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Endocrinology and Reproductive Systems > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

How do the response and signal compare in a negative feedback loop?

A

the response opposes the stimulus (decreases a variable when it gets too high; increases a variable when it gets too low)

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2
Q

How do the response and signal compare in a positive feedback loop?

A

The response amplifies the signal/stimulus (ex. cervical stretch, oxytocin and uterine contractions= parturition)

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3
Q

How does a positive feedback loop get shut off?

A

an outside factor is required (ex. delivery of baby in parturition stops the signal)

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4
Q

What is the purpose of feedforward regulation?

A

anticipatory/proactive; does not require a deviation signal

Accelerates response and minimizes fluctuation (circadian rhythm, salivation)

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5
Q

Which of the control mechanisms is a homeostatic reflex?

A

negative feedback

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6
Q

Which control mechanism is explosive in nature?

A

positive feedback

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7
Q

What is the mode of transmission of the endocrine system?

A

circulation

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8
Q

How do hormones affect functions in their target cells?

A

regulate, NOT initiate

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9
Q

What are the two post pit neuroendocrine hormones?

A

ADH and oxytocin

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10
Q

What are the 6 anterior pit trophic hormones?

A

FSH, LH, ACTH, TSH, GH, PRL

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11
Q

What are the 6 hypophysiotrophic hormones of the hypothalamus?

A

GnRH, GHRH, CRH, TRH, DA, SS

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12
Q

What are the two types of tyrosine derivatives?

A
  • Catecholamines (DA, Norepi, Epi in CNS/adrenal medulla) — exocytosis transport
  • Iodothryonines — diffusion transport
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13
Q

What are four places that steroid hormones are synthesized? What are they synthesized from?

A
  • cholesterol
  • adrenal cortex (aldosterone, cortisol, androstenedione)
  • gonads (testosterone, estradiol, progesterone)
  • placenta (progesterone, estrogens)
  • kidney (calcitriol)
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14
Q

How do steroid hormones behave in the body?

A
  • lipophilic (diffuse easily in and out)
  • bound to proteins in blood
  • intracellular receptors
  • can be administered orally
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15
Q

What is another name for somatostatin?

A

GHIH - GH inhibiting hormone

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16
Q

What are 3 glycoproteins and how do they differ?

A

LH, FSH, TSH - alpha subunits the same; beta subunits differ

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17
Q

How do peptide hormones behave in the body?

A
  • circulate unbound (except GH and IGF1)
  • polar
  • extracellular receptors
  • syn as preprohormones/prohormones
  • can be stored in cells as membrane bound granules
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18
Q

Which two peptide hormones CANNOT circulate unbound?

A

GH and IGF1

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19
Q

Which hormone type cannot be administered orally?

A

Peptide hormones

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20
Q

What is the rate limiting enzyme in steroid hormone synthesis from cholesterol?

A

side-chain cleavage enzyme (P450scc) which converts cholesterol to pregnenolone

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21
Q

What are the six major types of steroid hormones?

A

Vit D, progestin, mineralocorticoid, glucocorticoid, androgen, estrogen

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22
Q

What are two special things about the free portion of hormones in circulation? (Catecholamines, peptides, proteins)

A
  • biologically active

- controlled by homeostatic negative feedback control mechanism

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23
Q

Where are hormone binding proteins synthesized? Purpose?

A
  • liver

- hormone bound to BP’s is not available for metabolism, BUT serve as reservoir of readily-available hormone

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24
Q

What happens to free hormone levels right after an increased in BP as in pregnancy? Later on?

A
  • increased BP = increased bound hormone = decreased free hormone
  • negative feedback loop regulation kicks in and results in an increase in total hormone and no change in free hormone
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25
Q

How do protein and peptide hormones transmit their signal inside a cell?

