zantac

[Guest guest]

Hey do any of you brilliant pharmacisits know anything about zantac use and any

risk for

etg production? I have a possible duodenal ulcer that is acting up again, I am

in lots of

pain on and off, and I was told to take a H2 blocker by a GI doc I work with; I

read all I

could in my drug books, it says it is " less than 10% metabolized by the liver, "

mostly

excreted unchanged in urine and feces, has a short half life of like 2-4 H; The

books I

have don't go inot great detail, and I looked up Tylenol as well just to see how

it compared

in their explanation, and it wasn't really helpful. So my simple nurse mind

tells me that it

shouldn't be a problem right? Sorry so long, just paranoid as usual...BTW,

great blog on

etg Lorie...

[Guest guest]

hi amy,i think you are ok...see below...regards,r CLINICAL PHARMACOLOGY ZANTAC is a competitive, reversible inhibitor of the action of histamine at the histamine H 2 -receptors, including receptors on the gastric cells. ZANTAC does not lower serum Ca++ in hypercalcemic states. ZANTAC is not an anticholinergic agent. Pharmacokinetics: Absorption: ZANTAC is 50% absorbed after oral administration, compared to an intravenous (IV) injection with mean peak levels of 440 to 545 ng/mL occurring 2 to 3 hours after a 150-mg dose. The syrup and EFFERdose formulations are bioequivalent to the tablets. Absorption is not significantly impaired by the administration of food or antacids. Propantheline slightly delays and increases peak blood levels of ZANTAC, probably by delaying gastric emptying and transit time. In one study, simultaneous administration of high-potency antacid (150 mmol) in fasting subjects has been reported to decrease the absorption of ZANTAC. Distribution: The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%. Metabolism: In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there

are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability. amykellog <amykellog@...> wrote: Hey do any of you brilliant pharmacisits know anything about zantac use and any risk for etg production? I have a possible duodenal ulcer that is acting up again, I am in lots of pain on and off, and I was told to take a H2 blocker by a GI doc I work with; I read all I could in my drug books, it says it is "less than 10% metabolized by the liver,"

mostly excreted unchanged in urine and feces, has a short half life of like 2-4 H; The books I have don't go inot great detail, and I looked up Tylenol as well just to see how it compared in their explanation, and it wasn't really helpful. So my simple nurse mind tells me that it shouldn't be a problem right? Sorry so long, just paranoid as usual...BTW, great blog on etg Lorie...

[Guest guest]

Thank you so much Robin, always appreciated.

Amy

Hey do any of you brilliant

pharmacisits know

anything about zantac use and any risk for

> etg production? I have a possible duodenal ulcer that is acting up again, I am

in lots of

> pain on and off, and I was told to take a H2 blocker by a GI doc I work with;

I read all I

> could in my drug books, it says it is " less than 10% metabolized by the

liver, " mostly

> excreted unchanged in urine and feces, has a short half life of like 2-4 H;

The books I

> have don't go inot great detail, and I looked up Tylenol as well just to see

how it

compared

> in their explanation, and it wasn't really helpful. So my simple nurse mind

tells me that

it

> shouldn't be a problem right? Sorry so long, just paranoid as usual...BTW,

great blog on

> etg Lorie...

>