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Matrix > Respiratory > Flashcards

Respiratory Flashcards

- did not include from CXRs onwards in Melanie's ppt

1
Q

What is the definition of asthma?

A

Chronic reversible obstructive airways disease associated with airway hyper-responsiveness, bronchospasm and increased mucous secretion.

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2
Q

What are the pathological findings for asthma?

A
  1. Goblet cell hyperplasia with mucous plugging
  2. Thickened basement membrane
  3. Inflammatory infiltrate (eosinophils, lymphocytes)
  4. Smooth muscle hyperplasia
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3
Q

What are the triggers of asthma?

A
  • Allergens
  • Beta-blocker
  • Cold air
  • Drugs (aspirin, NSAIDs)
  • Exercise, emotions
  • Flu, URTI
  • GORD
  • Hormones (estrogen e.g. pregnancy)
  • Irritants (smoke, perfume, isocyanates)
  • Jobs (isocyanates, wood dust)
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4
Q

What is atopy?

A

Genetic predisposition to produce high amounts of IgE antibodies in response to allergens in the environment

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5
Q

What are the investigations for asthma?

A
  1. Peak flow meter
  2. Spirometry (FEV1/FVC ratio <80%)
    • FEV1 indicates severity of airflow obstruction
      • 60-80% mild
      • 40-59% moderate
      • <40% severe
    • Post-bronchodilator FEV1 increase >200mL & >12%
  3. ABG
  4. CXR
  5. Bronchial challenge test
  6. Skin prick test
  7. Blood radio-allergosorbent test (RAST)
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6
Q

How do you assess the severity of acute asthma?

A
  • Conscious level
  • Physical exhaustion
  • Cyanosis
  • Work of breathing - accessory muscle use, tracheal tug, subcostal recession
  • Ability to speak in sentences
  • O2 saturation
  • Silent chest - absent breath sounds
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7
Q

What is the management of an acute asthma attack

A
  • Inhaled bronchodilator (MDI with spacer/nebuliser)
  • Start ipatropium bromide if severe (MDI through spacer/nebuliser)
  • Oxygen therapy (if severe, maintain O2 sat >95%)
  • Corticosteroids (oral prednisolone or IV hydrocortisone/methyprednisolone)
    • Give oral corticosteroids within first hour Mx for acute asthma flare up

Consider add-on Tx at 1hr if severe or life-threatening:

  • IV magnesium sulphate
  • IV salbutamol
  • IV aminophylline
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8
Q

What is the long term management of asthma in terms of lifestyle and education?

A
  1. Lifestyle
    1. Avoid exposure to known allergens
    2. Patient education (features of disease, goals of treatment, self-monitoring)
  2. Pharmacological
  3. Educational
    1. Check inhaler technique
    2. Adherence to medications
    3. Asthma control
    4. Asthma management plan
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9
Q

What is the long-term pharmacological management of asthma?

A
  1. SABA (prn)
  2. Add on inhaled corticosteroids
  3. Add LABA or switch to combination inhaler (Seretide, Symbicort)
  4. Add on therapy
    1. Increase ICS
    2. Oral leukotriene inhibitor (montelukast)
    3. Inhaled mast cell stabiliser (sodium cromoglycate)
  5. Monoclonal antibodies (omalizumab)
  6. Step down therapy
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10
Q

When should asthma medication be stepped down?

A

If asthma is stable and well controlled for 2 - 3 months

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11
Q

How is asthma medication stepped down?

A
  • Reduce dose of ICS (25-50% dose reduction) every 2 - 3 months (after re-assessment of asthma control)
  • Stop LABA if ICS dose already low
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12
Q

What are indications to step up asthma medication?

A
  • Clinical symptoms >2x/week
    • Daytime, nocturnal
  • Usage of relievers >2x/week
  • Symptoms at night or waking
  • Any limitation in activity
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13
Q

What are the risk factors for potentially fatal asthma?

A
  • Previous ICU admission
  • Hospital admission due to asthma in the last year
  • Recurrent presentation to ED in the last year
  • Requiring ≥ 3 classes of asthma maintenance
  • Frequent SABA use
  • Poor lung function test
  • Other psychosocial/behavioural problems (non-compliance, substance abuse, depression/psychiatric illness)
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14
Q

What is the long term pharmacological management of asthma?

A
  1. SABA (prn)
  2. Add ICS
  3. Add LABA or switch to combination inhaler
  4. Add on therapy:
    1. Increase ICS
    2. Oral leukotriene inhibitor (montelukast)
    3. Inhalaed mast cell stabiliser (sodium cromoglycate)
  5. Monoclonal antibodies (omalizumab)
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15
Q

What are combination inhalers?

