Physiological Analysis Of Homeostatic Control Mechanisms, Acute Glomerulonephritis, And Third-degree Burns - An Essay.

(1)In this worksheet you will be asked to comment on the homeostatic control mechanisms which operate during increased activity,  Dan is undertaking a five mile road run.  During the run his heart rate increases to 154bpm; his respiration rate increases to 50 respirations per minute and his temperature rises to 39?c.  There is an increase in cellular respiration and energy use.  Analyse the change in each of the physiological readings; include in your analysis a discussion of the normal homeostatic control mechanisms for each.

(2) Assess the impact of acute glomerulonephritis on the structure and function of the kidneys and on the process of osmoregulation.

(3) Third-degree burns are full-thickness burns involving the entire thickness of the skin.  Explain the effects of this serious injury on the normal function of the skin, and its structures.  Consider the effects of hyperthermia and hypothermia in the body; noting how the body works to bring the temperature within the homeostatic range for body temperature.

Analysis of Homeostatic Control Mechanisms during Increased Activity

• The process of homeostatic regulation during the increased activity includes the detection by cell receptors followed by a message sent to the control center. After this, the control center activates the effector cells to restore the changes to normal(Waterhouse, 2013).
  
  
• There are three physiological changes noticed in Dan while he was running a road run of 5 miles.The first is an increment in the heart rate to 154bpm compared to a normal heart rate of 60-100bpm because while running the brain helps in stimulating and resulting in the increase of the adrenaline hormones from the adrenal gland. Then the impulses were sent to the nervous system branch of sympathetic nerves and then to the other organs and heart as the effect of it the heart starts to beat faster to meet the high need of oxygen and minerals by the skeletal muscles compromising the flow of blood to digestive system and skin(Waterhouse, 2013)..

Second is the elevation in the respiration rate from normal 12-20 respirations per minute to 50 respirations in one minute.The carotid artery and aorta have chemoreceptors which aid in detecting lower levels of oxygen as it is sensitive to oxygen and increment in carbon dioxide level as well as hydrogen ions. It is followed by sending of the message to the center of respiration “medulla” to increase respiration rate to increase oxygen and release the excess carbon dioxide and restoration of the normal oxygen level(Waterhouse, 2013)..

Third the body temperature of Dan is increased fromnormal 37 degree Celsius to 39 degree Celsius secondary to the greater amount of blood flow to the skeletal muscles and other skin cells to meet the needs of high energy and oxygen levelsand dilation of peripheral blood vessels to radiate heat out of the skin resulting in increase of body temperature.The highest rate of metabolism is also one of the reasons for it(Waterhouse, 2013).. 

• The control mechanism employed by the cells of the body to restore to normal happens after the running of 5 miles is completed. Adrenaline hormone or fight response hormone helped Dan to run faster and when it completes the level of hormone goes down and impulses generated by sympathetic nerve also die which consequently lowers the heart rate to normal. The respiration rate decreases after the activity is ceased as it lowers the requirement of oxygen in food breakdown to produce energy, thereby respiration rate restores to normal. When the increased activity has stopped the rate of metabolic activity decreases, thereby causing lowering of body temperature(Waterhouse, 2013)..

