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Resp Year 1 > Pathology Part 1 > Flashcards

Pathology Part 1 Flashcards

1
Q

Features of acute asthma

A

Worsening dyspnoea, wheeze and cough that is not responding to salbutamol

Maybe triggered by a respiratory tract infection

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2
Q

Why is a normal CO2 in acute asthma not a good sign?

A

Indicates exhaustion and should, therefore, be classified as life-threatening.

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3
Q

Moderate acute asthma attack features

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

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4
Q

Severe acute asthma attack features

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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5
Q

Life-threatening acute asthma attack features

A 
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
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6
Q

The classification of acute asthma

A

Moderate
Severe
Life-threatening

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7
Q

When is a chest x-ray indicated in acute asthma attacks?

A

life-threatening asthma
suspected pneumothorax
failure to respond to treatment

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8
Q

When is hospital admission indicated in acute asthma attacks?

A
  1. Life-threatening asthma attack
  2. Severe asthma features if they don’t respond to initial treatment
  3. Previous near-fatal asthma attack
  4. Pregnancy,
  5. Presentation at night
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9
Q

When is oxygen indicated in acute asthma attacks?

A

Acutely unwell should be started on 15L of supplemental via a non-rebreathe mask, which can then be titrated down to a flow rate where they are able to maintain a SpO₂ 94-98%.

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10
Q

Criteria for discharge after acute asthma attacks

A

Stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours

Inhaler technique checked and recorded

PEF >75% of best or predicted

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11
Q

Management of acute asthma attacks

A
  1. SABA
  2. All patients given 40-50mg of prednisolone orally (PO) daily, continued for at least five days or until the patient recovers from the attack
  3. Nebulised ipratropium bromide given 3rd line if needed
  4. IV magnesium sulphate
  5. IV aminophylline after consultation with senior medical staff
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12
Q

Acute bronchitis

A

A type of chest infection which causes inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.

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13
Q

Leading cause of acute bronchitis

A

Viral infection

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14
Q

How long does acute bronchitis last?

A

Usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time.

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15
Q

Features of acute bronchitis

A

Typically present with an acute onset of:
> cough: may or may not be productive
> sore throat
> rhinorrhoea
> wheeze
> Low grade fever (may/may not be present)

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16
Q

Chest examination findings in acute bronchitis

A

Majority of patients with have a normal chest examination, however, some may have Low-grade
fever & Wheeze

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17
Q

Differentiating acute bronchitis from pneumonia

A

Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.

Examination: No other focal chest signs in acute bronchitis other than wheeze. Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.

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18
Q

Investigations in acute bronchitis

A

Typically a clinical diagnosis

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19
Q

Management of acute bronchitis

A
  1. analgesia
  2. good fluid intake
  3. consider antibiotic therapy
  4. doxycycline first-line - cannot be used in children or pregnant women - amoxicillin is alternative
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20
Q

When is antibiotic therapy indicated in acute bronchitis?

A
  1. Systemically very unwell
  2. Pre-existing co-morbidities
  3. CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
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21
Q

What antibiotic is first line in acute bronchitis?

A

Doxycycline - cannot be used in children or pregnant women - amoxicillin is alternative

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22
Q

Features Acute exacerbation of COPD

A
  1. Increase in dyspnoea, cough, wheeze
  2. Increase in sputum suggestive of an infective cause
  3. May be hypoxic and in some cases have acute confusion
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23
Q

The most common bacterial organisms that cause infective exacerbations of COPD

A

Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis

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24
Q

Most common bacteria that causes infective exacerbations of COPD

A

Haemophilus influenzae

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25
Q

Management of infective exacerbations of COPD

A

Increase frequency of bronchodilator use and consider giving via a nebuliser

Prednisolone 30 mg daily for 5 days

Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line

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26
Q

When are antibiotics indicated in infective exacerbations of COPD?

A

Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line

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27
Q

What are the first-line antibiotics for infective exacerbations of COPD?

A

Amoxicillin or clarithromycin or doxycycline first-line

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28
Q

Acute respiratory distress syndrome (ARDS)

A

Caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli - life-threatening condition where the lungs cannot provide the body’s vital organs with enough oxygen.

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29
Q

Causes of Acute respiratory distress syndrome (ARDS)

A 
infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
cardio-pulmonary bypass
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30
Q

Features of Acute respiratory distress syndrome (ARDS)

A 
>   Acute onset and severe
>   dyspnoea
>   elevated respiratory rate
>   bilateral lung crackles
>   low oxygen saturations
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31
Q

Key investigations in Acute respiratory distress syndrome ARDS

A

A chest x-ray and arterial blood gases

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32
Q

Management of Acute respiratory distress syndrome ARDS

A
  1. ITU
  2. Oxygenation/ventilation to treat the hypoxaemia
  3. Treat underlying cause e.g. antibiotics for sepsis
  4. Strategies such as prone positioning and muscle relaxation shown to improve outcome in ARDS
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33
Q

Adult respiratory distress syndrome

A

Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia (PaO2/FiO2 ratio < 200) in the absence of evidence for cardiogenic pulmonary oedema.

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34
Q

Adult respiratory distress syndrome causes

A

Sepsis
Direct lung injury
Trauma
Acute pancreatitis
Long bone fracture or multiple fractures (through fat embolism)
Head injury (causes sympathetic nervous stimulation which leads to acute pulmonary hypertension)

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35
Q

The two stages of Adult respiratory distress syndrome

A

Early stages consist of an exudative phase of injury with associated oedema.

The later stage is one of repair and consists of fibroproliferative changes. Subsequent scarring may result in poor lung function.

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36
Q

Features of Adult respiratory distress syndrome

A

Acute dyspnoea and hypoxaemia hours/days after event
Multi organ failure
Rising ventilatory pressures

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37
Q

Management of Adult respiratory distress syndrome

A

> Treat the underlying cause
Antibiotics (if signs of sepsis)
Negative fluid balance i.e. Diuretics
Recruitment manoeuvres such as prone ventilation, use of positive end expiratory pressure

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38
Q

Allergic bronchopulmonary aspergillosis

A

Results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.

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39
Q

Allergic bronchopulmonary aspergillosis features

A
  1. Bronchoconstriction: wheeze, cough, dyspnoea.
  2. Patients may have a previous label of asthma
  3. Bronchiectasis (proximal)
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40
Q

Investigations in Allergic bronchopulmonary aspergillosis

A

> eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE

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41
Q

Management Allergic bronchopulmonary aspergillosis

A
  1. oral glucocorticoids

2. itraconazole as a second-line agent

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42
Q

Three main types of altitude-related disorders

A

Acute mountain sickness (AMS), which may progress to High altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE).

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43
Q

Features of Acute mountain sickness

A

Develop gradually over 6-12 hours and potentially last a number of days:
> headache
> nausea
> fatigue

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44
Q

HAPE/HACE features

A

Some people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions
> HAPE presents with classical pulmonary oedema features
> HACE presents with headache, ataxia, papilloedema

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45
Q

Management of high altitude pulmonary oedema (HAPE)

A
  1. descent
  2. nifedipine, dexamethasone, acetazolamide,
  3. phosphodiesterase type V inhibitors*
  4. oxygen if available
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46
Q

Management of high altitude cerebral oedema (HACE)

A
  1. descent

2. dexamethasone

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47
Q

Alpha-1 antitrypsin (A1AT) deficiency

A

Common inherited condition caused by a lack of a protease inhibitor normally produced by the liver.

The role of A1AT is to protect cells from enzymes such as neutrophil elastase. It classically causes emphysema in patients who are young and non-smokers.

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48
Q

What disease does Alpha-1 antitrypsin (A1AT) deficiency cause?

A

Causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.

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49
Q

The role of Alpha-1 antitrypsin

A

To protect cells from enzymes such as neutrophil elastase.

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50
Q

Inheritance of Alpha-1 antitrypsin (A1AT) deficiency

A

Autosomal recessive

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51
Q

Features of Alpha-1 antitrypsin (A1AT) deficiency

A
  1. Usually have PiZZ genotype
  2. Panacinar emphysema, mostly in lower lobes of lungs
  3. Liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
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52
Q

Investigations in Alpha-1 antitrypsin (A1AT) deficiency

A
  1. A1AT concentrations

2. spirometry: obstructive picture

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53
Q

Management of Alpha-1 antitrypsin (A1AT) deficiency

A
  1. no smoking
  2. supportive: bronchodilators, physiotherapy
  3. IV alpha1-antitrypsin protein concentrates
  4. Lung volume reduction surgery
  5. lung transplantation
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54
Q

Normal PaO2 levels

A

Pa02 on air should be >10 kPa

Less than this is hypoxaemic

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55
Q

Acidaemic and alkalaemic pH

A

Acidaemic (pH <7.35)

Alkalaemic (pH >7.45)

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56
Q

PaCO2 > 6.0 kPa

A

Suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)

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57
Q

PaCO2 < 4.7 kPa

A

Suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

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58
Q

Bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)

A

Suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)

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59
Q

Bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)

A

Suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)

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60
Q

Low pH + high PaCO2

A

Acidosis

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61
Q

High pH + low PaCO2

A

Alkalosis

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62
Q

Low pH + low bicarbonate

A

Acidosis

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63
Q

High pH + high bicarbonate

A

Akalosis

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64
Q

Asbestos

A

Can cause a variety of lung disease from benign pleural plaques to mesothelioma.

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65
Q

Pleural plaques

A

Benign and do not undergo malignant change. They, therefore don’t require any follow-up. Most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.

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66
Q

Pleural thickening

A

Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.

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67
Q

Asbestosis

A

The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis.

A chronic lung condition that is caused by prolonged exposure to high concentrations of asbestos fibers in the air.

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68
Q

Lung changes in Asbestosis

A

Typically causes lower lobe fibrosis

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69
Q

Asbestosis features

A

As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.

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70
Q

Mesothelioma

A

A malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form. Mesothelioma can occur even with very limited exposure to asbestos

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71
Q

Features of Mesothelioma

A
  1. progressive shortness-of-breath
  2. chest pain
  3. pleural effusion
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72
Q

Aspiration pneumonia

A

A pneumonia that develops as a result of foreign materials gaining entry to the bronchial tree, usually oral or gastric contents such as food and saliva.

