endocrine and reproductive exam Flashcards
(441 cards)
1
Q
function involves the secretion of hormones
A
endocrine
2
Q
a chemical substance that is secreted into the circulation in small
amounts and delivered to target tissues where they produce physiologic responses
distributed everywhere, but only have an effect where there is a receptor expressed
synthesized and secreted by endocrine cells, usually found in
endocrine glands
A
hormone
3
Q
what do hormones do
A
Hormones Help Maintain Homeostasis
Some function of
Hormones:
* Growth
* Development
* Reproduction
* Blood pressure
* Ion concentration and
osmolarity
* Behavior
4
Q
3 classes of hormones
A
- peptide/protein hormones
- amine hormones
- steroid hormones
5
Q
- Chain of amino acids
- Most hormones are this
- Rapid response
- insulin, glucagon, ghrelin, leptin
A
Peptide / Protein hormones
6
Q
- Derivatives of the amino acid tyrosine
- Catecholamines (epinephrine, norepinephrine, and dopamine) and thyroid hormones
- Catecholamines have a rapid response, but Thyroid Hormones have a Slow Response
A
amine hormones
7
Q
- Derivatives of cholesterol
- Cortisol, aldosterone, estradiol/estriol/estrone, progesterone, testosterone, and 1,25-
dihydroxycholecalciferol (aka calcitriol, active vit. D) - Slow Response
A
steroid hormones
8
Q
location of peptides and catecholamines receptors and rate of metabolism
A
location: plasma membrane
metabolism: fast (minutes)
9
Q
location of steroid and thyroid hormone and rate of metabolism
A
location: intracellular
metabolism: slow (hours/days)
10
Q
what receptors do steroid hormones bind to and why is it possible
A
Steroid hormones are lipophilic
and may diffuse across the
plasma membrane
bind to:
- receptors in the cytosol (cytosolic
receptors)
- receptors in the nucleus (nuclear
receptors)
11
Q
Hormones that bind to intracellular receptors are typically ________, allowing them to diffuse directly through the cell membrane.
examples:
A
lipid soluble
Examples: Steroid hormones (e.g., estrogen, testosterone, cortisol), thyroid hormone
12
Q
Hormones that bind to extracellular receptors are usually _______, requiring a cell surface receptor to transmit the signal inside the cell.
Examples:
A
water soluble
Examples: Protein hormones (e.g., insulin, growth hormone), peptide hormones
13
Q
peptide/protein hormones are synthesized as polypeptides from _______
A
amino acids
14
Q
amine hormones like epinephrine and norepinephrine are derived from _______
A
the amino acid tyrosine
15
Q
steroid hormones are derived from _________
A
cholesterol
16
Q
how to maintain homeostasis
A
the secretion of hormones must be
turned on and off as needed
Control of Plasma Concentrations
of Hormones is induced by the
concentration of hormones or
substances, (or some condition)
17
Q
presence of hormone or substance inhibits the hormone production and release
A
negative feedback
18
Q
Presence of hormone or substance increases hormone production and release.
A
positive feedback
19
Q
Examples of positive feedback
A
- depolarization induces more sodium permeability and more polarization
- Oxytocin, the cervix, and childbirth
20
Q
the ____________regulates the functions of the thyroid, adrenal, and reproductive glands and also controls growth, milk production and ejection, and osmoregulation
A
hypothalamic-pituitary unit
21
Q
the ______pituitary lobe is
derived from neural tissue
originating in the hypothalamus.
A
posterior
22
Q
The _______ pituitary is a
collection of endocrine cells
activated by hypothalamic tropic
hormones
A
anterior
23
Q
The hypothalamus releases several hormones including:
A
corticotropin-releasing hormone (CRH)
growth hormone-releasing hormone (GHRH)
gonadotropin-releasing hormone (GnRH)
Thyrotropin-releasing hormone (TRH)
dopamine
somatostatin
24
Q
how are hormones released from the hypothalamus
A
The hypothalamus produces these hormones which then travel to the pituitary gland via a network of blood vessels, stimulating the pituitary to release corresponding hormones into the bloodstream
25
anterior pituitary hormones
TSH
FSH
LH
ACTH
growth hormone
prolactin
26
posterior pituitary hormones
vasopressin (ADH)
oxytocin
27
* Released by somatotrophs of the anterior pituitary
* Protein structure of 191 amino acids (structurally related to prolactin)
* secreted throughout life.
* Most important hormone for normal growth to adult stature.
* Increases protein synthesis
* Mobilizes fatty acids from storage
* Antagonizes effects of insulin
* Stimulates gluconeogenesis in the liver (insulin stimulates glucose storage as glycogen)
growth hormone
28
- decreased glucose concentration
- decreased free fatty acid concentration
- arginine
- fasting or starvation
- hormones of puberty (estrogen/testosterone)
- exercise
- stress
- stage 3 and 4 sleep alpha adrenergic agonists
growth hormone stimulatory factors
29
- increased glucose concentration
- increased free fatty acid concentration
- obesity
- senescence
- somatostatin
- somatomedins
- growth hormone beta adrenergic agonists
- pregnancy
growth hormone inhibitory factors
30
how is growth hormone secreted
in a pulsatile pattern with bursts of secretion every 2 hours
31
when is the largest secretory growth hormone burst
within 1 hour of falling asleep
32
is growth hormone rate constant over a lifetime
no
33
steady increase of growth hormone from ______ to ________
birth to early childhood
34
when is there a dramatic boost of growth hormone that is responsible for a growth spurt
puberty
35
growth spurt in puberty triggered by
estrogen or testosterone
36
what does growth hormone releasing hormone (GHRH) from hypothalamus to anterior pituitary do
triggers release of growth hormone: stimulates somatotrophs to synthesize and release more growth hormone
37
- secreted by hypothalamus
- inhibits growth hormone
somatostatin (SRIF)
38
growth hormone regulation occurs by negative feedback in 3 ways
1. GHRH decreases release of GHRH
2. Somatomedins: byproducts of GHRH activity decrease release from pituitary
3. Both of these trigger somatostatin
release from the hypothalamus
39
specific effects of GH occur through growth factor byproducts called __________. they are insulin like growth factors and production of these peptides is triggered by GH
somatomedin
40
what are the specific effects of growth hormone
1. anti insulin effect
2. increased protein synthesis and organ growth
3. increased linear growth
41
growth hormone deficiency can lead to
dwarfism
42
what if you have a growth hormone secreting tumor
acromegaly
43
excess levels of GH prior to puberty (linear growth)
gigantism
44
what happens with gigantism after puberty
nonlinear enlargement of bones, increased organ size,
enlargement of tongue, facial features, and insulin resistance
45
what is the treatment for excess GH
somatostatin analogs like
octreotide (inhibits growth hormone secretion)
46
Major hormone responsible for milk production during lactation and
pregnancy
also involved in breast development
prolactin
47
prolactin is produced in the anterior pituitary by endocrine cells called _________
lactotrophs
48
what stimulates prolactin secretion from the anterior pituatary
thyrotropin releasing hormone (TRH)
49
if not pregnant or lactating, prolactin is inhibited by ______ released from hypothalamus
dopamine
50
dopamine comes from 3 sources:
1. hypothalamic neurons that secrete dopamine into the hypothalamic-hypophysial portal veins
2. small amount from posterior lobe
3. small amount from cells in anterior lobe
51
major stimulants for prolactin secretion
pregnancy and breast feeding
52
what causes a dramatic increase in prolactin
suckling
53
prolactin inhibits its own secretion by stimulating _______ release from the hypothalamus
dopamine
54
dopamine agonist that can inhibit milk production
bromocriptine
55
is stress a stimulatory factor of prolactin
yes
56
prolactin actions
1. breast development/mammary ducts
2. pregnancy: mammary alveoli which produces milk
3. induces synthesis of milk components
4. inhibits ovulation
57
what to keep in mind about antipsychotics
block dopamine receptors and may cause lactation (galactorrhea)
58
does the posterior pituitary synthesize oxytocin and ADH?
no it only secretes them
59
involved in milk ejection reflex of nursing mothers and emotional bonding
oxytocin
60
involved in regulation of water balance and osmolarity
ADH (vasopressin)
61
* Regulation of body fluid osmolarity
* Secreted by the posterior pituitary in response to an increased in serum osmolarity
* Increases reabsorption in the late
distal tubule and collecting duct
* Potent vasoconstrictor
- increases BP
ADH (vasopressin)
62
primary stimulus for increasing ADH secretion
increased plasma osmolarity
63
sensation of a decrease in blood pressure signals to the hypothalamus to ________
secrete ADH
64
what inhibits ADH
- decreased serum osmolarity
- ethanol
65
* Has effects at kidney and vascular
smooth muscle
* Vasopressin V2 receptor binding
increases water permeability at late
distal tubule and collecting duct by
insertion of aquaporin 2
* Vasopressin V1 receptor binding
causes contraction of vascular smooth muscle
* Vasopressin is a powerful vasoconstrictor
actions of ADH
66
what disease can you develop if you done make ADH
diabetes insipidus (you pee more)
67
failure of pituitary to release ADH
central diabetes insipidus
68
cells of the collecting duct are not responsive to ADH
nephrogenic (kidneys) diabetes insipidus
69
* Produce small volumes of concentrated urine
* Excess ADH is secreted from an autonomous site. Often associated with tumors.
syndrome of inappropriate ADH (SIADH)
70
* Produces the “letdown” reflex: Stimulates myoepithelial cells lining
milk ducts to eject milk during suckling
* Sight, sound, or smell of an infant may trigger release and
letdown.
* Causes uterine contractions at low concentrations
oxytocin
71
how is oxytocin release synthesized
- Major stimulus is suckling
- Sensory neurons in the nipple
transmit signals to the
hypothalamus.
72
what control oxytocin release (positive feedback)
dilation of the cervix
73
how does oxytocin analog Pitocin play a role in labor
labor inducer
74
synthesized and secreted by epithelial cells of the thyroid
gland
thyroid hormones
75
Epithelial cells surround a follicle
containing colloid, mainly comprised of a glycoproteins called
thyroglobulin
76
role of thyroglobulin
77
functions of thyroid
- growth and development
- Increases basal metabolic rate
- Increased glucose uptake into cells, ATP production and hydrolysis, temperature
- Increased lipid metabolism (and fatty acid production)
78
two active thyroid hormones
* Thyroxine (T4): 4 iodines
* Triiodothyronine (T3): 3 iodines
79
which thyroid hormone is more active
T3
80
which thyroid hormone is more abundant
T4
81
how does the body deal with the difference in T3 and T4
Target tissues convert T4 to T3
82
why are thyroid hormones capable
of diffusing into cells and binding cytosolic or nuclear receptors
Lipophilic (hydrophobic, nonpolar) structure
83
what is thyroid hormone synthesized by
follicular epithelial cells that are arranged in circular follicles
84
colloid is primarily composed of a protein called
thyroglobulin
85
Thyroglobulin is a protein that contains large quantities
of the amino acid
tyrosine
86
Thyroglobulin is synthesized in the follicle cells and then
moved to
the colloid lumen
87
________ are transported via sodium cotransport into the follicle cells and then into the colloid lumen
iodide anions
88
thyroid peroxidase catalyzes the following steps:
* In the lumen, I- is oxidized to I2 by thyroid peroxidase
* Thyroid peroxidase catalyzes the formation of monoiodotyrosine (MIT) and diiodotyrosine (DIT)
* DIT combines with DIT to form T4 (faster), or DIT combines with MIT to form T3.
89
* NOTE that _______ blocks thyroid peroxidase function and there by blocks thyroid synthesis
propylthiouracil (PTU)
90
what happens after the formation of T3 and T4 on thyroglobulin
* activation will cause the complex to move into the cell where it is cleaved and then secreted as active thyroid hormone.
* MIT and DIT is recycled.
91
Most T3 and T4 hormone is transported in blood bound to
thyroxinebinding globulin (TBG)
- small amount bound to albumin
- smaller amount unbound and free floating
92
what T3 and T4 is active
only free, unbound T3 and T4
- This means that the protein-
bound form must dissociate before diffusing into cells
93
what can increase levels of free T3 and T4
Because TGB is made in the liver, liver failure can reduce TGB, which increases levels of free T3 and T4. Consequently, negative feedback will result in inhibited synthesis
94
T4 is converted to T3 in target cells by
the enzyme 5’-iodinase
95
what happens to enzyme 5’-iodinase during starvation
it is inhibited which decreases metabolic rates (protective against starvation)
96
what happens to the brain form of enzyme 5’-iodinase during starvation
metabolic processes are not inhibited in the brain during starvation
97
is a tripeptide synthesized and released by cells of the hypothalamus
thyroid releasing hormone
98
a protein released by the pituitary in response to TRH.
thyroid stimulating hormone (TSH)
99
causes growth of the thyroid gland and secretion of thyroid hormones
TSH
100
an overgrowth of the thyroid gland
goiter
101
The presence of ______ mediates the negative feedback effect (possible because the anterior pituitary has the thyroid iodinase enzyme to
convert T4 to T3).
free T3
102
Binding of T3 with receptors
occurs in the target cell _____
nucleus
103
thyroid effects on Basal Metabolic Rate (BMR) and Metabolism
* Increased oxygen consumption and increased energy and resource use
* Increased glucose absorption and mobilization, increased ATP production (uses oxygen and glucose), and then increased Na/K ATPase activity (burns ATP).
* Increased protein synthesis, including key metabolic enzymes, and protein degradation (net
decrease in muscle mass).
* Increased protein production and degradation is a futile cycle that increases O2 consumption in
hyperthyroidism
* Increased lipid metabolism (and fatty acid production)
* Increased BMR leads to higher body temperature and heat intolerance
104
thyroid effects on cardiovascular and respiratory
* Increased ventilation
* Increased cardiac output by induction of beta-adrenergic receptor upregulation.
105
thyroid effects on growth
Thyroid hormones work synergistically with growth hormones and somatomedins to promote bone formation
106
thyroid effects on Central Nervous System (CNS) and Autonomic activity
* Thyroid hormones interact with the sympathetic nervous system
* Thyroid hormones are responsible for normal maturation of the CNS.
