Dental Physiology-The Endocrine System

Front 1

Endocrine glands include?

Back 1

 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

Front 2

List 4 type of hormones

Back 2

endocrine; neurocrine; paracrine; autocrine

Front 3

what are endocrine hormones?

Back 3

released from glands into blood, travel to target organs at distant sites

Front 4

what are neurocrine hormones?

Back 4

released from synaptic end bulbs of neurons into blood. eg ADH

Front 5

what are paracrine hormones?

Back 5

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)

Front 6

what are the autocrine hormones?

Back 6

act locally, receptors are located on the very same cell that released the hormone in the first place. eg,growth factors like PDGF

Front 7

typically hormone concentrations

Back 7

10^-9 M to 10^-12 M

Front 8

T/F?
some organs produce more than one hormones, but one cell type only produce one hormone.

Back 8

False. FSH and LH produced both produced by one cell type. This is the only exception

Front 9

List two example of positive feed back in female reproduction system.

Back 9

child birth and ovulaiton

Front 10

List three ways to maintain final hormones level

Back 10

long loop feedback
short loop feedback
ultrashort loop feedback.

Front 11

how to make a cell to less responsive to hormones (3 ways)

Back 11

reduce # of receptors(destroy or endocytosis into vesicles);
reduce the synthesis of the receptors;
inactive the hormone receptors.

Front 12

list three main type of hormones based on chemical structural

Back 12

1. proteins/peptides
2. amines
3. steroids

Front 13

what are peptide/protein hormones

Back 13

synthesized from aa. monomers. usually synthesized in an inactive prehormone or preprohormone form. Majority of hormones are peptides and proteins.

Front 14

List 12 peptide/protein hormones

Back 14

oxytocin; ADH; TSH; FSH; LH; ACTH; GH; PTH; Proclactin; hCG; Calcitonin; somatostatin

Front 15

what are amine hormones?

Back 15

derivative of aa tyrosine. eg. Catecholamine (epinephrine/norepinephrine and dopamine); thyroid hormones (T3 and T4)

Front 16

what are the steroid hormones?

Back 16

derivatives of cholesterol. include cortisol, aldosterone, estradiol and testosterone.

Front 17

which types of hormone need transport proteins while in the blood?

Back 17

steroids because they are hydrophobic and not easily dissolved in water.
T3 and T4 also need transport proteins.

Front 18

For amine hormones, which act more like protein hormones?

Back 18

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

Front 19

what are the function of hormone binding proteins?

Back 19

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

Front 20

brief two types of G protein signaling transduction with second messenger

Back 20

1. G protein coupled cAMP and PKA pathway (Gs)
2. G protein coupled DAG/IP3 and PKC/Ca2+ pathway (Gq)

Front 21

describe G protein coupled cAMP cascade

Back 21

Front 22

Describe G-protein coupled PIP2 pathway.

Back 22

Front 23

describe the steroid hormone signal pathway

Back 23

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

Front 24

Hormonal rhythms

Back 24

1. Periodicity (minutes to years)
2. Needed for normal function
3. Circadian (24 hour cycle)
4. Pulsatile rhythms are superimposed on circadian

Front 25

list the potential fate of hormones

Back 25

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

Front 26

what is the master hormone gland and where it is located

Back 26

Pituitary gland! located inferior to the hypothalamus and is connected by infundibulum

Front 27

which part of the pituitary gland is primarily endocrine cells?

Back 27

anterior lobe (adenohypophysis)

Front 28

which part of the pituitary gland is primarily neural tissue?

Back 28

posterior lobe (neurohypophysis) which produce Oxytocin and ADH.

Front 29

what is special about blood vessels around hypothalamus and pituitary gland

Back 29

the capillary bed of hypothalamus is connected to the capillary bed of anterior pituitary via "hypothalamic-hypophysial portal vessels"

Front 30

what hormones are produced by posterior pituitary gland? and their major role

Back 30

Oxytocin: female reproduction
ADH (antidiuretic hormone): also called vasopressin. function is to conserve water.

Front 31

what is the another name for ADH

Back 31

vasopressin

Front 32

where does Oxytocin hormone been produced

Back 32

paraventricular nuclei of hypothalamus

Front 33

where does ADH been produced

Back 33

supraoptic nuclei of hypothalamus.

Front 34

How does the ADH been released? (when/where/how)

Back 34

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.

Front 35

T/F
ADH release is only controlled by hypothalamus

Back 35

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.

