Respiratory Conditions Flashcards

1
Q

What is asthma

A

A chronic inflammatory airway disease characterised by episodic exacerbations of bronchoconstriction causing an obstruction to airflow going in and out of the lungs
This is a reversible airway obstruction which typically responds to bronchodilators scubas a salbutamol.

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2
Q

What is bronchoconstriction

A

Where the smooth muscles of the airways (the bronchi) contract, causing a reduction in the diameter in the airways

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3
Q

What causes bronchoconstriction in asthma

A

Airway hypersensitivity and can be triggered by environmental factors

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4
Q

What are the typical triggers of asthma

A
Infection
Night time or early morning
Exercise
Animals
Cold, damp or dusty air
Strong emotions
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5
Q

How does asthma present

A

Episodic symptoms
Diurnal variability, typically worse at night
Dry cough with wheeze and SOB
A history of other atopic conditions
Family history
Bilateral widespread polyphonic wheeze heard on auscultation

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6
Q

How is suspected asthma investigated

A

First line:

  • Fractional exhaled nitric oxide
  • Spirometry with bronchodilator reversibility

Follow up if uncertainty over diagnosis:

  • Peak flow variability (diary of several measurements a day for 2-4 weeks)
  • Direct bronchial challenge test with histamine or methacholine
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7
Q

How is asthma managed long term

A

Key treatments are:

  • Short acting beta 2 adrenergic receptor agonists (eg. salbutamol)
  • Inhaled corticosteroids (eg. beclometasone)
  • Long acting beta 2 agonists (eg. salmeterol)
  • Long acting muscarinic antagonists (eg. tiotropium)
  • Leukotriene receptor antagonists (eg. montelukast)
  • Theophylline
  • Maintenance and reliever therapy
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8
Q

How do short acting beta 2 adrenergic receptor agonists work in asthmatic patients

A

Work quickly but effect only lasts for an hour or two
Adrenalin acts on the smooth muscles of the airways to cause relaxation
This results in dilation of the bronchioles and improves the bronchoconstriction present in asthma
Used as reliever or rescue medication during acute exacerbations of asthma

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9
Q

How do inhaled corticosteroids work in asthmatic patients

A

Reduce the inflammation and reactivity of the airways

Used as maintenance or preventer medications and are taken regularly, even when well

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10
Q

How do long acting beta 2 agonists work in asthmatic patients

A

Adrenalin acts on the smooth muscles of the airways to cause relaxation
This results in dilation of the bronchioles and improves the bronchoconstriction present in asthma (same as short acting but have a much longer action)

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11
Q

How do long acting muscarinic antagonists work in asthmatic patients

A

Block acetylcholine receptors which are stimulated by the parasympathetic system and cause contracting of bronchial smooth muscles.
Blocking these receptors leads to bronchodilation

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12
Q

How do leukotriene receptor antagonists work in asthmatic patients

A

Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways.
These work by blocking the effects of leukotrienes

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13
Q

How does theophylline work in asthmatic patients

A

Relaxes the bronchial smooth muscle and reduces inflammation
Has a narrow therapeutic window and can be toxic in excess so monitoring plasma theophylline levels in the blood is required
Done 5 days after start of treatment and 3 days after each dose change

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14
Q

How does maintenance and reliever therapy work in asthmatic patients

A

A combination inhaler containing a low does inhaled corticosteroid and a fast acting LABA
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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15
Q

What is the stepwise ladder for asthma treatment according to NICE guidelines

A
  1. SABA as required for infrequent wheezy episodes
  2. Add a regular low dose inhaled corticosteroid
  3. Add an oral leukotriene receptor antagonist
  4. Add a LABA inhaler (continue only if good response)
  5. Consider changing to combined MART
  6. Increase inhaled corticosteroid to a moderate dose
  7. Consider increasing the inhaled corticosteroid to a high dose or oral theophylline or an inhaled LAMA
  8. Refer to specialist
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16
Q

