Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Life Cycles > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Sacrotuberous ligament

connects _______ to _______

creates the _______ foramen through which ________, ________, and _________ pass ______ (superficial/deep) to sacrotuberous ligament to enter the perineum

A

ischial tuberosity → sacrum/coccyx

Creates greater sciatic foramen (pudendal nerve and internal pudendal a/v pass deep to ST lig to enter perineum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sacrospinous ligament

connects _______ to _______

creates the _______ foramen through which ________, ________, and _________ pass ______ (superficial/deep) to sacrospinous ligament to enter the perineum

A

ischial spine → sacrum/coccyx

Creates greater and lesser sciatic foramen (pudendal n and internal pudendal a/v pass superficial to SP lig to enter perineum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Obturator membrane

A

covers obturator foramen

Attachment for obturator internus/obturator externus muscle

Superior gap provides exit of obturator n, a, and v (supplies medial thigh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

True pelvis

A

between pelvic inlet and pelvic outlet

Contents supported inferiorly by pelvic diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Greater pelvis/False pelvis

A

superior to pelvic inlet (contain abdominal viscera)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Perineum

A

inferior to pelvic diaphragm, contains external genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gubernaculum

A

fibrous tract guiding descent of gonads

Connected to abdominal wall at deep inguinal ring → testes enter and descend through deep ring

Degenerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Male embryonic development:

28th week: testes pass through _________ and enter _______ following ______ (anterior/posterior) to processus vaginalis (NOT through it)

→ Testes ensheathed in layers from abdominal wall

A

28th week: testes pass through inguinal canal and enter scrotum following POSTERIOR to processus vaginalis (NOT through it)

→ Testes ensheathed in layers from abdominal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Processus Vaginalis

A

peritoneal diverticulum, transverses developing inguinal canal to developing scrotum carrying with it layers of muscle and fascia from abdominal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tunica Vaginalis

A

remnant of processus vaginalis

Closed peritoneal sac surrounding testes with 2 pleural layers separated by potential space (like lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cryptorchidism

A

undescended testes, often unilateral, often self-resolves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Spermatic cord:

Contents: (5)

A

1) Ductus deferens
2) Testicular artery (direct branch from abdominal aorta)
3) Pampiniform venous plexus (converges into R/L testicular vein → R side goes to IVC, L side goes to L Renal Vein)
4) Vestige of processus vaginalis
5) Artery of ductus deferens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Layers of spermatic cord (3) and from which layer of the abdominal wall they originate

A

Internal spermatic fascia (from transversalis fascia)

Cremasteric fascia and muscle (from internal oblique)

External spermatic fascia (from external oblique)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sperm travels (8)

A

Seminiferous tubules of testes → rete testis → epididymis → ductus deferens → ejaculatory duct → prostate (prostatic urethra) → Penile urethra → external urethral orifice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tunica albuginea

A

tough outer surface of testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Seminiferous tubules

A

long, highly coiled tubes in which sperm are produced - joined to rete testis by straight tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rete Testis

A

collects sperm from tubules, passes them to efferent ductules → epididymis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Epididymis

A

posterior side of testes, concentrates sperm before it passes to ductus deferens for expulsion
Head → Body → Tail (continuous with ductus deferens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ductus deferens

A

continuation of epididymis

Thick muscular wall, narrow lumen

Ascends via spermatic cord → enter abdominal cavity via inguinal canal → join duct of seminal gland (posterior/inferior to bladder) → forms ejaculatory duct

Key relationships: anterior and superior to ureter and anterior to external iliac artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ejaculatory duct

A

where ductus deferens terminates

Burrow into back of prostate gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Seminal glands (vesicle)

A

secretes thick alkaline fluid with fructose and coagulant that mixes with sperm as they pass into the ejaculatory ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bulbourethral glands

A

paired glands that produce mucus-like secretion during sexual arousal

Secrete into spongy urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Testicular torsion

A

wisting of spermatic cord → obstruct venous drainage → edema → block arterial supply to testis

Associated with congenital malformation of processus vaginalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Varicocele

A

enlargement/dilation of pampiniform plexus of veins in spermatic cord

Cause: incompetent/absent valves in testicular veins → pooling/backflow

More common on left side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fallopian Tubes:

Four parts:

A

1) Infundibulum: catches egg, distal end has fimbriae projections
2) Ampulla: where fertilization typically occurs
3) Isthmus: narrows and thickens to enter uterine horn
4) Uterine part: within walls of uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ovarian ligament

A

remnant of upper gubernaculum, connects ovary to uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Suspensory Ligament of ovary

A

peritoneal fold continuous with mesovarium

Contains ovarian blood vessels, lymph vessels, nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Round Ligament of the Uterus

A

Ligamentum teres

Remnant of female lower gubernaculum

Attaches uterus near junction of uterine tube and labia majora via inguinal canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Broad ligament: 3 parts

A

1) Mesovarium: broad ligament that suspends ovaries
2) Mesosalpinx: broad ligament around uterine tubes
3) Mesometrium: largest part of broad ligament, mesentery for uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Blood supply to ovaries

A

ovarian artery from abdominal aorta (via suspensory ligament of ovary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Blood supply to uterus

A

Uterine artery from internal iliac artery

Anastomoses with ovarian artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Blood supply to vagina

A

Vaginal branch from uterine artery (superior and middle)

Inferior pudendal artery (inferior)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Indirect inguinal hernia

A

make up 2/3s of inguinal hernias

Herniated loop of intestine (usually small intestine) traverses entire Inguinal Canal, from DEEP INGUINAL RING to superficial inguinal ring

**Originates LATERAL to inferior epigastric vessels

Hernia located within persistent processus vaginalis, thus inside spermatic cord → MAY EXTEND INTO SCROTUM**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Direct inguinal hernia

A

Originates within INGUINAL TRIANGLE, MEDIAL to inferior epigastric vessels

Herniated intestine pushes directly through abdominal wall, follows medial part of Inguinal Canal to Superficial Inguinal Ring

Herniated loop lies parallel to spermatic cord, NOT within it → RARELY ENTERS SCROTUM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Normal Differentiation of Testis/Ovary

A

Chromosomal sex → gonad development → hormone production → differential development of internal duct systems and external genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Bipotential process of testes/ovary differentiation

A

undifferentiated structures either male or female direction, but current biological environment determines path (may change) at each stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Sex Determining Region of Y

A

KEY to sexual dimorphism is Y chromosome (SRY → short arm of Y chr)

protein transcription factor which activates other transcription factors and initiates testicular differentiation from indifferent gonad

  • Activates SOX-9
  • Inhibits WNT-4 and RSPO1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Process of Gonad Development:

1) Undifferentiated gonads appear at ___-____ wks as paired _________

Formed from proliferation of _______ and condensation of underlying ________

Just medial to developing _________ (1st kidney)

A

1) Undifferentiated gonads appear at 4-5wks as paired genital ridges

Formed from proliferation of epithelium and condensation of underlying mesenchyme

Just medial to developing mesonephros (1st kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Key transcription factors expressed early in gonadal development (2)

A

WNT-1

SF1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

WT-1

what is it?

what happens if there is a deletion/mutation?

