TEst II Flashcards

Exam

1
Q
  1. Describe the ureter and how it transports urine from the kidney to the bladder.
A
  1. Describe the ureter and how it transports urine from the kidney to the bladder.

The ureter descends from the kidneys and opens into the posterior base of bladder deep to peritoneum (serous lining that forms membrane).

The urine is propelled by peristalsis of smooth muscle (3 layers)

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2
Q
  1. Describe how the bladder fills in terms of histological changes and autonomic controls
A
  1. Describe how the bladder fills in terms of histological changes and autonomic controls

Bladder & Urinary tract histology
• Transitional epithelium: stratified cells that
accommodate extension during filling
• Invaginated plaques in cell surfaces flatten during cell
stretching; prevent overstretching of cell membranes

BLADDER PHYSIOLOGY
1. Bladder filling is mediated by the
sympathetic nervous system
• Baroreceptor sensory neurons bladder
stimulates sympathetic activity (L1,2) to:
– Relax detrusor muscle (β2)
– Constrict internal urethral sphincter
(α1) to allow filling.
2. Micturition reflexes
• Parasympathetic (S 2,3,4) responses to
baroreceptors trigger alternating
pattern of detrusor contraction and
relaxation (muscarinic).
• Produces pressure waves

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3
Q
  1. What are the pressure waves the precede urination? How are they generated by the ANS?
A
  1. What are the pressure waves the precede urination? How are they generated by the ANS?

Pressure Waves
• With increased expansion, several
reflexes can occur. Contractions
become more forceful until the bladder
can no longer be contained.
3. Voluntary micturition mediated by both
parasympathetic and somatic nerves.
• Parasympathetic activity relaxes the
internal urethral sphincter and contracts
the detrusor muscle.
• Contraction of abdominal muscles
compresses bladder which stimulates
stretch receptors initiating the
micturition reflex
• Pudendal nerve (somatic from S 2,3,4);
voluntary control of external urethral
sphincter.

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4
Q
  1. Describe the anatomy of the uterus, its position in the pelvis, and how that position is maintained.
A
  1. Describe the anatomy of the uterus, its position in the pelvis, and how that position is maintained.

FEMALE INTERNAL
REPRODUCTIVE SYSTEM
Uterus (Sagittal & horizontal views)
• Broad ligament (peritoneum)
• Anteversion - tipped forward
• Anteflexion - fundus pointing foward relative to cervix

• Uterine position maintained by ligaments:
– Cardinal (transverse cervical) ligament
– Uterosacral ligament
– Round ligament of uterus

Uterus (Coronal view)
• Body, isthmus, cervix, fundus
• Endometrium, myometrium
Ovary
• Suspensory ligs.
• Ovarian ligs.
Uterine (Fallopian) tube or oviduct
• Ampulla, infundibulum, fimbria

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5
Q
  1. Describe the anatomy of the uterus, its position in the pelvis, and how that position is maintained.
A
  1. Describe the anatomy of the uterus, its position in the pelvis, and how that position is maintained.

FEMALE INTERNAL
REPRODUCTIVE SYSTEM
Uterus (Sagittal & horizontal views)
• Broad ligament (peritoneum)
• Anteversion - tipped forward
• Anteflexion - fundus pointing foward relative to cervix

• Uterine position maintained by ligaments:
– Cardinal (transverse cervical) ligament
– Uterosacral ligament
– Round ligament of uterus

Uterus (Coronal view)
• Body, isthmus, cervix, fundus
• Endometrium, myometrium
Ovary
• Suspensory ligs.
• Ovarian ligs.
Uterine (Fallopian) tube or oviduct
• Ampulla, infundibulum, fimbria

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6
Q
  1. Describe the different parts of the uterus, uterine tube, and vagina
A
  1. Describe the different parts of the uterus, uterine tube, and vagina

Vagina
• Fornices (sing. fornix): anterior & posterior
• Mucosal layer: rugae
• Smooth muscle forms inner circular and external longitudinal layers

Uterus (Coronal view)
• Body, isthmus, cervix, fundus
• Endometrium, myometrium
Ovary
• Suspensory ligs.
• Ovarian ligs.
Uterine (Fallopian) tube or oviduct
• Ampulla, infundibulum, fimbria

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7
Q
  1. Describe the different parts of the uterus, uterine tube, and vagina
A
  1. Describe the different parts of the uterus, uterine tube, and vagina

Vagina
• Fornices (sing. fornix): anterior & posterior
• Mucosal layer: rugae
• Smooth muscle forms inner circular and external longitudinal layers

Uterus (Coronal view)
• Body, isthmus, cervix, fundus
• Endometrium, myometrium
Ovary
• Suspensory ligs.
• Ovarian ligs.
Uterine (Fallopian) tube or oviduct
• Ampulla, infundibulum, fimbria

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8
Q
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.
A
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.

MALE INTERNAL REPRODUCTIVE SYSTEM
Testis
• Tunica albuginea
• Seminiferous tubules: 1-4 of them contained within 250 lobules
• Rete testes
• Efferent ductules
• Epididymis

Seminiferous tubules
• Spermatogonia → spermatocytes →
spermatids → spermatozoa → mature
sperm cells
• Sertoli cells support sperm generation
• Leydig cells secrete testosterone

Epididymis
• Site for sperm maturation.
• Head, body and tail
• Highly coiled tube 4-6 m long
• Pseudostratified columnar ciliated epithelium

Ductus deferens (bilateral)
• Pass through spermatic
cord and inguinal canal
(see below) to enter
abdomen
• Behind the bladder, they
join with ducts from
seminal vesicles to form
the ejaculatory ducts
• Ejaculatory ducts
penetrate through the
prostate gland into the
prostatic urethra
Semen consists of
• Sperm from testes
• Seminal vesicle secretion
• Prostatic secretion

PROSTATE GLAND
• Gland surrounds prostatic urethra and is
itself surrounded by a CT capsule
– Ejaculatory ducts penetrate through
gland and enter prostatic urethra
• 30-50 tubuloalveolar glands
• Simple columnar epithelial cells secrete
prostatic acid phosphatase (PAP),
fibrinolysin (to liquefy semen), citric acid
and prostate-specific antigen (PSA).
– PSA: indicator for cancer.
• Peripheral zone: Main glands
– Inflammation and cancer
• Central zone: Submucosal glands
• Transitional zone: Mucosal glands
– BPH (benign prostatic hyperplasia)
occurs mainly in central and
transitional zones; can restrict urine
flow.