A
  • hormones bind to extracellular receptor which induces a conformational change = signal
  • change activates one or more intracellular 2nd messengers that bind effector proteins which result in hormone’s action = SIGNAL TRANSDUCTION PATHWAY
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26
Q

What are 3 types of intracellular messengers?

A
  • cyclic nucleotides: bind effector kinases
  • ions: direct or indirect (calbindin) regulation of effector proteins
  • Lipids: DAG activates protein kinase C; IP3 increases intracellular calcium; BOTH from phospholipase C activation
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27
Q

What are four protein hormone receptor types?

A
  • receptors that gate channels
  • receptors that activate enzymes (kinases and phosphatases)
  • GPCR
  • integrin receptors
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28
Q

What are two types of tyrosine kinases activated by protein hormone receptors?

A
  • growth factor subtype: receptor is tyrosine kinase

- cytokine subtype: receptor associated with JAK kinase

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29
Q

What are three G protein subtypes?

A
  • Gs = stimulates adenylyl cyclase
  • Gi = inhibits adenylyl cyclase
  • Gq = activates phospholipase c
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30
Q

Why do steroid hormones act more slowly than protein hormones?

A

action requires genomic transcription and subsequent translational processes

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31
Q

What are steroid receptors? What superfamily do they belong to?

A
  • intracellular receptors acting as transcription factors

- nuclear receptor superfamily

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32
Q

What is the action of the hormone receptor complex?

A
  • binds to specific DNA sequence = hormone response element
  • binding alters rate of gene transcription
  • can activate/repress transcription by recruiting co-activators or co-repressors
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33
Q

What is a major example of a negative feedback loop?

A
  • Hypo-pit-target gland axis
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34
Q

How do changes in receptor sensitivity and response differ?

A
  • response = change in receptor number

- sensitivity = change in receptor affinity; less common

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35
Q

what are 3 endogenous hormone release patterns?

A
  • diurnal
  • ultradian: pulsatile release patterns prevent down-reg of receptors
  • responses to specific stimuli
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36
Q

How does stress affect hormone levels?

A

Increases level of hormone/feedback set point but does not affect the diurnal/ultradian/circadian patterns of release

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37
Q

Where do axons and terminals of posterior pituitary originate?

A

hypothalamus via pituitary stalk - from oxy/ADH neurons of supraoptic and paraventricular nuclei via hypothalamohypophyseal tract

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38
Q

Post pit - where do hormones come from? blood supply? hormones are released where?

A
  • hypothalamic neurons (post pit acts as storage site = Herring bodies)
  • direct arterial blood supply
  • releases into systemic circulation (detectable in peripheral blood)
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39
Q

What are the 3 families of hormones associated with the ant pit?

A
  • glycoprotein family (TSH, FSH, LG)
  • GH/prolactin family
  • Proopiomelanocortin (POMC) family
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40
Q

What is POMC?

A

prohormone from which ACTH is cleaved

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41
Q

What controls the anterior pituitary?

A

hormone release controlled by hypothalamic releasing and inhibiting hormones that access ant pit via stalk portal capillaries (diffusion from secondary capillary plexus) – hypo hormones not detectable in peripheral blood

42
Q

How does GnRH affect ant pit hormones?

A

stimulates release of LH and FSH

43
Q

How does GHIH affect ant pit hormones?

A

inhibits release of GH and TSH

44
Q

How does TRH affect ant pit hormones?

A

stimulates release of TSH and PRL

45
Q

How does dopamine affect ant pit hormones?

A

inhibits release of PRL

46
Q

How does corticotropin releasing hormone affect ant pit hormones?

A

stimulates release of ACTH (from POMC family)

47
Q

If hypothalamic control of ant pit is lost, what happens to hormone levels?

A

LH, FSH, TSH, GH, and ACTH decrease; PRL will increase (no longer inhibited by dopamine)

48
Q

How does long-loop negative feedback control of HPA work?

A

Hormones produced by endocrine gland inhibit hypothalamic and ant pit hormone function

49
Q

What is Kallmann’s syndrome and what is it often associated with?

