Respiratory Flashcards
Zero to finals resp
1
Q
What is the most common type of lung cancer?
A
Non-small cell lung cancer = 80% of lung cancers. of these, 40% are adenocarcinomas, 20% are SCC and 10% are LCC.
2
Q
What is small cell lung cancer?
A
20% of lung cancers. Secrete neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.
3
Q
How does lung cancer present?
A
Shortness of breath Cough Haemoptysis (coughing up blood) Finger clubbing Recurrent pneumonia Weight loss Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
4
Q
What investigations would you do for lung cancer and what would they show?
A
- CXR -
Hilar enlargement
“Peripheral opacity” – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse - Contrast CT chest abdo pelvis - staging, LN involvement, mets.
- PET-CT - radioactive tracer attached to glucose molecules, pictures taken using CT scanner + gamma ray detector. Shows how metabolically active tissues are –> identify mets.
- Bronchoscopy with endobronchial ultrasound (EBUS) - assessment of tumour and uss guided biopsy
- Biopsy for histology - bronchoscopy or percutaneously
5
Q
How is non small cell lung cancer managed?
A
MDT
- Surgery - lobectomy, segmentectomy, wedge resection
- radiotherapy can be curative if early enough
- adjuvant chemotherapy - palliative or improve outcomes.
6
Q
How is small cell lung cancer managed?
A
MDT
- Chemo
- Radiotherapy
- Endobronchial treatment - stents/debulking palliative treatment to relieve obstruction.
7
Q
Which type of lung cancer has the worst prognosis?
A
Small cell.
8
Q
Give 5 extrapulmonary manifestations of lung cancer.
A
Recurrent laryngeal nerve palsy- hoarse voice caused by the cancer pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.
Phrenic nerve palsy - due to nerve compression causes diaphragm weakness, SOB
Superior vena cava obstruction (SVCO)
Horner’s syndrome
SIADH (ectopic ADH - SCLC)
Cushing’s syndrome (ectopic ACTH - SCLC)
Hypercalcaemia (ectopic PTH - squamous cell carcinoma)
Limbic encephalitis.
Lambert-Eaton myasthenic syndrome.
9
Q
What is Pemberton’s sign?
A
Raising the hands over the head causes facial congestion and cyanosis. –> SVCO - medical emergency.
10
Q
What is Horner’s syndrome?
A
Partial ptosis, anhidrosis and miosis. It is caused by a Pancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.
11
Q
Why does lung cancer lead to hyponatraemia and what type does this?
A
Syndrome of inappropriate ADH (SIADH) caused by ectopic ADH secretion by a small cell lung cancer –> hyponatraemia.
12
Q
What type of lung cancer leads to hypercalcaemia?
A
Squamous cell carcinoma –> ectopic PTH
13
Q
What would anti-Hu antibodies in someone with lung cancer mean?
A
Limbic encephalitis: Paraneoplastic syndrome where the small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.
14
Q
What is Lambert-Eaton Myaesthenic syndrome?
A
=LEMS: antibodies produced by the immune system against SCLC cells.
These antibodies also target and damage voltage-gated calcium channels (VGCCs) on the presynaptic terminals in motor neurones. This leads to weakness, esp proximal muscles, also intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia. Also autonomic –> dry mouth, blurred vision, impotence, dizziness.
Reduced tendon reflexes with post-tetanic potentiation: they become temporarily normal for a short period following a period of strong muscle contraction. For example, the patient can maximally contract the quadriceps muscle for a period, then have their reflexes tested immediately afterwards, and display an improvement in the response.
Think sclc in older smokers with LEMS symptoms
15
Q
What type of lung cancer is linked to asbestos inhalation?
A
Mesothelioma - mesothelial cells of the pleura. Latent period between exposure and cancer up to 45 years. Poor prognosis, chemotherapy can improve survival but it is essentially palliative.
16
Q
What is the definition of community acquired pneumonia?
A
Pneumonia developed outside of hosp
17
Q
What is hospital acquired pneumonia?
A
Pneumonia developed more than 48h after hospital admission.
18
Q
How does pneumonia present?
A
Shortness of breath Cough productive of sputum Fever Haemoptysis Pleuritic chest pain (sharp chest pain worse on inspiration) Delirium Sepsis
19
Q
Give 5 signs of sepsis secondary to pneumonia.
A
Tachypnoea Tachycardia Hypoxia Hypotension Fever Confusion
20
Q
What would you find on examination in pneumonia?
A
Bronchial breath sounds - harsh breath sounds equally loud on inspiration + expiration caused by consolidation.
Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.
Dullness to percussion due to lung tissue collapse and/or consolidation.
21
Q
What’s in the CURB65 score and what does the result mean?
A
C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65
Predicts MORTALITY (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%).
Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment
22
Q
What is the most common causative organism of pneumonia in adults?
A
50% streptococcus pneumoniae
20% haemophilus influenzae (smokers)
23
Q
What causes pneumonia in patients with COPD/immunocompromised?
A
Moraxella catarrhalis
24
Q
Give 2 organisms which cause pneumonia in patients with CF?
A
P aeruginosa (also bronchiectasis), staph aureus
25
What are 5 causes of atypical pneumonia? Give one associated feature for each.
Legions of psittaci MCQs -
Legionella pneumophilia - SIADH --> hyponatraemia, infected air conditioning units/water supplies (cheap hotels)
Chlamydia psittaci - birds/parrots
Mycoplasma pneumoniae - erythema multiforme (target lesions), neuro symptoms
Chlamydophila pneumoniae - school age, wheeze
Coxiella burnetii (Q fever) - animals/farmers
26
What causes pneumonia in patients with low CD4 count?
Pneumocystis jiroveci (PCP) pneumonia. Dry cough without sputum, SOBOE, night sweats. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.
27
How is pneumonia investigated?
CRB 2 or more - hosp admission -->
CXR- consolidation
FBC - raised WCC
U+Es - urea
CRP - raised. Nb not in immunocompromise.
Sputum cultures, blood cultures, urinary antigens for legionalla/pneumococcal.
28
How is pneumonia managed?
Abx for local area guidelines.
Mild: 5 days oral amoxicillin OR macrolide
Mod/severe: IV 7-10 days of BOTH. changed to oral guided by clinical improvement or improvement in WCC.
29
Give 5 complications of pneumonia.
```
Sepsis
Pleural effusion
Empyema
Lung abscess
Death
```
30
What is reversibility testing?
Doing spirometry before and after giving a bronchodilator eg salbutamol. Eg asthma is reversible but COPD is not.
31
What is the FEV1? What does reduction in FEV1 mean?
Forced expiratory volume in 1 second - reduced in obstruction to air flow out of the lungs.
32
What is FVC? What does reduction in FVC mean?
Forced vital capacity - total amount of air a person can exhale after a full inhalation. Reduced in restriction on the capacity of the lungs.
33
What type of pattern is seen on spirometry for obstructive lung disease? Give an example.
FEV1: FVC ratio <75% - air can go in but not out.
| Eg COPD, asthma. Asthma is reversible with bronchodilators.
34
What type of pattern is seen on spirometry in restrictive lung disease? Give an example.
Reduced FVC AND FEV1, with normal FEV1:FVC ratio (>75%).
| Eg interstitial lung disease, neurological eg MND, scoliosis or chest deformity, obesity.
35
What is peak flow?
Peak or fastest point of expiration. Asks Peak Expiratory Flow Rate (PEFR).
Demonstrates how much obstruction is present.
Varies between people so % predicted is used.
36
What is asthma?
Chronic inflammatory condition of airways causing episodic bronchoconstriction. Reversible airway obstruction. Caused by hypersensitivity.
37
Give 5 potential triggers for asthma.
```
Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
```
38
Give 5 features that would help you differentiate between asthma and another diagnosis eg viral induced wheeze.
Asthma: episodic, diurnal variability, worse at night, dry cough, wheeze, SOB, atopy, FHx, bilateral widespread polyphonic wheeze
Reconsider diagnosis: wheeze related to coughs and colds (VIW), isolated or productive cough, normal Ix, no response to treatment, unilateral wheeze (focal lesion/infection).
39
How is asthma diagnosed?
NICE guidelines 2017 advise definitive testing at a 'diagnostic hub', with:
Fractional exhaled nitric oxide (FENO),
Spirometry with bronchodilator reversibility.
If uncertain can go on to PF diary, direct bronchial challenge test with histamine or methacholine.
However the BTS and SIGN guidelines only suggest testing when there is clinical uncertainty.
40
Describe the long-term management of asthma.
1. SABA (salbutamol) - reliever, blue PRN
2. ICS (beclomethasone) - preventer, brown
3. LRA (montelukast)
4. LABA (salmeterol)
5. Consider Maintenance and reliever therapy (MART) = ICS + LABA.
6. Increase corticosteroid
7. LAMA (tiotropium)/theophylline
8. Refer to specialist
lifestyle - exercise, avoid smoking
check adherence+ technique
yearly review + flu jab
NICE 2017 (BTS/sign is different)
41
How does acute asthma present?
Progressively worsening shortness of breath
Use of accessory muscles
Fast respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation with reduced air entry
42
How is moderate acute asthma defined and managed?
PEFR 50 – 75% predicted
Nebulised salbutamol 5mg repeated as often as required ('back to back'). Monitor K+ as salbutamol causes hypokalaemia.
Nebulised ipratropium bromide
Oral prednisolone or IV hydrocortisone 5 days
Antibiotics if bacterial infection
43
How is severe acute asthma defined and managed?
PEFR 33-50% predicted
Resp rate >25
Heart rate >110
Unable to complete sentences
Senior input
Oxygen if required to maintain sats 94-98%
Aminophylline infusion
IV salbutamol
```
Remember OSHITME for treating asthma attack:
Oxygen
Salbutamol
Hydrocortisone IV
Ipratropium (senior)
Theophylline (senior)
Mag sulphate (senior)
Escalate
```
44
How is life-threatening asthma defined and managed?
33, 92 CHEST
```
PEFR <33%
Sats <92%
Cyanosis
Hypotension
Exhaustion/Tiring
Silent chest: airways are so tight that there is no air entry at all.
Tachycardia
```
IV magnesium sulphate infusion
HDU / ICU
Intubation in worst cases, but decide early because difficult to intubate with severe bronchoconstriction
45
What would ABG show in acute asthma?
Resp alkalosis due to 'blowing off CO2'.
Tiring --> normal CO2 or hypoxia.
Resp acidosis = high CO2, very bad sign
46
How would you monitor the response to treatment in acute asthma?
```
Respiratory rate
Respiratory effort
Peak flow
Oxygen saturations
Chest auscultation
```
47
What is COPD?
non-reversible, long term obstructive airway disease caused by damage to lung tissue (usually smoking)
48
How does COPD present?
```
chronic SOB
cough
sputum
wheeze
recurrent RTIs esp in winter
often smoker.
Differential - cancer, fibrosis, heart failure.
COPD does NOT cause clubbing, haemoptysis or chest pain
```
49
MRC Dyspnoea scale is recommended by NICE - give the grades and what they mean.
Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness
50
What would be seen on spirometry in COPD?
Obstructive picture - FEV1/FVC ratio <0.7, not reversible with bronchodilators.
51
How is COPD staged?
Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted
52
What investigations would you do for COPD?
CXR - exclude cancer etc
FBC - polycythaemia (hypoxia -> more EPO -> more Hb) or anaemia.
BMI as a baseline to later assess weight loss (e.g. cancer or severe COPD) or weight gain (e.g. steroids).
Sputum culture to assess for chronic infections such as pseudomonas.
ECG and echocardiogram to assess heart function.
CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis.
Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency. Deficiency leads to early onset and more severe disease.
Transfer factor for carbon monoxide (TLCO) is decreased in COPD. It can give an indication about the severity of the disease and may be increased in other conditions such as asthma.
53
Describe the management of COPD.
Stop smoking
One-off pneumococcal + annual flu vax
1. SABA/SAMA
2. LABA plus:
a. steroid responsive --> + ICS eg Seretide
b. not steroid responsive --> + LAMA eg Anoro Ellipta
3. LABA +LAMA +ICS (Trelegy Ellipta)
4. Other options:
nebs, theophylline, mucolytics (carbocisteine), prophylactiv azithromycin, LTOT
54
Indications and contraindications of LTOT?
Long term oxygen therapy is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale). It can’t be used if they smoke as oxygen plus cigarettes is a significant fire hazard.
55
What does the ABG show in COPD?
Acute: Resp acidosis due to retaining CO2.
Chronic: Raised HCO3 (metabolic compensation).
In an acute exacerbation, the kidneys can’t keep up with the rising level of CO2 so they become acidotic despite having a higher bicarbonate than someone without COPD.
56
What investigations would you do for acute exacerbation of COPD?
Chest xray to look for pneumonia or other pathology
ECG to look for arrhythmia or evidence of heart strain (heart failure)
FBC to look for infection (raised white cells)
U&E to check electrolytes which can be affected by infection and medications
Sputum culture if significant infection is present
Blood cultures if septic
57
How can you work out whether someone with COPD retains CO2 (and is dependent on hypoxaemia for their respiratory drive)?
Bicarb will be abnormal in CO2 retainers. If it is abnormal give oxygen with aim of 88-92%.
If normal bicarb, aim for oxygen >94%.
O2 sats and repeat ABGs to optimise pO2 without increasing PCO2.
58
How are acute exacerbations of COPD treated (at home, in hospital, and severe cases)?
At home:
Prednisolone 30mg once daily for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection
In hospital:
Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)
Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
Antibiotics if evidence of infection
Physiotherapy can help clear sputum
Oxygen - 88-92% in CO2 retainers
Severe:
IV aminophylline
Non-invasive ventilation (NIV)
Intubation and ventilation with admission to intensive care
Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate
59
What is non-invasive ventilation?
Non-invasive ventilation (NIV) involves using a full face mask or tight fitting nasal mask to blow air forcefully into lungs and ventilate them without intubation. Middle point between oxygen and intubation.
Can be BiPAP or CPAP.
60
What is BiPAP? How does it work?
Bilevel positive airway pressure. Cycle of high and low pressure to correspond to patients inspiration and expiration.
BiPAP = IPAP + EPAP (inspiratory + expiratory positive airway pressure).
61
When should BiPAP not be used? What should you do before starting?
Pneumothorax (CXR first), structural abnormality of face, airway or GIT.
Plan for in case BiPAP fails - escalation? palliation?
62
When is BiPAP indicated?
T2 resp failure, when pH <7.35, PaCO2 >6, despite adequate medical treatment.
(2 things wrong = T2 = BIpap)
63
What is CPAP?
Continuous positive airway pressure - continuous air being blown into lungs, keeps airways expanded. Used when airway prone to collapse.
64
When should CPAP be used?
T1 resp failure
Obstructive sleep apnoea
Congestive cardiac failure
Acute pulmonary oedema
65
What is interstitial lung disease (ILD)?
Broad term for conditions affecting lung parenchyma, causing inflammation and fibrosis (scarring, reduced elasticity). Irreversible, poor prognosis.
66
How is ILD diagnosed?
Clinical
High-res CT thorax (HRCT) --> ground glass appearance.
Lung biopsy and histology
67
How is ILD managed?
Poor prognosis, irreversible, supportive Rx/stop it getting worse.
Remove or treat the underlying cause
Home oxygen where they are hypoxic at rest
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate
Lung transplant
68
What is idiopathic pulmonary fibrosis and how does it present?
Progressive pulmonary fibrosis with no clear cause. Insidious onset SOB and dry cough >3 months. Usually affects those > 50 years. Examination: bibasal fine inspiratory crackles, finger clubbing.
69
Give 5 causes of interstitial lung disease.
```
Idiopathic
Drug induced
Secondary
Hypersensitivity pneumonitis
Cryptogenic organising pneumonia
Asbestos
```
70
How is IPF managed?
Pirfenidone - antifibrotic, anti-inflammatory
Nintedanib - mab against tyrosine kinase
Prognosis is poor with a life expectancy of 2-5 years from diagnosis.
71
Give 4 drugs that cause pulmonary fibrosis.
```
Think Manchester
Methotrexate
Nitrofurantoin
Amiodarone
Cyclophosphamide
(bad CHEST)
```
72
Give 4 diseases that cause secondary pulmonary fibrosis.
A1-AT def
Autoimmune:
RA SLE, systemic sclerosis
73
What is hypersensitivity pneumonitis? How is it diagnosed?
Aka extrinsic allergic alveolitis.
Type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in sensitive people.
Dx: bronchoscopy --> bronchoalveolar lavage --> wash airways --> test the fluid --> raised lymphocytes and mast cells.
74
How is hypersensitivity pneumonitis managed?
Remove allergen
Oxygen if hypoxic
Steroids
75
What is bird-fancier's lung?
Hypersensitivity pneumonitis reaction to bird droppings.
76
What is farmer's lung?
Hypersensitivity pneumonitis reaction to mouldy spores in hay
77
What is mushroom worker's lung?
Hypersensitivity pneumonitis reaction to mushroom antigens
78
What is malt workers lung?
Hypersensitivity pneumonitis reaction to mould on barley.
79
What is cryptogenic organising pneumonia?
Previously known as bronchiolitis obliterans organising pneumonia. It involves a focal area of inflammation of the lung tissue. This can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.
Presents as pneumonia, diagnosed by lung biopsy
80
How is cryptogenic organising pneumonia treated?
Systemic corticosteroids
81
What is asbestosis?
Lung fibrosis from absestos inhalation. Asbestos is fibrogenic and oncogenic. Causes fibrosis, pleural thickening + plaques, adenocarcinoma and mesothelioma.
Death with asbestos exposure = coroner.
82
What is a pleural effusion? How is it classified?
Collection of fluid in the pleural cavity.
Protein >3: exudate
Protein <3: transudate
83
Give 3 exudative causes of pleural effusion.
Protein leaking out of tissues into the pleural space, causing high protein count (>3g/dL). Usually inflammatory eg lung ca, pneumonia, RA and TB.
84
Give 3 transudative causes of pleural effusion.
Fluid moving across into pleural space, causing low protein count (<3g/dL).
CCF
Hypoalbuminaemia
Hypothyroidism
Meig's syndrome (right-sided pleural effusion with ovarian malignancy)
85
How would pleural effusion present?
SOB, dullness to percussion, reduced breath sounds, tracheal deviation and mediastinal shift if massive
86
What would pleural effusion show on X ray?
Blunting of costophrenic angle
Fluid in lung fissures
Large - meniscus (curving upwards where it meets chest wall and mediastinum)
Tracheal and mediastinal deviation if massive
87
How is pleural effusion investigated?
CXR
Aspiration/chest drain to take pleural fluid sample --> analyse for protein count, cell count, pH, glucose, LDH, microbiology.
88
How is pleural effusion treated?
Small --> conservative management, treat underlying cause
| Large --> aspiration or chest drain if recurrent.
89
What is empyema and how is it diagnosed?
Infected pleural effusion. Suspect in patient with improving pneumonia but ongoing/new fever.
Pleural aspiration - pus, pH <7.2, low glu, high LDH.
Treated by chest drain and abx
90
What is pneumothorax? What causes it?
Air in pleural space. Can be spontaneous or secondary:
trauma
iatrogenic eg lung biopsy, mechanical ventilation or central line insertion
lung pathology eg infection, asthma or COPD
91
How does pneumothorax present?
Usually tall, thin young man, sudden SOB, pleuritic chest pain, possibly after trauma/sports.
92
How is pneumothorax investigated?
Erect chest X ray - line demarcating edge of lung where lung marking ends and pneumothorax begins.
Measure size of the pneumothorax.
CT thorax can be used to detect smaller pneumothorax or assess size accurately.
93
How is pneumothorax managed?
If no SOB and there is a <2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.
If SOB and/or there is a >2cm rim of air on the chest xray then it will require aspiration and reassessment.
If aspiration fails twice it will require a chest drain.
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.
(BTS 2010)
94
What is tension pneumothorax?
Tension pneumothorax is caused by trauma to the chest wall that creates a one-way valve that lets air in but not out of the pleural space. The one-way valve means that during inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space. Therefore more air keeps getting drawn into the pleural space with each breath and cannot escape. This is dangerous as it creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.
95
How would you identify tension pneumothorax on examination?
Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension
96
How is tension pneumothorax managed?
Insert a large bore cannula into the second intercostal space in the midclavicular line. Then chest drain in the triangle of safety.
97
Where/how do you insert a chest drain?
inside the triangle of safety formed by:
The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)
Insert needle above rib to avoid neurovascular bundle that runs just below the rib.
Then get a chest x ray to check the positioning.
98
What is a pulmonary embolism?
Pulmonary embolism (PE) = clot (thrombus) in pulmonary arteries. Usually from a DVT in legs which has embolised to the R heart then to the pulmonary arteries --> block blood flow to lung tissue and create right heart strain.
99
What is VTE?
Venous thromboembolism - DVTs and PEs.
100
Give 5 risk factors for VTE.
```
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
```
101
How is VTE prevented?
All patients admitted to hosp risk-assessed and anticoagulated with sc LMWH and compression stockings if indicated.
102
What are contraindications to LMWH?
Active bleeding
| Anticoagulation already eg with warfarin or NOAC
103
How does PE present?
```
Need high index of suspicion.
Shortness of breath
Cough +/- haemoptysis
Pleuritic chest pain
Hypoxia
Tachycardia
Tachypnoea
Low grade fever
Haemodynamic instability causing hypotension
DVT symptoms eg unilateral leg swelling, tenderness
```
104
How is VTE investigated and diagnosed?
Hx, ex, CXR
Wells score -
Likely (>/=2) --> CTPA
Unlikely (<2) --> D-Dimer --> CTPA if positive
V/Q scan if patient has renal impairment, contrast allergy or at risk from radiation. PE --> perfusion worse than ventilation.
105
What would be seen on an ABG in PE?
Resp alkalosis due to hyperventilation --> less CO2 in blood.
pO2 is low.
106
How is PE managed?
Supportive Management:
Admit, Oxygen, Analgesia, monitor
Initial Management:
DOAC eg Apixaban or rivaroxaban.
LMWH eg enoxaparin if DOAC not suitable, or in antiphospholipid syndrome.
Long term anticoagulation:
DOAC
Warfarin with target INR of 2-3. When switching to warfarin continue LMWH for 5 days or the INR is 2-3 for 24 hours on warfarin (whichever is longer).
LMWH long term is first line treatment in pregnancy or cancer.
Continue anticoagulation for:
3 months if there is an obvious reversible cause (then review)
Beyond 3 months if cause unclear/recurrent VTE/irreversible underlying cause such as thrombophilia.
6 months in active cancer (then review)
107
When is thrombolysis indicated?
Thrombolysis = injecting a fibrinolytic such as alteplase or streptokinase. Consider in
massive PE with haemodynamic compromise. Significant risk of bleeding.
108
How is thrombolysis performed?
Intravenously using a peripheral cannula.
OR
Catheter-directed thrombolysis - catheter is inserted into the venous system, through the right side of the heart and in to the pulmonary arteries. The operator can then administer the thrombolytic agent directly into the location of the thrombus. Special equipment can also be used to physically break down the thrombus and aspirate it. There is a risk of damaging the pulmonary arteries doing this.
109
What is pulmonary hypertension and what are the complications?
Increased resistance and pressure of blood in the pulmonary arteries. Causes strain on the right side of the heart trying to pump blood through the lungs. and back pressure of blood into the systemic venous system.
110
What causes pulmonary hypertension?
Group 1 – Primary pulmonary hypertension or connective tissue disease (SLE)
Group 2 – Left heart failure - MI, HTN
Group 3 – Chronic lung disease (COPD)
Group 4 – Pulmonary vascular disease (PE)
Group 5 – Misc - sarcoidosis, glycogen storage disease and haematological disorders
111
How does pulmonary hypertension present?
```
Shortness of breath = main symptom
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema
```
112
What ECG changes occur in pulmonary htn?
R sided heart strain ->
Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)
Right axis deviation
Right bundle branch block
113
What X ray changes occur in pulmonary htn?
Dilated pulmonary arteries
| Right ventricular hypertrophy
114
What investigations would you do for pulmonary htn?
ECG
XR
NT-proBNP - raised in RV failure
Echo - pulmonary artery pressure
115
How is pulmonary htn managed?
Poor prognosis - 30-40% 5-year survival from diagnosis. This can increase to 60-70% where specific treatment is possible.
Primary pulmonary hypertension:
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
Secondary pulmonary hypertension - treat cause eg PE/SLE
Supportive treatment for complications such as respiratory failure, arrhythmias and heart failure.
116
What is sarcoidosis?
granulomatous inflammatory condition with systemic symptoms
117
What are granulomas?
nodules of inflammation full of macrophages
118
How does sarcoidosis present?
Resp sx in 90%: SOB, dry cough
| Bimodal distribution - young adults + age 60. More common in Black people.
119
Give 5 extrapulmonary manifestations of sarcoidosis.
Systemic - fever, fatigue, wt loss
Liver (20%)- liver nodules, cirrhosis, cholestasis
Eyes (20%) - uveitis, conjunctivitis, optic neuritis
Skin (15%): Erythema nodosum (shins), lupus pernio (face), granulomas in scar tissue
Heart (5%): Bundle branch block, heart block, myocardial muscle involveent
Kidneys (5%): Kidney stones (hypercalcaemia), nephrocalcinosis, interstitial nephritis
CNS (5%): nodules, pituitary (DI), encephalopathy
Bones (2%): arthralgia, arthritis, myopathy.
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What is Lofgren's syndrome?
Specific presentation of sarcoidosis. Triad of:
Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)
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What investigations would you do in sarcoidosis and what would they show?
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Blood Tests:
Raised serum ACE
Hypercalcaemia
Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins
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Imaging
CXR - hilar lymphadenopathy
High-resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules
MRI can show CNS involvement
PET scan can show active inflammation in affected areas
Tests for other organ involvement:
U&Es for kidney involvement
Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
LFTs for liver involvement
Ophthalmology review for eye involvement
ECG and echocardiogram for heart involvement
Ultrasound abdomen for liver and kidney involvement
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What is seen on histology in sarcoidosis?
Histology from biopsy is gold-standard dx. This is done using bronchoscopy with USS-guided biopsy of mediastinal lymph nodes.
Shows non-caseating granulomas with epithelioid cells.
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How is sarcoidosis treated?
No treatment if no or mild symptoms as the condition often resolves spontaneously.
Oral steroids if treatment is required - give for 6-24 months. Patients should be given bisphosphonates to protect against osteoporosis whilst on such long term steroids.
Second line options are methotrexate or azathioprine
Lung transplant is rarely required in severe pulmonary disease
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What is the prognosis of sarcoidosis?
Sarcoidosis spontaneously resolves within 6 months in around 60% of patients. In a small number of patients it progresses with pulmonary fibrosis and pulmonary hypertension, potentially requiring a lung transplant. Death in sarcoidosis is usually when it affects the heart (causing arrhythmias) or the central nervous system.
125
Give 5 differentials for sarcoidosis.
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Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis
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126
Which organ system is predominantly affected by sarcoidosis and how?
Lungs - Mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules.
127
What is obstructive sleep apnoea (OSA)?
Episodes of apnoea (not breathing) for up to a few minutes periodically during sleep, caused by collapse of the pharyngeal airway.
128
Give 5 risk factors for OSA.
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Middle age
Male
Obesity
Alcohol
Smoking
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How does OSA present?
Partner usually notices apnoea episodes or snoring, patient is unaware.
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness (use Epworth Sleepiness Scale and ask about job eg HGV driver affects urgent referral)
Concentration problems
Reduced oxygen saturation during sleep
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What are the complications of severe OSA?
Hypertension, heart failure and can increase the risk of myocardial infarction and stroke.
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How is OSA diagnosed?
ENT specialist or a specialist sleep clinic - sleep studies. This involves the patient sleeping in a laboratory whilst staff monitor their oxygen saturations, heart rate, respiratory rate and breathing to establish any apnoea episodes and the extent of their snoring.
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How is OSA managed?
1. correct reversible risk factors - stop drinking alcohol, stop smoking, lose weight.
2. CPAP
3. Surgery - significant surgical restructuring of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).