SEMINAL VESICLES
• Secretes viscous whitish-yellow fluid containing
fructose, prostaglandins, etc that flushes sperm
through urethra
• Ejaculatory & prostatic ducts open out into
prostatic urethra

BULBOURETHRAL
(COWPER’S) GLAND
• Embedded in the external
urethral sphincter and
opens into penile urethra
• Preseminal fluid that
lubricates penile urethra

Spermatic cord passes through inguinal canal & into
scrotum
• Ductus deferens
• Testicular artery from aorta
• Cremaster
• Pampiniform Plexus
Round Ligament of the Uterus:
• Equivalent of the spermatic cord in the female
• Passes through inguinal canal to labia majora

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9
Q
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.

Picture: seminiferous tubules

A
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.

MALE INTERNAL REPRODUCTIVE SYSTEM
Testis
• Tunica albuginea
• Seminiferous tubules: 1-4 of them contained within 250 lobules
• Rete testes
• Efferent ductules
• Epididymis

Seminiferous tubules
• Spermatogonia → spermatocytes →
spermatids → spermatozoa → mature
sperm cells
• Sertoli cells support sperm generation
• Leydig cells secrete testosterone

Epididymis
• Site for sperm maturation.
• Head, body and tail
• Highly coiled tube 4-6 m long
• Pseudostratified columnar ciliated epithelium

Ductus deferens (bilateral)
• Pass through spermatic
cord and inguinal canal
(see below) to enter
abdomen
• Behind the bladder, they
join with ducts from
seminal vesicles to form
the ejaculatory ducts
• Ejaculatory ducts
penetrate through the
prostate gland into the
prostatic urethra
Semen consists of
• Sperm from testes
• Seminal vesicle secretion
• Prostatic secretion

PROSTATE GLAND
• Gland surrounds prostatic urethra and is
itself surrounded by a CT capsule
– Ejaculatory ducts penetrate through
gland and enter prostatic urethra
• 30-50 tubuloalveolar glands
• Simple columnar epithelial cells secrete
prostatic acid phosphatase (PAP),
fibrinolysin (to liquefy semen), citric acid
and prostate-specific antigen (PSA).
– PSA: indicator for cancer.
• Peripheral zone: Main glands
– Inflammation and cancer
• Central zone: Submucosal glands
• Transitional zone: Mucosal glands
– BPH (benign prostatic hyperplasia)
occurs mainly in central and
transitional zones; can restrict urine
flow.

SEMINAL VESICLES
• Secretes viscous whitish-yellow fluid containing
fructose, prostaglandins, etc that flushes sperm
through urethra
• Ejaculatory & prostatic ducts open out into
prostatic urethra

BULBOURETHRAL
(COWPER’S) GLAND
• Embedded in the external
urethral sphincter and
opens into penile urethra
• Preseminal fluid that
lubricates penile urethra

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10
Q
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.
A
  1. Describe in gross and histological terms the anatomy of the testes, how sperm are made and transported out of the seminiferous tubules.

MALE INTERNAL REPRODUCTIVE SYSTEM
Testis
• Tunica albuginea
• Seminiferous tubules: 1-4 of them contained within 250 lobules
• Rete testes
• Efferent ductules
• Epididymis

Seminiferous tubules
• Spermatogonia → spermatocytes →
spermatids → spermatozoa → mature
sperm cells
• Sertoli cells support sperm generation
• Leydig cells secrete testosterone

Epididymis
• Site for sperm maturation.
• Head, body and tail
• Highly coiled tube 4-6 m long
• Pseudostratified columnar ciliated epithelium

Ductus deferens (bilateral)
• Pass through spermatic
cord and inguinal canal
(see below) to enter
abdomen
• Behind the bladder, they
join with ducts from
seminal vesicles to form
the ejaculatory ducts
• Ejaculatory ducts
penetrate through the
prostate gland into the
prostatic urethra
Semen consists of
• Sperm from testes
• Seminal vesicle secretion
• Prostatic secretion

PROSTATE GLAND
• Gland surrounds prostatic urethra and is
itself surrounded by a CT capsule
– Ejaculatory ducts penetrate through
gland and enter prostatic urethra
• 30-50 tubuloalveolar glands
• Simple columnar epithelial cells secrete
prostatic acid phosphatase (PAP),
fibrinolysin (to liquefy semen), citric acid
and prostate-specific antigen (PSA).
– PSA: indicator for cancer.
• Peripheral zone: Main glands
– Inflammation and cancer
• Central zone: Submucosal glands
• Transitional zone: Mucosal glands
– BPH (benign prostatic hyperplasia)
occurs mainly in central and
transitional zones; can restrict urine
flow.

SEMINAL VESICLES
• Secretes viscous whitish-yellow fluid containing
fructose, prostaglandins, etc that flushes sperm
through urethra
• Ejaculatory & prostatic ducts open out into
prostatic urethra

BULBOURETHRAL
(COWPER’S) GLAND
• Embedded in the external
urethral sphincter and
opens into penile urethra
• Preseminal fluid that
lubricates penile urethra

Picture: epididymis

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11
Q

Puberty a. know the basic changes for all people (what comes before what; basic

concepts more than specific steps) b. understand which hormones are responsible for what changes in whom;

know where the hormones come from (ie: hypothalamus vs. ant pit) and what regulates them (releasing hormones, positive and negative feedback etc…)

FEMALE!

