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MEDICINES AFFECTING THE BLOOD SYSTEM
Kharkov National Medical UniversityDepartment of Pharmacology and Medical Prescription
assistant Gordiychuk D.
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•Peripheral blood (circulating in vessels)•Bloodforming (Hemopoietic) organs:
the red bone marrow,
lymphatic nodes, and
spleen•Bloodbreaking organs (liver, spleen)•Neurohumoral regulation system
THE SYSTEM OF BLOOD CONSISTS OF:
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BLOOD CONSTITUENTS
Drugs acting on haemopoiesis
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Red Blood Cells Erythrocytes
• Place of formation – the red bone marrow
• Period of life ≈ 120 days• Functions:- Transport (respiratory, nutritional, excretory
function)- Defense- Regulation of blood рН
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Anemia can be considered to be a syndrome, not a diagnosis
The main types of anaemias are as follows:─ Iron deficiency, ─ B12-vitamin and folic acid deficiency, ─ Hypoplastic anaemia─ Hemolytic anaemia
DISORDERS OF ERYTHROPOIESISANEMIAS
Anaemia is a decrease of erythrocytes and/or hemoglobin in blood
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Hypochromic anemia
Rather wide-spread type of anemia
Decreased amount of iron in the organism makes it not possible to synthesize nessisary amount of hemoglobin
Iron deficiency is a common problem, especially for women
5% of women between the ages of 20 and 49 have iron deficiency with anemia and 11% have iron deficiency without anemia
1. IRON DEFICIENCY ANEMIA
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SYMPTOMS OF ANEMIA
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IRON ABSORBTION IN THE GASTROINTESTINAL TRACT
• Only ionized iron can be absorbed
Fe2+ is absorbed best of all• HCl facilitates absorption
as it converts elemental iron into ionized form• Ascorbic acid facilitates absorption
as it converts Fe3+ into Fe2+ • calcium, antacids, tetracycline and
chloramphenicol inhibit Fe2+ absorption • Fe2+ binds to apoferritin and in the form of ferritin
(with Fe3+) crosses intestinal epithelium
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Step 2 in blood
only Fe2+ is included in hemoglobin
but Fe3+ is transported by
transferrin !
IRON METABOLISM:
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For parenteral – only Fe3+ !
What iron compounds should be used as drugs for parenteral administration: Fe2+ or Fe3+ ?
PHARMACOLOGICAL CORRECTION OF THE HYPOCHROMIC ANEMIA -
IRON SUPPLEMENTATION
and for peroral – Fe2+ and Fe3+ is possible
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NB! Iron-containing drugs for peroral administration should never be administered at one time with iron-containing drugs for parenteral administration !
Transferin is in a limited amount!When transferrin is saturated by iron coming from the GIT poisoning by iron administered parentally is highly possible because it would be present in blood in free form that is toxic !
Why ?
