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Phase 2a > Respiratory COPY > Flashcards

Respiratory COPY Flashcards

1
Q

What is chronic obstructive pulmonary disease? What is its pathophysiology? How is it different to asthma? What may COPD patients experience? What are the two main types?

A
  • NON-REVERSIBLE long-term deterioration in air flow through the lungs, caused by damage to lung tissue (almost always due to SMOKING)
  • Px: obstructed airflow through the airways → difficulty ventilating the lungs → short of breath and prone to infection
  • Unlike asthma, NOT REVERSIBLE with bronchodilators i.e. salbutamol.
  • Patients may experience exacerbations; if due to infections, these are called INFECTIVE EXACERBATIONS (IE COPD)
  • 2 main types:

– Chronic Bronchitis

– Emphysema

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2
Q

What are the risk factors for COPD?

A
  • Smoking
  • Age - symptoms usually present between 40-60
  • Secondhand smoke exposure
  • Occupational exposure - mining, dust, cotton, wood
  • Pollution - heating fuel, outdoor pollutants
  • Genetics - Alpha-1-antitrypsin deficiency. A1AT is a protein made by the liver and functions to protect the lungs from damage caused by infection, inflammation and smoking
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3
Q

What are the classic presenting features of COPD? What does COPD not cause?

A
  • LONG-TERM SMOKER
  • SHORTNESS OF BREATH
  • Cough
  • Sputum production
  • Wheeze
  • RECURRENT RESPIRATORY INFECTIONS
  • COPD does NOT cause clubbing
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4
Q

How is COPD graded?

A
  • Grade 1: Breathless on strenuous exercise
  • Grade 2: Breathless on walking up hill
  • Grade 3: Breathless that slows on the flat
  • Grade 4: Stop to catch breath after 100m walking on flat
  • Grade 5: Unable to leave house due to breathlessness
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5
Q

How is COPD diagnosed? What is the value of the FEV1/FVC ratio in COPD? What does COPD not respond to? How can the severity of airways obstruction be measured?

A
  • COPD diagnosed by using CLINICAL PRESENTATION + SPIROMETRY
  • Spirometry will show an ‘OBSTRUCTIVE PICTURE’ - overall lung capacity is better than their ability to forcefully expire air quickly
  • FEV1/FVC ratio = <0.7
  • Does not respond to reversibility testing with SABA, e.g. salbutamol
  • FEV1 can be used to grade severity of airways obstruction i.e. Stage 1 = >80% of predicted, Stage 4 = <30% of predicted
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6
Q

Apart from clinical presentation and spirometry, what are the other investigations for COPD?

A
  • Chest X-ray (exclude lung cancer/other pathologies)
  • FBC (chronic hypoxia → polycythemia)
  • BMI (weight loss i.e. Lung Ca)
  • ECG - if concerns with cardiac function
  • Serum Alpha-1-antitrypsin levels
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7
Q

What would be shown on a CXR for COPD?

A
  • Hyperinflation
  • Bullae
  • Flat hemidiaphragm
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8
Q

What are the symptoms and complications of emphysema?

A
  • ‘Pink puffers’
  • Symptoms:
  • Dyspnoea/tachypnoea
  • Minimal cough
  • Pink skin, pursed-lip breathing
  • Accessory muscle use
  • Cachexia
  • Hyperinflation (barrel chest)
  • Weight loss (due to increased work of breathing and cachexia)
  • Complications = pneumothorax due to bullae
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9
Q

What are the symptoms of chronic bronchitis?

A
  • ‘Blue bloaters’
  • Symptoms:
  • Chronic productive cough - purulent sputum
  • Dyspnoea
  • Cyanosis (hypoxaemia) - can cause secondary polycythemia, may develop pulmonary hypertension (reactive pulmonary vasoconstriction)
  • Peripheral oedema
  • Obesity
  • Haemoptysis
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10
Q

What is the long-term management of COPD?

A
  • General:
  • STOP SMOKING!!! Refer to smoking cessation
  • Pneumococcal vaccine
  • Annual flu vaccine
  • Step 1:
  • SABA (i.e. salbutamol or terbutaline) OR SAMA (ipratropium bromide)
  • Step 2:
  • If no asthmatic / steroid response:
  • LABA (i.e. salmeterol) + LAMA (i.e. tiotropium), switch SAMA to SABA
  • If asthmatic / steroid response:
  • LABA (i.e. salmeterol) + ICS (i.e. budesonide), switch SAMA to SABA. If still S.O.B. then LAMA + LABA + ICS
  • Step 3:
  • Long-term oxygen therapy (LTOT)
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11
Q

Under what circumstances would we give long-term oxygen therapy?

A
  • FEV1 < 30% predicted
  • Cyanosis
  • Polycythaemia
  • Peripheral oedema
  • Raised JVP
  • O2 less than or equal to 92% on room air
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12
Q

What is the acute management for COPD?

A

1) Bronchodilators and O2
2) Oral prednisolone
3) CPAP before intubation and ventilation

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13
Q

What is the clinical presentation of IE COPD?

A

Presents with acute worsening of symptoms i.e. SoB, sputum, wheeze. Usually triggered by infection

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14
Q

What are the investigations for IE COPD?

A
  • ABG:
  • CO2 retention → acidosis
  • Are they in type 1 or 2 failure?
  • Normal pCO2 + low pO2 = T1RF
  • Raised pCO2 + low pO2 = T2RF
  • Chest X-Ray, sputum culture + sensitivities for antibiotic therapy, FBC + U&E
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15
Q

Describe the management for IE COPD.

A
  • STEROIDS (hydrocortisone / prednisolone) + NEBULISED BRONCHODILATORS (salbutamol / ipratropium bromide) + ANTIBIOTICS
  • Physiotherapy → sputum clearance
  • If severe: IV aminophylline (bronchodilator), non-invasive ventilation (CPAP / BIPAP)
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16
Q

What is tuberculosis caused by? What are its features?

A
  • Tuberculosis (TB) is caused by mycobacterium tuberculosis bacteria:
  • Aerobic, non-motile, non-sporing, slightly curved bacilli with a thick waxy capsule
  • Acid-fast bacilli – turns red/pink with Ziehl-Neelsen stain
  • Slow growing
  • Resistant to phagolysosomal killing and able to remain dormant
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17
Q

What is the epidemiology of tuberculosis?

A
  • Majority of cases in Africa and Asia (India and China)
  • Cause of death for most people with HIV
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18
Q

What is the pathophysiology of TB?

A
  • TB spread via respiratory droplets as it is an airborne infection
    1. Alveolar macrophages ingest bacteria and the rods proliferate inside
    2. Drain into hilar lymph nodes 🡪 present antigen to T lymphocytes 🡪 cellular immune response
    3. Delayed hypersensitivity reaction 🡪 tissue necrosis and granuloma formation: caseating
    a. PRIMARY GHON FOCUS - seen as a small, calcified nodule in the upper parts of the lower lobes or the lower parts of the upper lobes
    b. GHON COMPLEX – Ghon focus + lymph nodes
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19
Q

What is the clinical presentation of tuberculosis?

A
  • Systemic symptoms: weight loss, low grade fever, anorexia, drenching night sweats, malaise
  • Pulmonary symptoms: productive cough, haemoptysis, cough >3 weeks (dry or productive), breathlessness, sometimes chest pain
  • Signs: signs of bronchial breathing, dullness to percuss, decreased breathing, fever, crackles
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20
Q

What are the investigations for tuberculosis?

A
  • Ziehl-Neelsen stain on Lowenstein-Jensen agar
  • CXR: primary or reactivated = patchy consolidation, fibronodular opacities on upper lobe, disseminated military TB = ‘millet seeds’
  • Biopsy: shows caseating granuloma
  • Diagnosing latent TB:
  • MANTOUX TEST - tuberculin injected into intradermal space, >5mm = positive result
  • INTERFERON-GAMMA RELEASE ASSAYS (IGRA) - person with previous contact with TB will have WBCs that release interferon-gamma
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21
Q

What is the appearance of different types of TB on a chest x-ray?

A
  • Primary TB: patchy consolidation, pleural effusions and hilar lymphadenopathy
  • Reactivated TB: patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones
  • Disseminated Miliary TB: MILLET SEEDS
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22
Q

Describe the management for TB.

A
  • Acute pulmonary TB (RIPE):
  • Rifampicin for 6 months. Bacteriacidal - blocks protein synthesis. SE: RED URINE, hepatitis
  • Isoniazid for 6 months. Bacteriacidal - blocks cell wall synthesis. SE: neuropathy
  • Pyrazinamide for 2 months. Bacteriacidal initially, less effective later. SE: gout, arthralgia, rash, hepatitis
  • Ethambutol for 2 months. Bacteriostatic, blocks cell wall synthesis. SE: optic neuritis
  • Latent TB - otherwise healthy patients do not need treatment, but isoniazid can be used for patients at risk of reactivation of TB
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23
Q

A patient is started on RIPE for acute pulmonary tuberculosis. What should also be prescribed? Why?

