Week 3 Flashcards

Question 1

Q

21 year old pre-med student presents to the clinic for intermittent palpitations with associated shortness of breath and a tingling sensation in her hands. She confirms anxiety and has lost 6 lbs unintentionally.

what is going on in this part of her life?
is she burnt out?
what other sxs could you see

Answer

A

high stress=high cortisol level
not yet, but on way
Some people gain or lose weight -> It tends to deposit centrally; Some people tend to feel sick

Question 2

Q

What hormones come out of the cortex?

Answer

A

○ Glucocorticoids (cortisol)
○ Androgens
- Mineralocorticoids (aldosterone)

Question 3

Q

stress response

process called when body is burdened with stress
phases
1st phase
what curve looks like and what it means

Answer

A

General adaptation syndrome
alarm, resistance, exhaustion
alarm: light initiating phase that kind of knocked her off course where you can see the curve go downward just a little
body having the stressful event and it hasn’t kicked in anything from the adrenals yet, so the stress kind of knocked the person down a little bit, and then as the curve starts to go upward, that’s where cortisol is jumping on board as well as the catecholamines coming from the adrenal glands

Question 4

Q

HPA axis

mechanism of ACTH at the adrenal cortex
pathway at the adrenals
one effect of ACTH binding adrenals
how does it result in cortisol
As you increase levels of cortisol, what does that do to your axis?

Answer

A

From the hypothalamus, it releases CRH from the paraventricular nuclei–> CRH binds to corticotropes on the anterior pituitary –> ACTH from POMC is released –> stimulates adrenal cortex to release cortisol

peptide, receptor is on the membrane (G protein coupled receptor) and called MCR2
This is a G alpha-s receptor –> adenyl cyclase –> triggers cAMP –> activation of PKA
ACTH causes the activation of cholesterol-ester-hydrolase which increases cholesterol bioavailability and increases the activity of STAR (transports cholesterol to inner mitochondrial membrane)
These are the rate limiting steps, and eventually you’ll get the production of pregnenolone –> this then allows the production and release of cortisol –> cortisol has its effects on target organs
It inhibits it by binding to the anterior pituitary as well as back on the hypothalamus –> this negatively inhibits that axis –> decreases the amount of CRH released, decreases ACTH released

Question 5

Q

When do cortisol levels increase?

when are they highest
ACTH
why is time important?
what happens if you’re a night worker

Answer

A

They’re highest in the morning and lowest at night
You should normally have cortisol levels early on in the morning, and it will peak around 8am; then as you go on about the day, cortisol levels decrease
ACTH is pulsatile, so you have about 7-15 episodes per day and that’s going to stimulate a cortisol release in about 15 minutes of a surge
If you’re only taking cortisol levels at 2pm, you may not see what’s really going on throughout that axis –> This is why when we look at lab values, we have to look at specific time points
If you slept during the day and worked at night, your circadian rhythm would change – Your cortisol levels would be flipped

Question 6

Q

Why do we want high cortisol in the morning?

- What’s the point of it?

Answer

A

You want cortisol to be released in the morning to wake up and increase energy, but fasting is also going on during this time so you want cortisol to be released so that you can increase glucose levels in blood to be able to use it as energy
The point is to increase blood glucose in the body so that you have it energy

Question 7

Q

How is cortisol transported in the blood?

why is it important?
when can it bind?

Answer

A

It’s transported with a binding globulin
Cortisol has a short half-life, so it wants to bind to a protein so that it can help extend its half-life when it’s not being used
Cortisol is active and can bind to its receptor when it’s not bound, so any cortisol that’s bound cannot bind to its receptor –> keeps its bioavailability a lot longer so that it’s not degraded since it’s not being used up

Question 8

Q

Cellular mechanism of cortisol at its target organ

where does it bind
effect on water balance
other factors that help kidney

Answer

A

Cortisol will be bound to its binding globulin –> when it gets close to the cell then it releases its binding globulin –> cortisol crosses into the membrane –> cortisol binds to its intracellular receptor –> causes heat shock proteins to be released –> receptor dimerizes –> crosses into the nucleus –> binds to its response element –> undergoes transcription and translation –> production of proteins and whatever is needed for that response at those particular cells of the target organ
can bind to its receptor on cells but can also bind to mineralocorticoid receptors found in the collecting ducts of the kidney
It would throw water balance off by causing more reabsorption of sodium
cortisol being bound to a globulin protein helps to allow mineralocorticoid activity to overcome the cortisol activity (aldosterone is going to win out in the kidney), and the other part is that aldosterone dissociates a lot slower than cortisol from its receptor

Question 9

Q

How do you create cortisone from cortisol?

what is cortisone
importance of this form

Answer

A

11 beta hydroxy-steroid-dehydrogenase type II converts cortisol to cortisone
inactive form of cortisol
In the kidney, there’s high levels of 11 beta hydroxy-steroid- dehydrogenase type II, so when cortisol gets to that area, it’s converted into cortisone and then it can’t bind to the receptor and affect kidney

Question 10

Q

What does 11 beta hydroxy-steroid-dehydrogenase type I do?

Answer

A

converts from cortisone to cortisol

Question 11

Q

What are the early physiological effects of cortisol? At these target organs what is cortisol doing?

At the liver
Skeletal muscle
Adipose tissue
Pancreas
Bone
Skin
Reproductive tract
Immune response
CV
Adrenal medulla and sympathetics

Answer

A

Increased gluconeogenesis & glycogenolysis
Increases in proteolysis & glycogenolysis; cortisol can affect GLUT4 upregulation so you get a decrease glucose uptake and decrease in protein synthesis
Increase lipolysis & release of FFA and glycerol
Increase in glucagon, decrease in insulin
Decreased bone formation, Increased bone resorption, Decrease in osteoblast
Inhibit fibroblast activation and proliferation and decrease collagen formation
Decrease function
Decreases
Increase adrenergic receptors (Alpha 1 receptors, beta receptors in the heart) –> will increase CO and peripheral vascular resistance
Increase catecholamines

Question 12

Q

What are stress hormones?

- importance of multiple

Answer

A

cortisol, catecholamines, epi, and glucagon, GH

- you have to think about all the other hormones that are being upregulated

Question 13

Q

Exercise

what kind of response
what hormones
glucose use -> how?

Answer

A

stress response
Dealing w/ cortisol, epi, glucagon, and exercise
The combo of glucagon, epi, GH, cortisol will allow for glucose to be uptaken and utilized where it need to be
upregulation of GLUT4 in the exercising muscles due to increased AMP kinase to allow for utilization of the glucose

Question 14

Q

Relaxation techniques

autogenic training
centering prayer
clinical hypnosis
exercise
guided imagery
meditation
music therapy
progressive muscle relaxation
tai chi
therapeutic breathing
yoga
point of this technique

Answer

A

decreased sympathetic tone by visualizing bodily sensations
contemplative/mindful prayer using mantra
individualized suggestions paired with guided visualizations
coordination of physical activity with breathing
visualizations to cultivate relaxing thoughts ad emotions
active practice developing “let-it-be” mindset
uses sounds and harmonies to induce relaxation
contraction and relaxation of one muscle group at a time
slow, intentional movements coordinated with breathing
abdominal breathing, RR <6/min
coordination of physical postures with breathing
these techniques were trying to get out of that default mode network of thinking to a higher level of brain wave activity (alpha wave on ECG), which is a more meditative thought pattern

Question 15

Q

Late effects of chronically elevated cortisol?

liver
Fat
blood glucose
bones
skin
flushed face
decreased reproductive function
immune system
CV effects

Answer

A

Increase glycogen synthesis; Proteolysis - breakdown of muscle which can lead to thin extremities, weakness
Bc of increases in insulin you are no longer breaking down the fat.. You are storing the fat centrally -> central obesity;
still upregulated, but we are also increasing insulin so now in combination with the obesity we can get insulin resistance
When you have long term bone resorption –> bone density decreased –> could have osteoporosis
With chronic cortisol skin becomes very thin, and you’ve lost matrix –> capillary support goes away –> the capillaries can bust which leads to the bruising and striae can occur
Flushed face - aka plethora related to the alterations in collagen
Decrease in GnRH –> decrease in FSH/LH and eventually estrogen and that can cause infertility, decreased libido
At risk for recurrent infections
Increasing peripheral vascular resistance systemically for a longer period of time –> can now present w/ HTN

Question 16

Q

what is considered chronic cortisol elevation

- is there a transition period?

Answer

A

At least a few weeks (could be a few months or a few years) to really see many of the end effects manifesting themselves
yes, but prob don’t know when that happens or the length of the period.

Question 17

Q

What the diff etiologies of hypercortisolism?

ACTH dependent
ACTH independent

Answer

A

Can either be from a secondary condition (pituitary adenoma), Or can be ectopic (not from the axis at all) such as carcinoma in the lung that is over producing ACTH
Not dependent upon ACTH, Primary condition prob at the adrenal gland itself, Or could be through exogenous source, Such as glucocorticoids

Question 18

Q

How to determine etiology of patients underlying endocrine disorder

based off
why?
what should you see?
why that drug?
what does it mean with no response?
what does it mean with no response to low dose but having a response with high dose
what is CRH stimulation used for?

Answer

A

dexamethasone test
is an exogenous form of cortisol
Should go under neg feedback to decrease ACTH and then decrease amount of cortisol being released
Crosses the blood brain barrier, so we can see it make its way to hypothalamus
that the cortisol is ectopic
it means that the cells secreting ACTH are not as responsive as normal
confirms that axis works

Question 19

Q

Dx for labs that show

no response to low dose dexamethasone, a response to high dose dexamethasone, and increase in ACTH and cortisol with CRH stimulation
what kind of problem is this?

Answer

A

ACTH dependent pituitary adenoma

- secondary

Question 20

Q

Pit adenoma

kinds
tx

Answer

A

micro and macro; majority are micro, macro are usually non-functional and present because of mass effect
cut it out

Question 21

Q

Difference between cushing syndrome and dx

Answer

A

syndrome: anything that causes sxs from excess gluco-corticoids
dx: pituitary adenoma

Question 22

Q

ACTH dependent etiologies

Answer

A

pituitary adenoma

- ectopic ACTH

Question 23

Q

ACTH independent etiologies

Answer

A

adrenal adenoma, carcinoma

- iatrogenic

Question 24

Q

Treatment for iatrogenic etiology

- type to give

Answer

A

taper dose of steroid until you get to physiologic level for that person
hydrocortisone

Question 25

Q

Types of steroids

long term
short term
cross blood brain barrier

Answer

A

hydrocortisone
prednisone
dexamethasone

Question 26

Q

Pt with dysuria, and dipsticknotable for infection. This is second UTI in few months. Patient has weight gain.

what is causing UTI (direct)
indirect cause of UTI

Answer

A

increased cortisol is causing immune repression–leaves patient prone to infection
increased cortisol -> increase glucosuria -> make patient more susceptible to UTI

Question 27

Q

Resistance phase of general stress adaptation

caused by
how do we help?

Answer

A

higher amount of stress for longer amount of time

- needs something to tone down

Question 28

Q

Adaptogens for adrenal resistance

Ashwaganda
Siberian Ginseng
Vit B complex
Vit C

Answer

A

pre-eminent adaptogen, take daily basis, helpful with thyroid
initially studied for physical stamina for russian olympians but helpful with mental stamina too
Co factor for neuro transmission and helps reduce cortisol; use P5P for sleep, titrate until patient starts having dreams again
Vitamin C: co factor for metabolism of neurotransmitters -> adrenals need most vit C

Question 29

Q

33 yr old female with fatigue, unintentional weight loss, nausea, diffuse arthralgias, light headedness, and problems with memory, depression, and decreased libido. PE shows decreased BP and tanned skin.

importance of tanned skin
dx
etiology
other name

Answer

A

high ACTH levels–POMC is precursor for ACTH and stimulates melanocytes –> so elevated POMC= increase in ACTH and increase in stimulation for melanocytes
addisons dx
adrenal cortex destruction and in developed countries it is usually autoimmune
Adrenal insufficiency

Question 30

Q

What is the Cosyntropin test

function
what is it
expected results with normal
what happens if nothing is seen

Answer

A

trying to stimulate adrenals
it is sythetic ACTH
If the adrenal gland was responsive you would get increase of cholesterol and STAR and then increase cortisol production
problem is at the level of the adrenal gland (primary)

Question 31

Q

oligospermia

Answer

A

Oligo=few

- low sperm count

Question 32

Q

GnRH

where is it produced?
size
process
timing
signaling
binds to?
what inhibits its release
what stimulates its release
What determines whether a GnRH analogue stimulates or suppresses gonadotropins?

Answer

A

arcuate nuclei
decapeptide- 8 AA
gene product is a prepro GnRH, then gets ride of signal peptide and some of the peptides like GAP (GnRH Associated Peptide) present in it. Gets rid of that in the ER to produce the final decapeptide GnRH
pulsatile; Longer pulses of GnRH favor FSH production, and shorter pulses of GnRH favor LH production
gonadotrophs; GalphaQ
Beta endorphins, IL-1, prolactin hormone, GABA and dopamine
Leptin, norepinephrine, neuropeptide
Administration strategy: Pulsatile/intermittent dosing—stimulates GnRH release; continuous would suppress GnRH

Question 33

Q

LH and FSH

produced by?
are both produced from one cell or 1 from different cell?
kind of protein
longer half life?
when are they produced?
target organs in male and receptor type?
end product
inhibition
activation

Answer

A

gonadotrophs
Some can produce one or the other, and some can do both
glycoproteins
FSH
pulsatile; Longer pulses of GnRH favor FSH production, and shorter pulses of GnRH favor LH production
LH In male: acts on Leydig cells; FSH in male: acts on Sertoli cells; G alpha s
production of testosterone
inhibin B inhibits FSH -> produced by sertoli cells
activin from the sertoli cels

Question 34

Q

testosterone

end products?
Site of synthesis
stimulation for synthesis
1st pathway of conversion
2nd pathway of conversion

Answer

A

estradiol and DHEA
Testes; specifically the Leydig cells -> in the interstitial spaces around the blood vessels between the seminiferous tubules
LH (GalphaS)–> CREB initiates transcription of StAR and CYP11A1 –> converts cholesterol to pregnenolone
by cleaving the sidechain and converts C27 to a C21
Delta 5: 17-alpha-hydroxylase converts pregnenolone to17-alpha hydroxypregnenolone ->
17,20-Lyase converts to dehydroepiandrosterone (DHEA) -> DHEA can also be converted to androstenedione via 3beta HSD or 17-betaOH steroid dehydrogenase converts DHEA to androstenediol which then uses 3 beta HSD converts androstenediol to testosterone
-Delta 4: Conversion of pregnenolone to progesterone through 3 beta hydroxysteroid dehydrogenase–> Progesterone will go down to make testosterone

Question 35

Q

Difference between strucutal forms of GnRH, FSH/LH, and testosterone

Answer

A

○ GnRH is a peptide
○ LH and FSH are glycoproteins
○ Testosterone is a steroid

Question 36

Q

Leptin and male reproductive system

- action

Answer

A

activates GnRH

Question 37

Q

What does too much estradiol do in men?

Answer

A

gynecomastia

Question 38

Q

Sertoli cells

function
end result
other production

Answer

A

Mature the sperm- both meiosis I & II are gonna be ongoing through Sertoli cells as the provde nutrition for the spermocytes and phagocytose the remnant bodies of the sperm
spermatazoa by helping spermatid shed excess cytoplasm so it can be slim and trim

Question 39

Q

Androgen binding protein

Answer

A

binds to testosterone and helps to maintain active levels l of testosterone in seminiferous tubule which is very essential to maintain spermatogenesis.

Question 40

Q

How does testosterone effect sperm count?

Answer

A

low testosterone-> less active testosterone in seminiferous tubules-> low spermatogenesis-> oligospermia
Mullerian inhibitory substance and transferrin (plasma unbinding protein that caries iron in it) required in seminal fluid.

Question 41

Q

blood-testes barrier

function
importance
Who maintains the blood testes barrier?

Answer

A

acts as barrier between blood and testes; protect testes from substances and inhibits some hormones from acting on the testes and has immune protection as well.
protects luminal compartment of your seminiferous tubules from exposure to blood borne toxins, chemicals or even immune cells. The lumen of the seminiferous tubules has all your advanced sperm cells like spermatids and spermatazoa.
If immune cells were able to come directly into luminal compartment, it would lead to anti-sperm antibodies which would then eat up the sperms. This could be another cause for infertility.
Sertoli cells via tight junctions between them. They control entry of various components from the blood, which is close to the basement membrane, on the basal compartment of the seminiferous tubules into the luminal compartment.

Question 42

Q

DHT

stands for?
how is it made?
receptor it binds to?
function

Answer

A

dihydrotestosterone
converted in peripheral target cells by 5- alpha reductase.
Intracellular (not plasma bound) Androgen receptors
cytoplasmic receptors are in inactive form, they have DNA binding domain and ligand binding domain and are bound to heat shock protein which keep them in inactive form. As soon as ligand binds it-> heat shock proteins let go-> receptor activated-> travels into nucleus-> dimerizes-> DNA binding motive becomes active-> binds to androgen response elements to target gene-> helps in transcription of target gene.

Question 43

Q

Meds to use when you need decrease of testosterone

Answer

A

Finasteride is a 5-alpha reductase inhibitor so it stops the conversion of testosterone-> DHT bc DHT is more active form of testosterone that binds androgen receptors.
Flutamide- competitively inhibits androgen receptor itself-> prevents transcription effects of testosterone

Question 44

Q

physiologic functions of testosterone

Answer

A

• Axillary hair growth
• facial hair
• development of secondary sex organs- growth of penis &amp; seminal vesicles
• deepening of voice
• Spermatogenesis
• Libido
- increased muscle mass, etc.

Question 45

Q

actions of DHT?

Answer

A

Embryotic development of prostate
Testis descension
Pubic/axillary hair development
Activity of sebaceous glands
Male pattern balding

Question 46

Q

Main action of testes vs DHT

Answer

A

s internal male genital tract differentiation is major function of testosterone. Whereas external genitalia and prostatic growth is mainly because of DHT.

Question 47

Q

Spermatogenesis

steps
controlled by?
what do you see?
depends on?

Answer

A

Mitosis of spermatogonia -> primary spermatocyte -> meiotic division forming secondary spermatocyte- > 2nd meiotic division forming spermatid -> spermatazoa
FSH and testosterone -> increase spermatogonia proligeration and increase sertoli androgen binding protein
At any given time, all steps of spermatogenesis can be identified in the testis.
FSH acting at Sertoli cells and Intratesticular testosterone level has to be relatively high

Question 48

Q

Relate the key event in spermiogenesis to functional importance of sperm function

nuclear chromatin condensation
acrosome development
repositioning of spermatids; development and growth of flagellum
formation of mito sheath around flagellum

Answer

A

haploid chromatin carriers either X or Y chromosome
Acrosome contains enzymes needed for mucus penetration and fertilization
microtubular structure provides motility, allowing sperm movement through genital tract
provides energy for flagellar movement

Question 49

Q

Normal Semen parameters for fertility in adults

Answer

A

Needs to be in alkaline environment in order to be functional
Normal volume- 20mL
Sperm count- 40 million per ejaculate–> 20 million/mL

Question 50

Q

Basis for male conctraception

Answer

A

Progestin inhibits FSH and LH below the levels that are required for spermatogenesis

Question 51

Q

What are some pharmaceuticals that are used to increase spermatogenesis?

Answer

A

○ Pulsatile GnRH analogs like leuprolide
○ Estrogen receptor antagonists that inhibit gonadotropin release
○ FSH
HCG (human chorionic gonadotropin) has been shown to increase spermatogenesis

Question 52

Q

SHBG

stands for
function
synthesis
effect on testosterone
effect on time
same thing as ABP?

Answer

A

transports all sex hormones in the blood to their target cell
sex/steroid hormone binding globulin
in the liver
Bound form of testosterone is non-functional (inactive) because it has to transport through the plasma membrane to get thru the cell, and when bound, it can’t b/c of the protein
creates a buffer so that testosterone stays longer in circulation and it protects it from degradation (increases half-life of hormone)
no

Question 53

Q

ABP

function
importance

Answer

A

made by Sertoli cells and binds testosterone and keeps it active in seminiferous tubule and seminal fluid, while SHBG is binding protein in the blood
In the seminiferous tubule, testosterone does not have any specific receptors but there needs to be an active concentration of it there for the process to occur. So the role of testosterone is obligatory, but indirect in regards to spermatogenesis.

Question 54

Q

Metabolization of testosterone

Answer

A

When testosterone gets metabolized, it will be converted to ketosteroids which can be added to glucuronic acid which will make it more water soluble, or it can be added to sulfate and then eliminated via the urine

Question 55

Q

Free testosterone

what does that mean?
how much?
what keeps it from being free?

Answer

A

testosterone that is not bound to anything else and is active in the blood
2%
will bind both albumin and SHBG

Question 56

Q

Testosterone replacement

why not oral?
how to make it last? importance?
transdermal/topical gel

Answer

A

do not do well with first pass metabolism
add esters to prolong the effects of testosterone -> have to be hydrolyzed into their active form
bypasses the first metabolism so goes right into systemic circulation

Question 57

Q

Kallmann syndrome

classification
what is the problem?
common sxs? why?

Answer

A

Hypogonadotropic hypogonadism
GnRH neurons embryologically start in olfactory nerve in the cribriform plate, and if there’s some type of underdevelopment, they don’t descend properly, and you don’t get primary menarche
decreased smell, usually GnRH secreting neurons migrate from primordial, olfactory tissue to their correct location in the hypothalamus.

Question 58

Q

Parts of male reproductive tract in sequence through which sperm passes through? and role if any

Answer

A

Seminiferous tubules: location of sertol and leyding cells
Epididymis: H+ secretion which decreases luminal pH
Vas Deferens
Ejaculatory Duct
Urethra
Penis

Question 59

Q

Role of

-

Answer

A

Seminal vesicles: Secretion and storage of fructose-rich product, prostaglandins, ascorbic acid, fibrinogen, and thrombin-like proteins
Prostate: Secretion and storage of fluid rich in acid phosphatase and protease (prostate specific antigen=PSA)
Cowper glands: Secrete mucus upon arousal

Question 60

Q

Steps for Erection

results from?
innervation?
end result?

Answer

A

corporeal smooth muscle relaxation mediated by a spinal reflex involving central nervous processing allowing for increased blood flow into the corpus cavernosum
Corporeal vasodilatation is mediated by the parasympathetic nervous system. Parasympathetic fibers directly innervating the corporeal smooth muscle and sinusoidal endothelial cells releaseacetylcholine, stimulating the production of constitutive endothelialnitric oxide which then act on smooth muscle and induce relaxation through activation of guanylate cyclase and increased production of cyclic guanosine monophosphate (cGMP) by cGMP-dependent protein kinase (PKG) activation culminating in a reduction in intracellular Ca2+concentration and a decrease in the sensitivity of the contractile system to Ca2+.
Smooth muscle relaxation leads to corporeal vasodilation which increases blood flow into the penis which causes erection to occur

Question 61

Q

Steps for Ejaculation

2 sequential processes and what are they?
how do they happen?
innervation

Answer

A

emission and ejaculation
Emission: the deposition of seminal fluid into the posterior urethra and is mediated by simultaneous contractions of the ampulla of the vas deferens, the seminal vesicles, and the smooth muscles of the prostate
Ejaculation: results in expulsion of the seminal fluid from the posterior urethra through the penile meatus.
controlled by sympathetic innervation of the genital organs and occurs as a result of a spinal cord reflex arc

Question 62

Q

Steps for Detumescence

innervation
how?
definition

Answer

A

produced by sympathetic corporeal in the absence of sexual arousal.
Produced by sympathetic corporeal vasoconstriction and corporeal smooth muscle contraction by noradrenergic, neuropeptide Y, and endothelin-1 fibers.
Detumescence definition: the process of subsiding from a state of tension, swelling, or (especially) sexual arousal.

Question 63

Q

ED treatment

usual one, durg class, and MOA
other type? MOA
last type?

Answer

A

Viagra/sildenafil: PDE5 inhibitor; inhibits the degradation of cAMP by PDE5 –> increase in cGMP which causes dephosphorylation of MLC which leads to relaxation in the corpora cavernosa to increase BF
PGE (prostaglandin) analogs: Act via GalphaS and can cause increased vasodilation to smooth muscle
Alpha-adrenergic receptor antagonists: inhibit sympathetic outflow that causes vasoconstriction, so it induces vasodilation

Question 64

Q

Hypo gonadism

causes
clinical presentation childhood
clinical presentation adults

Answer

A

Kallmann syndrome, Adrenal hypoplasia, Pituitary tumors (including prolactinoma), Mutations in GnRH receptors, FSH or LH Beta-subunits, trauma/surgery
Early childhood onset: short stature, lack of deepening voice, female distribution of secondary hair, anemia, underdeveloped muscles, genitalia with delayed or absent onset of spermatogenesis and sexual function
○ Adults (after normal virilization has occurred): decreased bone density, decreased bone marrow activity –> anemia, alterations in body composition associated with muscle weakness and atrophy, changes in mood and cognitive function, regression of sexual function and spermatogenesis, loss of libido, ED

Answer 65

A

○ Hypothalamic tumors
○ Activating mutations of the LH receptors
○ Congenital adrenal hyperplasia (CAH)
Androgen-producing tumors

Answer 66

A

when a specific hormone at the end of an axis travels to the origins in the axis to downregulate production of those hormones

Answer 67

A

when a specific hormone at the end of an axis travels to the origins in the axis to upregulate production of those hormones

Answer 68

A

get positive feedback, the increased levels of estradiol that are being produced causes increased levels of FSH and LH to help development
estradiol levels start to have a negative feedback on the axis and so now you start to get decreases in FSH and LH
lose that negative feedback and get surge of LH again

Answer 69

A

oogenesis
germ cells (oogonium) undergo rapid mitosis to increase their number
immature follicles
Meiosis I is reduction division-your homologous chromosomes separate out
Meiosis II is similar to mitosis-it is separation of chromatids
prophase of meiosis I; primary oocyte; primary follicle
maernal LH and FSH

Answer 70

A

Negative feedback –> suppresses the axis
Axis is starting to be activated again, you start to get positive feedback
Estradiol starts to increase, which increases FSH and LH levels which leads to increase in prepubertal and pubertal change

Answer 71

A

Variable-on average around age 8 or 9
race and genetics
thelarche (breast budding)-can be unilateral and this is common for about up to 6 months from starting puberty
adrenarche:Maturation of adrenal system in relation to androgens -> You get body odor, axillary hair growth, acne, pubarche (pubic hair)
Peak height velocity (growth spurt), followed by menarche, followed by maturation of all the secondary sex characteristics
This process occurs over 4.5 years
Period usually starts about 2 to 3 years after thelarche (breast budding)
Tanner stages
The breast development and pubic hair Tanner stages aren’t always at the same stage

Answer 72

A

0-what all children under the age of 7 look like
5-adult distribution of everything
2-breast budding (you see breast nodule right below areola)
4-Mound on mound (areola sticks out a little more than breast, but breast is also slightly enlarged)
3 is gonna be in the middle

Answer 73

A

0-no pubic hair
2-sparse, thin, light colored pubic hair coming in
3-switches to coarser darker hair
4-adult type hair
5-adult hair spreads to medial thighs

Answer 74

A

estradiol
Follicular: Starts at day 1 of menses; estradiol levels are low and there’s also negative feedback on HPG axis so there’s low levels of FSH ad LH
Ovulatory: Starts about day 13 to 14 -> Ovulation occurs; dominant follicle starts to produce more estrogen, estradiol levels increase, and there’s now increased responsiveness of ant pit to GnRH so there’s positive feedback -> increase LH and FSH -> lead to ovulation
Luteal: At day 14 to day 28 -> now even though estrogen and estradiol levels are now elevated, the axis becomes negative inhibition and FSH and LH levels start to decrease

Answer 75

A

proliferative phase (which menses is a part of)

- Secretory phase

Answer 76

A

primordial follicle: oocyte and 1 layers of granulosa cells
primary follicle: fully grown oocyte, zona pellucida, and granulosa cells
secondary follicle: fully grown oocyte, zona pellucida, granulosa cells and theca cells –> after puberty in the ovaries during menstural cycle; high FSH which bind to granulosa to slowly start increasing the estradiol
early tertiary follicle: fully grown oocyte, zona pellucida, granulosa cells w/ antrum, theca interna and exerna -> thecal cells are responding to LH; granulosa and thecal cells work together to produce estradiol; FSH is low because of inhibin
graafian follicle: fully grown oocyte, zona pellucida, corona radiata, cumulus oophorus, granulosa cells w/ antrum, theca interna and exerna

Answer 77

A

concentrates a lot of FSH, estradiol, growth factor, and plasminogen activating factor.
prevents follicular atresia -> so, the follicle that is selected to grow all the way into the graafian follicle will have a very well developed antrum with trapped gonadotropins and growth factors inside

Answer 78

A

LH surge
grafian folllicle
selected follicles will have primary oocytes finish meosis I -> reduction division (diploid to haploid)
meosis II begins with secondary oocyte but stops at metaphase
upon fertilization/ penetration of sperm
forms corpus luteum

Answer 79

A

FSH–> Gαs–> cAMP–> PKA–> P450 aromatase–> androstenedione and/or testosterone has to come over to the granulosa cells to undergo aromatization–> converted to estradiol
very slow increase in estradiol -> positive feedback on FSH until a certain point then it goes to negative feedback
LH receptors–> LH binds–> Gαs–> cAMP–> PKA–> CYP11A1 activated–> Cholesterol converted to Pregnenolone–> 17 α hydroxylase converts pregnenolone to 17OH pregnenolone–> 17, 20 lyase converts 17OH pregnenolone to dehydroepiandrosterone–> continues to androstenedione and testosterone which diffuses to the granulosa cells to be turned into estradiol
granulosa cells do not have 17α-hydroxylase so cant convert pregnenolone into 17-hydroxypregnenolone so will not make androstenidione -> has to get it from theca cells
made by granulosa cells in response to LH

Answer 80

A

Day 9
Negative feedback–> increased levels of estradiol as well as inhibin so FSH is starting to go down… but as the estradiol levels start to increase through the rest of the follicular phase, it’s now positive feedback on LH and the surge can occur
non-dominant follicles undergo atresia and the dominant follicle can survive -> so ovary is in follicular phase with increased capillary density to increase cholesterol delivery
Endometrium is in the proliferative phase, and in response to estradiol it is undergoing hyperplasia and hypertrophy of the stromal and epithelial cells causing a thickening of the endometrium -> causing elongation of endometrial glands and increase vascularization of the uterus
none

Answer 81

A

Day 14
LH surge due to estradiol positive feedback -> Increased responsiveness of the anterior pituitary to GnRH
by the Increased number of GnRH receptors and increased pulsitivity–> LH and FSH are increasing–> effect on ovary
This surge is important because we’re trying to cause rupture of the follicle in the ovaries -> Ovarian capillary density is increased and LH causes an increase in vasodilators (bradykinin and histamine) which increases blood flow and primary follicle is becoming edematous and hyperemic. FSH is also increasing proteolytic enzymes which causes disaggregation of granulosa cells and the basement membrane between theca and granulosa cells start to fall apart and granulosa cells luteinize. Oocyte starts to detach. Thinning of follicular walls.–> all leads up to rupture of the follicle.
Highly vascularized, Glands becoming coiled, Storing glycogen, Release carbohydrate-rich mucus Thickening up and prepping for implantation in the instance that fertilization were t, o occur
Cramping on one side, Increase cervicle mucus, Increase body temperature, Increased libido, Breast tenderness

Answer 82

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Day 26
LH and FSH are low (negative feedback) -> Decreased pulsitivity of GnRH
Since she is not pregnant… regression of the corpus luteum occurs; Ovary in luteal phase
Menstruation, Shedding of endometrial lining due to low progesterone; Cut off blood supply/ischemia–> tissue necrosis–> shedding endometrial tissue
Mild-severe cramping, Moody, Food cravings, Muscle aches, joint aches, Fatigue, Migraines, Diarrhea/constipation (ovaries and uterus are releasing prostaglandins which can act on the intestinal tract which are anatomically in close proximity–> IBS symptoms

Answer 83

A

changing pulse frequency by giving the patient an elevated dose of either estrogen and progesterone or progesterone by itself. This means that now you would not see the ovary and endometrium changes that happened before. You may not get follicular development, no ovulation, and less bleeding. Cervical mucus can also change, making it hard for sperm to survive.
Ovaries= suppressing ovulation, depressing ovarian function, minimizing follicular development
Uterus= thicker, less copious cervical fluid. Stimulating proliferation of the endometrium.
Breast= breast enlargement due to estrogen
Overall endocrine function= inhibiting the HPG axis. Also, RAAs is also increased, cortisol binding globulin is increased, thyroxine binding globulin is increased
Clotting, stroke, nausea, breast tenderness, headaches (from estrogen), weight gain (from progesterone), acne (estrogen can help acne while certain progesterones are more androgenic and tend to be worse for acne), gallbladder, depression, break-through bleeding (more common in progestin-only OCPs)
History of thrombotic disease, Smokers, especially smokers over the age of 35, Breast cancer or tumor that is responsive to estrogen, Migraine with aura, Hepatic adenomas

Answer 84

A

Increased quantity and capacity of the cervical mucus as well as favorable electrolytes made it ideal for fertilization, Prostaglandins in the seminal fluid help induce uterine contractions to help propel the sperm closer to the egg, Acrosomal reaction–> lysosome help the sperm penetrate the egg and fertilization occur
She’s pregnant and maintaining the corpus luteum which is continuing progesterone production
Corpus luteum is growing
The embryonic trophoblast is going to produce hCG which maintains this area so implantation can occur, Embryo implants on the endometrial wall
Cramps, Minor spotting, Nausea, vomiting, GI symptoms, bloating (thank you prostaglandins), Mood swings

Answer 85

A

Secondary sex characteristics before the age of 8 for girls and 9 for males
Heterosexual precocious puberty and Isosexual precocious puberty
GnRH stimulation test to determine the pseudosexual vs the complete/true isosexual, For CAH, you can test for the different enzyme deficiencies, You can also test LH and FSH, for true precocious puberty order an MRI of the brain
Suppress puberty with a GnRH agonist like glucuronide
Earlier growth spurt, taller than peer initially but will finish growing sooner and be a shorter adult height

Answer 86

A

Start to exhibit secondary sex characteristics opposite of what your genetic sex chromosomes are
CAH (congenital adrenal hyperplasia), Virilizing tumor, Medications/ exogenous androgens

Answer 87

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Secondary sex characteristics are consistent with your actual genotypic sex
Complete can also be referred to as true, central, or gonadotropin dependent
Can be caused by things in the hypothalamus or pituitary (like CNS tumors, hydrocephalus, or something intracranial), Incomplete (isolated premature thelarche, pubarche, or adrenarche)
Sometimes called peripheral, or gonadotropin independent-> Can be caused by exogenous estrogen, ovarian tumor-secreting estrogen, severe hypothyroidism
Can see café au lait spots and fibrous dysplasia of the bone

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