A

TF expressed in developing genital ridge, kidney, gonads → activates SRY

WT1 deletion/mutation → gonadal dysgenesis, Wilms tumor, nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

NR5A (Steroidogenic Factor, SF1)

what is it?

what happens if there is a deletion/mutation?

A

expressed in developing genital ridge - regulates transcription of genes involved in gonadal and adrenal development, steroidogenesis and reproduction

SF1 deletions → gonadal dysgenesis, adrenal failure, persistent Mullerian structures (low AMH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Process of Gonad Development:

2) Germ cells migrate from _______ and invade ________ at wk 6

If germ cells don’t migrate…_________

Before/during germ cell invasion, epithelium of genital ridge proliferates and penetrates mesenchyme → ___________.
-These become__________ in males

A

2) Germ cells migrate from yolk sac and invade genital ridge at wk 6

If germ cells don’t migrate, gonads do not develop

Before/during germ cell invasion, epithelium of genital ridge proliferates and penetrates mesenchyme → primitive (medullary) sex cords.
-These become seminiferous tubules in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

3) Different for males/females

Males: ______ expressed at 6 weeks →

1) Primitive sex cords continue to proliferate and penetrate into _______ to form _______ (medullary cords)
2) Migration of _________ cells into developing testis
3) Differentiation of _______ cells (from surface epithelium, supporting cells) and differentiation of ________ cells (testosterone producers)

A

Males: SRY expressed at 6 weeks →

1) Primitive sex cords continue to proliferate and penetrate into medulla to form testis (medullary cords)
2) Migration of mesonephric cells into developing testis
3) Differentiation of sertoli cells (from surface epithelium, supporting cells) and differentiation of leydig cells (testosterone producers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Leydig cells begin production of testosterone by ______ wk

Located where?

A

8th week

between testis cords in seminiferous tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Important transcription factors in male/female differentiation (5)

A

1) SOX-9
2) SRY
3) DAX
4) WNT-4
5) RSPO1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

SOX-9

A

upregulated by SRY

essential for normal testis formation

elevates AMH concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Deletion/mutation in SOX-9 causes what?

A

Campomelic dysplasia–>

  • Severe skeletal dysplasia
  • Gonadal dysgenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

WNT-4 and RSPO1

A

expressed in females, activate B-catenin pathway, inhibit testis development, promote ovary development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

DAX

-single vs. double DAX gene

A

single DAX → testicular development

double DAX → activate ovarian development, inhibit testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is required for female differentiation

2 things + 4 TFs

A

1) requires 2 X chromosomes and absent Y
2) Requires migration of primitive germ cells
3) Important genes: DAX1 (2 copies), WNT-4, RSPO1, FOXL2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

The gonads of both males and females develop from the __________

In males the ________ form the testes

In females the cortex develops into the ________, while the medulla _________

A

germ cells in the urogenital ridge

In males the medullary cords form the testes

In females the cortex develops into the ovaries, while the medulla degenerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Internal ducts differentiation determines ______________

Initially, both ________ (Wolffian) and __________ (Mullerian) ducts develop in both sexes

A

phenotypic sex

Initially, both mesonephric (Wolffian) and paramesonephric (Mullerian) ducts develop in both sexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Male internal duct differentiation:

wolffian ducts –> what 3 structures

A

Wolffian ducts → 1) epididymis, 2) vas deferens, 3) seminal vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Male internal duct differentiation:

Duct differentiation requires testicular secretions:

1) High _________ produced by _______ cells = _________ effect

2) ________ hormone produced by ________ cells
→ Mullerian duct regression
Must be expressed before end of wk ______

A

Duct differentiation requires testicular secretions:

1) High LOCAL [testosterone] produced by Leydig cells = PARACRINE effect

2) Antimullerian hormone (AMH) produced by Sertoli cells
→ Mullerian duct regression
Must be expressed before end of wk 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Internal duct differentiation of females:

requires ABSENCE of _______ and _______

_________ ducts regress

A

Requires absence of local testosterone and AMH

Wolffian ducts regress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Internal duct differentiation of females:

Paramesonephric (Mullerian ducts) →what 3 structures?

A

Paramesonephric (Mullerian ducts) → 1) Fallopian tubes, 2) midline uterus, 3) upper portion of vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

External Genitalia differentiation:

Develop from three initially indifferent structures:

1) Genital tubercle → __________
2) Urethral folds → ___________
3) Labial-scrotal swellings → __________

A

1) Genital tubercle → glans penis/clitoris
2) Urethral folds → penile urethra/labia minora
3) Labial-scrotal swellings → scrotum/labia majora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Male external genital differentiation relies on _________, especially for the formation of the _________

Male external genital differentiation is complete by _____ weeks

Gonadal descent (testes reach scrotum) occurs by ______ weeks

A

Dependent on DHT (T → DHT via 5a-Reductase) especially formation of penile urethra

Complete by 13 weeks

Gonadal descent: testes reach scrotum by 33 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Male external genital differentiation:

During first trimester, _________ stimulates Leydig cells to make ________

After → requires ___________ for continued testosterone production

A

During first trimester, placental HCG stimulates Leydig cells to make testosterone

After → requires Hypothalamic-Pituitary-Testicular axis for continued testosterone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

In females, excessive androgen exposure…

before 13 weeks can cause what?
after 13 weeks can cause what?

A

Excessive androgen exposure after 13 weeks can cause cliteromegaly, but cannot result in posterior labial fusion or penile urethra

PRIOR to 13 wks → affects urogenital sinus and causes insertion of urethra into vagina (more androgen exposure = more severe defect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Rokitansky Syndrome

A

Mullerian duct abnormality

absent or underdeveloped mullerian (paramesonephric) structures in 46 XX female → presents as primary amenorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Persistent mullerian ducts in 46 XY

caused by what 2 things?

presentation?

