Respiratory Flashcards

1
Q

What is asthma?

A

A chronic inflammatory airway disease, it is characterised by intermittent airway obstruction and hyper reactivity, it is a disease of the small airways with a variable expiratory airflow.

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2
Q

What would you give for type 1 asthma and give examples

A

You would give short acting beta agonists, these cause bronchodilation.

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3
Q

What would you give someone with second stage asthma?

A

Corticosteroids

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4
Q

What are the main pathological features of asthma?

A

Airway smooth muscle:
Hyperresponsiveness
Constriction
Thickening

Sub epithelial inflammation and fibrosis

Mucus hypersecretion and an impaired mucus clearance

Increased eosinophils and/or neutrophils in the airway lumen

The above all contribute to narrow the airways.

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5
Q

Is asthma type 1 or type 2 resp failure?

A

It is type 1 resp failure- Low pO2, however can become type 2 with a low pO2 and high PCO2.

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6
Q

How would asthma present in a patient, and what leads to an onset of asthma?

A

Asthma presents as: wheeze, breathlessness, chest tightness, cough (dry and nocturnal)

Precipitating factors include: 
Allergens- pollens/lets 
Dust 
Cigarette smoke 
Cold weather 
Exercise 
Infection aerosols
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7
Q

What would you notice on examination of asthma?

A
Do the resp rate would be increased 
Pulse would be increased 
Oxygen says would be low 
Wheeze 
Atopy (hayfever, eczema)
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8
Q

How would you diagnose asthma?

A

Peak flow

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9
Q

How would you differentiate between asthma and COPD?

A
Asthma 
Dry cough 
Wheeze 
History of atopy 
Obstructive patter- good reversibility with bronchodilator 
COPD 
PRODUCTIVE cough 
Productive cough 
Wheeze 
History of smoking 
Obstructive pattern- poor reversibility
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10
Q

How do you recognise asthma, acute severe vs life threatening?

A
Acute severe: breathless, wheeze, O2 is greater than 92% 
RR >25 breaths per min 
Tachycardia 
Difficulty finishing sentences 
HR greater or equal to 110 
Life threatening 
Tired 
Drowsy 
Cyanosis 
Reduced effort 
Bradycardic
o2 less than 92% 
PF < 33% (peak flow)
Decreased BP/HR 
Altered consciousness
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11
Q

What are the 3 layers of the cortex of the adrenal gland and what do they secrete?

A

So it’s , go find Rex, make good sex,
ZONA glomerulosa-
mineralcorticoids- aldosterone

ZONA fasiculata-
Glucocorticoids- cortisol

ZONA reticularis- oestrogens

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12
Q

How do corticosteroids work?

A

Corticosteroids cause two actions: either causes or inhibits the transcription and hence translation of mRNA.

Transactivation of…
B2 receptors

Transrepression of... 
inflammatory mediators 
Cytokines 
Chemokines 
Adhesion molecules
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13
Q

What are the side effects of beta agonists?

A

Adrenergic- tachycardia, palpitations and tremor

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14
Q

When shouldn’t you you use beta agonists?

A

Don’t use when someone has hypertension/ACE inhibitors

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15
Q

Why might someone not respond to corticosteroids?

A

If they don’t have eosinophilia asthma, patients with eosinophilia asthma have a better response to inhaled steroids than non eosinophilic patients.

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16
Q

Before doing step 3, which is an add on therapy to the inhaled corticosteroids and beta agonist what should you check?

A

You should check the patients compliance
Check the patient knows how to use the inhaler
Eliminate the trigger factors (smoking, pets, damp, aerosols)

17
Q

What is the potency of A drug and what measurement is used to show it?

A

So potencies are the concentrations of a drug needed to cause an effect, the less concentration needed the higher the potency.
EC50 can be used to show this= concentration needed to produce half the max response.

18
Q

What is the step 3/add on therapy for asthma?

A

The first choice would be long acting B2 agonists (salmeterll/formoterol)
Add in LABA when patients are not controlled in 400mcg/day ICS

19
Q

What are the role of long acting beta agonists?