A

Pyridoxine (vitamin B6). This is because isoniazid has a side effect on peripheral neuropathy

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24
Q

What is cystic fibrosis? What is it caused by?

A
  • Cystic fibrosis = an AUTOSOMAL RECESSIVE genetic condition affecting the mucus glands
  • It is caused by a genetic mutation of the CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATORY GENE on chromosome 7
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25
Q

What are the key consequences of cystic fibrosis?

A
  • THICK PANCREATIC AND BILIARY SECRETIONS that cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract
  • LOW VOLUME THICK AIRWAY SECRETIONS that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections
  • CONGENITAL BILATERAL ABSENCE OF THE VAS DEFERENS in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility
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26
Q

Both parents are healthy, one sibling has cystic fibrosis and a second child does not have the disease, what is the likelihood of the second child being a carrier of cystic fibrosis?

A

2/3 - we know that the child doesn’t have the condition

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27
Q

How is cystic fibrosis generally diagnosed? What is often the first sign of cystic fibrosis?

A
  • CF is screened for at birth with the NEWBORN BLOODSPOT TEST
  • MECONIUM ILEUS is often the first sign - first stool (always black) is thick and sticky, causing it to get stuck and obstruct the bowel
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28
Q

If not diagnosed at birth, how does cystic fibrosis present later on in childhood?

A
  • RECURRENT LOWER RESPIRATORY TRACT INFECTIONS
  • FAILURE TO THRIVE
  • PANCREATITIS
  • Chronic cough
  • Thick sputum production
  • Steatorrhoea
  • ‘SALTY’ to kiss - concentrated salt in sweat
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29
Q

What are the three key methods for establishing a diagnosis of cystic fibrosis?

A
  • NEWBORN BLOOD SPOT TESTING is performed on all children shortly after birth and picks up most cases
  • SWEAT TEST = gold standard for diagnosis
  • Genetic testing for CFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling, or as a blood test after birth
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30
Q

Patients with cystic fibrosis struggle to clear the secretions in their airways. This creates a perfect environment with plenty of moisture and oxygen for colonies of bacteria to live and replicate. Give two important examples of key colonisers.

A

Staphylococcus aureus and pseudomonas aeruginosa

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31
Q

Describe the management of cystic fibrosis.

A
  • Chest physiotherapy to clear mucus and reduce risk of infection
  • Exercise and high calorie diet
  • Nebulised DNase (dornase alfa)
  • CREON tablets to digest fats in those with pancreatic insufficiency
  • Prophylactic flucloxacillin to reduce the risk of bacterial infections (particularly staph. aureus)
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32
Q

What is pneumonia? What does it cause? What is the aetiology of pneumonia? What are the different types of pneumonia?

A
  • Pneumonia = inflammation of the alveoli caused by infection
  • Aetiology: typically caused by a bacterial infection of the distal airways and alveoli with the formation of an inflammatory exudate
  • Different types:
  • Community acquired pneumonia
  • Hospital acquired pneumonia
  • Atypical pneumonia
  • Pneumonia in immunocompromised patients
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33
Q

What is community acquired pneumonia? What is its epidemiology? What are its commonest causes? What is responsible for producing rusty sputum?

A
  • Community acquired pneumonia = pneumonia acquired outside the hospital or healthcare facilities
  • Epidemiology:
  • Commoner in the extremes of age
  • Commonest causes: STREPTOCOCCUS PNEUMONIAE, HAEMOPHLIUS INFLUENZAE, mycoplasma pneumoniae
  • RUSTY SPUTUM IS CHARACTERISTIC OF STREP. PNEUMONIAE
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34
Q

What is hospital acquired pneumonia? What are its causes?

A
  • Hospital acquired pneumonia = an acute lower respiratory tract infection that is acquired after at least 48 hours of admission to hospital and is not incubating at the time of admission
  • Causes:
  • Most cases are caused by bacteria that are AEROBIC GRAM-NEGATIVE BACILLI. Examples (PEK): Pseudomonas aeruginosa, E. coli and Klebsiella pneumoniae
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35
Q

What is atypical pneumonia? What are its common causative organisms? What are its characteristic symptoms?

A
  • Bacterial pneumonia caused by atypical organisms that are not detectable on Gram stain and cannot be cultured using standard methods
  • Common organisms (MCL): Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila
  • Characteristic symptoms: headache + low-grade fever + cough + malaise
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36
Q

What is pneumocystis jirovecii pneumonia caused by? Who does it cause disease in?

A
  • Cause by fungus pneumocystis jirovecii
  • Causes disease in severely immunocompromised such as HIV +ve patients with CD4 < 200
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37
Q

What is the pathophysiology of pneumonia?

A

Invasion and overgrowth of a pathogen in lung parenchyma -> overwhelming of host immune defences -> production of intra-alveolar exudates

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38
Q

What are the symptoms and signs of pneumonia?

A
  • Dyspnoea
  • Pleuritic chest pain (sharp chest pain worse on inspiration)
  • Fever
  • Productive cough
  • SEPSIS
  • Signs: dull to percussion, decreased O2 sats, increased resp rate & heart rate, low BP + increased tactile fremitus
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39
Q

What are the signs on auscultation for pneumonia?

A
  • Decreased air entry
  • Wheezing
  • Course crackles
  • Bronchial breath sounds
  • Increased vocal resonance
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40
Q

What is used to measure the severity of pneumonia? What does it stand for?

A
  • CURB-65:
  • Confusion
  • Urea >7
  • Respiratory rate >30
  • Blood pressure < 90 systolic or < 60 diastolic
  • 65 - age > 65
  • 0-1= outpatient treatment, 2 = short-stay inpatient treatment OR hospital-supervised outpatient treatment, and 3-5 = manage as high-severity pneumonia
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41
Q

Describe the investigations for pneumonia.

A
  • FBC - increased WBC, increased urea, increased CRP
  • Sputum culture
  • Chest X ray = gold standard: localised/widespread consolidation, effusion, abscesses, empyema:

o Multi-lobar – strep pneumoniae, s. aureus

o Multiple abscesses – s. aureus

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42
Q

Describe the treatment for pneumonia.

A
  • Maintaining O2 Sats between 94-98%. In COPD patients: maintain O2 sats between 88-92%
  • Analgesia: paracetamol or NSAIDs
  • IV fluids
  • CURB-65 guided treatments:
  • 0 – 1: AMOXICILLIN 5 DAYS 500MG at home
  • 2: AMOXICILLIN (IV or oral) + macrolide (clarithromycin, erythromycin)
  • 3+ : consider ITU, IV CO-AMOXICLAV + MACROLIDE
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43
Q

What are the complications of pneumonia?

A
  • Sepsis
  • Pleural effusion
  • Empyema
  • Lung abscess
  • Death
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44
Q

What is bronchiolitis? What is it usually caused by? What is its epidemiology?

A
  • Bronchiolitis = inflammation and infection in the bronchioles
  • This is usually caused by a virus. RESPIRATORY SYNCYTIAL VIRUS (RSV) is the most common cause
  • Epidemiology: generally considered to occur in children <1 year (most common in children <6 months)
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45
Q

Why does a virus in the airways affect children more?

A

When a virus affects the airways of adults, swelling and mucus are proportionally small = little noticeable effect on breathing. The airways of infants are very small to begin with, so even the smallest amount of inflammation and mucus in the airway has a significant effect on the infants ability to circulate air to the alveoli and back out. This causes the harsh breath sounds, wheeze and crackles heard on auscultation when listening to a bronchiolitic baby’s chest

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46
Q

What is the clinical presentation of bronchiolitis?

A
  • CORYZAL SYMPTOMS (running or snotty nose, sneezing, mucus in throat and watery eyes)
  • Signs of respiratory distress
  • Dyspnoea
  • Tachypnoea
  • Wheeze and crackles on auscultation
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47
Q

What are the signs of respiratory distress in children?

A
  • Raised respiratory rate
  • Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
  • Intercostal and subcostal recessions
  • Nasal flaring
  • Head bobbing
  • Tracheal tugging
  • Cyanosis (due to low oxygen saturation)
  • Abnormal airway noises
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48
Q

Most infants with bronchiolitis can be managed at home. What are some reasons for admission?

A
  • Aged <3 months or any pre-existing condition such as prematurity, Downs syndrome or cystic fibrosis
  • 50 – 75% or less of their normal intake of milk
  • Clinical dehydration
  • Respiratory rate above 70
  • Oxygen saturations below 92%
  • Moderate to severe respiratory distress, such as deep recessions or head bobbing
  • Apnoeas
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49
Q

Describe the general management for bronchiolitis.

