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RESPIRATORY > COPD > Flashcards

COPD Flashcards

1
Q

what are the receptors in the airways

A

muscarinic acetylcholine receptors

M1, M2, M3

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2
Q

location of M1 receptor in the airways

A

Ganglia

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3
Q

role of M1 receptor

A

Facilitate fast neurotransmission mediated by ACh acting on nitcotinic receptors (nAChR)
Increase action potential frequency from nicotinic receptor stimulation

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4
Q

location of M2 receptors

A

postganglionic neurone terminals

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5
Q

role of M2 receptors

A

inhibitory autoreceptors reduce release of Ach (blockade)

Increase release of Ach

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6
Q

Location of M3 receptors

A

airway smooth muscle

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7
Q

role of M3 receptors

A

mediate contraction in response to Ach

present on mucus secreting cells causing increased secretion

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8
Q

what is COPD

A

increased resistance to airflow during expiration (no problem breathing in only on exhalation)

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9
Q

why does a person with COPD struggle to exhale

A

airways + alveoli lose elastic quality
walls between alveoli destroyed
airway walls inflamed
airways clogged by mucus

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10
Q

what causes COPD and airway obstruction to progress

A

muscular dysfunction
inflammation
Tissue damage

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11
Q

what two conditions contribute to COPD

A

emphysema + chronic bronchitis

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12
Q

what is emphysema

A 
Alveolar destruction (loss of alveoli walls)
Impaired gas exchange 
Loss of bronchial support
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13
Q

emphysema is reversible/irreversible

A

irreversible

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14
Q

how does emphysema occur

A

protease -> alveolar destruction -> emphysema

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15
Q

what is chronic bronchitis

A

chronic neutrophilic inflammation
Mucus hypersecretion
Mucociliary dysfunction
Altered lung microbiome

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16
Q

what cells are a marker for COPD

A

neutrophils

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17
Q

chronic bronchitis is reversible/irreversible

A

(partly) reversible

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18
Q

what effect does chronic bronchitis have on airway smooth muscle

A

smooth muscle spasm + hypertrophy

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19
Q

who gets COPD

A

smokers, those exposed to smoking, pollutants, chemical fumes, dusts or AAT deficient people

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20
Q

list the symptoms

A 
Daily mucus/sputum cough
Progressive Breathlessness
Wheezing (chronic bronchitis)
Chest tightness
Lips & fingers blue/grey = hypoxic
Exacerbations 
Reduced lung function
Chronic symptoms: not episode
reduced breath sounds (emphysema)
Dysponea (difficult/laboured breathing)
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21
Q

main symptoms of chronic bronchitis

A

wheezing

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22
Q

main symptom of emphysema

A

reduced breath sounds

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23
Q

what tests are used to diagnose COPD

A 
spirometry (pulmonary function test)
Chest X ray
Chest CT scan 
Arterial blood gas test (measures O2)
Blood Test: neutrophils present
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24
Q

how is spirometry carried out

A

patient blows into spirometer after max inspiration as hard and fast as possible

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25
Q

how is spirometry used to tell if a patient has COPD

A

airways more constrictive in COPD so FVC reduced due to gas trapping/decreased residual volume
FVC & FEV1 both reduced

26
Q

In a patient with COPD their FEV1 in response to a B2 agonist is

A

less than 15%

27
Q

what effect does smoking cessation have as treatment for COPD

A 
FEV1 falls gradually in non-smokers, FEV1 in smoker is rapid, FEV1 cannot be restored but ht falling FEV1 rate can be reverted to normal after long period of not smoking
early screening 
nicotine patches
bupropion
Varenicline
28
Q

What immunisations help protect against COPD patients

A

pneumococcal

influenza

29
Q

what is the aim O2 sats for a COPD patient

A

88% - 92%

30
Q

what mask must COPD patients get O2 from

A

venturi

31
Q

what percentage of oxygen must COPD patients be given

A

24% - 28%

32
Q

why must COPD patients be given controlled Oxygen

A

prevent hypercarbia (COPD patients cannot efficiently get rid of CO2 - poor ventilation - so CO2 builds up) causing respiratory acidosis

33
Q

how does renal compensation work

A

high conc of CO2 in blood detected by kidneys and renal secretion of HCO3 to counterbalance

34
Q

how are muscarinic antagonists used to treat COPD

A

inhaled
block post junctional end plate M3 receptor activation by preventing contraction (bronchoconstriction) by preventing Ach binding to receptor
Antagonist of M3 smooth muscle receptor activation in response to ACh released from postganglionic parasympathetic fibres and epithelial cells

