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Emily Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is COPD?

A

Describes progressive and irreversible obstructive airway disease. It is a combination of emphysema and chronic bronchitis

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2
Q

Describe the epidemiology of COPD

A

1.2 million people in the UK
4th leading cause of death globally

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3
Q

What are the risk factors for developing COPD?

A

Tobacco smoking (biggest risk factor)
Air pollution
A1AD
Occupational exposure such as dust, coal, cotton, cement and grain

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4
Q

What are the two things that make up COPD?

A

Emphysema and bronchitis

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5
Q

What is emphysema?

A

Alveolar air sacs become damaged or destroyed:
- They become enlarged and lose their elasticity.
- Individuals have difficulty exhaling which depends heavily on lung recoil

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6
Q

Describe the pathophysiology of emphysema

A

When lung tissue is exposed to irritants it triggers an immune response

This attracts various immune cells such as elastases and collagenases which causes a loss in elastin in the alveoli

The elastin loss causes collapse meaning:
- air is trapped distal to the point of collapse
-lungs become more compliant when air is inhaled, the lungs expand easily and hold onto air
- Breakdown if the thin alveolar walls, which reduces the surface area for gas exchange

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7
Q

What are some signs of emphysema?

A

Barrel shaped chest due to air trapping and hyperinflation
Downward displacement of liver due to hyperexpansion of the lungs

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8
Q

What is bronchitis

A

Inflammation of the bronchial tubes of the lungs. It is said to be chronic when it causes a productive cough for at least 3 months every year for 2 or more years

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9
Q

Describe the pathophysiology of chronic bronchitis?

A

-Due to chemicals and irritants the squamous epithelium may become ulcerated and when it heals it is replaced with columnar cells (metaplasia). Irritants also stimulate hypertrophy and hyperplasia of mucinous glands so there is an increase in mucus production in bronchioles with narrow lumen this can cause obstruction

This inflammation is also followed by scarring and thickening of the walls which narrows the small airways and makes cilia shorter making it harder to move mucus meaning coughing is the only way to remove it

Overall, there is airway narrowing due to hyperplasia, inflammation and oedema.

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10
Q

Why is there V/Q mismatch in COPD?

A

Due to damage and mucus plugging of smaller airways. This leads to a fall in PaO2 and increased respiration. CO2 will remain unaffected until patient can no longer maintain respiratory effort

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11
Q

What is the usual drive for respiration and how does this change in how does this change in COPD?

A

The usual drive for respiration is CO2 however body becomes desensitised to high CO2.
- Hypoxaemia (low arterial blood oxygen) becomes the new drive for respiration.

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12
Q

What are the signs of COPD?

A

Tachypnoea
Barrel chest
Cyanosis
Quiet breath sounds and wheeze

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13
Q

What are the symptoms of COPD

A

Dyspnoea
Productive cough
Wheeze
Chest tightness
Weight loss

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14
Q

What are signs of CO2 retention?

A

Drowsy
Asterixis (flapping tremor of hands)
Confusion

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15
Q

What are the differentials for COPD?

A

Lung cancer, lung fibrosis or heart failure
COPD does not cause clubbing or haemoptysis/chest pain

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16
Q

What is the MRC dyspnoea scale?

A

5 point scale for assessing impact of breathlessness.

Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

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17
Q

What is FEV1 and FVC?

A

FEV1 = forced expiratory volume in one second
FVC = forced vital capacity

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18
Q

What would happen to FVC (max air exhaled in one breath) in COPD?

A

It would be lowered

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19
Q

What would happen to FEV1 (first second of air breathed out in a single breath) in COPD?

A

Lowered more than FVC

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20
Q

What would happen to TLC in COPD?

A

Increased due to air trapping

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21
Q

How would you make a diagnosis of COPD?

A

Clinical presentation plus spirometry

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22
Q

What would spirometry show for COPD?

A

FEV1/FVC ratio less than 0.7

Important to note that it does not show a dramatic response to reversibility testing with salbutamol (beta-2 agonist). If it does then consider asthma as a differential

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23
Q

What is used to classify the severity of airway obstruction?

A

GOLD classification
Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

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24
Q

What other investigations might you perform for COPD?

A

Chest x-ray to rule out other pathology
BMI for a baseline to asses weight loss/weight gain form steroids
ECG
CT thorax to rule out fibrosis, cancer or bronchiectasis
Serum alpha-1 antitrypsin

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25
Q

What is the initial management for COPD?

A

STOP SMOKING

Annual flu vaccine and the pneumococcal vaccine (this is a one off vaccine)

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26
Q

What are the GOLD groups in COPD?

A

GOLD A = 1 or less exacerbations per year not requiring admission with mild symptoms, >80% FEV1
GOLD B = 1 or less exacerbations per year not requiring admission severe symptoms, 50-79%
GOLD C = 2 exacerbations per year or 1 per year requiring admission with mild symptoms, 30-49%
GOLD D = 2 exacerbations per year or 1 per year requiring admission with severe symptoms, <30%

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27
Q

What are the different bronchodilators used to treat COPD?

A

SABA:short-acting beta-agonist (e.g. salbutamol)
SAMA: short-acting muscarinic antagonist (ipratropium)
LABA: long-acting beta-agonist (e.g. salmeterol)
LAMA: long-acting muscarinic antagonist (e.g. tiotropium)

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28
Q

What is the treatment for GOLD group A?

A

Any short or long acting bronchodilator

(saba/laba)

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29
Q

What is the treatment for GOLD group B?

A

LAMA/LABA

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30
Q

What is the treatment for GOLD group C?

A

LAMA

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31
Q

What is the treatment for GOLD group D?

A

LAMA or LABA+LAMA or LABA+ICS
(ICS: inhaled corticosteroid e.g. beclomethasone)

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32
Q

When is long term oxygen therapy used to treat COPD?

A

Long term oxygen therapy
- is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale).
- It can’t be used if they smoke as oxygen plus cigarettes is a significant fire hazard.

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33
Q

What other treatments can be given alongside inhalers?

A

Mucolytics (carbocisteine)
Systemic corticosteroids (prednisolone)
Phosphodiesterase- 4 inhibitors (roflumilast)
Azithromycin
Long term antibiotics

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34
Q

What are the pros and cons of adding ICS to an bronchodilator?

A

Pro:
- history of hospitalisation for exacerbations of COPD
- >2 moderate exacerbations of COPD per year
- bloody eosinophils >300 cells

Cons:
- repeated pneumonia events
- blood eosinophils < 100 cells
- history of mycobacterial infection

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35
Q

What is an exacerbation of COPD?

A

COPD presents as an acute worsening of symptoms such as cough, shortness of breath, sputum production and wheeze

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36
Q

What causes an exacerbation of COPD?

A

Usually triggered by viral or bacterial infection
Can be heart failure, pulmonary embolism or medications

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37
Q

What would an exacerbation look like on an ABG?

A

CO2 will make blood more acidotic. This will show as a type 2 respiratory acidosis high CO2 and low oxygen with low pH

If this chronic there will be some metabolic compensation by kidneys releasing more bicarbonate to try and neutralise pH

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38
Q

What is the treatment for an exacerbation of COPD where the patient is well enough to stay at home?

A

Prednisolone for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is presence of infection

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39
Q

What is the treatment for an exacerbation of COPD where the patient is in hospital?

A

Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)

Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)

Antibiotics if evidence of infection

Physiotherapy can help clear sputum

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40
Q

What are the treatment options for an exacerbation of COPD not responding to treatment?

A

IV aminophylline
Non-invasive ventilation
Intubation and ventilation
-Doxapram can be used as a respiratory stimulant if ventilation not appropriate

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41
Q

Why should you not give beta blockers to someone with asthma?

A

Beta blockers = bronchoconstriction
e.g. atenolol

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42
Q

Why do you have to be careful giving oxygen to someone with COPD and how would you manage this?

A

Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive.

Venturi masks are designed to deliver specific percentage concentrations of oxygen

If retaining CO2 aim for oxygen saturations of 88-92% titrated by Venturi mask

If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%

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43
Q

What is the difference between COPD and asthma?

A

Spirometry:
COPD = always abnormal
Asthma = may be normal

Serial Peak Flow
COPD = minimal variation
Asthma = day to day + diurnal variation

Reversibility
COPD = usually <15%
Asthma = usually > 15%

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44
Q

What is asthma

A

A chronic inflammatory airway disease characterised by intermittent airway obstruction and hyperreactivity

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45
Q

What are the two types of asthma?

A

Allergic/eosinophilic
Non-allergic e.g. exercise, cold air and stress

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46
Q

What are some risk factors for developing asthma?

A

History of atopy (allergies)
Viral URTI
Occupational exposur

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47
Q

What causes asthma?

A

There is often an excessive reaction for the Th2 cells against specific antigens. Allergens from environmental triggers are picked up by dendritic cells and presented to Th2 cells leading to the release of cytokines.

