Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
RUSMpsychopharm5
Alcohols
| Question | Answer |
|---|---|
| What is the cause of the diuresis seen when drinking heavily (ie; "breaking the seal") | inhibition of ADH (vasopressin) from the post. PG |
| Clinical use of phenol injection | sometimes used to stop bleeding. |
| Cause of gynecomastia associated with alcoholism | Failure of the liver.... estrogens are no longer able to be broken down effectively. |
| ACUTE ingestion of alcohol (binge drinking) has what effect on medications being taken concurrently? | Decreased breakdown ---> increased drug activity. This is because all the available NAD+ and NADP+ associated with the enzymes of metabolism are being used up for EtOH metabolism |
| CHRONIC ingestion of alcohol (alcoholism) has what effect on medications being taken concurrently? (assuming no liver damage) | Increased breakdown of drugs ---> diminished effects. This is due to CP450 induction |
| Serious liver damage (ie; cirrhosis) has what effect on medications being taken concurrently? | Decreased drug breakdown --> increased activity of drug. |
| What is cocaethylene and how is it formed? | It is a compound that is formed as a result of concurrent ingestion of cocaine and alcohol... it is a dopamine reuptake inhibitor (increased DA levels--> dependence on both drugs. |
| EtOH has what effect on GABA and NMDA receptors | Amplifies GABA-A and blocks NMDA. |
| What is thought to be a contributing factor to the microencephaly seen in fetal alcohol syndrome? | Blockage of M3 receptors on astroglial cells ---> inhibits the proliferation of astroglial cells which may be a cause of the microencephaly |
| MOA of disulfiram | blocks aldehyde DH and dopamine hydroxylase |
| PTs with hx of what psych d/o are c/i for disulfiram? | Pt with hx of schizophrenia. Disulfiram blocks dopamine hydroxylase (enzyme that converts DA-->NE ), causing DA to accumulate in the CNS and PNS |
| The toxicity of methanol ingestion is due primarily to what metabolite? | Formic acid on the optic nerve a(nd formaldehyde on the retina). Formic acid is the end product metabolite |
| Ethylene glycol poisoning rx? | fomepizole. Does not depress the CNS and does not cause hypocalcemia. |
| Indication for fomepizole? | ethylene glycol poisening. (coolant, industrial solvent) |
| EtOH is commonly associated with what kind of behavior? | Aggressive. |
| Two causes of hyperuricemia in EtOH use. | 1) Consumption of beer, lager, port: microbial breakdown involves oxidation to uric acid 2) Depletion of NAD due to accumulation of NADH in alcohol metabolism: NADH --> NAD+ is favored by lactic acid fermentation rather that pyruvate. Glycolysis -> lctate |
| Fomepezole targets ______ while disulfiram tagets _______ (ezymes) | Fomepezole: alcohol DH and disulfiram: aldehyde DH. |
| tx of EtOH withdrawal. Rx? Why are these drugs effective? | diazepam, chlordizepoxide, oxazepam. They act at the benzodiazepine receptors in the same manner as alcohol. (cross tolerant) |
| 3 examples of other drugs besides EtOH who's metabolism is inhibited by disulfiram | Anticoags, phenytoin and warfarin |
| Definitive finding of ethylene glycol poisening? | oxalic acid crystals (also presents with large anion gap, and metabolic acidosis) Renal failure is major danger. |
| Major danger of ethylene glycol poisening | renal failure. tx with fomepizole |
Created by:
rkirchoff
Popular Pharmacology sets