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First Aid > Endocrine 1 > Flashcards

Endocrine 1 Flashcards

1
Q

Where does the thyroid diverticulum arise from?

A

The thyroid diverticulum arises from the floor of the primitive pharynx.

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2
Q

Where does the thyroid diverticulum descend into?

A

The thyroid diverticulum descends into the neck.

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3
Q

What connects the thyroid diverticulum to the tongue?

A

The thyroid diverticulum is connected to the tongue by the thyroglossal duct.

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4
Q

What may persist from the thyroglossal duct?

A

The thyroglossal duct may persist as cysts or a pyramidal lobe of the thyroid.

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5
Q

What is the normal remnant of the thyroglossal duct?

A

The normal remnant of the thyroglossal duct is the foramen cecum.

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6
Q

What is the most common site for ectopic thyroid tissue?

A

The most common ectopic thyroid tissue site is the tongue (lingual thyroid).

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7
Q

What can removal of lingual thyroid tissue result in?

A

Removal may result in hypothyroidism if it is the only thyroid tissue present.

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8
Q

How does a thyroglossal duct cyst present?

A

A thyroglossal duct cyst presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue.

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9
Q

How does a thyroglossal duct cyst differ from a branchial cleft cyst?

A

A thyroglossal duct cyst is an anterior midline neck mass that moves with swallowing or protrusion of the tongue, while a branchial cleft cyst arises from a persistent cervical sinus in the lateral neck.

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10
Q

From which germ layer are thyroid follicular cells derived?

A

Thyroid follicular cells are derived from endoderm.

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11
Q

From which origin are parafollicular cells derived?

A

Parafollicular cells (C cells) are derived from neural crest.

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12
Q

What is the origin of the adrenal cortex?

A

The adrenal cortex is derived from mesoderm.

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13
Q

What is the origin of the adrenal medulla?

A

The adrenal medulla is derived from neural crest.

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14
Q

What are the zones of the adrenal cortex?

A

The zones of the adrenal cortex are Zona Glomerulosa, Zona Fasciculata, and Zona Reticularis.

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15
Q

What does GFR stand for in relation to adrenal cortex zones?

A

GFR stands for Salt (mineralocorticoids), Sugar (glucocorticoids), Sex (androgens).

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16
Q

What primarily regulates the zona glomerulosa?

A

The primary regulator of the zona glomerulosa is AT II.

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17
Q

What hormone class does the zona glomerulosa produce?

A

The zona glomerulosa primarily produces mineralocorticoids.

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18
Q

What is the primary hormone produced by the zona glomerulosa?

A

The primary hormone produced by the zona glomerulosa is aldosterone.

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19
Q

What primarily regulates the zona fasciculata?

A

The primary regulators of the zona fasciculata are ACTH and CRH.

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20
Q

What hormone class does the zona fasciculata produce?

A

The zona fasciculata primarily produces glucocorticoids.

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21
Q

What is the primary hormone produced by the zona fasciculata?

A

The primary hormone produced by the zona fasciculata is cortisol.

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22
Q

What primarily regulates the zona reticularis?

A

The primary regulators of the zona reticularis are ACTH and CRH.

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23
Q

What hormone class does the zona reticularis produce?

A

The zona reticularis primarily produces androgens.

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24
Q

What is the primary hormone produced by the zona reticularis?

A

The primary hormone produced by the zona reticularis is DHEA (Dehydroepiandrosterone).

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25
Q

What hormones does the anterior pituitary secrete?

A

The anterior pituitary secretes FSH, LH, ACTH, TSH, Prolactin, GH, and β-endorphin.

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26
Q

Where is Melanotropin (MSH) secreted from?

A

Melanotropin (MSH) is secreted from the intermediate lobe of the pituitary.

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27
Q

What are ACTH, MSH, and β-endorphin derivatives of?

A

ACTH, MSH, and β-endorphin are derivatives of proopiomelanocortin (POMC).

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28
Q

What is the origin of the adenohypophysis?

A

The adenohypophysis is derived from Rathke’s pouch.

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29
Q

What is the common subunit of anterior pituitary hormones?

A

The common subunit is the hormone subunit common to TSH, LH, FSH, and hCG.

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30
Q

What determines the specificity of anterior pituitary hormones?

A

The specific subunit of anterior pituitary hormones determines hormone specificity.

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31
Q

Which anterior pituitary hormones are secreted by basophils?

A

Basophils secrete FSH, LH, ACTH, and TSH.

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32
Q

Which anterior pituitary hormones are secreted by acidophils?

A

Acidophils secrete GH and PRL.

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33
Q

What hormones does the posterior pituitary store and release?

A

The posterior pituitary stores and releases vasopressin (ADH) and oxytocin.

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34
Q

Where are vasopressin and oxytocin made?

A

Both are made in the hypothalamus (supraoptic & paraventricular nuclei).

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35
Q

How are vasopressin and oxytocin delivered to the neurohypophysis?

A

They are delivered via neurophysins (carrier proteins).

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36
Q

What is the origin of the posterior pituitary?

A

The posterior pituitary is derived from neuroectoderm.

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37
Q

What are Islets of Langerhans?

A

Islets of Langerhans are collections of endocrine cells that arise from pancreatic buds.

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38
Q

What do alpha pancreatic cells produce and where are they located?

A

Alpha pancreatic cells produce glucagon and are located peripherally within the islets of Langerhans.

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39
Q

What do beta pancreatic cells produce and where are they located?

A

Beta pancreatic cells produce insulin and are located centrally within the islets of Langerhans.

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40
Q

What do delta pancreatic cells produce and where are they located?

A

Delta pancreatic cells produce somatostatin and are interspersed within the islets of Langerhans.

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41
Q

What is the synthesis process of insulin?

A

Preproinsulin (synthesized in RER) undergoes cleavage of ‘presignal’ to proinsulin (stored in secretory granules), then cleavage of proinsulin leads to exocytosis of insulin and C-peptide equally.

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42
Q

In what scenarios would levels of both insulin and C-peptide be increased?

A

Levels of both insulin and C-peptide would be increased in insulinoma and sulfonylurea use.

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43
Q

What happens to levels of insulin and C-peptide with exogenous insulin use?

A

Only insulin increases, as exogenous insulin lacks C-peptide.

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44
Q

How does insulin bind to its receptors?

A

Insulin is released from pancreatic beta cells, binds insulin receptors with tyrosine kinase activity, and induces glucose uptake into insulin-dependent tissue and gene transcription.

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45
Q

What are the insulin-dependent glucose transporters?

A

GLUT4 is the insulin-dependent glucose transporter found in adipose tissue and striated muscle.

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46
Q

How can exercise affect GLUT4 expression?

A

Exercise can increase GLUT4 expression.

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47
Q

What are the insulin-independent glucose transporters?

A

GLUT1, GLUT2 (bidirectional), GLUT3, GLUT5 (Fructose), SGLT1/SGLT2 (Na+-glucose cotransporters).

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48
Q

Which tissues express GLUT1?

A

GLUT1 is expressed in RBCs, brain, cornea, and placenta.

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49
Q

Which tissues express GLUT2?

A

GLUT2 is expressed in islet cells, liver, kidney, and small intestine.

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50
Q

Which tissues express GLUT3?

A

GLUT3 is expressed in the brain and placenta.

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51
Q

Which tissues express GLUT5?

A

GLUT5 is expressed in spermatocytes and the GI tract.

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52
Q

Which tissues express SGLT1/SGLT2?

A

SGLT1/SGLT2 is expressed in the kidney and small intestine.

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53
Q

What does the brain utilize for metabolism during starvation?

A

The brain utilizes glucose for metabolism but ketone bodies during starvation.

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54
Q

What do RBCs utilize for energy?

A

RBCs utilize glucose for energy as they lack mitochondria for aerobic metabolism.

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55
Q

What tissues have insulin-independent glucose uptake?

A

Tissues with insulin-independent glucose uptake include Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet cells, Placenta, and Spermatocytes.

