Factors That V Leiden Thrombophilia

Factors That V Leiden Thrombophilia
Factor V Leiden Thrombophilia Thrombophilia is a disorder that contains several genetic
components that can cause an individual to form arterial and venous thrombi more readily. Many
serious medical complications can result from thrombus formations that are often times fatal. In fact,
a venous thromboembolism (VTE) is relatively common and a thrombosis of the deep veins of the
legs or pelvis can lead to morbidity and mortality. Small portions of this patient population even
develop pulmonary emboli (PE), which can be fatal. This major medical problem affects 1 in 1,000
persons per year and approximately 1 in 130 Americans younger than age 65 develop a VTE (Crow,
2003; Kujovich, 2011). Interestingly enough, inherited thrombophilia can be identified in half of the
patients presenting with VTE (Kujovich, 2011). In 1993, European investigators Dahlback and his
colleagues recognized a new mechanism for familial thrombophilia. Their research was initiated in
order to investigate the cause for a number of young adults that presented with VTE, who had a
family history of thrombosis but no detectable genetic link. As a result, a previously unrecognized
mechanism associated with activated protein C resistance (APCR) was found – Factor V Leiden
mutation (Crow, 2003). Factor V Leiden is considered the single most common cause of hereditary
thrombophilia and is often linked to thrombosis due to hereditary hypercoagulability. Studies have
indicated that factor V Leiden is a
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Analysis Of Hemostatic Agents And Their Applications
Analysis of Hemostatic Agents and their Applications in Treating Hemorrhage in Emergency
Combat and Civilian Situations
Author: Philip Sang
Literature Paper Reader: Dr. Whitney
Introduction
– Put in the general infoo about hemorrhage data in combat siutations...
– Talk about problems currently present
– Other shit
– Prompt hemorrhage hemostasis is not only paramount to survival but also long term recovery. If
patients survive and blood loss is controlled, the large blood loss can lead to
hypothermia/coagulopathy/infection/acidosis/multiple organ failure/ and fatal hypotension.
– Talk about need for stability during movement
– Talk about need for devices that don't require compression.
– Need junctional stuffs
– ... Show more content on Helpwriting.net ...
Kaolin is very easy to refine and produce due to the abundant available quantities of its unrefined
form, kaolinite. And since kaolin is inert in its clinical form it does not cause an immune response
when introduced into a biological system, however it is not biodegradable so it must be removed
after use (Bennett et al., 2014; Trabattoni et al., 2010). Kaolin has been an attractive hemostatic
agent due to its ability to form clots and being inexpensive to produces, however a major drawback
is that it does not work when the host is in a state of coagulopathy.
Chitosan:
Chitosan is a polysaccharide made of polymers of β–(1–4)–linked D–glucosamine and N–acetyl–D–
glucosamine (NAG), and is produced from a component of the exoskeleton of crustacean shells
called chitin. Chitosan's hemostatic effects are due to its amino groups reacting with the membranes
of circulating cells in the host's blood, leading to eventual clot formation that occurs independently
of the innate coagulation cascade. The positively charged residues present on chitosan attract the
negatively charged cell membranes of erythrocytes and thrombocytes, creating a cross–linkage of
said cells and then the formation of a thrombus. Chitosan is also biodegradable and is broken down
inside the host. It also induces an immune response that activates macrophages and stimulates cell
proliferation leading to faster wound healing

AAV Gene Therapy
In a study titled "AAV–mediated factor IX gene transfer to skeletal muscle in patients with severe
hemophilia B," 8 patients were enrolled to further investigate the safety of intramuscular injection of
adeno–associated viral vector. The study was also analyzed to determine the effectiveness and
duration of F.IX levels. Seven of the 8 patients were also previously infected with Hepatitis C.
Hence, muscle–directed gene therapy reduced the potential of certain complications compared to
liver–directed gene therapy. 4.1 Methods The patients were divided up into three groups depending
on the amount of injection sites with a limited dose of 1.5 x 1012 vector genomes (vg)/site. The
vector was administered into one or both of the vastus lateralis muscles located along the outside of
the thigh. The number of sites for three patients in the low–dose cohort was 10 and 20. Three other
patients in the medium–dose cohort were given 30 to 50 injections. Two patients in the high–dose
cohort were given a total of 80 to 90 shots in the vastus lateralis muscles, deltoid, and the soleus.
Bethesda assays were performed on equal volumes of test plasma and normal pooled plasma, which
determined the residual F.IX activity after incubation. Additionally, Western blot was also performed
to detect anti–F.IX antibodies. Polymerase chain reaction (PCR) assay ... Show more content on
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The studies could not be performed on all of the muscle biopsies due to insufficient tissue. Only two
biopsies were available for analysis for the 6–month and 10–month time periods. Vector DNA was
detectable on Southern blot of injected tissue as a high–molecular weight form for 5 of the 9
biopsies at 2 months. The gene copy number was about 0.5 to 4 copies/diploid genome at doses of
about 1.5 x 1012 vg/site. The copy number and expression were consistent for the samples observed
at each of the time

Plaque Synthesis
A major proportion of AMI occur in plaques that have not revealed clinically prior to the infarction,
that is have not initiated adequate degree of luminal obstruction results angina, which obfuscates
screening and interventional primary preventive procedures (38,44,45). Plaque distraction is the core
remarkable reason of AMI. The procedure there the fibrous cap of a plaque ruptures plus reveal the
blood for primary pro–thrombotic yields and following thrombus development is convoluted
(39,44). Lessened collagen synthesis or amplified mortification of extracellular matrix all subsidize
to this course. A lesser degree of smooth muscle cells (with attendant declined matrix production) as
well as a extreme degree of lipids, inflammatory cells ... Show more content on Helpwriting.net ...
Binding of vWF to platelets is mediated primarily by the GpIb/IX/V complex. Collagen also binds
to platelets via the GpIb/IX/V complex as well as through other collagen binding receptors on the
platelet surface (like GpIa/IIa and GpVI). The GpIb/IX/V complex also binds to other proteins like
thrombin and other proteins in the coagulation cascade and is critical for initial platelet response
(50–52). These vWF/collagen bound platelets form a monolayer of activated platelets that secrete
their granules and activate other platelets, which triggers the extension phase. Important mediators
in this process include thromboxane A2 (inhibited by aspirin), ADP (inhibited by P2Y12–inhibitors)
and thrombin ( inhibited by bivalirudin, dabigatran, heparin and low–molecular weight heparin) (
53). The final downstream step of platelet activation is the expression of to bind other activated
platelets (52,53). The platelet clot formation afterwards undergoes the stabilization phase, wherein
the platelets form a close network. Several receptors have been implicated in this process, including
the previously mentioned GPIIb/IIIa–receptors as well as CD40 and its ligand (CD40L) (51). The
final step in thrombus formation is the activation of the coagulation cascade with the deposition of
fibrin to stabilize the thrombus. This process is started by exposure of tissue factor to the
coagulation system, thrombin generation and final conversion of insoluble fibrinogen into fibrin

Pathophysiology: Disseminated Intravascular Coagulation (T
Disseminated intravascular coagulation
Pathophysiology
Disseminated intravascular coagulation (DIC) is an acquired syndrome that occurs when a stimulus
pathologically activates intravascular coagulation and fibrinolysis resulting in an unbalanced
hemostasis (Cunningham, 1999; Huether & McCance, 2008; Wada, 2008). The initiation of DIC
starts with the release of tissue factor (TF) by the endothelial cells or white blood cells (WBCs). TF
are present on many different cell types including lungs, brain, and placenta. The release of TF is
subsequent to a variety of causes including trauma, ischemia, excessive metabolic stress, tumors,
infectious organisms, exposure to cytokines and endotoxins (Baglin, 1996; Vinay, Abul, Nelson, &
Richard, 2007). The release of endotoxin is the means by which ... Show more content on
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In this specific patient with gram–negative sepsis leading to DIC may present with spontaneous
bruising, prolonged bleeding from venipuncture sites, and bleeding from three different sites. There
are also many other possible sites including the nose, gums, mucosa, eyes, arterial lines, or surgical
wounds (Bliss & Wallace–Jonathan, 2008; Wada, 2008). Depending on where the fibrin clots have
deposited, other symptoms may manifest as ischemia or organ failure occurs such as in the kidneys,
heart, lungs, or in the brain. There is a possibility of hemorrhaging into a closed compartment,
which may lead to shock (Huether & McCance, 2008).
Lab values during DIC are also of great importance. There is no specific test for DIC but a
combination of PT (prothrombin time), aPTT (activated partial thromboplastin time), fibrinogen,
platelet count and d–dimmer are used to assist in the diagnosis of DIC (Cunningham, 1999). Since
many disorders can cause an increase of each of these lab values, it is important to use the whole
picture to make the diagnosis.

The Body 's Clotting Of Clotting Factors
Until around 2003, the medical community attributed the coagulopathy of trauma to excessive
consumption of clotting factors, hemodilution by intravenous crystalloids, all while compounded by
hypothermia and acidosis. A group of physicians at the Royal London hospital authored a paper
hypothesizing that this was not entirely true and that the syndrome they labeled as Acute Traumatic
Coagulopathy(ATC) manifests itself by simultaneously activating protein C, decreasing available
fibrinogen, and inhibiting platelet function (Brohi, Singh, Heron, Coats, 2003; Kutcher et al., 2012).
Many other factors contribute to the systemic alteration in coagulation; however, these three
separate entities highlight pathophysiologically what happens during ... Show more content on
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In the face of hemorrhagic and ischemic shock with endothelial damage, fibrinogen levels fall
dramatically. Decreased fibrinogen levels directly alter the body's ability to form the fine meshwork
needed to achieve hemostasis. Normally, thrombin breaks down fibrinogen into fibrin to assist in
providing the scaffolding for clotting. When severe tissue injury occurs, the lack of fibrin cannot
form the mesh needed to assist in clot formation. The 2010 RCT CRASH–2 study displays the
strongest evidence proving that administering tranexamic acid(TXA) to severely shocked trauma
patients(MAP <75 mmHg) reduces the amounts of death from bleeding in this population from
18.4% to 14.9% (Napolitano, Cohen, Cotton, Schrieber, & Moore, 2013). Simply put, TXA prevents
plasminogen's conversion to plasmin. The inactivated plasminogen will then allow the clot to
become more secure. Because of plasmin's inherent ability to degrade fibrinogen, the patient's d–
dimer which measures fibrin degradation products, the patient with ATC will have elevated d–dimer
levels. Low fibrinogen levels in a patient with ATC warrants cryoprecipitate infusion and has been
associated with increased survival outcomes (Rourke, 2012). Impaired platelet function has been
described prospectively by Kutcher et al. in response to traumatic tissue injury. This describes the
primary hemostatic mechanism in which platelet dysfunction can alter platelet adhesion

Idarucizumab Research Paper
Idarucizumab for Dabigatran Reversal Authors: Charles V. Pollack, Jr., M.D., Paul A. Reilly, Ph.D.,
John Eikelboom, M.B., B.S., et al. Institution: Patients participating in the study were included from
184 centers in 35 countries. Journal: The New England Journal of Medicine. Funding: Boehringer
Ingelheim, Bristol–Myers Squibb /Pfizer Alliance (Eliquis) and Medtronic, Inc. Journal citation:
Pollack, C., et al. (2015, June 22). Idarucizumab for Dabigatran Reversal. Retrieved July 10, 2015,
from http://www.nejm.org/doi/full/10.1056/NEJMoa1502000 Primary objective: The primary
objective was to demonstrate reversal of the anticoagulant effect of Dabigatran and the safety of
intravenous idarucizumab. Design: Prospective cohort study with a duration ... Show more content
on Helpwriting.net ...
A surgery or procedure, which is elective or where the risk of uncontrolled or unmanageable
bleeding is low. 2.Contraindications to study medication including known hypersensitivity to the
drug or its excipients. Dropouts: 1 patient withdrew informed consent and 1 patient declined follow
up after the treatment. Method: The study design was a multicenter prospective cohort study. There
was no control group. The study included two treatment groups Group A and Group B as described
above. Both groups received a total of 5g of IV idarucizumab. The dose was divided into two 50 ml
bolus infusion. Each infusion contained 2.5g of idarucizumab. The two infusions were delivered
within 15 min after the initial dose. Blood samples were collected from the patients at baseline after
the initial dose and then at 10, 30 min, 1, 2, 4, 12 and 24 hours. The patients were followed for at
least 1 month or until death occurred. Study end points: The primary endpoint was the maximum
percent reversal of the anticoagulant effect of dabigatran, which was determined at any point from
the end of the first infusion to 4 hours after the second infusion. Dilute thrombin time and ecarin
clotting time were used to determine the percent

Hemophilia Essay
Hemophilia A is a disorder in which the blood doesn't clot normally due to the lack of blood
clothing factor VIII. Hemophilia A is also known as the 'Classic Hemophilia.' According to the
CDC, hemophilia will occur in approximately 1 in 5,000 live births. It is called classic hemophilia
due to the fact that this hemophilia is four times more common as hemophilia B. This disorder is
mainly a hereditary bleeding disorder which is caused by an inherited X linked recessive trait. Some
acquired forms do exist as well, largely in older patients, due to autoantibodies directed against
factor VIII. The defected gene is located on the X chromosome. And it results from a heterogeneous
mutation in factor VIII gene that maps for Xq28.
Hemophilia A is more common in males because males have one X and one Y chromosome. Since a
male's DNA contain only one X chromosome, hemophilia affects mostly males. Hemophilia was
first ... Show more content on Helpwriting.net ...
It includes complete blood count, aPTT, PT, fibrinogen, and clothing fact tests. CBC measures the
amount of hemoglobin, number of red cells and whites blood cells along with platelets. CBC is
usually normal in a person with hemophilia A. Activated partial thromboplastin time (aPTT)
measures how long it takes for blood to clot. It measures the clotting ability of factor XII, XI, IX,
VIII and this would be abnormal in a individual with hemophilia A since hemophilia A is associated
to factor VIII. Prothrombin time also measure the clotting ability but for factor X, VII, V, II, and I.
This would be normal in individuals with hemophilia A. Fibrinogen test helps doctors to assess a
patients ability to form a clot. Lastly, clotting factor test also known as factor assay is used to
determine the type and the severity of hemophilia. The testing mentioned above is the traditional
testing that's used to diagnose hemophilia

Hemophilia Case Study
. This factor VIII is also associated with hemophilia. It is the factor that is either damaged or
missing12. Factor Vlll can be in two states: active and inactive. When it is in its inactive state, it will
bind to VWF in the blood. If this factor does not bind VWF while it is in circulation, it will degrade.
After VWF is made, it can follow a number of pathways. It can either be released into the plasma,
released into the subendothelium or it can also be stored in organelles in the cytoplasm. If VWF is
stored, it can be released when it is needed depending on the physiological status of the
individual10. When VWF is exposed to an injury in the blood vessel in the endothelium, the platelet
receptors will be activated. This activation, will ... Show more content on Helpwriting.net ...
One of the main fibrinolysis enzymes is plasmin, this is an enzyme that comes from plasminogen,
the conversion of plasminogen to plasmin will incorporate 2 serine proteases. These serine proteases
are tPA and uPA. The enzyme tPA, is made and released from the endothelial cells, while uPA is
made by monocytes and macrophages. Two enzymes also differ in the fact that uPA has a lower
affinity for plasminogen compared to tPA. This process will stop and inhibit the buildup of fibrin, it
also allows the thrombus to be removed. The activation of plasminogen will form plasmin and this
will degrade the thrombus. Plasmin will terminate the clotting process. During this process, fibrin
degradation products (FDPs) will begin to form. These FDPs will include fibrinopeptide B and other
fibrin degradation dimers. These products will be released and will degrade the fibrin18. This
process will remove the

