r e s p i r a t o r y Flashcards

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
what is the inheritance pattern being CF
autosomal recessive
26
what are the clinical features of CF
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
27
what are the clinical signs associated with CF
Clubbing ± HPOA  Cyanosis  Bilateral coarse creps
28
what are the common resp organisms in CF
Early  S. aureus  H. influenza Late  P. aeruginosa: 85%  B. cepacia: 4%
29
describe how CF is dx
sweat test: Na and Cl > 60mM  Genetic screening for common mutations  Faecal elastase (tests pancreatic exocrine function)  Immunoreactive trypsinogen (neonatal screening)
30
describe the lx required in CF
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)
31
how is CF managed
``` 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 ```
32
describe the sx of lung Ca
``` Cough and haemoptysis  Dyspnoea  Chest pain  Recurrent or slow resolving pneumonia  Anorexia and ↓wt.  Hoarseness ```
33
what are the signs of lung Ca
``` 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 ```
34
what are the complications of lung Ca
``` 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 ```
35
what are the investigations for lung Ca
``` 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
36
what is type 1 resp failure
PaO2 <8KPa and PaCO2 <6KPa |  V/Q mismatch and diffusion failure
37
what is type 2 resp failure
PaO2 <8KPa and PaCO2 >6KPa |  Alveolar hypoventilation ± V/Q mismatch
38
what are the causes of V/Q mismatch
``` Vascular  PE  PHT  Pulmonary Shunt (R → L)  Asthma (early)  Pneumothorax  Atelectasis ```
39
what are the obstructive causes of alveolar hypoventilation
``` COPD  Asthma  Bronchiectasis  Bronchiolitis  Intra- and Extra-thoracic (Ca, LN, epiglottitis...) ```
40
what are the restrictive causes of alveolar hypoventilation
``` ↓ drive: CNS sedation, trauma, tumour  NM disease: cervical cord lesion, polio, GBS, MG  Chest: flail, kyphoscoliosis, obesity  Fluid and fibrosis ```
41
what are the causes of diffusion failure
``` Fluid  Pulmonary oedema  Pneumonia  Infarction  Blood  Fibrosis ```
42
how do you manage type 1 and type 2 resp failure
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)
43
what are the various types of oxygen masks and how much oxygen do they deliver
``` 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% ```
44
what is the asthma
Episodic, reversible airway obstruction due to bronchial hyper-reactivity to a variety of stimuli.
45
describe the pathophysiology of asthma
Mast cell-Ag interaction → histamine release |  Bronchoconstriction, mucus plugs, mucosal swelling
46
what are the causes asthma
``` 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 ```
47
wear are the sx of asthma
ough ± sputum (often at night)  Wheeze  Dyspnoea  Diurnal variation ̄c morning dipping
48
what are the questions to ask in hx for asthma
``` Precipitants  Diurnal variation  Exercise tolerance  Life effects: sleep, work  Other atopy: hay fever, eczema  Home and job environment ```
49
what are the signs of asthma
``` Tachypnoea, tachycardia  Widespread polyphonic wheeze  Hyperinflated chest  ↓ air entry  Signs of steroid use ```
50
what are the ddx for asthma
Pulmonary oedema (cardiac asthma)  COPD
51
what investigations are required
``` 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
describe general measures behind management asthma
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
describe the drug ladder for chronic asthma
1. SABA 2. SABA + ICS (budesonide) 3. SABA + ICS + LTRA 4. increasing dose of ICS
54
describe the acute management of asthma
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
what defines severe acute asthma
``` any one of  PEFR <50%  RR>25  HR >110  Can’t complete sentence in one breath ```
56
what defines life threatening asthma
``` 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
what defines fatal acute asthma
PCO2 increasing
58
ddx for asthma
pneumothorax acute exacerbation of COPD pulmonary oedema
59
when do you discharge pt after acute asthma attack
Been stable on discharge meds for 24h |  PEFR > 75% ̄c diurnal variability < 20%
60
what things are required in pt with asthma as part of discharge plan
TAME pt.  PO steroids for 5d  GP appointment w/i 1 wk.  Resp clinic appointment w/i 1mo
61
how are pleural effusions classified
