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pituitary gland aka

hypophysis

Pars nervosa

major part of neural tissue

Adenohypophysis

Anterior pit (pars tuberalis, pars distalis, pars intermedia)

Neurohypophysis

posterior pit (pars nervosa, infundibulum)

Pars distalis

major part of adenohypophysis

Diencephalon

Downgrowth from neurohypophysis

Raphe's pouch

roof of mouth -- turns into adeno

Alpha melanocyte stimulating hormone (alpha MSH)

in pars intermedia

Corticotropin

alternate name: Adrenocorticotropic hormone (ACTH)

Hormone synthesizing cells

suffix: tropes; ex: gonadotropes (synthesize LH, TSH)

Acidophilic cells

stain with acid dyes (GH, PRL cells)

Basophilic

stain with basic dyes (TSH, FSH, LH, ACTH)

Chromophobes

Show little staining (ACTH)

Category 1 hormones (GH, PRL)

similar size (191/199); common AA

GH fxns

stimulate growth, extracellular deposition of bones, lipases that convert triglycerides to FFAs and body fat

Somatomedin hypothesis

says GH actions are mediated by somatomedins produced in liver and other tissue; Ex: insulin like growth factors (IGF)

GH secretion

highest during sleep, hypothalamic control, hypoglycemia stimulus released

GH related dz

Dwarfism (underproduction); Gigantism (excess GH, linear bone growth); Acromegaly (excess GH in adults)

Tx for GH deficiency

Genotropsin ex of hGH, excess GH long acting analogs of SST

PRL fxns

diverse in vertebrates (reproduction, growth and development, water/electrolyte balance, integument (skin, hair feathers)

Effects of PRL on reproduction

mammary gland developmt and secretion in mammals; luteotropic effect in rodents; crop milk production in birds (brood patch development)

PRL secretion

inc during sleep/pregnancy; stimulated by nursing; inhibited by dopamine

Category 2 horm's (FSH, LH, TSH)

double chained w/ 2 subunits (alpha and beta; alpha same w/i spp, B determines hormone specificity)

FSH fxns

F (stimulate development of ovarian follicles) M (stimulate synthesis of androgen binding protein in sertolli cells, formation of LH receptors in Leydig cells)

LH fxns

F (stimulates ovulation, corpus luteum formation, estrogen synthesis) M (stimulates T synthesis by Leydig cells)

TSH fxns

stimulates thyroid gland

Category 3 horm's (ACTH, aMSH, BLPH)

derived from pro-opiomelanocortin (POMC)

ACTH fxn

stimulates glucocorticoid synthesis in adrenal cortex

aMSH fxn

affects pigmentation via cation of malanophores

BLPH fxn

stimulates lipolysis in fat cells, source of endorphins such as B endorphins

Hyposecretion

panhypopituitarism - total loss of secretion

Hypersecretion

Neoplastic tumor of hormone producing cells, most common in microadenonas

Parvocellular neurosecreatory neurons of hypothalamus

small size, in many hyponuclei, produce hypophysiotropic hormones that regulate the anterior pituitary fxn, axons extend to the primary plexus of median eminence

Hypophysiotropic horms

regulate activity of endocrine cells of hypophysis

Neurovascular hypothesis

hormonal rather than direct neural control of AP gland; Geoffrey Harris supporter;

Exceptions to NV hypothesis

increase amount of hormone released: Prolactin (synthesis and release inhibited by dopamine), aMSH (controlled by dopamine)

Evidence for NV hypothesis

interruption of vascular system altered horm secretion; reciprocal transplantation of pit gland between M and F rats indicated that hypothalamus controls AP fxn (not gender specific)

Hypophysiotropic neurohormones

neurohorms produced by neurosecratory neurons of hypothalamus that regulate release of AP horms

Guillemin and Schally

Discovered sxr of hypophysiotropic horms: (pyro) glu his pro nh2 -- correct sxr of TRH

TRH fxns

stimulate release of TSH in homeotherms (mammals/birds); useful to test ability of pituitary to produce TSH

GnRH fxn (gonadotropin RH)

decapeptide; fxns to release FSH,LH; neuroregulation of GnRH: dopaminergic neurons stimulate secretion, encephalinergic neurons inhibit secretion

Clinical importance GnRH

induce ovulation; treat oligospermia, constant exposure causes gonadotrope desensitization; GnRH longacting analogs = antifertility agent

