2/12-15: Pituitary Hormones Flashcards

1
Q

What is a true endocrine gland?

A

Anterior pituitary gland

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2
Q

What gland contains axon terminals of hypothalamic neurons?

A

Posterior pituitary gland

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3
Q

What hormones does the pituitary gland secrete?

A

Peptide hormones

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4
Q

What hormones are in the anterior pituitary?

A
  • Growth Hormone
  • Adrenocotricotropin (ACTH)
  • Thyroid-Stimulating
    Hormone (TSH)
  • Follicle-Stimulating
    Hormone (FSH)
  • Luteinizing Hormone (LH)
  • Prolactin
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5
Q

What hormones are in the posterior pituitary?

A
  • Antidiuretic Hormone
    (ADH)/Vasopressin
  • Oxytocin
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6
Q

What do somatotrophs secrete?

A

GH

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7
Q

What do corticotrophs secrete?

A

ACTH

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8
Q

What do thyrotrophs secrete?

A

TSH

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9
Q

What do gonadotrophs secrete?

A

LH and FSH

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10
Q

What do mammotrophs secrete?

A

Prolactin

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11
Q

What do adenomas involving somatotropic cells cause?

A

gigantism if occurring in
children before closure
of the long bones’
epiphyseal plates or
acromegaly in adults,
with musculoskeletal,
neurologic, and other
medical consequences

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12
Q

What do neurons in the hypothalamus do?

A

Synthesize and secrete hypothalamic releasing and inhibiting hormones that control the endocrine cells in the anterior pituitary

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13
Q

Where are hypothalamic hormones released into?

A

Primary capillary plexus in the median eminence

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14
Q

What do hypothalamic-hypophyseal portal blood vessels carry?

A

The hypothalamic hormones to the sinuses of the anterior pituitary gland

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15
Q

What hormones stimulate release?

A

TRH (thyrotropin releasing hormone)
GnRH (gonadotropin releasing hormone)
CRH (corticotropin releasing hormone)
GHRH (growth hormone releasing hormone)
PRH (prolactin releasing hormone)

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16
Q

What hormones inhibit release?

A

GHIH (somatostatin)
PIH (prolactin inhibiting hormone - dopamine)

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17
Q

What do hypothalamic regulatory hormones bind to?

A

G-protein coupled receptors in various endocrine cells of the anterior pituitary

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18
Q

How do hypothalamic regulatory hormone stimulate or inhibit AP hormone secretions?

A

Through generation of second messenger

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19
Q

What kind of hormone is GH?

A

Peptide hormone

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20
Q

What does GH release?

A

Insulin-like growth factor-1 (IGF-1)

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20
Q

What does GH act on?

A

Target tissues and as a tropic hormone to the liver

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21
Q

What is pulsatile secretion?

A

Lower concentrations during the day with highest levels a few hours after sleep

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22
Q

What is growth hormone secretion stimulated by?

A

starvation
(protein deficiency), fasting
(hypoglycemia), stress,
exercise, and excitement

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23
Q

When is secretion of the growth hormone?

A

neonatal period but decreases in childhood. Peak levels during puberty and then they decline with age

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24
Q

What are growth and metabolic effects of GH produced by?

A

IGFs (also called somatomedins)

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25
Q

Where is IGF-1 produced?

A

Most tissues

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26
Q

What does IGF-1 act on?

A

Neighboring cells in a paracrine manner

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27
Q

What is the major site of IGF-1 synthesis?

A

The liver

28
Q

How many different IGF binding proteins are there?

A

6 (IGFBP-1 and IGFBP-3)

29
Q

Growth in nearly all tissues in the body (increased size of cells, mitosis and differentiation of bone and muscle cells) acts mainly via?

A

IGF 1
↑Organ size
↑Organ function
↑Linear growth

30
Q

What does amino acid uptake and protein synthesis in most cells do?

A

↑Lean body mass

31
Q

What does reduced glucose utilization cause?

A

decreased uptake, increased hepatic glucose production and increased insulin secretion (insulin resistance;
diabetogenic)

32
Q

What does mobilization of fatty acids from adipose tissue result in?

A

Increased FFA in blood and use of FFA for energy

33
Q

What are the main mechanisms of action of GH and IGF-1?

A

↑Organ size
↑Organ function
↑Linear growth
↑Lean body mass
↓ adiposity

34
Q

What do GH and IGF-1 stimulate?

A

Stimulate chondrogenesis
and widening of the epiphyseal plates,
followed by bone matrix deposition stimulating linear growth

35
Q

In adults, GH and IGF-1 play a role in regulating the normal physiology of bone formation by

A

increasing bone
turnover (increasing bone deposition via the activation of OSTEOBLASTS and also increasing bone resorption via activation of OSTEOCLASTS, though to a lesser extent)

36
Q

What is growth hormone excess called in children and adults?

A

Gigantism in children
Acromegaly in adults

37
Q

What are symptoms of growth hormone excess?

A

Kyphosis
Paresthesias
Hyperthidrosis and oily skin
Coarse facial features, large fleshy nose, frontal bossing, jaw malocclusion
Coronary heart disease
Diabetes mellitus

38
Q

What is treatment for pituitary microadenoma?

A

Surgical resection of the tumor (adenomectomy)
via transphenoidal approach followed by
medication (somatostatin (GHIH) receptor ligand
or GH receptor antagonist).

