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The protracted withdrawal syndrome from benzodiazepines, opioids, alcohol and other addictive substances can produce symptoms identical to generalized anxiety disorder as well as panic disorder. Due to the sometimes prolonged nature and severity of benzodiazepine, opioid and alcohol withdrawal, abrupt cessation is not advised.
Venlafaxine has also been implicated to create withdrawal symptoms regardless of dosage. [15] Venlafaxine has been implicated in causing the most severe withdrawal symptoms after cessation of use, possibly due to its short half-life. [16] To simplify identifying the principal signs and symptoms, the mnemonic FINISH may be used: Flu-like ...
The scarring of the small blood vessels, called capillary sclerosis, is the initial lesion of analgesic nephropathy. [7] Found in the renal pelvis, ureter, and capillaries supplying the nephrons, capillary sclerosis is thought to lead to renal papillary necrosis and, in turn, chronic interstitial nephritis.
Drug withdrawal, drug withdrawal syndrome, or substance withdrawal syndrome [1] is the group of symptoms that occur upon the abrupt discontinuation or decrease in the intake of pharmaceutical or recreational drugs. In order for the symptoms of withdrawal to occur, one must have first developed a form of drug dependence.
Psychoactive substance-induced psychotic disorders outlined within the ICD-10 codes F10.5—F19.5: F10.5 alcohol: [8] [9] [10] Alcohol is a common cause of psychotic disorders or episodes, which may occur through acute intoxication, chronic alcoholism, withdrawal, exacerbation of existing disorders, or acute idiosyncratic reactions. [8]
The rebound effect, or pharmaceutical rebound phenomenon, is the emergence or re-emergence of symptoms that were either absent or controlled while taking a medication, but appear when that same medication is discontinued, or reduced in dosage.
Type A: augmented pharmacological effects, which are dose-dependent and predictable [5]; Type A reactions, which constitute approximately 80% of adverse drug reactions, are usually a consequence of the drug's primary pharmacological effect (e.g., bleeding when using the anticoagulant warfarin) or a low therapeutic index of the drug (e.g., nausea from digoxin), and they are therefore predictable.
Individuals who have had more withdrawal episodes are at an increased risk of very severe withdrawal symptoms, up to and including seizures and death. Long-term activation of the GABA receptor by sedative–hypnotic drugs causes chronic GABA receptor downregulation as well as glutamate overactivity, which can lead to drug and neurotransmitter ...