Organ System Correlation Assignment - I mmune system and the Endocrine system .

Question

Organ System Correlation Assignment - Immune system and the Endocrine system.

List the function of the organ system being studied this week. ( 1 point)

List some common signs/symptoms seen in diseases and conditions that involve this particular organ system ( 3 points)

List the ways in which the function/status of this organ system can be assessed (include physical exam and diagnostic/lab tests) ( 3 points)

List common therapeutic interventions used to treat diseases and conditions of this particular organ system(be general with the category of medications etc., be sure to include lifestyle interventions as well) (3 points)

Explanation / Answer

The multiple activities of the cells, tissues, and organs of the body are coordinated by the interplay of several types of chemical messenger systems: 1. Neurotransmitters are released by axon terminals of neurons into the synaptic junctions and act locally to control nerve cell functions. 2. Endocrine hormones are released by glands or specialized cells into the circulating blood and influence the function of target cells at another location in the body. 3. Neuroendocrine hormones are secreted by neurons into the circulating blood and influence the function of target cells at another location in the body. 4. Paracrines are secreted by cells into the extracellular fluid and affect neighboring target cells of a different type. 5. Autocrines are secreted by cells into the extracellular fluid and affect the function of the same cells that produced them. 6. Cytokines are peptides secreted by cells into the extracellular fluid and can function as autocrines, paracrines, or endocrine hormones. Examples of cytokines include the interleukins and other lymphokines that are secreted by helper cells and act on other cells of the immune system . Cytokine hormones (e.g., leptin) produced by adipocytes are sometimes called adipokines.

Hormones That Act Mainly on the Genetic Machinery of the Cell

Steroid Hormones Increase Protein Synthesis Another means by which hormones act—specifically, the steroid hormones secreted by the adrenal cortex, ovaries, and testes—is to cause synthesis of proteins in the target cells. These proteins then function as enzymes, transport proteins, or structural proteins, which in turn provide other functions of the cells.

The sequence of events in steroid function is essentially the following: 1. The steroid hormone diffuses across the cell membrane and enters the cytoplasm of the cell, where it binds with a specific receptor protein.

2. The combined receptor protein–hormone then diffuses into or is transported into the nucleus.

3. The combination binds at specific points on the DNA strands in the chromosomes, which activates the transcription process of specific genes to form mRNA.

4. The mRNA diffuses into the cytoplasm, where it promotes the translation process at the ribosomes to form new proteins. To give an example, aldosterone, one of the hormones secreted by the adrenal cortex, enters the cytoplasm of renal tubular cells, which contain a specific receptor protein often called the mineralocorticoid receptor. Therefore, in these cells, the sequence of events cited earlier ensues. After about 45 minutes, proteins begin to appear in the renal tubular cells and promote sodium reabsorption from the tubules and potassium secretion into the tubules. Thus, the full action of the steroid hormone is characteristically delayed for at least 45 minutes—up to several hours or even days. This is in marked contrast to the almost instantaneous action of some of the peptide and amino acid–derived hormones, such as vasopressin and norepinephrine.

Thyroid Hormones Increase Gene Transcription in the Cell Nucleus:

The thyroid hormones thyroxine and triiodothyronine cause increased transcription by specific genes in the nucleus.

To accomplish this, these hormones first bind directly with receptor proteins in the nucleus; these receptors are activated transcription factors located within the chromosomal complex, and they control the function of the gene promoters.

Two important features of thyroid hormone function in the nucleus are the following:

1. They activate the genetic mechanisms for the formation of many types of intracellular proteins—probably 100 or more. Many of these are enzymes that promote enhanced intracellular metabolic activity in virtually all cells of the body.

2. Once bound to the intranuclear receptors, the thyroid hormones can continue to express their control functions for days or even weeks.

Diabetes Mellitus

Diabetes mellitus is a syndrome of impaired carbohydrate, fat, and protein metabolism caused by either lack of insulin secretion or decreased sensitivity of the tissues to insulin.

There are two general types of diabetes mellitus: 1. Type I diabetes, also called insulin-dependent diabetes mellitus (IDDM), is caused by lack of insulin secretion.

