Block 13 Thyroid Parathyroid Steroid Adrenal MCQ's

The correct association is A, where I is associated with euthyroidism, II is associated with primary hypothyroidism (1˚ hypothyroidism), and III is associated with secondary hypothyroidism (2˚ hypothyroidism).

If a patient presents with signs of hypothyroidism and suffers from iodine deficiency, the expected results would be a reduction in T4 levels and an elevation in TSH levels. This is because iodine is necessary for the production of thyroid hormones, including T4. When there is an iodine deficiency, the thyroid gland is unable to produce enough T4, leading to a reduction in its levels. In response to the low levels of T4, the pituitary gland releases more TSH to stimulate the thyroid gland to produce more thyroid hormones, resulting in an elevation in TSH levels.

Glucocorticoids have immunosuppressive effects by reducing inflammation and suppressing the immune response. TNF (tumor necrosis factor) is a pro-inflammatory cytokine produced by macrophages. By reducing the production of TNF in macrophages, glucocorticoids decrease the inflammatory response and contribute to their immunosuppressive effect. This action helps to dampen the immune system and reduce inflammation in various conditions such as autoimmune diseases and organ transplant rejection.

In patients with a benign thyroid adenoma (toxic nodule), the adenoma itself produces excessive amounts of thyroid hormone (T4), leading to elevated levels of T4. However, the excessive production of T4 suppresses the release of thyroid-stimulating hormone (TSH) from the pituitary gland, resulting in reduced levels of TSH. Therefore, in this scenario, the expected results would be T4 elevated and TSH reduced.

The correct relationship between changes in plasma levels of T3 & T4 and the release of TRH and TSH is that an increase in T3 & T4 levels leads to a decrease in the release of TRH and TSH. This is because T3 & T4 act as negative feedback signals to the hypothalamus and pituitary gland, inhibiting the release of TRH and TSH. Therefore, when T3 & T4 levels are high, the release of TRH and TSH is suppressed, resulting in a decrease in their plasma levels.

Thyroid hormones are known to modulate transcription of selected genes in the nucleus. This means that they can influence the expression of specific genes by either increasing or decreasing their transcription. By doing so, thyroid hormones can regulate various physiological processes in the body, such as metabolism, growth, and development. This mechanism of action allows thyroid hormones to have widespread effects on different tissues and organs in the body.

A pheochromocytoma is a tumor that originates from the adrenal glands and produces excessive amounts of catecholamines, such as adrenaline and noradrenaline. These hormones are synthesized from the amino acid tyrosine. By inhibiting the enzyme tyrosine hydroxylase, which is responsible for the conversion of tyrosine to dopamine (a precursor for catecholamines), the production of excessive catecholamines can be reduced. Therefore, a tyrosine hydroxylase inhibitor would be the most suitable drug for the treatment of pheochromocytoma.

Thyroid peroxidase is an enzyme involved in the synthesis of thyroid hormones. It catalyzes the coupling of two molecules of diiodotyrosine (DIT) to form thyroxine (T4), which is the main form of thyroid hormone produced by the thyroid gland. This process is essential for the production of T4, which is then converted to the active form of thyroid hormone, triiodothyronine (T3), in peripheral tissues. The other statements are incorrect: type II deiodinase is not involved in iodine oxidation, anions such as perchlorate inhibit iodide transport, plasma iodide is transported by active transport, and TSH promotes proteolysis of iodinated thyroglobulin.

The correct answer is that thyroid follicular cells secrete T4 hormone. This is characteristic of the thyroid gland because it is responsible for producing and secreting thyroid hormones, including T4 (thyroxine). T4 hormone plays a crucial role in regulating metabolism, growth, and development in the body. The other statements are incorrect. The thyroid gland is derived from the 4th pharyngeal pouch, not the 3rd. It does not secrete parathyroid hormone, which is produced by the parathyroid glands. Chief cells are involved in the production of parathyroid hormone, not calcitonin. The colloid in the thyroid gland is primarily composed of thyroglobulin, not calcitonin and T3.

The correct answer is D. Thyroid hormones increase the expression of cardiac Na+,K+-ATPase. This enzyme is responsible for maintaining the balance of sodium and potassium ions in cardiac cells, which is crucial for normal cardiac function. By increasing the expression of this enzyme, thyroid hormones enhance the ability of the heart to pump blood, leading to an increase in cardiac output.

In this scenario, the patient's levels of both T3 and T4 are significantly lower than normal, indicating a deficiency in the production or availability of thyroid hormones. Since TSH levels are normal and the thyroid gland is of normal size without palpable masses, it suggests that the problem lies outside of the thyroid gland itself. Thyroxin-binding globulin (TBG) is a protein that binds to and transports thyroid hormones in the blood. A deficiency in TBG would lead to decreased levels of T3 and T4 in the blood, explaining the patient's laboratory findings.

