Study Guide - Endocrine System Course
A comprehensive review of every topic covered in the endocrine system course. Use this guide for exam prep, quick revision, or as a reference while studying.
Test your knowledge with the Endocrine System Game.
| Term | Definition |
|---|---|
| Endocrine system | Network of ductless glands that secrete hormones into the bloodstream to regulate body functions |
| Hormone | Chemical messenger produced by endocrine glands - travels via blood to target cells with specific receptors |
| Hypothalamus | Brain region linking the nervous and endocrine systems - controls pituitary hormone release |
| Anterior pituitary | Adenohypophysis - secretes GH, TSH, ACTH, FSH, LH, and prolactin under hypothalamic control |
| Posterior pituitary | Neurohypophysis - stores and releases ADH and oxytocin produced by the hypothalamus |
| Growth hormone (GH) | Stimulates growth, cell reproduction, and IGF-1 release from the liver |
| Thyroid-stimulating hormone (TSH) | Anterior pituitary hormone that stimulates T3 and T4 production by the thyroid gland |
| Adrenocorticotropic hormone (ACTH) | Anterior pituitary hormone that stimulates cortisol release from the adrenal cortex |
| Follicle-stimulating hormone (FSH) | Gonadotropin promoting follicle development in ovaries and spermatogenesis in testes |
| Luteinizing hormone (LH) | Gonadotropin triggering ovulation in females and testosterone production in males |
| Prolactin | Anterior pituitary hormone stimulating milk production in mammary glands |
| Antidiuretic hormone (ADH) | Posterior pituitary hormone promoting water reabsorption in renal collecting ducts |
| Oxytocin | Posterior pituitary hormone stimulating uterine contractions and milk ejection |
| Triiodothyronine (T3) | Active thyroid hormone - regulates metabolism, heart rate, and body temperature |
| Thyroxine (T4) | Thyroid prohormone converted to T3 in peripheral tissues - more abundant but less active |
| Calcitonin | Thyroid C-cell hormone that lowers blood calcium by inhibiting osteoclast activity |
| Parathyroid hormone (PTH) | Raises blood calcium via osteoclast activation, renal reabsorption, and vitamin D activation |
| Cortisol | Glucocorticoid from the adrenal cortex - anti-inflammatory, raises blood glucose, stress response |
| Aldosterone | Mineralocorticoid from the adrenal cortex - promotes Na+ reabsorption and K+ excretion in kidneys |
| DHEA | Adrenal androgen - weak precursor to testosterone and estrogen |
| Epinephrine | Catecholamine from the adrenal medulla - fight-or-flight response, increases heart rate and glucose |
| Norepinephrine | Catecholamine from the adrenal medulla - vasoconstriction, raises blood pressure |
| Insulin | Pancreatic beta-cell hormone - lowers blood glucose by promoting cellular uptake and glycogenesis |
| Glucagon | Pancreatic alpha-cell hormone - raises blood glucose via glycogenolysis and gluconeogenesis |
| C-peptide | Byproduct of proinsulin cleavage - clinical marker of endogenous insulin production |
| GLUT4 | Insulin-dependent glucose transporter in skeletal muscle and adipose tissue |
| Islets of Langerhans | Endocrine cell clusters in the pancreas containing alpha, beta, delta, and PP cells |
| Negative feedback | Primary regulatory mechanism where a hormone inhibits its own further release |
| HPA axis | Hypothalamic-pituitary-adrenal axis - regulates cortisol release and stress response |
| RAAS | Renin-angiotensin-aldosterone system - regulates blood pressure, fluid balance, and electrolytes |
| Diabetes mellitus | Metabolic disorder of impaired insulin secretion (type 1) or insulin resistance (type 2) |
| Graves disease | Autoimmune hyperthyroidism caused by TSH receptor-stimulating antibodies |
| Hashimoto thyroiditis | Autoimmune hypothyroidism with lymphocytic infiltration and thyroid destruction |
| Cushing syndrome | Chronic cortisol excess - causes moon face, central obesity, striae, and hyperglycemia |
| Addison disease | Primary adrenal insufficiency - low cortisol and aldosterone, hyperpigmentation |
Hypothalamus
Releasing/inhibiting hormones, links nervous and endocrine systems
Pituitary Gland
GH, TSH, ACTH, FSH, LH, prolactin, ADH, oxytocin
Thyroid & Parathyroid
T3, T4, calcitonin (thyroid) - PTH (parathyroid)
Adrenal Glands
Cortisol, aldosterone, DHEA (cortex) - epinephrine, norepinephrine (medulla)
Pancreas
Insulin (beta cells), glucagon (alpha cells), somatostatin (delta cells)
| Class | Solubility | Receptor Location | Speed of Action | Examples |
|---|---|---|---|---|
| Peptide/Protein | Water-soluble | Cell surface (membrane) | Fast (seconds-minutes) | Insulin, GH, ADH, PTH, glucagon |
| Steroid | Lipid-soluble | Intracellular (nuclear) | Slow (hours-days) | Cortisol, aldosterone, estrogen, testosterone |
| Amino acid-derived | Varies | Surface or intracellular | Varies | T3/T4 (intracellular), epinephrine (surface) |
| Condition | Gland | Hormone | Key Features |
|---|---|---|---|
| Graves disease | Thyroid | T3/T4 excess | Exophthalmos, weight loss, tachycardia, heat intolerance, diffuse goiter |
| Hashimoto thyroiditis | Thyroid | T3/T4 deficiency | Fatigue, weight gain, cold intolerance, anti-TPO antibodies |
| Cushing syndrome | Adrenal cortex | Cortisol excess | Moon face, buffalo hump, central obesity, purple striae, hyperglycemia |
| Addison disease | Adrenal cortex | Cortisol/aldosterone deficiency | Hyperpigmentation, hypotension, hyperkalemia, salt craving |
| Acromegaly | Anterior pituitary | GH excess (adult) | Enlarged hands/feet/jaw, coarsened facial features, insulin resistance |
| Diabetes insipidus | Posterior pituitary | ADH deficiency/resistance | Polyuria, polydipsia, dilute urine, hypernatremia |
| Type 1 diabetes mellitus | Pancreas (beta cells) | Insulin deficiency | Autoimmune beta-cell destruction, ketoacidosis, onset in childhood |
| Type 2 diabetes mellitus | Pancreas/peripheral | Insulin resistance | Obesity-associated, hyperinsulinemia early, gradual beta-cell failure |
| Pheochromocytoma | Adrenal medulla | Catecholamine excess | Episodic hypertension, headache, diaphoresis, palpitations |
| SIADH | Posterior pituitary | ADH excess | Hyponatremia, concentrated urine, fluid retention, no edema |
| Primary hyperparathyroidism | Parathyroid | PTH excess | Hypercalcemia - stones, bones, groans, psychiatric overtones |
| Conn syndrome | Adrenal cortex | Aldosterone excess | Hypertension, hypokalemia, metabolic alkalosis, low renin |
Q1.A patient presents with weight gain, cold intolerance, constipation, and elevated TSH. What is the most likely diagnosis, and why is TSH elevated?
The most likely diagnosis is primary hypothyroidism (e.g., Hashimoto thyroiditis). TSH is elevated because low T3/T4 levels remove negative feedback on the anterior pituitary, causing increased TSH secretion in an attempt to stimulate the failing thyroid gland.
Q2.Compare the mechanisms by which peptide hormones and steroid hormones exert their effects on target cells.
Peptide hormones are water-soluble and cannot cross the cell membrane. They bind to cell-surface receptors and activate intracellular second messenger cascades (e.g., cAMP, IP3/DAG), producing rapid effects. Steroid hormones are lipid-soluble and diffuse across the membrane to bind intracellular or nuclear receptors, forming hormone-receptor complexes that act as transcription factors to alter gene expression - producing slower but longer-lasting effects.
Q3.Explain the role of the HPA axis in the stress response and describe how negative feedback regulates cortisol levels.
Stress activates the hypothalamus to release CRH, which stimulates the anterior pituitary to secrete ACTH. ACTH travels to the adrenal cortex and stimulates cortisol release. Cortisol raises blood glucose, suppresses immune function, and mobilizes energy stores. Rising cortisol levels feed back to inhibit both CRH release from the hypothalamus and ACTH release from the anterior pituitary, completing the negative feedback loop and preventing chronic cortisol excess.
Q4.A patient has low cortisol, low aldosterone, elevated ACTH, and skin hyperpigmentation. Distinguish between primary and secondary adrenal insufficiency based on these findings.
This presentation is consistent with primary adrenal insufficiency (Addison disease). The adrenal gland itself is damaged, so cortisol and aldosterone are both low. ACTH is elevated because the loss of cortisol removes negative feedback on the anterior pituitary. ACTH shares a precursor molecule (POMC) with melanocyte-stimulating hormone (MSH), so elevated ACTH causes hyperpigmentation. In secondary adrenal insufficiency, the problem is at the pituitary - ACTH would be low, there would be no hyperpigmentation, and aldosterone is usually preserved because it is primarily regulated by RAAS rather than ACTH.
Q5.Describe how insulin and glucagon work together to maintain blood glucose homeostasis after a carbohydrate-rich meal versus during fasting.
After a carbohydrate-rich meal, blood glucose rises, stimulating pancreatic beta cells to secrete insulin. Insulin promotes GLUT4 translocation in skeletal muscle and adipose tissue, facilitating glucose uptake. It also stimulates glycogenesis in the liver and inhibits gluconeogenesis. During fasting, blood glucose drops, reducing insulin secretion and stimulating alpha cells to release glucagon. Glucagon promotes hepatic glycogenolysis and gluconeogenesis to raise blood glucose. This push-pull relationship maintains glucose within the normal range of approximately 70-110 mg/dL.
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