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Seminar
on
Drug Affecting Blood and Blood Formation: Coagulant and
Anticoagulant
 A seminar for the partial fulfillment of the requirement for
the Degree of Bachelor of Pharmacy In Sant Gadge Baba
Amravati University.
 Submitted By-
 Shruti Rajeev Gautam
 (B.Pharmacy 4th year 7thSemester)
 Guide-
 Prof. Dr. S.D.Pande
 Vidya Bharati College of Pharmacy, Amravati.
 2018-2019
Index
 Coagulant
 Mechanism
 Pathway
 Drug
 Anticoagulant
 Drugs
Coagulation
 Coagulation (also known as clotting) is the process by
which blood changes from a liquid to a gel, forming a
blood clot.
 It potentially results in hemostasis, the cessation of
blood loss from a damaged vessel, followed by repair.
Mechanism
 There is an injury to the blood vessel wall a primary
mechanism operates to form platelets plugs followed by
the secondary mechanism of haemostasis or blood
coagulation which operate to form the fibrin clot
Primary mechanism
Vessel wall injury
(endothelial cell)
Expose to collagen
Adherence of platelet to collagen
(platelet surface interaction )
Release of ADP
PLATELET aggregation
(platelet-platelet interaction )
Platelet mass
(Platelet plug )
Coagulation factors
FACTOR
FACTOR I Fibrinogen
FACTOR II Prothrombin
FACTOR III Tissue thromboplastin
FACTOR IV Calcium
FACTOR V Proaccelerin
FACTOR VI (not an independent factor)
FACTOR VII Proconvertin
FACTOR VIII Anithaemophilic globulin (AHG-A)
FACTOR IX Christmas factor (AHG -B)
FACTOR X Stuart-prower factor
FACTOR XI Plasma thromboplastin antecedent
(AHG-C)
FACTOR XII Hageman factor
FACTOR XIII Fibrin stabilizing factor
Intrinsic & Pathway Extrinsic
Drug used to restore
coagulation
 Classification
 Vitamin K
K1(from plants fat soluble) : Phytonadione
(phyllquinone )
K3 (Synthetic )
Fat soluble : Menadione , acetomenaphthone
Water soluble : menadione sod.bisulfite, menadion
sod. Diphosphate
 Miscellaneous
Fibrinogen
Antihaemophilic factor
Desmopressiin
Adrenochrome monosemicarbazone
Rutiin
Ethamsylate
Vitamin K :-
 It is fat soluble principle required for the synthesis of
clotting factors
 Action: vit k act as a cofactor at a late stage in the
synthesis by liver of coagulation protein –prothrombin ,
factor VII, IX and X
 utilization : fat soluble form of vit k are absorbed from
the intestine via lymph and require bile salt for
absorption while water soluble form are absorbed
directly into portal blood
 Deficieny : deficieny of vit k occur due to liver disease
,obstructive jaundice , malabsorption ,long term
antimicrobial thearpy which alters intestial flora
 Uses: dietary deficieny, prolonged antimicrobial
therapy,obstructive jaundice , liver disease
 Advers effect: allergic reaction
DRUG INTERACTIONS
 Temporary resistance to prothrombin-depressing
anticoagulants may result, especially when larger doses
of phytonadione are used. If relatively large doses have
been employed, it may be necessary when reinstituting
anticoagulant therapy to use somewhat larger doses of
the prothrombin- depressing anticoagulant, or to use
one which acts on a different principle, such as heparin
sodium.
Anticoagulant
 Anticoagulants, commonly referred to as blood
thinners, are chemical substances that prevent or
reduce coagulation of blood, prolonging the clotting
time.
 Drug used to reduce the coagulability of blood
Drug
 Used in vivo
 A) Parental Anticoagulants
(1) Indirect Thrombin Inhibitor: Heparin ,low molecular
weight heparin , fondaparinux , danapariod
(2) Direct Thrombin Inhibitor : Lepirudin , Bivalirudin,
Argatroban
 B.) Oral anticoagulant
(1) Coumarin Derivatives: Bishydroxycoumarin, Warfarin
sod , Acenocoumarol, Ethylbiscoumacetate
(2) Indandione derivative : Phenindione
(3) Direct factor Xa inhibitors : Rivaroxaban
(4) Oral direct thrombin inhibitor : Dabigatran etexilate
 Used in vitro
 A) Heparin
 B) Calcium Complexing Agent :
Sodium citrate
Sodium Oxalate
Sodium edetate
HEPARIN
HEPARIN
 Heparin is a non uniform mixture of straight chain
mucopolysaccharides with MW10,000 to 20,000
 Heparin carries strong electronegative charges and is
the strongest organic acid present in the body
 Is present in all tissue containing mast cell richest
source are lung ,liver and intestinal mucosa
 Action :
 Anticaogulant: Heparin is a powerful and instanteously
acting anticoagulant effective both in vivo and in virto.