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56
Q

What is insulin’s effect once in the placenta?

A

Unlike glucose, insulin does not cross the placenta.

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57
Q

What are the anabolic effects of insulin?

A

Insulin promotes glucose transport in skeletal muscle and adipose tissue, glycogen synthesis and storage, triglyceride synthesis, Na+ retention in kidneys, protein synthesis in muscles, cellular uptake of K+ and amino acids, and inhibits glucagon release.

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58
Q

What is the major regulator of insulin release?

A

The major regulator of insulin release is glucose.

59
Q

Why is there a different insulin response with oral vs IV glucose?

A

The difference is due to incretins (e.g., GLP-1, GIP), which are released after meals and increase beta cell sensitivity to glucose.

60
Q

What are incretins?

A

Incretins include glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are released after meals and enhance beta cell sensitivity to glucose.

61
Q

Which receptors regulate insulin secretion?

A

Insulin release is stimulated by GLP-1 and inhibited by somatostatin.

62
Q

What is the mechanism of insulin secretion by pancreatic beta cells?

A

Glucose enters beta cells, generating ATP from glucose metabolism, which closes K+ channels, depolarizes the cell membrane, opens voltage-gated Ca2+ channels, and stimulates insulin exocytosis.

63
Q

What is the source of glucagon?

A

Glucagon is made by alpha cells of the pancreas.

64
Q

What is the function of glucagon?

A

Glucagon promotes glycogenolysis, gluconeogenesis, lipolysis, and ketone production, elevating blood sugar levels during fasting.

65
Q

How is glucagon regulated?

A

Glucagon is secreted in response to hypoglycemia and inhibited by insulin, hyperglycemia, and somatostatin.

66
Q

What is the function of ADH?

A

ADH increases water permeability of distal convoluted tubule and collecting duct cells in the kidney to enhance water reabsorption.

67
Q

What is the stimulus for ADH secretion?

A

The stimulus for ADH secretion is plasma osmolality, except in cases of SIADH.

68
Q

What is the function of CRH?

A

CRH stimulates ACTH, MSH, and β-endorphin secretion.

69
Q

What decreases CRH levels?

A

CRH levels decrease in chronic exogenous steroid use.

70
Q

What is the function of dopamine?

A

Dopamine inhibits prolactin and TSH secretion.

71
Q

What can dopamine antagonists cause?

A

Dopamine antagonists can cause galactorrhea due to hyperprolactinemia.

72
Q

What is the function of GHRH?

A

GHRH stimulates GH secretion.

73
Q

What is GHRH analog used to treat?

A

GHRH analog (tesamorelin) is used to treat HIV-associated lipodystrophy.

74
Q

What is the function of GnRH?

A

GnRH stimulates FSH and LH secretion.

75
Q

What suppresses GnRH?

A

GnRH is suppressed by hyperprolactinemia.

76
Q

What is the effect of tonic vs pulsatile GnRH?

A

Tonic GnRH suppresses the HPG axis, while pulsatile GnRH leads to puberty and fertility.

77
Q

What is the function of MSH?

A

MSH stimulates melanogenesis by melanocytes.

78
Q

Why does MSH cause hyperpigmentation in Cushing disease?

A

MSH and ACTH share the same precursor molecule, proopiomelanocortin.

79
Q

What is the function of oxytocin?

A

Oxytocin causes uterine contractions during labor and is responsible for the milk letdown reflex in response to suckling.

80
Q

What is the function of prolactin?

A

Prolactin stimulates milk production in the breast and inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release.

81
Q

What symptoms does pituitary prolactinoma cause?

A

Pituitary prolactinoma causes amenorrhea, osteoporosis, hypogonadism, and galactorrhea.

82
Q

What is the function of somatostatin?

A

Somatostatin inhibits GH and TSH secretion.

83
Q

What are somatostatin analogs used to treat?

A

Somatostatin analogs are used to treat acromegaly.

84
Q

What is the function of TRH?

A

TRH stimulates TSH and prolactin secretion.

85
Q

What can increase TRH secretion?

A

TRH may increase prolactin secretion in primary or secondary hypothyroidism.

86
Q

Where is prolactin secreted from and what is it structurally homologous to?

A

Prolactin is secreted mainly by the anterior pituitary and is structurally homologous to growth hormone.

87
Q

What is the function of PRL?

A

PRL stimulates milk production in the breast and inhibits ovulation and spermatogenesis.

88
Q

What inhibits prolactin secretion?

A

Prolactin secretion is tonically inhibited by dopamine from the tuberoinfundibular pathway of the hypothalamus.

89
Q

How does prolactin inhibit its own secretion?

A

Prolactin inhibits its own secretion by increasing dopamine synthesis/secretion from the hypothalamus.

90
Q

What effect does TRH have on PRL secretion?

A

TRH increases prolactin secretion.

91
Q

What can inhibit prolactin secretion and be used to treat prolactinoma?

A

Dopamine agonists (e.g., bromocriptine) can inhibit prolactin secretion.

92
Q

What drugs stimulate prolactin secretion?

A

Dopamine antagonists (e.g., most antipsychotics) and estrogens (e.g., OCPs, pregnancy) stimulate prolactin secretion.

93
Q

Where is growth hormone (somatotropin) secreted from?

A

Growth hormone is secreted by the anterior pituitary.

94
Q

What is the function of growth hormone (GH)?

A

GH stimulates linear growth and muscle mass through IGF-1 secretion by the liver.

95
Q

What is a side effect of growth hormone?

A

GH can cause insulin resistance (diabetogenic).

96
Q

How is GH released?

A

GH is released in pulses in response to growth hormone-releasing hormone (GHRH).

97
Q

When is GH secretion increased?

A

GH secretion increases during exercise, deep sleep, puberty, and hypoglycemia.

98
Q

What inhibits GH secretion?

A

GH secretion is inhibited by glucose and somatostatin release via negative feedback by somatomedin.

99
Q

What can excess secretion of GH cause?

A

Excess GH secretion may cause acromegaly in adults or gigantism in children.

100
Q

How is excess GH treated?

A

Excess GH is treated with somatostatin analogs (e.g., octreotide) or surgery.

101
Q

What is the function of ghrelin?

A

Ghrelin stimulates hunger (orexigenic effect) and GH release via GH secretagogue receptor.

102
Q

Where is ghrelin produced?

A

Ghrelin is produced by the stomach.

103
Q

How does ghrelin exert its effects?

A

Ghrelin acts via the lateral area of the hypothalamus to stimulate appetite.

104
Q

How do sleep deprivation and Prader-Willi syndrome affect ghrelin?

A

Sleep deprivation or Prader-Willi syndrome increases ghrelin production.

105
Q

What is the function of leptin?

A

Leptin is a satiety hormone produced by adipose tissue.

106
Q

How does leptin exert its effects?

A

Leptin acts via the ventromedial area of the hypothalamus to decrease appetite.

107
Q

What effect does a mutation of the leptin gene have?

A

A mutation of the leptin gene can lead to congenital obesity.

108
Q

What effect does sleep deprivation have on leptin?

A

Sleep deprivation or starvation decreases leptin production.

109
Q

What is the effect of endocannabinoids?

A

Endocannabinoids act at cannabinoid receptors in the hypothalamus and nucleus accumbens to increase appetite.

110
Q

What is the source of ADH (vasopressin)?

A

ADH is synthesized in the hypothalamus (supraoptic and paraventricular nuclei) and stored/secreted by the posterior pituitary.

111
Q

What does ADH regulate and which receptors does it use?

A

ADH regulates serum osmolality via V2-receptors and blood pressure via V1-receptors.

112
Q

What can cause nephrogenic DI?

A

Nephrogenic DI can be caused by a mutation in the V2-receptor.

113
Q

What is the primary function of ADH?

A

The primary function of ADH is serum osmolality regulation.

114
Q

What is the source of ADH (vasopressin)?

A

Synthesized in hypothalamus (supraoptic and paraventricular nuclei), stored/secreted by posterior pituitary.

115
Q

What does ADH regulate and which receptors does it use?

A

Regulates serum osmolality (V2-receptors) and blood pressure (V1-receptors).

116
Q

What can cause nephrogenic diabetes insipidus (DI)?

A

Mutation in V2-receptor.

117
Q

What is the primary function of ADH?

A

Regulates serum osmolality (ADH ? serum osmolality, ? urine osmolality) via regulation of aquaporin channel insertion in principal cells of renal collecting duct.

118
Q

How do ADH levels differ in central vs nephrogenic diabetes insipidus (DI)?

A

ADH level is decreased in central DI, normal or decreased in nephrogenic DI.

119
Q

What is desmopressin used to treat?

A

Central diabetes insipidus and nocturnal enuresis.

120
Q

What regulates ADH secretion?

A

Osmoreceptors in hypothalamus and hypovolemia.

121
Q

What enhances the conversion of cholesterol into pregnenolone?

A

Steroidogenic acute regulatory protein (STAR) enhances this conversion by mediating cholesterol transport from outer to inner mitochondrial membrane.

122
Q

What is synthesized in the zona glomerulosa?

A

Mineralocorticoids.

123
Q

What is the first step in the mineralocorticoid synthesis pathway?

A

Cholesterol desmolase catalyzes the conversion of cholesterol to pregnenolone.

124
Q

What regulates cholesterol desmolase activity?

A

ACTH enhances the activity of cholesterol desmolase.

125
Q

What drug inhibits the conversion of cholesterol to pregnenolone?

A

Ketoconazole (azole antifungal, blocks several steps in steroidogenesis).

126
Q

What is synthesized in the zona fasciculata?

A

Glucocorticoids.

127
Q

What drug inhibits the conversion of 11-deoxycortisol to cortisol?

A

Metyrapone inhibits 11?-hydroxylase.

128
Q

What drug inhibits the conversion of cortisol to cortisone?

A

Glycyrrhetinic acid (found in black licorice).

129
Q

What is synthesized in the zona reticularis?

A

Androgens.

130
Q

What is the conversion of androstenedione in peripheral tissue?

A

Androstenedione converts to estrone (aromatase) and testosterone converts to estradiol (aromatase) or dihydrotestosterone (DHT) (5? reductase).

131
Q

What drugs inhibit the conversion of androstenedione to estrone and testosterone to estradiol?

A

Aromatase antagonists such as anastrozole and exemestane.

132
Q

What drug inhibits the conversion of testosterone to DHT?

A

5? reductase antagonist: finasteride.

133
Q

What regulates aldosterone synthase?

A

Angiotensin II (ATII) upregulates aldosterone synthase.

134
Q

What characterizes all congenital adrenal enzyme deficiencies?

A

Skin hyperpigmentation (due to increased MSH production) and bilateral adrenal gland enlargement (due to increased ACTH stimulation).

135
Q

What is the effect of 17?-hydroxylase deficiency on mineralocorticoids?

A

Mineralocorticoids: decreased.

136
Q

What is the effect of 17?-hydroxylase deficiency on cortisol?

A

Cortisol: decreased.

137
Q

What is the effect of 17?-hydroxylase deficiency on sex hormones?

A

Sex hormones: decreased.

138
Q

What is the effect of 17?-hydroxylase deficiency on blood pressure?

A

Blood pressure: increased.

139
Q

What is the effect of 17?-hydroxylase deficiency on potassium levels?

A
140
Q

What is the lab finding for 17?-hydroxylase deficiency?

A

Labs: increased androstenedione.

141
Q

What is the presentation of 17?-hydroxylase deficiency in XY individuals?

A

Ambiguous genitalia and undescended testes.

142
Q

What is the presentation of 17?-hydroxylase deficiency in XX individuals?

A

Lacks secondary sexual development.

143
Q

What is the most common steroidogenic enzyme deficiency?

A

Not specified in the provided text.

First Aid (18 decks)

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