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Respiratory Flashcards

How can I breathe with no air

1
Q

What scale can be used to assess breathlessness?

A

The MRC (Medical Research Council) Dyspnoea Scale is a 5-point scale for assessing breathlessness:
🔹Grade 1: Breathless on strenuous exercise
🔹Grade 2: Breathless on walking uphill
🔹Grade 3: Breathlessness that slows walking on the flat
🔹Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
🔹Grade 5: Unable to leave the house due to breathlessness

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2
Q

What spirometry result suggests COPD?

A

Obstructive picture with FEV1:FVC ratio < 70%
little or no response to reversibility testing with beta-2 agonists (e.g. salbutamol)

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3
Q

How can severity of COPD be graded?

A

The severity can be graded using the forced expiratory volume in 1 second (FEV1):

🔹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

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4
Q

What is the management of COPD?

A

Non-pharm: smoking cessation, pneumococcal and flu vaxx, pulmonary rehab

Medical: SABA (salbutamol) or SAMA (ipratropium bromide)

2nd line: determine if asthmatic or steroid responsive features
if NO features => LABA/LAMA e.g. anoro ellipta
if YES => LABA/ICS e.g. fostair, symbicort, seretide

3rd line: LABA/LAMA/ICS e.g. timbow, trelegy ellipta

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5
Q

What monitoring is needed for patients on azithromycin?

A

ECG
LFT

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6
Q

What are the indications for LTOT in COPD?

A

🔹chronic hypoxia (sats <92%)
🔹polycythaemia
🔹cyanosis
🔹cor pulmonale

smoking is C/I - fire risk

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7
Q

What is cor pulmonale?

A

Right sided HF caused by resp disease
Pulm HTN limits RV in pumping into pulm arteries => bac pressure into RA, VC, and venous system

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8
Q

What are some causes of cor pulmonale?

A

🔹COPD (most common)
🔹PE
🔹ILD
🔹CF
🔹Pulm HTN

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9
Q

What are symptoms of cor pulmonale?

A

most are asymptomatic
🔹SOB
🔹peripheral oedema
🔹SOBOE
🔹syncope
🔹CP

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10
Q

What are signs of cor pulmonale?

A

🔹hypoxia
🔹cyanosis
🔹raised JVP
🔹peripheral oedema
🔹parasternal heave
🔹loud second HS
🔹murmurs
🔹hepatomegaly

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11
Q

What can be seen on an ABG in ECOPD?

A

resp acidosis - ROME:
🔹low pH
🔹low pO₂
🔹raised pCO₂
🔹raised HCO₃⁻

set sats target to 88-92%

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12
Q

What is the management of ECOPD?

A

1st line:
🔹reg salb and ipra nebs
🔹prednisolone 30mg OD for 5 days
🔹Abx if infective

resp physio

severe ECOPD:
🔹IV aminophylline
🔹NIV
🔹intubation and ventilation + ITU

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13
Q

What are the criteria for NIV? What are some contraindications?

A

🔹Persistent resp acidosis (pH < 7.35 + PaCO₂ > 6)
🔹Potential to recover
🔹Acceptable to the pt

Contraindications
🔹untreated pneumothorax
🔹structural abnormality or pathology affecting the face/airway/GI tract

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14
Q

How can OSA be assessed?

A

Epworth Sleepiness Scale
Sleep studies
- simple sleep study - sats monitor overnight
- resp polygraphy - machine monitor RR, flow rate, sats, HR
- complex sleep study at sleep centre with polysomnography may inc EEG EMG ECG

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15
Q

How long before a pneumonia is classified as a HAP?

A

after >48hrs in hospital

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16
Q

What are the typical bacterial causes of pneumonia?

A

STREP PNEUM (most common)
🔹Haem influenza

🔹morazella catarrhalis (immunocomp or chronic resp diseases)
🔹pseudomonas aeruginosa - CF/bronchiectasis
🔹staph aureus - CF
🔹MRSA - HAP

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17
Q

What is atypical pneumonia? What antibiotics are used?

A

Atypical pneumonia is caused by organisms that cannot be cultured in the normal way or detected using a gram stain. Treatment with penicillin is ineffective. They are treated with macrolides (e.g., clarithromycin), fluoroquinolones (e.g., levofloxacin) and tetracyclines (e.g., doxycycline).

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18
Q

What are some causative organisms of atypical pneumonia?

A

Legionella pneumophila (Legionnaire’s disease) - inhaling infected water from water system e.g. AC => can cause SIADH . test with legionella urinary antigen

Mycoplasma pneumoniae - can cause erythema multiforme (“target”)

Chlamydophila pneumoniae - mild-mod chronic pneumonia and wheezing in school-age children

Coxiella burnetti (Q fever) - exposure to bodily fluid of animals e.g. farmer with a flu-like illness

Chlamydia psittaci - infected birds

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19
Q

What is PCP?

