Learning objectives AH1 - Respiratory Flashcards by keenin stone

Learning objectives for respiratory medicine:

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Use of PFTs?

Indications?

Contraindications?

Risks?

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What is normal FEV1/FVC?

What does ratio indicated obstruction?

What is the ratio in restrictive lung disease?

What is your DDX for obstructive PFTs?

What is your DDx for restrictive PFTs?

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What value do flow volume loops have?

What is it based on?

What are the findings on flow volume loop of an obstructive condition?

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What is meant by Reversibility in PFTs with asthma? E.g what are the values that would indicated this when pt given salbutamol?

What is your differential diagnosis for restrictive lung disease? - think - interstial pleuram NM, chest wall disease.

What are the findings you would expect on PFTs+ Flow volume loop in restrictive lung conditions?

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Outline a stepwise approach to interpreting PFTs:

Whats the importance of RV and TLC in obstructive?

How do you assess small airways?

Whats the importance of DlcO?

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What is the Diffusion lung Carbon monoxide test (DLCO)

How is the test done? How long do they hold their breath? What is the normal range?

What conditions cause an decrease diffusion capacity? Which can be increased

What conditions have normal PFTS but decreased DLCO test?

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What is Bronchectasis? What is the definition of it?

What are the eitologies? Congenital? Post-infectious? Obstruction?

Pathogens commonly involved in bronchiectasis?

Pathogenesis?

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What are the clinical features associated with Bronchiectasis?

Consititutional? Respiratory ?Signs of exacerbations(2/3) needed?

What examination findings would you expect?

Inspection, Vitals, Peripheries, JVP, Chest?

What are diagnostic investigations? (CT diagnostic)

What are CXR findings associated with Bronchiectasis? CT Findings? - 2 marks

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What investigations should be done to determine underlying cause of bronchiectasis?

What are the general Management measures? Abx? Bronchodilators? Ongoing monitoring? Closing?

What role does palliative care have in Bronchiectasis? (what do they provide)

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What is the definition of COPD? Overview read

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Case examples for patients with COPD: BMJ

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History and examination findings in COPD: Outline:

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What are spirometry values needed for diagnosis of COPD?

What are the GOLD criteria for severity of COPD? (FEV1 score)

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What are 4 key factors on history and 8 on examination which could be expected in COPD?

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More factors on examination for COPD?

What are major risk factors for COPD? List 5

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First line investigatons in COPD? (3 marks)

Investigations to consider? Ongoing

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Differential diagnosis for COPD? (pt presenting with COPD like symptoms) List 6 (3 marks)

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What do you need to continually address and monitor when managing a patient with COPD? (think symptoms, use of medications (puffers +steroid), no of exacerbation, vaccination, exposures etc)

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What is the intial pharmacological interventions in COPD?

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COPD management continued: Read - based on severity

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What is COPD X? What does it stand for? Explain

What are risk factors for COPD?

C – confirm diagnosis (FEV/FVC <70%)

O – Optimised function:

Pharmacological intervention
Pulmonary rehabilitation
Exercise and healthy eating

P – Prevent deterioration

Smoking cessation
Vaccines (influenza and pneumococcal)
Long term low flow oxygen therapy

D - Develop supportive networks and self-management skills

Written COPD action plans are an important component of comprehensive self-management.

X - Exacerbation management

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C- COPD X - Confirm diagnosis -

How is a diagnosis of COPD made, what investigations will support this diagnosis?

Diagnosis made on combination of

History

Exam findings

Spirometry
FEV1/FVC <70%
Irreversible with bronchodilator
RV + TLC increased
DLCO reduced
COPD Assessment Score (CAT)
Validated questionnaire

Others

CXR - features, rule out LuCa
COPD Assessment Score (CAT)
ABG - CO2 retainers have chronically ↑PaCO2 with compensatory ↑HCO3 and normal pH

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How do you differentiate COPD from Asthma? Hx? Examination findings? Clinical signs. (Outline assessment findings COPD vs asthma)

How do you determine the severity of COPD? (think symptoms, exacerbations, other comorbidites) What self assessment scores can be used to determine severity?

Outline overall management of COPD: Non-pharmacological? (smoking, vaccination, action plan, physio, excercise, pulmonary rehabiliatation) Pharmacological management? Mild, moderate, severe-palliative Ongoing monitoring?

Complications of COPD? + Comorbidities to consider

Important complications and comorbidities include: * CVD: * Cardio-selective ß-blockers are generally safe and well tolerated for patients with COPD * Avoid ßB if significantly overlapping asthma. * Anxiety and depression: * Associated with worse prognosis and increased hospitalisations. * Pulmonary rehab –\> reduces symptoms of both anxiety and depression. * Osteoporosis: * BMD is 10% lower on average than controls. * Manage as osteoporosis guidelines. * Diabetes * COPD –\> increased risk of DM & increased risk of diabetic complications 2º to ICS * Regularly monitor BSLs * Limit short courses of PO corticosteroids +/- escalation of hypoglycaemic therapy during course. * pHTN & Cor Pulmonale: * mild-mod pHTN is common complications * pVasculature remodelling 2º hypoxia, inflammation and loss of capillaries . * Severe pHTN – rare; diagnosed if pulmonary artery pressure \>35mmHg and is disproportionally high compared to current level of lung damage. * Cor Pulmonale: * Consider if – peripheral oedema, eJVP; systolic parasternal heaves; loud P2 * Assess need for long-term O2 * Consider diuretics if oedema. **Other complications of COPD:** * **Secondary Pneumothorax due to rupture of bullae** * **Chronic respiratory failure** * **Acute exacerbation of COPD**

O -Optimise function: Where to start? What non-pharm strategies are recommended?

* Assessment is the first step to optimising function * a validated assessment tool is a convenient way to measure baseline functional status and to measure response to treatment

O - Optimise continued- Approach to prescribing pharmacological therapies: Key points.

O - Optimise continued- Approach to prescribing pharmacological therapies: Key points. When should inhaler technique be reviewed? When Should treatment of comorbidities be optimised?

Stepwise approach: • For all patients, check: Adherence with COPD management strategies involves patients’ knowledge of their non-pharmacological and pharmacological treatment strategies, motivation, skill and physical ability with inhaler technique, health literacy, cost of medicines, willingness to pay, use of multiple inhalers and treatment for comorbidities. - adherence with non-pharmacological (e.g. smoking cessation, immunisation, exercise and oxygen therapy) and pharmacological treatment strategies regularly, preferably at each visit. SR ME - inhaler technique at each visit, especially in older, frail and cognitively impaired patients. SR ME • Consider a home medicines review by a consultant pharmacist.

When should referral to specialist be made with patients with COPD?

P- Prevent deterioration Whats the importance of giving smoking cessation advice; What is the 5 'as strategy- Brief intervention? How can exacerbations risk be reduced? What immunizations are needed for patients with COPD?

Why give smoking cessation advice? * Smoking cessation is the most important intervention to prevent worsening of COPD * Smoking cessation reduces the rate of decline in lung function [I]. * Smoking cessation advice from health professionals can increase quit rates [II]. * The major effect is to help motivate a quit attempt. (Zwar 2014) * Personalising smoking cessation advice based on lung age and the lung age * calculator may increase cessation rates [III]. (Parkes 2008) * Anxiety and depression are associated with high rates of smoking and reduce the likelihood of success of smoking cessation [III-2]. (Jimenez-Ruiz 2015) * Counselling combined with nicotine replacement therapy, bupropion, varenicline is more effective than counselling alone [I-II]. (Tashkin 2011) * In more nicotine dependent smokers, the combination of a nicotine patch with a rapid delivery form of nicotine replacement (e.g. gum) is more effective than one form alone [I]. (Stead 2012) * Based on a small number of trials, varenicline is more effective than nicotine replacement monotherapy but equally effective as a nicotine replacement combination therapy. • Flag current smokers for brief smoking cessation advice or referral to local programs. • Refer to best practice for brief smoking cessation counselling which is summarised in the 5-A strategy: - Ask and identify smokers at every visit. - Assess nicotine dependence and motivation to quit. - Advise about the risks of smoking and benefits of quitting. - Assist cessation by offering behavioural counselling and pharmacotherapy. - Arrange follow-up within a week of the quit date and one month after. A combination of pharmacological interventions and non-pharmacological strategies such as counselling and exercise improve effect.

P-Prevent deterioration- What immunizations are needed for patients with COPD? Why immunize against these? When should be mucolytics be used? Who benefits from long term oxygen in COPD

D - Develop a care plan: What good chronic disease care? How can health professionals improve quality of life and reduce disability? (what does this entail at GP level)

D - Develop a care plan: What is self-management support and how can patients with COPD benefit? (e.g there action plan, self management education, excercise training, psychosocial support) read What other services can a patient with COPD benefit? When and how should end stage palliative care be considered?

End-Stage & Palliative Care **Prognosis:** * Each exacerbation requiring hospitalisation increases the subsequent mortality risk * Consider end-of-life discussion and palliative care treatment when: * FEV1 \<25% * O2 dependence * Respiratory failure * Heart failure or other comorbidities * Weight loss or cachexia * Decreased functional status * Increased dependence on others * Advanced age. **Discussions:** * Include resuscitation and intubation wishes * Advanced care planning in outpatient setting. * Medical EPOA appointment. * Ensure patient and caregivers are aware of palliative care services **Treatment Offerings / Symptom Management:** * Physiotherapy +/- OT for chest clearance * Low-dose opioids +/- anxiolytics (lorazepam) * Palliative oxygen therapy – must not be smoking. Create at home care plan, so many of the symptoms can be managed at home preventing hospitalisation End-Stage & Palliative Care **Prognosis:** * Each exacerbation requiring hospitalisation increases the subsequent mortality risk * Consider end-of-life discussion and palliative care treatment when: * FEV1 \<25% * O2 dependence * Respiratory failure * Heart failure or other comorbidities * Weight loss or cachexia * Decreased functional status * Increased dependence on others * Advanced age. **Discussions:** * Include resuscitation and intubation wishes * Advanced care planning in outpatient setting. * Medical EPOA appointment. * Ensure patient and caregivers are aware of palliative care services **Treatment Offerings / Symptom Management:** * Physiotherapy +/- OT for chest clearance * Low-dose opioids +/- anxiolytics (lorazepam) * Palliative oxygen therapy – must not be smoking. Create at home care plan, so many of the symptoms can be managed at home preventing hospitalisation

X- Manage Exacerbations: How is a COPD exacerbation defined? What are the benefits of early diagnosis and treatment of exacerbations: What is the role of an COPD action plan?

How is a COPD exacerbation defined? * **A COPD exacerbation is characterised by a change in the patient’s baseline dyspnoea, cough and / or sputum that is beyond normal day-to-day variations, is acute in onset and may warrant a change in regular medicine or hospital admission.** * The greatest predictor of an exacerbation is a history of exacerbations as these events cluster in time and become more frequent as the severity of COPD worsens * Exacerbations become more frequent in those with a history of prior exacerbations, more severe disease (based on FEV1) and other predictors (including history of heartburn, poorer quality of life and elevated white cell count) * Triggers for exacerbations include viral or bacterial respiratory infection, left ventricular failure, psychosocial stressors and air pollution [III-2]. * Pulmonary embolism should be considered in patients who require hospitalisation for an acute exacerbation

X- Manage exacerbations: When should a patient with COPD be hospitalised? (list 4-6 reason) 2-3 marks: Can patients with an excerbation be treated at home?

X- Manage exacerbations: Are inhaled bronchodilators effective for excerbations? When, how and what doses should be given? What role does oral corticosteroids have for treating excerbations?

X- Manage Excerbations When are antibiotics beneficial in treating a patient with an excerbation? (e.g clinical features of infection)? Is oxygen beneficial in treating a patient with an excerbation? (e.g treat hypoxaemia!) When is non-invasive ventilation effective? (think ABG) Following an excerbation how soon can pulmoary rehabilitation be started?

X: Manage excerbations: What is the best approach to post-hospital care after an excerbation? (discharge plan, intergrated care approach, self management etc)

What is the Modified medical research council dyspnoea scale? (what are the gradigs and what do they represent)

COPD STEPWISE MANAGEMENT OF STABLE COPD: (stepwise management model) Mild, Moderate, Severe? Confirm diagnosis: Optimise function+Develop care plan Non-Pharm interventions: Pharmacological interventions:

Algorithm: Managing excerbation: COPD X: Outline approach: What to do initially when patient is having increased symptoms (sputum, cough, sob all increasing) What is the first option? Second option (COPD action plan)? When to send to hospital? (list 5) 2.5 marks

Managing a COPD Excerbation checklist: (COPD X) what should be done in 1) Hospital (List 6) 2) Prior to leaving the hospital (List 8) 3) Ongoing care (1-4 weeks post discharge) (list 6)

**Acute excerbations of COPD:** What are the major features to diganose or suspect this? Eitology: Infective vs Non infective? What are three common bacteria? (H.influenzae, m,cattarhalis, S.pneumoniae) Differential diagnosis? What should you rule out??? (PE, LVHF) Clinical features? History?

**Acute excerbations of COPD:** What are your examination findings? (3 marks) What Investigations need to be completed? List 6-8 (3-4 marks) Explain what your looking for in each Investigation: How is an infective excerbation diagnosed? How is a non-infective excerbation diagnosed? When should a patient be admitted?

What is the acute management? Medical (Bronchodilators, systemic corticosteroids, antibiotics, nebulised mucolytics + chest physiotherapy) + Supportive management? (4 marks:

Pulmoary function tests: Compare Obstrutive vs restrictive volume flow loops: What would you expect TLC to be in each? What are 4 ddx for obstructive picture? (2 marks) What are 4 DDx for restrictive lung picture?

Interpreting CXR: Consolidation: Signs on CXR- What are common DDX (3 marks) Reticular (interstial disease)- What are signs on CXR? What are 6 diseases that cause this picture? 3 Marks Nodular- Cavitary vs non-cavitary - What is you DDx- Think ((Neoplasm/infectious/inflammatory (RA, sarcoid, GPA, IPF))

Airways * Start at the top in the midline and review the airways. * trace down the trachea to the carina * is it straight and midline? * is there any narrowing? * trace down both main bronchi * is the carina wide (more than 100 degrees)? * is there bronchial narrowing or cut-off? * is there any inhaled foreign body? * Read more: chest x-ray assessment of the airways Breathing * Look for lung and pleural pathology. * both lungs should be well expanded and similar in volume * can you count 10 posterior ribs bilaterally? * is one lung larger than the other? * compare the apical, upper, middle and lower zones in turn * are they symmetrical? * are there areas of increased density? * trace the lung vessels * do they branch out progressively and uniformly? * can you see the retrocardiac and retrodiaphragmatic lung vessels? * are there extra lines in the periphery that aren't vessels? * trace the lateral margins of the lung to the costophrenic angles * are the costophrenic angles crisp? * trace the hemidiaphragms in to the vertebra * can you see the whole of the hemidiaphragm? * trace the cardiac borders * can you clearly see the left and right heart border? * can you see the descending aorta? * Read more: chest x-ray assessment of lungs and pleural spaces Circulation * Look at the heart and vessels (systemic and pulmonary). * check the cardiac position * is 1/3 to the right and 2/3 to the left? * assess cardiac size * is the cardiothoracic ratio \< 50%? * check the position and size of the aortic arch and pulmonary trunk * check the width of the upper mediastinum * look at the hilar vessels * can you see them clearly on both sides? * are they at a similar height? * can you see a preserved hilar point bilaterally? * Read more: chest x-ray assessment of the cardiomediastinum Disability * Check for any bony pathology (fracture or metastasis). * trace along each posterior (horizontal) rib on one side of the chest * is there a fracture or abnormal area? * repeat with the other side of the chest * now trace lateral and anterior ribs on the first side * repeat on the other side * now, check the clavicles and shoulders * can you trace around the cortex of the bones? * finally the check the vertebral bodies * are they all rectangular and of a similar height? * can you see 2 pedicles per vertebral body? * are there disc spaces? Read more: chest x-ray assessment of the bony thorax **Everything else** * Review the upper abdomen, soft tissues and take a look at some final check areas. * is there free gas under the diaphragms? * is there subcutaneous emphysema? * is the gastric bubble in the correct place? * is there a hiatus hernia? * is there an absent breast shadow? * are there any surgical clips? * check again... * are the lung apices clear? * is there any retrocardiac or retrodiaphragmatic pathology?

Arterial Blood gases: Outline step by step approach: 1) Ph 2) What is the metabolic disturbance? (metabolic vs respiratory) 3) Is there compensation? 4) If patient has metabolic acidosis- What is the anon gap and osmolar gap? (what does an abnormal osmolar gap indicate) ? 5) if Anion gap is increased, is the change in Bicarbonate the same as the change in anion gap? (if not consider a mixed metabolic picture Differential diagnosis of Respiratory acidosis? (increase PaCo2 secondary to hypoventilation) - E.g Lung diseases (all, Drugs, trauma, stroke, COPD) Differential diagnosis for Respiratory alkalosis? (decrease PaC02 secondary to hyperventilation)

Approach to hypoxaemia: What is the A-a gradient? (decreased DLco) - What do you do (management) give 02! When is DLCo decreased? Ddx? (think ILD, anaemia, emphysema) DCLo increased? (think) (asthma, obesity, polycythemia)

PFTS- Obstructive vs restrictive: How do you define restrictive conditons from PFTs? What is alpha-1 antitrypsin deficency?

What is Asthma? - Define: How does it clinically present? How is asthma defined? (atopic, non-atopic (intrinsic) Eitology (Atopic disease)? Risk factors for asthma?

Pahtogenesis of asthma: Sensitization, Early phase response, Late phase response. How does asthma result in a respiratory acidosis? (airway obstruction causes V/Q mismatch) Gross pathology? (mucus plugs, inflammed bronchi)

DDx for Acute wheeze and dyspnoea (Asthma) 1) Children 2) Adults What is the natural history of asthma attack? What are triggers for asthma? What are the clinical features of asthma? (list 6 atleast) what is the hallmark? - WHat are typical features of asthma?

What needs to be covered in a History in patient with asthma? (consider DDx when taking history) SOCRATES, triggers, associated, DDX, Pmhx, medications, immunizations, allergies, social (big in this) family hx) - 6 marks

What are expected examination findings in Acute asthma attack? Inspection (ABCEDEF), VS, Hands, face, neck, chest, auscultation: (5 marks) What is Status asthmaticus? What is the cause?

How is a diagnosis of asthma made? think Hx, exam, Ruling out other casues, PFT, bronchial challenge test, PEFR (diurnal variation): How is PEFR done? Whats its use? What are the expected results from day to night?

How is asthma severity determined? (mild, moderate, severe)

What is the emergency ACUTE management of acute asthma attack: Risk factors for severe asthma? (1 mark) What is the 4 by 4 approach for children? (2 marks) What are red flags to go to ED (DANGER)? (list 4) Outline Assessment of acute asthma attack: How do we assess? (think vitals, WOB, RR\< O2, behaviour LOC) Mild? Moderate? Severe asthma signs clincally? List life threatening signs in Asthma? What are investigations should be considered in acute asthma?

Asthma attack; First line therapy and management: 1) DRSABC 2) 1st line 3) 2nd line or things to consider 4) After 1 hour reassess 5) Post acute care and discharge after resolution: (think- non pharm 5 a's ) Medictions? Closing?

Maintenance Management of Asthma in adults: THINK (symptom control, education and non pharmological, Medical (preventers, relievers, pred) Saftey net and follow up. What are signs of poor asthma control? (DANGER) need to know ! What are the non-pharm/education 5 as of asthma management? (action plan, avoid triggers, annual vaccines, and educated )

What is an asthma action plan? What needs to be included on it? Drs details, check up dates When well? (regular medication) When not well? (asthma intefering with usual activity) If symptoms get worse? (plan for severe asthma- when to go to hospital)

Pharmacological management of Asthma: What is the stepped approach to asthma management? Step 1, Step 2, Step 3, Step 4, Step 5. What is a common starting regimen for asthma? What other very important things need to be taught and explinaed regarding use of MDI

How do you assess and manage poorly controlled asthma? What need to be assessed (think 5 as of asthma) How do you manage excercise induced asthma? Children under 6 with newly diagnosed reactive airways disease: Management prinicple:

How and when do you review asthma? (Monitor for DANGER symptoms) What is defined as poor asthma control? How often should an asthma action plan be reviewed? How is MDI with a spacer used? (adults 6+) (NOTE always use a spacer) What other things (e.g cleaning spacer etc)

OSCE example: Childs asthma not well controlled: Assess this patient: Think... Hx (symptoms,triggers, dangers, Pmhx, social, asthma history Management: Review entire management plan: Non-pharm (5as) - 2.5 marks? Medical management?

What are important medications in the mangement of Asthma? MOA? Indications (use)? Adverse effects? Beta agonists (beta 2 agonists) Anticholinergics (sama/lama) Corticosteroids? Cromolyns? Montelukast?

**Respiratory tract infections:** URTIs vs LRTIs (children vs adults) Acute bronchitis? What is defined as? (does not have crackles Eitology? Clinical signs? Investigations? Management? What is respiratory synctial virus? Who does it affect? Management?

How are pneumonia (s) classified? What is an Community acquired pneumonia? Epidemiology? Risk factors? Risk factors for severe infection? Aeitology: Viral (list 4) 2 marks? Bacterial (list 4-6) 2 marks? Atypical? (1.5 marks)? What is a tropical pneumonia? What are the risk factors? What are several types?

Community Acquired Pneumonia CAP is a lower respiratory infection due to one or more pathogens acquired outside of a healthcare setting, **Epidemiology:** * Incidence increases with age after 65yo. * Risk factors: * Chronic comorbidities – lung, renal, heart, liver, DM, PPI (treatment) * Behavioural factors – smoking and ETOH * Risk factors of drug-resistant organisms: * Severity of illness * Recent Abx or hospitalisation * Poor functional status * Immunosuppression. **Aetiology/Microbiology:** * Strep. Pneumonia * Atypical bacteria – mycoplasma pneumonia, Chlamydophila pneumoniae, legionella spec. * Viruses – influenza, RSV, parainfluenza, adenovirus.

What is your differential diagnosis for CAP? (resp, cv, systemic?) What are the 4 most common organisms causing CAP? What are Special features of each? (4 marks) What are risk factors for CAP? What is the Presentation/ clinical features of CAP? What are complications of CAP? What are first line investigations for CAP? (3 marks, explain each) bedside, bloods, imaging, other:?

Assessment **Clinical Features:** * Fevers & chills * Cough, increased sputum production, chest pain, SOB * Decreased breath sounds, crackles, egophony, and tactile fremitus overlying area of consolidation. **Investigations:** * Bedside – SpO2 * Bloods – FBC, UECs, LFTs, BC, ?CRP * CXR * Urine – Urinary antigen test (Strep. Pneumonia & legionella), dipstick (?UTI) * Other: * Sputum M/C/S – 40% success rate. * NPA * ABG – appropriate in patietns with high-severity CAP, hypoxaemia or comorbid lung disease.

Atypical CAP: What is it? Why is it called atypical? What are three major organisms causing this? Who do they affect? Clinical features? Management? What are the clinical features? (similiar to cap) What are some specific features for atypical pneumonias? (legionella, mycoplasma,) Investigations and expected findings? Management?

What is Defintion of Pneumoina?' (Toronto notes) Eitology and risk factors? Common organisms in Pneumonia? Clinical features? Investigations and reason+expected result? Treatment? Criteria for hospitilisation? What scoring systems to determine severity of CAP (1 mark)

What are red flags for hospital admission in CAP? What is CURB 65? Whats its use? What is the PSI? Use? What is SMART COP? CORB? uses? Lobar pneumonia, Bronchopneumonia, interstial pneumonia

**Red Flags –\> Hospital Admission:** Patients with the following parameters need close observation and warrant inpatient management. It doesn’t indicate that broader-spectrum empirical Abx are needed. * Tachypnoea (\>22 breaths/min) * Tachycardia \>100bpm * Hypotension (SBP\<90mmHg) * Acute onset confusion * O2 \<92% on RA (or lower than baseline in patients with comorbid lung disease) * Multilobar involvement on CXR * Blood lactate concentraiton \>2mmol/L **CRB-65 & CURB-65** CRB-65 and CURB-65 identify low-risk patients who can usually be safely managed in the community and higher-risk patients requiring admission to hospital. * Limitation = doesn’t account for hypoxaemia, may underestimate severity in younger demographic. * CRB-65 doesn’t require blood tests and therefore may be used in the primary care setting. * Predicts 30-day mortality rate. * N.B CURB-65 has greater specificity than Pneumonia Severity Index (PSI), its alternative scoring method. **SMARTCOP & CORB** * SMART-COP and CORB identify patients that need assessment for intensive care support. * SMART-COP uses more variables, which generally increase sensitivity. * CORB is a simple alternative to SMART-COP and can be used without the collection of blood samples. * SMART-COP: * Assess the likelihood patient with CAP will require invasive respiratory or vasopressor support (IRVS). * It is an appropriate measure of risk stratification in tropical Australia. ###

SMART COP and interpretation + CORB interpretation: Read (risk stratification)

**Interpretation** * 0-2 = low risk of requiring intensive respiratory or vasopressor support (IRVS) * 3-4 = moderate risk of requiring IRVS * 5-6 = high risk of needing IRVS * 7+ = very high risk of needing IRVS Severe CAP = 5+ CORB * Benefit - can do bedside * 1 point for each of * Confusion * O2 ≤90% * RR ≥30 * BP - sBP\<90 or dBP\<60 Interpretation Severe CAP = 2+ * 0-1 = outpatient * 2-3 = inpatient * 3-4 = consider ICU

Assessment of pneumonia: (think red flags- THINK SMART COP) Hx? (3 Marks important points) Examination findings? Auscultation: (5 marks- need to explain each)

What are important first line investigations for patients with suspected CAP? Bedside? Labs? Sputum? Urine? NPA/ CXR?

Management of CAP: Think. ABC, Principles of empirical Antibiotics therapy? Non-supportive measures? IN terms of severity: Mild? Moderate? Severe?

* Low-severity (mild) CAP: * 1) Amoxycillin 1g PO, TDS for 5 to 7 days, OR Doxycycline 100 mg PO, BD for 5 to 7 days * Use clarithromycin if mycoplasma pneumonia is suspected. * Failure to Respond **or suspect that you cannot review patient in 48 hours**: * Combinational therapy – amoxicillin + doxycycline OR admit. * Moderate CAP: * 1) admit to hospital * 2 ID pathogen if possible –\> BC and sputum M/C/S prior to Abx. * 3) empirical Abx: 2-drug regimen: * benzylpenicillin 1.2 g IV, 6hrly until improvement * + Doxycycline PO for 7 days * \*\*Allergic to penicillin –\> Use Ceftriaxone + Doxycycline or clarithromycin. * 4) Step down from IV to oral therapy once clinically stable. * Amoxicillin + doxycycline (or clarithromycin) * 5) timing: * Improvement within 2-3 days =\> 5 days of ABx (IV+orla) * Slow improvement =\> 7 days of ABx (IV+Oral) * Long Abx courses if lung abscess, empyema or parapneumonic effusion. * Severe CAP: * 1) Admit to ICU +/- Ventilator +/- Vasopressor supports. * 2) Empirical Abx within 1hr with cultures. * Ceftriaxone 1g IV + Azithromycin 500mg IV daily * 3) Duration = 7 days (IV+PO). * Severe CAP + Staph aureus: * Warning signs of Staph aureus – rapid progression to sepsis,cavitary, or necrotic pneumonia, multilobular consolidation, post-influenza pneumonia * Empirical Tx = Vancomycin * Severe CAP + Pseudomonas = pip/tax + Azithromycin + gentamycin (if sepsis/septic shock). * Severe aspirational – assumed to be anaerobes: * Empirical = metronidazole 500mg IV q12hrly.

Empirical Aantibiotics flow Chart for CAP: What is directed therapy in penumonia? How long should be given IV? Antibiotics for penumonia: Macrolides SEs? Doxycyline SEs?

Directed therapy * Change according to results of cultures/PCR Duration * IV for 24-48h and clinically improved --\> step down to oral Repeat CXR * At 6 weeks for underlying malignancy Children * Age dependent - need to look up guidelines Neonates * Pathogens- GBS and E coli from maternal perineum * Abx = benzylpenicillin + gentamicin Children after neonatal period * Usually viral Abx for pneumonia Macrolides * Common- azithromycin, erythromycin, clarithromycin SEs * GIT - C.difficile, N&V, diarrhoea, abdominal pain * Headache * CV - prolonged QT, arrhythmias * Hepatic and renal impairment DoxycyclineSEs * GI upset - N&V, diarrhoea * Hepatotoxicity * Photosensitivity rash * Teratogenic * Fanconi syndrome * Stunted growth in children * Hypersensitivity

What is a Hospital acquired penumonia? Definition? Transmission? Pathogens? What GN bacilli? MDR? Viruses? Risk factors for HAP? Risk factors for MRSA? Clinical features of HAP?

Hospital Acquired Pneumonia * Pneumonia that develops in a patient who has been hospitalised for longer than 48 hours, or within 48hrs of discharge. Intubation greatly increases risk of HAP (and these patients may develop ventilation associated pneumonia). * Common causes: gram negative enterobacteriae/ staph aureus. Also pseudomonas, Klebsiella, bacteroides, and anaerobes * In immunocompromised hospital patients: strep pneumoniae, H. Influenzae, S. aureus, M. catarrhalis, M. pneumoniae, gram negative bacilli, and pneumocystitis jirovecii **Risk of MDR/MRSA Infection:** * Depends on – admission ward, length of hospital stay and other factors: * Increased risk if – LOS \>5 days in high-risk ward (ICU, HDU, etc). * These patients require broader spectrum regimen earlier in disease course: * Empirical = Piperacillin + tazobactam * Decreased risk if LOS\<5 days: * Mild disease – amoxycillin + clavulanate (Augmentin). If penicillin allergy cefuroxime * Aspiration pneumonia = Metronidazole IV

Differential diagnosis for HAP? Investigations and reason? Diagnosis? Risk stratification?

**Risk of MDR Infection:** * Depends on – admission ward, length of hospital stay and other factors: * Increased risk if – LOS \>5 days in high-risk ward (ICU, HDU, etc). * These patients require broader spectrum regimen earlier in disease course: * Empirical = Piperacillin + tazobactam * Decreased risk if LOS\<5 days: * Mild disease – amoxycillin + clavulanate (Augmentin). If penicillin allergy cefuroxime * Aspiration pneumonia = Metronidazole IV

Management of HAP and VAP (ventilator associated pneumonia)? What must HAP cover that CAP does not? Mild, Moderate, Severe? Treatment algorithmn: ETG

HAP and VAP management pathways ETG: Review at 48 hours and 72 hours: What must be reviewed?

What are Pathogens common in immunocompromised patients with pneumonia? What would show local infiltrates? What would should diffuse infiltrates? How do you describe Consolidation on CXR? What is the hallmark

Several CXR examples: Lobar Broncho Interstial

Lobar pneumonia examples: RLL, RML, What are complications?

Complications * pulmonary abscess * pleural effusion * parapneumonic effusion - fibrinous inflammatory reaction to the adjacent pulmonary inflammation * empyema - purulent fibrinous inflammatory reaction due to infectious spread into the pleural space- note that both bland and purulent effusions may result in subsequent scarring/adhesions depending on the degree of fibroblastic organisation 2 * disseminated infection * bacteraemia * multiorgan infection

Bronchopneumonia? What is it? CXR findings?

What does an atypical pneumonia look like on CXR? (list 3) What does atelectasis look like on CXR? Aspiration pneumonia?

What is aspiration pneumonia assocaited with? What are the characteristics of an aspiration pneumonia? What are risk factors for aspiration pneumonia? Management? Management of recurrent aspirational pneumonitis? (think speechie, oral hygiene, immunisation, positioning, PEG)

Aspiration Pneumonia * Aspiration pneumonia is usually associated with bulbar dysfunction, impaired consciousness, stroke, myasthenia, and oesophageal disease * Aspiration pneumonitis is characterised by acute chemical injury to the lungs **within hours of aspirating gastric contents.** * Antibiotics are not required in classical aspiration pneumonitis (as gastric contents are normally sterile). * However, aspiration pneumonitis **can develop into aspirational pneumonia.** * Risk factors for aspiration pneumonia include gastric acid suppression and bowel obstruction * Key difference between **aspiration pneumonitis and pneumonia = time of onset**: * Aspiration pneumonitis = **within hrs** * Aspiration pneumonia = **1-2 days.** **Management:** * 1) Manage aspiration pneumonia as community- or hospital-acquired pneumonia initially. * 2) Consider stopping antibiotic therapy if the patient has improved as aspiration pneumonitis is a more likely diagnosis. * Aspiration pneumonitis generally resolves in 24-48hrs. * 3) Failure to respond within 48hrs leads to: * Empirical Abx – Amoxicillin 1g PO q8hrly + Metronidazole 400mg PO q12hrly Management of recurrent aspirational pneumonia: * Swallowing rehabilitation with a speech pathologist * Oral hygiene * Immunisation against Streptococcus pneumoniae * Management of gastro-oesophageal reflux—see Gastro-oesophageal reflux * Positioning the patient to minimise aspiration (eg elevating the head of the bed) * Insertion of a percutaneous endoscopic gastrostomy (PEG) tube.

Aspiration pneumonia: History? List 2 major features (on presentation e.g decline on ward) Key diagnostic factors? (things that make it likely) Risk factors for Aspiration pneumonia?

Pneumonia in Immunosuppressed patients: ETG

What is Directed therapy for pneumonia?

Acute excerbations of COPD: Notes How is this defined? Aeitology? Assessment: History, Clinical features (examination), Clinical features indicating bacteria-thus abxs- Investigation and reasons? Treatments: ABC, O2, SABAs+SAMA/LAMA, Systemic corticosteroids, antibiotics: indicators for admission?

Acute Exacerbation of COPD Acute exacerbation of COPD is characterized by an acute worsening in baseline symptoms (such as cough, dyspnoea, and/or sputum production) beyond normal daily variations to the extent where it requires a change in therapy. * increasing dyspnoea * reduced exercise tolerance * tachypnoea. An exacerbation may also be associated with: * increasing cough frequency * increasing sputum volume and/or purulence, with or without fever * right heart failure, manifesting as ankle oedema. N.B Can be difficult to distinguish between cardiovascular and COPD exacerbation – breathlessness, fatigue and chest discomfort. **Epidemiology:** * 2^nd leading cause of preventable hospitalisation. * Significant morbidity, mortality and healthcare costs. **Aetiology:** * 80% Infection – * Viral – RSV (64%); influenza, * Bacterial – Haemophilus influenza, Moraxella catarrhalis or strep. Pneumonia * Congestive heart failure * PE * Unidentified cause * Drugs – beta blockers * Air pollution * Stress Assessment **History** * Severity of underlying COPD * Duration of worsening or new symptoms * Number of previous exacerbations (total; note how many required hospitalisation) * Comorbidities * Current treatment regimen * Previous need for mechanical ventilation * Recent increased oxygen requirements (if applicable) * Recent degree of difficulty with activities of daily living **Clinical Features:** * Use of accessory respiratory muscles * Paradoxical chest wall movements * Worsening or new-onset central cyanosis * Development of peripheral oedema * Haemodynamic instability * Deteriorated mental status **Clinical Features Suggesting Bacterial Infection & ABx** All three of the following features is suggestive of bacterial infection * Increased sputum volume * Sputum purulence or change in sputum colour * Fever. N.B evidence only supports the use of antibiotics in ICU admissions with little supporting evidence for use in the community or ward based setting. American Guidelines: * ≥3 of – dyspnoea, increased sputum volume, and increased sputum purulence. * Of ≥2 if one is increased sputum purulence. **Investigations:** * Pulse oximetry * CXR * ECG * NPA * Bloods – FBC, UCE, LFTs * Sputum culture – not routine * Spirometry – ? follow up. Treatment **Management:** * ABCs * O2 therapy – aim = 88-92% saturations in patients with hypercapnic respiratory failure. * NIV = standard of care if associated with hypercapnic respiratory failure and acidosis. * SABAs +/- Anticholinergics (as the preferred bronchodilators) * Efficacy is equal; but salbutamol has faster onset. * pMDI with spacer is equally effective as nebuliser if FEV1 ≥30% of predicted. * Systemic corticosteroids: * Prednisone 30-50mg PO Mane for 5/7 * OR Hydrocortisone 100mg IV 6hrly until oral meds are feasible. * Antibiotics if indicated: * 1^st line = amoxicillin or doxycycline * 2^nd line = amoxicillin + clavulanate * 3^rd line = IV antibiotics & treatment following pneumonia guidelines. **Indicators for Admission:** * Marked increase in intensity of symptoms, such as sudden development of resting dyspnoea * Severe underlying COPD * Onset of new physical signs (eg cyanosis, peripheral oedema) * Failure of an exacerbation to respond to initial medical management * Presence of serious comorbidities (eg heart failure, newly occurring arrhythmias) * History of frequent exacerbations * Older age * Insufficient home support.

Respiratory failure: Type 1: Hypoxaemia: Causes (rapiddrop) Aeitlogy: Physiology: Pathogenesis: Clinical features:

* high altitude * PE (V/Q mismatch) * ARDS * Pneumonia * Pulmonary oedema (APO) * Acute NMJ disease (hypoventilation)

Type 2 Respiratory failure: Classifications: Aeitologys? Pathogenesis? Factors limiting CO2 exchange? Management?

Type 2 – Hypercapnia * Hypercapnic acute respiratory failure (T2) – imbalance between load on respiratory muscles and muscle pump capacity –\> PaCO2 \>45mmHg and pH\<7.35. * Classifications: * Acute – no/minor evidence of pre-existing respiratory disease with high PaCO2, low pH, and normal bicarb levels. * Acute on chronic – acute deterioration in patient with pre-existing hypercarpnic disease with high PaCO2, low pH but not as low as in acute hypercapnic ARF, and elevated bicarbonate levels. * Chronic – evidence of chronic respiratory disease with high PaCO2, near normal pH, and elevated bicarbonate levels. * Aetiology: * Obstructive lung disease – AE of COPD, Severe acute asthma, CF, non-CF bronchiectasis * Neuromuscular disorders – myasthenia gravis, phrenic nerve injury * Obesity hypoventilation syndrome * Chest wall disorders (i.e. kyphoscoliosis) * Pulmonary oedema * Drug intoxication and/or poisoning. * Pathogenesis: 2 mechanisms * Reduction of alveolar ventilation (pump respiratory failure) due to * Increase in dead space * Reduction of minute-ventilation – most common mechanism resulting from imbalance of respiratory neuromuscular capacity and respiratory muscle load. * Increased rate of CO2 production (less common) * Factors limiting CO2 exchange: * Poor ventilatory muscle function – neuromuscular disorders or drugs * Obstructions of airway/alveoli – acute asthma, COPD, pulmonary oedema * Secretions in small airways/alveoli – COPD and cystic fibrosis. * Chest wall abnormalities (obesity and kyphoscoliosis) Management * ABCs * T1 = Target SpO2 between 94-98% * T2 = target SpO2 between 88-92%. * Stabilisation & perform evaluation – Hx, PEx, Ix Treat underlying cause

What are the most common causes of tropical pneumonias? (e.g list top 4 causative organisms) What is Meliodosis? Pathogen? Where is it found? Transmission? Risk factors for disease? Differential diagnosis? Investigations? Management?

What is acinetobacter baumanni? Risk factors? Clinical? Dx? Rx? Lung abscess: DDX? Ix? Management? (active+follow up)

Aspiration Pneumonia: Notes: What is its? What are risk factors (list 6) Clinical features? (apiration pneumonia vs pnumonitis) Diagnosis? Prevention?

Management of aspiration pneumonia: Acute aspiration: Management: DRS ABC: Active management, ongoing monitoring, supportive, closing) Aspiration pneumonia managament: Clinically what do you expect? Principles? Empirical antibiotics What is aspiration pneumonitis?

What is an interstial lung disease? What is the basis of diagnosis? (Describe PFTs findings) 2 marks What is the pathophysiology? Clinical features (1.5 marks) (3 c's) What is the eitology of different ILD?

Clinical features of Interstitial lung disease: (list 4) 2 marks Diagnosis? Other investigations: plus think, underlying cause (SLE, RA, goodpasturs, GPA)

Idiopathic pulmoary fibrosis: Overview: Pathogenesis: Clinical features? Investigations? Management:

What are radiologyical CRX findings of ILD?

What is hypersensitivity pneumonitis? Clinical features? Presentation? Acute vs chronic: Diagnosis? Management?

What is a penumoconioses? What are three major types? What causes them? Basic patho: Management? What is CWP: Coal workers pneumoconioses? Clinical features? Ix? Managemement?

Silicosis: Eitology: Patho, CXR findings? Asbestosis: Eitology, pathology: Clinical features? Complications? Ix: Findings?

What is Sarcoidosis? Define: Who does it affect? Clinical features: (similar to TB) - Extrapulmonary? Investigations? CXR findings? Management:

Management * Most resolves spontaneously * Steroids - treat symptoms, lung disease, hypercalcemia and other extrapulmonary disease * Methotrexate - severe disease

What is pulmoary eosinphillia? What are the different types? Investigations?

What is a PE? Define: What are three pathological changes? Eitology? Risk factors: List 6 (3 marks) Pathophysiology: Differential diagnosis for Dyspnoea? (list 8) (4 marks)

Clinical features of PE- List 6 features ( 3 marks) What are the various types of PEs? Exmination findings in PE (list General inspect, VS, Exam (signs of RV overload) - 4 marks

How do you Work up a PE? What is the Wells scores? How do you interpret it? What is the PERC rule?

PE Assessment **Investigations:** Pre-test probability scores are intended to replace empirical assessment of patients with suspected pulmonary ebolism Rule in: * Wells Criteria * Geneva Score Rule out: * PERC Apply the PERC rule to those at low probability (Well’s \<3) to confidently rule out the chance of a PE: PERC Criteria * age \< 50 years * pulse \< 100 beats min * SaO2 \>or= 95% * no hemoptysis * no estrogen use * no surgery/trauma requiring hospitalization within 4 weeks * no prior venous thromboembolism (VTE) * no unilateral leg swelling Mnemonic – “**HAD CLOTS”** * **H**ormone * **A**ge \>50 * **D**VT/PE history * **C**oughing blood * **L**eg swelling * **O**2 \< 95% * **T**achycardia 100+ * **S**urgery/trauma \<28 day If all 8 PERC criteria are negative than the risk of PE is considered to be statistically remote enough to not warrant further investigations. Limitation of PERC is any patient with respiratory or cardiac symptoms will likely not pass the criteria. **Investigations include:** * If pre-testing score is at high risk: * D-dimer is not indicated * CTPA (or V/Q Scan if CTPA is contraindicated) * If pre-testing score is at intermediate risk: * D-dimer is indicated * +ve D-dimer –\> CTPA * If pre-testing score is low risk: * PERC * If all 8 –ve –\> no further investigations * If any are positive –\> D-Dimer * +ve D-dimer –\> CTPA If patient is haemodynamically unstable, echocardiogram may be used to confirm diagnosis. Other investigations include: * Bloods – coagulation studies, FBC, U&E’s * CXR * ECG * ABG **Diagnosis:** Pulmonary embolism can be diagnosed through imaging – CTPA, V/Q Lung Scan and echocardiogram

Diagnosis of PE: (plus expected findings) Bedside investigations? Bloods? Imaging? Doppler, CXR, V/Q scan, echo:

V/Q scan and CXR examples in PE: What are complications in PE? think RV dysfunction) Examination findings PE?

Complications * RS HF * Hypoxemia * Cardiovascular collapse and shock RV dysfunction * Clinical - JVP elevated * ECG - RV strain * Troponin - elevated * CTPA - RV dilated

Management of PE: **Resus, Immediate grading, thrombolysis, anticoagulation, NOACs- duration. Surgical.** When is thrombolysis indicated? Anticoagulation: - Indications? Acute,, duration needed (provoked vs unprovoked)

Pulmonary embolism can be diagnosed through imaging – CTPA, V/Q Lung Scan and echocardiogram Treatment **Deep Distal DVT:** * Less supporting evidence * Mx =\> * Treat as though deep distal DVT * OR conservative Mx with surveillance USS if risk of bleeding is high. * N.B 15% will progress to involve proximal vein. **Acute Anticoagulant therapy for Proximal DVT and PE (stable)** * 1) ABCs – if unstable proceed to next subheading * 2) Pre-anticoagulation screening: * Bloods – Coags (INR and aPTT), FBC, LFTs, UECs, ß-HCG * 3) First line therapy: * Oral Warfarin or NOAC * Preferred – Factor X inhibitors (apixaban & rivaroxaban) – no parenteral anticoagulation required * Apixaban cannot be used if CrCl\<25mL/min; Rivaroxaban \<30mL/min * Apixaban = 10mg BD for 7 days then 5mg BD * Rivaroxaban = 15mg BD for 7 days then 20mg BD * Dabigatran – requires 5 days of parenteral anticoagulation * Warfarin + parenteral anticoagulation – aim for INR of 2-3 * Parenteral anticoagulation: * Dalteparin (CrCl 30 mL/min or more) 200 units/kg subcutaneously, once daily, or 100 units/kg twice daily * **OR** Enoxaparin (has renally adjusted dosing). * 2^nd line * Unfractionated Heparin – useful if risk of bleeding is high and reversal may be required, and severe kidney disease * 80units/kg loading + 15mg/kg infusion. * Exception – pregnancy and cancer-associated VTE * Duration of therapy * Proximal DVT or PE caused by a major provoking factor that is no longer present – 3/12 * Isolated distal DVT caused by a major provoking factor that is no longer present – 6/52 * For patients with unprovoked distal DVT, proximal DVT or PE – 3/12 * Evidence supports ongoing use for reducing VTE events from present episode, but no evidence suggesting reduced risk of recurrence. * Extended anticoagulation therapy – indicated if **multiple prior unprovoked episodes of DVT or PE**, continue with full-dose anticoagulant therapy * Options = maintenance dose of NOAC or warfarin (INR=2-3) **Oral Anticoagulation Contraindications:** * Common: * Contraindicated in severe active bleeding or disease states with an increased risk of severe bleeding * Spinal injection or puncture * Surgery * Pregnancy * Elderly **Risk Factors for Bleeding:** Factors that predict increased likelihood of bleeding include a patient having: * A prior bleeding episode * Active peptic ulcer disease * Oesophageal varices. **Risk Factors for Disease Recurrence:** * Prior VTE * Active cancer * Unprovoked VTE—no provoking factor in the 3 months before the development of VTE (eg surgery, medical illness with reduced mobility, trauma, oestrogen therapy) * Proximal DVT or PE (rather than distal DVT) * Male sex * Certain thrombophilias—antithrombin deficiency, protein C or S deficiency **Fibrinolysis and interventional procedures for haemodynamically unstable PE** * Patient mortality due to pulmonary embolism (PE) complicated by shock is high * Treatments include: * Systemic fibrinolytic therapy * Catheter-directed fibrinolytic therapy * Thrombus aspiration * Surgical thrombectomy * Use of extracorporeal membrane oxygenation * 1) Fibrinolytic therapy – Alteplase or tenecteplase * Associated with increase risk of bleeding especially in older patients. * 2) Following fibrinolytic therapy – Parenteral anticoagulation * Dalteparin or Enoxaparin ALT = Unfractionated heparin – high risk of bleeding or severe renal impairment

List the 4 major types of pulmonary vasculitis? (think GPA, EGPA, anti-gbm, Rheuamtoid disease)

Medistinum mass: DDX? Clinical features? Ix?

Pleural effusion: Eitology: Transudate vs Exudate, Haemothorax, chylothroax, pleural empyema Clinical features: Symptoms+signs: Investigations: - Bloods, imaging, thoracocentesis:

EtiologyTransudate Transudate - usually bilateral due to systemic disease Common causes * Increased pressures - CHF, CKD, overload * Reduced oncotic pressure - hypoalbuminemia (nephrotic syndrome, cirrhosis), hypothyroidism Exudate * Bilateral or unilateral usually due to local disease * Patho - ↑permeability of pleural capillaries Common causes * Infectious - pneumonia, TB, abscess * Malignant - LuCa, lymphoma, metastases * Inflammatory - PE, RA, SLE, drug reaction * Intra-abdominal - pancreatitis, subphrenic abscess Haemothorax * Severe trauma, surgery Chylothorax (lymph) * Trauma or surgery of thoracic duct, carcinoma involving thoracic duct Pleural empyema * Pneumonia, abscess, bronchiectasis, TB, penetrating chest wound ClinicalSx * Often asymptomatic * Dyspnoea * Pleuritic chest pain Signs * Trachea - trachea displaced contralateral (massive effusion) * Expansion - reduced expansion of affected side * Percussion - stony dull * Breath sounds - reduced or absent,] * Vocal resonance - reduced or absent Ix Bloods * FBC, UECs, LFTs (albumin), glucose, LDH Imaging * CXR - detects pleural effusion \>200mL (less on lateral) --\> blunting of costophrenic angle, opacification with concave meniscus, if supine will appear as generalised haziness * CT chest - underlying pathology * Thoracocentesis * Pleural aspirate for analysis

What is "lights criteria", for pleural effusion analysis: What are the things measured in the pleural fluid? What indicates further investigation of pleural fluid (e.g MCS, RF, ANA, cell coutn differential)

PLeural Effusion: Notes: Know- Transudate vs exudate. Clinical features? Investigations? Lights criteria? Management: What is a parapneumonic effusion? When do they occur?

Pleural Effusion * Pleural effusion is an accumulation of excess fluid in pleural space. * Fluid can either be: * Transudate – heart failure, hypoalbuminaemia (Liver failure, Nephrotic syndrome) * Exudate – due to pleural disease or disease surrounding the lung * Infection, malignancy, pulmonary infarct (PE), autoimmune diseases i.e. Rheumatoid arthritis, drugs, radiation, pancreatitis. Assessment **Clinical Features:** * Symptoms – SOB, cough, pleuretic chest pain. * Signs: * Reduced expansion on affected side * Trachea and apex beat displaced away from lesion. (Massive) * Decreased or absent tactile fremitus * Stoney dull percussion * Decreased breath sounds * Bronchial breath sounds above affected region. **Investigations:** * CXR * Bloods * Diagnostic thoracentesis is [Analysis of the pleural fluid](https://www.amboss.com/us/knowledge/Pleural_effusion#xid=F50gNg&anker=Z854abb32b00d7b5310cd19f08f9b9644) (via [thoracentesis](https://www.amboss.com/us/knowledge/Pleural_effusion#xid=F50gNg&anker=Z233af6b707f6c16ceeb5369d2f281419)) is usually required to definitively establish the underlying etiology but may not be necessary if there is already a clear diagnosis of an underlying condition (e.g., known [CHF](https://www.amboss.com/us/knowledge/Congestive_heart_failure#xid=rS0faf&anker=Z07d22fa4c3f9da63ddf39683e4eaa845) or [connective tissue disease](https://www.amboss.com/us/knowledge/Connective_tissue_diseases#xid=WT0Pp2&anker=Z6975632047fb6dfa0329e9fb091527c5)). * Thoracentesis sample should be sent to the labs to analyse the serum protein, lipid and LDH **Light’s Criteria:** * Determines likelihood of exudative vs transudative effusion likely to be exudative or not. If the following criteria are met, then the fluid is highly likely to be exudative * Pleural fluid protein: serum protein ratio of **\>0.5** * Pleural fluid lactate dehydrogenase: serum LDH of **\>0.6** * Pleural fluid level **more than 2/3** of the normal upper value for serum LDH Management * Identify and **treat underlying cause** * Use direct USS guidance to sample pleural fluid by aspiration. * Send asprite for pH, LDH, protein, glucose * Consider **therapeutic** thoracentesis, tube thoracostomy, pleurodesis * Pleurodesis –\> used to prevent re-accumulation of pleural fluid. Obliterates the pleural space by inducing inflammation. * Common agents – talc and bleomycin * Administered through chest drain following drainage of pleural effusion. parapneumonic Effusion * Pleural effusion occurring with pneumonia * Occurs in 50% of pneumonias * Usually sterile, but not managed appropriately can develop into empyema. Should be directly sampled and cultured * If it developed into an empyema, it must be drained and treated with Abx: * Empirical – amoxicillin + clavulanate * IF gram -ve suspected – clindamycin * Systemic features despite drainage + oral Abx –\> IV pip/taz * Intrapleural enzyme therapy can also be administered to reduce the viscosity of pleural pus. * Alteplase + dornase alpha. Malignant pleural effusions * 2º to lung malignancy * Managed with drainage + pleurodesis with talc/bleomycin. Other subtypes & Variants * Cylothorax – lymphatic fluid form thoracic dyct (chlye) accumulates in pleural cavity. * Pseudochylothorax – accumulation of cholesterol-rich fluid in the pleural cavity due to chronic inflammation. * Haemothorax – accumulation of blood in the pleural cavity.

Pneumothorax: Overview: Eitology: Primary pneumothorax, Secondary pneumothorax, traumatic (List 4 causes of secondary pneumothorax) Tension pneumothorax: Reg flags for tension (2 marks) Symptoms/Signs of pneumothorax: 4 marks Investigations and findings of pneumothorax:

Pneumothorax Pneumothorax = air in the pleural space. May be spontaneous, traumatic, iatrogenic (pleural aspiration, lung biopsy, etc.) **Spontaneous Pneumothorax:** * Spontaneous pneumothoraces are subdivided into: * Primary—where there is no evidence of underlying lung disease * Secondary—where lung disease is present, most commonly COPD, but also asthma, interstitial lung disease, CF or HIV-associated infection. * Associated with sudden onset pleuritic chest pain, dyspnoea. Diagnosed on erect CXR * Signs: absent breath sounds, tachypnoea, decreased chest wall movement, hyper-resonance to percussion, decreased vocal resonance, and tracheal deviation to the opposite side **Tension pneumothorax:** * Intrapleural air accumulates progressively in such a way as to exert positive pressure on mediastinal and intrathoracic structures resulting in respiratory or haemodynamic compromise * Can rapidly decompensate –\> dyspnoea, hypoxaemia, hypotension, CV Collapse * Diagnosed clinically not radiologically. Assessment Clinical Features: * Chest Pain - Sharp, sudden onset pleuretic pain, maximum at onset and laterally located. * 1º spontaneous - symptoms resolve in 24hrs usually * 2º spontaneous - symptoms are more severe and don't resolve without Tx. * Dyspnoea * Decreased lung expansion * Hyper-resonance on percussion * Decreased/absent breath sounds on affected side * Subcutaneous emphysema. Investigations: * CXR +/- CT * Baseline bloods * ?ABG

Management of Primary Spontaneous Pneumothorax: What 3 things to determine- to determine management? Stable vs unstable Primary survey#?

Management **Primary Spontaneous pneumothorax:** Principles: * Primary spontaneous pneumothorax is usually a nuisance rather than a dangerous condition. Symptoms commonly resolve within 24 to 48 hours without treatment. * Aim for conservative therapy whenever possible. * Drainage – painful, carries risk (damage to internal organs, bleeding, infection) * If interventional treatment – **aspiration preferred over insertion of intercostal drain** * Lower complication rate. Management: * ABCs * Analgesia – improves breathlessness. * Oxygen – 10L/min via face mask – increases rate of intrapleural air resorption. * Conservative Management: Usually resolves in 2 weeks. * Small pneumothorax \<2cm * PLUS clinically stable – no SOB, full sentences, RR\<24, HR\<120, BP = normal. * Interventional therapy – failure of any of the above criteria. * Aspiration – 1^st line * Intercostal drain – 2^nd line Prognosis: * Recurrence rate for spontaneous pneumothorax = 30-50% (higher in smokers.) * To avoid future recurrence –\> pleurodesis (thoracoscopy + talc insufflation/pleural abrasion) can be used. **Secondary Spontaneous Pneumothorax Management:** * Early active intervention + hospitalisation for intervention. * Intercostal drainage is recommended in secondary spontaneous pneumothorax. * Simple aspiration is less likely to be successful **Pneumothorax Decompression in Tension Pneumothorax:** * Urgent Needle decompression (Needle thoracostomy): * 1) Insert a cannula above the third rib in the mid-clavicular line. * 2) Remove the needle from the cannula. * 3) A gush of air confirms the diagnosis. * 4) Once complete, insert a thoracostomy tube expeditiously. * Catheter Aspiration (thoracentesis) * Inject local anaesthetic subcutaneously first, until reaching the pleural space. * Then insert a small-bore catheter inserted above the 3rd rib in mid-clavicular line. * Aspirate until no air is returned. * Leave the catheter in situ and then repeat CXR. * If no air returned after 4 hours, discharge and advise to return if symptoms return. * Intercostal tube drainage (tube thoracostomy/ Chest drain): * Specialist procedure. * Indicated for secondary pneumothoraxes, most traumatic pneumothorax’s, tension pneumothoraxes and pneumothoraxes that failed earlier lines of treatment.

