PBL Topic 2 Case 3 Flashcards

1
Q

Outline four characteristics of COPD

A
  • Airflow limitation
  • Not fully reversible
  • Progressive
  • Abnormal inflammatory response
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2
Q

What are the main cause of COPD in developed countries and developing countries respectively?

A
  • Cigarette smoking

- Smoke from biomass fuels

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3
Q

Outline the pathophysiology of COPD

A
  • Mucus gland hyperplasia
  • Infiltration of neutrophils and CD8 lymphocytes
  • Squamous metaplasia
  • Loss of interstitial support
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4
Q

Define emphysema

A
  • Abnormal, permanent enlargement of air spaces
  • Distal to the terminal bronchioles
  • Accompanied by destruction of their walls without obvious fibrosis
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5
Q

Describe centri-acinar emphysema

A
  • Destruction concentrated around the respiratory bronchioles
  • Distal alveolar ducts and alveoli well preserved
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6
Q

Define pan-acinar emphysema

A
  • Destruction of the whole acinus

- Associated with a1-Antitrypsin deficiency

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7
Q

Outline the other type of emphysema

A
  • Irregular emphysema

- Damaging and scarring of lungs in a patchy manner independent of acinar structure

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8
Q

Identify 2 ways in which Va/Q mismatch occurs in emphysema

A
  • Mucous plugging of smaller airways from inflammation

- Closure of small airways due to loss of elastic support

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9
Q

Explain why hypoxaemia develops in emphysema

A
  • Va/Q mismatch leads to increased work of ventilation
  • PaCO2 increases
  • Patients become insensitive to CO2 and come to depend on hypoxaemia to drive their ventilation

(in normal people, the drive for ventilation is high CO2, though these patients become insensitive so low O2 drives their ventilation)

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10
Q

Explain why polycythaemia develops in emphysema

A
  • Renal hypoxia

- Fluid retention and erythrocyte production

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11
Q

Identify the clinical features of polycythaemia

A
  • ‘Blue Bloater’
  • Barrel chest and dyspneic
  • Hunched over
  • Breathes through pursed lips ‘pink puffers’
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12
Q

What is the role of a1-Antitrypsin

A
  • Antiprotease secreted by liver
  • Inhibits neutrophil elastase
  • Maintain lung elasticity
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13
Q

What is the effect of cigarette smoke on a1-Antitrypsin?

A
  • Inactivates a1-Antitrypsin

- Leads to emphysema

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14
Q

Respiratory failure is said to occur when:

  • PaO2 < [A]
  • PaCO2 > [B]
A
  • [A] = 8 kPa (60 mm Hg)

- {B] = 7 kPa (55 mm Hg)

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15
Q

What are the effects of hypoxia and hypercapnia?

A
  • Constriction of pulmonary arterioles

- Pulmonary hypertension (Cor Pulmonale)

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16
Q

What is the cause of pulmonary hypertension (cor pulmonale)

A
  • Renal hypoxia
  • Failure of excretion of sodium and water
  • Leads to fluid retention
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17
Q

What are the clinical features of pulmonary hypertension (cor pulmonale)

A
  • Cyanosed and breathless
  • Ankle oedema
  • Parasternal heave
  • Elevated JVP due to incompetence of pulmonary valve
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18
Q

‘During nocturnal hypoxia, PaO2 may fall as low [A], especially during the [B] phase of sleep’

A
  • [A] = 2.5 kPa (19 mm Hg)

- [B] = Rapid Eye Movement (REM)

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19
Q

During nocturnal hypoxia, outline three causes that result in alveolar hyperventilation

A
  • Inhibition of intercostal and accessory muscles in REM sleep
  • Shallow breathing
  • Increase in upper airway resistance due to reduced muscle tone
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20
Q

What is the main cause of death in COPD patients?

A
  • Most deaths occur at night
  • From cardiac arrhythmias
  • Due to hypoxaemia
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21
Q

Explain why patients with nocturnal hypoxia suffer from daytime sleepiness?

