Respiratory Flashcards

1
Q

Pulmonary hypertension may be defined as

A

a sustained elevation in mean pulmonary arterial pressure of greater than 20 mmHg at rest.

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2
Q

Group 3: Pulmonary hypertension secondary to lung disease/hypoxia

Clue: CISH

A
  • COPD
  • Interstitial lung disease
  • Sleep apnoea
  • High altitude
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3
Q

Respiratory acidosis may be caused by a number of conditions:

SOAP CN

A

Sedative drugs: benzodiazepines, opiate overdose
Obesity hypoventilation syndrome
Asthma– Life-threatening
Pulmonary oedema

COPD
Neuromuscular disease

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4
Q

respiratory depression leading to hypoventilation leads to what blood gas

A

respiratory acidosis.

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5
Q

What is STEP 1 in managing Asthma newly diagnosed in adults

A

Step 1 NICE
anti-inflammatory reliever (AIR) therapy which is

a low-dose inhaled corticosteroid (ICS)/formoterol combination inhaler to be taken as needed for symptom relief

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6
Q

IN STEP 1 of asthma Mx if the patient presents highly symptomatic (for example, regular nocturnal waking) or with a severe exacerbation what can be added with ICS

A

start treatment with low-dose MART (maintenance and reliever therapy)

treat the acute symptoms as appropriate (e.g. a course of oral corticosteroids may be indicated)

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7
Q

STEP 2 in Asthma Mx

A

Step 2 NICE
a low-dose MART

MART describes using an inhaled corticosteroid (ICS)/formoterol combination inhaler for daily maintenance therapy and the relief of symptoms as needed, i.e. regularly and as required

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8
Q

Step 3 in Asthma Mx

A

STEP 3 – from step 2 LOW DOSE Mart to moderate

a moderate-dose MART

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9
Q

Step 4
What to do if after checking the fractional exhaled nitric oxide (FeNO) level if available, and the blood eosinophil count NICE
if either of these is raised,

A

refer to a specialist in asthma care

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10
Q

if neither FeNO nor eosinophil count is raised in Asthma Mx

A

consider a trial of either a leukotriene receptor antagonist (LTRA) or a long-acting muscarinic receptor antagonist (LAMA) used in addition to moderate-dose MART

if control has not improved, stop the LTRA or LAMA and start a trial of the alternative medicine (LTRA or LAMA)

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11
Q

Who should LTOT be offered to?

A

LTOT should be offered to patients with a pO2 of < 7.3 kPa

or to those with a pO2 of 7.3 - 8 kPa

and one of the following:
secondary polycythaemia
nocturnal hypoxaemia
peripheral oedema
pulmonary hypertension

SNPP

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12
Q

Cor pulmonale features include

A

features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2

use a loop diuretic for oedema,

consider long-term oxygen therapy

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13
Q

What is a CI to Lung transplantation? CF Specific

A

chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation

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14
Q

Allergic bronchopulmonary aspergillosis - key finding

Clue bronchoconstriction: wheeze, cough, dyspnoea

A

bronchiectasis and eosinophilia.

positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE

Patients may have a previous label of asthma

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15
Q

Recommended Diet in CF

A

high calorie diet, including high fat intake

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16
Q

Allergic bronchopulmonary aspergillosis- Management

A

oral glucocorticoids
itraconazole is sometimes introduced as a second-line agent

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17
Q

What is Alpha-1 antitrypsin deficiency?

A

A common inherited condition caused by a lack of a protease inhibitor normally produced by the liver

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18
Q

What is the primary role of Alpha-1 antitrypsin?

A

To protect cells from enzymes such as neutrophil elastase

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19
Q

What condition is classically caused by Alpha-1 antitrypsin deficiency?

A

Emphysema (chronic obstructive pulmonary disease)

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20
Q

On which chromosome is the gene for Alpha-1 antitrypsin located?

A

Chromosome 14

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21
Q

How is Alpha-1 antitrypsin deficiency inherited?

