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Diseases > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Incidence of Lung Cancer?

A

Lung cancer is the third most common cancer in the UK behind breast and prostate

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2
Q

What is the biggest cause of lung cancer?

A

Cigarette smoking

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3
Q

WHat type of cancer is more common

Non small cell

small cell

A

Non small cell

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4
Q

Name examples of non small cell lung cancer?

A

Adenocarcinoma (around 40%)

Squamous cell carcinoma (around 20%)

Large-cell carcinoma (around 10%)

Other types (around 10%)

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5
Q

What are Small Cell Lung Cancer (SCLC)

A

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

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6
Q

Signs and Symptoms of Lung Cancer?

A
  • Shortness of breath
  • Cough
  • Haemoptysis (coughing up blood)
  • Finger clubbing
  • Recurrent pneumonia
  • Weight loss
  • Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
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7
Q

What is the first line investigation in suspected lung cancer.

A

CXR

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8
Q

SIgn on CXR that support lung cancer diagnosis?

A

Hilar enlargement

“Peripheral opacity” – a visible lesion in the lung field

Pleural effusion – usually unilateral in cancer

Collapse

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9
Q

Other Ix for Lung cnacer?

A

Staging CT scan- check for lymph node involvement and metastasis

PET-CT (positron emission tomography)

Bronchoscopy with endobronchial ultrasound (EBUS)

Histological diagnosis

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10
Q

What is first line treatment option for non small cell lung cancer?

A

Lobectomy (removing the lung lobe containing the tumour) is first line.

Segmentectomy or wedge resection (taking a segment or wedge of lung to remove the tumour) is also an option.

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11
Q

other Tx for non small cell lung cancer?

A

Radiotherapy can also be curative in non-small cell lung cancer when early enough.

Chemotherapy can be offered in addition to surgery or radiotherapy in certain patients to improve outcomes (“adjuvant chemotherapy”) or as palliative treatment to improve survival and quality of life in later stages of non-small cell lung cancer.

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12
Q

Tx for small cell lung cancer?

A

Treatment for small cell lung cancer is usually chemotherapy and radiotherapy. Prognosis is generally worse from small cell lung cancer than non-small cell lung cancer.

Endobronchial treatment with stents or debulking can be used as part of palliative treatment to relieve bronchial obstruction caused by lung cancer.

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13
Q

Lung cancer is associated with a lot of extrapulmonary manifestations and paraneoplastic syndromes.

Name some exmples

A

Recurrent laryngeal nerve palsy

Phrenic nerve palsy

Superior vena cava obstruction

Horner’s syndrome- caused by a Pancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.

Syndrome of inappropriate ADH (SIADH)

Cushing’s syndrome

Hypercalcaemia- ctopic parathyroid hormone from a squamous cell carcinoma.

Limbic encephalitis

Lambert-Eaton myasthenic syndrome.

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14
Q

Which associated diseases are with small cell lung cancer

A

Syndrome of inappropriate ADH (SIADH) caused by ectopic ADH secretion by a small cell lung cancer and presents with hyponatraemia.

Cushing’s syndrome can be caused by ectopic ACTH secretion by a small cell lung cancer.

Limbic encephalitis. This is a paraneoplastic syndrome where the small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas.It is associated with anti-Hu antibodies.

Lambert-Eaton myasthenic syndrome.

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15
Q

What is Pemberton’s sign and what is it associated with?

A

Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.

Superior vena cava obstruction

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16
Q

What is Lambert-Eaton Myasthenic Syndrome

A

Lambert-Eaton myasthenic syndrome is a result of antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones

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17
Q

Lambert-Eaton Myasthenic Syndrome symptoms and signs

A

This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

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18
Q

WHat is Mesothelioma

A

Mesothelioma is a lung malignancy affecting the mesothelial cells of the pleura. It is strongly linked to asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival but it is essentially palliative.

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19
Q

What is Pneumonia

WHat can you see in CXR

A

Pneumonia is simply an infection of the lung tissue. It causes inflammation of the lung tissue and sputum filling the airways and alveoli.

Pneumonia can be seen as consolidation on a chest xray.

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20
Q

What are the types of pneumonia?

A

community acquired pneumonia

hospital acquired pneumonia

aspiration pneumonia ( after inhaling foreign material such as food)

Atypical Pneumonia

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21
Q

Presentation of Pneumonia

A

Shortness of breath

Cough productive of sputum

Fever

Haemoptysis (coughing up blood)

Pleuritic chest pain (sharp chest pain worse on inspiration)

Delirium (acute confusion associated with infection)

Sepsis

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22
Q

SIgns of Pneumonia

A

There may be a derangement in basic observations. These can indicate sepsis secondary to the pneumonia:

Tachypnoea (raised respiratory rate)

Tachycardia (raised heart rate)

Hypoxia (low oxygen)

Hypotension (shock)

Fever

Confusion

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23
Q

chest signs of pneumonia?

