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CP1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Signs of pneumothorax on examination

A

From the end of the bed the patient may be tachypnoeic.

Diminished breath sounds on side of PTX on auscultation, and hyper-resonant on percussion.

Reduced chest expansion may be evident on side of PTX.

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2
Q

What would a CXR of a tension PTX show?

But why would this not usually be seen?

A

the heart and mediastinum will be being pushed to the opposite side due to the high pressure on the side of the PTX

should not be seen because the aim is to make a diagnosis based on symptoms in order to not delay treatment

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3
Q

what happens in a tension PTX?

A

A “one-way valve” establishes itself which allows air into the pleural cavity on inspiration, but closes on expiration to cause an increase in pressure

This will continue until the patient’s venous return to the heart is compressed and obstructed causing cardiac output failure and the patient will arrest

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4
Q

how to make a clinical diagnosis of tension PTX

A

Severe tachypnoea, may be cyanotic

Tachycardic, hypotensive

Raised JVP

Tracheal deviation

Absent breath sounds, hyper-resonant and hyperexpanded chest unilaterally

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5
Q

Immediate management of tension PTX

A

Large bore (14 or 16 gauge) needle decompression – 2nd intercostal space, mid-clavicular line.

Followed by tube thoracostomy

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6
Q

Primary vs. Secondary PTX

A

Primary occurs in otherwise healthy lung tissue

Secondary occurs due to underlying lung disease

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7
Q

What is asthma?

A

a disease involving bronchoconstriction and inflammation

causes variable and reversible increases in airway resistance

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8
Q

What FEV1:FVC ratio suggests increased airway resistance?

A

a ratio of less than 70-80%

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9
Q

Timing of symptoms of asthma

A

Symptoms tend to worsen at night or early in the morning, and symptoms tend to vary over time

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10
Q

Asthma symptoms

A

wheeze, shortness of breath, chest tightness and cough

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11
Q

Non-specific triggers for asthma

A 
Viral infections
Cigarette smoke
Pollution
Cold weather
Emotion
Exercise (sometimes)
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12
Q

Specific triggers for asthma

A

Pets
Pollen
Other allergens
Occupational pollutants

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13
Q

Important HPC/PMH points for asthma

A

Known precipitants

Diurnal variation in symptoms

Acid reflux symptoms (known association).

History of atopy.

History of these episodes (and establish whether they required hospital/ITU)

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14
Q

Relevant DHx for asthma

A

NSAIDs (particularly aspirin) and beta-blockers, as these can cause asthma

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15
Q

Relevant FH and SH for asthma

A

FH of atopy

Very important to ask about occupation (as there can be occupational pollutants such as flour or chemicals).
Days off work/school.
Smoking.

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16
Q

Diagnosis of asthma

A

Requires a structured clinical assessment to see if:

Episodes are recurrent
Symptoms are variable
PMH/FH of atopy.
Recorded observation of expiratory wheeze.
Variable peak expiratory flow or FEV1
Absence of symptoms of an alternative diagnosis.

If these give a high probability of asthma – diagnose as suspected asthma and initiate treatment

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17
Q

When is a diagnosis of asthma confirmed?

A

When there is objective improvement after initiating treatment.

if response to treatment is poor, refer for spirometry to test for airway obstruction with bronchodilator reversibility (FEV1/FVC <70% with bronchodilator reversibility is diagnostic)

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18
Q

Diagnosis of asthma in children

A

Children <5 with suspected asthma should have symptoms treated based on observations and clinical judgement and be reviewed regularly until they are old enough to do objective testing

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19
Q

Extrinsic Asthma:

A

Type I hypersensitivity reaction

Most frequently occurs in atopic individuals who show positive skin prick tests to common allergens, implying a definite extrinsic cause.

Tends to be early-onset

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20
Q

Intrinsic Asthma

A

Non-immune mechanisms

Occurs in middle-aged individuals, when no causative agent can be identified

Generally more severe, and associated with quicker deterioration of lung function.

Tends to be late-onset

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21
Q

Pathophysiology of asthma

A
  1. Spasmogens will act rapidly to cause smooth muscle contraction of the airways, leading to bronchospasm.
  2. Chemotaxins are released to stimulate eosinophils and mononuclear cells to go to the airways, causing an inflammatory response a few hours later.
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22
Q

Persistant airway obstruction in asthma

A

can become indistinguishable from COPD

more common in intrinsic asthma

bronchoconstriction due to increased responsiveness of bronchial smooth muscle, and hyper-secretion of mucous that plugs the airways

Sputum will contain Charcot-Leyden crystals (from eosinophil granules) and Curschman spirals (mucous plugs from small airways).

Can eventually lead to pulmonary hypertension

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23
Q

what is the basis of asthma treatment?

A

The use of bronchodilators reverses the bronchospasm and provides rapid relief – “relievers”.

There are also treatments to prevent more attacks – “preventers” – which are usually anti-inflammatory steroids

=> aim is to have no daytime symptoms, no night time waking, no need for rescue medication and no limitations on activity.

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24
Q

beta2-adrenoceptor agonists in asthma

A

typically the first-choice drug for relief.

Can be short-acting/long-acting (SABA / LABA)

Acts on beta2-adrenoceptors on smooth muscle, which causes relaxation and in turn an increase in FEV1.

given by inhalation; localising the action and providing a rapid effect.

Prolonged use may lead to receptor down-regulation – the beta2-adrenoceptors become less responsive

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25
Q

Long-acting beta agonists

A

given for long term prevention and control (e.g. overnight), as it stays bound to the receptors for a lot longer than salbutamol (SABA)

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26
Q

corticosteroids in asthma

A

Preventative, they do not reverse an attack.
Takes 2-3 days to have an effect.

Anti-inflammatory by activation of intracellular receptors, leading to altered gene transcription (decrease cytokine production) and production of lipocortin/annexin A1.

It is thought that lipocortin/annexin A1’s action is to inhibit phospholipase A2, and therefore inhibiting the synthesis of PGs and LTs by preventing the arachidonic acid pathways from occurring.

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27
Q

Leukotriene receptor antagonists (LTRAs) in asthma

A

e.g. Montelukast

Increased role as add on therapy.

Have both preventative and bronchodilator uses.

