exam 2- pituitary hormones Flashcards by Madyson Flax

true endocrine gland

anterior pituitary

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contains axon terminals of hypothalamic neurons

posterior pituitary gland

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neurohypophysis:
adenohypophysis:

n: posterior
a: anterior

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anterior pituitary secrete:

FLAT PEG

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

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pituitary hormone secretes

antidiuretic hormone (ADH)/vasopressin
oxytocin

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the hypothalamic hormones are released into the _____________ in the __________

primary capillary plexus

in the median eminence

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

hypothalamic-hypophyseal portal blood vessels

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what are the hypothalamic releasing and inhibiting hormones?
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2
3
4
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(TRH) thyrotropin releasing hormone
(GnRH) gonadotropin releasing hormone
(CRH) corticotropin releasing hormone
GHIH (somatostatin): inhibitor
(GHRH) growth hormone releasing hormone
(PIH) prolactin inhibiting hormone aka DOPAMINE
(PRH) prolactin releasing hormone

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what hormones have break and release?

GHIH/GHRH, PRH/PIH

TRH, GnRH, CRH do not! just stimulates

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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

G-protein coupled receptors

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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)

growth hormone GH

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what are stimulants of GHRH and what are inhibitors?

stimulates: sleep, hypoglycemia, acute stress

inhibitors: aging, disease, glucose, chronic stress

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

lowest: during day
highest: few hours after sleep

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what is GH stimulated by?

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

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inhibitors of GH release

somatostatin (GHIH)
IGF-1
glucose
FFA

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many growth and metabolic effects of GH are produced by:

IGFs alo called somatomedins

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

IGF-1

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what is the major site of IGF-1 synthesis

liver

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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

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

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amino acid uptake and protein syn in most cells

action/result of GH secretion

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

action/result of GH

also decrease adiposity but increase lipoloysis

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

insulin resistance ;diabetogenic (too much GH)

result of GH secretion

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

chondrogenesis

linear growth

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

increasing bone turnover (osteoblasts->osteoclasts)

what can growth hormone excess cause: (tumor in pituitary or actions in anterior pituitary)

gigantism in children acromegaly in adults

treatment for a pituitary microadenoma. surgical resection of the tumor (adenomectomy) via transphenoidal approach follow by medications:

that are GHIH(somatostatin) or GH receptor antagonist

oral manifestations of GH EXCESS

-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

causes of GH dificiency: disorders: mutations:

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)

neurons in the hypothalamus synthesize and secrete

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

clinical manifestations of GH dificiency.

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

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

achondroplasia

oral manifestations of GH deficiency. disproportionate delayed growth of the

skull and facial skeletion-> small facial appearance

oral manifestations of GH deficiency. tooth formation and growth of alveloar regions of jaw= smaller anatomic structures:

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

when is solitary median maxillary central incisor happening

with defiency of GH

when are primary and secondary dentition delayed

GH def

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

paraventricular nucleus(oxytocin) and supraoptic nucleus (ADH/AVP) secrete: antiduretic hormone ADH/arginine vasopressin AVP and oxytocin

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

V1 receptors

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)

binds to V2 receptors in the late distal tubule and collecting duct -aquaporin-2 (AQP-2) proteins water reabosorption

KNOW! what are the stimuli for ADH secretion:

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

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

ADH

decreased/absent feeling of thirst, which results in reduced intake of water and can cause (increase sodium Na levels!!)

hypodipsia causes hypernatremia (increased ECF sodium levels)

neurogenic/central

decrease ADH secretion

diabetes insipidus (DI)

issue with ADH

nephrogenic/peripheral

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

syndrome of inappropriate ADH (SIADH) adh levels:

high ADH

excretion of large volumes of urine that is hypotonic and tasteless -this is present in Diabetes Insipidus

polyuria

diagnostic test for DI includes

dehydration test in controlled environment

other causes of polyuria

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

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

syndrome of inappropriate ADH (SIADH) -decrease ECF sodium -decrease nerve and muscle excitability

stimulates contraction of the uterus towards the end of gestation -causes milk ejection from breasts POSITIVE FEEDBACK

oxytocin from post pit.