A
  • Lack of GnRH neuron migration out of olfactory placodeand no GnRH
  • deficiency of LH and FSH synthesis and secretion results in hypogonadism
  • anosmia
50
Q

Pathophysiology of Sheehan’s syndrome?

A

portal caps operate at low pressure and thus are at risk for clotting/infarction under conditions of low BP - shock, hemorrhage

51
Q

How do prolactin levels change in Sheehan’s?

A
  • initially increase due to lack of dopamine regulation

- then levels drop when ant pit cells die

52
Q

Tumors of pituitary commonly cause what type of visual deficit?

A

bitemporal hemi-anopsia

53
Q

What type of injury can completely sever the pituitary stalk?

A

whiplash (ADH affected = diabetes insipidus; drink and pee a lot)

54
Q

What is the importance of thyroid hormone in growth control?

A

essential for normal GH secretion and GH receptors; permissive to GH actions; important for CNS development

55
Q

What is the importance of gonadal estrogen in growth of both sexes?

A
  • pubertal growth spurt

- epiphyseal closure

56
Q

What is insulin’s role in growth?

A

enhances growth and is required for normal growth

57
Q

What is cortisol’s role in growth?

A

increases GH release and is required for normal growth

58
Q

What hormones control fetal growth?

A

insulin, other unknown factors

59
Q

What hormones control juvenile growth?

A

GH, thyroid hormones, insulin, cortisol

60
Q

What hormones control adolescent growth?

A

GH, sex steroids, thyroid hormones, insulin, cortisol

61
Q

Why do diabetic mothers have larger infants?

A

Increased blood glucose increases insulin levels and insulin enhances growth/controls fetal growth

62
Q

During what 2 periods are growth rates fastest?

A
  • in utero

- neonatal period (1st 2 years)

63
Q

Plasma level increases in what 3 hormones cause the pubertal growth spurt?

A
  • GH
  • IGF1
  • estrogens aromatized into androgens in boys and girls
64
Q

When does rate of growth plateau?

A

high estrogen levels cause epiphyseal closure inat the end of puberty and growth plateaus in adulthood

65
Q

What is the most abundant hormone in the ant pit?

A

GH, species specific, plasma concentrations vary throughout day

66
Q

What circulating hormone can be used as a good indicator of growth rate?

A

circulating IGF levels in single samples

67
Q

What is the GH receptor type?

A

tyrosine kinase receptor cytokine subtype (JAK-kinase-Stat TF)

68
Q

What are the 4 direct actions of GH?

A
  • generally oppose insulin

- increased lipolysis, gluconeogenesis, ketogenesis, and protein

69
Q

What are the indirect actions of GH and how are they mediated?

A
  • stimulate growth and protein synthesis in bone and splanchnic organs
  • IGF1 (somatomedin C)
70
Q

How does IGF1 regulate GH levels?

A

negative feedback control on hypothalamus and anterior pituitary

71
Q

What five factors cause a responsive increase in GH levels?

A
  • intense exercise
  • hypoglycemia
  • stress
  • amino acids (Arginine)
  • sleep rhythms
72
Q

What type of dwarf results from decreased GH only?

A

sexual ateliotic dwarf

73
Q

What type of dwarf results from a decrease in all anterior pituitary hormones?

A

panhypopituitary dwarf

74
Q

What type of dwarf results from a defect in expression of GH receptors? GH and IGF1 levels?

A
  • Laron dwarf

- normal or high GH and LOW IGF-1

75
Q

What type of dwarf results from a defect in IGF response to pubertal increase in GH? GH and IGF1 levels?

A
  • African pygmy

- normal GH and IGF1

76
Q

What are the symptoms associated with decreasing GH with age?

A
  • increased proportion of body fat
  • decreased proportion of muscle
  • muscle weakness and early exhaustion
77
Q

What are 3 tests used for GH secretion?

