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1st Year Medicine > Asthma > Flashcards

Flashcards in Asthma Deck (49):
0

How many people does asthma affect?

5 - 10% of the population.

1

What is bronchial asthma?

A chronic inflammatory disorder characterised by hyper active airways leading to episodic reversible bronchoconstriction.
Recurrent and reversible (in the short term) obstruction in response to normally harmless stimuli or may be due to a chronic inflammatory response in the airways.

2

Do asthmatics find inspiration or expiration easier and why?

Inspiration as the bronchioles widen and vice versa.

3

What are the symptoms of asthma?

Wheeze, cough and dyspnoea.

4

What changes occur in the airways of chronic asthmatics?

Hyperplasia and hypertrophy of smooth muscle.
Airway oedema.
Increased mucus secretion.
Epithelial shedding from long term inflammation. Causes damage exposing sensory nerve endings.

5

Describe neurogenic inflammation in asthma.

Sensory nerves have multiple branches. A blow sends an action potential to the CNS and around the branches. Causes release of inflammatory substances (substance P and calcitonin gene related peptide -CGRP). Histamine works on sensory endings and excite them causing bronchi spasm.

6

What causes bronchial hyper responsiveness in asthma?

Epithelial damage exposes sensory nerve endings (C-fibre irritant receptors). Airways are increasingly sensitive and may have neurogenic inflammation. Two components: hypersensitivity and hyperreactivity.

7

What drugs are used in asthma provocation tests?

Spasmogens e.g. Histamine and methacholine (muscarinic ach receptor agonist).

8

What do provocation tests look for?

Falls in FEV1 compared to the inhalation of the bronchiconstrictor.

9

What is an aero allergen?

Allergen in the air e.g. Pollen.

10

How can we tell if a patient is suffering from allergic asthma?

After allergen is phagocytosed by dendritic cell. Atopic individuals will have a strong Th2 antibody mediated IgE response. Non atopic will have a low level Th1 response with cell mediated immunity using IgG and macrophages.

11

What happens in the immediate phase of allergic asthma?

Allergen binds to IgE on the surface of mast cells and de granulation causes release of histamine causing: bronchospasm, inflammatory eosinophil influx and mucosal inflammation and oedema. The inflammatory infiltrate tends to lead to chronicity.

12

What happens in late phase asthma?

Chemotaxins and chemokines released during early phase infiltrate cytokine releasing Th2 cells and monocytes, activate inflammatory cells particularly eosinophils. This cause epithelial damage, airway inflammation, airway hyper reactivity and bronchospasm.

13

What forms of airway obstruction are common in asthma?

Airway lumen narrowing due to spasm and inflammation and mucus plugs.

14

How can asthma obstruction become irreversible?

If collagen is deposited and the airways become remodelled.

15

What does early/late onset mean in reference to asthma?

Refers to age.

16

What does atopic/non-atopic mean In reference to asthma?

Refers to allergic status.

17

What does extrinsic mean in reference to asthma?

The response to an inhaled antigen.

18

What does intrinsic mean in reference to asthma?

It has a non immune mechanism e.g. Cold, exercise or aspirin.

19

What is the asthma triad?

Reversible airflow obstruction
Airway inflammation
Airway hyperresponsiveness.

20

What kind of hypersensitivity is allergic asthma?

Type 1.

21

What is chronicity?

Lasting for a long length of time or marked by frequent recurrence.

22

What do eosinophils secrete which contributes to the affects of asthma?
What do these substances cause?

Platelet activating factor (PAF) and products like eosinophilic basic protein which stimulate chronic inflammation, epithelial damage and bronchial hyper responsiveness.

23

What are the pathological findings in asthma?

Narrowed oedematous airways.
Mucus plugs
Inflammatory cell infiltrate
Epithelial cell damage.

24

What happens during the inflammatory cascade in asthma?
Causes, results and mediators.

A genetic predisposition combined with a trigger factor causes airway inflammation. This is mediated by TH2 cytokines e.g. Histamine and leukotrines which cause twitching of the smooth muscle.

25

What drugs can we use to block the mediators stage in asthma?

Anti leukotrine,p and anti IL/4/5/13.

26

What drugs can we give to stop the inflammatory stages of asthma?

Corticosteroids.

27

What drugs do we give to relax the smooth muscle in asthma?

Beta 2 antagonists.

28

How long must patients stop smoking for before they can receive home oxygen?

6 weeks.

29

When we not intubation seriously ill patients?

If they have. DNAR or it is not realistic that we will ever be able to extubate them.

30

What problem should we always think of if we are presented with a severely hypoxic patient?

Blood clots.

31

What drugs can reduce the steroid burden?
How do they do this?

Omilozomab.
It has anti-IgE which reduces the inflammatory cascade.

32

Why should we not give beta antagonists before steroids in asthma?

As patients build up a tolerance to beta antagonists over time.

33

What microscopic hallmarks of airway remodelling can be seen?

Thickening of the basement membrane, collagen deposition in the submucosa and hypertrophy in the smooth muscle.

34

How does asthma normally evolve in the long term?

Bronchoconstriction causes brief symptoms, then chronic inflammation leads to exacerbations and airway hyper responsiveness which leads to airway remodelling causing fixed airway obstruction.

35

If we are clerking a patients with asthma what should we ask them about?

Triggers such as dust and dander.

36

How do we diagnose asthma?

History and examination.
Diurnal variation of peak flow rate.
Look for reduced forced expiratory ratio of under 75%
Provocation testing combined with reversibility to salbutamol of over 15%
Look for family history
Look for other signs of atopy.

37

How do we do provocation testing?

Give them an allergen or drug like methyl choline, see how many doses it takes to achieve a 20% drop in FEV1. The number of doses reflects the severity of the asthma. Then give salbutamol for reversibility.

38

What is the primary cell involved in the inflammatory exudate of asthma?

Eosinophils.

39

What are the differences between asthma and COPD in the below categories?
Smoking.
Allergy.
Onset.
Duration of symptoms?
Cough
Inflammatory cells.
Variability
Drug response
Spirometry response.
Gas exchange.

Asthma vs COPD.
Non-smokers vs. smokers.
Allergies vs non.
Any onset vs late onset.
Intermittent vs chronic symptoms.
Non productive vs productive cough.
Eosinophilic vs. neutrophillic inflammation.
Diurnal variability vs none.
Good corticosteroid and bronchodilator response vs poor response to both.
Preserved FVC and TLCO vs reduced of both.
Normal gas exchange vs impaired gas exchange.

40

What diurnal variation do asthmatic show?

Marked morning dipping of peak flow.

41

What tests do we do for an acute asthma attack?

Peak flow, sputum culture, FBC, U and E, CRP, blood cultures, ABG's

42

What associated symptom do asthmatics commonly get that if we treat can improve spirometry? What does treating it do to asthma symptoms?

Acid reflux. Treatment doesn't improve symptoms.

43

What should we do if the PaO2 of an asthmatic patient I'd normal but they are hyperventilating?

Watch carefully and repeat the PaO2 later.

44

What does an ABG normally show for a patient having an asthma attack?

Slightly reduced PaO2 and a low PaCO2

45

What should we do if the PaCO2 of a patient having an asthma attack is raised? And why?

Transfer to HDU or ITU for ventilation as this signifies failing respiratory effort.

46

What is the differential diagnosis of asthma?

Pulmonary oedema, COPD, airway obstruction, pneumothorax, PE or bronchiectasis.

47

How do we monitor chronic asthmatics?

Peak flows, spirometry and can do allergen testing.

48

What are the steps in asthma drug treatment?

Step 1 - occasional use of short acting beta 2 adrenoceptor antagonists.
Step 2 - low dose inhaled corticosteroids.
Step 3 - low to moderate dose inhaled corticosteroids plus long acting beta 2 adrenoreceptor antagonists.
Step 4 - high dose inhaled corticosteroids and regular bronchodilators and leukotriene receptor antagonists or theophylline.
Step 5 - regular oral corticosteroids.