Clinical Lectures Flashcards
Angle of Louis
T4/T5 intervertebral disc
Bifurcation of trachea
Start and end of aortic arch
Azygous vein enters SVC
Lung cancer
Mainly non small cell lung cancer NSCLC 81%, small cell 13%
Clinical features: smoker, heamoptysis, weight loss, dyspnoea, cough, chest pain, hoarse voice
Examination findings: features suggesting metastases, finger clubbing, cervical/supraclavicular lymphadenopathy, SVC obstruction
How do we find it: CXR then CT chest to confirm cancer, staging via bronchoscopy, biopsy, PET, endobronchial ultrasound EBUS
Treat: surgery, radiotherapy, chemotherapy
complications: SVC obstruction (raised JVP, cyanosis lips, collaterals), Horners syndrome (miosis, ptosis, enopthalmos), pleural effusion, recurrent laryngeal nerve palsy
Pleural effusion
Clinical features: dyspnoea, pain, reduced expansion, dull percussion note, reduced vocal resonance
Leakage into the pleural space produced by pathology in pleural space
Managing: tap fluid, aspirate, drain
Mesothelioma
Cancer of pleura related to asbestos exposure
Risk professions
Common presentations: pain, pleural effusion, diagnostic path similar to Lung cancer
Treatment: chemotherapy, radiotherapy, surgery (pleurectomy), immunotherapy, gene therapy
What is the pulmonary interstitium
Interstitial compartment is the portion of the lung sandwiched between epithelium and endothelial basement membrane, section that surrounds alveolar sac and space between capillary
Only visible radiographically when disease increases its volume and attentuation
Loose connective tissue
Bronchovascular division
Parenchymal division
Subpleural division
interstitium is where diffusion for gas exchange occurs
Pulmonary fibrosis
Type of interstitial lung disease
Restrictive disease, low FVC normal FEV1/FVC because fev1 and FVC reduced, low RV low TLC, spirometry, CXR, CT thorax. Subpleural reticular shadows, honeycombing, lung biopsy
DLCO- diffusing capacity is low
Scarring of the lung parenchyma usually following inflammation
Symptoms: dry cough, dyspnoea, fine end inspiratory crackles
Common in: 60-70 males, smokers, family history
Treatment: pirfenidone- anti-fibrotic, ambulatory O2/ lung transplant
Complications: poor prognosis: median survival rate 2.5-3.5 years
Sarcoidosis interstitial lung disease
Inflammatory condition defined by presence of ‘non-caseating granulomas’ these are small patches of red and swollen tissue
Clinical features: cough, gradual onset SOB, polyarthralgia, Löfgrens syndrome
Who: Afro-Caribbean, young adults, females, family history
Diagnosis: routine bloods, calcium raised, CXR, CT chest (ground glass appearance)
Treatment: observation or steroids, maybe immunosuppression (methotrexate)
Complications: pulmonary hypertension, respiratory failure fibrosis
Usual interstitial pneumonia UIP
Basal
Peripheral/sub-pleural
Not much ground glass
Honeycombing
Nil on antibodies etc
Non-specific interstitial pneumonia NSIP
Anything non specific
Generally better prognosis than classical UIP
Bronchoscopy may help, cell types on washing BAL
No honeycombing, only mild inflammatory changes
Management of interstitial lung diseases
Depends on cause, histology, severity, rapidity of progression
IPF- pirfenidone or nintedanib antifibrotics
Progressive pulmonary fibrosis nintendamib
Autoimmune disease-> immunosuppression
Transplantation
Monitor using PFTs pulmonary function tests
COP- corticosteroids
Smoking related ILD- respiratory bronchiolitis ILD RB-ILD etc smoking cessation
Hypersensitivity pneumonitis- avoidance of causative agent, corticosteroids
CTD-ILD- immunosuppression- corticosteroids
Sarcoidosis -corticosteroids
Treatments for IPF- antifibrotics
Pirfenidone:
5-methyl-1-phenylpyridin-2-one
Inhibits TGF-beta stimulated collagen synthesis
Decreases extracellular matrix
Inhibits fibroblast proliferation
Nintedanib:
BIBF 1120
Intracellular tyrosine kinase inhibitor
Extrinsic ‘allergic’ alveolitis EAA/ hypersensitive pneumonitis
Caused by inhalation of organic particles
Antibody formation ‘precipitins’ & T cell sensitisation
-leads to type III/ type IV hypersensitivity lung damage
Acute- may be confused with asthma or bronchitis dry cough, hypoxia, fevers, myalgia
Chronic- progressive dyspnoea, irreversible lung damage
Sub acute
Presentation determined by type exposure
Short and intense= acute, pigeon breeder etc
Long and low grade= chronic, fibrosis parrot owner
Diagnosis- identification potential antigen, characteristic radiological findings. Treatment- antigen avoidance, steroids
Granulomatous lung disease
Bugs: TB , fungi
Inflammatory: sarcoidosis , extrinsic allergic alveolitis
Vasculitic: Churg-strauss, Wegeners- granulomatosis with polyangiitis, polyarteritis nodosa
Löfgren’s syndrome
Triad:
-BHL- bilateral hilar lymphadenopathy
-erythema nodosum- skin inflammation red painful lumps most common front of legs
-polyarthralgia
Vasculitis
Inflammation of blood vessels
May obstruct vessels or cause bleeding
Often multisystemic, commonly renal
Eg Wegeners granulomatosis, goodpastures disease
Pulmonary haemorrhage
Dyspnoea, haemoptysis, looks opaque on CXR, PFTs show high gas transfer, visualise at bronchoscopy
Granulomatosis with polyangiitis (inflammation vessels)
Upper airway: granulomas- bleeding, sinusitis, saddle nose- septal destruction
Lungs: haemorrhage, cavities
Airway disease
Disease predominantly of the airways of the lung (bronchi, bronchioles, alveoli) where gas/air travels in inspiration and expiration. Include asthma, copd, bronchitis
Variable airflow limitation
Airway hyper responsiveness
Chronic airflow limitation
Airway inflammation
Measurements in airways diseases
Spirometry with the effect of an inhaled beta agonist it measure reversibility
PEF to measure diurnal variation of airflow limitation
Post beta agonist spirometry for chronic airflow limitation
Methacholine tests to measure airway responsiveness
Measures inflammation- exhaled NO, blood eosinophils, total IgE
FEV1/FVC ratio comparison
Obstruction: FEV1/FVC<0.7 low
Restriction: normal or high FEV1/FVC
Obstructive have a scooped out flow volume loop
Asthma
Chronic inflammatory disorder of the airways leading to airflow obstruction
Variable airflow obstruction increased FEV1 post bronchodilator diurnal variability in PEFR
Airway hyper responsiveness
Associated with atopy/allergy
Inflammation and bronchoconstriction
Coughing, wheezing, chest tightness, SOB
What happens in an asthma attack: airway narrowing caused by contraction smooth muscles, swelling of epithelium, increase mucous production
Triggers: allergens, irritants, cold air, exercise etc
Occupational asthma ask maintain PEFR at work
Inhaled asthma therapy
Long acting anti muscarinic eg tiotropium- bronchodilator targets Parasympathetic receptors
B2 agonist eg salbutamol, salmeterol- bronchodilator targets smooth muscle contraction
Steroids- fluticasone, targets inflammation
Oral steroids in asthma
Rarely needed in maintenance therapy used for exacerbations
Keep dose as low as possible
COPD
Chronic obstructive pulmonary disease: characterised by airflow obstruction that’s not fully reversible
Emphysema and chronic bronchitis commonly seen
Risk factors: smoking, asthma, occupational exposure to dusts and chemicals, exposure to fumes from bringing fuel, genetics
Activates inflammatory cells releases proteases and oxidants leads to parenchymal damage and mucous hypersecretion
Mucociliary dysfunction, structural changes, airflow limitation, systemic component
Increased SOB, sputum volume and green sputum, crackles in chest
Managing COPD
Maximise bronchodilation- improves symptoms ensures mucous clearance reduce inflammation and bacterial colonisation
Short acting b agonist SABA- salbutamol
Long acting muscarinic antagonist LAMA eg tiotropium
Combination long acting bronchodilators
Add an inhaled steroid in selected patients
Exacerbations COPD
Respiratory tract infections
Peaks of air pollution
Interruption of maintenance therapy
Idiopathic
Mimics/aggravators: pneumonia, pulmonary embolism, pleural effusion, arrhythmia/ congestive cardiac failure, pneumothorax
Management:
-steroids- prednisolone , nebulised bronchodilators salbutamol and ipratropium, oxygen, theophyllines, antibiotics, noninvasive ventilation
Increased breathlessness, increased sputum, green sputum
Obstructive sleep apnoea
Sleep related breathing disorder characterised by recurrent episodes of complete or partial obstruction of upper airway during sleep these can cause apnoea (complete airflow obstruction with temporary absence or cessation of breathing) or hypopnoea decreased airflow)
Classically middle aged obese man with loud snoring and excessive sleepiness in day
Who: increasing age, man, obesity, family history, enlarged tonsils, NMD
How do we find it: sleep studies (polysomnography) to confirm diagnosis refer to sleep clinic
Treat: continuous positive airway pressure CPAP, lifestyle changes such as weight loss and smoking cessation, inform DVLA
Pneumothorax
Abnormal accumulation of air within the pleural space
Sudden chest pain, sudden SOB, sweating, reduced breath sounds
Who: trauma, tall slender young people, underlying lung disease
Diagnosis; CXR unless very unstable then treat immediately
Treatment: aspirate at 2nd intercostal space at midclavicular line using 14G needle
Complications: cardiac arrest pressure on heart so it cant function effectively
Pulmonary embolism
Obstruction of pulmonary vasculature secondary to an embolus these emboli typically originate in lower extremities most commonly secondary to deep vein thrombosis
Pleuritic chest pain, SOB dsypnoea, haemoptysis, DVT
Signs: often none, may be pleural rub
Who: post surgery, flights, immobility, cancer, OCP, pregnancy, smoking, factor V leiden, protein S or C deficiency (FH).
Diagnosis: look at symptoms, D-dimer blood test, CT pulmonary angiogram, VQ scan - mismatch multiple PE
CXR: grossly normal, basal atelectasis +/- effusion, pleural based wedge shape of increased opacity= hamptons hump, oligaemia/hypovolaemia= westermarks signs, rarely infarction with cavitation
Treatment: thrombolysis, normally just need anticoagulation- LMWH then NOAC or warfarin requires INR monitoring ,
Pulmonary hypertension
Pulmonary artery pressure >25mmhg
SOB, fatigue, syncope/dizziness, R heart failure, peripheral oedema, ascites, loud 2nd heart sound, tricuspid regurgitation- pansystolic murmur
Who: rare, most common cause is COPD, more women, idiopathic,
Diagnosis: ECG, echocardiogram more accurate by right heart catheter, CT chest
Treatment: highly specialist management, drugs can target pulmonary vascular function PDE type 5 inhibitor
Managing r heart failure and pulmonary hypertension associated with lung disease is mostly about correcting hypoxia
Pneumonia
Typical vs atypical
Typical: pre existing disease, abrupt onset, purulent sputum, pleuritic pain, marked systemic upset, localised signs, responds to beta lactams
Atypical: previously well, insidious onset, dry cough, SOB, wheeze, mild systemic upset, no response to beta lactams
Organisms (strep pneumoniae/ haem influenzae)
Severity CURB65
Complications: respiratory failure, lung abscess, parapneumonic effusion, empyema
Consolidation on X-rays
Tuberculosis
Caused by mycoplasma tuberculosis
Night sweats, fever, weight loss, productive cough, haemoptysis, may be latent or active, reactivation
Diagnosis by testing sputum for acid fast bacilli AFB, if lymph nodes involved aspirate, bronchoscopy if no sputum, test for HIV
Treatment: RIPE therapy 4 antibiotics: rifampicin, isoniazid, pyrizinamide, ethambutol. Resistance, hepatitis
Blood borne spread TB: meninges, musculoskeletal, genitourinary, gastrointestinal, pericardial
Controlling TB: housing/overcrowding, nutrition/child health, immunisation, chemoprophylaxis
Bronchial infections
Acute: previously well, usually viral, not always sputum production, cough, may be complicated by secondary bacterial infection
Recurrent: cough with sputum, more likely bacterial, no features of chronic bronchitis, look for underlying sinus infection, post nasal drip and bronchiectasis
Bronchiectasis
A cycle of chronic bronchial widening, poor mucous clearance, and recurrent infections
Crackles in chest sometimes clubbing, cough, thick mucous production
Who: post infections, immune deficiency, poor mucociliary clearance Cystic fibrosis
Diagnosis: CXR, sputum culture, consider cause/risk factor
Treatments: physiotherapy (postural drainage), bronchodilators, long term antibiotics nebulised or inhaled colomycin, tobramycin, oral macrolides- azithromycin
Complications: widespread use antibiotics, resistance
Respiratory failure
Defined as PaO2 <8.0kpa while breathing air or PaCo2>6.5kpa
Type 1: low oxygen hypoxaemia