A

Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway.

Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.

Dullness to percussion due to lung tissue collapse and/or consolidation.

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24
Q

Severity Assessment of pneumonia?

A

C – Confusion (new disorientation in person, place or time)

U – Urea > 7

R – Respiratory rate ≥ 30

B – Blood pressure < 90 systolic or ≤ 60 diastolic.

65 – Age ≥ 65

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25
Q

Explain the scoring system for CURB 65

A

Score 0/1: Consider treatment at home

Score ≥ 2: Consider hospital admission

Score ≥ 3: Consider intensive care assessment

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26
Q

Common causes pneumonia?

A

Streptococcus pneumoniae (50%)

Haemophilus influenzae (20%)

Other Causes and Associations

Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease

Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis (also hospital acquired)

Staphylococcus aureus in patients with cystic fibrosis

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27
Q

What is Atypical Pneumonia

A

The definition of atypical pneumonia is pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain. They don’t respond to penicillins

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28
Q

Atypical pneumonia does not respond to peicillins and can be treated with_____

A

macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).

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29
Q

Example of atypical pneumonia caused by an organism that cannot be cultured

A

Legionella pneumophila

Mycoplasma pneumoniae.

Chlamydophila pneumoniae

Coxiella burnetii AKA “Q fever”.

Chlamydia psittaci

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30
Q

Which type of pneumonia typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH

Typical presentation?

A

Legionella pneumophila

The typical exam patient has recently had a cheap hotel holiday and presents with hyponatraemia.

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31
Q

THis type of pneumonia causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.

A

Mycoplasma pneumoniae

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32
Q

What is the presentation of Chlamydophila pneumoniae.

A

The presentation might be a school aged child with a mild to moderate chronic pneumonia and wheeze. Be cautious though as this presentation is very common without chlamydophilia pneumoniae infection

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33
Q

Coxiella burnetii AKA “Q fever” is linked to?

A

exposure to animals and their bodily fluids.

he MCQ patient is a farmer with a flu like illness.

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34
Q

Chlamydia psittaci is contracted contact with?

A

This is typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.

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35
Q

Fungal Pneumonia is associated is what type?

A

Pneumocystis jiroveci (PCP)

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36
Q

Fungal Pneumonia commonly presents which type of patients?

Tx?

A

patients that are immunocompromised. It is particularly important in patients with poorly controlled or new HIV with a low CD4 count. It usually presents subtly with a dry cough without sputum, shortness of breath on exertion and night sweats.

Treatment is with co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.

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37
Q

Ix for pneumonia

A

Chest xray

FBC (raised white cells)

U&Es (for urea)

CRP (raised in inflammation and infection)

Sputum cultures

Blood cultures

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

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38
Q

Tx for Pneumonia?

A

Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)

Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)

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39
Q

Complications of pneumonia?

A

Sepsis

Pleural effusion

Empyema

Lung abscess

Death

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40
Q

What is asthma?

A

Asthma is a chronic inflammatory condition of the airways that causes episodic exacerbations of bronchoconstriction.

In asthma there is reversible airway obstruction that typically responds to bronchodilators such as salbutamol. This bronchoconstriction is caused by hypersensitivity of the airways and can be triggered by environmental factors.

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41
Q

Typical Triggers of Asthma

A

Infection

Night time or early morning

Exercise

Animals

Cold/damp

Dust

Strong emotions

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42
Q

Presentation Suggesting a Diagnosis of Asthma

A
  • Episodic symptoms
  • Diurnal variability. Typically worse at night.
  • Dry cough with wheeze and shortness of breath
  • A history of other atopic conditions such as eczema, hayfever and food allergies
  • Family history
  • Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
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43
Q

What symptoms suggest something else other than asthma

A

Wheeze related to coughs and colds more suggestive of viral induced wheeze

Isolated or productive cough

Normal investigations

No response to treatment

Unilateral wheeze. This suggests a focal lesion or infection.

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44
Q

NICE Guidelines on Diagnosis on Asthma

A

First line investigations:

  • Fractional exhaled nitric oxide
  • Spirometry with bronchodilator reversibility

If there is diagnostic uncertainty after first line investigations these can be followed up with further testing:

  • Peak flow variability measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
  • Direct bronchial challenge test with histamine or methacholine
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45
Q

Long Term Management of asthma adult

A
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46
Q

What is Maintenance and Reliever Therapy (MART).

A

This is 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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47
Q

BTS/SIGN Stepwise Ladder (adapted from 2016 guidelines)

Asthma

A
  1. Add short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes.
  2. Add a regular low dose corticosteroid inhaler.
  3. Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.
  4. Consider a trial of an oral leukotriene receptor antagonist (i.e. montelukast), oral beta 2 agonist (i.e. oral salbutamol), oral theophylline or an inhaled LAMA (i.e. tiotropium).
  5. Titrate inhaled corticosteroid up to “high dose”. Combine additional treatments from step 4. Refer to specialist.
  6. Add oral steroids at the lowest dose possible to achieve good control.
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48
Q

Yearly Asthma management

A

Each patient should have an individual asthma self-management programme

Yearly flu jab

Yearly asthma review

Advise exercise and avoid smoking

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49
Q

What is an acute exacerbation of asthma

A

An acute exacerbation of asthma is characterised by a rapid deterioration in symptoms. This could be triggered by any of the typical asthma triggers such as infection, exercise or cold weather.

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50
Q

Presentation of acute asthma

A
  • Progressively worsening shortness of breath
  • Use of accessory muscles
  • Fast respiratory rate (tachypnoea)
  • Symmetrical expiratory wheeze on auscultation
  • The chest can sound “tight” on auscultation with reduced air entry
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51
Q

Grading Acute Asthma

Moderate

A

PEFR 50 – 75% predicted

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52
Q

Grading Acute Asthma

Severe

A
  • PEFR 33-50% predicted
  • Resp rate >25
  • Heart rate >110
  • Unable to complete sentences
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53
Q

Grading Acute Asthma

Life threatening

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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54
Q

Treatment for Acute Asthma

Moderate?

A
  • Nebulised beta-2 agonists (i.e. salbutamol 5mg repeated as often as required)
  • Nebulised ipratropium bromide
  • Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days
  • Antibiotics if there is convincing evidence of bacterial infection
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55
Q

Treatment for Acute Asthma

Severe

A
  • Oxygen if required to maintain sats 94-98%
  • Aminophylline infusion
  • Consider IV salbutamol
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56
Q

Treatment for Acute Asthma

Life Threatening

A
  • IV magnesium sulphate infusion
  • Admission to HDU / ICU
  • Intubation in worst cases – however this decision should be made early because it is very difficult to intubate with severe bronchoconstriction
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57
Q

What can you see on an ABG that indicates asthma?

A

Initially patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2

A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma. A respiratory acidosis due to high CO2 is a very bad sign in asthma.

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58
Q

How do you monitor the response to acute asthma treatment

A

use:

Respiratory rate

Respiratory effort

Peak flow

Oxygen saturations

Chest auscultation

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59
Q

What electrolyte do you monitor when on salbutamol

A

Monitor serum potassium when on salbutamol as it causes potassium to be absorbed from the blood into the cells. Salbutamol also causes tachycardia (fast heart rate).

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60
Q

What is Chronic obstructive pulmonary disease (COPD)

A

Chronic obstructive pulmonary disease (COPD) is a non-reversible, long term deterioration in air flow through the lungs caused by damage to lung tissue. This lung damage is almost always the result of smoking. The damage to the lung tissues causes an obstruction to the flow of air through the airways making it more difficult to ventilate the lungs and making them prone to developing infections.

61
Q

Presentation of COPD

A

Suspect COPD in a long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.

Always consider differential diagnoses such as lung cancer, fibrosis or heart failure. COPD does NOT cause clubbing. It is unusual for it to cause haemoptysis (coughing up blood) or chest pain. These symptoms should be investigated for a different cause.

62
Q

What is MRC (Medical Research Council) Dyspnoea Scale

A

This is a 5 point scale that NICE recommend for assessing the impact of their breathlessness:

Grades:

  • 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
63
Q

Diagnosis of COPD

A

Diagnosis is based on clinical presentation plus spirometry.

Spirometry will show an “obstructive picture”.

FEV1/FVC ratio <0.7

The obstructive picture does not show a dramatic response to reversibility testing with beta-2 agonists such as salbutamol during spirometry testing. If there is a large response to reversibility testing them consider asthma as an alternative diagnosis.

64
Q

The severity of the airflow obstruction can be graded using the FEV1:

Explain the stages

A
  • 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
    *
65
Q

Other Investigations used for COPD

A

Chest xray to exclude other pathology such as lung cancer.

Full blood count for polycythaemia or anaemia. Polycythaemia (raised haemoglobin) is a response to chronic hypoxia.

Body mass index (BMI) as a baseline to later assess weight loss (e.g. cancer or severe COPD) or weight gain (e.g. steroids).

Sputum culture to assess for chronic infections such as pseudomonas.

ECG and echocardiogram to assess heart function.

CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis.

Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency. Deficiency leads to early onset and more severe disease.

