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Resp Flashcards

1
Q

Management of mild CAP

A
  • Monotherapy, home. - PO Amoxicillin (500mg TDS) or macroloid e.g. Clarithromycin (500mg BD) in allergy - 5 days unless no improvement after day 3 - 7d
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2
Q

Management of moderate CAP

A
  • Dual therapy, consider hospital tx - PO/IV Amoxicillin (500mg TDS) + macroloid e.g. clarithromycin (500mg BD) - 7-10 days
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3
Q

Management of severe CAP

A
  • Dual therapy, hospital admission - IV beta-lactamase stable beta-lactam (e.g. co-amoxiclav 1.2g TDS) + IV macroloid e.g. Clarithryomycin (500mg BD) - OR: Cefuroxamine (1.5mg TDS) IV + clarithromycin (500mg BD) - 7-10 days
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4
Q

Which cause of penumonia is assocaited with a facial rash (Horder’s spots)? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

Chlam. Psitacci Aswell as Splenomegaly, epistaxis, hepatitis, nephritis and meningio-encephalitis. Treat with Clarythro.

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5
Q

Which cause of pneumonia is associated with Mediterranean travel? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

F. Legionella 50% of cases occur after travel, predominately in Mediterranea countries. It is associated with water containing systems such as air conditioning.

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6
Q

Which cause of pneumonia is associated with a previous or coincidentant influenza infection? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

B. Staph areus

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7
Q

Which cause of pneumonia is associated with cavitating lesions in the upper lobes? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

C. Klebisella Tx with Cefotaxamine

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8
Q

Which cause of pneumonia is associated with Low sodium? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

F. Legionella Tx with Clarithromycin +/- rifampacin

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9
Q

Which two causes of pneumonia can be diagnosed on a urinary antigen? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

A. Strep pneumonia Tx with amoxicillin F. Legionella Tx with Clarithromycin +/- rifampacin

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10
Q

Which cause of pneumonia is associated with herpes labialis? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

A. Strep pneumonia

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11
Q

What CXR finding would you most commonly expect to see on a patient with PCP penumonia? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Bilateral Perihilar interstitial shadowing
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12
Q

What CXR finding would you most commonly expect to see on a patient with Strep penumonia? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Lobar consolidation
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13
Q

What CXR finding would you most commonly expect to see on a patient with Staph aerus? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Cavitating lesions bilaterally
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14
Q

What CXR finding would you most commonly expect to see on a patient with Legionella? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Bi-basal consolidation
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15
Q

What CXR finding would you most commonly expect to see on a patient with Clamyd. psitacci? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Patchy consolidation
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16
Q

What CXR finding would you most commonly expect to see on a patient with Mycoplasma (select more than one)? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Patchy consolidation, OR 4. Reticulo-nodular shadowing
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17
Q

What CXR finding would you most commonly expect to see on a patient with Klebisella? 1. Bilateral Perihilar interstitial shadowing 2. Patchy consolidation 3. Bi-basal consolidation 4. Reticulo-nodular shadowing 5. Cavitating lesions bilaterally 6. Cavitating lesions in the upper lobes 7. Lobar consolidation

A
  1. Cavitating lesions in the upper lobes
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18
Q

Which two causes of pneumonia is associated with jaudice? A. Strep pneumonia B. Staph Aeurs C. Klebisella D. Pseudomonas E. Mycoplasma F. Legionella G. Chlamydiophila penumonia H. Chlamydiophila psittaci I. PCP

A

E. Mycoplasma F. Legionella Usually cholestatic

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19
Q

Complications of pneumonia (nine)

A
  1. Respiratory failure 2. Hypotension 3. AF 4. Plueral effusion 5. Empyema 6. Lung abscess 7. Sepsis 8. Pericarditis/myocarditis 9. Jaudice (legionella, mycoplasma)
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20
Q

Causes of clubbing

A
  • Unilateral - AVM or aneurysm of the upper limb
  • Bilateral:
    • Primary - familial
    • Secondary
      1. Respiratory
        • Carcinoma (mesothelioma or bronchial),
        • Chronic lung suppuration ( bronchiectasis, CF, empyema, abscess),
        • Fibrosis (idiopathic, TB)
      2. Cardiac
        • Atrial myxoma,
        • Congenital cyanotic heart disease,
        • Infective endocarditis
      3. GIT - 4 Cs
        • Coeliac,
        • Crohns and UC,
        • Cancer (GI lymphoma),
        • Cirrhosis
      4. Endocrine - thyroid acropachy
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21
Q

Define cyanosis

A

Blue discolouration of the skin or mucosal membranes occurring when deoxygenated Hb is greater than 5g/dL

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22
Q

Deoxygenated Hb is greater than ____g/dL results in cyanosis

A

5g/dL

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23
Q

Classification of cyanosis

A

Central (lips, tongue) or peripheral (nails)

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24
Q

Causes of cyanosis

A
  1. Respiratory
  • Decreased ventilation - COPD/MSK -
  • Decreased exchange - fibrosis, oedema -
  • V/Q mismatch - PE or AVM
  1. Cardiac/vascular
  • Insufficient output - AS, heart failure -
  • Decreased perfusion - Raynauds or DVT -
  • Congenital - Fallots, TGA
  1. Hb - hereditary or acquired low affinity Hb
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25
Q

SIRS definition and criteria

A

Systemic inflammatory response syndrome - a non specific inflammatory response to a number of insults. Criteria = 2 or more of: 1. Temp: more than 38 or less than 36 2. HR: more than 90 3. Resp: more than 20 or PaCO2 less than 4.6KPa 4. WCC: More than 12, less than 4 or more than 10% bands

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26
Q

Sepsis definition

A

SIRS + unidentified source of infection

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27
Q

Severe sepsis defintion

A

Sepsis (SIRS + infective source) + at least one organ dysfunction or hypoperfusion

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28
Q

Septic shock defintion

A

Severe sepsis with refractory hypotension

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29
Q

What is MODS

A

Multiorgan dysfuntion - dysfunction of at least two organs and failure to maintain haemostats without intervention.

