• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/88

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

88 Cards in this Set

  • Front
  • Back
Hormone
long-range chemical messengers, produced by endocrine glands
-regulate cellular functions
Endocrine
hormone is secreted into the blood by a gland
Paracrine
cell signaling in which the target cell is near ("para" = near) the signal-releasing cell
-hormones diffuse to nearby cells
Autocrine
cell secretes a hormone or chemical messenger binds to autocrine receptors on the same cell, leading to changes in the cells
What hormones are secreted from the posterior pituitary?
-vasopressin (ADH)
-oxytocin
Where are vasopressin and oxytocin synthesized?
hypothalamus
What are the effects of vasopressin
(on kidneys, and on arterioles)?
-kidney tubules: increases H20 reabsorption,
-Arterioles: produces vasoconstriction
What stimulates release of vasopressin?
dehydration stimulates osmoreceptors in hypothalamus
What are the effects of oxytocin (on uterus and on mammory glands)?
Uterus: stimulates contractions of the uterus during childbirth
Mammory glands: stimulates contractions of the alveoli and ducts of the mammary glands (causes milk ejection)
What stimulates release of oxytocin?
mechanoreceptors at nipple and cervix
What hormones are produced by hypothalamus?
-vasopressin and oxytocin
-CRH
-GRH
-Prolactin-inhibiting hormone
-Somatostatin
-TRH
-GHRH
Corticotropin Releasing Hormone
stimulates secretion of adrenocorticotropic hormone (ACTH)
Gonadotropin-releasing hormone
stimulates secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
Prolactin-inhibiting hormone
inhibits prolactin secretion
Somatostatin
inhibits growth hormone (GH) secretion