Essay on Point-of-Care Coagulation Platforms for...
Thrombophilia defines inherited and acquired conditions associated with an increased thrombotic
risk, which predispose to venous thromboembolism (VTE), cardiopulmonary bypass (CPB) and
stroke. Thromboembolic events have long been treated with the most commonly used anticoagulant
drug, heparin that is rapidly replaced by low molecular weight heparin (LMWH). A variety of point–
of–care (POC) coagulation platforms have been commercially available for many years now,
providing more control over the patient's anticoagulation management such as heparin and warfarin.
While the measurement for anticoagulation by POC devices has relied mainly on the clotting time
tests, innovative platelet function tests, and factor–specific assays based on ... Show more content on
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While the prevention of a thrombotic event achieved by an anticoagulant, over– or under–dosing
can give rise to excessive bleeding or severe clotting respectively, therefore closely link therapy
with monitoring is essential. Several techniques have been developed to address the disadvantages
of large sample volumes, by multiplexing of the assays in which various parameters or analytes are
measured concurrently from a single sample.
While laboratories became unable to provide results in time frames needed to allow rapid
turnaround that would allow timely intervention of anticoagulant therapy, the requirement for POC
coagulation monitoring techniques became essential (Harris, Castro–López and Killard, 2013).
In this review, I will focus on the availability of POC diagnostic tests for monitoring the
anticoagulant therapy for thrombophilia. I will first describe the conventional clot–based assays and
then, I will attempt to address current advances in microfluidic POC tests used for monitoring
thromboembolic–related events and highlight new fluorescence–based anti–Factor Xa (FXa)
microfluidic POC assay platform for monitoring both unfractionated and low molecular weight
heparins and fluorescence–based blood coagulation assay platform for monitoring activated partial
thromboplastin time (aPTT). Also, I will

Tissue Injury
In the normal extrinsic blood coagulation cascade, tissue injury causes expression of tissue factor.
Tissue injury also causes exposure of the subendothelial components, which includes Von
Willebrand Factor (vWF) and collagen. vWF holds platelets together and is a carrier protein for
fVIII in plasma. Tissue factor binds to factor VIIa (fVIIa) to form a complex that cleaves fX into
fXa to activate it. Prothrombin is then converted into thrombin by the promthrombinase complex
formed from fXa and fVa. Clotting requires both calcium and a phospholipid surface. The intrinsic
coagulation cascade and coagulation factors that're activated increase the amount of clotting there is.
When platelets are activated, they amplify clotting through localization ... Show more content on
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aureus coagulases are the virulence factors responsible for the pathogenesis of the bacteria. Their
pathogenic roles require staphylococci to be close to the resulting coagulation product. Double coa–
vwb mutant mice had significantly decreased abscesses and lethal sepsis as compared to controls. S.
aureus coagulases assist abscess formation, which is the classic sign of a S. aureus infection.
Abscesses formed from S. aureus infection are surrounded by prothrombin, fibrin, and fibrinogen.
They contain the coagulases Coa and vWbp. More specifically, these coagulases prevent phagocytes
from clearing S. aureus during an infection. While there is neutrophil recruitment during an
infection, not many of these recruited immune cells can phagocytose the bacteria. This leads to the
hypothesis that coagulation of staphylococci allows these bacteria to escape phagocytic activity.
Additionally, it is also possible that clots formed by S. aureus serve to allow the bacteria access to
vital nutrients within the host. Furthermore, they may exist in order to systematically place virulence
factors near their own communities and to spread to other parts of the

Disadvantages Of Hemostatic Dressings
CHAPTER 1
INTRODUCTION
According to World Health Organisation (WHO), on an average, motor vehicle crashes have killed
about 1.25 million people every year and also it has been observed that 90% of the world's fatalities
on the roads occur in low–income and middle–income countries. India accounts for about 10% of
road crash fatalities worldwide [45]. The control of hemorrhage (massive bleeding) is a critical step
in first aid and field trauma care. This control is essentially done by applying pressure, elevation of
bleeding site, usage of elastic field dressings, tourniquets and novel haemostatic dressings [29].
Among these methods, hemostatic dressings are used as last alternative, but it is the resourceful
system of all. In this report, various forms of hemostatic materials and the products available in the
market are reviewed.
Fig 1: A simplified hemorrhage control algorithm [31]
An ideal hemostatic dressing must have the subsequent characteristics: [29, 38]
Biocompatible, biodegradable and bio absorbable
Ease of storage
Easily removed without leaving residues
Easy administration
Flexible enough to fit complex wounds
Long shelf life, lightweight
Low cost
No adverse effects to healing
No thromboembolic complications
Prolonged stability even ... Show more content on Helpwriting.net ...
American Red Cross Holland Laboratory, Rockville, MD) consists of higher concentrations of
human fibrinogen, human thrombin and calcium chloride affixed in a mesh. These agents were in
increasingly used at the end of World War II but fell out and were consequently abandoned due to
the transmission of hepatitis. It was re–visited again in the early 1990s by the US Army and the Red
Cross to assist in hemostasis. Although not approved by the US Food and Drug Administration, it
was used under an investigational drug protocol by US forces in Iraq and Afghanistan and has
proven to be successful in combat because of its simple application, stability, and bio absorbability

Endothelial Cell Injury Essay
Thrombomodulin release and endothelial cell injury in Systemic lupus erythematosus
SLE is an autoimmune disease characterized by the formation of immune complexes (ICs), which
contain a complex mixture of autoantigens nucleic acids, nucleic acids–associated proteins and
corresponding autoantibodies (Sun et al., 2013) .
In SLE, the circulating ICs are deposited in the vascular walls of multiple organs and activate the
complement pathways. The resulting complement products stimulate leucocytes to injure the
vascular endothelium, leading to blood vessel destruction and organ injury (e.g. glomerulonephritis
and vasculitis). It has been suggested that expression of adhesion molecules primes the vascular
endothelium for subsequent injury that increase the release of TM into the circulation (HO et al.,
2003).
Soluble TM is an endothelial marker presents in large quantities on the surface of the endothelium,
particularly in the ... Show more content on Helpwriting.net ...
So increase levels of sTM in serum after endothelial injury has been reported as an evidence for a
pro–thrombotic state in SLE (Chan et al., 2006) .
It also has been used as a marker of microvascular endothelial injury and thrombotic events in
various diseases, such as disseminated intravascular coagulation, multiple sclerosis and rheumatic
diseases. Previous studies have reported that elevated sTM is associated with the disease activity of
SLE, nephritis and vasculitis. So, it is an established marker of endothelial cell damage (HO et al.,
2003) sTM which is normally a component of vascular EC membrane easily released to plasma in
patients with active SLE due to persisting EC detachment in active SLE patients. It was suggested
that elevated sTM levels reflect EC damage rather than activation, because EC–leucocyte adhesion
and interaction after the activation of inflammatory cytokines might result in the release of TM from
the EC surface (Fiedler and Augustin,

Comparing Positive And Positive Feedback
Compare and contrast negative and positive feedback, giving examples of each. Explain why
negative rather than positive feedback is required for maintenance of homeostasis.
In order to maintain a constant internal environment, organisms require mechanisms for maintaining
internal stability in spite of intrinsic or extrinsic changes. Negative feedback is a corrective
mechanism that opposes a variation from normal limits. It is required for the maintenance of
homeostasis in the body. However, positive feedback is a mechanism that increases a deviation from
normal limits after an initial stimulus. Homeostasis is the existence of a stable internal environment,
and maintaining it is extremely vital to an organism's survival. Failure to maintain it can lead to
illness or even death (Martini et al. 2014). There are different examples of negative and positive
feedback that are fundamental in every day life. Maintenance of blood glucose levels, and
thermoregulation, are both examples of negative feedback. Often positive feedback is more harmful
than beneficial, but examples when it is useful are during childbirth and clot formation.
Regulation of homeostasis consists of three parts: the first is a receptor. This detects changes in the
environment, and responds to a change in stimuli. The second part is a control centre. This receives
information from the receptor, and sends commands to the effector, which is the third part. The
effector is a cell or organ that will respond to

