HPRS 2201 Chapter 4 Part 1 Narrated

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[00:00:00]Hello. Today we're going to talk about the endocrine system. The endocrine system is a series of, it's a ductless system. They release specific chemical messengers called hormones directly into the bloodstream.

[00:00:18]Now hormones produce their effects by binding to receptors, which are recognition sites on the various target tissues on which the hormones act. Each hormone has its own receptor and these are the ones we're going to talk about.

[00:00:32]Now in the first part of this lecture we're going to cover the pineal gland, thymus, thyroid, and the parathyroid glands. The pineal gland. It's located in the central portion of the brain. It produces melatonin; it supports the body's biological clock; possibly induces sleep. Melatonin secretion increases with the deprivation of light, and is inhibited by sunlight. The thymus gland is located behind the sternum in the mediastinum. This is a centrally located area outside of and between the lungs. It contains the heart, aorta, trachea, esophagus, thymus gland, bronchial tubes, and many lymph nodes. The thymus contains lymphatic tissue and T-cell lymphocytes. Now thymosin aids in the development of immune responses in newborns. It is large in childhood and shrinks in adulthood.

[00:01:48]Now let's talk about the thyroid gland. So the thyroid gland covers the larynx, which is the Adam's apple. So let's move on. Now this is the hypothalamus-pituitary-thyroid gland feedback loop. So as you can see in the hypothalamus, something happens. There's some type of stimulus either cold or stress, and the hypothalamus releases TRH, which is thyrotropin-releasing hormone. This TRV, TRH sorry, I can't talk today, tells the anterior pituitary to release TSH. TSH stimulates the thyroid gland to produce T4 and then once the T4 is where it needs to be, then it tells the hypothalamus okay back off now we don't need to produce anymore okay.

[00:02:57]Now the T4 is produced in the thyroid gland, then the T4 goes to the liver where it is iodinated and one of the iodine's will come off and that becomes T3. Alright so here's the structure. T3 and T4 both have a tyrosine base okay.

[00:03:24]There's your tyrosine. Now see how they have four iodine's on, well--that's T4 and when you take one of them off, it makes it t3 okay.

[00:03:36]Now T4 is 5 times more plentiful than T3, but T3 is more biologically active.

[00:03:47]T4 and T3 are bound to thyroxine-binding proteins such as albumin and prealbumin.

[00:03:54]Now thyroglobulin is the pro hormone for T4, and T4 is the pro hormone for T3 okay. So you need thyroglobulin to make T4 and you need T4 to make T3. An increase or decrease in thyroglobulin will cause a concomitant rise or fall in T3 or T4. So some examples of conditions where you have increased thyroglobulin levels: oral contraceptives, infectious and chronic active hepatitis, biliary cirrhosis, and you have decreased thyroglobulin levels with nephrotic syndrome, androgen therapy, glucocorticoid therapy, or major systemic illnesses okay.

[00:04:48]The thyroid gland. They are two lobes on either side of the trachea just below the thyroid cartilage. Thyroxine, a tetraiodothyronine, is T4, and triiodothyronine is T3. Both maintain a normal level of metabolism in all body cells. T3 and T4 aid cells in their uptake of oxygen, which supports the metabolic rate. Cells need oxygen to burn fuel and release energy stored there.

[00:05:20]OK the other hormone that the thyroid gland produces is calcitonin, and that stimulates the calcium to leave the blood and enter the bone. OK so that's secreted when calcium levels in the blood are high. There is a nasal spray of calcitonin for osteoporosis.

[00:05:46]The thyroid gland. Okay let's talk about some of the diseases.

[00:05:50]The first one is hyperthyroidism and this is Graves disease. It's an autoimmune process, and this is primary hyperthyroidism. So if the problem occurs in the thyroid gland, its primary hyperthyroidism. If it occurs in the anterior pituitary, its secondary hyperthyroidism, and if something's happening in the hypothalamus to cause a problem with the thyroid, then it's called tertiary hyperthyroidism. But Graves is primary. So you have increased thyroid antibodies; you have hyperplasia of the thyroid parenchyma, and it produces excessive amounts of hormones. The cellular metabolic rate increases leading to sweating, weight loss, rapid and irregular heartbeat, diarrhea, and warm and moist skin. Now a sudden exacerbation or in the symptoms (increase of symptoms) may signal thyrotoxicosis or a thyroid storm, and that you got to be careful because you know your heart rate's going up. Everything's going at a much faster rate. Now you see this exophthalmos, where the eyes kind of look buggy-eyed, this is due to swelling of the tissue behind the eyeball pushing it forward. Now to make the diagnosis you have a decreased TSH and increased T3 T4.

[00:07:23]The thyroid scan will show an increased uptake of radioiodine, and that's diagnostic for it, and then you have increased anti-thyroid antibodies okay.

