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GROUP 2

Report

BLOOD DRUGS

Submitted to:

Dr. Sherwin Banan

Submitted by:

Alonzo, Carmela

Pacual, JP Brando

Galang, Roan Eina

Olivas, Nanette

Labbuanan, Kristell Anne

Sanao, Bryan Jay

Domingo, Rafael

Santos, Bryan

Baculi, Daryll

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NAMES

NO ATTENDANCE

NO CONTRIBUTION

NO REPORT

NO GRADE

Alonzo, Carmela

Pascual, JP Brando,

Galang, Roan

Olivas, Nanette

Santos, Bryan

Domingo, Rafael

Labbuanan, Kristell Ann

Sanao, Bryan

Baculi, Daryll

February 15, 2015

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BLOOD DRUGS

I. OVERVIEW

The vascular system delivers oxygen and nutrients to all body cells and removes waste

products from tissues. This closed system functions as a pressure system, with blood flowing

continuously from high-pressure to low-pressure areas. Injury of a blood vessel compromises

the closed system, causing blood to flow out of the injured vessel (now a low-pressure area).

With severe injury to a vessel, the entire circulatory system may be compromised and the

patient could die.

Blood vessel injuries are common, occurring, for instance, when someone hits the edge of a

table, coughs too hard, or falls down. They initiate a series of normal reactions that stops blood

flow and maintains balance within the system. The reactions include:

reflex vasoconstriction

platelet aggregation

blood coagulation (clot formation), which causes blood to solidify

clot resolution, which returns blood to the fluid state.

In many clinical situations, drugs are used to slow or stop this process, with the goal of

preventing tissue damage from the decreased blood flow that occurs when the clotting process

cuts off blood supply to an area. The succeeding discussion reviews the processes the body uses

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to maintain the cardiovascular system and discusses the mechanisms of action, benefits, and

risks of drugs used to alter coagulation.

After an injury to a blood vessel, the vessel constricts. With a small injury, constriction

typically seals the open space, allowing blood to flow and helping the vessel to heal. A larger

injury exposes endothelial cells lining the vessel to blood flowing through it, causing platelets to

adhere to the injured area.

When a platelet adheres, it releases chemicals that attract more platelets, in turn drawing

even more platelets to the area in a process called platelet aggregation. Consequently, a

platelet plug forms. In some cases, this is enough to seal the leak and keep pressures stable

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while the vessel heals. In more severe injuries, the vessel wall injury activates Hagemann factor,

a clotting factor. Activated Hagemann factor triggers activation of other clotting factors,

initiating the clotting cascade. The cascade ends in conversion of prothrombin to thrombin;

activated thrombin initiates clot formation.

All clotting factors are made in the liver and require vitamin K for their formation. Calcium is

the catalyst that speeds the clotting cascade. Activated thrombin breaks down fibrinogen into

fibrin. An insoluble protein, fibrin forms a clot at the site. The change of blood from fluid to

solid form stops blood flow in the vessel.

In this process, called the intrinsic process, a clot forms within the vessel. A similar process,

the extrinsic process, occurs in blood that has leaked out of the vessel at the injury site. This

process produces a seal within the vessel, along with a seal outside the vessel. While this allows

the vessel wall to seal and heal, it could interrupt blood flow to tissues beyond that point,

causing ischemia or even cell death. When Hagemann factor is activated and triggers the

clotting cascade, it also causes plasminogen conversion to plasmin. Plasmin dissolves fibrin and

returns blood to the fluid state. This is the body’s clot-dissolving mechanism. Plasminogen,

made in the liver, also is activated by such conditions as stress, fever, and various enzymes. This

process protects against the harmful effects of clot formation.

Indications for drugs that alter coagulation

In certain clinical situations for instance, coronary artery disease, immobility, atrial

fibrillation, and joint replacement interfering with coagulation helps prevent clots that could

impede blood flow and cause tissue damage or death. Patients with coronary artery disease, for

example, have narrowed vessels. An immobile patient loses the protective massaging of veins

caused by muscle fiber contractions; also, blood pools and doesn’t return to the heart

efficiently. With atrial fibrillation, blood pools in the heart’s auricles and may clot. The artificial

parts of a hip or knee replacement initially may damage a blood vessel, leading to clotting.