A
  • Desaturation is terminated by waking up
  • This occurs many times in the night
  • Amount of sleep is therefore reduced
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22
Q

Outline the main treatment of nocturnal hypoxia and why sleeping tablets should not be given.

A
  • Nocturnal administration of oxygen by nasal mask and BiPAP

- Sleeping tablets further depress respiratory drive

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23
Q

Outline characteristic symptoms of COPD

A
  • Cough with clear sputum
  • Wheeze and breathlessness
  • Infections with purulent symptoms
  • All made worse by cold / foggy weather
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24
Q

Outline characteristic signs of COPD

A
  • Tachypnea
  • Hyperinflation of lungs
  • Heart failure and oedema as terminal events
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25
Q

Diagnosis of COPD requires demonstration of flow obstruction by spirometry and is established when:

A
  • FEV1 < 80% predicted value

- FEV1/FVC ratio < 70%

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26
Q

Outline the management of COPD

A
  • Smoking cessation
  • Bronchodilators (B-adrenergic agonists, theophylline, antimuscarinic drugs)
  • Anti-inflammatories (corticosteroids, phosphodiesterase type 4 inhibitors)
  • Antibiotic treatment
  • Oxygen therapy
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27
Q

Outline when oxygen therapy will be beneficial to patients:

A
  • PaO2 < 55 mm Hg
  • PaO2 < 60 mm Hg with secondary polycythaemia
  • Carboxyhaemoglobin < 3%
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28
Q

What is the BODE Index?

A
  • Determine prognosis of COPD
  • B = Body Mass
  • O = Obstruction
  • D = Dyspnoea
  • E = Exercise Capacity
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29
Q

How does a BODE index of 0-2 differ to that of a BODE index of 7-10

A
  • 0-2: 4 year mortality rate of 10 %

- 7 - 10: 4 year mortality rate of 80%

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30
Q

Define bronchiectasis

A
  • Permanently dilated airways
  • Irreversible damage of airways
  • Impaired mucociliary transport mechanism
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31
Q

Outline two causes of bronchiectasis

A
  • Genetic defect e.g. cystic fibrosis

- Infection e.g. tuberculosis

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32
Q

Outline four clinical features of bronchiectasis

A
  • Clubbing
  • Yellow or green sputum (following infection)
  • Breathlessness (airflow limitation)
  • Haemoptysis
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33
Q

Identify investigations carried out for bronchiectasis

A
  • HRCT/CXR = Dilated Airways
  • Sputum culture = Bacterial Infection
  • Sinus X rays
  • Sweat test = Cystic Fibrosis
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34
Q

Outline the treatment of bronchiectasis

A
  • Postural drainage
  • Ceftazidime for P.aeruginosa
  • Flucloxacillin for S.aureus
  • Surgery: embolisation and surgical resection
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35
Q

Outline complications of bronchiectasis

A
  • Pulmonary Tuberculosis
  • Pneumonia
  • Pneumothorax
  • Emphysema
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36
Q

What is Pneumonia

A
  • Inflammation of the substance of the lungs
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37
Q

Identify three classifications of Pneumonia

A
  • Community-acquired (CAP)
  • Hospital-acquired (HAP)
  • Immunocompromised host
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38
Q

Who is most likely to be affected by CAP?

A
  • Those at the extremes of age
39
Q

Which organism is most responsible for CAP?

A
  • Pneumococcus
40
Q

Identify the two types of CAP

A
  • Lobar pneumonia affecting one or more lobes

- Diffuse pneumonia affecting the lobules

41
Q

How are the micro-organisms that cause CAP mainly spread?

A
  • Respiratory droplets
42
Q

Outline four clinical features of CAP

A
  • Cough
  • Breathlessness
  • Swinging Fever
  • Chest pain that is pleuritic in nature
43
Q

How is severity of CAP assessed?

