Respiratory COPY COPY COPY Flashcards

1
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A

Progressive irreversible airway obstruction characterised by persistent airflow limitation caused by long term damage to lung tissue.

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2
Q

What are the conditions that are classed as COPD?

A

Chronic Bronchitis
Emphysema

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3
Q

What is the epidemiology of COPD?

A

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.

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4
Q

What are the risk factors for COPD?

A

Cigarette smoking
Air pollution
Occupational exposure to dusts, chemical agents, and fumes
A1AT deficiency - can lead to early onset COPD

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5
Q

What is the most important cause/aetiological factor for COPD?

A

Cigarette smoking

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6
Q

Define Chronic Bronchitis?

A

A inflammatory lung condition that develops over time in which the bronchi and bronchioles become inflamed and scarred.

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7
Q

What is Chronic Bronchitis as a clinical definitions?

A

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.

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8
Q

What is Emphysema as a pathological Definition?

A

Refers to abnormal air space enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis.

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9
Q

What is the pathophysiology of Chronic Bronchitis?

A
  • 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.
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10
Q

What are the pathological changes that occur in Chronic Bronchitis?

A

Goblet cell hyperplasia
Mucus hypersecretion
Chronic inflammation and fibrosis
Narrowing of small airways

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11
Q

What are the symptoms of chronic bronchitis?

A

Chronic Cough - high sputum production

Dyspnoea

Wheeze

Recurrent respiratory tract infections - due to mucus plugging

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12
Q

What are the Signs of Chronic Bronchitis?

A

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

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13
Q

What is Emphysema?

A

A lung disease characterised by dilatation and destruction of the lung tissue causing enlarged air spaces distal to the terminal bronchioles

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14
Q

What is the Pathophysiology of Emphysema?

A

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.

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15
Q

What are the different types of Emphysema?

A

Centriacinar Emphysema

Panacinar Emphysema:

Paraseptal Emphysema:

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16
Q

What is Centriacinar Emphysema?

A

Most common

Damage to central/proximal acini due to smoking

Typically affects upper lobes

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17
Q

What is Panacinar Emphysema?

A

Entire acinus affected

Due to A1AT Deficiency (protease inhibitor deficiency) cannot prevent breakdown.

Typically affects Lower lobes

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18
Q

What is Paraseptal Emphysema?

A

Affects peripheral lung tissue.
Peripheral ballooned alveoli can rupture causing pneumothorax

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19
Q

What are the pathological changes seen in emphysema?

A

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

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20
Q

How is Chronic Bronchitis and Emphysema classified differently?

A

Chronic Bronchitis is defined by clinical features

Emphysema is defined by structural changes (enlarged alveoli)

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21
Q

What are the symptoms of Emphysema?

A

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

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22
Q

What are the main features of COPD phenotypes (emphysema/chronic Bronchitis)?

A

Pink puffer - emphysema
- Weight loss
- Breathless
- Emphysematous
- Maintained pO2

Blue bloater – chronic bronchitis
- Cough
- Phlegm
- Cor pulmonale
- Type 2 Respiratory failure

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23
Q

How does Emphysema lead to pulmonary hypertension?

A

Widespread Hypoxic vasoconstriction.

Too many blood vessels are constricted increasing the pressures in others.

Leads to pulmonary hypertension.

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24
Q

What is the cause of the barrel shaped chest in COPD?

A

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.

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25
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
26
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"
27
Who typically presents with COPD?
Older Px Long term smokers Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain
28
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
29
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
30
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
31
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.
32
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
33
Who typically presents with COPD?
Older Px Long term smokers Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain
34
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
35
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
36
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)
37
How is Breathlessness assessed in COPD?
Using the MRC Dyspnoea Scale: 1. Breathlessness on strenuous exercise. 2. Breathlessness on hurrying or slight hill. 3. Walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace. 4. Stops to catch breath after 100 metres OR a few minutes of walking 5. Breathlessness on minimal activity (dressing) or unable to leave the house due to breathlessness
38
How does Asthma respond to Reversibility testing?
Bronchodilator (salbutamol) will increase FEV1 by >12% AND must increase FEV1 by 200ml
39
What is FVC?
Forced Vital Capacity: The total amount of air forcibly expired
40
What is FEV1?
Forced Expiratory Volume in 1 second
41
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
42
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
43
What does a low FVC suggest?
Airway Restriction
44
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.
45
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.
46
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
47
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
48
What are the management Principles for COPD?
Education Smoking cessation Vaccination Pulmonary rehabilitation Self-management plans Management of co-morbidities Pharmacotherapy
49
What is the treatment of COPD?
Stop risk factors - smoking Prophylactic Vaccines - Pneumonia Medication: 1. SABA (Salbutamol) OR SAMA (Ipratropium Bromide) 2. (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
50
What management can be provided for severe COPD?
Nebulisers - Salbutamol and/or ipratropium Long term Oxygen therapy
51
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.
52
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
53
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.
54
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
55
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
56
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
57
Define Asthma?
Chronic reversible inflammatory airway condition characterised by reversible airway obstruction, airway hyperresponsiveness and inflamed bronchioles
58
What are the types of Asthma?
Eosinophilic (Allergic) (70%) - Extrinsic IgE mediated T1 Hypersensitivity Non-Eosinophilic (Non Allergic) (30%) - Intrinsic non IgE mediated.
59
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.
60
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.
61
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
62
What is the cause of asthma
Causes are unknown: Genetics may play a factor Environmental Factors: Hygiene hypothesis
63
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
64
What are the risk factors for asthma?
History of Atopy FHx of asthma Allergens - pollen, fur, smoke Occupation Obesity Premature Birth
65
What are some triggers for asthma?
Infection Night time or early morning Exercise Animals Cold/damp Dust Strong emotions Drugs
66
What drugs can trigger asthma?
Aspirin Beta blockers
67
How can aspirin trigger asthma?
Aspirin inhibits COX1/2 Shunts more arachidonic acid down LPOX pathway. Produces leukotrienes (LTB4, 5, 6) These are proinflammatory
68
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
69
What are the symptoms of asthma?
Chest tightness Episodic Dyspnoea/SOB Wheeze Dry Cough (typically but can be wet)
70
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
71
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
72
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.
73
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
74
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.
75
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
76
What is Samter's Triad
Nasal Polyps Asthma Aspirin sensitivity
77
What is Atopic Triad?
Atopic Rhinitis (Hayfever) Allergic Asthma (Asthma) Atopic Dermatitis (Eczema)
78
How is asthma classified?
According to: Frequency of symptoms (night/early morning) FEV1 PEFR (peak expiratory flow rate) Frequency of medication use
79
What are the classifications of asthma?
Intermittent Mild Persistent Moderate Persistent Severe Persistent
80
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
81
What are the targets of treating asthma?
Dampen inflammation: Corticosteroids LRTAs biologics Macrolides Relax Smooth Muscle Airways: Bronchodilators Antimuscarinics Theophylline
82
What is the Treatment algorithm for Chronic asthma?
16+: Avoid Triggers 1. SABA (salbutamol) 2. SABA + ICS (beclomethasone) 3a. Before adding more drugs assess inhaler technique and compliance 3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast) 4. SABA + ICS + LABA (Salmeterol) +/- LTRA 5. Consider change to MART (maintenance and reliever therapy) 6. Increase ICS Dose
83
What is the first line treatment for an acute asthma exacerbation?
Oxygen Driven Salbutamol Nebuliser
84
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
85
What are the complications of Asthma?
Asthma Exacerbation Pneumothorax
86
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
87
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
88
What are the main conditions that are caused by Lower respiratory Tract Infections (LRTL)?
Tuberculosis Pneumonia
89
What is Tuberculosis?
An infectious disease caused by Mycobacteria characterised by caseating granulomas.
90
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)
91
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)
92
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
93
How is TB infection spread?
Via airborne transmission
94
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
95
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
96
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
97
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
98
How does TB resist gram staining?
High lipid content with mycolic acids in cell wall makes mycobacteria resistant to gram stain
99
Is latent TB symptomatic?
No - ASx as bacteria is contained within granuloma and causes no Sx
100
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
101
What are the signs of TB?
Auscultation - often normal (may have crackles) Consolidation in lung Lung Collapse Clubbing
102
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
103
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)
104
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
105
What would you see on CXR in TB?
Patchy Consolidation Ghon Complex Granulomatous Lesions Hilar Lymphadenopathy Pleural Effusion
106
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
107
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)
108
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
109
Why is TB Treatment given for so long?
To ensure the TB is cleared to prevent re-occurrence Also to prevent Drug resistance developing.
110
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
111
What must be done if TB is diagnosed?
Inform Public Health England
112
How can TB be prevented?
Vaccination - BCG vaccine for neonates Detection and Tx of latent TB via Mantoux Test and Treat
113
What is the treatment for Latent TB?
6 months of isoniazid with pyridoxine (6H) or 3 months of isoniazid (with pyridoxine) and rifampicin (3HR)
114
What is Pneumonia?
Infection of the lung parenchyma leading to inflammation of the lung tissue and fluid exudation (sputum) collecting in the alveoli.
115
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
116
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
117
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
118
Define Community Acquired Pneumonia (CAP)?
Pneumonia that develops out in the community or <48hrs after hospital admission
119
Define Hospital Acquired Pneumonia (HAP)?
Pneumonia that develops more than 48 hours after hospital admission.
120
Define Aspiration pneumonia?
Pneumonia that develops as a result of inhaling foreign material (food etc)
121
What is the main type of organism that causes pneumonia?
Bacterial infection Can also be Viral (Influenza/CMV) or fungal (P. jirovecii)
122
What are the main cause of CAP?
S. pneumonia (50%) H. influenzae (20%) Mycoplasma pneumoniae (Atypical pneumonia) H. Influenzae Legionella
123
What are some less common causes of CAP?
S. aureus Legionella (atypical) Moraxella Chlamydia pneumoniae (atypical)
124
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
125
What are the risk factors for HAP?
Elderly Ventilator associated Post Operative
126
What are the main causes of HAP?
P. aeruginosa E. coli S. aureus Klebsiella
127
What is the concern of treating HAP?
Most of the causative organisms have multi drug resistance
128
What is the main cause of aspiration pneumonia?
Klebsiella
129
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.
130
What are the causes of atypical pneumonia?
Legionella Chlamydia psittaci Mycoplasma pneumoniae Chlamydophila pneumonia Q fever (Coxiella)
131
What is the main cause of fungal pneumonia?
Pneumocystis jiroveci (PCP) Occurs in immunocompromised Px AIDS defining illness
132
How is PCP treated?
Co-trimoxazole (combination of Trimethoprim and Sulphamethoxazole)
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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
134
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
135
What is the pathogenesis of atypical pneumonia?
Bacteria invades Infection and inflammation Exudate forms in interstitium of alveoli Dry cough
136
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
137
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
138
What are some classical symptoms of Pneumonia infection?
Fever Sweats Rigors
139
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
140
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
141
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)
142
What organisms may show multi-lobar pneumonic lesions on CXR?
S. pneumoniae S. aureus Legionella
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What organisms may show Multiple abscess pneumonic lesions on CXR?
S. aureus
144
What organisms may show upper lobe pneumonic lesions on CXR?
Klebsiella (but first exclude TB)
145
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)
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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.
147
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
148
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
149
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
150
What are the major complications of pneumonia?
Sepsis - Used to grade severity - CURB65 Parapneumonic Pleural effusion in 57% of CAP Empyema Lung abscess Death
151
What is Cystic Fibrosis?
An autosomal recessive condition that affects the mucus glands multi-systemically
152
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.
153
What is the prevalence of CF?
1 in 25 are carriers of the gene 1 in 2500 are affected by CF
154
What are the risk factors for CF?
FHx Known parental carriers Caucasian (CF is the most common inherited condition in caucasians)
155
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
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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.
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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
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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
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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
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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
161
How can CF lead to male infertility?
CFTR mutation can cause atrophy of the vas deferens leading to infertility
162
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)
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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
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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
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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)
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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.
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What are the key microbial organisms that colonise the respiratory tract in CF?
S. aureus P. aeruginosa +Haemophilus influenza Klebsiella pneumoniae Escherichia coli
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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.
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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
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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
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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
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What are the risk factors for Bronchiectasis?
Post Infection (TB/Pneumonia) Increased Age Smoking Females Genetics
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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.
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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.
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What are the symptoms of Bronchiectasis?
Dyspnoea/SOB Productive cough with Copious sputum production Haemoptysis (maybe) Wheeze Chest Pain
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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
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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)
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What are some differential Diagnoses for Bronchiectasis?
COPD Asthma TB Chronic sinusitis Pneumonia Pulmonary fibrosis Inhalation of foreign body
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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)
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What are some complications of Bronchiectasis?
Infective exacerbation Chronic respiratory failure Haemoptysis (may be massive and life-threatening) Cor pulmonale Pneumothorax Chest pain
181
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
182
What are the different types of Pleural effusion?
Whether the fluid is: Exudative - high protein count (>3g/dL) Transudative - lower protein count (<3g/dL)
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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
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What are the Exudative causes of pleural effusion?
Related to inflammation: Trauma Lung cancer Pneumonia Empyema Rheumatoid arthritis Tuberculosis
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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
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What is Meig's Syndrome?
right sided pleural effusion with ovarian malignancy
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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
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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
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What is the most common cause of Exudative pleural effusion?
Pneumonia and malignancy
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What is the most common cause of Transudative pleural effusion?
(congestive) Heart failure
191
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
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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
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What may be a differential diagnosis with a hyper resonant percussion?
Pneumothorax
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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
195
Where would you see transudates or exudates on CXR in pleural effusion?
Transudates - Bilateral (TB) Exudates - Unilateral (EU)
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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
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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
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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
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What is Empyema?
An infected Pleural Effusion (pus collects in pleural cavity)
200
What does Empyema Show on pleural aspiration?
PHAL: Pus, High LDH. Acidic pH (pH < 7.2), Low glucose
201
What is the treatment for Empyema?
chest drain to remove the pus and antibiotics
202
What is a Pneumothorax?
An excess accumulation of air within the pleural space causing ipsilateral lung collapse.
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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
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What are the causes of Pneumothorax?
Spontaneous Trauma Iatrogenic - lung biopsy, mechanical ventilation or central line insertion Lung pathology - infection, asthma or COPD
205
What are the risk factors for a pneumothorax?
Tall thin males Connective tissue disorders (MF, EHD) FHx Smoking Underlying Lung disease - COPD, Asthma RA
206
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
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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
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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
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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)
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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
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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
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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
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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.
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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
215
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.
216
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)
217
What is an Interstitial Lung Disease (ILD)?
Umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.
218
Give some examples of ILDs?
Idiopathic Pulmonary Fibrosis Pneumonoconiosis Sarcoidosis Hypersensitivity Pneumonitis
219
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
220
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
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What is Pulmonary Fibrosis?
Progressive fibrosis and scarring of the lung parenchyma.
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What are the different types of pulmonary fibrosis?
Idiopathic PF Drug induced PF Secondary PF
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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.
224
What drugs can induce pulmonary fibrosis?
Amiodarone Cyclophosphamide Methotrexate Nitrofurantoin
225
What are secondary causes of Pulmonary Fibrosis?
Alpha-1 antitripsin deficiency Rheumatoid arthritis Systemic lupus erythematosus (SLE) Systemic sclerosis
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What are the risk factors for Idiopathic Pulmonary FIbrosis?
Smoking Occupational causes (dust) Increased age (60-70s) Male FHx
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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.
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What can cause pulmonary fibrosis in the upper respiratory zones?
Pneumonoconiosis Silicosis Hypersensitivity Pneumonitis Cystic Fibrosis Sarcoidosis Tuberculosis
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What can cause Pulmonary Fibrosis in the Lower Respiratory Zones?
Idiopathic Pulmonary Fibrosis Drug Induced PF Connective tissue Disorders (SLE)
230
What are the symptoms of pulmonary fibrosis?
Progressive Dyspnoea Dry cough (no sputum) Malaise
231
What are the signs of pulmonary fibrosis?
Bibasal fine inspiratory crackles (end respiratory) Finger clubbing Cyanosis + Sx of underlying pathology if Secondary PF
232
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
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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
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What is the prognosis like for IPF?
IPF has a poor prognosis, with median survival ranging from 2.5 - 3.5 years after diagnosis.
235
What is Pneumonoconiosis?
Interstitial lung fibrosis that occurs secondary to inhalation of occupational triggering antigens that cause an inflammatory reaction.
236
What are some different types of pneumonoconiosis?
Silicosis - Inhalation of silicon dioxide Asbestosis - Inhalation of asbestos
237
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
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What are the risk factors for pneumonoconiosis?
Male Increasing age Substance exposure - Coal, dust, silicon, asbestos etc
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What are the symptoms of pneumonoconiosis?
Exertional Dyspnoea Dry Cough Haemoptysis Wheezing Weight loss
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What does asbestosis increase the risk of developing?
Mesothelioma
241
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
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what is the management for Pneumonoconiosis?
Conservative Mx as incurable: Stop smoking Avoid exposure
243
What is Sarcoidosis?
A Type of Interstitial Lung disease A multi-systemic Granulomatous inflammatory condition characterised by non-caseating granulomas depositing in many tissues
244
What is the cause of sarcoidosis?
Unknown: Thought to be a type 4 Hypersensitivity reaction. Idiopathic
245
What are the risk factors for sarcoidosis?
Afro-Caribbean and Scandinavian ethnicity Young adults: 20-40 yrs Female gender Family history
246
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.
247
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
248
What are the Chest symptoms of sarcoidosis?
Dry cough Dyspnoea Mediastinal lymphadenopathy Constitutional Sx: Weight loss, Fatigue and fever
249
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
250
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)
251
What are some differential diagnoses of sarcoidosis?
Tuberculosis (caseating) Lymphoma Hypersensitivity pneumonitis HIV Toxoplasmosis Histoplasmosis
252
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
253
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)
254
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
255
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
256
What are the potential complications of Sarcoidosis?
Can progress to Pulmonary Fibrosis Pulmonary HTN
257
What is Hypersensitivity pneumonitis?
Type 3 hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction.
258
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
259
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
260
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
261
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**
262
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
263
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
264
What is the treatment for hypersensitivity pneumonitis?
Remove the allergen Steroids (glucocorticoids) can help with symptoms Give oxygen if necessary
265
What is Goodpasture's Syndrome?
An autoimmune disease characterised by Anti-GBM autoantibodies that attack the lungs and kidneys. A type of Pulmonary Vasculitis
266
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.
267
What are the risk factors for Goodpasture's syndrome?
Genetics - HLA-DR15 infection Smoking Oxidative stress
268
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
269
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
270
What is the treatment for Goodpasture's Syndrome?
Corticosteroids Immunosuppressants - Cyclophosphamide Plasmapheresis
271
what is the normal pulmonary blood pressure at rest?
8-20mmHg
272
What is defined as pulmonary hypertension?
Resting mPAP >25mmHg at rest.
273
How is Pulmonary HTN normally measured?
Right heart catheterisation.
274
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.
275
What are the different groups of causes of pulmonary HTN?
1. Primary pulmonary HTN - Idiopathic/CT disorders (MF, EHD) 2. Left heart disease - VHD, HF, HOCM 3. Chronic Lung disease - COPD, Asthma 4. Pulmonary vascular disease - PE/Tumour 5. Unclear/multifactorial - Sarcoidosis, Haematological disorders
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What is the most common cause of secondary pulmonary HTN?
COPD
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What are the symptoms of Pulmonary HTN?
Progressive breathlessness Exertional Dizziness/syncope Fatigue Sx of underlying pathology
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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
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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
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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)
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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
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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
283
What is a Mesothelioma?
A malignant neoplasm of the mesothelial cells of the pleura
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What is the primary cause of Mesothelioma?
Asbestos Exposure Typically doesnt present until decades after the exposure
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What are the risk factors for Mesothelioma?
Asbestos Exposure (85% of cases have Hx) Increasing age (40-70) Males
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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
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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
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Why may a patient with a mesothelioma have a hoarse voice?
Tumour presses on recurrent laryngeal nerve
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What are the signs of a Mesothelioma?
Finger clubbing Reduced breath sounds Stony Dull Percussion Ascites (if peritoneal disease present)
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What are the primary investigations for mesothelioma?
First Line: Imaging: CXR - pleural thickening +/- effusion Contrast Enhanced CT Bronchoscopy + Biopsy (Gold Standard for Dx)
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What is the treatment for Mesothelioma?
Surgery (if operable) otherwise Palliative: Extrapleural pneumonectomy Pleurectomy with decortication Rarely curative +/- Chemotherapy: Cisplatin Pemetrexed +/- Radiotherapy
292
What is the Main malignancy of the lung parenchyma?
Primary Bronchial Carcinomas
293
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%)
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What are the primary metastasis sites for Lung cancers?
Bones Liver Adrenal Glands Brain Lymph Nodes
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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)
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What are the risk factors for Primary lung Cancer?
Smoking (BIGGEST CAUSE) Asbestos Coal Ionising radiation Underlying lung disease Increasing age FHx
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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
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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.
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Who is typically affected by SCLC?
Exclusively smokers
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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)
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What is the most common NSCLC?
Adenocarcinoma
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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
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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
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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
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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
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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
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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
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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
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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
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Which is a more aggressive cancer, SCLC or NSCLC?
SCLC is more aggressive
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What is the treatment for SCLC?
Often Diagnosed late and Px have metastatic disease: Therefore Chemo/radiotherapy (Cisplatin) palliative care
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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)
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What are some complications for lung cancer?
Recurrent laryngeal nerve palsy Horner’s syndrome (Pancoast tumour) SVC obstruction Paraneoplastic Syndromes Bone pain/Hypercalcaemia
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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.
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What are the common causes of secondary lung cancer?
Mets from: Breast Kidney Bowel Bladder
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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
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What syndrome does a Pancoast tumour cause?
HORNERS Syndrome characterised by: Ptosis - Droopy eyelids Myosis - Excessive Pupil Constriction Anhidrosis - Lack of sweating
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What is a Pulmonary Embolism?
Obstruction of the pulmonary vasculature, secondary to an embolus.
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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)
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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
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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)
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What are the signs of PE?
Hypotension Tachypnoea Tachycardia Raised respiratory rate Low grade fever Haemodynamic instability causing hypotension Raised JVP Hypoxia
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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%
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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
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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
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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
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What is the treatment of PE is the Px is haemodynamically unstable (Massive PE)?
Thrombolysis (clot busting) - Alteplase If fails - Catheter embolectomy
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What can be used as prophylaxis for a PE?
Compression Stockings Regular walking SC LMWH
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Define Dyspnoea?
A symptom of difficult or laboured breathing
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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
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What are the main acute respiratory causes of Dyspnoea?
Pneumonia Asthma PE Pneumothorax
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What are the main Chronic respiratory causes of Dyspnoea?
COPD Idiopathic Pulmonary Fibrosis Bronchiectasis
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What are the main cardiac causes of Dyspnoea?
ACS Stable angina Chronic HF Pericarditis
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What are some less common respiratory causes of Dyspnoea?
Pleural Effusion Lung Cancer Interstitial Lung Disease (pneumonoconiosis)
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What are some less common cardiac causes of Dyspnoea?
Carditis (end, myo, peri) Valvular dysfunction Cardiomyopathy Acute HF
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What are some other systemic causes of Dyspnoea?
Musculoskeletal Anxiety Metabolic acidosis: - DKA - Acute renal failure
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What can cause respiratory failure?
1. Low oxygen delivery - anaemia, high altitude 2. Airway obstruction - Asthma, COPD 3. Gas exchange limitation - lung fibrosis, IDLs 4. V/Q Mismatch - Pneumonia, PE, Pulm HTN 5. Alveolar hypoventilation - emphysema, reduced resp drive, obesity, Muscular weakness
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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.
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What is Type 1Respiratory Failure?
Type 1 = 1 change (O2) * pO2 (partial O2 pressure) is low * pCO2 (partial CO2 pressure) is low or normal
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What condition is the most common cause for Type 1 Respiratory failure?
Pulmonary Embolism Pneumonia
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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
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What is Type 2 Respiratory Failure?
Type 2 = 2 changes (O2 & CO2) * pO2 is low * pCO2 is high
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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)
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What are the signs of Hypercapnia seen in type 2 respiratory failure?
* Bounding pulse * Flapping tremor (asterixis) * Confusion * Drowsiness * Reduced consciousness
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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
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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
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What causes a high DLCO?
Pulmonary haemorrhage - can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available
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What causes a low DLCO?
- Severe emphysema - Fibrosing alveolitis - Anaemia - Pulmonary hypertension - Idiopathic pulmonary fibrosis - COPD
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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)
350
What are the main Upper Respiratory Tract Infections (URTI)?
Epiglottitis. Laryngitis. Pharyngitis (sore throat). Sinusitis (sinus infection). Whooping Cough Croup (Otitis Media)
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Where does an URTI go from?
Between the nose to the larynx above the vocal cords
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What are some risk factors impairing Lung Defences?
Old age Smoking Alcohol use ETT/nasotracheal intubation Respiratory therapy Hypoxaemia Acidosis Toxin inhalation Immunosuppression Malnutrition
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What is the epidemiology of URTIs?
Adults will have 2-3 URTIs each year. Most commonly caused by Viruses (rhinovirus)
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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%
355
What are the general Symptoms of a URTI?
Coryzal Sx: Nasal stuffiness, runny nose, sneezing, sore throat, and cough.
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What is Pharyngitis?
Inflammation of the pharynx w/wo exudate production
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What are the causes of pharyngitis?
Viral (70-80%) - Rhinovirus, Adenovirus, EBV/HIV Bacteria (20%) - Group A Strep (S. pyogenes)
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What are the signs of pharyngitis?
Sore throat Fever Cough (viral + bacterial) Nasal congestion (viral) Exudate (bacterial)
359
What must be ruled out if a Px (especially child) has pharyngitis?
Rheumatic fever (typically 2-4 weeks post S. pyogenes infection.
360
What is the treatment for pharyngitis?
Viral - self limiting Bacterial - Amoxicillin/Flucloxacillin Likely Strep pyogenes so amoxicillin
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What is Sinusitis?
inflamed mucosa of nasal cavity and nasal sinuses
362
What causes sinusitis?
Viral infection - Most common Bacterial infection - S. Pneumo / H. Influ
363
What are the signs and symptoms of sinusitis?
Symptoms Fontal headache Facial pain Fever Signs Purulent nasal discharge Tenderness
364
What is the treatment for Viral sinusitis?
Self limiting Usually lasts <10 days and has non-purulent discharge Inhalation of water vapour can help
365
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)
366
What is Otitis Media?
Middle ear infection and inflammation (commonly affects children) Presents with ear pain
367
What are the causes of Otitis media?
Bacterial or Viral
368
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.
369
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
370
What is Acute Epiglotitis?
Epiglottitis refers to inflammation and localised oedema of the epiglottis, which can result in potentially life-threatening airway obstruction.
371
What is the most common cause of Epiglottitis?
Haemophilus Influenza B Often secondary to immunocompromisation (such as following HIV)
372
What are the risk factors for Epiglottitis?
Peak age 6-12 (can occur at any) Male gender Unvaccinated Immunocompromised
373
What are the symptoms of Epiglottitis?
Rapid Onset: Dysphagia Dysphonia (stridor) Drooling Distress
374
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
375
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
376
What is the treatment for Epiglottitis?
EMERGENCY First Line: - Secure airway - Nebulised adrenaline - IV antibiotics - Doxycycline, Co-Amoxiclav, Erythromycin, Second Line: - Dexamethasone
377
What is Croup?
Acute infective upper respiratory infection causing oedema in the larynx (Acute Larygnotracheobronchitis)
378
Who is typically affected by croup?
Children between 6 months and 2 years old
379
What are the causes of Croup?
Main cause: Parainfluenza virus Influenza Adenovirus Respiratory Syncytial Virus (RSV)
380
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
381
What is the treatment of Croup?
Oral Dexamethasone (single dose 150mcg/kg)
382
What is Whooping Cough?
Upper respiratory tract infection caused by Bordetella pertussis
383
Who is affected by Whooping cough?
Mainly children 90% <5yrs
384
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
385
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
386
What is the characteristic symptom of whooping cough?
Whoop sound caused sharp inhalation of breath during coughing bout
387
What are the investigations of Whooping cough?
Nasopharyngeal swab/aspirate: Culture/PCR Anti-pertussis toxin immunoglobulin G (IgG) serology
388
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
389
What are the complications of Whooping cough?
Pneumonia Encephalopathy Otitis media Injuries from coughing - pneumothorax Seizures.
390
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
391
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
392
How are upper respiratory viral infections diagnosed?
Green Viral Throat swab + PCR Some Point of Care tests for some viruses (influenza, SARS-CoV-2)