What additional management should be provided for asthmatics

A

Self-management programme
Yearly flu jab
Yearly asthma review
Advise exercise and avoid smoking

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17
Q

What is acute asthma

A

An acute exacerbation asthma is characterised by a rapid deterioration in asthmatic symptoms which can be triggered by the typical asthma triggers

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18
Q

How does acute asthma present

A

Progressively worsening SOB
Use of accessory muscles
Fast respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
Chest can sound tight on auscultation with reduced air entry

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19
Q

How is acute asthma categorised

A

Moderate:
-PEFR 50-75% predicted

Severe:

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

Life-threatening:

  • PEFR <33%
  • O2 sats <92%
  • Becoming tired
  • No wheeze (airways so tight no air entry at all, AKA a ‘silent chest’)
  • Haemodynamic instability (ie. shock)
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20
Q

How is moderate acute asthma treated

A

Nebulised beta-2 agonist (salbutamol 5mg as often as necessary)
Nebulised ipratropium bromide
Oral prednisolone or IV hydrocortisone, continued for 5 days
Antibiotics if evidence of bacterial infection

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21
Q

How is severe acute asthma treated

A

O2 as required to maintain sats 94-98%
Aminophylline infusion
Consider IV salbutamol

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22
Q

How is life-threatening acute asthma treated

A

IV magnesium sulphate infusion
Admission to ICU or HDU
Intubation (decision to intubate should be made early as it is very difficult to intubate in sever bronchoconstriction

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23
Q

What will ABGs show in acute asthma

A

Initially, respiratory alkalosis as tachypnoea causes a drop in CO2

A normal pCO2 or hypoxia is concerning as it means patient is tiring and indicated life-threatening asthma

A respiratory acidosis due to high CO2 is a very bad sign

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24
Q

How are patients with acute asthma monitored for response to treatment

A
Respiratory rate
Respiratory effort 
Peak flow
O2 sats
Chest auscultation 

Also monitor serum potassium when on salbutamol as it causes potassium to be absorbed from blood into the cells and can also cause tachycardia

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25
Q

What is COPD

A

Chronic Obstructive Pulmonary Disease

A non-reversible, long term deterioration in air flow through the lungs, caused by damage to lung tissue due to smoking. The damage to the lung tissue causes an obstruction to the flow of air through the airways, making it more difficult to ventilate the lungs and making them more prone to infection

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26
Q

How does COPD present

A
Common:
Cough
Shortness of breath
Sputum production
Exposure to risk factors
Recurrent respiratory infections, especially in winter
Barrel chest
Hyper-resonance on percussion
Distant breath sounds on auscultation
Poor air movement on auscultation
Wheezing on auscultation
Coarse crackles
Uncommon:
Tachypnoea
Asterixis
Distended neck veins
Lower-extremity swelling
Fatigue
Weight loss
Muscle loss
Headache
Pursed lip breathing
Cyanosis
Loud P2
Hepatojugular reflux
Hepatosplenomegaly
Clubbing
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27
Q

What are the risk factors for COPD

A

Strong:
Cigarette smoking
Advanced age
Genetic factors

Weak:
White ancestry
Exposure to air pollution
Exposure to burning solid or biomass fuel
Occupational exposure to dusts, chemicals, vapors, fumes, or gases
Developmentally abnormal lung
Male sex
Low socio-economic status
Rheumatoid arthritis
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28
Q

What is the MRC (Medical Research council) dyspnoea scale

A

5 point scale for assessing the impact of patient’s breathlessness

Grades:

  1. Breathless on strenuous exercise
  2. Breathless on walking up hill
  3. Breathlessness that causes patient to slow when walking on flat
  4. Stop to catch breath after walking 100 meters on the flat
  5. Unable to leave the house due to breathlessness
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29
Q

