Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MRCP P1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What condition is bronchiolitis obliterans associated with?

A

Rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the features of bronchiolitis obliterans?

A
  1. Progressive dyspnoea
  2. Obstructive spirometry
  3. Centrilobular nodules, bronchial wall thickening on CT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Caplan’s syndrome?
How does it manifest?

A

Rheumatoid pneumoconiosis. Characterised by intrapulmonary nodules that appear homogeneous and well-defined on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes Caplan’s syndrome?

A

Occurs in patients with both RA and pneumoconiosis related to mining dust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the investigation of choice for upper airway compression?

A

Flow volume loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is a normal flow volume loop often described?

A

Triangle on top of a semicircle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is silicosis?

A

Fibrosing lung disease caused by inhalation of fine particles of crystalline silicone dioxide (silica)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which occupations are at risk of silicosis?

A
  1. Mining, quarrying
  2. Slate works
  3. Foundries
  4. Potteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What areas of the lungs does silicosis affect?

A

Upper zone fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of silicosis on CXR?

A
  1. Upper zone fibrosis (diffuse upper lobe reticular shadowing
  2. Egg-shell calcification of the hilar lymph nodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the features of silicosis on CT?

A
  1. Diffuse multiple small nodues accompanied by calcifications
  2. Mass like scarring with calcification and volume loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does egg shell calcification indicate?

A

Silicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is hypersensitivity pneumonitis also known as?
What type of hypersensitivity reaction predominates the acute phase of this condition?

A

Extrinsic allergic alveolitis = type 3 hypersensitivity reaction. Some type 4 hypersensitivity activity too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of particles cause hypersensitivity pneumonitis (AKA extrinsic allergic alveolitis)?

A

Organic particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give 4 examples of EAA/hypersensitivity pneumonitis.

A
  1. Bird fanciers lung
  2. Farmers lung
  3. Malt workers lung
  4. Mushroom workers lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes bird fanciers lung

A

Avian proteins from bird droppings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What bacteria causes farmers lung?

A

Spores from Saccharopolyspora rectivirgula (from wet hay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What organism causes malt workers lung?

A

Aspergillus clavatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What organisms are implicated in mushroom workers lung?

A

Thermophilic actinomycetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does extrinsic allergic alveolitis present in the acute phase?

A

Dyspnoea
Dry cough
Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does chronic hypersensitivity pneumonitis/EAA present?

A
  1. Lethargy
  2. Dyspnoea
  3. Productive cough
  4. Anorexia and weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What areas of the lungs are fibrosed in EAA/hypersensitivity pneumonitis?

A

Upper/mid-zone fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What would you find on bronchoalveolar lavage for EAA/hypersensitivity pneumonitis?

A

Lymphocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What investigations can you do for EAA/hypersensitivity pneumonitis?

A
  1. Imaging
  2. Bronchoalveolar lavage
  3. Serologic assays for specific IgG antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Would you find eosinophilia in EAA/hypersensitivity pneumonitis?

A

No eosinophilia in EAA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is EAA managed?

A

Avoid precipitating factors
Oral glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List chemicals associated with occupational asthma

A
  1. Isocyanataes e.g. toluene diisocyanate
  2. Platinum salts
  3. Soldering flux resin
  4. Glutaraldehyde
  5. Flour
  6. Epoxy resins
  7. Proteolytic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which type of lung cancer is most associated with cavitating lung lesions?

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which cancer gives the appearance of “cherry red ball” on bronchoscopy?

A

Carcinoid tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which smoking cessation drug should be avoided in depression?

A

Varenicline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which smoking cessation drug should be avoided in epilepsy?

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Gene polymorphisms encoding for what are linked to asthma?

A

Cytokines
Chemokines
Toll-like receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List innate immune cells involved in asthma inflammatory response.

A

Mast cells
Dendritic cells
Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List adaptive immune cells involved in asthma inflammatory response.

A

T helper type 2 lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which mediators are implicated in asthma?

A

Histamine
Leukotrienes
Cytokines (IL 4, 5, 9, and 13)
Chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe some structural changes that occur in asthmatic airways.

A
  1. Hypertrophy and hyperplasia of smooth muscle
  2. Thickening of the basement membrane
  3. Angiogenesis
  4. Increased mucous gland size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which T-helper cell is involved in eosinophilic asthma?

A

Th2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which T-helper cells are involved in neutrophilic asthma?

