Respiratory AS Flashcards

1
Q

What are the stages of clubbing?

A

Important nail sign of systemic disease linked with underlying pulmonary, cardiovascular, neoplastic etc.

Described as bulbous uniform swelling of soft tissue of the terminal phalanx of digit between nail and nail bed.

  1. Periungual erythema and softening of the nail bed (Bogginess + fluctuance of nail bed).
  2. increase in angle between proximal nail fold and nail plate. (loss of concave nail fold angle
  3. increased longitudinal and transverse curvature
  4. soft tissue expansion at distal phalanx (drumstick)
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2
Q

Causes of Clubbing?

A
Respiratory 
- Carcinoma (Bronchial + Mesothelioma) 
- Chronic lung suppuration Empyema, abscess
Bronchiectasis, CF
- Fibrosis 
Idiopathic pulmonary fibrosis
TB

Cardiac

  • Infective endocarditis
  • Congenital cyanotic heart disease
  • Atrial myxoma

GIT

  • Cirrhosis
  • Crohns’ UC
  • Coeliac
  • Cancer: GI lymphoma
Other
- Familial 
- Thyroid acropachy 
- Upper limb AVMs or aneurysm
Unilateral clubbing
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3
Q

What is cyanosis?

A

Blue discolouration of mucosal membranes or skin

Deoxygenated Hb >5g/dl

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4
Q

Classification of cyanosis?

A

Peripheral: cold, blue nails
Central: blue tongue, lips

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5
Q

Causes of cyanosis? Pathophysiology

A

Think of O2 cascade - The OC is the process of diminishing or declining O2 tension from the atmospheric environment down to the cellular level, specifically the mitochondria.

As it moves down through the body to the cell, O2 will be diluted down, extracted or lost, so that at cellular level the PO2 may be 3 or 4 mm/Hg.

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6
Q

Causes of Cyanosis

A

Respiratory

  • Hypoventilation: COPD, MSK
  • Decreased diffusion: Pulmonary oedema, fibrosing alveolitis
  • V/Q mismatch: PE, AVM (HHT) - Some areas of the lungs receive perfusion but no oxygen, or some receive oxygen but no perfusion.
  • inadequate transport of oxygen by haemoglobin

Cardiac

  • Congenital: Transposition of great arteries, Tetralogy of Fallot
  • Decreased Cardiac Output: Mitral stenosis, Systolic LVF
  • Vascular: Raynaud’s, DVT

RBC
- Low affinity Hb, may be hereditary or acquired

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7
Q

What is pneumonia?

A

Inflammation of the lungs with consolidation or interstitial lung infiltrates, categorised by causative organism.

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8
Q

Anatomical classification of pneumonia?

A

Bronchopneumonia
- Patchy consolidation of different lobes

Lobar Pneumonia

  • Fibrosuppurative consolidation of a single lobe
  • Congestion (vasculuar congestion + alveolar oedema) –> red (erythrocytes, neutrophils, desquamated epithelial cells)–> grey (fibrinopurulent exudate) –> resolution
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9
Q

Aetiological classification - community acquired pneumonia? Organisms?

A
  • Pneumonia acquired outside hospital.
  • Group of signs + symptoms related to LRTI with fever >38, cough, expectoration, chest pain, dyspnoea, and signs of invasion of alveolar space.

Typical Bacteria

  • Streptococcus Pneumoniae (most common CAP).
  • Haemophilus influenza
  • Staphylococcus aureus
  • Moraxella Catarrhalis

Atypical bacteria

  • Mycoplasma pneumoniae
  • Chlamydophilia pneumoniae
  • Legionella pneumophilia
  • Chlamydia psittaci

Virus

  • Influenza A/B
  • RSV
  • Adeno/Rhin
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10
Q

Aetiological classification - Hospital Acquired Pneumonia? Organisms?

A

HAP is an acute LRTI this is by definition acquired after at least 48hr of admission to hospital and is not incubated at time of admission.

Bacteria cause most HAP (mostly aerobic gram-negative bacilli)

  • Pseudomonas Aeruginosa
  • Escherichia coli
  • Klebsiella Pneumoniae
  • Acinetobacter
  • MRSA
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11
Q

Aetiological classification - Aspiration Pneumonia?

A

= Results from inhalation of oropharyngeal content into lower airways that leads to bacterial infection. Commonly due to recent intubation on ITU.

  • Commonly due to altered swallow/gag. increased risk from patients with stroke, bulbar palsy, decreased GCS, GORD, Achalasia.
  • Aspiration causes an inflammatory reaction called pneumonitis, results in damage to lung parenchyma. Leads to inflammatory reaction and ultimately aspiration pneumonia.
  • Often Strep Pneumoniae, Staphylococcus aureus, Haemophilus influenza, Pseudomonas aeruginosa.
  • Used to be anaerobes (Bacteroides, Porphyromonas).
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12
Q

Immunocompromised Pneumonia?

A

Pneumocystis Jirovecii Pneumonia (PCP), Aspergillosis, TB, CMV/HSV.

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13
Q

Symptoms of Pneumonia?

A
  • Fever, Rigors
  • Malaise, anorexia
  • Dyspnoea
  • Cough, purulent sputum, haemoptysis
  • Pleuritic pain
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14
Q

Signs of Pneumonia?

A
  • Increased RR
  • Increased HR
  • Cyanosis
  • Confusion
  • Consolidation (filled with liquid not air)
    Decreased expansion
    Dull Percussion
    Bronchial breathing
    Decreased air entry
    Crackles
    Pleural rub
    Increased vocal fremitus
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15
Q

Risk factors of pneumonia?

A
Age >65
COPD
Exposure to ciggy smoke
Alcohol abuse
HIV
use of steroids, antipsychotics, PPIs.
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16
Q

Investigations for Pneumonia?

A

Bloods: FBC (WBC) , U+E (severity scoring),
LFT (risk factor for patients with cirrhosis, CLD),
CRP (raised) - normally lags in comparison to WCC in treatment of bacterial infection.
Culture (pre-treatment),
ABG (if SpO2 to indicate severity) low, glucose can be elevated.

Urine: Ag test (pneumococcal, legionella)
Sputum: MC+S
Imaging: CXR (infiltrates, cavities, effusion, consolidation)

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17
Q

Special Tests of Pneumonia?

A
Special test 
- Paired sera Abs for atypicals 
Mycoplasma, Chlamydia, 
Legionella 
- Serum Procalcitonin
- Immunofluorescence (PCP) 
- BAL 
- Pleural tap - pleural effusion
- Rapid antigen testing for virus)
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18
Q

Assess severity of pneumonia?

A

Severity: CURB-65 (only if x-ray changes)

  • Confusion (AMT <8)
  • Urea >7
  • resp Rate >30/ mins
  • BP <90/60
  • > 65 yr old

Score of 0-1 –> home management
2 –>Hospitalisation
3-5 –> ICU admission 30 day mortality 15-30%.

CRP < 20 mg/L - do not routinely offer antibiotic therapy
CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
CRP > 100 mg/L - offer antibiotic therapy

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19
Q

General Management of pneumonia - Outpatient?

A
  • Consider limitations of severity score
    Ability to maintain oral intake, history of substance abuse, severe comorbid illness, cognitive impairment, impaired functional status, availability of outpatient support resources
  • Advise not to smoke, to rest, stay hydrated.
  • Advise them to report any chest pain, SOB or lethargy.
  • Reassess at 48hrs.
  • Repeat examination after 10-14 days
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20
Q

General Management of pneumonia - Inpatient?

A
- If hospital admission needed
Abx 
O2: Pa02 >8, SpO2 94-98% 
Monitor Sats
Fluids
Analgesia
Chest Physio
Consider ITU if shock, hypercapnea, hypoxia

F/up @ 6 weeks with CXR to allow for radiological changes.

Do not routinely discharge if in the past 24hr they have 2 more more

  • Temp 37.5
  • RR 24
  • HR >100
  • SBP 90
  • O2 <90
  • Abnormal mental status

1 week - Fever should be gone
4 weeks - chest pain + sputum production should have substantially reduced
6 weeks - cough + breathlessness reduced
3 months - most symptoms resolved maybe some fatigue
6 months - most feeling normal

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21
Q

Antibiotic management for outpatient pneumonia?

A

If CURB-65 = 0
Amoxicillin - 1g PO TDS OR doxycycline 100mg PO BDS OR clarithromycin 500mg PO BDS (where resistance)

If CURB-65 1 or 2 = Amoxicillin + clarithromycin OR doxycyclin 200mg on first day.

  • Consider influenza antiviral cover (Tamiflu)

If comorbidies (DM, chronic heart, liver, renal disease give co-amoxiclav + clarithyromycin

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22
Q

Antibiotic management for inpatient pneumonia?

A
  • IV cefuroxime/ceftriaxone (1-2g IV every 8hr, every 24hr for ceftriaxone) + clarithromycin 500mg orally BDS.
  • Add fluclox if staph suspected.
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23
Q

Antibiotics for MRSA cover?

A

Vancomycin (15mg/kg IV every 12hrs) - consider teicoplanin.
Linezolid (600mg IV every 12hrs) (second line.

MRSA swabbing - nasal and skin lesion or wounds.

Suppression of MRSA once carrier found - mupirocin in white soft paraffin.
Chlorhexidine gluconate.

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24
Q

Antibiotics for pseudomonas cover?

A

Tazocin 4.5mg IV every 6hr

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25
Atypical bacterial pneumonia management?
Generally speaking - Clarithromycin Azithromycin 500mg orally, then 250mg OD for 4 days - For Psittacosis and Q fever (Coxiella burnetii) use doxycyline 100mg orally - Legionella/Chlamydia pneumonia - Azithromycin 500mg, levofloxacin 750mg OD, IV - PCP - Co-trimoxazole 80/400mg (trimethoprim + sulfamethoxazole)
26
Hospital-acquired pneumonia management?
If within 5 days of admission. First line - Non severe = Co-amoxiclav 500/125mg 3x a day then review. Then consider Doxycyline/Cefalexin. ``` If more than 5 days after admission. If septic/high risk of resistance - PipTaz - Ceftriaxone - Meropenem ``` If patient has no risk factor for resistance pathogen - likely to be Strep Pneumonia, Haemophilis influenza, Staph A, E.coli, Klebsiella, Enterobacter, Proteus. - Pseudomonas management = tazocin/ceftazidime. Severe HAP - Likely to be Pseudomonas aeruginosa, K pneuonaemia (ESBL), Acinetobacter, MRSA, Legionella. Need Ceftazidime, imipenem/meropenem, piptaz. OR Tazocin ± vanc ± gent for 7 days.
27
Antibiotic for gram negative HAPS (Pseudomonas, Klebsiella)
``` Cephalosporin - ceftazidime Carbapenam - meropenem/ imipenem/colastatin Beta-lactamase inhibitor (pip-taz) Fluoroquinolone (cipro/levofloxacin) Gentamicin ```
28
Antibiotics with gram positive pathogen HAPS?
MRSA = Vancomycin or linezolid
29
ESBL HAP?
Carbapenem | Then Fluoroquinolone
30
Pneumovax?
Vaccine for pneumococcus for hi-risk adults. >65 yrs old Chronic renal, heart, kidney failure or conditions DM Immunosuppression: hyposplenism, chemo, HIV CI: P, B, Fever Revaccinate every 5yrs
31
Complications of Pneumonia - respiratory failure?
Respiratory Failure - Type 1: PaO2 <8kPa + PaCO2 <6kPa (acute hypoxic respiratory failure) - Type 2: PaO2 <8kPa + PaCO2 >6kPa (hypercapnic resp failure + hypoxia). Type 1 - Severe hypoxaemia (fluid in alveoli, collapse of alveoli etc) Type 2 - Hypercapnic (poor ventilatory muscle, obstruction of airways (COPD), secretion in small airways (Cystic fibrosis) Management: oxygen, ventilation
32
Other complications of pneumonia - Hypotension?
Hypotension - septic vasodilation + Dehydration - Management = if SBP <90 --> Fluid challenge 250ml over 15mins If no improvement: central line + IV fluids If refractory: ITU for inotropes
33
Other complications of pneumonia - AF?
Usually resolves with Rx | Management: digoxin or B-B for rate control
34
Other complications of pneumonia - pleural effusion?
Indicator of pneumonia severity. - Exudate - Mx: tap and send for MC+S, cytology and chemistry Complicated pleural effusion - Should be treated, on its way to becoming an empyema. f
35
Other complications of pneumonia - Empyema?
- Pus in the pleural space - Associated with pneumonia. - Patients have signs of infection and a significant pleural effusion. - Anaerobes, Staph, Gm-ve - Assoc with recurrent aspiration - Pt with resolving pneumonia develops recurrent fever - Tap : turbid, pH <7.2, decreased glucose, increased LDH Management: US guided chest drain must be inserted+ Abx.
36
Lung Abscess causes?
A circumscribed collection of pus in lung leading to cavity formation usually with an air-fluid level visible on chest x-ray. - Aspiration (altered consciousness + NG tubes) - Bronchial obstruction: tumour, foreign body - Septic emboli: sepsis, IVDU, RH endocarditis - Pulmonary infarction and secondary infection - Subphrenic/hepatic abscess - Complication of pneumonia
37
Features of a lung abscess?
- Swinging fever (high grade) - Cough, foul purulent sputum (indicative of anaerobes) - haemoptysis - Murmur due to cardiac murmur (bacterial endocarditis) - Cavernous breath sounds - Malaise, weight loss - Pleuritic pain - Clubbing - Empyema
38
Tests for a lung abscess?
- Blood: FBC (WBC), ESR, CRP, cultures - Sputum: micro, culture, cytology - CXR: cavity with fluid level, consolidation with central cavitation and air-fluid level. - Consider CT and bronchoscopy - usually a round cavity with irregular margins - no signs of compression of surrounding lung. - Bronchoscopy (proximal airway obstruction by tumour).
39
Management of lung abscess?
- Abx according to sensitivies (ceftriaxone + clindamycin) - Aspiration + postural drainage. - Surgical excision
40
Other complications of pneumonia?
- Sepsis - Pericarditis/myocarditis - Jaundice (usually cholestatic) due to sepsis, drugs (fluclox, augmentin), mycoplasma, legionella.
41
Sepsis criteria?
Updated version: Low risk - Normal RR (<21), BP (SBP >100), HR (<90), Urine output, temp, no non-blanching rash. Moderate risk / (high risk) - Altered behaviour - Impaired immunity, trauma or surgery - RR 21-24 (high = >25) - SBP 91-100 (high = <90) - HR 91-130 (high = >130) - No urine passed in previous 12-18 hrs. - Signs of infection - Mottled appearance/ non-blanching rash Outdated version >2 = - Temperature >38 or <36, - HR >90 - RR >20, or PaCo2 <4.6 - WCC: >12x10^9, <4 x10^9
42
Sepsis definition?
SIRS caused by infection (Systemic inflammatory response syndrome)
43
Severe sepsis definition
Sepsis with at least 1 organ dysfunction or hypoperfusion
44
Septic shock
Severe sepsis with refractory hypotension - (persistent hypotension requiring vasopressors to maintain MAP >65 - Serum lactate level >2mmol despite adequate volume resuscitation
45
Specific pneumonia - pneumococcus - gram positive diplococcus
RF: Elderly, EToH, immunosuppresed, CHF, pulmonary disease. Rapid onset, high fever, pleuritic chest pain, herpes labialis. Pulmonary features: Lobar consolidation. Extrapulmonary: Herpes labialis. Causes reactivation of herpes simplex virus resulting in cold sores. Management - Amoxicillin, BenPen, cephalosporins
46
Specific pneumonia | - S.aureus?
RF: Influenza infection, IVDU, Co-morbidities. Commonly occurs after patients have had an influenza virus. Pulmonary features - Bilateral cavitating bronchopneumonia Management: Fluclox or Vanc alongside amoxicillin.
47
Specific pneumonia | - Klebsiella?
RF: Rare, elderly, ETOH, DM Pulmonary features: cavitating pneumonia, especially upper lobes. Red-currant jelly sputum. May also cause an empyema Management: Cefotaxime
48
Specific pneumonia | - Pseudomonas?
RF: Bronchiectasis, CF Management: Taz
49
Specific pneumonia | - Mycoplasma
RF: epidemics Prolonged onset. Pulmonary features: Dry cough, reticulo-nodular shadowing or patchy consolidation Extra-pulmonary - Flu-like prodrome: headache/myalgia/arthralgia - Known to cause immune-mediated neurological disease. May also cause paraesthesia or neuropathic pain. - Haemolysis Presents with erythema multiforme. ``` Cold agglutinins --> AIHA (Autoimmune haemolytic anaemia) Cryoglobulin Erythema multiforme SJS GBS Hepatitis ``` Diagnosis: Serology. X-ray shows bilateral consolidation on x-ray. Typically does not respomd to penicillin or cephalosporin. Treatment: Doxy/Clarithro/Cipro
50
Specific pneumonia | - Legionella?
RF: Travel, Air conditioning Pulmonary Features: Dry Cough/Dyspnoea, bi-basal consolidation Extra-pulmonary: flu-like prodrome, anorexia, D+V, hepatitis, renal failure, confusion, SIADH --> Decreased Na. Management: lymphopenia, decreased Na, deranged LFTs. Dx: urinary antigen or serology Clarithro ± rifampacin
51
Specific pneumonia | - Chlamydia pneumoniae?
Pulmonary Features: Pharyngitis, otitis --> pneumonia Extrapulmonary: Sinus pain Management: diagnosis with serology, then clarithromycin
52
Specific pneumonia | - Chlamydia psittica?
RF: Parrots Pulmonary features: Dry cough, patchy consolidation Extra-pulmonary: Horder's spots ~ rose spots. Splenomegaly, epistaxis, hepatitis, nephritis, meningo-encephalitis. Dx: serology then clarithro
53
Specific pneumonia | - PCP?
- Immunocompromised/HIV - Pulmonary Features Dry Cough, exertional dyspnoea, bilateral creps - CXR: normal or bilateral perihilar interstitial shadowing Dx: Diagnosed from induced sputum - Visualisation from BAL, Sputus, biopsy High dose co-trimoxazole or pentamidine Prophylaxis if CD4 <200 or after 1st attack.
54
What is bronchiectasis?
- Permanent dilation of Bronchi due to destruction of the elastic and muscular components of the bronchial wall. Often causes as a consequence of recurrent and/or severe infections secondary to underlying disorder. - Majority of patients will present with a chronic cough and sputum production. - Retained inflammatory secretions and microbes --> airway damage + recurrent infection - Because of H.influenza, pneumococcus, s.aureus, pseudomonas
55
Cause of bronchietasis
- Idiopathic in 50% - Congenital CF (mainly upper lobe infiltration) Kartagener's/PCD Young's syndrome (azoospermia + bronchiectasis). May also have dextrocardia. May also have recurrent sinusitis. - Post-infectious Measles, pertussis, pneumonia, TB, bronchiolitis ``` - Immunodeficiency Hypogammaglobulinaemia X-linked agammaglobulinaemia: Bruton's CVID IgG subclass deficiency IgA HIV ``` - Allergic bronchopulmonary aspergillosis - Bronchial obstruction: LNs, tumour, foreign body - Connective Tissue Disorders RA Sjogren's - IBD UC, Crohns ``` - Yellow nail syndrome Yellow nail discoloration and dystrophy Lymphoedema Pleural effusion Bronchiectasis ```
56
Symptoms of bronchiectasis?
Presence of RF: cystic fibrosis, immunodeficiency, previous infection, PCD, alpha-1 antitrypsin, IBD. - Persistent cough with purulent sputum - Haemoptysis - Fever - Weight loss - Dyspnoea
57
Signs of bronchiectasis?
- Clubbing - Coarse inspiratory crepitation/crackles - squeaks and pops - Crackles - Wheeze - Purulent sputum - Cause Situs Inversus (+PCD = Kartagener's syndrome) Splenomegaly: immune deficiency
58
Complications of bronchiectasis?
- Pneumonia - Pleural effusion - Pneumothorax - Pulmonary HTN - Massive haemoptysis - Cerebral abscess - Amyloidosis
59
Investigations for bronchiectasis?
- Sputum MCS (gram-positive/gram-negative) - Bloods: FBC: WBC (eosinophil high = bronchopulmonary aspergillosis, neutrophilia may be infection) NNO level in primary ciliary dyskinesia Aspergillus precipitins, RF, a1-AT level Test Ig response to pneumococcal vaccine - Sweat chloride test (abnormal test >60mmol/L CF is likely) ± CFTR protein gene mutation. - CXR: thickened bronchial walls (tramlines and rings) - Spirometry: obstructive pattern (reduced FEV1, elevated RV/TLC) (obstructive = COPD, Asthma, Emphysema, bronchiectasis) = Restrictive (FEV1 reduced, FVC reduced (FEV1/FVC ratio normal (>0.7). due to pulmonary fibrosis, pulmonary oedema, lobectomy, parenchymal lung tumours, guillian barre, myasthenia gravis, motor neuron disease, ARDS, Sarcoidosis) - HRCT chest CT (High resolution) - thickened, dilated airways with/without air fluid levels. Cysts and/or tree-in-bud pattern. - Bronchoscopy + mucosal biopsy: Focal obstruction PCD
60
Management of bronchiectasis?
- Chest physio: Expectoration, draining, pulmonary rehab (postural drainage, percussion, vibration). - ABx for exacerbations: e.g cipro for 7-10days - Consider azithromycin for pseudomonas - Bronchodilators: nebulised salbutamol/ipratroprium/tiotropium - Inhaled hypertonic saline - Treat underlying cause CF: DNAase ABPA: Steroids ±azole antifungal Immune deficiency; IVIg or Inhaled tobramycin/gentamicin - infected with pseudomonas. - Consider surgery for those with recurrent infections, severe haemoptysis or focal disease. This can be resection of bronchiectatic area. or lung transplant in patients with FEV <30% or a rapid decline in FEV.
61
What is the pathogenesis of cystic fibrosis?
- Autosomal recessive - Mutation of CFTR gene on Chr 7 (delta F508) (anion channel found in the apical membrane of epithelial cells) - decrease luminal CL secretion and increase Na reabsorption --> Viscous secretions - In sweat glands, decreased Cl and Na reabsorption --> salty sweat
62
Clinical features of cystic fibrosis in neonates?
- FTT (failure to thrive) - Meconium ileus - Rectal prolapse
63
Clinical features of cystic fibrosis in children/young adults - NOSE?
- Nose: nasal polyps, sinusitis
64
Clinical features of cystic fibrosis in children/young adults - Resp?
- Resp: cough (prolonged colds, coughing) , wheeze, recurrent infection, bronchiectasis, haemoptysis, pneumothorax, cor pulmonale
65
Clinical features of cystic fibrosis in children/young adults - GI + other?
GI - Pancreatic insufficiency: DM, steatorrhoea, voracious appetite - Distal intestinal obstruction syndrome - Gallstones - Cirrhosis (secondary to biliary obstruction)/ Splenomegaly Other - Male infertility, osteoporosis, vasculitis - CLUBBING
66
Signs of Cystic fibrosis?
- Clubbing ± HPOA (hypertropic osteoarthropathy) - Cyanosis - Bilateral coarse crackles
67
Common respiratory organism in Cystic Fibrosis?
- Early S.aureus H.influenza Late - P.aeruginosa: 85% - B.cepacia: 4%
68
Diagnosis of cystic fibrosis?
- Sweat test: Na and Cl >60mM - Genetic screening for common mutations - Faecal elastase (tests pancreatic exocrine function) - Immunoreactive trypsinogen (neonatal screening)
69
Investigations of cystic fibrosis.
- 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)
70
Management of Cystic Fibrosis - General?
- MDT: Physician, GP, Physio, dietician, specialist nurse - Neonate management? lactulose to avoid obstruction.
71
Chest management for cystic fibrosis?
- Physio: postural drainage, forced expiratory techniques - Abx: acute infections and prophylaxis (inhaled tobramycin or IV tobramycin/piptaz/ceftazatidime). - Mucolytics: DNAse (dornase alfa + hypertonic saline inhaled. - Bronchodilators (salbutamol in inhaler) - Vaccinate