This leads to the production of IgE antibodies which lead to histamine release

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48
Q

What are some genetic causes of asthma ?

A

Genes controlling cytokines IL-3 -4 -5 -9 -13

ADAM33 is associated with airway hyper-responsiveness and tissue remodelling

Generally asthma before 12 is more genetic after this it is more environmental

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49
Q

What is the hygiene hypothesis?

A

Reduced early immune-system exposure to bacteria and viruses might increase the risk of later developing asthma, possibly by altering the overall proportion of immune cell subtypes.

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50
Q

What are the signs and symptoms of asthma?

A

Episodic
Diurnal variability- worse at night and in the morning
Dry cough with wheeze and shortness of breath
Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
Family history of other ectopic disease such as eczema and hayfever

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51
Q

What are the primary investigations for asthma?

A

Fractional exhaled nitric oxide a value of >40 ppb is positive

Spirometry = will show a FVC/FEV1 ratio of less than 70% but will improve by 12% and increase by >200ml when using a bronchodilator

FBC = look for eosinophils

Skin prick tests

Bronchial hyperesponsivness to e.g. histamine

Sputum eosinophil count

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52
Q

What tests would you perform if you were unsure of a diagnosis of asthma?

A

PEFR: measured multiple times a day over a 2-4 week period. Variability of >20% throughout the day is diagnostic

Airway hyperreactivity testing: a histamine or methacholine direct bronchial challenge

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53
Q

What are Short acting beta 2 adrenergic receptor agonists?

A

They work quickly but the effect only lasts for an hour or 2. Nor Adrenalin acts on smooth muscle of airways to cause relaxation.

Reliver or rescue medication salbutamol

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54
Q

What are Long-acting beta 2 agonists (LABA)?

A

Same as short acting but last for longer salmeterol

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55
Q

What are Long-acting muscarinic antagonists (LAMA)?

A

block acetylcholine receptors
- stimulated by the parasympathetic nervous system which cause bronchoconstriction.

E.g. tiotropium

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56
Q

What are Inhaled corticosteroids (ICS)?

A

They reduce inflammation and reactivity of the airways. They are used for maintenance and prevention.

Beclomethasone

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57
Q

What are Leukotriene receptor antagonists?

A

Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion.

Montelukast

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58
Q

What is MART?

A

Maintenance and Reliever Therapy (MART).
- a combination inhaler = containing a low dose inhaled corticosteroid and a fast acting LABA.

  • This replaces all other inhalers and the patient uses this single inhaler both regularly as a “preventer” and also as a “reliever” when they have symptoms.
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59
Q

What is the BTS/SIGN stepwise ladder for treatment of asthma?

A
  1. SABA as required for wheezy episodes
  2. Regular low dose ICS inhaler
  3. Add LABA e.g. salmeterol
  4. Consider LTRA e.g. Montelukast or oral beta 2 agonist, oral theophylline or an inhaled LAMA (i.e. tiotropium).
  5. Titrate up ICS
  6. Add oral steroids at lowest possible dose
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60
Q

What is the NICE Guidelines (adapted from 2017 guidelines) for asthma

A
  1. SABA as required or wheezy episodes
  2. Regular lose dose ICS inhaler
  3. Add LTRA e.g. Montelukast
  4. Add LABA
  5. Consider MART
  6. Increase steroid dose
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61
Q

What are the triggers for an asthma attack?

A

Allergy exposure
Viral infection
Smoking exposure
Pollution
Exercise

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62
Q

What is the presentation of an asthma attack?

A

Fast respiratory rate
Symmetrical wheeze
Tight sounding chest with reduced air entry

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63
Q

What is investigated in an asthma attack?

A

PEFR
ABG: patients will initially have respiratory alkalosis. Abnormal or high PCO2 is concerning as it implies the patient is tiring

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64
Q

What would be considered an moderate asthma attack?

A

PEFR 50-75% of predicted

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65
Q

What would be considered a severe asthma attack?

A

PEFR 33-50%
Resp rate >25
Heart rate above 110
unable to complete sentences

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66
Q

What would be considered a life threatening asthma attack?

A

PEFR <33%
Sats <92%
Becoming tired

No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.

Haemodynamic instability (i.e. shock)

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67
Q

What is the treatment for a moderate asthma attack?

A

Nebulised salbutamol
Nebulised ipratropium bromide
Steroids oral continue for 5 days after

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68
Q

What is the treatment for a severe asthma attack?

A

Oxygen is required to maintain stats
Aminophylline infusion
Consider IV salbutamol

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69
Q

What is the treatment for a life threatening asthma attack?

A

IV magnesium sulphate
Admission to ICU
Intubation in worst cases

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70
Q

What is dyspnoea?

A

Shortness of breath

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71
Q

What is the MRC dyspnoea scale?

A

Grade 1
Not troubled by breathlessness except on strenuous exercise

Grade 2
Short of breath when hurrying or walking up a slight hill

Grade 3
Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace

Grade 4
Stops for breath after walking about 100 metres or after a few minutes on level ground

Grade 5
Too breathless to leave the house, or breathless when dressing or undressing

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72
Q

What are the causes of dyspnoea?

A

Cardiac:
Acute pulmonary oedema
Cardiac arrhythmia
Cardiac tamponade
Chronic heart failure
MI

Pulmonary:
Asthma
Bronchiectasis
COPD
Interstitial Lung disease
Pleural effusion
lung collapse
Pneumonia
pulmonary embolism

other:
Anaemia
anaphylaxis
anxiety
diaphragmatic splinting (ascites, obesity, pregnancy)

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73
Q

What is type 1 respiratory failure?

A

Hypoxemia
- failure of lungs to provide adequate O2 to meet metabolic needs

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74
Q

What are the causes of type 1 respiratory failure?

A

R-L shunt
V/Q mismatch
Alveolar hypoventilation
Diffusion defect
Inadequate FIO2
e.g. Asthma, ILD, cardiac septal defect, COPD, PE

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75
Q

What is the criteria for type 1 respiratory failure?

A

PaO2 < 60mmHg on FiO2 or pO2 <8kpa

Low PaO2 with normal or low PaCO2

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76
Q

What is type 2 respiratory failure?

A

the failure of the lungs to eliminate adequate CO2

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77
Q

What are the causes of type 2 respiratory failure?

A

Pump failure
Increased Co2 production
R-L shunt
Increased deadspace
e.g. COPD, drug OD, obesity, chest wall deformity, neuromuscular weakness

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78
Q

What is the criteria for a type 2 respiratory failure?

A

Acute increase in PaCO2 > 50mmHg

Low PaO2 with raised PaCO2

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79
Q

What are the signs of hypercapnia in type 2 respiratory failure?

A

Bounding pulse
Flapping tremor
Confusion
Drowsiness
Reduced consciousness

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80
Q

What is DLCO a measure of?

A

Transfer Coefficient of oxygen/CO

Measure of ability of oxygen to diffuse across the alveolar membrane

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81
Q

How is DLCO measured?

A

Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill)
hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured

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82
Q

What causes a high DLCO?

A

Pulmonary haemorrhage
- can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available

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83
Q

What causes a low DLCO?

A

Severe emphysema
Fibrosing alveolitis
Anaemia
Pulmonary hypertension
Idiopathic pulmonary fibrosis
COPD

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84
Q

What is the pleura? and the layers?

A

Lining of the lung
—
1. Visceral pleura – forms the
outer covering of the lung
2. Parietal pleura – forms the inner lining of the chest wall

Between the 2 linings is the pleural space
In health this space is almost non-existent, contains 5- 10mls of fluid

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85
Q

What is the purpose of the pleura?

A

Allows for optimal expansion and contraction of the lungs
Pleural fluid allows for visceral and pareital pleurae to glide over without friction during respiration

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86
Q

What is pneumothorax?

A

‘collapse of the lung’

Presence of air in the pleural
space

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87
Q

what occurs during a pneumothorax?

A

Air enters due to
- Hole in the lung/pleura —
- Chest wall injury

intrapluerla pressure is negative, leads to air beinf sucked into cavity

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88
Q

What are the causes of a pneumothorax?

A
  • primary spontaneous pneumothorax
  • secondary spontaneous pneumothorax
  • traumatic pneumothorax
  • iatrogenic pneumothorax
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89
Q

What is primary spontaneous pneumothorax? and risk factors?

A
  • No underlying lung disease
  • Rupture of apical pleural bleb

Risk Factors
Male
Smoker
Tall (lung stretched)
Age 20-40 y/o

Annual incidence 9 per 100,000 —
Risk of recurrence high

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90
Q

What are the causes of secondary spontaneous pneumothorax?