* Beta blockers (-olol drugs) may be effective in treating some symptoms of hyperthyroidism
107
autoimmune disease (Type II hypersensitivity)
* Increased Thyroid Immunoglobulins activate TSH receptors. Thyroid immunoglobulins are antibody proteins made by the immune system. Antibodies usually attack and cause destruction of their target antigen (such as a virus), but in this case, they are targeting TSH receptors on the Thyroid gland and increasing their activity.
graves disease
108
* Weight loss (with increased appetite)
* Hair loss
* Arrhythmia and breathlessness on exertion
* Bone loss
* Heat intolerance (increased heat production)
* Sleep Disturbances
* Goiter due to overstimulation of the thyroid gland
* Sweating, tremor, nervousness, weakness
* Exophthalmos
symptoms of hyperthyroidism
109
Protruding eyes due to connective
tissue deposits
exophthalmos
110
If the cause of hyperthyroidism
originates from the
hypothalamus or pituitary, then
TSH levels will be _____
increased
111
If hyperthyroidism originates
outside the hypothalamus or
pituitary, then TSH levels will be ________
low due to negative feedback
112
Decreased metabolism
hypothyroidism
113
Autoimmune destruction of the thyroid gland
thyroiditis
114
* Decreased metabolic rate
* Weight gain
* Hair loss
* Goiter
* Iodine deficiency
* Cold intolerance
* Reduced heart rate
* High cholesterol
* Fatigue, slowed mental activity
Symptoms of hypothyroidism
115
Hashimoto is associated with
hypothyroidism
116
If the cause of hypothyroidism
originates from the hypothalamus
or pituitary, then TSH levels will be
decreased
117
If hypothyroidism originates in the
thyroid gland, then TSH levels will
be
high due to negative feedback
118
some causes of goiter
- graves disease
- TSH secreting tumor
- autoimmune thyroiditis
- iodine deficiency
119
* Inner zone of the adrenal gland
* Approximately 20% of the tissue
* Neural origin and secretes epinephrine and norepinephrine
adrenal medulla
120
* Outer zone with 3 distinct layers
Secretes:
* Mineralocorticoids (i.e. Aldosterone)
* Glucocorticoids (i.e. Cortisol)
* Androgens (i.e Androstenedione)
adrenal cortex
121
Precursor for all adrenocortical steroids is
cholesterol
122
Enzymes are uniquely present in each layer of the gland to produce
the specific hormones for that layer (except cholesterol desmolase which is in all 3)
123
all layers of adrenocortical steroids contain _____
cholesterol desmolase because that is the first step for all products (also the rate limiting step)
124
Cholesterol desmolase is stimulated
by
Adrenocorticotropic Hormone
(ACTH) from the anterior pituitary
125
stimulates aldosterone
production at the last enzymatic step unique to aldosterone production (other enzymes are shared with cortisol pathway)
angiotensin 2
126
Testosterone and Estrogens are made from androstenedione, but primarily occurs in the
gonads
127
Called glucocorticoids because they are associated with
an increase in blood glucose.
128
Major glucocorticoid produced in humans
Produced in the zona fasciculata/reticularis (inner zones) along with adrenal androgens
cortisol
129
a glucocorticoid
If part of the cortisol pathways is blocked, then function can continue through an alternate, corticosterone
pathway.
Corticosterone
130
is needed to synthesize both cortisol and corticosterone. A medication (metyrapone) inhibits both pathways for this reason. Ketoconazole inhibits several steps (including those of fungal organisms which is why it is an antifungal
11-beta hydroxylase
131
Hypothalamus releases ________ to anterior pituitary
cortisol releasing hormone (CRH)
132
Anterior pituitary releases
________ to adrenal cortex
adrenocorticotropic hormone (ACTH)
133
what does ACTH do
* stimulates adrenal cell growth and activity
* initiates processing of cholesterol
* Stimulates Cytochrome p-450 proteins and other enzymes for cortisol, androgen, (and aldosterone) processing
134
Negative feedback by cortisol directs to
both the hypothalamus and to the pituitary
135
what is the pulsatile pattern of ACTH
average of 10 secretory bursts in a 24 hour period
136
when is the lowest rate of ACTH
occur during the evening hours and just after falling asleep
137
when are cortisol tests scheduled
There is an early morning rise in cortisol levels. Occurs just before waking
* The morning burst accounts for ½ of daily cortisol secretion
* Cortisol tests are scheduled for early morning
138
Increased secretion of __________ is associated with stressful events or threats (stress hormone).
cortisol
139
Actions of Glucocorticoids in stimulation of gluconeogenesis
* Increases protein catabolism in muscle and decreases new protein synthesis to
provide more amino acids to the liver for glucose synthesis
* Increases lipolysis for gluconeogenesis
* Decreases glucose utilization by tissues
140
actions of glucocorticoids in suppression of immune response
suppresses t-cell proliferation
* Corticosteroids may be used as immunosupressants (arthritis, organ rejection, etc)
* Synergistic response with catecholamines to vasoconstrict and increase BP
* Inhibits bone formation
* Increases REM sleep, increases slow-wave sleep, increases awake time
141
Adrenal cortex produces androgenic compounds
* Dehydroepiandrosterone (DHEA)
* Androstenedione
142
In males, androgens play a ______ role because synthesis in the testes is much greater
minor
143
In females, these are the major androgens and produce:
* development of pubic and axillary hair and for libido
* Increased levels lead to masculinization of female
144
affect minerals (sodium, potassium, etc.)
mineralocorticoids
145
Major mineralocorticoid in humans
aldosterone
146
minerolocorticoids are only synthesized in
the outer zone (zona glomerulosa)
147
stimulates the first step in aldosterone synthesis (cholesterol
desmolase)
ACTH
148
is the primary regulator of
aldosterone secretion from the adrenal cortex
Renin-Angiotensin-Aldosterone system
149
Increases in________ will also directly increase aldosterone
secretion.
serum potassium
* High potassium causes depolarization and an influx of cholesterol desmolase
enzyme to the outer zone (zona glomerulosa)
* Synthesis of more Na/K pumps increases potassium secretion, lowering
potassium serum levels
150
Regulation of ACTH secretion may be related to
glucocorticoids (cortisol), androgens, or mineralocorticoids (aldosterone)
150
actions of mineralocorticoids
* Insertion of sodium/potassium ATPase
- Increases potassium secretion
- Increases sodium reabsorption
* Increased activity of Hydrogen ATPase
- Increases hydrogen secretion
* Fluid volume expansion and increased blood pressure
151
promotes gluconeogenesis
* Excess: hyperglycemia.
Deficiency: hypoglycemia
cortisol
152
causes K+ secretion, Na+ reabsorption
* Excess:
* Hypokalemia and associated symptoms
* Increased Na reabsorption and volume expansion (higher BP)
* Deficiency:
* Hyperkalemia and associated symptoms
* Decreased Na reabsorption and volume contraction (lower BP
aldosterone
153
* Excess: masculinization in females
* Deficit: loss of pubic hai
adrenal androgens
154
Hypoglycemia, anorexia, weight loss, nausea and vomiting,
weakness
low cortisol
155
Commonly, autoimmune destruction of all zones of the adrenal gland
Decreased circulating levels of cortisol, aldosterone, and adrenal
androgens
Addison Disease
Primary Adrenocortical Insufficiency
156
hyperkalemia, metabolic acidosis, hypotension
low aldosterone
157
Low DHEA and androstenedione results in decreased
pubic and axillary hair and decreased libido
low adrenal androgens
158
ACTH levels would be low if the source was due to _______ deficits in
hypothalamic (CRH) or pituitary (ACTH) function
secondary
158
Hyperpigmentation due to increased melanocyte stimulating hormone release caused by
high CRH/ACTH
159
* Caused by excess production of glucocorticoids:
* Over-production of cortisol by the adrenal cortex
* Administration of pharmacologic doses of exogenous glucocorticoids
* caused by a pituitary tumor
* Symptoms are most related to excess cortisol and excess adrenal androgens (Aldosterone only has a small effect)
Cushing syndrome
160
Hyperglycemia, increased proteolysis and muscle wasting, increased lipolysis and thin extremities, central obesity, round face, supraclavicular fat, buffalo hump, poor wound healing, osteoporosis, and striae (like stretch marks but caused by a loss of
connective tissue). Cortisol increases sympathetic activity to cause blood pressure increases
excess cortisol
161
virilization (development of male sex characteristics such as muscle, body hair, and deep voice). Also may cause menstrual disorders
Some aldosterone effects could also contribute to increased BP.
