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Hugh's MD1 Respiratory > Respiratory Drugs > Flashcards

Respiratory Drugs Flashcards

1
Q

What are LABAs combined with?

A

GCS

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2
Q

Which are more effective bronchodilators in asthma, beta adrenoceptors agonists or muscarinic receptor agonists?

A

Beta adrenoceptor agonists

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2
Q

What is theophylline?

A

Phosphodiesterase inhibitor

Smooth muscle relaxant

Adenosine inhibitor

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3
Q

What are LABAs? and uLABAs?

A

Long acting beta2 adrenoceptors agonists

uLABA - ultra long acting beta2 adrenoceptor agonist

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3
Q

What are some adverse effects of oral GCS?

A

Osteoporesis

Diabetes,

Muscle wasting

Hypertension

Growth suppression

Suppresion of adrenal, hypothalamus and pituitary axis

Need to wean off them

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4
Q

How does transrepression work?

A

GCS bound to its receptor bind to AP-1 downstream from its activation by inflammatory cytokines - the inhibits AP-1 activating inflammatory transcription factors

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5
Q

What are SAMAs and LAMAs?

A

Short and long acting murcarinic receptor agonists

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5
Q

How does GCS transactivation work on a molecular level?

A

They diffuse into cells >

Dimerize with a co-factor >

Activate transcription factors that encode anti-inflammatory products

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6
Q

T/F, combining inhaled GCS and LABAs improves symptoms, quality of life and exacerbation rate more than their use individually?

A

True

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6
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

None available

O2

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7
Q

Which are more effective are providing symptomatic relief, SABAs or LABAs?

A

LABAs

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8
Q

The end of GCS transrepression is …

A

Repressed transcription of:

Cytokines and their receptors

Inducible enzymes for inflammatory mediators (eg COX-2)

Adhesions molecules

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8
Q

Compare the histopathology of severe asthma and COPD

A

Asthma:

More SM

More BM

COPD

More fibrosis

Loss of alveolar tethering

Both:

High Inflammation

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9
Q

Which are more effective bronchodilators in COPD, beta adrenoceptors agonists or muscarinic receptor agonists?

A

Muscarinic are equally or more effective than adrenoceptor

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9
Q

When are phosphodiesterase inhibitors used?

A

In severe and very severe COPD as it can reduce exacerbations

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10
Q

What are the clinical effects of GCS treatment in COPD patients?

A

Improves symptoms

Better quality of life

Less frequent exacerbations

But it is associated with an increased risk of pneumonia

11
Q

What are the most important inhaled GCSs?

A

Budesonide

Fluticasone propionate

They are available in combinations with LABAs

13
Q

What is the difference between indacaterol, and salmeterol and formoterol

A

Indacaterol lasts an extra 12 hours (24 cf to 12hours)

14
Q

Where are muscarinic receptor in airways?

A

Smooth muscle (M3)

15
Q

What is the effect of LABAs?

A

Not 100% clear but they reduce the rate of exacerbations

Maybe anti-inflammatory

Chronically bronchodilate

17
Q

What ligand acts on muscarininc receptors in the airways?

A

ACh

19
Q

What are some other interventions for COPD?

A

Exercise

O2

Pulmonary rehab

Lung transplantation

20
Q

What are the two ways GCS are administered?

A

Inhaled (topical)

Oral (systemic)

22
Q

When are LABAs indicated?

A

Asthma, COPD

Prophylaxis only

24
Q

What are three LABAs?

A

Salmeterol and Formoterol and Indacaterol

25
Q

Why don’t anti-histamines work for asthma?

A

Because there are many mediators in these conditions, histamine isn’t an importnat mediator of bronchospasm
in asthma despite it working on H1 receptors on smooth muscle. Cystenile leukotriene can constrict the muscle for a much longer time, parasympathetic, comple
ment system.

26
Q

Do GCS only transactivate?

A

No, they can also perform tranrepression

27
Q

What are some anti-inflammatory products that GCS activate the expression of?

A

Annexin-1 - turns off on going inflammation and recruitment

Serpin A3 - anti-protease

Beta2-adrenoceptor - to maintain agonist’s effects

28
Q

Do LABAs improve survival in COPD patients? Why/why not?

A

No, because they don’t prevent remodelling

29
Q

When are GCS indicated?

A

If inhaled beta agonists are required >3 times per week

30
Q

Glucocorticoids overall affect in asthma is to

A

Reduce inflammatory cell number and activation

Decrease the probability and severity of episodes of asthma

31
Q

What are some adverse effects of inhaled GCS?

A

Dysphonia

Oral candidiasis

Reduced serum cortisol

32
Q

What are some other treatments for COPD?

A

Antibiotics - for infections

Antioxidants agents

Mucolytics agents

Antitusives

Vasodilators (for hypertension)

34
Q

What makes LABAs long acting?

A

They are lipid soluble

35
Q

When are oral GCS indicated in asthma

A

Acute exascerbations

Severe chronic asthma

36
Q

What is the difference between salmeterol and formoterol?

A

Salmeterol has a slow onset while formoterol has a fast onset

37
Q

What are the 4 effects of glucocorticoids on the inflammatory cells in asthma?

A

Reduce activity, recruitment and survival of eosinophils and T cells

Reduce mast cell cytokine production

Reduce macrophage cytokine production

Reduce proliferation, cytokine production and collagen production by fibroblasts and smooth muscle cells

38
Q

Does tolerance to LABAs develop? If so then how?

A

Yes

Reduced number of receptors

39
Q

What is the most common SABA?

A

Salbutamol

Hugh's MD1 Respiratory (15 decks)

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