Pob Case

Pob Case
Clinical Overview (Module 2.5) includes Efficacy summary, safety summary, justification of dosing
recommendations, appropriateness of product information, future plans for pediatric development,
any risk to different peoples, and benefit–risk ratio. For the given product the following objectives
need to take into consideration during the benefit–risk analysis. Doses of the Pob (investigational
drug) for different age groups, Side effects on the different age groups, Side effects of the pregnant
woman, Side effect on people of different origins, Effectiveness of the drugs, Maximum dose
allowance, t ½ time for Pob and others. In this particular case this investigational drug Pob is
investigated for the prophylactic treatment of congenital FXIII
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The Stages Of Acute Cutaneous Wound Healing
The stages of acute cutaneous wound healing and why some processes may be altered in diabetic
patients
"The process by which tissue repair takes place is termed wound healing and is comprised of a
continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory
cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore
a semblance of their usual discipline and having done so resume their normal function". ("The
Cellular Biology of Wound Healing" 2016)
Wound healing has 3 distinct stages, an inflammatory response, a proliferation phase and a
maturation phase, however wound healing is not a linear process and a patient can move back and
forth throughout the stages.
After the occurrence of a wound the inflammatory process immediately begins and can last up to 3
days ("Wound Healing" 2016), the initial injury causes the small vessels around the wound site to be
disturbed resulting in bleeding, the body's first response is a haemodynamic one in that it restricts
these vessels in order to prevent blood loss. There then comes a rapid release of preformed
inflammatory mediators from the cells surrounding the injury, the first thing this causes is the
aggregation of platelets, these platelets adhere to extracellular surface structures which are exposed,
such as collagen and basement membranes, this in turn causes serotonin from platelet stores to be
stimulated. (Kirk, Phillips and Murray 2001)
As well as

Hemophilia Research Paper
Hemophilia (sometimes spelled haemophilia) is a rare genetic blood disorder which prevents blood
from clotting normally. There are two types of hemophilia, and they are hemophilia A and
hemophilia B. Hemophilia A is also called classic hemophilia, and is caused by a mutated or missing
factor VIII, which is a clotting protein. Hemophilia B is sometimes called Christmas disease,
because the disorder was first reported in a patient with the last name Christmas. Hemophilia B is
caused by a mutated or missing factor XI, which is also a clotting protein. Although it wasn't named
yet, hemophilia was recognized in the 2nd century AD, in a collection of Jewish Rabbinical
writings. A 12th century physician named Albucasis wrote about a family

Altepalase Research Paper
2. Dora is right in believing that there is a medication that helps patients that are experiencing a
stroke. This medication is given to patients that are having an ischemic stroke. This medication is a
tissue plasminogen activator also known as a TPA, which is a thrombolytic and it breaks up clots
(Stroke Treatment). There are two fibrinolytics that can be used, alteplase and tenecteplase (Bledsoe,
p.g. 112). This medication improves the chances of recovering from an ischemic stroke. Alteplase is
an enzyme called serine protease that has the same property of fibrin enhanced conversion of
plasminogen into plasmin. "It produces limited conversion of plasminogen in the absence of fibrin.
Alteplase binds to fibrin in a thrombus and converts the ... Show more content on Helpwriting.net ...
The muscles then begin to spasm and further begin to violently shake and convulse (Silverman,
Isaac E). Tonic clonic is the most common major motor seizure and involves rhythmic bilateral
contractions of the muscles and extension of the extremities with an immediate loss of
consciousness (Grossman, p.g.521). Following the contraction and relaxation phase, the individual
will remain unconscious until the reticular activating system becomes functional again (Grossman,
p.g.521). These seizures typically last 60–90 seconds and incontinence of the bowel and bladder are
common and may occur during this time (Grossman, p.g.521). It is common to experience a seizure
after a hemorrhagic stroke and strokes are the most common cause of seizures in older people
(Silverman, Isaac E). The seizure is a sign of brain injury and are caused by a sudden onset of
disorganized electrical activity in the brain. The increase in intracranial pressure causes Cushing's
response. Cushing's response is changes that the body experiences to compensate for the rising
intracranial pressure ("Intracranial Pressure and Cushing Response). Donald is also experiencing
Cushing's triad which is three

Symptoms And Symptoms Of Sjogren Syndrome
Pulmonary histologic manifestation of Sjogren syndrome include nonspecific interstitial pneumonia
, organizing pneumonia , usual interstitial pneumonia , lymphocytic interstitial pneumonia, primary
pulmonary lymphoma , non caseating granuloma, bronchiolitis and diffuse interstitial amyloidosis.
Acute fibrinous and organizing pneumonia (AFOP) is a histological pattern characterized by intra–
alveolar fibrin deposition and associated organizing pneumonia. AFOP has been associated with
rheumatologic disorders in the literature but has not been described in association with Sjogren's
syndrome. We present a case of a 75 year old female with history of Sjogren's syndrome who was
not compliant with her medications. She presented to our clinic ... Show more content on
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The histological pattern are devoid of hyaline membrane, eosinophils, granulomatous inflammation
or extensive pneumonia or abscess1. Other minor features include acute or chronic inflammation,
type 2 pneumocyte hyperplasia and alveolar expansion with myxoid tissue1. This entity was first
published by Beasley et al in 2002. The case of 17 patients showed male and Caucasian
predominance with average age of 62 years. Average time to onset of symptoms was 19 days, and
the most common symptoms includes cough, shortness of breath and constitutional symptoms like
fatigue or malaise1. AFOP etiology could be idiopathic or due to a wide range of medical conditions
including rheumatologic diseases like systemic lupus erythematous, ankylosing spondylitis,
polymyositis, polymyalgia and juvenile dermatomyositis 1,2. Sjogren's syndrome is a slowly
progressive autoimmune disorder that affect many organ systems. Patients with Sjogren's syndrome
represent about 2 percent of the population and most commonly present with symptoms related to
diminished lacrimal and salivary gland function 3. Pulmonary involvement in Sjogren's syndrome is
common. Histological pattern seen include nonspecific interstitial pneumonia , organizing
pneumonia , usual interstitial pneumonia ,

What Are Possible Impacts Of FGF2 On Osteogenesis And Bone...
Bones: Possible impacts of FGF2 on osteogenesis and bone recovery have additionally been
accounted for. (Lisignoli et al.) refined BMSC's got from rats inside a hyaluronate–based polymer
framework with or without FGF2 . They found that the nearness of FGF2 firmly improved the
statement of osteogenic targets/markers and generalization, showing a conceivable part in bone
recovery. (Tabata et al.) Contemplated the part of FGF2 in a rabbit skull imperfection demonstrate.
Gelatin hydro–gel was additionally used to consolidate FGF2 to frame a polyionic complex and
capacity as a successful transporter. At 9 weeks, the inserts indicated emotional change in
imperfection conclusion, bone mineral thickness, and bone recovery in bunches treated with ...
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The materiel used was appeared to draw out the life expectancy of FGF2 upon managed discharge
for up to 20 days in vitro. The embed tests following three months were found to initiate incredible
improvement in new–bone development and mechanical solidness on the Matrigel–FGF2–treated
gathering when contrasted with bunches treated with FGF2 or Matrigel alone. The attending of
osteo–chondral complex tissue was similarly studied in vivo utilize a complex framework formed
HA/collagen primer FGF2. FGF2 was infused inside the HA/collagen platform and after that
enclosed into the osteo–chondral perfection in a rabbit femoral knee. In the times of implantation
through 4 to 25 weeks, FGF2–treated platform amass showed incredibly improved bone recovery
and attractive ligament recovery, proposing that the HA/collagen composite is a decent possibility
for conveying FGF2 amid the recovery of osteochondral deformity. While there has been some
accord with respect to change of the proliferation capability of osteoblasts, some unfriendly impacts
of FGF2 on the osteogenic separation and generalization have likewise been recognized.(Bosetti et
al.) examined the striking of different FGFs (FGF2, FGF4, and FGF6) on the behavior of human–
necessary osteoblasts. They examined that all FGFs activated in culture medium at 0.8 μM incited
osteoblast enlargement yet stopped ALP motion and generalization. When it comes to Vitamin D, it
was

What Is The Role Of FXI As A Therapeutic Strategy For...
FXI play a crucial role in coagulation, thromboembolism, and peripheral vascular disease mediated
by venous thrombus growth in an endothelial denudated vessel and/or blood stasis. Promotion of the
platelet aggregation and fibrin formation at low shear stress by the interaction of FXI and thrombin
signify the role of FXI in thromboembolism [47]. Further, reduction in the thrombus formation in a
denuded vessel with anti–FXI antibody indicates FXI to be a promising target in coagulation
cascade to prevent thromboembolic events [47,48]. Many studies has demonstrated the reduced
thrombus formation without increasing the risk of bleeding with antisense oligonucleotide (ASO)
along with increased number of fluorescent platelets shed from the ... Show more content on
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Factor XII inhibition and atherothrombosis
The role of FXII and FXIIa in atherothrombosis and inflammation has been documented in various
studies. Since inflammation does play a role in the pathogenesis of plaque formation and plaque
rupture resulting in thrombus formation, inhibiting FXII/FXIIa might abrogate the ongoing
inflammation and thrombus formation [7,29]. The findings of substantially less infarcted brain
without an increase in infarct–associated hemorrhage in FXII–deficient and FXII inhibitor treated
mice after transient middle cerebral artery occlusion suggest FXII to be dispensable for hemostasis
but instrumental in fibrin formation. This effect was due to impaired pathological fibrin formation
after FXII inhibition without increased bleeding [53]. Additionally, minimized trauma–induced
microvascular thrombus formation and ischemic injury with factor XII inhibitor rHA–Infestin–4 in
mice signify the thromboprotective effect of FXII inhibition [54] (Figure 2). These studies support
that FXII inhibition might be a safe and selective thromboprotective strategy [15].
To date, several classes of inhibitors of FXII and FXIIa including antibodies, biological inhibitors,
recombinant proteins, synthetic peptides, and antisense oligonucleotides along with their mode of
action, concurrent side–effects and the animal models in which