Transfer factor for carbon monoxide (TLCO) is decreased in COPD. It can give an indication about the severity of the disease and may be increased in other conditions such as asthma.

66
Q

Long Term Management of COPD

A
67
Q

What do you on ABG on COPD patients

A

Remember that CO2 makes blood acidotic by breaking down into carbonic acid (H2CO3). Low pH (acidosis) with a raised pCO2 suggests they are acutely retaining (not able to get rid of) more CO2 and their blood has become acidotic. This is a respiratory acidosis.

Raised bicarbonate indicates they chronically retain CO2 and their kidneys have responded by producing more bicarbonate to balance the acidic CO2 and maintain a normal pH. In an acute exacerbation, the kidneys can’t keep up with the rising level of CO2 so they become acidotic despite having a higher bicarbonate than someone without COPD.

68
Q

What is the difference between type 1 and type 2 resp failure

A

Low pO2 indicates hypoxia and respiratory failure

Normal pCO2 with low pO2 indicates type 1 respiratory failure (only one is affected)

Raised pCO2 with low pO2 indicates type 2 respiratory failure (two are affected)

69
Q

Other investigations of COPD

A

Chest xray to look for pneumonia or other pathology

ECG to look for arrhythmia or evidence of heart strain (heart failure)

FBC to look for infection (raised white cells)

U&E to check electrolytes which can be affected by infection and medications

Sputum culture if significant infection is present

Blood cultures if septic

70
Q

A general rule regarding target oxygen saturations in COPD is:

A
  • 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%
71
Q

Medical Treatment of an Exacerbation of COPD

at home

A
  • Prednisolone 30mg once daily for 7-14 days
  • Regular inhalers or home nebulisers
  • Antibiotics if there is evidence of infection
72
Q

Medical Treatment of an Exacerbation of COPD

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
73
Q

Medical Treatment of an Exacerbation of COPD

Options in severe cases not responding to first line treatment

A
  • IV aminophylline
  • Non-invasive ventilation (NIV)
  • Intubation and ventilation with admission to intensive care
  • Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate
74
Q

What is Interstitial Lung Disease

A

Interstitial lung disease is an umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis. Fibrosis involves the replacement of the normal elastic and functional lung tissue with scar tissue that is stiff and does not function effectively.

75
Q

Diagnosis of Intestitial lung disease

A

Diagnosis of interstitial lung disease requires a combination of clinical features and high resolution CT scan of the thorax. HRCT shows a “ground glass” appearance with interstitial lung disease. When diagnosis is unclear lung biopsy can be used to take samples of the lung tissue and confirm the diagnosis on histology.

76
Q

Management of interstitial lung disease

A

Generally there is a poor prognosis and limited management options in interstitial lung disease as the damage is irreversible. Generally the treatment is supportive and where possible to prevent further progression of the disease. Options are:

  • Remove or treat the underlying cause
  • Home oxygen where they are hypoxic at rest
  • Stop smoking
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and flu vaccine
  • Advanced care planning and palliative care where appropriate
  • Lung transplant is an option but the risks and benefits need careful consideration
77
Q

What is Idiopathic Pulmonary Fibrosis

A

This is a condition where there is progressive pulmonary fibrosis with no clear cause. It presents with an insidious onset of shortness of breath and dry cough over more than 3 months. It usually affects adults over 50 years old. Examination can show bibasal fine inspiratory crackles and finger clubbing. Prognosis is poor with a life expectancy of 2-5 years from diagnosis.

78
Q

Idiopathic Pulmonary Fibrosis

Medications

A

Two medications are licensed that can slow the progression of the disease:

  • Pirfenidone is an antifibrotic and anti-inflammatory
  • Nintedanib is a monoclonal antibody targeting tyrosine kinase
79
Q

Drug Induced Pulmonary Fibrosis

There are several drugs that can cause pulmonary fibrosis. Key medication that are worth remembering are:

A

Amiodarone

Cyclophosphamide

Methotrexate

Nitrofurantoin

80
Q

Pulmonary fibrosis can occur secondary to other conditions like

A

Alpha-1 antitripsin deficiency

Rheumatoid arthritis

Systemic lupus erythematosus (SLE)

Systemic sclerosis

81
Q

What is Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A

Hypersensitivity pneumonitis is a type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people that are sensitive to that allergen. Bronchoalveolar lavage involves collecting cells from the airways during bronchoscopy by washing the airways with fluid then collecting that fluid for testing. This shows raised lymphocytes and mast cells in hypersensitivity pneumonitis.

82
Q

Management of Hypersensitivity Pneumonitis

A

Management is by removing the allergen, giving oxygen where necessary and steroids

83
Q

Examples of specific causes of Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A
  • Bird-fanciers lung is a reaction to bird droppings
  • Farmers lung is a reaction to mouldy spores in hay
  • Mushroom workers’ lung is a reaction to specific mushroom antigens
  • Malt workers lung is a reaction to mould on barley
84
Q

WHat is Cryptogenic Organising Pneumonia

Presentation

Diagnosis

A

It involves a focal area of inflammation of the lung tissue. This can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

presentation is very similar to infectious pneumonia with shortness of breath, cough, fever and lethargy. It also presents on similarly to pneumonia on a chest xray with a focal consolidation.

Diagnosis is often delayed due to the similarities to infective pneumonia. Lung biopsy is the definitive investigation. Treatment is with systemic corticosteroids.

85
Q

Asbestosis

What is it

A

Asbestosis is lung fibrosis related to the inhalation of asbestos. Asbestos is fibrogenic, meaning it causes lung fibrosis. It is also oncogenic, meaning it causes cancer. The effects of asbestos usually take several decades to develop.

86
Q

Asbestosis inhalation causes several problems:

A

Lung fibrosis

Pleural thickening and pleural plaques

Adenocarcinoma

Mesothelioma

87
Q

What is pleural effusion

A

A pleural effusion is a collection of fluid in the pleural cavity. This can be exudative meaning there is a high protein count (>3g/dL) or transudative meaning there is a relatively lower protein count (<3g/dL). Whether it is exudative or transudative helps determine the cause.

88
Q

Exudative Causes of Pleural effusion

A

Exudative causes are related to inflammation. The inflammation results in protein leaking out of the tissues in to the pleural space (ex- meaning moving out of). Think of the causes of inflammation:

  • Lung cancer
  • Pneumonia
  • Rheumatoid arthritis
  • Tuberculosis
89
Q

Transudative Causes of Pleural Effusion

A

Transudative causes relate to fluid moving across into the pleural space (trans- meaning moving across). Think of the causes of fluid shifting:

  • Congestive cardiac failure
  • Hypoalbuminaemia
  • Hypothroidism
  • Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
90
Q

Presentation of pleural effusion

A
  • Shortness of breath
  • Dullness to percussion over the effusion
  • Reduced breath sounds
  • Tracheal deviation away from the effusion if it is massive
91
Q

Investigations of pleural effusion

CXR shows?

other Ix?

A

Chest xray shows:

  • Blunting of the costophrenic angle
  • Fluid in the lung fissures
  • Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum.
  • Tracheal and mediastinal deviation if it is a massive effusion

Taking a sample of the pleural fluid by aspiration or chest drain is required to analyse it for protein count, cell count, pH, glucose, LDH and microbiology testing

92
Q

Treatment of pleural effusion

A

Conservative management may be appropriate as small effusions will resolve with treatment of the underlying cause. Larger effusions often need aspiration or drainage.

Pleural aspiration involves sticking a needle in and aspirating the fluid. This can temporarily relieve the pressure but the effusion may recur and repeated aspiration may be required.

Chest drain can be used to drain the effusion and prevent it recurring

93
Q

What is Empyema

A

Empyema is where there is an infected pleural effusion. Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever. Pleural aspiration shows pus, acidic pH (pH < 7.2), low glucose and high LDH. Empyema is treated by chest drain to remove the pus and antibiotics.

94
Q

What is a Pneumothorax

A

Pneumothorax occurs when air gets into the pleural space separating the lung from the chest wall. It can occur spontaneously or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology. The typical patient in your exams is a young, tall, thin young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports.

air in the pleural space

95
Q

Causes Pneumothorax

A
  • Spontaneous
  • Trauma
  • Iatrogenic such as due to lung biopsy, mechanical ventilation or central line insertion
  • Lung pathology such as infection, asthma or COPD
96
Q

What type of chest x ray is used in Pneumothorax

A

Erect chest xray is the investigation of choice for a simple pneumothorax.

A chest xray will show an area between the lung tissue and the chest wall where there are no lung markings. There will be a line demarcating the edge of the lung where the lung markings ends and the pneumothorax begins.

no lung markings and edge of lung

97
Q

Management of pneumothorax

A

This is based on the 2010 guidelines from the British Thoracic Society:

If no SOB and there is a < 2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.

If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.

If aspiration fails twice it will require a chest drain.

Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

98
Q

Tension Pneumothorax

What is it

A

Tension pneumothorax is caused by trauma to chest wall that creates a one-way valve that lets air in but not out of the pleural space. The one-way valve means that during inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space. Therefore more air keeps getting drawn into the pleural space with each breath and cannot escape. This is dangerous as it creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.

