Respiratory Flashcards

1
Q

How does acute bronchitis present?

A

Symptoms typically peak after 2-3 days and then gradually clear → this can take 3-4 weeks.

  • Cough → main symptom
    • May be productive with clear, white, or discoloured sputum.
    • May have substernal or chest wall pain when coughing
  • Fever
  • Headache
  • Cold symptoms
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2
Q

If appropriate (eg, immunocompromised or failing to improve), what antibiotic is first-line for acute bronchitis?

A

Doxycycline

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3
Q

What is the most common cause of bacterial pneumonia across all ages?

A

Streptococcus pneumoniae

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4
Q

What bacteria is associated with pneumonia in those with COPD?

A

haemophilus influenzae

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5
Q

How is the severity of pneumonia assessed?

A
  • CRB-65 is used in the community & CURB-65 in hospital. Predicts mortality & is used when deciding management. Consider hospital admission if CRB-65 is more than 0.
  • C - Confusion → new disorientation in person, place, or time
  • U - Urea >7 mmol
  • R - Respiratory rate >30
  • B - Blood pressure <90/60
  • 65 - Age >65
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6
Q

What are the main causes of pulmonary hypertension?

A
  • Idiopathic pulmonary hypertension, or connective tissue disease (SLE)
  • Left heart failure → MI, systemic HTN
  • Chronic lung disease → COPD, pulmonary fibrosis
  • Pulmonary vascular disease → PE
  • Other → sarcoidosis, haematological disorders
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7
Q

How does pulmonary hypertension present?

A

Symptoms:

  • Due to gradually worsening right ventricular function
  • SOB
  • Weakness & fatigue
  • Chest pain
  • Syncope

Signs:

  • Loud S2
  • 3rd heart sound
  • Pansystolic murmur (tricuspid regurgitation) & diastolic murmur (pulmonary regurgitation)
  • Later signs
    • Ascites
    • Peripheral oedema
    • Parasternal heave
    • Elevated JVP
    • Hepatomegaly
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8
Q

What investigations are done for pulmonary hypertension?

A
  • ECG: signs of R-sided heart strain (p pulmonale, RVH, RAD, RBBB)
  • CXR: dilated pulmonary arteries
  • Raised BNP
  • Right heart catheterisation: gold standard as allows the pulmonary arterial pressure to be measured
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9
Q

What are the risk factors of asthma?

A
  • Non-modifiable
    • Personal or family history of atopy
    • Male sex (asthma development) or female sex (persistence to adulthood)
    • Prematurity & low birth weight
    • Maternal smoking during pregnancy
  • Modifiable
    • Exposure to smoke & dust
    • Obesity
    • Social deprivation
    • Infections in infancy
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10
Q

What are some triggers of asthma?

A
  • Respiratory infections
  • Allergens → dust, animals, food
  • Pollutants → smoke
  • Cold air
  • Exercise
  • Medications → NSAIDs, beta-blockers (particularly non-selective ones, eg propranolol)
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11
Q

What is the order of investigations recommended for an asthma diagnosis? What is a positive finding for each?

A

Initial Investigations:

  • Fractional Exhaled Nitric Oxide (FeNO) - >40ppb
  • Spirometry with bronchodilator reversibility -> FEV1/FVC ratio <70%, with >12% reversibility

Next Steps:

  • Peak flow variability - >20% variability positive
  • If still uncertainty then do a direct bronchial challenge test
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12
Q

What supportive management is indicated in asthma?

A
  • Asthma plan → treatment, treatment escalation, when to seek help
  • Annual asthma reviews
  • Vaccinations → childhood, pneumococcal, influenza, covid
  • Lifestyle measures → smoking cessation, weight loss, avoid triggers if possible
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13
Q

What is the progression of asthma treatment?

A
  1. Short-acting beta-2 agonist (salbutamol) + low-dose inhaled corticosteroid
  2. Add long-acting beta-2 agonist (salmeterol) OR change to maintenance & reliever therapy (MART)
  3. Increase the ICS, OR add a leukotriene receptor antagonist (montelukast)
  4. Specialist management
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14
Q

When should asthma treatment be reviewed for additional management?

