| xx | x | x |
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| Alcohol, phenytoin and aspirin follow _____-order kinetics | |
| _______ causes nausea, facial flushing, dizziness, and headache during alcohol metabolism. | |
| Alcohol is similar to water, thus distributes to all _______ spaces. | |
| Two major neuronal targets of ethanol are increased GABA activity and decreased _______ receptor activity. | |
| _____ receptor is the most extensively researched but may not be the most important ethanol site. | |
| Acute ethanol effect on smooth muscle is vaso_____, smooth muscle relaxation, hypothermia in cold environements. | |
| _____ dependence - need for continued drug exposure to avoid withdrawal symptoms. | |
| A reduced effect upon repeated exposure to a constant drug dose, or the need for an increased dose to maintain an effect | |
| The compulsive desire to use a drug despite adverse consequences; this craving can exist without drug tolerance or dependence | |
| There is a __% increased risk of alcoholism if there is a family history. | |
| Type I alcoholic involves the ______ pathway. Less severe, found in both males and females. | |
| Type 2 alcoholic inoves the _______ pathway. It is males only, early onset, and more heritable. | |
| Chronic tolerance of alcohol involves decreased _____ binding and affinity. | |
| CAGE- C= cut down, A= annoyed, G= Guilty, E= ______ | |
| Long term ethanol exposure increase the number and _____ of enzymes that metabolize ethanol. | |
| ________ Hypothesis: The brain then responds to this disruption by inducing an opposing chemical adaptation that tends to restore the neurochemical balance. | |
| Chronic tolerance of alcohol results in decreased Calcium uptake and increased dihydropyridine binding- channel antagonist that reduce ______ symptoms in animal models. | |
| Acute tolerance of alchol results in increased intracellular Calcium and ________ calcium influx. No effect on dihydropyridine binding. | |
| | xx | x | x |
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| Chronic alcohol tolerance ______ cAMP | |
| Chronic alcohol abuse is the number 1 cause of _____ and the need for liver transplant. | |
| Symptoms: opthalmoplegia, gait ataxia and confusion, memory loss. Cause: Vitamin B1 deficiency (thiamin) | |
| Opioid receptor antagonist. Reduces subjective “high” associated with alcohol | |
| Competitive inhibitor of NMDA receptors. Reduces craving in many addictive disorders. More effective when given in combination with naltrexone | |
| Toxicities of this drug includes visual disturbances, blurred vision, formaldehyde on breath or urine, bradycardia. It is metabolized by alcohol dehydrogenase to formaldehyde. | |
| _____ neuropathy: The effect observed are weakness, gait ataxia, paresthesia, muscle cramps, numbness and burning dysethesia, which may be produced by nutritional deficiency and by | |
| Heavy alcohol consumption for long durations results in ________ cardiomyopathy. Binge drinking or withdrawal result in ventricular arrythmias. | |
| Chronic alcohol consumption results in increased risk of mouth, pharynx, larynx, esophagus, and _____ cancer. | |
| Name a permanent effect of Fetal Alcohol Syndrome. | |
| In Fetal Alchohol Syndrome, alcohol may increase neuronal _________. | |
| Management of acute intoxication with alcohol involves rehydration with _____ solutions if the patient is vomiting. | |
| Name a symptom of alcohol withdrawal. | |
| ________ are most commonly used to reduce alcohol withdrawal syndrome. | |
| Inhibits Aldehyde dehydrogenase. Toxicities include inhibited metabolism of other drugs and hepatotoxitcity. | |
| _______ poisoning: patient comes in with elevated anion and osmolar gap. Patient has severe acidosis and retinal damage. | |
| Ethylene glycol is converted by alcohol dehydrogenase into _______ acid crystals in renal tubules. | |
| Alcohol dehydrogenase inhibitor. Used for methanol or ethylene glycol toxicity. | |
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Periodic Table
Multiplication Table
Minute Math (Addition)
