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Psyc 342 > final review first half of course > Flashcards

final review first half of course Flashcards

1
Q

2 types of hormones released by hypothalamus

A
  1. releasing hormones
  2. inhibiting hormones
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2
Q

hypothalamus: 6 releasing hormones

A
  1. thyrotropin-releasing hormone (TRH)
  2. growth hormone-releasing hormone (GHRH/somatocrinin)
  3. gonadotropin-releasing hormone (GnRH)
  4. melanotropin-releasing hormone (MRH)
  5. corticotropin-releasing hormone (CRH)
  6. kisspeptin

ALL OF THESE ARE EXCITATORY (releasing hormones)

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3
Q

hypothalamus: 3 inhibiting hormones

A
  1. somatostatin (growth hormone-inhibiting hormone/GHIH)
  2. gonadotropin inhibitory hormone (GIH)
  3. dopamine

ALL OF THESE ARE INHIBITORY

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4
Q

CRH

A

corticotropin-releasing hormone

stimulates secretion of ADRENOCORTICOTROPHIC hormone

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5
Q

‘tropic’ means…

A

nourishing

ie. adrenocorticotrophic means a hormone that nourishes the adrenal gland

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6
Q

GRH

A

gonadotropin-releasing hormone

controls release of…
a. luteneising hormone (LH)
b. follicle stimulating hormone (FSH)

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7
Q

TRH

A

thyrotropin-releasing hormone

tells pituitary to release more TSH (thyroid stimulating hormone)

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8
Q

MRH

A

melanotropin-releasing hormone

stimulates secretion of melanotropin

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9
Q

kisspeptin

A

initiates secretion of GnRH at start of PUBERTY

involved in sexual maturation, but unclear exactly how

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10
Q

dopamine

A

dopamine is usually excitatory

but in endocrine system it’s inhibitory

prolactin-inhibitory hormone

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11
Q

somatostatin

A

inhibits secretion of:

a. growth hormone (GH)
b. thyroid-stimulating hormone (TSH)

also inhibits production of insulin, glucagon, secretin

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12
Q

3 main anterior pituitary hormones

A

recall: ant pit is involved in controlling hormone secretions from adrenal glands, thyroid and gonads

  1. corticotropin-related peptides (painkillers, stress response)
    a. ACTH, MSH, beta-endorphins
  2. somatomammotropins (breast milk, growth)
    a. growth hormone (GH/somatotropin), prolactin
  3. glycoproteins (thyroids, gonads, sex hormones)
    a. TSH, LH, FSH
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13
Q

way to remember the 3 anterior pituitary hormones

A
  1. painkillers/stress response
    (ACTH, MSH, beta-endorphins)
  2. growth
    (somatostatin/GH, prolactin)
  3. sex
    (TSH, LH, FSH)
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14
Q

corticotropin-related hormones (class of hormones released by anterior pituitary)

A
  1. ACTH

^stimulates things to be released from adrenal glands: glucocorticoids, mineralocorticoids, steroids

  1. beta-endorphins

^endogenous opioids resembling opiates through action as “natural pain killer”

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15
Q

why are anterior pituitary hormones often considered poplypeptide-tropic hormones?

A

because they stimulate various physiological processes

either by acting directly on tissue or by causing other endocrine glands to release hormones

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16
Q

somatomammotropin hormones (class of hormones released by anterior pituitary)

A
  1. GH

^promotes linear growth and enhances amino acid uptake and mRNA transcription/translation (increased protein synthesis)

  1. prolactin

^promotes breast development, initiates milk synthesis

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17
Q

glycoproteins (class of hormones released by anterior pituitary)

A
  1. TSH

^works on thyroid to stimulate uptake of iodide and release of thyroid hormones

  1. LH and FSH

^bind to receptors in ovaries and testes, regulate gonadal function, stimulate sex steroid production and gamete development

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18
Q

posterior pituitary hormones

A

oxytocin and vasopressin

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19
Q

posterior pituitary hormone release

A
  1. neurosecretory cell bodies produce vasopressin and oxytocin and transport them to the posterior pituitary
  2. vasopressin and oxytocin are transported and stored in vesicles at axon terminals
  3. released in response to neural signals via exocytosis and enter the bloodstream this way

so posterior hormones can be released as quick as neural impulses

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20
Q

anterior pituitary hormone release

A

slower than posterior

  1. axon terminals of hypothalamic neurons release neurohormones near capillaries that give rise to portal vessels
  2. neurohormones from portal vessels stimulate or inhibit the release of hormones from anterior pituitary cells
  3. anterior pituitary hormones leave gland via the blood
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21
Q

oxytocin/vasopressin release is as fast as…

A

neural impulses

released from vesicles via exocytosis

super quickly in response to neural impulses

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22
Q

vasopressin

A

anti-diuretic hormone (makes us retain water/not pee)

causes blood vessel constriction to help deal with blood loss

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23
Q

5 points on oxytocin

A
  1. influences mammal REPRODUCTIVE function
  2. important during BIRTH
  3. causes UTERINE CONTRACTIONS
  4. used to INDUCE LABOUR
  5. involved in SUCKLING REFLEX
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24
Q

what does the pineal gland secrete?

A

melatonin

produced by pinealocytes

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25
Q

thyroid gland

A

large bilateral structure in the neck

consists of many spherical follicles

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26
Q

what does thyroid gland produce

A

T3 and T4

iodinated substances - their production relies on dietary levels of iodate

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27
Q

low levels of dietary iodate

A

reduced thyroid function

hypertrophy

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28
Q

hypertrophy manifests how?

A

swelling in the neck

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29
Q

what do thyroid hormones do?

A

increase OXIDATION RATES in tissues

3 general effects in mammals:

a. metabolism
b. growth and differentiation
c. reproduction

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30
Q

2 thyroid hormones

A

T3: triiodothyronine

T4: thyroxine

both are fat soluble and diffuse rapidly across membrane but need carrier protein to get through blood

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31
Q

4 key functions of T3 and T4

A
  1. regulation of METABOLISM
  2. control BRAIN and NS DEVELOPMENT
  3. sexual MATURATION
  4. TEMPERATURE regulation
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32
Q

hyper and hypothyroidism

A

hyperthyroidism: too much T3 and T4

^weight loss, fast HR, weak menstrual cycle, shaky hands

hypothyroidism: not enough T3 and T4

^weight gain, constipation, cold sensitivity

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33
Q

Ronaldo has…

A

hypothyroidism

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34
Q

parathyroid glands

A

located at rear of thyroid

release PTH (parathyroid hormone)

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35
Q

PTH

A

parathyroid hormone

released by parathyroid, produced by C cells of the thyroid

elevates CALCIUM LEVELS in the BLOOD

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36
Q

what makes PTH

A

C cells of the thyroid gland

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37
Q

how does PTH increase blood calcium levels?

A
  1. increases reabsorption of calcium from bone and gut
  2. inhibits phosphate reabsorption from kidney (reduces calcium clearance)
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38
Q

C cells

A

cells in the thyroid

make PTH and calcitonin

^modulate blood calcium levels

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39
Q

CT

A

calcitonin

released from thyroid’s C cells

works in opposition to PTH

lowers blood calcium levels by INHIBITING CALCIUM RELEASE from bone

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40
Q

CT and PTH are both directly controlled by…

A

blood calcium levels

no releasing hormones are involved in their concentrations

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41
Q

endocrine cells of the pancreas

A

most of the pancreas is exocrine: exocrine cells produce/release digestive juices

but islets of Langerhans are endocrine, and are nested among the exocrine cells

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42
Q

islets of Langerhans

A

islands of endocrine tissue nested within the exocrine cells of pancreas

4 types of cells within these islands

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43
Q

4 types of cells within islets of Langerhans

A
  1. alpha
  2. beta
  3. theta
  4. polypeptide-secreting cells
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44
Q

alpha cells

A

in islets of Langerhans of pancreas

release glucagon

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45
Q

what does glucagon do once it’s released from pancreas?

A

travels to liver

starts glycogenolysis

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46
Q

glycogenolysis

A

caused by glucagon action in liver

breakdown of stored glycogen (into glucose)

acts in opposition to insulin to increase blood glucose levels

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47
Q

glucagon, glycogen and glucose

A

glucagon is released from alpha cells

glucagon causes glycogen to convert to glucose

results in higher blood levels of glucose

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48
Q

ultimately, alpha cells…

A

increase blood levels of glucose

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49
Q

what do beta cells produce?

