Endocrine Physiology & Hormone Regulation Quiz

Thyroid hormone includes T3 and T4, both synthesized from tyrosine. They regulate metabolism, heart rate, and blood pressure. T3 is the biologically active hormone, while T4 serves mainly as a circulating precursor converted to T3 within target cells.

T3 and T4 levels are controlled through two feedback loops: TRH from the hypothalamus stimulates TSH, which stimulates thyroid hormone release. Rising T3/T4 suppress TRH and TSH. This closed-loop regulation stabilizes metabolic control.

A goiter forms when low thyroid hormone fails to inhibit TSH production. Excess TSH continuously stimulates gland growth. This typically occurs in hypothyroidism, often due to iodine deficiency or impaired hormone synthesis, causing visible swelling below the chin.

Graves’ disease is an autoimmune hyperthyroid disorder where antibodies activate the TSH receptor, driving constant T3/T4 production despite normal feedback signals. This results in elevated metabolism, heat intolerance, tachycardia, and often exophthalmos.

The HPA axis ends with cortisol released from the adrenal cortex. CRH triggers ACTH, which stimulates cortisol synthesis. Cortisol regulates stress responses, immunity, metabolism, and exerts negative feedback to stabilize the system.

Deiodinase enzymes remove iodine atoms from T4, converting it into the more active T3 form. This tissue-level conversion provides precise metabolic control and allows T4 to act as a stable circulating reservoir.

Steroid hormones are lipophilic and diffuse into cells, binding nuclear receptors. These receptors modify transcription directly, allowing long-lasting regulatory effects on metabolism, growth, and stress responses.

Addison’s disease is adrenal cortex failure, resulting in low cortisol and aldosterone. Symptoms include fatigue, low blood pressure, weight loss, and salt craving. It reflects inadequate adrenal steroid production.

Cortisol is a steroid synthesized from cholesterol within the adrenal cortex. Cholesterol serves as the common precursor for all steroid hormones including aldosterone, cortisol, progesterone, and sex steroids.

Aldosterone release is triggered by low blood pressure via the renin-angiotensin-aldosterone system. Angiotensin II stimulates aldosterone to increase sodium retention, restoring blood volume. High potassium also stimulates its release.

Somatostatin suppresses GH by inhibiting pituitary somatotroph cells. It acts as a brake on GH and TSH secretion, providing fine hormonal regulation.

Cushing syndrome arises from chronic elevated cortisol, either due to ACTH excess, adrenal tumors, or external steroid use. Effects include central obesity, muscle wasting, thin skin, and hypertension.

The pineal gland secretes melatonin, a hormone regulating sleep-wake cycles. Light exposure suppresses melatonin; darkness promotes its release, aligning circadian rhythms.

PTH increases blood calcium by stimulating bone resorption, enhancing intestinal absorption via vitamin D activation, and boosting renal calcium reabsorption. Bone is its primary rapid-response target.