A

Th1 or Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What physical examination findings in acute asthma attack?

A

Prolonged expiratory phase
Use of accessory muscles
Hyperinflation of the chest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Post-bronchodilator improvement in spiro/PEFR of what level suggests asthma?

A

> 12%, >200ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How to investigate for asthma?

A

Spiro with BD reversibility and FeNO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Methacholine challenge: How much decrease in FEV1 indicates hyperreactive airways (asthma)?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Explain how NO is produced in asthma

A
  1. nitric oxide produced by 3 types of nitric oxide synthesases.
  2. inducible NOS found in eosinophils and other inflammatory cells
  3. levels of NO correlate with levels of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

List the step wise approach for long term asthma management

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA +/- LTRA
  5. SABA + MART +/- LTRA (MART = fast acting LABA + low dose ICS)
  6. SABA + MART with medium dose ICS +/- LTRA
  7. SABA + high dose ICS + LABA, trial LAMA/theophylline
    Specialist referral if necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What PEFR in moderate acute asthma?

A

> 50-75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

PEFR in acute severe asthma?

A

33-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

PEFR in life threatening asthma?

A

<33%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the features of acute severe asthma?

A
  1. PEFR 33-50
  2. HR >=110
  3. RR >=25
  4. Can’t speak in full sentences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the features of life threatening asthma attack?

A
  1. PEFR <33%
  2. Normal pCO2
  3. Tiring/exhaustion/reduced resp. effort
  4. Confusion
  5. Reduced GCS
  6. Cyanosis
  7. Hypotension
  8. New arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What differentiates between life-threatening asthma and near-fatal asthma?

A

CO2 level normal in life-threatening, raised in near-fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Should you continue routine inhalers while on acute asthma treatment?

A

yes, including ICS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a common complication of mechanical ventilation in asthmatics?

A

hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which childhood infections can predispose to asthma in later life?

A

RSV
rhinovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which immunoglobulin in atopy/allergy?

A

IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do tobacco and marijuana combined affect COPD risk?

A

synergistic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Give an example of indoor pollution linked to COPD

A

biomass smoke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Give an example of outdoor pollution linked to COPD

A

PM2.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Give example of occupational exposure linked to COPD

A

coal dust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which gene polymorphisms are linked to COPD?

A
  1. CFTR (cystic fibrosis transmembrane conductance regulator)
  2. transforming growth factor beta-1
  3. serpine-2
  4. antioxidant enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does matrix metalloproteinase dysregulation lead to COPD?

A

increased MMP-12 is linked to emphysema and reduced lung function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How is asthma linked to risk of COPD?

A

chronic airway inflammation and atopy increases risk of copd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How does bronchopulmonary dysplasia link to COPD?

A

chronic airflow limitation
bronchopulmonary dysplasia occurs due to preterm birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Which infections predispose to COPD?

A

TB, RSV, HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Which vitamin deficiencies linked to COPD?

A

antioxidants - vit C and E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which gender is more predisposed to COPD?

A

females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are elastase levels linked to COPD?

A

excess elastase linked to copd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How does excess elastase link to COPD?

A

imbalance between elastases and their inhibitors (eg. alpha 1 antitrypsin) leads to premature emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Give examples of proteases

A

neutrophil elastase
matrix metalloproteinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Give example of antiproteases

A

alpha-1-antitrypsin
tissue inhibitors of metalloproteinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How does protease activity link to COPD?

A

excess protease activity degrades extracellular matrix components, leads to destruction of lung parenchyma and emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

How does smoking lead to oxidative stress?

A
  1. pollutants such as cigarette smoke induces production of reactive oxygen species.
  2. this results in oxidative stress
  3. oxidative stress causes direct cellular damage and impairs antiprotease activity, and promotes inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How does oxidative stress link to copd pathogenesis?

A
  1. impairs antiprotease activity
  2. direct cellular damage
  3. promotes inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What spirometry result confirms COPD?

A

POST-BRONCHODILATOR
FEV1/FVC <0.7 confirms persistent airflow limitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What CXR findings in COPD?

A

hyperinflation
bullae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is FEV1 in stage 1 mild COPD?

A

FEV1>80%, if has symptoms of copd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is FEV1 in stage 2 moderate COPD?

A

FEV1 50-79%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is FEV1 in stage 3 severe COPD?

A

FEV1 30-49%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is FEV1 in stage 4 very severe COPD?

