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Anatomy and Physiology > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q

endocrine system function

A

regulate physiologic functions via chemical messengers in plasma
- uses HORMONES to control and coordinate your body’s metabolism, energy level, reproduction, growth and development, and response to injury, stress, and mood

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2
Q

endocrine system communication

A

via chemical hormones

  • hormones released from endocrine glands
  • some released from specialized cells
  • hormones circulate in blood stream and bind with target organ cell receptors to affect a change in target cell
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3
Q

endocrine system requires what

A

the bloodstream from the hormones to travel in

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4
Q

endocrine glands

A

LACK ducts because the hormones are secreted directly into the blood stream

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5
Q

hormone effect depends on

A

the target cell and receptor type

- where they are and contact w/ the hormone

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6
Q

type of endocrine hormones

A
  1. amines
  2. peptide hormones
  3. steroid hormones
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7
Q

Amines hormones

A

derived from tyrosine (solubility varies)

  • thyroid hormone = lipid
  • adrenal catecholamines = water
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8
Q

Peptide hormones

A

peptides, polypeptides, and proteins

  • WATER soluble ( need a receptor to pass membrane, cant pass alone)
  • hypothalamus hormones
  • pituitary gland hormones
  • pancreas hormones
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9
Q

steroid hormones

A 
derived from cholesterol 
- LIPID soluble ( can pass through membrane alone) 
- adrenocortical 
- gonadal 
- vitamin D
these hormones modify cholesterol
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10
Q

water vs lipid soluble hormones

A

water cannot cross membrane without a receptor
lipid can cross the membrane freely
*hormone structure dictates how it communicates with the target cell

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11
Q

water soluble hormone

A
  • small peptides removed by kidneys, so they have a shorter relative half-life
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12
Q

G proteins

A

there are DIFFERENT TYPES of G proteins

- not all activate AC

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13
Q

benefit of secondary messenger system

A

AMPLIFICATION of signal

- a single hormone can have a HUGE effect!

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14
Q

lipid soluble hormones

A

can have direct gene activation mechanism

ex. steroids, stress, testosterone, estrogen hormones
- metabolized by the liver so they have a relatively longer half-life

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15
Q

half life in lipid vs. water soluble hormones

A

water soluble are small peptides and are easier to be excreted in filtration of urine and kidneys

  • water soluble = shorter half-life
  • lipid soluble = longer half-life
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16
Q

target cell activation depends on three factors:

A
  1. hormone levels in the blood
  2. number of receptors present on target cells (less receptors = small chance of connection w hormone)
  3. affinity of binding between receptor and hormone
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17
Q

types of hormone release mechanisms

A
  1. humoral stimulus
  2. neural stimulus
  3. hormonal stimulus
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18
Q

humoral stimulus

A

hormone release caused by altered levels of certain critical ions or nutrients
- endocrine gland has sensors for the body and makes changes

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19
Q

neural stimulus

A

hormone release caused by neural input

- release of epin. or nor. from the medulla gland

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20
Q

hormonal stimulus

A

hormone released caused by another hormone (a tropic hormone)

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21
Q

hypothalamus and pituitary

A

the hypothalamus is “the boss” of the pituitary gland

- it regulates hormone release by the pituitary

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22
Q

neurohypophysis

A

posterior pituitary

  • hypothalamus makes hormones that the posterior pituitary releases
  • oxytocin and ADH
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23
Q

Oxytocin in posterior pituitary

A

made in paraventricular cells of hypothalamus and is stored in the PP

  • allows milk let down- suckling stimulates release
  • uterine contractions in child birth
  • positive feedback
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24
Q

Antidiuretic hormone (ADH) in posterior pituitary

A

produced in hypothalamus and is stored in the PP

  • makes DCT and collecting duct more permeable to water
  • water reabsorbed and urine output decreased
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25
Q

adenohypophysis

A

anterior pituitary

- hypothalamus regulates AP hormone release by synthesizing releasing and inhibiting hormones