Cattle Byproducts Research Paper
When most people think of cattle byproducts, they think of steak and leather, but are either forgetful
or unaware of the other essential and inedible byproducts cattle provide society with. Many remain
unaware that beef also contributes to vital goods and services. From airplane lubricants to piano
keys produced from cattle bones, hormones and other products, arguably one of the most important
cattle byproducts is medicine. Diabetes and other diseases populate the earth in modern society.
Diabetes is a large recurring autoimmune disease in the United States where the pancreas stops
producing a hormone, insulin, that enable the body to gain energy from food. This disease requires
multiple insulin injections daily. As many as 1.25 million Americans

Recent Advances During Management Of Anti Coagulation
Recent advances in management of anti–coagulation in Atrial Fibrillation
Role of anti–coagulation in prevention of stroke in Atrial Fibrillation
Atrial fibrillation (AF) is the most common cardiac arrhythmia. It is more prevalent in men with
increasing age. ( 11343485). Hypertensive heart disease and coronary heart disease are most
common underlying disorders in patients with AF in developed countries. AF is classified based on
2014 AHA/ACC/HRS guidelines into Paroxysmal AF (AF that terminates spontaneously in less than
7 days), persistent AF (AF that fails to terminate in 7 days), long standing persistent AF (AF more
than 12 months) and permanent AF (AF that is considered not amenable to rhythm control strategy).
This classification ... Show more content on Helpwriting.net ...
(20569748).
For non–valvular AF with CHAD2S2–Vasc score 2 or more than 2, benefits of oral anti–coagulation
therapy (OAC) exceeds risk as shown in several studies. (22514252, 19721017, 21789337,
22186961). Scores of 1 entails various approaches for anti–coagulation depending on several factors
including but not limited to patient's age, safety, bleeding risks etc. For patients with score of 0, the
risk of anti–coagulation outweighs the benefits, so no anti–coagulation is needed. Based on these
findings, OAC is class 1 indication for patients with CHA2DS2–VASc score of 2 or more.
(23558044, 22922413).
Benefits of New non–vitamin K oral anti–coagulants
Traditionally, warfarin has been the drug of choice for long term anti–coagulation in AF after initial
bridging with heparin. Recently, newer non–vitamin K oral anti–coagulants (NOACs) are available
for long term anti–coagulation in AF. These drugs inactivate both circulating and clot bound
activated coagulation factors.(see figure 1 for mechanism of action). The two major class of NOAC
available are direct thrombin inhibitor (DTI) and factor Xa inhibitor. Parenteral direct thrombin
inhibitors include bivalirudin, argatroban and lepirudin. Oral direct thrombin inhibitors include
dabigatran. Oral factor Xa inhibitors

Mediated Clot Reaction Process
Differences in the integrin αIIbβ3–mediated clot retraction process between PECAM–1–/– and
wild–type platelets
At the experiment outset, the PECAM–1 deficient mouse population was healthy and displayed
normal Mendelian inheritance ratios.12 In addition, the population was within a haematologically
normal range and displayed normal platelet production.12 During the first months of life, when
compared to the age–and sex–matched population of wild mice, the homozygous PECAM–1
knockout mouse population struggled to grow, with lower average body weights.17 Research
performed by Mahooti et al,18 which assessed tail bleeding duration, suggested that the PECAM–
1–/– group displayed longer bleeding times and, therefore, an in–vivo bleeding defect. In sharp
contrast, similar research by Vollmar et al19 suggested that the PECAM–1 deficient population
displayed normal tail bleeding times. Initially, it was proposed that the potential reason for this
difference was an artefact created by different experimental techniques. Further investigation, using
hematopoietic reconstitution of irradiated PECAM–1–/– mice to evaluate any reversal of prolonged
tail bleeding, showed that the discrepancy was probably caused by an underlying endothelial defect
rather than a platelet defect.18
In vitro evidence suggested that modulation of integrin αIIbβ3–mediated functions was influenced
by engagement of the PECAM–1 group, so the next stage involved testing if a fundamental integrin
αIIbβ3 platelet

A New Generational Anticoagulant Drug
A New Generational Anticoagulant
For many year's patients with atrial fibrillation have been treated with anticoagulants such as
Warfarin to prevent strokes and embolisms. Unfortunately, Warfarin must be closely monitored and
that is an irritant for some patients. In October 2010, the FDA approved a new generational
anticoagulant drug called Dabigatran (Pradaxa). This alternate medication gives patients the benefit
of no dietary restrictions since dabigatran is not affected by certain foods. Another benefit of taking
dabigatran is a monthly blood test is not required to measure its effectiveness, so for this particular
reason many patients switch from taking other anticoagulants to dabigatran (Talati & White, 2011).
Since this medication does not require close monitoring, some wonder if is it truly a better option or
can more harm than good come from taking it. While the benefits of using dabigatran have shown
significant improvement over warfarin, there are still risks associated with using dabigatran. Atrial
fibrillation is the most common arrhythmia that puts patients at high risk for ischemic strokes.
Doctors will diagnosis atrial fibrillation by performing an electrocardiogram. The majority of
patients that develop atrial fibrillation are over the age of 65 years old and male. Atrial fibrillation
can be characterized by episodes of either paroxysmal or intermittent depending on frequency and
length of time before spontaneously stopping. It can also be persistent or

The Human Body Transports Oxygen And Nutrients Throughout...
The human body transports oxygen and nutrients throughout the body using the vascular system1.
When a person acquires an injury that causes him/her to bleed, the body has a natural defense to
repair it1; this is the basis of hemostasis, the formation and/or dissolution of blood clots2.
Localizing and amplifying coagulation proteases and their subsequent cofactor complexes maintain
hemostasis3. The inhibition and/or modification of these same coagulation proteases throughout the
rest of the body, away from the trauma site, also helps to maintain hemostasis3.
Coagulation, a cascade system abundant in fibrin and thrombin proteins that are vital to
hemostasis4, mainly occurs on the vascular surface because the rupture on the surface causes a
successive activation of trypsin–like serine proteases which lead to the release of thrombin and clot
formation3. The coagulation system may be activated via the intrinsic pathway, where plasma factor
XII triggers coagulation to begin, or the extrinsic pathway, where thromboplastin released from
tissues stimulates plasma factor VII –– once each pathway activates plasma factor X, a common
pathway leads to the conversion of fibrinogen to fibrin4 (this conversion is a function of which
thrombin is responsible for3). To prevent excessive bleeding (which occurs when there is a scarcity
of thrombin5) and/or unwanted blood clots (which occurs when there is a plethora of thrombin5),
coagulation must therefore be highly regulated3.
If hemostasis is

Thrombin Research Paper
Thrombin is a naturally occurring protein that is present in the blood of humans and animals. The
main function of thrombin is as an intermediate step during hemostasis, which slows bleeding by
forming blood clots. Thrombin acts as an enzyme during an injury, converting fibrinogen to fibrin,
which then causes blood clots to form. Due to its properties, thrombin's application to the medical
field includes topical surgery in the case of minor injuries as well as various other medical
procedures such as neurosurgical operations. Apart from applications in the medical field, thrombin
also plays significant roles by directly interacting with endothelial cells throughout the body. The
precursor to thrombin is prothrombin, an inactivated protein produced in the liver. Upon injury
prothrombin converts to thrombin with the purpose of catalyzing the conversion of fibrinogen to
fibrin. The process changes the blood plasma soluble fibrinogen to fibrin, which is not plasma
soluble. In order to do this the interaction removes two peptide chains from the ends of fibrinogen.
Once this reaction is complete fibrin will begin to form a blood clot around the site of injury. While
the interaction between fibrinogen is important it is not the only major ... Show more content on
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A common use is for minor wounds, which are too small to mend by other standard surgical
methods. One method to deal with bleeding is to use fibrin glue on the site of the wound. The glue
contains both fibrinogen and thrombin and once applied to the site of the injury forms fibrin
monomers and eventually a fibrin clot. Alternatively, administration of a hemostatic carrier with
thrombin so topical treatment is not necessary if not desired. Medical professionals also use pure
thrombin applied in a mist after dissolving it in a saline solution. This final method is typically only
for wounds that cover a large