A

FEV1 <30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What vaccines for COPD?

A

annual flu
one off pneumococcal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is general management for COPD?

A

smoking cessation
annual flu vax
one off pneumococcal vax
pulm rehab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What meds in initial mgmt of COPD?

A

SABA or SAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is second line management of COPD if not controlled on SABA or SAMA and steroid responsive?

A

if steroid responsive: add ICS + LABA, can continue to take either LABA or LAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

If not steroid responsive, what is second line management for COPD not controlled on SABA/SAMA?

A

LABA + LAMA.
PRN SABA only. No LAMA with SAMA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is third line mgmt of all COPD patients if not controlled with ICS or with LAMA+LABA?

A

triple therapy:
LAMA + LABA + ICS + SABA PRN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

When would you reduce oral theophylline dose?

A

if going to give macrolide (eg clarithromycin) or fluoroquinolones (eg levofloxacin) alongside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Why is azithromycin given as prophylaxis in COPD (re: properties)?

A

Both antimicrobial and immunomodulatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What screening prior to azithromycin, and what monitoring?

A
  1. CT to exclude TB
  2. LFT
  3. ECG for QTc
  4. hearing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Which medication can be used to prevent COPD exacerbations, and what class of meds?

A

phosphodiesterase-4 inhibitor - roflumilast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the clinical examination findings of Cor pulmonale?

A
  1. peripheral oedema
  2. systolic parasternal heave
  3. loud P2
  4. raised JVP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How to treat oedema as a result of Cor pulmonale?

A

loop diuretics eg furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How does COPD link to Cor pulmonale?

A
  1. chronic hypoxia leads to small pulmonary arteries constricting in order to redirect blood flow to better ventilated airways of lungs
  2. increased pulm pressure (ie pulm hypertension)
  3. chronic pulm htn causes increased RV pressure = cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the features of RV strain/cor pulmonale on CTPA?

A
  1. flattened intraventricular septum
  2. pulmonary trunk enlargement (bigger than aorta)
  3. reflux of contrast into IVC
  4. enlarged RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What can improve survival in copd patients?

A

LTOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the indications for LTOT?

A

evidence of chronic hypoxia
1. cyanosis
2. polycythaemia
3. peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What pO2 levels needed for LTOT?

A

pO2 <7.3kPa on 2 occasions at least 3 weeks apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

If pO2 7.3-8kPa, what features would make you consider LTOT?

A
  1. polycythaemia
  2. cyanosis
  3. features of RV strain - oedema, raised JVP, pulm HTN.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the extrapulmonary complications of COPD?

A
  1. cardiac - cor pulmonale, arrhythmias, IHD
  2. depression/anxiety
  3. weight loss/malnutrition
  4. osteoporosis if many steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Why weight loss in copd?

A

increased energy expenditure and reduced appetite.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is lung compliance?

A

Change in lung volume per unit change in airway pressure
ie. the lungs’ ability to stretch and expand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How does pulmonary oedema affect lung compliance?

A

Pulmonary oedema reduces lung compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

How do kyphosis and pneumonectomy affect lung compliance?

A

reduces

102
Q

Give example of condition that causes low lung compliance.

A

fibrosis - (thick balloon)

103
Q

Give example of condition that causes high lung compliance.

A

emphysema - plastic bag

104
Q

How does age affect lung compliance?

A

Age increases lung compliance

105
Q

What type of molecule is alpha-1 antitrypsin?

A

protease inhibitor

106
Q

What does A1A inhibit?

A

neutrophil elastase

107
Q

Where is A1A produced?

A

Liver

108
Q

Where is the gene for A1A?

A

Chromosome 14

109
Q

How is A1AT inherited?

A

Autosomal recessive/co-dominant

110
Q

How are the alleles classified in A1AT?

A

Electrophoretic mobility
M = normal
S = slow
Z = very slow

111
Q

What does heterozygous PiMZ signify in terms of emphysema risk and inheritance?

A

Low risk of emphysema if no-smoking
May pass on A1AD gene to children

112
Q

What are the A1AT levels in PiSS?

A

50%

113
Q

What are the A1AT levels in PiZZ?

A

10%

114
Q

How does A1AT present in lungs?

A

Panacinar emphysema, predominantly lower lobes

115
Q

How does A1AT affect liver in children?

A

Cholestasis

116
Q

How does A1AT affect liver in adults?

