Endocrine Flashcards
1
Q
Two major systems for physiological activities
A
Endocrine and CNS
2
Q
ENDOCRINE SIGNALING involves hormone secretion into the blood by an
A
endocrine gland
3
Q
The hormone is transported to a distant target site by
A
the blood stream
4
Q
Synthesis and release of the hormone is done by
A
endocrine cells (or neurons)
5
Q
Detection of the hormone or neurohormone by a
A
specific
receptor protein on the target cells
6
Q
A change in cellular metabolism triggered by
A
the hormonereceptor interactions
7
Q
Removal of the hormone results in
A
cellular
response
8
Q
“Classical”
Endocrine
Organs
A
Hypothalamus Anterior and posterior pitutary Thyroid and parathyroid glands Atrial natruretic peptides Adreal Glands (coretex and medulla) Pancreas (Islets of Langerhans) Ovaries (females) Testis (Male)
9
Q
Hypothalamic - Pituitary Signaling occurs by the
A
blood vessels of the pituitary stalk
10
Q
Hypothalamic-Hypophyseal Portal system is from the
A
the hypothalamus to the anterior pituitary.
11
Q
releasing factors
A
releasing hormones
12
Q
inhibiting factors
A
inhibiting
hormones
13
Q
-hypothalamic neurohormones
A
activate or inhibit activity of one of the six types of hormone - producing cellsin the anterior pituitary
14
Q
GLYCOPROTEINS Examples
A
FSH, LH, TSH
15
Q
POLYPEPTIDES Examples
A
ACTH, GH, Insulin, Glucagon, IGFs, oxytocin, calcitonin
16
Q
STEROIDS Examples
A
aldosterone, cortisol, estradiol, progesterone, testosterone, vitamin D
17
Q
AMINES Examples
A
T4, T3
18
Q
SYNTHESIS OF PROTEIN HORMONES: Ribosome
A
Preprohormones
19
Q
SYNTHESIS OF PROTEIN HORMONES: Rough ER
A
Preprohormones to prohormones
20
Q
SYNTHESIS OF PROTEIN HORMONES: Golgi Apparatus
A
prehormones packaged into secretory vesicles
prehormone to hormone and other peptide
21
Q
SYNTHESIS OF PROTEIN HORMONES: Vesicles
A
Storage of hormone
22
Q
PROPERTIES OF HORMONE RECEPTORS
A
SPECIFICITY: Recognition of single hormone or hormone family
AFFINITY: Binding hormone at its physiological concentration
SATURABILITY: A finite number of receptors
MEASUREABLE BIOLOGICAL EFFECT: A measurable biological response due to interaction of hormone with its receptor
23
Q
RECEPTOR REGULATION (2)
A
(A) RECEPTORS CAN BE UPREGULATED EITHER BY INCREASING THEIR ACTIVITY
IN RESPONSE TO HORMONE OR THEIR SYNTHESIS.
(B) RECEPTORS CAN BE DOWNREGULATED EITHER BY DECREASING THEIR
ACTIVITY OR THEIR SYNTHESIS
24
Q
3 mechanisms by which a hormone
can exert effects on target cells:
A
(1) Direct effects on function at the cell membrane.
(2) Intracellular effects mediated by second messenger systems.
(3) Intracellular effects mediated by genomic or nuclear action.
25
Hormone secretion is precisely regulated by
feedback mechanisms
26
An excess of hormone, or excess hormonal activity, leads to a
diminution of
| hormone secretion
27
a deficiency of hormone leads to an
increase in hormone
| secretion
28
PITUITARY GLAND Tissues
anterior pituitary, posterior pituitary
29
the anterior pituitary is _______ tissue.
endocrine
30
The posterior pituitary
| is ______ tissue
neural
31
Which hormone structure is unlike the others? why
Dopamine; it is Short
32
Hormone Structure
Long peptide chain
33
Neurohypophysis
Posterior Pituitary Gland
34
Posterior Pituitary Gland
- outgrowth of
- connected
- hypothalamus
| - by the pituitary stalk
35
Location that secretes oxytocin and vasopressin
Posterior Pituitary Gland
36
vasopressin also known as
antidiuretic hormone -ADH
37
supraoptic nucleus synthesizes
vasopressin or ADH
38
paraventricular nucleus synthesizes
Oxytocin
39
supraoptic nucleus and
| paraventricular nucleus axons run
down the pituitary stalk and
terminate in the posterior pituitary
close to capillary blood vessels
40
Prohormones processed in
secretory
| granules during axonal transport
41
neurophysins
- carrier molecules that transport the hormones oxytocin and vasopressin
- Mature hormones liberated from
42
Neurophysins half lives
1-3 minutes
43
What is the uterus sensistivr to during Parturition? When is paturation?
uterus extremely sensitive to oxytocin at end of pregnancy
44
dilation of uterine cervix by fetal head causes
release of oxytocin →
| uterine contraction, which assists the expulsion of fetus and then placenta
45
uterine contraction assists
the expulsion of fetus and then placenta
46
Milk ejection
response to the stimulus of suckling, in lactating mother
47
What hormone causes milk filled ducts to contract and squeeze milk out
Oxytocin
48
Behavioural effects of oxytocin in females
Local oxytocin release in the brain reduces anxiety
| and enhances bonding and pro-social behaviour
49
Ejaculation
Oxytocin surge during sexual activity assists epididymal
| passage of sperm and ejaculation
50
Behavioural effects of oxytocin in males
Local oxytocin release in the brain reduces anxiety
| and enhances bonding and pro-social behaviour.
51
Size of Thyroid Gland and how it varies
15 to 20g, varies size with sex, age, diet, reproductive state, etc.
52
Which sex is Thyroid Gland larger in?
Larger in females than males
53
Amount of healthy thyroid needed to maintain euthyroid state
only 39g
54
major component of the colloid
thyroglobulin
55
thyroglobulin
a large protein of 700,000Da
56
thyroglobulin converts
T4 to T3
57
thyroglobulin contains
thyroid hormones thyroxine (T4) and triiodothyronine (T3).