it acts indirectly by activating plasma antithrombin III
 Antiplatelet: Heparin in higher doses inhibits platelet
aggregation and prolong bleeding time
 Lipaemia clearing : injection of hepain clears turbid post
prandil lipaemia plasma by releasing a lipoprotein
lipase from vessel wall and tissue
HEPARIN
Mechanism of action
 Heparin binds to the enzyme inhibitor antithrombin III
(AT), causing a conformational change that results in its
activation through an increase in the flexibility of its
reactive site loop. The activated AT then inactivates
thrombin, factor Xa and other proteases. The rate of
inactivation of these proteases by AT can increase by up
to 1000-fold due to the binding of heparin.Heparin
binds to antithrombin via a specific pentasaccharide
sulfation sequence contained within the heparin
polymer
Pharmacokinetic data
a) Bioavailability :erratic
b) Metabolism :liver
c) Elimination half life :1.5hr
d) Excretion:urine
Adverse effect
 A serious side-effect of heparin is heparin-induced
thrombocytopenia(HIT), caused by an immunological
reaction that makes platelets a target of immunological
response, resulting in the degradation of platelets,
which causes thrombocytopenia. This condition is
usually reversed on discontinuation, and in general can
be avoided with the use of synthetic heparins. Also, a
benign form of thrombocytopenia is associated with
early heparin use, which resolves without stopping
heparin
DRUG INTERACTION
 Oral anticoagulants
 Heparin sodium may prolong the one-stage
prothrombin time Therefore, when heparin sodium is
given with dicumarol or warfarin sodium, a period of at
least 5 hours after the last intravenous dose should
elapse before blood is drawn if a valid prothrombin time
is to be obtained.
 Platelet inhibitors
 Drugs such as acetylsalicylic acid, dextran,
phenylbutazone, ibuprofen, indomethacin,
dipyridamole, hydroxychloroquine and others that
interfere with platelet aggregation reactions (the main
hemostatic defense of heparinized patients) may induce
bleeding and should be used with caution in patients
receiving heparin sodium.
Drug/Laboratory Test
Interactions
 Significant elevations of aminotransferase (SGOT [S-AST]
and SGPT [SALT]) levels have occurred in a high
percentage of patients (and healthy subjects) who have
received heparin. Since aminotransferase
determinations are important in the differential
diagnosis of myocardial infarction, liver disease, and
pulmonary emboli, rises that might be caused by drugs
(like heparin) should be interpreted with caution
Antidote to heparin
 Protamine sulfate has been given to counteract the
anticoagulant effect of heparin (1 mg per 100 units of
heparin that had been given over the past four hours).
It may be used in those who overdose on heparin or to
reverse heparin's effect when it is no longer needed
WARNING:-
 Heparin is not intended for intramuscular use.
 Cardiovascular —subacute bacterial endocarditis.
Severe hypertension.
 Surgical — During and immediately following (a) spinal
tap or spinal anesthesia or (b) major surgery, especially
involving the brain, spinal cord or eye.
 Hematologic — Conditions associated with increased
bleeding tendencies, such as hemophilia,
thrombocytopenia and some vascular purpuras.
 Gastrointestinal — Ulcerative lesions and continuous
tube drainage of the stomach or small intestine.
 Other — Menstruation, liver diseasewith impaired
hemostasis.
Warafarin sodium
Warafarin sodium
 It is most popular oral anticoagulant
 The commercial perparation of warafarin mixture of R
and S enantiomer .S form is more potent than R
 Crystalline warfarin sodium occurs as a white, odorless,
crystalline powder that is discolored by light. It is very
soluble in water, freely soluble in alcohol, and very
slightly soluble in chloroform and ether.
 It is commonly used to treat blood clots such as deep
vein thrombosis and pulmonary embolism and to
prevent stroke in people who have atrial fibrillation,
valvular heart disease or artificial heart valves. Less
commonly it is used following ST-segment elevation
myocardial infarction (STEMI) and orthopedic surgery. It
is generally taken by mouth but may also be used by
injection into a vein
 Warfarin first came into commercial use in 1948 as a rat
poison .
