PHYS 335 Unit 2

Tropic vs. Trophic Action

Tropic: affect secretion of another hormone Trophic: promote the growth and development of targets

Steroid Hormones -properties -characteristics

HYDROPHOBIC: 1. Major form found in plasma: attached to protein 2. Location of Receptors: intracellular 3. Most Common Signaling Mechanism: -intracellular receptors alter gene transcription 4. Rate of Excretion/Metabolism: slow (hours/days) 5. Synthesized from CHOLESTEROL molecules; source material: (presence or absence of specific enzymes in specific location of the cortex determines what hormone is ultimately produced) 6. Synthesized in either: -Adrenal Cortex: A. Cortisol B. Aldosterone -Gonads: A. Testerone B. Estradiol C. Progesterone Enzymatic modification: (testosterone --aromatase--> estradiol)

Early to Middle Follicular Phase Hormonal control

Hypothalamus: --GnRH-- v Anterior Pituitary: --FSH and LH-- v Ovaries: 1.FSH acts on Granulosa cells to secrete Inhibin and influences oocytes 2. LH acts on Theca cells to secrete Androgens 3. Androgens and Granulosa cells produce Estrogen v Reproductive Tract and other organs: -respond to estrogen- FEEDBACK: 1. Estrogen has local positive feedback on Granulosa cells 2. Inhibin has negative feedback on anterior pituitary, inhibits secretion of FSH 3. Estrogen has negative feedback on Hypothalamus and Anterior Pituitary 4. Both estrogen and progesterone needed to inhibit LH

Myosin vs. Actin -structural -functional

MYOSIN: thick filament - extension called cross bridges span gap between thick and thin filaments -each cross bridge has 2 globular heads that contain a binding stie for actin and extend towards overlapping actin; enzymatic site that splits ATP (myosin ATP-ase) -each cross bridge head has two binding sites- one for actin and on for ATP, ATP binding site serves as an enzyme that hydrolyzes ATP ACTIN: think filament -anchored to z-lines at each end of sarcomere -free ends overlap with myosin in the A band at the center of sarcomere -contains Troponin and Tropomyosin.

Anterior vs. Posterior Pituitary Gland secretions: -hormones name -abbreviation -major target/effect on body

POSTERIOR PITUITARY GLAND: 1. *Oxytocin*; contraction of uterine smooth muscle during birth milk secretion from breast tissue upon suckling, bonding behaviors in both male/female 2. *Anti-directuric Hormone* (ADH) (Vasopressin): water retention via kidney - ADH, constriction of smooth muscle in blood vessels -vasopressin ANTERIOR PITUITARY GLAND: 1. GnRH: gonads 2. GHRH: liver, organs 3. SST: liver, organs 4. TRH: thyroid 5. DA: Breasts 6. CRH: adrenal cortex

Major ovarian events during menstrual cycle -follicular phase -luteal phase

*28- day cycle is elaborate hormonal pacemaker starting at puberty and stopping at menopause (can be interrupted by pregnancy & medication) *with onset of puberty, ovary alternates between 2 phases: FOLLICULAR PHASE: produce mature follicle 1. bleeding begins 2. multiple follicles develop 3. one follicle becomes dominant 4. Dominant follicle matures OVULATION LUTEAL PHASE: prepare for pregnancy if fertilization occurs 1. corpus luteum forms and functions 2. corpus luteum degenerates >estrogen is secrete by granulosa cells and corpus luteum > progesterone secreted by granulosa and theca cells before ovulation >inhibin by granulosa cells and corpus luteum

Hormonal profile for ovarian events during menstrual cycle

*Days 1-5:* FSH and LH secretion increase as plasma estrogen concentration is low and exerting little negative feedback *Days 1-5:* multiple antral follicles begin to enlarge and secrete estrogen. androgens secreted by theca cells and granulosa cells make estrogen. *Day 5:* Plasma estrogen concentration begins to rise from enlarging theca and granulosa cells *Day 5:* One follicle becomes dominate and secretes large amounts of estrogen (dominant follicle is thought to have more estrogen synthesis) *Day 10:* Plasma estrogen increase ALOT *Day 10:* FSH secretion and plasma FSH concentration decrease causing atresia of non-dominant follicles *Day 12:* Increasing plasma estrogen exerts a positive feedback on gonadotropin secretion (hypothalamus and anterior pituitary). Increases LH secretion from Ant Pit. FSH is still inhibited by Inhibin. *Day 13:* LH surge triggered by estrogen & oocyte finishes first meiotic division *Day 14:* Ovulation *Day 17:* corpus luteum forms and begins to secrete large amounts of estrogen and progesterone. (steroid factory) *Day 21:* plasma estrogen and progesterone increase *Day 23:* FSH and LH secretion are inhibited and plasma concentration decrease, estrogen and progesterone exert negative feedback on the hypothalamus and anterior pituitary *Day 25:* Corpus luteum begins to degenerate and decrease its hormone secretion *Day 26:* Plasma estrogen and progesterone concentrations decrease as the corpus luteum dies from low LH concentrations (negative feedback) *Day 27:* FSH and LH secretions begin t increase and new cycle begins ( no more negative feedback)

Hypophysiotropic Hormones of the Hypothalamus -name -abbreviation -chemical class -affect on anterior pituitary -major target/effect on body

*all tropic* 1. Gonadtropin releasing Hormone (GnRH): peptide hormone; AP releases FSH and LH (gonadotroph cells); targets gonads to for germ development and secreting hormone (estradiol, progesterone, testerone) 2. Growth Hormone Releasing Hormone (GHRH): peptide hormone; AP releases GH (somatotroph cells); targets organs for protein synthesis and carb and lipid metabolism, ALSO targets liver to release hormone IGF-1 (insulin like growth factor) 3. Somatostatin (SST): peptide hormone; AP inhibited the release of GH (somatotroph cells); target cells do not release IGF-1 and no protein synthesis 4. Thyroid Releasing Hormone (TRH): peptide hormone; AP releases TSH (thyrotroph cells); targets thyroid to secrete T3 and T4 hormones 5. Dopamine (DA): catecholamine hormone; AP releases Prolactin (lactotroph cells); targets breasts to increase milk production and stimulates development 6. Cortisol Releasing Hormone (CRH): peptide hormone; AP releases ACTH (corticotroph cells); targets adrenal cortex to release cortisol from the zona fasciulata

