Term
| EtOh absorption occurs by ___ in the ___ but also through the ___ |
|
Definition
Simple diffusion
Proximal intestine
Stomach |
|
|
Term
| Delays in ___ slow the absorption rate of EtOh |
|
Definition
|
|
Term
| Rate of EtOh absorption is ___. Presence of ___ or ___ dilutes available alcohol. |
|
Definition
Concentration dependent
Food or liquids |
|
|
Term
| EtOH effects on endocrine/repro: acute (2), chronic (2) |
|
Definition
Acute
-Inhibition of ADH = diuresis
-Inhibition of oxytocin secretion, impaired LH secretion, decreased serum testosterone
Chronic
-Testicular atrophy, impotence, sterility, gynecomastia
-FAS |
|
|
Term
| EtOH is first delivered to the ___ and then to the ___. |
|
Definition
|
|
Term
| Typical BAC peaks ___ after ingestion |
|
Definition
|
|
Term
| Most EtOH is metabolized to ___ and ___ by ___ and ___. |
|
Definition
CO2 and H2O
Gastric and hepatic enzymes |
|
|
Term
| First step of EtOH metabolism |
|
Definition
| Gastric mucosal alcohol dehydrogenase (20%) |
|
|
Term
| Second step of EtOH metabolism (2) |
|
Definition
Hepatic alcohol dehydrogenase = primary (boys > girls 2x)
Microsomal enzyme oxidizing system = secondary |
|
|
Term
| Alcohol dehydrogenase is inactivated by ___ |
|
Definition
|
|
Term
| MEOS can be induced by ___ |
|
Definition
| Chronic, high levels of EtOH = 2x in alcoholic |
|
|
Term
| Alcohol dehydrogenase depends on ___ while MEOS does not |
|
Definition
| NAD+ = rate limiting factor |
|
|
Term
| EtOH rate of oxidation follow ___ kinetics |
|
Definition
| Zero order = independent of time and concentration = 1 drink/hr (7-10g EtOH) |
|
|
Term
| BAC of 0.08 means that... |
|
Definition
| You've reached the limit of the enzymes |
|
|
Term
|
Definition
Quantity ingested and rate
Speed of absorption
Body weight and %body water
Rate of metabolism |
|
|
Term
| Non-specific effects of EtOH act on the ___ |
|
Definition
| Membrane: disturbs the membrane proteins that participate in signaling (Na/K ATPase, adenyl cyclase, PKC, Ca/NA voltage-gated ion channels) |
|
|
Term
| Specific effects of EtOH act on ___ |
|
Definition
|
|
Term
| At lower concentrations of EtOH there is ___ (NT effects) |
|
Definition
Increased neuronal signaling = stimuation
-Decreases GABA influence = disinhibition
-Increases DA release in nucleus accumbens |
|
|
Term
| At higher concentrations of EtOH there is ___ (NT effects) |
|
Definition
Decreased neuronal signaling = depressant
-Enhanced GABA influence
-Inhibition of glutamate at NMDA-R |
|
|
Term
| EtOH effects on CNS: acute (2), chronic (3) |
|
Definition
Acute
-Low concentrations: disinhibition = stimulation
-High concentrations = impairment of reticular activating system = depression
Chronic
-Serious neuro and mental issues: cerebral and cerebellar atrophy, memory loss, sleep disturbances, psychoses
-VitB deficiency and neuropathies
-Increased risk of stroke |
|
|
Term
| EtOH effects on CV and respiratory systems: acute (2), chronic (2) |
|
Definition
Acute
-Low concentrations: cutaneous VD (direct smooth muscle relaxant), increased HR/BP and platelet aggregation
-High concentrations: myocardial, central vasomotor, and respiratory depression
Chronic
-HTN and worsening of existing HTN
-Irreversible cardiomyopathy |
|
|
Term
| EtOH effects on liver: acute (5), chronic |
|
Definition
Acute: metabolizing EtOH reduces NAD to NADH + H, the excess H:
-Transient hyperglycemia (enough glycogen) or hypoglycemia (decreased gluconeogenesis)
-Hyperlacticacidemia
-Hyperuricemia since lactic acid is preferentially eliminated
-Hyperlipidemia
-Ketoacidosis
Chronic: NADH inhibits glycerophosphate dehydrogenase causing increased glycerophosphate and esterification of FA/TG
-Decreased FA oxidation leads to increased hepatic fat |
|
|
Term
EtOH effects on GI: acute
(2), chronic (2) |
|
Definition
Acute
-Low concentrations: increase gastric acid secretion and appetite
-High concentrations = >40%: gastric irritation and pylorospasm, which slows absorption
Chronic: acts as organic solvent
-Erosive gastritis and esophageal/duodenal varices
-Pancreatitis (due to increased secretions) |
|
|
Term
| Acute toxicty of EtOH (2) |
|
Definition
Effects related to BAC causing CNS and respiratory depression
Treatment is supportive |
|
|
Term
| Chronic toxicity of EtOH (3) |
|
Definition
Increased mortality
-Liver disease: fatty liver, hepatitis, cirrhosis
-CNS issues
-Cancer |
|
|
Term
|
Definition
| Increased capacity to metabolize EtOH due to induction of liver enzymes |
|
|
Term
| Tolerance: cellular/pharmacodynamic |
|
Definition
Cellular: membranes affected by alcohol have reduced response
Pharmacodynamic: increased toxicity threshold |
|
|
Term
| Dependence: psych and physical (3) |
|
Definition
Psych: driven by DA levels
Physical: NT levels have changed due to the chronic depression caused by EtOH
-Downregulated GABA
-Upregulated glutamate
-Increased central NE |
|
|
Term
| Characteristics of physical dependence/withdrawal (1.3) |
|
Definition
| Forced reduction/discontinuation = withdrawal syndrome -Seizures -Sweating -Delirium tremors |
|
|
Term
| Physical dependence treatment |
|
Definition
| Disulfiram: inhibits alcohol dehydrogenase (acetaldehyde builds up, which causes unpleasant S/E!) = deterrent |
|
|
Term
| EtOH is bad for these diseases (8) |
|
Definition
Hepatic
Kidney
Skeletal
Cardiac
Peptic ulcer
Pancreatitis
Gout
Epilepsy/seizures |
|
|
Term
| EtOH can alter the bioavailability of drugs (2) |
|
Definition
Increase solubility of BZ and aminoglycosides = increased bioavailability
High concentrations/pylorospasm = decrease levels or delay onset of drugs absorbed in the proximal intestine |
|
|
Term
| EtOH can alter the metabolism of other drugs (2) |
|
Definition
Increased (chronic) or decreased (acute) metabolism: barbies and phenytoin
Increased (chronic): morphine, BZs |
|
|
Term
| EtOH can potentiate the effects of other drugs (4) |
|
Definition
Any CNS depressant
Salicylate = GI irritation
Sulfonylureas = hypoglycemia
Nitrates = hypotension |
|
|
Term
| Methanol and ethylene glycol are both metabolized by ___, and their toxicity can be reversed by administering ___ and treating ___ |
|
Definition
Alcohol dehydrogenase
EtOH (preferred substrate for the enzyme = displace the bad alcohols)
Metabolic issues |
|
|
Term
| Methanol metabolized to ___ causing (6) |
|
Definition
Formic acid
Headache, vomiting, dyspnea, metabolic acidosis
Blurring and blindness (destruction of ganglion cells) |
|
|
Term
| Ethylene glycol is metabolized to ___, causing (3) |
|
Definition
Glycoaldehyde then glycolic acid then glyoxylic acid then oxalic acid
CNS depression, metabolic acidosis
Nephrotoxicity if deposited in renal tubules |
|
|