 In 1954 it was approved for medical use in the United
States.[4] It is on the World Health Organization's List of
Essential Medicines, the most effective and safe
medicines needed in a health system
 Warfarin is used to decrease the tendency for
thrombosis or as secondary prophylaxis (prevention of
further episodes) in those individuals who have already
formed a blood clot . Warfarin treatment can help
prevent formation of future blood clots and help reduce
the risk of embolism
 Warfarin, sold under the brand name Coumadin
Pharmacokinetic data
a) Bioavailability :79-100% (by mouth)
b) Metabolism :liver
c) Elimination half life : 1 week (active half-life is 20-60
hours)
d) Excretion: kidney
e) Protein binding :99%
Mechanism of action
 warfarin is one of several drugs popularly referred to as
a "blood thinner"; this is a misnomer since it does not
affect the viscosity of blood.
 Warfarin inhibits the vitamin K-dependent synthesis of
biologically active forms of the calcium-dependent
clotting factors II, VI, IX and X, as well as the regulatory
factors protein C, protein S, and protein Z
Adverse effect
 Bleeding
 The only common side effect of warfarin is bleeding.
The risk of severe bleeding is small but definite (a
typically yearly rate of 1-3% has been reported)[and any
benefit needs to outweigh this risk when warfarin is
considered. All types of bleeding occur more commonly,
but the most severe ones are those involving the brain
(intracerebral hemorrhage/hemorrhagic stroke) and the
spinal cord.Risk of bleeding is increased if the INR is out
of range (due to accidental or deliberate overdose or
due to interactions). This risk increases greatly once the
INR exceeds 4.5
Warfarin necrosis
 A rare but serious complication resulting from
treatment with warfarin is, warfarin necrosis which
occurs more frequently shortly after commencing
treatment in patients with a deficiency of protein C.
Protein C is an innate anticoagulant that, like the
procoagulant factors that warfarin inhibits, requires
vitamin K-dependent carboxylation for its activity. Since
warfarin initially decreases protein C levels faster than
the coagulation factors, it can paradoxically increase the
blood's tendency to coagulate when treatment is first
begun , leading to massive thrombosis with skin
necrosis and gangrene of limbs. Its natural counterpart,
purpura fulminans, occurs in children who are
homozygous for certain protein C mutations
Osteoporosis
 After initial reports that warfarin could reduce bone
mineral density, several studies have demonstrated a
link between warfarin use and osteoporosis-related
fracture. A 1999 study in 572 women taking warfarin for
deep venous thrombosis, risk of vertebral fracture and
rib fracture was increased; other fracture types did not
occur more commonly] A 2002 study looking at a
randomly selected selection of 1523 patients with
osteoporotic fracture found no increased exposure to
anticoagulants compared to controls, and neither did
stratification of the duration of anticoagulation reveal a
trend towards fracture.
Purple toe syndrome
 Another rare complication that may occur early during
warfarin treatment (usually within 3 to 8 weeks of
commencement) is purple toe syndrome.This condition
is thought to result from small deposits of cholesterol
breaking loose and causing embolisms in blood vessels
in the skin of the feet, which causes a blueish purple
colour and may be painful.
 It is typically thought to affect the big toe, but it affects
other parts of the feet as well, including the bottom of
the foot (plantar surface). The occurrence of purple toe
syndrome may require discontinuation of warfarin.
Drug interaction
 Warfarin interacts with many commonly used drugs,
and the metabolism of warfarin varies greatly between
patients.Some foods have also been reported to
interact with warfarin.
 When taken with nonsteroidal anti-inflammatory drugs
(NSAIDs), warfarin increases the risk for gastrointestinal
bleeding. This increased risk is due to the anti-platelet
effect of NSAIDs as well as the possible damage to the
gastrointestinal mucosa
 Many commonly used antibiotics, such as
metronidazole or the macrolides, will greatly increase
the effect of warfarin by reducing the metabolismof
warfarin in the body.