Antagonises the actions of LTs by blocking their receptors

Also useful against symptoms of hayfever and eczema

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28
Q

Xanthines in asthma

A

e.g. theophylline, aminophylline.

These are also bronchodilators, but not as good as beta2-adrenoceptor agonists (therefore only 2nd line use).

Oral (or IV aminophylline in emergency)

Adenosine receptor antagonist.

Phosphodiesterase inhibitors, preventing the breakdown of cAMP.

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29
Q

Pharmacological treatment of SUSPECTED asthma

A

All patients with suspected asthma should receive a SABA.

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30
Q

Pharmacological treatment of CONFIRMED asthma

A 
SABA + ICS
=>
Add LABA
(or LTRA/xanthine if this fails).
=>
Increase dose of ICS
=>
Add oral steroid

if salbutamol inhaler is used more than 2 times a week, this indicates that their current control is inadequate, and the care needs to move up a step

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31
Q

Moderate Acute Asthma

A

Increasing symptoms
PEF 50-75%
No features of acute severe asthma

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32
Q

Acute Severe Asthma

A 
Requires any one of:
•	PEF 33-50% predicted
•	RR >25/min
•	HR >110
•	Inability to complete sentences in one breath
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33
Q

Life-threatening Asthma

A 
Any one of:
•	PEF <33% predicted
•	SpO2 <92%
•	PO2 <8kPa
•	Normal PaCO2 (4.6-6)
•	Silent chest
•	Cyanosis
•	Poor respiratory effort
•	Arrhythmia
•	Exhaustion 
•	Altered consciousness
•	Hypotension
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34
Q

Emergency management of asthma

A

If a patient has ANY life-threatening feature, an arterial blood gas is the only immediate investigation required whilst treatment is initiated.

  1. O2 to maintain sats at 94-98% (88-92% in COPD, 92-94% in Covid)
  2. Salbutamol nebuliser (add ipratropium if required).
  3. Steroids (PO prednisolone or IV hydrocortisone)
  4. IV magnesium sulphate
  5. IV aminophylline (senior review)
  6. Referral to ITU for patients who are not improving.
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35
Q

What blood gas features are markers of a life-threatening asthma attack?

A

Normal PaCO2 (should normally be low due to hyperventilation).

Severe hypoxia <8 kPa

A low pH

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36
Q

What is COPD?

A

= Chronic Obstructive Pulmonary Disease.

Characterised by airflow obstruction, which is usually progressive and not fully reversible.

Obstruction does not change markedly over several months.

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37
Q

What causes COPD?

A

significant exposure to noxious particles/gases.

> 90% caused by damage to the lungs from smoking.

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38
Q

pathological changes in COPD

A
  • Chronic inflammation – chronic response to irritants

* Structural change – repeated injury and repair

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39
Q

physiological changes in COPD

A

Mucous hypersecretion

Ciliary dysfunction

Airflow limitation, resulting in alveolar hyperinflation.

Impaired gas exchange

Pulmonary hypertension – due to remodelling of pulmonary arteries and veins.

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40
Q

Risk factors for COPD

A

SMOKING!!!!!!

Indoor air pollution

Occupational toxins

(Outdoor air pollution)

Genetic factors – alpha-1 antitrypsin deficiency.

Infections – measles, whooping cough.

Socio-economic factors – significant association with socio-economic deprivation.

Asthma and airway hyperreactivity

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41
Q

Clinical features of COPD

A

Chronic progressive dyspnoea
A chronic cough
Regular sputum production
Wheezing and chest tightness

These symptoms become exacerbated in acute infective episodes.

In severe cases, there may be fatigue, weight loss, anorexia, cough, syncope, depression/anxiety

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42
Q

Complications of COPD

A
  • Acute exacerbations
  • Polycythaemia
  • Respiratory failure
  • Cor pulmonale
  • Pneumothorax
  • Lung carcinoma
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43
Q

COPD - OE: observations

A
  • Tachypnoea
  • Possible cyanosis
  • Flapping tremor (if CO2 retainer, >10 kPa)
  • Cachexia
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44
Q

COPD - OE: inspection

A
  • Hyperinflation
  • Intercostal recession on inspiration
  • Lip pursing on expiration
  • Signs of respiratory distress.
  • Raised JVP
  • Peripheral oedema
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45
Q

COPD - OE: palpation

A

• Poor chest expansion

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46
Q

COPD - OE: percussion

A
  • Hyper-resonant throughout

* Loss of cardiac/hepatic dullness.

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47
Q

COPD - OE: auscultation

A
  • Widespread/polyphonic wheeze, or
  • Decreased breath sounds
  • Prolonged expiratory phase.
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48
Q

“Pink Puffer”

A

Patients remaining sensitive to CO2, thus keep a low CO2 and near-normal O2.

Tachypnoeic, tachycardic, using accessory muscles to increase ventilation.

Breathless but not cyanosed.

Very thin – large amounts of calories used to breathe.

Can progress to type 1 respiratory failure.

More emphysematous.

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49
Q

“Blue Bloater”

A

Patients are insensitive to CO2.

Severe chronic bronchitis/COPD.

Not particularly breathless but are cyanosed and oedematous (cor pulmonale).

Blood gas will show type 2 respiratory failure (low oxygen, retaining CO2.

Oxygen should be given with care to these patients.

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50
Q

What main investigations would you order for suspected COPD?

A

FBC
CXR
Spirometry

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51
Q

What additional investigations could be ordered in suspected COPD?

A 
Serial peak flow, 
Alpha 1 antitrypsin, 
Transfer factor for carbon monoxide.
Pulse oximetry, 
CT thorax
ECG
Echo

ABG – normal in mild disease, developing to type 1/2 respiratory failure.

Sputum culture – abnormal organisms suggest bronchiectasis.

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52
Q

COPD - FBC

A

Secondary polycythaemia

Any anaemia?

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53
Q

Secondary polycythaemia

A

= the overproduction of red blood cells

due to chronic hypoxaemia, which triggers increased production of EPO by the kidneys

causes your blood to thicken, which increases the risk of a stroke.

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54
Q

COPD - CXR

A

Hyperinflation (>6 anterior and >10 posterior ribs)

Flattened hemidiaphragm

Rule out malignancy/other diagnoses

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55
Q

Staging of COPD by spirometry

A

Stage 1 – FEV1 >80% predicted (clinical diagnosis); mild.

