Patho Exam 4 Thyroid Disease

Goiter is the correct answer because it refers to the abnormal enlargement of the thyroid gland. This condition can be caused by various factors such as iodine deficiency, autoimmune diseases, or thyroid nodules. Goiter can lead to symptoms like swelling in the neck, difficulty swallowing or breathing, and changes in voice. Treatment options for goiter depend on the underlying cause and may include medication, iodine supplements, or surgery.

Serum TSH is the most sensitive test for early hypothyroidism because it measures the levels of thyroid-stimulating hormone in the blood. In hypothyroidism, the thyroid gland does not produce enough thyroid hormones, causing an increase in TSH levels as the body tries to stimulate the thyroid gland. Therefore, measuring serum TSH levels can detect even subtle changes in thyroid function and diagnose hypothyroidism at an early stage. Serum LH, Serum FSH, and Serum TH are not directly related to thyroid function and would not be as sensitive in detecting early hypothyroidism.

Patients with Graves disease typically suffer from autoimmune disorders. Graves disease is an autoimmune disorder that affects the thyroid gland, causing it to produce excessive amounts of thyroid hormone. This condition is characterized by symptoms such as weight loss, irritability, heat intolerance, and an enlarged thyroid gland. Since Graves disease itself is an autoimmune disorder, it is common for patients with this condition to also have other autoimmune disorders, such as rheumatoid arthritis, lupus, or type 1 diabetes.

Thyroid-stimulating hormone (TSH) is a hormone that stimulates the thyroid gland to produce and release thyroid hormones. The anterior pituitary gland is responsible for secreting TSH. This gland is located at the base of the brain and controls the release of various hormones in the body. TSH is released in response to signals from the hypothalamus, which produces thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary gland to release TSH, which then acts on the thyroid gland to regulate its function. Therefore, the correct answer is the anterior pituitary gland.

Hashimoto's thyroiditis is the most common cause of hypothyroidism. It is an autoimmune disorder where the body's immune system mistakenly attacks the thyroid gland, leading to inflammation and damage. This results in a decrease in thyroid hormone production, leading to hypothyroidism. Graves' disease, on the other hand, is an autoimmune disorder that causes hyperthyroidism, not hypothyroidism. Thyroid storm is a life-threatening condition characterized by an excessive release of thyroid hormones, also not causing hypothyroidism. Abnormal iodine metabolism can contribute to thyroid disorders, but it is not the most common cause of hypothyroidism.

The statement is false because the thyroid actually has one of the highest rates of blood flow per gram of tissue compared to other organs. The thyroid gland requires a high blood supply in order to receive the necessary nutrients and hormones for its proper functioning. This high blood flow helps in the production and secretion of thyroid hormones, which play a crucial role in regulating metabolism and other bodily functions.

Patients with hyperthyroidism show an increase in osteoblastic and osteoclastic activity. This is because the excess thyroid hormone stimulates bone turnover, leading to increased osteoblast (bone-building cells) and osteoclast (bone-resorbing cells) activity. As a result, there is an accelerated bone remodeling process, which can lead to bone loss and an increased risk of osteoporosis in these patients.

T4 is composed of two di-iodotyrosine molecules coupled together. This means that two molecules of di-iodotyrosine are connected to form T4.

T3 induces increased production of beta-adrenergic receptors. T3 is a thyroid hormone that regulates metabolism, and one of its effects is to increase the expression of beta-adrenergic receptors. Beta-adrenergic receptors are a subtype of G-protein coupled receptors found on the cell membrane. These receptors are involved in various physiological processes such as heart rate regulation and mobilization of energy reserves. Therefore, the increased production of beta-adrenergic receptors induced by T3 can enhance the responsiveness of cells to adrenaline and other catecholamines, leading to increased metabolic activity.

TSH receptor autoantibody (TSH-R Ab) is an agonist because it binds to the TSH receptor and activates it, mimicking the action of the thyroid-stimulating hormone (TSH). This leads to an increased production and release of thyroid hormones by the thyroid gland. As an agonist, TSH-R Ab enhances the signaling pathway of the TSH receptor, resulting in increased thyroid hormone levels.

Transient hyperthyroidism refers to a temporary state of excessive thyroid hormone production. It is known to occur before the development of hypothyroidism, which is a condition characterized by an underactive thyroid gland and decreased production of thyroid hormones. Therefore, the correct answer is hypothyroidism, as transient hyperthyroidism precedes its development.

Men with hyperthyroidism typically have normal sperm counts, but their sperm motility is decreased. Hyperthyroidism can affect the function of the testes and the production of sperm, leading to lower motility. This means that although the number of sperm may be normal, they may have difficulty swimming and reaching the egg for fertilization.

Thyroid follicular cells collect and transport iodine to the colloid. Iodine is an essential element required for the synthesis of thyroid hormones, T3 (triiodothyronine) and T4 (thyroxine). These hormones are produced by the thyroid gland and play a crucial role in regulating metabolism, growth, and development in the body. The follicular cells actively take up iodine from the bloodstream and transport it into the colloid, which is a gel-like substance within the thyroid gland. This iodine is then utilized by the gland to synthesize thyroid hormones.

The appearance of cells in an active thyroid includes small follicles and cuboidal lining. This is because the thyroid gland is composed of many small follicles, which are small spherical structures that contain thyroid hormone. The lining of these follicles is made up of cuboidal epithelial cells, which are cube-shaped cells that are specialized for secretion and absorption. This arrangement allows for efficient production and release of thyroid hormone into the bloodstream.

T3 and T4 are thyroid hormones that are synthesized in the colloid of the thyroid gland. The process by which iodine is added to the amino acid tyrosine to form T3 and T4 is called iodination. This process involves the enzyme thyroid peroxidase, which catalyzes the reaction between iodine and tyrosine residues on thyroglobulin, a protein found in the colloid. Iodination is an essential step in the production of thyroid hormones, as it allows for the incorporation of iodine into the structure of T3 and T4, which is necessary for their biological activity.

The approximate half-life of T4 is 6-7 days, which means that it takes around 6-7 days for half of the T4 in the body to be eliminated. On the other hand, the approximate half-life of T3 is 30 hours, which means that it takes around 30 hours for half of the T3 in the body to be eliminated. Therefore, the correct answer is 6-7 days and 30 hours.

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TSH secretion typically peaks after midnight. The circadian pattern of TSH secretion follows a rhythm where it is lowest in the afternoon and evening, starts to rise during the night, and reaches its peak after midnight. This peak in TSH secretion is a normal physiological response in the body's hormonal regulation.

TSH (thyroid-stimulating hormone) is secreted by the pituitary gland and plays a role in regulating thyroid function. During stressful situations, the body releases cortisol, which can inhibit the secretion of TSH. This is because cortisol suppresses the hypothalamic-pituitary-thyroid axis, leading to a decrease in TSH production. Therefore, TSH secretion is inhibited by stress.

Graves disease/hyperthyroidism occurs when the immune system mistakenly targets the TSH receptors in the thyroid gland. One possible explanation for this is molecular mimicry, where a viral antigen shares similarities with the TSH receptors, causing the immune system to attack both. This phenomenon occurs when the immune system is unable to distinguish between self and non-self antigens, leading to autoimmune diseases like Graves disease.