You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is In alcoholics which vitamin should be replenished with carbohydrates? and explain in detail?
Ans. c (Thiamin) (Ref: Harrison's Internal medicine 18th/ch. 275 and fig. 275-7)WERNICKE'S SYNDROME# Due to Thiamine deficiency, seen in alcoholic patients.# See for.- Global confusion- Ophthmaparesis- Ataxia# Site of lesion:- Demylination and atrophy of mamillary bodies- DM nuclei of thalamus# PATHOGENESIS: Thiamine is a cofactor of several enzymes, including transketolase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase. Thiamine deficiency produces a diffuse decrease in cerebral glucose utilization and results in mitochondrial damage. Glutamate accumulates owing to impairment of alpha-ketoglutarate dehydrogenase activity and, in combination with the energy deficiency, may result in excitotoxic cell damage.# CEMRI :reveals abnormal enhancement of the mammillary bodies, typical of acute Wernicke's encephalopathy.# TREATMENT: It is a medical emergency. It requires immediate administration of thiamine, in a dose of 100 mg either IV or IM. The dose should be given daily until the patient resumes a normal diet and should be begun prior to treatment with IV glucose solutions. Glucose infusions may precipitate Wernicke's disease in a previously unaffected patient or cause a rapid worsening of an early form of the disease. For this reason, thiamine should be administered to all alcoholic patients requiring parenteral glucose.Wernicke-Korsakoff syndrome--confusion, ophthalmoplegia, ataxia (classic triad) + confabulation, personality change, memory loss (permanent). May progress to irreversible memory loss, confabulation, personality change (Korsakoff psychosis).Amygdala (bilateral)Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior).Associated with HSV-1.Frontal lobeDisinhibition and deficits in concentration, orientation, and judgment; may have reemergence of primitive reflexesRight parietal-temporal cortexSpatial neglect syndrome (agnosia of the contralateral side of the world)Left parietal-temporal cortexAgraphia, acalculia, finger agnosia, and left-right disorientation(Gerstmann syndrome).Reticular activating system (midbrain)Reduced levels of arousal and wakefulness (e.g., coma)Mammillary bodies (bilateral)Wernicke-Korsakoff syndrome: confusion, ophthalmoplegia, ataxia; memory loss(anterograde and retrograde amnesia), confabulation, personality changes.Associated with thiamine (Bl) deficiency and excessive EtOH use; can be precipitated by giving glucose without Bl.Basal gangliaMay result in tremor at rest, chorea, or athetosisCerebellar hemisphereIntention tremor, limb ataxia, and loss of balance; damage to the cerebellum results in ipsilateral deficits; fall toward side of lesionCerebellar vermisTruncal ataxia, dysarthriaSubthalamic nucleusContralateral hemiballismusHippocampus (bilateral)Paramedian pontine reticularAnterograde amnesia--inability to make new memoriesformationEyes look away from side of lesionFrontal eye fieldsEyes look toward lesion