 Thyroid activity also appears to influence warfarin
dosing requirements;hypothyroidism (decreased
thyroid function) makes people less responsive to
warfarin treatment,while hyperthyroidism(overactive
thyroid) boosts the anticoagulant effect. Several
mechanisms have been proposed for this effect,
including changes in the rate of breakdown of clotting
factors and changes in the metabolism of warfarin
Contraindications
 Warfarin is contraindicated in pregnancy, as it passes
through the placental barrier and may cause bleeding in
the fetus; warfarin use during pregnancy is commonly
associated with spontaneous abortion, stillbirth,
neonatal death, and preterm birth. Coumarins (such as
warfarin) are also teratogens, that is, they cause birth
defects
Reference
 Essential Of Medical Pharmacology –K.D. Tripathi 7
edition
 Essential Of Pharmacotherapeutics – F.S.K. Barar 4
edition
 https://www.rxlist.com/heparin-drug.htm#interactions
 https://www.rxlist.com/search/rxl/coumadin
Thank you

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Coagualnts and Anticoagulant

  • 1. Seminar on Drug Affecting Blood and Blood Formation: Coagulant and Anticoagulant  A seminar for the partial fulfillment of the requirement for the Degree of Bachelor of Pharmacy In Sant Gadge Baba Amravati University.  Submitted By-  Shruti Rajeev Gautam  (B.Pharmacy 4th year 7thSemester)  Guide-  Prof. Dr. S.D.Pande  Vidya Bharati College of Pharmacy, Amravati.  2018-2019
  • 2. Index  Coagulant  Mechanism  Pathway  Drug  Anticoagulant  Drugs
  • 3. Coagulation  Coagulation (also known as clotting) is the process by which blood changes from a liquid to a gel, forming a blood clot.  It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair.
  • 4. Mechanism  There is an injury to the blood vessel wall a primary mechanism operates to form platelets plugs followed by the secondary mechanism of haemostasis or blood coagulation which operate to form the fibrin clot
  • 5. Primary mechanism Vessel wall injury (endothelial cell) Expose to collagen Adherence of platelet to collagen (platelet surface interaction ) Release of ADP PLATELET aggregation (platelet-platelet interaction ) Platelet mass (Platelet plug )
  • 6. Coagulation factors FACTOR FACTOR I Fibrinogen FACTOR II Prothrombin FACTOR III Tissue thromboplastin FACTOR IV Calcium FACTOR V Proaccelerin FACTOR VI (not an independent factor) FACTOR VII Proconvertin FACTOR VIII Anithaemophilic globulin (AHG-A) FACTOR IX Christmas factor (AHG -B) FACTOR X Stuart-prower factor FACTOR XI Plasma thromboplastin antecedent (AHG-C) FACTOR XII Hageman factor FACTOR XIII Fibrin stabilizing factor
  • 8. Drug used to restore coagulation  Classification  Vitamin K K1(from plants fat soluble) : Phytonadione (phyllquinone ) K3 (Synthetic ) Fat soluble : Menadione , acetomenaphthone Water soluble : menadione sod.bisulfite, menadion sod. Diphosphate
  • 10. Vitamin K :-  It is fat soluble principle required for the synthesis of clotting factors  Action: vit k act as a cofactor at a late stage in the synthesis by liver of coagulation protein –prothrombin , factor VII, IX and X  utilization : fat soluble form of vit k are absorbed from the intestine via lymph and require bile salt for absorption while water soluble form are absorbed directly into portal blood
  • 11.  Deficieny : deficieny of vit k occur due to liver disease ,obstructive jaundice , malabsorption ,long term antimicrobial thearpy which alters intestial flora  Uses: dietary deficieny, prolonged antimicrobial therapy,obstructive jaundice , liver disease  Advers effect: allergic reaction
  • 12.
  • 13. DRUG INTERACTIONS  Temporary resistance to prothrombin-depressing anticoagulants may result, especially when larger doses of phytonadione are used. If relatively large doses have been employed, it may be necessary when reinstituting anticoagulant therapy to use somewhat larger doses of the prothrombin- depressing anticoagulant, or to use one which acts on a different principle, such as heparin sodium.
  • 14. Anticoagulant  Anticoagulants, commonly referred to as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time.  Drug used to reduce the coagulability of blood
  • 15.
