Fluid management techniques and related nursing care are also covered. Body fluids are mainly water and electrolytes, and the three main organs that regulate fluid balance are the brain, the adrenal glands and the kidneys Tortora and Grabowski, One-third of the total is circulatory fluid, sometimes known as extracellular fluid ECF ; the remainder is intracellular fluid ICF contained within cells Docherty and McIntyre, ; Edwards The anatomy and physiology of homeostasis are covered in part one of this series.
Most tissues contain a lot of water bones and adipose tissue are the two main exceptions. It has many functions, including Tortora and Grabowski, ; Adam and Osborne, :. When fluid volume decreases, the concentration of sodium in the blood will increase increased osmolarity, the amount of solute per unit volume , which in turn stimulates the hypothalamus Tortora and Grabowski, The hypothalamus is an osmoreceptor - a sensory end organ that reacts to changes in osmotic pressure and has an effect on the pituitary gland.
In response, the posterior pituitary gland releases antidiuretic hormone ADH, sometimes called vasopressin into the bloodstream, resulting in the kidneys retaining water. This in turn results in more concentrated urine and an increase in water returned to the ECF, thus correcting the volume depletion Tortora and Grabowski, ; Edwards, Fig 1. When sodium concentration in the blood decreases the adrenal cortex is stimulated into secreting the hormone aldosterone, which instructs the distal nephrons of the kidney to retain more sodium.
When the osmolarity of blood changes it is more or less dilute , water diffusion into and out of the osmoreceptor cells changes. That is, the cells expand when the blood plasma is more dilute and contract with a higher concentration.
When the osmoreceptors detect high plasma osmolarity often a sign of a low blood volume , they send signals to the hypothalamus, which creates the biological sensation of thirst. Osmoreceptors also stimulate vasopressin ADH secretion, which starts the events that will reduce plasma osmolarity to normal levels. The hypothalamus : The hypothalamus is the thirst center of the human body.
Another way through which thirst is induced is through angiotensin II, one of the hormones involved in the renin—angiotensin system. The renin—angiotensin system is a complex homeostatic pathway that deals with blood volume as a whole, as well as plasma osmolarity and blood pressure. The macula densa cells in the walls of the ascending loop of Henle of the nephron is another type of osmoreceptor; however it stimulates the juxtaglomerular apparatus JGA instead of the hypothalamus.
When the macula densa is stimulated by high osmolarity, The JGA releases renin into the bloodstream, which cleaves angiotensinogen into angiotensin I. ACE is a hormone that has many functions. Angiotensin II acts on the hypothalamus to cause the sensation of thirst. It also causes vasoconstriction, and the release of aldosterone to cause increased water reabsorption in a mechanism that is very similar to that of ADH. Note that the renin—angiotensin system, and thus thirst, can be caused by other stimuli besides increased plasma osmolarity or a decrease in blood volume.
For example, stimulation of the sympathetic nervous system and low blood pressure in the kidneys decreased GFR will stimulate the renin—angiotensin system and cause an increase in thirst. Fluid can leave the body in three ways: urination, excretion feces , and perspiration sweating. The hormones ADH anti-diuretic hormone, also known as vasopressin and aldosterone, a hormone created by the renin—angiotensin system, play a major role in this balance.
If the body is becoming fluid deficient, there will be an increase in the secretion of these hormones that causes water to be retained by the kidneys through increased tubular reabsorption and urine output to be reduced. Conversely, if fluid levels are excessive, the secretion of these hormones is suppressed and results in less retention of fluid by the kidneys and a subsequent increase in the volume of urine produced, due to reduced fluid retention. When blood volume becomes too low, plasma osmolarity will increase due to a higher concentration of solutes per volume of water.
Osmoreceptors in the hypothalamus detect the increased plasma osmolarity and stimulate the posterior pituitary gland to secrete ADH. ADH causes the walls of the distal convoluted tubule and collecting duct to become permeable to water—this drastically increases the amount of water that is reabsorbed during tubular reabsorption. ADH also has a vasoconstrictive effect in the cardiovascular system, which makes it one of the most important compensatory mechanisms during hypovolemic shock shock from excessive fluid loss or bleeding.
Aldosterone is a steroid hormone corticoid produced at the end of the renin—angiotensin system. To review the renin—angiotensin system, low blood volume activates the juxtaglomerular apparatus in a variety of ways to make it secrete renin. Renin cleaves angiotensin I from the liver -produced angiotensinogen.