58
Where do T4 and T3 split off?
thyroglobulin
59
Where do T4 and T3 enter and bind to after being split off?
blood where
| they bind to special plasma proteins
60
synthesis of thyroglobulin is under the control of... where
TSH of pituitary gland
61
What does thyroglobulin provide?
a type of
| storage for T4 and T3 prior to release
62
What element do Thyroid hormones contain
Thyroid hormones contain iodine
63
What is the availability of iodine to terrestrial vertebrates?
limited
64
thyroid follicular cells are able to
trap iodide and transport it across the cell against a chemical gradient
(active transport)
65
Iodine (I2) used for
iodination of tyrosine residues of
| thyroglobulin (TGB)
66
iodination
of tyrosine residues of
thyroglobulin (TGB) is used to form
monoiodotyrosine (MIT) and
| diiodotyrosine (DIT)
67
Oxidative coupling of two DIT forms
thyroxine (T4)
68
oxidative coupling of one MIT with one DIT forms
triiodothyronine (T3)
69
T4 and T3 are stored linked to
thyroglobulin
70
rate of all steps of T4 and T3
| the formation is increased by
TSH
71
thyroid activity without TSH
Without TSH, thyroid has very low
| turnover of thyroid hormones
72
Synthesis and release of TSH controlled by
hypothalamic thyrotropin releasing hormone (TRH)
73
-When T4 and T3 in blood increase they
exert a negative feedback at both hypothalamic and pituitary levels
74
a negative feedback at both hypothalamic and pituitary levels results to
decrease release of TRH and TSH
75
What does TSH lead to?
increased production of T4 and T3
76
What does TSH do to increase the production of T4 and T3?
interacts with specific receptors
| located on follicular cells of the thyroid gland
77
How does iodine deficiency affect thyroid hormones?
When the supply of iodide is deficient, synthesis of thyroid hormones
decreases andT4 andT3 in circulation decrease.
78
Iodine deficiency affects on TSH release?
Release of TSH increases and the thyroid follicular cells are constantly
stimulated
79
How does Iodine deficiency affect thyriod gland?
-Thyroid enlarges
80
goiter
a visible lump when the thyroid enlarges
81
What results from an enlarged thyroid due to the iodine deficiency?
is unable to synthesize biologically active
thyroid hormones, known as non-toxic
goiter
82
What hormone stimulates calorigenesis in most cells?
Thyroid hormones
83
How does thyroid hormones promote normal growth?
Promote neural branching and myelinization of nerves
Promote development and maturation of the nervous system
Stimulate growth hormone (GH) secretion; Promote bone growth; Promote IGF-I production
by the liver
84
What results from stimulation of calorigenesis in most cells?
Increase cardiac output: rate and strength of cardiac contractions
Increase oxygenation of blood
Increase rate of breathing; Increase number of red blood cells in the circulation
85
How does thyroid hormones affect carbohydrate metabolism?
Promote glycogen formation in the liver; Increase glucose uptake into adipose and muscle
86
How does thyroid hormones affect lipid turnover?
Increased lipid synthesis; Increased lipid mobilization; Increased lipid oxidation
87
How does thyroid hormones affect protein metabolism?
Stimulate protein synthesis
88
What hormone increases Basal Metabolic Rate
Thyroid hormones
| Both T4 and T3 increase BMR
89
BMR
the rate at which the organism burns up its stores of fuel to produce energy in the form of heat or
calories
90
T4 and T3 have profound effects on the metabolism of which macromolecules?
carbohydrates, lipids and proteins
91
How does thyroid hormones affect CNS?
Required for normal development of the brain
| absence decreases neuronal development
92
Absence of thyroid hormones at early stages of development leads to
irreversible mental retardation
93
What hormone stimulates the synthesis of the nerve growth factor (NGF)?
Thyroid hormones
94
nerve growth factor
| (NGF) induces
dendritogenesis and regeneration of sympathetic neurons.
95
What do T3 and T4 bind to when they enter their target cell nucleus?
cognate nuclear receptor
96
What does the binding of T3 and T4 to their cognate nuclear receptor do?
Alters the transcription of specific genes, and thus levels of encoded proteins
97
With the specific receptor for T4 and T3 located in the mitochondrial membrane, what may result?
Thyroid hormones may induce some effects by interactions with plasma
membrane & mitochondria.
-Not blocked by inhibitors of protein synthesis: i.e. de novo gene expression and
protein synthesis not necessary
98
How does the T4/T3 interact with the plasma membrane? What is this effect independent of?
T4/T3 act directly at plasma membrane and increase uptake of amino acids.
This
effect is also independent of protein synthesis
99
hypothyroidism
Hypofunction of the thyroid gland characterized by low levels of thyroid hormones.
100
hyperthyroidism
Hyperfunction of the thyroid gland characterized by high levels of thyroid hormones.
101
(Hyper/Hypo) thyroidism:
| T4-T3 levels (elevated/decreased)
Hyper --> Elevated
| Hypo --> Decreased
102
(Hyper/Hypo) thyroidism:
BMR
(elevated/decreased)
Hyper --> Elevated
| Hypo --> Decreased
103
(Hyper/Hypo) thyroidism:
Pulse
(increased/decreased)
Hyper --> increased
| Hypo --> Decreased
104
(Hyper/Hypo) thyroidism:
body temperature
(increased/lowered)
Hyper --> increased
| Hypo --> lowered
105
(Hyper/Hypo) thyroidism:
weight
(loss/gain)
Hyper --> loss
| Hypo --> gain
106
(Hyper/Hypo) thyroidism:
- Carotenemia
- Exophtalmos
Hyper --> Exophtalmos
| Hypo --> Carotenmia
107
(Hyper/Hypo) thyroidism:
| -Goiter
Hyper --> Goiter (primary or secondary origin)
| Hypo --> Goiter (may or may not be present)
108
Primary hypothyroidism
Myxedema
| At the level of the thyroid; an inability to synthesize active thyroid hormones.
109
Primary hypothyroidism (Male vs Female; young vs old)
-More common in women than in man; appears at about 40-60 years of age
110
Primary hypothyroidism Causes
(1) Atrophy of the thyroid .
(2) Autoimmune Thyroiditis:
(3) Goitrous Hypothyroidism or Non-Toxic Goitre: )
111
Autoimmune Thyroiditis:
Destruction by antibodies against cellular components of thyroid
A.K.A. autoimmune thyroiditis or Hashimoto’s disease. More common in women.
112
Goitrous Hypothyroidism or Non-Toxic Goitre:
blockage in a step ofT4/T3 synthesis.
| -thyroid gland increases in size and there is goitre formation (non-toxic goitre).
113
Secondary hypothyroidism
-At level of the pituitary; synthesis of little or no thyroid stimulating hormone (TSH).