Desferal is an antidote for iron
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Erythropoiesis stimulants (antianaemics)1. IRON-CONTAINING MEDICINES
FOR ENTERAL ADMINISTRATION
Fe2+ compoundsFerrous sulphate
Ferro-gradumet
Ferrous glucanate
Fe3+ compoundsFerrous saccharate
Ferrous hydroxide polymaltose complex
Ferrous protein-acetyl-aspartylate
Combined drugs:
Ferroplex
Feramide
Hemopheron
Sorbifer durules
FOR PARENTERAL ADMINISTRATION
Fe3+ compounds
Ferrous hydroxide polymaltose complex
Ferrous saccharate
Ferrum-lek (dextrane containing complex)
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Pharmacodynamics (effects) → IndicationsIncreases amount of the erythrocytesIncreases saturation of erythrocytes
by haemoglobin Improvement of the tissues
oxygenationThe reduction of symptoms of anemia
(weakness, paleness, tachycardia etc.) which begins in 5-7 days after the start of treatment
Prevention and treatment
of iron deficiency
in hypochromic anaemias
IRON-CONTAINING MEDICINES
Iron-containing medicines are donors of an iron ion and stimulate the synthesis of haemoglobin
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Side effects → ContraindicationsDyspepsia, pain in the epigastric area, intestinal colics, seldom - ulceration of the GIT
Constipation (resulting from binding of iron to H2S in the intestine and bowels)
Teeth darkness (resulting from binding of iron to H2S in the oral cavity and forming of black compound FeS)
Black colour of feces imitating intestinal bleeding
Nausea, vomiting, hemosiderosis, hypotension – in parenteral administration
Diseases of the GIT, anaemias that are not connected with the deficiency of iron in the organism
IRON-CONTAINING MEDICINES SIDE EFFECTS
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• Hyperchromic anemias• Characterized by presence of megaloblasts in
blood
• Lack of vitamin B12 or folic acid leads to the disorder of erythropoisis due to the
supression of DNA synthesis (megaloblasts – abnormally large cells are formed because of disorder of cell division and imbalance
between nucleus and cytoplasm development)
Note that blood cells are one of the most intensively renewed in the body
so they are one of the first to suffer in DNA and protein synthesis suppression
2. B12-DEFICIENCY AND FOLIC ACID DEFICIENCY ANAEMIAS
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Possible symptoms of hyperchromic anemia:
• Disorders of peripheral sensitivity or tingling
• Glossitis
• CNS disorders (loss of balance, personality changes)
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B12 binds to intrinsic Castle
factor in the stomach and is
absorbed by endocytosis in the intestine
and concentrates in the liver,
storage supply in the liver is enough for
several years
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Folic acid is water-soluble
and is absorbed in
small intestine and
concentrates in the liver, but storage
supply in the liver is enough
for several months only
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CYANOCOBALAMINE (VITAMIN B12) PROPERTIES
• transforms megaloblastic hemopoiesis into normoblastic one, normalizes the amount of erythrocytes, leucocytes and thrombocytes in blood
• takes part in the synthesis of myelin and acetylcholine, decreases neurological disturbances connected with megaloblastic anemia
• takes part in the function of the epithelium and decreases disturbances in tongue mucosa
The mechanism of actionpromotes the synthesis of the DNA Intensifies the cells’ division
and the formation of erythrocytesas well as other highly divisible cells
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INDICATIONSFOR CYANOCOBALAMINE
(VITAMIN B12)
Hyperchromic megaloblast anemia
Hypoplastic anemia
Radiation sickness
Neurological diseases
Liver diseases
Dystrophy in children
Glossitis
Side effects: allergy, hypercoagulation, tachycardia, pain in the heart, worsen in angina pectoris
FOR FOLIC ACID (VITAMIN Bc)
Hyperchromic megaloblast anemia
Chronic gastro-enteritis
In pregnancy for the prophylaxis of neurological pathology of the fetus and newborn
Note that folic acid in hyperchromic anemias should be used only in combination with B12!
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Erythropoietin is the glycopeptide hormone that stimulates erythropoiesis
It is produced by kidneys as a response for hypoxiaThe higher level of the renal hypoxia is, the more erythropoietin is produced
Nowadays with the help of the genetic engineering human erythropoietins α, β, ώ have been obtained
They are mainly used to normalize erythropoiesis in patients with chronic kidney diseases
ERYTHROPOIETIN
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Pharmacodynamics (effects) → Indications Increase in erythrocytes and reticulocytes amount, increase in the level of hemoglobin
Anaemias caused by the chronic renal insufficiency, HIV- infection, after usage of cytostatics, in preterm born infants, hypo- and aplastic anaemias
Side effects → Contraindications Increase of BP Hypertension
The mechanism of actionStimulation of proliferation and differentiation of cells of the red bone marrow because of activation of the specific erythropoietin’s receptors
ERYTHROPOIETIN
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-Sodium phosphate solution labeled by phosphorus-32 --Imiphos
The mechanism of actionsuppresses the erythropoietic part of the bone marrow
Side effect: Anemia
Contraindications: Erythropenia, HIV-infection
ERYTHROPOIESIS INHIBITORS
Indication:Erythremia - it is an increased amount of immatured, inferior erythrocytes in blood because of their increased production by the red bone marrow
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WHITE BLOOD CELLS
•Place of formation – the red bone marrow, thymus, lymph nodes
•Period of life – from few days to 10 years
•Function: defence- Phagocytosis- Immunity (cellular and humoral)- Synthesis of antibodies with antibacterial and antitoxic properties- Synthesis of enzymes that increase permeability of capillaries
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FORMATION OF BLOOD CELLS
Leukopoiesis is the process of leukocytes formation and maturation.Leukopenia is the decreased amount of leukocytes in blood. Lymphogranulomatosis is a malignant tumour of the lymphoid tissue.
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The deficient production of leukocytes and decrease of their
amount in blood (leukopenia, agranulocytosis)
leukopoiesis stimulants and colony-stimulating factors that accelerate the formation of leukocytes in the bone marrow are used
an increased production of inferior leukocytes
(leukosis, leukemia)
leukopoiesis inhibitors are needed
DISORDERS OF LEUKOPOIESIS AND THEIR CORRECTION
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Leukopoiesis stimulants –Nucleic acid derivatives Sodium nucleinate– Pyrimidine derivatives Methyluracilum Pentoxilum– Colony-stimulating factors (CSF) Lenograstim Molgrastim
The mechanism of actionThey bind to specific receptors of myeloid cell-precursors of the neutrophilic group, which are necessary for the matured leukocytes formation. It leads to increase of the matured leukocytes synthesis.
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Pharmacodynamics (effects) → Indications
Leukopoiesis stimulants: the increase of the matured leukocytes amount in blood
Leukopenia including those caused by the therapy with antitumour medicines, radiation sickness, HIV-infection
Side effects → Contraindications
Leukopoiesis stimulants: dyspepsia
Diseases of the GIT
Leukopoiesis stimulants
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Leukopoiesis inhibitors
Methotrexate
Mercaptopurine
Prednisolone
Leukopoiesis inhibitors that suppress the formation of leukocytes.
Pharmacodynamics (effects) → Indications Leukopoiesis inhibitors: decrease of the leukocytes amount in blood
Leukemias, lymphogranulomatosis
Side effects → Contraindications Leukopoiesis inhibitors: inhibition of hemopoiesis, dysfunction of liver and kidneys
Leukopenia, anaemia, thrombocytopenia, diseases of liver and kidneys
Teratogenecity and embryotoxicity Pregnancy, lactation
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Drugs acting on haemostasis
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• Place of formation – the red bone marrow
• Period of life – 8-12 days
• Function:
The blood clotting
THROMBOCYTES
Physiological propertiesPhysiological properties::AdhesionAdhesion – – ability to stick to the foreign and damaged surfaceability to stick to the foreign and damaged surface
AggregationAggregation – – ability to form a clump (cork)ability to form a clump (cork)
AgglutinationAgglutination – – pasting of thrombocytes one with anotherpasting of thrombocytes one with another
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damage of vessels 1 phase of blood clotting – vasoconstriction
2 phase – formation of thrombocytes cork
3 phase – thromb (clot) formation from fibrin
(marked yellow) and blood cells
THE BLOOD CLOTTING
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COAGULATION HEMOSTASIS
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I – formation of blood activator of plasminogen– extrinsic and intrinsic pathways
II –conversion of plasminogen to plasmin
III – plasmin disunites fibrin to peptides and amino acids (splits fibrin)
FIBRINOLYSISIt is the process of fibrin dissolution
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I – A decrease in blood coagulation and/or increase in fibrinolysis
RESULT IN BLEEDING
II – An increase in blood coagulation and/or decrease in fibrinolysis
RESULT IN THROMBOSIS, thromboembolism, syndrome of disseminated intravasal blood
coagulation
PATHOLOGY OF HEMOSTASIS AND FIBRINOLYSIS
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Drugs acting on hemostasis
• I. Drugs promoting haemostasis • 1. Procoagulants• 2. Fibrinolysis inhibitors• 3. Heparin antagonist• II. Drugs preventing clot formation• 1. Anticoagulants• 2. Antiplatelet drugs (Antiaggregants)• III. Thrombolytics
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ANTICOAGULANTS these are drugs decreasing blood
coagulation
1. Direct acting
- heparins (Heparin, LMW heparins: Enoxaparin, Fraxiparine,
Dalteparin sodium)
- factor Xa inhibitors (Rivaroxaban, Apixaban)
- thrombin inhibitors (Lepirudin, Desirudin, Bivalirudin)
2. Indirect acting
• coumarins
• indandiones
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Direct-acting anticoagulants
Systemic-acting Local-acting
HIGH MOLECULAR HEPARINS HeparinLOW MOLECULAR HEPARINS
Calcium adroparin
Fraxiparine
Heparin ointment
The mechanism of action
Direct-acting anticoagulants have highly negative charge, which promote the formation of the complex with positively charged coagulation proteins. As a result, coagulation proteins are inhibited.