-(also known as Growth Hormone Inhibiting Hormone [GIHI])
Thyrotropin-releasing hormone
stimulates secretion of thyroid-stimulating hormone (TSH)
Growth hormone releasing hormone
stimulates secretion of growth hormone (GH)
Thyroid stimulating hormone (TSH)
stimulates T3 and T4 secretion
Adrenocorticotropic hormone
stimulates cortisol secretion
Growth hormone
essential but not solely responsible for growth,
-promotes protein synthesis and growth,
-promotes lipolysis,
-promotes increased blood glucose
Follicle stimulating hormone
-promotes follicular growth and development;
-stimulates estrogen secretion
Luteinizing hormone
males - stimulates sperm production and testosterone secretion
females - stimulates ovulation, corpus luteum development, and estrogen & progesterone secretion
Prolactin
promotes breast development
-stimulates milk secretion
What hormones are released from the anterior pituitary?
TSH
AcTH
GH
FSH
LH
-Prolactin
Where are hormones released from the anterior pituitary synthesized?
in the anterior pituitary
Dwarfism
Hyposecretion of GH
Gigantism
Hypersecretion of Gh prior to closing of growth plates
Acromegaly
Hypersecrtion of GH after closing of growth plates
What hormones are produced by the thyroid gland?
T3 & T4
What is the difference between T3 and T4?
Most of thyroid hormone released from thyroid is in the form of T4. Most of the T4 is then converted (in the tissues) to T3 which is more active than T4.
What do thyroid hormones do?
-increases metabolic rate and heat production by enhancing sympathetic activity,
-stimulates protein synthesis and growth (through increased gene expression)
Cretinism
hypothyroidism in infants and young children characterized by low metabolic rate, growth retardation, mental retardation, hypothermia
Myxedema
adult hypothyroidism
Grave's disease
thyroid stimulating immunoglobulins bind to the TSH receptor and stimulate the thyroid, -increased metabolic rate, poor heat tolerance, decreased body weight, muscle weakness, exophthalmos (bulging eyes), goiter
Goiter
swelling in the thyroid gland which can lead to swelling of the larynx
2 types of Goiter
1) Endemic Goiter: due to iodide deficiency
2) Grave's Disease Goiter: Thyroid tumor, symptom of Grave's Disease
Where do corticosteroids come from?
adrenal cortex
What is the precurser for corticosteroids?
Cholesterol
What are the 3 classes of corticosteroids?
Mineralocorticoids (aldosterone)
Glucocorticoids (cortisol)
Sex Hormones (DHEA)
aldosterone
-helps in reabsorption of water and sodium (increase blood pressure), -controlled by amount of angiotensin II in the blood
Cortisol
-increases blood glucose, protein degradation and lipolysis,
-stimulated by ACTH
dehydroepiandrosterone (DHEA)
-makes androgens
-leads to precocious puberty or ambiguous sex development
-more is made if there is a 21-hydroxylase deficiency
Cushings Disease
-too much CRH, ACTH or cortisol
-leads to
*increased blood glucose, fat deposits (moon face & buffalo hump)
*muscle weakness
*stretch marks
*poor wound healing
*mental retardation in youth
Congenital Adrenal Hyperplasia
increased DHEA leads to more androgens due to deficiency in 21-hydroxylase.
Leads to precocious puberty (males) or ambiguous sex development (females)
21-hydroxylase
-converts pregenolone to cortisol
-leads to congenital adrenal hyperplasia if deficient
3 major secretions of pancreas
Glucagon
Insulin
Somatostatin
3 types of cells in islets of langerhands, and what each secretes
Alpha: Glucagon
Beta: Insulin
Delta:Somatostatin
actions of glucagon
increase blood glucose levels, decreases glycogen production, increases glycogen breakdown and glucose made,
decreases fat made
increases fat breakdown and ketones made,
glucose from proteins,
increase protein breakdown
slow protein creation
what controls the release of glucagon?
low blood sugar levels
actions of insulin
increase uptake of glucose into cells,
decrease blood glucose levels,
increases glycogen production,
decreases glycogen breakdown and glucose made,
increases fat made and decreases fat breakdown,
stop glucose from proteins, decrease protein breakdown increase protein creation
(essentially, opposite of glucagon)
Glut-4
increases glucose uptake
(insulin binds to receptors, releases a chemical (IRS-1 --> PI3K) that causes Glut-4 to move to and insert in cell membrane, creating passages for glucose to enter cell)
What triggers insulin secretion?
High blood sugar levels
Diabetes
increased urine
Diabetes Mellitus
"sweet tasting" diabetes
-elevated fasting blood glucose
-elevated urine glucose
Type I Diabetes
-due to autoimmune destruction of the beta cells of the pancreatic islets
-results in insulin deficiency
-patient must take insulin to survive
Type II Diabetes
-90% of all diabetics
-due to insulin resistance
-increased insulin secretion compensates for insensitivity in early stages,
-insulin deficiency occurs in later stages leading to hyperglycemia,
-average age >35, 90% are obese
Exercise effect
-muscle contraction has an insulin-like effect, by stimulating Glut-4 translocation
-exercise increases insulin sensitivity of muscle
AMPK
increases capacity for ATP synthesis (GLUT4 and mitochondrial enzymes) in response to endurance training
What the three classes of hormones?
Peptide Hormones
Amino Hormones
Steroid Hormones
Peptide Hormones
-examples
-how carried
-where receptors are located
-pituitary hormones, angiotensin, insulin, glucagon, IGF-1
-not protein bound
-in membrane
Amino Acid Hormones
-examples
-how carried
-where receptors are located
-epinephrine and thyroid hormones
-bound to carrier proteins
-in nucleus
Steroid Hormones
-examples
-how carried
-where receptors are located
-Aldosterone, Estradiol, Adrenal Cortical Hormones, Sex hormones
-bound to carrier proteins
-in nucleus
genetic sex
determined by X and Y chromosomes
phenotypic sex
determined by the presence or absence of masculinizing hormones
5a-reductase
changes testosterone to dihydrotestosterone
What happens if a male is deficient in 5a reductase?
male will have organs internally but not externally
What happens if a male is deficient in testosterone receptors?
genetically a male but not internal organs for either sex, and externally looks like a woman (pseudohermaphroditism)
pseudohermaphroditism
genetically a male but not internal organs for either sex, and externally looks like a woman
Testes
Produce sperm, secrete testosterone
Epididymus/Ductus Deferens
Path out of testes,
(epid.) site for sperm maturation
(epid.) concentrate and store sperm
Seminal Vesicle
-Supplies fructose,
-secretes prostglandins, semen, and precursors for semen
Prostate Gland
Alkaline secretion
triggers semen clotting
Bulbourethral Gland
Secretes Mucus (lubrication)
Seminiferous Tubules
produce sperm (inside testes)
Ovaries
Produce ova
secrete estrogen and progesterone
Oviducts
Transport ova
site of fertilization
Uterus
Maintain fetus during pregnancy
expel fetus during childbirth
Vagina
Site of sperm deposit
passageway for delivery of baby during childbirth
Leydig Cells
produce testosterone
What controls testosterone release?
-Fetal: placental hCG stimulates testosterone in leydig cells
-Puberty: GnRH is produced by hypothalamus which causes ant. pituitary to release LH which stimulates the leydig cells to produce testosterone
Spermatogenesis
Spermatagonium develops in the tight junction of a sertoli cell and through several intermediates turn into spermatozoon
-occurs in between sertoli cells
GnRH
-produced in hypothalamus, released from anterior pituitary
-produces LH, FSH
Testosterone
-Causes Wolffian Ducts to develop
-stimulates sertoli cells to begin spermatogenisis and release inhibin
-causes formation of male external genitalia
MIF
-mullarian inhibiting factor
-causes mullarian ducts to degenerate in males
FSH
stimulates sertoli cells
LH
stimulates leydig cells to produce testosterone
Sertoli cells
-in the seminiferous tubules
-provide nutrients and hormones for the production of sperm
Inhibin
produced by sertoli cell
-inhibits production of LH and FSH, therefore inhibit spermatogenesis. and leydig production of testosterone