Asthma Flashcards

1
Q

Define Asthma

A

“Asthma is a chronic inflammatory disorder of the airways.

inflammatory symptoms are usually associated with widespread but variable airflow obstruction and an increase in airway responsiveness to a variety of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

difference in airway obstruction in COPD and asthma

A

the airway obstruction in Asthma is often reversible

􏰉 the airway obstruction in COPD is not fully reversible -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is asthma classified?

A

ATOPIC & NON-ATOPIC

atopic> evidemce of allergen sensitization, often in patients w/ a histroy of allergic rhinitis and eczema

Non-atopic> w/ out evidence of allergen sensitization,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

different catagories of asthma and examples for each

A

Atopic asthma > allergen induced (oftem gave FH of asthma)

Non-atopic> non allergen, cause by respiratory infections

Drug-induced> aspirin and NSAIDS

Occupational> fumes (plastics) chemical dusts ( wood, cotton, platinium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does aspirin induce asthma?

A

inhibit the cycloxygenease pathway of AA w/ OUT AFFECTING THE LIPOXYGENEASE ROUTE!

thus tipping the balance toward the elaboration of bronchoconstrictor leukotrines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology of ASthma

A

Asthma is a chronic inflammatory process driven by Th2 cells

Macrophages process and present antigens to T lymphocytes.

This ‘activates’ T cells, with TH2 cells being preferentially activated.

TH2 cells release cytokines, which attract and activate inflammatory cells, including mast cells and eosinophils. TH2 cells also activate B cells, which produce IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

sensitized atopic asthmatic, exposure to antigen results in a

2 phase response :

name them

A

immediate response (reaching max in about 20 mins) followed by a late phase response ( 3 – 12 hours later).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is immediate response caused by?

A

is an example of type 1 hypersensitivity.

It is caused by interaction of the allergen & specific IgE antibodies, leading to mast cells degranulation and release of mediators (histamine, tryptase, prostaglandin D2 and leukotriene)

which cause bronchial smooth muscle contraction lading to bronchoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe Late phase response

A

an example of type 4 hypersensitivity.

involved in recruitment of inflammatory cells:

  • eosinophils,
  • mast cells,
  • lymphocyte
  • neutrophils

which release mediators and cytokines, which cause airway inflammation.

leukocyte recruitment is stimulated by the chemokines produced by the mast cells.

this 2nd wave of mediators stimulates the late reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what major substance does eosinophils release?

what does this cause?

A

release Leukotriene C4 and other mediators, some of which are toxic to epithelial cells

causes shedding of epithelial cells. !!!

(Eosinophils are very sensitive to steroid therapy).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does the the air way inflammation causes reduced airway calibre (airway narrowing) ?

due to what ?

A
  • 􏰉 Mucosal swelling (oedema) due to vascular leak,
  • 􏰉 Thickening of bronchial walls due to infiltration of inflammatory
  • cells
  • 􏰉 Mucous over production; the mucus is also abnormal- it is thick, tenacious & slow moving. The cough is therefore usually dry or only productive of scanty, white sputum. In severe cases many airways are occluded by mucus plugs.
  • 􏰉 Smooth muscle contraction
  • 􏰉 The epithelium is shed and is incorporated into the thick mucus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The inflammation also causes hyper responsiveness of airways.

what does this mean?

A

Because of airway hyper-responsiveness, non-allergic stimuli like cold air & fumes can also trigger attacks

in nonatopic asthma, respiratory infection like (rhinovirus, parainfluenza virus) r common triggers in non atopic asthma.in these patient hyperirritability of the bronchial tree probably lies in their asthma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what can Long term poorly controlled asthma lead to?

A

can lead to airway remodelling some of which may not be fully reversible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Long term poorly controlled asthma, can lead to airway remodelling some of which may not be fully reversible.

The changes include?

A

The changes include:

􏰉 hypertrophy & hyperplasia of smooth muscle,

􏰉 hypertrophy of mucus glands

􏰉 thickening of the basement membrane .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Effect of airways narrowing on spirometry & symptoms?

