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Major diseases Flashcards

1
Q

What is cystic fibrosis?

A

an inherited disease that causes abnormal secretions so build-up of mucus

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2
Q

Who does cystic fibrosis affect?

A

young people and 1 in 2000-3000 newborns

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3
Q

What causes cystic fibrosis?

A

autosomal recessive mutations of CFTR which is a transmembrane chloride channel found in the respiratory epithelium, exocrine ducts and sweat ducts

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4
Q

What does the CFTR protein do?

A

controls the movement of sodium and water our of the cell into the mucous layer by transporting chloride ions across the cell membrane
if it is not present or not working then chloride ions can’t flow so the mucus becomes thick and sticky

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5
Q

What are the two types of mutation that can occur on the CFTR protein?

A

homozygous or heterozygous (two different mutations one on each chromosome) result in cells producing mucus with high sodium and chloride content and viscosity that impairs mucociliary clearance

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6
Q

What ducts can become blocked in CF?

A

pancreatic ducts which can cause pancreatic damage and failure

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7
Q

What are the symptoms and signs of CF?

A
  • chronic bronchial colonisation with pathogenic bacteria
  • progressive bronchiectasis with small airways obstruction
    there will be respiratory failure so
  • clubbing
  • low BMI
  • extensive crepitations
  • obvious signs of airways obstruction
    also pancreatic insufficiency leading to malabsorption and glucose intolerance
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8
Q

What are the major complications of CF?

A
  • bronchiectasis
  • respiratory failure
  • lobar collapse
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9
Q

What are the tests for CF?

A
  • postnatal tests
  • measure sweat chloride concentration which will be high in CF patients
  • nasal potential difference tests
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10
Q

How is CF diagnosed?

A

genetic testing for CFTR mutations

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11
Q

What is the treatment for CF?

A
  • frequent antibiotics for bronchial infections
  • regular physiotherapy supported by a chest clearance device
  • regular use of inhaled beta-agonists
  • flucloxacillin is used prophylactically against chronic s. aureus as well as azithromycin
  • nebuliser DNase and hypertonic saline slows decline in lung function
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12
Q

What is the prognosis for CF?

A

death by slowly progressing type 2 respiratory failure but occasionally lung transplant is curative

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13
Q

What is a PE?

A

blockage of an artery of the lungs by a substance that has moved from elsewhere

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14
Q

What is acute PE?

A

signs and symptoms in a few hours or days

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15
Q

What is chronic PE?

A

multiple small emboli cause dyspnoea and pulmonary hypertension over weeks or months

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16
Q

How common is PE?

A

110 per 100,000, major cause of sudden death and diagnosis is often missed

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17
Q

What is another name for the pathogenesis of PE?

A

Virchow’s triad

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18
Q

What are the components of Virchow’s triad?

A
  • alterations to the constituents of blood
  • injury to the vascular endothelium
  • changes in blood flow
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19
Q

What are the risk factors for PE?

A
  • acquired altered blood constituents (malignancy, trauma, pregnancy and smoking)
  • inherited altered blood constituents (antithrombin deficiency, protein S and C deficiency)
  • endothelial wall damage (central venous catheter, trauma, drug use or surgery)
  • altered blood flow (surgery, pregnancy and prolonged immobility)
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20
Q

What are the signs and symptoms of acute PE?

A
  • dyspnoea
  • pleuritic chest pain
  • cough
  • haemoptysis
  • central cyanosis
  • tachypnoea
  • tachycardia
  • pleural rub
  • small effusion
  • loud P2 on auscultation
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21
Q

What are the signs and symptoms of massive PE?

A

(associated with cardiac arrest or life-threatening shock)

  • syncope
  • hypotension
  • severe dyspnoea
  • acute right ventricular failure
  • increased JVP
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22
Q

What are the signs and symptoms of chronic PE?

A
  • progressive dyspnoea over weeks/ months
  • sometimes with chest pain or haemoptysis
  • central cyanosis in sever cases
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23
Q

What will be seen in a respiratory exam for massive or chronic PE?

A

normal respiratory exam

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24
Q

What does decreased oxygenation and sudden onset dyspnoea suggest?

A

PE

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25
Q

What do blood tests for PE show?