A
  • ICS + LABA:
    • Seretide = fluticasone + salmeterol
    • Symbicort = budesonide + eformeterol
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16
Q

What characterises centri-acinar emphysema compared to pan-acinar emphysema?

A
  • associated with smoking
  • gross changes less severe
  • predominantly affects respiratory bronchioles & upper lobes
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17
Q

What characterises panacinar emphysema compared to centriacinar emphysema?

A
  • diffuse throughout asinus
    • resp bronchiole, alveolar duct, terminal alveoli
  • lower lobes
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18
Q

What is the significance of A1 anti-trypsin?

A
  • A1 anti-trypsin is a protease inhibitor produced/secreted into blood by liver, which then circulates to lungs.
    • Inhibits lung neutrophil elastase (proteolytic enzyme that destroys alveolar CT)
    • If A1 anti-trypsin deficient, elastase not broken down –> alveolar CT destroyed
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19
Q

When is oxygen therapy indicated in a COPD patient?

A
  • PaO2 < 55 mmHg
  • PaO2 < 65 mmHg with cor pulmonale or polycythaemia
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20
Q

What is the non-pharmacological management of COPD?

A
  • Smoking cessation
  • Influenza & pneumococcal vaccination
  • Pulmonary rehabilitation
  • Oxygen therapy
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21
Q

What is the pharmacological management of COPD?

A
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22
Q

What are the investigations for COPD?

A
  1. Spirometry
    1. FEV1 < 70% predicted
    2. FEV1/FVC < 70% predicted
    3. Insignificant response to bronchodilator
  2. DLCO
  3. FBE (Increased Hct)
  4. ABG
  5. Pulse oximetry
  6. A1 anti-trypsin level
  7. CXR
  8. CT
  9. Exercise - exertional hypoxaemia (advanced disease)
  10. Sleep study (elevated apnoea/hypopnoea index, nocturnal hypoxaemia)
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23
Q

What are the bacterial causes for an acute exacerbation of COPD?

A
  • Haemophillus influenzae
  • Moraxella catarrhalis
  • Strep pneumoniae
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24
Q

Aside from an infection, what are other causes of acute exacerbation of COPD?