99
Q

Signs of Tension Pneumothorax

A
  • Tracheal deviation away from side of pneumothorax
  • Reduced air entry to affected side
  • Increased resonant to percussion on affected side
  • Tachycardia
  • Hypotension
100
Q

Management of Tension Pneumothorax

A

The management sentence you need to learn and recite in your exams is: “Insert a large bore cannula into the second intercostal space in the midclavicular line”

If a tension pneumothorax is suspected do not wait for any investigations. Once the pressure is relieved with a cannula then a chest drain is required for definitive management.

.

101
Q

Where are chest drain is inserted

A

“triangle of safety”

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)

102
Q

What is a PE

A

Pulmonary embolism (PE) is a condition where a blood clot (thrombus) forms in the pulmonary arteries. This is usually the result of a deep vein thrombosis (DVT) that developed in the legs and travelled (embolised) through the venous system and the right side of the heart to the pulmonary arteries in the lungs. Once they are in the pulmonary arteries they block the blood flow to the lung tissue and create strain on the right side of the heart. DVTs and PEs are collectively known as venous thromboembolism (VTE).

103
Q

What are the risk factors for PE

A

There are a number of factors for developing a DVT or PE. In many of these situations we give patients prophylactic treatment with low molecular weight heparin to reduce the risk.

  • Immobility
  • Recent surgery
  • Long haul flights
  • Pregnancy
  • Hormone therapy with oestrogen
  • Malignancy
  • Polycythaemia
  • Systemic lupus erythematosus

Thrombophilia

104
Q

In your exams when a patient is presenting with possible features of a DVT or PE, ask about risk factors such as

A

periods of immobility, surgery and long haul flights to score extra points from your examiners.

105
Q

Explain the VTE Prophylaxis

A

Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE). If they at increased risk of VTE they should receive prophylaxis with a low molecular weight heparin such as enoxaparin unless contraindicated. Contraindications include active bleeding or existing anticoagulation with warfarin or a NOAC. Anti-embolic compression stockings are also used unless contraindicated. The main contraindication for compression stockings is significant peripheral arterial disease.

106
Q

Presentation of PE

A

Pulmonary embolism can present with subtle signs and symptoms. In patients with potential features of a PE, risk factors for PE and no other explanation for their symptoms have a low threshold for suspecting a PE. Presenting features include:

  • Shortness of breath
  • Cough with or without blood (haemoptysis)
  • Pleuritic chest pain
  • Hypoxia
  • Tachycardia
  • Raised respiratory rate
  • Low grade fever
  • Haemodynamic instability causing hypotension
107
Q

WHat is Wells Score

A

The Wells score predicts the risk of a patient presenting with symptoms actually having a DVT or pulmonary embolism. It takes in to account risk factors such as recent surgery and clinical findings such as tachycardia (heart rate >100) and haemoptysis.

108
Q

Diagnosis of PE

A

NICE recommend assessing for alternative causes with a:

  • History
  • Examination
  • Chest xray

Perform a Wells score and proceed based on the outcome:

  • Likely: perform a CT pulmonary angiogram
  • Unlikely: perform a d-dimer and if positive perform a CTPA

There are two main options for establishing a definitive diagnosis: CT pulmonary angiogram or ventilation–perfusion (VQ) scan.

109
Q

Whar does CT pulmonary angiogram (CTPA) involve

A

CT pulmonary angiogram (CTPA) involves a chest CT scan with an intravenous contrast that highlights the pulmonary arteries to demonstrate any blood clots. This is usually the first choice for investigating a pulmonary embolism as it tends to be more readily available, provides a more definitive assessment and gives information about alternative diagnoses such as pneumonia or malignancy.

110
Q

What is Ventilation-perfusion (VQ) scan involve?

A

Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera to compare the ventilation with the perfusion of the lungs. They are used in patients with renal impairment, contrast allergy or at risk from radiation where a CTPA is unsuitable. First, the isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation. Next a contrast containing isotopes is injected and a picture is taken to demonstrate perfusion. The two pictures are then compared. With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.

111
Q

Patients with a pulmonary embolism often have a _______ ______ when an ABG is performed.

A

Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed.

112
Q

Management of PE

Supportive Management

A
  • Admission to hospital
  • Oxygen as required
  • Analgesia if required
  • Adequate monitoring for any deterioration
113
Q

Initial Management (LMWH) of PE

A

The initial management guidelines from NICE were updated in March 2020. The initial recommended treatment is apixaban or rivaroxaban. Low molecular weight heparin (LMWH) is an alternative where these are not suitable, or in antiphospholipid syndrome. It should be started immediately before confirming the diagnosis in patients where DVT or PE is suspected and there is a delay in getting the scan. Examples are enoxaparin and dalteparin.

114
Q

What are the options for long term anticoagulation in VTE

A

warfarin, a NOAC or LMWH.

