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Clotting Cascade Case Study

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Essay 112: Vitamin K and the Coagulation Cascade The human blood clotting cascade consists of a tightly regulated network of enzymes designed to contain damage to the blood vessels by means of coagulation, thus restoring vascular integrity. Briefly, when a blood vessel suffers penetrating trauma, blunt force trauma, or an internal rupture the clotting cascade swings into action. The various proteins activate one another culminating in the formation of a clot composed of a platelet plug and cross linked strands of fibrin. The clot, or thrombus, acts as damage control, stopping further loss of blood through the wound. Physiologists divide the clotting cascade into three branches: the extrinsic pathway, consisting of Factors III and …show more content…

The best characterized of these disorders include deficiencies of Antithrombin III, Protein C, Protein S, and Factor V Leiden mutation. The treatment for these disorders is heparin injections in the acute setting. Long term treatment consists of anticoagulation with warfarin for patients with Protein C, S, or Factor V Leiden deficiency. People who are homozygous for Protein C deficiency require periodic transfusions of blood plasma rather than oral warfarin …show more content…

This vitamin was designated "K" stemming from the German word for coagulation, or blood clotting. Although some Vitamin K is produced by intestinal bacteria, the majority is obtained from dietary sources. The human body requires this vitamin to produce functional blood clotting proteins, in particular Factor II (prothrombin), as well as Factors VII, IX, and X. Each of these proteins is a serine protease, an enzyme that cleaves certain peptide bonds in its target protein(s). As it turns out, these particular clotting factors must bind calcium in order to become fully activated. The ability to bind calcium, in turn, requires that these proteins undergo a modification at certain glutamate residues known as gamma carboxylation. The amino acid glutamate normally contains a single negatively charged COO-, or carboxylic acid group in its side chain. An additional COO- group allows glutamate to bind positively charged calcium ions much more effectively. Vitamin K is an essential cofactor in the enzymatic reaction producing gamma

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Hypoprothrombinemia caused by vit K malabsorption Adult: PO/IM 2.5-25 mg, may repeat or increased to 50 mg, Child: PO/IM 5-10 mg, Infant: PO/IM 2mg. Hypoprothrombinemia caused by oral anticoagulants Adult and child: PO/SC/IM

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402 Words | 2 Pages

Vitamin B12 (Cobalmin) is a water soluble vitamin and plays a key role in the normal functioning of the brain and nervous system, and in the formation of red blood cells. Vitamin B12 deficiency can occur if the body does not absorb enough vitamin B12 from the gastrointestinal tract or when there is not enough dietary intake of the vitamin. One common cause of deficiency is as a result of pernicious anaemia which is an autoimmune disorder that results in inflammation and damage to the stomach lining, and loss of parietal cells. The parietal cells produce intrinsic factor, a protein needed for absorption of Vitamin B12 in the gut.

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There are two types of Warfarin, one activates clotting factor and the other slows down the clotting factor. Warfarin works against the liver to produce Vitamin K, which is needed for the proteins that help blood clotting. The treatment for Warfarin is an increase of Vitamin K to help clot internal bleeding. By increasing the vitamin K it should neutralize the effects of the

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IV bolus of unfractionated Heparin or Subcutaneous injection of low molecular weight heparin (LMWH) may be used to prevent the formation of new blood clots. Nursing consideration: Require regular monitoring of activated partial thromboplasitn time (aPTT) and needed frequent heparin dose changes (Brunner and Suddarth’s, et al, 2010: 765). Fibrinolytic therapy: This therapy is given to dissolve the thrombus in the artery and restore the blood flow. There are two fibrinolytic drugs which are streptokinase and Recombinant tissue plasminogen activators (r-TPA) which includes Alteplase, reteplase and tenecteplase (Brunner and Suddarth’s, et al, 2010: 772).