All drugs that alter coagulation interfere with the normal protective reflexes. As a nurse,

you need to be aware of the dangers of eliminating these reflexes, which could include serious

or even fatal bleeding episodes. Drugs that alter coagulation include platelet inhibitors and

anticoagulants

Platelet inhibitors are often the first line of defense in preventing vascular clots; they

don’t affect clots that already have formed. These drugs block platelets’ ability to adhere and

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aggregate to form the platelet plug, the first step in sealing the vascular system and preventing

blood loss into body tissues.

Current platelet inhibitors include abciximab (ReoPro), anagrelide (Agrylin), aspirin,

cilostazol (Pletal), clopidogrel (Plavix), dipyridamole (Persantine), eptifibatide (Integrilin),

ticlopidine (Ticlid), ticagrelor (Brilinta), and tirofiban (Aggrastat). These drugs are used to treat

cardiovascular diseases in which vessels become occluded, as well as to maintain venous and

arterial grafts and prevent cerebrovascular occlusion. They’re also given as adjuncts to

thrombolytic therapy in treating myocardial infarction (MI) and preventing post-MI reinfarction.

Ticagrelor, released in 2011, is indicated only to prevent thromboembolic events in acute

coronary syndrome. Its black-box warning cites the risk of excessive bleeding and dangers of

sudden withdrawal, which can trigger an acute cardiovascular event.

Most platelet inhibitors block receptors on platelets to prevent adhesion; anagrelide

prevents platelet formation in the bone marrow. Bleeding (including bleeding caused by

toothbrushing and excessive bleeding after injury) is the most common adverse effect. Easy

bruising also may occur.

II. THROMBUS VS. EMBOLUS

Thrombosis is the formation of an unwanted blood clot in the vessel and is the most common

abnormality of homeostasis. Thrombotic disorder treated with drugs such as: anticoagulant and

fibrinolytics.

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o Acute myocardial infarction- the blood clots blocks the coronary arteries which may

produce a heart attack.

o Deep vein thrombosis-is the formation of a blood clot or thrombus within a deep vein,

predominantly in the legs.

o Pulmonary embolism- is a condition in which a part of a blood clot in a vein breaks away

and travel through the heart and into the pulmonary circulatory system

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o Acute ischemic stroke- the blood supply to part of the brain is cut off because

atherosclerosis or a blood clot has blocked a blood vessel.

Bleeding disorders involving the failure of homeostasis are less common than

thromboembolic disease:

Hemophillia, the blood does not clot properly and bleeding persists. Blood does not clot

normally because it lacks sufficient blood clotting protein (clotting factor). These are treated

with dietary supplement of vitamin k. Anemia; red blood cell count stays persistently low, or

below 4million. Iron deficiency anemia is a common complication of pregnancy. It is treated

with iron supplement and iron rich foods including egg, cereals, green leafy vegetable and meat

specially the liver.

THROMBUS vs EMBOLUS

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Thrombus is a clot that adheres to a vessel wall immobile. Embolus is an intravascular

clot that floats in the blood. Mobile, thus a detached thrombus becomes an embolus. Both

thrombi and emboli are dangerous, because they may occlude blood vess els and deprive

tissues of oxygen and nutrients.

Arterial thrombosis most often occurs in medium-size vessels rendered thrombogenic

by surface lesions on endothelial cells caused by atherosclerosis. In contrast, Venous

thrombosis, is triggered by blood stasis or inappropriate activation of the coagulation cascade,

frequently result of a defect in the normal hemostatic defense mechanisms.

III. PLATELET RESPONSE TO VASCULAR INJURY

Physical trauma to the vascular system, such as a puncture or a cut, initiates a complex

series of interactions between platelets, endothelial cells, and the coagulation cascade. These

interactions lead to hemostasis or the cessation of blood loss from a damaged blood vessel.

Platelets are central in this process. Initially there is vasospasm of the damaged blood vessel to

prevent further blood loss. The next step involves the formation of a platelet-fi brin plug (clot)

at the site of the puncture. The creation of an unwanted thrombus involves many of the same

steps as normal clot formation, except that the triggering stimulus is a pathologic condition in

the vascular system rather than an external physical trauma.