A

increased D-dimers due to clot breakdown but this could be raised for other reasons

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26
Q

What would an ABG show for PE?

A

type 1 respiratory failure and respiratory alkalosis

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27
Q

What would ECG show for PE?

A

sinus tachycardia, T-wave inversions in right ventricular leads

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28
Q

What is seen on a CXR with PE?

A

excludes other diseases but can’t show emboli, occasionally wedge-shaped consolidation is seen and sometimes reduced blood vessel markings and small pleural effusions

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29
Q

What will a VQ scan show for PE?

A

mismatches, normal scan means no PE but difficult to determine in patients with chronic lung disease

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30
Q

What is the first line test for PE?

A

CTPA and this also shows other lung diseases

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31
Q

What is the problems with angiography for PE?

A

invasive and highly skilled

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32
Q

What test can show DVT?

A

venous ultrasound and electrocardiography

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33
Q

What will echo show with massive PE?

A

right ventricular dilation, decreased right ventricular function or tricuspid regurgitation

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34
Q

What is the treatment for acute PE?

A
  • oxygen
  • analgesics for pleuritic chest pain
  • fluid for hypotension
  • LMWH subcutaneous for 5-7 days for anti-coagulation
  • warfarin for long term
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35
Q

What is the treatment for massive PE?

A

embolectomy

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36
Q

What prevents recurrent PE in persistent DVT?

A

inferior vena cava filter

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37
Q

What is mortality rate for untreated PE?

A

30% (reduced by treatment)

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38
Q

What type of PE has the highest mortality?

A

massive PE

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39
Q

What increases mortality rate of PE?

A
  • right ventricular thrombus

- history of cancer

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40
Q

What is pulmonary hypertension?

A

when mean systolic is over 25 at rest or 30 during exercise

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41
Q

What are the different types of pulmonary hypertension?

A
  • primary caused by pathological processes that affect pulmonary circulation
  • secondary caused by gradual changes in pulmonary circulation due to chronic lung disease
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42
Q

What disease leads to secondary pulmonary hypertension?

A

chronic hypoxic disease

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43
Q

What is primary pulmonary hypertension caused by and how common is it?

A

PE and is rare

44
Q

What is the pathogenesis of pulmonary hypertension?

A
  • increase pulmonary vascular resistance
  • pulmonary venous pressure
  • pulmonary vascular flow
45
Q

What are the causes of pulmonary hypertension?

A
  • thickening of pulmonary artery walls due to cell proliferation
  • increased left atrial pressure
  • chronic pulmonary vasoconstriction in response to hypoxia and acidosis
  • loss of pulmonary vessels by scarring or alveolar wall destruction
  • occlusion of pulmonary vessels
  • increased pulmonary vascular flow by left to right shunt
46
Q

What are the main symptoms of pulmonary hypertension?

A
  • progressive dyspnoea on exertion
  • fatigue
  • chest pain on exertion because of right ventricular hypertrophy
47
Q

What are the signs of pulmonary hypertension?

A
  • raised pulmonary artery pressure so a loud P2, raised JVP with V wave
  • right ventricular hypertrophy so parasternal heave and an additional S3/4
  • right-sided cardiac failure so peripheral oedema, pleural effusion and tricuspid regurgitation
48
Q

What is the main clinical features of pulmonary hypertension?

A
  • unexplained SOB

- deterioration of existing lung disease with no other explanation

49
Q

What is seen on an ECG with pulmonary hypertension?

A

this can measure pulmonary artery pressure non-invasively and shows right ventricular hypertrophy and tricuspid regurgitation

50
Q

What will be seen on a CXR with pulmonary hypertension?

A

normal but sometimes enlarged central pulmonary arteries or other diseases that are causing the hypertension can be seen

51
Q

What will a pulmonary function test show for pulmonary hypertension?

A

decreased transfer factor

52
Q

What will a VQ scan show for pulmonary hypertension?

A

can find a pulmonary emboli that could be causing it

53
Q

What will right heart catheterisation show for pulmonary hypertension?

A

accurate measure of pulmonary artery pressure but it is invasive

54
Q

What is the treatment for pulmonary hypertension?

A
  • diuretics to reduce oedema due to right heart failure
  • oxygen therapy to reduce pressure by reversing hypoxia-driven vasoconstriction
  • anticoagulation to prevent PE
  • sever is treated with vasodilators
  • surgically remove PE
55
Q

What are examples of the vasodilator drugs used to treat pulmonary hypertension?

A

sildenafil or oral calcium channel blocker

56
Q

What is the prognosis fo pulmonary hypertension?

A

death within five years of diagnosis

57
Q

What is sarcoidosis?

A

an inflammatory disorder of unknown cause characterised by non-caseating granulomas

58
Q

What type of disease is sarcoidosis?

A

type 4 hypersensitivity

59
Q

How common is sarcoidosis?

A

5-10/100000 people

60
Q

What type of person usually gets sarcoidosis?

A

mostly 40 year olds, more common in women

61
Q

What is the pathology of sarcoidosis?

A

cell-mediated immunological response that causes granulomas and fibrosis in affected organs

62
Q

What is the cause of sarcoidosis?

A

unknown cause but genetics is a known factor

63
Q

What is the presentation of acute sarcoidosis?

A

bihilar lymphadenopathy associated with erythema nodosum, low-grade fever and arthralgia

64
Q

What is the presentation of chronic sarcoidosis?

A

insidious onset

65
Q

What are the symptoms of sarcoidosis in the lungs?

A

dry cough, dyspnoea and sometimes fine end respiratory crackles

66
Q

What are the four stages of CXR for sarcoidosis?

A

1) bilateral hilar lymphadenopathy
2) parenchymal infiltrates and bilateral hilar lymphadenopathy
3) parenchymal infiltrates only
4) advanced pulmonary fibrosis

67
Q

What type of diagnosis is needed for sarcoidosis?

A

histological diagnosis of non-caseating granulomas is needed

68
Q

What are the differential diagnoses of sarcoidosis?

A

TB
hypersensitivity pneumonitis
fungal infection

69
Q

What will be seen in a blood test for sarcoidosis?

A

increased serum ACE

70
Q

What is an essential test for sarcoidosis?

A

HRCT

71
Q

How do you biopsy for sarcoidosis and what will be seen in the results?

A

endobronchial ultrasound or biopsies of skin lesions to test for non-caseating granulomas

72
Q

What is the treatment for sarcoidosis?

A

for severe..

  • corticosteroids
  • hydroxychloroquine and methotrexate
  • infliximab
73
Q

What is the prognosis for sarcoidosis?

A

acute resolves within two years but chronic can cause severe disability and occasionally death

74
Q

What is pulmonary fibrosis?

A

a disease where the alveoli and the lung interstitium are infiltrated by mesenchymal cells and increased amounts if extracellular matrix and collagen

75
Q

What does pulmonary fibrosis result in?

A

impaired lung function, progressive breathlessness and characteristic appearances on CXR

76
Q

How common is pulmonary fibrosis?

A

5/100000

77
Q

What type of person gets pulmonary fibrosis?

A

much more common in men than in women and usually presents in around 70 year olds

78
Q

What is the pathophysiology of pulmonary fibrosis?

A

abnormal alveolar epithelium
epithelium turns to mesenchymal so there is increased production of extracellular matrix proteins so there is destruction of the lung tissue and scarring

79
Q

What are the two patterns of pneumonia that are seen in people with IPF?

A
  • interstitial pneumonia which has areas of normal lung, interstitial inflammation and honeycombing from fibroblasts and fibrotic cysts (treatment resisitant)
  • non-specific interstitial pneumonia with thickening of the alveolar sputum, variable inflammation and fibrosis
80
Q

What are the six causes of pulmonary fibrosis?

A

1) IPF (60% of patients) which is characterised by usual interstitial pneumonia
2) connective tissue disease which comes along with rheumatoid arthritis and systemic sclerosis (non-specific)
3) drugs eg chemotherapy
4) radiotherapy when pneumonitis progresses to mature pulmonary fibrosis
5) acute respiratory distress syndrome
6) other causes are hypersensitivity pneumonitis, sarcoidosis, pneumoconiosis, chronic aspiration and asbestosis

81
Q

How does pulmonary fibrosis present?

A

progressive dyspnoea over months and a dry cough

82
Q

What will be seen on examination with pulmonary fibrosis?