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It was also shown that diammonium glycyrrhizinate suppresses Keap1 therefore allowing Nrf2 to protect the hepatic cells from the increase in antioxidants. It also decreased the levels of NF-kappa B in order to decrease inflammation due to the proinflammatory

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On the other hand, the plasmin flows in the plasma and dissolves all fibrin forms. The degradations of fibrin are labeled as follows: E, D, Y, X, and D-dimer. E, D, Y, and X come from fibrin polymers, monomers, or fibrinogen while D-dimer comes from the cross-linked form of fibrin. The polymer form of fibrin activates the platelets, which motivates the coagulation pathway and causes thrombocytopenia. In the meantime, protein S, C, and antithrombin are lost upon the

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There may be certain factors that may interfere with the body’s normal ability to make platelets. There is times when the

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In Scottsdale January 1st, 2016, at approximately 11:35pm, two female witnesses found a pool of blood alongside a decapitated left hand with a knife in its grip, which was beside the garbage can. The local police called a search for a man with a missing left hand and after closer examination the police discovered the corpse that belonged to Earnest Earl with a knife wound in his chest and a note in his left pocket that said. "Earnest Earl, do you know Gods of death love apples." (This seems to be a message taunting the local police.) Authorities tested blood samples and fingerprints on the note.

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We are asked to see Mr. Preston. He is a pleasant 70-year-old gentleman recently diagnosed with myeloma, who is found to have a creatinine around 2.0. He appears to have been worked up in Florida for the creatinine around 2, and myeloma with 20% plasma cells was found. He was transferred here for chemotherapy. On review of his old record, he was diagnosed in the Butner systems based on our excellent electronic medical record in 02/2011 with hypertensive nephropathy.

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Vitamin B3 helps your body to use protein, fat and carbohydrate to make energy and helpsenzymes work right. Biotin allows your body to use protein, fat and carbohydrate from food. Vitamin B6helps your body to make and use protein and glycogen and helps form hemoglobin which carries oxygenin your blood. Vitamin B12 works with the vitamin folate to make DNA and

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The endothelium is the thin layer of squamous cells that lines the interior surface of blood vessels and lymphatic vessels, and it is the injury to this which leads to thrombosis. It can be damaged in a number of way, like through surgery or heart disease. Even so, the changes to the vessel wall are the least understood of the three factors of Virchow’s Triad. Section

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Often dubbed, “hemophilia C,” a hereditary Factor XI deficiency that interferes with thrombin production and affects both sexes has an average occurrence rate of 1:100,000 and usually only affects those with serious injuries or surgeries (Pemberton 81). An acquired form of hemophilia (AH) also exists - the presence of autoantibodies (antibodies that target internal tissue) against FVIII occurs once per roughly every 1.5 million (Lebegue 312). Approximately 50% of cases are idiopathic, and the disease carries a mortality between 8-22% (Ibid.). It is treated using bypassing factors, which target the antibody or inhibitor, and long-term treatment with immunosuppressive steroids like prednisone and cyclophosphamide - treatments also more commonly used to treat rejection of FFP or recombinant clotting

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“Aspartate and glutamate are found in aspartame and behave as neurotransmitters in the brain. Having an excess of these neurotransmitters kills certain neurons by allowing the inundation of calcium. This influx provokes excessive amounts of free radicals which kill the cells.” (Edward, PHD). Aspartate kills brain cells and disrupts neurons in the brain.

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A treatment option for those who have suffered an ischaemic stroke is thrombolysis. As 85% of strokes are ischaemic this is a treatment option for many (Fitzpatrick and Birns,2004).The goal of thrombolysis is to disintegrate the thrombus/embolus occluding the vessel and reduce the scale of tissue damage (Fitzpatrick and Birns,2004).It is important to note that thrombolysis using ateplase should only be used to treat acute ischaemic stroke once intracranial bleeding has been ruled out by diagnostic imaging, and within 4.5hours of onset by

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Degradation of fibrin is termed fibrinolysis. The fibrinolytic pathway is a complex physiological pathway controlled by action of a series of cofactors, inhibitors, receptors. Dysregulation of this pathway is associated with different pathologies (e.g. coagulopathies, disseminated intravascular coagulation (DIC) or congenital bleeding disorders). Degradation of fibrin is performed by serine protease plasmin, which is present in blood as a proenzyme, plasminogen, and needs to be activated by tissue plasminogen activator (tPA) and urokinase. Disturbance in haemostasis with abnormal bleeding may be caused by thromocytopenia, platelet function disorder, or defects in blood coagulation.

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