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Physiology > Asthma > Flashcards

Asthma Flashcards

(55 cards)

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1
Q

prevalence of asthma

A

1/12 adults

1/11 children

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2
Q

classification of asthma

A

extrinsic

intrinsic

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3
Q

what is extrinsic asthma?

A

allergic

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4
Q

what is intrinsic asthma?

A

non-allergic

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5
Q

different types of asthma

A 
chronic
severe acute
early/ late onset
episodic/ seasonal 
exercise induced
type 1 and 2 brittle
eosinophilic/ non-eosinophilic
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6
Q

type 1 brittle

A

rare but severe form of asthma, on medication but still experience asthma attacks

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7
Q

type 2 brittle

A

rare but severe form of asthma, experience severe life-threatening attacks with no warning

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8
Q

eosinophilic and non-eosinophilic asthma

A

same as allergic and non-allergic

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9
Q

triggers of asthma

A 
exercise
pollen
bugs in home
chemical fumes
cold air
fungus spores
dust
smoke
strong odours
pollution
anger
stress
pets
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10
Q

Immunological mechanism of asthma

A

mediated by IgE
formed in response to an allergen
first exposure - sensitisation occurs
re-exposure - allergen binds to specific IgE molecule on mast cell surface
degranulation of mast cells releasing histamines, chemokines, cytokines etc.

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11
Q

Airway narrowing

A

smooth muscle goes into spasm - narrows airway
lining of the lungs become inflamed
mucus production is increased
in some parts of the airway mucus can form plugs that block the airway

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12
Q

Histology of section asthmatic lung

A

thickening of basement membrane
mucous hyperplasia and hypersecretion
volume of smooth muscle increased

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13
Q

phases of asthma attack

A
  1. early phase

2. late phase

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14
Q

what happens in early phase of an asthma attack?

A

degranulation of mast cells, spasmogens released causing bronchospasm.
Chemotaxins and chemokines released leading to late phase

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15
Q

what happens in late phase of an asthma attack?

A

infiltration of Th2 cells, activation of inflammatory cells, cysLTs and other mediatorys, more eosinophils . Airway inflammation, more bronchospasm, airway hyper-reactivity and eosinophils cause epithelial damage

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16
Q

signs and symptoms of asthma

A

coughing
wheezing/ whistling noise in chest
shortness of breath
tightness in chest - dyspnoea

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17
Q

initial assessment of asthma

A

clinical history
physical examination
lung function tests

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18
Q

moderate asthma

A 
PEF> 50-75% 
oxygen sats > 92% 
speech normal
respiration <25/m 
pulse <110bpm
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19
Q

acute severe asthma

A 
PEF 33-50%
oxygen sats >92%
cannot complete sentences
respiration > 25/m
pulse >110bpm
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20
Q

life-threatening asthma

A 
PEF <33%
oxygen sats <92%
silent chest
cyanosis
poor respiratory effort 
arrhythmia 
hypotension
exhaustion
altered consciousness
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21
Q

treatment goals

A 
minimise or eliminate symptoms
maximise lung function
prevent exacerbations
minimise need for medication
minimise adverse effects of treatment 
promote adherence with medication
provide enough information and support to facilitate self-management
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22
Q

non-pharmacological measures for treating asthma

A 
avoidance of triggers
desensitisation to specific allergen
house dust mite control measures
smoking cessation
weight reduction
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23
Q

