Pharm- Pharmacodynamics Flashcards

1
Q

Pharmacodynamics

A
  • Action of drug on body
  • Influence of drug on magnitude of response (intended/ toxic)
  • Most effects ( beneficial/ harmful) result of interactions between drug and receptor on or inside cell

*not all drugs works via receptors (antacids)

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2
Q

Signal Transduction

A

Ligand- drug or natural molecule that acts as signal

Receptor- acts as signal detector

-in Pharm- any biological molecule to which drug binds and produces measurable response

Receptor states: Active/ inactive

* different ligands cause different actions depending on receptor

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3
Q

Ligand-gated ion channels

A

-Response very rapid

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4
Q

G protein- coupled receptors

A
  • Ligand binding activates G proteins causes dissociation and subsequent interaction with other intracellular molecules
  • Molecules then activate second messengers causing cellular response
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5
Q

Enzyme- linked receptors

A

-Ligand binding activates/ inhibits cytosolic enzyme activity

Duration: minutes - hours

-Effect metabolism, growth, and differentiation

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6
Q

Intracellular receptors

A
  • Ligand must be lipophilic (get thru membrane)
  • Primary target= transcription factors
  • Hours to months to outcome

Ex: hormones. corticosteroids

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7
Q

3 Adaptations of receptors/ Signal Transduction

A
  1. Signal amplification
    - small input -> large response
    - Important to receptos responding to hormones, neurotransmitters, peptides
  2. Desensitization/ down-regulation of receptors
    - receptor-endocytosis-recycled
    - receptor degraded- reduces receptor amount
    - dysregulation of receptors- bring disease (DMII)
  3. Up regulation
    - Occurs when receptor blocking drugs given over time in high dose
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8
Q

Agonists

A

Agonist binds to receptor-influences normal physiologic response

Two types:

  • Full: activate receptor- reults in normal response of endogenous ligand
  • Partial: partially activates receptor- result in response less than normal ( withdrawal)
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9
Q

Antagonists

A

Bind to receptors-block binding of endogenous ligand ( dont activate receptors)

Types:

  • Competitive/ reversible
  • Irreversible
  • Functional/ chemical
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10
Q

Competative Antagonism

A
  • Both antagonist and agonist can bind to receptor- they compete
  • Drug affinity determines binding
  • Competitive antagonist prevent agonist from binding- maintain receptor in inactive form unless competition too strong
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11
Q

Irreversible Antagonism

A
  • Drug binds covalently (high affinity) to active site on receptor- prevent anything else from activating receptor
  • Effects of irreversible antagonism only overcome by synthesis of new receptors
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12
Q

Functional/ Chemical Antagonism

A

Functional: physiologic response/interaction of different receptor sites result in opposing effects

-Ex: histamine at H1 receptor v epi at B2- adrenergic receptor in bronchial muscle

Chemical: chemical modifies agonist so its incapable of binding to activate receptor

Ex: protamine sulfate protein (+) binds to heparin (-)

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13
Q

Therapeutic index (window)

A
  • Relation of toxic dose to clinically effective dose
  • Want large TI
  • Measure of drugs safety
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14
Q

Tolerance

A
  • Loss of therapeutic effect over time
  • Often dose dependent ( overcome by higher dose)
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15
Q

Tachyphylaxis

(fast- blunted response)

A
  • Rapid tolerance ( decreased physiologic response)
  • Note dose dependent
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16
Q

ADRs

(adverse drug rxns)

A
  • Unintended/ harmful rxns to meds at therapeutic dose
  • Among leading cause of death in many countries
  • Most preventable
  • No med without risk
17
Q

Types of ADRs

A

Extension of therapeutic effect

  • drug has desirable effect
  • too much of good thing is not better
  • predictable

Ex: low BP after antihypertensive, fungal overgrowth after antibiotics

Non- Therapeutic

  • allergy- IgE mediated response
  • idiosyncratic ( extreme sensitivity, prolonged drug effect, resistance)

Iatrogenic (medical error)

  • caused by provider
  • patient education is key
18
Q

ADR: Prescriber responsibility

A
  • Use minimally effective dose
  • eval patient and fam hx
  • eval possible interactions
  • patient education
19
Q

Pharmacogenomics

A
  • How genetic makeup affects individual response to drug
  • CYP450 gene

Poor metabolizer

  • decreased expected serum conc. of metabolite
  • increased expected parent drug serum conc.

Extensive (normal)

-expected serum conc. of parent drug/ metabolite

Ultrarapid

  • increased expected serum conc. of metabolite
  • decreased expected parent drug conc.
20
Q

Drug Type

A

Prodrug- needs metabolism to work

Active drug- metabolized to inactive drug