A
  • 􏰉 causes wheezing & other clinical features of asthma
  • 􏰉 results in an obstructive pattern on Spirometry (↓ FEV/FVC ratio < 70% ) & typical flow volume loops; which shows reversibility with bronchodilators, or over a period of time
  • 􏰉 air trapping with increased RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does asthma Effect gas exchange:

A

Airway narrowing leads to reduced ventilation of the affected alveoli → this causes a ventilation / perfusion mismatch in the affected area.

17
Q

how can the lungs compensate for the ventilation / perfusion mismatch?

A

Hyperventilation of better ventilated areas of the lung cannot compensate for the hypoxia,

but can compensate for CO2 retention by increased breathing out of CO2

18
Q

how is asthma classified?

A
19
Q

what r the findings in mild to moderate asthma

A

↓pCO2 and ↓pO2 = type 1 respiratory failure

it starts off as type 1, cuz lal7een aku healthy bits of the lungs to comoensate for the high PCO2 that accumlate due to obstruction, but as disease progresses more areas r effected and ur lungs evetually cannot compensate!

20
Q

findings in severe attacks

A

↑pCO2 and ↓pO2 = type 2 respiratory failure

lungs cannot vompensate anymore and cant puff out excess CO2

21
Q

Therefore increasing pCO2 is a sign of life threatening Asthma. !!!

(Disease is severe & extensive and patient is exhausted— these patients often require assisted ventilation)

A
22
Q

what r Asthma Triggers ?

A

Allergens - pollen, animals (animal hair/dander), house dust, faeces

 Cold air

 exercise

 fumes - Car exhaust

 cigarette smoke

 perfumes

 chemicals - Isocyanates and acid anhydrides (varnish/paint)

 drugs - NSAIDS and beta blockers

 emotional distress;

23
Q

symtoms of asthma

and signs in examination

A
24
Q

Treatment of asthma?

A
25
Q

Why are inhalers preferred to oral formulations?

A
26
Q

Describe in outline how to recognise and treat acute severe asthma & life threatening asthma.

A

increasing pCO2 is a sign of life threatening Asthma.

27
Q

treatment of acute asthma attack

A
28
Q

Treatment of acute severe asthma includes

A

Treatment of acute severe asthma includes

nebulised 􏰎2 agonists & ipratropium delivered in oxygen

IV steroids followed by a short course of high dose oral prednisolone.

29
Q
A
30
Q

What is the difference between specific and non-specific triggers of
asthma?

A
  • Specific triggers* – antigens: only affect those that are sensitised
  • Non-specific triggers* - smoke, cold air, exercise: may affect anybody
31
Q

Mneumonic for treatment of asthma

O SHIT MATE

A

O SHIT MATE

  • Oxygen
  • Salbutamol>> nebuli withe oxygen
  • Hydrocortisone
  • Ipotropium bromide >> antimuscuranic in lung
  • Theophylline >> phosphodiesterase inhibitor
  • Magnesium>> decrease vagal tone -increase ca uptake in SR
  • Escalate>>
32
Q

What clinical features, if present, suggest life threatening asthma?

A

o Silent chest due to minimal air movement

o Central Cyanosis

o Disturbance of consciousness- confusion, coma

o Arterial pO2 less than 8 kPa (Oxygen saturation < 92%)

o Arterial pCO2 greater than 5.5 kPa

o Pulsus paradoxus

o Bradycardia, Hypotension

o Arrhythmia

o Feeble Respiratory effort, exhaustion

33
Q
A
34
Q

Physical examination finding of asthma

A

The most frequent finding is wheezing on auscultation, especially
on forced expiration

Wheezing may be absent during severe asthma exacerbations
(‘silent chest’)

35
Q

How can we measure Airway inflammation

(3)

A
36
Q

What can cause Breathlessness?

acute and chronic

(Think differential diagnosis!)

A
37
Q
A
38
Q

Differemt cells in copd and asthma

A
39
Q

Why is Jane’s asthma worse at night?

A

There is higher vagal activity at night.
Parasympathetic nerves are bronchoconstrictor in nature.
Posture: lung volume is lower when supine, therefore airways narrower.
Less cortisol at night>>