A
  • Typically patients only require supportive management. This involves:
  • Ensuring adequate intake
  • Saline nasal drops and nasal suctioning
  • Supplementary oxygen if the oxygen saturations remain below 92%
  • Ventilatory support if required - capillary blood gases are useful in severe respiratory distress and in monitoring children who have ventilatory support
  • PALIVIZUMAB = MAb given to high risk babies
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50
Q

What is bronchiectasis? What are its causes?

A
  • Bronchiectasis is the permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall
  • Causes:
  • Cystic fibrosis
  • Airway obstruction, e.g. cancer
  • Infections, e.g. aspergillosis, H.influenzae (most common)
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51
Q

What is the clinical presentation of bronchiectasis?

A
  • Cough
  • Sputum production
  • Crackles
  • Haemoptysis
  • Recurrent chest infections
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52
Q

What are the investigations for bronchiectasis?

A
  • CXR - KERLEY B LINES - increased bronchial markings at lung periphery
  • Sputum culture - H. influenzae most common
  • High resolution CT - dilated bronchi/bronchioles
  • FBC
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53
Q

Describe the treatment for bronchiectasis.

A
  • Bronchodilators - beta-2 agonists, e.g. albuterol
  • Inhaled corticosteroids, e.g. fluticasone
  • Antibiotics (1st line in acute exacerbation), e.g. amoxicillin
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54
Q

What is a pleural effusion? What are the two types?

A
  • Pleural effusion = collection of fluid in the pleural cavity (between visceral and parietal pleura)
  • Can be EXUDATIVE (high protein count) or TRANSUDATIVE (low protein count)
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55
Q

What is the pathophysiology of pleural effusion?

A

Rate of fluid formation > rate of fluid removal = fluid accumulates = pleural effusion

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56
Q

What are the 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
  • RA
  • TB
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57
Q

What are the 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)
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58
Q

What is the clinical presentation of pleural effusion?

A
  • SHORTNESS OF BREATH (effusion occupies space in the thoracic cavity and decreases lung volume)
  • Cough
  • Stony dullness to percussion over the effusion
  • Reduced breath sounds
  • Tracheal deviation away from the effusion if large effusion
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59
Q

What are the investigations for pleural effusions?

A
  • 1st line = CXR
  • Thoracocentesis identifies and diagnoses underlying cause
  • Pleural ultrasound
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60
Q

How does pleural effusion appear on a chest x-ray?

A
  • BLUNTING of the COSTOPHRENIC ANGLE
  • FLUID in lung fissures
  • Meniscus
  • Tracheal and mediastinal deviation if large effusion
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61
Q

Describe the treatment for pleural effusion.

A
  • Dependent on cause:
  • Fluid overload or congestive HF - diuretic
  • Infective - antibiotics
  • Large effusions often need aspiration or drainage
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62
Q

In which individuals do we tend to find pneumocystis jirovecii pneumonia in? What is its clinical presentation? Describe its treatment.

A
  • Pneumocystis jirovecii pneumonia occurs in patients that are immunocompromised - particularly those with poorly controlled or new HIV with CD4 < 200
  • 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
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63
Q

What is pharyngitis? What is its aetiology?

A
  • Acute pharyngitis is characterised by the rapid onset of sore throat and pharyngeal inflammation (with or without exudate)
  • Common viral causes:
  • EBV
  • Adenoviruses
  • Enteroviruses
  • HIV, chlamydia and gonorrhoea should be considered in sexually active people, especially those negative for Group A strep.
  • Also can be caused by GROUP A STREPTOCOCCUS
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64
Q

What is the clinical presentation of pharyngitis? Which factors suggest a Group A strep. infection compared to a viral infection?

A
  • Sore throat
  • Fever
  • Headache, myalgia skin rashes, swollen lymph nodes in the neck
  • Viral = runny nose, blocked nose, sneezing, cough
  • Group A strep. (bacterial) = pharyngeal exudates, cervical lymphadenopathy, fever, absence of cough or rhinorrhoea
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65
Q

What are the investigations for pharyngitis?

A

Clinical symptoms consistent with Group A strep infection:

  • Rapid antigen detection tests for Group A strep
  • Conventional throat culture
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66
Q

Describe the treatment for pharyngitis.

A

Confirmed Group A strep?

NO = supportive care (paracetamol and ibuprofen)

YES = phenoxymethylpenicillin (or clarithromycin if penicillin allergy) for 7-10d

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67
Q

What is otitis media? What is its aetiology?

A
  • Otitis media: infection in the middle ear
  • Most common bacterial cause = STREPTOCOCCUS PNEUMONIAE. Others = H.influenzae, Moraxella catarrhalis, Staph. aureus
  • Viral causes: RSV, rhinovirus, adenovirus, influenza virus
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68
Q

What are the risk factors for otitis media?

A
  • Young age
  • Male sex
  • Smoking
  • Frequent contact with other children
  • Family history
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69
Q

What is the pathophysiology of otitis media?

A
  • Infection of nasal passages, eustachian tube and middle ear causes inflammation and impairs mucociliary action and ventilatory function of the eustachian tube
  • Middle ear effusion develops and bacteria grows
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70
Q

What is the clinical presentation of otitis media?

A
  • Otalgia
  • Preceding URTI symptoms, e.g. Coryzal symptoms
  • Fever
  • Hearing issues
  • Sleep disturbance
  • Irritability in children
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71
Q

What are the investigations for otitis media?

A

Otoscope - bulging and erythema of the tympanic membrane

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72
Q

Describe the management of otitis media.

A

*Consider admitting children younger than 3 months, children 3- 6 months with T >39

  • 1st line = regular analgesia: ibuprofen/paracetamol - most cases will resolve in 3-7 days without antibiotics
  • For people who do not require admission but systemically unwell/ would benefit from antibiotics:
  • Amoxicillin 5-7 day course, clarithromycin (in penicillin allergy) and erythromycin (in pregnant women allergic to pencillin)
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73
Q

What is sinusitis? What is its aetiology?

A
  • Inflammation of the mucous membrane of the nasal cavity and paranasal sinuses - also known as acute rhinosinusitis. It is very common
  • Aetiology:
  • Common cause is a viral infection
  • Some cases progress onto acute bacterial sinusiti: Strep. pneumoniae, H. influenzae, Moraxella catarrhalis
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74
Q

What are the risk factors for sinusitis?

A
  • Nasal pathology, e.g. septal deviation or nasal polyps
  • Recent local infection, e.g. rhinitis or dental extraction
  • Swimming/diving
  • Smoking
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75
Q

What is the pathophysiology of sinusitis?

A

Viral infection = inflammatory response within sinonasal mucosa = ↑oedema and mucus production which blocks ventilation and drainage = ↓mucocilliary clearance and stasis of secretions = secondary bacterial infection

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76
Q

What is the clinical presentation of sinusitis?

A
  • Viral = symptoms <10 days: clear nasal discharge, fever, sore throat
  • Bacterial = symptoms >10 days: purulent nasal discharge, nasal obstruction, dental/ facial pain, headache
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77
Q

What are the investigations for sinusitis?

A
  • Diagnosis is clinical. Distinguish between viral and bacterial infection:
  • Viral: peak early and gradually resolve, symptoms for <10 days, clear nasal discharge, fever, sore throat
  • Bacterial: symptoms for >10 days, purulent nasal discharge, nasal obstruction, dental/facial pain, headache
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78
Q

Describe the management for sinusitis.

A
  • Acute viral sinusitis - analgesia and nasal decongestants, intranasal corticosteroids if symptoms over 10 days
  • Acute bacterial sinusitis - PHENOXYMETHYLPENICILLIN in 1st line if severe
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79
Q

What is epiglottitis? How common is it? What is its aetiology?

A
  • Epiglottitis = inflammation and swelling of the epiglottis caused by infection = airway emergency, especially in children
  • Now rare due to routine vaccination programme, which vaccinates all children against haemophilus
  • Aetiology: infection of supraglottis classically with H.influenzae type B, although others such as S.pneumoniae
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80
Q

What is the pathophysiology of acute epiglottitis?

A

Infection of epiglottis - swelling of the epiglottis which then obstructs the airways

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81
Q

What is the clinical presentation of acute epiglottitis?

A
  • Acute onset high fever 39-40
  • SORE THROAT and STRIDOR
  • TRIPODING (sat forward with a hand on each knee)
  • Toxic appearance
  • Dysphagia
  • Difficulty breathing
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82
Q

What are the investigations for acute epiglottitis?

A
  • If patient is acutely unwell and epiglottitis is suspected then investigations SHOULD NOT be performed
  • Laryngoscopy during intubation in an operating theatre
  • Lateral neck radiography if laryngoscopy not possible - THUMB PRINT SIGN
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83
Q

Describe the management of epiglottitis.

A
  1. Secure airway:
    - Direct rigid laryngoscopy and intubation is most useful
    - Mask ventilation follows commonly
  2. IV antibiotics, e.g. cefotaxime, ceftriaxone
  3. Supplemental O2 and possibly heliox as a temporising measure and maybe corticosteroids
    - DO NOT DISTURB CHILD WITH ORAL EXAMINATION OR TRYING FOR IV ACCESS AS IT CAN RESULT IN RESPIRATORY DISTRESS
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84
Q

What is croup? Which individuals does it typically affect? What is its aetiology?

A
  • Croup is an acute infective respiratory disease affecting young children. It is an upper respiratory tract infection causing oedema in the larynx
  • It typically affects children aged 6 months to 2 years, however they can be older
  • Aetiology:
  • PARAINFLUENZA VIRUS
  • RESPIRATORY SYNCYTIAL VIRUS (RSV)
  • Influenza
  • Adenovirus
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85
Q

What is the clinical presentation of croup?

A
  • Increased WORK OF BREATHING
  • “BARKING” cough, occurring in clusters of coughing episodes
  • Hoarse voice
  • Stridor
  • Low grade FEVER
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86
Q

Describe the management for croup.

A
  • Most cases can be managed at home with supportive treatment (fluids and rest)
  • Oral DEXAMETHASONE is very effective
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87
Q

What is empyema? What are the risk factors? What is the mortality?

A
  • Empyema = the presence of pus in the pleural space
  • Risk factors: pneumonia, iatrogenic intervention in the pleural space, diabetes, and alcohol abuse
  • Mortality is 15-20%
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88
Q

What is the clinical presentation of empyema?

A
  • Pyrexia and rigors
  • Productive cough
  • Pleuritic chest pain
  • Dyspnoea
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89
Q

What are the investigations for empyema?

A
  • Blood cultures
  • CRP
  • WBC count
  • CXR
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90
Q

Describe the management of empyema.

A
  • Awaiting culture results:
  • 1st line = IV empirical antibiotics (cefuroxime or ceftriaxone) PLUS chest tube drainage
  • Culture results available:
  • Antibiotics according to culture sensitivity PLUS chest tube drainage PLUS supportive care
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91
Q

What is asthma? What is its aetiology?

A
  • Asthma = chronic, inflammatory condition, causing episodes of reversible airway obstruction, due to bronchoconstriction and excessive secretion production
  • Aetiology: bronchoconstriction caused by hypersensitivity of the airways - triggered by various factors:
  • Cold air, exercise
  • Cigarette smoke
  • Air pollution
  • Allergens: pollen, cats, dogs, horses, mould
  • Time of day: early morning, night
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92
Q

What is the clinical presentation of asthma?

A
  • Episodes of wheeze (BILATERAL, WIDEPSREAD POLYPHONIC), breathlessness, chest tightness and dry cough
  • Atopy (family/personal history)
  • Diurnal variability
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93
Q

What are the investigations for asthma?

A
  • 1st line investigations:
  • SPIROMETRY WITH REVERSIBILITY TESTING (>5 years). Obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7
  • FRACTIONAL EXHALED NITRIC OXIDE (adults >40pbb, child- >35pbb)
  • If there is diagnostic uncertainty after the first line investigations these can be followed up with further testing:
  • Peak flow measurement
  • Direct bronchial challenge test with histamine or methacholine
94
Q

Describe the treatment for asthma.

A
  • KNOW THIS (Med school love it):
    1. SABA (e.g. salbutamol)
    2. Inhaled corticosteroid (ICS, e.g. budesonide)
    3. Leukotriene receptor antagonist (e.g. montelukast)
    4. LABA (e.g. salmeterol). In adults we STOP LTRA, in children we CONTINUE LTRA if needed
    5. Increase ICS dose
95
Q

Describe the management for an acute asthma attack.

A

O SHIT ME:

  • Oxygen
  • Salbutamol nebulisers
  • Hydrocortisone IV (or oral prednisolone)
  • Ipratropium bromide nebulisers
  • Theophylline
  • IV Magnesium Sulphate
  • Escalate to anaesthetist for I+V

This isn’t exact - salbutamol and ipratropium can be given together, magnesium often before aminophylline

96
Q

What is pneumothorax? What is the typical patient in an exam?

A
  • Pneumothorax occurs when air gets into the pleural space
  • Typical patient in exams is a tall, thin young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports
97
Q

What are the different causes of pneumothorax?

A
  • Spontaneous (spontaneous pneumothorax)
  • Trauma (traumatic pneumothorax - TENSION PNEUMOTHORAX is caused by trauma to the chest that creates a one-way valve)
  • Iatrogenic (iatrogenic pneumothorax)
  • Lung pathology, e.g. infection, asthma, COPD
  • Tension
98
Q

What are the risk factors for pneumothorax?

A
  • Smoking
  • Family history
  • Male
  • Tall and slender build
  • Young age
  • Presence of underlying lung disease
99
Q

What is the pathophysiology of pneumothorax?

A
  • Normally intrapleural pressure is negative
  • When there is a bridge between alveoli and pleural space or atmosphere and pleural space
  • Flow of air in until communication closed or gradient closed
100
Q

What is the clinical presentation of pneumothorax?

A
  • Stable patient
  • Sudden onset pleuritic patient chest pain, dyspnoea or cough
101
Q

What are the investigations for pneumothorax? What will they show?

A
  • 1st line = ERECT CHEST X-RAY. Reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall
  • Other investigations:
  • Bloods - clotting
  • US - if patient immobile
  • CT - if CXR uncertain
  • ABG if sats <92% on RA
102
Q

Describe the management for pneumothorax.

A
  • No shortness of breath and less than a 2cm visible rim of air on the chest x-ray:
  • NO TREATMENT is required as it will spontaneously resolve
  • Follow up in 2 – 4 weeks is recommended
  • Shortness of breath and/or more than a 2cm visible rim of air on the chest x-ray:
  • Aspiration followed by reassessment
  • When aspiration fails twice, a chest drain is required (into the TRIANGLE OF SAFETY)
103
Q

What is tension pneumothorax?

A
  • Trauma to the chest creates a ONE-WAY VALVE mechanism - air can enter the pleural space but cannot exit
  • Increased positive pressure within the chest
  • This pressure will push the MEDIASTINUM across, kink the big vessels in the mediastinum and cause CARDIORESPIRATORY ARREST
104
Q

What is the clinical presentation of tension pneumothorax?

A
  • Cardiopulmonary deterioration: hypotension - imminent cardiac arrest, respiratory distress, low sats, tachycardia, shock
  • Severe chest pain
  • TRACHEAL DEVIATION to the contralateral side
  • Ipsilateral reduced breath sounds
  • Hyperresonance on percussion
  • Hypoxia
105
Q

Describe the management of tension pneumothorax.

A
  • If a tension pneumothorax is suspected do not wait for any investigations
  • Need to learn: INSERT A LARGE BORE CANNULA INTO THE PLEURAL SPACE THROUGH THE SECOND INTERCOSTAL SPACE IN THE MID-CLAVICULAR LINE
  • Once the pressure is relieved with a cannula then a chest drain is required for definitive management
106
Q

What is whooping cough? What is it caused by? Why is it called whooping cough? Are people vaccinated against this?

A
  • Whooping cough = upper respiratory tract infection caused by Bordetella pertussis (a gram negative bacteria). It is called “whooping cough”, because the coughing fits are so severe that the child is unable to take in any air between coughs and subsequently makes a loud whooping sound as they forcefully suck in air after the coughing finishes
  • Children and pregnant women are vaccinated against pertussis
107
Q

What is the clinical presentation of whooping cough?

A
  • Typically starts with mild coryzal symptoms, low grade fever and mild dry cough
  • Severe coughing fits starts after a week or more - paroxysmal cough. Patient typically produces a large, loud inspiratory whoop when the coughing ends
108
Q

What are the investigations for whooping cough?

A
  • A nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks of the onset of symptoms
  • Where the cough has been present for more than 2 weeks patients can be tested for the ANTI-PERTUSSIS TOXIN IMMUNOGLOBULIN G
109
Q

Describe the management for whooping cough.

A
  • Pertussis is a notifiable disease. Therefore, PHE need to be notified of each case
  • Management typically involves simple supportive care
  • MACROLIDE ANTIBIOTICS, e.g. erythromycin and clarithromycin can be beneficial within the first 21 days or invulnerable patients. Co-trimoxazole is an alternative to macrolides.
  • Close contacts with an infected patient are given PROPHYLACTIC ANTIBIOTICS if they are in a vulnerable group, e.g. pregnant women
110
Q

Name a key complication of whooping cough.

A

Bronchiectasis

111
Q

What is interstitial lung disease? What are the different diseases to study?

A
  • Interstitial lung disease = umbrella term used to describe conditions that affect the lung parenchyma (tissue) causing inflammation and fibrosis (replacement of normal elastic lung tissue with stiff scar tissue):
  • Idiopathic pulmonary fibrosis (IPF)
  • Sarcoidosis
  • Occupational lung disorders: silicosis, asbestosis, hypersensitivity pneumonitis
  • Systemic disease: granulomatosis with polyangiitis, Goodpasture’s syndrome
112
Q

What is idiopathic pulmonary fibrosis? What is its epidemiology?

A
  • Idiopathic pulmonary fibrosis = formation of scar tissue in the lungs with no known cause
  • Epidemiology: most common interstitial lung disease. 2/3 >60 when presenting, M>F. Poor prognosis - life expectancy of 2-5 years from diagnosis
113
Q

What is the clinical presentation of idiopathic pulmonary fibrosis?

A
  • BIBASAL FINE INSPIRATORY CRACKLES and FINGER CLUBBING
  • Dyspnoea
  • Dry cough
114
Q

What are the investigations for idiopathic pulmonary fibrosis?

A

High resolution CT: GROUND GLASS appearance

115
Q

Describe the treatment for idiopathic pulmonary fibrosis.

A
  • Pharmacological: pirfenidone and nintedanib (MAb targeting tyrosine kinase)
  • Non-pharmacological: smoking cessation, physiotherapy, vaccines up to date
  • Lung transplantation = last resort
116
Q

What is silicosis/asbestosis?

A

Lung fibrosis related to the inhalation of silicone/asbestos

117
Q

What is the clinical presentation of silicosis/asbestosis?

A
  • Dyspnoea on exertion, dry cough, normal chest on auscultation
  • Onset >10 years after initial exposure in asbestosis
  • Bibasal inspiratory crackles in asbestosis
118
Q

What are the investigations for silicosis/asbestosis?

A
  • CXR
  • Spirometry (restrictive pattern)
  • HRCT
119
Q

Describe the treatment for silicosis/asbestosis.

A
  • Remove exposure
  • Smoking cessation
  • Symptom treatment
120
Q

What are the complications of asbestosis?

A
  • Pleural thickening
  • Mesothelioma
121
Q

What is hypersensitivity pneumonitis?

A

Type III hypersensitivity reaction, causing alveolar and bronchial inflammation, after exposure to an inhaled allergen (also called pigeon fancier’s, farmer’s, mushroom worker’s lung etc. = IF THEY HAVE EXPOSURE TO BIRDS THEN IT’S HYPERSENSITIVITY PNEUMONITIS

122
Q

What is the clinical presentation of hypersensitivity pneumonitis?

A
  • Dyspnoea
  • Cough
  • Fever
  • Malaise
  • Weight loss
123
Q

What are the investigations for hypersensitivity pneumonitis?

A

Bronchoalveolar lavage: raised lymphocytes, mast cells

124
Q

Describe the treatment for hypersensitivity pneumonitis.

A
  • Remove allergens
  • Steroids
125
Q

What is sarcoidosis? What is its epidemiology?

A
  • Sarcoidosis is a granulomatous inflammatory condition (granulomas are nodules of inflammation full of macrophages)
  • Epidemiology: two spikes (young adulthood and >60), women, black people (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)
126
Q

What is the clinical presentation of sarcoidosis?

A
  • Sarcoidosis can affect almost any organ in the body, but predominantly affects the lungs
  • Lungs: mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules
  • There is a specific presentation of sarcoidosis (Lofgren’s syndrome). It is characterised by:
  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Polyarthralgia (joint pain in multiple joints)
127
Q

What are some differential diagnoses for sarcoidosis?

A
  • Tuberculosis
  • Lymphoma
  • Hypersensitivity pneumonitis
  • HIV
128
Q

What are the investigations for sarcoidosis? What will they show?

A
  • Blood tests: raised serum ACE (this is often used as a screening test), hypercalcaemia is a key finding, raised serum soluble interleukin-2 receptor, raised CRP
  • CXR and CT shows hilar lymphadenopathy
  • Gold standard = biopsy. Histology shows NON-CASEATING GRANULOMAS with EPITHELIOID CELLS
129
Q

Describe the treatment for sarcoidosis.

A
  • NO TREATMENT is considered 1st line in patients with no or mild symptoms as resolves
  • ORAL STEROIDS = 1st line in patients who require treatment. Should be given bisphosphonates to protect against osteoporosis as long-term steroid course
  • Second line = methotrexate or azathioprine
130
Q

What is Goodpasture’s syndrome?

A

Autoimmune ANTI-GLOMERULAR BASEMENT MEMBRANE disease, where ANTIBODIES ATTACK the BASEMENT MEMBRANE in LUNGS AND KIDNEYS → bleeding from lungs, glomerulonephritis and kidney failure

131
Q

What is the clinical presentation of Goodpasture’s syndrome?

A
  • Haemoptysis
  • Haematuria
  • Dyspnoea
  • Glomerulonephritis
  • Chest pain
  • Fever
  • Fatigue
132
Q

What are the investigations for Goodpasture’s syndrome?

A

Lung and kidney biopsy - anti-GBM antibodies

133
Q

Describe the treatment for Goodpasture’s syndrome.

A
  • Supportive
  • Corticosteroids (i.e. pred)
  • Immunosuppressant (cyclophosphamide)
  • Plasmapheresis (removal/replacement of plasma)
134
Q

What is granulomatosis with polyangiitis? What is it associated with?

A
  • Systemic vasculitis involving small and medium vessels. Classically ENT, lung and kidney involvement (ELK)
  • Associated with c-ANCA
  • Formerly called Wegener’s granulomatosis
135
Q

What is the clinical presentation of granulomatosis with polyangiitis?

A
  • General: malaise, fatigue, fever, night sweats, arthralgias
  • ENT: rhinorrhoea, chronic ear infections, conjunctivits, scleritis, hoarseness
  • Lung: cough, dyspnoea, wheeze
  • Kidney: haematuria
136
Q

What are the investigations for granulomatosis with polyangiitis?

A
  • c-ANCA (anti-neutrophil cytoplasmic antibody)
  • Urinalysis
  • CT chest
137
Q

Describe the treatment for granulomatosis with polyangiitis.

A
  • Corticosteroids (methylprednisolone, prednisolone)
  • Immunosuppression (rituximab, methotrexate)
  • Prophylactic ABx
138
Q

What is alpha-1-antitrypsin? What is alpha-1-antitrypsin deficiency?

A
  • Alpha-1-antitrypsin is a protease inhibitor mainly produced in the liver, which inhibits neutrophil elastase (an enzyme that digests connective tissues). Coded for on chromosome 14
  • Alpha-1-antitrypsin deficiency is where there is an abnormality in the gene for A1A
  • It basically causes early-onset COPD and bronchiectasis
139
Q

Which organs does alpha-1-antitrypsin deficiency affect?

A
  • Affects the liver (cirrhosis >50 y/o) and lungs (bronchiectasis/emphysema after 30 y/o):
  • Lung: the lack of ‘normal’ A1AT → excess protease enzymes → attacks lung tissue
  • Liver: mutant A1AT builds up → tissue damage → cirrhosis → HCC
140
Q

What are the liver signs and symptoms of A1AT deficiency?

A
  • Tiredness
  • Loss of appetite
  • Weight loss
  • Oedema
  • Jaundice
  • Haematemesis/blood in stools
141
Q

What are the lung signs and symptoms of A1AT deficiency?

A
  • S.O.B.
  • Excessive cough with sputum production
  • Wheeze
  • Decreased exercise capacity, persistent fatigue
  • Chest pain (worse on inhalation)
142
Q

What are the investigations for A1AT deficiency?

A
  • Low SERUM A1AT (screening test of choice)
  • Liver BIOPSY shows cirrhosis and acid-Schiff-positive staining globules (this stain highlights the mutant alpha-1-antitrypsin proteins) in hepatocytes
  • Genetic testing for the A1AT gene
  • High resolution CT thorax diagnoses bronchiectasis and emphysema
143
Q

Describe the management for A1AT deficiency.

A
  • No cure :(
  • If they smoke - STOP (1st line for low plasma AAT)
  • Symptomatic treatment (inhalers, O2 therapy)
  • Organ transplant for end-stage liver/lung disease
  • Augementation* - limited evidence for benefit of replacement A1AT
  • Monitor for HCC
144
Q

What is pulmonary hypertension? What is it characterised by? What does it result in? What value does the pressure have to be above?

A
  • Pulmonary hypertension is increased resistance and pressure of blood in the pulmonary arteries
  • Characterised by vascular proliferation and remodelling
  • Results in a progressive increase in pulmonary vascular resistance (PVR)
  • The pressure must be above 25mmHg
145
Q

Describe the pathophysiology of pulmonary hypertension.

A
  • Increasing the pressure and resistance in the pulmonary arteries causes strain on the right side of the heart supplying O2 to the lungs -> hypertrophy -> O2 demand eventually exceeds supply -> right-sided heart failure
  • This also causes a back pressure of blood into the systemic venous system
146
Q

Describe the aetiology of pulmonary hypertension.

A
  • Group 1 – PRIMARY PULMONARY HYPERTENSION or connective tissue disease such as SLE - abnormal increase in PVR = increased strain on right side of heart
  • Group 2 – left heart failure usually due to myocardial infarction or systemic hypertension - backup of blood into the pulmonary veins, increased pressure in pulmonary artery
  • Group 3 – chronic lung disease such as COPD - hypoxic vasoconstriction = shunting of blood away from damaged areas
  • Group 4 – pulmonary vascular disease, e.g. pulmonary embolism
  • Group 5 – miscellaneous causes, e.g. sarcoidosis, glycogen storage disease and haematological disorders
147
Q

Describe the clinical features of pulmonary hypertension.

A
  • EXERTIONAL DYSPNOEA
  • LETHARGY AND FATIGUE
  • Ankle swelling
  • Accentuated pulmonic component to the 2nd heart sound
  • Tricuspid regurgitation murmur
  • Fatigue, peripheral oedema, cyanosis
148
Q

What are the investigations for pulmonary hypertension?

A
  • Initial tests:
  • CXR (dilated pulmonary arteries, right ventricular hypertrophy)
  • ECG (right ventricular hypertrophy, right axis deviation, right bundle branch block)
  • Trans-thoracic echocardiogram
  • Diagnostic test: RIGHT HEART CATHETERISATION
149
Q

Give 2 signs of pulmonary hypertension on a chest x-ray.

A

Elevated cardiac apex due to right ventricular hypertrophy and enlargement of the pulmonary arteries

150
Q

Describe the management of pulmonary hypertension.

A
  • PRIMARY pulmonary hypertension can be treated with:
  • CCBs (e.g. amlodipine). If contraindicated:
  • 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, e.g. treat underlying cause, oral anticoagulants, if fluid retention then give diuretics, supplemental oxygen
151
Q

What are the different types of lung cancer?

A
  • Lung cancer split into:
  • Small cell lung carcinoma (20%)
  • Non-small cell lung carcinoma (~ 80%):
  • Adenocarcinoma (around 40% of total lung cancers)
  • Squamous cell carcinoma (around 20% of total lung cancers)
  • Large-cell carcinoma (around 10% of total lung cancers)
  • Other types (around 10% of total lung cancers)

The presentations of these lung cancer are similar

152
Q

What do small cell lung carcinomas contain? What does this make them responsible for?

A

Small cell lung cancer carcinomas contain NEUROSECRETORY GRANULES that can release neuroendocrine hormones. This makes SCLC responsible for multiple PARANEOPLASTIC syndromes

153
Q

What are small cell lung cancers associated with? Where do they arise from? What do they secrete? What is the treatment?

A
  • Strongly associated with cigarette smoking
  • Arises from endocrine cells typically in the central bronchus
  • Secretes polypeptide hormones
  • Treatment: chemotherapy
154
Q

What are squamous cell carcinomas most strongly associated with? Where do they arise from? What are they associated with?

A
  • MOST strongly associated with cigarette smoking
  • Arises from epithelial cells typically in the central bronchus
  • Associated with production of keratin
155
Q

In which individuals are adenocarcinomas most common? Where do they originate from? Where do they metastasise to?

A
  • MOST COMMON CELL-TYPE IN NON-SMOKERS
  • Originate from mucus-secreting glandular cells
  • Metastasises to: pleura, lymph nodes, brain, bone , adrenals
156
Q

What is a mesothelioma? What is it strongly linked to? What is the prognosis and treatment?

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
157
Q

Where are the sites of metastatic spread in lung cancer?

A
  • LBAB:
  • Liver
  • Bone
  • Adrenal glands
  • Brain
158
Q

Regarding secondary lung cancer, where can cancer spread to the lungs from?

A
  • Breast
  • Bowel
  • Bladder
  • Kidney
  • Prostate
159
Q

What is the epidemiology of lung cancer? What are the risk factors?

A
  • Third most common cancer in the UK behind prostate and breast cancer
  • Risk factors: SMOKING, asbestos, coal and products of coal combustion, radon exposure, pulmonary fibrosis, HIV, genetic factors
160
Q

What is the clinical presentation of lung cancer?

A
  • Symptoms of local disease: PERSISTENT COUGH, S.O.B., HAEMOPTYSIS, WEIGHT LOSS, CHEST PAIN, SUPRACLAVICULAR LYMPHADENOPATHY, wheeze, recurrent infections
  • Symptoms of metastatic disease: bone pain, headache, seizures, neuro deficit, abdominal pain
  • Paraneoplastic changes: FINGER CLUBBING, hyperparathyroidism (↑PTH), SIADH (↑ADH), Cushing’s disease (↑ACTH)
  • Extrapulmonary manifestations: recurrent laryngeal nerve palsy (horase voice), superior vena cava obstruction (facial swelling, PEMBERTON’S SIGN)
161
Q

What are two key examination findings that would automatically indicate an urgent chest x-ray?

A

Finger clubbing and supraclavicular lymphadenopathy

162
Q

What are the investigations for lung cancer?

A
  • First line: CXR
  • GOLD STANDARD: PERCUTANEOUS OR BRONCHOSCOPIC BIOPSY AND HISTOLOGY
  • CT chest, liver & adrenal glands – for staging
  • Sputum cytology - malignant cells in sputum
  • Bronchoscopy with endobronchial ultrasound = detailed ultrasound of the tumour
163
Q

What would we find on a chest x-ray for lung cancer?

A
  • Opacified lesion
  • Hilar enlargement
  • Pleural effusion (usually unilateral in cancer)
  • Collapse
164
Q

Describe the treatment for lung cancer.

A
  • MDT meeting:
  • First line for isolated non-small cell lung cancer = surgery (segmentectomy, lobectomy, pneumonectomy)
  • Non-small cell lung cancer = radiotherapy and adjuvant or palliative chemotherapy
  • Small cell lung cancer = chemotherapy or radiotherapy
165
Q

What is the major complication of DVT? Explain how this occurs.

A

Pulmonary embolism - thrombus travels back to heart through vena cava, right atrium, right ventricle, and gets stuck in the pulmonary artery

166
Q

What are the risk factors for pulmonary embolism?

A
  • Increased age
  • Immobility, e.g. post surgery
  • Pregnancy
  • Active malignancy
  • DVT
  • Family history of VTE
167
Q

What is key to a pulmonary embolism? Describe this triad.

A

Virchow’s Triad:

– Vessel wall damage

– Venous stasis

– Hypercoagulability

168
Q

What are the signs and symptoms of a pulmonary embolism?

A
  • ACUTE ONSET SHORTNESS OF BREATH
  • Unilateral pleuritic chest pain
  • Leaning forward to breathe
  • Tachycardia
  • Tachypnoea
  • Haemodynamic instability - pallor, hypotension, shock, collapse
  • Haemoptysis
  • Signs of concurrent DVT
169
Q

What are the investigations for a pulmonary embolism?

A

COMPUTED TOMOGRAPHIC PULMONARY ANGIOGRAPHY (CPTA)! If Wells score >4 then immediate CPTA, <4 = D-dimer (Wells score: >4 = PE likely, <4 = PE unlikely)

  • Echocardiography
  • D-dimer
  • FBC
  • ABG
  • CXR and ECG - look for alternate causes
170
Q

Describe the treatment for a pulmonary embolism.

A
  • If PE suspected but unable to investigate, start anticoagulation: APIXABAN (DOAC) or RIVAROXABAN (both 1st line) or LMWH for 5 days followed by DABIGATRAN
  • If delay on CTPA give LMWH, e.g. Delteparin
  • Patient presenting with hypotension and raised JVP = acutely unwell. Offer O2 if <90%, continuous UNFRACTIONATED HEPARIN and THROMBOLYSIS - senior decision - ALTEPLASE, consider IV fluids
  • Surgical pulmonary embolectomy
  • Major complications can occur in pregnant women
171
Q

What are the differential diagnoses for a pulmonary embolism?

A
  • Unstable angina
  • MI
  • Pneumonia
  • Acute bronchitis
  • Pneumothorax
172
Q

What is respiratory failure? What is type I respiratory failure? What causes type I respiratory failure?

A
  • Respiratory failure = failure of gas exchange, inability to maintain normal blood gases. Either acute (rapid) or chronic (over time)
  • Type I:
  • PaO2 = low (hypoxia)
  • PaCO2 = low/normal (hypocapnia/normal)
  • Caused by problem with oxygenation, e.g. high altitude, shunting. Pulmonary embolism (form of ventilation-perfusion mismatch) most commonly causes Type I
173
Q

What is type II respiratory failure? What is it caused by?

A
  • PaO2 = low (hypoxia)
  • PaCO2 = high (hypercapnia)
  • Caused by poor ventilation, e.g. COPD, asthma
174
Q

How do we classify airways obstruction and restriction?

