Endocrine Flashcards
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
Other t3, t4 effects
Required for proper:
- CNS function
- female reproduction function
- GI function
- skin hydration
- skin sebum production
Required for development of:
- NS
- skeletal system
- muscular system
t3, t4 disorders (hyper)
Hyperthyroidism
-> Graves’ disease
Causes:
- autoimmune
- > immune system makes antibodies that mimic TSH
Symptoms
- increased temperature
- flush
- increased swearing
- nervousness
- weight loss
- exopthalmos -> bulging eyes
t3, t4 disorders (hypo)
Hypothyroidism
- decreased t3,t4
Causes:
- goiter -> iodine deficiency
- I131 poisoning
- hashimitos thyroiditis -> autoimmune
Symptoms
In adults: myxedema
- decreased BMR
- decreased temperature
- weight gain
- mental sluggishness
- dry skin
- hair loss
- constipation
- edema -> tissue swelling
In children: cretinism
- severe mental impairment
- retarded development of muscle and bone
Calcitonin
Secreted by parafollicular cells
Overall effect: decrease calcium in blood
- important in growing children
Also..
- stimulates osteoblasts
- inhibits osteoclasts
- increased calcium loss in urine
- inhibits secretion of PTH (parathyroid h)
Control of calcitonin secretion
If:
Increased levels of calcium
- detected by -> parafollicular cells
- > increase calcitonin sec.
- vice versa
Parathyroid glands secrete
Parathyroid hormone (PTH)
Effect: increased calcium in blood
PTH -
- stimulates osteoclasts
- increased calcium
(destroys bone = more ca+ in blood)
- inhibits osteoblasts
- decreased calcium loss in urine
- increased calcium concentration from GI
Control of PTH
If:
Decreased levels of calcium in blood
-detected by->
Parathyroid glands
-> increased output of PTH (parathyroid h)
** vise versa
Parathyroid hormone disorders (hyper)
*chart in notes
Hyper secretion of PTH
- > hypercalcemia
- > high levels of calcium
- increased risk of developing nephrolothiasis
(kidney stones)
- CNS depression
- bone leeching
- Osteitis Fibrosa Cystica
-> bone replaced by DFCT
Parathyroid hormone disorders
Hypo PTH
- > hypocalcemia
- decreased calcium
- increased bleeding
- > blood won’t clot as well
- tetany
- > skeletal muscles locking up
- > can lead to respiratory arrest
Adrenal glands
*pic in notes
Help the body deal with stress
Adrenal capsule -> DFCT
Adrenal cortex
- stratified cuboidal epithelial cells - produces steroid hormones
Adrenal medulla
- neurons (sympathetic) - catecholamines
Adrenal cortex zones
Outer zone -> zona glomerulosa
Middle zone -> zona fasciculata
Inner zone -> zona reticularis
Zona glomerulosa
Mineralcorticoids
-> aldosterone
Main effect of aldosterone is to increase sodium retention by the kidneys
-> = retain more water
Also stimulates a decrease in potassium retention by the kidneys
Control of secretion of aldosterone
- If decreased sodium and/or increased potassium
- detected by zona glomerulosa
- > increased aldosterone secretion
- detected by zona glomerulosa
- Stress
-> hypothalamus
-> releases CRH (corticotropin RH)
Anterior pituitary
-> increases ACTH output on to->
(adrenocorticotropin hormone)
Adrenal cortex
- increases aldosterone sec.
- increases cortisol sec.
- increased androgens
** aldosterone causes increase in blood pressure
- (most important)
Renin - angiotensin mechanism
If:
- decreases BP,
- decreased sodium,
- increased potassium
- decreased plasma osmorality
- > juntaglomerulosa apparatus - > renin
Angiotensinogen
- does nothing until stimulates by the enzyme Renin, then becomes active protein
—> turns into Angiotensinogen 2
- > stim zona glomerulosa
- > increased aldosterone
Aldosterone disorders (hypo)
Hyposecretion
- > primary adrenal insufficiency
- > Addison’s disease
Addison’s disease
- decreased aldosterone
- decreased cortisol
Symptoms
- decreased sodium
- increased potassium
- hypoglycemia
- decreased BP
- weight loss
- wasting
- bronzing -> tan appearance
Aldosterone disorders (hyper)
Hyper secretion
- > aldosteronism
- > increased sodium retention
- > leads to increased H2O retention
- > increased fluid volume
- increased BP
- edema (tissue swelling)
- > increased sodium retention
Zone fasciculata
Produces the hormone
-> glucocorticoids
-> cortisol
-> maintains increased glucose in blood
during times of stress
Control
- stress
- decreased glucose in blood
- decreased cortisol
Detected by hypothalamus
-> released CRH on ->
Anterior pituitary
-> released ACTH on ->
Zona fasciculata
-> increased cortisol
Cortisol - specific effects
- stimulates fat breakdown
-> released fatty acids into the
blood - stimulates protein breakdown
- > releases amino acids into the blood
- stimulates gluconeogenesis
-> creation of new glucose from non
carbohydrate molecules - gluconeogenesis
- > converts liberated fatty acids and amino acids into glucose
Cortisol - Other systematic effects
- stimulates vasoconstriction
- > increases BP
- enhances effects of catecholamines
- anti inflammatory agent**
Cortisol disorders (hypo)
Addison’s disease
Cortisol disorders (hyper)
(Overdose) - cushing’s disease/syndrome
Symptoms
- fluid retention
- increased BP
- edema
- weight gain (obesity)
- redistribution of adipose deposition
- “moon face”
- pot belly
- buffalo hump
- immunosuppressive
- loss or muscle and bone
Zona reticularis
Gonadocorticoids
-> androgens
Effects:
Females -> libido
Males -> no effect
Control:
- via ACTH, however, no androgen feedback
Zona reticularis disorders
Hypo: no effect
Hyper secretion:
a. ) female fetal pseudohermaphrodism
- > generic female fetus whose mother produces excess androgens during gestational period
-> children have male reproductive development in female
b.) adrenogenital syndrome
-> adult female
- produces excess cortical androgens s
-> causes Virilization
Virilization -> development of male secondary characteristics
c. ) precocious puberty
- > in young boys
- excess cortical androgens
- early puberty (ages 5-6)
