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
both a hormone & NT.
Nitric oxide (NO)
26
- 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.
Water-soluble
27
Amino acid derivatives, serotonin, histamine, and catecholamines (collective term):
Epi, NE, and dopamine.
28
— antidiuretic hormone (ADH) or vasopressin, oxytocin.
Peptides
29
insulin and growth hormone.
Proteins
30
prostaglandins and leukotrienes.
Eicosanoid hormones
31
• 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.
CONTROL OF HORMONE SECRETIONS
32
Release occurs in short bursts.
CONTROL OF HORMONE SECRETIONS
33
a. Example: adrenal medulla release of epinephrine.
Signals from nervous system
34
a. Example: blood Ca2+ affects parathyroid hormone.
Chemical changes in blood
35
a. Example: ACTH (adrenocorticotropic hormone) from pituitary stimulates release of cortisol from adrenal cortex.
Other hormones
36
ACTH
adrenocorticotropic hormone
37
• 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.
HYPOTHALAMUS AND PITUITARY
38
Serve as major link between nervous and endocrine systems.
HYPOTHALAMUS AND PITUITARY
39
ADH
antidiuretic hormone
40
• 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.
PITUITARY
41
Pituitary is attached to hypothalamus by stalk
infundibulum
42
SEVEN ANTERIOR PITUITARY HORMONES
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)
43
• 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.
HUMAN GROWTH HORMONE (hGH)
44
- most numerous cell in the anterior pituitary.
Released by somatotrophs
45
hGH (most abundant) promotes synthesis of insulin- like growth factors (IGFs)
somatomedins.
46
IGFs
insulin- like growth factors
47
Regulation - By hypothalamic hormones
a. Somatocrinin or Growth hormone-releasing hormone (GHRH) b. Somatostatin or Growth hormone-inhibiting hormone (GHIH)
48
Regulation - By blood glucose levels.
a. Low blood glucose levels → release of GHRH.
49
Growth hormone-releasing hormone (GHRH).
Somatocrinin
50
Growth hormone-inhibiting hormone (GHIH)
Somatostatin
51
a. Maintains muscle and bone mass. b. Promotes healing of injuries, tissue repair.
Stimulates protein synthesis.
52
a. Causes fat breakdown (“baby fat”) and release of fatty acids into blood. b. Breaks down liver glycogen → releases glucose into blood.
Makes “fuel” (ATP) available for growth.
53
• 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.
THYROID-STIMULATING HORMONE (TSH)
54
TRH
Thyrotropin-releasing hormone
55
T4
Thyroxine
56
T3
triiodothyronine
57
• 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.
FOLLICLE STIMULATING HORMONE (FSH) AND LUTEINIZING HORMONE (LH)
58
a. Starts egg production. b. Starts estrogen production from follicle cells.
FSH starts follicle development
59
a. Completion of egg and its ovulation. b. Secretion of progesterone + estrogen
LH stimulates formation of corpus luteum.
60
- FSH → sperm production in testes. - LH → release of testosterone from testes.
In males
61
- 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.
Regulation (feedback mechanism)
62
• 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
PROLACTIN (PRL)
63
Ejection of milk depends on
oxytocin
64
Hypersecretion → erectile dysfunction
Unknown function in males
65
Initiates and maintains milk production by mammary glands.
PROLACTIN (PRL)
66
• 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.
ADRENOCORTICOTROPIC HORMONE (ACTH)
67
Controls the production and secretion of glucocorticoids from adrenal cortex.
ADRENOCORTICOTROPIC HORMONE (ACTH)
68
CRH
Corticotrophin releasing hormone
69
from hypothalamus stimulates secretion of ACTH.
Corticotrophin releasing hormone (CRH)
70
Stress-related stimuli can also
stimulate ACTH release.
71
Glucocorticoids inhibit
CRH and ACTH release
72
- Corticotrophin releasing hormone (CRH) from hypothalamus stimulates secretion of ACTH. - Stress-related stimuli can also stimulate ACTH release. - Glucocorticoids inhibit CRH and ACTH release.
Regulation of ACTH
73
controlling effect on salt and water balance and helps control blood pressure.
Glucocorticoids
74
ACTH also used to regulate the level of steroid hormone cortisol, which is ___________
released from the adrenal gland.
75
controls blood sugar level, regulates metabolism, reduce inflammation, and assist with memory formulation.
Cortisol
76
• Small amounts in blood stream. • Excess amounts cause skin darkening.
MELANOCYTE STIMULATING HORMONE (MSH)
77
• 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.
POSTERIOR PITUITARY
78
Hormones made in hypothalamus pass down axons to posterior pituitary.
