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Pharmacology > Respiratory Disorders > Flashcards

Respiratory Disorders Flashcards

1
Q

asthma characteristics

A
  • inflammation of airways
  • bronchial hyper-reactivity
  • reversible airways obstruction
  • airways sensitive to stimulants
  • bronchospasm, propagate chronic inflammation response
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2
Q

asthma pathophysiology (general)

A
  • involves differentiation and activation of eosinophils, IgE production and release
  • IgE receptor expression on mast cells and eosinophils
    Immunoglobulin E, inflammatory mediators
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3
Q

asthma pathophysiology (immediate phase)

cause?
what cells release mediators?
what are some mediators involved? (2 things)

A

Bronchospasm

  • initial response to allergen provocation
  • mainly caused by spasm of bronchial smooth muscle
  • allergen interaction with mast cell causes release of inflammatory mediators (histamine, leukotriene B4, prostaglandin D2, interleukins, tumor necrosis factor alpha)
  • release of chemotaxins and chemokines attracts leukocytes (eosinophils) that propagate late phase
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4
Q

asthma pathophysiology (late phase)

what time?
which cells lead to the pathway?
what mediators are released

A

Inflammation

  • primarily nocturnal
  • a progressive inflammatory reaction
  • Th2 lymphocytes (T helper lymphocytes) express cytokines (eosinophils) and secretes inflammatory factors and cells
  • inflammatory cells (activated eosinophils) release cysteinyl leukotrienes, interleukins, other mediators that cause damage to and loss of epithelium
  • inflammatory cells also release growth factors that cause hypertrophy and hyperplasia of airway smooth muscle cells
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5
Q

Bronchodilators (general)

purpose?
4 types

A
  • reverse bronchospasm of immediate phase
    1. B-adrenoceptor agonists
    2. theophylline/aminophylline (caffeine like)
    3. cysteinyl leukotriene receptor antagonists
    4. muscarinic receptor antagonists (used for COPD)
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6
Q

Bronchodilators - B-adrenoceptor agonists

MOA (3 things)

A
  • dilate bronchi via direct action of smooth muscle cell B2-adrenoceptors
  • B2 adrenoceptors are G-protein coupled receptors that activate adenylate cyclase and increase cAMP levels (2nd messenger)
    - increased cAMP generation leads to activation
    of protein kinase A (PKA), reducing intracellular
    calcium levels leading to bronchodilation
  • also inhibit mediator release from mast cells and TNFa release from monocytes
  • increase mucus clearance (obstructs airway) by acting on cilia
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7
Q

Bronchodilators - B-adrenoceptor agonists

dosage form

A
  • usually given by inhalation or aerosol, powder, nebulized solution
  • in some cases, orally or via injection
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8
Q

Bronchodilators - B-adrenoceptor agonists

short acting

2 examples?
duration of action?

A
  • salbutamol (ventolin)
  • terbutaline
  • 3-5 hours
  • as needed basis to control symptoms, reach max effect within 30 min
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9
Q

Bronchodilators - B-adrenoceptor agonists

long acting

2 examples?
duration of action?

A
  • salmeterol
  • formoterol
  • 8-12 hours
  • usually taken as adjunctive therapy in pts with asthma inadequately controlled by glucocorticoids
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10
Q

salbutamol

terbutaline

A

Short acting B-adrenoceptor agonists

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11
Q

salmeterol

formoterol

A

Long acting B-adrenoceptor agonists

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12
Q

Bronchodilators - B-adrenoceptor agonists

side effects (3)

A
  • tachycardia
  • dysrhythmias
  • tremor

peripheral vasodilation, hypokalemia, hyperglycemia

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13
Q

Bronchodilators - Theophylline/aminophylline

dosage form
MOA (inhibits 2 things + effect)?

A
  • orally as a sustained-released preparation

MOA

  • methylxanthine based agent
  • inhibits phosphodiesterase (PDE), prevents breakdown of cAMP (increase cAMP levels)
  • inhibits adenosine receptors (competitive antagonist)
  • inhibits release of intracell. Ca2+ and thereby reduces smooth muscle contraction

Extra pharmacokinetics

  • narrow therapeutic window
  • metabolized by CYP450 enzymes
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14
Q

Bronchodilators - Theophylline/aminophylline

side effects (2)

A 
cardio (*dysrhythmia)
CNS toxicities (headaches and *seizures)
GI upset (nausea, vomiting)
stimulatory effects  (insomnia, restlessness)
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15
Q

Bronchodilators - cysteinyl leukotriene receptor antagonists

2 examples

MOA (which receptor in particular)?
efficacy compared to B2?

A

Montelukast
Zafirlukast
- derivative of arachidonic acid, Gq protein
- taken by mouth and usually in combo with inhaled corticosteroid

MOA

  • antagonize CysLT1 receptor only
  • reverses effects of bronchoconstriction, hyperresponsive airways, mucosal edema, mucous hypersecretion
  • less effective than B2 agonists at relaxing airways (additive together)
  • may reduce active rxns in aspirin sensitive patients
    • pt hypersensitive to aspirin secrete more
      leukotrienes and airways are more responsive
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16
Q

Montelukast
Zafirlukast

Side effects (generalizations?)

A

Bronchodilators - cysteinyl leukotriene receptor antagonists

  • mostly well tolerated
  • headache, GI disturbances
  • Zafirlukast inhibits CYP3A4 (may increase warfarin effects)
17
Q

Anti-Inflammatory Agents - Glucocorticoids

Function?
Name 5 inhaled ones
Name 1 oral one

A
  • prevent the progression of chronic asthma and are effective in acute severe asthma
  • often used with B2-adrenoceptor agonists

Inhaled: (-asone, -ide)

  • beclometasone
  • budenoside
  • flucticasone
  • mometasone
  • ciclesonide

Oral:
- prednisolone reserved for pt with severest disease

18
Q

Anti-Inflammatory Agents - Glucocorticoids

MOA?

  • general (1)
  • 2 mechanisms to control gene expression (where do ligands bind to)
A
  • bind intracellular receptors that then dimerize, allowing for nuclear translocation and modification of gene transcription (transcription factors)
  • receptor can go into nucleus to modify transc

A. Basic transactivation
- ligand binds to GR dimer (glucocorticoid receptor) and upregulates transcription

B: Basic transrepression
- ligand binds to GR dimer, which binds a nGRE (negative glucocorticoid receptor response element) and turns off transcription

19
Q

Anti-Inflammatory Agents - Glucocorticoids

MOA in asthma? (3)

What mediators do they reduce? (3-4)

A
  • inhibit proliferation of Th cells by reducing the transcription of the IL-2 gene
  • this leads to reduced formation of Th2 cytokines, reducing recruitment and activation of eosinophils
  • inhibit allergen induced influx of eosinophils into lung (by decreasing IL-5, IL-13)
    - IL-5 proliferates eosinophils to airways
    - IL-3 activates mast cells
  • reduce production of IgE and expression of IgE receptors
20
Q

Anti-Inflammatory Agents - Glucocorticoids

Adverse effects

Inhaled? (1)
Oral?

Is risk of systemic side effects high?

A

Inhaled steroids

  • *thrush (oropharyngeal candidiasis): fungal overgrowth in mouth and throat due to T lymphocytes unable to fight off fungal infections
  • dysphonia (croaky)
  • adrenal suppression (children) mainly by beclomethasone and budesonide

Oral steroids
- increased risk of infection, hyperglycemia (gluconeogenesis, osteoporosis

Risk of systemic side effects low due to low sys absorption, bioavailability

21
Q

Anti-IgE Treatment - Omalizumab

MOA?
Why is it used?
Dosage form?
Other uses?

A
  • humanized monoclonal anti-IgE antibody binds to IgE and prevents interaction with IgE receptors
  • severe allergic asthma that does not respond to high doses of corticosteroids
  • adverse effects: anaphylaxis
  • subq once every 2-4 weeks
  • use in urticaria, allergic rhinitis, atopic dermatitis
  • works only if IgE is not already bound to receptor
22
Q

Omalizumab

A

Anti-IgE Treatment - severe allergic asthma that does not respond to high doses of corticosteroids

23
Q

IL-5 Inhibition

Mepolizumab
Reslizumab

A
  • humanized monoclonal antibodies that bind and inhibit IL-5 which differentiates and recruits eosinophils
  • eosinophilic asthma

AE: headache, injection site rxn, oropharyngeal pain

24
Q

COPD characteristics (3)

A
  • main cause is smoking
  • morning cough
  • chronic cough with intermittent exacerbations
  • upper resp infection, discharge can contain pus
25
Q

IL-5 Inhibition - stop activation and prolif of eosinophils (name 2)

A

Mepolizumab

Reslizumab

26
Q

COPD pathophysiology (3)

A
  • fibrosis of small airways
  • obstruction/destruction of alveoli and elastin fibers in lung parenchyma (emphysema) - shortness of breath
  • chronic inflammation (bronchities) in small airways and lung parenchyma, not as well defined as in asthma
27
Q

COPD treatment

non-pharm treatment (1)
what is not that effective?

A
  • not a lot of drugs reverse it
    1. stop smoking (fibrosis of small airways)
  1. glucocorticoids - transrepressor
    - generally ineffective, but can try if asthma is also ther
    - they interact with histone deacetylases (hDAC) which makes DNA no longer condensed and transcription factors cannot bind DNA
    - smoking inhibits hDAC, so glucocorticoids aren’t effective
  2. Bronchodilators
    - doesn’t deal with underlying inflamm, useful palliation
    - short acting: salbutamol, ipratropium
    - long acting: salmeterol, formoterol
28
Q

COPD treatment - Inhaled Anticholinergics

short-acting (1)
long-acting (1)
AE

A
  • also used for asthma

Short-acting: ipratropium (derived from atropine)
Long-acing: tiotropium

AE: minimal, local rxns like dry mouth, nasal irritation, nose bleeds

29
Q

COPD treatment - Inhaled Anticholinergics

MOA

  • receptors (1)
  • action (2)
  • selectivity of tiotropium vs ipra
A
  • parasymp stimulation of muscarinic receptors on bronchioles causes bronchoconstriction, induces bronchial secretions
    need to block receptors!
  • mediated by M3 receptors (little M1)
  • M3 also involved in mucus secretion, need to decrease it
  • tiotropium has greater selectivity for M3, ipratropium is non-specified for M1-M3
30
Q

COPD treatment - Roflumilast

MOA

A
  • long-acting inhibitors of PDE4, increases cAMP
  • reduce inflamm
  • adjunct to bronchodilators for severe COPD
  • orally

AE: GI symptoms, weight loss, naus, headache, insomnia

Pharmacology (12 decks)

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