Asthma Flashcards

1
Q

Immune cells involved in immediate phase asthma

A

Mast cells which produce spasmogens (histamine PGD2 etc)

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2
Q

Immune cells involved in late phase asthma

A

TH2 cells activate eosinophils

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3
Q

Immediate phase asthma treatments

A

Bronchodilators (salbutamol, salmeterol)
CycLT1 receptor antagonists (zafirlukast, montelukast)
Cromoglicate
Nedocromil

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4
Q

Late phase treatment

A

Inhaled glucocorticoids

Oral glucocorticoids

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5
Q

Beta-2 agonists types

A

Long acting salmeterol

Short acting salbutamol/terbutaline

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6
Q

Beta-2 agonist MOA

A

Binds to cause smooth muscle relaxation and bronchodilation

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7
Q

beta-2 agonist SE

A

Tremor, nervous tension, tachycardia but all rare when given by inhalation

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8
Q

Muscarinic antagonist MOA

A

Atropine/ipratropium inhibit ACh bronchoconstriction

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9
Q

Xanthines MOA

A

Theophylline is an oral PDE-4 inhibitor, which breaks down cAMP which is needed for bronchodilation in smooth muscle

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10
Q

Xanthines SE

A

Nausea, headache, insomnia, GI discomfort

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11
Q

Why do NSAIDs cause asthma

A

Leukotrienes made instead of prostaglandins as arachidonate precursor in excess

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12
Q

FLAP inhibitors MOA

A

Zileuton is 5-lipoxygenase inhibitor which blocks arachidinic acid conversion to LTA4

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13
Q

Leukotriene receptor antagonist MOA

A

Zafirlukast, Montelukast block leukotriene receptor to reduce LT bronchoconstricor and inflammatory effects

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14
Q

SAIDs used in

A

Main therapy for moderate-severe asthma, inhalation first then for more severe oral if necessary

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15
Q

Inhaled SAIDs

A

Beclometasone/budesonide

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16
Q

Oral SAIDs

A

dexamethasone, prednisonlone

17
Q

Cromoglicate/Nedocromil MOA

A

Inhaled mast cell stabiliser and T cell inhibitor, prophylactic only but less effective than inhaled corticosteroid prophylaxis

18
Q

Omalizumab MOA

A

Anti-IgE antibody, prevents cross-linking which leads to degranulation

19
Q

Omalizumab downsides

A

Expensive, variable results (works in limited number of patients)