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30
Q

What is bronchiectasis

A

Chronic infection of the bronchioles/bronchi causing permanent dilatation, the production and retention of inflammatory secretion and microbes resulting in airway damage and recurrent infections.

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31
Q

What causes bronchiectasis

A
  1. Idiopathic (50%) 2. Congenital - lung sequestration 3. Mucocilliary clearance abnormalities: Kartageners, CF (#1 casein developed countries) and Young’s syndrome 4. Infective - severe pneumonia, whooping cough, TB and non-TB mycobacterium 5. Immune-deficiencies - 1º - hypogammaglobinaemias (Brutons, CVID, IgA, IgG) or 2º HIV, CLL, nephrotic syndrome 6. Toxic insults: aspiration, inhalation (gas/chemical) 7. Mechanical insult - carcinoma, enlarged LN, foreign body 8. Other - ABPI, yellow nail syndromeº
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32
Q

What is yellow nail syndrome

A
  1. Yellow/discoloued nails 2. Bronchiectasis 3. Pleural effusions 4. Lymphedema
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33
Q

List some complications of bronchiectasis

A
  1. Severe haemoptysis (25% mortality) 2. Pneumonia 3. Pleural effusion 4. Pneumothorax 5. Pulmonary HTN 6. Cerebral abscess 7. Amyloidosis
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34
Q

What is the usual cause of death in bronchiectasis?

A

Cor pulmonale and respiratory failure.

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35
Q

Essential investigations in ?brochiectasis

A
  1. CXR - tramlines and rings 2. HRCT - GOLD. Dilated and thickened airways. Saccular dilatations in clusters with pools of mucus 3. Lung function 4. Sweat test - need to rule out CF 5. Sputum cultures 6. IgA, IgM, IgG 7. Aspergillus precipitins maybe AFB in London
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36
Q

Management of bronchiectasis

A
  1. Chest physio 2. Abx for exacerbations (e.g. cirpo 7-10days) 3. Bronchodilators (neb Beta agonist) 4. Tx underlying cause 5. Antimicrobial chemo if necessary (intermittent or long-term)
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37
Q

Disease progression/symtoms of bronchiectasis

A
  1. Yellow/green sputum produced after infections 2. Persistent halitosis, recurrent febrile episodes and episodes of pneumonia 3. Continuous production of fowl smelling sputum (thicl and Khaki coloured) +/- haemoptysis +/- breathlessness May have associated fever and weight loss
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38
Q

Signs of bronchiectasis

A
  • Clubbing
  • Coarse inspiratory creps
  • Wheeze
  • Purulent sputum
  • Clues of the cause: situs inversus (kartageners) or splenomegaly in immune deficiency.
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39
Q

The main pathogens that colonise sufferers of bronchiectasis are…?

A

PIPS + klebisella

Pseudomonas H. Influenza Pneumococcus Staph areus

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40
Q

Pathogenesis of CF

A

An AR mutation in Ch7 of the CFTR gene which encodes a chlorine transporter. This causes luminal decreased secretions of Cl- and increased resorption of Na+ giving thick secretion. It also causes decreased resorption of Cl- and Na+ in sweat leading to salty sweat

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41
Q

Features/symptoms of CF

A

Neonates - meconium illeus, failure to thrive Children: 1) Nose - nasal polyps and recurrent sinusitis 2) Lung - wheeze, recurrent infections, thick secretions, cough, bronchiectasis, haemoptysis, pneumothorax and cor pulmonate 3) GI - - Pancreatic - DM, steatorrhoea - Distal intestinal obstruction syndrome - Gallstones - Cirrhoses (2º to billiard) 4) Bone - osteoporosis 5) Repro - male infertility 6) Vascular - vasculitis

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42
Q

Common respiratory organisms in CF

A

PI(P)S + B. Cepacia Pseudonomas H. Influenza Staph areus

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43
Q

Diagnosis of CF

A
  1. Prenatally - 1 T - villous sampling, 2T decreased ALP in amniotic fluid 2. At birth - heel prick - immunoreactive trypsinogen 3. Sweat test - pilocarpine ionotrophoresis (Na+ >60, Cl >50) Also fecal elastase and genetic screening
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44
Q

Investigations to do in CF sufferers (Post-diagnostic testing)

A
  1. Lung function:
  • CXR - bronchiectasis, pneumothorax…
  • HRCT - bronchiectasis
  • Sputum MCS -
  • Spirometry
  • Aspergillus serology (20% develop ABPA)
  1. GI
    • Bloods: LFTs, clotting, ADEK, glucose levels
    • US: cirrhosis, fatty liver, pancreatitis…
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45
Q

Management of CF

A

MDT approach: GP, specialist nurses, specialist doctors, physiotherapist, counsellors, genetics/family planning advice, dietician…

  1. Lungs
    1. Infection
        • Acute infections - longer course and increased dose -
      2. Pseudomonas (torbamysin or colistin bd neb) -
      3. vaccines: pneumococcus and H.Ifluenza.
    2. Mucus
        • Physio
        • Mucolytics - recombinant DNase -
      3. Hyeprtonic saline (7%)
    3. C) Other
        • Macrolides
        • anti-inflammatory -
      3. IVACAFTOR - CFTR potentiator
  2. GIT
    1. Pancreatic insufficiency
        • Enzymes (CREON)
      2. Vitamins (ADEK)
      3. Insulin
    2. HB - deoxycolic acid
  3. Bone - DEXA +/- calcium and vit
  4. End stage: steroids, Oxygen therapy and lung transplants.
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46
Q

Pulmonary aspergillus infections encompases a range of disease. What are these?