115
Q

The target INR for warfarin is

A

2-3

116
Q

LOng term anticoagulation

When switching to warfarin continue LMWH for _ days or the INR is 2-3 for 24 hours on warfarin (whichever is longer).

A

5

117
Q

They are an alternative option for anticoagulation that does not require monitoring. (instead of warfarin)

A

NOACs or DOACs

118
Q

Example of DOACs

A

apixaban, dabigatran and rivaroxaban.

119
Q

first line treatment for pregnancy or cancer with suspected PE

A

LMWH long term is first line treatment in pregnancy or cancer.

120
Q

DVT/PE

Continue anticoagulation for:

A
  • 3 months if there is an obvious reversible cause (then review)
  • Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.
  • 6 months in active cancer (then review)
121
Q

Where there is a massive PE with haemodynamic compromise there is a treatment option called

A

thrombolysis

122
Q

What does Thrombolysis involve?

A

Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. It is only used in patients with a massive PE where the benefits outweigh the risks

123
Q

Some examples of thrombolytic agents

A

streptokinase, alteplase and tenecteplase.

124
Q

There are two ways thrombolysis can be performed:

What are they?

A
  • Intravenously using a peripheral cannula.
  • Directly into the pulmonary arteries using a central catheter. This is called catheter-directed thrombolysis.
125
Q

What is a catheter-directed thrombolysis?

A

In catheter-directed thrombolysis a catheter is inserted into the venous system, through the right side of the heart and in to the pulmonary arteries. The operator can then administer the thrombolytic agent directly into the location of the thrombus. Special equipment can also be used to physically break down the thrombus and aspirate it. There is a risk of damaging the pulmonary arteries doing this.

126
Q

What is Pulmonary Hypertension

A

Pulmonary hypertension is increased resistance and pressure of blood in the pulmonary arteries. Increasing the pressure and resistance in the pulmonary arteries causes strain on the right side of the heart trying to pump blood through the lungs. This also causes a back pressure of blood into the systemic venous system.

127
Q

Causes of pulmonary hypertension

The causes of pulmonary hypertension can split into 5 groups:

What are they?

A

Group 1 – Primary pulmonary hypertension or connective tissue disease such as systemic lupus erythematous (SLE)

Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension

Group 3 – Chronic lung disease such as COPD

Group 4 – Pulmonary vascular disease such as pulmonary embolism

Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders

128
Q

Signs and Symptoms of pulmonary hypertension

A

Shortness of breath is the main presenting symptom.

Other signs and symptoms are:

  • Syncope
  • Tachycardia
  • Raised JVP
  • Hepatomegaly
  • Peripheral oedema.
129
Q

Ix for pulmonary hypertension

A

ECG Changes

The right sided heart strain causes ECG changes such as:

Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)

Right axis deviation

Right bundle branch block

Chest Xray Changes

Dilated pulmonary arteries

Right ventricular hypertrophy

Other investigations

A raised NT-proBNP blood test result indicates right ventricular failure

Echo can be used to estimate pulmonary artery pressure

130
Q

Management for pulmonary hypertension?

A

Primary pulmonary hypertension can be treated with:

  • IV prostanoids (e.g. epoprostenol)
  • Endothelin receptor antagonists (e.g. macitentan)
  • Phosphodiesterase-5 inhibitors (e.g. sildenafil)

Secondary pulmonary hypertension is managed by treating the underlying cause such as pulmonary embolism or SLE.

Supportive treatment for complications such as respiratory failure, arrhythmias and heart failure.

131
Q

What is Sarcoidosis

A

Sarcoidosis is a granulomatous inflammatory condition. Granulomas are nodules of inflammation full of macrophages. The cause of these granulomas developing is unknown.

132
Q

Sarcoidosis is associated with

A

It is usually associated with chest symptoms but also has multiple extra-pulmonary manifestations such as erythema nodosum and lymphadenopathy. Symptoms can vary dramatically from asymptomatic (in up to 50%) to severe and life-threatening

133
Q

What is the typical MCQ exam patient for sacordoisis patient

A

The typical MCQ exam patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum.

