The ethanol present in _____ ml of expired air is equal to the amount in 1 ml of blood.
2100 ml of expired air
Ethanol is primarily metabolized by (alcohol dehydrogenase/cytochrome P450 system).
Ethanol is metabolized to ________________ by alcohol dehydrogenase.
Acetaldehyde is metabolized by ________________.
Acetaldehyde is metabolized to ________________ by aldehyde dehydrogenase.
What is the rate limiting step in ethanol metabolism?
Conversion of ethanol to acetaldehyde
________ is the cytochrome P450 enzyme responsible for a portion of ethanol metabolism.
(T/F) Almost 100% of ethanol is metabolized and enters the citric acid cycle.
In Arkansas, the legally drunk limit is _____ g/dL.
What is the mechanism of action for ethanol?
Enhances activity of GABA at GABAa receptor
Inhibits excitatory glutamate receptors
Enhances Ca2+-activated potassium channels
- Inhibits N- and P/Q-type Ca2+ channels
Replaces water in cavities of protein structure causing allosteric effects
A reduction in drug effect as a result of a lowered drug concentration at the receptor is referred to as ____________.
What are some causes for dispositional tolerance?
- Changes in Absorption
- Changes in Distribution
- Changes in Excretion
- Changes in Metabolism
A reduction in drug effect without a change in drug concentration is referred to as __________.
What are some causes of pharmacodynamic tolerance?
- Down regulation of receptor
- Change in drug-receptor coupling
- Change in components distal to receptor, such as signaling cascade or secondary messengers
When a patient or subject learns to negate the physical or mental side effects of a drug, it is referred to as ___________.
Behavioral Tolerance (Learned Tolerance)
The phenomenon in which impairment is greater at a given blood alcohol level when BAC is increasing than for the same blood alcohol level when BAC is decreasing is known as the _________________.
(T/F) Tolerance developed to a given BAC achieved in a slower rate of consumption may not help moderate the effects of alcohol when the same BAC is achieved by binge drinking.
Extensive physiological disturbances upon abrupt discontinuation of drug intake are a sign of __________.
The severity of physical dependence symptoms is proportional to the:
Level of intake and duration of substance use
Ethanol may cause the (vasoconstriction/vasodilation) of peripheral vessels and subsequent (hypothermia/hyperthermia).
Death from alcohol use most often occurs from (hypothermia/respiratory depression/liver failure).
What changes may ethanol cause within the liver and GI tract?
- Induction of the P450 system
- Fatty degeneration of liver
- Erosive gastritis
(T/F) Ethanol produces substantial effects on nearly every endocrine system, interfering with the release of prolactin, growth hormone, and antidiuretic hormone.
The increase in urine production associated with ethanol intake is attributed to decreased release of __________.
Antidiuretic hormone (ADH; vasopressin)
Most often beginning around a BAC of ________, patients present with emesis, anesthesia, coma, severe hypotension, decreased cardiac contractility, and respiratory depression.
How is an acute ethanol overdose treated?
- Gastric lavage
- Hemodialysis in extreme cases
Liver damage is seen in ____% of chronic alcoholics.
________________ is a condition sometimes seen in alcoholics that results from lesions in the medial thalamic nuclei, mamillary bodies, periaqueductal and periventricular brainstem nuclei, and superior cerebellar vermis. It is caused by inadequate intake of thiamine (vit. B1).
Fetal alcohol syndrome (FAS) is diagnosed based off a cluster of 3 features. What are they?
- Prenatal growth deficiency
- Short palpebral fissures
Disulfiram inhibits the enzyme _____________, causing extreme "hangover" like symptoms on ingestion of alcohol.
___________ acts as an opioid inhibitor and antagonist. By occupying the opioid receptor, ___________ decreases the endogenous "reward" elicited by alcohol. This prevents cravings and alcoholics seeking "just one more drink".
NalTrexone = Tipsy = Alcohol treatment
_____________ modulates the release of glutamate, an excitatory neurotransmitter. Glutamate is often overproduced in alcoholics and over time may elicit symptoms such as shaking, hypertension, or seizures. _____________ prevents this by competing for glutamate receptors (NMDA receptors).
_____________ is a toxic impurity often encountered in antifreeze, solvent, fuels, or "moonshine" production. It utilizes the same metabolism mechanisms as ethanol, but yields more toxic metabolites. Poisoning with this toxin initially presents as a mild drunken state before progressing to visual disturbances, GI distress, shortness of breath, and respiratory arrest (often the cause of death).
Methanol is first metabolized to _______________ by alcohol dehydrogenase.
Formaldehyde is metabolized to ______________ by formaldehyde dehydrogenase.
Alcohol dehydrogenase has a (higher/lower) affinity for ethanol than methanol.
Higher affinity for ethanol
(T/F) Ingestion of a high dose of ethanol is utilized in methanol toxicity in order to compete for alcohol dehydrogenase.
____________ is a pharmacological competitive inhibitor of alcohol dehydrogenase. It is relatively non-toxic, and is the antidote of choice for methanol and ethylene glycol poisoning.
What is the typical treatment for methanol poisoning?