72
GI management for cystic fibrosis?
- Pancreatic enzyme replacement: pancreatin (Creon) - ADEK supplements Insulin - Urosdeoxycholic acid for impaired hepatic function (stimulates bile secretion) Oral bile acids. - PPI or Antacid to produce more alkaline environent for pancreatic enzyme supplement.
73
Management of advanced lung disease in cystic fibrosis?
- O2 - Diuretics for cor pulmonale - NIV - Heart/lung transplantation
74
Other management requirements for cystic fibrosis?
- Management of complications: e.g DM - Fertility and genetic counselling - DEXA osteoporosis screen
75
What are the pulmonary aspergillus diseases?
1. Asthma: T1HS reaction to spores 2. ABPA Hypersenstivity reaction to aspergillus antigens. Typically seen in patients with longstanding asthma 3. Aspergilloma (mycetoma Intracavity mass in the lung consistent of massos of aspergillus mycelia. 4. Invasive aspergillosis Local and systemic infiltration (in immunocompromised patients) 5. Extrinsic Allergic Alveolitis
76
What is Allergic Bronchopulmonary aspergillosis?
T1 and T3 HS reaction to Aspergillus fumigatus - Bronchoconstricton --> Bronchiectasis - Patients usually have a prior diagnosis of atopy, asthma or cystic fibrosis. - Presents with broncial obstruction, airway inflammation leading to bronchiectasis, fibrosis and respiratory compromise.
77
Symptoms of ABPA?
- Wheeze (underlying asthma and bronchial hyperreactivity) - Productive cough - Dyspnoea - Mucus plugs RF: History of Asthma/CF
78
Investigations for ABPA?
- CXR: bronchiectasis (upper and middle lobe infiltrates) - Aspergillus in sputum (black on silver stain) - Aspergillus skin test of IgE RAST (positive wheal and flare reaction) - Increased IgE and increased eosinophils
79
Management of ABPA?
- Pred 40mg/d + itraconazole for acute attacks (200mg) - Environmental control - Pred maintenance 5-10 mg/d - Bronchodilators for asthma
80
What is an aspergilloma (mycetoma)
- Fungus ball within a pre-existing cavity (TB or sarcoid)
81
Features of aspergilloma?
Usually asymptomatic Can --> Haemoptysis (may be severe) Lethargy, decreased weight
82
Investigations for aspergilloma?
- CXR: round opacity within a cavity, usually apical - Sputum culture - Aspergillus skin test/RAST
83
Management of aspergilloma?
Consider exicision for solitary lesions/severe haemoptysis
84
What is invasive aspergillosis?
Causes by filamentous fungi of the Aspergillus species. | Aflatoxins --> Liver cirrhosis and HCC (especially A.flavus)
85
What are the risk factors for Invasive Aspergillosis?
Immunocompromise: HIV, leukaemia, Wegener's | post-broad spectrum abx
86
Investigations of invasive aspergillosis?
- CXR: consolidation, abscess, cavities - Sputum MCS - Aspergillus species - BAL - show hypal elements or aspergillus - Serial galactomannan (two positive results)
87
Management of Aspergillosis?
Voriconazole for confirmed or amphotericin B for suspected.
88
What is Extrinsic Allergic Alveolitis?
= Inflammation of alveoli and sital bronchiales caused by immune response to inhaled allergens. - Occupational exposure to organic dust. - Sensitivity to aspergillus clavatus --> Malt worker's lung - Bird fancier's lung - Famer's lung: Saccharopolyspora rectivirgula - Mushroom workers: thermophilic actinomycetes
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Key points in a history for EAA? (as part of a hypersensitivty pneumonitis)
- Exposure to avian protein antigen - Mould in work environment - Occupational exposure to chemicals - Productive/non-productive cough. - Fevers, malaise, weight loss, diffuse rales, clubbing. - Restrictive picture - Chest x-ray: upper/mid-zone fibrosis - Bronchoalveolar lavage: lymphocytosos - NO eosinophilia
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EAA management?
Corticosteroid taper + avoidance of antigen. First line is avoidance, then corticosteroid avoidance.
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Types of Lung Cancer?
``` Non-small cell - Squamous Cell Carcinoma (PTH - hypercalcaemia ,clubbing HPOA, hyperthyroidism. - Adenocarcinoma Gynaecomastia, HPOA. - Large cell carcinoma ``` Small cell Carcinoma (rapid presentation) - ADH, ACTH, Lambert Eaton Syndrome
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Epidemiology and behaviour of sqaumous cell carcinoma
35% of all LC. M>F Smoking + Radon Gas Pathology - Centrally located with evidence of squamous differentiation (keratinisatioN). Behaviour - Locally invasive + metastasis late (via LN) - Release PTHrP --> increased Ca2+
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Epidemiology and behaviour of adenocarcinoma?
25% of all LC Females, non-smokers, far east. Peripherally located - Histo shows glandular differentiation (gland formation + mucin production). - common extrathoracic mets and early. - 80% presents with mets.
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Epidemiology and behaviour of large cell carcinoma
10% - Peripheral or central | Large, poorly differentiated cells with a poor prognosis.
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Epidemiology and behaviour of small cell carcinoma?
Central location near the bronchi - Histo: poorly differentiated cells. - 80% present with advanced disease. Very chemosensitive but v.poor prognosis. Ectopic hormone secretion. - Rapid presentation + have paraneoplastic
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What other lung tumours do you know?
- Adenoma: 90% are carcinoid tumours - Hamartoma - Mesothelioma
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What is the epidemiology of all lung cancers?
19% of all cancers | 27% of all cancer deaths
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What are the symptoms of lung cancer?
- cough and haemoptysis. New or persistent cough in a current or former smoker. - dyspnoea - Dyspnoea because of underlying COPD, pneumonia, or airway obstruction. - Chest pain - Most patients with chest pain have tumours invading the pleura or chest wall. - Recurrent or slow resolving pneumonia - Anorexia and weight loss - hoarseness due to recurrent laryngeal nerve palsy.
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Signs in the chest of lung malignancy?
- Consolidation - Collapse - Pleural effusion
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General signs of lung malignancy?
- Cachexia - Anaemia - Clubbing and HPOA (painful wrist swelling) more common in adenocarcinoma - Supraclavicular and/or axillary LNs (Horner's syndrome presenting with ptosis, miosis, ipsilateral anhydrosis)
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Signs of metastasis
- Bone tenderness - Hepatomegaly - Confusion, fits, focal neuro - Addison's - Cannon-ball mets = most commonly caused by renal cell cancer - CT abdomen is most appropriate to investigate this.
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Complications of lung cancer - local?
- Recurrent laryngeal nerve palsy - Phrenic nerve palsy - SVC obstruction - Horner's (Pancoast tumour) common in NSCLC - AF
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Paraneoplastic complications of lung cancer endo?
Endocrinology - Mostly found on SCLC - ADH --> SIADH (euvolaemic decreased in Na) due to small cell lung cancer. - ACTH - Cushing's syndrome - Serotonin --> Carcinoid (flushing, diarrhoea) - PTHrP --> primary HPT (increased Ca, bone pain) Mainly in squamous cell carcinoma. Lambert-Eaton syndrome in SCLC - autoimmune attack on VGCC.
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Paraneoplastic complications of lung cancer rheum?
Dermatomyositis/polymyositis
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Paraneoplastic complications of lung cancer Neuro?
- Cerebellar degenerations (due to Purkinje cells | - Peripheral neuropathy
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Paraneoplastic complications of lung cancer dermatology?
- Acanthosis nigricans (hyperpigmented body folds) - Trousseau syndrome: thrombophlebitis migrans (pancreas and lung). vessel inflammation due to blood clots in different part of the body. May present with visually swollen vessels.
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Metastatic complications of lung cancer?
- Pathological features - Hepatic failure - Confusion, fits, focal neurology - Addison's disease
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Investigations for Lung cancer - blood and sputum?
Bloods: FBC (anaemia) , U+E (SIADH + hyponatraemia) , Ca2+ (squamous cell carcinoma), LFTs (metastases) Cytology: Sputum (malignant cells in sputum), pleural fluid (patients that present a pleural effusion so would want to sample to look for malignant cells) Lung function tests - Assess treatment fitness?
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Imaging for lung cancer?
Offer urgent X-ray (2 weeks) to assess for lung cancer in people 40 or over with 2 or more unexplained symptoms (cough, fatigue, SOB, chest pain, weight loss, appetite loss). CXR - coin lesions - Hilar enlargement - Consolidation, collapse - effusion - bony secondaries - Contrast-enhanced volumetric CT (neck, thorax + upper abdo) Useful for staging, shows location + extent of primary tumour and evaluates hilar/mediastinal lymphadenopathy + distant mets. Consider - PET-CT: Exclude distant mets - Radionucleotide bone scan
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Types of biopsy for lung cancer?
- Percutaneous FNA: peripheral lesions and LN - Bronchoscopy: biopsy and assess operability - Endoscopic bronchial US biopsy: mediastinal LNs
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What are the differentials for a CXR coin lesion?
FANGS - Foreign body - Abscess: Staph, TB, Klebsiella, Mycetoma - Neoplasia (primary or secondary) - Granuloma: RA, Wegener's, TB, Sarcoid - Structural, AVM
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What is the staging for a non-small cell lung carcinoma?
TNM staging - Tx = Malignancy cells in bronchial secretions - Tis = CIS (carcinoma in situa) - T0 = None evidence - T1 = <3cm in lobar or more distal airways - T2 = >=3cm and >2cm from carina or pleural involvement - T3 = <2cm from carina or involves chest wall, diaphragm or >1 tumour in same lobe of lung - T4 = Involves mediastinum or malignant effusion in present, or more than 1 lobe. ``` N0 = none involved N1 = Peribronchial or ipsilateral hilum N2 = Ipsilateral mediastinum N3 = contralateral hilum or mediastinum or supraclavicular ```
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General management of lung cancer?
Refer using suspected 2ww - If they have chest x-ray finding suggesting lung cancer - Age 40 and over with unexplained haemoptysis. MDT: Respiratory physician, oncologist, radiology, histopathologist, specialist nurse, palliative care, GP. Assess risk of operative mortality: Thoracoscore + cardioresp function + comorbidities Advise smoking cessation
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NSCLC management?
Contra-indications to surgery - Stage IIIb or IV (mets) - FEV1 <1.5 litres considered general cut-off - Malignant pleural effusion - Tumour near hilum - Vocal cord paralysis - SVC obstruction Surgical resection - Management of choice for peripheral lesions with no metastatic spread = Stage I/II (~25%) - Requires good cardiorespiratory function - Wedge resection, lobectomy or pneumonectomy ± adjuvant chemo (cisplatin-based) preoperatively for stage II) and post-operatively for Stage 1B and 11. If not suitable use radiotherapy - if cardioresp reserve is poor. Chemo±radi for more advanced disease - Platinum-based regimes - If N2 or less consider surgery. For palliative: Consider MAbs targeting EGFR (cetuximab) or nintedanib (TKI), bevacizumab, ramucirumab (VEGFR) , pembrolizumab (programmed death-1 receptor)
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Management of SCLC?
- Typically disseminated @ presentation | - May respond to chemo but invariably relapses therefore use cisplatin + radiotherapy
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Management of palliation in SCLC?
- Radiotherapy: bronchial obstruction, haemoptysis, bone or CNS mets - SVC obstruction: stenting + Radio + dexamethasone - Endobronchial therapy: -Stenting, brachytherapy (radioactive material inside body) - Pleural drainage - Analgesia
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Prognosis of Lung malignancy?
SCLC 5 yr = 12% to 24% | NSCLC 5 yr = Stage 1 = 67%, Stage 3 = 23/25%.
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What is the pathogenesis of ARDS?
- May result from direct pulmonary insult or be secondary to sever systemic illness. - Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness - Inflammatory mediators --> increased capillary permeability and non-cardiogenic pulmonary oedema.
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Clinical features of ARDS?
``` Tachypnoea Cyanosis Bilateral fine creps SIRS/Sepsis Fever/cough/pleuritic chest pain ``` Rx: sepsis, aspiration, severe trauma etc
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Investigations for ARDS?
Bloods: ABG (low partial oxygen pressure PaO2/FiO2 inspired oxygen ratio of <300 on PEEP), sputum culture (sepsis), blood culture for sepsis, amylase/lipase for pancreatitis CXR: Bilateral opacities not explained by effusion or collapse.
