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ENDOCRINE SYSTEM Flashcards

1
Q

a molecule that is released in one part of the
body but regulates the activity and growth of cells in other parts of the body.

A

Hormone

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2
Q
  • Help regulate.
    a. Chemical composition and volume of internal
    environment (extracellular fluid).
    b. Metabolism and energy balance.
    c. Contraction of smooth and cardiac muscle fibes.
    d. Glandular secretions.
    e. Some immune system activities
  • Control growth and development.
  • Regulate operation of reproductive systems.
  • Help establish circadian rhythms.
A

Functions of Hormone

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3
Q

• Neurons release neurotransmitters at
synapses, neuromuscular or
neuroglandular
junctions.
• Effectors include
other neurons,
muscles, glands.
• Rapid responses from
effectors.

A

NERVOUS SYSTEM

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4
Q

• Releases hormones
into interstitial fluid
→ blood → general
circulation.
• Effectors: virtually
any type of body cell,
so can have
widespread effects
on diverse aspects of
metabolism.
• Slower, long-lasting
responses as
hormones linger in
blood.

A

ENDOCRINE SYSTEM

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5
Q

Neurons release
neurotransmitters at
synapses,
neuromuscular or
neuroglandular
junctions.

A

NERVOUS SYSTEM

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6
Q

Effectors include
other neurons,
muscles, glands.

A

NERVOUS SYSTEM

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7
Q

Effectors include
other neurons,
muscles, glands.

A

NERVOUS SYSTEM

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8
Q

Rapid responses from
effectors.

A

NERVOUS SYSTEM

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9
Q

Releases hormones
into interstitial fluid
→ blood → general
circulation.

A

ENDOCRINE SYSTEM

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10
Q

Effectors: virtually
any type of body cell,
so can have
widespread effects
on diverse aspects of
metabolism.

A

ENDOCRINE SYSTEM

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11
Q

Slower, long-lasting
responses as
hormones linger in
blood.

A

ENDOCRINE SYSTEM

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12
Q

• Secretion enters
interstitial fluid and
then → bloodstream.
• Stay in the body:
endo-
• Examples: all
hormones such as
growth hormone,
insulin, adrenalin,
estrogen,
testosterone.

A

ENDOCRINE GLANDS

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13
Q

Secretion enters
interstitial fluid and
then → bloodstream.

A

ENDOCRINE GLANDS

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14
Q

• Stay in the body:
endo-
• Examples: all
hormones such as
growth hormone,
insulin, adrenalin,
estrogen,
testosterone.

A

ENDOCRINE GLANDS

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15
Q

Secrete substances
that enter ducts.

A

EXOCRINE GLANDS

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16
Q

• Ultimately exit the
body (exo-)
• Examples: mucus,
saliva, and other
digestive secretions,
sweat, tears.

A

EXOCRINE GLANDS

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17
Q

• In endocrine glands
- Pituitary, thyroid, parathyroid, adrenal, pineal.
• In cells within organs that do produce hormones but also have other functions.
- Hypothalamus, thymus, pancreas, ovaries, testes, kidneys, stomach, liver, small intestine, skin, heart, adipose tissue, and placenta.

A

ENDOCRINE CELLS THAT MAKE HORMONES

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18
Q

In endocrine glands

A

Pituitary, thyroid, parathyroid, adrenal, pineal.

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19
Q

In cells within organs that do produce hormones but
also have other functions.

A

Hypothalamus, thymus, pancreas, ovaries, testes,
kidneys, stomach, liver, small intestine, skin, heart,
adipose tissue, and placenta.

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20
Q

• Hormones are carried in blood stream.
• But only certain cells can be affected by hormones.
- These target cells have 1000’s of receptors specific
for a particular hormone.
- Response determined by responding cell: different
cells may respond differently to the same hormone.
- Cell may have > 1 type of receptor, so can respond
to more than one hormone.

A

HORMONE ACTION

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21
Q

• Lipid-soluble
- Steroids, such as testosterone, estrogens.
- Thyroid hormones: T3 (triiodothyronine) and T4
(thyroxine) – synthesized by attaching iodine to amino
acid tyrosine.
- Nitric oxide (NO) – both a hormone & NT.

• Water-soluble
- Amino acid derivatives, serotonin, histamine, and
catecholamines (collective term): Epi, NE, and dopamine.
- Peptides: antidiuretic hormone (ADH) or vasopressin,
oxytocin.
- Proteins: insulin and growth hormone.
- Eicosanoid hormones: prostaglandins and leukotrienes.
• General action depends on chemistry.

A

HORMONE CHEMISTRY

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22
Q
  • Steroids, such as testosterone, estrogens.
  • Thyroid hormones: T3 (triiodothyronine) and T4
    (thyroxine) – synthesized by attaching iodine to amino acid tyrosine.
  • Nitric oxide (NO) – both a hormone & NT.
A

Lipid-soluble

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23
Q

such as testosterone, estrogens.

A

Steroids

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24
Q

T3 (triiodothyronine) and T4 (thyroxine) – synthesized by attaching iodine to amino acid tyrosine.

A

Thyroid hormones

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25
Q

both a hormone & NT.

A

Nitric oxide (NO)

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26
Q
  • Amino acid derivatives, serotonin, histamine, and
    catecholamines (collective term): Epi, NE, and dopamine.
  • Peptides: antidiuretic hormone (ADH) or vasopressin,
    oxytocin.
  • Proteins: insulin and growth hormone.
  • Eicosanoid hormones: prostaglandins and leukotrienes.
A

Water-soluble

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27
Q

Amino acid derivatives, serotonin, histamine, and
catecholamines (collective term):

A

Epi, NE, and dopamine.

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28
Q

— antidiuretic hormone (ADH) or vasopressin,
oxytocin.

A

Peptides

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29
Q

insulin and growth hormone.

A

Proteins

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30
Q

prostaglandins and leukotrienes.

A

Eicosanoid hormones

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31
Q

• Release occurs in short bursts.
• Regulated by:
- Signals from nervous system
a. Example: adrenal medulla release of epinephrine.
- Chemical changes in blood
a. Example: blood Ca2+ affects parathyroid hormone.
- Other hormones
a. Example: ACTH (adrenocorticotropic hormone) from pituitary stimulates release of cortisol from adrenal cortex.

A

CONTROL OF HORMONE SECRETIONS

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32
Q

Release occurs in short bursts.

A

CONTROL OF HORMONE SECRETIONS

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33
Q

a. Example: adrenal medulla release of epinephrine.

A

Signals from nervous system

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34
Q

a. Example: blood Ca2+ affects parathyroid hormone.

A

Chemical changes in blood

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35
Q

a. Example: ACTH (adrenocorticotropic hormone) from pituitary stimulates release of cortisol from adrenal cortex.

A

Other hormones

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36
Q

ACTH

A

adrenocorticotropic hormone

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37
Q

• Serve as major link between nervous and endocrine
systems.
• Hypothalamic cells synthesize:
- Many releasing and inhibiting hormones.
- Two hormones (oxytocin and ADH – antidiuretic
hormone) that are then stored and released from the
posterior pituitary.
• Anterior pituitary synthesizes 7 hormones.
• Regulate growth, development, metabolism, and
homeostasis.

A

HYPOTHALAMUS AND PITUITARY

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38
Q

Serve as major link between nervous and endocrine
systems.

A

HYPOTHALAMUS AND PITUITARY

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39
Q

ADH

A

antidiuretic hormone

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40
Q

• Located in depression in sphenoid bone just inferior
to the brain.
• Pituitary is attached to hypothalamus by stalk
(infundibulum).
• Pituitary has 2 lobes: anterior and posterior.

A

PITUITARY

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41
Q

Pituitary is attached to hypothalamus by stalk

A

infundibulum

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42
Q

SEVEN ANTERIOR PITUITARY HORMONES

A
  1. Human growth hormone (hGH)
  2. Thyroid-stimulating hormone (TSH)
  3. Follicle-stimulating hormone (FSH)
  4. Luteinizing hormone (LH)
  5. Prolactin
  6. Adrenocorticotropic hormone (ACTH)
  7. Melanocyte-stimulating hormone (MSH)
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43
Q

• Released by somatotrophs - most numerous cell in the anterior pituitary.
• hGH (most abundant) promotes synthesis of insulin-
like growth factors (IGFs) = somatomedins.
- Secreted by liver, muscle, cartilage, bone cells.
- Actions of IGFs much lie those of insulin.
• Regulation
- By hypothalamic hormones.
a. Growth hormone-releasing hormone (GHRH).
b. Growth hormone-inhibiting hormone (GHIH)
- By blood glucose levels.
a. Low blood glucose levels → release of GHRH.
• Actions of hGH
- Stimulates protein synthesis.
a. Maintains muscle and bone mass.
b. Promotes healing of injuries, tissue repair.
- Makes “fuel” (ATP) available for growth.
a. Causes fat breakdown (“baby fat”) and release of fatty
acids into blood.
b. Breaks down liver glycogen → releases glucose into
blood.

A

HUMAN GROWTH HORMONE (hGH)

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44
Q
  • most numerous cell in the anterior pituitary.
A

Released by somatotrophs

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45
Q

hGH (most abundant) promotes synthesis of insulin-
like growth factors (IGFs)

A

somatomedins.

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46
Q

IGFs

A

insulin- like growth factors

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47
Q

Regulation
- By hypothalamic hormones

A

a. Somatocrinin or Growth hormone-releasing hormone (GHRH)
b. Somatostatin or Growth hormone-inhibiting hormone (GHIH)

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48
Q

Regulation
- By blood glucose levels.

A

a. Low blood glucose levels → release of GHRH.

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49
Q

Growth hormone-releasing hormone (GHRH).

A

Somatocrinin

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50
Q

Growth hormone-inhibiting hormone (GHIH)

A

Somatostatin

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51
Q

a. Maintains muscle and bone mass.
b. Promotes healing of injuries, tissue repair.

A

Stimulates protein synthesis.

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52
Q

a. Causes fat breakdown (“baby fat”) and release of fatty acids into blood.
b. Breaks down liver glycogen → releases glucose into
blood.

A

Makes “fuel” (ATP) available for growth.

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53
Q

• Stimulates the formation and secretion of thyroid
hormones (T3, T4) by thyroid gland.
• Regulations of TSH (negative feedback).
- Low blood levels of T3, T4 →
- Hypothalamus → Thyrotropin-releasing hormone (TRH)
→
- TRH stimulates release of TSH (thyroid-stimulating
hormone).
- TSH stimulates thyroid production of T3, T4.

A

THYROID-STIMULATING HORMONE (TSH)

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54
Q

TRH

A

Thyrotropin-releasing hormone

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55
Q

T4

A

Thyroxine

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56
Q

T3

A

triiodothyronine

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57
Q

• In females
- FSH starts follicle development →
a. Starts egg production.
b. Starts estrogen production from follicle cells.
- LH stimulates formation of corpus luteum.
a. Completion of egg and its ovulation.
b. Secretion of progesterone + estrogen

• In males
- FSH → sperm production in testes.
- LH → release of testosterone from testes.

• Regulation (feedback mechanism).
- Gonadotrophin-releasing hormone (GnRH) from
hypothalamus → release of FSH or LH from anterior
pituitary.
- FSH → increases estrogen in females.
- LH → increases estrogen (E) and progesterone (P) in
females and testosterone (T) in males.
- High levels of these ovarian or testicular hormones (E, P, and T) suppress production of GnRH.

A

FOLLICLE STIMULATING HORMONE (FSH) AND
LUTEINIZING HORMONE (LH)

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58
Q

a. Starts egg production.
b. Starts estrogen production from follicle cells.

A

FSH starts follicle development

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59
Q

a. Completion of egg and its ovulation.
b. Secretion of progesterone + estrogen

A

LH stimulates formation of corpus luteum.

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60
Q
  • FSH → sperm production in testes.
  • LH → release of testosterone from testes.
A

In males

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61
Q
  • Gonadotrophin-releasing hormone (GnRH) from
    hypothalamus → release of FSH or LH from anterior
    pituitary.
  • FSH → increases estrogen in females.
  • LH → increases estrogen (E) and progesterone (P) in
    females and testosterone (T) in males.
  • High levels of these ovarian or testicular hormones (E, P, and T) suppress production of GnRH.
A

Regulation (feedback mechanism)

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62
Q

• Initiates and maintains milk production by mammary glands.
- Ejection of milk depends on oxytocin.
• Regulation
- Prolactin inhibiting hormone (PIH) suppresses prolactin release.
- High levels of estrogen → PRH (prolactin releasing
hormone → prolactin release.
• Unknown function in males
- Hypersecretion → erectile dysfunction

A

PROLACTIN (PRL)

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63
Q

Ejection of milk depends on

A

oxytocin

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64
Q

Hypersecretion → erectile dysfunction

A

Unknown function in males

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65
Q

Initiates and maintains milk production by mammary
glands.

A

PROLACTIN (PRL)

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66
Q

• Controls the production and secretion of
glucocorticoids from adrenal cortex.

• Regulation of ACTH
- Corticotrophin releasing hormone (CRH) from
hypothalamus stimulates secretion of ACTH.
- Stress-related stimuli can also stimulate ACTH release.
- Glucocorticoids inhibit CRH and ACTH release.
- Glucocorticoids – controlling effect on salt and water
balance and helps control blood pressure.
- ACTH also used to regulate the level of steroid hormone
cortisol, which is released from the adrenal gland.
a. Cortisol – controls blood sugar level, regulates
metabolism, reduce inflammation, and assist with
memory formulation.

A

ADRENOCORTICOTROPIC HORMONE (ACTH)

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67
Q

Controls the production and secretion of
glucocorticoids from adrenal cortex.

A

ADRENOCORTICOTROPIC HORMONE (ACTH)

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68
Q

CRH

A

Corticotrophin releasing hormone

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69
Q

from hypothalamus stimulates secretion of ACTH.

A

Corticotrophin releasing hormone (CRH)

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70
Q

Stress-related stimuli can also

A

stimulate ACTH release.

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71
Q

Glucocorticoids inhibit

A

CRH and ACTH release

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72
Q
  • Corticotrophin releasing hormone (CRH) from
    hypothalamus stimulates secretion of ACTH.
  • Stress-related stimuli can also stimulate ACTH release.
  • Glucocorticoids inhibit CRH and ACTH release.
A

Regulation of ACTH

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73
Q

controlling effect on salt and water balance and helps control blood pressure.

A

Glucocorticoids

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74
Q

ACTH also used to regulate the level of steroid hormone cortisol, which is ___________

A

released from the adrenal gland.

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75
Q

controls blood sugar level, regulates
metabolism, reduce inflammation, and assist with
memory formulation.

A

Cortisol

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76
Q

• Small amounts in blood stream.
• Excess amounts cause skin darkening.

A

MELANOCYTE STIMULATING HORMONE (MSH)

77
Q

• Hormones made in hypothalamus pass down axons
to posterior pituitary.
- Nerve impulses there cause release of hormones.

• Two hormones released:
- Oxytocin causes:
a. Smooth muscle contraction of uterus during
childbirth. (synthetic oxytocin – under the brand
name Pitocin – given to induce labor, increase
uterine tone and control hemorrhage).
b. Causes “letdown” of milk from glands to ducts.
c. Some sexual pleasure during sexual activity.
- Antidiuretic hormone (ADH) = vasopressin – a
substance that decreases urine production.
a. Causes kidneys to retain more water.
b. Causes vasoconstriction → increases blood
pressure.
c. Dehydration, pain, stress → increase ADH
secretion.

• Absence of antidiuretic hormone = causes urine
output to increase more than tenfold (1 – 2 liters per
day (normal) → 20 liters per day = leads to
dehydration) = diabetes insipidus.

A

POSTERIOR PITUITARY

78
Q

Hormones made in hypothalamus pass down axons
to posterior pituitary.

A

POSTERIOR PITUITARY

79
Q

Two hormones released:

A
  1. Oxytocin
  2. Antidiuretic hormone (ADH)
80
Q

a. Smooth muscle contraction of uterus during
childbirth. (synthetic oxytocin – under the brand
name Pitocin – given to induce labor, increase
uterine tone and control hemorrhage).
b. Causes “letdown” of milk from glands to ducts.
c. Some sexual pleasure during sexual activity.

A

Oxytocin causes

81
Q

under the brand name Pitocin – given to induce labor, increase uterine tone and control hemorrhage

A

synthetic oxytocin

82
Q

vasopressin

A

Antidiuretic hormone (ADH)

83
Q

a substance that decreases urine production.

A

Antidiuretic hormone (ADH)

84
Q

a. Causes kidneys to retain more water.
b. Causes vasoconstriction → increases blood
pressure.
c. Dehydration, pain, stress → increase ADH
secretion.

A

Antidiuretic hormone (ADH) = vasopressin

85
Q

causes urine output to increase more than tenfold (1 – 2 liters per day (normal) → 20 liters per day = leads to dehydration) = diabetes insipidus.

A

Absence of antidiuretic hormone

86
Q

3P’s of diabetes

A

• Polyphagia – insatiable hunger.
• Polyuria – excessive urination.
• Polydipsia – excessive thirst.

87
Q

insatiable hunger.

A

Polyphagia

88
Q

excessive urination.

89
Q

excessive thirst

A

Polydipsia

90
Q

• Location: inferior to larynx: two lobes
• Structure and function

  • Follicular cells produce hormones and store them in
    follicles.
    a. Thyroxin (T4)
    b. Triiodothyronine (T3) – most active than T4.
  • Parafollicular cells (C-cells) produce
    a. Calcitonin (CT)
A

THYROID GLAND

91
Q

Location: inferior to larynx: two lobes

A

THYROID GLAND

92
Q

Follicular cells produce hormones and store them in
follicles.

A

a. Thyroxin (T4)
b. Triiodothyronine (T3) – most active than T4.

93
Q

most active than T4.

A

Triiodothyronine (T3)

94
Q

Parafollicular cells (C-cells) produce

A

Calcitonin (CT)

95
Q

• T4 (thyroxine) and T3 increase basal metabolic rate,
protein synthesis, and growth.
- Blood level (T4 and T3) is controlled by TRH
(thyrotropin-releasing hormone from hypothalamus)
and TSH (thyroid-stimulating hormone from the
anterior pituitary gland).
- Increase in the body’s demand for ATP can also raise
blood levels (T4 and T3).

• Calcitonin (CT) inhibits osteoclasts.
- Inhibits osteoclasts. Effects:
a. Strengthens bones.
b. Decreases blood Ca2+
- Feedback control based on Ca2+ blood levels.

A

THYROID HORMONES: ACTIONS

96
Q

increase basal metabolic rate,
protein synthesis, and growth.

A

T4 (thyroxine) and T3

97
Q

inhibits osteoclasts.

A

Calcitonin (CT)

98
Q

Inhibits osteoclasts. Effects:

A

a. Strengthens bones.
b. Decreases blood Ca2+

99
Q

• Small round masses in posterior of thyroid gland.
• Release parathyroid hormone (PTH)
- Increases blood Ca2+ in three (3) ways.
a. Increases number and activity of osteoclasts that
break down bone/increasing bone resorption.
b. Slows loss of Ca2+ and Mg2+ (Magnesium) in
urine.
c. Promotes production of calcitriol (vitamin D) →
increases rate of Ca2+, Mg2+ and HPO42−
absorption in GI tract → increase blood Ca2+
- Decreases blood HPO42− (hydrogen phosphate) by
decreasing loss of HPO42− in urine.
- Increases loss of phosphate from the blood into
urine, and because more phosphate is lost in the
urine than what is gained from the bones, PTH
decreases the blood phosphate level and increases
the Ca2+ and Mg2+ level.

A

PARATHYROID GLANDS

100
Q

Small round masses in posterior of thyroid gland.

A

PARATHYROID GLANDS

101
Q

PTH

A

parathyroid hormone

102
Q

Release parathyroid hormone (PTH)

A

PARATHYROID GLANDS

103
Q

a. Increases number and activity of osteoclasts that
break down bone/increasing bone resorption.
b. Slows loss of Ca2+ and Mg2+ (Magnesium) in
urine.
c. Promotes production of calcitriol (vitamin D) →
increases rate of Ca2+, Mg2+ and HPO42−
absorption in GI tract → increase blood Ca2+

A

Increases blood Ca2+ in three (3) ways

104
Q

dissolve bone → calcium release.

A

Osteoclasts

105
Q

builds the bone

A

Osteoblast

106
Q

• Flattened organ in curve of duodenum.
• Mostly an exocrine organ that secretes digestive
enzymes.
• Endocrine cells in pancreatic islets (of Langerhans).
• Several cell types:
- Alpha cells → glucagon.
- Beta cells → insulin.

107
Q

Flattened organ in curve of duodenum.

108
Q

Alpha cells →

109
Q

Beta cells →

110
Q

• Low blood glucose stimulates glucagon release.
- Glucagon (hormone) stimulates liver to release
glucose (through glycogenolysis) → increases blood
glucose.

• High glucose levels stimulate insulin release.
- Insulin (hormone) increases glucose transport into
skeletal muscle and adipose cells → decreased blood
glucose.
- Insulin promotes amino acid uptake, protein
synthesis, and lipid storage.

• ANS also modulate hormone release.

A

ACTIONS OF INSULIN AND GLUCAGON

111
Q
  • Glucagon (hormone) stimulates liver to release
    glucose (through glycogenolysis) → increases blood
    glucose.
A

Low blood glucose stimulates glucagon release.

112
Q
  • Insulin (hormone) increases glucose transport into
    skeletal muscle and adipose cells → decreased blood
    glucose.
  • Insulin promotes amino acid uptake, protein
    synthesis, and lipid storage.
A

High glucose levels stimulate insulin release.

113
Q

Hepatocytes

A

Liver cells

114
Q

_____________stimulates alpha cells to secrete → GLUCAGON

A

Low blood glucose (hypoglycemia)

115
Q

______________ stimulates beta cells to secrete → INSULIN

A

High blood glucose (hyperglycemia)

116
Q

Convert glycogen into glucose

A

Glycogenolysis

117
Q

Form glucose from certain amino acids

A

Gluconeogenesis

118
Q

Speed conversion of glucose into glycogen

A

Glycogenesis

119
Q

Speed synthesis of fatty acids

A

Lipogenesis

120
Q

breakdown of glucose to produce energy (ATP).

A

Glycolysis

121
Q

• Location: on top of kidneys.
• Two separate gland structures:
- Adrenal cortex: 3 zones make steroids.
a. Outer zone → mineralocorticoids (aldosterone).
b. Middle zone → glucocorticoids (cortisol)
c. Inner zone → androgens (testosterone).
- Adrenal medulla: produces epinephrine (adrenalin)
and norepinephrine.

A

ADRENAL GLANDS

122
Q

Location: on top of kidneys.

A

ADRENAL GLANDS

123
Q

Two separate gland structures:

A

• Adrenal cortex
• Adrenal medulla

124
Q

3 zones make steroids.

A

Adrenal cortex

125
Q

Adrenal cortex

A

a. Outer zone → mineralocorticoids (aldosterone).
b. Middle zone → glucocorticoids (cortisol)
c. Inner zone → androgens (testosterone).

126
Q

produces epinephrine (adrenalin) and norepinephrine.

A

Adrenal medulla

127
Q

Outer zone (Zona Glomerulosa)

A

mineralocorticoids (aldosterone)

128
Q

Middle zone (Zona Fasciculata)

A

glucocorticoids (cortisol)

129
Q

Inner zone (Zona Reticularis)

A

androgens (testosterone)

130
Q

• Aldosterone is the major form.

• Action:
- Stimulates Na+ and H2O reabsorption from urine to
blood.
- Stimulates excretion of K+ into urine.

• Part of renin-angiotensin-aldosterone pathway
(RAAS).
- Decreased BP → release of renin from kidney.
- Renin causes angiotensinogen → angiotensin I
- In lungs, angiotensin converting enzyme (ACE) causes
angiotensin → angiotensin II.
- Angiotensin II stimulates aldosterone release.

A

MINERALOCORTICOIDS (Zona Glomerulosa)

131
Q

is the major form.

A

Aldosterone

132
Q
  • Stimulates Na+ and H2O reabsorption from urine to
    blood.
  • Stimulates excretion of K+ into urine.
A

Action of MINERALOCORTICOIDS

133
Q
  • Decreased BP → release of renin from kidney.
  • Renin causes angiotensinogen → angiotensin I
  • In lungs, angiotensin converting enzyme (ACE) causes angiotensin → angiotensin II.
  • Angiotensin II stimulates aldosterone release.
A

Part of renin-angiotensin-aldosterone pathway
(RAAS)

134
Q

is an enzyme in the juxtaglomerular cells of the kidney that catalyzes the conversion Angiotensinogen
to Angiotensin I

A

Renin (angiotensinogenase)

135
Q

converts the hormone Angiotensin I to the active vasoconstrictor Angiotensin II.

A

Angiotensin Converting Enzymes (ACE)

136
Q

ACE

A

Angiotensin Converting Enzymes

137
Q

• Increases rate of protein breakdown.
• Stimulates liver formation of glucose.
• Breaks down triglycerides in adipose.
• Anti-inflammatory effects.
- Inhibit white blood cells.
• Depresses immune system.
• Regulated by negative feedback: CRH (corticotrophin releasing hormone) and ACTH (adrenocorticotropic hormone).

A

GLUCOCORTICOID (CORTISOL) ACTIONS (Zona Fasciculata)

138
Q

• Small amount secreted from adrenal cortex in both
females and males.
- At puberty, in both genders, androgens
a. Stimulate axillary and pubic hair growth.
b. Contribute to adolescent growth spurt.
- In females, androgens
a. Contribute to libido.
b. Are converted to estrogens by other body
tissues.

A

ANDROGENS (Zona Reticularis)

139
Q

Small amount secreted from adrenal cortex in both
females and males.

A

ANDROGENS (Zona Reticularis)

140
Q

a. Stimulate axillary and pubic hair growth.
b. Contribute to adolescent growth spurt.

A

At puberty, in both genders, androgens

141
Q

a. Contribute to libido.
b. Are converted to estrogens by other body
tissues.

A

In females, androgens

142
Q

• Inner portion of adrenal glands.
• Part of sympathetic (fight, fright, flight response)
nervous system.
- Consists of sympathetic postganglionic cells.
- Stimulated by preganglionic sympathetic neurons.
- Releases epinephrine and norepinephrine.
- Actions mimic sympathetic nerves in stress.
a. Increases heart rate and blood pressure.
b. Increases blood glucose, dilates airways.

A

ADRENAL MEDULLA

143
Q

Inner portion of adrenal glands.

A

ADRENAL MEDULLA

144
Q

Part of sympathetic (fight, fright, flight response)
nervous system.

A

ADRENAL MEDULLA

145
Q

• Produce gametes: sperm and oocytes.

• Produce hormones.
- Testosterone in males.
- Estrogen and progesterone in females.
- Inhibin that inhibits FSH (follicle stimulating
hormone) release.
- Relaxin (hormone) during pregnancy: facilitates
birth.
- Relaxin – facilitates birth process by causing softening and lengthening of the cervix and pubic symphysis. It also inhibits the contraction of the uterus and important in determining the timing of delivery.

• Regulated by:
- GnRH (gonadotropin releasing hormone) from
hypothalamus.
- FSH (follicle stimulating hormone) + LH (luteinizing
hormone) from anterior pituitary.

A

GONADS: OVARIES AND TESTES

146
Q

Produce gametes: sperm and oocytes.

A

GONADS: OVARIES AND TESTES

147
Q

___________ that inhibits FSH (follicle stimulating
hormone) release.

148
Q

(hormone) during pregnancy: facilitates
birth.

149
Q

facilitates birth process by causing softening and
lengthening of the cervix and pubic symphysis. It also
inhibits the contraction of the uterus and important in determining the timing of delivery.

150
Q

• Small gland attached to roof of third ventricle of
brain.
• Produces melatonin (regulates circadian rhythm).
• Sets body’s biological clock.
- More released in darkness, less in sunlight.

A

PINEAL GLAND

151
Q

Small gland attached to roof of third ventricle of
brain.

A

PINEAL GLAND

152
Q

regulates circadian rhythm

A

Produces melatonin

153
Q

More released in darkness, less in sunlight.

A

Sets body’s biological clock.

154
Q

• Thymus: thymosin – T lymphocytes.

• GI tract
- Gastrin
- Glucose-dependent insulinotropic peptide (GIP_
- Secretin
- Cholecystokinin (CCK)

• Kidney: erythropoietin (EPO)

• Heart: atrial natriuretic peptide (ANP).

• Adipose tissue: leptin (tells our brain that we have
energy stored in our fat cells).

• Placenta: human chorionic gonadotropin (hCG)
(produced by syncytiotrophoblast, which is a
component of the fertilized egg after conception).

• Prostaglandins (PG) and leukotrienes (LT)
- Derived from fatty acids.
- Act locally in most tissues and released from most
body cells.
- LTs stimulate white blood cells and mediate
inflammation.
- PGs affect many visceral functions, modulate
inflammation, promote fever, and intensify pain.

A

OTHER HORMONES

155
Q

thymosin – T lymphocytes.

156
Q
  • Gastrin
  • Glucose-dependent insulinotropic peptide (GIP)
  • Secretin
  • Cholecystokinin (CCK)
157
Q

erythropoietin (EPO)

158
Q

atrial natriuretic peptide (ANP)

159
Q

leptin (tells our brain that we have energy stored in our fat cells).

A

Adipose tissue

160
Q

human chorionic gonadotropin (hCG)
(produced by syncytiotrophoblast, which is a
component of the fertilized egg after conception)

161
Q

hCG

A

human chorionic gonadotropin

162
Q
  • Derived from fatty acids.
  • Act locally in most tissues and released from most
    body cells.
  • LTs stimulate white blood cells and mediate
    inflammation.
  • PGs affect many visceral functions, modulate
    inflammation, promote fever, and intensify pain.
A

Prostaglandins (PG) and leukotrienes (LT)

163
Q

• Response to stressors

• When successful leads to extra physiological capacity and long-term adaptation.

• Three stages:
1. Initial “fight-or-flight” response.
- Nerve mediated response - sympathetic.
- Aldosterone: to raise blood pressure.
2. Resistance (slower) → → →
3. Exhaustion (may occur eventually).

A

STRESS RESPONSES

164
Q

Three stages of STRESS RESPONSES

A
  1. Initial “fight-or-flight” response.
  2. Resistance (slower) → → →
  3. Exhaustion (may occur eventually).
165
Q

Nerve mediated response

A

sympathetic.

166
Q

to raise blood pressure.

A

Aldosterone

167
Q

• Some decrease in function with aging.
- Loss of negative feedback sensitivity so decline in
circulating thyroid hormones.
- PTH (parathyroid hormone) levels rise → loss of bone mass.
- Less glucocorticoid production.
- Slower release of insulin.
- Thymus declines after puberty.
- Ovarian response to gonadotropins stops.
- Slow decline in testosterone production.

168
Q

Some decrease in function with aging.

169
Q

• Pituitary Gland Disorders
- Pituitary dwarfism, gigantism, and acromegaly.

• Diabetes Insipidus
- Defects in antidiuretic hormone (ADH) receptors or
an inability to secrete ADH.

• Thyroid Gland Disorders
- Congenital hypothyroidism (cretenism) –
hyposecretion of thyroid hormones that is present at
birth.
- Hypothyroidism during the adult years produces
myxedema (severe form of hypothyroidism).

• Hyperthyroidism.
- Grave’s disease – an autoimmune disorder in which
the person produces antibodies that mimic the
action of TSH (thyroid stimulating hormone).
- The antibodies continually stimulate the thyroid
gland to grow and produce thyroid hormones.
- A primary sign: enlarged thyroid, a peculiar edema
behind the eyes called exophthalmos.

• Goiter – enlarged thyroid gland. It may be associated with hyperthyroidism, hypothyroidism, or
euthyroidism.
- Dietary iodine intake is inadequate.

A

DISORDERS: HOMEOSTATIC IMBALANCES

170
Q

Pituitary dwarfism, gigantism, and acromegaly.

A

Pituitary Gland Disorders

171
Q

Defects in antidiuretic hormone (ADH) receptors or
an inability to secrete ADH.

A

Diabetes Insipidus

172
Q
  • Congenital hypothyroidism (cretenism) –
    hyposecretion of thyroid hormones that is present at
    birth.
  • Hypothyroidism during the adult years produces
    myxedema (severe form of hypothyroidism).
A

Thyroid Gland Disorders

173
Q
  • Grave’s disease – an autoimmune disorder in which
    the person produces antibodies that mimic the
    action of TSH (thyroid stimulating hormone).
  • The antibodies continually stimulate the thyroid
    gland to grow and produce thyroid hormones.
  • A primary sign: enlarged thyroid, a peculiar edema
    behind the eyes called exophthalmos.
A

Hyperthyroidism.

174
Q

an autoimmune disorder in which
the person produces antibodies that mimic the
action of TSH (thyroid stimulating hormone).

A

Grave’s disease

175
Q

A primary sign: enlarged thyroid, a peculiar edema
behind the eyes called

A

exophthalmos.

176
Q

enlarged thyroid gland. It may be associated
with hyperthyroidism, hypothyroidism, or
euthyroidism.

177
Q

Dietary iodine intake is

A

inadequate.

178
Q

• Cushing’s syndrome – hypersecretion of cortisol by
the adrenal cortex.
- Causes: tumor of the adrenal gland that secretes
cortisol, or elsewhere that secretes ACTH
(adrenocorticotropic hormone).
- Characterized by breakdown of muscle proteins and
redistribution of body fat, resulting in spindly arms
and legs accompanied by a rounded “moon face”,
buffalo hump” on the back, and pendulous (hanging)
abdomen.

• Addison’s disease (chronic adrenocortical
insufficiency) – hyposecretion of glucocorticoids and
aldosterone causes.
- The skin may have a “bronzed” appearance.
- Treatment consists of replacing glucocorticoids and
mineralocorticoids and increasing sodium in the diet.

• Pheochromocytomas
- Usually, benign tumors of the chromaffin cells of the
adrenal medulla, cause hypersecretion of
epinephrine and norepinephrine.

A

ADRENAL GLAND DISORDERS

179
Q

hypersecretion of cortisol by
the adrenal cortex.

  • Causes: tumor of the adrenal gland that secretes
    cortisol, or elsewhere that secretes ACTH
    (adrenocorticotropic hormone).
  • Characterized by breakdown of muscle proteins and
    redistribution of body fat, resulting in spindly arms
    and legs accompanied by a rounded “moon face”,
    buffalo hump” on the back, and pendulous (hanging)
    abdomen.
A

Cushing’s syndrome

180
Q

hyposecretion of glucocorticoids and
aldosterone causes.

  • The skin may have a “bronzed” appearance.
  • Treatment consists of replacing glucocorticoids and
    mineralocorticoids and increasing sodium in the diet.
A

Addison’s disease (chronic adrenocortical
insufficiency)

181
Q

Usually, benign tumors of the chromaffin cells of the
adrenal medulla, cause hypersecretion of
epinephrine and norepinephrine.

A

Pheochromocytomas

182
Q

• Diabetes mellitus – caused by an inability to produce or use insulin.
- Symptoms: “polys”: polyuria (increase in urination),
polydipsia (increase in thirst), & polyphagia (increase
in eating).
- Type 1 diabetes (IDDM – insulin dependent diabetes
mellitus/juvenile onset) – person’s immune system
destroys the pancreatic beta cells. The pancreas
produces little or no insulin.
- Type 2 diabetes (NIDDM – non-insulin dependent
diabetes mellitus/adult onset) – diabetes arises not
from a shortage of insulin but because target cells
become less sensitive to it due to down-regulation of
insulin receptors.
- Gestational diabetes mellitus (GDM) – condition in
which a hormone made by the placenta prevents the
body from using insulin effectively.

A

PANCREATIC ISLET DISORDERS

183
Q

caused by an inability to produce
or use insulin.

A

Diabetes mellitus

184
Q

“polys”:
polyuria (increase in urination),
polydipsia (increase in thirst), &
polyphagia (increase in eating).

A

Symptoms of Diabetes mellitus

185
Q

IDDM

A

insulin dependent diabetes mellitus/juvenile onset

186
Q

NIDDM

A

non-insulin dependent
diabetes mellitus/adult onset

187
Q

— person’s immune system destroys the pancreatic beta cells. The pancreas produces little or no insulin.

A

Type 1 diabetes (IDDM)

188
Q

– diabetes arises not from a shortage of insulin but because target cells become less sensitive to it due to down-regulation of insulin receptors.

A

Type 2 diabetes (NIDDM)

189
Q

— condition in which a hormone made by the placenta prevents the body from using insulin effectively.

A

Gestational diabetes mellitus (GDM)

ANAPHY (17 decks)

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