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64 Cards in this Set
- Front
- Back
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Where is EtOH absorbed?
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Proximal Intestine (via simple diffusion)
Stomach mucosa (20-30%) |
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What does a delay in gastric emptying do the the absorption rate of EtOH in the Proximal Intestine?
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Slows
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The rate of EtOH absorption is ______________ dependent.
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Concentration
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Concentrated EtOH solutions greater than 40% can produce _______________ and _____________ which _________ absorption
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Gastric irritation
Pylorospasm Slows |
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The presence of foods or liquids in the stomach _________ available alcohol.
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Dilutes
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An Anticholinergic would have what affect on EtOH absorption rate?
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slow down gastric emptying --> slow absorption
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Where does EtOH distribute once it is absorbed?
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Entire body water
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Typical peak BAC occurs ______ minutes after ingestion (depending on absorption rate)
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30-90
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Over 90% of ethanol is completely oxidized to _____ & _____ by gastric and hepatic enzyme systems.
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CO2 & H20
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What is the first step in Ethanol metabolism?
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metabolism by gastric Alcohol Dehydrogenase
*20% |
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Where cell is the gastric alcohol dehydrogenase enzyme located in?
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Parietal Cells
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What is the second step in ethanol metabolism?
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metabolism of ethanol by hepatic alcohol dehydrogenase into acetaldehyde
metabolism of acetaldehyde by hepatic aldehyde dehydrogenase to acetate & subsequently CO2 & H20 |
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What is the rate-limiting factor in hepatic Ethanol metabolism?
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availability of NAD+
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At what BAC will the MEOS (microsomal enzyme oxidizing system) kick in and start metabolizing Ethanol?
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100 mg/dL
*MEOS does NOT depend on NAD+ |
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What can induce MEOS?
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Chronic, high levels of ethanol
*see increased metabolism of other substrates for MEOS |
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What is the "tertiary" hepatic enzymatic mechanism for metabolizing Ethanol?
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Catalase
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What are the routes of elimination of the byproducts of Ethanol metabolism?
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Eliminated as CO2 & H20
Expired quantitatively in respiratory gases |
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What does the blood alcohol concentration reflect?
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Consumption rate & quantity ingested
Absorption speed Distribution--body weight and % of TBW Metabolism |
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How can BAC be measured?
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Directly: from blood via gas chromatograph analysis or enzyme analysis
Indirectly: via breath or saliva analysis |
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What are the membrane effects (non-specific effects) of Ethanol?
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Generalized perturbation of membrane proteins that participate in neuronal signaling
Enzymes: Na/K ATPase, adenyl cyclase, PKC Voltage-gate ion channels: Ca and Na channels |
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What effects does Ethanol have on neurotransmitter systems at LOWER concentrations?
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Increased neuronal signaling (Stimulatory effects):
-decreased actions of GABA (disinhibition) -increased release of Dopamine in the Nucleus Accumbens (mediates the pleasurable effects of EtOH) |
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What effects does Ethanol have on neurotransmitter systems at HIGHER concentrations?
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Decreased neuronal signaling (depressant effects)
-facilitation of the effects of GABA to enhance inhibitory signaling -inhibition of Glutamate effects at the NMDA receptor |
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What are the acute effects of Ethanol on the CNS?
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Low Concentrations--disinhibition of cortical inhibitory control mechanism--produces stimulation
Higher Concentrations--impairment of the Reticular Activating System leading to generalized depression of neuronal function |
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What are the chronic effects of Ethanol on the CNS?
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memory loss, sleep disturbances, psychoses
w/ concomitant B vitamin deficiency--peripheral neuropathies |
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What are the acute effects of Ethanol on Cardiovascular & Respiratory systems?
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Small doses--cutaneous vasodilation
Toxic doses--myocardial depression, central vasomotor & respiratory depression |
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What are the chronic effects of Ethanol on the Cardiovascular & Respiratory systems?
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Hypertension
Worsening of existing hypertension Irreversible cardiomyopathy |
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What are the acute effects of Ethanol on the Hepatic System?
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Excess reducing equivalents (H+) formed from metabolism increases the hepatic NADH/NAD ratio
Metabolic consequences: -transient hyperglycemia (when glycogen stores are adequate) or hypoglycemia w/ decreased gluconeogenesis -hyperlacticacademia -hyperuricemia -hyperlipidemia & ketoacidosis |
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What are the chronic effects of Ethanol on the Hepatic System?
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NADH-induced inhibition of Glycerophosphate dehydrogenase leads to increased Glycerophosphate & esterification of FAs (triglycerides)
Decreased oxidation of FAs Hepatic accumulation of "neutral" fat (fatty Liver) |
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What are the acute effects of Ethanol on the GI system?
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Low concentrations--increase gastric acid secretion
High concentrations--greater than 40%--produce gastric irritation & possibly pylorospasm |
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What are the chronic effects of Ethanol on the GI system?
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Erosive gastritis
Esophageal varices Duodenal abnormalities Pancreatitis |
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What are the acute effects of Ethanol on the Endocrine system?
