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1
Q

describe the classification of pneumonia anatomically

A

Bronchopneumonia
 Patchy consolidation of different lobes
Lobar Pneumonia
 Fibrosuppurative consolidation of a single lobe
 Congestion → red → grey → resolution

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2
Q

describe the aetiological classification of pneumonia and causative microbes

A

Community Acquired Pneumonia
 Pneumococcus, mycoplasma, haemophilus
 S. aureus, Moraxella, Chlamydia, Legionella
 Viruses: 15%

Hospital Acquired Pneumonia
 >48hrs after hospital admission
 Gm-ve enterobacteria, S. aureus
Pneumonia

Aspiration pneumonia

immunocompromised = usual suspects PCP, TB, fungi, CMV/HSV

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3
Q

what increases risk of aspiration

A

↑ Risk: stroke, bulbar palsy, ↓GCS, GORD, achalasia

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4
Q

what are the sx of pneumonia

A 
Fever, rigors
 Malaise, anorexia
 Dyspnoea
 Cough, purulent sputum, haemoptysis
 Pleuritic pain
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5
Q

what are signs of pneumonia

A 
↑RR, ↑ HR
 Cyanosis
 Confusion
 Consolidation
 ↓ expansion
 Dull percussion
 Bronchial breathing  ↓ air entry
 Crackles
 Pleural rub
 ↑VR
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6
Q

what investigations are required in pneumonia

A 
Bloods: FBC, U+E, LFT, CRP, culture, ABG (if ↓SpO2)  Urine: Ag tests (Pneumococcal, Legionella)
 Sputum: MC&S
 Imaging: CXR
 infiltrates, cavities, effusion  Special
 Paired sera Abs for atypicals
 Mycoplasma, Chlamydia, Legionella
 Immunofluorescence (PCP)  BAL
 Pleural tap
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7
Q

how do you assess severity of pneumonia

A 
Confusion (AMT ≤ 8)
 Urea >7mM
 Resp. rate >30/min
 BP <90/60
 ≥65

score 0-1 - home rx
score 2 hospital rx
score 3 or more = consider ITU

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8
Q

describe the general management for pneumonia

A 
Abx
 O2: PaO2≥8, SpO2 94-98%
 Fluids
 Analgesia
 Chest physio
 Consider ITU if shock, hypercapnoea, hypoxia
 F/up @ 6wks  ̄c CXR
 Check for underlying Ca
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9
Q

what are the abx used in mild, moderate, severe CAP and PCP

A

amoxicillin (or and clarithromycin) for mild/ moderate

severe = co amoxiclav and clarithromycin (add fluclox if staph suspected)

atypical = PCP - tetracycline

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10
Q

what abx are used in HAP

A 
mild = co amoxiclav 
severe = tazocin w vancomycin w gentamicin
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11
Q

what abx are used in aspiration pneumonia

A

co amoxiclav

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12
Q

what vaccination is given against pneumonia and what are the indications for this

A

pneumovax

≥65yrs
 Chronic HLKP failure or conditions
 DM
 Immunosuppression: hyposplenism, chemo, HIV

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13
Q

what are the contraindications to pneumovax

A

CI: P, B, fever

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14
Q

what are the complications of pneumonia

A

resp failure = type 1 and type 2 . manage with oxygen therapy, ventilation

hypotension = dehydration and septic vasodilation. management 250ml fluid challenge over 15min, ITU for inotropes if refractory, central line with iv fluids if no improvement

AF - usually resolves. give digoxin or b-blocker for rate control

pleural effusion = exudate - tap and send for MCS, cytology and chemistry

empyema = USS guided chest drain with abx

lung abscess

sepsis

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15
Q

what are the complications of pneumonia

A

resp failure = type 1 and type 2 . manage with oxygen therapy, ventilation

hypotension = dehydration and septic vasodilation. management 250ml fluid challenge over 15min, ITU for inotropes if refractory, central line with iv fluids if no improvement

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16
Q

describe the pathophysiology of bronchiectasis

A

Chronic infection of bronchi/bronchioles → permanent dilation

Retained inflammatory secretions and microbes → airway damage and recurrent infection

