The phenomenon of homeostasis is understood as the ability the body has to stabilise its internal environment despite the ever changing external conditions (Waterhouse, 2007). This internal environment is an atmosphere which surrounds the cells and is therefore the medium in which the cells are in direct contact with in the body (Sherwood, 2001). The internal environment is essential for cell survival because cells require a constant supply of oxygen and food which is exchanged from the external to the internal environment and then to the cell.
Cells also require the removal of toxic wastes like carbon dioxide which is released in the internal and then the external environment (Sherwood, 2001). In addition these enzyme-mediated processes work only within restricted temperature, pH and ion concentrations therefore internal environments should be preserved (Waterhouse, 2004). This preservation mechanism is controlled by a feedback loop system which is said to be the backbone of homeostasis (Waterhouse, 2004). Feedback loop sequences occur when a change in the internal environment deviates.
This deviation is sensed by a receptor which sends a signal to the control centre that contains the set value points required for normal function. Effectors then take effect to control the deviation (Waterhouse 2004). See illustration below: [pic] The series of events occurring in a negative feedback loop system aim to return low or high set point deviations to normal perimeters through a series of events (Jones, 2001). In a few instances however the deviation is increased from the ideal value resulting in a positive feedback.
This according to Jones (2001) does not play any part in keeping things constant, therefore positive feedback cannot be used as a homeostatic mechanism. Homeostasis is used as a survival tool because it enables animals to adapt to the ever changing environment (Tortora 1999). Without this ability death may occur, unless medical treatment is executed to bring about the natural occurrence of a feedback system (Clancy 2002). Disease will also result when there is a failure in the homeostatic control system because according to Clancy (2002) homeostasis provides a basis for health.
A body system which plays an important role in the control of homeostasis is the endocrine system which has the primary role of producing hormones that regulate the function of other organs. This system is responsible for the control of blood glucose levels which heavily depend on the secretion of insulin and glucagon (see fig 2). These hormones are produced in the pancreas, within specialist cells called Islets of langerhans containing alpha cells for glucagon production and beta cells for insulin production.
The pancreas also contains the receptors responsible for monitoring blood glucose levels. [pic] Fig 2 www. science aid. co. uk Glucose is essential in the production of ATP, which according to Clancy (2002) will fluctuate therefore glucose levels available should be regulated in order to maximise its energy making potential. The two hormones produced by the pancreas target the liver every time there is an increase or decrease of glucose production. In cases where glucose levels rise usually after a meal due to the carbohydrates being absorbed, the pancreas releases less glucagon and more insulin.
A decrease in glucose levels will however initiate the production of more glucagon and less insulin by the pancreas. Glucose levels can reduce by undertaking vigorous exercise. Fig 3 gives an illustration of the negative feedback control in the control of glucose levels. [pic] Because the liver is the main target organ for insulin it therefore acts as storage for glycogen. This is because the secretion of insulin promotes the conversion of glucose into glycogen, where the excess glucose can be stored for later date in the liver.
The secretion of glucagon however encourages the conversion of glycogen into glucose therefore increasing the amount of glucose available. As stated glucose levels are monitored by receptors in the pancreas which aim to keep the levels at about 3. 5-5. 5mmolg/ (fasting) (Clancy 2002). Conditions such as diabetes mellitus will rise in cases where there is a continuous rise in the amount of blood glucose levels. Diabetes can be insulin dependant diabetes mellitus (type 1) meaning that the patient has got no insulin production or type 2 which is non insulin dependant.
Type 1 diabetes occurs in at an early age. Patients with this condition have poor or no insulin production therefore blood glucose levels are high. The lack of insulin production is usually caused by antibodies produced by the immune system. These antibodies begin to attack the beta cells in the pancreas resulting in the disorder. Type 2 diabetes on the other had affects adults over 40. These patients can produce insulin but develop diabetes because they are unable to produce enough insulin needed by the body or the cells in the body do not use the insulin properly.
With type 2 diabetes the cells in the body become resistant to normal levels of insulin in the and therefore need more insulin than normal to keep the blood glucose down. Diabetes can lead to many life threatening and disabling complications. In diabetes the main causes of lower limb disease are peripheral neuropathy, foot deformities and peripheral arterial disease (PAD) (Pataky 2007). Boulton 2006 goes on to state that foot problems account for the majority of hospitalisation of patients with diabetes. He also goes on to say that diabetes is the single most cause of lower limb amputations.
High blood glucose levels are said to cause reduced sensation to the feet and also narrowing of arteries. High glucose levels even in moderation can cause nerve damage over time. This causes lack of sensation which can be a risk to ulceration. If a patient cannot feel beneath there feet they can easily step on to a sharp object causing ulceration. Wounds in some diabetic patients might not heel. The inability of these wounds or ulcers to heal is due to decreased blood and nutrient flow to the lower limb caused by peripheral vascular disease.
Diabetics also have an increased risk in developing furring of the arteries. This is caused by fatty deposits called atheroma. They build up in the inside of the arteries lining causing a reduced blood flow to various parts of the body. When affecting the feet it can cause poor circulation to the feet. This causes skin to be thin making it more prone to damage and it does not heal very quickly. Most diabetic wounds therefore will not heal quickly and might become bigger, increasing the chances of mputation in the lower limbs. Because some ulcers do not heal they may be come gangrenous and the only option will be to amputate in order to avoid life threatening infections (Boulton 2006). As stated above Motor, sensory and autonomic fibres may all be affected in people with diabetes. Because of these sensory deficits, diabetic patients do not have protective symptoms to guard against pressure and heat therefore the slightest trauma can initiate the development of leg ulcers (Jeffcoat 2003).
The lack of pain sensation also adds to the risk of ulcer formation because patients are unable to feel sharp objects and therefore injury to the leg might not be noticed until ulceration gets to an untreatable stage. Other cause s of ulceration are due to mechanical forces in high pressure areas which in diabetic patients can be due to motors changes giving way to new anatomical deformities (Edmonds 1999). These anatomical deformities range from highly arched feet, claw and hammer toes which all increase localised pressure to certain weight bearing surfaces.
And because the skin is fragile the slightest trauma can cause ulceration ( Cavanagh et al 2005) Diabetic foot ulcer are usually painless, punched-out ulcers in areas of thick callus and can be characterised by superadded infection, pus, oedema, erythema, crepitus, mal-odour. See fig 4 Fig 4. Neuropathic ulcer. (Livingston, 2006). Neale’s disorders of the foot People with diabetes develop foot ulcers because of neuropathy, ischemia or both. The initiating injury may be from acute mechanical or thermal trauma or from repetitively or continuously applied mechanical stress.
Peripheral neuropathy this is as a result of abnormal forces being applied to the foot. The skin is less able to with stand these pressures due to ischemia therefore giving way for ulceration. See illustration below. Once the skin is broken, many processes contribute to defective healing, including bacterial infection, tissue ischemia, continuing trauma, and poor management. Autonomic neuropathy- It affects blood flow perspiration and skin hydration. Neuroeschaemic foot- In diabetic patient it affects the popliteal, the tibial and the peroneal arteries. The ulceration is over the lateral aspect of the foot [pic]
Fig 5. Neuro-ischaemic ulceration. (Livingston, 2006). Neale’s disorders of the foot. Neuropathic oedema-swelling of the feet and lower legs associated with severe peripheral neuropathy and this can lead to ulcers which can form on the plantar surface of the foot Ischemic foot-Ulceration in the ischemic foot is often painful although it varies from patient to patient. Charcot foot The Charcot foot is characterised by bone and joint degeneration which can lead to a devastating deformity. Slight trauma triggers fracture of a weakened bone, which increases the load on adjacent bones, leading to gross destruction.
The process is self-limiting but the persisting deformity greatly increases the risk of secondary ulcer REFFERENCES 1. Tortora, G. J. 1999. Introduction to the human body. 3rd Ed. The essentials of Anatomy & Physiology. 2. Clancy J. McVicar A. 2002 Physiology and anatomy an homeostatic approach 2nd ed 3. Campbell N, Reece J. B. 2005. Biology. 7th ed 4. Jones M Gregory. 2001. Biology 2 5. Z. Pataky, U. Vischer. Diabetic foot disease in the elderly Diabetes & Metabolism, Volume 33, Supplement 1, April 2007, Pages S56-S65 6. Andrew JM Boulton .
The diabetic foot. Medicine, Volume 34, Issue 3, 1 March 2006, Pages 87-90 7. Jeffcoate WJ, Harding KG; Diabetic foot ulcers. Lancet. 2003 May 3;361(9368):1545-51. 8. Cavanagh PR, Lipsky BA, Bradbury AW; Treatment for diabetic foot ulcers. Lancet. 2005 Nov 12;366(9498):1725-35. 9. Bernard, C. 1813-1878. Physiological homeostasis. Publication, Thibodeau, G. A and Patton, K. T. Anatomy& Physiology 2nd ed pp15 10. James Waterhouse Homeostatic control mechanisms Anaesthesia & intensive care medicine, Volume 5, Issue 7, 1 July 2004, Pages 236-240 .