A
  • FVC: >80% than predicted value = normal. Low value indicates airways restriction
  • FEV1/FVC ratio of <70% = airways obstruction
  • FEV1: >80% than predicted value = normal
175
Q

What are the gas and pH levels like for respiratory alkalosis and acidosis?

A
176
Q

Give the diagnosis for each of these patients:

a) 60 yo male smoker with progressively worsening SoB
b) 32 yo female with ear infection, cough, dyspnoea and haematuria with purpuric rash on her arm
c) 51 year old non-smoker with severe shortness of breath and ascites

A

a) COPD
b) Granulomatosis with polyangiitis
c) Alpha-1 antitrypsin deficiency

177
Q

You are asked to review a 70 year old female who has been admitted with shortness of breath. You note she is on 5L of oxygen via nasal cannula. ABG results are below. What does it show?

  • pH: 7.29
  • PaO2: 7.0 kPa
  • PaCO2: 9.1kPa
  • HCO3-: 35 mmol/L
  • BE: +3

A.Type I respiratory failure

B.Type 2 respiratory failure

C.Acute respiratory acidosis

D.Acute respiratory alkalosis

E.Chronic respiratory alkalosis

A

B. Type 2 respiratory failure

  • pH: 7.35 – 7.45
  • PaCO2: 4.7 – 6.0 kPa || 35.2 – 45 mmHg
  • PaO2: 11 – 13 kPa || 82.5 – 97.5 mmHg
  • HCO3–: 22 – 26 mEq/L
  • Base excess (BE): -2 to +2 mmol/L
178
Q

A 24 year old female is due her asthma review. She currently takes salbutamol as needed, and regular beclometasone. She feels her asthma is not under control however, and has frequent asthma attacks. What could you prescribe her alongside her regular medication?

A. Montelukast

B. Theophylline

C. Increase steroid dose

D. Check medication adherence

E. Tiotropium

A

A. Montelukast

179
Q

A 60 year old man presents to his GP with a 1 year history of worsening SOB and a non-productive cough. He has also noticed some unintentional weight loss. He mentions he used to work as a builder. On examination, he has bibasal crackles, but no other findings of note. What is the most likely diagnosis?

A. Idiopathic pulmonary fibrosis

B. Asbestosis

C. Silicosis

D. COPD

E. Granulomatosis with polyangiitis

A

B. Asbestosis

180
Q

A 54-year-old smoker Sarah with diabetes, hypertension, coronary artery disease presents with a 2-day history of a productive cough with yellow sputum, chest tightness, and fever. Physical examination reveals fever; lung sounds are quiet but clear, with crackles at the left base. Chest x-ray reveals a left lower lobe infiltrate. FBC shows elevated white cell count.

What is the most likely diagnosis?

a) Pneumonia
b) Myocardial infarction
c) Heart failure
d) Tuberculosis

A

a) Pneumonia. Given the short history of symptoms we can rule out TB (it could be but that is not on top of your differential list). Heart failure wouldn’t present with fever usually and you wouldn’t expect the WCC to be elevated. MI would present with central crushing chest pain, nausea and vomiting, sweating - more acute presentation!

181
Q

John is a 65 year old non-smoker presenting to the GP with gradually worsening shortness of breath. He has also had a cough for a few weeks which sometimes brings up blood, but puts this down to allergies. His wife noticed that his clothes are a bit looser than usual. He has not noticed any other symptoms. He has always lived in England, and has never left the country.

What is the first-line investigation you would want to do?

a) Mantoux test
b) Interferon gamma release assay
c) Chest X-ray
d) CT chest

A

c) Chest X-ray

182
Q

John is a 65 year old non-smoker presenting to the GP with gradually worsening shortness of breath. He has also had a cough for a few weeks which sometimes brings up blood, but puts this down to allergies. His wife noticed that his clothes are a bit looser than usual. He has not noticed any other symptoms. He has always lived in England, and has never left the country.

What is the most likely diagnosis for this patient?

a) Squamous Cell Carcinoma
b) Adenocarcinoma
c) Tuberculosis
d) Pneumonia

A

b) Adenocarcinoma. This man has le adenocarcinoma. His symptoms are suggestive of a long term issue so it can be things like cancer, and TB. This patient however, does not have any other symptoms such as fevers which would be more suggestive of an infection. He also hasn’t left the country ever which makes TB less likely. So you’re thinking more cancer in which case it’s between a and b. He is a non-smoker and so adenocarcinoma is the most common lung cancer in non-smokers. First line investigation for all lung cancers is CXR.

183
Q

Thomas is 35 year old man, who is presenting to his GP as a temporary patient with a productive cough for the past 8 weeks. He has also been spiking some temperatures, and sweating profusely at night. He has also noticed that his clothes are hanging off him. He’s a non smoker. He recently moved from India and has been living in hostels with others.

What is the most likely diagnosis for this patient?

a) Multiple Myeloma
b) Tuberculosis
c) Adenocarcinoma
d) Pneumonia

A

b) Tuberculosis. Key points in this history is that he is rather young, so less likely to be cancer. Has an 8 week history of breathlessness, productive cough, fever, and night sweats and weight loss. Which suggestive of tuberculosis. This is then reaffirmed by the fact he has recently moved from India and living in hostels which an area that can have high prevalence of TB

184
Q

You diagnose Thomas with TB and start him on the standard management. A few weeks later he attends an appointment complaining of blurry vision.

What is the most likely cause of his blurry vision?

a) Multiple sclerosis
b) Pyrazinamide
c) Rifampicin
d) Ethambutol

A

d) Ethambutol. Optic neuritis which is inflammation of the myelin of the optic nerve which is a side effect of ethambutol - TB drug.

185
Q

64 year old female presenting with sudden onset of shortness of breath and left-sided chest pain which is worse on inspiration. She has no fevers, nausea or vomiting but felt a bit faint when it initially started. She underwent a hip replacement last week and was on bed rest for the past week.

On examination, you notice one of her calves is swollen, red and tender to touch. Her HR is 105, BP 120/80.

What is the next step in managing this patient?

a) D-dimer
b) CTPA
c) Give O2 and discharge
d) ECG

A

b) CTPA

186
Q

64 year old female presenting with sudden onset of shortness of breath and left-sided chest pain which is worse on inspiration. She has no fevers, nausea or vomiting but felt a bit faint when it initially started. She underwent a hip replacement last week and was on bed rest for the past week.

On examination, you notice one of her calves is swollen, red and tender to touch. Her HR is 105, BP 120/80.

Which of the following is NOT a risk factor for PE?

a) Pregnancy
b) Active malignancy
c) Combined OCP
d) Thrombocytopenia

A

d) Thrombocytopenia

187
Q

25 year old male, presenting with sudden shortness of breath and pleuritic chest pain while playing basketball. He does not recall hitting his chest anywhere and is experiencing mild discomfort. On examination there is no visible trauma but there is mild hyperexpansion of the chest, hyperresonance on percussion and reduced breath sounds on the left hemithorax.

What is the most likely diagnosis for this patient?

a) Pulmonary Embolism
b) Pleural Effusion
c) Tension Pneumothorax
d) Pneumothorax

A

d) Pneumothorax

188
Q

25 year old male, presenting with sudden shortness of breath and pleuritic chest pain while playing basketball. He does not recall hitting his chest anywhere.On examination there is no visible trauma but there is mild hyperexpansion of the chest, hyperresonance on percussion and reduced breath sounds on the left hemithorax.

What would suggest a tension pneumothorax?

a) Tracheal deviation to the opposite side to the pneumothorax
b) Tracheal deviation to the same side as the pneumothorax
c) Hyperresonant chest on the opposite side of the pneumothorax
d) Patient well and speaking normally, haemodynamically stable

A

a) Tracheal deviation to the opposite side of the pneumothorax

189
Q

A 36-year-old woman presents with a 6-month history of gradually progressive dyspnoea on exertion and fatigue. On physical examination, her vital signs are normal and she appears not to be in any distress. Her lungs are clear to auscultation. Her cardiac examination shows a raised JVP and a murmur best heard at the left sternal border.

What is the diagnostic test for the suspected condition?

a) Chest CT
b) Right-heart catheterization
c) CTPA
d) ECG

A

b) Right-heart catheterization

190
Q

A patient presents with a persistent cough for the last 6 weeks. Upon further questioning you find that they also have experienced unintentional weight loss and occasionally cough up bloody sputum. They also have signs and symptoms consistent with pleural effusion.

An aspirate is taken from the pleural space, what is the most likely composition of this aspirate?

a) Transudate
b) Exudate

A

b) Exudate

191
Q

A 7-year-old girl presents with abrupt onset of fever, nausea, vomiting, and sore throat. The child denies cough, rhinorrhoea, or nasal congestion. On physical examination, oral temperature is 38.5°C, and there is an exudative pharyngitis with enlarged, tender anterior cervical lymph nodes.

What is the most likely cause of her symptoms?

a) EBV
b) Group A streptococcus
c) Adenoviruses
d) Strep agalactiae

A

b) Group A streptococcus

192
Q

59 year old man with a 12 year history of progressive dyspnoea, dry cough and fatigue, he is now short of breath at rest for the past few months. He has no chest pain or peripheral oedema. He has no smoking history and denies any family history or exposure to asbestos. He has previously bred and raced pigeons for 20 years, now hasn’t done this activity for 5 years.

What type of hypersensitivity reaction is he experiencing?

a) Type 1
b) Type 2
c) Type 3
d) Type 4

A

c) Type 3

193
Q

Which of the following does NOT cause a reduction in transfer factor?

A. Idiopathic Pulmonary Fibrosis

B. Pulmonary Hypertension

C. Asthma

D. Anaemia

E. COPD

A

C. Asthma

194
Q

Which of the following is NOT a pathological description of findings seen in Interstitial Lung Disease?

A. Usual interstitial pneumonia

B. Non-specific interstitial pneumonia

C. Desquamative interstitial pneumonia

D. Obliterative bronchiolitis

E. Diffuse alveolar damage

A

D. Obliterative bronchiolitis

195
Q

Which of the following radiological features is NOT commonly seen with lobar collapse?

A. Triangular opacity with apex at the hilum

B. Veil like opacity over right hemithorax

C. “Sickle sign” of air around the aortic knuckle

D. Loss of right hemidiaphragm

E. The “sail sign”

A

B. Veil like opacity over right hemithorax

196
Q

Which of the following is not seen in Sarcoidosis?

A. Glaucoma

B. Heart Block

C. Lymphnode enlargement

D. Skin nodules

E. Nephrocalcinosis

A

A. Glaucoma

197
Q

Which of the following lung conditions does not commonly have an occupational component?

A. Asthma

B. Idiopathic Pulmonary Fibrosis

C. Sarcoidosis

D. Pigeon fancier’s lung

E. COPD

A

D. Pigeon fancier’s lung

198
Q

To establish a diagnosis of COPD, which of the following is not necessary?

A. Substantial smoking history

B. Progressive airflow obstruction

C. Lack of reversibility

D. Reduced FEV1/FVC ratio

E. Lack of change over several months

A

A. Substantial smoking history

199
Q

Which is a correct criteria for home O2 in COPD?

A. PaCO2 <7.3

B. Assessed while stable

C. Assessed twice, 6 weeks apart

D. Assessed off treatment

E. PaO2 > 7.3

A

B. Assessed while stable

200
Q

Which of the following is true?

A. 80% of all lung cancers are SCLC

B. 10 year survival is 10%

C. Traditional radiotherapy is as good as daily treatment

D. Chemotherapy for NSCLC gives a 4% increase in 2 year survival compared to traditional treatment

E. Performance status 4 is associated with a good 1 year survival

A

D. Chemotherapy for NSCLC gives a 4% increase in 2 year survival compared to traditional treatment

201
Q

Which is not a common side effect of radiotherapy?

A. Nausea

B. Cough

C. Fatigue

D. Oesophagitis

E. Anorexia

A

A. Nausea

202
Q

Which is compatible with respiratory acidosis?

A. pH 7.35

B. pH 7.25

C. pCO2 8.5

D. pCO2 2.3

E. BE -1.3

A

A. pH 7.35

B. pH 7.25

C. pCO2 8.5

E. BE -1.3

203
Q

Pick the true response:

A. 4.2 million people in the UK have an occupational illness

B. Most of these are respiratory

C. An occupational history is not worth the time it takes to ask

D. A diagnosis of occupational lung disease always solves employment problems

E. At least 10% of asthma is thought to be occupational

A

E. At least 10% of asthma is thought to be occupational

204
Q

Which of the following occupations are not associated with lung disease?

A. Baker

B. Lab technician

C. Joiner

D. Metal worker

E. Prawn sheller

A

C. Joiner

205
Q

In pulmonary embolism:

A. Shock is heralded by pleuritic chest pain and haemoptysis

B. DVT is usually seen

C. Prophylaxis is overused

D. Idiopathic PEs usually require 6 months of treatment

E. Treatment with NOACs is better than heparin in cancer

A

D. Idiopathic PEs usually require 6 months of treatment

206
Q

In bronchiecstasis:

A. A genetic cause is usually identified

B. A prompt course of antibiotics prevents the need for long courses of treatment

C. Immune dysfunction is usually the cause

D. There is a progression of microbiology from common pathogens like Pseudomonas to rarer ones like Moraxella

E. Immune dysfunction is sometimes the cause

A

C. Immune dysfunction is usually the cause

207
Q

CFTR:

A. Is coded for by Ch7

B. Is a sodium channel

C. Commonly has an amino acid substitution at position 508

D. Mutations can be cured by gene therapy

E. Mutations can cause mild disease

A

E. Mutations can cause mild disease

208
Q

The healthy pleural space contains:

A. No fluid

B. 15 mls fluid

C. Approx. 20-40mls fluid

D. Neutrophils

E. Dividing mesothelial cells

A

C. Approx. 20-40mls fluid

209
Q

Epidemic flu:

A. Crosses international boundaries

B. Caused by antigenic drift

C. 2 or more linked cases

D. Prevented by Tamiflu

E. Prevented by immunisation

A

B. Caused by antigenic drift

210
Q

A 25-year-old presents to the Emergency Department with worsening shortness of breath. Supportive O2 therapy is commenced. On examination she is wheezy and talking in short sentences.

  • Respiratory rate 26
  • Heart rate 115
  • SpO2 94%

What is the severity of this episode and therefore what is the most appropriate initial management?

a) Life-threatening – Nebulised salbutamol and PO prednisolone
b) Life-threatening – Nebulised salbutamol and tiotropium + PO prednisolone
c) Severe – Nebulised salbutamol and PO prednisolone
d) Severe – Nebulised salbutamol and tiotropium + PO prednisolone

A

C) Severe - nebulised salbutamol and PO prednisolone

No signs of life-threatening features e.g. silent chest or PaO2 < 92

D actually wouldn’t be unreasonable but tiotropium generally reserved for life-threatening disease

211
Q

A patient receiving chemotherapy for breast cancer has developed acute onset right chest pain and shortness of breath. She is tachycardic at 120bpm and goes on to have one episode of haemoptysis. You administer O2 and notice that she has become confused and drowsy.

What is the most appropriate initial management?

a) CTPA and immediate apixaban
b) Immediate CTPA
c) Immediate D-dimer
d) Thrombolysis with alteplase

A

D) Thrombolysis with alteplase

This is one of the rare cases of PE leading to haemodynamic instability

Signs of haemodynamic instability essentially = signs of reduced organ perfusion e.g. confusion or angina + tachycardia and hypotension

Bonus question = how long would this patient need to be anticoagulated for?

≥6-months

212
Q

You receive a phone call in the GP practice from the daughter of one of your patients. She is worried about her 70 year-old dad, who has developed a worsening cough over the past 4 days which is now productive of sputum. She reports he is not confused but increasingly distressed with the shortness of breath and chest pain. He has a Hx of osteoarthritis and mild dementia. His blood pressure monitor shows the following, what is the most appropriate initial management?

  • BP 120, HR 98, RR 28
    a) Admit for IV Tazocin
    b) Admit for PO amoxicillin
    c) No further management necessary
    d) Prescribe amoxicillin and manage in the community
A

B) Admit for PO amoxicillin

CRB = 1, when you don’t have a urea in the community 1 = use clinical judgement, as to whether they need admission or not. This patient has OE and mild dementia, so is unlikely to do well at home with increasing distress.

213
Q
A

A. The pulmonary artery is anterior to the main bronchus in the left lung

214
Q
A

D. External intercostal muscles

215
Q
A

B. 5th intercostal space, anterior border of latissimus dorsi, lateral border of pectoralis major and base of axilla

216
Q
A

B. Larynx

217
Q
A

E. All of the above

218
Q
A

D. FVC = normal, FEV1 = decreased, FEV1/FVC ratio = decreased

219
Q
A

a. Carbon dioxide (CO2)

220
Q
A

c. Long-acting beta agonist (LABA)

221
Q
A

d. Short-acting beta-2 agonist

222
Q
A

e. Decreased PO2, increased PCO2

223
Q
A

d. Raised temperature

224
Q
A

d. Silent chest

225
Q
A

c. Lung cancer

226
Q
A

e. Pulmonary embolism

227
Q
A

d. 15L via a non-rebreather mask

228
Q
A

a. Respiratory acidosis with metabolic compensation

229
Q
A

d. The pulmonary circulation is a high-pressure system

230
Q
A

e. Pulmonary oedema

Phase 2a (25 decks)

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