Phys Exam II Study Guide

A substance secreted by one cell that interfere with another cell or itself

• Anatomcial description of cells producing hormone, target cells and their environmetn and distance of separation
• Chemical Structure
• details of hormone biosynthesis
• How hormone ges to target cell
• Detailed mechanism of how target uses receptors to detect hormone
• Transduction pathway (second messengers) to initiate and sustain a biologicl response (Recall cAMP, IP3)
• How target communicates with hormone- producing cell to indicate an adequate presence of hormone (feedback loops)

• Pineal gland melatonin
• Pituitroy gland (hypophysis): adenohypophysis or Anterior Pituitory (LH, GH, TSH), Neurohypophysis or POsterior Pituitor Pituitary )VP OX
• Thyroid Gland: thyroid hormones, calcitonin
• Parathyroid gland: PTH
• Fat: leptin
• Heart: atrial natriureti peptide
• Skin: Vitamin D
• Gastro-entero-pancreatic system: stomach (gastrin), intestines (seretin), Pancreati Islets (Insulin, glucagon)
• Adrenal Gland (Epinephrine, Corticoids)
• Kidney, Liver (Renin-angiotension; Vitamin D3)
• Testis (Testosterone, Inhibin)
• Ovary (Estrogen, Progesterone)
• Placenta (Chorioni gonadotropin)

• Systemic
• Autocrine
• Paracrine
• Pheromones
• Nuerohormones

Peptide hormone precursors (pre-prohormones) are then processed in several stages, typically in the endoplasmic reticulum, including removal of the N-terminal signal sequence and sometimes glycosylation, resulting in prohormones. The prohormones are then packaged into membrane-bound secretory vesicles, which can be secreted from the cell by exocytosis in response to specific stimuli e.g. increase of calcium and cAMP concentration in cytoplasm

• Derived from cholesterol, which is modified by enzymes to make steroids
• VERY small changes is chemical structures can have profound physiological changes

physiological phenomenon by which a tissue produces a specific substance, which can either be introduced into the blood, or seep to the surface of a mucus or be secreted by an excretory channel

Look at slide 15 from endocrinology notes

• Supraoptic Nucleus (SON): Gonadotropin Releasing Hormone
• Paraventricular Nucleus (PVN): Corticotropin Releasing hormone
• Preoptic Area (POA):
• Arculate Nuclues: Growth Hormone-Releasing Hormone, Dopamine (Prolactin inhibition)
• Suprachiasmatic Nuclues:

IS the system of blood vessels that link the hypothalmus and the anterior pituitory in the brain

• Adenohypophsis
• Pars Distalis
• Pars Intermedia

• Adrenocorticotropin (ACTH): stimulates cell of the adrenal gland to increase steroid synthesis and secretion
• Thyroid-Stimulating Hormone (TSH) : Acts on thyroid follicle cells stimulating thyroid hormone synthesis
• Growth Hormone (GH) : General anabolic stimulant increases the release of insulin like growth factor, stimulating cell growth
• Prolactin (PRL): Stimulates differentiation of mmmary gland cells, stimulating milk synthesis
• Lutenizing Hormone (LH) : Increase ovarian progesterone synthesis, luteinization, acts on Leydig cells of the testes to increase the testosterone synthesis and increase interstitial cell development
• Follicle Stimulating Hormone (FSH): Ovarian follicle development and ovulation, increases estrogen production, acts on the Sertoli cells of semiferous tubule to increase spermatogenesis

Melanocyte-Stimulating Hormone, pigmentation

• Oxytocin: Uterine contraction, causes milk ejection in lactating females, respond to suckling reflex and estradiol
• Vasopressin: (Antidiuretic hormone ADH, Arginine vasopressin AVP) Responds to osmoreceptor which senses [Na+] blood pressure regulation , INcrease reabsorption from the distal tubules in kidneys

the process in the ovary that results in the production of female gametes

Is the maturation of the ovarian follicule

Tubules of the interior testes where sperm is produced

Cells in the testes that secrete testosterone, located between the semiferious tubules of the testes

• Secretes inhibin
• Somatic cell where spermotids develop in the tubuls of the testes

• Convert angrogen to estrogen
• is a somatic cell of the sex cord that is closely associated with the developing female gamete (called an oocyte or egg) in the ovary of mammals

• Comprise a layer of the ovarian follicules, tertiary follicules
• A surge from LH makes thecal cells migrate into antral space

The sex determination gene on the y chromosome

A duct in the embryo that becomes the vas deferons in males and forms vestignal structures in females

The duct from the embryonic pronephros, which in later development in mammals becomes the oviduct in females and disappears in males

• Luteolysis: is the structural and functional degradation of the corpus luteum that occurs at the end of the luteal phase of both the estrous and menstral cycles in the absence of pregnancy
• PGF2a is released the endometrium to lyse the corpus luteum

• LH acts on the theca cells to stimulate the production of androgens (little E)
• FSH acts on granulosa cells to convert androgen to estrogen,

Fetal ovaries produce estradiol, which supports follicular maturation but plays little part in other aspects of prenatal sexual differentiation, as maternal estrogen floods fetuses of both sexes

A sufficient amount of any androgen can cause external masculinization. The most potent is dihydrotestosterone (DHT), generated from testosterone in skin and genital tissue by the action of 5α-reductase. A male fetus may be incompletely masculinized if this enzyme is deficient. In some diseases and circumstances, other androgens may be present in high enough concentrations to cause partial or (rarely) complete masculinization of the external genitalia of a genetically female fetus

• Testosterone is converted into either Estradiol by aromatase, or Dihydroxytestosterone by 5alpha reductase
• SRY and other genes induce differentiation of supporting cells into Sertoli cells and (indirectly) steroidogenic cells into Leydig cells to form testes

Look at slide 2 of reproduction notes

• 1. Occurs 16 to 24 hours after LH peaks
• 2. Mature follicule secretes colagenase, which dissolves collagen in connective tissue that holds follicular cells together
• 3. Breakdown product of collagen create an inflammatory response attracking leukocytes that secrete prostaglandins into follcle: paracrine
• 4. The next is not clear, possible that prostaglandin causes smooth muscle cells in outer theca to contrac, rupturing follicle wall at weakest point
• 5. Egg is swept into fallopian tube

• The corpus luteum develops from an ovarian follicle during the luteal phase of the menstrual cycle
• Luteal phase: A surge in LH makes thecal cells migrate into antral space mingling with granulosa cells and filling cavity
• Both cels, under influence of LH, transform into luteal cells of corpus luteim
• Stop secreting estradiol and start to release progesterone
• Progesterone pontently inhibits GnRH secretion

Estrogen exerts a negative feedback on the LH/FSH but the number of thecal and granulosa cells are increasing and the number of LH/FSH receptors are increasing as well estrogen level are able to rise with a negative feedback

Rising estrogen drives a preovulatory surge in GNrH thus causing a surge in LH

ask ta

The person is deficient in 5 alpha reductase

A deficient aromatase

See slide 2 of the adrenal notes

The super ficial layer of the cortex and secretes aldosterone

Is the middle layer of the cortex, secretes corticoids (cell in bundles fasicles)

IS the deep layer of the adrenal cortex, secretes androgens

• Situated along the perimeter of the adrenal gland, the adrenal cortex mediates the stress response through the production of mineralocorticoids and glucocorticoids, including aldosterone and cortisol respectively. It is also a secondary site of androgen synthesis
• An endocrine organ that secretes corticosteroids for metabolic functions: aldosterone for sodium retention in the kidneys, androgens for male sexual development, and oestrogens for female sexual

• Cortisol inhibits the GLUT4 transporter in muscle
• Cortisol stimulates gluconeogenesis directly and through insulin increased FFAS
• Cortisol may stimulate FFA formation directly
• Cortisol stimulates muscle catabolism

• ACTH stimulates the Adrenal cortex, a stimulated adrenal cortex releases cortisol.
• Cortisol inhibit the pituitary gland, inhibits CRH (PVN) (Corticotropin releasing hormone)(Paraventricular nuclues) (in the Hypothalmus), inhibits the signal that is going to the PVN that is going to stimulate it.

• The first step is hydrophobic cholesterol is transferred to inner mitochondrial membrane by StAR protein (steroidgenic acute regulatory)
• StAR protein synthesis in glomerulosa induced by Angiotension II
• StAR makes pregnenolone from cholesterol
• CYP17: pregnenolone to progesterone, progesterone to 17 OH Progesterone
• CYP12: 17 OH Progesterone to Desoxycortisol
• CYP11: Desoxycortisol to Cortisol

• CAH, Congenital Adrenal Hyperplasia
• When adrenal gland is synthesizing cortisol, aldosterone, and androgen and a minimal level they are all equalling synthesized, but when the adrenal cortext is a maximial syntesizing it makes tons of androgen and mimimal aldosterone, and cortisol

• Stimulates synthesis and release of glucocorticoids and androgens via Gs
• Immediate effects: Increase cholesterol esterase, Increase StAR, Increase cholesterol binding to P450scc
• Subsequent effect: Induce sterogenic enzymes, hypertrophy, hyperplasia

Activates Melanocortin I Receptor, the activation of this recptor leads to increased melanin synthesis and melanocyte proliferation

• Cortisol inhibits GLUT4 in the muscle cell
• Cortisol simulates gluconeogenesis directly

i have no idea what the heck he is talking about

Cortisol inibits glut4 in the muscle cell, glut4 is responsible for insulin regulated translocation of glucose

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• Nelson's, the removal of the adrenal glands, Increased ACTH stimulates cutaneous melanocytes-hyperpigmentation
• Addison's hyperadrenalism, abrupt cessation of exogenous glucocorticoids
• Cushings disease, Cushing's syndrome as caused by a tumor of the pituitary gland, a glandular disorder caused by excessive ACTH resulting in greater than normal functioning of the adrenal gland; characterized by obesity
• Poor wound healing, cortisol blocks cytokine production, reducing the number of T-cells, reduced antibody production

• Atrial Natriuretic Peptide: Inhibits Na+ reabsorption, Inhibits Vasopressin, aldosterone and renin secretion and increase Glomerular filtration
• Vasopressin: released to increased osmolality (osmolality depends on the number of active ions in a solution), decreases solute free water clearance by the kidney, stimulate the production fo aquaporins in tublar cells of distal tubule, so keep water but lose salts
• Aldosterone: stimulates active uptake of Na+ and consequently H2O from distal tubules of kidneys, therefore increasing BP
• Aldosterone in slide 32 of arenal notes zzz

• Thyroid peroxidase (TPO) H2O2 converts iodide to active iodine, Iodine actively transported across apical surface
• Incorporated into tyrosine rediues of thyroglobulin molecules to form mono and di-iodotyrosine residues
• Secretion of thyroid hormones occurs by endocytosis, Fusion with lysosome, hydrolysis of thyroglobulin and release of T4 and T3, there is 10 fold more T4 secreted vs T3

• T3 and T4 have relatively long half lives in humans, due to extensive binding to plasma proteins
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See slide 2 of thyroid notes and draw it out

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• Increase the number and the size of mitochondira
• Stimulating synthesis of enzymes in respiratory chain
• Increasing membrane Na+/K+ ATPase concentrations of cells resting energy expenditure is used to maintain electrochemical gradient, thus increasing Na+/K+ ATPase, increses RMR
• Increase Beta-adrenergic receptors
• Increase glycogen synthesis and glyconenolysis as well as glucocneogenesis and glucose oxidation

• Primary means the thyroid gland is over-functioning
• Secondary, means the gland is hyperfunctioning because is is overstimulated by too much TSH
• Tertiary means there is too much TSH as a result of too much TRH
• Graves disease is an autoimmune diseases that makes anitbodies to the TSH receptor

Hashimoto's disease, deals with T-lymphocyte, lead to destroying the thyroid gland

Cretin: iodine deficiency pre and post natally

is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones (congenital hypothyroidism) due to maternal nutritional deficiency of iodine

High blood sugar concentration

Dificiency of blood sugar in the blood stream

• Type I diabetes, insulin dependent diabetes
• The pancreas secrete enough insulin to allow for efficient uptake usage and storage of sugar in the body
• Type II, INsulin resistant diabetes or non-insulin dependent
• Basically anything that interfers with the insulin pathway

in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy

• GLUT2 moves glucose into the cell, has a high Km for glucose
• GLUT4 is in the muscle which has a lower Km than GLUT2, insulin increases GLUT4 concetrations

• Increases the amount of GLUT4 receptors
• Induces the production of the dehydrogenase which converts glyceraldehyde 3 phosphate to glycerol-3-phosphate
• Stimulates lipoprotein lipase release the fatty acids from chylomicrons and VLDL complexes
• Inhibits adipose tissue lipase which breaks down triglycerides

• Released when glood glucose is low
• Glucagon: activates the cAMP pathway this activating PKA which activates phosphorylates kinase therefore activating glycogen breakdown and inactivates glycogen synthesis

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• High Blood glucose induces insulin release
• As blood sugar increases glucose (first step involves glucokinase)
• Results less K+ going through ATP-sensitive K+ channels

are responsible for bone formation

• Responsible for bone reabsorption
• Calcitonin inhibits osteoclast

In bones and teeth calcium phosphate occurs in form of submicroscopic crytals calle hydroxyapaptite deposited on organic matrix composed of collagen fibers called osteoids

• Vitamin D is a secosteroid, which are those in which one of the rings of the classic steroid undergone fission by breakage of C-C bond
• Is needed for Ca2+ absorption

• It is a hypercalcemic factor its actions cause an elevation in level of plasma Ca++, also effect osteoclast but its effect is indirect
• Increases the reabsorption of Ca++ in the ascending loop of henle and distal tubule by increasing uptake of Ca++ by a Ca-ATPase and a Na+-Ca++ antiporter

• Inhibits osteoclasts
• Antagonist actions of PTH on bone
• It is a hypocalcemic factor- action cause a decrease in level of plasma Ca++
• Secreted by parafollicular or C cells of thyroid

• Activates ATPase
• When Ca++ binds to calbindin it does not increase the concentrations of Ca++

Look at slides 4 to 6 Ca and Vit D notes

• Osteoclast:
• Metstatic: release OAF
• Osteoblast: release OAF ( osteoclast activating factor)

• PTH increases 1-25 Vitamin D production in kidney by stimulating 1-hydroxylase biosynthesis, Indirectly increasing gut Ca++uptake
• Actions of PTH on bone requires 1-25D
• Feedback loop of 1-35D on PTH production

• When Ca++ binds it can activate either pathway depending on the concentration of Ca++
• High concentration of Ca++ stimulates the IP3 pathway and PTH secretion is inhibited
• Low Concentration of Ca++ stimulates the adenylyl cyclase pathway and PTH secretion is stimulated

• They produce less VD3 in skin also there is more lactose intolerant
• There dark skin doesnt make as much VD3

Vitamin D is required for calcium absorption

PTH secretion is inhibited by high Ca++ concentrations

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• The metastatic cell releases OAF osteoclast activating factor therefore releasing Ca++ into the blood stream
• Tumors produce hormone termed PTH-related peptide (PTHrp) that acts like PTH, rarley tumors secrete PTH itself

• PTH
• increases 1-25D3
• production in kidney by stimulating 1-hydroxylase biosynthesis. Indirectly
• increases gut Ca2+
• uptake