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exam 2- pituitary hormones Flashcards

1
Q

true endocrine gland

A

anterior pituitary

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2
Q

contains axon terminals of hypothalamic neurons

A

posterior pituitary gland

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3
Q

neurohypophysis:
adenohypophysis:

A

n: posterior
a: anterior

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4
Q

anterior pituitary secrete:

A

FLAT PEG

folllicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
adrenocotricotropin (ACTH)
thyroid stimulating hormone (TSH)
prolactin
Growth hormone

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5
Q

pituitary hormone secretes

A

antidiuretic hormone (ADH)/vasopressin
oxytocin

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6
Q

the hypothalamic hormones are released into the _____________ in the __________

A

primary capillary plexus

in the median eminence

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7
Q

what carry the hypothalamic hormones to the SINUSes of the anterior pituitary gland

A

hypothalamic-hypophyseal portal blood vessels

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8
Q

what are the hypothalamic releasing and inhibiting hormones?
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7

A
  1. (TRH) thyrotropin releasing hormone
  2. (GnRH) gonadotropin releasing hormone
  3. (CRH) corticotropin releasing hormone
  4. GHIH (somatostatin): inhibitor
  5. (GHRH) growth hormone releasing hormone
  6. (PIH) prolactin inhibiting hormone aka DOPAMINE
  7. (PRH) prolactin releasing hormone
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9
Q

what hormones have break and release?

A

GHIH/GHRH, PRH/PIH

TRH, GnRH, CRH do not! just stimulates

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10
Q

the hypothalamus regulatory hormones bind to ___________ in the various endocrine cells of the anterior pituitary. then, through generation of second messengers (ex. cAMP, IP3, DAG) they either stimulate or inhibit AP hormone secretion

A

G-protein coupled receptors

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11
Q

a peptide hormone, acts directly on target tissues and as a tropic hormone to the liver, which releases IGF-1 (insulin-like growth factor -1)

A

growth hormone GH

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12
Q

what are stimulants of GHRH and what are inhibitors?

A

stimulates: sleep, hypoglycemia, acute stress

inhibitors: aging, disease, glucose, chronic stress

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13
Q

pusatile secretion; when are lower concen of GH and highest levels

A

lowest: during day
highest: few hours after sleep

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14
Q

what is GH stimulated by?

A

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

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15
Q

inhibitors of GH release

A

somatostatin (GHIH)
IGF-1
glucose
FFA

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16
Q

many growth and metabolic effects of GH are produced by:

A

IGFs alo called somatomedins

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17
Q

this is produced in most tissues and acts on neighboring cells in paracrine manner

A

IGF-1

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18
Q

what is the major site of IGF-1 synthesis

A

liver

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19
Q

IGF-1 accounts for nearly all growth of tissues in the body (increased cell size, mitosis and differentiation of bone and muscle cells etc) by INHIBITION

A

increase organ size
increase organ function
increase linear growth
increase lean body mass

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20
Q

amino acid uptake and protein syn in most cells

A

action/result of GH secretion

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21
Q

mobilization of Fatty Acids from adipose tissue (lipolysis) resulting in increased FFA in blood and use of FFA for energy so

A

action/result of GH

also decrease adiposity but increase lipoloysis

22
Q

reduced glucose utilization with IGF-1 =decreased uptake, increased hepatic glucose production and increased insulin secretion

A

insulin resistance ;diabetogenic (too much GH)

result of GH secretion

23
Q

before fusion of the epiphyseal plates, GH and IGF-1 stimulate ___________
and widening of the epiphyseal plates, followed by bone matrix deposition stimulating ________

A

chondrogenesis

linear growth

24
Q

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

A

increasing bone turnover (osteoblasts->osteoclasts)

25
Q

what can growth hormone excess cause:

(tumor in pituitary or actions in anterior pituitary)

A

gigantism in children
acromegaly in adults

26
Q

treatment for a pituitary microadenoma.

surgical resection of the tumor (adenomectomy) via transphenoidal approach follow by medications:

A

that are GHIH(somatostatin) or GH receptor antagonist

27
Q

oral manifestations of GH EXCESS

A

-thick rubbery skin, enlarged nose, and thick lips
-macrocephaly
-macrognathia
-disproportionate mandibular growth (mandibular prognathism and generalized diastemata)
-anterior open bite and malocclusion
-macroglossia, dyspnea, dysphagia, dysphonia, sialorrhea
-enlarged pharyngeal and laryngeal tissues-> sleep apnea

28
Q

causes of GH dificiency:
disorders:
mutations:

A
  1. hypothalamic disorders
  2. mutations in GHIH, GH gene, GH receptor, IGF-1 receptor
  3. radiation
  4. psychosocial deprivation (increases GHIH)
  5. combined pituitary hormone deficiencies (down in ath and gh)
29
Q

neurons in the hypothalamus synthesize and secrete

A

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

30
Q

clinical manifestations of GH dificiency.

A

-slow linear growth rate
-normal skeletal proportions
-pudgy, youthful appearance
-in the setting of cortisol deficiency-> hypoglycemia

31
Q

most common form of dwarfism
-autosomal
-mutation makes receptor overly active and inhibits cartilage growth at growth plates so limb growth is reduced NOT trunk

A

achondroplasia

32
Q

oral manifestations of GH deficiency.

disproportionate delayed growth of the

A

skull and facial skeletion-> small facial appearance

33
Q

oral manifestations of GH deficiency.

tooth formation and growth of alveloar regions of jaw= smaller anatomic structures:

A
  1. tooth crowding and malocclusion
  2. high tendency for plaque
  3. difficultly maintaining good oral hygiene
  4. prone to gingivitis and periodontal disease
34
Q

when is solitary median maxillary central incisor happening

A

with defiency of GH

35
Q

when are primary and secondary dentition delayed

A

GH def

36
Q

posterior pituitary/neurohypophysis contains unmyelinated axons of neurons who cell bodies are in hypothalamus:

and these secrete:

A

paraventricular nucleus(oxytocin) and supraoptic nucleus (ADH/AVP)

secrete:
antiduretic hormone ADH/arginine vasopressin AVP
and
oxytocin

37
Q

AVP action on blood vessels:
constriction of vascular smooth muscle(blood vessels) via:

A

V1 receptors

38
Q

ADH action on renal tubules:
binds to _____ receptors in the _____________
________proteins are then inserted into the apical membrane of tubular epithelial cells, allowing for ____________________ (along with AQP-3 and AQP-4 on basolateral membrane)

A

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

-aquaporin-2 (AQP-2) proteins

water reabosorption

39
Q

KNOW!

what are the stimuli for ADH secretion:

A
  1. decreased Blood volume (isotonic)
  2. increased osmolarity (isovolemic)
  3. decreased blood pressure
40
Q

normal changes in osmolarity stimulate ____- secretion by the posterior pituitary

A

ADH

41
Q

decreased/absent feeling of thirst, which results in reduced intake of water and can cause

(increase sodium Na levels!!)

A

hypodipsia

causes hypernatremia (increased ECF sodium levels)

42
Q

neurogenic/central

A

decrease ADH secretion

43
Q

diabetes insipidus (DI)

A

issue with ADH

44
Q

nephrogenic/peripheral

A

INCREASE ADH
lack of kidney response
-adh is made but kidney doesnt know how to respond
(kidney problem)

45
Q

syndrome of inappropriate ADH (SIADH) adh levels:

A

high ADH

46
Q

excretion of large volumes of urine that is hypotonic and tasteless

-this is present in Diabetes Insipidus

A

polyuria

47
Q

diagnostic test for DI includes

A

dehydration test in controlled environment

48
Q

other causes of polyuria

A
  1. primary ingestion of excess fluid: primary polydispia
  2. increased metabolism of ADH (ex. pregnancy)
49
Q

increased and uncontrolled secretion of ADH that causes volume expansion and hyponatremia
-can result from surgery, pain, stress etc

A

syndrome of inappropriate ADH (SIADH)

-decrease ECF sodium
-decrease nerve and muscle excitability

50
Q

stimulates contraction of the uterus towards the end of gestation

-causes milk ejection from breasts

POSITIVE FEEDBACK

A

oxytocin from post pit.

phys (16 decks)

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