  • 16. Drug  Used in vivo  A) Parental Anticoagulants (1) Indirect Thrombin Inhibitor: Heparin ,low molecular weight heparin , fondaparinux , danapariod (2) Direct Thrombin Inhibitor : Lepirudin , Bivalirudin, Argatroban
  • 17.  B.) Oral anticoagulant (1) Coumarin Derivatives: Bishydroxycoumarin, Warfarin sod , Acenocoumarol, Ethylbiscoumacetate (2) Indandione derivative : Phenindione (3) Direct factor Xa inhibitors : Rivaroxaban (4) Oral direct thrombin inhibitor : Dabigatran etexilate
  • 18.  Used in vitro  A) Heparin  B) Calcium Complexing Agent : Sodium citrate Sodium Oxalate Sodium edetate
  • 20. HEPARIN  Heparin is a non uniform mixture of straight chain mucopolysaccharides with MW10,000 to 20,000  Heparin carries strong electronegative charges and is the strongest organic acid present in the body  Is present in all tissue containing mast cell richest source are lung ,liver and intestinal mucosa  Action :  Anticaogulant: Heparin is a powerful and instanteously acting anticoagulant effective both in vivo and in virto. it acts indirectly by activating plasma antithrombin III  Antiplatelet: Heparin in higher doses inhibits platelet aggregation and prolong bleeding time  Lipaemia clearing : injection of hepain clears turbid post prandil lipaemia plasma by releasing a lipoprotein lipase from vessel wall and tissue
  • 22. Mechanism of action  Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop. The activated AT then inactivates thrombin, factor Xa and other proteases. The rate of inactivation of these proteases by AT can increase by up to 1000-fold due to the binding of heparin.Heparin binds to antithrombin via a specific pentasaccharide sulfation sequence contained within the heparin polymer
  • 23. Pharmacokinetic data a) Bioavailability :erratic b) Metabolism :liver c) Elimination half life :1.5hr d) Excretion:urine
  • 24. Adverse effect  A serious side-effect of heparin is heparin-induced thrombocytopenia(HIT), caused by an immunological reaction that makes platelets a target of immunological response, resulting in the degradation of platelets, which causes thrombocytopenia. This condition is usually reversed on discontinuation, and in general can be avoided with the use of synthetic heparins. Also, a benign form of thrombocytopenia is associated with early heparin use, which resolves without stopping heparin
  • 25. DRUG INTERACTION  Oral anticoagulants  Heparin sodium may prolong the one-stage prothrombin time Therefore, when heparin sodium is given with dicumarol or warfarin sodium, a period of at least 5 hours after the last intravenous dose should elapse before blood is drawn if a valid prothrombin time is to be obtained.  Platelet inhibitors  Drugs such as acetylsalicylic acid, dextran, phenylbutazone, ibuprofen, indomethacin, dipyridamole, hydroxychloroquine and others that interfere with platelet aggregation reactions (the main hemostatic defense of heparinized patients) may induce bleeding and should be used with caution in patients receiving heparin sodium.
  • 26. Drug/Laboratory Test Interactions  Significant elevations of aminotransferase (SGOT [S-AST] and SGPT [SALT]) levels have occurred in a high percentage of patients (and healthy subjects) who have received heparin. Since aminotransferase determinations are important in the differential diagnosis of myocardial infarction, liver disease, and pulmonary emboli, rises that might be caused by drugs (like heparin) should be interpreted with caution
  • 27. Antidote to heparin  Protamine sulfate has been given to counteract the anticoagulant effect of heparin (1 mg per 100 units of heparin that had been given over the past four hours). It may be used in those who overdose on heparin or to reverse heparin's effect when it is no longer needed
  • 28. WARNING:-  Heparin is not intended for intramuscular use.  Cardiovascular —subacute bacterial endocarditis. Severe hypertension.  Surgical — During and immediately following (a) spinal tap or spinal anesthesia or (b) major surgery, especially involving the brain, spinal cord or eye.  Hematologic — Conditions associated with increased bleeding tendencies, such as hemophilia, thrombocytopenia and some vascular purpuras.  Gastrointestinal — Ulcerative lesions and continuous tube drainage of the stomach or small intestine.  Other — Menstruation, liver diseasewith impaired hemostasis.
  • 30. Warafarin sodium  It is most popular oral anticoagulant  The commercial perparation of warafarin mixture of R and S enantiomer .S form is more potent than R  Crystalline warfarin sodium occurs as a white, odorless, crystalline powder that is discolored by light. It is very soluble in water, freely soluble in alcohol, and very slightly soluble in chloroform and ether.  It is commonly used to treat blood clots such as deep vein thrombosis and pulmonary embolism and to prevent stroke in people who have atrial fibrillation, valvular heart disease or artificial heart valves. Less commonly it is used following ST-segment elevation myocardial infarction (STEMI) and orthopedic surgery. It is generally taken by mouth but may also be used by injection into a vein
  • 31.  Warfarin first came into commercial use in 1948 as a rat poison .  In 1954 it was approved for medical use in the United States.[4] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system  Warfarin is used to decrease the tendency for thrombosis or as secondary prophylaxis (prevention of further episodes) in those individuals who have already formed a blood clot . Warfarin treatment can help prevent formation of future blood clots and help reduce the risk of embolism  Warfarin, sold under the brand name Coumadin
  • 32.