A. Resting Platelets

Platelets act as vascular sentries, monitoring the integrity of the endothelium. In the

absence of injury, resting platelets circulate freely, because the balance of chemical signals

indicates that the vascular system is not damaged.

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B. Platelet Adhesion

When the endothelium is injured, platelets adhere to and virtually cover the exposed

collagen of the subendothelium. This triggers a complex series of chemical reactions, resulting

in platelet activation.

C. Platelet Activation

Receptors on the surface of the adhering platelets are activated by the collagen of the

underlying connective tissue. This causes morphologic changes in platelets and the release of

platelet granules containing chemical mediators, such as adenosine diphosphate (ADP),

thromboxane A2, serotonin, platelet-activation factor, and thrombin. These signaling molecules

bind to receptors in the outer membrane of resting platelets circulating nearby. These

receptors function as sensors that are activated by the signals sent from the adhering platelets.

The previously dormant platelets become activated and start to aggregate. These actions are

mediated by several messenger systems that ultimately result in elevated levels of calcium and

a decreased concentration of cAMP within the platelet.

D. Platelet Aggregation

The increase in cytosolic calcium accompanying activation is due to a release of

sequestered stores within the platelet. This leads to:

1) the release of platelet granules containing mediators, such as ADP and serotonin that

activate other platelets;

2) activation of thromboxane A2 synthesis; and

3) activation of glycoprotein (GP) IIb/IIIa receptors that bind fibrinogen and, ultimately,

regulate platelet-platelet interaction and thrombus formation. Fibrinogen, a soluble plasma GP,

simultaneously binds to GP IIb/IIIa receptors on two separate platelets, resulting in platelet

cross-linking and platelet aggregation.

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This leads to an avalanche of platelet aggregation, because each activated platelet can

recruit other platelets.

E. Formation of a Clot

Local stimulation of the coagulation cascade by tissue factors released from the injured

tissue and by mediators on the surface of platelets results in the formation of thrombin (Factor

IIa). In turn, thrombin, a serine protease, catalyzes the hydrolysis of fibrinogen to fibrin, which

is incorporated into the plug. Subsequent cross-linking of the fibrin strands stabilizes the clot

and forms a hemostatic platelet-fibrin plug.

F. Fibrinolysis

During plug formation, the fibrinolytic pathway is locally activated. Plasminogen is

enzymatically processed to plasmin (fibrinolysin) by plasminogen activators in the tissue.

Plasmin limits the growth of the clot and dissolves the fibrin network as wounds heal. At

present, a number of fibrinolytic enzymes are available for treatment of myocardial infarctions,

pulmonary emboli, and ischemic stroke.

IV. PLATELET AGGREGATION INHIBITOR

Platelet aggregation inhibitors decrease the formation or the action of chemical signals

that promote platelet aggregation.

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The platelet aggregation inhibitors inhibit cyclooxygenase-1 (COX-1) or block GP IIb/IIIa

or ADP receptors, thereby interfering in the signals that promote platelet aggregation. Since

these agents have different mechanisms of actions, synergistic or additive effects may be

achieved when agents from different classes are combined.

A. Aspirin

Stimulation of platelets by thrombin, collagen and ADP results in activation of platelet

membrane phospholipases that liberate arachidonic acid from membrane phospholipids.

Arachidonic acid is first converted to prostaglandin H2 by COX-1; prostaglandin H2 is further

metabolized to thromboxane A2, which is released into plasma.

B. Ticlopidine and clopidogrel

These drugs irreversibly inhibit the binding of ADP to its receptors on platelets and, thus,

inhibit the activation of the GP IIb/IIIa receptors required for platelets to bind to fibrinogen and

to each other.

Ticlopidine is approved for the prevention of transient ischemic attacks and strokes for patients

with prior cerebral thrombotic event. Adveres Drug reaction includes:

Neutropenia/Agranulocytosis

Thrombotic Thrombocytopenic Purpura (TTP)

Aplastic anemia

Clopidogrel is used to prevent thrombotic events associated with percutaneous coronary

intervention with or without coronary stent.

C. Abciximab

Stimulating platelet aggregation directed attempts to block this receptor on activated

platelets.

D. Eptifibatide and tirofiban

Similar to Abciximab

E. Dipyridamole

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Increases intracellular levels of cAMP by inhibiting cyclic nucleotide phosphodiesterase,

resulting in decreased thromboxane A2 synthesis. It may potentiate the effect of prostacyclin to

antagonize platelet stickiness and, therefore, decrease platelet adhesion to thrombogenic

surfaces.

