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Physiology > Asthma > Flashcards

Asthma Flashcards

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

A
  1. relievers

2. preventers

24
Q

what are relievers

A

beta 2 agonists
antimuscarinics
methylxanthines

25
Q

what are preventers

A

corticosteroids
leukotriene receptor antagonists
cromones

26
Q

methylxanthines

A

e.g. theophylline

additive effect when used in conjunction with small doses of beta 2 agonists

27
Q

what do Short-acting beta 2 agonists do?

A

relaxes smooth muscles - bronchodilation by stimulation of beta 2 receotors on airway smooth muscle

28
Q

example of short-acting beta 2 agonist

A

salbutamol and terbutaline

29
Q

adverse effects of short-acting beta 2 agonist

A 
fine tremor in hands
nervous tension
headache
tachycardia
hypokalaemia at high doses - modification of ATPase at Na+/K+
30
Q

what is the mechanism of beta 2 agonists

A

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
Q

what are antimuscarinics

A

2 classes

32
Q

example of antimuscarinics

A

ipratropium

33
Q

how do antimuscarinics work?

A

blocks muscarinic receptors as they cause bronchoconstriction

34
Q

how are antimuscarinics administered?

A

by inhalation

maximal effect occurs 30-60 mins after use and lasts 3-6 hours

35
Q

what are the adverse effects of antimuscarinics?

A 
dry mouth 
constipation
diarrhoea
cough
headache
caution needed in prostatic hyperplasia, bladder outflow, obstruction, angle closure glaucoma - blocks tubes
36
Q

examples of corticosteroids

A

beclomethasone
budesonide
fluticasone

37
Q

how do corticosteroids work?

A

reduce bronchial inflammatory reactions - reduce oedema and mucous hypersecretion
inhibit production of inflammatory mediators acting as transcription factor

38
Q

administration of corticosteroids

A

metered inhalation

must be used regularly for maximum benefit

39
Q

what are the adverse effects of inhaled corticosteroids?

A

fewer systemic effects
hoarse voice
reflex coughing after inhalation
oral candidiasis

40
Q

use of oral corticosteroids

A

more severe, less controlled asthma treated by oral corticosteroids
for acute attacks and chronic asthma

41
Q

administration of oral corticosteroids

A

associated with many serious adverse effects
taken as a single dose in the morning
enough cannot be inhaled to be beneficial

42
Q

examples of oral corticosteroids

A

hydrocortisone IV injection in emergency treatment of severe acute asthma
e.g. prednisolone

43
Q

example of long-acting beta 2 agonists

A

salmeterol and formoterol

44
Q

what are long-acting beta 2 agonists used for?

A

use with regularly inhaled corticosteroids
role in long-term control of chronic asthma
not for relief of asthma attack

45
Q

administration of long-acting beta 2 agonists

A

combination inhalers available with corticosteroids and long-acting beta 2 agonists
e.g. symbicort

46
Q

examples of leukotriene receptor antagonists

A

montelukast and zafirlukast

47
Q

use of leukotriene receptor antagonists

A

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
Q

examples of Cromones

A

sodium cromoglicate

nedocromil sodium

49
Q

use of cromones

A

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
Q

omalizumab

A

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
Q

well-controlled asthma

A

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
Q

patient counselling

A

knowledge of disease state
knowledge of medicines
knowledge of how to monitor condition

53
Q

monitoring of asthma

A

compliance
pulmonary function
theophylline

54
Q

mechanism of action of methylxanthines?

A

Inhibits phosphodiesterase

phosphodiesterase breaks down cAMP, so by inhibiting phosphodiesterase it increases cAMP concentration

55
Q

Administration of methyxanthines

A

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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