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Phase 2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Define inspiratory reserve volume (IRV).

A

The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.

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2
Q

Define expiratory reserve volume (ERV).

A

The additional volume of air that can be forcibly exhaled after a tidal volume expiration.

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3
Q

Define forced vital capacity (FVC).

A

The maximum volume of air that can be forcibly exhaled after maximal inhalation.

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4
Q

Define total lung capacity.

A

The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.

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5
Q

Define residual volume (RV).

A

The volume of air remaining in the lungs after a maximal exhalation.

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6
Q

Define functional residual capacity (FRC).

A

The volume of air remaining in the lungs after a tidal volume exhalation.

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7
Q

Define tidal volume (TV).

A

The volume of air moved in and out of the lungs during a normal breath.

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8
Q

Define FEV1.

A

The volume of air that can be forcibly exhaled in 1 second.

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9
Q

When is FEV1 abnormal

A

When FEV1 is less than 80% if the predicted value = obstruction

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10
Q

Define forced vital capacity

A

Total amount of air a person can exhale after full exhalation

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11
Q

When is FVC abnormal

A

When is is less than 80% of the predicted value

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12
Q

When is obstructive lung disease diagnosed in terms of lung function tests

A

FEV1/FVC <0.7
FEV1 lower than FVC
Suggests that there is some obstruction slowing the passage of air getting out of the lungs

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13
Q

What are the two main obstructive lung diseases

A

Asthma - narrowed airway due to bronchoconstriction

COPD - Chronic airway and lung damage causing obstruction

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14
Q

Describe the lung function test results for restrictive lung diseases

A

FEV1/FVC above 0.7
FVC and FEV1 equally reduced below 80% predicted volume
Restriction to the ability of the lungs to expand and take in air

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15
Q

Define peak expiratory flow (PEF).

A

The greatest rate of airflow that can be obtained during forced expiration. Age, sex and height can all affect PEF.

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16
Q

What is the transfer coefficient?

A

The ability of O2 to diffuse across the alveolar membrane.

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17
Q

How can you find the transfer coefficient?

A

Low dose CO is inspired, the patient is asked to hold their breath for 10s at TLC, the amount of gas transferred is measured.

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18
Q

Name 3 diseases that might have a low transfer coefficient.

A
  1. Emphysema.
  2. Anaemia.
  3. Fibrosing alveolitis.
  4. Pulmonary hypertension
  5. Idiopathic pulmonary fibrosis
  6. COPD
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19
Q

Name a disease that might have a high transfer coefficient.

A
  1. Pulmonary haemorrhage.
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20
Q

What happens in respiratory acidosis

A

Fail to get rid of CO2 resulting in a decrease in pH

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21
Q

What are the causes of respiratory acidosis

A 
Hyperventilation 
COPD
Any cause of respiratory failure 
 - Type 1 = PE 
 - Type 2 = hypoventilation
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22
Q

Describe the renal compensation to respiratory acidosis

A

Kidneys increase H+ secretion in form of NH4+ and will release more HCO3- into the plasma which increases pH

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23
Q

Define respiratory alkalosis

A

Too much CO2 lost resulting in an increased pH as CO2 is lost

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24
Q

What are the causes of respiratory alkalosis

A

CO2 depletion due to hyperventilation
Hypoxia
T1 respiratory failure due to PE

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25
Q

What is the renal compensation for respiratory alkalosis

A

Kidneys decrease H+ secretion thereby retaining H+ and helping the pH return to normal

Decrease in H+ secretion will result in a decrease in HCO3- reabsorption resulting in HCO3- excretion and thus a fall in plasma HCO3-

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26
Q

What is metabolic acidosis

A

Excess acid production resulting in a decrease in pH

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27
Q

What are the causes of metabolic acidosis

A

Renal failure
GI HCO3- loss
Dilution of the blood
Failure of H+ excretion - hypoaldosteornism

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28
Q

What is the respiratory compensation to metabolic acidosis

A

Decrease in pH will stimulate chemoreceptors of the lung resulting in enhanced respiration resulting in a fall in CO2 resulting in a increase in pH

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29
Q

What are the causes of a metabolic alkalosis

A 
Increase in pH 
Vomiting (Due to loss of gastric secretions)
Volume depletion 
Alkali ingestion 
Hyperaldosteronism
Hyperkalaemia
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30
Q

What is the respiratory compensation for metabolic alkalosis

A

Increase in pH inhibits chemoreceptors of the lung thereby reducing respiration thereby increasing CO2 resulting in a decrease in pH

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31
Q

What are the natural defences of the upper respiratory tract against pathogens

A

Mucosal defences

  • Cough reflex
  • Mucus barrier and respiratory cilia
  • Surface secretions (Defensins and complement)

Innate immunity

  • macrophages
  • neutrophils

Adaptive immunity

  • B-cells
  • T cells
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32
Q

Name 2 upper respiratory tract infections.

A 
Rhinovirus = cold, bronchitis, sinusitis 
Influenza = flu 
Coronavirus = colds but sometimes severe respiratory illness 
Adenovirus = URTI, pharyngitis, bronchitis, pneumonia
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33
Q

Name some emergency respiratory infections

A

Severe acute respiratory distress syndromes (SARS)
Middle East respiratory syndrome novel coronavirus
Avian influenza

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34
Q

What viruses can cause pneumonia?

A

Adenoviruses, influenza A and B, measles, VZV.

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35
Q

What are the causative agents of the common cold

A

Rhinovirus and coronavirus

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36
Q

What are the symptoms of rhinitis or sinusitis

A 
Blocked/runny nose 
Sore throat 
Cough 
Sneezing
Pain, swelling and tendernesss around sinuses 
Facial pain 
Fever
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37
Q

What is the management of rhinitis and sinusitis

A

Nasal decongestants = xylometazoline

Broad spectrum antibiotics = Co-amoxiclav

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38
Q

Is sinusitis usually bacterial or viral?

A

Viral.

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39
Q

What are the causative agents of bacterial sinusitis

A

Streptococcus pneumoniae

Haemophilus influenzae

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40
Q

What are the symptoms of bacterial sinusitis

A

Unilateral pain
Purulent discharge
Fever

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41
Q

What are the complications of sinusitis

A

Brain abscess, sinus vein thrombosis, orbital cellulitis

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42
Q

Is pharyngitis normally caused by bacterial or viral infection?

A

Viral e.g. rhinovirus, adenovirus etc.

Rarer causes = EBV and acute HIV

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43
Q

What bacteria might sometimes cause pharyngitis?

A

Streptococcus pyogenes.

Rare = mycoplasma pneumoniae, N. gonorrhoea, C.diptheriae

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44
Q

What are the symptoms of pharyngitis

A 
Painful throat 
Dry/scratchy throat 
Pharyngeal erythema 
Dry cough 
lymphadenopathy 
Fever 
Tonsils inflamed and swollen
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45
Q

What is the Centor criteria used for?

A

It determines the likelihood that a sore throat is bacterial or viral

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46
Q

What signs make up the Centor criteria?

A
  1. Tonsillar exudate.
  2. Tender/enlarged anterior cervical lymph nodes.
  3. Fever (>38°C).
  4. Absence of cough.
    (3 or 4 of these = 50% chance of bacterial infection).
    (0-2 = viral infection)
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47
Q

What is the management of pharyngitis

A

Self limiting disease
Symptomatic treatment
No antibiotics
Persistent and severe tonsillitis treated with phenoxylmethylpenicillin

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48
Q

What is the causative agent of acute epiglottis

A

Haemophilus Influenza B

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49
Q

What are the symptoms of acute epiglottis

A

Odynophagia (Pain on swallowing)
Sore throat
Inspiratory stridor (High pitched wheezing noise when she breathes it in)
Febrile

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50
Q

What is the management of acute epiglottis

A 
Prevention = HiB vaccine 
Treatment = amoxicillin --> Doxycycline or co-amoxiclav
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51
Q

What is the causative agent of whooping cough

A

Bordatella pertussis - childhood disease with 90% cases below the age of 5

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52
Q

What type of bacteria is Bordetella pertussis?

A

Gram negative bacilli.

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53
Q

What is the disease course of whooping cough

A

7-10 day incubation
1-2 wk catarrhal stage
1-6wk paroxysmal stage

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54
Q

What are the symptoms of whooping cough in adults?

A
  • Chronic paroxysmal cough = sudden and severe

- Inspiratory ‘whoop’ posttussive vomiting (Vomiting after cough)

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55
Q

What are the complications of whooping cough

A

Pneumonia
Encephalopathy
Sub-conjunctival haemorrhage

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56
Q

What antibiotics might you use in someone with bordetella pertussis infection?

A

Clarithromyocin.

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57
Q

What agar would you culture bordetella pertussis on?

A

Bordet Gengou agar.

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58
Q

When is someone vaccinated against bordatella pertussis?

A

A child is vaccinated at 8, 12 and 16 weeks and at 3 years 4 months with dTaP vaccine.

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59
Q

What is the causative agent in influenza

A 
Influenza A (Severe outbreaks) 
Influenza B and C
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60
Q

What are the main antigens on influenza A?

A
  • Hemagglutinin (H).

- Neuraminidase (N).

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61
Q

What is the function of hemagglutinin?

A

‘Grappling hook’; grabs onto cells.

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62
Q

What is the function of neuraminidase?

A

‘Bolt cutters’; cuts newly formed virus loose from infected cells.

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63
Q

Which influenza pathogen is commonly behind severe and extensive outbreaks? Why?

A

Influenza A; it replicates a lot and mutations are common.

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64
Q

What are the two types of genetic variability in influenza

A

Antigenic drift

Antigenic shift

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65
Q

Define antigenic drift.

