Respiratory Flashcards
Define chronic obstructive pulmonary disease (COPD)
Chronic obstructive pulmonary disease (COPD) is a progressive, irreversible obstructive lung disease characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.
What is emphysema?
Emphysema involves loss of alveolar integrity due to an imbalance between proteases and protease inhibitors (e.g. alpha-1 antitrypsin). Elastase breaks down elastin > increased loss of elastin. Triggered by chronic inflammation, such as smoking.
What is chronic bronchitis?
Bronchitis involves excessive mucus secretion secondary to ciliary dysfunction and increased goblet number and size → lung parenchymal destruction → impaired gas exchange. Chronic bronchitis is long-term bronchitis.
What are the risk factors for developing COPD?
- Age: usually diagnosed after the age of 45
- Tobacco smoking: greatest risk factor
- Air pollution
- Occupational exposure: such as dust, coal, cotton, cement and grain
- Alpha-1 antitrypsin deficiency: younger patients present with features of COPD
What signs and symptoms might patients with COPD present with?
The disease can range from mild to severe.
Mild symptoms - occasional bronchodilator
Severe symptoms - frequent exacerbation need hospital admission.
1) Symptoms
- Dyspnoea: particularly on exertion
- Cough: often productive
- Wheeze
2) Signs
- Tachypnoea
- Barrel chest (bulging of the chest)
- Hyperresonance on percussion
- Tar staining of fingers with peripheral cyanosis
3) Evidence of an exacerbation:
- Significant dyspnoea, wheeze and cough
- Coarse crepitations (lung crackles)
- Pyrexia
- Evidence of cor pulmonale (right-sided heart failure due to severe COPD): e.g. peripheral oedema
What investigations/tests are used to diagnose COPD?
Primary investigations:
1) Spirometry: FEV1/FVC <0.70 + bronchodilator reversibility (BDR): lack of reversibility post-bronchodilator is indicative of COPD (not required for diagnosis)
2) Chest X-ray: flattened diaphragm, hyperinflation and bullae. Carried out to detect lung cancer.
3) FBC: COPD causes chronic hypoxia, which may result in secondary polycythaemia (high levels of RBC).
4) FBC is also required to determine is eosinophilia (abnormally high eosinophil levels) is present
5) Calculate body mass index (BMI)
What is FEV1/FVC?
FEV1: forced expiratory volume; the volume of air exhaled in the first second of forced exhalation
FVC: forced vital capacity; the volume exhaled after maximal expiration following full inspiration
Normal FEV1/FVC = above 0.75-85
What does an FEV1/FVC ratio of <0.7 indicate?
Obstructive disease e.g. COPD or asthma
What are the general management principles for COPD?
Smoking cessation
Pulmonary rehabilitation: for patients who are self-perceived as functionally disabled by COPD (e.g. MRC grade ≥3)
Vaccinations: one-off pneumococcal and annual influenza
Initial therapy:
All patients will be started on a short-acting bronchodilator PRN (pro ra nata - as needed) (e.g. salbutamol) and may have additional long-acting agents
What is the GOLD classification for COPD?
Global Initiative for Chronic Obstructive Lung Disease (GOLD) groups patients according to severity to guide treatment.
Stage 1: Mild
Post-bronchodilator FEV1/FVC: <0.70
FEV1 (% of predicted): ≥80%
Stage 2: Moderate
Post-bronchodilator FEV1/FVC: : <0.70
FEV1 (% of predicted): 50-79%
Stage 3: Severe
Post-bronchodilator FEV1/FVC: : <0.70
FEV1 (% of predicted): 30-49%
Stage 4: Very severe
Post-bronchodilator FEV1/FVC: :<0.70
FEV1 (% of predicted): <30%
What are the medications used in managing COPD?
1) SABA: short-acting beta-adrenoceptor agonist (e.g. salbutamol) - leads to bronchodilation
2) SAMA: short-acting muscarinic antagonist (ipratropium) - inhibits smooth muscle contractions
3) LABA: long-acting beta-adrenoceptor
agonist (e.g. salmeterol) - leads to bronchodilation
4) LAMA: long-acting muscarinic antagonist (e.g. tiotropium) - inhibits smooth muscle contraction
5) ICS: inhaled corticosteroid (e.g. beclomethasone)
What are the medications used in managing asthma?
1) SABA (short-acting beta-agonist); e.g. salbutamol
2) ICS (inhaled corticosteroid); e.g. beclomethasone.
3) LTRA (leukotriene receptor antagonist); e.g. montelukast (reduces inflammation, not a steroid)
4) LABA (long-acting beta-agonist); e.g. salmeterol
5) MART (maintenance and reliever therapy); combined fast-acting LABA and ICS for symptomatic relief and maintenance in a single inhaler.
DDx for COPD
- Asthma
- Congestive heart failure
- Bronchiectasis
Salmeterol
1) Use
2) MOA
3) Side effects
1) Reversible airways obstruction in COPD, asthma for patients needing long-term bronchodilation
2) Activation of β adrenergic receptors leading to relaxation of smooth muscle in the lung, and dilation and opening of the airways
3) Arrhythmias; headache; palpitations; tremor
What is the management plan for COPD according to the GOLD classifcation?
GOLD A
Exacerbations: ≤1 per year not requiring admission
Symptoms between exacerbations: mild
Inhaler: any bronchodilator (short or long-acting)
GOLD B
Exacerbations: ≤1 per year not requiring admission
Symptoms between exacerbations: severe
Inhaler: LABA or LAMA
GOLD C
Exacerbations: ≥ 2 per year OR 1 requiring admission
Symptoms between exacerbations: mild
Inhaler: LAMA
GOLD D
Exacerbations: ≥ 2 per year OR 1 requiring admission
Symptoms between exacerbations: severe
Inhalers:
LAMA or
LAMA + LABA or
LABA + ICS
What are the NICE guidelines for managing COPD?
In clinical practice, GOLD classification used more often to manage COPD.
NICE guidelines are based on whether the patients have asthma symptoms.
Initial managment: COPD diagnosis = SAMA or SABA
Scenario 1: if symptoms persist AND asthma symptoms/previously diagnosed asthma > commence LABA & ICS
Scenario 2: if symptoms persist but no asthma > commence LABA & LAMA
If above therapies ineffective > commence LAMA, LABA & ICS
Define asthma
Asthma is a chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity.
What is the aetiology of asthma in adults?
A complex interaction between genetic and environmental factors.
Asthma usually starts with a genetic susceptibility which predisposes patients to airway hyper-responsiveness. It is then triggered by environmental factors such as viral infection, allergens (the main cause in children), cold and exercise
What is the aetiology of asthma in children?
In children, the cause is commonly atopy (genetic tendency to develop allergic diseases) and exposure to allergens (pollen, dust mites, animal fur, pollution).
Associated atopic conditions are eczema, hayfever.
What is the pathophysiology of asthma in adults?
Much like asthma in children, the inflammatory response in asthma is driven by Th2 cells → secretion of inflammatory mediators (IL-3, IL-5, IL-10, IL-13)
This results in eosinophil activation, IgE production and mast cell degranulation.
Ultimately this causes smooth muscle contraction > bronchiole constriction and increased mucus production > initially reversible airflow obstruction > irreversible over time due to fibrosis and tissue damage > permanent reduction in airway diameter
What is the pathophysiology of asthma (osmosis)?
Chronic asthma (PTS SAQ) - The primary abnormality in asthma is narrowing of the airway, which is due to smooth muscle contraction, thickening of the airway wall by cellular infiltration and inflammation, and the presence of secretions within the airway lumen
A trigger (e.g. cigarette smoke) detected by dendritic cells > present antigen to T-helper 2 cells
TH2 cells produce IL-4 and IL-5
IL-4 stimulates production of IgE which cause mast cell degranulation e.g. histamine
IL-5 stimulate eosinophils which release inflammatory mediators and leukotrienes
Minutes after exposure > bronchiole smooth muscles contract + increased mucus > airway narrowing and difficulties breathing
Also increase in vascular permeability >
recruitment of additional immune cells from the blood.
Hours after exposure, eosinophils release chemical mediators that damage the lung endothelium.
Initially, the damage is reversible but over time become irreversible.
Oedema, scarring, and fibrosis > permanent reduction in airway diameter
What are the risk factors for asthma in adults?
History of atopy: such as eczema and allergic rhinitis (IgE-mediated atopic conditions)
Family history
Allergens: such as tobacco smoke, pets, outdoor air pollution
Viral upper respiratory tract infection
Other triggers: cold weather and exercise
Occupational exposure (10-15%): e.g. spray paint, flour (bakers), people involved in plastic, foam and glue manufacturing. Requires a specialist referral
What are the risk factors for developing asthma in children?
1) Personal or family history of atopy: e.g. eczema and allergic rhinitis
2) Passive smoking
3) Antenatal factors: maternal smoking, RSV infection during pregnancy
4) Low birthweight
5) Bottle-fed (rather than breastfed)
6) Significant allergen exposure: e.g. dust mites, pets, tobacco smoke or air pollution
7) Childhood infection with a respiratory syncytial virus (RSV) MIGHT increase asthma risk
8) ‘Hygiene hypothesis’: reduced exposure to the developed world is theorised to lead to reduced ability of the child’s body to differentiate between harmful and harmless substances > increased asthma risk
Reduced exposure causes a Th2-predominant response.
What signs and symptoms might an adult patient with asthma present with?
Symptoms
1) Episodic shortness of breath with diurnal variation, i.e. worse at night and early morning
2) Dry cough
3) Wheeze and ‘chest tightness.’
4) History of exposure to a trigger
Signs:
1) Diural peak expiratory flow rate (PERF - the volume of air forcefully expelled from the lungs in one quick exhalation)
2) Dyspnoea and expiratory wheeze
3) Samter’s triad: sinus inflammation (nasal polyps), aspirin sensitivity and asthma
What signs and symptoms might a paediatric patient with asthma present with?
Symptoms:
1) Episodic shortness of breath
2) Dry cough
3) Wheeze and ‘chest tightness’
4) Features of atopic disease: e.g. eczema
Signs:
1) Diurnal peak expiratory flow rate (PEFR) variation
2) Dyspnoea and wheeze
What investigations/tests are used to diagnose asthma in adults?
Primary investigations:
- Spirometry: FEV1/FVC <70% suggests obstruction. If obstruction is found, BDR should be carried out
- Bronchodilator reversibility (BDR): improvement of FEV1 by ≥12% and increase ≥200ml in volume post-bronchodilator (bronchodilator irreversible would indicate COPD instead)
- Peak expiratory flow rate (PEFR) - measured multiple times a day over 2-4 weeks.
- PEFR - Morning lower, evening higher. Diurnal variation
- Variability of >20% throughout the day is diagnostic - compared with patient’s PB or normal values for age, height and gender
What investigations/tests are used to diagnose asthma in children?
Children aged < 5 years:
- Diagnose and treat based on clinical judgement, with regular reviews until ≥ 5
Children aged 5-16 years:
- Spirometry is 1st investigation; FEV1/FVC <70% is a positive result (obstructive)
- Bronchodilator reversibility (BDR): consider if obstructive spirometry is present; an improvement of FEV1 by ≥12% = positive
- PEFR often performed in adult but inconclusive in children
What is the management plan for asthma in adults?
Occupational exposure = they should be referred to a specialist.
Occupational asthma = symptoms and reduced PEFR during the working week and improvement when not at work.
Step 1: Newly-diagnosed asthma: SABA (PRN)
Step 2: If symptoms not controlled through SABA: SABA + low-dose ICS
Step 3: SABA + low dose ICS + LTRA
Step 4: SABA + low dose ICS + LABA +/- LTRA dependent on response
What is the management plan for asthma in children?
Children < 5 years old: clinical judgement must also be used
Step 1: newly-diagnosed asthma = SABA
Step 2: not controlled on the previous step
= SABA + trial paediatric moderate dose ICS for 8 weeks + review after
Step 3: SABA + paediatric low dose ICS + LTRA
Step 4: Stop LTRA + seek expert opinion
Children 5 - 16= similar management as adults:
Step 1: SABA
Step 2: SABA + ICS
Step 3: SABA + ICS + LTRA
Step 4: SABA + ICS + LABA (STOP LTRA)
DDx for asthma
Adults
- Cystic fibrosis
- COPD
- Chronic rhinosinusitis
Children
- Bronchiolitis
- Episodic (viral) wheeze triggered only by viral infection
- Inhaled foreign body
What is asthmatic exacerbation?
When triggers such as pollen, pollution, infection and exercise cause bronchoconstriction and inflammation in patients with asthma.
Patients with asthma have hyperreactive airways, which makes them more suspectable to the above triggers.
The inflammatory response is usually driven by Th2 cells, particularly if the trigger is an allergen.
Type 1 hypersensitivity reaction
What is the management plan for asthmatic exacerbations in adults?
1) Immediate management:
- Oxygen: SpO2 94-98%
- Nebulised bronchodilators: salbutamol 5mg is first-line
- Corticosteroids: prednisolone 40mg OD or 100mg hydrocortisone IV. Patients should continue on their inhaled corticosteroids.
- ICU and IV bronchodilator if above ineffective
Discharge:
Patients can be discharged once their PEFR > 75%
Given a course of oral steroids, inhaled steroids, and inhaled bronchodilator
GP appointment within 48 hours of discharge and an asthma plan
What is the management plan for asthmatic exacerbations in children?
1) General management for all severities:
Oxygen: in life-threatening asthma or if SpO2 <94%
Bronchodilators: Inhaled salbutamol (1st line) +/- ipratropium bromide:
Corticosteroids:
Oral prednisolone is given if the child is alert and able to swallow; otherwise, offer IV hydrocortisone
Usually 3-day course, but spends on the severity
2) Severe or life-threatening exacerbation:
Intravenous bronchodilation: magnesium sulphate may be needed if the child does not respond to the above
Other IV bronchodilators: second-line options include IV salbutamol and aminophylline
Ventilation: non-invasive ventilation or intubation if no response to above
Other considerations:
3) Antibiotics: may be used where the underlying trigger is a suspected bacterial infection
Define tuberculosis (TB)
Primary TB: a granulomatous disease caused by Mycobacterium tuberculosis.
Secondary TB: reactivation after becoming immunocompromised
What is the pathophysiology of primary TB?
Mycobacterium tuberculosis can thrive in the body because macrophages struggle to clear M. tuberculosis due to its waxy mycolic acid capsule, which confers protection. Same reason it can only be stained with Ziehl-Neelsen stain and not gram-stain as it is acid-fast.
1) Initial exposure
2) Formation of caseating granuloma (a collection of epithelioid histiocytes) in the lower lobe called Ghon focus. Ghon complex = granuloma + associated hilar lymph lobe)
3) The granuloma has caseous necrosis in the centre due to dead tissue > containing infection and will undergo fibrosis > dormant
If the patient is immunocompromised - Ghon focus reactivated > more areas of caseating granuloma > cavities = spread
4) This inflammatory process is a type 4 hypersensitivity reaction.
Primary infection is often asymptomatic.
What is a latent TB infection
This occurs after primary infection, patients remain asymptotic with a negative sputum test but a positive Mantoux test.
Might proceed to secondary TB infection if the patient is immunocompromised.
What is secondary TB?
When latent TB reactivates in immunocompromised patients because the immune system cannot contain the infection.
It can then spread systemically, resulting in miliary TB.
What are the risk factors for developing TB?
1.7 billion people worldwide have latent TB [
1) Contact with a person with active TB
2) Endemic regions: South Asian or sub-Saharan Africa
3) Homelessness
4) Alcohol or drug abuse
5) Immunocompromised: e.g. secondary to HIV, steroid use or malnutrition
What signs and symptoms might a patient with active TB disease present with?
Latent TB is asymptomatic and not infectious, unlike active disease:
Symptoms
1) Haemoptysis
2) Dyspnoea
3) Systemic symptoms:
- Fever
- Weight loss
- Night sweats
- Lymphadenopathy
Signs:
1) Auscultation: often normal; crackles may be present
2) Clubbing: if long-standing
What investigations/tests are used to diagnose TB?
1) Latent disease
- Mantoux screening: for high risk patients
2) Active disease
- 1st line is CXR: Ghon complex is visible in latent disease, whilst upper zone cavitating lesions are seen in active disease
- Microbiology: 3 deep cough sputum samples, analyse with Ziehl-Neelsen stain and Mycobacterium culture
- Nucleic-Acid Amplification Test (NAAT): rapid diagnostic test conducted on sputum or urine if HIV or at risk of MRSA
- HIV and hepatitis status: assess for co-infection
DDx for TB
Pulmonary
- COVID-19
- Community-acquired pneumonia
- Lung cancer
Extrapulmonary
- Lymphoma
- Sarcoidosis
What is the Mantoux test (tuberculin skin test (TST))?
Detects previous immune response to TB. This indicates possible previous vaccination, latent or active TB.
Intradermal injection of tuberculin and the site is inspected 48-72 hours later.
If positive, a type IV hypersensitivity reaction occurs, measured as a diameter of induration (lump) that occurs across the forearm
What is the management plan of latent and active TB?
1) Management of Latent TB:
Patients at risk of reactivation of latent TB can be treated with either:
- Isoniazid and rifampicin for 3 months
- Isoniazid for 6 months
2) Management of active pulmonary TB - coordinated MDT and TB specialist
RIPE - the combination of 4 drugs
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
Negative follow-up sputum test = successful treatment
3) Other Management Considerations:
- Test for other infectious diseases (HIV, hepatitis B and hepatitis C).
- Test contacts for TB.
- Notify Public Health of all suspected cases.
- Patients with active TB isolated until established on treatment (~2 weeks)
- Negative pressure rooms used in hospitals, these rooms have ventilation that removes air to prevent spread to the wards.
What are some extrapulmonary manifestations of TB?
1) Central nervous system: TB meningitis; the most serious complication
2) Vertebral bodies: Pott’s disease (MSK TB)
3) Adrenals: Addison’s disease
4) Gastrointestinal tract
5) Renal system
6) Genitourinary: e.g. tuberculous epididymitis
What is the treatment for TB meningitis?
Active tuberculosis of the central nervous system:
A longer continuation phase of antibiotics (rifampicin and isoniazid) for ≥ 10 months
Dexamethasone or prednisolone is also required.
Define cystic fibrosis
Cystic fibrosis (CF) is an inherited, autosomal recessive, multi-system disease due to mutations in the CF transmembrane conductance regulator (CFTR) gene on chromosome 7, CFTR is a chloride channel found in cells lining the lungs, intestines, pancreatic ducts, sweat glands, and reproductive organs.
What is the aetiology of cystic fibrosis?
Δ-F508 is the most common mutation, where the codon for phenylalanine (F) in the CFTR gene is deleted, resulting in proteolytic degradation.
CFTR is a chloride channel, and mutation causes dysfunctional Na+ and Cl- movement across membranes, resulting in the numerous systemic manifestations of the disease.
What are the risk factors for developing cystic fibrosis?
- Family history of CF
- Known carrier status of both parents
- Ethnicity - white
What is the pathophysiology of cystic fibrosis?
CFTR is an epithelial cAMP-regulated chloride channel and mutation causes dysfunctional Na+ and Cl- movement across membranes.
Resulting systemic manifestation:
1) Respiratory system
- Dry airways and impaired mucociliary clearance: results in cough, dyspnoea and recurrent pneumonia
- Increased risk of bacterial colonisation e.g. Staphylococcus aureus & Pseudomonas aeruginosa (worsens prognosis)
- Inflammation: chronic inflammatory response leads to bronchiectasis
2) Gastrointestinal
- Thickened secretions within small and large bowel: presents with failure to pass meconium (newborn first poop) and can cause bowel obstruction
3) Pancreatic insufficiency
- Defects in ion transport impede the secretion of crucial enzymes: resulting in malabsorption
3) Liver cirrhosis
Thickened biliary secretions: may block the bile ducts resulting in liver fibrosis, cirrhosis and portal hypertension
Right heart failure
Occurs due to pulmonary hypertension, resulting in cor pulmonale
What are the key infective microorganisms that colonise the respiratory system in cystic fibrosis?
Staph aureus and pseudomonas aeruginosa
Patients with cystic fibrosis take long-term prophylactic flucloxacillin to prevent staph aureus infection.
Pseudomonas aeruginosa should be remembered as a particularly troublesome coloniser that is hard to treat and worsens the prognosis of patients with cystic fibrosis.
What signs and symptoms might a patient with cystic fibrosis present with?
- Chronic cough
- Thick sputum production
- Recurrent respiratory tract infections
- Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
- Abdominal pain and bloating
- Parents may report the child tastes salty due to the concentrated salt in the sweat
- Poor weight and height gain (failure to thrive)
Signs
- Low weight or height on growth charts
- Nasal polyps
- Finger clubbing
- Crackles and wheezes on auscultation
- Abdominal distension
What signs and symptoms might a neonatal with cystic fibrosis present with?
- Prolonged jaundice
- Meconium ileus (bowel obstruction due to thickened meconium)
What signs and symptoms might an adult patient with cystic fibrosis present with?
- Recurrent chest infections
- Atypical asthma
- Diabetes mellitus (pancreatic insufficiency
- Male infertility: absence of vas deferens
- Female subfertility
What is the gold standard investigation for diagnosing cystic fibrosis?
Sweat test
A skin patch is chosen for the test, typically on the arm or leg.
Pilocarpine is applied to the skin and electrodes pass electrical currents, causing the skin to sweat. The sweat is absorbed with a special gauze or filter paper > lab tests for the chloride concentration.
cystic fibrosis > 60mmol/l chloride concentration (normal <40mmol/l)
What other primary investigations are used to diagnose cystic fibrosis?
Guthrie test: heel-prick test for serum immunoreactive trypsinogen (IRT) at 5-days old
Genetic testing: Δ-F508 is the most common mutation (80% of cases in the UK).
What is the management plan for cystic fibrosis?
1) 1st line: Chest physiotherapy several times a day
2) Plus: Bronchodilators such as salbutamol inhalers for bronchoconstriction and nebulised hypertonic saline (thins mucus)
3) Plus: inhaled mucolytic: nebulised DNase (dornase alfa) - enzyme that can break down DNA material in respiratory secretions, making it less thick and easier to clear
Consider the following
- Exercise improves respiratory function and reserve, and helps clear sputum
- Prophylactic flucloxacillin
- Treat chest infections
- Vaccinations including pneumococcal, influenza and varicella
GI disease
- High-calorie, high-fat diet
- CREON tablets to digest fats in patients with pancreatic insufficiency (these replace the missing lipase enzymes)
What are some other treatment options for cystic fibrosis?
1) Lung transplantation in end-stage respiratory failure
2) Liver transplant in liver failure
3) Fertility treatment involving testicular sperm extraction for infertile males
4) Genetic counselling
Define pneumonia
Pneumonia is an infection of the lung tissue. It causes inflammation of the lung tissue and sputum fills the airways and alveoli. Pneumonia can be seen as consolidation on a chest x-ray.
What is community-acquired pneumonia?
Pneumonia acquired outside of healthcare facilities (most common).
What is hospital-acquired pneumonia?
Occurs ≥ 48 hours after hospital admission.
What is the aetiology of community-acquired pneumonia (CAP)?
1) Streptococcus pneumoniae (pneumococcus):
- The most common cause of pneumonia (80%)
- Associated with rapid-onset and a high fever
- Pneumococcal vaccination is available.
2) Haemophilus influenza - associated with COPD
3) Staphylococcus aureus
- Commonly causes secondary bacterial infection after a viral URTI or the flu and can result in an abscess and empyema (pockets of pus).
What is atypical CAP?
Atypical CAP is caused by atypical organisms which are hard to gram stain and culture. Often presents with minimal respiratory symptoms and causes interstitial inflammation, meaning CXR is often normal.
What is the aetiology of atypical CAP?
1) Mycoplasma pneumoniae - commonly seen in young adults and is associated with Rauyand’s, autoimmune haemolytic anaemia and erythema multiforme
2) Legionella pneumophila - history of exposure to water source e.g. air conditioning. Associated with hyponatraemia, lymphopenia and deranged LFTs
3) Chlamydia psittaci - exposure to birds
What is the aetiology of hospital-acquired pneumonia (HAP)?
- Pseudomonas aeruginosa
- E.coli
- Staphylococcus aureus
May require broad-spectrum antibiotics
What are the risk factors for developing pneumonia?
1) Extremes of age: young children and the elderly are particularly at risk
2) Preceding viral infection
3) Immunosuppressed: e.g. due to steroid use
4) Intravenous drug abuse: Staphylococcus aureus
5) Respiratory conditions: asthma, COPD, malignancy, cystic fibrosis
What signs and symptoms might a patient with pneumonia present with?
Symptoms
- Productive cough
- Red currant jelly sputum is classically seen in Klebsiella pneumoniae
- Pleuritic chest pain
- Dyspnoea
Signs:
- Reduced breath sounds, and coarse crepitations
- Hypoxia
- Tachycardia
- Pyrexia
What investigations/tests are used to diagnose pneumonia?
- Definitive diagnostic test: CXR - classic finding is localised/widespread consolidation caused by inflammatory exudate within alveoli and bronchioles.
- FBC- ↑ WCC, ↑ urea, ↑ CRP (sign of inflammation)
- U + E - deranged in severe disease
- Sputum culture - causative organism
- ABG: perform if hypoxic to assess for respiratory failure
What is the CURB-65 score?
CURB -65 score is used to assess the severity of pneumonia, 1 point each for:
- Confusion (Abbreviated Mental Test Score ≤ 8, or disorientation in person, place or time)
- Urea > 7mmol/l
- Respiratory rate ≥ 30/min
- BP < 90mmHg systolic and/or<60mmHg diastolic
- Age ≥ 65
0-1 – outpatient treatment (home)
2 – consider hospital admission or close outpatient management
>3 – consider intensive care
What are the general principles for managing pneumonia?
- Maintain O2 sats at 94-98% (COPD 88-92%)
- Antibiotics
- Analgesia
- Fluids
What is the management plan for community-acquired pneumonia?
1) Low severity (CURB ≤ 1): oral amoxicillin OR doxycycline/clarithromycin if penicillin-allergic or atypical microorganism - 5-day course
- 1st line during COVID-19 = doxycycline
2) Moderate severity (CURB 2): amoxicillin; add clarithromycin if an atypical pathogen is suspected; usually a 5-day course
3) High severity (CURB ≥ 3): IV co-amoxiclav and clarithromycin
What is the management plan for hospital-acquired pneumonia?
1) Low severity: oral co-amoxiclav
2) High severity: a broad-spectrum antibiotic, such as IV tazocin or ceftriaxone
3) Suspected or confirmed MRSA: add vancomycin
Define bronchiectasis
Bronchiectasis is a chronic, debilitating lung disease characterised by the permanent dilation of the bronchi.
What is the aetiology of bronchiectasis?
Bronchiectasis is typically caused by chronic bronchial inflammation caused by previous infection(s) or systemic inflammatory conditions (e.g. cystic fibrosis, RA or IBD) or lung cancer.
What is the pathophysiology of bronchiectasis?
Chronic inflammation in bronchiectasis activates proteases, which break down elastin and other structures, leading to the dilatation of bronchi.
Dilated bronchi increase the risk of persistent microbial colonisation, which perpetuates inflammation, leading to increased mucus secretion and mucus trapping due to the dilated bronchi.
Due to the dilation and obstruction of the airways, an obstructive pattern is seen on spirometry.
