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Medical conditions > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the first step in diagnosing asthma in adults with suspected Asthma (age > 16 years).

List 2 tests – either one positive then diagnose.

A
  1. Measure blood eosinophil count or FeNO
    Raised eosinophil count → Diagnose asthma
  2. FeNO ≥ 50 ppb → Diagnose asthma
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2
Q

What is the first step in diagnosing asthma in children and young adults aged 5-16 years?

A

Measure FeNO.

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3
Q

What should be done if asthma is not confirmed by FeNO level or FeNO cannot be measured?

A

Measure bronchodilator reversibility with spirometry. Or peak flow if unavailable.

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4
Q

What FEV1 increase indicates a diagnosis of asthma?

A

FEV1 increase ≥ 12% and ≥200 ml compared to measurement pre-bronchodilator.

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5
Q

What should be performed if asthma is not confirmed by any of the tests (FeNO, spirometry, peak flow)? List 2.

A
  1. Perform skin prick testing for house dust mite allergy.
  2. FBC - serum eosinophil count.

Negative then exclude. If still uncertain > paed specialist.

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6
Q

What is a major change in asthma management guidelines in 2024?

A

SABA-Free Pathways and regular ICS use.

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7
Q

What the first step in medical management of asthma (2024) in patients aged > 12?

What is it now called?

A

PRN - Low-dose ICS + formoterol (LABA) combination inhaler used as-needed.

This is referred to as anti-inflammatory reliever (AIR) therapy.

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8
Q

What does MART stand for in asthma management?

A

Maintenance and reliever therapy (MART).

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9
Q

List 3 medications used as ICS for asthma.

A

Beclomethasone, budesonide, fluticasone

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10
Q

What is Step 2 in the asthma management guideline (2024)?

E.g. Name the specific drugs.

A

MART: ICS + Formoterol used for daily maintenance and as needed.

Change: AIR therapy now PRN and maintenance.

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11
Q

What is Step 3 in the asthma management guideline (2024)?

E.g. patient not controlled despite low-dose MART.

A

Moderate-dose MART.

Increase MART dose.

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12
Q

What is Step 4 and 5 in the asthma management guideline (2024)?

E.g. patient not controlled despite moderate-dose MART.

A

Step 4: Check adherence to medications and then FeNO and eosinophil count. If FeNO or eosinophil count is raised, refer to secondary care. If not raised, proceed to the following step.

Step 5: Add LRTA or LAMA on top of MART.

Oral leukotriene receptor antagonist trial (LRTA) or a long-acting muscarinic receptor antagonist (LAMA) + moderate-dose MART. After 8-12 weeks:
- Asthma controlled → Continue this treatment.
- Asthma partially controlled but not adequately → Continue this treatment but try the other medication not used.
- Asthma control not improved → Stop LTRA or LAMA and try the other medication not used.

If not controlled: specialist advice.

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13
Q

For how long should the 5th step of asthma management be tried before adjusting/ referring to a specialist?

i.e. LRTA + moderate dose MART

A

8-12 weeks

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14
Q

Why is someone with asthma prone to exacerbations?

A

Chronic inflammation of the airways leads to bronchial hyperresponsiveness.

which causes bronchial constriction and mucus hypersecretion.

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15
Q

Causes of acute asthma exacerbation. (List 3)

A
  1. Cold air, exercise
  2. Respiratory infection
  3. Irritants and allergens: pollution, smoke, dust, strong odour

SOB, wheeze, chest tightness, cough.

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16
Q

List 2 medications that can precipitate asthma

A

NSAIDs, beta-blockers

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17
Q

How do you determine treatment of an acute asthma attack?

A

Grade it by severity.

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18
Q

Three severities of an asthma attack that don’t respond to initial AIR therapy.

A
  1. Moderate
  2. Severe
  3. Life-threatening
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19
Q

What are your bedside investigations for suspected asthma exacerbation?

Start from examination.

