Respiratory Flashcards
Causes of ARDS?
(SHAFT)
Sepsis
Head injury (sympathetic nervous stimulation which then leads to pulmonary HTN)
Acute pancreatitis
Fractures of long bone or multiple fractures (through fat embolism)
Trauma/ direct lung injury
How do you exclude Pulmonary Oedema?
normal pulmonary capillary wedge pressure
How would you describe ARDS
acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary oedema
causes of upper lobe fibrosis?
CHARTS
Coal workers’ pneumoconiosis
Histiocytosis
Ankylosing spondylitis/Allergic bronchopulmonary aspergillosis
Radiation
Tuberculosis
Silicosis (progressive massive fibrosis), sarcoidosis
Describe Chronic Bronchitis
productive cough for more than 3 months in two consecutive years
Describe Emphysema
Destruction of lung parenchyma - abnormal airspace enlargement from distal to terminal bronchioles + alveoli destruction
What does chronic bronchitis lead to?
1) chronic inflammation / fibrosis
2) goblet cell hyperplasia
3) mucuous hypersecretion
4) narrowing of small airways
Causes of Emphysema?
Smoking A1AT deficiency (uninhibited neutrophil elastase breaks down alveoli)
What is Cor Pulmonale and what are the signs?
RV impairment due to pulmonary disease
1) peripheral oedema
2) left heave (RVH)
3) Raised JVP
4) Hepatomegaly
Difference in inflammation between COPD and Asthma?
COPD - inflammayion with neutrophils, CD8 T lymphocytes and macrophages
Asthma - Mainly eosinophilic infiltration with CD4+ T lymphocytes
CO2 retention signs?
Asterixis
Drowsy
Confusion
Symptoms of COPD
Wheeze Sputum Cough breathless Bronchitis
Signs of COPD?
Dyspnoea
Pursed lips
Coarse crackles
bronchial sounds
Diagnosis on Spirometry?
FVC decreased
FEV1 decreased
FEV1 / FVC <70%
How is COPD staged?
FEV1% of prediced
1 >80%
2 50-79%
3 30-49%
4 <30%
Medical management of COPD?
1st - SABA/SAMA
2nd - Asthmatic features = LABA + ICS
No asthmatic features = LABA + LAMA
3rd - Triple Therapy = LABA, LAMA , ICS
give examples of SAMA and LAMA
SAMA - Ipratropium
LAMA - Tiotropium / Glycopyrronium
Give examples of a Mucolytic
Mucinex (guaifenesin)
Carbocisteine.
What is Seretide made up of
LABA + ICS (Salmeterol + Fluticasone)
What is Trimbow made up of
LABA + LAMA + ICS (formoterol, glycopyrronium, beclometasone)
What is Ultibro made up of
LABA + LAMA (indacaterol + glycopyrronium)
Appropriate bedside tests for COPD
O2 sats sputum pot ECG ABG BMI
When should someone be admitted to hospital if they have a COPD exacerbation
- cant cope at home
- severe co-morbidities
- severe symptoms (low sats <90%)
- confined to bed
- already on LTOT
- CXR changes
what are the PaCO2 and PaO2 figures in T2RF?
PaO2 <8kPa
PaCO2 >6.7kPa
further complications of COPD?
Pneumona Pneumothorax Polycythaemia / anaemia Depression respiratory failure
Describe the 5 stages of the MRC Dyspnoea Scale
1 - breathless on strenuous exercise 2 - " a hill / hurrying 3 - " normal walk 4 - " after 100m / few minutes of walk 5 - " minimal activity (dressing etc - cant leave house)
Treatment of COPD Exacerbation?
Oxygen (aim for 88-92% sats) Salbutamol (2.5mg neb) Ipratropium bromide (500mcg neb) Prednisolone (30mg for 5 daysa) Doxycycline (200g stat then 100mg for 7 days)
What is Obstructive Sleep Apnoea
collapse of the pharyngeal airway during sleep. It is characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes.
Obstructive Sleep Apnoea
Risk Factors?
Middle age Male Obesity Alcohol Smoking
macroglossia: acromegaly, hypothyroidism, amyloidosis
Obstructive Sleep Apnoea
Features?
Partner complains of excessive snoring and apnoea episodes
- morning headache
- daytime sleepiness
Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.
Obstructive Sleep Apnoea
Assessment of sleepiness?
Diagnosis?
Epworth Sleepiness Scale
sleep studies (polysomnography)
Obstructive Sleep Apnoea
Treatment?
indication of urgent referral?
weight loss
continuous positive airway pressure (CPAP) is first line
Patients that need to be fully alert for work, for example heavy goods vehicle operators, require urgent referral
ASTHMA
How does inhalation of allergens lead to histamine release?
Inhalation of allergens results in type 1 hypersensitivity which causes IgE antibody release
IgE bind to mast cells which degranulate to cause histamine release
ASTHMA
How does histamine release cause airway obstruction
1) Smooth muscle contraction
2) Bronchoconstriction
3) Mucous production
all cause obstruction
ASTHMA
How is it diagnosed
Spirometry and peak flow
Fractional Exhaled Nitric Oxide (FeNO)
ASTHMA
How are FeNO results interpreted?
> 40ppb = dx of asthma
25-39ppb = suggestive of dx
ASTHMA
Management (7 steps)
1) SABA
2) SABA + ICS
3) SABA + ICS + LTRA
4) SABA + ICS + LABA (+/- LTRA)
5) SABA + MART
6) SABA + Moderate dose MART (increase ICS dose)
7) additional theophylline or MRA
ASTHMA
Management of under 5 years?
1) SABA
2) 8 week trial of ICS
3) Add LTRA
ASTHMA
Acute management?
- Oxygen
- Salbutamol nebulisers
- Ipratropium bromide nebulisers
- Hydrocortisone IV OR Oral Prednisolone
- Magnesium Sulfate IV
- Aminophylline/ IV salbutamol
When can a patient after an acute asthma attack be discharged?
If peak flow is >75% of best with <25% diurnal variation
If peak flow <50% then 5 days minimum prednisolone required
BRONCHIECTASIS
What is it?
Irreversible and abnormal dilation of the airways
Commonly secondary to cystic fibrosis
BRONCHIECTASIS
how does infection lead to further predisposition to infection?
infection - inflammation - destruction - dilation - further predisposition
BRONCHIECTASIS
Causes?
immunodeficiency
primary ciliary dyskinesia / kartagener syndrome
airway obstruction
young syndrome
Allergic bronchopulmonary aspergillosis (sensitive to fungus Aspergillus)
What is Young Syndrome?
condition characterized by
- male infertility
- bronchiectasis
- sinusitis
What is Kartagener’s syndrome?
autosomal recessive genetic ciliary disorder comprising the triad of:
- situs inversus
- chronic sinusitis
- bronchiectasis
BRONCHIECTASIS
clinical features?
Persistent sputum production + cough
+ dyspnoea
+ haemoptysis
+ weight loss
BRONCHIECTASIS
Signs on examination?
Wheeze
high pitch inspiratory crackles
BRONCHIECTASIS
Gold standard dx?
CT of chest (Signet Ring Sign = dilated bronchus)
CXR (tramtrack airways + ring shadows)
BRONCHIECTASIS
Basic necessary investigations?
sputum / blood cultures
kidney function
serum immunoglobulins
BRONCHIECTASIS
Management?
1) Airway clearance techniques
2) Mucolytic agents
3) Antibiotic prophylaxis
What mucoactive should NOT be used in Bronchiectasis
Recombinant human DNase
BRONCHIECTASIS
Long terrm antibiotics are given if a patient has over 3 exacerbations a month. Which should be given?
Pseudomonas aeruginosa colonised :
1st - Inhaled Colistin / gentamicin
2nd - Oral Macrolides
Non P. aeruginosa:
1) Macrolides
2) Inhaled Gent
+ bronchodilators
BRONCHIECTASIS
Complications?
haemoptysis
Respiratory failure
Cor Pulmonale
Pneumothorax
LUNG CANCER
Types?
Non small cell (NSCLC)
- Adenocarcinoma
- Squamous cell carcinoma
- large cell
Small Cell (SCLC)
LUNG CANCER
Describe Adenocarcinoma
e. g
- % of incidence
- where cancer tends to be
Most common type (38%) - cancer of mucous secreting cells
tends to be lung peripheries
LUNG CANCER
Describe squamous cell carcinoma
e. g
- % of incidence
- where cancer tends to be
- how it presents
- mets?
(20% incidence)
SMOKING - most common cause
Tends to be central - often presents with pneumonia secondary to obstructed bronchus
mets tend to be LATE and histology shows keratin
LUNG CANCER
What is large cell and does it metastasise early or late
Metastises early and large cell LC is undifferentiated neoplasms with poor prognosis
LUNG CANCER
Describe small cell LC
cancer of ..
% of incidence
mets early or late
15%
Cancer if APUD cells (neuroendocrine cells in lung so causes paraneoplastic syndromes)
early mets with POOR prognosis
LUNG CANCER
Possible symptoms
SVCO cough malaise haemoptysis weight loss
How is SVCO clincially diagnosed and what is it?
Superior vena cava obstruction due to compression by tumour or mediastinal lymphadenopathy
diagnosed by presence of neck and facial swelling and distended veins over the anterior chest wall.
LUNG CANCER
Signs on examination?
Lymphadenopathy Stridor Clubbing HPOA Signs of effusion
What is HPOA
Hypertrophic pulmonary osteoarthropathy (HPOA) syndrome characterized by the triad
- periostitis
- digital clubbing
- painful arthropathy of the large joints (especially lower limbs)
LUNG CANCER
Likely mets?
Bone (bone pain + raised ALP)
Brain
Liver (abnormal mets)
Adrenal glands
LUNG CANCER
Signs of Pancoast tumour?
Tumour of the apex
horners syndrome
hoarseness due to pressure on recurrent laryngeal nerve
pain/ atrophy of upper limb + oedema
What cancer does Asbestos cause
Mesothelioma classically and adenocarcinoma
Name some Paraneoplastic Syndromes
Hypercalcaemia
SiADH Hyponatraemia Cushings Lambert Eaton HPOA
What is the incidence of Hypercalcaemia in various lung cancers?
50% in SCC
20% in adenocarcinoma
15% in small cell
how can Lung Cancer cause Cushings?
Lung cancer producing ectopic ACTH (SCLC)
What is Lambert Eaton Syndrome?
Antibodies form to Calcium gated channels in the nerves to muscles resulting in PROXIMAL and OCULAR WEAKNESS
LUNG CANCER
Investigations?
CXR - CT - PET
Tissue biopsy via Bronchoscopy
Cytology from aspiration / washings / secretions
LUNG CANCER
How are NSCLC and SCLC staged?
NSCLC - TMN
SCLC - VALSG
LUNG CANCER
Management of NSCLC and SCLC?
NSCLC - Surgical for stage 1/2
chemo
palliative radio to improve symptoms
SCLC - surgical only if early enough (<5% cases even in T1/2)
LUNG CANCER
5 year survival?
16% - poor prognosis
highest cancer related death
LUNG CANCER
5 year survival?
16% - poor prognosis
highest cancer related death
Murmur heard in Patent ductus Arteriosus?
continuous machinery murmur
What is Barlow syndrome?
click murmur heard in mitral valve prolapse found in 5-10% of world population
What is Austin Flint murmur
Rumbling diastolic murmur heard in AR
What is Graham Steell Murmur
early diastolic murmur due to pulmonary incompetence caused by pulmonary hypertension
What is Carey Coombs murmur
Mid diastolic (mitral stenosis from rheumatic fever)
What is the mutation in Cystic Fibrosis
Mutation to CFTR gene on chromosome 7
Cystic Fibrosis
Why is there mucociliary dysfunction
Dehydration of airway surface fluid causes this as well as impaired biliary and pancreatic drainage
What does impaired biliary and pancreatic drainage in CF lead to?
Impaired digestion and malabsorption
What does mucociliary dysfunction lead to?
1) Reduced mucous clearance
2) Airway obstruction
3) predisposition to infection - leads to Bronchiectasis
Associated problems as well as respiratory CF?
Pancreatic insufficiency - (Steatorrhoea due to pancreatic blocking of exocrine digestive enzymes)
CF related diabetes
Infertility
CF
How is it diagnosed early on?
Skin heel prick on day 5 OR
Meconium Ileus / constipation in first few days of life
How is CF confirmed?
Sweat test (chloride over 60mmol/L)
immunoreactive trypsin test
How is CF pulmonary disease managed?
1) Airway clearance techniques
2) Mucolytic agents
3) Antibiotic prophylaxis
4) Bilateral sequential lung transplant
Name some mucolytic agents
rhDNase (not used in bronchiectasis)
hypertonic saline
mannitol dry powder
Management of CF extra pulmonary disease?
1) Pancreatic enzyme replacement
2) Liver screening annually + ursodeoxycholic acid
3) Diabetes screening (OGTT / CGM)
What is the name of new CF drugs?
what is the median age of life?
CFTR modulator drugs
49 years
Idiopathic Pulmonary Fibrosis
Name some symptoms
Chronic exertional dyspnoea
Dry cough
fatigue
Idiopathic Pulmonary Fibrosis
Name some signs
Bilateral inspiratory crackles
Clubbing
Acrocyanosis (peripheral discolouration)
Idiopathic Pulmonary Fibrosis
What pattern is shown on lung function testing
Restrictive
Reduced lung volume
reduced DLCO
Idiopathic Pulmonary Fibrosis
What does CT show?
honeycombing
reduced lung volume
reticular opacities
(seen in bases and peripheries)
Idiopathic Pulmonary Fibrosis
Methods of gathering pathological specimens?
bronchoalveolar lavage
Transbronchial biopsy
Surgical lung biopsy
Idiopathic Pulmonary Fibrosis
Management of breathlessness?
Oxygen
Physio
Idiopathic Pulmonary Fibrosis
Name some IPF modifying drugs and when they can be given
Pirfenidone
Nintedanib
If FVC is 50-80% of predicted
Idiopathic Pulmonary Fibrosis
Name some medication that can be given for symptomatic relief
Benzos and Opioids
PLEURAL EFFUSION
Sign on X-ray?
Blunting of costophrenic angles
PLEURAL EFFUSION
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
PLEURAL EFFUSION
Why may fluid enter the pleural space?
1) Microvascular pressure (increased hydrostatic pressure in venous system - HF)
2) Vasculature permeability (leaky vessels - infection/malignancy)
3) Decreased plasma oncotic pressure (hypoproteinaemia)
PLEURAL EFFUSION
Transudate and Exudates
Whats the difference and are they bilateral or unilateral
Transudates tend to be bilateral and minimal protein
Exudates tend to be unilateral and protein count of >30g/L
PLEURAL EFFUSION
Transudate causes?
- Heart failure
- Hypoalbuminaemia
- Constrictive pericarditis
- Peritoneal dialysis
- Meig’s syndrome (benign ovarian tumour)
PLEURAL EFFUSION
why might someone have hypoalbuminaemia and what type of effusion does it cause
Nephrotic syndrome
liver disease / cirrhosis
malabsorption
Transudate
PLEURAL EFFUSION
Exudate causes
- Connective tissue disease (RA, SLE)
- Cancer/ Malignancy (lung / breast)
- TB
- Pneumonia (secondary to MOST COMMON)
- PE
- Pancreatitis
CC T TRIPLE P
PLEURAL EFFUSION
Signs on examination?
REDUCED:
breath sounds
vocal resonance
chest expansion
DULL percussion
Tracheal deviation AWAY from effusion
PLEURAL EFFUSION
Imaging?
Initially X-ray
Contrast CT for investigating cause
PLEURAL PARACENTESIS
US with aspiration to reduce complication rate
PLEURAL EFFUSION
Management?
What should the fluid be sent for:
ASPIRATION
- 21G needle and 50ml syringe should be used
fluid should be sent for ; pH protein lactate dehydrogenase (LDH) cytology and microbiology
PLEURAL EFFUSION
Management if infected?
pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling
If the fluid is purulent or turbid/cloudy = CHEST TUBE
if the fluid is clear but the pH is less than 7.2 in suspected infection = CHEST TUBE
PLEURAL EFFUSION
Transudate management?
Treat with diuretics - aspiration should be avoided
PNEUMONIA
Common organism in CAP?
Strep pneumoniae
H. influenza
What type of bacteria is Strep Pneumoniae
Gram POSITIVE alpha haemolytic strep
PNEUMONIA
Common organism in HAP?
What patients is this organism common in CAP?
Pseudomonas Aureginosa
IN CF and Bronchiectasis - common in CAP
PNEUMONIA
Types of Atypical Pneumonia?
Mycoplasma
Legionella
Chlamydophila
Psittacosis (BIRDS e.g parrots)
Q fever
Tularemia
What is Q fever?
a disease caused by the bacteria Coxiella burnetii
infected farm animals
Extrapulmonary symptoms of Mycoplasma?
HAEM
Haemolytic Anaemia
Arthralgia
Erythema Multiforme
Myocarditis / Pericarditis
Extrapulmonary symptoms of Legionella?
How is it diagnosed?
Hyponatraemia secondary to SiADH
Hypophosphataemia and Raised serum ferritin
Diagnosed with urinary antigen testing
How can Klebsiella causing Pneumonia be recognised?
‘red currant jelly’ sputum
What is PCP and its antibiotic treatment?
Pneumocystis jirovecii - fungi causing pneumonia - aids defining illness
Treated with Co - trimoxazole
What is Co- trimoxazole made up of
Trimethoprim and Sulfamethoxazole
PNEUMONIA
Which patients is aspiration pneumonia more common in
Those with reduced conscious level / neuro disorders
PNEUMONIA
Signs on examination?
Dull percussion
Bronchial breathing
Coarse crepitations
PNEUMONIA
Investigations?
CXR
blood and sputum Cultures
FBC, U+Es, CRP
PNEUMONIA
What is CURB-65
Method of determining severity of pneumonia
0: low risk (less than 1% mortality risk)
1 or 2: intermediate risk (1-10% mortality risk)
3 or 4: high risk (more than 10% mortality risk- urgent admission)
Confusion Urea >7mmol Respiratory rate >30 BP <90 systolic or <60 diastolic >65 years old
PNEUMONIA
Management?
Fluids, Analgesics, Antibiotics:
Low risk : amoxicillin / doxycycline / clarithromycin
Intermediate: Amoxicillin + Macrolide (clarithromycin)
High : an IV beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam + Macrolide (clarithromycin)
Link between Pneumonia and Lung cancer?
11% of patients who smoke over the age of 50 with pneumonia have lung cancer
Major risk factors of PE?
- DVT
- Previous VTE
- Active Cancer
- Recent surgery / immobilisation / flight
- Pregnancy
- COCP
- Thrombophilia
- Obesity
What is Virchows Triad
3 factors that are critically important in the development of venous thrombosis:
(1) venous stasis,
(2) activation of blood coagulation (hypercoaguable state) (3) vein damage (endothelial injury)
Symptoms of PE?
Dyspnoea Pleuritic chest pain (worse on inspiration) Cough Haemoptysis Syncope leg swelling
Frequency of clinical signs in PE?
Tachypnea (respiratory rate >16/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%
Signs of Right heart failure?
Increased JVP
Hypotension
Pansystolic tricuspid regurgitation murmur
Split S2
Describe the 2- level PE Wells Score
/12.5
if >4 points do immediate CTPA
if <4 points do d-dimer, if positive do CTPA
Score itself: \+3 signs of DVT \+3 PE most likely dx \+1.5 Immobilised for >3 days / recent surgery/ flight \+1.5 Previous DVT/ PE \+1 Haemoptysis \+1 Malignancy <6 months
What should be done if Wells under 4 points and the d-dimer is negative?
Stop anticoagulation and consider alternative diagnosis
What should be given if PE suspected
immediate anticoagulation
LMWH is empirical but DOAC recommended
What anticoagulation should be given if PE diagnosed and:
Stable?
Unstable?
Active cancer?
Renal impairment?
Stable - Apixiban / Rivaroxaban
Unstable - Thrombolysis / UFH
Active cancer- Edoxaban, 2nd line - LMWH
Renal impairment - CrCl <15ml/min offer LMWH/ UFH followed by VKA
What should be given if Apixiban / Rivaroxaban not suitable in PE?
LMWH followed by dabigatran or edoxaban
OR
LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
How long should anticoagulation in PE last?
At least 3 months
If unprovoked at least 6 months and test for thrombophilia / cancer
Indications for thrombolysis in PE?
Cardiac arrest with confirmed PE
No improvement after anticoagulation
haemodynamically unstable (e.g. BP under 90 for over 15 mins)
PULMONARY HYPERTENSION
How does it occur?
Increased resistance / pressure in pulmonary arteries leads to right heart strain and back pressure into venous system
PULMONARY HYPERTENSION
Causes?
GROUP 1: Primary pulmonary HTN (connective tissue disorders e.g. SLE)
2: Left heart failure due to MI / systemic hypertension
3: chronic lung disease (COPD)
4: Vascular (PE)
5: Miscellaneous (sarcoidosis)
PULMONARY HYPERTENSION
Signs?
SHORTS SOB Hepatomegaly Oedema Raised JVP Tachycardia Syncope
PULMONARY HYPERTENSION
Signs on ECG?
Signs of RVH on ECG?
Right heart strain - RVH, RAD, RBBB
RVH :
V1-3 larger R waves
V4-6 deeper S waves
PULMONARY HYPERTENSION
Signs on X-ray?
which blood marker is classically raised?
Dilated pulmonary arteries
RVH
RAISED BNP (NT proBNP)
PULMONARY HYPERTENSION
Give examples of?
Prostanoids
Epoprestenol
PULMONARY HYPERTENSION
Primary treatment?
1) IV Prostanoids
2) Endothelin Receptor Antagonists
3) Phosphodiesterase - 5 - inhibitors
PULMONARY HYPERTENSION
Give examples of?
Phosphodiesterase - 5 - inhibitors
Sildenafil
PULMONARY HYPERTENSION
Give examples of?
Endothelin receptor Antagonists
Macitentan
Signs of Acute Bronchitis?
normal CXR with clear sputum and low grade fever
When should antibiotic therapy be given in acute bronchitis?
Which Abx is first line
1) Systemically unwell
2) Pre existing co morbidities
3) CRP >100
if CRP 20-100 give delayed prescription
DOXYCYCLINE
What is Heerfordt’s Syndrome?
Uveoparotid fever
Parotid enlargement and uveitis secondary to Sarcoidosis
+ facial nerve palsy
Stages of Pulmonary Sarcoidosis?
1- Biliteral hilar lymphaedenopathy (BHL)
2- BHL + interstitial infiltrates
3 - diffuse interstitial infiltrates
4 - diffuse fibrosis
Signs of Diffuse fibrosis?
what may it lead to?
Fine inspiratory crackles, clubbing and exertional desaturation
may lead to pulmonary hypetension and cor pulmonale
Sarcoidosis spirometry findings?
RESTRICTIVE (reduced FVC)
Treatment and causes of secondary Pneumothorax?
<1cm - observe
1-2cm - treat with needle aspiration
>2cm - small bore chest drain
causes - pre-existing lung disease e.g. COPD fibrosis asthma bronchiectasis TB Sarcoidosis
What is goodpastures syndrome now known as?
What is it?
Anti Glomerular basement membrane disease (GBM)
type 2 hypersensitivity small vessel vasculitis more common in men (20-30s, 60-70s)
ANTI-GBM DISEASE
Classical disease?
Pulmonary haemorrhage (haemoptysis)
Rapid progressive glomerulonephritis / rapid onset AKI
systemically unwell: fever, nausea
ANTI-GBM DISEASE
Cause?
Associated HLA?
Anti GBM antibodies against type 4 collagen - small vessel vasculitis
HLA-DR2
Signs of Eosinophilic granulomatosis with polyangiitis?
asthma blood eosinophilia (e.g. > 10%) paranasal sinusitis mononeuritis multiplex pANCA positive in 60%
What is Churg Strauss Syndrome?
Eosinophilic granulomatosis with polyangiitis
ANCA associated small-medium vessel vasculitis
Eosinophilic granulomatosis with polyangiitis
What may precipitate disease?
Leukotriene receptor antagonists
ANTI-GBM DISEASE
Investigations?
Renal biopsy - linear IgG deposits on basement membrane
Increased transfer factor secondary to pulmonary haemorrhage
ANTI-GBM DISEASE
Management?
plasma exchange (plasmapheresis)
steroids
cyclophosphamide
What is Wegener’s Granulomatosis known as now?
Granulomatosis with Polyangiitis
Management of Granulomatosis with Polyangiitis ?
Same as Anti GBM:
plasma exchange (plasmapheresis)
steroids
cyclophosphamide
ANTI-GBM DISEASE
Factors which increase the likelihood of Pulmonary Haemorrhage?
smoking lower respiratory tract infection pulmonary oedema inhalation of hydrocarbons young males
Features of Granulomatosis with Polyangiitis ??
upper respiratory tract: epistaxis, sinusitis, nasal crusting
lower respiratory tract: dyspnoea, haemoptysis
kidneys: rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
saddle-shape nose deformity
also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
Investigations of Granulomatosis with Polyangiitis ?
cANCA positive in 90%
renal biopsy shows epithelial crescents in Bowman’s capsule
What is Granulomatosis with Polyangiitis ?
autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting:
1) upper and lower respiratory tract
2) kidneys.
Prophylactic Abx of choice in a patient with COPD who has frequent exacerbations?
Azithromycin
KEY SYMPTOMS of:
Mitral stenosis?
Dyspnoea
Atrial Fibrillation
Malar flush on cheeks
Mid-diastolic murmur
KEY SYMPTOMS of:
Aspergilloma?
Often past history of TB
Haemoptysis may be severe
CXR shows rounded opacity
KEY SYMPTOMS of:
Pulmonary Oedema?
Dyspnoea
Bibasal crackles
S3
What may be seen on X-ray in idiopathic pulmonary fibrosis?
bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’
Causes of lower lobe fibrosis?
- idiopathic pulmonary fibrosis
- most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
- drug-induced: amiodarone, bleomycin, methotrexate
- asbestosis
