Respiratory Flashcards

1
Q

Describe cystic fibrosis in lay terms

A

An inherited condition that causes sticky mucus to build up in the lungs and digestive system. Causes lung infections and problems with digesting food

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

Inheritance of cystic fibrosis

A

autosomal recessive

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

Gene implicated cystic fibrosis

A

CFTR

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

Describe key pathogenesis of cystic fibrosis

A

High sodium sweat: primary secretion of sweat duct is normal but CFTR does not absorb chloride ions, which remain in the lumen and prevent sodium absorption (therefore sweat testing used in diagnosis)

Pancreatic insufficiency: relative dehydration of pancreatic secretions, causing their stagnation in the pancreatic ducts.

Biliary disease: defective ion transfer across the bile duct causes reduced movement of water in the lumen so that bile becomes concentrated, causing plugging and local damage.

Gastrointestinal disease: low-volume secretions of increased viscosity, changes in fluid movement across both the small and large intestine and dehydrated biliary and pancreatic secretions cause intraluminal water deficiency.

Respiratory disease: dehydration of the airway surfaces reduces mucociliary clearance

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

What does CFTR gene do

A

Codes a cAMP-regulated chloride channel

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

Which chromosome most commonly affected in cystic fibrosis

A

Delta F508 on long arm of chromosome 7

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

Carrier rate cystic fibrosis

A

1 in 25

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

Why should those with CF minimise contact with each other (what bug(s))

A

Brukholderia cepacia complex and psudeomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Whats first line in those with pseudomonas aeruginosa who have failed eradication with antibiotics?

A

Nebulised colistimethate sodium

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

Contraindication to lung transplant in cystic fibrosis

A

Chronic infection with brukholderia cepacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Drug used for those homozygous for delta F508 mutation (CF) - explain mechanism

A

Lumacaftor/Ivacaftor (Orkambi)

Lumacaftor increases the number of CFTR proteins that are transported to the cell surface

Ivacaftor is a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management COPD acute exacerbation

A

Pred 30mg
Ipratropium bromide 500mcg 5mg NEB
Salbutamol 5mg NEB

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

Ipratropium MOA

A

Blocks muscarinic acetylcholine receptors - relaxes bronchial smooth muscle. Tiotropium long acting

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

Theophylline MOA

A

Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP

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

Montelukast MOA

A

Block leukotriene receptors
(apparently useful in aspirin induced asthma) –> antiinflammatory and bronchodilatory properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Features of eosinophilic granulomatosis (small - medium vessel vasculitis)

A

Asthma
Blood eosinophilia (e.g. > 10%)
pANCA positive in 60%
Mononeuritis multiplex

Sinusitis
Vasculitis
Dyspnoea

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

Precipitant of eosinophilic granulomatosis

A

LTRA

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

Features of granulomatosis with polyangitis

A

Renal failure
Epistaxis/haemoptysis
cANCA
Saddle shaped nose deformity

Sinusitis (+nasal crusting)
Vasculitis
Dyspnoea

also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions,
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)

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

Is granulomatosis with polyangitis largely cANCA +ve or pANCA +ve?

A

cANCA

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

Renal biopsy granulomatosis with polyangitis

A

Epithelial crescents in bowman’s capsule

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

Management granulomatosis polyangitis

A

Steroids
Cyclophosphamide
Plasma exchange
Median survival 8-9 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is idiopathic pulmonary fibrosis?

A

Lung fibrosis when no underlying cause can be identified

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

Transfer factor IPF

A

Reduced

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

Gold standard investigation IPF

A

CT - honeycombing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Management IPF
Pulmonary rehab, some evidence for pirfenidone (antifibrotic)
26
What is kartageners?
Primary ciliary dyskinesia, autosomal recessive problem with impaired mucocilliary clearance
27
Pathogenesis kartageners
Dynein arm defect results in immotile cilia
28
Features kartageners
Dextrocardia or complete situs inversus (quiet hear sounds, small volume complexes in lateral leads) Bronchiectasis Recurrent sinusitis Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
29
Features of kelbsiella pneumonia
More common in alcoholic and diabetics May occur following aspiration 'Red-currant jelly' sputum Often affects upper lobes (abscesses, empyema)
30
Motelukast is associated with development of what syndrome?
Eosinophilic granulomatosis with polyangiitis
31
What is lofgren's syndrome?
Acute form sarcoidosis
32
Characteristics of logren's syndrome
Bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia
33
RF for lung abscess
Poor dental hygiene, prev stroke, reduced consciousness
34
Rarer causes lung abscess
Haematogenous spread eg 2ndary to IE, direct extension from empyema, bronchial obstruction eg lung tumour
35
Monomicrobial causes of lung abscess
Staphylococcus aureus Klebsiella pneumonia Pseudomonas aeruginosa
36
What is carcinoid lung ca?
NE tumours, arising from the amine precursor uptake and decarboxylation (APUD) system, like small cell tumour. Account for 1% of carcinoid tumours
37
Features lung carcinoid
Slow growing - long history. Often central and not seen on CXR. "Cherry red ball" often seen on bronchoscopy
38
What is carcinoid syndrome
Seen in those who have a carcinoid tumour when it spreads to the liver releasing serotonin - skin flushing, facial lesions, diarrhoea, dyspnoea, tachycardia
39
Contraindications to lung ca surgery
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
40
Small cell lung ca paraneoplastic features
ADH -> hypoN ACTH - (cushings) not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc Lambert-Eaton syndrome (antibodies to voltage gated calcium channels causing myasthenic like syndrome)
41
Squamous cell lung ca paraneoplastic features
Parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia Clubbing Hypertrophic pulmonary osteoarthropathy (HPOA) Hyperthyroidism due to ectopic TSH
42
Adenocarcinoma lung ca paraneoplastic feautres
Gynaecomastia Hypertrophic pulmonary osteoarthropathy (HPOA)
43
Is coal dust a RF for lung ca?
No
44
What cell type does small cell lung ca arrise from?
APUD cells (Amine - high amine content Precursor Uptake - high uptake of amine precursors Decarboxylase - high content of the enzyme decarboxylase)
45
Fibrosis affecting upper zones
C - Coal worker's pneumoconiosis H - Histiocytosis/ hypersensitivity pneumonitis (Extrinsic allergic alveolitis) A - Ankylosing spondylitis R - Radiation T - Tuberculosis S - Silicosis/sarcoidosis
46
Fibrosis affecting lower zones
IPF Most connective tissue disorders (except ankylosing spondylitis) e.g. SLE Drug-induced: amiodarone, bleomycin, methotrexate Asbestosis
47
Microscopic polyangitis features (small vessel ANCA vasculitis)
renal impairment: raised creatinine, haematuria, proteinuria fever other systemic symptoms: lethargy, myalgia, weight loss rash: palpable purpura cough, dyspnoea, haemoptysis mononeuritis multiplex
48
pANCA/cANCA microscopic polyangitis
pANCA (against MPO) - positive in 50-75% cANCA (against PR3) - positive in 40%
49
What causes Middle East respiratory syndrome?
Betacoronavirus MERS-CoV
50
Risk factor for MERS-CoV
Contact with camels (including camel products such as milk)
51
Indications for non-invasive ventilation
COPD with respiratory acidosis pH 7.25-7.35 (pH<7.25 it can be used with increased monitoring, but lower threshold for intubation and ventilation) Type 2 resp failure Sleep apnoea Cardiogenic pulmonary oedema unresponsive to CPAP Weaning from tracheal intubation
52
Recommended initials settings for bi-level pressure support in COPD
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O back up rate: 15 breaths/min back up inspiration:expiration ratio: 1:3
53
Predisposing factors sleep apnoea
Obesity Macroglossia: acromegaly, hypothyroidism, amyloidosis Large tonsils Marfan's syndrome
54
Consequences of sleep apnoea
Daytime somnolence Compensated respiratory acidosis hypertension
55
Management sleep apnoea
Weight loss CPAP Intra oral devices eg mandibular advancement DVLA should be informed if excessive
56
What is olamizumab used for?
Severe persistent confirmed allergic IgE-mediated asthma as an add on to optimised standard therapy in people aged 6 years and older: who need continuous or frequent treatment with oral corticosteroids (defined as 4 or more courses in the previous year)a, given as an injection every 2 to 4 weeks
57
What type of drug is olamizumab?
Monoclonal antibody
58
Adverse effects olamizumab
Abdominal pain Headache Fever Churg-Strauss syndrome: may present with eosinophilia, vasculitic rash, worsening respiratory symptoms and peripheral neuropathy
59
What is the oxygen dissociation curve?
Describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration.
60
If oxygen dissociation curve shifts left what does this mean? What causes this?
For given oxygen tension there is increased saturation of Hb with oxygen i.e. decreased oxygen delivery to tissues. Shifts to L → Lower oxygen delivery, caused by Low [H+] (alkali) Low pCO2 Low 2,3-DPG Low temperature
61
If oxygen dissociation curve shifts right what does this mean? What causes this?
For given oxygen tension there is reduced saturation of Hb with oxygen i.e. enhanced oxygen delivery to tissues 'CADET, face Right!' for CO2, Acid, 2,3-DPG, Exercise and Temperature
62
Oxygen management in COPD patients
Prior to availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis. Adjust target range to 94-98% if the pCO2 is normal
63
Transudate pleural effusion causes
Heart failure (most common transudate cause) Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption) Hypothyroidism Meigs' syndrome Transudate = failures of organs + meigs
64
Exudate pleural effusion
Infection: pneumonia (most common exudate cause), TB, subphrenic abscess Connective tissue disease: RA, SLE Neoplasia: lung cancer, mesothelioma, metastases Pancreatitis Pulmonary embolism Dressler's syndrome Yellow nail syndrome
65
Pleural aspiration from pleural effusion - what is sent for?
pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
66
What criteria differentiates transudate and exudate causes?
Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L If the protein level is between 25-35 g/L, Light's criteria should be applied. An exudate is likely if at least one of the following criteria are met: pleural fluid protein divided by serum protein >0.5 pleural fluid LDH divided by serum LDH >0.6 pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
67
Pleural fluid with low glucose might indicate
rheumatoid arthritis, tuberculosis
68
Pleural fluid with raised amylase might indicate
pancreatitis, oesophageal perforation
69
Pleural fluid with heavy blood staining might indicate
mesothelioma, pulmonary embolism, tuberculosis
70
When should a chest drain be placed pleural effusion?
If the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage If the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed
71
Management options of recent pleural effusion
Recurrent aspiration Pleurodesis Indwelling pleural catheter drug management to alleviate symptoms e.g. opioids to relieve dyspnoea
72
Describe CRB65 (primary care)
C: Confusion (abbreviated mental test score <= 8/10) R: Respiration rate >= 30/min B: Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg 65: Aged >= 65 years
73
What score of CRB 65 merits hospital admission
Considered if >2, Urgent if 3 or above
74
Management of severe CAP
Amox+macrolide dual therapy
75
What findings may block a person's discharge with pneumonia
Temperature higher than 37.5°C Respiratory rate 24 breaths per minute or more Heart rate over 100 beats per minute Systolic blood pressure 90 mmHg or less Oxygen saturation under 90% on room air Abnormal mental status Inability to eat without assistance
76
Over what time periods should patients expect to feel better post pneumonia?
1 week - fever should have resolved 4 weeks - chest pain and sputum production reduced 6 weeks - cough and breathlessness should have reduced 3 months - most symptoms should have resolved, may be fatigued 6 months - most back to normal
77
Following pneumonia when should a repeat CXR be done?
6 weeks after clinical resolution
78
RF for pneumothorax
Pre-existing lung disease (secondary) Connective tissue disease Ventilation including non invasive
79
What is a catamenial pneumothorax?
Cause of 3-6% of spontaneous pneumothorax, occurring in menstruating women
80
Management of primary penumothorax
If rim of air <2cm and patient not short of breath then consider discharge, otherwise aspiratino If fails or >2cm chest drain insertion
81