Stage 2 – FEV1 50-79% predicted; moderate.

Stage 3 – FEV1 30-49% predicted; severe.

Stage 4 – FEV1 <30% predicted; very severe.

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56
Q

Management of COPD

A

Patient education - how to recognise and manage exacerbation

Lifestyle advice - diet, exercise, STOP SMOKING

Pneumococcal vaccine

Medical management

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57
Q

Medical management of COPD

A

Short-acting bronchodilators (SABA or SAMA)

If no features of asthma/steroid responsiveness:

  • Add a long-acting beta-agonist (LABA) and muscarinic agonist (LAMA)
  • Add inhaled corticosteroids if still symptomatic
  • Remove ICS after 3 months if no improvement.

If features of asthma/steroid-responsiveness are present – LABA + ICS.
- LABA + LAMA + ICS if ongoing symptoms.

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58
Q

What are features of asthma/steroid-responsiveness in COPD?

A

Previous diagnosis of asthma/atopy, blood eosinophilia, substantial variation in FEV1 over time or diurnally.

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59
Q

Specialist treatments for COPD

A

Pulmonary rehabilitation – consider if someone is functionally disabled by COPD.

Oral aminophylline/theophylline – if still symptomatic after trial of triple therapy.

Mucolytics – e.g. carbocysteine

Roflumilast – PDE4 inhibitor

Nutritional supplements – consider for low BMI

Long-term oxygen therapy

Surgery

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60
Q

Acute exacerbation of COPD

A

Exacerbations are frequently caused by bacterial/viral infections, or exposure to pollutants.

Dyspnoea and wheeze will become worse, with increased production of purulent sputum.

Patient should have rescue medications.

Hospital admission in severe breathlessness, rapid symptom onset, acute confusion, cyanosis, low oxygen sats, or worsening peripheral oedema.

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61
Q

Steps for smoking cessation

A
  1. ASK about smoking at every opportunity.
  2. ADVISE all smokers to stop smoking.
  3. Offer ASSISTANCE to all smokers to stop.
  4. ARRANGE smoking cessation follow-up.
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62
Q

What are some useful things to do when helping someone to stop smoking.

A
  • Set a date to stop completely
  • Specialised stop-smoking clinics
  • Review previous quit attempts (what helped/hindered)
  • Plan for problems and how to manage them
  • Plan for how to handle alcohol drinking situations
  • Try smoking cessation treatments
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63
Q

What are some treatments to help smoking cessation?

A

Nicotine replacement therapy

Bupropion

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64
Q

Epidemiology of Lung Cancer

A

Lung cancer is the third most common cancer in the UK.

Incidence increases with age

Lung cancer is the most common cause of cancer deaths in the UK (accountable for ~1 in 5)

79% of lung cancers are preventable.

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65
Q

Risk factors for developing lung cancer

A

Smoking
Second-hand/environmental smoking
Old age
Air pollution
Radon
Occupational hazards (e.g. asbestos, silica)
Family History of lung cancer in a close relative.

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66
Q

Lung cancer - Clinical Features

A
  • Persistent cough – non-specific sign.
  • Haemoptysis – less common but more specific.
  • Dyspnoea
  • Dysphagia
  • Hoarseness
  • Chest pain – pleural/chest wall involvement.
  • Fatigue, Weight loss, Appetite loss, Fever
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67
Q

Lung cancer - On Examination

A
  • Clubbing
  • Cachexia
  • Signs of anaemia
  • Chest signs of collapse/consolidation/effusion
  • Signs of metastases.
  • Hypertrophic pulmonary osteoarthropathy – a paraneoplastic syndrome
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68
Q

What is the rough split between incidence of small cell and non-small cell lung cancers

A

Small-cell - 15%

Non-small cell - 85%

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69
Q

Small cell (“oat cell”) carcinomas

A

Rarer but highly malignant, grow very quickly and metastasise early.

Rare in non-smokers.

Usually centrally located.

Originate mostly from bronchial epithelium, but differentiate into neuroendocrine cells (e.g. secreting ADH, ACTH, etc.) and causing paraneoplastic syndrome.

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70
Q

Squamous cell carcinoma

non-small cell

A

Arise from squamous metaplasia of the normally pseudostratified ciliated columnar epithelium

Occur mainly in response to cigarette smoke exposure.

Usually central, close to the carina.

May secrete PTH, causing hypercalcaemia (can also be due to secondary bone metastases).

Can often be diagnosed with sputum cytology.

Tends to cause cavitating lesions.

Slow growing, may be resectable.

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71
Q

Adenocarcinoma

non-small cell

A

Equal gender incidence, and less related to smoking.

Characteristically originate in peripheral locations (potentially areas of previous lung scarring).

Associated with asbestos exposure.

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72
Q

Large cell carcinoma

non-small cell

A

Features showing small cell/adenocarcinomatous origins may be seen, but they are not differentiated enough to eb classified.

Poor prognosis, often widely disseminated at diagnosis.

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73
Q

Bronchoalveolar carcinoma

A

a special type of adenocarcinoma,

Rare but associated with better prognosis.

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74
Q

Metastatic lung tumours

A

the lungs are a common site of metastasis of many cancers.

secondary lung tumours will be made up of cells of the primary tumour.

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75
Q

Local complications of lung tumours

A

SVC compression
Recurrent laryngeal nerve palsy
Horner syndrome

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76
Q

Distant metastasis of lung tumours

A

Most common sites – brain, bone, liver, adrenal glands.

Symptoms will be associated to the specific organ affected

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77
Q

Lung tumours - SVC compression

A

Raised JVP, raised arm BP/swelling, facial swelling.

Common presenting feature of lung cancer.

Often due to local nodes rather than the tumour itself

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78
Q

Lung tumours - Recurrent laryngeal nerve palsy

A

voice hoarseness and left vocal cord paresis.

If present, indicates tumour inoperability.

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79
Q

Lung tumours - Horner syndrome

A

Miosis, ptosis, anhidrosis

Destructive lesions of the thoracic inlet, often involving the brachial plexus.

Due to Pancoast tumour

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80
Q

CXR in suspected lung cancer

A

For anybody with suspected lung cancer - first investigation is a CXR.

Also, ANY patient with haemoptysis should have a CXR

Symptomatic tumours are almost always visible.