2. Type II diabetes, also called non-insulin-dependent diabetes mellitus (NIDDM), is initially caused by decreased sensitivity of target tissues to the metabolic effect of insulin. This reduced sensitivity to insulin is often called insulin resistance. In both types of diabetes mellitus, metabolism of all the main foodstuffs is altered.

The basic effect of insulin lack or insulin resistance on glucose metabolism is to prevent the efficient uptake and utilization of glucose by most cells of the body, except those of the brain. As a result, blood glucose concentration increases, cell utilization of glucose falls increasingly lower, and utilization of fats and proteins increases.

Type I Diabetes—Deficiency of Insulin Production by Beta Cells of the Pancreas Injury to the beta cells of the pancreas or diseases that impair insulin production can lead to type I diabetes. Viral infections or autoimmune disorders may be involved in the destruction of beta cells in many patients with type I diabetes, although heredity also plays a major role in determining the susceptibility of the beta cells to destruction by these insults. In some instances, there may be a hereditary tendency for beta cell degeneration even without viral infections or autoimmune disorders.

The usual onset of type I diabetes occurs at about 14 years of age in the United States, and for this reason it is often called juvenile diabetes mellitus. However, type I diabetes can occur at any age, including adulthood, following disorders that lead to destruction of pancreatic beta cells.

Type I diabetes may develop abruptly, over a period of a few days or weeks, with three principal sequelae: (1) increased blood glucose, (2) increased utilization of fats for energy and for formation of cholesterol by the liver, and (3) depletion of the body’s proteins. Approximately 5 to 10 percent of people with diabetes mellitus have the type I form of the disease. Blood Glucose Concentration Rises to High Levels in Diabetes Mellitus. The lack of insulin decreases the efficiency of peripheral glucose utilization and augments glucose production, raising plasma glucose to 300 to 1200 mg/100 ml. The increased plasma glucose then has multiple effects throughout the body. Increased Blood Glucose Causes Loss of Glucose in the Urine. The high blood glucose causes more glucose to filter into the renal tubules than can be reabsorbed, and the excess glucose spills into the urine. This normally occurs when the blood glucose concentration rises above 180 mg/100 ml, a level that is called the blood “threshold” for the appearance of glucose in the urine. When the blood glucose level rises to 300 to 500 mg/100 ml—common values in people with severe untreated diabetes—100 or more grams of glucose can be lost into the urine each day. Increased Blood Glucose Causes Dehydration. The very high levels of blood glucose (sometimes as high as 8 to 10 times normal in severe untreated diabetes) can cause severe cell dehydration throughout the body. This occurs partly because glucose does not diffuse easily through the pores of the cell membrane, and the increased osmotic pressure in the extracellular fluids causes osmotic transfer of water out of the cells. In addition to the direct cellular dehydrating effect of excessive glucose, the loss of glucose in the urine causes osmotic diuresis. That is, the osmotic effect of glucose in the renal tubules greatly decreases tubular reabsorption of fluid. The overall effect is massive loss of fluid in the urine, causing dehydration of the extracellular fluid, which in turn causes compensatory dehydration of the intracellular fluid.Thus, polyuria (excessive urine excretion), intracellular and extracellular dehydration, and increased thirst are classic symptoms of diabetes. Chronic High Glucose Concentration Causes Tissue Injury. When blood glucose is poorly controlled over long periods in diabetes mellitus, blood vessels in multiple tissues throughout the body begin to function abnormally and undergo structural changes that result in inadequate blood supply to the tissues. This in turn leads to increased risk for heart attack, stroke, end-stage kidney disease, retinopathy and blindness, and ischemia and gangrene of the limbs. Chronic high glucose concentration also causes damage to many other tissues. For example, peripheral neuropathy, which is abnormal function of peripheral nerves, and autonomic nervous system dysfunction are frequent complications of chronic, uncontrolled diabetes mellitus. These abnormalities can result in impaired cardiovascular reflexes, impaired bladder control, decreased sensation in the extremities, and other symptoms of peripheral nerve damage. The precise mechanisms that cause tissue injury in diabetes are not well understood but probably involve multiple effects of high glucose concentrations and other metabolic abnormalities on proteins of endothelial and vascular smooth muscle cells, as well as other tissues. In addition, hypertension, secondary to renal injury, and atherosclerosis, secondary to abnormal lipid metabolism, often develop in patients with diabetes and amplify the tissue damage caused by the elevated glucose.

Diabetes Mellitus Causes Increased Utilization of Fats and Metabolic Acidosis. The shift from carbohydrate to fat metabolism in diabetes increases the release of keto acids, such as acetoacetic acid and ?-hydroxybutyric acid, into the plasma more rapidly than they can be taken up and oxidized by the tissue cells. As a result, the patient develops severe metabolic acidosis from the excess keto acids, which, in association with dehydration due to the excessive urine formation, can cause severe acidosis. This leads rapidly to diabetic coma and death unless the condition is treated immediately with large amounts of insulin.

All the usual physiological compensations that occur in metabolic acidosis take place in diabetic acidosis. They include rapid and deep breathing, which causes increased expiration of carbon dioxide; this buffers the acidosis but also depletes extracellular fluid bicarbonate stores. The kidneys compensate by decreasing bicarbonate excretion and generating new bicarbonate that is added back to the extracellular fluid.

Insulin resistance is part of a cascade of disorders that is often called the “metabolic syndrome.” Some of the features of the metabolic syndrome include (1) obesity, especially accumulation of abdominal fat; (2) insulin resistance; (3) fasting hyperglycemia; (4) lipid abnormalities, such as increased blood triglycerides and decreased blood high-density lipoprotein-cholesterol; and (5) hypertension. All of the features of the metabolic syndrome are closely related to accumulation of excess adipose tissue in the abdominal cavity around the visceral organs.

The usual methods for diagnosing diabetes are based on various chemical tests of the urine and the blood.

Urinary Glucose. Simple office tests or more complicated quantitative laboratory tests may be used to determine the quantity of glucose lost in the urine. In general, a normal person loses undetectable amounts of glucose, whereas a person with diabetes loses glucose in small to large amounts, in proportion to the severity of disease and the intake of carbohydrates.

Fasting Blood Glucose and Insulin Levels.

The fasting blood glucose level in the early morning is normally 80 to 90 mg/100 ml, and 110 mg/100 ml is considered to be the upper limit of normal. A fasting blood glucose level above this value often indicates diabetes mellitus or at least marked insulin resistance.

In type I diabetes, plasma insulin levels are very low or undetectable during fasting and even after a meal. In type II diabetes, plasma insulin concentration may be severalfold higher than normal and usually increases to a greater extent after ingestion of a standard glucose load during a glucose tolerance test .

Glucose Tolerance Test. a “glucose tolerance curve,” when a normal, fasting person ingests 1 gram of glucose per kilogram of body weight, the blood glucose level rises from about 90 mg/100 ml to 120 to 140 mg/100 ml and falls back to below normal in about 2 hours.

Treatment of Diabetes Effective treatment of type I diabetes mellitus requires administration of enough insulin so that the patient will have carbohydrate, fat, and protein metabolism that is as normal as possible. Insulin is available in several forms. “Regular” insulin has a duration of action that lasts from 3 to 8 hours, whereas other forms of insulin (precipitated with zinc or with various protein derivatives) are absorbed slowly from the injection site and therefore have effects that last as long as 10 to 48 hours. Ordinarily, a patient with severe type I diabetes is given a single dose of one of the longer-acting insulins each day to increase overall carbohydrate metabolism throughout the day. Then additional quantities of regular insulin are given during the day at those times when the blood glucose level tends to rise too high, such as at mealtimes. Thus, each patient is provided with an individualized pattern of treatment. In persons with type II diabetes, dieting and exercise are usually recommended in an attempt to induce weight loss and to reverse the insulin resistance. If this fails, drugs may be administered to increase insulin sensitivity or to stimulate increased production of insulin by the pancreas. In many persons, however, exogenous insulin must be used to regulate blood glucose. In the past, the insulin used for treatment was derived from animal pancreata. However, human insulin produced by the recombinant DNA process has become more widely used because some patients develop immunity and sensitization against animal insulin, thus limiting its effectiveness.

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