Management of a secondary pneumothorax
Admit all If >50 years old and rim of air is >2cm or SOB then chest drain If rim of air 1-2cm then aspiration attempted If <1cm O2
82
Management of iatrogenic pneumothorax
Most will resolve with observation, can aspirate if not Ventilated and some with COPD may need chest drains
83
Lifestyle advice following pneumothorax
Avoid smoking to avoid risk of recurrence, Fly 2 weeks after successful drainage/ 1 week post CXR Can't scuba dive
84
Fever with history of bird contact you think of which type of pneumonia
Chlamydia psittaci
85
Presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics - which bug
Chlamydia psittaci
86
Management of chlamydia psittaci pneumonia
1st-line: tetracyclines e.g. doxycycline 2nd-line: macrolides e.g. erythromycin
87
Causes of pulmonary eosinophilia (conditions)
Churg-Strauss syndrome Allergic bronchopulmonary aspergillosis (ABPA) Loffler's syndrome Eosinophilic pneumonia Hypereosinophilic syndrome Tropical pulmonary eosinophilia Less common: Wegener's granulomatosis
88
Causes of pulmonary eosinophilia (drugs)
Nitrofurantoin, sulphonamides 
89
What is Loffler's syndrome
A disease in which eosinophils accumulate in the lung in response to a parasitic infection (Ascaris lumbricoides). Generally self limiting
90
Management eosinophilic pneumonia
Highly responsive to steroids
91
What is tropical pulmonary eosinophilia caused by (typically)
Wuchereria bancrofti infection
92
Obstructive lung disease on PFT
FEV1 - significantly reduced (<70) FVC - reduced or normal  FEV1% (FEV1/FVC) - reduced
93
Examples obstructive lung disease
Asthma COPD Bronchiectasis Bronchiolitis obliterans
94
Restrictive lung disease on PFT
FEV1 - reduced FVC - significantly reduced FEV1% (FEV1/FVC) - normal or increased
95
Examples restrictive lung disease
Pulmonary fibrosis Asbestosis Sarcoidosis Acute respiratory distress syndrome Infant respiratory distress syndrome Kyphoscoliosis e.g. ankylosing spondylitis Neuromuscular disorders Severe obesity
96
What is pulmonary hypertension (PAH)
Sustained elevation in mean pulmonary arterial pressure of greater than 25 mmHg at rest
97
Group 1 pulmonary arterial hypertension (PAH
- idiopathic - familial - associated conditions: collagen vascular disease, congenital heart disease with systemic to pulmonary shunts, HIV, drugs and toxins, sickle cell disease - persistent pulmonary hypertension of the newborn
98
Group 2 pulmonary hypertension
With left heart disease - left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation
99
Group 3 pulmonary hypertension
Secondary to lung disease/hypoxia - COPD - interstitial lung disease - sleep apnoea - high altitude
100
Group 4 pulmonary hypertension
Thromboembolic disease
101
Group 5 pulmonary hypertension
Miscellaneous conditions - lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis
102
Causes of respiratory acidosis
COPD Decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema Neuromuscular disease Obesity hypoventilation syndrome sedative drugs: benzodiazepines, opiate overdose
103
Causes of respiratory alkalosis
Anxiety leading to hyperventilation Pulmonary embolism Salicylate poisoning* CNS disorders: stroke, subarachnoid haemorrhage, Encephalitis Altitude Pregnancy *salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
104
What is tidal volume?
Volume inspired or expired with each breath at rest 500ml in males, 350ml in females
105
What is inspiratory reserve volume?
Maximum volume of air that can be inspired at the end of a normal tidal inspiration inspiratory capacity = TV + IRV
106
What is expiatory reserve volume?
Maximum volume of air that can be expired at the end of a normal tidal expiration
107
What is residual volume?
Volume of air remaining after maximal expiration Increases with age RV = FRC - ERV
108
What is functional residual capacity?
The volume in the lungs at the end-expiratory position FRC = ERV + RV
109
What is vital capacity?
Maximum volume of air that can be expired after a maximal inspiration 4,500ml in males, 3,500 mls in females Decreases with age VC = inspiratory capacity + ERV
110
What is total lung capacity?
The sum of the vital capacity + residual volume
111
What is caplan's syndrome?
Combination of rheumatoid arthritis (RA) and pneumoconiosis - massive fibrotic nodules with occupational coal dust exposure
112
What respiratory conditions are associated with rheumatoid?
Pulmonary fibrosis Pleural effusion Pulmonary nodules Bronchiolitis obliterans Complications of drug therapy e.g. methotrexate pneumonitis Pleurisy Caplan's syndrome Infection (possibly atypical) secondary to immunosuppression
113
Features of sarcoidosis
Acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia Insidious: dyspnoea, non-productive cough, malaise, weight loss Skin: lupus pernio (malar rash) Hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
114
What is Lofgren's syndrome
Acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
115
What is Mikulicz syndrome
Enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma
116
What is Heerfordt's syndrome
(uveoparotid fever) There is parotid enlargement, fever and uveitis secondary to sarcoidosis
117
Diagnostic tests sarcoidosis
ACE levels (monitoring rather than diagnosis) CXR: 1 - BHL 2 - BHL + interstitial infiltrates 3 - Diffuse interstitial infiltrates 4 - Diffuse fibrosis
118
Indication for steroids in sarcoidosis
CXR stage 2 or 3 with symptoms Hypercalcaemia Eye, heart or near involvement PUNCH parenchymal lung involvement Uveitis Neuro involvement Cardio involvement Hypercalcaemia
119
Prognosis of sarcoidosis
Remits in around 2/3 without treamtent
120
Signs of poor prognosis sarcoidosis
Insidious onset, symptoms > 6 months Absence of erythema nodosum Extrapulmonary manifestations: e.g. lupus pernio, splenomegaly CXR: stage III-IV features black people
121
What is silicosis?
Fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica)
122
Features of sarcoidosis on cxr
Egg-shell calcification of the hilarity lymph nodes
123
How long should smoking cessation be prescribed for?
2 weeks after the target stop date. If unsuccessful not to offer a repeat prescription within 6 months unless special circumstances
124
Adverse effects nicotine replacement therapy?
Nausea & vomiting, headaches and flu-like symptoms
125
What is varenicline?
A nicotinic receptor partial agonist, shown to more effective that bupropion
126
How long is a typical course varenicline?
12 weeks
127
SE varenicline?
Nausea, headache, insomnia, abnormal dreams. Use with caution in those with history of depression and self harm. CI in pregnancy and breast feeding
128
What is bupropion?
A norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist
129
SE bupropion
Small risk of seizures
130
Contraindications to bupropion
Contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication
131
Management of smoking cessation pregnant women
Apparently all tested with CO detectors! CBT, motivational interviewing, self help Can use NRT
132
What is transfer factor?
The rate at which a gas will diffuse from alveoli into blood
133
Whats the difference between TLCO and KCO?
Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)
134
Causes of raised TLCO?
Asthma - due to hyperinflation Pulmonary haemorrhage (Wegener's, Goodpasture's) Left-to-right cardiac shunts Polycythaemia Hyperkinetic states male gender, exercise
135
Cause of lower TLCO
Pulmonary fibrosis Pneumonia Pulmonary emboli Pulmonary oedema Emphysema Anaemia Low cardiac output
136
Conditions that may lead to increased KCO with normal/reduced TLCO
Pneumonectomy/lobectomy Scoliosis/kyphosis Neuromuscular weakness ankylosis of costovertebral joints e.g. ankylosing spondylitis
137
What is allergic bronchopulmonary aspergillosis?
Allergic bronchopulmonary aspergillosis results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.
138
Investigations allergic bronchopulmonary aspergillosis?
Flitting CXR changes, positive radioallergosorbent (RAST) test to Aspergillus, positive IgG precipitins (not as positive as in aspergilloma. - aspergilloma being a fungus ball), raised IgE
139
Management bronchopulmonary aspergillosis
Oral glucocorticoids Itraconazole is sometimes introduced as a second-line agent (a triazole)
140
Criteria for life threatening asthma
PEFR < 33% Oxygen sats < 92% Silent chest, cyanosis or feeble respiratory effort Bradycardia, dysrhythmia or hypotension Exhaustion, confusion or coma Normal pCO2 (exhaustion)
141
Indications CXR acute asthma
Life-threatening asthma Suspected pneumothorax failure to respond to treatment
142
Indication ABG acute asthma
Sats <92%
143
Management acute asthama
Oxygen, nebuliser salbutamol, pred 40mg, if no response to this ipratropium bromide
144
Criteria for discharge acute asthma
Been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours Inhaler technique checked and recorded PEF >75% of best or predicted
145
Most common bacterial organisms COPD exacerbation
Haemophilus influenzae (most common cause) Streptococcus pneumoniae Moraxella catarrhalis
146
What's ARDS
Caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema.
147
Causes of ARDS
Infection: sepsis, pneumonia Massive blood transfusion Trauma Smoke inhalation Acute pancreatitis Cardio-pulmonary bypass
148
Criteria for ARDS diagnosis
Acute onset (within 1 week of a known risk factor) Pulmonary oedema: bilateral infiltrates on chest x-ray ('not fully explained by effusions, lobar/lung collapse or nodules) Non-cardiogenic (pulmonary artery wedge pressure needed if doubt) pO2/FiO2 < 40kPa (200 mmHg)
149
What's pulmonary artery wedge pressure?
pulmonary artery wedge pressure gives an indirect estimate of left arterial pressure. Measured by putting a catheter in a peripheral vein and advancing to RA->RV->PA->branch of PA
150
What is alpha 1 antitrypsin deficiency?
Caused by a lack of a protease inhibitor (Pi) normally produced by the liver. The role of A1AT is to protect cells from enzymes such as neutrophil elastase. Classically causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.
151
A1AT what chromosome?
14
152
Inheritance of A1AT
Autosomal recessive / co-dominant fashion*
153
Describe genotypes for A1AT?
Alleles classified by their electrophoretic mobility - M for normal, S for slow, and Z for very slow normal: PiMM heterozygous: PiMZ homozygous PiSS: 50% normal A1AT levels homozygous PiZZ: 10% normal A1AT levels
154
Which genotype of A1AT typically manifests disease?
PiZZ genotype, paracinar emphysema
155
What are the three types of altitude related disorder?
Acute mountain sickness (AMS), which may progress to… High altitude pulmonary oedema (HAPE) or High altitude cerebral oedema (HACE)
156
Features of acute mountain sickness?
Features of AMS start to occur above 2,500 - 3,000m, developing gradually over 6-12 hours and potentially last a number of days: headache nausea fatigue
157
Prevention of acute mountain sickness
Ascend no more than 500m per day, acetazolamide (a carbonic anhydrase inhibitor) (it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation)
158
Presentation and management of High altitude pulmonary oedema (HAPE)
Pulmonary oedema features descent nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors oxygen if available
159
Presentation and management of high altitude cerebral oedema (HACE)
headache, ataxia, papilloedema descent and dexamethasone
160
Most dangerous form asbestos
Crocidolite (blue)
161
Types of asbestos disease
Pleural plaques (benign), pleural thickening, asbestosis (lower lobe fibrosis), mesothelioma
162
New asthma diagnosis test
Emphasis on fractional exhaled nitric oxide (FeNO). Nitric oxide is produced by 3 types of nitric oxide synthases (NOS). One of the types is inducible (iNOS) and levels tend to rise in inflammatory cells, particularly eosinophils. Levels of NO therefore typically correlate with levels of inflammation.
163
What is considered a positive FeNO test?
In adults level of >= 40 parts per billion (ppb) is considered positive In children a level of >= 35 parts per billion (ppb) is considered positive
164
Considered positive for asthma in reversibility testing
In adults, a positive test is indicated by an improvement In FEV1 of 12% or more and increase in volume of 200 ml or more
165
Management asthma - steps
1. SABA 2. SABA + ICS 3. SABA + ICS + LTRA 4. SABA + low-dose ICS + long-acting beta agonist (LABA), Continue LTRA depending on patient's response to LTRA 5. SABA +/- LTRA, Switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose ICS 6. SABA +/- LTRA + medium-dose ICS MART, OR consider changing back to a fixed-dose of a moderate-dose ICS and a separate LABA 7. SABA +/- LTRA + one of the following options: Increase ICS to high-dose (only as part of a fixed-dose regime, not as a MART) A trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline) seeking advice from a healthcare professional with expertise in asthma
166
What is MART
A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)
167
What are the doses of low, medium and high corticosteroid doses asthma
<= 400 micrograms budesonide or equivalent = low dose 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose > 800 micrograms budesonide or equivalent= high dose.
168
Most common cause occupational asthma
Isocyanates eg spray painting and foam moulding using adhesives GF at PEPSI factory Platinum salt Epoxy resins Proteiolytic enzymes Solodering flux resins Isocynayes
169
Whats atelectasis?
Common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions. Within 72hrs
170
Causes of bilateral hilarity lymphadenopathy
The most common causes are sarcoidosis and tuberculosis. Other causes include: * lymphoma/other malignancy * pneumoconiosis e.g. berylliosis (a form of metal posioning - berillyium) fungi e.g. histoplasmosis (bad/bird droppings), coccidioidomycosis ("valley fever" - southwest america and mexico)
171
What is bronchiectasis?
Permanent dilatation of the airways secondary to chronic infection or inflammation.
172
Triad of Youngs syndrome
Male infertility, sinusitis, bronchiectasis
173
Triad of yellow nail syndrome
Yellow nail discolouration, lymphoedema, bronchiectasis
174
What's bronchiolitis
Acute bronchiolar inflammation, most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against RSV.
175
Contraindications chest drain insertion
INR > 1.3 Platelet count < 75 Pulmonary bullae - focal regions of emphysema Pleural adhesions
176
What intercostal space is a chest drain inserted
5th
177
Complication chest drain insertion
Failure of insertion - the drain may be leaning on the apical pleura Bleeding Infection Penetration of the lung Re-expansion pulmonary oedema
178
Whats re-expansion pulmonary oedema?
When a lung re-expands quickly. May be preceded by the onset of a cough and/or shortness of breath. Chest drain should be clamped and an urgent chest x-ray should be obtained. To avoid re-expansion pulmonary oedema, it is recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours)
179
When should chest drain be removed?
Fluid drainage - no output for > 24 hours and imaging shows resolution of the fluid collection. Pneumothorax - when drain no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax. Drains inserted in cases of penetrating chest injury should be reviewed by the specialist to confirm an appropriate time for removal.
180
CXR signs COPD
hyperinflation, bullae, flat hemidiaphragm (lungs push against the diaphragm puhsing it downwards)
181
Severity of COPD stages
Stage 1 - FEV1 >80% Stage 2 - FEV1 50-79% Stage 3 - 30-49% Stage - <30%
182
Criteria for LTOT?
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 Assess if stage 3
183
How frequent are gases for LTOT assessment?
Measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management
184
Management COPD if no asthmatic features or features suggesting steroid responsiveness
SABA or SAMA No asthmatic features/features suggesting steroid responsiveness: -add a LABA + LAMA -if already taking a SAMA, discontinue and switch to a SABA
185
What drugs should not be given alongside theophylline
Macrolide or fluroquinones
186
Who qualifies for prophylactic antibiotic therapy in COPD
Azithromycin for those who don't smoke, optimised treatment, exacerbations (need CT and sputum culture). Not can prolong QT
187
Features fo cor pulmonale
Peripheral oedema, raised JVP, systolic parasternal heave, loud P2
188
Management cor pulmonale
Use a loop diuretic for oedema, consider long-term oxygen therapy
189
Whats cryptogenic organising pneumonia?
Diffuse interstitial lung disease that affects the distal bronchioles, respiratory bronchioles, alveolar ducts and alveolar walls. Aetiology unknown
190
Presentation of cryptogenic organising pneumonia
Cough, shortness of breath, fever and malaise. With no response to abx Bloods show a leukocytosis and an elevated ESR and CRP. Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities. Transfer factor reduced
191
Which lung ca most likely in a smoker
Squamous - caviating and associated with hypercalcaemia
192
Which lung ca most likely in a non smoker
Adeonocarcioma
193
Typical presentation alveolar cell lung ca
Productive cough with copious sputum and fluffy infiltrates on chest x-ray
194
Presentation small cell carcinomas
Fast growing, may well be mets
195
Presentation small cell carcinomas
Fast growing, may well be mets
196
Most common organisms bronchiectasis
Haemophilus influenzae (most common) Pseudomonas aeruginosa Klebsiella spp. Streptococcus pneumoniae
197
Most suitable way of assessing compression of upper airway
Flow volume loop
198
How much does smoking increase risk of lung ca by
Factor of 10
199
How much does asbestos increase risk of lung ca by
Factor of 5
200
COPD management when asthmatic features/steroid responsiveness
Asthmatic features/features suggesting steroid responsiveness: LABA + ICS - if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS (if already taking a SAMA, discontinue and switch to a SABA)
201
How is asthma/steroid responsiveness features assessed in COPD?
Prev diagnosis of asthma or atopy Higher blood eosinophil count Substantial variation in FEV1 over time (at least 400ml) Substantial diurnal variation in peak exploratory flow
202
Gene association bronchiectasis
HLA-DR1
203
Gene association SLE
HLA DR2
204
Gene association autoimmune hepatitis, sjogre, T1DM, SLE
HLA DR3
205
Gene association rheumatoid arthritis, T1DM
HLA DR4
206
Gene association ankylosing spondylitis, post gonococcal arthritis, acute anterior uveitis
HLA B27
207
A good prognostic factor in sarcoidosis
Erythema nodosum