A

Pneumocystis jirovecii pneumonia - fungal
immunocompromise, HIV, low CD4 count
dry cough + SOBOE + night sweats

Tx with co-trimoxazole

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20
Q

How is COVID-19 transmitted?

A

Primarily through respiratory droplets
Contact with contaminated surfaces
Aerosol transmission in certain settings

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21
Q

How does SARS-CoV-2 enter host cells?

A

The virus binds to the ACE2 receptor on host cells, facilitating entry and replication.

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22
Q

What are common clinical features of COVID-19?

A

Fever, cough, fatigue, loss of taste or smell, myalgia

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23
Q

What is the incubation period for COVID-19?

A

The incubation period is 2-14 days, with a median of 5 days.

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24
Q

What is the gold standard for diagnosing COVID-19?

A

RT-PCR is the gold standard for detecting viral RNA

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25
Q

What imaging findings are common in severe COVID-19?

A

Chest X-ray: Bilateral infiltrates
CT Scan: Ground-glass opacities and consolidation

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26
Q

What are the main pharmacological treatment options for COVID-19?

A

Antivirals: Remdesivir for hospitalized patients
Corticosteroids: Dexamethasone for severe respiratory distress
Immunomodulators: Tocilizumab in cases of systemic inflammation

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27
Q

What causes Tuberculosis (TB)?

A

TB is caused by Mycobacterium tuberculosis, a slow-dividing, rod-shaped bacillus with high oxygen requirements.

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28
Q

Why is Mycobacterium tuberculosis referred to as an “acid-fast bacilli”? What staining is needed?

A

It has a waxy coating, making gram staining ineffective and resistant to acids in the staining process, requiring Ziehl-Neelsen staining.

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29
Q

What is the outcome of Ziehl-Neelsen staining for TB?

A

TB bacilli appear bright red against a blue background.

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30
Q

What are the possible outcomes after inhaling TB bacteria?

A
  1. Immediate clearance
  2. Primary active TB
  3. Latent TB
  4. Secondary TB (reactivation)
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31
Q

What is miliary tuberculosis?

A

It refers to disseminated and severe disease when TB spreads and the immune system cannot control the infection.

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32
Q

What are common sites for extrapulmonary TB?

A

Lymph nodes, pleura, CNS, pericardium, GI system, genitourinary system, bones and joints, skin (cutaneous TB).

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33
Q

What is a “cold abscess” in TB?

A

A firm, painless abscess, usually in the neck, without inflammation or redness typical of acute infection.

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34
Q

What investigations are used for diagnosing TB?

A

Mantoux test
IGRA (Interferon-Gamma Release Assay)
Chest x-ray
Sputum cultures

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35
Q

What does a positive Mantoux test indicate?

A

Induration of 5mm or more at the injection site indicates a positive result, suggesting TB infection.

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36
Q

What are the typical chest x-ray findings for TB?

A

Primary TB: Patchy consolidation, pleural effusions, hilar lymphadenopathy
Reactivated TB: Nodular consolidation with cavitation, typically in upper zones
Miliary TB: Small nodules resembling “millet seeds” scattered throughout the lung fields.

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37
Q

What is the treatment regimen for latent tuberculosis?

A

Isoniazid and rifampicin for 3 months,
or
Isoniazid for 6 months

38
Q

What does the RIPE mnemonic stand for in TB treatment?

A

R: Rifampicin (6 months)
I: Isoniazid (6 months)
P: Pyrazinamide (2 months)
E: Ethambutol (2 months)

39
Q

What are common side effects of TB treatment drugs?

A

Rifampicin: Red/orange secretions - “red-I’m-pissin’”
Isoniazid: Peripheral neuropathy (prevented with pyridoxine or Vitamin B6) - “I’m-so-numb-azid”
Pyrazinamide: Hyperuricaemia (gout)
Ethambutol: Colour blindness and reduced visual acuity - “eye-thambutol”

40
Q

What is the importance of nucleic acid amplification tests (NAAT) in TB?

A

NAAT detects TB DNA quickly and provides information about drug resistance.

41
Q

What is a key examination finding in asthma?

A

A widespread “polyphonic” expiratory wheeze.

42
Q

Which medications can worsen asthma symptoms?

A

Non-selective beta-blockers (e.g., propranolol) and non-steroidal anti-inflammatory drugs (e.g., ibuprofen or naproxen).

43
Q

What test is used to measure lung function in asthma?

A

Spirometry

44
Q

What is the significance of a FEV1 ratio of less than 70% in spirometry?

A

It suggests obstructive pathology, such as asthma or COPD.

45
Q

How does reversibility testing support the diagnosis of asthma?

A

A greater than 12% increase in FEV1 after a bronchodilator supports a diagnosis of asthma.

