Respiratory COPY

Question 1

Pleural effusion definition and presentation

Answer 1

Abnormal accumulation of fluid in the pleural cavity

Dyspnea
Reduced exercise tolerance
Chest pain

Question 2

Pleural effusion examination findings

Answer 2

Tachypnoea
Cyanosis
Lymphadenopathy
Stony dull percussive sound on affected side
Reduced/absent breath sounds
Bronchial breathing at upper border
Vocal resonance reduced over the effusion
Reduced chest expansion

Question 3

Exudative pleural effusions

Answer 3

Protein content >35g/l

More likely to be unilateral
Caused by diseases that increase capillary permeability, such as:

Infections (parapneumonic effusion)
Malignancy
Inflammatory conditions
Pulmonary infarction
Pancreatitis
Chylothorax (collection of lymph in pleural space, usually secondary to trauma to the lymphatic system)

Question 4

Transudative pleural effusions

Answer 4

Protein content <35g/l

Caused by imbalance in Starling forces governing interstitial fluid:

Heart failure (most common transudate cause)
Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
Hypothyroidism
Meigs’ syndrome

Question 5

Light’s criteria

Answer 5

Developed to help distinguish between a transudate and an exudate

Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
If the protein level is between 25-35 g/L, Light’s criteria should be applied

An exudate is likely if at least one of the following criteria are met:
Pleural fluid protein divided by serum protein >0.5
Pleural fluid LDH divided by serum LDH >0.6
Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

Question 6

Pleural effusion investigations

Answer 6

Bloods - FBC, U&E, LFT, clotting
CXR (first line)
Thoracic ultrasound
CT scan with contrast
Pleural fluid sampling:

sent for biochem, cytology and microbiology
Also Glucose - most commonly low in rheumatoid arthritis or empyema
pH – <7.2 in empyema
Amylase – raised in pancreatitis
Cholesterol and triglycerides – raised in chylothorax
Immunology

Question 7

Recurrent pleural effusion management

Answer 7

Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
Drug management to alleviate symptoms e.g. opioids to relieve dyspnoea

Question 8

Asthma pathophysiology

Answer 8

Reversible airway obstruction

Often associated with family history of atopy, which includes the atopic triad of asthma, allergic rhinitis, and atopic eczema

Involves a type 1 hypersensitivity reaction, with allergens stimulating Type 2 helper T cells to produce cytokines like IL-4, IL-5, and IL-13. The inflammation of the respiratory airways results in bronchial hyperresponsiveness and reversible bronchoconstriction

Question 9

Asthma risk factors

Answer 9

Family history
Personal history of atopy
Maternal smoking
Viral infections
Lower socioeconomic status

Question 10

Asthma symptoms/signs

Answer 10

Wheeze
Dyspnoea
Cough (may be nocturnal)
Chest tightness
Diurnal variation (symptoms worse in the morning)

Symptoms may worsen following exercise, weather changes or following the use of nonsteroidal anti-inflammatory drugs (NSAIDs)/beta blockers

Tachypnoea
Hyperinflated chest
Hyper-resonance on chest percussion
Decreased air entry
Wheeze on auscultation

Question 11

Chronic asthma investigations

Answer 11

Peak flow diary (readings will be lower in variation the morning due to diurnal - variability >20% is diagnostic)

Bloods - total IgE and eosinophils
CXR to exclude other causes
Spirometry - FEV1/FVC <0.7, reversible with bronchodilator
FeNO - >40 in adults or >35 in children

Question 12

Chronic asthma management - non-pharmacological

Answer 12

Smoking cessation
Avoidance of precipitating factors (eg. known allergens)
Review inhaler technique

Question 13

Chronic asthma management - pharmacological

Answer 13

Step 1: short-acting inhaled β2 agonist (eg. salbutamol)

Step 2: add low-dose inhaled corticosteroid steroid (ICS)

Step 3: add long-acting β2 agonist (eg. salmeterol).

if no benefit, stop this and increase ICS dose
if benefit but inadequate control, continue and increase ICS dose

Step 4: trial of oral leukotriene receptor antagonist, high-dose steroid, oral β2 agonist, oral theophylline

Patients escalated to steps 3 and 4 should be referred to a respiratory specialist.

