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Endocrine > Biochem & Phys > Flashcards

Biochem & Phys Flashcards

1
Q

What is the principal regulator of adrenomedullary secretion of catecholamines?

A

ACh release from preganglionic sympathetic fibers of the splanchnic nerves

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2
Q

somatic innervation of the penis (both motor & sensory)

A

pudendal nerve (S2-S4)

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3
Q

nerve plexuses that supply sympathetic motor fibers (5) to the male sex organs

A
  1. celiac (this is a “pass through)
  2. superior mesenteric
  3. inferior mesenteric
  4. superior hypogastric
  5. inferior hypogastric or pelvic (receives sympathetic supply from hypogastric nerve)
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4
Q

where does the spermatic ganglion receive sympathetic fibers?

A

lumbar sympathetic nerves & other ganglia

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5
Q

prolonged meiosis arrest in prophase I

A

dictyotene stage

These are primary oocytes.

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6
Q

primary oocyte with a surrounding single layer of pregranulosa cells

A

primordial follicle

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7
Q

larger oocyte surrounded by a single layer of cuboidal granulosa cells

A

primary follicle

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8
Q

Primary oocyte surrounded by several layers of cuboidal granulosa cells. Formation of capillaries and increased vascular supply to developing follicular units is also present.

A

secondary follicle

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9
Q

from stromal cells that differentiate and surround the follicle

A

theca cells

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10
Q

Which cells secrete fluid into the antrum?

A

granulosa cells

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11
Q

stage of follicular development when the antrum is present

A

tertiary follicle

The second antral stage is preovulatory: Graafian follicle

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12
Q

mucopolysaccharides immediately surrounding the oocyte

A

zona pellucida

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13
Q

most metabolically active follicular cells which are farthest from the center of the follicle and contain large quantities of LH receptors

A

mural granulosa cells

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14
Q

Cells that become the large luteal cells of the corpus luteum

A

antral granulosa cells

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15
Q

What regulates the concentration of SHBG?

A

Estrogen increases it. Testosterone decreases it. Women have twice as much SHBG as men.

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16
Q

Estrogen is metabolized to what less active steroids by the liver?

A

Estriol and estrone

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17
Q

How does the ovary synthesize estrogen?

A

LH stimulates the theca cells to synthesize androgens which diffuse to granulosa cells that synthesize estrogen under the stimulation of FSH. Granulosa cells contain aromatase. Theca cells have CYP17 activity.

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18
Q

What inhibits milk production during pregnancy?

A

High levels of progesterone

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19
Q

Why is hormone secretion pulsatile?

A

Prevent downregulation of the receptor

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20
Q

Serum proteins that bind thyroxine

A

Thyroxine binding globulin

Transthyretin

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21
Q

Why is the level of cortisol highest in the morning?

A

to prepare you to get up

it’s lowest in the evening.

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22
Q

Main regulator of ADH release

A

increased plasma osmolality (mainly hypernatremia) and decreased blood volume (hypovolemia)

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23
Q

Neurons that synthesize and release ADH and oxytocin

A

magnacellular neurons of the PVN & SON (supraoptic nuclei)

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24
Q

Causes central diabetes insipidus

A

decreased release of ADH

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25
Q

Causes nephrogenic diabetes insipidus

A

decreased renal responsiveness to ADH -> mutation of V2R and/or AQP2

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26
Q

SIADH manifestations

A
  1. central edema or coma from decreased plasma osmolality causing intracellular fluid shift
  2. increased expression of AQP2 causing water retention & hyponatremia (Na 125-135)
  3. increased GFR from increased water retention therefore more sodium excretion
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27
Q

symptoms associated with sodium 125-135

A

nausea, loss of appetite, fatigue, headache

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28
Q

symptoms associated with sodium < 120

A

weakness, confusion, sleepiness, vomiting

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29
Q

second messenger for insulin, GH and IGF1, prolactin & insulin receptors

A

tyrosine kinase

these receptors are dimers

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30
Q

hormone and binding protein complex formation serves what functions?

A
  • provides a reservoir poor of hormone minimizing fluctuations in concentration
  • extends the half-life of the hormone
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31
Q

effects of increased synthesis of T4 binding globulin in pregnancy

A
  • increases level of TSH secretion

- increases plasma T4 (not free!)

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32
Q

amine hormones (derivatives of tyrosine)

A

epinephrine
norepinephrine
dopamine
thyroid hormones

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33
Q

positive feedback loop of estrogen

A

During the follicular phase of the menstrual cycle, estrogen released by the ovaries acts on the anterior pituitary to rapidly release a burst of LH and FSH. FSH and LH burst causes ovulation and release of more estrogen.

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34
Q

positive feedback of oxytocin

A

Dilation of the cervix causes release of oxytocin by the posterior pituitary. Oxytocin stimulates uterine contractions, causing further dilation of the cervix.

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35
Q

hormone concentration that causes 50% of maximal response

A

sensitivity

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36
Q

methods of downregulation of receptors

A

decrease numbers

decrease affinity for hormone

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37
Q

Which subunit of G proteins binds to GDP or GTP

A

alpha
G proteins have alpha, beta and gamma subunits
binding to GTP makes it “active”

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38
Q

Hormones that utilize cAMP second messenger (12)

A
  1. ACTH
  2. LH
  3. FSH
  4. TSH
  5. ADH (V2)
  6. hCG
  7. MSH
  8. CRH
  9. calcitonin
  10. PTH
  11. Glucagon
  12. beta receptors (beta1 & beta2)
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39
Q

Hormones that use phospholipase C second messenger (7)

A
  1. GnRH
  2. TRH
  3. GHRH
  4. ANG II
  5. ADH (V1)
  6. Oxytocin
  7. alpha1 receptors
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40
Q

type of hormone receptor that uses Janus kinase downstream messengers

A

GH

activation of STAT (signal transducers and activators of transcription) causes synthesis of proteins

41
Q

Connects the hypothalamus to the pituitary gland

A

infundibulum

42
Q

hypothalamic nuclei that synthesize ADH

A

supraoptic nuclei (SON)

43
Q

hypothalamic nuclei that synthesize oxytocin

A

paraventricular (PVN)

44
Q

supply most of the blood to the anterior pituitary

A

portal blood vessels

Most of the blood supply to the anterior pituitary is venous

45
Q

hormones that have same alpha subunits but different beta subunits

A

hCG, LH, FSH, and TSH

46
Q

preprohormone for ACTH and MSH

A

POMC = preproopiomelanocortin

47
Q

anterior pituitary cells that synthesize GH

A

somatotrophs

48
Q

hormones that share 75% and 80% homology with GH, respectively

A

prolactin and human placental lactogen

49
Q

potent stimuli for GH secretion

A

starvation
hypoglycemia
Other: exercise, fever, trauma, anesthesia, stage III & IV sleep

50
Q

When is GH secretion rate the highest?

A

puberty

51
Q

Inhibit GH secretion

A

obesity, hyperglycemia, increased FA concentration, senescence, SOMATOSTATIN, GH, beta agonists, pregnancy

52
Q

somatomedin C

A

IGF-1

The growth-promoting effects of GH are mediated mostly through production of IGF-1. IGF-1 is produced in the liver.

53
Q

Effects of GH

A 
insulin resistance (hyperglycemia)
lipolysis
increased protein synthesis (increased lean muscle mass & increased organ size)
increased linear growth
cartilage metabolism -> growth
54
Q

Postpubertal signs of excess GH

A 
increased periosteal bone growth
increased organ size
increased hand and foot size
tongue enlargement
coarse facial features
insulin resistance
glucose intolerance
55
Q

treatment for GH excess

A

somatostatin analogs (octreotide)

56
Q

most common cause of excess GH

A

pituitary adenoma

57
Q

Which hormone is tonically inhibited by dopamine?

A

prolactin
Anything that interrupts the connections between the hypothalamus & the pituitary (disrupts the infundibulum) and halts the inhibitory action of dopamine causes milk production (galactorrhea).
**Prolactin is the ONLY pituitary hormone that is tonically inhibited!

58
Q

treatment for excess prolactin

A

bromocriptine (dopamine agonist)

59
Q

How does prolactin inhibit ovulation?

A

inhibition of release of GnRH -> causes infertility

60
Q

Inhibit ADH release

A

ethanol, ANP, alpha agonists

61
Q

stimulate ADH secretion

A

pain, nausea, hypoglycemia, nicotine, opiates, antineoplastic drugs

62
Q

location of V2 receptor

A

principal cells of the distal tubule and collecting ducts

63
Q

location of V1 receptor

A

vascular smooth muscle

64
Q

low ADH, large volumes of dilute urine, concentrated plasma -> due to failure of the posterior pituitary to secrete ADH

A

central diabetes insipidus

65
Q

principal cells are unresponsive to ADH due to defect in the V2 receptor; excretion of large volumes of dilute urine, increased serum osmolality; increased ADH level from increased serum osmolality

A

nephrogenic diabetes insipidus

tx: thiazide diuretic

66
Q

excess ADH secretion from an ectopic site (small cell carcinoma of the lung), dilute serum; concentrated urine

A

SIADH

Tx: demeclocycline (ADH antagonist) & water restriction

67
Q

produces milk ejection

A

oxytocin

in addition to stimulation by suckling, oxytocin is secreted in response to cervical dilation and orgasm

68
Q

responsible for I- into the follicular cell via the Na/I cotransporter

A

Na EC gradient

69
Q

oxidizes I- to I2

A

thyroid peroxidase

70
Q

blocks synthesis of thyroid hormones by inhibiting thyroid peroxidase

A

propylthiouracil (PTU)

71
Q

releases DIT and MIT from thyroglobulin

A

lysosomal enzymes

72
Q

enzyme that converts T4 to T3 in the target tissues

A

5’ iodinase
starvation inhibits this enzyme in skeletal muscle, lowering O2 consumption and BMR during times of decreased caloric intake

73
Q

hypothalmic nucleus that secretes TRH

A

PVN

74
Q

actions of TSH

A

regulate growth of the thyroid gland

secretion of thyroid hormones

75
Q

Why is the thyroid gland enlarged in Graves disease?

A

IgG to TSH receptor causes activation, producing the same response as if TSH is bound: thyroid hormone synthesis & release plus hyperplasia/hypertrophy

76
Q

mechanism of action of thyroid hormones

A

growth, bone maturation, increased activity of Na/K ATPase, increase O2 consumption, increased heat production, increased BMR, increased glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, protein synthesis, CO

77
Q

Why are beta blockers effective treatment for thyrotoxicosis?

A

thyroid hormone causes increased expression of beta receptors in heart (beta1), skeletal muscle & adipose, making them more sensitive to sympathetic stimulation

78
Q

accumulation of osmotically active mucopolysaccharides in the interstitial fluid, seen in hypothyroidism

A

myxedema

79
Q

decreased thyroid hormone synthesis due to antibodies to peroxidase; goiter present due to increased TSH from lack of negative feedback from hormones.

A

autoimmune thyroiditis

80
Q

Anti-inflammatory effects of cortisol

A
  • induces synthesis of lipocortin which inhibits phospholipase A2
  • inhibits IL-2 and T cell proliferation
  • inhibits release of histamine & serotonin from mast cells & platelets
  • note inhibition of IL-2 and T cells also serves immunosuppressive role
81
Q

How does cortisol maintain vascular responsiveness to catecholamines?

A

upregulation of alpha1 receptors (increased synthesis)

82
Q

How does cortisol inhibit bone formation?

A
  • decreases synthesis of type I collagen (main component of matrix)
  • decreases osteoblast activity
  • decreases GI calcium absorption
83
Q

What are the expected physiologic changes to aldosterone deficiency (ie adrenal insuff)?

A
  • decreased sodium absorption
  • decreased K+ and H+ secretion
  • ECF volume contraction
  • hypotension
  • hyperkalemia
  • metabolic acidosis
84
Q

What enzyme converts cortisol to cortisone?

A

11 beta HSD

85
Q

What is the difference between Cushing syndrome and Cushing diease?

A

Cushing disease is caused by hypersecretion of ACTH from a pituitary adenoma, driving the adrenal cortex to produce excess cortisol. Cushing syndrome is from chronic excess of corticosteroids.
Disease: increased ACTH
Syndrome: decreased ACTH from neg feedback

86
Q

Why does HTN occur with Cushing disease?

A

cortisol is a weak mineralocorticoid and it also upregulates alpha 1 receptors

87
Q

primary hyperaldosteronism caused by aldosterone-secreting tumor; see increased sodium, volume expansion, increased potassium secretion (metabolic alkalosis) and HTN

A

Conn syndrome

88
Q

Destruction of all layers of the adrenal cortex

A

Addison disease

89
Q

In a female fetus: causes masculinization of the external genitalia, penis-like clitoris, and scrotum-like labia. In childhood the excess androgens increase linear growth, cause precocious puberty and suppress gonadal function

A

21 beta hydroxylase deficiency
* low cortisol production results in increased ACTH and cause a trophic effect on the adrenal cortex: congenital adrenal hyperplasia

90
Q

absence of cortisol and adrenal adrogens, shunting steroid synthesis toward mineralocorticoid synthesis; Results in HTN, hypokalemia, metabolic alkalosis

A

17 alpha hydroxylase deficiency
Note: aldosterone is actually low in this syndrome because of the increase in 11-DOC and corticosterone, both of which have MR activity. HTN decreases renin release therefore aldosterone release.

91
Q

negative feedback for GnRH and LH is by what?

A

estrogen

92
Q

negative feedback for FSH is by what?

A

inhibin

93
Q

In menopause, do LH & FSH increase or decrease?

A

Increase due to loss of feedback inhibition by estrogen since estrogen is decreased.

94
Q

ethicities prone to type 1 DM

A 
African American
Latino
Native American
Asian American 
Pacific Islander
95
Q

childhood virus associated with increased incidence of IDDM

A

Rubella

96
Q

short-acting insulin dosing should be based on what?

A

carbohydrate intake of meals and snacks

97
Q

oral glucose load given and GH measured. Normal is GH < 1 ng/mL

A

test for acromegaly
IGF-1 produces negative feedback to prevent pituitary release of GH. This inhibition of GH release is mediated by release of somatostatin. Remember: glucose inhibits GH release. Hypoglycemia stimulates GH release!

98
Q

To what tissue does IGF1 bind?

A

Skeletal muscle

99
Q

Why is galactorrhea present with acromegaly?

A

GH can interact with the PRL receptor

Endocrine (11 decks)

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