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Endocrine Part 2
| Question | Answer |
|---|---|
| What are the three general classes of hormones? | The three general classes of hormones are steroids, amino-acid derived hormones (monoamines), and catecholamines. |
| From what substance are steroid hormones derived? | Steroid hormones are derived from cholesterol. |
| What types of hormones are included in the steroid class? | Steroids include sex steroids and corticosteroids. |
| What are some examples of peptide and glycoprotein hormones? | Examples include oxytocin, ADH, all releasing and inhibiting hormones of the hypothalamus (except dopamine), and most anterior pituitary hormones. |
| Which hypothalamic releasing or inhibiting hormone is an exception to being a peptide/glycoprotein? | Dopamine is the hypothalamic exception. |
| From what precursor are monoamines (biogenic amines) derived? | Monoamines are derived from amino acids. |
| Which specific hormones belong to the monoamine class? | Monoamines include catecholamines (norepinephrine, epinephrine, dopamine) and thyroid hormones that act like steroids. |
| How do different steroid hormones structurally differ from one another? | Steroid hormones are synthesized from cholesterol and differ in the functional groups attached to their 4-ringed steroid backbone. |
| From which amino acid are almost all monoamines synthesized? | All monoamines are synthesized from tyrosine, except for melatonin. |
| Which amino acid is used to synthesize melatonin? | Melatonin is synthesized from tryptophan. |
| Which unusual mineral is required for thyroid hormone synthesis? | Thyroid hormone synthesis requires the mineral iodine. |
| What is the composition of thyroid hormone at the molecular level? | Thyroid hormone is composed of two tyrosine molecules (DIT + MIT = T3). |
| In what proportion are T4 and T3 released into the blood? | Thyroid hormone is released into the blood as 90% T4 and 10% T3. |
| What structural feature gives monoamines their class name? | Monoamines are made of amino acids and retain one amino group, which gives the class its name. |
| What does peptide hormone synthesis involve? | Peptide hormone synthesis is the same as for any peptide and may involve preprohormone and prohormone steps, as in insulin. |
| Why do monoamines and peptides mix easily with blood plasma? | Monoamines and peptides are hydrophilic, so they mix easily with blood plasma. |
| Why must steroids and thyroid hormones bind to transport proteins in the blood? | Steroids and thyroid hormones are hydrophobic and require transport proteins for transport through blood plasma. |
| What is a bound hormone? | A bound hormone is a hormone attached to a transport protein. |
| What are the benefits of a hormone being bound to a transport protein? | Binding to a transport protein prolongs the hormone's half-life to weeks and protects it from degradation by enzymes and kidney filtration. |
| Which form of a hormone can leave capillaries to reach target cells? | Only an unbound hormone can leave a capillary to reach a target cell. |
| What is the typical half-life of an unbound hormone? | The half-life of an unbound hormone is a few minutes. |
| What are three transport proteins in blood plasma that bind to thyroid hormone? | Blood plasma transport proteins include albumin, thyretin, and thyroxine-binding globulin (TBG). |
| Why do hypothyroid symptoms take 2 weeks to appear after surgical removal of the thyroid gland? | Binding to transport proteins prolongs thyroid hormone's half-life, so symptoms do not appear for 2 weeks after thyroid removal. |
| What specific transport proteins do steroid hormones bind to? | Steroid hormones bind to globulins, such as transcortin. |
| Does aldosterone bind to a transport protein, and what is its half-life? | Aldosterone has no transport protein and has a half-life of 20 minutes. |
| Where are hormone receptors located in or on a target cell? | Hormone receptors are located on the plasma membrane, on mitochondria and other organelles, or in the nucleus. |
| Approximately how many receptors exist for a given hormone on a target cell? | There are usually thousands of receptors for a given hormone. |
| What action do hormone receptors perform when a hormone binds? | Receptors turn metabolic pathways on or off when a hormone binds. |
| What two key properties do hormone receptors exhibit? | Hormone receptors exhibit specificity and saturation. |
| How do hydrophobic/lipophilic hormones enter target cells? | Hydrophobic hormones (steroids and thyroid hormone) penetrate the plasma membrane and enter the nucleus. |
| Did lipophilic hormones require transport proteins in the blood? | Yes, lipophilic hormones required transport proteins while traveling in the blood. |
| Why must hydrophilic hormones bind to cell-surface receptors? | Hydrophilic hormones (monoamines and peptides) cannot pass through the plasma membrane, so they must bind to cell-surface receptors. |
| Did hydrophilic hormones require transport proteins in the blood? | No, hydrophilic hormones did not need transport proteins in the blood. |
| What effect does thyroid hormone (TH) have when binding to mitochondrial receptors? | TH binding to mitochondrial receptors increases the rate of aerobic respiration. |
| What effect does TH have when binding to receptors on ribosomes and chromatin? | TH binding to ribosomes and chromatin increases protein synthesis. |
| Which specific protein produced by TH action generates heat? | Na+-K+ ATPase is produced, which generates heat. |
| What happens to T4 inside target cells? | T4 is converted into T3 inside target cells. |
| How does thyroxine (T4) travel to target cells? | Thyroxine (T4) travels to target cells bound to thyroxine-binding globulin (TBG). |
| Is all released T3 bound to carrier proteins in the blood? | No, some T3 is released unbound to a carrier, acting as "free iodine". |
| Where are thyroid hormone receptor proteins located? | Receptor proteins are located inside the nucleus bound to DNA. |
| Describe the two half-sites of the thyroid hormone response element on DNA. | The response element has two half-sites: one for a T3 receptor and one for a 9-cis-retinoic acid receptor (a Vitamin A derivative). |
| What structure is formed when T3 and 9-cis-retinoic acid receptors bind to DNA, and why? | They form a heterodimer because two different receptors are involved. |
| What happens to corepressors and coactivators when T3 binds to its receptor? | The binding of T3 causes corepressor proteins to be removed and coactivator proteins to be recruited. |
| Which other substances act similarly to thyroid hormone in target cells? | Vitamin D and steroid action in the cell are similar to thyroid hormone action. |
| What role does cAMP play in the action of hydrophilic hormones? | cAMP acts as an intracellular second messenger. |
| What are the sequential steps of the cAMP second messenger pathway? | 1) Hormone binding activates a G protein; 2) G protein activates adenylate cyclase; 3) Adenylate cyclase produces cAMP; 4) cAMP activates kinases; 5) Kinases activate enzymes; 6) Activated enzymes catalyze metabolic reactions |
| What is enzyme amplification? | Enzyme amplification is the process by which a single hormone molecule can lead to the production of billions of reaction product molecules. |
| Where do peptides and catecholamines bind on target cells? | Peptides and catecholamines bind to receptors located in the cell membrane. |
| What are the three possible second messenger mechanisms used by surface-binding hormones? | The three second messenger mechanisms are Adenylate cyclase (cAMP), Phospholipase C, and Tyrosine kinase. |
| Which hormones use the Adenylate Cyclase (cAMP) system? | Epinephrine and norepinephrine use the Adenylate Cyclase system. |
| Which receptor type do epinephrine and norepinephrine bind to in the cAMP system? | They bind to a beta-adrenergic receptor. |
| What step occurs immediately after receptor binding in the cAMP system? | The G-protein dissociates. |
| Which G-protein subunit activates adenylate cyclase? | The alpha subunit activates adenylate cyclase. |
| What substrate does adenylate cyclase use to create cAMP? | Adenylate cyclase uses ATP to make cAMP. |
| What is the target of cAMP in the adenylate cyclase system? | cAMP activates protein kinase. |
| How does protein kinase alter cell metabolism? | Protein kinase phosphorylates proteins in the target cell to alter cell metabolism. |
| How is cAMP inactivated? | cAMP is inactivated by phosphodiesterase. |
| What secondary molecule can some cells use that operates similarly to cAMP? | Some cells can use cGMP. |
| What alternative receptor type does epinephrine bind to in the Phospholipase C system? | Epinephrine binds to alpha-adrenergic receptors. |
| What two molecules are produced by Phospholipase C activity? | Phospholipase C produces IP3 and DAG. |
| What is the effect of IP3 and DAG production on intracellular calcium? | IP3 and DAG liberate Ca2+ from the endoplasmic reticulum. |
| What protein is activated by liberated Ca2+ in the Phospholipase C pathway? | Ca2+ activates calmodulin. |
| What is the final cellular outcome of calmodulin activation? | Calmodulin activates protein kinases to modify cell enzymes. |
| Which hormones or factors utilize the Tyrosine Kinase system? | Insulin and growth factors use the Tyrosine Kinase system. |
| What dual structural function does the receptor serve in the Tyrosine Kinase system? | The receptor itself is also the enzyme tyrosine kinase. |
| How are the binding site and enzyme region oriented on the Tyrosine Kinase receptor? | The ligand-binding site is on the outside of the cell, while the enzyme portion faces the cytoplasm. |
| How is the enzyme portion of the Tyrosine Kinase receptor activated? | The enzyme portion is activated via phosphorylation. |
| What does the activated Tyrosine Kinase receptor phosphorylate? | The activated receptor phosphorylates insulin receptor substrate molecules, triggering an enzymatic activity cascade. |
| Which organs are responsible for taking up, degrading, and excreting hormones? | The liver and kidneys take up and degrade hormones, which are then excreted in bile or urine. |
| What is the rate of hormone clearance called? | The rate of hormone clearance is called the metabolic clearance rate (MCR). |
| How is a hormone's half-life defined? | Half-life is defined as the time required to clear 50% of a hormone from the body. |
| How can target cells modulate their sensitivity to a hormone? | Target cells modulate sensitivity through upregulation and downregulation. |
| What is upregulation, and what is an example? | Upregulation is increasing the number of receptors to increase hormone sensitivity (e.g., oxytocin). |
| What is downregulation, and what is an example? | Downregulation is decreasing the number of receptors to reduce sensitivity (e.g., LH and the testis). |
| Under what conditions might downregulation occur, and what are its potential risks? | Downregulation may occur with pharmacological doses of hormones, along with risks of excess hormone binding to foreign receptors or conversion into a different hormone. |
| What are the three types of interactive hormone effects? | The three types of interactive effects are synergistic, permissive, and antagonistic. |
| What is a synergistic hormone effect, and what is an example? | Synergistic effects occur when two hormones work together to produce a greater effect, such as FSH and testosterone working together in sperm production. |
| What is a permissive hormone effect, and what is an example? | Permissive effects occur when one hormone enhances the response to a second hormone, such as estrogen and progesterone in the uterus. |
| What is an antagonistic hormone effect, and what is an example? | Antagonistic effects occur when one hormone counteracts the effect of another, such as insulin and glucagon. |
| How is stress defined in physiology? | Stress is defined as any situation that upsets homeostasis and threatens one's physical or emotional well-being. |
| Which hormones are elevated during the general adaptation syndrome (GAS)? | GAS typically involves elevated levels of epinephrine and glucocorticoids (cortisol). |
| What occurs during the Alarm Reaction stage of GAS? | Norepinephrine and epinephrine prepare the body for fight-or-flight, depleting glycogen. |
| What physiological processes occur during the Stage of Resistance in GAS? | Hours into stress, cortisol is secreted to break down fat and protein for gluconeogenesis; protein synthesis and immune function are inhibited (increasing illness risk), while generated glucose is spared for the brain. |
| What happens during the Stage of Exhaustion in GAS? | Months later, body fat is depleted, muscle wasting occurs, leading to rapid physiological decline and death. |
| What are paracrine secretions? | Paracrine secretions are chemical messengers that diffuse short distances to stimulate nearby cells. |
| How do paracrines differ from neurotransmitters and hormones? | Unlike neurotransmitters, paracrines are not produced in neurons; unlike hormones, paracrines are not transported in the blood. |
| What is the source and function of histamine as a paracrine secretion? | Histamine is secreted by mast cells in connective tissue and causes the relaxation of blood vessel smooth muscle. |
| What is the source and function of nitric oxide as a paracrine secretion? | Nitric oxide is secreted by blood vessel endothelium and causes vasodilation. |
| What is the source and function of somatostatin in the pancreas? | Somatostatin is secreted by delta cells and inhibits secretion from pancreatic alpha and beta cells. |
| Give an example of paracrine diffusion involving catecholamines. | Catecholamines diffuse locally from the adrenal medulla to the adrenal cortex. |
| From what precursor fatty acid are eicosanoids derived? | Eicosanoids are paracrine secretions derived from arachidonic acid. |
| What function do leukotrienes serve, and what enzyme produces them? | Lipoxygenase converts arachidonic acid into leukotrienes, which mediate allergic/inflammatory reactions and cause asthma symptoms. |
| What function does prostacyclin serve, and what enzyme produces it? | Cyclooxygenase converts arachidonic acid into prostacyclin, which is produced by blood vessel walls to inhibit blood clotting and vasoconstriction. |
| Where are thromboxanes produced, and what is their physiological function? | Thromboxanes (such as Thromboxane A2) are produced by platelets after injury to override prostacyclin and stimulate vasoconstriction and blood clotting. |
| What is the function of PGI2 prostaglandins? | PGI2 prostaglandins inhibit blood clotting and promote vasodilation. |
| What functions do PGE prostaglandins perform? | PGEs relax smooth muscle in the bladder, intestines, bronchioles, and uterus, while stimulating blood vessel contraction. |
| How do PGF prostaglandins compare to PGEs? | PGFs exert opposite effects to PGEs. |
| What causes noticeable symptoms in endocrine disorders? | Variations in hormone concentration and target cell sensitivity produce noticeable effects. |
| What is hyposecretion, and what causes it? | Hyposecretion is inadequate hormone release, often caused by a tumor or lesion destroying a gland. |
| How can head trauma lead to diabetes insipidus? | Head trauma damages the pituitary gland's ability to secrete ADH, resulting in diabetes insipidus characterized by chronic polyuria. |
| What is hypersecretion, and what causes it? | Hypersecretion is excessive hormone release caused by tumors or autoimmune disorders. |
| What is the mechanism behind toxic goiter (Grave's disease)? | Autoimmune antibodies mimic the effect of TSH on the thyroid gland, leading to hypersecretion. |
| What is acromegaly? | Acromegaly is adult hypersecretion of growth hormone causing thickening of bones and soft tissues. |
| What growth disorders occur from GH imbalance in childhood/adolescence? | Oversecretion of GH causes gigantism, while hyposecretion causes pituitary dwarfism. |
| Who was Robert Pershing Wadlow, and what caused his condition and death? | He was the tallest person in recorded medical history (8' 11.1") due to a GH-producing pituitary tumor; he died from an infection caused by a sore from a poorly fitting leg brace. |
| Who is Sultan Kosen? | Sultan Kosen (b. 1982) is the tallest living person (8' 3") due to a pituitary tumor. |
| What caused Brenden Adams' extreme growth, and how was it treated? | Brenden Adams grew to 7'8" due to a Chromosome 12 defect (not a pituitary tumor); he was treated with testosterone to induce early puberty and close his epiphyseal growth plates. |
| What are the symptoms of infant congenital hypothyroidism? | Symptoms include abnormal bone development, thickened facial features, low body temperature, lethargy, and brain damage. |
| What is Myxedema, and what are its clinical symptoms? | Myxedema is adult hypothyroidism causing low metabolic rate, sluggishness, sleepiness, weight gain, constipation, dry skin/hair, cold sensitivity, elevated blood pressure, and tissue swelling. |
| What causes endemic goiter, and why does the thyroid gland grow? | Dietary iodine deficiency prevents TH synthesis, eliminating negative feedback; elevated TSH acts as a tropic hormone, causing the thyroid gland to enlarge. |
| What is toxic goiter (Grave's disease) and its distinct physical sign? | Toxic goiter occurs when antibodies masquerade as TSH to elevate TH levels; a key sign is exophthalmos (bulging eyes). |
| What are the hormonal titers of TH, TRH, and TSH in endemic goiter? | TH is low, which causes TRH and TSH levels to be elevated. |
| What are the hormonal titers of TH, TRH, and TSH in Grave's disease? | TH is elevated, which causes both TRH and TSH titers to be low due to negative feedback. |
| What causes hypoparathyroidism, and what is its fatal complication? | Hypoparathyroidism is caused by accidental surgical removal during thyroid surgery, resulting in fatal tetany within 3–4 days. |
| What causes hyperparathyroidism, and how does it affect bone and blood chemistry? | It is caused by a gland tumor that excessively pulls Ca2+ from bones into the blood, causing soft, fragile, deformed bones. |
| What renal complication is associated with hyperparathyroidism? | Excess blood Ca2+ leads to renal calculi (kidney stones). |
| What is Cushing syndrome, and what are its primary symptoms? | Cushing syndrome is excess cortisol secretion causing hyperglycemia, hypertension, weakness, edema, muscle/bone loss, and abnormal fat deposition ("buffalo hump" and "moon face"). |
| What is Adrenogenital syndrome (AGS), and how does it affect children and women? | AGS is hypersecretion of adrenal androgen (often accompanying Cushing syndrome) that causes enlarged external genitalia/early puberty in children and masculinizing effects (deeper voice, beard growth) in women. |
| What are the primary signs and symptoms of diabetes mellitus? | Signs include polyuria, polydipsia, polyphagia, hyperglycemia, glycosuria, and ketonuria. |
| How does excess blood glucose cause osmotic diuresis in diabetes mellitus? | Glucose levels exceed the transport maximum of kidney tubules, preventing full reabsorption; glucose remaining in the urine increases osmolarity and draws extra water into the urine. |
| What is glycosuria? | Glycosuria is the spilling of excess glucose into the urine when renal reabsorption capacity is exceeded. |
| What causes Type 1 diabetes mellitus, and how is it managed? | Type 1 (10% of cases) involves autoimmune destruction of beta cells preventing insulin production; diagnosed around age 12 and managed with diet, exercise, blood glucose monitoring, and insulin injections or pumps. |
| What causes Type 2 diabetes mellitus, and what are its major risk factors? | Type 2 (90% of cases) is caused by insulin resistance; major risk factors are heredity, age (40+), and obesity. |
| How is Type 2 diabetes treated? | Type 2 diabetes is treated with weight-loss programs (diet and exercise) and oral medications that improve insulin secretion or target cell sensitivity. |
| What acute metabolic shifts and symptoms occur in untreated diabetes? | Cells rely on fat/protein catabolism (causing weight loss and weakness), raising blood free fatty acids and ketone bodies; ketonuria causes electrolyte loss (Na+, K+) and ketoacidosis (lowering blood pH), leading to dyspnea and diabetic coma. |
| What chronic pathologies develop from long-term hyperglycemia? | Chronic hyperglycemia causes neuropathy, cardiovascular damage from atherosclerosis, retinal and kidney failure (common cause of death in Type 1), coronary artery atherosclerosis/heart failure (common cause of death in Type 2), and gangrene. |
| What causes hyperinsulinism, and what immediate symptoms occur? | Hyperinsulinism is caused by insulin overdose or a pancreatic islet tumor, causing hypoglycemia, weakness, hunger, anxiety, sweating, and elevated heart rate. |
| Which compensatory hormones are secreted during hyperinsulinism? | Hypoglycemia triggers the secretion of epinephrine, growth hormone (GH), and glucagon. |
| What happens if hyperinsulinism is left uncorrected? | Uncorrected hyperinsulinism leads to insulin shock, characterized by disorientation, convulsions, or unconsciousness. |
| What is the structure of a steroid hormone-response element on DNA? | It consists of two half-sites (each six nucleotide bases long) separated by a three-nucleotide spacer segment. |
| How do steroid receptors bind to the DNA response element? | One steroid-bound receptor attaches to one half-site, and a second steroid-bound receptor attaches to the adjacent half-site. |
| What is receptor dimerization? | Dimerization is the process of two receptor units coming together at the two DNA half-sites. |
| Why is a steroid receptor pair called a homodimer? | It is called a homodimer because both receptor units in the pair are identical. |
| What happens once steroid receptor dimerization takes place? | The activated nuclear receptor complex stimulates transcription of specific target genes. |
| How many regulatory proteins are required for estrogen action? | Estrogen action requires more than 20 different regulatory coactivator and corepressor proteins in addition to the estrogen receptor. |
| What chaperone protein is removed when a steroid hormone binds to its nuclear receptor? | Binding at the ligand-binding domain causes the removal of a heat shock protein. |
| What was the function of the heat shock protein prior to hormone binding? | The heat shock protein previously prevented the nuclear receptor from binding to DNA. |
| What occurs after heat shock protein removal? | The receptor binds to DNA and recruits coactivator proteins to promote DNA transcription (RNA synthesis). |
| Where are thyroid hormone receptors located when no ligand is present? | Thyroid hormone receptors are located inside the nucleus bound to DNA even in the absence of hormone. |
| How does DNA half-site binding differ between thyroid receptors and steroid receptors? | The thyroid receptor (for T3) binds to only one half-site, while the other half-site binds to a receptor for 9-cis-retinoic acid (a Vitamin A derivative). |
| Why is the thyroid hormone receptor complex on DNA termed a heterodimer? | It is called a heterodimer because it is composed of two different receptors (TR and RXR). |
| What do thyroid hormone receptors recruit in the absence of T3? | In the absence of T3, thyroid receptors recruit corepressor proteins that inhibit gene transcription. |
| What happens to corepressors and coactivators when T3 binds to the thyroid receptor? | Corepressors are removed and degraded by proteasomes, and coactivators are recruited to stimulate genetic transcription. |
| Where does intracellular T3 originate? | While some T3 enters directly from blood plasma, most intracellular T3 is produced within the cell by conversion from T4. |
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