A
  1. known lung disease = COPD, Asthma. lung cancer, cystic lung disease (cyst pops)
  2. infection = PCP/TB, lung abscess
  3. genetic predisposition = Marfan’s, Birt- Hogg Dube, lymphangioleiomyomatosis LAM
  4. Catamenial pneumothorax = occur with menstruation + PCOS (only in females)
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91
Q

What are the difference in traumatic and iatrogenic causes of pneumothorax?

A

Traumatic
— Penetrating chest wall injury
— Puncture from rib
— Rupture bronchus/ oesophagus

Iatrogenic:
‘Doctor induced’ —
Risk
— Pacemakers,
— CT lung biopsies,
— Central line insertion —
Mechanic ventilation —
Pleural aspiration

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92
Q

What is the presentation for a pneumothorax?

A

Asymptomatic
— Acute/ sudden
— Breathlessness
— Pleuritic chest pain —
Cough
— Life threatening resp failure/ cardiac arrest
sweating

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93
Q

What are the signs of a pneumothorax?

A

Tachyopnoea
— Hypoxia
— Unilateral chest wall expansion —
Reduced breath sounds
— Hyper-resonant percussion note

Tension penumothorax:
— Deviated trachea (away)
— Surgical emphysema
— Distended neck veins
— Cardiovascular compromise

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94
Q

What is a tension pneumothorax?

A
  • air pushing against the healthy lung, squashing it
  • displaces mediastinum and cardiac compromise
  • medical emergency
  • requires urgent decompression
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95
Q

What is the first line investigation for a pneumothorax?

A

If tension pneumothorax is suspected then don’t wait

Chest x-ray would be first line and would show:
- no pleural edge with no lung markings
- Look for mediastinal shift in tension

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96
Q

What is the gold standard investigation for a pneumothorax?

A

CT chest:
will show an accurate size of the pneumothorax will be rarely used though

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97
Q

What is the management for a pneumothorax?

A
  1. No intervention
    — Reabsorb spontaneously 2% volume a day —
    Consider high flow oxygen (10L)
  2. Pleural Aspiration
    — Up to 1.5Litre of air can be aspirated
  3. Ambulatory devices
    stick one way valve on chest and send home
  4. Chest Drain
    — Needed for most secondary pneumothoraxes
  5. Surgery
    — For persistent and recurrent pneumothorax
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98
Q

What is the management for a tension pneumothorax?

A

Initially inset a large bore cannula into the second intercostal space in the midclavicular line do not wait to do this

Once the pressure is relieved then use a chest drain

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99
Q

Where are chest drains usually inserted?

A
  • The 5th intercostal space (or the inferior nipple line)
  • The mid axillary line (or the lateral edge of the latissimus dorsi)
  • The anterior axillary line (or the lateral edge of the pectoris major)
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100
Q

Why is a tension pneumothorax dangerous?

A

Air is drawn in to the pleural space with each breath and cannot escape.

This is dangerous as it creates pressure in the thorax and will push the mediastinum across kinking the big vessels causing cardiorespiratory arrest

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101
Q

What is general advice to prevent future pneumohtoraxes?

A

(very high re-occurence rate)

stop smoking
no air flight until 6 week after resolution
no scuba diving ever

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102
Q

What is a pleural effusion?

A

collection of fluid in the pleural space
- fluid presses against lung, compressing it and making it smaller

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103
Q

What are the 2 types of pleural effusions?

A

(light’s criteria)
Transudates
- pleural fluid protein < 30g/L or 1/2 serum protein
- low protein count fluid moving across into the pleural space (fluid shifting)
(increased hydrostatic pressure or reduced osmotic pressure in microvascular circulation)

Exudates
- pleural fluid protein > 30g/L or 1/2 serum protein
- high protein count caused by inflammation proteins leak out of tissue
(increase capillary permeability and impaired reasborption)

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104
Q

What are the causes of transudative pleural effusion?

A

Congestive heart failure
Hypoalbuminemia
Hypothyroidism
Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
(cirrhotic liver disease)

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105
Q

What are the causes of exudative causes of pleural effusion?

A

Lung cancer
Pneumonia
Rheumatoid arthritis
TB
(inflammation increase protein levels)

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106
Q

What are the symptoms for a pleural effusion?

A

Asymptomatic
— Breathlessness
— Cough
— Pain
— Fever

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107
Q

What are the signs for pleural effusion)

A

Reduced chest wall
expansion
— Quiet breath sounds
— “Stony” Dull Percussion
— Reduced tactile/ vocal fremitus
— Mediastinal shift away from affected side

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108
Q

What investigations are done for a pleural effusion?

A

X-ray = blunting of diaphragm + costcophrenic angle, fluid, larger effusions, tracheal + medialstinal deviation
Thoracic USS = before doing needle aspiration, to exclude other causes
pleural aspiration = take sample of fluid

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109
Q

What do the appearances of the pleural fluids signify?

A
  • straw coloured = transudate/exudate
  • turbid/foul smelling= empyema/parapneumonic effusion
  • milky = chylothorax
  • blood stained = trauma, cancer, PE
  • food particles = oesophageal rupture
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110
Q

What tests are done on the lung fluid?

A

Biochemistry —
pH
— Protein
— LDH
— Glucose
— (Amylase)

Microscopy and culture —
- AAFB

Cytology

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111
Q

What is a medical thoracoscopy?

A
  • local anaesthetic
  • put tube in and draw out all the fluid
  • and take some biopsies
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112
Q

What is the management for a pleural effusion?

A

Depends on size, symptoms and underlying cause —

Small effusions often treated conservatively

Pleural infection/empyema
- Antibiotics
- Chest drain if pus/ complex infection

Malignant effusion
- Consider chest drain if symptomatic (+/- talc)
- If re-current consider long term chest drain

Treat underlying cause e.g.
— Diuretics for heart failure
— Dialysis for renal failure
— NSAIDS/ steroids for SLE effusion

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113
Q

What is the criteria for a pleural infection?

A

Criteria that would support a diagnosis of
pleural infection
—pH < 7.2
— Glucose < 3.4mmol/L
— PF LDH > 1000 IU/L
— Bacterial growth on culture
— Macroscopic appearance of pus (can do a chest drain straight away)

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114
Q

What is the progression of a pleural infection?

A
  1. Simple parapneumoni effusion
  2. complex parapneumonic effusion
  3. Empyema (pus)
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115
Q

What is a complication of pleural effusion?

A

Empyema

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116
Q

What is empyema?

A

pus in the pleural space

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117
Q

What are the causes of empyema?

A

community/acquired
- S. milleri/ S. pneumo/ S. Aureus/
Anaerobes

Hospital Acquired
— MRSA/ S. Aureus/ Enterococcus

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118
Q

What are the symptoms for empyema?

A

Symptoms
— Patient unwell/ not improving —
Swinging fevers/ rigor
— Cough/ Chest Pain

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119
Q

What is the treatment for empyema?

A

Antibiotics (prolonged course) —
Chest Drain
Surgery

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120
Q

What is the treatment for malignant effusions?

A

Drain and ‘pleurodesis’
- chest drain (talc via drain)
- thoracoscopy (spray talc - cause inflammatory response making lung expand and stick to pleura to stop from refilling with fluid)

if recurrent = indwelling pleural catheter (IPC)

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121
Q

What is a haemothorax?

A

Blood in pleural cavity
(haemocrit ratio >50%)

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122
Q

What are the causes of a haemothorax?

A

Trauma
— Post-operative
— Bleeding disorders
— Lung cancer
—PE
— Aortic rupture
— Thoracic endometriosis

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123
Q

What is the management for haemothorax?

A
  • Large bore chest drain
  • Possible vascular intervention = embolise vessel to stop bleed
  • Surgical opinion
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124
Q

What is a hydropneumothorax? A

A

air and fluid in pleural space

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125
Q

What are the causes for a hydropneumothorax?

A

Iatrogenic
Gas forming organisms
Thoracic trauma

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126
Q

What is the cause of thickening of pleura?

A
  • Related to asbestos exposure
  • Following infection/ empyema/ chest trauma/ haemothorax
  • Cancer (Consider if nodular/ >1cm depth)
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127
Q

What is a pneumomediastinum?

A

Air in mediastinum
- Air from lungs/ trachea/ oesophagus/ peritoneal cavity

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128
Q

What are the features and causes of a pneumomediastinum?

A

Can track to neck/ face and abdomen
Often seen with surgical emphysema/ pneumothorax
Oesophageal rupture (Boerhaave’s syndrome - also get mediastinitis)

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129
Q

What is a normal alveolar-arterial gradient?

A

normally less than 2kPa

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130
Q

What are the causes of a raised A-a gradient?

A
  1. V/Q mismatch (ventilation perfusion)
  2. Diffusion limitation
  3. Shunt (right-to-left)
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131
Q

What are the features and treatment of a high altitude pulmonary oedema?

A

1%at4000m
* 2-3 days after ascent
* Exaggerated hypoxic pulmonary vasoconstriction
* Treatment: Descent, oxygen, pulmonary vasodilators

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132
Q

What are the classfications for obstructive and restrictive lung conditions?

A

Obstructive vs. Restrictive
* Low FEV1 (< 80% predicted)
* FEV1/FVC ratio (< 0.7 aka 70%) = obstructive
* FEV1/FVC ratio normal = restrictive

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133
Q

What is transfer factor?

A

Diffusing capacity
- the extent to which oxygen passed from the air sac of the lungs into the blood

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134
Q

What does a low or high Transfer factor of the lungs for Carbon Monoxide (TLCO) indicate?

A

Low TLCO
* Thickening of the alveolar-capillary membrane
* Reduced lung volumes
Raised TLCO
* Increased capillary blood volume
* Pulmonary haemorrhage

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135
Q

What conditions have low TLCO?

A

Pulmonary fibrosis

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136
Q

What conditions have a high TLCO?

A
  • Alveolar haemorrhage (blood is sitting there so has more time to diffuse)
  • left to right intracardial shunt (blood goes past twice)
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137
Q

What is the difference between pneumonia, pulmonary fibrosis, pulmonary TB, emphysema, asthma and bronchitis?

A

Pneumonia = alveoli fill with thick fluid, making gas exchange harder

Pulmonary fibrosis = fibrous connective tissue build up in lung, reduce elasticity

Pulmonary TB = TB encapsulate bacteria + elasticity reduced

Emphysema = alveoli burst and fuse into enlarged air spaces reducing surface area

Asthma = airways are inflamed due to irritation and bronchioles constrict due to muscle spasms

Bronchitis = airways are inflamed due to infection or irritants

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138
Q

What are the advantages of inhaled medicines?

A
  • lungs are robust
  • large surface ares
  • rapid absorption
  • fewer systemic side effects (as drug is ending up just in lungs where you want it)
  • non-invasive
  • act directly on the lung or enter the systemic circulation
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139
Q

What are the different delivery systems for inhaled devices?

A
  • pressurised metered dose inhalers
  • spacer devices = slow down particles so more of drug can be inhaled
  • dry powder inhalers = person needed sufficient inspiratory effort to breathe in powder
  • Nebuliziers = less coordination needed
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140
Q

What occurs during bronchoconstriction?

A

Constriction of the airways due to:
- tightening of airway smooth muscle (ASM)
- lumenal occlusion by mucus and plasma
- airway wall thickening

Leads to airflow obstruction.

Most commonly seen in asthma & COPD
Reversible vs non-reversible

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141
Q

How do airway smooth muscle cells react in asthma?

A

ASM is both primed to contract and is resistant to relaxation

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142
Q

What are the two categories of bronchodilators?

A

Adrenergic (sympathetic)
bronchodilation

Anti-cholinergic (parasympathetic)
Block bronchoconstriction

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143
Q

How do b2-adrenergic agonists work? Examples?

A

act on b2-adrenoceptors to cause smooth muscle relaxation and bronchodilation.
- Also inhibit histamine release from lung mast cells

SABA e.g. salbutamol
LABA e.g. formoterol

144
Q

How do anticholinergics work? Examples?

A

Block acetylcholine binding to muscarinic receptors (would activate smooth muscle contraction)

e.g. Atropine, ipratropium bromide

145
Q

WHat do you use to treat lung inflammation?

A

Glucocorticoids (inhaled corticosteroids ICS)
- suppress inflammation
- most effective for asthma
- can prevent irreversible airway changes

ineffective in COPD
people with asthma can become resistant

146
Q

How do ICS reduce inflammation?

A

Reduce number of inflammatory cells in the airways
- suppress the production of chemotactic mediators
- Reduce adhesion molecule expression
- Inhibit inflammatory cell survival in the airway

  • suppress inflammatory gene expression in airway epithelial cells e.g. via IKB-alpha
147
Q

What are the side effects of ICS?

A

Titrating to lowest effective dose reduces side effects

high-dose ICS are OFTEN used in COPD.

Loss of bone density
Adrenal suppression
Cataracts, glaucoma

148
Q

How do B2 agonist and ICS work together?

A

ICS
- Glucocorticoids increase the transcription of the b2-receptor gene, resulting in increased expression of cell surface receptors

B2
Long-acting b2-Agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids

149
Q

Why can monoclonal antibodies not be inhaled?

A

cannot cross mucus barrier

150
Q

What is bronchiectasis?

A

Obstructive lung disease w/ abnormal Dilation of the bronchi

  • excessive sputum production, chest pain
  • Permits infection
  • Associated with Cystic Fibrosis (CF)
  • excessive and persistent inflammation in the lung
151
Q

What are the causes of bronchiectasis?

A
  • Severe pneumonia
    – TB
    – Whooping cough
    – Obstruction
    – Fibrosis
    – traction bronchiectasis
    – Ciliary dysfunction = primary ciliary dyskinesia
    – Immunosuppression
  • pseudomonas aeruginosa
152
Q

What are the symptoms for bronchiectasis?

A

– Productive cough
* Green mucoid sputum
* Large volumes
* Postural element
* Worse in infections
– Haemoptysis
– Hallitosis. (bad breath)
- wheezing
- inspiratory crackles

153
Q

What are the signs of bronchiectasis?

A

– Clubbing
– Crackles
– Hyperexpanded chest
– Purulent sputum
– Signs of cor pulmonale

154
Q

What are the first-line investigations for Bronchiectasis?

A

CXR = will show dilated airways with thickened walls that appear as tram tracks
Sputum cultures
Spirometry will show obstructive FEV1/FVC <0.7

155
Q

What is the gold standard test for Bronchiectasis?

A

High resolution CT chest: shows bronchial dilation and bronchial wall thickening (Signet ring cell)

156
Q

How to treat bronchiectasis?

A

Hard to treat - aim to reduce symptoms

Mucolytics treat hyersecretion
B2 agonists most useful in COPD/ASTHMA/bronchiectasis overlap syndromes
Anticholinergics have limited effect
ICS have limited effect

157
Q

What is lung fibrosis?

A

excessive fibrous connective tissue leads to permanent scarring, airway wall thickening and breathing difficulties.
A common end-stage of a number of heterogenous conditions

158
Q

What are the symptoms of fibrosis?

A

Insidious onset of SOB
Dry cough

159
Q

What are the signs of fibrosis?

A

Fine crepitations (crackling in lungs)
Clubbing
Cyanosis

160
Q

What are the causes of fibrosis?

A
  • Drugs (amiodarone, methotrexate, bleomycin)
  • Autoimmune disease (Rheumatoid arthritis, SLE, scleroderma)
  • Cryptogenic (usual interstitial pneumonitis)
  • Occupational (asbestosis, pneumoconiosis, silicosis)
  • Others (sarcoid, HP, OP)
161
Q

What is the treatment for fibrosis?

A
  • transplantation is best option
  • Pirfenidone = reduce fibroblast and collagen proliferation
  • Nintedanib = tyrosine kinase inhibitor
162
Q

Why is lung expansion reduced in restrictive lung diseases?

A
  1. Altered lung parenchyma
  2. Pleural disease
  3. Neuromuscular disease
  4. Chest wall disease
163
Q

What is cystic fibrosis?

A

An inherited autosomal recessive multi-system disease affecting the mucus glands

164
Q

A mutation on what gene causes CF?

A

cystic fibrosis transmembrane conductance regulatory gene on chromosome 7

165
Q

How does a mutation to the CFTR gene cause disease?

A
  • The CFTR protein gets misfolded and can’t migrate from the RER to the cell membrane
  • The CFTR is a channel protein that pumps chloride ions into various secretions helping to thin them out meaning secretions are left overly thick
166
Q

How does CF cause respiratory problems?

A
  • Results in dry airways and impaired mucociliary clearance
  • The low volume thick airway secretions result in reduced airway clearance increasing chances of infection and this chronic inflammation can lead to bronchiectasis
167
Q

dWhat are the GI problems associated with CF?

A

Thickened secretions within small and large bowel can make it difficult to pass stools resulting in bowel obstruction

168
Q

What are the pancreatic problems associated with CF?

A

Thick pancreatic and bile secretions
- block the pancreatic ducts
- resulting in a lack of digestive enzymes
- can also result in pancreatitis and diabetes

169
Q

What are the liver problems associated with CF?

A

Thickened biliary secretions may block the bile ducts resulting in liver fibrosis and cirrhosis

170
Q

What are some other problems associated with CF?

A
  • Can result in pulmonary hypertension leading to right sided heart failure
  • In males there is bilateral absence of vas deferens so it means there is male infertility
171
Q

What if often the first sign of CF in a baby

A

meconium ileus

172
Q

What is meconium ileus?