A

Cirrhosis
Hepatocellular carcinoma

117
Q

What is the mechanism behind ARDS?

A

Increased alveolar permeability leading to alveolar fluid accumulation (pulmonary oedema, non-cardiogenic)

118
Q

How is A1AT treated?

A
  1. No smoking
  2. Supportive - bronchodilators, physio
  3. IV alpha-1 antitrypsin protein concentrates
  4. Lung volume reduction surgery/endobronchial valve surgery, lung transplant
119
Q

How is A1AT investigated?

A

Spirometry - obstructive picture
A1AT concentrations

120
Q

How would ARDS present?

A
  1. Tachypnoea, Dyspnoea
  2. Hypoxia
  3. Bilateral crepitations
121
Q

What are the American-European Consensus Conference criteria for diagnosing ARDS?

A
  1. Acute onset (within 1 week)
  2. Pulmonary oedema (bilateral infiltrates on CXR)
  3. Non-cardiogenic (pulmonary wedge pressure required if uncertain)
  4. pO2/FiO2 < 40kPa (300 mmHg)
122
Q

What are some triggers for ARDS?

A
  1. Large blood transfusion
  2. Cardiopulmonary bypass
  3. Infections, sepsis
  4. Trauma
  5. Covid-19
  6. Acute pancreatitis
  7. Smoke inhalation
123
Q

What are the key investigations in suspected ARDS?

A

CXR and ABG

124
Q

What can be used to confirm non-cardiogenic pulmonary oedema in ARDS?

A

Pulmonary wedge pressure

125
Q

What is pulmonary wedge pressure and how is it measured?

A

Catheter wedged into tapering branch of a pulmonary artery

126
Q

How is ARDS treated?

A
  1. Treat underlying cause eg Abx in sepsis
  2. Oxygenation/ventilation
  3. Organ support, vasopressors
  4. Prone positioning, muscle relaxation
127
Q

What does pulmonary wedge pressure estimate?

A

Left atrial pressure.

128
Q

Which conditions predispose to ABPA?

A

Atopic/asthma
CF

129
Q

What investigations/findings for ABPA?

A
  1. Eosinophilia
  2. Flitting CXR changes
  3. IgE levels raised
  4. Positive IgG precipitins (not as raised as in aspergilloma)
  5. Positive Radioallergosorbent (RAST) test to aspergillus
130
Q

What is ABPA?

A

Allergy to aspergillus spores

131
Q

What is a bronchocoele, and how are they linked to ABPA?

A

Impacted mucoid secretions within the bronchial tree.
ABPA is a cause of non-obstructive bronchocoele.

132
Q

Where is bronchiectasis in ABPA?

A

proximal

133
Q

How is ABPA treated?

A
  1. Oral glucocorticoids
  2. Can add on itraconazole as second-line
134
Q

What is an aspergilloma?

A

Mycetoma (fungus ball) which colonises a pre-existing lung cavity e.g. secondary to lung cancer, CF, tuberculosis

135
Q

What are the clinical features of an aspergilloma?

A

Cough
Haemoptysis

136
Q

How would aspergilloma present on CXR?

A

Fungal ball cavity surrounded by crescent sign

137
Q

What investigations for aspergilloma?

A

CXR
High titres of aspergillus precipitins

138
Q

What is cryptogenic organising pneumonia?

A

Type of ILD

139
Q

Where does cryptogenic organising pneumonia affect?

A
  1. Distal bronchioles
  2. Respiratory bronchioles
  3. Alveolar ducts
  4. Alveolar walls
140
Q

How does cryptogenic organising pneumonia present?

A

Cough
SoB
Fever
Malaise
Symptoms present for weeks-months
Non-response to antibiotics

141
Q

How does cryptogenic organising pneumonia present on imaging?

A

Bilateral patchy consolidation/ground glass changes

142
Q

How does cryptogenic organising pneumonia present on lung function tests?

A

Restrictive picture, reduced TLCO

143
Q

How is cryptogenic organising pneumonia treated?

A

Watch and wait if mild
Steroids if severe

144
Q

What is Churg-Strauss also known as?

A

Eosinophilic granulomatosis with polyangiitis

145
Q

Which ANCA is Churg-Strauss?

A

pANCA (only in 60% of patients)

146
Q

What are the main clinical features of Churg-Strauss?

A
  1. Asthma
  2. Eosinophilia
  3. Nerve lesions (mono or polyneuropathy)
  4. Paranasal sinusitis
147
Q

What can precipitate Churg-Strauss?

A

LTRAs (montelukast)

148
Q

What antibodies in Churg-Strauss?

A

Anti myeloperoxidase antibodies in Churg Strauss

149
Q

What does ANCA stand for?

A

Anti Neutrophil Cytoplasmic Antibody

150
Q

What are the pathophysiological phases in Churg-Strauss?

A
  1. Prodromal allergic phase - similar to asthma/allergy symptoms
  2. Eosinophilic phase - accumulation of Eos in lungs/GI tract - causes pneumonia/gastroenteritis
  3. Vasculitic phase - necrotizing small-medium vessel vasculitis
151
Q

How does the vasculitic phase of Churg-Strauss manifest?

A
  1. Purpura
  2. Neuropathies
  3. Organ damage - renal/cardiac.
152
Q

How does Acute Mountain Sickness present?

A
  1. Nausea
  2. Headache
  3. Fatigue
153
Q

How is Acute mountain sickness prevented? Explain the mechanism of action of this drug

A

Acetozolamide
Carbonic anhydrase inhibitor
Causes a metabolic acidosis
Body tries to compensate by causing a respiratory alkalosis
This increases resp rate (to blow off CO2)
Increased resp rate increases oxygenation

154
Q

How is acute mountain sickness treated?

A

descent

155
Q

What is the pathophysiological mechanism behind High Altitude Pulmonary oEdema (HAPE)?

A

Hypobaric hypoxia causes uneven pulmonary vasoconstriction
Areas of lung with greater blood flow experience increase in capillary pressure
Causes alveolar oedema
Hypoxia also increases capillary permeability, more fluid leaks into alveoli

156
Q

How does HAPE present?

A

Typical pulmonary oedema symptoms

157
Q

How is HAPE treated?
What is the proposed mechanism of action for these drugs?

A

Descent

Nifedipine
Dexamethasone
Acetozolamide
PDE5 inhibitors

Drugs reduce systolic pulmonary artery pressure

158
Q

What is High Altitude Cerebral oEdema (HACE)?

A

Hypoxia causes cerebral vasodilation
Elevated cerebral blood volume -> fluid leaks out

Hypoxia increases BBB permeability -> more fluid in extracellular space

159
Q

How does HACE present?

A

Headache
Ataxia
Papilloedema

160
Q

How is HACE managed?

A

Descent
Dexamethasone

161
Q

What is omalizumab?

A

MAB to treat severe confirmed allergic IgE mediated asthma.
Binds to IgE
Add on to optimised standard therapy
SC Injection every 2-4 weeks

Can also be used in ABPA

162
Q

List 5 ways that asbestos can affect the lung.

A
  1. Pleural plaques
  2. Pleural thickening
  3. Asbestosis
  4. Lung cancer
  5. Mesothelioma
163
Q

What is asbestosis?

A

Lung fibrosis secondary to asbestos exposure.
Severity of asbestosis is directly proportional to length of asbestos exposure

164
Q

What is the latent period for asbestosis?

A

10-15 years after exposure

165
Q

What area of lung is affected in asbestosis?

A

Lower lobe fibrosis

166
Q

How does asbestosis present?

A

Like other ILD

Dyspnoea on exertion
Clubbing
Bilateral end inspiratory crackles
Restrictive spiro with reduced TLCO

167
Q

How is asbestosis treated?

A

Conservative management. No current interventions offer a significant benefit

168
Q

What is mesothelioma?

A

Malignant disease of pleura

169
Q

How does mesothelioma present?

A
  1. Chest pain
  2. Progressive dyspnoea
  3. Pleural effusion
170
Q

What is the most dangerous form of asbestos in mesothelioma?

A

Crocidolite (blue) asbestos

171
Q

How is mesothelioma treated?

A

Palliative chemo
May be offered surgery/radiotherapy

172
Q

How does asbestos exposure link to smoking in the risk of developing lung cancer?

A

Smoking has a synergistic effect with asbestos - massively increases risk of developing lung Ca.

173
Q

What is atelectasis?

A

Collapse of lung alveoli
Occurs when airways obstructed by bronchial secretions

174
Q

When does atelectasis usually occur?

A

72 hours post-op

175
Q

How does atelectasis present?

A

Dyspnoea
Hypoxia

176
Q

How is atelectasis treated?

