Lecture 17 Endocrine 2 Flashcards by Sarah underwood

Q

Hypothalamus

A

Tropic Hormones (inhibiting and releasing hormones)
part of the brain (diencephalon) controls pituitary gland

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Q

Pituitary gland

A

also called hypophysis

major endocrine gland; infundibulum attaches to hypothalamus

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Q

Anterior Pituitary Gland Releases

A

TSH, ACTH, FSH, LH, GH, prolactin

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Q

Posterior Pituitary Gland Releases

A

ADH, oxytocin

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Q

Pineal Gland Releases

A

Melatonin

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Q

Thyroid Gland releases

A

thyroxine (T4), triiodothronine (T3); calcitonin

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Q

parathyroid glands

A

4 on the back of the thyroid gland
secrete PTH (parathyroid hormone)
regulation of Calcium

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Q

Thymus

A

thymosin, thymopoietin

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Q

Adrenal Cortex Secretes

A

aldosterone, cortisol, androgens

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Q

Adrenal Medulla

A

epinephrine and norepinephrine

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Q

Pancreas

A

Pancreatic Islets

insulin, glucagon

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Q

Ovaries/Testes

A

Females: Estrogen, progesterone
Males: Androgens (testosterone)

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Q

Placenta

A

estrogen and progesterone, hCG

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Q

Secondary Endocrine Organs

A

GI organs, heart, kidneys, liver, skin

GI hormones ANP, erythropoietin, Vitamin D3, etc.

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Q

Posterior Pituitary

A

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

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Q

Anterior Pituitary

A

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

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Q

Hypothalamus-Anterior Pituitary Axis

TRH

A

Hypothalamus releases TRH + -> TSH from anterior pituitary -> thyroid gland (target endocrine gland)

Q

Hypothalamus-Anterior Pituitary Axis

CRH

A

Hypothalamus releases CRH + -> ACTH from anterior pituitary -> adrenal cortex (target endocrine gland)

Q

Hypothalamus-Anterior Pituitary Axis

GnRH

A

Hypothalamus releases GnRH + -> FSH & LH from anterior pituitary -> ovaries/testes (traget endocrine gland)

Q

Hypothalamus-Anterior Pituitary Axis

GHRN

A

Hypothalamus releases GHRN + -> growth hormone from anterior pituitary -> liver, bone, muscle, etc. (target endocrine gland/tissue)

Q

Hypothalamus-Anterior Pituitary Axis

PRH

A

hypothalamus releases PRH + -> prolactin from anterior pituitary -> breasts (target endocrine organ)

Q

Effects of thyroid hormones

A

increase basal metabolic rate
stimulate protein synthesis
developmental effects: nervous and reproductive systems

Q

Adrenal Cortex

Mineralocorticoids

A

(aldosterone)

promotes Na+ retention and K+ excretion by kidneys

Q

Adrenal Cortex

Glucocorticoids

A

(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