A

When there are small mutations and minor antigenic variation. Antigenic drift can cause seasonal epidemics.

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66
Q

Define antigenic shift.

A

When there are larger mutations and major antigenic variation. Antigenic shift can cause pandemics!

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67
Q

How can influenza virus be transmitted?

A
  • Aerosol: coughing and sneezing, inhale particles.

- Droplet: hand to hand.

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68
Q

What is the reproduction number?

A

The average number of secondary cases generated from a primary case.

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69
Q

What are the symptoms of influenza

A

URT infections = cough, sore throat, runny nose

Systemic symptoms = fever, headache and myalgia

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70
Q

What are the complications of influenza

A

Bacterial pneumonia

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71
Q

What is the treatment for influenza?

A

Supportive care! Antiviral medications might be used to reduce the risk of transmission.

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72
Q

Define outbreak.

A

> 2 linked cases.

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73
Q

Define epidemic.

A

More cases in a region/country.

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74
Q

Define pandemic.

A

Epidemics that span international boundaries.

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75
Q

What are the possible consequences of pandemics?

A
  1. High morbidity.
  2. Excess mortality.
  3. Social disruption.
  4. Economic disruption.
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76
Q

What factors are there to suggest that future pandemics may be likely?

A
  1. More travel.
  2. Increasing world population.
  3. Rise in intensive farming.
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77
Q

What factors are there to suggest that future pandemics may be unlikely?

A
  1. Healthier population due to medical advances.
  2. Better healthcare.
  3. Vaccination.
  4. Antivirals.
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78
Q

Where are a high proportion of cases of TB found?

A

The indian sub continent e.g. India, Bangladesh, Pakistan etc.

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79
Q

What are the 4 main mycobacterial species

A

Mycobacterium tuberculosis
Mycobacterium bovis
Mycobacterium africanum
Mycobacterium microti

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80
Q

Describe mycobacterium tuberculosis.

A
  1. Acid fast bacilli.
  2. Has a waxy capsule.
  3. It grows slowly and therefore is hard to culture in a lab.
  4. It can resist phagolysosomal killing resulting in granulomatous disease.
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81
Q

What mycobacterium can cause abdominal tuberculosis?

A

Mycobacterium bovis.

- Can be found in unpasteurised milk.

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82
Q

Give 5 risk factors for TB.

A
  1. If you live in a high prevalence area.
  2. IVDU.
  3. Homeless.
  4. Alcoholic.
  5. HIV+.
  6. smoking
  7. Prisons and malnutrition
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83
Q

How is TB transmitted?

A

Aerosol transmission - mycobacterium TB bacilli are inhaled and enter the lung.

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84
Q

Describe pulmonary infection of TB.

A

Bacilli settle in lung apex. Macrophages and lymphocytes mount an effective immune response that encapsulates and contains the organism forever.

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85
Q

Describe the pathogenesis of pulmonary TB disease.

A
  1. Bacilli and macrophages form primary focus.
  2. Mediastinal lymph nodes enlarge.
  3. Primary focus and enlarged lymph nodes = primary complex.
  4. Granuloma develops into a cavity.
  5. The cavity is filled with TB bacilli - these are expelled when the patient coughs.
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86
Q

TB disease: Where in the lung is a granuloma cavity most likely to develop?

A

Most likely to develop in the apex of the lung as there is more air and less blood supply/immune cells.

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87
Q

Presentation of TB: what systemic symptoms might you see?

A
  1. Weight loss.
  2. Night sweats.
  3. Anorexia.
  4. Malaise.
  5. Fever
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88
Q

Presentation of TB: what pulmonary TB symptoms might you see?

A
  1. Cough for more than 3 weeks in a year
  2. Chest pain.
  3. Breathlessness.
  4. Haemoptysis.
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89
Q

What are the extra pulmonary symptoms of TB

A

Lymph node TB with swelling and discharge

Bone pain and swelling in the joint

Abdominal TB = ascites and abdominal lymph nodes

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90
Q

What tests might you do in someone with suspected TB

A

Inflammatory markers = raised CRP, hyperalbuminaemia, thrombocytosis
Microbiology = Ziehl neelsen on sputum/biopsy
Tuberculin skin test (Mantoux test for latent TB) = stimulates T4 hypersensitivity reaction
CXR

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91
Q

What might you see on a CXR taken from someone with TB?

A
  1. Consolidation.
  2. Collapse.
  3. Pleural effusion.
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92
Q

Name 6 places where TB might spread to?

A
  1. Bone and joints - pain and swelling.
  2. Lymph nodes - swelling and discharge.
  3. CNS - TB meningitis.
  4. Miliary TB - disseminated.
  5. Abdominal TB - ascites, malabsorption.
  6. GU TB - sterile pyuria, WBC in GU tract.
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93
Q

What test might you do to diagnose latent TB?

A

Mantoux test - stimulates type 4 hypersensitivity reaction.

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94
Q

What drugs are given in the treatment of TB?

A

Rifampicin (6 months).
Isoniazid (6 months).
Pyrazinamide (2 months).
Ethambutol (2 months).

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95
Q

TB treatment: which 2 drugs are taken for the entire 6 months in active TB?

A
  1. Rifampicin.

2. Isoniazid.

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96
Q

TB treatment: which 2 drugs are taken for only the first 2 months for active TB?

A
  1. Pyrazinamide.

2. Ethambutol.

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97
Q

Which drug is taken for 6 months for latent TB

A

Isoniazid

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98
Q

Which drug is taken for 3 months for latent TB

A

Rifampicin

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99
Q

Give 3 potential side effects of Rifampicin.

A
  1. Red urine.
  2. Hepatitis.
  3. Drug interactions; rifampicin is an enzyme inducer.
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100
Q

Give 2 potential side effects of Isoniazid.

A
  1. Hepatitis.

2. Neuropathy.

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101
Q

Give 3 potential side effects of Pyrazinamide.

A
  1. Hepatitis.
  2. Gout.
  3. Rash.
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102
Q

Give 1 potential side effect of Ethambutol.

A
  1. Optic neuritis.
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103
Q

Compliance in taking TB medication is critical. Why?

A

Resistance and relapse may be likely if the patient is non-compliant.

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104
Q

Why does TB treatment need to last for 6 months?

A

TB treatment lasts for at least 6 months to ensure all the dormant bacteria have ‘woken up’ and been killed.

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105
Q

What is the acronym commonly used for the drugs taken in TB treatment?
HRZE.

A 
HR = 6 months. 
ZE = 2 months. 
- H - isoniazid. 
- R - rifampicin. 
- Z - pyrazinamide. 
- E - ethambutol.
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106
Q

TB treatment: Give 4 factors that can increase the risk of drug resistance?

A
  1. If the patient has had previous treatment.
  2. If they live in a high risk area.
  3. If they have contact with resistant TB.
  4. If they have a poor response to therapy.
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107
Q

What are the problems associated with drug resistance in TB treatment?

A
  1. TB becomes more difficult to treat.
  2. Medication course > 20 months.
  3. Increased risk of side effects.
  4. Increased relapse rate.
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108
Q

How can TB be prevented?

A
  1. Active case finding - reduce infectivity.
  2. Detect and treat latent TB.
  3. Vaccination - BCG.
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109
Q

A special culture medium is needed to grow TB. What is the medium called?

A

Lowenstein Jensen Slope.

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110
Q

Lowenstein Jensen Slope is a medium used to grow TB. What is special about this medium?

A
  1. It contains growth factors that promote mycobacterial growth.
  2. It contains small amounts of penicillin that prevent pyogenic bacteria growth.
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111
Q

What might a lymph node biopsy from someone with TB show?

A

Caseating granuloma.

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112
Q

Why does TB cause hypercalcaemia?

A

Granulomatous diseases -> increased vitamin D production and so increased bone resorption, increased absorption from gut and increased re-absorption from kidney.
This is also seen in sarcoidosis.

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113
Q

State the name of the pathological lesion that characterises primary tuberculosis?

A

Ghon complex.

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114
Q

State two socioeconomic factors that are associated with an increased prevalence of tuberculosis.

A
  1. Overcrowding.
  2. Poverty.
  3. Lower socio-economic class.
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115
Q

Define pneumonia

A

Infection of the lung tissue

= acute lower respiratory chest infection

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116
Q

Name 5 groups of people who might be at increased risk on pneumonia.

A
  1. The elderly.
  2. Children.
  3. People with COPD.
  4. Immunocompromised people.
  5. Nursing home residents.
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117
Q

What are the two anatomical classifications of pneumonia

A

Bronchopneumonia = patchy consolidation of different lobes

Lobar pneumonia = Fibrosuppurative consolidation of a single lobe

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118
Q

Describe in 3 steps the pathogenesis of pneumonia.

A
  1. Bacteria translocate to normally sterile distal airway - alveolar macrophage response
  2. Resident host defence is overwhelmed.
  3. Macrophages, chemokines and neutrophils produce an inflammatory response leading to airway exudate and parenchyma damage
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119
Q

What intrinsic factors can affect pneumonia?

A

Cold temperature, infection, stress, exercise, various pollutants.

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120
Q

Describe the process of pneumonia resolution?

A

Bacteria are cleared and inflammatory cells are removed by apoptosis.