A

Review when using >3 doses of SABA a week or using >1 inhaler device in a month

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15
Q

What are some side effects of SABA inhalers?

A
  • Tachycardia
  • Vasodilation
  • Arrhythmia
  • Tremor
  • Hypokalaemia
  • Insomnia
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16
Q

What are the different severities of an acute exacerbation of asthma?

A

Moderate exacerbation features:

Peak flow 50 – 75% best or predicted

Severe exacerbation features:

Peak flow 33-50% best or predicted
Respiratory rate above 25
Heart rate above 110
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Life-threatening exacerbation features:

Peak flow less than 33%
Oxygen saturations less than 92%
PaO2 less than 8 kPa
Becoming tired
Confusion or agitation
No wheeze or silent chest
Haemodynamic instability (shock)

17
Q

What are the medical management options for an acute exacerbation of asthma?

A
  • Oxygen → if hypoxic
  • SABA → high dose, either with inhaler + spacer, nebulisers, IV
  • Corticosteroids → 40-50mg prednisolone PO for 5 days
  • Ipratropium bromide → if severe or failure to respond
  • IV magnesium sulphate → for severe, life-threatening
18
Q

What is COPD defined as?

A

= a long-term, progressive lung disease characterised by emphysema, chronic bronchitis, and small airway fibrosis.

Definitions:

  • Chronic bronchitis → a productive cough for at least 3 months in 2 consecutive years.
  • Emphysema → damage & dilatation of the alveolar sacs & alveoli, decreasing the surface area for gas exchange.
19
Q

What is the medical management of COPD?

A
  1. SABA + SAMA (ipratropium bromide)
  2. If asthmatic/steroid responsive features → LABA + ICS (fostair). If no asthmatic features →LABA + LAMA (anoro ellipta)
  3. LABA + LABA + ICS → trimbo, trelegy ellipta
20
Q

What are the common causes of COPD exacerbation?

A
  • Bacterial
    • H.influenzae
    • S.pneumoniae
    • M.catarrhalis
  • Viruses
    • Rhinovirus
    • Influenza
21
Q

How is a COPD exacerbation managed?

A
  • Regular inhalers or nebulisers
  • Steroids → 30mg OD for 5 days
  • Antibiotics
  • Respiratory physiotherapy to help clear sputum
  • If severe:
    • IV amiophylline
    • NIV
    • Intubation & ventilation
22
Q

What is bronchiectasis & how does it develop?

A

= a chronic respiratory disease characterised by permanent dilation of the bronchi, due to irreversible damage to the bronchial wall.
Pathophysiology:

  • Poorly understood
  • An initial insult results in immune cells being recruited to the bronchi → these secrete cytokines & proteases, leading to inflammation
  • This inflammation damages the muscle & elastin → bronchial dilation
  • Normally, this bronchial dilation is reversible after the resolution of the initial insult to the bronchi → in bronchiectasis, several factors prevent the bronchial dilation from reversing
  • Dilated bronchi are predisposed to persistent microbial colonisation, as mucus is trapped.
  • Vicious cycle of microbial colonisation causing inflammation, which worsens the bronchiectasis, which increases the risk of further colonisation
23
Q

How does bronchiectasis present on imaging?

A
  • CXR
    • Tram-track opacities
    • Ring shadows
  • High-resolution CT → gold-standard imaging test
    • Signet ring sign
24
Q

How is bronchiectasis managed?

A

General:

  • Vaccines
  • Chest physio
  • Smoking cessation
  • Long-term antibiotics → if >3 exacerbations per year, azithromycin
  • LABA → for breathlessness
  • LTOT → if chronically reduced saturations
  • Surgical lung resection or transplant

Infective Exacerbations:

  • Sputum culture
  • Extended course of antibiotics
    • 7-14 days
    • Ciprofloxacin → usual choice for exacerbations caused by pseudomonas aeruginosa
25
Q

What does interstitial lung disease show on imaging?

A
  • CXR → reticular (fine) opacities
  • High-resolution CT → honeycombing, dilated airways
26
Q

What are the two medications that slow disease progression in someone with idiopathic pulmonary fibrosis?

