Pgy 412G Endocrine Physiology

Front 1

What does hormones never do?

Back 1

Initiate cellular responses -- they only modulate -speed up or slow down

Front 2

What does hormones help the body do?

Back 2

1. maintain homeostasis
2. adapt to change
3. perform coordinated complex processes

Front 3

Whats the difference between exocrine and endocrine?

Back 3

exocine - secreted into a luman (gland and goes to a specific place)
endocrine- secreted into the blood

Front 4

At what concentration does hormones circulate in the blood?

Back 4

very small concentration

Front 5

What is a primary endocrine gland?

Back 5

Its main function is to secrete hormones

Front 6

What hormones are made in the adrenal cortex? medulla?

Back 6

Cortex -- 1. cortisol, androgens, aldosterone

Medulla - epi and nor

Front 7

What hormones does the placenta secrete?

Back 7

1. human chorionic gonadotropin
2. estogen
3. progesterone
4. human placental lactogen

Front 8

Hormones of the thyroid?

Back 8

1. T3 2. T4 3. Calcitonin

Front 9

What are the 3 main groups of hormones?

Back 9

1. amino 2. peptide 3. steroid

Front 10

What is the order of organelles that hormones travel to become active?

Back 10

Starts as pre-pro then goes to ER to become pro. then to golgi to become active then goes into secretory vessicals

Front 11

What is inside the secretory vessicle?

Back 11

both the hormone and the copeptide (what was bound to it as pro hormone

Front 12

What AA are amino acid hormones derived from?

Back 12

Tyrosine

Front 13

Whats another name for amine hormones?

Back 13

catecholamines

Front 14

tyrosine hydroxylase -

Back 14

converts tyrosine to DOPA -(this is the rate limiting step to make Epi)

Front 15

PNMT-

Back 15

coverts NE to E

Front 16

What 2 peptide hormones bind to proteins in the blood?

Back 16

GH and IGF

Front 17

What amine hormone needs to be bound to a protein?

Back 17

Thyroid hormones -t3 and t4

Front 18

Where is the first enzymatic step to make steroid hormone?

Back 18

in the mitochondria

Front 19

What are the rate limiting steps to make steroid hormones?

Back 19

1. transport of cholesterol into the mito
2. activity of P450 that catalyzes conversion of cholesterol into pregnenolone

Front 20

Give an example of a glucocorticord, mineralocorticoid, androgen that is secreted from the adrenal cortex?

Back 20

glucocorticord-- cortisol
mineralocorticoid--aldosterone
androgen --DHEA and androstendione

Front 21

What causes receptor down regulation?

Back 21

a chonic exposure to a high level of the hormone leads to a lowered max response --diabeties type 2

Front 22

Where are catecholamines (amine hormones) released from?

Back 22

neurons and adrenal medulla

Front 23

What is the pathway from Tyrosine to E with enzymes

Back 23

Tyrosine (tyrosine hydroxylase) DOPA, DA, NE (PNMT) E

Front 24

What 3 catecholamines are stored in secretory vessicles?

Back 24

DA, NE, E

Front 25

What are secretory vessicles secreted in response to:?

Back 25

Secetogogues that increase intracellular Ca

Front 26

What proteins bind to Thyroid hormones?

Back 26

thyroxine binding globulin and albumin

Front 27

Where is the first step to make steroid hormones from cholesterol?

Back 27

in the mitochondria

Front 28

What are the rate limiting steps in the formation of steroid hormones?

Back 28

1. cholesterol transport to mitochondira
2. activity of P450 - catalyzes conversion of cholesterol to pregnenolone

Front 29

What does enzyme P450 do?

Back 29

converts cholesterol into pregnenolone

Front 30

Where does the rest of the steps of steroid synthesis take place?

Back 30

in the mitochondia or smooth ER

Front 31

cholesterol esterase-

Back 31

what removes the cholesterol from the LDL

Front 32

What is the purpose of the signal peptide?

Back 32

to send the protein to the ER

Front 33

What is steroidogenesis controlled by?

Back 33

trophic hormones that bind G proteins coupled receptors

Front 34

What tissues produces steroids? and what steroids?

Back 34

adrenal cortex -- aldosterone, cortisol, DHEA
gonads-- testosterone and estradiol

Front 35

Glucocorticoids- example and what they do

Back 35

cortisol - increase glucose levels

Front 36

mineralocorticolds

Back 36

Aldosterone -enhance water and NaCl reabsorption

Front 37

What is weaker DHEA or testosterone?

Back 37

DHEA

Front 38

What is the main estrogen?

Back 38

estradiol

Front 39

What is a weak estrogen secreted by placenta?

Back 39

estriol

Front 40

What type of hormones are stored?

Back 40

Peptide and amine -- thyroid and steroid diffuse out of cell after synthesis

Front 41

How does thyroid and steroid mostly circulate in the blood?

Back 41

binded to the plasma binding globulins

Front 42

What is actually measured when measuring hormone concentration?

Back 42

the free H --what is maintained at a set point

Front 43

What serves as a reservior for the steroid and thyroid hormones?

Back 43

H:BG

Front 44

What 2 things must be working to have a hormone response?

Back 44

receptor and hormone

Front 45

Sensitivity of a hormone -defined as

Back 45

[H] that creates the half max response

Front 46

A more sensitive receptor would shift to the ___

Back 46

Left -- less hormone needed to create the same response

Front 47

Which way does receptor down regulaton shift the hormone concentration Hormone effect graph"?

Back 47

decreases the hormone effect -- so shifts it down

Front 48

Receptor sensitivity may change due to __ and shift the graph__ in the case of diametes

Back 48

1. genetics 2. inhibitors 3. activators
shifts graph to the right -requires more hormone for the same response

Front 49

How does receptor down regulation work?

Back 49

The chronic exposure to the target hormone decreases the number of receptors on the cell

Front 50

What type of hormones lead to generation of second messengers like cAMP, cGMP, Ca++, activation of kinases leading to P of proteins?

Back 50

Both peptide and catacholamines

Front 51

What hormones are in blood attached to binding proteins?

Back 51

all steroid, thyroid and GH

Front 52

What 3 major tissues/organs make and store energy?

Back 52

liver, muscle, fat

Front 53

intermediary metabolism-

Back 53

sum of anabolism and catabolism

Front 54

Anabolism -When does anabolism occur?

Back 54

build up of moleculesduring the absorptive phase -- requires energy

Front 55

Catabolism - when?

Back 55

the break down of larger molecules - releases energy --during post absorptive phase or fasting

Front 56

glycogenesis -

Back 56

Glucose to glycogen

Front 57

Where does gluconeogensis happen?

Back 57

liver and sometimes kidney

Front 58

What 3 tissues participate in intermediary metabolism?

Back 58

liver, muscle and fat

Front 59

What does lipolysis start with and then produce?

Back 59

TG --> Glycerol 3P and 2 FA

Front 60

What is ketogensis? where does it happen?

Back 60

FFA to Ketones in liver

Front 61

Where is insulin produced?

Back 61

Beta cells in pancreas

Front 62

What hormone levels increase when fasting?

Back 62

glucagon, epi, GH, and cortisol -- all act to increase blood glucose

Front 63

Fasting causes what in respect to innervation of liver and adipose tissue?

Back 63

Increases the activity of the sympathetic nerves in liver and adipose

Front 64

What is the storage form of fat muscle, and liver tissue?

Back 64

fat- fat
muscle - muscle glycogen
liver- glycogen

Front 65

When is the absorptive phase?

Back 65

Lasts 4 hours after eating

Front 66

What are the insulin opposing hormones? and where are they produced

Back 66

GH (anterior pit), cortisol (adrenal cortex), epi (adrenal medulla), and glucagon (pan - alpha cells)

Front 67

What is the main energy source ffor all cells during absorptive phase?

Back 67

Glucose

Front 68

What dictates the metabolic events during absorptive phase?

Back 68

Insulin

Front 69

What are 3 effects of insulin?

Back 69

1. decreases sympathetic activity
2. increases digestion
3. stimulates anabolic events in liver, muscle, and fat

Front 70

What tissues are insulin dependent?

Back 70

muscle and fat - requires GLUT 4

Front 71

What GLUT does the liver have? How does glucose in liver still depend on insulin?

Back 71

Liver =GLUT2
Insulin still increases the glucose uptake in liver by increasing glucose kinase (glucose --> G6P

Front 72

Why is the increased activity of glucose kinase help to bring more glucose into the cell?

Back 72

Lowers the concentration of glucose so more will flow in

Front 73

What is excess glucose changed into in the liver? - where does it travel and then what is it changed into ?

Back 73

VLDL - exported to the blood and then hydrolyzed into monoglycerides and FFA

Front 74

VLDL is hydrolyzed to what? by what? and where?

Back 74

VLDL changed into FFA and monoglycerides by LPL at the adipocyte capillaries

Front 75

After the formation of FFA where do they go? and form/

Back 75

FFA then enters the adipocyte and combine with glycerol phosphate to form fat

Front 76

When the fat cells uptakes excess glucose what forms?

Back 76

fat --TG

Front 77

What is the final location of absorbed triglycerides in plasma chylomicrons?

Back 77

follow the same path as VLDL and goes to form fat (TG) in adipocytes

Front 78

What is LPL activated by and when?

Back 78

Insulin the absorptive phase (4 hours after eating)

Front 79

What is the path of absorbed amino acids?

Back 79

go to make new protein

stored energy as protein in muscle

Front 80

What does LPL do?

Back 80

strips a TG from the VLDL and then breaks it down into FFA and 2 glycerols

Front 81

What carries the TGs from the liver to the fat cells?

Back 81

VLDL and chylomicrons

Front 82

Post absorptive phase-when? enzymes?

Back 82

Between meals - decreased insulin and increased glucagon, GH, epi, and cortisol

Front 83

How does the body maintain glucose levels?

Back 83

by gluconeogensis and having non CNS cells use FFA and ketones-- glucose sparing

Front 84

What can be used as energy for CNS?

Back 84

ketones and glucose -- FFA can not cross the blood brain barrier

Front 85

What is glucagons main target?

Back 85

the liver

Front 86

How does the 4 insulin antagonist hormones work together?

Back 86

each hormone works on a different pathway

Front 87

Why is cortisol needed?

Back 87

to upregulate uptake of epi

Front 88

FFA are turned into what in the post absorptive phase? where?

Back 88

Ketone bodies in the liver

Front 89

What is the final product of glycogen break down in skeletal? why/

Back 89

lactic acid or pyruvate -- because no G6Pase -- an enzyme in glycolysis

Front 90

TG is broken down in to? by what? where?

Back 90

TG - FFA and glycerol3P Hormone sensitive lipase - in the fat cell

Front 91

What inhibits HSL?

Back 91

insulin

Front 92

What is limited at the start of fasting?

Back 92

protein catabolism -- strategy the body uses to withstand a long fast

Front 93

What is the cause of cushions syndrome?

Back 93

increased cortisol

Front 94

Diabetes Mellitus --

Back 94

a condition which insulin production 1 or function 2 is imparied

Front 95

What is an effect of diabetes?

Back 95

hungry cells because the glucose cant be taken in - so high blood glucose

Front 96

What are some symptoms of diabetes?

Back 96

polyuria, polyphagia, polydepisa, weight loss, blurry vision, numbness,

Front 97

Type 1 diabetes-

Back 97

due to beta cell destruction by auto immune disease - normal or super sensitive insulin function

Front 98

Type 1.5 diabetes-

Back 98

delayed onset of type 1

Front 99

Type 2 diabetes-

Back 99

insulin insensitivity-receptor problem, genetics, obesity, normal or high insulin levels in plasma, leads to beta cell exhaustion

Front 100

Gestational diabetes0

Back 100

pregnant women - like type 2 insulin resistance

Front 101

If you have a GH secreting hormone what effect on blood glucose?

Back 101

increases it

Front 102

Does cushings syndrome cause higher or lower blood glucose?

Back 102

Cushings = cortisol secreting tumor =higher blood glucose

Front 103

What is one mandated activity for diabetes patients? Why?

Back 103

excercise - contraction of skeletal muscle can stimulate translocation of vesicles with GLUT4 to plasma membrane -feeds into the same pathway as insulin

Front 104

What diabetic symptoms could excercise aleaveate?

Back 104

problems due to hyperglycemia

Front 105

What is the pathway that excercise feeds into called?

Back 105

Contraction induced signals

Front 106

How does our body control food intake and weight? where?

Back 106

through central integrating center located in hypothalamus

Front 107

Short term control of weight and food intake includes-

Back 107

ghrelin - from stomach stimulates hunger center in hypothalamus

Front 108

What hormones stimulate the satiety center as short term control?

Back 108

glucose, insulin, and gut hormones

Front 109

How does the body do long term control of body weight and food intake?

Back 109

fat inhibits appetite by secreting leptin

Front 110

What does CRH inhibit? What is CRH?

Back 110

CRH is from the hypothalamus and stimulates the secretion of ACTH- adrenocorticotropic hormone --CRH inhibits the hunger center

Front 111

What nervous system does fasting stimulate? eating

Back 111

Eating- parasympathic - rest and digest
Fasting sympathic

Front 112

Where is the hypothalamus, posterior pituitary, and anterior pituitiary derivered from?

Back 112

hypothalamus - embryonic brain tissue
posterior pituitary-embryonic brain tissue
anterior pituitiary-roof of the mouth

Front 113

What tissue types is the pituritary a hybrid of?

Back 113

endocrine tissue (anterior) and neural (posterior)

Front 114

How does the anterior pituitary receive the releasing hormones from the hypothalamus?

Back 114

through the hypothalamic pituitary portal system --hormones released from hypo and travel to median eminence, travel through capillaries to AP

Front 115

How does the posterior receive blood?

Back 115

directly arterial blood supply

Front 116

At what concentrations are the hypothalamus hormone levels in portal vessel? systemic circulation?

Back 116

portal - pM to nM
systemic - not dectable

Front 117

What is the only pituitary hormone under chronin inhibition? how are others controlled

Back 117

prolactin others by negative feedbakc

Front 118

What increases the size of the target tissue of anterier pituitary hormones?

Back 118

if you increase the AP hormones

Front 119

Sheehan's syndrome --

Back 119

blockage in the hypothalamic portal vessel from mother who just delivered baby -lots of blood loss vessel collapse

Front 120

Why does prolactin only have negative feed back?

Back 120

because DA goes straight to prolactin - no intermediate

Front 121

Sheehans syndrome would do what to the anteteior pituitary levels?

Back 121

decrease all except prolactin

Front 122

Primary disfunction of homeostatic hormonal regulation --

Back 122

happens with the target h

Front 123

Tertiary disfunction?
Secondary/

Back 123

Happens with hypothalamus
2- anterier pituitary

Front 124

What is the posterier pituitary composed of?

Back 124

axons and terminals of neurons that are originiated from the SON and PVN --the cell bodys (somas) are in hypothalamus

Front 125

Where are posterior pituitary hormones released? stored? created?

Back 125

directly into venous circulation -stored in the posterier pit - created in the hypothalamus

Front 126

What are SON and PVN?

Back 126

Dendrites in the hypothalamus responding to stimulus

Front 127

What hormones are made in posterier?

Back 127

ADH and oxytocin

Front 128

What is the infundibulum?

Back 128

Connects the hypothalamus to pituitary. - where the axons to the pp are found

Front 129

What does oxytocin do?

Back 129

stimulats smooth muscle growth and modulates the activity of many neurons - helps facilitate species propagation

Front 130

What does the release of PP hormones require?

Back 130

an Action potential in the hypothalus to get release

Front 131

How many effects can the hypothalamic pituitary axis produce from 1 signal?

Back 131

Same signal can stimulate secretion from both PP and AP through 2 distinctly different pathways ex- oxytocin and prolactin

Front 132

What needs to happen to get milk synthesis and ejection?

Back 132

Anterior P - stops producing DA because its inhibitory so more prolactin is now there -- PP - neurons signal to secrete more oxytocine

Front 133

What type of hormone is somatostain?

Back 133

PEPTIDE

Front 134

What is the only nonpeptide regulatory protein?

Back 134

DA

Front 135

What are the 3 pillars that are involved in balancing physiology? how?

Back 135

1. thyroid- metabolic rate
2. adrenal - restores homeostasis after physiological stress
3. sex - development and maintance

Front 136

Where is thyroid? what is beside it/

Back 136

beside trachea - just below larnx - contains 4 parathyroid glands

Front 137

what does the parathyroid do/

Back 137

secrete PTH- increases plasma Ca and decreases PO4

Front 138

Where is the site of thyroid hormone synthesis?

Back 138

a single layer of follicular cells that surround a pool of colloid --hormones made in the lumen of the follicular cell

Front 139

When the thyroid is hyperactive what happens?

Back 139

the colloid increases and you get a goiter

Front 140

What are the 3 steps in TH synthesis?

Back 140

1. addition of I to tyrosine residues in thyroglobulin in luman
2. coupling to make TH on thyroglobulin
3. cleaving TH from thyroglobulin and send it back to the follicular cell

Front 141

Where is thyroglobulin (TG) made? and then sent to?

Back 141

made in the follicular cell and then sent to the follicular cell lumen wo I can bind to it

Front 142

How does I get into the follicular cell? what type of transporter?

Back 142

I comes from the circulation - and then is symported with Na in a 2ndary active transporter

Front 143

What is a 2ndary active transporter-

Back 143

doesnt directly use ATP - uses the energy from some other process

Front 144

What does the conjugation of I into tyrosine residues of TG produce?

Back 144

MIT - monoiodotyrosine or DIT - diiodontyrosine

Front 145

How does MIT or DIT produce T3 or T4?

Back 145

Either MIT and DIT form T3 or 2 DIT form T4

Front 146

How are T3 and T4 secreted back into the follicular cell?

Back 146

with the TG still attached

Front 147

Which is stronger T3 or T4? What is secreted more? whos half life is longer?

Back 147

T3 - much more potent
T4 is secreted more
T4 lasts longer

Front 148

What converts T4 to T3? where?

Back 148

deiodinase in the liver and target cells

Front 149

Where are Thyroid receptors found?

Back 149

in most cells in the body

Front 150

What does TH do?

Back 150

1. increase BMR main function
2. increase sympathetic responses - beta adrenergic responses - increases epi so increased heart rate

Front 151

What are THs required for?

Back 151

neuron development and function --formation of nerve terminals and synpases
--increases GH secretions
-normal reproduction in adults
--proper nerve/muscle reflexes
--normal recognition

Front 152

Would plasma TSH levels of a subject with inactive thyroid receptors be higher or lower?

Back 152

higher - because your taking away the negative feedback

Front 153

What is the most obvious thing that indicates a thyroid dysfunction?

Back 153

a goiter -but a goiter could be caused by something else too

Front 154

When does a goiter form?

Back 154

When chronically stimulated by TSH/TSH like substances - the thyroid glands (coloid) increases

Front 155

hyperplasia- define - what does it cause

Back 155

increase in the number of cells
causes a goiter

Front 156

What does colliod droplets contain in follicular cell?

Back 156

T3 or T4 with bound TG

Front 157

How does TH increase BMR?

Back 157

by stimulating moblization of energy substrates, O2 consumption, and Na/K ATPase activity

Front 158

What could hyperthyroidism be caused by?

Back 158

A TSH secreting tumor

Front 159

Grave's Disease -

Back 159

presence of immunoglobulins that bind and activate TSH receptors -which leads to high TH and then lower levels of actual TSH but still have goiter b/c of immunoglobins

Front 160

What does a thryrotrope do/

Back 160

produces TSH

Front 161

What is a cause of hypothyroidism?

Back 161

death of thyrotropes -- you cant make TSH so thyroid atrophys without stimulation

Front 162

Does chronic I deficiency result in a goiter?

Back 162

Yes - Low TH removes neg feedback and increases TSH

Front 163

What can thyroiditis cause? lead to?

Back 163

causes slow or rapid inflammation of the thyroid gland -- eventually hypothyridism

Front 164

What is another name for hyperthyroidism?

Back 164

Thyrotoxicosis

Front 165

What are some symptoms of hyperthyroidism?

Back 165

exopthalmos (grave's diease--eyes) fine tremor,tachycardia, weight loss, heat intolenance

Front 166

symptoms of hypothyroidism-

Back 166

cretinism for congenitial deficiency, growth stunt, cold intoleance, bradycardia, weight gain

Front 167

What is the effect of defective TH receptors?

Back 167

cannot activate TH receptors on TSH or TRH - so increase in TH and increase in TSH -- but you would have the symptoms of hypo because TH cant do anything bc of defective receptors

Front 168

What secretes catacholamines? What are they?

Back 168

sympathetic nervous system and adrenal medulla -- epi and nor

Front 169

What does the adrenal cortex secrete? function?

Back 169

cortisol - increase blood glucose, anti inflam, anti immune and anti stress

Front 170

What is the adrenal gland a hybrid of?

Back 170

endocrine cortex and neural medulla

Front 171

Where is the adrenal glands?

Back 171

superior pole of the kidney

Front 172

How is blood supplied to the adrenal glands/

Back 172

1st to the cortex (outside) then medulla

Front 173

What kind of nerves are supplied to the medulla?

Back 173

modified ganglion of the sympathetic nervous system

Front 174

What are the different layers of the adrenal cortex glands and what do they secrete?

Back 174

OUTER
1.Zona glomeralosa- Aldosterone
2.Zona fasciculate - Cortisol and androgens
3. Zona Reticularis - androgens(DHEA) and cortisol
INNER

Front 175

What do all things secreted from cortex have in common?

Back 175

All steroid hormones

Front 176

What does the medulla secrete

Back 176

amine hormones - Epi and Nor the catachoamines

Front 177

What is the rate limiting step of forming Epi/

Back 177

Tyrosine to DOPA by tyrosine hydrolase

Front 178

What happens with DHEA levels with aging?

Back 178

they decrease - some take as antiaging supplement

Front 179

What are adrenal steriods derived from? rate limiting step?

Back 179

cholesterol = conversion of cholesterol to prenenolone by P450 located in inner mit membranne

Front 180

What do both epi and cortisol protect the body from?

Back 180

stress - maintain plasma glu levels

Front 181

What does cortisol do normally? at high levels?

Back 181

maintains glu levels by gluconeogensis and lipolysis
high levels -- stimulates protein breakdown

Front 182

Why give pregnant women who are goin to have a premie a cortisol shot?

Back 182

to stimulate lung maturation---surfactant production

Front 183

What is the active form of cortisone?

Back 183

hydrocortisone

Front 184

When is cortisol levels the highest? how does the pattern change when stressed? a ACTH secreting tumor?

Back 184

when you first wake = stressed =same pattern but highre

ACTH tumor - flat line

Front 185

What are some therapeutic uses of cortisol?

Back 185

1. bee stings
2. arthritis
3. prevent rejection of organ transplant

Front 186

Why would you have hyposection of cortisol?

Back 186

autoimmune destruction of adrenal cortex -- loss of both aldosterone and cortisol

Front 187

Addison's Disease -

Back 187

destruction of adrenal cortex - hypotension, hypoglycemia, fatigue, and weakness

Front 188

What causes impaired cortisol secretion?

Back 188

congenital adrenal hyperplasia -- cant convert cholesterol to cortisol

Front 189

Cushings syndrome caused by? symptoms?

Back 189

caused by - hypersection of cortisol - hypertension, muscle weakness, immunosuppressive,

Front 190

What does high concentrations of cortisol do?

Back 190

stimulates protein degradation and inhibits bone formation and stimulates bone resorption (can lead to osteoprosis

Front 191

What molecules could causes a growth stunt?

Back 191

high glucocorticoids

Front 192

What is congenital adrenal hyperplasia?

Back 192

A definciency in 21 alpha OHase which changes cholesterol to cortisol - so the ACTH increases which increases DHEA

Front 193

What hormones increase during stress?

Back 193

Aldsterone- retain Na
,ADH - retain h20
GH- mobilze stored energy
epi and nor -pain killing
glucagone- increase blood glucose

Front 194

What hormones decrease during stree?

Back 194

insulin and reproductive

Front 195

What are the primary reproductive organs? another name? What happens here?

Back 195

gonads -ovaries and testes - gametogeneisis and steroid hormone production

Front 196

What are accessory reproductive organs?

Back 196

duct systems and related secretory glands - gamete transport or storage -- can be internal or external genetials

Front 197

What are the major steroids from testes and ovaries?

Back 197

testosterone and estradiol

Front 198

What tissues secrete estrogens?

Back 198

ovaries, fat, and placent

Front 199

What tissues secrete testosterone?

Back 199

testes and non gonadal tissue

Front 200

What is more potent that testosterone? the enzyme?

Back 200

DHT formed from testosterone by 5alpha reductase

Front 201

What converts testosterone to estradiol?

Back 201

armatase

Front 202

Name the cell types in meiosis in males in order

Back 202

Spermatogonium, Primary spermatocyte, Secondary spermatocyte, spermatids, sperm

Front 203

How long does it take to make 1 sperm from the begininng?

Back 203

60 days

Front 204

At what cell stage does the sperm become haploid?

Back 204

Spermatid

Front 205

What happens at puberty to signal spermatogenesis?

Back 205

awakening of the hypothalamic axis - anterior pit secretes GH and enlarges testes

Front 206

How many sperm do you get out of spermatogenesis?

Back 206

4

Front 207

What are women born with? at what stage are that arrested? When are they arrested until

Back 207

A fixed number of oocytes arrected at prophase 1 until puberty

Front 208

What is the first phase of spermogenisis?

Back 208

mitosis

Front 209

At birth how many oocytes? puberty?

Back 209

400,000 and continuely die off 200,000

Front 210

What stage is an ovulated egg in?

Back 210

Secondary oocyte arrested at metaphase 2

Front 211

When can nondisjunction happen?

Back 211

during M1 or M2

Front 212

Name the disorder
XO
21 tri
XXY

Back 212

XO - Turners syndrome
21 tri - downs syndrome
XXY - Kleinefelts

Front 213

XO -

Back 213

female but no 2ndary sex characterists and will not go through puberty

Front 214

XXY -

Back 214

Kleinefelts - functioning male but infertile

Front 215

When does sex determination happen/

Back 215

5-10 weeks

Front 216

-Thalidomide-

Back 216

sold to prevent morning sickness-but it produced teratogen a exogenous chemical that can disrupt a growing fetus - no arms

Front 217

Sex differentiation involves -

Back 217

transformation of mullerian ducts (female) or wolffian(male) ducts to either male or female

Front 218

How does males break the female default?

Back 218

by producing SRY gene on the Y chromosome

Front 219

What does SRY od? what is it/

Back 219

formation of testes through the wolffian duct -- its is a transcription factor that breaks M cycle

Front 220

testes secrete-- and they do?

Back 220

testosterone and MIH - together inhibit female and stimulate formation of male

Front 221

What is testosterone to by? and then what does it do?

Back 221

testosterone to DHT by 5alpha reductase -- induces differentiation of urogenital sinus to male

Front 222

What binds to androgen receptors?

Back 222

both T and MIH

Front 223

What is the main hormone that is responsible for forming male external genitalia?

Back 223

DHT

Front 224

What causes the testes to decend?

Back 224

Testosterone

Front 225

What causes androgen insensitivity?

Back 225

defective androgen receptors - neither T or DHT can activate the receptors --still has SRY

Front 226

What will form with androgen insensitivity?

Back 226

the testes b/c you still have SRY and the hormones from testes will be secreted but will have no function

Front 227

What hormones will still have function in androgen insensitivity?

Back 227

MIH - so no internal gental b/c you have MIH which stops female and no DHT or test functioning

Front 228

What inhibits LH?

Back 228

Testosterone