COPD Flashcards

1
Q

what is a pack year

A

number of packs x number of years smoked

20 cigs = 1 pack

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2
Q

what is COPD?

A

airflow obstruction with little to no reversibility

includes chronic bronchitis and emphysema

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3
Q

what is chronic bronchitis

A

cough and sputum production on most days for 3 months, of 2 successive years

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4
Q

what is emphysema

A

enlarged air spaces distal to terminal bronchioles; destruction of alveolar walls

may join together to form a bullae that ruptures and causes a pneumothorax

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5
Q

difference between COPD and asthma

A

both obstructive diseases but asthma is reversible

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6
Q

what are the causes of COPD

A

genetics:
- alpha-1-anti-trypisin deficiency (Still need to smoke) = A1AT protects against tissue damage from neurtrophil elastase which is induced by smoking

other gene polymorphisms eg those against metaloproteinases that protect lung against inflammation

active and passive smoking, cannabis, biomass fuels

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7
Q

what are the 3 pathological changes to the lungs and the main features of COPD

A

goblet cell hyperplasia, causing cough and sputum
airway narrowing causes breathlessness and wheeze
alveolar destruction

main features: bronchoconstriction, musocal oedema and mucosal hypersecretion

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8
Q

pathogenesis of COPD?

A

epithelial cells allows entry of cig smoke
macrophages and dendritic cells = activation of IS
proteases cause mucus production
damage lungs
fibroblasts scar airways

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9
Q

why do you get type 2 resp failure in COPD?

A
  • loss of elastic recoil
  • gas trapping and reduce excretion of CO2
  • forms carbonic acid in blood
  • progressive CO2 retention = compensation by kidneys reabsorbing more bicarbonate to neutralise it

-but CO2 will always be high and SOB = low oxygen levels

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10
Q

what are the symptoms of COPD?

A

smoker or ex-smoker >35

exertional breathlessness
chronic cough
regular sputum production
winter exacerbations
wheeze
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11
Q

what are the physical signs of COPD

A
tar staining
central cyanosis 
tachypnea 
chest hyperexpansion = BARREL SHAPED
cor pulmonale
wheeze
palpable liver edge
use of acessory muscle on inspiration
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12
Q

how do you stage COPD

A

GOLD stages, based on FEV1 ratio

1>80%
2 50-79%
3 30-49%
4<30%

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13
Q

what is the BODE index?

A

predicts survival in COPD patients, based on FEV1% of predicted, 6 minute walk distance, BMI, and mMRC dyspnea scale

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14
Q

what are the investigations you do for COPD?

A

spirometry
ABGS
CXR
CT

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15
Q

how are ABGS used in COPD

A
  • always check pH first
  • may find both types of resp failure
  • after that, check compensation:
  • compensated if HCO3 is abnormal; if raised = degree of chronicity but if pH is low it has not compensated

BE = metabolic component? if infection, BE is low

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16
Q

what is type 1 resp failure

A
  • low oxygen
  • hypoxaemic failure, <8kPa
  • underlying pathology with LUNGS eg infection, oedema or shunt
17
Q

what is type 2 resp failure and what are the clinical features?

A

low oxygen and high co2
-may lead to low pH and high CO3

-dilated pupils, bounding pulse, hand flap, myoclonus, confusion and drowsiness

18
Q

what would you see on a CXR of COPD

A

often normal but exclude other conditions

low, flattened diaphragms
nipple shadows 
smaller heart size
horizontal ribs 
hyper-expansion
19
Q

what would you see on a CT scan of COPD

A

holes or bullae suggesting emphysema (in apices)

bronchial wall thickening

20
Q

how is COPD used in spirometry

A

measures VC and FVC (refer to asthma flashcards)

21
Q

how do you differentiate between asthma and COPD?

A

using spirometry

  • asthma will have:
  • a large response >400ml to bronchodilators or 30mg oral prednisolone daily for 2 weeks
  • serial peak flow measurements showing >20% diurnal variability
  • night time waking with breathlessness or wheeze
22
Q

what happens if a COPD patient stops smoking?

A

lung function stops declining as quickly but not reversible so symptoms will still prevent but just later in life

23
Q

what is cor pulmonale and why do you get it

A

it is right sided heart failure as a result of chronic hypoxic lung disease

  • hypoxia
  • pulmonary arterial vasoconstriction
  • increased pulmonary artery pressure
  • RV hypertrophy
  • RV failure
24
Q

how do you treat COPD?

A

-STOP SMOKING

  • start SABA
  • if still breathless, add LABA or anti-muscarinic in preference to SAMA (LAMA)
  • if FEV1 ratio <50% or frequent exacerbations add inhaled CCS in combined inhaler with LABA
  • if still breathless consider pulmonary rehab, theophylline or high dose bronchodilators
25
Q

what other non-pharmacological treatments can you give to COPD patients

A
  • flu and pneumococcal vaccine
  • oxygen short burst for symptoms if >15 hours a day
  • physio for breathing

may need bullectomy, lung volume reduction surgery or lung transplantation

26
Q

what are the complications of COPD

A
exacerbations
pneumonia
pneumothorax 
RVF
peripheral neuropathy 
cachexia
27
Q

what causes a COPD exacerbation

A

viruses and bacteria such as H.influenzae, S.pnemonia, pseudomonas

28
Q

what are the symptoms of a COPD exacerbation

A
preceding coryzal symptoms 
increased breathlessness
increased cough 
increased sputum
sputum purulence 
ankle swelling
29
Q

wha investigations would you do in a COPD exacerbation

A
CXR
ABG or o2 sats
ECGs
FBC, U&Es, CRP
sputum culture
30
Q

how do you manage a COPD exacerbation

A
  • oxygen, SaO2 not more than 94% in selected cases if hypercapnic
  • high dose SABA, nebulised
  • high dose CCS (prednisolone 40mg/day - 7 days) to reduce inflammation
  • antibiotic ONLY if purulent sputum

reassess after an hour

31
Q

what do you do if, after an hour, a COPD exacerbation patient is still in resp acidosis?

A
  • IV bronchodilator: salbutamol or theophylline
  • ICU
  • non invasive ventilation
  • then intubation or assisted ventilation
32
Q

what are the 3 ways of oxygen delivery devices

A

nasal cannulae: 60% delivery, max oxygen 5L oxygen/minute

non-rebreathing mask - control of acute patients, 15L/min = 85% of FiO2
- cannot regulate amount of inspired oxygen but once initial assessment is complete, reduce oxygen to appropriate target sats of 94-98%

venturi mask - exact control of FiO2, and avoids over-oxygenation