There are also now biologic therapies in the form of monoclonal antibodies

Question 14

Acute asthma presentation - severe attack

Answer 14

inability to speak in complete sentences
respiratory rate >25 breaths per minute
peak flow 33–50% predicted
heart rate >110 bpm

Question 15

Acute asthma presentation - life-threatening attack

Answer 15

peak flow <33% of predicted
silent chest
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

Question 16

Acute asthma investigations

Answer 16

Routine bloods inc FBC and CRP to look for underlying cause
CXR to exclude other diagnoses
ABG:

in a tachypnoeic patient
respiratory alkalosis is expected – owing to hyperventilation causing low paCO2
paO2 will likely be high

a falling respiratory rate is a sign of patient fatigue
paCO2 will return towards normal – this is a very concerning sign and the patient requires urgent escalation
type 2 respiratory failure (low paO2 and high paCO2) due to hypoventilation is a sign of a life-threatening attack

Question 17

Management of acute asthma

Answer 17

ABCDE approach

Ensure a patent airway
Ensure oxygen saturations of 94–98%
Nebulisers (eg. salbutamol, ipratropium)
Steroids – oral prednisolone or IV hydrocortisone (if severe asthma or unable to swallow)

If severe
Single dose of IV magnesium sulphate
IV aminophylline (if inadequate response to nebulised bronchodilator)

Question 18

Pneumonia definition

Answer 18

inflammatory condition of the lungs caused by infection. This leads to fluid and blood cells leaking into the alveoli. The infection spreads across the alveoli and eventually the lung tissue becomes consolidated, impairing the gas exchange due to reduced ventilation

Question 19

Common causes of pneumonia

Answer 19

streptococcus pneumonia (usually community acquired)
Haemophilus influenzae
Mycoplasma pneumoniae

Question 20

Pneumonia symptoms

Answer 20

Fever
Malaise
Rigors
Cough
Purulent sputum
Pleuritic chest pain
Haemoptysis

Question 21

Pneumonia signs

Answer 21

Tachypnoea
Tachycardia
Hypotension
Cyanosis
Pyrexia
Dull percussion
Increased vocal resonance/ tactile vocal fremitus
Bronchial breathing - this is a higher pitch and inspiration and expiration are equal. There is an audible pause between inspiration and expiration
Pleural rub is an audible sound heard in patients with pleurisy. It is caused by the layers of pleura rubbing against each other

Question 22

Hospital acquired pneumonia definition

Answer 22

lower respiratory tract infection that develops more than 48 hours after hospital admission. The most common organisms are Pseudomonas aeruginosa, Staphylococcal aureus, and Enterobacteria

Question 23

Aspiration pneumonia definition

Answer 23

occurs in patients with an unsafe swallow. Risk factors include stroke, myasthenia gravis, bulbar palsy, alcoholism, and achalasia. On chest x-ray the right lung is most commonly affected, as the right bronchus is wider and more vertical than the left bronchus, making it more likely to facilitate the passage of aspirate.

Question 24

Staphylococcal pneumonia

Answer 24

A bilateral cavitating bronchopneumonia due to staphylococcal aureus, a gram-positive cocci found in clusters.
It is found in intravenous drug users, elderly patients, or patients who already have an influenza infection.

Question 25

Klebsiella pneumonia

Answer 25

Primarily affects the upper lobes resulting in a cavitating pneumonia, presenting with “red-currant” sputum.
It is caused by a gram-negative anaerobic rod.
Furthermore, there is an increased risk of developing complications including empyema, lung abscesses and pleural adhesions.
Patients at risk of Klebsiella pneumonia are those with weakened immune systems such as elderly, alcoholics, and diabetics.
Additional at-risk groups include patients with malignancy, chronic obstructive pulmonary disease, long term steroid use and renal failure.

Question 26

Mycoplasma pneumonia

Answer 26

Presents with flu like symptoms consisting of flu, arthralgia, myalgia, dry cough and headache.
It primarily affects younger patients.
Additional features include auto-immune manifestation due to cold agglutinins causing an autoimmune haemolytic anaemia.
Complications that are associated with this pneumonia include: erythema multiforme; Stevens-Johnson Syndrome; Guillain-Barre Syndrome and meningoencephalitis

Question 27

Legionella pneumonia

Answer 27

Fever, myalgia and malaise followed by a dyspnoea and a dry cough. It is associated with Legionnaire’s disease, usually in patients who have been exposed to poor hotel air conditioning.

Look for hyponatraemia and deranged LFTs on blood tests. Legionella antigen may be present in the urine

Question 28

Chlamydophila psittaci pneumonia

Answer 28

Chlamydophila psittaci is an intracellular bacteria that results in psittacosis. It is acquired from contact with infected birds such as parrots, cattle, horse and sheep.
Features include lethargy, arthralgia, headache, anorexia, dry cough and fever.
Additional features include: hepatitis; splenomegaly; nephritis; infective endocarditis; meningoencephalitis and a rash

Question 29

Pneumocystis pneumonia

Answer 29

This is associated with patients who are immunosuppressed (malignancy or chemotherapy) or HIV positive.
The causative organism is known as pneumocystis jiroveci and is a fungus. In patients who are HIV-positive the risk of PCP increases when the CD4+ <200 cells/uL.
Symptoms include exertional dyspnoea, dry cough, and fever

Question 30

Pneumonia investigations

Answer 30

ABG
Bloods – FBC, U&E, LFT, ESR, CRP
Blood culture
Sputum for microscopy & culture
Polymerase chain reaction: for mycoplasma pneumonia
Urine antigen: for legionella and pneumococcal pneumonia
Chest X-ray: identify lobar, multi-lobar, cavitation and signs of pleural effusion

Question 31

Pneumonia scoring severity

Answer 31

CURB-65

C – confusion: An abbreviated mental test of ≤8

U – urea: >7mmol/L

R - Respiratory rate: ≥30/ min

B - blood pressure <90 systolic and/ or <60mmHg diastolic

65 - age: >65year old

Question 32

Pneumonia management

Answer 32

Oxygen to keep O2 saturations above 94%

Fluid management

Analgesia if patients have pleuritic chest pain. Paracetamol 1g/6 hours (Max. 4g 24hours)

Antibiotics can be given orally for patients who are not nil by mouth and are managed in the community. However, for severe pneumonia Intravenous route is required

Follow up appointments are organized for 6 weeks and CXR could be repeated at this time if there are complications or symptoms have not resolved

Question 33

Pneumothorax definition

Answer 33

the presence of air in the pleural space

Question 34

Pneumothorax signs/symptoms

Answer 34

Sudden onset shortness of breath
Pleuritic chest pain

Tachypnoea
Respiratory distress
Reduced chest expansion on affected side
Hyper-resonant percussion on affected side
Vocal resonance reduced on affected side
Tachycardia
Hypotension
Tracheal deviation to contralateral side

Question 35

Pneumothorax investigations

Answer 35

CXR

Question 36

Pneumothorax management - primary

Answer 36

rim of air <2cm and patient not short of breath then discharge or aspirate
If fails, insert chest drain

Question 37

Pneumothorax management - secondary

Answer 37

if patient >50 year old and/or rim of air is >2cm and/or patient short of breath

insert chest drain and admit for 24 hours

Question 38

Tension pneumothorax definition

Answer 38

Life-threatening emergency

ongoing, one-way leak into pleural space

as the pressure in this space increases, it will begin to displace the mediastinum, impeding venous return and cardiac output

this will eventually cause cardiovascular collapse and cardiac arrest

in a simple pneumothorax, air does not continue entering the pleural cavity in this way, so it does not cause tension

Question 39

Tension pneumothorax management

Answer 39

Initially ABCDE

High flow oxygen 15l/min via a non-rebreather mask
open thoracostomy followed by a chest drain
otherwise a needle decompression can be used with a 16-gauge cannula, which is inserted at the second intercostal space, mid-clavicular line, on the affected side

Question 40

Recurrent pneumothorax management

Answer 40

Smoking cessation
Avoid scuba diving

pleurodesis
bullectomy

Question 41

Lung cancer risk factors

Answer 41

Smoking (tobacco and cannabis)
Passive smoking
Occupational exposure (asbestos, silica, welding fumes, coal)
HIV
Organ transplantation
Radiation exposure (X-ray, gamma rays)
Beta-carotene supplements in smokers

Question 42

Lung cancer symptoms

Answer 42

Cough
Haemoptysis
Dyspnoea
Chest pain
Weight loss
Nausea and vomiting
Anorexia

Question 43

Lung cancer signs

Answer 43

Cachexia

Finger clubbing

Hypertrophic pulmonary osteoarthropathy

Anaemia

Horner syndrome (if the tumour is apical)

Examination of the chest:

consolidation (pneumonia)
collapse (absent breath sounds, ipsilateral tracheal deviation)
pleural effusion (stony dull percussion, decreased vocal resonance and breath sounds)
Enlargement of supraclavicular and axillary lymph nodes

Paraneoplastic syndromes:

Cushing syndrome – suggests small cell
syndrome of inappropriate ADH production (SIADH) – suggests small cell
Lambert–Eaton syndrome – suggests small cell
hyperparathyroidism – suggests squamous cell

Question 44

Features of squamous cell carcinoma

Answer 44

most common
presents as obstructive lesions of the bronchus leading to infection
occasionally cavitates
Hypercalcaemia (high PTHrp)
Clubbing
hypertrophic pulmonary osteoarthropathy

Question 45

features of adenocarcinoma

Answer 45

Commonly invades the mediastinal lymph nodes and the pleura, and spreads to the brain and bones
Does not usually cavitate
Proportionally more common in nonsmokers, women and people from the Far East – least likely to be related to smoking
Most likely to cause pleural effusion

Question 46

Features of small cell carcinoma

Answer 46

Arises from endocrine cells (Kulchitsky cells, which are APUD cells), so these tumours secrete many polypeptides, mainly adenocorticotrophic hormone (ACTH)
Can cause various presentations, such as Addison’s disease and Cushing syndrome
Spread very early – almost always inoperable at presentation
Do respond to chemotherapy, but the prognosis is generally poor

Question 47

Lung cancer investigations

Answer 47

Sputum cytology
CXR:
nodules
lung collapse
pleural effusion
consolidation
bony metastases
contract CT including adrenals and liver to check for metastases
Bronchoscopy – used to obtain a sample for histology

Endobronchial ultrasound transbronchial needle aspiration (EBUS-TBNA) – allows biopsy of lymph nodes, paratracheal and bronchial lung lesions for histology

Cardiovascular review and lung function tests should also be performed to assess the patient’s suitability for different treatment options

Question 48

COPD definition

Answer 48

Irreversible, usually progressive airway obstruction
Encompasses chronic bronchitis (hypertrophy and hyperplasia of the mucus glands in the bronchi) and emphysema (enlargement of the air spaces and destruction of alveolar walls)

Question 49

COPD symptoms

Answer 49

Productive cough
Recurrent respiratory infections
Wheeze
Dyspnoea
Reduced exercise tolerance
Weight loss

Question 50

COPD signs

Answer 50

Accessory muscle use for respiration
Prolonged expiratory phase
Pursed lip breathing
Tachypnoea
Hyperinflation – reduction of the cricosternal distance
Reduced chest expansion
Hyper-resonant percussion
Decreased/quiet breath sounds
Wheeze
Cyanosis
Cor pulmonale (signs of right heart failure)

Question 51

COPD investigations

Answer 51

Bloods

FBC – polycythaemia due to chronic hypoxia
ABG – reduced paO2 +/– raised paCO2 (may be acute or compensated type 2 respiratory failure)

ECG

P-pulmonale (right atrial hypertrophy)
Right ventricular hypertrophy, if there is cor pulmonale

Chest X-ray

Hyperinflated chest (>6 anterior ribs)
Bullae
Decreased peripheral vascular markings
Flattened hemidiaphragms

Spirometry – can be performed at diagnosis or to monitor progression

FEV1/FVC ratio <0.7
Increased TLC
Low TLCO – seen in patients who have significant emphysema without a significant chronic bronchitis element
Reversibility testing is not required unless history/examination fails to differentiate between asthma and COPD

Other tests:

Sputum culture – to identify exacerbating organisms
Brain natriuretic peptide (BNP) + echocardiogram – to assess for heart failure
Serum alpha-1 antitrypsin – to assess for genetic cause in young patients
Consider high-resolution CT (HRCT) scan if the diagnosis remains ambiguous

Question 52

COPD pharmacological management

Answer 52

Step 1: short-acting β2 agonist/short-acting muscarinic antagonist – these are continued as the patient goes up the management steps

Step 2: for patients with persistent exacerbations but no asthmatic features or evidence of steroid responsiveness

add a long-acting β2 agonist AND a long-acting muscarinic antagonist
for patients with persistent exacerbations with asthmatic features or evidence of steroid responsiveness

increase management to a combination of long-acting β2 agonist and ICS

Step 3: for patients on a long-acting β2 agonist + long-acting muscarinic antagonist combination who are still getting daily symptoms that affect their activities of daily living

consider a 3-month trial of long-acting muscarinic antagonist + long-acting β2 agonist + ICS (triple therapy)
if this does not work, revert back to long-acting β2 agonist + long-acting muscarinic antagonist
for any patient on step 2 who is getting more than one severe or two moderate exacerbations in a year

start long-acting muscarinic antagonist + long-acting β2 agonist + ICS

Step 4: if patients are still symptomatic, consider specialist referral

Question 53

COPD acute exacerbation management

Answer 53

Ensure a patent airway

Ensure oxygen saturations of 88–92% (if there is a history of CO2 retention)

Oral prednisolonw

Nebulisers – salbutamol, ipratropium

Steroids – oral prednisolone or IV hydrocortisone (if severe)

Antibiotics if any evidence of infection (eg. fever or raised inflammatory markers)

Monitor closely for signs of type 2 respiratory failure: drowsiness, asterixis, agitation as this may indicate the need for non-invasive ventilation (BiPaP)

Question 54

Chronic bronchitis pathophysiology

Answer 54

Chronic exposure to noxious particles such as smoking or air pollutants causes hypersecretion of mucus in the large and small bronchi
Airway inflammation and fibrotic changes result in narrowing of the airways and subsequently chronic airway obstruction
Cigarette smoke interferes with the action of cilia in removing noxious particles
Cigarette smoke also dampens the ability of leukocytes in eliminating the bacteria in the airways

Question 55

Emphysema pathophysiology

Answer 55

Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls
This reduces the alveolar surface area thus impeding efficient gaseous exchange
Cigarette smoke stimulates accumulation of neutrophils and macrophages which produce neutrophil elastase that destroys alveolar walls
In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase. However, in emphysema, the normal balance of proteases and antiproteases is lost. The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin
This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping

Question 56

COPD FEV1 severity scale

Answer 56

Stage 1 (mild): FEV1 more than 80% of predicted
Stage 2 (moderate): FEV1 50-79% of predicted
Stage 3 (severe): FEV1 30-49% of predicted
Stage 4 (very severe): FEV1 less than 30% of predicted

Question 57

Ratio of FEV1 to FVC below 70%

Answer 57

Obstructive lung disease

Question 58

Ratio of FEV1 to FVC above 70%

Answer 58

Restrictive lung disease

Question 59

Obstructive vs restrictive lung disease

Answer 59

Obstructive = difficulty with exhalation
Restrictive = difficulty with inhalation

Question 60

Type 1 respiratory failure

Answer 60

Pa O2 <8kPa, PaCO2 normal

Due to V/Q mismatch - volume of air passing in and out of the lungs is comparatively smaller than the volume of blood perfusing the lungs

Asthma
Congestive Cardiac Failure
Pulmonary embolism
Pneumonia
Pneumothorax
Low V/Q: areas that have poor ventilation with oxygen but are well perfused by blood. E.g. bronchoconstriction (Asthma), airway collapse in emphysema, mucus plug, congestive cardiac failure
High V/Q: areas of the lung with adequate ventilation but are lacking blood perfusion E.g. Pulmonary embolism

Question 61

Type 2 respiratory failure

Answer 61

PaO2 <8kPa, PaCO2 >6kPa

Due to alveolar hypoventilation - lungs fail to effectively oxygenate and blow off carbon dioxide

Obstructive lung diseases – Chronic obstructive pulmonary disease
Restrictive lung diseases - idiopathic pulmonary fibrosis
Depression of the respiratory center – opiates
Neuromuscular disease – Guillan-Barre syndrome, motor neuron disease
Thoracic wall disease – rib fracture

Question 62

PE definition

Answer 62

formation of a blood clot in the pulmonary arterial vasculature, typically stemming from an underlying deep vein thrombosis (DVT) in the lower limbs

Question 63

PE risk factors

Answer 63

Immobility (eg. bed-rest, long-haul flights)
Pregnancy
Oestrogen-containing medications – combined oral contraceptive pill, hormone replacement therapy (HRT)
Obesity
Age
Malignancy
Thrombophilia
Recent lower limb surgery or injury
Smoking

Question 64

PE signs/symptoms

Answer 64

triad of symptoms, although all three features are rarely present:
Sudden-onset shortness of breath
Pleuritic chest pain
Haemoptysis
Syncope is a concerning symptom indicating massive PE
A small PE may be asymptomatic

Tachypnoea
Tachycardia – may be the only presenting sign
Hypoxia
Low-grade pyrexia (possibly)

A massive PE may present with:
Hypotension
Cyanosis
Signs of right heart strain (eg. a raised JVP, parasternal heave and loud P2)

Question 65

PE investigations

Answer 65

ECG findings:

Normal or sinus tachycardia
In a massive PE, there may be evidence of right-heart strain – P pulmonale, right axis deviation, right bundle branch block, and nonspecific ST/T wave changes
The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III and inverted T waves in lead III) is relatively uncommon – <20% of patients

Bloods:

D-dimer - is highly nonspecific but has a 95% negative predictive value (ie. it is useful in ruling out a PE if negative)
FBC – the patient may be anaemic if the PE has caused haemoptysis
CRP – may be raised
U&E – to assess renal function before a CTPA
Clotting function – important if the patient is to be started on low-molecular weight heparin (LMWH)/warfarin

ABG - may be normal or show a type 1 respiratory failure and/or a respiratory alkalosis (from hyperventilation secondary to hypoxia)

Chest X-ray -typically normal in PE but helpful in ruling out differentials (eg. pneumonia, pneumothorax)

possible findings include:

Fleischner sign – an enlarged pulmonary artery
Hampton’s hump – a peripheral wedge shaped opacity
Westermark sign – regional oligaemia

CT pulmonary angiogram (CTPA) – the diagnostic test of choice for a PE, will show a filling defect in the pulmonary vasculature

V/Q scan – preferred if the patient has renal impairment, contrast allergy or is pregnant

Lower limb Duplex – helpful if a DVT is thought to be the cause of the PE (note: this investigation is first-line – before a CTPA – in pregnancy)

Bedside echocardiogram – used to check for signs of right heart strain/hypotension in intermediate to high-risk PE, done to assess suitability for thrombolysis

Question 66

Well’s coring system

Answer 66

3 points
clinical signs and symptoms of a DVT
if no alternative diagnosis is more likely than a PE

1.5 points
tachycardia (heart rate >100 beats/minute)
if the patient has been immobile for more than 3 days or has had major surgery within the last month
if the patient has had a previous PE or DVT

1 point
if the patient presents with haemoptysis
if there is an active malignancy

If 4 or less, measure D-dimer to rule out PE

If more than 4, diagnostic imaging required

Question 67

PE general management

Answer 67

Oxygen if hypoxic
Consider fluids if hypotensive
Analgesia
Consider IV fluids if the systolic blood pressure is <90 mmHg

Question 68

PE anticoagulation

Answer 68

administered if there is high clinical suspicion

can be started while awaiting confirmation on CTPA

First-line treatment = direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban

if neither suitable, dabigatran, edoxaban or warfarin (with low molecular weight heparin bridging), LMWH or unfractionated hepartin can be considered

In inpatient/emergency setting, low molecular weight heparin is usually started instead as it is shorter acting

provoked PE (identifiable risk factors, such as surgery or peripartum) should be treated for 3 months

An unprovoked PE should be treated for 6 months
If there is an ongoing cause (eg. thrombophilia), the patient should be treated for life
recurrence of venous thromboembolism in a patient already on warfarin requires an increase in the target INR (to 3–4)

Question 69

Massive PE management

Answer 69

defined as systolic blood pressure <90 mmHg (or >40 mmHg below patient’s baseline BP) for >15 minutes

treatment is thrombolysis (an IV bolus of Alteplase®)

there is an associated risk of haemorrhage but this it lower than the risk of death from PE
There is ongoing debate over whether Alteplase® should be administered in an intermediate–high risk (or submassive) PE

This should be considered on a case-by-case basis

Question 70

In COPD acute exacerbation give

Answer 70

Prednisolone for 5 days

Amoxicillin if purulent sputum or clinical signs of pneumonia

Question 71

Pneumectomy definition and CXR findings

Answer 71

Surgical procedure to remove a lung

opacified hemithorax with mediastinal and tracheal shift towards the affected side
Crowding of the ribs over the affected side with compensatory overinflation of normal lung is also seen
NB. filled with air for first ~6 months then fills with fluid

Question 72

The Centor criteria

Answer 72

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

to determine if a sore throat is bacterial in origin and should be treated via antibiotics (if 3 or more are met)