A normal CXR in a symptomatic patient should warrant further investigation for central tumours

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81
Q

Blood tests in suspected lung cancer

A

FBC - anaemia/secondary polycythaemia
U&E - hypercalcaemia, hyponatraemia
LFTs - liver mets?

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82
Q

What are the steps in suspected lung cancer?

A

CXR
Bloods

Any patient presenting with any suspicion of lung cancer requires a 2-week wait referral to a lung cancer clinic for further investigation

Specialist referral for:

  • sputum/pleural cytology
  • contrast-enhanced CT staging
  • bronchoscopy
  • pulmonary function tests
  • PET scan if suspected metastasis.
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83
Q

How much fluid is normally within the pleural cavity?

A

~15 mL of serous pleural fluid

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84
Q

What is pleural effusion?

A

the build-up of excess fluid between the layers of the pleura outside the lungs

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85
Q

How does pleural effusion differ from pulmonary oedema?

A

the location of the fluid

Pleural effusion - fluid in pleural space
Pulmonary oedema - fluid in alveolar spaces and lung tissue

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86
Q

Haemothorax

A

= accumulation of blood, due to trauma

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87
Q

Empyema/pyothorax

A

= accumulation of pus, due to infection

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88
Q

Chylothorax

A

= accumulation of lymph, due to thoracic duct leakage

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89
Q

Fluid effusion

A

= fluid accumulation, transudative or exudative

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90
Q

Transudate

A

Occur due to increased hydrostatic pressure/decreased oncotic pressure

Causes – cardiac failure, liver failure, renal failure, peritoneal dialysis.

Rarer causes – hypothyroidism, ovarian tumours.

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91
Q

What is the protein concentration of transudate?

A

Protein concentration <30 g/L

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92
Q

Exudate

A

Occur due to increased capillary permeability

  • Infections – bacterial pneumonia, TB
  • Neoplasm – lung primary/secondary, mesothelioma.
  • Pulmonary Embolism
  • Autoimmune disease – RA/SLE
  • Abdominal disease
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93
Q

What is the protein concentration of transudate?

A

Protein concentration >30 g/L

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94
Q

If protein level of pleural fluid is 25-30 g/L, what criteria are needed to suggest it is an exudate (not transudate)?

A

one positive element of Light’s criteria will suggest an exudate:

  • Pleural fluid protein/serum protein >0.5.
  • Pleural fluid LDH/serum LDH >0.6.
  • Pleural fluid LDH more than two-thirds the upper limit of normal serum LDH.
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95
Q

Symptoms of pleural effusion

A

A small amount of fluid is completely asymptomatic

As the volume of fluid increases, the patient will experience:
•	Shortness of breath
•	Cough
•	Pleuritic chest pain
•	Reduced exercise tolerance
96
Q

Pleural effusion - percussion

A

dull due to underlying fluid

97
Q

Pleural effusion - auscultation

A

quieter breath sounds and vocal fremitus

98
Q

What is the first-line investigation on suspicion of a pleural effusion?

A

CXR

99
Q

What is the issue in using a CXR in ?pleural effusion

A

PA and AP erect X-ray films are insensitive to small amounts of fluid – as much as 250-600 mL of fluid is required before it becomes evident.

100
Q

CXR features indicating pleural effusion

A
  • blunting of the costophrenic angle
  • blunting of the cardiophrenic angle
  • fluid within the horizontal or oblique fissures
  • eventually, a meniscus will be seen (note: if a hydropneumothorax is present, no such meniscus will be visible)
  • with large volume effusions, mediastinal shift occurs away from the effusion
101
Q

Pleural effusion - ultrasound

A

allows the detection of small amounts of pleural locular fluid, with positive identification of amounts as small as 3-5 mL.

It is it is effective in guiding thoracocentesis (even in small fluid collections) and can be used to assess pleural fluid volume.

102
Q

Treatment of pleural effusion

A

The treatment of pleural effusions is usually targeted to the underlying condition.

Ultrasound-guided aspiration is reliable and fast and enables loculated effusions to be drained. Symptomatic patients with large effusions may be treated by therapeutic aspiration/pleural tap.

Fluid can be sent to microbiology and also be assessed for clinical chemistry (protein, LDH, glucose) and cytology. It can also be run through a blood gas machine to assess pH.

103
Q

Community-acquired pneumonia definition

A

Clinical lower respiratory tract infection AND

New pneumonic changes on CXR AND

Onset of symptoms in the community OR within 48 hours of hospital admission.

104
Q

CAP is more common in…

A
  • Males
  • Winter/early spring

• The elderly – peak age 50-70 years; most severe in age >65.

  • Alcoholics
  • Smokers
  • People with established chronic disease
105
Q

CAP presentation

A

The patient presents with symptoms of LRTI – cough, sputum, breathlessness, pleuritic chest pain, occasionally haemoptysis

These symptoms are similar to bronchitis, and for a diagnosis of CAP you need evidence of lung parenchymal involvement (confirmation with CXR).

106
Q

CAP presentation in the elderly

A

Elderly populations may present with very few symptoms, but be very unwell and usually acutely confused

107
Q

Causes of CAP

A 
Conventional bacteria (60-80%)
=> S. pneumoniae, H. influenzae

‘Atypical’ bacteria (10-20%)

Viruses (10-20%)

108
Q

What are the “atypical” bacteria causing CAP?

A

Mycoplasma pneumoniae,
Chlamydia pneumoniae
Legionella pneumophila

109
Q

CAP - on examination

A

Inspection:
• Tachypnoea

Palpation:
• Decreased chest expansion on the affected side.

Percussion:
• Dullness over the affected area

Auscultation:
• Coarse crackles and pleural rub over the affected area
• Bronchial breathing
• Increased vocal resonance – “111” / “99” can be heard better due to consolidation.

ALSO there can be upper abdominal tenderness in lower lobe pneumonia.

110
Q

Investigations for CAP

A
  • Confirm diagnosis – CXR
  • Assess severity of disease – CURB65

• Identify complications
=> Often linked to respiratory failure (T1RF/T2RF)
=> Can lead to multi-organ failure, septic shock and death.
=> Will the patient need supplementary oxygen therapy to maintain PO2 >94 (or >88 COPD)?
=> Bloods – LFTs, FBC, CRP, Arterial Blood Gas.

