absorbed with gauze or filter paper
- It is tested for chloride concentration
- CF = chloride conc >60mmol/L

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118
Q

How can genetic testing for the CFTR gene be carried out?

A
  • Amniocentesis or chorionic villus sampling (pregnancy)
  • Blood test after birth
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119
Q

What is the treatment for CF?

A
  • Chest physiotherapy
  • Exercise
  • High calorie diet
  • CREON tablets (digests fat)
  • Bronchodilators e.g. salbutamol
  • Nebulised DNase
  • Nebulised hypertonic saline
  • Vaccinations e.g. pneumococcal, influenza and varicella
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120
Q

What is nebulised DNase?

A

Enzyme that breaks down DNA material in respiratory secretions - makes CF patients’ secretions less viscous and easier to clear

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121
Q

What is done to reduce the risk of microbial colonisers in patients with CF?

A
  • Long-term prophylactic flucloxacillin (for staphylococcus aureus and others)
  • Patients with CF should avoid contact with each other to reduce the risk of spreading pseudomonas aeruginosa
  • Long-term nebulised antibiotics e.g. tobramycin or oral ciprofloxacin (for pseudomonas aeruginosa)
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122
Q

What monitoring is undergone for patients with CF?

A
  • Regular monitoring (6 months) of sputum for colonisation of bacteria
  • Monitoring and screening for diabetes, osteoporosis, vitamin D deficiency, liver failure
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123
Q

What is the median life expectancy for patients with CF?

A

47 years

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124
Q

What are 5 complications of CF?

A
  1. Significantly increased morbidity and mortality if pseudomonas colonisation
  2. 90% of patients develop pancreatic insufficiency
  3. 50% of adults develop CF-related diabetes and require insulin
  4. 30% of adults develop liver disease
  5. Most males are infertile due to absent vas deferens
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125
Q

What is bronchiectasis?

A

Chronic respiratory disease characterised by permanent bronchial dilation due to irreversible damage to the bronchial wall

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126
Q

Describe the epidemiology of bronchiectasis

A
  • 3/100 people in the UK
  • 60% of diagnoses are in patients >70
  • More common in females
127
Q

What are 5 causes of bronchiectasis?

A
  1. Idiopathic (40%)
  2. Post-infectious (recurrent resp tract infections, pulmonary TB, allergic bronchopulmonary aspergillosis (ABPA))
  3. Pulmonary disease (COPD, asthma, lung cancer)
  4. Congenital (CF, primary ciliary dyskinesia, A1AT deficiency)
  5. Connective tissue disease (rheumatoid arthritis, SLE, sarcoidosis)
128
Q

What are 3 risk factors for bronchiectasis?

A
  1. Age >70
  2. Female
  3. Smoking history
129
Q

Describe the pathophysiology of bronchiectasis

A
  • Initial insult to bronchi (e.g. infection) results in immune cells being recruited to the bronchi
  • Immune cells secrete cytokines and proteases, leads to inflammation in the bronchi
  • Inflammation damages the muscle and elastin found in the bronchial walls, leading to bronchial dilation
  • Dilated bronchi are predisposed to persistent microbial colonisation (as mucus traps in the dilated bronchi)
130
Q

What are 6 clinical presentations of bronchiectasis?

A
  1. Daily cough with production of mucopurulent sputum
  2. Haemoptysis
  3. Dyspnoea
  4. Fatigue
  5. Rhinosinusitis symptoms e.g. nasal discharge, nasal obstruction, facial pressure
  6. Finger clubbing
131
Q

What 3 things are heard in patients with bronchiectasis?

A
  1. Coarse crepitations in both expiration and inspiration (caused by sudden opening/closing of airways)
  2. Rhonchi (low pitched noises - caused by movement of secretions in the large airways)
  3. High-pitched inspiratory squeaks and pops
132
Q

What are 8 investigations for patients with bronchiectasis?

A
  1. CXR (Kerley B/septal lines)
  2. Chest CT (gold standard imaging - bronchial dilation with/without airway thickening)
  3. Pulse oximetry
  4. Sputum culture
  5. Lung function tests (obstructive FEV1/FVC <70%)
  6. Echocardiogram
  7. FBC (raised WBCC)
  8. CRP (raised)
133
Q

What is treatment for bronchiectasis?

A
  • Smoking cessation
  • Vaccinations e.g. pneumococcal, influenza
  • Pulmonary rehabilitation (physical training)
  • Postural drainage
  • Mucoactive agents
  • Long-term antibiotics e.g. azithromycin
  • Long acting bronchodilators e.g. formoterol
  • LTOT
  • Surgery
134
Q

What do mucoactive agents do and give 2 examples?

A

Aid the clearance of sputum e.g. nebulised saline and carbocisteine

135
Q

What surgery can be done for patients with bronchiectasis?

A
  • Lung resection for localised bronchiectasis
  • Lung transplant
136
Q

What are 2 complications of bronchiectasis?

A
  1. Respiratory failure
  2. Massive haemoptysis (often due to a rupture of a bronchial artery into a bronchus)
137
Q

What is a pleural effusion?

A

Collection of fluid in the pleural cavity (between parietal and visceral pleural surfaces of thorax)

138
Q

What are the 2 types of pleural effusion and what is the difference?

A

Exudative and transudative:
- Exudative = alteration of local factors, inflammation, high protein count (>3g/dL) and high LDH
- Transudative = mediated by systemic factors, low protein count (<3g/dL) and low LDH

139
Q

What are 4 causes of exudative pleural effusion?

A

Inflammation results in protein leaking out of tissues into the pleural space
1. Lung cancer
2. Pneumonia
3. Rheumatoid arthritis
4. TB

140
Q

What are 4 causes of transudative pleural effusion?

A
  1. Congestive cardiac failure
  2. Hypoalbuminemia
  3. Hypothyroidism
  4. Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
141
Q

Describe the pathophysiology of pleural effusion

A

Rate of fluid formation > rate of fluid removal

142
Q

What are 5 clinical presentations of pleural effusion?

A
  1. Dyspnoea
  2. Dullness to percussion over effusion
  3. Pleuritic chest pain
  4. Reduced breath sounds
  5. Tracheal deviation away from the effusion (if massive)
143
Q

What are 3 investigations for pleural effusion?

A
  1. CXR
  2. Pleural fluid sample by aspiration or chest drain (analyse for protein count, cell count, pH, glucose, LDH and microbiology testing)
  3. Pleural ultrasound
144
Q

What does a CXR look like in patients with pleural effusion?

A
  • Blunting of costophrenic angle
  • Fluid in the lung fissures
  • Larger effusions will have a meniscus
  • Tracheal and and mediastinal deviation (if massive effusion)
145
Q

What is a meniscus in a CXR?

A

Curving upwards where it meets the chest wall and mediastinum

146
Q

What is the treatment for pleural effusion?

A
  • Conservative management (for small effusions)
  • Loop diuretics for congestive HF
  • Antibiotics
  • Therapeutic thoracentesis
  • Pleural aspiration
  • Chest drain
147
Q

What is empyema?

A

Infected pleural effusion

148
Q

When should you suspect empyema?

A

In a patient who has improving pneumonia but new or ongoing fever

149
Q

How do you investigate empyema?

A

Pleural aspiration:
- Shows pus, acidic pH (pH <7.2)
- Low glucose
- High LDH

150
Q

What is the treatment for empyema?

A
  • Chest drain to remove pus
  • Antibiotics
151
Q

What is a pneumothorax?

A

When air gets into the pleural space

152
Q

What are 3 causes of pneumothorax?

A

Can occur spontaneously
Secondary to:
1. Trauma
2. Medical interventions (iatrogenic - lung biopsy, mechanical ventilation, central line insertion)
3. Lung pathology (infection, asthma, COPD)

153
Q

What is the difference between a simple and tension pneumothorax?

A

Simple = air moves in and out of pleural space
Tension = one way valve created

154
Q

Describe the pathophysiology of a tension pneumothorax

A
  • Trauma to chest wall
  • One way valve created that lets air in but not out of the pleural space
  • During inspiration, air is drawn in but trapped during expiration
  • Air continues to be drawn in
  • Pressure increases inside the thorax
  • Pushes mediastinum across
  • Kinks the big vessels in the mediastinum
  • Causes cardiorespiratory arrest (RHF)
155
Q

What is the typical patient for pneumothorax?

A

Young, tall, thin man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports

156
Q

What are 5 clinical presentations of tension pneumothorax?

A
  1. Tracheal deviation away from side of pneumothorax
  2. Reduced air entry to affected side
  3. Increased resonant to percussion on affected side
  4. Tachycardia
  5. Hypotension
157
Q

What are 2 investigations for patients with pneumothorax?

A
  1. Erect CXR
  2. CT thorax
158
Q

What does a CXR look like in patients with pneumothorax?

A
  • No lung markings between lung tissue and chest wall
  • Line demarcating the edge of the lung where the lung markings ends and the pneumothorax begins
159
Q

How is a pneumothorax measured?

A

Measure horizontally from the lung edge to the inside of the chest wall at level of the hilum

160
Q

Why is a CT thorax done in patients with pneumothorax?

A
  • Can detect a small pneumothorax that is too small to see on a CXR
  • Can be used to accurately assess the size of the pneumothorax
161
Q

What is the treatment for simple pneumothorax?

A
  • No treatment required if no SOB and <2cm rim of air on CXR (will resolve spontaneously - follow up in 2-4 weeks)
  • Aspiration and reassessment if SOB and/or >2cm rim of air on CXR
  • Chest drain if aspiration fails or in unstable patients/bilateral/secondary pneumothoraces
162
Q

What is the treatment for tension pneumothorax?