POSTERIOR PITUITARY
79
Two hormones released:
1. Oxytocin 2. Antidiuretic hormone (ADH)
80
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.
Oxytocin causes
81
under the brand name Pitocin – given to induce labor, increase uterine tone and control hemorrhage
synthetic oxytocin
82
vasopressin
Antidiuretic hormone (ADH)
83
a substance that decreases urine production.
Antidiuretic hormone (ADH)
84
a. Causes kidneys to retain more water. b. Causes vasoconstriction → increases blood pressure. c. Dehydration, pain, stress → increase ADH secretion.
Antidiuretic hormone (ADH) = vasopressin
85
causes urine output to increase more than tenfold (1 – 2 liters per day (normal) → 20 liters per day = leads to dehydration) = diabetes insipidus.
Absence of antidiuretic hormone
86
3P’s of diabetes
• Polyphagia – insatiable hunger. • Polyuria – excessive urination. • Polydipsia – excessive thirst.
87
insatiable hunger.
Polyphagia
88
excessive urination.
Polyuria
89
excessive thirst
Polydipsia
90
• 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)
THYROID GLAND
91
Location: inferior to larynx: two lobes
THYROID GLAND
92
Follicular cells produce hormones and store them in follicles.
a. Thyroxin (T4) b. Triiodothyronine (T3) – most active than T4.
93
most active than T4.
Triiodothyronine (T3)
94
Parafollicular cells (C-cells) produce
Calcitonin (CT)
95
• 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.
THYROID HORMONES: ACTIONS
96
increase basal metabolic rate, protein synthesis, and growth.
T4 (thyroxine) and T3
97
inhibits osteoclasts.
Calcitonin (CT)
98
Inhibits osteoclasts. Effects:
a. Strengthens bones. b. Decreases blood Ca2+
99
• 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.
PARATHYROID GLANDS
100
Small round masses in posterior of thyroid gland.
PARATHYROID GLANDS
101
PTH
parathyroid hormone
102
Release parathyroid hormone (PTH)
PARATHYROID GLANDS
103
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+
Increases blood Ca2+ in three (3) ways
104
dissolve bone → calcium release.
Osteoclasts
105
builds the bone
Osteoblast
106
• 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.
PANCREAS
107
Flattened organ in curve of duodenum.
PANCREAS
108
Alpha cells →
glucagon.
109
Beta cells →
insulin.
110
• 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.
ACTIONS OF INSULIN AND GLUCAGON
111
- Glucagon (hormone) stimulates liver to release glucose (through glycogenolysis) → increases blood glucose.
Low blood glucose stimulates glucagon release.
112
- Insulin (hormone) increases glucose transport into skeletal muscle and adipose cells → decreased blood glucose. - Insulin promotes amino acid uptake, protein synthesis, and lipid storage.
High glucose levels stimulate insulin release.
113
Hepatocytes
Liver cells
114
_____________stimulates alpha cells to secrete → GLUCAGON
Low blood glucose (hypoglycemia)
115
______________ stimulates beta cells to secrete → INSULIN
High blood glucose (hyperglycemia)
116
Convert glycogen into glucose
Glycogenolysis
117
Form glucose from certain amino acids
Gluconeogenesis
118
Speed conversion of glucose into glycogen
Glycogenesis
119
Speed synthesis of fatty acids
Lipogenesis
120
breakdown of glucose to produce energy (ATP).
Glycolysis
121
• 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.
ADRENAL GLANDS
122
Location: on top of kidneys.
ADRENAL GLANDS
123
Two separate gland structures:
• Adrenal cortex • Adrenal medulla
124
3 zones make steroids.
Adrenal cortex
125
Adrenal cortex
a. Outer zone → mineralocorticoids (aldosterone). b. Middle zone → glucocorticoids (cortisol) c. Inner zone → androgens (testosterone).
126
produces epinephrine (adrenalin) and norepinephrine.
Adrenal medulla
127
Outer zone (Zona Glomerulosa)
mineralocorticoids (aldosterone)
128
Middle zone (Zona Fasciculata)
glucocorticoids (cortisol)
129
Inner zone (Zona Reticularis)
androgens (testosterone)
130
• 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.
MINERALOCORTICOIDS (Zona Glomerulosa)
131
is the major form.
Aldosterone
132
- Stimulates Na+ and H2O reabsorption from urine to blood. - Stimulates excretion of K+ into urine.
Action of MINERALOCORTICOIDS
133
- 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.
Part of renin-angiotensin-aldosterone pathway (RAAS)
134
is an enzyme in the juxtaglomerular cells of the kidney that catalyzes the conversion Angiotensinogen to Angiotensin I
Renin (angiotensinogenase)
135
converts the hormone Angiotensin I to the active vasoconstrictor Angiotensin II.
Angiotensin Converting Enzymes (ACE)
136
ACE
Angiotensin Converting Enzymes
137
• 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).
GLUCOCORTICOID (CORTISOL) ACTIONS (Zona Fasciculata)
138
• 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.
ANDROGENS (Zona Reticularis)
139
Small amount secreted from adrenal cortex in both females and males.
ANDROGENS (Zona Reticularis)
140
a. Stimulate axillary and pubic hair growth. b. Contribute to adolescent growth spurt.
At puberty, in both genders, androgens
141
a. Contribute to libido. b. Are converted to estrogens by other body tissues.
In females, androgens
142
• 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.
ADRENAL MEDULLA
143
Inner portion of adrenal glands.
ADRENAL MEDULLA
144
Part of sympathetic (fight, fright, flight response) nervous system.
ADRENAL MEDULLA
145
• 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.
GONADS: OVARIES AND TESTES
146
Produce gametes: sperm and oocytes.
GONADS: OVARIES AND TESTES
147
___________ that inhibits FSH (follicle stimulating hormone) release.
Inhibin
148
(hormone) during pregnancy: facilitates birth.
Relaxin
149
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.
Relaxin
150
• 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.
PINEAL GLAND
151
Small gland attached to roof of third ventricle of brain.
PINEAL GLAND
152
regulates circadian rhythm
Produces melatonin
153
More released in darkness, less in sunlight.
Sets body’s biological clock.
154
• 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.
OTHER HORMONES
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thymosin – T lymphocytes.
Thymus
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- Gastrin - Glucose-dependent insulinotropic peptide (GIP) - Secretin - Cholecystokinin (CCK)
GI tract
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erythropoietin (EPO)
Kidney
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atrial natriuretic peptide (ANP)
Heart
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leptin (tells our brain that we have energy stored in our fat cells).
Adipose tissue
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human chorionic gonadotropin (hCG) (produced by syncytiotrophoblast, which is a component of the fertilized egg after conception)
Placenta
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hCG
human chorionic gonadotropin
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- 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.
Prostaglandins (PG) and leukotrienes (LT)
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• 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).
STRESS RESPONSES
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Three stages of STRESS RESPONSES
1. Initial “fight-or-flight” response. 2. Resistance (slower) → → → 3. Exhaustion (may occur eventually).
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Nerve mediated response
sympathetic.
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to raise blood pressure.
Aldosterone
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• 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.
AGING
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Some decrease in function with aging.
AGING
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• 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.
DISORDERS: HOMEOSTATIC IMBALANCES
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Pituitary dwarfism, gigantism, and acromegaly.
Pituitary Gland Disorders
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Defects in antidiuretic hormone (ADH) receptors or an inability to secrete ADH.
Diabetes Insipidus
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- Congenital hypothyroidism (cretenism) – hyposecretion of thyroid hormones that is present at birth. - Hypothyroidism during the adult years produces myxedema (severe form of hypothyroidism).
Thyroid Gland Disorders
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- 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.
Hyperthyroidism.
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an autoimmune disorder in which the person produces antibodies that mimic the action of TSH (thyroid stimulating hormone).
Grave’s disease
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A primary sign: enlarged thyroid, a peculiar edema behind the eyes called
exophthalmos.
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enlarged thyroid gland. It may be associated with hyperthyroidism, hypothyroidism, or euthyroidism.
Goiter
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Dietary iodine intake is
inadequate.
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• 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.
ADRENAL GLAND DISORDERS
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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.
Cushing’s syndrome
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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.
Addison’s disease (chronic adrenocortical insufficiency)
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Usually, benign tumors of the chromaffin cells of the adrenal medulla, cause hypersecretion of epinephrine and norepinephrine.
Pheochromocytomas
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• 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.
PANCREATIC ISLET DISORDERS
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caused by an inability to produce or use insulin.
Diabetes mellitus
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“polys”: polyuria (increase in urination), polydipsia (increase in thirst), & polyphagia (increase in eating).
Symptoms of Diabetes mellitus
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IDDM
insulin dependent diabetes mellitus/juvenile onset
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NIDDM
non-insulin dependent diabetes mellitus/adult onset
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— person’s immune system destroys the pancreatic beta cells. The pancreas produces little or no insulin.
Type 1 diabetes (IDDM)
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– diabetes arises not from a shortage of insulin but because target cells become less sensitive to it due to down-regulation of insulin receptors.
Type 2 diabetes (NIDDM)
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— condition in which a hormone made by the placenta prevents the body from using insulin effectively.
Gestational diabetes mellitus (GDM)