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IRON, VITAMINB12, FOLIC
ACID, ANTICOAGULANTS
GROUP IX
NALUKWAGO DORCUS
OKIA JACOB
BWAMBALE FESTO
IRON
INTRODUCTION
• Iron deficiency is the most common cause of chronic anemia. Like other forms of
chronic anemia, iron deficiency anemia leads to pallor, fatigue, dizziness,
exertional dyspnea, and other generalized symptoms of tissue hypoxia.
• The cardiovascular adaptations to chronic anemia—tachycardia, increased cardiac
output, vasodilation, can worsen the condition of patients with underlying
cardiovascular disease.
• Iron forms the nucleus of the iron-porphyrin heme ring, which together with
globin chains forms hemoglobin. Hemoglobin reversibly binds oxygen and
provides the critical mechanism for oxygen delivery from the lungs to other
tissues.
• In the absence of adequate iron, small erythrocytes with insufficient
hemoglobin are formed, giving rise to microcytic hypochromic
anemia. Iron containing heme is also an essential component of
myoglobin, cytochromes, and other proteins with diverse biologic
functions
Pharmacokinetics
CONT…
Elimination
• There is no mechanism for excretion of iron. Small amounts are lost in the
feces by exfoliation of intestinal mucosal cells, and trace amounts are
excreted in bile, urine, and sweat.
Indications for the Use of Iron
• The only clinical indication for the use of iron preparations is the treatment
or prevention of iron deficiency anemia.
• Iron deficiency is common in infants (premature), pregnant and lactating
women; and patients with chronic kidney disease who lose erythrocytes at
a relatively high rate during hemodialysis
• Inadequate iron absorption also can cause iron deficiency. This is seen after
gastrectomy and in patients with severe small bowel disease that results in
generalized malabsorption.
Formulations
• Oral iron therapy and Parenteral iron therapy
SIDE EFFECTS
• Therapeutic doses - dose related nausea, upper abdominal pain,
constipation or diarrhea
• Iron overdose (1-2 g) can lead to circulatory collapse and death. Non-
intentional iron overdose has been a leading cause of fatal poisoning
in children <6 years old. Keep out of reach of children.
• Iron overdose can be treated by gastric lavage with a phosphate
solution and deferoxamine (iron chelator).
• Acute Iron Toxicity which causes necrotizing gastroenteritis with
vomiting, abdominal pain, and bloody diarrhea
• Chronic iron toxicity (iron overload), also known as hemochromatosis
DRUG INTERATIONS
• The risk or severity of adverse effects can be decreased when Iron is
combined with Captopril.
• Cimetidine can cause a decrease in the absorption of Iron resulting in
a reduced serum concentration and potentially a decrease in efficacy.
CONTRAINDICATIONS
• Patients with hemochromatosis, hemosiderosis or hemolytic anemia
VITAMIN B12
INTRODUCTION
• Vitamin B12 (cobalamin) serves as a cofactor for several essential biochemical
reactions in humans. Plays an essential role in red blood cell formation, cell
metabolism, nerve function and the production of DNA, the molecules inside cells
that carry genetic information
• Deficiency of vitamin B12 leads to megaloblastic anemia ,gastrointestinal
symptoms, and neurologic abnormalities.
• The chief dietary source of vitamin B12 is microbially derived vitamin B12 in
meat (especially liver), eggs, and dairy products. Vitamin B12 is sometimes called
extrinsic factor to differentiate it from intrinsic factor, a protein secreted by the
stomach that is required for gastrointestinal uptake of dietary vitamin B12.
Cont…
• Vitamin B-12 injections or nasal spray might be prescribed to treat
vitamin B-12 deficiency
• Left untreated, a vitamin B-12 deficiency can lead to anemia, fatigue,
muscle weakness, intestinal problems, nerve damage and mood
disturbances.
• The recommended daily amount of vitamin B-12 for adults is 2.4
micrograms. higher doses have been found to be safe. Your body
absorbs only as much as it needs, and any excess passes through your
urine.
Pharmacokinetics
• Vitamin B12 is produced only by bacteria; this vitamin cannot be synthesized by multicellular
organisms.