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73
Q

Risk factors for the development of aspiration pneumonia

A 
Poor dental hygiene
Swallowing difficulties
Prolonged hospitalization or surgical procedures
Impaired consciousness
Impaired mucociliary clearance
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74
Q

Lung changes in Aspiration pneumonia

A

The right middle and lower lung lobes are the most common sites affected, due to the larger calibre and more vertical orientation of the right main bronchus.

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75
Q

Most common bacteria to cause infection in Aspiration pneumonia

A

Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa

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76
Q

Most common chronic respiratory disorder encountered in clinical practice

A

Asthma

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77
Q

Asthma

A

Defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity. Symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.

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78
Q

Risk factors for Asthma

A
  1. personal or family history of atopy
  2. Maternal smoking, viral infection during pregnancy 3. Low birth weight
  3. Not being breastfed
  4. Maternal smoking around child
  5. Exposure to high concentrations of allergens
  6. Air pollution
  7. ‘hygiene hypothesis’
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79
Q

Patients with asthma also suffer from other IgE-mediated atopic conditions; what are they?

A
  1. atopic dermatitis (eczema)

2. allergic rhinitis (hay fever)

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80
Q

Occupational asthma

A

Type of asthma caused by exposure to inhaled irritants in the workplace. Diagnosed by observing reduced peak flows during the working week with normal readings when not at work.

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81
Q

Symptoms and signs of asthma

A
  1. cough: often worse at night
  2. dyspnoea
  3. ‘wheeze’, ‘chest tightness’
  4. expiratory wheeze on auscultation
  5. reduced peak expiratory flow rate (PEFR)
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82
Q

Spirometry

A

Test which measures the amount (volume) and speed (flow) of air during exhalation and inhalation.

Categorizes respiratory disorders as either obstructive or restrictive.

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83
Q

FEV1

A

Forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration

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84
Q

FVC

A

Forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration

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85
Q

Typical spirometry results in asthma

A

FEV1 - significantly reduced
FVC - normal
FEV1% (FEV1/FVC) < 70%

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86
Q

Investigations in asthma patients over 17

A

Spirometry with a bronchodilator reversibility test
All patients should have a FeNO test
Chest x-ray: particular in older patients or those with a history of smoking

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87
Q

Short-acting beta-agonists (SABA)

A

Salbutamol

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88
Q

Inhaled corticosteroids (ICS)

A

Beclometasone
Dipropionate
Fluticasone
Propionate

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89
Q

Long-acting beta-agonists (LABA)

A

Salmeterol

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90
Q

Leukotriene receptor antagonists

A

Monteleukast

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91
Q

Maintenance and reliever therapy (MART)

A

A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.

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92
Q

Side effects of Short-acting beta-agonists (SABA)

A

> Trembling, particularly in the hands.
Nervous tension.
Headaches
Suddenly noticeable heartbeats (palpitations)
Muscle cramps

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93
Q

Inhaled corticosteroids (ICS) side effects

A

Candidiasis and stunted growth in children

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94
Q

LABA side effects

A 
Shaking of a part of your body that you cannot control
headache
nervousness
dizziness
cough
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95
Q

Investigations in asthma patients under 16

A

All patients should have spirometry with a bronchodilator reversibility (BDR) test

FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test

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96
Q

Management of asthma

A 
>   SABA
>   SABA + low-dose ICS
>   SABA + low-dose ICS + LTRA
>   SABA + low-dose ICS + LABA
>   Continue LTRA depending on response to LTRA
>   SABA +/- LTRA
>   Switch ICS/LABA for a low-dose ICS MART
>   SABA +/- LTRA + medium-dose ICS MART
>   SABA +/- LTRA + high-dose ICS MART
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97
Q

Low dose ICS

A

<= 400 micrograms budesonide or equivalent

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98
Q

Moderate dose ICS

A

400 micrograms - 800 micrograms budesonide or equivalent

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99
Q

High dose ICS

A

> 800 micrograms budesonide or equivalent

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100
Q

Common chemicals that cause occupational asthma

A 
ocyanates - spray painting and foam 
moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes
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101
Q

Atelectasis

A

A common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.

A complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid. Atelectasis is one of the most common breathing (respiratory) complications after surgery

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102
Q

Atelectasis features

A

Should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively

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103
Q

Atelectasis management

A

> positioning the patient upright

> chest physiotherapy: breathing exercises

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104
Q

Most common causes of bilateral hilar lymphadenopathy

A

Sarcoidosis and tuberculosis

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105
Q

All causes of bilateral hilar lymphadenopathy

A 
>   lymphoma/other malignancy
>   pneumoconiosis e.g. berylliosis
>   fungi e.g. histoplasmosis, coccidioidomycosis
>   Sarcoidosis 
>   Tuberculosis
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106
Q

Bronchiectasis

A

Describes a permanent dilatation of airways secondary to chronic infection or inflammation