V. BLOOD COAGULATION

The coagulation process that generates thrombin consist of two interrelated pathways,

the extrinsic and intrinsic system.

Extrinsic system more important system in vivo is initiated by the activation of clotting factor

VII by tissue factor or thromboplastin.

Intrinsic system triggered by the activation of clotting factor XII, following its contact in vitro

with glass or highly charged surface.

FORMATION OF FIBRIN

Both the extrinsic and intrinsic system involve in cascade of enzyme reaction that

sequentially transform various plasma factor(proenzyme) to their active (enzymatic) form. If

thrombin is not formed or , coagulation is inhibited. Each step in the activation process is

catalytic,(for example, one unit of activated factor Xa can potentially generate 40units of

thrombin, which will result to the production of large amount of fibrin at the site of injury)

ROLL OF CELL SURFACES

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Phospholipid-based protein-protein complex-consist of membrane surfaces provided by

phospholipid of activated platelets or activated endothelial cell, an enzyme, a substrate, and a

cofactor.

Calcium is essential to this process, bridging anionic phospholipid and y-carboxyglutamic

acid resisues of the clotting factor.

INHIBITORS OF COAGULATION

It is important that coagulation is restricted to the local site of the vascular injury,

Inhibitors of coagulation factors:

Protein C

Protein S

Antithrombin III

Tissue factor pathway imhibitor

The mechanism of action of several anticoagulant agents, including hrparin and heparin related

products, involves actiovation of these endogenous inhibitor(primarily Antithrombin III)

VI. ANTICOAGULANT

Anticoagulant medicines reduce the ability of the blood to clot (coagulation means

clotting). This is necessary if the blood clots too much, as blood clots can block blood vessels

and lead to conditions such as a stroke or a heart attack.

A. HEPARIN

Heparin injection is an anticoagulant. It is used to decrease the clotting ability of the

blood and help prevent harmful clots from forming in blood vessels. This medicine is sometimes

called a blood thinner, although it does not actually thin the blood. Heparin will not dissolve

blood clots that have already formed, but it may prevent the clots from becoming larger and

causing more serious problems.

Heparin is used to prevent or treat certain blood vessel, heart, and lung conditions.

Heparin is also used to prevent blood clotting during open-heart surgery, bypass surgery,

kidney dialysis, and blood transfusions. It is used in low doses to prevent the formation of blood

clots in certain patients, especially those who must have certain types of surgery or who must

remain in bed for a long time. Heparin may also be used to diagnose and treat a serious blood

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condition called disseminated intravascular coagulation. This medicine is available only with

your doctor's prescription.

This product is available in the following dosage forms:

Injectable

Solution

B. OTHER PARENTERAL ANTICOAGULANTS

1. LEPIRUDIN

Lepirudin is used in thinning the blood and preventing blood clots in patients with low

blood platelets caused by heparin. It may also be used for other conditions as determined by

your doctor.

Lepirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which

helps to prevent the formation of blood clots.

2. FONDAPARINUX

Fondaparinux is an anticoagulant medication chemically related to low molecular weight

heparins.

Fondaparinux is similar to enoxaparin in reducing the risk of ischemic events at nine

days, but it substantially reduces major bleeding and improves long-term mortality and

morbidity.

Fondaparinux is given subcutaneously daily. Clinically, it is used for the prevention

of deep vein thrombosis in patients who have had orthopedic surgery as well as for the

treatment of deep vein thrombosis and pulmonary embolism.

C. VITAMIN K ANTAGONIST

Vitamin K antagonists (VKA) are a group of substances that reduce blood clotting by

reducing the action of vitamin K. They are used as rat poisons but also

as anticoagulant medications in the prevention of thrombosis.

Mechanism of Action

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These drugs deplete the active form of the vitamin by inhibiting the enzyme vitamin K

epoxide reductase and thus the recycling of the inactive vitamin K epoxide back to the active

reduced form of vitamin K. The drugs are structurally similar to vitamin K and act as competitive

inhibitors of the enzyme. The term "vitamin K antagonist" is a misnomer, as the drugs don't

directly antagonise the action of vitamin K in the pharmacological sense, but rather the

recycling of vitamin K.Vitamin K is required for the proper production of certain proteins

involved in the blood clotting process.

