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Flashcards in Asthma Deck (44):
1

What is asthma?

A chronic inflammatory disorder of the airways, inflammatory symptoms are usually associated with widespread but variable airflow obstruction and an increase in airway response to a variety of stimuli. Obstruction is often reversible, either spontaneously or with treatment

2

How many people currently in the UK are receiving treatment for asthma?

5.4 million

3

how much does the NHS spend treating asthma?

1 billion

4

is it boys or girls that have a higher prevalence of wheeze and diagnosed asthma?

Boys

5

what percentage of asthma deaths are preventable if correct treatment is given early enough?

90%

6

asthma mortality rate?

0.4 PER 100,000

7

What is the pathology of Asthma?

Inflammation of the bronchial tree with hyper-reactivity of the lungs to one or more stimuli.
Airways narrowing, secondary to bronchoconstriction and mucosal oedema with elevated mucus production

8

What are the long-term effects of asthma?

Airway remodelling- Structural changes include subepithelial fibrosis, increased smooth muscle mass, enlargement of submucosal glands, neovascularization and epithelial alterations

9

what stimuli can trigger or worsen an asthma attack?

allergens- cause around 1/3 of attacks (common allergens include pollens, mould, house dust mite faeces)
Infection- URTVI exacerbate asthma (extra steroid use may be needed)
pollutants- e.g. cigarette smoke and sulphur dioxide

10

List triggers that cause an asthma attack?

Occupational- manufacture of chemicals e.g paints, epoxy resins wood or grain dust,flour, solvents, solder fumes etc
Drugs- NSAIDs e.g.aspirin, ibuprofen (3-10% population sensitive, risk of bronchospasm) + beta blockers e.g. propanolol
Exercise- may cause or exacerbate (recommend swimming as constriction may be due to loss of heat and moisture)

11

Discuss the pathology of Allergic asthma?

EARLY PHASE:
-Allergen interacts with mast cell-fixed IgE causing release of histamine, cysteinyl-leukotrienes and prostaglandin D
-these chemicals cause spasm of the bronchial smooth muscle
-various chemokines and chemotaxins are released , which attract leucocytes (eosinophils + mononuclear cells) to the area
LATE PHASE:
-A progressive inflammatory reaction, initiated during early phase
-Activated cytokine releasing T-helper lymphocytes infiltrate and release further leukotrienes, cytokines,chemokines and toxic proteins
-toxic proteins cause damage and loss of

12

what is episodic/seasonal asthma?

Occurs at intervals throughout the year e.g. when fungal spores are released

13

what is chronic asthma?

Persistent disease state, with acute exacerbations periodically

14

what is exercise induced asthma?

airways sensitive to colder drier air from mouth-breathing

15

what is childhood asthma?

asthma which is often due to allergic reactions, resolution is common as child ages

16

what is late-onset asthma?

Asthma presenting for the first time in adult life.
More likely to be female patients, non-allergic and require higher dose of corticosteroid to control (can be unresponsive to treatment)

17

what is status asthmaticus (severe acute asthma)?

a long-lasting severe acute attack- aggresive early treatment needed (can be fatal and unresponsive to late intervention)

18

What is Extrinsic asthma?

Common in childhood, associated with a genetic predisposition and precipitated by known allergens

19

what is intrinsic asthma?

Develops in adulthood, symptoms triggered by non-allergenic factors e.g. viral infection, irritants (causing epithelial damage/mucosal inflammation), emotional upset (mediates excessive parasympathetic input) or exercise (water and heat loss triggers mediator release from mast cells)

20

What is brittle asthma?

Acute catastrophic severe asthma

21

What must be remembered about the symptoms of asthma when performing a diagnosis?

-intermittent
-variable
-worse at night or early in the morning
-provoked by triggers

22

What are the symptoms of asthma?

-Wheeze
-cough
-SOB
-Chest tightness

23

How is a diagnosis of asthma achieved?

PEF- greater than or equal 20% variation in PEF on 3 or more days in one week over a 2 week period
-reversibility tests: measure function before and after administration of beta 2 agonist e.g. salbutamol
-skin tests- specific allergens can be identified e.g.mould, pollen
-Chest radiograph: hyperinflation of the lungs due to air trapping as a result of mucus plugging

24

how is a diagnosis of acute severe asthma achieved?

-Respiratory rate of 25 or more breaths per minute
-heart rate of over 100 beats per minute
-PEF 33-50% best or predicted
-Inability to complete sentences in one breath
other signs;
hypercapnia- increased CO2 levels
Cyanosis- bluish coloration due to lack of O2
Absence of wheezing- no air passing in or out

25

What are the non-pharmacological approaches to asthma treatment?

-Avoidance of triggers
-desensitisation to specific allergen- immunotherapy
-House dust mite control measures
-smoking cessation-including parents
-weight reduction

26

Should chronic use of bronchodilators be used on there own to treat asthma?

NO, without anti-inflammatory agent it may let more allergen in!

27

How do Beta 2 adrenoreceptor agonist work?

stimulation of beta 2 receptors increases intracellular cAMP leading to airway relaxation through relaxation of smooth muscle

28

when is a preventer needed when you are on a Beta 2 adrenoreceptor agonist

If you are using your reliever greater than 3 times a week

29

What may occur when high doses of Beta 2 adrenoreceptor agonist are used?

selectivity may be lost resulting in beta 1 receptor stimulation i.e cardiac stimulation

30

What methods are used to administer Beta 2 adrenorecptor agonists?

main route is inhaled but can also be administered orally e.g. bambuterol (pro drug terbutaline) but this results in increased risk of side effects.

31

what types of Beta 2 adrenorecptor agonists are there?

SABA- salbutamol t1/2 3-5 hours +terbutaline
LABA- salmeterol/formoterol

32

Is it suitable to use a SABA or LABA for the treatment of an acute attack

NO!

33

When can LABA be prescribed?

Can be prescribed if the patient is already on an ICS and the ICS should be continued

34

what is the ideal treatment using a LABA?

A combination inhaler, ICS + LABA as this aids adherence and means LABA is not taken without ICS

35

name a LABA with a fast onset of action and discuss why this may be beneficial for patients 18+

Formoterol has a rapid onset of action and can be combined with a steroid to give an inhaler that is both a reliever and a preventer (maintenance therapy)

36

what are hte adverse effects of Beta 2 adrenorecptor agonists?

1)tremor
2)tachycardia
3)Cramps
4)hypokalemia

37

what type of specific asthma may LABAs be useful for?

Nocturnal asthma

38

Name the most used methylxanthine?

Theophylline

39

What is the most common formulation of methylxanthine?

sustained release

40

what routes of administration are available for methylxanthines?

given orally (s/r theophylline) or very slow IV infusion (aminophylline)

41

What is aminophylline?

IV Methylxanthine
stable mixture of theophylline and ethylenediamine

42

How do methylxanthines work?

inhibit phosphodiesterase and therefore results in increase cAMP and causes airways to relax

43

are mthylxanthines more or less effective than Beta 2 agonists?

they are less effective but may have a synergistic effect

44

What are the issues with methylxanthines?

-Hepatically metabolised (CYP1A2) therefore susceptible to interactions e.g. cimetidine and erythromycin increase t1/2 + smoking decreases t1/2
-NTW (10-20mcg/ml)
-life threatening toxicity if ememrgency