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PM2C2 > Respiratory therapeutics - Asthma week 1 > Flashcards

Respiratory therapeutics - Asthma week 1 Flashcards

1
Q

what is asthma?

A

inflammatory disease of the airway caused by:

  1. recurrent reversible obstruction in response to irritant stimuli
  2. hypersecretion (increased) of mucus by bronchial epithelial cells
  3. eosinophil infiltration (WBC)
  4. bronchial smooth muscle cells hyperplasia causing hyper-responsiveness and bronchospasm (increased sensitivity to stuff in airway and bronchospasm means increased contraction)
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2
Q

what happens in asthma (airways) and in asthma attack?

A

with asthma, increased airway smooth muscle

in asthma attack:
airway is constricted due to contracted airway smooth muscle

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3
Q

what causes asthma?

A

exact causes not sure:

  1. genetic
  2. environmental
  3. combination of factors

increased chances to develop the conditions:

  1. family history
  2. bronchiolitis as a kid
  3. exposure to tobacco smoke
  4. being born prematurely
  5. type of job
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4
Q

asthma triggers

A 
dust
pest
fungi 
smoke
some drugs like salicylic acid
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5
Q

what are symptoms of asthma?

A

wheeze
breathlessness
cough
chest tight

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6
Q

what are the objective tests for asthma?

A

lung function tests

airway inflammation measurement

airway hyper-reactivity measurement

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7
Q

what is the airway inflammation measurement?

A

measure Fractional exhaled nitric oxide (FeNO) in the breath

positive tests:
FeNO level of 40 parts per billion (ppb) or more in adult

during inflammation, the epithelial cells increase production of NO.

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8
Q

tell me about lung function tests?

A

spirometry can be used to measure lung function

forced expiratory volume 1 sec = volume of air exhaled during the first second of the FVC

forced vital capacity = maximal amount of air that can be exhaled after a maximal breath

positive test for obstructive airway disease: FEV1/FVC <70% or below the lower limit of normal

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9
Q

BDR (bronchodilator reversibility test)

A

you do a spirometry after inhaling a short-acting B2AR agonist

positive test for reversibility: an improvement in FEV1 of 12% or more, and with an increase in volume of 200ml or more

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10
Q

peak flow - lung function

A

positive test of more than 20% variability

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11
Q

airway hyperreactivity measures?

A

direct bronchial challenge test with histamine or methacholine

positive test: provocatine concentration of methacholine causing a 20% fall in FEV1 (pc20) of 8mg/ml or less

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12
Q

pathobiology of asthma

A
  1. immediate phase of asthma attack - (bronchial hyper-reactivity of and spasm)

triggers (allergens, air pollutants) can cause an asthma

this causes release of spasmogens (e.g. histamine, LTC4, LTD5 etc) and causes bronchospasm

also release chemotaxins (cytokines) which causes the delayed phase of asthma:

  1. delayed phase:
    influx of inflammatory cells which relaase: cytokines, eosinophil etc which cause:
    bronchospasm, wheezing and coughing

and also increase hyperreactivity & inflammation, increased mucus

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13
Q

chronic asthma: non pharmacological management

primary prevention ?

A

mainly supported by observational studies:

multifaceted approach to avoid indoor asthma

aeroaallergen and food avoidance

weight-loss interventions for overweight and obese adults and children with asthma

microbial exposure and hygiene hypothesis

avoid smoking and air pollution

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14
Q

chronic asthma: non pharmacological management

secondary prevention ?

A

house dust mite avoidance: should not be routinely recommended

breathing exercise programmes

family therapy with pharmacotherapy

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15
Q

asthma management:

pharmacological treatment:
relievers

A

relievers

what: bronchodilators:

inhaled short-acting fast onset b2 adrenoreceptor agonists

inhaled long-acting fast onset b2 adrenoreceptor agonists as MART ONLY

why: fast control of symptoms given the fast onset of action less than 7 mins
when: to relieve asthma symptoms and for asthmatic patient with infrequent, short lived wheeze and normal lung function

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16
Q

asthma management:

pharmacological treatment:
preventers

A

what: long acting bronchodilators and anti-inflammatory drugs

inhaled long acting b2 adrenoreceptor agonists

inhaled and systemic corticosteroids

leukotriene receptor antagonists

long-acting muscarinic receptor antagonists

theophylline

why: control symptoms and reduce inflammation
when: regular maintenance therapy to improve symptoms, lung function and prevent asthma

17
Q

B2 adrenoreceptor agonist - mechanism of action

A

activate b2AR in airway smooth muscle

cause airway smooth muscle relaxation by cAMP-dependent (and independent mechanisms)