A

Positioning patient upright
Chest physio

177
Q

List some causes of bilateral hilar lymphadenopathy

A
  1. Sarcoidosis
  2. TB
  3. Lymphoma/malignancy
  4. Pneumoconiosis e.g. berylliosis
  5. Fungi e.g. histoplasmosis, coccidioidomycosis
178
Q

List causes of bronchiectasis.

A
  1. Post-infective
  2. CF
  3. Bronchial obstruction due to foreign body/tumour
  4. Immune deficiency - Hypogammaglobulinaemia, selective IgA
  5. ABPA
  6. Ciliary dyskinetic syndromes: Kartagener, Young’s syndrome
  7. Yellow nail syndrome
179
Q

What is bronchiectasis?

A

Permanent dilatation of the airways secondary to chronic infection or inflammation.

180
Q

Which organisms most commonly isolated from bronchiectasis patients?

A
  1. Haemophilus influenzae
  2. Pseudomonas aeruginosa
  3. Klebsiella spp.
  4. Streptococcus pneumoniae
181
Q

Where should chest drains be inserted?

What borders make up the triangle of safety?

A

“Triangle” of safety (square fr)

Anterior border of latissimus dorsi
Base of the axilla
Lateral edge of pectoralis major
5th intercostal space (nipple line)

182
Q

Which type of lung cancer is associated with cavitating lung lesions?

A

Squamous cell carcinoma

183
Q

What cancers are associated with cannonball mets?

A

Renal
Prostate
Choriocarcinoma

184
Q

Which cancers cause calcified lung mets?

A

Chondrosarcomas
Osteosarcomas

185
Q

Where is the gene for CF located?

A

Long arm of Chromosome 7

186
Q

What is the most common mutation for CF patients in the UK?

A

Delta F508

187
Q

How does CFTR mutation cause thickened secretions in CF?

A
  1. Dysfunctional CFTR protein causes Cl- and H2O retention in cells
  2. This leads to increased extracellular Na concentration.
  3. This prompts reabsorption of Na and H2O together into cells.
  4. Leads to dehydrated and thickened secretions
188
Q

How does CF cause lung damage over time?

A
  1. Thickened mucus causes impaired mucociliary clearance, allows bacteria to colonise
  2. This leads to chronic infections and inflammation in the airways
  3. Chronic inflammation and mucoid obstruction over time lead to bronchiectasis and structural changes
  4. Eventually leads to respiratory failure
189
Q

How does CF affect the GI system?

A
  1. Pancreatic blockage - leads to malabsorption and steatorrhoea
  2. Intestinal obstruction - meconium ileus/distal intestinal obstruction syndrome in adults
  3. Liver involvement - blocked bile ducts leads to focal biliary cirrhosis
190
Q

How can CF affect fertility?

A

In males: congenital bilateral absence of vas deferens (obstructive azoospermia)
In females: thickened cervical mucus, irregular menses

191
Q

How does CF cause dehydration?

A
  1. CFTR dysfunction causes reduced reabsorption of chloride and sodium from sweat.
  2. Salty sweat increases dehydration and electrolyte imbalance esp in exercise
192
Q

What respiratory symptoms in CF?

A
  1. Chronic cough
  2. Wheezing and dyspnoea
  3. Recurrent respiratory infections
  4. Chronic sinusitis and nasal polyps
193
Q

What are the most common organisms which cause infections in CF patients?

A
  1. Staph Aureus
  2. Pseudomonas aeruginosa
  3. Burkholderia cepacia
  4. Haemophilus influenzae
194
Q

Which vitamin deficiencies commonly found in CF?

A

Fat soluble vitamins
ADEK

195
Q

What GI symptoms in CF?

A
  1. Meconium ileus, distal intestinal obstruction syndrome in adults
  2. Pancreatic insufficiency
  3. Biliary cirrhosis
  4. GORD
196
Q

What is distal intestinal obstruction syndrome?

A

Partial or complete intestinal obstruction due to inspissated faecal material.

197
Q

How does CF affect liver?

A

bile duct obstruction
leads to cirrhosis and portal hypertension and potential liver failure

198
Q

How does GORD affect CF patients?

A

Increased prevalance in CF.
Exacerbates pulmonary complications

199
Q

How does CF lead to haemoptysis and how is this treated?

A

Bronchial wall erosion due to chronic inflammation/infection
May need pulmonary artery embolisation

200
Q

Give 2 endocrine manifestations of CF.

