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Bio > Ch. 5: The Endocrine System > Flashcards

Ch. 5: The Endocrine System Flashcards

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1
Q

defn: glands

A

organs that secrete hormones

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2
Q

defn + func: hormones

A

signaling molecules that are secreted directly into the bloodstream to distant target tissues

bind to receptors at target tissues inducing a change in gene expression or cellular function

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3
Q

what are the three categories of hormones?

A
  1. peptides
  2. steroids
  3. amino acid derivatives
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4
Q

char(3): peptide hormones

A
  1. made up of amino acids
  2. large range of sizes
  3. all derived from larger precursor polypeptides that are cleaved during posttranslational modification
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5
Q

what is the process by which larger precursor polypetides become peptide hormones? (3)

A
  1. cleaved during posttranslational modification
  2. smaller units are transported to the Golgi apparatus for further mods that activate the hormones and direct them to the correct cell locations
  3. such hormones are released by exocytosis after being packaged into vesicles
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6
Q

why must peptide hormones bind to an extracellular receptors?

A

because they are charged and cannot pass through the plasma membrane

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7
Q

defn: first vs. second messenger (peptide hormones)

A

FIRST messenger = peptide hormone

SECOND messenger = the second signal that is triggered by the peptide hormone binding to the receptor

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8
Q

defn: signaling cascade

A

the connection between the hormone at the surface and the effect brought about by second messengers within the cell

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9
Q

why is there the possibility of amplification at each step?

A

each receptor may activate multiple enzymes, each of which will trigger the production of large quantities of second messengers –> each step can result in an increase in signal intensity

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10
Q

what are three common second messengers for peptide hormones?

A
  1. cAMP: cyclic adenosine monophosphate
  2. IP3: inositol triphosphate
  3. calcium
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11
Q

how is a G-protein couple receptor activated?

A
  1. the binding of a peptide hormone triggers the receptor to either activate or inhibit adenylate cyclase
  2. this raises or lowers the levels of cAMP accordingly
  3. cAMP can bind to intracellular targets, such as protein kinase A, which phosphorylates transcription factors like cAMP response element-binding protein (CREB) to exert the hormone’s ultimate effect
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12
Q

func: adenylate cyclase

A

an enzyme that raises or lowers the levels of cAMP

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13
Q

diagram + summary: mechanism of action of a peptide hormone

A

peptide hormones bind to membrane-bound receptors to initiate a signal cascade, using second messengers like cAMP

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14
Q

how do the effects of peptide and steroid hormones differ? why?

A

PEPTIDE = rapid, short-lived –> bc they act through second messenger cascades (transient) –> it’s quicker to turn them on and off (compared with STEROID) but their effects do not last without relatively constant stimulation

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15
Q

are peptide hormones water or lipid soluble? what does this imply?

A

water-soluble

they can travel freely in the bloodstream and usually do not require carriers

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16
Q

are steroid hormones water or lipid soluble?

A

lipid-soluble

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17
Q

summary: mechanisms of peptide hormones vs. steroid hormones

A

PEPTIDE = have surface receptors and act via second messenger systems

STEROID = bind to intracellular receptors and function by binding to DNA to alter gene transcription

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18
Q

defn: steroid hormones

A

derived from cortisol and produced primarily by the gonads and the adrenal cortex

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19
Q

why can steroid hormones easily cross the cell membrane?

A

because they are derived from nonpolar molecules

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20
Q

where are steroid hormone receptors (2)?

A

intracellular (in the cytosol)

intranuclear (in the nucleus)

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21
Q

what happens to steroid hormones when they bind to their receptor?

A

undergo complex conformational changes so that they can bind directly to DNA, resulting in either increased or decreased transcription of particular genes, depending on the identity of the hormone

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22
Q

defn: dimerization

A

pairing of 2 receptor-hormone complexes

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23
Q

why are the effects of steroid hormones slower but longer lived than peptide hormones?

A

because steroid hormones participate in gene regulation, causing alterations in the amount of mRNA and protein present in a cell by direct action on DNA

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24
Q

mechanism of action of steroid hormone (summary)

A

influences cell behavior by modifying transcription

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25
Q

what impact does the fact that steroid hormones are not water-soluble have?

A

they must be carried by proteins in the bloodstream to travel around the body, some of which are very specific and carry only one hormone

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26
Q

what is an example of a carrier protein that is specific to only one hormone? what is an example of one that is nonspecific?