Angiotensin II has a variety of effects such as increasing thirst but it also causes release of aldosterone from the adrenal cortex. Aldosterone has a number of effects that are involved in the regulation of water output. This causes greatly increased reabsorption of sodium and water which follows sodium osmotically by cotransport , while causing the secretion of potassium into urine.
Aldosterone increases water reabsorption; however, it involves an exchange of sodium and potassium that ADH reabsoption regulation does not involve. Aldosterone will also cause a similar ion -balancing effect in the colon and salivary glands as well. A schematic diagram of the renin—angiotensin system : Overview of the renin—angiotensin system that regulates blood pressure and plasma osmolarity. This disorder is not related to the more common diabetes , which affects the level of the hormone insulin in your blood.
If the condition is acute, you may have a headache , nausea , or vomiting. In severe cases, coma and convulsions can occur. Nephrogenic diabetes insipidus is another very rare disorder that may affect ADH levels. The signs and symptoms are similar to central diabetes insipidus.
They include excessive urination, which is called polyuria, followed by extreme thirst, which is called polydipsia. Testing for this disorder will likely reveal normal or high ADH levels, which will help distinguish it from central diabetes insipidus.
Nephrogenic diabetes insipidus is not related to the more common diabetes mellitus, which affects the level of insulin hormone in the blood. A healthcare provider will draw blood from your vein, usually on the underside of the elbow. During this process, the following occurs:. Many medications and other substances can affect the levels of ADH in your blood.
Before the test, your doctor may ask you to avoid:. An ADH test alone is usually not enough to make a diagnosis. Your doctor will probably need to perform a combination of tests. Some tests that may be performed with an ADH test include the following:. Excessive urination volume or polyuria occurs when you urinate more than normal. Urine volume is considered excessive if it equals more than 2. Most performance enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies including the International Olympic Committee, the U.
The side effects of synthetic hormones are often significant and non-reversible, and in some cases, fatal. Androgens produce several complications such as liver dysfunctions and liver tumors, prostate gland enlargement, difficulty urinating, premature closure of epiphyseal cartilages, testicular atrophy, infertility, and immune system depression.
The physiological strain caused by these substances is often greater than what the body can handle, leading to unpredictable and dangerous effects and linking their use to heart attacks, strokes, and impaired cardiac function.
In females, FSH stimulates development of egg cells, called ova, which develop in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production.
LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries, as illustrated in Figure Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle. The posterior pituitary releases the hormone oxytocin , which stimulates uterine contractions during childbirth.
The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete.
Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary. Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels.
Additional regulation is mediated by the thyroid hormones. Cells of the body require nutrients in order to function, and these nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake and utilizing reserves when necessary, the body uses hormones to moderate energy stores.
Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise for example, after a meal is consumed. Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production.
It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use.
Insulin also increases glucose transport into certain cells, such as muscle cells and the liver. This results from an insulin-mediated increase in the number of glucose transporter proteins in cell membranes, which remove glucose from circulation by facilitated diffusion.
As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. However, this does not occur in all cells: some cells, including those in the kidneys and brain, can access glucose without the use of insulin.
Insulin also stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins. This animation describe the role of insulin and the pancreas in diabetes. Impaired insulin function can lead to a condition called diabetes mellitus , the main symptoms of which are illustrated in Figure This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin.
This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia high sugar. High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system.
Oversecretion of insulin can cause hypoglycemia , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.
When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis.
Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis.
Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin.
Which of the following statement about these two conditions is true? The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine , also known as tetraiodothyronine or T 4 , and triiodothyronine , also known as T 3.
These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria resulting in increased ATP production. In the nucleus, T 3 and T 4 activate genes involved in energy production and glucose oxidation. T 3 and T 4 release from the thyroid gland is stimulated by thyroid-stimulating hormone TSH , which is produced by the anterior pituitary.
TSH binding at the receptors of the follicle of the thyroid triggers the production of T 3 and T 4 from a glycoprotein called thyroglobulin.
Thyroglobulin is present in the follicles of the thyroid, and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported into the thyroid follicle from the bloodstream.
A peroxidase enzyme then attaches the iodine to the tyrosine amino acid found in thyroglobulin. T 3 has three iodine ions attached, while T 4 has four iodine ions attached. T 3 and T 4 are then released into the bloodstream, with T 4 being released in much greater amounts than T 3.
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