How is a diagnosis of COPD made

A

Based on clinical presentation and spirometry

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30
Q

What will show on a COPD patient’s spirometry

A

An obstructive picture
Overall lung capacity (FVC) is not as bad as ability to quickly exhale air out of lungs (FEV1)
This is due to damage to airways causing airway obstruction
FEV1/FVC ratio <0.7
Also no dramatic response to reversibility testing with beta-2 agonists during spirometry test (if responsive then consider asthma as differential)

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31
Q

What does FVC stand for

A

Forced vital capacity

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32
Q

What does FEV1 stand for

A

Forced expiratory volume in 1 second

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33
Q

How is the severity of COPD graded

A

Using FEV1

  1. > 80% of predicted
  2. 50-79% of predicted
  3. 30-49% of predicted
  4. <30% of predicted
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34
Q

What investigations can be done in a case of suspected COPD

A
Spirometry
Chest x ray
FBC
BMI
Sputum culture
ECG
Echocardiogram
CT thorax
Serum Alph-1 antitrypsin
Transfer factor for carbon monoxide
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35
Q

What is the long term management of COPD

A

Smoking cessation is essential
Pneumococcal and anual flu vaccines

  1. short acting bronchodilators (beta 2 agonists) or short acting antimuscarinics

2.If not asthmatic or steroid responsive then have a combined LABA and a LAMA
If they are asthmatic or steroid responsive then have a LABA plus an ICS, if not enough then step up to LABA, LAMA and ICS combination inhaler

  1. In more severe cases options are:
    - Nebulisers
    - Oral theophylline
    - Oral mucolytic therapy to break down sputum
    - Long term prophylactic antibiotics
    - Long term oxygen therapy at home
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36
Q

When is long term oxygen therapy used in COPD

A

Severe COPD that is resulting in chronic hypoxia, polycythaemia, cyanosis, or heart failure secondary to pulmonary hypertension (cor pulmonale)
Cannot be used if they smoke as significant fire hazard

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37
Q

What is an exacerbation of COPD

A

An acute worsening of symptoms, such as a cough, SOB, sputum production, and wheeze, which is usually caused by a viral or bacterial infection

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38
Q

What are Venturi masks

A
Oxygen masks that are designed to deliver a specific concentration of oxygen by allowing some of the oxygen to escape out the side of the mask and normal air to be inhaled along with oxygen 
Blue: 24% O2
White: 28% O2
Orange: 31% O2
Yellow: 35% O2
Red: 40% O2
Green: 60% O2
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39
Q

What is the general rule regarding target o2 sats in COPD patients

A

If CO2 retaining, aim for O2 sats of 88-92% titrated by Venturi mask
If not CO2 retaining and normal bicarbonate (meaning do not normally retain CO2) then aim for O2 sats over 94%

40
Q

Why should a patient who is CO2 retaining be on lower dose of O2

A

Too much oxygen in someone that is prone to retaining CO2, can depress respiratory drive, slowing their breathing rate and effort and leading to retaining more CO2

41
Q

What is the treatment for an exacerbation of COPD

A

Home:

  • prednisolone 30mg daily for 7-14 days
  • regular inhalers or home nebulisers
  • antibiotics if evidence of bacterial infection

Hospital:

  • nebulised bronchodilators
  • steroids (eg 200mg hydrocortisone or 30-40mg prednisolone)
  • antibiotics if evidence of bacterial infection
  • physiotherapy to help clear sputum

In severe or unresponsive to treatment cases:

  • IV aminophylline
  • Non-invasive ventilation (NIV)
  • Intubation and ventilation with admission to ICU
  • Doxapram as a respiratory stimulant when NIV or intubation not appropriate
42
Q

What are the differentials for COPD

A
Asthma
Congestive heart failure
Bronchiectasis
Tuberculosis
Bronchiolitis
Upper airway dysfunction
Chronic sinusitis/ postnasal drip
Gastro-oesophageal reflux disease (GORD)
ACE inhibitor induced chronic cough
Lung cancer
43
Q

What are the types of lung cancer

A

Non-small cell lung cancer:

  • Squamous cell carcinoma (35%)
  • Adenocarcinoma (25%)

Small cell lung cancer (20%):

  • contain neurosecretory granules that release neuroendocrine hormones
  • responsible for multiple paraneoplastic syndromes
44
Q

How common is lung cancer

A

Third most common cancer in the UK behind breast and prostate

45
Q

What are the signs and symptoms of lung cancer

A
SOB
Cough
Haemoptysis
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy (often supraclavicular nodes are the first to be found on examination)
46
Q

How is lung cancer investigated

A

Chest Xray is first line:

  • Hilar enlargement
  • Peripheral opacity (a visible lesion in the lung field)
  • Pleural effusion (usually unilateral in cancer)
  • Lung collapse

Staging CT scan of chest, abdomen and pelvis to establish the stage and check for lymph node involvement and metastasis. This should be contrast enhanced to give more detailed information about the different tissues

PET-CT (positron emission tomography):

  • inject a radioactive tracer (usually attached to glucose molecules)
  • takes images using a combination of CT scanner and a gamma ray detector to visualise how metabolically active the tissues are
  • useful in identifying areas that the cancer has spread

Bronchoscopy with endobronchial ultrasound:

  • endoscopy with ultrasound equipment on the end of the scope
  • allows detailed assessment of the tumour and ultrasound guided biopsy

Histological diagnosis:

  • to check the types of cells in the cancer requires biopsy
  • can be done by bronchoscopy or percutaneously (through the skin)
47
Q

How is lung cancer treated

A

Surgery:

  • first line for isolated non-small cell lung cancer
  • intention is to cure the cancer
  • lobectomy (removing the lung lobe containing the tumout) is first line
  • segmentectomy or wedge resection (taking a segment or wedge of lung to temove the tumour) is another option

Radiotherapy:
-Can also be curative in non-small cell lung cancer when diagnosed early enough

Chemotherapy:

  • Offered in addition to surgery or radiotherapy (adjuvant chemotherapy)
  • Or as palliative treatment to improve survival and QOL in later stages of non-small cell lung cancer (palliative chemotherapy)

Treatment for small cell lung cancer:
-Usually chemotherapy and radiotherapy

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

48
Q

What is the prognosis for lung cancer patients

A

Prognosis is generally worse for small cell lung cancer compared with non-small cell lung cancer

Extrapulmonary manifestations:

Recurrent laryngeal nerve palsy:

  • presents with a hoarse voice
  • caused by the cancer pressing on or affecting the nerve as it passes through the mediastinum

Phrenic nerve palsy:

  • due to nerve compression
  • causes diaphragm weakness
  • presents as SOB

Superior vena cava obstruction:

  • complication of lung cancer
  • caused by direct compression of the tumour on the superior vene cava
  • presents with facial swelling, difficulty breathing, distended veins in the neck and upper chest
  • Pemberton’s sign is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency

Horner’s syndrome:

  • a triad of partial ptosis, anhidrosis and miosis
  • can be caused by a pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion

Syndrome of inappropriate ADH (SIADH):

  • caused by ectopic ADH secretion by a small cell lung cancer
  • presents with hyponatraemia

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

Hypercalcaemia:
-caused by ectopic parathyroid hormone from a squamous cell carcinoma

Limbic encephalitis:

49
Q

What is mesothelioma

A
  • Lung malignancy affecting the mesothelial cells of the pleura
  • Strongly linked to asbestos inhalation
  • Huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years
  • The prognosis is very poor
  • Chemotherapy can improve survival but it is essentially palliative
50
Q

What is limbic encephalitis

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
  • causes symptoms such as short term memory impairment, hallucinations, confusion and seizures
  • associated with anti-Hu antibodies
51
Q

What is Horner’s syndrome

A
  • a triad of partial ptosis, anhidrosis and miosis

- can be caused by a pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion

52
Q

What are the risk factors for lung cancer

A
Tobacco smoking
Second hand smoke
Radon exposure 
Asbestos exbosure
Exposure to other carcinogens
Arsenic in drinking water
Previous radiation therapy to the lungs
Air pollution 
PMH or FH of lung cancer
53
Q

What is a pneumothorax

A

Pneumothorax occurs when air gets into the pleural space, separating the lung from the chest wall.

