Phys 2- Test 2

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Phys 2- Test 2
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2011-08-15 15:15:26
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Phys 2- Test 2one
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  1. zones of the adrenal gland
    • zona glomerulosa
    • zona fasiculata
    • zona reticularis
    • medulla
  2. aldosterone secreted from
    zona glomerulosa
  3. cortisol and androgens secreted from
    zona fasiculata
  4. androgens are secreted from
    zona reticularis
  5. norepi and epi are secreted from
    adrenal medulla
  6. the adrenal gland is located:
    • at the 12th throacic level
    • above the kidney
  7. adrenal cortex is stimulated by:
    • ACTH from anterior pituitary
    • reninangiotensin
  8. adrenal medulla is stimulated by:
    sympathetic nervous system
  9. chromaffin cells
    • located in the adrenal medulla
    • secrete norepi and epi
  10. Adenocorticoid hormones
    from cholesterol from LDL
  11. ACTH and adenocorticoid hormones
    • increase LDL receptors on adenocortical cells
    • increases cholesterol from LDL
  12. Angiotensin 2 and adenocorticoid hormones
    cholesterol causes pregenvlolone causes cortisol, sex hormones, and aldosterone
  13. glucocoricoids
    • can bind to cortisol r/c
    • agonist
  14. Cortisol
    • glucocorticoid
    • produced during stress
    • r/cs in almost all cells
  15. cortisol control
    • ACTH: stimulated by CRH, secreted by stress and circadian rhythm
    • CRH: diurnal, highest before waking
  16. normal cortisol - feedback
    • inhibits CRH from hypothalamus
    • inhibits ACTH from anterior pituitary
    • OVERRIDEN BY STRESS
  17. cortisol circulation
    • mostly bound to CBG (corticosteroid binding globulin) and albumin
    • slow elimination
    • resovior
  18. cortisol metabolism
    • occurs in the liver
    • 25%- bile/feces
    • 75%- kidneys/urine
  19. lack of cortisol effects:
    • cells, organs, systems cant respond to signals and stress
    • causes death
  20. excess cortisol
    • supresses immune and inflammatory responses
    • breakdown of CT and bone
    • increase diabetes mellitus
  21. Cortisol effects to increase and maintain blood glucose
    • increase liver gluconeogenesis (glu from AAs and lipids)
    • increase mobilization of AAs
    • decrease glucose uptake
    • lipolysis in adipose (FA for energy)
  22. cortisol effects as antagonist to insulin
    • increase gluconeogenesis
    • increase glycogen storage in liver
    • decrease glucose utilization
  23. overall cortisol effects
    • increase in circulating glucose causing insulin secretion
    • causes decrease in insulin effectiveness and sensetivity
    • DIABETOGENIC
  24. cortisol causes a decrease in protein storage:
    • EXCEPT in the liver
    • decrease protein catabolism causing muscle weakness
    • decrease protein synthesis causing decrease immunity
  25. lipolysis caused by cortisol
    • increase free FA (better for FA oxidation)
    • use of FA for energy instead of glucose
  26. cortisol can cause obesity
    • increase appetite
    • increase leptin
    • increase visceral fat deposition
  27. cortisol and immunity
    cortisol weakens immunity
  28. cortisol and anti-inflammatory
    • blocks inflammatory process
    • rapid resolution
    • speedy healing
    • stabalizes lysosomal membranes
    • inhibits tissue destruction
    • decreases capillary permeability
    • attenuates fever
  29. cortisol and mineralocoticoid activity
    • binds to aldosterone r/c in kidney
    • normally converted to cortison, which doesnt bind
    • -inhibited by liquorice
  30. other cortisol effects
    • decreases bone formation
    • creates memories from short term exposure
    • fetal maturation- surfactant
  31. hydrocortisone
    • theraputic uses
    • anti-inflammatory
    • chronic use may impair anabolic process (cushing's syndrome)
  32. cushing syndrom
    hypercortisolism, adrenalism, and adenocorticism
  33. s/sx of cushings syndrom
    • truncal weight gain
    • moon-like face
    • acne and hiruitism
    • hypertension
    • high blood glucose
    • weakness
    • purple stria
    • osteoporosis
    • menstral irregularities
  34. Cushing's disease
    adenomas of anterior pituitary
  35. cushings treatment
    • labs
    • primary- high cortisol, low ACTH
    • secondary- high cortisol, high ACTH
  36. ADdisons disease
    • failure of adrenals to produce hormones
    • usually autoimmune problem
    • low aldosterone
    • low cortisol
    • steroid treatment
  37. s/sx of low aldosterone
    • low fluid
    • high RBCs, low plasma
    • decreased cardiac output
  38. s/sx of low cortisol
    • decreased metabolic functions
    • sluggish, weakness
    • increase ACTH
    • increase melanin
  39. aldosterone
    • mineralocorticoid
    • from zona glomerulosa
    • from cholesterol stimulated by ACTH
    • stimulated by the concentration of angiotensisn 2 and K+
  40. Aldosterone increases Na retention and K secretion
    • in the collecting ducts and tubules
    • atrial natriuetic peptide inhibits aldosterone
  41. what increases aldosterone secretion
    • increased [K]
    • increase renin-angiotensin system
    • ACTH
  42. what decreases aldosterone secretion
    decreased [Na]
  43. aldosterone defficiency
    • death
    • renal Na wasting causing decreased blood volume and cardiac output
  44. aldosterone excess
    • adrenal tumor
    • increased Na/H2O retention
    • hypertension
    • muscle weakness
  45. alkalosis symptoms
    • confusion
    • twitching
    • nausea
    • light-headed
  46. Conn's syndrome
    • primary aldosteronism
    • from zona glomerulosa tumor
    • excess aldosterone production
  47. adrenal sex hormones
    • important during fetal development and puberty
    • DHEA, androstendine (precursor to testosterone)
    • progesterone and estrogen
  48. fight or flight reaction
    • increases:
    • contraction/cardiac output
    • breathing rate
    • sweating
    • anxiety
    • metabolism
  49. pheochromocytoma
    • chromaffin cell tumor
    • overproduction of norepi and epi
    • usually benign
    • treatment to nromalize blood pressure
  50. pheochromocytoma from genetic defect
    • multiple endocrine neoplasia 2
    • pheochromocytoma with meduallary thyroid cancer or hyperparathyroidism= MEN 2A
    • pheochromocytoma wiht tumors of Ns in lips, mouth and eyes = MEN 2B
  51. diagnosis of pheochromocytoma
    • labs show:
    • increased epi, norepi and metanephrines
    • abnromal CT/MRI
  52. untreated hypertension from pheochromocytoma:
    • MI
    • heart failure
    • stroke
    • kidney failure
    • vison impairment
    • death
  53. hypertension crisis
    • release of excess catecholamines causing HR 250/150
    • causes stroke, congestive heart failure
    • increased risk of diabetes
  54. pancreas- cell types
    • islets of langerhans
    • beta cells
    • alpha cells
    • delta cells
    • polypeptide cells
  55. beta cells secrete:
    • insulin
    • amylin (inhibits insulin)
  56. alpha cells secrete:
    glucagon
  57. delta cells secrete:
    somatastatins (inhibit glucagon and insulin
  58. polypeptide cells secrete:
    pancreatic polypeptide
  59. insulin
    • the dominant hormone in regulating blood sugar
    • increases when engery's abundant
    • increases energy storage
    • increases to reduce blood sugar
  60. insulin causes:
    • storage of CHOs as glycogen in liver and MS
    • stores protein as AAs
  61. insulin synthesis
    • translated/synthesiszed as preprohormone
    • cleaved in ER to proinsulin
    • cleaved in golgi to insulin
    • packaged and secreted into blood
    • cleared in 10-15 minutes
    • degredaded by insulinase
  62. insulin action
    • binds to r/c, initiates enzymatic cascade
    • increases cells glucose uptake to adipose and Ms
    • phosphorylates glucose for CHO metabolism
    • increases membrane permeability to AA, K, and Phosphate
  63. insulin action- liver
    • noninsulin regulated GKUT-2 r/c
    • increased glycogen synthetase
    • decreased glycogen phosphylation
  64. insulins CHO effects
    • increase glucose uptake
    • increase glucogenesis
    • decreased gluconeogenesis
  65. insulin- fat effects
    • increased tri-g synthesis
    • decreased tri-g breakdown
  66. insulin- protein effects
    • increased synthesis
    • decreased breakdown
  67. insulin secretion
    • Glu-6-P causes Ca+ influx causing insulin secretion from beta cells
    • primary factor is increased blood Glu sensed by GLUT-2 r/c on beta cells
    • increased glucagon, AA, GI hormones after a meal, ACh, and sulfonurea drugs
  68. high CHO meal causes:
    • increased glucose= increased insulin= increased uptake and storage of Glu
    • b/t meals insulin needs to be low so glucose can go to the brain
  69. glucose is the only nutrient used by:
    the brain
  70. insluin: FA synthesis
    • promotes in liver
    • glucose to pyruvate to acetal-CoA to FAs
    • packaged in VLDL to the blood, stored as fat
  71. Ms using Glu for energy:
    • during exercise without insulin
    • after meals with increased Glu
  72. insulin and growth
    insulin + GH causes dramatic growth
  73. Glucagen
    • hyperglycemic hormone
    • increases with low blood glucose
    • opposes insulin (causes high blood glucose to correct hypoglycemia)
  74. Glucagen causes:
    • glycogenolysis- breakdown of liver glucose
    • gluconeogenesis- in liver, uptake of AA
    • increased adipose breakdown
    • decreased tri-g storage in liver
  75. glucagon secretion increased by:
    • decreased blood glucose
    • exercising
    • increased serum AA after high protein meal
  76. glucagon secretion decreased by:
    • high blood glucose
    • somatostatin
  77. somatostatin
    • secreted from delta cells
    • inhibits insulin and glucagon
  78. somatostatin secretion increased by:
    • ingestion of food
    • blood glucose
    • AA
    • FA
    • GI hormones
  79. goal of somatostatin
    • extend time for nutrients to get into blood
    • decrease use of absorbed nutrients by tissues
  80. Lack of insulin on CHO leads to
    low blood glucose causing shock, coma, death
  81. lack of insulin on PRO
    protein wasting causing wakness and organ dysfunction
  82. lack of insulin on fat
    • more fat used for energy
    • atherosclerosis from increased free FAs
    • formation of ketone bodies in the liver
    • death
  83. diabetes mellitus
    • impaired CHO, PRO, and fat metabolism
    • caused by:
    • -lack of insulin secretion (IDDM, type 1)
    • -decreased insulin sensetivity of tissues (NIDDM, type 2)
  84. Type 1 DM
    • beta cell failure/destruction
    • 5% of cases
    • genetic predistposition
    • onset usually during childhood
    • developes abruptly
    • increased blood glucose to urine
    • polyol pathway
  85. causes of type 1 DM
    • genetic
    • auto-immune
    • viral infection
  86. polyol pathway
    • glycated protein/ frosted
    • loss of normal function
    • s/sx: polyuria, increased thirst
  87. chronic high blood glucose
    • causes tissue damage
    • polyol pathway
  88. chronic high blood glucose causes:
    • altherosclerosis
    • blindness
    • gangrene
    • peripheral neuropathey
    • hypertension
    • fat metabolism leading to death
  89. type 2 DM
    • loss of insulin sensetivity, later loss of beta cells
    • 95% of cases
    • usual onset >30
    • develops gradually
    • associated with high insulin causing decreased sensetivity and more insulin secretion
  90. causes of type 2 DM
    over eating
  91. s/sx of tkype 2 diabetes
    • obesity
    • abdominal fat
    • reactive hypoglycemia
    • insulin resistance
    • fasting hyperglycemia
    • increased tri-g, decreased HDL
    • hypertension
  92. if you have DM, you have cardiovascular disease
  93. causes of insulin resistance
    • chronic inculin exposure causing r/c down regulation
    • obesity
    • excess cortisol/GH
    • pregnancy
    • polycystic ovarian syndrome
    • hemochromatosis
  94. if the beta cells burn out in type 2 DM you get:
    IDDM
  95. type 2 DM treatment
    • deit
    • excersize
    • weightloss
    • drugs
  96. glucose/insulin tolerance labs would show what for DM 1
    low/undetectable insulin
  97. glucose/insulin tolerance labs would show what for DM 2?
    high insulin early, low late
  98. insulinoma
    • tumor of beta cells causing hypersecretion of insulin
    • can lead to insulin shock (hypoglycemia-coma)
  99. fasting hypoglycemia caused by:
    • drugs
    • hormone deficiencies
    • liver failure
    • critical illness
    • endogenous hyperinsulinism
    • auto-immune disease
  100. post prandial hypoglycermia caused by:
    • congenital deficiency of enzyme of CHO metabolism
    • GI
  101. genetic sex
    determined by chromosomes
  102. gonadal sex
    determined by testes/ovaries
  103. phenotypic sex
    determined by hormones and secondary sex characteristics
  104. male development
    • mullerian inhibiting hormone- inhibits growth of paramesonephric ducts
    • testosterone- causes deveolopemnt of mesonephric ducts
  105. female development
    • ovaries secrete estrogen and progesterone
    • no testosterone so mesonephric ducts wither
  106. hypothalamic pituitary axis
    • hypothalamus
    • anterior pituitary
    • gonads
  107. hypothalamic pituitary axis regulates
    • gametogenesis
    • hormone secretion

    • hypothalamus- GnRH
    • anterior pituitary- LH and FSH
  108. GnRH (gonadotropin releasing hormone)
    • from hypothalamus
    • released in pulsatile fashion
    • binds to r/c on gonadotropes
    • feedback by LH and FSH
    • also controlled by stress, pheramones, light/dark cycles
  109. LH and FSH (gonadotropins)
    • from anterior pituitary
    • bind and activate G-protein and cAMP
    • promotes gametogenesis and gonadal hormone secretion
  110. hormone levesl at gestation
    • week 4- GnRH secretion (low till puberty)
    • week 10-12- LH and FSH secretion (peak at mid-gestation, low until puberty)
  111. hormone levels during childhood
    LH and FSH levels rise slowly
  112. hormone levels during puberty
    • pulsitile secretion of GnRH
    • increased LH and FSH secretion
  113. hormone levels during senescence
    • increase in LH and FSH due to down regulation of r/cs (no negative feedback)
    • more gradual in males
  114. puberty
    • plasma levels increase (estrogen, testosterone, and inhibin)
    • r/cs become more responsive resulting in the development of secondary sex characteristics
  115. female puberty
    • ovaries produce estradiol
    • budding of breasts
    • hair growth
    • menarche
    • growth spurts
  116. male puberty
    • leydig cell proliferation
    • lowering of voice
    • spermatogenesis begins
    • growth spurt
  117. male reproduction
    • regulation, synthesis, and secretion of hormones
    • spermatogenesis
    • sex
  118. testes
    • leydig cells
    • sertoli cells
  119. leydig cells
    • located in CT
    • secrete testosterone
    • stimulated by LH
  120. sertoli cells
    • in seminiferous tubules
    • stimulated by FSH
    • produce sperm
    • testosterone r/cs
    • secrete inhibin (inhibits GnRH and FSH)
  121. epididymis
    • testes to vas deferens
    • maturation of sperm
    • lined by cilia
  122. seminal vesicles
    • secretes 70% of semen fluid
    • energy
  123. prostate gland
    • 5 lobes
    • produces seminal fluid
    • contracts during emission
  124. semen
    • pH 7.5
    • clotting enzymes
    • fibrinolysis
  125. sperm
    • head- acrosome
    • tail- glagellum

    • mature in epididymis
    • stored in vas deferense
  126. sperm abnormalities
    • increased temp causes decreased spermatogenesis
    • cryptorchidism- failure of testes to descend
    • <20 million= infertility
  127. hormones from the testes
    androgens (testosterone, dihydrotestosterone, androstenedione)
  128. which hormones cause spermeogenesis
    FSH and testosterone
  129. inhibin
    • produced by sertoli cells
    • supresses FSH via negative feedback
  130. control of spermatogenesis
    via FSH
  131. steps in spermatogenesis
    spermatogonia -> primary spermatocyte -> secondary spermatocyte -> spermatid -> spermatozoa

    • stimulated at puberty by FSH
    • GH controls metabolic function of testes
    • sertoli cells produce androgen binding protein
  132. androgens
    • = steroid promoting growth and decvelopment of genital tract
    • 95% from leydig cells
    • 5% from adrenals
  133. testosterone
    most abundant androgen
  134. dihydrotestosterone
    from testosterone
  135. androstenedione
    precurosor to testosterone
  136. testosterone secretion
    • diurnal
    • low at night, high in the morning
  137. age patterns of testosterone secretion
    • fetal- high
    • childhood- low
    • puberty- high
    • adulthood- high, decreases after 60
  138. androgen transport
    • most circulate bound to proteins (sex-hormone binding globumin and albumin)
    • 2% free and active
    • converted in liver to dehydroepiandosterone for excretion
  139. action of testosterone
    • binds to cytoplasmic r/cs
    • enters nucleus (transcription and translation)
    • production of proteins everywhere in the body
    • androgen actions
  140. testosterone metabolites
    • estradios via aromatase
    • dehydrotestosterone via 5-alpha-reductase
  141. fetal functions of testosterone
    • stimulated by hCG
    • supresses female genetalia
    • makes hypothalamus more male
  142. puberty functions of testosterone
    developement of primary and secondary sex characteristics
  143. reproduction functions of testosterone
    • secretions
    • libido
    • sperm materation
    • semen production
  144. testosterones anabolic activity produces the male body type
  145. female reproductive tract
    • prepares for conception
    • pregnancy
  146. female hormones
    • FSH and LH stimulate estrogen and progesterone from ovary
    • FSH and LH inactve until puberty
  147. ovary anatomy
    • oogonia formed in fetus by hCG, Gh, and gonadotropins
    • granulosa cells surround ovun- primordial follicle
    • gransulosa cells secrete oocyte inhibiting factor until puberty
    • FSH stimulates 6-12 follicles
    • outer granulosa cells form thecal cells
  148. thecal cells
    • have LH receptors
    • produce androstenediaon and testosterone
  149. inner granulosa cells
    • have FSH receptors
    • have aromatase to convert androstenedion to estradiol
  150. developing follicle
    • theca internaa produces estrogen, progesterone, and theca externa
    • growth via estrogen
    • LH and estrogen cause increased theca secretions
    • 1 mature follicle per month
  151. corpus luteum maintained by:
    LH
  152. corpus albicans form because of:
    low levels of LH and FSH when unfertilized
  153. endometium
    • influenced by estrogen and progesterone
    • if corpus albicans form, menstral phase occurs, sloughing off of endometrium
    • high estrogen prior to ovulation causes endometrial proliferation
    • high progesterone after ovulation causes secretory development
  154. secondary sex characteristics formed by:
    estrogen levels become high and cyclic
  155. estrogen in menopause
    • ovarian burn-out
    • estradiol secretion ceases
    • FSH and LH levels rise b/c of no negative feedback
  156. most important estrogen
    estradiol
  157. most important progestin
    progesterone
  158. function of estrogens
    • proliferation
    • promote growth and development of reproductive tract
    • secondary sex characteristics
  159. function of progestins
    • secretory
    • prepare uterus for pregnancy
    • prepare breasts for lactation
  160. follicular phase
    progesterone and testosterone synthesized but then converted to estrogen by aromatase in granulosa cells
  161. luteal phase
    progesterone levels high
  162. transport of estrogen/progesterone
    • 98% bound to sex hormone binding protein or albumin
    • loose binding, hormones easily released
  163. metabolism of estrogen/progesterone
    • mainly in liver
    • converts E1 and E2 to E3 (inactive)
  164. 3 types of estrogens
    • E2- beta estradiol- most potent/common- non pregnant
    • E1- estrone- from conversion of testosterone to estrogen
    • E3- estriol- from oxidation of others in liver
  165. effects of estrogen on reproductive tract
    • ovaries: follicular growth
    • uterus: proliferation of endometrium
    • vagina: growth, reduces pH
    • fallopian tube: growth , ciliary action to uterus
    • external genetalia: growth
    • breasts: growth, development
    • cervical mucus: thinner, increased pH, sperm transport
  166. other effects of estrogen
    • anabolic
    • stimulates bone growth
    • increased skin thickness
    • sodium and water retention
  167. excess estrogen causes:
    • cramps
    • nausea
    • edema
    • enlarged uterus
    • fibrocystic breasts
    • menorrhagia
  168. estrogen deficiency causes:
    • scant menses
    • small uterus
    • small breasts
    • spotting
  169. types of progestins
    • progesterone- most inportant
    • 17-alpha-hydroxyprogesterone- aganist to progesterone
  170. effects of progesterone
    • endometrial secretory changes
    • decreased contraction of uterus
    • secretion of fallopian tubes
    • breast enlargement
    • maintains pregnancy
  171. other effects of progesterone
    • thermogenic effect (increased basal body temp)
    • CNS effects
  172. excess progesterone causes:
    • edema
    • bloating
    • headach
    • depression
    • weight gain
    • tiredness
    • varicose veins
  173. progesterone deficiency causes
    • prolonged menses
    • heavey menses
    • cramps
    • luteal spotting
  174. fertilization
    • fertilized secondary oocyte completes meiosis 2 -> ovum
    • chromosomes align
  175. implantation
    • 3-5 days after fertilization
    • progesterone relaxes smooth muscle
    • implantation of blastocyst
    • requires low estrogen and high progesterone levels
  176. factors secreted by placenta
    placenta: hCG, estrogens, progesterone, hCS
  177. hCG
    • human chorionic gonadotropin
    • prevents involution of corpus luterum
    • development of alveoli in breasts
    • development of male fetus
  178. pattern of secretion of hCG
    • from syncytiotrophoblasts 2-3 days post plantation
    • detection used for pregnancy tests
    • maximum secretion wekk 10-12
    • low levels weeks 16-20
  179. hCS
    • human chorionic somatomammotropin
    • secreted around week 5 in proportion to fetal weight
  180. actions of hCS
    • development of breasts
    • decreased insulin sensetivity for more blood glucose for baby
    • release of free FA for moms energy
  181. progesterone synthesis
    • secreted by corpus luteum
    • week 12- secreted by syncytiotrophoblast
    • increased 10X during pregnancy
    • produced from cholesterol by placenta
  182. progesterone during pregnancy
    • develupment of decidual cells
    • decreases contractility of myometrium
    • cleaveage of embryo
    • prepares breasts for lactation
  183. estrogen synthesis
    • from syncytiotrophoblast cells
    • requires dehydroepiantrosterone- from fetal adrenals
  184. estrogen during pregnancy
    • enlargement of uterus
    • enlargement of breasts
    • enlargement of external genitalia
    • relaxation for parturition
  185. other pregnancy hormones
    • increased CRH, TRH, and prolactin
    • increased clucocorticoids
    • increased aldosterone
    • thyroid enlargement
    • PTH- Ca absorption and lactation
    • relaxin- softens cervix
    • oxytocin- increases in uterine contraction reflex
  186. pregnancy changes in mom
    • weight gain
    • increase metabolic rate (increased temperature)
    • anemia from deficiency
    • increased cardiac output
    • increased blood volume
    • increased respiratory rate
    • increased urination
    • preclampsia
  187. preclampsia
    • hypertension with proteinuria
    • -salt and water retention
    • -low blood flow
    • caused by: aldosterone, autoimmune, low blood to placenta
  188. placenta action
    • fetal nutrition
    • diffusion of oxygen
    • removal of CO2
    • steroid hormone secretion
  189. diffusion of O2 thru placenta
    • maternal PO2= 50
    • fetal PO2= 30
    • fetal hemoglobin has high binding affinity
    • Borr effect
  190. parturition hromones
    • progesterone- inhibits contractions
    • increased estrogen- causes uterine contractions, increased gap junctions
    • oxytocin- positive feedback for contractions
  191. lactation
    • estrogen develops ducts
    • progesterone develops secretory characteristics
    • prolactin promates secretion of milk
    • oxytocin promotes ejection of milk into ducts

    hypothalamus inhibits prolactin - dopamine

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