Front 36

what cause the ADH to be released? in detail.

Back 36

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.

Front 37

How target cell response to ADH? in detail

Back 37

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.

Front 38

what is diabetes insipidus?

Back 38

occurs when the body is UNABLE to produce adequate levels of ADH or defect in the ADH receptor

Front 39

List two type of diabetes insipudus and their features

Back 39

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

Front 40

List 6 hormones released from anterior pituitary gland

Back 40

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.

Front 41

TRH source, target and down stream response

Back 41

hypothalamus-> stimulate TSH and PRL(prolactin) in Anterior pituitary->1. thyroid gland release T3 (triiodothyronine) and T4 (thyroxine or tetraiodothyronine); 2. mammary glands

Front 42

GHRH/GHIH source, target and down stream response

Back 42

released from hypothalamus-> +/- GH in anterior pituitary->liver and other tissues->IGFs (insulin-like growth factors, also called Somatomedins)

Front 43

CRH source, target and down stream response

Back 43

hypothalamus->ACTH (adrenocorticotropic H.) in anterior pituitary->adrenal cortex->mineralcorticoids-aldosterone(minor); glucocorticoids-cortisol; androgens-dehydroepiandrosterone(DHEA)

Front 44

PIH(dopmine) source, target and down stream response

Back 44

hypothalamus-> inhibit PRL in anterior pituitary->mammary gland

Front 45

GnRH source, target and down stream response

Back 45

hypothalamus-> stimulate FSH (follicle stimulating H.) and LH ( luteinizing H.) release in anterior pituitary-> gonads (testes&ovaries) release testosterone and estradiol/progesterone.

Front 46

what type of cell release following hormone?
TSH; GH; ACTH; PRL; FSH; LH

Back 46

Thyrotropes; somatotropes; corticotropes; lactotropes; gonadotropes; gonadotropes.

Front 47

what are the main sites of action from hormones

Back 47

liver, adipose tissue and muscle.

Front 48

what is the normal blood glucose level

Back 48

90-120 mg%

Front 49

what tissue/cell are heavily rely on glucose for energy

Back 49

brain, nervous tissue and red blood cell

Front 50

T/F
Despite the importance of glucose as an energy source, very little glucose is stored in the body as glycogen (~1%)

Back 50

True

Front 51

what are the two type of energy storage?

Back 51

fat 76% and protein 23%

Front 52

matching fed and fasting state with following:
a. glycogenesis; b. lipogenesis; c. gluconeogenesis; d. protein synthesis; e. glycogenolysis; f. lipolysis; g proteolysis

Back 52

Fed state: a. glycogenesis; b. lipogenesis; d. protein synthesis;
Fasting state: c. gluconeogenesis; e. glycogenolysis; f. lipolysis; g proteolysis

Front 53

when and where does the ketone body come from

Back 53

after 5-6 weeks starvation, body will use fat to produce energy thus accumulate ketone body during the process.

Front 54

what is ketoacidosis

Back 54

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.

Front 55

what is isthmus

Back 55

structure connect two lobes of thyroid.

Front 56

where does the thyroid hormones are produced in thyroid gland?

Back 56

thyroid gland is divided into two lobes and further divided into segments called follicles , where thyroid hormones are produced by its epithelial cells.

Front 57

what hormones thyroid gland produce? full name.

Back 57

T3, tri-iodo-thyro-nine
T4, tetra-iodo-thyro-nine, also called thyroxine

Front 58

which is more active, T3 or T4, reverse T3?

Back 58

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.

Front 59

does synthesis of thyroid hormones happened in intracellular or extracellular

Back 59

both!

Front 60

T/F
iodide are combined with TGB in extracellular space to from T1~T4.

Back 60

False. Iodine combine with TGB. Iodide is absorbed from blood plasma and transferred into follicular cell through Na+-I- symporter.

Front 61

List three major component when synthesis thyroid hormone

Back 61

1. iodide form diet
2. aa. thyrosine
3. protein thyroglobulin (TGB)

Front 62

where does T3 and T4 stored in thyroid gland?

Back 62

in colloid

Front 63

which enzyme convert iodide to iodine

Back 63

thyroid peroxidase

Front 64

synthesis of thyroid hormones

Back 64

Front 65

8 steps of thyroid hormone synthesis

Back 65

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

Front 66

which enzyme convert T4 to T3?

Back 66

mono-de-iodinase

Front 67

T/F
Thyroxine bind to nuclear receptors and modifies gene transcription within the target cell.

