Respiration Flashcards
What is COPD?
Disease state characterised by airflow limitation that is not fully reversible
Airflow limitation usually both progressive and associated with an abnormal inflammatory response of lungs in noxious particles or gases
Associated with development of chronic bronchitis and emphysema
What causes COPD?
Tobacco smoking cause and related to daily average smoked and years smoking
Chronic exposure to - pollutants at work, outdoor pollution, inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas
Rarely symptomatic before middle-age
Alpha-1 antitrypsin
- Early onset COPD
What can increase your risk of getting COPD?
Age Cigarette smoke Occupational dust and chemicals Environmental tobacco smoke (passive smoking) Indoor and outdoor air pollution Genes Infection Socio-economic status of parents (in utero development) - low birth weight infants with poorly developed lungs
What is the pathophysiology of COPD?
Increased number of mucus-secreting goblet cells within bronchial mucosa
Bronchi overtly inflamed and pus seen in lumen
Most have emphysema and chronic bronchitis leading to severe airflow limitation
V/Q mismatch partly due to damage and mucus plugging of smaller airways from chronic inflammation and partly due to rapid closure of smaller airways in expiration owing t loss of elastic support
Fall in PaO2 and increase work or respiration
CO2 excretion less affected by V/Q mismatch and many patients have low-normal PaCO2 due to hyperventilation to fix hypoxia
Others fail to maintain respiratory effort and PaCO2 levels increase
Short term - rise in CO2 leads to stimulation of respiration, often become insensitive to CO2 and depend on hypoxaemia to drive ventilation
What is the pathophysiology of chronic bronchitis?
Airways narrowing and hence airflow limitation due to hypertrophy and hyperplasia of mucus secreting glands of bronchial tree
Bronchial wall inflammation and mucosal oedema
Microscopically - infiltration in walls of bronchi and bronchioles with acute and chronic inflammatory cells
Epithelial layer may become ulcerated and squamous epithelium replaces columnar cells when ulcer heals
Inflammation followed by scarring and thickening of walls narrowing small airways
Small airways particularly affected in early disease - initially no SOB
Initial inflammation reversible and accounts for improvement of airway function if smoking stopped early
Later - inflammation continues even if smoking stopped
Blue bloaters
What is the pathophysiology of emphysema?
Dilatation and destruction of lung tissue distal to terminal bronchioles
Loss of elastic recoil that normally keeps airways open during expiration
Expiratory flow limitation and air trapping
Loss of alveoli decreases capacity for gas transfer
Pink puffers
What are the different types of emphysema?
Centri-acinar emphysema - distention and damage of lung tissue concentrated around respiratory bronchioles, more distal alveolar ducts and alveoli tend to be well preseved
Pan-acinar emphysema - distension and destruction affecting whole acinus and in severe cases lung just collection of bullae, associated with alpha-1 antitrypsin deficiency
Irregular emphysema - scarring and damage affecting lung parenchyma patchily, independent of acinar structure
What does cigarette smoke do to your lungs?
Causes hypertrophy of mucus glands in larger airways and increases neutrophils, macrophages and lymphocytes in airways and walls of bronchi and bronchioles
Release of inflammatory mediators that attract inflammatory cells, induce structural changes and break down connective tissue in lung resulting in emphysema
Inactivates major protease inhibitor alpha-1 antitrypsin
How does COPD present?
Productive cough with white/clear sputum
Wheeze/SOB
Colds settle on chest
Frequent infective exacerbations with purulent sputum
Symptoms worsened by cold/damp weather and atmospheric pollution
Systemic effects - hypertension, osteoporosis, depression, weight loss, reduced muscle mass with general weakness
Rest with prolonged expiration
Poor chest expansion and hyperinflated lungs
Pursed lips on expiration help prevent alveolar and airway collapse
Later develop respiratory failure - PaO2 < 8 kPa, PaCO2 > 7 kPa
Pulmonary hypertension due to excretion of Na and water by hypoxic kidney
What is a possible differential for COPD?
Asthma Congestive HF Bronchiectasis Allergic fibrosing alveolitis Pneumoconiosis Asbestosis
How is COPD diagnosed?
Hx of SOB and sputum production in chronic smoker
Absence of Hx of smoking then asthma more likely unless FHx of alpha-1 antitrypsin deficiency
Lung function tests
- Progressive airflow limitation with increasing severity and SOB
- FEV1 < 80% predicted
- FEV1/FVC < 0.7 (obstruction)
- Stage 1 - FEV1 < 80%
- Stage 2 - FEV1 50-79%
- Stage 3 - FEV1 30-49%
- Stage 4 - FEV1 < 30%
- Multiple peak flow measurements needed to exclude asthma
CXR
- May be normal or show evidence of hyperinflated lungs indicated by low, flattened diaphragm and long narrow heart shadow
- Reduced peripheral lung markings
High res CT
Hb and PCV high due to persistent hypoxaemia and secondary polycythaemia
ABGs normal/hypoxia with/without hypercapnia
ECG normal
Alpha-1 antitrypin levels and genotypes
How is COPD treated?
Smoking cessation - slow rate of deterioration and prolong time before disability and death
Bronchodilators
- Inhaled tiotropium bromide (long acting muscarinic agent) with rescue short-acting B2 agonist
- Long acting B2 agonist if SOB
Corticosteroids
- Prednisolone for 2 wks with measurements of lung function before and after treatment period
- If improved then discontinue prednisolone and move to inhaled corticosteroid
Prevention of infection
- Exacerbations often due to bacterial or viral infection
- Pneumococcal vaccine and annual flu vaccine
- Prompt antibiotic treatment
O2 therapy
- For patients who no longer smoke
- O2 for 19 hrs per day, every day via nasal prongs to increase PaO2 > 90%
Anti-mucolytic agents
Diuretics
Pulmonary rehabilitation to increase exercise capacity with diminished sense of SOB and improved general well being
Good diet to reduce weight and obesity
Alpha-1 antitrypsin replacement
What is asthma?
Chronic condition whose cause is incompletely understood
How common is asthma?
Commonly starts in childhood between 3-5 and may either worsen or improve during adolescence
Peak prevalence 5-15
More common in developed countried
What are the different types of asthma?
Allergic/eosinophilic (70%) - allergens and atophy
- Extrinsic (atopic) - childhood asthma often accompanied with asthma
- Intrinsic - often starts in middle age and attacks usually triggered by respiratory infections, often had extrinsic asthma as a child, positive allergen skin tests, or caused by sensitisation to occupational agents eg toluene, diisocyanate, intoleracne to NSAIDs
Non-allergic/non-eosinophilic (30%)
- Exercise, cold air, stress
- Smoking and non-smoking associated
- Obesity associated
What can cause asthma?
Genetics - several genes in combination with environmental factors, genes controlling production of cytokines IL3, 4, 5, 9 and 13, ADAM33 associated with airway hyerpresponsiveness and tissue remodelling
Environmental factors - early childhood exposure to allergens and maternal smoking has influence on IgE production, growing up in clean environment may predispose towards IgE response to allergens
What can increase your risk of getting asthma?
Personal Hx of atopy FHx of asthma or atopy Obesity Inner-city environment Premature birth Socio-economic deprivation
What is the pathophysiology of asthma?
Airflow limitation - usually reversible spontaneously or with treatment
Airway hyper-responsiveness
Bronchial inflammation with T lymphocytes, mast cells, eosinophils and associated with plasma exudation, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage
Atopy - IgE developed against common environmental antigens such as house-dust mites, grass pollen, fungal spores
Serum IgE levels affected by several genetic and environmental factors
Primary abnormality - narrowing of airway die to SM contraction, thickening of airway wall by cellular infiltration and inflammation and presence of secretions within airway lumen
What are the precipitating factors of asthma?
Occupational sensitisers - wood dust, bleaches, dyes, isocyanates, latex
Cold air and exercise
Atmospheric pollution and irritant dusts
Diet - more fruit and veg protective
Emotion - high risk asthma attacks in anxious individuals
Drugs - NSAIDs, beta-blockers direct parasympathetic innervation resulting in bronchoconstriction
Allergen induced asthma
What causes inflammation in asthma?
Mast cells - increased in epithelium, SM and mucous glands, sensitised when IgE binds to mast cell receptor and mast cell responds to allergen if allergen on IgE
Mast cell releases histamine within seconds resulting in bronchoconstriction and inflammation, tryptase, prostaglandin 2 within minutes, cysteine leukotirens within minutes and more potent that histamine, cytokines TNF-alpha, IL-3, 4 and 5 within hours increasing the number of mast cells resulting in inflammation and airway remodelling
All act on SM, small vessels, mucus secreting cells and sensory nerves causing immediate asthmatic reaction
Eosinophils - in bronchial wall and secretions, attracted to airways by IL3 and 5
Release LTC4 and proteins that are toxic to epithelial cells
Number and activity decreased by corticosteroids
Dendritic cells and lymphocytes in mucous membranes and alveoli
Dendritic cells APCs to lymphocytes of allergen
T helper lymphocytes activate and release cytokines key in mast cell activation
What changes are there in the lung after challenge from allergen?
30 mins - bronchoconstriction
3 hours - initial bronchoconstriction decreases, inflammation occurs due to vasodilation which decreases blood flow leading to build up of WCC, increased vascular permeability and unregulated adhesion molecules
6 hours - worsening inflammation resulting in eosinophils releasing mediators resulting in second wave of bronchoconstriction
How does the airway remodel after an asthma attack?
Characteristic feature of chronic asthma alteration of structure and function of formed elements of airways
SM hypertrophy and hyperplasia so larger fraction of wall SM
Thickening of wall by deposition of repair collagens and matrix proteins below BM
Expansion of submucosa due to deposition of matrix proteins, swelling and cellular infiltration so for every degree of SM shortening excess airway narrowing
Epithelium stressed and damaged with loss of ciliated columnar cells
Metaplasia occurs with increase in number of mucus secreting goblet cells
Damage to epithelium makes it more vulnerable to infection
How does asthma present?
Intermittent SOB
Wheeze
Cough especially nocturnal
Sputum
Symptoms worse at night
Provoking factors - allergens, infections, menstrual cycle, exercise, cold air
During attack - reduced chest expansion, prolonged expiratory, time, bilateral expiratory polyphonic wheezes, tachypnoea
Uncontrolled asthma PEFR < 50%, RR < 25, pulse < 1000, normal speech
Severe attack - inability to complete sentences, pulse > 100, RR > 25
Life threatening attack - silent chest, confusion, exhaustion, cyanosis PaO2 < 8 kPa, bradycardia, PEFR < 33%
What is a possible differential diagnosis of asthma?
Pulmonary oedema COPD (may co-exist) Large airway obstruction caused by foreign body/tumour Pneumothorax Bronchiectasis
How is asthma diagnosed?
RCP3 Qs - recent nocturnal waking, usual asthma symptoms in a day, interference with activities of daily living
Asthma control test - 25 well controlled, 20-24 on target, < 20 off target
Lung function tests - PEFR (on waling, prior to taking bronchodilator and before bed after taking bronchodilator), spirometry, CO test normal, must be > 15% improvement of FEV1 or PEFR on bronchodilator inhalation
Exercise tests
Trail or corticosteroids
Exhaled NO - measures eosinophilic inflammation and index of corticosteroid response
Blood and sputum tests - increased eosinophils in peripheral blood, sputum eosinophilia more specific
Hx tells a lot
Distinguish from COPD
- Later disease and dominated by smokers
- Relentless progressive SOB with wheeze
- Less day-to-day variation
- Winter symptoms and sputum production
- Overlap possible
What is the immediate management of an asthma attack?
O2 therapy to maintain O2 94-98%
Nebulised 5mg salbutamol - repeat/IV infusion
Prednisolone with/without hydrocortisone IV
ABGs and repeat within 2 hours if severe attack/patient deteriorating
CXR if fails to respond
PEFR within 15-30 mins/regularly
Oximetry to ensure SaO2 > 92%
What are the aims of asthma treatment?
Abolish symptoms
Restore normal/best possible lung function
Reduce risk of severe attacks
Enable normal growth to occur in children
Minimise absence from school/employment, patient and family education about asthma and treatment
Avoidance of identified causes if possible
Use of lowest effective doses of medication to minimise short-term and long-term side effects
How is asthma treated?
Control of extrinsic factors when specific allergen triggers identified Bronchodilators - Beta-2 agonists - Long acting beta agonists - Muscarinic antagonists - Methylxanthines Anti-inflammatory steroids Other agents - Leukotriene receptor antagonist - Oral corticosteroid for those not controlled on inhaled Steroid sparing agents - Methotrexate - Ciclosporin - IV immunoglobulin - Anti-IgE monoclonal antibody
How common is bronchial carcinoma?
Most common malignant tumour worldwide with around 1.4 million deaths annually
3rd most common cause of death in UK after IHD and CVD
Slightly more common in men than women but incidence in women increasing due to smoking habits
What are the two main types of bronchial carinoma?
Small cell lung carcinoma Non-small cell - Squamous carcinoma - Adenocarcinoma - Large cell and differentiated carcinoma - Carcinoid tumours Difference of histological phenotype Distinction necessary with respect to behaviour of tumour, providing prognostic information and determining best treatment
What can increase your risk of bronchial carcinoma?
Cigarette smoking (including passive) 90% Occupational - Asbestos - Coal and products of coal combustion - Chromium - Arsenic - Nickel - Petroleum products - Iron oxide Environmental - Radon exposure - Ionising radiation Host factors - Pre-existing lung disease such as pulmonary fibrosis - HIV infection - Genetic factors
What is the pathology of small cell lung carcinoma?
Strongly associated with cigarette smoking Often spread by time of presentation Often arises in central bronchus Arises from endocrine cells Secretes polypeptide hormones Early development of widespread metastases Chemotherapy primary treatment Poor prognosis
What is the pathology of non-small cell lung carcinoma?
Associated with cigarette smoking
May have metastasised by time of diagnosis
Often treated best by surgical ablation with lymph node sampling
Chemotherapy and radiotherapy
More susceptible to new therapy such as tyrosine kinase therapy
What is the pathology of squamous cell carcinoma?
Most strongly associated with cigarette smoking
Tumours usually central location and frequently cavitate with central necrosis
Arise from epithelial cells, associated with production of keratin
Cause obstructive lesions of bronchus with post-operative infection
Local spread common
Metastasise relatively late
What is the pathology of adenocarcinoma?
Most common
Central/peripheral
Single lesions but can be multi-focal pattern, sometimes bilaterally
Originate from mucus secreting glandular cells
Most common cell type in non-smokers
Often cause peripheral lesions on CXR/CT
Metastases common especially to pleura. lymph nodes, brain, bones, adrenal glands
Associated with asbestos
What is the pathology of carcinoid tumours?
Present at earlier age and have characteristic neuroendocrine secreting cells and relatively low rate of invasion and growth
Still malignant
What is the pathology of lymphomas in the lung?
Involve lung primarily but usually part of disseminated disease
Main lung lymphoma BALTOMA - bronchus associated tissue lymphoma, B cell lymphoma and responds to chemo
What is the pathology and name of a benign lung tumour?
Hartoma
Irregular proliferations of benign/normal tissues not normally found in this pattern in lung tissue, commonest chondroid harmartoma that incorporated cartilage, glandular tissue, fat fibrous tissue and blood vessels
What sites can lung cancer metastasise to?
Liver - anorexia, nausea, weight loss, RUQ pain radiating across abdomen
Bone - bony pain and pathological fractures
Adrenals - asymptomatic
Brain - space occupying lesion
Spread within chest and involve pleura and ribs resulting in pain and fractures
What cancers can spread to lung?
More common than lung metastasising elsewhere Breast Bowel Kidney (most common) Bladder
What are the symptoms of bronchial carinoma?
Cough 3 wks merits CXR SOB on exertion Haemoptysis Chest pain Wheeze Recurrent infections Clubbing Metastatic disease - bone pain, headache, seizure, neurological deficit, hepatic pain, abdominal pain Paraneoplastic changes (10%) - secretion of PTH, SIADH, secretion of ACTH, hypertrophic pulmonary osteoarthropthy, finger clubbing, non-infective endocarditis, DIC
What is the TNM classification for bronchial carcinoma?
T1 < 3cm
T2 > 3cm
T3 invasion of chest wall, diaphragm and pericardium
T4 invasion of mediastinum, heart, great vessels, trachea, oesophagus, vertebrae, carina, malignant effusion, metastases in same lobe
N0 no nodes
N1 hilar nodes
N2 same side mediastinal nodes of subcarinal
N3 contralateral mediastinal nodes/supraclavicular
M1a tumour of same side
M1b tumour elsewhere
How is bronchial carinoma diagnosed?
CXR - round shadow, edge has fluffy, spiked appearance, hilar enlargement, consolidation, lung collapse, pleural effusion
CT for staging
Bronchoscopy for histology and assessing operability +/- endobronchial USS for assessment and biopsy
Cytology sputum and pleural fluid
Bloods FBC
How is non-small cell lung carcinoma treated?
Surgical excision for peripheral tumours with no metastatic spread
Curative radiotherapy for alternative if respiratory reserve poor
Chemotherapy +/- radiotherapy for more advanced disease with monoclonal antibodies targeting epidermal growth factors receptor
How is small cell lung carcinoma treated?
Chemo and radiotherapy
Extensive - chemo
Usually relapse
Palliation to relieve symptoms radiotherapy for bronchial obstruction, haemoptysis, bone pain, cerebral metastases
SVC stent and radiotherapy and dexamethasone for SVC obstruction
Endobronchial therapy - trachial stenting, cryotherapy, brachytherapy for airway narrowing
Pleural drainage
Analgesia, steroids, antiemetics, codeine, bronchodilators, antidepressants
What can cause a pulmonary embolism?
Clots breaking off, passing through veins to IVC then into right side of heart before lodging in pulmonary circulation R ventricular thrombus Septic emboli Fat embolus Air embolism Amniotic fluid embolism Neoplastic cells Parasites Foreign material during IV drug misuse
What can increase your risk of a pulmonary embolism?
Change in blood flow - Immobility, obesity, pregnancy Change in blood vessel - Smoking, hypertension Change in blood constituents - Dehydration, malignancy, high oestrogen, polycythaemia, nephrotic syndrome, inherited Recent surgery especially abdominal/pelvic/hip or knee replacement Leg fracture > 60 years
What is the pathology of pulmonary embolism?
Circulatory stasis, endothelial injury and hypercoagulable states predispose you to clot
Arise from venous thrombus in pelvis/legs
Clot breaks off and passes through veins -> IVC -> RA -> RV -> pulmonary circulation where lodged in small capillaries supplying alveoli resulting in PE
Lung tissue ventilated but not perfused so intrapulmonary dead space and impaired gas exchange
After a few hours, non-perfused lung no longer produces surfactant resulting in alveolar collapse exaggerating hypoxaemia
Primary haemodynaic consequence is reduction in cross-sectional area of pulmonary bed causing elevation in pulmonary arterial pressure due to increased resistance and reduction in CO
RV ischaemia detected with elevations of troponin and creatinine kinase
Associated with adverse outcomes
Small emboli in more distal/terminal vessels can be clinically silent unless lead to infarction
How does PE present?
Depends on number/size/distribution of emboli Large often fatal Sudden onset, unexplained SOB Pleuritic chest pain Haemoptysis Dizziness Risk factors Past/FHx Pyrexia Cyanosis Tachypnoea/tachycardia Hypotension Raised JVP Pleural rub/effusion
What is a possible differential diagnosis of PE?
Asthma COPD MI Pneumonia HF
How is PE diagnosed?
CXR
- Often normal
- Decreased vascular markings, blunting of costophrenic angle, wedge shaped areas of infarction, pulmonary oligaemia
- Make sure not MI/pneumothorax
ECG
- Sinus tachycardia, R atrial dilation (small peaked P waves in lead II), RBBB, R ventricular strain (inverted T wave in V1-4)
Blood gases - hypoxiaemia T1 resp failure
Plasma D dimer
USS of leg and pelvis looking for clots
CT pulmonary angiography
How is PE treated?
High flow O2 (60-100%) not if significant lung disease
Anticoagulated with LMW heparin
IV fluids and inotrophic agents
Thrombolysis
Surgical embolectomy
VC filter in those who develop PE even on anticoagulation
How do you prevent PE long term?
Vitamin K antagonist
Target INR between 2-3
Patients mobilised
TED stockings
How is a massive PE managed?
Oxygen if hypoxic
Morphine
Antiemetic
Immediate thrombolysis if critically ill
IV access for heparin
Systolic BP < 90mmHg rapid colloid infusion, still low dobutamine, still low noradrenaline, still low after 30-60 mins definitely PE begin thrombolysis
Systolic BP > 90mmHg warfarin and confirm diagnosis
What is acute epiglottistis?
Epiglottis inflammation
What can cause acute epiglottitis?
Adults - most severe H influenzae, also from causes of pharyngitits, additional pathogens in immunocompromsied
Rare due to Hib vaccine
How does acute epiglottitis present?
High fever Severe airflow obstruction Meningitis Septic arthritis Osteomyeltitis
How is acute epiglottitis treated?
Urgent endotracheal intubation
IV antibiotics ceftazidime
What is croup?
Occasional complication of upper respiratory tract infections
Particularly those caused by parainfluenza viruses and measles
Acute laryngotracheobronchitis
What causes croup?
Parainfluenza viruses
Most severe in children under 3
What is the pathology of croup?
Inflammatory oedema extends to vocal cords and epiglottis causing narrowing of airway
Progressive airway obstruction with recession of soft tissue of neck and abdomen during inspiration and in severe cases central cyanosis
How does croup present?
Voice hoarse with barking cough
Audible stridor (high pitched wheeze on inspiration)
Febrile - high RR and cyanosis
Intercostal recession
How is croup treated?
Nebulised adrenaline for short term relief
Oral/IM corticosteroids eg dexamethasone with O2 and fluids
What is pharyngitis?
Infection of throat
What is tonsilitis?
Infection of tonsils
What can cause pharyngitis and tonsilitis?
Most common viral cause adenoviruses of which 32 serotypes
Rhinovirus, EBV, acute HIV infection
Lancefield group A beta-haemolytic streptococci
How does pharyngitis and tonsilitis present?
Sore throat Tender glands in neck Fever Stable vital signs Large tonsils with exudate Tender anterior cervical lymph nodes enlarged within 1-2 days Oropharynx and soft palate reddened
How is pharyngitis and tonsilitis treated?
Self-limiting disease
Symptomatic treatment
No antibiotic required
Persistent and severe tonsilitis treated with phenoxylmethylpenicillin or cefaclor
What can cause respiratory viral infections?
Rhinovirus - common cold, bronchitis, sinusitis
Influenza A virus- flu
Coronaviruses - colds but occasionally sever respiratory illnesses
Adenoviruses - upper respiratory tract infection, pharyngitis, bronchitis and occasionally pneumonia
Respiratory syncytial viruses - bronchiolitis in young children, severe illness in nursing home residents and pneumonia in immunocompromised
What can cause emergency respiratory infections?
SARS
- Coronavirus
- Outbreak from China
- Severe respiratory illness with respiratory failure
MERS-nCV
- Middle East
- Similar to SARS but low person to person spread
Avian inflenza
- Novel form of Influenza A
- Occasional human cases with severe illness
- Seen in South Asia associated with poultry exposure
- Low person to person spread
What are the complications of respiratory viral infections?
Pharyngitis Sinusitis Otitis media Bronchitis Pneumonia Bacterial superinfection
What is sinustitis?
Infection of paranasal sinuses that is bacterial or occasionally fungal
What causes sinustitis/
Bacterial - streptococcus pneumoniae (40%), H influenzae (30-35%)
How does sinustitis present?
Fever, facial pain with tenderness, purulent nasal discharge
Frontal headache
Purulent rhinorrhoea
Bacterial sinusitis - unilateral pain and purulent discharge with/without fever for more than 10 days
How is sinusitis treated?
Nasal decongestants = xylometazoline
Broad spectrum antibiotics such as co-amoxiclav
What are the possible complications of sinusitis?
Brain abscess
Sinus vein thrombosis
Orbital cellulitis
What is whooping cough?
Bordatella pertussis - gram negative coccobacillus
Bordatella parapertussis and bronchiseptica produce milder infections
When is whooping cough most common?
Childhood 90% cases are under 5
No age exempt as antibody levels fall over years
What is the pathology of whooping cough?
Highly contagious
Spread by droplet infection
In early stages, indistinguishable from other upper respiratory tract infections
Multiple virulence factors
- Filamentous haemagglutinin and fimbrae aid adherence
- Adenylate cyclase toxin inhibits phagocyte chemotaxis and T cell activation
- Pertussis toxin A/B toxin that ADP ribosylates G proteins and inhibits alveolar macrophage host defence
- Tracheal cytotoxin and dermonectroic toxin cause epithelial necrosis
Lymphoid hyperplasia and Th17 skewing of immune response contributes to inflammation and cough
How does whooping cough present?
Chronic cough Febrile Sub-conjuntival haemorrhage Catarrhal phase (1-2 wks) - Highly infectious - Cultures from respiratory cultures positive in 90% cases - Malaise - Anorexia - Rhinorrhoea - Conjuntivitis Paroxysmal phase (1-6 wks) - Coughing spasms - 1 wk after catarrhal phase - Classic inspiratory whoop in younger people with compromised respiratory tract with mucous secretion and oedema - Coughing spasms terminated in vomiting - Cough for more than 14 days - Associated with complications - pneumonia, encephalopathy, sub-conjuntival haemorrhage
How is whooping cough diagnosed?
Chronic cough with one clinical feature indicating pertussis
Chronic cough with Hx of contact/microbial diagnosis
Suggested clinically by whoop and Hx of contact with infected individual
PCR test
Culture of nasopharyngeal swab for definitive diagnosis
How is whooping cough treated?
Antimicrobials such as macrolides (clarithromycin) eliminate carriage of bacteria and reduce symptoms in catarrhal stage and early paroxysmal
In paroxysmal - antibiotics play little role
Vaccination - acellular pertussis part of dTap vaccine (diptheria, tetanus and acellular pertussis) at 2, 3, 4 months and 3-4 years
What is pneumonia?
Inflammation of substance in lungs
Acute lower respiratory tract infection
Usually caused by bacteria but can also be caused by viruses and fungi
Usually due to infection affecting distal airways and alveoli with formation of inflammation exudate
What is community acquired pneumonia?
No underlying immunosuppression or malignancy
Occurs across all ages but commoner at extremes
Primary/secondary to underlying disease
Streptococcus pneumoniae commonest cause
Rarer - S aureus, Legionella spp, Moraxella cararrhalis, Chlamydia (not susceptible to beta-lactams)
Infection can be localised
Can be diffuse when lobules of lungs mainly affected, often due to infection centred on bronchi and bronchioles - bronchopneumonia
What is hospital acquired pneumonia?
New onset cough with purulent sputum along with completeable x-ray demsonstrating consolidation in patients beyond 48 hrs initial admission or been in healthcare setting in last 3 months
Elderly, ventilator associated and post-operative
HAP second most common hospital acquired infection after UTI
Aerobic gram-negative bacilli - P aerguinosa, E coli, K pneumoniae
S aureus particularly MRSA
HAP due to S aureus more common in patients with DM or head trauma and those in ITU
What are the causes of pneumonia in immunocompromised patients?
Unusual organisms and opportunistic pathogens
Symptoms may resemble CAP or be non-specific
Pneumocystitis jiroveci most common
What is aspiration pneumonia?
Acute aspiration of gastric contents into lungs
Severe sometimes fatal due to intense destructiveness of gastric acid
Seen in those with stroke, myasthenia gravis, bulbar palsies and lack of consciousness
Can complicated anaesthesia, particularly pregnancy
What can cause CAP?
S pneumoniae
H influenzae
Atypical - mycoplasma pneumoniae, Chlamydia pneumoniae
Enteric gram negative bacteria E coli, K pneumoniae
What can increase your risk of getting pneumonia?
Under 16 Over 65 Co-morbidities - HIV infection, DM, CF, COPD, bronchiectais Excess alcohol Smoking IVDU Immunosuppressant therapy
What is the pathology of pneumonia?
Spread by respiratory droplets
Pneumococcal pneumonia typically acute in onset with prominent respiratory symptoms and fever
Atypical pathogens tend to have slower onset with more prominent extra-pulmonary symptoms and complications
Do not respond to penicillin as lack cell wall
Translocate to normally sterile airway
Overwhelm resident host defence
Alveolar macrophages ingest bacteria and produce hormonal factors
Antibodies produces with mircobial factros and bacteria destroyed
Host defences overwhelmed and alveolar macrophages change roles and instead co-ordinate response
Stimulate neutrophils to fill alveolar space and produce pus
Normally resolved and bacteria cleared with inflammatory cells being removed by apoptosis
Severe disease results if excessive inflammation, lung injury, failure to resolve without lung damage
How does pneumonia present?
Symptoms of fever, night sweats, raised RR, productive cough and absence of URT symptoms Low BP Rigors Malaise and anorexia SOB - alveoli filled with pus and debris, imparing gas exchange, coarse crackles on ascultation due to consolidation of lung parenchyma Signs of consolidation - Dull to percussion - Decreased air entry - Bronchial breath sounds Dry productive cough Purulent sputum Pleuritic chest pain Cyanosis Confusion
What is a differential diagnosis of pneumonia?
TB
Lung cancer
How is pneumonia diagnosed?
CXR - radiological abnormalities can lag behind clinical findings
- Normal CXR repeated after 2-3 days if CAP suspected
- Air bronchogram in consolidated areas
- Multi-lobar (S pneumoniae, S aureus, Legionella)
- Multiple abscesses S aureus
- Upper lobe cavity then K pneumoniae must exclude TB
Bloods
- FBC - WBC elevated in S pneumoniae, marker of severity
- ESR/CRP raised
Biochemisty - U&Es and LFTs
Pulse oximetry and ABGs if O2 < 94%
HIV tests
Microbial tests
- Sputum culture and antibiotic sensitivities +/- gram stain
- Blood culture
- Serology for viruses and atypical organisms
CURB65 to assess severity of CAP
What is CURB65?
One point for each
- Confusion
- Urea > 7mmol/L
- RR > 30/min
- BP < 90mmHg systolic and/or 60mmHg diastolic
- Age > 65
Implications
- 0-1 mild only admit if social circumstances/single worrying feature
- 2 moderate admit
- 3-5 severe, admit and monitor closely
- 4-5 consider admission to critical care
How is pneumonia treated?
Maintain O2 sats between 94-98%
In COPD 88-92%
First dose antibiotics administered within 4 hrs presentation in hospital and treatment not delayed whilst investigations underway
Analgesia - paracetamol/NSAIDs for pleuritic chest pain
Narrow spectrum antimicrobials if mild amoxicillin 5-7 days
IV antibiotics if severe co-amoxiclav/clarithromycin 7-10 days
Special cases
- Legionella fluoroquinolone (ciprofloxacin) with/without clarithromycin
- Necrotising pneumonia - IV linezolid, clindamycin, rifampicin
- Pseudomonas aeruginosa IV ceftazidime with gentamycin/tobramycin
How do you prevent pneumonia?
Polysaccharide pneumococcal vaccine
Influenza vaccine for those > 65, immunocompromised or with medical co-morbidities
Smoking cessation
What are the complications of pneumonia?
Respiratory failure
Hypotension - dehydration and vasodilation due to sepsis
Parapneumonic effusion and empyema
Lung absecesses
