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Individual differences |
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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
An adverse drug reaction (abbreviated ADR) is an expression that describes the unwanted, negative consequences associated with the use of given medications. An ADR is a particular type of adverse effect. The meaning of this expression differs from the meaning of "side effect", as this last expression might also imply that the effects can be beneficial. The study of ADRs is the concern of the field known as pharmacovigilance.
For psychologist two particular classes of reaction are relevent:
ADRs may be classified by e.g. cause and severity.
- Type A: Augmented pharmacologic effects
- Type B: Bizarre effects (or idiosyncratic)
- Type C: Chronic effects
- Type D: Delayed effects
- Type E: End-of-treatment effects
- Type F: Failure of therapy
- Hospitalization (initial or prolonged)
- Disability - significant, persistent, or permanent change, impairment, damage or disruption in the patient's body function/structure, physical activities or quality of life.
- Congenital Anomaly
- - or -
- Requires Intervention to Prevent Permanent Impairment or Damage
Overall Drug RiskEdit
- Red (High Risk)
- Orange (Elevated Risk)
- Yellow (Guarded Risk)
- Blue (General Risk)
- Green (Low Risk)
Adverse effects may be local, i.e. limited to a certain location, or systemic, where a medication has caused adverse effects throughout the systemic circulation.
As research better explains the biochemistry of drug use, less ADRs are Type B and more are Type A. Common mechanisms are:
- Abnormal pharmacokinetics due to
- genetic factors
- comorbid disease states
- Synergistic effects between either
- a drug and a disease
- two drugs
Comorbid disease statesEdit
Phase I reactionsEdit
Phase II reactionsEdit
Interactions with other drugsEdit
These interactions are usually transient and mild until a new steady state is achieved. These are mainly for drugs without much first-pass liver metabolism. The prinicple plasma proteins for drug binding are:
- α1-acid glycoprotein
Patients have abnormal metabolism by cytochrome P450 due to either inheriting abnormal alleles or due to drug interactions. Tables are available to check for drug interactions due to P450 interactions..
An example of synergism is two drugs that both prolong the QT interval.
- Note that an ADR should not be labeled as 'certain' unless the ADR abates with dechallenge and recurs with rechallenge are true.
A more complicated scale is the Naranjo algorithm.
Many countries have official bodies that monitor drug safety and reactions. On an international level, the WHO runs the Uppsala Monitoring Centre, and the European Union runs the European Medicines Agency (EMEA). In the United States, the Food and Drug Administration (FDA) is responsible for monitoring post-marketing studies.
- Adverse effect (medicine) parent concept
- Drug interaction
- Evidence-based medicine
- EudraVigilance (European Union)
- Medical prescription
- Paradoxical reaction
- Responsible drug use
- The Medical Letter on Drugs and Therapeutics
- Yellow Card Scheme (UK)
- ↑ 1.0 1.1 Nebeker JR, Barach P, Samore MH (2004). Clarifying adverse drug events: a clinician's guide to terminology, documentation, and reporting. Ann. Intern. Med. 140 (10): 795-801.
- ↑ Rawlins MD, Thompson JW. Pathogenesis of adverse drug reactions. In: Davies DM, ed. Textbook of adverse drug reactions. Oxford: Oxford University Press, 1977:10.
- ↑ Aronson JK. Drug therapy. In: Haslett C, Chilvers ER, Boon NA, Colledge NR, Hunter JAA, eds. Davidson's principles and practice of medicine 19th ed. Edinburgh: Elsevier Science, 2002:147-63. ISBN 0-44307-035-0.
- ↑ MedWatch - What Is A Serious Adverse Event?. URL accessed on 2007-09-18.
- ↑ includeonly>"'Traffic-light' medicine risk website to launch", The Guardian, 2007-10-02.
- ↑ Rang, H. P. (2003). Pharmacology, Edinburgh: Churchill Livingstone. Page 146
- ↑ Clinical Drug Use. URL accessed on 2007-09-18.
- ↑ Phillips KA, Veenstra DL, Oren E, Lee JK, Sadee W (2001). Potential role of pharmacogenomics in reducing adverse drug reactions: a systematic review. JAMA 286 (18): 2270–9.
- ↑ Goldstein DB (2003). Pharmacogenetics in the laboratory and the clinic. N. Engl. J. Med. 348 (6): 553–6.
- ↑ Drug-Interactions.com. URL accessed on 2007-09-18.
- ↑ 11.0 11.1 11.2 Weinshilboum R (2003). Inheritance and drug response. N. Engl. J. Med. 348 (6): 529–37.
- ↑ 12.0 12.1 Evans WE, McLeod HL (2003). Pharmacogenomics--drug disposition, drug targets, and side effects. N. Engl. J. Med. 348 (6): 538–49.
- ↑ DeVane CL (2002). Clinical significance of drug binding, protein binding, and binding displacement drug interactions. Psychopharmacology bulletin. 36 (3): 5–21.
- ↑ Benet LZ, Hoener BA (2002). Changes in plasma protein binding have little clinical relevance. Clin. Pharmacol. Ther. 71 (3): 115–21.OVID full text summary table at OVID
- ↑ 15.0 15.1 Sands CD, Chan ES, Welty TE (2002). Revisiting the significance of warfarin protein-binding displacement interactions. The Annals of pharmacotherapy 36 (10): 1642–4.
- ↑ Drug-Interactions.com. URL accessed on 2007-09-18.
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