Phys Exam II Study Guide

  1. Define: hormone
    A substance secreted by one cell that interfere with another cell or itself
  2. Define the 7 stages of what comprises an endocrine system
    • 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)
  3. List the known endocrine organs and their hormones
    • 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)
  4. List the divisions of how hormonal systems are classified
    • Systemic
    • Autocrine
    • Paracrine
    • Pheromones
    • Nuerohormones
  5. Describe peptide hormone production
    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
  6. Describe steroid hormone production
    • Derived from cholesterol, which is modified by enzymes to make steroids
    • VERY small changes is chemical structures can have profound physiological changes
  7. Describe secretion
    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
  8. List the specific “axes” of neuroendocrinology
    Look at slide 15 from endocrinology notes
  9. List the nuclei of the hypothalamus and note which neuroendocrine hormonal cell bodies are located in these nuclei
    • 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:
  10. Describe the functions of the hypophyseal portal system
    IS the system of blood vessels that link the hypothalmus and the anterior pituitory in the brain
  11. What are fenestrations?
  12. List the hormones of the anterior pituitory gland
    • Adenohypophsis
    • Pars Distalis
    • Pars Intermedia
  13. What are the hormones of the Pars Distalis?
    • 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
  14. What is the hormone of the Par Intermedia?
    Melanocyte-Stimulating Hormone, pigmentation
  15. List the hormones of the Neurohypophysis
    • 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
  16. Define: oogenesis
    the process in the ovary that results in the production of female gametes
  17. Define: follicular growth
    Is the maturation of the ovarian follicule
  18. Define Semiferious tubules
    Tubules of the interior testes where sperm is produced
  19. Define: Leydig cells
    Cells in the testes that secrete testosterone, located between the semiferious tubules of the testes
  20. Define Sertoli cells
    • Secretes inhibin
    • Somatic cell where spermotids develop in the tubuls of the testes
  21. Define: Granulosa cell
    • 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
  22. Define Thecal Cell
    • Comprise a layer of the ovarian follicules, tertiary follicules
    • A surge from LH makes thecal cells migrate into antral space
  23. Define the SRY gene
    The sex determination gene on the y chromosome
  24. Define the wolffian duct
    A duct in the embryo that becomes the vas deferons in males and forms vestignal structures in females
  25. Define the Mullerian duct
    The duct from the embryonic pronephros, which in later development in mammals becomes the oviduct in females and disappears in males
  26. Decribe the role PGF2a in luteolysis
    • 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
  27. Describe the steroidal genesis of estradiol
    • LH acts on the theca cells to stimulate the production of androgens (little E)
    • FSH acts on granulosa cells to convert androgen to estrogen,
  28. What is the role of estrogen in sexual development?
    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
  29. What is the role of dihydroxytestosterone in sexual development?
    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
  30. How is male made from female?
    • 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
  31. To draw the hypothalamo-pituitary-gonadal axes of the male and female
    Look at slide 2 of reproduction notes
  32. Explain how ovulation occurs
    • 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
  33. Explain Luteogenesis
    • 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
  34. Explain the changes in GnRH/LH and FSH secretion over the menstrual cycle
  35. Explain how estrogen levels can rise although it is exerting negative feedback in the follicular
    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
  36. Explain how estrogen drives a surge in LH secretion
    Rising estrogen drives a preovulatory surge in GNrH thus causing a surge in LH
  37. Explain why constant release of implant of GnRH shuts down the reproductive axis
    ask ta
  38. Explain how an anatomical female can occur in a XY person
    The person is deficient in 5 alpha reductase
  39. Explain how an anatomical male can occur in a XX person
    A deficient aromatase
  40. Draw the hypothalmo-pituitary-adrenal axis
    See slide 2 of the adrenal notes
  41. Define: zona glomerulosa
    The super ficial layer of the cortex and secretes aldosterone
  42. Define: Zona Fasiculata
    Is the middle layer of the cortex, secretes corticoids (cell in bundles fasicles)
  43. Define: Zona Reticularis
    IS the deep layer of the adrenal cortex, secretes androgens
  44. Describe the structure and function of the adrenal cortex
    • 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
  45. Decribe the secretory path of cortisol and its importance
    • 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
  46. Describe the HPA axis
    • 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.
  47. Explain the biosynthesis of aldosterone, cortisol, adrenal androgens.
    • 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
  48. Explain how effects in the biosynthesis of adrenal androgens gives rise to CAH
    • 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
  49. Explain the effects of ACTH on the adrenal, the immediate and subsequant effects
    • 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
  50. Explain the effects of ACTH (MSH) on the skin
    Activates Melanocortin I Receptor, the activation of this recptor leads to increased melanin synthesis and melanocyte proliferation
  51. Explain the effects of cortisol on high blood sugar
    • Cortisol inhibits GLUT4 in the muscle cell
    • Cortisol simulates gluconeogenesis directly
  52. Explain the effects of cortisol on adiposity in the mideline
    i have no idea what the heck he is talking about
  53. Explain the effects of cortisol on muscle wasting
    Cortisol inibits glut4 in the muscle cell, glut4 is responsible for insulin regulated translocation of glucose
  54. Explain why cortisol must be converted corticosterone in the kidney
  55. Explain the specific consequences and the therapy of high ACTH and cortisol and adrenal androgen disorders
    • 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
  56. Explain The role of aldosterone, vasopressin (AVP or ADH) and atrial natriuretic peptide (ANP) in blood pressure regulation.
    • 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
  57. Describe the synthesis and release of thyroid hormones (T4 and T3)
    • 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
  58. Explain the transport of thyroid hormone in plasma
    • T3 and T4 have relatively long half lives in humans, due to extensive binding to plasma proteins
    • zzz
  59. Draw the hypothalamo-pituitary-thyroid axis
    See slide 2 of thyroid notes and draw it out
  60. Draw the functioning thyroid follicle
  61. Explain thyroid hormone feedback control
  62. Explain the effects of the thyroid hormone
    • 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
  63. Explain hyperthyroidism and Graves Disease
    • 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
  64. Explain hypothyroidism and Hashimoto's disease
    Hashimoto's disease, deals with T-lymphocyte, lead to destroying the thyroid gland
  65. Explain iodine deficiency
    Cretin: iodine deficiency pre and post natally
  66. Explain cretinism
    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
  67. Define: hyperglycermia
    High blood sugar concentration
  68. DefinE: Hypoglycemia
    Dificiency of blood sugar in the blood stream
  69. Define: primary and secondary diabetes mellitus
    • 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
  70. Define: Gestational Diabetes
    in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy
  71. Define: Glucose transporter
    • 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
  72. Explain the effects of insulin
    • 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
  73. Explain the effects of glucagon
    • 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
  74. Explain the control of blood glucose in the fedding and fasting state
  75. Explain the specific consequences of high blood glucose
    • High Blood glucose induces insulin release
    • As blood sugar increases glucose (first step involves glucokinase)
    • Results less K+ going through ATP-sensitive K+ channels
  76. Define: osteoblast
    are responsible for bone formation
  77. Define: osteoclast
    • Responsible for bone reabsorption
    • Calcitonin inhibits osteoclast
  78. Define: osteoid and hydroxyapaptite
    In bones and teeth calcium phosphate occurs in form of submicroscopic crytals calle hydroxyapaptite deposited on organic matrix composed of collagen fibers called osteoids
  79. Define Vitamin D
    • 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
  80. Define: Parathyroid hormone
    • 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
  81. Define: Calcitonin
    • 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
  82. Define: Calbindin
    • Activates ATPase
    • When Ca++ binds to calbindin it does not increase the concentrations of Ca++
  83. Describe Ca++ reabsorption and bone formation
    Look at slides 4 to 6 Ca and Vit D notes
  84. Describe the Ca++ cells of the parathyroid and thyroid
    • Osteoclast:
    • Metstatic: release OAF
    • Osteoblast: release OAF ( osteoclast activating factor)
  85. Describe how 1-25 Vitamin D is made
    • 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
  86. Describe the Ca++ receptor in the parathyroid
    • 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
  87. Explain why rickets is on the rise in people in african heritage
    • They produce less VD3 in skin also there is more lactose intolerant
    • There dark skin doesnt make as much VD3
  88. Explain how vitamin D effects calcium concentrations
    Vitamin D is required for calcium absorption
  89. Explain how PTH effects calcium concentrations
    PTH secretion is inhibited by high Ca++ concentrations
  90. Explain the interplay between PTH and Vitamin D
  91. Explain how calcitonin effects calcium concentrations in humans and other mammals
  92. Explain why cancer causes high concentration of Ca++
    • 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
  93. Explain Ca uptake from the Gut
    • PTH
    • increases 1-25D3
    • production in kidney by stimulating 1-hydroxylase biosynthesis. Indirectly
    • increases gut Ca2+
    • uptake
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Phys Exam II Study Guide
Phys exam II study guides