Respiratory Medicine Flashcards

1
Q

What are some causes of nodules on a CXR?

A

Infective Causes: Aspergilosis, Tuberculosis, Lung Abscess, Round pneumonia

Non-infective Causes: RA, Sarcoidosis, Wegener’s (GPA), lung tumour.

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2
Q

What are some risk factors for PE?

A
  • recent surgery (especially abdominal, pelvic or hip/knee replacement)
  • thrombophilia
  • leg fracture
  • prolonged bed rest/ reduced motility
  • malignancy
  • pregnancy/postpartum
  • pill/HRT
  • previous PE
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3
Q

Describe PE, it’s symptoms, relevant tests and management

A

Venous thrombi, usually from DVT, pass into pulmonary circulation and blocks blood flow to lungs.

Symptoms: acute dyspnoea, pleuritic chest pain, syncope, haemoptysis

Signs: hypotension, tachycardia, increased JVP, tachypnoea, cyanosis, AF

Tests:

  • d dimer if wells score less than 3 to exclude PE
  • FBC, U+E, ABG may show decreased PaO2 and PaCO2.
  • ECG may show RBBB, right ventricular strain (inverted t wave in v1-v4) RAD

Imaging:

  • CTPA 1st line for diagnosis
  • if haemodynamically unstable Transthoracic echocardiogram looking for evidence of right ventricular dysfunction

Management:

  • oxygen if hypoxic
  • morphine and antiemetic if in pain
  • if critically ill or unstable consider thrombolysis
  • Anticoagulation with LMWH and start warfarin once confirmed . (Start LMWH before imaging if intermediate/high clinical risk)
  • Stop heparin when INR > 2 and continue warfarin for 3 months (aim for INR 2-3)
  • Testing for thrombophilia should be considered in patient afed under 50 with recurrent PE or those with strong family history of VTE.
  • Investigations for occult cancer are indicated for unprovoked PE.

Prevention: thrombophylaxis and compression stockings

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4
Q

Describe Asthma, its symptoms and signs, tests, and non-emergency treatment

A

Asthma is characterised by recurrent episodes of dyspnoea, cough and wheeze caused by reversible airways obstruction. Three factors contribute to airway narrowing:

  • Bronchial muscle contraction
  • Mucosal inflammation
  • Increased mucus production

Signs and symptoms: Intermittent dyspnoea, wheeze, cough (often nocturnal) and sputum. Tachypnoea, audible wheeze, hyperinflated chest, hyperresonant percusion notes, decreased air entry, widespread polyphonic wheeze.

Tests: decreased PEF, Spirometry shows obstructive defect (Decreased FEV1/FVC) with reversibility I.e. improvment in FEV1 following B2 agonists.

Treatment:
-Step 1: SABA
-Step 2: SABA + low-dose ICS (First step if symptoms 3/wk or night time waking)
-Step 3: SABA + Low-dose ICS + LTRA
-Step 4: SABA + low-dose ICS + LABA (Continue LRTA depending on patients response to LRTA)
-Step 5 SABA +/- LRTA and switch Low-dose ICS/LABA for a Maintenance and Reliever Therapy (MART), that includes a low-dose ICS.
-Step 6: SABA +/- LRTA + Medium-dose ICS MART. (May consider switching back to fixed dose of moderate-dose ICS and a separate LABA)
-Step 7: SABA +/- LRTA + High-dose ICS (Not in MART) OR a trial of additaional drug e.g. LAMA or theophylline OR seek advice from asthma specialist
-Omalizumab is used in severe asthma with Raised IgE, and Mepolizumab can be used in severe asthma with eosinophilia
(Low-dose ICS is less than 400micrograms, medium is 400-800 and High is over 800)

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5
Q

Describe COPD, its symptoms, signs, complications, tests and treatment.

A

A common progressive disorder characterised by airway obstruction (FEV1 less than 80%, FEV1/FVC les than 0.7) with little or no reversibility. It includes chronic bronchitis (cough and sputum for most days for 3 months of 2 successive years) and emphysema which is histologically enlarged air spaces. Pathologically there is mucous gland hypertrophy, goblet cell hyperplasia, and squamous metaplasia of respiratory epithelium.

Signs and symptoms: Cough, sputum, dyspnoea, wheeze, tachypnoeic, use of accessory muscles of respiration, hyperinflation, decreased cricosternal distance (less than 3cm), hyper resonant percussion notes, cor pulmonale.

Complications: Acute exacerbations +/- infection, polycythaemia, respiratory failure, cor pulmonale (oedema, raised JVP), pneumothorax (ruptured bullae), lung carcinoma

Tests:

  • FBC may show increased packed cell volume.
  • CXR shows hyperinflation (more than 6 anterior ribs), flat hemidiaphragms.
  • ECG may show right atrial and ventricular hypertrophy (cor pulmonale).
  • ABG shows decreased PaO2 +/- hypercapnia
  • Spirometry shows obstructive (FEV1/FVC less than 0.7) severity graded by FEV1, greater than 80% is stage 1 mild, 50-79% is stage 2 moderate, 30-49% is stage 3 severe, and less than 30% is stage 4 very severe

Treatment:

  • Conservative: Smoking cessation advice, encourage exercise, Flu and pneumococcal vaccinations, pulmonary rehabilitation programme
  • Pharmcological: Step 1 = PRN short acting anti-muscarinic or B2-agonist. Step 2 = inhaled long-acting anti-muscarinic or B2-agonist if FEV1 greater than 50% Step 3 = combination long-acting B2-agonist + corticosteroid Or long-acting anti-muscarinic. Step 4 = combination long-acting B2-agonist + corticosteroid, + long-acting anti-muscarinic.
  • Roflumilast is an Long-acting PDE-4 Inhibitor used in severe COPD in those with FEV1 less than 50% and 2 or more exacerbation in a year despite triple therapy.
  • If severe PaO2 less than 8kpa or pulmonary hypertension consider Long-Term Oxygen Therapy (LTOT) in non-smokers.’
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6
Q

Define Chronic Bronchitis

A

Chronic bronchitis is defined clinically as cough with sputum production on most days for 3 months of 2 successive years.

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7
Q

What are the stages of severity of COPD?

A

Stage 1 Mild = FEV1 >80% Pred
Stage 2 Moderate = FEV1 50-79% Pred
Stage 3 Severe = FEV1 30-49% Pred
Stage 4 Very Severe = FEV1 less than 30%

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8
Q

Describe Bronchiectasis, it’s causes, symptoms, and tests, and management

A

Chronic infection of the bronchi and bronchioles leading to permanent dilatation of these airways. Three main types cylindrical (Most common), Varicose and Cystic.

Causes:

  • congenital e.g. CF, youngs syndrome, kartageners syndrome
  • post infection e.g. Measles, pertussis, bronchiolitis, pneumonia, TB, HIV
  • Other e.g. Bronchial obstruction, RA, UC, idiopathic

Symptoms: persistent cough, copious purulent sputum, intermittent haemoptysis, clubbing, coarse inspiratory crepitations, wheeze

Tests: Sputum culture (commonly Haem Influzenzae, strep p, staph a, pseudomonas), CXR shows thickened bronchial walls (Tramlines and ring shadows). HRCT assesses extent and distribution of disease. Spirometery shows obstructive picture.

Management:

  • Postural drainage should be performed twice daily
  • Antibiotics guided by culture, if more than 3 exacerbations consider long-term antibiotics.
  • Bronchodilators in patients with underlying asthma, COPD, CF
  • Surgery may be needed in localised disease or to control severe haemoptysis.
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9
Q

Describe Interstitial lung disease, its symptoms and classification

A

A term used to describe a number of conditions characterised by chronic inflamation and or/progressive interstitial fibrosis

Symptoms: dyspnoea on exertion, non-productive paroxysmal cough, abnormal breath sounds, abnormal CXR or HRCT (fibrosis) restrictive pulmonary spirometry.

Classification:

  • Occupational e.g. asbestosis, berylliosis, silicosis, cotton workers lung (byssinosis)
  • drugs e.g. nitrofuratoin, bleomycin, amiodarone, sulfasalazine
  • hypersensitivity reactions e.g. extrinsic allergic alveolitis
  • infections - TB, fungi, viral
  • GORD
  • Those associated with systemic disorders e.g. sarcoidosis, RA, SLE, systemic sclerosis, sjrogren syndrome, UC, Renal tubular acidosis, autoimmune thyroid disease
  • Idiopathic e.g. idiopathic pulmonary fibrosis, cryptogenic organising pneumonia, lymphocytic interstitial pneumonia
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10
Q

Describe pleural effusion, its causes, symptoms, signs, tests and management

A

A pleural effusion is fluid in the pleural space. They can be divded by their protein concentration into transudates (protein les than 25g/L) and exudates (protein greater than 35g/L). Blood in the pleural space is a haemothorax, pus in the pleural space is an empyema.

Causes of transudates:

  • increased venous pressure (Cardiac failure, constrictive pericarditis, fluid overload)
  • hypoproteinaemia (cirrhosis, nephrotic syndrome, malabsorption)
  • hypothyroidism

Causes of exudates:
-leakiness of pleural capillaries due to infection (TB, pneumonia) inflammation (RA, SLE) or malignancy (Bronchogenic carcinoma, lung metastases, lymphoma, mesothelioma)

Symptoms: Asymptomatic or dyspnoea and pleuritic chest pain.

Signs: decreased expansion, stony dull percussion note, diminished breath sounds occur on affected side. vocal resonance is decreased. trachea deviation away from large effusion.

Tests: CXR show blunting of costophrenic angles abd water-dense shadows with meniscus.

Management:

  • drainage and fluid analysis
  • pleurodesis with tetracycline, bleomycin or talc may be helpful for recurrent effusions. Thorascopic talc pleurodesis is most effective for malignant effusions.
  • Surgery may be needed for persistent collections and increasing pleural thickness.
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11
Q

Describe simple pneumothorax, its causes, features, and management.

A

Causes:
-Primary (especially in young thin men) due to rupture of a subpleural bulla
Secondary:
-chronic lung disease e.g. asthma, copd, lung fibrosis, sarcoidosis
-infection e.g. TB, pneumonia, lung abscess
-traumatic including iatrogenic
-carcinoma
-connective tissue disorders e.g. marfans or ehlers-danlos

Features: Pleuritic chest pain, SOB

Management:
Primary:
-less than 2cm, and patient not short of breath, discharge with follow up
-rim of air 2cm or more, or breathless it needs needle aspiration
-if needle aspiration fails (i.e. Still more 2cm air or symptomatic) then a chest drain should be inserted.
-those that are admitted for observation high flow oxygen increases the absorption of the pneumothorax
Secondary:
-all patients should be admitted for at least 24hours.
-If patient over 50 and rim of air over 2cm or breathless then chest drain
-aspiration if 1-2cm, if it fails (pneumothorax still greater than 1cm) a chest drain should be inserted
-those that are admitted for observation high flow oxygen increases the absorption of the pneumothorax if tolerated

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12
Q

Describe type 1 respiratory failure and its management

A

Defined as hypoxia (PaO2 less than 8kPa) with a normal or low PaCO2. It is caused primarily by ventilation/perfusion mismatch e.g. Pneumonia, pulmonary oedema, PE, asthma, emphysema, pulmonary fibrosis, ARDS.

Management:

  • treat underlying cause
  • Give oxygen to correct hypoxia
  • Assisted ventilation if PaO2 less than 8kPa despite 60% oxygen.
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13
Q

Describe type 2 respiratory failure and its management

A

Defined as hypoxia (PaO2 less than 8kPa) with hypercapnia (PaCO2 greather than 6kPa). Caused by alveolar hypo ventilation causes include pulmonary disease such as asthma, COPD, pneumonia, end-stage pulmonary fibrosis, obstructive sleep apnoea, reduced respiratory drive e.g. Sedative drugs CNS tumour or trauma, neuromuscular disease or thoracic wall disease.

Management:

  • Treat underlying cause
  • Controlled oxygen therapy beware hypoxic drive.
  • Recheck ABG after 20 min if PaCO2 steady or lower continue monitoring if increasing consider NIPPV, contact ITU
  • If this fails consider intubation and artificial ventilation

Respiratory drive may be driven by hypoxia aim for sats 88-92% and monitor blood gases. If oxygen therapy not improving and CO2 rising consider NIPPV and failing that intubation and ventilation.

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14
Q

Describe sarcoidosis, its symptoms, tests, prognostic factors, and management.

A

It is a multisystem granulomatous disorder of unknown cause. Usually affects adults aged 20-40yrs and is more common in women. Afro-carribeans are more frequently and severly affected.

Symptoms: dry cough, progressive dyspnoea, chest pain. Non-pulmonary signs include lymphadenopathy, hepatomegaly, splenomegaly, lupus pernio, erythema nodosum.

Tests: Raised ESR, lymphopenia, raised serum ACE. Hypercalcaemia. 90% have abnormal 24 urine collection shows hypercalcaemia. CXR may show the following changes:

  • Stage 0: Normal
  • Stage 1: Bilateral Hilar Lymphadenopathy
  • Stage 2: BHL + interstitial infiltrates
  • Stage 3: Diffuse interstitial infiltrates only
  • Stage 4: diffuse fibrosis

Poor prognostic factors:

  • Insidious onset, symptoms longer than 6 months
  • Absence of erythema nodosum
  • Extrapulmonary manifestations e.g. lupus pernio, splenomegaly
  • CXR stage III-IV features
  • Afro-carribean

Management:

  • patients with Bilateral hilar lymphadenopathy do not need treatment, acute sarcoid requires bed rest and NSAIDs.
  • indication for predinsolone (40mg/24h PO) are uveitis, parenchymal lung disease, hypercalcaemia or neurological or cardiac involvement.
  • in severe disease immunosuppressants may be tried (methotrexate, hydroxychloroquine, ciclosporin, cyclophosphamide).
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15
Q

Describe Obstructive Sleep Apnoea, its symptoms, investigations, and management

A

Characterised by intermittent closure/collapse of the pharyngeal airway causing apnoeic episodes during sleep. These are terminated by partial arousal.

Symptoms: Obese, middle-aged man apnoeic episodes during sleep. loud snoring, daytime somnolence, poor sleep quality, morning headache, decreased libido, reduced cognitive performance

Complications: Pulmonary hypertension, type II respiratory failure, risk factor of hypertension

Investigations: Sleep studies (O2 sats, airflow at nose and mouth, ECG, EMG chest and abdominal wall movement during sleep) 15 or more epsiodes during 1h of sleep indicates significant sleep apnoea, TFTs (hypothyroidism is treatable cause)

Management:

  • Weight reduction, avoidance of tobacco and alcohol
  • mandibular advancement device if mild
  • CPAP via nasal mask during sleep for moderate to severe
  • surgery to relieve pharyngeal obstruction is occasionally needed refer to chest physician for assessment, bariatric surgery
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16
Q

Describe Costochondritis (Tietze’s syndrome), its symptoms, and managements

A

Symptoms:
Localised pain/tenderness at the costosternal junction, enhanced by motion, coughing, or sneezing. The 2nd rib is most often affected. The diagnostic key is localised tenderness which is marked (flinches on prodding).

Management:

  • Reassure patient, it is benign, usually clears up after a few weeks
  • Simple analgesia e.g. NSAIDs
  • In lengthy illness local steroid injections may be used
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17
Q

What is pleurodesis?

A

A medical procedure in which the pleural space is artificially obliterated, it involve the adhesion of the two pleurae. It can be done chemically or surgically, it prevents recurrence or pneumothorax or pleural effusion. Chemicals such as bleomycin, tetracycline or talc can be introduced into the pleural space through a chest drain, it is painful procedure so patients are often premedicated with sedative and analgesics.

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18
Q

What is the sail sign?

A

Triangular opacity over heart which indicates left lower lobe collapse commoner in asthmatics.

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19
Q

Describe Mesothelioma, its symptoms, investigations, types, and management.

A

A tumour of mesothelial cells that usually occurs in the pleura, and rarely in the peritoneum or other organs. It is associated with occupational exposure to asbestos. 90% report previous exposure to asbestos but only 20% of patients have pulmonary asbestosis. Compensation is available.

Symptoms: Chest pain, dyspnoea, weight loss, finger clubbing, recurrent pleural effusions, signs of metastases (lymphadenopathy, hepatomegaly, bone pain, abdominal pain/obstruction.

Investigations: CXR/CT show pleural thickening, diagnosis made on histology following thorascopy.

Types: there are three main histiological subtypes:

  • Epitheliod - Most common, best prognosis, Characterised by high levels of calretinin
  • Sarcomatous - less common, worst prognosis, Does not express high levels of calretinin
  • Biphasic

Management:

  • Pemetrexed + Cisplatin chemotherapy can improve survival.
  • Pleurodesis may help recurrent effusions.
  • Prognosis is poor, median survival 12 months
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20
Q

Describe Atelectasis, its symptoms, investigations, and management.

A

Collapse/closure of a lung. A common post-operative complication, also foreign body, tumour (usually squamous cell carcinoma), mucus plug.

Symptoms: SOB, chest pain, effusion, low O2 sats, cyanosis, tachycardia.

Investigations: CXR, CT, Bronchoscopy

Management:

  • ABCDE
  • CPAP
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21
Q

What are the different causes of tracheal deviation?

A

Pulled: Pneumonectomy, lung collapse, pulmonary hypoplasia

Pushed: Tension pneumothorax, Pleural effusion, diaphragmatic hernia, large thoracic mass.

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22
Q

What are the types of fibrosis predominately affecting upper zones?

A
BREAST:
Berylliosis, silicosis, pneumoconiosis
Radiation
Extrinsic allergic alveolitis
Ankylosing Spondylitis, Amiodarone
Sarcoidosis
TB
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23
Q

Which types of fibrosis typically affect the lower zones?

A
RAID:
Rheumatoid Arthritis/SLE
Asbestosis
Idiopathic pulmonary fibrosis
Drug induced e.g bleomycin, methotrexate
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24
Q

What is the Golden S sign on CXR?

A

Curves from lobar collapse then a counter curve caused by displacement by central mass. It’s significantly associated with bronchogenic carcinoma.

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25
Q

Describe Pulmonary Aspiration, its features, investigations, and management.

A

Aspiration of solid or liquid material into the upper and lower airways is likely when:

  • decreased GCS
  • decreased cough/gag reflexes
  • tendency to regurgitate/vomit (Last meal?)

Features: large food particles may cause complete airway obstruction (choking, stridor, cyanosis, loss of concisouness) vomit leads to sudden onset of severe SOB, wheeze and cyanosis, the acidity causes severe damage to the alveolar-capillary membrane, with desaturation of pulmonary surfactant and increased pulmonary permeability with oedema and atelectasis.

Investigations:

  • ABG shows hypoxemia initially with decreased CO2 due to hyperventilation until Pulmonary compliance and increased work of breathing lead to hypoventilation.
  • CXR abnormalities may take hours to develop, Right lower lobe most commonly affected, diffuse bilateral infiltrates and pulmonary oedema similar to ARDS appearance.

Management:

  • Prevention is key, in at risk patients pass an NG tube to empty the stomach
  • correct hypoxia and give nebulised salbutamol. Although secondary infection is common use of antibiotics or steroids in initial management is not routinely indicated.
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26
Q

Describe Pulmonary contusion, its features, and management.

A

Caused by high energy transfer during blunt injury e.g. RTA or high falls. Suspect in all patients with flail segments, or multiple rib fractures.

Features: Causes ventilation-perfusion mismatch and so hypoxia and respiratory distress. CXR may show patchy opacification which tend to become more prominent over time.

Management:
-Mostly supportive, high flow oxygen and monitor ABG to help assess need for GA, tracheal intubation and IPPV.

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27
Q

In terms of Pleural Fluid Analysis what is lights criteria?

A

Lights criteria determines presence of exudates with protein and LDH levels, there are 3 main criterion:

1) Pleural fluid protein to serum protein ratio is greater than 0.5
2) Pleural fluid LDH to serum LDH ratio is greater than 0.6
3) Pleural fluid LDH is over 2/3 of upper value
4) Serum Albumin - Pleural Fluid albumin is less than 1.2g/dL

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28
Q

Describe Pulmonary Hypertension, its causes, features, investigations, and management.

A

An increase in mean pulmonary arterial pressure of greater than 25mmHg at rest or 30 mmHg after exercise. (Normally 8-20mmHg).

Causes:
Pulmonary Arterial Hypertension Group 1: Idiopathic, inherited (autosomal dominant mutation in BMPR2 gene), drug-induced (cocaine, SSRIs, Interferon), congenital heart disease, HIV, connective tissue disease, portal hypertension (Normal PCWP)

Group 2: Left heart disease e.g. Left ventricular systolic dysfunction, left ventricular diastolic dysfunction, valvular heart disease, cardiomyopathy (Raised PCWP)

Group 3 secondary to lung disease: COPD, ILD, Sleep apnoea, Chronic high altitude

Group 4 thromboembolic: Blood clots in pulmonary arterial system

Group 5 unclear or multifactorial: e.g. Myeloproliferative disorders, systemic disorders e.g. Vasculitis, metabolic disorders e.g. Thyroid disease

Features: Progressive SOB, Odema, Ascites, left parasternal heave, Loud P2, pulmonary regurgitation, triscupid regurgitation, raised JVP,

Investigations: LFTs, TFTs, Autoimmune screen, CXR, echo,

Management:

  • Treat underlying condition.
  • acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilator such as IV epoprostenol or inhaled nitric oxide
  • For those with a positive response to acute vasodilator testing oral Ca-Channel blockers,
  • For those with a negative response to acute vasodilator testing, Prostacyclin analogues e.g. treprostinil, iloprost, Or Endothelin receptor antagonists e.g. bosentan. Or phosphodiesterase inhibitors e.g. sildenafil.
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29
Q

Describe Acute Respiratory Distress Syndrome, its causes, features, and management

A

An acute condition characterised by bilateral pulmonary infiltrates and severe hypoxaemia (PaO2/FiO2 ratio under 200) in the absence of evidence for cardiogenic pulmonary oedema (clinically or pulmonary capillary wedge pressure (CVP) less than 18mmHg

Causes: Sepsis, aspiration, trauma, acute pancreatitis, fat embolism, head injury (sympathetic stimulation leads to acute pulmonary HTN)

Features: Acute dyspnoea and hypoxaemia, hours/days after event. Multi-organ failure, rising ventilatory pressures.

Management:

  • treat underlying cause
  • antibiotics if signs of sepsis/aspiration
  • negative fluid balance (diuretics)
  • recruitment manoeuvres such as prone ventilation, use of positive end expiratory pressure
  • mechanical ventilation with LOW tidal pressures (conventional tidal pressures may cause lung injury)
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30
Q

Describe Hereditary Angioedema, its features, and management.

A

Aka C1 esterase inhibitor deficiency. C1 esterase inhibitor is a member of the serum protease inhibitors and acts to inhibit the classical pathway of complement cascade. In the absence of C1 esterase inhibitor activation of complement leads to increased levels of vasoactive peptides that increase capillary permeability, most notably, bradykinin. This patients taking ACE-i leads to further increase of bradykinin. This is mast-cell independent so there is no itching or erythema.

Features: Facial oedema, laryngeal oedema, with subsequent airway obstruction. No Urticaria. Episodes may be provoked by traum to mucosal membranes e.g. sexual intercourse or dental work.

Management:

  • patients may not respond to adrenaline and ultimately need C1 esterase inhibitor concentrate.
  • intubate and involve ITU for supportive treatment
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31
Q

Describe Cystic Fibrosis, its presentation, investigations, and management.

A

An autosomal recessive disease, reflecting mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR) on chromosome 7, which codes for a cAMP-regulated sodium/chloride channel. Neonates are screened for immuno reactive trypsin on the Guthrie card, then DNA analysis if raised. 85% coverage.

Presentation: 10% present with meconium ileus as neonates, most present later with recurrent pneumonia (+/- clubbing), steattorrhoea, or slow growth. Meconium ileus present with failure to pass stol or committing in the 1st 2 days of life. Distended loops of bowel are see through abdominal wall. Initially patients become infected with Staph Aureus, before subsequent colonisation with gram -ve bacteria most commonly Burkholderia cepacia and pseudomonas aeruginosa

Investigations:

  • sweat test
  • CXR may show shadowing suggestive of bronchiectasis especially in upper lobes.

Management:

  • (meconium ileus may require nasogastric drainage, washout enemas and excision of the gut containing meconium).
  • genetic counselling
  • antibiotics and good nutrition key to long-term survival.
  • May need enzymes due to pancreatic malabsorption.
  • Omeprazole helps absorption by increasing duodenal pH. Low fat diet may be needed if these measures fail to control steattorrhoea.
  • monitor glucose tolerance and insulin may be need later in life. Optimise diet.
32
Q

What are the causes of deranged kCO on lung function testing?

A

Increased kCO: Alveolar haemorrhage e.g. Goodpastures, GPA, Chung-Strauss, SLE

Decreased kCO: Destroyed alveoli e.g. Emphysema, pulmonary fibrosis.

33
Q

What is Heerfordt’s Syndrome?

A

Uveoparotid fever, there is parotid enlargement, fever and uveitis secondary to sarcoidosis

34
Q

Describe Allergic Bronchopulmonary Aspergillosis, its features, investigations, and management.

A

Results from an allergy to aspergillosis spores.

Features: Bronchoconstriction (wheeze, cough, dyspnoea), bronchiectasis (proximal)

Investigations:

  • Eosinophilia
  • Flitting CXR changes
  • Positive Skin prick to Asperigillus most specific
  • Positive RAST test to aspergillus
  • Positive IgG precipitins
  • Raised IgE

Management:

  • Steroids
  • Itraconazole is sometimes used as second-line agent
35
Q

Describe silicosis, it’s risk factors and features

A

Silicosis is a fibrosing lung disease caused by the inhalation of crystalline silicon dioxide. It is a risk factor for developing TB.

Risk Factors: Mining, Slate works, Foundries, Potteries

Features:
Fibrosing lung disease typically affecting upper lobes
‘Egg-shell’ calcification of hilar lymph nodes

36
Q

Describe Alpha-1-Antitrypsin Deficiency, its features and management.

A

Common autosomal recessive / co-dominant condition caused by a lack of protease inhibitor normally produced by the liver. A1AT protects cells from enzymes such as neutrophil elastae. A1AT located on chromosome 14. Alleles classified by their electrophoretic mobility M for normal S for slow and Z for very slow e.g. PiMM is normal, Homozygous PiZZ 10% normal A1AT levels.

Features:

  • Lungs: Panacinar emphysema, most marked in lower lobes
  • Liver: cirrhosis and hepatocellular carcinoa in adults, cholestatis in children.

Management:

  • A1AT concentration
  • No smoking
  • Supportive: bronchodilators, physiotherapy
  • IV A1AT concentrate
  • Surgery for volume reduction/ lung transplantation
37
Q

Describe Allergic Bronchopulmonary Aspergillosis, its features, investigations, and management.

A

Results from an Allergy to Aspergillus spores. Exam questions often give a history of bronchiectasis and eosinophilia.

Features:

  • Bronchoconstriction: wheeze, cough, dyspnoea
  • Bronchiectasis

Investigations:

  • Eosinophilia
  • Flitting CXR changes
  • Positive RAST test to Aspergillus
  • Positive IgG precipitins
  • Raised IgE

Management:

  • Steroids
  • Itranconazole is sometimes introduced second line
38
Q

Describe High Flow Nasal Cannulae (HFNC) its indications and contraindications.

A

Aka Optiflow, able to deliver high FiO2 humidified oxygen. Also has. A CPAP effect due to mechanical splinting of the nasopharynx and low levels of PEEP which contribute to alveolar recruitment and improved compliance and decreased work of breathing. Observational data suggest it outperforms face masks for relieving respiratory distress preventing the need for NIV or intubation.

Indications: Hypoxic respiratory failure e.g. CAP, Acute asthma, Cardiogenic pulmonary oedema, pulmonary embolism, interstitial pneumonia, carbon monoxide poisoning.

Contraindications: epistaxis (also a complication), base of skull fracture, surgery to nose, Nasal obstruction.

39
Q

Describe Chylothorax, its causes, and management.

A

A type of pleural effusion that results from lymphatic fluid accumulating in the pleural cavity due to either disruption or obstruction of the thoracic duct. Can be identified by its turbid, milky white appearance, and high levels of triglycerides. Important to distinguish chlyothroax from psuedochylothroax which is an effusion high in cholesterol.

Causes:

  • Traumatic e.g. Direct laceration from surgery e.g. Open heart surgery.
  • nontraumatic most common is malignancy e.g. Lymphoma, left-heart failure, infections and developmental abnormalities e.g. Down syndrome and noonan syndrome.

Treatment:

  • Drainage
  • pleuroperitoneal shunting
  • Pleurodesis
  • omitting fat from the diet.
40
Q

Describe Extrinsic Allergic Alveolitis, its causes, features, and management..

A

In sensitised individuals inhalations of allergens provokes a hypersensitivity reaction. In the acute phase the alveoli are infiltrated with acute inflammatory cells. With chronic exposure granuloma formation and obliterative bronchiolitis occurs.

Causes:

  • Bird-fancier’s lung (Proteins in bird droppings)
  • Farmer’s Lung (Micropolyspora Faeni, Thermoactinomyces vulgaris)
  • Malt Worker’s Lung (Aspergillus clavatus)
  • Bagassosis or Sugar Worker’s lung (thermactinomyces sacchari)
  • Nitrofuratoin

Features:

  • Acute: Fever, rigors, myalgia, dry cough, dyspnoea, crackles
  • Chronic: Increasing dyspnoea, weight loss, type 1 respiratory failure, cor pulmonale
  • Bloods: neutrophilia, raised ESR,
  • CXR: Upper zone fibrosis Hilary lymphadenopathy

Management:
-remove allergen and give O2
-prednisolone 40mg OD followed by reducing dose
:

41
Q

Describe Pulmonary Emobilism Severity Index (PESI)

A

Predicts 30-day outcome of patients with pulmonary emobilism using 11 clinical criteria.

If the patient is considered very low (Less than 65) or low risk (66-85) by the PESI score, patient has an overall low risk of mortality or severe morbidity and outpatient management should be considered

If the patient is considered intermediate (86-105), high risk (106-15) or very high risk (over 125) by the PESI the patient has an overal high risk of mortality and severe morbidity and higher levels of care e.g. ICU should be considered.

42
Q

What factors shift the Oxygen Dissociation Curve to the Left?

A

Oxygen dissociated curve shift to the left means lower oxygen delivery.

The L rule:
Low H+ (Alkali)
Low pCO2
Low 2,3-DPG
Low temperature

And HbF, Methaemoglobin, Carboxyhaemoglobin.

43
Q

What factors shift the Oxygen Dissociation Curve to the right?

A

Oxygen dissociation curve shift to the right means raised oxygen delivery.

‘CADET, Face Right’

CO2 raised
Acid - Raised H+
DPG - Raised 2,3-DPG
Exercise
Temperature - Raised
44
Q

Describe Crack Lung, its features, and management.

A

Features: Patients present with sympathetic hyperactivity such as tachycardia, Hypertension, dilated pupils and chest pain, productive cough, dyspnoea and hypoexamia along with fever, haemoptysis and respiratory failure. There may be pneumothorax, pneumomediastinum, Pulmonary haemorrhage usually due to the vaslava manoeuvre performed whilst smoking.

Management:
-Most cases are conservative may require ventilatory supports or corticosteroids may have a role.

45
Q

What are the mechanisms of hypoxia?

A

Hypoventilation e.g. CNS depression, Obesity hypoventilation, muscular weakness, poor chest wall elasticity.

V/Q mismatch i.e. increased A-a gradient e.g. COPD, Asthma, pulmonary vascular disease, ILD

Right-to-left shunt (Shunt equation Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2). Causes may be anatomical e.g. AVM, Intracardiac shunt, Hepatopulmonary syndrome, or physiological e.g. pneumonia, ARDS

Diffusion Limitation e.g. ILD or exercise, lack of time for oxygenation to occur.

Reduced inspired oxygen tension e.g.s altitude

46
Q

What is TLCO (Transfer factor)?

A

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

Causes of a raised TLCO:

  • Asthma
  • Pulmonary Haemorrhage (Wegener’s, Goodpasture’s)
  • Left-to-right cardiac shunts
  • Polycythaemia
  • Hyperkinetic states
  • Male gender, exercise

Causes of a lower TLCO:

  • Pulmonary Fibrosis
  • Pnemonia
  • Pulmonary Embolism
  • Pulmonary Oedema
  • Emphysema
  • Anaemia
  • Low cardiac output

KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO:

  • Pneumonectomy/lobectomy
  • Scoliosis/Kyphosis
  • Neuromuscular weakness
  • Ankylosis of costovertebral joints e.g. ankylosing spondylitis.
47
Q

Describe Tracheostomy, its indications, and complications.

A

A tracheostomy is a surgical procedure which consist of making an incision on the anterior aspect of the neck and opening a direct away through the incision into the trachea.

Indications:

  • After a period of time following intubation with an endotracheal tube
  • reduced sedation
  • improved patient communication
  • possible reduction in laryngeal damage
  • nursing care potentially easier
  • Facilitation of weaning.

Complications:

  • Displacement or obstruction - Evidenced by failing gas exchange, unexpected ventilator pressures, patient may be able to talk despite cuff inflated. If available use capnography to detect oscillating FiCO2 and determine if obstructed or not. Remove inner tube, and check for secretion build up. try passing suction catheter.
  • Infection early or late good stoma care should prevent this
  • Bleeding, local erosion at entry site, damage from vigorous suctioning, more seriously erosion by tracheostomy tip or high pressure balloon cuff rarely into the innominate artery which lies anteriorly.
48
Q

Describe NIV, its indications, Contradindications, implementation, and weaning.

A

Indications:

  • pH less than 7.35, pCO2 over 6
  • COPD
  • Neuromuscular disease
  • Obesity hypoventilation syndrome

Contra-indications:

  • Vomiting
  • Facial burns/trauma/recent surgery
  • Fixed upper airways obstruction
  • Undrained pneumothorax
  • Relative contraindications: life-threatening hypoxaemia, severe co-morbidity, confusion/agitation, inability to protect airway, Haemodynamically unstable, copious secretion.

Implentation:

  • In COPD start at 15/4 then increase to 20/4 in first 30mins. Repeat ABG if no significant improvement increase to 22/4, and if still no improvement continue to increase up to 30/4.
  • In Neuromuscular disease start at 10/4, increase to 12/4 in first 30mins. Repeat ABG if no significant improvement increase to 14/4 and if still no improvement continue to increase up to 16/4.
  • In obesity hypoventilation syndrome start at 15/6 and increase to 20/6 in first 30 mins. Repeat ABG if no significant improvement increase to 24/8 and if still no improvement continue to increase to 30/8.

Weaning:
-Once pH has normalised begin weaning, starting with meal breaks for 24 hours with overnight continuous NIV, then 2hrly breaks, then 4hrly breaks then just overnight NIV. Assess weaning each day with repeat ABG.

49
Q

What is the Hering-Breurer Reflex?

A

A reflex triggered to prevent over-inflation of the lung. Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching by sending action potentials via the vagus nerve to the inspiratory area in the medulla and apneustic area of the pons. In response the insularity area is inhibited directly and the apneustic area is inhibited from activating the inspiratory area this inhibits inspiration, allowing expiration to occur.

50
Q

What are the different lung segments?

A

Right lung is divided into three lobes and ten segments:

  • Right upper lobe - Apical, Posterior, Anterior
  • Right Middle lobe - Lateral, medial
  • Right Lower lobe - superior, medial, anterior, lateral, posterior.

The left lung is divided into two lobes and eight segments:

  • Left Upper lobe - Apicoposterior, Anterior, Superior lingular, Inferior lingular
  • Left Lower lobe - Superiorm anteriomedial, lateral, posterior.
51
Q

What is Lofgren’s syndrome?

A

Acute sarcoidosis characterised by bilateral hilarity lymphadenopathy, erythema nodosum, fever and polyarthralgia. It typically occurs in young females and carries an excellent prognosis.

52
Q

What is the mechanism leading to hypecalcaemia in Sarcoidosis?

A

1-alpha-hydroxylase is activated by macrophages in sarcoid granulomas and Converts 25-hydroycitamin D3 to 1,25 dihydroxyvitamin D3, the active form of the vitamin leading to absorption of calcium from the gut and increased renal calcium absorption from the distal tubule.

53
Q

Describe the PERC rule for pulmonary embolism.

A

Rules out PE if no criteria are present and pre-test probability is less than 15%.

The PERC rules can be applied to patients where the diagnosis of PE is being considered but the patient is deemed low-risk.

PERC 1 point for:

  • Age over 50
  • HR over 100
  • SpO2 less than 95%
  • Unilateral leg swelling
  • Haemoptysis
  • Recent surgery or trauma (1 month)
  • Prior PE/DVT
  • Hormone use

A single point means the patients will likely require well’s criteria and D-dimer to further evaluate. If this criteria scores 0 can be safely discharged without FU or D-Dimer.

54
Q

Describe Chronic Thromboembolic Pulmonary Hypertension, its features, investigations, and management.

A

Only potential curable form of pulmonary hypertension. Pulmonary hypertension secondary to chronic PE.

Features: Progressive Dyspnoea, exercise intolerance.

Investiations:

  • V/Q scan imaging of choice the. Right Heart Catheterisation / Pulmonary angiography.
  • Diagnosis depends on pulmonary hypertension present i.e. PAP over 25mmHg in absence of elevated PCWP (i.e. less than 15mmHg).
  • Evidence of thromboembolic occlusion in the proximal or distal vasculature.

Management:
-pulmonary endarectomy

55
Q

Describe Cryptogenic Organising Pneumonia, its causes, and features

A

A form of non-infectious pneumonia, more specifically an inflammation of the bronchioles and surrounding lung tissue.

Cause: It is often a complications of existing chronic inflammatory disease such as RA, Dermatomyositis, or a side effect of medications such as Amiodarone.

Features: Radiological features of pneumonia, That tends to affect different areas on serial imaging. SOB, fevers, fatigue, cough.

56
Q

Describes Bronchiolitis Obliterans and its features.

A

Aka popcorn lung. Causes include toxic fumes, Connective tissue disorder, or complications following bone marrow or heart-lung transplant.

Features: Dry cough, SOB, wheezing, Lethargy.

Investigations: HRCT, Lung function tests, Biopsy. Chest X-ray is often normal.

57
Q

Describe Byssinosis, and its features

A

Aka Brown lung disease, an occupational lung disease caused by exposure to cotton. Occurs in workers of yarn and fabric manufactures thought to be due to endotoxins from walls of gram-negative bacteria that grow on cotton.

Features: Breathing Difficulties, chest tightness, wheezing, cough.

58
Q

What is the sniff test?

A

The fluoroscopic sniff test, also known as diaphragm fluoroscopy, is used most often to confirm absence of muscular contraction of the diaphragm during inspiration in patient with phrenic nerve palsy or breathing difficulties following a stroke.

During a sniff the diaphragm contract during inspiration (moves downwards) and relapses during expiration and both hemidiaphrams move together. If there is a diaphragmatic palsy the affected diaphragm does not move downwards during inspiration and even paradoxical motion can occur.

59
Q

What are the normal values for Lung function testing?

A

In 70kg man:

Peak Expiratory flow 520-700l/min
Total Lung capacity 5-6.5L
Functional Residual Capacity 2-3L
Tidal Volume 500 - 700mL
Inspiratory reserve volume 3300mL
60
Q

What are the monoclonal antibodies used in severe asthma?

A

Omazilzumab is used in severe asthma with raised IgE

Mepolizumab is used in severe asthma with eosinophilia

61
Q

Describe idiopathic pulmonary haemosiderosis

A

Characterised by alveolar capillary bleeding and accumulation of haemosiderin in the lungs. May be associated with circulating anti-GBM antibodies and cow’s milk hypersensitivity

Features: Haemoptysis, Diffuse parenchyma infiltrates on chest radiographs and IDA. Usually found in children. 2-8

Management:

  • Corticosteroids
  • steroid sparing immunotherapies.
62
Q

Describe Aspergilloma, its features and management

A

Features: Fevers, cough, Haemoptysis CXR shows consolidation in cavity with halo sign ring of air around fungus ball.

Management:
-Surgical resection is first line unless poor lung function in which case oral itraconazole is used.

63
Q

Describe Chronic Eosinophilic Pneumonia, its features, and its management

A

Eosinophilic pneumonia is a rare respiratory pathology characterised by pulmonary infiltrates and pulmonary eosinophilia. It can be idiopathic or secondary to parasites, drugs or systemic diseases such as vasculitis. The peripheral Eosinophil count is not always raised. The serum IgG is raised in two-thirds of patients and the ESR is elevated. Sputum and Bronchoalveolar Lavage often show and eosinophilia.

Features:
This presents over months to years, usually occurs in those aged in their 50s with a. Female to male ration 2:1. It can be irreversible. About 60% of patients with CEP have asthma and 90% are non-smokers. Patients present with constitutional symptoms, cough, wheeze, and fever. Chest X-RAY often shows the opposite of pulmonary oedema with bilateral pulmonary infiltrates in the out two thirds of the lung.

Management:
Steroids.

64
Q

Describe Usual Interstitial Pneumonia, its features and causes.

A

A histopathologic and radiologic pattern of interstitial lung disease which is the hallmark pattern of idiopathic Pulmonary Fibrosis.

Features: On imaging, UIP usually presents with a lung volume loss and a craniocaudal gradient of peripheral septal thickening, bronchiectasis and honeycombing.

Causes:

  • Idiopathic Pulmonary fibrosis
  • rheumatoid Arthritis (UIP is the most dominant pattern)
  • Systemic Sclerosis (NSIP more common than UIP)
  • Polymysitis (A UIP, NSIP or COP pattern)
  • mixed connective tissues disease (Either UIP or NSIP)
  • Asbestosis
  • Chronic Hypersensitivity Pneumoniitis
  • Radiation pneumonitis
  • Amiodarone lung
  • Hermansky-Pudlak Syndrome
65
Q

Describe Non-Specific Interstitial Pneumonia, its types, features and causes.

A

The second most common morphological and pathological pattern of interstitial lung diseases.

Types:

  • Fibrotic Type: Most Common, worse outcome
  • Cellular type: Less common, better prognosis due to good treatment response.

Features: Symmetric Bilateral ground-glass opacities with associated fine reticulations and volume loss resulting in traction Bronchiectasis. Immediate Subpleural sparing is considered very specific for NSIP.

Causes: Connective Tissue disorders, RA, PBC, Hashimoto’s Thyroiditis, Chemotherapy induced lung disease, Hypersenitivity lung disease. HIV, IgG4 disease. MDS.

66
Q

What are the main differentiating features between UIP and NSIP?

A

NSIP: Bilateral Ground-glass Opacities with fine reticulations and sparing of the immediate subpleural space.

UIP: Macroscopic Honeycombing

67
Q

What are the physiological effects of CPAP?

A

Improved gas exchange ( Particularly oxygenation)

Reduced work of breathing

Offloads the left ventricle as the positive pressure applied counteracts the normal negative pressure which normally cause LVEDV to increase impairing cardiac function. The positive pressure leads to Lower LVEDV and increased stroke volume

68
Q

What is pressure support?

A

The difference between IPAP and EPAP

69
Q

Describe the principles of adjusting NIV therapy

A

If hypoxaemic increase CPAP up to 10cmh20 and increase FiO2

If tachypneoic and acidotic increase IPAP in 2cmh20 increments as tolerated

If asynchronous check mask fit, assess intrinsic PEEP or trigger sensitivity

70
Q

Describe the management of Empyema

A
  • Broad-spectrum IV Antibiotics
  • Urgent Intrapleural chest drainage
  • If not resolving within 48hrs consider discussing with Thoracic surgeons:
  • VATS /Open Thoracotomy.
  • TPA/DNAase may be used in loculated lesions, MIST 2 Protocol showed reduction in need for Surgery and reduced length of stay when used.
71
Q

Describe Hermansky-Pudlák syndrome and its features.

A

An extremely rare autosomal recessive condition which results in oculocutaenous albinism, bleeding problems, and storage of an abnormal fat protein compound. Affects 1 in 500000 and more common in Puerto Rican’s ( 1 in 1800).

Features:

  • albinism and eye problems, individuals will have varying amounts of melanin. This leads to photophobia, impaired vision, strabismus and nystagmus
  • bleeding disorders, platelet dysfunction leads to abnormal clotting.
  • cellular storage disorders, wa lax substance to accumulate in the lungs and kidneys leading to fibrosis.
72
Q

Describe the DECAF score for Acute exacerbation of COPD.

A

For use in patients over 35yrs old hospitalised with IECOPD.

1) (On a good day, within the last 3 months) Extended MRC Dyspnoea scale
- score 1-4 = 0 Points,
- score 5a (Too dysgenic to leave the house but independent with washing/dressing) +1
- Too dyspneic to leave the house and wash/dress 5b = +2

2) Eosinopenia Eos less than 0.05 = +1
3) Consolidation on CXR = +1
4) Acidaemia pH less than 7.3 = +1
5) AF on ECG or Hx of AF = +1

A score of 0-1 is associated with a mortality risk of 0-1.5% and these patients can be considered for early discharge.

A score of 2 is associated with 5.4% in-hospital mortality these patients require clinical judgement regarding early discharge.

A score of 3-6 is associated with 15.3%-50% mortality these patients should not only be kept in hospital but might benefit from early ITU involvement or Palliative care.

73
Q

What is Caplan’s syndrome?

A

A combination of Rheumatoid Arthritis and Pneumoconiosis that manifests as intrapulmonary nodules which appear homogenous and well defined on CXR. Occurs in dust-exposed persons with RA or subsequently develop RA within 5-10years. Usually related to mining dust (Coal, Asbestos, Silica)

Features: Cough, SOB, Joint Pain/ Swelling

Management:
-Exclude TB and manage with steroids.

74
Q

Describe the management of Pulmonary nodules.

A

If CT shows Solid non-calcified nodules and there are clear features of benign disease (e.g. Hamartoma, typical peri-fissures nodule), or nodule less than 5mm diameter (or 80mm3) or patient unfit for any surgery they can be discharged.

If the nodule is less than 8mm diameter or 300mm3 they can under go CT Surveillance. Otherwise they need to be risk assessed using Brock Model.

If less than 10% risk of malignancy with brock model they can undergo CT Surveillance, if over 10% they require PET-CT with risk assessment using Herder Model.

If the risk of malignancy is less than 10% with Herder model they can undergo CT Surveillance, 10-70% risk should be considered for CT-Guided biopsy or excision biopsy, or CT Surveliannce guided by individual risk and patient preference. If the risk is over 70% excision or non-surgical treatment (+/- image guided biopsy) should be considered.

CT Surveillance depends on the initial size. If 5-6mm CT 1 year after baseline and calculate the Volume Doubling Time (VDT). If Volume over 80mm3 or 6mm diameter repeat CT in 3 months.

If VDT less than 400days or clear evidence of growth further work up is needed. If stable in diameter repeat CT at 2 years, if stable in volume discharge. If VDT over 600 days consider discharge. If VDT 400-600 consider biopsy or further surveillance.

75
Q

Describe Brock Model for pulmonary nodule assessment.

A

A scoring calculator that outputs a Malignacy probability based on nodule size and number, type (Solid, pure ground glass, part solid), Location, speculation, and patient demographics such as age, sex, FHx and presence of emphysema.

76
Q

Describe the Herder Model score for pulmonary nodules

A

A scoring system which outputs a probability of malignancy in patients who have under gone PET-CT.

It takes into account, age, smoking status, history of malignancy, nodule size and location, spiculation. And PET Activity (No, Faint, Moderate or Intense FDG)