A

specific: sex hormone-binding globulin

non-specific: albumin

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27
Q

char (2) of hormones while attached to a carrier protein

A

generally inactive
must dissociate from the carrier to function

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28
Q

what does the level of carrier proteins have an impact on? + example

A

the levels of active hormone

example: some conditions increase the quantity of a protein that carries thyroid hormones (thryoxine-binding globulin) –> this causes the body to perceive a lower level of thyroid hormone because the increase quantity of TBG binds a larger proportion of the hormone, meaning there is less free hormone available

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29
Q

defn: amino acid-derivative hormones

A

less common than peptide and steroid hormones, but still important

derived from one or two amino acids, usually with a few additional modifications

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30
Q

what are 4 important amino acid-derivative hormones?

A
  1. epinephrine
  2. norepinephrine
  3. triiodothyronine
  4. thryoxine
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31
Q

chemistry of amino acid-derivative hormones

A

considerably less predictable

epinephrine and norepinephrine bind to G protein-coupled receptors, have extremely fast onset, and are short-lived (think of adrenaline rush)

thyroid hormones bind intracellularly, have slower onset, but a longer duration

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32
Q

defn: direct hormones vs. tropic hormones

A

DIRECT = are secreted and then act directly on a target tissue

TROPIC = require an intermediary to act; usually originate in the brain and anterior pituitary gland, allowing for the coordination of multiple processes within the body

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33
Q

nomenclature: peptide and amino acid-derivate hormone suffixes

steroid hormone suffixes

A

peptide and amino acid-derivate hormone suffixes: - IN or -INE

steroid hormone suffixes: -ONE, -OL, or -OID

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34
Q

what are the 8 endocrine glands?

A
  1. hypothalamus
  2. pituitary
  3. thyroid
  4. parathyroid glands
  5. adrenal glands
  6. pancreas
  7. gonads
  8. pineal glands
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35
Q

defn + func + diagram: endocrine glands

A

each of these organs is capable of synthesizing and secreting one or more hormones into the bloodstream to act on distant target tissues

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36
Q

what are 4 organs that have collections of cells within them that serve important endocrine rolls?

A
  1. kidneys
  2. gastrointestinal glands
  3. heart
  4. thymus
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37
Q

func (6): hypothalamus

A
  1. the bridge between the nervous and endocrine systems
  2. regulates the pituitary gland through tropic hormones, and thus has organism-wide effects
  3. receives input from a wide variety of sources
  4. helps to control sleep-wake cycles
  5. responds to blood osmolarity
  6. regulate appetite and satiety
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38
Q

where is the hypothalamus located? (3)

A
  1. in the forebrain
  2. directly above the pituitary gland
  3. directly below the thalamus
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39
Q

what impact is had by the fact that the hypothalamus and the pituitary are close to each other?

A

the hypothalamus controls the pituitary through paracrine release of hormones into a portal system that directly connects the 2 organs

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40
Q

what are the 3 sections of the hypothalamus?

A
  1. lateral
  2. ventromedial
  3. anterior hypothalamus
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41
Q

what are the 6 roles of the nuclei in the 3 sections of the hypothalamus?

A
  1. emotional experience
  2. aggressive behavior
  3. sexual behavior
  4. metabolism
  5. temperature regulation
  6. water balance
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42
Q

what regulates the release of hormones by the hypothalamus?

A

negative feedback

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43
Q

defn + func: negative feedback

A

defn: occurs when a hormone (or product) later in the pathway inhibits hormones (or enzymes) earlier in the pathway

func: maintains homeostasis and conserves energy by restricting production of substances that are already present in sufficient quantities

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44
Q

why are the hypothalamus and pituitary gland inextricably linked?

A

the pituitary gland has an anterior and posterior component, each with a unique interaction with the hypothalamus

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45
Q

where does the hypothalamus secrete compounds into? (4 step path) + where are they NOT found

A
  1. the hypophyseal portal system (portal bloodstream)
  2. then down the pituitary stalk and then
  3. bind to receptors in the anterior pituitary, stimulating the release of other hormones

cannot be found in appreciable concentrations in the systemic circulation

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46
Q

defn + diagram: hypophyseal portal system

A

a blood vessel system that directly connects the hypothalamus with the anterior pituitary

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47
Q

defn: hypophysis

A

an alternative term for the pituitary

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48
Q

does the hypothalamus secrete direct or tropic hormones?