A

Puberty a. know the basic changes for all people (what comes before what; basic

concepts more than specific steps) b. understand which hormones are responsible for what changes in whom;

know where the hormones come from (ie: hypothalamus vs. ant pit) and what regulates them (releasing hormones, positive and negative feedback etc…)

FEMALE

B. Female

  1. Timing a. Average for girls is ages 8-13 for onset 2. Initiation of puberty a. Body composition important 1. Fat to lean ratio as well as fat to total body weight a. 20-30% over ideal weight usually have early onset menarche b. Malnutrition will delay menarche c. Well-nourished females with strenuous exercise regimens (thus decreased body fat) have delayed puberty.b. Hormones
  2. Prepubertal: low estrogen causes negative feedback loop with hypothalamic/pituitary (H/P) axis, so low FSH and LH — opposite of post puberty
  3. At pubarche: as critical wt/ body comp achieved, H/P axis less sensitive to low estrogen negative feedback, and GnRH is secreted in increasing amounts
  4. Increased GnRH causes increased gonadotrophins
  5. Adrenal androgens are not strong enough to cause masculinization
  6. Secondary sex characteristics in the female (See Tanner’s Stages illustrations) a. breast tissue changes 1. The first sign of puberty in the female 2. Hormonally stimulated 3. Ultimate size and shape are genetically and nutritionally determined b. Typical feminine body proportions develop
  7. Other physical/ anatomical changes a. Enlargement of labia minora and majora b. Dulling of vaginal mucosa c. Increased vaginal secretion d. Uterine changes e. Ovarian enlargement f. Growth spurt g. Skin changes h. Menarche
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12
Q

Puberty a. know the basic changes for all people (what comes before what; basic

concepts more than specific steps) b. understand which hormones are responsible for what changes in whom;

know where the hormones come from (ie: hypothalamus vs. ant pit) and what regulates them (releasing hormones, positive and negative feedback etc…)

MALES

A

Puberty a. know the basic changes for all people (what comes before what; basic

concepts more than specific steps) b. understand which hormones are responsible for what changes in whom;

know where the hormones come from (ie: hypothalamus vs. ant pit) and what regulates them (releasing hormones, positive and negative feedback etc…)

MALES

C. Male

  1. Timing a. Average for boys is ages 9-14 years for onset
  2. Hormones Controlling Puberty a. Androgens 1. androgen 2. Mostly testicular; mostly testosterone. b. Testicular androgens: testosterone, dihydrotestosterone, androstenedione 1. Testosterone is considered the primary testicular androgen 2. Testosterone is produced in the Leydig cells of the testicles (aka interstitial cells of Leydig) 3. Responsible for male secondary sex characteristics (see below)
  3. In fetal lifea. placental HCG stimulates testes to produce testosterone
  4. Production in puberty stimulated by Ant Pit secretion of gonadotropic hormones 6. Excess testosterone causes epiphyses to close prematurely
  5. Increases basal metabolic rate by up to 15%
  6. Increases red blood cell count
  7. Inhibition of gonadotropins c. Other androgens
  8. Adrenals secrete at least five androgens d. Estrogen 1. Small quantity 2. Probably formed by Sertoli cells and in other tissues (like the liver) and seems to be made by converting testosterone to estradiol e. Initiation of puberty 1. Hypothalamus secretes GnRH which stimulates ant pit to produce FSH and LH2. LH is primary stimulus for testosterone production in the testes 3. FSH stimulates spermatogenesis
  9. Secondary sex characteristics in the male a. Laryngeal changes b. Hair c. Protein anabolism d. Increased sex drive and possibly aggression e. Skin and glandular changes 4. Other physical/ anatomical changes a. Growth spurt 1. Increased GH and IGF-1(insulin-like growth factor) in puberty2. Sex steroids stimulate IGF-1 by increasing GH (which stimulates production if IGF-1) and directly stimulating cartilage to produce IGF-1 b. Change in body composition 1. While males and females are about equal prepuberty, males have about 1.5 times as much lean body mass, skeletal mass, and muscle mass post puberty 2. Increased bone density
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13
Q

II. Gametogenesis a. know the hormones that regulate these processes for everyone b. know the basic terminology (dominant follicle, spermatocyte.. that sort of

thing) and when eggs and sperm are considered functional c. understand the role of: dominant follicle, sertoli cells, corpus luteum,

ejaculation contents d. know the basic features of: mature egg and sperm (ie: zona pellucida,

vitelline membrane, acrosome, head, tail) e. know where sperm are made and stored, what else is ejaculated with them,

and what each fluid contributes to ejaculate

FEMALE!

A

II. Gametogenesis a. know the hormones that regulate these processes for everyone b. know the basic terminology (dominant follicle, spermatocyte.. that sort of

thing) and when eggs and sperm are considered functional c. understand the role of: dominant follicle, sertoli cells, corpus luteum,

ejaculation contents d. know the basic features of: mature egg and sperm (ie: zona pellucida,

vitelline membrane, acrosome, head, tail) e. know where sperm are made and stored, what else is ejaculated with them,

and what each fluid contributes to ejaculate

FEMALE

II. Gametogenesis A. Female (the ovarian cycle) 1. Hormones a. Change daily to create the monthly cycle b. Ovulation requires FSH and LH c. FSH and LH act using second messenger system, activating cAMP d. IGF-1 and IGF-2 stimulate gonadotropin-induced production of steroids, especially progesterone and E2 (estradiol) e. Ovary produces three primary steroids: estradiol, progesterone, androstenadione

