Resp Flashcards
Asthma What? Presentation? Common allergens? Drug cautions?
Chronic inflammatory airway disease characterised by intermittent obstruction and hyperreactivity
Recurrent wheezing, breathlessness, chest tightness, coughing
Allergic: house dust mite, pet fur, grass pollen -> IgE
Non: exercise, cold air, stress, strong emotion, viral infx, smoking
Beta blockers - B2 cause airway constriction
NSAIDS or aspirin block COX-1 -> decrease prostaglandins + overproduction of pro-inflammatory leukotrienes
Pathophysiology of asthma
Early phase
Exposure to allergen in presensitised individual
X-link IgE on mast cells
Release inflammatory mediators histamine, leukotrienes and TNFa ->
Increase in vascular permeability and autonomic hypersecretion of mucus -> airway oedema
Increase in airway tone and increased smooth muscle responsiveness
Both lead to narrowed airways
Constriction at 30 mins, inflammation at 3 hours
Late phase: eosinophil mediated (recruited by IL4 and IL5) at 6 hours
Increased goblet cells
Epithelial denudation -> airway hyperresponsiveness
Deposition of matrix proteins and swelling -> airway remodelling and smooth muscle hyperplasia
Presentation of Asthma
Worse at night and early morning Wheeze (polyphonic and expiratory) Episodic SOB Chest tightness Cough - *worse at night FHx atopy/nasal polyposis Diurnal variation - *worse in morning
Assessment of asthma control
How often felt SOB? How often woken from sleep? How often used reliever? How often interfered with normal activities e.g. school/work? How rate asthma control? Asthma control questionnaire Inhaler technique
Ix for asthma
PEFR (peak flow rate) - diurnal variation >20%, according height/weight
Reversibility testing FEV1 improves by 15% with SABA (or PEF - 20%)
Spirometry
FEV1 < 80% + *FEV1/FVC < 70% = obstructive
CXR: normal or hyperinflation
Step wise management of asthma
SABA \+ low ICS (800ug) \+ LTRA (montelukast) \+LABA (May remove or keep LTRA) \+ Higher does of ICS (200ug) \+ 40mg Pred Hospital admission
Antimuscarinic agents - Ipratropium/Triotopium can be used as adjuctive therapy.
Acute asthma management
Moderate - PEF 50-75%
Severe - PEF 33-50%, RR>25, HR>110, inability to complete sentences (one of)
Life threatening - PEF<33%, SpO2 <92%, PaO2 < 8kPa, silent chest, exhaustion
Steroids within 1 hour
O2 aim 94-98%
Nebulised salbutamol
Reassess severity -> repeat salbutamol (every 20 mins) up to 3
If poor response add nebulised ipratroprium bromide up to 3
Within 1 hour: oral pred (mild) or IV hydrocortisone (sev/lt)
If PEF < 50% IV MgSO4 IV theophylline IV salbutamol Intubate + ventilate if exhaustion
COPD
What?
Pathophysiology (2 parts)?
Aetiology
Chronic obstruction with irreversible airflow obstruction -> air trapping and hyperinflation
Narrowing of airways and mucosal oedema -> mucus hypersecretion -> cough and excessive mucus for 3M per year for >2y
Elastin breakdown: Permanent destruction and enlargement of alveoli
Cigarette smoking -> inactivation of A1AT
Occupational (particles and gases)
A1ATD
COPD
Symptoms
Signs
Pink puffer vs Blue bloater
SOB (initially with exercise but progresses) + cough (morning)
Barrel chest, CO2 flap, hyperresonant percussion, distant breath sounds (over bullae, hyperinflation and trapping), coarse crackles (exacerbation), wheeze (exacerbation)
Pink puffer: emphysema -> CO2 retention -> old and thin, use of accessory muscles
Blue bloater: peripheral oedema and overweight from RHF
COPD complications
Cor pulmonale - RHF secondary to long standing COPD - raised JVP, distended neck veins, hepatomegaly - Rx: LTOT + loop diuretic
Pneumonia - pneumococcal vaccine and yearly influenza vaccine
Depression*
Polycythaemia
Respiratory failure:
T1: PaO2 < 8 (Ventilation/perfusion mismatch)
T2: PaO2 < 8 + PaCO2 > 6.0 (Alveolar hypoventilation)
Ix of COPD
4 x ray changes.
Spirometry: Classification based upon FEV1 Obstructive pattern: FEV1/FVC < 0.7 Non-reversible Decreased pulse oximetry ABG: may see hypoxia +- hypercapnia CXR: Flattened diaphragm Increased intercostal spaces Hyperlucent lungs Increased AP diameter FBC: may see polycythaemia (HCT > 0.55) + Hb rise
Management of COPD
Patient education + vaccination + depression screen + COPD nurse
Smoking cessation, exercise, obesity mgmt (pulmonary rehabilitation)
Inhaled therapy
LTOT (*15hrs) IF PaO2 <7.3 or 7.3-8 with SaO2 < 88 or CHF or oedema or PCV
Inhalers if no significant improvement.
Infective exacerbation of COPD
Management
SABA + SAMA neb (salbuamol + ipratropium) + O2 (24% venturi aim for 88-92%)
Oral corticosteroid (prednisolone) - prevents recurrence
Airway clearance - mucolytics + physio
BIPAP if respiratory insufficiency
Blood culture and sputum culture + gram stain
Community (less severe)
Narrow spectrum: amoxicillin or doxycycline
Hospital
Broad spectrum: ?IV vancomycin or tazocin
Cell differences in COPD vs Asthma
Neutrophils + macrophages = COPD
Mast cells + eosinophils = Asthma
CURB 65
CURB 65 Confusion Urea > 7 RR > 30 BP < 90 or < 60 diastolic 65
Score
0-1 - low risk, recommend outpatient care
2 - moderate risk - to hospital
3-5 - high risk = to ITU (30 day mortality = 15-40%)
Pneumonia Ix & Chest xray changes
FBC, CRP (raised WCC, raised CRP)
ABG: may be low oxygenation
Sputum culture and sensitivity - for causative
CXR - lobar
Air bronchograms
Consolidation: homogenous opacification in lobe
Atelectasis if small airway obstruction (incomplete obstruction)
If atypical = diffuse reticular or reticulonodular opacities (affects interstitium)
Blood culture - for causative organism
*Urinary antigen: for legionella and pneumococcus
Pneumonia management Low/Mod/Severe Hospital aq Legionella Chlamydia
O2 if needed + IV fluids if needed +
Low risk (0-1) CAP: Oral 5 day amoxicillin
Mod (2) CAP: Oral 7-10 days amoxicillin + clarithromycin (doxycycline if allergic)
Mod and high risk (2+) CAP: 7-10 day dual therapy:
Co-amoxiclav + clarithromycin (IV) if penicillin allergic = cefotaxime
HAP: IV cefotaxime + gentamicin
Legionella: Clarithromycin + fluoroquinolone
Chlamydia: Doxycycline
Complications of Pneumonia
Septic shock
ARDS - non-cardiogenic pulmonary oedema
Pleural effusion (50%) + empyema
*Hepatisation (histologically)
Bilateral hilar lymph enlargement
Sarcoid
TB
Lymphoma
TB aetiology
Risk factors
Organisms
Birth endemic (asia etc), immunocompromised (e.g. HIV), exposure (v.infective)
Poor nutrition, overcrowding, IVDU, homeless, prisons
M. tuberculosis, m. bovis
TB Pathophysiology
MP @ midzone of lun engulfs bacteria
MP + LC -> granuloma -> Ghon Focus
MP presents antigen to T cell -> caseation
Caseation heals and calcifies -> some bacilli -> regional LN (mediastinal) -> Ghon complex (calcified focus + associated LN)
Secondary lesions form @lung apices -> fewer WBC (usually at year 1 or 2)
TB Presentation
Cough (+haemoptysis) + fever + weight loss + night sweats + weight loss + RF
Pleuritic chest pain + erythema nodosum
Crackles, bronchial breathing
Ix for TB
CXR:
Primary: consolidation + ipsilateral hilar enlargement (lymphadenopathy)
Healed primary: Ghon focus: large round calcified lesion near hilum
Post primary: fibronodular upper zone opacities with cavitation + calcification + consolidation to hilum
3 x sputum acid fast bacilli smear Ziehl-Neelsen stain - pink Sputum culture No growth or solid medium = 4-8 weeks or liquid medium = 1-3 weeks FBC - leukocytosis and anaemia NAAT - +ve for m.tuberculosis
Medical TB management
Infectivity TB management
6M Rifampicin: liver tox, orange secretions, induces hepatic enzymes (accelerate oestrogens, steroids, anticoagulants, phenytoin)
6M Isoniazid: liver tox, peripheral neuropathy (give w/ pyridoxine B6)
2M Pyrazinamide: liver tox, hepatitis
2M Ethambutol: *visual disturbance: optic neuritis, loss of acuity
Isolate patient e.g. negative pressure room
Contact tracing and treatment
Decreased infectivity after 2 weeks of treatment + 3 consecutive -ve AFB smears
Screen household and close contacts
Extra pulmonary TB (8)
Pleura - pleural TB leads to pleural effusion
LN - scrofula - swelling and discharge
GU - frequency/dysuria/haematuria
Bone - osteomyelitis starting in growth plates of bone Pott’s disease - vertebral fracture associated with TB
Brain - TB meningitis - Rich foci
Abdomen - ascites (peritoneal) and abdominal LN
Miliary TB: millet seed appearance on CT: liver/spleen/lung - by haematogenous spread
DVT
Clot forming triad
Risk Factors
Virchow’s triad: venous stasis, vessel injury, activation of clotting system (hypercoaguable state)
Thromboembolic risk factors:
Cancer, trauma, major surgery, hospitalisation, immobilisation, oral contraception, obesity/preg (high oestrogen), recent flight (immobilisation)
Genetic risk factors: (Family history)
Factor V leiden, protein C deficiency, protein S deficiency, antithrombin deficiency, antiphospholipid
Wells scoring for DVT Ix pathway
0 or 1 = D dimer If D dimer negative = No DVT. D dimer positive/2 or more Wells = USS <4hours If positive = Treat. If negative = Repeat @6-8 days
Types of pulmonary embolism
Thrombus formation in distal veins -> 50% will embolise Amniotic fluid embolus Fat embolus (at long bone fracture) Air embolus Tumour embolus
X ray appearance of PE
Wedged shaped opacity set against the pleura.
PE Wells scores
DVT = 3 Most likely = 3 TachyC (>100) = 1.5 Immobilisation (bed > 3 days or surg in 4 weeks) = 1.5 Hx DVT/PE = 1 Haemoptysis = 1 Malig (6 months) = 1 4 points = PE likely
Ix for PE
ECG: sinus tachycardia, S1Q3T3, RBBB D dimer + CTPA CXR: Decreased vascular markings, atelectasis, small pleural efusion Late sign: wedge shape infarction ABG: reduced PaO2, high lactate
