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MRCP - Pastest Book > Respiratory Medicine > Flashcards

Respiratory Medicine Flashcards

1
Q

What reduces pulmonary compliance? (2)

A

Pulmonary venous engorgement + alveolar oedema

Atelectasis

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2
Q

Which cells release pulmonary surfactant?

A

Type 2 alveolar epithelial cells -> This lowers surface tension of the fluid lining the alveoli increasing lung compliance

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3
Q

What causes respiratory distress syndrome?

A

Lack of surfactant

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4
Q

Where does the greatest resistance to flow occur in the airways?

A

Medium-sized bronchi

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5
Q

What can happen to small airways at low lung volumes? Where is most susceptible to this?

A

They can close completely which can lead to areas of atelectasis

This particularly occurs at the lung bases

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6
Q

What is hypoxic vasoconstriction?

A

This is when vasoconstriction occurs in small arterioles of a hypoxic region of the lung

This helps divert blood away from areas of poor ventilation to ensure ventilation and perfusion is matched

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7
Q

Where are central and peripheral chemoreceptors found? what do they respond to?

A

Central - Medulla (Increases in H+ in the CSF secondary to increased pCO2 in blood)

Peripheral - Carotid + aortic bodies (Low O2, High CO2 and pH changes)

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8
Q

What is Cheyne-Strokes breathing?

A

Periods of apnoea followed by hyperventilation

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9
Q

When does Cheyne-Strokes breathing occur? (3)

A

Severe heart failure

Severe brain damage

High altitudes

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10
Q

What is the normal FEV1 : FVC ratio?

A

70-80%

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11
Q

What conditions show reduced FEV1 with normal FVC (reduced ratio)?

A

Occurs in airway obstruction eg asthma and COPD

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12
Q

What conditions show reduction in FVC with preserved FEV1 : FVC ratio?

A

Restrictive disease eg. pulmonary fibrosis, neuromuscular disease, obesity and pleural disease

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13
Q

How can TLC, RV and FRC be measured? (3)

A

Helium dilution
Nitrogren washout
Body box

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14
Q

What are the different causes of hypoxaemia? (7)

A

Hypoventilation (Opiate overdose, Respiratory muscle paralysis)

V / Q mismatch (PE)

Low inspired pO2 (High altitudes)

Impaired diffusion (Pulmonary oedema, interstitial lung disease)

Bronchiolar-alveolar cell carcinoma

Shunts (Pulmonary AV malformations, cardiac right to left)

Breathing in hypoxic mixtures

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15
Q

What does right shift of the oxygen dissociation curve represent? What can trigger this? (4)

A

Right shift increases how easily O2 offloads in the tissues

Caused by high temp, acidosis, increase in pCO2 and increased 2,3-diphosphoglycerate (2,3-DPG)

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16
Q

What does left shift of the oxygen dissociation curve represent? What can trigger this? (6)

A

O2 held on more closely by the Hb

Caused by low temp, alkalosis, decrease in pCO2, decrease in 2,3-diphosphoglycerate (2,3-DPG), COHb and fetal Hb

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17
Q

What are some early responses to altitude of the body? (2)

A

Hyperventilation due to hypoxic stimulation of peripheral chemoreceptors

The subsequent resp alkalosis is corrected via renal excretion of bicarb

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18
Q

What are some later changes in response to high altitude? (3)

A

Hypoxaemia -> EPO via kidneys -> polycythaemia thus incerased O2 carriage by blood

Increased 2,3-DPG production -> right shift of O2 dissocation curve -> better offloading to tissues

Hypoxic vasoconstriction -> increased pulmonary artery pressure -> RVH (nb. pulmonary HTN can be associated w/ pulmonary oedema - altitude sickness)

19
Q

Most important allergens responsible for asthma? (5)

A

House dust mite
Dog allergen
Cat allergen
Pollen
Grasses
Moulds

20
Q

Which drugs can trigger asthma attacks?

A

B-blockers

NSAIDs inc aspirin

21
Q

What are the features of early stages of asthma? (3)

A

Airways narrowed by a combination of:
1. Bronchiolar smooth muscle contraction
2. Mucosal oedema
3. Mucus plugging

In early stages, these changes are reversible

22
Q

What are the features of chronic asthma? (3)

A

Same features as early asthma however stuctural changes develop and lead to irreverisble fibrosis of airways

Structural changes:
1. Thickening of basement membrane
2. Goblet cell hyperplasia
3. Smooth muscle hypertrophy

23
Q

What causes sputum to be yellow / green in asthma?

A

Presence of eosinophils

24
Q

What are some features that suggest someone’s asthma may respond to steroids?

A

Sputum eosinophils >2 %

FENO >50 parts/billion

24
Q

What are some lung function tests that support asthma? (4)

A

Significant diurnal PEFR variability (>20%) for 3 or more days / week for 2 weeks

Significant improvement in PEFR (>15%)+ FEV1 (400ml+) with bronchodilator / steroids

Reduced FEV1 (Decreased FEV1:FVC ratio)

Raised exhaled nitric oxide concentration (FENO)

25
Q

When should patient with acute asthma be referred to ICU? (7)

A

Worsening PEFR
Persistent / worsening hypoxia
Rising pCO2
Decreasing pH
Exhaustion
Altered conciousness
Respiratory arrest

25
Q

Features of life threatening asthma? (10)

A
  • Hypoxaemia
  • PEFR <33% of predicted
  • Exhaustion
  • Bradycardia (pulse <60 beats/min) or arrhythmmia
  • Hypotension
  • A silent chest
  • Altered consciousness
  • Poor respiratory effort
  • Cyanosis
  • A normal or raised PCO2.
26
Q

Discharge criteria for patient with asthma? (5)

A
  • PEFR should be at least 75% of the patient’s best or predicted value
  • PEFR diurnal variability on monitoring should be <25%
  • The patient should have required no nebulised bronchodilators for at least 24 hours
  • The patient should have a written asthma action plan
  • The patient should have follow-up in primary or secondary care within 30 days of discharge
27
Q

What other respiratory condition do most patients with allergic bronchopulmonary aspergillosis have?

A

Asthma but can also occur in those without asthma

28
Q

What feature determines long term prognosis in those with COPD? What is a better way?

A

Post-bronchodilator FEV1 however this is poor in isolation

BODE index (BMI, airflow obstruction, dyspnoea, exercise) - 7 or more is 31% 2y mortality

29
Q

Can COPD progress if the person stops smoking?

A

Yes

30
Q

Causes of COPD? (5)

A
  • Smoking (usually a history of at least 20 pack-years)
  • Air pollution
  • Low birthweight and low socio economic status
  • Dust exposure
  • α1-Antitrypsin deficiency
31
Q

What is chronic bronchitis?

A

Chronic cough + sputum production for at least 3 months in 2 consecutive years in the absence of other causes

32
Q

What is emphysema?

A

Abnormal, permenant enlargement of airpaces distal to terminal bronchioles

It is accompanied with destruction of their walls without obvious fibrosis

33
Q

What are the different types of emphysema? (4)

A

Centriacinar (affects upper lobes, associated w/ smoking)

Panacinar (more common in a1-antitrypsin deficiency - whole acinus affected: alveoli, bronchioles + blood vessels)

Paraseptal

Scar emphysema (Localised around scars)

34
Q

What happens to DLCO in emphysema?

A

Reduced - which means reduced gas transfer

35
Q

How is COPD severity measured using FEV1? (4)

A
  • Mild: FEV1 ≥80% predicted
  • Moderate: FEV1 50–79% predicted
  • Severe: FEV1 30–49% predicted
  • Very severe: FEV1 <30% predicted
36
Q

What are the signs of Cor pulmonale?

A

Raised JVP

R Ventricular heave

Loud P2

Tricuspid regurg

Peripheral oedema

Hepatomegaly

37
Q

Does adding inhaled steroids in addition to LA bronchodilators in COPD impact disease progression?

A

No

38
Q

Why are inhaled steroids used in COPD management alongside long-acting bronchodilators?

A

They reduce frequent of exacerbations and improve QoL in patients w/ severe or v. severe COPD

39
Q

Which patients with COPD can be considered for lung transplants?

A

Under 65 with FEV1 and DLCO <20% of predicted

History of hospitalisation with exaccerbation associated with pulmonary hypertension +- cor pulmonale despite O2 therapy

40
Q

Which patients with COPD should be referred for pulmonary rehab? Why?

A

All motivated patients regardless of severity

Increases exercise tolerance + improve QoL

41
Q

When are abx indicated in COPD exacerbations?

A

If 2 of the following are present:
* Increased breathlessness
* Increased sputum volume
* Increased sputum purulence.

42
Q

What needs to be done in COPD exacerbation if hypercapnia and acidosis is present on inital ABG?

A

Treated as normal for hour

Repeat ABG

If acidosis with hypercapnia persists non-invasive positive pressure ventilation should be started via face mask

MRCP - Pastest Book (2 decks)

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