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Pharmacodynamics (effects) → Indications Direct-acting anticoagulants
Anticoagulant (inhibition of blood coagulation at all phases)
Myocardial infarction, direct blood transfusion, surgery on the heart or vessels. Prophylaxis and treatment of embolism and vascular thrombosis
Fibrinolysis activation, improvement of blood rheological properties
Prophylaxis of thrombosis after coronary vessels shunting and prosthetics of the heart valves
Antiaggregant (inhibition of adhesion and aggregation of thrombocytes and erythrocytes, normalization of the blood rheological properties, improvement of microcirculation of the brain, myocardium, retina etc.)
Thrombophlebitis, hypercoagulation syndrome
Hypolipidemic (decrease of the lipid level in blood)
Prophylaxis and treatment of atherosclerosis
Coronarodilating (improvement of blood circulation in the coronary vessels)
Myocardial infarction, stable angina of tension
Immunosuppressive Direct blood transfusion, surgery on the heart or vessels, rheumatism, bronchial asthma, glomerulonephritis, hemolytic anemia, renal transplantation, endocarditis
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HeparinMechanism of action
• Heparin binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that results in its activation up to 1000-fold .
• The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa.
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Is administered intravenously (IV), intramuscularly (IM), subcutaneously (SC), topically
begins to act immediately after IV administration and acts during 4-6 hours
begins to act in 15-30 min after IM administration and acts during 6-8 hours
begins to act in 30-60 after SC administration and acts during 8-12 hours
Is metabolized in the liver by heparinase and is excreted with urine
HEPARINE PHARMACOKINETICS
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SIDE EFFECTS OF HEPARINEBleeding
Hematomes
Micro- and macrohematuria
Thrombocytopenia
Allergy
Osteoporosis
Hair silvering
Protamine sulfate is an antidote for heparin
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low molecular weight heparin
do not inhibit thrombin (acts through supression of Xa factor), so the control of activated partly thromboplastin time (laboratory analysis) is not needed
Is administered subcutaneously once a day
has higher bioavailability, longer duration of action, less binding to plasma proteins (in comparison with heparin)
is used for the treatment of thromboflebitis, prevention of thrombus formation after surgeries
FRAXIPARINE
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Factor Xa ihibitors
• Rivaroxaban• ApixabanMechanism: they act directly upon Factor X
in the coagulation cascade, without using antithrombin as a mediator
Advantages over LMW heparins and indirect acting anticoagulants:
1. Oral administration 2. Absence of hypoprothrombinemia
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Warfarin
Ethyl bisoumacetate
Acenocumarol
Fenindion
Indirect-acting anticoagulants have no influence on coagulation factors directly in the bloodThey supress the biosynthesis of coagulation proteins (proconvertin and prothrombin) in the liver as a result of antagonism with vitamin K.
The mechanism of action
INDIRECT-ACTING ANTICOAGULANTSNote that these
drugs are vitamin K antagonists!
Pharmacological effects
─ a decrease in blood coagulation ─ an increase in fibrinolysis─ a decrease in lipids concentration in blood
Oral Anticoagulants Vitamin K Antagonists (Coumarins)Vitamin K Antagonists (Coumarins)
• Vitamin K is co-factor for the hepatic synthesis of clotting factors II, VII, IX & X
Vit. K Vit. K epoxide (active form)
By Vit.k reductase
warfarin
Warfarin inhibits Vit. K reductase no active form of Vit. K no synthesis of clotting factorsWarfarin inhibits Vit. K reductase no active
form of Vit. K no synthesis of clotting factors
Vitamin K AntagonistsWarfarin
Warfarin has 100% oral bioavailability, high plasma protein binding & long plasma t1/2 of 36 hours
A high loading dose followed by an adjusted maintenance dose
Warfarin is contraindicated with pregnancy as it crosses the placental barrier and is teratogenic in the first trimester & and induce intracranial hemorrhage in the baby during delivery
Warfarin is metabolized by hepatic Cytochrome P450 enzymes with half-life of 40 hrs
Warfarin Drug Pharmacokinetic & Pharmacodynamic Interactions
Potentiating warfarin Inhibitors of hepatic P450
enzymes (cimetidine, cotrimoxazole, imipramine, amiodarone)
Platelet aggregation inhibitors (NSAIDs e.g. aspirin)
3rd generation cephalosporins* Drugs displacing warfarin from
binding sites (NSAIDs) Drugs reducing the availability of
vitamin K Hepatic disease(↓ clotting factors)&
hyperthyroidism (↑ basal metabolic rate)
Inhibiting Warfarin Vitamin K in some
parenteral feed Inducers of hepatic P450
enzymes (rifampicin, barbiturates, … etc)
Reduction of GIT absorption (cholestyramine)
Diuretics Hypothyroidism
*Cephalosporins potentiate warfarin’s effect by killing vit.k producing normal flora
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INDICATIONS and SIDE EFFECTS FOR INDIRECT-ACTING ANTICOAGULANTS
Prophylaxis and treatment of venous and arterial thrombosis, thromboembolism, thrombophlebitis, obliterating endarteritis, hypercoagulation syndrome, coronary insufficiency, miocardial infarction, ischemic insult, prevention of thrombosis after surgeries
Side effects:BleedingForming of hematomes
Hematuria
Dyspepsia
Supression of the liver function
Allergy
Nb!
Index of prothrombin
(laboratory value) should be
controlled for the safety of the
therapy!
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Pharmacodynamics - Indications
Fibrinolytic - dissolution of fibrin filaments of the recent (up to 3 days) thrombs
Venous and arterial thrombosis, acute myocardial infarction, pulmonary embolism
FIBRINOLYTIC DRUGS (THROMBOLYTIC DRUGS)Direct-acting: Fibrinolysin
Indirect-acting: Urokinase
Streptokinase
Alteplase
Note that these drugs are able to produce the lysis of the blood clot!
Fibrinolytics (fibrinolysis activators) transform profibrinolysine (plasminogen) into its active form - fibrinolysine (plasmin), decrease the level of fibrinogen in the blood plasma, inhibit aggregation of thrombocytes and the activity of natural blood procoagulants, i.e. they activate the fibrinolytic system (fibrinolysis)
The mechanism of action
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Is the protein from the donor’s plasma,the active factor of fibrinolysis
Is administered by intravenous infusion
has a direct action on fibrin and dissolves fibrin clot in the first hours after its formation
Is used for the treatment of acute thrombosis, acute miocardial infarction, thrombophlebitis
may cause bleeding resulting from an increase in fibrinolysis, allergy, anaphylaxis, arrhytmia, hypotension
contraindicated in bleeding, a cerebral vascular accident, recent trauma of the brain, surgery, noncontrolled hypertension
FIBRINOLYSIN
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Is the proteolytic enzyme from hemolytic streptococcushas a plasma half life of 23 min, is administered by intravenous infusion (intracoronary infusion in myocardial infarction)
acts indirectly,promotes the conversion of plasminogen to plasmin, causes systemic activation of fibrinolysis and degradation both of fibrin and fibrinogen resulting in dissolving of the thrombus
is more potent than fibrinolysindoes not cause arrhytmia
STREPTOKINASE
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Is a tissue plasminogen activator,product of biotechnology
has a half life of 5 min, is administered by intravenous infusion
has a high affinity for fibrin
act selectively on plasminogen bound with thrombus
ALTEPLASE (ACTILISE)
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DRUGS THAT DECREASE PLATELET AGGREGATION (ANTIAGGREGANTS)
–COX-inhibitorsAcetylsalicylic acid (aspirin)
–Inhibitors of phosphodiesterase Dipyridamole
–Inhibitors of ADP-mediated aggregationTiclopidine (Ticlid)Clopidogrel
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Acetylsalicilic acid blocks synthesis of thromboxane A2 by inhibiting COX1
Dipiridamol increases cAMP concentrations in the platelets that supresses clotting associated with TXA2
Clopidogrel and ticlopidine block ADP-receptors in the platelet membrane
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Anti-platelet effect occurs in low doses
100-300 mg
The effect lasts more than 48 hrs (till 7 days)
ANTI-PLATELET EFFECT OF ASPIRINE
The inhibition of COX-1 is irreversible Why?
Platelets have no nucleus and they can not synthesize new COX-1
So the platelet that has once contacted with aspirin never would take part in blood clotting
And average period of platelet’s life is 7 days
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ANTI-PLATELET EFFECT OF DIPYRIDAMOLE
Dipyridamole inhibits adenosine desaminase and phosphodiesterase in platelets, increases cAMP concentrations in the platelets and inhibits TXA2 synthesis that leads to decrease in platelet aggregation
It also increases prostacycline level
Remember antianginal drugs!Dipyridamole also increases myocardial oxygen supply by dilating coronary vessels but causes «stealing sydrome» - redistribution of coronary blood flow in favour of the normal areas of myocardium with the worsening of blood supply in the area of ischemia
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ANTI-PLATELET EFFECT OF TICLOPIDINE
Ticlopidine irreversibly blocks purinergic receptors for ADP in platelet membranes
The inhibition of ADP-induced expression of glycoprotein IIa/IIIa receptors in the platelet membranes decreases platelet aggregation
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Antiaggregants • Dipyridamol• Ticlopidine• Acetylsalicylic acid
Pharmacodynamics - Indications
Antiaggregant effect
Prophylaxis and treatment of the hypercoagulation syndrome, chronic coronary insufficiency.
Prophylaxis of ischemic stroke and encephalopathies
Side effects → Contraindications
Bleedings, thrombocytopenia
Low blood coagulability, increased permeability of vessels, peptic ulcer
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THE PHARMACOLOGICAL “FACE” OF ANTICOAGULANTS AND ANTIAGGREGANTS
• * - nadroparin is more safe than heparin;• ** - dipyridamol`s activity is similar to aspirin, and ticlopidine is more active
than aspirin.
Medicines Route of administration
Onset of effect
Duration of effect
Heparin i/v 5 min 2-6 h
i/m 15-30 min 2-8 h
s/c 30-40 min 4-12 h Nadroparin* s/c 3-4 h up to 6 h Acenocumarol per os 24-48 h 2-4 days Fenindion per os 10-24 h 24-72 h Dipyridamol** per os, i/v Ticlopidine** per os 1-2 days 8-10 days Acetylsalicylic acid
per os 20-30 min up to 7 days
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Medicines that increase blood coagulation promote stopping bleedings they may be used locally as well as for resorptive action
Antifibrinolytic agents (inhibitors
of fibrinolysis)
Hemostatics Coagulants of the synthetic, animal,
plant origin Systemic-acting
Local-acting
Aminocapronic acidTranexaemic acidTrasylol (Aprotinin)
Fibrinogen
Calcium chloride
Menadion
Thrombin
Hemostatic sponge
Vicasol
Gelatin medical
Water pepper herb
Nettle herb
MEDICINES INCREASING BLOOD COAGULATION(HEMOSTATICS, ANTIHEMORRHAGIC MEDICINES)
Classification of medicines
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Antifibrinolytic agents inhibit the action of plasminogen and the action of plasmin;
suppress the kinins’ system and the activity of fibrinolysis
Hemostatics are the natural components of the blood coagulation system.
