Respiratory Flashcards

Question

Medication post-transplant? (M)

Answer 1

Steroids, MMF, CNIs (e.g. tacrolimus) Prophylactic medication to prevent opportunistic infection

Answer 2

-Not dyspnoeic at rest -Dry cough -Finger clubbing -Bruising possibly secondary to steroid therapy -Fine-end inspiratory crepitations at both bases ILD (Aetiology e.g. sclerodactyly) (Pulmonary HTN e.g. loud P2) Other differentials: -Pulmonary oedema (however no other features HF) -Bronchiectasis (however cough was dry and crackles did not alter with coughing) -COPD (no tar staining, no prolonged expiratory phase, no wheeze)

Answer 3

History (occupational, environmental, drug, systems review for CTD) Bloods (including FBC, CRP, U+Es, LFTs, bone profile, ESR and autoimmune screen, consider serum ACE) and urine dip **ABG (T1RF)** **Sputum culture if expectorating** CXR (reticulonodular changes, loss of definition of either heart border, small lungs) HRCT (bi-basal subpleural honeycombing typical of UIP, widespread ground-glass shadowing more likely NSIP which is often associated with AI disease, if apical think sarcoidosis, ABPA, old TB, hypersensitivity pneumonitis) PFTs (FEV1/FVC >0.8, low TLC and reduced TLCO and KCO) and 6 minute walk test ECG and echo (pulmonary hypertension) **Consider:** Bronchoalveolar lavage (exclude infection prior to any immunosuppressants, if lymphocytes > neutrophils indicates better response to steroids and better prognosis) Occasionally lung biopsy if diagnostic uncertainty (though morbidity 7%)

Answer 4

**MDT approach (including respiratrory physicians, specialist nurses):** -Smoking cessation team input is crucial -Immunisations and nutrition important -PR team input -Consider LTOT team **Medical:** -Discontinue toxic medications -Treatment of infections promptly -Immunosuppression if likely to be inflammatory e.g. steroids -Referral to ILD service for consideration of an antifibrotic agent if FEV1 50-80% **Surgical:** -Single lung transplant **End stage:** -Palliative care for symptom control e.g. opiates

Answer 5

Variable as depends on aetiology Highly cellular with ground-glass infiltrate responds to immunosuppression 80% 5-year survival Honeycombing on CT no response to immunosuppression 80% 5 year mortality Increased risk of bronchogenic carcinoma

Answer 6

CAID: Connective tissue diseases (e.g. scleroderma which tends to cause more NSIP) and autoimmune disease (RA which tends to cause more UIP) Asbestosis/Aspiration (right main bronchus is shorter, wider and straighter so foreign bodies more likely to enter) IPF Not in textbook but: Drugs (bleomycin, nitrofurantoin, amiodarone)

Answer 7

TRASH: TB Radiation Ankylosing spondylitis/**ABPA** Sarcoidosis/Silicosis/Berrylliosis Hypersensitivity pneumonitis

Answer 8

Idiopathic e.g. IPF Hypersensitivity diseases e.g. HP or ABPA Autoimmune e.g. AS, scleroderma, RA, dermatomyositis, ANCA Sarcoidosis Infectious such as TB Iatrogenic such as radiation or drugs Pneumoconioses such as asbestosis, silicosis or berryliosis Others such as Langerhans Cell Histiocytosis

Answer 9

SLE, RA, scleroderma, dermatomyositis

Answer 10

-Respiratory failure -Pneumonia -Pulmonary hypertension and cor pulmonale -Lung Ca

Answer 11

PPPP BBC I -Pulmonary fibrosis (UIP more common, trials using anti-fibrotics used in IPF) -Pulmonary nodules -Pleural effusion (exudate) -Pleurisy -Bronchiolitis obliterans (obstructive pattern on spirometry centrilobular nodules, bronchial wall thickening) -Bronchiectasis -Caplan's syndrome (massive fibrotic nodules with occupational coal dust exposure) -Infection (possibly atypical) secondary to immunosuppression

Answer 12

**Progressive and irreversible airflow obstruction** due to chronic bronchitis (clinical diagnosis) or emphysema (pathological diagnosis, enlargement of distal air spaces air spaces and destruction of their walls) Results from imbalance between protease and anti-protease activity, triggered by smoking

Answer 13

-Breathless at rest with pursed lip breathing during prolonged expiration -Nicotine staining -There is no CO2 retention asterixis and the pulse is not bounding -There is reduced cricoid notch distance and some tracheal tug with accessory muscle use -Hyperinflated chest -Hyper-resonant percussion note -Quiet breath sounds with polyphonic expiratory wheeze (No signs PH) Differentials include: -Asthma -Bronchiectasis (can cause wheeze but would expect coarse crepitations also) -ILD (would expect fine inspiratory crepitations and no prolonged expiratory phase)

Answer 14

Environmental: smoking and industrial dust exposure Genetic: alpha-1 antitrypsin deficiency (deficiency in enzyme which inhibits neutrophil elastases, different phenotypes with ZZ most severe)

Answer 15

-Infection (60%) Viruses (rhinovirus, influenza, parainfluenza, coronavirus) Bacteria (Haemophilus, Moraxella, streptococcal) -Environmental (10%) -Unknown (30%)

Answer 16

Loud S2 Parasternal heave S3 TR Features of RHF include ascites, peripheral oedema, elevated JVP, hepatomegaly

Answer 17

PAH Eisenmenger's

Answer 18

History (smoking history, number of exacerbations per year, malignancy red flags) Bloods (WCC, Hb for secondary polycythaemia, alpha-1 antitrypsin, albumin) **ABG (type II respiratory failure)** **Sputum culture** CXR (hyper-expanded with flattened hemidiaphragms, bullae, prominent pulmonary vasculature, pneumothorax) Spirometry (obstructive), minimal reversibility, and gas transfer (low TLCO) **ECG (RVH +/- strain and MAT) and echo if ?PH**

Answer 19

**MDT management:** -Smoking cessation single most beneficial management strategy so review by smoking cessation team crucial -Vaccinations and nutrition important -PR team -Consider LTOT team **Medical treatment:** -According to GOLD classification of severity (which looks at number of exacerbations and symptoms with MRC/CAT): -Mild GOLD A: short or long-acting bronchodilator -Moderate GOLD B: LABA/LAMA -Severe GOLD E: LABA/LAMA (plus ICS if eosinophils over 300) -Consider theophylline, roflumilast, azithromycin or mucolytics (TRAM) under specialist guidance -Also consider home nebulisers and rescue packs **Surgical treatment:** -Bullectomy if occupying at least 30% of the hemithorax -Lung reduction surgery -Endobronchial valve insertion -Single lung transplant **End stage:** -Palliative care involvement

Answer 20

To treat acute exacerbation: -Controlled oxygen -Bronchodilators -Antibiotics -Steroids -NIV/IMV Discharge planning with community COPD treatment team and smoking cessation

Answer 21

DECAF score predicts in-hospital mortality for acute exacerbation of COPD MRC dyspnoea scale **BODE index for 4 year survival**

Answer 22

Acute exacerbation have 15% mortality

Answer 23

COPD Asthma Pulmonary oedema Bronchiolitis obliterans Bronchiectasis

Answer 24

Polyphonic: asthma or COPD Monophonic: SOL or foreign body

Answer 25

-Non-smoker (carboxyhaemoglobin <3%) -PaO2 <7.3 RA **-PaCO2 which doesn't rise excessively on oxygen** -If evidence of cor pulmonale PaO2 <8.0 -2-4L/min via NC for at least 15 hours/day -Improves average survival by 9 months

Answer 26

GOLD criteria, based on FEV1: >80% mild 50-80% moderate 30-50% severe <30% very severe Or MRC dyspnoea scale

Answer 27

1) Chronic hypoxia 2) Hypoxic vasoconstriction 3) Pulmonary hypertension 4) Right-heart failure --- Treatment: LTOT Diuretics

Answer 28

-Not breathless at rest -Productive cough -Finger clubbing -Normal chest expansion -Coarse inspiratory crepitations which alter on coughing -Widespread expiratory wheeze (in 1/3) (Aetiology e.g. CF, RA) (No signs PH) Differentials would be: -Bilateral pneumonia -COPD (no tar staining, no prolonged expiratory phase) -Pulmonary oedema (however no other features HF) -ILD (fine crepitations) N.B. Percussion note and vocal fremitus variable

Answer 29

History (childhood infections, past medical history) Bloods **ABG if hypoxic** **Sputum culture and cytology** CXR (tramlines and ring shadows) HRCT ('signet ring sign' which is thickened dilated bronchi larger than adjacent vascular bundle) **Then investigate cause:** -Immunoglobulins IgG and IgA (hypogammaglobulinaemia) -Rheumatoid serology **-Alpha-1 antitrypsin** -Aspergillus RAST or skin prick testing (ABPA if bronchiectasis affects upper lobe) -Nasal nitric oxide (PCD) -Sweat chloride test or genetic screening (CF) **-HIV test** N.B. PFTs may be normal or may be obstructive (if airway obstruction due to secretions or co-existent obstructive airways disease)

Answer 30

-Post-infectious e.g. childhood measles or pertussis **-Congenital (ciliary dyskinesia e.g. in Kartagener's; CF)** -Immune OVERactivity (ABPA, IBD-associated or rheumatoid arthritis) -Immune UNDER activity (hypogammaglobulinaemia, CVID or HIV) -Aspiration if localised to RLL (alcoholics, post-stroke) In addition: traction bronchiectasis in fibrosis

Answer 31

NRT (patch, gum, lozenge, inhalator) Varenicline Bupropion | Can't use the latter 2 in pregnancy and can't use bupropion in epilepsy

Answer 32

**MDT management:** -Chest physiotherapy input crucial -Smoking cessation team -Immunisations and nutrition -PR team -Consider review by LTOT team **Medical:** -Prompt antibiotic therapy for exacerbations -Long-term treatment with low-dose azithromycin three x/week -Pseudomonas eradication if isolated -Bronchodilators/ICS if any airflow obstruction -Mucoactive agents e.g. nebulised saline **Surgical:** -Surgical resection if localised disease -Transplant -Bronchial artery embolisation if massive haemoptysis

Answer 33

-Respiratory failure -Pneumonia and empyema **-Collapse** -Pulmonary hypertension and cor pulmonale **-Secondary amyloidosis** -Massive haemoptysis

Answer 34

Bronchial wall dilatation Caused by destruction of muscular and elastic components of bronchial walls Causes impaired clearance of secretions which causes colonisation and infections

Answer 35

H. influenza Pseudomonas

Answer 36

Pseudomonas Staph. Aureus MRSA S. Maltophillia H. Influenzae Can also become colonised with Cepacia (high mortality), M. Abscessus and Aspergillus

Answer 37

-Plombage (polystyrene balls into thoracic cavity) -Thoracoplasty (rib removal, lung not resected) -Apical lobectomy

Answer 38

-Rifampicin: hepatitis and increased metabolism of COCP -Isoniazid: peripheral neuropathy (Rx pyridoxine) and hepatitis -Pyrazinamide: hepatitis -Ethambutol: retrobulbar neuritis and hepatitis

Answer 39

-Deviated trachea -Reduced chest expansion on R/L -Dull percussion note at R/L base extending up to mid-zone with reduced vocal fremitus -Breath sounds diminished with an area of bronchial breathing above the area of dullness Aetiology?

Answer 40

Transudate (<30) CCCHH: -CCF -Chronic renal failure -Chronic liver failure -Hypoalbuminaemia (and nephrotic syndrome) -Hypothyroidism Exudate (>30 protein) NIIIPY: -Neoplasm (primary or secondary) -Infection (pneumonia and TB) -Infarction -Inflammation (RA and SLE) -Pancreatitis -Yellow nail syndrome/Meigs syndrome | Peritoneal dialysis would cause transudate

Answer 41

Recurrent malignant effusions Recurrent pneumothoraces

Answer 42

History (infective symptoms, malignancy red flags) Bloods (FBC, U+Es, LFTs, protein and LDH, BNP, amylase, TFTs, autoimmune profile) **ABG if hypoxic** **Sputum culture if expectorating** CXR and USS (loculated, smaller effusions) Pleural tap (protein, LDH, glucose, pH, amylase, cholesterol, cytology, microscopy and culture, ZN staining, RF) **In addition:** -CT-TAP, biopsy, bronchoscopy (malignancy) -CT-PA (if PE suspected) -Echo (CCF)

Answer 43

Light's criteria (exudate if one or more present, protein between 25-35): -Pleural fluid protein divided by serum protein >0.5 -Pleural fluid LDH divided by serum LDH >0.6 -Pleural fluid LDH >2/3 the upper limits of normal serum LDH Empyema if pH <7.2, exudate and low glucose

Answer 44

MEAT Malignancy Empyema RA (very low) TB

Answer 45

Malignancy Empyema RA

Answer 46

Malignancy TB

Answer 47

-Pleural effusion -Pleural thickening -Collapse -Consolidation -Raised hemidiaphragm -Lower lobe lobectomy

Answer 48

Treat underlying cause e.g. CCF, infection Pleural drainage (pH <7.2, frank pus when aspirating, culture positive, large effusion, symptomatic) If recurrent consider indwelling catheter or pleurodesis

Answer 49

-Pain -Inappropriate placement -Infection -Bleeding -Pneumothorax -Re-expansion pulmonary oedema -Tube blocks, displaces or surgical emphysema -Organ puncture

Answer 50

Collection of pus within the pleural space Most frequent organisms anaerobes, staphylococci and gram negative organisms Associated with bronchial obstruction e.g. carcinoma, recurrent aspiration, poor dentition and alcohol dependence

Answer 51

Tumour affecting the pleura Associated with asbestos exposure in 80% of cases, pleural plaques on CXR and effusions

Answer 52

Autosomal recessive condition affecting 1/2500 live births It involves chromosome 7q, and affects he gene which encodes the CFTR Cl- channel Secretions are thickened and block the lumens of various structures: -Bronchioles (bronchiectasis) -Pancreatic ducts (loss of exocrine and endocrine function i.e. CFRD, pancreatic enzyme insufficiency) -Gut (distal intestinal obstruction syndrome) -Seminal vesicles and fallopian tubes (infertility) Also causes liver disease, gallstones, osteoporosis, sinusitis

Answer 53

**Screen at heel prick test at birth (low immunoreactive trypsin)** Sweat test (Na >60 with false positive in hypothyroidism and Addison's) Genetic screening HRCT will confirm bronchiectasis --- **For complications:** -Infection: inflammatory markers, sputum culture and CXR -Diabetes: HbA1c, fundoscopy, urine ACR and U+Es -Pancreatic exocrine: faecal elastase -DIOS: AXR -Liver: LFTs, coagulation and USS liver -Bone: bone profile, PTH, vitamin D, DEXA

Answer 54

**MDT management:** -Chest physiotherapy is crucial for postural drainage and active cycle breathing techniques -Smoking cessation team if required -Immunisations should be offered in community -Nutrition team input (pancreatic enzymes with PPI and fat-soluble vitamin supplements and consideration of gastrostomy) -DSN teams -PR team -Consideration of LTOT **Medical:** -CFTR modulators (Ivacaftor) if suitable CFTR mutations -Prompt antibiotic therapy for exacerbations -Long-term treatment with low-dose azithromcyin three x/week -Pseudomonas eradication if isolated -Bronchodilators/ICS -Mucoactive agents e.g. hypertonic saline DNase **Surgical:** -Double lung transplant -Embolisation if massive haemoptysis -Surgical team input if DIOS | Ivacaftor improves production and function of the receptor, improves int

Answer 55

Medial survival is 40 years but rising Poor prognosis if becomes infected with Cepacia

Answer 56

-Bloods (WCC, CRP, urea) -ABG **Culture everything!** -Blood culture -Sputum culture -Urine for atypical screen (and haemoglobinuria as mycoplasma causes haemolysis) -Respiratory viral swabs -CXR consolidation, abscess and effusion -Consider CT chest if e.g. cavitation, effusion or multifocal consolidation -Consider pleural tap and culture if effusion

Answer 57

Streptococcus pneumoniae 50% Mycoplasma pneumoniae 6% Haemophilus influenzae (especially in COPD)

Answer 58

CURB-65 -Oxygen if hypoxic -IV fluids if volume deplete -Antibiotics (note cover for Staph. aureus if post-influenza, anaerobes if aspiration, fungal/PCP/CMV if immunocompromised) -Analgesia -Optimise nutrition -pLMWH -ITU if required -Follow-up in CAP clinic -Vaccinations to at-risk groups -Smoking cessation

Answer 59

-Septic shock and multi-organ failure -ARDS -C. difficile -Para-pneumonic effusion or empyema -Lung abscess

Answer 60

>72 hours after admission to hospital Gram negative bacilli, Pseudomonas, anaerobes

Answer 61

Bloods (FBC, **autoimmune screen for scleroderma and SLE**, TFTs, LFTs, HIV test, BNP) **ABG (LTOT if pO2 <8)** Echo (RV size and function, TR velocity to estimate PASP) CT-PA for proximal chronic thrombi but also parenchymal lung disease **PFTs for underlying lung disease (ILD versus COPD)** Right heart catheter to confirm raised pulmonary pressures plus estimation of LA pressures (wedge pressure) and vasodilator testing

Answer 62

Group 1: PAH (idiopathic, heritable, congenital, porto-pulmonary, drugs (amphetamines), connective tissue, HIV) Group 2: left heart disease Group 3: lung disease Group 4: chronic thromboembolic disease Group 5: miscellaneous (thyrotoxicosis, long-term HD, sickle cell)

Answer 63

Group 1: phosphodiesterase 5 inhibitors (sildenafil), endothelin receptor antagonists (ambrisentan), prostacyclin analogues (iloprost), double lung transplant if refractory Group 4: lifelong anticoagulation, riociguat, pulmonary endarterectomy (if proximal), balloon pulmonary angioplasty (if distal) Groups 2, 3 and most of 5: treat the underlying cause **In addition:** -Diuretics -Consider LTOT -Supervised exercise training -Vaccinations and psychosocial support -Counselling on risks associated with pregnancy

Answer 64

Death from right heart failure Atrial arrhythmias Dilation of proximal pulmonary artery (stretching of recurrent laryngeal nerve, external compression of LAD causing angina-like CP, external compression of right middle lobe bronchus causing localised bronchiectasis)

Answer 65

RFs include exposure to infection, immunosuppression (including HIV), silicosis, malignancy, birth in an endemic country Ix: -CXR -Sputum AFB and cultures -NAAT -Bronchoscopy -FBC and HIV test Tx: -ID-guided -RIPE (duration determined by site of infection)

Answer 66

Primary Secondary: -Underlying lung disease e.g. COPD, asthma, bronchiectasis, ILD -CTD e.g. Marfan's **-Iatrogenic e.g. pleural procedures, PPM** -Trauma

Answer 67

-Tracheal deviation to opposite side -Mediastinal shift (apex beat displaced) -Raised JVP --- -Manage with A through E -Oxygen -Large bore cannula into second intercostal space mid axillary line -Prompt insertion of intercostal drain

Answer 68

Lateral CXR

Answer 69

After 48 hours for persistent air leak or failure to expand Low pressure used

Answer 70

If asymptomatic: For conservative If symptomatic: **-If high risk and safe to intervene, for chest drain** -If not high risk but safe to intervene, manage taking into account the patient's priority (rapid relief versus procedure avoidance) i.e. aspiration +/- drain versus conservative --- If persistent air leak or inadequate expansion: Thoracic suction, converting to larger-bore chest drain, blood patch or chemical pleurodesis, endobronchial valves or thoracic surgery

Answer 71

Dyspnoea Headache Nasal stuffiness Head, facial, arm swelling Symptoms worsen on bending down, coughing

Answer 72

Elevate head Steroids Stenting If malignancy: Chemotherapy Radiotherapy If thrombosis: Thrombolysis or anticoagulation

Answer 73

Inspiratory = extrathoracic obstruction -Epiglottitis -Anaphylaxis -Tracheal/laryngeal/pharnygeal pathology Expiratory = intrathoracic -Foreign body -Bronchial pathology N.B. Wheeze is turbulent airflow through smaller airways Stridor is through larger airways Wheeze is predominantly expiration Stridor predominantly inspiration

Answer 74

Thickened, dystrophic or discoloured nails Bronchiectasis and/or pleural effusion Lymphoedema

Answer 75

History Bloods (FBC (eosinophils) CRP IgE) ABG (if hypoxic in acute setting) Sputum culture if expectorating CXR Peak expiratory flow diary (reduced in early mornings, **>20% variability**) Spirometry (obstructive, BDR improvement in **FEV₁ of 12% or more in response to beta agonists and increase in volume of 200 mL**) **Allergy testing** FeNO (increased) Consider referral for bronchial challenge

Answer 76

**MDT:** -Patient education from the asthma nurses is crucial -Patient should be counselled on how best to control their environment and should be advised on inhaler technique -Smoking cessation team involvement if needed **Medical:** Stepwise approach, changed in November 2024: 1) Low-dose inhaled corticosteroid (ICS)/formoterol (as-needed AIR therapy) 2) Low-dose MART 3) Moderate-dose MART 4) Add LTRA (montelukast) or LAMA Then referral to specialist (consideration of theophylline, oral steroids or biologics)

Answer 77

N.B. BOS causes obstruction