| Drug
Interaction |
| Drug
1 |
Drug
2 |
Nature
of Interaction |
Mechanism
|
| ACE
inhibitors |
+ Potassium
sparing
diuretics |
Hyperkalemia may occur.
|
Aldosterone
causes sodium retention and increased K+ and H+
excretion. ACE inhibitors reduces K+ excretion
by reducing aldosterone levels. Potassium sparing diuretics,
through different mechanism, conserve K+. So ACE
inhibitors together with potassium sparing diuretic may lead
to hyperkalemia. |
| Acetaminophen
|
+Alcohol |
Severe liver damage,
fatality may occur in alcoholics; seems to have no risk for
moderate drinkers. |
Persistent heavy
drinking stimulates cytochrome P-450 dependent mixed function
oxidase system allowing production of large amount of hepatotoxic
metabolites. Glutathione, when insufficient, is unable to detoxify
these metabolites resulting in binding of these toxic metabolities
to hepatic macromolecules causing hepatocellular damage. |
|
+ Anticholenergics
|
Delayed onset of
analgesic/ antipyretic action of acetaminophen. |
Anticholinergics
slow the rate of gastricemptying with reduced rate of absorption
in the gut. |
| |
+ Oral contraceptives
(O.C) |
Expected analgesic
effects are reduced; there is also increased absorption
of` ethinyloestradiol by 21.6%. |
Oral contraceptives
increase hepatic metabolism of acetaminophen resulting in its
rapid clearance; acetaminophen, on the other hand, reduces metabolism
of O.C. by the gut wall during absorption. |
|
+ Narcotic
analgesics (morphine/diamorphine) |
Delayed and
reduced plasma acetaminophen level. |
Opiate analgesics
delay gastric emptying reducing the rate of absorption. |
| |
+ Zidovudine
|
Haematological
abnormalities eg. anaemia, neutropenia, leukopenia etc. are
common. |
Acetaminophen
may compete with zidovudine for glucuronidation resulting in
increased mes New Roman; mso-ansi-language: EN-US; mso-fareast-language:
EN-US; mso-bidi-language: AR-SA">
zidovudine serum level and causing toxicity. |
