Respiratory Flashcards
(107 cards)
1
Q
Pulmonary hypertension may be defined as
A
a sustained elevation in mean pulmonary arterial pressure of greater than 20 mmHg at rest.
2
Q
Group 3: Pulmonary hypertension secondary to lung disease/hypoxia
Clue: CISH
A
- COPD
- Interstitial lung disease
- Sleep apnoea
- High altitude
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
4
Q
respiratory depression leading to hypoventilation leads to what blood gas
A
respiratory acidosis.
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
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)
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
8
Q
Step 3 in Asthma Mx
A
STEP 3 – from step 2 LOW DOSE Mart to moderate
a moderate-dose MART
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
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)
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
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
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
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
15
Q
Recommended Diet in CF
A
high calorie diet, including high fat intake
16
Q
Allergic bronchopulmonary aspergillosis- Management
A
oral glucocorticoids
itraconazole is sometimes introduced as a second-line agent
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
18
Q
What is the primary role of Alpha-1 antitrypsin?
A
To protect cells from enzymes such as neutrophil elastase
19
Q
What condition is classically caused by Alpha-1 antitrypsin deficiency?
A
Emphysema (chronic obstructive pulmonary disease)
20
Q
On which chromosome is the gene for Alpha-1 antitrypsin located?
A
Chromosome 14
21
Q
How is Alpha-1 antitrypsin deficiency inherited?
A
In an autosomal recessive / co-dominant fashion
22
Q
What are the alleles classified by their electrophoretic mobility?
A
- M for normal * S for slow * Z for very slow
23
Q
What is the genotype for normal Alpha-1 antitrypsin levels?
A
PiMM
24
Q
What is the genotype for heterozygous Alpha-1 antitrypsin levels?
A
PiMZ
25
What is the risk of developing emphysema for non-smokers with Alpha-1 antitrypsin deficiency?
Low risk of developing emphysema but may pass on A1AT gene to children
26
What are the A1AT levels for homozygous PiSS genotype?
50% normal A1AT levels
27
What are the A1AT levels for homozygous PiZZ genotype?
10% normal A1AT levels
28
Which genotype usually manifests the disease?
PiZZ genotype
29
What lung condition is associated with Alpha-1 antitrypsin deficiency?
Panacinar emphysema, most marked in lower lobes
30
What liver conditions can occur in adults with Alpha-1 antitrypsin deficiency?
* Cirrhosis * Hepatocellular carcinoma
31
What liver condition can occur in children with Alpha-1 antitrypsin deficiency?
Cholestasis
32
What investigations are done for Alpha-1 antitrypsin deficiency?
A1AT concentrations
Spirometry showing obstructive picture
33
What is a key management strategy for patients with Alpha-1 antitrypsin deficiency?
No smoking
34
What supportive treatments are available for Alpha-1 antitrypsin deficiency?
* Bronchodilators * Physiotherapy
35
What specific therapies can be used for Alpha-1 antitrypsin deficiency?
* Intravenous alpha1-antitrypsin protein concentrates * Surgery options like lung volume reduction surgery and lung transplantation
36
What are some adverse effects of nicotine replacement therapy?
Nausea & vomiting, headaches, flu-like symptoms
## Footnote
These effects can vary in severity among individuals.
37
What does NICE recommend for individuals with a high level of dependence on nicotine?
A combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge, or nasal spray)
## Footnote
This approach is recommended for those who found single forms of NRT inadequate in the past.
38
What is varenicline?
A nicotinic receptor partial agonist
## Footnote
It is used as a smoking cessation aid.
39
When should varenicline be started?
1 week before the patient's target date to stop
## Footnote
This timing helps increase the likelihood of successful cessation.
40
What is the recommended course of treatment with varenicline?
12 weeks
## Footnote
Patients should be monitored regularly and treatment continued only if not smoking.
41
How does varenicline compare to bupropion in effectiveness?
Varenicline has been shown to be more effective than bupropion
## Footnote
This finding is based on clinical studies.
42
What is the most common adverse effect of varenicline?
Nausea
## Footnote
Other common problems include headache, insomnia, and abnormal dreams.
43
In which patients should varenicline be used with caution?
Patients with a history of depression or self-harm
## Footnote
There are ongoing studies regarding the risk of suicidal behavior in these patients.
44
Is varenicline contraindicated in pregnancy?
Yes
## Footnote
It is also contraindicated during breastfeeding.
45
What type of medication is bupropion?
A norepinephrine-dopamine reuptake inhibitor and nicotinic antagonist
## Footnote
It differs from many antidepressants by having minimal effect on serotonin.
46
When should bupropion be started?
1 to 2 weeks before the patient's target date to stop
## Footnote
This helps prepare the patient for cessation.
47
What is the small risk associated with bupropion?
Seizures (1 in 1,000)
## Footnote
This risk necessitates careful patient selection.
48
What are the contraindications for bupropion?
Epilepsy, pregnancy, breastfeeding
## Footnote
Having an eating disorder is a relative contraindication.
49
What did NICE recommend regarding smoking in pregnant women?
All pregnant women should be tested for smoking using carbon monoxide detectors
## Footnote
This is partly due to the pressure not to smoke during pregnancy.
50
What should happen if a pregnant woman has a CO reading of 7 ppm or above?
She should be referred to NHS Stop Smoking Services
## Footnote
This applies to women who smoke or have stopped smoking within the last 2 weeks.
51
What are the first-line interventions in pregnancy for smoking cessation?
Cognitive behaviour therapy, motivational interviewing, structured self-help, support from NHS Stop Smoking Services
## Footnote
These approaches are recommended before considering NRT.
52
What is the evidence regarding the use of NRT in pregnancy?
The evidence is mixed but often used if first-line measures fail
## Footnote
There is no evidence that NRT affects the child's birthweight.
53
What should pregnant women do with nicotine patches before going to bed?
Remove the patches
## Footnote
This practice aims to minimize potential risks during sleep.
54
Are varenicline and bupropion recommended for pregnant women?
No, both are contraindicated
## Footnote
Safety during pregnancy is a primary concern.
55
What is extrinsic allergic alveolitis also known as?
Hypersensitivity pneumonitis
56
What causes extrinsic allergic alveolitis?
Hypersensitivity induced lung damage due to inhaled organic particles
57
What type of hypersensitivity is largely responsible for tissue damage in EAA?
Type III hypersensitivity
58
Which additional type of hypersensitivity is thought to play a role in chronic EAA?
Type IV hypersensitivity
59
What is an example of EAA related to bird droppings?
Bird fanciers' lung
60
What causes farmer's lung?
Spores of Saccharopolyspora rectivirgula from wet hay
61
What is the causative agent of malt workers' lung?
Aspergillus clavatus
62
What is the causative agent of mushroom workers' lung?
Thermophilic actinomycetes
63
What are the acute symptoms of EAA?
Dyspnoea, dry cough, fever
64
How long after exposure do acute symptoms of EAA occur?
4-8 hours
65
What are the chronic symptoms of EAA?
Lethargy, dyspnoea, productive cough, anorexia and weight loss
66
How long after exposure do chronic symptoms of EAA occur?
Weeks to months
67
What imaging finding is associated with EAA?
Upper/mid-zone fibrosis
68
What does bronchoalveolar lavage reveal in patients with EAA?
Lymphocytosis
69
What serologic test is used in the investigation of EAA?
Serologic assays for specific IgG antibodies
70
What blood finding is NOT typically seen in EAA?
Eosinophilia
71
What is a key management strategy for EAA?
Avoid precipitating factors
72
What medication is commonly used in the management of EAA?
Oral glucocorticoids
73
High altitude pulmonary oedema (HAPE): key pathophysiological step is
uneven hypoxic pulmonary vasoconstriction is a key pathophysiological step
74
high altitudes diseases 3
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
Prevention and treatment of AMS
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
Management of HACE
descent
dexamethasone
77
Management of HAPE
descent
nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available
78
Sarcoidosis CXR stages 1 to 4
Sarcoidosis CXR
1 = BHL
2 = BHL + infiltrates
3 = infiltrates
4 = fibrosis
79
Sarcoidosis
Other investigations
spirometry:
Other investigations
spirometry: may show a restrictive defect
80
Sarcoidosis
Other investigations
tissue biopsy
tissue biopsy: non-caseating granulomas
81
Contraindications to lung cancer surgery
SFMV
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
Asthmatic features/features suggesting steroid responsiveness in COPD:
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
Bronchiectasis: causes
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
Bronchiectasis: management
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
Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
86
Insertion of a chest drain is relatively contraindicated in patients with any of the following:
INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions
87
Offer LTOT 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
peripheral oedema
pulmonary hypertension
88
kartagener's syndrome (also known as primary ciliary dyskinesia
Features
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
89
Kartagener's syndrome (also known as primary ciliary dyskinesia)
Pathogenesis
Pathogenesis
dynein arm defect results in immotile cilia
90
Psittacosis is infection caused by
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
Psittacosis TX
Treatment:
1st-line: tetracyclines e.g. doxycycline
2nd-line: macrolides e.g. erythromycin
92
Causes of pulmonary eosinophilia
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
Respiratory acidosis
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
Respiratory alkalosis
Respiratory alkalosis
Common causes
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
95
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
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
CXR Sarcoidosis
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
Sarcoidosis
Factors associated with poor prognosis
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
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).
Occupations at risk of silicosis
mining
slate works
foundries
potteries
upper zone fibrosing lung disease
'egg-shell' calcification of the hilar lymph nodes
99
Varenicline
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
Bupropion
a norepinephrine-dopamine reuptake inhibitor and nicotinic antagonis
contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication
101
Transfer factor
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
Causes of a raised TLCO
asthma
pulmonary haemorrhage (e.g. granulomatosis with polyangiitis, Goodpasture's)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
103
Causes of a lower TLCO
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
104
Acronym for causes of upper zone fibrosis:
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
Fibrosis predominately affecting the lower zones
idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
106
What are the most appropriate initial settings for the ventilator?
IPAP 10, EPAP 5 H20
107
Light's criteria: Effusion LDH level greater than 2/3rds the upper limit of serum LDH points to exudate
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.