Corticosteroids primarily exert their effects by binding to specific nucleotide sequences of the DNA. This binding leads to the activation or inhibition of gene transcription, resulting in the production of proteins that mediate the anti-inflammatory, immunosuppressive, and metabolic effects of corticosteroids. This mechanism of action allows corticosteroids to regulate a wide range of physiological processes and modulate the immune response. G-protein coupled receptors, tyrosine kinase receptors, ion channel coupled receptors, specific nucleotide sequences of RNA, and specific nucleotide sequences of ribosomes are not the primary targets for corticosteroid action.

Thyroid follicles do not include parafollicular cells that release calcitonin into the colloid.

Thyroid hormone receptors are integral membrane proteins that bind T3 or T4 on their extracellular domains. They then facilitate the entry of T3 or T4 into the cell. Once inside the cell, the receptors bind T3 or T4 with their ligand binding domain and function in the nucleus. This allows them to regulate gene expression and ultimately impact various physiological processes in the body.

The patient's symptoms, including episodic weakness, paresthesias, constipation, and low plasma K+ level, are consistent with hyperaldosteronism caused by excess fludrocortisone. Fludrocortisone is a synthetic corticosteroid that acts as a mineralocorticoid, increasing sodium reabsorption and potassium excretion in the kidneys. This can lead to hypokalemia, which can cause weakness and paresthesias. Additionally, excess aldosterone can cause hypertension, which is supported by the patient's elevated blood pressure. Cortisol-induced hyperglycemia, inadequate therapy of adrenal insufficiency, cortisol-induced myopathy, and essential hypertension are not the best explanations for the patient's symptoms.

A tyrosine hydroxylase inhibitor would slow down the formation of 3-methoxy-4-hydroxymandelic acid because tyrosine hydroxylase is the enzyme responsible for converting tyrosine into norepinephrine. If tyrosine hydroxylase is inhibited, there would be less norepinephrine available for breakdown, leading to a decrease in the formation of 3-methoxy-4-hydroxymandelic acid.

The most probable cause of this patient's illness is primary hyperplasia. Primary hyperplasia is a condition in which all four parathyroid glands become enlarged and overactive, leading to increased levels of parathyroid hormone. This results in high serum calcium levels and low phosphate levels. The fact that the patient's serum creatinine is normal suggests that renal failure is not the cause of the elevated parathyroid hormone. Parathyroid adenoma and parathyroid carcinoma would typically only involve one gland, rather than all four. Lung carcinoma would not directly cause these symptoms. Therefore, primary hyperplasia is the most likely explanation.

The patient presented with signs and symptoms consistent with Cushing's syndrome, which is caused by excessive cortisol production. The presence of an adrenal adenoma further supports this diagnosis. Surgery to remove the adenoma would result in a sudden decrease in cortisol levels, which could lead to adrenal insufficiency. Therefore, cortisol would be given during and after surgery to ensure adequate adrenal function and prevent adrenal crisis. Fludrocortisone is a mineralocorticoid and would not address the cortisol deficiency. Spironolactone is an aldosterone antagonist and would not be appropriate in this case. Aminoglutethimide, mifepristone, and ketoconazole are all medications used to inhibit cortisol synthesis and would not be given in this situation.

Annexin is also known as *** lipocortin.**** Lipocortins suppress phospholipase A2. This is the mechanism by which glucocorticoids (primarily cortisol) inhibit inflammation.

Annexin A-I seems to be one of the most heavily involved annexins in anti-inflammatory responses. Upon infection or damage to tissues, annexin A-I is believed to reduce inflammation of tissues by interacting with annexin A-I receptors on leukocytes. In turn, the activation of these receptors functions to send the leukocytes to the site of infection and target the source of inflammation directly. As a result, this inhibits leukocyte (specifically neutrophils) extravasation and down regulates the magnitude of the inflammatory response. Without annexin A-I in mediating this response, neutrophil extravasation is highly active and worsens the inflammatory response in damaged or infected tissues. Annexin A-I has also been implicated in apoptotic mechanisms in the cell. When expressed on the surface of neutrophils, annexin A-I promotes pro-apoptotic mechanisms. Alternatively, when expressed on the cell surface, annexin A-I promotes the removal of cells that have undergone apoptosis. Moreover, annexin A-I has further medical implications in the treatment of cancer. Annexin A-I can be used as a cell surface protein to mark some forms of tumors that can be targeted by various immunotherapies with antibodies against annexin A-I.

The correct answer is that oral bioavailability is generally very good, substantial absorption does occur through the skin, and their biological half-lives can be long (up to 72 hours). Corticosteroids are well-absorbed when taken orally, and they can also be absorbed through the skin when applied topically. Their long half-lives mean that they stay in the body for an extended period of time before being eliminated. However, they do not distribute easily into the brain due to the blood-brain barrier, and they are not mainly excreted unchanged by the kidney.

Glucocorticoids have several effects on carbohydrate metabolism. One of these effects is increased glycogen synthesis in the liver, which means that more glucose is converted into glycogen and stored in the liver. Another effect is decreased glucose uptake by adipose tissue, meaning that adipose tissue takes up less glucose from the blood. These effects help to regulate blood glucose levels and ensure that glucose is available for other tissues that require it, such as skeletal muscle.