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STEP 1 (2) > Endocrine Embryo and Anatomy > Flashcards

Endocrine Embryo and Anatomy Flashcards

1
Q

How does the thyroid gland develop?

A

the thyroid diverticulum arises from the floor of the primitive pharynx and descends into the neck, connected to the tongue by the thyroglossal duct which normally dissappears but may persist as the pyramidal lobe of the thyroid

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2
Q

What is the remnant of the thyroglossal duct?

A

the foramen cecum

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3
Q

What is the most common ectopic thyroid tissue site?

A

the tongue

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4
Q

What does the adrenal cortex derive from?

A

the mesoderm

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5
Q

What does the adrenal medulla derive from?

A

the neural crest

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6
Q

What are the three zones of the adrenal cortex from out to in?

A

Zona glomerulosa

Zona Fasciculate

Zone Reticularis

“Salt (Na+), Sugar (glucocorticoids), Sex (androgens)- the deeper you go, the sweeter it gets”

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7
Q

What is the priamry regulator and products of the zone glomerulosa?

A

renin-angiotension, and produces aldosterone

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8
Q

What is the primary regulator and products of the zone fasciculata?

A

ACTH, CRH; cortisol, and sex hormones

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9
Q

What is the primary regulator and products of the zone reticularis?

A

ACTH, CRH; sex hormones

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10
Q

What is the main cell of the adrenal medulla?

A

the chromaffin cells

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11
Q

What is the primary regulator of the adrenal medulla and its products?

A

regulator is preganglionic sympathetic fibers and products are catecholamines (epi and nor)

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12
Q

What are the most common adrenal medulla tumors in a) adults and b) children

A

a) pheochromocytoma
b) neuroblastoma

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13
Q

What are the hormones of the anterior pituitary (aka adenohypophysis)?

A

FSH, LH, ACTH, TSH, prolactin, and GH

FLAT PiG

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14
Q

What is the anterior pituitary derived from?

A

oral ectoderm (Rathke pouch)

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15
Q

What are the acidophilic hormones of the anterior pituitary?

A

GH and prolactin

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16
Q

What are the basophilic hormones of the anterior pituitary?

A

B-FLAT

FSH, LH, ACTH, TSH

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17
Q

Describe the subunits of the anterior pituitary hormones

A

a subunit is common to TSH, LH, FSH, and hCG

b subunit determines hormone specificity

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18
Q

What are the hormones of the posterior pituitary (aka neurohypophysis)?

A

vasopressin (ADH) and oxytocin. These are made in the hypothalamus (supraoptic and paraventicular nuclei, respectively) and transported to the posterior pituitary via neurophysins (carrier proteins)

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19
Q

The posterior pituitary is derived from what?

A

the neuroectoderm

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20
Q

Melanotropin (MSH) is secreted from what?

A

the intermediate pituitary

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21
Q

What are the products of a,B, and d cells in the islets of langerhans in the pancreas?

A

a- glucagon (peripheral)

b- insulin (central)

d- soamtostatin (interspersed)

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22
Q

How is insulin made?

A

preproinsulin is synthesized in the RER of B cells and then cleavage of a presignal yieds proinsulin which is stored in secretory granules. Cleavage of proinsulin results in exocytosis of insulin and C-peptide in equal amounts

Note that insulin AND C-peptide are elevated in insulinomas and sulfonylurea use, but exogenous insulin lacks C-peptide

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23
Q

How does insulin act?

A

it binds to insulin receptors (tyrosine kinase activity), inducing mobilization of GLUT-4 receptors to internalize glucose

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24
Q

Where are GLUT-4 receptors found?

A

adipose tissue, striated muscle

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25
Q

What are the main effects of insulin?

A
  • lower BG via GLUT-4 upregulation
  • increase glycogen synthesis and decrease glucagon
  • increase TAG and protein synthesis
  • Na+ retention at the kidneys
  • increase cellular uptake of K+ and AAs
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26
Q

Does insulin cross the placenta?

A

No, unlike glucose

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27
Q

Where are GLUT-1 receptors located?

A

RBCs, brain, cornea

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28
Q

Where are GLUT-2 receptors located?

A

B-islet cells, liver, kidney, and small intestine

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29
Q

Where are GLUT-3 receptors located?