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

Essay On Wound Regeneration
The greatest challenge in clinical research trials is the development of bioactive surgical additives to
reduce the post operative signs and symptoms by regulating inflammation and increase the speed of
healing process. [1] An extensive intra cellular and extra cellular set of event are carried out in the
healing of soft and hard tissue which are medicated by signalling proteins. [2]Yet complete self–
regeneration in many tissues and organs after injury is limited. In endogenous regenerative
medicine, tissue recovery is stimulated by blood plasma, growth factors and cytokines from
platelets. [3, 4] Several studies are focusing on the development of innovative technologies for
tissue regeneration based on the use of different graft ... Show more content on Helpwriting.net ...
PRP is the precursor of another autologous derivates, the platelet–rich fibrin (PRF), a solid fibrin–
based biomaterial. [13]
A recent classification divided plasma concentrates into four different categories depending on their
leukocytes and fibrin content: pure platelet–rich plasma (P–PRP), such as cell separator PRP,
Vivostat PRF or Anitua's PRGF; leucocyte– and platelet–rich plasma (L–PRP), such as Curasan,
Regen, Plateltex, SmartPReP, PCCS, Magellan or GPS PRP; pure plaletet–rich fibrin (P–PRF), such
as Fibrinet and leucocyte– and platelet–rich fibrin (L–PRF), such as Choukroun's PRF. This
classification helps to analyse the successes and failures that have occurred so far in oral surgery,
and direct research towards further applications of these technologies in daily clinical practise. [14–
16]
PLATELET RICH FIBRIN:
Platelet–rich fibrin (PRF) is an autologous biomaterial which is the second generation of platelet
concentrates. It is the successor of platelet–rich plasma (PRP), having multiple benefits [17]. The
benefits of working with PRF are quicker preparation, availability for every patient and minimal
trauma. Several works related to the issue of the use of PRP and PRF in periodontal, oral,
maxillofacial and plastic surgery as well as in otorhinolaryngology have been published [18]. Some
of the application in oral and maxillofacial are: sinus augmentation after maxillary sinus floor

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

Fibrin Microthreads
Pre – Lab 2 1. Fibrin microthreads and fibrin gels differ in that fibrin gels are weaker than fibrin
microthreads. Fibrin microthreads are mechanically stronger than fibrin gels because they can be
braided together to form larger porous structures. Fibrin microthreads are also more similar to tissue
already found in the body and therefore are a better structure for processes such as cell attachment.
Fibrin gels can be used in the development of biomaterials because they can be used in surgery and
be used in the process of wound healing. 2. UV treatment increased the mechanical strength of the
fibrin microthreads, decreased the swelling ratio, and decreased cell proliferation. UV treatment
increased the mechanical strength of the threads the most at around 17 J/cm^2, and the UTS of the
threads increased after treatment. Swelling ratio of the threads decreased from around four times
more than dry threads to around 2.5 times more after UV treatment. Cell proliferation decreased
because while the number of cells on non UV treated threads continued to ... Show more content on
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According to the data I collected, accuracy and precision do remain for the most part constant for
the different volumes. I was the most accurate during one of my measurements of 200 µL, but I was
the most precise with my measurements of 25 µL and 50 µL. 4. The slope of the linear fit of the data
is 1.0049. What this tells me about the water is that it is increasing at a close to constant rate – while
my results were not completely accurate because the slope of the line was not one it was fairly close
to the target

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

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

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

Septic Arthritis Research Paper
Septic Arthritis
Septic arthritis is a common cause of severe lameness in cattle. Most commonly the distal
interphalangeal joint is involved, but septic arthritis of proximal joints (fetlock, carpus, tarsus, stifle
etc.) have been reported on a much lower frequency. Bacteria can colonize the joint in 3 different
ways: (1) through a wound directly invading the joint, (2) by close proximity of a primary infection
site to the joint and migration the bacteria within the inflamed tissue into the joint, and (3) by
hematogenous spread from bacteremia. In this manner, joints can become infected remotely from
the primary source of infection. Adult cows tend to suffer more from the first 2 etiologies of septic
arthritis and therefore a single joint is ... Show more content on Helpwriting.net ...
Septic arthritis induces a high intensity nociceptive stimulus. In addition to the treatment options
above, anti–inflammatory drugs are utilized for cases of septic arthritis. These NSAIDs (e.g. flunixin
meglumine, ketoprofen, carprofen, meloxicam) are administered for 3 days, and are used for
inhibition of the inflammatory mediators, for reduction of the inflammatory swelling, and to help
make the animal feel better overall so hopefully they continue to eat. If pain is unaffected by
administration of nonsteroidal anti–inflammatory drugs, a multimodal pain management plan should
be attempted to allow the animal to be more comfortable, but also to allow the joint to be mobilized
with the maximal range of

