Respiratory medicine.

Respiratory medicine

Phase 2a Revision Session
Jonny Jackson (3a) & Rob Chan (3a) The Peer Teaching Society is not liable for false or misleading information…

Basic respiratory physiology & histology
Functional unit of gas exchange = alveolus Conducting airways 16th generation of bronchi/bronchioles Ends with terminal bronchioles (columnar or low cuboidal epithelium) Histology of the trachea Mucosa - columnar ciliated pseudostratified epithelium & goblet cells. Supported by the elastic lamina propria (elastin) Submucosa – sero-mucinous glands. Ventilatory airways = acinus (collection of alveoli) Respiratory bronchioles – ciliated cuboidal epithelium Clara cells (secrete surfactant component) – non-ciliated cells. No cartilage plates or glands/diffuse lymphatic tissue in bronchioles. Normal V/Q (4l/min)/(5l/min = CO) ~ 0.8. Postural V/Q mismatch when standing = higher V/Q due to RELATIVE decrease in blood supply due to gravity at APEX. There are regional V/Q changes. The Peer Teaching Society is not liable for false or misleading information…

Respiratory failure ‘Inadequate gaseous exchange leading to hypoxia’ ~ PaO2 <8kPa [ ] Causes: ‘LAVISH’ (see notes) Ventilation/perfusion mismatch [V/Q mismatch] Type 1 RF = hypoxia + normal/low PaCO2 [normal value = 4.5-6] E.g. pulmonary embolism, pulmonary oedema, pneumonia (physiological shunting*) Alveolar hypoventilation (decreased minute ventilation) Global reduction in oxygen delivery Type 2 RF = hypoxia + hypercapnia (PaCO2 > 6kPa) Clinical importance in ‘chronic retainers’ and O2 therapy (88-92% target SATS) E.g. MND, Guillain–Barré syndrome, COPD exacerbation (acute on chronic RF) , severe asthma (status asthmaticus), drug toxicity, stroke & reduced GCS Abnormal diffusion (parenchymal) e.g. ARDS, pulmonary fibrosis, sarcoidosis L-R cardiac shunting E.g. Patent ductus arteriosus, VSD, ASD and AVSD Q ~ reversal of long-standing L-R cardiac shunt? *infection in the lung decreases regional ventilation therefore the V/Q is decreased. Which drugs are commonly associated with respiratory depression? OPIODS (pin-point pupils on examination). Nb effects of V/Q mismatch may be reduced to an extent by hypoxic vasoconstriction. Answer to Q: Eisenmenger's syndrome – pulmonary hypertension (scarring of lung tissue and pulmonary vasculature damage) > R-sided cardiac hypertrophy > R pressure then becomes greater than left pressure > shunt reversal and therefore cyanosis. ‘LAVISH’ Low inspired O2 ( decreased PiO2) – e.g at altitiude Alveolar hypoventillation Ventilation/perfusion (V/Q) mismatch Impaired diffusion SHunt e.g. pulmonary AV shunt The Peer Teaching Society is not liable for false or misleading information…

Respiratory failure - COMPLICATIONS
Why? Complications arise if there is a ‘LOAD’ vs. ‘CAPACITY’ mismatch/TIPPING-POINT! Pulmonary: Pulmonary embolism Pulmonary hypertension Barotrauma (ARDS patients e.g. pneumothorax, pneumoperitoneum) Pulmonary fibrosis Pneumonia Extra-pulmonary: GI hemorrhage Right ventricular failure Renal failure Infection Thrombocytopenia/ polycythemia LOAD = resistive loads (bronchospasm, oedema, upper airway obstruction) , lung elastic loads (alveolar oedema, atelectasis, infection) , chest wall elastic loads (ascites, abdominal distention, obesity, pleural effusion, rib #) and minute ventilation loads (hypovolaemia, PE, sepsis) CAPACITY – NEUROMUSCULAR COMPETENCE e.g impaired respiratory drive (OD, brain stem lesion) , impaired neurotransmission (GBS, MND, MG, phrenic nerve palsy) , muscle weakness (fatigue, hypoxaemia (e.g. anaemia), myopathy, undernutrition) The Peer Teaching Society is not liable for false or misleading information…

Obstructive vs. Restrictive
OBSTRUCTIVE (problem getting air Out) Increased resistance to AIRFLOW ↓FEV1/FVC < 70% & increased RV ↓ Radial traction – leading to airway collapse Examples: Acute obstruction such as a foreign body, mucus plug or tumour. Leads to distal collapse of the lung = obstructive atelectasis COPD Asthma Bronchiectasis Cystic fibrosis Sleep apnoea Cor pulmonale RESTRICTIVE Reduced lung VOLUMES STIFF LUNG! Decreased residual volume (RV) FEV1/FVC > 80% & reduced TLC (VC) Examples: Lung parenchyma – granulomatosis, systemic connective tissue disorders, EAA, diffuse progressive pulmonary fibrosis. Chest wall – rib fractures, Kyphoscoliosis, Ankylosing spondylitis, pneumothorax, pleural effusion and disorders. Restrictive disorders of the newborn Neonatal Respiratory Distress Syndrome (NRDS) Remember that some patient may have a MIXED disease pattern. The Peer Teaching Society is not liable for false or misleading information…

Obstructive vs. Restrictive [2]
Obstructive lung disorders - lung volume alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue. High lung volumes are associated with greater traction and decreased airway resistance. Patients with increased airway resistance (asthma) learn to breathe at higher lung volumes to offset the high airway resistance associated with there disease.” In a patient with obstructive lung disease there isn't enough fibrous tissue to apply radial traction on the walls of the bronchioles, therefore they tend to collapse in hence obstruct the airway. At the same time because of the lesser amount of fibrous tissue there is lesser recoil of lung compared to the negative intra-thoracic pressure so here the negative intrapleural pressure wins over the recoil force and the lung volume exapands so this increase in volume would somewhat help the patient to help relieve the airway resistance because the air passages will open somewhat at high volumes offsetting at least some of the increased airway resistance The Peer Teaching Society is not liable for false or misleading information…

Bronchiectasis [1] ‘Abnormal, permanent dilatation of the airways’
Dilatation (‘ectasia’) – pooling of secretions – scarring and inflammation of surrounding tissues. Ciliary dysfunction +/- ulceration Persistent severe inflammation (bronchitis), obstruction and destruction of lung parenchyma. Associated with chest sepsis, septicemia, metastatic abscess formation, R-sided cardiac failure and amyloid deposition. Types LOCALISED (obstruction, focal severe infection) e.g. measles, staphylococcus aureus, klebsiella infection, streptococcus pneumoniae and pseudomonas aeruginosa (CF?) DIFFUSE (cystic fibrosis, ciliary dyskinesias e.g PCD) Consider underlying primary IMMUNE DEFICIENCY syndromes e.g. Common Variable Immune Deficiency (CVID)! *post-infectious = commonest identifiable cause of bronchiectasis CVID – a type of “late onset” hypogammaglobulinemia. Usually presents in the 3rd of 4th decades of life. Compared to other human immune defects, CVID is a relatively frequent form of primary immunodeficiency, found in about 1 in 25,000 persons; this is the reason it is called “common.” The degree and type of deficiency of serum immunoglobulins, and the clinical course, varies from patient to patient, hence, the word “variable.” In some patients, there is a decrease in both IgG and IgA; in others, all three major types of immunoglobulins (IgG, IgA and IgM) are decreased. In still others there are defects of the T-cells, and this may also contribute to increased susceptibility to infections as well as autoimmunity, granulomata and tumors. P aeruginosa is an opportunistic pathogen. It rarely causes disease in healthy persons. In most cases of infection, the integrity of a physical barrier to infection (eg, skin, mucous membrane) is lost or an underlying immune deficiency (eg, neutropenia, immunosuppression) is present. Adding to its pathogenicity, this bacterium has minimal nutritional requirements and can tolerate a wide variety of physical conditions. The Peer Teaching Society is not liable for false or misleading information…

Bronchiectasis [2] Cylindrical is the most common type ~ 47% Varicose ~ 10% post-infective (most common) necrotising bacterial pneumonia, e.g Staph. aureus, Klebsiella, B. pertussis granulomatous disease, e.g tuberculosis, MAIC, histoplasmosis allergic bronchopulmonary aspergillosis (ABPA) measles The Peer Teaching Society is not liable for false or misleading information…

Bronchiectasis [3] Clinical features: Persistent COUGH
One of the causes of CLUBBING (suppurative lung dx + can you name another cause?) Purulent SPUTUM – BUT some patients may have a non-productive cough Dyspnoea No history of smoking + young age of onset = raises suspicion of BE Hemoptysis +/- recurrent pulmonary infections (LRTIs) w/ long recovery times May be referred as ‘treatment resistant asthma’ or a ‘lung cancer’ Investigations: Include: Spirometry, sputum culture, CXR, immunology, serology, functional ciliary studies and bronchoscopy. Q: What is the gold standard for imaging? Q: What is the mainstay of treatment in BE? Q: Name two complications of BE? Q: What is the gold standard for imaging? High-resolution CT (HRCT) Thickened, dilated bronchi and cysts at the end of the bronchioles Airways larger than associated blood vessels = big brochoarterial ratio Q: What is the mainstay of treatment in BE? Antibiotic therapy, physiotherapy (e.g postural drainage) & airway pharmacotherapy (mucolytics, Inhaled corticosteroids (anti-inflammatory agents) (in adults) ect.) Q: Name two complications of BE? empyema and lung abscess The Peer Teaching Society is not liable for false or misleading information…

Bronchiectasis [4] Signet ring sign on CT – cylindrical type bronchiectasis The Peer Teaching Society is not liable for false or misleading information…

COPD [1] Definition: ‘Chronic airflow obstruction secondary to chronic bronchitis and/or emphysema that is NOT fully reversible’ Emphysema Destruction of lung parenchyma - enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls (histology) Centrilobular (commoner = UPPER LOBE) or panacinar pattern (commoner in A1AT = LOWER LOBE). Lobules are MACROSCOPIC structures. If there are confluent areas of destruction > macroscopic BULLAE > increases AIR TRAPPING. Bronchitis – cough & sputum production on most days for 3 months of 2 successive yrs. Submucosal bronchial gland enlargement Goblet cell metaplasia (abnormal change) & mucus hypersecretion Airway oedema Inflamed bronchial tree Smooth muscle and connective tissue hypertrophy Airway epithelial squamous metaplasia & ciliary dysfunction The Peer Teaching Society is not liable for false or misleading information…

