|Type of paper:||Case study|
Diabetes Mellitus (DM) is metabolic anarchy typified by the occurrence of chronic hyperglycemia accompanied by larger or smaller impairment in the metabolism of lipids, proteins, and carbohydrates. It is possibly among the oldest ailments familiar to man. The disease was initially reported in the Egyptian document around three-thousand years ago. A clear difference between type 1 and type 2 Diabetes Mellitus was made in 1936. In 1988, type 2 DM was primarily depicted as a constituent of metabolic syndrome. The source and etiology of Diabetes Mellitus could profoundly differ, but at some point in the course of the disease, it always includes faults in either insulin secretion or response. In most cases, people with diabetes mellitus have immune-mediated diabetes. The most prevalent type of diabetes is type 2, and it is distinguished by insulin resistance, comparative insulin deficit, and hyperglycemia. It is a product of the association between three risk factors which are behavioral, genetic and environmental. Diabetes can as well have a link to hereditary defects, infections, gestational hormonal environment and particular drugs.
Pathophysiological Basis of Diabetic Foot Ulcers and Impact of Infection on Glucose
Individuals suffering from diabetes mellitus commonly suffer from diabetic foot ulcer which is a harsh complication with a cumulative life span occurrence of up to 25%. As a result of the heightening diabetes rates worldwide, foot ulcers have become a main and escalating issue of public health. Some effects of foot ulcers include low quality of life, considerable morbidity, and huge economic losses due to high treatment costs ( Baker, 2014). Several factors associated with weakened levels of glucose metabolism and neurovascular complications tend to delay the healing of wounds. Diabetic foot ulcers may willingly turn into chronic, and in most cases, these wounds do not primarily heal.
The physiological course of wound healing has convention partitions of four stages. They include hemostasis, inflammation, proliferation, and maturation also known as remodeling. Cellular and humoral aspects slightly interact causing the steps to orchestrate. After one hour of being hurt, clotting and vasoconstriction take place, and these features distinguish hemostasis which is the initial step. Platelets play various roles in the process of wound healing. They instigate clotting cascade, secret development feature as well as cytokines responsible for initiating recovery. The following stage is inflammation and it lasts until the seventh day after the injury. It intercedes via neutrophil granulocytes that help in thwarting the contagion of bacteria and cleaning up the damage from cell debris. Chemotactic features contribute to the attraction of monocytes to the injury, and this makes the separate to injury macrophages. Monocytes remove nonviable and bacteria by phagocytosis and also release a range of growth factors necessary for stimulation of fibroplasia and angiogenesis thus presenting the foundation for configuration of ECM. In day two of damage, proliferation stage starts, and it lasts for twenty days. Angiogenesis takes place at this stage whereby tissue granulation and creation of new blood cells takes place. Aspects of platelet-derived growth factors, angiotensin, and macrophage angiogenesis features encompass the angiogenesis process (Clerici & Faglia, 2016). What follows is the initiation of concomitant epithelialization which helps in covering the granulation layer with a cellular obstruction. After a week of the injury until six months, there is extensive remodeling of tissues, and this indicates the final stage. It is at this stage that proteoglycan and collagen molecules replace the provisional wound matrix. There is an arrangement of collagen molecules into firm bundles ensuing in sturdier and inflexible scar tissue.
Intrinsic and extrinsic aspects surrounding an injury and its biology impair the recovery of wounds in diabetic people (Clerici & Faglia, 2016). A foot is in an exposure of common shocks or mechanical pressure causing it to be insensitive as a result of neuropathy because of macro or microvascular disease and these shows the external features. The basement membrane of capillaries, as well as arterioles, coagulates in diabetic patients and this leads to weakened injury recovery and importunate formation of ulcers (Game, 2014).
In type 2 Diabetes Mellitus, free fatty acids play a significant role in encouraging loss of insulin sensitivity, but the causal mechanism remains ambiguous. The pathophysiology of type 2 DM is distinguished by peripheral insulin resistance also known as insulin sensitivity, impaired regulation of the production of hepatic glucose, glucose transport dysfunction, surplus toxicity, cell damage, and superfluous oxidation. When type 2 Diabetes primarily develops as a result of hyperglycemia, some significant cells are affected. These cells include liver cells, fat, blood cells, and glycated red blood cells. The cells have been designed to obtain glucose out of the blood, absorb it into the cells and convert it into energy. Insulin is necessary for the cells to enable the absorption of glucose through insulin receptors and GLUT4 transporters. Notably, in a non-diabetic individual, once the pancreas produces insulin, the insulin connects the insulin receptors on the cells' outer edge. Conversely, at the cellular level of a diabetic person, the insulin does not join the insulin receptors on the cell's outer edge on the production of insulin by the pancreas. As a result, the blood glucose begins rising. Failure of the cells to absorb blood sugar increases the level of blood sugar because the sugar remains in the blood. The high levels of sugars tend to injure the red blood cells. Glycation is a crystalline formed by the attachment of sugar molecules to the exterior part of red blood cells. Due to the crystalline red blood cells, injuries are prevalent in the entire circulatory system which destroys the capillaries and arteries. The liver manufactures cholesterol that amends the destruction causing arterial plaque formation. The coarse red blood cells lead to elevated injury in dense capillary regions like feet and hands.
Practice Guidelines and Antimicrobial Therapy for Diabetic Foot Infections
The medication prescribed for the treatment of the infection is sensitive. Lisinopril is used in the treatment of high blood pressure or rather hypertension in mature individuals and children who have attained six years and above. It is also effective in congestive heart failure and progress survival after a person has a heart attack. Hydrochlorothiazide also lowers the level of blood pressure, averts strokes, heart attack and kidney failures. It functions by making an individual urinate several times thus getting rid of extra salt and water. It minimizes additional fluid in the body a condition known as edema cause. It reduces s symptoms like breath shortness and feet swelling. The infection is composed of replicating microorganism that causes host injury. Cephalexin belongs to the cephalosporin family, and it's an antibiotic that treats bacteria-caused infections. Most of the drugs offered for Jeff's treatment are aimed at lowering the blood pressure. Examples of organisms sensitive to the medication prescribed include Pseudomonas, E.coli, Staphylococcus aureus, Proteus, Stenotrophomonas, and Acinetobacter. Self-testing blood sugar is a vital tool in the management of treatment plan and preventing complications that come as a result of diabetes. Drugs are not always the best option especially if there is a natural alternative to cure. Missing out on meals or eating often results in unhealthy highs o low glucose levels (Porth, 2015). Eating a healthy diet and incorporating nutrition therapy is very crucial. Some of the prescriptions for Jeff's care tend to play similar roles, and therefore they should not all be used. A drug like Atorvastatin lessens harmful cholesterol and fats in the blood. Healthy diet and exercise can act as an alternative to Jeff's treatment.
Naproxen Sodium and Congruence with Practice Guidelines
Pain-relieving, antipyretic and anti-inflammatory properties characterize naproxen. Just like the rest of NSAIDS, the mechanism of action in Naproxen is not entirely comprehended but entails inhabitation of cyclooxygenase (COX-1 and COX-2). The drug could cause cardiovascular thrombotic happenings as well as myocardial infarction and stroke which can be deadly. To reduce the probable risk for an unfavorable CV occurrence in NSAID- treated patient, you should make sure to utilize the lowest effective dose for the shortest time possible. Doctors and patients ought to be alert for the emergence of these events throughout the complete treatment course even if the previous CV signs are absent. Patients should be aware of the symptoms of severe CV events and the procedure to undergo in case of occurrence. Evade using Narprelan in people with a current MI except when the advantages are anticipated to overshadow risk of recurrent CV thrombotic events. If used, it is vital to monitor patients for symptoms of cardiac ischemia. Administering more than one NSAID at the same time is dangerous. Signs of GI ulceration and bleeding could occur, and therefore you should remain alert to note them. Naproxen agrees with the treatment of back pains. Majority of back pains tend to be self-limiting dissolving in days. The appropriate treatment should involve medicines that minimize pain, inflammation accompanied by muscle intensification exercises that reinstate proper use and prevent reappearance ( Orlyk, Povorozniuk, & Kreslov, 2015).
Food, Drug and Herb Interactions
Not all foods should be consumed while taking St. John's Wort. While taking the drug, it is imperative that Jeff avoid taking or drinking foods and drinks that have high levels of tyramine. The reason behind this is that the meals could raise the blood pressure to hazardous levels thus leading to life-threatening symptoms.
Baker, N. (2014). Chapter-09 The Assessment and Management of Plantar Ulcers and Offloading the Diabetic Foot. Contemporary Management of the Diabetic Foot, 63-77. doi:10.5005/jp/books/11997_9
Clerici, G., & Faglia, E. (2016). Diabetic Foot Ulcers. Ulcers of the Lower Extremity, 181-235. doi:10.1007/978-81-322-2635-2_12
Game, F. (2014). Chapter-15 Diabetic Foot Ulcers: Short- and Long-term Outcomes. Contemporary Management of the Diabetic Foot, 134-138. doi:10.5005/jp/books/11997_15
Porth, C. M. (2015). Essentials of pathophysiology: Concepts of altered health states (4th ed.). Philadelphia, PA. Wolters Kluwer Health|Lippincott Williams & Wilkins.
Orlyk, T., Povorozniuk, V., & Kreslov, Y. (2015). Comparative evaluation of the effectiveness of NSAIDs in the treatment of patients with back pain depending on the bone mineral density. ORTHOPAEDICS, TRAUMATOLOGY and PROSTHETICS, 0(3), 71. doi:10.15674/0030-59872015371-77
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