A

INSERT A LARGE BORE CANNULA INTO THE SECOND INTERCOSTAL SPACE IN THE MIDCLAVICULAR LINE
- followed by chest drain

163
Q

Where is a chest drain inserted?

A

Into the triangle of safety:
- 5th intercostal space (inferior nipple line)
- Mid axillary line
- Anterior axillary line
Needle inserted just above the rib to avoid the neurovascular bundle

164
Q

What is interstitial lung disease?

A

Groups of conditions that affect the lung parenchyma causing inflammation and fibrosis

165
Q

What are 6 examples of interstitial lung diseases?

A
  1. Idiopathic pulmonary fibrosis
  2. Hypersensitivity pneumonia
  3. Cryptogenic organising pneumonia
  4. Asbestosis
  5. Sarcoidosis
  6. Goodpasture’s syndrome
166
Q

Describe the epidemiology of idiopathic pulmonary fibrosis

A
  • Most common interstitial lung disease
  • More common in males
  • Usually affects adults >50
167
Q

What are 3 causes of interstitial lung disease?

A
  1. Idiopathic
  2. Drug induced
  3. Secondary
168
Q

What are 4 drugs that can cause interstitial lung disease?

A
  1. Amiodarone
  2. Cyclophosphamide
  3. Methotrexate
  4. Nitrofurantoin
169
Q

What are 4 causes of secondary interstitial lung disease?

A
  1. A1AT deficiency
  2. Rheumatoid arthritis
  3. SLE
  4. Systemic sclerosis
170
Q

Describe the pathophysiology of interstitial lung disease

A

Replacement of normal elastic and functional lung tissue with scar tissue that is stiff and doesn’t function properly

171
Q

What are 3 clinical presentations of idiopathic pulmonary fibrosis?

A
  1. Insidious (gradual) onset of SOB and dry cough over more than 3 months
  2. Finger clubbing
  3. Bibasal fine inspiratory crackles
172
Q

What are 2 investigations for patients with interstitial lung disease (specifically idiopathic pulmonary fibrosis)?

A
  1. High resolution CT thorax (ground glass appearance)
  2. Lung biopsy
173
Q

What is the treatment for interstitial lung disease?

A
  • Treat underlying cause
  • Medications to slow the progression of the disease
  • Home oxygen
  • Smoking cessation
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and flu vaccine
  • Lung transplant
174
Q

What are 2 medications that slow the progression of interstitial lung disease (specifically idiopathic pulmonary fibrosis)?

A
  • Pirfenidone (antifibrotic and anti-inflammatory)
  • Nintedanib (monoclonal antibody that targets tyrosine kinase)
175
Q

What is the life expectancy of idiopathic pulmonary fibrosis?

A

2-5 years from diagnosis

176
Q

What is hypersensitivity pneumonitis?

A

Type of interstitial lung disease - type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and damage

177
Q

What are 4 causes of hypersensitivity pneumonitis?

A
  1. Bird-fanciers lung (reaction to bird droppings)
  2. Farmers lung (reaction to mouldy spores in hay)
  3. Mushroom workers lung (reaction to specific mushroom antigens)
  4. Malt workers lung (reaction to mould on barley)
178
Q

What is the investigation for patients with hypersensitivity pneumonitis?

A

Bronchoalveolar lavage:
- Collect cells from the airways during bronchoscopy by washing the airways with fluid and then collecting that fluid for testing
- Shows raised lymphocytes and mast cells

179
Q

What is the treatment for hypersensitivity pneumonitis?

A
  • Remove allergen
  • Oxygen
  • Steroids
180
Q

What is cryptogenic organising pneumonia?

A

Type of interstitial lung disease - focal area of inflammation of lung tissue (previously known as bronchiolitis obliterans organising pneumonia)

181
Q

What are 6 causes of cryptogenic organising pneumonia?

A
  1. Idiopathic
    Triggered by:
  2. Infection
  3. Inflammatory disorders
  4. Medications
  5. Radiation
  6. Environmental toxins/allergens
182
Q

What are 4 clinical presentations of cryptogenic organising pneumonia?

A

Similar to infectious pneumonia:
1. SOB
2. Cough
3. Fever
4. Lethargy

183
Q

What are 2 investigations for patients with cryptogenic organising pneumonia?

A
  1. CXR (focal consolidation)
  2. Lung biopsy (definitive)
184
Q

What is the treatment for cryptogenic organising pneumonia?

A

Systemic corticosteroids

185
Q

What are 3 examples of occupational lung disorders?

A
  1. Silicosis
  2. Asbestosis
  3. Hypersensitivity pneumonitis
186
Q

What is asbestosis?

A

Type of interstitial lung disease - lung fibrosis related to the inhalation of asbestos

187
Q

Why is asbestos bad?