111
Q

Microbiological investigations for CAP

A

• Sputum analysis and culture

• Immunofluorescence on sputum/nasopharyngeal samples
=> Viruses (influenza), mycoplasma, legionella

• Blood cultures

• Urinary pneumococcal and legionella antigen
=> For any patient with moderate/severe CAP!

112
Q

CURB65 criteria

A

Confusion – mini-mental test score of 8 or less (new)
Urea >7 mmol/L (new)
Respiratory Rate >30 breaths per minute
Blood Pressure – systolic BP <90 mmHg or diastolic BP <60 mmHg
65 or more years old

113
Q

Low-severity CAP

A

CURB score 0 or 1

114
Q

Management of Low-severity CAP

A

PO Amoxicillin, managed as outpatients.

PO doxycycline if penicillin allergy.

115
Q

Moderate-severity CAP

A

CURB score 2

116
Q

Management of Moderate-severity CAP

A

Higher mortality – ~5-10%

PO amoxicillin + clarithromycin, usually admitting the patient

117
Q

Severe CAP

A

CURB score >2

118
Q

Management of Severe CAP

A

Can be >20% mortality if established failure in another organ system.

Requires admission to at least Level 01 unit or even HDU/ICU.

IV co-amoxiclav + clarithromycin.

Penicillin allergy/MRSA suspicion – vancomycin and levofloxacin.

Treatment for at least 10 days.

119
Q

Pneumonia follow-up

A

Patients should always have a follow-up CXR at 6 weeks to ensure resolution of consolidation and assess for persistent abnormalities of the lung parenchyma

120
Q

CAP non-resolution

A

?endobronchial obstruction as cause of pneumonia (e.g. lung cancer)

121
Q

Definition of hospital-acquired pneumonia

A

Clinical lower respiratory tract infection AND

New pneumonic changes on CXR AND

onset of symptoms > 48 hours after admission OR admission in the last 7 days

122
Q

when is there increased risk of HAP?

A

prolonged hospital stays, poor mobility, age >70 years and severe underlying disease.

123
Q

What are the causes of HAP?

A

Tends to be more gram negative pathogens

Enteric gram-negative bacilli – ~60% HAP cases

Also:
Strep. pneumoniae
H. influenzae
Staph. aureus

124
Q

Management of HAP

A

Assess MRSA risk factors
Assess HAP severity

Mild HAP – oral doxycycline.
Severe HAP – IV Tazocin.

125
Q

Aspiration pneumonia

A

Aspiration of gastric contents leading to chemical inflammation and infection.

126
Q

When should you suspect aspiration pneumonia?

A

Does not always show on CXR!!

Suspect it for example in someone who has a low GCS and evidence of vomiting (so at risk of aspirating).

127
Q

What should you do in suspected aspiration pneumonia?

A

If suspected can add metronidazole for HAP or CAP – this is to cover anaerobic bacteria.

128
Q

Complications of pneumonia

A

Sepsis
Septic shock
Lung abscess
Empyema

129
Q

Complications of pneumonia - empyema

A

= pus-filled collection in the pleural space.

Seen especially in streptococcus pneumonia

130
Q

Complications of pneumonia - lung abscess

A

= pus-filled collection in the lung parenchyma

Seen especially in Staph. aureus pneumonia.

131
Q

When should you suspect lung abscess/empyema?

A

if there is a persistent swinging pyrexia and rising CRP despite treatment.

132
Q

characteristics of Mycobacterium tuberculosis

A

an aerobic bacillus:

Non-motile

Cell envelope which resists gram staining.

Known as “acid fast bacilli” or AFBs

Very slow growing.

133
Q

In which groups in the UK is TB particularly common?

A

immigrant ethnic groups,
the socially disadvantaged,
HIV +,
Londoners

134
Q

How is TB transmitted?

A

The person with pulmonary TB can cough and expel infectious droplets. Infectious particles can remain suspended in the air for several hours and inhaled aerosolised droplets lodge in the alveoli.

135
Q

What are factors that determine the probability of TB transmission?

A

Susceptibility of exposed person - e.g. HIV+
Infectiousness - number of bacilli expelled into the air
Environment - e.g. enclosed spaces
Exposure - proximity, frequency, duration

136
Q

Primary TB infection

A

occurs when a non-immune host (never met TB before) is exposed to M. tuberculosis

137
Q

The process of primary TB infection

A
  1. TB containing droplets reach the alveoli and are taken up by macrophages
  2. If macrophages fail to kill TB, primary infection occurs.
    => TB bacilli then slowly multiply inside the macrophages.
    => macrophages can carry TB to local lymph nodes or further around the body.
    => granulomatous lesions beginning to develop in the lungs.
  3. At this point a complex interplay between host and bacteria occurs to determine whether active or latent disease occurs.
    => Factors such as number of TB bacteria inhaled and whether the host is immunocompetent.
138
Q

When do the caseating granulomas of TB develop?

A

The tissue reaction in the lungs and lymph nodes changes to form caveating granulomas ~1-2 weeks after infection.

139
Q

Latent TB infection

A

LTB occurs when the host defences are able to contain the TB infection.

Over around 2-6 weeks the adaptive immune response kicks in and and a granuloma forms to contain the TB infection.

The TB within the granuloma is DORMANT, therefore, latent TB can always be reactivated

but people with LTB do not have active disease and are not infectious

140
Q

Post-primary TB infection

A

occurs when latent TB becomes reactivated.

This may stay local or spread to more distant sites, causing extra-pulmonary TB.

Cavities and progressive lung destruction lead to cough and systemic symptoms (patient is infectious again)

141
Q

Which people are at a higher risk of TB reactivation?

A

Untreated HIV+

Immunosuppressed for other reasons – e.g. long-term steroids, organ transplant.

Comorbidities – e.g. diabetes and CKD

Aging

142
Q

% risk of LTB reactivation

A

LTB + no risk factors – 10% risk of reactivation over lifetime

LTB + untreated HIV – 7-10% risk of reactivation per year.

143
Q

Investigating TB

A
  1. Culture:
    => Pulmonary TB – several sputum samples (at least one in early morning) to look for acid fast bacilli down the microscope and then culture.

=> PCR if rapid diagnostic results required or suspected MDR-TB

=> Culture is gold-standard test but takes 6 months.