A

In an autosomal recessive / co-dominant fashion

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22
Q

What are the alleles classified by their electrophoretic mobility?

A
  • M for normal * S for slow * Z for very slow
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23
Q

What is the genotype for normal Alpha-1 antitrypsin levels?

A

PiMM

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24
Q

What is the genotype for heterozygous Alpha-1 antitrypsin levels?

A

PiMZ

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25
Q

What is the risk of developing emphysema for non-smokers with Alpha-1 antitrypsin deficiency?

A

Low risk of developing emphysema but may pass on A1AT gene to children

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26
Q

What are the A1AT levels for homozygous PiSS genotype?

A

50% normal A1AT levels

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27
Q

What are the A1AT levels for homozygous PiZZ genotype?

A

10% normal A1AT levels

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28
Q

Which genotype usually manifests the disease?

A

PiZZ genotype

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29
Q

What lung condition is associated with Alpha-1 antitrypsin deficiency?

A

Panacinar emphysema, most marked in lower lobes

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30
Q

What liver conditions can occur in adults with Alpha-1 antitrypsin deficiency?

A
  • Cirrhosis * Hepatocellular carcinoma
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31
Q

What liver condition can occur in children with Alpha-1 antitrypsin deficiency?

A

Cholestasis

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32
Q

What investigations are done for Alpha-1 antitrypsin deficiency?

A

A1AT concentrations

Spirometry showing obstructive picture

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33
Q

What is a key management strategy for patients with Alpha-1 antitrypsin deficiency?

A

No smoking

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34
Q

What supportive treatments are available for Alpha-1 antitrypsin deficiency?

A
  • Bronchodilators * Physiotherapy
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35
Q

What specific therapies can be used for Alpha-1 antitrypsin deficiency?

A
  • Intravenous alpha1-antitrypsin protein concentrates * Surgery options like lung volume reduction surgery and lung transplantation
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36
Q

What are some adverse effects of nicotine replacement therapy?

A

Nausea & vomiting, headaches, flu-like symptoms

These effects can vary in severity among individuals.

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37
Q

What does NICE recommend for individuals with a high level of dependence on nicotine?

A

A combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge, or nasal spray)

This approach is recommended for those who found single forms of NRT inadequate in the past.

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38
Q

What is varenicline?

A

A nicotinic receptor partial agonist

It is used as a smoking cessation aid.

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39
Q

When should varenicline be started?

A

1 week before the patient’s target date to stop

This timing helps increase the likelihood of successful cessation.

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40
Q

What is the recommended course of treatment with varenicline?

A

12 weeks

Patients should be monitored regularly and treatment continued only if not smoking.

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41
Q

How does varenicline compare to bupropion in effectiveness?

A

Varenicline has been shown to be more effective than bupropion

This finding is based on clinical studies.

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42
Q

What is the most common adverse effect of varenicline?

A

Nausea

Other common problems include headache, insomnia, and abnormal dreams.

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43
Q

In which patients should varenicline be used with caution?

A

Patients with a history of depression or self-harm

There are ongoing studies regarding the risk of suicidal behavior in these patients.

44
Q

Is varenicline contraindicated in pregnancy?

A

Yes

It is also contraindicated during breastfeeding.

45
Q

What type of medication is bupropion?

A

A norepinephrine-dopamine reuptake inhibitor and nicotinic antagonist

It differs from many antidepressants by having minimal effect on serotonin.

46
Q

When should bupropion be started?

A

1 to 2 weeks before the patient’s target date to stop

This helps prepare the patient for cessation.

47
Q

What is the small risk associated with bupropion?

A

Seizures (1 in 1,000)

This risk necessitates careful patient selection.

48
Q

What are the contraindications for bupropion?

A

Epilepsy, pregnancy, breastfeeding

Having an eating disorder is a relative contraindication.

49
Q

What did NICE recommend regarding smoking in pregnant women?

A

All pregnant women should be tested for smoking using carbon monoxide detectors

This is partly due to the pressure not to smoke during pregnancy.

50
Q

What should happen if a pregnant woman has a CO reading of 7 ppm or above?

