Goodman & Gilman's The Pharmacological Basis of Therapeutics¶
Brunton, L. L., Hilal-Dandan, Randa, & Knollmann, B. C. (2018). Goodman & Gilman's The Pharmacological Basis of Therapeutics. McGraw-Hill.
Cited by¶
11 citations across 11 artifacts.
Each citation links to the sentence it supports in the citing article.
Primes¶
- Bioaccumulation
- … on maintaining tissue concentration within a therapeutic or safe window through dose adjustment and periodic biomonitoring, an approach codified across the cardiovascular and antiarrhythmic chapters of Goodman & Gilman's The Pharmacological Basis of Therapeutics (Brunton, Hilal-Dandan, & Knollmann, 2018, 13th ed.).
This sourceCanonical pharmacology reference covering chronic management and therapeutic drug monitoring of long-half-life cardiac drugs (amiodarone, digoxin)
- … on maintaining tissue concentration within a therapeutic or safe window through dose adjustment and periodic biomonitoring, an approach codified across the cardiovascular and antiarrhythmic chapters of Goodman & Gilman's The Pharmacological Basis of Therapeutics (Brunton, Hilal-Dandan, & Knollmann, 2018, 13th ed.).
- Dose-Response Relationship
- Every dose-response articulation, as systematized in the canonical pharmacological reference of Brunton, Hilal-Dandan, and Knollmann (2018), specifies (1) the dose metric—concentration, cumulative exposure, rate, scheduling pattern—and its measurement scale (often logarithmic because response varies over orders of magnitude); (2) the response metric and its measurement (quantal responses—yes/no at population level—versus graded responses within individuals; therapeutic effect versus adverse effect); (3) the functional form—linear, sigmoidal (Hill equation, log-logistic), threshold, U-shaped (hormetic), biphasic—that best describes the observed relationship and its theoretical grounding; and (4) the key parameters of the curve: ED50 or EC50 (dose producing 50% of maximal response), Emax (maximal response), slope factor (Hill coefficient), and threshold or no-observed-effect level.
This sourceCanonical pharmacology reference; supports D47-017 (a dose-response articulation specifies the dose metric and scale, the response metric, the functional form, and the curve's key parameters: ED50/EC50, Emax, Hill slope, threshold). NOTE: the pre-existing annotation about phenytoin/CYP2C9 saturable metabolism is mis-pasted from another prime and does not describe the D47-017 claim.
- Every dose-response articulation, as systematized in the canonical pharmacological reference of Brunton, Hilal-Dandan, and Knollmann (2018), specifies (1) the dose metric—concentration, cumulative exposure, rate, scheduling pattern—and its measurement scale (often logarithmic because response varies over orders of magnitude); (2) the response metric and its measurement (quantal responses—yes/no at population level—versus graded responses within individuals; therapeutic effect versus adverse effect); (3) the functional form—linear, sigmoidal (Hill equation, log-logistic), threshold, U-shaped (hormetic), biphasic—that best describes the observed relationship and its theoretical grounding; and (4) the key parameters of the curve: ED50 or EC50 (dose producing 50% of maximal response), Emax (maximal response), slope factor (Hill coefficient), and threshold or no-observed-effect level.
- Elasticity
- In medicine, dose–response elasticity frames the therapeutic window: steep elasticity near a threshold means a narrow window.
This sourceFrames the dose–response curve and therapeutic window — a steep dose–response slope near threshold means a narrow window.
- In medicine, dose–response elasticity frames the therapeutic window: steep elasticity near a threshold means a narrow window.
- Gain Control
- In endocrine and homeostatic systems receptor downregulation and sensitivity changes retune responses to ambient hormone levels, with pharmacological tolerance as the same pattern.
This sourceThe standard pharmacology text; describes receptor downregulation and desensitization as adaptive responses to sustained agonist exposure and the basis of pharmacodynamic tolerance — cellular gain control on hormone/drug signaling, with tolerance and drug-holiday resets as the same pattern.
- In endocrine and homeostatic systems receptor downregulation and sensitivity changes retune responses to ambient hormone levels, with pharmacological tolerance as the same pattern.
- Potentiation
- It stands as the direct opposite of tolerance, with which it shares structural logic but inverted direction: both are time-dependent response changes under repeated exposure, but potentiation amplifies while tolerance dampens.