pharmacological treatment of asthma

Study These Flashcards
A
  1. relievers

2. preventers

24
Q

what are relievers

Study These Flashcards
A

beta 2 agonists
antimuscarinics
methylxanthines

25
what are preventers
corticosteroids leukotriene receptor antagonists cromones
26
methylxanthines
e.g. theophylline | additive effect when used in conjunction with small doses of beta 2 agonists
27
what do Short-acting beta 2 agonists do?
relaxes smooth muscles - bronchodilation by stimulation of beta 2 receotors on airway smooth muscle
28
example of short-acting beta 2 agonist
salbutamol and terbutaline
29
adverse effects of short-acting beta 2 agonist
``` fine tremor in hands nervous tension headache tachycardia hypokalaemia at high doses - modification of ATPase at Na+/K+ ```
30
what is the mechanism of beta 2 agonists
stimulates GalphaS receptor activates adenylate cyclase lots of cAMP produced cAMP inhibits myosin light chain kinase by inhibiting calcium elease inhibits contraction - causing bronchodilation
31
what are antimuscarinics
2 classes
32
example of antimuscarinics
ipratropium
33
how do antimuscarinics work?
blocks muscarinic receptors as they cause bronchoconstriction
34
how are antimuscarinics administered?
by inhalation | maximal effect occurs 30-60 mins after use and lasts 3-6 hours
35
what are the adverse effects of antimuscarinics?
``` dry mouth constipation diarrhoea cough headache caution needed in prostatic hyperplasia, bladder outflow, obstruction, angle closure glaucoma - blocks tubes ```
36
examples of corticosteroids
beclomethasone budesonide fluticasone
37
how do corticosteroids work?
reduce bronchial inflammatory reactions - reduce oedema and mucous hypersecretion inhibit production of inflammatory mediators acting as transcription factor
38
administration of corticosteroids
metered inhalation | must be used regularly for maximum benefit
39
what are the adverse effects of inhaled corticosteroids?
fewer systemic effects hoarse voice reflex coughing after inhalation oral candidiasis
40
use of oral corticosteroids
more severe, less controlled asthma treated by oral corticosteroids for acute attacks and chronic asthma
41
administration of oral corticosteroids
associated with many serious adverse effects taken as a single dose in the morning enough cannot be inhaled to be beneficial
42
examples of oral corticosteroids
hydrocortisone IV injection in emergency treatment of severe acute asthma e.g. prednisolone
43
example of long-acting beta 2 agonists
salmeterol and formoterol
44
what are long-acting beta 2 agonists used for?
use with regularly inhaled corticosteroids role in long-term control of chronic asthma not for relief of asthma attack
45
administration of long-acting beta 2 agonists
combination inhalers available with corticosteroids and long-acting beta 2 agonists e.g. symbicort
46
examples of leukotriene receptor antagonists
montelukast and zafirlukast
47
use of leukotriene receptor antagonists
blocks the effects of cysteinyl leukotrienes in airways effective late on in late phase response effective alone or with inhaled corticosteroids well-tolerated with no common side effects
48
examples of Cromones
sodium cromoglicate | nedocromil sodium
49
use of cromones
no longer in guidelines question over the effectiveness but still available mechanism of action is unclear may be of value in allergic asthma prophylactic drug - no value in acute attacks has side effects must be withdrawn gradually over 1 week otherwise adverse effects
50
omalizumab
recombinant humanised monoclonal antibody selectively binds to IgE forming a complex recommended by NICE for use in adults and young people over 12 with severe persistent allergic (IgE mediated) asthma who meet specific criteria
51
well-controlled asthma
no daytime symptoms no night time awakening due to asthma no need for rescue medication no limitations on activity, including exercise normal lung function with minimal side effects FEV1 and PEF greater than 80% of predicted
52
patient counselling
knowledge of disease state knowledge of medicines knowledge of how to monitor condition
53
monitoring of asthma
compliance pulmonary function theophylline
54
mechanism of action of methylxanthines?
Inhibits phosphodiesterase | phosphodiesterase breaks down cAMP, so by inhibiting phosphodiesterase it increases cAMP concentration
55
Administration of methyxanthines
given orally or very slow IV infusion - needs to be monitored as risk of toxicity watch for interactions - hepatically metabolised adverse effects - narrow therapeutic range, nausea, headaches, insomnia, abdominal discomfort, toxic effects above 25mg/L - seizures

Physiology (46 decks)

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