A
  • CURB-65 Score
  • C = Confusion present
  • U = Urea level
  • R = Respiratory rate
  • B = Systolic BP
  • 65 = > 65
  • Score of 0-1 = Outpatient
  • Score 2 = Admit to hospital
  • Score 3+ = ICU
44
Q

Outline the management of CAP

A
  • Supplemental oxygen
  • Intravenous fluid for hypotensive patients
  • Intravenous antibiotics
  • Thromboprophylaxis (heparin)
45
Q

Outline two complications of CAP, how they are diagnosed and treated

A
  • Empyema, diagnosed using thoracocentesis and Light’s criteria, treated by drainage and antibiotic treatment
  • Lung abscess, diagnosed based on CT scan and worsening pneumonia, treated by surgical drainage
46
Q

When is HAP diagnosed?

A
  • Cough and purulent sputum in patients who:
  • Are beyond 2 days of initial admission /
  • Attending a haemodialysis unit /
  • Resident in nursing home or long-term care facility
47
Q

Which organisms are most attributable to HAP?

A
  • Gram negative bacteria (Escherichia, Pseudomonas, Klebsiella)
  • Staphylococcus aureus
  • Anaerobes
48
Q

Outline the treatment for HAP

A
  • Cephalosporins and aminoglycoside for gram negative

- Vancomycin for MRSA

49
Q

What is the cause of aspiration pneumonia?

A
  • Aspiration of gastric content into the lungs
50
Q

What is Mendelson’s syndrome?

A
  • Aspiration of gastric content during anaesthesia

- Particularly during pregnancy

51
Q

What is the treatment of aspiration pneumonia and why?

A
  • Co-amoxiclav

- Covers Gram-negatives and anaerobes

52
Q

Which type of pathogens cause pneumonia in immunocompromised patients?

Provide one example of this type of pathogen

A
  • Opportunistic pathogens

- Pneumocystis jiveroci

53
Q

Identify the symptoms and treatment of Pneumocystis pneumonia

A
  • Shortness of breath
  • Fever
  • Bilateral diffuse interstitial shadowing
  • Co-trimoxazole
54
Q

What is the importance of induced sputum?

A
  • Safe method of obtaining microbiological samples

- Most patients are too ill for bronchoscopy

55
Q

What are interstitial lung diseases?

A
  • Heterogenous group of conditions
  • Whose presentation may differ widely
  • But share similar symptoms, signs and pulmonary function abnormalities
56
Q

Outline the pathogenesis of idiopathic pulmonary fibrosis

A
  • Patchy fibrosis of interstitium
  • Minimal or absent inflammation
  • Collagen deposition and honeycombing
  • Absence of type 1 pneumocytes in favour of type 2 pneumocytes
57
Q

How does fibroblastic foci develop?

A
  • Micro-injuries to alveolar cells secrete TGF-Beta

- Which secrete fibroblasts which differentiate into myofibroblasts.

58
Q

Outline the clinical features of Idiopathic Pulmonary Fibrosis

A
  • Progressive breathlessness
  • Bilateral end-inspiratory crackles
  • Finger clubbing in 2/3 of cases
59
Q

Outline the investigations carried out for Idiopathic Pulmonary Fibrosis

A
  • Chest X-ray shows a glassy appearance
  • Blood gases show hypoxaemia
  • Blood tests show anti-nuclear antibodies and rheumatoid factors with ESR and immunoglobulins mildly elevated
60
Q

Identify the effect of smoking on large airways

A
  • Increase in submucosal gland volume
  • Increase in number of goblet cells
  • Chronic inflammation
  • Metaplasia and dysplasia of surface epithelium
61
Q

Identify the effect of smoking on small airways

A
  • Increase in number and distribution of goblet cells
  • Airway inflammation and fibrosis
  • Epithelial metaplasia / dysplasia
  • Carcinoma
62
Q

Identify the effect of smoking on lung parenchyma

A
  • Proximal acinar scarring
  • Increase in alveolar macrophage numbers
  • Emphysema
63
Q

Identify the two components of cigarette smoke that are potent carcinogens

A
  • Polycyclic aromatic hydrocarbons

- Nitrosamines

64
Q

Identify the dangers of maternal smoking

A
  • Decrease in birthweight of infant
  • Increase in fetal and neonatal mortality
  • Increase risk in asthma
65
Q