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107
Q

Causes of Bronchiectasis

A

Post-infective: tuberculosis, measles, pertussis, Pneumonia
Cystic fibrosis
Bronchial obstruction e.g. lung cancer/foreign body
Immune deficiency: selective IgA, Hypogammaglobulinaemia
Allergic bronchopulmonary aspergillosis (ABPA)
Yellow nail syndrome

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108
Q

Management of Bronchiectasis

A

Physical training (e.g. inspiratory muscle training)
Postural drainage
Antibiotics for exacerbations + long-term rotating antibiotics in severe cases
Bronchodilators in selected cases
Immunisations
Surgery in selected cases (e.g. Localised disease)

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109
Q

Most common organisms isolated from patients with bronchiectasis

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

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110
Q

Most common bacteria isolated from patients with bronchiectasis

A

Haemophilus influenzae

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111
Q

Chest drain

A

A tube inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.

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112
Q

Chest drain indications

A 
>   Pleural effusion
>   Empyema
>   Haemothorax
>   Haemopneumothorax
>   Chylothorax
>   Pneumothorax not suitable for conservative management or aspiration
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113
Q

Chest drain contraindications

A
  1. INR > 1.3
  2. Platelet count < 75
  3. Pulmonary bullae
  4. Pleural adhesions
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114
Q

Insertion of chest drain

A

Patient should be positioned in a supine position or at a 45º angle.

Forearm may be positioned behind the patient’s head to allow easy access to the axilla.

Identify the 5th intercostal space in the midaxillary line.

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115
Q

Chest drain complications

A
  1. Failure of insertion
  2. Bleeding
  3. Infection
  4. Penetration of the lung
  5. Re-expansion pulmonary oedema
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116
Q

Re-expansion pulmonary edema

A

Uncommon complication following drainage of a pneumothorax or pleural effusion. Symptoms include cough, chest discomfort and hypoxemia; if the edema is severe, shock and death may ensue.

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117
Q

How to prevent re-expansion pulmonary oedema

A

Recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours).

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118
Q

When are large bore chest drains used?

A

Trauma and haemothorax drainage

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119
Q

When are smaller diameter chest drains used?

A

Pneumothorax or pleural effusion drainage

120
Q

Differentials for Chest x-ray: cavitating lung lesion findings

A 
Abscess 
Squamous cell lung cancer
Tuberculosis
Wegener's granulomatosis
Pulmonary embolism
Rheumatoid arthritis
Aspergillosis, histoplasmosis, Coccidioidomycosis
121
Q

Common causes of lobar collapse

A
  1. Lung cancer
  2. Asthma (due to mucous plugging)
  3. Foreign body
122
Q

Most common cause of lobar collapse in older adults

A

Lung cancer

123
Q

The general signs of lobar collapse on a chest x-ray

A
  1. Tracheal deviation towards the side of the collapse
  2. Mediastinal shift towards the side of the collapse
  3. Elevation of the hemidiaphragm
124
Q

Chest x-ray findings for lung metastases

A

Multiple, round well-defined lung secondaries are often referred to as ‘cannonball metastases’. Commonly seen with renal cell cancer but may also occur secondary to choriocarcinoma and prostate cancer.

125
Q

Causes of actual mediastinal widening

A 
vascular problems: thoracic aortic aneurysm
lymphoma
retrosternal goitre
teratoma
tumours of the thymus
126
Q

How can nasogastric tube position be assesed?

A

Chest x ray

127
Q

Complications of misplaced nasogastric tubes

A

Aspiration pneumonia and death

128
Q

Chest x-ray pulmonary oedema changes

A
  1. interstitial oedema
  2. bat’s wing appearance
  3. upper lobe diversion (increased blood flow to the superior parts of the lung)
  4. Kerley B lines
  5. pleural effusion
129
Q

Chest x-ray: white lung lesions causes

A 
consolidation
pleural effusion
collapse
pneumonectomy
specific lesions e.g. tumours
fluid e.g. pulmonary oedema
130
Q

Trachea pulled toward the white-out (Chest x-ray: white lung lesions)

A

Pneumonectomy
Complete lung collapse
Pulmonary hypoplasia

131
Q

Trachea pushed away from white-out (Chest x-ray: white lung lesions)

A

Pleural effusion
Diaphragmatic hernia
Large thoracic mass

132
Q

Trachea central in white lung lesion findings

A

Consolidation
Pulmonary oedema (usually bilateral)
Mesothelioma

133
Q

Cardiac causes of finger clubbing

A

Cyanotic congenital heart disease
Bacterial endocarditis
Atrial myxoma

134
Q

Respiratory causes of finger clubbing

A 
Lung cancer
Cystic fibrosis
Bronchiectasis
Abscess
Empyema
Tuberculosis
Asbestosis, mesothelioma
135
Q

Coal workers’ pneumoconiosis

A

An occupational lung disease caused by long term exposure to coal dust particles. Commonly experienced by those who have been involved in the coal mining industry and severity is linked to the extent of exposure.

136
Q

Pathophysiology of Coal workers’ pneumoconiosis

A

Dust reaches the terminal bronchioles and is engulfed by alveolar and interstitial macrophages.

