Physio Exam 2 Flashcards

1
Q

Gonadotropin dependent precocious puberty

A

Blame the Anterior Pituitary
Tx: Long acting GnRH Agonist
(causes desensitization)

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2
Q

Gonadotropin independent precocious puberty

A

Blame the gonads

Tx: Remove the tumor on the ovaries/testes

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3
Q

LH and FSH

A

tell the gonads to do their job during puberty

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4
Q

LH and FSH are controlled by

A

Anterior Pituitary

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5
Q

Hypogonadotropic

A

problem is in CNS

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6
Q

Hypergonadotropic

A

problem is with gonads

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7
Q

Kallmans

A

can’t smell
Tx: Estrogen or Testosterone replacement
Later, can start with GnRH to help Ant Pit work again for fertility

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8
Q

Kallmans

A

Kall can’t smell

problem with Ant Pit

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9
Q

Turner syndrome

A
absence of X chromo [XO]
No gonads 
Short stature or delayed/absent puberty
Amenorrhea
LH and FSH really high bc no negative feedback from Estrogen from gonads

Tx: Estrogen supp and then supplemental sex steroids

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10
Q

Turner syndrome

A

will never be fertile

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11
Q

Klinefelters

A

XXY
Failure of normal testicle function (no testosterone release)—> absence of negative feedback to the pituitary
Feminization occurs
Complications: germ cell tumor, breast CA, osteoporosis

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12
Q

Klinefelters

A

Tx: GH first (Testosterone) and then supplemental steroids

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13
Q

Tx for Turner and Klinefelters

A

the same

GH first and then supplemental sex steroids

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14
Q

Acrosome reaction

A

After sperm has passed Zona Radiata, it reaches the Zona Pellucida (gel)

Hydrolytic enzymes are released into Pellucida so that sperm can pass through

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15
Q

Zona Pellucida (gel)

A

has ZP3 protein that Sperm receptors bind to

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16
Q

Sperm (fertilin) binds to

A

Integrin receptor on Ovum

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17
Q

A bunch of sperm help to degrade the Pellucida (gel), BUT once the sperm reaches the cell membrane,

A

only one contributes its genetic material

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18
Q

Zona Reaction

A

Release of granules containing enzymes to degrade the ZP3 protein so that the Pellucida (gel) layer will harden back up!

prevent multiple sperm from getting to the final step

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19
Q

Zona reaction

A

granules degrade ZP3
ALSO,
Final maturation of oocyte- signals for completion of 2nd Meiotic division

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20
Q

After Zona reaction

A

Head of sperm is fully inside of Oocyte

Pronuclei of sperm will eventually fuse with Pronuclei of Oocyte

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21
Q

Binding of Integrin on Ovum to Fertilin on Sperm triggers

A

Zona reaction

harden gel layer back up and complete 2nd meiotic division of ovum

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22
Q

Estrogen during pregnancy

A

requires healthy Placenta AND baby

uses baby Adrenal gland to convert Chol –> DHEA Sulfate –> Estriol

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23
Q

Estrogen during pregnancy functions:

A
Growth of myometrium (muscles for delivery)
Develop ductile system of breasts
Prolactin release
Relax pelvic ligaments
Inhibit lactation
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24
Q

Progesterone during pregnancy

A

Requires only healthy placenta

made from mother cholesterol

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25
Progesterone functions
Makes the uterus a secretory gland Inhibit premature contractions Inhibit premature Lactose (baby milk) synthesis
26
First two trimesters
Progesterone keeps the uterus quiet (aka no contractions)
27
Levels of High Estrogen as women prepare for parturition (birth)
- Gap jx increase uterus - Oxytocin receptors increase - Prostaglandins --> cervical softening
28
Placenta carries
CRH --> Fetal Ant Pit --> ACTH --> Fetal Adrenal Cortex --> Cortisol and DHEA production
29
Cortisol
Fetal lungs --> increase pulmonary surfactant -->
30
DHEA
placenta --> DHEA --> Estrogen
31
CRH
"placental clock"
32
Triggers to premature pregnancy
Bacterial infection Allergic rxn Multiple fetal pregnancies (twins, triplets)
33
Role of Nuclear Factor in uterus
NF-B caused by stretching, increased production of Macrophages as a result of increased Pulm Surfactant NF-B stimulates production of inflammatory cytokines (IL-8) and prostaglandins --> cervical softening PREMATURE DELIVERY
34
Prolactin
enzymes for Milk synthesis
35
Estrogen and Progesterone
helps develop mammary glands but inhibits milk synthesis until baby is born
36
Prolactin
stimulates secretion of milk
37
Oxytocin
milk ejection
38
Removal of steroids at birth
initiate lactation
39
Estrogen and Progesterone
block the action of Prolactin on the breast DURING pregnancy
40
Estrogens
Ductal growth | DUCTS
41
Progesterone Prolactin Hcs
Lobules and Alveoli of breast
42
Prolactin and Hcs
milk enzymes
43
Anterior pituitary
release Prolactin (leading to more milk production)
44
Posterior pituitary
release Oxytocin (leading to contraction and milk "let down")
45
Stress can affect the Post Pit and inhibit
Oxytocin release | inhibiting "let down"
46
Prolactin (milk synthesis) release is regulated by
Dopamine (inhibitory) | Thyrotropin-releasing hormone: TRH (stimulatory)
47
Prolactin
inhibits GnRH thus inhibiting FSH and LH No ovarian cycling!!
48
Irreg menses, very heavy Dark coarse hair on face, upper arm, abdomen Persistent acne Cant get pregnant
High testosterone levels High LH and FSH Ovarian enlargement with too MANY follicles, but none dominant (eventually they turn into cysts) PCOS
49
PCOS
The follicles turn into cysts | Cysts produce many Androgens
50
PCOS
"Stein-Leventhal Synd" Primary product of ovary is Testosterone instead of normal hormones Testosterone interferes with normal female cycle
51
46XX 21 hydroxylase deficiency Virilization
Virilization (masculinization) | Extra levels of Testosterone --> DHT (enlarged clitoris)
52
46XX
Low glucose and Low cortisol | High ACTH and Testosterone
53
46XX | 21 hydroxylase def
Low cortisol d/t lack of 21-hydroxylase cannot be converted into Cortisol, so the precursors instead get made into Testosterone
54
46XX | 21 hydroxylase def
more precursors left over SO Low Cortisol High Testosterone
55
46XX
can be lethal if low levels of Cortisol are not corrected
56
Optimal Spermatogenesis requires both sufficient levels of
Testosterone | FSH
57
Spermatogenesis also requires sufficient
Sertoli cells (which are stimulated by both Testosterone and FSH)
58
Hormone with a pleiotropic effect
meaning several effects
59
Hormone with a trophic effect
meaning regulates: - Hormone secretion by ANOTHER gland - Growth and integrity of that endocrine gland
60
TRH example of hormone with a Trophic effect
tells pit to stimulate TSH, goes into bloodstream, targets thyroid gland, releases thyroid hormone (secretory) and maintains normal growth of thyroid gland
61
Endocrine
dumped into plasma to act distally on receptor cell
62
Paracine effect
hormone regulates processes in NEIGHBORING cells
63
Autocrine effect
hormone "acts back" , leaves cell but comes back to to regulate process WITHIN CELL OF ORIGIN acts on those receptors
64
Intracrine
act on cell of origin but DOESNT EVEN LEAVE CELL at all
65
Neurocine
hormone that is released from neuron, travels down axon carried distally either by blood vessel or synaptic transmission
66
"Classic" endocrine glands
``` Hypoth Pit Pineal Thyroid and Parathyroid Placenta, ovaries, testes Pancreas GI tract Thymus Adrenal cortex and medulla ```
67
"Novel" endocrine glands
Adipose tissue Heart (epicardial fat) Skeletal muscle
68
Chemical structure categories
Peptide (gene is transcribed into mRNA) Amine (tyrosine) Steroid (cholesterol)
69
Peptide (the majority) | water loving
gene mRNA
70
Amine
derived from tyrosine
71
Steroid
derived from cholesterol
72
Majority of hormones are:
Peptide hormones (produced from gene that is transcribed into mRNA)
73
Peptide hormones hydrophillic water loving
gene, mRNA | derived from Amino Acids
74
Tyrosine is in
Adrenal medulla, | used to make Catecholamines
75
Tyrosine is the parent A.A. for
Catecholamines and Thyroid hormones
76
Thyroid hormone is made by
Two tyrosine and Iodine atoms
77
Catecholamines are made by
modifying the side groups of Tyrosine
78
Amines
``` Epi NE Dopamine T4 (Thyroxine) T3 (Triiodothyronine) ```
79
Steroids
``` Aldosterone Cortisol Estradiol Estrogen Testosterone DHEA Vit D ```
80
Majority or hormones are
PEPTIDE | Glycoproteins fall under the peptide family
81
Glycoproteins (type of peptide)
``` FSH TSH LH hCG have a slight modification: CARB moiety critical in secretion and activity of this hormone ```
82
Hydrophillic- water loving- reach target tissue via Cardiovascular system
Peptide hormones and Catecholamines
83
Hydrophobic
Steroid and Thyroid- need carrier protein
84
Hydrophillic
dissolved and transported in bloodstream
85
Concentration of hormone in plasma is determined by:
Production/release of plasma binding proteins Feedback mechanisms Glucuronidation Sulfate conjugation (increases water solubility for excretion) Peripheral conversion Internalization of hormone/receptor in peripheral tissue
86
Group 1 mechanism: Steroid and Thyroid STD goes right through steroid and thyroid
Hydrophobic | Dissolve RIGHT THROUGH membrane and bind to nucleus
87
Group 1 mechanism: Steroid and thyroid
do not have any fancy signal transduction mechanisms bc they can dissolve through and go right to the nucleus
88
Steroid hormone synthesis
Cholesterol --> Cytosol, ER, mitochondria --> immediately dumped into circulation (no storage)
89
Amines
Tyrosine --> Enzymatic in cytosol (catecholamines) and Follicular cell and colloid (for thyroid) --> stored in granules or inside the Follicular cells
90
Follicular cells are found
in the Thyroid gland
91
Peptide hormone synthesis (the big class)
Specific gene that directs mRNA --> Ribosomes, golgi, ER --> stored in granules until needed
92
Synthesis of peptide
Gene for hormone transcribed into mRNA (in nucleus) then leaves Preprohormone --> prohormone (in Endoplasmic Reticulum) Prohormone --> hormone (in Golgi) Hormone is stored in secretory vesicles until it is released
93
Leaving the ER
we have Prohormone
94
Leaving the Golgi
we have normal Hormone
95
ER
preprohormone--> prohormone
96
Peripheral conversion
transfer to something else to increase biological activity
97
Skin: Vitamin D3
hydroxylation on Liver and Kidney--> 1,25 Dihydroxyviamin D3
98
Testes: testosterone
Androgens formed conversiont ot E2 in brain and testes DHT and E2 final products
99
Thyroid: Thyroxine T4
Conversion in most tissues to make T3 (final product) Triiodothyronine
100
T3
active form
101
Humoral release
activated by blood borne substrate
102
Humoral release
the concentration of substrate is above or below "setpoint" | i.e. Ca levels low, trigger PTH release from Parathyroid gland
103
Neural release
``` Psychological stress Emotion Fight or flight Exercise Hypoglycemia Shock Hemorrhage Heart dz CNS is secreting the hormones ```
104
Examples of Humoral release
Calcium and PTH | Glucose and Insulin
105
Neural release
Adrenal gland releases hormones (Epi and NE)
106
Hormonal release
Classic endocrine gland | Network of hormonal connection starting at Hypoth
107
Hormonal release
Hormones regulate the secretion of OTHER hormones
108
Long example of Hormonal release
TRH stimulate pituitary secretion of TSH which stimulates endocrine gland (thyroid) to release thyroid hormone (T3/T4)
109
What types of hormones have to bind to receptor on the cell surface?
Peptides and catecholamines (hydrophobic, cant get through)
110
What types of hormones diffuse through and go straight to nucleus?
Steroid and Thyroid hormones
111
Decrease in max response
Decrease in target cells | Decrease signal transduction mechanisms
112
Decrease in sensitivity (max response can still be reached)
More hormone needed in order to get max response Decrease in affinity Decrease in receptor #
113
Example of decrease in sensitivity
Insulin and obesity
114
Permissiveness
Hormone cannot exert its effect unless it has help from another (needing a bathroom buddy in order to be able to pee)
115
Autologous up/down regulation
hormone regulates its own receptor affinity/number
116
Heterologous up/down regulation
hormone regulates number/affinity of ANOTHER hormone's receptor
117
Anterior pituitary
``` Metabolism Growth Reproduction Lactation Response to stress ```
118
Posterior pituitary
``` Water balance Birth and lactation (lactation is in both) Regulate BP Cardiac fx Diuresis ```
119
Main products of posterior pituitary
Oxytocin | AVP/ADH
120
Main products of Anterior Pituitary
``` ACTH Growth hormone TSH Prolactin FSH ```
121
Post pit
Magnocellular neurons --> downt Infundibular process --> end in Post pit --> hormones into capillary bed
122
Ant Pit
Parvicellular neurons --> median eminence with releasing hormones--> hypothalamo-hypophyseal portal vessels --> Ant Pit --> regulate secretion of Tropic hormones
123
Ant pit
either inhibiting or releasing hormones Vascular link from hypothalamus and Ant PIt
124
Parvicellular | Ant Pit
Secrete hormones that are either inhibitory or stimulatory
125
GHRH
Growth hormone releasing hormone Act on somatotrophs, which release Growth Hormone
126
TRH
stimulating hormone Thyrotropin releasing hormone acts on Thyrotrophs Target thyroid gland T3 and T3 Also maintains growth (trophic effect)
127
Somatostatin
INHIBITORY | causes decrease in GH and TSH
128
TRH
also involved in Prolactin glands- mammary glands- breast development and milk synth
129
GnRH
stimulates production of LH and FSH (in gonads)
130
LH
Synth of Estrogen | Secretion of Testosterone form Leydig cells
131
FSH
Development of follicle | Initiate spermatogenesis
132
CRH
acts on Corticotrophs, makes ACTH which then acts on Adrenal glands Trophic Result: growth of Adrenal gland, synth of Corticosteroids
133
PRF
Prolactin releasing factor mammary glands breast develop and milk synth
134
Dopamine
INHIBITORY | inhibits prolactin release (inhibits milk synth and breast development)
135
Hormones of post pit
ADH and Oxytocin
136
Oxytocin and ADH are made by two types of neurons in the Hypoth
Supraoptic | Paraventricular
137
ADH and Oxytocin
Peptide hormones
138
Oxytocin
binds NP1
139
ADH
binds NPII
140
Central Diabetes Insipidus
absence of NeurophysinII can lead to no ADH being released into blood
141
Neurophysins
keep the hormone in the axon for as long as it needs to be, then allows it to be released
142
messed up Neurophysins or deficiency
leads to low levels of the hormone ADH example Diabetes Insipidus
143
ADH
VERY sensitive to changes in Plasma Osmolarity anything above 280-284
144
Homeostatic adjustments for dehydration Re-establish plasma osmolarity
ADH secretion Water reabsorp Decrease urine output Stimulate thirst
145
ADH is less sensitive to volume depletion
than osmolarity
146
Changes in blood volume (specifically loss here)
Baroreceptors also activates ADH secretion if BP is too low
147
Distention of cervix and Uterine contraction
Stimulates Oxytocin release
148
Oxytocin is also important cardiovascular and cardiometabolic
cardio renal axis | Regulating BP
149
Oxytocin
produced in heart receptors in heart Part of Oxytoxin- natriuretic peptide NO axis
150
OT in heart
stimulates ANP/BNP release from cardiomyocytes and then ANP stimulates release of NO from vascular endothelium Protective
151
Nucleus Tractus Solitarius NTS
is in the Medulla Oblongata
152
What activates the Cardio-Renal axis? baroreceptors?
HTN and | Hypervolemia
153
Oxytocin is cardioprotective because
decreases work of heart by decreasing BOTH Chronotropy and Ionotropy Opening up blood vessels opening up flood gates of Kidney to allow diuresis
154
Local oxytocin system in the heart
OT receptors Locally produced oxytocin Pituitary produced oxytocin Either one causes same effect: NO release Bradycardia Negative ionotropy Increased glucose uptake
155
Oxytocin effect in heart
like insulin!!! but different mechanism. | increased in glucose uptake BY THE HEART!
156
Sertoli cells secrete:
Anti-mullerian hormone Androgen binding protein Inhibin
157
Leydig cells secrete:
Testosterone
158
Where are germ cells and Sertoli cells?
Seminif tubule
159
Where are leydig cells?
connective tissue
160
Two essential products of testes
Sperm | Testosterone
161
Spermiogenesis occurs in the walls of:
Seminif tubules
162
Spermatogonia (diploids) become
Spermatozoa sperm (haploid)
163
After 2 rounds of Mitosis in males
Create 4 diploid spermatocytes Double strand DNA
164
After 2 rounds of MEIOSIS in males
Now have 16 haploid spermatocytes/spermatids Single strand DNA
165
Tight jxb /w Sertoli cells
Blood-testes barrier Prevents immune cells from accessing spermatozoa, REQUIRED for fertility
166
Early sperm cells have more communication with outside world, but once they pass the Blood-Testes barrier,
Now entirely dependent on the Seminiferous Tubules for nutrients an EXLUSIVE area inside the seminif tubules
167
Gap jx
allow for nutrients to be exchanged b/w sertoli cells
168
tight jx
hold young sperm in place together, not ready to be released yet
169
Cytoplasmic bridge
allows genetic info txr from X--> Y
170
What two hormones stimulate Sertoli cells?
Testosterone | FSH
171
From "cell like" Spermatids --> "animal like" Spermatozoa
SpermIOgenesis
172
Spermiation | "Release!"
release sperm from sertoli cells syncytium into the Seminif tubules
173
Spermiation
pass thru Rete testes
174
Where are sperm stored and further matured?
Epididymis "maturation area"
175
SpermATOgenesis
germ cells --> spermatozoa
176
SpermIOgenesis
packaging "cell like" spermatids --> "animal like" spermatozoa
177
SpermIATION
release from Sertoli cells tight jx
178
Kiss1 neuron in ARC nucleus in MALES
always stimulate GnRH
179
Kiss1neuron in ARC nucleus in FEMALES
can be inhibitory or stimulatory
180
FSH
Tells Sertoli cells to secrete Inhibin and Androgen binding protein
181
LH
tells Leydig cells to produce Testosterone
182
Inhibin regulates
FSH
183
Testosterone regulates
LH and FSH by negative feedback
184
What enzyme is vital for any steroid hormone?
Cholesterol desmolase- rate limiting
185
What stimulates Cholesterol desmolase to do its thing?
LH
186
T --> DHT via
5-a-reductase
187
T--> E2 via
Aromatase
188
DHT effects | external
Diff of penis, scrotum, and prostate Hair/baldness Prostate Sebaceous
189
Testosterone effects
Diff of Epididymis, vas deferens, and Seminal vesicles Deep voice Neg fdbk on Ant pit Libido (sex drive)
190
Rate of sperm production is set by
Retinoic acid signaling within the Sertoli cells timing controlled by Vit A
191
When do Sertoli cells cease proliferation?
End of puberty
192
What determines the spermatogenic potential of the testes?
of sertoli cells
193
Average sperm count
20-40 million per ml/ejacu
194
Oligospermia (little)
<15 million
195
Taking too much Testosterone (Aka steroids) messes with sperm production bc
You are causing Testosterone to have a negative feedback on FSH (which would usually tell Sertoli cells to do their thing AKA make sperm)
196
synergistic effect on spermiation? (Release of sperm)
FSH and Testosterone
197
DHEA
An androgen produced from Adrenal glands
198
DHT
Male pattern baldness
199
ppl with deficiency of 5-a-reductase
DONT GO BALD bc they cant convert T--> DHT
200
5-a-reductase activity
leads to baldness
201
Beard growth
DHT and IGF-1
202
Who does NOT go bald?
Androgen-insensitivity Castrated 5-a-reductase deficient
203
DHT and TGF-B1
Lead to thinning of hair!!
204
Propecia (finasteride)
``` block 5-a-reductase Non-competitive blocker (does not let go) blocks T --> DHT Treats: Enlarged prostate Baldness ```
205
Propecia (finasteride)
Baldness | Enlarged prostate
206
Propecia (finasteride)
Erectile dysfx Loss libido Reduced ejaculate
207
Propecia (finasteride) DO NOT GIVE TO PREGNANT WOMEN
dangerous bc blocking DHT in utero can have profound effects on MALE BABY DEVELOPMENT
208
What organ makes up most of the ejaculate? (60%)
Seminal vesicles - Fructose - Prostaglandins - Clotting factors
209
Prostate produces 20% of ejaculate
Secretes | -Alkaline fluid to counteract acidic vagina
210
Bubourethral glands produce 10% of ejaculate
Lubrication
211
Seminal vesicles
Fructose Prostaglandins Clotting factor
212
Prostate
Alkaline fluid (for pH)
213
Bulbourethral glands
Lubrication
214
3 main dz of prostate
1. BPH 2. Prostatitis- infection 3. CA of prostate
215
How many corpus cavernosa do males have?
Two
216
How many corpus spongiosum do males have?
One
217
Integration site in CNS of erectoin
MPOA- medial preoptic area
218
Order of information in erection
Amygdala info --> MPOA integration --> Paraventricular nuclei of hypoth --> grey matter S2-S4
219
Erection achieved by (3 possibilities)
Higher brain activity (thinking) Mechanical stimulation of glans provides sensory fdback to S2-S4 Periodic parasymp impulses from sacral erection generation center
220
NO
activates guanyl cyclase increases cGMP LOWERS ca release vasodilation
221
Increase of flow into cavernosa and prevent blood flow out
Increase BF to cavernosa thanks to cGMP AND contraction of muscles around base of penis to keep blood from getting out
222
Flaccid state
BF into penis is limited d/t contraction of Helicine arteries and Trabecular sm.muscle
223
Erection state
Relaxation of Helicine arteries
224
Compression of what reduces venous outflow during erection?
Subtunical venules
225
Pathway of sperm ejaculation
Vas deferens --> Ampulla --> Urethra
226
Role of the Internal urethral muscle/sphincter
Prevents retrograde sperm ejaculation into the bladder
227
What degrades cGMP?
Phosphodiesterase
228
PDE5
Phosphodiesterase inhibitor can treat Erectile Dysfx
229
PDE5
Viagra/Sildenafil Cialis/Tadalafil Levitra/Vardenafil Maintain high levels of cGMP
230
Vasectomy
ligation of vas deferens accessory gland functions are unnaffected semen (BUT NO SPERM) are still produced T not affected
231
Vasectomy
Sperm can no longer move thru the ejaculatory duct- are degraded by phagocytosis
232
Vasecotomy, what will semen have in it?
everything normal but NO SPERM (sperm was degraded by phagocytes bc it could not get through the ejac duct)
233
LH stimulates Thecal cells to convert Cholesterol ------chol.desmolase----> Androgens
Androgens then diffuse over to Granulose cells where FSH stimulates the conversion of Androgens -------aromatase----->Estradiol
234
FSH
less frequent pulse from GnRH hypoth
235
LH
more frequent pulse from GnRH hypoth
236
As follicular phase proceeds, the levels of Estrogen in amtrum are building up
eventually causes a switch from negative feedback (-) to positive feedback (+) on the anterior pituitar
237
Buildup of Estrogen during follicular phase and switch to positive feedback (+) leads to
More GnRH released --> more FH and LSH released as a result, BUT Inhibin is keeping FSH in check so we just have a LH SURGE
238
Thx to LH surge
``` Primary --> Secondary oocyte Meiosis resumed Enzymes help follicle get thru 2 layers Increase prostaglandins Remainder parts turn into Corpus Luteum ```
239
What restores the normalcy of feedback after LH surge?
Progesterone has a negative feedback on hypoth and pit which suppresses the (+) of Estrogen, SUPPRESSING A 2nd LH SURGE!
240
Suppression of 2nd LH surge
Progesterone
241
If any changes in woman cycle occurs, which stage is it?
First half | Follicular phase which corresponds to Uterine Proliferative phase
242
After day 14
Physiologically, the Luteal and Progestational/Secretory phases are pretty consistent.
243
Rise in Estrogen means
Rise in RECEPTORS for Progesterone. Estrogen does a great job at prepping the body for Progesterone.
244
Progesterone
"hormone of Pregnancy"
245
Progesterone acts on Estrogen primed tissue and
antagonizes Estrogen's effects
246
Prostaglandins are responsible for
Contraction of Uterus during Menses Cramps GI discomfort
247
PMDD
Premenstrual Dysphoric Disorder (bloating, wt gain, breast tend, mood swing, depression, unable to work effectively) 5% of women Meds
248
No TDF
Ovaries develop
249
Testes produce
Testosterone ---> DHT and Wolffian
250
DHT
External male genitalia
251
Wolffian ducts
Male internal reproductive tract
252
Absence of testoterone
female External genitalie
253
Absence of Mull-Inh factor
Female internal reproductive tract
254
What secretes Anti- Mull hormone?
Seroli cells
255
5-a-reductase deficiency
all of a sudden male develops at Puberty male internally all along, but not enough DHT--> testosterone conversion to make Male external until puberty
256
Hormones important for "growth spurt"
IGF-1 and GH
257
Gonadotropin dependent
Meaning depending on the gonadotropins- problem with CNS increased gonadotropins (LH and FSH)
258
Gonadotropin independent
Blame the gonads | Increased gonadal hormones
259
Kallmans
Can't smell CNS problem Hypo Hypo
260
Klinefelter and Turner
Hyper hypo | Blame the gonads
261
Kallman
Can't smell
262
Tx for Kallman
Supp sex steroids (FIRST, this is unique) Estrogen or Progesterone later GnRH
263
Tx for Klinefelter and Turner
GH first, | then Supp sex steroids
264
Once sperm reaches the alkaline pH of the cervix (alkaline thx to Estrogen) it is activated by
Cholesterol withdraw Surface protein redistribution Ca influx (motility)
265
What triggers Acrosomal reaction?
Receptors on the sperm bind to ZP3 protein in the Zona Pellucida
266
Acrosomal rxn
breakage of this cap so that the enzymes can be release and break down the egg wall
267
Acrosomal rxn
an "army" of sperm help break down, but only one gets through to actually fertilize the egg
268
Zona rxn
the re-hardening of zona pellucida, making sure only 1 sperm fertilizes the egg
269
Zona rxn
degrade ZP3 | completion of final maturation of Oocyte!
270
Ovulation
day 14
271
Optimal implanatoin
day 20-24
272
hCG
rescues Corpus luteum and maintains until Placenta takes over
273
In order for the placenta to make Estrogen, requires
BOTH fetus and placenta Needs fetus Adrenal glands (DHEA) and fetal Liver
274
What does the placenta need in order to make Progesterone?
only placenta
275
Fetal Adrenal gland
DHEA | CRH "placental clock"
276
CRH leads to production of
ACTH which tells Adrenal cortex to produce: Cortisol --> pulm surfactant, and DHEA --> Estrogen