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121
Q

What are different etiological classifications of pneumonia

A

Community acquired pneumonia
Hospital acquired pneumonia
Aspiration pneumonia
Immunocompromised pneumonia

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122
Q

What are the three main causes of community acquired pneumonia

A

Streptococcus pneumococcus
Mycoplasma pneumoniae
Haemophilus influenzae

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123
Q

What are the atypical causes of community acquired pneumonia

A

S.aureus
Moraxella cattarrhalis
Chlamydia pneumoniae
Legionella pneumonphilia

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124
Q

What are the main causative agents of hospital acquired pneumonia

A

> 48 hours since hospital admission
S.aureus
Pseudomonas Aeruginosa
Klebsiella pneumoniae

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125
Q

Which groups are at greater risk of aspiration pneumoniae

A

Patients with stroke, bulbar palsy, decreased GCS, GORD

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126
Q

What causes of immunocompromised pneumonia

A

S.pneumococcus
M.pneumoniae
H. Influenza

Rarer causes

  • Pneumocystis Jirevecii
  • TB
  • Aspergillus
  • CMV/HSV
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127
Q

What symptoms might you see in someone with pneumonia?

A
  • Productive cough with purulent sputum (Rusty) and haemoptysis
  • Sweats and rigor
  • Fever.
  • Breathlessness.
  • Pleuritic chest pain.
  • Anorexia, malaise
  • Myalgia, headache, arthralgia suggests atypical pneumonia.
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128
Q

What signs might you see in someone with pneumonia?

A 
Tachycardia + Tachypnoea 
Cyanosis 
Confusion 
Consolidation 
 - Dull percussion due to lung collapse 
 - Bronchial breathing (Harsh breathing on insp and exp due to consolidation)
 - Crackles (Air passing through sputum)
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129
Q

What investigations might you do on someone to determine whether or not they have pneumonia?

A
  • CXR - look for air bronchogram in consolidated area, infiltrates, cavities
  • FBC (look at WBC’s).
  • U+E.
  • ABG
  • Liver function tests.
  • CRP (marker of inflammation).
  • Microbiology: sputum culture, blood culture, serology etc
  • Sera Abs for atypicals ie mycoplasma, chlamydia and legionella
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130
Q

How can pneumonia be prevented?

A

How can pneumonia be prevented?

  • Children are given PCV.
  • Smoking cessation is encouraged.
  • Influenza vaccines are given to children and the elderly.
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131
Q

What is CURB65 used for?

A

It is a way of assessing the severity of community acquired pneumonia. It predicts mortality.

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132
Q

What does CURB65 stand for?

A 
Confusion.
Urea >7mmol/L. 
RR >30/min. 
BP reduced - systolic <90mmHg, diastolic <60mmHg.
Age >65.

1 point for each
0-1 = home Mx
2 = hospital Mx
>3 = consider ICU

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133
Q

Why is CRB65 often used in the community?

A

Because facilities to measure urea are often not available.

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134
Q

What is the treatment for pneumonia

A

Abx
O2
Analgesia if pleurisy
Chest physio

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135
Q

Which antibiotics are used for mild pneumonia

A

Amoxicillin OR clarithromycin

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136
Q

What antibiotics are used for moderate pneumonia

A

Amoxicillin AND Clarithromycin

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137
Q

What antibiotics are used for severe pneumonia

A

Co-amoxiclav/cefuroxime AND clarithromycin

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138
Q

What antibiotics are used for atypical pneumonia

A 
Chlamydia = tetracycline 
PCP = Co-trimoxazole 
Legionella = Clarithro + Rifampicin
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139
Q

What groups of people may develop pneumonia caused by klebsiella pneumoniae?

A
  • Homeless people.
  • Alcoholics.
  • People in hospital.
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140
Q

What are the complications of pneumonia

A 
Respiratory failure 
Hypotension (Due to dehydration and septic vasodilatation) 
Atrial fibrillation 
pleural effusion 
Empyema
Lung abscesses 
Sepsis 
Myocarditis/pericarditis 
Jaundice
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141
Q

What is empyema?

A

Pockets of pus that have collected in a body cavity e.g. in the pleural cavity

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142
Q

What bacteria can cause empyema

A

Anaerobes
Staph
Gm -ve
Associated with recurrent aspiration

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143
Q

Give 3 signs of empyema.

A
  1. WBC/CRP don’t settle with antibiotics.
  2. Pain on deep inspiration.
  3. Pleural collection.
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144
Q

What is the usual treatment for empyema?

A

Drainage.

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145
Q

What might you see in tap of someone with empyema

A

Turbid
pH <7.2
Decrease glucose
Yellow

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146
Q

What are lung abscesses

A

Severe localised suppuration within the lung associated with cavity formation

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147
Q

What are the causes of lung abscesses

A

Aspiration
Bronchial obstruction by tumour or foreign body
Septic emboli

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148
Q

What are the features of lung abscesses

A 
Swinging fever 
Cough, foul purulent sputum and haemoptysis 
Malaise and wt loss 
Pleuritic pain 
Clubbing 
Empyema
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149
Q

What is the management of lung abscesses

A

Aspiration
Abx
Surgical excision

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150
Q

Name 3 groups of people who might be at risk of hospital acquired pneumonia.

A
  1. Elderly.
  2. Ventilator associated.
  3. Post operative patients.
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151
Q

A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L.

a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient.

A

a) Their CURB65 score is 5.
b) This patient should be treated in hospital and admitted to critical care.
c) The patient should be given IV clarithromyocin and co-amoxiclav.

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152
Q

How can less common ‘atypical’ pathogens responsible for causing pneumonia be identified?

A

They are hard to grow in culture and so serology and antigen tests are often used.

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153
Q

What antibiotic might be used against less common ‘atypical’ pathogens responsible for causing pneumonia?

A

Macrolides like clarithromyocin as they are often resistant to beta lactams.

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154
Q

What can cause acute airway obstruction?

A

Tumour or foreign bodies with distal collapse of the lung.

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155
Q

If the trachea, bronchi and bronchioles are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Obstructive.

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156
Q

If the lung parenchyma are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive.

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157
Q

If the chest wall is involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive.

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158
Q

What happens to the FEV1, FVC and FEV1/FVC ratio in an obstructive lung disease?

A
  • FEV1 is < 80% predicted.
  • FVC is normal.
  • FEV1/FVC ratio < 0.7.
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159
Q

What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?

A
  • FVC reduced.

- FEV1/FVC ratio normal or increased

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160
Q

Give an example of a reversible obstructive lung disease.

A

Asthma.

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161
Q

Give an example of an irreversible obstructive lung disease.

A

COPD.

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162
Q

What is the affect of COPD on residual volume and total lung capacity?

A

RV and TLC are increased.

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163
Q

Give an example of a restrictive lung disease.

A

Pulmonary fibrosis.

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164
Q

What is bronchiectasis?

A

chronic infection of the bronchi/bronchioles leading to Permanent dilation of bronchi leading to a build-up of excess mucus and predisposes someone to chest infections.

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165
Q

Describe the pathogenesis of bronchiectasis.

A

Failed mucocilliary clearance and impaired immune function mean that a microbe can easily invade and cause infection. This leads to inflammation and therefore progressive lung damage. Bronchitis -> bronchiectasis -> fibrosis.

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166
Q

What can cause bronchiectasis?

A
  1. Often post-infective e.g. previous pneumonia, TB or whooping cough, measles
  2. Congenital causes e.g. primary ciliary dyskinesia/CF/Kartenger’s
  3. 50% idiopathic.
  4. Hypogammaglobinaemia
  5. Bronchial obstruction (Tumour, foreign body)
  6. Ulcerative colitis and Rheumatoid arthritis
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167
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenzae.
  2. Streptococcus Pneumococcus
  3. Pseudomonas aeruginosa.
  4. Staphylococcus aureus.
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168
Q

Give 6 symptoms of bronchiectasis.

A
  1. Chronic productive cough with purulent sputum
  2. Recurrent chest infections.
  3. Fever and wt loss
  4. Dyspnoea and wheeze.
  5. Recurrent exacerbations.
  6. Chest pain.
  7. Haemoptysis.
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169
Q

What are the signs of Bronchiectasis

A

Clubbbing
coarse inspiratory wheeze (Crackles)
Wheeze
Purulent sputum

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170
Q

Complications of bronchiectasis

A

Pneumonia
Pleural effusion
Pneumothorax
Pulmonary HTN

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171
Q

What investigations might you do on someone to determine whether they have bronchiectasis?

A
  • High resolution CT scan showing dilated and thickened airways
  • Spirometry - would be obstructive.
  • Sputum culture.
  • CXR showing thickened bronchial walls (Tramlines and rings)
  • Bloods (Serum Abs for aspergillus, RF, a1-AT)
  • Bronchoscopy
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172
Q

What is the treatment/management for bronchiectasis?

A
  1. Education.
  2. Smoking cessation.
  3. Annual influenza and pneumococcal vaccinations.
  4. Antibiotics.
  5. Anti-inflammatories.
  6. Bronchodilators - salbutamol
  7. Improved mucus clearance e.g. physiotherapy = postural drainage
  8. Treat underlying cause
    - Mucus = DNAse
    - Immune deficiency = IVIg
  9. Surgical lung resection
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173
Q

What antibiotic is used for P.aeruginosa

A

Ciprofloxacin

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174
Q

What antibiotic is used for H.influenza

A

Amoxicillin
Co-amoxiclav
Cephalosporin

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175
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a neonate likely to be colonised with?

A

s.aureus.

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176
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a child likely to be colonised with?

A

h.influenzae.

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177
Q

The airways in a person with bronchiectasis often become chronically colonised. What is the airway of an adult likely to be colonised with?

A

pseudomonas aeruginosa.

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178
Q

A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?

A

Bronchiectasis.

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179
Q

Define CF.

A

An autosomal recessive disease resulting in abnormal exocrine gland function.

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180
Q

Which chromosome codes or CFTR?

A

Chromosome 7.

181
Q

Describe the pathogenesis of cystic fibrosis.

