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48 Cards in this Set

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  • Back

ADH (Name and Chemical Class and Organ that releases)

Anti Diuretic Hormone, Peptide, Cell bodies in supra optic nucleus releases from posterior pituatary

ADH (Stimulation)

Angiotensin II and hyperosmotic plasma (water leaving cells)

ADH(Target Tissue and Physiological effects)

Kidney, Increases water retention, blood presure

ADH (mechanism of Action)

Cell Surface Receptor, cAMP and negative feedback loop

Oxytocin(Chemical class and Organ location)

Peptide, Cell bodies in paraventricular nucleus releases from posterior pituatary

Oxytocin(stimulation)

Childbirth, suckling, sight and smell of newborn all stimulate. Stress, catecholamines inhibit.

Oxytocin(Target Tissue and physiological effects)

Contraction of uterus and causes milk let down.

Oxytocin(mechanism of action)

gprotiento phospholipase c, IP3 from ip4 which is for uterine muscle contraction. Thesecondary diacylglycerol leads to protein kinase c which breaks down the plasmamembrane and creates arachidonic acid through cox pathway the myoepitheal cellsconstrict leading to milk let down

GH(Name, Chemical Class, Organ Location)

Growth Hormone, Peptide, Anterior pituitary

GH(Stimulation)

Stimulated by GHRH. inhibited by GHIH. Stimulated by hypoglycemia. Inhibited by GH, somatostatin, Somatomedins, and hyperglycemia.

GH(feedback loops)

Short: GHRH from hypothalmus is negative feed back to the hypothalmus


Medium: From the growth hormone it is positive feedback for the hypothalmus to produce Somatostatin which is a negative feedback for the ant pit.


Long: Target tissues of the GH produce Somatomedins(igf) which negative feedback straight to Ant Pit. Also positive feedbacks the hypothalmous to produce somatostatin which negative feebacks ant pit.

GH(Target tissue and Physiological effect)

Effects Muscle, Liver, and adipose = direct ifit goes to the liver it can make IF and go to bone.




Increasenutrient availability elevates blood glucose and fats, Increases protein synthesisand organ growth, Increases linear bone growth.

GH(Mechanism of Action)

ThroughThyrosine kinase enzyme causes phosporalation of enzyme produces secondmessanger which increases transcription and metabolisim

Prolactin(chemical class and Organ Location)

Peptide Anteriory Pit

Prolactin(stimulation)

Tonically inhibited by dopamine(PIH) also inhibited by prolactin. TRH, pregnancy, breastfeeding, and stress stimulate.

Prolactin (target tissue and Physiological effects)

Breast development in pregnancy, Synthesis of milk. Inhibits Ovulation.

Prolactin (mechanism of action)

Tyrosinekinase enzyme activates and produces mapk and STAT which leads to proliferationand differation

Thyroid stimulating Hormone(Chemical Class and location)

peptide, Ant pit

Thyroid Hormone (stimulation)

TRH Stimulates, T3 and T4 inhibit

Thyroid Hormone(target tissue, mechanisim of action, physiological effects)

Thyroid, thyroidgland which releases t3(active) and t4, Thyroid hormone is permissive of GH. Actions– growth, BMR increase, Maturation of CNS, increase metabolisim, increasecardiac output.

T3 and T4

T3 and T4 enter into a target cell and bind a cytosolicreceptor. T3 and T4 are produced in follicle cells of thethyroid gland. These cells take upiodide from the blood and oxidize it into iodine. The iodine is pumped into a region of thethyroid known as the colloid, which is surrounded by follicle cells. Once T4 is converted into T3,it can move into the nucleus where it binds a nuclear receptor and stimulatesprotein synthesis.

Gonadotropic hormone Female (name two and their chemical class)

Lutenizing hormone and Follicle stimulating hormone both peptides. in the Ant pit

FSH

Ovary,FSHinitiates growth of granulosa cells, follicle cell to produce an egg. It creates inhibin secretion which is a negative feedback to the ant pit

LH

Produces Androgen secretion which leads to estrogen secretion. Assist is follicular development and increases plasma estrogen which feeds back negativly to the ant pit and hypothalmus

Female cycle stages

1. Follicular


2. Mid cycle


3. Luteal

Hypothalamic hormones

GHRH- growth hormone releasing hormoneGHIH – Growth hormone inhibitory hormone orsomatostatinTRH – Thyroid releasing hormoneCRH – Corticotropin releasing hormoneGonadotropin releasing hormone – GnRH


PIH- prolactin inhibitory hormone

Estrogen

secondarysex charateristics, follicle development

Progesterone

maintinenceof pregnancy and development of placenta and prepares uterus for implantation

Ovulatory(midcycle)

During the ovulatory phase, estrogen begins tofeed back positively to the anterior pituitary, leading to increased release ofLH. The LH elevates the levels ofestrogen, which elevates the level of LH.

Luteal Phase

During the late luteal phase of the reproductivecycle, progesterone (a steroid) is produced and feeds back negatively at theanterior pituitary.

Corpus Luteum

the follicle cell that produced the egg fillswith fat and produces progesterone, that characterizesthis last phase of the cycle. If no pregnancy occurs, the corpus luteum diesafter about a week and is resorbed and menstruation occurs. If pregnancy does occur, the zygote beginsproducing another hormone known as human chorionic gonadotropin (HCG). HCG “rescues” the corpus luteum, which staysaround and produces protesterone for the first several months ofpregnancy. Once the placenta is fullydeveloped, it takes over the job of producing progesterone, which is necessaryfor the growth and development of the fetus.

Follicular phase

Estraogenfeeds back negative to anterior pituitary

Gonadotropin Males (two and their type)

FSH and LH peptides

FSH Males

Stimulates Sertoli cells which comprise the seminiferous tubles to produce androgen binding protein and inhibin which is a negative feedback to the ant pit

LH Males

stimulates the leydig cells, which are locatedin between the seminiferous tubules, to produce testosterone.

Testosterone

Steroid. causes sperm production by cells in theseminiferous tubules. negative feedback to ant pit and hypothalmus

Cortisol(chemical class, location, stimulation)

Steroid produced at Adrenal cortex. Stimulated by ACTH from pituatary. release is cyclic and pulsatile, with mostsecretions occurring during the early part of the day

Cortisol effects

1.Gluconeogenesis


2.Anti-inflammatory- blocks phospholipase A2 (thefirst enzyme in the arachadonic acid pathway)


3.Anti-immune – inhibits T cells, IL-2


4.Up-regulates alpha-1- BP5.Decreases bone formation


6.Increases GFR- dilates afferent


7.CNS- limbic system (stress), decrease REM

Cortisol MOA

As a steroid, cortisol readily enters targetcells and travels to the nucleus, where it binds a receptor. It turns on certain genes and leads toprotein syntheses.

Aldosterone (chemical class, Location, Stimulation, Target Tissue)

Steroid, Adrenal Cortex, Stimulatedby Renin-angiotensin system, and High K+, Targets the kidneys abosrobtion of Na+ and K+ balance

Aldosterone(MOA and effect)

Entersand binds to cytoplasmic receptor, which leads to protein sysnthesis whichcreates new K+ outpumps and Na+ uptakes. Increased renal Na+ reabsorption, Increased K+secretion

Epinephreine(Location, chemical Class, stimulation, target tissue)

Adrenal Medulla, Steroid, sympathetic response, Targets whole body sympathetic response.

Epinephrine MOA and effect

In all cases where epinephrine stimulates betareceptors, it works through the adenylate cyclase pathway to produce the secondmessenger, cAMP. When it stimulatesalpha receptors, it works through the phospholipase C pathway to produce IP3and DAG as second messengers.




stimulatesbeta-1 receptors in heart to increase cardiac output. Stimulate beta-2receptors on blood vessels to cause vasodialation. If there is a high enoughrelease it can stimulate alpha-1 receptors to cause vasoconstriction. Causesliver to release glucose into blood. And causes fight or flight and exercise response.

Angiotensin II

renin with angiotensin creates angiotensin 1, plus ACE creates angiotensin 2. . Angiotensin II is a vasoconstrictor. It isalso works to release aldosterone and activates activity of neuron athypthalmus to produce ADH. Angiotensin is through second messangersystem.

Insulin

Beta cell from Pancreas, protein, Controlledby glucose, when glucose is high it enters beta cells and turns to ATP betacell depolarizes which allows in calcium which leads to exocytosis and createsinsulin. Also with FFA and amino acids

Insulin MOA and Effects

cellsurface receptor which associates with thyrosine kinase, which leads to glucosetransfer uptake.


decreaseblood glucose and fatty acid and AA, increase glycogen storage

Glucagon

Pancreas Alpha cell, peptide, stimulated by low blood glucose, targets the liver

Glucagon MOA and effects

cAMP mechanisim that breaks down glycogen




elevateblood glucose and F.A