The action of this class of anticoagulants may be reversed by administering vitamin K for

the duration of the anticoagulant's residence in the body, and the daily dose needed for

reversal is the same for all drugs in the class. However, in the case of the second generation

"super warfarins" intended to kill warfarin resistant rodents, the time of vitamin K

administration may need to be prolonged to months, in order to combat the long residence

time of the poison. The vitamin K antagonists can cause birth defects (teratogens).

VII. THROMBOLYTIC DRUGS

Acute thromboembolic disease in selected patients may be treated by the

administration of agents that activate the conversion of plasminogen to plasmin-a serine

protease that hydrolyzes fibrin and, thus, dissolves clots. Streptokinase, one of the first such

agents to be approved, causes a systematic fibrinolytic state that can lead to bleeding

problems. Alteplase acts more locally on the thrombotic fibrin to produce fibrinolysis. In the

case of acute myocardial infarction, the thrombolytic drugs are reserved for those instances

when angioplasty is not an option or until the patient can be taken to a facility that performs

percutaneous coronary interventions. Fibrinolytic drugs may lyse both normal and pathologic

thrombi.

Common characteristics of thrombolytic agents

Mechanism of action: All act either directly or indirectly to convert plasminogen to plasmin,

which in turn cleaves fibrin, thus lying thrombi. Clot dissolution and reperfusion occur with a

higher frequency when therapy is initiated early after clot formation, increased local thrombi

may occur as the clot dissolves, leading to enhanced platelet aggregability and thrombosis.

Strategies to prevent this include administration of antiplatelet drugs, such as aspirin, or

antithrombotics, such as, heparin.

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Therapeutic uses: Originally used for the treatment of deep-vein thrombosis and serious

pulmonary embolism, thrombolytic drugs are now being used less frequently for these

conditions. Their tendency to cause bleeding has also blunted their used in treating acute

myocardial infarction or peripheral arterial thrombosis. However, thrombolytic agents are

helpful in restoring catheter and shunt function, by lying clots causing occlusions. Thrombolytic

agents are also used to dissolve clots that result in strokes.

Pharmacokinetics: For myocardial infarction, intracoronary delivery of the drugs is the most

reliable in terms of achieving recanalization. However, cardiac catheterization may not be

possible in the 2-to-6 hour “therapeutic window”, beyond which significant myocardial salvage

becomes less likely. Thus, thrombolytic agents are usually administered intravenously, because

this route is rapid, is inexpensive, and does not have the risks of catheterization.

Adverse effects: The thrombolytic agents do not distinguish between the fibrin of an unwanted

thrombus and the fibrin of a beneficial hemostatic plug. Thus, hemorrhage is a major side

effect. For example, a previously unsusoected lesion, such as a peptic ulcer, may hemorrhage

following injection of a thrombolytic agent. These drugs are contraindicated in patients with

healing wounds, pregnancy, history of cerebrovascular accident, or metastic cancer. Continued

presence of thrombogenic stimuli may cause rethrombosis after lysis of the initial clot.

1. Alteplase. Alteplase (formerly known as tissue plasminogen activator, or tPA) is a serine

protease originally derived from cultured human melanoma cells. It is now obtained as a

product of recombinant DNA technology.

Mechanism of Action

Alteplase has a low affinity for free plasminogen in the plasma, but it rapidly activates

plasminogen that is bound to fibrin in a thrombus or a hemostatic plug, thus, alteplase is said to

be “fibrin selective,” and at low doses, it has the advantage of lysing only fibrin, without

unwanted degradation of other proteins-notably fibrinogen.

Therapeutic uses

Alteplase is approved for the treatment of myocardial infarction, massive pulmonary

embolism, and acute ischemic stroke. Alteplase seems to be superior to streptokinase in

dissolving older clots and ultimately, may be approved for other applications. Alteplase ,

administered within 3 hours of the onset of ischemic stroke, significantly improves clinical

outcome-that is, the patient’s ability to perform activities of daily living. Reteplase is simila r to

alteplase can be uses as an alternative.