Managemnt of different types of Pneumothorax: Tension pneumothorax: Stable and small with minimal symptoms: Large:? Supportive, ongoing, long term (advise), safety net?: Managment of Secondary pneumothorax: Technique for needle aspiration: Indications? Procedure? Chest drain(intercostal catheter)

Pneumothorax clincal pathway:

What is respiratory failure: How is each define? (hypoxaemic type 1, Hypercapnic type 2) Clinical signs? Investigations? List 4 causes of hypoxic resp failure:

What is hypercapnic respiratory failure (type 2)? Causes? (think alveolar hypoventilation) (overproduction of c02) Management?

What is ARDs? (acute respiratory distress syndrome) Overview: What characterizes it? Eitology? Pathogenesis? Gross/microscopic histology: What is the Berlin criteria? Clinical features (acute)-exudative phase:

What are CXR fingdings in ARDS? Management: Think Ventilation: (PEEP, circulation, active treatment) What is respiratory distress syndrome?

Cystic fibrosis: Epidemiology: Eitology: Pathophysiogy: Multi system disease: Prognosis: Diagnosis:

Clinical features of CF? (3 marks) Multi-system Complications: (2 amrks) Examination findings: Investigations?

CXR findings in CF:

Differential diagnosis: Recurrent chest infections and failure to thrive in children? Think systems

Management of CF- Referal, non pharm, medical, management of GI disease, monitoring, closing, prognosis.

What screening occurs in carriers? Whats risk of inheritance? Risks of CF in pregnancy? Antenatal care for mother with CF?

Lung cancers: Epidemiology: Australia, Smokers. Classification of lung cancers (1.5 marks)? Risk factors? (2 marks) Pathogenesis: Read

Morpholgical changes and pre-cursor lesions: (read)

Clinical features of lung cancers: 3 marks Symptoms/signs- 3 marks Symptoms due to metastasis- local spead? hameatogenous? Paraneoplastic syndrome(s)?

Lung caer à Accounts for 25% of cancer deaths **Risk factors** * Cigarette smoking (active and passive) * Exposure to: * Asbestos * Metals - chromium, iron oxides, arsenic * Radiation **Types** *Primary* * Bronchogenic carcinoma: Epithelial lung tumours * Small cell (20%) * Non-small cell * Squamous cell (35%) * Adenocarcinoma (25%) * Large cell * Alveolar cell * Benign epithelial lung tumours * Papilloma * Adenoma **Clinical features** à May be due to primary lesion, metastasis, or paraneoplastic syndrome *Primary lesion* * Cough: beware of chronic cough that changes in character * Dyspnoea * Chest pain * Haemoptysis * Other pain * Clubbing * Constitutional symptoms: anorexia, weight loss, fever, anaemia *Metastasis* * Lung, hilum, mediastinum, pleura: pleural effusion, atelectasis, wheezing * Pericardium: pericarditis, pericardial tamponade * Oesophageal compression: dysphagia * Phrenic nerve: paralyzed diaphragm * Recurrent laryngeal nerve: hoarseness * Superior vena cava syndrome: * Lung apex (Pancoast tumour): Horner’s syndrome, brachial plexus palsy (most commonly C8 and T1 nerve roots) * Rib and vertebrae: erosion * Distant metastasis to brain, bone, liver, adrenals *Paraneoplastic syndromes* * A group of disorders associated with malignant disease, not related to the physical effects of the tumour itself * Most often associated with SCLC * Neurological * Confusion * Fits * Cerebellar syndrome

Lung cancer: Secondary Clinical features: Hypercalcemia? SIADH? Cushings? Haematological syndromes? Pancoast tumors: Fetaures? Others?

Investigations for suspected lung Ca? Diagnosis (1.5 marks) Staging (bloods/imaging/screening) What basis does cell cytology have in Lung Ca? What are the morphological changes seen on cytology associated with: 1) Adenocarcinoma: 2) Squamous Cell Carcinoma? 3) Small cell?

Describe Characteristics of the following 1) Adenocarcinoma 2) SCLC 3) SCC 4) Large cell carcinoma Risk factors?

Signs and symptoms of lung Ca: Toronto notes: read again:

Paraneoplastic syndrome: Tornoto notes: Investigations? Initial? Staging?

Assessment/ Examination OSCE: of Lung cancer/COPD patient: Outline: General, VS, Hands, face, neck, chest, IPPA, CVS, Lower limb, others.

Outline: Origin (cell type), Smoking correlation, Location (CXR), histology, Clincal features: Of each 1) Small cell (SCLC) 2) Squamous cell (SCC) 3) Adenocarinoma

Basic management principles for Lung Ca: Localised? Palliative care options:

What are the general features of on CXR of the lung cancers (generally) , and specific SCC Sqamous cell Adenocarcinoma

Lung Ca CXR examples:

Lung Cancer CXR Adenocarcinoma CXR

Small cell carcinoma: Gross morphology: Microscopic histology:

Squamous cell carcinoma: Gross morphological features:

Squamous cell carcinoma: Microscopic features (2 marks)

Adenocarcinoma: Gross features: (1.5 marks) Microscopic features Features of metastasis: on CXR?

General principles to management of Lung Ca: SCLC NSLCL Surgery? Chemotherapeutic options? Acute issues? Chronic issues? Other lung Ca.

Approach to pulmonary nodule: Differential diagnosis? Benign/malignant? Investigations? (4 marks)

What is sleep apnoea? What are the 2 major types? What are risk factors for OSA? (2.5 marks) What is the pathogenesis of OSA? What are associated risks having OSA?

What are the clinical features of OSA? Signs/symptoms? Complications? Examination findings: Investigations: What is a good questionaire for OSA? What are the indications for overnight polysonography? What is the basis of severity?

Management of OSA: Non pharm: SNAP + Meds: Dental splints: CPAP: Benefits? risks? Surgery:

Pleural infections: What is the common cause? What do you have to determine? Why is it important to identify? What are the bacteria that commonly cause it? Hospital causes? What does an effusion look like on CXR? What is you differential ddx for effusion? What is a loculated effusion?

What are the clinical features/presentation of effusion? What does imaging show? USS? What role does thoracocentesis have? When sending the pleural fluid for analysis what do you need to send for? (e.g Cell count, chemistry (protien, glucose, LDH) ph, etc)

Differential diagnosis of pleural fluid exudate: Think: Infectious, iatrogenic, malignancy, other inflammatory disorders, CT, endocrine, lymphatics, movement of lquid from abomen to)

How is a diagnosis made: Pleural effusion: imaging+analysis How are they classified? uncomplicated vs complicated vs empyema

CXR findings in APO: List 3 marks:

How is APO catergorized? What can precipitate symptomatic HF leading to APO- THINK - HEART FAILED How does APO present? What is your differential diagnosis acute dyspnoea? (Cardiac, non cardiac, resp, others)

HEART FAILED * HTN\* (common) * Endocarditis/Pericarditis * Anemia\* * RHD * Thyrotoxicosis * Failure to take CHF meds\* * Arrhythmia * Infection/Ischemia\* * Lung - COPD, pneumonia, PE * Endocrine - hyperaldosteronism etc. * Diet - fluid overload from salt or fluid increase intake

Outline assessment of APO History: Ix: bedside, labs, imaging: Managament of acute cardiogenic pulmoary oedema: (LMNOPP) DRABCD + non pharm management If unresponsive? Monitoring? Supportive?

What is Non-invasive ventilation? What are the benefits of it? list: hameodynamics, respiration:

What is pulmonary hypertension: How is it defined? How is is diagnosed? Patho: Eitology: List 4 (2 marks) How is it classified?

WHO functional classification of pulmonary HTN: How does pulmonary HTN present? (2 marks) Examination findings? (3 marks) Investigations? (ECG findings: 2 marks atleast) Echo: What is idopathic PAH? Other causes of P HTN?

Learning objectives AH1 - Respiratory Flashcards

(167 cards)