A

normal virilization, with unilateral hernia

Defect in AMH synthesis
Defect in AMH receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Disorder (difference) of Sex Development (DSD)

A

congenital conditions in which development of chromosomal, gonadal, or phenotypic sex is atypical

Genital ambiguity

Discordance between genital appearance and prenatal karyotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Classification of DSDs (2)

A

1) 46XX DSD: virilized XX fetus

2) 46XY DSD: undervirilized XY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

46XX DSD

4 possible causes?

A

virilized XX fetus

1) Congenital adrenal hyperplasia (95% of cases)
2) 46 XX sex reversal (SRY translocation) - baby looks male
3) Ovotesticular DSD
4) Gestational hyperandrogenism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

46XY DSD

3 possible categories of causes

A

1) Abnormal testicular development
2) Defects in adrenal and testicular steroidogenesis
3) Defects in testosterone/androgen metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

5a-Reductase deficiency

A

AR cause of 46XY DSD

  • T not converted to DHT
  • -> Wolffian ducts differentiated (normal) and testes normal, BUT external genitalia undervirilized (ambiguous at birth)
  • Testes in inguinal canal or labial-scrotal folds
  • Spontaneous virilization at puberty possible
  • Typically male gender identity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Androgen insensitivity syndrome

A

Mutation in androgen receptor on X chromosome

can be complete or incomplete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Complete androgen insensitivity

A
  • Gonads intraabdominal or in inguinal canal
  • ->Bilateral inguinal hernias common
  • blind vaginal pouch (Testicular Feminization)
  • Spontaneous breast development at puberty
  • Little/no pubic/axillary hair
  • Female gender identity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Types of Congenital Adrenal Hyperplasia (CAH)

5

A

1) 21 hydroxylase deficiency: 95% of CAH cases
2) 11B hydroxylase deficiency
3) StAR protein deficiency
4) 3B-Hydroxysteroid dehydrogenase deficiency
5) 17a hydroxylase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

21 hydroxylase deficiency

what is blocked, what is overactivated?

normal function of enzyme?

A

21 hydroxylase normally converts progesterone → 11-deoxycorticosterone and 17-OH progesterone to 11-deoxycortisol

Aldo and cortisol pathways blocked, androgen pathway overstimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

21 hydroxylase deficiency

features (4)

A

1) Virilization → female (virilization of external genitalia), male (no genital abnormalities)
- Degree of androgen exposure determines degree of virilization

2) Hyperpigmentation (too much ACTH and POMC)

3 and 4) Hyponatremia/Hyperkalemia due to aldo deficiency

Mild forms may present later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

21 hydroxylase deficiency

diagnosis and treatment

A

Diagnosis:

  • Virilized XX infant or XY infant with hyperkalemia/hyponatremia
  • 17-OH progesterone tested on newborn screen

Treatment:

  • Surgery in females
  • Replace hormones and suppress ACTH overproduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

11B hydroxylase deficiency

normal function of enzyme

what is overproduced, what is blocked?

A

11B hydroxylase normally converts 11-deoxycorticosterone → corticosterone and 11-deoxycortisol → cortisol

increased 11-deoxycorticosterone
increased androgens
decreased cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

11B hydroxylase deficiency

features (3)

A

1) Virilization similar to 21-OH
2) NO salt wasting because 11-deoxycorticosterone has mineralocorticoid activity
3) HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

StAR protein deficiency

normal protein function?

A

Steroidogenic Acute Regulatory Protein

Normally transfers cholesterol from outer to inner mitochondrial membrane allowing for conversion of cholesterol → pregnenolone

deficiency causes build up of cholesterol esters in adrenocortical tissues (Congenital Lipoid Hyperplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

StAR protein deficiency

features (3)

A

1) UNDERVIRILIZATION - Females have normal genitalia, Males have female external genitalia
2) Salt wasting
3) Fatal if not detected early in infancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

3B-Hydroxysteroid dehydrogenase deficiency

normal enzyme function?

A

Normally involved in conversion of:

pregnenolone → progesterone

17-OH pregnenolone → 17-OH progesterone

DHEA → androstenedione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

3B-Hydroxysteroid dehydrogenase deficiency

features (3)

A

1) Virilization in girls
2) Undervirilization in boys
3) Salt wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

17a hydroxylase deficiency

A

Normally converts pregnenolone → 17-OH pregnenolone and progesterone → 17-OH progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

17a hydroxylase deficiency

features (4)

A

1) HTN (increased 11-deoxycorticosterone)
2) Hypokalemia

3) Females born with normal genitalia and present at puberty with failure to develop secondary sex characteristics
- Males born undervirilized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Four Cardinal Steps in Mullerian Development:

A

1) Elongation
2) Fusion
3) Canalization
4) Septal resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Four Cardinal Steps in Mullerian Development:

1) Elongation

A

1) Elongation:
Formation: 37 days after fertilization, Mullerian ducts (paramesonephric ducts) first appear lateral to Wolffian ducts (mesonephros)
→ Elongation of Mullerian duct: occurs medially and caudally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Four Cardinal Steps in Mullerian Development:

2) Fusion

A

2) Fusion: Mullerian ducts fuse in midline and subsequently fuse with urogenital sinus at Muller tubercle
Wolffian ducts regress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Four Cardinal Steps in Mullerian Development:

3) Canalization

A

3) Canalization: Mullerian duct initially solid structures, but will canalize and become tubes

Metanephric ducts (kidneys) fully develop and establish connection with cloaca/bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Four Cardinal Steps in Mullerian Development:

4) Septal Resorption

A

septum separating uterus into two is resorbed → uterus joins with urogenital sinus to form lower vagina

Sinovaginal bulb elongates and develops into full vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

After septal reapsorption step of Mullerian development what happens?

A

Mullerian system (cephalad) fuses with urogenital sinus (caudad)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Imperforate hymen

A

failure of caudal end of sino-vaginal bulbs to canalize → cyclical pain and build up of menstrual blood upon starting menstruation

thin membrane covering vaginal opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Transverse vaginal septum

A

failed canalization of the vaginal plate (where mullerian ducts meet urogenital sinus)

Vagina ends in pink tissue

Presents with cyclical pain

more involved surgery to repair than imperofrate hymen –> remove septum, sew vagina closed with possible graft to prevent pain with intercourse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Vaginal atresia

A

failure of urogenital sinus to canalize below vaginal plate

Presents with cyclical pain

Treatment: vaginal dilators or surgical vaginoplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Mullerian Agenesis or Hypoplasia

A

Class I Mullerian defect

Most severe form
*Failure of elongation - Mullerian structure never came down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Mullerian Agenesis or Hypoplasia presentation

A

amenorrhea

Blind ending vagina - NO UTERUS or FALLOPIAN TUBES but do have ovaries so develop secondary sex characteristics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Unicornuate uterus

A

Class II Mullerian defect

Failure of one mullerian duct to elongate or reach urogenital sinus with contralateral duct

typically have normal menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Uterine didelphys

A

Class III Mullerian defect

  • Occurs if Mullerian ducts completely fail to fuse in midline
  • Completely separate cavities with 2 distinct endometrial cavities and cervixes, each with one fallopian tube

Can occur with obstructed hemivagina if septum comes down and obstructs one uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Bicornuate Uterus

A

Class IV Mullerian defect

Incomplete fusion of midline Mullerian ducts during embryogenesis partially or completely divides the endometrial cavity into two longitudinal halves

Complete or partial

Occurs at 9th week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Septate Uterus

A

Class V Mullerian defect

Failure of septum resorption

Fibrous or fibromuscular septum may extend partially into the uterine cavity or may extend the entire length

Usually asymptomatic

MOST COMMON type of mullerian anomaly (55% of cases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Arcuate Uterus

A

Class VI Mullerian defect

  • Variant of normal
  • Near complete resorption of utero-vaginal septum with some remnant
  • Asymptomatic
  • Normal external contour
  • No adverse reproductive outcomes
  • No surgical intervention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

DES Drug Related Mullerian Defect

A

Class VII Mullerian defect

Diethylstilbestrol-induced uterine anomalies

69% of women with DES exposure had uterine anomalies
→ T shaped uterus (most common), fundal constriction rings, hypoplastic uterus, intrauterine adhesions

Also associated with cervical hypoplasia, vaginal adenosis, and clear-cell vaginal adenocarcinoma, SAB, EP, and cervical incompetence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Reproductive implications of DES drug related Mullerian defect (5)

A 
Endometriosis
Recurrent miscarriage
Preterm delivery
Malpresentation
Associated renal anomalies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Sertoli Cells function (6)

A

1) Form blood-testis barrier (tight junctions)
2) Nurture developing sperm
3) Secrete androgen binding protein (APB) → maintain high local level of testosterone
4) Convert androgens to estrogen (via aromatase)
5) Secrete inhibin and other growth factors
6) Respond to FSH through GPCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Role of Leydig Cells:

A

1) Required for spermatogenesis
2) Synthesis of testosterone (via 5a-reductase)

3) Synthesis of steroidogenic acute regulatory protein (StAR) and sterol carrier protein (SCP)
- -> Transport cholesterol to mitochondrial side chain cleavage enzyme

4) Stimulate steroidogenesis
5) Respond to LH through GPCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

BOTH leydig and sertoli cells are necessary for _____________

A

testicular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

hCG looks like what?

A

TSH and LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Androgens inhibit ______, _______, and ________

Inhibin suppreses _________

Activin activates _________

Follistatin binds and controls activity of _________

A

Androgens (testosterone) inhibit GnRH release

Androgens (and estrogen) inhibit LH and FSH release

Inhibin suppresses FSH production

Activin → activates FSH

Follistatin → binds and controls activity of activin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

DHT

A

most potent, highest affinity for AR

Receptors for DHT in external genitalia, sebaceous glands, hair follicles

Generated from testosterone via 5a-reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Male Puberty:

A

Increased growth hormone

Increased testosterone

Pubertal growth spurt (11 inches) - later in puberty than female growth spurt

Prepuberty males/females have equal body mass, skeletal mass, and body fat →

POST puberty males have:
150% female muscle mass, 150% female skeletal and lean body mass, 200% female muscle cell number, 50% female body fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Consequence of steroid abuse:

A 
Infertility, decreased sperm production
Gynecomastia - breast development
Testicular atrophy
Baldness and excessive body hair
Short stature
Tendon rupture
Increase LDL, decreased HDL → atherosclerosis
High BP
Heart attack and stroke
Enlargement of LV
Liver cancer, blood filled cysts
Severe acne, cysts, oily scalp
Fluid retention, kidney failure
Psychiatric disturbances Mania, delusions, irritability, insomnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Growth hormone vs. sex steroids in bone growth:

A

Growth hormone: causes BALANCED growth and ossification
-Bones continue to lengthen through childhood and pubertal ages under its influence in absence of sex steroids

Testosterone and estrogen: stimulates bone growth, accelerates bone maturation, promotes epiphyseal closure

  • NARROWs growth window limiting long-bone growth
  • Growth “levels off” after puberty
109
Q

Effects of androgens in puberty:

1) androgenic effects (3)
2) Anabolic effects (4)
3) Interactions with GH and IGF1 (3)

A

1) Androgenic effects:
- Growth and development of male reproductive tract
- Secondary sexual characteristics
- Behavioral responses

Anabolic effects:

  • Growth of somatic tissues
  • Linear body growth (long bones)
  • Nitrogen retention, protein synthesis
  • Muscle development

Interacts with insulin like growth factor (IGF-1) and growth hormone axis

  • GH/IGF1 → stimulate gonadal function
  • IGF1 → stimulate GnRH secretion
  • Testosterone and estrogen → stimulate GH secretion and growth
110
Q

First signs of puberty

A

testicular enlargement (FSH/LH mediated) or breast bud development

111
Q

7 Estrogen stimulated changes in puberty

A
  1. Breast development
  2. Genital growth (labia minora)
  3. Maturation of vaginal mucosa
  4. Uterine/endometrial growth
  5. Body composition changes (female fat distribution)
  6. Menarche (estrogen and progesterone) - occurs mid-late puberty
  7. Growth acceleration (mediated by ESTROGEN) - not as fast as boys
112
Q

Testosterone mediated changes in puberty (7)

A

occur up to a year after growth of testes

  1. Scrotal changes
  2. Sexual hair (upper lip, chin, sideburns, axilla, pubic area)
  3. Penile growth
  4. Prostatic/seminal vesicle growth
  5. Deepening of voice
  6. Increase in muscle mass
  7. Linear growth acceleration mediated by increased GH (mediated by ESTROGEN)
113
Q

Normal age of pubertal onset for boys

A

9-14

114
Q

Normal age of pubertal onset for girls

A

8-13

115
Q

What occurs durin pubertal onset

A

:re-emergence of hypothalamic GnRH secretion → stimulates gonadotrope secretion of FSH and LH → bind receptors in ovaries/testes → gonadal maturation and production of sex steroids (gonadarche** = breast development, testicular enlargement)

116
Q

Puberty: Night time increases in GnRH pulses →

A

predominantly LH response

Prepuberty: FSH > LH

Puberty: LH > FSH

117
Q

What eventually happens to GnRH pulses in puberty?

A

GnRH pulses eventually continue throughout the da

118
Q

Test of pubertal axis maturation

A

Can test if pubertal axis has matured with leuprolide stimulation test (GnRH analog) to measure LH response

LH > 5 → puberty has begun

Primary response is FSH → prepubertal

119
Q

Adrenarche

A

maturation of adrenal gland (zona reticularis) and production of adrenal androgens (DHEA-S and androstenedione)

Cause the physical signs of pubic hair, axillary hair, body odor, and acne in both boys and girls

120
Q

Juvenile pause

A

HPG axis is active in fetal development and infancy, but enters quiescent state after infancy

121
Q

Delayed puberty

A

lack of onset or lack of normal progression of puberty

Signs:

Boys: no testicular enlargement by age 14

Girls: no breast development by age 13 or no menses after pubertal onset or by age 16 years

122
Q

Causes of delayed puberty

A

lack of pubertal maturation of HPG axis or gonadal dysfunction

123
Q

Hypergonadotropic hypogonadism

GnRH level?
FSH/LH level?

A

(high GnRH)

high FSH and/or LH + impotence

primary gonadal failure

124
Q

Congenital causes of hypergonadotropic hypogonadism (5)

A
  1. Klinefelter’s
  2. Turner
  3. 46 XX or 46 XY gonadal dysgenesis
  4. Testicular regression syndrome
  5. Noonan syndrom
125
Q

Klinefelters:

what is the defect?
what cells are absent, what cells are intact?

Levels of FSH, LH, and testosterone?

A

genetic defect of XXY

Failing testes with no spermatogenic elements

-Dysgenesis of seminiferous tubules –> decreased inhibin B –> increased FSH

Abnormal Leydig cell function –> low testosterone, increased LH, increased estrogen.

HIGH FSH (no inhibin) + NORMAL LH + LOW/NORMAL TESTOSTERONE

126
Q

Testicular regression syndrome is usually due to ___________

A

vascular event

127
Q

Acquired causes of hypergonadotropic hypogonadism (7)

Levels of FSH, LH, and testosterone?

A
  1. Chemo (especially alkylating agents)
  2. Irradiation to pelvic region
  3. Galactosemia
  4. Autoimmune oophoritis
  5. Testicular torsion, trauma
  6. Mumps orchitis
  7. Cryptorchidism

HIGH FSH (early, loss of inhibin), HIGH LH (later), LOW TESTOSTERONE (later)

128
Q

Hypogonadotropic hypogonadism

Level of LH, FSH, and testosterone?

A

LOW GnRH→ congenital or acquired deficits of GnRH and/or LH/FSH (hypothalamic or pituitary problem, central)

low LH, FSH, and Testosterone + impotence

129
Q

Hypogonadotropic hypogonadism is usually due to

A

Usually constitutional delay of growth and puberty (timing/progression of puberty goes with bone age)

Low FSH and LH

TX: testosterone

130
Q

Reversible disorders of hypogonadotropic hypogonadism

A

chronic illness, malnutrition, stress, excessive exercise, anorexia nervosa, hyperprolactinemia, hypothyroidism

-OSA, narcotics, repeated glucocorticoid injections

Hypothyroidism → Low FSH and LH, elevated TSH

131
Q

5 congenital causes of hypogonadotropic hypogonadism

A
  1. Isolated gonadotropin deficiency
  2. Kallman syndrome
  3. Congenital hypopituitarism
  4. Midline CNS defects
  5. prader-willi (why my balls are small. Sorry Maddie)
132
Q

Acquired CNS lesions causing hypogonadotropic hypogonadism

A

1) Pituitary or hypothalamic tumor (prolactinoma)
2) Infiltrative disease (e.g. hemochromatosis)
3) Trauma, irradiation, infection, autoimmune hypophysitis

133
Q

Isolated gonadotropin deficiency

A

Low GnRH in absence of any structural abnormalities of hypothalamus/pit.

Low FSH and LH

134
Q

Kallman syndrome

A

(GnRH deficiency + anosmia)
Agenesis or hypoplasia of olfactory sulci/lobes
Low FSH and LH

135
Q

Evaluation of hyper vs hypogonadism

A

Hypergonadotropic hypogonadism → primary gonadal failure, no negative feedback of sex steroids to brain

Hypogonadotropic hypogonadism → low GnRH levels

136
Q

Other tests for hypogonadotropin

A

Bone age, Pubertal staging, Sense of smell, Thyroid panel, ESR, CBC, BMP, prolactin, testosterone, estradiol, karyotype (if hypergonadotropic)

137
Q

Tx of hypogonadism

A

testosterone replacement therapy (boys), low dose estrogen replacement + cyclic therapy with estrogen and progestin (girls)

138
Q

Precocious puberty

A

pubertal development begins before age 8 (girls) or age 9 (boys)

139
Q

Complete precocious puberty

A

early onset AND progression of pubertal development with evidence of linear growth acceleration and bone age advancement

→ early closure of growth plates, compromised final height

140
Q

incomplete precocious puberty:

A

signs of puberty not progressive= benign premature thelarche, benign premature adrenarche
No treatment required

141
Q

Benign premature adrenarche:

A

pubic hair, acne, etc. development but NO breast or height changes

Prepubertal with FSH > LH
No advanced bone age

142
Q

Premature benign thelarche:

A

no height changes, no pubic hair development, do get breast development

143
Q

Central precocious puberty

A

(gonadotropin-dependent):

premature activation of HPG axis
More common in girls

BOTH breast and pubic hair development or enlargement of testes + growth acceleration

Pubertal response with LH > FSH

Advanced bone age

TX = continuous GnRH agonist

144
Q

Peripheral precocious puberty

A

(gonadotropin-independent): independent of GnRH and gonadotropin stimulation

145
Q

Peripheral precocious puberty in boys (6)

A
  1. Familial toxicosis
  2. hCG secreting tumor
  3. Leydig cell tumor
  4. Congenital adrenal hyperplasia
  5. Adrenal tumor
  6. Exogenous androgens
146
Q

Familial testotoxicosis

A

Mutation of LH receptor causing it to be constitutively activated → Leydig hyperplasia

  • Testes enlarged
  • Penile enlargement, pubic hair development

Suppressed GnRH, elevated testosterone

147
Q

Tx of familial testotoxicosis

A

aromatase inhibitor + androgen blocker/ketoconazole

148
Q

hCG secreting tumor

A

hCG acts like LH and TSH → increased testicular size, with no/decreased adrenarche → disproportionately low degree of virilization

149
Q

Leydig cell tumor

A

Assymetric testes

150
Q

Congenital adrenal hyperplasia

A

secondary sex characteristics (virilization, penile enlargement) without testes enlargement (LH not elevated)

151
Q

Tx of CAH

A

glucocorticoids (suppresses androgens)

152
Q

Peripheral precocious puberty in girls (3)

A

excess estrogens caused by ovarian cyst, ovarian granulosa cell tumor, exogenous estrogens

153
Q

Ovarian cyst

A

signs of estrogenization (breast development, dark areola), no pubic hair, no height acceleration

SHORT time frame of estrogenization

No advanced bone age

Suppressed/prepubertal GnRH in stim test

TX = watchful waiting

154
Q

Peripheral precocious puberty in both boys and girls

A
  1. Hypothyroidism

2. McCune Albright Syndrom

155
Q

Hypothyroidism and precocious puberty

A

TSH > 500

TSH can act like FSH and stimulate FSH receptor → estrogen production (females), enlarged testes/normal T (males)

156
Q

McCune Albright Syndrome

A

cafe-au-lait spots, polyostotic fibrous dysplasia, precocious puberty (breast development, menarche, but NO adrenarche),

due to activating mutation in a-subunit of G protein

Can also get high GH and TH (G-protein mechanism)
Advanced bone age
Suppressed/prepubertal GnRH stim test

157
Q

Tx of McCune Albright

A

Aromatase inhibitor

158
Q

Bilateral testicular enlargement →

A

central precocious puberty, activation of LH receptor by HCG tumor, testotoxicosis, McCune-Albright Syndrome

159
Q

Unilateral testicular enlargement

A

Testicular tumor

160
Q

Evaluation of precocious puberty

A
  1. Bone age, height, growth rate
  2. LH, FSH,
  3. estradiol/testosterone
  4. GnRH stimulation test
  5. Cranial MRI (with central)
  6. Testicular/ovarian ultrasound
161
Q

GnRH Stimulation test:

  • pubertal LH response to GnRh
A

Central precocious puberty

162
Q

GnRH Stimulation test:

  • prepubertal LH response to GnRH
A

Peripheral precocious puberty

163
Q

Goal of tx of precocious puberty

A

arrest/cause regression of signs of puberty, alleviate psychosocial stress of early puberty, slow bone age advancement, preserve final adult height

164
Q

GnRh analogues

A

(IM leuprolide acetate, histrelin implant) used for CENTRAL precocious puberty → down regulate pituitary GnRH receptors → decrease GnRH secretion

165
Q

Aromatase inhibitors

A

(McCune Albright Syndrome) → block conversion of androgens to estrogens

166
Q

Ketoconazole + androgen blocker + aromatase inhibitor

A

→ familial testotoxicosis

167
Q

Conditions of androgen excess

A

Prostate cancer, BPH, androgenetic alopecia, precocious puberty, hirsutism

168
Q

Finasteride

A

inhibits type II 5a-reductase (prevents conversion of T → DHT)
Used to treat prostate cancer

169
Q

Propecia

A

inhibits 5a-reductase

Used to treat hair loss

170
Q

Dutasteride

A

Type I and II 5a reductase inhibitor

Used to treat prostate cancer

171
Q

Conditions of androgen deficiency

A
  • Androgen replacement therapy in hypogonadal boys and men
  • Osteoporosis
  • Muscle wasting with AIDS
  • Hormone replacement therapy in aging men (controversial)
172
Q

MOA testosterone

A

diffuses across membrane → interact with cytosolic receptor → dimerization and binding to DNA response elements → alteration of target gene transcription → growth, differentiation, synthesis of enzymes/functional proteins

Only free, unbound, hormone active

173
Q

Actions of testosterone

A

synthesized in testes (95%) and adrenal (5%) (in women most synthesized in adrenal)

Converted to DHT by 5a-reductase

Converted to Estradiol by aromatase

174
Q

Principles of testosterone tx

A

ONLY in men distinctly subnormal T (<200-300 ng/dL) with multiple occasions with symptoms

Symptoms = low libido, decreased morning erections, low bone mineral density, gynecomastia, small testes, fatigue, depression, anemia, reduced muscle strength, increased fat**

** Mnemonic: Charlie

175
Q

“Hey doc, my spermatogenesis is impaired. Will you prescribe me some of that testosterone stuff?”

A

HELL NO

NOT indicated for impaired spermatogenesis as T suppression of GnRH secretion would further impair spermatogenesis

176
Q

Intramuscular testosterone

A

given every 1-3 weeks

Testosterone ethane, Testosterone cypionate

Less frequent injections → greater fluctuations in serum T levels

177
Q

Transdermal testosterone gel

A

given every 24 hours
Advantage: maintain most stable T levels throughout dosing period

Most expensive

178
Q

Transdermal testosterone patch

A

androderm, applied once daily

Advantage: maintain stable T levels throughout dosing period

Can cause severe rash in ⅓ of patients

179
Q

Subcutaneous testosterone

A

Testopel (pellets) given every 3-4 months as implanted pellets in subdermal fat of buttocks

180
Q

Buccal testosterone

A

tablet 2x a day

181
Q

Nasal testosterone

A

gel administered to nostrils via metered pump 3x daily

182
Q

Oral testosterone

A

methyltestosterone

Hepatic side effects

183
Q

Adverse effects of testosterone

A
  1. Avoid androgens in infants and young
  2. Decreased spermatogenesis:
    - Decreases LH/FSH release (testicular shrinkage)
    - Conversion of androgens to estrogens (gynecomastia)
    - Return to normal function after discontinuation
  3. Reversible cholestatic jaundice (higher with oral agents)
  4. Edema → weight gain
  5. Increased susceptibility to arterial thrombosis (dec. HDL, inc. LDL)
  6. Prostate enlargement
184
Q

MOA Finasteride-dutasteride

A

5a-reductase inhibitors (decreased DHT)

185
Q

Use of Finasteride Dutasteride

A

BPH, androgenetic alopecia

186
Q

Pharmacokinetics of finasteride-dutasteride

A

Orally 1x daily

187
Q

ADR of finasteride dutasteride

A

decreased libido, ejaculatory or erectile dysfunction, weakness

188
Q

MOA Bicalutamide/flutamide

A

androgen receptor antagonist

189
Q

Use bicalutamide/flutamide

A

prostate cancer, hirsutism of PCOS

190
Q

Phamacokinetics of biclutamide/flutamide

A

orally 1x daily

191
Q

ADRs of biclutamide/flutamide

A

androgen deprivation effects (loss of libido, gynecomastia), nausea, transient abnormal LFTs

192
Q

MOA leuprolide

A

GnRH analog

193
Q

Phamacokinetics leuprolide

A

SC or IM

Duration of 1-3-4-6 months

194
Q

Use of leuprolide

A

continuous administration for prostate cancer, precocious puberty in boys

195
Q

ADRs leuprolide

A

headache, nausea, injection site reaction, hypogonadism with prolonged treatment

196
Q

Spirinolactone MOA

A

androgen receptor antagonist

197
Q

Use of spirinolactone

A

prostate cancer, hirsutism in PCOS

198
Q

Pharmacokinetic of spirinolactone

A

orally 1x daily

199
Q

ADRs spirinolactone

A

hyperkalemia, gynecomastia

200
Q

MOA ketoconazole (in reference to antiandrogen effects)

A

inhibits 17a-hydroxylase, inhibits testosterone synthesis

201
Q

Type A spermatogonia: ___N?

A

4N

202
Q

Type A spermatogonia

A

undergo initial mitotic division

Outer region of tubules

True stem cells that can divide mitotically to totipotent progenitors

203
Q

Type B spermatogonia: ___N ?

A

2N

204
Q

Type B spermatogonia

A

commited to meiosis

205
Q

Primary spermatocytes

A

4C (4 chromatids)

Large nuclei
Develop as primary spermatocytes for about 3 weeks → complete meiosis I (crossing over occurs)

206
Q

Secondary spermatocytes

A

primary spermatocytes that have completed meiosis II, only around for about 2 hrs before they become spermatids

207
Q

Spermatids

A
  • haploid, different stages of nuclear condensation toward central part of tubules
  • Have residual body connected (taken up by sertoli cells)
  • Cells derived from a given spermatogonium, remain linked as a syncytium with connected cytoplasmic bridges → RNA exchange between developing haploid spermatids
  • Surrounded by supportive Sertoli cells
208
Q

Sertoli cells (8)

A
  1. have tight junctions, form blood-testes barrier that seal off spermatocytes from immune system
  2. Surround developing spermatid
  3. Spermatogonia at base of seminiferous epithelium are not contained in this barrier
  4. Secrete androgen binding protein into these compartments → sequester high levels of T required for spermatogenic process
  5. Have FSH receptors
  6. Produce inhibin
  7. Provide nutrient to developing spermatocytes and spermatids
  8. Phagocytose residual bodies and degenerating cells
209
Q

Location of Leydig cells

A

outside seminiferous tubules

210
Q

Rete Testes:

A

contain non-motile spermatozoa

  • Lined by cuboidal epithelium with cells have a single cilium
  • Contain connective tissue with myoid cells → contract and aid in moving sperm through channels
211
Q

Ductuli efferentes

A
  • tubule leading from Rete to epididymis
  • Lined by cells that are a mixture of columnar ciliated cells (move immotile sperm along) and cuboidal absorptive cells
  • Coni vasculosi
212
Q

Coni vasculosi

A

part of ductuli efferentes that are outside the testes,
- highly coiled, fuse to form a single epididymal duct

  • Contain band of circularly arranged smooth muscle around each ductule to propel spermatozoa into epididymis
213
Q

Spermatozoa _____ when leaving testes, gain motility en route along _____

A

Spermatozoa non motile when leaving testes, gain motility en route along epididymis

214
Q

Spermatozoa NOT fully capacitated (able to fertilize) until they enter ______

A

Spermatozoa NOT fully capacitated (able to fertilize) until they enter female reproductive tract

215
Q

Epididymis is Lined by _________ epithelium with layer of ________ outside basal lamina → propel spermatozoa along tube

A

Lined by pseudostratified columnar epithelium with layer of smooth muscle outside basal lamina → propel spermatozoa along tube

216
Q

Vas deferens Conducts spermatozoa to ejaculatory duct by ________

A

peristaltic contraction

217
Q

3 layers of muscle in vas deferes

A

inner longitudinal, medial circular, outer longitudina

218
Q

Innervation of vas deferens

A

sympathetic nerves to expel contents into urethra during ejaculation

219
Q

Vas deferens is lined by _____ with _______

A

columnar epithelium

microvillar surface

220
Q

Seminal vesicles

A
  • Paired glands leading to a single vas deferens
  • Glandular structure, highly irregular extension of tissue lined with pseudostratified columnar epithelium with a microvillar surface
  • Outer muscular layer that contracts during ejaculation
221
Q

Prostate glands

A
  • Where ejaculatory duct meets the urethra

- Peripheral glandular tissue which empties via small ducts into urethra and contributes fluid to semen

222
Q

Primordial germ cells in fetus divide to produce ____ → ______ (arrested in ______)
Ceases at around ___ months gestation

A

oogonia → oocytes (arrested in meiosis I)

6 months gestation

223
Q

Primordial follicles

A

4C oocytes surrounded by single layer of flattened follicular cells → over several years acquire outer arrangement of flattened thecal cells

224
Q

After menarche, primary follicles → ____ follicles → ____ proliferate, ____ cells increase and enlarge → ______ follicles

A

After menarche, primary follicles → antral follicles → granulosa cells proliferate, thecal cells increase and enlarge → Graafian follicles

225
Q

Thecal cells contain____

A

vasculature

226
Q

Monthly, one large ______ becomes dominant, increasing in volume to ovulatory stage

A

Graafian follicle

227
Q

Hours prior to ovulation, meiosis___ completed → ___ oocyte → first polar body released

A

Hours prior to ovulation, meiosis I completed → 2C oocyte → first polar body released

228
Q

Second polar body released after

A

oocyte penetrated by sperm → Oocyte then haploid

229
Q

oocyte penetrated by sperm → Oocyte then haploid

A

follicular cells become cuboidal

230
Q

Secondary (preantral) follicles:

A

contain more than one layer of granulosa cells

231
Q

Antral (Graafian) follicles:

A

after puberty, some primary follicles develop to antral follicles → advanced antral (Graafian) follicles due to FSH

232
Q

Atretic follicles:

A

fate of the majority of primary follicles

233
Q

Corpus luteum:

A

after ovulatory follicle releases oocyte, remaining granulosa/thecal cells remodeled into endocrine group of cells

  • Occurs monthly
  • Driven by LH production at Day 12 into cycle = Luteinization
  • Cells become distended by lipid, secrete progesterone and estrogen ⇒ prepare uterine endothelium for implantation
234
Q

No implantation of corpus luteum->

A

corpus albicans

235
Q

Implantation of corpus luteum->

A

enlarges, influenced by HCG to maintain pregnancy

236
Q

Corpus albicans:

A

degenerated corpus luteum if implantation does not occur

237
Q

Germinal epithelium:

A 
mesothelial layer (thin) that lines ovary
Thin so that oocyte can exit ovary
238
Q

Zona pellucida:

A

structured region around oocyte with nutrients

239
Q

Corona radiata

A

ayer of granulosa cells, stay with oocyte even after ovulation

240
Q

Oviduct

A

aka Fallopian tube

Contain fimbriae that embrace ovary, conduct egg to uterus

241
Q

Infundibulum → ______ → ______

A

Infundibulum → ampulla → isthmus

242
Q

Fertilization occurs where?

A

Ampulla

243
Q

Lining of oviduct

A

Mucosal lining highly folded (most in ampulla, least in isthmus)

Ciliated in infundibulum

244
Q

Musculature of oviduct

A

inner circular + outer longitudinal layer of smooth muscle

Contract/agitate inner compartment

Peristalsis + cilia → move egg toward uterus

245
Q

Oviduct, estrogen sensitive or resistant>

A

Sensitive

246
Q

Secretory cells of fallopian tube

A

release protein, sugar, etc. important for egg and sperm viability and fertilization

247
Q

2 zones of endometrium

A

Functionalis and basalis

248
Q

Zona functionalis of endometrium

A

hormonally responsive, cycles monthly from puberty to menopause

  • Contains coiled, tubular glands, lined by epithelium
  • Proliferates as follicle develops in ovary
  • No implantation → menstrual phase
249
Q

Zona basalis of endometrium

A

not shed, contains basal region of endometrial glands

250
Q

Proliferative stage and endometrium

A

zona functionalis proliferates and stroma expands

251
Q

Secretory stage and endometrium

A

driven by progesterone, gland becomes highly coiled, secretes glycoprotein, becomes thicker

  • Spiral arteries develop within uterine stroma
  • No adequate estrogen/progesterone → arteries contract, become kinked → ischemia, necrosis → bleeding
252
Q

Myometrium

A

Bundles of smooth muscle

Hypertrophy and hyperplasia during pregnancy

253
Q

Cervical portion:

A

lined by single layer of tall epithelial cells that extend into deep slit-like invaginations along wall (endocervical mucus glands)

Ends at endo cervix (stratified squamous)

254
Q

Mammary glandular structure:

Before lactation:

A

Glandular tissue arranged as acini with ducts leading to larger ducts → nupple
Acini lined with secretory epithelial cells with outer layer of myoepithelial cells, connective tissue, and adipose tissue

255
Q

Mammary glandular structure:

During lactation:

A

prolactin stimulates milk production → extensive elaboration of glandular tissue filled with milk

Myoepithelial cells under influence of oxytocin contract and propel milk into lactiferous sinuses

256
Q

Spermatogenesis:

spermatogonium (__ploid, _N, _C) stem cell → [Interphase] → primary spermatocyte (__ploid, _N, _C) → [Meiosis I] → secondary spermatocyte (__ploid, _N, _C) → [Meiosis II] → spermatid (__ploid, _N, _C)

A

Spermatogenesis: spermatogonium (diploid, 2N, 2C) stem cell → [Interphase] → primary spermatocyte (diploid, 2N, 4C) → [Meiosis I] → secondary spermatocyte (haploid, 1N, 2C) → [Meiosis II] → spermatid (haploid, 1N, 1C)

257
Q

Proliferative phase of spermatogenesis

A

spermatogonia → spermatocytes

258
Q

3 Types of spermatogonial cells

A
  • Type Ad (dark) → can differentiate into Type Ap
  • Type Ap (pale) → divide by mitosis and give rise to type B
  • Type B → divide to produce preleptotene spermatocytes that enter meiosis
259
Q

Meiotic phase of spermatogenesis

A

spermatocytes undergo meiosis (2C→ 1C)

Spermatid contains prominent round nucleus, golgi apparatus, centrioles, and mitochondria

260
Q

Spermiogenic phase of spermatogenesis

A

spermatids undergo significant morphological changes and mature into spermatozoa

261
Q

Spermatogenesis from spermatogonia → spermatozoa takes __ days

A

64

262
Q

Spermiogenesis

A

spermatid (haploid, 1N, 1C) → mature spermatozoon (haploid, 1N, 1C)

Spermatid matures, elongates, develops flagellum
Once spermatid matures, sperm released into seminiferous tubule out rete testis

263
Q

4 stages of spermiogenesis

A

1) Golgi Phase: formation of acrosomal vesicles by Golgi apparatus → cause centrioles to move to opposite end of nucleus
2) Cap Phase: Acrosomal vesicles become acrosomal cap → will allow the sperm to penetrate egg corona
3) Acrosomal Phase: centriole continues to extend away from nucleus to form flagellum
4) Maturational phase

264
Q

Post-testicular sperm maturation

A

occurs in epididymis

Develop motility, become capable of fertilizing

265
Q

Hormonal Control of Spermatogenesis:

A

Sertoli cells express FSH receptors → FSH stimulation from pituitary
→ androgen binding protein (binds T) → maintain high [androgen] within seminiferous tubules
→ secrete inhibin → negative feedback on FSH from pituitary

Leydig cells → secrete androgens (primarily T) → negative feedback on pituitary to control release of LH

266
Q

Hemochromatosis can cause hypogonadotropic hypogonadism how?

A

Production/release of pituitary LH/FSH blocked
Iron deposits selectively in gonadotropes

+ liver disease, diabetes, CHF

267
Q

Klinefelter’s syndrome

Presentation

A

Presentation: small testes, delayed/incomplete puberty, gynecomastia, eunuchoid body habitus, infertility

  • Tubular fibrosis and destruction of Leydig cells over time
  • Increased risk of breast cancer

HIGH FSH (no inhibin) + NORMAL LH + LOW/NORMAL TESTOSTERONE

268
Q

Congenital anorchia and Vanishing testes syndrome

Levels of LH, FSH, and testosterone

A

insult to fetus before 10-12 weeks gestation interrupts testicular development

HIGH LH AND FSH + LOW TESTOSTERONE

269
Q

Levels of LH, FSH, testosterone, and estradiol in complete androgen insensitivity

A

HIGH LH, FSH, TESTOSTERONE AND ESTRADIOL

No clinical effects of testosterone due to receptor insensitivity/mutation

Life Cycles (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions