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Respiratory Conditions Flashcards

1
Q

Define ARDS

A

Non-cardiogenic pulmonary oedema and diffuse lung inflammation.

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2
Q

What do you need to see to diagnose ARDS

A

Acute onset
Bilateral infiltrates
Opacity on CXR

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3
Q

What Conditions lead to ARDS?

A 
T - Trauma
O - Opiate overdose
A - Aspiration
S - Sepsis
T - Transplantation
P - Pneumonia
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4
Q

Risk Factors for ARDS

A 
Critical illness
Smoking
Alcohol
Sepsis
Aspiration
Blood transfusion
Lung transplant
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5
Q

Investigations for ARDS

A

CXR - Bilateral infiltrates
ABG (Hypoxaemia)
Cough with frothy sputum
Echo - Severe aortic or mitral valve dysfunciton
Sputum/blood/urine culture - positive if underlying infection

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6
Q

Signs of ARDS

A 
Cyanosis
Tachycardia
Tachypnoea
Bilateral diffuse inspiratory crackles
Hypoxaemia refractory to O2
Peripheral vasodilation
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7
Q

Symptoms of ARDS

A

SOB
Respiratory distress
Cough

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8
Q

What investigations are done for ARDS?

A 
CXR ( B/L infiltrate)
ABG (Decreased O2)
Sputum culture, Blood culture, Urine culture (Positive for underlying cause)
Amylase + Lipase (if pancreatitis)
Consider: BNP, Echo
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9
Q

What is asbestos-related lung disease?

A

Industrial dust diseases (Asbestosis, Mesothelioma)

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10
Q

What is Asbestosis?

A

Long-term inflammation and scarring of lungs caused by inhalation of asbestos fibres

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11
Q

What is Mesothelioma?

A

Aggressive tumour of mesothelial cells that occurs in the Pleura (90%) and sometimes in the peritoneum, pericardium or testes

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12
Q

What is the cause of asbestosis?

A

3 different types of asbestos chrysotile (White), Crocidolite (Blue), Amosite (Brown).
Commonly used in building trade (Shipyard workers!)
Degree of asbestosis depends on degree of fibrosis
Inflammation gradually causes mesothelial plaques in pleura
Increased risk of bronchial adenocarcinoma and mesothelioma

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13
Q

What is the cause of mesothelioma?

A

Associated with occupational exposure
45 year latency period
Malignant mesothelioma spreads to distant sites, most present with locally advanced disease

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14
Q

What are the risk factors of abestos-related lung disease?

A

Cumulative asbestos inhalation

Often occupational

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15
Q

What are the symptoms of asbestos related lung disease?

A 
Asbestosis - progressive dyspnoea
Mesothelioma: 
SOB, Chest pain, weight loss
Fatigue
Fever
Night sweats
Bone pain
Abdominal pain
Sometimes, bloody sputum
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16
Q

What are the signs of asbestos related lung disease?

A

Asbestosis:
Clubbing
Fine end-inspiratory crackles

Mesothelioma:
Occasional palpable chest wall mass
Clubbing
Recurrent pleural effusion
Signs of mets: Lymphadenopathy, hepatomegaly, bone tenderness
Abdominal pain/obstruction
Rarely cause pneumothorax
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17
Q

What is Aspergillus lung disease?

A

Lung disease associated with Aspergillus fungal infection

5 different ways this group of fungi can affect your lungs

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18
Q

What are the 5 ways that aspergillus fungi can affect the lungs?

A 
Asthma
Allergic bronchopulmonary aspergillosis
Aspergilloma
Invasive aspergillosis 
Extrinsic allergic alveolitis
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19
Q

How does aspergillus cause asthma?

A

Type I hypersensitivity (atopic) reaction to fungal spores

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20
Q

How does it cause Allergic bronchopulmonary aspergillosis (ABPA)?

A

Type I and III hypersensitivity reactions to aspergillus fumigatus

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21
Q

How does aspergillus cause aspergilloma (mycetoma)?

A

A fungus ball within a pre-existing cavity (often caused by sarcoidosis or TB)

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22
Q

How do aspergillus fungi cause extrinsic allergic alveolitis(EAA)?

A

Due to sensitivity to aspergillus clavatus

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23
Q

What is Malt workers lung?

A

EAA caused by aspergillus clavatus

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24
Q

What causes aspergilloma?

A

Growth of A.fumigatus mycetoma ball in a pre-existing lung cavity

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25
Q

What causes ABPA?

A

Colonisation of the airways by aspergillus fumigatus leads to IgE and IgG-mediated immune response
Occurs in asthmatics and CF patients
Release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage, initially causing bronchoconstriction but as inflammation persists, permanent damage occurs as bronchiectasis

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26
Q

What causes invasive aspergillosis?

A

Invasion of aspergillus into lung tissue and fungal dissemination
Occurs in immunosuppressed patitnes (e.g. Neutropenia, Steroids, AIDS) or after broad-spectrum antibiotic therapy

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27
Q

What are the Risk factors for aspergillus lung disease?

A 
Allogenic stem cell transplant/solid organ transplant
Prolonged neutropenia (>10 days)
Immunosuppression
Chronic Granulomatous Disease
Aplastic anaemia
Acute leukaemia
Pre-existing cavity (aspergilloma)
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28
Q

What are the symptoms of Aspergilloma?

A

Asymptomatic

May cause cough, haemoptysis, lethargy, weight loss

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29
Q

What are the symptoms of ABPA?

A

Difficult to control asthma

Recurrent episodes of pneumonia with wheeze, cough, sputum, dyspnoea, fever and malaise

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30
Q

What are the symptoms of invasive aspergillosis?

A

Dyspnoea
Rapid deterioration
Septic picture

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31
Q

What are the signs of aspergillus lung disease?

A

Tracheal deviation (only with very large aspergillomas)
Dullness in affected lung
Reduced breath sounds
Wheeze (in ABPA)
Cyanosis (Possible in invasive aspergillosis)

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32
Q

What are the investigations for Aspergilloma?

A

CXR (Round mass with a crescent of air around it) - usually found in the upper lobes
CT/MRI - used if CXR unclear
Strongly positive serum precitpitins
Aspergillus skin test +ve in 30%

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33
Q

What are the investigations of ABPA?

A

Immediate skin test reactivity to aspergillus
Aspergillus-specific IgE radioallergosorbent test (RAST)
Eosinophilia
Raised total serum IgE
Raised specific serum IgE and IgG to A. fumigatus
Aspergillus in sputum
CXR (Patchy shadows, segmental collapse or consolidation, distended mucous-filled bronchi, Signs of complications (Fibrosis in upper lobes, bronchiectasis)
CT (lung infiltrates, central bronchiectasis)
Lung function test (Reversible airflow limitation, Reduced lung volumes/gas transfer)

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34
Q

What investigations are done for invasive aspergillosis?

A

Apergillus detected in cultures or by histological examination
Bronchoalveolar lavage fluid or sputum may be used diagnostically
Chest CT (nodules surrounded by ground-glass appearance [halo sign], caused by haemorrhage into tissue surrounding fungal invasion)

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35
Q

What is Asthma?

A

Chronic inflammatory airway disease characterised by paroxysmal airway obstruction and hyper-reactivity.

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36
Q

What three things occur in asthma?

A

Bronchospasm (smooth muscle spasm narrowing arteries)
Excessive production of secretions (plugging ariways)
Mucosal swelling/inflammation, caused by mast cell and basophil degranulation

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37
Q

What causes Asthma?

A

Airway inflammation secondary to a complex interaction of inflammatory cells, mediators and other cells and tissues in the airway.
Trigger leads to release of inflammatory mediators leading to a consequent activation and migration of other inflammatory cells
Inflammatory reaction is a Th2 lymphocyte response.
Th2 inflammation characterised by CD4 + lymphocytes that secrete IL-4/5/13, chemokine eotaxin, TNF-alpha and LTB4
This Th2 response is important in initiation and prolongation of the inflammatory cascade

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38
Q

What are the Risk factors for asthma?

A 
Family history
History of allergy/atopy
Inner city environment
Socio-economoic deprivation
Nasal polyposis
Obesity
GORD
Premature/low birthweight
Smoking/maternal smoking
Early exposure to broad spectrum ABx
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39
Q

What are possible predictive factiors of Asthma?

A

Breast-feeding
Vaginal birth
Lots of siblings
Farming environment

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40
Q

How do people with asthma present?

A

> 1 of following symptoms: Wheeze, breathlessness, chest tightness and cough
Beta blocker
Atopic history
Wheeze on auscultation
Low FEV1 or PEF
Unexplained eosinophilia
Cold air, viral infection, drugs, exercise, emotions, allergens, smoking/passive smoking, pollution all prelude it

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41
Q

What are the signs of Asthma?

A 
Tachycardia
Resp Rate >25
Sats <92
Inspiratory:Expiratory of 1:2
Hyperinflated chest
Chest deformity in chronic asthma (Harrison's sulci)
Intercostal recession with Respiratory distress
Diffuse wheeze
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42
Q

What are the investigations are indicated for Asthma?

A 
Peak flow (unreliable if they are under 5) - best of 3, biggest number
Spirometry - preferred for confirmation. Repeat when symptomatic 
CXR - normal even with asthma
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43
Q

What is the management for asthma based on?

A

Based on 4 principles:

  1. Control symptoms, including nocturnal symptoms and those related to exercise
  2. Prevent exacerbation and need for rescue medication
  3. Achieve the best possble lung function (especially FEV1 and/or PEFR >80% predicted)
  4. Minimise side-effects
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44
Q

What must be considered when treating asthma?

A

Upper respiratory tract infections

Very difficult to treat asthma if co-existing allergic rhinitis

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45
Q

What types of inhalers are there?

A

Measured dose inhaler

Dose Prepared inhaler

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46
Q

What are the drug treatments for asthma?

A

Step 1: Salbutamol
Step 2: Regular inhaled steroids (Beclometasone diproprionate)
Step 3: LABA (not without oral steroids - budesonide) and increase to 800 micrograms of Beclometasone
Step 4: Increase to 2000 micrograms/day and a 4th drug (leukotriene receptor antagonist)
Step 5: Continuous or frequent use of oral steroids [Recommends omalizumab in severe persistent allergic IgE-mediated asthma]

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47
Q

What are the triggers for adding steroids?

A

Exacerbation in last 2 years
Use Blue Inhaler >3 times a week
Symptomatic >3 times a week
Waking due to asthma >1 time a week

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48
Q

How do you control exercise induced asthma?

A

Regularly inhaled steroids beyond anticipatory use of a bronchodilator when preparing for sport.
Consider adding LABAs, Leukotriene inhibitors, oral B2 agonists

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49
Q

What are the complications of Asthma?

A 
Pneumonia
Pneumothorax
Pneumomediastinum
Respiratory failure
Arrest 
Chest wall deformity
Growth retardation
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50
Q

What are predictors for controlled wheeze after school?

A 
Presentation over 2
Male sex in pre pubertal
Frequent or severe episodes of wheezing
Personal or Family history of atopy
Abnormal lung function
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51
Q

What is Bronchiectasis?

A

Permanent dilatation of bronchi due to destruction of the elastic and muscular components of the bronchial wall. Often caused as a consequence of recurrent and/or severe infections secondary to an underlying disorder

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52
Q

What causes Bronchiectasis?

A

Chronic lung inflammation leads to fibrosis and permanent dilatation of the bronchi due to destruction of the elastic and muscular components of the bronchial wall
Leads to pooling of mucous, predisposes to further cycles of infection, damage and fibrosis of bronchial walls

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53
Q

What conditions cause bronchiectasis?

A

Idiopathic (50%)
Congenital (CF, Young’s syndrome, Primary ciliary dyskinesia, Kartagener’s syndrome)
Post-infectious (Pneumonia, whooping cough)
Host immunodeficiency (HIV)
GORD
Bronchial obstruction
ABPA

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54
Q

What are the risk factors for Bronchiectasis?

A 
Cystic fibrosis
Host immunodeficiency
Previous infections
Congenital disorders of the bronchial airways
Primary ciliary dyskinesia
Alpha-1 antitrypsin deficiency
Connective tissue disease
IBD
Aspiration or inhalation injury
Focal bronchial obstruction
Tall, thin, white females aged 60 or over
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55
Q

What are the symptoms of Bronchiectasis?

A 
Purulent cough with copious sputum - worse laying flat
Intermittent haemoptysis
Breathlessness
Chest pain
Malaise
Fever
Weight loss
Symptoms benign after acute respiratory illness
Worsen during exacerbations
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56
Q

What are the signs of Bronchiectasis?

A

Clubbing
Coarse inspiratory crackles (at bases) - shift with coughing
Wheeze - high pitched inspiratory crackles

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57
Q

What investigations are done for Bronchiectasis?

A 
FBC (Eosinophilia, ABPA, Neutrophilia)
Rheumatid factors (Positive)
Specific IgE or skin prick test for A. fumigatus
CXR 
High-resolution CT
Nasal nitric oxide
Spirometry (obstructive image)
6-minute walk test (reduced in significantly reduced lung function)
Serology (HIV, immunoglobulins)
Serum alpha-1-antitrypsin phenotype
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58
Q

How do you manage acute bronchiectasis?

A

Lung damage irreparable
Treat underlying cause and co-existing medical problems
Exercise and improved nutrition + airway clearance therapy w/ inhaled bronchodilator and mucoactive agent

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59
Q

How do you manage ongoing bronchiectasis?

A

Mild to moderate causes: short term oral ABx + increased airway clearance (clear mucous) + continue maintenance

Severe underlying disease: Short term IV ABx + increased clearance + continue maintenance therapy

3 or more exacerbations per year despite maintenance therapy: Reassess physiotherapy +/- muco-active treatment + continue maintenance therapy w/ long-term ABX with surgery

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60
Q

What are the complications of Bronchiectasis?

A

Massive Haemoptysis
Respiratory failure
Cor Pulmonale
Ischaemic stroke

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61
Q

What is Cor pulomanle?

A

Abnormal enlargement of the right side of the heart due to underlying lung disease

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62
Q

what is COPD?

A

It is a common progressive disorder characterised by airway obstruction with little or no reversibility.
Includes: Emphysema & Chronic bronchitis
Usually have COPD or asthma not both

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63
Q

What are the signs and symptoms of COPD?

A

Respiratory distress (Tachypnoea, breathlessness on exertion, increased use of accessory muscles on breathing, pursed lips)
Abnormal posture (Lean forward for ease of breathing)
Drowsiness (Flapping tremor and confusion)
Other: Underweight, ankle oedema, cyanosis, hyperinflation of chest, downward displacement of liver
Cough
Sputum
Dyspnoea
Wheeze

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64
Q

What is the staging of COPD?

A

Stage 1: >/= 80% of FEV1
Stage 2: 50-79% of FEV1
Stage 3: 30-49% of FEV1
Stage 4: <30% of FEV1

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65
Q

What investigations are done for COPD?

A

FBC (Raised Hct, Possibly raised leucocytes)
Spirometry (FEV1/FVC <0.7)
ABG (PaCO2 >50mmHg and/or PaO2 <60mmHg)
CXR (Hyperinglation, flattened diaphragm, increased intercostal space)
ECG (R. ventricular hypertrophy, arrhythmia, ischaemia)

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66
Q

How do you manage COPD?

A

Generally: Stop smoking, encourage exercise, treat malnutrition, influenza and pneumococcal vaccinations, pulmonary rehab or palliative care
Mild/moderate: LAMA (tiotropium) or LABA
Severe: LABA + Corticosteroids or tiotropium
If still symptomatic: Tiotropium + inhaled steroids + LABA

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67
Q

How do you treat more advanced COPD?

A

Pulomnary rehabilitation
Indication for surgery (recurrent pneumothoraces, isolated bullous disease, lung volume reduction surgery)
NIIV
Air travel risky if FEV1 <50% or PaO2 <6.7kPa

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68
Q

What are the complications of COPD?