Type 2: low oxygen and high CO2 hypoxaemia and hypercapnia
Need to find underlying cause: sepsis, pneumonia, pulmonary embolism, IECOPD, pulmonary oedema. Investigate with ABG, blood tests, CXR, ECG
Management: hypoxaemia kills first so give oxygen first and fix co2 and pH later
Oxygen therapy
Nasal cannula
Simple mask low flow rate means you can rebreathe CO2
Venturi: different sized adaptors most ore is oxygen concentrations good for chronic lung disease
Non-rebreathe one way valve highest possible oxygen therapy
Assisted ventilation
Respiratory arrest
Respiratory fatigue
Airway compromise due to decreased consciousness
Bilevel positive airway pressure ventilation BiPap: non invasive form of mechanical ventilation provided by means of nasal prongs or a full face mask
Invasive mechanical ventilation: replaces the respiratory muscle pump
Goal for assisted ventilation: improve ventilation by optimising gas exchange, rest respiratory muscles, assistance for neural or muscle dysfunction
Management of CAP
Non-severe cases: oral amoxycillin and macrolide or levofloxacin or moxifloxacin
Severe cases: Iv co-amoxiclav and macrolide, cefuroxime and macrolide, benzylpencillin and levofloxacin
Severity: CURB65: confusion, urea, respiratory rate, Bp, over 65
Management of empyema
Antibiotics: penicillins, anaerobic
Drainage
Surgery: break adhesions, decortication (remove fibrous tissue), open drainage
Cystic fibrosis
Abnormal membrane chloride channel
Impaired mucous clearance, obstruction pancreatic duct, in utero obstruction of male reproductive tract, focal biliary cirrhosis
Bronchiectasis, pancreatic insufficiency, infertility
Investigations: sweat test, genetic testing
Aggressive management of bronchiectasis
Pancreatic enzyme supplements
Insulin
Nutrition
Lung transplantation
How breathing rate increases in exercise
During exercise metabolism is increased which results in a build up of carbon dioxide and a reduction in the supply of oxygen
These changes are detected by chemoreceptors and impulses are sent to the respiratory control centre in the brainstem
Signals are sent to the diaphragm and intercostal muscles to increase the rate of ventilation (this process is involuntary)
As the ventilation rate increases CO2 levels in the blood will drop restoring blood pH (also O2 levels will rise)
Brain injury
More likely to affect respiratory function if it affects breathing centres in brainstem
Chemoreceptors on ventral side of medulla oblongata effectively detect CO2
Brainstem lesions
Affect our most basic functions
-unconscious patient
-look for cranial never signs to locate it
Difficult to see on CT scans better on MRI
Brainstem may be affected by larger lesions above it pushing downwards leading to respiratory failure
Sedative drugs
Decrease respiratory drive so decrease ventilation
Post surgery
Overdoses
Morphine and other opiates
Benzodiazepines
Neuromuscular disease
MND
Duchenne muscular dystrophy
Usually causes chronic deterioration
Tests include:
-spirometry—> low FVC
-transcutaneous CO2 monitoring overnight
-arterial blood gas- type 2 respiratory failure
Motor neurone disease
Degeneration of the ventral horns in spinal cord where UMN meets LMN, mix of LMN and UMN pathology
Usually starts with limbs or bulbar muscles
Can result in diaphragmatic weakness-> respiratory failure
Poor swallowing -> recurrent aspiration
Progressive- usually fatal 2-5 years from diagnosis
Managing respiratory failure: non-invasive ventilation, reduces CO2, extends life and probably improves QOL
When happens when we sleep
Cycle between NREM and REM sleep
REM: decrease muscle tone, increase sympathetic nervous system activity
Measure apnoea Hypopnea index AHI- measures number combine average of apnoeas and hypopneas per hour of sleep
>30 is severe OSA
Clinical features OSA
Associated with obesity and Craniofacial abnormalities
Usually snoring
Daytime sleepiness
Choking overnight
Morning headaches
Can occur in down syndrome and acromegaly
Micrognathia (Lower jaw undersized) in Treacher-Collins syndrome surgical correction
Managing OSA
Continuous positive airway pressure CPAP at night
Use >4 hours/ night
Provides a continuous airflow to ensure airways are open helps to counteract some metabolic risk factors