A

In babies the first stool passed is called the meconium and it is black and sticky and should be passed within 48 hours

In babies with CF the meconium does not pass as it is too sticky so it causes bowel obstruction occurs in 20% of babies with CF

173
Q

What are some signs of CF?

A

Low weight
Nasal polyps
Finger clubbing
Crackles and wheezes
Abdominal distension

174
Q

What are the symptoms of CF?

A

Chronic cough
Thick sputum production
Recurrent respiratory infections
Loose, greasy stools (steatorrhea) due to a lack of fat digesting lipase enzymes
Abdominal pain and bloating
Poor weight and height gain (failure to thrive)

Parents may report the child tastes particularly salty when they kiss them, due to the concentrated salt in the sweat

175
Q

When is CF most often diagnosed?

A

It is found during the heel-prick/Guthrie test which screens for CF in babies by looking for serum immunoreactivity trypsinogen

176
Q

What is the gold standard test for CF?

A

The sweat test

177
Q

What is the sweat test?

A

test for CF

Pilocarpine is applied to the skin and electrodes are placed either side of the patch with small current to cause skin to sweat

The sweat is absorbed and sent to lab for testing a diagnostic test of chloride
- concentration above **60 mmol/l is diagnostic

178
Q

What are common microbial colonisers in CF?

A

Staphylococcus aureus - patients take long term prophylactic flucloxacillin

Pseudomonas aeruginosa - can be harder to treat and worsen the prognosis

179
Q

what is the new miracle cure for CF?

A

Kaftrio:
- triple combination treatment combining three drugs which perform different functions
1. ivacaftor
2. tezacaftor
3. elexacaftor

and tackles the underlying causes of the disease, by helping the lungs work effectively.

180
Q

What is the management for the respiratory symptoms of CF?

A
  • Chest physiotherapy at least twice a day to remove mucus
  • Exercise
  • Salbutamol
  • Nebulised DNase (dornase alfa wolf) an enzyme that breaks down DNA material in respiratory secretions
  • Nebulised hypertonic saline
181
Q

What is the treatment for the GI symptoms of CF?

A
  • CREON tablets helps to digest fats in patients with pancreatic insufficiency (missing lipase)
  • High calorie diet to make up for malabsorption and calories needed for respiratory effort
182
Q

What is the prognosis for CF?

A
  • 90% of patients with CF develop pancreatic insufficiency
  • 50% of adults with CF develop cystic fibrosis-related diabetes and require treatment with insulin
  • 30% of adults with CF develop liver disease
    Most males are infertile due to absent vas deferens
183
Q

What are the different types of parenchymal disease?

A

Diffuse Interstitial Pulmonary Fibrosis
* Pneumoconiosis
* Sarcoidosis
* Lung resection
* Atelectasis (collapse or closure of a lung)
* (Congestive Cardiac Failure)

184
Q

What is the pathophysiology of interstitial lung disease?

A
  1. oxygen uptake reduced
  2. reduction in transfer factor of the lung for carbon monoxide
    3.
185
Q

What is interstitial lung disease?

A

An umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis.

This means normal elastic and functional lung tissue is replaced with scar tissue that is stiff and does not function

186
Q

What are the different types of interstitial lung diseases?

A
  1. Idiopathic
  2. Autoimmune
  3. Sarcoidosis
  4. exposure related
  5. hypersensitvity pneumonitis
187
Q

What is pulmonary fibrosis (PF)?

A

It describes the interstitial fibrosis of the lung parenchyma and has a number of causes. The most common cause is idiopathic

188
Q

What are some causes of drug induced PF?

A

Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

189
Q

What are some causes of secondary PF?

A

Alpha-1 antitrypsin
Rheumatoid arthritis
SLE
Systemic sclerosis
Asbestosis

190
Q

What is the pattern created by lung fibrosis called?

A

The loss of alveoli, creates cysts surrounded by thick walls this is called HONEYCOMBING

191
Q

What is the pathophysiology of idiopathic pulmonary fibrosis?

A
  1. fibroblasts repair damaged tissue
  2. fibroblasts migrate to the lungs and become myofibroblasts
  3. myofibroblasts deposit collagen in the extracellular matrix
  4. In IPF, these fibroblasts are resistant to apoptosis
  5. myofibroblasts proliferate and form fibroblastic foci
  6. the thickened tissue leads to lower gas exchange efficiency in the lungs
192
Q

What are the key features in the lungs of idiopathic pulmonary fibrosis?

A

Collections of fibroblasts (fibroblastic foci)
* Thickening of alveolar interstitium
* Destruction (honeycombing) of alveoli
* Affects periphery and base of lungs
* Spatial heterogeneity (normal lung tissue next to abnormal tissue)

193
Q

What are the symptoms of idiopathic PF?

A

Progressive dyspnoea
Non-productive cough
Malaise

194
Q

What are the signs of idiopathic PF?

A

Bibasal fine end-inspiratory crackles
Clubbing
Cyanosis

It has an insidious onset

195
Q

What is the primary investigation for PF?

A

High resolution CT scan of the thorax.
- It will show a ground glass/honeycomb appearance with interstitial lung disease

196
Q

What test is performed when CT scan is unclear for PF?

A

Lung biopsy

197
Q

What antibodies may be present in PF?

A

Antinuclear antibodies (ANA) and rheumatoid factor (RF):

ANA is positive in 30% and RF is positive in 10-20%, but this does not confirm that the fibrosis is secondary to connective tissue disease

198
Q

What is the management for PF?

A

Remove/treat underlying cause
Home oxygen when hypoxic at rest
Stop smoking
Physiotherapy
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate

199
Q

What are some drugs that can slow the progression of IPF?

A

Pirfenidone = antifibrotic + anti-inflammatory
Nintedanib = monoclonal antibody targets tyrosine kinase

200
Q

What is the prognosis for IPF?

A

IPF has a poor prognosis, with median survival ranging from 2.5 - 3.5 years after diagnosis.

Respiratory failure due to progressive disease is the most common cause of death.
- Most patients undergo subacute deterioration (worsening over > 4 weeks - months) before their death.

201
Q

What is hypersensivity Pneumonitis?

A

Type 3 hypersensivity reaction (immune complexes)
- prior sensitisation is required
- causes parenchymal inflammation and destrcution in people sensitive to that allergen

202
Q

What are some of the causes of hypersensitivity pneumonitis?

A

Bird-fanciers lung
Farmers lung
Mushroom workers lung
Malt workers lung
Louis Ertl lung
Bronchoscopy will show raised lymphocytes and mast cells

203
Q

What is the treatment of hypersensitivity pneumonitis?

A

Main treatment is identification and removal of antigen
- sometimes steroids used

204
Q

What is sarcoidosis?

A

It is a granulomatous inflammatory multi-systemic disease where any organ can be affected but it predominately affects the lungs

205
Q

What are the risk factors for sarcoidosis?

A

Afro-Caribbean
Young adults
Female gender
Family history

206
Q

What would a typical presentation of sarcoidosis be?

A

A 20-40 year old black women presenting with a dry cough and shortness of breath. They may have nodules on their shins

207
Q

Describe the pathophysiology of sarcoidosis

A
  • It is a type IV hypersensitivity reaction against an unknown antigen.
  • A T cell-mediated immune response to an antigenic stimulus attracts immune cells and causes the formation of granulomas
  • The granulomas in sarcoidosis are non-caseating meaning there is no tissue necrosis at the centre,
  • Macrophages fuse together to form a single large multi-nucleated cell called a Langhans giant cells.
208
Q

What are the pulmonary symptoms of sarcoidosis?

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules
Dry productive cough
Dyspnoea

209
Q

What are the signs of sarcoidosis on the skin?

A

Erythema nodosum
Lupus pernio (raised, purple skin lesions commonly on cheeks and nose)
- Granulomas develop in scar tissue

210
Q

What other organs are affected in sarcoidosis and what are the symptoms

A

Liver 20% (cirrhosis and nodules)
Eyes 20% (uveitis, conjunctivitis and optic neuritis)
Heart 5% (Heart blocks)
Kidney 5% (Kidney stones (due to hypercalcaemia) Nephrocalcinosis Interstitial nephritis)

211
Q

What are some syndromes associated with sarcoidosis?

A

Lofgren’s = an acute form of sarcoidosis that is associated with polyarthritis, erythema nodosum and bilateral hilar lymphadenopathy

Heefordt’s syndrome = causes facial nerve palsy fever, uveitis and parotitis

Mikulicz’s disease = bilateral parotid and lacrimal gland enlargement; can also occur due to TB and lymphoma.

212
Q

What are some differentials for sarcoidosis?

A

Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
Toxoplasmosis
HIV

213
Q

What are the blood tests for sarcoidosis?

A

Raised serum ACE. Often used as a screening test
Hypercalcaemia is a key finding
Raised serum soluble interleukin 2 receptor
Raised CRP

214
Q

What would imaging for sarcoidosis show?