114
Tertiary hypothyroidism
At the level of the hypothalamus; synthesis of little or no thyrotropin-releasing hormone (TRH)
115
Infantile hypothyroidism
-Absence of thyroid gland or incomplete development of thyroid gland at birth
116
T4/T3 levels of Infantile hypothyroidism at birth
At birth infant is normal since the fetus uses mother’s T4/T3.
117
Physical affects of Infantile hypothyroidism after a few months
```
exhibits decreased physical growth & mental development
growth retardation (dwarfism) and the mental retardation associated with cretinism.
```
118
Treatment for hypothyroidism
administration of thyroid hormones
119
Primary hyperthyroidism
at the level of the thyroid gland
120
Toxic Diffuse Goiter (Graves Disease):
Autoimmune disease characterized by presence of substance produced by lymphocytes
called Long Acting Thyroid Stimulator (LATS)
121
Long Acting Thyroid Stimulator (LATS)
an antibody that mimics the action of TSH and
| stimulating release of T3 and T4
122
toxic goitre
Formation of goitre
| synthesizes biologically active T4/T3 from constant stimulation by LATS increases mass of thyroid leading to the
123
Thyroid adenoma or thyroid cancer
-synthesize of thyroid hormones independent ofTSH stimulation
124
Secondary hyperthyroidism
```
level of anterior pituitary gland
no negative feedback from increased levels of T3/T4 and synthesize autonomously thyroid
stimulating hormone (TSH). Often due to the presence of a pituitary tumor
```
125
Tertiary Hyperthyroidism:
at level of the hypothalamus
No negative feedback of high T3/T4 to decrease synthesis of thyrotropin releasing hormone
(TRH) Often it is due to the presence of a hypothalamic tumor.
126
Treatment for Hyperthyroidism
1. Surgery plus replacement therapy (administration of thyroid
hormones) .
2. Administration of radioactive Iodide (131I) about 5 mCi.
3. Administration of antithyroid drugs such as propylthiouracil
127
What do antithyroid drugs (propylthiouracil) do?
blocks addition of iodine to thyroglobulin
128
Specific care requirements for the administration of antithyroid drugs
Care must be taken not to inhibit the synthesis of thyroid hormones to a great extent and cause
hypothyroidism.
129
What does radioactive Iodide (131I) do?
The radioactive iodide concentrates in the cells of the thyroid follicles and destroys them. Replacement therapy may be administered as needed.
130
What are calcium ions essential for?
- essential structural component of the skeleton.
- important in normal blood clotting.
- with Na+ and K+ helps maintain transmembrane potential of cells.
- important in excitability of nervous tissue
- important in contraction of muscles
- important in release of hormones and neurotransmitters.
131
Concentration of calcium in cellular and extracellular fluid
~10mg/100ml.
132
Where does the calcium ions exist in circulation
50% free, 50% bound to albumin
133
Where is about 99 % of the body’s calcium?
Bone
134
What does bone serve as for calcium?
Bone thus serves as a calcium reservoir
135
Maintenance of plasma calcium is achieved mainly by
exchange between bone and plasma
| under influence of hormones
136
How do hormones affect the intestines and kidneys?
Hormones affect intestinal absorption of calcium and excretion of by kidneys
137
Where is Parathyroid hormone (PTH) produced?
protein and is produced by parathyroid glands
138
What does Parathyroid hormone (PTH) do?
increases circulating levels of Ca++
139
What does Calcitonin do?
-lowers the circulating levels of Ca++
140
What does Vitamin D do? (calcium)
-Increases the circulating levels of Ca++
141
Where is Calcitonin (PTH) produced?
protein and is produced by the parafollicular or “C” cells of the thyroid gland
142
Where is calcium obtained?
obtained in the diet; milk, cheese, eggs, butter etc.
143
Where is calcium absorbed?
-absorbed from the digestive tract primarily in the duodenum and upper jejunum.
144
What increases the absorption of calcium?
Its absorption is increased by vitamin D and PTH
145
From the plasma, where does the calcium go?
- some of the calcium will be deposited in bone or cells of other tissues
- some will go through the kidney and into the urine
146
What hormone increases calcium deposition
| in bone?
calcitonin
147
What hormone increases calcium loss through kidneys into urine?
calcitonin
148
What occurs when calcium plasma concentration is below 10mg/100ml?
PTH will stimulate reabsorption
| of calcium from the kidney and removal of calcium from the bone (bone resorption)
149
Stable concentrations of calcium in blood is achieved mainly by exchange between
calcium between
| bone and plasma under hormonal influence
150
Where is the parathyroid hormone secreted?
from parathyroid chief cells
| embedded in surface of thyroid
151
Where are parathyroid glands located?
back side of the thyroid gland
152
What results from the Removal of parathyroids
severe drop
in plasma calcium levels causing
tetanic convulsions and death
153
PTH amino acid structure
84 amino acid polypeptide - only Nterminal 34 amino acids important for
full activity.
154
What is PTH synthesized as part of?
a larger
| protein, preproparathyroid hormone,
155
How does preproparathyroid produce PTH?
undergoes proteolytic cleavage
156
Half-life of PTH
-Very short half-life – 3-18 minutes
| depending on individual
157
FUNCTIONS OF PTH (3)
1. Increase the concentration of plasma calcium :
2. Control of PTH release
3. Mechanism of PTH activity
158
What is the release of PTH controlled by?
controlled directly by the circulating concentration of calcium
159
What mechanism of PTH controls the activity?
binding to cognate receptor on target cells exerts
160
PTH impact on bone resorption
increases bone demineralization -increases Ca++in body
| fluids
161
PTH impact on kidney
increase the reabsorption of Ca++ in proximal convoluted tubule
162
PTH impact on Vitamin D synthesis
stimulates the conversion of 25-hydroxyvitamin D3 to
1,25-dihydroxyvitamin D3 (1,25D3; biologically active form of vitamin D)
primarily in kidney
163
PTH impact on gut
PTH and 1,25D3, facilitate the absorption of Ca++ from the gut
164
hypoparathyroidism
low levels of PTH in circulation
165
Symptoms of hypoparathyroidism
-low plasma calcium
-production of biological active vitamin D is decreased
Tetany, convulsions more serious clinical problems of hypoparathyroidism
166
hypocalcemia
low plasma calcium
167
convulsions
Spasms of laryngeal muscles may lead to death by asphyxiation.
168
Tetany
Ca++ <7mg/100ml -increased neural overexcitability - muscle spasms
169
hyperparathyroidism
high levels of PTH in circulation
170
hyperparathyroidism is often caused by
parathyroid adenoma of parathyroid producing too much PTH
171
hyperparathyroidism 1,25D3 levels
-high production of 1,25D3.
