Endocrinology Quiz: Thyroid Disorders

ACE inhibitors (ACEi) and Angiotensin II Receptor Blockers (ARBs) reduce afterload on the left ventricle (LV) by counteracting the vasoconstrictive effects of Angiotensin II (AT II) on peripheral arterioles.

Although Angiotensin II has a minor impact on the afferent arterioles, its primary effect is vasoconstriction of the efferent arterioles. This causes a rise in filtration fraction and sustains glomerular filtration rate (GFR) even when renal blood flow is reduced.

Fibromuscular dysplasia (FMD) is characterized by tunica media proliferation, typically affecting women between 20 and 50 years old. This leads to decreased renal perfusion, stimulating renin secretion by the juxtaglomerular cells (JGC), and ultimately activating the RAAS.

Renal artery stenosis, caused by atherosclerosis, is often associated with:

*Intermittent claudication *History of coronary artery bypass grafting (CABG) *Long-term smoking

Addison's disease (primary hypoadrenalism) is often characterized by:

*Hyperpigmentation of the forearms *Eosinophilia (elevated eosinophil count) *Fatigue *Low blood pressure (BP)

Addison's disease is caused by decreased production of aldosterone and cortisol. The lack of cortisol leads to decreased negative feedback on the hypothalamus and anterior pituitary, resulting in low levels of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH).

In Addison's disease, adrenocorticotropic hormone (ACTH) and α-melanocyte-stimulating hormone (α-MSH) are both derived from pro-opiomelanocortin (POMC). ACTH and α-MSH contribute to hyperpigmentation in Addison's.

ACTH and Cortisol levels will not decrease with high-dose dexamethasone in patients with Cushing syndrome caused by a non-pituitary source, such as small cell lung cancer.

Lambert-Eaton myasthenic syndrome is a rare autoimmune disorder that affects the nerves that control the muscles. This can cause muscle weakness and fatigue.

Cushing syndrome is a disorder caused by prolonged exposure to high levels of cortisol.

The zona fasciculata is the middle layer of the adrenal cortex. It produces cortisol.

A cortisol-secreting adenoma is a benign tumor in the adrenal gland that produces excessive cortisol.

Negative feedback is a process where the output of a system inhibits the input of the system.

High glucocorticoid levels can lead to potassium wasting in the distal kidney, potentially causing hypokalemia.

Patients with Cushing syndrome often present with central obesity, purple striae, and an adrenal mass visualized on CT scan.

High-dose dexamethasone is used to suppress cortisol production in patients with Cushing syndrome. This is a diagnostic test to help differentiate between different causes of Cushing syndrome.

Myasthenia gravis is an autoimmune disorder that affects communication between nerves and muscles. This can cause muscle weakness and fatigue.

Prednisone, a synthetic glucocorticoid, is a cortisol analog. It's commonly used to treat various conditions, including autoimmune diseases like Systemic Lupus Erythematosus (SLE), Inflammatory Bowel Disease (IBD), and Rheumatoid Arthritis (RA).

Prednisone, a synthetic glucocorticoid, inhibits the production of both ACTH and cortisol via negative feedback. ACTH is a hormone released by the pituitary gland and stimulates cortisol production in the adrenal gland.

In a patient receiving exogenous glucocorticoids, like prednisone, the body's natural production of cortisol is suppressed, even though the patient exhibits Cushingoid features, indicating high levels of circulating cortisol.

Waterhouse-Friderichsen syndrome is a severe complication of meningococcal sepsis characterized by bilateral adrenal hemorrhage. The hemorrhagic necrosis damages the adrenal glands, disrupting the production of cortisol and aldosterone.

Waterhouse-Friderichsen syndrome results in low levels of serum aldosterone and cortisol due to adrenal hemorrhage. The lack of cortisol prevents the upregulation of alpha-1 receptors on arterioles, leading to reduced vasoconstriction and hypotension.

In patients with Waterhouse-Friderichsen syndrome, the deficiency in cortisol leads to a lack of vasoconstriction, resulting in low blood pressure (hypotension). This occurs because cortisol usually enhances the effectiveness of norepinephrine and epinephrine in vasoconstriction.

In primary hyperparathyroidism, serum calcium is elevated due to increased PTH secretion, but increased calcium reabsorption in the distal tubules also leads to high urinary calcium excretion.

Hydrocortisone is a synthetic cortisol analogue commonly used to treat adrenal insufficiency, including cases like Waterhouse-Friderichsen syndrome. It acts as a replacement for the deficient cortisol, providing the necessary hormones to restore function.

Despite increased PTH reabsorption of calcium in the distal tubules, the high serum calcium in hyperparathyroidism results in an overall increase in urinary calcium excretion. The body filters more calcium due to the high serum levels.

Waterhouse-Friderichsen syndrome causes a decrease in serum bicarbonate (HCO3-), leading to metabolic acidosis. This is due to the lack of cortisol, which normally contributes to sodium reabsorption and potassium excretion in the kidneys, influencing acid-base balance.

The calcium-sensing receptors in parathyroid glands act as negative feedback mechanisms. When calcium levels rise, they suppress PTH secretion. If these receptors are less sensitive, they are less effective at suppressing PTH, which in turn leads to higher PTH levels.

High Parathyroid hormone (PTH) levels in hypocalciuric hypercalcemia lead to increased urinary cAMP due to PTH's action on G-proteins. PTH activates adenylyl cyclase, which in turn increases cAMP levels.

Familial hypocalciuric hypercalcemia is a genetic condition characterized by a mutation in the calcium-sensing receptor of the parathyroid glands, causing reduced sensitivity. This results in high serum calcium and low urinary calcium excretion due to persistent PTH stimulation.

In primary hyperthyroidism, the thyroid gland is overactive, producing too much thyroid hormone. This leads to low TSH levels (hypothalamus and pituitary are suppressed due to high T3/T4) and high T3 and T4 levels.

In secondary hyperthyroidism, the problem lies in the pituitary or hypothalamus, causing them to overproduce TSH. This leads to high levels of TSH, T3, and T4.

Primary hypothyroidism occurs when the thyroid gland itself is underactive, producing too little thyroid hormone. This leads to high TSH levels (due to the lack of negative feedback), and low T3 and T4 levels.

Secondary hypothyroidism occurs when the pituitary or hypothalamus are not producing enough TSH, causing the thyroid to be underactive. This results in low TSH, T3, and T4 levels.

Graves disease is the most common cause of primary hyperthyroidism. It is an autoimmune disease where the body attacks the thyroid gland, leading to increased thyroid hormone production.

In Graves disease, TSH levels are low, T3 and T4 levels are high, and radioiodine uptake is increased due to hyperactivity of the thyroid gland.

Sheehan syndrome is a condition where the pituitary gland is damaged, usually due to postpartum hemorrhage. It can lead to decreased production of various hormones, including TSH.

Hashimoto thyroiditis is an autoimmune disease where the body attacks the thyroid gland, leading to decreased thyroid hormone production and eventually hypothyroidism.

Exophthalmos, tremulousness, and type I diabetes mellitus are clinical features commonly found in patients with Graves disease.

In Graves disease, the thyroid gland is hyperactive, leading to increased uptake of radioiodine.