Identify the dangers of passive smoking

A
  • Risk of asthma, pneumonia and bronchitis in infants of smoking parents
  • Increase in cough and breathlessness in people with COPD and asthma
  • Increased cancer risk
66
Q

Identify the likely cause of yellow or green sputum

A
  • Presence of neutrophils or eosinophils

- Infection / bronchiectasis

67
Q

Identify the likely cause of sputum that is rusty in appearance

A
  • Lobar pneumonia
68
Q

Identify the likely cause of sputum that is pink and frothy in appearance

A
  • Pulmonary oedema
69
Q

Identify the likely cause of sputum that is purulent

A
  • Bronchiectasis
70
Q

Identify the likely cause of massive haemoptysis

A
  • Bronchiectasis

- Tuberculosis

71
Q

Identify the likely cause of firm plugs of sputum

A
  • Allergic bronchopulmonary aspergillosis
72
Q

Describe the function and purpose of exercise tests

A
  • 6 minute walk along measured track
  • Additional information can be obtained by pulse oximetry
  • In order to assess the degree of disability of breathlessness
73
Q

Identify an example of a macrolide

A
  • Erythromycin
74
Q

Outline the mechanism of action of macrolides

A
  • Bind to P site on 50s subunit

- Inhibition of incoming tRNA and its attached amino acid

75
Q

Which bacteria are susceptible to macrolides?

A
  • Gram-positive bacteria
  • Spirochaetes
  • Some Gram-negative bacteria e.g mycoplasma pneumoniae and legionella
76
Q

Identify unwanted effects of erythromycin

A
  • Gastrointestinal disturbances

- Hypersensitivity reactions e.g. rashes and fever

77
Q

Identify an example of a second-generation cephalosporin

A
  • Cefuroxime
78
Q

Outline the mechanism of action of cephalosporins

A
  • Bind to penicillin-binding proteins
  • Inhibit transpeptidation enzyme
  • Activate autolytic enzymes
  • Leading to lysis of bacterium
79
Q

Identify unwanted effects of cephalosporins

A
  • Hypersensitivity reactions
80
Q

Outline the Moral Model of Addiction

A
  • An addict is behaving excessively

- Is therefore deserving of punishment

81
Q

Outline the Biomedical Approach

A
  • First disease concept, focus for the illness is the substance
  • Second disease concept, focus for the illness is the individual
82
Q

Outline Behaviourism

A
  • Classical conditioning, learning by association
  • Operant condition, learning by reinforcement
  • Social Learning Theory, learning by observing role models
83
Q

Outline predictors of initiation and maintenance of addiction

A
  • Fun pleasure, calming nerves, building confidence

- Parental smoking, peer group pressure and attitudes of the school towards smoking

84
Q

Outline interventions for smoking cessation

A
  • Clinical interventions, nicotine patches and replacement therapy
  • Self help movements, including aversion therapies and cue exposure procedures
  • Public health interventions, including doctor’s advice, governments interventions (banning advertisement, raising the cost, raising the cost, banning smoking in public places)
85
Q

Outline external and internal cues for a high risk situation

A
  • External cues, someone else smoking

- Internal cues, such as anxiety

86
Q

Outline coping strategies in a high risk situation

A
  • Avoiding the situation
  • Using a substitute behaviour
  • Remembering to abstain
87
Q

What is the difference between positive and negative outcome expectancies

A
  • Positive = Smoking will make me feel less anxious

- Negative = Smoking will be bad for my health

88
Q

What is empyema and what is its cause?

A
  • Collection of pus in the pleural cavity

- Due to bacterial infections

89
Q

What is the indicator that a patient has empyema?

A
  • Swinging fevers
90
Q

Why do patients with pneumonia have chest pain?

A
  • Inflammation of pleura

- Pleural rub may be heard

91
Q

What is lung consolidation?

A
  • Region of lung tissue is filled with liquid rather than air
92
Q

Why are patients with pneumonia treated with intravenous fluids?

A
  • Hypotension

- Inflammation causes vasodilation

93
Q

Explain the clinical significance of cefuroxime in relation to resistance

A
  • Beta lactamase resistant