“Hypoparathyroidism” plus 2 more nursing article(s): NursingCrib.com Updates |  |
| Posted: 18 Oct 2010 07:12 PM PDT
Hypoparathyroidism Hypoparathyroidism is a condition where a marked decrease, reduction or diminished secretion of parathyroid hormones is noted. This disorder occurs less frequently than hyperparathyroidism. A genetic factor is sometimes involved in the occurrence of this disorder where the kidneys develop insensitivity to parathyroid hormones leading to a condition known as pseudohypoparathyroidism (HPH). Parathyroid glands are small nodular endocrine tissue located at the posterior surface of the thyroid glands. There are around 2-8 glands found on the on the thyroid lobes. However, typically four to six are found. These glands are responsible for the production of parathyroid hormones. The chief cells of parathyroid glands synthesize this peptide hormone that is also called a parathormone (PTH). Only few of these hormones are stored because after it is synthesized, secretion follows immediately. The main function of parathormone (PTH) is to regulate the serum calcium level. That is why this is the most important regulator of maintaining the blood homeostasis in relation to calcium level. The secretion of PTH is relatively dependent on calcium concentration. Very low degree of serum calcium stimulates the parathyroid glands to synthesize and increase the secretion of parathormone. Normal serum calcium level is 9-11 mg/dl. Any drop below the minimum range Increase levels of parathormones would increase calcium levels. Thus, PTH is also called a hypercalcemic hormone. The one that acts opposite to PTH is called calcitonin which is secreted by the thyroid glands that causes increase deposition of calcium in the bones and low in the blood plasma. Thereby, calcitonin is called a hypocalcemic hormone. The feedback interaction between these two hormones is very vital in achieving calcium homeostasis in blood. Increase levels of parathormones would increase calcium levels. Thus, PTH is also called a hypercalcemic hormone. The one that acts opposite to PTH is called calcitonin which is secreted by the thyroid glands that causes increase deposition of calcium in the bones and low in the blood plasma. Thereby, calcitonin is called a hypocalcemic hormone. The feedback interaction between these two hormones is very vital in achieving calcium homeostasis in blood. The mechanisms on how calcium is elevated with increase PTH secretion are the following:
Result: release of calcium deposited in bones When calcium levels drop parathyroid hormones activates osteoclasts inside the bone. Osteoclasts are cells that stimulate bone cell destruction. This is primarily done by the body to cause a breakdown in the bone matrix so that calcium from the bone will be released to the blood, making more calcium available.
Result: decrease phosphate levels Increase parathormone secretion due to low calcium level triggers the body to undergo another mechanism which is the escalation of phosphate elimination in kidneys. This is effective in maintaining calcium in plasma because when calcium and phosphate are both elevated, they are incorporated into the bones. Presence of calcium alone does not have this effect, therefore, elimination of phosphate would prevent calcium bone deposition and the calcium released from the bones remains in the extracellular fluid (ECF).
Result: increase calcium in extracellular fluid (ECF)
Result: increase calcium absorption in the intestinal tract This mechanism will lead to the addition of calcium in the blood plasma from the diet or food intake of a person. Vitamin D is a fat soluble vitamin that is needed for the absorption of calcium. Without this vitamin, calcium will not be used by the body. If a person's diet contains enough calcium such as milk products, green leafy vegetables, shrimp, salmon, clams, tofu, legumes and fortified orange juice he/she will just excrete the calcium on the condition that vitamin D is lacking. Foods rich in Vitamin D are dairy products, eggs, and fatty fish. Once PTH is present this vitamin found in the gastrointestinal tract will be activated thereby, increasing calcium absorption. Etiology
A resulting low calcium concentration in the plasma (hypocalcemia) due to the mentioned etiological factors can cause extreme weakness, defective muscular function and altered mental processes. Related posts: |
| Posted: 18 Oct 2010 06:47 PM PDT
Glycosylated Hemoglobin Test Glycosylated hemoglobin test indicates the average plasma glucose concentration over two (2) to three (3) months. The word "glycosylated" denotes the attachment of a blood glucose molecule to hemoglobin. It is abbreviated as HbA1c. Normally, the result ranges from 4% – 8%. In people with poorly controlled serum glucose levels (diabetes), the levels are markedly elevated. Red blood cells (RBCs) contain an iron bearing protein called hemoglobin. Hemoglobin molecules contain amino acid chains and are responsible for the carrying and transportation of oxygen from the blood. When blood sugar rises, a glucose molecule would attach itself to hemoglobin inside an erythrocyte, the hemoglobin is now called glycosylated or glycated hemoglobin (glycohemoglobin).  