Chapter 16: Endocrine System Flashcards
Exocrine Glands:
o Secrete non-hormone chemicals into ducts, then into skin, mucous membranes, and body cavities.
o Extracellular Effects.
o Examples: Sweat glands, salivary glands, pancreatic secretions/ducts.
Endocrine Glands:
o Secrete hormones from the endocrine gland/cell into the IF, then diffuses from the IF into capillaries.
o Glands have a rich vascular supply and lymphatic drainage that receives these hormones from the IF.
o No ducts!!
o Intracellular effect in target tissue.
o Example: Thyroid Gland.
Can Some Glands be Both Endocrine and Exocrine?
Yes
The 2 Organ Systems That Regulate Homeostasis:
o Endocrine System.
o Nervous System.
The 4 Types of Cell-to-Cell Communication:
o 1) Gap Junctions: “stuff” flows directly from the cytoplasm of one cell to the cytoplasm of the next cell.
o 2) Neurotransmitters: Neurons release NT into a synaptic cleft to bind to receptors on target cells.
o 3) Autocrine and Paracrine Hormones: Endocrine cells release hormones into IF to act on local cells (or same cell) displaying receptor for hormone. (Some believe they’re not true hormones)
o 4) Systemic Hormones: Endocrine cells release hormones into the blood, hormones travel in the blood until they interact with tissues/organs which display a receptor for that hormone. (Many intrecellular/metabolic effects!)
Local Hormones:
o Paracrine Hormones:
o Endocrine cell releases a hormone that stimulates a nearby cell. (don’t travel in the blood to its target tissue)
o Most Eicosanoids (leukotrienes, prostaglandins), and act as paracrine hormones.
o Example: Somatostatin (peptide hormone) is released by cells in pancreas. Functions locally to inhibit the release of insulin from beta cells of pancreas.
o Autocrine Hormones:
o Hormones are released from a cell then attach to a receptor on the same cell.
o Hormone acts on cell that released it.
Systemic Hormones:
o Hormone released into IF that then diffuses into blood or lymph vessels.
o Hormones are transported in blood in free form or in bound form (attached to a plasma protein).
o Hormones attach to either a cell surface receptor or a receptor inside the target cell.
o Hormones attach only to cells that have a specific receptor for that hormone.
o Cells can then: synthesize new molecules, change permeability of membrane, alter rates of metabolic reactions, secrete stuff, or undergo mitosis( divide).
The 3 Interactions Between Hormones:
o Synergistic: Effect greater with 2 or more hormones.
o Permissive: Hormone enhances target cell’s response to 2nd hormone secreted later.
o Antagonistic: Hormone opposes action of second hormone.
Half Life of Hormones:
o Hormone half-life is brief, between seconds to 30 minutes.
o Factors that decrease half-life of a hormone: Excretion, metabolism, active transport, conjugation.
o Factors that increase half-life of a hormone: Binding to large plasma protein, structure, liver or kidney disease.
The 3 Causes of Hormone Release:
o Humoral Stimuli: A change in the blood level of some nutrient of other chemical triggers the release of a hormone.
o Neural Stimuli: Neurons release NT onto endocrine glands/cells that cause them to release hormones.
o Hormonal Stimuli: An endocrine gland/cell releases its hormone into the blood then travels to a second endocrine gland/cell to cause the release of a different hormone.
Control of Hormone Secretion:
o Regulated by signals from nervous system (neural stimuli), chemical changes in the blood (humoral stimuli), or by other hormones (hormonal stimuli), or by combination.
o Negative Feedback Control (Most common): Decrease/Increase in blood level is reversed.
o Positive Feedback Control: The change produced by the hormone causes more hormone to be released.
o Disorders involve either hyposecretion or hypersecretion of a hormone.
Lipid-Soluble Hormones:
o Steroids: Lipids derived from cholesterol. Different functional groups attached to core or structure to provide uniqueness. ALL come from Cholesterol. Examples: Progesterone, testosterone, estrogens, cortisol, aldosterone, calcitriol.
o Thyroid Hormones: Tyrosine ring plus attached iodines are lipid-soluble.
o Nitric Oxide: Gas.
Action of Lipid-Soluble Hormones:
o 1) Hormone diffuses through phospholipid bilayer and into cell.
o 2) Hormone Binds to Receptor turning on/off specific genes.
o 3) Genes direct production of new protein that alters the cell’s activity.
Water-Soluble Hormones:
o Amine, peptide, and protein hormones:
o Modified amino acids or amino acids put together.
o Serotonin, melatonin, histamine, some glycoproteins.
o Eicosanoids:
o Derived from arachidonic acid.
o Protaglandins or leukotrienes.
Production of Peptide Hormones:
o Ribosomes follow directions of mRNA to make preprohormone.
o Guided into the rER and changed into prohormone.
o Transferred to Golgi Complex and modified to mature systemic hormone.
Action of Water-Soluble Hormones:
o Can’t diffuse through plasma membrane of capillary endothelial cells. o Must go through pores or clefts in capillaries to get into IF. o Capillary Endothelium serving organs regulated by protein hormones have large pores. o Binds to receptors on the surface of cell membrane because it can’t diffuse. o Ligand (1st messenger), then receptor, then G Protein, then enzyme, then 2nd messenger.
Second Messengers:
o Some hormones increase the synthesis of cAMP: ADH, TSH, ACTH, Glucagon, and EP.
o Some hormones decrease the level of cAMP: Growth hormone inhibiting hormone (GHIH).
o Other substances can act as second messengers besides cAMP: Calcium ions, cGMP, IP3 (inositol triphosphate), DAG (diacylglycerol).
o Same hormone may use different second messengers in different target cells.
Amplification of Hormone Effects:
o Single molecule of EP binds to receptor on hepatocyte cell membrane.
o This 1 hormone molecule activates 100 G-proteins.
o Each G-protein activates an adenylate cyclase molecule, which then produces 1000 cAMP, so far we have 100,000 second messengers of cAMP.
o Each cAMP activates a protein kinase, which may act upon 1000’s of substrate molecules.
o One molecule of epinephrine may result in breakdown of millions of glycogen molecules into glucose molecule.
Anatomy of Pituitary Gland:
o Pea-shaped, found in sella turcica of sphenoid bone.
o Anterior Lobe: 75% of weight of pituitary. Develops from roof of mouth. Makes “controlling” hormones.
o Posterior Lobe: 25% of weight of pituitary. Composed of axons of 10,000 neurons whose cell bodies are found in hypothalamic nuclei.
Hypothalamus Control:
o Hypothalamus regulates both the ANS and Endocrine System. It receives input from the cerebral cortex, thalamus, limbic system, and internal organs.
o Hypothalamus controls the anterior pituitary gland with many different releasing and inhibiting hormones.
o Hypothalamus controls the posterior pituitary via neuron axons traveling through the infundibulum.
o Both the hypothalamus and the pituitary gland are important endocrine glands since their hormones control other endocrine glands.
Flow of Blood to Anterior Pituitary:
o Controlling hormones enter blood capillaries from hypothalamus.
o Then travel through portal veins.
o Then enter anterior pituitary at capillaries.
o Lastly Hypophyseal portal system.
Hypothalamus-Pituitary-3rd Gland Axis:
o The many Releasing and Inhibiting Hormones from the Hypothalamus control the release of hormones from the anterior pituitary.
o Many hormones produced from the target glands of the anterior pituitary hormones also feedback to control the release of hormones from the anterior pituitary.
o This hypothalamus-pituitary-target gland feedback loop is complex but critical in fine-tuning the endocrine system.
Important Axes:
o HPA axis = Hypothalamic to Pituitary to Adrenal cortex.
o HPT axis = Hypothalamic to Pituitary to Thyroid gland.
o HPG axis = Hypothalamic to Pituitary to Gonadal gland.
Specific Anterior Pituitary Hormones:
o hGH: Human Growth Hormone. o TSH: Thyroid Stimulating Hormone. o ACTH: Adrenocorticotrophic Hormone. o FSH: Follicle Stimulating Hormone. o LH: Leutinizing Hormone. o PRL: Prolactin. o MSH: Melanocyte Stimulating Hormone.
Human Growth Hormone (hGH) and IGFs:
o Secreted by: Anterior Pituitary (released in bursts, especially during deep sleep!)
o Stimulus for release: Increased GHRH from hypothalamus, Hypoglycemia, Decreased fatty acids in blood, Increased amino acids in blood, Increased sympathetic activity (stress & exercise—esp. intense bursts of exercise), Increased ghrelin (hormone from stomach).
o Inhibited by GHIH (somatostatin) from hypothalamus (released if hyperglycemia).
o Growth Hormone Direct Effects:
o Promotes synthesis/secretion of IGFs from LIVER.
o Enhances liver gluconeogenesis and glycogenolysis.
o Targets adipose tissue to increase fat catabolism.
o Target Tissues of IGFs (many cells!):
o Skeletal muscle (promotes protein synthesis).
o Bone (promotes protein synthesis and growth).
o Cartilage (promotes uptake of sulfur needed for synthesis of cartilage matrix).
o Enhanced protein synthesis.
o Mitosis and cell growth.
Diabetogenic Effect of Human Growth Hormone (hGH):
o Excess of growth hormone o Acts as an insulin antagonist!!! o Raises blood glucose concentration. o Pancreas releases insulin continually. o Beta-cell burnout… permanent diabetes. o Very difficult to manage medically.
Imbalances of Human Growth Hormone (hGH):
o Hyposecretion of hGH:
o Pituitary Dwarfism: seen in kids before epiphyseal plate closes. Short, but proportional.
o Hypersecretion of hGH:
o Gigantism: seen in kids before epiphyseal plate closes, very tall, but proportional.
o Acromegaly: seen in adults after epiphyseal plate closes, soft tissues thicken, increased bone deposition in hands, feet, and facial bones, often diabetes.
Thyroid Stimulating Hormone (TSH):
o Secreted by: Anterior pituitary.
o Stimulus for Release: TRH (thyrotropin releasing hormone) from the hypothalamus.
o Target tissue: thyroid gland.
o Stimulates synthesis and secretion of T4 and T3 (thyroid hormones).
Adrenocorticotrophic Hormone (ACTH):
o Secreted by: Anterior Pituitary.
o Stimulus for Release: Increased CRH from hypothalamus because of:
o Stress, Trauma, Hypoglycemia.
o Target tissue: Adrenal Cortex
o Effect: Increased release of corticosteroids, especially glucocorticoids (cortisol) from zona fasciculate leads to cortisol effects.
Follicle Stimulating Hormone (FSH):
o Secreted by: Anterior pituitary.
o Stimulus for Release: Increased GnRH from hypothalamus.
o Target Tissues: Gonads.
o Initiates the maturation of follicles within ovary.
o Stimulates follicle cells to secrete estrogen.
o Stimulates sperm production in testes (spermatogenesis).
Luteinizing Hormone (LH):
o Secreted by: Anterior pituitary. o Stimulus for Release: Increased GnRH from hypothalamus. o Target Tissues: gonads o In females, LH stimulates o Secretion of estrogen. o Triggers ovulation. o Formation of corpus luteum. o Secretion of progesterone. o In males, LH stimulates interstitial cells to secrete testosterone.
Prolactin (PRL):
o Secreted by: Anterior pituitary.
o Stimulus for Release:
o Increased PRH from hypothalamus.
o Inhibited by PIH from hypothalamus (DA).
o Target Tissue: Mammary Glands
o Effect:
o Stimulates production of breast milk.
o In males, makes testes more sensitive to LH.
o Imbalance: Galactorrhea (usu. from pituitary tumor).
o Under right conditions, prolactin causes milk production.
o Mammary glands must first be primed by estrogen and progesterone, hGH, insulin and T4.
o Suckling reduces levels of hypothalamic inhibition (decrease PIH) and prolactin levels rise along with milk production.
o In non-pregnant females and males, PIH predominates increase PRL secretion in males, causes breast enlargement & impotence.
Melanocyte Stimulating Hormone (MSH):
o Secreted by: intermediate lobe & anterior pituitary (adult humans do not have functioning intermediate lobe).
o Stimulus for Release: increased CRH from hypothalamus or high ACTH; inhibited by dopamine.
o Target tissue: Skin + ???
o Effect: Function not certain in humans (increases skin pigmentation in frogs) do see darkening of skin in humans with Addison’s dz (lack of corticosteroids, with hypothalamus releasing lots of CRH to try to compensate).
o May be involved in appetite regulation pathways.
Posterior Pituitary Gland:
o Does not make hormones (just storage).
o Consists of axon terminals of hypothalamic neurons.
o Neurons release two neurotransmitters that enter capillaries as hormones.
o Oxytocin and ADH (antidiuretic hormone).
Oxytocin:
o Two target tissues: both involved in neuroendocrine reflexes.
o During delivery: Baby’s head stretches cervix, hormone release enhances uterine muscle contraction, baby and placenta are delivered.
o After delivery: Suckling and hearing baby’s cry stimulates milk ejection hormone causes uterine smooth muscle contraction and milk ejection.
o PITOCIN = synthetic oxytocin used to induce labor.
o Breast feeding stimulates oxytocin, which ALSO helps uterus contract to pre-pregnancy size.
o Involved in the human response to STRESS, it seems to be a down-regulator of the body’s stress axis system, smaller, briefer stress response.
o There are oxytocin receptors on muscle stem cells.
o Cuddle Hormone:
o Released in men and women during sexual climax
o In animals, fosters parental caretaking behavior toward young offspring AND monogamous parental behavior, block receptors for oxytocin and prairie voles become promiscuous.
Antidiuretic Hormone (ADH):
o Secreted by: posterior pituitary gland
o Stimulus for Release: High bl. Osmolarity, low blood pressure, stress, trauma, pain, anxiety, certain drugs (nicotine, tranquilizers, morphine, some anesthetics).
o Regulation of ADH:
o Dehydration: ADH releases, save water/ pee less.
o Overhydration: ADH inhibited, lose water/pee more.
o Target Tissues: Kidneys (principal cells), Sweat glands, Arteriole smooth muscle (VASOPRESSIN), Brain NT (arginine vasopressin).
o Effects: Decrease urine production via water reabsorption, Decrease sweating, Increase BP.