A

pirfenidone & nintedanib

27
Q

What investigations are done for suspected pneumothorax?

A

Bedside:

  • Pulse oximetry
  • RR, HR

Laboratory Investigations:

  • FBC & clotting screen → in trauma cases, in case of transfusion
  • ABG → respiratory alkalosis secondary to hyperventilation, or it may show type 1 respiratory failure

Imaging:

  • Erect CXR → first line for a suspected simple pneumothorax
  • CT Thorax → can detect a pneumothorax that is too small to be seen on CXR.
28
Q

How is a simple pneumothorax managed?

A
  • Management is mainly guided by symptoms & the degree of physiological compromise.
  • High-risk characteristics means a chest drain is required. (haemodynamically unstable, significant hypoxia, bilateral, underlying lung disease, >50yrs old with significant smoking history)
  • Low risk with <2cm → conservative management
  • Low risk with >2cm → management based on patient’s priority (proceudure avoidance - conservative, symptom relief - needle aspiration or ambulatory device)
29
Q

When is surgical intervention required for a simple pneumothorax, and what are the options?

A
  • Required if → chest drain fails to correct the pneumothorax, the drain is persistently leaking, the pneumothorax reoccurs.
  • Abrasive pleurodesis → creates an inflammatory reaction in the pleural lining sticks together & the pleural space becomes sealed.
  • Chemical pleurodesis → talc power
  • Pleurectomy
30
Q

What staining is required for TB culture?

A

Zeihl-Neelsen stain → a special staining which turns them bright red against a blue background.

31
Q

What is the disease course of TB?

A
  • Spread → inhaling saliva drops from infected people
  • Once in the body, there are several possible outcomes:
    • Immediate clearance of the bacteria (70% cases)
    • Primary active TB (active infection after exposure)
    • Latent TB (presence of bacteria without being symptomatic or contagious)
    • Secondary TB (reactivation of latent TB to active infection)
  • Miliary TB → when the immune system cannot control the infection, causing disseminated & severe disease.
32
Q

What two tests are used to check for an immune response to TB?

A

Mantoux Test:

  • Tuberculin is injected into the intradermal space on the forearm (no live bacteria)
  • The infection creates a bleb under the skin → after 72hrs the test is checked, and if >5mm then this is a positive result

Interferon-Gamma Release Assays:

  • A blood sample is mixed with antigens from M.TB bacteria
  • After previous contact with TB, WBCs become sensitised to the bacteria antigens & will release interferon-gamma during the test → this is a positive result
33
Q

How will TB look on a CXR?

A
  • Primary TB → patchy consolidation, pleural effusions, hilar lymphadenopathy
  • Reactivated TB → patchy, nodular consolidation with cavitation, typically in the upper zones
  • Disseminated miliary TB → millet seeds uniformly distributed across the lung fields
34
Q

How is latent TB managed?

A
  • Isoniazid + rifampicin → 3 months
  • or Isoniazid → 6 months
35
Q

How is active TB managed?

A
  • R - rifampicin (6 months)
  • I - isoniazid (6 months)
    • Pyridoxine (vitamin B6) co-prescribed to reduce risk of peripheral neuropathy
  • P - pyrazinamide (2 months)
  • E - ethambutol (2 months)
36
Q

What are the side effects of Rifampicin?

A
  • Red/orange discolouration of secretions, such as urine & tears
  • Inducer of cytochrome P450 enzymes, reduces the effect of the COCP
  • Hepatotoxicity
  • “red-im-pissing”
37
Q

What are the side effects of Isoniazid?

A
  • Peripheral neuropathy
  • Pyridoxine (vitamin B6) prescribed to reduce the risk
  • Hepatotoxicity
  • “I-so-numb-azid”
38
Q

What are the side effects of pyrazinamide?

A
  • Hyperuricaemia, resulting in gout & kidney stones
  • Hepatotoxicity
39
Q

What are the side effects of ethambutol?

A
  • Colour blindness & reduced visual acuity
  • “eye-thambutol”