Discuss the Beneficial Effects of Activated Protein C in...
Sepsis is a potentially fatal medical condition where the blood is overwhelmed by the presence of
bacteria; activating the immune response and potentially causing organ dysfunction due to the
disruption of homeostasis, tissue perfusion and limited oxygen supply. Systemic inflammatory
response syndrome can be a key to the recognition of the illness. This condition can be treated with
antibiotics intravenously or by draining the infected fluid. However, treating the infection with
appropriate anti–microbial medication does not always cure the illness. Understanding the activation
of inflammation, coagulation and fibrinolysis in the pathophysiology of sepsis, has allowed further
research and development of therapeutic agents in its clinical ... Show more content on
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It inhibits thrombosis by inactivating co–factors Va, and VIIIa (Neyrinck, 2009). When deficient,
Factor V can cause excessive blood clotting and Factor VIII, being an essential clotting factor, can
cause blood to profusely move out of tissues once cut or damaged (Faust, 2001 and Yan, 2001).
Thrombin may become limited, one reason being the decrease of plasma D–dimer, which again
stimulates fibrinolysis (Bernard, 2001).
Animal models have been used to test the effectiveness of Protein C as a treatment for severe sepsis;
one example is an experiment carried out to investigate the coagulation effects of Protein C which
was tested using baboons (Taylor FB, 1987). Studies of this type have initiated the development of
recombinant human protein C; the activated form also termed drotrecogin alfa (activated).
A variety of variables are considered throughout the research of many experiments in investigating
whether Protein C is a beneficial treatment of severe sepsis. Animal models, specifically sheep, were
used to observe the clinical significance of APC in the work of Wang.Z et al. The results indicate the
beneficial consequence of APC on gaseous exchange and lactic acidosis; a considerably higher
arterial pressure is observed, as well as, higher thoracopulmonary compliance and PaO2/FIO2

Setting Up A Pcr Assay For Fv Cambridge Mutation
MEDS2140/2142 – LITERATURE REVIEW
TITLE OF PROJECT: SETTING UP A PCR ASSAY FOR FV CAMBRIDGE MUTATION, THIS
INCLUDES A FULL EVALUATION OF THE METHOD AND THE ESTIMATION OF THE
INCIDENCE OF THE MUTATION IN THE BLOOD DONOR POPULATION.
Name: Lisa Nguyen
Student Number: 3330181
Due Date: 31/08/14
Demonstrator: Dr Cindy O'Malley INTRODUCTION
The haemostatic system is a process that keeps the blood in balance between bleeding and
thrombosis. In a healthy individual, blood is maintained in a stable flowing state and is able to
rapidly form a haemostatic plug that will prevent unrestricted bleeding when a vessel is ruptured.
The coagulation cascade is involved in fibrin formation and it consists of the common, intrinsic and
extrinsic ... Show more content on Helpwriting.net ...
Factor V mutations include: Factor V Leiden, Factor V Cambridge and Factor V Hong Kong.
Studies have been conducted to see the prevalence of these mutations in patients who have been
diagnosed with venous thrombosis and its association with activated protein C resistance.
COAGULATION
Coagulation is a process where there is a blood clot formation at the site of an injured blood vessel.
Once there has been an injury to the blood vessel wall, vasoconstriction immediately occurs, and
then we get primary haemostasis. Platelet activation occurs in this process and they adhere to the
subendothelial complex. There is a formation of fibrin in this process and this leads to a haemostatic
plug being formed at the site of injury. Secondary haemostasis also occurs simultaneously with
primary haemostasis. In this process, tissue factors are involved in the initiation of the coagulation
cascade. The end result of the coagulation cascade is the activation of thrombin. Thrombin is an
important enzyme in haemostasis as it is needed for the conversion of fibrinogen to an insoluble
fibrin monomer to form the matrix of the clot and also it is important for further platelet activation.
(Khan and Dickerman, 2006; Hoffman, 2003; Clemetson, 2012; Arnout et al., 2006; Hawiger, 1987;
Green, 2006)
FACTOR V
The location of the

Soft Tissue Repair Case Study
Soft Tissue Repair Case Study: The Four Phase of Soft Tissue Healing and Therapeutic
Interventions that can be used to Aid Progression of Repair.
In this essay we will discuss the four different phases of the soft tissue healing process and also
explain all the components of each particular phase and how it functions. This will also include sport
therapeutic interventions that may contribute to the healing process and that may maximise healing
of soft tissue.
First Phase – Bleeding
This particular phase is immediate and depending on the vascularity of the tissue that is damaged
although it only happens during the first few hours as demonstrated by (Watson, 2006) in this
illustration of the length of each phase. >
The bleeding occurs following trauma to the tissue this could be an overload of a tissue or even
external force. One of the bodies first initial haemodynamic responses to bleeding is
vasoconstriction which narrows the blood vessels causing decreased blood velocity, in 2008
(Watson) states that this is due to the release of noradrenaline(norepinephrine); the reaction last lasts
only a few seconds to a minute. It is also explained by (Terkeltaub & Ginsberg, 1988) that both
lymphatic and blood vessels are plugged to limit any fluid loss and platelet, aggregation is
stimulated by the presence of thrombin. Vasoconstriction responds primarily to haemostasis which is
a response to prevent blood loss and a platelet plug is formed to support the prevention of excessive

Hemostasis: A Case Study
Hemostasis will begin immediately after the injury to the knee. Hemo=Blood and
Stasis=stopping/keeping. There will be three sequences of events occurring during this "stop
bleeding" event: Mechanism 1) Vascular Spasm (squeeze step–––blood vessels around the wound
will constrict to bound blood escape) Mechanism 2) Formation of a platelet plug (known as the plug
step whereby platelets come to the scrapped area of knee and adhere to exposed collagen fibers 3)
Blood clotting (Coagulation phase –––Coagulation cascade converts inactive proteins to active
forms and blood clotting begins)
During this step, the body has one primary goal; Stop the bleeding (coagulate the blood). In order to
reach this goal, as series of clotting factor proteins have ... Show more content on Helpwriting.net ...
Tissue factor has an essential role to play in inflammation because the launch of the extracellular
blood coagulation signaling passageway will launch an intracellular inflammation signaling
passageway. Inflammation is the body's way of attracting and accumulating leukocytes at the site of
the tissue injury ultimately leading to phagocytosis and destroying harmful bacteria that could cause
infection.
Events of inflammation:
Vasodilation and increased blood flow. Blood vessel and arterioles around the injured area of the
knee will dilate as the first event. Because the arterioles dilate more blood flows to the affected area.
Signs of redness and swelling will soon appear.
Vascular permeability increases. Because of the trauma to the knee, the endothelium will more
freely exchange the plasma proteins, antibody molecules, and leukocytes needed from the blood into
the tissue spaces. The emigration of these leukocytes into the tissue space causes swelling (edema)
of the area.
Leucocytic exudation and Chemotaxis. Leukocytes including an abundance of neutrophils and
monocytes ooze from the blood vessels and accumulate in massive numbers to the scrapped area of
the knee. Neutrophils prevail in the first day and are replaced by monocytes in one to two

The Use Of Anticoagulant Therapy And Its Effects On The...
Introduction
Epistaxis is defined as the occurrence of haemorrhage from the nose, which is relatively common
and does not always need professional medical attention. However, prolonged or repeated events of
nosebleeds, also known as 'recurrent idiopathic epistaxis ' may indicate certain bleeding disorders or
potential adverse effects from the use of anticoagulant therapy. Warfarin (Coumadin) is a common
anticoagulant that affects clotting factors that are produced in the liver. It is often administered after
an myocardial infarction in order to prevent thrombosis and thromboemobolism which could lead to
the development of a stroke, most of which are ischemic in origin. Despite its effectiveness,
warfarin has been implicated in 50 ... Show more content on Helpwriting.net ...
His laboratory tests showed an abnormal coagulation profile, which is perhaps attributed to his daily
medication regime. Prothrombin time(PT) was significantly prolonged, whereas partial
thromoboplastin time(PTT) was only mildly prolonged. The tests also revealed a lower than normal
haematocrit, that being a direct result of prolonged bleeding. Also, his stool sample was tested
positive for blood.
Homeostasis of Hemostasis
Blood coagulation is the process whereby a blood clot (thrombus) is formed. The formation of a
thrombus represents the second stage of hemostasis, following vasoconstriction and platelet
aggregation at the site of injury. The clotting process is very complex and its role is to maintain
vascular integrity and to induce rapid clot formation after a vascular injury. It is vital to be able to
regulate the production of thrombin, in order to prevent thrombosis, as well as maintaining normal
blood circulation.
As shown by figure 1, the coagulation cascade is a protein based system which is initiated through
the activation of two separate pathways designated extrinsic and intrinsic. These two pathways
proceed through the common pathway of coagulation until fibrin is formed. The extrinsic pathway is
generally the first pathway to be activated, and it is stimulated by tissue factor 'thromboplastin '
coming into direct contact with factor VII. Factor VII is

An Antagonist Of Vitamin And Its Effect On The Formation...
All three of the drugs being studied do to some degree affect fundamental processes within a
'coagulation cascade'.
If one of the in vivo processes is altered within the cascade the cycle cannot complete with the
formation of Thrombin. [Figure 2]
Warfarin is an antagonist of vitamin K used to treat reoccurrence of DVT and pulmonary
embolisms. 'Stenflo & Nelsestuen, 1974' showed prothrombin 'the precursor to thrombin' to contain
a number of glutamate residues relating to the amino acid γ–carboxyglutamic acid (Gla).
Antagonism in the production of this residue by Warfarin is the key reason for its anticoagulant
action and is shown in red in [Figure 1].
Warfarin affects a VKOR enzyme which would normally ... Show more content on Helpwriting.net
...
(Bügel, 2003)
Enoxaparin is a parenteral low molecular weight heparin used in the treatment of venous
thromboembolisms. (Hirsch et al, 2001) Its mode of action is to increase the rate of antithrombin
(ATlll) a 'suicide substrate' for proteases. Inhibition is brought about as protease cleaves select Arg–
Ser peptide bonds in the centre becoming fixed in a stable 1:1 complex. This in–turn renders (Factor
Xa) 'which sits at the junction of the extrinsic and intrinsic pathways' inactive. This further disrupts
the cascade cycle as Xa can no longer separate prothrombin into the desired thrombin needed for
fibrogen formation.
Apixaban is an oral reversible medicament taken primarily for prevention of stroke and systemic
embolisms for those with atrial fibrillation. It is used commonly in post–operative orthopaedic
surgery (AHFS, 2014). Similarly to Enoxaparin, Apixaban is a direct inhibitor of Xa and follows the
same process of inhibition as Enoxaparin.
Both Enoxaparin and Apixaban affect the coagulation cascade much later on in the mechanism than
that of Warfarin and thus have a faster onset of effect: Enoxaparin (Tmax)= 15mins and Apixaban
(Tmax)= 1–3 hours, with Warfarin (Tmax)= 24–48 hours. (BMA, 2008) This is particulary useful in
emergencies to prevent further clotting when a clot has already reached the lungs or brain for
example.
II. Chemistry
The physiochemical properties of: Log P/D, pKa, S/R and MW

Platelet-Rich Fibrin
Choukroun et al. (130) developed the, platelet–rich fibrin (PRF), which is a second generation
platelet concentrate widely used to accelerate soft and hard tissue healing. Its advantages over the
better known (PRP) include ease of preparation and application, minimal expense, and lack of
biochemical modification (no bovine thrombin or anticoagulant is required).
"The major role of fibrin in wound repair is hemostasis, but fibrin also provides a matrix for the
migration of fibroblasts and endothelial cells that are involved in angiogenesis and responsible for
remodeling of new tissue. Platelet activation in response to tissue damage and vascular exposure
results in the formation of a platelet plug and blood clot as well as the secretion of biologically
active proteins. The fibrin matrix supporting the (PRF) certainly constitutes the determining element
responsible for its therapeutic potential of however platelets and leukocyte cytokines play an
important part in the biology of this biomaterial (131_132)
Platelet–rich fibrin overcomes platelet–rich plasma in the ethical ... Show more content on
Helpwriting.net ...
Second, the integration of this fibrin network into the regenerative site facilitates cellular migration,
particularly for endothelial cells necessary for the neo–angiogenesis, vascularization and survival of
the graft. Third, the platelet cytokines (PDGF, TGF– 3, IGF–1) are gradually released as the fibrin
matrix is resorbed, thus creating a permanent process of healing. Lastly, the presence of leukocytes
and cytokines in the fibrin network can play a significant role in the self–regulation of inflammatory
and infectious phenomena within the graft

Fibrinogen Lab Report
Fibrinogenolytic activity
Fibrinogen is a soluble, large and complex glycoprotein which helps in formation of blood clot 241.
The glycoprotein has two sets of disulfide bridged Aα, Bβ and γ chains. Each molecule has two
outer D domains which is connected to E domain (a central domain) by coiled coil segment 242–
244. The experiment was conducted to observe any effect of crude N. kaouthia venom on various
chains of bovine fibrinogen. In brief, bovine fibrinogen (2mg/ml) was dissolved in 50mM TrisHCl
buffer, pH 7.4, 0.15M NaCl for overnight. Various amounts of crude venom from 1–10µg in 150 µl
of buffer (Tris–Cl buffer, pH 7.4, 0.15M NaCl) were incubated with 300µl of dissolved fibrinogen
for different time intervals (0, 30, 60, 120, 240, 480, 960 and 1440mins) at 37°C 240. The collected
mixtures at various time intervals were then run on a 12.5% SDS–PAGE to observe any changes in
the protein bands of fibrinogen. Staining was done with 1.2% coommassie brilliant blue R250 and
destained with Methanol: Acetic acid: Water (40:10:50) to observe any effect on the Aα, Bβ and γ
chains of bovine fibrinogen.
2.2.12 In–vitro coagulant assays
2.2.12.1 Recalcification time
Recalcification time test was performed according to ... Show more content on Helpwriting.net ...
Activated partial thrombin time was determined using APTT reagent obtained from STAGO
(France) according to the manufacturers' protocol. Various concentrations of crude N. kaouthia
venom/ purified toxin (Nk–3FTx) (0.0042 to 4.2µg/ml) were assayed to determine its effect on
APTT of harvested PPP. The crude venom was pre–incubated with 50µl PBS, 50µl of human PPP
and 50µl of APTT reagent for 3mins at 37oC on a coagulation analyzer (STAGO, France). Further,
50µl of 0.025M CaCl2 was added to the reaction mixture to determine clot formation time. The clot
formation time with PBS was considered as normal clotting

Acute Coronary Syndrome ( A Group Of Conditions With...
Acute coronary syndrome (ACS) refers to a group of conditions with clinical symptoms similar to
acute myocardial ischemia, including pressure–like chest pain associated with nausea and sweating
(1). It includes non–ST segment elevation myocardial infarction (NSTEMI), ST–segment elevation
myocardial infarction (STEMI), and unstable angina (UA). ACS patients are at increased risk of
myocardial infarction and death, therefore, the moderate– to high–risk patients with ACS are treated
with early cardiac catheterization followed by prompt revascularization (1, 2). In order to prevent
peri–procedural thrombotic problems during the percutaneous coronary intervention (PCI)
anticoagulation is required (3). Anticoagulation remains the core of ... Show more content on
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This review will aim to integrate our current understanding of the pharmacology of bivalirudin
along with the clinical trials of bivalirudin reported to date. Pharmacokinetics and
Pharmacodynamics Bivalirudin is a short–acting direct anti–thrombin belonging to DTI class of
compounds. DTIs are structurally related to hirudin molecule (3). Bivalirudin is a hirudin analog
that is a 20 amino acid synthetic polypeptide (3). It displays linear pharmacokinetics with low oral
bioavailability (13, 14). Due to the low oral bioavailability, bivalirudin is given as an intravenous
infusion. There is little distribution of volume with a short half–life of 25 minutes (13–15).
Bivalirudin clearance is independent of gender and dose but renal function dependent (16). The drug
is cleared mainly by intracellular proteolysis and 20% of the unchanged drug is cleared renally (17).
Bivalirudin pharmacokinetics and pharmacodynamics have been studied in the setting of renal
impairment (16). In mild renal impairment, plasma clearance of bivalirudin was not significantly
decreased when compared with normal kidney function. However, in moderate and severe renal
impairment, the plasma clearance of bivalirudin reduced 21% and 24%, respectively (16).
Mechanism of Action Thrombin is generated from prothrombin after initiation of the

Enoxoparin Sodium Injection ( Low Molecular Weight Heparin )
Lovenox (Enoxoparin Sodium Injection) Classification: Anticogaulant (Low Molecular Weight
Heparin)
MW: 1134.899 g/mol pKa1 –2.4 pKa2 –4.4
Chemical Formula: C26H42N2O37S5 IUPAC name 6–[6–[6–[5–acetamido–4,6–dihydroxy–2–
(sulfooxymethyl)oxan–3–yl]oxy–2–carboxy–4–hydroxy–5–sulfooxyoxan–3–yl]oxy–2–
(hydroxymethyl)–5–(sulfoamino)–4–sulfooxyoxan–3–yl]oxy–3,4–dihydroxy–5–sulfooxyoxane–2–
carboxylic acid Description
Enoxaparin is a highly acidic mucopolysaccharide. It is an anticoagulant drug that is used primarily
for prophylaxis of deep vein thrombosis (DVT) or for patients that exhibit pulmonary embolism
(PE) that have underwent specific surgery. Enoxaparin functions as a serine–type endopeptidase
inhibitor and targets antithrombin–III. It binds to it and creates a vertex that irreversibly inactivates
clotting factor Xa. Enoxaparin binding to antithrombin–III also accelerates the activity of
antithrombin–III which is a serine protease inhibitor that modulates the activation of blood
coagulation. Enoxaparin inhibits the production of prothrombin to thrombin. Antithrombin–III
inhibits thrombin, factors Xa, IXa, and XIa, as well as matripatase–3/TMPRSS7. With the presence
of enoxaparin its inhibitory activity is increased greatly. With the Xa being catalyzed by the
attachment of enoxaparin, the translation of prothrombin to thrombin is decreased.

Xylocaine Report
The battle to properly label manufactured goods has been an ongoing debate between governments
and manufacturers worldwide and evidence has been documented as far back as early 13th century
England's first food regulatory law, the Assize of Bread (LTD, 2008). The purpose of labeling is to
protect the consumer and prevent misbranded or false prompts from harming said consumer. A
properly labeled medication should tell what the medicine is, what it is supposed to do, who should
or shouldn't take it, and how to use it. This report will cover the prescription labeling and usage for
Xylocaine with Epinephrine, Thrombin, and Dantrium Sodium. Xylocaine by itself is the brand
name for the generic drug lidocaine and it is classified as a local anesthetic ... Show more content on
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Unlikely, but the most common side effects and adverse reactions (incidence ≥ 2%) are
hypersensitivity, bleeding, anemia, post–operative wound infection, thromboembolic events,
hypotension, pyrexia, tachycardia and thrombocytopenia. For normal healthy adults, where bleeding
is profuse, the dose of Thrombin–JMI is usually concentrations of 1,000 International Units per mL
and dental extractions, skin grafting, etc. solutions containing approximately 100 International
Units/mL are frequently used (Chuna, 2016). Dantrium is the trade name for a generic drug called
dantrolene–sodium which is classified as a direct–acting skeletal muscle relaxant. This drug is
available for use in both intravenous and capsule form, the following information if for the
intravenous product

Hepatic Portal Vein Obstruction ( Ehpvo )
Introduction: Extra–hepatic portal vein obstruction (EHPVO), i.e., in the absence of liver cirrhosis
or abdominal cancer, is a rare manifestation of venous thrombosis that often leads to portal
hypertension1.After prothrombin, factor V, next most common cause of thrombophilia is high
plasma levels of coagulation factor VIII, which are present in approximately 20% of patients with
deep vein thrombosis (DVT) of the lower limbs and increase the risk of the disease in a dose–
dependent manner 2. Like fibrinogen, factor VIII is an acute phase reactant whose concentration
rises in plasma in the presence of inflammation. However, high factor VIII levels are associated with
an increased risk of DVT independently of the acute phase reaction3.
Case report: A 21–year–old male in good health and with no significant past medical history
presented with abdominal pain for 2 months in epigastric and left hypochondrium. He is not on any
drugs. History of similar complaints in his younger sister and she died 2 years back without any
evaluation. A contrast enhanced computed tomography scan of the abdomen showed superior
mesenteric vein thrombosis with multiple collaterals in perigastric and porta hepatis. A coagulation
profile work–up was done. His factor VIII activity concentration was found to be 260% of normal
(normal: 60–150). Analyses for prothrombin O20210A

School Of Pharmacy : Memo
TTUHSC School of Pharmacy
Memo
To: John Zoidberg
From: Tuong Nguyen
Date: December 4, 2015
Re: Information on Pradaxa Dr. Zoidberg,
Thank you for your request for information regarding Pradaxa (dabigatran etexilate). As you stated,
you have a patient named PF, who is planned to have hip arthroplasty in 2–4 weeks due to
degenerative joint disease that is unresponsive to either physical therapy or simple pain relievers.
Mr. PF is a 79 year–old male with hypertension and hyperlipidemia. His current medications include
naproxen 220 mg po bid, tramadol 50 mg po tid, and enalapril 10 mg po qd. In addition, Mr. PF has
the codeine allergy. Because of Mr. PF's severe fear of giving himself shots, your concern is whether
or not Mr. PF can have Pradaxa orally instead of enoxaparin 40mg subcutaneously for DVT
prophylaxis and still receives the similar efficacy and safety.
The dabigatran etexilate (DE) is a prodrug that directly competes for the active site of thrombin.1
This direct inhibition inactivates both fibrin–bound and free form of thrombin. Because of its rapid
onset and offset of action, there is no need for the initial parenteral anticoagulant treatment in
patients with acute thrombosis.1 On the other hand, the enoxaparin indirectly inhibits factor Xa.2 It
has a shorter duration of action (12h vs 24h) and a shorter half–life (4.5–7h vs 12–14h) in
comparison to DE. The DE and the enoxaparin have no interaction with diet and alcohol. There is no
routine monitoring required

Pharmacology : An Important Aspect Of The Surgical...
Pharmacology is an important aspect of the surgical environment. Many different medications are
used for a variety of indications at the sterile field; as a surgical technologist you are responsible for
verifying and properly labeling all medications included in the surgical procedure. The three
medications this paper will focus on are topical thrombin, heparin, and Xylocaine® with
epinephrine; all are commonly used during surgical procedures for very different reasons. Topical
thrombin, also known under the brand name of Thrombin–JMI®, is bovine in origin (PDR,
Thrombin). It is classified as a hemostatic agent (Snyder, 2017), which requires a doctor's order and
is placed in category C for pregnant women and should only be administered ... Show more content
on Helpwriting.net ...
In surgery it is most often used in the dry, powder form and is dusted onto oozing surfaces as
needed. For reconstituted thrombin, the recommended dosage is 1,000 to 2,000 International Units
per milliliter (King, FDA, 2016). Vials come in total volumes of 5,000 units with a 5 mL diluent and
20,000 units with a 20 mL diluent (Medscape, thrombin). Thrombin is for topical use only (Snyder,
2017). This product should never be directly injected into the circulatory system, used in patients
with antibodies to bovine thrombin or Factor V, have a history of hypersensitivity to thrombin or
bovine products, or for severe arterial bleeding (PDR, Thrombin). Antibodies may develop in
patients with repeated exposure to topical thrombin. Side effects include: bleeding, thrombosis,
hypersensitivity, anemia, postoperative wound infection, hypotension, pyrexia, tachycardia, and
thrombocytopenia (PDR, thrombin). Adverse effects, which may be life threatening, include
anaphylaxis and extensive intravascular clotting if it enters large blood vessels (King, FDA 2016).
At the opposite end of the spectrum from thrombin is heparin sodium. Heparin sodium; which is
also known as Heparin Sodium Injection, USP, Fragmin®, Innohep®, and Lovenox®. Fragmin,
Innohep, and Lovenox are low molecular weight heparin products (Snyder, 2017). Heparin sodium
is classified as a glycosaminoglycan anticoagulant, which requires a doctor's

Symptoms And Treatment Of Acute Coronary Syndrome
Introduction Acute coronary syndrome (ACS) refers to a group of conditions with clinical symptoms
similar to acute myocardial ischemia, including pressure–like chest pain associated with nausea and
sweating (1). It includes non–ST segment elevation myocardial infarction (NSTEMI), ST–segment
elevation myocardial infarction (STEMI), and unstable angina (UA). ACS patients are at increased
risk of myocardial infarction and death, therefore, the moderate– to high–risk patients with ACS are
treated with early cardiac catheterization followed by prompt revascularization (1,2). In order to
prevent peri–procedural thrombotic problems during the percutaneous coronary intervention (PCI)
anticoagulation is required (3). Anticoagulation remains the core of treatment in patients with ACS.
The most frequent anticoagulation used during early phase of ACS and PCI is low molecular weight
heparins (LMWHs) and unfractionated heparin (UFH) (3). The combination of antithrombotic and
antiplatelet agents are efficient in containing ischemic events in relation to PCI, but have been noted
to have higher rates of bleeding complications (4–10). Bivalirudin has shown to have a better safety
profile when compared with heparin along with glycoprotein IIb/IIIa (GP) administration (11).
Bivalirudin for this reason is considered the anticoagulant of choice in patients with ACS.
Bivalirudin is a direct thrombin inhibitor (DTI) that is effective against clot–bound thrombin, unlike
UFH and LMWHs (12).

The Field Of Cosmetics And The Treatment Of Injuries,...
Today, the field of cosmetics and the treatment of injuries, skin, and hair ailments have gained the
attention of doctors all over the world. While multiple treatment methods have been examined,
preference remains for the safest and the most effective method. Recently, treatment with PRP has
been established as an effective medical treatment in many fields, such as oral surgery, neurosurgery,
cosmetic surgery, sports medicine, and orthopedics. Platelets are one of the essential components
found in blood, known best for their importance in coagulation. They contain proteins known as
growth factors that play an essential role in healing damaged tissue (Lubkowska et al., 2012). The
normal range of platelets in healthy human blood ranges from ... Show more content on
Helpwriting.net ...
Despite these variations, all protocols follow the same sequence: blood sample collection, a soft spin
for separating blood components, followed by a hard spin for concentrating the platelets, in the
presence or absence of anticoagulants, and growth factor activators.
Kececi, Ozsu, and Bilgir (2014) examined the effect of the number of spins on the platelet recovery
during centrifugation. Both single and double centrifugation methods were used to prepare the PRP.
Two sets of blood samples were drawn from 10 adult New Zealand rabbits. The blood samples were
added into 10% sodium citrate and centrifuged; The first group was single centrifuged at 160 G for 6
minutes at room temperature, while the second group was double centrifuged, the first spin was at
160 G for 20 minutes at room temperature, followed by the second spin at 400 G for 15 minutes.
Average platelet amount collected from the second group (1,986,875 ± 685,020/μl) was greater than
the first group (781,875 ± 217,693/μl). According to Amable et al. (2013) different centrifugal forces
have been applied to obtain pure PRP from the blood samples obtained of healthy donors (4.5 ml of
WB), using a refrigerated high speed centrifuge, with speeds reaching up to 30,000 rpm (rotation per
minute). Since the lower centrifugal force (less than 300 x g) did not release a sufficient amount of
PRP, 300 × g for 5 minutes at 18°C

Hemostasis Research Paper
Hemostasis is the process that causes bleeding to stop. It also changes blood from a liquid to a gel. It
consists of three processes, vascular spasm, platelet plug formation and blood coagulation. Vascular
spasm is the first step in heeling in the wound. Vascular spasm is when the damaged blood vessels
constrict due to tightening of muscle cells on the inside wall. This helps decrease blood flow, thus
minimizing blood loss. Then platelet plug formation occurs. This is when platelets adhere to the
damaged endothelium and form a plug. Normally platelets do not stick to the endothelial lining but
during an injury collagen is exposed. The exposed collagen activates the platelets to stick together
and form a plug. Once the platelets are stuck together

Exercise 40 Chi Squared Essay
Researchers routinely choose an ◊–level of 0.05 for testing their hypotheses. What are some
experiments for which you might want a lower ◊–level (e.g., 0.01)? What are some situations in
which you might accept a higher level (e.g., 0.1)?
An alpha level of 0.05 is arbitrary and was set as a standard by scientists. One of the key concepts in
hypothesis testing is that of significance level or, the alpha level, which specifies the probability
level for the evidence to be an unreasonable estimate. Unreasonable means that the estimate should
not have taken its particular value unless some non–chance factor(s) had operated to alter the nature
of the sample such that it was no longer representative of the population of interest. (Price, 2000) ...
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(2000). What Alpha Level? In I. Price, Inferential Statistics (p. Chapter 5). New England: University
of New England.
University of Texas–Houston Health Science Center . (2013). Hypothesis Testing . Retrieved March
21, 2013, from Biostatistics for the Clinician :
http://www.uth.tmc.edu/uth_orgs/educ_dev/oser/L2_2.HTM
4DQ1
How would you explain the analysis of variance, assuming that your audience has not had a
statistics class before?
When examining the differences between two or more groups, you can use the analysis of variance
which is known as ANOVA. This is a statistical technique that is used to compare the means or
averages of more than two groups. There are three uses of ANOVA which are the one–way, the two–
way and N–way Multivariate ANOVA. (Solutions, 2013) The determining factor when to use one of
the "ways" is dependent upon how many "treatments" are used in the study. We use the term
treatment because ANOVA originated in the 1920's to test different treatments of fertilizers' crop
yields. ("Analysis of Variance," 2012, p. 2) Here, we will cover the one–way and the two–way
ANOVA.
The one–way between groups, ANOVA is used when you want to test the difference between two or
more groups. This is the simplest version of ANOVA. (Crossman, 2013) This could be used for
example in a study on the ages of patients on different cardiac medications. Here we are only
looking at

Anticoagulation Therapy
Anticoagulation therapy is indicated for the prevention of stroke and systemic embolism in patients
with chronic atrial fibrillation (AF), and for the treatment of arterial and venous thromboembolism.
The vitamin K antagonist warfarin has been the most commonly used anticoagulant for the
prevention of AF related thromboembolic complications for the past 60 years. Warfarin's
effectiveness is complicated by its variable pharmacokinetic profile, narrow therapeutic index, and
numerous food and drug interactions. These limitations have led to the development of more ideal
target–specific oral anticoagulants. Four target–specific oral anticoagulants (TSOACs), also
commonly referred to as novel oral anticoagulants (NOACs), have been approved by the ... Show
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FDA (2014) conducted its own observational study of 134,000 Medicare beneficiaries ages 65 and
older, comparing dabigatran and warfarin for rates of ischemic stroke, intracranial hemorrhage,
major gastrointestinal bleeding, myocardial infarction, and death. They found that dabigatran was
associated with a lower risk of ischemic stroke, intracranial hemorrhage, and death compared with
warfarin. They observed an increased risk of major gastrointestinal bleeding compared to warfarin.
These findings echo those of the RE–LY trial. Based on this data, the FDA did not adjust
dabigatran's label or recommendations for use, but advises health care professionals and patients to
report adverse side effects to the FDA MedWatch program (U.S. FDA,

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