A

There is a defect in chromosome 7 coding CFTR protein leading to increased Na+ reabsorption and decreased luminal Cl- secretion. there is production of thickened mucus secretions due to increased water reabsorption

182
Q

How is cystic fibrosis passed on?

A

It is an autosomal recessive condition.

1 in 25 people are carriers.

183
Q

A common mutation in which gene can cause CF?

A

A mutation in ∆F508.

184
Q

Why do patients with CF have salty sweat

A

Because in the sweat glands there is decreased Cl and Na+ reabsorption

185
Q

What are the clinical features of CF in neonates

A

Failure to thrive
Meconium ileus (Sticky intestine)
Rectal prolapse

186
Q

What are the respiratory clinical features of CF in children and young adults

A 
Nasal polyps and sinusitis 
Resp
 - Cough 
 - Wheeze 
 - Recurrent infections
 - Bronchiectasis 
 - Haemoptysis 
 - Pneumothorax 
 - Cor pulmonale
187
Q

What are the gastrointestinal clinical features of CF in children and young adults

A 
Pancreatic insufficiency = DM and steatorrhea 
Distal intestinal obstruction syndrome 
Gallstones 
Cirrhosis 
male infertility 
Osteoporosis 
Vasculitis 
Arthritis
188
Q

What are the signs of CF

A

Clubbing
Hypertrophic pulmonary osteoarthropathy
Cyanosis
Bilateral coarse crepitus

189
Q

What are the common causative respiratory agents in early CF

A

S.aureus

H.Infleunza

190
Q

What are the common causative respiratory agents in late CF

A

P.aeruginosa

B.cepacia

191
Q

How is CF diagnosed

A

Sweat test = Na+ and Cl- >60mM
Genetic screening for common mutations
Faecal elastase test for pancreatic exocrine function

192
Q

What investigations might you do In someone with CF

A

Bloods
Sputum MCs
CXR shows bronchiectasis + hyperinflation
Abdo US shows fatty liver, cirrhosis and pancreatitis
Spirometry shows obstructive defect

193
Q

What is the management of CF

A

Physio = postural drainage and forced expiratory technique
Abx = acute infections and prophylaxis
Mucolytics = DNAse
Bronchodilators
Vaccinate
Pancreatic enzyme replacement ADEK supplements
Insulin
Ursodeoxycholic acid for impaired hepatic function

194
Q

State why cystic fibrosis increases the viscosity and tenacity of the bronchial mucus?

A

Failure to excrete Cl- leads to Na+ retention. This then leads to H2O retention.

195
Q

Malignant bronchial tumours can be divided into two groups; what are they?

A
  1. Non small cell cancer (Squamous cell carcinoma, adenocarcinoma, large cell)
  2. Small cell cancer.
196
Q

Which type of malignant bronchial tumour tends to have a worse prognosis?

A

Small cell cancer.

197
Q

Give 5 causes of lung cancer.

A
  1. SMOKING!
    - Occupational:
  2. Asbestos exposure.
  3. Radon exposure.
  4. Coal tar exposure.
  5. Chromium exposure.
198
Q

Which type of NSCC is most common in smokers?

A

Squamous cell carcinoma.

199
Q

Describe the pathology of squamous cell carcinoma

A

Central located

Evidence of squamous differentiation with keritanisation

200
Q

Which type of NSCC is most common with non smokers

A

Adenocarcinoma

201
Q

Describe the pathology of adenocarcinoma

A

Peripherally located with glandular differentiation leading to gland formation and mucus production with mets to the pleura, lymph nodes, brain, bone and adrenal glands

202
Q

From what cells are Small Cell Cancers derived from and what is the significance of this?

A

Neuroendocrine cells centrally located near bronchi

Can secrete peptide hormones such as ACTH, PTHrP, ADH and HCG.

203
Q

What are three rare lung tumour types

A

Adenoma
Hamartoma
Mesothelioma

204
Q

The 5 year lung cancer survival rate is 8-10%. Why is this?

A

People often present very late with lung cancer and so treatment is much harder.

205
Q

Give 3 main cell types that make up non small cell lung cancer?

A
  1. Squamous cell (20%).
  2. Adenocarcinoma (40%).
  3. Large cell.
206
Q

Give 6 symptoms of local disease lung cancer.

A
  1. Chest pain.
  2. Wheeze.
  3. Breathlessness.
  4. Cough.
  5. Haemoptysis.
  6. Recurrent chest infections - pneumonia
  7. Anorexia and wt loss
  8. Hoarseness
207
Q

What are the signs of lung cancer

A

Chest consolidation, collapse and pleural effusion
Cachexia
Anaemia
Clubbing and hypertrophic pulmonary osteoarthropathy

208
Q

Give 6 symptoms of lung cancer that has metastasised.

A
  1. Bone pain, especially waking up in the night from pain.
  2. Headache and confusion
  3. Seizures.
  4. Neurological deficit.
  5. Hepatic and/or abdominal pain - hepatomegaly
  6. Weight loss.
209
Q

Name 5 places that lung cancer might metastasise to.

A
  1. Bone.
  2. Brain.
  3. Liver.
  4. Lymph nodes.
  5. Adrenal glands.
210
Q

Name 5 places that cancer might metastasise to the lung from

A

Brain, prostate, kidney, thyroid , melanoma, lymphoma

211
Q

What are paraneoplastic syndromes?

A

Disorders triggered by immune response to a neoplasm.

212
Q

Give 5 examples of paraneoplastic syndromes.

A
  1. Finger clubbing.
  2. Anorexia.
  3. Weight loss.
  4. Hypercalcemia.
  5. Hypernatremia.
213
Q

Endocrine paraneoplastic syndromes include

A

ADH = SIADH
ACTH = Cushing’s syndrome
Serotonin = Carcinoid (Flushing and diarrhoea)
PTHrP

214
Q

Rheumatoid paraneoplastic syndromes include

A

Dermatomyositis/polymyositis

215
Q

Neuronal paraneoplastic syndromes include

A

Purkinje cells leading to cerebellar degeneration

Peripheral neuropaty

216
Q

What are the complications of lung cancer

A 
Recurrent laryngeal N palsy 
Phrenic nerve palsy 
SVC obstruction 
Horner's 
Atrial fibrillation
217
Q

What investigations might you do on someone to determine whether they have lung cancer?

A
  • CXR (Coin lesion, hilar enlargement, consolidation, collapse, effusion)
  • CT scan for staging
  • Bronchoscopy.
  • Surgical and percutaneous biopsy.
  • Bloods.
218
Q

What does TNM stand for?

A
  1. T: tumour (T1-4).
    Tis = carcinoma in situ
    T0 = none evident
    T1 = <3cm in lobar or more distal airway
    T2 = >3cm and >2cm from carina or pleural involvement
    T3 = <2cm from carina and involves chest wall and diaphragm
    T4 = Involves mediastinum or malignant effusion is present
  2. N: nodal involvement (N0-3).
    N0 = none involved
    N1 = Peribronchial or ipsilateral hilum
    N2 = Ipsilateral mediastinum
    N3 = Contralateral hilum or mediastinum or supraclavicular
  3. M: metastases (M0-1).
    M0 = non
    M1 = distant metastasis
    - Increased staging = decreased survival.
219
Q

What tests might you do on a patient to determine whether they’re fit for operation?

A
  1. ECG.
  2. Lung function tests.
  3. Determine performance status.
220
Q

What are the treatment options for NSCLC

A
  1. Surgical resection for peripheral lesions with no mestastatic spread
  2. Curative radiotherapy
  3. Chemo and radiotherapy for more advanced disease
221
Q

What is the treatment for SCLC

A

Typically disseminated @ presentation and may respond to chemo

222
Q

What are the palliation options for lung cancer

A 
Radiotherapy for bronchial obstruction, haemoptysis, bone and CNS mets 
Stenting and radio for SVC obstruction 
Endobrachial therapy 
Pleural drainage 
Analgesia
223
Q

Secretion of which hormones might result in paraneoplastic changes?

A
  1. PTH.

2. Increased ADH (SIADH).

224
Q

Why is the prognosis for small cell lung cancer normally very poor?

A

Small cell cancers often metastasise and so prognosis is poor.

225
Q

What does the medulla detect?

A

The pH (H+ conc) of the CSF.

226
Q

What do carotid and aortic bodies detect?

A

Chemoreceptors respond to increased CO2 and decreased O2.

227
Q

What is type 1 respiratory failure?

A

Hypoxia - decreased PaO2.

PaCO2 is normal or slightly low due to hyperventilation.

228
Q

What is type 2 respiratory failure?

A

Hypoxia and hypercapnia - decreased PaO2 and increased PaCO2.
There is alveolar hypoventilation.

229
Q

Give 3 signs of hypercapnia.

A
  1. Bounding pulse.
  2. Flapping tremor.
  3. Confusion
  4. Headache
  5. Flushing and peripheral vasodilation
230
Q

What are the signs of acute hypoxia

A

Dyspnoea
Agitation
Confusion
Cyanosis

231
Q

What are the chronic signs of hypoxia

A

Polycythaemia
PHT
Cor pulmonale

232
Q

What can cause type 1 respiratory failure?

A
  1. Airway obstruction.
  2. Failure of O2 to diffuse into the blood.
  3. V/Q mismatch.
  4. Alveolar hypoventilation.
233
Q

What can cause type 2 respiratory failure?

A

Alveolar hypoventilation.

234
Q

Give examples of diseases that obstruct the airway and so could lead to type 1 respiratory failure.

A
  1. COPD.
  2. Obstructive sleep apnoea.
  3. Asthma.
    (Can’t get O2 in but can get CO2 out).
235
Q

What are the obstructive causes of alveolar hypoventilation

A

COPD
Asthma
Bronchiectasis
Bronchiolitis

236
Q

What are the restrictive causes of alveolar hypoventilation

A

Decreased respiratory drive due to sedation, trauma or tumour
Neuromuscular disease ie. MND, GBS, Myasthenia gravis
Chest wall deformity ie. kyphoscoliosis, obesity

237
Q

Give examples of diseases that lead to a failure of O2 to diffuse into the blood and so could cause type 1 respiratory failure.

A
  1. Emphysema.

2. ILD e.g. IPF, sarcoidosis.

238
Q

Give examples of diseases that lead to V/Q mismatch and so could cause type 1 respiratory failure.

A
  1. Cardiac failure.
  2. PE (dead space, V/Q = ∞)
  3. Shunt (V/Q = 0)
  4. Pulmonary hypertension.
239
Q

What is the management of T1 respiratory failure

A

Give O2 to maintain SpO2 94-98%

Assisted ventilation if PaO2 <8Kpa

240
Q

What is the management of T2 respiratory failure

A

Controlled O2 therapy

241
Q

What treatments might be given for V/Q mismatch?

A

Ventilation support e.g. CPAP and BIPAP.

242
Q

What is continuous positive airway pressure (CPAP)? When might it be used?

A

Ventilation support often given to people with Obstructive Sleep Apnoea. It improves gaseous exchange by providing a continuous positive airway pressure.

243
Q

What is bilevel positive airway pressure (BIPAP)? When might it be used?

A

Ventilation support often given to people who have had acute exacerbations of COPD. It causes pressure to decrease when you breathe out and increase when you breathe in therefore improving ventilation to perfused alveoli.

244
Q

Define asthma

A

Episodic reversible airway obstruction causing dyspnoea, cough and wheeze due to bronchial hyper-reactivity to a variety of stimuli

245
Q

What are the three processes that aid bronchial constriction

A

Bronchial muscle contraction
Mucosal swelling and inflammation
Increased mucus production

246
Q

Describe the epidemiology of asthma

A

Peaks at 5yrs and most outgrow by adolescence

247
Q

What 2 categories can asthma be divided into?

A
  1. Allergic asthma (extrinsic); atopic. IgE and mast cell involvement.
  2. Non allergic asthma (intrinsic).
248
Q

What is allergic asthma?

A

When an innocuous allergen triggers an IgE mediated response. The immune recognition processes are faulty and so there is increased IgE, IL-3,4 and 5 production.

249
Q

What is non-allergic asthma?

A

Airway obstruction induced by exercise, cold air and stress.

250
Q

What factors can commonly exacerbate asthma?

A

1.Cold weather.
2. Exertion.
3. Fumes.
4. Often worse at night
5. Allergens
6. Stress.
viral infections
7. Cigarette smoke
8. Drugs

251
Q

Extrinsic asthma: what happens when IgE binds to mast cells?

A

Vasoactive substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.

252
Q

Describe the pathophysiology of acute asthma

A

Mast cell and allergen interaction leading to histamine release, bronchoconstriction, mucus plugs and mucosal swelling

253
Q

Describe the pathophysiology of chronic asthma (12hr)

A

Th2 cells release IL-3,4,5 causing mast cells, eosinophil and B cell recruitment leading to airway remodelling

254
Q

What are the causes of asthma

A
  1. Atopy = T1 hypersensitivity to variety of antigens (Dust mites, pollen, food, animals, fungus)
  2. Stress = Cold air, Viral URTI, Exercise, emotion
  3. Toxins = smoking, pollution, Drugs (NSAIDs and beta blockers
255
Q

What occupations may be associated with an increased risk of developing asthma?

A
  1. Paint sprayers - exposure to fumes.
  2. Animal breeders.
  3. Bakers.
  4. Laundry workers.
256
Q

What are the symptoms of asthma?

A
  1. Breathlessness.
  2. Diurnal variation - often worse in the morning.
  3. Cough with sputum
  4. Episodic wheeze.
  5. Chest tightness.
257
Q

What are the signs of asthma

A

Tachycardia and tachypnoea
Widespread polyphonic wheeze
Hyperinflated chest
decreased air entry

258
Q

What investigations might you do on someone to determine whether they have asthma?

A
  1. PEFR (Dinural variation and morning dipping)
  2. Spirometry should show an obstructive pattern; FEV1 < 80%, FEV1/FVC < 0.7, PEFR - variable.
    - >15% improvement in FEV1 with Beta agonist
  3. Test for atopy; RAST, skin prick test.
  4. CXR - hyperinflation
  5. Eosinophil count.
  6. O2 saturation
  7. Bloods
    - FBC
    - Increased IgE
    - Aspergillus serology
259
Q

How can reversibility be tested in asthma?

A

When given a beta agonist there will be a 400ml increases in FEV1 OR a 20% improvement in PEFR.

260
Q

What tool can be used to assess the severity of asthma?

A 
RCP3 
- Recent nocturnal waking? 
- Usual asthma symptoms during the day? 
- Interference with ADL's? 
May also want to ask about whether the patient has used any rescue medications.
261
Q

What is the function of RCP3?

A

It is used to assess the severity of asthma.

262
Q

What are the 2 principles of asthma treatment?

A
  1. Alleviate symptoms.

2. Target inflammation.

263
Q

What are the general measures used in the treatment of asthma

A

Technique for inhaler use
Avoidane: allergens, smoking, dust
Monitor (Peak flow diary)
Educate

264
Q

What is the first pharmacological option for chronic asthma

A

Short acting beta agonist ie. Salbutamol for symptomatic relief

265
Q

What is the second pharmacological option for chronic asthma

A

Low dose inhaled corticosteroid ie beclometasone or budesonide

266
Q

What is the third pharmacological option for chronic asthma

A

Long acting beta agonist ie. Salmeterol or formoterol

267
Q

What are the fourth pharmacological options for chronic asthma

A

Increase inhaled steroid dose
Leukotriene receptor antagonist (Montelukast/zafirlukast)
Theophylline

268
Q

what is the 5th pharmacological option for chronic asthma

A

Prednisolone

269
Q

How to B2 agonists work

A

SABA or LABA

Stimulate the B2 adrenergic receptors in the smooth muscle of the airway which increases cAMP production which decreases intracellular calcium leading to smooth muscle relaxation and bronchodilation

270
Q

What are the side effects of B2 agonists

A 
Fine tremor 
increases HR and Palpitations 
Anxiety 
Headache 
muscle cramps 
Decreased K+
271
Q

Name two SABA

A

Salbutamol

Terbutaline

272
Q

Name 2 LABA

A

Salmeterol

Formoterol

273
Q

Name some corticosteroids used in the treatment of asthma

A 
Hydrocortisone (Cortisol)
Prednisolone (Longer lasting cortisol)
Dexamethasone 
Beclometasone 
Budesonide
274
Q

How do corticosteroids work in the treatment of asthma

A

Lipophilic molecule which passes through the phospholipid bilayer and binds to nuclear glucocorticoid or mineralocorticoid receptor causes altered protein synth

Leads to altered anti-inflammatory effects due to increased lipocortin-1 which decreases phospholipase A2 which decreases eicosanoid production including prostaglandins, thromboxanes and leukotrienes

275
Q

What are the side effects of inhaled corticosteroids

A

Oral candidiasis

Dysphonia

276
Q

What are the side effects of oral glucocorticoids

A 
Cushing's 
Increased appetite
Increased weight 
GI ulcers and acute pancreatitis 
Osteoporotic fractures 
Skin thinning 
Hypertension 
Diabetes
277
Q

Describe how theophylline works

A

Phosphodiesterase inhibitor that causes decreases intracellular calcium leading to airway smooth muscle relaxation

278
Q

What are the SE of theophylline

A

Nausea and vomiting
Arrhythmias
Seizures
Decreases K+

279
Q

Name a short acting muscarininc antagonist

A

Ipratropium

280
Q

Name a long acting muscarinic antagonist

A

Tiotropium

281
Q

Describe how muscariininc antagonists work in the treatment of asthma

A

Acting on M3 receptors by preventing ACh from binding the M3 receptor and preventing phospholipase C conversion to DAG which stops protein kinase C activation and prevents smooth muscle contraction

282
Q

What is the first line treatment for acute severe asthma?

A

Nebulised salbutamol with oxygen.

IV corticosteorids and abx if evidence of infection.

283
Q

What 4 measurements can be used to diagnose acute severe asthma?

A
  1. RR > 25.
  2. HR > 110.
  3. PEFR 35-50% predicted.
  4. Unable to complete a sentence in one breath.
284
Q

What are the 3 characteristic features of asthma?

A
  1. Airflow obstruction.
  2. Hyper-responsive airways to a range of stimuli.
  3. Bronchial inflammation.
285
Q

Describe the process of airway remodelling in asthma.

A
  1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen.
  2. Deposition of collagen below the BM thicken the airway wall.
  3. Eosinophils also play a role in remodelling.
286
Q

Give 3 histo-pathological changes that occur in asthma.

A
  1. Basement membrane thickening.
  2. Epithelium metaplasia; increased no. of goblet cells leads to mucus hypersecretion.
  3. Increase in inflammatory gene expression on many cell types.
287
Q

What are the signs of asthma?

A
  1. Secretions.
  2. Obstructive spirometry.
  3. Variable PEFR.
  4. Reversibility when given beta-2-agonist, FEV1 > 20%.
  5. Diurnal variation.
288
Q

What can chronic obstructive pulmonary disease be sub-divided into?

A
  1. Chronic bronchitis.

2. Emphysema.

289
Q

Is chronic bronchitis reversible?

A

Chronic bronchitis is irreversible.