A

Fibrogenic (causes lung fibrosis) and oncogenic (causes cancer)

188
Q

What can asbestos inhalation cause?

A
  • Lung fibrosis
  • Pleural thickening and pleural plaques
  • Adenocarcinoma
  • Mesothelioma
189
Q

What is silicosis?

A

Type of interstitial lung disease - lung fibrosis related to the inhalation of silica

190
Q

Crystalline silica dust is found naturally in what?

A

Certain types of stone, rock, sand and clay

191
Q

People working in which 6 industries are most at risk of silicosis?

A
  1. Stone masonry and stone cutting
  2. Construction and demolition
  3. Worktop manufacturing and fitting
  4. Pottery, ceramics and glass manufacturing
  5. Mining and quarrying
  6. Sand blasting
192
Q

What does silica inhalation cause?

A

Lung inflammation and fibrosis

193
Q

What are 3 symptoms of silicosis?

A
  1. Persistent cough
  2. Persistent shortness of breath
  3. Weakness and tiredness
194
Q

What is sarcoidosis?

A

Type of interstitial lung disease - granulomatous inflammatory condition

195
Q

Describe the epidemiology of sarcoidosis

A
  • Spikes in incidence in young adulthood and around 60
  • More common in females
  • More common in black people
196
Q

What are granulomas?

A

Nodules of inflammation made of WBCs (macrophages) and other tissue

197
Q

What is the typical patient for sarcoidosis?

A

Young, black woman with a cough

198
Q

What is Lofgren’s syndrome?

A
  • A specific presentation of sarcoidosis
  • Characteristic triad of:
  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Polyarthralgia
199
Q

What are the 10 general areas that sarcoidosis can produce symptoms in?

A

Can be asymptomatic (in up to 50%)
1. Lungs (90%)
2. Systemic
3. Liver (20%)
4. Eyes (20%)
5. Skin (15%)
6. Heart (5%)
7. Kidneys (5%)
8. Central nervous system (5%)
9. Peripheral nervous system (5%)
10. Bones (2%)

200
Q

What are 3 things that can occur in the lungs due to sarcoidosis?

A
  1. Mediastinal lymphadenopathy
  2. Pulmonary fibrosis
  3. Pulmonary nodules
201
Q

What are 3 systemic symptoms of sarcoidosis?

A
  1. Fever
  2. Fatigue
  3. Weight loss
202
Q

What are 3 things that can occur in the liver due to sarcoidosis?

A
  1. Liver nodules
  2. Cirrhosis
  3. Cholestasis
203
Q

What are 3 things that can occur in the eyes due to sarcoidosis?

A
  1. Uveitis
  2. Conjunctivitis
  3. Optic neuritis
204
Q

What are 3 things that can occur in the skin due to sarcoidosis?

A
  1. Erythema nodosum (tender, red nodules on shins)
  2. Lupus pernio (raised, purple skin lesions on cheeks and nose)
  3. Granulomas develop into scar tissue
205
Q

What are 3 things that can occur in the heart due to sarcoidosis?

A
  1. Bundle branch block
  2. Heart block
  3. Myocardial muscle involvement
206
Q

What are 3 things that can occur in the kidneys due to sarcoidosis?

A
  1. Kidney stones (due to hypercalcaemia)
  2. Nephrocalcinosis
  3. Interstitial nephritis
207
Q

What are 3 things that can occur in the central nervous system due to sarcoidosis?

A
  1. Nodules
  2. Pituitary involvement (diabetes insipidus)
  3. Encephalopathy
208
Q

What are 2 things that can occur in the peripheral nervous system due to sarcoidosis?

A
  1. Facial nerve palsy
  2. Mononeuritis multiplex
209
Q

What are 3 things that can occur in the bones due to sarcoidosis?

A
  1. Arthralgia
  2. Arthritis
  3. Myopathy
210
Q

What are 3 investigations for patients with sarcoidosis?

A
  1. Bloods
  2. Imaging (CXR/CT/MRI/PET)
  3. Histology from biopsy (GOLD STANDARD)
211
Q

What do bloods show in patients with sarcoidosis?

A
  • Raised serum ACE
  • Hypercalcaemia
  • Raised serum soluble interleukin-2 receptor
  • Raised CRP
  • Raised immunoglobulins
212
Q

What does imaging show in patients with sarcoidosis?

A
  • CXR = hilar lymph adenopathy
  • CT thorax = hilar lymph adenopathy and pulmonary nodules
  • MRI = can show CNS involvement
  • PET scan = active inflammation
213
Q

What does histology from a biopsy show in patients with sarcoidosis?

A
  • Done via bronchoscopy with ultrasound guided biopsy of mediastinal lymph nodes
  • Show characteristic non-caseating granulomas with epithelioid cells
214
Q

What is the treatment for sarcoidosis?

