Pulmonology Flashcards
1
Q
What Spirometry Values Indicate Obstructive Lung Disease?
A
FEV1:FVC ratio <0.7
FVC<0.8 of normal value.
2
Q
What Spirometry Values Indicate Restrictive Lung Disease?
A
FEV1:FVC ratio is normal
FVC<0.8 of normal value.
3
Q
Examples of obstructive lung diseases
A
Airway conditions - asthma, COPD
4
Q
Example of restrictive lung diseases
A
Parenchymal conditions - idiopathic pulmonary fibrosis, sarcoidosis, wegener’s granulomatosis.
5
Q
Cause of High Alveolar-Arterial Gradient
A
V/Q mismatch
Defects in diffusion
Right-left shunt e.g ASD
6
Q
Causes of Normal Alveolar-Arterial Gradient but Low PaO2
A
Means PAO2 must be low
Can be due to hypoventilation, low FiO2 (high altitudes)
7
Q
Pathophysiology of High Altitude Pulmonary Oedema
A
In higher altitudes there is widespread hypoxia in the lungs which can lead to widespread pulmonary vasoconstriction.
Causes fluid to be forced out of vessels and result in oedema.
8
Q
Management of High Altitude Pulmonary Oedema
A
Descent, administer oxygen, bronchodilators.
9
Q
Causes of Low TLCO
A
Thickening of alveolar-capillary membrane
Decreased lung volumes
10
Q
Causes of Raised TLCO
A
Increased lung volumes
Pulmonary haemorrhage
11
Q
What is the function of the pleural space?
A
Reduces friction between pleura during expansion and contraction of the lung.
12
Q
What is Pleural Effusion?
A
Excess fluid accumulation between the parietal and visceral pleura.
13
Q
What are the 2 Types of Pleural Effusion Fluid?
A
Fluid is either transudative or exudative.
14
Q
Aetiology of Transudative Pleural Effusion
A
More systemic causes
CHF
Hypoalbuminaemia - nephrotic syndrome
Liver cirrhosis
15
Q
Pathophysiology of Transudative Pleural Effusion
A
Fluid has less protein content (<50% of serum protein)
Occurs due to increased hydrostatic pressure or decreased oncotic pressure in pulmonary microvasculature.
16
Q
Aetiology of Exudative Pleural Effusion
A
More local causes
Pneumonia
TB
Lung cancer
Post-cardiac surgery (Dressler’s syndrome)
Pulmonary embolism.
17
Q
Pathophysiology of Exudative Pleural Effusion
A
Can be due to inflammation resulting in increased vascular permeability and reduced reabsorption.
18
Q
Clinical Presentation of Pleural Effusion
A
Dyspnoea
Pleuritic chest pain
Cough
Fever
Reduced chest wall expansion upon inspiration.
19
Q
Examination of Pleural Effusion
A
Stony dull chest sounds on ipsilateral side upon auscultation.
Reduced breath sounds.
20
Q
Investigation of Pleural Effusion
A
FL: CXR
GS: Thoracic ultrasound
Thoracentesis - pleural aspiration
Thoracoscopy - camera inside thoracic cavity to visualize.
21
Q
What can be seen on an X-ray with Pleural Effusion?
A
Decreased costophrenic angle
Large amount of white fluid.
Can have contralateral tracheal deviation.
22
Q
Aetiology of Turbid Thoracentesis Sample
A
Infection, pleural empyema.
23
Q
Aetiology of Milky Thoracentesis Sample
A
Chylothorax - accumulation of lymph fluid in chest cavity.
24
Q
Aetiology of Food Particles in Thoracentesis Sample
A
Oesophageal rupture.
25
Aetiology of Bloody Thoracentesis Sample
P.E, trauma, cancer.
26
Management of Pleural Effusion
Chest Drain
If recurrent - pleurodosis (surgical fusing of pleural layers).
27
Infective Aetiology of Pleural Infection
S.milleri
S.pneumoniae
S.aureus
28
Pathophysiology of Pleural Infection/Empyema
Original chest infection can cause infected pleural fluid resulting in a pleural infection.
29
Investigation of Pleural Infection/Empyema
Thoracentesis
Low pH < 7.2
Low glucose <3.4 mmol/L
LDH > 1000
Macroscopic appearance of pus
Bacterial growth on culture.
30
Management of Pleural Infection/Empyema
Chest drain
Empirical Antibiotics - ceftriaxone if community acquired, vancomycin if hospital acquired.
31
Management of Malignant Pleural Effusions
Pleurodesis
Chest drain/thoracoscopy with talc administration.
If pleurodesis fails and recurrent effusion, insert indwelling pleural catheter.
32
What are the 5 Types of Pneumothorax?
Primary spontaneous pneumothorax
Iatrogenic pneumothorax
Trauma pneumothorax.
Tension pneumothorax
Secondary spontaneous pneumothorax
33
Risk Factors/Aetiology of Primary Spontaneous
Tall, thin male - lungs can stretch, causing weakness
Age 20-40 years old.
Smoking
Connective tissue disorders e.g Marfan’s, Ehler-Danlos
Pleural fistula
Rupture of apical pleural bleb.
34
Risk Factors/Aetiology of Secondary Spontaneous Pneumothorax
Known lung disease - COPD, ILD, asthma, CF.
Infection - TB, lung abscess
Genetic predisposition - Birt-Hogg Dube, Lymphangioleiomyomatosis.
Catamenial pneumothorax - occurs with periods, esp in females with endometriosis.
35
Risk Factors/Aetiology of Traumatic Pneumothorax
Penetrating chest wall injury
Puncture from rib fracture
36
Pathophysiology of Simple Pneumothorax
Intrapleural is negative, hence a breach can cause air to be sucked into the pleural cavity.
This increases intrapleural pressure can cause ipsilateral lung collapse
37
Pathophysiology of Tension Pneumothorax
Pleural injury acts as a one-way valve.
Air enters pleural space but does not leave.
Hence inspiration increases intrapleural pressure making situation worse.
38
Clinical Presentation of Simple Pneumothorax
One-sided acute pleuritic chest pain
Dyspnoea
Cough
39
Clinical Presentation of Tension Pneumothorax
Symptoms of simple pneumothorax +
Surgical emphysema - air under the skin, cannot open eyes.
Distended neck veins
Pain worsening with inspiration.
40
Examination of Pneumothorax
Hyper-resonant chest sounds
Reduced/absent breath sounds.
41
Investigation of Pneumothorax
CXR - one side is dark due to collapsed lung and excess air.
Potential contralateral tracheal deviation.
42
Investigation of Tension Pneumothorax
CXR - contralateral tracheal deviation to that of collapsed lung.
One side is darkened
43
Conmplications of Tension Pneumothorax
Obstructive shock - increased intrathoracic pressure can cause medistinal IVC kinking, causing reduced CO and JVD.
44
Lifestyle Management of Simple Pneumothorax
Smoking cessation
No air travel
No scuba diving.
45
Clinical Management of Simple Pneumothorax
If small - self healing: 2% volume reabsorbed per day.
If larger - pleural aspiration, chest drain.
If recurrent - surgical: pleurodesis.
46
Management of Tension Pneumothorax
Needle decompression.
47
What is a Haemothorax?
Blood in the pleural cavity
Pleural fluid haematocrit > 50%.
48
Aetiology of Haemothorax
Penetrating chest trauma
Iatrogenic - central line placement, surgery.
49
Aetiology of Pleural Thickening
Asbestos exposure
Pleural infection/empyema
Haemothorax
Mesothelioma
50
What is a Pneumomediastinum?
Presence of air in the mediastinum
51
Aetiology of Pneumomediastinum
Surgical emphysema
Pneumothorax
Penetrating chest trauma
52
What is COPD?
Group of conditions that cause progressively worsening, irreversible airway obstruction.
53
What Conditions Come Under COPD?
Chronic Bronchitis
Emphysema
54
Risk Factors/Aetiology of COPD
Alpha-1-antitrypsin deficiency
Smoking
Air pollution exposure
Increasing age
Male gender
55
Pathophysiology of Chronic Bronchitis
Hypertrophy and hyperplasia of respiratory mucous glands - key hallmark.
Along with inflammation of the bronchi/bronchioles.
Inflammation can cause fibrosis resulting in thickening and narrowing of lumen.
There is also mucus hypersecretion and ciliary dysfunction.
56
Pathophysiology of Emphysema
Destruction of tissue distal to respiratory bronchioles.
Elastin keeps respiratory bronchiole and alveolar walls open during expiration through bernoulli's principle.
Loss of elastin causes loss in elastic recoil and alveolar collapse.
Bullae formation due to air being trapped distal to collapsed segments.
57
What are the 2 types of Emphysema?
Centrilobular and Panacinar
58
What is Centrilobular Emphysema?
Emphysema that only affects respiratory bronchioles
59
Risk Factor for Centrilobular Emphysema
More common in smokers
60
What is Panacinar Emphysema?
Emphysema that affects both respiratory bronchioles and alveoli.
61
RIsk Factor for Panacinar Emphysema
A1ATD
62
Pathophysiology of A1ATD Induced COPD
A1AT degrades neutrophil elastase enzyme which breaks down elastin.
In deficiency there is now excess elastin breakdown resulting in panacinar emphysema.
If no PMH of smoking - consider A1ATD.
63
Clinical Presentation of Chronic Bronchitis
Blue Bloater
Chronic, productive cough
Purulent sputum
Cyanosis - chronically raised PaCO2
Obesity
64
Clinical Presentation of Emphysema
Pink Puffer
Pinkish skin
Breathing with lips pursed - increases airway pressure to prevent collapse.
Visible use of accessory breathing muscles
Barrel chest
65
Investigation of COPD
FBC - Polycythaemia
Spirometry - FEV1:FVC ratio <0.7 indicates obstructive airway disease.
Decreased DLCO (diffusion capacity of CO across lung)
ABG - can show T2RF (hypoxia and hypercapnia)
66
How is COPD Graded?
GOLD system
Mild: FEV1 > 80% predicted value
Moderate: FEV1 is 50-80% predicted value
Severe: FEV1 is 30-50% predicted value
Very Severe: FEV1 is < 30% predicted value
67
Lifestyle Management of COPD
Smoking cessation
Pulmonary rehabilitation - exercise training programs
Wearing of PPE
68
Pharmacological Management of COPD
FL: Short acting beta 2 agonist (SABA) e.g salbutamol inhaler
SL: Add LABA e.g salmeterol + LAMA e.g tiotropium bromide inhaler.
OR if suggestive of steroid responsiveness - LABA + ICS
TL: LABA + LAMA + ICS
69
Bronchodilator Effects in Asthma vs COPD
If >12% increase in FEV1 after bronchodilator, then reversible obstruction e.g asthma.
If <12 increase in FEV1 after bronchodilator, then irreversible obstruction e.g COPD.
70
Management of Acute COPD Exacerbation
Maintain O2 sat at 88-92%.
Administer nebulised salbutamol and ipratropium (SAMA)
Non-invasive ventilation
71
Why Should Low O2 Saturations be Maintained in Hospitalized COPD Patients?
Patients are CO2 retainers and so rely on hypoxic drive to breath.
Increasing O2 saturation can take away the drive, causing hypoventilation leading to hypercapnia and respiratory acidosis and T2RF.
72
Pharmacodynamics of Beta-2 Agonists
Active the beta 2 adrenergic receptors which increase intracellular cyclic AMP to promote airway smooth muscle relaxation and bronchodilation.
73
Examples of Short Acting Beta 2 Agonists (SABA)
Salbutamol, terbutaline
74
Examples of Long Acting Beta 2 Agonists (LABA)
Salmeterol, formoterol
75
Contraindications of Beta-2 agonists
Hyperthyroidism
Arrythmias, Hypertension
Hypokalaemia
Diabetes - minor risk of DKA
76
Side effects of Beta-2 agonists
Fine tremor
Palpitations
Glaucoma - esp in those using nebulized versions.
77
Pharmacodynamics of Anti-muscarinics
Antagonists to the muscarininc M3 receptor which prevents parasympathetic bronchoconstriction, gland secretion and enhances neurotransmitter release.
78
Example of Short Acting Muscarine Antagonists (SAMA)
Ipratropium bromide
79
Example of Long Acting Muscarine Antagonists (LAMA)
Tiotropium bromide,
80
Contraindications of Anti-muscarinics
Pregnancy
Breastfeeding
BPH
Renal failure
81
Side effects of Anti-muscarinics
Palipitations, bronchospasm, headache.
82
Pharmacodynamics of Inhaled Corticosteroids (ICS)
Reduce the number of inflammatory cells in the airways through inhibiting their survival.
Suppress production of inflammatory mediators
Reduce expression of adhesion molecules
Binds to cell nucleus and prevents DNA synthesis and inflammatory gene expression in cells.
83
Examples of Inhaled Corticosteroids
Fluticasone, budesonide
84
What are LABAs and ICS Prescribed Together?
Glucocorticoids increase the transcription of the B2 receptor gene, increasing cell surface receptor expression.
Long-acting b2-Agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids = beta agonists help ICS to work
85
Examples of Interstitial Lung Diseases
Sarcoidosis, Idiopathic Pulmonary FIbrosis, Hypersenstivity Pneumonitis
86
What is the Most Common ILD?
Idiopathic Pulmonary Fibrosis
87
Risk Factors for Idiopathic Pulmonary Fibrosis
Smoking
Old age
Occupational exposure e.g dust, asbestos.
Drugs e.g methotrexate
Male gender
88
Pathophysiology of Idiopathic Pulmonary Fibrosis
Fibroblasts migrate into the lungs and become myofibroblasts which deposit collagen.
In IPF the fibroblasts are resistant to apoptosis.
Causes myofibroblast proliferation and formation of fibroblastic foci.
Results in excess collagen deposition and fibrosis.
Can result in T1RF.
89
Clinical Presentation of Idiopathic Pulmonary Fibrosis
Exertional dyspnoea
Dry, unproductive cough
Finger clubbing
90
Examination of Idiopathic Pulmonary Fibrosis
Fine, bi-basal end inspiratory crackles on auscultation.
91
Investigation of Idiopathic Pulmonary Fibrosis
ABG: Low PaO2
Spirometry - indicative of restrictive lung disease where FEV1:FVC > 0.7, but FVC < 0.8 of normal value.
CXR: Interstitial shadowing.
GS: CT chest - honeycombing, ground glass appearance
Lung biopsy - interstitial pneumonia.
Reduced DLCO
92
Management of Idiopathic Pulmonary Fibrosis
Smoking cessation
Pirfenidone + nintedanib.
Lung transplant.
93
Pharmacodynamics of Pirfenidone
Inhibits TGF-beta which decreases myofibroblast proliferation.
94
Pharmacodynamics of Nintedanib
Tyrosine kinase inhibitor - reduces PDGF, FGF, VEGF levels to decrease myofibroblast proliferations.
95
Pathophysiology of Hypersensitivity Pneumonitis
T3 hypersensitivity reaction which immune complex deposition in lung causing an immune response.
Requires prior sensitization.
96
Risk Factors/Aetiology of Hypersensitivity Pneumonitis
Farming - moldy hay can cause farmer’s lung.
Bird-keeping - droppings can cause pigeon fancier’s lung
Mold
97
Investigation of Hypersensitivity Pneumonitis
Bronchoalveolar lavage - lymphocytosis
Lung biopsy - lymphocyte rich infiltrate.
98
Management of Hypersensitivity Pneumonitis
Removal of stimulus.
Steroids and immunosuppression.
99
Risk Factors of Sarcoidosis
Female gender
Middle aged
Afro-Caribbean descent
100
Pathophysiology of Sarcoidosis
Patches of non-caseating granulomatous inflammation in the lung.
101
Clinical Presentation of Sarcoidosis
Fever, Fatigue
Dyspnoea
Dry cough
Anterior uveitis,
Lupus pernio - purple nodules on cheeks and nose.
Erythema nodosum
102
Investigation of Sarcoidosis
CXR - bilateral hilar lymphadenopathy + pulmonary infiltrates.
GS: Lung biopsy - non-caseating granulomas with schaumaunn and asteroid bodies.
Elevated serum ACE - marker for granulomatous inflammation.
103
Management of Sarcoidosis
Corticosteroids e.g prednisolone.
104
Drug-Induced Aetology of Interstitial Lung Disease
Nitrofurantoin
Methotrexate
Amiodarone
Bleomycin
105
What are the 3 classes of primary lung tumours
Mesothelioma
Bronchial carcinomas
Carcinoid tumours
106
What are the 2 types of bronchial carcinomas
Non-small cell and small-cell carcinoma
107
Examples of non-small cell carcinoma
Adenocarcinoma - most common
Squamous cell carcinoma
Large cell carcinoma
Can only be distinguished histologically.
108
What are sources of secondary/metastatic lung cancers?
Kidney, Breast, Bowel, Bladder cancers likely to metastasize.
109
Why are secondary/metastatic lung cancers more common than primary ones?
Secondary metastasis to the lung more common because all blood goes through pulmonary circulation.
110
What sites can lung cancer commonly metastastize to?
Metastatic Sites of Lung Cancer
Bone
Adrenals
Brain
Lymph nodes
111
Aetiology/Risk Factors for Mesothelioma
Asbestos exposure
Male gender
40-70 years
112
Clinical Presentation of Lung Cancers
Weight loss
Night sweats
Fever
Cough - continuous, more than 3 weeks
Dyspnoea
Haemoptysis
Chest pain
Recurrent chest infections - tumour can cause stasis and buildup of fluid and mucous.
113
Investigation of Mesothelioma
FL: Imaging - CXR + CT chest
Can show pleural thickening, pleural effusion.
Elevated serum CA-125
GS: Pleural biopsy
114
Management of Mesothelioma
Surgery
Palliative chemotherapy + radiotherapy.
115
Aetiology/Risk Factors of Bronchial Carcinomas
Smoking - squamous cell carcinoma most common in smokers, SCLC is seen exclusively in smokers.
Asbestos - adenocarcinoma
Coal
Ionising radiation
116
Pathophysiology of Squamous Cell Carcinoma
Can causes central lung lesions with central necrosis.
Can cause release of PTH related protein (PTHrP) which can result in hypercalcaemia.
117
What cells do lung adenocarcinomas arise from?
Arises from mucus secreting glandular epithelial cells.
118
Paraneoplastic effct of a large cell carcinoma
Can produce hCG and result in gynaecomastia.
119
Paraneoplastic effects/disease associations of small cell carcinomas
Ectopic ADH production - SIADH
Ectopic ACTH production - Cushing’s
Lambert-Eaton’s syndrome
Encephalitis
120
Investigation of Bronchial Carcinomas
FBC: Anaemia
FL: Imaging - CXR + CT Chest
GS: Bronchoscopy + biopsy
121
What would be seen on biopsy of a squamous cell carcinoma?
Keratin pearls
122
What would be seen on a biopsy of a large cell carcinoma?
Giant cells
123
Management of Small Cell Carcinoma
Early GS: radiotherapy + chemotherapy
Late - palliative care
124
Management of Non-Small Cell Lung Carcinoma
Early GS - surgical excision
Late - Chemotherapy/radiotherapy,
Can use monoclonal antibodies as cetuximab
125
Complication of Non-Small Cell Lung Carcinoma
Pancoast tumour causing Horner's Syndrome
126
Pathophysiology of Horner's Syndrome
Pancoast tumour causes compression of thoracic sympathetic chain.
127
Clinical Presentation of Horner's Syndrome
Ptosis
Meiosis
Anhydrosis
Hoarse voice - RLN compression.
Pemberton's sign - raising arms causes facial flushing and redness.
128
What is Occupational Lung Disease?
Occupational lung diseases represent a wide-range of respiratory conditions caused by inhaling a harmful substance in the workplace
129
Types of inhaled particles that can cause occupational lung disease
Dusts
Solid particles 1-1000 microns
E.g chiselling stone, cutting wood.
Fumes
Solid particles suspended in air
Soldering electronics, welding.
Mists
Liquid particles suspended in air
Metalworking coolant mist.
Inhaled vapours/gases
Paint spraying vapours, gas leaks
130
What is the most common occupational lung disease?
Occupational Asthma
Develops after a latent period.
131
Examples of Chemicals Can Cause Occupational Lung Disease
Asbestos
Coal
Beryllium
Silicon
132
What is Pneumoconiosis
Accumulation of dust in the lungs with associated tissue reactions.
133
Types of Coal-Worker’s Pneumoconiosis
Simple pneumoconiosis
Progressive massive fibrosis.
134
Pathophysiology of Simple Pneumoconiosis
Coal exposure causes macrophage death resulting in inflammation and lung fibrosis.
135
Investigation of Simple Pneumoconiosis
CXR: Micronodular shadowing, especially on upper lobes.
136
Pathophysiology of Progressive Massive Fibrosis
Development of fibrotic masses in the upper lobes.
Can have necrotic centers.
137
Clinical Presentation of Coal Worker’s Pneumoconiosis
Black sputum
Exertional dyspnoea.
138
Which type of asbestos is most commonly associated with pneumoconiosis?
Crocidolite (blue asbestos)
139
Aetiology/Risk Factors for High Asbestos Exposure
Roofing
Plumbing
Ship-building.
140
Asbestos-Related Lung Diseases
Mesothelioma
Asbestosis
Pleural effusions
Bronchial adenocarcinoma
141
Pathophysiology of Asbestos-Induced Mesothelioma Lung Disease
Can cause formation of pleural plaques - calcified collagen deposits.
Can result in pleural thickening.
142
Pathophysiology of Asbestosis
Cellular infiltration and deposition of asbestos can cause inflammation and fibrosis.
143
Investigation of Asbestos-Related Lung Disease
CXR: Ivory white calcified pleural and supradiaphragmatic plaques.
Bronchoalveolar lavage/sputum sample - golden/brown asbestos bodies.
144
Aetiology/Risk Factors for Silicon Exposure
Sandblasting
Mining
Foundry work
Ceramic work
145
Silicon-Related Lung Diseases
Silicosis
COPD
TB
146
Types of Silicosis
Chronic simple silicosis
Chronic complicated silicosis - can cause progressive massive fibrosis.
Accelerated silicosis
147
Pathophysiology of Silicosis
Alveolar macrophages respond to silica exposure by release of fibrogenic factors to causes fibrosis.
148
Investigation of Silicosis
CXR: Thin streaks (Eggshell-like) of calcification of hilar lymph nodes.
149
What is Asthma?
Obstructive, often reversible inflammatory airway disease which can occur in episodes.
150
Clinical Presentation of Asthma
Symptoms are episodic
Dyspnoea
Wheezing - originally laminar flow of air is now turbulent.
Dry Cough
Chest tightness
Symptoms are often nocturnal.
151
Aetiology of Asthmatic Attacks
Occupational sensitizers e.g wood dust,
Air pollution
Drugs - beta blockers, NSAIDs esp aspirin
Allergens - pollen
152
Pathophysiology of Allergen Induced Asthma
Chronic airway inflammation which can lead to episodic bronchospasm.
A subset of asthmatics can have non-episodic, fixed airflow obstruction due to airway remodelling.
Dendritic cell detect allergen and present to naive T cells.
Cause differentiation into Th2 cells and cytokine release.
Results in plasma B cells producing IgE
IgE causes mast cell degranulation and release of histamine, cysteine leukotrienes, prostaglandins and cytokines.
Causes eosinophilia and eosinophil migration.
Net effect is airway inflammation and contraction of airway smooth muscle.
153
What factors are released in mast cell degranulation during asthma?
Histamine
Cystine leukotriene
Prostaglandins
Cytokines
154
What granulocyte is mainly associated with allergen induced asthma?
Eosinophils
155
What granulocyte is mainly associated with non-allergen induced asthma?
Viral infections and other stimuli can cause a neutrophilic response.
156
Investigation of Asthma
Testing for Airway Obstruction:
Spirometry
Bronchial Challenge Test
Peak Flow Test
Testing For Airway Inflammation:
Total Serum IgE
Eosinophil Count
Skin Prick Testing
FeNO MeasurementDLCO
DLCO is NORMAL in ASTHMA
157
What can spirometry show in asthma?
FEV1:FVC < 0.7 - obstructive lung disease.
Reversibility test - If 200ml FEV1 improvement & >12% increase in FEV1 after bronchodilator, then reversible obstruction e.g asthma.
158
What can the bronchial challenge test show for asthma?
Inhalation of mannitol, an osmotic agent causes dryness/irritation of the airways.
Incremental doses + spirometry
If there is >15% drop in FEV1, test is positive.
159
What can peak flow tests show in asthma?
Normally should have minimal variation.
In asthmatics there can be diurnal variation.
160
What would serum IgE and eosiniphil levels show in asthma?
There would be high levels.
High IgE indicates atopy - higher tendency to have allergic disease.
161
What would skin prick testing show in allergic asthma?
An inflammatory response when the allergen is injected.
162
What would FeNO Measurements show in asthma?
Inflammation can cause increased NO production.
163
2 Classifications of Asthma
T2 Hi (Allergic)
Higher activity of Th2 cells.
Mainly early onset, allergic asthma.
T2 Lo (Non-Allergic)
Lower activity of Th2 cells.
Presents later, can be associated with factors like smoking, COPD.
164
What would inflammatory asthma investigations show in T2 Hi asthma?
High serum IgE, eosinophils, FeNO, and positive skin prick response.
165
Lifestyle Management of Asthma
Smoking cessation
Weight loss
Physiotherapy – breathing pattern control
Speech therapy – inducible laryngeal obstruction
Allergen avoidance
Avoidance of air pollutants
166
Management of Chronic Asthma
SABA
SABA + ICS
SABA + ICS + LTRA
SABA + ICS + LABA +/- LTRA
MART - ICS + Fast Acting LABA (formeterol) in single inhaler.
LTRA = Leukotriene receptor antagonist (oral)
167
Pharmacodynamics of leukotriene receptor antagonists
Prevent bronchoconstriction by inhibiting cysteine leukotriene released from mast cells binding to receptors in smooth muscle.
168
Examples of leukotriene receptor antagonists
Montelukast.
169
Examples of biologics in asthma treatment
Anti-IgE - omalizumab
Anti IL5/IL5 receptor - mepolizumab
Anti IL13 - dupilumab
Anti TSLP (alarmins) - tezepelumab
170
Management of Acute Asthma Attack
O SHIT
Oxygen (40-60%)
Salbutamol nebulised
Hydrocortisone (ICS)
IV magnesium sulfate
Thyophiline IV
Antibiotics
BIPAP Ventilation if needed.
171
What is the atopic triad?
Asthma, eczema and hay fever.
172
Viral Aetiology of Respiratory Tract Infections
CAPRRI
Coronaviruses (10-15%)
Adenoviruses (5-10%)
Parainfluenza viruses (5%)
Rhinoviruses (45-50%)
Respiratory Syncytial viruses (5%) - affects infants and severely immunocompromised.
Influenza A virus (25-30%)
173
Management of Influenza (Flu) Viruses
Oseltamivir (tamiflu) - start within 48 hours of symptom onset.
Zanamivir - start within 36 hours of symptom onset.
174
Viral Aetiology of Pharyngitis
pHaRAEngitis
Rhinovirus
Adenoviruses
EBV, HIV
175
Bacterial Aetiology of Pharyngitis
Streptococcus pyogenes - group A strep.
Neisseria gonorrhoea - history of oral sex
Corynebacterium diphtheriae
176
Management of S.Pyogenes Infection
FL: Amoxicillin
If allergic, clarithromycin.
177
Clinical Presentation of C.Diphtheriae Infection
Neck lymphadenopathy
Greyish membrane on tonsils.
178
Management of Diphtheriae Infection
FL:Clarithromycin
SL: Erythromycin
179
Centor Criteria
Indicates likelihood of a sore throat being of bacterial origin.
Tonsilar exudate (pus)
Tender anterior cervical adenopathy
Fever over 38°C (100.5°F) by history
Absence of cough.
180
Aetiology of Sinusitis
Mainly viral - rhinovirus
Bacterial - s.pneumonia, h.influenzae
181
Clinical Presentation of Sinusitis
Frontal headache/facial pain
Fever
Purulent nasal discharge
182
Management of Bacterial Sinusitis
Empiral: Co-Amoxiclav
H.influenzae - Doxycycline
S.pneumoniae - Amoxicillin
183
Complications of Bacterial Sinusitis
Brain abscesses
Sinus vein thrombosis
Orbital cellulitis
184
What Organism can Cause Acute Epiglottitis?
H.influenzae type B
185
Clinical Presentation of Acute Epiglottitis
Inspiratory stridor
Pain on swallowing - odynophagia
186
Management of Acute Epiglottitis
ABCDE
IV ceftriaxone
187
Management of H.Influenzae Infection
Doxycycline
Vaccination
188
Aetiology of Whooping Cough
Bordatella pertussis - Gram neg bacilli
189
Pathophysiology of Bordatella Pertussis
Infection causes release of pertussis toxin which increases cAMP. Also causes lymphocytosis Th17 skewing of immune response contribute to chronic inflammation and cough.
190
Clinical Presentation of Whooping Cough
Catarrhal Phase: Fever, mucosal inflammation.
Paroxysmal Phase: Periods of coughing followed by a long inspiration
191
Management of B.pertussis Infection
Macrolides e.g Clarithromycin
Vaccination - is part of DTaP
192
What age group dose Croup Affect?
Affects children 3 months - 3 years.
193
Aetiology of Croup
Mainly Parainfluenza viruses
RSV
Influenza A
194
Clinical Presentation of Croup
Barking cough
Hoarse voice
Respiratory stridor
Central cyanosis
195
Management of Croup (Laryngo-Tracheobronchitis)
Nebulised adrenaline for short term relief.
Oral/IM corticosteroids e.g dexamethasone.
196
Investigation of Respiratory Viruses
Green viral throat swab
Multiplex PCR
197
Types of Pneumonia
Community acquired pneumonia - lobar pneumonia, bronchopneumonia
Hospital/healthcare acquired pneumonia
Aspiration pneumonia
Atypical (walking pneumonia)
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Risk Factors for Community Acquired Pneumonia
HIV
Cigarette smoking
IVDU
Immunosuppression e,g steroid use.
<16 or >65 age.
199
Bacterial Aetiology of Community-Acquired Pneumonia
S.pneumoniae - most common
K.pneumoniae
H.influenzae
Moraxella catarrhalis
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Bacterial Aetiology of Atypical/Walking Pneumonia
Leigonella pneumophiliae
Mycoplasma pneumoniae - Reynaud’s
Chlamydophila pneumoniae
Chlamydophila psittaci - birds, parrots
Coxiella burnetti - sheep
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Pathophysiology of Community Acquired Pneumonia
Infection causes bacterial overwhelming of immune defence.
Resulting in inflammation and accumulation of pus and exudate to form consolidations in the lung.
202
Clinical Presentation of Pneumonia
Fever
Sweats
Fatigue, malaise
Dyspnoea
Productive Cough - rust colored sputum = s.pneumoniae
Pleuritic chest pain - s.pneumoniae
Tachycardia, high RR, hypotension.
203
Symptoms of s.pneumoniae associated community acquired pneumoniae
Rust colored sputum
Pleuritic chest pain
204
Extrapulmonary Clinical Presentations of Pneumonia
Pericarditis - mycoplasma pnuemoniae
GI symptoms e.g abdominal pain, vomiting - leigonella pneumophilia.
205
Examination of Pneumonia
Upon auscultation:
Dull percussion
Localized coarse crackling due to consolidation.
Increased tactile fremitus (vibration) when speaking
Bronchial breath sounds
206
Investigation of Pneumonia
CXR: Lung consolidation with air-bronchograms.
Multi-lobar consolidation - s.pneumoniae, l.pneumophilia.
Multiple abscesses - S.aureus
Upper lobe only consolidation - k.pneumoniae
FBC: leukocytosis
Raised ESR/CRP
U+E - renal function check
Sputum culture
Blood cultures
Urinary antigens
PCR
207
What is the CURB65 Score
Used to describe severity of pneumonia.
1 point for each:
Confusion
Urea > 7 mmol/L
RR > 30
BP, <90 systolic, <60 diastolic
Age > 65
0-1 = mild, only admit if social circumstances or single worrying feature
2= moderate, admit to hospital
3-5 = severe, admit and monitor closely,
4-5 consider admission to critical care unit
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Empirical Management of Community Acquired Pneumoniae
CRB65 0-1, oral amoxicillin 500 mg OR clarithromycin if allergic.
CRB65 2 - oral amoxicillin + oral clarithromycin
CRB65 3-5 - IV co-amoxiclav + IV clarithromycin
209
Organism Specific Management of Pneumoniae
S.pneumonia - IV amoxicillin/co-amoxiclav and clarithromycin.
H.influenzae - co-amoxiclav + doxycycline
S.aureaus - fluxcloxacillin
K.pneumoniae - amoxicillin + cephalosporins
210
Management of Hospital Acquired Pneumoniae
Empirically Co-Amoxiclav
211
Management of Atypical Pneumonia
Macrolides such as clarithromycin.
212
Travel to what country is commonly known to cause Leigonella pneumophilia infections?
Spain
213
In what conditiions and methods is Leigonella pneumophilia known to infect people?
Air conditioning, mold, warm water infection.
214
What vaccine is given to adults 65 and over against pneumonia?
Polysaccharide pneumococcal vaccine
215
What vaccine is given to children adults against pneumonia?
Pneumococcal conjugate vaccine
216
What is the condition for pneumonia to be classified as hospital acquired?
Must be diagnosed 48 hours post-admission into hospital.
217
Bacterial Aetiology of Hospital-Acquired Pneumonia
ESKAPE
Enterococcus faecium
S.aureus (MRSA)
Klebsiella pneumoniae
Acinetobacter baumanni
P.aeruginosa
Enterobacter
218
Aetiology/Risk Factors for Hospital Acquired Pneumonia
Ventilator associatd
Post-operativeI
Immunocompromised patients
Elderly patients
219
Management of Early Onset Hospital Acquired Pneumonia
Metronidazole or use beta lactamase inhibitor e.g co-amoxiclav/piperacillin-tazobactam.
220
Management of Late Onset Hospital Acquired Pneumonia
MRSA - vancomycin
P.aeruginosa - ciprofloxacin
221
Complications of Pneumonia
Respiratory failure
Parapneumonic effusion & empyema
Sepsis
222
Risk Factors/Aetiology of Lung Abscess
IVDU - clot infection
Gastric content aspiration
Lack of dental hygiene
Right heart metastasis
223
Bacterial Aetiology of Lung Abscess
S.viridans
K.pneumoniae
S.aureus - IVDU
224
Management of Lung Abscess
Chest drain
6 week antibiotics
225
Aetiology of bronchiolitis
RSV
226
Aetiology of Acute Bronchitis
Usually viral - adenoviruses, rhinoviruses, parainfluenza viruses.
Mycoplasma pneumoniae
Chlamydia pneumoniae
Bordatella pertussis
227
Bacterial Aetiology of TB
M.tuberculosis
M.bovis
228
Risk Factors for TB
HIV
Air pollution exposure
Smoking
Immunosuppression e.g steroids
229
How is TB transmitted?
Aerosol transmission (respiratory droplets)
230
Pathophysiology of Primary TB
Primary TB
Most people are infected with TB bacteria, but do not actually have the disease.
Bacilli are taken by alveolar macrophages into hilar lymph nodes.
Delayed hypersensitivity reaction resulting in caseous granuloma formation to starve bacteria.
Granulomas known as Ghon focus.
More likely to form in lung apex.
231
Pathophysiology of Latent TB
Granulomas can calcify, causing bacteria within them to become dormant for years.
There is persisting cell mediated immune response that is still detectable on tuberculin skin test.
232
Pathophysiology Of Pulmonary Tuberculosis
If bacterial growth is strong enough, granulomas can enlarge into into cavities and form abscesses.
Can form a Ghon complex, which is a combination of Ghon focus (lung granulomas) and mediastinal lymphadenopathy.
Ghon focus and complex most likely to form in lung apex.
233
Which Stage of TB is there a Ghon focus formation?
Primary
234
What is a Ghon complex and which stage of TB does it form in?
Combination of ghon focus (lung granuloma and mediastinal lymphadenopathy.
Forms in pulmonary TB.
235
Systemic Clinical Presentation of Tuberculosis
Weight loss
Fever
Night sweats
Malaise
Lymphadenopathy
236
Pulmonary Clinical Presentation of Tuberculosis
Cough
Haemoptysis
Chest pain
Dyspnoea
237
Extra-Pulmonary Manifestations of TB
Bone: Pott's disease, joint swelling.
Abdominal: Ascites, malabsorption.
GU: Dysuria, haematuria
CNS: Meningitis, CN palsy
Miliary: Widespread diffuse TB
238
Investigation of Active TB
FBC: Normocytic normochromic anaemia
Raised ESR/CRP
CXR: Consolidation, cavitation.
Lung & lymph node biopsy/histology: Caseating granuloma with ZN stain.
Sputum culture: Acid fast bacili on ZN stain.
239
Investigationof Latent TB
Mantoux/Tuberculin Skin Test
TB antigen injected intradermally.
Stimulates T4 delayed hypersensitivity reaction.
Positive if inflammatory response within 48 hours.
Interferon Gamma Release Assays (IGRAs)
Obtaining blood sample and mixing it with bacterial antigens.
Analysing amount of IFN-gamma released to determine if there is latent TB.
240
Management of TB
RIPE
Rifampicin - 6 months
Isoniazid - 6 months
Pyrazinamide - 2 months
Ethambutol - 2 months
241
Side Effects of Rifampicin
Hepatitis, Red urine
242
Side Effects of Isoniazid
Hepatitis, peripheral neuropathy
243
Side Effects of Pyrazinamide
Hepatitis, arthralgia, rash.
244
Side Effects of Ethambutol
Optic neuritis
245
Which TB antibioticvs are bactericidal?
Rifampicin, Isoniazid
246
Which TB antibiotics are bacteriostatic?
Pyrazinamide and ethambutol.
247
Complications of TB
Pleural effusion - due to rupture of ghon complex into the pleural cavity.
Bronchopneumonia - granulomatous erosion into bronchus
Pericardial effusion - lymphatic node rupture introducing bacteria into pericardium.
248
What is Bronchiectasis?
Chronic airway dilation often caused by, and can lead to further chronic lung infection and inflammation.
249
Aetiology/Risk Factors of Bronchiectasis
Post pneumonia TB
Idiopathic pulmonary fibrosis
Cystic fibrosis
Primary ciliary dyskinesia
250
Infectious Aetiology of Bronchiectasis
H.influenzae
P.aeruginosa
251
Pathophysiology of Bronchiectasis
Chronic pulmonary inflammation and infection can lead to fibrosis and bronchial dilation.
Can also result in ciliary dysfunction & mucociliary transport causing further infection and inflammation.
252
Clinical Presentation of Bronchiectasis
Chronic productive cough with purulent sputum
Dyspnoea
Mild haemoptysis
Finger clubbing
Recurrent infections
253
Examination of Bronchiectasis
Coarse crackles heard upon auscultation.
254
Investigation of Bronchiectasis
Spirometry: FEV1:FVC <0.7
CXR: Dilated bronchi with thickened walls.
GS: High resolution CT scan (HRCT) - tram-track airway appearance with signet ring sign - increased bronchioarterial ratio.
Nasal nitric oxide - PCD screening
255
Anti-Inflammatory Management of Bronchiectasis & CF
Anti-Inflammatory
Oral azithromycin/ibuprofen.
256
Aetiology of Cystic Fibrosis
Autosomal recessive mutation in CFTR gene on chromosome 7.
257
Pathophysiology of Cystic Fibrosis
CFTR encodes for a chloride channel on epithelial cells.
Actively transports chloride into lung and GI mucous, and sweat glands.
Na passively follows Cl, so lack of Cl + Na secretion from cells causes osmotic intracellular water movement.
Leads to secretion of viscous mucous.
Can lead to mucosal stasis which pre-disposes to increased infections and bronchiectasis.
258
Clinical Presentation of Cystic Fibrosis
Dyspnoea
Recurrent infections
Nasal polyps
Nail clubbing
Steatorrhea -Pancreatic insufficiency
259
Investigation of Cystic Fibrosis
GS: Sweat test - Na and Cl > 60 mmol/L
Immunoreactive trypsinogen test in newborns - raised IRT.
Genetic testing for CTFR gene mutation.
260
Management Objectives for CF and Bronchiectasis
AIrway clearance
Anti-microbial treatment
Anti-inflammatory treatment
261
Airway Clearance in Bronchiectasis and CF
Airway clearance therapy - autogenic drainage, activated breathing cycle technique.
Mucolytics: Nebulised saline for both along with:
Carbocisteine in bronchiectasis
Dornase alfa in CF
262
Antibiotic Management in Bronchiectasis & CF
P.aeruginosa - oral ciprofloxacin - CF only
H.influenzae - oral doxycycline
263
Anti-Inflammatory Management in Bronchiectasis & CF
Oral azithromycin/ibuprofen.
264
Differential Diagnoses for Haemoptysis
TB
Small cell carcinoma of the lung
Pulmonary embolism
265
Differential Diagnoses of Productive Cough
Pneumonia infection
Chronic bronchitis
Bronchiectasis
COPD
Cystic fibrosis
266
Differential Diagnoses of Dry Cough
Idiopathic pulmonary fibrosis
Sarcoidosis
Whooping cough
Croup (laryngotracheobronchitis)
267
Which Obstructive Lung Disease have a normal DLCO?
Asthma
Chronic Bronchitis
268
Which Obstructive Lung Disease have a reduced DLCO?
Emphysema
269
Which Restrictive Lung Diseases have a reduced DLCO?
Parenchymal ones e.g IFP, sarcoidosis
270
What is Pulmonary Hypertension?
Mean pulmonary pressure > 25 mmHg
271
Pre-capillary causes of PH
Idiopathic PH
Pulmonary embolus
272
Capillary causes of PH
COPD
Asthma
273
Post-capillary causes of PH
LV failure
274
Pathophysiology of PH
Pre & post-capillary: Backup causes increaed pressure.
Capillary: Hypoxic pulmonary vasoconstriction causes increased pressure.
Can lead to right-sided hypertrophy.
275
Clinical Presentation of PH
Exertional dyspnoea, fatigue
RHF symptoms: Oedema, jugular venous distension with cannon A waves
276
Investigation of PH
GS: Right heart catheter for BP measurement.
277
Management of PH
Sildenafil (PDE5 inhibitor)
