You are absolutely right.
...

I am pretty certain she doubled up on her meds the day before I had to have
her hospitalized. But the bruising didn't occur until she was already in
the hospital almost a week and I am pretty certain they reduced or
cancelled her Coumadin.

That's alright, this is alt.cancer.support, not alt.cancer.treatment :-) so
I am just bouncing ideas off you guys so I'll be better prepared to face
the doctor with intelligent questions (which I will promptly forget when I
need them)

CLINICAL PHARMACOLOGY

An anticoagulation effect generally occurs within 24 hours after drug
administration. However, peak anticoagulant effect may be delayed 72 to 96 hours.
The duration of action of a single dose of racemic warfarin is 2 to 5 days. The
effects of COUMADIN may become more pronounced as effects of daily maintenance doses
overlap.

Absorption
COUMADIN is essentially completely absorbed after oral administration with peak
concentration generally attained within the first 4 hours.

Metabolism

The elimination of warfarin is almost entirely by metabolism. COUMADIN is
stereoselectively metabolized by hepatic microsomal enzymes (cytochrome P-450) to
inactive hydroxylated metabolites (predominant route) and by reductases to reduced
metabolites (warfarin alcohols). The warfarin alcohols have minimal anticoagulant
activity. The metabolites are principally excreted into the urine; and to a lesser
extent into the bile. The metabolites of warfarin that have been identified include
dehydrowarfarin, two diastereoisomer alcohols, .4-, 6-, 7-, 8- and
10-hydroxywarfarin. The cytochrome P-450 isozymes involved in the metabolism of
warfarin include 2C9,2C19,2C8,2C18,1A2,and 3A4. 2C9 is likely to be the principal
form of human liver P-450 which modulates the in vivo anticoagulant activity of
warfarin.

Excretion

The terminal half-life of warfarin after a single dose is approximately one week;
however, the effective half-life ranges from 20 to 60 hours, with a mean of about 40
hours. The clearance of R-warfarin is generally half that of S-warfarin, thus as the
volumes of distribution are similar, the half-life of R-warfarin is longer than that
of S-warfarin. The half-life of R-warfarin ranges from 37 to 89 hours, while that of
S-warfarin ranges from 21 to 43 hours. Studies with radiolabeled drug have
demonstrated that up to 92% of the orally administered dose is recovered in urine.
Very little warfarin is excreted unchanged in urine. Urinary excretion is in the
form of

CLINICAL PHARMACOLOGY

COUMADIN and other coumarin anticoagulants act by inhibiting the synthesis of
vitamin K dependent clotting factors, which include Factors II,VII,IX and X, and the
anticoagulant proteins C and S. Half-lives of these clotting factors are as follows:
Factor II - 60 hours, VII - 4-6 hours, IX - 24 hours, and X - 48-72 hours. The
half-lives of proteins C and S are approximately 8 hours and 30 hours, respectively.
The resultant in vivo effect is a sequential depression of Factors VII,IX,X and II
activities. Vitamin K is an essential cofactor for the post ribosomal synthesis of
the vitamin K dependent clotting factors. The vitamin promotes the biosynthesis of
-carboxyglutamic acid residues in the proteins which are essential for biological
activity. Warfarin is thought to interfere with clotting factor synthesis by
inhibition of the regeneration of vitamin K1 epoxide. The degree of depression is
dependent upon the dosage administered. Therapeutic doses of warfarin decrease the
total amount of the active form of each vitamin K dependent clotting factor made by
the liver by approximately 30% to 50%.

An anticoagulation effect generally occurs within 24 hours after drug
administration. However, peak anticoagulant effect may be delayed 72 to 96 hours.
The duration of action of a single dose of racemic warfarin is 2 to 5 days. The
effects of COUMADIN may become more pronounced as effects of daily maintenance doses
overlap. Anticoagulants have no direct effect on an established thrombus, nor do
they reverse is chemic tissue damage. However, once a thrombus has occurred, the
goal of anticoagulant treatment is to prevent further extension of the formed clot
and prevent secondary thromboembolic complications which may result in serious and
possibly fatal sequelae.

Pharmacokinetics

COUMADIN is a racemic mixture of the R- and S-enantiomers. The S-enantiomer exhibits
2-5 times more anticoagulant activity than the R-enantiomer in humans, but generally
has a more rapid clearance.

Absorption

COUMADIN is essentially completely absorbed after oral administration with peak
concentration generally attained within the first 4 hours.

Distribution

There are no differences in the apparent volumes of distribution after intravenous
and oral administration of single doses of warfarin solution. Warfarin distributes
into a relatively small apparent volume of distribution of about 0.14 liter/kg. A
distribution phase lasting 6 to 12 hours is distinguishable after rapid intravenous
or oral administration of an aqueous solution. Using a one compartment model, and
assuming complete bioavailability, estimates of the volumes of distribution of R-
and S-warfarin are similar to each other and to that of the race-mate.
Concentrations in fetal plasma approach the maternal values, but warfarin has not
been found in human milk (see WARNINGS: Lactation). Approximately 99% of the drug is
bound to plasma proteins.

Metabolism

The elimination of warfarin is almost entirely by metabolism. COUMADIN is
stereoselectively metabolized by hepatic microsomal enzymes (cytochrome P-450) to
inactive hydroxylated metabolites (predominant route) and by reductases to reduced
metabolites (warfarin alcohols). The warfarin alcohols have minimal anticoagulant
activity. The metabolites are principally excreted into the urine; and to a lesser
extent into the bile. The metabolites of warfarin that have been identified include
dehydrowarfarin, two diastereoisomer alcohols, .4-, 6-, 7-, 8- and
10-hydroxywarfarin. The cytochrome P-450 isozymes involved in the metabolism of
warfarin include 2C9,2C19,2C8,2C18,1A2,and 3A4. 2C9 is likely to be the principal
form of human liver P-450 which modulates the in vivo anticoagulant activity of
warfarin.