39
Q

What are oral manifestations of GH excess?

A
  • Thick rubbery skin, enlarged nose,
    and thick lips
  • Macrocephaly
  • Macrognathia
  • Disproportionate mandibular growth
    o Mandibular Prognathism
    o Generalized Diastemata
  • Anterior open bite and malocclusion
    (macrognathia and tooth migration)
  • Macroglossia, Dyspnea,
    Dysphagia, Dysphonia, Sialorrhea
  • Hypertrophy of the pharyngeal and
    laryngeal tissues -> sleep apnea
40
Q

What are causes of growth hormone deficiency?

A
  • hypothalamic disorders
  • mutations
  • Combined pituitary hormone deficiencies (panhypopituitarism)
  • Radiation
  • Psychosocial deprivation
41
Q

What are mutations that cause GH deficiency?

A

GHRH receptor, GH gene, GH receptor, IGF-1 receptor

42
Q

What do complete clinical manifestations depend on?

A

The time of onset and the severity of hormone deficiency

43
Q

What does complete GH deficiency manifest as?

A
  • slow linear growth rates
  • normal skeletal proportions
  • pudgy, youthful appearance (decreased lipolysis)
  • in the setting of cortisol deficiency -> hypoglycemia
44
Q

What is the most common form of dwarfism?

A

Achondrodisplasia

45
Q

What is achondrodisplasia?

A

autosomal dominant condition that results from a mutation of FGF-3 receptor in cartilage and brain

46
Q

What does a mutation in FGF-3 cause>

A

This mutation makes
the receptor overly active and it inhibits cartilage growth at growth plates so limb growth is
reduced (growth of the trunk of the body is not impacted)

47
Q

What are oral manifestations of GH deficiency?

A

Disproportionate delayed growth of the skull & facial skeleton -> small facial appearance

48
Q

What happens to tooth formation in a GH deficiency?

A

Tooth formation & growth of the alveolar regions of the jaws are
abnormal and may be disproportionately smaller than adjacent
anatomic structures, I
- tooth crowding and malocclusion
- a high tendency for plaque accumulation
- difficulty maintaining good oral hygiene
- prone to gingivitis and periodontal disease

49
Q

What is a common oral condition in someone who has a GH deficiency?

A

Solitary median maxillary central incisor

50
Q

What is management of solitary median maxillary central incisor?

A

correct dental & skeletal malocclusions

51
Q

What does the posterior pituitary/neurohypophysis secrete?

A

(1) Antidiuretic Hormone
(ADH)/Arginine Vasopressin
(AVP)
(2) Oxytocin

52
Q

What is the mechanism of action of ADH/AVP in blood vessels?

A

Contraction of vascular
smooth muscle via V1
receptors

53
Q

What does ADH/AVP bind to in renal tubules?

A

Binds to V2 receptors in
the late distal tubule and
collecting duct

54
Q

What is the mechanism of action of ADH/AVP in renal tubules?

A

Aquaporin-2 (AQP-2)
proteins are then
inserted into the apical
membrane of tubular
epithelial cells, allowing
for water reabsorption
(along with AQP-3 and
AQP-4 on the basolateral membrane)

55
Q

What are stimuli that would lead to the body secreting ADH?

A

Decreased Blood Volume (Isotonic)
Increased Osmolarity (Isovolemic)
Decreased Blood Pressure

56
Q

What do normal changes in osmolarity sitmulate?

A

ADH secretion by the posterior pituitary

57
Q

What is hypodipsia?

A

Decreased or absent feeling of thirst, which results in
reduced intake of water

58
Q

What can hypodipsia cause?

A

Hypernatremia

59
Q

What is hypodipsia associated with?

A

A common problem in elderly people, but is also
associated with lesions in the hypothalamus (thirst
center), head trauma, occult hydrocephalus or
subarachnoid hemorrhage

60
Q

What are ADH imbalances?

A
  • Diabetes Insipidus (DI)
    – Neurogenic/Central
    – Nephrogenic/Peripheral
  • Syndrome of Inappropriate ADH (SIADH)
61
Q

What is diabetes inspidus due to?

A

insufficient production (Neurogenic/Central) or lack
of kidney response (Nephrogenic/Peripheral) to ADH

62
Q

What is diabetes insipidus present with?

A

Polyuria: Excretion of a large volumes of
urine that is hypotonic and tasteless (insipid)

63
Q

What is a diagnostic test of diabetes inspidus?

A

dehydration test in a controlled
environment

64
Q

What are other causes of polyuria?

A
  1. Primary ingestion of excess fluid: Primary Polydispia
  2. Increased metabolism of ADH (ex. pregnancy)
65
Q

What is syndrome of inappropriate ADH (SIADH)?

A

Increased and uncontrolled secretion of ADH that causes
volume expansion and hyponatremia

66
Q

What can syndrome of inappropriate ADH (SIADH) result from?

A

surgery, pain, stress, temperature changes,
tumor, TB, Pneumonia, positive pressure breathing,
Hydrocephalus, Meningitis, HIV, etc

67
Q

What does oxytocin stimulate?

A

Contraction of the uterus towards the end of gestation

68
Q

What does oxytocin cause?

A

Milk ejection from the breasts in lactation