290
Q

Define COPD

A

Airway obstruction
FEV1 <80%
FEV1:FVC <0.70

291
Q

Define chronic bronchitis

A

Cough and sputum production on most days for 3 months o 2 successive years

292
Q

Define emphysema

A

Histological diagnosis of enlarged air spaces distal to the terminal bronchioles leading to destruction of alveolar walls

293
Q

Describe the pathophysiology of chronic bronchitis

A

Exposure to irritants and chemicals e.g. smoke -> hypertrophy and hyperplasia of mucus secreting glands -> increased mucus -> airway obstruction. Neutrophil and macrophage involvement -> bronchi become inflamed.

294
Q

How is airway obstruction defined by spirometry?

A
  • FEV1 < 80% predicted.

- FEV1/FVC < 0.7.

295
Q

What are the main causes of COPD?

A

Occupational factors (Dust/chemicals)
Smoking
Pollution
Alpha1 Anti trypsin deficiency

296
Q

Deficiency of what protease inhibitor can cause emphysema?

A

Alpha 1 anti-trypsin deficiency.

297
Q

What is the function of alpha 1 anti-trypsin?

A

It inhibits neutrophil elastase

298
Q

What can cause chronic bronchitis?

A

It is often tobacco smoking induced and can be aggravated by pollution and infections.

299
Q

What can happen over time in a patient with chronic bronchitis?

A

The patient might become hypercapnic, hypoxic and have progressive right sided cardiac failure (cor pulmonale) due to pulmonary vasoconstriction. There is fibrosis and tissue destruction.

300
Q

What is the pathology of emphysema?

A

Irritants and chemicals trigger inflammatory mediators to release matrix destructive enzymes -> elastin destruction and enlargement of alveolar air spaces -> air trapping.

301
Q

What can cause emphysema?

A

It is often tobacco smoking induced. It can also be associated with alpha-1-antitrypsin deficiency and coal dust exposure.

302
Q

What are the symptoms of COPD?

A
  1. Breathlessness.
  2. Wheeze.
  3. Chronic cough.
  4. Sputum (White/clear)
  5. Wt loss
303
Q

Give 5 signs of emphysema.

A
  1. Tachypnoea
  2. Prolonged expiratory phase
  3. Barrel chest (Hyperinflation)
  4. Early inspiratory crackles
  5. Cyanosis
  6. Cor pulmonale/ increased jugular venous pressure
304
Q

Would a patient with emphysema be a ‘pink puffer’ or a ‘blue bloater’?

A

They would be a ‘pink puffer’.
These patients often present with symptoms of weight loss; breathlessness; barrel chest; pursed lip breathing; CO2 retention.

305
Q

Describe the pathology of pink puffer emphysema

A

Increased ventilation so they are breathless but not cyanosed

Means PaO2 is normal
PaCO2 is normal or low

Progresses to T1 respiratory failure

306
Q

Would a patient with chronic bronchitis be a ‘pink puffer’ or a ‘blue bloater’?

A

They would be a ‘blue bloater’.
These patients often present with symptoms of chronic cough, phlegm, cor pulmonale, hypoxia and hypercapnia, wheeze, crackles and cyanosis.

307
Q

Describe the pathology of blue bloater in chronic bronchitis

A

Decreased alveolar ventilation so they are cyanosed by not breathless so there is decreased PaO2 but increased PaCO2 leading to T2 respiratory failure and cor pulmonale

308
Q

What scale might be used to assess breathlessness?

A

MRC dyspnoea scale; scored from 1-5.
(5 statements that describe the entire range of respiratory disability from none to almost complete incapacity).

  1. Dyspnoea worse only on vigorous exercise
  2. SOB on hurrying or walking up stairs
  3. Walks slowly or has to stop for breath
  4. Stops for breath after <10m
  5. Too breathless to leave house or SOB upon dressing
309
Q

What are the complications of COPD

A

Cor pulmonale
Acute exacerbations and infection
Polycythaemia
Pneumothorax

310
Q

Give 3 factors that can be used to establish a diagnosis of COPD?

A
  1. Progressive airflow obstruction.
  2. FEV1/FVC ratio < 0.7.
  3. Lack of reversibility.
311
Q

Aside from COPD, what might be a differential diagnosis for breathlessness?

A
  1. Heart failure.
  2. PE.
  3. Pneumonia.
  4. Lung cancer.
312
Q

What investigations might you do in someone with suspected COPD

A

Bloods (Polycythaemia, a1-AT level, ABG)
CXR (Hyperinflation and prominent pulmonary arteries and bullae)
ECG (RVH, RAH)
Spirometry where FEV1 <80% and FEV1:FVC <0.70

313
Q

Describe the classification system for COPD severity

A

Mild = FEV1 <80% but FEV1/FVC <0.7 and symptomatic

Moderate = FEV1 50-79%

Severe = FEV1 30-49%

Very severe = FEV1 <30%

314
Q

What are the treatments for COPD?

A
  1. Smoking cessation!
  2. Pulmonary rehabilitation.
  3. SABA/LABA for symptom relief.
  4. Mucolytics
  5. Inhaled Corticosteroid.
  6. Long term oxygen therapy
  7. Lung volume reduction surgery - quite rare.
315
Q

Define exacerbation.

A

An acute event characterised by worsening symptoms beyond normal day to day variation. It often leads to a change in medication.

316
Q

Give 5 potential consequences of exacerbations of COPD/asthma.

A
  1. Worsened symptoms.
  2. Decreased lung function.
  3. Negative impact on Q.O.L.
  4. Increased mortality.
  5. Huge economic cost.
317
Q

What is the likely cause for an exacerbation of COPD?

A

Viral infection e.g. RSV, influenza, parainfluenza, rhino and coronaviruses.

318
Q

What is the treatment for an exacerbation of COPD?

A
  1. Oxygen.
  2. Bronchodilators.
  3. Systemic steroids.
  4. Antibiotics if there is breathlessness and sputum production.
319
Q

What are the aims of treatment for exacerbations of COPD?

A
  1. Minimise the impact of the current exacerbation.

2. Prevent subsequent exacerbations.

320
Q

Give 3 ways in which subsequent exacerbations be prevented.

A
  1. Smoking cessation.
  2. Vaccination.
  3. LABA/LAMA/ICS.
321
Q

What broad class of drugs are commonly used to alleviate symptoms?

A

Bronchodilators.

322
Q

What broad class of drugs are commonly used to target inflammation?

A

Steroids.

323
Q

Name 3 types of bronchodilators that are commonly used.

A
  1. Beta agonists.
  2. Muscarinic antagonists.
  3. Methylxanthines.
324
Q

What makes LABA long acting?

A

They have increased lipophilicity.

325
Q

What type of beta adrenergic receptors are found in the lungs?

A

Beta 2.

326
Q

Where are beta 1 adrenergic receptors found?

A

In the heart.

327
Q

Where are beta 3 adrenergic receptors found?

A

In adipose tissue.

328
Q

Describe the process of PKA synthesis from beta 2 receptor activation.

A

Beta 2 interacts with Gs. This activates adenylate cyclase. Adenylate cyclase converts ATP to cyclic AMP, this then leads to PKA synthesis -> bronchodilation.

329
Q

Give 2 functions of cAMP.

A
  1. Stabilisation of mast cells, inhibits mast cell mediator release.
  2. Relaxes airway smooth muscle.
330
Q

What happens following activation of the M3 receptor?

A

M3 interacts with Gq. Phospholipase C is activated, this leads to DAG and IP3 production which further leads onto Ca2+ and PKC production = bronchoconstriction

331
Q

How do muscarinic antagonists work?

A

They prevent M3 receptor activation and so there is a reduction in Ca2+ activation. This means less MLC kinase is produced and you have reduced muscle contraction.

332
Q

How do methylxanthines work?

A

They are PDE inhibitors. They increase cAMP production and therefore PKA production. PKA inhibits MLC kinase and you have reduced muscle contraction.

333
Q

Where is PDE4 found?

A

In the airways and inflammatory cells.

334
Q

What is the function of MLC kinase?

A

MLC kinase phosphorylates MLC which causes muscle contraction.

335
Q

What inhibits Myosin Light Chain kinase?

A

PKA.

336
Q

What activates MLC kinase?

A

Calmodium.

Calmodium is produced from Ca2+

337
Q

Using the myosin light chain, explain how beta agonists and methyxanthines work to alleviate symptoms.

A

Beta agonists and methylxanthines result in increased cAMP and therefor PKA. MLC kinase is inhibited and you have less smooth muscle contraction in the airway -> bronchodilation.

338
Q

Using the myosin light chain, explain how muscarinic antagonists work to alleviate symptoms.

A

Muscarinic antagonists block M3 receptor activation and so you have a reduction in Ca2+ production. Less MLC is activated and so you have less smooth muscle contraction in the airway -> bronchodilation.

339
Q

Where are anti-inflammatory steroids produced?

A

Adrenal cortex.

340
Q

Where in the adrenal cortex are mineralocorticoids produced and give an example of one.

A
  • Zona glomerulosa.

- Aldosterone.

341
Q

Where in the adrenal cortex are glucocorticoids produced and give an example of one.

A
  • Zona fasciculata.

- Hydrocortisone.

342
Q

Give 3 potential side effects of prolonged hydrocortisone use.

A
  • Muscle wasting.
  • Osteoporosis.
  • Increased risk of infection.
343
Q

What are the main cells responsible for inflammation in asthma?

A

Mast cells and eosinophils.

344
Q

What are the main cells responsible for inflammation in COPD?

A

Neutrophils and macrophages.

345
Q

How does anti IgE therapy work?

A

Ab binds to and neutralises free IgE; this prevents IgE binding and results in decreased mast cell sensitisation. Allergens are unable to activate mast cells.