A

tropic!

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49
Q

what are 4 hormones released by the hypothalamus and the corresponding hormones released by the anterior pituitary in response? what is the one exception to this pattern? + summary of what is happening with the tropic hormones

A
  1. Gonadotropin-releasing hormone (GnRH) —-> follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
  2. Growth hormone-releasing hormone (GHRH) –> growth hormone (GH)
  3. Thyroid-releasing hormone (TRH) –> thyroid-stimulating hormone (TSH)
  4. Corticotropin-releasing factor (CRF) –> adrenocorticotropic hormone (ACTH)

EXCEPTION:
1. Prolactin-inhibiting factor (dopamine) –> decreases prolactin secretion

summary: each of the tropic hormones causes the release of another hormone from an endocrine gland that has negative feedback effects

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50
Q

corticotropin-releasing factor (CRF) from the hypothalamus will stimulate the anterior pituitary to secrete ACTH, what happens after that?

A

ACTH causes the adrenal cortex to increase the level of cortisol being secreted into the blood

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51
Q

how is excess cortisol secretion prevented? why does this makes sense?

A

cortisol inhibits the hypothalamus and anterior pituitary from releasing CRF and ACTH, respectively

this makes sense because CRF and ACTH have already accomplished their desired effect (getting more cortisol into the blood)

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52
Q

are there cortisol receptors in the hypothalamus and pituitary? why or why not?

A

yes because these organs need to be able to recognize that cortisol levels have increased

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53
Q

defn + 2 examples: axes

A

three-organ systems that engage in negative feedback loops

  1. hypothalamic-pituitary-adrenal (HPA) axis
  2. hypothalamic-pituitary-ovarian (HPO) axis
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54
Q

diagram: hypothalamic negative feedback mechanism

A
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55
Q

how does the posterior pituitary receive hormones? how DOESNT the posterior pituitary receive hormones?

A

DOES NOT: through the hypophyseal portal system

DOES: neurons in the hypothalamus send their axons down the pituitary stalk directly into the posterior pituitary

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56
Q

what 2 hormones does the posterior pituitary release?

A
  1. oxytocin
  2. antidiuretic hormone
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57
Q

func (3): oxytocin

A
  1. stimulates coordinated uterine smooth muscle contractions during labor
  2. stimulates milk letdown during lactation (promotes milk ejection through contraction of smooth breast muscle) and is promoted by suckling
  3. may be involved in bonding behavior
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58
Q

func + aka: antidiuretic hormone

A

aka: vasopressin

increases reabsorption of water in the collecting ducts of the kidneys

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59
Q

what is ADH secreted in response to? (2)

A
  1. increased plasma osmolarity
  2. increased concentration of solutes within the blood
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60
Q

what effect does a tumor of the pituitary gland have?

A
  1. may result in compression of the portal system that connects the pituitary to the hypothalamus
  2. block the ability of PIF to reach the pituitary and exert its effect so
  3. more prolactin will be released
  4. this may result in lactation (in males or nonpregnant women)
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61
Q

how many products does the anterior pituitary synthesize and secrete?

A

7 different hormones (4 tropic, 3 direct)

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62
Q

mnemonic: products of the anterior pituitary

A

Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Adrenocorticotropic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Prolactin
Endorphins
Growth hormone (GH)

FLAT = tropic hormones
PEG = direct hormones

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63
Q

what do FSH and LH act on?

A

testes and ovaries (gonads)

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64
Q

what does ACTH act on?

A

the adrenal cortex

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65
Q

what does TSH act on?

A

the thyroid

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66
Q

func: prolactin

A

stimulates milk production in the mammary glands

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67
Q

what effect does the release of dopamine from the hypothalamus have on prolactin?

A

dopamine decreases the secretion of prolactin

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68
Q

explain the relationship between the levels of estrogen, progesterone, dopamine, and lactation and plantecal drop

A

HIGH levels of estrogen and progesterone –> development of milk ducts in preparation for lactation

shortly after placental expulsion, estrogen, progesterone, and dopamine levels drop, there is no longer a block on milk production, and lactation begins

69
Q

when does milk ejection occur?

A

when the newborn latches onto the breast

70
Q

what does nipple stimulation cause activation of?

A

the hypothalamus, resulting in two different reactions

71
Q

what 2 reactions result from hypothalamus activation due to nipple stimulation?

A
  1. oxytocin is released from the posterior pituitary, resulting in contraction of the smooth muscle of the breast and milk ejection through the nipple
  2. the hypothalamus stops releasing dopamine onto the anterior pituitary, allowing prolactin release, causing milk production and milk supply regulation
72
Q

func: endorphins

A

decrease the perception of pain

73
Q

func (2) + char (2): growth hormone

A

func: 1. promotes growth of bone and muscle
2. prevents glucose uptake in certain tissues (those that aren’t growing) and stimulates the breakdown of fatty acids, increasing glucose availability overall for muscle and bone to use

char: 1. energetically expensive growth
2. requires large quantities of glucose

74
Q

what is GH release stimulated by?

A

growth hormone-releasing hormone (GHRH) from the hypothalamus

75
Q

where does bone growth originate in the body? what happens to these spots during puberty?

A

originates in special regions of the bone (epiphyseal plates)

these seal shut during puberty

76
Q

what causes gigantism? dwarfism?

A

GIGANTISM = an excess of GH released in childhood

DWARFISM = a deficit of GH in childhood

77
Q

what causes acromegaly + char?

A

GH excess in adulthood

the long bones are sealed, but GH still has an effect, so it is primarily in the smaller bones (hands, feet, head)

78
Q

struct: posterior pituitary

A

contains the nerve terminals of neurons with cell bodies in the hypothalamus

79
Q

what is ADH secreted in response to (from the posterior pituitary)? + what senses this

(2)

A
  1. low blood volume (sensed by baroreceptors)
  2. increased blood osmolarity (sensed by osmoreceptors)
80
Q

impact (4): ADH

A
  1. increases the permeability of the collecting duct to water
  2. this increases the reabsorption of water from the filtrate in the nephron
  3. this results in greater retention of water
  4. this results in increased blood volume and higher blood pressure
81
Q

diagram: antidiuretic hormone

A
82
Q

does the posterior pituitary synthesize hormoens?

A

no, the hormones that are released by the posterior pituitary are MADE in the hypothalamus

83
Q

explain the positive feedback loop of oxytocin

A

the release of oxytocin promotes uterine contraction, which promotes more oxytocin release, which promotes stronger uterine contractions, etc.

“spiraling forward”

definitive endpoint: delivery

84
Q

what is the thyroid controlled by?

A

thyroid-stimulating hormone from the anterior pituitary

85
Q

where is the thyroid?

A

on the front surface of the trachea, at the base of the neck

86
Q

2 major func: thyroid + how does it carry out each effect

A
  1. setting basal metabolic rate (by releasing T3 and T4)
  2. promoting calcium homeostasis (through the release of calcitonin)
87
Q

how are T3 and T4 produced?

A

by the iodination of the amino acid tyrosine in the follicular cells of the thyroid

88
Q

how are thyroid hormones capable of resetting the basal metabolic rate?

A
  1. making energy production more or less efficient
  2. altering the utilization of glucose and fatty acids
89
Q

impact of increased T3 and T4 (3)

A
  1. increased cellular respiration
  2. this leads to increased protein and fatty acid turnover due to increased synthesis and degradation of these compounds
  3. when high in plasma: lead to decreased TSH and TRH synthesis (negative feedback)
90
Q

diagram: thyroid hormone negative feedback mechanism

A
91
Q

cause + defn + symptoms (5): hypothyroidism

A

CAUSE = a deficiency in iodine or inflammation of the thyroid

DEFN: thyroid hormones are secreted in insufficient amounts or not at all

SYMPTOMS: 1. lethargy
2. decreased body temp
3. slowed respiration and heart rate
4. cold intolerance
5. weight gain

92
Q

what are thyroid hormones required for in children?

A

appropriate neurological and physical development

93
Q

why are most children tested for thyroid hormones at birth?

A

a deficiency will result in intellectual disability and developmental delay (cretinism)

94
Q

cause + defn + symptoms (5): hyperthyroidism

A

CAUSE: may result from a tumor or thyroid over-stimulation

DEFN: excess of thyroid hormone

SYMPTOMS: 1. heightened activity level
2. increased body temperature
3. increased respiratory and heat rate
4. heat intolerance
5. weight loss

95
Q

what 2 types of cells are within the thyroid and what products do they correspond to?

A

follicular cells –> make thyroid hormones

C-cells (parafollicular cells) –> make calcitonin

96
Q

in what 3 ways does calcitonin decrease plasma calcium levels?

A
  1. increasing calcium excretion from the kidneys
  2. decreasing calcium absorption from the gut
  3. increasing storage of calcium in the bone
97
Q

what do high levels of calcium in the blood stimulate?

A

secretion of calcitonin from the C-cells

98
Q

mnemonic: calcitonin effect

A

calciTONin TONes down calcium levels in the blood

99
Q

what are the 6 important functions of calcium?

A
  1. bone structure and strength
  2. release of neurotransmitters from neurons
  3. regulation of muscle contraction
  4. blood clotting (calcium is cofactor)
  5. cell movement
  6. exocytosis of cellular materials
100
Q

struct/loc + what hormone do they produce: parathyroids

A

four small pea-sized structures that sit on the posterior surface of the thyroid

produces: parathyroid hormone (PTH)

101
Q

func (4): PTH

A
  1. serves as an antagonistic hormone to calcitonin, raising blood calcium levels
  2. decreases excretion of calcium by the kidneys, increasing absorption of calcium in the gut via vit D and increases bone resorption, thereby freeing up calcium
  3. promotes phosphorus homeostasis by increasing the resorption of phosphate from bone and reducing reabsorption of phosphate in the kidney (thus promoting its excretion in the urine)
  4. activates vitamin D
102
Q

explain how PTH is subject to feedback inhibition

A

as levels of plasma calcium rise, PTH secretion is decreased

103
Q

diagram: calcium and phosphorus homeostasis

A
104
Q

what is the overall effect of PTH?

A

a significant increase in blood calcium levels with little effect on phosphate (the absorption of phosphate in the gut and its excretion in the kidney somewhat cancel each other)

105
Q

how can we think of calcitonin and PTH as a pair?

A

they are antagonistic to each other

and have the primary function of regulating calcium levels in the blood

PTH increases serum calcium levels, whereas calcitonin decreases calcium levels

106
Q

structure + location: adrenal glands

A

located on top of the kidneys

each consists of a cortex and a medulla, each of which is responsible for the secretion of different hormones

107
Q

what does the adrenal cortex secrete?

A

corticosteroids

108
Q

what are the 3 classics of corticosteroids?

A
  1. glucocorticoids
  2. mineralocorticoids
  3. cortical sex hormones
109
Q

defn: glucocorticoids

A

steroid hormones that regulate glucose levels and affect protein metabolism

110
Q

what are 2 glucocorticoids?

A
  1. cortisol
  2. cortisone
111
Q

func (2): cortisol and cortisone

A
  1. raise blood glucose by increasing gluconeogenesis and decreasing protein synthesis
  2. decrease inflammation and immunologic responses
112
Q

func (2): cortisol

A
  1. stress hormone because it is released in times of physical or emotional stress
  2. increases blood sugar and provides a ready source of fuel in case the body must react quickly to a dangerous stimulus
113
Q

how is glucocorticoid release controlled? (3 steps)

A

corticotropin-releasing factor from the hypothalamus –> adrenocorticotropic hormone from anterior pituitary –> glucocorticoid release from adrenal glands

114
Q

func + organ affected: mineralocorticoids

A

func: used in salt and water homeostasis

organ: most profound effects on kidneys

115
Q

what is the most noteworthy mineralocorticoid + its func (3)?

A

aldosterone

  1. increases sodium reabsorption in the distal convoluted tubule and collecting duct of the nephron
  2. water follows the sodium cations into the bloodstream, increasing blood volume and pressure
  3. decreases the reabsorption of potassium and hydrogen ions in these same segments of the nephron, promoting their excretion in the urine
116
Q

how do the effects of ADH contrast the effects of aldosterone?

A

ALDOSTERONE: increases sodium reabsorption, but water and sodium ions flow together, so plasma osmolarity remains unchanged

ADH: increases water reabsorption only, so plasma osmolarity decreases

117
Q

what system is aldosterone under the control of?

A

the renin-angiotensin-aldosterone system

118
Q

explain the parts of the renin-angiotensin-aldosterone system (5 + diagram)

A
  1. decreased blood pressure causes the juxtaglomerular cells of the kidney to secrete renin, which 2. cleaves an inactive plasma protein, angiotensinogen, to its active form, angiotensin I
  2. angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE) in the lungs
  3. angiotensin II stimulates the adrenal cortex to secrete aldosterone
  4. once blood pressure is restored, there is a decreased drive to stimulate renin release, serving as negative feedback mechanism for the system
119
Q

what organ makes the cortical sex hormones (androgens and estrogens)?

A

the adrenal glands

120
Q

why does adrenal testosterone play a small role in male physiology?

A

because the testes already secrete large quantities of androgens

121
Q

why are females more sensitive than males to cortical sex hormone production disorders? + example

A

the ovaries secrete far smaller amounts of androgens than the testes

example: certain enzyme deficiencies in the synthetic pathways of other adrenal cortex hormones result in excess androgen production in the adrenal cortex

this deficiency would have no phenotypic effects in a male fetus, but a female might be born with ambiguous or masculinized genitalia due to the presence of excess cortical sex hormones

122
Q

mnemonic: functions of the corticosteroids

A

the 3 S’s

Salt (mineralocorticoids)
Sugar (glucocorticoids)
Sex (cortical sex hormones)

123
Q

fun: adrenal medulla

A

responsible for the production of the sympathetic hormones epinephrine and norepinephrine

the specialized nerve cells in the medulla can secrete these compounds directly into the bloodstream

124
Q

what group of hormones do epinephrine and norepinephrine belong to?

A

catecholamines

125
Q

func (2): epinephrine

A
  1. increase the breakdown of glycogen to glucose (glycogenolysis) in both liver and muscle
  2. increase the basal metabolic rate
126
Q

func (3): both epinephrine and norepinephrine

A
  1. increase heart rate
  2. dilate the bronchi
  3. shunt blood flow to the systems that would be used in a sympathetic response (vasodilation of blood vessels leading to increased bloodflow to the skeletal muscle, heart, lungs, and brain; vasoconstriction decreases bloodflow to the gut, kidneys, and skin)
127
Q

impact of cortisol vs. catecholamines + relationship of the 2

A

CORTISOL = mediate long-term (slow) stress responses

CATECHOLAMINES = control short-term (fast) stress responses

cortisol increases the synthesis of catecholamines

128
Q

exocrine and endocrine funcs: pancreas

A

EXOCRINE: pancreas produces a number of digestive enzymes

ENDOCRINE: small clusters of hormone-producing cells are grouped together into islets of Langerhans throughout the pancreas

129
Q

func: exocrine tissues

A

secrete substances directly into ducts

130
Q

3 types of cells in islets in pancreas + what each type secretes

A

alpha cells –> glucagon

beat cells –> insulin

delta cells –> somatostatin

131
Q

diagram: pancreas anatomy

A
132
Q

when is glucagon secreted?

A

during fasting

133
Q

what happens when glucose levels are low? high?

A

LOW: glucagon increases glucose production by triggering glycogenolysis, gluconeogenesis, and the degradation of protein and fat

HIGH: glucagon release is inhibited

134
Q

what thing, other than low blood glucose concentrations, increases glucagon release?

A

certain GI hormones (like cholecystokinin and gastrin)

135
Q

mnemonic: high glucagon levels

A

GLUCAGON levels are high when GLUCOSE is GONE

136
Q

when is insulin secreted?

A

when blood glucose levels are high (it is antagonistic to glucagon)

137
Q

func (2): insulin

A
  1. induces muscle and liver cells to take up glucose and store it as glycogen for later use
  2. stimulates anabolic processes such as fat and protein synthesis
138
Q

diagram + summary: insulin relationship with blood glucose concentration

A

when blood glucose levels are high, insulin levels rise, and cells take up glucose from the blood

when blood glucose levels are low, insulin levels remain low as well

139
Q

cause + char: hypoglycemia

A

cause: excess insulin
char: low blood glucose concentration

140
Q

cause (3) + char: diabetes mellitus

A

cause:
1. underproduction of insulin
2. insufficient secretion of insulin
3. insensitivity to insulin

char: hyperglycemia (excess glucose in blood)

141
Q

what happens in the kidneys when there is excessive glucose? (3)

A
  1. excessive glucose in the filtrate overwhelms the nephron’s ability to reabsorb glucose, resulting in it being in the urine
  2. because it is an osmotically active particle and does not readily cross the cell membrane, glucose in the filtrate leads to excess excretion of water and an increase in urine volume
  3. so diabetes patients often have polyuria and polydipsia
142
Q

defn: polyuria vs. polydipsia

A

polyuria = increased frequency of urination

polydipsia = increased thirst

143
Q

cause + treatment: type I diabetes

A

insulin-dependent

cause: autoimmune destruction of the beta-cells of the pancreas, resulting in low or absent insulin production

treatment: regular injections of insulin to prevent hyperglycemia and to permit uptake of glucose into cells

144
Q

cause + treatment: type II diabetes

A

non-insulin dependent

cause: receptor-level resistance to the effects of insulin; partially inherited and partially environmental (like high-carb diets and obesity)

treatment: certain oral medicine can be taken to help the body better use the insulin it produces

145
Q

when do type II diabetics need to take insulin?

A

when their bodies can no longer control glucose levels, even when aided by medications

146
Q

how do the following things affect plasma glucose?

insulin

glucagon

growth hormone

glucocorticoids

epinephrine

A

insulin: decreases

glucagon, growth hormone, glucocorticoids, epinephrine: increases

147
Q

defn: somatostatin

A

an inhibitor of both insulin and glucagon secretion

148
Q

what 2 things stimulate somatostatin secretion?

A
  1. high blood glucose
  2. high amino acid concentrations
149
Q

what is somatostatin produced by and what impact does it have here in addition to its effects on insulin and glucagon?

A

produced by the hypothalamus where it decreases growth hormone secretion

150
Q

what do testes secrete in response to what?

A

secrete testosterone in response to stimulation by gonadotropins (LH and FSH)

151
Q

func (2): testosterone

A
  1. sexual differentiation of the male during gestation
  2. promotes the development and maintenance of secondary sex characteristics in male (axillary and pubic hair, deepening of the voice, and muscle growth)
152
Q

what do ovaries secrete in response to what?

A

estrogen and progesterone in response to gonadotropins

153
Q

func (2): estrogen

A
  1. development of the female reproductive system during gestation
  2. promotes the development and maintenance of secondary sex characteristics in females (axillary and pubic hair, breast growth, body fat redistribution)
154
Q

func (2): estrogen and progesterone

A
  1. govern the menstrual cycle
  2. govern pregnancy
155
Q

location: pineal gland

A

deep within the brain

156
Q

main func: pineal gland

A

secretes melatonin (which is involved in circadian rhythms)

157
Q

what impact does the retina have on the pineal gland?

A

the pineal gland receives projections directly from the retina, but is not involved in vision

hypothesis: the pineal gland responds to decreases in light intensity by releasing melatonin

158
Q

where (2) in the GI tract can endocrine tissue be found?

A
  1. the stomach
  2. the intestine
159
Q

what are 3 important GI peptides?

A
  1. secretin
  2. gastrin
  3. cholecystokinin
160
Q

what is the stimulus for the release of most GI peptides?

A

the presence of specific nutrients

161
Q

explain how kidneys play a role in water balance (2)

A
  1. ADH increases water permeability in the collecting duct
  2. the renin-angiotensin-aldosterone system increases sodium and water reabsorption in the distal convoluted tubule and collecting duct
162
Q

what produces + func + what is it secreted in response to: erythropoietin

A

produced by the kidneys

func: stimulates bone marrow to increase production of erythrocytes (red blood cells)

secreted in response to low oxygen levels in the blood

163
Q

func (3) + what releases it + what causes it to be released: atrial natriuretic peptide (ANP)

A

when cells in the atria (heart) are stretched from excess blood volume they release ANP

  1. released to help regulate salt and water balance
  2. promotes excretion of sodium and 3. thus increases urine volume
164
Q

what and why is ANP functionally antagonistic to?

A

to aldosterone because it lowers blood volume and pressure and has no effect on blood osmolarity

165
Q

location: thymus

A

located directly behind the sternum

166
Q

what does the thymus release and what is the function?

A

releases thymosin

func: important for proper T-cell development and differentiation

167
Q

what happens to the thymus and thymosin in adulthood?

A

the thymus atrophies
thymosin levels drop

168
Q

table: full list of hormones in their actions (see p. 205)

A

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