=> Non-Pulmonary TB – a sample from the suspected site to culture

  1. Histology – classically will find caseating granuloma
  2. Imaging
    => CXR – different findings for primary, latent and post-primary, but also significant overlap!
144
Q

CXR in Primary TB

A

Caseating granulomas/Ghon focus
=> These represent healing of a primary TB infection.

Lobar or patchy consolidation

Effusions and regional lymphadenopathy

145
Q

Ghon focus and complex

A

Calcified caseating granulomas

if seen with regional lymphadenopathy then called Ghon complex

146
Q

miliary TB

A

where the TB spreads rapidly though the body

looks like ‘Millet seeds’ on CXR

more common if immunosuppressed

147
Q

CXR in Post-primary TB

A

characterised by:

  • necrosis and cavitation formation
  • Progressive lung destruction

Cavities now tend to be apical (more oxygen).

148
Q

CXR in latent TB

A

Should be normal!

Very occasionally a few nodules.

There should be no signs of active TB disease.

149
Q

When would you investigate for Latent TB?

A

close contacts of active TB patient (contact tracing);

someone who has come from a high incidence TB country

150
Q

How do you investigate for latent TB?

A

Mantoux test/tuberculin skin test
=> can get false positives if prior BCG vaccine or false negatives with HIV infection

Interferon-gamma release assay (IGRA) test
=> no false negatives with HIV or cross reaction with BCG

Positive results should lead to assessment for active TB (as these tests cannot differentiate between active/latent disease). If no evidence of active TB, treat as latent TB.

151
Q

Presentation of pulmonary TB

A

Cough
Haemoptysis
Fever
Systemic symptoms – night sweats, weight loss, fatigue.

152
Q

Presentation of extra-pulmonary TB

A

Common sites include the larynx, pleura, brain, kidneys and bone.

Presentation varies, as it depends on the site

153
Q

Management of active TB

A

Therapy consists of 6 months of treatment, which can be divided into:

  1. “bactericidal” phase in which the majority of organisms are killed = four drugs for two months
  2. “sterilising” phase in which persisting organisms are eliminated = two drugs for four months.

Standard therapy in the UK (BTS 1998) is:

  1. Rifampicin, isoniazid, pyrazinamide and ethambutol given for a two-month period.
  2. Followed by Rifampicin and isoniazid for four months.
154
Q

What is given as a supplement with isoniazid?

A

given with pyridoxine supplements to prevent peripheral neuropathy.

155
Q

Why is combination therapy essential in treating active TB?

A

Mycobacteria mutate to develop single drug resistance.

in a bacillary population of sufficient size, single drug therapy will always select resistant organisms.

156
Q

Management of latent TB

A

Isoniazid for 6 months
OR
Rifampicin and Isoniazid for 3 months

157
Q

TB resistance / MDR TB

A

The most common drug resistance in the UK is isolated Isoniazid resistance, with rifampicin being the marker for multi-drug resistant TB

158
Q

Who is at risk of MDR TB?

A

Individuals previously treated for TB

Known contact with a case of drug resistant TB

Acquisition of infection in a country or group with high prevalence of drug resistance (e.g. Tanzania).

Patients who fail to make a satisfactory response to adequate conventional treatment

Co-existing HIV infection

159
Q

What is bronchiectasis?

A

a disease involving inflammation which causes permanent dilation of the subsegmental airways (bronchi and bronchioles)

leads to a build-up of excess mucous.

160
Q

How is there a two-fold effect of deadspace created in bronchiectasis?

A
  1. The damage will significantly reduce the surface area to volume ratio.
  2. Airways become filled with secretion, so less oxygen can reach the alveoli.
161
Q

What are the types of bronchiectasis?

A

Cylindrical (most common)
Varicose
Cystic (most severe, least common)

162
Q

Cylindrical bronchiectasis

A

airways are widened, but structure tends to be the same

163
Q

Varicose bronchiectasis

A

architecture is also damaged as well as widened ariways

164
Q

Cystic bronchiectasis

A

development of out-pouches/bulges, which can impinge on healthy airways

165
Q

Vicious cycle hypothesis of bronchiectasis

A

an initial insult leads to the start of the chain reaction of:

Respiratory tract infection
&
Bronchial Inflammation
&
Respiratory tract damage
166
Q

What can be the initial insult of bronchiectasis?

A

Congenital (e.g. CF)

Infective (viruses, bacteria, fungi)

Obstruction (e.g. COPD, tumours, foreign bodies, irritants)

Other (e.g. Idiopathic)

167
Q

Long-term consequences of bronchiectasis

A

Recurrent pneumonia

Pleural effusions – accumulated inflammatory transudate.

Secondary pneumothorax

Massive haemoptysis – larger vessel eroded by chronic disease

Right heart failure – increased pulmonary resistance.

Rarely – cerebral abscess and amyloidosis

168
Q

Typical Presentation of bronchiectasis

A

Shortness of Breath

Fatigue

Copious amounts (“cupfuls”) of sputum, sometimes with blood.
=> Productive cough

Previous infection/history of lung disease – e.g. pneumonia

169
Q

Atypical Presentation of bronchiectasis

A

Idiopathic bronchiectasis – no history of lung disease.

Dry bronchiectasis – no excessive sputum production

COPD-bronchiectasis overlap

170
Q

What is the difference between the early stages of COPD and bronchiectasis?

A

COPD is a functional/physiological diagnosis – due to poor reversible airflow obstruction.

Bronchiectasis is a structural diagnosis – presence of airway dilatation on CT
=> initially restrictive due to widening of airways,
=> then obstructive as airways fill up with fluid/mucous,
=> eventually mixed deficit towards the advanced stages of disease

171
Q

Bronchiectasis - on examination

A

Acute signs:

  • Rronchi (loud expiratory wheezing)
  • Mid-inspiratory squeaks
  • Coarse crackles

Chronic signs – maybe acute signs, but also potentially:

  • Generalised wheezing
  • Clubbing
  • RHF (raised JVP, oedema)
172
Q

Bronchiectasis - investigations

A

Routine bloods – FBC, U&E, CRP, coagulation.

Sputum Microbiology – identify causative or propagating organism
=> Treat with broad spectrum initially, target once known.
=> If negative, consider fungal infection.