A

insulin

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50
Q

what does insulin do?

A

lowers blood sugar

controls efficient movement of energy from blood into the cells

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51
Q

glucagon and insulin

A

work in opposition

glucagon increases blood sugar

insulin lowers blood sugar

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52
Q

2 causes of diabetes

A

type 1: insulin deficiency
(pancreatic islets are destroyed by autoimmune response)

type 2: decreased insulin response
(potensh from eating too much sugar or from your insulin not working right)

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53
Q

what do theta cells release?

A

somatostatin

somatostatin inhibits glucagon and insulin release locally in the pancreas

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54
Q

adrenal glands 2 parts

A
  1. adrenal cortex
  2. adrenal medulla
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55
Q

adrenal cortex

A

distinct cellular zones with distinct functional roles

  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
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56
Q

zona glomerulosa

A

whorls of epithelial cells

aldosterone

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57
Q

zona fasciculata

A

orderly bands of cells

glucocorticoid

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58
Q

zona reticularis

A

disorganized cells

sex hormones

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59
Q

adrenal medulla

A

made of chromaffin cells

chromaffin cells come from embryonic development, they’re derived from primitive neural tissue

releases monoamine hormones in response to neural signals

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60
Q

chromaffin cells

A

derived from primitive neural tissue

make up the adrenal medulla

part of ANS

respond to signals from the spinal cord

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61
Q

monoamine hormones released by adrenal medulla

A
  1. epinephrine
  2. norepinephrine
  3. dopamine

also release enkephalins (proteins)

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62
Q

why is adrenal medulla important in fight or flight?

A

because it releases epinephrine and norepinephrine

and because chromaffin tissue receives neural signals super fast (part of ANS since derived from primitive neural tissue)

receives info through direct spinal cord innervations

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63
Q

how does adrenal cortex receive info?

A

through the blood - so it’s slower

(reminder: it releases aldosterone, glucocorticoids and sex hormones)

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64
Q

2 functions of gonads

A
  1. hormone production
  2. gamete production
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65
Q

3 functions of steroid hormones

A
  1. gamete development
  2. behaviours that bring sperm and egg together
  3. development of secondary sex characteristics
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66
Q

seminiferous tubules

A

part of testes

where spermatogenesis occurs

contains sertoli and leydig cells

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67
Q

sertoli cells

A

located along base of seminiferous tubules

facilitate progression from germ cells to spermatozoa

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68
Q

leydig cells

A

interstitial cells between seminiferous tubules

produce androgens/testosterone in response to LH from anterior pituitary

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69
Q

leydig cells produce androgens/testosterone in response to…

A

LH from the anterior pituitary

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70
Q

what does it mean to say the ovaries are “compartmentalized”?

A

its different areas have different functions

follicles, stroma, corpora lutea

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71
Q

germinal epithelia in fetal ovary

A

fetal ovary has germinal epithelia that will eventually develop into primordial follicles

infant ovaries have 500 000 immature follicles

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72
Q

how many immature follicles in infant ovaries?

A

500 000

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73
Q

how many eggs do women ovulate between puberty and menopause?

A

400

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74
Q

atresia

A

continual degeneration of follicles throughout life

no additional gametes are formed postnatally

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75
Q

stroma

A

neoendocrine connective tissue of endocrine glands

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76
Q

follicles

A

epithelial cell-lined sacs that contain an egg

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77
Q

egg/ovum

A

haploid female gamete

contained in follicles

78
Q

corpora lutea

A

endocrine structures that form from remnants of ovarian follicles after egg has been released

secrete progestins

79
Q

progestins

A

secreted by corpora luteum

prepare uterine lining for blastocyst implantation

80
Q

each primary follicle consists of…

A

an ovocyte (immature egg)

81
Q

granulosa cells

A

epithelial cells that surround each ovocyte

produce activin and inhibin (peptide hormones)

82
Q

theca cells

A

surround granulosa cells during follicular maturation

participate in estrogen synthesis

83
Q

antrum

A

space between ovum and surrounding epithelial cells

filled with fluid prior to ovulation

84
Q

ovum is called what as the antrum enlarges?

A

tertiary follicle

85
Q

antrum fluid

A

rich in steroid hormones

aka follicular fluid

86
Q

follicle at its maximum size

A

Graafian follicle

87
Q

granulosa and theca cells after ovum release

A

undergo rapid mitosis

capillaries generated by theca cells vascularize the granulosa cells

88
Q

corpora lutea formation

A

forms from the rapid mitosis of the theca and granulosa cells after ovum release

(and vascularization of granulosa cells)

89
Q

zona pellucida

A

multiple layers of epithelial cells that surround the follicle

90
Q

what does placenta form from?

A

tissues from blastocyst and maternal uterus

91
Q

what does placenta do for fetus?

A
  1. maintains nutritional, excretory and respiratory functions
  2. supplies steroid and peptide hormones for mother and fetus
92
Q

placenta tie to pregnancy tests

A

pregnancy tests measure HCG (human chorionic gonadotropin)

HCG is a hormone produced by rudimentary placenta right after blastocyst implantation

93
Q

HCG

A

hormone produced by rudimentary placenta

right after blastocyst implantation

94
Q

relaxin

A

produced by corpora lutea during pregnancy

softens pelvic ligaments

to allow enough stretch for passage of fetus head through pelvis

95
Q

what do supplementary tropic hormones of the placenta do?

A

stimulate…

gonadal, mammary, adrenal and thyroid functions

96
Q

supplementary tropic hormones released by placenta

A
  1. chorionic gonadotropin
  2. chorionic somatommamotropin (placental lactogen)
  3. chorionic corticotropin
  4. chorionic thyrotropin
97
Q

chorionic gonadotropin (hCG)

A
  1. maintains corpora luteum function (progestin secretion) during pregnancy
  2. inhibits ovulation during pregnancy
98
Q

what hormone helps inhibit ovulation during pregnancy?

A

hCG - chorionic gonadotropin

99
Q

how are the endocrine cells of the gastrointestinal tract organized?

A

primitive organization

scattered around the gut

100
Q

gastrointestinal tract: what kind of endocrine communication?

A

intracrine/autocrine

gastrointestinal hormones regulate the cells in which they’re produced

(considered more primitive process than endocrine mediation)

101
Q

main gastrointestinal hormones

A
  1. secretin
  2. cholecystokinin
  3. ghrelin

act to supplement ANS during digestion

102
Q

blastocyst

A

cluster of dividing cells made by fertilized egg

early stage of embryo

103
Q

secretin

A

released by duodenal mucosa

in response to food passing into small intestine

stimulates pancreas to produce secretions to aid in digestion

104
Q

cholecystokinin (CKK)

A

released by lining of small intestine

may be involved in satiation of food intake

causes exocrine pancreas to secrete digestive enzymes

causes gallbladder to contract/release bile

105
Q

where outside of gut has CKK been found?

A

brain

neuromodulator and neurotransmitter

106
Q

gastrin

A

peptide hormone

secreted by mucous layer of stomach (produced in antral glands of stomach)

induces water and electrolyte secretion from stomach, liver, pancreas

107
Q

ghrelin stimulates release of what?

A

GHRH from anterior pituitary

108
Q

where is ghrelin made?

A

endocrine cells in stomach

109
Q

what happened when ghrelin was injected into mice?

A

food intake increased

fat deposition increased

110
Q

what happens if you give humans ghrelin?

A

food intake increases by about 30%

111
Q

when do ghrelin concentrations peak?

A

before a meal

decrease after a meal

112
Q

2 pattern types for internal hormonal regulation

A
  1. regulation by physiological by-products generated in response to hormonal action (thermostat)

^ie. parathyroid hormone is released when blood calcium levels drop and stops when the levels have normalized

  1. regulation by stimulatory/inhibitory effects of other hormones

^ie. GnRH is regulated by negative feedback chain

113
Q

negative feedback

A

key part of hormonal regulation

regulatory system that stabilizes a process by reducing its output once a certain level has been reached

114
Q

positive feedback

A

part of hormonal regulation

regulatory system that accelerates a process by increasing output

generally less frequent, must be tightly controlled

ie. short term stress response (can continue for too long)

115
Q

methods by which hormones can affect the levels of their own receptors

A
  1. up regulation - similar to positive feedback

^hormone causes increase in its amount of receptors

  1. down regulation - similar to negative feedback

^hormone causes decrease in its amount of receptors

116
Q

how do hormonal messengers invoke intracellular responses?

A

via signal transduction

chemical hormonal message is transformed into intracellular events that ultimately affect cell function

begins with hormone binding to receptor, ends with final response in target cell

117
Q

signal transduction in steroid hormone cells

A

steroid hormone receptors are located in the cell (nucleus or cytosol)

steroids are lipid-soluble so pass cell membrane to bind with the intracellular receptors

hormone binds their receptor and travel to nucleus

here, they regulate gene transcription

118
Q

signal transduction in peptide/protein hormones

A

peptide/protein receptors are located in cell membrane

2 types of activity

a. intrinsic enzymatic activity: enzymes in cytoplasm activate intracellular proteins

b. second messenger: g-coupled proteins activate when hormone binds receptor which activates proteins

119
Q

example of species that produces asexually

A

white spotted bamboo shark

disadvantage: less genetic diversity

120
Q

sex differences and evolutionary flexibility

A

sex differences result in more evolutionary flexibility

because of increased genetic diversity

through separation of haploid gametes and recombination in offspring

having a combination of genetic material means more flexibility

121
Q

what mating system produces more sexual dimorphism?

A

polygamous (more than monogamous)

ie. prairie voles are monogamous and it’s almost impossible to tell them apart

ie. elk are polygamous and they have clear differences

122
Q

nature or nurture? sexually dimorphic behaviours

A

product of both

reflect role of biology and environment (socialization)

ie. boys more likely to hang out in large groups, rough and tumble pay

ie. girls are more likely to hang out in twos and threes, more verbal communication

123
Q

5 levels of mammalian sexual differentiation

A
  1. chromosomal sex
  2. gonadal sex
  3. hormonal sex
  4. morphological sex
  5. behavioural sex

each level affects the next one

124
Q

how is chromosomal sex determined

A

by whether the male contributes an x or y

(because female always contributes an x)

xx: female
xy: male

125
Q

germinal ridge

A

bipotential primordial gonad, which is essentially a thickening of the germinal ridge

each undifferentiated fetus has this

turns into either ovaries or testes

126
Q

what is needed for germinal ridge to develop into testes?

A

SRY gene from the Y chromosome

it produces TDF (testis determination factor)

127
Q

SF-1

A

steroidogenic factor 1

in combination with TDF, produces a transcription factor

this transcription factor regulates expression of S09X gene

128
Q

protein products of SRY and SOX9 leads to…

A

germinal ridge turning into the testis

if they’re absent, the germinal ridge turns into the ovaries

129
Q

testis development requires

A

SRY gene > TDF

SF-1 > transcription factor > SO9X

130
Q

what gene might be required for normal ovarian development?

A

Wnt4

this is important because used to be thought that mere absence of SOX9 and SRY would leave to development of ovaries

but this suggests there might be another gene that must be present for ovaries to develop

131
Q

what do hormonal secretions from the developing gonads determine?

A

whether fetus develops in male or female-typical manner

mammalian testes produce androgens

mammalian ovaries don’t produce any hormones in high levels

132
Q

in presence of ovaries or complete absence of any gonads, what will happen to development?

A

will follow a female-typical pathway

133
Q

interesting finding: sexually dimorphic transcription of over 50 genes in brains of mice at 10.5 days post conception

A

50 chromosomal genes were different between males and females

even at 10.5 days post-conception, wayyyyy before gonads were developed

suggests that sex genes are mediated by chromosomes, not gonads

134
Q

interesting finding: cell culture from XY mice contain more cells expressing tyrosine hydroxlyase than XY mice, irrespective of the gonadal sex of the embryos from which the cells were taken

A

again, suggests that chromosomes are mediating sex to a certain degree

independently from gonads

135
Q

morphological sex

A

Mullerian (female) and Wolffian (male) systems are both present early on in embryonic development

dual anlagen

136
Q

dual anlagen

A

rudimentary basis of accessory sex organs

apparatus for both male and female accessory organs

137
Q

mullerian duct system develops into…

A

fallopian tubes

uterus

upper vagina

(and Wolffian ducts regress)

138
Q

wolffian duct system develops into…

A

seminiferous tubules

vas deferens

(and Wolffian ducts regress)

139
Q

male accessory organs require…

A
  1. Mullerian inhibitory hormone (MIH)
  2. testosterone

^both are products of the embryonic testes

140
Q

roles of testosterone and MIH

A

testosterone: stimulates Wolffian duct development (masculinization)

MIH: causes regression of Mullerian system (defeminization)

141
Q

what’s responsible for differentiation of external genitalia?

A

androgens

142
Q

what happens to external genitalia in response to androgens?

A
  1. urethral groove fuses
  2. penis develops from genital tubercle
  3. scrotum develops from fusion of genital folds
143
Q

what happens to external genitalia in absence of androgens?

A
  1. clitoris develops from genital tubercle
  2. labia develop from genital folds
144
Q

what do accessory sex organs look like at 6 weeks?

A

still undifferentiated

  1. urethral groove
  2. urogenital sinus
  3. anal fold
145
Q

male vs female external genitalia

A

male: penis, scrotum

female: labia, clitoris

146
Q

what controls mating behaviour in both sexes?

A

gonadal steroid hormones

147
Q

castrated male mice

A

castration stops mounting behaviour

but replacement therapy restores mounting behaviour to regular levels

148
Q

does injecting adult female rats with testosterone cause them to display mounting behaviour?

A

no

suggests that at some point in development, female rats lose the potential to exhibit male typical behaviour

149
Q

do male rats injected with estrogen display female behaviour?

A

no

150
Q
A
151
Q

Charles Phoenix study phase 1 - effect on genitalia

A

LARGER dose mother’s female offspring: external genitalia indistinguishable from males

SMALLER dose mother’s female offspring: no visible changes to external genitalia (“unmodified females”)

152
Q

Charles Phoenix study phase 2 - groups

A

3 groups of males and females

a. smaller dose prenatal testosterone

b. larger dose prenatal testosterone

c. control

153
Q

Charles Phoenix study phase 2 steup

A

all 3 groups were:

  1. gonadectomized
  2. injected with estrogen and progesterone (to stimulate female sexual behaviour)
  3. paired with male guinea pig
  4. later, all injected with androgens (to stimulate male behaviour)
  5. paired with female guinea pig
154
Q

Charles Phoenix study findings

A

androgens given to guinea pigs prenatally…

a. decreased tendency of both small and large dose females to display lordosis

b. increased tendency of both small and large dose females to display mounting in response to testosterone therapy

c. caused no deleterious effects on mounting behaviour or other masculine traits in males who were treated

155
Q

Charles Phoenix study takeaway

A

there’s a clear distinction between prenatal hormonal action which causes organization of neural substrates for behaviour

and the actions of hormones in adulthood that cause the activation of these behaviours

led to the organization-activation hypothesis of sexually dimorphic behaviours

156
Q

organizational/activational hypothesis of sexually dimorphic behaviour

A
  1. sex hormones work during prenatal stage to permanently organize the nervous system in a sex-specific manner
  2. during adulthood, these same hormones have activation effects
157
Q

cyclic vs tonic gonadal function

A

cyclic: in females

^cycles in mating behaviour

tonic: in males

^continuous willingness to mate

158
Q

LH profile in males and females

A

males:
a. steady pulsatile release

females:
a. pulsatile release
b. negative feedback is broken
c. big increase in FSH and LH secretion
d. after ovulation, pulsatile release resumes

159
Q

what controls LH levels?

A

gonadotropins secreted from anterior pituitary

GnRH > LH > gonadal function

160
Q

LH affects what in males and females

A

males: testis and testosterone

females: ovaries and estrogen/progesterone

161
Q

females: GnRH negative feedback is altered how?

A

on a cyclical basis

162
Q

females: breaking GnRH negative feedback loop

A

females escape negative GnRH feedback loop on a cyclical basis

  1. estrogen levels increase
  2. surge of GnRH in response
  3. GnRH stimulates anterior pituitary to release FSH and LH (ovulation
  4. after ovulation, negative feedback system re-engages
163
Q

GnRH and negative feedback

A

happens in both males and females

high GnRH levels feedback to gonads, anterior pituitary and hypothalamus

this slows GnRH, gonadotropin and gonadal steroid secretion

164
Q

chromosomal to gonadal sex

A

Y chromosome contains SRY gene

SRY gene causes expression of TDF

TDF (when combined with SOX9 which needs SF1) leads to development of the testis

without TDF and SOX9, the ovaries develop

165
Q

partial SRY expression

A

leads to incomplete gonadal differentiation

166
Q

chromosomal XY but no SRY

A

male mice develop ovaries

167
Q

chromosomal XX but insert SRY

A

female mice develop testes

168
Q

Swyer syndrome

A

no sex glands develop (no testes or ovaries)

in individuals with XY chromosomes that lack SRY gene

don’t experience puberty without intervention

external female genitalia, but no menstruation

functionless gonads

169
Q

Swyer syndrome is classified as…

A

a disorder of sexual development (DSD)

DSDs encompass any condition where chromosomal, gonadal or anatomic sex is abnormal

170
Q

Swyer syndrome treatment

A

hormonal replacement therapy

171
Q

hormonal to morphological sex

A

if individual is XY, testosterone and MIH must be secreted at the correct time

if MIH isn’t secreted at the correct time, Mullerian system will develop

depending on hormonal secretion, it’s possible for both systems or for neither to develop

172
Q

intersex

A

variety of conditions in which reproductive/sexual anatomy doesn’t fit definition of male or female

ie. discrepancies between external genitalia and internal sexual organs

ie. when both systems develop (either separately or intertwined)

173
Q

is intersex a medical problem?

A

no, but it may signal underlying metabolic concern

used to be considered a problem and people would be surgically altered

174
Q

spectrum of hormonal to morphological sex

A

two intersecting continua

  1. masculinization to de-masculinization
  2. feminization to de-feminization

potential for multiple diff outcomes

175
Q

Prader scale

A

scoring system for grading degrees of genital masculinization

0: un-virilized female

5: completely virilized female

176
Q

completely virilized female

A

5 on Prader scale

female who appears male at birth

but empty scrotum because no testicals

177
Q

what’s responsible for external genitalia differentiation?

A

androgens

androgenic metabolites

178
Q

androgenic metabolite that’s crucial for genital fusion process

A

5 alpha-dihydrotestosterone (5 DHT)

testosterone is converted to 5 DHT by an enzyme

179
Q

high 5 DHT in females

A

leads to development of male external genitalia

180
Q

5 DHT deficiency

A

genetic males (XY)

a. ambiguous genitalia

b. small, undescended testes

c. considered female at birth and raised female

d. testosterone masculinizes body at puberty

181
Q

puberty and people with DHT deficiency

A

testosterone masculinizes body

a. male-typical musculature

b. auxiliary hair growth

c. genitalia develop to resemble penis and scrotum

182
Q

Turner syndrome

A

congenital condition

lack second chromosome (X0) or damage to second chromosome

female external appearance

limited ovarian development

don’t reach puberty without treatment

183
Q

congenital adrenal hyperplasia

A

caused by lack of 21-hydroxylase enzyme

leads to overproduction of adrenal androgens

(progesterone also needs 21-hydroxylase to create other important hormones)

184
Q

congenital adrenal hyperplasia: congenital males versus females

A

males: causes no problems

females: causes moderate/severe masculinization of genitalia

185
Q

androgen insensitivity syndrome

A

absence of functional androgen receptors

XY individuals with this syndrome have normal appearing female external genitalia

but vagina is often short, no menstruation occurs, and they’re sterile

sexed and reared as girls

186
Q

when do people discover they have androgen insensitivity syndrome?

A

puberty

when menstruation fails to occur

187
Q

3 trisomic anomalies

A
  1. XXY - Klinefelter syndrome
  2. XYY
  3. XXX
188
Q

Klinefelter syndrome

A

XXY

extra X chromosome

presence of Y chromosome is sufficient for SRY to act and for masculinization to occur

usually sterile because of decreased sperm production

often severe learning disabilities

189
Q

what are people with Klinefelter syndrome sexed as at birth?

A

males

190
Q

Klinefelter syndrome mainly reflects

A

variation in the androgen receptors

191
Q

modern organizational-activational hypothesis of sexual differentiation

A
  1. expands variables that affect sex differences

a. genes
b. hormones
c. environment

  1. expands time period in which organizational effects occur

a. to pre-pubertal period

essentially, modern version sees things as much less fixed

192
Q

sex differences in behaviour often show significant overlap between the sexes…

A

but there are often greater differences in behaviour between members of the same sex

than between individuals of the opposite sex

essentially, there’s considerable overlap between the sexes

Psyc 342 (10 decks)

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