Structure and Function 2- Exam 1

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Last updated 11:21 PM on 4/29/26
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122 Terms

1
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What are the 2 ways the human body can maintain homeostasis

nervous and endocrine systems

2
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what is the endocrine system

made of organs/ tissues that release hormones into the bloodstream and attach to the target cell to produce a response

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what is a hormone

the signaling molecules of the endocrine system

4
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what are target cells/ tissues

cells that receive the hormonal signal and are able to respond to it. a target cell has to have the correct receptor for a hormone (not all cells are target cells for all hormones)

5
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target cell response is dependent on...

concentration of hormones and number of receptors (sensitivity)

6
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t/f in general the more hormone you have the greater the response

true (and vice versa is also true)

7
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t/f the response of a target tissue is proportional to the concentration of hormone and the number of receptors available

true

8
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t/f the number of receptors can change

true

9
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describe up and down regulation

if a tissue is exposed to prolonged high levels of hormone, the cells in the tissue will "down-regulate" (decrease the number of receptors) this causes a decrease in sensitivity and responsiveness to the hormone. But if hormone levels drop, cells can increase the number of receptors, called up regulation, to increase sensitivity and responsiveness to the hormone

10
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Describe additive hormone interactions

if 2+ hormones are released at the same time and have the same responses, the overall effect is equal to the sum of the effect of each individual hormone

11
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Describe synergism hormone interactions

the overall effect of 2+ hormones is greater than the sum of individual effects

12
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Describe antagonism hormone interactions

hormone produce opposite effects (ex insulin and glucagon)

13
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Describe permissiveness hormone interactions

the effect of hormone "A" does not occur unless hormone "B" is present

14
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hydrophilic (protein based) cannot cross the lipid bilayer alone, thus the receptors are on the ______ of the cell

outside

15
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lipophilic (hydrophobic) receptors are on the ______ of the cell

inside (most often often in/on the nucleus)

16
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What types of hormones are lipid soluble

steroid hormones, thyroid hormone

17
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what types of hormones are water soluble

all amino acid-based hormones except thyroid hormone

18
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can lipid soluble hormones be stored inside a cell

no- they would diffuse right back out, thus you cannot store the active form of the hormone

19
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can water soluble hormones be stored inside a cell

yes

20
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how do lipid soluble hormones travel in blood

bound to a transport protein

21
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how to water soluble hormones travel in blood

freely in plasma

22
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what is the half life of lipid soluble hormones

long (because of they are protected by transport proteins)

23
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what is the half life of water soluble hormones

short (most get excreted easily in kidneys)

24
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what is the mechanism of action for lipid soluble hormones

stimules genes, causing protein synthesis

25
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what is the mechanism of action for water soluble hormones

acts through 2nd messenger systems in which when bound to target cell it activated things in the cell to make a response

26
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how long is the onset of response for a lipid soluble hormone

slow (has to get inside the cell, interact with DNA and form a new protein)

27
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how long is the onset of response for a water soluble hormone

fast (just "turns on" cell)

28
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when are hormones released?

when they are needed, the organ releasing them must be stimulated

29
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what are the 3 types of hormone stimuli

other hormones, humoral factors (chemicals in blood),and the nervous system

30
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t/f high hormone at the end of a pathway will turn off the pathway (negative feedback), low hormone at the end of a pathway will turn on the pathway (positive feedback)

true

31
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t/f the pituitary gland is 2 separate glands, with no functional connection between the 2 other than they are both controlled by the hypothalamus

true

32
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what type of cells is the anterior pituitary gland made of

epithelial cells

33
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what type of cells is the posterior pituitary gland made of

neurons

34
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The paraventricular nucleus of the posterior pituitary gland makes what hormone

oxytocin

35
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The supraoptic nucleus of the posterior pituitary gland makes what hormone

antidiuretic hormone (ADH)

36
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Once the nuclei of the posterior pituitary gland makes its hormone in the _________ is travels to the posterior pituitary gland via the _________________

hypothalamus; hypothalamic-hypophyseal tract

37
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________ is the "stalk" connecting hypothalamus to both lobes of the pituitary gland

infundibulum

38
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t/f no hormones are made in the posterior pituitary gland only in the 2 nuclei and are stored in the gland

true

39
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what are the effects of oxytocin in both males and females

smooth muscle contraction, bonding, reduces anxiety, decreases cortisol, released during sexual arousal/ orgasm

40
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what are the effects of oxytocin in females

uterine contractions (labor), milk "let down", mom/baby bonding

41
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what are the effects of oxytocin in males

contractions of male reproductive system to aid in moving sperm during ejactualtion, bonding with partner

42
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does ADH increase or decrease urinary output

decreases (promoted water conservation)

43
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what are the stimuli for ADH

increases plasma osmolarity (high concentration of salt to water, above 300 mOsml), low blood volume (thus low bp)

44
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describe the pathway for ADH

stimulus (high plasma osmolarity, or low blood volume), detected by hypothalamus, ADH is released from posterior pituitary gland, travels to kidney (target tissue), water reabsorption, prevents further increases in osmolarity or BV drop

45
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describe the "big picture" process of hormones from the anterior pituitary gland

neurons of the hypothalamus produce hormones, when the neurons are stimulated, the hormone "A" is released into the H-H portal system, which carries them to the anterior pituitary gland. They diffuse out of the portal vessels and bind to their receptors on their target cells in the ant. pit. This stimulates or inhibits the release of hormone "B" into the blood stream

46
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describe the hypothalamic-hypophyseal portal system

hormone "A" enters the capillaries in the hypothalamus, travels down the portal vein and then diffuses out of the capillaries in the anterior pituitary gland

47
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what does growth hormone do

increases nutrient availability, stimulates growth (increase protein synthesis, and decreases protein catabolism), increases mitosis and cell growth, lipolysis, gluconeogensis (makes sugar), glycogenolysis (breaks down glycogen), anti-insulin effect except in brain (provides sugar for the brain)

48
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what type of growth does GH stimulate in kids? adults?

interstitial growth (height, chondrocyte division), appositional growth and remodeling (bone density, osteoblasts)

49
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what is the stimuli for growth hormone

age, time of day, increased need for proteins (starvation, tissue trauma, exercise), nutrient levels (high amino acids, low fatty acids, low blood glucose),

50
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describe the pathway for growth hormone

stimulus, hypothalamus released GHRH (growth hormone releasing hormone), GHRH goes through portal system and binds to somatotropes (target cells in ant. pit), then GH is released into blood stream to bind to target cells (muscle, cartilage, bone, adipose, and liver). Once GH binds to liver, IGF-1 is released which binds to its target cells (muscle, cartilage, bone, adipose)

51
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why do we need GH and IGF-1

GH half life in 6-20 minutes, which IGF-1 half life in 20 hours

52
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what time of day does GH peak

first few hours of sleep

53
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Describe the pathway if there are high levels of IGF-1

stimulus (high IGF-1), hypothalamus releases somatostatin, travels through portal binds to somatotropes and turns off the pathway

54
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t/f GHRH and somatostatin share the same receptors, but are antagonist hormones

true (GHRH turns on pathway, somatostatin turns off pathway)

55
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what is gigantism

tumor in the somatotropes that causes overproduction of GH. the tumor must begin in childhood before the growth plates close. causes intersistal growth (very tall)

56
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what is acromegley

tumor in the somatotropes that causes huge increases in appositional growth. the tumor began after growth plates closed.

57
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what is the purpose of thyroid hormone

increase the body's metabolic rate, increases nutrient and oxygen availability, increase body temp, increase calorie burn and weight loss, increase HR and breathing rate. required for normal fetal and childhood growth and development (nervous system of baby, if too high of T3/T4 the growth plates can close early)

58
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what is the stimuli for thyroid hormones

cold body temp (loss of body heat), pregnancy, low T3/T4

59
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describe the pathway for thyroid hormone

stimuli, hypothalamus releases TRH (thyrotropin releasing hormone) into portal system, binds to thyrotropes (target cells on ant. pit.), that causes the release of TSH (thyroid stimulating hormone), that binds to thyroid gland (target tissue), which releases T3 and T4 and travels to all cells in the body

60
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t/f 90% of thyroid hormone is T4

true

61
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what is a goiter

abnormal enlargement of the thyroid gland

62
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what causes a goiter/ the thyroid gland to grow

too much TSH

63
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What is Hashimoto's thyroiditis?

autoimmune destruction of thyroid gland (hypothyroidism)

64
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what will the levels of TRH, TSH, and T3/T4 be in someone who has hashimotos

high TRH, high TSH, low T3/T4 (the thyroid gland is attacked and cannot make enough thyroid hormone, but trh and tsh are high bc TH is so low), goiters are common in this disease

65
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what would be symptoms of someone with hashimotos

weight gain, cold body temp

66
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what is graves disease

the body is making antibodies that mimic TSH, causing high levels of T3/T4 (hyperthyroidism)

67
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what will the levels of TRH, TSH, and T3/T4 be in someone who has graves disease

low TRH, low TSH (high "fake" TSH), high T3/T4

68
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what would be symptoms of someone with graves disease

weight loss, high body temp

69
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what is the purpose of cortisol

body respond to stress by mobilizing nutrients (every type of nutrient) and modulating the immune system and inflammatory response

70
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what are the stimuli for cortisol

time of day (right before/ as you wake up), decreased cortisol level (you have a baseline level of cortisol), stress (emotional, physical)

71
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describe the pathway for cortisol

stimuli causes the hypothalamus to release CRH (corticotropin releasing hormone) into the portal system which binds to the corticotrophes (ant pit.) which releases ACTH (adrenocorticotrophic hormone) which binds to the adrenal cortex (target cells) which releases cortisol and that binds to most cells in the body

72
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what are the 2 types of corticosteroids

glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

73
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what are the problems with long-term elevation of cortisol

protein breakdown, connective tissue breakdown at joints and bones. glycogenolysis, gluconeogensis and anti-insulin effect (hyperglycemia esp in diabetics). immune suppression, anti-inflamatory effects, exogenous use after 2+ weeks can turn off HPA (hypothalamic-pituitary-adrenal cortex) and body's own production of cortisol

74
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what are some clinical uses for corticosteroids

immunosuppression (like before an organ transplant), anti-inflammatory effects, pain

75
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what is the difference between endogenous and exogenous

endogenous is when the body makes its own hormone and exogenous is when it comes from outside the body (like a shot or pill)

76
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t/f short-term stress uses epinephrin, long-term stress uses cortisol

true

77
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what is cushing's disease and cushing's syndrome

both are too much cortisol for a long period of time. disease is endogenous, when the body is producing too much. syndrome is taking too much exogenous sources. symptoms include "moon pie face" (fat and fluid in face) and "buffalo hump" (fat between shoulder blades and neck)

78
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what is addison's disease

the body does not produce ACTH, thus cannot produce cortisol. people with this disease must take exogenous cortisol hormones

79
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describe the FSH-LH pathway

the hypothalamus releases GnRH (gonadotropin releasing hormone) into the portal system which binds to gonadotropes (ant. pit.) which releases FSH and LH, those travel to its effector tissues the ovaries or testes

80
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what does FSH and LH do for females in the ovaries

FSH stimulates follicular development and estradiol production, LH stimulates ovulation and estradiol and progesterone production

81
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what does FSH and LH do for males in the testes

FSH stimulates ABP production (androgen binding protein, also called nurse cells) and LH stimulates testosterone production (libido, secondary sex characteristics, sex organs). ABP + testosterone= sperm production

82
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t/f androgen means male hormone

true

83
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what hormone is released in males if sperm count it too high which turns off the FSH-LH pathway

inhibin (binds to gonadotropes), this turns off FSH only and does affect testosterone

84
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if testosterone levels get above nornal, LH receptors down-regulate which decreases the effect of LH which RAISES or LOWERS testosterone production

lowers

85
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PIH (prolactin inhibiting hormone) is released all the time in females (it is thought to be dopamine) but when they need to nurse that is turned off. describe that pathway

stimulating factors (like trying to nurse) stimulate the hypothalamus which releases estrogen binds to mamatrophes (ant. pit) and releases PRL (prolactin) and turns off PIH

86
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ALL hypothalamic hormones affecting the anterior pituitary glands are tropic hormones, what does tropic mean

hormones that affect the release of other hormones

87
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t/f all anterior pituitary hormones are released in response to another hormone

true

88
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What hormone lowers blood calcium? raises?

Calcitonin, PTH (parathyroid hormone)

89
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Describe the pathway of calcitonin

is calcium levels are too high (stimulus), the c-cells in the thyroid release calcitonin which binds to its target cells (bones, intestines, kidney's) which increases bone deposition (osteoblasts), increases calcium loss in feces and urine

90
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Describe the pathway of PTH

if calcium levels are too low (stimulus), the parathyroid gland releases PTH, which binds to its target cells (bones, kidneys) which increases osteoclast activity, calcium reabsorption in kidneys and activation of vit D by kidney (allows for absorption of dietary calcium)

91
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What is hypoparathyroidism

low PTH levels, this causes hypocalcemia as there is no way to raise blood calcium. this lowers the threshold and raises NM excitability

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what is hyperparathyroidism

high PTH levels, this causes hypercalcemia. this raises threshold and lowers NM excitability (stiff, weak bones)

93
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what is the purpose of aldosterone

salt and water balance. blood volume and blood pressure regulation

94
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what are the stimuli for aldosterone

low blood volume, high potassium, low sodium

95
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describe the aldosterone pathway

stimuli (low blood volume, high K, low Na) causes the adrenal cortex to release aldosterone into the bloodstream which goes to its target cells on the kidney. that causes Na reabsorption (thus water reabsorption as water follows salt) and a decreases urinary output (that helps raise bv thus bp). also, potassium is excreted in the urine

96
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what is the stimuli for renin (renin-angiotensin-aldosterone system)

low BV and low BP

97
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Describe the renin-angiotensin-aldosterone system (RAAS)

the stimuli (low BV and BP) cause the kidney to release renin which causes the inactive angiotensinogen to convert to angiotensin I, then ACE (angiotensin converting enzyme) converts that to angiotensin II which the active form that is released into the blood stream and acts as a powerful vasoconstrictor (raises BP) and stimulates aldosterone release

98
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What is hyperaldosteronism?

over production of aldosterone. this causes hypernatremia (high Na) which causes high BV and high BP (bad for heart) and hypokalemia (low K) which affects resting membrane potential (more negative, low NM excitability)

99
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What is hypoaldosteronism?

low aldosterone. this causes hyponatremia (low Na) causes low BV and BP (cardiovascular collapse) and hyperkalemia (high K) which causes a raise in RMP and high NM excitability

100
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Describe type I diabetes mellitus

destruction of pancreatic Beta cells. it is an autoimmune disease (some genetic component). they body is unable to synthesize insulin, thus cells "starve" because there is no insulin thus no glucose intake. It is commonly diagnosed in children and teens. DKA