Dust particles are then moved by the macrophages via the mucociliary elevator and removed from the body as mucus.

In coal miners who are exposed over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli, which starts an immune response, causing damage to the lung tissue.

137
Q

The two presentations for Coal workers’ pneumoconiosis

A

Simple pneumoconiosis:

Progressive Massive Fibrosis

138
Q

Simple pneumoconiosis

A

Commonest type of pneumoconiosis
Patients are often asymptomatic
Increases the risk of lung diseases
May lead to Progressive Massive Fibrosis (PMF)

Pneumoconiosis is one of a group of interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs

139
Q

Commonest type of pneumoconiosis

A

Simple pneumoconiosis

140
Q

Progressive Massive Fibrosis

A

Round fibrotic masses most commonly in the upper lobes.

The exact pathogenesis is not known.

Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.

141
Q

Progressive Massive Fibrosis symptoms

A

Often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.

142
Q

Coal workers’ pneumoconiosis

A

Chest x-ray: upper zone fibrosis

Spirometry: restrictive picture on lung function tests

143
Q

Pneumoconiosis

A

Accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.

144
Q

Most common cause of COPD

A

Smoking

145
Q

Causes for COPD

A 
Smoking
Alpha-1 antitrypsin deficiency
Cadmium (used in smelting)
Coal
Cotton
Cement
Grain
146
Q

What is COPD?

A

Refers to a group of diseases that cause airflow blockage and breathing-related problems. It includes emphysema and chronic bronchitis.

147
Q

COPD features

A

Cough: often productive
Dyspnoea
Wheeze
Severe cases, right-sided heart failure

148
Q

Investigations in COPD

A
  1. Spirometry (obstructive picture)
  2. Chest x-ray
  3. Full blood count
  4. Body mass index (BMI) calculation
149
Q

Chest x-ray changes in COPD

A

> hyperinflation
bullae
flat hemidiaphragm
also important to exclude lung cancer

150
Q

Stage 1 COPD (mild)

A

FEV1/FVC < 0.7

FEV1 of predicted >80%

151
Q

Stage 2 COPD (moderate)

A

FEV1/FVC < 0.7

FEV1 of predicted = 50-79%

152
Q

Stage 3 COPD (severe)

A

FEV1/FVC < 0.7

FEV1 of predicted 30-49%

153
Q

Stage 4 COPD (very severe)

A

FEV1/FVC < 0.7

FEV1 of predicted <30%

154
Q

General management for all COPD patients

A

> Smoking cessation advice
Annual influenza vaccination
One-off pneumococcal vaccination
Pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD

155
Q

First line management for COPD

A

SABA or SAMA

156
Q

Second line management for COPD patients

A

Breathless or have exacerbations despite SAMA/SABA the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

No asthmatic features/features suggesting steroid responsiveness
add LABA + LAMA - already taking a SAMA, discontinue and switch to a SABA

Asthmatic features/features suggesting steroid responsiveness
LABA + inhaled corticosteroid (ICS)

157
Q

Third line treatment for COPD in patients with and without asthma features

A

LABA + LAMA + ICS

158
Q

When is oral prophylactic antibiotic therapy recommeneded in COPD patients?

A

Patients should not smoke, have optimised standard treatments and continue to have exacerbations

159
Q

What antibiotic is used for oral prophylactic antibiotic therapy in COPD patients?

A

Azithromycin

160
Q

When are mucolytics indicated in COPD?

A

Should be ‘considered’ in patients with a chronic productive cough and continued if symptoms improve

161
Q

Anion gap calculation

A

(Na+ + K+) - (Cl- + HCO3-)

162
Q

Normal chloride ion levels

A

The normal range = 10-18 mmol/L

163
Q

Normal anion gap ( = hyperchloraemic metabolic acidosis) causes

A
  1. Bicarbonate loss: diarrhoea, fistula
  2. Renal tubular acidosis
  3. Drugs: e.g. acetazolamide
  4. Ammonium chloride injection
  5. Addison’s disease
164
Q

Raised anion gap causes

A
  1. Lactate: shock, hypoxia
  2. Ketones: diabetic ketoacidosis, alcohol
  3. Urate: renal failure
  4. Acid poisoning: salicylates, methanol
165
Q

Metabolic alkalosis

A

A rise in plasma bicarbonate levels.

Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.

Caused by a loss of hydrogen ions or a gain of bicarbonate.

166
Q

Causes of metabolic alkalosis

A 
Vomiting / aspiration 
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia
167
Q

Mechanism of metabolic alkalosis

A

Activation of RAAS is a key factor

Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule

ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels

In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality

168
Q

Causes of Respiratory acidosis

A

COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose

169
Q

Causes of Respiratory alkalosis

A 
>    Anxiety leading to hyperventilation
>    Early salicylate poisoning*
>   Stroke, subarachnoid haemorrhage, 
>    encephalitis
>    Pregnancy
>    Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
170
Q

Respiratory alkalosis mechanism

A

Hyperventilation resulting in excess loss of carbon dioxide - result in increasing pH

171
Q

Respiratory acidosis mechanism

A

Rise in carbon dioxide levels usually as a result of alveolar hypoventilation

172
Q

Methylxanthines (e.g. theophylline) mechanism of action

A

Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP

173
Q

Monteleukast, zafirlukast mechanism of action

A

Blocks leukotriene receptors

174
Q

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

A

An ANCA associated small-medium vessel vasculitis

175
Q

Another name for Eosinophilic granulomatosis with polyangiitis

A

Churg-Strauss syndrome

176
Q

Features of Eosinophilic granulomatosis with polyangiitis

A 
asthma
blood eosinophilia 
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%
177
Q

Extrinsic allergic alveolitis

A

A condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. Thought largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.

