Lecture 17 Endocrine 2 Flashcards
Hypothalamus
Tropic Hormones (inhibiting and releasing hormones) part of the brain (diencephalon) controls pituitary gland
Pituitary gland
also called hypophysis
major endocrine gland; infundibulum attaches to hypothalamus
Anterior Pituitary Gland Releases
TSH, ACTH, FSH, LH, GH, prolactin
Posterior Pituitary Gland Releases
ADH, oxytocin
Pineal Gland Releases
Melatonin
Thyroid Gland releases
thyroxine (T4), triiodothronine (T3); calcitonin
parathyroid glands
4 on the back of the thyroid gland
secrete PTH (parathyroid hormone)
regulation of Calcium
Thymus
thymosin, thymopoietin
Adrenal Cortex Secretes
aldosterone, cortisol, androgens
Adrenal Medulla
epinephrine and norepinephrine
Pancreas
Pancreatic Islets
insulin, glucagon
Ovaries/Testes
Females: Estrogen, progesterone
Males: Androgens (testosterone)
Placenta
estrogen and progesterone, hCG
Secondary Endocrine Organs
GI organs, heart, kidneys, liver, skin
GI hormones ANP, erythropoietin, Vitamin D3, etc.
Posterior Pituitary
Also called Neurohypophysis
direct neural connection to hypothalamus
neurosecretory cells originate in hypothalamus
axons in infundibulum
axon terminals in posterior pituitary secrete neurohormones
ADH (vasporessin) and oxytocin
Anterior Pituitary
also called Adenohypophysis
Circulatory connection to hypothalamus via hypothalamic -hypophyseal portal system
Neurosecretory cells orignate in hypothalamus, axons in infundibulum, axon terminals in posterior pituitary secrete neurohomrones
anterior pituitary secretes trophic hormones that control other endocrine glands
Hypothalamus-Anterior Pituitary Axis
TRH
Hypothalamus releases TRH + -> TSH from anterior pituitary -> thyroid gland (target endocrine gland)
Hypothalamus-Anterior Pituitary Axis
CRH
Hypothalamus releases CRH + -> ACTH from anterior pituitary -> adrenal cortex (target endocrine gland)
Hypothalamus-Anterior Pituitary Axis
GnRH
Hypothalamus releases GnRH + -> FSH & LH from anterior pituitary -> ovaries/testes (traget endocrine gland)
Hypothalamus-Anterior Pituitary Axis
GHRN
Hypothalamus releases GHRN + -> growth hormone from anterior pituitary -> liver, bone, muscle, etc. (target endocrine gland/tissue)
Hypothalamus-Anterior Pituitary Axis
PRH
hypothalamus releases PRH + -> prolactin from anterior pituitary -> breasts (target endocrine organ)
Effects of thyroid hormones
increase basal metabolic rate
stimulate protein synthesis
developmental effects: nervous and reproductive systems
Adrenal Cortex
Mineralocorticoids
(aldosterone)
promotes Na+ retention and K+ excretion by kidneys
Adrenal Cortex
Glucocorticoids
(cortisol)
stress hormones, promotes gluconeogenesis
anti-inflammatory
Cortisol
stimulates gluconeogenesis
reduces inflammation
suppress immune response (theraputic uses)
Stress hormone
Adrenal cortex also secretes
Androgens like testosterone
Adrenal Medulla
connection to sympathetic ANS
chromaffin cells secrete epinephrine (e) and norepinephrine (NE)
Epi and NE act via adrenergic receptors on target cells
(alpha adrenergic receptors - constriction of blood vessels)
(beta adrenergic receptors - B1 increase heart rate, B2 bronchodilation)
Pancreas
endocrine portion consists of pancreatic islets (islets of langerhans)
beta cells- secrete insulin
alpha cells- secrete glucagon
insulin and glucagon are major actors in the maintenance of glucose homeostasis
exocrine - acini
endocrine - pancreatic islets
What cells are most abundant in the pancreas
beta cells
Fed (absorptive) State
high blood glucose
right after a meal nutrients are absorbed into the blood
blood glucose levels increase
beta cells secrete insulin
insulin acts to decrease blood glucose levels
Fasted (post absorptive) State
hours after a meal
blood glucose levels decreasing
alpha cells secrete glucagon
glucagon acts to increase blood glucose levels
Results of fed state
parasympathetic division insulin: glucose uptake glucose oxidation glycogen synthesis fat synthesis protein synthesis
Results of Fasted state
sympathetic division
glycogenolysis
gluconeogenesis
ketogenesis
Insulin
secreted during absorptive state when blood glucose and a.a levels are high
stimulates glucose uptake (facilitated diffusion) into most body cells
stimulates synthesis of glycogen, protein, and lipids (energy storage)
decreases plasma glucose concentration
Glucagon
secreted during postabsorptive state when blood glucose levels are low
stimulates glycogenolysis and gluconeogenesis in liver (releases glucose into blood)
stimulates lipolysis in adipose tissue (mobilizes energy stores, spares glucose)
increases plasma glucose concentration
Type one diabetes
insulin dependent (IDDM)
juvenile onset
not secreting enough insulin
Type two diabetes
non insulin dependent (NIDDM)
adult onset
receptor deficiency, receptors are down regulated
Hyperglycemia
high blood glucose levels
glycosuria
excretion of glucose in the urine
osmotic effect results in excessive urinary water loss (diuresis)
Elevated ketones and ketoacidosis
cells are “glucose starved” because of insufficient glucose uptake
-> increased fat and protein catabolism -> excess production of ketone bodies
*other effect of Diabetes is vascular degeneration