excess adrenal androgens
162
Adrenal cortex insufficiency
* May be autoimmune
* Tuberculosis
Addisons
163
Overproduction of Cortisol
Increased Medications (like
prednisone) or pituitary
tumors are common
Cushing
164
what hormones do the pancreas release into the bloodstream
glucagon
insulin
somatostatin
165
where are pancreatic hormones released from
islets of langerhans
166
hormone associated with alpha cells
glucagon
167
hormone associated with beta cells
insulin
168
hormone associated with delta cells
somatostatin
169
where are alpha cells mostly found
around the outer rim of islets
170
delta cells (somatostatin) may serve a __________ paracrine role within the islets
paracrine
171
release Insulin when they detect high blood glucose levels (or when triggered by gut-derived hormone released by the stomach after eating)
beta cells
172
release glucagon when they detect low blood glucose levels (such as between meals)
alpha cells
173
produce somatostatin which extends the time food is in the stomach and blocks insulin and glucagon release to give time
for cells to absorb nutrients
delta cells
174
Beta cells release _______ when they detect high blood glucose levels (or
when triggered by gut hormones released after eating)
insulin
175
insulin consists of
2 chains (A and B) made from a longer prepro and proinsulin
176
how to measure beta cell function and production of insulin
the connecting peptide (C peptide) is cleaved off
177
more effective way to monitor beta cell function than directly measuring insulin, because it works even when the patient is still taking exogenous insulin.
C peptide
178
most important factor of stimulation and inhibition affecting insulin secretion
glucose concentration
179
Oral glucose increases several
___________, which increases insulin
release.
gastrointestinal factors (including
GIP)
This is why oral glucose is a more
effective stimulator of insulin release
than IV glucose.
180
There are ___________ on
beta cells that will inhibit insulin
release
adrenergic receptors
181
what transports glucose into the beta cells
glucose transporter type 2
182
what will more glucose in the blood result in
more glucose being transported into beta cells
183
what does high glucose cause potassium channels to do
close
184
what happens to the cell when potassium collects in the cells
the cell depolarizes
185
what happens when the cell depolarizes
the calcium channels open which causes the vesicle containing insulin to fuse with the membrane and release insulin
186
how do the cell membrane receptors get activated
insulin binds to the alpha subunits
187
what happens to the the receptors after activation
the receptors are internalized and with either be degraded or recycled
188
what is a partial factor in insulin resistance in obesity and type 2 diabetes
inappropriate down regulation of receptors (insulin down regulates its own receptor)
189
what happens after insulin binds to and activates a receptor on target cells
Intracellular signals are generated that result in the insertion of a GLUT
(Glucose Transporters) into the cell
membrane
Glucose is transported across the cell membrane through the GLUT
Increasing the number of glucose transporters allows glucose to enter the target cells, which decreases blood glucose
190
Excess glucose is stored as a complex chain of glucose molecules
called
glycogen
191
When glycogen stores are full, glucose is converted to fatty acids to
form
triglycerides
192
the production of new glucose from other molecules such as amino acids, glycerol, or fatty acids
gluconeogenesis
(happens when glucose levels are depleted)
193
When fatty acids, glycerol and amino acids are catabolized to make ATP, they form
acidic ketones often resulting in ketoacidosis (the blood pH falls – more acidic)
194
what is the overall action of insulin
increase storage of energy into cells (hormone of abundance)
194
what does insulin do to potassium
increases potassium uptake into cells
195
what 3 cell types does insulin effects
- adipose tissue
- skeletal muscle
- liver
196
what effect does insulin have on adipose tissue
* Increases Glucose Uptake
* Increases fatty acid uptake
* Triglyceride Synthesis
* Decrease Lipolysis
197
what effect does insulin have on skeletal muscle
* Uptake of Glucose
* Increases Glycogen storage
* Increases uptake of amino acids and protein synthesis
198
what effect does insulin have on the liver
– Increases glycogen synthesis
– Increases Triglyceride Synthesis
– Decreases Gluconeogenesis
199
insulin effect on blood levels
– Decreased Glucose
– Decreased Fatty acids
– Decreased Ketoacids
– Decreased Amino Acids
200
Abnormality in blood glucose regulation and nutrient storage related to an absolute or relative
deficiency of insulin and/or resistance to the actions of insulin
Essentially, the patient can’t release insulin or can’t respond to it
diabetes mellitus
201
* Usually caused by an autoimmune destruction of beta cells
* 5-10% of all patients
type 1diabetes mellitus
– Insulin Dependent Diabetes Mellitus (IDDM)
202
Associated with Insulin Resistance: High blood glucose, relative lack of insulin. (about 90-95% of
diabetics are Type 2)
type 2 diabetes mellitus
203
associated with pregnancy
gestational diabetes
204
does diabetes insipidus have an effect on glucose levels
no, it is associated with ADH release
205
destruction of pancreatic beta cells prevents release of insulin
Type 1- IDDM
206
* Autoimmune destruction of beta cells
* Genetic predisposition with environmental trigger leads to T lymphocyte-mediated hypersensitivity reaction
* More common in young persons, but can occur at any age
* Absolute insulin deficiency - need insulin replacement
* Prone to ketoacidosis
Type 1A (autoimmune)
207
what is type 1A IDDM characterized by
* Increased blood glucose
* Increased blood fatty acid and ketoacid concentration
* Increased blood amino acid concentration
* Less lean body mass and loss of adipose tissue
208
More common in type 1
acute complication
Mechanism:
* Lack of insulin results glucose not being moved into cells (blood glucose levels are high, but the
cells are starving).
* Glucagon triggers breakdown of triglycerides into fatty acids & glycerol which leads to increased
production of ketones in the liver.
