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197 Cards in this Set

  • Front
  • Back
Endocrine glands include?
 Pituitary,thyroid, parathyroid, adrenal and pineal glands
 Hypothalamus,thymus, pancreas, ovaries, testes, kidneys, stomach, liver, small intestine, skin, heart, adipose tissue, and placenta not exclusively endocrine glands
List 4 type of hormones
endocrine; neurocrine; paracrine; autocrine
what are endocrine hormones?
released from glands into blood, travel to target organs at distant sites
what are neurocrine hormones?
released from synaptic end bulbs of neurons into blood. eg ADH
what are paracrine hormones?
released from local cell and travel a short distance through the interstitial space to another cell in the immediate area, do not enter blood typically. eg somatostatin ( in pancreas inhibit alpha and beta cell release hormones)
what are the autocrine hormones?
act locally, receptors are located on the very same cell that released the hormone in the first place. eg,growth factors like PDGF
typically hormone concentrations
10^-9 M to 10^-12 M
some organs produce more than one hormones, but one cell type only produce one hormone.
False. FSH and LH produced both produced by one cell type. This is the only exception
List two example of positive feed back in female reproduction system.
child birth and ovulaiton
List three ways to maintain final hormones level
long loop feedback
short loop feedback
ultrashort loop feedback.
how to make a cell to less responsive to hormones (3 ways)
reduce # of receptors(destroy or endocytosis into vesicles);
reduce the synthesis of the receptors;
inactive the hormone receptors.
list three main type of hormones based on chemical structural
1. proteins/peptides
2. amines
3. steroids
what are peptide/protein hormones
synthesized from aa. monomers. usually synthesized in an inactive prehormone or preprohormone form. Majority of hormones are peptides and proteins.
List 12 peptide/protein hormones
oxytocin; ADH; TSH; FSH; LH; ACTH; GH; PTH; Proclactin; hCG; Calcitonin; somatostatin
what are amine hormones?
derivative of aa tyrosine. eg. Catecholamine (epinephrine/norepinephrine and dopamine); thyroid hormones (T3 and T4)
what are the steroid hormones?
derivatives of cholesterol. include cortisol, aldosterone, estradiol and testosterone.
which types of hormone need transport proteins while in the blood?
steroids because they are hydrophobic and not easily dissolved in water.
T3 and T4 also need transport proteins.
For amine hormones, which act more like protein hormones?
Catecholamines (eg. NE and EPI) because they do not cross cell membrane; T3 and T4 cross membrane and bind to intracellular receptors and require carrier protein
what are the function of hormone binding proteins?
1. typically associated with hormones exhibiting long term effects
2. 99.99% of T4 in circulation is bind to binding protein
3. provide reservoir and extend half life(bound T4: 7-8 days; free T4 about several minutes)
4. so body just regulate the free and unbound hormones
5. needed for thyroid hormone, IGFs, GH and sterioid
brief two types of G protein signaling transduction with second messenger
1. G protein coupled cAMP and PKA pathway (Gs)
2. G protein coupled DAG/IP3 and PKC/Ca2+ pathway (Gq)
describe G protein coupled cAMP cascade
Describe G-protein coupled PIP2 pathway.
describe the steroid hormone signal pathway
Steroid hormone enter cell and bind to receptors in the cytosol or nucleus, exert transcriptional effects on cell. eg of protein product can be Na+-K+ ATP pump
Hormonal rhythms
1. Periodicity (minutes to years)
2. Needed for normal function
3. Circadian (24 hour cycle)
4. Pulsatile rhythms are superimposed on circadian
list the potential fate of hormones
1. bind to the hormone receptor and initial effects
2. activated in the blood/tissue(bind to the receptor)
3. inactivated in blood, kidney, liver, etc
4. excreted in urine/feces
what is the master hormone gland and where it is located
Pituitary gland! located inferior to the hypothalamus and is connected by infundibulum
which part of the pituitary gland is primarily endocrine cells?
anterior lobe (adenohypophysis)
which part of the pituitary gland is primarily neural tissue?
posterior lobe (neurohypophysis) which produce Oxytocin and ADH.
what is special about blood vessels around hypothalamus and pituitary gland
the capillary bed of hypothalamus is connected to the capillary bed of anterior pituitary via "hypothalamic-hypophysial portal vessels"
what hormones are produced by posterior pituitary gland? and their major role
Oxytocin: female reproduction
ADH (antidiuretic hormone): also called vasopressin. function is to conserve water.
what is the another name for ADH
where does Oxytocin hormone been produced
paraventricular nuclei of hypothalamus
where does ADH been produced
supraoptic nuclei of hypothalamus.
How does the ADH been released? (when/where/how)