Acute Glomerulonephritis can be defined as the inflammation of the glomerular region and cellular proliferation due to the mechanism of the immune system and as the name indicates acute that is occurring for a short interval of time. The reasons of this disease arean infection and non-steroidal drug intake.These sometimes affect the immune cells in such a way that it starts affecting its own cells. A glomerulus is a group of several numbers of nerve endings, tiny blood vessels and it is present in the end region of a tubule of the kidney. As we know that the nephron is the basic cell which is present in millions in the kidney to purify and regulate the balance of water and ions in the body. Nephron consists of two parts, namely glomerulus containing cup-like structure “Bowmen’s capsule”that holds a lot of blood capillariesand renal tubule which receives the fluid from the former part(Gattone, 2009).The structural changes in the kidney due to acute glomerulonephritis include primarily cellular proliferation resulting in the increment of the cell numbers in the glomerular part secondary to the proliferation of mesangial, endothelial, and epithelial.These take place either inside the capillaries of glomerulus or outside the capillaries of epithelial cells of Bowman space. The indicators of leukocyte proliferation are the presence of monocytes and neutrophils.The thickening of the membrane of glomerular basement appears secondary to the complex process of immune response(Glomerulonephritis with Neulasta, 2015). Hyalinization or the process of eating of self-immune cells denote irreversible injury.These changes in the structure of the kidney are segmental, diffuse or global. The kidney may become bigger in size of about half of its size as compared to normalbean-shaped kidney which is 11 cm in length in the top region of posterior lumbar(Diadyk et al., 2016).

Impact of Acute Glomerulonephritis on Kidney Structure and Function

The changes in the function of the kidney included alarge amount of protein in the urinecalled proteinuria, and blood in the urine called hematuria, reduction in Glomerular Filtration Rate (i.e., oligoanuria), and RBC casts and RBC contributes to the active urine sediment. Glomerulus acts as a filter which helps to remove water and ions from the blood into Bowmen’s capsule thereby retaining macromolecules and blood. It receives blood from the efferent artery and the nephron structure is completed surrounded by blood capillaries to allow reabsorption of essential fluid elements such as ions as well as water and it is directly connected to the proximal tubule of the nephron(VanDeVoorde, 2015).It supports in the maintenance of water and ion balance and sends the blood through veins to the body after the levels of them are equilibrated. The decreased of GFR increases the retention of nephron salt and water causing expansion in volume of intravascular vessels, high blood pressure, pH imbalance,affect the volume of urine produce either it is reduced or increased based the hormone levels of ADH(anti-diuretic hormone) and swelling of extremities etc. The glomerulus is unable to maintain the proper water and ion balance in the body which is attributed to cell proliferation in the capillaries of glomerulus and could lead to congestive heart failure, kidney failure, and pulmonary oedema(Makhova, Vikhodseva and Novicova, 2016).

The building up of excess fluids and salts in the blood secondary to the dysfunction of the glomerulus.This can result in the complications of elevated blood pressure and kidney failure in some cases(Ponticelli and Glassock, 2009).Osmoregulation is the vital function of the kidney which balances the concentration of water and salt ions in the body such as sodium ions and potassium ions. Water is balanced with the help of ADH hormone and osmotic pressure development in the capillaries. When the water level of cells is high, osmotic pressure decrease which decreases the amount of ADH produced which leads to excretion more water from the cells. However, when there is less water than the osmotic pressure rises and leads to increase ADH hormone, thereby decreasing the water excretion from the capillaries. The sodium ion is regulated by the release of aldosterone from adrenal cortex when the concentration of potassium ions increases in the blood and helps to manage blood pressure and blood volume.Glomerulonephritis disturbs and reduces the secretion of ADH and aldosterone thereby resulting in undesirable changes in the process of osmoregulation(Melnyk, 2016).

Effects of Third-degree Burns on Skin Function and Structure

Third-degree burns are indicated by the doctors when the body is burnt 50 percent. The skin consists of several layers of cells and tissues(Basaran et al., 2008). It includes epidermis the outer layer which is thin, which contains many layers such as Stratum Corneum (made up of keratin protein), Stratum Lucidum(a layer of transparent cells), Stratum Granulosum (a layer of granular cells), Stratum Spinosum, Stratum Germanitivum(the deepest layer of cells). Each layer has a particular function and occurrence in the body. In third degree burns the majority of these layers is destroyed. Third-degree burn results in the destruction of up dermis and epidermis of the skin. It covers the burns of hands, feet, groin, and face or genital area. It also can burn and cause damage to the underlying muscles, tendons, and bones(L et al., 2016). The sensation at the burn site is negligible as the nerves present there was destroyed by burns. The burnt area appears white; skin becomes disfigured, and scarring of tissues occurs(Watkins, 2013).

