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GER UNIT 8 > Physio > Flashcards

Physio Flashcards

1
Q

what hormones does the hypothalamus produce?

A
  • CRH
  • TRH
  • GnRH
  • GHRH
  • Somatostatin
  • Dopamine
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2
Q

what hormones does the anterior pituitary produce?

A

GLAMP ForTwo

  • GH
  • LH
  • ACTH
  • MSH
  • Prolactin
  • FSH
  • TSH
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3
Q

what hormones does the posterior pituitary produce?

A
  • oxytocin
  • ADH
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4
Q

what hormones does the thyroid produce?

A
  • T3, T4
  • Calcitonin
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5
Q

what hormones does the parathyroid produce?

A
  • PTH
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6
Q

what hormones does the pancreas produce?

A
  • insulin
  • glucagon
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7
Q

what hormones does the adrenal medulla produce?

A
  • norepi
  • epi
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8
Q

what hormones does the kidney produce?

A
  • renin
  • 1,25-dihydroxycholecalciferol
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9
Q

what hormones does the adrenal cortex produce?

A
  • aldosterone
  • adrenal androgens
  • cortisol
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10
Q

what hormones does the testes produce?

A
  • testosterone
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11
Q

what hormones does the ovares produce?

A
  • progesterone
  • estradiol
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12
Q

what hormones does the corpus luteum produce?

A
  • estradiol
  • progesterone
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13
Q

what hormones does the placenta produce?

A
  • progesterone
  • HPL
  • HCG
  • estriol
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14
Q

what are the differences between peptide/amine hormones and steroid hormones?

A

peptide/amine hormones

  • ​stored in secretory vesciles
  • receptors within cell membrane
  • activate signaling ascades
  • fast acting (seconds/minutes)

steroid hormones

  • produced on demand
  • diffuses through cell membrane
  • receptors in nucleus (sometimes cytoplasm)
  • up/down regulate transcription
  • slow acting (hours/days)
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15
Q

pseudohypoparathyroidism

A

excess PTH because of genetic defect in GPCR PTH receptor on kidney→unable to transduce PTH signal to regulate body Ca2+ and phosphorus homeostasis

  • hypocalcemia and tetany
  • hyperphosphatemia
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16
Q

what is the difference between long loop and short loop negative feedback regulation of hormonal secretion?

A
  • long loop: hormones released from peripheral glands feeds back onto hypothalamic-pituitary axis
  • short loop: anterior pituitary feeds back on hypothalamus
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17
Q

how is the secretion of anterior pituitary hormones regulated by hypothalamus?

A

releasing factors are delivered from hypothalamus to the anterior pituitary via hypothalamic-hypophysial portal system

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18
Q

how is the secretion of posterior piturary hormones regulated by the hypothalamus?

A

nerve cell bodies in hypothalamus synthesize hormones which are transported in vesicles down axons to posterior pituitary for release

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19
Q

describe the nature of the blood supply to the anterior and posterior pituitary

A
  • anterior pituitary recieves venous blood carrying neuropeptides from hypothalamus and pituitary stalk
  • posterior pituitary receives arterial blood
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20
Q

what are the differences in the nature of the hormones released by the anterior vs. the posterior pituitary?

A
  • ​anterior pituitary hormones are proteins and glycoproteins
  • posterior pituitary hormones are smaller molecular mass peptides associated with neurophysins (carrier proteins which transport the oxytocin and vasopressin to posterior pituitary from hypothalamus)
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21
Q

the release of most anterior pituitary hormones is controlled by hypothalamic releasing factors EXCEPT…

A

prolactin; under tonic inhibitory control by dopamine

  • circulating prolactin increases if infundibulum is severed
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22
Q

what are effects of GHRH from hypothalamus?

A
  • stimulates GH transcription and release
  • stimulates production of GHFH receptor
  • stimulates somatostatin release (negative feedback)
  • inhibits GHRH secretion (negative feedback)
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23
Q

what are the effects of somatostatin release from the hypothalamus?

A
  • inhibits pulse frequency of GH
  • inhibits pulse amplitude of GH
  • inhibits release of GH
  • has NO impact on synthesis of GH
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24
Q

how does the pulsatile secretion of GH change during puberty?

A

number of pulses per day are constant but there is a larger pulse amplitude

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25
Q

what kinds of things stimulate GH secretion?

A
  • deep sleep
  • exercise
  • sex hormones
  • fasting/hypoglycemia
  • stress
  • dopamine agonists (suppress in acromegaly)
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26
Q

what kinds of things inhibit GH secretion?

A
  • IGF-1 (negative feedback)
  • GH (negative feedback)
  • obesity
  • hyperglycemia
  • pregnancy
  • somatostatin
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27
Q

what are the net effects of GH?

A

counteracts insulin

  • decreases glucose uptake into cells (diabetogenic)
  • decreases glucose utilization in muscle
  • increased protein synthesis in muscle
  • increased lipolysis
  • increased IGF-1 production
  • (inhibits its own secretion by stimulating somatostatin from hypothalamus)
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28
Q

what is the direct effect of GH on the liver?

A
  • stimulates release of IGF-1 (acts on GHRH and anterior pituitary to reduce GH production)
  • stimulates hepatic glucose production
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29
Q

what is the direct effect of GH on adipocytes?

A

releases and oxidizes free FA especially during fasting, mediated by reduction of lipoprotein lipase activity (reduced lipogenesis)

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30
Q

what is the relationship between GH and IGF?

A

IGF-1 is primary mediator of the effects of GH

  • tyrosine kinase IGF-1 receptor dimerizes and autophosphorylates→recruits phosphotyrosine binding proteins IRS-1 and Shc→P13K and Ras/MAP kinase regulation of transcription
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31
Q

how does IGF account for longitudinal growth?

A

action of GH via IGF is responsible for linear growth

  • IGF-1 induces clonal expansion of early chondrocytes and maturation of later chondrocytes
  • increases protein synthesis in muscle and organs
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32
Q

laron syndrome

A
  • low IGF-1→post-natal growth failure (similar phenotype to STAT5b mutation)
  • normal/elevated GH
  • reduction in cancer and diabetes BUT do not live longer (epilepsy and obesity)
  • treat: rhIGF-1
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33
Q

what is the mechanism of GH receptor activity?

A

hormone/cytokine receptor with no inherent tyrosine kinase activity

  • GH binds→conformational change of receptor dimer→activates JAK2→phosphorylates/ activates STAT TF
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34
Q

what are the effects of ghrelin from the stomach and pancreas on GH secretion?

A

ghrelin acts on the hypothalamus and anterior pituitary to stimulate GH release

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35
Q

acromegaly

A
  • occurs in adults with GH-secreting adenomas
  • protruding jaw, macroglossia, englarged hands/feet
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36
Q

how does nutritional deficiency affect growth?

A

nutritional deficiency slows growth through reduction of IGF-1 levels

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37
Q

hypothyroidism

A
  • low TH→decreased BMR, thermogenesis, gluconeogenesis, glycogenolysis, protein synthesis, proteolysis, lipogenesis, lipolysis
  • normal serum glucose
  • increase serum cholesterol
  • non pitting edema
  • bone age
  • reduced GH production (thyroid hormone response element is upstream of GH transcription start site)
  • cretinism in infants (mental, growth retardation)
  • treat with thyroxine (T4): longer half-life and greater stability (tighter binding/lower metabolic clearance)
    • excessive treatment→bone loss/osteoporosis
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38
Q

what are the implications of GH-deficiency on CVD?

A
  • not as impactful as obese and sedentary but same trend
  • increases: visceral adipose tissue, carotid intima-media thickness, inflammatory markers of CVD, clotting factors, insulin resistance, LDL
  • decreases: myocardial function, HDL
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39
Q

describe the regulation of thyroid hormone by TRH and TSH

A
  • TRH from hypothalamus→anterior pituitary to produce TSH by activing GPCR linked to PLC→IP3
  • TSH stimulates TH synthesis/release by GPCR linked to adenylate cyclase→cAMP
  • TSH increases uptake up iodide, synthesis of TG, storage of TH in colloid, increases endocytosis of colloid
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40
Q

what are the biologically active forms of thyroid hormone?

A
  • T4: “prohormone”
  • T3: biologically potent form derived from T4
  • rT3: not biologically active
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41
Q

how does the body overcome the fact that the formation of T4 is preferred over production of T3 (active form)?

A

target tissues are able to convert T4 to T3 using peripheral deiodinases

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42
Q

what is the mechanism of action of thyroid hormone

A
  • peripheral deiodinases generate T3 and rT3 from T4
  • free T4 and T3 enters cell→5’/3’-monodeiodinase converts most T4 to T3 (cytoplasmic levels of T4 and T3 are about equal)→TH receptor binds DNA at thyroid response elements in promoter region regulated by THs
  • result: protein/enzyme production to increase metabolic rate and O2 consumption; catabolism
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43
Q

hyperthyroidism

A
  • high TH→increased BMR, thermogenesis gluconeogenesis, glycogenolysis, protein synthesis, proteolysis, lipogenesis, lipolysis
  • muscle wasting, no exopthalmus
  • normal serum glucose
  • low serum cholesterol
  • increased expression of ßadrenoreceptors (increased senstitivity to catecholamines)
  • treatment: PTU (blocks thyroid peroxidase activity)
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44
Q

describe the formation of T3 and T4 from TG

A
  1. thyroglobulin from tyrosine
  2. Na+/I- cotransport
  3. oxidation of I-→I2 in lumen, organification of I2
  4. coupling of MIT and DIT
  5. stimulation by TSh→endocytosis from lumen
  6. lysosomal enzymes digest thyroglobulin, releasing T3 and T4
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45
Q

describe the negative feedback process of of thyroid hormone

A

T3 (especially) and T4 exert negative feedback on anterior pituitary and hypothalamus by downregulating TRH receptors

  • dopamine and somatostatin also inhibit effects on TSH release
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46
Q

what three enzymes are responsible for both mineralocorticoid and glucocorticoid synthesis?

A
  1. 3ßhydroxysteroid dehydrogenase
  2. 21ßhydroxylase
  3. 11ßhydroxylase
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47
Q

what are the effects of glucocorticoids on target tissues?

A
  • stimulates gluconeogenesis
  • increase protein breakdown in muscle (to provide a.a for gluconeogenesis)
  • decreases glucose utilization (except in brain, inhibits Glu4 recruitment–brain uses Glu3)
  • increases lipolysis
  • anti-inflammatory: inhibits cytokines and chemoattractants
  • immunosuppressant: suppresses T cells, inhibits IL-2
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48
Q

if cortisol binds mineralocorticoid receptors with the same affinity as glucocorticoid receptors, why does it have little mineralocorticoid activity?

A

11ßhydroxysteroid dehydrogenase II in kidney and colon convert cortisol into cortisone which does not bind MR

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49
Q

how are steroid hormones regulated?

A

CRH from PVN in hypothalamus→hypothalamic-hypophysial portal blood→corticotrophs in ant. pituitary→POMC→ACTH

  • **ACTH: ** increases cholesterol desmolase activity, promotes adrenal cortex cell proliferation, upregulates ACTH receptor
50
Q

describe the mechanism of negative feeback on ACTH

A
  • feedback inhibition only exerted by glucocorticoids
  • inhibits expression of CRH receptor (and thus ACTH synthesis) from corticotrophs of ant. pituitary
51
Q

when is cortisol secreted?

A

circadian control of cortisol secretion because CRH→ACTH→cortisol

  • highest just before waking
  • cortisol is major hormone related to stress (e.g., biochemical stress like hypoglycemia)
52
Q

addison’s disease

A

hypoadrenal function due to autoimmune diease or TB→destruction of adrenal cortex; symptoms: skin hyperpigmentation

  • decreased aldosterone: hypertension, hypokalemia, metabolic acidosis
  • decreased cortisol: increased ACTH, weight loss, poor stress tolerance
  • decreased sex hormones
53
Q

cushing’s disease

A

excess ACTH from pituitary gland tumor→excess cortisol

  • symptoms: upper body obesity, buffalo hump, poor wound healing
  • increased aldosterone: hypertension
  • increased cortisol: increased blood glucose
  • increased androgens
54
Q

cushing’s syndrome

A

any etiology of excess cortisol that is NOT a pituitary gland tumor; ACTH levels will thus be low because of feedback

55
Q

dexamethasone (glucocorticoid) suppression test

A

differentiates Cushing’s by taking advantage of the feedback inhibition on ACTH secretion

  • normal: low cortisol→low ACTH
  • adrenal tumor: high cortisol→low ACTH
  • ACTH producing tumor: high cortisol→high ACTH (if you increase the dose then low cortisol→low ACTH)
56
Q

graves disease

A
  • most common cause of hyperthyroidism
  • **autoimmune: TSH receptor antibodies (LATs) bind tighter and longer than TSH→chronic T3/T4 production **
  • TSH levels fall because negative feedback loop is working
  • symptoms: exophthalmos, fatigue, weight loss with increased appetite, tachycardia, muscle wasting
57
Q

hashimoto’s disease

A
  • most common cause of hypothyroidism
  • elevated thyroid antibodies
  • elevated TSH
58
Q

what is the overall action of PTH?

A
  • increases serum Ca2+
  • decreases serum PO4
59
Q

what is the primary target of PTH?

A

kidney

  • increases reabsorption of Ca2+ from distal tubule via Ca channel in luminal membrane
  • decreases resorption of PO4 in proximal tubule
  • increases synthesis of active vitamin D (leads to more Ca2+ absorption)
60
Q

what is the effect of PTH on bone?

A

increases osteoclastic resorption via receptors on osteoblasts→increased Ca2+ and PO4 in ECF and plasma

  • osteoblasts sends out cytokines (RANKL) that activates nearby osteoclasts to form new osteoclasts
61
Q

what is the primary target of vitamin D?

A

intestine

  • increases Ca2+ and PO4 absorption by increasing synthesis of calbindin (transporter)
62
Q

what is the effect of vitamin D on bone?

A

stimulates osteoclastic resorption via receptors on osteoblasts→increased Ca2+ and PO4

63
Q

what are the effects of vitamin D on the parathyroid and kidney?

A
  • parathyroid: suppresses PTH (negative feedback)
  • kidney: aids increased reabsorption of Ca2+ in distal tubule by increasing calbindin/Ca2+ transport and efflux at basal side of tubule
64
Q

rickets

A

chronic vitamin D and/or Ca2+ and/or PO4 during early development→poor mineralization of bone→weakened and mechanically distorted long bones and abnormal growth plates

65
Q

osteomalacia

A

chronic vitamin D and/or Ca2+ and/or PO4 deficiency→poor quality bone formed during remodeling

66
Q

primary hyperparathyroidism

A

excess PTH secretion (usually parathyroid adenoma)

  • hypercalcemia
  • hypophosphatemia
  • increased phosphaturia (high alk phos) and calciuria
  • increased bone resorption
67
Q

secondary hyperparathyroidism

A

primary hypocalcemia (due to low D, renal failure, diet, etc…)→high PTH to stimulate Ca2+ resorbtion in kidney and bone

68
Q

hypoparathyroidism

A

usually due to surgical damage on parathyroid→decreased PTH

  • hypocalcemia and tetany
  • hyperphosphatemia
69
Q

humoral hypercalcemia of malignancy

A

Ca2+ is high due to release of PTHrp by lung tumor cells (analog of PTH)

  • same as hyperparathyroidsm except LOW PTH due to feedback inhibition
70
Q

follicular phase of ovarian cycle

A

day 0-14: FSH stimulates development of follicles

  • includes menstrual and most of proliferative phase of uterine cycle
  • estrogen dominates and primes uterus for progesterone (induces progesterone receptors)
  • primordial follicle→graafian follicle
71
Q

ovulatory phase of ovarian cycle

A

day 14: burst of estrogen synthesis that has positive feedback on FSH and LH→LH surge→rupture of graafian follicle​

72
Q

luteal phase of ovarian cycle

A

day 14-28: LH converts rupture follicle to corpus luteum which synthesizes estrogens and progesterone

  • progesterone dominates→conversion of uterus to secretory type (promotes glycogen storage/secretion of carb-rich mucus), increased vascularity, increased temp
  • characterized by negative feedback on GnRH release
73
Q

menstrual phase of uterine cycle

A
  • prostaglandin→vasoconstriction of spiral arteries and local ischemic injury/inflammation, regresion of corpus luteum
  • abrupt withdrawal of estrogen and progesterone→sloughing off of endometrium
74
Q

what are the roles of hypothalamic and pituitary hormones in regulation of ovarian function?

A

pusatile GnRH→ant. pituitary→FSH (during follicular phase) and LH (during luteal phase)

  • FSH: binds receptors on granulosa cells→synthesis of aromatase, activins, and inhibins
  • LH: binds to receptors on theca cells→synthesis of progestins and androgens→granulosa cells and are converted to estrogens
75
Q

describe the LH surge during the late follicular phase

A

positive feedback when high circulating estrogens “sensitize” ant. pituitary gonadotrophs to stimulation by GnRH→LH surge necessary for rupture of follicle→ovulation

76
Q

two-cell, two-gonadotropin model

A

granulosa cells have aromatase necessary for estrogen synthesis but do not have enzyme to make androgen precursors (those are synthesized in theca)

  • testosterone diffuses from theca to granulosa
  • vascularization of corpus luteum makes LDL available to granulosa cells which enables both granulosa and theca cells to make progesterone
77
Q

hormonal changes in female puberty

A
  • before puberty: release of GnRH inhibited by low sex steroids
  • during puberty: pulsatile secretion of GnRH (observed first at night then duing the day as well)→upregulation of its own receptor on anterior pituitary
  • thelarche, adrenarche, menarche
78
Q

the menopause

A
  • no more follicles to respond to FSH and LH→decrease in circulating sex steroids
    • rise of FSH and LH (no negative feedback and lack of inhibin)
  • larger women may not be as symptomatic because estrone is produced peripherally by muscle and adipose tissue
  • estrogen treatment increases risk for certain cancers/diseases; mix with progesterone
79
Q

polycystic ovary disease

A
  • bunch of follicles with no dominant follicle→no ovulation, no conversion of proliferative→ secretory
  • reduced estrogen and progesterone
  • continued production of androgen by thecal cells→facial hair and acne
  • treat with birth control or clomiphene (partial estrogen receptor agonist, restores ovulation)
80
Q

where is the most dangerous place for ectopic pregnancy?

A

interstitial region of uterine tube; puts patient at risk for major hemorrhage because of its proximity to the area where the uterine vasculature enters the uterus

81
Q

how does ß-hCG change during pregnancy?

A
  • doubles every 48 hours until its peak
  • low in ectopic pregnancy
82
Q

what do you use to diagnose menopause?

A

rise of FSH (due to lack of negative feedback)

83
Q

capacitation of sperm

A

functional maturation of the spermatozoon; removal of a glycoprotein layer make receptors available on the sperm cell membrane; area of acrosomal cap is also so altered, enabling acrosome reaction

84
Q

acrosomal reaction

A

triggered by sperm binding to an egg glycoprotein; Ca-dependent process in which the acrosome (large organelle in sperm head) fuses with the sperm cell plasma membrane (exocytosis)

  • causes second Ca rise in egg that triggers cortical reaction (exocytosis of granules that hardens zona pellucida to prevent polyspermy)
85
Q

how long does it take the blastocyst to move from the fallopian tube to the uterus?

A

3-5 days; 1-2 days before implantation

86
Q

how is the corpus luteum rescued from regression?

A

trophoblasts→synciotrophoblasts that produce HCG (similar to LH)

  • sustains corpus luteum for 8-10 weeks as maternal LH declines, before placenta takes over steroid production
87
Q

what hormone is measured in a pregnancy test?

A

HCG

88
Q

how do fetal adrenal-placental interactions produce estrogen?

A

fetal adrenal gland​ makes DHEA-S which is then hydroxylated in the fetal liver, intermediates are transferred to the placenta where it is converted to estrogens

89
Q

where is progesterone produced during the first and second trimesters of pregnancy?

A
  • first: corpus luteum
  • second: placenta
90
Q

ferguson reflex

A

positive feedback of oxytocin whereby baby’s head stretches cervix→fundic contraction due to oxytocin→stretches cervix more→more contractions

91
Q

what are the roles of estrogen/progesterone, oxytocin, and prostaglandin during parturition?

A
  • increased ratio of estrogen/progesterone makes uterus more sensitive to contractile stimuli
  • estrogen increases number of oxytocin receptors on myometrial tissue in uterus (enables ferguson reflex)
  • prostaglandins initiate contractions and are sustained by oxytocin and more prostaglandins
92
Q

what hormones are mammogenic?

A
  • estrogen
  • progesterone
  • cortisol
  • prolactin
93
Q

what hormones are lactogenic?

A
  • prolactin
94
Q

what hormones are galactokinetic?

A
  • oxytocin
95
Q

what hormones are galactopoietic?

A
  • prolactin
96
Q

how is ovulation suppressed during breast feeding?

A

prolactin acts to

  • inhibit GnRH secretion
  • inhibits action of GnRH on anterior pituitary (thus inhibiting LH and FSH)
  • antagonizes actions of LH and FSH on ovaries
97
Q

how is secretion of breast milk inhibited during pregnancy?

A

estrogen and progesterone black action of prolactin on the breast

98
Q

how does suckling maintain lactation?

A

suckling triggers neuroendocrine response that causes release of oxytocin while inhibiting release of GnRH

99
Q

colostrum

A

fluid initially produced during breast feeding; concentrated, low-volume form of nutrition for neonate’s immature GI tract (has little/no fat and antibodies)

100
Q

describe the blood supply to the fetus

A

placenta receives 50% of combined CO from iliac arteries→spiral arteries from mother empty directly into intervillous space→umbilical vein

101
Q

what is the difference between HbF and Hb?

A

placenta has 50% more HbF than mother

  • HbF has same PO2 as HbF has a higher saturation
102
Q

describe the path of blood after gas exchange occurs in the placenta

A

gas exchange in placenta→umbilical vein (highly oxygenated)→ductus venosus→IVC→atria

  • 40% of blood flows through foramen ovale from RA→LA
  • 66% to RV→pulmonary artery→ductus arteriosis→aorta
  • 34% to LV (heart and brain)
103
Q

how is circulation maintained in the fetus?

A
  • circulating prostaglandin is 5x that of adult
  • lower PO2 allows cells of ductus arteriosa to be relaxed
  • lungs are collpase due to hypoxic vasocontriction, lack of inflaction, relative acidosis→high vascular resistance
104
Q

what are the mechanisms involved in transitioning from fetal to neonatal to adult circulations

A
  • clamp umbilical cord→BP in aorta increases→sudden increase in systemic vascular resistance)→back pressure in LV and LA and pressure in RA decreases
    • closure of foramen ovale caused by reversal of R/L atrial pressure
  • first breath: alveoli of neonate are oxygenated, decreased PVR, and pulmonary blood flow increases and becomes equal to CO
    • constriction of vascular smooth muscle (due to increased PO2, decreased prostaglandin, and brandykinin) causes closure of ductus arteriosis
  • ductus venosus closes
105
Q

what are the dangers of delivering a baby at high altitudes?

A

ductus arteriosis cannot close due to low PO2→hypoxia→ vasoconstriction of lung→persistent fetal circulation

  • treat: O2 and endomethycin (inhibits COX which inhibits prostaglandin)
106
Q

genotypic vs. gonadal vs phenotypic sex

A

genotypic: presence of Y chromosome
gonadal: presence of SRY gene (encodes testes determining factor)
phenotypic: hormones→gonads

107
Q

describe the role of FSH in testicular function

A

FSH→testes→sertoli cells→

  • increased transcription of androgen binding protein, P450 aromatase, growth factors
  • inhibin: negative feedback on ant. pituitary and suppress FSH secretion (suppresses leydig cell proliferation)
108
Q

describe the role of LH in testicular function

A

LH→testes→leydig cells→testosterone→

  • increased transcription of enzymes involved in testosterone synthesis
  • stimulate sertoli cells
  • negative feedback on hypothalamus and ant. pituitary
109
Q

describe the role of testosterone in sex differentiation

A

testosterone→wolffian duct→male internal genitalia (vas deferens, semnal vesicles, and ejaculatory duct)

  • without testosterone, wolffian duct degenerates (female)

testosterone→DHT→external genitalia and prostate

110
Q

describe the role of AMH in sex differentiation

A

AMH (from sertoli cells)→mullerian duct→degeneration of mullerian ducts

  • no androgens=no AMH→mullerian duct becomes fallopian tubes, cervix, and uterus
111
Q

kallman syndrome

A
  • hypogonadotropic hypogonadism; lack of LH and FSH, patient presents with failure to enter puberty
  • congenital anosmia: mutations prevent neurosensory neurons from extending axons into brian AND preventing migration of GnRH neurons into hypothalamus
112
Q

male pseudohermaphroditism

A

deficit in mechanims by which androgens act in genetic males

  • 5a-reductase deficiency: low DHT (no external genitalia or prostate) but normal testosterone
  • androgen insensitivity: normal testosterone and DHT but absent/defective androgen receptors→female development (except AMH→degeneration of mullerian ducts)
113
Q

describe why the pubertal growth spurt occurs first in girls

A

bone maturation occurs indirectly through estradiol metabolites and is more gradual in men than in women; estradiol levels rise earlier and reach higher levels in women than in men

114
Q

kennedy’s disease (spinobulbar muscular atrophy)

A

x-linked LMN disease caused by mutations in androgen receptor; CAG repeat expansion→weakness of tongue and mouth, fasciculations, progressive weakness of limbs

115
Q

what are the neural components of erection and ejaculation?

A

“Point and Shoot”

  • parasymp: responsible for vasodilation and smooth muscle relaxation→tumescence (erection)
  • symp: maintains tedumescence, responsible for emission and ejaculation
116
Q

IVF procedures

A
  • controlled ovarian hyperstimulation
  • embryo retrieval using ultrasound
  • IVF
  • embryo transfer
  • luteal phase support
117
Q

clomiphene citrate

A

estrogen antagonist, inhibits negative feedback of estrogen on hypothalamust→increased secretion of GnRH and FSH/LH; used during controlled ovarian hyperstimulation so that more than 1 mature oocyte is produced

118
Q

ovarian hyperstimulation syndrome

A

excessive response to medicines (especially gonadotropins) used to stimulate follicle growth due to large number of growing follicles (>25) along with high estradiol levels→bloating, nausea, weight gain due to transufation of protein rich fluid

119
Q

how old are embryos when they are transferred into the uterus during IVF

A
  • day 5 (blastocyst): preferred because of higher rates of implantation survival
  • day 3 (cleavage stage): suited to patients with less than 6 embryos, low quality embryos or previous IVF failures
120
Q

luteal phase support

A

progesterone supplementation daily or hCG once or more during the luteal phase to promote development of endometrium

GER UNIT 8 (3 decks)

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