A
  • arginine
  • dopamine
  • insulin-induced hypoglycemia
78
Q

How does excess GH affect blood glucose?

A

high GH –> increased blood glucose

  • excess GH is diabetogenic
79
Q

How does excess GH affect plasma IGF1 levels?

A

HIGH

80
Q

Which two hormones bind to their hormone response element’s on DNA to initiate transcription?

A

Vit D3 and Thyroid (gene transcription is repressed when hormones aren’t bound)

81
Q

What 3 hormones are secreted by the thyroid?

A
  • calcitonin
  • T4 thyroxine
  • T3 triiodothyronine
82
Q

Two Tx options for GH deficiency syndrome in children caused by hypothalamic defect?

A
  • recomb hGH = somatropin, somatrem

- synthetic GHRH = sermorelin acetate (less effective than somatropin)

83
Q

AE’s of using synthetic GHRH sermorelin acetate to tx GH deficiency syndrome in children caused by hypothalamic defect?

A

headache, dizziness, scoliosis due to rapid growth

84
Q

Why must AR Laron syndrome be treated differently than typical GH deficiency?

A

GH resistant dwarfism

85
Q

Tx for Laron syndrome? AE? Contra?

A
  • mecasermin = IGF1
  • intracranial hypertension
  • cancer
86
Q

What is the cause and Tx of GH deficiency syndrome in adults?

A
  • defects in pit function (pit adenoma)

- somatropin (not sermorelin bc it is GHRH and pit isn’t working and can’t make GH anyway)

87
Q

AE’s and contra in somatropin Tx in adults?

A
  • arthralgia, myalgia, thirst, hunger headache

- cancer

88
Q

Three Tx options for GH excess?

A
  • pit surgery
  • octreotide/pasierotide = syn somatostatin analog
  • pegvisomant = GH analog that binds receptor BUT w/ no dimerization/signaling (doesn’t decrease GH levels)
89
Q

AE’s of synthetic somatostatins octreotide and pasireotide?

A
  • GI, gallstones

- liver tox, ACTH suppression

90
Q

AE of GH analog pegvisomant?

A

reversible abnml liver f(x) test

91
Q

Function and regulation of prolactin?

A
  • stimulates breast development/lactation; inhibits gonadotropin secretion
  • increased by TRH/suckling, decreased by dopamine
  • no feedback control
92
Q

Three causes of hyperprolactinemia?

A
  • pit/hypo disorder (tumor)
  • renal failure (dec PRL clearance)
  • chest trauma (autonomic response)
93
Q

Symptoms of hyperprolactinemia in men? Women?

A
  • infertility, enlarged breasts, libido loss, impotence

- infertility, amenorrhea, lactation in non-pregos

94
Q

What is an example of a DA receptor agonist used to Tx hyperprolactinemia? AE’s? Contra?

A
  • bromocriptine (Parkinson’s)
  • NV, dizziness, insomnia
  • uncontrolled hypertension
95
Q

What are the 3 gonadotropins?

A

FSH, LH, placental chorionic gonadotropin

96
Q

What drug can be used to treat steroid hormone excess conditions?

A

ketoconazole - inhibits steroid biosynthesis

97
Q

FSH functions in men and women?

A
  • stimulates spermatogenesis

- stimulates follicle development

98
Q

LH functions in men and women?

A
  • increases testosterone secretion

- stimulate mat. of follicle to corpus luteum; required for ovulation

99
Q

Menotropins vs. urofollitropins?

A
  • FSH and LH in urine from post-men women

- purified FSH

100
Q

Two AE’s of tx of decreased gonadotropin production?

A
  • multiple births

- OHSS = ovarian hyperstimulation syndrome – fluid in peritoneal cavity, pericardium, thorax

101
Q

Population and caused of increased gonadotropin production?

A
  • mostly males

- constitutively active AD mutation of LH receptor

Endocrinology and Reproductive Systems (1 decks)

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