Chapter 16: Endocrine System

Question 1

Exocrine Glands:

Answer 1

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.

Question 2

Endocrine Glands:

Answer 2

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.

Question 3

Can Some Glands be Both Endocrine and Exocrine?

Answer 3

Yes

Question 4

The 2 Organ Systems That Regulate Homeostasis:

Answer 4

o Endocrine System.

o Nervous System.

Question 5

The 4 Types of Cell-to-Cell Communication:

Answer 5

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!)

Question 6

Local Hormones:

Answer 6

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.

Question 7

Systemic Hormones:

Answer 7

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).

Question 8

The 3 Interactions Between Hormones:

Answer 8

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.

Question 9

Half Life of Hormones:

Answer 9

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.

Question 10

The 3 Causes of Hormone Release:

Answer 10

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.

Question 11

Control of Hormone Secretion:

Answer 11

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.

Question 12

Lipid-Soluble Hormones:

Answer 12

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.

Question 13

Action of Lipid-Soluble Hormones:

Answer 13

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.

Question 14

Water-Soluble Hormones:

Answer 14

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.

Question 15

Production of Peptide Hormones:

Answer 15

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.

Question 16

Action of Water-Soluble Hormones:

Answer 16

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.

Question 17

Second Messengers:

Answer 17

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.

Question 18

Amplification of Hormone Effects:

Answer 18

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.

Question 19

Anatomy of Pituitary Gland:

Answer 19

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.

Question 20

Hypothalamus Control:

Answer 20

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.

Question 21

Flow of Blood to Anterior Pituitary:

Answer 21

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.

Question 22

Hypothalamus-Pituitary-3rd Gland Axis:

Answer 22

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.

Question 23

Important Axes:

Answer 23

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.

Question 24

Specific Anterior Pituitary Hormones:

Answer 24

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.

Question 25

Human Growth Hormone (hGH) and IGFs:

Answer 25

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.

Question 26

Diabetogenic Effect of Human Growth Hormone (hGH):

Answer 26

``` 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. ```

Question 27

Imbalances of Human Growth Hormone (hGH):

Answer 27

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.

Question 28

Thyroid Stimulating Hormone (TSH):

Answer 28

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).

Question 29

Adrenocorticotrophic Hormone (ACTH):

Answer 29

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.

Question 30

Follicle Stimulating Hormone (FSH):

Answer 30

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).

Question 31

Luteinizing Hormone (LH):

Answer 31

``` 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. ```

Question 32

Prolactin (PRL):

Answer 32

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.

Question 33

Melanocyte Stimulating Hormone (MSH):

Answer 33

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.

Question 34

Posterior Pituitary Gland:

Answer 34

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).

Question 35

Oxytocin:

Answer 35

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.

Question 36

Antidiuretic Hormone (ADH):

Answer 36

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.

Question 37

Disorders of ADH:

Answer 37

o Hyposecretion: o Diabetes Insipidus, with polyuria and hypernatremia without adequate replacement fluid. o Alcohol intake inhibits ADH secretion. o Hypersecretion: o SIADH (syndrome of inappropriate ADH secretion), over-retention of fluid, weight gain, hypoosmolarity of blood. o High blood pressure (vasopressin!)

Question 38

Thyroid Gland:

Answer 38

o Two lateral lobes (isthmus in between lobes). o Weighs 1 oz and has rich blood supply. o Follicle = sac of stored hormone (colloid) surrounded by follicular cells that produced it. o Produces T4 and some T3 (most T3 is formed inside target tissues). o Target tissues: almost every cell in body! o Parafollicular cells are located in between the follicle cells. o They produce a different hormone (CALCITONIN) which lowers blood calcium levels when they are too high.

Question 39

Formation of Thyroid Hormone:

Answer 39

o Iodide trapping by follicular cells. o Synthesis of thyroglobulin (TGB) and release into colloid. o Iodination of tyrosine in colloid. o Formation of T3 and T4 by combining T1 and T2 together. o Uptake and digestion of TGB by follicle cells. o Secretion of T3 and T4 into blood. o Transport on TBG = thyroxine binding protein.

Question 40

General Effects of T3 and T4:

Answer 40

o Stimulates synthesis of additional Na+/K+ ATP-ase pumps …this requires ATP, generates heat! o Stimulates enzymes concerned with glucose oxidation and it mobilizes fats for F.A. oxidation…both increase O2 consumption and increase BMR. o Important regulator of tissue growth and development, esp. skeletal, nervous, reproductive systems (thyroid deficiency in fetus = mental retardation = cretinism). o Essential for protein synthesis. o Enhances effects of sympathetic nervous system.

Question 41

Control of T3 and T4 Secretion:

Answer 41

o Negative feedback system. o Low blood levels of T4 and T3 stimulate hypothalamus to release TRH. o TRH stimulates pituitary to release TSH. o TSH stimulates gland to increased release T4 and T3.

Question 42

Thyroid Gland Disorders:

Answer 42

o Hypothyroidism= hyposecretion of T4 and T3: o During infancy results in dwarfism & retardation called CRETINISM (short, disproportionate body). o Hypothyroidism in adult produces: o Sensitivity to cold and low body temperature. o Constipation. o Weight gain. o Thick/dry skin and puffy eyes. o Lethargy/myalgias/hypoactive reflexes. o Low HR/dyslipidemias and increased risk CVD. o Mental dullness/memory impairment/depression. o Myxedema = severe or prolonged adult hypothyroidism. o Hyperthyroidism = hypermetabolic state secondary to ↑ thyroid hormone levels. o Symptoms: o HTN. o Tachycardia. o Insomnia. o Tremor. o High body temperature. o Wt. loss with increased appetite. o Increased sweating. o GRAVE’S DZ = autoimmune dz with weight loss, nervousness, irregular heart beat, sweating, tremor and exophthalmos (edema behind eyes).

Question 43

Goiters:

Answer 43

o A goiter is just an enlarged thyroid gland. It can be from any number of causes: o Lack of iodine in the diet (endogenous goiter) (in this case, nothing is wrong with the thyroid gland at all…just no building blocks!). o Hypothyroidism, low levels of T3 and T4 cause an increased secretion of TRH and TSH. o Grave’s Disease, weird antibody complex formed in this autoimmune disease mimics the effects of TSH.

Question 44

Calcitonin:

Answer 44

o Secreted by: thyroid gland (parafollicular cells). o Stimulus for Release: high blood calcium levels (must be about 20 percent above normal). o Target Tissue: bone. o Inhibits osteoclastic activity, decreases bone resorption o Promotes bone deposition. o Appears to be most important in kids whose skeleton is growing quickly… only a weak hypocalcemic agent in adults. o MIACALCIN = calcitonin extract derived from salmon that is 10X more potent than human calcitonin.

Question 45

Parathyroid Glands:

Answer 45

o 4 pea-sized glands found on back of thyroid gland. | o Can be as many as 8, rarely even in thorax/neck!

Question 46

Parathyroid Hormone (PTH):

Answer 46

o Secreted by: parathyroid glands . o Stimulus for Release: low blood calcium levels (release inhibited by hypercalcemia). o Target Tissues: o Skeleton: stimulates osteoclasts, Ca++ and phosphate released into blood. o Kidneys: o 1. Enhances Ca++ and Mg++ reabsorption and secretion of phosphate. o 2. Also activates Vit. D to CALCITRIOL, which promotes absorption of Ca++, Mg++, and phosphates from the digestive tract.

Question 47

Disorders of Parathyroid Hormone:

Answer 47

o Hyperparathyroidism: o Usually caused by a parathyroid gland tumor. o Calcium is leached from the bones leads to bones soften and mineral salts are replaced by fibrous c.t. leads to hypercalcemia. o HYPERCALCEMIA causes depression of nervous system with abnormal reflexes. o Calcium deposits form in soft tissues throughout body leads to kidney stones common. o “Painful bones, renal stones, abdominal groans, and psychic moans.” o Hypoparathyroidism: o Usually caused by trauma to the parathyroid gland, surgical removal, or autoimmune processes. o Rarely caused by an extreme dietary deficiency of Mg++ (required for secretion). o Causes HYPOCALCEMIA, with hyperexcitable nervous system, muscle spasm, tetany, convulsion. • Trousseau’s sign. • Chvostek’s sign.

Question 48

Adrenal Glands:

Answer 48

o One on top of each kidney…really 2 glands in one! o Adrenal cortex produces 3 different types of hormones from 3 zones of cortex. o Adrenal medulla produces epinephrine & norepinephrine (trace of dopamine). o 3 X 3 X 1 cm in size and weighs 5 grams total! o Adrenal Cortex o Zona glomerulosa: Produces mineralcorticoids (Aldosterone). o Zona fasciculata: Produces glucocorticoids (Cortisol). o Zona reticularis: produces gonadocorticoids (DHEA). o Adrenal Medulla: Produces Catecholamines (80 percent epinephrine, 20 percent norepinephrine, trace of dopamine.

Question 49

Mineralocorticoids: Aldosterone

Answer 49

o 95 percent of hormonal activity due to aldosterone. o Secreted by: Adrenal cortex (zona glomerulosa). o Stimulus for Release: o High blood potassium (hyperkalemia). o Low blood sodium (hyponatremia, not as potent). o Angiotensin II (from renin-angiotensin system responding to low blood pressure or low blood volume). o Target Tissues: Kidney (principal cells) o Sodium reabsorption, Potassium excretion. o Aldosterone also promotes H+ excretion in urine. o Aldosterone can also target the sweat glands, the salivary glands, colon and gastric glands, enhancing sodium reabsorption in all of these target tissues! o Aldosterone also targets the heart, causing proinflammatory and profibrotic changes that result in left ventricular hypertrophy and remodeling. o Aldosterone’s effects are fairly brief…last only about 20 minutes. This means that lyte balance can be more PRECISELY controlled and modified continuously. o All the corticosteroids (including mineralocorticoids like aldosterone) help our body cope with extremely stressful situations, so there are other ways to regulate aldosterone.

Question 50

Regulation of Aldosterone:

Answer 50

o Humoral stimulation (plasma K+ and Na+). o Hormonal regulation: o Renin-angiotensin system (most important). o ANP, increased ANP blocks renin secretion and blocks aldosterone secretion directly. o ACTH, usually has very little effect on the zona glomerulosa (main effect of ACTH is on the zona fasciculata and cortisol production), but if SEVERE stress, then hypothalamus increases secretion of CRH, which increases ACTH, which increases aldosterone secretion to a small extent.

Question 51

Imbalances of Aldosterone:

Answer 51

``` o Hyperaldosteronism (Conn’s dz): o Too much aldosterone secreted, usually from a tumor of the adrenal gland. o Sx = HTN, edema (excessive Na+ retention), hypokalemia (excessive K+ loss in urine) with muscle weakness and nonresponsive neurons. o Hypoaldosteronism: o Not enough aldosterone secretion, Na+ not reabsorbed, severe dehydration, hypotension, hyperkalemia. o Usually in conjunction with inadequate cortisol secretion in ADDISON’S DZ. ```

Question 52

Glucocorticoids: Cortisol

Answer 52

o 95 percent of hormonal activity is due to cortisol. o Secreted by: Adrenal cortex (zona fasciculata). o Stimulus for Release: o Released in bursts driven by patterns of eating and activity…definite pattern throughout day…cortisol peaks just after getting up in the morning. o This “normal” pattern is overturned if STRESS of any variety: infections physical trauma, hemorrhage, emotional trauma. o Stress stimulates sympathetic N.S., triggers release of CRH, triggers release ACTH, triggers release of cortisol. Cortisol = hydrocortisone. o Target tissues: influences METABOLISM of most body cells, especially skeletal muscle, adipose tissue, and liver. o Protein breakdown to liberate amino acids (especially in skeletal muscle). o For gluconeogenesis, probably cortisol’s primary effect. o For synthesis of critical proteins needed from the “stress”. o Gluconeogenesis (especially in the liver). o Lipolysis (especially in adipose tissue). o Provides resistance to stress by making nutrients available for ATP production. o Raises BP by vasoconstriction (makes blood vessels more sensitive to hormones that cause vasoconstriction). o Depresses immune response, used in organ transplants (why stress reduces resistance). o Anti-inflammatory effects: o Reduces release of histamine from mast cells. o Decreases capillary permeability. o Depresses phagocytosis. o Unfortunately, this retards tissue repair.

Question 53

Imbalances of Cortisol:

Answer 53

o Cortisol = Hydrocortisone = steroid hormone = can be given p.o. (by mouth) o Excessive cortisol in the blood (either from drugs or from a body “out of balance”) has many side effects: o Increased bone loss, leading to osteoporosis. o Decreased cartilage formation. o Negative nitrogen balance (body protein loss). o Sodium retention and edema. o Potassium, magnesium, and calcium loss. o Hyperglycemia. o Poor wound healing. o GI bleeding.

Question 54

Cushing's Syndrome:

Answer 54

o Excessive amounts of glucocorticoids. o Usually caused by excessive steroid use (meds like prednisone), but can also be caused by a tumor that secretes ACTH (in the pituitary, or ectopically in the lungs, pancreas, kidneys)… could also be a tumor of the adrenal cortex that hypersecretes cortisol. o Signs and Symptoms: o Hyperglycemia, loss of muscle tone, redistribution of fat to abdomen, moon face, buffalo hump, osteoporosis, Na+/water retention, edema and HTN, easy bruising, poor wound healing.

Question 55

Addison's Disease:

Answer 55

o Deficient amounts of glucocorticoids and aldosterone. o Signs and symptoms: o Weight loss, Hypoglycemia, Muscle weakness, Major dehydration due to decreased Na+ in blood, Low blood pressure (hypotension), Hyperkalemia (with potential cardiac arrest), High ACTH that mimics skin darkening effects of MSH.

Question 56

Androgens from Zona Reticularis:

Answer 56

o Small amount of male hormone produced, primarily a precursor to testosterone = DHEA = dehydroepiandrosterone o Males: probably insignificant compared to amounts of testosterone made during late puberty/adulthood o Females: o May contribute to sex drive in females. o Is converted to estrogen in postmenopausal females. o Children: Gonadocorticoids rise continuously in both sexes between the ages of 7 and 13, may have something to do with onset of puberty.

Question 57

Congenital Adrenal Hyperplasia:

Answer 57

o Disorder where person lacks an enzyme to make cortisol, blood cortisol levels are low. o This feeds back to the hypothalamus, increase in CRH, Increase in ACTH, causes abnormal growth of the entire adrenal cortex. o Precursor molecules (including DHEA) accumulate, causes VIRILISM (masculinization). o Prepubertal boys: precocious puberty. o Females: develop beard, masculine patterns of hair and musculature, clitoris grows to resemble a small penis.

Question 58

Adrenal Medulla:

Answer 58

o Chromaffin cells receive direct innervation from sympathetic nervous system (splanchnic nerve). o Develop from same tissue as postganglionic neurons. o Produce CATECHOLAMINES: epinephrine, norepinephrine, and (trace) of dopamine. o Catecholamines are sympathomimetic. o Effects mimic those of sympathetic NS. o Cause fight-flight behavior. o Acetylcholine increases catecholamine secretion by adrenal medulla (acts on nicotinic receptors).

Question 59

Epinephrine and Norepinephrine:

Answer 59

o Secreted by: Adrenal medulla (chromaffin cells). o Stimulus for Release: Stress (fight or flight). o Target tissues: Most body cells…variable effects: o Increased heart rate and strength of contraction. o Increased blood pressure. o Glycogenolysis with increased blood sugar. o Bronchodilation of airways and increased rate/depth respirations. o Decreased blood flow to digestive tract and urinary system to maximize blood flow to brain, skeletal muscle, liver and adipose tissue. o Brief Response.

Question 60

Pheochromocytoma:

Answer 60

o Disease causing excessive amounts of catecholamines to be secreted into blood o Cause is usually a tumor of the adrenal medulla o Signs and symptoms: o Hyperglycemia. o Hypermetabolism (increased metabolic rate). o Headache. o HTN. o Hyperhidrosis (increased sweating). o Heart palpitations and increased heart rate. o Intense nervousness. o Massive sympathetic N.S. effects.

Question 61

Disorders of Endocrine System: Prolactinoma

Answer 61

Production of too much prolactin.

Question 62

Disorders of Endocrine System: Cretinism

Answer 62

Mental retardation from thyroid deficiency.

Question 63

Disorders of Endocrine System: Diabetes Mellitus II

Answer 63

Insufficient insulin.

Question 64

Disorders of Endocrine System: Addison's Disease

Answer 64

Insufficient aldosterone and cortisol.

Question 65

Disorders of Endocrine System: Conn's Disease

Answer 65

Too much aldosterone.

Question 66

Disorders of Endocrine System: Cushing's Syndrome

Answer 66

Too much cortisol.

Question 67

Disorders of Endocrine System: Trousseau's Sign and Chvostek's Sign

Answer 67

Hypercalcemia.

Question 68

Disorders of Endocrine System: Pheochromocytoma

Answer 68

Too many catecholamines.

Question 69

Disorders of Endocrine System: Acromegaly

Answer 69

Abnormal increase in width of bones.

Question 70

Hormones Secreted by Adipose Tissue:

Answer 70

``` o Leptin: o Increases BMR. o Decreased appetite. o Resistin: o Decreased cell response to insulin. o Adiponectin: o Increased cell response to insulin ( Decreased amt. if Increased adiposity). ```

Question 71

Hormones Secreted by the Digestive Tract:

Answer 71

``` o Stomach: o Gastrin. o Histamine. o Serotonin. o Ghrelin. o Gut-brain peptides: o GIP. o VIP. o Substance P. o Neuropeptide Y. o CCK (small amounts). ```

Question 72

Hormones Secreted by the Liver:

Answer 72

``` o TPO: o Increased thrombopoiesis. o EPO (tiny amount): o Increased erythropoiesis. o Hepcidin: o Decreased iron absorption. o IGFs. o Precursors: o Angiotensinogen. o Calcidiol. ```

Question 73

Hormones Secreted by the Small Intestine:

Answer 73

o CCK: o Increased dig. enzyme secretion from panc. acinar cells. o Increased contraction GB. o Relaxes Sphincter of Oddi. o Secretin: o Increased alkaline juices from panc. and liver duct cells. o Increased bile secretion. o VIP. o Enteroglucacon and Glucagon-like peptide (GLP-1).

Question 74

Glucagon-Like Peptide (GLP-1):

Answer 74

o GLP-1: o Enhances release of insulin from pancreas. o Decreases secretion of glucagon from pancreas. o Delays gastric emptying and decreases appetite. o GIP (aka glucose-dependent insulinotropic peptide): o Enhances release of insulin from pancreas. o Delays gastric emptying and decreases HCl production.

Question 75

New Diabetic Medications:

Answer 75

o Incretin mimetics (e.g., Byetta: gila monster saliva). o DPP-4 enzyme inhibitors: o GLP-1 and GIP have very short half lives (less than 10 minutes). o They are broken down by DPP-4 enzymes. o DPP-4 enzyme inhibitor meds allow Increase’s levels incretins. • Januvia (sitagliptin). • Nesina (alogliptin). • Tradjenta (linagliptin). • Onglyza (saxagliptin).

Question 76

Anatomy of Pancreas:

Answer 76

o Organ (5 inches) consists of head, body and tail. o Cells (99 percent) in acini produce digestive enzymes. o Endocrine cells in pancreatic islets produce hormones. o Histology: o 1 to 2 million pancreatic islets. o Contains at least 4 types of endocrine cells.

Question 77

Cell Types of the Pancreatic Islets:

Answer 77

o Alpha cells (20 percent) produce glucagon. o Beta cells (70 percent) produce insulin. o Beta cells produce amylin. o Decreases gastric emptying. o Increased satiety. o Decreases glucagon secretion. o Delta cells (5 percent) produce somatostatin. o F cells produce pancreatic polypeptide. o These cells are tiny “fuel” sensors… they secrete hormones independently of each other based on fed or non-fed states.

Question 78

Humoral Regulation of Glucagon and Insulin Secretion:

Answer 78

o Low blood glucose stimulates release of glucagon. | o High blood glucose stimulates secretion of insulin and amylin.

Question 79

Glucagon:

Answer 79

o Secreted by: pancreas (alpha cells) o Stimulus for Release: o Falling blood glucose and increasing a.a. in blood. o Sympathetic stimulation (beta-2 receptors). o Catecholamines. o Target tissue: Liver and Adipose Tissue. o Glycogenolysis and gluconeogenesis. o Lipolysis. o Subsequent release of glucose and F. A. into blood. o Imbalance: Too much glucagon in DM (not enough insulin to inhibit glucagon release).

Question 80

Insulin:

Answer 80

o Secreted by: pancreas (beta cells) o Stimulus for Release: Rising blood glucose (also increasing amino acids and F.A. in blood) AND MANY OTHER THINGS. o Target tissues: All body cells (although liver, kidney, and brain do not require insulin for glucose uptake). o Enhances entry of glucose into cells via stimulating cell to insert glucose transport molecules into cell membrane DECREASES BLOOD GLUCOSE. o Increases oxidation of glucose for ATP (glycolysis). o Increases glycogenesis (inhibits glycogenolysis). o Converts excess glucose to fat (triglyceride) for storage (and inhibits lipolysis). o Stimulates amino acid uptake, increased protein synthesis.

Question 81

Diabetes Mellitus:

Answer 81

``` o Type I DM = inadequate or no insulin secretion. o Type II DM = problem in cell signaling cascade OR inadequate or ineffective insulin secretion OR decreased numbers/effectiveness of insulin receptors OR insufficient/ineffective glucose transporters OR too much resistin hormone OR too much liver output of glucose. o Cardinal symptoms of Type I at time of dx: o Polyuria (increased urination from glucose in urine dragging water along with it). o Polydipsia (increased thirst and fluid consumption). o Polyphagia (increased appetite and food intake). o Uncontrolled diabetes mellitus can lead to DKA (diabetic ketoacidosis--usually in Type I). ```

Question 82

Treatment for Type I Diabetes:

Answer 82

o Insulin injections/insulin pumps. o Insulin inhalers. o Insulin patches in development stage. o Pancreatic islet beta cell transplants. o New hormone discovered April 2013: BETATROPHIN. • Mice can produce beta cells at 30 times the normal rate.

Question 83

Treatment for Type II Diabetes:

Answer 83

o Weight loss o Exercise and increased activity o Low glycemic-index diet o Medications o Meds that inhibit gluconeogenesis/glycogenolysis (e.g., biguanides--metformin, glucophage) and DPP-4 inhibitors that enhance incretins. o Meds that stimulate insulin release (e.g., sulfonylureas--glyburide, glipizide, glucotrol, amaryl and meglitinides (e.g., Prandin) and incretin mimics (Byetta) and DPP-4 inhibitors (e.g., Januvia). o Meds that improve insulin sensitivity (e.g., TZDs = Thiazolidinediones)(Actos). o Meds that decrease glucose absorption in gut (e.g., Precose, Glyset). o Meds that inhibit SGLT in kidney: Invokana.

Question 84

Long-Term Complication of Chronic Uncontrolled DM:

Answer 84

o Peripheral neuropathy: Impotence, Incontinence, Loss of sensation in affected areas; amputations. o Retinal disease leads to blindness. o Kidney disease leads to chronic renal failure. o Cardiovascular disease: o Increased atherosclerosis. o Increased CAD and increased risk MI. o Contributes to gangrene.

Question 85

Abnormal Disorder: Hyperinsulinism

Answer 85

o Etiology: o Insulin overdose o Inadequate food intake with normal insulin dose o Excessive exercise with normal insulin dose o (rarely) pancreatic islet cell tumor o Effect: o Low blood sugar = hypoglycemia leads to weakness, disorientation, convulsions, coma. o Triggers release of hyperglycemic hormones, Ep, glucagon, hGH, increased catecholamines can lead to anxiety, nervousness, tremors, sweating, headache.

Question 86

Ovaries and Testes:

Answer 86

o Ovaries o Estrogen, progesterone and inhibin. o Regulate reproductive cycle, maintain pregnancy and prepare mammary glands for lactation. o Testes o Produce testosterone and inhibin. o Regulate sperm production and secondary sexual characteristics.

Question 87

Hormones from Placenta:

Answer 87

``` o hCG: human chorionic gonadotropin. o Maintains corpus luteum in ovary. o Promotes normal placental development. o hPL: human placental lactogen (aka human chorionic somatomammotropin). o Stimulates maturation of breasts o Glucose-sparing effect in mother o Relaxin: o Relaxes pelvic ligaments. o Widens pubic symphysis; increases flexibility. o Estrogen and Progesterone. ```

Question 88

Melatonin and Pineal Gland:

Answer 88

o Secreted by: pineal gland. o Stimulation for Release: darkness (bright light suppresses melatonin secretion). o Target tissues: Not completely understood o Melatonin responsible for setting the biological clock of hypothalamus (suprachiasmatic nucleus). o Strong antioxidant. o May have an antigonadotropic effect (may inhibit precocious sexual maturation, affecting the timing of puberty).

Question 89

Seasonal Affective Disorder (SAD):

Answer 89

o Depression that occurs during winter months when day length is short. o Due to overproduction of melatonin. o Therapy; o Exposure to several hours per day of artificial light as bright as sunlight. o Speeds recovery from jet lag.

Question 90

Thymus Gland:

Answer 90

o Important role in maturation of T cells o Hormones produced by gland promote the proliferation and maturation of T cells. o Thymosin. o Thymic humoral factor. o Thymic factor. o Thymopoietin.

Question 91

Eicosanoids:

Answer 91

o Local hormones released by all body cells. o Leukotrienes influence WBCs and inflammation. o Prostaglandins alter. o Smooth muscle contraction, glandular secretion, blood flow, platelet function, nerve transmission, metabolism etc. o Ibuprofen and other nonsteroidal anti-inflammatory drugs treat pain, fever and inflammation by inhibiting prostaglandin synthesis.

Question 92

Aging and the Endocrine System:

Answer 92

o Production of human growth hormone decreases o Muscle atrophy and other changes in body composition. o Production of TSH increase with age in effort to stimulate thyroid . o Decrease in metabolic rate, increase in body fat and hypothyroidism. o Thymus after puberty is replaced with adipose. o Adrenal glands produce less cortisol and aldosterone. o Receptor sensitivity to glucose declines. o Decreased testosterone in both sexes. o Ovaries no longer respond to gonadotropins. o Decreased output of estrogen (osteoporosis and atherosclerosis). o Increased levels of FSH and LH.