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

Explain The Biological Process Of Osseointegration
The biological process of osseointegration following the creation of an osteotomy site includes
blood clot formation and the release of growth factors (BMP's, VEGF etc.); this is followed by new
blood vessel formation (Angiogenesis). The presence of a fibrin scaffold between the osteotomy site
and the surface of the implant serves as a transition between the bone marrow (where the
osteoprogenitor cells are located) and the surface of the implant, which is a very important factor in
the migration of osteoprogenitor cells into the bone–implant interface zone. When the cells get
there, they begin the deposition of lamellar bone and then the formation of a more mature bone on
the surface of the implant to achieve a good osseointegration. The reason

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

Differences Between Pla And Pla
Investigations into 2D material substrates were designed to include a number of principles
associated with a 3D biodegradable scaffold surface. Firstly cytoskeletal tensions are known to
influence MSC lineage commitment on substrates of different elasticities. Figure 8 1 demonstrates
hypothetical differences in substrate elasticity as a result of agglomeration.
Results from chapter 5 did not specifically address the differences in substrate elasticity due to
difficulties with HAp dispersion within PLA. However one cell viability assay demonstrated no
significant difference between PLA and PLA (non–dispersed) HAp. Further investigations are
required in order to determine any potential effects of this principle. However, it is likely that the
inherent stiffness of PLA hides any elasticity changes caused by HAp inclusion to the MSC.
Results from chapter 6 demonstrate MSC responses to fibrin and fibrin/HAp filled substrates. As
was evident from SEM and TEM images, the HAp within the fibrin was agglomerated. Results from
morphological analysis of MSC demonstrated some decrease in cell spreading on fibrin/HAp
compared with fibrin substrates. Fibrin is a softer material, and it is more probable that differences
observed between fibrin and fibrin/HAp substrates is due to changes in substrate elasticity.
Secondly, protein adhesion is a fundamental facilitator of cell adhesion. Figure 8 2 demonstrates
hypothetical differences in protein binding on HAp filled and coated substrates.

Pathophysiology of Stroke
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References Bryant, B & Knights, K 2011, Pharmacology for health professionals, 3rd edn., Elsevier,
Australia. Craft, J Gordon, C 2011, 'Alterations in neurological function across the life span', in J
Craft, C Gordon, A Tiziani (eds), Understanding pathophysiology, Elsevier Mosby, Chatswood,
NSW, pp. 188–226. Brain foundation 2011, A–Z of disorders, Stroke, Brain Foundation, Sydney,
viewed 30 June 2011, . 3. Would it be appropriate to consider treating this patient with tissue
plasminogen activator (tPA, alteplase)? How does this drug work? Treating Mrs Smith with tissue
plasminogen activator (tPA) or alteplase would be advisable after the evidence from the magnetic
resonance imagery (MRI) scan confirmed no haemorrhagic conditions existed, even though the
presenting symptoms greatly suggest a transient ischaemic attack (TIA) has occurred (Brain
Foundation 2011). Tissue plasminogen activator is a fibrinolytic drug which is used to treat
thromboembolic disorders, such as ischaemic strokes. These agents initiate secondary fibrinolysis to
occur; altering the haemostatic capability. The primary purpose of this agent is to clear occluded
blood vessels within the systemic circulation (Bryant & Knights 2011, pp.534–536). The occlusion,
caused by a haemostatic plug or thrombus is comprised of a fibrous protein called fibrin. This
protein polymerises to create a tightly woven mesh, trapping platelets within the fibrin fibre
meshwork, resulting in the

Why Does Pneumonia Develop?
How does (typical) Pneumonia develop?
–Most of the time the body will filter the organisms
–keeps the lungs from becoming infected.
–But sometimes organisms enter the lungs and grow, and they can cause infections.
–This is more likely to occur when: the immune system is weak. the organism is very strong. the
body fails to filter the organisms
Pathogenesis
The lower respiratory tract is normally sterile by physiologic defense mechanisms including
(Mucociliary clearance)
Lobar Pneumonia:
–caused by mainly bacteria called Strep pneumonia
–Rare due to antibiotic treatment.
Can be caused by Mycobacterium tuberculosis, if pulmonary pneumonia is left untreated
Four stages of lobar pneumonia
Congestion:
–Presence of a proteinaceous exudate,

Factor Vs Juavian
The Genetics of Factor V Leiden
Factor V Leiden as named after the Dutch city Leiden in which it was discovered. Factor V Leiden
is a genetic blood clotting disorder that results from a mutation of the Factor V gene. Most of the
time you will inherit Factor V Leiden from your family. If kept under control blood clots are mostly
harmless, but if left uncared you can have a piece of the blood clot break and enter your lung there it
will cause serious damage like a heart attack or stroke. The main job for our blood is to transport
important nutrients and oxygen to all the body tissues. Your blood must remain in liquid form to so
it can flow easily through your body. When a person gets a injury the blood will flow and form a
plug is this know