18
Q

short acting b2 adrenoceptor angonists

A

salbutamol: hydrophilic, it enters the binding site of B2AR, fast onset but short action (3-6 hours)

use:
occasional reliever for acute asthma

monitor and repeat treatment if needed

inhaled but also oral, s.c., slow IV

salmeterol:
long, lipophilic side chain binds to exosite: active portion of the molecule remains at the receptor site
- slow onset but longer duration of action (12 hours)

formeterol:
moderately liphophilic, taken into depot at cell membrane
fast onset

19
Q

b2-adrenergic agonists

A

salbutamol - hydrophilic short duration, fast onset

formoterol - intermediate, long duration, fast onset

salmeterol - lipophilic, long duration, slow onset

20
Q

long acting b2 adrenoceptor agonists

A 
use:
inhaled
chronic asthma 
Maintenance And Reliever Therapy  - formoterol 
only in combination with ICS

Advantages:
allow reduction of corticosteroid dose
reduction of symptoms and improvement of lung function

disadvantages:
risk increase of asthma exacerbation, hospitalisation, death

21
Q

adverse effects of B2 adrenoceptor agonuists

A

arrthymias, angina precipitation, palpitation, tachycardia

peripheral vasodilation

headache

tumour mortality/morbidity (LABA)

contraindications:
cardiovascular diseases
pregnancy

interactions with other drugs:
hypokalaemia

22
Q

corticosteroids - most effective anti inflammatory therapy for asthma

A

mechanism of action - TRANS REPRESSION

switch off multiple activated inflammatory genes and decrease transcription of:

cytokines (IL1, TNFs)
chemokine (IL8)
inflammatory enyzmes (COX2, iNOS)
inflammatory receptors
others

TRANS-ACTIVATION - activate anti inflammatory gene expression and increase transcription of:

B2-adrenergic receptor
IL-1 receptor antagonist
others

23
Q

corticosteroids - further information

A

inhaled:
beclometasone dipropionate
budesonide
use: recommended preventer drug for adults and children for achieving overall treatment goals

oral:
prednisolone
use: acute and severe asthma

parenteral:
hydrocortisone (i.v.)
use: life-threatening acute asthma

24
Q

corticosteroids: unwanted/side effects ?

A

with long term use: many

reduction of bone mineral density, osteoporosis

hypertension

cataracts and glaucoma

hyperglycaemia, diabetes

weight gain

increased vulnerability to infection - lower respiratory tract infections

thinning of the skin and easy bruising

hoarseness, dysphonia, throat irritation and candidiasis - local deposition of inhaled glucocorticoid in the oropharynx and larnyx

25
Q

what does cyst Ts do?

LTC4, LTD4, LTE4

A

AHR

myofibroblast accumulation

increased collagen deposition

eosinophil chemotaxis activation - decreased apoptosis

increased mucus secretion

plasma leak

bronchoconstriction smooth, smooth muscle hyperplasia

26
Q

LTB4

A

AHR

neutrophil chemotaxis

increased mucus secretion

plasma leak

27
Q

leukotriene receptor antagonists (LTRA) mechanism of action:

A

block cysteinyl-leukotrienes receptors on bronchial tissue (and other cells) to reduce bronchoconstriction, mucus, secretion, edema,

treatment:
montelukast & zafirlukast

use: oral asthma preventer NOT as reliever/rescue remedy

28
Q

anticholinergic agents

A

mechanism of action:

Antagonist of muscarinic acetylcholine receptors - blockage of M3 receptors reduce bronchoconstriction (promoting relaxation of pulmonary smooth muscle and bronchodilaton) and reduces secretion

tiotropium bromide: long acting muscarinic antagonist (LAMA)

USE: recently approved for maintenance treatment for asthma:
in combination with ICS and LABA
BIGGER ROLE IN MANAGEMENT OF COPD

29
Q

Theophylline - mechanism of action

A

non-selective phosphodiesterase inhibitor (increase cAMP)

Non-selective antagonist at adenosine receptors

activates histone deacetylases (HDACs)

others unknown

induces relaxation of the smooth muscle of bronchial airways reducing airways obstruction and airway responsiveness

inhibits release of inflammatory mediators

use:
oral and parenteral, for chronic and acute asthma

very small therapeutic windows - extensively metabolised by the liver. serum levels must be monitored to avoid toxicity

30
Q

severe persistent allergic asthma: Anti-IgE

A

mechanisms of action:
antibody binds to circulating IgE decreasing binding if iGE to the high-affinity IgE receptor (FceRI) in mast cells

OMALIZUMAB

use: subcutaneous injections every 4 weeks, severe persistent IgE-mediated asthma

NOTE effect is not immediately apparent: 12 weeks treatment required

PM2C2 (2 decks)

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