172
high PTH affect on bone and kidneys
high PTH stimulates bone resorption and calcium reabsorption from kidney.
173
1,25D3 affect on intestines
-1,25D3 increases calcium absorption from the intestines.
174
hyperparathyroidism calcium levesls
-elevated calcium in circulation.
175
formation of kidney stones is a common symptom of
hyperparathyroidism
176
Severe cases of hyperparathyroidism can result in
cardiac arrhythmias, depressed neuromuscular excitability,
| calcium deposition on walls of blood vessels and cartilaginous regions of bones
177
Treatment of hyperparathyroidism
```
removal of (affected) parathyroids and replacement therapy of 1,25D3
and Ca++
```
178
Treatment of hypoparathyroidism
removal of (affected) parathyroids and replacement therapy of 1,25D3 and Ca++
179
Where do we get VITAMIN D from?
- available from limited dietary sources (cod liver oil, fatty fish).
- can be synthesized from a cholesterol metabolite,
180
VITAMIN D is synthesized by
1. UVB light + 7-dehydrocholesterol in skin.
2. 25-hydroxylation in liver followed by…
3. 1-hydroxylation in kidney and several peripheral tissues-> 1,25-dihydroxyvitamin D3.
181
PHYSIOLOGICAL FUNCTIONS of VITAMIN D: (3)
1. primary function: increase calcium absorption from the intestine.
2. regulates the immune system -> protects against infection, anti-inflammatory
3. anticancer properties
182
REGULATION OF VITAMIN D SYNTHESIS IN KIDNEY IN conditions of low calcium
- increased in conditions of low calcium, when PTH is also increased
- depressed by high calcium
183
Vitamin D affect in northern countries
In northern countries, absence ofUVB may lead to vitamin D deficiency and deficient bone mineralization
184
Rickets in growing individuals
deficient bone mineralization
| baldness
185
Skin colour affect on vitamin D
vitamin D deficiency is more severe in dark-skinned people.
186
Low vitamin D in adults leads to
osteomalacia (soft bone).
187
Hereditary vitamin D
| -resistant Rickets is due to
– due to inactivating
mutation in the vitamin D
receptor
188
CALCITONIN peptide structure
32 amino-acid calcium-lowering peptide hormone
189
Where is calcitonin manufactured?
-manufactured in parafollicular or “C” cells of the thyroid gland
190
How does calcitonin lower the plasma calcium?
by promoting transfer of Ca++ from blood to bone,
| and increasing urinary excretion of Ca
191
Impact of increase in plasma calcium to calcitonin?
-rise in plasma Ca++ increases release of calcitonin.
-decrease in plasma calcium concentration decreases the release of
calcitonin
192
Absence of calcitonin impact on calcium homeostasis?
Absence of calcitonin does not compromise calcium homeostasis in man,
suggesting that its biological importance is limited.
193
Location of Adrenal Glands
-located adjacent to upper surface of kidneys
194
Adrenal Glands size in male vs female
-heavier in the male than in the female
195
two distinct types of tissue in adrenal glands
cortex and medulla
196
Histologic appearance of Cortex
large-lipid containing epithelial cells
197
Histologic appearance of Medulla
chromaffin cells-fine brown granules when fixed with potassium
bichromate
198
Origin of Cortex
derived from mesoderm
199
Origin of Medulla
derived from neural crest
200
Function of Cortex
Produces steroid hormones; glucocorticoids (major one being
cortisol in human) and mineralocorticoids (e.g.
aldosterone), and progestins
201
Function of Medulla
Produces catecholamines epinephrine and norepinephrine
& some peptide hormones (enkephalins, dynorphins and atrial natriuretic
peptides)
202
Adrenal Cortex layers
- zona glomerulosa
- zona fasciculata
- zona reticularis
203
zona glomerulosa produces
mostly mineralocorticoids (aldosterone).
204
zona fasciculata produces
produces mainly glucocorticoids (cortisol).
205
zona reticularis produces
glucocorticoids, progestins, androgens & estrogens
206
Synthesis of adrenal steroids controlled by
pituitary hormone adrenocorticotropin (ACTH).
207
18-hydroxylase is synthesized of
mineralocorticoid
| aldosterone
208
18-hydroxylase is only present in
zona glomerulosa
209
17a-hydroxylase is absent in
zona glomerulosa
210
Does the zona glomerulosa produce glucocorticoids
zona glomerulosa does not produce
| glucocorticoids.
211
Function of steroid
| hormones
to regulate (increase or
decrease) the transcription of
hormone/receptor-specific target
genes
212
Physiological role of Aldosterone
```
Sodium metabolism
- increases the
reabsorption of Na+ by the kidney
- Also affects the plasma concentration of K+ and H+
- loss of K+ and H+
in urine balance
reabsorption of Na+.
```
213
Main Glucocorticoids in humans
Cortisol
214
Glucocorticoids affect on salt retention
Some activity but less effective than aldosterone. Can be important under pathological
conditions when plasma cortisol remains elevated
215
Glucocorticoids effects on protein and carbohydrate metabolism
- Stimulate the synthesis of a number of gluconeogenic enzymes in hepatocytes, and several enzymes that breakdown proteins in muscle and other tissues
- released amino acids enter liver and are converted to glucose and glycogen (gluconeogenesis).
- Decrease glucose uptake by muscle and adipose tissue and decrease glycolysis (glucose oxidation) to conserve glucose for other tissues.
- leads to increased blood glucose levels -> increased insulin secretion *
216
adrenal diabetes
Increased blood glucose due to excess of glucocorticoid activity
– if prolonged, may lead to destruction of beta-cells of pancreas and true diabetes mellitus.
217
Glucocorticoids on Lipid metabolism
maintain or increase the levels of lipolytic enzymes in the adipose tissue cells and augments lipolytic action of other hormones, e.g. epinephrine
218
Excess of what can lead to hyperlipidemia and hypercholesterolemia
excess of glucocorticoids
219
Anti-inflammatory and immunosuppressive actions of glucocorticoids:
-Reduce inflammatory responses: e.g. at sites of injury.
-Cause atrophy of the lymphatic system (lymph nodes, thymus, spleen)
-decreased levels of circulating lymphocytes and reduced antibody formation. Therefore
glucocorticoids used in organ transplantation
-decrease histamine formation and thus decrease allergic reactions.
220
Effects of glucocorticoids on bone
-decrease the protein matrix of the bone through their protein catabolic effect. As a result,
increased loss of Ca++ from the bone leading to osteoporosis
221
osteoporosis
weakens bones to the point where they break easily
222
Control of glucocorticoid secretion is done by
pituitary adrenocorticotropin
| ACTH
223
```
pituitary adrenocorticotropin
(ACTH) structure
```
39 amino acid polypeptide
224
What is 39 ACTH synthesized as part of
larger protein known as
| proopiomelanocortin (POMC)
225
feedback control of cortisol secretion is via
hypothalamus and anterior pituitary
226
In cases of enzyme deficiencies (lack of 11bhydroxylase) where cortisol is not produced; how is ACTH secretion impacted
ACTH secretion is unchecked
227
Enzyme deficiencies where cortisol is not produced can result from
congenital adrenal hyperplasia
228
treatment for congenital adrenal hyperplasia
administration of cortisol, which (a)
corrects the deficiency and (b) normalizes the
ACTH secretion
229
What/where does ACTH bind to?
binds to specific ACTH receptor
| on membranes of zona fasciculata and zona reticularis cells
230
ACTH stimulation of adenylyl cyclase leading to
| increased production of
cyclic AMP
231
Daily rhythm of plasma cortisol and ACTH levels at night /morning
- diurnal rhythm of ACTH and cortisol secretion
- minimum at midnight and
maximum in the morning.
232
the daily rhythm of plasma cortisol and ACTH compared to sleep
-rhythm may be independent of sleep and
| abolished by stress and Cushing’s disease.
233
activation steroidogenic enzymes leads to
increased synthesis and release of steroid
| hormones
234
What activates steroidogenic enzymes
ACTH
235
How does stress, affect syntheisis and release of CRH, ACTH, and cortisol
increase
236
Common types of physiological stresses
pain, fear, exercise, hunger, cold, hemorrhage
237
Release of cortisol during stress advantageous impacts
- provides energy and
| amino acids through the breakdown of tissue proteins, especially under conditions where normal feeding not feasible
238
Release of cortisol during stress disadvantageous impacts
cortisol inhibits wound healing.
239
Prolonged stress would maintain constantly high levels of
glucocorticoids
240
constantly high levels of glucocorticoids can lead to
```
increased blood glucose (true diabetes mellitus), decreased
immune responses (individual will become susceptible to infections), loss of
bone etc
```
241
Addison’s Disease
hypofunction of adrenal cortex
242
What is Addison's disease characterized by ?
characterized by failure of the adrenal
| cortex to produce adrenocortical hormones
243
What effect may the gland have with addison's disease
involve total destruction of the gland
244
What does Addison's disease mostly results from?
autoimmune attack on the
adrenal glands, but can also be caused by
tuberculosis.
245
Cushing’s Disease
hyperfunction of adrenal cortex
246
What is Cushing’s Disease characterized by ?
by hyperplasia of the
adrenal cortex due to increased circulating
levels of ACTH.
247
In Cushing’s Disease, how are the productions of glucocorticoids and mineralocorticoids impacted?
excessive production of glucocorticoids
as well as increased production of
mineralocorticoids.
248
Location of the pancreas
located behind the stomach
249
Percentage of pancreas that is exocrine
99 % of pancreas is exocrine and secretes the digestive enzymes
250
Islets of Langerhans
scattered within the exocrine pancreas are small endocrine structures, compact mass of cells with good vascularization
251
beta-cells
synthesize insulin
| About 60 % of the cells of the islets of Langerhans
252
alpha-cells
synthesize glucagon
| About 25 % of the cells of the islets
253
Insulin and glucagon
small protein hormones and both control of glucose
| concentration in blood
254
Why is insulin very important?
insulin is more important than glucagon and insulin deficiency or absence compromises
significantly the well-being of the individual and if not treated may lead to death
255
Only hormone that acts primarily to
| decrease blood glucose
-Insulin
256
Where is glucose always present?
In the blood
| - 80 mg/100 mL
257
Where is there little free glucose ?
in tissues
258
How must glucose enter cells
Where is glucose always present?
259
What is glucose converted into in the liver and muscle cells
glycogen
260
What is glucose converted into in the adipose tissue cells?
to fat and stored for later use
261
What happens to glucose in many cells of the body cells?
oxidized to produce
| energy
262
Insulin receptor
Membrane receptor, stimulates
insertion of glucose transport proteins stored in
cytoplasm into plasma membrane
263
How does the insertion of glucose transport proteins into plasma membrane affect glucose uptake
increases glucose uptake
264
Results when the b-cells are destroyed
Insulin deficiency
265
Insulin deficiency
Results when the b-cells are destroyed
266
What can Insulin deficiency lead to
Diabetes Mellitus
267
Diabetes Mellitus
most tissues cannot take
up glucose efficiently, glucose accumulates in
circulation.
268
Can Insulin deficiency occur if there is no glucose in diet
Occurs even if no glucose in diet because of
increased gluconeogenesis (e.g. protein
breakdown to amino acids and synthesis of
glucose)
269
During Insulin deficiency what is the principal source of energy?
free fatty acids (FFA) - increased lipolysis
270
What occurs when fat is inefficiently used
incomplete
oxidation of FFA and increased circulating
acetoacetic acid and b-hydroxybutyric acid
(metabolic acidosis) and acetone (ketosis -
acetone smell in breath of untreated diabetics).
271
How does increased lipolysis affect blood pH
leads to decreased blood pH, and death unless treatment is provided
272
pH affect from diabetic coma
decreased blood pH
273
glycosurea
presence of reducing sugars in the urine
274
At >180mg% what happens to glucose
glucose spills over into urine
275
How does diabetes mellitus effect the water in urine
-leads to loss of water in urine, causing polyurea
276
polyurea
- dehydration and increased thirst
277
polydipsia
increased thirst
278
What leads to ketosis, and metabolic
| acidosis?
untreated diabetes
279
Treatment of diabetes Mellitus
-administration of insulin is needed to restore individual back to normal.
280
in diabetic comas, what must be corrected in addition to insulin administration?
acidosis and associated electrolyte imbalance
281
diabetes insipidus
persons suffering from
| antidiuretic hormone deficiency
282
Two types of diabetes
type 1 insulin-dependent or type 2 insulin independent
283
type 1 diabetes
deficiency of insulin
284
type 2 diabetes
hyporesponsiveness to insulin
285
what happens to b-cells during type 1 diabetes?
Destruction of the b-cells in the pancreas
286
Destruction of the b-cells of pancreas causes
Type 1 diabetes where synthesis of insulin does not occur
287
Treatment for Destruction of the b-cells of pancreas
administration of insulin is needed associated with proper diet
288
Defective insulin release causes
Type 1 diabetes where insulin is not released
289
Defective insulin release treatment
Drugs stimulating insulin release could be
| administered again associated with proper diet and exercise.
290
Affect on brain when blood glucose reaches 20-30mg/100ml?
the availability
of glucose for the brain is not sufficient and the individual may fall into a coma known as insulin shock or hypoglycemic coma
291
insulin shock or hypoglycemic coma
To little glucose in brain
292
insulin shock or hypoglycemic coma treatment
treated with
immediate administration of glucose, otherwise death or permanent brain
damage may occur
293
Insulin levels in TYPE 2 DIABETES
Insulin levels normal or abnormally high
294
problem in type 2 diabetes
hyporesponsiveness of target cells to insulin
295
insulin resistance often
| due to
decreased number of insulin receptors on target cells
296
What type of diabetes is associated with obsiety?
Type 2
297
overeating affect on insulin/ insulin receptor levels?
```
prolonged high insulin levels decrease
number receptors (downregulation)
```
298
treatment for type 2 diabetes
- proper diet and exercise
| - decreased caloric intake, decreased insulin, upregulation of receptors
299
how do insulin receptors change in response to endurance?
insulin receptors increased in response to frequent endurance exercise,
independent to changes in body weight
300
JUVENILE DIABETES MELLITUS
Juvenile diabetes mellitus appears in childhood and is insulin dependent
301
B cells in JUVENILE DIABETES MELLITUS
The b-cells
| of pancreas do not produce insulin
302
Treatment of JUVENILE DIABETES MELLITUS
Treatment requires administration of insulin
303
Glucose tolerance test
Blood Glucose Concentration compared Time
304
How is glucose tolerance changed in diabetes?
Glucose tolerance is decreased in diabetes
(low or absence of insulin) and is increased in
hyperinsulinism
305
How did blood glucose change in normal vs diabetic individuals?
increase in blood glucose is
| greater and returns to normal more slowly
306
Purpose of insulin section feedbacks?
control of insulin release to avoid hypoglycemia.
307
beta cells responding to levels of blood glucose is a
negative feedback mechanims
308
beta cells affect on insulin section
secreting little or no
| insulin when blood glucose low, secreting much more when the blood glucose is high
309
The release of what (2) induce insulin release
release of gastrin and vagal impulses to the beta-cells induce insulin release, as
a result insulin starts to leave the pancreas even before the blood glucose begins to
rise during meals
310
What peptide hormone is synthesized and released by alpha cells of pancreas.
Glucagon
311
-Metabolic functions of glucogon compared to insulin
opposite
312
metabolic function of glucogon
Raises blood sugar
313
How does glucagon raise blood sugar in the liver?
by promoting glycogenolysis (breakdown of glycogen) and
| gluconeogenesis (synthesis of glucose) in the liver.
314
How does glucagon raise blood sugar in adipose tissue?
glucagon increases rate of lipolysis leading to increased
| concentration of free fatty acids in circulation
315
What is glucagon release controlled by?
concentration of glucose in circulation
316
What does low blood glucose stimulate in pancreatic alpha cells?
to increase synthesis and release of glucagon
317
What does high blood glucose stimulate in pancreatic alpha cells?
high blood glucose content decreases release and synthesis
318
Is more glucagon super important for increased blood glucose content?
Glucagon not as important as insulin, other hormones increase blood glucose content such as cortisol (glucocorticoids) as well as epinephrine, nor-epinephrine etc
319
Where is growth hormone produced?
anterior lobe of the pituitary
320
What is growth hormone responsible for?
growth
321
Somatotropin is also known as
growth hormone
322
What is growth hormone do? (2)
-Increases protein synthesis in many tissues such as bone, muscle, kidney, liver by
enhancing amino acid uptake by cells and by accelerating the transcription and
translation of mRNA
- increases the rate of lipolysis and utilization of free fatty acids as a source of energy
323
What direct affect of growth hormone is not mediated by somatomedins?
increases the rate of lipolysis and utilization of free fatty acids as a source of
energy
324
Where are somatomedins produced?
liver
325
What condition are somatomedins produced?
under stimulation of GH
326
How do somatomedins compare to insulin?
structurally similar to insulin
327
Another name for somatomedins
insulin-like growth factors I and II (IGFI and IGF-II)
328
IGFI and IGF-II
bind to insulin receptors and insulin at high
| concentrations may bind to somatomedin receptors)
329
What do somatomedins do?
increase protein synthesis and stimulate growth
330
The GH released is controlled by
mediated
| by two hypothalamic neurohormones
331
What two hypothalamic neurohormones control GH release
- growth hormone releasing hormone
- somatostatin (growth hormone
inhibiting hormone
332
somatoliberin
growth hormone releasing hormone
(GRH) also known as somatoliberin,
which stimulates growth hormone
release
333
somatostatin
(growth hormone inhibiting hormone), which inhibits
| growth hormone release
334
How are GRH and somatostatin regulated?
tightly regulated by
an integrated system of neural, metabolic,
and hormonal factors
335
GH Deficiency in young leads to ?
In the young, absence of growth hormone leads to decreased physical growth
336
Excess GH in young leads to ?
In young individual leads to gigantism.
337
Excess GH in later in life (adult) leads to what condition?
condition of acromegaly
338
acromegaly
many bones get longer and heavier
| particularly at the cartilaginous regions of the bones
339
primary reproductive organs
the gonads, testes in the male, ovaries in the female
340
Two functions of the gonads
Gametogenesis
| Secretion of sex hormones (specific steroids)
341
Gametogenesis
the production of reproductive cells known as gametes;
the spermatozoa in the male
ova in the female
342
Name of male reproductive cells (gametes)?
spermatozoa
343
Name of female reproductive cells (gametes)?
ova
344
Male sex hormone
testosterone (androgen) in the male
345
Female sex hormone
estrogen and progesterone in the female
346
Are the differences in reproductive endocrinology in males and females, quantitative or
qualitative
is quantitative and not
| qualitative
347
Are androgens unique to males?
No
348
Are estrogens unique to females?
No,
349
What can produce small amounts of estrogen
Testes
| produce small amounts of estrogen
350
What can androgens be converted into?
androgens can be converted into estrogens by
| a single enzymatic step in several non gonadal tissues (bone, for example)
351
Where are androgens usually produced in females (amounts too)?
produced in small amounts in ovaries and in larger amounts by the adrenals
352
How is estrogen produced in males?
locally in tissues by the conversion by aromatase
| of testosterone the estrogen estradio
353
Estrogen deficiency in males results in
(i) Leads to increased body fat.
| (ii) Contributes to sexual desire and erectile function.
354
Gonadotropin releasing hormone (GnRH) is secreted by
hypothalamus
355
How does Gonadotropin releasing hormone (GnRH) travel?
travels to anterior
| pituitary via hypothalmo-pituitary portal vessels
356
What stimuilates the release of pituitary gonadotropins
follicle-stimulating hormone
| FSH) and luteinizing hormone (LH
357
FSH and LH stimulates
development of spermatozoa or ova, and secretion of sex
| steroids
358
Where do sex steroids exert effects
effects in gonads, in other
parts of the reproductive system, and body
(e.g. estrogen maintains bone density; i.e.
prevention of osteoporosis)
359
where is inhibin protein produced?
Gonads
360
What does inhibin protein do?
feeds back on the anterior pituitary
361
-The principal function of testes
production of mature germ cells
(spermatogenesis) , and steroid hormones
(steroidogenesis) .
362
Females supplyy of ova
e females, who at birth has her
| whole life’s supply of ova,
363
Males supply of precursor germ cells
```
the male
continually renews his pool of precursor
germ cells (spermatogonia) so that a
relatively constant supply is available
throughout life
```
364
The process of spermatogenesis takes
| place within the
Coiled seminiferous
| tubules of the testes
365
The time it takes for maturation from immature spermatogonia to the mature spermatozoon
approximately 60
| days in humans
366
Two cell types are critical for
| maturation of spermatozoa
Leydig cells and Sertoli cells
367
Where are Leydig cells located?
outside the seminiferous
| tubules
368
In response to LH, what do Leydig cells do?
synthesize androgens
369
Where are Sertoli cells located?
within the seminiferous
| tubules
370
What are Sertoli cells intially involved in?
sperm maturation process
371
In response to FSH, what do Sertoli cells do?
synthesize
| Androgen Binding Protein (ABP) and inhibin
372
What is Spermatogenesis dependent on? where? how much?
```
critically dependent on androgen
concentrations
-within seminiferous tubules,
- 10 times higher
than androgen concentration in circulation
```
373
What happens if less than 10 times higher concentration in seminiferous tubules than circulation?
otherwise spermatogenesis ceases
374
What ensures high androgen concentration
| within seminiferous tubules
presence of ABP synthesized by Sertoli cells
375
Testicular androgen synthesis regulated by
two negative feedback loops:
376
two negative feedback loops for Testicular androgen synthesis
Hypothlamic-pituitary-Leydig cell axis
Hypothalamic-pituitary-seminiferous-tubules axis:
377
Hypothlamic-pituitary-Leydig cell axis
GnRH stimulates release of LH and FSH -
stimulate Leydig cells and Sertoli cells. Leydig cells produce androgen, which
inhibit the release of GnRH , LH and FSH
378
Hypothalamic-pituitary-seminiferous-tubules axis
non steroidal inhibin
| secreted by the sertoli cells inhbits FSH release only
379
Principal functions of ovary
production of mature
| eggs, and steroid hormones
380
What do mature eggs, and steroid hormones do
regulate the reproductive tract and influence sexual behavior
381
Where are germs cells at brith
At birth ovary contains non-proliferating
| pool of germ cells or oocytes
382
Number of ova at birth vs pubery
about 2 million), which are its whole life supply of ova.
| At puberty only ~400,000 ova left
383
The oocytes are surrounded by a
single layer
of granulosa cells and a basement membrane
making up the structures called primordial
follicles -
384
fundamental reproductive units of
| the ovary
primordial follicles
385
Growth of primordial follicles is controlled by? until?
gonadotropins and
steroid hormones until the follicles either
ovulate or degenerate (atresia).
386
Follicular development leads to one of two events
1. Follicular Atresia
| 2. Ovulation
387
Follicular Atresia
Although many follicles initiate growth and development in each
reproductive cycle, in humans usually only one follicle will ovulate in each
reproductive cycle - remaining secondary follicles degenerate in a process
known as atresia
388
atresia
process of remaining secondary follicles
389
Ovulation
follicular rupture
390
What happens to ruptured follicle?
Ruptured follicle transformed into Corpus
| Luteum
391
What does Corpus Luteum do
secretes progesterone
392
What cell/s cells contribute to
| formation of the corpus luteum
Both theca and granulosa cells
393
a temporary
| endocrine structure within the ovary? what does it synthesize?
corpus luteum
| progesterone and estrogens
394
Progesterone and estrogens amounts following ovulation? what happens after?
Progesterone and estrogens are produced in large
amounts by corpus luteum for few days following
ovulation but then drop off unless implantation of
the fertilized ovum occurs
395
-Upon implantation, corpus luteum transformed
| into
corpus luteum of pregnancy
396
corpus luteum of pregnancy is responsable for
synthesis of progesterone and estrogens and
creation of proper endocrine environment for maintenance of pregnancy until progesterone and
estrogen synthesis by placenta established
397
In absence of implantation what happens to corpus luteum?
Luteolysis occurs
| life span of corpus luteum limited
398
What induces luteal regression?
prostaglandins which decrease LH binding and thus
| steroidogenesis
399
What may be trigger for initiation of next
| reproductive cycle
Decrease of plasma progesterone and
| estrogen
400
Prior to day 1 of the menstrual cycle what happens to the endometrium? under the influence of what?
-Prior to day one, endometrium thickens under influence of estradiol
401
What induces the appearance of specialized glycogen-secreting glands
progesterone
402
What occurs on day 1 of menstrual cycle?
first day of detectable vaginal bleeding
| deterioration of uterine endometrium
403
When does menses begin?
when estradiol and progesterone very low in circulation, when
the blood vessels supplying endometrium constrict reducing the blood supply
404
When the endometrium deteriorates where does it flow?
flows through the cervix into the vagina
405
How long does bleeding last? what happens to the ovaries?
Bleeding occurs for ~5 days during which, ovaries are endocrinologically rather inactive
406
Low estradiol and progesterone lead to secretion of what hormone and decreases what
to increased
pituitary FSH secretion (lack of –ve feedback loop)
decrease in non-steroidal ovarian inhibin
407
What does non-steroidal ovarian inhibin do?
selectively inhibits secretion of FSH, may
| contribute to elevation in FSH release
408
What happens to ovarian follicles under influence of FSH
Under influence of FSH, cohort of ovarian follicles
| develop.
409
What does FSH stimulate in menstrual cycle?
granulosa cells of follicles to proliferate
410
How does the stimulation of granulosa cells of follicles to proliferate affect estrogen levels? and granulose cells?
production of estrogen, which further stimulates granulosa cell proliferation
411
What occurs on day 8 of the menstrual cycle?
one follicle becomes dominant and
committed to further development. Remaining
follicles begin to degenerate by atresia
412
What does the dominant follicle produce? effects?
produces increasingly more estradiol
| increasing estradiol stimulates uterine endometrium proliferation
413
What happens to the endotherium by day 13?
the endometrium very thick
414
What induces the production of endometrial progesterone receptors?
Estradiol
415
Moderate estradiol concentrations on FSH release
negative feedback
416
What does moderate estradoil concentraions stimulate? which in turn stimulates?
stimulate synthesis of LH by pituitary and increase sensitivity of pituitary to GnRH
stimulates LH synthesis
417
Under influence of developing follicles at high estradiol concentrations what happens?
estrogen concs.
| continue to build
418
Elevated estrogen concs. stimulate
LH release - LH surge
419
On day 14 what happens to FSH
small increase in FSH release also occurs
420
What happens to LH synthesis by day 14.
Stimulation of LH synthesis by estradiol and increased sensitivity of the anterior pituitary to GnRH leading to increased LH synthesis by anterior pituitary known as estrogen +ve feedback control mechanism
421
What feedbacks does estrogen exert?
-ve feedback - decreased GnRH and LH release
+ve feedback -
increased sensitivity of anterior pituitary cells to GnRH and increased LH synthesis
422
At day 14, what is the size of the follicle and why does it rupture? cause on ovum
the follicle has become huge.
The sudden surge of LH causes the
follicle to rupture and the ovum is ejected
423
Oral contraceptives contain
estrogen and progesterone
424
What do Oral contraceptives do
maintain moderate circulating levels of estrogen and progesterone suppress the release of LH and FSH from the pituitary and prevent ovarian
follicles from maturing and being ovulated
425
Under the influence of LH the follicle becomes
corpus luteum
426
Under the influence of LH the follicle produces
large amounts of
| estradiol and progesterone
427
The production of large amounts of
| estradiol and progesterone induces
endometrial growth of the uterus
| the endometrium becomes glandular
428
The luteal Phase occurs when there is
no fertilization
429
What happnes during the luteal Phase? how long does it last?
- egg degenerates, corpus luteum degenerates (luteolysis)
| 14 days
430
What happens after 14 days in absence of implantation?
- corpus luteum
- steriod levels
- uterune endometrium
- menstruation
- FSH secretion
After 14 days in absence of implantation corpus luteum degenerates, steroid levels drop,
uterine endometrium degenerates, menstruation begins and pituitary starts to increase its
secretion of FSH,
431
At ovulation where is the unfertilized egg taken? where is it propelled towards?
unfertilized egg is taken by the fimbria of the oviduct (or fallopian tube)
Is being propelled towards the lumen of the uterus
432
If sexual intercourse takes place around the ovulation time what happens
```
fertilization!
some spermatozoa
deposited in the vagina will travel as
far as the oviduct and one of these will
fertilize the egg
```
433
After fetilization what happens to the egg? where is it transported?
Egg starts dividing to the stage of
blastocyst during its transport down
the oviduct into the uterine lumen
434
After implantation, the Blastocyst differentiates into (2)? which becomes the?
Blastocyst differentiates into trophoblast (becomes
the placenta) and the inner cell mass (which will form
the embryo)
435
Around time of implantation, trophoblast starts to
| synthesize
human chorionic gonadotropin (HCG)
436
human chorionic gonadotropin (HCG) has similar properties to
LH-like properties
437
WHat does HCG stimiute
the corpus
| luteum to continue secreting gonadal steroids
438
After about 12th week of pregnancy endocrine function of corpus luteum is taken over by
placenta
439
The plcenta with the developing fetus forms the
fetoplacental unit
440
HCG appears in what? and what is the levels used for?
```
HCG quickly appears
in blood and urine
where it forms the
basis for the biological
or immunological
pregnancy test
```
441
lactation
The secretion of milk by the breast
442
What. is required for lactation
Normal mammary
| development under endocrine control
443
Ductal
Mature non-pregnant mammary glands
444
marked
| enhancement of duct growth and duct branching in puberty occurs because of
increasing levels of estrogens
445
in prescence of estrogen, marked enhancement of duct growth and duct branching
but relatively little development of the
alveoli
446
What stimulates the growth of the aveoli
Progesterone
447
most breast enlargement due to
fat deposition under the glandular tissue
448
What causes both
| ductal and alveoli structures to fully develop
Under influence of several hormones, including estrogen,
| progesterone, prolactin, human placental lactogen
449
Milk production during pregnancy controlled by
prolactin
450
What inhibits milk secretion
high estrogen levels
451
What induces milk synthesis and the alveoli secrete
| milk, filling the ducts
Prolactin
452
What causes ducts contract to cause milk ejection.
under action of oxytocin
453
What do ferent
| fibers (nerves) from nipple stimulate
Prolactin from anterior pituitary and oxytocin from posterior pituitary
454
What sustains milk production?
Prolactin
455
What causes milk letdown or ejection
oxytocin
456
Milk contains
water, protein, fat and carbohydrate lactose and antibodies
457
What can be transmitted from mother to infant through breast milk?
infectious agents
| such as viruses and drugs
458
Lactational amenorrhea
Maintained nursing stimulates prolactin production, which inhibits the secretion of FSH
and LH
459
What does Lactational amenorrhea block
The resumption of the reproductive cycle
460
Menopause
loss of ovarian steroid production
461
Effect on hormones from Depletion of follicles
loss of capacity for steroid (estrogen and progesterone)
| hormone production by the ovary
462
What induces the following symptoms?:
hot flashes, dry vagina,
restlessness, bone loss (osteoporosis - long term)
-Lack of estrogens
463
What eliminates–ve feedback loop and rise in
| levels of plasma gonadotropins FSH and LH
Cessation of ovarian steroid hormone production
464
The constantly high levels of plasma FSH is
| most reliable indicator for
onset of menopause