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Pharmacokinetics: Alteplase has a very short half-life (about 5 minutes) and therefore, is

administered as a total dose equal to 0.9 mg/kg.

Adverse effects: Bleeding complications, including gastrointestinal and cerebral haemorrhages,

may occur.

2. Streptokinase. Streptokinase is an extracellular protein purified from culture broths of

group C β-hemolytic streptococci.

Mechanism of action

Streptokinase has no enzymic activity. Instead, it forms an active one-to-one complex

with plasminogen. This enzymatically active complex coverts uncomplex plasminogen to the

active enzyme plasmin.

Therapeutic uses

Streptokinase is approved for use in acute pulmonary embolism, deep-vein thrombosis,

acute myocardial infarction, arterial thrombosis, and occluded access shunts.

Pharmacokinetics

Streptokinase therapy is instituted within 4 hours of myocardial infarction and is infused

for 1 hour. Its half-life is less than half an hour.

Adverse effects

Bleeding disorders: Activation of circulating plasminogen by streptokinase leads to

elevated levels of plasmin, which may precipitate bleeding by dissolving hemostatic

plugs. In the rare instance of life –threatening hemorrhage, aminocaproic acid may be

administered.

Hypersensitivity: Streptokinase is a foreign protein and is anti-genic. Rashes, fever, and

rarely, anaphylaxis occur. Because most individuals have had a streptococcal infection

sometime in their lives, circulating antibodies against streptokinase are likely to be

present in most patients.

3. Anistreplase ( anisoylated plasminogen streptokinase activator complex. Anistreplase

is a performed complex of streptokinase and plasminogen and it is considered to be a

prodrug. Streptokinase must be released, and only plasminogen to which it was

associated will get converted to plasmin.

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VIII. DRUG USED TO TREAT BLEEDING

Bleeding problem may have their origin in naturally occurring pathologic conditions such

as hemophilia (a serious disease that causes a person who has been cut or injured bleeding for

a very long period of time) or result of fibrinolytic states (that may rise after GI surgery or

prostatectomy).

The use of anticoagulants may also give rise to hemorrhage.

Certain natural proteins and Vitamin K, as well as synthetic antagonists, are effective

controlling this bleeding. For example, hemophilia is a consequence of a deficiency in plasma

coagulation factors, most frequently Factors VIII and IX.

Blood transfusion is also an option for treating severe hemorrhage.

A. Aminocaproic Acid and Tranexamic Acid. Fibrinolytic states can be controlled by the

administration of aminocaproic acid or tranexaminc acid. These drugs are synthetic,

which they inhibits plasminogen activation, are orally active and excreted in the urine. A

side effect of this treatment is intravascular thrombosis.

B. Protamine sulfate is an agent that antagonizes the anticoagulant effect of heparin. This

protein derived from the fish sperm or testes and is high in arginine content. The

adverse effects of drug administration include hypersensitivity as well as dyspnea,

flushing, bradycardia, and hypotension.

C. Vitamin K or Phytomenadione is a fat-soluble vitamins the human body needs

for complete synthesis of certain proteins that are required for blood coagulation, and

also certain proteins that the body uses to manipulate binding of calcium in bone and

other tissues. The vitamin K-related modification of the proteins allows them to

bind calcium ions, which they cannot do otherwise. Without vitamin K, blood

coagulation is seriously impaired, and uncontrolled bleeding occurs. Low levels of

vitamin K also weaken bones and promote calcification of arteries and other soft tissues.

D. Aprotinin, is a serine protease inhibitor that stops bleeding by blocking plasmin. It can

inhibit streptokinase. This agent may cause renal dysfunction and hypersensitivity

reaction. In addition, this agent should not be administered to patients who have

already been exposed to the drug within the previous 12 months due to the possibility

of anaphylactic reaction.

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IX. AGENTS USED TO TREAT ANEMIA

Anemia is defined as a below-normal plasma hemoglobin concentration resulting from a

decreased number of circulating red blood cells or an abnormally low total hemoglobin content

per unit of blood volume. In other words anemia is a condition in which your blood has a lower

than normal number of red blood cells.

The following are causes of Anemia:

o Chronic blood loss

o Bone marrow abnormalities

o Increased hemolysis

o Infections

o Malignancy

o Endocrine deficiencies

o Renal failure

Anemia can be at least temporarily corrected by transfusion of whole blood.