diabetic ketoacidosis (DKA)
209
Clinical presentation
* Slow onset, prolonged recovery
* History of 1-2 days of polyuria, polydipsia, nausea, vomiting, marked fatigue; may progress to stupor & coma
* Characteristic fruity breath because of the presence of volatile ketoacids
* Metabolic acidosis (insulin resistance accompanies severe acidosis => low dose insulin
therapy is indicated with frequent monitoring of serum glucose levels)
* Compensatory mechanisms: tachycardia, tachypnea
diabetic ketoacidosis
210
* Characterized by Insulin Resistance and increased glucose production by the liver
* The pancreas produces insulin, but the insulin has little or no effect
* Over time, the beta cells may be damaged, impairing insulin release, possibly requiring insulin
injections
* Over 90% of newly diagnosed cases
* Usually occurs in people over 30 years of age (that age is decreasing)
* Progressive
* Non-pharm treatment is usually caloric restriction and weight reduction
type 2 non insulin dependent diabetes mellitus
211
medications that increase pancreas secretion of insulin
sulfonylureas
212
drugs that up regulate insulin receptors and decrease insulin resistance
biguanides (metformin)
213
glucagon is produced by _______ of the islets of langerhans
alpha cells
214
what is glucagon triggered by
decreases in blood concentration
(insulin decreases the activity of glucagon)
215
roles of glucagon
* Maintains blood glucose between meals and during periods
of fasting
* Able to initiate glycogenolysis in the liver for quick increase in
glucose (breakdown of glycogen to release glucose monomers)
* Able to stimulate gluconeogenesis in liver to build new glucose from amino and fatty acids
* Increases blood fatty acid and ketoacid concentrations
(contributes to diabetic ketoacidosis)
216
how does glucagon mobilize energy
1) Glycogen --> glucose (glycogenolysis)
2) Fat --> fatty acids for energy (lipolysis)
3) Amino acids --> glucose (gluconeogenesis)
217
what is the hormone of starvation
glucagon
217
* Triggered by decreased nutrients
between meals (or during fasting)
* Mobilizes energy stores to maintain continuous availability of energy
glucagon
218
* Secreted by delta cells of the islets of Langerhans
* Stimulated by the ingestion of all forms of nutrients, by several GI
hormones, by glucagon, and by alpha-adrenergic agonists
somatostatin
219
Function:
* Inhibits secretion of insulin and glucagon within the islets of
Langerhans (paracrine action)
* Secreted in response to a meal
* Modulates response to ingestion of food
Other functions we have talked about:
* Inhibits growth hormone
* Inhibits thyroid stimulating hormone
* Decreases stomach and gut motility
somatostatin
220
extracellular calcium is vital to
muscle contraction (including cardiac) and neurotransmitter release from neurons (and many other structural and physiologic functions)
221
Decrease in extracellular (plasma) Ca2+ (hypocalcemia) causes what
* Hyperreflexia, twitching, muscle cramps, tingling, numbness
* Chvostek sign: twitching of facial muscles when tapping on facial nerve
* Trousseau sign: carpopedal (hand) spasm upon inflation of a BP cuff
222
Hypercalcemia: Increase in extracellular (plasma) Ca2+ causes what
Hyporeflexia, lethargy, constipation, polyuria, polydipsia, coma and death
223
__________ is carried in the blood, but
about 40% is bound to plasma
proteins (albumin)
* 60% is filterable, 10% of which is
bound to anions, particularly
phosphate
* 50% is free, ionized Ca2+
calcium
224
what happens to calcium when there is increased blood proteins
increase total blood calcium
225
what happens to calcium if phosphate anions (HPO42- and
H2PO4-) increase
then more calcium will be
bound, which decreases free Ca2+
226
calcium competes with ________ for
albumin binding sites
hydrogen
227
lower plasma calcium
acidemia
228
higher plasma calcium
alkalemia
228
what 3 organs control calcium homeostasis
- bone (calcium storage)
- kidney
- intestine
229
what three hormones involved in calcium homeostasis
- parathyroid hormone
- calcitonin
- Active form of Vitamin D (1,25-
Dihydroxycholecalciferol)
230
* Increases resorption from bone and reabsorption from the kidney
* Directs activation of vitamin D in kidney
parathyroid hormone
231
Reduces bone resorption
calcitonin
232
* Increases bone resorption (inhibited by calcitonin)
* Increases absorption in intestines
Active form of Vitamin D (1,25-
Dihydroxycholecalciferol)
233
what is secreted by
the parathyroid glands: (4 small glands located in the neck on the posterior part of the thyroid gland)
parathyroid hormone (PTH)
234
* critically important for regulation of calcium levels in extracellular fluid
* When calcium concentration decreases, it is secreted by the parathyroid glands.
* has effects on bone, kidney, and
intestine to increase calcium
PTH
235
* Parathyroid hormone is an 84 amino acid polypeptide
* PTH secretion varies to help maintain calcium levels within a normal range
* Calcium sensing receptors on PTH membranes monitor extracellular calcium
* The presence of calcium prevents release of PTH. When calcium levels are low, PTH is
secreted.
PTH
236
primarily made of a Calcium Phosphate lattice structure called
hydroxyapatite
bone
237
responsible for bone formation
osteoblasts
238
responsible for breakdown of bone
osteoclasts
239
increases osteoclast activity and resorption of calcium (and
phosphate) from bone
PTH
240
PTH's 2 actions on the kidney
* PTH stimulates Calcium reabsorption in the distal convoluted tubule
* PTH Inhibits phosphate reabsorption by inhibiting sodium/phosphate cotransport
241
what happens to calcium levels when you excrete phosphate
calcium remains unbound in the plasma, increasing calcium levels
242
PTH effect on small intestine
Indirect effect by activating vitamin D
* PTH stimulates the renal enzyme to convert 25-hydroxycholecalciferol to the active form, 1,25 dihydroxycholecalciferol.
* Activated Vitamin D stimulates intestinal calcium absorption
242
what is reabsorption of phosphate blocked by
cAMP mechanism
243
Usually caused by a parathyroid adenoma (benign tumor)
Primary hyperparathyroidism
can cause:
- hypercalcemia
- hypophosphatemia
- increased calcium in urine
- constipation
- increased risk of osteoporosis
244
due to increased bone resorption and renal reabsorption
hypercalcemia
245
due to increased excretion
Hypophosphatemia
245
may lead to kidney stones (renal calculi)
Increased Calcium in urine
246
from reduced intestinal motility
constipation
247
Usually a consequence of thyroid surgery (for hyperthyroidism)
or parathyroid surgery (for hyperparathyroidism)
* Hypocalcemia from decreased bone resorption and renal reabsorption
* Hyperphosphatemia from increased phosphate reabsorption
* May be treated with active vitamin D and calcium
hypoparathyroidism
248
The primary action is to inhibit osteoclast mediated bone resorption, decreasing plasma calcium levels
calcitonin
249
* 32 amino acid polypeptide
* Released by cells of the Thyroid Gland
* Release is stimulated by increased plasma calcium
* does not have a major impact on minute-to-minute calcium homeostasis
* Thyroidectomy and Thyroid tumors do not have a significant impact on
calcium regulation
calcitonin
250
Role is to increased plasma concentrations of both calcium and phosphate to promote the mineralization of new bone
vitamin D
251
Provided in diet and manufactured in the skin from cholesterol
fat soluble vitamin D
251
vitamin D:
active vitamin D:
cholecalciferol
1,25-dihydroxycholecalciferol
252
where does vitamin D activation occur
occurs in the kidney by renal enzyme
– this step is directed by PTH
253
actions of vitamin D on intestine
increase calcium and phosphate absorption
Mechanism is from production of a calcium binding protein
(calbindin) that can bind 4 calcium ions and then release them
into the bloodstream
253
actions of vitamin D on kidney
Stimulates calcium and phosphate
reabsorption.
**Remember that PTH caused phosphate excretion**
254
actions of vitamin D on bone
Stimulates remodeling and formation of new bone.
Vitamin D stimulates osteoclasts to promote the resorption of
old bone. The phosphate and calcium are then used to build
new bone
255
vitamin D deficiency
* Insufficient calcium and phosphate are available for growing bones
* Manifests as growth failure and skeletal deformities
rickets
256
The kidney is unable to produce the active form of vitamin D.
* Vitamin D supplements do not help. The active form is required.
* Chronic kidney disease (CKD) patients are often prescribed 1,25-dihydroxycholecalciferol
(active form of vitamin D) since they are unable to produce it
vitamin D resistance
256
vitamin D deficiency in adults
osteomalacia
257
Estrogen and testosterone are needed for maintenance of
bone mass
In older age, declines in these hormones is a risk factor
osteoporosis
258
is defined by the presence of male or female gonads
* Testes
* Ovaries
gonadal sex
258
is directed By Our Genome
* Humans have 23 pairs of chromosomes (23 from mom, 23 from dad)
* 22 pairs of autosomes
* X and Y = 1 pair of sex chromosomes. XX is genetically female. XY is genetically male.
* Having pairs of chromosomes can be beneficial because if a gene on one chromosome does not
function properly, the gene on the other chromosome can compensate. This is also the basis of
genetic diseases
genetic sex
259
is defined by the physical characteristics of the internal genital
tract and the external genitalia
phenotypic sex
259
male phenotypic sex
Internal Genital tract
* Prostate
* Seminal Vesicles
* Vas deferens
* Epididymis
External genitalia
* Scrotum
* Penis
260
female phenotypic sex
Internal Genital tract
* Fallopian Tubes
* Uterus
* Upper 1/3 of vagina
External genitalia
* Clitoris
* Labia majora
* Labia minora
* Lower 2/3 of the vagina
261
what is gender determined by
genetic inheritance of two
chromosomes known as the sex chromosomes (X and Y).
261
sex chromosomes males possess
X Y
262
sex chromosomes females possess
X X
262
when and how is sex of the fetus expressed
During the seventh week of fetal development the Sex Determining Region of Y (SRY) gene located on the Y chromosome is expressed
263
SRY turns ______ genes for male development and turns _____ genes for female development
on, off
264
what happens when there is no SRY expression
the fetus goes on to become a girl
264
what stimulates the development of testes
presence of SRY
265
where is testosterone secreted from
leydig cells
266
what is secreted from Sertoli cells
antimullerian hormone
266
testosterone from leydig cells in the developing testes stimulates ______________ into __________
maturation of wolfian duct
vas deferens
267
what does antimullerian hormone do
disintegration of the Mullerian duct, which would otherwise become the fallopian tube, uterus, and cervix).
268
Growth and development of external male genitalia depend
on the conversion of
androgen to dihydrotestosterone
(DHT) in the testes. Note that androgen receptors are
required for this process
269
what happens to gonadal females without SRY
develop ovaries that
produce estrogen, but do not secrete antimüllerian hormone or testosterone
270
what happens without antimüllerian
hormone or testosterone
Internal and external development progresses to female without these hormones
271
Sertoli cells produce
antimullerian hormone
272
During development the testes form in the abdominal cavity and then descend through the ________
inguinal canal
Although the path closes up, it
creates a weak point in the lower
part of the abdomen
* Inguinal Hernia
272
leydig cells produce
testosterone
273
in the absence of testosterone and antimullerian hormone
the fetus continues to produce a female
274
genetic males develop a uterus and have external female genitalia (Swyer Syndrome)
loss of function Y
274
ambiguous genitalia
Mutations with partial function
275
males without a Y (46XX)
Displacement of SRY to X chromosome
276
If a gonadal female is exposed to androgens in utero, when external genitalia are differentiating, then
a male phenotype results.
If it occurs later, then a female
phenotype is retained. This may be seen with excessive androgen secretion from the adrenal gland or ovaries, or from hormonal medications
277
The absence of androgen receptors in a gonadal male will result in
development of female external genitalia
278
what reproductive hormone does the hypothalamus produce
Gonadotropin releasing hormone (GnRH)
279
what hormones come from the Anterior pituitary gonadotropins:
* Luteinizing hormone (LH)
* Follicle stimulating hormone (FSH)
280
what do Gonads (testes and ovaries) produce
steroid and peptide hormones
* Gonads are the main source of sex steroid
281
Hormones produced by the gonads feed back to the________ to inhibit release
pituitary and hypothalamus
282
what will continuous release of GNRH do to gonadotropins (LH and FSH).
decrease release of the gonadotropins (LH and FSH). Synthetic forms are used as a treatment for androgen-sensitive
prostate cancer
283
Many reproductive and developmental processes,
including puberty are directed by the hypothalamic- pituitary axis:
* Gonadotropin Releasing Hormone (GnRH) from the Hypothalamus
* Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) from the pituitary gland
* Secretion of GnRH begins at gestational week 4, but levels remain low until puberty
* Secretion of LH and FSH begins between gestational weeks 10-12. Levels are also low until Puberty (during childhood FSH is relatively higher)
* The release patterns change during puberty and throughout the reproductive years
284
Pulsatile release of GnRH begins at _________ (and as a consequence, also FSH and LH) and continues through reproductive years.
puberty
285
Upregulation of GnRH receptors in the pituitary increase the sensitivity of
LH and FSH, (LH levels are now greater than FSH)
286
what does Increased FSH and LH do
increase the production and release of testosterone and estradiol.
287
what is Testosterone and estradiol responsible for
appearance of secondary sex characteristics
287
The onset of puberty has been shown to be
genetically programmed
Age of onset is similar for parents and their children
288
The mechanisms that trigger the onset of pulsatile GnRH secretion is
unknown
289
what are the events of puberty initiated by
pulsatile secretion of GnRH, FSH, and LH
290
what will GnRH deficiency do
delay puberty
Treatment with exogenous, pulsatile GnRH will initiate puberty (long-
acting GnRH will not)
290
Pubic and axillary hair is due to increased production of
adrenal androgens (adrenarche). Begins early, or before puberty
291
boys characteristics of puberty
* Leydig cell proliferation (make testosterone)
* Growth of testes (increased number of seminiferous vesicles where
sperm are made)
* Growth of sex accessory organs (e.g. prostate)
291
girls characteristics of puberty
* Onset of puberty is earlier
* Budding of breasts occurs, followed approximately 2 years later by
menarche (onset of menstrual cycles)
* Estradiol secretion from ovaries is increased
292
* Sperm production occurs in the testes
* Emission and ejaculation through the urethra of the
penis
spermatogenesis
293
Hormone Production takes place in the
testes
294
produce testosterone and other hormones
leydig cells (activated by LH)
295
provide nutrients and other factors for the development of sperm from germ cells to mature sperm (also called nurse cells or sustentacular cells)
Sertoli cells (activated by FSH)
296
where does developing sperm move to
move into the seminiferous
tubules (makes up 80% of the mass of the testes)
297
where does spermatogenesis occur
along the length of the seminiferous tubules
297
phases of spermatogenesis
Mitotic Divisions
* Many cell divisions to produce the cells that will become sperm
Meiotic divisions
* Decrease chromosome number to 23 (including either X or Y)
Produce unique, haploid spermatids (only one set of
chromosomes. No longer in pairs)
* These are unique combinations of the initial pairs of chromosomes
Spermiogenesis
* The last step is loss of the cytoplasm and formation of the flagella
tail. Final maturation takes place in the epididymis, where mature
sperm are viable for several months.
* Process takes 65-75 days
* Each day about 100-300 million sperm complete spermatogenesis
* Normal sperm production requires a temperature 2-3°C below core
body temperature
* Cremaster and dartos muscle contract or relaxe to move testes up
or down
298
normal sperm production requires a temperature
2-3 degrees celsius below core body temperature
298
what does the head of the sperm produce
Head contains the nucleus and acrosome:
* Nucleus with 23 chromosomes (haploid or n)
* Acrosome – vesicle filled with oocyte
penetrating enzymes
299
contains centrioles forming microtubules that comprise remainder of tail
neck of sperm
300
contains mitochondria to provide
ATP energy
middle piece of sperm
301
longest portion of tail
principal piece of sperm
301
terminal, tapering portion of tail
Once ejaculated, sperm do not survive more than 48 hours in female reproductive tract
end piece of sperm
302
starting molecule for Pathways for Steroid Hormones in gonads
Starting molecule is cholesterol. LH activates the first enzymatic step
303
enzyme for synthesis of estrogens from testosterone
Aromatase
304
enzyme for synthesis of DHT from testosterone
5-alpha reductase
305
Target cells may be activated by
testosterone or dihydrotestosterone
(DHT)
306
Conversion of testosterone to
DHT is by
5-alpha reductase
306
5-alpha reductase inhibitors
(finasteride) are sometimes used
to treat
enlarged prostate gland
(benign prostatic hyperplasia,
BPH) or topically for baldness
307
when does secretion of gonadotropin-releasing hormone
(GnRH) increase
puberty
308
GnRH stimulates anterior pituitary to increase secretion of
luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
* FSH and LH are protein hormones
309
LH stimulates Leydig cells to secrete
testosterone
* Testosterone is synthesized from cholesterol
* Testosterone suppresses secretion of LH and GnRH via negative
feedback
* Testosterone also functions in a paracrine fashion to support
spermatogenesis in Sertoli Cells
310
The enzyme_________ converts testosterone into
dihydrotestosterone (DHT) in Leydig cells
5 alpha-reductase
311
___________ act on Sertoli cells
to stimulate spermatogenesis
FSH and testosterone
312
_____ are where spermatogenesis is initiated:
Sertoli cells
* Sertoli cells form a barrier to prevent mixing of sperm and blood (blood-testes barrier). This protects sperm from immune destruction
* Sertoli cells provide nutrients to differentiating sperm (because sperm are isolated from blood).
* Secrete fluid into seminiferous tubules to help transport sperm
* Synthesize and secrete Androgen Binding Protein (ABP) into the seminiferous tubules to bind
testosterone and keep levels high for continued sperm development
313
Sertoli cells release __________ which inhibits FSH release from the anterior pituitary without inhibiting LH release
inhibin
Allows testosterone production from Leydig cells to continue, while limiting sperm production
314
_______ carries sperm
semen
314
Sperm leave the testes through ________
ducts
315
Semen is produced in:
* Seminal Vesicle
* Bulbourethral gland
* Prostate gland (note that the prostate
surrounds the urethra and ejaculatory
duct. BPH pts often have difficulty
emptying their bladder)
315
Sperm and semen are carried by:
* Vas Deferens (ductus deferens)
* The left and right vas deferens
converge at the ejaculatory duct
* Urethra through the penis
316
Accessory glands contribute _______ of semen volume, as well as the following:
99%
317
Prostate gland (30%)
– buffers (bases), citric
acid, proteolytic enzymes, calcium
317
Seminal vesicles (60%)
– fructose, vitamin C,
prostaglandins, clotting agents
Prostaglandins may make cervical mucous more penetrable and may increase peristaltic contractions in the reproductive trace to help move sperm
318
Bulbourethral gland (5%)
mucus, buffers (high pH)
319
when vas deferens is cut or tied (vasectomy), what happens to the semen
semen will still be made due to the location of the glands, but it will lack sperm
319
accumulation of sperm cells and
secretions of the prostate gland and seminal vesicles in the urethra
emission
320
Emission is controlled by ____________centers in spinal cord
sympathetic
* Accumulation in urethra sends sensory information to spinal cord
* Peristaltic contractions of reproductive ducts coming from the testes
* Seminal vesicles and prostate release secretions
321
constriction of internal
sphincter of urinary bladder so semen and urine do not mix
sympathetic
321
to skeletal muscles and base
of penis causing rhythmic contractions that force semen out of urethra: ejaculation
somatic motor
322
what does Erection require
inhibition of sympathetic
activity so parasympathetic will dominate
(Recall that ejaculation is a sympathetic reflex)
323
Medications that increase arterial
vasodilation through maintenance of nitric oxide help with achieving erection. Also used for pulmonary hypertension)
(PDE5 inhibitors – Sildenafil)
323
A positive feedback mechanism helps maintain an erection:
As the penis fills with blood, the veins are compressed which prevents blood from draining, further
maintaining the erection
324
Development of oocytes occurs within follicles in the ovaries
* If fertilized, it will
attach to the uterine wall
324
what is nitric oxide
vasodilator
325
Production of a mature oocyte - Essentially the same steps as spermatogenesis but occur at different times
oogenesis
325
when does meiosis begin
Meiosis begins prior to birth but is
interrupted until puberty, leaving a
primary oocyte
325
how many oocytes at birth and remain at puberty
About 200,000 to 2,000,000 at birth
About 40,000 remain at puberty
326
when does meiosis 1 take place
during follicle development
327
how many oocytes mature during a lifetime
400
327
when do the final divisions of meiosis 2 take place
after fertilization
327
when does the ovary stop developing the remaining eggs
menopause
327
Hypothalamus releases
Gonadotropin Releasing
Hormone (GnRH)
327
Progesterone feed back is
negative
327
Hormones from the hypothalamus and anterior pituitary stimulate the
ovaries
327
Estrogen feedback is
negative but will switch
to positive at ovulation
(midcycle)
327
The ovaries release _______
in varying patterns during each cycle
estrogen and progesterone
327
Anterior Pituitary releases
Follicle Stimulating Hormone
(FSH) and Luteinizing Hormone (LH)
327
Ovulation releases a _______ monthly
mature oocyte
327
_________ prepare the uterus
for possible pregnancy
Estrogen and progesterone
328
LH stimulates
thecal cells
328
FSH affects
granulosa cells
328
* LH stimulates thecal cells to produce _________
androgens and progesterone
328
what stimulates the initial enzyme
for hormone production
Luteinizing hormone (LH)
329
Androstenedione, produced in thecal cells, moves into
granulosa cells
330
Follicle stimulating hormone (FSH) activates __________
to stimulate the conversion of testosterone into estrogen
(17-beta Estradiol) in ovarian granulosa cells
aromatase
331
Ovulation releases a mature
oocyte monthly
Ovaries are the location of sex
hormone production
ovarian cycle
332
The uterus prepares to nurture a
fertilized egg by forming an
endometrium that will sustain the
developing embryo
Associated with menstruation
uterine cycle
333
3 phases of the ovarian cycle
1. Follicular Phase: The Follicle containing the oocyte develops
Primarily Stimulated by Follicle Stimulating Hormone (FSH)
2. Ovulation: The Ripened follicle bursts, releasing the oocyte
Caused by a surge in LH - also makes sense because that starts the:
3. Luteal Phase: The ruptured follicle
develops into a corpus luteum (lasts 14 days following ovulation)
334
If fertilization takes place, the corpus luteum _________
remains
335
If no fertilization, the corpus luteum _________
deteriorates
336
_________ are produced in the Ovaries by the developing follicle and corpus luteum
hormones
337
Thecal cells produce
progesterone
338
Granulosa cells surrounding the follicle produce
estrogen
338
As the follicle develops, more and more estrogen and progesterone are made
The corpus luteum produces _________ progesterone if pregnancy occurs
more
339
FSH stimulates
follicular development
Events in ovaries
* Under FSH influence, several primordial follicles develop into
primary follicles and then into secondary follicles
* Takes several months
* Follicle that begins to develop in one cycle may not mature for several
cycles later
* Left or right ovary release is not very consistent
Maturation to secondary and tertiary follicles
340
Estrogen begins to ________- as the developing follicle matures
increase
341
Normally, estrogen __________ LH from being released
due to negative feedback
* HOWEVER, at some point the higher levels of estrogen
(>200 picograms per mL) actually cause more LH to be
released (switches from negative feedback to positive
feedback – it’s not known precisely how).