CXR
=> ?pneumonia, ?effusion,
=> might see some bronchial thickening,

Pulmonary function tests – will show obstructive picture (FEV1/FVC <0.7)

173
Q

What would a high resolution CT scan of a patient with bronchiectasis show?

A

Signet ring pattern

174
Q

Restrictive Lung Disease

A

= physical reduction in potential maximum lung volume

Can be:

  • A problem of compliance – e.g. fibrosis
  • An increase in dead space – e.g. effusion, pus
175
Q

Obstructive lung disease

A

= increased effort to reach near-normal lung volume, due to narrowing of airways

Can be:

  • obstruction of large airways – asthma, COPD, bronchitis
  • obstruction of small airways – bronchiolitis, bronchiectasis
176
Q

What is FEV1?

What is considered normal?

A

= the volume exhaled in the first second after deep inspiration and forced expiration

Normal is >80%

177
Q

What is FVC?

What is considered normal?

A

= the total volume of air that can be forcibly exhaled in one breath from maximal inhalation

Normal is >80%

178
Q

What is FEV1/FVC?

What is considered normal?

A

a ratio used to identify restrictive/obstructive deficit.

Normal is >70%

179
Q

Spirometry in obstructive lung disease

A

FEV1 <80%
FVC >80%
FEV1/FVC <0.7

180
Q

Spirometry in restrictive lung disease

A

FEV1 <80%
FVC <80%
FEV1/FVC >0.7 (i.e. normal)

181
Q

What causes non-lung related restrictive deficit?

A

Pregnancy, obesity, kyphoscoliosis

182
Q

What is pulmonary fibrosis?

A

a condition in which there is diffuse scarring of the lung parenchyma

183
Q

Focal pulmonary fibrosis

A

The occupational Lung Diseases (OLD)

=> affects lymphoid tissue

184
Q

Interstitial pulmonary fibrosis

A

Extrinsic Allergic alveolitis

=> affects parenchyma

185
Q

Replacement pulmonary fibrosis

A

RA, TB, connective tissue disorders

=> direct damage due to disease

186
Q

Apical pulmonary fibrosis

A TEA SHOP

A 
Allergic Bronchopulmonary Aspergillosis
Tuberculosis
Extrinsic allergic alveolitis
Ankylosing Spondylosis
Sarcoid
Histiocytosis
Occupational (berylliosis, silicosis)
Pneumoconiosis
187
Q

Basal pulmonary fibrosis

DR CIA

A 
Drugs
Rheumatoid Arthritis
Connective Tissue Disease
Idiopathic Pulmonary fibrosis 
Asbestosis
188
Q

Which drugs can cause pulmonary fibrosis?

A

amiodarone, bleomycin, busulfan, methotrexate, vincristine, nitrofurantoin

189
Q

Which occupational lung diseases cause direct fibrosis?

A

Berylliosis – beryllium inhalation
Silicosis – silica/silicon inhalation
Asbestosis – asbestos inhalation

190
Q

Which occupational lung diseases cause extrinsic allergic alveolitis?

A

Pigeon Fancier’s Lung – Bird dander/droppings

Farmer’s Lung – hay/crop mould

Malt worker’s lung – hop moulds

Hot tub lung – M. avium from hot tub mist.

Saxophonist’s lung – mixed fungi from uncleaned instruments

191
Q

Pulmonary fibrosis - investigations

A

Bloods:
• ABG
• CRP
• Special tests

Imaging:
• CXR – reduced lung volume
• CT – classic signs of fibrosis: honeycombing.

Spirometry – restrictive deficit.

Lung biopsy – to assess for any fibrotic change ONLY if the CT scan and other tests are equivocal and diagnosis is uncertain.

192
Q

what does pulmonary fibrosis look like on a high resolution CT?

A

Honeycombing

193
Q

Prognosis of pulmonary fibrosis

A

Condition is progressive and life-limiting - prognosis is poor if untreated.

Treatment depends on the cause, and is often very limited.

Lung transplants can be done, but there is still risk of developing fibrosis in the new lung.

194
Q

What are the three main buffering systems for H+ in the body?

A
  1. Intra- and extracellular buffers
  2. Ventilation
  3. Renal regulation of H+ and HCO3-
195
Q

How does the body deal with an excess of H+?

A

buffers can combine with H+ to reduce levels

ventilation can increase to excrete CO2

Excreting H+ as free hydrogen ions or in phosphate/ammonia buffers

196
Q

What pH is acadaemia and what pH is alkalaemia?

A

<7.35 is acidaemic

>7.45 is alkalaemic

197
Q

Steps to interpreting an ABG

A
  1. How is the patient?
  2. Assess oxygenation
  3. Determine the pH
  4. Determine the respiratory component
  5. Determine the metabolic component
  6. Is there any evidence of compensation?
  7. Base excess
198
Q

What should oxygenation on an ABG be?

A

PaO2 should be >10kPa on air, or

PaO2 should be ~10kPa less than the % inspired concentration.

199
Q

What would respiratory acidosis look like on an ABG?

A

acidaemic

PaCO2 >6

200
Q

What would respiratory alkalosis look like on an ABG?

A

alkalaemic

HCO3- >26

201
Q

What does base excess look like on an ABG?

A

Negative in metabolic acidosis

Positive in metabolic alkalosis

202
Q

What is base excess?

A

the theoretical amount of acid needed to bring a patient’s fully oxygenated blood to normal pH at room temperature

203
Q

Respiratory Acidosis

A

Decrease in gaseous exchange leading to retention of CO₂

High PCO₂ leads to renal retention of bicarbonate to buffer excess H⁺

Compensation by the kidneys results in an increase in secretion of H⁺ over 3-5 days leading to increase in plasma bicarbonate level

204
Q

Causes of respiratory acidosis

A

Drugs e.g. morphine and sedatives
Stroke
Infection

Asthma
COPD

Pneumoconiosis
Bronchitis
Acute respiratory distress syndrome (ARDS)

Poliomyelitis
Kyphoscoliosis
Myasthenia gravis
Muscular dystrophies

Obesity
Hypertension

205
Q

Respiratory Alkalosis

A

Alveolar hyperventilation leads to excess exhalation of CO₂, resulting in low PCO₂

Compensation by the kidneys results from decreased ammonium (NH₄⁻) excretion, leading to a fall in bicarbonate

206
Q

Causes of respiratory alkalosis

A 
Pain, anxiety, psychosis
Fever
Cerebrovascular accident/stroke
Meningitis/encephalitis
Trauma
High altitude
Pneumonia
Pulmonary oedema
Aspiration
Severe anaemia

Pregnancy, progesterone
Salicylates

Haemothorax, flail chest
Cardiac failure, PE

Septicaemia
Mechanical hyperventilation
Hepatic failure, heat exposure

207
Q

Metabolic Acidosis

A

Results from the body producing too much acid or the kidneys failing to excrete enough H⁺.

Initially this creates a decrease in bicarbonate as carbonic acid is produced to buffer the H⁺

The lungs compensate by hyperventilation and blowing of the CO₂

The anion gap can be used to differentiate causes – if gap is normal, bicarbonate is being lost either by GI loss (e.g. diarrhoea) or renal disease allowing loss.

High anion gap results from increased production of acids (e.g. lactic acid, urate or diabetic ketoacidosis) or large amounts of acid (e.g. aspirin overdose)

208
Q

Causes of metabolic acidosis

A

HIGH anion gap

Lactic acidosis
Ketoacidosis – diabetic, alcohol abuse, starvation
Renal failure – acute/chronic
Toxins – e.g. methanol, salicylates

NORMAL anion gap

Bicarbonate loss from GI tract
Renal acidosis (proximal/distal tubular acidosis)
Drug-induced (NSAIDs, ACEi, spironolactone, etc)
Rapid saline infusion

209
Q

Metabolic Alkalosis

A

Results from increased bicarbonate due to either decreased H⁺ concentration (e.g. due to vomiting) or a direct increase in bicarbonate.

Bicarbonate shift can occur from retention, an intracellular shift in H⁺ or by ingestion of large amounts of alkali (e.g. antacids).

The lungs compensate by slower breathing to retain more CO₂

210
Q

Causes of metabolic alkalosis

A 
Milk-alkali syndrome
Vomiting
Nasogastric suction
Villous adenoma
Hypercalcaemia 
Recovery from lactic acidosis/ketoacidosis
High renin – renal artery stenosis
Accelerated hypertension
Aldosteronism
Cushing’s Syndrome
Steroids
211
Q

ABG - type 1 respiratory failure

A

PaO2 <10

PaCO2 <6

212
Q

ABG - type 2 respiratory failure

A

PaO2 <10

PaCO2 >6

213
Q

Respiratory History - Dyspnoea

A

When did it start?
Sudden or gradual?

How long has this been going on for?

can they speak in full sentences?
Is it impacting on day-to-day activities?
How far can they walk?

Does it fluctuate?
Does anything make it better or worse?

214
Q

Respiratory History - specific PMH

A

Asthma/COPD or other respiratory conditions
Hx of atopy
Recurrent chest infections in childhood

215
Q

Respiratory History - relevant drug history

A

Inhalers – reliever/preventer

Beta-blockers/NSAIDs – bronchoconstriction
ACE inhibitors – dry cough
Cytotoxic agents – interstitial lung disease
Oestrogen – increased risk of PE
Amiodarone/methotrexate – pleural effusions/ interstitial lung disease

216
Q

Respiratory History - relevant family history

A

e.g. asthma / atopy / lung cancer / CF

217
Q

How many cigarettes are 1 pack year?

A

20 cigarettes/day

218
Q

Respiratory History - social history

A

Smoking status - current/past/never
Alcohol
Illicit drugs - cannabis increased risk of lung cancer

Employment - occupational lung disease
Hobbies pets (e.g. bird fancier disease)

Overseas travel - long haul flights (PE), TB risk

Ability to complete activities of daily living (ADL)

219
Q

What type of cells line the respiratory tract normally?

A

Columnar epithelial cells

220
Q

How will emphysema appear histologically?

A

there will be loss of the solid architecture (“moss eaten” appearance)

also unequal size and enlargement of the alveoli (due to dilatation).

221
Q

What is the difference between congenital and functional alpha1-antitrypsin deficiency?

A

Congenital - gene defect causes inactivation of antiproteiases

Functional - Smoking causes reactive oxygen species/free radicals, which cause inactivation of antiproteases

222
Q

Saddle embolism

A

a large pulmonary embolism that straddles the bifurcation of the pulmonary trunk extending to the left and right pulmonary arteries

223
Q

What pathogens tend to cause interstitial pneumonia?

A

The atypical organisms

SARS coronaviruses

224
Q

What is the most likely organism causing pneumonia in a previously healthy individual?

A

S. pneumoniae

225
Q

What is the most likely organism causing pneumonia in pre-existing viral infection?

A

Staph. aureus or S. pneumoniae

226
Q

What is the most likely organism causing pneumonia in COPD?

A

Haemophilus influenzae or S. pneumoniae

227
Q

What is the most likely organism causing pneumonia in HIV+?

A

Pneumocystis carinii, cytomegalovirus, TB

228
Q

What is the most likely organism causing pneumonia in Cystic Fibrosis?

A

Pseudomonas, Berkholderia species

229
Q

What is the most likely organism causing pneumonia in a child?

A

Haemophilus influenzae

230
Q

What is the most likely organism causing pneumonia in someone who also has a maculopapular skin rash in their extremities?

A

Mycoplasma pneumoniae

extra-pulmonary manifestations are common

231
Q

What is the most likely organism causing pneumonia developed during hospital admission?

A

E. coli, Klebsiella spp., proteus spp., S. pneumoniae, S. aureus (MSSA or MRSA).

232
Q

what is a the lead time between asbestos exposure and development of mesothelioma?

A

normally >20 years

233
Q

which sites does mesothelioma most commonly spread to from the pleural cavity?

A

other pleural cavity
lung
hilar lymph nodes

234
Q

what type of room is best to prevent the spread of airborne microbes?

A

negative pressure isolation room

235
Q

What is a cavitating lung mass?

what are the causes?

A

= gas-filled spaces surrounded by consolidation, a lung mass or nodule.

Causes:

  • bacterial lung abscess
  • metastatic squamous cell carcinoma
  • granulomatosis
  • pulmonary infarct
236
Q

what organisms may cause a caveatting lung abscesS?

A

anaerobic spp.

mycobacterium tuberculosis

CP1 (12 decks)

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