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Therapeutics > W20 - COPD > Flashcards

W20 - COPD Flashcards

1
Q

what is COPD

A

COPD is the preferred term for patients who were previously diagnosed with chronic bronchitis or emphysema and in place of COLD and COAD

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2
Q

What does COPD stand for

A

Chronic
Obstructive - (Narrowing of airways)
Pulmonary - (Small airways or alveoli destruction)
Disease

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3
Q

what is COPD characterized by

A

airflow limitation that is not fully reversible

progressive abnormal inflammatory response of the lungs to noxious particles and gases

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4
Q

what is airflow limitation caused by

A

mixture of small airway disease and parenchymal destructions

Chronic bronchitis and emphysema

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5
Q

how potent is COPD

A

third leading cause of death worldwide

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6
Q

what are the risk factors of COPD

A 
smoking
environmental
genetic factor
occupational exposure
frequent infections of the airways
age >35
socio economical deprivation
poor diet
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7
Q

what are the symptoms of COPD

A

progressive and exertional breathlessness (Dyspnea)

chronic cough

sputum production

wheezing and chest tightness

frequent winter bronchitis

upper respiratory infection

pulmonary hypertension

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8
Q

what are the symptoms of severe COPD

A

weight loss

anorexia

asymptomatic rib fractures

ankle swelling

depression

anxiety

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9
Q

what factors do we take into account when making a COPD diagnosis

A

AGE >35
RISK SMOKING
RESPIRATORY SYMPTOMS
TEST AIRFLOW OBSTRUCTION

AGE
RISK
RESPIRATORY
TEST

ARRT

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10
Q

what is bronchitis

A

inflammation of central airways and smaller airways

hypertrophy and hyperplasia occur to mucus secreting glands and smooth muscle in smaller airways (bronchioles)

These then become obstructed by intraluminal mucus, mucosal oedema and airways wall fibrosis

The obstruction and the mucus increase resistance to airflow and chronic viral and bacterial colonisation in the retained mucus

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11
Q

what is emphysema

A

persistent inflammation destroys alveoli at the end of small airways.

permanent enlargement of airspaces distal to the terminal bronchiole

accompanied by destruction of their walls

destruction of the parenchyma decrease the area for gas exchange + lung elasticity

hypertrophy of capillaries reduces ability to absorb oxygen and may increase blood pressure

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12
Q

what are the3 stages of pathogenesis of COPD

A

inflammatory cells and mediators - chronic inflammation

oxidative stress, reactive oxygen and nitrogen species

protease antiprotease imbalance

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13
Q

what are cytokines

A

redundant secreted proteins with growth, differentiation and activation functions which regulate the nature of immune responses and control immune cell trafficking and the cellular arrangement of immune organs

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14
Q

what are the aims to manage stable COPD

A

prevent and control symptoms

reduce the frequency and severity of exarcerbations

improve general health status and exercise tolerance

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15
Q

what non pharmacological management should be given

A

offer treatment and support to stop smoking

offer pneumococcal and influenza vaccinations

offer pulmonary rehab if indicated

co develop a personalised self management plan

optimise treatment for comorbidities

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16
Q

when should inhaled therapies be given

A

all the above interventions have been offered (if appropriate)

people have been trained to use inhalers and can demonstrate satisfacotry technique

17
Q

what are inhaled therapies used for

A

to relieve breathlessness and exercise limitation

18
Q

what does SABA stand for

A

short acting beta agonist

19
Q

what does SAMA stand for

A

short acting muscarinic agonist

20
Q

describe the mechanism of action for a short acting beta agonist

A

upon activation the beta agonist bind to the beta agonist active site, activating adenyl cyclase through G(alpha)s leading to an increase in cAMP levels.

The surge in cAMP activates PKA which phosphorylates myosin light chain kinase to inhibit contraction

PKA also actives the K+ channel inducing membrane hyperpolarization

this countaracts electrical excitation leading to contraction

cAMP inhibits Ca2+ release from intracellular store

All of which aid relaxation of the airway smooth muscle

21
Q

how do muscarinic 1 receptors help mediate bronchodilation

A

release of relaxing agent from the respiratory epithelia or pulmonary nerves

22
Q

what do muscarinic 2 receptors do

A

found on post ganglionic cholinergic nerves and they provide negative feedback to reduce acetylcholine release

23
Q

what do muscaric 3 receptors do

A

found on airway, smooth muscle cells and glads

they mediate bronchoconstriction and mucus secretions

24
Q

what is the mechanism of action of anticholinergic drugs

A

block muscarinic acetylcholine receptors causing bronchodilation and reduce mucus secretion

25
Q

when is the peak affect in SAMA

A

onset after 20 mins with peak effect with 30 to 60 minutes

26
Q

what is the duration of SAMA

A

3 - 6 hours

27
Q

what is the peak effect of long acting muscarinic drugs

A

onset of 30-40 mins

peak effect 3 - 4 hours

28
Q

duration of LAMA

A

24 hour duration of action

29
Q

what are the side effects of inhaled anticholinergics drug

A

Common: dry mouth; arrhythmias;cough;dizziness;headache;nausea

Uncommon: Constipation; dysphonia; glaucoma; palpitations; skin reactions; stomatitis; urinary disorders; vision blurred

30
Q

what cautions do we have when taking inhaled anticholinergics

A

tiotropium: can cause arrythmia, heart failure or myocardial infarction

31
Q

what other treatment options are available

A

oral corticosteroid

mucolytic drug therapy

long actin phosphodiesterase 4 inhibitor

32
Q

when is mucolytic drug therapy considered

A

considered in patients with a chronic cough, productive of sputum

33
Q

what is the treatment plan

A

non pharmacological

Saba or Sama

LABA + LAMA or LABA + ICS

LABA + LAMA + ICS

Therapeutics (50 decks)

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