A
  • No treatment (resolves spontaneously in about 60% of patients)
  • Oral steroids with bisphosphonates to protect against osteoporosis (1st line)
  • Methotrexate or azathioprine (second line)
  • Lung transplant (in rare, severe cases)
215
Q

What are 3 complications of sarcoidosis?

A
  1. Pulmonary fibrosis
  2. Pulmonary hypertension
  3. Death (when it affects the heart of CNS)
216
Q

What is Goodpasture’s syndrome?

A

Type of interstitial lung disease and glomerulonephritis - autoimmune anti-glomerular basement membrane disease

217
Q

Describe the pathophysiology of Goodpasture’s syndrome

A

Autoantibodies (anti-GBM) to type IV collagen in glomerular and alveolar basement membranes

218
Q

What are 9 clinical presentations of Goodpasture’s syndrome?

A
  1. SOB (dyspnoea)
  2. Oliguria
  3. Haemoptysis
  4. Haematuria
  5. Chest pain
  6. Fever
  7. Fatigue
  8. Glomerulonephritis
  9. Pulmonary haemorrhage
219
Q

What is the investigation for patients with Goodpasture’s syndrome?

A

Lung and kidney biopsy/bloods = anti-GBM antibodies

220
Q

What is the treatment for Goodpasture’s syndrome?

A
  • Corticosteroids e.g. prednisolone
  • Immunosuppressants e.g. cyclophosphamide
  • Plasmapheresis
221
Q

What is pulmonary hypertension?

A

Increased resistance and pressure of blood in the pulmonary arteries

222
Q

What are the 5 main causes of pulmonary hypertension?

A
  1. Group 1 (primary pulmonary hypertension)
  2. Group 2 (due to left heart failure)
  3. Group 3 (due to chronic lung disease)
  4. Group 4 (due to pulmonary vascular disease)
  5. Group 5 (due to unknown/miscellaneous causes)
223
Q

Give an example of a group 1 cause of pulmonary hypertension

A

Connective tissue disease e.g. systemic lupus erythematosus

224
Q

Give 2 examples of group 2 causes of pulmonary hypertension

A
  1. Myocardial infarction
  2. Systemic hypertension
225
Q

Give an example of a group 3 cause of pulmonary hypertension

A

COPD

226
Q

Give an example of a group 4 cause of pulmonary hypertension

A

Pulmonary embolism

227
Q

Give 3 examples of group 5 causes of pulmonary hypertension

A
  1. Sarcoidosis
  2. Glycogen storage disease
  3. Haematological disorders
228
Q

Describe the pathophysiology of pulmonary hypertension

A
  • Increased pressure and resistance in the pulmonary arteries causes strain on the right side of the heart
  • Causes a back pressure of blood into the systemic venous system
229
Q

What are 6 clinical presentations of pulmonary hypertension?

A
  1. SOB (main)
  2. Syncope
  3. Tachycardia
  4. Raised JVP
  5. Hepatomegaly
  6. Peripheral oedema
230
Q

What are 4 investigations for patients with pulmonary hypertension?

A
  1. ECG
  2. CXR
  3. NT-proBNP blood test (raised indicates right ventricular failure)
  4. Echocardiogram (can be used to estimate pulmonary artery pressure)
231
Q

What does an ECG look like in patients with pulmonary hypertension?

A
  • Right ventricular hypertrophy (larger R waves on right sided chest leads (V1-3) and S waves on left sided chest leads (V4-6))
  • Right axis deviation
  • Right bundle branch block
232
Q

What does a CXR look like in patients with pulmonary hypertension?

A
  • Dilated pulmonary arteries
  • Right ventricular hypertrophy
233
Q

What is the prognosis for patients with pulmonary hypertension?

A

30-40% 5 year survival from diagnosis

234
Q

What is the treatment for primary pulmonary hypertension?

A
  • IV prostanoids e.g. epoprostenol
  • Endothelin receptor antagonists e.g. macitentan
  • Phosphodiesterase-5 inhibitors e.g. sildenafil
235
Q

What is the treatment for secondary pulmonary hypertension?

A

Treat underlying cause

236
Q

Describe the epidemiology of lung cancer

A

3rd most common cancer in the UK (behind breast and prostate)

237
Q

What is the main cause/risk factor for lung cancer?

A

Cigarette smoking - around 80% of lung cancers are thought to be preventable

238
Q

Describe the pathophysiology of non-small cell lung cancer

A
  • Around 80%
  • Adenocarcinoma (40%)
  • Squamous cell carcinoma (20%)
  • Large cell carcinoma (10%)
  • Other types (10%)
239
Q

Describe the pathophysiology of small cell lung cancer

A
  • Contain neurosecretory granules that can release neuroendocrine hormones
  • Responsible for multiple paraneoplastic syndromes
240
Q

What are 7 clinical presentations of lung cancer?