  • 33. Pharmacokinetic data a) Bioavailability :79-100% (by mouth) b) Metabolism :liver c) Elimination half life : 1 week (active half-life is 20-60 hours) d) Excretion: kidney e) Protein binding :99%
  • 34. Mechanism of action  warfarin is one of several drugs popularly referred to as a "blood thinner"; this is a misnomer since it does not affect the viscosity of blood.  Warfarin inhibits the vitamin K-dependent synthesis of biologically active forms of the calcium-dependent clotting factors II, VI, IX and X, as well as the regulatory factors protein C, protein S, and protein Z
  • 35. Adverse effect  Bleeding  The only common side effect of warfarin is bleeding. The risk of severe bleeding is small but definite (a typically yearly rate of 1-3% has been reported)[and any benefit needs to outweigh this risk when warfarin is considered. All types of bleeding occur more commonly, but the most severe ones are those involving the brain (intracerebral hemorrhage/hemorrhagic stroke) and the spinal cord.Risk of bleeding is increased if the INR is out of range (due to accidental or deliberate overdose or due to interactions). This risk increases greatly once the INR exceeds 4.5
  • 36. Warfarin necrosis  A rare but serious complication resulting from treatment with warfarin is, warfarin necrosis which occurs more frequently shortly after commencing treatment in patients with a deficiency of protein C. Protein C is an innate anticoagulant that, like the procoagulant factors that warfarin inhibits, requires vitamin K-dependent carboxylation for its activity. Since warfarin initially decreases protein C levels faster than the coagulation factors, it can paradoxically increase the blood's tendency to coagulate when treatment is first begun , leading to massive thrombosis with skin necrosis and gangrene of limbs. Its natural counterpart, purpura fulminans, occurs in children who are homozygous for certain protein C mutations
  • 37.
  • 38. Osteoporosis  After initial reports that warfarin could reduce bone mineral density, several studies have demonstrated a link between warfarin use and osteoporosis-related fracture. A 1999 study in 572 women taking warfarin for deep venous thrombosis, risk of vertebral fracture and rib fracture was increased; other fracture types did not occur more commonly] A 2002 study looking at a randomly selected selection of 1523 patients with osteoporotic fracture found no increased exposure to anticoagulants compared to controls, and neither did stratification of the duration of anticoagulation reveal a trend towards fracture.
  • 39.
  • 40. Purple toe syndrome  Another rare complication that may occur early during warfarin treatment (usually within 3 to 8 weeks of commencement) is purple toe syndrome.This condition is thought to result from small deposits of cholesterol breaking loose and causing embolisms in blood vessels in the skin of the feet, which causes a blueish purple colour and may be painful.  It is typically thought to affect the big toe, but it affects other parts of the feet as well, including the bottom of the foot (plantar surface). The occurrence of purple toe syndrome may require discontinuation of warfarin.
  • 41.
  • 42. Drug interaction  Warfarin interacts with many commonly used drugs, and the metabolism of warfarin varies greatly between patients.Some foods have also been reported to interact with warfarin.  When taken with nonsteroidal anti-inflammatory drugs (NSAIDs), warfarin increases the risk for gastrointestinal bleeding. This increased risk is due to the anti-platelet effect of NSAIDs as well as the possible damage to the gastrointestinal mucosa
  • 43.  Many commonly used antibiotics, such as metronidazole or the macrolides, will greatly increase the effect of warfarin by reducing the metabolismof warfarin in the body.  Thyroid activity also appears to influence warfarin dosing requirements;hypothyroidism (decreased thyroid function) makes people less responsive to warfarin treatment,while hyperthyroidism(overactive thyroid) boosts the anticoagulant effect. Several mechanisms have been proposed for this effect, including changes in the rate of breakdown of clotting factors and changes in the metabolism of warfarin
  • 44. Contraindications  Warfarin is contraindicated in pregnancy, as it passes through the placental barrier and may cause bleeding in the fetus; warfarin use during pregnancy is commonly associated with spontaneous abortion, stillbirth, neonatal death, and preterm birth. Coumarins (such as warfarin) are also teratogens, that is, they cause birth defects
  • 45. Reference  Essential Of Medical Pharmacology –K.D. Tripathi 7 edition  Essential Of Pharmacotherapeutics – F.S.K. Barar 4 edition  https://www.rxlist.com/heparin-drug.htm#interactions  https://www.rxlist.com/search/rxl/coumadin