Pathology Part 1 Flashcards
Features of acute asthma
Worsening dyspnoea, wheeze and cough that is not responding to salbutamol
Maybe triggered by a respiratory tract infection
Why is a normal CO2 in acute asthma not a good sign?
Indicates exhaustion and should, therefore, be classified as life-threatening.
Moderate acute asthma attack features
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
Severe acute asthma attack features
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
Life-threatening acute asthma attack features
PEFR < 33% best or predicted Oxygen sats < 92% Silent chest, cyanosis or feeble respiratory effort Bradycardia, dysrhythmia or hypotension Exhaustion, confusion or coma
The classification of acute asthma
Moderate
Severe
Life-threatening
When is a chest x-ray indicated in acute asthma attacks?
life-threatening asthma
suspected pneumothorax
failure to respond to treatment
When is hospital admission indicated in acute asthma attacks?
- Life-threatening asthma attack
- Severe asthma features if they don’t respond to initial treatment
- Previous near-fatal asthma attack
- Pregnancy,
- Presentation at night
When is oxygen indicated in acute asthma attacks?
Acutely unwell should be started on 15L of supplemental via a non-rebreathe mask, which can then be titrated down to a flow rate where they are able to maintain a SpO₂ 94-98%.
Criteria for discharge after acute asthma attacks
Stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
Inhaler technique checked and recorded
PEF >75% of best or predicted
Management of acute asthma attacks
- SABA
- All patients given 40-50mg of prednisolone orally (PO) daily, continued for at least five days or until the patient recovers from the attack
- Nebulised ipratropium bromide given 3rd line if needed
- IV magnesium sulphate
- IV aminophylline after consultation with senior medical staff
Acute bronchitis
A type of chest infection which causes inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.
Leading cause of acute bronchitis
Viral infection
How long does acute bronchitis last?
Usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time.
Features of acute bronchitis
Typically present with an acute onset of:
> cough: may or may not be productive
> sore throat
> rhinorrhoea
> wheeze
> Low grade fever (may/may not be present)
Chest examination findings in acute bronchitis
Majority of patients with have a normal chest examination, however, some may have Low-grade
fever & Wheeze
Differentiating acute bronchitis from pneumonia
Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
Examination: No other focal chest signs in acute bronchitis other than wheeze. Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
Investigations in acute bronchitis
Typically a clinical diagnosis
Management of acute bronchitis
- analgesia
- good fluid intake
- consider antibiotic therapy
- doxycycline first-line - cannot be used in children or pregnant women - amoxicillin is alternative
When is antibiotic therapy indicated in acute bronchitis?
- Systemically very unwell
- Pre-existing co-morbidities
- CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
What antibiotic is first line in acute bronchitis?
Doxycycline - cannot be used in children or pregnant women - amoxicillin is alternative
Features Acute exacerbation of COPD
- Increase in dyspnoea, cough, wheeze
- Increase in sputum suggestive of an infective cause
- May be hypoxic and in some cases have acute confusion
The most common bacterial organisms that cause infective exacerbations of COPD
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
Most common bacteria that causes infective exacerbations of COPD
Haemophilus influenzae
Management of infective exacerbations of COPD
Increase frequency of bronchodilator use and consider giving via a nebuliser
Prednisolone 30 mg daily for 5 days
Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line
When are antibiotics indicated in infective exacerbations of COPD?
Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line
What are the first-line antibiotics for infective exacerbations of COPD?
Amoxicillin or clarithromycin or doxycycline first-line
Acute respiratory distress syndrome (ARDS)
Caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli - life-threatening condition where the lungs cannot provide the body’s vital organs with enough oxygen.
Causes of Acute respiratory distress syndrome (ARDS)
infection: sepsis, pneumonia massive blood transfusion trauma smoke inhalation acute pancreatitis cardio-pulmonary bypass
Features of Acute respiratory distress syndrome (ARDS)
> Acute onset and severe > dyspnoea > elevated respiratory rate > bilateral lung crackles > low oxygen saturations
Key investigations in Acute respiratory distress syndrome ARDS
A chest x-ray and arterial blood gases
Management of Acute respiratory distress syndrome ARDS
- ITU
- Oxygenation/ventilation to treat the hypoxaemia
- Treat underlying cause e.g. antibiotics for sepsis
- Strategies such as prone positioning and muscle relaxation shown to improve outcome in ARDS
Adult respiratory distress syndrome
Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia (PaO2/FiO2 ratio < 200) in the absence of evidence for cardiogenic pulmonary oedema.
Adult respiratory distress syndrome causes
Sepsis
Direct lung injury
Trauma
Acute pancreatitis
Long bone fracture or multiple fractures (through fat embolism)
Head injury (causes sympathetic nervous stimulation which leads to acute pulmonary hypertension)
The two stages of Adult respiratory distress syndrome
Early stages consist of an exudative phase of injury with associated oedema.
The later stage is one of repair and consists of fibroproliferative changes. Subsequent scarring may result in poor lung function.
Features of Adult respiratory distress syndrome
Acute dyspnoea and hypoxaemia hours/days after event
Multi organ failure
Rising ventilatory pressures
Management of Adult respiratory distress syndrome
> Treat the underlying cause
Antibiotics (if signs of sepsis)
Negative fluid balance i.e. Diuretics
Recruitment manoeuvres such as prone ventilation, use of positive end expiratory pressure
Allergic bronchopulmonary aspergillosis
Results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.
Allergic bronchopulmonary aspergillosis features
- Bronchoconstriction: wheeze, cough, dyspnoea.
- Patients may have a previous label of asthma
- Bronchiectasis (proximal)
Investigations in Allergic bronchopulmonary aspergillosis
> eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE
Management Allergic bronchopulmonary aspergillosis
- oral glucocorticoids
2. itraconazole as a second-line agent
Three main types of altitude-related disorders
Acute mountain sickness (AMS), which may progress to High altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE).
Features of Acute mountain sickness
Develop gradually over 6-12 hours and potentially last a number of days:
> headache
> nausea
> fatigue
HAPE/HACE features
Some people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions
> HAPE presents with classical pulmonary oedema features
> HACE presents with headache, ataxia, papilloedema
Management of high altitude pulmonary oedema (HAPE)
- descent
- nifedipine, dexamethasone, acetazolamide,
- phosphodiesterase type V inhibitors*
- oxygen if available
Management of high altitude cerebral oedema (HACE)
- descent
2. dexamethasone
Alpha-1 antitrypsin (A1AT) deficiency
Common inherited condition caused by a lack of a protease inhibitor normally produced by the liver.
The role of A1AT is to protect cells from enzymes such as neutrophil elastase. It classically causes emphysema in patients who are young and non-smokers.
What disease does Alpha-1 antitrypsin (A1AT) deficiency cause?
Causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.
The role of Alpha-1 antitrypsin
To protect cells from enzymes such as neutrophil elastase.
Inheritance of Alpha-1 antitrypsin (A1AT) deficiency
Autosomal recessive
Features of Alpha-1 antitrypsin (A1AT) deficiency
- Usually have PiZZ genotype
- Panacinar emphysema, mostly in lower lobes of lungs
- Liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
Investigations in Alpha-1 antitrypsin (A1AT) deficiency
- A1AT concentrations
2. spirometry: obstructive picture
Management of Alpha-1 antitrypsin (A1AT) deficiency
- no smoking
- supportive: bronchodilators, physiotherapy
- IV alpha1-antitrypsin protein concentrates
- Lung volume reduction surgery
- lung transplantation
Normal PaO2 levels
Pa02 on air should be >10 kPa
Less than this is hypoxaemic
Acidaemic and alkalaemic pH
Acidaemic (pH <7.35)
Alkalaemic (pH >7.45)
PaCO2 > 6.0 kPa
Suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
PaCO2 < 4.7 kPa
Suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
Bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)
Suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
Bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)
Suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)
Low pH + high PaCO2
Acidosis
High pH + low PaCO2
Alkalosis
Low pH + low bicarbonate
Acidosis
High pH + high bicarbonate
Akalosis
Asbestos
Can cause a variety of lung disease from benign pleural plaques to mesothelioma.
Pleural plaques
Benign and do not undergo malignant change. They, therefore don’t require any follow-up. Most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis.
A chronic lung condition that is caused by prolonged exposure to high concentrations of asbestos fibers in the air.
Lung changes in Asbestosis
Typically causes lower lobe fibrosis
Asbestosis features
As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
A malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form. Mesothelioma can occur even with very limited exposure to asbestos
Features of Mesothelioma
- progressive shortness-of-breath
- chest pain
- pleural effusion
Aspiration pneumonia
A pneumonia that develops as a result of foreign materials gaining entry to the bronchial tree, usually oral or gastric contents such as food and saliva.
Risk factors for the development of aspiration pneumonia
Poor dental hygiene Swallowing difficulties Prolonged hospitalization or surgical procedures Impaired consciousness Impaired mucociliary clearance
Lung changes in Aspiration pneumonia
The right middle and lower lung lobes are the most common sites affected, due to the larger calibre and more vertical orientation of the right main bronchus.
Most common bacteria to cause infection in Aspiration pneumonia
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Most common chronic respiratory disorder encountered in clinical practice
Asthma
Asthma
Defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity. Symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.
Risk factors for Asthma
- personal or family history of atopy
- Maternal smoking, viral infection during pregnancy 3. Low birth weight
- Not being breastfed
- Maternal smoking around child
- Exposure to high concentrations of allergens
- Air pollution
- ‘hygiene hypothesis’
Patients with asthma also suffer from other IgE-mediated atopic conditions; what are they?
- atopic dermatitis (eczema)
2. allergic rhinitis (hay fever)
Occupational asthma
Type of asthma caused by exposure to inhaled irritants in the workplace. Diagnosed by observing reduced peak flows during the working week with normal readings when not at work.
Symptoms and signs of asthma
- cough: often worse at night
- dyspnoea
- ‘wheeze’, ‘chest tightness’
- expiratory wheeze on auscultation
- reduced peak expiratory flow rate (PEFR)
Spirometry
Test which measures the amount (volume) and speed (flow) of air during exhalation and inhalation.
Categorizes respiratory disorders as either obstructive or restrictive.
FEV1
Forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration
FVC
Forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration
Typical spirometry results in asthma
FEV1 - significantly reduced
FVC - normal
FEV1% (FEV1/FVC) < 70%
Investigations in asthma patients over 17
Spirometry with a bronchodilator reversibility test
All patients should have a FeNO test
Chest x-ray: particular in older patients or those with a history of smoking
Short-acting beta-agonists (SABA)
Salbutamol
Inhaled corticosteroids (ICS)
Beclometasone
Dipropionate
Fluticasone
Propionate
Long-acting beta-agonists (LABA)
Salmeterol
Leukotriene receptor antagonists
Monteleukast
Maintenance and reliever therapy (MART)
A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.
Side effects of Short-acting beta-agonists (SABA)
> Trembling, particularly in the hands.
Nervous tension.
Headaches
Suddenly noticeable heartbeats (palpitations)
Muscle cramps
Inhaled corticosteroids (ICS) side effects
Candidiasis and stunted growth in children
LABA side effects
Shaking of a part of your body that you cannot control headache nervousness dizziness cough
Investigations in asthma patients under 16
All patients should have spirometry with a bronchodilator reversibility (BDR) test
FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test
Management of asthma
> SABA > SABA + low-dose ICS > SABA + low-dose ICS + LTRA > SABA + low-dose ICS + LABA > Continue LTRA depending on response to LTRA > SABA +/- LTRA > Switch ICS/LABA for a low-dose ICS MART > SABA +/- LTRA + medium-dose ICS MART > SABA +/- LTRA + high-dose ICS MART
Low dose ICS
<= 400 micrograms budesonide or equivalent
Moderate dose ICS
400 micrograms - 800 micrograms budesonide or equivalent
High dose ICS
> 800 micrograms budesonide or equivalent
Common chemicals that cause occupational asthma
ocyanates - spray painting and foam moulding using adhesives platinum salts soldering flux resin glutaraldehyde flour epoxy resins proteolytic enzymes
Atelectasis
A common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
A complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid. Atelectasis is one of the most common breathing (respiratory) complications after surgery
Atelectasis features
Should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively
Atelectasis management
> positioning the patient upright
> chest physiotherapy: breathing exercises
Most common causes of bilateral hilar lymphadenopathy
Sarcoidosis and tuberculosis
All causes of bilateral hilar lymphadenopathy
> lymphoma/other malignancy > pneumoconiosis e.g. berylliosis > fungi e.g. histoplasmosis, coccidioidomycosis > Sarcoidosis > Tuberculosis
Bronchiectasis
Describes a permanent dilatation of airways secondary to chronic infection or inflammation
Causes of Bronchiectasis
Post-infective: tuberculosis, measles, pertussis, Pneumonia
Cystic fibrosis
Bronchial obstruction e.g. lung cancer/foreign body
Immune deficiency: selective IgA, Hypogammaglobulinaemia
Allergic bronchopulmonary aspergillosis (ABPA)
Yellow nail syndrome
Management of Bronchiectasis
Physical training (e.g. inspiratory muscle training)
Postural drainage
Antibiotics for exacerbations + long-term rotating antibiotics in severe cases
Bronchodilators in selected cases
Immunisations
Surgery in selected cases (e.g. Localised disease)
Most common organisms isolated from patients with bronchiectasis
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
Most common bacteria isolated from patients with bronchiectasis
Haemophilus influenzae
Chest drain
A tube inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.
Chest drain indications
> Pleural effusion > Empyema > Haemothorax > Haemopneumothorax > Chylothorax > Pneumothorax not suitable for conservative management or aspiration
Chest drain contraindications
- INR > 1.3
- Platelet count < 75
- Pulmonary bullae
- Pleural adhesions
Insertion of chest drain
Patient should be positioned in a supine position or at a 45º angle.
Forearm may be positioned behind the patient’s head to allow easy access to the axilla.
Identify the 5th intercostal space in the midaxillary line.
Chest drain complications
- Failure of insertion
- Bleeding
- Infection
- Penetration of the lung
- Re-expansion pulmonary oedema
Re-expansion pulmonary edema
Uncommon complication following drainage of a pneumothorax or pleural effusion. Symptoms include cough, chest discomfort and hypoxemia; if the edema is severe, shock and death may ensue.
How to prevent re-expansion pulmonary oedema
Recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours).
When are large bore chest drains used?
Trauma and haemothorax drainage
When are smaller diameter chest drains used?
Pneumothorax or pleural effusion drainage
Differentials for Chest x-ray: cavitating lung lesion findings
Abscess Squamous cell lung cancer Tuberculosis Wegener's granulomatosis Pulmonary embolism Rheumatoid arthritis Aspergillosis, histoplasmosis, Coccidioidomycosis
Common causes of lobar collapse
- Lung cancer
- Asthma (due to mucous plugging)
- Foreign body
Most common cause of lobar collapse in older adults
Lung cancer
The general signs of lobar collapse on a chest x-ray
- Tracheal deviation towards the side of the collapse
- Mediastinal shift towards the side of the collapse
- Elevation of the hemidiaphragm
Chest x-ray findings for lung metastases
Multiple, round well-defined lung secondaries are often referred to as ‘cannonball metastases’. Commonly seen with renal cell cancer but may also occur secondary to choriocarcinoma and prostate cancer.
Causes of actual mediastinal widening
vascular problems: thoracic aortic aneurysm lymphoma retrosternal goitre teratoma tumours of the thymus
How can nasogastric tube position be assesed?
Chest x ray
Complications of misplaced nasogastric tubes
Aspiration pneumonia and death
Chest x-ray pulmonary oedema changes
- interstitial oedema
- bat’s wing appearance
- upper lobe diversion (increased blood flow to the superior parts of the lung)
- Kerley B lines
- pleural effusion
Chest x-ray: white lung lesions causes
consolidation pleural effusion collapse pneumonectomy specific lesions e.g. tumours fluid e.g. pulmonary oedema
Trachea pulled toward the white-out (Chest x-ray: white lung lesions)
Pneumonectomy
Complete lung collapse
Pulmonary hypoplasia
Trachea pushed away from white-out (Chest x-ray: white lung lesions)
Pleural effusion
Diaphragmatic hernia
Large thoracic mass
Trachea central in white lung lesion findings
Consolidation
Pulmonary oedema (usually bilateral)
Mesothelioma
Cardiac causes of finger clubbing
Cyanotic congenital heart disease
Bacterial endocarditis
Atrial myxoma
Respiratory causes of finger clubbing
Lung cancer Cystic fibrosis Bronchiectasis Abscess Empyema Tuberculosis Asbestosis, mesothelioma
Coal workers’ pneumoconiosis
An occupational lung disease caused by long term exposure to coal dust particles. Commonly experienced by those who have been involved in the coal mining industry and severity is linked to the extent of exposure.
Pathophysiology of Coal workers’ pneumoconiosis
Dust reaches the terminal bronchioles and is engulfed by alveolar and interstitial macrophages.
Dust particles are then moved by the macrophages via the mucociliary elevator and removed from the body as mucus.
In coal miners who are exposed over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli, which starts an immune response, causing damage to the lung tissue.
The two presentations for Coal workers’ pneumoconiosis
Simple pneumoconiosis:
Progressive Massive Fibrosis
Simple pneumoconiosis
Commonest type of pneumoconiosis
Patients are often asymptomatic
Increases the risk of lung diseases
May lead to Progressive Massive Fibrosis (PMF)
Pneumoconiosis is one of a group of interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs
Commonest type of pneumoconiosis
Simple pneumoconiosis
Progressive Massive Fibrosis
Round fibrotic masses most commonly in the upper lobes.
The exact pathogenesis is not known.
Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
Progressive Massive Fibrosis symptoms
Often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
Coal workers’ pneumoconiosis
Chest x-ray: upper zone fibrosis
Spirometry: restrictive picture on lung function tests
Pneumoconiosis
Accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.
Most common cause of COPD
Smoking
Causes for COPD
Smoking Alpha-1 antitrypsin deficiency Cadmium (used in smelting) Coal Cotton Cement Grain
What is COPD?
Refers to a group of diseases that cause airflow blockage and breathing-related problems. It includes emphysema and chronic bronchitis.
COPD features
Cough: often productive
Dyspnoea
Wheeze
Severe cases, right-sided heart failure
Investigations in COPD
- Spirometry (obstructive picture)
- Chest x-ray
- Full blood count
- Body mass index (BMI) calculation
Chest x-ray changes in COPD
> hyperinflation
bullae
flat hemidiaphragm
also important to exclude lung cancer
Stage 1 COPD (mild)
FEV1/FVC < 0.7
FEV1 of predicted >80%
Stage 2 COPD (moderate)
FEV1/FVC < 0.7
FEV1 of predicted = 50-79%
Stage 3 COPD (severe)
FEV1/FVC < 0.7
FEV1 of predicted 30-49%
Stage 4 COPD (very severe)
FEV1/FVC < 0.7
FEV1 of predicted <30%
General management for all COPD patients
> Smoking cessation advice
Annual influenza vaccination
One-off pneumococcal vaccination
Pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD
First line management for COPD
SABA or SAMA
Second line management for COPD patients
Breathless or have exacerbations despite SAMA/SABA the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’
No asthmatic features/features suggesting steroid responsiveness
add LABA + LAMA - already taking a SAMA, discontinue and switch to a SABA
Asthmatic features/features suggesting steroid responsiveness
LABA + inhaled corticosteroid (ICS)
Third line treatment for COPD in patients with and without asthma features
LABA + LAMA + ICS
When is oral prophylactic antibiotic therapy recommeneded in COPD patients?
Patients should not smoke, have optimised standard treatments and continue to have exacerbations
What antibiotic is used for oral prophylactic antibiotic therapy in COPD patients?
Azithromycin
When are mucolytics indicated in COPD?
Should be ‘considered’ in patients with a chronic productive cough and continued if symptoms improve
Anion gap calculation
(Na+ + K+) - (Cl- + HCO3-)
Normal chloride ion levels
The normal range = 10-18 mmol/L
Normal anion gap ( = hyperchloraemic metabolic acidosis) causes
- Bicarbonate loss: diarrhoea, fistula
- Renal tubular acidosis
- Drugs: e.g. acetazolamide
- Ammonium chloride injection
- Addison’s disease
Raised anion gap causes
- Lactate: shock, hypoxia
- Ketones: diabetic ketoacidosis, alcohol
- Urate: renal failure
- Acid poisoning: salicylates, methanol
Metabolic alkalosis
A rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate.
Causes of metabolic alkalosis
Vomiting / aspiration Diuretics Liquorice, carbenoxolone Hypokalaemia Primary hyperaldosteronism Cushing's syndrome Bartter's syndrome Congenital adrenal hyperplasia
Mechanism of metabolic alkalosis
Activation of RAAS is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
Causes of Respiratory acidosis
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose
Causes of Respiratory alkalosis
> Anxiety leading to hyperventilation > Early salicylate poisoning* > Stroke, subarachnoid haemorrhage, > encephalitis > Pregnancy > Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
Respiratory alkalosis mechanism
Hyperventilation resulting in excess loss of carbon dioxide - result in increasing pH
Respiratory acidosis mechanism
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
Methylxanthines (e.g. theophylline) mechanism of action
Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP
Monteleukast, zafirlukast mechanism of action
Blocks leukotriene receptors
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
An ANCA associated small-medium vessel vasculitis
Another name for Eosinophilic granulomatosis with polyangiitis
Churg-Strauss syndrome
Features of Eosinophilic granulomatosis with polyangiitis
asthma blood eosinophilia paranasal sinusitis mononeuritis multiplex pANCA positive in 60%
Extrinsic allergic alveolitis
A condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. Thought largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.
Classifications of Extrinsic allergic alveolitis
- bird fanciers’ lung
- farmers lung
- Malt workers’ lung
- mushroom workers’ lung
Cause of farmers lung (Type of EAA)
Spores of Saccharopolyspora rectivirgula from wet hay
Cause of Malt workers’ lung (type of EAA)
Aspergillus clavatus
Causes of mushroom workers’ lung (type of EAA)
Thermophilic actinomycetes*
Acute presentation of EAA
Occurs 4-8 hrs after exposure
dyspnoea
dry cough
fever
Chronic presentation of EAA
Occurs weeks-months after exposure lethargy dyspnoea productive cough anorexia and weight loss
Investigations in EAA
Imaging: upper/mid-zone fibrosis
Serologic assays - specific IgG antibodies
Blood: NO eosinophilia
EAA chest x-ray changes
Upper/mid-zone fibrosis
Management of EAA
- avoid precipitating factors
2. oral glucocorticoids
Granulomatosis with polyangiitis (Wegener’s granulomatosis)
An autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.
Features of Granulomatosis with polyangiitis (Wegener’s granulomatosis)
- Epistaxis, sinusitis, nasal crusting
- Dyspnoea, haemoptysis
- Rapidly progressive glomerulonephritis
- Saddle-shape nose deformity
Another name for Granulomatosis with polyangiitis
Wegener’s granulomatosis
Investigations in Granulomatosis with polyangiitis
cANCA positive in > 90%, pANCA positive in 25%
Renal biopsy - epithelial crescents in Bowman’s capsule
Management of Granulomatosis with polyangiitis
> steroids
cyclophosphamide (90% response)
plasma exchange
Renal biopsy findings in Granulomatosis with polyangiitis
Epithelial crescents in Bowman’s capsule
Idiopathic pulmonary fibrosis
A chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis, IPF is used when no underlying cause exists.
Epidemiology of Idiopathic pulmonary fibrosis
Typically seen in patients aged 50-70 years and is twice as common in men.
Features of Idiopathic pulmonary fibrosis
Progressive exertional dyspnoea
Bibasal fine end-inspiratory crepitations
Dry cough
Clubbing
Investigations in Idiopathic pulmonary fibrosis
Restrictive results on spirometry
Impaired gas exchange: reduced TLCO
Imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
ANA positive in 30%,
Imaging findings in Idiopathic pulmonary fibrosis
Bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray
High-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
Management of Idiopathic pulmonary fibrosis
Pulmonary rehabilitation
Many patients will require supplementary oxygen and eventually a lung transplant
Klebsiella pneumoniae
A Gram-negative rod that is part of the normal gut flora. Can cause a number of infections in humans including pneumonia and urinary tract infections.
Features of Klebsiella pneumonia
More common in alcoholic and diabetics
May occur following aspiration
‘red-currant jelly’ sputum
Often affects upper lobes
Small cell lung cancer features
Usually central
ADH → hyponatraemia
ACTH → Cushing’s syndrome & can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome
Squamous cell lung cancer features
Parathyroid hormone-related protein secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH
Adenocarcinoma features
Gynaecomastia
HPOA
Investigations for lung cancer
Chest x-ray CT Bronchoscopy PET scanning Bloods
When is PET scanning used in lung cancer?
Typically done in non-small cell lung cancer to establish eligibility for curative treatment
When is bronchoscopy used in lung cancer?
Allows a biopsy to be taken to obtain a histological diagnosis sometimes aided by endobronchial ultrasound
Lung cancer: non-small cell management
Only 20% suitable for surgery
Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement
Curative or palliative radiotherapy
Poor response to chemotherapy
Lung cancer classifications
Small cell lung cancer (SCLC)
Non-small cell lung cancer (NSCLC)
Non-small cell lung cancer (NSCLC) further classifications
adenocarcinoma squamous large cell alveolar cell carcinoma bronchial adenoma
Most common type of lung cancer
Adenocarcinoma
What lung cancer is seen in non-smokers?
Adenocarcinoma & alveolar cell carcinoma
Acronym for causes of upper zone fibrosis
C - Coal worker's pneumoconiosis H - Histiocytosis/ hypersensitivity pneumonitis A - Ankylosing spondylitis R - Radiation T - Tuberculosis S - Silicosis/sarcoidosis
Fibrosis predominately affecting the lower zones
idiopathic pulmonary fibrosis
most connective tissue disorders
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
What drugs cause lung fibrosis of lower lungs?
amiodarone, bleomycin, methotrexate
Contents of Superior mediastinum
Superior vena cava Brachiocephalic veins Arch of aorta Thoracic duct Trachea Oesophagus Thymus Vagus nerve Left recurrent laryngeal nerve Phrenic nerve
Contents of middle mediastinum
Pericardium Heart Aortic root Arch of azygos vein Main bronchi
Contents of Anterior mediastinum
Thymic remnants
Lymph nodes
Fat
Contents of Posterior mediastinum
Oesophagus Thoracic aorta Azygos vein Thoracic duct Vagus nerve Sympathetic nerve trunks Splanchnic nerves
Mesothelioma
A cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure.
Microscopic polyangiitis
A small-vessel ANCA vasculitis
Non-invasive ventilation - key indications
- COPD with respiratory acidosis pH 7.25-7.35
- Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
- Cardiogenic pulmonary oedema unresponsive to CPAP
Predisposing factors for Obstructive sleep apnoea/hypopnoea syndrome
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome
Assessment for sleepiness in Obstructive sleep apnoea/hypopnoea syndrome
Epworth Sleepiness Scale
Multiple Sleep Latency Test (MSLT)
Diagnosis of Obstructive sleep apnoea/hypopnoea syndrome
Sleep studies (polysomnography
Management of Obstructive sleep apnoea/hypopnoea syndrome
> Weight loss
CPAP
DVLA should be informed
Oxygen dissociation curve
Describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration
The L rule in Oxygen dissociation curve (shifts to left)
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature
Oxygen dissociation curve (shifts to right?
Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG*
Raised temperature
What does it mean when the Oxygen dissociation curve shifts to the right?
Raised oxygen delivery
What does it mean when the Oxygen dissociation curve shifts to the left?
Lower oxygen delivery
Oxygen saturation targets
Acutely ill patients: 94-98%
Patients at risk of hypercapnia (e.g. COPD patients): 88-92%
Pleural effusion classifications
Transudate
Exudate
Pleural effusion
Build-up of excess fluid between the layers of the pleura outside the lungs. The pleura are thin membranes that line the lungs and the inside of the chest cavity and act to lubricate and facilitate breathing.
Transudate causes of pleural effusions
(< 30g/L protein) heart failure hypoalbuminaemia hypothyroidism Meigs' syndrome
Most common transudate cause of pleural effusion
Heart failure
Exudate causes of pleural effusions
Exudate (> 30g/L protein) infection: pneumonia, TB, subphrenic abscess connective tissue disease: RA, SLE neoplasia: lung cancer, mesothelioma, metastases pancreatitis pulmonary embolism Dressler's syndrome yellow nail syndrome
Most common exudate cause of pleural effusion
Pneumonia
Exudate protein concentration
(> 30g/L protein)
Transudate protein concentration
(< 30g/L protein)
Features of Pleural effusions
Dyspnoea, non-productive cough or chest pain
Classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion
Pleural aspiration for pleural effusions
Ultrasound is recommended to reduce the complication rate
A 21G needle and 50ml syringe should be used
Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
Managing patients with recurrent pleural effusions include
recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms
Investigations for pleural effusion
Posterioranterior (PA) chest x-rays
Ultrasound
Contrast CT
Pleural aspiration
Heavy blood staining in pleural effusion causes
Mesothelioma, pulmonary embolism, tuberculosis
Low glucose pleural effusion causes
rheumatoid arthritis, tuberculosis
Raised amylase pleural effusion causes
pancreatitis, oesophageal perforation
Pleural infection management
All patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling
if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage
if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed
Most common type of pneumonia
Bacterial
Causes of pneumonia
Bacterial, viral & fungal
Pneumonia
Describes any inflammatory condition affecting the alveoli of the lungs, but in the vast majority of patients this is secondary to a bacterial infection.
Idiopathic interstitial pneumonia
A group of non-infective causes of pneumonia - Examples include cryptogenic organizing pneumonia which describes a form of bronchiolitis that may develop as a complication of rheumatoid arthritis or amiodarone therapy.
Community-acquired pneumonia (CAP)
Develop pneumonia within the community, i.e. outside of hospital
Signs and symptoms of pneumonia
Cough Sputum Dyspnoea Pleuritic chest pain Fever Tachycardia Reduced oxygen saturations Reduced breath sounds Bronchial breathing
Chest x-ray changes in pneumonia
Consolidation
Investigations in Pneumonia
Chest x-ray - consolidation Full blood count - Neutrophilia in bacterial infections Urea and electrolytes CRP - raised in response to infection Arterial blood gases
Management of Pneumonia
- Antibiotics: treat underlying infection
- Oxygen therapy if hypoxaemic
- IV fluids if hypotensive/dehydration
CURB-65
Risk stratification process using a scoring system called CURB-65 - grades the severity of community-acquired pneumonia and risk of death
CURB65 calculation
C Confusion (abbreviated mental test score <= 8/10)
U Urea > 7
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years
Management of Pneumonia depending on CURB65 score
Home-based care for patients with a CRB65 score of 0 - oral amoxicillin is generally used first-line
Hospital assessment for all other patients, particularly those with a CRB65 score of 2 or more.
Risk factors of Pneumothroax
Pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
Connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
Ventilation
Symptoms of Pneumothorax
> dyspnoea > chest pain: often pleuritic > sweating > tachypnoea > tachycardia
Primary pneumothorax management
If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
Otherwise, aspiration should be attempted
If this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
Primary Pneumothorax
Primary if there is no underlying lung disease and secondary if there is.
Secondary pneumothorax management
If the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
Otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted.
All patients should be admitted for at least 24 hours - if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
Contraindications after treated for pneumothroax
- Smoking
- Fitness to fly - may travel 2 weeks after successful drainage if there is no residual air.
- Scuba diving
Restrictive lung disease
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
Obstructive lung disease
FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
Obstructive lung disease causes
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
Restrictive lung disease causes
Pulmonary fibrosis Asbestosis Sarcoidosis Acute respiratory distress syndrome Infant respiratory distress syndrome Kyphoscoliosis e.g. ankylosing spondylitis Neuromuscular disorders Severe obesity
Expiratory reserve volume
maximum volume of air that can be expired at the end of a normal tidal expiration
Inspiratory reserve volume (IRV)
maximum volume of air that can be inspired at the end of a normal tidal inspiration
Tidal volume (TV)
volume inspired or expired with each breath at rest
Residual volume (RV)
volume of air remaining after maximal expiration
increases with age
Functional residual capacity (FRC)
the volume in the lungs at the end-expiratory position
FRC = ERV + RV
Vital capacity (VC)
maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females
Decreases with age
Total lung capacity (TLC)
The sum of the vital capacity + residual volume
Centor criteria
presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough
Sarcoidosis
A multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent
Sarcoidosis features
Erythema nodosum bilateral hilar lymphadenopathy, swinging fever polyarthralgia dyspnoea non-productive cough malaise weight loss Hypercalcaemia
Why is there hypercalcaemia in sarcoidosis?
Macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
Lofgren’s syndrome
An acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
Mikulicz syndrome
There is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma
Heerfordt’s syndrome
(uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis
Investigations in Sarcoidosis
A chest x-ray
Spirometry: may show a restrictive defect
Tissue biopsy: non-caseating granulomas
Sarcoidosis stages on chest x-ray
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
Indications for steroids in Sarcoidosis
Chest x-ray stage 2 or 3 disease who are symptomatic.
Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
Hypercalcaemia
Eye, heart or neuro involvement
Silicosis
A fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing TB (silica is toxic to macrophages).
Occupations at risk of silicosis
mining
slate works
foundries
potteries
Features of silicosis
fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes
What is a disease that can develop with silicosis?
TB (silica is toxic to macrophages).
Tension pneumothorax
May occur following thoracic trauma when a lung parenchymal flap is created. This acts as a one way valve and allows pressure to rise.
The trachea shifts and hyper-resonance is apparent on the affected side.
Treatment of Tension pneumothorax
Treatment is with needle decompression and chest tube insertion.
Features of tension pneumothorax
The trachea shifts and hyper-resonance is apparent on the affected side.
Transfer factor
Describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.
Causes of a lower TLCO
pulmonary fibrosis pneumonia pulmonary emboli pulmonary oedema emphysema anaemia low cardiac output
Causes of a raised TLCO
asthma Wegener's, Goodpasture's left-to-right cardiac shunts polycythaemia hyperkinetic states male gender, exercise