A
  1. SOB
  2. Cough
  3. Haemoptysis
  4. Finger clubbing
  5. Recurrent pneumonia
  6. Weight loss
  7. Lymphadenopathy
241
Q

What are 5 investigations for patients with lung cancer?

A
  1. CXR (first line)
  2. Staging CT scan with contrast of chest, abdomen and pelvis
  3. PET-CT scan
  4. Bronchoscopy with endobronchial ultrasound
  5. Histology from biopsy
242
Q

What does a CXR look like in patients with lung cancer?

A
  • Hilar enlargement
  • Peripheral opacity (visible lesion in lung field)
  • Pleural effusion (usually unilateral in cancer)
  • Collapse
243
Q

What does a staging CT scan with contrast look for in patients with lung cancer?

A
  • Establishes the stage
  • Checks for lymph node involvement and metastases
244
Q

What does a staging CT scan with contrast look for in patients with lung cancer?

A
  • Establishes the stage
  • Checks for lymph node involvement and metastases
245
Q

What does a PET-CT scan look for in patients with lung cancer?

A
  • Radioactive tracer injected
  • Images visualise how metabolically active various tissues are
  • Useful in identifying areas that the cancer has spread to
246
Q

What does a bronchoscopy with endobronchial ultrasound and histology from biopsy look for in patients with lung cancer?

A
  • Allows for detailed assessment of the tumour and ultrasound guided biopsy
  • Checks the type of cells in the cancer
  • Biopsy taken via bronchoscopy or percutaneously
247
Q

What is the treatment for non-small cell lung cancer?

A
  • Surgery when the disease is isolated to a single area (lobectomy/segmentectomy/wedge resection)
  • Radiotherapy
  • Chemotherapy
248
Q

What is the treatment for small cell lung cancer?

A
  • Worse prognosis (mostly palliative)
  • Radiotherapy
  • Chemotherapy
249
Q

What is the palliative treatment for lung cancer?

A
  • Radiotherapy
  • Chemotherapy
  • Endobronchial treatment (stents/debulking to relieve bronchial obstruction)
250
Q

What is lung cancer associated with?

A

Extrapulmonary manifestations and paraneoplastic syndromes

251
Q

Name 10 extrapulmonary manifestations/paraneoplastic syndromes that are associated with lung cancer

A
  1. Recurrent laryngeal nerve palsy
  2. Phrenic nerve palsy
  3. Superior vena cava obstruction
  4. Horner’s syndrome
  5. SIADH
  6. Cushing’s syndrome
  7. Hypercalcaemia
  8. Limbic encephalitis
  9. Lambert-Eaton myasthenic syndrome
  10. Mesothelioma
252
Q

Describe the association between lung cancer and recurrent laryngeal nerve palsy

A
  • Caused by cancer pressing on/affecting the recurrent laryngeal nerve as it passes through the mediastinum
  • Presents with hoarse voice
253
Q

Describe the association between lung cancer and phrenic nerve palsy

A
  • Nerve compression causes weakness in the diaphragm
  • Presents with SOB
254
Q

Describe the association between lung cancer and superior vena cava obstruction

A
  • Caused by direct compression of the tumour on the superior vena cava
  • Presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest
  • Pemberton’s sign (medical emergency - raising the hands over the head causes facial congestion and cyanosis)
255
Q

Describe the association between lung cancer and Horner’s syndrome

A
  • Caused by a Pancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion
  • Triad = partial ptosis, anhidrosis, miosis
256
Q

Describe the association between lung cancer and SIADH

A
  • Caused by ectopic ADH secretion by a small cell lung cancer
  • Presents with hyponatraemia
257
Q

Describe the association between lung cancer and Cushing’s syndrome

A

Caused by ectopic ACTH secretion by a small cell lung cancer

258
Q

Describe the association between lung cancer and hypercalcaemia

A

Caused by ectopic parathyroid hormone from a squamous cell carcinoma

259
Q

Describe the association between lung cancer and limbic encephalitis

A
  • Paraneoplastic syndrome
  • Small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation
  • Short term memory impairment, hallucinations, confusion, seizures
  • Associated with anti-Hu antibodies
260
Q

Describe the association between lung cancer and Lambert-Eaton myasthenic syndrome

A
  • Result of antibodies produced by the immune system against small cell lung cancer cells
  • Antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones
261
Q

Describe the association between lung cancer and mesothelioma

A
  • Lung malignancy affecting the mesothelial cells of the pleura
  • Strongly linked to asbestos inhalation
  • Huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years
  • Poor prognosis
  • Chemotherapy is mostly palliative
262
Q

What is dyspnoea?

A

Shortness of breath/breathlessness

263
Q

What are 9 causes of dyspnoea?

A
  1. Asthma
  2. Chest infection
  3. Being overweight
  4. Smoking
  5. Panic attack
  6. COPD
  7. Idiopathic pulmonary fibrosis
  8. Heart failure
  9. Lung cancer
264
Q

What is respiratory failure?

A

When alveolar ventilation is not sufficient to maintain arterial blood gasses
PaO2 <8kPa
PaCO2 >7kPa

265
Q

What are 6 causes of type I respiratory failure?

A

Restrictive lung disease:
1. Pulmonary oedema
2. Pneumonia
3. ARDS
4. Idiopathic pulmonary fibrosis
5. Pneumothorax
6. Pulmonary embolism

266
Q

What are 7 causes of type II respiratory failure?

A

Obstructive lung disease:
1. COPD
2. Asthma
3. Emphysema
4. Drug effects
5. Extreme obesity
6. Chronic bronchitis
7. Neuromuscular problems

267
Q

Describe the pathophysiology of respiratory failure

A
  • Disturbances in ventilation and perfusion in pulmonary disease leads to V/Q mismatch and so the balance of PaO2 and PaCO2 become disrupted
  • = disturbance in acid-base balance
268
Q

What is V/Q mismatch?

A

When the perfusion of blood in the capillaries doesn’t match the ventilation of the alveoli

269
Q

Describe the pathophysiology of type I respiratory failure

A
  • Respiratory system cannot adequately provide oxygen to the body
  • Leads to hypoxemia
  • Low O2, normal CO2
270
Q

Describe the pathophysiology of type II respiratory failure

A
  • Respiratory system cannot sufficiently remove carbon dioxide from the body
  • Leads to hypercapnia
  • Low O2, high CO2
271
Q

What are 3 symptoms of respiratory failure?

A
  1. SOB
  2. Drowsiness/dizziness
  3. Cyanosis (bluish colour of extremities)
272
Q

What are the normal PaO2 and PaCO2 levels?

A

PaO2 = 11-13kPa
PaCO2 = 4.7-6kPa

273
Q

What is the treatment for respiratory failure?

A

Oxygen

274
Q

What are upper respiratory tract infections and give 6 examples?

A

Infections affecting the sinuses and throat:
1. Common cold
2. Sinusitis
3. Tonsilitis
4. Laryngitis
5. Croup
6. Whooping cough

275
Q

What is sinusitis?

A

Inflammation of the paranasal sinuses in the face often following upper respiratory tract infections

276
Q

What are 5 causes of sinusitis?

A
  1. Infection, particularly following viral upper respiratory tract infections
  2. Allergies e.g. hayfever
  3. Obstructions of drainage e.g. due to a foreign body, trauma, polyps
  4. Smoking
  5. Bacterial infection
277
Q

What are 5 bacterial causes of sinusitis?

A
  1. Group A streptococcus (mainly strep. pyogenes)
  2. Streptococcus pneumoniae
  3. Haemophilus influenza
  4. Morazella catarrhalis
  5. Staphylococcus aureus
278
Q

What is a risk factor for sinusitis?

A

Patients with asthma

279
Q

Describe the pathophysiology of sinusitis

A
  • Inflammation of the paranasal sinuses
  • Paranasal sinuses produce mucous and drain into the nasal cavities via holes called ostia
  • Blockage of the ostia prevents drainage of the sinuses, resulting in sinusitis
  • Usually accompanied by inflammation of the nasal cavity (rhinosinusitis)
280
Q

What is the difference between acute and chronic sinusitis?

A

Acute = <12 weeks
Chronic = >12 weeks

281
Q

What is the typical presentation of acute sinusitis?

A

Recent viral upper respiratory tract infection with:
- Nasal congestion
- Nasal discharge
- Facial pain or headache
- Facial pressure
- Facial swelling over affected areas
- Loss of smell

282
Q

What are 5 clinical presentations of sinusitis?

A
  1. Tenderness to palpitation of affected areas
  2. Inflammation and oedema of nasal mucosa
  3. Discharge
  4. Fever
  5. Other signs of systemic infection e.g. tachycardia
283
Q

How does chronic sinusitis present?

A
  • Similarly to acute sinusitis with symptoms lasting longer than 12 weeks
  • May be associated with nasal polyps
284
Q

What are 2 investigations for patients with sinusitis?

A

Not necessary in most cases
1. Nasal endoscopy
2. CT scan

285
Q

What is the treatment for sinusitis?

A
  • Most cases are caused by a viral infection and resolve within 2-3 weeks
  • Don’t upper antibiotics to patients with symptoms for up to 10 days
  • Patients with systemic infection or sepsis require admission to hospital for emergency management
286
Q

What is the treatment for sinusitis if symptoms don’t improve after 10 days?

A
  • High dose steroid nasal spray for 14 days e.g. mometasone
  • Delayed antibiotic prescription, used if worsening or not improving within 7 days (phenoxymethylpenicillin first line)
287
Q

What is the treatment for chronic sinusitis?

