Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is atopy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When should asthma medication be stepped down?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are combination inhalers?

A
  • ICS + LABA:
    • Seretide = fluticasone + salmeterol
    • Symbicort = budesonide + eformeterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What characterises panacinar emphysema compared to centriacinar emphysema?

A
  • diffuse throughout asinus
    • resp bronchiole, alveolar duct, terminal alveoli
  • lower lobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When is oxygen therapy indicated in a COPD patient?

A
  • PaO2 < 55 mmHg
  • PaO2 < 65 mmHg with cor pulmonale or polycythaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the non-pharmacological management of COPD?

A
  • Smoking cessation
  • Influenza & pneumococcal vaccination
  • Pulmonary rehabilitation
  • Oxygen therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the pharmacological management of COPD?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A
  • Haemophillus influenzae
  • Moraxella catarrhalis
  • Strep pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A
  • Heart failure
  • PE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the management of an acute exacerbation of COPD?

A
  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
Q

What are the typical pathogens for community acquired pneumonia?

A
  • Strep pneumoniae
  • Haemophillus influenzae
  • Moraxella catarrhalis
  • Staph aureus
27
Q

What are the atypical pathogens for community acquired pneumonia?

A
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Chlamydia psittaci
  • Legionella pneumophilla
  • Coxiella burnetti
  • Influenza, RSV, parainfluenza
28
Q

Bug causing rusty sputum in pneumonia

A

Strep pneumoniae

29
Q

Bugs causing pneumonia in exacerbation of COPD?

A
  • Moraxella catarrhalis
  • Haemophilus inlfuenza
30
Q

Bugs giving bird fancier pneumonia

A

Chlamydia psitacci

31
Q

Pneumonia - abbatoir workers, MSM, Q fever

A

Coxiella burnetti

32
Q

Pneumonia - alcoholics, red currant jelly, aspiration pneumonia, lung abscesses

A

Klebsiella pneumoniae

33
Q

Pneumonia - HIV, immunodeficiency

A

Pneumocystitis jiroveci

34
Q

Pneumonia - erythema multiforme, cold agglutin haemolysis

A

Mycoplasma pneumoniae

35
Q

Pneumonia - air conditioning

A

Legionella pneumophila

36
Q

Pneumonia - IVDU, health care associated

A

Staph aureus

37
Q

Pneumonia - bronchiectasis

A

Pseudomonas

38
Q

Which pathogens does a rapid urinary antigen test for?

A
  • Legionella
  • Strep pneumoniae
39
Q

What pathogen does IgM serology test for?

A

Mycoplasma

40
Q

What pathogen does cold agglutin test test for?

A

Mycoplasma

41
Q

What pathogen does PCR of nasopharyngeal aspirate test for?

A
  • Influenza A & B
  • Parainfluenza
  • RSV
42
Q

What is an air bronchogram?

A
  • 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
Q

What are the causes of air bronchograms?

A
  • Pulmonary consolidation
  • Pulmonary oedema
  • Non-obstructive atelectasis
  • Severe ILD
  • Cancer: bronchioalveolar, pulmonary lymphoma
  • Pulmonary infarct
  • Normal expiration
44
Q

How does one assess the severity of pneumonia?

A
  • CU(O)RB65:
    • Confusion
    • Uraemia >7mmol OR O2 sat <92%
    • RR >30/min
    • BP <90/60mmHg
    • Age >65
  • ≤ 1 = outpatient
  • 2 - 3 = inpatient
  • ≥ 4 = admit to ICU
45
Q

What is the empirical management of community acquired pneumonia, stratified by severity?

A
  • 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
Q

What is the definition of pneumonia?

A

LRTI with pulmonary ssx and:

  • ≥ 1 systemic presentation or temperature > 38oc
  • new CXR infiltrate
47
Q

What constitutes community acquired pneumonia compared to hospital acquired pneumonia?

A

Pneumonia in a patient who has not in the last 14 days:

  • been hospitalised OR
  • in a long term facility
48
Q

What constitutes hospital acquired pneumonia compared to community acquired pneumonia?

A

Patient develops pneumonia >48 hours after admission

49
Q

What are some pathogens associated with hospital acquired pneumonia?

A
  • MRSA
  • E. coli
  • Pseudomonas
  • Klebsiella
50
Q

What is the management of HAP stratified according to severity?

A
  1. Low risk MDR organisms:
    • Mild: augmentin (oral)
    • Moderate: ceftriaxone/cefotaxime (IV)
  2. High risk MDR organisms:
    1. Tazocin (piperacillin + tazobactam; IV)
51
Q

What are the pathogens associated with aspiration pneumonia?

A
  • Enterococcus
  • Strep pneumoniae
52
Q

What is the management of aspiration pneumonia stratified according to severity?

A
  • Mild: amoxycillin (oral/IV)
  • Moderate: Benpen (IV)
  • Severe: Ceftriaxone/cefotaxime (IV) + metronidazole (IV)
53
Q

When should metronidazole be added in treatment of pneumonia?

A
  • 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
Q

What is Light’s criteria for pleural effusion?

A

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
Q

What are some causes of transudative pleural effusions?

A
  • Heart failure
  • Kidney disease (nephrotic syndrome)
  • Liver failure
  • Hypothyroidism
  • Hypoalbuminaemia
  • Malabsorption
56
Q

What are some causes of exudative pleural effusions?

A
  • 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
Q

What are transudative pleural effusions associated with?

A
  • Increased hydrostatic pressure
  • Decreased plasma oncotic pressure
58
Q

What are exudative pleural effusions associated with?

A
  • Increased permeability of capillaries –> proteins leak out
  • Bilateral OR unilateral
59
Q

What are the investigations of a pleural effusion?

A
  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
Q

Where is the pleural aspiration/thoracocentesis/pleurodesis for a pleural effusion done?

A

Percuss for the upper border of the pleural effusion and choose a site 1-2 intercostal spaces below

61
Q

What are the causes of clubbing?

A
  • Cyanotic heart disease
  • Lung stuff - Abscess, Bronchiectasis, CF, Don’t say COPD, Empyema, Fibrosis
  • Ulcerative colitis, Crohn’s
  • Billiary cirrhosis
  • Birth defects
  • Infective endocarditis
  • Neoplasm - e.g. lung CA
  • Gastrointestinal malabsorption (Coeliac)
62
Q
A

Matrix (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions