Download Endocrine System 2 - Napa Valley College

Biology 219 – Human Physiology
Clemens
Endocrine System 2
Text: Ch. 7
A. Summary of Endocrine Glands and Hormones
1a. Primary endocrine organs
Hormones
hypothalamus
trophic hormones (releasing and inhibiting hormones)
pituitary gland ( = hypophysis)
anterior pituitary
TSH, ACTH, FSH, LH, GH, prolactin
posterior pituitary
ADH, oxytocin
pineal gland
melatonin
thyroid gland
thyroxine (T4), triiodothyronine (T3); calcitonin
parathyroid gland
PTH
thymus
thymosin, thymopoietin
adrenal gland
adrenal cortex
aldosterone, cortisol, androgens
adrenal medulla
epinephrine & NE
1b. Primary endocrine glands in other organs
pancreas (pancreatic islets)
insulin, glucagon
ovaries / testes
♀: estrogen & progesterone / ♂: androgens (testosterone)
placenta
estrogen & progesterone, hCG
2. Secondary endocrine organs
GI organs, heart, kidneys, liver, skin GI hormones, ANP, erythropoietin, vitamin D3, etc.
B. Hypothalamus and Pituitary Gland
hypothalamus - part of the brain (diencephalon), controls the pituitary gland
pituitary gland - major endocrine gland; infundibulum attaches to hypothalamus
1. Posterior pituitary (neurohypophysis)
- direct neural connection to hypothalamus
- neurosecretory cells originate in hypothalamus, axons in infundibulum,
axon terminals in posterior pituitary secrete neurohormones
- ADH (vasopressin) and oxytocin
2. Anterior pituitary (adenohypophysis)
- circulatory connection to hypothalamus via hypothalamic-hypophyseal portal system
- neurosecretory cells in the hypothalamus secrete releasing hormones into portal system
which control anterior pituitary secretion
- anterior pituitary secretes trophic hormones that control other endocrine glands and tissues
Hypothalamus-Anterior Pituitary Axis
hypothalamus
TRH
CRH
GnRH
GHRH
somatostatin
PRH
dopamine
+
+
+
+
–
+
–
→
→
→
→
→
anterior pituitary
TSH
ACTH
FSH & LH
growth hormone
“
prolactin
“
→
→
→
→
target endocrine gland/tissue
thyroid gland
adrenal cortex
ovaries/testes
liver, bone, muscle, etc.
→
breasts
C. Thyroid Gland
1. Production of thyroid hormones T3 and T4 (thyroxine)
2. Effects of thyroid hormones
- increase basal metabolic rate
- stimulate protein synthesis
- developmental effects: nervous and reproductive systems
3. Feedback control of thyroid hormone secretion
D. Adrenal Gland
1. Adrenal cortex
a) mineralocorticoids (aldosterone) - promotes Na+ retention and K+ excretion by kidneys
b) glucocorticoids (cortisol) - “stress hormones”, promote gluconeogenesis, anti-inflammatory
c) androgens (testosterone, etc.)
2. Adrenal medulla
- connection to sympathetic ANS
- chromaffin cells secrete epinephrine (E) and norepinephrine (NE)
- Epi and NE act via adrenergic receptors on target cells
a. alpha-adrenergic receptors
α1 → constriction of blood vessels
b. beta-adrenergic receptors
β1 → increase in heart rate and contractility
β2 → bronchodilation
E. 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
1. 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
2. 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
3. Diabetes mellitus – insulin deficiency disease
a. Type 1 diabetes - insulin dependent (IDDM), “juvenile onset”
b. Type 2 diabetes - non-insulin dependent (NIDDM), “adult onset”
Effects and complications:
- 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
- vascular degeneration