b. What are the stages of MODS? (see also sepsis and SIRS [systemic inflammatory response syndrome])
MODS starts off as an infection localized to a specific area. Eventually with treatment failure and or neglect of an infected area by the patient, the infection can turn into sepsis which is an inflammatory state generated by a systemic response to bacteria. (Merck 19th 2299)
Hypovolemic shock is the beginning of MODS in which the intravascular volume is decreased. Venous return, ventricular filling and stroke volume are all diminished as well. Cardiac output is diminished by the effects of the intravascular volume decrease. Heart rate increases in order to increase cardiac output. Hypovolemic shock is usually caused by a severe hemorrhage
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What are the effects of these hormone imbalances in a person with MODS?
a. Hypersecreted hormones b. Hyposecreted hormones
4. a. How is the heart affected by MODS?
With the heart having low pressure baroreceptors and chemoreceptors will cause an increase in heart rate, because it increases cardiac output. The extreme low pressure will cause tachycardia, because the heart will be pumping faster to try to bring cardiac output back of homeostasis (BOOK, 731).
b. What heart symptoms would a MODS patient most likely exhibit?
A MODS patient will begin to fail due to pulmonary edema, which is a fluid backup in the lungs (Multiple Organ Dysfunction Syndrome).
c. Explain why these changes are occurring.
The lungs then fail to circulate oxygenated blood. This will causes cardiopulmonary collapse In cases of septic shock, where the pressure of blood is so low it cannot deliver blood to the liver, kidneys, or lungs adequately, death will occur when these organs cannot maintain enough blood to continue functioning (Multiple Organ Dysfunction Syndrome).
5. a. How are blood vessels affected by MODS? Peripheral arteriole resistance is decrease due to dilated arteries and arterioles. (Berkow et al. 2300)
b. Explain why these changes are
The immunologic events that are happening at the local level during Carlton's acute inflammatory response would be:
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, hypoxia, which is a lack of oxygen, is another pathological physiological outcome of sepsis as less oxygen is reaching the tissue; this is due to the fact that there is less oxygen in the blood.
In an arterial system, the input impedance of the vessel varies with changes in the vessel’s size and properties. For compliant arteries, whic...
Septic shock is a condition and/or state of hypoperfusion that derives from another condition called sepsis; Sepsis the infection of the bloodstream. In order to acquire septic shock one must obtain an infection of the bloodstream. Any type of pathogen can cause that infection. The main factor is bacteria and while fungi and viruses have been known to be able to cause septic shock the occurrence is much more rare than through bacteria.The cause of septic shock lies within
Qiao T, Liu C and Ran F. (2005) The impact of gastrocnemius muscle cell changes in chronic venous insufficiency. Eur J Vasc Endovase Surg 30; 430-436.
“Immune Response: MedlinePlus Medical Encyclopedia.” National Library of Medicine - National Institutes of Health. Web. 18 Dec. 2011. .
When the first line of defense fails, the bodies second line of defense kicks in. Natural killer cells, neutrophils, macrophages, inflammation, fever and transferrin and lactoferrin kick in to eliminate microbes. These also prevent infectious diseases. Keeping infection out of the intravenous site is very important. As long as the bodies defense mechanisms are working properly and aren’t compromised, the process is made
Capriotti & Frizzell (2016) explain that sepsis is often seen in those who have a weak immune system. These individuals are at an increased risk of developing sepsis from microorganisms that a healthy immune system would normally fight off (Capriotti et al. 2016). The elderly, infants, and immunosuppressed patients are the most at risk for developing the condition (Capriotti et al. 2016). Sepsis can be caused by any microbe, but is most often caused by bacteria (Capriotti et al. 2016). Since sepsis has such a broad reach and can develop as a secondary infection after an initial injury or illness, Capriotti & Frizzell (2016) further explain the di...
Yung,, L.M., Laher, I., Chen, Z.Y., Huang, Y. and Leaung , F.P. (2009) Exercise, Vascular Wall and Cardiovascular Diseases. Sports Medicine. Vol. 39, No. 1: 45-63
The incidence of mastitis is associated with impaired PMN function (Cai et al., 1994) since the resolution of the disease is dependent on the ability of PMN for recognition of the pathogen, migration to the site of infection, phagocytic ability and its elimination (Vangroenweghe et al., 2005), and dependable of the generation of ROS by PMN (Heyneman et al., 1990).
Sepsis is defined as a systemic inflammatory response caused by an infective process such as viral, bacterial or fungal (Holling, 2011). Assessment on a patient and starting treatment for sepsis is based on identifying several factors including the infective source, antibiotic administration and fluid replacement (Bailey, 2013). Because time is critical any delay in identifying patients with sepsis will have a negatively affect the patients’ outcome. Many studies have concluded every hour in delay of treatment mortality is increased by 7% (Bailey, 2013). Within this assignment I will briefly discuss the previous practice and the recent practice including the study based on sepsis. I will show what enabled practice to change and I will use the two comparisons of current practice and best practice.
The heart is a pump with four chambers made of their own special muscle called cardiac muscle. Its interwoven muscle fibers enable the heart to contract or squeeze together automatically (Colombo 7). It’s about the same size of a fist and weighs some where around two hundred fifty to three hundred fifty grams (Marieb 432). The size of the heart depends on a person’s height and size. The heart wall is enclosed in three layers: superficial epicardium, middle epicardium, and deep epicardium. It is then enclosed in a double-walled sac called the Pericardium. The terms Systole and Diastole refer respectively and literally to the contraction and relaxation periods of heart activity (Marieb 432). While the doctor is taking a patient’s blood pressure, he listens for the contractions and relaxations of the heart. He also listens for them to make sure that they are going in a single rhythm, to make sure that there are no arrhythmias or complications. The heart muscle does not depend on the nervous system. If the nervous s...
This first period is called the Incubation period. This is from the point a pathogen inters your body up until the first minor symptoms occur. The second period is called the prodromal period; this starts when the first minor symptoms occur up until the major symptoms occur because of the pathogen creating infection. Some minor symptoms are headache, nausea, and dizziness. The third period is the period of illness; this is when the major symptoms occur because the infection is growing. Some major symptoms are diarrhea, vomiting, and inflammation. If a patient is infected with a lethal pathogen it is possible the patient has a chance of death in the period of illness if not treated with antibiotics right away. The fourth period is the period of decline; this is when the symptoms begin to go away. The fifth, and last period, is called the convalesce period; this is when the previously infected patient regains strength and is