endocrine wk5

• Released from zona fasciculata of the adrenal cortex
• Stimulated by ACTH from anterior pituitary
• inhibits tissues (muscle, fat) from absorbing glucose
• promotes glyconeogenesis from amino acids and lipids, especially in the liver
• promotes muscle breakdown and release of fats from adipose tissue (theorized to provide raw materials for wound healing).

• inhibitory effect over several proinflammatory cytokines, thus exerting an inhibitory influence over the immune system. This is believed to be a manner in which pain and inflammation are reduced during an emergency situation.
• net effect: increases glucose in bloodstream

• adrenal cortex, zona reticularis
• converted to estrogen or testosterone in gonadal tissues

• released from adrenal medulla chromaffin cells
• Dilated pupils

Elevated heart rate

Elevated blood pressure

Dilated respiratory tract

• Shunting of blood from skin to skeletal muscle
• Increased metabolic rate

Elevated blood sugar

• inhibits TSH and ACTH release from the pituitary gland
• inhibits Alpha and Beta islet cells secretion.

Tri-iodothyronine (T3) Tetra-iodothyronine (T4, also known as thyroxine

• ACIDOPHILS
• Most numerous in adenohypophysis
• Protein-based hormonal products inside vesicles
• Brownish-red color
• GH, prolactin

• BASOPHILS
• Glycoprotein-coated secretory products
• Stain brightly basophilic or purplish with PAS
• POMC (cleaved into ACTH), TSH, FSH, LH

• Derived from nervous tissue and behaves like it
• Cells here don't synthesize hormones
• Neurosecretory cells within hypothalamic nuclei synthesize vasopressin and oxytocin
• Send those products down axons that terminate on fenestrated capillaries in the post pit
• Vasopressin: maintains blood pressure, kidney fluid resorption, arteriole smooth muscle tone
• Oxytocin: response to infant nursing, milk to be secreted by mammary glands, social/emotional behaviors
• Herring bodies: Basophilic-staining, non-cellular objects, Elaborated axons from the neurosecretory cells
• Pituicytes: Specialized glial cells, Cytoplasmic extensions surround axon termianls of neurosecretory cells from hypothalamus

• outermost layer of adrenal cortex
• Mineralocorticoids: aldosterone
• Stimulates resorption of Na and K by kidneys
• Release regulated by renin-angiotensin system
• Thin layer relative to middle layer
• Spherical arrangement of cells

• Gonadocorticoids: DHEA, androstenedione
• Hormones taken up by gonadal tissues and converted to testost/estrogen
• Small minority of the sex hormones for an individual
• Stains darker than other layers with H&E
• Cells contain lots of pigment called lipofuscin, breakdown product of lipid metabolism

• Alpha cells: glucagon
• Signals liver to undergo glycolysis to raise blood glucose
• Beta cells: insulin
• Signals muscle/liver/adipose to take up glucose
• Signals muscle to take up AAs
• Delta cells: somatostatin
• Inhibits TSH and ACTH release from the pituitary
• Inhibits alpha/beta islet cells

• Fatigue
• Weight gain
• Dry brittle hair
• Decreased HR
• Joint pain
• Decreased sweating
• Constipation

• Large spherical thyroid follicles surrounded by follicular cells
• Filled with substance called colloid in lumen
• Colloid is reservoir for iodine (bound by protein called thyroglobulin) cells
• Secrete calcitonin, promotes calcium absorption in bone
• Stain lightly with H&E, but darkly with lead hematoxylin

• Principal cells
• Lightly staining, numerous
• Synthesize PTH
• Oxyphil cells
• Highly eosinophilic cytoplasm
• Unknown function
• Large number of capillaries

• Four small bean shaped glands, deep surface of the thyroid gland
• Secrete parathyroid hormone PTH
• Elevate serum calcium
• Stimulates osteoblasts which stimulate osteoclasts to catabolize bone, liberating sequestered calcium from the bone matrix
• Acts on kidneys to increase calcium reabsorption
• Small intestine to increase calcium uptake

• Kidneys - increase Ca2+ reabsorption, decrease PO4 reabsorption
• stimulate osteoblasts in bone -> M-CSF released + RANK ligand binds to osteoclast precursor
• Osteoclasts break down bone
• increase plasma Ca2+, PO4 -> neg feedback on PTH glands
• increase urine PO4 -> Vit D, incr. plasma Ca2+ and PO4

• Ca2+: 1kg, almost all in bone (65% mineral phase, 35% organic matrix) - about 50% ionized. When total [Ca2+] goes down, the percentage adjusts so that the same amt of [Ca2+] is free
• PO4-: 600g, almost all in bone, <20% intracellular, 80% ionized
• Mg2+: 10g

• PTH: kidney, bone. PTH changes greatly with change in [Ca2+]
• 5-10% of Ca2+ reabsorption occurs in DCT, regulated by PTH
• Vit D: intestine, bone, kidney. Activated in skin, liver, kidney

• Stimulated by: incr. PTH, decr Ca2+, decr PO4
• Inhibited by: decr PTH, incr Ca2+, incr PO4

• 25-(OH)D, calcidiol is used
• 1,25(OH)2D, calcitriol, has a shorter half life

• 80% have no symptoms (primary hyperparathyroidism)
• GI: dry mouth, thirst, polydipsia, vomiting, nausea, constipation
• Genitourinary: polyuria, nocturia, renal stones, renal failure

• Malignancy - bone metastasis, humoral hypercalcemia
• Viatmin D intoxication
• Sarcoidosis (1,25(OH)2-vit D)
• Renal reabsorption: Familial hypocalciuric hypercalcemia, thiazide diuretics, lithium

• promotes proliferation and apoptosis of chondrocytes
• required for normal bone development
• malignancy marker

• Low serum albumin (apparent)
• Chronic renal failure
• Magnesium deficiency
• Hypoparathyroidism
• Pseudohypoparathyroidism
• Osteomalacia due to Vitamin D deficiency
• “Hungry bone” syndrome-after parathyroidectomy
• Acute hemorrhagic/edematous pancreatitis
• Hyperphosphatemia

• renal failure
• cell lysis
• excessive PO4 administration
• hypoparathyroidism/pseudohypoparathyroidism

• hypocalcemia - secondary hyperparathyroidism
• hyperphosphatemia
• decreased production of active vit D
• elevated BUN, creatinine
• usually elevated PTH

• Caused by tumor of pituitary or hypothalamus/ectopic tumors
• acromegaly: excess of GH, adult onset
• thickening of skin on face, hands, feet
• lethargy, sweating, headaches
• incr. incidence of HTN, diabetes
• gigantism: onset before fusion of epiphyseal plates

• diagnosis: incr. IGF-1, failure to suppress GH levels with glucose
• treatment: surgery, octreotide (somatostatin analog), B-adrenergic agonists

• GH deficiency caused by congenital defect in GH, GHRH, GH receptor, IGF-1, IGFR, abnormality of pituitary or hypothalamus; or acquired (tumors, pituitary trauma, psychosocial deprivation)
• Clinically: short, plump, retarded bone age
• Injection of GH or IGF-1

• Turner's syndrome
• renal failure
• dwarfism

low mood, reduced E, obesity, reduced bone density

• Pulsatile/nocturnal
• Stimulated by: hyppoglycemia, stress, sleep, aa's, sex steroids, ACh, fasting, alpha-adrenergic
• Inhibited by: obesity, B-adrenergic, glucocorticoids, high FFA, hyperglycemia, hypothyroidism, IGF-1

• GH stimulates production of somatostatin, inhibits more GH release
• Thyroid hormones stimulate GH release and activity
• GHRH stim by sleep, stress
• Can have insulin-like and anti-insulin like effects based on binding to JAK2->IRS (insulin receptor substrate) and interfering w/insulin's actions

• synthesis induced by GH, prenatal and postnatal growth
• produced by liver and other tissues
• binds insulin receptor or IGFR
• regulation by soluble IGF-binding proteins to extend half-life (GH has similar reg)

• homology to GH
• GH-like anti-insulin activity
• contributes to gestational diabetes

• cortisol can bind and activate the mineralcorticoid receptor (aldosterone), but is normally inactivated by 11beta-OH DH
• people w/mutated 11beta-OH DH have high blood pressure

• Essential hypertension: effects 25% adult population.
• Primary aldosteronism: Adrenal tumor. Overproduction of aldosterone leads to hypertension.
• Malignant hypertension: Renal damage leads to loss of control of renin secretion and increased plasma renin
• levels.
• Liver disease: aldosterone is not degraded normally.
• Addisons disease: destruction of adrenals (source of aldosterone)
• Congenital Adrenal Hypertension Type II: mutation in 11 hydroxylase

• ACE inhibitors
• Antagonists of MR (in kidney tubules)
• Antagonists of AT1 angiotensin II receptor (smooth muscle cells and adrenal cells)

• increased muscle mass
• increase blood pressure
• increased cholesterol (LDL) and lower HDL
• increased risk of liver and heart damage
• gynecomastia (enlarged male breast tissue)
• increased risk of prostate cancer
• acne on the face and body
• shrunken testicles
• reduced sperm count
• mood swings and increased aggressive behavior