This sourceCanonical pharmacology reference: documents phenytoin as the archetypal case of saturable hepatic CYP2C9 metabolism producing non-linear pharmacokinetics, dose-dependent half-life, and the transition from first-order to zero-order elimination near therapeutic concentrations.
- It stands as the direct opposite of tolerance, with which it shares structural logic but inverted direction: both are time-dependent response changes under repeated exposure, but potentiation amplifies while tolerance dampens.
- Receptor Saturation
- As Brunton, Hilal-Dandan, and Knollmann (Goodman & Gilman, 2018) describe in their treatment of phenytoin pharmacokinetics,
This sourceCanonical pharmacology reference: documents phenytoin as the archetypal case of saturable hepatic CYP2C9 metabolism producing non-linear pharmacokinetics, dose-dependent half-life, and the transition from first-order to zero-order elimination near therapeutic concentrations.
- As Brunton, Hilal-Dandan, and Knollmann (Goodman & Gilman, 2018) describe in their treatment of phenytoin pharmacokinetics,
- Synergy and Antagonism
- The isobologram framework precisely quantifies both directions and permits dose-optimization without trial-and-error.
This sourceCanonical pharmacology reference: documents phenytoin as the archetypal case of saturable hepatic CYP2C9 metabolism producing non-linear pharmacokinetics, dose-dependent half-life, and the transition from first-order to zero-order elimination near therapeutic concentrations.
- The isobologram framework precisely quantifies both directions and permits dose-optimization without trial-and-error.
- Therapeutic Window
- The width of this window is a defining property of the intervention and a first-class design target.
This sourceCanonical pharmacology reference: documents phenytoin as the archetypal case of saturable hepatic CYP2C9 metabolism producing non-linear pharmacokinetics, dose-dependent half-life, and the transition from first-order to zero-order elimination near therapeutic concentrations.
- The width of this window is a defining property of the intervention and a first-class design target.
- Tolerance
- A time-indexed sequence of identical exposures produces responses whose magnitude declines progressively across the sequence, formalized—as Brunton, Hilal-Dandan, and Knollmann (2018) develop in their treatment of receptor pharmacology—as a rightward shift of the dose-response curve, where the dose required to achieve a target effect (e.g., 50% maximum response) increases over time.
This sourceCanonical reference for clinical pharmacology: develops tolerance as rightward shift of the dose-response curve driven by receptor downregulation, enzyme induction, and behavioral compensation; chapters on opioid analgesics treat rotation, dose holidays, and adjuvant strategies as mechanism-specific responses to tolerance.
- A time-indexed sequence of identical exposures produces responses whose magnitude declines progressively across the sequence, formalized—as Brunton, Hilal-Dandan, and Knollmann (2018) develop in their treatment of receptor pharmacology—as a rightward shift of the dose-response curve, where the dose required to achieve a target effect (e.g., 50% maximum response) increases over time.
Domain-specific¶
- Contraindication
- The prohibition rule is the restriction itself, which clinical medicine codes in two gradations: absolute contraindications (the treatment must not be given under the conditioning context, with no room for compensating adjustments) and relative contraindications (the risk-benefit ratio worsens enough to require serious alternative consideration or protective co-intervention, but clinical judgment may still permit the treatment with appropriate safeguards)
This sourceStandard reference for the risk-benefit framing that defines a contraindication; the absolute-versus-relative gradation is clinical convention rather than a distinction this text or the FDA labelling rule (21 CFR 201.57(c)(5)) formally draws. Covers the beta-blocker/asthma and ACE-inhibitor/pregnancy contraindications and their mechanisms; the live-vaccine limb rests on the CDC/ACIP General Best Practice Guidelines for Immunization, which bar live vaccines in most forms of altered immunocompetence because of uninhibited growth of the attenuated organism.
- The prohibition rule is the restriction itself, which clinical medicine codes in two gradations: absolute contraindications (the treatment must not be given under the conditioning context, with no room for compensating adjustments) and relative contraindications (the risk-benefit ratio worsens enough to require serious alternative consideration or protective co-intervention, but clinical judgment may still permit the treatment with appropriate safeguards)
Mechanisms¶
- Dosage Window Protocol
- This is the therapeutic window
This sourceDefines the pharmacological dose-response, therapeutic-index, and safety-margin concepts that bound beneficial and harmful drug exposure.
- This is the therapeutic window
Verification¶
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Links previously used in the corpus¶
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- https://accesspharmacy.mhmedical.com/book.aspx?bookid=2189 ×1
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