A

CXR would show hilar lymphadenopathy

High-resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules

215
Q

What is the gold standard test for sarcoidosis?

A

Histology from a biopsy which is done using bronchoscopy with ultrasound guided biopsy.

216
Q

What would the histology of sarcoidosis show?

A

Non-caseating granulomas with epithelioid cells

217
Q

What is the treatment for sarcoidosis?

A

(1st is no treatment with mild symptoms)
First line is corticosteroids, e.g. inhaled budesonide or oral prednisolone
Second line is immunosuppressants such as methotrexate and azathioprine 187

218
Q

What is TB?

A

Is an infectious disease caused mycobacterium tuberculosis

219
Q

What type of bacteria is mycobacterium tuberculosis?

A

It is a small rod shaped bacteria. They are resistant to acids used in staining procedure so known as acid-fast bacilli.

Require a Zeihl-neelsen stain and is red

220
Q

Describe the epidemiology of TB

A

1.7 billion people worldwide have latent TB
Common in South Asia and sub-Saharan Africa
Prevalent in immunocompromised patients

221
Q

What are the risk factors for TB?

A
  • contact with a person with active TB
  • homelessness
  • alcohol or drug abuse
  • immunocompromised e.g. HIV (worsens each other), steroid use, malnutrition
  • silicosis = impairs macrophage function
222
Q

How to catch TB

A
  1. spread in aerosol from infected individual’s lung ti another lung
    OR drink milk from cow with M.bovis
  2. droplet cannot be too big otherwise will get stuck and coughed up
  3. aerosol droplets of about 5m contain a few bacilli
  4. lodge in alveoli or small airways
  5. majority of people mount an effective immune response (only macrophage) that encapsulate and contain organism forever
  6. bacilli taken in lymphatic to hilar lymph nodes
  7. granulomata form in lung apex
  8. macrophage + lymphocytes seal in and kill majority of infected bacilli (try to surround and kill TB - but some TB just go to sleep and don’t use nutrients ‘latent’)
  9. granuloma grows into cavity
  10. cavity full of TB bacilli, expelled when patient coughs (spreads)
223
Q

What is primary (Ghon) focus?

A

bacilli + macrophages coalesce to form a granuloma
(circular shape on X-ray)

primary focus + mediastinal lymph nodes = Ghon complex

224
Q

How does TB cause disease?

A
  • Macrophages struggle to clear TB due to its waxy mycolic acid capsule.
  • A focal caseating granuloma typically forms in the lower lobe known as a Ghon focus. This creates a type IIII hypersensitivity reaction
  • The TB bacteria are very slow dividing with high oxygen demands.
  • It spreads via respiratory droplets from patients with active disease
225
Q

What is latent TB?

A

Occurs after primary infection patients will remain asymptomatic and the bacteria remain dormant, resulting innegative sputumcultures but apositive Mantoux test.

The patient is not infectious but it can reactivate in immunocompromised individuals

226
Q

What is secondary TB?

A

Reactivation typically occurs in thelung apexwhere pO2is highest, as mycobacteria are aerobic.

The bacteria can spread locally, to form caseating granulomata, or systemically (miliary TB).

227
Q

What is miliary TB?

A

Occurs due to lympho-hematogenous spread to multiple organs e.g. heart, lungs, spleen, liver, bone marrow, pancreas and brain

228
Q

What is the BCG vaccine?

A
  • Involves an intradermal infection of live attenuated TB.
  • It offers protection against severe and complicated TB
  • Prior to vaccine patients are tested with Mantoux test
229
Q

Who is offered the BCG vaccine?

A

BCG vaccine is offered to patients that are at higher risk of contact with TB:

  • Neonates born in areas of the UK with high rates of TB
  • Neonates with relatives from countries with a high rate of TB
  • Neonates with a family history of TB
  • Unvaccinated older children and young adults (< 35) who have close contact with TB
  • Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
  • Healthcare workers
230
Q

What differentiates TB from a cough or chest infection?

A
  • Lasted longer than pneumonia or chest infection
  • has more systemic symptoms
  • presence of risk factors = race, where they’re form
231
Q

What is the main presentation of TB?

A

cough up blood

232
Q

What are the signs and symptoms of TB?

A

Lethargy
Fever or night sweats
Weight loss (can be confused with cancer)
Cough
Lymphadenopathy
Erythema nodosum
Spinal pain in spine TB also know as Pott’s disease of the spine

233
Q

What is the presentation of pulmonary TB?

A

cough > 3/52 (most other causes resolve by then)
Chest pain
Breathlessness
Haemoptysis

234
Q

How does TB spread from pulmonary to other locations?

A
  1. Primary complex, focus + regional glands in lungs
  2. rupture of focus into pleural space with effusion, serous + occasionally purulent
  3. erosion into bronchus inhalation and area of TB bronchopneumonia
  4. pericardial effusion post rupture of node through pericardium
235
Q

Pathway of TB

A
  1. primary infection
  2. primary or progressive primary disease
  3. latent TB
  4. post primary
  5. Re-infection
  6. new disease
  7. latent Tb
  8. death = most die with latent TB never realising they had it
236
Q

What is the Mantoux test?

A

(only useful for diagnosing latent TB)

This involves injecting tuberculin into the intradermal space on the forearm.
- Tuberculin is a collection of tuberculosis proteins that have been isolated from the bacteria.
- The infection does not contain any live bacteria.

Injecting the tuberculin creates a bleb under the skin. After 72 hours the test is “read”. T
- his involves measuring the induration of the skin at the site of the injection.

NICE
5mm or more = positive result.

After a positive result they should be assessed for active disease.

237
Q

What is the Interferon-Gamma Release Assays (IGRAs) test?

A

The test involves taking a sample of blood and mixing it with antigen from the TB bacteria.

In a person who has had previous contact with TB there WBC will have become sensitised and they will release interferon gamma as part of an immune response

(pro = doesn’t respond to response from TB vaccine)

238
Q

What are the tests performed in active TB?

A
  • CXR
  • Bacterial culture collected from = sputum, blood culture or lymph node aspiration
  • NAAT rapid diagnostic test done on sputum or urine
239
Q

How to diagnose latent TB?

A

Not going to find the bacteria
- need to detect an immune memory response to organism
- Tuberculin skin test (TST)/mantoux test = stick in skin, if T cells recognise it cause inflammation within 2 days (shows previous exposure - delayed Type 4 hypersensitivity)

240
Q

What would a CXR show for TB?

A

Primary TB
- patchy consolidation,
- pleural effusions
- hilar lymphadenopathy

Reactivated TB
- patchy or nodular consolidation
- with cavitation (gas filled spaces in the lungs) in the upper zones

Disseminated Miliary TB
- “millet seeds” uniformly distributed throughout the lung fields

241
Q

What is the management for latent TB?

A

Isoniazid and rifampicin for 3 months
Isoniazid for 6 months only

Isoniazid can often cause peripheral neuropathy. Pyridoxine (vitamin B6) is prescribed to prevent this

242
Q

What is the management of acute pulmonary TB?

A

R- Rifampicin for 6 months
I- Isoniazid for 6 months
P- Pyrazinamide for 2 months
E- Ethambutol for 2 months

RI6PE2- all these drugs are associated with hepatotoxicity

(cannot use just one antibiotic as will just cause TB to become antibiotic resistant)
12 months if in CNS

243
Q

Why is the treatment so long for TB?

A

Amount of TB bacteria goes down quickly
- but some then becomes dormant again to protect itself
- so need 4 more months with less medicines so each time TB wakes up you kill them
- this stops a patient from having a secondary infection a few years later

244
Q

What are the side effects of rifampicin?

A

Reduces the effect of drugs metabolised by cytochrome p450 e.g. contraceptive pill

hepatitis

Causes red/orange discoloration of secretions (urine)

245
Q

What are the side effects of isoniazid?

A

Peripheral neuropathy
- hepatitis

246
Q

What are the side effects of pyrazinamide?

A

Can cause hyperuricaemia resulting in gout
- rash
- arthralgia
- hepatitis

247
Q

What are the side effects of ethambutol?

A

Can cause colour blindness and reduced visual activity
- optic neuritis

248
Q

What are the complications of TB?

A

Empyema
Aspergilloma
Bronchiectasis
Pneumothorax
Miliary TB
Extra-pulmonary disease

249
Q

What is the prognosis for TB?

A

5% mortality with treatment
and 50% without

250
Q

What is pneumonia?

A

A infection of the ling tissue and sputum filling the airways and alveoli. Can be seen as consolidation on a chest x-ray

251
Q

What are the different types of pneumonia?

A

Community acquired
Hospital acquired if it occurs more than 48 hours after admission
Aspiration pneumonia if it occurs after inhaling foreign material

252
Q

What are the main causes of CAP?