A
  • Resp exam: inspection of breathing effort, auscultation for wheeze and breathing.
  • Vital signs: O2, heart rate, respiratory rate
  • ** Peak expiratory flow** test (measure against predicted value)
  • **ABG **if life-threatening.
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20
Q

Important investigation for patients with suspected life-threatening asthma..

A

ABG

SpO2 might be > 92% which is dangerous

Look at CO2 and pH as well.

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21
Q

Describe the features of moderate, severe, and life-threatening exacerbations.

Start from presentation e.g. Speech, exam, vital signs, PEFR etc.

A

Moderate: can speak, but PEFR 50-75%, slightly raised RR and HR

Severe: Can’t complete full sentences, PEFR 35-50%, RR > 25 and HR>110

Life-threatening: Can’t speak, may have altered mental status, silent chest, cyanosis PEFR <35%, PaO2 <92%

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22
Q

Red flags for life-threatening exacerbation of asthma. (List 4)

A
  • Unable to speak/ depressed conscious state
  • Cyanosis, silent chest, feeble respiratory effort
  • O2 sats <92%
  • PEFR < 35%

Any one present requires hospital admission. E.g. patient may have good O2 sats but is completely unable to speak and looks really unwell.

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23
Q

A patient with a history of asthma presents acutely SOB despite inhaler.

What warrants immediate referral and admission to hospital for treatment?

A

Severe and life-threatening asthma. Esp with pregnant women.

Often patients can’t speak properly and has deranged vital signs. PEFR < 50%.

Mild-moderate may be managed in community.

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24
Q

List 2 management options of moderate acute asthma exacerbation in the community.

A

Salbutamol (spacer or nebulised)

Prednisolone 40-50mg if needed.

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25
Q

Management options of acute, severe asthma in hospital.

A
  • Oxygen - aim for target saturations of 94-98%
  • Nebulised (oxygen driven) salbutamol 5mg
  • 40-50mg prednisolone oral (IV if not responding) for 5 days

Main addition is oxygen therapy.

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26
Q

Management options of life-threatening asthma in hospital. (List 3 essential therapeutics)

Consider A-E, meds, non-meds

A
  1. O2 supplementation targeting 94-98%
  2. Salbutamol (SABA) and Ipratropium (SAMA) - combined, nebulised.
  3. Hydrocortisone IV (100mg) or prednisolone PO (40-50mg)

If not responding:
5. Magnesium IV infusion
6. ICU/ expert help

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27
Q

What should be checked, to complete the management of an asthma exacerbation once patient is stable?

A

Inhaler technique
Review management plan e.g. if step-up needed. (By GP)

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28
Q

Definition of chronic bronchitis

A

Cough with sputum production for at least 3 months a year for 2 consecutive years.

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29
Q

What causes the pathophysiological changes found in COPD?

A

Chronic inflammation (caused by inhlaed particles i.e. smoking)

Inflammatory cells (neutrophil, macrophages and lymphocytes) release inflammatory mediators. This leads to airway remodelling, mucus hypersecretion and tissue destruction.

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30
Q

What are the 3 pathophysiological changes found in COPD that causes obstructive airflow?

A
  • Airway remodelling: thickened airways due to increased smooth muscle and fibrosis
  • mucus hypersecretion: stimulated by chronic inflammation
  • tissue destruction: parenchymal destruction —emphysema. Alveoli are progressively destroyed.
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31
Q

How does COPD affect the capillary pressure in the lungs and the heart?

A

Chronic hypoxia leads to thickening of vessel walls and narrowing of pulmonary arteries.

This can increase pulmonary arterial pressure and lead to pulmonary hypertension. > R-sided ventricular hypertrophy/failure, peripheral oedema etc.

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32
Q

Apart from smoking, list 4 other risk factors for COPD?

A
  • Occupation exposure of dust, fumes, chemicals (mining, construction and manufacturing.)
  • Air pollution
  • Alpha-1-antitrypsin deficiency
  • Asthma
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33
Q

When should you suspect COPD in a patient?

A

NICE says to suspect COPD in people >35 with a risk factor and one or more of the symptoms e.g. progressive, breathlessness, worse on exertion, chronic productive cough, wheeze, frequent lower respiratory tract infections e.g. during winter.

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34
Q

List some signs of COPD upon examination (from observation etc.)

A
  • Cyanosis
  • Accessory muscle use, pursed lip breathing
  • Raised JVP
  • Peripheral oedema
  • Hyperinflation of chest
  • On percussion: hyperresonance
  • On auscultation: wheeze, crackles
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35
Q

How do you describe breathlessness that is worse on exertion?

A

Exertional breathlessness

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36
Q

How is COPD diagnosed?

A

Spirometry. FEV1/FVC < 0.7 post-bronchodilator

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37
Q

What is the role of spirometry in COPD patients?

A
  • Diagnosis
  • Monitoring disease progression/severity
38
Q

What additional test may be performed for patients who have early-onset COPD? They may also have liver disease.

A

Serum alpha-1-antitrypsin

39
Q

What should you explain to patients upon a diagnosis of COPD?

A
  • What it is —an irreversible and progressive lung conditions
  • Disease progression/complications and ways to manage it: conservative and medical
  • Education on how to use inhalers and what to expect e.g. side effects.
40
Q

List 3 self-management options for COPD

A
  • Smoking cessation
  • Pulmonary rehabilitation e.g. Keeping healthy e.g. diet, weight loss, exercise, education
  • Vaccination: annual flu and pneumococcal vaccine to reduce risk of infection and exacerbation
41
Q

What is the first-line medical treatment of COPD?

A

Short acting beta-2- agonist (salbutamol)
or
Short acting muscarinic antagonist (ipratropium bromide)

SABA or SAMA; for relief of breathlessness or exercise limitations

42
Q

What are the second-line treatments for COPD if there are persistent symptoms after first-line treatments?

Which feature determines whether to add steroids or not?

A

Continue or switch to SABA
AND
start maintenance therapy: LABA + inhaled corticosteroid if with asthmatic features or LABA+LAMA

43
Q

List some asthma features/steroid responsive features in COPD patients.

A
  • Previous diagnosis of asthma or atopic illness
  • FEV1 variation >400mls
  • Peak flow diurnal variability or >20%
  • Elevated blood eosinophil count
44
Q

What is triple inhaled therapy? When is it indicated?

A

LABA + LAMA + ICS

Indicated for patients with severe COPD e.g. grade 3-4 with day-to-day symptoms and exacerbations, despite dual therapy.

45
Q

What are some long-acting beta agonists?

A

Salmeterol, formeterol

46
Q

Give an example of a SAMA and LAMA.

A
  • SAMA: ipratropium
  • LAMA: Tiotropium, aclidinium, umeclidinium
47
Q

What is a common combination inhaler brand?

A

Ellipta (LABA+LAMA)

48
Q

How do muscarinic antagonists e.g. SAMAs/LAMAs improve COPD?

A
  • Bronchodilation: relaxes airway smooth muscle
  • Reduces inflammation
  • Decreases mucus production.

By blocking M3 mAchRs.

49
Q

What are common side effects of inhaled B2 agonists? Which electrolyte imbalance might it cause?

A

Tremors, tachycardia, palpitations, headache, and muscle cramps.

Can also cause hypokalaemia.

50
Q

How should you instruct a patient on how to use a metered-dose inhaler?

A
  1. Shake the inhaler
  2. Take a deep breath out before closing your lips around the mouthpiece of the inhaler
  3. Press the dose-release button and breathe in slowly and deeply.
  4. Hold your breath for about 10 seconds
  5. Breathe out slowly.
  6. Wait 30-60s if another dose is needed.

Ask patient to repeat after.

Propellent is used in the mist

51
Q

What are the differences between dry-powdered inhalers?

A

There is no need to press a dose-release button, but requires patient’s sharp and deep inhalation.

52
Q

Why is good inhaler technique important and how would you explain this to a patient?