A
  1. CF related diabetes due to reduced insulin secretion in pancreas + insulin resistance
  2. Growth problems - delayed growth and puberty due to malabsorption, chronic inflammation, and increased energy expenditure
201
Q

What diagnostic tests for CF?

A
  1. Newborn heelprick - immunoreactive trypsinogen
  2. Chloride sweat test
  3. Genetic testing
202
Q

What substance in CF newborn heelprick test?

A

Immunoreactive trypsinogen

203
Q

What are three other clinical features of CF (aside from lung/GI)

A
  1. Clubbing due to chronic hypoxia
  2. Osteoporosis (reduced Vit D absorption, chronic inflammation and freq. steroids)
  3. Salt loss syndrome
204
Q

What is salt loss syndrome in CF?

A

Excessive NaCl loss in sweat leads to hyponatraemic dehydration
Also metabolic alkalosis, particularly in children

205
Q

How to improve airway clearance in CF?

A
  1. Chest physio/positioning
  2. High frequency chest wall oscillation
  3. Exercise
206
Q

List some pharmacological interventions that can help in CF.

A
  1. Mucolytics - dornase alfa, hypertonic saline
  2. Bronchodilators
  3. Antibiotics (inhaled in Pseudomonas colonisation), rotational prophylaxis
  4. Anti-inflammatories - steroids and NSAIDs
  5. CFTR modulators - ivacaftor, lumacaftor, elexacaftor
207
Q

List CFTR modulators

A

ivacaftor
lumacaftor
elexacaftor

208
Q

How are nutritional manifestations of CF managed?

A
  1. Pancreatic enzyme supplementation
  2. High fat, high calorie diet
  3. Fat soluble vitamin supplements (ADEK)
209
Q

How can CF liver disease be managed?

A

Regular LFT monitoring
Early UDCA
Can consider liver transplant in severe cases

210
Q

List 4 respiratory complications of CF.

A
  1. Bronchiectasis
  2. Pneumothorax
  3. Haemoptysis due to bronchial wall erosion - may need bronchial artery embolisation
  4. Respiratory failure - may need supplemental oxygen/lung transplant to extend life
211
Q

List 3 other complications of CF (not lung/GI/endo).

A
  1. Sinusitis/nasal polyps
  2. Bone disease (osteoporosis)
  3. Kidney stones due to dehydration, alkaline urine, and hyperoxaluria
212
Q

What causes nephrolithiasis in CF?

A

Combination of:
1. Dehydration
2. Alkaline urine
3. Hyperoxaluria

213
Q

How do ipratropium and tiotropium work?

A

Anti-muscarinic
Block acetylcholine receptors

214
Q

What class of drug is theophylline and how does it work?

A

Methylxanthines
Non-specific inhibitor of PDE, increases cAMP

215
Q

List triad of systems implicated in Wegener’s

A
  1. Upper respiratory tract
  2. Lower respiratory tract
  3. Glomerulonephritis
216
Q

How does Wegener’s manifest in the upper respiratory tract?

A
  1. Chronic sinusitis
  2. Nasal crusting/discharge
  3. Epistaxis
  4. Subglottic stenosis - hoarseness/stridor
  5. Otitis media, hearing loss, ear pain

Can have oral ulcers

217
Q

How does Wegener’s manifest in the lower respiratory tract?

A
  1. Cough, dyspnoea
  2. Haemoptysis
  3. Pleuritis
  4. Pulmonary infiltrates/nodules
218
Q

How does Wegener’s manifest in the kidneys?

A
  1. Microscopic haematuria
  2. Urinary sediment
  3. Pauci-immune Rapidly progressing glomerulonephritis, can lead to CKD
219
Q

How can Wegener’s affect the eye?

A
  1. Ocular pseudotumours - proptosis, diplopia, visual loss
  2. Episcleritis/scleritis
220
Q

How can Wegener’s manifest in skin?

A
  1. Leukoclastic angiitis - purpura, ulceration, vesicles
221
Q

List neurological manifestations of Wegener’s

A
  1. Mononeuritis multiplex
  2. Peripheral sensorimotor polyneuropathy
  3. Cranial nerve palsies
222
Q

List investigations for Wegener’s

A
  1. cANCA positive in >90%, pANCA positive in 25%. (specifically anti-proteinase 3)
  2. CXR - nodular changes, cavitating lesions
  3. Endothelial crescents in Bowman’s capsule on renal biopsy
223
Q

Which proteinase implicated in Wegener’s

A

proteinase 3

224
Q

What is the gold standard for diagnosis in Wegener’s?

A

Histopathological confirmation of necrotising granulomatous inflammation from affected organ

225
Q

How is Wegener’s treated?

A
  1. Steroids
  2. Cyclophosphamide
  3. Plasma exchange
226
Q

What prophylaxis alongside Wegener treatment?

A

Osteoporosis prophylaxis
Pneumocystis prophylaxis

227
Q

List 3 respiratory complications of Wegener’s

A
  1. Pulmonary haemorrhage
  2. Otitis media, chronic sinusitis
  3. Pulmonary fibrosis
228
Q

How can orbital pseudotumour present in Wegener’s

A

Proptosis
Diplopia
Eye pain

229
Q

How does IPF present?

A
  1. Progressive exertional dyspnoea
  2. Bibasal fine end-inspiratory crackles
  3. Clubbing
  4. Dry cough
230
Q

What are the features of IPF on HRCT?

A

Bilateral patchy irregularities, small, peripheral
Initially ground-glass, progressing to honeycombing

231
Q

What investigations in IPF?

A
  1. HRCT
  2. Spirometry - restrictive + reduced TLCO
  3. ANA positive in 30%, RF positive in 10%
232
Q

How is IPF treated?

A
  1. Pulmonary rehabilitation
  2. Antifibrotics - nintedanib, pirfenidone
  3. May need oxygen supplementation, lung transplant
233
Q

What are some respiratory complications of IPF?

A
  1. Respiratory failure
  2. Pulmonary hypertension and cor pulmonale
  3. Lung infections
  4. Lung Ca
234
Q

What are some complications of IPF (not respiratory)?

A
  1. VTE
  2. GORD
235
Q

What is Loffler syndrome?

A

Eosinophilic pneumonia

236
Q

What are common triggers for Loffler’s syndrome?

A
  1. Parasitic infections (Ascaris lumbricoides, Strongyloides stercoralis) - Type 2 hypersensitivity
  2. Drug induced - NSAIDs, antibiotics, anticonvulsants
  3. Idiopathic
237
Q

How is Loeffler’s treated?

A
  1. Treat underlying cause - antiparasitics if indicated
  2. Steroids
    Oxygen if required
238
Q

What is Kartagener’s syndrome?

A

Primary ciliary dyskinesia

239
Q

What is the pathophysiology of Kartagener’s?

A

Defects in dynein arm leads to immotile cilia

240
Q

What are the features of Kartagener’s?

A

Dextrocardia or complete situs invertus
Bronchiectasis
Recurrent sinusitis
Subfertility

241
Q

How does dextrocardia present in exam questions?

A

Quiet heart sounds
Small volume complexes in lateral leads

242
Q

What is the mechanism behind subfertility in Kartagener’s?

A

Males: impaired sperm motility
Females: impaired ciliary motility in Fallopian tubes

243
Q

How is Kartagener’s managed?

A
  1. Chest physio
  2. Mucolytics such as N-Acetylcisteine
  3. Bronchodilators
  4. Antibiotics (both prophylactic and treatment)
  5. Sinus management (saline irrigation, topical steroids)
  6. Surgery - lobectomy in localised bronchiectasis, sinus surgery if recurrent
  7. Vaccinations against resp. organisms (flu/pneumococcal)
244
Q

Where is Klebsiella normally found?

A

Klebsiella is part of normal gut flora

245
Q

What type of pneumonia is commonly caused by Klebsiella?

A

Aspiration pneumonia

246
Q

In what groups does Klebsiella pneumonia tend to occur?

A
  1. Alcohol excess
  2. Diabetes
247
Q

Where in lungs does Klebsiella tend to affect?

A

Upper lobes

248
Q

How is Klebsiella sputum often described?

A

Red currant jelly sputum = klebsiella

249
Q

What are the complications of Klebsiella pneumonia?

A
  1. Lung abscess
  2. Empyema
250
Q

Which receptors are blocked by LTRAs (montelukast, zafirlukast)?

A

CysLT1

251
Q

What is Lofgren’s syndrome?

A

Form of sarcoidosis characterised by:
1. Bilateral hilar lymphadenopathy
2. Erythema nodosum
3. Fever
4. Polyarthralgia

252
Q

What is the prognosis of Lofgren’s syndrome?

A

Lofgren = Excellent prognosis

MRCP P1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions