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The role of homeostasis is to maintain a constant internal environment within the body despite changes in the external environment. For example, the body is able to keep its core temperature, blood sugar levels and water balance relatively constant.This ensures the survival and functioning of cells, organs and tissues. If homeostasis were to cease and the human body drop or rise in temperature, the vital organs crucial to for humans to survive would be severely damaged. Additionally the tissue fluid must remain constant if the cells within are to remain functioning and able. Homeostasisis a complex and delicate process as cells can cease to function and die from minimal changes in energy sources, temperature, electrolyte balance and pH (Saylor, 2012). This makes homeostasis one of the most important physiological functions of the human body, which is frequently exposed to changes in condition, temperature and nutritional provision (Saylor, 2012).
The components responsible for maintaining homeostasis are known as the homeostatic control mechanisms. All of the body’s systems and organs are involved in this and need to have the appropriate control mechanisms available when needed. These mechanisms will respond to changing needs to restore and maintain the ideal internal environment. For this self-regulation to continue the body requires a complex communication system called the feedback control loop (Saylor, 2012) and information is communicated by the neuroendocrine system. These feedback control loops will always have the same fundamental components and work in a near identical way despite facilitating different information for different functions (Saylor,2012).
The control systems are composed of three components: the detector, control centre and effector. The control centre regulates the limits in which the variable factor should be maintained. The detector is what sends the input to the control centre, which then integrates the information. If the incoming signal indicates a required adjustment then the control centre will respond to alter its output to the effector. This process allows constant readjustment of a variety of physiological variables. The impact that effectors can have on sensors will be either negative or positive feedback. This means that homeostatic control mechanisms will be categorised into negative or positive feedback systems (Saylor, 2012).
Negative feedback systems are needed to ensure the body is in a consistent internal environment. An action is activated that will counter a change that triggered the system (Saylor, 2012). Positive feedback is not designed to assist the body in maintaining a homeostatic condition. Due to this it can be harmful or even lethal to the functioning of the body. Whilst negative feedback will oppose changes in the internal environment, positive feedback will increase the changes. Using the domestic house temperature example, positive feedback would detect the lowering temperature and react by decreasing the temperature further, creating a loop where the temperature is consistently lowering. Should this occur, body functions would cease to occur properly and homeostasis would be disrupted.This means negative feedback is the most crucial and used of the two homeostatic control mechanisms. However positive feedback does have uses on occasion. Examples include the formation of blood clots, meaning positive feedback can occasionally promote-survival.
There are two ways that signals are sent throughout the body. One of these ways is via nerves in the nervous system. Signals are sent as nerve impulses that travel through nerve cells known as neurons (Long, 2015). These impulses are sent to other neurons or specific target cells at a specific location of the body that the neuron extends to. Most of the signals that the body uses for temperature regulation are sent via the nervous system. The second way is through the circulatory system, where, specific molecules called hormones produced by the endocrine glands (diagram 1) travel through the circulatory system, and transmit signals (Long, 2015).
Forthermore regulation the detectors are skin and hypothalamus thermoreceptors. The controller is the hypothalamus’ heat loss and generation centre and the effectors include sweat glands, arteriole muscles, hair follicles and the hormones adrenalin and thyroxin. When body temperature is too high, the thermodetectorssignal the hypothalamus to initiate cooling mechanisms. The hypothalamus then sends signals to the circulatory system to vasodilate arterioles and produce sweat through the sympathetic nervous system. This allows the body to lose heat more quickly. It also stops adrenalin and thyroxin form being produced which lowers basal metabolic rate and muscle activity. This means less heat is generated when resting. When body temperature is too low the thermodetectors signals the hypothalamus to initiate mechanisms raising its temperature. It then signals the circulatory system to start vasoconstriction to keep more body heat in (diagram 7). It also signals the adrenal glands to produce adrenaline, which increase BMR, and so the creation of body heat. It will also cause shivering and piloerection where the hair stands on end to trap a layer of air over the skin keeping it warm and increase thermogenesis.
The negative feedback loops between detectors, control and effects keep the body’s actions to move body temperature up or down proportionate to the current variance from normal body temperature at all times.
The human body maintains glucose levels via hormone signalling. Glucose is a monosaccharide and the main source of fuel for our bodies but is too big to diffuse into cells alone. The pancreas produces insulin, a hormone that facilitates glucose transport into cells. By facilitating glucose transport into cells via the bloodstream, insulin lowers blood glucose levels and inhibits glucose production from amino acids, fatty acids and glycogen. Insulin also stimulates glycogen formation from glucose. All functions of insulin help lower blood glucose levels in the bloodstream. Glucagon is a hormone also produced from the pancreas that raises blood glucose levels by stimulating the breakdown of glycogen into glucose, stimulating glucose production from fatty and amino acids and stimulating the release of glucose from the liver (Morris, 2014). This means that insulin and glucagon have antagonistic effects against one another, with glucagon promoting glucose production and release into the bloodstream whilst insulinpromotes the transport of glucose into cells from the bloodstream whilst inhibiting glucose production (diagram 2). Glucose levels in the blood are usually measured in milligrams per decilitre with a normal rang of 70 to 110 mg/dl(Morris, 2014). If glucose levels stray out this range, the pancreases will adjust the amounts of insulin and glucagon accordingly to bring glucose levels back into the set range. The pancreases will always be producing insulin and glucagon, endeavouring to find a balance between glucose releases into the blood and glucose uptake into the cells, defining this process as homeostasis.
In blood glucose control the detectors are glucose sensitive cells in the hypothalamus. The controllers are the islets of Langerhans and the effects are the hormones insulin and glucagon.