Hemophilia Research Paper
Hemophilia is a lot more than just a cut that doesn't stop bleeding. For starters, the word hemophilia
is a combination of the Greek words for "blood" and "love", which is a way of saying people with
hemophilia "love to bleed"or just can't stop to blood. Why is that? A large part about the disease
comes from the effect it has on the cardiovascular system, but more importantly the hemostasis of
the body. Normally, when damage occurs to a blood vessel walls, there's an immediate narrowing of
the blood vessel which limits the amount of blood flow. Which leads for some platelets adhere to the
damaged vessel wall, and become activated that then recruit additional to form a plug. This platelet
plug is the result of the primary hemostasis. Leading up to the coagulation cascade to be activated.
In 2010, Chris Pallister and Malcolm Watson best summarized coagulation cascade as: ... Show
more content on Helpwriting.net ...
These are the contact activation pathway (also known as the intrinsic pathway), and the tissue factor
pathway (also known as the extrinsic pathway) which both lead to the same fundamental reactions
that produce fibrin. The pathways are a series of reactions, in which a zymogen (inactive enzyme
precursor) of a serine protease and its glycoprotein co–factor are activated to become active
components that then catalyze the next reaction in the cascade, ultimately resulting in cross–linked
fibrin. Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended
to indicate an active form. The coagulation factors are generally serine proteases (enzymes), which
act by cleaving downstream proteins. The exceptions are FIII, FV, FVIII, FXIII. FIII, FV and FVIII
are glycoproteins, and Factor XIII is a transglutaminase.

The Effects Of Wound Healing On Diabetic Patients
eous wound healing and why some processes may be altered in diabetic patients
"The process by which tissue repair takes place is termed wound healing and is comprised of a
continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory
cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore
a semblance of their usual discipline and having done so resume their normal function". ("The
Cellular Biology of Wound Healing" 2016)
Wound healing has 3 distinct stages, an inflammatory response, a proliferation phase and a
maturation phase, however wound healing is not a linear process and a patient can move back and
forth throughout the stages.
After the occurrence of a wound the inflammatory process immediately begins and can last up to 3
days ("Wound Healing" 2016), the initial injury causes the small vessels around the wound site to be
disturbed resulting in bleeding, the body's first response is a haemodynamic one in that it restricts
these vessels in order to prevent blood loss. There then comes a rapid release of preformed
inflammatory mediators from the cells surrounding the injury, the first thing this causes is the
aggregation of platelets, these platelets adhere to extracellular surface structures which are exposed,
such as collagen and basement membranes, this in turn causes serotonin from platelet stores to be
stimulated. (Kirk, Phillips and Murray 2001)
As well as attracting further

Fibrinogen Case Study
At least in mice it does. In this issue of Blood, Machlus et al investigated the effects of high
fibrinogen levels using a combination of murine models of thrombosis and in vitro studies, to show
that high fibrinogen leads to increased formation of thrombi that are more resistant to proteolytic
degradation.1 These findings are important because it has long been debated whether elevated
fibrinogen causes thrombosis or not. There are clearly a number of mechanisms by which higher
levels of fibrinogen could cause thrombosis, including increased blood viscosity, increased fiber
density of the fibrin clot, increased resistance of the fibrin clot to fibrinolysis, and altered
mechanical properties of the fibrin clot (see figure). While clinical ... Show more content on
Helpwriting.net ...
Fibrin is the main structural component of the thrombus. The conversion of fibrinogen to fibrin by
thrombin leads to one of the most remarkable processes in biology in which fibrin spontaneously
forms a gel by producing fibers that grow longitudinally as well as laterally, with branch points
forming and interconnecting the fibers leading to the formation of a 3–dimensional network that
binds platelets and traps other blood cells. Even after the gel point, the architecture of the fibrin
network can change quite dramatically.7 Other plasma proteins such as factor XIII, α2–antiplasmin,
and fibronectin interact with the fibrin and alter its structural and functional properties. Once the
fully organized thrombus is formed, its life span is determined by the resistance of the fibrin clot to
proteolysis by plasmin. The generation of plasmin from plasminogen by tissue plasminogen
activator is enhanced by the presence of fibrin, particularly after partial degradation by plasmin. The
structure of the fibrin clot has been reported to significantly modulate both the rate of proteolysis of
fibrin by plasmin as well as the rate of plasmin formation.8 Two previous murine in vivo studies
point to an

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

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
Helpwriting.net ...
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

The Danger of Deep Vein Thrombosis
Deep vein thrombosis (DVT) is a type of cardiovascular disease. DVT is a blood clot that forms in
the large deep veins in the leg or pelvis area and grows toward the heart. Including the veins in the
calf and thighs, the femoral, popliteal, and iliofemoral vein are also the sites of DVT development. It
is a mainly common and dangerous condition (Kesieme et al., 2011). Some DVTs may cause no
pain or swelling, whereas others might be quite painful and result in a lot of swelling. Mortality is
not high with prompt diagnoses and treatment for most DVTs. However some can be a threat to your
life, especially the ones that develop in the deep veins as compared to the clots that develop in the
visible superficial veins. Clot which forms in the deep veins is more likely to break free and travel
through the veins, which is then called an embolus. When an embolus travels from the legs or pelvis
area and lodges into the lung artery, the condition is known as a pulmonary embolism or PE. This is
a potentially fatal condition if it is not treated immediately and can lead to death. As high as 50% of
the time a DVT can progress to pulmonary embolism. Collectively, DVT and PE are known as
venous thromboembolism (VTE). DVT and PE are highly preventable (Kesieme et al., 2011). Both
DVT and PE are a major public health problem worldwide. DVT affects approximately 0.1% of
persons per year. The overall average age and sex adjusted annual incidence of VTE is 117 per
100,000, with higher rates among