A
  1. Asthma
  2. ABPA - allergic bronchopulmonary aspergillosis
  3. Aspergilloma (mycetoma), also CCPA chronic cavitary pulmonary aspergilloma
  4. Invasive aspergillosis
  5. Extrinsic allergic alveoli’s
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47
Q

What is the pathogenesis behind ABPA

A

A type I and III hypersensitivity reaction to aspergillus fumigatus moulds (which can be isolated from the air of most houses). IgG and IgE reactions to aspergillum leading to bronchoconstriction and bronchiectasis.

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48
Q

What are the symptoms of ABPA

A
  • Cough (productive) - Wheeze - Dyspnoa
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49
Q

What are the diagnostic criteria of ABPA

A

Top 4 1. Long Hx of asthma 2. CXR showing bronchiectasis 3. Positive skin prick or RAST test for aspergillum 4. Postive se precitipins (IgG to aspergillus) Others: - aspergillus in sputum - High IgE and eosinophils - Lung infiltrates

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50
Q

Management of ABPA

A

Essentially treat as asthma adding an anti-fungal Steroids: 5-10mg/d, increased to 40mg during acute attack Bronchodilators as needed. Anti-fungal: itraconazole (monitor LFTs - liver dysfunction)

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51
Q

What is an aspergilloma

A

Formation of a fungi ball in a previously formed cavity (e.g. from sarcoid or TB). If there are several this is termed Chronic Cavitating Pulmonary Aspergilloma.

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52
Q

What is CCPA

A

Chronic Cavitating Pulmonary aspergilloma - presence of several aspergilloma

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53
Q

Clinical features of Aspergilloma

A

Usually asymptomatic. May present with haemoptysis or systemic symptom of chronic disease (fever, Wt. loss, malaise, lethargy, chest pain)

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54
Q

Management of aspergilloma

A
  1. If a solitary lesion - may not require treatment, or consider resection particularly if severe haemoptysis. 2. Itroconazole or Voriconazole can help systemic symptoms or CPAP 3. Treat haemoptysis which may be life threatening.
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55
Q

What is invasive aspergillosis?

A

Invasion of tissue by aspergillus hyphae. - Route of entry is probably lungs, spreading to the brain, sinuses, heart, eyes and skin. - Alfatoxin production can lead to liver cirrhosis and HCC

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56
Q

What are the risk factors for invasive aspergillosis

A
  1. Immunosuppression: HIV, leukaemia, wegeners 2. Post-borad spectrum Abx. 3. Neutropenia and steroid use
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57
Q

Treatment of invasive asperillosis

A

Voriconazole IV

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58
Q

SE of voriconazole

A

deranged LFT, rash and visual disturbance

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59
Q

SE of itroconazole

A

deranged LFTs - liver dysfuntion

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60
Q

____% mortality in invasive aspergillosis

A

30%

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61
Q

What is extrinsic allergic allveolitis

A

Hypersensitivity to various proteins including

  • Aspergillum species - Aspergillus clavatus - malt workers (mouldy barley)
  • Farmers lung
  • Humidifiers lung
  • Compost lung
  • Mushroom workers lung etc.
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62
Q

Common lung cancer types

A
  1. Non-small cell lung cancer - SCC (35%) - Aden (25%) - Large cell cancer (10%) 2. Small cell lung cancer (20%) Others: adenoma, mesothelioma, hamartoma…
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63
Q

What lung cancers is smoking a risk factor for?

A
  • Small cell lung cancer - SCC - NOT adeno
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64
Q

Common locations within the lungs of the common lung cancer types?

A

Peripheries: Large cell and adeno Centrally: SCC, Large cell and small cell

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65
Q

Differences in histology of the common lung cancer types

A
  1. SCC - evidence of squamous differentiation - keratinised 2. Adeno - gandular differentiation - gland formation and mucin production 3. Large cell - large poorly differentiated cells 4. Small cell - small poorly differentiated cells
66
Q

Which lung cancer types metastasise early and which late?