A

Streptococcus pneumonia (50%)
H. Influenzae (20%)

253
Q

What are the main causes of HAP?

A

P.aeurginosa
E.coli
S.aureus
Klebsiella

254
Q

What is the main cause of aspiration acquired pneumonia?

A

Klebsiella

255
Q

What is the pathophysiology of pneumonia?

A

Pneumonia refers to any inflammatory reaction affecting the alveoli it is most commonly secondary to infection

The inflammation brings water into the lung tissue which makes it harder to breathe

256
Q

What is atypical pneumonia?

A

It is a pneumonia caused by an organism that cannot be cultured in the normal way or detected on a gram stain.

257
Q

What are the 5 causes of atypical pneumonia

A
  1. Legionella pneumophila (Legionnaires’ disease).
    - infected water supplies or air conditioning units.
    - cause hyponatraemia (low sodium) by causing an SIADH.
  2. Mycoplasma pneumoniae
    - causes a rash = erythema multiforme (varying sized “target lesions” formed by pink rings with pale centres.) - neurological symptoms in young patient in the exams
  3. Chlamydophila pneumoniae
    - school aged children with pneumonia
  4. Q fever
    - exposure to animals and their bodily fluids
  5. Chlamydia psittaci.
    - infected birds.
    - The MCQ patient is a from parrot owner.
    - Legions of psittaci MCQs
258
Q

What are the symptoms of pneumonia?

A

SOB
Cough productive of sputum
Fever
Haemoptysis
Pleuritic chest pain (worse on inspiration)

LOOK FOR SEPSIS

259
Q

What are the signs of pneumonia?

A

raised heart rate
raised respiratory rate
low blood pressure
dull to percussion
decreased air entry
crackles +/- wheeze
increased vocal resonance

260
Q

What is the presentation of atypical pneumonia?

A

Dry cough
Mild dyspnoea
Flu-like symptoms
Mild or no fever

261
Q

What are the 3 characteristics chest signs of pneumonia?

A
  1. Bronchial breath sounds = these are harsh breath sounds equally loud on inspiration and expiration
  2. Focal coarse crackles = air pasing through the sputum causes sound
  3. Dullness to percussion due to lung tissue collapse
262
Q

What are the primary investigations for pneumonia?

A

CXR- will show consolidation (atypical pneumonia causes interstitial inflammation instead so may not show)
Chest x-ray
FBC (raised white cells)
CRP (raised in inflammation and infection)

263
Q

What other investigations would be performed for more severe cases of pneumonia?

A

Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)

264
Q

What is used to test the severity of pneumonia?

A

C- Confusion
U- Urea >7
R- Respiratory rate >30
B- Blood pressure below 90/60
65- age over 65

If score of 1 then consider treatment at home
If score of 2 or more then consider hospital admission
If score of 3 or more than consider intensive care assessment

265
Q

What is the treatment for CAP?

A
  1. Low severity: oral amoxicillin or doxycycline/clarithromycin if penicillin allergy (5 days)
  2. Moderate severity: amoxicillin and clarithromycin
  3. High severity: IV co-amoxiclav and clarithromycin
266
Q

What is the treatment for HAP?

A

Low severity = Oral co-amoxiclav

High severity = broad-spectrum e.g. IV tazocin or ceftriaxone add vancomycin if MRSA suspected

267
Q

What is the prognosis for pneumonia?

A

CURB-65 of 0-1: low risk (<3% mortality)
CURB-65 of 2: intermediate risk (3-15% mortality)
CURB-65 of 3-5: high risk (>15% mortality)

268
Q

What is pneumocystis pneumonia?

A

An opportunistic respiratory infection caused by the fungus, Pneumocystis jirovecii.

269
Q

Who is at risk of pneumocystis pneumonia?

A

People with HIV/AIDS or who are immunosuppressed

270
Q

What is the treatment for pneumocystis pneumonia?

A

1st: Trimethoprim/sulfamethoxazole (co-trimoxazole)

Prednisolone = indicated if hypoxic with pO2< 9.3 kPa, to reduce the risk of respiratory failure (< 50% risk) and death

IV/ nebulised pentamidine = this is reserved for severe cases where co-trimoxazole is contraindicated or has failed

271
Q

What is pulmonary hypertesnion?

A

A mean pulmonary arterial pressure that is greater than 25 mmHg

272
Q

What are the group 1 causes of PHT?

A

Primary pulmonary hypertension
Connective tissue disease e.g. SLE

273
Q

What is the cause of group 2 PHT?

A

Left heart failure die to MI or systemic hypertension

274
Q

What is the cause of group 3 PHT?

A

Chronic lung disease such as COPD

275
Q

What is the cause of group 4 PHT?

A

Pulmonary vascular disease such as PE

276
Q

What is the cause of group 5 PHT?

A

Miscellaneous causes
- sarcoidosis,
- glycogen storage disease
- haematological disorders

277
Q

What is cor pulmonale?

A
  • When high pressure in the pulmonary artery maker it harder for the right ventricle to pump blood and over time it causes hypertension.
  • When the right side of the heart becomes too big for oxygen supply causes right side heart failure. Known as cor pulmonary if caused by chronic lung disease
278
Q

What are the signs and symptoms of pulmonary hypertension?

A

SOB- main symptom
Chest pain
Syncope
Tachycardia
Hepatomegaly
Oedema
Raised JVP

279
Q

What changes would be show on an ECG for PHT?

A

Right sided heart strain can cause:

Right ventricular hypertrophy will show larger R waves on V1-3 and S waves on V4-6
Right axis deviation
Right bundle branch block

280
Q

What would a CXR show for PHT?

A

Dilated pulmonary arteries
Right ventricular hypertrophy

281
Q

What other tests would be performed for PHT?

A

A raised NT-proBNP blood test result indicates right ventricular failure
Echo can be used to estimate pulmonary artery pressure

282
Q

What is the management for primary PHT?

A

IV prostanoids = epoprostenol

Endothelin receptor antagonists = macitentan

Phosphodiesterase-5 inhibitors = sildenafil

283
Q

What is the prognosis for PHT?

A

The prognosis is quite poor with a 30-40% 5-year survival from diagnosis.
- This can increase to 60-70% where specific treatment is possible.

284
Q

How common is lung cancer?

A

Third most common cancer behind breast and prostate

285
Q

What % of lung cancers are related to smoking?

A

Around 80% this includes other preventable causes

286
Q

What are the two main categories lung cancers are split in to?

A

Small cell- 20%
Non-small cell lung cancer- 80%

287
Q

What are the different types NSCLC?

A

Adenocarcinoma (40%)
Squamous cell (20%)
Large-cell carcinoma (10%)

288
Q

Describe the pathophysiology of SCLC?

A
  • A central lesion near the main bronchus. They are derived from neuroendocrine Kulchitsky cells
  • They contain neurosecretory granules that can release neuroendocrine hormones
  • They grow rapidly and patients present in an advanced stage
289
Q

What are the paraneoplastic syndromes that can be caused by SCLC?

A
  • SIADH causing hyponatremia
  • Ectopic ACTH causing Cushing’s
  • Lambert-Eatonmyasthenic syndrome
  • Limbic encephalitis = this causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.
290
Q

What is Lambert-eaton syndomre?

A
  • Antibodies produced against cancer cells damage voltage gated calcium channels sited on pre-synaptic terminals in motor neurones.
  • weakness in proximal muscles
  • can affects intraocular muscles = double vison ptosis
  • affect pharyngeal muscles = slurred speech + dysphagia (difficulty swallowing).

dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

291
Q

Describe the pathophysiology of Squamous cell carcinomas

A

Location: central lesion
Cells produce keratin
They can cause hypercalcaemia by secretion of ectopic parathyroid hormone

292
Q

Describe the pathophysiology of adenocarcinomas

A

Location: peripheral lesion
Originate from mucus-secreting glandular cells
Can cause gynaecomastia

293
Q

Describe the pathophysiology of large cell carcinomas

A

Location: peripheral lesion commonly, but found throughout lungs
Lack both glandular and squamous differentiation
Can cause ectopic β-HCG secretion

294
Q

Describe the pathophysiology of carcinoid tumours

A

They can cause carcinoid syndrome
- secretion of hormones
= serotonin which leads to increased peristalsis, diarrhoea and bronchoconstriction

295
Q

What are the signs and symptoms of lung cancer?

A

SOB
Cough
Haemoptysis
Finger clubbing
Recurrent pneumonia
Weigh loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination

296
Q

What are some extrapulmonary signs and symptoms of lung cancer?

A

Fever
Night sweats
Hoarseness
Facial plethora and swelling due to SVC obstruction

297
Q

What is the first-line investigation and what will it show for lung cancer?