FXII And FXI Case Study
The role of FXII and FXIIa in atherothrombosis and inflammation has been documented in various
studies. Since inflammation does play a role in the pathogenesis of plaque formation and plaque
rupture, resulting in thrombus formation, inhibiting FXII/FXIIa might abrogate the ongoing
inflammation and thrombus formation [5,36]. The findings of a substantially less infarcted brain
without an increase in infarct–associated hemorrhage in FXII–deficient and FXII inhibitor treated
mice after transient middle cerebral artery occlusion suggest FXII to be dispensable for hemostasis
but instrumental in fibrin formation. This effect was due to impaired pathological fibrin formation
after FXII inhibition without increased bleeding [55]. Additionally, ... Show more content on
Helpwriting.net ...
There was no effect on the initial formation of the thrombus, however, the size of the thrombus at a
later time (2 and 10 minutes after plaque rupture) and stability were reduced with the use of corn
trypsin inhibitor or r–HA–infestin–4 to inhibit factor XIIa [32] (Figure 2).
Efficient inhibition of the fibrin deposition and thrombus formation by plasma protease FXIIa–
neutralizing antibody, 3F7, by binding specifically to the enzymatic pocket of FXIIa in an
extracorporeal membrane oxygenation (ECMO) system similar to heparin but without treatment
associated increase in hemorrhage signifies thromboprotective properties of 3F7. Further, inhibition
of the thrombus formation without impairing the hemostasis indicates FXII as a potential target for
prevention of atherothrombosis. The use of ECMO simulating the clinical settings signifies the
meaningful importance of this study to use in clinics. However, the prevention of the contact–
induced FXIIa formation, thrombus formation in mice and rabbits and coagulation in–vitro with 3F7
has also been documented [59,60,61] (Figure 2). FXII activation is also mediated by inorganic
polymer polyphosphate (polyP), which is stored in platelets and secreted on platelet activation [36].
Reduced fibrin accumulation and attenuated thrombus formation without increased risk

Hemostasis Research Paper
Hemostasis is a physiological body response to the event of a vascular injury or a damaged vessel.
On the other hand, thrombosis is a pathological response when the hemostatic mechanisms are
incorrectly activated leading to blood clots formation 1.
The main blood component engaged in hemostasis, and subsequently in thrombosis too, are the
platelets. Platelets during hemostasis adhere to the injured vessel wall creating a barrier that blocks
the blood loss. The initial platelet adhesion is followed by platelet aggregation and platelet–platelet
adhesion which are induced by cytokines released by the activated platelets. As a final step in
hemostasis, the coagulation cascade is stimulated with final result thrombin and fibrin formation at
the site of damage. 1,2 ... Show more content on Helpwriting.net ...
Thrombus formation is generated by vessel damage and the subsequent thrombogenic stimuli
exposure and consists of activated platelets and fibrin protein. 3 This barrier that is created limits the
blood flow through coronary vessels causing myocardial ischemia. Thus coronary blood vessel
thrombosis is related to pathologic events of acute coronary syndromes which include unstable
angina, myocardial infarction, and sudden ischemic death. 3,4
Uncontrolled platelet aggregation has been associated with thrombosis and subsequently with acute
coronary syndromes; therefore the development of therapeutic interventions has been focused on
interrupting one or several stages in hemostasis, platelet aggregation and/or coagulation. 3
Eptifibatide is a cyclic heptapeptide which originated from a protein found in the venom of the
southeastern pygmy rattlesnake (Sistrurus miliarus barbouri) and selectively blocks the platelet
glycoprotein IIb/IIIa receptor. It belongs to the class of the so called arginin–glycin–aspartat–
mimetics and reversibly binds to

Assessment Of Acute Phase Protein
DEPARTMENT OF BIOCHEMISTRY
FACULTY OF MEDICINE
UNIVERSITY OF KHARTOUM
Assessment of acute phase protein (plasminogen activating inhibitor) levels and in type 2 Sudanese
diabetic patients
A research proposal for master degree of medical biochemistry
By Khalid M.Elhassan Osman Abdelsamad Supervisor Dr. Khalid Hussein
Introduction and literature review: Diabetes mellitus is a metabolic disorder of multiple etiologies. It
is characterized by chronic hyperglycemia together with disturbances of carbohydrate, fat and
protein metabolism resulting from defects of insulin secretion, insulin action or both.(1) Type 2
diabetes (formerly called non–insulin–dependent or adult onset diabetes) is caused by the body's
ineffective use of insulin. It often results from excess body weight and physical inactivity. The
expected number of diabetic patients 438 million by 2030, an increase of 54% compared to
predicted figures for 2010(2). Macro vascular diseases such as coronary artery disease are one of
complications of both type 1 and type 2 diabetes mellitus. The prevalence of diabetes is increasing,
now diabetes also affects adolescents and younger adults, thus promoting the earlier development of
long term cardiovascular complications. Diabetes itself accounts for 75 – 90% of the excess
coronary artery disease (CAD) risk and enhances the effects of other cardiovascular risk factors.
Death from stroke and myocardial infarction (MI) are the leading

Rheumatoid Arthritis Essay
The pathophysiology of Rheumatoid Arthritis or RA includes cartilage damage. The cartilage
damage results in; neutrophils and cells in the synovial fluid being activated and the surface layer of
articular cartilage degraded, cytokines and tumor necrosis factor alpha result chondrocytes to attack
cartilage, and the synovium. The phagocytes of inflammation ingest immune complexes and
degrade synovial tissue and articular cartilage. In addition, the immune systems B and T
lymphocytes are activated. The B lymphocytes produce more RFs and the T lymphocytes produce
enzymes that amplify and perpetuate the inflammatory response. There is a large supply of the
targeted self–antigens that perpetuate the inflammatory response and formation of immune
complexes. Both the ... Show more content on Helpwriting.net ...
Moreover, the synovial inflammation results in small venules being occluded, which results in
decreased vascular flow to the synovial tissue. The comprised circulation and increased metabolic
needs result in hypoxia and metabolic acidosis. The erosion of the articular cartilage and the
inflammation in the supporting ligaments and tendencies stimulated by acidosis. Inflammation
results in hemorrhage, coagulation, and fibrin deposition on the synovial fluid. Also, the fibrin
becomes pannus. So, it is believed that as the RA progresses the pannus extends into the adjacent
articular cartilage and destroys it. Also, it is believed that the pannus forms on articular cartilage
after the cartilage has been destroyed by inflammation. RA has systematic symptoms which include;
fever, fatigue, weakness, anorexia, weight loss, and aching or stiffness. Local symptoms include
painful, tender and stiff joints. Complications of RA are cysts in the articular cartilage or
subchondral bone. Another complication is a rupture of a cyst or the actual synovial
joint.Furthermore, both loss of motion and deformities are other complications that come from

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.

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

Retepalase Research Paper
Approved in 1996 by the FDA, Reteplase is designed for the treatment of acute myocardial
infarction due to coronary artery obstruction (heart attack), improving ventricular function after a
myocardial infarction, reduces the incidence of congestive heart failure as well as reduces the rate of
mortality associated with this type of infarction. Reteplase is designed to be more potent and has a
faster action then many other types of drugs that treat myocardial infarction this is due to its unique
binding site as well as its half–life when introduced into the body. Reteplase, a third generation
thrombolytic agent, is a type of recombinant tissue plasminogen activator that is genetically
engineered in modified Escherichia coli. Reteplase contains 355 of the 527 amino acids present in
tissue plasminogen activator (tPA); this is, in fact, designed to increase the half–life of the molecule
when introduced within the body as well as allowing for different ... Show more content on
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Reteplase a selective thrombolytic molecule that only activates when fibrin, a protein involved in
the clotting of blood, is present. Activation of plasminogen by reteplase is stimulated in the presence
of fibrin and occurs through what is known as the kringle–2 domain, a type of binding mediator that
regulates the breakdown of proteins. Reteplase does this by acting on an endogenous fibrinolytic
system; by breaking the bond between arginine and valine to convert plasminogen to plasmin.
Plasmin degrades fibrin and fibrinogen, as well as the coagulation factors in this process. The
activity of reteplase depends on the presence of fibrin and in the absence of this, only small amounts
of the plasminogen are transformed into fibrin. While in the presence of a clot, the reteplase
penetrates the inside and activates the plasminogen, while the tissue plasminogen activator binds to
the fibrin matrix and accumulates on the surface of the

Disseminated Intervascular Coagulation
Disseminated Intervascular Coagulation (DIC) is a clinicopathologic syndrome characterized by
widespread intravascular fibrin formation in response to excessive blood protease activity that
overcomes the natural anticoagulant mechanisms (Harrison, T. 1974).The mechanism of DIC is a
generation of thrombin that is uncontrolled from exposure of blood to levels of tissue factors
pathologically. Two factors that add to the deposition of fibrin in small and midsize vessels and also
speed up the process are, simultaneous suppression of physiologic anticoagulant mechanisms and
abnormal fibrinolysis (Harrison, T. 1974). Fibrin deposition can interfere with the blood supply of
many major organs such as the lung, kidney, liver, and brain, all causing ... Show more content on
Helpwriting.net ...
2015). These blood test can show the number of platelets in the blood sample has dropped and that
the blood is taking a long time to clot. The diagnosis of DIC is confirmed if test results show large
amounts of plasma d–dimer and often a low or decreasing level of fibrogen. The d–dimer indicates
more clots are being produces and broken down than usual (Sharp, M. 2015).

Final Maturation Stage Research Paper
final maturation stage, the collagen is remodeled over time. When the body is inflicted with a
penetrating wound, vessels and tissue fibers are ripped and broken. The area is then filled with
leaking blood from the surrounding vessels and the outermost blood flow begins to form a scab. The
surrounding vessels at that time constrict to minimize the blood leakage in a process known as
vasoconstriction. The first step of the body is to clot the blood and achieve hemostasis, or blood
clotting to impede blood leakage. The blood also coagulates, forming into a gel–like substance from
its liquid state. The area of damage undergoes the coagulation cascade in which a fibrin clot is made.
Blood platelets begin to release inflammatory factors and express glycoproteins on the cell
membranes, a sticky–like protein, in order to aggregate. The area then forms a fibrin matrix via
fibrin and fibronectin fibers, which provide the scaffold for incoming cells. this fibrin clot plays a
crucial role in clotting the surrounding area as well as trapping essential proteins and cells.
(https://en.wikipedia.org/wiki/Wound_healing)
(http://www.nature.com/nature/journal/v453/n7193/full/nature07039.html) The matrix serves as the
primary structural support of the wounded area until it is replaced by collagen and later granulation
tissues. ... Show more content on Helpwriting.net ...
The growth factors increase the rate of cell division of cells in the surrounding areas. Inflammatory
chemicals such as serotonin and histamine cause the blood vessels in the surrounding area to dilate
and become more porous in a process known as vasodilation. This dilation and increase of
porousness facilitates the flow of essential cells, nutrient, and water into the extravascular space. A
variety of control mechanisms tightly regulate the growth factors from going out of hand and
potentially developing into

Von Willebrand Disease ( Vwd )
Von Willebrand disease (VWD) is a genetic disorder that will occur when an individual has limiting
amounts of the von Willebrand factor (VWF) or they have abnormal forms of it. This disease can
also be associated with having low plasma levels. It is one of the world's most common bleeding
disorders. It is so common, that it can be found all over the world, it is known to affect 1% of the
world's population. VWD is also a very unique disorder because it can affect various animal species
like dogs and pigs. is known as one of the most common bleeding disorders. It is known to affect
1can also be found in various animal species, like dogs and pigs. This is a silent disease because
many people don't even know they have it. But, when someone who is suffering from VWD starts
bleeding, they will undergo severe bleeding. Just because an individual might not present with
symptoms, doesn't mean they won't suffer from the severe bleeding consequences. This lack of
knowledge is due to the fact that the symptoms of VMD are so mild. This factor can either be
missing or it can just be defective. VWF is known as a clotting protein
(https://www.hemophilia.org/Bleeding–Disorders/Types–of–Bleeding–Disorders/Von–Willebrand–
Disease). The Finnish doctor, Erik von Willebrand was the man who found this disease. He
discovered this disease by observing families in the Aland Islands. When observing this families, he
was able to describe this disease, but he wasn't able to distinguish it from a

Investigation on NyQuil
Area of Interaction II: Anatomy & Physiology
Toxicology
Though NyQuil is an over the counter drug that treats cold symptoms, if consumed more than
recommended servings, severe symptoms may occur with an overdose. An overdose on NyQuil can
induce general effects on the brain such as a feeling of anxiety, restlessness or nervousness, and
perhaps dizziness and drowsiness as well (Busse). However, the two main ingredients of NyQuil,
acetaminophen and dextromethorphan, are what induce the more severe effects. Respectively,
consumption of large amounts of acetaminophen has been known to cause severe liver damage and
other stomach complications, such as nausea, vomiting, and a loss of appetite. According to Busse
from Livestrong.com, overdosing ... Show more content on Helpwriting.net ...
The most important organ of the circulatory system is the heart. This, fist sized, organ has the all–
important job of providing the body with all the blood and oxygen needed to sustain human life.
Though, the heart is one of the most vital organs your body needs, it is prone to various defects or
complications throughout its lifecycle. According to Durani from KidsHealth.org, "More than 64
million Americans have some type of cardiac problem." Perhaps the most deadly of all the heart's
complications is a heart attack. A heart attack is the leading killer in men and women in the United
States, with an estimate 1 million heart attacks alone in the United States (NHLBI). A heart attack
occurs when the heart is unable to obtain oxygen, due to a section of heart muscle becoming blocked
and preventing oxygen–rich blood to flow properly. The leading cause of heart attacks is coronary
heart disease, also known as coronary artery disease. Coronary heart disease is a result of plague, a
waxy like substance, building up inside the coronary arteries, the arteries that are responsible for
providing blood to the heart (NHLBI). Overtime, the built up plaque can rupture inside of an artery
causing a blood clot to form, which prevents blood from reaching heart muscles. Portions of heart
muscle once fed by this now blocked artery begin to die if blockage is not treated in time. Many
drugs, whether they be prescribed or over the counter, all have the

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