• It is absorbed from the gastrointestinal tract in the presence of intrinsic factor, a product of the
parietal cells of the stomach. Plasma transport is accomplished by binding to transcobalamin II.
• Vitamin B12 is stored in the liver in large amounts; a normal individual has enough to last 5 yrs.
• The 2 available forms of vitamin B12, cyanocobalamin and hydroxocobalamin, have similar
pharmacokinetics, but hydroxocobalamin has a longer circulating half-life.
Pharmacodynamics
• Vitamin B12 is essential in 2 reactions: conversion of methylmalonylcoenzyme A (CoA) to
succinyl-CoA and conversion of homocysteine to methionine.
• The second reaction is linked to folic acid metabolism and synthesis of deoxythymidylate (Dtmp)),
a precursor required for DNA synthesis.
• In vitamin B12 deficiency, folates accumulate as N5-methyltetrahydrofolate; the supply of
tetrahydrofolate is depleted; and the production of red blood cells slows. Administration of folic
acid to patients with vitamin B12 deficiency helps refill the tetrahydrofolate pool and partially or
fully corrects the anemia.
• However, the exogenous folic acid does not correct the neurologicdefects of vitamin B12
deficiency
side effects
High doses of vitamin B-12, such as those used to treat a deficiency,
might cause:
• Headache
• Nausea and vomiting
• Diarrhea
• Fatigue or weakness
• Tingling sensation in hands and feet
Interactions:
• Aminosalicylic acid (Paser). Taking this drug used to treat digestive problems
might reduce your body's ability to absorb vitamin B-12.
• Colchicine (Colcrys, Mitigare, Gloperba). Taking this anti-inflammatory drug used
to prevent and treat gout attacks might decrease your body's ability to absorb
vitamin B-12.
• Metformin (Glumetza, Fortamet, others). Taking this diabetes drug might reduce
your body's ability to absorb vitamin B-12.
• Proton pump inhibitors. Taking omeprazole (Prilosec), lansoprazole (Prevacid) or
other stomach acid-reducing drugs might decrease your body's ability to absorb
vitamin B-12.
• Vitamin C (ascorbic acid) supplements. Taking vitamin B-12 with vitamin C might
reduce the available amount of vitamin B-12 in your body. To avoid this
interaction, take vitamin C two or more hours after taking a vitamin B-12
FOLIC ACID
INTRODUCTION
• Folate and folic acid: are forms of vitamin B9 used for deficiency and to
prevent pregnancy complications. Folic acid is the synthetic form of folate,
which is a naturally occurring B vitamin.
• Like vitamin B12, folic acid is required for normal DNA synthesis, and its
deficiency usually presents as megaloblastic anemia.
• In addition, deficiency of folic acid during pregnancy increases the risk of
neural tube defects in the fetus.
• Many foods contain folate or have folic acid added. Foods that are naturally
high in folate include; leafy vegetables, okra, asparagus, certain fruits,
beans, yeast, mushrooms, animal liver and kidney, orange juice, and
tomato juice. Folic acid is also available as a supplement, and is often used
in combination with other B vitamins
INDICATIONS
• Consuming folic acid 600-800 mcg by mouth daily during pregnancy reduces the
risk of these Neural tube birth defects.
• Toxicity caused by the drug methotrexate. Taking folic acid by mouth seems to
reduce nausea and vomiting from methotrexate treatment.
• High levels of homocysteine in the blood (hyperhomocysteinemia). This condition
has been linked to heart disease and stroke. Taking folic acid by mouth lowers
homocysteine levels in people with normal or high homocysteine levels and in
people with kidney failure.
• Depression
• Stroke; taking folic acid supplements can reduce the risk of stroke.
• Decline in memory and thinking skills more so in elderly
• Gum enlargement caused by the drug phenytoin.
Pharmacokinetics
• Folic acid is readily absorbed from the gastrointestinal tract. Only modest
amounts are stored in the body, so a decrease in dietary intake is followed
by anemia within a few months
• Folic acid appears in the plasma approximately 15 to 30 minutes after an
oral dose; peak levels are generally reached within 1 hour. After intravenous
administration, the drug is rapidly cleared from the plasma. Cerebrospinal
fluid levels of folic acid are several times greater than serum levels of the
drug.
