Asthma Flashcards

1
Q

What physiological adaptations can occur with a person that has chronic asthma?

A

Increased mucus secretion.
Increased smooth muscle mass.
Sub-epithelial fibrosis.
Epithelial damage that leads to exposed nerve endings that leads to hyperreactivity and hypersensitivity.

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2
Q

What is in the asthma triad?

A

Airway inflammation.
Reversible airway blockage.
Airway hyperresponsiveness.

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3
Q

Describe the treatment you would use for an acute asthma attack?

A

OSHITME
Oxygen 100% through non rebreather mask.
Salbutamol - nebulised (4-6 litres oxygen if your giving them both at the same time.)
Hydrocortisone IV (oral prednisolone if they can tolerate).
Ipratropium - nebulised.
Theophylline (Aminophylline) IV - Bronchodilator
Magnesium sulfate - only if they haven’t had a large response to dilator.
Escalate care.

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4
Q

Describe the build up of treatment of long term asthma?

A

1 - SABA - salbutamol (continuously increase the SABA throughout. (move up if they are having to use three times a week).
2 Add on ICS - Beclomethasone/budesonide
3 add on LABA (combined inhaler with the ICS) - Salmeterol/ Formoterol. (Maintenance and reliever therapy (MART)).
4 - If no response to the LABA stop the LABA and try increase ICS does (if it does help a bit keep the LABA and just increase the dose, or add a leukotriene antagonists (montelukast)).
5 - Try ICS such as prednisolone (ICS used for severe asthma), or leukotriene receptor antagonists - montelukast or oral salbutamol, or a methyl-xanthines like oral theophylline

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5
Q

What do ICS do?

A

They are anti inflammatories that reduce the inflammation in the airway.

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6
Q

What other drugs might you try to use during the build up of treatment when you stop the LABA and are trying other things?

A

CysLT1s - Monteleukast
Methyl-xanthines - Theophylline/aminophyline.
Monoclonal antibody directed IgE agonist - omalizumab.
Anti-inflammatory anti IL5 - mepolizumab.

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7
Q

Describe the pharmacological action of glucocorticosteroids.

A

They decrease the transcription of inflammatory proteins like mast cells, IgE antibodies and TH2 cytokines.

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8
Q

What is the name given to a peak flow that is worse at night than in the morning?

A

Diurnal peak flow.

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9
Q

What are the main symptoms of asthma?

A

Tight chest.
Wheezing.
Dry Cough.
Breathlessness.

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10
Q

Describe the pharmacology of Leukotriene receptor antagonists?

A

They block the effect of leukotrienes.
Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways.

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11
Q

Describe the pharmacology of SABA’S

A

They contain adrenaline, adrenaline causes bronchodilation in the smooth muscles of the airway to cause relaxation - this helps relieve the bronchoconstriction aspect of asthma.

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12
Q

What is the difference between a SABA and a LABA?

A

SABA’s are relivers that act for a short period of time.

LABA’s work for longer periods of time and are preventers.

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13
Q

Describe the pharmacology of oral theophylline?

A

Relaxes bronchial smooth and reduces inflammation, has narrow therapeutic window though (it can be toxic in excess).

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14
Q

What is FVC and FEV1

A

Forced vital capacity - maximum volume of air that can be expelled from the lungs following a maximal inspiration.
Forced expiratory volume in 1 second - the maximum amount of air that can be expelled from the lungs in one second.

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15
Q

In asthma what would the FEC1% (FEV1/FVC) be like and what would the FEV1 and FVC be?

A

It would be reduced (less than 70%).
FEV1 - Significantly reduced.
FVC - normal or slightly reduced.

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16
Q

If the FEV1/FVC pattern is below 75% what does this suggest?

A

An obstructive disease pattern (Asthma, COPD).

17
Q

What type of hypersensitivity is asthma associated with?

A

Type 1 hypersensitivity - IgE.

18
Q

If a patient is doing peak flow at different times of the day over a few days, when is it likely to be worst?

A

In the morning, its called diurnal variability.

19
Q

What is a side effect of B2 agonists (SABAs/LABAs)

A

Fine tremor.

20
Q

What are some of the best distinguishing symptoms between asthma and COPD?

A

A - Non-productive cough/ C - productive cough.
A - Non-smokers/C -smokers.
A -early or late onset/ C - Late onset.
A - eosinophilic inflammation/ C - neutrophilic inflammation
A - good response to corticosteroids and bronchodilators/ C - not to either of those.

21
Q

How would an acute exacerbation of asthma present?

A

Progressively worsening shortness of breath.
Use of accessory muscles.
Fast respiratory rate (tachypnoea).
Symmetrical expiratory wheeze upon auscultation.

22
Q

What is the usual ABGs of a patient that had come in with an asthma attack?

A

Respiratory alkalosis as they are tachypnoea and this causes a drop in CO2.
Normal PCO2 or hypoxia is a concerning sign as they are tiring, this indicates life threatening asthma.
Respiratory acidosis as it means that they have high CO2 due to them being exhausted and don’t have the effort to breath.

23
Q

What investigations would you do for investigating asthma

A

Full blood count - eosinophilic inflammation.

Peak flow - look to see if it is less and also if it has diurnal variation.

24
Q

What is a side effects of ICS

A

Hypertension.
Hyperglycemia.
Oral thrush.
Osteoporosis.

25
Q

Describe the PEFR (Peak expiratory flow rate) in a moderate exacerbation of Asthma?

A

PEFR 50-75% of their best.

26
Q

Why do they monitor serum potassium when on salbutamol in an asthma attack?

A

Salbutamol causes potassium to be absorbed into the cells.

27
Q

Describe the PEFR (Peak expiratory flow rate) in a severe exacerbation of Asthma?

A

33-50% of their best.

resp rate > 25.

28
Q

Describe the PEFR in a severe exacerbation of asthma?

A

<33%