46
Q

What does a high FeNO (Fractional exhaled Nitric Oxide) level indicate in asthma diagnosis?

A

A FeNO level above 40 ppb supports a diagnosis of asthma due to airway inflammation.

47
Q

What is the purpose of peak flow variability testing in asthma?

A

To measure fluctuations in airway obstruction, where a variability of more than 20% supports the diagnosis of asthma.

48
Q

What are the signs of a life-threatening asthma exacerbation?

A

Peak flow less than 33%,
oxygen saturations less than 92%,
confusion or agitation,
silent chest, and
haemodynamic instability (shock).

49
Q

Why is the “silent chest” a critical sign in asthma?

A

A silent chest indicates severe bronchoconstriction with no air entry, signifying life-threatening asthma.

50
Q

What is the role of intravenous magnesium sulfate in severe asthma exacerbations?

A

IV magnesium sulfate helps to relax airway muscles and is used in severe exacerbations to relieve bronchoconstriction.

51
Q

What are the peak flow measurements for moderate, severe, and life-threatening asthma exacerbations?

A
  • Moderate: Peak flow > 50% predicted
  • Severe: Peak flow < 50% predicted
  • Life-threatening: Peak flow < 33% predicted
52
Q

What are the heart rate and respiratory rate thresholds for severe asthma exacerbations in children aged 1-5 years and older than 5 years?

A

Heart rate: > 140 (1-5 years) or > 125 (>5 years)

Respiratory rate: > 40 (1-5 years) or > 30 (>5 years)

53
Q

How are bronchodilators stepped up in acute asthma management?

A
  1. Inhaled or nebulised salbutamol
  2. Inhaled or nebulised ipratropium bromide
  3. IV magnesium sulfate
  4. IV aminophylline
54
Q

What is the stepwise approach to treating moderate to severe asthma exacerbations?

A
  1. salbutamol inhalers via a spacer
  2. nebulisers with salbutamol/ipratropium
  3. oral prednisone
  4. IV hydrocortisone
  5. IV magnesium sulfate
  6. IV salbutamol
  7. IV aminophylline
55
Q

What are common side effects of salbutamol in high doses?

A

Tachycardia (fast heart rate) and tremor.

56
Q

When can a child with asthma exacerbation be considered for discharge?

A

When they are well on 6 puffs 4-hourly of salbutamol and can be prescribed a reducing salbutamol regime for home use.

57
Q

What is the stepwise approach to managing asthma in children under 5 years?

A
  1. SABA
  2. low dose ICS or leukotriene antagonist
  3. low ICS + leukotriene antagonist
  4. Refer to a specialist if necessary.
58
Q

What is the stepwise approach to managing asthma in children aged 5-12 years?

A
  1. SABA
  2. add a low-dose corticosteroid
  3. add LABA
  4. inc ICS dose
  5. add ? leukotriene antagonists or theophylline.
59
Q

What investigation is typically used to diagnose a simple pneumothorax?

A

An erect chest x-ray, which shows an area without lung markings and a clear line demarcating the lung edge.

60
Q

How is the size of a pneumothorax measured on a chest x-ray?

A

By measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum, according to BTS guidelines.

61
Q

How is a pneumothorax managed if the patient has a <2 cm pneumothorax?

A

Conservative management with regular outpatient reviews, with no active treatment required.

62
Q

What options are available for managing a pneumothorax larger than 2 cm in lower-risk patients?

A

Options include conservative management, pleural vent ambulatory devices, needle aspiration, or chest drains based on the patient’s priority for procedure avoidance or rapid symptom relief.

63
Q

What is a pleural vent ambulatory device, and when is it used?

A

A catheter inserted into the pleural space with a device allowing air to exit but not return, used in outpatient management of pneumothorax for rapid symptom relief.

64
Q

Where is a chest drain inserted for treating pneumothorax?

A

In the “triangle of safety” formed by the 5th intercostal space, midaxillary line, and anterior axillary line, just above the rib to avoid the neurovascular bundle.

65
Q

What are signs that a chest drain is functioning correctly?

A

Air bubbling through the drain, swinging of water during respiration, and lung re-inflation on a repeat chest x-ray.

66
Q

What are two common complications of chest drains?

A

Air leaks around the drain site (persistent bubbling) and surgical emphysema (air collecting in the subcutaneous tissue).

67
Q

When is surgical intervention required in the management of pneumothorax?

A

When a chest drain fails, there is a persistent air leak, or for recurrent pneumothorax.

68
Q

What are the surgical options for treating recurrent pneumothorax?

A

Video-assisted thoracoscopic surgery (VATS) with options like pleurodesis (abrasive or chemical) or pleurectomy.

69
Q

What causes a tension pneumothorax, and why is it dangerous?

A

A one-way valve lets air into the pleural space but not out, causing pressure to build, potentially shifting the mediastinum and leading to cardiorespiratory arrest.