A

Reduce asthma exacerbation
Improve asthma symptoms
Improve lung function
They aren’t anti inflammatory on their own and must always be prescribed in conjunction with an inhaled steroid.

20
Q

What is better, folmoterol or salmeterol and why?

A

Formoterol has a stronger intrinsic B2 agonist activity than salmeterol, it also has a greater effect and less is needed to have the same effect.

21
Q

Now there is becoming single inhalers which can be used, which combine both LABA and ICS in a single inhaler, give the rational behind this…

A

Ease of use
Compliance
1 prescription, rather than two to worry about
Can be cheaper than 2 individual inhalers
They are also safer p- steroids you don’t get the immediate action (takes a while to affect the expression of proteins)

22
Q

What are some alternative step 3/4 add ins?

A

High dose ICS
Leukotriene receptor antagonists
Theophylline
Tiotropium

23
Q

What are leukotriene receptor antagonists, give the mechanism of action and examples…

A

Normally LTC4 release by mast cells and eosinophils can induce bronchoconstriction, mucosal secretion, mucosal oedema and promote inflammatory cell recruitment.
Therefore block this binding

24
Q

What are the side effects of using leukotriene receptor antagonists?

A
Angioedema 
Dry mouth (xanthalasma) 
Anaphylaxis 
Arthralgia ( joint pain) 
Fever 
Gastric disturbances
25
Q

What is Theophylline and how does it work?

A

This is a methylxanthine, it’s role is to antagonise adenosine receptors

26
Q

Is theophylline effective?

A

No methylxanthines are generally poorly efficacious, they have a very narrow therapeutic window and cause frequent side effects (nausea, headache and reflux), as well as potentially life threatening complications- arrhythmia sand fits.

27
Q

What should you notuse theophylline with and why?

A

It has important drug interactions with cytochrome P450 inhibitors eg: erythromycin and ciprofloxacin, levels will be increased.

28
Q

How do long acting anticholinergics work and give an example…

A

They are licensed for both COPD and asthma, they have relative selectivity for M3 muscarinic receptor
Reduces exacerbation in both COPD and asthma, you get small improvements in lung function and symptoms.
Has relative selectivity for M3 muscarinic receptor.

29
Q

How do LAMAs work?

A

So they bind to M3 receptors mainly in the airways and cause bronchodilation.

30
Q

What is the sign of acute sever asthma in adults?

A

Unable to complete sentences
A pulse greater than 110 beats/min
Resp rate greater than 25 per min (should be 2-20)
Peak flow 33-50% of best or predicted

31
Q

What do you need to look out for, for life threatening features of asthma?

A
Any of the acute severe symptoms (resp rate, pulse, peak flow, unable to complete sentences) plus any one of the following... 
1. Silent chest 
2. Cyanosis 
3. Feeble resp effort 
4. Hypotension, bradycardia, arrhythmia 
5. Exhaustion, confusion 
, coma
32
Q

How would you treat acute severe asthma?

A
  1. Oxygen, high flow with aim to kee O2 at 94-98%
  2. Nebuliser salbutamol- continuous if necessary
  3. Oral prednisolone (a steroid)
  4. If moderate exacerbation and not responding, or acute severe/life threatening then add nebuliser ipratropium bromide
  5. Consider IV aminophylline if no improvement and life threatening features not responding to above treatment
33
Q

When is iprotapium bromide important?

A

It is important as an add on in acute severe/life threatening asthma, or moderate exacerbation with a poor response to the initial therapy.
Bronchodilation develops more slowly and less intense than adrenergic agonists, responses can last for up to 6 hours.

34
Q

What is arachiodonic acid and why is it important in prostanoid synthesis?

A

Arachiodonic acid is involved in the mechanism of inflammation, it is released by phospholipids in the cell membrane by the phospholipase A2 enzyme, it is the substrate for two major enzymes COX-1 and COX-2 which are involved in production of prostanoids.