Endocrinology Flashcards
1
Q
Function of the endocrine system?
A
Regulates critical aspects of bodily function(ex. Respiration, digestion, excretion)
2
Q
Long distance communication in the endocrine system?
A
-releasing cells secrete chemical substances that interact with specific receptors on distant target cells
3
Q
Endocrine signaling?
A
- A hormone is secreted into the blood by an endocrine gland
- The hormone is then transported by the blood to a distant target
4
Q
What is a hormonal cascade?
A
The pathway a hormone takes, first it is released by an endocrine gland, then it is transported through the blood and then it binds to a target receptor leading to a physiological effect
5
Q
Source of hormones in neuroendocrine signaling?
A
Anterior pituitary contains neuronal cells that release the hormone
6
Q
Paracrine signaling?
A
Signaling between adjacent cells(close proximity)
Cells can be of the same type of different
7
Q
Autocrine signaling?
A
Individual cell release a substance and that substance binds to receptors on the cell that released it (cell talking to itself)
8
Q
Step 1 of communication by hormones(or neurohormones)?
A
- Synthesis of the hormone by endocrine cells(or neuronal cells in the case of neurohormones)
9
Q
Step 2 of communication by hormones(or neurohormones)?
A
- Release of the hormone by the endocrine cells(or neurohormones by the neurons)
10
Q
Step 3 of communication by hormones(or neurohormones)?
A
Transport of the hormone or neurohormone to the target site by the blood stream
-Hormone is often transported in the bloodstream bound to proteins
11
Q
Step 4 of communication by hormones(or neurohormones)?
A
Detection of the hormone or neurohormone by a specific receptor protein on the target cells
12
Q
Step 5 of communication by hormones(or neurohormones)?
A
A change in cellular metabolism triggered by the hormone-receptor interactions
13
Q
Step 6 of communication by hormones(or neurohormones)?
A
Removal of the hormone, this often terminates the cellular response
-Some of these hormones have short half lifes
14
Q
Classical Endocrine organs?
A
-Hypothalamus
-Anterior/posterior pituitary
-Thyroid/parathyroid glands
-Adrenal glands
-Pancreas
-Ovaries/Testis
15
Q
Hypothalamic-Hypophyseal Portal system?
A
A vascular network that connects the hypothalamus to the anterior pituitary. Allows rapid transport of hormones from the hypothalamus to the anterior pituitary
16
Q
Hypothalamic-Pituitary Signaling?
A
-Occurs via the Hypothalamic-Hypophyseal Portal system(blood vessels of the pituitary stalk)
17
Q
Hypothalamic neurohormones effect on the anterior pituitary?
A
-Can either activate or inhibit activity of one of the six types of hormone producing cells in the anterior pituitary
18
Q
Releasing vs inhibiting hypothalamic hormones?
A
Releasing hormones: Hormone released by the hypothalamus causes cells in the anterior pituitary to produce hormones
Inhibiting hormones: Hormone released by the hypothalamus causes cells in the anterior pituitary to stop releasing hormones
19
Q
Anterior pituitary ?
A
-Connected to the hypothalamus
-Source of multiple types of hormones
-All hormones released by the AP are controlled by the hypothalamus
20
Q
Posterior pituitary?
A
An extension of the hypothalamus
21
Q
Classes of hormones?
A
- Peptides and proteins
- Steroids(small molecules)
- Amines(small molecules)
22
Q
Protein/peptide hormones and examples?
A
-Genome encodes a gene for the hormone
-Ex. Insulin(production of insulin is initiated by transcription of the insulin gene)
23
Q
Small molecule hormones?
A
-No gene encodes these proteins
-There are genes that encode enzymes necessary for the biosynthesis of these small molecules
24
Q
Synthesis of protein hormones?
A
- Synthesized as a pre prohormones on ribosomes where there are N-terminal extensions of the protein coding sequence.
- During the secretory process prepro sequences are cleaved off
- When the polypeptide is released it is in its mature form lacking the pre pro sequence
25
Why is the protein hormone first synthesized as a prepro hormone?
The prepro hormone sequences help guide the polypeptide into the secretory system
26
Structure of aldosterone and cortisol?
-These steroid hormones have similar structures because they are both produced by the adrenal glands
27
Structure of estradiol and testosterone?
-These two steroid hormones also have very similar structures because they are both produced by the gonads
28
How is testosterone different from estradiol(role of aromatase)?
Testosterone aromatic-ring has a CH3 group preventing double bond
Aromatase: is an enzyme that removes the CH3 group and then testosterone spontaneously converts to estradiol
29
T/F: Testosterone is a precursor to estradiol?
True
30
Thyroid hormone structures and examples?
-Derived from tyrosine
-These hormones require iodine for production
-Ex. T4(made up of 4 iodine residues), T3(made up of 3 iodine residues)
31
What is rT3?
rT3 looks like a thyroid hormone however it cannot bind to thyroid hormone receptors
32
How to avoid thyroid hormone deficiency?
Add iodine to salt
33
Do T4 and T3 bind to thyroid hormone receptors?
Yes
34
"lock and key: mechanism for a hormone binding to a membrane receptor ?
1. The hormone has structure that is complementary to that of the receptor.
2. When the hormone binds to the receptor it induces a conformational change in the receptor that stimulates it activity
35
What happens once the receptor is activated by the hormone?
Receptors are often associated on the intracellular side of the cell to regulatory proteins that can lead to the activation of an enzyme or change in protein activity in cells(cascade)
36
Specificity of hormone receptors?
Receptors only recognize a single hormone or hormone family
37
Affinity of hormone receptors?
Hormone receptors bind hormones at their physiological concentration
38
Why do receptors bind hormones only at their physiological concentration?
Because if they were to just bind them whenever the hormone was present then the receptor would never be off unless we completely got rid of the hormone
39
Hormone receptors should show satiability?
Yes, hormone receptors shoulld have a finite number of receptors
40
Hormone receptors should have a measurable biological effect?
When the receptor is bound by the hormone it should result in a measurable biological effect
41
How can receptors be upregulated?
Receptors can be upregulated either by increasing their activity in response to hormone or their synthesis
42
How can receptors be downregulated?
Receptors can be downregulated either by decreasing their activity in response to hormone or their synthesis
43
3 mechanisms by which a hormone can exert effects on target cells?
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
44
Direct effects on function at the cell membrane how does the hormone do this?
There is a directi communication between the receptor and a regulatory subunit of the receptor
45
Intracellular effects mediated by second messenger systems
1. Hormone(first messenger) binds to the receptor which is coupled to a G-protein
2. Activation of the receptor causes ATP to convert to cAMP
3. cAMP binds to a protein kinase which becomes active and phosphorylates a number of target proteins within the cell
4. The phosphorylation changes the activity of those proteins either activates or represses them (signal is sent through second messenger)
46
Intracellular effects mediated by genomic or nuclear action?
This is signaling by nuclear receptors which bind steroid hormones
1. Steroid hormone can enter the cell and bind to receptors within the cytoplasm of the cell.
2. This induces translocation of the receptor into the nucleus where it will act to regulate transcription of a subset of genes
3. It changes the rate of transcription and protein content in the cell which changes the way the cell functions
47
T/F: Hormone secretion is regulated by feedback mechanisms?
True
An excess of hormone, leads to a diminuation of hormone secretion
Conversely, a deficiency of hormone leads to an increase in hormone secretion
48
Calcium feedback loop?
Low calcium leads to stimulation of parathyroid glands which leads to synthesis and release of parathyroid hormone. PTH secretion increases which leads to action on bone, kidney and gut that increase plasma calcium concentration
The increase in plasma calcium then inhbits stimulation of the parathyroid glands
49
CRH and ACTH?
Corticotopin releasing hormone
Adrenocorticotropic hormone
50
Negative feedback mechanism of cortisol?
51
Pituitary gland anatomy and their tissues?
-Anterior pituitary(endocrine tissue)
-Posterior pituitary(neural tissue)
Two completely distinct tissues
52
What hormone released by the hypothalamus causes FSH and LH to be released by the anterior pituitary?
Gonadotropin releasing hormone
53
Posterior pituitary hormones, what do they control(2)?
-Arignine vasopressin(BP SM)
-Oxytocin (birth SM)
These were made by gene duplication (similar structures) and they control SM tension
54
What are hypophyseotropic hormones?
Hormones released by the hypothalamus that target the anterior pituitary
55
Hypophyseotropic hormones(6)?
1. TRH
2. GnRH
3. Somatostatin
4. GRH
5. PIH(dopamine)
6.CRH
All of these are peptide hormones except PIH
56
What does the posterior pituitary gland release?
-Secretes oxytocin and vasopressin
(aka,. Antidiuretic hormone)
57
Where/how are oxytocin and vasopressin synthesized?
1. Synthesized in two hypothalamic nuclei, whose axons run down the pituitary stalk and terminate in the posterior pituitary close to capillary blood vessels
2. The prohormones are processed/cleaved in the secretory granules during axonal transport
3. Mature hormones are then liberated from the carrier molecules (neurophysins)
58
What is the circulating half-life of oxytocin and vasopressin?
1-3 minutes
59
Function of oxytocin in females for parturition(birth)?
Dilation of the uterine cervix by the fetal head causes release of oxytocin which leads to uterine contractions, which helps expulse the fetus and placenta
60
T/F: The uterus is extremely sensitive to oxytocin at the end of pregnancy?
True
61
Function of oxytocin in females for milk ejection?
In lactating mother oxytocin is released in repsonse to suckling
Oxytocin causes milk filled ducts to contract and squeeze milk out
62
Function of oxytocin in females/males behavioral effects?
Local oxytocin release in the brain reduces anxiety and enhances bonding, and pro-social behaviour
63
Function of oxytocin in male ejaculation?
Oxytocin surge during sexual activity assists passage of sperm and ejaculation
64
Thyroid gland (thyroglobulin)?
Thyroglobulin is a large protein found in the thyroid gland in a fluild filled space called the colloid
65
What is the function of thyroglobulin, what stimulates synthesis of it?
Thyroglobulin is crucial for the synthesis of thyroid hormones thyroxine(T4) and triiodothyronine(T3)
Synthesis of thyroglobulin is controlled by TSH (released by anterior pituitary)
66
T4 and T3?
Produced by the thyroglobulin in the thyroid gland these hormones then enter the bloodstream and bind to special plasma proteins. Prior to being released thyroglobulin provides a storage spot for these two hormones
67
Thyroid gland structure/size?
-15 to 20g
-Varies in size with age, sex, diet, reproductive state
-Larger in females
-Only 3g of healthy thyroid are needed to maintain euthyroid state(normal thyroid levels)
68
T/F: Availability of iodine to terrestrial vertebrates is limited?
True
69
How does the thyroid gland convserve iodine?
Overtime mechanisms have developed for concentration, utilization and conservation of iodine in the thyroid gland
Thyroid follicular cells are able to trap iodide and transport it across the cell against a chemical gradient(active transport)
70
How does the thyroid make T4?
1. Iodine is taken up as the iodide ion. It is then used to iodate tyrosine residues of thyroglobulin.
2. This forms DIT
3. Two molecules of DIT are then oxidatively coupled to form T4
4. T4 is then sotred in the thyroglobulin
71
How does the thyroid make T3?
1. Iodine is taken up as the iodide ion. It is then used to iodate tyrosine residues of thyroglobulin.
2. This forms MIT
3. Oxidative coupling of one MIT molecule then forms T3.
4. T3 is then sotred in the thyroglobulin.
72
What controls synthesis and liberation of T3 and T4 thyroid hormones?
Thyroid stimulating hormone which is released by the anterior pituitary in response to hypothalmic hormones
73
What happens when there is low TSH(thyroid stimulating hormone)?
Thyroid has low turnover rate of thyroid hormones
74
What hypothalamic hormone causes the release of TSH from the anterior pituitary?
Hypothalamic thyrotropin releasing hormone(TRH)
75
How does an increase in T4 and T3 in the blood affect the release of TSH and TRH?
An increase in T4 and T3 in the blood exerts a negative feedback at both the hypothalamic and pituitary levels to decrease release of TRH and TSH.
(double negative feedback loop)
76
TSH interacts with specific receptors located on follicular cells, leading to increased production of T4 and T3?
Yes, TSH acts on these cells leading to an increase in cAMP and Adenylyl cyclase which leads to inceased T4 and T3 production
77
How is thyroid hormone production affected by deficient iodide?
Synthesis of thyroid hormones and T4 and T3 in circulation decrease
78
What happens when you have an iodide deficiency?
1. Synthesis of thyroid hormones decrease
2. TSH and TRH release increases
3. During prolonged iodine deficiency, thyroid enlarges and may form a visivble lump(goiter)(hypertrophic)
79
Why is the thyroid goiter in iodine deficiency referred to as a non-toxic goiter?
Since it is unable to synthesize active thyroid hormones due to iodine deficiency
80
5 effects of thyroid hormones ?
1. Stimulation of calorigenesis in most cells
2. Effects on carbohydrate metabolism
3. Effects on lipid turnover
4. Effects on protein metabolism
5. Promote normal growth
81
What does stimulation of calorigenesis do?
- Increases cardiac output: rate/strength of cardiac contractions
-Increases oxygenation of blood
-Increases the rate of breathing and number of RBCs in circulation
82
What effects on carbohydrate metabolism do thyroid hormones have ?
-Promote glycogen formation in the liver
-Increase glucose uptake into adipose and muscle tissues
83
What effects on lipid turnover do thyroid homrones have ?
-Increased lipid synthesis for cells
-Increased lipid mobilization(used as a carbon source)
-Increased lipid oxidation
84
What effect on protein metabolism do thyroid hormones have?
-Stimulate protein synthesis
85
How do thyroid hormones promote normal growth?
-Promote neural branching and myelination of nerves
-Promote development and maturation of the nervous system
-Stimulate growth hormone secretion
-Promote bone growth
-Promote IGR-I production by the liver
86
Hyperthyroid?
A thyroid that is consuming calories at an elevated rate
87
T/F: Thyroid hormones control your basal metabolic rate(BMR)?
True
88
Basal metabolic rate?
Rate at which an organisms burns up its stores of fuel to produce energy in the form of heat or calories
89
How do T4 and T3 effect BMR?
They increase it
90
T/F: Thyroid hormones are needed for normal development of the brain?
True
91
How does an absence of thyroid homrones affect the CNS?
-Neuronal development is decreasd
-Absence of them at early development leads to irreversible mental retardation
92
How do thyroid hormones help with CNS development?
-Stimulate synthesis of the nerve growth factor(NGF), which induces dendritogenesiss and regeneration of sympathetic neurons
93
T/F: Thyroid receptors are part of the same family of receptors as the steroid receptors?
True, they function in the nucleus to regulate transcription of genes
94
Describe how T3 and T4 bind to their target receptor?
1. T3 and T4 enter the target cell nucleus and bind to their nuclear receptor
2. The receptor then alters transcription of specific genes
95
T/F: Thyroid hormones may induce some effects by interactions with plasma membrane & mitochondria?
True
96
Are T3 and T4 hormones dependent on protein synthesis or new gene expression?
NO, they are not blocked by inhibitors of protein synthesis
97
How do T4/T3 effect uptake of amino acids?
They act directl at the plasma membrane and increase uptake of amino acids
98
T/F: Radioactive iodine can bind to iodine receptors?
True
99
Hypothyroidism?
Low levels of thyroid hormones
100
Hyperthyroidism?
High levels of thyroid hormones
101
When do hyper and hypothyroidism occur?
May be presennt at birth or may occur later in life
102
Hyperthyroidism consequences/symptoms?
-Elevated BMR
-Weightloss
-Elevated T3/T4
-Goiter(primary or secondary origin)
103
Hypothyroidism symptoms?
-Low BMR
-Weight gain
-Goiter(may or may not be present)
104
Primary Hypothyroidism?
-Defect in the thyroid gland itself(level of the thyroid)
-More common in women
-Also called Myxedema
105
Causes of primary hypothyroidism?
-Atrophy of the thyroid
-Autoimmune Thyroiditis: destruction by antibodies against cellular components of the thyroid(hashimotos)
-Goitrous hypothyroidism/Non-toxic: blockage in a step of T3/T4 synthesis
(this causes thyroid to increase in size)
106
Secondary Hypothyroidism?
-At the level of the pituitary
-Synthesis of little to no thyroid stimulatiing hormone(TSH)
107
Tertiary hypothyroidism?
-At the level of the hypothalamus
-Synthesis of little or no thyrotropin releasing hormone(TRH)
108
Infantile hypothyroidism?
Absence of thyroid gland or incomplete development at birht
109
Effects of Infantile hypothyroidism?
At birth, the child will be normal sice since it uses th mother T3/T4. However, a few months later, child exhibits decreased physical growth & mental development
-Requires early treatment otherwise growth retardation and mental retardation lead to cretinism
110
Treatment of hypothyroidism?
Alll three types of hypothyroidisms are trearted by administration of thyroid hormones
111
Ectopic thyroid?
Thyroid gland in the wrong place
112
Primary Hyperthyroidism?
-At the level of the thyroid
113
Primary hyperthyroidism caused by toxic diffuse goiter?
-Graves Disease
-Autoimmune disease characterized by lymphocytes constantly releasing Long Acting Thyroid Stimulator(LATS)
-LATS mimic the action of TSH and stimulates release of T3/T4
-Negative feedback loop is working(no TRH or TSH being released)
114
Toxic goitre?
When the goitre produces thyroid hormone
115
Primary hyperthyroidism caused by thyroid adenoma or thyroid cancer?
-Synthesis of thyroid hormones independent of TSH stimulation
-The double negative feedback loop is not working
116
Secondary Hyperthyroidism?
-Level of the anterior pituitary gland
-No negative feedback from increased levels of T3/T4 to decrease synthesis of TSH
-Often due to a pituitary tumour
117
Tertiary hyperthyroidism?
-Level of the hypothalamus
-NO negative feedback of high T3/T4 to decrease synthesis of TRH
-Often due to presence of a hypothalamic tumour
118
Treatments for hyperthyroidism?
1. Surgery plus replacement therapy(remove thyroid then give thyroid hormones)
2. Administer radioactive iodide, it will concentrate the cells of the thyroid follicles and destroy them
3. Administration of antithyroid drugs which block addition of iodine to thyroglobulin
119
Propylthiouracil?
Antithyroid drug, don't want to administer too much or else you get hypothyroidism
120
Calcium ion plays a key role in many fundamental processe?
1. Important in normal blood clotting
2. Essential structural component of the skeleton
3. With Na+ and K+ helps maintain transmembrane potential of cells
4. Important in excitability of nervous tissue
5. Important in contraction of mucles
6. Important in release of hormones and neurotransmitters
121
Concentration of Ca2++ in cellular and ECF?
10mg/100ml
-50% are free in circulation
50% are bound to albumin in circulation
122
Where is the majority of the body's calcium?
-In bone
-Bone = calciium resevoir
123
Hormonal control of Ca2+?
-Maintenance of plasma calcium is mainly maintained by exchange between bone and plasma under influence of hormones
-Hormones also affect intestinal absorption of calcium and excretion by kidneys
124
Three hormones important for calcium homeostasis?
1. Parathyroid hormone
2. Calcitonin
3. Vitamin d
125
Parathyroid hormone and calcium?
PTH is a protein that is produced by the parathyroid glands
It increases circulating levels of Ca2+
126
Calcitonin and its effects on calcium?
-It is a portein produced by the parafollicular of "C" cells of the thyroid gland
-It lowers the circulating levels of Ca2+
-Not essential for homeostasis of Ca
Increase calcium deposition in bone
Increases calcium going through the kidney and leaving via urination
127
Vitamin D and its effects on calcium?
Increases circulating levels of Ca2+
Stimulates intestinal uptake of Ca2+
128
How do we get calcium?
-Obtainned in the diet from things like milk, cheese, eggs and butter
-It is then absorbed from the digestive tract primarily in the duodenum and upper jejunum
-Its absorption is increased by vitamin D and PTH
129
What happens when plasma concentration of calcium is below 1mg/100ml?
PTH will stimulate reabsorption of calcium from the kidney and removal of calcium from the bone
130
T/F: stable concentration in blood of calcium is acheived mainly by exchange of calcium between bone and plasma under hormonal influence?
True
131
Calcium cycle?
Low levels of calcium in the plasma:
- PTH and Vitaminn D stimulate absorption of Ca2+ from gut
-PTH stimulaties reabsoprtion from the bone and kiney
High levels of calcium in the plasma:
-Calcium is excreted into the feces by the gut
-Calcitonin leads to excretion of Ca2+ by kidneys into the urine
-Calcitonin leads to deposition into the bone
132
How many parathyroid glands are there and where are they?
-4 parathyroid glands, located on the back side of the thyroid gland
133
Effects of the removal of parathyroids?
-Severe drop in plasma calcium levels causing teetanic convulsions and death
134
Parathyroid hormone?
-Secreted from parathyroid cheif cells embedded in the surface of parathyroids
135
PTH structure?
-84 amino acid polypeptide, only N-terminal 34 amino acids are important for full activity
-Synthesized as part of a larger protein, preproparathyroid hormone, which then undegoes proteolytic cleavage to produce mature PTH
136
Half-life of PTH?
3-18 minutes
137
Functions of PTH?
1. Bone resportion : increases bone demineralization to increase Ca2+ in body
2. Kidney: increases the reabsorption of Ca2+ in proximal convoluted tubule
3. Vitamin D synthesis: stimulates the conversion of 25-hyroxyvitamin D3 to 1, 25-dihyrdoxyvitamin D3(active) in the kidney
4. Gut: PTH and 1,25-dihydroxyvitamin D3 facilitate the absorption of Ca2+ from the gut
138
Control of PTH release?
-Controlled by the circulating concentration of Calcium
-More Ca2+ = more bound to parathyroid receptors = less PTH released
139
Mechanism of PTH?
-Binds to receptor on target cells
140
Hypoparathyroidism?
-Low levels of PTH in circulation
141
Symptoms of Hypoparathyroidism?
-Low plasma calcium (hypocalcemia)
-Production of biological active vitamin D is decreased
-Tetany, convulsions more serious( Calcium concentration is less than 7mg/100ml causes increased neural overexcitability, muscle spasms, spasms of laryngeal muscles may lead to death by asphyxiation)
142
Treatment for hypoparathyroidism?
-Administration of 1,25-dihydroxyvitamin D and calcium supplements
143
Hyperparathyroidism?
High levels of PTH in the circulation
144
Causes of hyperparathyroidism?
-Parathyroid adenoma producing too much PTH
145
Results of hyperparathyroidism?
-High production of 1,25D3
-High PTH stimulates bone resorption and calcium reabsorption from kidney
-1,25D3 increases calcium absorption from intestine
-Elevated calcium in circulation
-Formation of kidney stones
Severe cases: Cardiac arrhtyhmias , depressed neuromuscular excitability, calcium deposition on walls of blood vessles and cartilaginous regions of bones
146
Treatment of hyperparathyroidism?
-Removal of affected parathyroids and replacement therapy of 1,25D3 and Ca2+
147
How do we get vitamin D?
- Cod liver oil, fatty fish
-Can be synthesized from a cholesterol metabolite(not a vitamin)
148
How do we get vitamin D from cholesterol?
1. Precursor cholesterol (70dehydrocholesterol) is found in the skin
2. Requires UVB to cleave a conjugated double bond and break the B ring to give active vitamin D
3. 25-hydroxylation then occurs in the liver followed by 1-hydroxylation in the kidney
149
Physiological function of vitamin D?
1. Primary function: increase calcium absorption from the intestine
2. Regulates the immune system(protects against infection, anti-inflammatory)
3. Anticancer properties
150
Regulation of vitamin D synthesis in kidney?
-Increased in conditions of low calcium, when PTH is also increased
-Depressed by high calcium
151
Rickets in growing individuals?
In northern countries, absence of UVB may lead to vitamin D deficiency and deficient bone mineralization. More severe in dark-skinned individuals
152
Low vitamin D in adults?
Leads to osteomalacia(soft bone)
-Bone does not have enough mineralized calcium
153
Hereditary vitamin D-resistant Rickets + symptoms?
-These children have rickets due to inheriting an inactivating mutation in the vitamin D receptor
Symptoms:
-Shortened clavicle
-BALD
154
Rickets caused by lack of enzyme to produce active form of vitamin D?
These patients have hair
155
Where is calcintonin produced and what is its structure?
-Producing in the parafollicular or "C" cells of the thyroid gland
-32 amino acid calcium lowering peptide hormone(all 32 amino acids are needed)
156
Regulation of calcitonin?
-Rise in plasma Ca2+ increases release of calcitonin(promotes transfer of Ca2+ from blood to bone and increases urinary excretion of the ion)
-Decrease in plasma Ca2+ decrease the release of calcitonin
157
Adrenal Glands?
-Located adjacent to upper surface of kidneys
-Heavier in males
-Two distinct tissue types - cortex and medulla
158
Histological appearance of the cortex vs medulla?
Cortex:
-Large-lipid containing epithelial cells
Medulla:
-Chromaffin cells-fine brown granules when fixed with potassium bichromate
159
Origin of cortex vs medulla?
Cortex: derived from mesoderm
Medulla: derived from neural crest
160
Function of cortex vs medulla?
Cortex: produces steroid hormones; glucocorticoids(cortisol in human) and mineralocorticoids(ex. aldosterone), and progestins
Medulla: produceds catecholamines epinephrine and norepinephrine & some peptide hormones (atrial natriuretic peptides)
161
Adrenal. cortex layers and what they produce?
-One produces mainly mineralocorticoids(aldosterone)
-One produces mainly glucocorticoids(cortisol)
-One produces mainl glucocorticoids, progestins, androgens & estrogens
Each lyer has specific enzmes for the biosyntheis of their respective molecules
162
Regulation of the synthesis of adrenal steroids?
-Controlled by pituitary hormone adrenocorticotropin(ACTH)
163
18-hydroxylase and 17a-hydroxylase?
18-hydroxylase
- present only in the layer that produces minerlocorticoids
17a-hydroxylase
- present only in the layers that produce glucocorticoids
164
Molecular mechanisms of action of steroid hormones?