* The release of inhibin begins prior to ovulation and
keeps FSH release lower than LH)
prevents
342
what induces ovulation
The Surge of LH
343
The surge of LH also causes the developing follicle to
change, creating the ________-
corpus luteum
344
The Corpus Luteum releases _______ in large amounts
progesterone
345
* Secretion of inhibin and progesterone begins
* Inhibin decreases FSH secretion to prevent a surge during ovulation
* Estrogen changes from negative to positive feedback
* Enhanced secretion of LH - the LH surge
* Ovulation
* Mature follicle secretes collagenase
* Inflammatory reaction produces
prostaglandins
* Follicle ruptures releasing mature oocyte
* Theca and granulosa cells change into luteal cells
late follicular phase
346
* Begins with Menses
* Endometrium Sheds
* First few days
day 1 of uterine cycle
346
If no implantation
* Corpus luteum undergoes
apoptosis after 12 days
* Hormone production by the
corpus luteum stops
* Lack of progesterone leads to
death of endometrium
* Menses = sloughing of the
dead endometrium
* FSH and LH secretion
resumes
late luteal phase
346
* After ovulation, the follicle “turns into” the corpus luteum
* Corpus luteum continues to develop and secretes progesterone and estrogen
* Progesterone and estrogen exert
negative feedback on hypothalamus
* Effects of progesterone
* Endometrium develops further
* Cervical mucus thickens
early mid luteal phase
347
* Proliferative Phase
* Endometrium Proliferates – grows
thicker
prior to ovulation
348
* Secretory Phase
* Endometrium becomes secretory
after ovulation
349
Uterine Cycle – Largely controlled by
ovarian hormones
350
builds up to prepare for implantation of fertilized oocyte
endometrial lining
351
Estrogen is primarily responsible for _________ the endometrium
building up
351
Progesterone is primarily responsible for developing
and ________ the endometrium and making it _______
maintaining, secretory
352
Uterine Phases, starting with menses:
1. Menses – first 5 days of cycle
2. Proliferative or follicular phase
(Endometrium proliferates; follicle in ovary matures) Varies, but is about 10 days for most women
3. Secretory or luteal phase (maturation and
secretion of uterine glands; presence of corpus luteum) Consistent - 14 days for most women
352
The endometrium secretes _________ and other factors to support the fertilized oocyte
hormones
352
Repeated proliferation and
shedding of endometrium – Occurs in uterus
menstrual cycle
353
Events in uterus during Menses
* Menstrual discharge occurs because declining levels of estrogens and progesterone stimulate release of prostaglandins causing uterine spiral
arterioles to constrict
* Cells deprived of oxygen begin to die
354
* If no implantation, Endometrium __________, so LH and FSH increase again due to a decrease of
Estrogen and Progesterone and their negative feedback
* Cycle starts over.
sloughs off
354
events of the menstrual cycle
* GnRH stimulates the release of FSH and LH from the anterior pituitary
* FSH stimulates ovarian follicles to develop (one takes over as the primary follicle)
* Estrogen (and progesterone) increase, keeping FSH and LH low
due to negative feedback
* Estrogen reaches a level where it suddenly changes to positive
feedback, leading to a surge in LH
* LH surge triggers ovulation
* The mature follicle that remains is transformed into a corpus luteum
* Corpus luteum secretes high levels of progesterone
Progesterone:
* Triggers proliferation of the endometrial lining of the
uterus
* Thickens mucous in the cervical canal (effectively closing it
off)
355
Site of egg development
ovary
356
Following Ovulation, Egg moves through
fallopian tube to uterus
357
* Sperm from penis deposited into vagina and move through the cervix
* Sperm swim to the fallopian tube
Fertilization usually takes place in the fallopian tube before moving down to the uterus
* Cervix (means “neck”) – opening to the uterus from the vagina
* Sperm moves through cervical canal
* (cervix dilates during birth as baby
pushes downward from the uterus)
fertilization
358
Sperm must move through
the cervical canal to the
fallopian (uterine) tube
359
promotes a mucus plug that prevents sperm from moving through, except for a time
prior to ovulation
progesterone
360
The first sperm to penetrate causes a depolarization reaction that blocks the rest
Only the head of the sperm will penetrate and deposit the sperm nucleus. The tail piece does
not enter. The mitochondria from the sperm will ______ enter the oocyte (why you have your mom’s
mitochondria)
not
361
moves through the fallopian tubes
and into the uterine cavity
where it will be implanted.
Takes about 4 days
floats in the uterine cavity for about a day before implantation
Implantation is dependent
on high progesterone
levels
blastocyst
362
Oocyte can be fertilized up to ________ after ovulation
24 hours
363
Sperm cells can be viable for as much as _______ in female tract (usually 2-4 days)
6 days
364
blastocyst divides
identical twins
365
Implantation occurs anywhere other than uterine cavity
ectopic pregnancy
366
two eggs
fraternal twins
367
do baby and mom have the same circulatory system
no
* Fetus and mother’s blood DO NOT MIX
* Mother’s blood engulfs the chorion and nutrients and oxygen cross membranes to supply
the fetus
368
tissue layer that encloses
the developing embryo
chorion
369
tissue layer that secretes
amniotic fluid, suspending the embryo
amnion
370
form a close connection with
blood vessels of the endometrium
chronic villi
371
is released from the Chorion. Basis for pregnancy tests!
Human Chorionic Gonadotropin (hCG)
372
embryonic development following implantation
* hCG produced in the chorion maintains corpus luteum (in the ovary)
* Corpus luteum secretes progesterone and estrogen
373
why is Human Chorionic Gonadotropin (hCG) reliable to measure for pregnancy tests
detected about one week after implantation.
Reliable because it is released from a sac associated with an embryo
374
Changes in Hormones During Pregnancy
* Progesterone and Estrogen
continue to rise until delivery
* hCG is only high for about 3-4
months
* hCG stimulates the corpus
luteum to NOT degenerate, but
to continue producing
progesterone
375
* Stretch of cervix as a stimulus
parturition (birth)
376
Role of oxytocin in labor
– Stretch stimulates release
– Oxytocin stimulates prostaglandin release for local stimulation of contractions
– Positive feedback (contractions
stimulate more oxytocin
release)
377
Organs of milk production
located within mammae or
breasts
Consist of glandular lobes and
adipose tissue
mammary glands
377
steps of birth
* Prior to labor: softening of the
cervix
Labor
– Rhythmic uterine contractions
– Positive feedback cycle of oxytocin
release
– Cervical dilation
* Delivery of the baby
* Placental release and expulsion
378
* Prior to pregnancy, prolactin-inhibiting hormone (PIH (dopamine))
blocks prolactin secretion (released by hypothalamus). During
pregnancy, prolactin levels increase to enhance mechanisms for
milk production.
* High sex steroid (estrogen) levels suppress milk production
before birth
378
how does milk move out of the breast
* Prolactin triggers development
and production
* Oxytocin triggers the letdown
reflex
* Milk is allowed to move out
378
* High prolactin & low estrogen lactation
* Recall that high estrogen prevented lactation prior to birth
* Breast milk = nutrients + immunity
after birth
379
* Inhibits PIH, allowing milk production
* Oxytocin stimulates “let-down reflex”
suckling
380
* Estrogen and Progestin (Progestin is synthetic
progesterone)
* Keeps Estrogen and Progesterone levels constant
* Suppress LH and FSH release from pituitary
combined oral contraceptives
381
what does not LH surge mean
no ovulation
382
progestin causes the endometrium to ______ and the cervical mucous to _______
thin, increase
382
inactive pills drop...
hormone levels so menses can occur
383
* All pills are active
* Can be taken everyday or can be injected
* Primary mechanism is thickening of cervical mucous
* Depending on dose, it may or may not prevent ovulation
* Thins the endometrium so
implantation is less likely
(this is a feature of synthetic progestin)
progestin only