70
Q

What are key signs of a tension pneumothorax?

A

Tracheal deviation away from the pneumothorax, reduced air entry, increased resonance on percussion, tachycardia, and hypotension.

71
Q

How is a tension pneumothorax managed in an emergency?

A

Insert a large-bore cannula into the second intercostal space in the midclavicular line or the 4th/5th intercostal space anterior to the midaxillary line.

72
Q

What are the normal values for pH, PaO2, PaCO2, HCO3, and lactate in ABGs?

A

pH: 7.35 – 7.45
PaO2: 10.7 – 13.3 kPa
PaCO2: 4.7 – 6.0 kPa
HCO3: 22 – 26 mmol/L
Lactate: 0.5 – 1 mmol/L

73
Q

What is the main difference between type 1 and type 2 respiratory failure?

A

Type 1: Low PaO2 with normal PaCO2.
Type 2: Low PaO2 with elevated PaCO2.

74
Q

How can you distinguish between respiratory and metabolic causes of acid-base imbalance?

A

Respiratory cause: Changes in PaCO2 (high CO2 for acidosis, low CO2 for alkalosis).
Metabolic cause: Changes in bicarbonate (HCO3) (low in acidosis, high in alkalosis).

75
Q

How does the kidney respond to chronic CO2 retention?

A

The kidneys produce more bicarbonate (HCO3) to buffer the acidic CO2, helping maintain a normal pH, which is seen in chronic conditions like COPD.

76
Q

What are some common causes of metabolic acidosis?

A

Raised lactate: Due to tissue hypoxia (e.g., shock).

Raised ketones: In diabetic ketoacidosis.

Increased hydrogen ions: Renal failure or rhabdomyolysis.

Reduced bicarbonate: Diarrhea or renal tubular acidosis.

77
Q

What are the common causes of metabolic alkalosis?

A

Loss of hydrogen ions from vomiting, or increased aldosterone activity (e.g., Conn’s syndrome, heart failure, cirrhosis).

78
Q

How do loop and thiazide diuretics contribute to metabolic alkalosis?

A

They increase aldosterone activity, leading to increased excretion of hydrogen ions in the kidneys.

79
Q

What ABG findings are typical in a patient with diabetic ketoacidosis?

A

Metabolic acidosis with low pH, low bicarbonate, and raised ketones.

80
Q

What ABG findings are expected in a patient with anxiety-induced hyperventilation?

A

Respiratory alkalosis with high pH, low PaCO2, and typically normal or high PaO2.

81
Q

What are the escalating options for supporting a patient’s respiratory system?

A
  1. Oxygen therapy
  2. High-flow nasal cannula
  3. Non-invasive ventilation (NIV)
  4. Intubation and mechanical ventilation
  5. Extracorporeal membrane oxygenation (ECMO)
82
Q

What is the primary goal of respiratory support?

A

Respiratory support buys time to manage the underlying problem, but it does not fix the root cause.

83
Q

What are the key features of Acute Respiratory Distress Syndrome (ARDS)?

A

Alveolar collapse (atelectasis)
Pulmonary oedema (non-cardiogenic)
Decreased lung compliance
Lung fibrosis (after ~10 days)

84
Q

What are the clinical signs of ARDS?

A

Acute respiratory distress

Hypoxia unresponsive to oxygen therapy

Bilateral infiltrates on a chest x-ray

85
Q

How is ARDS managed?

A

Respiratory support

Prone positioning

Careful fluid management

86
Q

What are the oxygen delivery methods and corresponding FiO2?

A

Nasal cannula: 24 – 44%
Simple face mask: 40 – 60%
Venturi masks: 24 – 60%
Non-rebreather mask: 60 – 95%

87
Q

What is Positive End-Expiratory Pressure (PEEP), and why is it important?

A

PEEP is the pressure applied at the end of exhalation to keep the airways inflated, reducing atelectasis and improving gas exchange.

88
Q

What is Continuous Positive Airway Pressure (CPAP) used for?

A

CPAP provides constant pressure to keep airways open, commonly used in obstructive sleep apnoea and conditions prone to airway collapse.

89
Q

What is the difference between CPAP and non-invasive ventilation (NIV)?

A

CPAP provides constant pressure without ventilating, while NIV uses varying pressures to assist both inhalation and exhalation, supporting ventilation.

90
Q

What does BiPAP stand for, and how does it work?

A

BiPAP (Bilevel Positive Airway Pressure) delivers two pressures: IPAP for inhalation and EPAP for exhalation, preventing airway collapse and supporting breathing.

91
Q

What is Extracorporeal Membrane Oxygenation (ECMO), and when is it used?

A

ECMO provides respiratory support by oxygenating blood outside the body. It is used in severe, reversible respiratory failure when mechanical ventilation is insufficient.

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