A

She should be referred to NHS Stop Smoking Services

This applies to women who smoke or have stopped smoking within the last 2 weeks.

51
Q

What are the first-line interventions in pregnancy for smoking cessation?

A

Cognitive behaviour therapy, motivational interviewing, structured self-help, support from NHS Stop Smoking Services

These approaches are recommended before considering NRT.

52
Q

What is the evidence regarding the use of NRT in pregnancy?

A

The evidence is mixed but often used if first-line measures fail

There is no evidence that NRT affects the child’s birthweight.

53
Q

What should pregnant women do with nicotine patches before going to bed?

A

Remove the patches

This practice aims to minimize potential risks during sleep.

54
Q

Are varenicline and bupropion recommended for pregnant women?

A

No, both are contraindicated

Safety during pregnancy is a primary concern.

55
Q

What is extrinsic allergic alveolitis also known as?

A

Hypersensitivity pneumonitis

56
Q

What causes extrinsic allergic alveolitis?

A

Hypersensitivity induced lung damage due to inhaled organic particles

57
Q

What type of hypersensitivity is largely responsible for tissue damage in EAA?

A

Type III hypersensitivity

58
Q

Which additional type of hypersensitivity is thought to play a role in chronic EAA?

A

Type IV hypersensitivity

59
Q

What is an example of EAA related to bird droppings?

A

Bird fanciers’ lung

60
Q

What causes farmer’s lung?

A

Spores of Saccharopolyspora rectivirgula from wet hay

61
Q

What is the causative agent of malt workers’ lung?

A

Aspergillus clavatus

62
Q

What is the causative agent of mushroom workers’ lung?

A

Thermophilic actinomycetes

63
Q

What are the acute symptoms of EAA?

A

Dyspnoea, dry cough, fever

64
Q

How long after exposure do acute symptoms of EAA occur?

65
Q

What are the chronic symptoms of EAA?

A

Lethargy, dyspnoea, productive cough, anorexia and weight loss

66
Q

How long after exposure do chronic symptoms of EAA occur?

A

Weeks to months

67
Q

What imaging finding is associated with EAA?

A

Upper/mid-zone fibrosis

68
Q

What does bronchoalveolar lavage reveal in patients with EAA?

A

Lymphocytosis

69
Q

What serologic test is used in the investigation of EAA?

A

Serologic assays for specific IgG antibodies

70
Q

What blood finding is NOT typically seen in EAA?

A

Eosinophilia

71
Q

What is a key management strategy for EAA?

A

Avoid precipitating factors

72
Q

What medication is commonly used in the management of EAA?

A

Oral glucocorticoids

73
Q

High altitude pulmonary oedema (HAPE): key pathophysiological step is

A

uneven hypoxic pulmonary vasoconstriction is a key pathophysiological step

74
Q

high altitudes diseases 3

A

acute mountain sickness (AMS), which may progress to high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE). All three conditions are due to the chronic hypobaric hypoxia which develops at high altitudes

75
Q

Prevention and treatment of AMS

A

the risk of AMS may actually be positively correlated to physical fitness
gain altitude at no more than 500 m per day
acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
treatment: descent

76
Q

Management of HACE

A

descent
dexamethasone

77
Q

Management of HAPE

A

descent
nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available

78
Q

Sarcoidosis CXR stages 1 to 4

A

Sarcoidosis CXR
1 = BHL
2 = BHL + infiltrates
3 = infiltrates
4 = fibrosis

79
Q

Sarcoidosis

Other investigations
spirometry:

A

Other investigations
spirometry: may show a restrictive defect

80
Q

Sarcoidosis

Other investigations
tissue biopsy

A

tissue biopsy: non-caseating granulomas

81
Q

Contraindications to lung cancer surgery

SFMV

A

Contraindications to lung cancer surgery include
assess general health

stage IIIb or IV (i.e. metastases present)