Functions of cortisol -unstressed -stressed

*cortisol is necessary for life* UNSTRESSED (Physiological): 1. metabolic effects: liver glucose production between meals (maintains enzymes involved in metabolic homeostasis)- glucocorticoid 2. permissiveness of adrenergic receptors in CV system (maintain adequate mean arterial blood pressure) 3. Anti-inflammatory and anti-immune (prevent hyper-response) 4. fetal development of brain, intestines, lungs, glands, production of surfactant in last months of gestation 5. maintain responsiveness of target cells to epinephrine, and norepinephrine STRESSED: 1. Metabolic effects: glucose sparing- metabolic shift of glucose usage to CNS away from body cells; mobilize glucose, FA, AA for fuel and tissue repair -- gluconeogenesis , lipolsis, decrease in insulin 2. Bone resorption: Ca2+ mobilization- breaking down of bones to mobilize Ca2+ for bone break prevention, prolonged leads to osteoporosis 3. Support sympathetic responses (flight, fight) keep MAP up, if prolonged high blood pressure 4. Stimulates erythropoietin (hormone from kidneys that replaces RBCs) bleeding wound, if prolonged polycythemia- many cells in the blood 4. Inhibits non-essential functions (reproduction, growth) 5. Enhanced vascularization 6. Anti-inflammatory/ Immunosuppression (helps in treatment to prevent rejection of transplanted organs) 7. Psychological/Analgesic: cortisol elevates mood (giddy), endorphins co-released with ACTH; inhibits pain

Stress stimuli

- surgery -trauma -cold -heavy exercise -infection -shock -low O2 supply -starvation -sleep deprivation -pain -fear -strong emotions

Steps between motor neuron action potential and skeletal muscle fiber contraction

1. AP is initiated and propagates to motor neuron axon terminal 2. Ca2+ enter axon terminal through voltage-gated channel 3. Ca2+ entry triggers release of Ach via exocytosis from terminal 4. Ach diffuses from terminal to motor end plate in muscle fiber 5. Ach binds to nicotinic receptor on motor end plate, increasing permeability of Na+ and K+ 6. more Na+ rushes into fiber than K+ moves out, depolarizing membrane and producing end-plate potential (EPP) which is large graded potential 7. local currents depolarize adjacent muscle cell plasma membrane to its threshold potential, generating AP that propagates over the muscle fiber surface and into the fiber along the T-tubules inside. 8. AP in T-tubules induces DHP receptors to pull open ryanodine receptor channels, allowing release of Ca2+ from terminal cisternae of SR 9. Ca2+ binds to troponin on the thin filaments, causing tropomyosin to move away from blocking position, uncovering cross-bridge sites on actin 10. energize myosin cross-bridges on thick filaments bind to actin [A + M * ADP * P] to [ A * M * ADP * P] 11. Cross-bridge binding triggers release of ATP hydrolysis products from myosin, producing an angular movement of each cross-bridge: [A * M * ADP * P] to [A * M + ADP + P] 12. ATP binds to myosin, breaking linkage between actin and myosin and thereby allowing cross-bridges to dissociate from actin: [A * M + ATP] to [A + M * ATP] 13. ATP bound to myosin is split, energizing the myosin cross-bridge: [A + M * ATP] to [A + M * ADP * P] 14. Crossbridges repeat 10-13 producing movement (sliding) of thin filaments past thick filaments. Cycles of cross-bridge movement continue as long as Ca2+ remains bound to troponin 15. Cytosolic [Ca2+] decreases as Ca2+ - ATPase actively transports Ca2+ back into SR 16. Removal of Ca2+ from troponin restores blocking action of tropomyosin, cross-bridge cycle ceases and muscle fiber relaxes

Disrupt Neuromuscular Junction 1. BoTox 2. Curare 3. Organophosphates

1. BoTox: protease inhibits Ach release by eating up the SNARE proteins that exocytosis Ach into synaptic cleft 2. Curare- poison (AchR antagonist): aka rocuronium and vecuronium; strongly binding to N-Ach receptor, doesn't open channel and block Ach binding to receptor. No EPP in motor end plate = no contraction, cannot breathe and paralysis 3. Organophosphates- pesticides, nerve gases: Ach released normally and binds to end plate but is not degraded (destroyed in the synaptic cleft); ion channels remain open and maintained depolarization. Receptors become desensitized causes paralysis

distinguishing features of 3 muscle types

1. Cardiac- heart -striated (rods) -single nucleus 2. Skeletal- attached to bones - striated (rods) -multi-nucleated -large diameter 3. Smooth- surrounds hollow cavities/tubes -smooth, spindles -single nucleus

Long Bone Growth

1. Cartilage being laid down in the plates by chondrocytes. -Hyperplasia: chondrocytes undergoing cell division at the top of epiphyseal growth plate -Hypertrophy: older chondrocytes enlarging, making cartilage 2. Simultaneously, osteoblasts at the shaft edge convert cartilage to bone As the plate gets wider, the bone gets longer -Epiphyseal Closure: Growth plates "fuse" after prolonged exposure to sex steroids (estrogen and testosterone) Growth stops when plates are completely converted to bone.

Hormonal Events in Late Follicular phase leading to LH surge

1. Dominant follicle matures and secretes lots of estrogen 2. increasing estrogen switches to positive on gonadotropin secretion 3. LH surge is triggered Hormal flowchart: Hypothalamus: --GnRH-- v Anterior Pituitary Gland: --LH and FSH-- v LH surge FSH continues to act on granulosa cells to secrete inhibin and estrogen FEEDBACK: 1. inhibin has negative feedback on ant pit to inhibit FSH (no "FSH surge") 2. Estrogen has positive feedback on hypothalamus and Ant Pit to secrete more LH *this induces ovulation then.. LUTEAL PHASE: rupture of follicle and corpus luteum forms causing a decrease in LH and FSH, creating a decrease in estrogen and an increase in progesterone

Sertoli Cells - functions

1. FSH stimulates sertoli cells (granulosa cells) 2. regulate spermatozoa maturation; form tight junctions from unbroken ring around the outer circumference of the semiferous tubule (blood-testes barrier) 3. "nurse cells" - nourish developing sperm Functions: 1. provide barrier to chemicals in plasma (sperm not considered "self") 2. Nourish developing sperm 3. Secrete luminal fluid, including androgen binding protein 4. Respond to stimulation by testosterone and FSH to secrete paracrine agents that stimulate sperm proliferation and differentiation 5. Secrete the protein hormone inhibin, which inhibits FSH secretion from ant pit 6. Secrete paracrine agents that influence the function of Leydig cells 7. Phagocytize defective sperm 8. Secrete anti-mullerian hormone (AMH), causes the primordial female duct system to regress during embryonic life.

Roles of ATP in skeletal muscle contraction

1. Hydrolysis of ATP by the Na+/K+-ATPase in the plasma membrane maintains Na+ and K+ gradients, which allows the membrane to produce and propagate AP 2. Hydrolysis of ATP by Ca2+-ATPase in SR provides the energy for the active transport of Ca2+ ion into the reticulum, lowering cytosolic [Ca2+] ending contraction and allowing muscle to relax 3. Hydrolysis of ATP by myosin-ATPase energizes the cross-bridges providing energy for force generation 4. Binding of ATP to myosin dissociates cross-bridges bound to actin allowing the bridges to repeat cycle.