A

Chest x-ray will show:

Hilar enlargement
peripheral opacity
Bilateral pleural effusion
Collapse

298
Q

What is the gold standard investigation for lung cancer?

A

CT Chest, abdomen and pelvis with contrast.

299
Q

If CT is suggestive of malignancy what test is perfomed?

A

PET-CT the scan involves injecting a radioactive tracer and taking images using CT scanner and gamma ray detector.
It shows how metabolically active each tissue is and shows where tumour may have spread

300
Q

What is used to stage lung cancer?

A

TMN staging

301
Q

What is used to treat non-metastatic (stage I to IIIa) NSCLC?

A

Usually involves surgery with an adjuvant of chemotherapy

302
Q

What are the surgeries to treat NSCLC?

A

Lobectomy removing the lung lobe where the tumour is present

Segmentectomy or wedge resection

303
Q

What is used to relieve bronchial obstruction in lung cancer?

A

Endobronchial treatment with stents or debulking

304
Q

What is Horner’s syndrome?

A

Horner’s syndrome is a triad
1. partial ptosis,
2. anhidrosis
3. miosis

It is caused by aPancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.

305
Q

What is the prognosis for lung cancer?

A

Prognosis for lung cancer is poor, with a 10-year survival rate of 5.5%.

SCLC has a poorer prognosis than NSCLC, as SCLC patients will likely have disseminated disease at the point of first presentation.

306
Q

What is a mesotheliomas?

A

An aggressive epithelial neoplasm arising from the lining of the lung, abdomen, pericardium, or tunica vaginalis.

307
Q

What are the risk factors for a mesothelioma?

A

Increasing age
Male gender
Asbestos exposure

308
Q

How does asbestos cause a mesothelioma?

A

Cancer develops around 20-40 years after exposure.
- The asbestos fibres make their way to the mesothelium where they get tangled up with the cell’s chromosome
- This causes DNA damage and modification in gene expression thus increasing the risk of cancer

309
Q

What is gold-standard for diagnosis in mesothelioma?

A

Thoracoscopy

310
Q

What is the prognosis for a mesothelioma?

A

The prognosis for mesothelioma is very poor, as only 5-10% of patients live beyond 5 years after their diagnosis. The median survival is only 12 months.

311
Q

What are the main Upper Respiratory Tract infections?

A

Epiglottis
Laryngitis
Pharyngitis
Sinusitis
Whooping cough
Croup

312
Q

What is pharyngitis?

A

Inflammation of the pharynx with exudate production

313
Q

What are the causes of pharyngitis?

A

Viral - EBV and adenovirus. (rhinovirus causes tonsillitis)

Bacteria - group A Strep (S.pyogenes)

314
Q

What are the signs of pharyngitis?

A

Sore throat
Fever
Cough
Nasal congestion (viral)
Exudate (bacterial)

315
Q

What must be ruled out if someone (especially a child has pharyngitis)?

A

Rheumatic fever
(typically 2-4 weeks post S.pyogenes infection)

316
Q

What is the treatment for pharyngitis?

A

Viral is self-limiting
Bacterial - amoxicillin/flucloxacillin

317
Q

What is the Centor Criteria?

A

The Centor criteria give an indication of the likelihood of a sore throat being due to bacterial infection.
The criteria are:

Tonsillar exudate
Tender anterior cervical adenopathy
Fever over 38°C (100.5°F) by history
Absence of cough.

318
Q

What causes sinusitis?

A

Viral infection most common
(Rhinovirus, parainfluenza virus, and influenza virus)

Can be caused by bacterial infection
(Streptococcus pneumoniae, haemophilus influenzae and staphylococcus aureus)

319
Q

What is the treatment for viral sinusitis?

A

Self-limiting. Usually lasts <10 days and has a non purulent discharge
If no improvement after 10 days then give high dose steroid nasal spray

320
Q

What is the treatment for bacterial sinusitis?

A

May have a purulent discharge and last for longer than 10 days

If no improvement after 10 days and likely bacterial cause then give delayed or immediate antibiotics e.g. amoxicillin

321
Q

What is otitis media?

A

Infection and inflammation of the middle ear

322
Q

What are the causes of otitis media?

A

Bacteria
- Streptococcus pneumoniae (most common), haemophilus influenzae, and staphylococcus aureus

Viral
- Respiratory syncytial virus, rhinovirus, adenovirus

323
Q

What is the diagnostic finding for otitis media?

A

Otoscopy examination will reveal a bulging tympanic membrane

324
Q

What is the treatment for otitis media?

A

Will usually resolve within 3-7 days
Can give amoxicillin
2nd line would be Co-amoxiclav

325
Q

What is acute epiglottitis?

A

Inflammation and localised oedema of the epiglottis which can result in life threating airway obstruction

326
Q

What is the most common cause of epiglotitis?

A

Caused by a bacterial infection of the epiglottis most commonly
- by Haemophilus influenzae B (gram-negative coccobacillus)
in children.
(rare now due to Hib vaccine)

327
Q

Why have incidence of epiglottitis decreased?

A

The introduction of the HiB vaccination has caused numbers to fall

328
Q

What are the risk factors for epiglottitis?

A

Peak age 6-12
Male gender
Unvaccinated
Immunocompromised

329
Q

What are the signs of epiglottitis?

A

Stridor
Muffled voice
Respiratory distress
Tripod position (the patient leans forward and supports their upper body with their knees)
Fever

330
Q

What are the symptoms of epiglottitis?

A

Fever
Sore throat
Dysphagia
Dysphonia
Drooling
Distress

331
Q

What is the primary investigation of epiglottitis?

A

DO NOT examine the airway or distress the child as this could lead to catastrophic airway occlusion and respiratory arrest

  1. Laryngoscopy- will show swelling and inflammation of the epiglottis or supraglottis
  2. Lateral neck radiography- secure the airway first but look for thumb sign on trachea useful for ruling out foreign body
332
Q

What is the treatment for epiglottitis?

A

First line:
- Secure airway
- Nebulised adrenaline
- IV antibiotics

Second line:
Dexamethasone

333
Q

What is croup?

A

Acute infective upper respiratory infection causing oedema in the larynx

334
Q

Who is typically affected by croup?

A

Children between 6 months and 2 years old

335
Q

What are the causes of Croup?

A

Main cause : Parainfluenza virus

Influenza
Adenovirus
Respiratory syncytial virus

336
Q

What are the signs of croup?

A

Pyrexia
Stridor
Respiratory distress

337
Q

What are the symptoms of croup?

A

Barking cough worse at night
Difficulty breathing
Fever
Coryza (inflammation of the nose) basically a blocked nose

338
Q

What is used to classify the severity of croup?

A

Most often a clinical diagnosis is made

-The Westley score is a classification system used to asses the severity

339
Q

What is the treatment for croup?

A

Oral dexamethasone (single dose 150mcg/kg)

340
Q

What is whooping cough?

A

URTI caused by Bordetella pertussis
- gram negative bacillus

341
Q

Who is affected by whooping cough?

A

Mainly children 90% are under 5

342
Q

What are the the stages of whooping cough?

A

Catarrhal stage (1-2 weeks)

Paroxysmal stage (1-6 weeks)

Convalescent stage (lasts up to 6 months)

343
Q

What is the catarrhal stage of whooping cough?

A

Dry unproductive cough
Low grade fever
Conjunctivitis
Coryzal symptoms

344
Q

What is the paroxysmal of whooping cough?

A

Coughing fits: typically consist of a short expiratory burst followed by an inspiratory gasp, causing the ‘whoop’ sound
Post-tussive vomiting

345
Q

What is the characteristic symptom of whooping cough?

A

Whoop sound caused by sharp inhalation of breath after coughing bout

346
Q

What are the investigations for whooping cough?

A

Nasopharyngeal swab/aspirate: culture/PCR

Anti-pertussis toxin IgG

347
Q

What is the treatment of whooping cough?

A

Notify PHE

Antibiotics marcolids clarithromycin or azithromycin
Stay off school as highly contagious

vaccination

348
Q

What are the complications of whooping cough?

A

Pneumonia
Encephalopathy
Otitis media
Injuries from coughing e.g., pneumothorax and seizures

349
Q

Define pneumomediastinum

A

accumulation of air around the heart

350
Q

What is a pocket of air within the lung tissue?

351
Q

Define atelectasis?

A

an area of collapsed lung

352
Q

How do you measure the severity of stable COPD?

A

FEV1 predicted

353
Q

What is the first investigation to assess acute asthma severity?

A

Clinical examination
- can’t do a peak flow when struggling to breathe

354
Q

What is the main cause of bronchiolitis?

A

common chest infection that affects babies and children
- respiratory syncytial virus (RSV)

355
Q

What is the treatment for flu?

A

Oseltamivir ‘tamiflu’
Zanamivir ‘Relenza’

Emily Phase 2a (15 decks)

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