  1. Making the ovum a. At birth, the ovary contains 1-2 million oocytes. 1. Oogenesis begins in fetal life. 2. Primordial germ cells (oogonia) migrate to genital ridge where they undergo mitosis. 3. in the 7th month of gestation, oogonia begin meiotic division (becoming haploid, 23X) and become primary oocytes a. Surrounded by follicular cells which multiply and become the cumulus oophorusb. GnRH acting at the ant pit causes release of FSH (and LH) which causes maturation of the primary oocyte into the follicle 1. initially, several follicles begin to develop, under the influence of FSH 2. local factors contribute to the development of a mature follicle 3. FSH stimulates the primordial follicle, causing it to mature into a preantral follicle (aka primary follicle). 4. Primary follicle produces estradiol, which does 3 things: a. Stimulates primary follicle growth b. Reduces follicle atresia c. Increases FSH action on the granulosa cells
  2. testosterone prevents preantral follicle growth and increases follicle atresia. 6. only one follicle will become the dominant follicle 7. at the same time, rising estradiol from the dominant follicle produces negative feedback at ant pit to decrease FSH production .c. Now we have a single dominant follicle 1. Dominant follicle continues to develop because of its increased density of FSH receptors 2. It also has increased vascularity of the theca cells 3. increasing uptake and use of FSH 4. As granulosa cells proliferate, they develop LH receptors 5. Fluid accumulates within the follicular cells 6. Oocyte and cumulus cells move to one side of the developing follicular cavity 7. Rapid accumulation of fluid in the antral cavity and growth of follicular cells causes further enlargement of the preovulatory or graafian follicle
  3. After ovulation 9. Leutenized granulosa cells form the corpus luteum a. CL survives for about 14 days if pregnancy does not occur, and then is gradually replaced by fibrous tissue10. If pregnancy occurs, the corpus luteum will remain functional, producing progesterone, until the placenta takes over this task
    d. Oocyte features 1. Zona pellucida surrounds developing oocyte 2. Under ZP is vitelline membrane, which surrounds ooplasm. Just below this membrane are cortical granules that form as the oocyte matures 3. Follicular fluid contains estrogens, androgens, and proteins

Picture: Month @ a Glance

Hormone, ovary, uterus

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14
Q

II. Gametogenesis a. know the hormones that regulate these processes for everyone b. know the basic terminology (dominant follicle, spermatocyte.. that sort of

thing) and when eggs and sperm are considered functional c. understand the role of: dominant follicle, sertoli cells, corpus luteum,

ejaculation contents d. know the basic features of: mature egg and sperm (ie: zona pellucida,

vitelline membrane, acrosome, head, tail) e. know where sperm are made and stored, what else is ejaculated with them,

and what each fluid contributes to ejaculate

MALE

A

II. Gametogenesis a. know the hormones that regulate these processes for everyone b. know the basic terminology (dominant follicle, spermatocyte.. that sort of

thing) and when eggs and sperm are considered functional c. understand the role of: dominant follicle, sertoli cells, corpus luteum,

ejaculation contents d. know the basic features of: mature egg and sperm (ie: zona pellucida,

vitelline membrane, acrosome, head, tail) e. know where sperm are made and stored, what else is ejaculated with them,

and what each fluid contributes to ejaculate

B. Male

  1. Hormones a. Controlled by hypothalamic/pituitary axis. b. GnRH is the primary controller, via LH, FSH 1. Secreted by arcuate nucleus of the hypothalamus 2. Controls release of LH and FSH 3. FSH & LH are both ant pit hormones, both glycoproteins. 4. FSH and LH act by second messenger system, activating cAMP in the target tissues which activates enzymes in the target cells 5. testosterone is only produced when LH stimulates the Leydig cells 6. testosterone from Leydig cells inhibits GnRH at hypothalamus and thus inhibits LH (& FSH), inhibiting testosterone. c. Specific spermatogenesis controlled by FSH and testosterone 1. FSH binds to receptors on Sertoli cells in seminiferous tubules 2. Testosterone diffuses from Leydig cells into the seminiferous. tubules. 3. Both FSH and testosterone are necessary to initiate spermatogenesis 4. If no sperm are produced by seminiferous tubules, FSH increases. If sperm are produced too fast, FSH is decreased. a. Inhibition: Sertoli cells produce inhibin when spermatogenesis happens too rapidly. 5. Estrogens are also produced by Sertoli cells when they are stimulated by FSH (not direct E production, this is by conversion of T into E). d. M/E factors are thought to contribute, with stress decreasing the output of GnRH. 2. making the super swimmers a. Occurs in seminiferous tubules of the testes b. Seminiferous tubules contain many germinal epithelial cells called spermatogonia
    c. In a nutshell (total of about 74 days): (1) type A spermatogoonium divides 4x —> (16) type B spermatogonia —> migrate to be among Sertoli cells —> 24 day progress among Sertoli cells to become primary spermatocyte —> each primary spermatocyte divides to become (2) secondary spermatocytes (first meiotic division; each now has 23 chromosomes, either 23X or 23Y) —> 2-3 days later, second meiotic division produces (4) spermatids for each primary spermatocyte —> Sertoli cells nurse each spermatid for a few weeks as they gradually become sperm d. Sertoli cells: 1. Large, with overflowing cytoplasmic envelopes that extend from spermatogonal layer to central lumen of seminiferous tubules. 2. Tight barrier of cell membranes to prevent large proteins like immune globulins from getting from capillary bed into tubules3. Envelop developing spermatogonia as they become spermatozoa 4. Spermatogenesis is initiated by FSH acting on Sertoli cells e. Sperm anatomy 1. As they develop from spermatids into sperm, they elongate and become more specialized 2. Head: nucleus of original spermatid thin cytoplasm and cell membrane anterior 2/3 has thick cap called acrosome 3. Tail: aka flagellum central skeleton (axoneme) made of microtubules thin membrane covering axoneme mitochondria surrounding the proximal portion (body) of the tailnormal sperm move in a straight line at about 1-4mm per minute f. After formation in the seminiferous tubules 1. Several day passage through 6 feet of epididymis 2. After 18-24 hours in epididymis, they are capable of motility, though they are kept non-motile until ejaculated 3. Ejaculate content a. Sperm 1. Produced in seminiferous tubules; about 120 million per day 2. mature in epididymis 3. A few are stored in the epididymis, but most are stored in the vas deferens and the ampulla of the vas deferens 4. Can remain fertile in storage for up to a month; with increased sexual activity, may be stored for few days 5. Maintained in a deeply inactive state due to inhibitory proteins in the ducts 6. Ejected from vas deferens, with other fluid form the vas, into ejaculatory duct; this forms 10% of ejaculate7. A few sperm will reach the upper end of the fallopian tube within 5 minutes of ejaculation 8. Sperm can live in the female genital tract for somewhere from 24-72 hours; some sources say possibly longer b. Other fluids in ejaculate & their sources 1. Prostate a. Secretes thin, milky alkaline fluid; about 30% of the total ejaculate b. Fluid contains: 1. Citrate ion 2. Calcium 3. Acid phosphatase 4. Clotting enzyme 5. Profibrinolysin c. Prostate ejects its fluid at the same time as the vas deferens d. Alkaline nature of prostatic fluid seems to be important in neutralizing vaginal pH and fertilizing the egg. 3. Seminal vesicles a. Secretory, not storage of sperm b. Secretes mucoid material that is rich in: 1. Fructose 2. Prostaglandins 3. Finbrinogen c. The last fluid ejected into ejaculatory duct just after vas deferens ejects sperm d. Provides 60% of fluid in ejaculate 4. Bulbourethral glands & other glands a. Secrete small quantity of mucus 4. Semen analysis info a. Statistics 1. Generally considered normal to have 60-150 million sperm per ml of ejaculate; normal ejaculate quantity 1.5-5.5 ml total 2. Considered below minimum standards if fewer than 20 million sperm per cc 3. Normal pH 7.8 - 8.0 4. Morphology (shape): should be more than 30% normal (according to WHO 1992), preferably more than 50% 5. Motility: preferably more than 50% motile6. Grade forward motion/ progression on a scale from 1-4; want to see 2 or better 7. No agglutination, WBCs, or increased viscosity 8. Also look at liquefaction time if the sample is collected in office. Should liquefy in 5-30 minutes after ejaculation b. Things that affect semen analysis 1. Days of abstinence prior to collection 2. Prefer to have average of 3 samples to establish a baseline 3. Method of collection a. Masturbation is preferred; coitus interruptus is acceptable b. Need wide-mouthed clean (not sterile) glass or plastic container c. Temperature during transit is crucial if specimen isn’t collected at the office d. Time from ejaculation to analysis is also important. Need to examine within one
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15
Q

Pituitary, ovarian, and endometrial cycles

A

Pituitary, ovarian, and endometrial cycles

The monthly cycle

a. Understand both ovarian and endometrial cycles and how they overlap (pay close attention to the “month at a glance,” “pituitary, ovarian, and endometrial cycles” and the “overview of hormone regulation/ menstrual & ovarian cycles” charts from your notes.)
b. You might consider being able to label hormones and events and feedback cycles on the handouts/ illustrations.
c. Know the hormones that regulate all of the cycles, the sources of these hormones, stimuli for their release, interactions with target tissues and other hormones, and general feedback loops

The uterine cycle is regulated by the ovarian cycle in healthy females. The ovarian cycle is regulated by hypotahalmus/pituitary axis.

HORMONES:

  1. Hypothalamus

A. GnRH: FSH/LH

  1. Anterior pituitary

A. FSH: Increases estrogen production and ovary

B. LH - stimulates ovulation from corpus luteum.

  1. Ovary

A. Estrogens

Also.. progesterone: secreted by corpus luteum

  1. Functions: Prepares the uterus for pregnancy (secretory phase of menstrual cycle)
  1. The Uterus’ month: the menstrual cycle (aka the endometrial cycle) a. Mean duration is 28 days +/- 7 days b. The month at a glance • days 1-4 or 5: bleeding estrogen & progesterone at their lowest levels due to degeneration of the corpus luteum due to drop in E & P, blood vessels in uterine lining constrict, causing ischemia of endometrium ischemia causes necrosis and desquamation– the bleeding (loss of about 65% on the endometrium in total). The entire functional layer of the endometrium is shed during this process. total blood loss: about 35cc and about 35cc of other fluids (serous fluid mainly), though there is a lot of variation fibrinolysis prevents clots unless there is excessive bleeding. Women with very heavy periods often note passage of clots.vasospasm causing cramps is probably caused by prostaglandins • days 6-13 or so: proliferation increasing estrogen (from granulosa cells of developing follicle) causes thickening of the remaining thin layer of basal tissue in the endometrium. At the end of the proliferative cycle, stringy fertile cervical mucus is secreted. Mucus should be spinnbarkeit at and for 1-2 days preceeding ovulation. FSH stimulates growth of several follicles; one becomes dominant and others undergo atresia increasing estrogen levels days 6-13 causes LH to increase about 2 days before ovulation LH surges about 24-36 hours before ovulation- very high level in a surge pattern, then it drops • day 14 (range generally 12-16; this is a 24-36 hour process): ovulation LH surge causes swelling and rupture of the follicle resulting in ejection of the egg cervical mucus: two types: fertile and non-fertile • days 15-28 or so (post-ovulation): secretory LH causes the follicular cells to become luteal cells, increasing production of progesterone and estrogen (there is still a fair quantity of estrogen produced, but progesterone is dominant in the second half of the cycle) estrogen and progesterone secreted by the corpus luteum slight continued endometrial proliferation due to estrogen progesterone produces increased glycogen and lipid in the endometrium and causes swelling and secretory development to prepare the endometrium for implantation of a fertilized egg E & P have negative feedback to ant pit and as their levels increase, FSH and LH are decreased. By day 22, there is marked edema of the functional layer By day 24, CL hormone production is declining and predecidual changes are beginningFunctional layer of the endometrium begins to shrink, making the endometrial glands become more torturous and saw-toothed Intermittent constriction of the spiral arteries leads to stasis in the capillaries of the functional layer of the endometrium, and this leads to ischemia, extravisation of blood into the stroma, and small hematomas. Eventually, desquamation follows (the bleeding; you’re back to day one) By day 26, lymphocytes (especially PMNs) infiltrate the functional layer As the corpus luteum involutes (when there is no implantation), E&P production decreases and the negative feedback loop is lost, allowing FSH and LH levels to begin to rise again 5. Changes in the event of a pregnancy a. If a blastocyst implants, serum HCG and progesterone increase b. Increase in progesterone produces decidualization of the endometrium. c. The corpus luteum does not involute d. HCG is produced by the chorionic villi of the placenta
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16
Q

Month @ a glance

Hormones, ovary, uterus

A

The monthly cycle

a. Understand both ovarian and endometrial cycles and how they overlap (pay close attention to the “month at a glance,” “pituitary, ovarian, and endometrial cycles” and the “overview of hormone regulation/ menstrual & ovarian cycles” charts from your notes.)
b. You might consider being able to label hormones and events and feedback cycles on the handouts/ illustrations.
c. Know the hormones that regulate all of the cycles, the sources of these hormones, stimuli for their release, interactions with target tissues and other hormones, and general feedback loops

The uterine cycle is regulated by the ovarian cycle in healthy females. The ovarian cycle is regulated by hypotahalmus/pituitary axis.

HORMONES:

  1. Hypothalamus

A. GnRH: FSH/LH

  1. Anterior pituitary

A. FSH: Increases estrogen production and ovary

B. LH - stimulates ovulation from corpus luteum.

  1. Ovary

A. Estrogens

Also.. progesterone: secreted by corpus luteum

  1. Functions: Prepares the uterus for pregnancy (secretory phase of menstrual cycle)
  1. The Uterus’ month: the menstrual cycle (aka the endometrial cycle) a. Mean duration is 28 days +/- 7 days b. The month at a glance • days 1-4 or 5: bleeding estrogen & progesterone at their lowest levels due to degeneration of the corpus luteum due to drop in E & P, blood vessels in uterine lining constrict, causing ischemia of endometrium ischemia causes necrosis and desquamation– the bleeding (loss of about 65% on the endometrium in total). The entire functional layer of the endometrium is shed during this process. total blood loss: about 35cc and about 35cc of other fluids (serous fluid mainly), though there is a lot of variation fibrinolysis prevents clots unless there is excessive bleeding. Women with very heavy periods often note passage of clots.vasospasm causing cramps is probably caused by prostaglandins • days 6-13 or so: proliferation increasing estrogen (from granulosa cells of developing follicle) causes thickening of the remaining thin layer of basal tissue in the endometrium. At the end of the proliferative cycle, stringy fertile cervical mucus is secreted. Mucus should be spinnbarkeit at and for 1-2 days preceeding ovulation. FSH stimulates growth of several follicles; one becomes dominant and others undergo atresia increasing estrogen levels days 6-13 causes LH to increase about 2 days before ovulation LH surges about 24-36 hours before ovulation- very high level in a surge pattern, then it drops • day 14 (range generally 12-16; this is a 24-36 hour process): ovulation LH surge causes swelling and rupture of the follicle resulting in ejection of the egg cervical mucus: two types: fertile and non-fertile • days 15-28 or so (post-ovulation): secretory LH causes the follicular cells to become luteal cells, increasing production of progesterone and estrogen (there is still a fair quantity of estrogen produced, but progesterone is dominant in the second half of the cycle) estrogen and progesterone secreted by the corpus luteum slight continued endometrial proliferation due to estrogen progesterone produces increased glycogen and lipid in the endometrium and causes swelling and secretory development to prepare the endometrium for implantation of a fertilized egg E & P have negative feedback to ant pit and as their levels increase, FSH and LH are decreased. By day 22, there is marked edema of the functional layer By day 24, CL hormone production is declining and predecidual changes are beginningFunctional layer of the endometrium begins to shrink, making the endometrial glands become more torturous and saw-toothed Intermittent constriction of the spiral arteries leads to stasis in the capillaries of the functional layer of the endometrium, and this leads to ischemia, extravisation of blood into the stroma, and small hematomas. Eventually, desquamation follows (the bleeding; you’re back to day one) By day 26, lymphocytes (especially PMNs) infiltrate the functional layer As the corpus luteum involutes (when there is no implantation), E&P production decreases and the negative feedback loop is lost, allowing FSH and LH levels to begin to rise again 5. Changes in the event of a pregnancy a. If a blastocyst implants, serum HCG and progesterone increase b. Increase in progesterone produces decidualization of the endometrium. c. The corpus luteum does not involute d. HCG is produced by the chorionic villi of the placenta
17
Q

The monthly cycle

a. Understand both ovarian and endometrial cycles and how they overlap (pay close attention to the “month at a glance,” “pituitary, ovarian, and endometrial cycles” and the “overview of hormone regulation/ menstrual & ovarian cycles” charts from your notes.)
b. You might consider being able to label hormones and events and feedback cycles on the handouts/ illustrations.
c. Know the hormones that regulate all of the cycles, the sources of these hormones, stimuli for their release, interactions with target tissues and other hormones, and general feedback loops

A

The monthly cycle

a. Understand both ovarian and endometrial cycles and how they overlap (pay close attention to the “month at a glance,” “pituitary, ovarian, and endometrial cycles” and the “overview of hormone regulation/ menstrual & ovarian cycles” charts from your notes.)
b. You might consider being able to label hormones and events and feedback cycles on the handouts/ illustrations.
c. Know the hormones that regulate all of the cycles, the sources of these hormones, stimuli for their release, interactions with target tissues and other hormones, and general feedback loops

The uterine cycle is regulated by the ovarian cycle in healthy females. The ovarian cycle is regulated by hypotahalmus/pituitary axis.

HORMONES:

  1. Hypothalamus

A. GnRH: FSH/LH

  1. Anterior pituitary

A. FSH: Increases estrogen production and ovary

B. LH - stimulates ovulation from corpus luteum.

  1. Ovary

A. Estrogens

Also.. progesterone: secreted by corpus luteum

  1. Functions: Prepares the uterus for pregnancy (secretory phase of menstrual cycle)
  1. The Uterus’ month: the menstrual cycle (aka the endometrial cycle) a. Mean duration is 28 days +/- 7 days b. The month at a glance • days 1-4 or 5: bleeding estrogen & progesterone at their lowest levels due to degeneration of the corpus luteum due to drop in E & P, blood vessels in uterine lining constrict, causing ischemia of endometrium ischemia causes necrosis and desquamation– the bleeding (loss of about 65% on the endometrium in total). The entire functional layer of the endometrium is shed during this process. total blood loss: about 35cc and about 35cc of other fluids (serous fluid mainly), though there is a lot of variation fibrinolysis prevents clots unless there is excessive bleeding. Women with very heavy periods often note passage of clots.vasospasm causing cramps is probably caused by prostaglandins • days 6-13 or so: proliferation increasing estrogen (from granulosa cells of developing follicle) causes thickening of the remaining thin layer of basal tissue in the endometrium. At the end of the proliferative cycle, stringy fertile cervical mucus is secreted. Mucus should be spinnbarkeit at and for 1-2 days preceeding ovulation. FSH stimulates growth of several follicles; one becomes dominant and others undergo atresia increasing estrogen levels days 6-13 causes LH to increase about 2 days before ovulation LH surges about 24-36 hours before ovulation- very high level in a surge pattern, then it drops • day 14 (range generally 12-16; this is a 24-36 hour process): ovulation LH surge causes swelling and rupture of the follicle resulting in ejection of the egg cervical mucus: two types: fertile and non-fertile • days 15-28 or so (post-ovulation): secretory LH causes the follicular cells to become luteal cells, increasing production of progesterone and estrogen (there is still a fair quantity of estrogen produced, but progesterone is dominant in the second half of the cycle) estrogen and progesterone secreted by the corpus luteum slight continued endometrial proliferation due to estrogen progesterone produces increased glycogen and lipid in the endometrium and causes swelling and secretory development to prepare the endometrium for implantation of a fertilized egg E & P have negative feedback to ant pit and as their levels increase, FSH and LH are decreased. By day 22, there is marked edema of the functional layer By day 24, CL hormone production is declining and predecidual changes are beginningFunctional layer of the endometrium begins to shrink, making the endometrial glands become more torturous and saw-toothed Intermittent constriction of the spiral arteries leads to stasis in the capillaries of the functional layer of the endometrium, and this leads to ischemia, extravisation of blood into the stroma, and small hematomas. Eventually, desquamation follows (the bleeding; you’re back to day one) By day 26, lymphocytes (especially PMNs) infiltrate the functional layer As the corpus luteum involutes (when there is no implantation), E&P production decreases and the negative feedback loop is lost, allowing FSH and LH levels to begin to rise again 5. Changes in the event of a pregnancy a. If a blastocyst implants, serum HCG and progesterone increase b. Increase in progesterone produces decidualization of the endometrium. c. The corpus luteum does not involute d. HCG is produced by the chorionic villi of the placenta
18
Q

IV. Sex a. Understand the triggers & mechanisms for arousal, plateau, orgasm, and

resolution for all genders b. Understand the neurological controls and hormonal controls of all the

above (in item a)

A

IV. Sex a. Understand the triggers & mechanisms for arousal, plateau, orgasm, and

resolution for all genders b. Understand the neurological controls and hormonal controls of all the

above (in item a)

IV. Sex A. Generalities (apply to all sexes) 1. Arousal a. Both psychological and physical stimulation required for successful arousal & completion of the sex act b. basic physiological changes include vasoconstriction and neuromuscular tension which do the following: 1. Vasoconstriction: increased blood to genital tissues 2. Neuromuscular tension: buildup of excitement throughout entire body

B. Her side 1. Sexual response cycle a. Desire 1. Varies during the month for women, with peak around ovulation b. Arousal (aka excitement phase) 1. Physical/ psych stimulus via nervous system 2. local stimulation of external structures via touch of a variety of sorts (massage, irritation)3. Parasympathetic activity causes changes in the local tissues a. Dilation of erectile tissues around introitus & eventually in vagina provide engorgement and lubrication b. Plateau phase (according to Masters & Johnson) c. Orgasm 1. Rhythmic contractions of perineal muscles and probably uterus and uterine tubes, followed by rapid relaxation 2. Dilation of cervical canal, allowing sperm to pass through more easily (lasts up to 30 minutes) d. Resolution 1. Vasoconstriction resolves as contractions pump blood out of tissues 2. Decrease in HR, RR, BP 3. Time required to reach end of resolution phase increases if no orgasm occursC. His side 1. Sexual response cycle a. Desire 1. No apparent monthly cycle b. Arousal 1. Physical / psych stimulus via nervous system 2. Local stimulation of all external genital structures 3. Parasympathetic activity causes changes in local tissues a. Erection (dilation of erectile tissues) b. Plateau phasec. Orgasm 1. Emission and ejaculation are separate functions 2. Emission is combination of contractions and secretions from various glands prior to ejaculation of semen from the penis 3. Ejaculation reflex d. Resolution

19
Q

V. Conception & the placenta

a. Understand the basic mechanisms of: ovulation, fertilization, egg transport, implantation, including the following:
i. When each will happen ii. How long they take if they take a span of time (ie: not really an

issue with ovulation, but is from fertilization to implantation) iii. Where each occurs iv. Hormonal and mechanical mechanisms mentioned in lecture to aid

fertilization, blastocyst development, sperm transport, implantation b. understand the hormones that support the implanted embryo where they

come from, and how they are maintained

A

V. Conception & the placenta

a. Understand the basic mechanisms of: ovulation, fertilization, egg transport, implantation, including the following:
i. When each will happen ii. How long they take if they take a span of time (ie: not really an

issue with ovulation, but is from fertilization to implantation) iii. Where each occurs iv. Hormonal and mechanical mechanisms mentioned in lecture to aid

fertilization, blastocyst development, sperm transport, implantation b. understand the hormones that support the implanted embryo where they

come from, and how they are maintained

V. Pregnancy A. Conception 1. Ovulation occurs and the ovum is moved from the peritoneal cavity into the ampulla of the fallopian tube 2. As many as 98% of ovulated ova are swept into the tube3. Fertilization a. After ejaculation, sperm move through uterus to the ampullae at the ovarian ends of the fallopian tubes b. Usually occurs very soon after ovum enters the ampulla c. Sperm penetrates corona radiata then binds to and penetrates the zona pellucida d. After sperm enters ovum, sperm head swells, forming a pronucleus 4. Transport and implantation a. It takes from 3-4 days from fertilization until the egg has traveled through the tube to the uterus b. Development along the way 1. Divides until it has about 100 cells 2. Called blastocyst 3. Fed by secretions from fallopian tube c. Once in the uterus 1. Remains in the uterine cavity for another 2-4 days 2. Implantation occurs around day 7 after ovulation 3. Progesterone is enriching the uterine environment 4. Columns of trophoblast cells (cytotrophoblasts) develop on the surface of the blastocyst to facilitate implantation a. secrete proteolytic enzymes b. Trophoblast cells multiply rapidly after implantation c. Where trophoblast attaches, part differentiates and becomes syncytiotrophoblast. This is the only part in direct contact with maternal circulation B. Hormones of early pregnancy 1. Corpus luteum is still pumping out progesterone and estrogen, and implantation causes production of hCG from the developing placenta 2. hCG produced within 24 hours of implantation 3. hCG produces positive feedback to ovary to sustain the corpus luteum 4. Increasing hCG causes increasing steroid production from the corpus luteum 5. Progesterone is the most important hormone for sustaining the pregnancy at this point 6. Eventually CL function declines, despite continued hCG production 7. Once CL is not supporting the pregnancy, the placenta should be functional and supports the pregnancy for the duration 8. CL also produces relaxin, a protein hormone that ripens the cervix, softens the pubic symphysis, and helps progesterone to prevent uterine contractions

20
Q

b. understand the hormones that support the implanted embryo where they

come from, and how they are maintainedc. know the basic functions of the placenta d. know where HCG is produced and what it does e. know, generally, what things can cross the placenta f. know what sort of placental problems can affect fetal growth (not a lot of

detail, but the basics)

A

b. understand the hormones that support the implanted embryo where they

come from, and how they are maintainedc. know the basic functions of the placenta d. know where HCG is produced and what it does e. know, generally, what things can cross the placenta f. know what sort of placental problems can affect fetal growth (not a lot of

detail, but the basics)

C. The placenta & the feto-placental unit 1. Basic A & P a. Main function is to establish and maintain communication between mother and fetus through the pregnancy in three basic ways: 1. Secretion of proteins and steroid hormones into maternal circulation2. Control of fetal endocrine function, growth, and development 3. Acting as a selective barrier b. Maintains immune and genetic integrity of the two individuals involved c. At the site of implantation, some cytotrophoblasts differentiate into the syncytiotrophoblast. 1. in direct contact with maternal circulation 2. major site of placental hormone production 3. Blastocyst implants in endometrium with embryonic pole toward the endometrium 4. Stromal (CT) cells at site of implantation have lots of glycogen and lipids to feed developing embryo 5. Lacunae (cavities in the syncytiotrophoblast) develop as fetus develops 6. Syncytiotrophoblast produces hCG d. Placenta is not a filter 1. Nutrients and oxygen from maternal blood 2. Waste products and carbon dioxide from fetal circulation 3. Basic structure allows for very large surface for gas/ nutrient exchange without actual mixing of maternal and fetal blood a. Maternal side 1. endometrial spiral arteries push blood into villous spaces 2. Blood eventually passes back into endometrial veins and back to maternal circulationb. Fetal side 1. Poorly-oxygenated blood from fetus goes into umbilical arteries 2. Well-oxygenated blood is passed into the umbilical vein c. Placenta’s intervillous spaces contain about 150 cc of blood; supply is replaced 3-4 times per minute 4. Fetal development is most dependent on adequate blood supply to chorionic villi. 5. Mechanisms of placental transport of substances a. The usual suspects: simple diffusion, facilitated diffusion, active transport, pinocytosis 6. Things that can pass through the placental barrier a. Most drugs, licit and illicit b. Many viruses & other infectious agents 1. See teratogenicity section at end of notes c. Nutrients d. Hormones e. Electrolytes f. Maternal antibodies g. Gases h. Waste products e. After the baby’s done with it, the placenta is shed

21
Q

VI. embryology

a. know the concepts underlying teratogenicity, but do not need to know the specific timing for damage to any organ or system.

A

VI. embryology

a. know the concepts underlying teratogenicity, but do not need to know the specific timing for damage to any organ or system.
a. The developing embryo does not develop birth defects in response to teratogens until 4 weeks gestation (2 weeks after conception) 2. structures are most vulnerable early in their development
4. Teratogenicity: three main concepts a. Is the agent present during a critical period of development? b. Is the dosage of the drug, chemical, or substance adequate to produce adverse effects in the fetus? c. Is the embryo genetically susceptible to this teratogen?

22
Q

Ovary in Ordinary Adult cycle

A

Ovary in Ordinary Adult cycle

General suggestions: Understand all hormones, their regulation (up and down), their sources and functions, where they act

Go for concepts and sequences more than for specific timing. For example, I don’t think it’s critical to know how many hours sperm spend in the vas deferens, but it is important to understand that they have a couple of long­ish periods of maturation required to become functional, and it’s important to know where those maturation periods occur more than exactly how long they take.

Refer to those illustrations mentioned. Be very familiar with them.