-Regulate the transcription of hormone/receptor-specific target genes
-Genes regulated vary with each target tissue, and relate specifically to those functions regulated by each steroid hormone and the physiological function of the tissue
165
Roles of the adrenal hormone aldosterone?
-regulates sodium metabolism(increases the reabsorption of Na+ by the kidney)
-Affects plasma concentration of K+ and H+
-Loss of K+ and H+ in urine balance reabsorption of Na+
166
Function of glucocorticoids(cortisol) for salt retention?
-Less effective than aldosterone
-Can be important under pathological conditions when plasma cortisol remains elevated
167
Function of glucocorticoids(cortisol) for protein and carbohydrate metabolism?
-Stimulates synthesis 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
-Decrease glucose uptake by muscle and adipose tissue and decrease glycolysis to conserve glucose for other tissues
-Increased blood glucose levels -- increase insulin secretion
168
Adrenal diabetes?
Increase blood glucose levels due to excess glucocorticoid activity
If prolonged, can lead to destruction of beta cell and diabetes mellitus
169
Function of glucocorticoids(cortisol) for lipid metabolism?
-Glucocorticoids maintain or increase the levels of lipolytic enzymes in the adipose tissue cells and augment lipoyltic action of other hormones
-Lipids are used by muscles as fuel
170
Hyperlipidemia and hypercholesterolemia?
Excess glucocorticoids leads to these
171
Function of glucocorticoids(cortisol) for anti-inflammatory and immunosuppressive actions?
-Reduce inflammatory responses
-Cause atrophy of the lymphatic system
-Descreased levels of circulating lymphocytes and reduced antibody formation (used in organ transplantation)
-Decrease histamine formation and decrease allergic reactions
172
Function of glucocorticoids(cortisol) on bone?
-Decrease the protein matrix of the bone through their protein catabolic effect(bones become less dense)
-This results in increased loss of Ca2+ from the bone leading to osteoporosis
173
Structure of glucocorticoid?
39 amino acid polypeptide, synthesized as part of a larger protein known as proopiomelanocortin
174
Feedback control of cortisol secretion?
Hypothalamus secretes CRH
CRH increases secretion of ACTH by the pituitary
ACTH then acts on the adrenal cortex causing synthesis and release of glucocorticoids
As cortisol levels in the plasma increase it has a negative feedback on the hypothalamus and pituitary
175
Congenital adrenal hyperplasia?
-Enzyme deficiencies where cortisol is not produced
-ACTH secretion is constant due to lack of cortisol
176
Treatment of congenital adrenal hyperplasia?
-Administration of cortisol, which corrects the deficiency and normalizes ACTH secretion
177
How does ACTH work?
1. Binds to specific ACTH receptors on membranes of zona fasciculata and zone reticularis cells
2. Stimulates adenylyl cyclase leading to increased production of cAMP
3. cAMP activates steroidogenic enzymes leading to increased synthesis and release of steroid hormones
178
Daily rhythm of plasma cortisol and ACTH?
Diurnal rhythm of ACTH and cortisol secretion
-minimum at midnight and maximum in the morning
179
Cushing's disease?
When the diurinal rhythym of ACTH and cortisol is independent of sleep due to stress
180
What can cause increase synthesis and release of CRH, ACTH and cortisol ?
Stress stimuli
ex. Pain, fear, exercise, hunger, cold
fight or flight
181
How can release of cortisol during stress be advantageous?
-Provides energy and amino acids through the breakdown of tissue proteins
182
How can release of cortisol during stress be disadvantageous?
Cortisol can inhibit wound healing
183
Prolonged stress?
-Leads to constantly high levels of glucocorticoids which could lead to increased blood glucose(diabetes mellitus), decreased immune response(susceptible to infections), loss of bone
184
Addison's Disease?
-Hypofunction of the adrenal cortex
-Failure of the adrenal cortex to produce adrenocortical hormones(cortisol + aldosterone)
185
Cause of Addision's Disease?
1. Severe conditions: results from destruction of the adrenal gland
2. Less severe: results due to autoimmune attack on the adrenal glands
3. Can also be caused by tuberculosis
186
Effects of Addison's Disease?
Glucocorticoid deficiency:
- Low blood sugar
-Decrease lipolysis
-Decrease gluconeogenesis
Mineralocorticoid deficiency:
-Low plasma concentrations of Na+, Cl- and H2O(lost in urine)
-High concentrations of K+ and H+(hyperkalemia + acidosis)(reabsorbed from urine)
187
Cushing's Disease?
-Hyperfunction of the adrenal cortex
-Excessive production of glucocorticoids as well as increased production of mineralocorticoids due to increased levels of ACTH(pituitary tumour) or arenal tumour
188
What causes Cushing's Disease?
-Hyperplasia of one adrenal cortex(adrenal tumour) or both (pituitary tumour)
189
Effects of Cushing's Disease?
Glucocorticoids increased:
-Increased blood glucose
-Increased insulin secretion
-Decreased protein synthesis
-Increased protein breakdown
-Osteopororis
Mineralocorticoid increased:
-Increase plasma Na+ , Cl- and H2O(moon face)(reabsorbed from urine)
-Decreased K+ and H+ (hypokalemia, Alkalosis)(lost in urine)
190
Treatment of Cushing's disease?
Surgery
-Remove the adrenal cortex
191
Cushing's Disease: Case Report
- Female presents with hypertension(does not respond to BP medication), moon face, high levels of circulating cortisol and ACTH is undectable
Where is the tumour?
She must have an adrenal tumour since this would prevent the adrenal cortex from releasing ACTH.
If she had a pituitary tumour ACTH would be high and she would have hyperplasia of both adrenals and the pituitary
192
How to fix the patient with cushing's disease?
-Surgery to remove the adrenal adenome
-However, this then results in Addison's due to severe atrophy of the other adrenal because of loss of ACTH(Addison's Disease)
Now we perscribe glucocorticoids and mineralocorticoids
193
The pancreas?
-Located behind the stomach
-99% of the pancreas in exocrine and secretes digestive enzymes
-Pancreas also consists of small endocrine structures(islets of Langerhans)
194
Islets of Langerhans cells?
-60% of the cells are known as beta cells and synthesize insulin
-25% of the cells are alpha cells and synthesize glucagon
195
Insulin and glucagon?
Small protein hormones and both control glucose concentration in the blood
196
T/F: Insulin is more important than glucagon?
True, insulin deficiencies or absence can lead to death if not treated
197
Oonly hormone that acts primarily to decrease blood glucose?
Insulin
198
How much glucose present in the blood?
-Glucose is always present in the blood (the fasting level is about 80mg/100ml)
-Very little is free in tissues
199
Glucose does not diffuse readily into most cells, how is it transported?
In the liver and muscle cells glucose is converted to glycogen
In the adipose tissue glucose is converted to fat and stored for later use
In many cells of the body glucose is oxidized to produce energy
200
Insulin receptor and increasing glucose uptake due to binding?
Glucose is hydrophilic and cannot cross the lipid bilayer, so it binds to an inulin receptor on the outside of the cell binding to the membrane receptor, stimulates insertion of glucose transport proteins stored in cytoplasm into plasma membrane to increase glucose uptake
201
Insulin deficiency results?
-Results when beta-cells are destroyed and will lead to Diabetes mellitus
-most tissues are unable to take up glucose efficiently which causes glucose to accumulate in the circulation
202
What happens in insulin deficiency if you don't consume glucose?
You still get accumulation of glucose in the circulation because of increased gluconeogenesis
203
Primary source of energy due to insulin deficiency?
-Free fatty acids become the principal source of energy(increased lipolysis)
-However, the fat is inefficiently used (incomplete oxidation of the fatty acids and increased circulation of acetoacetic acid and acetone)
-Causes ketosis which leads to acetone smell in breath
204
Why does insulin deficiency lead to decreased blood pH?
-Build up of short chain fatty acids leads to a decreased blood pH
-This can lead to a diabetic coma and even death
205
Process of insulin deficiency?
1. Tissues cannot take up glucose due to lack of glucose, so the cells become starved
2. This leads to breakdown of proteins to free AA and use of AA to make glucose
3. This leads to increased lipolysis and free fatty acids
4. This leads to decreased pH(metabolic acidosis) and increased acetone(ketosis)
206
Glycosurea?
Glucose concentrations increase and this leads to loss of glucose in the urine. This leads to loss of water in the urine(polyurea). Dehydration and thirst increased
207
How to fix diabetes?
-Administration of insulin
-In diabetic comas, along with insulin patients must correct electrolyte imbalance and acidosis
208
Causes of diabetes mellitus?
Type 1 insulin dependent diabetes: Due to a deficiency of insulin
Type 2 insulin independent diabetes:
Due to hyporesponsiveness to insulin
209
Type 1 insulin dependent diabetes and treatments?
-Destruction of beta-cells of pancreas (synthesis of insulin does not occur)
Treatment: administration of insulin
-Defective insulin release(drugs stimulating insulin release could be administered)
210
How low is too low of blood glucose?
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 (insulin shock), when too much insulin administered
211
Type 2 insulin independent diabetes?
-Insulin levels normal or abnormally high
-Insulin resistance often due to decreased number of insulin receptors on target cells
-Associated with obesity due to overeating (prolonged high insulin levels decrease number receptors)
212
Treatment for Type 2 diabetes?
-Proper diet and exercise
-Decreased caloric intake, decreased insulin, upregulation of receptors. Insulin receptors increase in response to frequent endurance exercise(independent to changes in body weight)
213
Juvenile Diabetes Mellitus?
-Appears in childhood and is insulin dependent
-Beta-cells of the pancreas do not produce insulin
-Requires insulin administration
214
Glucose tolerance in those with diabetes vs hyperinsulinism?
Diabetes: Patients have decreased tolerance to glucose
Hyperinsulinism: Patients have increased tolerance to glucose
215
Glucose tolerance test?
1. After an over night fast a patient is give 0.75-1.5g of glucose/kg body weight
2. Blood is taken prior to administration and at 30-60 minute interval after for 3-4 hrs(glucose is measured in blood)
216
Glucose tolerance test results in normal patients?
-Blood glucose increases in 1 hr from 80mg/100ml to 130mg/100ml
-After 2-3 hrs glucose returns to normal
217
Glucose tolerance test results in diabetic?
-Increase in blood glucose is greater than in the normal patient
-Blood glucose returns to normal more slowly
218
Most important mechanism controlling insulin secretion?
Beta cells response to levels of blood glucose
-They secrete little to no insulin when blood glucose is low
-They secrete a lot of insulin when blood glucose is high
219
Another mechanism controlling insulin secretion?
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.
220
Glucagon?
-Synthesized and released by alpha-cells of the pancreas
-Opposite metabolic functions as insulin
221
Function of glucagon?
Raises blood sugar by promoting glycogenolysis (breakdown of glycogen) and gluconeogenesis(synthesis of glucose) in the liver
-In the adipose tissue, glucagon increases rate of lipolysis leading to increased concentration of free fatty acids in circulation
222
Regulation of glucagon release?
-Controlled by concentration of glucose in the circulation
-Low blood glucose stimulates the alpha-cells to increase glucagon production, which high blood glucose decreases production
223
T/F: Glucagon is not as important as insulin?
True
224
Glucagon-like peptide-1(GLP-1)
-Derived from the same protein precursor as glucagon
-Produced by enteroendocrine L cells of the intestine
-Member of the hormone family, incretins, which means it is gut derived
225
GLP-1 action?
Muscle:(reduces glucose circulation levels)
-Increases glycogen synthesis
-Increases glucose oxidation
Adipose tissue:(reduces glucose circulation levels)
-Increases lipolysis
-Increases glucose uptake
Pancreas:
-Increase insulin secretion
Brain:
-Decreases appetite
-Increase satiety
Heart:
-Decreases BP, increase HR, increase cardioprotection
GIT:
-Slows down digestion to make you feel full longer
226
Ozempic vs GLP-1?
GLP-1 has a very short half-life where as semaglutide mimic GLP-1 but have a much longer half-life
GLP-1 only stimulates insulin release when glucose is present
227
Growth Hormone?
-Single chain polypeptide produced by anterior lobe of the pituitary
-Responsible for growth
-Somatotropin(STH)
228
Effects of Growth hormone?
-Increases protein synthesis in many tissues such as bone, kidney and liver by enhancing amino acid uptake by cells and accelerating transcription and translation
-Increases rate of lipolysis and utilization of free fatty acids as a source of energy
229
Somatomedins
-Produced by the liver under stimulation of GH
-Similar structure to insulin
-Named(insulin-like growth factors I and II)
-May bind insulin receptors and insulin at high concentrations
-Increase protein synthesis and stimulate growth
230
Control of GH release?
Growth hormone releasing hormone is a hypothalamic neruohormone that stimulates release of growth hormone from the anterior pituitary
Somatostatin hormons is a hypothalamic neruohormone that inhibits growth hormone release
231
What regulates somatostatin release?
Exercise, sleep, stress, low blood sugar
232
GH deficiency?
In young, absence of growth hormone leads to decreased physical growth
233
Excess GH?
In young leads to gigantism
In adults leads to acromegaly, in which many bones get longer(cartilaginous regions) and heavier
234
Primary reproductive organs?
-Gonads, testes, ovaries
235
Functions of the gonads?
1. Gametogenesis: production of reproductive cells known as gametes; the spermatozoa in male and ova in females
2. Secretion of sex hormones; testosterone(androgens) in males, and estrogen and progesterone in females
236
Differences in reproductive endocrinology in males and females is quantitative and not qualitative?
Androgens are not unique to males and estrogen is not unique to females.
Testes produce small amounts of estrogen, and androgens can be converted to estrogens by a single enzymatic step in non gonadal tissues. Androgens produced in small amount in ovaries and larger in adrenals
237
T/F: Estrogen maintains bone density in males?
True
238
How is estrogen produced in males?
Produced locally in tissues by the conversion by aromatase of testosterone to the estragen estradiol
239
Estrogen deficiency in males?
-Increased body fat
-Contributes to sexual desire and erectile function
240
Control of reproductive function?
1. Gonadotropin releasing hormone is secreted by the hypothalamus and travels to the anterior pituitary via hypothalamus-pituitary portal vessels
2. GnRH stimulates the release of pituitary gonadotropins: FSH and LH
3. FSH and LH stimulate the development of spermatozoa or ova, and secretion of sex steroids
4. Sex steroids exert effects in the gonads, in other parts of the reproductive system, and body
241
Inhibin?
Produced by the gonads it is a protein that feeds back on the anterior pituitary and prevents FSH release
242
Function of the testes?
- Production of mature germ cells (spermatogenesis)
-Steroid hormones (steroidogenesis)
243
Spermatogonia?
These are found in the testes and are precursor germ cells that help males continually renew their pool of sperm , so that a constant supply of sperm is available throughout life
244
Where does spermatogenesis take place?
Within th coiled seminiferous tubules of the testes
245
How long does the process of maturation from spermatogonia to mature spermatozoon take?
60 days in humans
246
Sertoli cells?
Located in the seminiferous tubules
Involved with the sperm maturation process-envelop the sperm cells throughout their development
In response to FSH, thse cells synthesize androgen binding protein(ABP) and inhibin
247
Leydig Cells?
Located outside the seminiferous tubules. In response to LH, leydig cells synthesize androgens
248
What does spermatogenesis depend on?
Androgen concentrations within the seminiferous tubules
The concentration must be 10 times higher than androgen concentration in circulation otherwise spematogenesis ceases
249
What ensures high concentrations of androgens in the seminiferous tubules?
ABP synthesized by the Sertoli cells ensures high concentration in the seminiferous tubules
250
Hypothalamic-pituitary-leydig cell axis?
Negative feedback loop regulating testicular androgen synthesis:
GnRH stimulates release of LH and FSH from the anterior pituitary which stimulates Leydig cells and Sertoli cells. Leydig Cells then produce androgen, which inhibits release of GnRH, LH and FSH
251
Hypothalamic-pituitary-seminiferous-tubules axis?
GnRH stimulates release of LH and FSH from the anterior pituitary which stimulates the Sertoli cells. Sertoli cells then produce inhibin which inhibits FSH release only
252
T/F: In males there is no positive feedback loop, but in females there is?
True
253
Principal function of ovaries ?
-production of mature eggs
-Production of steroid sex hormones, which regulate the reproductive tract and influence sexual behaviour
254
Ovary at birth?
At birth, the ovary contains non-proliferating pool of germ cells or oocytes(about 2 million), which are its whole supply of ova
255
At puberty how many ova do you have left?
About 400000
256
Structure of the oocytes?
Surrounded by a single layer of granulosa cells and a basement membrane making up the structures called primordial follicles
257
Primordial follicles?
Fundamental reproductive units of the ovary
258
Growth of primordial follicles into primary follicles?
Begins by an unknown initiating event (independent of pituitary)
Once initiated, growth is controlled by gonadotropins(LSH+FSH) and steroid hormones(estrogen) until the follicles wither ovulate or degenerate
259
Steps leading from oocyte to primary follicle?
1. Enlargement and differentiation of the oocyte, which gorws & elaborates zona pellucida(acellular layer rich in glycoproteins surrounding the oocyte)
2. Granulosa cells divide & increase to 2 or more layer(primary follicles). Influenced by FSH and estrogens. Estrogens are important for expression of LH receptors on granulosa cells.
260
Production of secondary follicle from primary follicle?
Under the influence of FSH and LH, primary follicle develops into a secondary follicle which expresses receptors for FSH, estrogens and LH.
Appearance of the follicular antrum which contains secretions from the granulosa cells.
261
Preovulatory follicle production?
Under the influence of FSH and LH the granulosa cells elaborate follicular fluid, which takes up the larger portion of the preovulatory follcile(known as late secondary follicle)
262
Production of theca cells?
As the follicle matures from primary to secondary, cells from ovarian stroma surrounding the follicle differentiate and become steroid prodcuing cells(theca cells)
263
Theca interna and the granulosa cells?
Collaborate for synthesis of higher amounts of estrogen
264
Follicular development leads to one of what two events?
1. Follicular Atresia
2. Ovulation
265
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. The remaining follicles degenerate in a process called atresia
266
Ovulation?
Mechanism of follicular rupture that is poorly understood
267
Luteinization(after ovulation)
1. Ruptured follicle is transformed into the Corpus Luteum which secretes progesterone
268
What cells contribute to the formation of the corpus luteum?
Both theca and granulosa cells
269
Corpus luteum?
Temporary structure in the ovary that synthesizes progesterone and estrogens.
270
Corpus luteum synthesis of hormones?
For the first few days following ovulation the corpus luteum produces large amounts of progesterone and estrogens but then production drops off unless implantation of fertilized ovum occurs
271
What happens to corpus luteum upon implantation?
Corpus luteum transforms into the corpus luteum of pregnancy. It is responsible for synthesis of progesterone and estrogens and creation of proper endocrine environment for maintenance of pregnancy until progesterone and estrogen synthesis by placenta is established.
272
Luteal phase of the cycle?
After ovulation, when the burst follicle transforms into the corpus luteum.
273
What induces the luteal phase?
LH
274
Role of estrogen and progesterone secreted by the corpus luteum?
Estrogen: thickens the endometrial wall to create a structure appropriate for implantation
Progesterone: helps estrogen to finish thickening of the ednometrial wall and make a place fit for implantation
275
What happens when there is no implantation/fertilization?
-Corpus luteum degenerates and is no longer a steroid hormone producing structure
-Steroid hormones fall
-Both estrogen and progesterone are no longer needed to maintain the corpus luteum
-On set of mensturation
276
Implantation?
Progesterone and estrogen are maintained to maintain the structure of the Corpus luteum
277
Prior to day one of the menstural cycle?
-Endometrium thickens under the influence of estradiol
-Progesterone induces the appearance of specialized glycogen-secreting glands
278
Day 1 of the menstural cycle?
-First day of detectable vaginal bleeding(deterioration of uterine endometrium)
-Bleeding begins when estradiol and progesterone are very low in circulation(blood vessels supplying the endometrium constrict reducing blood supply)
-Endometrium deteriorates and flows through the cevix into the vagina
279
How long is bleeding and what are the ovaries doing?
About 5 days and ovaries are endocrinologically inactive
280
What happens when estrogen dorps during bleeding?
Drop in estrogen leads to an uptake in the release of FSH due to feedback loop. This initiates the next round of follicular development
Also there is a decrease in inhibin which can lead to increased FSH secretion
281
Day 8 of the cycle?
This is when one follicle becomes dominant and commited to further development
Remaining follicles begin to degenerate via atresia
282
Dominant follicle?
Prodcues increasingly more estradiol, which becomes important in late stages of the cycle and stimulates uterine endometrium proliferation(thickening)
By day 13 the endometrium is very thick and the estradiol induces production of endometrial progesterone receptors
283
LH surge?
Dramatic spike in LH that induces ovulation
284
Effects of moderate estradiol concentrations?
-Negative feedback on FSH release
-stimulates synthesis of LH by the pituitary and increases sensitivity of pituitary to GnRH by increasing receptors
Stimulates synthesis of LH but inhibits its release, therefore LH accumulates to high levels in the pituitary
285
high estradiol concentrations?
-under the influence of the developing follicle estrogen conc. rises
286
Effects of high estradiol concentrations?
-Stimulates LH release - LH surge
-day 14 (small inc. in FSH also)
287
Estrogen +ve feedback control mechanism?
Stimulation of LH synthesis by estradiol and increased sensitivity of the anterior pituitary to GnRH leads to increase LH synthesis by anterior pituitary
288
T/F: estrogens exert negative feedback(decreased GnRH and LH release) and positive feedback (increased sensitivity of anterior pituitary to GnRH and increase LH synthesis) ?
True
289
What does the LH surge do?
Causes the follicle to rupture and the ovum is ejected
290
What do oral contraceptives contain?
estrogen and progesterone
291
What do oral contraceptives do?
Maintain moderate circulating levels of estrogen and progesterone and suppress the release of LH and FSH from the pituitary and prevent ovarian follicles from maturing and being ovulated
292
Ectopic pregnancy?
Implantation of the egg in the fallopian tube
293
Unfertilized egg at ovulation?
Taken by the fallopian tube and is propelled towards the lumen of the uterus
294
What happens to egg upon fertilization?
Once fertilization takes place a series of rapid divisions occur in the egg. Until it develops into a blastocyst structure and reaches the uterine lumen.
295
Blastocyst differentiates into?
Trophoblast: becomes the placenta
Inner cell mass: becomes the embryo
296
Trophoblast?
-Invades uterine mucosa to embed the developing embryo
-Around implantation trophoblast starts to synthesize HCG which has LH-like properties and stimulates the corpus luteum to continue secreting gonadal steroids(estrogen/progesterone)(keeps corpus luteum alive)
297
After the 12th week of pregnancy?
Endocrine function of corpus luteum is taken over by the placenta
298
Pregnancy test?
HCG appears in the blood/urine
299
T/F: After ejection of placenta estrogen and progesterone levels die quickly?
Yes
300
Lactation?
Secretion of milk by the breast
301
Maturation of non-pregnant mammary glands?
-With onset of puberty increasing levels of estrogen lead to enhancement of duct growth and duct branching but little development of the alveoli
-most breast enlargement due to fat deposition
302
maturation of pregnant mammary glands?
- Several hormones(estrogen progesterone, prolactin, human placental lactogen) lead to ductal and alveoli structures fully developping
303
Milk production. during pregnancy is controlled by?
Prolactin
304
What inhibits milk production?
High estrogen levels
305
Lactating mammary gland?
-After birth, estrogen levels decrease whiile levels of prolactin remain high
-Prolactin induces milk synthesis and the alveoli secrete milk, filling the ducts
306
Nursing effects of lactation?
Suckling = oxytocin = contraction of duct = milk ejection
307
Prolactin and oxytocin?
Stimulated by the afferent fibers from the nipple. Prolactin(anterior pituitary) sustains milk production and oxytocin(posterior pituitary) causes milk ejection
308
Milk
water, protein, fat, and carbohydrate lactose and antibodies
Viruses and drugs may also be transmitted from mother to baby
309
Lactational amenorrhea?
Maintained nursing stimulates prolactin production, which inhibits the secretion of FSH and LH. This blocks the reproductive cycle(natural method of contraception).
310
Factors that affect lactational amenorrhea?
Intensity and frequency of suckling are important for maintenance of the blockade on the reproductive cycle
311
What is menopause?
Loss of ovarian steroid production
No more follicles left, most have disappeared by atresia and a few hundred by ovulation
312
What does depletion of follicles do?
Results in the loss of capacity for steroid(estrogen and progesterone) hormone production by the ovary
313
Lack of estrogen symptoms due to menopause?
Hot flashes, restlessness, bone loss
314
Indicator for onset of menopause?
No production of estrogen eliminates the negative feedback loop which leads to a rise in FSH and LH
Constantly high levels of FSH are indicators for menopause
315
Estrogen replacement therapy?
Given to reduce osteoporosis but fertility cannot be recovered since all follicles have been depleted
316
Major circulating form of vitamin D?
25-hydroxy-vitamin D3
317
1,25-dihydroxyvitamin D3 biosynthesis steps?
1. 7-dehydrocholesterol is converted to vitamin D3 due to UVB (through skin)
2. Vitamin D3 then passes through the liver which converts it to 25-hydroxy-vitamin D3
3. It is then activated in the peripheral tissues to 1,25-dihydroxy vitamin D3
318
T/F: Children with Rickets are at increased risk of a number of immune related disorders ?
True due to lack of vitamin D which boosts your immune system
319
3 Diseases that have demonstrated north-south gradients (depend on deficiencies of Vitamin D)?
1. Cancers (digestive cancers and leukemia)
2. Autoimmune diseases (MS)
3. Infectious diseases
320
What happens to macrophages when they are exposed to bacterial cell wall components?
Macrophages ramp up production of 1-hydroxylase which is the enzyme that converts 25 vitamin D3 to the active form. This suggests that vitamin D is important for our immune system.
321
What happens when you treat cells with 1, 25-dihydroxyvitamin D3?
It induces secretion of antibacterial activity in the form of antimicrobial proteins
Two genes are stimulated by the vitamin D receptor that encode your body's own antibiotics, these help kill bacteria