54
Q

What is a tension pneumothorax

A

Tension pneumothorax is caused by trauma to the 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 in to 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 vessel in the mediastinum and cause cardiorespiratory arrest

55
Q

How common is a pneumothorax

A

In England and Wales, overall rate of presentation is 24/100,000 a year for men and 10/100,000 a year for women

56
Q

What causes pneumothorax

A
  • Spontaneous
  • Trauma
  • Iatrogenic (eg due to lung biopsy, mechanical ventilation, central line insertion)
  • Lung pathology (eg infection, asthma or COPD)
57
Q

What are the risk factors for pneumothorax

A
Strong:
Smoking
Family history of pneumothorax
Tall and slender body build
Age <40 y/o
Recent invasive medical procedure
COPD
Chest trauma
Acute severe asthma
Tuberculosis
AIDS-related Pneumocystis jirovecii infection
Cystic fibrosis
Lymphangioleiomyomatosis
Birt-Hogg-Dibe syndrome
Pulmonary Langerhans cell histiocytosis
Erdheim-Chester disease
Weak:
Marfan syndrome
Homocystinuria
Primary lung cancer
Metastatic cancer to the lungs
58
Q

How does pneumothorax present

A
Common:
Chest pain
Dyspnoea
Ipsilateral reduced breath sounds
Ipsilateral reduced breath sounds
Ipsilateral hyperinflation of the hemithorax with hyperresonance on percussion
Hypoxia
Uncommon:
Cardiopulmonary deterioration
Trachea shifted to the contralateral side
Sweating
Cough
59
Q

What are the signs of a tension pneumothorax

A
  • Tracheal deviation away from side of the pneumothorax
  • Reduced air entry on the affected side
  • Increased resonant percussion on the affected side
  • Tachycardia
  • Hypotension
60
Q

What are the differentials for a suspected pneumothorax

A
Acute asthma exacerbation
Acute COPD exacerbation
PE
Myocardial ischaemia
Pleural effusion
Bronchopleural fistula
Fibrosing lung disease
Oesophageal perforation
Giant bullae
61
Q

How is a suspected pneumothorax investigated

A

Erect chest X-ray:

  • first line for suspected simple pneumothorax
  • 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 end and the pneumothorax begins

Measuring the size of the pneumothorax:

  • on a chest xray
  • in accordance to the BTS guidelines from 2010
  • involves measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum

CT thorax:

  • can detect a pneumothorax that is too small to see on a chest xray
  • can also be used to accurately measure the size of the pneumothorax
62
Q

What are the important patient discussions to have with those diagnosed with pneumothorax

A

Explain that they are at increased risk of future pneumothoraces and so should seek immediate medical attention if their symptoms recur.

Advise smoking cessation

Can return to work and resume normal physical activity once symptoms have resolved

Instruct not to fly for at least 1 week after resolution of a pneumothorax

Resolution must be confirmed on chest xray

63
Q

What is the treatment plan for those diagnosed with pneumothorax

A

Simple pneumothorax:
-If no SOB and there is <2cm rim of air on the xray, then no treatment is required and 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, then will require a chest drain
  • Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain

Tension pneumothorax:

  • Insert a large bore cannula into the second intercostal space in the midclavicular line
  • If suspected, do not wait for supporting investigations
  • Once the pressure is relieved with a cannula then a chest draine is required for definitive management

Chest drain:

  • Inserted in the triangle of safety
  • Traingle formed by:
    • 5th intercostal space (or the inferior nipple line)
    • Mid axillary line (or the lateral edge of the latissimus dorsi)
    • Anterior axillary line (or the lateral edge of the pectoris major)
  • Needle is inserted just above the rib, to avoid the neurovascular bundle that runs just below the rib
  • Once the drain is inserted, obtain a chest xray to check the positioning
64
Q

What is the prognosis for those with a pneumothorax

A

Between 30-50% of patients will have an ipsilateral recurrent spontaneous pneumothorax

65
Q

What is a pleural effusion and the two types

A

A pleural effusion is a collection of fluid in the pleural cavity.
This can be exudative menaing there is a high protein count (more than 3g/l) or transudative menaing there is a relatively lower protein count (less than 3g/l)

66
Q

How common is a pleural effusion

A

~1.5 million people develop a pleural effusion in the US every year with the leading cause being congestive heart failure

67
Q

What causes a pleural effusion

A

Cause is determined by whether it is exudative or transudative

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

  • Lung cancer
  • Pneumonia
  • Rheumatoid arthritis
  • Tuperculosis

Transudative causes relate to fluid moving across into the pleural space (trans-meaning moving across) Causes:

  • Congestive cardiac failure
  • Hypoalbuminaemia
  • Hypothyroidism
  • Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
68
Q

What are the risk factors for pleural effusion

A

Strong:

  • Congestive heart failure
  • Pneumonia
  • Malignancy
  • Recent coronary artery bypass graft surgery

Weak:

  • Pulmonary embolism
  • Recent MI
  • Occupational lung disease
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Renal failure
  • Drug induced pleural effusion
  • Recent ovarian stimulation treatment
  • Chylothorax
69
Q

How does a pleural effusion present

A
  • Dyspnoea
  • Dullness to percussion over the effusion
  • Pleuritic chest pain
  • Cough
  • Quieter breath sounds
  • Decreased or absent tactile fremitus
  • Tracheal deviation away from the effusion if it is massive
70
Q

What are the differentials in suspected pleural effusion

A
Pleural thickening
Pulmonary collapse and consolidation
Elevated hemidiaphragm
Pleural tumours/ extrapleural fat
COVID-19
71
Q

How is a suspected pleural effusion investigated

A

Chest xray:

  • Blunting of costophrenic angle
  • Fluid in the lung fissures
  • Larger effusion will have a meniscus
  • 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:

  • proetin count
  • cell count
  • pH
  • glucose
  • LDH
  • microbiology testing
72
Q

What are the important discussions to have with patients diagnosed with pleural effusion

A

Patients who have a procedure that may insert air into the cavity surrounding their lung (thoracentesis, thoracoscopy, or tube thoracostomy) should be advised to avoid high altitudes, scuba diving, or flying in unpressurised aircraft until they are cleared by their physician.

73
Q

How is a pleural effusion treated

A

Conservative management:
-appropriate for small effusions as they will resolve with treatment of the underlying cause

Larger effusions often need aspiration or drainage

Pleural aspiration involves sticking a needle through the chest wall into the effusion and aspirating the fluid. This can temporarily relieve the pressure but the effucion may recur and repeated aspiration may be required

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

74
Q

What is pneumonia

A

An infection of the lung tissue.
It causes inflammation of the lung tissue and production of sputum that fills the airways and alveoli
Can be seen as consolidation on a chest xray

75
Q

What is the epidemiology of pneumonia

A

Globally, lower respiratory tract infections are the most deadly infectious disease, resulting in 3 million deaths worldwide in 2016

Community acquired pneumonia is a serious health problem with high morbidity and mortality in all age groups worldwide, and is a major burden on healthcare resources

76
Q

What causes pneumonia

A

Common causes:

  • Streptococcus pneumoniae (50%)
  • Haemophilius influenzae (20%)

Other causes:

  • Moraxella catarrhalis (in immunocompromised pts or those with chronic pulmonary disease)
  • Pseudomonas aeruginosa (in pts with cystic fibrosis or bronchiectasis)
  • Staphylococcus aureus (in pts with cystic fibrosis)
Atypical pneumonia causes:
(legions of psittaci MCQs)
Legions - Legionella pneumophila
Psittaci - Chlamydia psittaci
M - Mycoplasma pneumoniae
C - Chlamydophila pneumoniae
Qs - Q fever (coxiella burnetii)

Fungal pneumonia:
Pneumocystis jiroveci pneumonia (PCP) occurs in patients that are immunocompromised

77
Q

What are the risk factors for pneumonia

A

Strong:

  • Age >65 y/o
  • Residence ina gealthcare setting
  • COPD
  • Exposure to cigarette smoke
  • Alcohol abuse
  • Poor oral hygeine
  • Use of acid reducing drugs
  • Contact with children

Weak:

  • Diabetes
  • CKD
  • Chronic liver disease
  • Use of opioids
78
Q

How does pneumonia present

A

SOB
Cough producing sputum
Fever
Haemoptysis
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis

79
Q

What signs may a patient with pneumonia have on examination

A
Derangement in basic observations
Can indicate sepsis secondary to the pneumonia
-Tachypnoea (raised resp rate)
-Tachycardia (raised heart rate)
-Hypoxia (low oxygen)
-Hypotension (shock)
-Fever
-Confusion

Characteristic chest signs:

  • Bronchial breath sounds (harsh breath sounds equally loud on inspiration and expiration, caused by consolidation of lung tissue around the airway)
  • Focal coarse crackles (air passing through sputum in the airways similar to using a straw to blow air through a drink)
  • Dullness to percussion (due to lung tissue collapse and/or consolidation)
80
Q

What are the differentials in suspected pneumonia

A
COVID-19
Acute bronchitis
Congestive heart failure
COPD exacerbation
Asthma exacerbation
Bronchiectasis exacerbation
Tuberculosis
Lung cancer or lung metastases
Empyema
Pulmonary embolism
Pneumothorax
Hypersensitivity pneumonitis
81
Q

How is a patient with suspected pneumonia investigated

A

Chest Xray
FBC (raised white cells)
U and Es (for urea)
CRP (raised in inflammation and infection)

Patients with moderate or sever cases should also have:

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

Patients that are immuncompromised may not show an inflammatory response and may not have raised inflammatory markers despite severe infection

82
Q

What is the severity assessment for pneumonia

A

CURB-65 score in hospital
CRB-65 score in community (same but without Urea)

A CRB-65 score of anything other than 0 should be referred to hospital

C- confusion
U- urea >7
R- respiratory rate of at least 30
B- blood pressure <90 systolic or <60 diastolic
65- age at least 65

The CURB 65 score predicts mortality:

  • Score 1 = under 5%
  • Score 3 = 15%
  • Score 4/5 = over 25%
83
Q

How is pneumonia treated

A

Treat with antibiotics

Always follow your local area guidelines as created with local antibiotic resistance in mind
Typical abx course:
-Mild CAP: 5 day course of oral abx (amoxicillin or macrolide)
-Moderate to severe CAP: 7-10 day course of dual abx (amoxicillin and macrolide)

84
Q

What are potential complications of pneumonia

A
  • Sepsis
  • Pleural effusion
  • Empyema
  • Lung abscess
  • Death
85
Q

What is empyema

A

A collection of pus in the pleural space

86
Q

What is a pulmonary embolism

A

A condition where a blood clot (thrombus) forms in the pulmonary arteries.

87
Q

What causes a pulmonary embolism

A

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.