A

Explain this before instructing patient of inhaler technique.

Good technique is essential for ensuring the medication reaches their lungs for its therapeutic effects. It also reduces the chance of side effects associated with steroids e.g. oral thrush.

53
Q

Do all patients need to rinse their mouths after inhaler use?

A

No. Only those which has steroid.

54
Q

What are infective causes of COPD exacerbations? List 3 viral and 3 bacterial causes.

A
  • Rhinovirus
  • Influenza virus
  • Respiratory syncytial virus (RSV)
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
55
Q

List 4 non-infective causes of COPD exacerbation.

A
  • Psychological: stress and anxiety
  • Environmental: cold weather, air pollution
  • Allergens: pollen, dust mites, animal dander
  • Medication non-adherence
56
Q

What is an important feature in a COPD patient’s history that may suggest an infective exacerbation?

A

Recent upper respiratory tract infection (past 5 days)

57
Q

What are some symptoms that suggest COPD exacerbation?

A
  • Worsened dyspnoea (reduced air entry)
  • Worsened cough and sputum - plurulence, amount
  • Wheezing
  • Fatigue, malaise
58
Q

What is the name of right-sided heart failure that originates from lung disease? How may it present?

A

Cor pulmonale

May cause raised JVP, peripheal oedema, fatigue etc.

59
Q

What are complications of COPD exacerbations i.e. which conditions are patients at risk of?

A
  • Pneumonia
  • PE
  • Cardiac disease e.g arrythmias
  • Worsening diabetes
60
Q

What are 3 important bedside investigations for COPD exacerbation patients?

A
  • Vital signs: pulse oximetry
  • ECG - to rule out comorbidities and make sure there are no cardiac complications
  • Take sputum culture
61
Q

What are some blood tests and first line imaging for investigating COPD exacerbation?

A
  • FBC, UnE - might show infection, polycythaemia
  • ABG - for respiratory failure
  • Blood culture if feverish.
  • Chest X-ray
62
Q

What blood gas results may indicate a type two respiratory failure?

3 domains

A
  1. Respiratory acidosis (pH <7.35)
  2. PaO2 < 8 kPa
  3. PaCO2 > 6 kPA
63
Q

What are 3 components of managing COPD exacerbations?

A
  1. Oxygenation - target 88-92%
  2. Bronchodilation and reduction of inflammation
  3. Treatment of underlying or presumed infection.
64
Q

How might you achieve good oxygenation in COPD patients? Give 2 ways.

A
  • Venturi mask (24% at 2-3L or 28% at 4L) - These are lowest. Blue or white masks.
  • Nasal cannula flow rate 1-2L/min

88-92%

65
Q

What five colours do venturi masks come in? What is the lowest O2 concentration and what is the highest?

A
  • Blue: Imagine a calm blue sky, representing the lowest oxygen concentration (24%).
  • White: Think of a white cloud, slightly higher up in the sky (28%).
  • Yellow: Picture a bright yellow sun, providing more energy (35%).
  • Red: Visualize a red hot air balloon, higher and more intense (40%).
  • Green: Imagine a lush green forest, representing the highest concentration (60%)
66
Q

What are adjustements to short-acting bronchodilation therapy for COPD exacerbation? I.e. changes to salbutamol.

A

Increase frequency and dose. Use nebulisation if needed.

67
Q

What additional medication is given in COPD exacerbation. What dose for how many days?

A

PO 30mg prednisolone once daily for 5 days.

68
Q

First-choice antibiotics for COPD exacerbation.

A

Amoxicillin

69
Q

What is an additional drug that can be used as an adjunct if patient is not responding to nebulisedi bronchodilators?

What is a cautionary test?

A

Theophylline.

Should monitor theophylline levels

70
Q

What should be done before discharge of a COPD exacerbation patient?

A
  • Spirometry tests
  • Optimisation of maintenance therapy.
71
Q

During a review for COPD, what key elements should be discussed?

