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Physiology > Endocrine and reproduction > Flashcards

Endocrine and reproduction Flashcards

1
Q

What are the male equivalents of the mullerian ducts in females?

A

Wolffian ducts

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2
Q

Can the Y and X chromosomes cross-over?

A

Yes, but only within a short pairing region

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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

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4
Q

What is the significance of thesrygene? 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!)

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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

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6
Q

What sex phenotype can result if the srygene is transferred to an X chromosome?

A

An XX male

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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

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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

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9
Q

Which week of embryonic development is when the penis and scrotum differentiate?

A

Weeks 9-10

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10
Q

What hormone is created from testosterone using5α reductase that allows for differentation of the male external genitalia?

A

Dihydrotestosterone (DHT)

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11
Q

If there is no SRY gene, will the ovaries secrete AMH, testosterone, or produce DHT?

A

No to all

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12
Q

By what week of embryonic development is the fetus fully differentiated into a male?

A

week 12

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13
Q

What causes testicular feminization?

A

A defect in androgen receptors: the duct system is insensitive to androgens

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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

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15
Q

What disease causes masculinization of female external genitalia at birth?

A

Congenital adrenal hyperplasia

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16
Q

How does congenital adrenal hyperplasia cause masculinization of external genitalia?

A

Androgens are secreted by a hyperplastic adrenal gland

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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

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18
Q

What sex phenotype disorder is this representative of?

A

Congenital adrenal hyperplasia

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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

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20
Q

What hormone is released in pulses of increased frequency and amplitude to initiate puberty?

A

GnRH

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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

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22
Q

Of the pM, nM, μM and mM concentration ranges, which are most common for hormones?

A

pM and nM

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23
Q

In what two tissues are the enzymes related to steroid synthesis most prevalently expressed?

A

Adrenal cortex, gonads

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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++

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25
Q

The anterior pituitary arises from an evagination of what pouch?

A

Rathke’s pouch

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26
Q

What is the shortest hypothalamic peptide hormone?

A

TRH, with three amino acids

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27
Q

For each hormone(s), name the cell type in the pituitary that produces it.– ACTH– LH and FSH– TSH– PRL– GH

A

– ACTH: corticotroph– LH and FSH: gonadotroph– TSH: thyrotroph– PRL: lactotroph– GH: somatotroph

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28
Q

For each of the following pituitary cell types, name the hormone(s) that they release.– corticotroph– gonadotroph– thyrotroph– lactotroph– somatotroph

A

– corticotroph: ACTH– gonadotroph: LH & FSH– thyrotroph: TSH– lactotroph: PRL– somatotroph: GH

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29
Q

Hypothalamically secreted hormones acting via Gsproteins include[…], GnRH, ADH, GHRH, and oxytocin.

A

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and oxytocin.

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30
Q

Hypothalamically secreted hormones acting via Gsproteins includeTRH, […], ADH, GHRH, and oxytocin.

A

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and oxytocin.

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31
Q

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, […], GHRH, and oxytocin.

A

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and oxytocin.

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32
Q

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, […], and oxytocin.

A

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and oxytocin.

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33
Q

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and […].

A

Hypothalamically secreted hormones acting via Gsproteins includeTRH, GnRH, ADH, GHRH, and oxytocin.

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34
Q

Can serum amino acids stimulate GH release?

A

Yes

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35
Q

Are growth hormone receptors found only in the liver or throughout the body? What signalling protein is thought to faciitate indirect effects of GH?

A

Throughout the body; IGF-1, also called somatomedin

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36
Q

What is the standard treatment for growth hormone deficiency? Can a patient with Laron dwarfism be treated with it as well?

A

Growth hormone supplementation; no, because Laron dwarfism involves a receptor mutation

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37
Q

Which receptor does somatomedin act at? Is it a potential treatment for Laron dwarfism? Why or why not?

A

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)

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38
Q

Is the predominant regulation of prolactin via stimulated secretion or inhibition of primary tone?

A

Inhibition of primary tone

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39
Q

What neurotransmitter is prolactin inhibiting hormone chemically equivalent to?

A

Dopamine

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40
Q

What signal transduction pathway does prolactin’s receptor use?

A

Jak-Stat

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41
Q

What accounts for ~70% of pituitary tumors? What is the most common clinical feature that presentsspecifically?

A

Prolactinomas; galactorrhea (spontaneous discharge from mammary gland)

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42
Q

How are prolactinomas treated?

A

Dopamine agonists (bromocriptine, cabergoline)

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43
Q

In the pituitary-thyroid axis, what hormone is secreted by the hypothalamus? The anterior pituitary? The thyroid gland?

A

hypothalamus: TRH; anterior pituitary: TSH; thyroid: thyroid hormones

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44
Q

What two sets of nuclei contain hypothalamic neurons that release hormones into the posterior pituitary?

A

Paraventricular nuclei and supraoptic nuclei

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45
Q

What downregulates TRH receptors of thyrotropes? Where are thyrotropes found?

A

High intracellular T3; thyrotropes are in the anterior pituitary

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46
Q

What is TRH’s effect on prolactin? What is primary hypothyroidism’s effect on prolactin?

A

TRH positively regulates prolactin; therefore, primary hypothyroidism, where TRH is high, would associate with hyperprolactinemia

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47
Q

How many transmembrane domains are in a GPCR?

A

7

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48
Q

The α subunit of TSH shares homology with what three other peptide hormones?

A

FSH, LH, and hCG

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49
Q

What negatively regulates TSH secretion?

A

T3and T4

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50
Q

What type of receptor is the TSH receptor?

A

GPCR

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51
Q

What cotransport efficiently concentrates I-ion within thyroid cells? What enzyme catalyzes oxidation to I2?

A

Na+/I-cotransport; thyroid peroxidase

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52
Q

Which amino acids of thyroglobulin are substrates for iodine incorporation? At how many sites can iodine be incorporated?

A

Tyrosine; one or two

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53
Q

What hormone stimulates endocytosis of thyroglobulin into the follicular cells of the thyroid?

A

TSH

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54
Q

What two drugs competitively inhibit Na+/I-cotransport? What two drugs can inhibit thyroid peroxidase (TPO) activity?

A

Thiocyanate and perchlorate inhibit Na+/I-cotransport; methimazole and propylthiouracil (PTU) inhibit TPO activity

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55
Q

Is most T3and T4in serum protein-bound?

A

Yes, normally 99%

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56
Q

What enzymes can convert T4to T3or rT3?

A

Deiodinases

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57
Q

What does the number in T3or T4signify?

A

The number of iodine residues

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58
Q

Where does the thyroid receptor reside within cells? When it is bound to T3, what does it function as? Can T4bind with as great affinity?

A

It is nuclear; it acts as a transcription factor when active; T3binds with 10x greater affinity than T4

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59
Q

Where is the thyroid receptor expressed? What is the effect of thyroid hormone on O2consumption, basal metabolic rate, body temperature, synthesis of Na+/K+ATPase?

A

Essentially ubiquitously; all of these increase

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60
Q

Does thyroid hormone increase cardiac output via increased heart rate, contractility, both, or neither?

A

Both

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61
Q

What hormone(s) act in conjunction with growth hormone to promote growth?

A

Thyroid hormones

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62
Q

Is calcitonin secreted by the thyroid or the parathyroid? Which cell type secretes it?

A

Thyroid; C cells that are parafollicular

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63
Q

Is parathyroid hormone or calcitonin the primary modulator of blood Ca++?

A

Parathyroid hormone is primary

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64
Q

Is TSH elevated or low in primary hypothyroidism? What about secondary hypothyroidism?

A

Elevated in primary hypothyroidism, low in secondary hypothyroidism

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65
Q

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

A

– 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

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66
Q

What is the most common etiology of primary hypothyroidism? What causes it?

A

Hashimoto’s thyroiditis; autoimmune destruction of the thyroid gland

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67
Q

Defects in the TSH receptor, Na+/I-cotransport, thyroglobulin, and thyroid peroxidase can cause what endocrine disorder?

A

Congenital hypothyroidism

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68
Q

What endocrine disorder is depicted here?

A

Congenital hypothyroidism

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69
Q

What dietary condition causes hypothyroidism?

A

Iodine deficiency

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70
Q

What is this patient, who presents with tachycardia and jitters, suffering from? What is its etiology?

A

Grave’s disease; production of auto-antibodies that stimulate the TSH receptor (mimicking TSH)

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71
Q

What causes the exophthalmos of Grave’s disease?

A

TSH acts at the fibroblasts of the eye muscles, it is not related to the high levels of thyroid hormones

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72
Q

What peptide hormone is most homologous to oxytocin?

A

ADH (vasopressin)

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73
Q

What are two types of receptors that provide input for vasopressin secretion?

A

Osmoreceptors in the hypothalamus and cardiac baroreceptors

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74
Q

Does angiotensin II stimulate or inhibit ADH release?

A

Stimulate

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75
Q

Does increased plasma volume increase or decrease ADH secretion? Does increased plasma osmolality increase or decrease ADH secretion?

A

Increased plasma volume (hypervolemia) → ADH↓Increased plasma osmolality → ADH↑

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76
Q

Where are the two types of vasopressin receptors located?

A

V1receptor: vascular smooth muscle;V2receptor: kidney

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77
Q

What intracellular signaller participates in the insertion of aquaporin channels into the distal tubule and collecting duct upon ADH stimulation?

A

cAMP

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78
Q

What are the two principal mechanisms for diabetes insipidus? What is the presenting symptom?

A

Vasopressin deficiency or vasopressin resistance; polyuria (high dilute urinary volume)

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79
Q

What test distinguishes between central or nephrogenic diabetes insipidus?

A

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)

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80
Q

What does SIADH stand for? What is the presenting serum test abnormality for SIADH?

A

Syndrome of Inappropriate ADH; severe hyponatremia

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81
Q

What receptor type is shared by the receptors for ADH and oxytocin?

A

They are all GPCRs

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82
Q

Which part of the adrenal gland synthesizes steroids? Which part synthesizes catecholamines?

A

Cortex: steroids; medulla: catecholamines

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83
Q

What hormones are produced by cleavage of POMC(pro-opiomelanocortin)?

A

MSH, endorphin, lipotrophin, and ACTH

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84
Q

What does ACTH stand for?

A

Adrenocorticotropic hormone

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85
Q

Are steroids produced in a pulsatile or steady manner? Does production go up, down, or stay the same at night?

A

Pulsatile; it goes down at night

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86
Q

What is the common metabolic precursor for steroid hormones?

A

Cholesterol

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87
Q

What are the two major classes of adrenal enzymes?

A

Cytochrome P450 oxidases and hydroxysteroid dehydrogenase

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88
Q

Do steroid hormone receptors reside in the nucleus or cytoplasm when inactive?

A

Cytoplasm

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89
Q

What is the difference between cortisol and prednisone?

A

The ratio between glucocorticoids and mineralocorticoids; prednisone has more glucocorticoids

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90
Q

Which class of steroid hormones participates in the renin-angiotensin system?

A

Mineralocorticoids

91
Q

Are glucocorticoids proinflammatory or anti-inflammatory? Do they increase or decrease GFR?

A

Anti-inflammatory; they increase GFR

92
Q

What are the symptoms of acute adrenal crisis?

A

Abdominal pain and fever

93
Q

Can nausea, anorexia, and hypoglycemia indicate adrenal insufficiency? Is this combination specific for adrenal insufficiency?

A

Yes they are possible symptoms; no, most symptoms of adrenal insufficiency are non-specific

94
Q

What endocrine disorder results in this symptom?

A

Hyperpigmentation is suggestive of primary adrenal insufficiency

95
Q

What is autoimmune destruction of the adrenal gland called?

A

Addison’s disease

96
Q

What is Zellweger syndrome?

A

A metabolic etiology for adrenal destruction causing primary adrenal insufficiency

97
Q

What is the most common defect causing congenital adrenal hyperplasia? What modulation in steroid balance does this cause?

A

Loss of function of 21-hydroxylase; Cortisol deficiency and androgen excess

98
Q

What developmental disorder of the genitalia results from 21-hydroxylase deficiency? Why?

A

Ambiguous genitalia in XX females; overproduction of androgens

99
Q

What is the most common cause of secondary adrenal insufficiency?

A

Pharmacologic doses of steroids that cause central negative feedback

100
Q

Is mineralocorticoid deficiency a typical manifestion of secondary adrenal insufficiency?

A

No

101
Q

What causes Cushing syndrome?

A

Exposure to excessive glucocorticoids

102
Q

What endocrine disorder is this clinical presentation associated with?

A

Cushing syndrome

103
Q

What causes the glucocorticoid elevation driving Cushing syndrome?

A

Excess ACTH from a pituitary microadenoma

104
Q

What tissue type is the origin of an adenoma? What about a carcinoma?

A

Adenoma - glandular; carcinoma - endodermal or ectodermal derived tissue (usually a lining)

105
Q

What is Conn syndrome?

A

A primary hyperaldosteronism via a aldosterone-secreting tumor

106
Q

What is the embryonic origin of the adrenal medulla?

A

Neuroectodermal cells from the neural crest

107
Q

Does the adrenal medulla produce all of the circulating norepinephrine?

A

No, only 30%

108
Q

What is a pheochromocytoma?

A

A tumor of the adrenal medulla that causes high levels of catecholamines

109
Q

What are the three cell types of the islets of Langerhans?

A

α, β, and δ cells

110
Q

What peptide (that may have regulatory effects) is generated in equimolar amounts with insulin?

A

C-peptide

111
Q

What glucose transporter is in β cells of pancreatic islets?

A

GLUT2

112
Q

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?

A

ATP-dependent K+channel; membrane depolarization leads to influx of Ca++

113
Q

What drug can inhibit the ATP-dependent K+channels of pancreatic β cells?

A

Sulfonylurea

114
Q

How many phases of insulin secretion are there?

A

Two

115
Q

What class of receptor is the insulin receptor?

A

RTK

116
Q

Does insulin promote or inhibit lipolysis? What about amino acid uptake into cells (e.g. muscle)?

A

Inhibits lipolysis; stimulates amino acid uptake

117
Q

What kind of receptor is the glucagon receptor?

A

GPCR

118
Q

Is the preprohormone for glucagon only created in the pancreas?

A

No, it is used to make other substances in the intestine and brain

119
Q

Is glucagon released in conditions of low or high blood glucose? What other two conditions can stimulate its release?

A

Low blood glucose; certain amino acids, and α adrenergic stimulation

120
Q

What is glucagon’s effect on glycogenolysis? What about gluconeogenesis? What about lipolysis?

A

Promotes all threeof these

121
Q

What is the etiology of type 1 diabetes mellitus? What is the treatment?

A

Autoimmune destruction of pancreatic β cells; insulin replacement

122
Q

Do sulfonylureas increase or decrease insulin secretion? What do they bind to and inhibit?

A

Increase insulin secretion; ATP-dependent K+channels

123
Q

What does metformin activate to improve insulin resistance? What is the mechanism of thiazolinediones?

A

Metformin activates AMP kinase; thiazolinedione is a PPAR-agonist

124
Q

What ion is a cofactor for enzymes involved in blood clotting?

A

Ca++

125
Q

What percentage of Ca++moving through the nephron is reabsorbed?

A

98%

126
Q

What ionic imbalance triggers release of PTH?

A

Low serum Ca++

127
Q

How is PTH release self-regulated?

A

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
Q

What broad class of receptor is the Ca++-sensing receptor?

A

GPCR

129
Q

What type of receptor is the PTH receptor? What is its internal signalling mechanism?

A

GPCR; adenylyl cyclase increasing cAMP

130
Q

Which part of the loop of Henle does PTH act on to increase Ca++reabsorption?

A

The thick ascending limb

131
Q

Do osteoblasts express the PTH receptor? What about osteoclasts?

A

Yes osteoblasts do; no osteoclasts do not

132
Q

What must happen to multiple osteoclast precursors to activate them? How does PTH modulate this?

A

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
Q

What vitamin is activated by PTH? Via which enzyme?

A

Vitamin D; via renal 1α hydroxylase

134
Q

What gland synthesizes and secretes calcitonin? What cell type is responsible for this? Is this in reponse to high or low serum Ca++?

A

Thyroid synthesizes calcitonin; C cells; high serum Ca++

135
Q

What kind of receptor is the calcitonin receptor? What cell type expresses it and does it inhibit or activate their activity?

A

GPCR; osteoclasts express it and are inhibited by its activity

136
Q

Are cramping, paresthesia/tetany, seizures, and prolonged QT signs of hypocalcemia or hypercalcemia?

A

Hypocalcemia

137
Q

What sign is this (induced with the use of a blood pressure cuff)? What is it indicative of?

A

Trousseau sign; hypocalcemia

138
Q

What is the mnemonic for signs and symptoms of hypercalcemia?

A

Groans: constipationMoans: fatigue, lethargyBones: bone painStones: kidney stones (nephrolithiasis)Psychiatric Overtones: depression, confusion

139
Q

If hypercalcemia presents with low PTH (i.e. it is not hyperparathyroidism), what else could be causing it?

A

Vitamin D intoxication, granulomatous disease, neoplasia, other lytic disease

140
Q

What metabolic deficiency is a common etiology for hypocalcemia?

A

Vitamin D deficiency

141
Q

What secosteroid is needed for intestinal absorption of calcium and phosphate?

A

Vitamin D

142
Q

What endocrine disorder is suggested by these pictures?

A

Hypoparathyroidism, cased by DiGeorge syndrome or 22q11 microdeletion, which causes facial malformations

143
Q

What characterizes familial hypocalciuric hypercalcemia? What causes it?

A

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
Q

What is the most often cause of primary hyperparathyroidism?

A

Benign adenoma

145
Q

Are LH and FSH elevated, lower, or the same during menopause as compared to the reproductive years?

A

Elevated

146
Q

What hormones are secreted by the corpus luteum and the placenta to regulate the hypothalamic pituitary axis for LH and FSH?

A

Estrogen and progesterone

147
Q

Pulses of what hypothalamic hormone determine puberty?

A

GnRH

148
Q

How can an XY genotype individual present with female external genitalia but no internal genitalia?

A

Testicular feminization, caused by androgen receptor defect (androgen insensitivity)

149
Q

Which hormone is responsible for the formation of external female genitalia?

A

Estrogen

150
Q

What do the testes produce that prevents development of fallopian tubes, the uterus, and the upper part of the vagina?

A

Anti-mullerian hormone (AMH)

151
Q

Is testosterone directly responsible for formation of the internal or external male genitalia, or both?

A

Only the internal (Wolffian ducts)

152
Q

What precursor cells for gametes migrate from their origin in the hindgut to the gonads during embryogenesis?

A

Primordial germ cells

153
Q

When does mitosis for primordial germ cells in females stop?

A

Fetal life

154
Q

What proportion of oocytes are lost by atresia from birth until menopause? How many remain at menopause?

A

99.9%; about 1000 remain

155
Q

What ligament lies between the ovary and the uterus?

A

The mesovarium (ovarian ligament)

156
Q

At about what day of the menstrual cycle does estrogen peak? At about what day does proesterone peak?

A

Estrogen: 12 days (right before ovulation); progesterone: 19 days (after ovulation)

157
Q

What hormone peaks sharply only during the ovulation phase of menstruation?

A

LH

158
Q

What dimer protein complex is secreted by the granulosa cells of ovarian follicles that suppresses FSH?

A

Inhibin

159
Q

Which form of estrogen is the most prominent during the reproductive years?

A

Estradiol

160
Q

Where does inhibin act along the hypothalamic/pituitary axis?

A

It provides negative feedback at the pituitary and hypothalamus, decreasing GnRH, LH, and FSH levels.

161
Q

Name the arrow-marked features.

A

Clockwise from top left: granulosa cells, oocyte, zona pellucida, culumus oophorus

162
Q

Is the zona pellucida made of cells?

A

No, it is a non-cellular glycoprotein coat

163
Q

Which ovarian cell type provides feedback inhibition for FSH? Whichovariancell type provides feedback inhibition of LH?

A

Granulosa makes inhibin and estradiol to inhibit FSH; theca cell makes progesterone to inhibit LH

164
Q

What are the precursors for the estradiol made by the granulosa cell? Where do they come from?

A

They are androgens hormones; they are secreted by the theca cells

165
Q

How does the dominant follicle per menstrual cycle get picked, leaving the others to become atretic?

A

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
Q

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?

A

It becomes a positive feedback loop, causing the surge of LH that triggers ovulation

167
Q

What meitoic devision accompanies the surge of LH received by the follicle? Where does it re-arrest?

A

Meiosis I; arrests at metaphase II

168
Q

What span the zona pellucida to allow transport between cumulus cells and the oocyte? What happens when the LH surge is received?

A

Microvilli; they are withdrawn after the LH surge

169
Q

Before ovulation, where does the vasculature of the follicle reside? After ovulation, what changes occur in this layout?

A

Vasculature remains in thecal layers; after ovulation, thecal cells and blood vessels invade

170
Q

What is the terminal differentiation process that granulosa cells undergo to form the corpus luteum called?

A

Luteinization

171
Q

What hormone causes the increase in thickness (the proliferative phase) of the endometrium during the menstrual cycle?

A

Estradiol

172
Q

What is the total blood loss during a typical menstrual cycle?

A

60 mL

173
Q

How many “peaks” of estradiol are there throughout the menstrual cycle?

A

Two; one before ovulation, and one afterward, concurrent with the progesterone peak around day 19

174
Q

What enzyme produces estrogens from androgens in the granulosa cells? What hormone induces its activity?

A

Aromatase; FSH

175
Q

FSH induces the formation of receptors to what other hormone?

A

LH

176
Q

How long does it take for the oocyte to move from the ampulla to the uterus?

A

5-6 days

177
Q

Which part of this implanted embryo produces hCG? What does this hormone do to the corpus luteum?

A

The syncytium; it sustains growth of the corpus luteum

178
Q

What is the first thing that must be ruled out to determine the etiology of anovulation?

A

pregnancy

179
Q

What four “compartments” of integrated organs need to be examined in disorders of the female menstrual cycle?

A

CNS compartment, anterior pituitary, the gonad (ovary), and the target organ (uterus)

180
Q

What does this sonogram of an ovary indicate? Besides amenorhea, what overall effect can it have on sexual characteristics (hair growth, breasts, etc.)?

A

Polycystic ovary, determined by more than 12 antral follicles; can cause androgenization

181
Q

What period of time must one sustain intercourse without conceiving to indicate infertility?

A

One year

182
Q

What procedure is this?

A

Hysterosalpingogram

183
Q

What is this procedure, performed on day 2 or 3 of the menstrual cycle? Which picture is more indicative for female infertility?

A

Basal antral follicle count; right suggests lack of antral follicles, which is not good for fertility

184
Q

What is the major barrior to sperm number traveling through the female reproductive tract?

A

The cervical mucus

185
Q

What pharmacological strategy can be used to cause ovulation of multiple follicles, increasing the odds of pregnancy?

A

Ovarian hyperstimulation

186
Q

When does hCG production peak?

A

9 weeks post-fertilization

187
Q

How many stages of labor are there?

A

Three

188
Q

The placenta secretes what two hormones that encourage the growth of breasts throughout pregnancy?

A

Estrogen and progesterone

189
Q

Suckling stimulates production of what two hormones that encourage lactation?

A

Oxytocin and prolactin

190
Q

What nerves transmit the signal of suckling to the CNS?

A

4-6th intercostal nerves

191
Q

What is the average age of menopause?

A

51.7 years old

192
Q

Why do FSH and LH levels increase during menopause?

A

Lack of estrogen produced from the ovarian follicles, which have depleted, and so negative feedback on the hypothalamic/pituitary axis.

193
Q

What common skeletal disorder results after menopause? Why?

A

Osteoporosis; the deficiency of estrogen causes less stimulation of estrogen receptors on bones, causing more bone resorption

194
Q

Can the negative side effects of menopause be mitigated with hormone replacement therapy?

A

Trials were attempted in 2002 but the increased risk of coronary heart disease, stroke, and breast cancer outweighed the benefits

195
Q

Is it possible to cryopreserve oocytes from before menopause so they can be fertilized later?

A

It is difficult because mature oocytes have delicate meiotic spindles that are destroyed by ice crystals

196
Q

What is another name for the Cowper’s gland? What does it secrete?

A

Bulbourethral gland; A galactose-rich fluid that lubricates the urethra before ejaculation

197
Q

How many degrees below body temperature are the testes?

A

1 or 2 degrees

198
Q

When testosterone enters Sertoli cells, what hormone is it converted to?

A

Estradiol (estrogen)

199
Q

What organelles are rich throughout the acrosome of the sperm? What about the middle piece?

A

Lysosomes in the acrosome; mitochondria in the middle piece (to produce energy for motility)

200
Q

What zone of the oocyte is broken down by the acrosomal head of the sperm? In what space is the sperm nucleus released?

A

Zona pellucida; perivitelline space

201
Q

Are FSH and LH produced in males?

A

Yes

202
Q

What does LH stimulate in males? What hormone is produced by its target?

A

Interstitial cells of Leydig; testosterone

203
Q

What hormonal changes are present in hypogonadotropic hypogonadism (for a male)?

A

FSH, LH, and testosterone are all low, because the defect is in gonadotrophs in the anterior pituitary

204
Q

In the case of congenital absence of the vas deferens, how can sperm be retrieved for fertilization?

A

Directly from the testes, either percutaneously or via open microsurgery

205
Q

Do testes produce glucocorticoids or mineralocorticoids?

A

No, they lack the correct enzymes

206
Q

Which cells of the testes produce antimullerian hormone?

A

Sertoli cells

207
Q

What hormone causes male hair patterns and baldness?

A

Dihydrotestosterone

208
Q

What drug class is used to treat benign prostatic hypertrophy and male pattern baldness?

A

5 α-reductase inhibitors (e.g. Finasteride)

209
Q

What two proteins does testosterone bind to in blood?

A

Albumin and sex hormone binding globulin

210
Q

What does Klinefelter’s syndrome present as? What is the karyotypic change?

A

Primary hypogonadism; XXY

211
Q

Is hypogonadism characterized by a decreased size of the testicles or penis?

A

Not necessarily, it means decreased production of sex hormones, which may have nothing to do with external appearance

212
Q

What is the congenital cause of secondary hypogonadism (pituitary failure) in males called?

A

Kallmann’s syndrome

213
Q

Do testosterone levels decrease or increase with age in males?

A

Decrease

214
Q

Does visceral fat increase or decrease levels of circulating testosterone?

A

Decrease

215
Q

How does testosterone affect bone physiology? What is the mechanism?

A

It promotes osteogenesis; it encourages osteoblast differentiation, and inhibits osteoclast differentation

216
Q

As testosterone levels decline with age, what common skeletal injury can increase in men?

A

Hip fractures

217
Q

Does increased levels of circulating testosterone increase or decrease risk of coronary heart disease?

A

Decrease

218
Q

What is the standard treatment for hypogonadism in male? What are some of the adverse effects on the testicles, prostrate, and sexual characteristics?

A

Testosterone replacement; it can cause suppression of sperm production, prostrate grown, and increased plasma estrogen, causing gynecomastia

219
Q

Is erectile dysfunction correlated with a lesser or greater risk of heart attack?

A

Greater risk

220
Q

What is the sympathetic innervation of the penis? What is the parasympathetic/somatic innervation?

A

T10-L2 sympathetic; the remaining are S2-S4

221
Q

How does erectile tissue prevent outflow through the surrounding subtunical veins?

A

They are compressed, trapping the blood

222
Q

What key cellular signaller is involved in relaxation of the smooth muscle surrounding helicine arteries of erectile tissue?

A

Nitric oxide

223
Q

What do drugs like Viagra, Cialis, and Levitra inhibit to cause release of nitric oxide (NO)?

A

PDE5, which normally breaks down cGMP, an intracellular signaller that promotes NO release

Physiology (3 decks)

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