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Uk essay the pathophysiology of sepsis
Uk essay the pathophysiology of sepsis
Uk essay the pathophysiology of sepsis
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Introduction
Sepsis is a critical condition caused by an overreacting immune response to an infection. Most of the time, such infection are caused by bacteria. When a person is being infected, chemicals are released into the bloodstream to fight off infection. This may result in multiples inflammation found within the body. Inflammation can trigger a cascade of event which may cause multiple organ damage, leading to multiple failure of organs where the body is unable to function normally. In worst scenario, infection can lead to an increase in low blood pressure which rapidly leads to the failure of several organs causing death. Besides causing inflammation, it also causes increased in coagulation, decreased fibrinolysis and decreases the amount of activated protein C in the body (Tazbir, 2004).
Protein C is a soluble and vitamin K dependent (Toussaint and Gerlach, 2009) molecule that are produced in our body which aids in the prevention of blood clotting. These proteins are initially in an inactive form, and are being activated when thrombin binds to thrombomodulin (Tazbir, 2004). Protein C are able to act as an anticoagulant which inhibit clotting factors Va and VIIIa when it work together with its cofactor protein S (Yamakawa et al, 2011). It is understood that inflammation is brought about by cytokine production in our body. In order to reduce inflammation, activated protein C is trigger. It also leads to an increased in fibrinolysis by inactivating plasminogen activator inhibitor-1 (PAI-1) (Tazbir, 2004).
For human with sepsis, plasma levels of proteins C are decreased and thrombomodulin is downregulated. Since it is downregulated, thrombin will not be able to bind with it to form an activated protein C. This results in multi...
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...s could also lead to an increased in activated protein C.
Results
It is clearly stated that treatment with recombinant activated protein C is beneficial to sepsis. Researchers do make changes to the dose of DrotAA and the duration for such treatment. This may help in the decision-making of identifying the right amount to completely cure sepsis or in another words reduce the rate of mortality. It is stated that high doses and long infusion period results in a higher amount of protein C (Shorr et al, 2010). Although there are a few cases of bleeding occurred, it can actually be prevented by the use of activated protein C variants (Mosnier, Gale, Yegneswaran and Griffin, 2004). Mortality rate was also lower in patients treated with rhTM (Yamakawa et al, 2011). There was also another research done with all the patients survived after the treatment (Donati et al, 2013).
Currently, there is no official vaccine that is being used to protect patients against C. diff. Vaccines are currently being developed which targets the specific proteins of the organism that is essential for vaccine development. 5 These proteins produce an immune response when introduced to a host. 5 There are also recent clinical trials that have shown strains of C. diff that only produce toxin B exist and that developing an antitoxin B may be used in defense of an infection. 5 Researchers have also developed vaccine that contains purified versions of toxin A and B. Patients injected with this vaccine had a significant rise of antitoxins during the 30th day of the vaccination regimen. Although this vaccine did not create any adverse reaction and was deemed safe by the researchers it is still under clinical trial. 5
Sepsis is defined as an exaggerated, overwhelming and uncontrolled systemic inflammatory response to an initially localised infection or tissue injury, which may lead to severe sepsis and septic shock if left untreated (Daniels, 2009; Robson & Daniels, 2013; Dellinger et al, 2013; Perman, Goyal & Gaieski, 2012; Vanzant & Schmelzer, 2011). Septic shock can be classified by acute circulatory failure as a result of massive vasodilation, increased capillary permeability and decreased vascular resistance in the body, causing refractory hypotension despite adequate fluid resuscitation. This leads to irreversible tissue ischaemia, end organ failure and ultimately, death (McClelland & Moxon, 2014; Sagy, Al-Qaqaa & Kim, 2013, Dellinger et al, 2013).
The guidelines’ first focus is the definition of sepsis, which makes sense, because there is no way to effectively treat sepsis without an accurate and categorical definition of the term. The guidelines define sepsis as “the presence (probable or documented) of infection together with systemic manifestations of infection”. Such systemic manifestations can include fever, tachypnea, AMS, WBC >12k, among others; these manifestations are listed in full in Table 1 of the guidelines. The definition for severe sepsis builds on to the definition of sepsis, bringing organ dysfunction and tissue hypoperfusion (oliguria, hypotension, elevated lactate) into the picture; full diagnostic criteria is listed in Table 2. The guidelines recommend that all
Also, cytokines are used as they can destroy the infection, however there is a problem with this diagnosis as excessive production can cause tissue and organ damage. The pathological physiological outcomes of sepsis is that there is a multi-organ dysfunction that includes the heart, brain, kidneys and the lungs. Acute respiratory distress syndrome (ARDS) is a condition where there is a low oxygen level in the blood, this mostly affects the lungs, people who have sepsis will be affected by ARDS as their breathing rate will decrease. Another reason for multi-organ dysfunction is that there is a lack of blood being given to the organs, this causes low blood pressure or as it’s called hypotension, this mostly affects diabetic people which leads them to having sepsis.
As an ICU nurse I constantly watch how patients develop pressure ulcers, a pressure ulcer is an area of skin that breaks down due to having constant friction and pressure, also from having limited movement and being in the same position over a prolonged period of time. Pressure Ulcers commonly occur in the buttocks, elbows, knees, back, shoulders, hips, heels, back of head, ankles and any other area with bony prominences. According to Cox, J. (2011) “Pressure ulcers are one of the most underrated conditions in critically ill patients. Despite the introduction of clinical practice guidelines and advances in medical technology, the prevalence of pressure ulcers in hospitalized patients continues to escalate” (p. 364). Patients with critical conditions have many factors that affect their mobility and therefore predispose them to developing pressure ulcers. This issue is significant to the nursing practice because nurses are the main care givers of these patients and are the ones responsible for the prevention of pressure ulcers in patients. Nurses should be aware of the tools and resources available and know the different techniques in providing care for the prevention of such. The purpose of this paper is to identify possible research questions that relate to the development of pressure ulcers in ICU patients and in the end generate a research question using the PICO model. “The PICO framework and its variations were developed to answer health related questions” (Davies, K., 2011).
Signs of DIC are as varied as the diseases and conditions which precipitate it; the most universal sign is abnormal bleeding, such as excessive bleeding from venipuncture sites and petechiae or ecchymoses occurring spontaneously along the ventrum and inguinal body regions (Bassert 1161, Tilley 373). Three distinct phases of DIC are recognized: the chronic silent phase, the peracute hypercoagulability phase, and the acute consumptive phase (Bruchim). Each phas...
Hemophilia is a rare bleeding disorder that slows the blood clotting process, which is not normal. Some people with Hemophilia may just have a little bit of “clotting factor” or no clotting factor at all (National Institute of Health [NIH], 2013). Clotting factor is a protein in blood that controls bleeding and they are needed the blood to clot normally. In order to help the blood clot, clotting factors work with “platelets” (National Institute of Health [NIH], 2013). Platelets are small blood cell fragments that form in the bone marrow, a tissue in the bones that is similar to a sponge. The functions of platelets have a very important role in blood clotting; the role of a platelet is to stick together (by the help of clotting factors) to block cuts, break on the carriers of blood (veins or arteries) throughout the body, and stop the bleeding when “blood vessels” (National Institutes of Health [NIH], 2013) are injured. Blood vessels are tube like structures carrying blood through the tissues and organs, like a vein, artery, or capillary. People with hemophilia do not have enough “clotting factor VIII or IX” (World Federation of Hemophilia [WFH], 2013) in their blood, which results to prolonged bleeding or oozing, meaning that bleeding can last longer (though, not faster) than usual after surgeries, accidents, or having teeth pulled out at the dentist. Clotting factor VIII, which can also be called as “anti-hemophilic factor” (AHF, for short) (Patient.co.uk, 2011), is a blood clotting protein that is necessary for humans to have. Clotting Factor IX is a protein that i...
(2)Saudan,P.,Niederberger,M.,De Seigneux,S.,Romand,J.,Pugin,J.,Pernrger,T.,& Martin,P.Y(2006).Adding a dialysis dose to continuous hemofiltration increases survival in patients with acute renal failure .Kidney international,70(7),1312-1317.
The changes in f8 and f9 gene are responsible for hemophilia A and B. the f8 gene codes for a protein called coagulation 8. This protein is responsible for the blood clotting process. After an injury blood clots protect the body by sealing off the area of injury. Mutation in the f8 and f9 gene can lead to the abnormal form of the protein. Also can lead to a reduction of the coagulation pro...
1 in 3 Americans Adults are currently at risk for developing kidney disease. What is acute renal failure, when your kidneys functions all of a sudden stop working and your kidneys are the body’s filter which remove waste products and help balance water, salts and minerals especially electrolytes in your blood when your kidneys stop working you end up building all the products in your body that need to be filtered and eliminated. The pathophysiology of Acute Renal Failure are due to three main causes Pre-renal, Intra-renal, and Post renal. Pre-renal is a sudden drop in blood pressure or interruption of blood flow to the kidneys from illness or sever injury. Intra-renal is direct damage to the kidneys by inflammation of drugs, infection, toxins or reduced blood supply. Post-renal is a sudden obstruction of urine flow because of enlarged prostate bladder tumor, kidney stones, or injury.
There is a disease spreading out in the world called Hepatitis C. It affects the liver and may cause the liver to fail. This disease is caused by a virus called Hepatitis C virus which is also known as HCV. About 32,000 people are affected with this disease per year only in the United States area. Some It’s a disease with many symptoms and many causes. of these symptoms are easy bruising, upset stomach and fever. These are just some of the many symptoms that come from the virus. Hepatitis Cs nature of the causative agent is determined by many things. The biological data of this disease is filled so much information. It is estimated that over 180 million people have gotten Hepatitis C and it is growing.
Immediately after wounding, the first phase of hemostatsis sets in motion with vascular constriction which restricts the blood flow in the blood vessels followed by the platelets plug formation which creates a temporary blockage of blood flow and then coagulation takes place with fibrin clot formation. The clot and surrounding tissue release pro-inflammatory growth factors and cytokines such as transforming growth factor (TGF)-13, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and epidermal growth factor (EGF).
Hospital acquired infections are one of the most common complications of care in the hospital setting. Hospital acquired infections are infections that patients acquired during the stay in the hospital. These infections can cause an increase number of days the patients stay in the hospital. Hospital acquired infections makes the patients worse or even causes death. “In the USA alone, hospital acquired infections cause about 1.7 million infections and 99,000 deaths per year”(secondary).
“ Sepsis” according to the International Surviving Sepsis Campaign, is defined as the presence of infection together with systemic manifestations of infection (Dellinger et al., 2013) In todays modern society sepsis still accounts for 15% of maternal deaths a year worldwide (Dolea & Stein, 2003). Despite medical advances, aseptic technique, and antibiotic use, sepsis is the most common cause of direct maternal death in the UK. According to the CMACE report the maternal mortality rate increased from 0.85 deaths per 100,000 maternities in 2003–05 to 1.13 deaths in 2006–08 (Harper, 2011). Puerperal sepsis has a long history within obstetrics and midwifery, and yet despite this knowledge it has become, yet again, the leading cause of direct maternal death. Therefore due to the increased maternal mortality, I have chosen to focus on the care of a woman within ...
The white blood cells destroy any unfamiliar pathogens in the bloodstream and can cause inflammation. Therefore, the inflammation causes a surplus of white blood cells to clot the wound for healing.