A

Early: Adeno and small cell (80% advanced at presentation

Late: SCC (locally invasive)

67
Q

Typical symptoms of lung cancer

A
  1. cough
  2. poorly resolving pneumonia
  3. haemoptysis
  4. Breathlessness
  5. Systemi: wt loss, anorexia, lethargy…
  6. Chest pain
  7. hoarseness

Of metastasis: bone tenderness, hepatomegaly, confusion/fits, addison’s

68
Q

Signs of lung cancer

A
  1. In the lungs: consolidation, collapse, pleural effusion 2. Generally: cachexia, anaemia, clubbing and HPOA, suclavicular/axillary LN 3. Of metastasis: bone tenderness, hepatomegaly, confusion/fits, addison’s…
69
Q

Complications of lung cancer

A
  1. Local - nerve palsies (recurrent laryngeal and phonic), SVC obstruction, horner’s syndrome, AF
  2. Paraneoplastic - Endo (ADH, serotonin, ACTH, PTHrP) - Rheum (dermatomyositis/polymyositis) - Neuro (peripheral neuropathies and cerebral degeneration - Derm (acanthosis nigricans and trousseaus)
  3. Metastatic - bone fractures - hepatic failure - confusions/fits/focal neurology - Addisons
70
Q

CXR characteristics of lung cancer

A
  1. Coin lesions 2. Pleural effusion 3. Hilar enlargement 4. Consolidation/collapse 5. Bone secondaries
71
Q

Imaging to use in ?lung cancer

A
  1. CXR 2. Contrast-enhanced volumetric CT 3. PET-CT - distant mets 4. Radionuclide bone scan
72
Q

Biopsy option in ?Lung cancer

A
  1. Percutaneous FNA 2. Bronchoscopy - biopsy + operability? 3. Endoscopic bronchial US biopsy
73
Q

Differentials for coin lesion on CXR

A

“FANGS” F - foreign body A - abscess: TB, Kleb, Staph, Mycetoma N - neoplastic G - granuloma: RA, wegeners, TB, sarcoid… Structural - AVM

74
Q

Staging of lung non-small cell lung cancer

A

TMN staging Tis - in situ Tx - in bronchial secretions To - nil T1 - local, less than 3 cm T2 - more than 3 cm but more than 2cm from carina or pleural involvement T3 - less than 2cm from carina or pleural involvement T4 - Involvement of mediastinum or malignant effusion present No - nil N1 - local bronchial, ipsilateral hilar N2 - ipsilateral mediastinum N3 - contralateral or supraclavicular

75
Q

Management of Lung cancer (general)

A
  1. MDT approach: pulmonologist, oncologist, radiologists, palliative care team, specialist nurse, surgeon, GP… 2. Assess operative risk 3. Advice smoking cessation
76
Q

Management of NSCLC

A
  1. SURGICAL resection - Stage I or II and good cardio-rep function with no mets +/- adjuvant chemo 2. Curative radiotherapy 3. Chemo +/- radio for advanced disease: platinum based: cetuximab (EGFR), erlotinib (TKI)
77
Q

management of SCLC

A
  1. Chemotherapy (good response but rapid recurrence) 2. Palliation: a. analgesia b. pleural drainage c. Endobrochial therapy: stenting d. SVC obstruction: dexamethasone, stent, radio. e. Radio: bronchial obstruction, bone mets, haemoptysis or CNS mets,
78
Q

What is the pathogenesis of ARDS

A

Presence of inflammatory mediators increases permeability of the pulmonary vascular leading to a non-cariogenic pulmonary oedema

79
Q

Causes of ARDS

A
  1. Primary - lung insult
    1. Aspiration
    1. Pneumonia
    1. Contusion
    1. Inhalation injury
  1. Secondary - systemic
      1. Shock
      1. Sepsis
      1. Major haemorrhage with several transfusions
      1. DIC
      1. Liver failure
      1. Pancreatitis
      1. Trauma
      1. Obs: eclmapsia, amniotic embolism
      1. Drugs: aspirin and heroin.
80
Q

Clinical features of ARDS

A
  1. tachypnoea 2. cyanosis 3. bilateral fine crops 4. SIRS Of acute onset with no features of congestive heart failure.
81
Q

Investigations in ARDS

A

Bloods: amylase, FBC, U&E, clotting, CRP, cultures, ABG CXR: bilateral hilar infiltrates PaO2:FiO2 = less than 200.

82
Q

Management of ARDS

A

Intensive care admission and tx of underlying cause: 1) Ventilation - 6ml/Kg + PEEP 2) Circulation - Invasive BP monitoring. Maintain BP and DO2 using ionotropes if needed: nomad or dobutamin 3) Sepsis - abs 4) Nutritional support enteral best, or TPN

83
Q

Indications for ventilation in ARDS

A

PaCO2 more than 6, PaO2 less than 8 despite 60% FiO2

84
Q

Prognosis of ARDS

A

50-75% mortality.

85
Q

Differentials for Pulmonary Oedema

A
  1. Blood source a) Increased hydrostatic pressure - CCF, iatrogenic fluid overload, renal failure b) decreased capillary oncotic pressure - liver failure, nephrotic syndrome, malnutrition/malabsorbtion, protein loosing enteropathies 2. Interstital source Decreased lymphatic drainage - e.g. cancer
86
Q

Define the types of respiratory failure

A

Type 1 - PaO2 less than 8 with PaCO2 less than 6 Type II - Pa=2 less than 8 with PaCO2 more than 6

87
Q

Causes of respiratory failure

A
  1. V/Q mismatch -
    1. vascular (PE, PHT, Pulmonary shunt R to L),
    2. Early asthma,
    3. Pneumothorax, atelectasis.
  2. Alveolar hypoventilation
    • a) Obstructive: asthma, COPD, bronchiectasis, bronchiolitis, intra/extrathoracic (Ca, LN, epiglottitis)
    • b) Restrictive:
      • decreased drive (sedation malignancy or trauma),
      • NM disease (MG, GBS, polio, cervical lesion),
      • Chest (flail, kyphoscoliosis, obesity),
      • Fluid and fibrosis
  3. Diffusion failure
    1. Fluid: oedema, pneumonia, infection or blood
    2. Firbosis
88
Q

Clinical features of respiratory failure

A

Acute: cyanosis, dyspnoea, agitation, confusion Chronic: PHT, polycythaemia, cor pulmonale.