FEV1 < 1.5 litres is considered a general cut-off point*

malignant pleural effusion

tumour near hilum

vocal cord paralysis

SVC obstruction

82
Q

Asthmatic features/features suggesting steroid responsiveness in COPD:

A

previous diagnosis of asthma or atopy
a higher blood eosinophil count
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)

83
Q

Bronchiectasis: causes

A

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. There are a wide variety of causes are listed below:

Causes
post-infective: tuberculosis, measles, pertussis, pneumonia
cystic fibrosis
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
yellow nail syndrome

84
Q

Bronchiectasis: management

A

physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)

85
Q

Most common organisms isolated from patients with bronchiectasis:

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

86
Q

Insertion of a chest drain is relatively contraindicated in patients with any of the following:

A

INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions

87
Q

Offer LTOT to patients with a pO2 of

A

< 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:secondary polycythaemia
peripheral oedema
pulmonary hypertension

88
Q

kartagener’s syndrome (also known as primary ciliary dyskinesia

Features

A

dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

89
Q

Kartagener’s syndrome (also known as primary ciliary dyskinesia)
Pathogenesis

A

Pathogenesis
dynein arm defect results in immotile cilia

90
Q

Psittacosis is infection caused by

A

by Chlamydia psittaci

combination of typical fever with a history of bird contact (reported in 84%) or a presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics.

91
Q

Psittacosis TX

A

Treatment:
1st-line: tetracyclines e.g. doxycycline
2nd-line: macrolides e.g. erythromycin

92
Q

Causes of pulmonary eosinophilia

A

Churg-Strauss syndrome
allergic bronchopulmonary aspergillosis (ABPA)
Loffler’s syndrome
eosinophilic pneumonia
hypereosinophilic syndrome
tropical pulmonary eosinophilia
drugs: nitrofurantoin, sulphonamides
less common: Wegener’s granulomatosis

93
Q

Respiratory acidosis

A

Respiratory acidosis
Respiratory acidosis may be caused by a number of conditions:
COPD
decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
neuromuscular disease
obesity hypoventilation syndrome
sedative drugs: benzodiazepines, opiate overdose

94
Q

Respiratory alkalosis

A

Respiratory alkalosis
Common causes
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

95
Q

Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent

features

A

Features
acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: dyspnoea, non-productive cough, malaise, weight loss
ocular: uveitis
skin: lupus pernio
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

96
Q

CXR Sarcoidosis

A

A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

97
Q

Sarcoidosis
Factors associated with poor prognosis

A

Factors associated with poor prognosis
insidious onset, symptoms > 6 months
absence of erythema nodosum
extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
CXR: stage III-IV features
black African or African-Caribbean ethnicity

98
Q

Silicosis is a fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing tuberculosis (silica is toxic to macrophages).

A

Occupations at risk of silicosis
mining
slate works
foundries
potteries
upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes

99
Q

Varenicline

A

a nicotinic receptor partial agonist

nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams

varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline
contraindicated in pregnancy and breastfeeding

100
Q

Bupropion

A

a norepinephrine-dopamine reuptake inhibitor and nicotinic antagonis

contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication

101
Q

Transfer factor

A

Transfer factor
The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

102
Q

Causes of a raised TLCO

A

asthma
pulmonary haemorrhage (e.g. granulomatosis with polyangiitis, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise

103
Q

Causes of a lower TLCO

A

pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output

104
Q

Acronym for causes of upper zone fibrosis:

A

Acronym for causes of upper zone fibrosis:

CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis

105
Q

Fibrosis predominately affecting the lower zones

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

106
Q

What are the most appropriate initial settings for the ventilator?

A

IPAP 10, EPAP 5 H20

107
Q

Light’s criteria: Effusion LDH level greater than 2/3rds the upper limit of serum LDH points to exudate

A

Light’s Criteria for exudative effusion requires one of more of the following:
Pleural fluid protein / Serum protein >0.5
Pleural fluid LDH / Serum LDH >0.6
Pleural fluid LDH > 2/3 * Serum LDH upper limit of normal
Glucose is not used in Light’s Criteria.