A
  • finger clubbing
  • reduced bilateral chest expansion
  • fine late inspiratory crepitation
  • cyanosis
  • cor pulmonale (increased heart on right side)
83
Q

What is looked for in blood tests for pulmonary fibrosis?

A
  • rheumatoid factor, antinuclear antibodies
  • creatine kinase (connective tissue disease)
  • avian precipitins
  • serum ACE (sarcoidosis)
84
Q

What would pulmonary function test show for pulmonary fibrosis?

A

small lung volumes and a reduced transfer factor from the restrictive lung defect

85
Q

What does imaging show for pulmonary fibrosis?

A

diffuse basal reticulonodular shadowing

86
Q

What is seen in a HRCT for pulmonary fibrosis?

A
  • thickened interlobular septa
  • ground glass infiltration
  • honeycombing
87
Q

What test can help exclude other diagnoses for pulmonary fibrosis and what are these diagnoses?

A

bronchoscopy and bronchoalveolar lavage

to exclude sarcoidosis, hypersensitivity pneumonitis and infections

88
Q

What is the treatment for pulmonary fibrosis?

A

(treat underlying cause)

  • high dose corticosteroids
  • N-acetylcysteine
  • azathioprine cyclophosphamide or both
  • pirfenidone or nintedanib
89
Q

What can help relieve symptoms of pulmonary fibrosis?

A

pulmonary rehabilitation and oxygen therapy

90
Q

What is the prognosis for IPF?

A

five year survival feat of 10-15%
connective tissue disease PF has a better prognosis
chemo or radio induced PF can be fatal or it can stop progressing
from ARDS will improve over time

91
Q

What is hypersensitivity pneumonitis?

A

aka extrinsic allergic alveolitis

ILD caused by an immunological reaction to an inhaled antigen

92
Q

What is the most common form of hypersensitivity pneumonitis?

A

Bird fancier’s lung

93
Q

What decreases the risk of hypersensitivity pneumonitis?

A

smoking

94
Q

What does hypersensitivity pneumonitis consist of?

A

type four cell-mediated hypersensivity reaction leading to fibrosis in the upper lobes

95
Q

What does hypersensitivity pneumonitis present with?

A
  • acute = breathlessness, wheeze, cough, fever and crepitations 4-6 hours after exposure
  • chronic = progressive dyspnoea, cough, fatigue and weight loss
96
Q

What do pulmonary function tests show for hypersensitivity pneumonitis?

A

restrictive or mixed restrictive-obstructive defect with reduced transfer factor

97
Q

What does a CXR show for hypersensitivity pneumonitis?

A 
acute = patchy diffuse infiltrates
chronic = reticulonodular shadowing
98
Q

What does HRCT show for hypersensitivity pneumonitis?

A
  • ground glass consolidation
  • centrilobular nodules
  • mosaicism
  • fibrotic changes
99
Q

What does a biopsy show for hypersensitivity pneumonitis?

A
  • poorly-formed small non-caseating granulomas
  • mononuclear cell infiltrate
  • peribronchial fibrosis
100
Q

What is the treatment for hypersensitivity pneumonitis?

A

avoid antigen causing it if known

occasionally high dose corticosteroids work

101
Q

What is the prognosis for hypersensitivity pneumonitis?

A

acute doesn’t damage but repeated attacks lead to chronic damage which can progress to end-stage PF

102
Q

What is pneumonia?

A

Pneumonia is signs and symptoms of a lower respiratory tract infection with consolidation on a chest x ray

103
Q

What are the different types of pneumonia?

A
  • Lobar pneumonia is when whole lobes are infected
  • Bronchopneumonia is wide-spread patches of consolidation in both lungs which is common in patients with S. aureus
  • Interstitial pneumonia presents with bilateral subtle interstitial infiltrates on CXR
  • Aspiration pneumonia is as a result of vomiting when drunk
104
Q

How common is pneumonia?

A

2-5/1000 per year

Risk is higher in children under 5 and in elderly

105
Q

What is the pathogenesis of pneumonia?

A

Inflammatory response causing the alveoli to sill with extracellular fluid
Right to left shunting of deoxygenated blood resulting in hypoxia

106
Q

What is the presentation of sarcoidosis?

A

erythema nodosum
bilateral hilar lymphadenopathy
arthralgia
Afro-Caribbeans

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