W20 - Asthma Flashcards

1
Q

what is an inflammatory disease of the airways characterized by

A

recurrent reversible airway obstruction in response to irritant stimuli

hypersecretion of mucus by bronchial epithelial cells

Eosinophil infiltration

Bronchial smooth muscle cells hyperplasia causing airway hyper responsiveness and bronchospasm

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2
Q

what is hyperplasia

A

increase in number of cells in an organ or tissue

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3
Q

what is hypertrophy

A

increase in size of smooth muscle suspected contribute to the irreversible airflow obstruction and permanently impaired pulmonary function observed in patients with chronic asthma

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4
Q

what is bronchospasm

A

abnormal contraction of the smooth muscle of the bronchi resulting in an acute narrowing and obstruction of the respiratory airway

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5
Q

what happens to the airway in an asthmatic attack

A

increased smooth muscle contracts meaning hard to breathe

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6
Q

what factors are the chances to develop the condition

A
a family history 
bronchiolitis as a child
exposure to tobacco smoke
being born prematurely 
type of job occupational exposures
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7
Q

what are some triggers of asthma

A
indoor environment
house dust mites
moulds + fungi
pollen
food
drugs
stress or even a fit of laughter
cold and viral infection
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8
Q

what is intrinsic asthma

A

asthma caused by substances within the body

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9
Q

do people with intrinsic asthma benefit from allergy shots or allergy medications

A

nop

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10
Q

what is extrinsic asthma

A

asthma caused by inhaling or ingesting foreign substane from without the body.

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11
Q

what are the symptoms of asthma

A
wheeze
breathlessness
cough
daily or seasonal variation
chest tightness
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12
Q

what are some tests we can use to diagnose asthma

A

airway inflammation measurement
lung function tests
airway hyperreactivity measurement

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13
Q

what does airway inflammation measure

A

fractional exhaled nitric oxide

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14
Q

what is a potive test on the airway inflammation

A

40 parts per billion +

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15
Q

what is a positive test of the obstructive airway test

A

<70%

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16
Q

what is forced vital capacity

A

maximal amount of air that can be exhaled after a maximal breath

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17
Q

what is the thought process behind obstructive airway

A

measure lung volumes and capacity to determine the presence of an obstructive or a restirctive disease

changes will differ depending on type of disease

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18
Q

what is a positive test on the bronchodilator reversibility test

A

FEV1 12 or more

+

Increase in volume of 200 ml or more

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19
Q

what is FEV1

A

forced expiraytory volume 1 second

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20
Q

what is a postive test on a peak flow variability test

A

20% +

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21
Q

what is a positive test on bronchial challenge test

A

provocative concentration of methacholine causing a 20% fall in FEV1 of 8mg / ml or less

22
Q

describe the mechanism behind an asthma attack

A

a trigger occurs e.g. pollen

causes release of mast cell spasmogens e.g. histamine
+ chemotaxins

spasmogens causes bronchospasm

Chemotaxins cause influx and activation of inflammatory cells which release leuktriens, cytokines,eosinophil proteins

these can cause

  • Bronchospasm
  • wheezing
  • cough
  • increase of hyper reactivity and inflammation

leading to reduction in size of lumen of bronchiole

23
Q

what are the two phases of an asthma attack

A

immediate

delayed

24
Q

describe immediate phase of asthma attack

A

trigger

release mast cell spasmogen + chemotaxin

spasmogen cause bronchospasm

25
describe delayed phase of an asthma attack
influx of inflamatory cells which release leikotrienes cytokines eosinophil protein etc these can cause - Bronchospasm - wheezing - cough - increase of hyper reactivity and inflammation leading to reduction in size of lumen of bronchiole
26
what primary prevention (non pharmacological methods do we have to manage chronic asthma
multifcaceted approach to avoid indoor asthma Aeroallergen and food avoidance Weight loss interventions for overweiht and obese adults and children with asthma Microbial exposure and hygiene hypothesis avoid smoking and air pollution
27
what secondary prevention do we have to manage chronic asthma
house dust mite avoidance should not be routinely recommended breathing exercise programmes can be offered to adult to improve quality of life and reduce symptoms family therapy with pharmacotherapy
28
what can be used to relieve asthma
inhaled short acting fast onset beta adrenoceptor agonists inhaled long acting fast onset beta adrenoceptor agonists as MART only
29
why are relievers used
they are used to relieve asthma symptoms and for asthmatic patients with infrequent short lived wheeze and normal lung function to control the symptoms quickly
30
what can be used to control + prevent
long acting bronchodilators and anti inflammatory drugs - inhaled long acting beta 2 adrenoceptor agonists in combination with ICS - inhaled and systemic corticosteroids - leukotriene receptor antagonists - long acting muscarinic receptor antagonists - theophylline
31
why are controllers used
regular maintenance therapy to improve symptoms lung function and prevent asthma attack
32
what is salbutamol used for
occasional reliever and for acute asthma attacks it is suitable for this due to the fast onset, however it has short action
33
what is salmeterol onset compared to salbutamol
longer but longer duraiton
34
what are the advantage of long acting adrenceptor agonists
allow reduction of corticosteroid dose | reduction of symptoms and improvement of lung functions
35
what are the disadvantage of long acting adrenoceptor agonists
risk increase of asthma exarcerbation hospitilization and death
36
what does MART stand for
maintenance and reliever therapy and is a combined form of ICS and LABA treatment
37
what are the adverse affect of beta 2 adrenoceptor agonists
arrythmias angina precipitation palpitation tachycardia peripheral vasodilation headache tremor
38
what are contraindications and use with caution in regards to beta 2 adrenoceptor agonists
cardiovascular diseases | pregnancy
39
what might interact with other drugs beta 2 adrenoceptor agonists
hypokalaemia
40
what are the most effective anti inflammatory therapy for asthma
corticosteroids
41
what are the two mechanisms of action
trans repression | trans activation
42
What is trans repression
switch off multiple activated inflammatory genes and decrease transcription of cytokines chemokines inflammatory enzymes inflammatory receptors others
43
what is trans activation
activate anti inflammatory gene expression and increase transcription of beta adrenergic receptor
44
what are the unwanted side effects of long term corticosteroid use
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
45
what do blt1 and 2 mediate
chemotaxis and immunomodulation in several leukocyte populations and are in addition expressed on non myeloid cells such as vascular smooth muscle and endothelial cells.
46
what do cysLT1 and 2 exhibit
distinct expression patterns in human tissues, mediating for example smooth muscle cell contraction, regulation of vascular permeability and leukocyte activation
47
describe the mechanism of action for leuktriene receptor antagonists
block csyteinyl leukotrine receptors on bronchial tissue + others to reduce bronchoconstriction, mucus secretion, edema, eosinophil migration
48
Mechanism of action of anticholinergic agents
Antagonist of muscarinic acetylcholine receptors. -Blockage of M3 receptors reduces bronchoconstriction (promoting relaxation of pulmonary smooth muscle and bronchodilation) and reduces mucus secretion
49
Mechanism of action of theophylline
Non-selective phosphodiesterase inhibtor (=↑cAMP) Non-selective antagonist at adenosine receptors Activates histone deacetylases (HDACs) Others unknown
50
mechanism of action of Anti lgE
Antibody binds to circulating IgE decreasing binding of IgE to the high-affinity IgE receptor (FceRI) in mast cells.