Steps of thyroid hormone synthesis, storage, and secretion

1. Iodide is co-transported with Na+ into the follicle cell from the interstitial fluid 2. Iodide is diffuse from the follicular cell (shoreline) to the colloid (lake) 3. Iodide is transported to colloid, oxidized and attached to rings of tyrosine (thyroid hormones derived from tyrosine) on thyroglobulin (TG-has tyrosine) 4. Another iodinated ring is added to the first. to make T3, T4 5. Release molecule from storage in the colloid (lake) via endocytosis to follicular cell (shoreline) of thyroglobulin protein containing T3 and T4 6. Lysosomal enzymes release T3 and T4 hydrophobic hormones from TG protein 7. T3 and T4 are secreted from the follicular cell (shoreline) to the bloodstream 8. TG is recycled 9. Free thyroid hormone bound to carrier in blood *all synthetic steps in T3 and T4 are stimulated by TSH (uptake of iodide where it is trapped in follicle) *TSH causes growth (hypertrophy) of thyroid tissues

Leydig Cells (interstitial cells)

1. LH stimulates leydig cells (theca cells) 2. in small connective tissues between tubules secrete testosterone 3. make and release androgen steroids

Long Bone Anatomy

1. Long bones elongates at growth "plates" next to their epiphyses where rapid mitosis and differentiation occur under the influence of BOTH local and circulating hormones to convert cartilage to bone.

Neuromuscular Junction events

1. Motor neuron axon potential travels to axon terminal 2. Ca2+ enters voltage gated channels in axon terminal 3. Ach released via exocytosis 4. Ach binding opens ion channels 5. Na+ enters through ion channels and depolarizes muscle fiber (end plate potential) *EPPs occur along entire motor end plate 6. Local current between depolarized end plate and adjacent muscle plasma membrane 7. Muscle fiber AP initiation 8. AP propagates in muscle plasma membrane down T-tubule , AP can travel in both directions since synapse is in the middle of the muscle fiber *a single AP sufficient to produce AP in skeletal muscle fiber [EPPs are HUGE graded potentials, 1 alpha motor neuron per 1 motor fiber is a safety factor] *EPPs are always excitatory (inhibition come from CNS) * synapse can be disrupted by toxins, drugs, disease

Functional anatomy of female reproductive system

1. Ovary: -oogenesis (maturing ovum=egg) - steroid sex hormone secretion (estrogen and progesterone) 2. Fallopian tubes (oviducts)- allowing for tavelling of egg by the current in fimbriae 3. Uterus- source of menstrual flow and fetus development -endometrium (shed monthly) -myometrium (contracts during labor) 4. Cervix- opening of the uterus, can cause mucus plug 5. Vagina 6. Fimbriae- fingerlike projects that create current to move egg

Hydrophilic Hormones: receptor locations

1. Plasma-bound hydrophilic molecules unable to diffused through lipid bilayer

Gametogenesis: Ovaries

1. Primary Oocyte: 46 chromosomes 2. First meiotic division includes crossing over- nonsister chromatids exchange 3. Homologous chromosome pairing - one chromosome from each pair 4. Secondary Oocyte : 23 chromosomes with 2 chromatids and First polar body (23 chromosomes-just DNA no cytoplasm) 5. Second meiotic division -- occurs after fertilization 6. Zygote (46 chromosomes), and second polar body (23 chromosomes) *polar bodies degenerate

Gametogenesis: Testes

1. Primary Spermatocyte: 46 chromosomes 2. First meiotic division includes crossing over- nonsister chromatids exchange 3. Homologous chromosome pairing - one chromosome from each pair 4. Secondary Spermatocyte : 23 chromosomes with 2 chromatids 5. Second meiotic division -- occurs after puberty 6. Spermatids with 23 chromosomes with 1 chromatid 7. Sperm Cells

steps of the Crossbridge Cycle

1. Resting muscle: -Actin and myosin not bound. Tn pushing on Tm to cover binding sites. -Energized cross-bridge on myosin with ADP + Pi attached [A + M * ADP * P] 2. [Ca2+] rises and cross-bridge binds to actin; myosin head bending touching actin [ A * M * ADP * P] 3. Powerstroke: ADP + P released and cross-bridge moves [A * M ] 4. ATP binds to myosin causing cross-bridge to detach [A + M * ATP] 5. Hydrolysis of ATP energizes cross-bridge [ A + M * ADP * P] -if you die, rigor mortsis occurs No ATP is available to detach cross-bridge after the powerstoke thus actin and myosin stay bound together = stiffening of muscles [A * M] as plasma membrane degrades and myosin becomes naked detaches cross-bridge without the use of ATP *repeat cycle, each cycle produces small increment of movement

Peptide hormones sequential synthesis and secretion

1. SYNTHESIS: Occurs on ribosomes of endocrine cells. Peptide hormones are processed by enzymes from *preprohormones* containing a signal peptide, to *prohormones* 2. PACKAGING: Occurs by the Golgi. Prohormone processing results in one or more active hormones that are stored in secretory vesicles. STORAGE: hormone is stored in secretory vesicle until needed. SECRETION: hormone is exocytosis with any "pro" fragments . Ex: Insulin is synthesized as a preprohormone that is cleaved to a prohormone. A proteolytic enzyme cleaves the prohormone into insulin and C-peptide, this results in two chains of insulin, connected by disulfide bridge.

Effects of Progesterone in female:

1. converts the estrogen-primed endometrium to an actively secreting tissue suitable for implantation of an embryo 2. Induces thick, sticky cervical mucus 3. Decreases contractions of fallopian tubes and myometrium 4. Decreases proliferation of vaginal epithelial cells 5. Stimulates breast growth, particularly glandular tissue 6. Inhibits milk-inducing effects of prolactin 7. Has feedback effects on hypothalamus and anterior pituitary gland 8. Increases body temp

Five Important characteristics of hormone receptors

1. determine which tissues respond to an endocrine "broadcast" 2. High sensitivity (10-12 M) 3. Huge signal amplification - because of signal transduction mechanisms (2nd messengers) 4. Hormone levels influence expression of their ownPos receptors: - High [H]: down-regulation (decrease receptor number) - Low [H]: up-regulation (increase receptor number) 5. Permissive effect on expression of other hormones' receptors

Male testis Anatomy

1. efferent ductules: penetrate covering of testes 2. Epididymis: collection of efferent ductules into vas deferens 3. Seminiferous tubule: makes sperm ; contain sertoli cells and leydig cells 4. Rete testis: collection point Tubular wall is composed of developing germ cells and supporting cells (sertoli)

Hydrophobic Hormones: receptor locations

1. intracellular hydrophobic molecules are able to diffuse through lipid bilayer

Granulosa cell function during menstrual cycle

1. nourish oocyte 2. secrete chemical messengers that influence the oocyte and theca cells 3. secrete antral fluid 4. site of action for estrogen and FSH in the control of follicle development during early and middle follicular phases 5. express aromatase, which converts androgen (theca cells) to estrogen 6. Secrete inhibin, which inhibits FSH secretion via action on anterior pituitary gland 7. site of action for LH induction of changes in the oocyte and follicle culminating in ovulation and formation of the corpus luteum

Days 7-12 in menstrual cycle

1. plasma estrogen increases because of secretion by the dominant follicle -larger granulosa and theca cells secreting androgens and converting to estrogen via aromatase Therefore: - endometrium stimulated to proliferate (grow) 2. LH and FSH decrease due to estrogen and inhibin negative feedback Therefore: -degeneration (atresia) of nondominant follicles occur

Consequences of LH surge

1. primary oocyte completes first meiotic division and undergoes cytoplasmic changes that prepare ovum for implantation for fertilization (proliferation -snuggly nest); LH effects on oocyte are mediated by messengers released from granulosa cells 2. Antrum size (fluid volume) and blood flow to follicle increase ALOT 3. Granulosa cells begin releasing progesterone and decreasing release of estrogen, accounts for midcycle decrease in [estrogen] and small rise in [progesterone] before ovulation 4. Enzymes and prostaglandins synthesized by granulosa cells, break down in the follicular ovarian membranes. Weakened membranes rupture allowing the oocyte and surrounding granulosa cells to be carried out on to the surface of ovary. 5. remaining granulosa and theca cells of ruptured follicle transformed in to corpus luteum, begins releasing progesterone and estrogen.

Effects of Testosterone in Male

1. required for initiation and maintenance of spermatogenesis (acts via Sertoli cells-local feedback) 2. negative feedback on hypothalamus decreases GnRH secretion 3. Inhibits LH secretion via a direct action on the anterior pit gland 4. Induces differentiation of male accessory reproductive organ and maintains their function 5. Induces male secondary sex characteristics; opposes action of estrogen on breast growth 6. Stimulates protein anabolism, bone growth, and cessation of bone growth (bone plates fuse) 7. Required for sex drive and aggressive behavior 8. Stimulates erythropoietin secretion by kidneys

Transport of Sperm

1. semiferous tubules, sperm passes to epididymis concentrated and become mature 2. epididymis and van deferens store sperm, seminal vesicles and prostate semen 3. erection occurs 4. ejaculation includes emission- empty semen in urethra andexpulsion of semen from urethra

Effects of Estrogen in female:

1. stimulates growth of ovary and follicles (local effects) 2. stimulates growth of smooth muscle and proliferation of epithelial linings of reproductive tract; in addition: -fallopian tubes: increases contractions and ciliary activity -uterus: increases myometrial contractions and responsiveness to oxytocin; stimulates secretion of abundant watery cervical mucus; prepares endometrium for progesterone's actions by inducing progesterone receptors -vagina: increases layering of epithelial cells 3. stimulates external genitalia growth, (puberty) 4. stimulates breast growth (ducts and fat deposition during pregnancy) 5. stimulates female body configuration development during puberty; narrow shoulders, broad hips, female fat distribution (deposition on hips and breasts) 6. stimulates fluid secretion from lipid (sebum) producing skin glands (sebaceous glands) - anti-acne effects 7. stimulates bone growth and ultimate cessation of bone growth (closure of epiphyseal plates); protects from osteoporosis; doesn't have anabolic effect of skeletal muscle 8. vascular effects (deficiency = hot flashes) 9. Feedback effects on hypothalamus and anterior pituitary gland 10.s stimulates prolactin secretion but inhibits prolactin's milk-inducing action on breasts 11. protects from atherosclerosis (cholesterol)

Day 25-28 of menstrual cycle

Corpus luteum degenerates (if implantation of embryo doesn't occur) Therefore: 1. plasma estrogen and progesterone concentrations decrease rapidly Thus: endometrium begins to slough at conclusion of day 28 and new cycle begins.

Uterine changes during menstrual cycle

3 uterine phases aline with 2 ovarian phases: 1. Menstrual 2. Proliferative 3. Secretory -restart cycle- 1. Menstrual FOLLUICULAR PHASE: 1. MENSTRUAL: *Days 5-7:* -corpus luteum degrades causing decreased estrogen and progesterone causes the release of potent prostaglandins, which cause vasoconstriction of uterine blood vessels. Then dilation and hemorrhage. -endometrium dies and sloughs off and exits body. -endometrial thickness decreases 2. PROLIFERATIVE: *Days 5-15:* -increase estrogen stimulates growth/proliferation of endometrium, glands, blood vessels of endometrium and myometrium -increase in theca cells -endometrial thickness increases LUTEAL PHASE: 3. SECRETORY/PROGESTATIONAL: *Days 15-28:* -increased progesterone -endometrium and myometrium is thickened even further -increased vascularization -becomes filled with stored glycogen to support embryo -when implantation can occur -If no embryo is implanted corpus luteum dies and cycle restarts -inhibit uterine contactions -progesterone acts upon estrogen-primed endometrium to convert it to an actively secreting tissue

Catecholamine Hormones -properties -characteristics

HYDROPHILLIC: 1. Major form found in plasma: free (unbound) 2. Location of Receptors: plasma membrane 3. Most Common Signaling Mechanism: -2nd messengers (ex: cAMP, Ca2+) -enzyme activation by receptor (ex: JAK) -intrinsic enzymatic activity of receptor (ex: tyrosine autophosphorylation) 4. Rate of Excretion/Metabolism: fast (minutes) 5. Synthesized: from tyrosine KNOW: 1. Norepinephrine 2. Epinephrine 3. Dopamine

Possible fates/actions of a hormone after is is secreted by the endocrine cell

A. Endocrine cell secretes hormone B. Hormone circulates blood fates: 1. excreted in urine/feces (peptide) 2. inactivated by metabolism (catecholamine) 3. activated by metabolism (steroids) 4. target cells: bind to receptor and produce a cellular response (thyroid)

How do you distinguish primary from secondary disorder?

measurements of the hormone and any tropic hormone under both basal conditions and during experiments where there is stimulation of each hormone's secretion (first injecting tropic hormone). If gland doesn't respond to the increase in tropic hormone then you know it is primary

Sliding Filament Theory

As a muscle shortens: -cross-bridge and thin filament move = shorter muscle length - cross-bridges rotate and pull in. -Actin is being pulled into H-zone (origin) = decreasing H-zone - Actin pulls on Z-lines ( decrease length of sarcomere) - I-bands decreases as actin overlaps with myosin - A- band remains unchanged because thick myosin filaments stay same position - Z-line remains the same width *No change of myofilament length just a change in position

Cortisol hormone cascade

neural inputs v hypothalamus: --CRH-- v anterior pituitary gland: --corticotrophic cells release ACTH--- v adrenal cortex: --cortisol (steroid) -- v target cells *cortisol exerts negative feedback on the hypothalamus and the anterior pituitary gland* *epinephrine is also a stress hormone depending on type of stress

Osteoblasts

BLAST = BUILD bone forming cells at the shaft edge of the epiphysis growth plate that convert the cartilaginous tissue at edge to bone.

Neuroendocrine Signaling

neurohormones diffuse into the bloodstream and trigger responses in target cells anywhere in the body

Adrenal Gland -secretion of layers -chemical class

CORTEX: 3 layers.. 1. Zona Glomerulosa: releases aldosterone; steroid (mineralocorticoid);Kidney's Na+/K+ levels 2. Zona Fasciculata: releases cortisol and small amounts of androgens; steroid (glucocorticoid); glucose levels 3. Zona Reticularis: releases androgens (DHEA) and small amounts of cortisol; steroid; female testerone MEDULLA: releases epinephrine and norepinephrine; catecholamine

Neurotransmitter signaling

neuron or effect cell in close proximity to site of neurotransmitter release

Steroid hormones synthesis and secretion -adrenal cortex -gonads

Cortisol- glucocorticoids Aldosterone- mineralocorticoid Steps of general steroid synthesis: 1. NT binds to receptor activates G proteins to convert GDP to GTP, 2. GTP activates adenylyl cyclase to convert ATP to cAMP (2nd messenger) . 3. cAMP activates PKA to make cholesterol 4. Cholesterol goes through several enzymatic conversions to the final steroid hormone 5. steroid hormone diffuses from cell into the blood. ADRENAL GLAND: comprises of two zones... 1. Cortex: comprises of 3 layers... A. Zona glomerulosa -- Aldosterone B. Zona fasciculata -- Cortisol C. Zona reticularis -- Androgens 2. Medulla: epinephrine and norepinephrine GONADS: 1. Testes-- testosterone 2. Ovaries -- estradiol testosterone --aromatase--> estradiol

Cushing Syndrome vs. Cushing Disease

Cushing Syndrome: blanket! -chronically increased cortisol- -Primary: adrenal tumor Cushing Disease: specific -increased cortisol due to ACTH secreting anterior pituitary tumor (secondary disease) -Symptoms for both: hypertension, high blood sugar, redistribution of fat- face, obesity, muscle and bone weakness, immunosuppression, osteoporosis

Feedback effects of Estrogen, Progesterone and Inhibin

ESTROGEN: 1. low [estrogen]: negative feedback on Hypothalamus (less GnRH) and anterior pit (less FSH and LH secretion) -- early to middle follicular phase 2. high [estrogen]: positive feedback on hypothalamus (increase GnRH secretion) and anterior pit (increase FSH and LH secretion) -- results in LH surge triggers ovulation PROGESTERONE: 1. high [progesterone]: in presence of estrogen negative feedback on hypothalamus (decrease GnRH secretion) and anterior pit (decrease FSH and LH) -- results in prevention of LH surges during luteal phase and pregnancy, decrease of LH leads to death of corpus luteum INHIBIN: 1. peptide hormone released by granulosa cells that exerts negative feedback on ant pit to inhibit secretion of FSH -- no FSH surge

Reproductive roles of Estrogen vs. Progesterone 1. endometrium 2. myometrium 3. cilia/fimbria 4. cervical muscles 5. breast (pregnancy) 6. follicle 7. body temperature

ESTROGEN: 1. proliferation- follicular phase 2. increase growth of smooth muscle 3. increase activity (in sync with ovary) 4. thin, watery, lots 5. duct development 6. increase development 7. no change PROGESTERONE: 1. secretory-luteal phase 2. decrease contractility 3. decrease activity 4. viscous, little 5. lobules/alveoli (promotes milk production) 6. decrease development 7. increase by .5 Celsius

Hypo vs Hyper thyroidism -goiter

Goiter is the enlargement of thyroid gland. HYPOTHYROIDISM: not enough thyroid hormone being produced. Causes: 1. damage to thyroid gland 2. lack of iodide in the diet 3. auto-immune thyroiditis (hashimoto's)- antibodies attack thyroid gland Symptoms: low BMR, cold, fatigue, weight gain, decrease cognitive function GOITER: decreased T3 & T4; no negative feed back on TRH, increase TRH, increase TSH (has trophic action, no tropic action) HYPERTHYROIDISM: too much thyroid hormone being produced. Causes: 1. Grave's Disease- auto-immune stimulation of TSH receptors, TSI antibodies mimic TSH Symptoms: high BMR, hot, irritable, weight loss, constant fight or flight state, exopthalmos (bulging eyes) GOITER: TSI antibodies attach to TSH receptors, increase T3 & T4 hormone, negative feedback on TRH and TSH, however not antibodies, they continue to attack

Peptide/Protein Hormones -properties -characterisitcs

HYDROPHILLIC: 1. Major form found in plasma: free (unbound) 2. Location of Receptors: plasma membrane 3. Most Common Signaling Mechanism: -2nd messengers (ex: cAMP, Ca2+) -enzyme activation by receptor (ex: JAK) -intrinsic enzymatic activity of receptor (ex: tyrosine autophosphorylation) 4. Rate of Excretion/Metabolism: fast (minutes) 5. Synthesized: In ER and Golgi 6. Stored: packaged into storage vesicles (ex: insulin) *most numerous

Adrenal Insufficiency -symptoms -causes -diagnostic hormone profiles

Hypo-secretion of adrenal gland hormones 1. *Primary adrenal insufficiency:* adrenal gland (primary gland) doesn't produce cortisol or aldosterone Causes: -destructive tumors -infection (tuberculosis) - auto-immune destruction (ex: Addison's disease- adrenal destruction) Symptoms: hypotension (low bp), hypoglycemia (low blood sugar), high plasma ACTH (tropic hormone from Ant. Pit) 2. *Secondary adrenal insufficiency:* problem with trophic hormone from the Anterior Pituitary gland, ACTH Causes: -loss of ACTH in plasma Symptoms: hypotension, hypoglycemia, low plasma ACTH

Hypothalamus-Pituitary relationship

Hypothalamus regulates activity of cells in anterior lobe of pituitary gland and neurohormone release from posterior lobe of pituitary gland. ANTERIOR PITUITARY GLAND: 1. nuclei send axons to median eminence 2. Median eminence in the infundibulum is connect by blood vessels and axons 3. Tropic hormones released by hypothalamus travel through the hypothalamo-hypophyseal portal vessels to anterior pituitary glands 4. Endocrine cells in anterior pituitary gland receive hormone and increase or decrease release trophic hormone to blood circulation POSTERIOR PITUITARY GLAND: 1. Hypothalamus axons of cell bodies terminate at the posterior pituitary gland 2. Action potentials propagate from hypothalamus to posterior lobe terminals trigger exocytosis (release) of neurohormone (oxytocin or vasopressin) into blood.

Hormonal flowchart of ovarian function during luteal phase

Hypothalamus: --GnRH-- v Anterior Pituitary: --FSH and LH-- (decreasing FSH) ------------------- Ovary: --corpus luteum secretes progesterone, estrogen, and inhibin-- FEEDBACK: 1. Inibin exerts negative feedback on anterior pit to decrease FSH 2. Estrogen and progesterone exert negative feedback on hypothalamus and anterior pit to decrease GnRH and FSH and LH *increasing negative feedback from increasing levels of progesterone during early to mid luteal phase LEADS to declining LH and FSH and loss of corpus luteum thus cycle termination. corpus luteum sheds at end of menstrual cycle.

Hormonal Control of Testes and spermatogenesis

Hypothalamus: --secretes GnRH-- v Anterior Pituitary: --FSH and LH-- v Testes: 1. FSH stimulates Sertoli cells to -stimulate spermatogenesis -secrete inhibin 2. LH stimulates Leydig cells to secrete testosterone (local feedback on sertoli cells) testosterone v Reproductive Tract and other organs -respond to testosterone- FEEDBACK: 1. Testosterone has negative feedback on hypothalamus and ant pit to decrease LH 2. Inhibin has negative feedback on ant pit to decrease FSH 3. Testosterone has local positive feedback on Sertoli cells to activate spermatogenesis and produce inhibin *LH has tropic effect on testes to stimulate testosterone secretion

CONTRACTIONS: Isometric vs Isotonic -eccentric -concentric

ISOMETRIC: -muscle stays the same length -tension development -Crossbridge cycle -rotation of powerstroke of myosin head in crossbridge cycle is absorbed within the fibers elastic elements ISOTONIC: -muscle changes in length (flex or extend) -tension development -Crossbridge cycle -Types: 1. Concentric : shortening (muscle tension > load) 2. Eccentric : lengthening (muscle tension < load) (cross-bridges still cycle) TENSION: force exerted by muscle on obj

Control of estrogen synthesis during early and middle follicular phase

LH and FSH are both peptides acting on ovarian follicle LH acts on the Theca cells to synthesize androgens which diffuse to Granulosa cells and convert androgens to estrogen via aromatase FSH acts on granulosa cells Thus FSH and LH are needed for estrogen production

Days 12-13 of menstrual cycle

LH surge is induced by increasing plasma estrogen secreted by the dominant follicle (positive feedback now) Therefore: 1. oocyte is induced to complete first meiotic division and undergo cytoplasmic maturation 2. Follicle is stimulated to secrete digestive enzymes and prostaglandins

LH

Luteinizing Hormone secreted by anterior pituitary gland in response to GnRH

Growth: -Growth Hormone's effect; metabolic effect -Other hormones

MAJOR EFFECTS OF GH: 1. Promotes growth: precursor cells in bone and other tissues (liver) to differentiate and secrete IGF-1 stimulating cell division. 2. Stimulates protein synthesis 3. Metabolic-- Anti-insulin effects: -adipocytes more responsive to stimuli that induce breakdown of triglycerides release FA into blood -stimulates gluconeogenesis -reduces insulin to stimulate glucose uptake HORMONES INFLUENCING GROWTH: 1. GH: stimulates postnatal growth 2. INSULIN: stimulates fetal growth, stimulates secretion of IGF-1, stimulates prot synthesis 3. THYROID: permissive with GH secretion and CNS; trophic effects 4. TESTOSTERONE: stimulates growth at puberty by stimulating GH, causes epiphyseal closure, prot synthesis in males 5. ESTRADIOL: stimulates growth at puberty by stimulating GH, causes epiphyseal closure 6. CORTISOL: inhibits growth and stimulates protein catabolism IGF-1 can be a autocrine, paracrine, or endocrine hormone

Skeletal Muscle contraction

Muscle Contraction: generation of force, the length of the muscle may (isotonic) or may not (isometric) change in length Relaxed Muscle: low cytosolic [Ca2+] -Tn pushes Tm to cover actin binding spot -Tm blocks crossbridge binding -cross bridge is energized waiting to bind Activated Muscle: high cytosolic [Ca2+]: -Calcium binds to Tn causes conformational change in shape -Tn stops pushing on Tm, Tm naturally wants to exposed actin binding spot so Tm moves away without Tn's force -cross bridge (myosin) binds to actin and generates force *an increase in Ca2+ means the myosin cross-bridge and actin can physically interact to cause the muscle to contract (not necessarily lengthen or shorten) CONTRACTION: activation of myosin cross-bridge to exert force on the thin filaments Contraction= active force generation (with use of ATP) = Tension development

Thyroid Hormone cascade

Neural Inputs v Hypothalamus: --TRH-- v Anterior Pit: --thyrotroph cells release TSH-- v Thyroid Gland: --follicular cells release hydrophobic amines: T3 & T4-- v Target Cells: T4 converted to T3; respond to increase T3 *TSH has both tropic and trophic affect on thyroid gland* - this is why a goiter can form with excess TSH *T3 and T4 have long loop negative feedback on Hypothalamus, and Anterior Pit gland*

Development of human oocyte and ovarian follicle -purpose of each change

Ovarian function: 1. before birth, primary oocytes exist as primordial follicles. (oocyte + granulosa cells- secrete progesterone) 2. In childhood and during menstrual cycle, portion of resting primary follicles progress to pre-antrial/early antrial follicles. Pre-antrial: thicker granulosa cells, early theca cells. Early antrial: development on atrium (fluid sac) --at this point primary oocyte is still in meiotic arrest/ 10-25 progress-- 3. In growing follicles, granulosa cells (& theca) secrete estrogen --FOLLICULAR PHASE-- 4. At beginning of menstrual cycle 10-25 of the early antral follicles enlarge, only dominant follicle survives Mature follicle: only one oocyte matures; atrum increases and oocyte sits on cumulus oophorous pedistal which separates cell wall in meiotic division- secondary oocyte 5. Throughout reproductive life, only ~400 follices reach mature follicle and release the oocyte (ovulation) --LUTEAL PHASE-- - remaining cells of dominant follicle differentiate into corpus luteum which lasts 2 weeks if pregnancy doesn't occur 6. Non-dominant follices undergo "atresia" death

Spermatogenesis -Sertoli cells -Leydig cells

Process does not occur until puberty begins Spermatogonia (46 chromo; 2 chromatids) 1. Mitosis differentiation - during this stage one spermatogonia drops out and is perserved as a stem cell for the next round Primary spermatocytes (46 chromo; 2 chromatids) 2. 1st meiotic division Secondary spermatocytes (23 chromo; 2 chromatids) 3. 2nd meiotic division Spermatids (23 chromo; 1 chromatid) 4. Differentiation- sertoli cells sperm proliferation/differentiation Spermatozoa (23 chromo: 1 chromatid) -sertoli cells regulate spermatozoa maturation; tight junctions protect sperm form immune attack *no polar bodies in gametogenesis

Skeletal Muscle sarcomere -bands -lines -zones

SARCOMERE: z-line to z-line; one unit of the repeating thin and thick filament pattern within myofibril; Functional Unit Bands: I BAND: light band, composed of actin A BAND: dark band, composed of myosin, does not change length Lines: Z-LINE: border of sarcomere; centered in I-band; where actin attaches M-LINE: center of A-band and center of H-zone; protein keeps myosin in proper position Zone: H-ZONE: center of A-band, area of light in the A-band; area of naked myosin no actin overlap

Negative feedback and tropic/trophic actions of hormones in 3-gland cascade

Stimulus v Gland 1: Hypothalamus secretes hormone 1 (hypophysiotropic) in hypothalamo-hypophyseal portal vessels v Gland 2: Anterior Pituitary secretes hormone 2 in the bloodstream v Gland 3: Endocrine Gland secretes hormone 3 v Gland 4: Target cells respond to hormone 3 *hormone 1: tropic *hormone 2: often tropic, all trophic *hormone 3: actions vary *gland 3: varies, may stop here LONG LOOP NEGATIVE FEEDBACK: - hormone 3 exerts negative feedback on anterior pituitary and hypothalamus SHORT LOOP NEGATIVE FEEDBACK: - hormone 2 exerts negative feedback on hypothalamus

Reproductive physiology hormone cascade

STIMULI v Hypothalamus: --GnRH-- v Anterior Pituitary: --gonadotroph cells secrete FSH and LH-- v Gonads: *Roles:* 1. gametogenesis (ovum and sperm) 2. steroid production (ovaries secrete estrogen, progesterone) & (Testes secrete testosterone) v Reproductive tract: -respond to sex hormones- *FSH stimulates 1. females- granulosa cells to release inhibin 2. males- sertoli cells release inhibin *inhibin has negative feedback on FSH *LH stimules 1. females- theca cells to release androgens 2. males- Leydig cells release androgen steroids Androgens + granulosa cells --> Estrogen *estrogen has long-loop negative feedback on anterior pituitary and hypothalamus *estrogen has local positive feedback on FSH *estrogen can have long-loop positive feedback on anterior pituitary during the LH surge.

Growth Hormone Cascade

STIMULUS: exercise, stress, fasting, low plasma glucose, sleep v Hypothalamus: --secretes GHRH or SST-- v Anterior Pituitary Gland: --somatroph cells secrete (GHRH)/inhibit (SST) GH release-- v Liver, Bones: --by GHRH somatomedins increase IGF-1-- v Target Cells: result in stimulating protein synthesis, burning fat, bones elongating *IGF-1 exerts TWO long-loop negative feedback on the hypothalamus and anterior pituitary gland: -DECREASES GHRH --> decreasing GH -INCREASES SST --> decreasing GH

membrane structures in skeletal muscle fibers

Sarcolema (plasma membrane) sends tubular extensions (T-tubules) throughout cross-section of cell. -T-tubules (transverse tubules) interact with terminal cisternae of sacroplasmic reticulum (Ca2+ is stored) -Sarcoplasmic reticulum = smooth (longitudinal) ER, terminal cisternae (ca2+ storage) -T-tubules contain ECF fluid -SR is meshed in between T-tubules surrounding the myofibrils within the muscle fiber

Short Loop vs. Long Loop Negative Feedback

Short Loop: -hormone 2 released from the anterior pituitary gland exerts negative feedback on the hypothalamus decreasing secretion of hormone 1 Long Loop: -hormone 3 released from the endocrine gland exerts negative feedback on the anterior pituitary gland and hypothalamus decreasing secretion of hormone 2 and 1.

Isometric twitch events (Single Skeletal muscle fiber contractile mechanism)

Single Skeletal muscle fiber contractile mechanism #1: isometric twitch (no change in length of muscle) TWITCH: mechanical response of a single fiber or a whole muscle to a single AP. 1. fast twitch: short contraction time 2. slow twitch: long contraction time In a twitch there is a short latent period (when the steps of EC -coupling occur) In this experiment the length is held constant and a single stimulus is sent. Tension is measure over time. CONTRACTION PERIOD: begin of contraction (after latent period) to the peak tension Factors that affect Twitch duration: 1. speed of cross-bridge cycle (myosin enzymatic rate) 2. speed of SR Ca2+-ATPase pump

steps of skeletal muscle Excitation-Contraction Coupling

Skeletal muscle fibers actively shorten, thin filaments propelled towards the center of sarcomere by movements of myosin cross-bridge that binds to actin. STEPS: 1. AP propagated along muscle cell membrane into T-tubule (filled with ECF) 2. DHP receptor (voltage-gated sensor) in T-tubule senses depolarization from AP and pulls on Ryanodine receptor which opens Ca2+ channel. 3. Ca2+ released from lateral sac of the terminal cisternae of the SR 4. Ca2+ binding to Troponin removes blcoking action of Tropomyosin 5. Cross-bridge binds and generates force from powerstroke (ATP needed) 6. Ca2+ removal from troponin restores tropomyosin blocking action; detaches crossbridge binding 6. Ca2+ transported back into SR by primary active transport pump Summary: increase in [Ca2+] is triggered by AP in plasma membrane. AP propagated into interior of fiber along T-tubule to the SR where DHP receptors sense the voltage change and pull open the ryanodine receptors, releasing Ca2+ ions from reticulum. Relaxtion occurs from active transport of Ca2+ into SR.

Actions of Thyroid Hormone

T4 main secretory product, but T3 is more active 1. T3 increases metabolic rate and promotes consumption of calories (calorigenic effect) --> heat production 2. Sympathetic nervous sys are potentiated by T3, *permissive action* of T3 3. permissive growth and development of the nervous system during fetal life and childhood -T3 up-regulates (permissive effect) beta-adrenergic epinephrine receptors in tissue (heart and nervous system) -symptoms are similar to increase in epinephrine and norepinephrine 4. Affects every cell by increasing gene transcription (intracellular receptor) and protein synthesis (metabolism related gene products) 5.Controls basal metabolic rate (BMR) and body temperature (cells burn ATP to main life functions)- increased by Na+/K+ ATPase pump 7. Essential for fetal CNS development and function -(ex: congenital hypothyroidism- lack of iodide in mother's diet leads to improper development of fetus)

Male Reproductive Tract

Testes (Gonads): produce steroids and gametogenesis; produce sperm in seminiferous tubule and secrete testosterone from Leydig cells 2. Epididymus: sperm storage 3. Vas Deferens: duct work vas deferns --> ejaculatory duct --> urethra 4. Seminal vesicles: fructose, prostaglandins 5. Prostate gland : alkaline mucus, clotting factors; secretes fluid through tiny opening in the side of the urethra 6. Bulbourethral glands: lubricating mucus 7. Penis: more ductwork 8. glandular secretions -nutrients -buffers for protecting sperm in acidic vaginal secretions - chemicals increase sperm mobility -prostaglandins 2-7 are specialized for delivery and survival of sperm in the female reproductive tract

Thyroid Gland Anatomy -colloid -follicular cells

Thyroid gland: tapioca bowtie gland Location: on the throat, overlapping the trachea below the larynx Composed of: primarily colloid-filled spheres enclosed by a single layer of follicular cells - A thyroid follicle contains colloid and thyroid hormone attached to thyroglobulin (thyroid hormones are protein-bound) Thyroglobulin: protein that attached to thyroid hydrophobic hormone to prevent its passing of the plasma membrane so it can be stored in colloid until need -follicular cells border thyroid follicle, where they secrete thyroid hormones (T3 and T4) -thyroid hormone is stored until stimulated to be secreted by TSH -Thyroid hormone is transported int the blood bound to carrier proteins -Thyroid hormone is lipophilic (hydrophobic amine hormone) and thus binds to receptors inside target cell.

muscle structure: organ to filament

Whole Skeletal Muscle (organ) v Muscle Fiber (one cell) v Myofibrils (cylinders of intracellular contractile structures arranged in repeating units) v Thick and thin filaments v Myosin and Actin Myosin and actin interact to create tension (the function of the unit) Tendons: attach muscle to bone (white connective tissue) Muscle: changes angle around joint

Role of hCG in pregnancy

hCG = Human Chorionic Gonadotropin produced by tropoblast *only if mature follicle is fertilized!* progesterone and estrogen are required to maintain the uterus during pregnancy, which come from the corpus luteum for the first two months, their secretion stimulated by HCG HCG: 1. secreted by developing embyro 2. Basis for pregnancy tests ( HCG in maternal urine) 3. Rescues corpus luteum (similar to LH) 4. Mediates implantation 5. Turns on testosterone production in male fetus testes 3 months after beginning last menstruation luteal placental shift occurs where the placenta takes over for secreting estrogen and progesterone -highest time for miscarriage High concentration of progesterone in the presence of estrogen inhibits GnRH so no menstrual cycle occurs

Gigantism Short Stature Acromegaly

all result from problem in growth cascade GIGANTISM: - too much GH before epiphyseal plates close (before puberty) -results in long bones ACROMEGALY: - too much GH after epiphyseal plates close (after puberty) -results in thick face, hands, bones, enlarged organs SHORT STATURE: can occur from too little GH or IGF-1 Causes: - too little GH, decrease IGF-1 - insensitive GH receptors -lack of IGF-1 secretion, GH is normal -Insensitive IGF-1 receptors -hyporesponsiveness in GH receptors

Neuromuscular Junction parts

alpha motor neurons synapse on skeletal muscle fibers near the fiber's center at a specialized synapse NMJ Motor end plate: highly folded region of the muscle's sarcolemma (plasma membrane) that lies directly beneath the alpha motor axon terminal at the NMJ One synapse per fiber Parts: 1. motor neuron myelinated by schwann cells synapse in the center of a muscle fiber 2. axon terminal contains: voltage-gated channels, Ach vesicles 3. ECF contains: Ca2+ and Na+ and K+ 4. muscle end plate contains: N-Ach receptor (Iontropic nonspecific cation channel), Ach esterase, voltage-gated Na+ channels.

Autocrine Signaling

autocrine substance acts on same cell that secreted the substance

Structure of Thyroid Hormone -T3 vs T4

colloid follicles trap iodide for the synthesis of thyroid hormone 1. T4 or Thyroxine: - 4 IODIDES -90% of thyroid hormone secreted -"storage pool" in blood -converted to T3 in target cells -not very active -bound to plasma membrane 2. T3 or Triiodothyronine: - 3 IODIDES - most active -most potent at target cell

Day 15-25 of menstrual cycle

corpus luteum forms and under the influence of low but adequate levels of LH, secretes estrogen and progesterone, increasing plasma concentrations of these hormones which have negative feedback on hypothalamus and ant pit to decrease FSH and LH concentrations Therefore: 1. secretory endometrium develops 2. secretion of FSH and LH from anterior pit gland inhibited by lowering their plasma concentrations Thus: no new follicles develop

Endocrine Disorder: Primary Disorder

defect in the cells that secrete the hormone (usually third gland)

Days 1-5 in menstrual cycle

estrogen and progesterone are low because the previous cycle's corpus luteum is degrading Therefore: 1. endometrial lining sloughs off 2. secretion of FSH and LH is released from inhibition and their plasma concentrations increase THUS: several growing follicles are stimulated to mature

FSH

follicle stimulating hormone secreted by anterior pituitary gland in response to GnRH

Permissive effect of hormone

number of presence of hormone receptors can be influenced by the presence of another hormone. Ex: thyroid (hydrophobic) hormone is permissive of epinephrine (hydrophilic catecholamine) effects thus thyroid hormone increases the number of epinephrine receptors on target cells. -when the thyroid hormone is alone, little fatty acids are released -when epinephrine is alone, some fatty acids released -when together large amounts of fatty acids are released why? Hydrophobic (thyroid) hormones change the genetic expression from their intracellular receptor and induced an increase expression of epinephrine receptors. The same dose of epinephrine will now bind to a larger number of receptors creating a greater effect.

Day 14 of menstrual cycle

ovulation is mediated by follicular enzymes and prostaglandins

Oogenesis

phases of the ova (egg) development in the ovary. 1. Before birth, oogonium divides mitotically to give rise to 2-4 million oogonia (proliferation differentiation). - 7 months after conception this process ends -46 chromosomes 2. Just before birth, oogenia begin first meiotic division but do not complete it, they are in meiotic arrest = primary oocytes -46 chromosomes 3. Prior to ovulation, the primary oocyte competes first meiotic division = secondary oocyte (only ~400 oocytes) -crossing over occurs here-- non-sister chromatids exchange -23 homologous chromosomes pairing-- one chromosome from each pair is taken - 1st polar body is formed (23 chromosomes no cytoplasm) --> degrades 4. The secondary oocyte is ovulated and fertilized if sperm is present -23 homologous chromosomes 5. Sperm entry to secondary oocyte triggers second meiotic division= zygote -second polar body (23 chromosomes) -46 chromosomes (23 from mom + dad) 5. No sperm present: remnants of dominant follicle form the corpus luteum, which lives for about 2 weeks then becomes corpus albicans

Endocrine Disorder: Hypo-responsiveness

receptors are down-regulated (decrease in number) or altered function within the second messenger cascade Ex: type 2 diabetes

Endocrine Disorder: Hyper-responsiveness

receptors are up-regulated (increase in number) or altered functions within the second messenger cascades Ex: hyperthyroidism

Day 7 in menstrual cycle

single follicle becomes dominant -has more estrogen production than non-dominants

Endocrine Signaling

take raw material from the blood and use them to build hormones that go back out into the blood and influence target cells that can be distance away.

Paracrine Signaling

target cells in close proximity to site of release of paracrine substance

Endocrine Disorder: Hyposecretion

too little secretion of a hormone. Causes: -glandular destruction -loss of key regulators -enzyme deficiency dietary deficiency (ex: iodide) -tumors that destroy nearby hormone secreting cells -auto-immunity -problem in signal transduction pathway)

Endocrine Disorder: Hypersecretion

too much hormone being secreted. Causes: 1. Primary: -gland secretes too much hormone 2. Secondary: -excessive stimulation of gland by tropic hormone - negative feedback ignored -tumor increases the number of cells secreting hormone - auto- immunity (ex: TSI mimic TSH receptors) - problem in signal transduction pathway

Endocrine Disorder: Secondary Disorder

too much or too little tropic hormone

Thyroid Hormone -properties -characteristics

very HYDROPHOBIC: iodides make it hydrophobic 1. Major form found in plasma: attached to protein 2. Location of Receptors: intracellular 3. Most Common Signaling Mechanism: -intracellular receptors alter gene transcription 4. Rate of Excretion/Metabolism: slow (hours/days) 5. Thyroid Hormone is an AMINE 6. Derived from Tyrosine KNOW: 1. Tetraiodothyronine (thyroxine, T4) 2. Triiodothyronine (T3)