Endocrine and Reproduction Flashcards
1
Q
What are the male equivalents of the mullerian ducts in females?
A
Wolffian ducts
2
Q
Can the Y and X chromosomes cross-over?
A
Yes, but only within a short pairing region
3
Q
Can the Y chromosome cross over with the X chromosome at any point along its length?
A
No, the pairing region is comparatively short
4
Q
What is the significance of the *sry *gene? Is it in the pairing region of the Y chromosome?
A
It is the sex determining region of the Y chromosome; no, it is in the non-pairing region (otherwise it could be transferred to X chromosomes!)
5
Q
If the SRY gene is deleted or mutant in an otherwise normal XY male, what will the primordial gonads differentiate into?
A
Ovaries
6
Q
What sex phenotype can result if the *sry *gene is transferred to an X chromosome?
A
An XX male
7
Q
What is the difference between genetic and gonadal sex?
A
Genetic is the configuration of X or Y chromosomes; gonadal is the presentation of a sex phenotype with formation of testes or ovaries
8
Q
What do fetal testes synthesize that oppose the formation of the Mullerian duct system? Is it secreted by fetal ovaries? What hormone supports formation of the Wolffian duct system instead?
A
AMH, anti mullerian hormone; no, AMH is not secreted by ovaries; testosterone supports formation of the Wolffian duct system
9
Q
Which week of embryonic development is when the penis and scrotum differentiate?
A
Weeks 9-10
10
Q
What hormone is created from testosterone using 5α reductase that allows for differentation of the male external genitalia?
A
Dihydrotestosterone (DHT)
11
Q
If there is no SRY gene, will the ovaries secrete AMH, testosterone, or produce DHT?
A
No to all
12
Q
By what week of embryonic development is the fetus fully differentiated into a male?
A
week 12
13
Q
What causes testicular feminization?
A
A defect in androgen receptors: the duct system is insensitive to androgens
14
Q
In androgen insensitivity disorder, do the uterus and fallopian tubes form? Do female external genitalia form?
A
No uterus of fallopian tubes, because AMH will still be released and effectively repress Mullerian duct formation; external female genitalia because testosterone and DHT cannot perform their actions
15
Q
What disease causes masculinization of female external genitalia at birth?
A
Congenital adrenal hyperplasia
16
Q
How does congenital adrenal hyperplasia cause masculinization of external genitalia?
A
Androgens are secreted by a hyperplastic adrenal gland
17
Q
What enzyme defect in the adrenal gland can cause increased androgen production? What sex phenotype disorder does this cause?
A
21 hydroxylase deficiency; congenital adrenal hyperplasia
18
Q
What sex phenotype disorder is this representative of?
A
Congenital adrenal hyperplasia
19
Q
What is the median age for puberty onset in American females? What about in American males?
A
10 years for females; 12 years in males
20
Q
What hormone is released in pulses of increased frequency and amplitude to initiate puberty?
A
GnRH
21
Q
Do levels of LH periodically cycle before a girl reaches her reproductive years? What hormone besides LH is elevated during puberty?
A
No; FSH is also elevated during puberty
22
Q
Of the pM, nM, μM and mM concentration ranges, which are most common for hormones?
A
pM and nM
23
Q
In what two tissues are the enzymes related to steroid synthesis most prevalently expressed?
A
Adrenal cortex, gonads
24
Q
Phosopholipase C, when activated by active α G-protein, performs what action on PIP2? What effect does this have on Ca++ cytosolic concentration, and how?
A
It cleaves it to form diacylglycerol (DAG) and IP3; IP3goes on to open calcium channels and increase cytosolic Ca++
25
The anterior pituitary arises from an evagination of what pouch?
Rathke's pouch
26
What is the shortest hypothalamic peptide hormone?
TRH, with three amino acids
27
For each hormone(s), name the cell type in the pituitary that produces it.
– ACTH
– LH and FSH
– TSH
– PRL
– GH
– ACTH: corticotroph
– LH and FSH: gonadotroph
– TSH: thyrotroph
– PRL: lactotroph
– GH: somatotroph
28
For each of the following pituitary cell types, name the hormone(s) that they release.
– corticotroph
– gonadotroph
– thyrotroph
– lactotroph
– somatotroph
– corticotroph: ACTH
– gonadotroph: LH & FSH
– thyrotroph: TSH
– lactotroph: PRL
– somatotroph: GH
29
Hypothalamically secreted hormones acting via Gs proteins include [...], GnRH, ADH, GHRH, and oxytocin.
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and oxytocin.
30
Hypothalamically secreted hormones acting via Gs proteins include TRH, [...], ADH, GHRH, and oxytocin.
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and oxytocin.
31
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, [...], GHRH, and oxytocin.
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and oxytocin.
32
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, [...], and oxytocin.
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and oxytocin.
33
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and [...].
Hypothalamically secreted hormones acting via Gs proteins include TRH, GnRH, ADH, GHRH, and oxytocin.
34
Can serum amino acids stimulate GH release?
Yes
35
Are growth hormone receptors found only in the liver or throughout the body? What signalling protein is thought to faciitate indirect effects of GH?
Throughout the body; IGF-1, also called somatomedin
36
What is the standard treatment for growth hormone deficiency? Can a patient with Laron dwarfism be treated with it as well?
Growth hormone supplementation; no, because Laron dwarfism involves a receptor mutation
37
Which receptor does somatomedin act at? Is it a potential treatment for Laron dwarfism? Why or why not?
It acts at IGF (the insulin receptor); it is a potential treatment for Laron dwarfism; this is because it acts at a different receptor than the one mutated in Laron dwarfism (GH receptor)
38
Is the predominant regulation of prolactin via stimulated secretion or inhibition of primary tone?
Inhibition of primary tone
39
What neurotransmitter is prolactin inhibiting hormone chemically equivalent to?
Dopamine
40
What signal transduction pathway does prolactin's receptor use?
Jak-Stat
41
What accounts for ~70% of pituitary tumors? What is the most common clinical feature that presents specifically?
Prolactinomas; galactorrhea (spontaneous discharge from mammary gland)
42
How are prolactinomas treated?
Dopamine agonists (bromocriptine, cabergoline)
43
In the pituitary-thyroid axis, what hormone is secreted by the hypothalamus? The anterior pituitary? The thyroid gland?
hypothalamus: TRH; anterior pituitary: TSH; thyroid: thyroid hormones
44
What two sets of nuclei contain hypothalamic neurons that release hormones into the posterior pituitary?
Paraventricular nuclei and supraoptic nuclei
45
What downregulates TRH receptors of thyrotropes? Where are thyrotropes found?
High intracellular T3; thyrotropes are in the anterior pituitary
46
What is TRH's effect on prolactin? What is primary hypothyroidism's effect on prolactin?
TRH positively regulates prolactin; therefore, primary hypothyroidism, where TRH is high, would associate with hyperprolactinemia
47
How many transmembrane domains are in a GPCR?
7
48
The α subunit of TSH shares homology with what three other peptide hormones?
FSH, LH, and hCG
49
What negatively regulates TSH secretion?
T3 and T4
50
What type of receptor is the TSH receptor?
GPCR
51
What cotransport efficiently concentrates I- ion within thyroid cells? What enzyme catalyzes oxidation to I2?
Na+/I- cotransport; thyroid peroxidase
52
Which amino acids of thyroglobulin are substrates for iodine incorporation? At how many sites can iodine be incorporated?
Tyrosine; one or two
53
What hormone stimulates endocytosis of thyroglobulin into the follicular cells of the thyroid?
TSH
54
What two drugs competitively inhibit Na+/I- cotransport? What two drugs can inhibit thyroid peroxidase (TPO) activity?
Thiocyanate and perchlorate inhibit Na+/I- cotransport; methimazole and propylthiouracil (PTU) inhibit TPO activity
55
Is most T3 and T4 in serum protein-bound?
Yes, normally 99%
56
What enzymes can convert T4 to T3 or rT3?
Deiodinases
57
What does the number in T3 or T4 signify?
The number of iodine residues
58
Where does the thyroid receptor reside within cells? When it is bound to T3, what does it function as? Can T4 bind with as great affinity?
It is nuclear; it acts as a transcription factor when active; T3 binds with 10x greater affinity than T4
59
Where is the thyroid receptor expressed? What is the effect of thyroid hormone on O2 consumption, basal metabolic rate, body temperature, synthesis of Na+/K+ ATPase?
Essentially ubiquitously; all of these increase
60
Does thyroid hormone increase cardiac output via increased heart rate, contractility, both, or neither?
Both
61
What hormone(s) act in conjunction with growth hormone to promote growth?
Thyroid hormones
62
Is calcitonin secreted by the thyroid or the parathyroid? Which cell type secretes it?
Thyroid; C cells that are parafollicular
63
Is parathyroid hormone or calcitonin the primary modulator of blood Ca++?
Parathyroid hormone is primary
64
Is TSH elevated or low in primary **hypo**thyroidism? What about secondary **hypo**thyroidism?
Elevated in primary hypothyroidism, low in secondary hypothyroidism
65
For each of the following symptoms, would hypothyroidism or hyperthyroidism be a more likely cause?
– decrease in metabolic rate
– loose stools
– jitteriness and tremor
– tachycardia
– cold intolerance and dry skin
– poor linear growth as a child
– decrease in metabolic rate: hypo
– loose stools: hyper
– jitteriness and tremor: hyper
– tachycardia: hyper
– cold intolerance and dry skin: hypo
– poor linear growth as a child: hypo
66
What is the most common etiology of primary hypothyroidism? What causes it?
Hashimoto's thyroiditis; autoimmune destruction of the thyroid gland
67
Defects in the TSH receptor, Na+/I- cotransport, thyroglobulin, and thyroid peroxidase can cause what endocrine disorder?
Congenital hypothyroidism
68
What endocrine disorder is depicted here?
Congenital hypothyroidism
69
What dietary condition causes hypothyroidism?
Iodine deficiency
70
What is this patient, who presents with tachycardia and jitters, suffering from? What is its etiology?
Grave's disease; production of auto-antibodies that stimulate the TSH receptor (mimicking TSH)
71
What causes the exophthalmos of Grave's disease?
TSH acts at the fibroblasts of the eye muscles, it is not related to the high levels of thyroid hormones
72
What peptide hormone is most homologous to oxytocin?
ADH (vasopressin)
73
What are two types of receptors that provide input for vasopressin secretion?
Osmoreceptors in the hypothalamus and cardiac baroreceptors
74
Does angiotensin II stimulate or inhibit ADH release?
Stimulate
75
Does increased plasma volume increase or decrease ADH secretion? Does increased plasma osmolality increase or decrease ADH secretion?
Increased plasma volume (hypervolemia) → ADH↓
Increased plasma osmolality → ADH↑
76
Where are the two types of vasopressin receptors located?
V1 receptor: vascular smooth muscle;
V2 receptor: kidney
77
What intracellular signaller participates in the insertion of aquaporin channels into the distal tubule and collecting duct upon ADH stimulation?
cAMP
78
What are the two principal mechanisms for diabetes insipidus? What is the presenting symptom?
Vasopressin deficiency or vasopressin resistance; polyuria (high dilute urinary volume)
79
What test distinguishes between central or nephrogenic diabetes insipidus?
Water deprivation test: after water deprivation, let plasma osmolality rise to 295 mmol/kg and then administer ADH, if urine osmolality rises there is a central ADH deficiency, otherwise ADH resistance (nephrogenic)
80
What does SIADH stand for? What is the presenting serum test abnormality for SIADH?
Syndrome of Inappropriate ADH; severe hyponatremia
81
What receptor type is shared by the receptors for ADH and oxytocin?
They are all GPCRs
82
Which part of the adrenal gland synthesizes steroids? Which part synthesizes catecholamines?
Cortex: steroids; medulla: catecholamines
83
What hormones are produced by cleavage of POMC (pro-opiomelanocortin)?
MSH, endorphin, lipotrophin, and ACTH
84
What does ACTH stand for?
Adrenocorticotropic hormone
85
Are steroids produced in a pulsatile or steady manner? Does production go up, down, or stay the same at night?
Pulsatile; it goes down at night
86
What is the common metabolic precursor for steroid hormones?
Cholesterol
87
What are the two major classes of adrenal enzymes?
Cytochrome P450 oxidases and hydroxysteroid dehydrogenase
88
Do steroid hormone receptors reside in the nucleus or cytoplasm when inactive?
Cytoplasm
89
What is the difference between cortisol and prednisone?
The ratio between glucocorticoids and mineralocorticoids; prednisone has more glucocorticoids
90
Which class of steroid hormones participates in the renin-angiotensin system?
Mineralocorticoids
91
Are glucocorticoids proinflammatory or anti-inflammatory? Do they increase or decrease GFR?
Anti-inflammatory; they increase GFR
92
What are the symptoms of acute adrenal crisis?
Abdominal pain and fever
93
Can nausea, anorexia, and hypoglycemia indicate adrenal insufficiency? Is this combination specific for adrenal insufficiency?
Yes they are possible symptoms; no, most symptoms of adrenal insufficiency are non-specific
94
What endocrine disorder results in this symptom?
Hyperpigmentation is suggestive of primary adrenal insufficiency
95
What is autoimmune destruction of the adrenal gland called?
Addison's disease
96
What is Zellweger syndrome?
A metabolic etiology for adrenal destruction causing primary adrenal insufficiency
97
What is the most common defect causing congenital adrenal hyperplasia? What modulation in steroid balance does this cause?
Loss of function of 21-hydroxylase; Cortisol deficiency and androgen excess
98
What developmental disorder of the genitalia results from 21-hydroxylase deficiency? Why?
Ambiguous genitalia in XX females; overproduction of androgens
99
What is the most common cause of secondary adrenal insufficiency?
Pharmacologic doses of steroids that cause central negative feedback
100
Is mineralocorticoid deficiency a typical manifestion of secondary adrenal insufficiency?
No
101
What causes Cushing syndrome?
Exposure to excessive glucocorticoids
102
What endocrine disorder is this clinical presentation associated with?
Cushing syndrome
103
What causes the glucocorticoid elevation driving Cushing syndrome?
Excess ACTH from a pituitary microadenoma
104
What tissue type is the origin of an adenoma? What about a carcinoma?
Adenoma - glandular; carcinoma - endodermal or ectodermal derived tissue (usually a lining)
105
What is Conn syndrome?
A primary hyperaldosteronism via a aldosterone-secreting tumor
106
What is the embryonic origin of the adrenal medulla?
Neuroectodermal cells from the neural crest
107
Does the adrenal medulla produce all of the circulating norepinephrine?
No, only 30%
108
What is a pheochromocytoma?
A tumor of the adrenal medulla that causes high levels of catecholamines
109
What are the three cell types of the islets of Langerhans?
α, β, and δ cells
110
What peptide (that may have regulatory effects) is generated in equimolar amounts with insulin?
C-peptide
111
What glucose transporter is in β cells of pancreatic islets?
GLUT2
112
What channel is blocked by the increased ATP-ADP ratio in pancreatic β cells after glucose import? What does this cause to stimulate exocytosis of insulin-containing granules?
ATP-dependent K+ channel; membrane depolarization leads to influx of Ca++
113
What drug can inhibit the ATP-dependent K+ channels of pancreatic β cells?
Sulfonylurea
114
How many phases of insulin secretion are there?
Two
115
What class of receptor is the insulin receptor?
RTK
116
Does insulin promote or inhibit lipolysis? What about amino acid uptake into cells (e.g. muscle)?
Inhibits lipolysis; stimulates amino acid uptake
117
What kind of receptor is the glucagon receptor?
GPCR
118
Is the preprohormone for glucagon only created in the pancreas?
No, it is used to make other substances in the intestine and brain
119
Is glucagon released in conditions of low or high blood glucose? What other two conditions can stimulate its release?
Low blood glucose; certain amino acids, and α adrenergic stimulation
120
What is glucagon's effect on glycogenolysis? What about gluconeogenesis? What about lipolysis?
Promotes all three of these
121
What is the etiology of type 1 diabetes mellitus? What is the treatment?
Autoimmune destruction of pancreatic β cells; insulin replacement
122
Do sulfonylureas increase or decrease insulin secretion? What do they bind to and inhibit?
Increase insulin secretion; ATP-dependent K+ channels
123
What does metformin activate to improve insulin resistance? What is the mechanism of thiazolinediones?
Metformin activates AMP kinase; thiazolinedione is a PPAR-agonist
124
What ion is a cofactor for enzymes involved in blood clotting?
Ca++
125
What percentage of Ca++ moving through the nephron is reabsorbed?
98%
126
What ionic imbalance triggers release of PTH?
Low serum Ca++
127
How is PTH release self-regulated?
Once PTH triggers release of Ca++ into blood from bone, kidney, and intestine, Ca++ inhibits the release of PTH via the Ca++ sensing receptors of the parathyroid
128
What broad class of receptor is the Ca++-sensing receptor?
GPCR
129
What type of receptor is the PTH receptor? What is its internal signalling mechanism?
GPCR; adenylyl cyclase increasing cAMP
130
Which part of the loop of Henle does PTH act on to increase Ca++ reabsorption?
The thick ascending limb
131
Do osteoblasts express the PTH receptor? What about osteoclasts?
Yes osteoblasts do; no osteoclasts do not
132
What must happen to multiple osteoclast precursors to activate them? How does PTH modulate this?
There is an interaction of RANK with RANKL on the osteoblasts that promotes fusion into the activated form; PTH increases the RANKL/OPG ratio on the osteoblasts
133
What vitamin is activated by PTH? Via which enzyme?
Vitamin D; via renal 1α hydroxylase
134
What gland synthesizes and secretes calcitonin? What cell type is responsible for this? Is this in reponse to high or low serum Ca++?
Thyroid synthesizes calcitonin; C cells; high serum Ca++
135
What kind of receptor is the calcitonin receptor? What cell type expresses it and does it inhibit or activate their activity?
GPCR; osteoclasts express it and are inhibited by its activity
136
Are cramping, paresthesia/tetany, seizures, and prolonged QT signs of hypocalcemia or hypercalcemia?
Hypocalcemia
137
What sign is this (induced with the use of a blood pressure cuff)? What is it indicative of?
Trousseau sign; hypocalcemia
138
What is the mnemonic for signs and symptoms of hypercalcemia?
Groans: constipation
Moans: fatigue, lethargy
Bones: bone pain
Stones: kidney stones (nephrolithiasis)
Psychiatric Overtones: depression, confusion
139
If hypercalcemia presents with low PTH (i.e. it is not hyperparathyroidism), what else could be causing it?
Vitamin D intoxication, granulomatous disease, neoplasia, other lytic disease
140
What metabolic deficiency is a common etiology for hypocalcemia?
Vitamin D deficiency
141
What secosteroid is needed for intestinal absorption of calcium and phosphate?
Vitamin D
142
What endocrine disorder is suggested by these pictures?
Hypoparathyroidism, cased by DiGeorge syndrome or 22q11 microdeletion, which causes facial malformations
143
What characterizes familial hypocalciuric hypercalcemia? What causes it?
Low urine calcium in the setting of high serum calcium; caused by loss-of-function mutation of Ca++ sensing receptor in parathyroid (therefore body always considers Ca++ low and releases lots of PTH)
144
What is the most often cause of primary hyperparathyroidism?
Benign adenoma
145
Are LH and FSH elevated, lower, or the same during menopause as compared to the reproductive years?
Elevated
146
What hormones are secreted by the corpus luteum and the placenta to regulate the hypothalamic pituitary axis for LH and FSH?
Estrogen and progesterone
147
Pulses of what hypothalamic hormone determine puberty?
GnRH
148
How can an XY genotype individual present with female external genitalia but no internal genitalia?
Testicular feminization, caused by androgen receptor defect (androgen insensitivity)
149
Which hormone is responsible for the formation of external female genitalia?
Estrogen
150
What do the testes produce that prevents development of fallopian tubes, the uterus, and the upper part of the vagina?
Anti-mullerian hormone (AMH)
151
Is testosterone directly responsible for formation of the internal or external male genitalia, or both?
Only the internal (Wolffian ducts)
152
What precursor cells for gametes migrate from their origin in the hindgut to the gonads during embryogenesis?
Primordial germ cells
153
When does mitosis for primordial germ cells in females stop?
Fetal life
154
What proportion of oocytes are lost by atresia from birth until menopause? How many remain at menopause?
99.9%; about 1000 remain
155
What ligament lies between the ovary and the uterus?
The mesovarium (ovarian ligament)
156
At about what day of the menstrual cycle does estrogen peak? At about what day does proesterone peak?
Estrogen: 12 days (right before ovulation); progesterone: 19 days (after ovulation)
157
What hormone peaks sharply only during the ovulation phase of menstruation?
LH
158
What dimer protein complex is secreted by the granulosa cells of ovarian follicles that suppresses FSH?
Inhibin
159
Which form of estrogen is the most prominent during the reproductive years?
Estradiol
160
Where does inhibin act along the hypothalamic/pituitary axis?
It provides negative feedback at the pituitary and hypothalamus, decreasing GnRH, LH, and FSH levels.
161
Name the arrow-marked features.
Clockwise from top left: granulosa cells, oocyte, zona pellucida, culumus oophorus
162
Is the zona pellucida made of cells?
No, it is a non-cellular glycoprotein coat
163
Which ovarian cell type provides feedback inhibition for FSH? Which ovarian cell type provides feedback inhibition of LH?
Granulosa makes inhibin and estradiol to inhibit FSH; theca cell makes progesterone to inhibit LH
164
What are the precursors for the estradiol made by the granulosa cell? Where do they come from?
They are androgens hormones; they are secreted by the theca cells
165
How does the dominant follicle per menstrual cycle get picked, leaving the others to become atretic?
It has the most FSH receptors and "consumes" the majority of the incoming FSH, meanwhile secreting estradiol from its granulosa cells to inhibit FSH production, "starving" the smaller follicles.
166
With high enough levels of estradiol, how does its effect on the female hypothalamic pituitary axis change? What surge does this cause and what does that surge trigger?
It becomes a positive feedback loop, causing the surge of LH that triggers ovulation
167
What meitoic devision accompanies the surge of LH received by the follicle? Where does it re-arrest?
Meiosis I; arrests at metaphase II
168
What span the zona pellucida to allow transport between cumulus cells and the oocyte? What happens when the LH surge is received?
Microvilli; they are withdrawn after the LH surge
169
Before ovulation, where does the vasculature of the follicle reside? After ovulation, what changes occur in this layout?
Vasculature remains in thecal layers; after ovulation, thecal cells and blood vessels invade
170
What is the terminal differentiation process that granulosa cells undergo to form the corpus luteum called?
Luteinization
171
What hormone causes the increase in thickness (the proliferative phase) of the endometrium during the menstrual cycle?
Estradiol
172
What is the total blood loss during a typical menstrual cycle?
60 mL
173
How many "peaks" of estradiol are there throughout the menstrual cycle?
Two; one before ovulation, and one afterward, concurrent with the progesterone peak around day 19
174
What enzyme produces estrogens from androgens in the granulosa cells? What hormone induces its activity?
Aromatase; FSH
175
FSH induces the formation of receptors to what other hormone?
LH
176
How long does it take for the oocyte to move from the ampulla to the uterus?
5-6 days
177
Which part of this implanted embryo produces hCG? What does this hormone do to the corpus luteum?
The syncytium; it sustains growth of the corpus luteum
178
What is the first thing that must be ruled out to determine the etiology of anovulation?
pregnancy
179
What four "compartments" of integrated organs need to be examined in disorders of the female menstrual cycle?
CNS compartment, anterior pituitary, the gonad (ovary), and the target organ (uterus)
180
What does this sonogram of an ovary indicate? Besides amenorhea, what overall effect can it have on sexual characteristics (hair growth, breasts, etc.)?
Polycystic ovary, determined by more than 12 antral follicles; can cause androgenization
181
What period of time must one sustain intercourse without conceiving to indicate infertility?
One year
182
What procedure is this?
Hysterosalpingogram
183
What is this procedure, performed on day 2 or 3 of the menstrual cycle? Which picture is more indicative for female infertility?
Basal antral follicle count; right suggests lack of antral follicles, which is not good for fertility
184
What is the major barrior to sperm number traveling through the female reproductive tract?
The cervical mucus
185
What pharmacological strategy can be used to cause ovulation of multiple follicles, increasing the odds of pregnancy?
Ovarian hyperstimulation
186
When does hCG production peak?
9 weeks post-fertilization
187
How many stages of labor are there?
Three
188
The placenta secretes what two hormones that encourage the growth of breasts throughout pregnancy?
Estrogen and progesterone
189
Suckling stimulates production of what two hormones that encourage lactation?
Oxytocin and prolactin
190
What nerves transmit the signal of suckling to the CNS?
4-6th intercostal nerves
191
What is the average age of menopause?
51.7 years old
192
Why do FSH and LH levels increase during menopause?
Lack of estrogen produced from the ovarian follicles, which have depleted, and so negative feedback on the hypothalamic/pituitary axis.
193
What common skeletal disorder results after menopause? Why?
Osteoporosis; the deficiency of estrogen causes less stimulation of estrogen receptors on bones, causing more bone resorption
194
Can the negative side effects of menopause be mitigated with hormone replacement therapy?
Trials were attempted in 2002 but the increased risk of coronary heart disease, stroke, and breast cancer outweighed the benefits
195
Is it possible to cryopreserve oocytes from before menopause so they can be fertilized later?
It is difficult because mature oocytes have delicate meiotic spindles that are destroyed by ice crystals
196
What is another name for the Cowper's gland? What does it secrete?
Bulbourethral gland; A galactose-rich fluid that lubricates the urethra before ejaculation
197
How many degrees below body temperature are the testes?
1 or 2 degrees
198
When testosterone enters Sertoli cells, what hormone is it converted to?
Estradiol (estrogen)
199
What organelles are rich throughout the acrosome of the sperm? What about the middle piece?
Lysosomes in the acrosome; mitochondria in the middle piece (to produce energy for motility)
200
What zone of the oocyte is broken down by the acrosomal head of the sperm? In what space is the sperm nucleus released?
Zona pellucida; perivitelline space
201
Are FSH and LH produced in males?
Yes
202
What does LH stimulate in males? What hormone is produced by its target?
Interstitial cells of Leydig; testosterone
203
What hormonal changes are present in hypogonadotropic hypogonadism (for a male)?
FSH, LH, and testosterone are all low, because the defect is in gonadotrophs in the anterior pituitary
204
In the case of congenital absence of the vas deferens, how can sperm be retrieved for fertilization?
Directly from the testes, either percutaneously or via open microsurgery
205
Do testes produce glucocorticoids or mineralocorticoids?
No, they lack the correct enzymes
206
Which cells of the testes produce antimullerian hormone?
Sertoli cells
207
What hormone causes male hair patterns and baldness?
Dihydrotestosterone
208
What drug class is used to treat benign prostatic hypertrophy and male pattern baldness?
5 α-reductase inhibitors (e.g. Finasteride)
209
What two proteins does testosterone bind to in blood?
Albumin and sex hormone binding globulin
210
What does Klinefelter's syndrome present as? What is the karyotypic change?
Primary hypogonadism; XXY
211
Is hypogonadism characterized by a decreased size of the testicles or penis?
Not necessarily, it means decreased production of sex hormones, which may have nothing to do with external appearance
212
What is the congenital cause of secondary hypogonadism (pituitary failure) in males called?
Kallmann's syndrome
213
Do testosterone levels decrease or increase with age in males?
Decrease
214
Does visceral fat increase or decrease levels of circulating testosterone?
Decrease
215
How does testosterone affect bone physiology? What is the mechanism?
It promotes osteogenesis; it encourages osteoblast differentiation, and inhibits osteoclast differentation
216
As testosterone levels decline with age, what common skeletal injury can increase in men?
Hip fractures
217
Does increased levels of circulating testosterone increase or decrease risk of coronary heart disease?
Decrease
218
What is the standard treatment for hypogonadism in male? What are some of the adverse effects on the testicles, prostrate, and sexual characteristics?
Testosterone replacement; it can cause suppression of sperm production, prostrate grown, and increased plasma estrogen, causing gynecomastia
219
Is erectile dysfunction correlated with a lesser or greater risk of heart attack?
Greater risk
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What is the sympathetic innervation of the penis? What is the parasympathetic/somatic innervation?
T10-L2 sympathetic; the remaining are S2-S4
221
How does erectile tissue prevent outflow through the surrounding subtunical veins?
They are compressed, trapping the blood
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What key cellular signaller is involved in relaxation of the smooth muscle surrounding helicine arteries of erectile tissue?
Nitric oxide
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What do drugs like Viagra, Cialis, and Levitra inhibit to cause release of nitric oxide (NO)?
PDE5, which normally breaks down cGMP, an intracellular signaller that promotes NO release