Pharmacodynamics
• Folic acid is converted to tetrahydrofolate by the action of
dihydrofolate reductase.
• One important set of reactions involving tetrahydrofolate and
dihydrofolate constitutes the dTMP cycle , which supplies the dTMP
required for DNA synthesis.
• Rapidly dividing cells are highly sensitive to folic acid deficiency. For
this reason, antifolate drugs are useful in the treatment of various
infections and cancers.
Side effects
When taken by mouth:
• cause stomach upset,
• Nausea, bad taste in the mouth
• Diarrhea
• Irritability
• confusion, behavior changes
• skin reactions,
• seizures, and other side effects
• Sleep pattern disturbance
Contraindications
• Type 2 diabetes
• Allergic reaction to folic acid
• Rheumatoid arthritis
• Inflammatory bowel disease
• Celiac disease
• Heart problem
• Cancer patients
• Vitamin B 12 deficiency anemia
• haemodialysis
Drug interactions
• Folic acid can increase how quickly the body breaks down phenytoin. Taking folic acid along with
phenytoin might decrease the effects of phenytoin for preventing seizures.
• Phenobarbital is used for seizures. Taking folic acid can decrease how well phenobarbital works for
preventing seizures.
• Pyrimethamine is used to treat parasite infections. Folic acid might decrease the effects of
pyrimethamine for treating parasite infections.
• Barbiturates drugs working on CNS is also affected
• Methotrexate, a cancer drug; its effectiveness is reduced by co-administration with folic acid
Dosage and formulation
• Dietary Folate Equivalents, or DFE tablet (5mg)
• The RDA in adults is 400 mcg DFE daily. In pregnancy, the RDA is 600
mcg DFE daily. When breastfeeding, the RDA is 500 mcg DFE daily. In
children, the RDA depends on age
ANTI COAGULANTS
BLOOD COAGULATION CASCADE
• Blood coagulates due to the transformation of soluble fibrinogen into insoluble
fibrin by the enzyme thrombin. Several circulating proteins interact in a cascading
series of limited proteolytic reactions .
• At each step, a clotting factor zymogen undergoes limited proteolysis and
becomes an active protease (eg, factor VII is converted to factor VIIa).
• Each protease factor activates the next clotting factor in the sequence, culminating
in the formation of thrombin (factor IIa). Several of these factors are targets for
drug therapy
ANTI COAGULANTS
Anticoagulants inhibit the formation of fibrin clots.
Three major types of anticoagulants are available:
heparin and related products, which must be used parenterally;
direct thrombin and factor X inhibitors, which are used parenterally or
orally;
the orally active coumarin derivatives (eg, warfarin).
HEPARIN
• Heparin is a large sulfated polysaccharide polymer obtained from animal sources. Each batch contains
molecules of varying size, with an average molecular weight of 15,000–20,000
• Heparin is highly acidic and can be neutralized by basic molecules(eg, protamine). Heparin is given
intravenously or subcutaneously to avoid the risk of hematoma associated with intramuscular injection.
• Low-molecular-weight (LMW) fractions of heparin (eg enoxaparin) have molecular weights of 2000–6000.
LMW heparins have greater bioavailability and longer durations of action than unfractionated heparin; thus,
doses can be given less frequently (eg, once or twice a day).
• Fondaparinux is a small synthetic drug that contains the biologically active pentasaccharide present in
unfractionated and LMW heparins. It is administered subcutaneously once daily.
MECHANISM
• The anticoagulation action of heparin depends on the presence of a specific serine protease inhibitor (serpin) of thrombin,
antithrombin III, in normal blood. Heparin binds to antithrombin III and induces a conformational change that accelerates
the interaction of antithrombin III with the coagulation factors.
• Heparin also catalyzes the inhibition of thrombin by heparin cofactor II, a circulating inhibitor. Smaller amounts of heparin
are needed to prevent the formation of free thrombin than are needed to inhibit the protease activity of clot-bound
thrombin. Inhibition of free thrombin is the basis of low-dose prophylactic therapy
• Unfractionated heparin binds to endogenous antithrombin III (ATIII) via a key pentasaccharide sequence. The heparin–
ATIII complex combines with and irreversibly inactivates thrombin and several other factors, particularly factor Xa .