35
Q

benefit of muscarinic antagonists acting against M3

A

high therapeutic ratio (Safe)

reduces exacerbations

36
Q

describe the steps of airway smooth muscle contraction Brought about by the binding of Ach to M3

A

Ach binds to M3 receptor, signal to Gq/11 signal to PLC causing PIP2 -> IP3, IP3 causes release of calcium from sacropasmic reticulum, intermediate steps involve calmodulin and MLCK leading to contraction

37
Q

types of muscarinic antagonsits

A

Ipratropium (SAMA - short acting)

LAMA: tiotropium, Glycopyrronium, Aclidinium, Umedlidinium, Aclidinium bromide

38
Q

how does ipratropium work

A

delayed bronchodilator - reduces bronchospasm

non-selective blocker of M1, M2, M3

39
Q

what is the effect of treating a patient with a LAMA or SAMA

A

decreased mucus secretion

no effect on COPD progression

40
Q

how is ipratropium given

A

high nebulised dose

41
Q

ipratropium and tiotropium have a quaternary ammonium group what is the benefit of this

A

reduces absorption/systemic exposure

avoids multiple AP adverse effects of a generalised parasympathetic block

42
Q

what does atropine posses

A

tertrial amine

43
Q

how do B2 agonists help COPD patients

A

b-adrenoceptors inhaled causing bronchodilation

44
Q

does salbutamol help reduce inflammation

A

NO! only bronchodilation

45
Q

what are the short acting B2 agonists

A

salbutamol 4-6h

46
Q

what are the long acting B2 agonists

A

salmeterol/formoterol (2x day)

indacaterol/olodaterol (ultra LABA) once daily

47
Q

most effective way to relax the airways of a COPD patient during exacerbation

A

LABA/LAMA combo inhaler
increases FEV1
both drugs in same airway location (act on same ligand)

48
Q

what treatment would be given to a COPD patient having few (<2 exacerbation)

A

Glycophyrronium/indacterol

49
Q

what treatment would be given to a COPD patient having sever/frequent (>2) exacerbations

A

LABA and/or LAMA + ICS (co-adminstered with glucocorticoid)

50
Q

what effect does administering a glucocorticoid have on COPD patient

A

reduces inflammation

51
Q

when would glucocorticoid be co-administered with LAMA/LABA

A

high eosinophil count

52
Q

when can glucocorticoid be unresponsive in COPD patients

A

Oxidative/nitrative stress due to chronic inhalation of tobacco or if HDAC2 reduced

53
Q

what is an adverse effect of co-administering a glucocorticoid

A

can cause pneumonia as local immune suppression altered microbiome and impairs MC clearance

54
Q

why is fluticasone more likely to cause predisposition to pneumonia

A

it causes prolonged lung retention

55
Q

give examples of ICS/LABA/LAMA triple inhaler

A

beclomethasone
formoterol
glycopyrronium

56
Q

when would a triple inhaler like beclomethasone, formoterol or glycopyrronium be used

A

once daily for moderate/severe COPD

NOT for asthma/acute bronchospasm

57
Q

what would be given as an add on therapy, given orally, to reduce exacerbations in people with severe COPD + chronic bronchitis

A

Rofumilast:

inhibitor of PDE4 (PDE4 expressed on neutrophils, T cells and macrophages surpasses inflammation and emphysema

58
Q

adverse effects of rofumilast

A

GI effects, nausea, headache

59
Q

What add on therapy is used to reduce exacerbations by reducing sputum viscosity and aide sputum expectoration

A

mucolytis: oral carbocisteine or erdosteine

60
Q

how would you treat a patient with acute COPD

A

nebulised high dose salbutamol (LABA) + ipratropium (LAMA)
oral prednisolone (steroid)
antibiotic (amoxycillin/doxycycline) if infection eg. high eosinophils
24-28% O2 via Venturi against PaO2/PaCO2
physic to aide sputum expectoration
Non-invasive ventilation allowing higher FiO2 (inspired O2)
ITU intubated assisted ventilation (only if reversible component eg. Pneumonia)

61
Q

what does the prognosis of COPD depend on

A

FEV1: higher the FEV1 = decreased exacerbations = good prognosis

62
Q

describe the chronic cascade in COPD

A

Progressive fixed airflow obstruction
Impaired alveolar gas exchange
Respiratory failure: decreased PaO2 Increased PaCO2
Pulmonary hypertension
Right ventricular hypertrophy/failure (i.e. cor pulmonale)
Death

RESPIRATORY (12 decks)

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