precursor of ADH is produced in supraoptic nuclei of hypothalamus and packed into vesicles; these vesicles travel down the axons into the posterior pituitary gland where they await for action potential for exocytosis.
ADH release is only controlled by hypothalamus
False. hypothalamus (osmoreceptors) is the main control. but other factors also regulate secretion: blood volume (low pressure receptors in atrial, great veins, and pulmonary vessels, baroreceptors of carotid sinus and aortic arch); pain; surgical stress; alcohol inhibits the release of ADH.
what cause the ADH to be released? in detail.
osmoreceptors in hypothalamus shrink when exposed in hypertonic solution during body dehydration. the osmoreceptors then stimulate the supraoptic nuclei of the hypothalamus to increase their AP and ADH is released. usually when plasma osmolatity rises above 290 mOsm and ECF decreases by greater than 5-10% or normal.
How target cell response to ADH? in detail
ADH binds to V2 receptor of principal cells in the late distal convoluted tubule and collecting duct. it stimulates the insertion of aquaporin-2 channel into the apical membrane and allows for reabsorption of water.
ADH also bind to V1 receptors in smooth muscle and acts through G protein coupled IP3/Ca2+ second messenger system and lead to vasoconstriction.
what is diabetes insipidus?
occurs when the body is UNABLE to produce adequate levels of ADH or defect in the ADH receptor
List two type of diabetes insipudus and their features
central diabetes insipidus (also called neurogenic )-damage to the posterior pituitary gland;
Nephrogenic diabetes insipidus- defect in the ADH receptor in the kidney. major causes in adult are lithium toxicity and hypercalcemia
List 6 hormones released from anterior pituitary gland
TRH: thyrotropin releasing H.
GHRH: GH releasing H.
GHIH(somatostatin): GH inhibiting H.
CRH: corticotropin releasing H.
PIH(dopamine): prolactin inhibiting H.
GnRH: gonadotropin releasing H.
TRH source, target and down stream response
hypothalamus-> stimulate TSH and PRL(prolactin) in Anterior pituitary->1. thyroid gland release T3 (triiodothyronine) and T4 (thyroxine or tetraiodothyronine); 2. mammary glands
GHRH/GHIH source, target and down stream response
released from hypothalamus-> +/- GH in anterior pituitary->liver and other tissues->IGFs (insulin-like growth factors, also called Somatomedins)
CRH source, target and down stream response
hypothalamus->ACTH (adrenocorticotropic H.) in anterior pituitary->adrenal cortex->mineralcorticoids-aldosterone(minor); glucocorticoids-cortisol; androgens-dehydroepiandrosterone(DHEA)
PIH(dopmine) source, target and down stream response
hypothalamus-> inhibit PRL in anterior pituitary->mammary gland
GnRH source, target and down stream response
hypothalamus-> stimulate FSH (follicle stimulating H.) and LH ( luteinizing H.) release in anterior pituitary-> gonads (testes&ovaries) release testosterone and estradiol/progesterone.
what type of cell release following hormone?
Thyrotropes; somatotropes; corticotropes; lactotropes; gonadotropes; gonadotropes.
what are the main sites of action from hormones
liver, adipose tissue and muscle.
what is the normal blood glucose level
90-120 mg%
what tissue/cell are heavily rely on glucose for energy
brain, nervous tissue and red blood cell
Despite the importance of glucose as an energy source, very little glucose is stored in the body as glycogen (~1%)
what are the two type of energy storage?
fat 76% and protein 23%
matching fed and fasting state with following:
a. glycogenesis; b. lipogenesis; c. gluconeogenesis; d. protein synthesis; e. glycogenolysis; f. lipolysis; g proteolysis
Fed state: a. glycogenesis; b. lipogenesis; d. protein synthesis;
Fasting state: c. gluconeogenesis; e. glycogenolysis; f. lipolysis; g proteolysis
when and where does the ketone body come from
after 5-6 weeks starvation, body will use fat to produce energy thus accumulate ketone body during the process.
what is ketoacidosis
Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids.Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Fasting leads to ketosis but not ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone.
what is isthmus
structure connect two lobes of thyroid.
where does the thyroid hormones are produced in thyroid gland?
thyroid gland is divided into two lobes and further divided into segments called follicles , where thyroid hormones are produced by its epithelial cells.
what hormones thyroid gland produce? full name.
T3, tri-iodo-thyro-nine
T4, tetra-iodo-thyro-nine, also called thyroxine
which is more active, T3 or T4, reverse T3?
Mostly T4 is secreted but T3 is more active (4 times) after activation at target organ. reverse T3 is not biologically active, but level increase during times of caloric restriction or stress.
does synthesis of thyroid hormones happened in intracellular or extracellular
iodide are combined with TGB in extracellular space to from T1~T4.
False. Iodine combine with TGB. Iodide is absorbed from blood plasma and transferred into follicular cell through Na+-I- symporter.
List three major component when synthesis thyroid hormone
1. iodide form diet
2. aa. thyrosine
3. protein thyroglobulin (TGB)
where does T3 and T4 stored in thyroid gland?
in colloid
which enzyme convert iodide to iodine
thyroid peroxidase
synthesis of thyroid hormones
8 steps of thyroid hormone synthesis
1. iodide trapping; 2. synthesis of TGB; 3. oxidation of iodide; 4. iodination of tyrosine; 5. coupling of T1 and T2; 6. pinocytosis and digestion of colloid (remove backbone); 7. secretion of thyroid hormones; 8. transport in blood with TBG
which enzyme convert T4 to T3?
Thyroxine bind to nuclear receptors and modifies gene transcription within the target cell.
False. T3 bind to nuclear receptor, not T4 which is thyroxine.
the major job of thyroid hormones and is accomplished mainly by which cellular mechanism?
increase the basal metabolic rate and oxygen consumption by increasing the synthesis and activity of the Na+/K+ ATPase. it has calorigenic effect and produce 40% of body heat.
thyroid hormone acts on virtually every organ system in the human body
what is the effect of thyroid hormone on bone formation? how about GH and IGFs?
thyroid hormone acts synergistically with GH and Somatomedins (IGFs) to increase bone formation
what is the effect of thyroid hormone on heart and lung?
increase cardic output (positive inotrope-contractility and chronotrope-rate) and increase respiratory rate. This is sympathomimetic effect (stimulate beta receptors.
what is Cretinism and cause/symptoms
Cretinism is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones (congenital hypothyroidism) usually due to maternal hypothyroidism.
thickened skin/enlarged tongue/protruding abdomen
symptoms of hypothyroidism
cold sensitivity; hypoventilation; lethargy =fatigue; myxedema =swollen of skin; weight gain; goiter (also in hyperthyroidism)
symptoms of hyperthyroidism
exophthalmos=protruding of eyes; increased basal metabolic rate, cardiac output and heat production; sweating; weight lose; goiter (also in hypothyroidism)
what is primary, secondary and tertiary hypo/hyper-thyroidism?
primary-origin is the thyroid gland(T3/T4)
secondary-origin is the anterior pituitary (TSH)
tertiary-origin is the hypothalamus (TRH)
what is Hashimoto's thyroiditis
or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by a variety of cell- and antibody-mediated immune processes. It was the first disease to be recognized as an autoimmune disease.Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism
what is ectopic-graves disease
an autoimmune disease in which the body produce thyroid-stimulating immunoglobulins (TSI) which are similar in structure to TSH, resulting stimulated thyroid gland and overproduction of thyroid hormone. often causing enlarged goiter. TRH and TSH actually low but TSI cause high T3 and T4
list one of the major causes of goiter development
iodine deficiencies often lead to hypothyroidism and goiter
what is the effect of high level estrogen to TBG, and to thyroid hormone? is this characterized as euthyroidism, hypo or hyper thyroidism?
During pregnancy, high levels of estrogen inhibit the breakdown of TBG by the liver, and TBG levels rise. Total T3/T4 will rise but free physiologically active T3/T4 will stay same and synthesis of T3/T4 also rise to compensate the lose of free T3/T4. This would be an euthyroidism.
Brief GH pathway (source, target)
GHRH(dominant hormone)/GHIH(less) from hypothalamus->GH from anterior pituitary->bind to the GH receptors on liver->IGFs produced from liver.
why GH has a dabetogenic effect?
1. decreases glucose uptake and use by muscle/adipose tissue; 2. increases lipolysis; 3. provides insulin resistance; 4. stimulate gluconeogenesis.
what is the indirect effect of GH?
GH binds to its receptors in the liver and lead to production of IGFs. IGF-1 is released throughout life; IGF-2 is released at puberty.
IGFs are produced primarily at NON-endocrine tissues such as the liver, kidney and muscle.
what is another name for IGFs
effect of somatomedins
1. growth of soft tissues and bones by increasing the uptake of aa.
2. stimulating synthesis of DNA, RNA and proteins.
what factors stimulate the release of GH?
(more like in fasting state)
low glucose; low free FA; fasting/stavation; exercise/stress; stages III-IV of sleep (1-2 hrs after onset); high aa or protein diet
what factors inhibit GH
high glucose; high FA; obesity.
How does hypersecrection of GH affect adult long bone?
periosteal bone growth after epiphyseal plate closure, causing Acromegaly.
what cause adult hypersecrection of GH
GH secrecting pituitary adenoma (tumor)
symptom of child hyposecrection of GH
Dwarfish; short stature; failure to growth; mild obesity; delayed puberty
hyposecrection of GH in adult will result mild hypoglycemia
what is Laron Dwarf? what's its GHRH/GHIH/GH/IGFs level?
an autosomal recessive disorder characterized by an insensitivity to growth hormone (GH), caused by a mutation of the growth hormone receptor. It causes short stature and a resistance to diabetes and cancer. high GHRH/GH level and low GHIH level. No IGFs because receptor mutation
what is pituitary dwarfism? what's its GHRH/GHIH/GH/IGFs level?
the body does not produce enough GH. low in GHIH/GH/IGFs but high GHRH because of negative feedback.
All endocrine glands are controlled by master gland pituitary gland.
Fasle. eg. pancreas is not controlled by hypothalamus and pituitary gland.
where is pancreas located?
in the retroperitoneal cavity behind the stomach
what the structure response for secreting pancreatic hormones?
islets of langerhans, which only comprise 1-2% of the pancreatic mass
how many islets of langerhans in the pancreas and how many cells each islet contain, approximately
one million islets and each islet contain 2,500 cells.
list three types of endocrine cells in the pancreas and what hormone they produce (ratio)
beta cell (65%)produce insulin;
alpha cell (20%) produce glucagon;
delta cell (10%) produce somatostatin
5% other cells produce polypeptide
insulin is response for____
high glucose in blood. (postprandial state=post meal)
what is C-peptide? any clinic application
Connecting peptide between proinsulin A chain and B chain.
Clinically as a marker for insulin produced by body. Normally 60% proinsulin is break down by liver, so C-peptide can be an indication of how body produce proinsulin/insulin
image the structure of proinsulin
List four glucose transporters type and where are they expressed. which type sensitive to insulin?
GLUT-1 & GLUT-3: constitutively expressed in most cells;
GLUT-2: found in hepatic, renal tubule and pancreatic beta cells;
GLUT-4: insulin sensitive glucose transporter found in skeletal and cardic muscle, adipose tissue.
how insulin is been released by pancreatic beta cell after rising of blood glucose concentration?
1. glucose bind to GLUT-2 on cell membrane and transferred into cell
2. glucokinase add Pi to it and then go through oxidation to produce ATP.
3. increased ATP production closes ATP sensitive K+ channel
4. cell accumulate K+ inside and depolarization, resulting voltage gated Ca2+ opening
5. increased cellular Ca2+ concentration stimulate exocytosis of vesicles containing insulin.
image the insulin secretion by beta cell.
what is the main effect of Sulfonylurea drugs (Glyburide) on beta cells
inhibit K+ channel so K+ stuck inside cell and depolarization cell. Resulting insulin release
what factors stimulate insulin release?
primarily high glucose in blood. Other factors like increased FA and ketoacid, glucagon, cortisol, glucose-dependent insulinotropic peptide (GIP, when eating), K+, Vagal stimulation(resting digestion), sulfonylurea drugs-Glyburide(inhibit K+ channel), obesity.
Also increased aa. stimulate both insulin and glucagon release.
what factors inhibit insulin release?
low blood glucose, fasting, exercise and somatostatin(very potent inhibitor actually inhibit both insulin and glucagon release)
what the insulin effects on blood glucose?
Decrease blood glucose level by:
1. increase glucose transport into target cell (GLUT-4);
2. formation glucogen/ inhibit glycogenolysis
3. inhibits gluconeogenesis
what the insulin effects on blood fatty acid?
Decrease blood FA and ketoacid level by:
1. stimulate fat deposition
2. inhibit lipolysis
what the insulin effects on blood protein/aa?
Decrease blood aa level by
1. increase aa and protein uptake
2. increase protein synthesis
3. inhibit proteolysis
what the insulin effects on K+?
increase K+ uptake into cells.
what is diabetes mellitus and how to diagnose?
a condition of hyperglycemia due to improper production or response to insulin.
1. fasting blood glucose level is >126 mg/dL on two occasion
2. random glucose > 200mg/dL with other clasic symptoms
3. sustained increase of >200 mg/dL glucose following a glucose tolerance test.
which will result a high insulin response? and why?
a. oral glucose intake
b. IV glucose injection
oral glucose intake. Because it will also stimulate GIP, which in turn stimulate insulin release.
In diabetes mellitus type II patients, why doesn't insulin deficiency usually lead to severe ketoacidosis?
in type II diabetes mellitus, beta cells response to high glucose is not complete diminished. the residual function of beta cell is the key difference to type I diabetes, where beta cell been destroyed and usually lead to severe ketoacidosis and death.
compare type I and type II diabetes mellitus:
Other Name:
Typical patient:
what factors stimulate glucagon release?
fasting; decreased glucose concentration; and/or increased aa concentration (arginine and allanine)-increased aa also stimulate insulin release
what factors inhibit glucagon release?
insulin; somatostatin; increased FA and ketoacid plasma concentration.
which signal pathway does glucagon use to increase blood glucose?
through G protein coupled receptor using adenylyl cyclase
which factors stimulate and inhibit somatostatin secretion? and what is the function of somatostain?
stimulated by: ingestion of nutrients; GI hormones; Glucagon

inhibited by insulin;

somatostain is considered to be a inhibitory hormone, which inhibit both insulin and glucagon secretion.
somatostatin is a small polypeptide hormone comprise of 29 aa produced by delta cells of pancreas. It acts in a paracrine fashion to decrease both insulin and glucogan secretion.
False. it is a 14 aa polypeptide hormone. Glucagon is a 29 poly peptide hormone. Other parts of the statement are true.
which part of adrenal gland is considered not essential on hormone secretion
adrenal medulla secret catecholamines(epinephrine, norepinephrine, dopamine), which can be produced at other sites of the body.
where are the adrenal glands are located
in the retroperitoneal cavity superior to each of the kidneys.
adrenal cortex contains 80% of the gland and releases hormones essential for life; while adrenal medulla contains remaining 20% of adrenal gland that releases hormones can be produced by other tissue of the body.
list three regions of adrenal cortex, what hormones they secret?
outmost: 1. zona glomerulosa produces mineralcorticoids such as aldosterone
middle: 2. zona fasciculata produces glucocorticoids like cortisol
inner: 3. zona reticularis produces androgens like DHEA and andro-stenedione.

"GFR vs Salt, suger and sex"
describe renin-angiotensin-aldosterone system
1. liver constant produce may proteins. One of them is angiotensinogen
2. kidney detect low perfussion pressure, low plasma Na+(macula densa) and high K+
3. kidney then release renin (enzyme/hormone) and travel into blood stream
4. renin convert angiotensinogen into angiotensin I
5. angiotensin converting enzyme (ACE, primary located in lung, 40%)convert angiotensin I into angiotensin II
6. angiotensin II can constrict blood vessels. It can also cause adrenal gland to release aldosterone.
7. aldosterone goes back to kidney (increases sodium reabsorption and potassium secretion at principal cells in the nephron; also increase H+ secretion from alpha intercalated cells in nephron) and to save sodium by increase synthesis of basal-lateral Na+/K+ ATPase, apical Na+ channels and the Na+/K+/Cl- cotransporter (TAL)
image of renin-angiotensin-aldosterone system
cortisol also has high affinity for mineralcorticoid receptor (where aldosterone bind in renal cells), how cell resolve this problem
renal cell contain an enzyme: 11-beta-hydroxy-steroid dehydrogenase that converts cortisol to cortisone, which has much lower affinity for the receptors
what is the peak release of cortisol?
usually during morning when people stress out.
How cortisol been released
in general, cortisol acts to mobilize energy stores in body.

hypothalamus releae CRH-> pituitary release ACTH->zona fasciculata release cortisol
what is the function of glucocorticoids in terms of glucose homeostasis
It stimulate gluconeogenesis, proteolysis(major muscle wasting hormone) and lipolysis

It inhibit glucose usage by tissues and insulin sensitivity of adipose tissue(inhibit glucose uptake)
cortisol is catabolic, diabetogenic and helpful during fasting...
other role of cortisol
1. reduce inflammation
2. suppress the immune response-inhibits IL-2 and proliferation of T cell
3. maintain vascular responsiveness to catecholamines-upregulates alpha one adrenergic receptors-constriction
4. inhibit bone formation-decrease synthesis of type I collage, osteoblast production and intestinal calcium absorption
5. increase GFR-vasodilation of afferent aterioles
6. affect the CNS-decrease REM sleep, increases slow wave sleep and awake time; alters mood and cognition.
what is andrenogenital syndrome
deficiency of the hormone 21 beta-hydroxylase in the steroid biosynthetic pathway. This will block the pathway to cortisol and aldosterone synthesis and end up with excessive production of androgens. clinically cause masculinization of the external genitalia during female development and virilization in adult females.
note in this syndrome, ACTH is elevated.
what is Addison's disease/ defect hormones and their symptoms
Primary adrencortical insufficiency; causes: ~70% cases are unknown and ~30% by adrenal gland destroyed by cancer, infections like tuberculosis;
Decreased aldosterone-hypotension, hyperkalemia, metabolic acidosis
Decreased cortisol-hypoglycemia, weight loss, nausea and weakness
Decreased androgens-decreased pubic and axillary hair in female, masculinization in females, decreased sexual desire.
Increased ACTH-stimulate melanocyte causing hyperpigmentation
what is Cushing's Disease/syndrome
Cushing's syndrome=Excess of glucocorticoids from adrenal cortex or exogenous sources
Cushing's Disease=excess glucocorticoids due to ACTH hypersecretion from pituitary adenoma.
Increased cortisol-hyperglycemia, central obesity(causing lipolysis and redistribute fat), round face, supraclavicular fat, buffalo bump, osteoporosis, muscle wasting, susceptibility to infections
Increased cortisol also cause hypertension-increases responsiveness of arterioles to catecholamines (constrictor) and has mild mineralcorticod activity.
increased androgens-unable to produce and menstrual disorders in female.
what cell produce catecholamines?
chromaffin cells in adrenal medulla
catecholamines synthesis pathway and modulators
sympathetic stimulation and cortisol simulation

tyrosine--> --> dopamine-->norepinephrine-->epinephrine(by hormone Phenylethanolamine-N-methyltransferase=PNMT)
which receptors epinephrine and norepinephrine bind to?
epinephrine binds to beta adrenergic receptors

norepinephrine binds to alpha adrenergic receptors.

both operate through G protein coupled signal transduction pathway.
Epinephrine only produced in kidney medulla.
the control of epinephrine and norepinephrine secretion is through direct negative feedback loop
false. by indirectly through monitoring of physiological end effects
what is the effect of epinephrine on blood glucose?
increase blood glucose by gstimulate glycogenolysis, gluconeogenesis, glucagon release and lipolyss. inhibits the release of insulin and uptake of glucose.
what is the normal calcium concentration in body? what hormones regulate the calcuim
~10 mg/ mL
parathyroid hormone (PTH)-increase [Ca2+]
Calcitonin ("down")-decrease [Ca 2+]
Vitamin D3-increase Ca2+ reabsorption
where type of hormone PTH belong to and where does it formed and site of action?
protein hormone that formed in Chief cells of PARATHYROID gland. site of action are bone and kidney (increase blood Ca2+)
where type of hormone Calcitonin belong to and where does it formed and site of action?
Protein hormone
formed in Parafollicular or C cells of the THYROID gland. site of action is bone and decrease Ca2+
where type of hormone vitamin D3 belong to and where does it formed and site of action?
Steroid hormone
formed at skin or from diet. site of action are intestine and bone.(stimulate Ca2+ reabsorption)
Where and when body release PTH
from the CHIEF cells of the parathyroid gland in response to low plasma calcium level
Action of PTH hormone (4 pts)
1. stimulate osteoclasts
2. inhibit osteoblasts
3.stimulate calcium reabsorption in the kidney at the loop of Henle (distal tubule)
4. and inhibit phosphate reabsorption (by lowering Tm) in PCT
what cause Calcitonin releasing and its action
hypercalcemia and postprandial state. Action is to inhibit osteoclast activity thus decrease blood Ca2+ level.
List two major sources of Vitamin D3
1. diet
2. formed in the skin from 7-dehydrocholesterol using UV rays
what is the role of Cholecalciferol?
Cholecalciferol is the product when UV light hit 7-dehydrocholesterol in skin(or from diet). It can be converted into 25-OH-Cholecalciferol in liver by 25-hydroxylase(inactive form), which can be further converted into 1,25- (OH)2-Cholecalciferol in kidney by 1-alpha-hydroxylase (stimulated by high PTH, Low Ca and Pi). 25-OH-Cholecalciferol can also be converted into inactive form of 24,25-(OH)2-Cholecalciferol in kidney by 24-hydroxylase.
Image of vitamin D3 synthesis
List three effect of vitamin D3 and its site of action
1. instestines- induces synthesis of Calbindin D-28K -> increase Ca reabsorption
2. Kidney- stimulate Ca resorption
3. Bone- stimulate reforming (stimulate osteoclast and bone resorption; and promotes mineralization of new bone)
match symptoms with disorder
Note decreased bone formation can be caused by either hyperparathyroidism or Vitamin D deficiency
Clinic effect of hyperparathyroidism
1. Bradycardia and arrhythmias
2. cardiac rigor- ventricular muscle contracts and can not relax
3. muscle weakness due to depressed neuromuscular excitability
Clinic concern of vitamin D deficiencies. In children and in adult
in children lead to rickets- growth failure and skeletal deformities

in adult lead to osteomalacia or bone softening

Osteoporosis can be associated with vitamin D deficiency. Vitamin C deficiencies also cause this disorder. In elderly women, reduced level of estrogen is another factor.
what is the exocrine function of male reproduction system (4 pts)
1. sperm; 2. prostate fluid; 3. seminal vesicle fluid; 4. bulbourethral gland (or Cowper's gland)
main role of male reproductive hormones (4 pts)
1. stimulate male pattern before birth; 2. control spermatogenesis; 3. promote male secondary sexual characteristics; 4. increase sexual drive (libido)
What play a vital role in regulate the temperature of testes?
cremaster and dartos muscles of the scrotum.
where does spermatozoa been produced?
seminiferous tubules in testes.
List three cell types in seminiferous tubule and their function.
1. Leydin cell- produce testosterone hormone
2. sperm cell- from spermatogenic cells
3. sertoli cell- nourish spermatozoa and form blood testes barrier.
where does spermatozoa become mature?
what is the route that spermatozoa pass through
testes(seminiferous tubules) -> epididymis -> vasdeferens -> ejaculatory duct -> urethra
what glands add seminal fluid to sperm secretion?
1. seminal vesicles; 2. prostate gland; 3. bulbourethral gland (Cowper's gland)
list 6 function of sertoli cell
1. blood testis barrier; 2. nourishment; 3. phagocytosis; 4. sperm transport; 5. secrete inhibin; 6. regulate effects of testosterone and FSH
1. inhibit FSH release; 2. inhibit LH; 3. male pattern; 4. GnRH inhibit; 5. Testosterone secretion; 6. spermatogenesis; 7. stimulate LH and FSH

a. inhibin; b. testosterone; c. LH; d. FSH; e. GnRH
a. inhibin=1. inhibit FSH release; b. testosterone=2. inhibit LH; b. testosterone=3. male pattern; Testosterone (inhibit)=4. GnRH inhibit; c. LH=5. Testosterone secretion; d. FSH and b.testosterone=6. spermatogenesis; e.GnRH=7. stimulate LH and FSH

a. inhibin; b. testosterone; c. LH; d. FSH; e. GnRH
Testosterone is response to what hormone and how does it released/regulated?
GnRh released from the hypothalamus and stimulate anterior pituitary gland to release LH, which travel to the leydig cells in the testes and stimulate testosterone release.

sertoli cell also secret "androgen binding protein" - (also called testosterone binding globulin) increases testosterone concentration in the seminiferous tubules to stimulate spermiogenesis (and keep high level of the androgen within local range)

Estradiol - aromatase from Sertoli cells convert testosterone to 17 beta estradiol to direct spermatogenesis
what does inhibin do and where does it come from
inhibit both FSH and LH release at anterior pituitary gland. But inhibit FSH more. Sertoli cell secret inhibin hromone.
what is the difference between dihydro-testosterone and testosterone?
in some tissue it more response for external male pattern; testosterone more response for internal male pattern
What are the negative feedback pathway in male hormone production? (3pts)
1. sertoli cell secret inhibin to inhibit FSH and LH release
2. testosterone inhibit LH release at anterior pituitary gland
3. testosterone inhibit GnRH release at hypothalamus.
what is the paracrine function of testosterone?
leydig cell secret testosterone will travel short distant to stimulate spermatogenic cells.
Male hormone feedback "map"
Male hormones stimulate anabolism and protein synthesis
what does female reproductive system consists(structures)? (6pts)
ovaries(site of oogenesis and ovulation)
Fallopian tubes(site of fertilization- ampula)
Uterus(zygote implantation andmenstruation)
Vagina(site of penetration and canal for child birth)
Pudendum(vulva-external genitalia)
Breasts(source of lactation)
Main roles of female reproductive hormones. (5pts)
1.Stimulate proper development of ovum and the surrounding follicular cells. eg. FSH
2.Regulate the ovulation of developing eggs from the ovaries. eg. FSH and LH
3.Provide a favorable environment for implantation of a zygote in the uterus. eg. progesterone and estrogens
4.Control embryonic maturation, fetal development, and parturition. eg. relaxin
5.Facilitate lactation. eg. estrogen, progesterone
where does corpus luteum coming form and its function? what is its fate w/ or w/o fertilization?
ruptured follicle release secondary oocyte and the remaining called corpus lutenum. It keep release female reproductive hormones (progesterone, estrogens, relaxin and inhibin) for at least two weeks.

if no fertilization after two weeks, it degenerates into the corpus albicans and menstruation occurs
if fertilization occurs, implanted egg release HCG (human chorionic gonadotropin) to keep corpus luteum working until placenta becomes capable of producing sufficient hormones.
where does inhibin secreted in male and female. Does it have same inhibition function on anterior pituitary gland?
in male secreted by sertoli cells; in female by corpus luteum.

both inhibits release of FSH and to a lesser extend LH.
what are the TOH in male and female
Male: testosterone; DHT; inhibin

Female: estrogens(estradiol);progesterone; relaxin; inhibin
what is the function of estrogens in female?
Promote development and maintenance of female sex characteristics
Increase protein anabolism
Lower blood cholesterol
MODERARE!!! levels inhibit release of GnRH, FSH and LH
(HIGH levels of estrogen will initiate positive feedback of LH-estrogen-GnRH system)
what is the function of progesterone
works with estrogens to prepare endometrium for implantation
Prepare mammary glands
Inhibits release of GnRH and LH
what is the function of relaxin
Inhibits contractions of uterine smooth muscle
During labor, increases flexibility of pubic symphysis and dilates uterine cervix
Female sex hormones and feedback map
In male and female, what hormones inhibit GnRH release?
Male: testosterone
Female: estrogen and progesterone
in male and female, what hormones inhibit FSH and LH release
Male; testosterone and inhibin
Female: estrogen, progesterone and inhibin
Image: Ovulation and hormonal change
if a woman has menstrual cycle of 35 days, roughly how many days is preovulatory phase
postovulatory phase is fairly constant in all female, which is 14 days. So in this case preovulatory phase will be 35-14=21 days
In female, if estrogen level increase, what happen to the LH level?
LH will also increase. This(ovulation) is one of the positive feedback of female reproductive system (another is oxytocin during child birth). LH level decrease after follicle rupture.
High level of estrogen will initiate negative feedback which will decrease GnRH and LH release
False. High level estrogen will initiate positive feedback.
Where does HCG been released and what is its function
released from the developing embryo that can rescue corpus luteum from degeneration
List the events of early pregnancy.
0 days: ovulation
1 day: fertilization
4 days: entrance of blastocyst into uterine cavity
5 days implantation
6 days attachmetn to endometrium
8 days onset of secretion of hCG
10 days hCG rescue corpus luteum
During which trimester hCG is high and when it reach peak
first trimester and peaking at 9 gestational week.
Besides female hormones, cortisol, prostaglandins and catecholamines are also involved in parturition.

parturition = child birth
what is PIH and its function
Prolactin inhibiting hormone, also called dopamine. It inhibit prolactin release, a major hormone stimulate production of milk.
what is the difference between prolactin and oxytocin regarding milk production?
prolactin stimulation production of milk

oxytocin stimulate milk ejaction
Describe oxytocin positive feedback
As a baby moves towards the birth canal, it presses against the pressure receptors in the muscular part of the uterus (cervix). These receptors evoke a release of oxytocin from the brain (and maybe also the placenta). When the oxytocin reaches responsive receptors in the muscles of the uterus it will increase muscular tension thus increasing stimuli to the pressure receptors. This goes on as "labor" until the pressure is relieved: the baby is born -- oxytocin is no longer evoked and labor contractions cease.
image: site of hormone secretion.