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Inhibition of ADH secretion causing diuresis of variable intensity & duration
Inhibition of Oxytocin secretion Impaired secretion of LH Decreased serum Testosterone levels |
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What are the chronic effects of Ethanol on the Endocrine-Reproductive system?
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Testicular atrophy
Impotence Sterility Gynecomastia Abuse during preggo: Fetal Alcohol Syndrome |
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What is responsible for the acute toxicity of Ethanol?
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BAC dependent CNS & Cardiovascular system depression
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What is the treatment for acute Ethanol toxicity?
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Largely supportive w/ prevention of aspiration
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What chronic toxicities are associated with Ethanol Abuse?
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Increased mortality
Liver disease--alcoholic fatty liver (reversible) progressing to alcohol hepatitis and, finally, cirrhosis CNS abnormalities including symmetrical peripheral neuropathies Increased risk of certain cancers (Pancreatic / Head&Neck) |
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What are the two types of Ethanol Tolerance?
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Metabolic
Pharmacodynamic |
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Metabolic tolerance to Ethanol is evidenced by:
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Increased capacity to metabolize alcohol
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What is the mechanism responsible for metabolic tolerance?
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Induction of hepatic cytochrome P450 2E-1 (amount can increase 2 fold)
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What is Pharmacodynamic tolerance?
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Cellular tolerance--membrane systems less affected, behavioral adaptation, significant increase in toxicity threshold
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What type of dependence develops first (physical/psychological)?
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Psychological--due to Dopamine released
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Physical dependence is characterized by adaptive changes in _____________.
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Neurotransmitter systems
*downregulation of GABA receptors *upregulation of NMDA receptors *increased central NE activity |
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What are characteristics of physical dependence?
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Forced reduction or discontinuation of Ethanol consumption results in a withdrawal syndrome
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Withdrawal syndrome is characterized acutely by:
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Hallucinations
Seizures Delirium Tremors (DT's) |
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In what diseases should Ethanol be avoided?
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Hepatic
Severe Renal disease Skeletal or Cardiac myopathies Peptic Ulcer disease Pancreatitis Gout |
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Disinhibition properties of Ethanol on the CNS inhibitory pathways predict potential adverse effects in patients with ____________
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Seizure disorders
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The solubility of what drugs are increased by low concentrations of Ethanol thus increasing bioavailability?
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Diazepam
Aminoglycoside antibiotics |
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Acutely high concentrations of Ethanol can interfere with the Hepatic metabolism of drugs such as:
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Pentobarbital
Phenobarbital Phenytoin |
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Chronic Ethanol can induce the hepatic cytochrome p450 microsomal system to enhance drug metabolism of:
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Phenytoin
Morphine Benzodiazepines Meprobamate |
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What drugs can inhibit hepatic Aldehyde Dehydrogenase leading to a buildup of Acetaldehyde in the body?
What are symptoms of "aldehyde syndrome"? |
Disulfram
Metronidazole Sulfonureas Aldehyde syndrome: cutaneous vasodilation, throbbing headache, respiratory difficulties, nausea, copious vomiting, sweating, chest pain, blurred vision, hypotension, orthostatic syncope, confusion |
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Ethanol in combination with any agent that has CNS depressant properties will result in?
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Enhanced sedation
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Ethanol can potentiate gastric irritation associated with __________.
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Salicylates
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Ethanol can potentiate the hypoglycemic response associated with __________.
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Sulfonylureas
Biguanides |
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Ethanol can potentiate the hypotensive response associated with ___________.
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Nitrates
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Methanol is rapidly absorbed in the ____________ and distributed to the total body water.
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Stomach
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Methanol is metabolised by ADH and subsequently AlDH into?
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ADH: formaldehyde
AlDH: formic acid |
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Methanol intoxication is associated with:
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Metabolic acidosis
Bilateral blindness (due to destructive inflammation of retinal ganglion cells) |
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What is the treatment for Methanol intoxication?
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Largely supportive
*Correction of acidosis is most important step in treatment* Ethanol & 4-methylpyrazole can be administered (both are substrates for ADH and block the metabolism of methanol to its toxic metabolites) |
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A fatal dose of Isopropyl alcohol is ____ ounces.
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4-8
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What are signs & symptoms of Isopropyl intoxication?
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similar to ethanol, but more prominent gastritis, pain and vomiting (and potential aspiration)
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What is Isopropyl metabolized to?
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Acetone
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Evidence of ____________ and _______ in the urine confirms intoxication.
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Ketoacidosis
Ketones |
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What is the pathway of Ethylene Glycol metabolism?
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Ethylene glycol --> glycoaldehyde --> glycolic acid --> glyoxylic acid --> oxalic acid
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The manifestations of Ethylene Glycol intoxication include?
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CNS depression (initial sign) followed by metabolic acidosis
Nephrotoxicity--deposition of oxalic acid crystals in the renal tubules |
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The treatment of Ethylene Glycol intoxication includes:
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Supportive w/ correction of metabolic acidosis
Formation of toxic metabolites can be reduced by administration of Ethanol or 4-methylpyrazole |