A

brain

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30
Q

Where are GLUT-5 (fructose) receptors located?

A

spermatocytes, GI tract

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31
Q

Glucose use in the brain and RBCs

A

the brain uses glucose for metabolism normally and ketone bodies during starvation

RBCs always use glucose because they lack mitochondria for aerobic metabolism

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32
Q

What are the insulin-independent glucose uptake organs?

A

BRICK L

brain, RBCS, intestine, cornea, kidneys, and liver

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33
Q

What two things increase insulin release?

A

GH and B2-agonists

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34
Q

How does glucose cause insulin release?

A

glucose enters B cells via GLUT-2 receptors and increases the ATP:ADp ratio which causes the closure of an ATP-sensitive K+ channel (Target of sulfonylureas) and depolarizes the B cell membrane casuing voltage-gated Ca2+ to open and cause Ca2+ influx which then stimulates insulin exocytosis

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35
Q

Glucagon is made by a cells. What does it do?

A

promotes glycogenolysis and gluconeogenesis, and lipolysis and ketone production

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36
Q

What is the function of CRH?

A

release ACTH, MSH, and B-endorphin (decreased in chronic exogenous steroid use by feedback)

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37
Q

What are the effects of dopamine on prolactin?

A

it decreases prolactin release (note that dopamine antagonists like some antiphsychotics can cause galactorrhea due to hyperprolactinemia)

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38
Q

What is the role of GHRH?

A

release of GH (note that an analog of GHRH, tesamorelin, is used to tx HIV-associated lipodystrophy)

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39
Q

What is the role of GnRH?

A

cause release of FSH and LH (prolactin inhibits GnRH levels)

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40
Q

Somatostatin inhibits what hormones?

A

insulin and glucagon

GH

TSH

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41
Q

TRH not only promotes TSH release but also ____

A

prolactin

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42
Q

Prolactin is mainly secreted by the anterior pituitary. What is its function?

A

stimulates milk production in the breast

inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release

decreases libido

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43
Q

How is prolactin regulated?

A

tonic suppression by dopamine from the hypothalamus. Prolactin in turn inhibits its own secretion by increasing dopamine synthesis

TRH can also promote prolactin release (e.g. in primary or secondary hypothyroidism)

estrogens can also cause prolactin release (e.g. OCPs, pregnancy)

44
Q

GH is also secreted from the anterior pituitary. What does it do?

A

stimulates linear growth and muscle mass through IGF-1 (somatomedin C) secretion and promotes insulin resistance (diabetogenic)

45
Q

How is GH released?

A

in pulses in response to GHRH. Secretion increased during exercise and sleep

46
Q

What does ghrelin do? Where is it made?

A

it is made in the stomach and makes you hungry and causes GH release

increased with sleep loss and Prader-Willi syndrome

47
Q

What is Prader-Willi syndrome?

A

a genetic disorder due to loss of function of specific genes on chromosome 15.

In newborns symptoms include weak muscles, poor feeding, and slow development. In childhood the person becomes constantly hungry which often leads to obesity and type 2 diabetes. There is also typically mild to moderate intellectual impairment and behavioral problems. Often the forehead is narrow, hands and feet small, height short, skin light in color, and they are unable to have children

48
Q

What does leptin do? Where is it made?

A

Made by adipose tissue and makes you full

49
Q

T or F. Lack of sleep makes you hungry

A

T. More ghrelin and less leptin

50
Q

ADH is synthesized in the hypothalamus in the supraoptic nuclei and released via the posterior pituitary. What does it do?

A

it helps decrease serum osmolarity by binding to V2-receptors and upregulating aquaporin channel expression in the principle cells of the renal collecting ducts

and increase blood pressure (V1 receptors) by causing vasoconstriction

51
Q

ADH levels are decreased in what?

A

central diabetes insipidus

52
Q

How is central diabetes insipidus tx?

A

desmopression acetate (ADH analog)

53
Q

How is pregnenolone made?

A

cholesterol is converted to pregnenolone via cholesterol desmolase in the zona glomerulosa via ACTH action

54
Q

What things inhibit the action of cholesterol demolase?

A

ketoconazole

55
Q

What things can happen to pregnenolone?

A

1) conversion to progesterone via 3B-HSD in the ZG
2) conversion to 17-hydroxypregnenolone via 17a-hydroxylase in the ZF

56
Q

What things can happen to pregesterone?

A

1) conversion to 11-deoxycorticosterone via 21-hydroxylase in the ZG
2) conversion to 17-hydroxyprogesterone via 17a-hydroxylase in the ZF

57
Q

How is aldosterone formed?

A

11-deoxycorticosterone converted to corticosterone via 11B-hydroxylase and then to aldosterone via aldosterone synthase all in the ZG

58
Q

What upregulates aldosterone synthase expression in the ZG?

A

angiotensin II

59
Q

What things can happen to 17-hydroxypregnenolone?

A

1) conversion to 17-hydroxyprogesterone in the ZF via 3B-HSD
2) conversion to DHEA in the ZR (no enzyme)

60
Q

How is cortisol made in the ZF?

A

1) 17-hydroxyprogesterone converted to 11-deoxycortisol via 21-hydroxylase
2) 11-deoxycortisol converted to cortisol via 11B-hydroxylase

61
Q

What happens to DHEA?

A

converted to androstenedione via 3B-HSD in the ZR (note that 17-hydroxyprogesterone can also be converted to androstenedione- no enzyme)

62
Q

What things can happen to androstenedione?

A

1) converted to estrone and then estradiol via aromatase
2) converted to testosterone

both in the ZR

63
Q

How is testosterone converted to DHT?

A

5a-reductase

64
Q

Describe 17a-hydroxylase deficiency

A
65
Q

Describe 21-hydroxylase deficiency

A

it causes decreased aldosterone and cortisol with increased sex hormones leading to low BP, hyperkalemia and sexual problems

66
Q

What labs are elevated in 21-hydroxylase deficiency?

A

increased renin and 17-hydroxyprogesterone

67
Q

Describe 11B-hydroxylase deficiency

A

results in decreased aldosterone (but increased 11-deoxycorticosterone which also acts like aldosterone so BP is elevated and hypokalemia exists), decreased cortisol, and increased sex hormones

68
Q

T or F. Renin activity is decreased in 11B-hydroxylase deficiency

A

T.

69
Q

Note that all congenital adrenal enzyme deficiencies are characterized by an enlargement of BOTH adrenal glands due to increased ACTH stimulation (due to decreased cortisol)

A
70
Q

Cortisol is made in the adrenal zona fasciculata. What are its main functions?

A

BIG FIB

  • increase BP
  • cause insulin resistance (diabetogenic)
  • increase gluconeogenesis, lipolysis, and proteolysis
  • decrease fibroblast activity
  • increase inflammatory and immune responses
  • decrease bone formation/osteoblast activity
71
Q

How does cortisol increase BP?

A

it upregulates a1-receptors on arterioles increasing the sensitivity to catecholamines and

at high conc can bind to aldosterone receptors

72
Q

How does cortisol decrease immune and inflammatory responses?

A
  • inhibits production of leukotrienes and prostaglandins
  • inhibits WBC adhesion (causes neutrophilia)
  • blocks histamine release from mast cells
  • reduces eosinophils
  • blocks IL-2 production
73
Q

Note that exogenous corticosteroids can cause reactivation of TB and candidiasis due to IL-2 blockage

A
74
Q

How is cortisol regulated?

A

CRH from the hypothalamus stimulates ACTH release from the pitutiary sitmulating cortisol production in the adrenal ZF

chronic stress and pregnancy also cause cortisol levels to increase

75
Q

What are the main forms of calcium?

A
  • ionized (45%)
  • albumin bound (40%)
  • anion bound (15%)
76
Q

How does pH affect calcium?

A

increased pH causes increased affinity of albumin to Ca2+ causing hypocalemia which presents as cramps, pain, paresthesias, etc.

77
Q

What is the source of vitamin D (cholecalciferol)?

A

D3 from sun and D2 from plants are both converted to 25-OH in the liver and 1,25-OH in the kidneys

78
Q

What does vitD do?

A

increases GI absorption of dietary Ca2+ and PO43-, as well as bone resorption of both

79
Q

How is vitD regulated?

A

increased PTH, or decreased Ca2+/PO4 lead to increased vitD levels

80
Q

What are the results of vitD deficiency?

A

rickets in children and osteomalacia in adults

81
Q

What are the effects of PTH?

A
  • increased Ca2+ reabsorption in the distal convoluted tubule
  • decreased PO4 reabsorption in the proximal convoluted tubule
  • upregulation of vitD via 1a-hydroxylase in proximal convoluted tubule
  • increased bone resorption of Ca2+ and PO43-
82
Q

What is PTH made?

A

chief cells of the parathyroid

83
Q

PTH increases serum Ca2+, decreases serum PO4, and increases urine PO4

A
84
Q

How does PTH cause Ca resorption?

A

it increases production of macrophage colony-stimulating factor and RANK-L (receptor activator of NF-kB). RANK-L (ligand) secreted by osteoblasts and octeocytes binds to RANK on osteoclasts to activate them

NOTE: low-dose PTH can be used for bone formation

85
Q

What things cause PTH release?

A

low Ca2+ and Mg2+

high PO4

NOTE: VERY low Mg2+ (in cases of diarrhea, diuretics, alcohol abuse, aminoglycosides) actually inhibits PTH secretion

86
Q

Where is calcitonin made?

A

parafollicular cells (C) of the thyroid

87
Q

What are the functions of calcitonin?

A

oppose PTH- decrease bone resorption of Ca2+ and lower serum Ca2+ (but not that important in adult Ca2+ homeostasis)

88
Q

What hormones work by increasing cAMP?

A

FLAT ChAMP GCG

FSH, LF, ACTH, TSH

CRH, hCG, ADH (V2 receptor), MSH, PTH

calcitonin, GHRH, glucagon

89
Q

What hormones work by increasing cGMP?

A

ANP, BNP, NO

90
Q

What hormones work by increasing IP3 (Gq mechanism)?

A

GnRH, Oxytocin, ADH (V1 receptor), TRH, Histamine (H1 receptor), Angiotensin II, Gastrin

GOAT HAG

91
Q

What hormones work by binding to an intracellular receptor?

A

vitD, Estrogen, Testosterone, T3/T4, cortisol, aldosterone, progesterone

VETTT CAP

92
Q

What hormones work by binding to a receptor with intrinsic tyrosine kinase activity (MAP kinase pathway)?

A

Insulin, IGF-1, FGF, PDGF, EGF

93
Q

What hormones work by binding to a receptor with receptor-associated tyrosine kinase activity (JAK/STAT pathway)?

A

Prolactin, Immunomodulators (e.g. IL-2, IL-6, IFN), GH, G-CSF, EPO, TPO

PIGGlET

94
Q

Note about steroid hormones

A
95
Q

How do OCPs and pregnancy affect SHBG?

A

they increase it with free estrogen levels remaining unchanged

96
Q

How are the thyroid hormones made?

A

Iodide enters follicular thyroid cells via the basolateral side and is oxidation on the apical side to I2 which then binds with thyroglobulin to form MIT or DIT, and then T3/T4 via thyroid peroxidase. These are then exocytosed back through the follicular cell into circulation

97
Q

What carries T3/T4 in blood?

A

thyroxine-binding globulin (TBG) (but only free hormone is active)

98
Q

When is TBG decreased? increased?

A

decreased- hepatic failure, steroids

increased- pregnancy or OCP use

99
Q

While T4 is the major thyroid product, T3 is the most active form. How is T4 covnerted to T3?

A

5’-deiodinase at the target tissue

100
Q

What are the roles of thyroid hormones?

A
  • Brain/CNS maturation
  • Bone growth (synergism with GH)
  • B-adrenergic effects via B1 binding causing increased CO, HR, and SV
  • increase Basal metabolic rate
101
Q

How do thryoid hormones increase BMR?

A

they increase NaKATPase activity leading to increased O2 consumption, RR, and body temp

they also increase glycogenolysis, gluconeogenesis, and lipolysis

102
Q

How are thyroid hormones regulated?

A

TRH causes TSH release from the pituitary

103
Q

What things decrease iodine uptake into follicular cells?

A

Anions like prechlorate, pretechnetate, and thiocyanate

104
Q

What things decrease thryoid peroxidase activity?

A

propylthiouracil (also inhibits 5’-deiodinase) and methimazole

105
Q

What is the Wolff-Chaikoff effect?

A

excess iodine temporarily inhibits thyroid peroxidase, decreasing iodine organification and causing hypothyroidism

STEP 1 (2) (16 decks)

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