Once in the pulmonary arteries the thrombus will 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)

88
Q

What are the risk factors for a PE

A
Increasing age
DVT diagnosis
Surgery within the last 2 months
Bed rest >5 days
Long haul flights
Previous VTE event
FH of VTE
Active malignancy
Recent trauma or fracture
Pregnancy/ postnatal period
Paralysis of the lower extremities
Factor V Leiden mutation
Prothrombin G20210A mutation
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Antiphospholipid antibody syndrome
Obesity
Smoking
COPD
Sepsis
89
Q

How does a PE present

A

SOB (dyspnoea)
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemoynamic instability causing hypotension
Positive Wells or Geneva score
Failure to meet PERC rule
Signs and symptoms of a DVT (eg. unilateral leg swelling and tenderness)

90
Q

What is the PERC rile

A
The pulmonary embolism rule-out criteria
Used when have low clinical suspicion of PE
Where risk of PE is considered to be lower than the risk of testing for PE
Rule is:
-Age <50y/o
-Heart rate <100bpm
-O2 sats >95% on air
-No unilateral leg swelling 
-No haemoptysis
-No recent surgery or trauma (<4 weeks ago)
-No prior PE or DVT
-No hormone use 

Request D-dimer testing for any patient in who the PERC rile fails to rule out a PE (ie. one or more criteria not fulfilled)

91
Q

What are the differentials in suspected PE

A
Unstable angina
NSTEMI
STEMI
Community acquired pneumonia
Acute bronchitis
Acute COPD exacerbation
Acute asthma exacerbation
Acute CHF exacerbation
Pericarditis
Cardiac tamponade
Pulmonary hypertension due to chronic thromboembolic disease
Pneumothorax
Costochondritis
Panic disorder
92
Q

How is a suspected PE investigated

A
History
Examination
Chest Xray
Perform a Wells Score:
-Likely: do a CT pulmonary angiogram
-Unlikely: do a d-dimer and if positive then do a CTPA

D-dimer is a sensitive but not specific blood test for VTE. Can be raised in:

  • DVT
  • PE
  • Pneumonia
  • Malignancy
  • Heart failure
  • Surgery
  • Pregnancy

Two main investigations for establishing cause:

  • CTPA
  • Ventilation Perfussion (VQ) scan

1st line investigations:

  • CTPA
  • Echo
  • D-dimer
  • FBC
  • ECG
  • U and Es
  • Coagulation studies
  • LFTs

Investigations to consider:

  • ABG
  • Chest Xray
  • Lower limb compression venous ultrasound
  • Cardiac biomarker
  • VQ scan
  • Further investigation for unprovoked PE

Emerging tests:

  • Biomarkers
  • Point of care D-dimer testing
  • D-dimer adjusted to clinical probability
  • Magnetic resonance angiograpy (MRA)
93
Q

What should be discussed with a patient diagnosed with PE

A

Patient education is essential before starting warfarin
Need to have regular INR testing and follow-ups
Make sure the patient is aware of the details of warfarin

94
Q

How is a PE treated

A

Supportive management:

  • Admission to hospital
  • O2 as required
  • Analgesia is required
  • Adequate monitoring for deterioration

Initial management:
-Treatment dose low molecular weight heparin (LMWH) started immiediately before confirming the diagnosis in patients where DVT or PE is suspected (eg Enoxaparin and dalteparin)

Switching to long term anticoagulation:
Options for long term anticoagulation in VTE are:
-Warfarin
-NOAC or DOACs (oral anticoagulations that are not warfarin which do not require monitoring. Main options are apixaban, dabigatran and rivaroxaban)
-LMWH

Thrombolysis:

  • Where there is a massive PE with haemodynamic compromise
  • Injects a fibrinolytic medication (they brake down fibrin)
  • Rapidly dissolves clots
  • Significant risk of bleeding which can make it dangerous
  • Only used where the benefits outweigh the risk
  • Some examples are streptokinase, alteplase and tenecteplase
  • Can be performed IV using a peripheral cannula
  • Or directly into the pulmonary arteries using a central catheter (catheter-directed thrombolysis)
95
Q

What are the potential complications of a PE

A
Acute bleeding during treatment
Pulmonary infarction
Cardiac arrest/ death
Chronic thromboembolic pulmonary hypertension
Heparin associated thrombocytopenia
Recurrent venous thromboembolic event
Death