The pancreas produces glucagon and insulin from alpha and beta cells of the islets of Langerhans. When sugar is too high the beta cells secrete insulin that opens binds to special receptors at the cell membranes allowing glucose to be actively transported into them. This lowers blood sugar levels and leads to glycogogenesis (making glycogen), lipogenesis (making fat) and faster protein synthesis.
When blood sugar is too low the alpha cells produce glucagon that causesglycogenolysis. Glycogen is broken down in glucose, in gluconeogenesis, which circulates in the blood stream and raises blood sugar levels. It also leads to ketogenesis (breaking down fats to form ketones) and proteolysis where protein is broken down into amino acids to make ATP. By negative feedback, the secretion of each hormone is adjusted to match the variance from normal blood sugar.
In water balance the detectors are osmoreceptors in the hypothalamus, the controller is the hypothalamus and the effectors are the hormones ADH and aldosterone.
Water balance in the human body is regulated by the renal system, mainly composed of the kidneys but also involving the connecting arteries, veins and urinary tract (diagram 3). The kidneys maintain the balance of water by controlling the concentration of blood plasma and salt levels. Within the kidneys are tiny filtering structures called nephrons (See diagram 4). These nephrons are the functional units of the kidneys, helping remove excess waste, water and other substances from the blood whilst returning substances such as potassium, phosphorus and sodium when supplies run low in the body (Saylor,-2012).
Anti-diuretic hormone (ADH) is a hormone produced by the pituitary gland to control blood volume. The more concentrated it is, the more is ADH released causing the kidneys to hold onto more water. In dehydration, osmoreceptors detect a drop in blood volumewhich the hypothalamus detects. It releases ADH through the pituitary gland where it goes into the bloodstream. When it reaches the kidneys it causes them to hold water which lowers urine volume (Diagram 5). As it rises the amount of ADH-in the blood lowers through negative feedback. When blood volume is too high ADH is not released into the blood. Therefore the kidneys do not reabsorb water and dilute urine is produced copiously which quickly lowers blood volume to normal levels. As it lowers more ADH will be realised to prevent low blood volume.
Aldosterone is another important hormonereleased by the adrenal cortex. Before it can be released renin must be released by the kidneys in response to low renal blood flow. Renin and angiotensin converting enzyme stimulate theadrenal cortex to releasealdosterone which regulates water and salt balance. When it is releasedand reaches the kidneys it makes them reabsorb water and sodium so less is lost in urine and blood volume is raised. As it raises less will be released into the blood (Diagram 6).
Diabetes occurs in people whose blood glucose is not regulated properly and efficiently by their body (Diabetes, 2015). Diabetes can either be type-1 or type-2. Both conditions are characterised with the person having blood sugar levels that are higher than normal. However, type-1 diabetes is often diagnosed in childhood, associated with higher levels of ketone and controlled with insulin injections. Type-2 is usually diagnosed in adults, associated with a higher than average body weight and blood pressure/cholesterol and treated with medication such as tablets. Additionally, people with type-2 diabetes can sometimes come off medication, especially if they lose weight, whilst there currently is no such long-term solution for type-1 diabetes (Diabetes, 2015).
The cause of condition also differs between type-1 and type-2. Type-1 diabetes is often inherited, meaning a possible autoimmune reaction could be genetic. In this case, the pancreas is completely unable to produce insulin as the person’s immune system identifies the cells in the pancreas as hostile and destroys them. People with type-2 on the other hand are able to produce insulin from their pancreas. However diabetes occurs when they do not produce enough or their body does not recognise and utilise the insulin efficiently (a condition known as insulin resistance). This means that glucose is unable to diffuse into the body’s cells and will build up in the bloodstream, damaging the body and depriving cells of the glucose they need, hindering their functioning (Diabetes, 2015).
The girl had high levels of blood glucose in her system and ketones present in her urine. Her blood glucose levels were abnormally high, measured at 35mmols/L whilst blood sugar level should be between 4 and 9mmols/L. This along with her age indicates that she has type-1 diabetes because of those with the disease ketones are far more common in those with type 1 who produce no insulin (NHS Choices, 2014). The diagnosis of type 1 diabetes will need to include checks for polyuria, polyphasia and polydipsia. Polyuria is where urine is made excessively because high blood sugar levels means that water passes through nephrons into the bladder instead of being reabsorbed. Polydipsia is unquenchable thirst caused by high blood sugar that pulls water out of cells by osmosis into it to equalise osmotic pressure. Polyphasia is uncontrollable hunger caused by the inability of cells to absorb glucose via insulin. If the girl has any or all of these symptoms it will increase the chance she has diabetes.
People with type-1 diabetes have to take insulin injections daily to prevent ketoacidosis and to control hyperglycaemia. Hyperglycaemia is the name given to the condition where the blood glucose concentration rises higher than the natural set level, commonly associated with untreated diabetes (NHS Choices, 2014).
The ketone in the urine suggestsshe hadketonuria, which occurs when high levels of ketone bodies are found in the urine, resulting from cells are broken down for access to the energy. People with type-1 diabetes produce little natural insulin. Since ketones are produced due to insufficient insulin, the patient is at a greater risk of developingketonuria (MedicineNet, 2013). Their bodies will produce more ketones if they go for extended periods of time without sufficient insulinasthe body breaks down tissue from fat and muscle to access the cells and energy to use as fuel instead. Therefore treatment for this patient should include: insulin, monitoring during her recovery and education on how she should consume a low glycaemic diet by managing her intake of refined sugars, certain chocolates and processed foods such as crisps whilst being taught how to eat foods low in glucose and high in water soluble fibre like brown rice and oat cereal. When she was discharged from the hospital she had been successfully treated as her blood glucose level stood at 7 and there was no ketones found in her urine.
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