A
  • Saline nasal irrigation
  • Steroid nasal sprays/drops e.g. mometasone, fluticasone
  • Functional endoscopic sinus surgery (FESS)
288
Q

What is croup?

A

Acute upper respiratory tract infection causing oedema in the larynx

289
Q

Describe the epidemiology of croup

A

Typically affects children aged 6 months to 2 years

290
Q

What are 5 causes of croup?

A
  1. Parainfluenza virus (most common)
  2. Influenza
  3. Adenovirus
  4. Respiratory syncytial virus (RSV)
  5. Diphtheria
291
Q

Describe croup caused by diphtheria

A
  • Used to be caused by diphtheria
  • Leads to epiglottitis and has a high mortality
  • Vaccination means that this is very rare in developed countries
292
Q

What are 6 clinical presentations of croup?

A
  1. Oedema in the larynx
  2. Increased work of breathing
  3. ‘Barking’ cough, occurring in clusters of coughing episodes
  4. Hoarse voice
  5. Stridor
  6. Low grade fever
293
Q

What is the treatment for croup?

A
  • Usually improves in less than 48 hours
  • Steroids e.g. dexamethasone, prednisolone
294
Q

What is the treatment for severe croup?

A
  • Oral dexamethasone
  • Oxygen
  • Nebulised budesonide
  • Nebulised adrenaline
  • Intubation and ventilation
295
Q

What is whooping cough?

A

Upper respiratory tract infection caused by Bordetella pertussis

296
Q

What is the cause of whooping cough?

A

Bordetella pertussis (a gram negative bacteria)

297
Q

What does presentation of whooping cough typically start with?

A
  • Mild coryzal symptoms
  • Low grade fever
  • Mild dry cough
298
Q

Describe coughing fits in whooping cough

A
  • Sudden and recurring attacks of coughing with cough free periods in between (paroxysmal cough)
  • Coughing fits are severe and keep building until the patient is completely out of breath
  • Patients produce a large, loud inspiratory whoop when the coughing ends
299
Q

What are 4 other clinical presentations of whooping cough?

A
  1. Infants may not ‘whoop’ and present with apneas rather than a cough
    Patients cough so hard they:
  2. Faint
  3. Vomit
  4. Develop a pneumothorax
300
Q

What are 2 investigations for patients with whooping cough?

A
  1. Nasopharyngeal or nasal swab with PCR testing or bacterial culture (can confirm the diagnosis within 2-3 weeks of the onset of symptoms)
  2. Anti-pertussis toxin immunoglobulin G test in oral fluid (aged 5-16) or blood (aged >17) (when the cough has been present for more than 2 weeks)
301
Q

What is the treatment for whooping cough?

A
  • Children and pregnant women are vaccinated against pertussis
  • Macrolide antibiotics e.g. azithromycin, erythromycin, clarithromycin
  • Co-trimoxazole
  • Close contacts with infected patients are given prophylactic antibiotics
302
Q

What is a complication of whooping cough?

A

Bronchiectasis

303
Q

What is otitis media?

A

Infection of the middle ear causing inflammation and a build-up of fluid behind the eardrum

304
Q

Describe the epidemiology of otitis media

A

Most commonly affects between 6-15 months old

305
Q

What are 6 causes of otitis media?

A
  1. Most commonly caused by viral infections
    Bacterial:
  2. Group A streptococcus (mainly streptococcus pyogenes)
  3. Streptococcus pneumonia
  4. Haemophilus influenzae
  5. Morazella catarrhalis
  6. Staphylococcus aureus
306
Q

What are 3 clinical presentations of otitis media?

A
  1. Ear pain
  2. Bulging red tympanic membrane
  3. Discharge from ear (if eardrum perforates)
307
Q

What is the treatment for otitis media (and sinusitis)?

A
  • Usually resolve without treatment over 1-3 weeks
  • Antibiotics should be reserved for immunocompromised patients, those with severe co-morbidities, those with severe infections/infections that fail to resolve
  • Amoxicillin (first line)
  • Clarithromycin/erythromycin (if penicillin allergy)
  • Co-amoxiclav (second line)
308
Q

What is pharyngitis?

A

Inflammation of the pharynx - sore throat (more a symptom than a condition)

309
Q

What are 3 causes of pharyngitis?

A
  1. Bacterial
  2. Viral
  3. Fungal
310
Q

What is acute epiglottitis?

A

Inflammation of the epiglottis which obstructs the airway

311
Q

Describe the epidemiology of acute epiglottitis

A

Common in children under 5 years

312
Q

What are 3 symptoms of acute epiglottitis?

A
  1. Tripodding (patient leans forward with mouth open and tongue out to breathe)
  2. Sore throat
  3. SOB
313
Q

What is the investigation for acute epiglottitis?

A

Laryngoscopy

Phase 2a (29 decks)

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