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26
Q

anterior pituitary

A

hypothalamic hormones released into special blood vessels

- releasing and inhibitory hormones of the hypothalamus affect AP hormone release

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27
Q

Growth hormone (somatotropic) in anterior pituitary

A

GHRH, stimulates and increases growth of body tissues and cell size

  • promotes glycogen breakdown
  • protein production in muscle increases mass
  • can lead to gigantism (GHRH) or dwarfism (GHIH = somatostasin)
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28
Q

adrenocorticotrophic hormone (ACTH)

A

anterior pituitary (adrenal cortex hormone)

  • acts on adrenal cortex to release glucocorticoids and mineralocorticoids
  • secretion regulated by hypothalamus corticotrophin (CRH)
    hypo. ->CRH-> AP -> ACTH -> adrenal cortex -> glucocorticoids and mineralcorticoids release
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29
Q

releasing hormone (CRH) in response to:

A
  1. STRESS
  2. cold, heat
  3. hypoglycemia
  4. toxemia
  5. dehydration
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30
Q

adrenal glands

A

located near kidneys, split into:

  1. adrenal cortex = corticosteroids
  2. adrenal medulla = catecholamines
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31
Q

adrenal glands: medulla

A

adrenal medulla produces catecholamines (water soluble)

- epinephrine and norepinephrine

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32
Q

adrenal glands: cortex

A

adrenal medulla produces corticosteroids (lipid soluble)

- glucocorticoids (cortisol) and mineralocorticids (aldosterone)

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33
Q

Aldosterone (mineraocorticoid)

A

enhances Na+ resorption and K+ secretion in the renal collecting ducts and DCT

  • release stimulated by the renin/angiotensisn system when BP is low or dehydration
  • results in Na+ resorption and water retention
  • blood volume increases
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34
Q

Cortisol (glucocorticoid)

A

released in response to ACTH stimulus (from pituitary)
triggered from:
- hypocalcemia = low blood sugar
- stress = very catabolic and breaks things down
* cortisol increases GLUCOSE in the bloodstream

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35
Q

negative feedback of glucocorticoids

A
  1. abundance of glucocorticoids (cortisol) in blood stream
  2. glucocorticoid receptors in hypothalamus bound
  3. release of CRH stopped
  4. no release of ACTH
  5. no adrenal stimulation
  6. no more glucocorticoids released
    * negative inputs back to hypothalamus and anterior pituitary
36
Q

hyperadrenocorticism

A

crushings disease
- Etiology: tumor (primary vs secondary) and iatrogenic
steroid diabetes: polyuria (increase in urination) and polydipsia (increase in thirst)

37
Q

effects of polyuria/polydipsia (steroid diabetes) and why these occur

A

why? increase in glucose in blood which increases urination and overwhelms convoluted tubules

  • think skin/hair loss
  • swollen liver
  • bone loss/weaken muscles
38
Q

thyroid stimulating hormone (TSH)

A

anterior pituitary

  • acts on the thyroid to release throid hormones
  • regulator of metabolic activity
  • secretion regulated by hypothalamus
  • depends of release of thyrotropin releasing hormone (TRH)
39
Q

thyroid gland

A

thyroid hormones are amine - derived from tyrosine

  • lipid soluble
  • thyroglobulin holds tyrosine and becomes iodinated to form active compounds
  • released into blood and bound to thyroxine-binding globulin to carry to target organs
  • T4 and T3
40
Q

T4 thyroid hormone

A

tetraiodothyronine (4 iodine bound to thyroglobulin) = throxine
- less makes it to cells but lasts longer

41
Q

T3 thyroid hormone

A

triiodothyronine (3 iodine bound to thyroglobulin)

- more potent but lasts longer

42
Q

iodine

A

taken in from your diet

- needed for the thyroid gland to make T3 and T4 hormones

43
Q

function of thyroid gland

A

increases metabolism and regulates carbs, proteins, and fat metabolism
- increases oxygen consumption

44
Q

thyroid hormone released stimulants by TSH from anterior pituitary

A
  1. low levels detected by the hypothalamus
  2. TRH released to pituitary
  3. pituitary releases TSH
  4. TSH works on thyroid gland to increase activity and release T4 and T3
45
Q

if too much T3 and T4 is release:

A

negative feedback system starts

46
Q

thyroid hormone is especially important for

A

normal development and regulating basal metabolic rate and temperature regulation

47
Q

T3 and T4 negative feedback loop act on:

A

the anterior pituitary and the hypothalamus

48
Q

thyroid hormone positive feedback system steps

A
  1. hypothalamus
  2. TRH
  3. anterior pituitary
  4. TSH
  5. thyroid
  6. T3 and T4 is released and affects basometabolic rate
49
Q

thyroid hormone deficiency effects

A

hypothyroidism - reduced BMW, increased weight

  • lethargy and mentally sluggish
  • cold feeling
  • overweight
  • edema
  • intellectual and physical challenges if at a young age
50
Q

Iodine deficiency

A

deficiency from decreased thyroid hormone production

  • hypothalamus sees low hormone and send to TRH to pituitary which send to TSH to thyroid gland
  • glands grow trying to make T3 and T4
51
Q

goiter

A

enlarged thyroid gland because there is no iodine to bind to T3 and T4 so loop continues

52
Q

hyperthyroidism

A

graves disease

- bulging eyes (exophthalmos)

53
Q

Calcitonin

A

another thyroid hormone produced from TG, NOT associated with feedback loop

  • HIGH blood calcium levels stimulate calcitonin release = hypercalcemia
  • calcitonin inhibits osteoclastic activity, increases Ca2+ in osteoblasts
54
Q

causes of hypercalcemia

A

high blood calcium levels

  • cancers
  • parathyroid tumor (rare)
  • bone lesions
55
Q

causes of hypocalcemia

A

low blood calcium levels

  • nutritonal
  • calcitriol deficiency
  • excessive demand (ex. birth)
  • lpw or high PTH
56
Q

Parathyroid

A

secreted from the parathyroid gland in response to HYPOcalcemia

  • raise blood Ca2+ levels, causes Ca2+ and phosphorous to be released from bone which enhances osteocastic activity
  • increases Ca2+ reabsorption in the kidneys
  • causes conversion of inactive vitamin D to active form, Calcitriol
57
Q

Calcitriol

A

active form of vitamin D

  • lipid soluble
  • increases small intestinal apical calcium channels and pumps
  • increases bone absorption
  • decreases PTH secretion
  • decreases renal Ca2+ excrertion
58
Q

hormones associated with bones

A
  1. GH (growth hormone + thyroid hormone)
  2. testosterone
  3. estrogen
  4. insulin
  5. cortisol
59
Q

testosterone

A

results in heavier bone growth by increasing GH secretion

- increased osteoblast activity and epiphysial losure

60
Q

estrogen

A

increased osteoblast activity

  • cessation of long bone growth
  • prevents osteoporosis
61
Q

insulin

A

stimulates osteoblast activity (bone formation)

62
Q

cortisol

A

dose dependent osteoclast inhibition

- stops/inhibits activity

63
Q

releasing and inhibitory hormones of the hypothalamus affect

A

anterior pituitary hormone release

64
Q

Prolactin

A

anterior pituitary hormone

  • water soluble
  • stimulates lactogenesis (milk production)
  • lactation requires prolactin and oxytocin (milk let down)
  • hypothalamus produces prolactin releasing hormone factors (PRH/PRF)
  • hypothalamus produces prolactin inhibiting hormone (dopamine;PIH) to stop lactogenesis
65
Q

Follicle stimulating hormone (FSH) and Luitenizing Hormone (LH)

A

anteriot pituitary hormones
- sex steroid stimulation
- hypothalamus produces gonatrophin releasing hormone (GnRH)
Males: testosterone will inhibit GnRH production
Females: Estrodial stimulates GnRH production

66
Q

Female Hypothalamic-Pituitary-Gondal Axis Steps

A
  1. Maturing follicle secretes estradiol
  2. Estradiol stimulates hypothalamus and anterior pituitary
  3. hypothalamus secretes GnRH
  4. GnRH and estradiol stimulate pituitary to secrete LH and FSH
  5. Oocyte complete meiosis 1; follicle radpidly enlarges and then ovulates
67
Q

Male Hypothalamic-Pituitary-Gondal Axis Steps

A
  1. GnRH from hypothalamus stimulates the anterior pituitary to secrete FSH and LH
  2. FSH stimulates nurse cells to secrete androgen-binding protein
  3. LH stimulates interstitial cells to secrete testosterone (androgen)
  4. presence of ABP, testosterone stimulates spermatogenesis
  5. testosterone also stimulates the libido and the development of secondary sex organs
  6. testosterone has negative feedback effects that reduce GnRH secretion and pituitary sensitivity to GnRH
  7. nurse cells also secrete inhibin which inhibits FSH secretion and reduces sperm production without reducing testosterone secretion
68
Q

in males, balance of hormones is achieved during

A

puberty and stabilizes in adulthood

69
Q

what does testosterone do in puberty

A

produce sperm by initiating spermatogenesis

  • reproductive structures grow to adult size
  • secondary sex characteristics
70
Q

menopause

A

cessation of ovulation and menstruation

- estrogen levels begin to decline as women reach later 40s

71
Q

sex steroids

A

have some non-reprodctive effects

  • help faciliatate Ca2+ uptake and reduce osteoclast activity
  • maintain bone density
72
Q

estrogen also promotes:

A

coagulation
increase in: plasma fibrinogen, coagulation factor, platelet activity
decrease in: anti-thrombin

73
Q

testosterone is important for

A

protein synthesis and building/maintaining muscle and helps with RBC production

74
Q

Pineal gland produces

A

melatonin

  • water soluble
  • prodcution occurs at night
75
Q

Pancreas endocrine gland cell types

A 
hormones produces by:
- alpha produce 
- beta produce 
glucose homeostasis:
- glucagon 
- insulin
76
Q

Endocrine hormones

A

produced by alpha and beta cells in the pancreatic islets

  • glucagon and insulin hormones
  • important for glucose homeostasis
77
Q

glucagon vs. Insulin

A

increases blood sugar vs. decrease blood sugar

78
Q

Insulin (water soluble)

A
  • peptide is produced/secreted from Beta Cells
  • allows glucose entry into a cell by facilitated diffusion
  • lowers blood glucose
  • promotes carbs and lipid storage (anabolic)
79
Q

insulin secretion is stimulated by

A
  1. glucose
  2. parasympathetic release of acetylcholine
  3. cholecystokinin
80
Q

diabetes mellitus

A

not enough insulin activity

  • decreased production (type 1)
  • insulin resistance (type 2)
81
Q

glucagon

A

opposite effects of insulin

  • secreted from alpha cells when blood glucose is LOW
  • catabolic
    1. initiates glycogenolysis (breakdown)
    2. initiates gluconeogenesis (production)
82
Q

homeostatic balance of blood glucose by

A

insulin (anabolic) and glucagon (catabolic)

83
Q

example of homeostatic imbalance

A

diabetes

  • either lack of insulin production (type 1)
  • improper response to stimulus (type 2)
84
Q

insulin is

A

anabolic and is secreted by Beta cells when blood glucose is high

85
Q

glucagon is

A

catabolic and produced by alpha cells when blood glucose is low

86
Q

In males, testosterone will

A

inhibit GnRH production, FSH feedback also involved hormone called inhibin

87
Q

In females, Estrodial

A

stimulates GnRH production

Anatomy and Physiology (6 decks)

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