Drugs for Pulmonary Disorders Flashcards

1
Q

what are the goals of asthma therapy?

A
  • reduce intensity and frequency of asthma symptoms

- reduce the risk of adverse effects associated with asthma

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2
Q

reduction of intensity and frequency of asthma symptoms include?

A
  • reducing symptoms (cough, SOB)
  • reducing need for short acting beta agonists
  • reduce- night time awakenings due to asthma
  • optimization of lung function
  • participation in normal daily activities
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3
Q

reduction of risk of adverse effects associated with asthma includes?

A
  • prevention of recurrent exacerbations and need for emergency department or hospital care
  • prevention of reduced lung growth in children, and loss of lung function in adults
  • optimization of pharmacotherapy with minimal or no adverse effects
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4
Q

what are the two main therapeutic strategies in asthma?

A
  • relievers and controllers
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5
Q

relievers include

A
  • beta adrenergic agonists

- muscarinic antagonists

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6
Q

controllers include

A
  • glucocorticoids
  • long acting beta adrenergic agonists
  • leukotriene antagonists and lipoxygenase inhibitors
  • methylxanthines
  • IgE antibodies and mast cell stabalizers
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7
Q

what two mediators induce bronchoconstriction?

A
  • histamine and leukotrienes
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8
Q

how does histamine induce bronchoconstriction?

A
  • IP3 levels increase within the mast cell and cause calcium to be released from sarcoplasmic reticulum
  • calcium causes mast cell degranulation and releases histamine
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9
Q

how do leukotrienes induce bronchoconstriction?

A
  • increase of calcium from sarcoplasmic reticulum also causes phospholipase A2 to be activated and causes formation of arachidonic acid
  • AA causes leukotrienes to be created which cause immune cell recruitment and bronchoconstriction
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10
Q

beta 2 adrenergic agonists

A
  • bind to beta 2 receptor associated with Gs
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11
Q

what are the routes of administration for beta 2 adrenergic agonists?

A
  • severe asthma attack (nebulizer)
  • inhaler (short and long acting)
  • oral (long acting, paediatric cases, night time control)
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12
Q

what are some adverse effects of beta 2 adrenergic agonists?

A
  • tremors and tachycardia
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13
Q

muscarinic antagonists

A
  • blocks muscarinic receptors in the smooth muscle of the bronchi
  • second line therapy (effective in 2/3 of clients with asthma, slower acting than SABA)
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14
Q

when are muscarinic antagonists used?

A
  • COPD, chronic bronchitis
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15
Q

what are some adverse effects of muscarinic antagonists?

A
  • dry mouth and sedation
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16
Q

can muscarinic antagonists be combined with short acting beta agonists?

A
  • yes
17
Q

how do allergens relate to asthma?

A
  • induce transcription factors to induce formation of inflammatory cytokines which recruit immune cells to lungs
  • immune cells produce cytotoxic compounds that will remodel air ways and cause bronchoconstriction
18
Q

what is the mechanism of action for glucocorticoids with asthma?

A
  • act at a level of of transcription factor , terminating the ability to act at the level of DNA and causing no cytokines to be formed
  • bind to receptor, the complex binds to response elements to cause down regulation of genes responsible for production of inflammatory cytokines, increased production of proteins that inhibit phospholipase A2
19
Q

what are the effects of daily administration of glucocorticoids?

A
  • suppresion of airway inflammation, reduces airway hyper responsiveness sand airway obstruction to prevent asthma attacks
20
Q

what are the routes of administration for glucocorticoids?

A
  • IV or oral for severe asthma

- inhalers for moderate to severe asthma

21
Q

what are some adverse effects of glucocorticoids?

A
  • low does; throat irritation and oral candidiasis

- high dose; adrenal insufficiency and osteoporosis

22
Q

what is the mechanism of action for leukotrienes receptor antagonists?

A
  • competitively bind to leukotriene receptors in bronchioles to induce bronchodilatory and immunodulatory effects
  • weaker effects compared to beta 2 adrenergic agonists
  • 2nd line therapy compared to glucocorticoids
  • cam be used in combination with glucocorticoids
23
Q

what are the routes of administration for leukotriene receptor antagonists?

A
  • oral (taken twice , available in chewable for paediatrics, taken at night
24
Q

what are some adverse effects of leukotrienes receptor antagonists ?

A
  • nausea , headache
25
Q

when are mast cell stabalizers used?

A
  • when someone is prone to asthma attacks when they are exposed predictably to a known allergen
  • prevent mast cells from releasing calcium in response to IgE receptor stimulation
26
Q

what is the mechanism of action of lipoxygenase inhibitors?

A
  • inhibit formation of all leukotrienes

- used for prevention of asthma attacks

27
Q

what type of patients are lipoxygenase inhibitors contraindicated with?

A
  • those with liver disease
28
Q

what is the mechanism of action of methylxanthines?

A
  • inhibit phosphodiesterase which degrades CAMP

- slow release; for the control of nocturnal asthma

29
Q

what are some adverse effects of methylxanthines?

A

-GI distress, irritability, insomnia, headache, nausea and vomiting

30
Q

what is the mechanism of action of IgE antibodies?

A
  • for allergic forms of asthma; reduces the production of IgE, down regulates IgE receptors, mast cell stabalizing effects
31
Q

when are IgE antibodies used and what type of patients?

A
  • moderate to severe allergic asthma

- who have failed step 1 to 4 of therapy (do not respond to glucocorticoids)

32
Q

what are some adverse effects of IgE antibodies?

A
  • pain, dizziness, fatigue, skin rash, anaphylaxis