346
Q

What is the advantage of having inhaled medications in the management of asthma?

A

Inhaled medications are more likely to reach the target sites and there is reduced chance of side effects.

347
Q

What is the function of inositol trisphosphate?

A

Inositol trisphosphate (IP3) increases free cytosolic Ca2+ by releasing Ca2+ from intracellular compartments. Ca2+ activates MLC kinase = bronchial smooth muscle contraction.

348
Q

What does activation of the M3 receptor cause?

A
  1. Bronchoconstriction.
  2. Vasodilation.
  3. Glandular secretions.
349
Q

Pulmonary embolism: where might an emboli arise from?

A

Emboli often arise from a dislodged DVT - from iliofemoral veins.

350
Q

What is the consequence of a small, peripheral PE?

A

Infarction!

There is ventilation but no perfusion; dead space.

351
Q

What is the consequence of a large, central PE?

A

Ischaemia!

There is resistance to flow which can also result in RHF.

352
Q

Give 5 risk factors for PE.

Spasmodical

A 
Sex: F
Pregnancy 
Age (Increased)
Surgery 
Malignancy 
Oestrogen (OCP)
DVT/PE previous history 
Immobility
Colossal size (Obesity)
Antiphospholipid Abs 
Lupus Anticoagulant
353
Q

What are the symptoms of PE

A

Dyspnoea
Pleuritic chest pain
Haemoptysis
Syncope and dizziness

354
Q

What are the signs of PE

A 
Fever 
Cyanosis 
Tachycardia 
Tachypnoea 
Hypotension 
Increased JVP
355
Q

What are symptoms of a small, peripheral PE?

A
  • Breathlessness.

- Pleuritic chest pain.

356
Q

What are symptoms of a large, central PE?

A
  • Severe central chest pain.

- Pale and sweaty.

357
Q

What investigations might you do in someone to determine whether they have PE?

A
  • CXR = dilated PA, linear atelectasis and oligaemia
  • ECG = sinus tachycardia and RBBB
  • D-dimer.
  • ABG = decreased PaO2 and decreased PaCO2
  • V/Q lung scan - shows ventilated areas with perfusion defects.
  • CTPA - can detect emboli.
358
Q

The Wells scoring system is used to work out the probability of a person having a PE. Name 5 factors that the scoring system uses.

A
  1. Clinical signs/symptoms of DVT.
  2. HR > 100bpm.
  3. Recent immobilisation.
  4. Previous DVT/PE.
  5. Haemoptysis.
  6. Malignancy.
    Score >4 - PE likely.
359
Q

Describe the treatment for PE.

A
  1. Thrombolysis is used for a large PE.
  2. LMWH (anti-coagulant) and oral warfarin.
  3. NOAC (anticoagulant).
  4. Analgesia for pain relief.
360
Q

How long is the treatment for an idiopathic pulmonary embolism?

A

At least 6 months.

361
Q

Give 4 signs of a large PE.

A
  1. Shocked.
  2. Central cyanosis.
  3. Raised JVP.
  4. Accentuation of second heart sound.
362
Q

Define Pneumothorax

A

Accumulation of air in the pleural space secondary to lung collapse

A defect in the visceral pleura causes air to enter the pleural space from the lungs. The elastic recoil of the lungs then causes them to deflate

363
Q

What are the three main types of pneumothorax?

A

Closed = Intact chest wall and air leaks from the lung into the pleural cavity

Open = Defect in the chest wall allows communication patient and exterior

Tension = air in the pleural cavity through one way valve that cannot escape leading to mediastinal compression

364
Q

What are the causes of pneumothorax

A

Spontaneous

Primary
- No underlying lung disease and often occurs in young thin men who are smokers

Secondary
- Underlying lung disease including COPD, TB, pneumonia

Traumatic (Penetrating

Iatrogenic

365
Q

What are the symptoms of pneumothorax

A 
Acute sudden onset SOB 
Dyspnoea 
Pleuritic chest pain 
Can be asymptomatic 
Tension = respiratory distress and cardiac arrest
366
Q

What are the signs of pneumothorax

A 
Decreased chest expansion 
Resonant percussion 
Decreased breath sounds 
Decreased vocal resonance 
Tension = increased JVP, mediastinal shift, increased HR
367
Q

What investigations would you do in someone with pneumothorax

A

CXR but skip in someone with suspected tension pneumothorax
Ultrasound
ABG

368
Q

What is the management for primary pneumothorac

A

usually self resolve otherwise needle aspiration

369
Q

What is the management for secondary pneumothorax

A

Conservative treatment if <1cm
Needle aspirate if 1-2cm
Chest drain if >2cm or SOB

370
Q

What is the management for tension pneumothorax

A

Resuscitate patient
No CXR
100% O2
Needle aspiration for instant relief then proceed to chest drain

371
Q

Describe the pathophysiology of a tension pneumothorax.

A

A pleural tear creates a 1-way valve through which air passes in inspiration -> increased intra-pleural pressure -> respiratory distress, shock and cardiac rest.

372
Q

What does pleural fluid contain?

A

Proteins e.g. albumin, globulin.

373
Q

What is the function of the pleura?

A

It allows movement of the lung and lung expansion against the chest wall.

374
Q

What produces and reabsorbs pleural fluid?

A

The parietal pleura.

375
Q

Name 3 diseases associated with the pleura.

A
  1. Pleural effusions.
  2. Pleural plaques.
  3. Pneumothorax.
376
Q

Define pleural effusion

A

Excess fluid in the pleural space

377
Q

What are the different classifications of pleural effusion

A

Transudate = <25g/L of protein and caused by organ failure

Exudate = >35g/L of protein and are due to the 4 I’s

378
Q

What are the causes of transudate pleural effusion

A

Increased venous pressure

  • Congestive cardiac failure
  • Constrictive pericarditis

Hypoproteinaemia
Renal failure
Meig’s syndrome
Hypothyroidism

379
Q

What are the causes of exudate pleural effusion

A 
Infection = pneumonia and TB
Infiltration = cancer of lung, breast, lymphoma, malignant mesothelioma 
Infarction = PE and MI
Inflammation = RA and SLE
380
Q

What are the symptoms of pleural effusion

A

SOB
Cough
Pleuritic chest pain

381
Q

What are the signs of pleural effusion

A 
Stony dull percussion 
Decreased breath sounds 
Decreased chest expansion 
Mediastinal shift 
Decreased vocal resonance 
Clubbing in lung cancer 
increased jugular venous pressure in HF
382
Q

What investigations would you do in someone that has suspected pleural effusion

A

Bloods
CXR = Blunt costophrenic margins, mediastinal shift
Diagnostic tap
Pleural biopsy

383
Q

What is the management of pleural effusions

A

Treat underlying cause
Use drainage or aspiration if symptomatic
May require a chest drain

384
Q

What is pleural fibroma?

A

Fibrous tumour of the pleura.

385
Q

What are the consequences of pleural fibroma?

A

Pleural fibromas can grow to a massive size and compress on lung tissue. Occasionally they can secrete insulin related factors and so produce hypoglycaemic symptoms.

386
Q

Define sarcoidosis

A

Non-caseating granulomatous disease that most commonly affects lung and lymph nodes

387
Q

What is the epidemiology of sarcoidosis

A

20-40yrs
F>M
Afro caribbean
HLA-DRB1 and DQB1 alleles

388
Q

What are the symptoms of sarcoidosis

A

20-40% disease presents incidentally on CXR

  1. Bi-lateral hilar lymphadeonopathy (BHL).
  2. Erythema nodosum.
  3. Uveitis, Keratoconjunctivitis and Sicca
  4. Non productive cough, SOB, wheeze., chest pain
  5. Metabolic affect of sarcoidosis = hyperacalcaemia -> nephrocalcinosis.
  6. polyArthalgia and dactylitis
  7. Hepatosplenomegaly.
  8. Neurological: inflammation of the meninges and seizures.
  9. Heart block.
  10. Lung fibrosis.
  11. Finger clubbing is rare!
  12. Fever, anorexia, wt loss
389
Q

What is the staging system for the respiratory symptoms of sarcoidosis

A

Stage 1 = bilateral hilar lymphadenopathy
Stage 2 = BHL + peripheral infiltrates
Stage 3 = Peripheral infiltrates alone
Stage 4 = Progressive mid zone fibrosis

390
Q

What investigations in sarcoidosis

A

Bloods = increased ESR, Ca, ACE and lymphopenia
CXR for staging
LFT’s = restrictive pattern
Tissue biopsy = non caveating granulomas

391
Q

What is the management for sarcoidosis

A

Patients with asymptomatic BHL don’t require Rx

Acute sarcoidosis = bed rest and NSAIDs

Chronic = Prednisolone

392
Q

Define interstitial lung disease

A

Disease affecting the lung interstitium = connective tissue between the alveolar epithethelium and the capillary endothelium = increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion

393
Q

What are the causes of interstitial lung disease

A 
Idiopathic pulmonary fibrosis 
Pneumoconiosis 
Hypersensitivity pneumonitis 
Infection = TB
Sarcoidosis 
Connective tissue disease ie. SLE, RA, systemic sclerosis and ankylosing spondylitis
394
Q

Which drugs can cause interstitial lung disease

A 
Bleomycin 
Amiodarone 
Radiation 
Methotrexate 
Aspirin and ACEi
Nitrofurantoin
395
Q

What are symptoms of ILD

A

Progressive SOB
Drug cough
Failure to respond to treatment of other conditions

396
Q

What are the signs of ILD

A 
Crackles - end inspiratory 
Tachypnoea 
Clubbing 
Peripheral cyanosis 
Decreased chest expansion
397
Q

What is the commonest cause of ILD

A

Idiopathic pulmonary fibrosis

398
Q

What is IPF characterised by

A

Dysregulated fibroblasts and myofibroblasts

399
Q

What is IPF

A

A disease characterised by chronic inflammation and permanent scarring in the alveoli. Respiratory ability is affected. Chest infection and hypoxic damage are likely.