• In the presence of heparin, ATIII proteolyzes thrombin and factor Xa approximately 1000-fold faster than in its absence.
Because it acts on preformed blood components, heparin provides anticoagulation immediately after administration.
INDICATIONS
• Because of its rapid effect, heparin is usedwhen anticoagulation is needed immediately (eg, when
starting therapy). Common uses include treatment of DVT, pulmonary embolism, and acute
myocardial infarction.
• Heparin is used in combination with thrombolytics for revascularization and in combination with
glycoprotein IIb/IIIa inhibitors during angioplasty and placement of coronary stents.
• Because it does not cross the placental barrier, heparin is the drug of choice when an anticoagulant
must be used in pregnancy.
• LMW heparins and fondaparinux have similar clinical applications.
Contraindications, Cautions, and Drug
Interactions
• Absolute contraindications include serious or active bleeding; intracranial bleeding; recent brain,
spinal cord, or eye surgery; severe liver or kidney disease; dissecting aortic aneurysm; and
malignant hypertension.
• Relative contraindications include active gastrointestinal hemorrhage, recent stroke or major
surgery, severe hypertension, bacterial endocarditis, threatened abortion, and severe renal or
hepatic failure.
• Drugs that inhibit platelet function (e.g., aspirin) or produce thrombocytopenia increase the risk of
bleeding when heparin is administered. Oral anticoagulants and heparin produce synergistic
effects. Many basic drugs precipitate in the presence of the highly acidic heparin (e.g.,
antihistamines, quinidine, quinine, phenothiazines, tetracycline, gentamicin, neomycin)
SIDE EFFECTS
• Increased bleeding is the most common adverse effect of heparin and related
molecules; the bleeding may result in hemorrhagic stroke.
• Protamine can lessen the risk of serious bleeding that can result from excessive
unfractionated heparin.
• Unfractionated heparin causes moderate transient thrombocytopenia in many
patients and severe thrombocytopenia and thrombosis(heparin-induced
thrombocytopenia or HIT)
• Prolonged use of unfractionated heparin is associated with osteoporosis.
COUMARIN DERIVATIVES
• Coumarin derivatives are derived from 4-hydroxycoumarin and
include dicumarol, warfarin sodium, and phenprocoumon. Of these
agents, warfarin has the best bioavailability and the least severe
adverse effects.
WARFARIN
• administered orally, has 100% bioavailability.
• Highly teratogenic and fetotoxic, with a t1/2 of 2.5 days, warfarin is
extensively (99%) bound to plasma albumin and can displace many
other drugs from this site.
PHARMOCODYNAMICS
• Coumarin derivatives indirectly interfere with γ-carboxylation of glutamate residues in
clotting factors II (prothrombin), VII, IX, and X, which is coupled to the oxidation of
vitamin K. Continued production of functional clotting factors requires replenishment of
reduced vitamin K from the oxidized form; this reduction is catalyzed by vitamin K
epoxide reductase; which is directly inhibited by coumarin derivatives.
• Clotting factors are still synthesized, but at reduced levels, and are undercarboxylated and
have greatly reduced biologic activity; clotting factors produced before coumarin therapy
decline in concentration as a function of factor half-life. This causes a latency period of
36–48 hours before effects are seen. It does not affect established thrombi.
Indications
• Treatment and prophylaxis of venous thrombosis and of pulmonary
embolism.
• Reduce thromboembolism
• in patients with mechanical heart valves.
• to treat patients with atrial fibrillation, whose risk for a stroke is
greatly increased.
Adverse effects
• Bleeding is a common adverse effect with oral anticoagulants;
prothrombin times should be frequently monitored.
• Warfarin causes hemorrhagic infarction in the breast, intestine, and
fatty tissues;
• it also readily crosses the placenta and can cause hemorrhage in the
fetus.
• Warfarin causes defects in normal fetal bone formation; its
teratogenic potential is high
Drug interactions
• Amiodarone and sulfinpyrazone inhibit the metabolism of the more active warfarin stereoisomer
and increase drug activity.
• Aspirin and salicylates increase warfarin action by inhibiting platelet function and displacement of
warfarin from plasma-binding sites.
• Antibiotics decrease microbial vitamin K production in the intestine.
• Barbiturates and rifampin decrease warfarin effectiveness by inducing microsomal enzymes.
• Oral contraceptives decrease warfarin effectiveness by increasing plasma clotting
• factors and decreasing antithrombin III

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Group pharmacology uuuuu. .pptx

  • 1. IRON, VITAMINB12, FOLIC ACID, ANTICOAGULANTS GROUP IX NALUKWAGO DORCUS OKIA JACOB BWAMBALE FESTO
  • 3. INTRODUCTION • Iron deficiency is the most common cause of chronic anemia. Like other forms of chronic anemia, iron deficiency anemia leads to pallor, fatigue, dizziness, exertional dyspnea, and other generalized symptoms of tissue hypoxia. • The cardiovascular adaptations to chronic anemia—tachycardia, increased cardiac output, vasodilation, can worsen the condition of patients with underlying cardiovascular disease. • Iron forms the nucleus of the iron-porphyrin heme ring, which together with globin chains forms hemoglobin. Hemoglobin reversibly binds oxygen and provides the critical mechanism for oxygen delivery from the lungs to other tissues.
  • 4. • In the absence of adequate iron, small erythrocytes with insufficient hemoglobin are formed, giving rise to microcytic hypochromic anemia. Iron containing heme is also an essential component of myoglobin, cytochromes, and other proteins with diverse biologic functions
  • 6. CONT… Elimination • There is no mechanism for excretion of iron. Small amounts are lost in the feces by exfoliation of intestinal mucosal cells, and trace amounts are excreted in bile, urine, and sweat. Indications for the Use of Iron • The only clinical indication for the use of iron preparations is the treatment or prevention of iron deficiency anemia. • Iron deficiency is common in infants (premature), pregnant and lactating women; and patients with chronic kidney disease who lose erythrocytes at a relatively high rate during hemodialysis • Inadequate iron absorption also can cause iron deficiency. This is seen after gastrectomy and in patients with severe small bowel disease that results in generalized malabsorption.
  • 7. Formulations • Oral iron therapy and Parenteral iron therapy
  • 8. SIDE EFFECTS • Therapeutic doses - dose related nausea, upper abdominal pain, constipation or diarrhea • Iron overdose (1-2 g) can lead to circulatory collapse and death. Non- intentional iron overdose has been a leading cause of fatal poisoning in children <6 years old. Keep out of reach of children. • Iron overdose can be treated by gastric lavage with a phosphate solution and deferoxamine (iron chelator). • Acute Iron Toxicity which causes necrotizing gastroenteritis with vomiting, abdominal pain, and bloody diarrhea • Chronic iron toxicity (iron overload), also known as hemochromatosis
  • 9. DRUG INTERATIONS • The risk or severity of adverse effects can be decreased when Iron is combined with Captopril. • Cimetidine can cause a decrease in the absorption of Iron resulting in a reduced serum concentration and potentially a decrease in efficacy.
  • 10. CONTRAINDICATIONS • Patients with hemochromatosis, hemosiderosis or hemolytic anemia
  • 12. INTRODUCTION • Vitamin B12 (cobalamin) serves as a cofactor for several essential biochemical reactions in humans. Plays an essential role in red blood cell formation, cell metabolism, nerve function and the production of DNA, the molecules inside cells that carry genetic information • Deficiency of vitamin B12 leads to megaloblastic anemia ,gastrointestinal symptoms, and neurologic abnormalities. • The chief dietary source of vitamin B12 is microbially derived vitamin B12 in meat (especially liver), eggs, and dairy products. Vitamin B12 is sometimes called extrinsic factor to differentiate it from intrinsic factor, a protein secreted by the stomach that is required for gastrointestinal uptake of dietary vitamin B12.
  • 13. Cont… • Vitamin B-12 injections or nasal spray might be prescribed to treat vitamin B-12 deficiency • Left untreated, a vitamin B-12 deficiency can lead to anemia, fatigue, muscle weakness, intestinal problems, nerve damage and mood disturbances. • The recommended daily amount of vitamin B-12 for adults is 2.4 micrograms. higher doses have been found to be safe. Your body absorbs only as much as it needs, and any excess passes through your urine.
  • 14. Pharmacokinetics • Vitamin B12 is produced only by bacteria; this vitamin cannot be synthesized by multicellular organisms. • It is absorbed from the gastrointestinal tract in the presence of intrinsic factor, a product of the parietal cells of the stomach. Plasma transport is accomplished by binding to transcobalamin II. • Vitamin B12 is stored in the liver in large amounts; a normal individual has enough to last 5 yrs. • The 2 available forms of vitamin B12, cyanocobalamin and hydroxocobalamin, have similar pharmacokinetics, but hydroxocobalamin has a longer circulating half-life.
  • 15. Pharmacodynamics • Vitamin B12 is essential in 2 reactions: conversion of methylmalonylcoenzyme A (CoA) to succinyl-CoA and conversion of homocysteine to methionine. • The second reaction is linked to folic acid metabolism and synthesis of deoxythymidylate (Dtmp)), a precursor required for DNA synthesis. • In vitamin B12 deficiency, folates accumulate as N5-methyltetrahydrofolate; the supply of tetrahydrofolate is depleted; and the production of red blood cells slows. Administration of folic acid to patients with vitamin B12 deficiency helps refill the tetrahydrofolate pool and partially or fully corrects the anemia. • However, the exogenous folic acid does not correct the neurologicdefects of vitamin B12 deficiency
  • 16. side effects High doses of vitamin B-12, such as those used to treat a deficiency, might cause: • Headache • Nausea and vomiting • Diarrhea • Fatigue or weakness • Tingling sensation in hands and feet
  • 17. Interactions: • Aminosalicylic acid (Paser). Taking this drug used to treat digestive problems might reduce your body's ability to absorb vitamin B-12. • Colchicine (Colcrys, Mitigare, Gloperba). Taking this anti-inflammatory drug used to prevent and treat gout attacks might decrease your body's ability to absorb vitamin B-12. • Metformin (Glumetza, Fortamet, others). Taking this diabetes drug might reduce your body's ability to absorb vitamin B-12. • Proton pump inhibitors. Taking omeprazole (Prilosec), lansoprazole (Prevacid) or other stomach acid-reducing drugs might decrease your body's ability to absorb vitamin B-12. • Vitamin C (ascorbic acid) supplements. Taking vitamin B-12 with vitamin C might reduce the available amount of vitamin B-12 in your body. To avoid this interaction, take vitamin C two or more hours after taking a vitamin B-12
  • 19. INTRODUCTION • Folate and folic acid: are forms of vitamin B9 used for deficiency and to prevent pregnancy complications. Folic acid is the synthetic form of folate, which is a naturally occurring B vitamin. • Like vitamin B12, folic acid is required for normal DNA synthesis, and its deficiency usually presents as megaloblastic anemia. • In addition, deficiency of folic acid during pregnancy increases the risk of neural tube defects in the fetus. • Many foods contain folate or have folic acid added. Foods that are naturally high in folate include; leafy vegetables, okra, asparagus, certain fruits, beans, yeast, mushrooms, animal liver and kidney, orange juice, and tomato juice. Folic acid is also available as a supplement, and is often used in combination with other B vitamins
  • 20. INDICATIONS • Consuming folic acid 600-800 mcg by mouth daily during pregnancy reduces the risk of these Neural tube birth defects. • Toxicity caused by the drug methotrexate. Taking folic acid by mouth seems to reduce nausea and vomiting from methotrexate treatment. • High levels of homocysteine in the blood (hyperhomocysteinemia). This condition has been linked to heart disease and stroke. Taking folic acid by mouth lowers homocysteine levels in people with normal or high homocysteine levels and in people with kidney failure. • Depression • Stroke; taking folic acid supplements can reduce the risk of stroke. • Decline in memory and thinking skills more so in elderly • Gum enlargement caused by the drug phenytoin.
  • 21. Pharmacokinetics • Folic acid is readily absorbed from the gastrointestinal tract. Only modest amounts are stored in the body, so a decrease in dietary intake is followed by anemia within a few months • Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour. After intravenous administration, the drug is rapidly cleared from the plasma. Cerebrospinal fluid levels of folic acid are several times greater than serum levels of the drug.
  • 22. Pharmacodynamics • Folic acid is converted to tetrahydrofolate by the action of dihydrofolate reductase. • One important set of reactions involving tetrahydrofolate and dihydrofolate constitutes the dTMP cycle , which supplies the dTMP required for DNA synthesis. • Rapidly dividing cells are highly sensitive to folic acid deficiency. For this reason, antifolate drugs are useful in the treatment of various infections and cancers.
  • 23. Side effects When taken by mouth: • cause stomach upset, • Nausea, bad taste in the mouth • Diarrhea • Irritability • confusion, behavior changes • skin reactions, • seizures, and other side effects • Sleep pattern disturbance
  • 24. Contraindications • Type 2 diabetes • Allergic reaction to folic acid • Rheumatoid arthritis • Inflammatory bowel disease • Celiac disease • Heart problem • Cancer patients • Vitamin B 12 deficiency anemia • haemodialysis
  • 25. Drug interactions • Folic acid can increase how quickly the body breaks down phenytoin. Taking folic acid along with phenytoin might decrease the effects of phenytoin for preventing seizures. • Phenobarbital is used for seizures. Taking folic acid can decrease how well phenobarbital works for preventing seizures. • Pyrimethamine is used to treat parasite infections. Folic acid might decrease the effects of pyrimethamine for treating parasite infections. • Barbiturates drugs working on CNS is also affected • Methotrexate, a cancer drug; its effectiveness is reduced by co-administration with folic acid
  • 26. Dosage and formulation • Dietary Folate Equivalents, or DFE tablet (5mg) • The RDA in adults is 400 mcg DFE daily. In pregnancy, the RDA is 600 mcg DFE daily. When breastfeeding, the RDA is 500 mcg DFE daily. In children, the RDA depends on age
  • 28. BLOOD COAGULATION CASCADE • Blood coagulates due to the transformation of soluble fibrinogen into insoluble fibrin by the enzyme thrombin. Several circulating proteins interact in a cascading series of limited proteolytic reactions . • At each step, a clotting factor zymogen undergoes limited proteolysis and becomes an active protease (eg, factor VII is converted to factor VIIa). • Each protease factor activates the next clotting factor in the sequence, culminating in the formation of thrombin (factor IIa). Several of these factors are targets for drug therapy
  • 29.
  • 30. ANTI COAGULANTS Anticoagulants inhibit the formation of fibrin clots. Three major types of anticoagulants are available: heparin and related products, which must be used parenterally; direct thrombin and factor X inhibitors, which are used parenterally or orally; the orally active coumarin derivatives (eg, warfarin).
  • 31. HEPARIN • Heparin is a large sulfated polysaccharide polymer obtained from animal sources. Each batch contains molecules of varying size, with an average molecular weight of 15,000–20,000 • Heparin is highly acidic and can be neutralized by basic molecules(eg, protamine). Heparin is given intravenously or subcutaneously to avoid the risk of hematoma associated with intramuscular injection. • Low-molecular-weight (LMW) fractions of heparin (eg enoxaparin) have molecular weights of 2000–6000. LMW heparins have greater bioavailability and longer durations of action than unfractionated heparin; thus, doses can be given less frequently (eg, once or twice a day). • Fondaparinux is a small synthetic drug that contains the biologically active pentasaccharide present in unfractionated and LMW heparins. It is administered subcutaneously once daily.
  • 32. MECHANISM • The anticoagulation action of heparin depends on the presence of a specific serine protease inhibitor (serpin) of thrombin, antithrombin III, in normal blood. Heparin binds to antithrombin III and induces a conformational change that accelerates the interaction of antithrombin III with the coagulation factors. • Heparin also catalyzes the inhibition of thrombin by heparin cofactor II, a circulating inhibitor. Smaller amounts of heparin are needed to prevent the formation of free thrombin than are needed to inhibit the protease activity of clot-bound thrombin. Inhibition of free thrombin is the basis of low-dose prophylactic therapy • Unfractionated heparin binds to endogenous antithrombin III (ATIII) via a key pentasaccharide sequence. The heparin– ATIII complex combines with and irreversibly inactivates thrombin and several other factors, particularly factor Xa . • In the presence of heparin, ATIII proteolyzes thrombin and factor Xa approximately 1000-fold faster than in its absence. Because it acts on preformed blood components, heparin provides anticoagulation immediately after administration.