89
Q

management of respiratory failure

A
  1. Tx underlying cause
  2. Type 1 - give O2 to maintain 94-96% sats. Assisted ventilation if PaO2 is less than 8 despite FiO2 60%
  3. Type 2 - give 24% O2 to main 88-92% sats and PaO2 more than 8. Check ABG after 20 min - check PaCO2 and may increase O2 if necessary.

If patient still hypoxic consider NIV or rep stimulus (doxapram)

90
Q

What is doxapram

A

A respiratory stimulator.

91
Q

Define asthma

A

An episodic, reversible airway obstruction caused by bronchial hyper-reactivity to a variety of stimuli

92
Q

Pathophysiology of asthma

A
  1. Acute (30min) - Mast cell-Ag interaction leading to histamine release. This causes bronchoconstriction, mucus plugging and mucosal swelling.
  2. Chronic (12h) - Th2 cell releasing IL-3, 4 and 5 causing mast cell, eosinophil and B cell recruitment. Airway remodelling.
93
Q

Causes of asthma

A
  1. Atopy: T1 hyersensitivity to pollen, dust mites, food, animals, fungus…
  2. Stress: cold air, URTI, exercise, emotion
  3. Toxins: smoking, pollution, facory
  4. Drugs: NSAIDs and beta-blockers
94
Q

Asthma associated respiratory diseases

A
  • GORD
  • ABPA
  • Churg-Strauss
95
Q

Top differentials for asthma

A
  • Pulomary oedema (cardiac asthma)
  • COPD
96
Q

Investigations in asthma

A
  1. Lung function tests. FEV1:FVC 75% with a 15% FEV1 improvement with a beta-agonist
  2. Bloods: IgE, FBC (eosinophilia), aspergillus serology
  3. CXR - hyperinflation
  4. PEFR monitoring showing diurnal variation more than 20% with mornig dippinh
  5. Atopy: RAST, skin prick.
97
Q

Management of Asthma

A

TAME the asthma + use the ladder

  1. T - teach correct inhaler technique
  2. A - avoide allergens, smoke, dust…
  3. M - monitor peak flow (diary 2-4x/d)
  4. E - educate: liase withspecialist nurse, explain need for compliance and produce emergency action plan
98
Q

BTS Asthma drug Ladder (non-acute)

A
  1. PRN beta agonists
  2. Low dose inhalded steroids (100-400micrograms BD). 200g BD is a good starting dose.
  3. Add LABA (e.g. salmetorol 50 micrograms BD)
    1. If good repsonse continue
    2. If poor response, increase steroid to 400BD.
    3. If no response: stop LABA, increase steroid (800) and try alternative: leutrokiene receptor antagonist or theophylline
  4. Trail
    1. Increase steroid to 1.000 micrograms BD
    2. Add 4th drug:
      1. Leukotreiene receptor antagonist
      2. Theophylline
      3. beta agonist PO
  5. Oral steroids: pred 5-10mg OD maintaining a high dose inhaled steroid (2.000) and REFER.
99
Q

Define acute severe asthma

A

Must have any of the following four features

  1. PEFV <50% best
  2. HR >110
  3. RR >25
  4. Cannot complete a full sentence in one breath
100
Q

Define life threatening asthma

A
  1. SpO2 <92%, O2 <8kPa, CO2 > 4.6kPa
  2. PEFV <33% best
  3. “CHEST”
    1. Cyanosis
    2. Hypotension
    3. Exhaustion/confusion
    4. Silent chest
    5. Tacy/brady/arrhythmia
101
Q

Admission criteria for acute asthma

A

Life threatening asthma or acute severe with a poor inital response to treatment. A patient may leave if after one hour PEFR > 75%

102
Q

Management of acute severe asthma

A
  1. ABC
    1. Airway - make sure it is not obstructed
    2. Breathing - oxygen to maintain SpO2 94-98%
    3. Circualtion - insert wide boar cannular
  2. Treatment:
    1. Nebulised, oxygen driven, salbutamol (2.5-5mg)
    2. Ipratropium bromide 0.5mg
    3. Steroids (as soon as possible): 40-50mg PO prednisolone
  3. Monitor
    1. PEFR
    2. O2 sats, pH and PCO2
    3. HR, RR
    4. Glucose, potassium
    5. CXR for pneumothorax or pneumonia
103
Q

How to treat asthma not responsive to steroids, beta agonist and anti-cholingerci therapy

A
  • IV magnesium sulphate 1.2-2g IV over 20 min
  • IV aminophylline 5mg/kg over 20 min
  • Fluids, antibiotics and adrenaline as needed.
104
Q

Discharge plan post serious asthma exacerbation

A
  • TAME: teach correct inhalaer technique, avoidacne of allergens/trriggers, Monitor with peak flow diary, Educate (emercy plan, specialist nurse…)
  • PO steroids for 5 days
  • GP appointment within the week
  • Specialist appointment within the month
105
Q

Definition of COPD

A
  1. Cough present on most days for at least 3 months of the successive two years
  2. Emphysema: histological diagnosis of enlarged ariway speaces and destruction of alveolar walls.
  3. Airway obstruction (FEV1 <80%, FEV1:FVC <0.7)
106
Q

Causes of COPD

A
  1. Smoking
  2. Pollution
  3. A1AT deficiency
107
Q

Scoring of dyspnoea severity

A

mMRC dyspnoea scale

  1. Dyspnoea on vigorous exercise
  2. Dyspnoea on mild exertion: hurrying or walking up stairs
  3. Walks slowly or needs to stop for breath
  4. Needs to stop after 100m or a few minutes walking (flat)
  5. Unable to leave the house or SOB on dressing
108
Q

Assessing the severity of COPD

A

GOLDS criteria

  • Mild: FEV1 > 80%, FEV1/FVC <0.7
  • Moderate: FEV1 50-80%, FEV1/FVC <0.7
  • Severe: FEV1 30-50%
  • V. Severe: FEV1 <30%
109
Q

Management of COPD

A
  1. STOP SMOKING
  2. Pneumococcal and haemophilusinfluenza
  3. If MRC >/= 3
    1. Inhaled therapies:
      1. SABA
      2. FEV1 >50% LABA or LAMA
      3. FEV1 <50% LABA + ICS
      4. Step up: LABA + LAMA + ICS
    2. Short term (only) oral therapies:
      1. Steroids
      2. Mucolytics
      3. Theophylline
    3. Oxygen therapy
      1. Short burst
      2. Long term - more than 15h/day
    4. Physiotherapy - positive expiratory pressure mask and active cycle breathign techniques.
110
Q

CXR features of COPD

A
  1. Hyperexpansion (more than 6 ribs anteriorly)
  2. Prominent pulmonary arteries
  3. Periferal oligaemia
  4. Bullae
111
Q

Predicting prognosis of COPD

A

BODE criteria (It doesnt BODE well…)

  • BMI
  • Obstruction, airway
  • Dyspnoea
  • Exercise tolerance
112
Q

Management of an acute exacerbtion of COPD

A
  1. Oxygen - 25% oxygen via a venturi mask. Vary FiO2 and SpO2 target according to ABG. Aim PaO2 >8 and PCO2 increase less than 1.5kPa
  2. Nebs: Salbutamol 5mg/4h and ipratropium bromide 0.5mg/6h
  3. Steroids (PO and IV): hydrocortisone 200mg IV and pred 40mg PO for 7-10 days
  4. Abx if necesary: 200mg doxy PO STAT, then 100mg PO OD for 5 days.

If no response try NIV, then invasive ventilation.

113
Q

Causes of COPD exacerbations

A
  1. Viral URTI (30%)
  2. Bacterial
  3. Pollution
  4. DEcrease in temperature.
114
Q

Causes of PE

A

SPASMODICAL

  • Surgery - mainly ortho, pelvic and abdo*
  • Pregnancy - c-setion and pre-eclmapsia too*
  • Age
  • Sex - female
  • Maligancy*
  • Oestrogen (OCP/HRT)
  • DVT/PE history*
  • Immobility - intensive care, long haul flight…*
  • Collosal size - obesity
  • Antiphospholipid syndrome
  • Lupus anticoagulant

* Major causes (5-10x increased risk)

115
Q

Presntation of PE

A

May e acute or chronic

  1. Acute
    1. Dyspnoea (75%)
    2. Haemoptysis with or without pleuritic chest pain
    3. Collapse - circulatory
    4. Syncope (10%) - usually PE in the elderly.
  2. Chronic - many minor emboli.
    1. Progressive dyspnoea over weeks or months of unexplained cause
    2. Sx of RV failure, pleural effusions and new onset AF.
116
Q

How to diagnose a PE? Routine investigations and gold standard.

A
  1. Bloods, U&E, FBC, clotting, D-dimers
  2. CXR - may be normal
  3. ABG - may be normal
  4. ECG S1, Q3 T3 - rare.
  5. Doppler US
  6. CTPA

GOLD STANDARD: WELL’s score

  1. Wells <4
    • D-dimer - negative exclude PE (94% NPV)
    • Positive do CTPA
  2. Wells >4 - likely
    • Do CTPA
117
Q

Determining prognosis post PE?

A

PESI score

30 day outcome post PE.

118
Q

Management of PE

A

ABCD…

  1. Oxygen (100%)
  2. Analgesia (+ metaloclopromide) if needed
  3. Consider thrombolysis is massive PE - alteplase 50mg bolus stat or surgical/interventional thrombolysis
  4. LMWH e.g. enoxoparin 1.5mg/kg/24hours SC. Continue for 5 days or INR >2 (whichever is later).
  5. If SBP <90 - colloid. If no response consider dobutamine, NORAD or thrombolysis.
119
Q

Defintion of a pneumothorax

A

Accumuation of air in the pleural space with secondary lung collpase.

120
Q

Causes of a pneumothorax

A

Spontaneous

  1. Primary
    • Tall skinny men (ruptures supleural bullae)
    • Smokers
  2. Secondary
    • COPD
    • Marfans/Ehler danlos
    • Plumonary firbosis or sarcoidosis

Trauma - penetrating or blunt with/without rib fractures

Iatrogenic

  1. Subclavian CVP
  2. Liver biopsy
  3. Transbrochial biopsy
  4. Positive pressure ventilation
121
Q

Classification of pneumothoraces

A
  • Closed - intact chest wall with air leaking from lung into the pleural cavity
  • Open - defect of the chest wall allows communication between the pleura space and the exterior
  • Tension - one way valve allowing air entry but not exit into the pleural space and casuing mediastinal shift.
122
Q

A 2cm rim on x-ray repsents a ____% loss in volume

A

50%

123
Q

Management of a ension penumothorax

A
  1. Resucitate pateint
  2. No CXR
  3. Large bore venflon inserted in the 2nd intercostal space midclavicular line
  4. Insert ICD
124
Q

Management of a traumatic penumothorax

A

Resucitate patient

Analgesia

3-sided dressing if sucking

Insert ICD

125
Q

management of a spontanous penumothorax

A

First decide if it is a 1º or 2º penumothrorax

  • Primary
    1. If not SOB or rim <2cm consider discharge
    2. If SOB and/or rim >2cm attempt aspiration
    3. If aspiration succesful consider discharge, otherwise insert ICD
  • Seconday
    1. If not SOB, <50 and rim <2cm, aspirate. If succesfull admit for 24hours. If not insert ICD.
    2. If SOB, >50 and/or rim >2cm, insert ICD.
126
Q

Where should one insert an intercostal chest drain?

A

In the 5th intercostal space, mid-axillary line. Inferior to the axilla, above the nipple line, anterior to the latissimus doris and posterior to the pectoralis major.

Aspiration of fluid or air would comfirm correct placement.

127
Q

Classification of pleural effusions

A

Trasnduate or exudate.

Transudate = protien less than 25

Exdudate = protein more than 35.

Otherwise use Lights criteria:

  1. Efussion: serum LDH is >0.6
  2. Effusion: serum protein >0.5
  3. Effusion LDH is >0.6 ULN serum value
128
Q

Causes of a pleural effusion

A

Divide into transudate and exudate

  1. Transudate
    1. Cardiac - LVF, mitral stenosis and constrictive pericarditis
    2. Pulmonary - PE (10-20%), atelectasis
    3. Metabolic (low albumin) - cirrhosis or nephrotic syndrome
    4. Endocrine - hypothyroidism
    5. Iatrogenic - peritoneal dialysis
    6. Other: Meig’s syndrome
  2. Exudate
    1. Pulmonary - malignancy, PE
    2. Rheumatoid - SLE, RA, wegeners, churg strauss, sacrcoid…
    3. Infectious - SPPE, TB
    4. Gastro - pancreatitis, oesophageal rupture.
129
Q

Management of a pleaural effusion

A
  • Admit + chest drain if: mailgnant effusion, Ph <7.3 or unwell with massive effusion.
  • Treat the underlying cause.
  • Can drain 2L/24hours if symtomatic
  • Chemical pleurodesis if reccurent malignant infection.
  • Persistent effusions may require surgery
130
Q

What are the clinical features of sarcoidosis

A

GRANULOMAS

  • G - general: weight loss, fevers, lethargy, lymphadenopathy
  • R - resp:
    • URTI: otitis and sinusitis
    • LRTI:
      • Stage 1 - BHL
      • Stage 2 - BHL + peripheral infiltrates
      • Stage 3 - Only peripheral infiltrates
      • Stage 4 - mid zone fibrosis and bullae
  • A - arthralgia: dactylitis and polyarthalgia
  • N - neuro: craniala and peripheral polyneuropathies, SoLs, meningitis and transverse myelitis
  • U - urine: high calcium - renal stones, nephrocalcinosis, DI
  • L - low hormones e.g. amenorrhoea
  • O - ophatlmic: uveitis, keratoconjunctivitis, sjorgens
  • M - myocardial: restrictive cardiomyopathies and pericardial effusions
  • A - abdominal: hepatomegaly with cholestatis LFTs and splenomegally
  • S - skin: lupus pernio and erythema nodosum
131
Q

Management of sarcoidosis

A

Asymtomatic BHL requires no treatment

Acute sarcoid usually reolves spontanously. NSAIDs and bed rest

Chronic sarcoid can be treated with 4-6 weeks of 40mg/day of prednisolone. Additional immunosupression may be added (methotrexate, cyclosporin, cyclophosphamide).

132
Q

What is sarcoidosis?

A

A multisystem non-casseating granulomatous disorder of unknown cause.

133
Q

Prognosis of sarcoidosis

A

60% of thoracic sarcoidosis resolves within 2 years

20% responds to steroids

20% sees no improvement despite steroids

134
Q

Differentials of BHL

A
  1. Infective: TB, mycoplasma
  2. Malignant: lymphoma, carcinoma
  3. Interstitial disease: EAA, silicosis
  4. Sarcoidosis
135
Q

Name some granulomatous diseases

A
  • Infectious: TB, leprosy, shypilis…
  • AI: PBC
  • Vasculitis: wegeners, PAN, GCA
  • Idiotpathic: sarcoid and crohns
  • Interstial lung: EAA, silicosis
136
Q

Clinical features of interstitial lung disease:

A
  • Dyspnoea
  • Dry cough
  • Abnormal CT/CXR
  • Restrictive spirometry
137
Q

Causes of interstitial lung disease

A

By location

  • Upper zone (A PENT house)
    • A - aspergillosis
    • P - penumoconiosis (coal, silica)
    • E - EAA
    • N - negative sero-arthopathies
    • T - TB
  • Lower zone (STAIRS)
    • S - sarcoid (mid zone)
    • T - toxins (BANS ME: bleomycin, amiodarone, nitrofuritoin, sulphazalazine, methotrexate)
    • A - asbestosis
    • I - idiopathic plumonary fibrosis
    • R - rheum associated (RA; SOE, scleroderma, sjorgens…)
138
Q

Investigations in ?interstitial lung disease and usual findings

A
  1. Spirometry - restrictive picture
  2. CXR - small pneumothoraces, reticular changes
  3. HRCT - aswell as CT according to NICE
  4. Pathology if indicated - honeycomb cahnges (poor prognosis)
  5. Bloods - inflammatory markers
139
Q

Causes of extrinsic allergic alveolitis

A
  1. Bird fanciers lung: droppings.
  2. Farmer/mushroom workers
  3. Malt workers lung: aspergillus clavatus
140
Q

Management of Extrinsic allergic alveolitis

A

Avoid exposure, steroids acutely and long-term, compensation may be payable.

141
Q

Causes of industrial lung disease

A
  1. Coal-workers pneumoconiosis
  2. Silicosis - quarries, sand blastin
  3. Asbestois - demolition, ship yards
142
Q

Presentation of mesothelioma and main RFx

A

Main RF - asbestosis

  • Pleuritic chest pain
  • weight loss, fever, lethargy, anorexia
  • Clubbing
  • Dsypnoea
  • Recurretn infectios
143
Q

What is idiopathic plumonary fibrosis (CFA)

A

The most common cause of interstitial lung disase. A restrictive defect causing Type 2 respiratory failure with bilateral reticulo-nodular shadowing and honeycobing on CXR.

144
Q

What are the complications of idiopathic pulmonary fibrosis

A

Increased risk of cancer

Type 2 repsiratory failure

145
Q

Investigations in ?Idiopathic pulmonary fibrosis and salient findings

A
  1. Spirometry - restrictive picture
  2. CXR - bilateral retiulo-nodular shadowing and honecombing
  3. Bloods: Raised CRP and Ig. 30% +ve ANA, 10% +ve RF. ABG of Type II Resp failure.
  4. BAL indicates disease severity.
  5. HRCT - similar finding to CXR.
146
Q

Prognosis and prognostic factors of idiopathic pulmonary fibrosis

A
  1. BAL - high eosinophils and PMN = bad prognosis. High lymphocytes = good prognsois
  2. 50% 5 year survival.
147
Q

Management of idiopathic pulmonary fibrosis

A
  • Supportive care
    • Stop smoking
    • Pulmonary rehab
    • Ocygen therapy
    • palliation
    • management of heart failure
  • Lung tx only cure
148
Q

Defintion of pulmonary hypertension

A

A PA pressure greater than 25mmHg

149
Q

Causes of Pulmonary hypertension

A
  1. Vascular
    • Idiopathic pulmonary hypertension
    • Acute/chronic PEs
    • Vasculitis: wegeners, SLE, scleroderma
    • Sickle Cell anameia
    • Portal hypertension
  2. Cardiac
    • LVF
    • Mitral stenosis
    • Mitral regurgication
    • L to R shunt
  3. Lung parenchyma (chronic hypoxia leads to vasoconstriction)
    • COPD
    • Asthma (severe or chronic)
    • Interstitial lung disease
    • Bronchiectasis and CF
  4. Chronic hypoxia
    • OSA
    • Thoracic deformities - kyphosis, scoliosis
    • Msk - Myasthenia gravis, MND, polio
    • Morbid obesity
150
Q

What is pickwickian syndrome

A

morbid pbesity causing hypoventilation chronically. This can lead to portal hypertension.

151
Q

Gold standard diagnosis of Pulmonary hypertension

A

Cardiac catheteraisation fo the right heart to determin:

  • Mean pulmonary arterial pressure
  • Pulmonary vascular resistance
  • CO
152
Q

Signs of right heart failure

A
  • Increased JVP witha prominent a wave
  • Left parasternal heave
  • S3 and loud P2
  • Pulsatile hepatomegaly
  • PR and TR murmurs
  • Fluid build up: ascites and peripheral oedema
153
Q

Defintion of cor pulmonale

A

RVF secondary to chronic pulmonary hypertension

154
Q

Management of cor pulmonale

A
  1. Treat the underlying cause of PTH
  2. Decrease the vascular resistance:
    • LTOT
    • CCD - nifedipine
    • Sildenafil
    • Prostacyclin analogues
  3. Treat the heart failure
    • ACE-I and beta blockers (care in asthma)
    • Diurectics
  4. Heart and lung transplant
155
Q

Prongosis of cor pulmonale

A

50% at 5 years

156
Q

Define obstructive sleep apnoea

A

Intermittent closure or collapse of the pharangeal airway causing apnoeic episodes during sleep

157
Q

What are the causes of obstructive sleep apnoea

A

OSA IS Not Sexy

  • O - obesity
  • S - smoking
  • A - alcohol
  • I - idiopathic pulmonary fibrosis
  • S - structural airway pathology - micrognathia
  • N - NM disease e.g. MND
  • S - sex, male
158
Q

Complciation of OSA

A
  1. Pulmonary hypertension
  2. Cor pulmonale
  3. Type 2 repsiratory failure
159
Q

Management of OSA

A
  • Modificationof risk factors (weight loss, stp alcohol adn smoking…)
  • CPAP at night
  • Surgery to correct pharangeal obstrutions
160
Q

Clincial features of OSA

A
  1. Daytime
    • Tiredness, irritability and depression
    • decreased concentration
    • mornign headache
    • somnolence
  2. Nightime
    • snoring
    • Chocking, gasping, apnoeic episodes.
161
Q

Options for facilitated smoking cessation

A
  • Nicotine replacement: patch or gum
  • Varenicline - selective partial nicotine receptor agonist - 23% abstince at one year verus 10% with placebo. NICE recommended Initiate while still smoking
  • Bupropion (dopamine/NA antagonist - antidepressant)

Medicine (6 decks)

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