Asthma Pharmacology Flashcards

1
Q

what are the drugs used as relievers

A

SABAs
LABAs
CystLT antagonists

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2
Q

What is the role of reliever drugs in asthma

A

Act as bronchodilators

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3
Q

What drugs are used as preventers in asthma

A

Glucocorticoids
Cromoglicate
Humanised monoclonal IgE

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4
Q

What is the role of preventer drugs in asthma

A

Act as anti-inflammatory

Reduce airway inflammation

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5
Q

Which drug is used for both relieving and prevention in asthma

A

Methylxanthines

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6
Q

what is the main role of beta 2 adrenoreceptor agonists

A

act as physiological antagonists of all spasminogens

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7
Q

What is an example of a SABA

A

Salbutamol

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8
Q

What is the first line treatment for mild, intermittent asthma

A

SABAs

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9
Q

What effects does a SABA cause on the airways

A

bronchial smooth muscle relaxation
increase mucus clearance
decrease mediator release from mast cells and monocytes

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10
Q

What are some side effects of SABAs

A

fine tremor
tachycardia
arrhythmia
hypokalaemia

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11
Q

What is an example of LABA

A

Salmeterol, formoterel

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12
Q

When would a LABA be prescribed

A

useful in nocturnal asthma

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13
Q

Which other drugs should LABAs be used with

A

Glucocorticoids

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14
Q

Why can asthmatics not use non-selective beta agonists (e.g. propranolol)

A

Risk of bronchospasm

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15
Q

What is an example of CysLT1 receptor antgonist

A

Montelukast

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16
Q

How do CysLT1 receptor antagonists work

A

They act competitively at CysLT1 receptors to block CysLTs causing smooth muscle contraction, mucus secretion and oedema

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17
Q

examples of CysLTs

A

LTC4
LTD4
LTE4

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18
Q

What are CysLTs derived from

A

mast cells

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19
Q

What is the result of using CysLT antagonist

A

bronchodilation (early phase)

Anti-inflammatory (late phase)

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20
Q

What types of asthma are CysLT1 receptor antagonists effective in

A

mild persistent asthma (as add on therapy)
severe asthma (in combination with corticosteroids)
Antigen induced and exercise induced bronchospasm

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21
Q

What are 2 examples of methylxanthines

A

theophylline and aminophylline

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22
Q

what is the effect of methyxantines

A

bronchodilation
anti-inflammatory
inhibit mediator release from mast cells
increase mucus clearance

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23
Q

how do methyanthines improve lung ventilation

A

increase diaphragmatic contractility and reduce fatigue

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24
Q

why are methylxanthines problematic

A

very narrow therapeutic window
adverse effects in both therapeutic and supra-therapeutic concentrations
numerous drug interactions

25
Q

what are the side effects of methylxanthines

A
dysrhythmia
seizures
hypotension
nausea
vomiting
abdominal discomfort
headache
26
Q

what are the 2 major classes of steroid hormone produced by adrenal cortex

A

glucocorticoid

mineralcorticoids

27
Q

which class of steroid hormone produced fro adrenal gland is used in treatment of asthma

A

glucocorticoid

28
Q

glucocorticoid increases/decreases inflammatory response

A

decreases

29
Q

glucocorticoid increases/decreases immune response

A

decreases

30
Q

glucocorticoid increases/decreases liver glycogen deposition

A

increases

31
Q

glucocorticoid increases/decreases gluconeogenesis

A

increases

32
Q

glucocorticoid increases/decreases glucose output from the liver

A

increases

33
Q

glucocorticoid increases/decreases glucose utilisation

A

decreases

34
Q

glucocorticoid increases/decreases protein catabolism

A

increases

35
Q

glucocorticoid increases/decreases bone catabolism

A

increases

36
Q

glucocorticoid increases/decreases gastric acid and pepsin secretion

A

increases

37
Q

what are some examples of synthetic derivatives of cortisol

A

beclometasone
budesonide
fluticasone

38
Q

why are glucocorticoids used in the prophylaxis of asthma

A

they have no direct bronchodilator effect when given acutely, hoover they can minimise adverse systemic effects

39
Q

what type of nuclear receptor do glucocorticoids signal via

A

GRalalpha

40
Q

are glucortcoids lipophilic or lipophobc

A

lipophilic

41
Q

how do glucocorticoids enter the cell

A

diffuse across the plasma membrane

42
Q

where do glucocorticoids combine with GRalpha

A

within the cytoplasm

43
Q

what happens with glucocorticoid combine with GRalpha

A

produce dissociation of inhibitory heat shock proteins and activates the receptor

44
Q

what do glucocorticoids do to genes when I the promoter region

A

transactivate (switch transcription on for anti-inflammatory genes)
trans-repressed (switch transcription off)

45
Q

where do glucocorticoids act to regulate genes

A

glucocorticoid response elements (GREs)

46
Q

where is the glucocorticoid response element

A

within the promotor region of specific genes

47
Q

What do glucocorticoids do to TH2 cytokines

A

decrease their formation

induce apoptosis

48
Q

How do glucocorticoids act on mast cells

A

reduce the number of cells and decrease Fce expression

49
Q

How do glucocorticoids act on immunoglobulins

A

prevent IgE production

50
Q

which inflammatory cells do glucocorticoids decrease

A
Eosinophil
T-lymphocyte cytokines
mast cells
Macriphage cytokines
Dendritic cells
51
Q

Which structural cells do glucocorticoids affect

A

epithelial - decease cytokines and mediaors
Endothelial cells - leak
Airway smooth muscle - increase beta 2 receptors and decrease cytokines
mucus gland - decrease secretion

52
Q

Common side effects of glucocorticoids

A

dysphonia

oropharyngeal candidiasis

53
Q

Which steroid is used in chronic, severe or rapidly deteriorating asthma

A

oral prednisolone in combination with inhaled steroid

54
Q

What is the action of cromones

A

they produce a weak anti-inflammatory effect

55
Q

when are cromones used

A

prophylactically in treatment of atopic asthma

56
Q

what is a specific cromone agent

A

sodium cromoglicate

57
Q

what is an example of monoclonal antibodies against IgE

A

Omalizumab

58
Q

how does Omalizumab work?

A

brinds to IgE via Fc t prevent attachment to FCe receptors on mast cells

59
Q

what is an example of monoclonal antibody against IL5

A

mepolizumab