Endocrine and Metabolic Disorders

In Barrter's syndrome there is a mutation, which inhibits the activity of the NaK2Cl cotransporter. It is the molecule normally inhibited by frusemide. The clinical effects of Barrter''s syndrome are therefore the same as excess frusemide and include loss of sodium, potassium and water. The bodies response to this is to raise aldosterone levels in an attempt to conserve sodium.

Exophthalmic goiter (Graves' disease) is caused by hypersecretion of thyroid hormones (thyroxine). Option B correctly identifies the thyroid gland, though 'thyriod' is misspelled. The thyroid is an endocrine gland, but not all endocrine glands cause this condition.

Affects 90-95% of people who have diabetes 

It is a chronic systemic disease characterized by either a deficiency of insulin or a decreased ability of the body to use insulin.

Hyperglycemia or high blood sugar is a condition in which an excessive amount of glucose circulates in blood plasma. High blood glucose happens when the body has too little insulin or when the body can't use insulin properly.

It occurs mainly in children and young adults, and the onset is usually sudden. The deficiency or absence of insulin is due to the destruction of islet cells. The causes are familial tendency and genetic involvement. In many cases antibodies to islet cells are present probably in cells previously damaged by infection.

Acromegaly is caused by excessive secretion of growth hormone in adults, leading to enlargement of bones in hands, feet, and face. In children, excess growth hormone causes gigantism. Grave's disease is thyroid-related, Gull's disease is hypothyroidism, and dwarfism is caused by growth hormone deficiency.

This is the correct option. Thyroid hormone causes myxoderma (in adults). Insulin hormone causes diabetes mellitus. Aldosterone hormone causes Addison's disease.

Mineralocorticoid excess (such as in Conn's syndrome or hyperaldosteronism) causes metabolic alkalosis through multiple mechanisms: increased H+ ion secretion in the renal tubules, hypokalemia (which leads to intracellular H+ shift), and increased urinary acid excretion. The opposite condition - mineralocorticoid deficiency - would cause metabolic acidosis, not alkalosis.

Thiazides DECREASE calcium excretion (they increase calcium reabsorption in DCT), making them useful in hypercalciuric stone formers. The question asks for what they DON'T cause. They DO cause hyperglycemia, increased uric acid (precipitating gout), and are useful in CHF for their diuretic effect.

Loop diuretics like furosemide actually DECREASE serum calcium by increasing urinary calcium excretion, so they do NOT cause hypercalcemia. Lithium causes hypercalcemia by increasing parathyroid hormone secretion. Vitamin D intoxication directly increases calcium absorption and bone resorption.

Glucocorticoids like prednisone cause hyperglycemia by promoting gluconeogenesis, reducing glucose uptake in peripheral tissues, and inducing insulin resistance. Beta blockers can mask hypoglycemia symptoms but don't directly raise blood glucose. NSAIDs have minimal effect on glucose metabolism.

SIADH (Syndrome of Inappropriate ADH) causes euvolemic or hypervolemic hyponatremia with concentrated urine and hypouricemia (increased renal uric acid excretion). Volume depletion causing hypotension is NOT seen in SIADH - that would occur in true volume depletion states like dehydration or hemorrhage. SIADH patients are typically normotensive.

Low dietary calcium intake leads to hypocalcemia, which stimulates the parathyroid glands to secrete more parathyroid hormone (PTH) via negative feedback. PTH acts to restore serum calcium by increasing bone resorption, enhancing renal calcium reabsorption, and stimulating renal 1-alpha-hydroxylase activity (not 24-hydroxylase). Calcitonin levels would decrease, not increase, as it responds to hypercalcemia. Phosphate levels typically decrease due to PTH's phosphaturic effect.

Cushing's disease typically causes sustained hypertension (not episodic) due to cortisol excess, along with central obesity, easy bruisability from skin fragility, and glucose intolerance from cortisol-induced insulin resistance. Episodic hypertension is more characteristic of pheochromocytoma. Episodic hypertension is the exception among these findings.