A
  • Disease progression and effects of treatment
  • Mental health
  • Management: smoking status and motivations, rehab activities e.g. diet and exercise, vaccines, inhaler technique

https://www.nice.org.uk/guidance/ng115/resources/chronic-obstructive-pulmonary-disease-in-over-16s-diagnosis-and-management-pdf-66141600098245#page45

72
Q

What is LTOT and what is the criteria for being started on it?

A

LTOT - administration of oxygen for more than 15 hours a day, aimed at increasing life expectancy, reducing complications, and improving quality of life.

Criteria: people with advanced COPD.
ABG taken at 2 occasions, 3 weeks apart of
1. PaO2 < 7.3 or
2. PaO2 <8 with complicated features e.g. cor pulmonale (pulmonary hypertension, peripheral oedema), secondary polycythaemia

In patients with stable COPD management and are not smoking.

Burns and fires - no smoking and neighbors smoking, including e-cigarettes.

73
Q

Length of anticoaulation therapy for a provoked VTE e.g. PE with a clear precipitating factor?

Such as surgery or immobilisation

A

3 months.

74
Q

A 58-year-old woman presents with suspected PE. Her left calf is swollen and tender. Her Wells score is calculated to be 6. However, a CTPA returns a negative result for PE.

What is the most appropriate next step for this patient?

A

Proximal leg vein ultrasound scan is the most appropriate next step if a CTPA is negative but there is still clinical suspicion of DVT, which could still be the source of emboli despite a negative CTPA.

75
Q

When is a D-dimer most helpful during the investigation for a PE?

A

When the Wells score for PE is ≤ 4, it indicates that PE is unlikely. In such cases, a D-dimer test is performed to rule out PE.

Consider alternative diagnosis if low clincal suspicion and D-dimer neg.

76
Q

Indications for V/Q perfusion scan instead of a CT-PA for suspected PE.

A

**Severe renal impairment (eGFR < 30 mL/min/1.73m²)
**

77
Q

When is CT-PA performed?

A

High suspicion of PE, with calculated Well’s score > 4

78
Q

Which triad is useful for conceptualising RFs for VTEs?

A

Virchow’s triad: Haemostasis, hypercoaguable states, endovascular injury.

79
Q

What would happen if you perform a CT-PA on a patient with GFR<20?

A

Contrast-induced nephropathy

80
Q

Length of anticoaulation therapy for an unprovoked VTE

A

6 months.

81
Q

Top 2 anticoagulation drug choices for PE/DVT

A

Apixaban or rivaroxaban.

82
Q

Threshold for leg scan for suspected DVT

A

Well’s score 2 or more. 3 or more is highly likely.

83
Q

Types of lung cancer (x3)

A

NSCLC: adenocarcinoma, squamous cell carcinoma, large cell carcinoma
SCLC

Non-small cell vs small cell

84
Q

Distribution of lung cancer (location)

A
  • Central
  • Peripheral
85
Q

Which lung cancers typically grow centrally?

A

Squamous cell carcinoma (smokers) and small-cell lung cancers.

Large cell carcinomas can grow anywhere

86
Q

Which lung cancer(s) grow peripherally?

A

Adenocarcinoma

Large cell carcinomas can grow anywhere

87
Q

Most common type of lung cancer.

A

Adenocarcinoma

Affects non-smokers

88
Q

Which cells do adenocarcinomas orignate from? Where are they found?

A

Glandular cells (mucus producing), found in the peripheries of lungs e.g. alveoli.

89
Q

Which cells do squamous cell lung carcinomas orignate from? Where are they found?

A

Bronchial flat cells (line the surface of the airways) and tends to grow near the lung’s centre.

THINK smoking : highest concentration of smoke.

90
Q

Which cells do small cell lung cancers originate from? Where are they found?

A

Neuroendocrine (Kulchitsky) cells of the lung. Often central, near bronchi.

91
Q

Which lung cancer is most aggressive?

A

SCLC

Medical conditions (25 decks)

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