A 
Chronic hypoxaemia
Pneumothorax
Respiratory failure
Arrhythmias e.g. atrial fibrillation
Infection
Secondary polycythaemia
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69
Q

What is Extrinsic allergic alveolitis?

A

Intersitital inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pnuemonitis

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70
Q

What causes extrinsic allergic alveolitis?

A

In sensitised individuals, repetitive inhalation of allergens provokes a hypersensitivity reaction which varies in intensity and clinical course depending on the antigen
In the acute phase, alveoli are infiltrated with acute inflammatory cells
Antigenic dusts include microbes and animal proteins
Early diagnosis and prompt allergen removal can halt and reverse disease progression, so prognosis can be good

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71
Q

What are examples of EAA?

A

Farmer’s lung (Caused by mouldy hay containing thermophilic actinomycetes)
Pigeon Fancier’s lung (Caused by blood on bird feathers and excreta)
Malt worker’s lung (Caused by barley or maltlings containign A. clavatus)
Bagassosis or sugar worker’s lung (Thermoactinomyces sacchari)

72
Q

What are the Risk Factors for EAA?

A

Smoking
Viral infection
Mould/Bacteria/avian protein/anhydride antigen exposure
Epoxy resin/pain/metal-working fluid/nitrofurantoin/methotrexate exposure

73
Q

What are the symptoms of Acute EAA?

A 
Present 4-12 hours after 
Dry cough
Dyspnoea
Malaise
Fever
Myalgia
Wheeze and productive cough if repeat high-level exposure
74
Q

What are the symptoms of chronic EAA?

A

Slowly increasing breathlessness
Decreased exercise intolerance
Weight loss
Exposure usually chronic, low-level and may be no history of previous acute episodes

75
Q

What are the signs of acute EAA?

A

Rapid shallow breathing
Pyrexia
Inspiratory crackles

76
Q

What are the signs of Chronic EAA?

A

Fine inspiratory crackles

Clubbing (rare)

77
Q

What are the investigations for EAA?

A

FBC (Neutrophilia, lymphopenia)
ESR (Raised)
Serology (Test for IgG to fungal or avial antigens)
ABG (Reduced PO2 adn PCO2)
CXR (Normal acutely, fibrosis in chronic cases (upper zone fibrosis and honeycomb lung))
High-resolution CT-T (Early change, patchy ground-glass shadowing and nodules, extensive fibrosis)
Pulmonary function tests (Low FEV1, Low FVC, Preserved or raised FEV1/FVC, reduced TLC)
Bronchoalveiolar lavage (Lymphocytes and mast cells)
Lung biopsy can be performed

78
Q

What is idiopathic pulmonary fibrosis?

A

Chronic inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium. With no known cause.

79
Q

What is the cause of idiopathic pulmonary fibrosis?

A

Recurrent injury to alveolar epithelial cells results in secretion of cytokines and growth factors by the pneumocytes, in particular TGFbeta1

Cytokine release causes fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and increased collagen synthesis and deposition

Leads to thickened interstitial layer causing problems with ventilation and oxygenation.

Restrictive disease as there is a restricted lung expansion due to fibrosis

Also loss of alveoli leading to fluid filled cysts surrounded by a thick wall (Honeycombing)

80
Q

What are the risk factors for Idiopathic Pulmonary fibrosis?

A 
Age
Male
Smoking
occupational exposure to metal or wood
Chronic microaspiration
Animal and vegetable dusts
81
Q

What are the symptoms of Idiopathic pulmonary fibrosis?

A 
Gradual onset, progressive dyspnoea on exertion
Dry irritating cough
NO wheeze!
May be preceded by a viral-type illness
Fatigue and weight loss are common
82
Q

What are the signs of IPF?

A

Clubbing
Bibasal fine late inspiratory crackles
Cyanosis
Sighs of Right heart failure in advanced stages of diseases

83
Q

What are the investigations of IPF?

A

CRP and immunoglobulin (Raised)
ANA and Rheumatoid factor (1/3 of patients are positive)
ABG (Normal early disease, PO2 decrease with exercise, normal PCO2, rises in late disease)
CXR (normal, early disease has ground glass shadowing, B/L lower zone reticulonodular shadowing)
High resolution CT
Pulmonary function tests (Restrictive features - reduced FEV1 and FVC with preserved or increased FEV1/FVC)
Lung biopsy - gold standard for diagnosis

84
Q

What is Lung cancer?

A

Primary malignant neoplasm of the lung
Classification of bronchocarcinoma: Small cell (20% - small cells that divide and spread rapidly)
Non-small cell (80% - Divide and spread slowly)

85
Q

What are the types of Lung cancer?

A

Small cell (central tumours, treat with chemo therapy, associated with Hyponatraemia)
Non-small cell (adenocarcinomas, squamous cell carcinomas, large cell carcinomas and carcinoid tumours)
Squamous cell carcinomas (Treat with radiotherapy, Associated with PTHrp release which leads to hypercalcaemia)
Adenocarcinoma (Located peripherally, more common than others in non-smokers)
Large cell (Poor prognosis)

86
Q

What causes lung cancer?

A

Smoking
Asbestos exposure
Other occupational exposure: Polycyclic hydrocarbons, nickel, radon gas, chromium, arsenic, iron oxides
Atmospheric pollution

87
Q

What are the symptoms of Lung cancer?

A 
Cough
Haemoptysis
Dyspnoea
Recurrent pneumonia
Brachial plexus invasion (shoulder/arm pain)
Left recurrent laryngeal nerve invasion (hoarse voice and bovine cough)
Dysphagia
Arrhythmias
Horner's syndrome (pancoast tumour)
Weight loss
Fatigue
Fractures
Bone pain
88
Q

What are the signs of Lung cancer?

A

Fixed monophonic wheeze
Signs of lobar collapse or pleural effusion
Signs of metastases (tenderness, confusion, fits, cerebellar symptoms)
Cachexia
Anaemia
Clubbing
Hypertrophic pulmonary osteoarthropathy causing wrist pain
Lymphadenopathy

89
Q

What are the investigations for Lung cancer?

A

CXR (Peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusion, bony secondaries)
Staging (Requires CT/MRI of head, chest and abdomen)
PET
Radionuclide bone scan if mets. suspected
Lung function tests assess lobectomy
FBC
U&Es
Calcium (Raised)
ALP (Bony mets)
LFT
Pre-op (ABG and pulmonary function tests)

90
Q

What is Obstructive sleep apnoea?

A

A disease characterised by recurrent prolapse of the pharyngeal airway (cessation of airflow for >10 seconds) during sleep, followed by partial arousal from sleep

91
Q

What causes Obstructive sleep apnoea?

A

Occurs due to narrowing of upper airways because of the collapse of soft tissues of the pharynx
Associated with: Weight gain, surgical swelling, smoking, alcohol, sedative use, macroglossia, marfan’s syndrome, craniofacial abnormalities

92
Q

What are the Risk Factors for obstructive sleep apnoea?

A 
Obesity/Large neck
Male/post-menopausal female
Maxillomandibular anomalies
Increased volume of soft tissues
Family history
Snoring
PCOS
Hypothyroidism
Down's syndrome
Age
Smoking
Black/hispanic/asian
93
Q

What are the symptoms of Obstructive sleep apnoea?

A 
Excessive daytime sleeping
Unrefreshing or restless sleep
Morning headaches
Dry mouth
Difficulty concentrating
Irritability and mood changes
Decreased libido and cognitive performance
Partner reporting loud snoring, nocturnal apnoeic episodes or nocturnal choking
94
Q

What are the signs of Obstructive sleep apnoea?

A 
Large tongue
Enlarged tonsils
Long or thick uvula
Retrognathia (pulled back jaws)
Neck circumference - more than 42cm in males
- More than 40 cm in females 
Obesity
Hypertension
95
Q

What investigations are done for Obstructive sleep apnoea?

A 
Simple studies: Pulse oximetry, video recording
Sleep study (polysomnography)
Bloods (TFTs [low], ABG)
Endoscopy
96
Q

What is Pneumoconiosis?

A

Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts

97
Q

What are the types of Pneumoconiosis?

A

Simple (Coal worker’s pneumoconiosis)
Complicated: Pneumoconiosis resulting in loss of lung function
Asbestosis: A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

98
Q

What causes Coal worker’s pneumoconiosis?

A

Inhalation of coal dust particles over 15-20 years. They are ingested by macrophages which die, releasing their enzymes and causing fibrosis

99
Q

What causes asbestosis?

A

A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

100
Q

What are the causes of Pneumoconioses?

A

Inhalation of particles: Cold dust, Silica, Asbestos

Often co-exists with chronic bronchitis

101
Q

What are the Risk Factors for Pneumoconiosis?

A

Occupational exposure
Risk is dependent on extent of exposure and the size/shape of particles
Smoking
TB

102
Q

What are the symptoms of Pneumoconiosis?

A

Occupational history is very important
Asymptomatic (picked up on CXR)
Symptomatic (onset SOB, Dry cough, Black sputum [produced occasionally in coal worker’s], pleuritic chest pain)

103
Q

What are the signs of pneumoconiosis?

A

Coalworker pneumoconiosis and sillicosis - decreased breath sounds
Asbestosis - End-inspiratory crackles, clubbing
Signs of pleural effusion or right heart failure (Cor pulmonale)

104
Q

What investigations are done for Pneumoconiosis?

A

CXR
Simple: micronodular mottling
Complicated: - Nodular opacities in upper lobes
- Macronodular shadowing
- Eggshell calcification of hilar lymph nodes (Characterisitc of silicosis)
- B/L lower zone reiculonodular shadowin and pleural plaques

CT scan - fibrotic changes can be visualised early

Bronchoscopy - Allows visualisation and bronchoalveolar lavage

Lung function tests - restrictive pattern

105
Q

What is Pneumonia?

A

Characterised by acute inflammation with an intense infiltration of neutrophils in and around the alveoli and the terminal bronchioles

106
Q

How can you categorise Pneumonia?

A 
Community acquired
Hospital acquired
Aspiration
Pneumonia in the immunocompromised
Typical
Atypical (Mycoplasma, chlamydia, legionella)
107
Q

What causes community acquired pneumonia?

A 
Most common: Streptococcus Pneumonia
Haemophilus influenzae
Mycoplasma pneumoniae
Moraxella catarrhalis (COPD patients)
Chlamydia pneumoniae
Chlamydia psittaci
Legionella (anywhere with air conditioning)
Staphylococcus aureus
Coxiella burnetii (Q fever)
TB
Viruses (15%)
108
Q

What causes Hospital acquired Pneumonia?

A

> 48 hours after Hospital admission
Most common: Gram negative enterobacteria!
(Pseudomonas, Klebsiella or S. Aureues)

109
Q

What causes aspiration Pneumonia?

A

Stroke, Myasthenia gravis, bulbar palsies, reduced consciousness, oesophageal diseases or poor dental hygeine - risk aspirating oropharyngeal anaerobes

110
Q

What causes pneumonia in immunocompromised patients?

A 
Streptococcus pneumoniae
Haemophilus influenzae
Staphylococcus Aureus
M catarrhalis
M pnerumoniae
Gram -ve bacilli
PCP (AIDS defining disease)
111
Q

What are the Risk factors for Pneumonia?

A 
Age
Smoking
Alcohol
Pre-existing lung disease
Immunodeficiency
Contact with patients with Pneumonia
112
Q

What are the symptoms of Pneumonia?

A 
Fever
Rigors
Sweating
Malaise
Dyspnoea
Cough
Purulent sputum
Haemoptysis
Pleuritis chest pain
Weight loss
Confusion (in severe cases or in the elderly)
Atypical pneumonia symptoms (Headache, myalgia, diarrhoea/abdominal pain, dry cough)
113
Q

What are the signs of Pneumonia?

A 
Pyrexia
Respiratory distress
Tachypnoea
Tachycardia
Hypotension
Cyanosis
Signs of consolidation: 
- Decreased chest expansion
- Dull to percuss over affected areas
Increased tactile vocal fremitus/vocal resonance over affected areas
- Bronchial breathing over affected area
- Coarse crackles on affected site
114
Q

How do you manage Pneumonia?

A

CURB-65 is the scoring system
Treat hypoxia (Sats <88%), starting at 24-28% if history of COPD
Treat hypotension/shock from infection
Assess for dehydration
Start empirical Abx (vary on cause)
Supportive treatment (O2, IV fluids, CPAP, drainage)

115
Q

What is the CURB-65 scoring system?

A

Allocate each a point:

  • Confusion (AMTS <8)
  • Urea (>7 mmol/L)
  • Respiratory rate >30
  • BP <90 systolic and/or <60 diastolic
  • Age greater than / equal to 65
116
Q

What score in CURB-65 denotes a mild, moderate or severe pneumonia?

A

0-1: Home treatment if possinle
2: Hospital therapy
3+: Severe pneumonia - consider ICU

117
Q

What Antibiotics should be used?

A

Mild pneumonia: Oral amoxicillin
Moderate: IV/Oral amoxicillin + clarithromycin
Severe: IV Co-amoxiclav + Clarithromycin
IF penicillin allergic, use cephalosporin instead
IF aspiration pneumonia: Cephalosporin IV + metronidazole IV

118
Q

What should be done if you suspect atypical pneumonias? (Legionella, Chlamydophilia, PCP)

A

Legionella pneumophilia: Add levofloxacin + rifampicin
Chlamydophilia species: Add tetracycline
PCP: High-dose co-trimoxazole

119
Q

How do you treat hospital acquired neutropenic disorder?

A

IV aminoglycloside e.g. gentamicin + antipseudomonal penicillin e.g. Ticarcillin

120
Q

What are the complications of community acquired pneumonia?

A 
Septic shock 
ARDS
Antibiotic-associated clostridium dificile colitis
Heart failure
Acute coronary syndrome
Cardiac arrhythmias
Necrotising pneumonia
Pleural effusion
Lung abscesses
Pneumothorax
121
Q

What are complications of Hospital acquired pneumonia?

A

Empyema or Lung abscess
Systemic inflammatory response syndrome or sepsis with multi-organ failure
Pulmonary embolism/infarction
Clostridium difficile colitis due to broad-spectrum antibiotic use

122
Q

What are complications of atypical pneumonia?

A 
Pleural/parapneumonic effusion
Rash
Neurological complications
Pericarditis
Atherosclerosis
123
Q

What is a Pneumothorax?

A

Collection of air in the pleural space, there are other variants in which other substances are found in the pleural space

  • Haemothorax (Blood)
  • Chylothorax (Lymph)
124
Q

What causes pneumothorax?

A

Primary spontaneous pneumothorax

  • Without preceding trauma or precipitating event, develops in a person without clinically apparent pulmonary disease
  • Most common in: Smokers, Those with marfan’s, Homocystinuria, Family history, Patients with primary spontaneous pneumothorax tends to be tall, slender, young males
125
Q

What causes secondary spontaneous pneumothorax?

A 
Complication of underlying disease
- PCP
- CF
- TB
Severity of lung dysfunction correlated with likelihood of developing a secondary spontaneous pneumothorax
126
Q

What causes a traumatic pneumothorax?

A

Penetrating or blunt injury to the chest

127
Q

What causes a tension pneumothorax?

A

Complicate primary and secondary spontaneous pneumothoraces as well as traumatic pneumothoraxes

128
Q

What are the symptoms of Pneumothorax?

A

May be asymptomatic
Sudden onset breathlessness
Pleuritic chest pain
Distress with rapid shallow breathing in tension pneumothorax
Patients on ventilation may present with hypoxia or increase in ventilation pressures

129
Q

What are the signs of Pneumothorax?

A 
None if small
Signs of respiratory distress
Hyper-resonance to percussion on affected side
Reduced breath sounds on affected side
Tension pneumothorax
- Severe respiratory distress
- Tachycardia
- Hypotension
- Cyanosis
- Distended neck veins
- Tracheal deviation away from the affected side
- Increased percussion note, reduced air entry/breath sounds on affected side
130
Q

What is the management of tension pneumothorax?

A 
Maximum O2
Needle decompression: Insert large-bore needle into 2nd intercostal space MCL on affected side
Aspirate up to 2.5L of air
Stop if they cough or resistance felt
Then chest drain
Follow up CXR 2hrs and 2 weeks later
131
Q

How do you manage primary spontaneous pneumothorax?

A

<50 years old

  • Small (supplemental O2 therapy and observation)
  • Breathless or large (supplemental O2 therapy and peructaneous aspiration w/ chest-tube thoracotomy w/ suction w/ video-assisted thoracoscopy or pleurodesis)
132
Q

How do you manage Secondary spontaneous pneumothorax?

A

Small:
- Hospitalisation with supplemental oxygen + observation
Moderate:
- Hospitalisation and supplemental oxygen + percutaneous aspiration w/ chest-tube thoracotomy w/ suction w/ video-assisted thoracotomy or pleurodiesis
Breathless or large: Hospitalisation with supplemental oxygen + chest-tube thoracotomy w/ suction w/ video-assisted thoracoscopy or pleurodiesis

133
Q

What is a catamenial pneumothorax?

A

Pneumothorax that occurs with menstrual periods

134
Q

How do you treat a catamenial pneumothorax?

A

Supplemental oxygen +/- percutaneous aspiratoin w/ tube thoracotomy drainage + ovarian suppression + video assisted thoracoscopy or open thoracotomy + chemical or mechanical pleurodiesis

135
Q

How do you treat a traumatic pneumothorax?

A

Hospitalisation and supplemental oxygen + percutaneous aspiration w/ chest tube thoracostomy w/ thoracotomy

136
Q

How do you treat a pneumothorax ex vacuo

A

Hospitalisation and supplemental oxygen w/ bronchoscopy

137
Q

How do you treat a pneumothorax in someone who is pregnant?

A

Recurrence more common in pregnancy

Observation and aspiration most common

138
Q

How do you treat someone with HIV who has had a pneumothorax?

A

Early intercostal tube drainage and surgical referral

Add appropriate treatment for HIV and p.jirovechi infection

139
Q

How do you treat a pneumothorax in someone with CF?

A

Pleural procedures

140
Q

What are the complciations of pneumothorax?

A

Re-expansion pulmonary oedema

Talc pleurodiesis-related ARDS

141
Q

How many people will a Pneumothorax recur in?

142
Q

What is a Pulmonary Embolism?

A

A consequence of a thrombus formation within a deep vein of the body, most frequently in lower extremities.

143
Q

What is the cause of Pulmonary embolism?

A

Virchow’s triad is the preferred aetiological model for DVT and PE

144
Q

What is Virchow’s triad?

A

Venous stasis
Vessel wall damage
Hypercoagulability

145
Q

What are Risk factors for Pulmonary embolism?

A 
Increasing age
Diagnosis of DVT
Surgery in the last 2 months
Bed rest >5 days
Surgery in the last 2 months
Family history of VTE
Active malignancy
Recent trauma or fracture
Varicose veins
Behcet's disease
Obesity
and many more
146
Q

What are the symptoms of pulmonary embolism?

A

Small PE - Asymptomatic
Moderate PE - Sudden SOB, Cough, Haemoptysis, Pleuritic chest pain
Large PE (as above) - severe pleuritic chest pain, shock, collapse, acute RHF, sudden death
Multiple small recurrent - symptoms of pulmonary hypertension

147
Q

What are the signs of Pulmonary embolism?

A

Severity of PE assessed based on associated signs

  • Small - no clinical signs
  • Sudden onset
  • Moderate - Tachypnoea, tachycardia, pleural rub, Low O2 saturation, pyrexia, hypotension
  • Massive PE - Shock, cyanosis, signs of right heat strain (Raised JVP, Left parasternal heave, accentruated S2 heart sound)
  • Multiple recurrent PE - signs of pulmonary HTN and RHF
148
Q

What are the investigations for Pulmonary embolism?

A 
Well's score determines the best investigation for PE!
If  4 or less - Do D-dimer
If >4 - Do CTPA and start on LMWH, if CT contraindicated use V/Q scanning
ABG (Low PaO2 and PaCO2)
ECG
Spiral CTPA
V/Q scan
Pulmonary angiography
149
Q

What is the well’s score?

A

Clinically suspected DVT - 3
Alternative diagnosis less likely than PE - 3
Tachycardia - 1.5
Immobilisation for >3 days or surgery in previous 4 weeks - 1.5
History of DVT/PE - 1.5
Haemoptysis - 1
Malignancy - 1

150
Q

How do you manage a Pulmonary embolism?

A

Initial resuscitation
Oxygen 100%
IV access, monitor closely
Give analgesia if needed
Assess circulation (massive PE if systolic BP <90)
- IF stable: O2, anticoagulation (LMWH), switch to oral warfarin (Maintain INR 2-3), Nalgesia

Embolectomy (Surgically), IVC filters

151
Q

What are the complications of a PE?

A 
Acute bleeding during treatment
Pulmonary infarction
Cardiac arrest/death
Chronic thromboembolic pulmonary hypertesnion
Heparin-associated thrombocytopenia
Recurrent venous thromboembolic event
152
Q

What is sarcoidosis?

A

Multisystem granulomatous (collection of macrophages) inflammatory disorder of unknown cause. Non-caseating therefore no necrosis. Affects lungs, skin and eyes.

153
Q

What is the cause of sarcoidosis?

A

Unknown associated with HLA-DRB1/DQB1

Unknown antigen presented in MHC2 complexes, causing cytokine release and granuloma formation

154
Q

What are the risk factors for sarcoidosis?

A 
20-40 years old
Family history
Scandinavian origin 
Female
Non-smokers
Black ancestry (US)
Puerto rican origin: Lupus pernio
European origin: Erythma nodosum
155
Q

What is Lupus pernio?

A

Chronic raised indurated lesion of the skin
Purplish in colour
Seen on nose, ears, cheeks, lips and forehead

156
Q

What are the signs and symptoms of Sarcoidosis?

A

Fever
Malaise
Weight loss
B/L parotid swelling
Pulmonary symptoms (dry cough and breathlessness)
Musculoskeletal symptoms
Eye symptoms (keratoconjunctivitis sicca, papilloedema)
Neurological symptoms
Cardiac symptoms (non-specific changes in rhythm)

157
Q

What are the skin symptoms of Sarcoidosis?

A

Lupus pernio
Erythema nodosum
Maculopapular eruptions

158
Q

What are the neurological symptoms of sarcoidosis?

A 
Lymphocytic meningitis
Pituitary infiltration
Cerebellar ataxia
Cranial nerve palsies
Peripheral neuropathy
Meningitis
159
Q

What are the invesitgations for Sarcoidosis?

A 
CXR
Serum ACE (Raised)
U&amp;Es (Raised)
AST/ALT (Raised)
Biopsy (Epitheloid cells, multinucleate langerhans cells, mononuclear cells)
Pulmonary functions test
ECG (abnormal)
PPD of tuberculin (negative)
160
Q

What is seen on CXR of someone with Sarcoidosis?

A 
Stage 0 - Normal
Stage 1 - B/L hilar lymphadenopathy
Stage 2 - Stage 1 + pulmonary infiltration
Stage 3 - Only pulmonary infiltrates
Stage 4 - Fibrosis and distortion
161
Q

What is Tuberculosis?

A

Granulomatous disease caused by mycobacterium tuberculosis

162
Q

What are the types of TB?

A

Primary
Miliary
Post-primary TB

163
Q

What is primary TB?

A

Initial infection may be pulmonary or GI (rare)

164
Q

What is miliary TB?

A

Haematogenous dissemination of TB

165
Q

What is Post-primary TB?

A

Caused by reinfection or reactivation

166
Q

What is the causes of tuberculosis?

A

Mycobacterium TB is an intracellular organism
Survives phagocytosis by macrophages.
3 weeks after, cell-mediated immnity leads to granuloma formation around the infected area of the alveoli.
In some cases, TB remains viable but latent and when their immune system is weakened, it reactivates in the upper loves - Miliary TB

167
Q

What does Miliary TB include:

A 
Kidney causing sterile pyuria
Meningitis
Lumbar vertebrae causing pott disease
Adrenals causing addison's
Liver causing hepatitis
Cervical lymph nodes
168
Q

What are the risk factors for Tuberculosis?

A 
Immunocompromised, especially HIV
Low CD4
High ESR
Co-infections
Poor nutrition
High viraemia
169
Q

What are the signs and symptoms for Primary TB?

A 
Mostly asymptomatic
Fever
Malaise
Cough
Wheeze 
Erythema nodosum
Phyloctenular conjunctivitis
170
Q

What are the signs and symptoms of Miliary TB?

A

Fever
Weight loss
Meningitis
Yellow caseious tubercles spread to other organs

171
Q

What are the signs and symptoms of Post-primary TB?

A 
Fever/night sweats
Malaise
weight loss
Breathlessness
Cough
Sputum
Haemoptysis
Pleuritic chest pain
Signs of pleural effusion
Collapse
Consolidation
Fibroids
172
Q

What are the signs and symptoms of Non-pulmonary TB?

A

Occurs mainly in the immunocompromised
Suppuration of cervical lymph nodes leading to abscesses or sinuses
CNS - Meningitis, tuberculoma
Skin - Lupus vulgaris
Heart - Pericardial effusion, constrictive pericarditis
GI - Subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites
Genitourinary - UTI symptoms, renal failure, epididymitis, endometrial or tubal involvement, infertility
Adrenal insufficiency
Bone/joint - osteomyelitis, arthritis, vertebral collapse, spinal cord compression

173
Q

What investigations are done for Tuberculosis?

A 
CXR:
Primary infection (Peripheral consolidation, hilar lymphadenopathy)
Miliary infection (Fine shadowing)
Post-primary (Upper lobe shadowing, streaky fibrosis and cavitation, calcification, pleural effusion, hilar lymphadenopathy)
174
Q

How do you treat TB? (Not in sofia notes 19/20)

A

RIPE
Rifampicin, Isoniazid, Pyrazinamide and ethambutol
First given for 6 months
Second for 2 months only
Sputum cultures repeated during treatment

175
Q

What are the investigations for Asbestos-related lung diseases?

A 
Asbestosis - History and exam
- CXR: Reticular-nodular shadowing +/- pleural plaques
Mesothelioma
- CXR/CT: Pleural thickening/effusion. Bloody pleural fluid. Show pleural mass and rib destruction
- MRI and PET
- Pleural fluid
- Pleural biopsy
- Diagnosis made on histology

Conditions (18 decks)

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