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Question 1

What is the mechanisim of activation that GnRH uses?

Answer 1

It activates Gq protein and IP3 second messenger

Question 2

What is the patteren of GnRH secretion at gestation,birth, and prior to puberty?

Answer 2

GnRH neurons are active during gestation, then ↓ at parturition/birth.

GnRH increases in infancy followed by a decade of low activity.

Question 3

What happens to GnRH in prepuberty?

Answer 3

In prepuberty → a sleep induced rise in GnRH

Question 4

What are two functions of LH?

Answer 4

LH stimulate cholesterol into mitochondria for steroidogenesis.

LH also increases gene expression and activity of the steroidogenic enzymes

(steroidogenic acute regulatory protein and P450scc[CYP]).

Question 5

What is testostrone bound to in plasma?

Answer 5

sex hormone binding globulin (SHBG) and albumin

Only free hormone is bioactive

Question 6

What is testostrone bound to in seminephrous tubules?

Answer 6

bound to androgen-binding protein (ABP) and concentrates in the lumen.

Question 7

What are three things that can happen to testosterone at target tissues?

Answer 7

1. testosterone can have a direct androgen receptor

2. be converted to 17β-estradiol (by aromatase)

3. to 5α-dihydrotestosterone (DHT) by 5α-reductase.

Question 8

What happens when there is increased SHBG in men, and decreased in women?

Answer 8

Question 9

What are the two different types of 5a-dihydrotestostrone?

Answer 9

Type 1 expresses at puberty, primarily in the skin and stimulates sebaceous gland activity and acne linked to puberty.

Type 2 activity initiate pubertal changes such as growth and activity of the prostate gland, growth of the penis, darkening and folding of the scrotum, growth of pubic and axillary hair, facial and body hair, and increased muscle mass

Question 10

What does finasteridine do what is it used to treat?

Answer 10

It is: selective 5 α -reductase-2 inhibitor

Used to treat: prostatic hypertrophy and prostatic cancer. May also be used in male pattern baldness.

Question 11

What is the state of the Cytoplasmic Androgen Receptor (AR) when no ligand is present?

Answer 11

It is bound to chaperone proteins, preventing it from entering the nucleus.

Question 12

What happens when testosterone or DHT binds to the Androgen Receptor (AR)?

Answer 12

The binding dissociates the chaperone proteins, allowing the AR to translocate to the nucleus.

Question 13

What happens to the AR-ligand complex when it first enters the nucleus?

Answer 13

It dimerizes.

Question 14

What do dimerized Androgen Receptors attach to in the DNA?

Answer 14

They attach to androgen-response elements (ARE).

Question 15

What role do co-regulatory proteins play after AR binds to ARE?

Answer 15

They assist in activating transcription of androgen-responsive genes.

Question 16

What stimulates the secretion of inhibin and from where is it secreted?

Answer 16

It is released from Sertoli cells in response to FSH.

Question 17

How does Inhibin B regulate FSH levels?

Answer 17

By negative feedback.

Question 18

What do Inhibin B levels correlate with and what does it serve as an index for?

Answer 18

Total sperm count and testicular volume; it serves as an index for spermatogenesis.

Question 19

What is the role of Activin at the pituitary gland?

Answer 19

It opposes inhibin’s actions and favors the synthesis of FSH.

Question 20

What enzyme converts testosterone to 17β-estradiol in the testes and adipose tissue?

Answer 20

Aromatase.

Question 21

Where is most estradiol produced in males?

Answer 21

By adipocytes.

Question 22

What factors are linked to aromatase activity in adipocytes?

Answer 22

Level of adiposity, cytokine levels, and glucocorticoid levels.

Question 23

Q: What physical symptoms may indicate anabolic steroid abuse in men?

A:

What mediates bone epiphyseal closure?

Answer 23

Aromatase conversion of testosterone to estradiol by osteoblasts and chondroblasts.

Question 24

What physical symptoms may indicate anabolic steroid abuse in men?

Answer 24

Acne, gynecomastia, and small testes.

Question 25

How does exogenous testosterone affect the hypothalamic-pituitary-gonadal axis?

Answer 25

It inhibits the axis, leading to ↓ intratesticular testosterone.

Question 26

What are common virilization symptoms in women due to anabolic steroid abuse?

Answer 26

Hirsutism, acne, breast atrophy, and male pattern baldness.

Question 27

What happens when there is a CYP19-aromatase deficiency in men?

Answer 27

Inability to produce estrogen occurs

Question 28

What is a notable physical consequence of CYP19-aromatase deficiency?

Answer 28

Tall stature due to lack of epiphyseal closure in long bones and osteoporosis.

Question 29

What role does estrogen play in insulin sensitivity?

Answer 29

Estrogen promotes insulin sensitivity.

Question 30

How does estrogen affect lipoprotein profiles?

Answer 30

It increases HDL and decreases triglycerides and LDL.

Question 31

What causes precocious puberty?

Answer 31

Excess androgens in childhood

Question 32

What are the age thresholds for precocious puberty in girls and boys?

Answer 32

Before age 8 years in girls and before age 9 years in boys.

Question 33

What does precocious puberty do to the height of the patient?

Answer 33

↑sex hormone exposure or production → ↑ linear growth, somatic and skeletal maturation (e.g., premature closure of epiphyseal plates → **short stature**).

Question 34

What are the two types of precocious puberty?

Answer 34

Central precocious puberty and Peripheral precocious puberty.

Question 35

What causes Central precocious puberty and how does it work?

Answer 35

Central precocious puberty (↑ GnRH secretion): idiopathic (most common; early activation of hypothalamic-pituitary gonadal axis), CNS tumors.

Question 36

What causes Peripheral precocious puberty and how does it work?

Answer 36

Peripheral precocious puberty (GnRH-independent); ↑ sex hormone production, as in congenital adrenal hyperplasia and Leydig cell tumor.

Question 37

What are the two main causes of hypogonadism?

Answer 37

Disorders of the hypothalamic–pituitary–gonadal axis (hypogonadotropic or secondary hypogonadism) or testicular dysfunction (hypergonadotropic or primary hypogonadism).

Question 38

What is hypogonadotropic hypogonadism?

Answer 38

A condition resulting from abnormal GnRH secretion or impaired gonadotropin secretion by the anterior pituitary.

Question 39

What are some potential causes of hypogonadotropic hypogonadism?

Answer 39

Genetic defects (e.g., Kallmann syndrome), mutations of the GnRH receptor, pituitary tumors (e.g., prolactinoma), trauma, or surgery.

Question 40

What condition can result from congenital adrenal hyperplasia related to hypogonadism?

Answer 40

Increased adrenal androgen production from 21-hydroxylase (CYP21A2) deficiency, leading to a lack of mineralocorticoids and glucocorticoids.

Question 41

What type of hypogonadism is Kallmann syndrome associated with?

Answer 41

Hypogonadotropic hypogonadism (lack of LH and FSH).

Question 42

What is the primary cause of Kallmann syndrome?

Answer 42

Lack of GnRH neurons in the hypothalamus.

Question 43

What additional sensory issue is associated with Kallmann syndrome?

Answer 43

Anosmia (loss of the sense of smell).

Question 44

Which sex is more frequently affected by Kallmann syndrome?

Answer 44

Males are more frequently affected than females.

Question 45

What common condition is seen in males with Kallmann syndrome?

Answer 45

Undescended testes (cryptorchidism).

Question 46

How does Kallmann syndrome affect Wolffian duct differentiation?

Answer 46

There is normal differentiation of the Wolffian duct due to androgens being stimulated by placental HCG instead of LH.

Question 47

What is a key developmental issue related to penis development in Kallmann syndrome?

Answer 47

Deficiencies in penis development can lead to microphallus due to a lack of LH-induced androgen synthesis and release.

Question 48

What type of hypogonadism is associated with Klinefelter syndrome?

Answer 48

Hypergonadotropic hypogonadism (high FSH and LH) due to testicular failure.

Question 49

What is the chromosomal pattern of an individual with Klinefelter syndrome?

Answer 49

Male with a 47 XXY karyotype and a Barr body.

Question 50

What physical features are commonly associated with Klinefelter syndrome?

Answer 50

Testicular atrophy, eunuchoid body shape, long extremities, gynecomastia, and female-pattern hair distribution.

Question 51

What are some sexual functions affected by Klinefelter syndrome?

Answer 51

Lack of libido and erectile dysfunction.

Question 52

What hormonal changes occur due to dysgenesis of seminiferous tubules in Klinefelter syndrome?

Answer 52

↓ inhibin B → ↑ FSH and abnormal Leydig cell function → ↓ testosterone → ↑ LH.

Question 53

What causes Androgen Insensitivity Syndrome (AIS)?

Answer 53

A defect in the gene on the X chromosome that expresses the androgen receptor.

Question 54

What is the karyotype of individuals with AIS?

Answer 54

Normal 46,XY karyotype.

Question 55

What hormones are produced by the testes in individuals with AIS?

Answer 55

Testosterone and Anti-Müllerian Hormone (AMH).

Question 56

Where do the testes of AIS patients typically descend?

Answer 56

Into the labia majora instead of the scrotum.

Question 57

Why must the testes be removed in AIS patients?

Answer 57

To prevent the risk of tumor development.

Question 58

What happens to the Wolffian duct in AIS patients?

Answer 58

It does not develop due to the absence of androgen receptors (AR).

Question 59

What effect does AMH have on the Müllerian duct in AIS patients?

Answer 59

The AMH causes the Müllerian duct to regress, leading to a lack of internal genitalia.

Question 60

What is the typical external phenotype of individuals with AIS?

Answer 60

The external genitalia typically develop as female, resulting in a female phenotype.