A
  • Heart failure
  • PE
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25
What is the management of an acute exacerbation of COPD?
1. ABC 2. **O2** (O2 sats 88-92%) 3. Bronchodilator - **SABA** + **ipatroprium** (via MDI with spacer/nebuliser) 4. Corticosteroids - IV **hydrocortisone** or oral **prednisilone** 5. **Abx** for supsected infection
26
What are the typical pathogens for community acquired pneumonia?
* Strep pneumoniae * Haemophillus influenzae * Moraxella catarrhalis * Staph aureus
27
What are the atypical pathogens for community acquired pneumonia?
* Mycoplasma pneumoniae * Chlamydia pneumoniae * Chlamydia psittaci * Legionella pneumophilla * Coxiella burnetti * Influenza, RSV, parainfluenza
28
Bug causing rusty sputum in pneumonia
Strep pneumoniae
29
Bugs causing pneumonia in exacerbation of COPD?
* Moraxella catarrhalis * Haemophilus inlfuenza
30
Bugs giving bird fancier pneumonia
Chlamydia psitacci
31
Pneumonia - abbatoir workers, MSM, Q fever
Coxiella burnetti
32
Pneumonia - alcoholics, red currant jelly, aspiration pneumonia, lung abscesses
Klebsiella pneumoniae
33
Pneumonia - HIV, immunodeficiency
Pneumocystitis jiroveci
34
Pneumonia - erythema multiforme, cold agglutin haemolysis
Mycoplasma pneumoniae
35
Pneumonia - air conditioning
Legionella pneumophila
36
Pneumonia - IVDU, health care associated
Staph aureus
37
Pneumonia - bronchiectasis
Pseudomonas
38
Which pathogens does a rapid urinary antigen test for?
* Legionella * Strep pneumoniae
39
What pathogen does IgM serology test for?
Mycoplasma
40
What pathogen does cold agglutin test test for?
Mycoplasma
41
What pathogen does PCR of nasopharyngeal aspirate test for?
* Influenza A & B * Parainfluenza * RSV
42
What is an air bronchogram?
* Air-filled bronchi (dark) being made visible by opacification of surrounding alveoli (grey/white) * Almost always caused by pathological airspace/alevolar process (something other than air fills alveoli) * Not visible if bronchi themselves opacified - therefore indicate patent proximal airways
43
What are the causes of air bronchograms?
* Pulmonary consolidation * Pulmonary oedema * Non-obstructive atelectasis * Severe ILD * Cancer: bronchioalveolar, pulmonary lymphoma * Pulmonary infarct * Normal expiration
44
How does one assess the severity of pneumonia?
* CU(O)RB65: * **C**onfusion * **U**raemia \>7mmol OR **O**2 sat \<92% * **R**R \>30/min * **B**P \<90/60mmHg * Age \>**65** * **≤ 1** = outpatient * **2 - 3** = inpatient * **≥ 4** = admit to ICU
45
What is the empirical management of community acquired pneumonia, stratified by severity?
* Mild = Oral **amoxy** + **doxy** (if suspect atypical) * Moderate = **IV BenPen** + oral **doxy** * Severe = **IV Ceftriaxone** +/- **IV azithromycin** * Suspect gram -ve: add gentamycin/ceftriaxone * Atypicals: azithromycin
46
What is the definition of pneumonia?
LRTI with pulmonary ssx and: * ≥ 1 systemic presentation or temperature \> 38oc * new CXR infiltrate
47
What constitutes community acquired pneumonia compared to hospital acquired pneumonia?
Pneumonia in a patient who has not in the last 14 days: * been hospitalised OR * in a long term facility
48
What constitutes hospital acquired pneumonia compared to community acquired pneumonia?
Patient develops pneumonia \>48 hours after admission
49
What are some pathogens associated with hospital acquired pneumonia?
* MRSA * E. coli * Pseudomonas * Klebsiella
50
What is the management of HAP stratified according to severity?
1. Low risk MDR organisms: * Mild: **augmentin** (oral) * Moderate: **ceftriaxone**/cefotaxime (IV) 2. High risk MDR organisms: 1. Tazocin (**piperacillin** + **tazobactam**; IV)
51
What are the pathogens associated with aspiration pneumonia?
* Enterococcus * Strep pneumoniae
52
What is the management of aspiration pneumonia stratified according to severity?
* Mild: amoxycillin (oral/IV) * Moderate: Benpen (IV) * Severe: Ceftriaxone/cefotaxime (IV) + metronidazole (IV)
53
When should metronidazole be added in treatment of pneumonia?
* Metronidazole targets anaerobic organisms * Pt has moderate disease and: * Putrid sputum, severe peridontal disease or history of chronic hazardous alcohol consumption * Develop lung abscess, empyema or necrotising pneumonia * Don't respond to initial empirical therapy
54
What is Light's criteria for pleural effusion?
Pleural effusion is classified as exudative if any one of: * Pleural fluid protein/serum protein \>0.5 * Pleural fluid LDH/serum LDH \>0.6 * Pleural fluid LDH \>2/3 upper limits of normal serum LDH
55
What are some causes of transudative pleural effusions?
* Heart failure * Kidney disease (nephrotic syndrome) * Liver failure * Hypothyroidism * Hypoalbuminaemia * Malabsorption
56
What are some causes of exudative pleural effusions?
* Infection - pneumonia, empyema, TB * Inflammation - SLE, RA * Malignancy - primary, mets, lymphoma * Intra-abdominal abscess * Subphrenic abscess * Pancreatic disease * Meig's syndrome (ovarian fibroma + ascites + pleural effusion)
57
What are transudative pleural effusions associated with?
* Increased hydrostatic pressure * Decreased plasma oncotic pressure
58
What are exudative pleural effusions associated with?
* Increased permeability of capillaries --\> proteins leak out * Bilateral OR unilateral
59
What are the investigations of a pleural effusion?
1. PA CXR (\>100mL) 2. Lateral CXR (\>50mL) 3. Pleural U/S 4. Pleural aspiration: 1. WCC + differential 2. pH 3. RBC count 4. protein 5. LDH 6. glucose 7. immunology 8. lipids 9. microbiology 10. cytology 5. Pleural biopsy
60
Where is the pleural aspiration/thoracocentesis/pleurodesis for a pleural effusion done?
Percuss for the upper border of the pleural effusion and choose a site 1-2 intercostal spaces below
61
What are the causes of clubbing?
* **C**yanotic heart disease * **L**ung stuff - **A**bscess, **B**ronchiectasis, **C**F, **D**on't say COPD, **E**mpyema, **F**ibrosis * **U**lcerative colitis, Crohn's * **B**illiary cirrhosis * **B**irth defects * **I**nfective endocarditis * **N**eoplasm - e.g. lung CA * **G**astrointestinal malabsorption (Coeliac)
62

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