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Diagnosis of ARDS?
- Acute onset - CXR shows bilateral opacities/infiltrates - No evidence of CCF - PaO2:FiO2 200 -300 = Mild 100-200 = Moderate <100 = Severe CLinical indicated of hypoxaemia as it is comparing inspired oxygen to arterial oxygen
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Management of ARDS?
- Admit to ITU for organ support and manage underlying cause Ventilation - Indications PaO2 <8kPa (normal is >10.6) despite 60% FiO2 - PaCO2 >6KPa Method - 4-8ml/kg + PEEP (e.g 10cm H20) - SE = VILI (ventilator induced lung injury), VAP (pneumonia), Weaning difficulty Circulation - Invasive BP monitoring - Maintain CO and DO2 with inotropes. Keep CVP <4cm H20. - Dobutamine Sepsis = Abs
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Causes of ARDS?
Pulmonary (alveolar damage + diffuse oedema) - Pneumonia - Aspiration - Inhalation injury - Contusion Systemic - Shock - Sepsis - trauma - Haemorrhage - Pancreatitis - Acute liver failure - DIC - Obs: Eclampsia, amniotic embolism - Drugs: aspirin or heroin
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What is a differential diagnosis of pulmonary effusion?
- Transudate = Forced through by hydrostatic pressure therefore low protein. Therefore ratio is high (SAAG = >1.2) - Exudate = Through inflammation therefore high protein. Therefore ratio is low as normal to blood (SAAG <1.2).
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Causes of Transudates?
Increased capillary hydrostatic pressure - CCF - Iatrogenic fluid overload - Renal failure - Relative high in negative pressure pulmonary oedema Decreased capillary oncotic pressure (opposite effect to hydrostatic, due to low protein levels) - Liver failure - Nephrotic syndrome - Malnutrition, malabsorption, protein-losing enteropathy Increased interstitial pressure - Decreased lymphatic drainage: e.d Ca Exudates - ARDS
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Define Type 1 Respiratory failure?
- PaO2 <8kPa and PaCo2 <6KPa (due to hypoxaemia) | V/Q mismatch and diffusion failure
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Define Type 2 Respiratory Failure?
- PaO2 <8kPa and PaCO2 >6KPa | - Alveolar hypoventilation ± V/Q mismatch.
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Causes of a V/Q mismatch and diffusion failure?
Either no oxygen or no blood to carry oxygen. Increased Alveolar-arterial gradient. ``` - Vascular due to PE (ventilation good but perfusion bad) PHT Pulmonary Shunt (R--> L) (perfusion problem) - Early Asthma - Pneumothorax - Atelectasis ``` ``` Diffusion failure - Fluid Pulmomnary oedema Pneumonia Infarction Blood ``` Fibrosis (both fluid and fibrosis can also cause alveolar hypoventilation and V/Q mismatch due to decreased compliance.
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Causes of alveolar hypoventilation therefore limit exchange of CO2 with atmosphere.
Obstructive - COPD - Asthma - Bronchiectasis - Bronchiolitis - Intra and Extra-thoracic (Ca, LN, epiglottitis) Restrictive - Decreased drive: CNS sedation, trauma, tumour - NM disease: cervical cord lesion, polio, GBS, MG - Chest: kyphoscoliosis, obesity - Fluid and fibrosis
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Clinical features of hypoxia?
Acute - Dyspnoea - Tachypnoea - Stridor - Cyanosis - Confusion - Agitation Chronic - Polycythaemia - PHT - cor pulmonale (increase in HR)
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Clinical features of hypercapnoea?
- Headache - Flushing and peripheral vasodilatation - Bounding pulse - Flap - Confusion --> Coma
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Management of Type 1?
Give O2 and maintain SpO2 94-98% | Assisted ventilation if PaO2 <8Kpa despite 60%
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Management of Type 2?
Controlled O2 therapy @24% oxygen aiming for SpO2 88-92%. Check ABG after 20 mins - If PaCO2 steady or lower can increased FiO2 if necessary - If PaCO2 increased >1.5KPa and patient still hypoxic, consider NIV or respiratory stimulant. - BiPAP can be helpful in hypercapnic.
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Principles of oxygen therapy?
- Critically ill patients should receive high conc O2 immediately. - O2 should be prescribed to achieve target SpO2. 94-98% for most patients 88-92% for those at risk of hypercapnic resp failure - In patients at risk of hypercapnic resp failure - Start O2 therapy at 25% and do an ABG - Blue Venturi @2-4L Clinically: decreased RR with O2 may be useful sign If PCO2 <6: increased target SpO2 to 94-98% If PCO2 >6kPa: maintain target SpO2.
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Mechanisms of Oxygen Therapy?
- Nasal Prongs: 1-4L/min = 24-40% - Simple Face mask - Non-rebreathing mask: reservoir bag allows delivery of high conc of O2. 60-90% at 10-15L. - Venturi Mask - Provides precise O2 concentration at high flow rates: Yellow: 5% White: 8% Blue: 24% Red: 40% Green: 60%
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Definition of chronic asthma?
Episodic, reversible airway obstruction due to bronchial hyper-reactivity to a variety of stimuli.
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Pathophysiology of asthma?
Acute - Mast cell-Ag interaction --> histamine release - Bronchoconstriction, mucus plugs, mucosal swelling Chroni - Th2 cells release IL3,4,5 --> mast cell ,eosinophil and B cell recruitment - Airway remodelling.
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Triggers of chronic asthma?
- T1 hypersenstivity to variety of antigens - Dust mites, pollen, food, animals, fungus. Stress - Cold air - Viral URTI - Exercise - Emotions Toxins - Smoking, pollution - Drugs; NSAIDs, B-B.
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Symptoms of asthma?
- Cough (often at night - Dry night-time cough. - Tachypnoea - Wheeze (polyphonic wheeze) - Localised wheeze suggests inhaled foreign body. - Dyspnoea - Diurnal variation with morning - dipping Features considers for asthma - recurrent episodes of symptoms: may be triggered by viral infection, allergen exposure, NSAIDs/beta-blockers and/or exacerbated by exercise, cold air and emotion/laughter in children - recorded observation of wheeze: due to varying use of language this usually means wheeze documented by a clinician - symptom variability: asthma is generally worse at night or early in the morning personal history of atopy: e.g. eczema/allergic rhinitis - absence of symptoms of alternative diagnosis: e.g. COPD, dysfunctional breathing or obesity* - historical record of variable peak flows or FEV1
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History of asthma?
- Precipitants - Diurnal variation - Exercise tolerance - Life effects: sleep, work - Other atopy: hay fever, eczema - Home + job environment
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Signs of asthma?
- Tachypnoea, tachycardia - Widespread polyphonic wheeze - Hyperinflated chest - Decreased air entry - Signs of steroid use
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Associated disease with asthma?
- GORD - Churg-Strauss - ABPA
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Differentials for Asthma?
- Pulmonary oedema (cardiac asthma) | - COPD
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Investigations for asthma?
Bloods: Fbc (eosinophilia), increased IgE, aspergillus serology CXR: hyperinflation A negative result on spirometry does not exclude asthma as a diagnosis. - FeNO: >40 Spirometry. Levels of NO correlate with inflammation. In children FeNO >35 - Obstructive pattern with FEV1:FVC <0.75 (this is because FEV is decreased whereas in restrictive, both FEV and FVC are reduced). Reversibility: - >12% improvement in FEV1 with B-agonist. Response to bronchodilator reversibility. or an increased in volume of 200ml in adults. Peak Expiratory Flow Rate - May be low with diurnal variation of >20% - Morning dipping Atopy: skin-prick, RAST All patients >=17 - patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma - All patients should have spirometry with a bronchodilator reversibility (BDR) test - All patients should have a FeNO test Patients 5-16 - all patients should have spirometry with a bronchodilator reversibility (BDR) test - a FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test <5 = Clinical judgement
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Management of asthma - General measures?
General Measure? TAME ``` - Technique for inhaler use - Remove cap, shake before delivery. Breath should be held for 10 s, then gap of 30 seconds. - Avoidance: allergens, smoking, dust - Monitor: Peak flow diary (2-4x/d) - Educate Liaise with specialist nurse NEed for Rx compliance Emergency action plan ```
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Management of asthma - drug ladder?
Step 1 - SABA PRN (100 micrograms) up to 4 times daily when required. If use >1/d or nocte symptoms --> Step 2 Step 2 - SABA + LD inhaled steroid: beclometasone 100-400microgram bd. (if symptoms >2x a week but 1 a day). If night-time symptoms ?2 a month. Step 3 SABA + Low-dose ICS + LTRA. montelukast 10mg) Step 4. SABA + low-dose ICS + LABA: salmeterol 50micrograms bd - If good response: contine - Benefit but control still poor: increase steroid to 400micrograms bd - Continue LTRA depending on patient's response to LTRA Moderate persistent is: daily symptoms, use of SABA daily, exacerbation >2x a week and may last for days. 4. Trials of - Increased inhaled steroid to up to 1000 micrograms bd - Leukotriene receptor antagonist (montelukast 10mg) + medium dose steroids. - SR Theophylline - MR B agonist PO 5. - Oral steroids e.g prednisolone 5-10mg - Use lowest dose necessary - Maintain high-dose inhaled steroid - Refer to asthma clinic Omalizumab - Severe, persistent, allergic asthma - Confirmed IgE -mediated allergy to perennial allergen. >2 exacerbations required hospital admission in the preceding year. Doses of inhaled corticosteroid dose - <=400 budesonide = low dose - 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose - > 800 micrograms budesonide or equivalent= high dose. Step down of asthma - reduce the dose of any steroid to 50% at a time.
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Presentation of an acute severe asthma attack?
Acute breathlessness and wheeze - Hx of precipitant: infection, travel, exercise - Decrease from baseline in objective measures of pulmonary function, such as PEFV and FEV1. - Usual and recent rx - Previous attack and severity: ICU? - best PEFR Patients with moderate acute severe asthma should be admitted to hospital in the presence of a previous near-fatal attack.
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Investigations for acute asthma attack?
PEV or FEV1 - Extent of asthma exacerbation can be determined by measuring peak flow as percentage of normal >80 = mild, moderade = 80-60%, severe = <60%. ``` ABG - PaO2 usually normal or slightly low - PaCO2 low - If PaCo2 high (>6): send to ITU for ventilation FBC, U+E, CRP, Blood cultures. ```
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Assessment of asthma attack? Severe?
If any of - PEFR <50% - RR >25 - HR >110 - Can't complete sentences in one breath (dyspnoea at rest) Life threatening: any one of - PEFR <33% - SpO2 <92%, PCO2 >6 kPa, PaO2 <8kPa - Cyanosis - Hypotension - Exhaustion, confusion - Silent chest, poor respiratory effort - Tachy/brady/arrhythmias
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Differentials for Acute Asthma Attack?
- Pneumothorax - Acute Exacerbation of COPD - Pulmonary Oedema
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Admission criteria for acute asthma attack?
- Life-threatening attack - Feature of severe attack persisting despite initial Rx - May discharge if PEFR >75% 1h after initial Rx.
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When to discharge a patient with an acute asthma attack?
- Been stable on discharge meds for 24hr | - PEFR >75% with diurnal variability <20%
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What is the discharge plan for a patient with an acute asthma attack?
- TAME patient Technique, avoidance, monitor and educate. - PO steroids for 5d - GP appointment w/i 1 week - Resp clinic appointment within 1 month.
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Initial management of acute exacerbation of asthma?
Mild - Inhaled SABA (4-8 puffs every 20 mins for up to 4 hrs, then every 1-4 hrs when required). - Prednisolone 40-80mg orally. Moderate to severe O2, Nebs and Steroids - Sit up - 100% O2 via non-rebreathe mask (aim for 94-98%) - Nebulised salbutamol (5mg) every 20 mins for 3 doses, followed by 2.5 to 10mg every 1-4 hrs when required - ipratropium (0.5mg) (anticholingeric) - Prednisolone 50mg PO (or both) - Write no sedation on drug chart Then consider - Magnesium sulphate - Aminophylline/ IV salbutamol
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Management of acute severe asthma if life threatening?
- Inform ITU - MgSO4 2g IVI over 20 mins - IV hydrocortisone 100mg every 8hrs - Nebulised salbutamol every 15 mins (monitor ECG).
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Management of Acute Asthma exacerbation If improving on management?
- Monitor SpO2 @ 92-94%, PEFR - Continue pred 40mg OD for 5 days which could settle her exacerbation. - Nebulised salbutamol every 4hr
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Management of acute asthma if no improvement in 15-30mins?
- Nebulised salbutamol every 15 mins (monitor ECG) - Continue ipratropium 0.5mg 406hr - MgSO4 2mg IV over 20 mins - Salbutamol IV 3-20 micrograms /min - ITU transfer for invasive ventilation - Consider aminophylline (Little evidence) Load: 5mg/kg IVI over 20mins Continue: 0.5mg/kg/hr Monitor levels
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MOnitoring for patient with acute severe asthma?
- PEFR every 15-30 mins Pre and post-B agonist - SpO2: keep >92% - ABG if initial PaCO2 normal or increased.
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Definition of COPD?
- Airway obstruction:FEV1:FVC <0.7, FEV1 can be >80. - Mild can be considered with a FEV1 >80% as mild. - Chronic bronchitis: cough and sputum production on most days for 3 months of 2 successive years - Emphysema: histological diagnosis of enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls
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Epidemiology of COPD?
Prevalence: 10-20% of >40yr
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Causes of COPD?
Smoking Pollution a1ATD - consider this in young person with emphysema-like illness.
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Symptoms of COPD?
- Cough + Sputum (chronic 3 months) - Exertional Dyspnoea - Wheeze - Weight loss - Regular sputum production - Regular winter bronchitis
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Signs of COPD?
- Tachypnoea - Prolonged expiratory phase (obstructive picture). Breath in and then out otu out, hear a squeeze. Silent chest has hyperinflation and obstructive disease. - Hyperinflation decreased cricosternal distance (normal = 3 fingers) Loss of cardiac dullness - hyperexpansion. Displaced liver edge - Wheeze - May have early-inspiratory crackles - Cyanosis - Cor pulmonale: increased JVP, oedema, loud P2. -Sign of steroid use
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What is a Pink Puffer?
In EmPhysema - Increased alveolar ventilation --> breathless but not cyanosed - Normal or near normal PaO2 - Normal or low PaCO2 - Progress --> T1 respiratory failure
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What is a blue bloater?
chronic Bronchitis - Decreased alveolar ventilation --> cyanosed byt not breathless - Decreased PaO2 and Increased PaCO2: rely on hypoxic drive - Progress --> T2 respiratory failure and cor pulmonale
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What criteria can you use for COPD?
All have obstructive picture FEV1/FVC <0.7 GOLD criteria? - Gold 1 - mild: FEV1 >80% predicted - Gold 2 - moderate: 50% - 80% predicted - Gold 3- severe: 30-50% predicted - Gold 4 - very severe: FEV1 <30% predicted
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Complications of COPD?
- Acute exacerbations ± infections - Polycythaemia - Pneumothorax (ruptured bullae) - When placing a chest drain - could mimic a pneumothorax. - Cor Pulmonale - Lung Carcinoma
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Investigations for COPD?
- BMI - Bloods: FBC (polycythaemia), a1-AT level, ABG (low oxygen sats - 88-90% acceptable, PaO2 <60mmHg suggests respiratory insufficiency). - CXR Hyperinflation (>6 ribs anteriorly) Flattened diaphragm Prominent pulmonary arteries Peripheral oligaemia Bullae - ECG R atrial hypertrophy: P pulmonale RVH, RAD - COPD is classified based on patient's FEV1. Result of FEV1/FVC ratio <7.0. or FEV <80% - Assess for reversibility - Gas transfer - Echo: PHT
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Chronic General Management of COPD?
- Assess severity ``` - General measures Stop Smoking Specialist nurse nicotine replacement therapy Bupropion, vareniciline Support programme ``` - Pulmonary rehab/exercise. At the earlier stages of COPD, recommended to start as soon as they feel short of breath. Improves exercise capacity. - Rx poor nutrition and obesity - Screen and manage comorbidities E.g cardiovascular, lung Ca, osteoporosis - influenza + pneumococcal vaccine - Review 1-2x/yr - Air travel risky if FEV1 <50%
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Specific management of COPD?
1) Breathlessness and/or exercise limitations - SABA (salbutamol) and/or SAMA (iptratropium) PRN - SABA PRN may continue at all stages 2) Exacerbations or persistent breathlessness (consider FEV, any previous atopy, higher eosinophil count, substantial diurnal variation in peak expiratory flow) - Consider asthmatic features suggesting steroid responsiveness: previous diagnosis of asthma, higher blood eosinophil count, substantial variation in FEV1 over time (at least 400ml), diurnal variation in peak expiratory flow (at least 20%). If no asthmatic features: consider LABA + LAMA. Stop SAMA, switch to SABA. If asthma features : LABA (salmeterol) + ICS combo or (LAMA (tiotropium) 3) THEN OFFER TRIPLE: Persistent exacerbations or breathlessness - LABA + LAMA + ICS - Roflumilast/theophylline may be considered - Consider home nebs 4) Oral Theophylline - After trials of long and short acting bronchodilators. +/- 5) Prophylactic antibiotics - 250mg azithromycin or 500mg 3x a week. Must do LFTs and ECG to exclude QT prolongation Recommended in COPD if they DO NOT SMOKE - optimised non-pharm management + inhaled therapies + referred for pulmonary rehab + continue to have 1 or more of the following + significant daily sputum production. : frequency 4 or more a year with sputum production Prolonged exacerbation with sputum production exacerbation resulting in hospitalisation +/- 5) Mucolytics - Consider if chronic productive cough - Not used to prevent exacerbation in people with stable COP - E.g Carbocisteine (CI in PUD) 6) LTOT - For chronic hypoxia, polycythaemia, pulmonary hypertension, peripheral oedema (cor pulmonale), FEV <30% predicted. Raised JVP. - Aim: PaO2 >8 for 15h/day (increased survival by 50%) - Clinically stable non-smokers with PaO2 <7.3 (stable on two occasions >3 weeks apart) - PaO2 7.3-9 + PHT/cor pulmonale (also use loop diuretics)/ polycythaemia/nocturnal hypoxaemia - Terminally ill pts 7) Surgery - Recurrent pneumothoraces - Isolated bullous disease - Lung volume reduction
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Acute Exacerbation of COPD causes?
- Viral URTI (30%) - Also bacterial infections - Haemophilus Influenza is the most common - Streptococcus pneumonia - Moraxella catarrhalis Staph aureus more likely in patients with post-viral pneumonia
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Acute Exacerbation COPD Presentations + history?
- Cough + sputum - Breathlessness - Wheeze - Smoking Status - Exercise capacity - Current treatment - Previous exacerbations
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Investigations for acute exacerbation of COPD?
- PEFR - oxygen sats (check patient baseline) - Bloods: FBC (may show elevated haematocrit + elevated WBC) , U+E, ABG (respiratory acidosis + compensatory metabolic alkalosis), CROP, cultures - CXR: Infections, pneumothorax, will show hyper-expansion, flattened diaphragm, increased retro-sternal air space, bullae. - ECG
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What are the differentials for Acute exacerbation of COPD?
- Pneumothorax - Pulmonary Oedema - PE - Asthma
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Plans for discharge for acute exacerbation of COPD?
- Spirometry - Establish optimal maintenance therapy - GP and specialist f/up - Prevention using home oral steroids and Abx - Rescue medication. - Pneumococcal Flu vaccine - Home assessment
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Management of Acute Exacerbation of COPD?
Controlled O2 Therapy - Sit up Any critically ill patient should initially be treated with high flow oxygen which is then titrated to achieve target sats. Do ABG, CXR, ECG, FBC, U+E, MCS, BC. - Then - 28% O2 via Venturi mask: SpO2 88-92% at 4L. - Vary FiO2 and SpO2 target according to ABG - Aim for PaO2 >8 and increase in PCO2 of <1.5kPa ``` Then Nebulised Bronchodilators - Air driven with nasal specs - Salbutamol 5mg/4h - Ipratropium 0.5mg/6hr ``` Then - Steroids (IV or PO) Hydrocortisone 200mg IV - Prednisolone 40mg PO for 7-14 days Abx - If evidence of infection, purulent sputum or signs of pneumonia. - Doxy 200mg PO STAT then 100mg OD PO for 5 days Or Amoxicllin etc Then consider NIV if no response (worsening baseline examination, ABG, lung function). - PaCO2 >6kPA, pH <7.35. Persistent respiratory acidosis Use of accessory respiratory muscles, cyanosis. If they have respiratory acidosis, severe dyspnoea, increased work of breathing. - Repeat nebs and consider aminophylline IV - Consider NIV (BiPAP) if pH <7.35 and/or RR >30. Useful for T2RF. IPAP and EPAP - Consider invasive ventilation if pH <7.26
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What is a pulmonary embolism
Consequence of the thrombus formation within a deep vein of the body mostly lower extremities. Occurs due to Virchow's triad.
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What causes a pulmonary embolism?
- Usually arises from DVT in proximal legs or iliac veins - Rarely (right ventricle post MI) - Septic emboli in right sided endocarditis
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What are the risk factors for a PE?
SPASMODICAL - Sex - Pregnancy - Age increased - Surgery (10d postop straining at stool) - Malignancy - Oestrogen: OCP/HRT - DVT/PE previous Hx - Immobility - Colossal size - Antiphospholipid Abx - Lupus Anti-Coagulant
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How does a PE present?
Symptoms and signs depend on size, number and distribution of emboli? Symptoms - Dyspnoea/Tachypnoea - Tachycardia - Pleuritic pain - Haemoptysis - Syncope Signs - Crackles - Fever - Cyanosis - Tachycardia, tachypnoea - RHF: hypotension, increased JVP, loud P2 - Evidence of cause: DVT
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Investigations of Pulmonary Embolism?
CXR - Must happen prior to CTPA or V/Q. Bloods: FBC, U+E (renal impairment before LMWH) , Clotting (baseline before treating), D-dimers (used to exclude PE in low risk patients - based on Well's) ABG: normal or decreased PaO2 and decreased PaCo2, increased pH. ECG: (used to assess Right ventricular function) Sinus tachycardia, RBBB, right ventricular strain (inverted T in V1-V4) S1,Q3,T3 is rare (deep 3 waves in 1, pathological Q waves in III, inverted T waves in III indicating right heart strain). Doppler US: thigh and pelvis (+ve in 60%) CTPA + venous phase of legs and pelvis V/Q is used to patients with renal impairment - scans use a contrast media that is nephrotoxic
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Diagnosis of PE?
Assess using Well's Score Criteria for Well's score - Clinical signs of DVT - Alternative diagnosis less likely than PE - Previous PE or DVT - HR >100bpm - Surgery or immobilisation within 4 weeks - Haemoptysis - Active cancer - Low probability --> (less than or equal to 4) perform D-dimers Negative = exclude PE Positive = CTPA ``` High probability (>4) = CTPA unless CKD then don't use contrast. ```
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Prevention of a PE?
- Risk assessment for all patients - TEDS - Prophylactic LMWH - Avoid OCP/HRT if @ risk
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Management of PE?
- Sit up - 100% oxygen via non-rebreather mask - Analgesia Morphine ± metoclopramide If critically ill with massive PE consider thrombolysis (SBP <90) - High flow oxygen/fluids (500ml saline) ± adrenaline if SBP <90 - Alteplase 100mg bolus over 2hrs - Surgical or interventional embolectomy Then Acutely Anticoagulate with LMWH or Unfractionated (preferred) (heparin and adjust does to APTT) + Warfarin 5mg orally adjust according to INR. Can be reversed with protamine (UFH) and stopped at an INR 2-3. Can also give fondaparinux Those at low risk can have rivaroxaban 15mg orally twice daily.
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Management of PE if BP refractory to treatment?
Dobumatine inotropes: aim for SBP >90 - Consider addition of norepinephrine. - Consider thrombolysis (medical or surgical)
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On-going management of PE
- TED stocking in hosptial - Graduated compression stocking for 2yrs if DVT prevents post-phlebetic syndrome - Continue LMWH until INR >2 (at least 5day) Then continue with warfarin for 3 months. - Target INR = 2-3 - Duration Remedial cause: 3months No identifiable cause: 6 months On-going cause: - VC filter if repeat DVT/PE despite anticoagulation (or with an absolute contraindication to anticoagulant therapy, or with patients experiencing major bleeding or with recurrent PE).
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What is a Pneumothorax
- Accumulation of air in the pleural space with 2ndry lung collapse
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What is the classification of pneumothorax?
Closed: intact chest wall and air leaks from lung into pleural cavity Open: Defect in chest wall allows communication between PTX and exterior: may be sucking Tension: air enters pleural cavity through one way valve and cannot escape leading to mediastinal compression
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What is a primary spontaneous pneumothorax?
Occurs without preceding trauma or precipitating event, and develops in a person without clinically apparent pulmonary disease. Most at risk are those who smoke, Marfan's. homocystinuria or FHx. - Young thin men
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What is a secondary spontaneous pneumothorax?
Complication of underlying pulmonary disease. COPD is most common from cigarette smoke. May also be PCP, Cystic fibrosis, TB. Pulmonary fibrosis, sarcoidosis
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Causes of pneumothorax?
- Spontaneous primary and secondary - Trauma (penetrating or blunt ± rib fracture) due to flail chest syndrome - Iatrogenic (subclavian CVP line insertion, positive pressure ventilation, transbronchial biopsy, liver biopsy).
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Presentation of pneumothorax?
Symptoms - Sudden onset - Dyspnoea - Pleuritic chest pain Signs - Decreased expansion of side affected - Resonant percussion (hyperresonant) ipsilateral - Decreased breath sounds ipsilateral - Decreased vocal resonance - Trachea shift in tension to the unaffected side) - Crepitus: surgical emphysema
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Presentation of tension pneumothorax?
- Respiratory distress - increased JVP, mediastinal shift, increased HR, decreased JVP - Hyper-resonant chest - Absent breath sounds - Trachea is deviated to the left away from pneumothorax. - Insert wide-bore cannula into second intercostal space - mid-clavicular line.
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Investigations for pneumothorax?
- ABG - US - CXR (expiratory film may be helpful) Translucency + collapse (2cm rim = 50% loss) Visualise line of pleura Mediastinal shift (away from PTX) Surgical emphysema Causes: rib fractures, pulmonary distress
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Management of a tension pneumothorax?
- Resuscitate patient - Oxygen therapy >10L/min via a non-rebreather face mask. - No CXR - Large bore 14G Venflon into 2nd ICS, mid-clavicular line - Insert intercostal chest drain Remember that 22G is paediatric and 14G is the largest.
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Management of traumatic pneumothorax?
- Resuscitate patient - Analgesia e.g morphine - 3-sides wet dressing if sucking - Insert ICD (intercostal chest drain)
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Management of a primary pneumothorax?
SOB and/or rim >2cm? If yes then aspirate + then if successful discharge. If unsuccessful chest drain. If no SOB or rim <2cm, then discharge. even following aspiration. Give oxygen to all 10L/min For those above 50 or have a significant smoking history, treat as you would 2ndry.
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Management of secondary pneumothorax?
- Admit - 10L oxygen/min - SOB and >50 yrs and rim >2cm? Yes then insert chest drain. - If not, then aspirate, and then decide to insert ICD. - If pneumothorax is less than 1cm then BTS guidelines suggest giving oxygen + admitting for 24hrs.
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What is a pleural effusion?
Fluid collects between the parietal and visceral pleural surfaces of the thorax. A thin layer of fluid is always present in this space for lubrication.
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How would you classify a pleural effusion?
Effusion protein <30g/L = transudate (through a strainer) Effusion protein >30g/L = exudate (through holes) If between 25-35 = Light's Criteria
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What is Light's Criteria?
Used to differentiate transudate from exudate. - an exudate has one of: Effusion: pleural protein to serum protein ratio >0.5 Effusion: serum LDH ratio >0.6 Effusion LDH is >2/3 upper limit of normal for serum. Other findings include: - Rheumatoid arthritis, tuberculosis - Raised amylase: pancreatitis, oesophageal perforation
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Causes of an exudate?
>30g/L Increased capillary permeability - Infection: pneumonia, TB - Neoplasm: bronchial, lymphoma, mesothelioma - Inflammation: RA, SLE - Pulmonary Embolism - Dressler's Syndrome - Yellow Nail syndrome
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Causes of an transudate?
``` Increased capillary hydrostatic or decreased oncotic pressure? - CCF - Renal failure - Decreased albumin: nephrosis, liver failure, enteropathy - Hypothyroidism - Meig Syndrome Right pleural effusion Ascites Ovarian fibroma ```
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Presentation of pleural effusion?
- Normally asymptomatic - Or presented with dyspnoea (difficult breathing) - Pleuritic chest pain Signs - Tracheal deviation away from effusion (towards deviation is in lung collapse or lobe fibrosis) - Decreased expansion - Stony dull percussion - Decreased air entry - Bronchial breathing just above effusion - Decreased vocal fremitus (air to water). Decreased breath sounds). Signs of associated disease - Cancer: cachexia, clubbing, HPOA, LNs, radiation - Chronic liver disease - Cardiac failure - RA, SLE - Hypothyroidism
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Investigations for Pleural effusion?
Diagnostic Tap - Percuss upper border and go 1-2 spaces below - Infiltrate down to pleura with lignocaine - Aspirate with 21G needle - Send for Chemistry: protein, LDH (exudate if ratio is >0.5, LDH to serum LDH is >0.6), pH, glucose, amylase Bacteriology: MCS, auramine stain, TB culture Cytology (malignant effusion) Immunology: SF, ANA, complement ``` Bloods: FBC (WBC), U+E, LFTs, TFTs, Ca, ESR PA CXR - Blunt costophrenic angles (key point) - Dense shadow with meniscus - Mediastinal shift away - Cause: coin lesion, cardiomegaly ``` US: Facilitates tapping and recommended. Volumetric/Contrast CT Consider Pleural biopsy if fluid inconclusive.
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What would Emypema, Ca, TB, RA and SLE show on pleural tap?
- Increased protein - Decreased glucose <3.3 - Decreased pH <7.2 - Increased LDH >0.6 x serum /ULN
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What would oesophageal rupture show?
Oesophageal rupture - decreased pH <7.2 - Increased amylase
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Management of pleural effusion?
- Manage underlying cause - May use drainage if symptomatic (<2L/24hr) Repeated aspiration of ICD - using pleural aspiration. - Chemical pleurodesis if recurrent malignant effusion - Persistent effusion may require surgery - Consider therapeutic thoracentesis - VATS? --> Video-assisted If pleural effusion is drained too quickly, a rare but important complication is a re-expansion pulmonary oedema. Once patient consent has been obtained and patient imaging assessed, the patient should be positioned in a supine position or at a 45º angle. The patient's forearm may be positioned behind the patient's head to allow easy access to the axilla. Identify the 5th intercostal space in the midaxillary line. The area should be anaesthetised using local anaesthetic injection (lidocaine, up to 3mg/kg). The drainage tube should then be inserted using a Seldinger technique. The drain tubing should then be secured using either a straight stitch or with an adhesive dressing. o avoid re-expansion pulmonary oedema, it is recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours).
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What is sarcoidosis?
Multisystem granulomatous disorder of unknown cause?
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What is the epidemiology of sarcoidosis?
Age: 20-40 Sex: F>M Geo: Afro Caribbean HLA-DRB1 and DQB1 alleles
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Clinical features of sarcoidosis - General?
GRAULOMAS - 20-40% the disease presents incidentally on CXR - Acute sarcoidosis: EN, fever, polyarthralgia, BHL General - Fever - Anorexia and weight loss - Fatigue - Lymphadenopathy and hepatosplenomegaly Lofgren's sydnrome: fever, hilar lymphadenopathy, polyarthritis. Acute form of the disease Heerfordt's syndrome - Parotid enlargement, fever and uveitis secondary to sarcoidosis.
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Respiratory features of sarcoidosis?
``` Upper: Otitis, sinusitis Lower (seen in 90%) - Dry cough, - SOB of gradual onset, - chest pain, - decreased lung function Stage 1: BHL Stage 2: BHL + peripheral infiltrates Stage 3: Peripheral infiltrates alone Stage 4: Progressive mid-zone fibrosis with bullae ```
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Arthralgic features of sarcoidosis?
- Polyarthralgia | - Dactylitis
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Neurological features of sarcoidosis?
- Peripheral and cranial polyneuropathy (esp. Bell's palsy) | - Meningitis, transverse myelitis, SOL
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Urine features of sarcoidosis?
Increased calcium --> renal stones, nephrocalcinosis, DI
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Low hormones of sarcoidosis?
Pituitary dysfunction: e.g amenorrhoea
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Ophthalmological features of sarcoidosis?
- Uveitis - Keratoconjunctivitis - Sicca/Mikulicz/Sjogren's Syndrome
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Myocardial features of sarcoidosis?
- restrictive cardiomyopathy sndry to granulomas and fibrosis - Pericardial effusions
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Abdominal features of sarcoidosis?
- Hepatomegaly + cholestatic LFTs | - Splenomegaly
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Skin features of sarcoidosis?
Erythema Nodosum: painful erythematous nodules on shins (paniculitis) Lupus pernio: Raised, dusky purple plaques on nose, cheeks, fingers. Non-itchy, frequently affecting the nose, cheeks, lips and ears.
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Investigations for sarcoidosis?
Bloods - Increased ESR - Increased Ca (dysregulated calcitriol by macrophages and granulomas) - Lymphopenia - Increased serum ACE - Increase Ig - Increased LFTs (elevated AST and ALT) CXR, CT, MRI for pulmonary involvement. Tuberculin skin test - Negative in 2/3 Lung functions test - Restrictive pattern with decreased FVC - Decreased transfer factor Tissue Biopsy - Lung, LNs, Skin nodules, liver - Diagnostic: non-caseating granulomas Ophthalmology assessment
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Management of sarcoidosis?
Pts with asymptomatic BHL do not require Rx Acute sarcoidosis - usually resolves spontaneously - Bed rest, prednisolone (if unable to breath/respiratory failure), NSAIDS Chronic Sarcoidosis - Steroids: Prednisolone 40mg/d for 4-6 weeks NICE recommends = indications for corticosteroid treatment are: parenchymal lung disease, uveitis, hypercalcaemia, neurological or cardiac involvement. - Consider second line - methotrexate, ciclosporin, cyclophosphamide Cutaneous disease - Topical corticosteroids (triamcinolone) or oral prednisolone 40mg
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Bilateral Hilar lymphadenopathy differential
- Sarcoidosis - Infection: TB, mycoplasma - Malignancy: lymphoma, carcinoma - Interstitial disease: EAA, Silicosis
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Interstitial lung disease
Large group of disorders for fibrosis of the lungs - Exposure related - Idiopathic - Sarcoidosis - Connective tissue disease
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Principle features of interstitial lung disease?
- Dyspnoea - Dry cough - Abnormal CXR/CT - Restrictive Spirometry
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Causes of interstitial lung disease?
``` Known Causes - Environmental: asbestosis, silicosis - Drug: BANS ME Bleomycin, Busulfan Amiodarone Nitrofurantoin* Sulfasalaine Methotrexate* , Methysergide - Hypersensitivity: EAA - Infection: TB, viral, fungi ``` Associated with systemic disease - Sarcoidosis - RA - SLE, systemic sclerosis, Sjorgren's, MCTD - UC, ankylosing spondylitis Idiopathic - Idiopathic pulmonary fibrosis
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Causes by Location for interstitial lung disease?
Upper Zone - A PENT - Aspergillosis: ABPA - Pneumoconiosis: coal, Silica - Extrinsic allergic alveolitis - Ank Spond - TB Lower Zone: STAIR (More common affect the bottom) - Sarcoidosis (mid zone) - Toxins: BANS ME Amiodarone, methotrexate, bleomycin - Asbestosis - Idiopathic pulmonary fibrosis - Rheum: RA, SLE, Scleroderma, Sjogren's, PM, DM
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Extrinsic allergic alveolitis?
Acute allergen exposure in sensitised pts --> T3HS Chronic exposure --> granuloma formation and obliterative bronchiolitis (T4Hs)
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Causes of extrinsic allergic alveolitis?
- Bird fancier's lung: proteins in bird droppings - Farmer's/mushroom workers - Malt worker's lung: Aspergillus clavatus
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Clinical features of EAA?
4-6hr post exposure - Fever, rigors, malaise - Dry cough, dyspnoea - Crackles (no wheeze) Chronic - Increasing dyspnoea - Weight loss - T1 respiratory failure - Cor pulmonale
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Investigations for EAA?
Ix - Bloods Acute: neutrophilia, elevated ESR +ve se precipitins - CXR Upper zone reticulonodular opacifications or fibrosis --> honeycomb lung BHL - Spirometry Restrictive defect Decreased transfer factor during acute attacks BAL - increased lymphocytes and mast cells
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Management for EAA?
- Avoid exposure - Steroids: acute/long-term - Compensation may be payable
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Industrial Lung Diseases?
Part of the Pneumoconioses - due to mineral dust exposure or metal. Activate macrophages on alveolus leading to fibrosis. Coal-workers Pneumoconiosis Silicosis Asbestosis
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Coal-Workers Pneumoconiosis?
Black lung disease = occupational lung disease caused by long term exposure to coal dust particles. -Most are male = due to coal mining. Coal dust enters lung - reaches terminal bronchioles and engulfed by interstitial macrophages. Macrophages get overwhelmed and accumulate in alveoli - causing damage to lung. Simple pneumoconiosis - Commonest type - Patients often asymptomatic - May lead to progessive massive fibrosis (Massive fibrotic masses several centimers - in the upper lobe). Category 1: some opacities but normal lung markings visible. Category 2: large number of opacities but normal lung markings visible. Category 3: large number of opacities with normal lung not visible. - Progressive massive fibrosis - Presents as progressive dyspnoea and chronic bronchitis - CXR: Upper zone fibrotic masses
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Silicosis?
From Quarrying, sand-blasting | Upper zone reticular shadowing and egg shell calcification of hilar nodes --> PMF
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Asbestosis
Demolition and ship building - Basal fibrosis, - pleural plaques - Benign + are calcified. PLeural thickening Asbestosis - lower lobe fibrosis Increased risk of mesothelioma - Chest pain, weight loss, clubbing, recurrent effusions, dyspnoea - CXR: Pleural effusions, thickening - Dx by histology of pleural biopsy Often palliative chemotherapy + there is also a limited role for surgery and radiotherapy.
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Management of pneumoconioses?
Oxygen therapy Pulmonary rehab Bronchodilator therapy
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Idiopathic Pulmonary Fibrosis (CFA)
Rare, life threatening disease that manifests over several years and characterised by formation of scar tissue within lungs and progressive dyspnoea.
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Epidemiology of Idiopathic pulmonary fibrosis?
- Commonest cause of interstitial lung disease - MIddle age - M>F = 2:1 - Associated with AI disease in 30%
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Presentation for IPF?
``` Presentation - Symptoms Dry cough - non-responsive to antitussives Dyspnoea - progressive over 6 months Malaise, weight loss Arthralgia OSA ``` ``` Signs - Cyanosis - Clubbing - Crackles: fine, end-inspiratory (coarse crackles typically louder, lowe pitch and early inspiratory. Indicate excess fluid due to pulmonary oedema, bronchitis) ```
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Complications for idiopathic pulmonary fibrosis?
Increase risk of Ca lung | - Type 2 respiratory failur and cor pulmonale
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Investigations for IPF?
Bloods - Increased CRP - Increased Ig - ANA+ (30%) - RF+ (10%) - ABG: decreased PaO2, increased PaCO2 CXR - Lung volume decreased - Bilateral lower zone reticulonodular shadowing - Honeycomb lung - Ground-glass - traction bronchiectasis HRCT - Shows similar changes to CXR - More sensitive Spiro - Restrictive defect - Decreased transfer factor ``` Other: Lung biopsy: usual interstitial pneumonia BAL: may indicate disease activity - Increased lymphocytes: good prognosis - PMN or eosinophils: bad prognosis ``` DTPA scan: may reflect disease activity
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Management of IPF?
Supportive care - Stop smoking - Pulmonary rehab - O2 therapy - Palliation - Rx symptoms of heart failure - New management Lung Tx offer only cure
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Pulmonary Hypertension
PA pressure >25mmHg
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Causes of pulmonary HTN?
Left heart disease - Mitral stenosis - Mitral regurg - Left ventricular failure - L--> R shunt ``` Lung parenchymal disease - Mechanism Chronic hypoxia --> hypoxic vasoconstriction Perivascular parenchymal changes COPD - Asthma: severe, chronic - Interstitial lung disease - CF, bronchiectasis ``` Pulmonary vascular disease - Idiopathic pulmonary hypertension - Pulmonary vasculitis: scleroderma, SLE, Wegener's - Sickle Cell - Pulmonary embolism: acute or chronic - Portal HTN: portopulmonary HTN Hypoventilation - OSA - Obesity - Thoracic cage abnormalitiy: Kyphosis, scoliosis - Neuromuscular: MND, MG, Polio
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Investigations for P HTN?
ECG - P pulmonale - PVH - RAD CXR - Attentuated peripheral vascular markings Echo - Velocity of tricuspid regurgitation jet - Right atrial or ventricular enlargement - Ventricular dysfunction - Valve Disease ``` Gold standard - Right heart catheterisation: gold standard Mean pulmonary artery pressure Pulmonary vascular resistance CO Vasoreactivity testing to guide Rx ```
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What is Cor Pulmonale?
RHF due to chronic PHT
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Symptoms of Cor Pulmonale?
- Dyspnoea - Fatigue - Syncope
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Signs of Cor Pulmonale?
1. Increased JVP with prominent a wave 2. Left parasternal heave 3. Loud P2 +S3 (due to P HTN) 4. Murmurs PR: Graham Steell EDM TR: PSM 5. Pulsatile hepatomegaly 6. Fluid: Ascites + Peripheral oedema
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Investigations of cor pulmonale?
- Bloods: FBC, U+E, LFTs, ESR, ANA,RF - ABG: hypoxia ± hypercapnoea - CXR Enlarged R atrium and ventricle Prominent pulmonary arteries Peripheral oligaemia ECG: P pulmonale (Peaked P wave) + RVH Echo: RVH, TR, increased Pa pressure Spirometry Right HEart catheterisation
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Management of Cor Pulmonale + PHTN?
Manage underlying condition - Decreased pulmonary vascular resistance - Long Term Oxygen therapy - CCB ( nifidipine) - Sildenafil (PDE-5 inhibitor_ - Prostacycline analogues - Bosentan (endothelin receptor antagonist) Cardiac failure - ACEi + b-B (cautio if asthma) - Diuretics Heart/Lung transplant
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OSA?
Intermittent closure/collapse of pharyngeal airway --> Apnoeic episodes during sleep. OSA - pharyngeal collapse - Central sleep apnoea - Often related to cerebrovascular, cardiac or neuro disease.
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Risk factors of OSA?
``` Obesity Male Smoker ETOH Idiopathic pulmonary fibrosis Structural airway pathology NM disease Hypothyroid Macroglossia ```
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Investigations OSA?
SpO2 Polysomnography is diagnostic Other investigations = ABG = respiratory metabolic therefore rebound metabolic alkalosis. MSLT = daytime hypersomnolence. How quickly patients fall asleep.
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Management of OSA?
Weight loss Avoid smoking + ETOH CPAP during sleep Epworth Sleepiness - ESS - Total score >10 or sleepiness in dangerous situation, even with normal ESS.
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Clinical features OSA?
Nocturnal - Snoring - Choking, gasping, apnoeic episodes Daytime - Morning headache - Drowsiness - Decreased memory and attention - Irritability, depression - Do you get refreshing sleep. - Unrefreshing sleep - Morning headache. Pickwickian - Obesity hypoventilation syndrome - Characterised by obesity, chronic hypercapnia, and sleep disorder breathing. - Approx 90% of patients also have OSA Management: nocutrual CPAP
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Complications of OSA?
``` Pulmonary HTN T2RF Cor pulmonale HTN Stroke Diabetes mellitus ```
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Management of OSA?
``` Decrease weight Stop smoking CPAP at night via nasal mask Surgery to releive pharyngeal obstruction. - Tonsillectomy Uvulopalatpharyngoplasty ```
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Smoking Cessation Advice?
Very Brief Advise - Ask: Enquire as to smoking status - Advise: best way to stop is with support and medication - Act: provide details of where to get help - NHS stop smoking helpline Facilitating Quitting - Refer to specialist stop smoking service - Nicotine replacement (for pregnancy) Gum, patches - Varenicline: selective partial nicotine receptor agonist. Not for pregnancy. Start whilst smoking - Bupropion (not for pregnancy and can reduce the epilepsy threshold.
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Gold standard for staging of COPD?
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
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Transfer factor?
The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO). Reduced ability of the lungs to perform gas exchange. Concentration of CO inhaled and exhaled. Reduction in Gas transfer occurs in both obstructive + restrictive. Restrictive becasue reduce lung volume. Therefore when transfer factor vs alveolar volume the ratio of transfer factor: alveolar volume is not reduced. In obstructive - loss of alveolar structure suggests that alveolar volume is not lost. Therefore transfer factor: alveolar volume is reduced.
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Causes of traised TLCO?
``` asthma pulmonary haemorrhage (Wegener's, Goodpasture's) left-to-right cardiac shunts polycythaemia hyperkinetic states male gender, exercise ```
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Causes of lower TLCO
``` Causes of a lower TLCO pulmonary fibrosis pneumonia pulmonary emboli pulmonary oedema emphysema anaemia low cardiac output ```
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KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO
pneumonectomy/lobectomy - Big scar, mediastinum shift towards pneumonectomy, decreased chest wall expansion, dull percussion, decreased breath sounds, decreased vocal fremitus. scoliosis/kyphosis neuromuscular weakness ankylosis of costovertebral joints e.g. ankylosing spondylitis
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Lobectomy
``` TB Bronchiectasis Malignancy Cystic fibrosis Lung Abscess Single Pulmonary Nodule - RA ```
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Lung Ca
Small cell - SIADH - ACTH - Lambert-Easton Squamous - Hypercalcaemia - PTHrP - Hpoerthyroidims - TSH Adeno - clubbing, HPOA, gynaeocomastia (produced HCG)
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NSCLC
Mostly operated on - adeno, squamous, large cell.
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Pancoast syndrome
- apical lung tumour involvement of the brachial plexus and cervical sympathetic nerves. - Pain in the shoulder/anterior chest wall and arm weakness. - Wasting of intrinsic muscles of the hand. - Ipsilateral Horner's syndrome (ptosis, miosis, anhydrosis and enopthalmos). May present with a history of hoarseness of voice. This can compress the recurrent laryngeal nerve causing hoarseness of voice. Normally in the apices of chest-x ray. CT scan of chest is diagnostic.
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Lung transplant
``` Emphysema Idiopathic pulmonary fibrosis idiopathic pulmonary hypertension Bronchiectasis Cystic fibrosis ```
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Complication of lung cancer - SVCO?
SVCO - Oedema of the face, neck and upper body. - Prominent neck and chest wall vessels - Facial plethora - Stridor - Headache - Dizziness Management - Oncologist and emergency radiotherapy.
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Aspergillus
Aspergilloma - risk with repv TB, sarcoid, COPD. fungal ball in cavity. ABPA - asthma lie ,raised IgE< proximal bronchiectasis. RAST, positive IGG precipitins. Invasive - immunodeficiency.
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Afro-carribean lady presents with breathlessness. She has vague symptoms, fevers, malaise, has a rash on her face. Her bloodworks show increased ACE activity.
Sarcoidosis - bilateral HLA - Afro-caribbean women - ACE, Ca, ESR - Non-caseating granuloma - Kveim test (Kveim - intradermal injection of splenic extraction followed by skin biopsy. - biopsy gold standard.
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Hoarse Voice
- Laryngeal issues - polyp, carcinoma, inflammation (sining, GORD, steroid inhalers - Candida. - Vocal cord paralysis: thyroid mass, lung cancer, ortner's - Laryngoscopy - ENT referral.
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What is tracheal tugging
Diaphragm is working hard, feel the trachea stretching. Indicative of respiratory distress
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Vesicular breathing
all that is left through transmission from bronchial breathing
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In Bronchial breathing
This is conducted because of consolidation. | Ask patient to breath through their mouth.
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Barrell Chest
Feel front and back and left and side and compare their diameter to see if barrel chest.
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Inhaled foreign body
End up passing through the right main bronchus as the most direct pathway. Mostly into the inferior or middle lobe bronchi.
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Indications for NIV?
- COPD with respiratory acidosis pH 7.25-7.35 - T2RF secondary to chest well deformity, neuromuscular disease, OSA. - cardiogenic pulmonary oedema unresponsive to CPAP - weaning from tracheal intubation
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Recommended initial settings for bi-level pressure support in COPD?
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O back up rate: 15 breaths/min back up inspiration:expiration ratio: 1:3
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Lobar collapse causes?
Lung cancer Asthma (due to mucous plugging) Foreign body Signs of lobar collapse - tracheal deviation towards the side of the collapse - mediastinal shift towards the side of the collapse - elevation of the hemidiaphragm
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Causes of respiratory alkalosis
- Hyperventilation - Pulmonary Embolism - Salicylate poisoning - CNS disorder: stroke, Sub Arachnoid (hyperventilation reduces ICP via hypocapnoeic vasoconstriction) - Altitude - Pregnancy
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Management of atelectasis
Presents with early postoperative shortness of breath, with a raised temperature. Due to basal alveolar collapse. Due to obstruction by bronchial secretions obstructing airways. Management = Chest physiotherapy.
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Differential for postoperative shortness of breath
Atelectasis Pneumonia PE
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Causes of respiratory acidosis?
- COPD - Decompensation in other respiratory conditions - life-threatening asthma - Neuromuscular disease - Obesity hypoventilation syndrome - Sedative: benzodiazepines, opiate overdose
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What is the transfer factor?
Describes the rate at which gas will diffuse from alveoli into blood. CO is used to test the rate of diffusion. Results are given as total gas transfer or that correct for lung volume (transfer coefficient, KCO). TLCO is an overall measure of gas transfer for the lungs from alveoli into capillaries and reflects how much O2 is being taken up. KCO is TLCO divided by the alveolar volume - measure of how efficient gas exchange is in relation to the alveolar-capillary surface to volume ratio. Therefore in a small alveolus, there is increased pulmonary blood flow which increases the relative surface area to volume ratio.
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What are the causes of a raised TLCO? (total lung gas transfer)
- Asthma - Pulmonary haemorrhage - Left-to-right cardiac shunts - Polycythaemia - Hyperkinetic state - Male gender This is because the problem is not affecting the alveoli directly or gas exchange, so the lungs try to compensate by improving gas exchange. KCO is TLCO divided by alveolar volume - this is increased because increased pulmonary blod flow which increases the number of cell which come in contact with gas.
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What are causes of lower TLCO
``` Pulmonary fibrosis Pulmonary emboli Pulmonary oedema Emphysema Anaemia Low cardiac output ```
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KCO?
Increases with age. These conditions increased KCO with a normal or reduced TLCO - Pneumonectomy/lobectomy - Scoliosis - Neuromuscular weakness - Ankylosis of costovertebral joints.
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Occupational asthma?
Serial measurements of peak expiratory flow are recommended at work and away from work. Consider referral to specialist
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Oxygen therapy
Acutely ill patient: 94-98% | COPD (hypercapnia patients): 88-92
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Alpha-1 antitrypsin deficiency
Inherited condition caused by lack of protease inhibitor normally produced by liver. - May present with emphysema, in the lower lobes. COPD presents with emphysema in the upper lobes. - Liver: cirrhosis and HCC in adults, cholestasis in children.
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Cavitating lung lesions differentials
``` Abscess (Staph A, Klebsiella, Pseudomonas) Squamous Cell lung cancer TB Wegener's Granulomatosis Pulmonary Embolism RA Aspergillosis ```
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Granulomatosis with polyangiitis
Autoimmune condition associated with a necrotizing granulomatous vasculitis. - URT: epistaxis, sinusitis, nasal crusting - LRT: dyspnoea - Glomerulonephritis - Saddle-shaped nose deformity - Vasculitis rash, eye, cranial nerve. WAGs CANCA Remember Churg-Strauss causes asthma, eosinophilia too. Therefore there are polyps in the nose - positive ANCA.
295
Presence of consolidation below the horizontal fissure
Suggests right middle lobe consolidation.
296
Nasogastric tube aspirate placement?
If aspirate obtained has a pH <5.5, the NG tube is safe to use. If aspirate >5.5, request a chest x-ray to confirm the position of the NG tube. If no aspirate can be obtained - Turn the patient on their left side Inject 10-20ml air offer a drink or mouth care and recheck aspirate in 15-20 mins Advance or withdraw the NG tube by 10-20cm.
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Chest X-ray lobar collapse causes?
Lung cancer Asthma (Mucus plugging) Foreign boy. General signs of lobar collapse - Tracheal deviation towards the side of the collapse - Mediastinal shift towards the side of the collapse - Elevation of the hemidiaphragm
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Pneumonectomy
Opacified left hemithorax with mediastinal and tracheal shift towards the affected side. Crowding of the ribs over the affected side with compensatory overinflation of normal lung is also seen.
299
Causes of trachea pulled towards with white out?
Pneumonectomy Complete lung collapse Pulmonary hypoplasia
300
Trachea pushed away from the white-out?
Pleural effusion Diaphragmatic hernia Large thoracic mass
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Trachea central with whiteout
Consolidation Pulmonary oedema Mesothelioma
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Predominant cough without lung function abnormalities?
pertussis
303
prominent dizziness, light-headedness, peripheral tingling
Dysfunctional breathing
304
Recurrent severe asthma attacks without objective confirmatory evidence
Vocal cord dysfunction
305
Predominant nasal symptoms without lung function abnormalities?
Rhinitis
306
Postural and food-related symptoms, predominant cough
GORD
307
Orthopnoea, paroxysmal nocturnal dyspnoea, peripheral oedema, preexisting cardiac disease
Cardiac failure
308
Chronic productive cough in the absence of wheeze or breathlessness
Bronchiectasis; inhaled foreign body; obliterative bronchiolitis; large airway stenosis
309
New onset in smoker, systemic symptoms, weight loss, haemoptysis
Lung cancer; sarcoidosis
310
Altitude disorders?
Acute mountain sickness High altitude pulmonary oedema High altitude cerebral oedema All due to chronic hypobaric hypoxia which develops at high altitudes.
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What is Acute mountain sickness
Start over 2500-3000. Over 6-12hr. - Headache - Nausea - Fatigue Prevention and treatment of AMS - the risk of AMS may actually be positively correlated to physical fitness - gain altitude at no more than 500 m per day - acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base - treatment: descent
312
HACE and HAPE
A minority of people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions HAPE presents with classical pulmonary oedema features HACE presents with headache, ataxia, papilloedema Management of HACE - descent - dexamethasone ``` Management of HAPE descent - nifedipine, - dexamethasone, - acetazolamide, - phosphodiesterase type V inhibitors* - oxygen if available ```
313
Mesothelioma?
Malignancy of mesothelial cells of pleura Metastases to contralateral lung and peritoneum Right lung affected more often than left - Features include occupational asbestos exposure - Family history - Latent period Typically present with - Dyspnoea - Clubbing - 30% secondary to pleural effusion (stony dull percussion note). - History of asbestos exposure Although a chest x-ray is usually the first modality performed - normally see unilateral pleural effusion/thickening. - the next step is normally a pleural CT - if a pleural effusion is present fluid should be sent for MC&S, biochemistry and cytology (but cytology is only helpful in 20-30% of cases) - local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%) - if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used ``` Management - Symptomatic Industrial compensation - Chemotherapy, Surgery if operable - Prognosis poor, median survival 12 months ```
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Causes of haemoptysis
Lung cancer - smoking, weight loss, anorexia Pulmonary oedema - dyspnoea, bibasal crackles + S3 TB - fever, night sweats, anorexia, weight loss PE - Pleuritic chest pain, tachycardia. LRTI - purulent cough Bronchiectasis - usually long history of cough daily + purulent sputum production MS - dyspnoea, AF, malar flush, mid-diastolic murmur Aspergilloma - past history of TB, haemoptysis, rounded opacity Granulomatosis with polyangiitis - URT (epistaxis, sinusitus) LRT (dyspnoea, haemoptysis, glomerulonephritis, saddle-shaped nose deformity Goodpastures - haemoptysis, glomerulonephritis, systemically unwell: fever, nausea
315
Causes of lung metastases?
``` Breast cancer Colorectal cancer Renal cell cancer Bladder cancer prostate cancer ```
316
Loss of the left heart border?
Left lingula consolidation
317
Bilateral hilar lymphadenopathy?
``` Lymphoma Pneumoconiosis Fungi TB Sarcoid ```
318
No antibiotic prescribing or delayed antibiotic prescribing for which resp conditions?
``` Acute otitis media Acute sore throat Acute pharyngitis Acute tonsillitis Common cold Acute rhinosinusitis Acute cough/acute bronchitis ```
319
Consider immediate antibiotic prescribing in which patients?
children younger than 2 years with bilateral acute otitis media children with otorrhoea who have acute otitis media patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present
320
What is the Centor criteria?
The Centor criteria* are as follows: Bacterial cause of sore throat. - presence of tonsillar exudate - tender anterior cervical lymphadenopathy or lymphadenitis - history of fever - absence of cough
321
Length of time for each Resp infection?
The guidelines also suggest that patients should be advised how long respiratory tract infections may last: acute otitis media: 4 days acute sore throat/acute pharyngitis/acute tonsillitis: 1 week common cold: 1 1/2 weeks acute rhinosinusitis: 2 1/2 weeks acute cough/acute bronchitis: 3 weeks
322
Respiratory causes of clubbing
``` Lung cancer Cystic fibrosis, bronchiectasis, abscess, empyema TB Asbestosis, mesothelioma Fibrosing alveolitis ```
323
Chest drain swinging?
Rises in inspiration Falls in expiration Insertion - Safe triangle Mid axillary line 5th intercostal space. Anterior edge of latissimus dorsi, lateral border of pectoralis major, line superior to the horizontal level of the nipple.
324
Thymoma causes what?
Myasthenia gravis.
325
Nicotine replacement?
- Patient should be offered NRT, varenicline, bupropion. NRT, varenicline, bupropion normally as part of commitment to stop smoking. - NRT, varenicline, bupropion should be sufficient to last only 2 weeks after target stop date. - If unsuccessful, do not offer repeat prescriptions within 6 months unless special circumstances have intervened. Do not offer NRT, varenicline, bupropion.
326
Adverse effects of NRT?
adverse effects include nausea & vomiting, headaches and flu-like symptoms NICE recommend offering a combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge or nasal spray) to people who show a high level of dependence on nicotine or who have found single forms of NRT inadequate in the past
327
What is varenicline?
- a nicotinic receptor partial agonist - should be started 1 week before the patients target date to stop - the recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking) has been shown in studies to be more effective than bupropion - nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams - varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline - contraindicated in pregnancy and breast feeding
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What is bupropion?
Bupropion a norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist should be started 1 to 2 weeks before the patients target date to stop small risk of seizures (1 in 1,000) - contraindicated in epilepsy, pregnancy and breast feeding. - Having an eating disorder is a relative contraindication
329
Respiratory syncytial virus
Bronchiolitis
330
Parainfluenza?
Croup
331
Rhinovirus
Common cold
332
Influenza
Flu
333
Strep Pneumonia
Most common cause of CAP
334
Haem Influenzae
CAP Most common cause of bronchiectasis exacerbation Acute epiglottitis
335
Staph Aureus
Pneumonia, particular following influenza