[00:07:35]Now guys this is, remember that feedback loop, so as the T3 T4 goes up in the body, the TSH comes down, and conversely when the TSH goes up. the T3 and T4 go down okay. So you got, so that's the way, you can remember that when you're studying for the test, the lab work. So if you have hyperthyroidism, you're going to have increased T3 T4. If you have increased T3 T4, you should have a decreased TSH. Now in Graves disease you have antibodies that mimic TSH and this has caused the thyroid gland to produce more T4 because it thinks it's TSH okay, and this TSH-R right there that's the thyroid- stimulating hormone receptor. This is a malfunction in the body's immune system. It releases abnormal antibodies that mimic TSH, and the treatment for this - you want to give them anti-thyroid drugs. They reduced the hormone levels by blocking the synthesis of these hormones, and radioactive iodine which destroys the overactive glandular tissue.

[00:09:01]This is goiter. You get hyperplasia or enlargement of the thyroid gland, and it's caused by a lack of iodine in the diet. As the hyperplasia increases, it produced, it presses on the esophagus causing difficulty swallowing. It can enlarge further, affecting the trachea causing dyspnea, which is trouble breathing. So in here you have decreased iodine levels, decreased T3 T4, and what do you think is going to happen with the TSH? That's right; it's going to increase.

[00:09:37]You'll have an increased TSH. Now let's talk about hypothyroidism. We have myxedema. This is advanced hypothyroidism in children or adults. You have atrophy of the thyroid gland. Practically no hormone is produced. The skin is dry and puffy due to a collection of mucus-like material under the skin, and it may also be secondary to failure of the pituitary to produce thyrotropin.

[00:10:12]You have, remember this is hypothyroidism right, so you would expect, what would you expect your T4 and T3 to be? Right. Decreased and you have a decreased free T4 and an increased TSH okay. So the reason the TSH is increased is because when the the body says oh oh my T4 is going down, so we need to get this loop going again. We need to produce more, and it's trying, but the thyroid gland is atrophied and so it's not going to help it, but it's still trying to produce it.

[00:10:56]Hashimoto's thyroiditis. It's also called chronic lymphocytic thyroiditis. It's the leading cause of goiter and hypothyroidism. The auto-antibodies appear to destroy the thyroid tissue. The gland enlarges as a result of an inflammatory process with massive infiltration by the lymphocytes and plasma cells. As a result, gland tissue is replaced by fibrous tissue okay.

[00:11:26]The diagnosis is an increased TSH, auto- antibodies to thyroid tissue, and radioactive iodine uptake will show slow uptake okay. So the auto-antibodies present are anti-thyroglobulin and anti-thyroid peroxidase antibodies. Now you may have seen that as written as TPO, and the treatment is lifelong replacement of the thyroid hormones. Now another form of cretinism, I mean of hypothyroidism, is cretinism. This is extreme hypothyroidism developing during infancy and childhood, and it leads to a lack of normal physical and mental growth. The child is obese, short and stocky, skeletal growth is more inhibited than soft tissue growth, and you have now this is hypothyroidism so you have decreased T4, increased TSH, and the thyroid scan confirms the absence of thyroid tissue. So this is just an overview of the thyroid gland. It produces T3 and T4, which increases metabolism. Remember it gets the oxygen to the cells, and it produces calcitonin, which decreases blood calcium so it takes calcium from the blood and puts it into the bone. Now we're going to talk about the parathyroid glands. These are four small oval bodies located on the dorsal aspect of the thyroid gland okay. They're right there.

[00:13:22]Calcium is necessary for proper functioning of body tissues especially muscles so the hormone that it produces is a it's called the parathyroid hormone or parathormone. It mobilizes calcium from the bone and puts it into the bloodstream. This hormone, like other hormones in the body, control homeostasis, which is an equilibrium or constancy in the body's internal environment. If a blood calcium decreases such as pregnancy or vitamin D deficiency, the PTH or the parathyroid hormone will increase, and this causes calcium to leave the bones and go into the bloodstream.

[00:14:04]Blood calcium levels are thus brought back to normal. Conversely, increased calcium in the bloodstream causes decreased PTH, causing calcium to leave blood and go into the bones. Now we have hyperparathyroidism and hypoparathyroidism. Hyperparathyroidism - you have an increased PTH. This will result in hypercalcemia. Remember because the calcium leaves the bone and goes into the bloodstream. You'll have osteoporosis due to calcium loss because it's going from the bone into the blood, and kidney stones.

[00:14:52]Also there's conduction defects of the heart due to the hypercalcemia. The diagnosis is made with an increase, that little "i" is in the intact PTH okay, hypercalcemia, hypophosphatemia. So you have an increased serum calcium, decreased serum phosphorous, hypocalcuria (decreased calcium in the urine), and the DXA scan shows bone demineralization, and DXA stands for dual energy x-ray absorptiometry (I can't talk today), and what it does it measures bone mineral density okay. Alright, and that's the end of part one.