The victim turns pale, anxious, confused, and frightened due to the pain caused by burning and may become unconscious. It causes a rapid fall in blood pressure resulting in cold extremities, pallor, and may eventually collapse. It also results in the fluid loss from the blood circulation; not just the fluid loss in the cells which are destroyed, but a liquid substance that leaks from the area of damaged cells secondary to the loss of skin protective cover.Burns not only kills and damages tissues but also allows their leakage of fluids and salts in the surrounding tissue. This also causes the disturbance in the levels of potassium and sodium salts which further results in changes of the osmotic balance of the body fluids and body. The burnt skin does not have the capability to fight infection, protection, heat regulations, the production of vitamin D, melanin formation, secretions and elimination etc(L et al., 2016).

The effects of third-degree burns on the skin are so severe that it destroys the ability of skin to regulate its homeostatic temperature. Environmental factors such as cold and heat affect the cardiovascular organs. An elevation of the body temperature (called hyperthermia) from approximately 36.5 degrees C to 39 degrees C leads toa doubling of the output of the cardiacorgans. In this condition, the skin thermal receptors and nerves send impulses to control center of temperature in the brain, which further activates the reflex process to release heat. The body loses heat by vasodilation for radiation of heat and vasodilation of the skin leads tosweating. This mechanism helps the body to restore its normal temperature gradually(Waterhouse, 2013). The risk factors, e.g. diabetes and age, lead to the decrease resistance to heat stress. When there is a reduction of the internal body temperature from 37 degrees C to 34 degrees C (called hypothermia), the thermal receptors sends impulses to the brain and in response, the blood vessel constriction and constriction of the skinoccurs to reduce the heat loss and conserve heat. But here cardiac output, respiratory rate decreases (Doshi and Giudici, 2015).

References

Basaran, K., Bicer, A., Beskardes, Y. and Ermis, I. (2008). Third-degree burn or a fried egg?. Burns, 34(3), pp.428-429.

Diadyk, O., Nekrasova, L., Taran, O., Siroshtanova, I. and Kominko, L. (2016). Acute Glomerulonephritis: Clinical and Pathologic Features (Case Report). KIDNEYS, 0(1.15), p.89.

Doshi, H. and Giudici, M. (2015). The EKG in hypothermia and hyperthermia. Journal of Electrocardiology, 48(2), pp.203-209.

Gattone, V. (2009). Kidney Structure and Function. Microscopy and Microanalysis, 15(S2), pp.74-75.

Glomerulonephritis with Neulasta. (2015). The Pharmaceutical Journal.

L, B., C, I., BH, K. and D, T. (2016). Third degree skin burns caused by a MRI conditional electrocardiographic monitoring system. Journal of Radiology and Imaging, 1(4), pp.29-32.

Makhova, E., Vikhodseva, G. And Novicova, L. (2016). Evaluation Of Disorders Of Hemostasis, Functional State Of The Kidneys And Renal Hemodynamics In Children With Nephrotic Syndrome Of Acute Glomerulonephritis. V Mire Nauchnykh Otkrytiy, 0(2), P.40.

Melnyk, O. (2016). Hemostatic System and its Regulation in Disorders of Renal Function. KIDNEYS, 0(3.17), p.57.

Ponticelli, C. and Glassock, R. (2009). Treatment of primary glomerulonephritis. 1st ed. Oxford: Oxford University Press.

VanDeVoorde, R. (2015). Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis. Pediatrics in Review, 36(1), pp.3-13.

Waterhouse, J. (2013). Homeostatic control mechanisms. Anaesthesia & Intensive Care Medicine, 14(7), pp.291-295.

Watkins, J. (2013). Skin rashes, part 1: Skin structure and taking a dermatological history. Practice Nursing, 24(1), pp.30-33.