400
Q

Give 4 risk factors for IPF.

A
  1. Smoking.
  2. Dust exposure.
  3. Exposure to infectious agents.
  4. Long term antidepressant use.
401
Q

What are the symptoms of IPF

A

Dry cough
Dyspnoea
Malaise and Wt loss
Arthralgia

402
Q

What are the signs of IPF

A

Cyanosis
Clubbing
Crackles - fine, end inspiratory

403
Q

What investigations would you do in someone with suspected IPF

A 
Bloods = increased CRP
ABG = decreased PaO2 and increased PaCO2
CXR = decreased lung volume, honeycomb lung 
Lung biopsy
Spiro = Restrictive 
BAL = Lymphocytes increased
404
Q

What is the management for someone with IPF

A

Stop smoking
Pulmonary rehabilitation
Steroids

405
Q

What is the effect of interstitial lung disease on lung volumes?

A

Reduced TCO, VC and FEV1. FEV1/FVC ratio and PEFR is normal.

406
Q

What is the treatment for interstitial lung disease?

A

Steroids and immunosuppressive agents. Lung transplantation may be required.

407
Q

When looking to diagnose IPF, what 3 findings would you look for on pulmonary function

A
  1. Reduced TLCO.
  2. Restrictive spiromerty: low FEV1 and FVC but normal ratio.
  3. Low/normal PaO2.
408
Q

What is hypersensitivity pneumonitis (EAA)?

A

Inhalation of allergen in sensitised patients leads to a type 3 hypersensitivity reaction; there is an inflammatory response in the alveoli and small airways

Chronic exposure leads to granuloma formation and obliterative bronchiolitis

409
Q

Name a cause of hypersensitivity pneumonitis (EAA).

A
  1. Farmer’s lung; due to mouldy hay and aspergillus spores.
  2. Bird fancier’s lung; due to proteins present in bird faeces
  3. Malt workers lung due to aspergillus clavatus
410
Q

What are the clinical features of EAA 4-6hr post exposure

A

Fevers, rigors, malaise
Dry cough and dyspnoea
Crackles (no wheeze)
Resolution 24-48 hours following antigen removal

411
Q

What are the clinical features of chronic EAA

A

Increasing dyspnoea
Wt loss
T1 respiratory failure
Cor pulmonale

412
Q

What investigations would you do in someone with EAA

A

Bloods = increased ESR, neutrophilia
CXR = honey comb lung
Spirometry = restrictive defect
Bronchoalveolar enlargement = increased lymphocytes and mast cells

413
Q

What is the management for EAA

A

Remove allergen/avoid exposure

Steroids (Hydrocortisone/prednisolone)

414
Q

What are occupational lung disorders?

A

Lung disorders due to a response to inhaling something at work e.g. fumes, dust, gas, aerosol.

415
Q

Give 5 damage mechanisms of occupational lung disorders.

A
  1. Direct injury.
  2. Infection.
  3. Allergy e.g. EAA.
  4. Chronic inflammation e.g. COPD.
  5. Destruction of lung tissue e.g. emphysema.
  6. Lung fibrosis.
  7. Carcinogenesis.
416
Q

Give 4 ways in which occupational lung disorders can be prevented.

A
  1. Risk assessment.
  2. Legal requirement under COSHH.
  3. Prevent and minimise exposure to harmful substances.
  4. Monitor worker’s health so health problems can be identified early.
417
Q

What are the potential consequences of occupational lung disorders?

A
  1. Increased morbidity and mortality.
  2. Loss of income.
    Occupational lung disorders are avoidable and easily missed! It is important to balance health and employment and seek advice as soon as you notice any signs of lung problems.
418
Q

What is the name of the lung disorder group that reflects inhaled dust/toxins?

A

Pneumoconiosis.

419
Q

Give an example of a pneumoconiosis?

A

Coal worker’s pneumoconiosis, silicosis, asbestos exposure, extrinsic allergic alveolitis.

420
Q

What is asbestosis

A

Due to inhalation of asbestos for a period >10years

421
Q

Pneumoconiosis: What might be the consequences of asbestos exposure?

A
  • Lung cancer.
  • Persistent pleural effusion.
  • Diffuse pleural fibrosis.
  • Diffuse interstitial lung fibrosis.
422
Q

What are the symptoms of asbestosis

A

Chest pain, wt loss, clubbing, dyspnoea

423
Q

What is silicosis

A

Inhalation of silica particles from quarrying and sand blasting

424
Q

What is coal workers pneumoconiosis

A

Inhalation of coal and dust particles which is ingested by macrophages which die and release enzymes causing fibrosis

425
Q

What can silicosis and coal workers pneumoconiosis lead to

A

Massive fibrosis in the upper lobe

426
Q

What does someone with silicosis have an increased risk of developing?

A

TB.

There is a borderline increased risk of cancer.

427
Q

Define mesothelioma

A

Cancer arising from the mesothelium, the epithelial layer of the serosa

428
Q

What is the major cause of mesothelioma

A

Asbestos

429
Q

What is the epidemiology of mesothelioma

A

M>W
Present between 40-70
Latent periods between exposure and development of tumour may be 45 years

430
Q

What are the signs and symptoms of mesothelioma

A 
SOB
Dull chest pain 
Weight loss 
Fever 
Fatigue 
Clubbing 
Lymphadenopathy 
Hepatomegaly
431
Q

What investigations might you do on someone to determine whether they have mesothelioma?

A
  • CXR = show pleural thickening
  • CT scan.
  • Pleural biopsy.
432
Q

What is the treatment for mesothelioma?

A
  1. Symptom control.
  2. Palliative chemotherapy or radiotherapy.
  3. Radical surgery (removal of tumour blood supply).
433
Q

What is the difference between radical radiotherapy and palliative radiotherapy?

A
  1. Radical: daily treatments for 4-6 weeks.

2. Palliative: the patient attends the minimum number of visits possible to control symptoms.

434
Q

Give one advantage and one disadvantage of adding chemotherapy to radiotherapy.

A
  • Advantage: survival advantage.

- Disadvantage: increased risk of toxicity.

435
Q

Give 5 side effects of radiotherapy.

A
  1. Fatigue.
  2. Anorexia.
  3. Cough.
  4. Oesophagitis.
  5. Systemic symptoms.
436
Q

What are the 3 main aims of palliative chemotherapy?

A
  1. Relieve symptoms.
  2. Improve quality of life.
  3. Shrink tumours.
437
Q

Give 4 side effects of chemotherapy.

A
  1. Alopecia.
  2. Nausea/vomiting.
  3. Peripheral neuropathy (nerve damage in extremities).
  4. Constipation or diarrhoea.
438
Q

Why is treatment of mesothelioma so difficult?

A

Mesothelioma is incurable as it is resistant to surgery, chemotherapy and radiotherapy. The average time from diagnosis to death is about 8 months.

439
Q

Define pulmonary hypertension.

A
  • mPAP > 25mmHg.

- Secondary RV failure.

440
Q

What can cause an increase in mPAP?

A

Increased resistance to flow.

Increased flow rate.

441
Q

Give 5 causes of pulmonary hypertension.

A
  1. Left heart disease (Mitral stenosis, mitral regurgitation)
  2. Lung parenchymal disease as chronic hypoxia leads to hypoxic vasoconstriction (COPD, asthma ILD, CF)
  3. Pulmonary vascular disease (Idiopathic pulmonary hypertension, pulmonary vasculitis, Pulmonary embolism)
  4. Hypoventilation (Kyphosis, scoliosis, MND, Myasthaenia gravis)
442
Q

Give 5 symptoms of pulmonary hypertension.

Initial symptoms:

A
  1. Dyspnoea on exertion.
  2. Lethargy.
  3. Fatigue.
  4. Syncope.
    Symptoms as RV failure develops:
  5. Pulmonary oedema.
  6. Abdominal pain.
443
Q

What investigations might you do in someone to determine whether they have pulmonary hypertension?

A
  1. ECG - see if there’s RV hypertrophy.
  2. Spirometry.
  3. CXR - enlarged proximal pulmonary arteries.
  4. Echocardiography.
444
Q

What might you notice in the ECG take from someone with pulmonary hypertension?

A

There might be signs of RV hypertrophy.

445
Q

What might you notice in a CXR take from someone with pulmonary hypertension?

A

There might be enlarged proximal pulmonary arteries which taper distally.

446
Q

Describe the usual treatment for someone with pulmonary hypertension.

A
  1. Initial treatment is O2.
  2. Warfarin (due to risk of thrombosis).
  3. Diuretics (for oedema).
  4. Ca2+ blockers (pulmonary vasodilators).
  5. Treat underlying cause.
447
Q

Why might someone with pulmonary hypertension experience peripheral oedema?

A

Blood accumulates in the pulmonary artery. The RV experiences a greater afterload and works harder to get blood out of the ventricle and into the pulmonary artery. There is RV hypertrophy and right heart failure. This results in peripheral oedema.

448
Q

Give 5 signs of pulmonary hypertension.

A
  1. RV hypertrophy (ECG).
  2. Loud pulmonary secondary sound.
  3. Right parasternal heave.
  4. Enlarged proximal pulmonary arteries (CXR).
  5. In advanced disease there are signs of RHF, elevated JVP, hepatomegaly and pleural effusion etc.

Phase 2 (16 decks)

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