Endocrine Flashcards
(46 cards)
Endocrine glands
Pile o cells
Exception to exocrine glands
- > goblet cells - unicellular exocrine gland
Mechanisms of Hormonal Action
-see pic
Binding of hormone causes G protein to shift and activate inactive enzyme
Activates ATP -> AMP
Hypothalamus
The “master master gland”
- Controls the anterior pituitary via the release of Releasing Hormones
- Controls posterior pituitary gland via direct neural stimulation
Pituitary Gland
The “master gland” - anterior pituitary controls other endocrine glands via the secretion of Tropic Hormones
Tropic hormones -> secreted by anterior pituitary gland and controls other glands
Hypothalamus & Pituitary structure
Infundibulum
Anterior pituitary
- epithelial cells - aka -> adenohypophysis
Posterior pituitary
- neurons - aka -> neurohypophysis
Pars intermedia
Hypophyseal Portal System
The hypothalamus communicates with the anterior pituitary gland via a vascular* connection called the hypophyseal portal system
Artery -> primary plexus (in hypo)->
veins -> secondary plexus (in ant p) ->
veins
Plexus -> capillaries
Hypothalamic Hypophyseal Tract
The hypothalamus communicates with the posterior pituitary gland via the Hypothalamic Hypophyseal Tract -> neural connection*
Cell bodies (in hypo) -> AP’s -> post p -> axon terminals (where secretion takes place)
Synaptic vesicles -> secrete
Posterior Pituitary hormones
- Synthesized in the hypothalamus
- Stored in the posterior pituitary
- Released from the posterior pituitary
a.) oxytocin
- comes from paraventricular cells in the
hypothalamus
b.) ADH
- antidiuretic hormone
- comes from cells called supraoptic
cells in the hypothalamus
Hypothalamic inhibiting hormones
Hypothalamic releasing hormones
Anterior pituitary hormones
Hypothalamic inhibiting hormones:
- GHIH -> growth inhibiting hormone
- PIH -> prolactin inhibiting hormone
Hypothalamic releasing hormones:
- GNRH (gonadotropin releasing hormone)
- TRH (thyroptropin releasing hormone)
- CRH (corticotropin releasing hormone)
- GHRH (growth hormone releasing hormone
- PRH (prolactin releasing hormone)
Anterior pituitary hormones:
GNRH -> FSH* LH*
TRH -> TSH* (thyroid stim hormone)
CRH -> ACTH* (adrenocorticotropin hormone)
GHRH -> GH (growth hormone)
PRH -> PRL (prolactin)
- ———> tropic hormone**
Growth hormone
Growth hormone -> somatotropin
Direct effects:
GH -> tissue effects
Indirect effects
GH -> skeletal muscle ->
liver -> somatomedins
bone -> -tissue effects
adipose ->
Growth hormone - direct effects
- increase in cellular lipolysis (fat breakdown)
- increase in lipoprotein transport in blood
- increase in lipid burning (muscle + liver)
- increases glycogen breakdown
- > glucose into blood
- > increased glucose blood concentration
- diabetogenic effect - decrease glucose uptake + burning
GH -> adipose breakdown
- > increased lipids in blood - > increased fat burning
Growth Hormone - indirect effects
Anabolic *
Somatomedins
- increased amino acid uptake
- sulfur uptake
->
-> both required for production of
proteins -> increased protein
production
Those proteins:
- increased cartilage production
- increased bone growth production
- increased skeletal muscle production
Control of Growth Hormone secretion
If there is:
- decreased GH
- decreased glucose
- decreased lipids
- increased amino acids
-detected by-> hypothalamus
Hypo -> increased release of GHRH on
anterior pituitary
anterior pituitary -> increased GH release
————————————————
If there is:
- increased GH
- increased somatomedins
- increased lipids
- increased glucose-detected by-> hypothalamus
Hypo -> GHIH (GH inhibiting hormone->
Anterior pituitary
-> decreased secretion of GH
Disorders of GH secretion
Hypersecretion
In children: giantism
- grow tall (> 7 feet)
In adulthood: acromegaly
Symptoms of acromegaly
- progressive distortion of face features
- overgrowth of:
- frontal
- nasal
- tongue expands
- mandible + maxilla
- heart -> decreased lifespan
- overgrowth of:
—————————
Hypo secretion
In children: pituitary dwarfism (< 4ft)
Posterior pituitary hormones
Oxytocin
- child birth
- lactation
ADH
- increased H2O retention by kidneys
(decreased urine output)
Control of secretion of ADH
If:
Increased solutes in blood plasma
(Dehydration)
-detected by ->
Hypothalamic Osmoreceptors (thirst*)
-impulses->
Posterior pituitary
-> increased output of ADH
————————
If: drink a lot of water
- decreased solutes in blood plasma
-detected by hypothalamus ->
-> decreased ADH output
(increased urination)
ADH and alcohol
Alcohol
—> decreases ADH output
—> this increases urination
Urination -> dilute urine
Secondary effect of ADH
- vasoconstriction (makes BP go up)
- vasopressin
Shock:
if you have a signification blood loss (> 10%)
this means decreased blood volume which
equals decreased blood pressure
-detected by->
Hypothalamus - stimulates thirst - big blast of ADH
Disorders of ADH secretion (hyper)
Hypersecretion of ADH:
-> SI ADH
(syndrome if inappropriate ADH)
Causes:
- hypothalamic damage
- cancer -> tumor cells secrete ADH
Symptoms:
- increased H2O retention
- > increased blood pressure
- > edema - hyponotremia
- > H2O intoxication
Disorders of ADH secretion (Hypo)
Hyposecretion
-> Diabetes Insipidus
- no ADH production
Causes
- hypothalamic damage
- genetic
Symptoms
- excess production of dilute urine
(dilute-> mostly water little solutes)
-> causes increase in concentration of
solutes —> causes thirst
Thyroid Gland
- pic in notes
Lumen
-> contains Thyroglobulin Colloid
Thyroglobulin Colloid -> large glycoprotein that stores Thyroxine (t3, t4)
Follicle cells (simple cuboidal)
Parafollicular cells (C) -> calcitonin
The synthesis, storage, and release of t3 and t4
- pic in notes
TSH, all amino acids (especially Tyrosine), and Iodine’s
-> enter follicle from capillary
Follicle cells synthesize colloid, release it into follicle via exocytosis
Colloid -> stored
TSH
-> enters follicle from capillary
TSH also stimulates follicle cells to absorb colloid, spilt off t3, t4 + release t3, t4 into the blood
t3, t4 in blood attach to Thyroid Binding Globulin
—> blood to tissues
Control of secretion if t3, t4
If: t3, t4 decreases
-detected by-> hypothalamus
Hypo -> releases TRH (Thyrotropin releasing hormone) on to ->
Anterior P -> increased TSH (thyroid stimulating hormone on Thyroid -> increased t3, t4 secretion
*** vice versa
(increased t3, t4 -> decreased TRH output)
t3, t4 effects
Stimulates an increase in oxidative respiration by cells
- controls BMR (basal metabolic rate)
** see formula in notes **
- increased oxygen consumption
- increased glucose consumption
- increased CO2 production
- increased heat production
- > calorigenic effect
- increased temp
- increased heat
- > calorigenic effect
- increased ATP production