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know which hormones are water-soluble and which are lipid-soluble - ANSWER water soluble: peptides- GH, insulin, leptin, PTH, prolactin glycoproteins- FSH, LH, TSH polypeptides: adrenocorticotropic hormone, ADH, calcitonin, endorphins, glucagon, hypothalamic hormones, lipotropins, melanocyte-stimulating hormone, oxytocin, somatostatin, thymosin, thyrotropin-releasing hormone amines: Epi, Norepi lipid soluble: Thyroxine: T3 and T steroids: Estrogen, glucocorticoids, mineralocorticoids, progestin, testosterone (all steroids are cholesterol based) derivatives of arachidonic acid (autocrine or paracrine action): Leukotrienes, Prostacyclins, prostaglandins, thromboxanes How are water-soluble hormones transported? - ANSWER Water-soluble hormones are proteins that are polarized with a high molecular weight. Because they cannot diffuse across the lipid cell plasma membrane, they must interact or bind with receptors in or on the cell membrane to activate a
second-messenger to mediate short-acting responses. How are lipid-soluble hormones transported? - ANSWER Lipid-soluble hormones diffuse freely across the cell and nuclear membrane and bind with cytosolic or nuclear receptors. (can also bind with receptors in or on the plasma membrane) know how protein hormones are transported in the blood - ANSWER peptide or protein hormones are water-soluble and circulate in free (unbound) forms why do water soluble hormones have a short half-life? - ANSWER because they are catabolized by circulating enzymes. Remember they are unbound. How long can lipid-soluble hormones remain in the blood? - ANSWER For hours to days. They last longer in the blood because they are bound to carrier/transport proteins. only free hormones can do what? - ANSWER initiate changes within a target cell How does the concentration of binding proteins affect the concentration of free hormones in the plasma? - ANSWER because equilibrium exists between the concentration of free hormones and hormones bound to plasma proteins What are the two main functions of the target cell hormone receptor? - ANSWER 1. To recognize and bind with high affinity to their particular hormones
- To initiate a signal to appropriate intracellular effectors *when a hormone is released into the circulatory system, it is distributed throughout the body, but only those cells with appropriate hormone receptors for that hormone are affected.
and reducing serum osmolality. what causes ADH to be secreted? - ANSWER when plasma osmolality increases, the osmoreceptors of the hypothalamus are stimulated- the rate of ADH secretion is increased causing more water to be absorbed by the kidneys- the plasma osmolality returns to its set point (280 mOsm/kg) How does ADH effect electrolytes? - ANSWER ADH does not directly effect electrolytes but due to the dilutional effect of increasing water absorption, serum electrolytes may decrease How does the body detect volume loss in order to stimulate receptors to release ADH? - ANSWER Baroreceptors in the L Atrium, carotid arteries, and aortic arch detect changes in intravascular volume. Once a volume loss of 7-25% is detected, receptors are stimulated. What can cause secretion of ADH? - ANSWER stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, and drugs (morphine) when does ADH secretion decrease? - ANSWER when plasma osmolality decreases/returns to normal, intravascular volume increases, with HTN, an increase in estrogen, progesterone, angiotensin II, and alcohol ingestion. How does ADH affect blood pressure? - ANSWER ADH acts on vasopressin (V1) receptors which cause vasoconstriction, - increasing blood pressure What is the target tissue and action of Thyrotropin-releasing hormone (TRH)? - ANSWER Anterior pituitary Stimulates release of TSH and Modulates prolactin secretion What is the target tissue and action of Gonadotropin-releasing hormone (GRH)? - ANSWER Anterior pituitary
Stimulates release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). What is the target tissue and action of Somatostatin? - ANSWER Anterior pituitary Inhibits release of growth hormone(GH) and TSH What is the target tissue and action of Growth hormone-releasing hormone (GHRH)? - ANSWER Anterior pituitary Stimulates release of GH What is the target tissue and action of Corticotropin-releasing hormone (CRH)? - ANSWER Anterior pituitary Stimulates release of adrenocorticotropic hormone (ACTH) and B-endorphin What is the target tissue and action of Substance P? - ANSWER Anterior pituitary inhibits synthesis and release of ACTH Stimulates secretion of GH, FSH, LH, and prolactin What is the target tissue and action of Dopamine? - ANSWER Anterior pituitary Inhibits synthesis and secretion of prolactin What is the target tissue and action of Prolactin-releasing (PRH)? - ANSWER Anterior pituitary Stimulates secretion of prolactin What is the target tissue and action of Prolactin-inhibiting hormone (PIH)? -
Promotes hypertrophy and hyperplasia of thymocytes What is the target organ and function of LH? - ANSWER In women: granulosa cells Ovulation, progesterone production In men: Leydig cells Testicular growth, testosterone production What is the target organ and function of FSH? - ANSWER In women: Granulosa cells Follicle maturation, estrogen production in men: Stertoli cells Spermatogenesis What is the target organ and function of B-Lipotropin? - ANSWER Adipose cells Fat breakdown and release of fatty acids What is the target organ and function of B-endorphins? - ANSWER Adipose cells and brain opioid receptors Analgesia, may regulate body temperature, food and water intake Where are hormone receptors located? - ANSWER they can be in or on the plasma membrane of the target cell or they can be in the intracellular
compartments of the target cell how do steroid hormones bind to their receptors? - ANSWER some bind to receptor molecules in the cytoplasm, then diffuse into nucleus. Others bind to receptors in the nucleus. Insulin - ANSWER Anabolic hormone that promotes synthesis of proteins, lipids, and nucleic acid How does insulin effect skeletal muscle cells? - ANSWER direct effect on skeletal muscle cells with insulin receptors, causing increased glucose transport into those cells How does insulin effect mammary cells? - ANSWER permissive effect of mammary cells, facilitating the response of these cells to direct effects of prolactin Glucagon - ANSWER Produced by alpha cells of the pancreas and by some cells lining the GI tract. Acts primarily on the liver to increase blood glucose by stimulating glycogenolysis and gluconeogenesis Insulin antagonist Amylin - ANSWER peptide hormone secreted with insulin in response to nutrient stimuli. Regulates blood glucose by delaying nutrient intake and suppressing glucagon secretion after meals. Has an antihyperglycemic effect through satiety Aldosterone - ANSWER Most potent of naturally occurring
the blood stream and putting it into bones Where is TSH synthesized and what are its target cells? - ANSWER TSH is a glycoprotein hormone synthesized and stored in the anterior pituitary. TSH binds with receptor sites on the thyroid follicular cells. What is the role of TSH? - ANSWER immediate increase in release of stored thyroid hormones increased iodide uptake and oxidation increase in thyroid synthesis increase in synthesis and secretions of prostaglandins by the thyroid increases growth of the thyroid gland by stimulating thymocyte hyperplasia, hypertrophy, and decreasing apoptosis. explain the negative feedback loop for TSH - ANSWER TRH is released from hypothalamus --> anterior pituitary releases TSH -> stimulate synthesis of TH -> TH rises causing negative feedback on hypothalamus inhibiting TRH, stops release of TSH, and TH synthesis/release is stopped What causes TRH levels to rise? - ANSWER exposure to cold stress decreased T4 levels What regulates the release of TSH? - ANSWER serum levels of T3 and T4. When T3 and T4 concentrations are low, TSH production is increased. What is PTH? - ANSWER hormone produced by parathyroid gland- single most important hormone in regulation of serum calcium levels
what is the role of PTH? - ANSWER increase serum calcium and decrease serum phosphate What stimulates production of PTH? - ANSWER decreased serum calcium levels ->stimulates PTH secretions -> PTH enters circulation in unbound form -> PTH attaches to plasma membrane receptors on target tissue and is mediated by activation of the adenylyl cyclase system How does PTH act directly on bones? - ANSWER low serum calcium stimulates secretion of PTH which stimulates osteoblasts to release receptor activator for nuclear factor (NF-kb), receptor activator (RANKL), and macrophage-colony stimulating factor (M-CSF) which stimulates osteoclasts maturation and release of acidic enzymes (capthepsin) which moves calcium from the bones into the blood stream. Intermittent PTH stimulation = bone formation continuous PTH stimulation= bone remodeling How does PTH act on the kidneys? - ANSWER by increasing calcium resorption by the distal nephron and decreasing phosphate (and bicarb) resorption by the proximal nephron PTH also stimulates hydrolase 1a in the renal tubules to increase Vit D and increase calcium resorption from the GI tract phosphorous - ANSWER mineral that combines with calcium to form bones and teeth. Phosphate is found in all cells in your body and is absorbed with help from Vit D Calcium - ANSWER stored in your bones
what do Delta cells secrete? - ANSWER gastrin and somatostatin What do F (or PP) cells secrete? - ANSWER pancreatic polypeptide that stimulates gastric secretion and antagonizes cholecystokinin (responsible for release of bile and pancreatic enzymes) to regulate protein, fat, and carb metabolism What stimulates the beta cells to secrete insulin? - ANSWER the parasympathetic nervous system (usually before a meal). After a meal, increased blood glucose levels, amino acids (leucine, argine, and lysine) and GI hormones (glucagon, gastrin, cholecystokinin, secretin) what causes a decrease in insulin secretion? - ANSWER low blood glucose levels high levels of insulin sympathetic stimulation of the beta cells prostaglandins Effect of insulin on potassium - ANSWER insulin facilitates the intracellular transport of potassium, phosphate, and magnesium what is aldosterone? - ANSWER Aldosterone is the most potent of the naturally occurring mineralocorticoids (secreted from the adrenal cortex) and acts to conserve sodium by increasing the activity of the sodium pump of the epithelial cells in the nephron. Renin-Angiotensin-Aldosterone system - ANSWER when blood pressure, renal blood flow, or serum sodium levels are low -> renin, an enzyme secreted by the kidneys is released. Renin stimulates the formation of angiotensin I (an inactive polypeptide). ACE from pulmonary vessels converts
angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction which elevates BP and stimulates secretion of aldosterone. Aldosterone promotes sodium and water reabsorption by the proximal tubules of the kidneys, conserving sodium. Aldosterone also stimulates secretion and excretion of potassium by the distal tubule of the kidney reducing potassium concentrations in the ECF. Restoration of sodium levels, blood volume, and renal perfusion then inhibit further release of renin. Other effects of aldosterone - ANSWER enhanced cardiac muscle contration stimlation of ectopic ventricular activity via 2ndary cardiac pacemakes in the ventricles stiffening blood vessels with increased vascular resistance decreased fibrinolysis (breakdown of the fibrin in blood clots) *elevated levels of aldosterone implicated in myocardial changes associated with heart failure where is Epi and Norepi synthesized? - ANSWER the chromaffin cells in the adrenal medulla store and secrete Epi and Norepi. Both are synthesized from the amino acid phenylaline. *30% of circulating Epi comes from the adrenal medulla, 70% is released from nerve terminals, the medulla is only a minor source) Epi and Norepi are both considered water-sol. amines What stimulates release of Epi and Norepi - ANSWER traumatic injury, hypoxia, hypoglycemia (catecholamines promote hyperglycemia via interferance with usual glucose regulatory feedback mechanisms)
CNS disorders: encephalitis, meningitis, intracranial hemorrhage, tumors, trauma including neurosurgery medications (especially in the elderly): hypoglycemic, antidepressants, antipsychotics, narcotics, general anesthetics, chemo agents, NSAIDs, synthetic ADH Patho of SIADH - ANSWER features of SIADH are the result of enhanced renal water retention. ADH increases renal collecting duct permeability to water by inducing the insertion of aquaporin2 (water channel protein), the tubular luminal membrane increases water reabsorption by the kidneys, expansion of extracellular fluid volume, dilutional hyponatremia, hypoosmalarity, and urine is reabsorbed clinical manifestations of SIADH - ANSWER hyponatremia causes hypervolemia and weight gain. symptoms resolve witht the correction of hyponatremia. Na decreases from 140 to 130 : thirst, impaired taste, anorexia, dyspnea on exertion, fatigue, dulled sensorium. *wt gain usually absent Na decreases from 130-120: vomiting, abd cramps, *wt gain from water retention Na levels 110-115: confusion, lethargy, muscle twitching, seizures, neurological damage
Diagnosing SIADH - ANSWER serum hypoosmalality (<280mOsm/kg) and hyponatremia (Na <135) urine hyperosmolarity (the urine osmolarity is always higher than the osmolality of the serum) urine sodium excretion that matches sodium intake normal renal, adrenal, and thyroid function absence of conditions that can alter volume status (recent diuretic use, heart or liver failure, hypervolemia from any cause, or renal insufficiency. *ADH is hard to measure in serum. Copeptin (an ADH precursor molecule) is used as a surrogate marker. Treatment of SIADH - ANSWER treatment of underlying problems fluid restriction when possible Na level monitorning and neuro checks careful administration of hypertonic saline Resolution usually occurs within 3 days with 2-3kg wt loss from enhanced free water clearance and correction of hyponatremia and salt wasting. *if hyponatremia is corrected too quickly, a severe neurologic syndrome (central pontine myelinolysis) can ensue *Demeclocycline (causes renal tubules to develop resistance to ADH. May be used to treat resistance or chronic SIADH *Vasopressin receptor antagonists (vaptans) may be effective in treating SIADH
lesion (brain tumor, aneurysm, thrombosis, infections, immunologic disorders) on the hypothalamus, pituitary stalk, or posterior pituitary. nephrogenic DI is caused by renal tubule insensitivity to ADH. Can be genetic or acquired (disorders or drugs that affect the renal tubule or affect the renal tubule's ability to generate cAMP) Neurogenic DI - ANSWER can be a complication on closed-head trauma or neuro (pituitary) surgery- can be transient or permanent Treatment of Neurogenic DI for symptomatic patients - ANSWER synthetic vasopressin drug desmopressin acetate (DDAVP). Can be taken intranasal or oral. Treatment of nephrogenic DI - ANSWER nephrogenic DI caused by drugs is reversible nephrogenic DI caused by disorders may not be reversible treatment includes correction of any reversible underlying disorders, discontinuation of medications, and correction of associated electrolyte disorders Disorders that may cause irreversible DI - ANSWER pyelonephritis amyloidosis destructive uropathies polycystic disease intrinsic renal disease Drugs that may cause (reversible) DI - ANSWER lithium
colchicine amphotericin B loop diuretics general anesthetics demeclocycline etiology of primary pituitary adenoma - ANSWER usually slow growing benign tumors that arise from cells of the anterior pituitary. The cause is unknown and the occurrence is sporadic. patho of primary pituitary adenoma - ANSWER hypothalamic and intra-pituitary factors altered expression of pituitary cell cycle genes, activiation of pituitary selective oncoproteins, or loss of pituitary suppressor factors Hormonal effects of primary pituitary adenoma - ANSWER hypersecretion from the adenoma itself and hyposecretion from surrounding pituitary cells The adenomatous tissue secretes the hormone of the cell type from which it arose (without regard to physiologic needs and without benefit of regulatory feedback mechanisms)
- Often associated with increased secretion of GH and prolactin ***If the tumor exerts sufficient pressure → thyroid and adrenal hypofunction r/t ↓in TSH and ACTH (with resultant hypothyroidism and hypocortisolism) pituitary microadenomas - ANSWER (<10mm)