glucose attaching itself to hemoglobin molecules Once hemoglobin is glycosylated (glucose attaching to hemoglobin) it remains that way for the entire life span of a red blood cell. Since the life cycle of an erythrocyte is 120 days, the glycosylated hemoglobin value detects glucose levels for about 120 days or 3 months. The duration of hyperglycemia, determines the amount of glucose that attaches to hemoglobin. If the elevated sugar level stays for a longer period in the blood, higher glycosylated hemoglobin would be the result. In cases where episodes of blood glucose elevation are intermittent or infrequent and the person a near-normal blood glucose level, the total value of HbA1c would also not be greatly increased. On the other hand, if hyperglycemic occurrence is frequent and persistent, the test result will significantly rise. Some patients are monitoring their blood glucose levels at home by using a special reagent strip and allowing a drop of blood to remain in it for about 1 minute (60 seconds) and visually comparing the color change of the strip to the standardized color code in the container. Others are using a glucometer where the strip is just inserted in a device and a digital display will show the serum glucose levels. With these self-monitoring tests, the blood glucose determined is during the time the procedure is done only (short term). Patient who have high glycosylated hemoglobin but are mostly obtaining normal results with self-monitoring tests at home might have a mistake with the methods executed. These instances include the flowing:
HbA1c or HbA1 is not affected by sudden changes in blood glucose levels. For instance if a patient has had an episode of hyperglycemia but has managed to keep his sugar level normal or near-normal most of the time, the glycosylated hemoglobin result will most likely be good. It is like a student who is top of the class. This intelligent individual got 7 out of 10 in one of the quizzes but most of the time he gets the perfect rating. At the end of the semester, he is still ranked as the best in his class. Glycosylated hemoglobin works this way. It evaluates not the short-term changes but rather the overall effectiveness of long-term therapy for diabetes and how well the person is doing in controlling the disease. In addition, a diabetes control card is helpful in interpreting the results obtain with glycosylated hemoglobin test. images from wellsphere.com, aurorabaycare.com,embeediagnostics.com Related posts: |
| Increased Intracranial Pressure Posted: 18 Oct 2010 06:42 PM PDT
Increased Intracranial Pressure Intracranial pressure (ICP) is the pressure in the skull that results from the volume of three essential components: cerebrospinal fluid (CSF), intracranial blood volume and central nervous system tissue. The normal intracranial pressure is between 5-15 mmHg. This is slightly lower than the mean systemic arterial pressure but considerably higher than venous pressure. The intact cranium is essentially inexpandable containing about 1400 grams of central nervous system (CNS) or brain tissue, 75 ml of blood and about 75 ml of cerebrospinal fluid (CSF). These three components of the cranial vault maintain a state of equilibrium. Their pressure and volume determine the condition of balance. According to Monro-Kellie hypothesis, any increase in one of these elements must be balanced or compensated by a proportional constriction either or both of the other two components such as decreasing the volume of cerebral blood flow, shifting CSF flow (into the spinal canal) or increasing CSF absorption. Absence of these compensatory changes results to increased intracranial pressure. Once ICP reaches around 25 mmHg marked elevation in intracranial pressure will be noted. CSF is formed from the blood by the choroid plexuses, which are hanging at the roof of the brain's ventricles. From the point where it is produced, it flows through the aqueduct of Sylvius to the fourth ventricles. Three apertures (opening) are found in the fourth ventricle which serves as passageway going to the subarachnoid spaces in the brain and spinal cord. These openings are Foramina of Magendie (median aperture) and two Foramina of Luschka (lateral apertures). A presence of tumor in choroid plexus may cause an overproduction of CSF. If the passageway of CSF is obstructed or brain tissue damage during surgery occurs, elevated ICP is inevitable. Normally, a change in CSF and blood volume occurs. For instance, during exhalation a temporary rise in intrathoracic pressure occurs. This impairs cerebral venous drainage and thereby reabsorption of CSF. An increase in ICP might likely occur, unless the blood will be expelled or the brain tissue will shrink (compensatory mechanism). If no compensation will occur, based on Monro-Kellie hypothesis, a slight increase in intracranial pressure will take place. The same process occurs during Valsalva maneuver (forcible exhalation against a closed glottis), sneezing, coughing and straining at stool. This is the main reason why people with increase ICP and at risk for cerebral hemorrhage are instructed to avoid these instances. Presence of carbon dioxide can also increase ICP. Carbon dioxide is a potent vasodilator that dilates aretrioles (including those in the chorionic plexus in the brain) which elevates cerebral blood volume and ICP. Etiology CSF – hydrocephalus
CNS tissue
Blood
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