Brainscape's Knowledge GenomeTM

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


See full index

Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD? [3]

A

Long term deterioration
Bronchitis - obstruction
Emphysema - hyperinflation

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

What is bronchitis?
What are the pathological changes you can see? [4]
Any changes on CXR?

A
  • Presence of productive cough for 3 months
  • Mucous gland hypertrophy = repeated infection
  • Increased goblet cells
  • Inflammation + fibrosis
  • Obstruction due to airway and alveoli damage
  • Normal CXR just inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Emphysema pathophysiology [5]

A
  • Inflammation causes increase in size of airspaces due to dilation and destruction of walls
  • Leads to collapse and trapped air = hyperinflation
  • Lung tissue for gas exchange destroyed
  • Increased compliance
  • Decreased recoil so expiration difficult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do each of the 3 main risk factors of COPD lead to lung inflammation?

A

Smoking

Environment - smoking / pollution / infection
Leads to free radicals
Anti-protease inactivated

Genetics (a1-AT deficiency)
Lungs unable to prevent damage

Leads to inflammation -increased cytokines, protease and oxidative stress

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

How is A1AT deficiency inherited?

A1AT pathogenesis

A

AR

A1AT protects cells from damage so if deficient cannot protect from damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A1AT pathophysiology, clinical manifestations [4]

Mx [3]

A 
Emphysema LL 
Cirrhosis and HCC
Cholestasis in children
Think in young person with COPD /asthma Sx refractory to Rx
Mx: 
- as for COPD
- IV A1AT protein concentrations
- lung volume reduction surgery, lung transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Smoking in pathogenesis of COPD [2]

A

Increases neutrophils and proteases which cause lung damage

Inactivate anti-proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms of COPD [6]

What happens in severe disease [2]

A 
SOB 
Rapid shallow breath 
Prolonged wheeze
Chronic cough sputum 
Frequent winter bronchitis
Minimal variation

If severe

  • Resp failure
  • RHF + peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are findings on examination [8]

A
  • Cachexia
  • Cyanosis
  • Reduced chest expansion
  • Accessory muscles, tachypnoea
  • Barrel chest, Hyperinflated chest
  • Decreased breath sounds
  • Tremor, pursed lip breathing (CO2 retention)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are signs of respiratory failure / RHF? [5]

A 
Cyanosis, Accessory muscles
Peripheral oedema
Increased JVP 
Ascites
Palpable liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is severity of COPD classed? [4]

A

FEV1 >80% = mild
50-79 = moderate
30-49 = severe
<30 = very severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is needed for diagnosis of COPD? [3]

What other investigations are needed? [5]

A
  • Partly clinical diagnosis
  • Spirometry - FEV1 <70
  • PEFR low with minimal reversibility
Others: 
CXR 
Serum a1AT (deficiency)
ECG + ECHO (cardiac failure)
BMI - for baseline 
FBC (anaemia or polycythaemia from chronic hypoxia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you manage COPD non-pharmacology? [7]

A 
Smoking cessation
Exercise
Inhaler technique
Vaccine - flu + pneumococcal
Pulmonary rehab to improve exercise capacity 
Nutrition 
Psychological support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rx COPD

First and second line

A
  1. SABA or SAMA as required
    2a. Asthmatic features present: LABA + ICS
    2b. No asthmatic features: LABA + LAMA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do you do in an exacerbation of COPD? [5]

A

Bundle
Are they a retainer? Check with ABG and use controlled O2 therapy as appropriate.
Nebulisers as regular: salbutamol 2.5-5mg and ipratropium 500 micrograms every 6 hours
Prednisolone 40-50mg for 5 days
CXR
Consider antibiotics for chest infection
VTE prophylaxis

2nd line
Aminophylline, magnesium
Referral to respiratory
Referral to ITU

COPD nurse input
Spirometry
Carbocisteine, nebulised saline
BMI weight, nutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are definite indications of LTOT [5]

Requirements for LTOT [3]

A 
Severe airflow obstruction
PO2 <7.3 after bronchodilator or nocturnal hypoxaemia
Oedema
Pulmonary hypertension 
Polycythaemia

Requirements:

  • Falls risk
  • Burns, fire risk
  • Cannot smoke on LTOT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why should you be careful when giving O2 in COPD and what is aim?

A

If elevated PaCO2 (Type 2 respiratory failure) then body goes in to hypoxic drive (relies on low O2 not CO2)
Further oxygen = reduced drive and will lead to retention in CO2
pH should not be allowed to fall below <7.25
Requires artificial ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cor pulmonale pathophysiology [4]

A
  • Hypoxic alveoli
  • Vasoconstrict causing pulmonary hypertension
  • Right ventricle hypertrophy
  • Right sided HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the signs of cor pulmonale [4]

A

Peripheral oedema
Raised JVP
Heave
Loud P2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do you treat cor pulmonale [2]

A

Management of heart failure like furosemide etc

LTOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are pink puffer COPD [4]

A
  • Increased alveolar ventilation
  • Normal PaO2 and normal or low PaCO2
  • SOB but no cyanosis
  • Type 1 respiratory failure
22
Q

What are blue puffer COPD [4]

A
  • Deceased ventilation
  • Low PaO2, High PaCO2
  • No SOB but Cyanosed
  • Insensitive to Co2
23
Q

What are asthmatic features on top of COPD [3]