Young black woman with a cough

134
Q

What are the organs affected with sarcoidosis

A

Sarcoidosis can affect almost any organ in the body. The most commonly affected are the lungs so sarcoidosis is usually managed by respiratory physicians

Lungs (affecting over 90%)

  • Mediastinal lymphadenopathy
  • Pulmonary fibrosis
  • Pulmonary nodules

Systemic Symptoms

  • Fever
  • Fatigue
  • Weight loss

Liver (affecting around 20%)

  • Liver nodules
  • Cirrhosis
  • Cholestasis

Eyes (affecting around 20%)

  • Uveitis
  • Conjunctivitis
  • Optic neuritis

Skin (affecting around 15%)

  • Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
  • Lupus pernio (raised, purple skin lesions commonly on cheeks and nose)
  • Granulomas develop in scar tissue

Heart (affecting around 5%)

  • Bundle branch block
  • Heart block
  • Myocardial muscle involvement

Kidneys (affecting around 5%)

  • Kidney stones (due to hypercalcaemia)
  • Nephrocalcinosis
  • Interstitial nephritis

Central nervous system (affecting around 5%)

  • Nodules
  • Pituitary involvement (diabetes insipidus)

Encephalopathy

  • Peripheral Nervous System (affecting around 5%)
  • Facial nerve palsy
  • Mononeuritis multiplex

Bones (affecting around 2%)

  • Arthralgia
  • Arthritis
  • Myopath
135
Q

What is Lofgren’s Syndrome

A

This is a specific presentation of sarcoidosis. It is characteristic by a triad of:

  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Polyarthralgia (joint pain in multiple joints)
136
Q

Differential Diagnosis of Sarcoidosis

A
  • Tuberculosis
  • Lymphoma
  • Hypersensitivity pneumonitis
  • HIV
  • Toxoplasmosis
  • Histoplasmosis
137
Q

Blood Tests of Sarcoidosis

A
  • Raised serum ACE. This is often used as a screening test.
  • Hypercalcaemia (rasied calcium) is a key finding.
  • Raised serum soluble interleukin-2 receptor
  • Raised CRP
  • Raised immunoglobulins
138
Q

Imaging for Sarcoidosis

A
  • Chest xray shows hilar lymphadenopathy
  • High-resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules
  • MRI can show CNS involvement
  • PET scan can show active inflammation in affected areas
139
Q

gold standard for sarcoidosis

A

The gold standard for confirming the diagnosis of sarcoidosis is by histology from a biopsy

140
Q

Sarcoidosis

WHat does biopsy show?

A

The histology shows characteristic non-caseating granulomas with epithelioid cells.

141
Q

Sarcoidosis

Tests for other organ involvement

A
  • U&Es for kidney involvement
  • Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
  • LFTs for liver involvement
  • Ophthalmology review for eye involvement
  • ECG and echocardiogram for heart involvement
  • Ultrasound abdomen for liver and kidney involvement
142
Q

Treatment for sarcoidosis

A
  • No treatment is considered as first line in patients with no or mild symptoms as the condition often resolves spontaneously.
  • Oral steroids are usually first line where treatment is required and are given for between 6 and 24 months. Patients should be given bisphosphonates to protect against osteoporosis whilst on such long term steroids.
  • Second line options are methotrexate or azathioprine
  • Lung transplant is rarely required in severe pulmonary disease
143
Q

What obstructive sleep apnoea

A

Obstructive sleep apnoea is caused by collapse of the pharyngeal airway during sleep. It is characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes. This is usually reported by the partner as the patient is unaware of these episodes.

144
Q

Risk Factors for sleep Obstructive sleep apnoea

A
  • Middle age
  • Male
  • Obesity
  • Alcohol
  • Smoking
145
Q

Features of sleep apnoea

A
  • Apnoea episodes during sleep (reported by partner)
  • Snoring
  • Morning headache
  • Waking up unrefreshed from sleep
  • Daytime sleepiness
  • Concentration problems
  • Reduced oxygen saturation during sleep
146
Q

Severe cases of OSA can cause _______,_____ ________ and can increase the risk of _________ _____ and ______

A

Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.

147
Q

Epworth Sleepiness Scale

A

The Epworth Sleepiness Scale is used to assess symptoms of sleepiness associated with obstructive sleep apnoea.

TOM TIP: If interviewing someone that you suspect has obstructive sleep apnoea ask about their daytime sleepiness and their occupation. Daytime sleepiness is a key feature that should make you suspect obstructive sleep apnoea. Patients that need to be fully alert for work, for example heavy goods vehicle operators, require urgent referral and may need amended work duties whilst awaiting assessment and treatment.

148
Q

Management of obstructive Sleep Apnoea

A

Referral to an ENT specialist or a specialist sleep clinic where they can perform sleep studies. This involves the patient sleeping in a laboratory whilst staff monitor their oxygen saturations, heart rate, respiratory rate and breathing to establish any apnoea episodes and the extent of their snoring.

The first step in management is to correct reversible risk factors by advising them to stop drinking alcohol, stop smoking and lose weight.

The next step is to use a continuous positive airway pressure (CPAP) machine that provides continuous pressure to maintain the patency of the airway.

Surgery is another option. This involves quite significant surgical restructuring of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).

Diseases (40 decks)

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