| Term 
 
        | Adverse Effects of Alcohol |  | Definition 
 
        | CNS: Peripheral Neuropathy Wernicke-Ataxia, Ophthalmoplegia Korsakoffs-Learning, Memory Problems CV: Vasodialation-Hypothermia Vasoconstriction-Heart/Brain HPTN, Dialated Cardiomyopathy GI: Gastrin->Acid->Peptic Ulcer Disease Liver: Increased NADH->Fatty Liver/Cirrhosis Acetomenophen Toxicity Renal: ADH decrease Sex: Premenopausal-Decrease Estrogen Postmenopausal-Increased Estrogen(cancer) Men-Decrease Test, Increased Estrogen Teratogenic: Decreased IQ, Microcephaly, Facial Abnormalities |  | 
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        | Term 
 
        | What are the enzymes that metabolize ethanol, which is inducable, which is blocked by disulfiram, and which is blocked by Fomepizol? |  | Definition 
 
        | Alcohol Dehydrogenase: Blocked by Fomepizole Aldehyde Dehydrogenase: Blocked by disulfiram CYP2E1: Inducible in heavy drinkers |  | 
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        | Term 
 
        | What are the treatments for alcohol withdrawal |  | Definition 
 
        | Benzodiazepines: lorazepam or oxazepam should be used if liver is damaged Haloperidol: Prevent hallucinations Beta-Block/Clonidine: Prevent Adrenergic |  | 
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        | Term 
 
        | How does alcohol use cause liver steatosis |  | Definition 
 
        | NADH decreases Beta-Oxitdation Hypoglycemia increases Keto-fatty Acids |  | 
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        | Term 
 
        | What drugs inhibit Aldehyde Dehydrogenase |  | Definition 
 
        | Cyclophosphamide Oral Hypoglycemics Metronidazole Disulfiram |  | 
        |  | 
        
        | Term 
 
        | What population shows more expression of the inactive form of aldehyde dehydrogenase |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What are the causes of metabolic acidosis in alcohol use? |  | Definition 
 
        | A)Lactic Acid production to maintain NAD/NADH ratio B)NADH reduces Gluconeogenesis causing hypoglycemia and a rise in Keto-Fatty acids   |  | 
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        | Term 
 
        | What are the mechanisms of Alcohol |  | Definition 
 
        | Potentiate GABAa Block NMDA->increase Dopamine(Accumbens) 5HT-3 increases Inhibition     |  | 
        |  | 
        
        | Term 
 
        | How is Pharmacodynamic and Pharmacokinetic tolerance to alcohol generated |  | Definition 
 
        | Pharmacokinetic: CYP2E1 Induction Pharmacodynamic: GABAa, NMDA-Glutamate Ca receptor increase |  | 
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        | Term 
 
        | What is the mechanism of Acetomenophen toxicity in alcoholics |  | Definition 
 
        | CYP2E1 induction generates more NAPQI Glutathione Depletion allows more damage |  | 
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        | Term 
 
        | What are the signs and treatment of Methanol toxicity |  | Definition 
 
        | Sign: Visual Disturbances Treatment: Fomepizol or Ethanol |  | 
        |  | 
        
        | Term 
 
        | What is the pathophysiology of ethylene glycol poisoning and how is it treated |  | Definition 
 
        | Path: Metabolic Acidosis Renal Insufficiency from Oxalate production Treatment: Fomepizol or Ethanol |  | 
        |  | 
        
        | Term 
 
        | How is gout precipitated by alcohol |  | Definition 
 
        | Lactic acid shows compete with urate for excretion transporter in the kidney |  | 
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        | Term 
 
        | What are the drugs used treat alcoholism and what is their mechanism of action |  | Definition 
 
        | Disulfiram: Block Aldehyde Dehydrogenase Naltrexone: Block alcohol reinforcement Acamprosate: Block NMDA Rimonobant: CB1 Agonist |  | 
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