A

Previous Dx asthma or atopy
High blood IgE
Variation in FEV1

24
Q

When should you consider a Dx [3]

A

> 35yo
Symptoms
Past or present smoker

25
Q

What does spirometry show [4]

A
  • PEFR reduced
  • FEV1 reduced <80%
  • FVC may be reduced
  • Ratio <70% even post bronchodilator indicates COPD as non reversible
26
Q

What does CXR show [5]

A 
Low diaphragm
Hyperinflated lungs
Hyperlucent lung field 
Bullae / holes in the lungs 
Decreased lung markings
27
Q

What will PFT show [2]

A

RV / TLC >30% due to hyperinflation

Decreased gas transfer

28
Q

Prophylactic antibiotic in chronic mx of COPD [2]

5 indications

A

Azithromycin 250mg 3x per week

  • Non-smoker
  • Optimised medical mx but continue to have >1 of:
  • > 4 exacerbations/year with sputum
  • Prolonged exacerbation with sputum
  • Exacerbations causing hospitalisation
29
Q

What should you do before Azithromycin [4]

A

CT (bronchiectasis)
Sputum C&S to exclude atypical / TB
LFT
ECG as prolong QT

30
Q

Summarise oral therapies (only to be tried after inhaled therapies have failed) [5]

A 
Prophylactic antibiotics
Theophylline
Muclytic therapy
Roflumilast
CCS
31
Q

Assessment for suitability of LTOT [2]

A

Assess with 2 ABG 3 weeks apart

32
Q

Complications of COPD [8]

A
  1. Hypoxaemia > Resp failure
    - Decreased ventilation of alveoli
    - Decreased gas exchange due to loss of parenchyma
  2. Hypercapnia
    - No recoil so takes longer to expire
    - Hyperinflation as air trapped
  3. Chronic increased HCO3
  4. Acute exacerbation / infection
  5. Polycythaemia due to chronic hypoxia so kidney secrete more EPO
  6. Cor pulmonale
  7. Pneumothorax
  8. Lung cancer
33
Q

What should you aim sats to be in COPD [3]

A

88-92%
94-98% if PCO2 normal
No high flow O2

34
Q

What is CI in asthma / COPD

A

BB as bronchospasm

35
Q

What improves long term outcome [3]

A

LTOT
Smoking cessation
Lung volume reduction - offer in late stages

36
Q

Causative organisms for acute exacerbations:
Bacterial [3] (indicate most common)
Viral infection [3]

A

Bacterial

  • H.influenza*
  • Strep pneumonia
  • Moraxella catarhalis

Viral

  • Rhinovirus
  • RSV
  • Influenza
37
Q

What are the symptoms [4]

A

Increase in:
SOB, Wheeze, Cough
Increase in sputum or purulence
Hypoxia, Confusion

38
Q

Indications for hospital admission [9]

A
  • Social difficulties can’t cope at home
  • Severe SOB, poor deteriorating condition, cyanotic
  • Poor level of activity or bedbound
  • Already receiving LTOT
  • Acute confusion
  • Rapid onset
  • SAO2 <90%
  • CXR changes
  • Respiratory distress eg pursed lip breathing
39
Q

What investigations when admitted [9]

A 
FBC, U+E, CRP
ABG, ECG, CXR
Blood culture if febrile
Sputum MC&amp;S if purulent
Theophylline level
40
Q

Which one do you treat first, hypoxia or hypercapnia?

How do you prescribe oxygen therapy for COPD acute admission? [3]

A

Give oxygen if sats low, hypoxia will kill faster than hypercapnia

Start at 28% Venturi mask on 4L/min in those at risk of hypercapnia but without hx respiratory acidosis
Do ABG within 1 hour of O2 therapy (adjust accordingly)
If critically unwell give with 15l non-rebreathe

41
Q

Rx acute COPD [3]

A
  • Give salbutamol and ipratropium bromide nebulizers back to back
  • Prednislone 30mg 1w
  • Antibiotics oral
42
Q

Antibiotic options for acute exacerbation [3]

A

Amox
Tetracycline
Clarithroymycin

43
Q

If still no response [6]

A 
If giving O2 worsens condition then any more will worsen further 
IV hydrocortisone
IV theophylline 
NIPPV - BiPAP 
Ventilation and intubation if fails 
Regular ABG
44
Q

Why is BiPAP used

A

More useful in type 2 as alters pressure

45
Q

When is CPAP used

A

Type 1 or pulmonary oedema as pushes fluid out

46
Q

What is important in preparation of nebulizer in COPD patient?

A

nebuliser should be delivered by air instead of oxygen if hypercapnia or acidosis

47
Q

What do you ask in Hx [4]

A

Usual and recent Rx
Home O2
Smoking status
Exercise capacity

48
Q

What do you do for discharge [3]

A

GP follow up
Smoking
Vaccines

49
Q

Indications for NIV [4]

A
  • Blood pH 7.25-7.35
  • Type 2 failure 2 to neuromuscular / OSA/ chest wall deformity
  • Cardiogenic pulmonary edema unresponsive CPAP
  • Weaning from tracheal ventilation
50
Q

How do you differentiate exacerbation of COPD from pneumonia

A

CXR - consolidation

51
Q

What is unusual for COPD to cause? [3]

A

Haemoptysis
Chest pain
DOES NOT cause clubbing

Respiratory (14 decks)

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