Effusion protein < 25g/L = transudate Effusion protein >35g/L = exudate
62
what are the exudative causes of pleural effusions
``` Exudates: ↑ capillary permeability  Infection: pneumonia, TB  Neoplasm: bronchial, lymphoma, mesothelioma  Inflammation: RA, SLE  Infarction ```
63
what are the transudatice causes of pleural effusions
↑ capillary hydrostatic or ↓ oncotic pressure  CCF Renal failure  ↓ albumin: nephrosis, liver failure, enteropathy  Hypothyroidism
64
how do pt with pleural effusion present
Asymptomatic  Dyspnoea  Pleuritic chest pain
65
where the signs of pleural effusion
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
what investigations are required in pleural effusions
``` 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
how do you manage pleural effusion
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
what is usually cause for PE
Usually arise from DVTs in proximal leg or iliac veins Rarely:  Right ventricle post MI  Septic emboli in right sided endocarditis
69
what are the rx factors associated with PE
``` 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
how do pt with PE present
Dyspnoea  Pleuritic pain  Haemoptysis  Syncope
71
what are the signs associated with PE
``` ever  Cyanosis  Tachycardia, tachypnoea  RHF: hypotension, ↑JVP , loud P2  Evidence of cause: DVT ```
72
what investigations are required in PE
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
How is PE dx
``` ssess probability using Wells’ Score 2. Low-probability → perform D-dimers  Negative → excludes PE  Positive → CTPA 3. High probability → CTPA ```
74
what things are done to prevent or reduce risk of PE
Risk assessment for all pts  TEDS  Prophylactic LMWH  Avoid OCP/HRT if @ risk
75
describe the acute management of PE
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
what is a pneumothorax
Accumulation of air in the pleural space ̄c 2O lung collapse
77
what is a tension pneumothorax
air enters pleural cavity through one-way valve | and cannot escape → mediastinal compression.
78
what are the causes of pneumothorax
``` 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
what are the investigations required in pneumothorax
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
what is the acute management of a pneumothorax
Resuscitate pt.  NoCXR  Large bore Venflon into 2nd ICS, mid-clavicular line  Insert ICD
81
what is COPD
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
what are the causes of COPD
Smoking  Pollution  α1ATD
83
what are the sx of COPD
Cough + sputum  Dyspnoea  Wheeze  Wt. loss
84
what are the clinical signs seen in COPD
``` Tachypnoea  Prolonged expiratory phase  Hyperinflation  Wheeze  Cyanosis  Cor pulmonale: ↑JVP , oedema, loud P2 ```
85
destine pink puffers vs blue bloaters in COPD
pink puffers = emPhysema = blue bloaters = chronic bronchitis
86
describe pink puffers COPD
↑ alveolar ventilation → breathless but not cyanosed  Normal or near normal PaO2  Normal or low PaCO2  Progress → T1 respiratory failure
87
describe blue bloaters COPD
alveolar ventilation → cyanosed but not breathless  ↓PaO2 and ↑ PaCO2: rely on hypoxic drive  Progress → T2 respiratory failure and cor pulmonale
88
What score is used in COPD for SOB and what are the stages
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
what are the complications of COPD
``` Acute exacerbations ± infection  Polycythaemia  Pneumothorax (ruptured bullae)  Cor Pulmonale  Lung carcinoma ```
90
what Lx are required in COPD and would each show
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
describe the management of chronic COPD
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
when is LTOT in COPD pt indicated
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
name a surgical option in COPD pts
lung volume reduction
94
describe acute management of COPD exacerbation
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
how does ILD present, clinical characteristics
Dyspnoea  Dry cough  Abnormal CXR / CT  Restrictive Spirometry
96
what are the causes of ILD
``` Environmental: asbestosis, silicosis  Drugs: BANS ME  Bleomycin, Busulfan  Amiodarone  Nitrofurantoin  Sulfasalazine  MEthotrexate, MEthysergide  Hypersensitivity: EAA  Infection: TB, viral, fungi can be idiopathic = IPF ```
97
what are systemic disease associated with ILD
sarcoidosis RA SLE, Sjogren's UC, AS
98
what are the causes of ILD by location ? upper zone?
``` A PENT  Aspergillosis : ABPA  Pneumoconiosis: Coal, Silica  Extrinsic allergic alveolitis  Negative, sero-arthropathy  TB ```
99
what are the causes of ILD by location ? lower zone?
``` STAIR  Sarcoidosis (mid zone)  Toxins: BANS ME  Asbestosis  Idiopathic pulmonary fibrosis  Rheum: RA, SLE, Scleroderma, Sjogren’s, PM/DM ```
100
what are the sx of IPF
``` Dry cough  Dyspnoea  Malaise, wt. loss  Arthralgia  OSA Signs ```
101
What are the signs of IPF
Cyanosis  Clubbing  Crackles: fine, end-inspiratory
102
what are the complications associated with IPF
↑ risk Ca lung |  Type 2 respiratory failure and cor pulmonale
103
Lx required and results expected in IPF
``` 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
how is IPF managed
``` Supportive care  Stop smoking  Pulmonary rehabilitation  O2 therapy  Palliation  Rx symptoms of heart failure  Lung Tx offers only cure ```
105
name 3 industrial lung diseases and their rx factors
coal workers pneumoconiosis silicosis asbestosis
105
name 3 industrial lung diseases and their rx factors
coal workers pneumoconiosis silicosis asbestosis
106
asbestosis has increased risk of ...
mesothelioma
107
how does asbestosis present and what changes are seen on CXR. how is it dx
Chest pain, wt. loss, clubbing, recurrent effusions, dyspnoea. CXR: pleural effusions, thickening  Dx by histology of pleural biopsy  <2yr survival
108
what is pulmonary HTN
108
what is pulmonary HTN
PA pressure greater than 25mmHg
109
what are the causes of pulmonary HTN
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
describe the mechanism of pulmonary HTN via lung parenchyma disease
Chronic hypoxia → hypoxic vasoconstriction  Perivascular parenchymal changes
111
Lx for pulmonary htn
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
what is cor pulmonale
RHF due to chronic PHT
113
what are the sx of cor pulmonale
Dyspnoea  Fatigue |  Syncope
114
what are the signs seen in cor pulmonale
↑ JVP ̄c prominent a wave 2. Left parasternal heave 3. LoudP2±S3 4. Murmurs 5. Pulsatile hepatomegaly 6. Fluid: Ascites + Peripheral oedema
115
lx for cor pulmonale
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
how is cor pulmonale managed
```  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
what is obstructive sleep apnoea
Intermittent closure/collapse of pharyngeal airway → apnoeic episodes during sleep.
118
rx for obstructive sleep apnoea
``` Obesity  Male  Smoker  EtOH  Idiopathic pulmonary fibrosis  Structural airway pathology: e.g. micrognathia  NM disease: e.g. MND Ix ```
119
Lx for obstructive sleep apnoea
SpO2 |  Polysomnography is diagnostic
120
how is it managed
Wt. loss  Avoid smoking and EtOH  CPAP during sleep
121
what are the clinical features of obstructive sleep apnea nocturnal
 Snoring |  Choking, gasping, apnoeic episodes
122
what are the clinical features of sleep apnoea day time
Morning headache  Somnolence  ↓ memory and attention  Irritability, depression
123
complications of sleep apnoea
 Pulmonary hypertension  Type 2 respiratory failure  Cor pulmonale
124
how is sleep apnoea managed
``` wt. loss  Stop smoking  CPAP @ night via a nasal mask  Surgery to relieve pharyngeal obstruction  Tonsillectomy ```
125
advice and management of pt who wants to stop smoking
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