Coagulants of the synthetic, animal and plant origin decrease permeability of the vascular wall, increase the blood viscosity, slow the blood flow, promote conditions for forming thrombi
MEDICINES INCREASING BLOOD COAGULATION(HEMOSTATICS, ANTIHEMORRHAGIC MEDICINES)
The mechanism of action
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Pharmacodynamics (effects) → Indications
Hemostatic effect: stoppage or decrease of bleedings
Inhibitors of fibrinolysis: bleedings caused by the increased fibrinolysis, thrombocytopenia, including ones caused by peptic and duodenal ulcer, postnatal bleedings
Hemostatics: bleedings in surgery, obstetrics, traumatology caused by deficiency of blood coagulation system factors: capillary, from parenchymal organs, local bleedings (nasal, extraction of teeth, etc.)
Coagulants of synthetic, animal and plant origin: hemorrhagic diathesis, metrorrhagia, nasal, renal, intestinal bleedings
Side effects → Contraindications
Increase of blood coagulation
Predisposition to thrombosis, thromboembolism
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THE PHARMACOLOGICAL “FACE” OF MEDICINES INCREASING THE BLOOD COAGULATION
Medicines The route of administration
Other effects / peculiarities
Aminocapronic acid per os, i/v Anti-inflammatory, anti-allergic
Fibrinogen i/v, locally It is a component of the blood coagulation system
Calcium chloride per os, i/v
Thrombin locally
Menadion per os, i/m, i/v A synthetic water soluble vitamin K analogue
Hemostatic sponge locally A mixture of CaCl2 and thrombin on the solid carrier
Carbazochrome locally, s/c, i/v A synthetic solid
Nettle herb per os Anti-inflammatory,
capillary-stabilizing
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PLASMA SUBSTITUTESClassification
I. Salines:- Isotonic NaCl (0,9%)- Ringer-Loc sol.- Acesol- TrysolII. Alkaline solutions:- Sodium hydrocarbonate (NaHCO3)III. Drug contains the components of human
blood:- human albumin- dry plasma
Classification
IV. Synthetic plasma expanders:
- Reopoliglukine
- Neogemodes
- Gekodes
V. Glucose:
- Isotonic Glucose sol. (5%)
- Hypertonic Glucose sol. (10-40%)
Indications for plasma expanders
• Salines: compensation for loss of fluid in burns, diarrhea, vomiting; detoxification, drug dissolution - antibiotics, analgesics, cardiac glycosides; violations of water-salt state, correction of hemodynamic.
Contraindications: threat of lung or brain edema, closed head injury with intracranial hypertension.
• Alkaline solutions: metabolic acidosis.
Indications for plasma expanders- Drug contains the components of human blood:
hemodynamic instability in bleeding, burns, liver diseases, malnutrition in children; protein deficiency, dystrophy, as an agents for detoxification and substitutes in hemophilia B.
Side effects: allergic reactions, caused by individual hypersensetivity.
• Synthetic plasma expanders: blood loss, shock, burns, microcirculation disturbances, peritonitis, sepsis, diseases of the liver, intoxication in purulent and other diseases, prevention of thrombosis.
Side effects: allergic reactions, lowering of blood pressure.
• Glucose: (5% sol.) - replenishing the blood stream as plasma substitute, normalization of blood osmotic pressure.
(10-40%) - dangerous swelling of tissues, brain, lungs; hypoglycemia, infectious processes, degeneration and atrophy of the liver, decompensated cardiac function, hemorrhagic diathesis, poisoning by narcotic analgesics, hydrogen cyanide, carbon monoxide, aniline, fosfogenom, shock and collapse.
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Thank you!