  • 33. INDICATIONS • Because of its rapid effect, heparin is usedwhen anticoagulation is needed immediately (eg, when starting therapy). Common uses include treatment of DVT, pulmonary embolism, and acute myocardial infarction. • Heparin is used in combination with thrombolytics for revascularization and in combination with glycoprotein IIb/IIIa inhibitors during angioplasty and placement of coronary stents. • Because it does not cross the placental barrier, heparin is the drug of choice when an anticoagulant must be used in pregnancy. • LMW heparins and fondaparinux have similar clinical applications.
  • 34. Contraindications, Cautions, and Drug Interactions • Absolute contraindications include serious or active bleeding; intracranial bleeding; recent brain, spinal cord, or eye surgery; severe liver or kidney disease; dissecting aortic aneurysm; and malignant hypertension. • Relative contraindications include active gastrointestinal hemorrhage, recent stroke or major surgery, severe hypertension, bacterial endocarditis, threatened abortion, and severe renal or hepatic failure. • Drugs that inhibit platelet function (e.g., aspirin) or produce thrombocytopenia increase the risk of bleeding when heparin is administered. Oral anticoagulants and heparin produce synergistic effects. Many basic drugs precipitate in the presence of the highly acidic heparin (e.g., antihistamines, quinidine, quinine, phenothiazines, tetracycline, gentamicin, neomycin)
  • 35. SIDE EFFECTS • Increased bleeding is the most common adverse effect of heparin and related molecules; the bleeding may result in hemorrhagic stroke. • Protamine can lessen the risk of serious bleeding that can result from excessive unfractionated heparin. • Unfractionated heparin causes moderate transient thrombocytopenia in many patients and severe thrombocytopenia and thrombosis(heparin-induced thrombocytopenia or HIT) • Prolonged use of unfractionated heparin is associated with osteoporosis.
  • 36. COUMARIN DERIVATIVES • Coumarin derivatives are derived from 4-hydroxycoumarin and include dicumarol, warfarin sodium, and phenprocoumon. Of these agents, warfarin has the best bioavailability and the least severe adverse effects.
  • 37. WARFARIN • administered orally, has 100% bioavailability. • Highly teratogenic and fetotoxic, with a t1/2 of 2.5 days, warfarin is extensively (99%) bound to plasma albumin and can displace many other drugs from this site.
  • 38. PHARMOCODYNAMICS • Coumarin derivatives indirectly interfere with γ-carboxylation of glutamate residues in clotting factors II (prothrombin), VII, IX, and X, which is coupled to the oxidation of vitamin K. Continued production of functional clotting factors requires replenishment of reduced vitamin K from the oxidized form; this reduction is catalyzed by vitamin K epoxide reductase; which is directly inhibited by coumarin derivatives. • Clotting factors are still synthesized, but at reduced levels, and are undercarboxylated and have greatly reduced biologic activity; clotting factors produced before coumarin therapy decline in concentration as a function of factor half-life. This causes a latency period of 36–48 hours before effects are seen. It does not affect established thrombi.
  • 39. Indications • Treatment and prophylaxis of venous thrombosis and of pulmonary embolism. • Reduce thromboembolism • in patients with mechanical heart valves. • to treat patients with atrial fibrillation, whose risk for a stroke is greatly increased.
  • 40. Adverse effects • Bleeding is a common adverse effect with oral anticoagulants; prothrombin times should be frequently monitored. • Warfarin causes hemorrhagic infarction in the breast, intestine, and fatty tissues; • it also readily crosses the placenta and can cause hemorrhage in the fetus. • Warfarin causes defects in normal fetal bone formation; its teratogenic potential is high
  • 41. Drug interactions • Amiodarone and sulfinpyrazone inhibit the metabolism of the more active warfarin stereoisomer and increase drug activity. • Aspirin and salicylates increase warfarin action by inhibiting platelet function and displacement of warfarin from plasma-binding sites. • Antibiotics decrease microbial vitamin K production in the intestine. • Barbiturates and rifampin decrease warfarin effectiveness by inducing microsomal enzymes. • Oral contraceptives decrease warfarin effectiveness by increasing plasma clotting • factors and decreasing antithrombin III