Somatostatin SST

produced by neurosecratory cells in hypothalamus: inhibits GH release from AP; Produced by G cells of GI tract and pancreatic islets: inhibits gastrin release, inhibits insulin/glucagon release; Long acting analogs treat acromegaly, PUD, diabetic retinopathy s/p DM

Somatocrinin

stimulates GH release from AP

Ghrelin

stimulates GH release from AP; produced in stomach, sm intestine, hypothalamic neurosecreatory neurons; regulates feeding behavior/energy homeostasis

CRH - Corticotropin releasing horm

stimulates ACTH release; stress stimulates CRH release; cholinergic pathways important, atropine can block pathways

Dopamine

neurotransmitter; inhibits prolactin release; agonists inhibit PRL release from AP, antagonists stimulate release; Hyperprolactinemia in 28% women with menstrual abnormalities, treat with dopamine agonists (parlodel, bromocryptine mesylate)

MSH release inhibiting hormone

dopamine inhibits MSH release, dopamine present in hypo portal system

Feedback control of pituitary horm excretion

Cortisol (neg feedback) Thyroxine, Estradiol/testosterone

Negative feedback

Hypothalamus releases CRH to AP, stimulates ACTH release

Autoinhibition/short loop feedback

inhibitory effects of release of ACTH

Long loop feedback

ACTH target, adrenal cortex releases cortisol (negative feedback at higher level: hypothalamus)

Neurohemal organ

axon endings, vascular bed, pituicytes

Nucleus

collection of nerve cell bodies in CNS; supraoptic and paraventricular (more oxytocin)

Magnocellular neurosecratory neurons

paraventricular nucleus, supraoptic nucleus, preoptic nucleus (PON)

Sxr of neurohypophysial hormones

nonapeptides, 12 different ones, 2 different horms in a spp (exceptions: cyclostomes, lamprey and hagfish -- only have arginine vasotocin)

Transport of neurohypophysial horms

via larger proteins called neurophysins: Vasopressin neurophysin = pressophysin, oxytocin NP = oxyphysin, cleaved off during axonal transport, secreted with neurohormones

OT (oxytocin) release

neuroendocrine reflex - result of sensory input to SC -> brain; neuron depolarization in AP of pars nervosa -> Ca entry -> exocytosis of OT; AP reach axon tips in 0.5-1.5m/s; ex of stimulus released coupling: rapid response

Fxns of neurohypophysial horms

osmoregulate, contractile regulation (vasopressin-osmo, OT -contractile activity: uterine, milk release, orgasm); Vasopressin - antidiuretic, ADH, increase permeability of collecting ducts to water

Mechanism of vasopressin

80% h2o uptake in proximal tubule by AVP independent means, other 20% by horms (AVP acting on collecting ducts, aldosterone acting on distal tubes)

Factors affecting AVP release: plasma osmolality

<280 = little/no release, >280 = increase release; release very sensitive to change; osmoreceoptors in anterior hypothalamus detect changes in blood Na

Factors affecting AVP release: blood volume/pressure

AVP less sensitive than response to changes in osmolality, 5% dec in BP, 8% dec in BV; important with hemorrhage and blood loss, location of arterial baroreceptors: aortic arch, carotid sinus, lt atrium

Factors affecting AVP release: Angiotensin II

component of rennin angiotensin system, acts on brain to stimulate AVP release

Inhibiting factors of AVP

atrial natruiuretic factor (ANF), ethanol, low temp

Arginine Vasotocin (AVT)

key neurohypophysial hormone, constricts preglomular arterioles in birds/reptiles, increase h2o permeability in the skin of frogs and urinary bladder of toads

Neurohypophysial contractile activity

pregnancy (OT release causes contraction during labor); mammary glands (OT causes milk release); mating (inc uterine activity, orgasm, milk ejection, inc sperm transport)

OT causes embryonic diapuse of kangaroos

suckling: OT release; OT inhibits P synthesis by corpus luteum or ovary -> development of blastocyte; AVT mediates egg laying in sea turtles

Neurohypophysial hormones and BP

OT causes umbilical arteries to contract; AVP causes contraction in some peripheral vascular beds: mediated via the V receptor, IP3 causes inc in intracellular Ca

Diabetes insipidus

Excess water loss in urine, inc volume of urine, hypernatremia, high plasma osmolality; 2 types (pituitary/neurogenic: failure to produce/release AVP, nephrogenic/AVP resistant) Ex: Brattleboror rat doesnt produe AVP due to mutuation

Syndrome of inappropriate vasopressin secretion

Continual AVP release independent of plasma osmolality; sxs: dec urine volume, hyponatremia, hypoosmality

Opiomelanotropins

aMSH from larger precursor; Peptides from pro-opiomelanocortin (POMC), heptapeptide sequence conserved

aMSH cleared from ACTH sections of POMC

Pars distalis (corticotrophs) -> ACTH; Pars intermedia (melanotrophs) ->ACTH and enzymes to break down ACTH to aMSH --> aMSH and CLIP

Pars intermedia

source of melanotropins; present in cyclostomes, amph, reptile and most mammals (well defined pars intermedia or lobe wtih MSH secreting cells); not present in birds, whales/dolphins, adult humans (present in fetus)

Chromatophores

pigment containing cells, present in all vertebrates, prominent in poikilotherms (dont use metabolism to regulate temp); fxns: camo, warning signals, sexual states, thermoreg, protection from solar radiation; ex: veiled chamelion

Melanophores

Melanin pigment; eumelanins (black/brown) and pehomelanins (yellow/red); pig's in melanostomes (fully melanized organelle); located in dermis/epidermis

Xanthophores

yellow/orange/red pigments; carotenoids/pteridines; located in dermis

Iridiphores

Iridescent pigment: reflects light, contains crytal purines; located in dermis

Physiological color change

rapid(min), pigment aggregates/disperses, typical of poikiotherms; change color with background; Affected by aMSH (MSH absent: light skin, MSH present: skin dark)

Dermal chromatophore unit

integrated functional units; important in rapid color change in amphibians and reptiles (ex: green anole lizard, brown vs green)

aMSH present

MSH binds to melanocortin1 receptor; inc in cAMP dec "free" Ca2+ causing relaxation of melanofilaments which allow melanosomes to spread, causing skin to darken

aMSH absent

dec in cAMP increase free Ca2+ causing contraction of melanofilaments whic hpull melanosomes into smaller area, causing lightened skin

Morphological color change

slow (days/weeks), inc pigment/# pigment cells, involves epidermal melanophores, aMSH stimulates melanin sythesis and/or inc number of melanophores

Epidermal melanin unit

consists of melanocyte and epidermal cell; impt in human skin/hair color, aMSH in humans not controlling amt of pigment produced usually, aMSH does play a role in other mammals

Pelage

fur color in mammals; ex: short tailed weasel, white fur in winter (inc aMSH), brown fur in summer (dec aMSH)

MSH stimulation of melanin sythesis

tyrosinase improtant in formmation of DOPA which is basic structure leading ot melanin

Neuro control of aMSH

inhibition (Dop hyperpolarizes aMSH secreting cells and inhibits MSH release) stimulation (Acetylcholine depolarizes MSH secreting cells and stimulates MSH release)

Color change with background

High albeto, inc reflectance, dec MSH, lighter skin; low albeto, dec reflectance, inc MSH, dark skin::: inc survival in dft environments

Neuroendocrine reflex regulating pigment dispersion

dark backgroun -> inhibit dopamine, inc MSH, dark skin; light backgroun, CNS stimulates dopamine, dec MSH, light background ::: track from retina through brain

Adrenal gland

human (MSH causes development of fetal zone prior to birht, ACTH causes development of cortex after birth) sheep (switch from MSH to ACTH increasing cortisol sythesis, which induces birth of lamb)

Food intake and MSH

aMSH binding to melanocortin4 reduces food intake (inc leptin, inc MSH); inhibition of Mc4r causes overeating and obesity (Agouti protein inhibits Mc4r)

Serum Ca

about 10mg/ml; free Ca biologically active; low Ca causes tetany (twitches)

Factors affecting serum Ca balance

GI absorption; storage in bone as Ca10(PO4)6(OH)2 (80% Ca in bone); relationship to P: [Ca] x [PO4] = K; PO4 stored in bone/tissue not carefully regulated

Hormones regulating Ca

Parathyroid (PTH), Calcitonin (CT), 1a,25dihydroxyvitamin D3 [1,25(OH)2D3] = VitD = calcitrol

PTH - parathyroid horm

polypeptide essential for life; fxns to inc blood CA levels, produced by chief cells of parathyroid gland;

Regulation of PTH release

low Ca2+ stimulates, high Ca2+ inhibits, 1,25(OH)2D3 inhibits PTH synthesis

Important bone cells

osteoblasts (new bone formation); osteoclasts (bone breakdown, 18% Ca in bone now replaced in one year)

PTH action on bone

increase Ca mobilization from bone; stimulate osteoblasts to release osteoclast diff inducing factore (IL-6) that cause osteoclasts to release acid proteases whichd digest bone matrix; stimulates differentiation of precursor cells to osteoclasts

PTH action on kidneys

inc tubular reabsorption of Ca into ascending loop of Henle; inc excretion of PO4, inhibits H+ secretion into tubules; inhibits bicarb reabsorption

PTH action on intestine

acts indirectly to inc CA2+ and PO4 uptake by activating 1a-hydroxylate enzyme required to form 1a,25(OH)2D3

PTH related peptide (PTHrp)

hypercalcemic agent produced by tumors, nl physio fxns in growth and development (inc fetal serum Ca, tooth eruption, mammary gland development)

Calcitonin (CT)

dec blood Ca by acting on bone to inhibit osteoclast activity; produced by C cells (parafollicular cells that arise from ultimobranchial glands in mammals, migrate to thyroid gland) located in thyroid gland

Regulation of CT release

Inc Ca stimulates release; gastrin stimulates release

Physiological fxns

prevent hypercalcemia after meals; mineralization of bone in pre-weaning young; protect against Ca loss in pregnancy, lactation and prolonged Ca deprivation

Vitamin D3/D2

Prehormones for 1,25(OH)2D3; Vit D3 (cholecalciferol) synthesized in skin from 7-dehydrocholesterol upon exposure to UVB, also in animal tissue; Ergocalciferol (D2) from plants can be used to form 1,25(OH)2D3

1a,25(OH)2D3

biologically active horm affecting Ca, synthesized from Vit D3, Vit D3 from diet/skin exposed to UV light

Formation of Vit D3

7-dehydrocholesterol: from liver to skin: is converted to Vit D3, enters blood, binds to protein, adds hydroxyl groups

Synthesis of 1,25(OH)2D3

Vit D3 binds to transcalciferin in blood, goes to liver with 25,hydroxylate forming 25(OH)Vit D3; blood moves to kidneys and reacts wtih 1a-hydroxylate stimulated by PTH, forming active 1,25(OH)2D3

Fxs of 1,25(OH)2D3

Intesting (stimulate sythesis of Ca-binding protein, inc # Ca channels) :: Kidney (inc Ca reabsorption) :: Bone (accretion of new bone during remodeling) :: PT gland ( inhibits PTH synthesis)

Feedback control of 1,25(OH)2D3

synthesis requiring sunlight; active hormone to gut causes + action of Ca and PO4; bone/kidney inc effects of reabsorption Ca/PO4; Ca to O high -> neg feedback, inhibits release from PTH

Binding of 1,25(OH)2D3 to HSPs

Can form heterodimers, ect

Hypoparathyroidism

dec in release of PTH; causes tetany and convulsions; tapping facial muscles detects latent tetany; pseudohypoparathyroidism - nl PTH levels, low Ca levels, failure to generate cAMP

Osteoporosis

dec bone density due to demineralization; postmenopausal (type 1) -- dec steroid hormone; senile (type 2) - lack of Vit D :: spinal osteoporosis - loss of mineralization, compression of vertebrae

Failures in nl bone mineralization

rickets (failure in kids) osteomalacia (in adults) Paget's dz ( weak bones due to excessive osteoclasts)

Therapies for Ca loss dz

CT tx; Biphosphonates (fosamax, boniva, actonel); selective estrogen recetpor modulator (SERMS); topical Vit D; lifestyle modifications (weight bearing exercise/ Ca uptake)

Fxn of GI hormones in digestive movements

enzye, acid/base secretion; smooth muscle contraction; horm release from pancreatic islets; growth promoting actions

Location of GI horms

distributed diffusely; clear cells tained by silver or chromium salts; termed: argyphil cells, argentaffin cells, enterochromaaffic cells, or enterochromaffin like cells(ECL); GI and pacreatic horms = gastroenteropancreatic horms

Gastrin family

gastrin (G) and cholecystokinin (CCK); share same 5AA at carboxyl end

CCK and G receptors

CCK-A in pancreas acinar cells, CCK-B in brain and stomach, G receptor similar to CCk-B

Mech of gastrin

CCK & G inc IP3 which inc free Ca2+, evolved from a CCk ancestral molecule :: fish/amph only have CCk, reptiles/birds/mammals have CCK and G

Secretin family

Secretin, glucagon, gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP); share AA sequences; inc cAMP

Gastrin release

food (peptides, AA, IFA), distention of stomach, activity of vagus nerve (GRP) inhibited by SST

Gastrin fxns

Primarily to increase HCL (release of H+ from stomach parietal cells) directly and indirectly (via stimulataing HCL cells to release histamine that stimulates the parietal cells via H2 receptors); inc calcitonin release and gastric mucosal growth

Cholecystokinin (CCK)

Produced by I cells of duodenum; stimulus for release: HCL, AA, FAs

CCK fxns

gallbladder contractions, relaxation of sphincter of oddi, inhibition of gastric emptying, inc pancreatic enzyme secretion and bicarb secretion, stimulates growth exocrine pancreas

CCK and feeding

inhibits feeding behavior; bulemic people release les CCk than nl people; anorexia of aging inc sensitivity to CCK and dec feeding

Secretin

S cells of dueodenum synthesize them; acid stimulates release (not release when pH >4.5)p; inc bicarb secretion from pancreas

GIP - gastric inhibitory peptide

aka glucose-dependent insulinotropic peptide, enterogastrone; made in K cells, small intestine; stimulus for release are fats and glucose

Fxn of GIP

insulin release in response to glucose; inhibits gastric acid secretion; anabolic action on adipose cells (FFA to triglycerides);

Glucagon like peptide-1 (GLP-1)

intestinal peptide encoded in proglucagon gene; produced by L cells of the intestine; stimulates insulin release in presence of glucose and suppresses glucagon secretion

Vasoactive Intestinal peptide (VIP)

in neurons of CNS and ANS; has vasodilator and hypotensive effects; mediates descending relaxation component of peristaltic reflex

Tumors

most originate in pancreatic islets and secrete insulin, glucagon, sometimes gastrin and VIP; Gastrin secreting tumor (gastinoma) -> Zollinger-ellison syndrome (ulcers); VIP secreting tumor (vipoma) -> pancreatic cholera (watery diarrhea); CCK in required for gallbladder fxn, pentagastrin for gastric acid secretion

Cells and hormones of islets of Langerhans

B cells (insulin) a cells (glucagon) D cells (SST) F cells (PP, pancreatic polypeptide)

Distribution of cells

B cells surrounded by a cells and SST secreting cells; blood flow from B to a cells, gap junctions

Glucose homeostasis

Flux in and out of blood in a controlling point; balance of glucose production and utilization; hormone regulators: insulin, glucagon, cortisol, epi, GH; improtant tissues that regulate glucose; liver, adipose tissue, muscle

Insulin

hypoglycemic hormone that dec BSG levels, inc m/m of glucose into cells

Glucagon

hyperglycemic horm that inc BSG levels, inc glucose m/m into blood, dec storage/utilization of glucose in cells :: Cortisol, GI, Epi also hypoglycemic hormones

Anabolism

insulin stimulates, glucagon inhibits; fuel source: diet; glycogenesis, lipogenesis, protein sythesis

Catabolism

insulin inhibits, glucagon stimulates; fuel source: storage depots; glycogenolysis, lipolysis, proteolysis

Gluconeogenesis

Glucose preduction from noncarb carbon substrates: AA from proteins, glycerol from fats

Glucose sparing

using substances other than blucose to generate energy: FFA from fats

Amino acids

glucogenic AA can be converted to carbs: alanin and glutamine most impt, leucine and lysine cant be used

Alanine transamination

Converts alanine to pyruvic acid which produces glucose (gluconeogenesis) and acetyl CoA (glucose sparing)

Triglycerides

Broken down by lipases to glycerol and FFA; Glycerol converted to glucose by gluconeogenesis, FFA converted to acetyl CoA by glucose sparing

Ketone bodies

Acetone, Acetoacetic acid, B-hydroxybutyric acid

Insulin sxr

2 chains (A chain, 21AA, B chain, 30 AA), 2 inter-chain disulphide bridges

Insulin metabolism

Haptic blutathione insulin dehydrogenase (liver) separates A and B chains; half life is about 5 min

Insulin action

RK activated receptor phosphorylates tyrosines of proteins; Glucose transporter systems;

GLUT-2:

insulin insensitive, in the liver and pancreas, bi-directional transport, direction depends on glucose concentration

GLUT-4

insulin sensitive; in skeletal and cardiac muscle, adipose tissue; insulin causes 20-40 fold inc in glucose transport rate; 80% of insulin mediated glucose uptake in skeletal muscle

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