COPD Flashcards by Ciara McGloin

what are the receptors in the airways

muscarinic acetylcholine receptors

M1, M2, M3

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location of M1 receptor in the airways

Ganglia

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role of M1 receptor

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

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location of M2 receptors

postganglionic neurone terminals

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role of M2 receptors

inhibitory autoreceptors reduce release of Ach (blockade)

Increase release of Ach

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Location of M3 receptors

airway smooth muscle

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role of M3 receptors

mediate contraction in response to Ach

present on mucus secreting cells causing increased secretion

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what is COPD

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

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why does a person with COPD struggle to exhale

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

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what causes COPD and airway obstruction to progress

muscular dysfunction
inflammation
Tissue damage

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what two conditions contribute to COPD

emphysema + chronic bronchitis

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what is emphysema

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

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emphysema is reversible/irreversible

irreversible

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how does emphysema occur

protease -> alveolar destruction -> emphysema

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what is chronic bronchitis

chronic neutrophilic inflammation
Mucus hypersecretion
Mucociliary dysfunction
Altered lung microbiome

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what cells are a marker for COPD

neutrophils

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chronic bronchitis is reversible/irreversible

(partly) reversible

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what effect does chronic bronchitis have on airway smooth muscle

smooth muscle spasm + hypertrophy

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who gets COPD

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

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list the symptoms

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

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main symptoms of chronic bronchitis

wheezing

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main symptom of emphysema

reduced breath sounds

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what tests are used to diagnose COPD

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

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how is spirometry carried out

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

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how is spirometry used to tell if a patient has COPD

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

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

less than 15%

what effect does smoking cessation have as treatment for COPD

``` 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 ```

What immunisations help protect against COPD patients

pneumococcal | influenza

what is the aim O2 sats for a COPD patient

88% - 92%

what mask must COPD patients get O2 from

venturi

what percentage of oxygen must COPD patients be given

24% - 28%

why must COPD patients be given controlled Oxygen

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

how does renal compensation work

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

how are muscarinic antagonists used to treat COPD

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

benefit of muscarinic antagonists acting against M3

high therapeutic ratio (Safe) | reduces exacerbations

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

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

types of muscarinic antagonsits

Ipratropium (SAMA - short acting) | LAMA: tiotropium, Glycopyrronium, Aclidinium, Umedlidinium, Aclidinium bromide

how does ipratropium work

delayed bronchodilator - reduces bronchospasm | non-selective blocker of M1, M2, M3

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

decreased mucus secretion | no effect on COPD progression

how is ipratropium given

high nebulised dose

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

reduces absorption/systemic exposure | avoids multiple AP adverse effects of a generalised parasympathetic block

what does atropine posses

tertrial amine

how do B2 agonists help COPD patients

b-adrenoceptors inhaled causing bronchodilation

does salbutamol help reduce inflammation

NO! only bronchodilation

what are the short acting B2 agonists

salbutamol 4-6h

what are the long acting B2 agonists

salmeterol/formoterol (2x day) | indacaterol/olodaterol (ultra LABA) once daily

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

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

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

Glycophyrronium/indacterol

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

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

what effect does administering a glucocorticoid have on COPD patient

reduces inflammation

when would glucocorticoid be co-administered with LAMA/LABA

high eosinophil count

when can glucocorticoid be unresponsive in COPD patients

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

what is an adverse effect of co-administering a glucocorticoid

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

why is fluticasone more likely to cause predisposition to pneumonia

it causes prolonged lung retention

give examples of ICS/LABA/LAMA triple inhaler

beclomethasone formoterol glycopyrronium

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

once daily for moderate/severe COPD | NOT for asthma/acute bronchospasm

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

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

adverse effects of rofumilast

GI effects, nausea, headache

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

mucolytis: oral carbocisteine or erdosteine

how would you treat a patient with acute COPD

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)

what does the prognosis of COPD depend on

FEV1: higher the FEV1 = decreased exacerbations = good prognosis

describe the chronic cascade in COPD

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