178
Q

Classifications of Extrinsic allergic alveolitis

A
  1. bird fanciers’ lung
  2. farmers lung
  3. Malt workers’ lung
  4. mushroom workers’ lung
179
Q

Cause of farmers lung (Type of EAA)

A

Spores of Saccharopolyspora rectivirgula from wet hay

180
Q

Cause of Malt workers’ lung (type of EAA)

A

Aspergillus clavatus

181
Q

Causes of mushroom workers’ lung (type of EAA)

A

Thermophilic actinomycetes*

182
Q

Acute presentation of EAA

A

Occurs 4-8 hrs after exposure
dyspnoea
dry cough
fever

183
Q

Chronic presentation of EAA

A 
Occurs weeks-months after exposure
lethargy
dyspnoea
productive cough
anorexia and weight loss
184
Q

Investigations in EAA

A

Imaging: upper/mid-zone fibrosis
Serologic assays - specific IgG antibodies
Blood: NO eosinophilia

185
Q

EAA chest x-ray changes

A

Upper/mid-zone fibrosis

186
Q

Management of EAA

A
  1. avoid precipitating factors

2. oral glucocorticoids

187
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

An autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.

188
Q

Features of Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A
  1. Epistaxis, sinusitis, nasal crusting
  2. Dyspnoea, haemoptysis
  3. Rapidly progressive glomerulonephritis
  4. Saddle-shape nose deformity
189
Q

Another name for Granulomatosis with polyangiitis

A

Wegener’s granulomatosis

190
Q

Investigations in Granulomatosis with polyangiitis

A

cANCA positive in > 90%, pANCA positive in 25%

Renal biopsy - epithelial crescents in Bowman’s capsule

191
Q

Management of Granulomatosis with polyangiitis

A

> steroids
cyclophosphamide (90% response)
plasma exchange

192
Q

Renal biopsy findings in Granulomatosis with polyangiitis

A

Epithelial crescents in Bowman’s capsule

193
Q

Idiopathic pulmonary fibrosis

A

A chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis, IPF is used when no underlying cause exists.

194
Q

Epidemiology of Idiopathic pulmonary fibrosis

A

Typically seen in patients aged 50-70 years and is twice as common in men.

195
Q

Features of Idiopathic pulmonary fibrosis

A

Progressive exertional dyspnoea
Bibasal fine end-inspiratory crepitations
Dry cough
Clubbing

196
Q

Investigations in Idiopathic pulmonary fibrosis

A

Restrictive results on spirometry

Impaired gas exchange: reduced TLCO

Imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF

ANA positive in 30%,

197
Q

Imaging findings in Idiopathic pulmonary fibrosis

A

Bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray

High-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF

198
Q

Management of Idiopathic pulmonary fibrosis

A

Pulmonary rehabilitation

Many patients will require supplementary oxygen and eventually a lung transplant

199
Q

Klebsiella pneumoniae

A

A Gram-negative rod that is part of the normal gut flora. Can cause a number of infections in humans including pneumonia and urinary tract infections.

200
Q

Features of Klebsiella pneumonia

A

More common in alcoholic and diabetics
May occur following aspiration
‘red-currant jelly’ sputum
Often affects upper lobes

201
Q

Small cell lung cancer features

A

Usually central

ADH → hyponatraemia

ACTH → Cushing’s syndrome & can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis

Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

202
Q

Squamous cell lung cancer features

A

Parathyroid hormone-related protein secretion causing hypercalcaemia

clubbing

hypertrophic pulmonary osteoarthropathy (HPOA)

hyperthyroidism due to ectopic TSH

203
Q

Adenocarcinoma features

A

Gynaecomastia

HPOA

204
Q

Investigations for lung cancer

A 
Chest x-ray
CT
Bronchoscopy
PET scanning
Bloods
205
Q

When is PET scanning used in lung cancer?

A

Typically done in non-small cell lung cancer to establish eligibility for curative treatment

206
Q

When is bronchoscopy used in lung cancer?

A

Allows a biopsy to be taken to obtain a histological diagnosis sometimes aided by endobronchial ultrasound

207
Q

Lung cancer: non-small cell management

A

Only 20% suitable for surgery

Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement

Curative or palliative radiotherapy

Poor response to chemotherapy

208
Q

Lung cancer classifications

A

Small cell lung cancer (SCLC)

Non-small cell lung cancer (NSCLC)

209
Q

Non-small cell lung cancer (NSCLC) further classifications

A 
adenocarcinoma
squamous
large cell
alveolar cell carcinoma
bronchial adenoma
210
Q

Most common type of lung cancer

A

Adenocarcinoma

211
Q

What lung cancer is seen in non-smokers?

A

Adenocarcinoma & alveolar cell carcinoma

212
Q

Acronym for causes of upper zone fibrosis

A 
C - Coal worker's pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
213
Q

Fibrosis predominately affecting the lower zones

A

idiopathic pulmonary fibrosis
most connective tissue disorders
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

214
Q

What drugs cause lung fibrosis of lower lungs?

A

amiodarone, bleomycin, methotrexate

215
Q

Contents of Superior mediastinum

A 
Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve
216
Q

Contents of middle mediastinum

A 
Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi
217
Q

Contents of Anterior mediastinum

A

Thymic remnants
Lymph nodes
Fat

218
Q

Contents of Posterior mediastinum

A 
Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves
219
Q

Mesothelioma

A

A cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure.

220
Q

Microscopic polyangiitis

A

A small-vessel ANCA vasculitis

221
Q

Non-invasive ventilation - key indications

A
  1. COPD with respiratory acidosis pH 7.25-7.35
  2. Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
  3. Cardiogenic pulmonary oedema unresponsive to CPAP
222
Q

Predisposing factors for Obstructive sleep apnoea/hypopnoea syndrome

A

obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome

223
Q

Assessment for sleepiness in Obstructive sleep apnoea/hypopnoea syndrome

A

Epworth Sleepiness Scale

Multiple Sleep Latency Test (MSLT)

224
Q

Diagnosis of Obstructive sleep apnoea/hypopnoea syndrome

A

Sleep studies (polysomnography

225
Q

Management of Obstructive sleep apnoea/hypopnoea syndrome

A

> Weight loss
CPAP
DVLA should be informed

226
Q

Oxygen dissociation curve

A

Describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration

227
Q

The L rule in Oxygen dissociation curve (shifts to left)

A

Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

228
Q

Oxygen dissociation curve (shifts to right?

A

Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG*
Raised temperature

229
Q

What does it mean when the Oxygen dissociation curve shifts to the right?

A

Raised oxygen delivery

230
Q

What does it mean when the Oxygen dissociation curve shifts to the left?

A

Lower oxygen delivery

231
Q

Oxygen saturation targets

A

Acutely ill patients: 94-98%

Patients at risk of hypercapnia (e.g. COPD patients): 88-92%

232
Q

Pleural effusion classifications

A

Transudate

Exudate

233
Q

Pleural effusion

A

Build-up of excess fluid between the layers of the pleura outside the lungs. The pleura are thin membranes that line the lungs and the inside of the chest cavity and act to lubricate and facilitate breathing.

234
Q

Transudate causes of pleural effusions

A 
(< 30g/L protein)
heart failure
hypoalbuminaemia 
hypothyroidism
Meigs' syndrome
235
Q

Most common transudate cause of pleural effusion

A

Heart failure

236
Q

Exudate causes of pleural effusions

A 
Exudate (> 30g/L protein)
infection: pneumonia, TB, subphrenic abscess
connective tissue disease: RA, SLE
neoplasia: lung cancer, mesothelioma, metastases
pancreatitis
pulmonary embolism
Dressler's syndrome
yellow nail syndrome
237
Q

Most common exudate cause of pleural effusion

A

Pneumonia

238
Q

Exudate protein concentration

A

(> 30g/L protein)

239
Q

Transudate protein concentration

A

(< 30g/L protein)

240
Q

Features of Pleural effusions

A

Dyspnoea, non-productive cough or chest pain

Classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion

241
Q

Pleural aspiration for pleural effusions

A

Ultrasound is recommended to reduce the complication rate

A 21G needle and 50ml syringe should be used

Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology

242
Q

Managing patients with recurrent pleural effusions include

A

recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms

243
Q

Investigations for pleural effusion

A

Posterioranterior (PA) chest x-rays
Ultrasound
Contrast CT
Pleural aspiration

244
Q

Heavy blood staining in pleural effusion causes

A

Mesothelioma, pulmonary embolism, tuberculosis

245
Q

Low glucose pleural effusion causes

A

rheumatoid arthritis, tuberculosis

246
Q

Raised amylase pleural effusion causes

A

pancreatitis, oesophageal perforation

247
Q

Pleural infection management

A

All patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling

if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage

if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed

248
Q

Most common type of pneumonia

A

Bacterial

249
Q

Causes of pneumonia

A

Bacterial, viral & fungal

250
Q

Pneumonia

A

Describes any inflammatory condition affecting the alveoli of the lungs, but in the vast majority of patients this is secondary to a bacterial infection.

251
Q

Idiopathic interstitial pneumonia

A

A group of non-infective causes of pneumonia - Examples include cryptogenic organizing pneumonia which describes a form of bronchiolitis that may develop as a complication of rheumatoid arthritis or amiodarone therapy.

252
Q

Community-acquired pneumonia (CAP)

A

Develop pneumonia within the community, i.e. outside of hospital

253
Q

Signs and symptoms of pneumonia

A 
Cough
Sputum
Dyspnoea
Pleuritic chest pain
Fever
Tachycardia
Reduced oxygen saturations
Reduced breath sounds
Bronchial breathing
254
Q

Chest x-ray changes in pneumonia

A

Consolidation

255
Q

Investigations in Pneumonia

A 
Chest x-ray - consolidation 
Full blood count - Neutrophilia in bacterial infections
Urea and electrolytes
CRP - raised in response to infection
Arterial blood gases
256
Q

Management of Pneumonia

A
  1. Antibiotics: treat underlying infection
  2. Oxygen therapy if hypoxaemic
  3. IV fluids if hypotensive/dehydration
257
Q

CURB-65

A

Risk stratification process using a scoring system called CURB-65 - grades the severity of community-acquired pneumonia and risk of death

258
Q

CURB65 calculation

A

C Confusion (abbreviated mental test score <= 8/10)
U Urea > 7
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years

259
Q

Management of Pneumonia depending on CURB65 score

A

Home-based care for patients with a CRB65 score of 0 - oral amoxicillin is generally used first-line

Hospital assessment for all other patients, particularly those with a CRB65 score of 2 or more.

260
Q

Risk factors of Pneumothroax

A

Pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia

Connective tissue disease: Marfan’s syndrome, rheumatoid arthritis

Ventilation

261
Q

Symptoms of Pneumothorax

A 
>   dyspnoea
>   chest pain: often pleuritic
>   sweating
>   tachypnoea
>   tachycardia
262
Q

Primary pneumothorax management

A

If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered

Otherwise, aspiration should be attempted

If this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

263
Q

Primary Pneumothorax

A

Primary if there is no underlying lung disease and secondary if there is.

264
Q

Secondary pneumothorax management

A

If the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

Otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted.

All patients should be admitted for at least 24 hours - if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

265
Q

Contraindications after treated for pneumothroax

A
  1. Smoking
  2. Fitness to fly - may travel 2 weeks after successful drainage if there is no residual air.
  3. Scuba diving
266
Q

Restrictive lung disease

A

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased

267
Q

Obstructive lung disease

A

FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced

268
Q

Obstructive lung disease causes

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

269
Q

Restrictive lung disease causes

A 
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
270
Q

Expiratory reserve volume

A

maximum volume of air that can be expired at the end of a normal tidal expiration

271
Q

Inspiratory reserve volume (IRV)

A

maximum volume of air that can be inspired at the end of a normal tidal inspiration

272
Q

Tidal volume (TV)

A

volume inspired or expired with each breath at rest

273
Q

Residual volume (RV)

A

volume of air remaining after maximal expiration

increases with age

274
Q

Functional residual capacity (FRC)

A

the volume in the lungs at the end-expiratory position

FRC = ERV + RV

275
Q

Vital capacity (VC)

A

maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females

Decreases with age

276
Q

Total lung capacity (TLC)

A

The sum of the vital capacity + residual volume

277
Q

Centor criteria

A

presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough

278
Q

Sarcoidosis

A

A multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent

279
Q

Sarcoidosis features

A 
Erythema nodosum
bilateral hilar lymphadenopathy, 
swinging fever
polyarthralgia
dyspnoea
non-productive cough
malaise
weight loss
Hypercalcaemia
280
Q

Why is there hypercalcaemia in sarcoidosis?

A

Macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

281
Q

Lofgren’s syndrome

A

An acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

282
Q

Mikulicz syndrome

A

There is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

283
Q

Heerfordt’s syndrome

A

(uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

284
Q

Investigations in Sarcoidosis

A

A chest x-ray
Spirometry: may show a restrictive defect
Tissue biopsy: non-caseating granulomas

285
Q

Sarcoidosis stages on chest x-ray

A

stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

286
Q

Indications for steroids in Sarcoidosis

A

Chest x-ray stage 2 or 3 disease who are symptomatic.

Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment

Hypercalcaemia

Eye, heart or neuro involvement

287
Q

Silicosis

A

A fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing TB (silica is toxic to macrophages).

288
Q

Occupations at risk of silicosis

A

mining
slate works
foundries
potteries

289
Q

Features of silicosis

A

fibrosing lung disease

‘egg-shell’ calcification of the hilar lymph nodes

290
Q

What is a disease that can develop with silicosis?

A

TB (silica is toxic to macrophages).

291
Q

Tension pneumothorax

A

May occur following thoracic trauma when a lung parenchymal flap is created. This acts as a one way valve and allows pressure to rise.

The trachea shifts and hyper-resonance is apparent on the affected side.

292
Q

Treatment of Tension pneumothorax

A

Treatment is with needle decompression and chest tube insertion.

293
Q

Features of tension pneumothorax

A

The trachea shifts and hyper-resonance is apparent on the affected side.

294
Q

Transfer factor

A

Describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.

295
Q

Causes of a lower TLCO

A 
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
296
Q

Causes of a raised TLCO

A 
asthma
Wegener's, Goodpasture's
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise

Resp Year 1 (2 decks)

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