Respiratory COPY COPY COPY Flashcards
What is Chronic Obstructive Pulmonary Disease (COPD)?
Progressive irreversible airway obstruction characterised by persistent airflow limitation caused by long term damage to lung tissue.
What are the conditions that are classed as COPD?
Chronic Bronchitis
Emphysema
What is the epidemiology of COPD?
1.2 million people with COPD in the UK
4th leading cause of death globally
Typically diagnosed >45 yrs
More common in males
Strongly related to Smoking.
What are the risk factors for COPD?
Cigarette smoking
Air pollution
Occupational exposure to dusts, chemical agents, and fumes
A1AT deficiency - can lead to early onset COPD
What is the most important cause/aetiological factor for COPD?
Cigarette smoking
Define Chronic Bronchitis?
A inflammatory lung condition that develops over time in which the bronchi and bronchioles become inflamed and scarred.
What is Chronic Bronchitis as a clinical definitions?
Chronic Bronchitis is a clinical term relating to a chronic productive cough for at least 3 months over 2 consecutive years.
Alternative explanations for the cough should also be excluded.
What is Emphysema as a pathological Definition?
Refers to abnormal air space enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis.
What is the pathophysiology of Chronic Bronchitis?
- Initial exposure to irritants and chemicals (cigarette smoke)
- Hypertrophy and hyperplasia of bronchial mucinous glands and goblet cells. There is also ciliary destruction.
- This increases the production of mucus in the lumen causing narrowing and obstruction
- Epithelial layer becomes ulcerated and there is the stimulation of immune cells causing inflammation of the bronchus and bronchioles.
- This leads to scarring and thickening of the walls further narrowing the airways.
- This causes air trapping causing poor exchange of O2 and CO2 and increases risk of infection.
What are the pathological changes that occur in Chronic Bronchitis?
Goblet cell hyperplasia
Mucus hypersecretion
Chronic inflammation and fibrosis
Narrowing of small airways
What are the symptoms of chronic bronchitis?
Chronic Cough - high sputum production
Dyspnoea
Wheeze
Recurrent respiratory tract infections - due to mucus plugging
What are the Signs of Chronic Bronchitis?
Wheeze - narrowing of airway creates higher pitch sound.
Crackles - popping open of small airways
Hypoxaemia and Hypercapnia - mucus plugs block airflow and lead to partial pressures of CO2 to rise and subsequent decline of O2.
Cyanosis (if hypoxaemia is really bad leading to the term blue bloaters).
Pulmonary Hypertension - due to Hypoxic vasoconstriction leading to increased pulmonary vascular resistance
What is Emphysema?
A lung disease characterised by dilatation and destruction of the lung tissue causing enlarged air spaces distal to the terminal bronchioles
What is the Pathophysiology of Emphysema?
Occurs in the ACINUS
Irritants/chemicals lead to damage and destruction of the alveoli wall.
Causes and inflammatory reaction and immune cell infiltration releasing Leukotriene B4, IL-8 and TNF-a
Proteases (elastases and collagenases) are also produced which break down alveolar wall structural proteins.
This leads to permanent enlargement of the alveoli and loss of their elasticity.
Alveolar wall septa break down reducing the total surface area. This leads to gas exchange dysfunction.
Loss of elasticity in the airways means that the airways collapse upon exhalation causing air trapping distally.
What are the different types of Emphysema?
Centriacinar Emphysema
Panacinar Emphysema:
Paraseptal Emphysema:
What is Centriacinar Emphysema?
Most common
Damage to central/proximal acini due to smoking
Typically affects upper lobes
What is Panacinar Emphysema?
Entire acinus affected
Due to A1AT Deficiency (protease inhibitor deficiency) cannot prevent breakdown.
Typically affects Lower lobes
What is Paraseptal Emphysema?
Affects peripheral lung tissue.
Peripheral ballooned alveoli can rupture causing pneumothorax
What are the pathological changes seen in emphysema?
Related to loss of Elastin:
Collapse: the alveoli are prone to collapse.
Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae
How is Chronic Bronchitis and Emphysema classified differently?
Chronic Bronchitis is defined by clinical features
Emphysema is defined by structural changes (enlarged alveoli)
What are the symptoms of Emphysema?
Dyspnoea - diminished gas exchange
( can improve this by exhaling slowly through pursed lips giving the name pink puffers)
Hypoxaemia
Weight loss
Cough - with some sputum
Pulmonary HTN
What are the main features of COPD phenotypes (emphysema/chronic Bronchitis)?
Pink puffer - emphysema
- Weight loss
- Breathless
- Emphysematous
- Maintained pO2
Blue bloater – chronic bronchitis
- Cough
- Phlegm
- Cor pulmonale
- Type 2 Respiratory failure
How does Emphysema lead to pulmonary hypertension?
Widespread Hypoxic vasoconstriction.
Too many blood vessels are constricted increasing the pressures in others.
Leads to pulmonary hypertension.
What is the cause of the barrel shaped chest in COPD?
Both chronic bronchitis and emphysema leads to air trapping within the Bronchi/acini.
This leads to Hyperinflation of the lungs giving a barrel chest appearance.
What are the main complications of COPD?
Recurrent Respiratory Tract Infections: S. pneumoniae/H. influenzae
Respiratory failure
Pneumothorax: rupture of bullous disease
Polycythaemia or anaemia
Depression
What is a the most serious complication of COPD?
Cor Pulmonale:
Both Chronic bronchitis and Emphysema will lead to pulmonary hypertension due to excessive hypoxic vasoconstriction.
This causes R sided ventricular hypertrophy which will eventually lead to RHF and “Cor Pulmonale”
Who typically presents with COPD?
Older Px
Long term smokers
Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain
What are the Symptoms of COPD?
Chronic cough: usually productive
Sputum production
Breathlessness: usually on exertion in early stages
Frequent episodes of ‘bronchitis’: usually in the winter
Wheeze
What are the Signs of COPD?
- Dyspnoea
- Pursed lip breathing: (prevents alveolar collapse by increasing the positive end expiratory pressure)
- Wheeze
- Coarse crackles
- Loss of cardiac dullness: due to hyperexpansion of lungs from emphysema
- Downward displacement of liver: due to hyperexpansion of lungs from emphysema
- Signs of C02 retention
Drowsy
Asterixis
Confusion
What symptoms may be concerning in a COPD patient that suggests an alternative pathology?
Weight loss
Haemoptysis
Anorexia
Chest pain
Lymphadenopathy
Finger clubbing
Unexplained fatigue
May suggest cancer
Do patients with COPD typically present with Chronic Bronchitis or Emphysema?
Often Px will present with both conditions as COPD due to the same triggers causing both.
What is an acute exacerbation of COPD?
Presents similarly to chronic stable COPD however there is an acute and sustained worsening of symptoms in the patient
Who typically presents with COPD?
Older Px
Long term smokers
Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain
How is COPD Diagnosed?
Clinical Dx with Spirometry Test for confirmation
Spirometry shows Obstruction:
FEV1/FVC ration <0.7
Negative Reversibility Testing: <12% Inc FEV1
Obstruction does not show good response to salbutamol.
CXR - Lung hyperinflation + Bullae
What other investigations may be done in COPD on top of spirometry?
Bloods: FBC (assess for anaemia) and A1AT levels
CXR: Hyperexpanded, flattened hemidiaphragms, hypodense, Saber sheath trachea
ECHO if Cor Pulmonale Suspected
What features of a Px are supportive of a COPD diagnosis?
Smoker or ex-smoker
Symptoms in older adults (> 35 years old)
Chronic productive cough
Persistent/progressive breathlessness
Night time waking with symptoms uncommon
Variability uncommon (diurnal or day-to-day)
How is Breathlessness assessed in COPD?
Using the MRC Dyspnoea Scale:
- Breathlessness on strenuous exercise.
- Breathlessness on hurrying or slight hill.
- Walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace.
- Stops to catch breath after 100 metres OR a few minutes of walking
- Breathlessness on minimal activity (dressing) or unable to leave the house due to breathlessness
How does Asthma respond to Reversibility testing?
Bronchodilator (salbutamol) will increase FEV1 by >12%
AND
must increase FEV1 by 200ml
What is FVC?
Forced Vital Capacity:
The total amount of air forcibly expired
What is FEV1?
Forced Expiratory Volume in 1 second
What is an Abnormal FEV1?
- The result is compared with the predicted values, if the FEV1 is 80% or
greater than the predicted value = NORMAL - Thus is the FEV1 is less than 80% of the predicted value = LOW i.e
abnormal
What is an Abnormal FVC?
- The result is compared with the predicted values, if the FVC is 80% or
greater than the predicted value = NORMAL - Thus is the FVC is less than 80% of the predicted value = LOW i.e
abnormal
What does a low FVC suggest?
Airway Restriction
What does a Low FEV1/FVC ratio suggest?
<0.7 = Airway Obstruction
If FEV1/FVC ratio is high/normal but FVC is low (<80%) then airway restriction.
Do patients with COPD typically present with Chronic Bronchitis or Emphysema?
Often Px will present with both conditions as COPD due to the same triggers causing both.
What other tests may be done to look for the cause of COPD?
DLCO (diffusing capacity of CO across lung):
Low in COPD, Normal in Asthma
Genetic testing for A1AT Def.
ABG - may show T2RF
ECG - heart function
CXR - flattened diaphragm
Bloods - anaemia
How is the severity of COPD and airflow graded?
Post Bronchodilator when FEV1/FVC ratio < 70%
Stage 1: Mild - FEV1 >80% of predicted
Stage 2: Moderate - FEV1 50-79% of predicted
Stage 3: Severe - FEV1 30-49% of predicted
Stage 4: Very Severe - FEV1 <30% of predicted
What are the management Principles for COPD?
Education
Smoking cessation
Vaccination
Pulmonary rehabilitation
Self-management plans
Management of co-morbidities
Pharmacotherapy
What is the treatment of COPD?
Stop risk factors - smoking
Prophylactic Vaccines - Pneumonia
Medication:
1. SABA (Salbutamol) OR SAMA (Ipratropium Bromide)
- (a = Non steroid Responsive. B = Steroid Responsive)
a. LABA (Salmeterol) + LAMA (Tiotropium
b. Steroid Responsive = LABA + ICS (Beclometasone)
3.
a. 3 Month Trial of LABA + LAMA + ICS
b. Steroid Responsive = LABA + LAMA + ICS
What management can be provided for severe COPD?
Nebulisers - Salbutamol and/or ipratropium
Long term Oxygen therapy
What is an Exacerbation of COPD?
worsening of symptoms such as cough, shortness of breath, sputum production and wheeze. It is usually triggered by a viral or bacterial infection.
How are Exacerbations of COPD treated?
At Home:
Prednisolone 30mg once daily for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection (Doxycycline / Co-amoxiclav)
In Hospital:
Oxygen - carefully monitored
Nebulised Bronchodilators
Prednisolone 30mg once daily for 7-14 days
Antibiotics if there is evidence of infection
Physiotherapy
What is the main risk of COPD exacerbations?
Respiratory Failure:
COPD patients are chronic retainers of CO2 and therefore their kidneys adapt to produce extra HCO3 to compensate the acidotic state.
In acute exacerbations the kidneys cannot produce enough HCO3 quickly leading to RF.
What are some Impacts of COPD exacerbations?
Negative impact on quality of life
Impact on symptoms and lung function
Increased economic costs
Increased mortality
Accelerated lung function decline
What are the differential Diagnoses of COPD?
Asthma
Heart Failure
Other causes of SOB:
Bronchiectasis (airways become abnormally widened resulting in build-up of excess mucus making lungs more susceptible to infection)
Allergic fibrosing alveolitis
Pneumoconiosis
Pulmonary Embolus
Lung cancer
Asbestosis
What are the indications for hospital admission in a Px with COPD?
Marked increases in symptom intensity
Severe underlying COPD
Onset of new physical signs
Failure of an exacerbation to respond to initial medical management
Presence of serious comorbidities
Frequent exacerbation
Older age
Insufficient home support
Define Asthma?
Chronic reversible inflammatory airway condition characterised by reversible airway obstruction, airway hyperresponsiveness and inflamed bronchioles
What are the types of Asthma?
Eosinophilic (Allergic) (70%) - Extrinsic IgE mediated T1 Hypersensitivity
Non-Eosinophilic (Non Allergic) (30%) - Intrinsic non IgE mediated.
Explain the pathophysiology IgE mediated asthma?
Environmental trigger against specific allergens leads to sensitisation reaction where IgE Abs against antigen bind to mast cells.
Secondary exposure leads to an immune system activation and activation of Th2 cells.
Th2 cells produce cytokines such as IL3, 4, 5, 13.
IL-4 leads to IgE Crosslinking and degranulation of mast cells releasing histamine and leukotrienes.
IL-5 leads to eosinophil activation and release of proteins
This leads to a Hypersensitivity Rxn which causes Smooth muscle bronchospasm and increased mucus production leading to narrow airways and airway obstruction.
What happens to the airways in chronic asthma?
Initially asthma and inflammation of the airways is reversible.
Over chronic asthma the inflammation in the airways causes irreversible damage such as scarring and fibrosis causing thickening of the epithelial BM causing permanent narrowing of the airways.
What pathological changes are responsible for airway narrowing in Asthma?
Increased number of and hypertrophy of smooth muscle
Constriction of smooth muscle cells (bronchoconstriction)
Increased mucous production
Swelling and inflammation (of mucosa)
Thickened basement membrane
Airway hyperreactivity, cellular infiltration
What is the cause of asthma
Causes are unknown:
Genetics may play a factor
Environmental Factors:
Hygiene hypothesis
What is the Hygiene Hypothesis?
Reduced early exposure of bacteria and viruses when young leads to an altered proportion of immune cells.
This can subsequently lead to later onset asthma
What are the risk factors for asthma?
History of Atopy
FHx of asthma
Allergens - pollen, fur, smoke
Occupation
Obesity
Premature Birth
What are some triggers for asthma?
Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
Drugs
What drugs can trigger asthma?
Aspirin
Beta blockers
How can aspirin trigger asthma?
Aspirin inhibits COX1/2
Shunts more arachidonic acid down LPOX pathway.
Produces leukotrienes (LTB4, 5, 6)
These are proinflammatory
What is the epidemiology of asthma?
5.4 Million in UK receiving treatment
More common in developed countries
More common in children/young people compared to COPD
Commonly starts age 3-5. Peak prevalence age 5-15
What are the symptoms of asthma?
Chest tightness
Episodic Dyspnoea/SOB
Wheeze
Dry Cough (typically but can be wet)
What are the signs of asthma?
Diurnal PEFR variation
Dyspnoea and Expiratory Polyphonic wheeze
Hyper resonant Percussion
Samter’s Triad: Nasal polyps, Aspirin sensitivity, Asthma
What are some addition signs of an acute asthma attack?
Signs of Respiratory Failure
Tachypnoea
Tachycardia
Inability to complete sentences
Exhaustion
Reduced respiratory effort
Silent chest
Altered conscious level
What may be found in sputum from an asthmatic?
Curschmann spirals:
Mucus plugs that look like casts of the small bronchi
Charcot-Leyden crystals:
From break down of eosiophils.
How may a patient present indicating asthma?
Episodic symptoms
Diurnal variability. Typically worse at night.
Dry cough with wheeze and shortness of breath
A history of other atopic conditions such as eczema, hayfever and food allergies
Family history
Bilateral widespread “polyphonic” wheeze
How may a patient present indicating a different diagnosis to asthma?
Wheeze related to coughs and colds more suggestive of viral induced wheeze
Isolated or productive cough
Normal investigations
No response to treatment
Unilateral wheeze. This suggests a focal lesion or infection.
What are the signs of asthma?
Diurnal PEFR variation
Dyspnoea and Expiratory Polyphonic wheeze
Samter’s Triad: Nasal polyps, Aspirin sensitivity, Asthma
Atopic Triad: Atopic Rhinitis, Asthma, Eczema
What is Samter’s Triad
Nasal Polyps
Asthma
Aspirin sensitivity
What is Atopic Triad?
Atopic Rhinitis (Hayfever)
Allergic Asthma (Asthma)
Atopic Dermatitis (Eczema)
How is asthma classified?
According to:
Frequency of symptoms (night/early morning)
FEV1
PEFR (peak expiratory flow rate)
Frequency of medication use
What are the classifications of asthma?
Intermittent
Mild Persistent
Moderate Persistent
Severe Persistent
What are the primary investigations for asthma?
NICE advise to carry out tests and not make a clinical Dx:
1st Line Ix:
- Spirometry w/ Bronchodilator Reversibility
(shows reversible obstruction 200ml AND 12% increase)
- if spirometry normal - do Bronchial challenge
2nd Line:
PEF variation measurements - 2-4 weeks
Direct bronchial challenge test with histamine or methacholine
What are the targets of treating asthma?
Dampen inflammation:
Corticosteroids
LRTAs
biologics
Macrolides
Relax Smooth Muscle Airways:
Bronchodilators
Antimuscarinics
Theophylline
What is the Treatment algorithm for Chronic asthma?
16+: Avoid Triggers
- SABA (salbutamol)
- SABA + ICS (beclomethasone)
3a. Before adding more drugs assess inhaler technique and compliance
3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast)
- SABA + ICS + LABA (Salmeterol) +/- LTRA
- Consider change to MART (maintenance and reliever therapy)
- Increase ICS Dose
What is the first line treatment for an acute asthma exacerbation?
Oxygen Driven Salbutamol Nebuliser
What is the treatment for acute asthma Exacterbations?
OSHITME:
O2 if oxygen sats are low
Saba (Salbutamol nebulised)
Hydrocortisone (ICS)
IV MgSO4
Theophyline (IV) - MgSO4 / Escalate
What are the complications of Asthma?
Asthma Exacerbation
Pneumothorax
What is the histological characterisation of asthma?
Characterised by eosinophilic inflammation:
Lots of inflammation
Smooth muscle hypertrophy
Basement membrane thickening
Little fibrosis and little alveolar disruption
What is the Histological Characterisation of COPD?
Characterised by neutrophilic inflammation:
Lots of inflammation
Lots of fibrosis
Lots of alveolar disruption
Little smooth muscle hypertrophy and basement membrane thickening
What are the main conditions that are caused by Lower respiratory Tract Infections (LRTL)?
Tuberculosis
Pneumonia
What is Tuberculosis?
An infectious disease caused by Mycobacteria characterised by caseating granulomas.
What are the organisms classified as Mycobacterium Tuberculosis Complex (MTC)?
MTC organisms = TB causing:
M. tuberculosis
M. africanum
M. microtis
M. bovis (from unpasteurised milk)
What is the morphology of M. TB?
Gram Positive Rod Bacilli
Non motile + non spore forming
Mycolic acid capsule: Acid fast staining (w/ ZN)
Resistant to phagocytic killing.
Slow growing (15-20 hrs)
What is the epidemiology of TB?
1.7Bn people have latent TB
Top infectious killer in the world and in top 10 killers in the world (of anything)
Affects immunocompromised more
More common in South Asia (India, China, Pakistan) and Sub-Saharan Africa
How is TB infection spread?
Via airborne transmission
What are the risk factors for TB infection?
Contact with someone w/ active TB
Country/recent travel to associated countries
Immunocompromised (HIV etc)
IVDU
Homelessness
Smoking and alcohol
Increased age
What are the different types of TB?
Active TB - active infection
Latent TB (95% of cases) - Previous infection where the immune system has encapsulated and prevented progression of TB
Secondary TB - When Latent TB reactivates
Miliary TB - Where immune system cannot control the infection and it becomes disseminated
Extrapulmonary TB - where TB infects other areas
What Extra-pulmonary sites can TB infect?
Lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Cutaneous TB affecting the skin
What is the pathogenesis of TB?
Infection of TB via droplets/aerosol
TB phagocytosed (but resistant to killing) and is taken to hilar lymph nodes
Immune cells are recruited and a granuloma forms. (typically in lung apex)
T cells recruited and Centre of granuloma undergoes caseating necrosis (1’ Ghon Focus)
Ghon Focus spreads to nearby lymph nodes forming a Ghon Complex
Latent TB:
In most people TB is contained within granuloma and becomes latent TB.
Miliary TB:
If TB spreads from Ghon complex
systemically then it becomes Miliary TB
How does TB resist gram staining?
High lipid content with mycolic acids in cell wall makes mycobacteria resistant to gram stain
Is latent TB symptomatic?
No - ASx as bacteria is contained within granuloma and causes no Sx
What are the symptoms of active TB?
Systemic Sx:
Fatigue
Fever + night sweats + weight loss (characteristic of TB)
Lymphadenopathy
Cough w/haemoptysis >3 weeks
Chest pain
Dyspnoea
Erythema Nodosum
What are the signs of TB?
Auscultation - often normal (may have crackles)
Consolidation in lung
Lung Collapse
Clubbing
What may be symptoms of Extrapulmonary TB?
Lymph Node TB (most common)
CNS - Meningism
Skin rash
Cardiac - TB pericarditis Sx
Bone - Join pain
Spinal Pain (spinal TB)
GU - Epididymitis, LUTS
Abdo - Ascites
What are some screening Tests for TB/diagnosis of latent TB?
Latent Disease - Mantoux Test
Interferon Gamma release assay
(This can distinguish between TB exposure and TB vaccine)
What are the primary investigations for Active TB?
CXR - patchy consolidation, pleural effusions, Granulomata in chest
Sputum culture and Microscopy:
Microscopy - AFB bright red on ZN stain.
PCR - NAAT/PCR
Culture - Solid Culture on Lowenstein-Jensen Agar
What would you see on CXR in TB?
Patchy Consolidation
Ghon Complex
Granulomatous Lesions
Hilar Lymphadenopathy
Pleural Effusion
What is the Mantoux Test?
Protein derived from organism (Tuberculin)
Inject intradermally
Stimulates type 4 delayed hypersensitivity reaction
- within 2 days the APCs and T cells would be activated if there has been exposure to Tb and an immune response would have occurred
Not sensitive – immunosuppressed or miliary TB won’t react (false negatives)
Only moderately specific (false positives)
Won’t easily distinguish infection from disease
Drawback of Tuberculin skin test:
If patient has had BCG vaccine, there will be a reaction
Cannot tell if patient has latent TB
What is the management of latent TB?
Doesnt necessarily need Tx
If risk of reactivation then:
6 months of isoniazid with pyridoxine (6H) or
3 months of isoniazid (with pyridoxine) and rifampicin (3HR)
What is the Treatment for Active TB?
When would Tx be given for 12 months?
RIPE: Combination Abx for 6-12 months
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for first 2 months
E – Ethambutol for first 2 months
Tx for 12 months if CNS TB
Why is TB Treatment given for so long?
To ensure the TB is cleared to prevent re-occurrence
Also to prevent Drug resistance developing.
What are the side effects of TB treatment?
Rifampicin - red/orange Urine + Hepatitis
Isoniazid - Peripheral Neuropathy / inhibitor of CYP450/ Hepatitis
Pyrazinamide - Hepatitis and gout
Ethambutol - Optic neuritis/eye problems
What must be done if TB is diagnosed?
Inform Public Health England
How can TB be prevented?
Vaccination - BCG vaccine for neonates
Detection and Tx of latent TB via Mantoux Test and Treat
What is the treatment for Latent TB?
6 months of isoniazid with pyridoxine (6H) or
3 months of isoniazid (with pyridoxine) and rifampicin (3HR)
What is Pneumonia?
Infection of the lung parenchyma leading to inflammation of the lung tissue and fluid exudation (sputum) collecting in the alveoli.
What is the Epidemiology of Pneumonia?
Incidence 350/100, 000/year (>1 in 300)
20-50% hospitalised, 5-10% require ITU
Hospitalisation average 6-8 days
Mortality
1% in community, 10% in hospital, 30% in ITU
UK 2012, 28,952, 5.1% of all deaths
Costs > £400 million/year to UK
Significant short- and long-term mortality from other causes after pneumonia
Who is at risk of developing pneumonia?
Extremes of age
COPD and other respiratory diseases
Immunocompromised
Nursing home residents
Impaired swallow
Diabetes
Congestive Heart Failure
Alcoholics
IVDU
What are the classifications of Pneumonia?
Classified by the setting in which a Px has contracted infection
Community Acquired Pneumonia
Hospital Acquired Pneumonia
Aspiration Pneumonia
Define Community Acquired Pneumonia (CAP)?
Pneumonia that develops out in the community or <48hrs after hospital admission
Define Hospital Acquired Pneumonia (HAP)?
Pneumonia that develops more than 48 hours after hospital admission.
Define Aspiration pneumonia?
Pneumonia that develops as a result of inhaling foreign material (food etc)
What is the main type of organism that causes pneumonia?
Bacterial infection
Can also be Viral (Influenza/CMV) or fungal (P. jirovecii)
What are the main cause of CAP?
S. pneumonia (50%)
H. influenzae (20%)
Mycoplasma pneumoniae (Atypical pneumonia)
H. Influenzae
Legionella
What are some less common causes of CAP?
S. aureus
Legionella (atypical)
Moraxella
Chlamydia pneumoniae (atypical)
Where is legionella caused pneumonia typically from?
Often from Spain/ warmer countries
Recent Travel Hx and staying in hotels with air conditioning.
Or WARM water
What are the risk factors for HAP?
Elderly
Ventilator associated
Post Operative
What are the main causes of HAP?
P. aeruginosa
E. coli
S. aureus
Klebsiella
What is the concern of treating HAP?
Most of the causative organisms have multi drug resistance
What is the main cause of aspiration pneumonia?
Klebsiella
What is atypical pneumonia?
How are they Tx?
pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.
They dont respond to penicillins
Tx with Macrolides, Fluoroquinolones and tetracyclines.
What are the causes of atypical pneumonia?
Legionella
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumonia
Q fever (Coxiella)
What is the main cause of fungal pneumonia?
Pneumocystis jiroveci (PCP)
Occurs in immunocompromised Px
AIDS defining illness
How is PCP treated?
Co-trimoxazole
(combination of Trimethoprim and Sulphamethoxazole)
What are the risk factors for pneumonia?
Extremes of age
Preceding infection (viral)
Immunosuppressed
IVDU
Smoking
CO-Morbidities - DM, HIV
Respiratory conditions - asthma, COPD, CF
What is the pathogenesis of typical pneumonia?
- Bacteria “translocate” to normally sterile distal airway - bacteria from URT that has either came in quickly or colonised for a while are micro-aspirated into lower lung
- Resident host cells become overwhelmed
- Develop an inflammatory response – neutrophils and inflammatory exudate fill alveolar space
- Pus collects in the lung causing consolidation
Resolution phase – when bacteria cleared
- Inflammatory cells removed by apoptosis
- Resolution phase leads to complete recovery
Simple:
Bacteria invades
Infection and inflammation
Exudate forms inside alveolar lumen
Sputum production
What is the pathogenesis of atypical pneumonia?
Bacteria invades
Infection and inflammation
Exudate forms in interstitium of alveoli
Dry cough
What are the symptoms of pneumonia?
Productive cough w/purulent sputum (classically rusty may suggest S. pneumonia)
Fever, Sweat and Rigors - due to infection
Pleuritic chest pain
SOB
Malaise
May cause confusion in elderly
Dry cough in atypical pneumonia
What are the signs of pneumonia?
Reduced breath sounds
Bronchial Breathing w/ coarse crepitations
Crackles and Wheeze
Consolidation
Dull Percussion
Hypoxia
Tachycardia
Pyrexia
Confusion
Cyanosis
What are some classical symptoms of Pneumonia infection?
Fever
Sweats
Rigors
What are the primary investigations of pneumonia?
1st Line:
CXR (diagnostic) shows consolidation
Sputum Microscopy culture and Sensitivities (MC+S) + Gram Stain to ID organism
FBC - Raised WCC
U&E - urea
CRP - raised due to inflammation
Legionella Urinary Antigen - Doesn’t respond well to Abx
How is pneumonia assessed for severity?
CURB65:
C – Confusion
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65
Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment
How can CURB65 be used to assess mortality in Pneumonia?
0 = Low risk (<1% mortality)
1-2 = Intermediate risk (1-10% mortality)
3-4 = High Risk (>10% mortality)
What organisms may show multi-lobar pneumonic lesions on CXR?
S. pneumoniae
S. aureus
Legionella
What organisms may show Multiple abscess pneumonic lesions on CXR?
S. aureus
What organisms may show upper lobe pneumonic lesions on CXR?
Klebsiella
(but first exclude TB)
What is the Initial treatment for CAP pneumonia?
Oxygen Saturation 94-98%
IV Fluids if dehydrated
Appropriate Analgesia - Paracetamol/NSAIDs
Antibiotics: Initially start on Broad Spec:
- Mild CAP (CURB65 0-1): Amoxicillin PO 5 days (clarithromycin/Doxycycline if allergic)
- Moderate-severe CAP (CURB65 2): Amoxicillin + Macrolide (clarithromycin) PO 7-10 days
- Admit to hospital
- Severe CAP (CURB65 3-5): IV Co-Amoxiclav + IV Macrolide (Clarithromycin) 7-10 days or 14-21 if S.aureus
(If legionella (notify PHE) and Clarithromycin)
After Treating Pneumonia, What should be done in the elderly (>50yrs)
Follow-up CXR to ensure that there is not a lung tumour causing the infection.
What is the treatment for pneumonia when the causative organism is known?
S. pneumoniae - Amoxicillin (Clarithromycin/Cefotaxime)
H. Influenzae - Doxycycline/Co-amoxiclav
S. aureus - Flucloxacillin (cefuroxime)
MRSA - Vancomycin
Klebsiella - Cephalosporins (cefotaxime) or carbapenems
P. Aeruginosa - Piperacillin-Tazobactam (Tazocin)
Atypical - Macrolides/Fluoroquinolones
What are the treatments for HAP?
Broader spectrum Empirical Tx first:
Early Onset <5 days - Metronidazole OR Co-amoxiclav/ Tazocin
Later Onset >5 days - Tazocin
Then once cultures ID organism - targeted Abx
What can be done to prevent pneumonia?
- Polysaccharide pneumococcal vaccine – protects against 23 serotypes
- Pneumonococcal Conjugate Vaccine
- Influenza vaccination to those >65, immunocompromised or with medical co-morbidities
- Smoking cessation
What are the major complications of pneumonia?
Sepsis - Used to grade severity - CURB65
Parapneumonic Pleural effusion in 57% of CAP
Empyema
Lung abscess
Death
What is Cystic Fibrosis?
An autosomal recessive condition that affects the mucus glands multi-systemically
What are the genetics for CF?
autosomal recessive mutation on Chromosome 7 affecting the CFTR protein.
There are multiple mutations but Del-F508.
(phenylalanine is deleted)
This affects chloride channels.
What is the prevalence of CF?
1 in 25 are carriers of the gene
1 in 2500 are affected by CF
What are the risk factors for CF?
FHx
Known parental carriers
Caucasian (CF is the most common inherited condition in caucasians)
What is the CFTR protein?
CFTR is an epithelial cAMP regulated chloride channel that normally actively secretes Cl- ions and passively secretes Na+ ions along with water into ductal secretions
This makes the ductal secretions thin and watery
What is the pathophysiology of CFTR protein?
Mutation in CFTR causes it to become dysfunctional.
CFTR has reduced function meaning that less Cl-, Na+ and water are released into ductal secretions leading to the thickening of the mucus secretion.
What is the pathophysiology of a CFTR dysfunction in relation to the lungs?
CFTR mutation leads to thick mucus secretions.
This causes impaired mucociliary clearance as the mucus is extra thick.
This leads to stagnation of mucus that contains pathogens which leads to increased infection risk.
The thicker mucus causes difficulty breathing
Trapping of mucosal pathogens can cause a inflammatory reaction which leads to an increased risk of bronchiectasis
What is the pathophysiology of a CFTR dysfunction in relation to neonates?
Can lead to Meconium Ileus:
Stool becomes too thick to pass through the bowel leading to bowel obstruction.
Failure to thrive
What is the pathophysiology of a CFTR dysfunction in relation to the GI Tract?
Thick secretions from the pancreas can lead to pancreatic duct obstruction.
Pancreatic insufficiency and malabsorption of foods.
Bowel obstructions
What is the pathophysiology of a CFTR dysfunction in relation to the Hepatobiliary system?
Thicker biliary secretions leads to an increased risk of biliary obstruction.
Could lead to liver cirrhosis
How can CF lead to male infertility?
CFTR mutation can cause atrophy of the vas deferens leading to infertility
What are the symptoms of CF?
Chronic cough w/Thick sputum production
Recurrent respiratory tract infections
Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
Abdominal pain and bloating
Most common cause of Meconium Ileus in infants
Parents may report the child tastes particularly salty when they kiss them, due to the concentrated salt in the sweat
Poor weight and height gain (failure to thrive)
What are the signs of CF?
Low weight or height on growth charts
Nasal polyps
Recurrent respiratory infections
Salty Sweat
Pancreatic Insufficiency
Finger clubbing
Crackles and wheezes on auscultation
Abdominal distention
What are the primary investigations for CF?
New-born Blood spot test (Immuno-reactive Trypsin Test)
Sweat Test (gold standard)
Genetic testing for CFTR mutation)
Faecal Elastase Test - Pancreatic Insufficiency
CXR - Hyperinflation, Increased Pulmonary Markings, Bronchiectasis
What is the CF Sweat test?
Pilocarpine and electrodes placed on skin make it sweat.
Tested for Chloride Concentration.
A result of > 60 mmol/L (sweat chloride) is positive and requires referral to a cystic fibrosis specialist (normal value < 40 mmol/Ll)
Why are people with CF at a massively increased risk of recurrent respiratory tract infections?
Patients with cystic fibrosis struggle to clear the secretions in their airways.
This creates a perfect environment with plenty of moisture and oxygen for colonies of bacteria to live and replicate.
What are the key microbial organisms that colonise the respiratory tract in CF?
S. aureus
P. aeruginosa
+Haemophilus influenza
Klebsiella pneumoniae
Escherichia coli
What is the management of CF?
Conservative:
- Chest physiotherapy
- Exercise
- No smoking
Medication:
- Anti-mucolytics - rhDNase
- Prophylactic Flucloxacillin (prevent S. aureus), Amoxicillin (H. Influ), Ciprofloxacin (p.aeur)
- Bronchodilators (SABA) + ICS
- Vaccinations - Pneumococcal, Influenza, Varicella
- Lung Transplant in progressive RF
Systemic Tx:
- Pancreatic enzyme replacement
- Vitamin Supplements
- High calorie diet.
What is Bronchiectasis?
Chronic inflammation of the bronchi and bronchioles leading to permanent dilatation of central and medium-sized airways. This is due to inflammatory destruction of airway walls resulting in persistently infected mucous.
Commonly occurs secondary to CF
What is the Epidemiology of Bronchiectasis?
More common in women than men
May develop after lung infections
Pathological end point of many disease
Presents at any age but incidence increase with age
What are the possible causes of Bronchiectasis?
Chronic bronchial inflammation caused by :
- Obstruction - Foreign bodies, Tumour, Thick Mucus
- Previous infection - P. aeruginosa, TB
- Allergy and Inflammatory conditions
- Immunodeficiency - AIDS, Immunoglobulin Deficiency
- Congenital - CF
What are the risk factors for Bronchiectasis?
Post Infection (TB/Pneumonia)
Increased Age
Smoking
Females
Genetics
What is the pathogenesis of Bronchiectasis?
Infection or chronic inflammatory conditions cause immune system activation.
This will secrete proteases that break down elastin in the bronchi walls leading to irreversible dilation of the bronchi
This leads to increased risk of microbial colonisation.
This causes mucus hypersecretion and trapping due to the dilated bronchi and damaged cilia there is impaired mucociliary escalator
This will lead to airway obstruction.
How are bronchiectasis and emphysema different?
Emphysema is dilation of the acini and alveoli due to loss of elastin.
Bronchiectasis is dilation of the bronchi due to loss of elastin.
What are the symptoms of Bronchiectasis?
Dyspnoea/SOB
Productive cough with Copious sputum production
Haemoptysis (maybe)
Wheeze
Chest Pain
What are the signs of Bronchiectasis?
Hx of Chronic Productive cough and recurrent Chest infections
Foul Smelling Sputum
Auscultation:
Coarse Crackles on inspiration
High pitched inspiratory squeaks
Ronchi - Low pitch snore
Finger Clubbing
What are the primary investigations for Bronchiectasis?
High resolution CT Chest: Gold Standard:
shows bronchial dilation and bronchial wall thickening (signet ring sign)
CXR - dilated airways with thickened walls appear as ‘tram-tracks’
Sputum cultures - infective organisms
Spirometry: Obstructive (FEV1/FVC < 0.7)
What are some differential Diagnoses for Bronchiectasis?
COPD
Asthma
TB
Chronic sinusitis
Pneumonia
Pulmonary fibrosis
Inhalation of foreign body
What is the treatment for Bronchiectasis?
Non curative: Tx underlying cause if present.
Reduce RFs (stop smoking) and Chest Physiotherapy
Mucoactive agent (carbocisteine)
Bronchodilator - for asthma/COPD sufferers
Prophylactic Abx for acute exacerbations: (Pseudo (Ciproflox), Haem (Doxyc), S.aureus (fluclox)
What are some complications of Bronchiectasis?
Infective exacerbation
Chronic respiratory failure
Haemoptysis (may be massive and life-threatening)
Cor pulmonale
Pneumothorax
Chest pain
Define a Pleural Effusion?
Excess fluid accumulation between the visceral and parietal pleura (pleural cavity)
Clinically detected when >500ml present
Detected on CXR when >300ml Present
What are the different types of Pleural effusion?
Whether the fluid is:
Exudative - high protein count (>3g/dL)
Transudative - lower protein count (<3g/dL)
What are the main pathology relating to a Exudative and Transudative Pleural Effusion?
Exudative:
Occurs due to increased permeability and therefore leakiness of pleural space and/or capillaries, usually as a result of inflammation, infection or malignancy
Transudative:
Occurs when the balance of hydrostatic forces in chest favour accumulation of pleural fluid i.e. increased pressure due to the backing up of blood in left-sided congestive HF
What are the Exudative causes of pleural effusion?
Related to inflammation:
Trauma
Lung cancer
Pneumonia
Empyema
Rheumatoid arthritis
Tuberculosis
What are the Transudative causes of Pleural effusion?
Fluid Moving (transport) across into the pleural space:
Increase Hydrostatic Pressure:
Congestive cardiac failure
Fluid Overload
Constrictive pericarditis
Meig’s syndrome
Decreased Oncotic Pressure:
Hypoalbuminaemia
Hypothroidism
Nephrotic Syndrome
What is Meig’s Syndrome?
right sided pleural effusion with ovarian malignancy
What is the pathophysiology of an Exudative pleural effusion?
Inflammation leading to increased vascular permeability
This leads to increased protein leaking out of the vessels and accumulates in the pleural cavity.
Increased pleural oncotic pressure draws fluid into the pleural cavity leading to pleural effusion
What is the pathophysiology of an Transudative pleural effusion?
Fluid shifting due to and increase in hydrostatic pressure (eg. in HF) or a decrease in oncotic pressure (eg.hypoalbuminaemia) causing leaking of fluid into pleural cavity
What is the most common cause of Exudative pleural effusion?
Pneumonia and malignancy
What is the most common cause of Transudative pleural effusion?
(congestive) Heart failure
What are the symptoms of Pleural effusion?
- Dyspnoea
- Pleuritic chest pain (often exudate due to pleural inflammation/irritation)
- Cough
Sx of underlying pathology:
Peripheral oedema - HF
Ascites - LF
Cough & fever - RTI
What are the signs of pleural effusion?
Reduced Chest expansion on affected side
Reduce breath sounds on affected side
Dull percussion (increased fluid)
Pleural friction rub/bronchial breathing
Tracheal Deviation
What may be a differential diagnosis with a hyper resonant percussion?
Pneumothorax
What are the primary investigations for pleural effusion?
GS + 1st Line: CXR:
Shows Blunting of Costophrenic angles
Fluid in lung fissures (fluid appears white)
Tracheal/Mediastinal deviation (if massive effusion)
Thoracocentesis (Pleural fluid aspiration):
pH, Lactate, WCC, Microscopy
Determine Transudate or Exudate
Where would you see transudates or exudates on CXR in pleural effusion?
Transudates - Bilateral (TB)
Exudates - Unilateral (EU)
What would you see in thoracocentesis to aid in determining whether a pleural effusion is exudative or transudative?
Transudate – clear
Exudate – cloudy
Lymphatic – looks like milk
What is the treatment for Pleural effusion?
Conservative Mx:
Small effusions can be treated by Tx of underlying cause (often Transudative)
Infective Effusions:
Chest Drain - remove fluid (often Exudative)
Non-malignant:
Thoracocentesis - needle drainage for Sx effusions.
Recurrent:
Pleurodesis - injection that adheres visceral and parietal pleural
What should be done if a patient is having chronic recurrent pleural effusions?
Pleurodesis:
Surgical fusing/injection that adheres the pleural layers together to prevent fluid accumulation between them
What is Empyema?
An infected Pleural Effusion (pus collects in pleural cavity)
What does Empyema Show on pleural aspiration?
PHAL:
Pus,
High LDH.
Acidic pH (pH < 7.2),
Low glucose
What is the treatment for Empyema?
chest drain to remove the pus and antibiotics
What is a Pneumothorax?
An excess accumulation of air within the pleural space causing ipsilateral lung collapse.
What is the Epidemiology of a Pneumothorax?
Occurs spontaneously or secondary to chest trauma
Spontaneous pneumothorax most common in young males
Generally, more common in males
Patients often tall and thin
Most commonly occurs between 20-40
What are the causes of Pneumothorax?
Spontaneous
Trauma
Iatrogenic - lung biopsy, mechanical ventilation or central line insertion
Lung pathology - infection, asthma or
COPD
What are the risk factors for a pneumothorax?
Tall thin males
Connective tissue disorders (MF, EHD)
FHx
Smoking
Underlying Lung disease - COPD, Asthma
RA
What is the Pathophysiology of a Pneumothorax?
Pleural space is normally a vacuum (no air) with a negative pressure
Breach in the pleura (trauma/CT disorders)
Leads to air entry into pleural cavity
Elastic recoil of the lung causes it to deflate
eg. Subpleural bullae burst
eg. Abnormal connection between pleural space and airways
What are the symptoms of a pneumothorax?
Sudden onset
Sharp Pleuritic Chest pain
SOB
As pneumothorax enlarges, patient becomes more breathless and may develop pallor and tachycardia
What are the signs of a pneumothorax?
Reduced breath sounds on affected side
Hyper resonant percussion (increased air)
Reduced chest expansion
Trachea Deviation away
Tachycardia/Tachypnoea
Hypotension - in Tension Pneumothorax
What is the primary investigation for a pneumothorax?
If suspected Tension Pneumothorax - Do not wait for Ix
GS + 1st Line: erect CXR
Excess air appears black
Tracheal Deviation to other side
CT thorax can be more sensitive for small pneumothoraxes (GS for smaller Pneumothoraxes)
What is seen on CXR in a pneumothorax?
When should you avoid requesting a CXR?
Loss of lung markings
Visible visceral pleural edge
Radiolucent space
Avoid request in Tension-Pneumothorax as this wastes time
What is the treatment for a Primary, secondary and Tension pneumothorax?
Primary:
- No SOB / <2cm - Self limiting and discharge
- SOB/>2CM - Needle aspiration
Secondary:
- NO SOB/<1cm - Self limiting and Discharge
- NO SOB/1-2cm - Needle Aspiration
- SOB & >2cm - Chest Drain (5th ICS)
Tension:
- Urgent Needle Decompression
- ABCDE Management
- High Flow Oxygen
What is a Tension Pneumothorax?
MEDICAL EMERGENCY:
Caused by trauma to the pneumothorax where air can flow into the pleural space but it cannot lead due to the creation of a one way valve
What is the pathogenesis of a Tension pneumothorax?
Trauma creates a one way valve
During inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space.
More air keeps getting drawn into the pleural space with each breath and cannot escape.
Creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.
What are the signs of a tension pneumothorax?
Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension
What is the treatment for a Tension Pneumothorax?
High Flow Oxygen and Urgent Needle Decompression
LEARN BY HEART:
“Insert a large bore cannula into the second intercostal space in the midclavicular line on the side of the pneumothorax.”
Once pressure is relieved then chest drain.
Where would you insert a chest drain?
Triangle of Safety:
The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)
What is an Interstitial Lung Disease (ILD)?
Umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.
Give some examples of ILDs?
Idiopathic Pulmonary Fibrosis
Pneumonoconiosis
Sarcoidosis
Hypersensitivity Pneumonitis
What test is generally used to diagnose ILD?
High resolution CT Thorax:
Shows Ground Glass appearance and honeycombing (mainly in the lower zones)
Spirometry - Restrictive Pattern
Lung Biopsy can confirm diagnosis on Histology
What is the general Management for ILD?
Generally the damage is irreversible and so supportive Tx to prevent progression.
Mx options:
Remove or treat the underlying cause
Home oxygen where they are hypoxic at rest
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
What is Pulmonary Fibrosis?
Progressive fibrosis and scarring of the lung parenchyma.
What are the different types of pulmonary fibrosis?
Idiopathic PF
Drug induced PF
Secondary PF
What is Idiopathic Pulmonary Fibrosis?
Condition of PF where there is no clear cause.
This is the most common ILD that is typically seen in older men who smoke.
What drugs can induce pulmonary fibrosis?
Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin
What are secondary causes of Pulmonary Fibrosis?
Alpha-1 antitripsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
What are the risk factors for Idiopathic Pulmonary FIbrosis?
Smoking
Occupational causes (dust)
Increased age (60-70s)
Male
FHx
What is the pathophysiology of Pulmonary fibrosis?
- Progressive chronic lung damage
- Causes Type II pneumonocytes to over proliferate during repair leading to excessive myofibroblast activation
- Leads to Replacement of damaged lung parenchyma with collagen.
- Causes excessive scarring and fibrosis.
- Lungs fail to expand on inhalation
- Thickens the interstitium between the capillary and alveoli causing impaired gas exchange
Can lead to Type 1 Respiratory Failure.
What can cause pulmonary fibrosis in the upper respiratory zones?
Pneumonoconiosis
Silicosis
Hypersensitivity Pneumonitis
Cystic Fibrosis
Sarcoidosis
Tuberculosis
What can cause Pulmonary Fibrosis in the Lower Respiratory Zones?
Idiopathic Pulmonary Fibrosis
Drug Induced PF
Connective tissue Disorders (SLE)
What are the symptoms of pulmonary fibrosis?
Progressive Dyspnoea
Dry cough (no sputum)
Malaise
What are the signs of pulmonary fibrosis?
Bibasal fine inspiratory crackles (end respiratory)
Finger clubbing
Cyanosis
+ Sx of underlying pathology if Secondary PF
What are the diagnostic investigations for pulmonary fibrosis?
Spirometry: Restriction (FVC reduced, FEV1/FVC normal)
CXR - non specific but can be used to exclude other DDx
Gold Standard:
High CT thorax to confirm diagnosis = Ground glass & Honeycombing
What is the treatment for Pulmonary Fibrosis?
Supportive Tx:
Smoking cessation
Pulmonary Rehabilitation
Oxygen Therapy
Vaccines
Antifibrotic Agents:
Pirfenidone or nintedanib (indicated if FVC is 50% - 80% of predicted)
Consider Lung Transplant
What is the prognosis like for IPF?
IPF has a poor prognosis, with median survival ranging from 2.5 - 3.5 years after diagnosis.
What is Pneumonoconiosis?
Interstitial lung fibrosis that occurs secondary to inhalation of occupational triggering antigens that cause an inflammatory reaction.
What are some different types of pneumonoconiosis?
Silicosis - Inhalation of silicon dioxide
Asbestosis - Inhalation of asbestos
Explain the pathogenesis of pneumonoconiosis?
Particles (Dust, asbestos, silica) are inhaled, they reach the terminal bronchioles and are ingested by interstitial and alveolar macrophages.
Dust particles are carried by macrophages and expelled as mucus.
In chronic exposure (occupation), this process is no longer functional and macrophages accumulate in alveoli,
Resulting in immune system activation and lung tissue damage.
Fibroblasts then arrive and deposit excess collagen to cause lung fibrosis
What are the risk factors for pneumonoconiosis?
Male
Increasing age
Substance exposure - Coal, dust, silicon, asbestos etc
What are the symptoms of pneumonoconiosis?
Exertional Dyspnoea
Dry Cough
Haemoptysis
Wheezing
Weight loss
What does asbestosis increase the risk of developing?
Mesothelioma
What are the diagnostic findings for Pneumonoconiosis?
CXR:
Coal Workers Lung - Nodular opacities in upper lobes
Silicosis - Eggshell calcification of hilar lymph nodes
Asbestosis - Pleural Thickening and Calcification
Spirometry: Restrictive and reduced DLCO
High-Res CT chest: interstitial fibrosis
Microscopic Exam - Ferruginous Bodies - Asbestos fibres coated in macrophages
what is the management for Pneumonoconiosis?
Conservative Mx as incurable:
Stop smoking
Avoid exposure
What is Sarcoidosis?
A Type of Interstitial Lung disease
A multi-systemic Granulomatous inflammatory condition characterised by non-caseating granulomas depositing in many tissues
What is the cause of sarcoidosis?
Unknown: Thought to be a type 4 Hypersensitivity reaction.
Idiopathic
What are the risk factors for sarcoidosis?
Afro-Caribbean and Scandinavian ethnicity
Young adults: 20-40 yrs
Female gender
Family history
What is the Typical presentation of Sarcoidosis?
Sx can range from ASx to life threatening
Typical patient:
patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum.
What part of the body is affected by Sarcoidosis?
Typically affects the lungs (90%)
But can present will many extra-pulmonary symptoms as it can affect any system of the body
What are the Chest symptoms of sarcoidosis?
Dry cough
Dyspnoea
Mediastinal lymphadenopathy
Constitutional Sx:
Weight loss, Fatigue and fever
What are the Common and Less common Extra-pulmonary symptoms of Sarcoidosis?
Common: (PESH)
- Peripheral lymphadenopathy
- Eye – anterior uveitis
- Skin –Erythema nodosa, skin papule
- Hepatosplenomegaly
Less common:
- Bone
- Heart – arrhythmias
- CNS
- Kidney
What is Lofgren’s Syndrome?
specific presentation of sarcoidosis. It is characteristic by a triad of:
Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)
What are some differential diagnoses of sarcoidosis?
Tuberculosis (caseating)
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis
What are the primary investigations for sarcoidosis?
First Line:
- CXR - Bilateral Hilar lymphadenopathy and pulmonary infiltrates/nodules
- CXR often used for staging
CT Chest (may also be used)
GS Diagnostic:
- Biopsy (non caseating granuloma)
Other:
- Spirometry - Restrictive
- Bloods:
- Hypercalcaemia - Excess Vit D produced by macrophage
- Elevated ACE due to granulomas
What would be seen on CXR to stage Sarcoidosis?
Staging
Stage 0 – no changes
Stage I – bilateral hilar lymphadenopathy
Stage II – bilateral hilar lymphadenopathy and diffuse interstitial disease
Stage III – interstitial disease only (reticulonodular pattern)
Stage IV – pulmonary fibrosis (honeycombing)
What other investigations would be done for sarcoidosis to check for extra-pulmonary involvement?
U&Es - kidney involvement
Urine dipstick - proteinuria indicating nephritis
LFTs - liver
Ophthalmology review - eye
ECG/ECHO - heart
Abdo USS - liver and kidney
What is the treatment of Sarcoidosis?
ASx/Mild: No Tx is 1st Line:
85% of stage 1 resolve spontaneously
50% of stage 2 resolve spontaneously
When Tx required:
1st Line: Oral Prednisolone (+bisphosphonates to protect against OP)
2nd Line: Methotrexate/Azathioprine
What are the potential complications of Sarcoidosis?
Can progress to Pulmonary Fibrosis
Pulmonary HTN
What is Hypersensitivity pneumonitis?
Type 3 hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction.
Explain the pathophysiology of Hypersensitivity pneumonitis?
Allergen is inhaled and picked up by alveolar macrophages which take it to the nearest lymph node.
antibodies against allergen (IgG) form Ab-Ag complexes.
These complexes get deposited in the lung tissues and alveoli.
Complement is activated which causes acute inflammation of the lung tissue causing pneumonitis
Chronically this can lead to pulmonary fibrosis
What are some different allergens/occupations that can lead to hypersensitivity pneumonitis?
Bird-fanciers lung is a reaction to bird droppings
Farmers lung is a reaction to mouldy spores in hay
Mushroom workers’ lung is a reaction to specific mushroom antigens
Malt workers lung is a reaction to mould on barley
What are the classifications of Hypersensitivity Pneumonitis?
Acute - Sx develop <12 hrs post exposure and resolve typically < 48 hrs
Chronic - Develop often after lower levels but prolonged exposure to allergens
What are the acute clinical manifestations of Hypersensitivity Pneumonitis?
Sx develop <12 hrs after a good amount of exposure and resolve after 48 hrs
- Fever
- Rigors
- Headache
- Myalgia
- Shortness of breath
- Cough
- Chest tightness
What are the Chronic clinical manifestations of Hypersensitivity Pneumonitis?
Sx develop over prolonged exposure (often lower levels for long time)
Progressive cough
Progressive Dyspnoea
Fatigue
Weight loss
Fibrosis is evident
How is Hypersensitivity pneumonitis diagnosed?
Bronchoscopy with Bronchoalveolar lavage:
Biopsy shows raised T Lymphocytes in bronchi, alveoli and non-caseating granulomas
High Res CT - Ground glass (upper lobes) and centrilobular nodules. Reticular opacity
Spirometry/ Pulmonary function test - Restrictive
Serology - Specific Igs
What is the treatment for hypersensitivity pneumonitis?
Remove the allergen
Steroids (glucocorticoids) can help with symptoms
Give oxygen if necessary
What is Goodpasture’s Syndrome?
An autoimmune disease characterised by Anti-GBM autoantibodies that attack the lungs and kidneys.
A type of Pulmonary Vasculitis
What is the pathophysiology of Goodpasture’s Syndrome?
Type II Hypersensitivity Reaction
Lung alveolar basement membranes and kidney glomerular basement membranes are made up of Type IV collagen (containing alpha 3, 4, and 5 strands)
Environmental toxins (smoking/infection) pass through the kidneys (via blood) or the lungs (inhalation) and damage the collagen exposing the strands.
Autoantibodies against the alpha3 chain of collagen bind and activate the Classical complement system.
This leads to inflammation of the lungs and kidneys that can cause pulmonary fibrosis and glomerular nephritis.
What are the risk factors for Goodpasture’s syndrome?
Genetics - HLA-DR15
infection
Smoking
Oxidative stress
What are the symptoms of Goodpasture’s Syndrome?
Constitutional Sx:
Lethargy
Fever
Anorexia
Weight loss
Myalgia
Pulmonary Sx:
Cough
Haemoptysis
Dypsnoea
Kidney Sx:
Haematuria and proteinuria
How is Goodpasture’s syndrome diagnosed?
Biopsy often of kidney /lung:
Shows inflammation of BM and fluorescence testing for auto Abs
Microscopy - Crescent Glomerulonephritis
Serology: Anti-GMB +tve
What is the treatment for Goodpasture’s Syndrome?
Corticosteroids
Immunosuppressants - Cyclophosphamide
Plasmapheresis
what is the normal pulmonary blood pressure at rest?
8-20mmHg
What is defined as pulmonary hypertension?
Resting mPAP >25mmHg at rest.
How is Pulmonary HTN normally measured?
Right heart catheterisation.
What is the pathophysiology of pulmonary HTN?
Reactive pulmonary vasoconstriction due to hypoxaemia
The increased resistance in the pulmonary vasculature leads to increased pressure in the right ventricle
This results in increased ventricular filling and stroke volume, which further increases pulmonary arterial pressure
Over time, right ventricular hypertrophy develops as it compensates for the increased afterload.
What are the different groups of causes of pulmonary HTN?
- Primary pulmonary HTN - Idiopathic/CT disorders (MF, EHD)
- Left heart disease - VHD, HF, HOCM
- Chronic Lung disease - COPD, Asthma
- Pulmonary vascular disease - PE/Tumour
- Unclear/multifactorial - Sarcoidosis, Haematological disorders
What is the most common cause of secondary pulmonary HTN?
COPD
What are the symptoms of Pulmonary HTN?
Progressive breathlessness
Exertional Dizziness/syncope
Fatigue
Sx of underlying pathology
What are the signs of pulmonary HTN?
Loud S2 heart sound - pulmonary side
Raised JVP
Pulmonary/Tricuspid regurgitation
Tachycardia
Hepatomegaly
Peripheral oedema
Right parasternal heave - due to RV hypertrophy
Signs of underlying pathology
What are the primary investigations for Pulmonary HTN?
1st Line: ECHO:
RV function, enlargement and Pressures
Gold Standard (diagnostic) Right heart Catheter
CXR - RVH, Enlarged proximal PA
ECG:
Right Ventricular Hypertrophy
Right axis deviation
Right bundle branch block
What does Right ventricular hypertrophy look like on an ECG?
Larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)
What is the treatment for pulmonary HTN?
Primary P HTN:
Phosphodiesterase-5 inhibitors (SILDENAFIL)
IV prostanoids (Epoprostenol)
Endothelin receptor antagonists (Macitentan)
Secondary P HTN:
Tx underlying cause
Supportive Tx for complications:
Respiratory failure, HF, arrythmias
What are the main complications of pulmonary HTN?
Right heart failure: due to increasing pulmonary pressures
(Can lead to biventricular failure)
Pericardial effusion and tamponade
Hepatic congestion: due to worsening right heart failure
What is a Mesothelioma?
A malignant neoplasm of the mesothelial cells of the pleura
What is the primary cause of Mesothelioma?
Asbestos Exposure
Typically doesnt present until decades after the exposure
What are the risk factors for Mesothelioma?
Asbestos Exposure (85% of cases have Hx)
Increasing age (40-70)
Males
What is the epidemiology of a Mesothelioma?
More common in men
Often presents between 40-70
Latent period between exposure and development of tumour may be up to 45 years
What are the symptoms of Mesothelioma?
SOB
Cough
Persistent Pleuritic chest pain
Constitutional Cancer Sx:
Fatigue, fever, night sweats, weight loss
Sx of metastases: bone pain etc
Why may a patient with a mesothelioma have a hoarse voice?
Tumour presses on recurrent laryngeal nerve
What are the signs of a Mesothelioma?
Finger clubbing
Reduced breath sounds
Stony Dull Percussion
Ascites (if peritoneal disease present)
What are the primary investigations for mesothelioma?
First Line: Imaging:
CXR - pleural thickening +/- effusion
Contrast Enhanced CT
Bronchoscopy + Biopsy (Gold Standard for Dx)
What is the treatment for Mesothelioma?
Surgery (if operable) otherwise Palliative:
Extrapleural pneumonectomy
Pleurectomy with decortication
Rarely curative
+/- Chemotherapy:
Cisplatin
Pemetrexed
+/- Radiotherapy
What is the Main malignancy of the lung parenchyma?
Primary Bronchial Carcinomas
How are Primary Lung cancers classified?
By Histology:
Small Cell Lung Cancer (SCLC): 20%
Non-Small Cell Lung Cancer (NSCLC): 80%
- Adenocarcinoma (40%)
- Squamous cell Carcinoma (20%)
- Large Cell Carcinoma (10%)
- Carcinoid/other (10%)
What are the primary metastasis sites for Lung cancers?
Bones
Liver
Adrenal Glands
Brain
Lymph Nodes
What is the epidemiology of Lung Cancer?
3rd most common cancer in the UK and 1/3rd of all cancer deaths
(behind breast and prostate)
Male:Female - 2:1
Kills 35,000 people in the UK
(more than Breast and Colorectal combined)
What are the risk factors for Primary lung Cancer?
Smoking (BIGGEST CAUSE)
Asbestos
Coal
Ionising radiation
Underlying lung disease
Increasing age
FHx
What are the causes of Lung Cancer?
SHOE:
Smoking (most common - 90%)
Host factors - Pre-existing lung disease, Genetics, HIV
Occupational - Coal, Asbestos, Nickel
Environmental - Ionising Radiation, Radon
What is a Small cell lung cancer?
15% of primary lung cancers.
Derived from neuroendocrine APUD cells
Has Central lung lesions
Rapidly grows and Px often present at an advanced stage.
Who is typically affected by SCLC?
Exclusively smokers
What are the features of a SCLC?
Number of cases:
Location:
Derivation:
Paraneoplastic Syndromes
No of Cases - 15% of Lung Cancer
Location - Central lesions near main bronchus
Derived - From neuroendocrine cells - makes them responsible for paraneoplastic syndromes
Paraneoplastic Syndromes:
Ectopic ACTH - Cushing’s
Ectopic ADH - SIADH
Lambert Eaton Syndrome (NMJ disorder)
What is the most common NSCLC?
Adenocarcinoma
What are the features of an Adenocarcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes
Number of cases: 40% of NSCLC
Location: Peripheral Lesion
Originates: Mucus Secreting Glandular Cells
Affects: Non-smokers mainly
Paraneoplastic Syndromes:
- Hypertrophic Pulmonary Osteoarthropathy
- Gynaecomastia
What are the Features of a Squamous Cell Carcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes
Number of cases: 20% NSCLC
Location: Central Lesion
Originates: From Lung Epithelium and has central necrosis
Affects: Smokers typically
Paraneoplastic Syndromes:
- Hypertrophic Pulmonary Osteoarthropathy
- PTHrp - Hypercalcaemia
What are the Features of a Carcinoid NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes
Number of cases: <10% NSCLC
Location: Rare Peripheral
Originates: From mature Neuroendocrine cells related to MEN1 mutation
Affects: MEN1 mutations and neurofibromatosis
Paraneoplastic Syndromes
Secretes Serotonin
What are the Features of a Large-cell Carcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes
Number of cases: <10% NSCLC
Location: Peripheral lesion commonly but can be found anywhere in lungs
Originates: Lacks both glandular and squamous differentiation
Paraneoplastic Syndromes
- Ectopic B-hCG production
What are the general Symptoms of Lung cancer?
Cough w/haemoptysis
Shortness of breath
Pleuritic Chest pain
Constitutional Sx of Cancer:
Fever
Night sweats
Weight loss
Loss of appetite
What are the general signs of Lung Cancer?
Reduced Breath sounds
Stony Dull Percussion - suggests malignant pleural effusion
Hoarseness (press on RLN)
Lymphadenopathy
Clubbing
Recurrent chest infections
Paraneoplastic Changes
What are the primary investigations for lung cancer?
First line: CXR
Hilar enlargement
Peripheral opacity – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse
Staging - CT Thorax with contrast scan if abnormal CXR
GS Diagnostic: Bronchoscopy + Biopsy
How are Lung Cancers Graded?
TNM classification
Tumour – how big it is
T1 – <3cm
T2 - >3cm
T3 – invades chest wall, diaphragm and pericardium
T4 – invades mediastinum, heart, great vessels, trachea, oesophagus, vertebra, carina
Nodes – how many and where they are
N0 - none
N1 – Hilar nodes
N2 – same side mediastinal nodes or subcarinal
N3 – contralateral mediastinum or supraclavicular
Metastases
0 - none
1a – tumour on same side
1b – tumour elsewhere
X - unknown
Which is a more aggressive cancer, SCLC or NSCLC?
SCLC is more aggressive
What is the treatment for SCLC?
Often Diagnosed late and Px have metastatic disease:
Therefore
Chemo/radiotherapy (Cisplatin)
palliative care
What is the treatment for NSCLC?
Early: Surgical Excision + adjuvant therapy
Late/Metastatic:
palliative treatment with immunotherapy, chemotherapy, and radiotherapy
(Nb. NSCLC has poor response to chemotherapy)
What are some complications for lung cancer?
Recurrent laryngeal nerve palsy
Horner’s syndrome (Pancoast tumour)
SVC obstruction
Paraneoplastic Syndromes
Bone pain/Hypercalcaemia
What is more common, Primary or secondary lung cancer?
Secondary are More common than Primary:
Lungs oxygenate 100% of blood and therefore they come into contact with all blood. This increases the risk of metastasis.
What are the common causes of secondary lung cancer?
Mets from:
Breast
Kidney
Bowel
Bladder
What is a Pancoast Tumour?
A tumour in the lung apex that commonly metastasises to the necks sympathetic plexus and can press on the sympathetic ganglion causing Horner’s Syndrome:
Triad of Ptosis, Miosis and Anhidrosis
What syndrome does a Pancoast tumour cause?
HORNERS Syndrome characterised by:
Ptosis - Droopy eyelids
Myosis - Excessive Pupil Constriction
Anhidrosis - Lack of sweating
What is a Pulmonary Embolism?
Obstruction of the pulmonary vasculature, secondary to an embolus.
What is the pathophysiology of a PE?
Embolus enters Right heart via IVC
It enters pulmonary vasculature
This causes occlusion of small blood vessels
Causes V/Q mismatch as blood cannot gas exchange.
Causes Hypoxic vasoconstriction and reactive bronchoconstriction.
Narrows airways leading to Dyspnoea
Hypoxic vasoconstriction increases pulmonary vascular resistance causing Pulm HTN.
This causes RV heart strain and hypertrophy.
Eventually this leads to RHF (Cor Pulmonale)
What are the risk factors of a PE?
Anything affecting Virchow’s Triad:
Endothelial Injury:
Smoking, HTN, Trauma
Venous Stasis:
Immobility, Post surgery, AF, Obesity
Hypercoagulability - OCP, Polycythaemia, Malignancy
What are the symptoms of PE?
Sudden onset Shortness of breath
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Dyspnoea/Tachypnoea
Syncope (RED FLAG)
What are the signs of PE?
Hypotension
Tachypnoea
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension
Raised JVP
Hypoxia
What are the common features that are highly suggestive of PE on examination?
Tachypnoea (RR >16/minute): 96%
Crackles: 58%
Tachycardia (HR >100): 44%
Fever (temp >37.8°C): 43%
How is PE diagnosed?
WELLS Score:
<4 Unlikely PE - perform D-dimer. - if >500ng/ml then perform CT Pulmonary Angiogram.
> 4 Likely PE - Perform CTPA (GS): Will diagnose PE clot.
CXR - Exclude other pathology (typically normal in PE)
ECG - S1Q3T3
What other investigations are performed for a PE?
ECG: S1Q3T3
Deep S waves in lead I
Deep Q waves in lead III
T waves inverted in Lead III
RBBB V1-3 & Sinus Tachycardia
CXR - usually normal
CTPA - GS diagnostic
Bloods:
D-Dimer
Anti-phospholipid Abs - in unprovoked DVT/PE
What is the treatment of PE is the Px is haemodynamically stable (non-massive PE)?
Anticoagulants:
1st Line:
DOAC (Rivaroxaban, Apixaban)
(LMWH if DOAC CI)
2nd Line: Warfarin
What is the treatment of PE is the Px is haemodynamically unstable (Massive PE)?
Thrombolysis (clot busting) - Alteplase
If fails - Catheter embolectomy
What can be used as prophylaxis for a PE?
Compression Stockings
Regular walking
SC LMWH
Define Dyspnoea?
A symptom of difficult or laboured breathing
What is the MRC Dyspnoea Scale?
Assess degree of baseline functional disability due to Dyspnoea
Grade 0: I only get breathless with strenuous exercise
Grade 1: I get short of breath when hurrying on level ground or walking up a slight hill
Grade 2: On ground level I stop for breath when walking at own pace
Grade 3: I stop for breath after walking about 100 yards or after a few minutes on level ground
Grade 4: I am too breathless to leave the house or I am breathless when dressing/undressing
What are the main acute respiratory causes of Dyspnoea?
Pneumonia
Asthma
PE
Pneumothorax
What are the main Chronic respiratory causes of Dyspnoea?
COPD
Idiopathic Pulmonary Fibrosis
Bronchiectasis
What are the main cardiac causes of Dyspnoea?
ACS
Stable angina
Chronic HF
Pericarditis
What are some less common respiratory causes of Dyspnoea?
Pleural Effusion
Lung Cancer
Interstitial Lung Disease (pneumonoconiosis)
What are some less common cardiac causes of Dyspnoea?
Carditis (end, myo, peri)
Valvular dysfunction
Cardiomyopathy
Acute HF
What are some other systemic causes of Dyspnoea?
Musculoskeletal
Anxiety
Metabolic acidosis:
- DKA
- Acute renal failure
What can cause respiratory failure?
- Low oxygen delivery - anaemia, high altitude
- Airway obstruction - Asthma, COPD
- Gas exchange limitation - lung fibrosis, IDLs
- V/Q Mismatch - Pneumonia, PE, Pulm HTN
- Alveolar hypoventilation - emphysema, reduced resp drive, obesity, Muscular weakness
What is the main pathophysiology of type 1 respiratory failure?
Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia.
What is Type 1Respiratory Failure?
Type 1 = 1 change (O2)
- pO2 (partial O2 pressure) is low
- pCO2 (partial CO2 pressure) is low or normal
What condition is the most common cause for Type 1 Respiratory failure?
Pulmonary Embolism
Pneumonia
What is the main pathophysiology of type 2 respiratory failure?
Type 2 respiratory failure occurs when the respiratory system cannot sufficiently remove carbon dioxide from the body, leading to hypercapnia
What is Type 2 Respiratory Failure?
Type 2 = 2 changes (O2 & CO2)
- pO2 is low
- pCO2 is high
What is the most common cause of Type 2 Respiratory Failure?
Hypoventilation:
Caused by Obstruction:
COPD
Alveolar Hypoventilation:
Neuromuscular weakness
Obesity
Chest wall deformity
Reduced respiratory drive (opiates)
What are the signs of Hypercapnia seen in type 2 respiratory failure?
- Bounding pulse
- Flapping tremor (asterixis)
- Confusion
- Drowsiness
- Reduced consciousness
What is DLCO a measure of?
Transfer Coefficient of oxygen/CO
the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries
How is DLCO measured?
Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill)
hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured
What causes a high DLCO?
Pulmonary haemorrhage - can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available
What causes a low DLCO?
- Severe emphysema
- Fibrosing alveolitis
- Anaemia
- Pulmonary hypertension
- Idiopathic pulmonary fibrosis
- COPD
Why in airway restriction is FVC low but FEV1 normal?
Due to restriction, lung volumes are small (lower TLC and therefore FVC) and most of breath is out in first second (normal FEV1)
What are the main Upper Respiratory Tract Infections (URTI)?
Epiglottitis.
Laryngitis.
Pharyngitis (sore throat).
Sinusitis (sinus infection).
Whooping Cough
Croup
(Otitis Media)
Where does an URTI go from?
Between the nose to the larynx above the vocal cords
What are some risk factors impairing Lung Defences?
Old age
Smoking
Alcohol use
ETT/nasotracheal intubation
Respiratory therapy
Hypoxaemia
Acidosis
Toxin inhalation
Immunosuppression
Malnutrition
What is the epidemiology of URTIs?
Adults will have 2-3 URTIs each year.
Most commonly caused by Viruses (rhinovirus)
What are the most common causes of URTIs?
Rhinoviruses (45-50%)
Influenza A virus (25-30%)
Coronaviruses (10-15%)
Parainfluenza viruses (5%)
Respiratory syncytial viruses (5%
What are the general Symptoms of a URTI?
Coryzal Sx:
Nasal stuffiness, runny nose, sneezing, sore throat, and cough.
What is Pharyngitis?
Inflammation of the pharynx w/wo exudate production
What are the causes of pharyngitis?
Viral (70-80%) - Rhinovirus, Adenovirus, EBV/HIV
Bacteria (20%) - Group A Strep (S. pyogenes)
What are the signs of pharyngitis?
Sore throat
Fever
Cough (viral + bacterial)
Nasal congestion (viral)
Exudate (bacterial)
What must be ruled out if a Px (especially child) has pharyngitis?
Rheumatic fever
(typically 2-4 weeks post S. pyogenes infection.
What is the treatment for pharyngitis?
Viral - self limiting
Bacterial - Amoxicillin/Flucloxacillin
Likely Strep pyogenes so amoxicillin
What is Sinusitis?
inflamed mucosa of nasal cavity and nasal sinuses
What causes sinusitis?
Viral infection - Most common
Bacterial infection - S. Pneumo / H. Influ
What are the signs and symptoms of sinusitis?
Symptoms
Fontal headache
Facial pain
Fever
Signs
Purulent nasal discharge
Tenderness
What is the treatment for Viral sinusitis?
Self limiting
Usually lasts <10 days and has non-purulent discharge
Inhalation of water vapour can help
What is the treatment for Bacterial Sinusitis?
May last >10 days and have purulent discharge
Symptoms for less than 10 days: No antibiotics.
No improvement after 10 days: 2 weeks of high-dose steroid nasal spray
No improvement after 10 days and likely bacterial cause: consider delayed or immediate prescription of antibiotics (Amoxicillin)
What is Otitis Media?
Middle ear infection and inflammation
(commonly affects children)
Presents with ear pain
What are the causes of Otitis media?
Bacterial or Viral
What is the diagnostic findings for otitis media?
Otoscopy examination will reveal a bulging red tympanic membrane.
If the ear drum perforates there can be discharge from the ear.
What is the treatment for otitis media?
Otitis media usually resolves within 3-7 days without antibiotics.
An appropriate initial antibiotic in the community:
Amoxicillin
Alternatives in penicillin allergy:
Clarithromycin
Erythromycin
2nd Line: Co-Amoxiclav
What is Acute Epiglotitis?
Epiglottitis refers to inflammation and localised oedema of the epiglottis, which can result in potentially life-threatening airway obstruction.
What is the most common cause of Epiglottitis?
Haemophilus Influenza B
Often secondary to immunocompromisation (such as following HIV)
What are the risk factors for Epiglottitis?
Peak age 6-12 (can occur at any)
Male gender
Unvaccinated
Immunocompromised
What are the symptoms of Epiglottitis?
Rapid Onset:
Dysphagia
Dysphonia (stridor)
Drooling
Distress
What are the signs of Epiglottitis?
Stridor - whistling
Tripod Position: A sign of respiratory Distress
Lean forward, mouth open, tongue out = max air in)
Pyrexia
What is the primary investigation of Epiglottitis?
If acutely unwell then NO Ix but immediate Tx
Laryngoscopy (GS):
swelling and inflammation of the epiglottis or supraglottis.
Lateral neck radiograph:
Thumb print sign
What is the treatment for Epiglottitis?
EMERGENCY
First Line:
- Secure airway
- Nebulised adrenaline
- IV antibiotics - Doxycycline, Co-Amoxiclav, Erythromycin,
Second Line:
- Dexamethasone
What is Croup?
Acute infective upper respiratory infection causing oedema in the larynx
(Acute Larygnotracheobronchitis)
Who is typically affected by croup?
Children between 6 months and 2 years old
What are the causes of Croup?
Main cause: Parainfluenza virus
Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)
What is the presentation of Croup?
Usually improves in <48 hours
Increased work of breathing
“Barking” cough, occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever
What is the treatment of Croup?
Oral Dexamethasone (single dose 150mcg/kg)
What is Whooping Cough?
Upper respiratory tract infection caused by Bordetella pertussis
Who is affected by Whooping cough?
Mainly children
90% <5yrs
What is the pathogenesis of Whooping cough?
Haemagglutinin and fimbriae adhere to cilia of URT.
Adenylate cyclase toxin inhibits phagocyte chemotaxis (Lots of virulence factors)
Pertussis toxin inhibits alveolar macrophages
Leads to lymphoid hyperplasia skewing the immune response
What are the stages of whooping cough presentation?
Catarrhal stage (1-2 weeks):
- Dry, unproductive cough
- Low-grade fever
- Conjunctivitis
- Coryzal symptoms
Paroxysmal stage (1-6 weeks):
- Coughing fits: typically consist of a short expiratory burst followed by an inspiratory gasp, causing the ‘whoop’ sound
- Post-tussive vomiting
Convalescent stage (lasts up to 6 months):
Gradual improvement in symptoms
What is the characteristic symptom of whooping cough?
Whoop sound caused sharp inhalation of breath during coughing bout
What are the investigations of Whooping cough?
Nasopharyngeal swab/aspirate:
Culture/PCR
Anti-pertussis toxin immunoglobulin G (IgG) serology
What is the treatment for Whooping cough?
Notify PHE
Hospital admission if severe
Antibiotics: if Cough Sx is within 21 days
Macrolids - Clarithromycin, Azithromycin
School work absence: highly contagious
What are the complications of Whooping cough?
Pneumonia
Encephalopathy
Otitis media
Injuries from coughing - pneumothorax
Seizures.
What can cause the oxygen dissociation curve to shift to the left?
Rule of L:
Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature
What can cause the oxygen dissociation curve to shift to the right?
‘CADET, face Right!’
For CO2, Acid, 2,3-DPG, Exercise and Temperature
Raised [H+] (acidic) (from exercise)
Raised pCO2
Raised 2,3-DPG*
Raised temperature
How are upper respiratory viral infections diagnosed?
Green Viral Throat swab + PCR
Some Point of Care tests for some viruses (influenza, SARS-CoV-2)