Diagnostic procedure: Blood Transfusion

Nutritional anemias are caused by dietary deficiencies of substances such as:

1. Iron. It is stored in intestinal mucosal cells as ferritin until needed by the body. Iron

deficiency results from a negative iron balance due to depletion of iron stores and/ or

inadequate intake, culminating in hypochromic microcytic anemia. The treatment of

deficiency in iron is supplementation of ferrous sulfate. The Adverse Effect is GIT

Disturbances.

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2. Folic Acid. The primary use of folic acid is in treating deficiency states that arise from

inadequate levels of the vitamin. Folate deficiency may be caused by increased demand,

poor absorption caused by pathology of the small intestines , alcoholism and treatment

with drugs that are dihydrofolate reductase inhibitors. The primary results of deficiency

are megaloblastic anemia and cyanocobalamin (Vitamin B12).

3. Cyanocobalamin. Deficiencies of vitamin B12 can result from either low dietary levels,

poor absorption of the vitamin due to the failure of gastric parietal cells to produce

intrinsic factor, or loss of activity of the receptor needed for intestinal uptake of the

vitamin.

4. Erythropoietin and Darbepoetin. Erythropoietin is a GP, normally made by the kidney,

which regulates red blood cell proliferation and differentiation in bone marrow.

Human erythropoietin is effective in the treatment of anemia caused by end stage renal

disease.

Darbepoetin is a long acting version of erythropoietin that differs from erythropoietin by

the addition of two carbohydrate chains, which improves its biologic activity.

Darbepoetin has no value in acute treatment of anemia due to its delayed onset of

action.

X. AGENTS USED TO TREAT SICKLE CELL DISEASE

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Sickle cell anemia has no widely available cure. However, treatments can help relieve

symptoms and treat complications. The goals of treating sickle cell anemia are to relieve pain;

prevent infections, organ damage, and strokes; and control complications (if they occur).

Blood and marrow stem cell transplants may offer a cure for a small number of people

who have sickle cell anemia. Researchers continue to look for new treatments for the disease.

Infants who have been diagnosed with sickle cell anemia through newborn screening are

treated with antibiotics to prevent infections and receive needed vaccinations. Their parents

are educated about the disease and how to manage it. These initial treatment steps have

greatly improved the outcome for children who have sickle cell anemia.

Specialists Involved. People who have sickle cell anemia need regular medical care.

Some doctors and clinics specialize in treating people who have the disease. Hematologists

specialize in treating adults and children who have blood diseases or disorders.

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Treating Pain

Medicines and Fluids

Mild pain often is treated at home with over-the-counter pain medicines, heating pads,

rest, and plenty of fluids. More severe pain may need to be treated in a day clinic, emergency

room, or hospital.

The usual treatments for acute (rapid-onset) pain are fluids, medicines, and oxygen

therapy (if the oxygen level is low). Fluids help prevent dehydration, a condition in which your

body doesn't have enough fluids. Fluids are given either by mouth or through a vein. Your

doctor may prescribe antibiotics if you have an infection.

Treatment for mild-to-moderate pain usually begins with acetaminophen (Tylenol®) or

nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. If pain continues or becomes

severe, stronger medicines called opioids might be needed. Talk with your doctor about the

possible benefits and risks of taking strong pain medicine, especially if the medicine will be used

for a long period.

Hydroxyurea

Severe sickle cell anemia can be treated with a medicine called hydroxyurea This

medicine prompts your body to make fetal hemoglobin. Fetal hemoglobin, or hemoglobin F, is

the type of hemoglobin that newborns have. In people who have sickle cell anemia, fetal

hemoglobin helps prevent red blood cells from sickling and improves anemia.

It is taken daily by mouth, hydroxyurea reduces how often painful sickle cell crises and

acute chest syndrome occur. Many people taking hydroxyurea also need fewer blood

transfusionsand have fewer hospital visits.

Preventing Complications

Blood transfusions are commonly used to treat worsening anemia and sickle cell

complications. A sudden worsening of anemia due to an infection or enlarged spleen is a

common reason for a blood transfusion. Some, but not all, people who have sickle cell anemia

need regular blood transfusions to prevent life-threatening problems, such as stroke, spleen

problems, or acute chest syndrome.