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Pharmacology > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

1
Q

What is the effect of histamine in allergy?

A

Hist–>H1R–>Gq–>IP3–>Ca

  • adds to PNS pathway
  • bronchiole constriction
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2
Q

Draw how an allergen causes inflammation in the respiratory tract.

A

Respiratory Pharm

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3
Q

IgE

A
  • primary ig involved in immunoresponses

- triggers mast cell degranulation

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4
Q

Histamine

A

stimulation of H1 R
lungs-vasoconstriction
vascular smooth muscle-relaxation

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5
Q

Leukotrienes

A
  • stimulate CysLT1 R

- vasoconstriction, bronchospasm, increased vascular permeability

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6
Q

What are 4 treatment strategies for inflammation in the respiratory tract, asthma and allergy?

A
  1. bronchodilators
  2. antiinflammatory agents/immune modulators
  3. Inhaled formulations
  4. systemic
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7
Q

What are 3 bronchodilators?

A
  1. beta2 AR agonists (salbutamol, salmeterol)
  2. anticholinergics (tiotropium)
  3. methylxanthines (theophylline)
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8
Q

What are 3 antiinflammatory agents/immune modulators?

A
  1. corticosteroids (flucticasone, prednisone)
  2. antileukotrienes (montelukast, zileuton)
  3. antihistamines (diphenhydramine, loratadine)
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9
Q

Explain inhaled formulations in their treatment of asthma and allergy?

A
  • applied topically to the lungs
  • drugs act locally
  • most have limited systemic absorption
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10
Q

Explain systemic in their treatment of asthma and allergy?

A
  • modulation of pro inflammatory mediators

- oral/IV steroids in more severe cases (asthma attacks)

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11
Q

What is the therapeutic approach for asthma?

A
  • patients started on SABA- used at onset of symptoms
  • as disease progresses or if symptoms not well controlled treatment is stepped up
  • SABA used as rescue medication
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12
Q

B2 adrenergic R agonists-SABA

A
  • short acting beta agonists
  • salbutamol
  • structurally similar to NE
  • onset= 5 min, duration=3-8 hr
  • administered as needed
  • overuse leads to red in clinical efficacy–> patients requiring >2 doses/ week have therapy stepped up
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13
Q

Desensitization & Downregulation of β2-AR

A
  1. Agonist binds to receptor, initiates response
  2. Activated receptor phosphorylated and bound to β-arrestin, prevents further response
  3. Receptor complex internalized (endocytosis)
  4. Dephosphorylation by phosphatase
  5. Recycling of receptor to cell surface • These steps cause desensitization
  6. Excessive stimulation can trigger receptors to be degraded
    • Resulting in down-regulation
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14
Q

What is the difference between GPCR desensitization vs downregulation

A

Desensitization
-Within minutes of exposure
-Reapplication of agonist generates full response
Downregulation
-Usually hours of exposure (varies)
-Reapplication of agonist generates partial or no response

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15
Q

Long Acting Beta Agonists (LABAs)

A
  • salmeterol
  • long C chain through to act as anchor in receptor, prolongs duration of action
  • onset-20 mins
  • duration-12 hrs
  • administered on a scheduled basis
  • cannot be used as rescue med-onset too slow
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16
Q

How does salmeterol prevent desensitization?

A
  • binds to B2 AR in a way that reduces beta arrestin binding
  • allows prolonged duration of action
17
Q

Methylxanthines-theophylline

A
  • structurally related to caffeine
  • promote bronchodilation (increased breakdown of cAMP)
  • administered orally 400-600mg/day
  • systemic side effects (CNS stimulation/heart palpitations)
18
Q

Anticholinergics-Tiotropium

A
  • block the actions of M3 cholinergic R in the lungs
  • inhaled
  • non selective
  • charged molecule reduces systemic absorption
  • often combined w/ beta2 AR for synergistic effect
19
Q

Corticosteroids

A
  • active intracell glucocorticoid R
  • modify gene Tc
  • primary therapeutic benefit are anti-inflammatory effects
20
Q

Systemic Corticosteroids (prednisone)

A
  • many useful indications

- high rate of side effects

21
Q

Inhaled corticosteroids (fluticasone)

A
  • localized effects in the lungs
  • reduce inflammation in the airways
  • administered daily to reduce and prevent inflammation
  • local immunosuppressive effects in the oral cavity (thrush infection)
22
Q

Antileukotrienes

A
  • long term use reduces the severity of the allergic response
  • oral admin provides ease of use and systemic response
  • leukotriene receptor antagonist: montelukast, competitive antagonist of CysLT1 R
23
Q

Zileutin

A

Antileukotriene

  • 5-lipoxygenase inhibitor
  • reduce production of LTA4
24
Q

Antihistamines

A

-inverse agonist of H1 receptors

25
Q

First Generation antihistamines

A
  • diphenhydramine
  • short duration of action 6-8 hr
  • has off target CNS and anticholinergic effects
26
Q

Second generation antihistamines

A
  • loratadine
  • active metabolite is desloratadine
  • 24 hr duration of action

Pharmacology (9 decks)

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