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17
Q

which organisms affect pt with bronchiectasis

A

H. influenza
 Pneumococcus  S. aureus
 Pseudomonas

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18
Q

what are the causes of bronchiectasis

A

causes = idiopathic
congenital = CF, kartagener’s, young’s syndrome
post infectious = measles, pertussis, pneumonia, TB, bronchiolitis

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19
Q

what are the sx of bronchiectasis

A

Persistent cough ̄c purulent sputum
 Haemoptysis (may be massive)
 Fever, wt. loss

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20
Q

what are the signs of bronchiectasis

A 
clubbing
 Coarse inspiratory creps
 Wheeze
 Purulent sputum
 Cause
 Situs inversus (+ PCD = Kartagener’s syn.)  Splenomegaly: immune deficiency
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21
Q

what are the complications of bronchiectasis

A 
Pneumonia
 Pleural effusion
 Pneumothorax
 Pulmonary HTN
 Massive haemoptysis
 Cerebral abscess
 Amyloidosis
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22
Q

what investigations are required

A

Sputum MCS
 Blood: Se Ig, Aspergillus precipitins, RF, α1-AT level
 Test Ig response to pneumococcal vaccine
 CXR: thickened bronchial walls (tramlines and rings)
 Spirometry: obstructive pattern
 HRCT chest
 Dilated and thickened airways
 Saccular dilatations in clusters ̄c pools of mucus
 Bronchoscopy + mucosal biopsy
 Focal obstruction
 PCD
 CF sweat test

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23
Q

how is bronchiectasis managed

A

Chest physio: expectoration, drainage, pulm. rehab
 Abx for exacerbations: e.g. cipro for 7-10d
 Bronchodilators: nebulised β agonists
 Treat underlying cause
 CF: DNAase
 ABPA: Steroids
 Immune deficiency: IVIg
 Surgery may be indicated in severe localised disease

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24
Q

describe the pathophysiology behind CF

A

Mutation in CFTR gene on Chr 7 (commonly ∆F508)
 → ↓ luminal Cl secretion and ↑ Na reabsorption →
viscous secretions.
 In sweat glands, ↓ Cl and Na reabsorption → salty sweat

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25
Q

what is the inheritance pattern being CF

A

autosomal recessive

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26
Q

what are the clinical features of CF

A

Neonate
 FTT
 Meconium ileus
 Rectal prolapse

Children / Young Adults
 Nose: nasal polyps, sinusitis
 Resp: cough, wheeze, infections, bronchiectasis,
haemoptysis, pneumothorax, cor pulmonale
 GI:
 Pancreatic insufficiency: DM, steatorrhoea  Distal Intestinal Obstruction Syndrome
 Gallstones
 Cirrhosis (2O biliary)
 Other: male infertility, osteoporosis, vasculitis

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27
Q

what are the clinical signs associated with CF

A

Clubbing ± HPOA
 Cyanosis
 Bilateral coarse creps

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28
Q

what are the common resp organisms in CF

A

Early
 S. aureus
 H. influenza

Late
 P. aeruginosa: 85%  B. cepacia: 4%

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29
Q

describe how CF is dx

A

sweat test: Na and Cl > 60mM
 Genetic screening for common mutations
 Faecal elastase (tests pancreatic exocrine function)
 Immunoreactive trypsinogen (neonatal screening)

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30
Q

describe the lx required in CF

A

Bloods: FBC, LFTs, clotting, ADEK levels, glucose TT  Sputum MCS
 CXR: bronchiectasis
 Abdo US: fatty liver, cirrhosis, pancreatitis
 Spirometry: obstructive defect
 Aspergillus serology / skin test (20% develop ABPA)

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31
Q

how is CF managed

A 
General
 MDT: physician, GP, physio, dietician, specialist nurse
Chest
 Physio: postural drainage, forced expiratory techniques
 Abx: acute infections and prophylaxis
 Mucloytics: DNAse
 Bronchodilators
 Vaccinate
GI
Advanced Lung Disease
 O2
 Diuretics (Cor pulmonale)
 NIV
 Heart/lung transplantation
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32
Q

describe the sx of lung Ca

A 
Cough and haemoptysis
 Dyspnoea
 Chest pain
 Recurrent or slow resolving pneumonia
 Anorexia and ↓wt.
 Hoarseness
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33
Q

what are the signs of lung Ca

A 
Chest
 Consolidation  Collapse
 Pleural effusion
General
 Cachexia
 Anaemia
 Clubbing and HPOA (painful wrist swelling)
 Supraclavicular and/or axillary LNs
Metastasis
 Bone tenderness
 Hepatomegaly
 Confusion, fits, focal neuro
 Addison’s
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34
Q

what are the complications of lung Ca

A 
Local
 Recurrent laryngeal N. palsy
 Phrenic N. palsy
 SVC obstruction
 Horner’s (Pancoast’s tumour)
 AF
Paraneoplastic  Endo
 ADH → SIADH ( euvolaemic ↓Na+)
 ACTH → Cushing’s syndrome
 Serotonin → carcinoid (flushing, diarrhoea)  PTHrP → 1O HPT (↑Ca2+, bone pain) – SCC
 Rheum
 Dermatomyositis / polymyositis
 Neuro
 Purkinje Cells (CDR2) → cerebellar degeneration  Peripheral neuropathy
 Derm
 Acanthosis nigricans (hyperpigmented body folds)
 Trousseau syndrome: thrombophlebitis migrans

Metastatic
 Pathological #
 Hepatic failure
 Confusion, fits, focal neuro
 Addison’s
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35
Q

what are the investigations for lung Ca

A 
bloods = FB, U+E, Ca, LFTs
cytology = sputum, pleural fluid

Imaging
 CXR. Coin lesion, Hilar enlargement
Consolidation, collapse  Effusion
 Bony secondaries

 Contrast-enhanced Volumetric CT
 Staging: lower neck, chest, upper abdomen

 Consider CT brain
 PET-CT: exclude distant mets
 Radionucleotide bone scan
Biopsy
 Percutaneous FNA: peripheral lesions and LNs
 Bronchoscopy: biopsy and assess operability

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36
Q

what is type 1 resp failure

A

PaO2 <8KPa and PaCO2 <6KPa

 V/Q mismatch and diffusion failure

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37
Q

what is type 2 resp failure

A

PaO2 <8KPa and PaCO2 >6KPa

 Alveolar hypoventilation ± V/Q mismatch

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38
Q

what are the causes of V/Q mismatch

A 
Vascular  PE
 PHT
 Pulmonary Shunt (R → L)
 Asthma (early)
 Pneumothorax
 Atelectasis
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39
Q

what are the obstructive causes of alveolar hypoventilation

A 
COPD
 Asthma
 Bronchiectasis
 Bronchiolitis
 Intra- and Extra-thoracic (Ca, LN, epiglottitis...)
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40
Q

what are the restrictive causes of alveolar hypoventilation

A 
↓ drive: CNS sedation, trauma, tumour
 NM disease: cervical cord lesion, polio, GBS,
MG
 Chest: flail, kyphoscoliosis, obesity
 Fluid and fibrosis
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41
Q

what are the causes of diffusion failure

A 
Fluid
 Pulmonary oedema  Pneumonia
 Infarction
 Blood
 Fibrosis
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42
Q

how do you manage type 1 and type 2 resp failure

A

Type 1
 Give O2 to maintain SpO2 94-98%
 Assisted ventilation if PaO2<8KPa despite 60% O2

Type 2
 Controlled O2 therapy @ 24% O2 aiming for SpO2 88-92% and a PaO2 >8kPa
 Check ABG after 20min
 If PaCO2 steady or lower can ↑ FiO2 if necessary
 If PaCO2 ↑>1.5KPa and pt. still hypoxic, consider
NIV or respiratory stimulant (e.g. doxapram)

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43
Q

what are the various types of oxygen masks and how much oxygen do they deliver

A 
Nasal Prongs: 1-4L/min = 24-40% O2
Simple Face Mask
Non-rebreathing Mask
 Reservoir bag allows delivery of high concentrations of O2.
 60-90% at 10-15L
Venturi Mask = Provide precise O2 concentration at high flow rates  Yellow: 5%
 White: 8%
 Blue: 24%
 Red: 40%
 Green: 60%
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44
Q

what is the asthma

A

Episodic, reversible airway obstruction due to bronchial hyper-reactivity to a variety of stimuli.

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45
Q

describe the pathophysiology of asthma

A

Mast cell-Ag interaction → histamine release

 Bronchoconstriction, mucus plugs, mucosal swelling

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46
Q

what are the causes asthma

A 
Atopy
 T1 hypersensitivity to variety of antigens
 Dust mites, pollen, food, animals, fungus
Stress
 Cold air
 Viral URTI
 Exercise
 Emotion
Toxins
 Smoking, pollution, factory
 Drugs: NSAIDS, β-B
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47
Q

wear are the sx of asthma

A

ough ± sputum (often at night)
 Wheeze
 Dyspnoea
 Diurnal variation ̄c morning dipping

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48
Q

what are the questions to ask in hx for asthma

A 
Precipitants
 Diurnal variation
 Exercise tolerance
 Life effects: sleep, work
 Other atopy: hay fever, eczema
 Home and job environment
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49
Q

what are the signs of asthma

A 
Tachypnoea, tachycardia
 Widespread polyphonic wheeze
 Hyperinflated chest
 ↓ air entry
 Signs of steroid use
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50
Q

what are the ddx for asthma

A

Pulmonary oedema (cardiac asthma)  COPD

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51
Q

what investigations are required

A 
Bloods
 FBC (eosinophila)
 ↑IgE
 Aspergillus serology
CXR: hyperinflation
Spirometry
 Obstructive pattern  ̄c FEV1:FVC < 0.75
 ≥15% improvement in FEV1  ̄c β-agonist
PEFR monitoring / diary
 Diurnal variation >20%
 Morning dipping
Atopy: skin-prick, RAST
52
Q

describe general measures behind management asthma

A

General Measures: TAME
 Technique for inhaler use
 Avoidance: allergens, smoke (ing), dust
 Monitor: Peak flow diary (2-4x/d)  Educate
 Liaise ̄c specialist nurse  Need for Rx compliance  Emergency action plan

53
Q

describe the drug ladder for chronic asthma

A
  1. SABA
  2. SABA + ICS (budesonide)
  3. SABA + ICS + LTRA
  4. increasing dose of ICS
54
Q

describe the acute management of asthma

A

Sit-up
2. 100% O2 via non-rebreathe mask (aim for 94-98%) 3. Nebulised salbutamol (5mg) and ipratropium (0.5mg) 4. Hydrocortisone 100mg IV or pred 50mg PO (or both) 5. Write “no sedation” on drug chart

back to back nebs, consider aminophylline

if lifethreatening = inform ITU, MgSO4 IVI over 20 min, nebs salbutamol every 15 mins monitor ECG

55
Q

what defines severe acute asthma

A 
any one of
 PEFR <50%
 RR>25
 HR >110
 Can’t complete sentence in one breath
56
Q

what defines life threatening asthma

A 
any one of
 PEFR <33%
 SpO2 <92%, PCO2 >4.6kPa, PaO2 <8kPa
 Cyanosis
 Hypotension
 Exhaustion, confusion
 Silent chest, poor respiratory effort
 Tachy-/brady-/arrhythmias
57
Q

what defines fatal acute asthma

A

PCO2 increasing

58
Q

ddx for asthma

A

pneumothorax
acute exacerbation of COPD
pulmonary oedema

59
Q

when do you discharge pt after acute asthma attack

A

Been stable on discharge meds for 24h

 PEFR > 75% ̄c diurnal variability < 20%

60
Q

what things are required in pt with asthma as part of discharge plan

A

TAME pt.
 PO steroids for 5d
 GP appointment w/i 1 wk.
 Resp clinic appointment w/i 1mo

61
Q

how are pleural effusions classified

A

Effusion protein < 25g/L = transudate

Effusion protein >35g/L = exudate

62
Q

what are the exudative causes of pleural effusions

A 
Exudates: ↑ capillary permeability
 Infection: pneumonia, TB
 Neoplasm: bronchial, lymphoma, mesothelioma
 Inflammation: RA, SLE
 Infarction
63
Q

what are the transudatice causes of pleural effusions

A

↑ capillary hydrostatic or ↓ oncotic pressure
 CCF
Renal failure
 ↓ albumin: nephrosis, liver failure, enteropathy
 Hypothyroidism

64
Q

how do pt with pleural effusion present

A

Asymptomatic
 Dyspnoea
 Pleuritic chest pain

65
Q

where the signs of pleural effusion

A

Chest
 Tracheal deviation away from effusion  ↓ expansion
 Stony dull percussion
 ↓ air entry
 Bronchial breathing just above effusion
 ↓VR Associated disease
 Ca: cachexia, clubbing, HPOA, LNs, radiation burn, radiation tattoo
 Chronic liver disease
 Cardiac failure
 RA, SLE
 Hypothyroidism

66
Q

what investigations are required in pleural effusions

A 
Blood: FBC, U+E, LFT, TFT, Ca, ESR  CXR
 Blunt costophrenic angles
 Dense shadow  ̄c meniscus
 Mediastinal shift away
 Cause: coin lesion, cardiomegaly
 US: facilitates tapping  Volumetric CT
Diagnostic Tap
 Percuss upper boarder and go 1-2 spaces below  Infiltrate down to pleura  ̄c lignocaine.
 Aspirate  ̄c 21G needle
 Send for
 Chemistry: protein, LDH, pH, glucose, amylase  Bacteriology: MCS, auramine stain, TB culture  Cytology
 Immunology: SF, ANA, complement
67
Q

how do you manage pleural effusion

A

Rx underlying cause
 May use drainage if symptomatic (≤2L/24h)
 Repeated aspiration or ICD
 Chemical pleurodesis if recurrent malignant effusion  Persistent effusions may require surgery

68
Q

what is usually cause for PE

A

Usually arise from DVTs in proximal leg or iliac veins

Rarely:
 Right ventricle post MI
 Septic emboli in right sided endocarditis

69
Q

what are the rx factors associated with PE

A 
SPASMODICAL
 Sex:F
 Pregnancy
 Age:↑
 Surgery (classically 10d post-op straining at stool)
 Malignancy
 Oestrogen: OCP/HRT
 DVT/PE previous Hx
 Immobility
 Colossal size
 Antiphospholipid Abs
 Lupus Anti-coagulant
70
Q

how do pt with PE present

A

Dyspnoea
 Pleuritic pain
 Haemoptysis
 Syncope

71
Q

what are the signs associated with PE

A 
ever
 Cyanosis
 Tachycardia, tachypnoea
 RHF: hypotension, ↑JVP , loud P2
 Evidence of cause: DVT
72
Q

what investigations are required in PE

A

Bloods: FBC, U+E, clotting, D-dimers
 ABG: normal or ↓PaO2 and ↓PaCO2, ↑pH
 CXR: normal or oligaemia, linear atelectasis
 ECG: sinus tachycardia, RBBB, right ventricular strain
(inverted T in V1-V4)
 S1, Q3, T3 is rare
 Doppler US: thigh and pelvis (+ve in 60%)
 CTPA + venous phase of legs and pelvis
 85-95% sensitivity

73
Q

How is PE dx

A 
ssess probability using Wells’ Score
2. Low-probability → perform D-dimers
 Negative → excludes PE
 Positive → CTPA
3. High probability → CTPA
74
Q

what things are done to prevent or reduce risk of PE

A

Risk assessment for all pts
 TEDS
 Prophylactic LMWH
 Avoid OCP/HRT if @ risk

75
Q

describe the acute management of PE

A
  1. oxygen via non rebreather mask
  2. morphine with metoclopramide
  3. alteplase bolus stat if critically ill with massive PE
  4. LMWH = enoxaprin
  5. SBP reduced = fluids, inotropes
76
Q

what is a pneumothorax

A

Accumulation of air in the pleural space ̄c 2O lung collapse

77
Q

what is a tension pneumothorax

A

air enters pleural cavity through one-way valve

and cannot escape → mediastinal compression.

78
Q

what are the causes of pneumothorax

A 
Spontaneous
 1O: no underlying lung disease
 Young, thin men (ruptured subpleural bulla)  Smokers
 2O: underlying lung disease  COPD
 Marfan’s, Ehler’s Danlos
 Pulmonary fibrosis, sarcoidosis
Trauma
 Penetrating
 Blunt ± rib #s
79
Q

what are the investigations required in pneumothorax

A

ABG
US
CXR (expiratory film may be helpful)
 Translucency + collapse (2cm rim = 50% vol loss)  Mediastinal shift (away from PTX)
 Surgical emphysema
 Cause: rib #s, pulmonary disease (e.g. bullae)

80
Q

what is the acute management of a pneumothorax

A

Resuscitate pt.  NoCXR
 Large bore Venflon into 2nd ICS, mid-clavicular line
 Insert ICD

81
Q

what is COPD

A

Airway obstruction: FEV1 <80%, FEV1:FVC <0.70

 Chronic bronchitis: cough and sputum production on
most days for 3mo of 2 successive years.

 Emphysema: histological diagnosis of enlarged air
spaces distal to terminal bronchioles ̄c destruction of alveolar walls.

82
Q

what are the causes of COPD

A

Smoking
 Pollution
 α1ATD

83
Q

what are the sx of COPD

A

Cough + sputum
 Dyspnoea
 Wheeze
 Wt. loss

84
Q

what are the clinical signs seen in COPD

A 
Tachypnoea
 Prolonged expiratory phase
 Hyperinflation
 Wheeze
 Cyanosis
 Cor pulmonale: ↑JVP , oedema, loud P2
85
Q

destine pink puffers vs blue bloaters in COPD

A

pink puffers = emPhysema =

blue bloaters = chronic bronchitis

86
Q

describe pink puffers COPD

A

↑ alveolar ventilation → breathless but not cyanosed
 Normal or near normal PaO2
 Normal or low PaCO2
 Progress → T1 respiratory failure

87
Q

describe blue bloaters COPD

A

alveolar ventilation → cyanosed but not breathless
 ↓PaO2 and ↑ PaCO2: rely on hypoxic drive
 Progress → T2 respiratory failure and cor pulmonale

88
Q

What score is used in COPD for SOB and what are the stages

A

mMRC Dyspnoea Score

  1. Dyspnoea only on vigorous exertion
  2. SOB on hurrying or walking up stairs
  3. Walks slowly or has to stop for breath
  4. Stops for breath after <100m / few min
  5. Too breathless to leave house or SOB on dressing
89
Q

what are the complications of COPD

A 
Acute exacerbations ± infection
 Polycythaemia
 Pneumothorax (ruptured bullae)
 Cor Pulmonale
 Lung carcinoma
90
Q

what Lx are required in COPD and would each show

A

Bloods: FBC (polycythaemia), α1-AT level, ABG  CXR
 Hyperinflation (> 6 ribs anteriorly)  Prominent pulmonary arteries
 Peripheral oligaemia
 Bullae
 ECG:
 R atrial hypertrophy: P pulmonale  RVH, RAD
 Spirometry: FEV1 <80%, FEV1:FVC <0.70, ↑TLC, ↑RV  Echo: PHT

91
Q

describe the management of chronic COPD

A

General Measures

 Stop smoking
 Specialist nurse
 Nicotine replacement therapy
 Bupropion, varenicline (partial nicotinic agonist)  Support programme
 Pulmonary rehabilitation / exercise  Rx poor nutrition and obesity
 Screen and Mx comorbidities
 e.g. cardiovasc, lung Ca, osteoporosis  Influenza and pneumococcal vaccine
 Review 1-2x/yr
 Air travel risky if FEV1<50%
Mucolytics
 Consider if chronic productive cough
 E.g. Carbocisteine (CI in PUD)
Breathlessness and/or exercise limitation
 SABA and/or SAMA (ipratropium) PRN
 SABA PRN may continue at all stages
Exacerbations or persistent breathlessness
 FEV1 ≥50%: LABA or LAMA (tiotropium) (stop SAMA)
 FEV1 <50%: LABA+ICS combo or LAMA
Persistent exacerbations or breathlessness
 LABA+LAMA+ICS
 Roflumilast / theophylline (PDIs) may be considered
 Consider home nebs

92
Q

when is LTOT in COPD pt indicated

A

Aim: PaO2 ≥8 for ≥15h / day (↑ survival by 50%)
 Clinically stable non-smokers ̄c PaO2 <7.3 (stable on
two occasions >3wks apart)
 PaO2 7.3 – 8 + PHT / cor pulmonale / polycythaemia /
COPD
nocturnal hypoxaemia  Terminally ill pts.

93
Q

name a surgical option in COPD pts

A

lung volume reduction

94
Q

describe acute management of COPD exacerbation

A

4% O2 via Venturi mask: SpO2 88-92%,
 Vary FiO2 and SpO2 target according to ABG
 Aim for PaO2 >8 and ↑ in PCO2 of <1.5kPa
Nebulised Bronchodilators
 Air driven ̄c nasal specs
 Salbutamol 5mg/4h
 Ipratropium 0.5mg/6h
Steroids (IV and PO)
 Hydrocortisone 200mg IV
 Prednisolone 40mg PO for 7-14d
Abx
 If evidence of infection
 Doxy 200mg PO STAT then 100mg OD PO for 5d
NIV if no response = consider back to back nebs very 15 mins

95
Q

how does ILD present, clinical characteristics

A

Dyspnoea
 Dry cough
 Abnormal CXR / CT
 Restrictive Spirometry

96
Q

what are the causes of ILD

A 
Environmental: asbestosis, silicosis
 Drugs: BANS ME
 Bleomycin, Busulfan  Amiodarone
 Nitrofurantoin
 Sulfasalazine
 MEthotrexate, MEthysergide
 Hypersensitivity: EAA
 Infection: TB, viral, fungi
can be idiopathic = IPF
97
Q

what are systemic disease associated with ILD

A

sarcoidosis
RA
SLE, Sjogren’s
UC, AS

98
Q

what are the causes of ILD by location ? upper zone?

A 
A PENT
 Aspergillosis : ABPA
 Pneumoconiosis: Coal, Silica
 Extrinsic allergic alveolitis
 Negative, sero-arthropathy
 TB
99
Q

what are the causes of ILD by location ? lower zone?

A 
STAIR
 Sarcoidosis (mid zone)
 Toxins: BANS ME
 Asbestosis
 Idiopathic pulmonary fibrosis
 Rheum: RA, SLE, Scleroderma, Sjogren’s, PM/DM
100
Q

what are the sx of IPF

A 
Dry cough
 Dyspnoea
 Malaise, wt. loss  Arthralgia
 OSA
Signs
101
Q

What are the signs of IPF

A

Cyanosis
 Clubbing
 Crackles: fine, end-inspiratory

102
Q

what are the complications associated with IPF

A

↑ risk Ca lung

 Type 2 respiratory failure and cor pulmonale

103
Q

Lx required and results expected in IPF

A 
Bloods
 ↑CRP
 ↑Ig
 ANA+ (30%)
 RF+ (10%)
 ABG: ↓PaO2, ↑PaCO2

CXR
 ↓ lung volume
 Bilat lower zone retic-nod shadowing  Honeycomb lung
HRCT
 Shows similar changes to CXR 
 More sensitive

Spiro

 Restrictive defect  ↓ transfer factor

104
Q

how is IPF managed

A 
Supportive care
 Stop smoking
 Pulmonary rehabilitation
 O2 therapy
 Palliation
 Rx symptoms of heart failure
 Lung Tx offers only cure
105
Q

name 3 industrial lung diseases and their rx factors

A

coal workers pneumoconiosis
silicosis
asbestosis

105
Q

name 3 industrial lung diseases and their rx factors

A

coal workers pneumoconiosis
silicosis
asbestosis

106
Q

asbestosis has increased risk of …

A

mesothelioma

107
Q

how does asbestosis present and what changes are seen on CXR. how is it dx

A

Chest pain, wt. loss, clubbing, recurrent effusions, dyspnoea.

CXR: pleural effusions, thickening
 Dx by histology of pleural biopsy
 <2yr survival

108
Q

what is pulmonary HTN

108
Q

what is pulmonary HTN

A

PA pressure greater than 25mmHg

109
Q

what are the causes of pulmonary HTN

A

left heart disease = mitral stenosis, mitral regurgitation, LVF, left to right shunt

lung parenchymal disease = COPD, asthma, ILD, CF, bronchiestasis

pulmonary vascular disease = idiopathic pulmonary HTN, sickle cell, PE, portal HTN

hypoventilation - morbid obesity, MND, polio

110
Q

describe the mechanism of pulmonary HTN via lung parenchyma disease

A

Chronic hypoxia → hypoxic vasoconstriction  Perivascular parenchymal changes

111
Q

Lx for pulmonary htn

A

ECG

 P pulmonale  RVH

Echo
 Velocity of tricuspid regurgitation jet
 Right atrial or ventricular enlargement  Ventricular dysfunction
 Valve disease

Right heart catheterisation: gold standard
 Mean pulmonary artery pressure

112
Q

what is cor pulmonale

A

RHF due to chronic PHT

113
Q

what are the sx of cor pulmonale

A

Dyspnoea  Fatigue

 Syncope

114
Q

what are the signs seen in cor pulmonale

A

↑ JVP ̄c prominent a wave 2. Left parasternal heave

  1. LoudP2±S3
  2. Murmurs
  3. Pulsatile hepatomegaly
  4. Fluid: Ascites + Peripheral oedema
115
Q

lx for cor pulmonale

A

Bloods: FBC, U+E, LFTs, ESR, ANA, RF  ABG: hypoxia ± hypercapnoea
 CXR

 ECG: P pulmonale + RVH
 Echo: RVH, TR, ↑ PA pressure
 Spirometry
 Right heart catheterisation

116
Q

how is cor pulmonale managed

A 
 Rx underlying condition
 ↓ pulmonary vascular resistance
LTOT
CCB: e.g. nifedipine
 Sildenafil (PDE-5 inhibitor)
Prostacycline analogues
Bosentan (endothelin receptor antagonist)

 Cardiac failure
 ACEi + β-B (caution if asthma)  Diuretics

 Heart-Lung Tx

117
Q

what is obstructive sleep apnoea

A

Intermittent closure/collapse of pharyngeal airway → apnoeic episodes during sleep.

118
Q

rx for obstructive sleep apnoea

A 
Obesity
 Male
 Smoker
 EtOH
 Idiopathic pulmonary fibrosis
 Structural airway pathology: e.g. micrognathia
 NM disease: e.g. MND
Ix
119
Q

Lx for obstructive sleep apnoea

A

SpO2

 Polysomnography is diagnostic

120
Q

how is it managed

A

Wt. loss
 Avoid smoking and EtOH
 CPAP during sleep

121
Q

what are the clinical features of obstructive sleep apnea nocturnal

A

 Snoring

 Choking, gasping, apnoeic episodes

122
Q

what are the clinical features of sleep apnoea day time

A

Morning headache
 Somnolence
 ↓ memory and attention
 Irritability, depression

123
Q

complications of sleep apnoea

A

 Pulmonary hypertension
 Type 2 respiratory failure
 Cor pulmonale

124
Q

how is sleep apnoea managed

A 
wt. loss
 Stop smoking
 CPAP @ night via a nasal mask
 Surgery to relieve pharyngeal obstruction
 Tonsillectomy
125
Q

advice and management of pt who wants to stop smoking

A

Ask: enquire as to smoking status
 Advise: best way to stop is with support and medication
 Act: provide details of where to get help
 E.g. NHS stop smoking helpline

 Refer to specialist stop smoking service
 Nicotine replacement
Gum or Patches

 Varenicline: selective partial nicotine receptor agonist

bupropion

M E D (18 decks)

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