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Respiratory > Asthma Drug Treatment > Flashcards

Asthma Drug Treatment Flashcards

1
Q

Two types of drug treatment for asthma?

A

Relievers and Controllers.

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2
Q

Difference between a reliever and a controller?

A

Relievers are fast acting and treat an acute attack whereas controllers have no effect during an acute attack and require long term usage.

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3
Q

4 types of relievers.

A

Slow Acting Beta2-adrenoceptor agonist (SABA)

Long acting beta2-adrenoceptors agonist (LABA)

Ultrs-LABA

CyLT1 receptor antagonists.

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4
Q

SABA drugs in treatment of asthma?

A

Salbutamol and Terbutaline.

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5
Q

Other name for Salbutamol?

A

Albuterol.

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6
Q

LABA drugs in treatment for asthma?

A

Salmeterol and Formoterol.

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7
Q

Why is salmeterol not used in acute attacks?

A

Slow acting.

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8
Q

What are LABAs usefor for treating?

A

Nocturnal asthma as they act for about 8 hours.

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9
Q

Most important things about LABAs?

A

CANNOT be administered alone.

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10
Q

What must LABAs be co-administered with?

A

Glucocorticoids. e.g. beclametosone

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11
Q

Effects of SABAs?

A

Relax bronchial smooth muscles.

Increase mucus clearance.

Decrease mediator release from mast cells and monocytes.

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12
Q

What are methylxanthines sometimes used as?

A

Both relievers and controllers.

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13
Q

Purpose of controllers?

A

With long term usage they reduce the frequency and severity of asthma attacks.

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14
Q

Examples of controllers?

A

Glucocorticoids,
Cromoglicate,
Humanised monoclonal IgE antibody (Expensive).

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15
Q

Beta2-adrenoceptor agonists act as…

A

Physiological antagonists for all spasmogens.

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16
Q

Why are non-selective beta-adrenoceptor agonists redundant in asthmatics?

A

Risk of bronchospasm.

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17
Q

What is the name of CysLT1 receptor antagonist and what does it act as?

A

Cysteinyl leukotriene receptor antagonists.

Bronchodilator.

18
Q

How does CysLT1 receptor antagonist act as a reliever?

A

CysLT1 act competitively on CysLT1 receptor. Competing with LTC4, LTD4 and LTE4 which are derived from mast cells and infiltrating inflammatory cells causing smooth muscle contraction, mucus secretion and oedema.

19
Q

What occurs if CysLT1 receptor antagonists do not bind to CysLT1 receptor?

A

CysLTs (LTC4, LTD4, LTE4) bind to receptor instead activating it and causing early phase bronchoconstriction followed by delayed phase inflammation.

20
Q

Examples of CysLT1 receptor antagonists?

Administration route?

Primary treatment or add on?

A

Montelukast, Zafirlukast.

Oral.

Suitable as an add on to treat bronchospasm.

21
Q

Why is CysLT1 receptor antagonists not recommended for relief of acute severe asthma?

Any side effects?

A

Not as effective as a SABA such as salbutamol.

Generally well tolerated but headaches and gastrointestinal upset reported.

22
Q

Methylxanthines molecular mechanism?

A

Unknown but thought to inhibit isoforms of phosphodiesterases (PDE3 & 4) which inactivate cAMP preventing binding to PKA and advancement to MLCK which results in relaxation of ASM.

23
Q

Effects of methylxanthines?

Primary or add on treatment?

Administration route?

Side effects?

A

Bronchodilator (high doses) and anti-inflammatory. Increased mucous clearance, increased diaphragmatic contractibility

Add on used in combination with Beta-2-adrenoceptor agonists and glucocorticoids.

Oral.

Very narrow therapeutic window, nausea, headache, vomiting reported and above TPW can cause seizures and hypotension.

24
Q

What could potentiate anti-inflammatory action of glucocorticoids?

A

Theophylline activates histone deacetylase.

25
Q

What are the 2 classes of steroid hormone?

Where are they synthesised?

Pre stored?

A

Glucocorticoids, Mineralocorticoids.

Adrenal cortex.

No, synthesised and released on demand.

26
Q

Main hormone in glucocorticoids?

Effects?

A

Cortisol (hydrocortisone).

< inflammatory response
< immunological response

27
Q

Main mineralocorticoid?

Effect?

A

Aldosterone.

Regulates sat and water retention by the kidneys.

28
Q

Why are glucocorticoids ineffective in an acute attack?

Administration route?

A

They have no direct bronchodilator action and therefore cannot relieve bronchospasm.

Usually inhaled to minimise adverse effects.

29
Q

What is an endogenous steroids?

A

Gluco and mineralocorticoid actions but the latter is unwanted in treatment of inflammatory conditions.

30
Q

Glucocorticoid molecular mechanism of action?

A

Signal via nuclear receptors (GRalpha).

Glucocorticoids are lipophilic and diffuse into cell across PM. In cytoplasm they combine with GRa producing dissociation of HSPs.

The activated receptor translocates to the nucleus via importins. Here the monomers assemble to homodimers and bind to Glucocorticoid response element (GRE). Transcription of specific genes is switched on (transactivated) or switched off (transrepressed) to alter mRNA levels and rate of synthesis of mediator proteins.

31
Q

How do glucocorticoids affect translation of inflammatory and ant-inflammatory genes?

A

Decrease inflammatory.

Increase anti-inflammatory.

32
Q

Why do glucocorticoids recruit HDACs?

A

To switch off transcription.

33
Q

What does expression of inflammatory genes involve?

A

Acetylation of histones by histone acetyltrasferases (HATs).

34
Q

What does acetylation of histones cause?

A

Unwinding of DNA from histones allowing transcription.

35
Q

Effect of HDAc and HAT on transcription?

A

HDAC = No transcription

HAT = Transcription.

36
Q

Effect of glucocorticoids on TH2 cytokines?

A

Decrease formation of eg IL4 IL5 and cause apoptosis.

37
Q

How are glucocorticoids usually administered?

A

By inhalation from a metered dose inhaler (to minimise adverse effects such as oropharyngeal candidiasis).

38
Q

What are cromones?

A

Drugs that supress histamine release from mast cells.

39
Q

What is the effect of cromones on bronchial smooth muscle?

A

None.

40
Q

What is sodium cromoglicate?

A

Specific cromone agent, delivered by inhalation and more effective in young people.

41
Q

Example of a monoclonal antibody directed on IgE?

Mechanism of action?

A

Omalizumab.

Requires IV administration.

Respiratory (7 decks)

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