Back 67

False. T3 bind to nuclear receptor, not T4 which is thyroxine.

Front 68

the major job of thyroid hormones and is accomplished mainly by which cellular mechanism?

Back 68

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.

Front 69

T/F
thyroid hormone acts on virtually every organ system in the human body

Back 69

True

Front 70

what is the effect of thyroid hormone on bone formation? how about GH and IGFs?

Back 70

thyroid hormone acts synergistically with GH and Somatomedins (IGFs) to increase bone formation

Front 71

what is the effect of thyroid hormone on heart and lung?

Back 71

increase cardic output (positive inotrope-contractility and chronotrope-rate) and increase respiratory rate. This is sympathomimetic effect (stimulate beta receptors.

Front 72

what is Cretinism and cause/symptoms

Back 72

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

Front 73

symptoms of hypothyroidism

Back 73

cold sensitivity; hypoventilation; lethargy =fatigue; myxedema =swollen of skin; weight gain; goiter (also in hyperthyroidism)

Front 74

symptoms of hyperthyroidism

Back 74

exophthalmos=protruding of eyes; increased basal metabolic rate, cardiac output and heat production; sweating; weight lose; goiter (also in hypothyroidism)

Front 75

what is primary, secondary and tertiary hypo/hyper-thyroidism?

Back 75

primary-origin is the thyroid gland(T3/T4)
secondary-origin is the anterior pituitary (TSH)
tertiary-origin is the hypothalamus (TRH)

Front 76

what is Hashimoto's thyroiditis

Back 76

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

Front 77

what is ectopic-graves disease

Back 77

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

Front 78

list one of the major causes of goiter development

Back 78

iodine deficiencies often lead to hypothyroidism and goiter

Front 79

what is the effect of high level estrogen to TBG, and to thyroid hormone? is this characterized as euthyroidism, hypo or hyper thyroidism?

Back 79

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.

Front 80

Brief GH pathway (source, target)

Back 80

GHRH(dominant hormone)/GHIH(less) from hypothalamus->GH from anterior pituitary->bind to the GH receptors on liver->IGFs produced from liver.

Front 81

why GH has a dabetogenic effect?

Back 81

1. decreases glucose uptake and use by muscle/adipose tissue; 2. increases lipolysis; 3. provides insulin resistance; 4. stimulate gluconeogenesis.

Front 82

what is the indirect effect of GH?

Back 82

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.

Front 83

T/F
IGFs are produced primarily at NON-endocrine tissues such as the liver, kidney and muscle.

Back 83

True!

Front 84

what is another name for IGFs

Back 84

somatomedins

Front 85

effect of somatomedins

Back 85

1. growth of soft tissues and bones by increasing the uptake of aa.
2. stimulating synthesis of DNA, RNA and proteins.

Front 86

what factors stimulate the release of GH?

Back 86

(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

Front 87

what factors inhibit GH

Back 87

high glucose; high FA; obesity.

Front 88

How does hypersecrection of GH affect adult long bone?

Back 88

periosteal bone growth after epiphyseal plate closure, causing Acromegaly.

Front 89

what cause adult hypersecrection of GH

Back 89

GH secrecting pituitary adenoma (tumor)

Front 90

symptom of child hyposecrection of GH

Back 90

Dwarfish; short stature; failure to growth; mild obesity; delayed puberty

Front 91

T/F
hyposecrection of GH in adult will result mild hypoglycemia

Back 91

True.

Front 92

what is Laron Dwarf? what's its GHRH/GHIH/GH/IGFs level?

Back 92

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

Front 93

what is pituitary dwarfism? what's its GHRH/GHIH/GH/IGFs level?

Back 93

the body does not produce enough GH. low in GHIH/GH/IGFs but high GHRH because of negative feedback.

Front 94

T/F
All endocrine glands are controlled by master gland pituitary gland.

Back 94

Fasle. eg. pancreas is not controlled by hypothalamus and pituitary gland.

Front 95

where is pancreas located?

Back 95

in the retroperitoneal cavity behind the stomach

Front 96

what the structure response for secreting pancreatic hormones?

Back 96

islets of langerhans, which only comprise 1-2% of the pancreatic mass

Front 97

how many islets of langerhans in the pancreas and how many cells each islet contain, approximately

Back 97

one million islets and each islet contain 2,500 cells.

Front 98

list three types of endocrine cells in the pancreas and what hormone they produce (ratio)

Back 98

beta cell (65%)produce insulin;
alpha cell (20%) produce glucagon;
delta cell (10%) produce somatostatin
5% other cells produce polypeptide

Front 99

insulin is response for____

Back 99

high glucose in blood. (postprandial state=post meal)

Front 100

what is C-peptide? any clinic application

Back 100

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

Front 101

image the structure of proinsulin

Back 101

Front 102

List four glucose transporters type and where are they expressed. which type sensitive to insulin?

Back 102

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.

Front 103

how insulin is been released by pancreatic beta cell after rising of blood glucose concentration?

Back 103

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.

Front 104

image the insulin secretion by beta cell.

Back 104

Front 105

what is the main effect of Sulfonylurea drugs (Glyburide) on beta cells

Back 105

inhibit K+ channel so K+ stuck inside cell and depolarization cell. Resulting insulin release

Front 106

what factors stimulate insulin release?

Back 106

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.

Front 107

what factors inhibit insulin release?

Back 107

low blood glucose, fasting, exercise and somatostatin(very potent inhibitor actually inhibit both insulin and glucagon release)

Front 108

what the insulin effects on blood glucose?

Back 108

Decrease blood glucose level by:
1. increase glucose transport into target cell (GLUT-4);
2. formation glucogen/ inhibit glycogenolysis
3. inhibits gluconeogenesis

Front 109

what the insulin effects on blood fatty acid?

Back 109

Decrease blood FA and ketoacid level by:
1. stimulate fat deposition
2. inhibit lipolysis

Front 110

what the insulin effects on blood protein/aa?

Back 110

Decrease blood aa level by
1. increase aa and protein uptake
2. increase protein synthesis
3. inhibit proteolysis

Front 111

what the insulin effects on K+?

Back 111

increase K+ uptake into cells.

Front 112

what is diabetes mellitus and how to diagnose?

Back 112

a condition of hyperglycemia due to improper production or response to insulin.
Diagnose:
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.

Front 113

which will result a high insulin response? and why?
a. oral glucose intake
b. IV glucose injection

Back 113

oral glucose intake. Because it will also stimulate GIP, which in turn stimulate insulin release.

Front 114

Back 114

Front 115

In diabetes mellitus type II patients, why doesn't insulin deficiency usually lead to severe ketoacidosis?

Back 115

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.

Front 116

compare type I and type II diabetes mellitus:
Other Name:
Cause:
Ketoacidosis:
Typical patient:

Back 116

Front 117

what factors stimulate glucagon release?

Back 117

fasting; decreased glucose concentration; and/or increased aa concentration (arginine and allanine)-increased aa also stimulate insulin release

Front 118

what factors inhibit glucagon release?

Back 118

insulin; somatostatin; increased FA and ketoacid plasma concentration.

Front 119

which signal pathway does glucagon use to increase blood glucose?

Back 119

through G protein coupled receptor using adenylyl cyclase

Front 120

which factors stimulate and inhibit somatostatin secretion? and what is the function of somatostain?

Back 120

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.

Front 121

T/F
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.

Back 121

False. it is a 14 aa polypeptide hormone. Glucagon is a 29 poly peptide hormone. Other parts of the statement are true.

Front 122

which part of adrenal gland is considered not essential on hormone secretion

Back 122

adrenal medulla secret catecholamines(epinephrine, norepinephrine, dopamine), which can be produced at other sites of the body.

Front 123

where are the adrenal glands are located

Back 123

in the retroperitoneal cavity superior to each of the kidneys.

Front 124

T/F
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.

Back 124

True

Front 125

list three regions of adrenal cortex, what hormones they secret?

Back 125

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"

Front 126

describe renin-angiotensin-aldosterone system

Back 126

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)

Front 127

image of renin-angiotensin-aldosterone system

Back 127

Front 128

cortisol also has high affinity for mineralcorticoid receptor (where aldosterone bind in renal cells), how cell resolve this problem

Back 128

renal cell contain an enzyme: 11-beta-hydroxy-steroid dehydrogenase that converts cortisol to cortisone, which has much lower affinity for the receptors

Front 129

what is the peak release of cortisol?

Back 129

usually during morning when people stress out.

Front 130

How cortisol been released

Back 130

in general, cortisol acts to mobilize energy stores in body.

hypothalamus releae CRH-> pituitary release ACTH->zona fasciculata release cortisol

Front 131

what is the function of glucocorticoids in terms of glucose homeostasis

Back 131

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)

Front 132

T/F
cortisol is catabolic, diabetogenic and helpful during fasting...

Back 132

True

Front 133

other role of cortisol

Back 133

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.

Front 134

what is andrenogenital syndrome

Back 134

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.

Front 135

what is Addison's disease/ defect hormones and their symptoms

Back 135

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

Front 136

what is Cushing's Disease/syndrome

Back 136

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.

Front 137

what cell produce catecholamines?

Back 137

chromaffin cells in adrenal medulla

Front 138

catecholamines synthesis pathway and modulators

Back 138

sympathetic stimulation and cortisol simulation

tyrosine--> --> dopamine-->norepinephrine-->epinephrine(by hormone Phenylethanolamine-N-methyltransferase=PNMT)

Front 139

which receptors epinephrine and norepinephrine bind to?

Back 139

epinephrine binds to beta adrenergic receptors

norepinephrine binds to alpha adrenergic receptors.

both operate through G protein coupled signal transduction pathway.

Front 140

T/F
Epinephrine only produced in kidney medulla.

Back 140

True

Front 141

T/F
the control of epinephrine and norepinephrine secretion is through direct negative feedback loop

Back 141

false. by indirectly through monitoring of physiological end effects

Front 142

what is the effect of epinephrine on blood glucose?

Back 142

increase blood glucose by gstimulate glycogenolysis, gluconeogenesis, glucagon release and lipolyss. inhibits the release of insulin and uptake of glucose.

Front 143

Back 143

Front 144

what is the normal calcium concentration in body? what hormones regulate the calcuim

Back 144

~10 mg/ mL
parathyroid hormone (PTH)-increase [Ca2+]
Calcitonin ("down")-decrease [Ca 2+]
Vitamin D3-increase Ca2+ reabsorption

Front 145

where type of hormone PTH belong to and where does it formed and site of action?

Back 145

protein hormone that formed in Chief cells of PARATHYROID gland. site of action are bone and kidney (increase blood Ca2+)

Front 146

where type of hormone Calcitonin belong to and where does it formed and site of action?

Back 146

Protein hormone
formed in Parafollicular or C cells of the THYROID gland. site of action is bone and decrease Ca2+

Front 147

where type of hormone vitamin D3 belong to and where does it formed and site of action?

Back 147

Steroid hormone
formed at skin or from diet. site of action are intestine and bone.(stimulate Ca2+ reabsorption)

Front 148

Where and when body release PTH

Back 148

from the CHIEF cells of the parathyroid gland in response to low plasma calcium level

Front 149

Action of PTH hormone (4 pts)

Back 149

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

Front 150

what cause Calcitonin releasing and its action

Back 150

hypercalcemia and postprandial state. Action is to inhibit osteoclast activity thus decrease blood Ca2+ level.

Front 151

List two major sources of Vitamin D3

Back 151

1. diet
2. formed in the skin from 7-dehydrocholesterol using UV rays

Front 152

what is the role of Cholecalciferol?

Back 152

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.

Front 153

Image of vitamin D3 synthesis

Back 153

Front 154

List three effect of vitamin D3 and its site of action

Back 154

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)

Front 155

match symptoms with disorder

Back 155

Note decreased bone formation can be caused by either hyperparathyroidism or Vitamin D deficiency

Front 156

Clinic effect of hyperparathyroidism

Back 156

1. Bradycardia and arrhythmias
2. cardiac rigor- ventricular muscle contracts and can not relax
3. muscle weakness due to depressed neuromuscular excitability

Front 157

Clinic concern of vitamin D deficiencies. In children and in adult

Back 157

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.

Front 158

what is the exocrine function of male reproduction system (4 pts)

Back 158

1. sperm; 2. prostate fluid; 3. seminal vesicle fluid; 4. bulbourethral gland (or Cowper's gland)

Front 159

main role of male reproductive hormones (4 pts)

Back 159

1. stimulate male pattern before birth; 2. control spermatogenesis; 3. promote male secondary sexual characteristics; 4. increase sexual drive (libido)

Front 160

What play a vital role in regulate the temperature of testes?

Back 160

cremaster and dartos muscles of the scrotum.

Front 161

where does spermatozoa been produced?

Back 161

seminiferous tubules in testes.

Front 162

List three cell types in seminiferous tubule and their function.

Back 162

1. Leydin cell- produce testosterone hormone
2. sperm cell- from spermatogenic cells
3. sertoli cell- nourish spermatozoa and form blood testes barrier.

Front 163

where does spermatozoa become mature?

Back 163

epididymis

Front 164

what is the route that spermatozoa pass through

Back 164

testes(seminiferous tubules) -> epididymis -> vasdeferens -> ejaculatory duct -> urethra

Front 165

what glands add seminal fluid to sperm secretion?

Back 165

1. seminal vesicles; 2. prostate gland; 3. bulbourethral gland (Cowper's gland)

Front 166

list 6 function of sertoli cell

Back 166

1. blood testis barrier; 2. nourishment; 3. phagocytosis; 4. sperm transport; 5. secrete inhibin; 6. regulate effects of testosterone and FSH

Front 167

matching:
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

Back 167

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

Front 168

Testosterone is response to what hormone and how does it released/regulated?

Back 168

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

Front 169

what does inhibin do and where does it come from

Back 169

inhibit both FSH and LH release at anterior pituitary gland. But inhibit FSH more. Sertoli cell secret inhibin hromone.

Front 170

what is the difference between dihydro-testosterone and testosterone?

Back 170

in some tissue it more response for external male pattern; testosterone more response for internal male pattern

Front 171

What are the negative feedback pathway in male hormone production? (3pts)

Back 171

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.

Front 172

what is the paracrine function of testosterone?

Back 172

leydig cell secret testosterone will travel short distant to stimulate spermatogenic cells.

Front 173

Male hormone feedback "map"

Back 173

Front 174

T/F
Male hormones stimulate anabolism and protein synthesis

Back 174

True

Front 175

what does female reproductive system consists(structures)? (6pts)

Back 175

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)

Front 176

Main roles of female reproductive hormones. (5pts)

Back 176

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

Front 177

where does corpus luteum coming form and its function? what is its fate w/ or w/o fertilization?

Back 177

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.

Front 178

where does inhibin secreted in male and female. Does it have same inhibition function on anterior pituitary gland?

Back 178

in male secreted by sertoli cells; in female by corpus luteum.

both inhibits release of FSH and to a lesser extend LH.

Front 179

what are the TOH in male and female

Back 179

Male: testosterone; DHT; inhibin

Female: estrogens(estradiol);progesterone; relaxin; inhibin

Front 180

what is the function of estrogens in female?

Back 180

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)

Front 181

what is the function of progesterone

Back 181

works with estrogens to prepare endometrium for implantation
Prepare mammary glands
Inhibits release of GnRH and LH

Front 182

what is the function of relaxin

Back 182

Inhibits contractions of uterine smooth muscle
During labor, increases flexibility of pubic symphysis and dilates uterine cervix

Front 183

Female sex hormones and feedback map

Back 183

Front 184

In male and female, what hormones inhibit GnRH release?

Back 184

Male: testosterone
Female: estrogen and progesterone

Front 185

in male and female, what hormones inhibit FSH and LH release

Back 185

Male; testosterone and inhibin
Female: estrogen, progesterone and inhibin

Front 186

Image: Ovulation and hormonal change

Back 186

Front 187

if a woman has menstrual cycle of 35 days, roughly how many days is preovulatory phase

Back 187

postovulatory phase is fairly constant in all female, which is 14 days. So in this case preovulatory phase will be 35-14=21 days

Front 188

In female, if estrogen level increase, what happen to the LH level?

Back 188

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.

Front 189

T/F
High level of estrogen will initiate negative feedback which will decrease GnRH and LH release

Back 189

False. High level estrogen will initiate positive feedback.

Front 190

Where does HCG been released and what is its function

Back 190

released from the developing embryo that can rescue corpus luteum from degeneration

Front 191

List the events of early pregnancy.

Back 191

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

Front 192

During which trimester hCG is high and when it reach peak

Back 192

first trimester and peaking at 9 gestational week.

Front 193

T/F
Besides female hormones, cortisol, prostaglandins and catecholamines are also involved in parturition.

Back 193

True:

parturition = child birth

Front 194

what is PIH and its function

Back 194

Prolactin inhibiting hormone, also called dopamine. It inhibit prolactin release, a major hormone stimulate production of milk.

Front 195

what is the difference between prolactin and oxytocin regarding milk production?

Back 195

prolactin stimulation production of milk

oxytocin stimulate milk ejaction

Front 196

Describe oxytocin positive feedback

Back 196

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.

Front 197

image: site of hormone secretion.

Back 197