Excretion

The terminal half-life of warfarin after a single dose is approximately one week;
however, the effective half-life ranges from 20 to 60 hours, with a mean of about 40
hours. The clearance of R-warfarin is generally half that of S-warfarin, thus as the
volumes of distribution are similar, the half-life of R-warfarin is longer than that
of S-warfarin. The half-life of R-warfarin ranges from 37 to 89 hours, while that of
S-warfarin ranges from 21 to 43 hours. Studies with radiolabeled drug have
demonstrated that up to 92% of the orally administered dose is recovered in urine.
Very little warfarin is excreted unchanged in urine. Urinary excretion is in the
form of metabolites.

Elderly

Patients 60 years or older appear to exhibit greater than expected prothrombin time
(PT)/International Normalized Ratio (INR) response to the anticoagulant effects of
warfarin. The cause of the increased sensitivity to the anticoagulant effects of
warfarin in this age group is unknown. This increased anticoagulant effect from
warfarin may be due to a combination of pharmacokinetic and pharmacodynamic factors.
Racemic warfarin clearance may be unchanged or reduced with increasing age. Limited
information suggests there is no difference in the clearance of S-warfarin in the
elderly versus young subjects. However, there may be a slight decrease in the
clearance of R-warfarin in the elderly as compared to the young. Therefore, as
patient age increases, a lower dose of warfarin is usually required to produce a
therapeutic level of anticoagulation.

Hepatic dysfunction can potentiate the response to warfarin through impaired
synthesis of clotting factors and decreased metabolism of warfarin.

The most serious risks associated with anticoagulant therapy with warfarin sodium
are hemorrhage in any tissue or organ and, less frequently (<0.1%), necrosis and/or
gangrene of skin and other tissues. The risk of hemorrhage is related to the level
of intensity and the duration of anticoagulant therapy.

t cannot be emphasized too strongly that treatment of each patient is a highly
individualized matter. COUMADIN (Warfarin Sodium), a narrow therapeutic range
(index) drug, may be affected by factors such as other drugs and dietary Vitamin K.
Dosage should be controlled by periodic determinations of PT/INR or other suitable
coagulation tests.

Caution should be observed when COUMADIN is administered in any situation or in the
presence of any predisposing condition where added risk of hemorrhage, necrosis,
and/or gangrene is present.

PRECAUTIONS

Periodic determination of PT/INR or other suitable coagulation test is essential.

Numerous factors, alone or in combination, including travel, changes in diet,
environment, physical state and medications, including botanicals, may influence
response of the patient to anticoagulants. It is generally good practice to monitor
the patient’s response with additional PT/INR determinations in the period
immediately after discharge from the hospital, and whenever other medications,
including botanicals, are initiated, discontinued or taken irregularly. The
following factors are listed for reference; however, other factors may also affect
the anticoagulant response.

Drugs may interact with COUMADIN through pharmacodynamic or pharmacokinetic
mechanisms. Pharmacodynamic mechanisms for drug interactions with COUMADIN are
synergism (impaired hemostasis, reduced clotting factor synthesis), competitive
antagonism (vitamin K), and altered physiologic control loop for vitamin K
metabolism (hereditary resistance). Pharmacokinetic mechanisms for drug interactions
with COUMADIN are mainly enzyme induction, enzyme inhibition, and reduced plasma
protein binding. It is important to note that some drugs may interact by more than
one mechanism.

The following factors, alone or in combination, may be responsible for INCREASED
PT/INR response

ENDOGENOUS FACTORS
(see the rest including a long list of foods and medicines that can interact)

Special Risk Patients
COUMADIN (Warfarin Sodium) is a narrow therapeutic range (index) drug, and caution
should be observed when warfarin sodium is administered to certain patients such as
the elderly or debilitated or when administered in any situation or physical
condition where added risk of hemorrhage is present.

Caution should be observed when COUMADIN (or warfarin) is administered concomitantly
with nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin, to be certain
that no change in anticoagulation dosage is required.

I am scared that cancer treatment would be the straw that breaks

Aren't you putting the cart in front of the horse? Chris's mother hasn't
been diagnosed with cancer. J mentions peritonitis is an inflammation of the
peritoneum, the thin membrane that lines the abdominal wall and covers most
of the organs of the body. There are two major types of peritonitis. Primary
peritonitis is caused by the spread of an infection from the blood and lymph
nodes to the peritoneum. This type of peritonitis is rare - less than 1% of
all cases of peritonitis are primary. The more common type of peritonitis,
called secondary peritonitis, is caused by the entry of bacteria or enzymes
into the peritoneum from the gastrointestinal or biliary tract. Both cases
of peritonitis are very serious and can be life-threatening if not treated
properly.  From the descriptiion a tap was done, if it was peritonitis she
would be in the hosptial on antibotics.

Cbris, why was your mother's belly tap?  Did they tell you why? I would
guess, and only a guess she had acities which is the presence of excess
fluid in the peritoneal cavity. It is a common clinical finding with a wide
range of causes, but develops most frequently as a part of the
decompensation of previously asymptomatic chronic liver disease. Also can be
caused by CHF. The nursing home physician well  versed in CHF due to the
patients s/he treats. if is severe it really doesn't matter if you mother
has cancer or not since her heart will go before the cancer takes over. When
they tapped your mother,did they send the fluid to cytology since  cancer
cells would show up if she had ovarian cancer.

Alex

And that is the prime thing I don't know.