COPD [2] 3. Small airway involvement (<2mm) = DON’T FORGET THIS
Involved in EARLY on in COPD – obstructive bronchiolitis = major site of airway obstruction Pulmonary vasculature changes Intimal thickening + endothelial destruction SM hypertrophy and collagen deposition + breakdown of collagen bed architecture. Leads to pulmonary hypertension, hypoxia and a decrease in TLCO and KCO Clinical presentation of COPD – DYSPNOEA that is persistent, progressive and worse with exercise. CHRONIC COUGH – may be intermittent and un-productive. Recurrent wheeze (POLYPHONIC). Chronic SPUTUM production. History or LRTIs + RFs + FHx of COPD. The Peer Teaching Society is not liable for false or misleading information…

COPD [3] - phenotypes Blue bloater = hypoxic drive as C02 retention due to increased dead space (for any given minute ventilation the greater the dead space = poorer the co2 elimination) (becomes insensitive to it) therefore not breathless. More likely to develop cor pulmonale due to vasoconstriction. Pink puffer = compensatory hyperventilation (increased minute ventilation), no cyanosis. Pulmonary capillary bed is damaged unlike bronchitis IN REALITY = SPECTRUM!! The Peer Teaching Society is not liable for false or misleading information…

COPD [4] Risk factors – NAME FIVE!! Tobacco smoking
Indoor & outdoor air pollution Occupational exposures e.g organic and inorganic dusts. Implicated in 20% of COPD diagnoses. Genetic factors – A1AT = <1% of COPD cases. Severe A1AT linked to accelerated and premature development in smokers and non-smokers. Suspect if patient <40 years old at age of onset Increasing age (onset = middle-aged generally) and female gender Poor lung development during gestation or childhood Severe childhood respiratory infections Lower SES COPD exacerbations – worsening of symptoms above normal variation for > 2 days, may require hospital ADMISSION (3-4% mortality rate). Exacerbations are NOT linked to the severity of the underlying disease process. Usually an infective cause. The Peer Teaching Society is not liable for false or misleading information…

COPD [5] - asessment GOLD – 2017 POCKET GUIDE (worth a read guys and girls). Assessment of a patient dyspnoea is either via the MRC score (learn this) or the COPD Assessment Test (CAT). Spirometry is POST-bronchodilator (15-20minutes). The Peer Teaching Society is not liable for false or misleading information…

COPD [6] Peripheral oedema Raised jugular venous pressure (JVP)
Investigations & Assessment (cont.) CXR e.g >6 anterior ribs seen above diaphragm in mid-clavicular line. RULE out DDx e.g. TB, CHF CT – areas of gross emphysema (BLACK areas) – allows assessment of severity & distribution FBC – rule out ANAEMIA Pulse oximetry/ ABG +/- sputum culture Exhaled NO (‘inflammometer’) – COPD w/ eosinophilic dominance? Assess for COR PULMONALE (includes ECG + ECHO) Peripheral oedema Raised jugular venous pressure (JVP) Systolic parasternal heave A loud pulmonary second heart sound (P2) Widening of the descending pulmonary artery on CXR Right ventricular hypertrophy on ECG The Peer Teaching Society is not liable for false or misleading information…

COPD [7] Treatment of COPD – overview: Smoking cessation!!
Diet advice + supplements = improves respiratory muscle functioning Antioxidant mucolytics – productive cough (selected patients) Rx for respiratory failure (e.g non-invasive ventilation – e.g. Rx of respiratory acidosis during an exacerbation) Screen for depression and anxiety Flu (annual) & pneumococcal (one-off) vaccinations +/- palliative care Pulmonary REHABILITATION (6-8 weeks, 2/3 times per week) MRC ≥ 3 or functional impairment INHALED THERAPIES Long-term O2 therapy (LTOT) – if Pa02 < 7.3 kPa + non-smoker OR PaCO pulmonary hypertension, polycythemia, peripheral oedema or nocturnal hypoxia. Surgery – recurrent pneumothoracies, isolated bullous disease (bullectomy), lung-volume reduction surgery (LVRS) A1AT – future role of AAT augmentation therapy (IV)?? The Peer Teaching Society is not liable for false or misleading information…

COPD [8] Stable COPD: B2 agonists – short acting (salbutamol) & long-acting (formoterol & indacaterol). Increase cAMP Antimuscarinics (M3 receptors) – Short-acting (ipratropium and oxitropium) & long-acting (tiotropium, aclidinium) Methylxanthines – theophylline & aminophylline = modest bronchodilator effects. Metabolized by CYP 450 and clearance decreases with age. ICS – e.g. beclomethasone, budesonide and fluticasone = anti-inflammatory agents. Used w/ LABA or as part of a triple therapy of LABA + LAMA + ICS. GOLD guidance – move towards early maximal bronchodilatation w/ LABA +/- LAMA Never use a regular ICS alone as increases the risk of PNEUMONIA by x2 (especially in severe dx) LABAs and LAMAs – reduce exacerbation rates and improve lung function, dyspnoea and health status. Other drugs used – PDE4 inhibitors (roflumilast 500µg OD), exacerbation prophylaxis with macrolide antibiotics (e.g. azithromycin), mucolytics (N-AC and carbocysteine), statins?? Leukotriene modifiers?? (phosphodiesterase type 4 inhibitor) PDE4 inhibition interferes with the breakdown of cAMP, leading to the accumulation of intracellular cAMP. In turn, an elevated concentration of intracellular cAMP activates protein kinase A, which enhances phosphorylation of proteins. This chain of biochemical reactions and physiological processes should: Inhibit numerous inflammatory cell functions, e.g. proliferation and release of cytokines and chemokines, reactive oxygen species, arachidonic acid metabolites, chemotaxis and proteases8 Modulate human airway epithelial cells that might support mucociliary clearance10 Modulate human lung fibroblasts to potentially prevent a fibrotic response12 Inhibit proliferation of pulmonary artery smooth muscle cells, and improve endothelial barrier integrity, thereby reducing pulmonary vascular remodelling.11 The Peer Teaching Society is not liable for false or misleading information…

COPD [8] GOLD – 2017 POCKET GUIDE (worth a read guys and girls). Assessment of a patient dyspnoea is either via the MRC score (learn this) or the COPD Assessment Test (CAT) The Peer Teaching Society is not liable for false or misleading information…

COPD [10] Note on ICS – emerging evidence that unless COPD patient has an eosinophil count of 4% or greater or 300 cells per μL then ICS have little therapeutic benefit with regards to exacerbation prevention = a more tailored approach to COPD rx in the future?? The Peer Teaching Society is not liable for false or misleading information…

COPD [11] COPD exacerbations: They are classified as:
Mild - treated with short acting bronchodilators only Moderate - treated with SABDs plus antibiotics and/or oral corticosteroids Severe – hospitalization (20% of cases) or visits the emergency room. Severe exacerbations may also be associated with acute respiratory failure. Signs of LIFE-THREATENING respiratory failure Respiratory rate > 30 breaths per minute Using accessory respiratory muscles Acute changes in mental status Persisting hypoxemia / need for high FiO2 (>40%) Hypercapnia i.e. PaCO2 increased compared with baseline or elevated> 60 mmHg Acidosis (pH <7.25) Mainstay of Rx – SABAs, SAMAs, systemic corticosteroids 7-14 days (prednisolone 30mg OD) +/- osteoporosis prophylaxis , antibiotics 5-7 days and NIV if required. NIV – BiPaP in COPD exacerbations associated with T2RF as will remove C02. Vs CPAP which is just used for treating hypoxaemia and reducing the work of breathing S.Pneumoniae, H.influenzae and M.catarrhalis = 3 common COPD exacerbation pathogens The Peer Teaching Society is not liable for false or misleading information…

??? Indistinct border + silhouette sign (Loss of silhouette sign more usefully = loss of lung/soft tissue interface e.g in this photo = R heart border loss = anterior pathology in the right middle lobe) + air bronchograms. Pneumonia = a RADIOLOGICAL diagnosis. LRTI = clinical. S.pneumoniae = lung cavitation and empyema potentially. The Peer Teaching Society is not liable for false or misleading information…

Pneumonia (CAP) Infection and inflammation (exudate) of the lung parenchyma – usually bilateral (streptococcus tends to be unilateral). Includes any pneumonia up to 48 hours into current hospital admission. Methods of spread: Inhalation of airborne particles Aspiration of gastric contents or nasopharyngeal flora – e.g. neuromuscular disorders/ reduced GCS/ stroke patients. Haematogenous spread e.g. septic arthritis Common pathogens: S.pneumoniae (RUSTY sputum), Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella sp, H.influenzae and Moraxella catarrhalis (10% of COPD exacerbations). Atypicals tend to have a more insidious onset with more prominent extra-pulmonary features. CAP can be viral (CMV, VZV, SARS) and fungal (PCP* - Pneumocystis jiroveci , aspergillosis, histoplasmosis ect.) Q: Give me some clinical signs of CAP/LRTI? Q: Relationship between AF and pneumonia? Q: Risk factors for CAP? Pneumonia increases risk of AF – origin in the pulmonary veins Question: what signs might you expect in pneumonia?? – intercostal recessions, reduced chest movement, decreased expansion, dull to percuss, crackles, absent/reduced breath sounds,+/- pleural rub early on (‘fresh snow’ sounds), bronchial breathing and whispering pectoriloquy + signs of SEPSIS and HYPOXIA if severe!! New onset cough, pleuritic chest pain, hemoptysis potentially and sputum RF Age <16 or >65 years Co-morbidities CF Asplenia Bronchiectasis COPD Lifestyle Cigarette smoking Excess alcohol IV drug use Iatrogenic Immunosuppressant therapy (including prolonged corticosteroids) The Peer Teaching Society is not liable for false or misleading information…

Pneumonia (CAP) Investigations – “UBEX Special”
Urine & Cultures – exclude UTI, legionella urinary antigen, strep. urinary antigen. Sputum and blood cultures especially if pyretic. Bloods (FBC, U+E’s, biochemistry and CRP) -/ + serological tests (HIV, mycoplasma IgM ect.) Endoscopy and Biopsy – bronchoalveolar lavage (BAL) if non-productive/ ventilated patient X – Imaging CXR +/- lateral view – NEW consolidation on CXR. Repeat in 6 weeks post-discharge to see if underlying malignancy!! ?Chest USS – parapneumonic effusion/ empyema ?CT chest – not usually indicated Special tests ECG – tachycardias, myocardial infarction and arrhythmias Diagnostic tap of pleural fluid – cytology, G-stain, cultures and sensitivities. *Differentials: HF, PE, malignancy, pulmonary TB, ILD *Monitor: CRP, procalcitonin, clinical picture and temperature, O2 sats (ABG if <92% = rule of thumb) The Peer Teaching Society is not liable for false or misleading information…

Pneumonia (CAP) Assessment – ‘CURB 65’ score – SEVERITY of disease!
Confusion (AMTS ≤ 8) Urea (BUN) > 19 mg/dL or > 7 mmol/L RR > 30/min BP – systolic <90 mmHg or diastolic ≤60 mmHg 65 years of age or older *Notes: Score of 2 = IV Abx. 4/5 = ITU/HDU admission Urea INCREASE – I believe this is due to renal insufficiency and dehydration essentially. The Peer Teaching Society is not liable for false or misleading information…

Pneumonia (CAP) Management: Supportive therapies & antibiotics
ABCD approach e.g. CPAP (T1RF and pneumonia), IV fluids, vasopressors (NAdr) – vasoconstriction and adequate glucose control Antibiotics – empirical initially then guided on MC&S Anaerobic cover if aspiration pneumonia e.g. metronidazole Uncomplicated CAP (mild): Amoxicillin (0.5g-1g TDS) or macrolide +/- flucloxacillin (s.aureus = virulent!) Complicated CAP Moderate severity – amoxicillin + macrolide PO/IV Severe – co-amoxiclav IV (1.2g TDS) +/- rifampicin or a macrolide. Thromboprophylaxis w/ LMWH if admitted for >12hours ANALGESIA!! Note: patients may take up to 6 months to fully recovers from CAP – residual symptoms. The Peer Teaching Society is not liable for false or misleading information…

Pneumonia (CAP) What might you see on a CXR and CT w/ PCP?
Question time : What might you see on a CXR and CT w/ PCP? How might a patient with PCP present (HINT: exercise)? Antibiotic of choice for PCP? 16- year old with CAP symptoms + COLD agglutinins? Patient is a HOT TUB enthusiastic who presents with abdominal pain, diarrhea, lymphocytopenia and hyponatremia? 5 complications of severe pneumonia? 3 organisms that are more commonly associated with HAP + one RF? 92 year old lady . 2/52Hx of ‘bad flu’ and acute on chronic confusion. Lives in a nursing home. Coarse crepitations at left lung base and multiple cavitating lesions on imaging (L-lung)? What % of CAP will have no identifiable pathogen? Difference between an empyema and an abscess? What might you see on a CXR w/ PCP? ‘ground glass appearance’ on CT (HRCT). PERI-HILAR OPACITIES on CXR & sub-pleural ‘blebs’ - chest radiographs classically demonstrate bilateral, diffuse, often perihilar, fine, reticular interstitial opacification, which may appear somewhat granular % of CXRs will ne normal. In the context of a CD4 count <200/mm3. How might a patient with PCP present (HINT: exercise)? Dry cough, EXERTIONAL dyspnoea (often profound), fever, often insidious onset. Co-existing opportunistic infections may also be present. Antibiotic of choice for PCP?High dose SEPTRIN (co-trimoxazole). Prophylaxis = co-trimoxazole or neb. pentamidine. 16 - year old with CAP symptoms + COLD agglutinins? Mycoplasma pneumoniae – atypical pneumonia – cold agglutinins = at cold temperatures <31 degrees C Abs (often IgM) vs RBCs lead to a AUTOIMMUNE hemolysis Patient is a HOT TUB enthusiastic who presents with abdominal pain, diarrhea, lymphocytopenia and hyponatremia? Legionnaires' disease – sputum culture and urinary antigen. Rx = flouroquinolone +/- clarithromycin. 5 complications of severe pneumonia? Septicaemia – spread from lung parenchyma, can lead to metastatic infection e.g. endocarditis Lung abcess – look for swinging fever, foul-smelling sputum, weight loss, haemoptysis, pleuritic chest pain Atrial fibrilation esp. in elderly, may require beta-blocker Pericarditis/myocarditis may complicate pneumonia Hypotension – may be due to dehydration and sepsis-induced vasodilatation Empyema – if recurrent fever, yellowish pleural effusion aspirated Respiratory failure – type 1 is common, act if PaCO2 >6kPa Other: worsening of pre-existing HF 7. 3 organisms that are more commonly associated with HAP? S.aureus, Klebsiella spp, Pseudomonas aeruginosa & other Enterobacteriaceae (E.coli etc.) – RFs include – increasing age, mechanical ventilation and respiratory tract obstruction. 8. 92 year old lady . 2/52Hx of ‘bad flu’ and acute on chronic confusion. Lives in a nursing home. Coarse crepitations at left lung base and multiple cavitating lesions on imaging (L-lung)? S.aureus infection 9. What % of CAP will have no identifiable pathogen? Around 30% 10. An empyema is a collection of pus in a pre-existing cavity/space such as the pleural space. Absecess e.g lung abscess is within the lung parenchyma (parenchymal necrosis). Empyema is defined as pus in the pleural space. It typically is a complication of pneumonia. However, it can also arise from penetrating chest trauma, esophageal rupture, complication from lung surgery, or inoculation of the pleural cavity after thoracentesis or chest tube placement. The Peer Teaching Society is not liable for false or misleading information…

?? What would you see/find on examination??
Meniscus sign on RHS – stony dull to percuss. May be mediastinal shift if v.large effusion. The Peer Teaching Society is not liable for false or misleading information…

Pleural effusion [1] The pleural space normally contains 0.3ml/kg of fluid 0r 10-20ml. This fluid is spread thinly between the visceral and parietal pleura and is reabsorbed and produced by the parietal pleura via lymphatic stoma. TOO MUCH = pleural effusion. Causes: 40+ causes BUT only need to be aware of a few & categorise them! TRANSUDATES (SYSTEMIC) – oncotic PRESSURE and hydrostatic force alteration [<25g/l] Very common – heart failure & liver cirrhosis (hypoalbuminaemia) Less common – nephrotic syndrome, hypothyroidism & peritoneal dialysis Rare – constrictive pericarditis, urinothorax and Meigs’ syndrome (U/L effusions and ovarian fibroma - can be classified as an exudate as well) EXUDATES (LOCAL) – altered PERMEABILITY of the vasculature = INFECTION, INFLAMMATION & MALIGNANCY [>30g/l] Common – malignancy (direct pleural invasion) , parapneumonic (s.pneumoniae = 20-60%) and Tb. Less common – PE (tissue necrosis), RA, lupus, ARDS, benign asbestos effusion, pancreatitis and post-MI (Dressler’s syndrome) LDH – marker of ongoing INFLAMMATION – classically high in exudates The Peer Teaching Society is not liable for false or misleading information…

Pleural effusion [2] Light’s Criteria: useful in pre-existing low protein states. The Peer Teaching Society is not liable for false or misleading information…

Pleural effusion [3] Management:
Importance of Hx – e.g. history of asbestos exposure – mesothelioma? Transudate – TREAT the UNDERLYING CAUSE e.g. trial of a diuretic for LVF before drainage Pleural aspiration w/ USS guidance +/- pleural biopsy, thoracoscopy and VATS Therapeutic medical or surgical pleurodesis e.g. using TALC – causes scarring and obliterates pleural space. Pleural fluid tests: WHAT DOES IT LOOK LIKE as DDx = empyema?? Biochemistry – LDH & protein MC&S – TB / parapneumonic – INFECTION? Cytology and differential cell count – malignancy, pneumonia, pancreatitis?? (AMYLASE?) pH – parapneumonic effusion (complicated or simple?) or acidosis <7.2 = empyema? hence drainage is needed – stops progression to FIBROSING PLEURITIS. Note: CRP >200 predicts progression to a parapneumonic effusion in pneumonia. Glucose – LOW in RA, Tb and infections TAGs and cholesterol – chylothorax Hematocrit/ appearance – diagnosis of haemothorax/ malignancy* CHF- related effusions – 75% will resolve with 2 days of diuretic Rx Parapneumonic effusions = priority Small effusions = therapeutic thoracentesis Complicated effusions or empyemas – tube thoracostomy The Peer Teaching Society is not liable for false or misleading information…

Pleural effusion [4] Lifeinthefastlane.com = really useful site to look at for this The Peer Teaching Society is not liable for false or misleading information…

??spot diagnosis Erythema nodosum - also occurs in IBD. Usually self-limiting in 2-6 weeks. Usually isolated to the extensor surfaces of the legs. RHS = lupus pernio (cutaneous sarcoidosis manifestation) = PATHOGNOMONIC of sarcoidosis – associated with poorer outcomes. Granulomatous infiltration The Peer Teaching Society is not liable for false or misleading information…

Sarcoidosis Skin – erythema nodosum Arthritis esp. of feet, hands
‘SARCOID’ – multisystem chronic inflammatory condition Skin – erythema nodosum Arthritis esp. of feet, hands Respiratory – bilateral hilar lymphadenopathy (BHL), pulmonary infiltrates Cardiac – heart block, VT, heart failure Ocular – anterior uveitis, can lead to blindness Intracranial (brain) – chronic meningitis, seizures, neuropathy Derangement of liver and renal function – hepatic granuloma (70% patients), hypercalcaemia (can lead to kidney stones and nephrocalcinosis) *LOFGREN Syndrome – acute form of sarcoidosis = BHL + erythema nodosum + arthralgia *Raised ESR (65% of cases) and raised serum ACE (limited use clinically and NOT for monitoring disease progression – secreted by NCGs) *HISTOLOGY – non-caseating granulomas (NCGs) . Granuloma definition – a collection of epithelioid histiocytes (macrophages). DDx: Infection, maliganacy, EEA, industrial dust disease, histocytosis and Tb Prognosis: the disease is known to be more severe in certain races, in black Americans mortality rates of 10% have been seen. Progressive fibrosis, pulmonary artery hypertension and cor pulmonale are the most frequent causes of death. Less commonly myocardial disease may result in death. The Peer Teaching Society is not liable for false or misleading information…

Sarcoidosis Investigations:
Bone profile - calcium, corrected calcium, albumin, total protein and alkaline phosphatase Serum ACE CXR Mantoux test to rule of TB (langhan’s giant cells) FBC etc. Bronchoalveolar lavage Transbronchial biopsy Treatment: Stage I-III (III=infiltrates alone, II= BHL & infiltrates I=BHL) = remission likely Stage IV (pulmonary fibrosis) ~ prednisolone 4-6wks (40mg/day) +/- bone protection DDx: Infection, maliganacy, EEA, industrial dust disease, histocytosis and Tb Prognosis: the disease is known to be more severe in certain races, in black Americans mortality rates of 10% have been seen. Progressive fibrosis, pulmonary artery hypertension and cor pulmonale are the most frequent causes of death. Less commonly myocardial disease may result in death. The Peer Teaching Society is not liable for false or misleading information…

??diffuse alveolar damage – Hx of severe burns
Widespread B/L pulmonary oedema and pulmonary hemorrhages The Peer Teaching Society is not liable for false or misleading information…

ARDS ‘SUDDEN & SEVERE lung damage’
Acute lung injury w/ DIFFUSE ALVEOLAR DAMAGE secondary to a direct pulmonary source or due to a severe systemic injury Leakage of fluid into the alveoli ~ non-cardiogenic pulmonary oedema (no response to diuretics!!) and reduced arterial oxygenation. Causes – some examples Pulmonary ARDS – trauma/lung contusion, fat embolism, DIC & viral pneumonia Extra-pulmonary – sepsis, multiple blood transfusions, pancreatitis, burns and hypovolemic shock *50% mortality – if it does resolve patients often have some pulmonary fibrosis and will develop a chronic lung disease. *CXR features develop 12-24hours after initial acute lung injury due to widespread interstitial oedema. ITU – treat underlying disease, NIV, conservative fluid management, Abx if infectious cause and sedation The Peer Teaching Society is not liable for false or misleading information…

Pneumothorax Air in the pleural space – due to the rupture of a pleural bleb (thin walled air containing spaces) usually APICAL, thought to be due to congenital defects in the connective tissue of the alveolar walls. Localised if adhesions have occurred between the visceral and parietal pleura or generalised 3 TYPES: 1. SIMPLE No communication w/ the atmosphere and no mediastinal shift & NON-expanding. Pleural cavity pressure LESS than the atmospheric pressure (unlike a tension pneumothorax) 2. TENSION - life-threatening!! Progressive build-up of air within the pleural space, usually due to a lung laceration which allows air to escape into the pleural space but not to return. Exacerbated by +IVE pressure ventilation. Air entry can persist if there is a bronchopleural fistula. BEWARE the BILATERAL tension pneumothorax! 3. COMMUNICATING (‘OPEN or ‘SUCKING CHEST WOUND’) Loss of integrity of the chest wall e.g. secondary to penetrating chest trauma. Leads to a paradoxical collapse of the affected lung during inspiration. The Peer Teaching Society is not liable for false or misleading information…

Pneumothorax Causes: 1. Primary spontaneous
No underlying lung disease – associated with Marfan’s syndrome and Ehlers-Danlos syndrome Patients often TALL & THIN. +/- familial component 2. Secondary spontaneous Underlying lung pathology or disease e.g. COPD (emphysema), asthma, CF, lung abscess and necrotic pneumonia. 3. Traumatic/iatrogenic Ventilator – associated, percutaneous biopsy and pulmonary laceration. Treatment depends on: SIZE of the pneumothorax, SYMPTOMS & background lung disease/respiratory reserve. Treatment options = no Rx and radiological follow up (<2cm) > needle aspiration (decompressive needle thoracostomy) > intercostal chest drain. The Peer Teaching Society is not liable for false or misleading information…

Tension pneumothorax - EMERGENCY
Signs ~ Presentation is variable and may initially have no symptoms. With time severe dyspnea, tachycardia and hypotension occur. Distended neck veins and tracheal deviation are also often present. Eventually impaired venous return results in cardiac arrest and death. This can occur within minutes. Signs – distended neck veins, shock, subcutaneous emphysema, hyper-resonant percussion note, tracheal displacement and cyanosis. The Peer Teaching Society is not liable for false or misleading information…

Resp. examination - summary
Important to rule out the following during primary survey: ‘ATOM FC’ Airway obstruction Tension pneumothorax Open pneumothorax Massive haemorrhage (>1500ml) Flail chest – abnormal breathing within lung tissue Cardiac tamponade The Peer Teaching Society is not liable for false or misleading information…

Asthma - Epidemiology & Aetiology
5.4 million people in the UK 1 in 11 children - aka 3 children in every classroom Commonly starts between ages 3-5 years Aetiology: Genetic - atopy triad - asthma, hayfever, eczema Environmental Hygiene hypothesis, maternal smoking Allergenic - childhood exposure to allergens, occupational exposure Hygiene hypothesis- growing up in a relatively clean environment may predispose towards an IgE response to allergens The Peer Teaching Society is not liable for false or misleading information…

Asthma - Triggers NSAIDs - Samter’s triad (asprin exacerbated respiratory disease) → block COX-1, decrease thromboxane + anti-inflam prostiglandins → increased pro-inflamatory prostaglandins BB - Beta-adrenoreceptors allow widening of airways The Peer Teaching Society is not liable for false or misleading information…

Allergenic Asthma - Pathophysiology
Immediate: Trigger IgE mediated type 1: hypersensitivity Mast cell degranulation Histamine + cytokines release Bronchoconstriction Mucus production Inflammation (Increased vascular permeability) Long-term: - Airways remodeling Repeated airway constriction → smooth muscle hyperplasia + hypertrophy Mucus gland hyperplasia + metaplasia → increase in goblet cells The Peer Teaching Society is not liable for false or misleading information…

Asthma - Symptoms and Signs
Intermittent dyspnoea Tachypnoea Wheeze Polyphonic wheeze Chest tightness Hyperinflated chest + hyperresonance Sputum Cough (often nocturnal) Ask about: Triggers Diurnal variation - worse at night? Other atopic symptoms RCP3: Daytime symptoms Effect on daily life (housework, school) Sleep (nocturnal waking, cough) Get students to remember triggers Students explain S&S due to pathophysiology The Peer Teaching Society is not liable for false or misleading information…

Asthma - Investigations
Peak expiratory flow- diurnal variation >20% on >3days/week for 2-4 weeks Bronchodilator reversibility testing: baseline spirometry → salbutamol → repeat spiro after 15min → ↑FEV1 by >15% Spirometry: decreased FEV1/FVC Therefore is what type of respiratory disease? Obstructive because FEV1/FVC < 0.7 The Peer Teaching Society is not liable for false or misleading information…

Asthma - Management SABA (short acting beta agonist) - Salbutamol
ICS (inhaled corticosteroid) - beclomethasone LABA - salmeterol increase ICS - up to 800mcg theophylline (aminophylline) or leukotriene antagonist (montelukast) Increase ICS (2000mcg), add theophylline Oral prednisolone Start at the step most appropriate to severity; move to next step if needed, or back if control is good for >3months The Peer Teaching Society is not liable for false or misleading information…

Asthma - Further Management
Conservative: Stop smoking Avoid precipitants Education: Ensure good inhaler technique PEFR monitoring Interventional: Possible bronchial thermoplasty The Peer Teaching Society is not liable for false or misleading information…

Asthma - Acute Management
Classifying asthma severity Life-threatening (PEFR <33%): 33,92 CHEST 33: PEFR <33% predicted 92: Sats <92% Cyanosis Hypotension Exhaustion Silent chest Tachycardia Severe (PEFR <50%): Can’t complete sentences, RR>25, PR>110 Moderate (PEFR <75%) Mild (PEFR >75%) ABCDE O SH*T ME! Oxygen- maintain sats at 94-98% Salbutamol Nebulised Hydrocortisone IV or oral prednisolone- oral daily, IV 6 hourly *Ipratropium bromide 4-6 hourly (if poor response/severe/life threatening) Theophylline- usually in ICU Magnesium sulphate- one off dose if life threatening (before theophylline) Escalate care (intubation and ventilation) ABCDE O SH*T ME = everything before the * give straight away, other elements if refractory to initial treatment Give all together initially Give if needed with senior input The Peer Teaching Society is not liable for false or misleading information…

Case 1 Janet is a 79-year-old Smokes cigarettes History of angina
Presents to your accident and emergency (A&E) department with chest pain worse on inspiration and shortness of breath The Peer Teaching Society is not liable for false or misleading information…

Pulmonary Embolism Definition: Blockage of pulmonary artery or one of its branches in the lung by a venous thromboembolism Aetiology/PP: DVT forms in leg (iliofemoral veins) → dislodges and travels to lung → occlusion; rarely R atrial emb Risk factors: OCP, age >65, immobility, pregnancy, malignancy, recent surgery (esp. pelvic/lower limb), prev VTE, obesity The Peer Teaching Society is not liable for false or misleading information…

Pulmonary Embolism - Signs and Symptoms
Headlines: dyspnoea, pleuritic chest pain, hemoptysis, shock Other: Cyanosis, fever, tachypnoea/cardia, hypoT, raised JVP, pleural rub, pleural effusion, collapse The Peer Teaching Society is not liable for false or misleading information…

Lung Blood Supply Q: Why do peripheral PE’s only cause ischaemia not infarction? The Peer Teaching Society is not liable for false or misleading information…

Possible PE, what do you do next?
The Peer Teaching Society is not liable for false or misleading information…

Case 1 Blood pressure is 132/86 mmHg, SpO2 95% on air, respiratory rate 16 breaths per minute, heart rate is 72 beats per minute temperature 36.2 There are no clinical signs of a DVT. Upon further questioning you identify that she sprained her ankle 5 days ago and has ‘been keeping her feet up’ since. The Peer Teaching Society is not liable for false or misleading information…

Hampton’s Hump = wedge shaped infarct

Westermark Sign  collapse of vasculature distal to PE leading to a sharp cut off

Fleischner sign  dilated central pulmonary vessel

Case 1 – PE ECG PE is identified on Helen’s V/Q SPECT scan. What would you do next? LMWH or fondaparinux Unfractionated Heparin if complex Renal failure Bleeding risk Hemodynamically unstable ECG changes in PE? The Peer Teaching Society is not liable for false or misleading information…

The D-dimer test is positive.
Case 1 The D-dimer test is positive. Her hospital records show that she had an allergic reaction to contrast media in the past, therefore you cannot offer CTPA. What other investigations could you offer? The Peer Teaching Society is not liable for false or misleading information…

Case 1 - Further Investigations
D-dimer CTPA ALTERNATIVE  V/Q radio-nucleotide scan (if CTPA C/I) The Peer Teaching Society is not liable for false or misleading information…

Saddle Embolus = MASSIVE PE

Case 1 - Management PE is identified on Helen’s V/Q SPECT scan. What would you do next? LMWH or fondaparinux Unfractionated Heparin if: Renal failure Bleeding risk Haemodynamically unstable ECG changes in PE? The Peer Teaching Society is not liable for false or misleading information…

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Respiratory medicine.

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