Sem 4 Week 12 Lec 3

Front 1

Structure of testosterone(T) ?

Back 1

4 rings like all steroids.

Front 2

DHEA is

Back 2

Not androgenic

Front 3

Where is T made?

Back 3

Leydig(interstitial) cells of testis and in ovary from cholesterol.

Front 4

T is metabolized into DHT by

Back 4

5 alpha reductase in target tissues.(prostae,hair follicles,genitals)

Front 5

DHT potency is > than T in some tissues.

Back 5

True

Front 6

What regulates T synthesis?

Back 6

LH from pituitary.

Front 7

DHEA and androstenedione are?

Back 7

Very weak adrenal androgens

Front 8

To go bald,

Back 8

you need DHT.

Front 9

Drugs that block 5 alpha reductase are used to

Back 9

treat prostate cancer/baldness.

Front 10

What are the androgens?

Back 10

-T
-DHT
-DHEA
-Androstendione

Front 11

Where are the above produced/

Back 11

-testis
-ovary
-Adrenal

Front 12

Androgenic effects ?

Back 12

-Control sexual diff. in male
-Regulate function in male reproduction.

Front 13

Anabolic effects ?

Back 13

Promote growth of bone,muscle,prostate,other tissues.

Front 14

Main androgen

Back 14

T

Front 15

Main function of T

Back 15

-masculinising function
-growth promoting function.
--> regulate reproduction in males.((expressed in utero,neonatal periods,puberty)

Front 16

T actions ?

Back 16

-sexual diff. of internal/external genitalia in utero
-puberty
-adult life:role in testis and role outside testis.

Front 17

How many phases of androgen activity?

Back 17

3

Front 18

What are the 3 main periods when pituitary gonadal axis is active?

Back 18

-midtrimester of fetal period
-during early neonatal period
-from puberty throughout reproductive years.

Front 19

SRY

Back 19

-switches on the Y chromosome
-testis determining factor on Y chrm.

Front 20

Being female is

Back 20

Default state.

Front 21

If SRY is active,

Back 21

Dev. gonad becomes a testis.

Front 22

What does testis secrete?

Back 22

-T
-AMH(anti mullerian hormone) or MIS

Front 23

What are the 2 duct systems present in embryo?

Back 23

-Wolfian duct has potential to develop into male genital tract.
-Mullerian duct has potential to dev. into female genital tract.

Front 24

Y chrm w/o SRY ?

Back 24

XY female

Front 25

Y chrm translocated onto X chrm ?

Back 25

XX male

Front 26

T initiates dev. of ?

Back 26

Male internal genitals(epididymis,vas deferens,seminal vesicles)

Front 27

DHT is required for ?

Back 27

Dev. of external male genitalia and prostate(prostate,urethra,penis,scrotum)

Front 28

AMS(MIH) causes ?

Back 28

regression of mullerian duct which otherwise dev. into--> fallopian tubes,uterus & upper third of vagina.

Front 29

What are the 2 types of cells from testis ?

Back 29

-Sertoli
-Leydig

Front 30

Sertoli cells produce

Back 30

MIS(AMH)

Front 31

Leydig cells produce

Back 31

T

Front 32

T + AR gives

Back 32

-Wolfian duct dev.
-Masculinization of internal organs
-Maintenance of spermatogenesis.

Front 33

DHT + AR gives ?

Back 33

-masculinization of external genitalia
-Dev. of prostate
-Dev. of secondary sexual characteristics.

Front 34

T actions during puberty?

Back 34

-Penis and testis enlarge
-Growth of facial hair
-Increased sebum production
-Pubic hair
-Growth in height and increase in muscle size
-vocal cords enlarge and larynx enlarge.

Front 35

High conc. of T are present in testis

Back 35

True-required for spermatogenesis.

Front 36

Role of T outside testis ?

Back 36

-Bone/muscle strength
-hair growth and baldness
-libido
-psycho function.
-aging ?

Front 37

XY baby with no androgen Receptor cannot dev. neither external nor internal genitali but testis working-->T not acting but MIH still produced with atrophy of vagina and uterus BUT still dev. like normal females at puberty.why ?

Back 37

Excess T metabolized to estrogen by aromatase at puberty.

Front 38

In human males,hormonal activity is only 1 factor of sexual behaviour.

Back 38

True

Front 39

Seminal vesicle atrophies w/o T.

Back 39

True

Front 40

hypogonadism

Back 40

not enough T in males.

Front 41

T actions in females

Back 41

-Pubic and axillary hair
-bone strength
-muscle strength(works better in females)
-Sexual function-libido
-Psychological function

Front 42

What happens when T levels increase in women?

Back 42

-baldness
-Hirsutism
-breasts atrophy
-Increase in size of genitals

Front 43

What can this be a sign of ?

Back 43

-Testicular secreting tumour of ovaries

Front 44

Dx of females pt with frontal baldness,deep voice,hirsutism,enlarged clitoris.

Back 44

ovarian tumour.

Front 45

Diff. between the various steroid hormone receptor superfamily lies in

Back 45

Diff. ligand binding domains.

Front 46

T action is via ?

Back 46

Protein synthesis.

Front 47

Androgen responsive systems?

Back 47

on almost all tissues of body.

Front 48

Androgen responsive systems in the erythropoietic system causes

Back 48

Increase in RBC

Front 49

Androgen responsive systems in reproductive/sex tissues responsible for ?

Back 49

-Genital dev.
-Prostate dev.
-Spermatogenesis
-Breast (-VE)

Front 50

Androgen responsive systems in brain/nervous system responsible for ?

Back 50

-Behavioural modulation
-motor neurones(KENNEDY's disease)

Front 51

What are the simple Androgen response elements ?

Back 51

-Consensus GRE
-Palindromic

Front 52

What are some complex AR binding sites?

Back 52

-multiple weak AREs
-non consensus binding sites.

Front 53

Androgen responsive genes

Back 53

regulate many genes:-
-growth factors
-secretory factors
-matrix/structural pz.

Front 54

Pituitary or testicular disease of T metabolism causes ?

Back 54

-Delayed puberty
-Hypogonadism in adults.

Front 55

Hypogonadism in adult males ?

Back 55

-Decreased libido
-Decreased muscle bulk
-Osteoporotic fractures
-Changes in personality
--> can be reversed by T replacement.

Front 56

Defects in 5 alpha reductase(T-->DHT) leads to

Back 56

-females external genitals at birth in XY pts
-masculinise at puberty

Front 57

We need DHT for

Back 57

External genitalia dev.

Front 58

XY females can have

Back 58

Testes

Front 59

What is Androgen insensitivity(AIS) ?

Back 59

Loss of function mutations in the androgen receptor.(genetic defect in T action)
-XY females
-testis
-male T levels
-female external genitalia
-no uterus nor fallopian tubes
-breasts at puberty

Front 60

In New Guinea,pts born females and masculinize at puberty.why?

Back 60

Increased levels of T and 5 alpha reductase at puberty.

Front 61

AR gene mutations cause loss of function in

Back 61

AIS(partial or complete)

Front 62

AR gene mutations cause GAIN in function in

Back 62

-prostate cancer(increased hormone responsiveness)
-Kennedy's disease
-Breasts cancer.

Front 63

Kennedy's disease ?

Back 63

-motor neuron disease
-Spino-bulbar muscular atrophy
-Trinucleotide repeat expansion in exon A
-> 40 triplets
-Increased length of Gln in Amino terminal domain
-Decreased transactivation

Front 64

Prostate cancer ?

Back 64

-AR mutations at specific sites in ligand binding domain
-Mutations in primary and secondary cancers
-receptor activation by adrenal androgens,anti-androgens & estrogens.

Front 65

Clinical uses of T ?

Back 65

-Replacement if inadequate production(pituitary disease/testicular disease)
-Contraception(doesnt work orally)
-Body building(illicit in sport)

Front 66

T is synthetized by

Back 66

testis and to small extent by ovary.

Front 67

T is converted locally to more potent DHT in

Back 67

Prostate

Front 68

T regulates :-

Back 68

-Sexual diff
-Maturation
-Spermatogenesis

Front 69

T is required for

Back 69

Dev of male internal genitalia

Front 70

DHT required for

Back 70

Dev. of prostate and external male genitalia.

Front 71

Androgens act by

Back 71

Binding to INTRAcR receptors which regulate gene expression.