repro Flashcards

(194 cards)

1
Q

name the parts of the hip bone

A
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2
Q

name the parts of the pelvic girdle
(anterior view)

hint:
* ischium: (2)
* pubic: (2)
* ischium + pubic: (2)
* ilium: (4)

A
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3
Q

name the parts of the pelvic girdle
(posterior view)

A
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4
Q

differences bet male and female pelvis

A
  • weight: bones of male are heavier
  • shape of pelvic cavity: male’s one is narrow and deep
  • pelvic inlet: male’s one is heart-shaped
  • subpubic angle: male’s one is more acute
  • coccyx: male’s one is less flexible and more curved
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5
Q

what structures form the borders of the pelvic outlet

A
  • pubic symphysis
  • coccyx
  • inferior ramus
    (or ischiopubic ramus)
  • sacrotuberous ligament
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6
Q

what structures form the borders of the pelvic inlet

A
  • pubic symphysis
  • promontory and ala of SACRUM
  • illiopectineal/arcuate lines
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7
Q

ligaments in pelvic wall

A
  • sacrospinous ligament: bet sacrum and ISCHIAL spine
  • sacrotuberous ligament: bet sacrum and ISCHIAK tuberosity
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8
Q

functions of ligaments in pelvic wall

A
  • provide stability to pelvis
  • form passageways (greater and lesser sciatic foramens) for neurovascular bundles to pass through and enter the gluteal, thigh and perineal regions

mainly connecting pelvis to glutes and perineum

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9
Q

muscles that make up the pelvic wall

A
  • piriformis
  • obturator internus

note: piriformis exits via GREATER sciatic foramen and attaches to the FEMUR

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10
Q

(anatomical facts about the pelvic diaphragm/floor:
* muscular partition (i.e. its muscles) consist of (…) and (…)
* innervated by (…) and (…)
* males: (…) hiatus
females: (…) hiatus

A

anatomical facts about the pelvic diaphragm/floor:
* muscular partition (i.e. its muscles) consist of levator ani and coccygeus
* innervated by perineal branch of S4 and pudendal nerve (S2-S4)
* males: 2 hiatus (urethral opening + anal canal)
females: 3 hiatus (extra vaginal opening)

levator ani consists of 3 separate paired muscles: puborectalis, pubococcygeus, iliococcygeus

note:
* the perineal branch of S4 does NOT pass through any foramens,
enter pelvis directly
* pudendal nerve exits through greater sciatic foramen and re-enters through lesser sciatic foramen (recap!)

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11
Q

what is the lateral origin of the levator ani
(i.e. where does it attach to laterally)

A

tendinous arch,
which is the thickened fascia of the obturator internus muscle

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12
Q

functions of pelvic diaphragm
(or pelvic floor)

A
  • support the pelvic viscera
  • resist rise in intra-abdominal and pelvic pressure (e.g. coughing, lifting, straining) by counteracting with CONTRACTION of levator ani
  • helps maintain continence via
    puborectalis keeping the anorectal angle sharp → preventing leakage
    and supporting anal sphincters
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13
Q

what is the part of the pelvis which serves at the main weight-bearing point
(i.e. the part you sit down on)

A

ischial tuberosity

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14
Q

anatomical facts abt pelvis:
* greater sciatic notch is located on (…) surface of (… portion of hip bone …)
* separated from lesser sciatic notch
(which is on (… portion of hip bone …))
by (…) (also on (… portion of hip bone …))

A

anatomical facts abt pelvis:
* greater sciatic notch is located on posterior surface of ilium bone
* separated from lesser sciatic notch
(which is on ischium)
by ischial spine (also on ischium)

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15
Q

what structures pass through the greater sciatic foramen

1 muscle, 2 NAV,1 nerve

A
  • piriformis
  • superior and inferior gluteal NAV
  • pudendal NAV (pudendal nerve + internal pudendal artery/vein)
  • sciatic nerve

  • superior and inferior gluteal NAV: motor innervation and blood supply to glute muscles
  • sciatic nerve: motor AND SENSORY innervation to leg and foot muscles

pudendal nerve EXITS via greater sciatic foramen and RE-ENTERS via lesser sciatic foramen

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16
Q

structures that pass through the lesser sciatic foramen

A
  • obturator internus and nerve supplying it
  • pudendal NAV (pudendal nerve + internal pudendal artery/vein)

  • pudendal NAV: motor (and sensory) innervation and blood supply to perineum, sphincters and external genitalia
    pudendal nerve EXITS via greater sciatic foramen and RE-ENTERS via lesser sciatic foramen

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17
Q

what is the difference between diagonal conjugate and true conjugate

A
  • diagonal conjugate: distance from sacral PROMONTORY to inferior portion of pubic SYMPHYSIS
    ⇒ what you can measure during a physical examination
  • true conjugate: distance from sacral PROMONTORY to closest point of pubic SYMPHYSIS
    narrowest point fetus has to pass through
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18
Q

clinical significance of diagonal and true conjugate

A

use in pelvimetry
* minus off 1.5cm from diagonal conjugate to estimate true conjugate
* if true conjugate < 10.5 cm
cephalopelvic disproportion
(clinically significant mismatch bet size and shape of fetus and maternal birth canal)
⇒ need Cesarean

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19
Q

autonomic innervation of pelvis:
* sympathetic fibers: (…)
* parasympathetic fibers: (…)
* visceral afferent fibers:
1. above (…) follow (…) fibers (lumbar splanchnic) back to T10-L2 spinal segments
⇒ referred pain to lower abdomen, flank, lumbar
2. below (…): follow (…) fibers (pelvic splanchnic) back to S2-S4 spinal segments
⇒ referred pain to perineum and sacral dermatomes

A
  • sympathetic fibers: lumbar splanchnic nerve
  • ParaSympathetic fibers: Pelvic Splanchnic nerve
  • visceral afferent fibers:
    1. above pelvic pain line: follow sympathetic fibers (lumbar splanchnic) back to T10-L2 spinal segments
    2. below pelvic pain line: follow parasympathetic fibers (pelvic splanchnic) back to S2-S4 spinal segments
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20
Q

main artery supplying pelvis

= supplying all the pelvic organs

A

branches of internal iliac artery

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21
Q

which lymph nodes drain the pelvis

= drain all pelvic organs

A

internal iliac lymph nodes

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22
Q

which lymph nodes drain the structures in the perineum

split into 3:
1. majority
2. glans penis and clitoris
3. ovaries and testes

A
  1. majority drained by superficial inguinal lymph nodes
  2. glans penis and clitoris drained by deep inguinal lymph nodes
  3. ovaries and testes drained by para-aortic lymph nodes
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23
Q

Perineum is divided into 2 triangles, urogenital triangle and anal triangle.
What separates them?

A

imaginary line between the 2 ischial tuberosities

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24
Q

what are the contents of the urogenital triangle

A
  • superficial perineal pouch
  • deep perineal pouch
  • external genitalia
  • perineal membrane
  • muscles (in the pouches)
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25
what are the contents of the anal triangle
* anal canal * 2 **ischiorectal fossa**: **fat**-filled spaces lateral to anal canal
26
what is the urogenital diaphragm | and what structures does it contain
* an area directly **inferior to the urogenital triangle** * includes: 1. anterior part of pelvic diaphragm (and fascia in between) 2. deep perineal space 3. perineal membrane 4. superficial perineal space 5. colles fascia
27
structures in deep perineal space
* deep transverse perineal muscles * urethra: specifically **membranous** portion for males * external urethral sphincter * males: **bulbourethral glands** (NOT the duct tho) females: part of **vagina**
28
what nerve is the external urethral sphincter controlled by
pudendal nerve
29
structures in superficial perineal space
* superficial transverse perineal muscles * ischiocarvernosus, bulbospongiosus * perineal branch of **pudendal** nerve and perineal branch of **internal pudendal** vessels * males: root of penis (bulb + cura) females: root of **clitoris** * females: Skene's (para-urethral) gland, greater vestibular gland
30
what does the ischiorectal fossa communicate with | and the clinical implications
* deep post anal space, **posteriorly** * potential space for the **spread of infections** from the anal canal or ischiorectal fossa
31
borders of ischiorectal fossa
32
ischiorectal abscesses: * formed as ischiorectal fossa have (...) * (local/systemic) antibiotics are used to treat it and why
ischiorectal abscesses: * formed as ischiorectal fossa have **poor blood supply** ⇒ predisposed to infection * **CANNOT** be treated by **systemic** antibiotics ← again poor blood supply * need **local** antibiotics and drainage
33
definition of perineal body | what it is + location
tendon located at **junction** of anus (NOT anorectal triangle) and urogenital triangle
34
function of perineal body
serves as point of **attachment** for muscle fibers of 1. external anal sphincter and levator ani 2. deep and superficial transverse perineal muscles 3. bulbospongiosus muscle ## Footnote NOT ischiocavernosus which is more **lateral** and anterior
35
anatomical facts about testes: * located in (...), which is an (...) of anterior abdominal wall * function: (...) * supplied by (...) arteries * drained by (...) → merge into (...) ⇒ drain into (...) ((...) vein drains **directly**, while (...) veins drains into (...) first)
* located in **scrotum**, which is an **outpoutching** of anterior abdominal wall * function: produce **sperm** * supplied by **testicular** arteries * drained by **pampiniform venous plexus** → merge into a pair of **testicular** veins ⇒ drain into **IVC** (**R** vein drains **directly**, while **L** veins drains into L **renal vein** first) ## Footnote Testicular arteries arise DIRECTLY from abdominal aorta, at level of **L2**
36
descent of testes: 1. where is it first located at 2. how does it descent
1. originate from **posterior** abdominal wall, **retroperitoneally** 2. **gubernaculum** anchors the **inferior** pole of the testis to scrotal SKIN 3. **peritoneum** evaginates to form **processus vaginalis** (which creates the future **inguinal canal**) 4. pathway of descent: deep inguinal ring → inguinal canal → superficial inguinal ring → scrotal sac 5. processus vaginalis **obliterates** a few weeks before birth (leaves behind a layer of peritoneum surrounding the testes = tunica vaginalis)
37
how is a **lower temp** maintained at testes | lower than body temp by **2 - 4 ºC**
* cremaster muscle and dartos muscle: (e.g. contraction → draws testes closer → reduce SA of scrotal skin exposed to cold ⇒ conserve heat) * pampiniform plexus: **countercurrent heat exchanger** in which blood flow is in **opp direction** from testicular arteries ⇒ cooler venous blood **cools arterial blood** before it reaches testes
38
difference bet cremaster muscle and dartos muscle | type of muscle + innervation
* cremaster: **skeletal** muscle, innervated by **genitofemoral** nerve * dartos: **smooth** muscle, innervated by **sympathetic** fibers
39
what is the cremasteric reflex: * stimulus * afferent and efferent pathways * spinal cord segments
* stimulus: gentle stroke on **inner thigh** * afferent pathway: **illioinguinal** nerve and *FEMORAL* branch of **genitofemoral** nerve * spinal cord segments involved: **L1 and L2** * efferent pathway: *GENITAL* branch of **genitofemoral** nerve
40
layers of testes
from superficial to deep: 1. skin 2. dartos fascia and muscle 3. colles fascia 4. external spermatic fascia 5. cremaster muscle and fascia 6. internal spermatic fascia 7. tunica vaginalis ## Footnote how does it correspond to layers of abdominal wall: 1. skin → skin 2. **camper's** fascia → **dartos** fascia and muscle 3. **scarpa's** fascia → **colles** fascia 4. external oblique muscle → external spermatic fascia 5. **internal oblique** muscle → **cremaster** muscle and fascia 6. transversalis fascia → internal spermatic fascia 7. tunica vaginalis transversus abdominis does NOT carry on
41
components of testes (including bigger structures and cells)
* tunica ALBUGINEA: (diff from tunica vaginalis) dense **connective tissue** which serves as **outer covering** of testes * **seminiferous** tubules: structures in which **spermatogenesis** takes place, contains **Sertoli cells** * interstitial space (bet tubules): contains **Leydig cells**
42
Sertoli cells: * shape * functions
* **columnal** cells * functions: 1. (MOST IMPT) **support** and **nutrition** of spermatogenic cells 2. form **blood testis barrier** 3. secrete **androgen binding protein** ⇒ keep **high** local conc of **testosterone**
43
Leydig cells: * function * structures they contain
* function: **testosterone** synthesis, produced in presence of **LH** * contain **abundant SER** for steroid hormone (testosterone) synthesis
44
process of spermatogenesis: * whole process takes (...) weeks * process starts during (...), in which **spermatogonium** (germ cells) undergo (...) → become (...) spermatocytes (23 chromosomes, 2C) * (...) spermatocytes (46 chromosomes, 4C) then undergo (...) → become (...) spermatocytes (23 chromosomes, 2C) * 2º spermatocytes then quickly undergo (...) → become (...) (23 chromosomes, C) * (...) then undergo (...) (= maturation/differntiation) in (...) to form (...)
* whole process takes **9-10 weeks** * process starts during **puberty**, in which **spermatogonium** (germ cells) undergo **mitosis** → become **1º** spermatocytes (23 chromosomes, 2C) * 1º spermatocytes (46 chromosomes, 4C) then undergo **1st meiotic division** → become **2º** spermatocytes (23 chromosomes, 2C) * 2º spermatocytes then quickly undergo **2nd meiotic division** → become **spermatids** (23 chromosomes, C) * spermatids then undergo **spermiogenesis** (= maturation/differntiation) in **epididymis** to form **mature spermatozoa** ## Footnote memory tips! * spermato**go**nium = **go**ing to become sperm cell => **germ cell** * spermato*zoon* = *zoom*ing towards oocyte => *final mature form*
45
epididymis: * location * function (overall, head, body, tail)
* located at **superior** and **posterolateral** side of each testes * function: transports sperm from testes **to vas deferens** via 1. head: **receives** SPERMATOZOA **from efferent ductules** 2. body: **maturation** of SPERMATOZOA (develop **motility**) 3. tail: **storage** of SPERMATOZOA until ejaculation
46
histology of epididymis
* **pseudostratified** COLUMNAR epithelium, consisting of 1. **prinicipal** cells which has **stereocilia** to absorb water and residual bodies from testis 2. **basal** cells which **produce new cells**
47
Hydrocele: * abnormal collection of (...) BETWEEN the 2 layers of the (...) of the testis * 2 types: (...) and (...)
* abnormal collection of **serous fluid** BETWEEN the 2 layers of the **tunica vaginalis** of the testis * 2 types: 1. Communicating: where **processus vaginalis** remains **patent**, and hydrocele **changes sizes** around the day (usually smaller in morning, bigger at night) 2. NON-communicating: where processus vaginalis is **closed**
48
what is a varicocele: * definition * cause * appearance * presenting features
* **enlargement** of **pampiniform** plexus * due to **valve failure** * bag of **worms** appearance * presents with sharp to dull **discomfort**, and **worsening** over the DAY
49
contents of spermatic cord
3x3 * arteries: *testicular* artery, artery to *vas deferens*, *cremasteric* artery * nerves: genital branch of genitofemoral nerve, sympathetic and parasympathetic fibers * others: **VAS DEFERENS**, lymphatics (para-aortic), pampiniform plexus ## Footnote * genital branch of genitofemoral: **motor** to cremaster, **sensory** to *scrotum* * sympathetic and parasympathetic: **vasomotor** and **visceral pain** to *testes and epididymis*
50
vas deferens: * structure * function
* **muscular** tube ⇒ strong **peristaltic contraction** to **expel** contents within a very short period * functions to transport sperm cells FROM **epididymis** to **prostatic urethra** * joins with ducts of **seminal vesicles** to open into prostatic urethra
51
histology of vas deferens
* **pseudostratified** COLUMNAR epithelium * epithelium and lamina propria are thrown into **multiple folds** ⇒ allowing **expansion** ## Footnote smooth muscle layer consists of: * inner AND outer longitudinal muscle * thick middle circular layer
52
Testicular torsion: * definition * presenting feature * a/w which abnormality
* **testicle** rotates → twisting **spermatic cord** ⇒ cutting off blood supply * presents w/ ABSENCE of **cremasteric reflex** on affected side * a/w **Bell Clapper abnormality** ⇒ treatment is **bilateral** orchidopexy ## Footnote Bell Clapper abnormality: * abnormally high insertion of tunica vaginalis on spermatic cord ⇒ **increased mobility** of testis * even if torsion occurs on ONE side, other side usually has the **same abnormality** ⇒ thus surgeons fix BOTH testes to the scrotal wall (orchidopexy) to prevent future torsion
53
Cryptorchidism: * definition * a/w (...) * should wait for (...) months in infants for descent before operating
* when testicle **HAS NOT** moved down into scrotum * a/w risk of infertility, testicular cancer, hernia and torsion * should wait for **6 months** in infants for descent before operating
54
prostate gland: * divided into 3 zones: transitional, peripheral and central 1) BPH most commonly @ (...) zone 2) Prostate cancer most commonly @ (...) zone * supplied by (...) and (...) arteries (branches of INTERNAL ILIAC artery) * drained by (...), which communicates with (...) => possible prostate cancer metastasis to (...)
* divided into 3 zones: transitional, peripheral and central 1) BPH most commonly @ **transitional** zone 2) Prostate cancer most commonly @ **peripheral** zone * supplied by **inferior vesicle** and **middle rectal** arteries (branches of INTERNAL ILIAC artery) * drained by **prostatic plexus**, which communicates with **vertebral venous plexus** (**VALVELESS**) => possible prostate cancer **metastasis to spine**
55
histology of prostate gland
* consists of tubuloacinar **glands** * which are double layered: 1) **pseudostratified** COLUMNAR epithelium consisting of **secretory** cells 2) **basal** cells in basement membrane * **corpora amylacea**, which are conc prostatic fluid + glycoproteins + keratan sulfate, may be seen in **lumen** of glands
56
composition of semen fluid (components + %)
* **seminal vesicle** fluid (*70-80%*) * **prostatic** fluid (*30%*) * secretions from **bulbourethral** gland (minor)
57
components of **prostatic** fluid and their functions
* ions: zinc, citric acid, calcium and phosphate → sperm **health** and **motility** * enzymes: **prostate-specific antigen** (PSA) → **liquifies semen** in ejaculate, ALSO used as marker in **prostatic cancer / inflammation** (elevated)
58
secretions of bulbourethral gland and their functions
pre-ejaculatory fluid → **NEUTRALISE ACIDIC** residue in urethra (from urine) AND **lubricates** urethra ## Footnote recall: bulbourethral **gland** is located in **DEEP** perineal pouch, but **duct** is in **SUPERFICIAL** perineal pouch ⇒ opens into **SPONGY** urethra (NOT membranous urethra)
59
components of seminal vesicle fluid and their functions
* FRUCTOSE → major **energy source** for spermatozoa * Prostaglandins → **softens mucus of cervix** ⇒ reduce viscocity and make it easier for sperm to pass through cervix
60
facts about urethra: * (...) is surrounded by the **internal** urethral sphincter while (...) is surrounded by the **external** urethral sphincter * (...) is the **broadest**, most dilatable part of the urethra * spongy urethra is surrounded by (...)
* **pre-prostatic** urethra is surrounded by the **internal** urethral sphincter while **membranous** urethra is surrounded by the **external** urethral sphincter * **prostatic** urethra is the **broadest**, most dilatable part of the urethra * *spongy* urethra is surrounded by **corpus *spongiosum***
61
what happens when there is a RUPTURE in the membranous urethra vs in the spongy urethra
* membranous: blood flows into **pelvic cavity** → **bladder and prostate floating** in blood and urine * spongy: blood flowing into superficial perineal pouch, scrotum, around penis and even **anterior abdominal wall** ## Footnote * **Colles**’ fascia (superficial perineal fascia) is **continuous with Scarpa’s** fascia of the anterior abdominal wall → provides a pathway for urine and blood to spread over penis, scrotum, and **anterior abdominal wall** * **perineal body** acts as a **posterior barrier**, so urine **CANNOT enter deep pelvis** (think of a dam in a river channel)
62
erectile tissues in penis
* corpus **spongiosum**: surrounds **urethra**, has **more elastic tissue** to prevent urethral compression * corpus **cavernosa**: surrounded by **tunica albuginea**
63
parts of penis
* root: **proximal** part, located in **superficial perineal pouch** * body: free part bet root and glans * glans: **bulbous expansion** of **CORPUS spongiosum**, covered by **prepuce** (foreskin)
64
muscles in penis
* ischio*cavernosus*: spirals over CORPORA *cavernosa*, aids **movement** and **support** of erect organ * bulbo*spongiosus*: spirals over CORPORA *spongiosum*, aids in **emptying urethra** (expulsion of semen, last few drops of urine)
65
anatomical facts about penis: * blood supply (artery + vein) * innervation of muscles | plus picture the overall structure of penis
* supplied by **DORSAL** artery * drained by **deep dorsal** vein * innervate by **PUDENDAL** nerve ## Footnote note that dorsal artery ← internal pudendal artery ← internal iliac (thus NOT a direct branch of internal iliac)
66
what is phimosis
inability to retract foreskin
67
mechanism of erection and ejaculation
"*Point* and **Shoot**" * *erection* : *Parasympathetic* fibers are activated (prostatic nerves plexus) → **relaxation** of smooth muscles in **trabeculae** AND **dilation of arteries** (dorsal artery) → **filling** of **cavernous spaces** with blood → blood-filled spaces **compress veins** against **tunica albuginea** ⇒ pool of blood in penis (erection) * **ejaculation**: **Sympathetic** fibers are activated (T11-L2) → closure of **internal urethral sphincter** ⇒ prevents **backflow of semen** into bladder
68
anatomical facts about ovaries: * ligaments * functions * arterial supply * venous drainage
* ligaments: 1. suspended (i.e. hanging off) **posterior** part of **BROAD ligaments** 2. **SUSPENSORY ligaments** of ovary contain ovarian vessels, lymphatics and nerves * functions: 1. produce and release **ova** through **oogenesis** 2. produce and release hormones (**estrogen, progesterone**) * supplied by **ovarian** artery and ovarian branch of **uterine** artery ⇒ form an extensive **anastomosis** * drained by L and R **ovary** veins → R ovary vein drains into **IVC** directly whie L ovary veins drains into L **renal vein** first ## Footnote note: suspensory ligaments of ovary is NOT considered a uterine supporting ligament as * its role is mainly vascular (a conduit for blood/lymph/nerve supply to ovary) * it does not help support the uterus
69
histology of ovaries: 6 components
from outer to inner: * germinal epithelium: **visceral peritoneum** over the tunica albuginea, DOES NOT produce germ cells * tunica albuginea: **surface** of ovary, basically condensed stroma * cortex: contains **ovarian follicles** in **different stages of development** * medulla: loose connective tissue with abundant **blood vessles, lymphatic vessels and nerve fibers** * stroma: found **throughout ovary**, functions as **structural support** and microenvironment for **development and function** * hilum: **entry and exit pt** for blood vessels
70
which part of the ovary is the most common site of origin for **ovarian cancer** | recall **6** components of ovaries!
germinal epithelium
71
describe oogenesis: 1. (...): primordial germ cells undergo (...) to form **1º oocyte** → which undergoes meiosis and is halted at (...) at (...) 2. (...): completes meiosis I to form **2º oocyte** → continues on to meiosis II , resulting in ONE 2º oocyte halted at (...) during (...) 3. (...): completes meiosis II to form (...)
1. **BEFORE birth**: **oogonium** (primordial germ cells) undergo **mitosis** to form **1º oocytes** (23 chromosomes, 2C) → 1º oocytes (46 chromosomes, 4C) then undergo meiosis and are halted at **prophase of meiosis I** at **time of birth** 2. **menstrual cycle**: stimulation by **FSH** allows meiosis I to continue and be completed → form **2º oocyte** (23 chromosomes, 2C) → continues on to meiosis II, resulting in **ONE** 2º oocyte halted at **metaphase of meiosis II** during **ovulation** 3. **fertilisation** (i.e. sperm penetrates oocyte): meiosis II is completed → **ovum** (23 chromosomes, C) is formed
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describe the ovarian cycle: 1. **primordial** follicle: **(...) oocyte** surrounded by **(...) layer(s)** of **(...) follicular** cells 2. **primary** follicle: **(...)** stimulates the primordial follicle to (...) AND (...) layer(s) of flattened cells -> **(...) layer(s)** of (...) cells (= (...) cells), outermost (...) cells form (...) cells 3. **secondary** follicles: a) follicular cells **continue proliferating** to form more layers b) (...) cells secrete fluid -> forms (...) c) (...) cells also convert (...) -> (...), while (...) cells produce (...) 4. **(...)/mature** follicle: a) **antrum increases** in size -> pushes oocyte (...) in follicle b) (...): **innermost** layer of granulosa cells which (...), adjacent to zona pellucida c) (...): **crowded** granulosa cells which **anchor oocyte** to follicle wall, **away from (...)** 5. **ovulation**: (...) follicle **ruptures**, releasing **(...) oocyte** along with (...) and (...) 6. **post-ovulation**: a) ruptured follicle becomes (...) and produces (...) b) if not fertilised, degenerates to form (...)
1. **primordial** follicle: **1º oocyte** surrounded by **single layer** of ***flattened* follicular** cells 2. **primary** follicle: **FSH** stimulates the primordial follicle to **increase in size** AND single layer of flattened cells → **multiple layers** of ***cuboidal/columnar* follicular** cells (= **granulosa** cells), outermost **stromal** cells form **theca** cells 3. **secondary** follicles: a) follicular cells **continue proliferating** to form more layers. b) **granulosa** cells secrete fluid ⇒ forms **follicular antrum** c) **granulosa** cells also convert **androgens → estrogen and progesterone**, while **theca** cells produce **testosterone** 4. **Graafian/mature** follicle: a) **antrum increases** in size ⇒ pushes oocyte **eccentrically** in follicle b) **corona radiata**: innermost layer of granulosa cells which **protects ovum**, adjacent to zona pellucida c) **cumulus oophorus**: crowded granulosa cells which **anchor oocyte** to follicle wall, **away from fluid cavity** 5. **ovulation**: mature/Graafian follicle **ruptures**, releasing **2º oocyte** along with **zona pellucida** and **corona radiata** 6. **post-ovulation**: a) ruptured follicle becomes **corpus luteum** and produces **progesterone** b) if not fertilised, degenerates to form **corpus albicans**
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fallopian tube: * lies BETWEEN the 2 layers of the (...) of the (...) * parts of the tube (lateral -> medial): (5) * fallopian tube opens into (...) through (...) * supplied by (...) * functions: 1) transport (...) 2) transport (...) * sterilisation method = (...)
* lies BETWEEN the 2 layers of the **upper margin** of the **broad ligament** * parts of the tube (lateral → medial): **fimbriae** (end processes of infundibulum) → **infundibulum** → **ampulla** → **isthmus** → **interstitium** * fallopian tube **opens into peritoneal cavity** through infundibulum * supplied by branches of **ovarian artery** * functions: 1) transport **ova** from ovary 2) transport **fertilised** egg to uterus * sterilisation method = **tubectomy** ## Footnote note: **longest** end process (fimbriae) is **attached to ovary** ⇒ helps **“guide” the oocyte** into the tube at ovulation
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histology of fallopian tube
* **simple** COLUMNAR epithelium * consisting of 1. **ciliated** cells (**lightly** stained): aids **movement of ovum** towards uterus 2. **secretory** cells (**dark** stained): secrete **glycoprotein** ⇒ **nutrient** for ovum
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uterus: * structure: (...) is bet uterus and cervix * position: 1) (...): bent over long axis of vagina 2) (...): bent over long axis of cervix * innervated by (...), which carries 1) (...) (sympathetic) 2) (...) (parasympathetic) * implantation site is (...) wall
* structure: INTERNAL **os** is bet uterus and **cervix** * position: 1) anter**Verted**: bent over long axis of **Vagina** 2) ante**fleXed**: bent over long axis of **cerviX** * innervated by **inferior hypogastric** PLEXUS, which carries 1) **lumbar** splanchnic nerve (**sympathetic**) 2) **Pelvic Splanchnic** nerve (**ParaSympathetic**) * implantation site is **upper** and **posterior** wall
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broad ligament: * location (runs from where to where) * function
* runs from **uterus** to **lateral wall** of pelvis * function: **not much support**, but rather contain **uterine vessels, lymphatics and ovarian ligament**
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cardinal ligament: * definition * functions
* thick connective tissue at **base of broad ligament** * functions: 1) **MAJOR support** to uterus 2) contains UTERINE **artery**, as well as UTERINE **veins** ## Footnote uterine artery ← internal iliac artery uterine veins → internal iliac vein
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facts about uterine artery: * uterine artery anastomoses with 1) (...) 2) (...) * runs through cardinal ligament, with (...) passing UNDER it
* uterine artery **anastomoses** with 1) **other** uterine artery 2) superiorly with **ovarian** artery * runs through cardinal ligament, with **ureter passing UNDER it**
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round ligament: * development * parts
* developed from **gubernaculum** * parts: 1) **cranial** end developed into **ovarian** ligament (medially wall of ovary to lateral wall of uterus) 2) **caudal** end developed into **round** ligament of UTERUS (uterus to **labia majora**) ## Footnote pathway of round ligament of uterus: begins at the **lateral** wall of the **uterus** → passes anterolaterally and enters deep inguinal ring → runs through **inguinal canal** → exits via superficial inguinal ring → ends by **merging** with labia majora
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histology of uterus: layers
* *endo*metrium (*innermost*): **simple** COLUMNAR epithelium, contains numerous **tubular glands** * *myo*metrium (*middle*): thick **smooth muscular** layer * *peri*metrium (*outermost*): **connective tissue**
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histology of *endo*metrium ## Footnote recall: *innermost* layer of uterus
from inner to outer: * stratum **basale**: more **cellular**, remains **constant** through whole cycle, **regenerates** endometrium for next cycle * stratum **functionale**: **proliferates, secretes** and **sheds** during menstrual cycle * **simple** COLUMNAR epithelium
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arterial supply of endometrium (5)
uterine artery → arcuate artery → radial artery → spiral and basal arteries * **arcuate** artery supplies **myometrium** * **spiral** arteries supply **functional endometrium** and **respond to hormonal** changes (e.g. drop in progesterone → constriction of arteries → ischaemia → shedding of endometrium ⇒ menses) * **basal** arteries supply **basal endometrium** and is **NOT responsive** to hormones
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changes in endometrium during menstrual cycle
* **proliferative** phase: under influence of **estrogen**, can be divided into 1) **early** proliferative: tubular **glands** and **endothelial cells** proliferate 2) **late** proliferative: glands **coil** and become **CLOSELY PACKED** => **thickening** of endometrium * **secretory** phase: under influence of **progesterone**, glands even **more complexly** coiled (**SAW TOOTH** appearance) => endometrium reaches **maximum thickness**, secretions rich in **glycogen** and **glycoprotein** ## Footnote * Glycogen = **energy** for embryo until placenta takes over * Glycoproteins = adhesion + **immune protection** for implantation
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function of myometrium
during pregnancy, it * **increases** in size through **hypertrophy and hyperplasia** * **muscular contractions** during labour to expel fetus, with **reinforcement** of the contractions by **oxytocin** ## Footnote also note that the contractions during labour reduce blood supply to placenta => thus precipitating its detachment
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parts of cervix (and their respective type of epithelium)
* *endo*cervix: *connects* to **uterus**, **simple** COLUMNAR epithelium * *ecto*cervix: projects ***into* vagina**, non-keratinised **stratified** SQUAMOUS epithelium * **transformation** zone (squamocolumnar junction)
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vagina: * which part is expanded and why * secretions? * pH?
* **upper** end **expanded** ← receives uterine cervix * **no secretory** glands or secretions, but opening is **lubricated** by secretions from **Bartholin's** gland (which lies in superficial perineal space) * **acidic** ⇒ protect from **external pathogens**
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which peritoneal pouch is MOST LIKELY to **accumulate fluid**
rectouterine (**Douglas**) pouch
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blood supply, innervation and lymphatic drainage of vagina
* arterial supply: divided by **pelvic floor**, 1. ABOVE pelvic floor: **uterine** and **vaginal** artery 2. BELOW pelvic floor: **internal pudendal** artery * nerve supply: divided into upper **4/5** and lower **1/5**, 1. UPPER 4/5: **inferior hypogastric** plexus (**stretch** only) 2. LOWER 1/5: **pudendal** nerve (**touch, temp**) * lymphatics: divided into upper **4/5** and lower **1/5**, 1. UPPER 4/5: **iliac** (external + internal) nodes 2. LOWER 1/5: **superficial inguinal** nodes
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histology of vagina
* non keratinised **stratified** SQUAMOUS epithelium * which has cells with a large amt of **cytoplasm** → filled with **glycogen** which they produce ⇒ helps to **maintain pH** ## Footnote how do they maintain pH? cells slough off → glycogen is released into the lumen → normal vaginal flora (Lactobacilli) metabolize glycogen → produce lactic acid ⇒ thus maintaining acidic vaginal pH (~4–4.5)
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external genitalia of female
* mons pubis: **hairy** skin and subcutaneous fat in front of **pubic symphysis** * labia majora: 2 **hair bearing EXTERNAL** skin folds + subcutaneous tissue * labia minora: 2 **hairless** skin folds **within** labia majora * vestibule: area **enclosed by labia minora**, containing opening of **vagina and urethra** * hymen: **covers** part of **vaginal** opening ## Footnote another diff bet labia MAJOR and labia MINORA is their histology! * labia majora: **KERATINISED** stratified squamous epithelium * labia minora: **NON-keratinised** stratified squamous epithelium
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erectile tissue in female
* corpora **cavernosa**: one on each side of urogenital triangle, form the **crura of the CLITORIS** -> each crus attached to **ischiopubic ramus** and anchored to **perineal membrane** * corpua spongiosum: originates from perineal body and splits into 2, form the 2 **bulbs of the vestibule** -> which join tgt to form **glans CLITORIS**
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what is an episiotomy
surgicial incision of **perineum** on **inferoposterior** wall → **enlarge opening** for **baby** to pass through ⇒ thus preventing **multiple tears** ## Footnote Layers incised 1. Skin 2. Subcutaneous tissue 3. Superficial and deep transverse perineal muscles 4. Part of levator ani 5. Posterior vaginal wall
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lymphatic drainage of urethra
* UPPER **1/4**: **internal iliac** nodes * LOWER **3/4**: **superficial** inguinal nodes
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What is the homologue of * scrotum (covering of reproductive organ) * prostate (accessory reproductive organ) * bulbourethral (Cowper's) glands (organ that secretes lubricating fluid during sexual arousal)
* labia **majora** * paraurethral (Skene) glands * greater vestibular (Bartholin's) glands
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What is the most impt gene for sex differentiation? and its gene pdt
sex region Y (**SRY**) gene on **Y chromosome** → encodes for testis determining factor (**TDF**) ## Footnote * other pro-male genes: **S**OX9 (also begin with **S**) * other pro-female genes: *F*OXL2, *W*NT4, *F*ST (all either begin with F or W = *F*emale or *W*omen)
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describe development of internal genital organs
up until 6 weeks: BOTH **wolffian duct** (male internal organs) and **mullerian duct** are present males: PRESENCE of **TDF** → formation of **Sertoli and Leydig** cells → a) **Sertoli** cells produce **Mullerian Inhibiting Substance** (MIS) ⇒ **regression of mullerian** duct b) **Leydig** cells produce **testosterone** ⇒ **wolffian duct develops** into male internal organs females: ABSENCE of TDF → NO Sertoli and Leydig cells → a) no Sertoli so no MIS ⇒ **mullerian duct develops** into female internal organs b) no Leydig so no testosterone ⇒ **regression of wolffian** duct
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breast: * location * lateral and medial borders * posterior muscles * layers
* **2nd to 6th** rib * lateral border: **axillary** tail * medial border: lateral border of **sternum** * posterior muscles: pectoralis major, serratus anterior, external oblique * layers (superficial to deep): 1. nipple, areola, breast 2. **retromammary space, pectoral fascia** 3. pec major, pec minor, chest wall
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arterial supply of breast
* branches of **axillary** artery: superior *thoracic*, acromio*thoracic*, lateral *thoracic* * perforating branches of **internal *thoracic*** * lateral branches of **posterior intercostal** arteries
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lymphatic drainage of breast: 2 main groups and where they drain into
* **superficial** lymphatics: **skin** of breast ⇒ drain into **axillary** lymph nodes * **deep** lymphatics: everything else (parenchyma, **nipple** and **areola**) ⇒ drain into **axillary** or **internal mammary** nodes (**medial** quadrants) * axillary nodes route: anterior, posterior, lateral nodes → **central** node → **apical** node ⇒ **supraclavicular** node * internal mammary nodes may result in **contralateral** spread (i.e. to other breast)
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histology of breast
* parts: 1. **glandular** elements: modified **apocrine sweat** glands 2. **stroma**: connective tissue, adipose tissue and cells (fibroblasts and plasma cells) 3. **STRATIFIED** SQUAMOUS epithelium at **nipple and areola** * what forms the "wall" of each gland? 1. **luminal** cells: **innermost** layer of epithelium, **PRODUCE milk** 2. **myoepithelial** cells: **outermost** layer of epithelium, **contract** for **MILK EJECTION** during lactation 3. basement membrane: produced by myoepithelial cells
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are mammograms more useful in younger or older female patients
older! * **adipose replace fibrous** tissue in stroma with increasing age ⇒ older women have **more adipose** tissue, and thus mammogram can **pick up masses** more easily ## Footnote further explanation: adipose tissue is radiolucent (darker) ⇒ calcifications and small masses (brighter) are detected more easily
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stages of mammary gland: inactive vs active
* inactive (non-pregnancy): normal lobules and stroma (**dense, irregular** interlobular connective tissue) * active (pregnancy and lactation): 1. **more glandular** tissue and less connective tissue 2. glandular tissue: INCREASE in **epithelial and myoepithelial** cells → form more secretory alveoli 3. **interlobular** connective tissue: MORE **plasma cells** → secrete **IgA** into breast milk
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describe 5⍺-reductase deficiency
* mutation of 5⍺-reductase gene → testosterone cannot be **converted** to DHT ⇒ absence of **DHT** * genetic sex: **XY** ⇒ **testes** present * has **testosterone** ⇒ development of **male internal genitalia** * NO **DHT** → **NO** developement of **male EXTERNAL genitalia** ⇒ predominantly **female phenotype** *before puberty* * has **testosterone** ⇒ development of **male secondary sexual characteristics** *after puberty*
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describe Androgen Insensitivity Syndrome (AIS)
* mutation of **androgen receptor** ⇒ inability to respond to androgens (testosterone, DHT) * genetic sex: **XY** ⇒ **testes** present * NON-FUNCTIONAL **testosterone** ⇒ **NO** development of **male internal genitalia** * NON-FUNCTIONAL **DHT** → **NO** development of **male external genitalia** ⇒ predominantly **female phenotype** *before puberty* * NON-FUNCTIONAL **testosterone** ⇒ **NO** development of **male secondary sexual characteristics**; testosterone receptors are unable to detect testosterone → **feedback** to produce **more** testosterone → **high testosterone** → converted to **estradiol** ⇒ development of **female secondary sexual characteristics** *after puberty*
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puberty: progress and its associated physical changes
1. *hypothalamus* **increases** secretion of **GnRH** 2. *anterior pituitary* responds by **progressive secretion** of **FSH and LH**, associated with **increased** secretion of **GH** ⇒ **somatic growth** 3. **increased** secretion of **testosterone/oestrogen** ⇒ development of **secondary sexual characteristics** occurs due to: * males: ***L*H** -(act on)→ ***L*eydig** cells → production of **testosterone**, **F*S*H** -(act on)→ ***S*ertoli** cells → **conversion** of testoterone to estradiol * females: **LH** -(act on)→ **Theca** cells → production of **testosterone**, **FSH** -(act on)→ **Granulosa** cells → **conversion** of testoterone to estradiol ## Footnote involves the Hypothalamic - Pituitary - Gonadal Axis: * Hypothalamus: GnRH * Pituitary: FSH and LH * Gonads: Sertoli, Leydig, Granulosa and Theca cells
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describe Klinefelter syndrome
* genotype: **XXY** => **impairment** of **testes** function, including **testosterone** production * functional hypothalamus and pituitary => *INCREASE FSH and LH* levels in response to **LOWER testosterone** * thus *HYPERgonadotropic* **hypogonadism**
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describe Kallmann syndrome
* mutations of multiple genes -> failure in **GnRH** function (hypothalamus level) => *IMPAIRED FSH and LSH* production * which will subsequently result in **IMPAIRED testosterone** production * thus *HYPOgonadotropic* **hypogonadism**
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difference between primary and secondary amenorrhoea | amenorrhoea = absence of menstrual cycle
* primary: failure of **ONSET** of menstrual cycle by **age 16** * secondary: **ABSENCE** of menstrual cycle for **6 months**
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fertilisation: * location * process: 1. sperm undergoes (...) reaction in female genital tract 2. sperm binds to (...) of egg -> (...) reaction is triggered 3. (...) break down -> allowing entry of sperm 4. 2º oocyte resumes meiosis II 5. male and female (...) are formed and fuse to form (...)
* usually occurs in **ampulla** of fallopian tube * process: 1. sperm undergoes **capacitation** reaction in female genital tract 2. sperm **binds to zona pellucida** of egg -> **acrosomal** reaction is triggered 3. zona pellucida and oocyte membrane **break down** -> allowing **entry of sperm** 4. 2º oocyte **resumes meiosis II** 5. **male and female pronuclei** are formed and **fuse** to form zygote ## Footnote polyspermy is prevented via oocyte preventing entry of more than one sperm via fast and slow block
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when there are **changes in length** of menstrual cycle, which **OVARIAN phase** is affected?
* **follicular** phase ← diff factors (e.g. weight loss, physical activity, stress levels) can affect **FSH secretion** and **follicular growth** rate * **luteal** phase remains **constant** ← **lifespan** of corpus luteum is constant (∼ 14 days)
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negative feedback in HPG axis
males: *testosterone* ⇒ **inhibitory** effect on BOTH hypothalamus and AP females: *oestrogen* ⇒ **inhibitory and stimulatory** effect on BOTH hypothalamus and AP AND *progesterone* ⇒ **inhibitory** effect on BOTH hypothalamus and AP *inhibin* ⇒ **inhibitory** effect on PITUITARY males: *follistatin* ⇒ **inhibitory** effect on PITUITARY females: *activin* ⇒ **stimulatory** effect on PITUITARY | main impt ones are sex hormones and inhibin! ## Footnote * effects of **estrogen**: 1. **majority** (= early-mid follicular + luteal): **inhibits** FSH (and LH) ⇒ prevent development of other follicles 2. ONLY in **midcycle** (= late follicular): **stimulates** LH (and FSH) ⇒ surge in LH for ovulation * all the other hormones (NOT sex hormones) are produced by **sertoli** and **granulosa** cells in males and females respectively
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describe menopause: * age * cause * hormonal changes * effects
* occurs at around **50** y/o * due to the **depletion of oogenesis** (i.e. no responsive follicles left) → ovaries **decrease** production of **oestrogen and progesterone** ⇒ **increase** in **FSH and LH** (loss of inhibitory effect from oestrogen and progesterone) * leads to symptoms like **osteoporosis**, hot flashes, insomnia, depression
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what is involved in implantation, A) zygote B) morula C) blastocyst
C) blastocyst * around **7-10 days** after ovulation * via it binding to endometrium through **special receptor binding** → **trophoblastic** cells (syncytiotrophoblast cells specifically) secreting enzymes to **digest uterine cells** ⇒ blastocyst **invading** into endometrium
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why does menstruation NOT occur when a woman is fully breastfeeding | i.e. lactational amenorrhoea
**increased prolactin** levels → **inhibit** production and secretion of **GnRH** → **decreased oestrogen** lvls → no surge in LH ⇒ NO **ovulation** | considered a **contraceptive** effect!
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how can we classify testicular neoplasms
* seminomatous: originate from **spermatogenic** cells (i.e. cells that form sperm) * sex-cord stroma: originate from **supporting** cells of **seminiferous tubules** * lymphomas: originate from **lymphoid** cells **infiltrating the testis**
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seminomatous vs non-seminomatous germ cell tumours
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important serum markers in testicular neoplasms: * **lactate dehydrogenase**, raised in (2) * alpha-fetoprotein (AFP), raised in (...) * beta human chorionic gonadotrophin (HCG), raised in (...)
* LDH: 1. seminomas 2. lymphomas * AFP: yolk sac tumour * HCG: choriocarcinoma likely MIXED germ cell tumour! | if **> 1** serum marker is elevated, ## Footnote * LDH is raised as 1. tumours **outgrow their blood supply** → **hypoxic** regions → cells rely less on aerobic metabolism and more on **anaerobic glycolysis** ⇒ which is catalysed by **LDH** 2. **reprogramming of energy metabolism** (recall: hallmark of cancer!) where cells **switch to aerobic glycolysis** even in the presence of oxygen (i.e. still have oxygen, but in pyruvate → lactate pathway) ⇒ which is catalysed by **LDH** 3. **high cell turnover** → more cell death/**necrosis** ⇒ **release** of **intracellular** enzymes (like **LDH**) into the bloodstream * choriocarcinoma originates from placenta tissue (trophoblast cells)
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characteristics of yolk sac tumour | think of *SAC*! ## Footnote recall: yolk sac tumour is a **germ cell** neoplasm, specifically **non-seminomatous** in males!
* *S*chiller-Duval bodies = central vessel surrounded by tumour cells (basically the one that looks like a fried egg) * *A*lpha-fetoprotein (AFP) levels raised * *C*hildren (esp neonates up to 6 months)
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pathophysio of BPH
* TOO MUCH **5-α reductase** → stimulate production of **growth factors** → INCREASED **proliferation** of **stroma cells** and DECREASED **cell death** ⇒ **imbalance** bet the two ## Footnote recall! * 5-α reductase helps in conversion of testosterone → DHT * 1 of the functions of DHT is development and growth of prostate gland
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histologic features of BPH
* **hyperplasia** of bilayered **glands** * AND hyperplasia of **stroma** * in *nodular* configuration | ⇒ gross: **enlarged** prostate with *nodules* ## Footnote * preservation of **BOTH layers** indicate that it is **benign**
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symptoms of BPH
compression of prostate on prostatic urethra → **obstruction** ⇒ *hesitation* (← delay in initiating stream), *weak stream* and *straining* (← **increased intra-abdominal pressure** to overcome obstruction) → **incomplete emptying** ⇒ *dribbling* and subsequently *frequency* (← residual urine remaining each time) and *urgency* (← compensatory **detrusor overactivity**) ## Footnote also NOCTURIA which has same mechanisms as **frequency** and *urgency* ← *reduced cortical inhibition* and **increased urine production** at night
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management of BPH
* drugs: 1) **5-α reductase inhibitors** 2) **α blockers** ⇒ mainly work to **relax** smooth muscles in **prostate** * lifestyle: modifications that will **decrease urine production** (less fluid, less alcohol/coffee) ## Footnote alcohol and coffee are diuretics!
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symptoms of prostatic cancer
* most commonly: **NO SYMPTOMS** * metastatic presentations: **back pain** * constitutional presentations (e.g. LOW) * LUTs: similar to BPH ## Footnote back pain: recall that prostate gland is drained by **prostatic plexus**, which has a **VALVELESS communication** with **vertebral venous plexus **
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investigations for prostatic cancer
* digital rectal examination: **hard, uneven** prostate (↔ *firm, smooth* prostate in BPH) * **PSA** levels: **elevated** ## Footnote PSA levels are **more sensitive than specific** bcos other conditions (e.g. BPH, prostatitis) could also present with elevated PSH → elevated PSH = NOT confirm have → does NOT rule *IN* ⇒ NOT *SP*ecific (*SPIN*)
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oestrogen vs progesterone: * effects on libido * effects on cancer risk * effects during pregnancy * effects on lactation
* **libido**: **estrogen increases** (← derivative of testosterone), progesterone decreases * cancer risk: **estrogen increases**, progesterone decreases * pregnancy: **progesterone** 1) maintains **endometrium** 2) reduces **maternal immune response** 3) **decreases** contractility of **uterine smooth muscle** while oestrogen 1) promotes **growth** of UTERUS and UTERINE **blood flow** 2) stimulate **breast cell proliferation** and fat deposition (→ prepare for lactation) * lactation: estrogen stimulate **breast cell proliferation** (i.e. more breast epithelial cells) and **fat deposition** (⇒ enlargement of breasts) while progesterone **converts epithelial cells into secrety cells**, BOTH **INHIBIT lactation**
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what triggers lactation after birth
sudden **reduction** in **oestrogen and progesterone**
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human chorionic gonadotropin (hCG): * produced by (2) * binds to (...) receptor on (...) * function: (...) * used in (...) test
* produced by **syncytiotrophoblasts**, which are initially in implanting **blastocyst** and later in **placenta** * binds to **LH receptor** on **corpus luteum** * function: maintain function of corpus luteum of secreting **progesterone** * used in **urine pregnancy tests** (detected via **immunoassay**) ## Footnote for urine pregnancy tests, * positive results can be as early as **6-8 days** after conception * **false (+)** could be due to malignancy (e.g. **hCG producing tumours** like choriocarcinoma)
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human placental lactogen (hPL): * produced by (...) * function: (...)
* produced by **syncytiotrophoblasts** in **placenta** (ONLY and not implanting blastocyst) * function: supports **foetal nutrition**
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prostaglandins during pregnancy: * produced by (...) * functions and MOA
* produced by **myometrium, decidua and chorion** * functions: 1. stimulate **uterine contractions** (via **increasing Ca2+** in **myometrial** cells to increase **actin and myosin activation**) 2. **cervical ripening** and **dilation**
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relaxin: * produced by (...) * functions and MOA
* produced by **placenta** * functions: bind to **relaxin receptors** on **smooth muscles** ⇒ 1. **cervical ripening** and **softening of pubic symphysis** 2. increase cardiac output, renal blood flow and arterial compliance (= basically **vasodilation**) ⇒ help with **expanded blood vol** and increased metabolic demands during pregnancy ## Footnote can think of it can RELAXin helps one to RELAX during pregnancy and childbirth by helping body adapt and thus making things easier
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oxytocin: * produced by (...) and stored in (...) * functions and MOA
* produced by cells of **SON and PVN** in **hypothalamus** and stored in **posterior pituitary** gland * main functions: 1. **uterine contractions** (via binding to **oxytocin receptors** on **myometrium and endometrium**) 2. milk ejection ## Footnote binding to receptors on endometrium has an **indirect** effect on uterine contractions: binding → stimulates production of **prostaglandins** ⇒ further **enhance** uterine contractions
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complications of placental infection
* intrauterine growth retardation * premature delivery * low birth weight * congenital abnormalities * deafness
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symptoms of eclampsia
* seizures ← **cerebral** vasoplasm and endothelial dysfunction * disseminated intravascular coagulation (DIC) ← activation of **coagulation** ## Footnote pathophysio: abnormal **trophoblast invasion** → spiral arteries remain narrow and high-resistance instead of becoming large and low-resistance → placenta becomes hypoperfused and **ischemic** → **release of factors** into maternal blood by placenta → widespread maternal **endothelial dysfunction** => **HTN** (<- widespread **vasospasm**), **proteinuria** and **edema** (<- increased vascular **permeability**) [triad of pre-eclampsia]
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complications of eclampsia
*HeLLP* syndrome: 1. *H*aemolysis ← **destruction of RBCs** as they pass through blood vessels obstructed by **clots** 2. *e*levated *L*iver enzymes ← **clots** obstructing renal blood flow and resulting in **liver injury** 3. *L*ow *P*latelets ← **platelets** used for **clot** formation | life-threatening, an emergency!
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describe different forms of abnormal placenta: a) abruptio b) percreta/increta/acreta c) previa 1) abnormal **adhesion** due to defective decidua (missing Nitabuch's layer which fns to limit trophoblast invasion) 2) placenta **block** baby as it implants low in the uterus 3) placenta **detaches** from uterus
* 1b * 2c * 3a ## Footnote for abnormal adhesion, * accreta = adhesion * increta = infiltration * percreta = penetration past myometrium into surrounding organs
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hydatidiform moles: * definition * risk factors (3) * types (2)
* caused by abnormal fertilisation -> proliferation of trophoblasts => abnormal placental growth * risk factors: 1. extremes of **pregnancies** (**super young/old**), with **older** patients at higher risk of developing **malignant** complications as well 2. **previous** mole (<-> previous normal pregnancies (= term pregnancies and live births) reduce risk) 3. asians/africans/latin americans * 2 types: 1. complete 2. partial ## Footnote trophoblasts * are outermost layer of cells on blastocyst * produce hCG
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complete vs partial mole
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types of vaginal cancer
* clear cell adenocarcinoma * rhabdomyo(sarco)ma
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# vaginal cancer! pathophysiology of clear cell adenocarcinoma
mother treated w/ **DES** (= synthetic oestrogen) -> **metaplasia** of stratified squamous epithelium into glandular structure in child
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# vaginal cancer! features of rhabdomyo(sarco)ma
* **grape**-like mass * presents in **infants and children**
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pre-cancerous lesion associated with cervix
cervical intraepithelial lesion (CIN)
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# pre-cancerous lesion in cervix risk factors for CIN
* sex * HPV **16** & **18** * co-infection with **HIV**
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# pre-cancerous lesion in cervix screening for patients w/ CIN
look for **HPV** * ages 25-29: **pap** smear cytology, every **3** years * ages > **30**: HPV **DNA** immunohistochemistry, every **5** years
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types of cervical cancer
* Squamous Cell Carcinoma (SCC) * adenocarcinoma
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# cervical cancer features of SCC
* most common cervical cancer! * **cauliflower**-like growth
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types of uterine cancer
* endometrial carcinoma * leiomyo(sarco)ma
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# uterine cancer type I vs type II endometrial carcinoma: * related gene * which has poorer prognosis
* type I: EXCESSIVE **oestrogen** -> hyperplasia => loss of **PTEN** * type II: loss of **P53**, poorer prognosis ## Footnote recall! * loss of PTEN = cells **resist apoptosis** * loss of P53 = cells keep dividing despite **DNA damage**
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risk factors for endometrial cancer
**oestrogen**-related: * **OBESITY** * peri/post-**menopausal** * 2º to oestrogen-producing tumours * oestrogen hormone therapy
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# uterine cancer symptoms for leiomyo(sarco)ma
related to its rapid **enlargement** DURING pregnancy * pain * haemorrhage * bladder compression * spontaneous abortion
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salpingitis: * inflammation of (...) * almost always a component of **PID** * most common cause: (...) — usually (...) and (...) * acute infection -> inflammation -> (...) => (...) resulting in: 1. (...) 2. (...)salpinx: tube fills with (...) 3. (...)salpinx: tube fills with (...) 4. infections spreading to (...) — (...), then to (...) — (...) and finally to (...) — (...)
salpingitis: * inflammation of **fallopian tube** * almost always a component of **PID** * most common cause: **STDs** — usually **chlamydia** trachomatis and neisseria **gonnorhoea** * acute infection -> inflammation -> **adhesions** => **blockage** of tube resulting in: 1. **ectopic** pregnancy 2. **hydro***salpinx*: tube *fills with* **serous fluid** 3. **pyo***salpinx*: tube *fills with* **pus** 4. infections spreading to **PERITONEUM** — peritonitis, then to **liver CAPSULE** — **Fitz-Hugh-Curtis** syndrome and finally to systemic circulation — **bacteraemia/septicaemia** ## Footnote * other causes include objects & fomites, iatrogenic * recall: FHC syndrome involves NORMAL LIVER parenchyma, but "violin-string" adhesions bet liver and abdominal wall, presents w/ RUQ pain
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how does actinomycotic salpingitis differ from the usual salpingitis ## Footnote caused by actinomyces israelii (filamentous, branched, gram pos bacteria)
* results in **CHRONIC invasive** infection instead of an acute mucosal infection * associated w/ **IUD** — intra-uterine device
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treatment for salpingitis
* ceftriaxone => kills N. gonorrhoea * azithromycin => stops growth of obligate *intracellular* C. trachomatis
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cause of a single ovarian cyst
simple ovarian cyst due to early maturation of **Graafian** follicle and then **failure to rupture** -> continuous accumulation of **serous fluid** in **antrum** => enlargement into cyst ## Footnote usually 1-5 cm
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what syndrome could **multiple** ovarian cysts be associated with + its symptoms
PolyCystic Ovarian Syndrome (PCOS) * acne * hirsutism * obesity * (sometimes) 1º amenorrhoea ## Footnote pathophysiology: 1. increased LH: FSH ratio -> theca cells are highly stimulated -> excessive amts of androgens => hirsutism and acne 2. insulin resistance -> hyperinsulinemia -> greater storage of fat => obesity
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which marker can be used to monitoring **epithelial** ovarian cancer?
Cancer-Antigen (CA) **125** <- can rmb as ovarian cancers have 3 categories: thecal (1), granulosa (2) and epithelial (5) ## Footnote not used for diagnosis as not very sensitive or specific e.g. high CA-125 can also be seen in other conditions such as endometriosis, PID, HF, etc
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types of epithelial ovarian cancer
* endometrioid * clear cell * serous * mucinous * Brenner ## Footnote epithelial = **germinal epithelium** which is pluripotent and thus can differentiate into various types of epithelium
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what type of epithelium does each epithelial ovarian cancer have | think abt the structures which they resemble
* endometrioid: **stratified** <- endometrial **glands** * serous: columnar, **ciliated** <- **fallopian tube** * mucinous: columnar, **mucin-producing** <- endocervix/GI * *B*renner: **urothelium** <- organs in urinary tract, e.g. *B*ladder
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compare gross features of the different types of epithelial ovarian cancers
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compare histological features of the different types of epithelial ovarian cancers
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which types of epithelial ovarian cancer are associated w/ endometriosis?
* endometrioid * clear cell * Brenner
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types of granulosa ovarian cancers
* granulosa cell tumour * Sertoli-Leydig cell tumour
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# ovarian cancer genetic mutation associated w/ granulosa cell tumour
FOXL2
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# ovarian cancer histological features of *granulosa* cell tumour
* **Call**-**exner** bodies: "**Call** *granny* **exner**" * Coffee-bean nuclei:
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# ovarian cancer symptoms of granulosa cell tumour
granulosa cells convert androgens -> oestrogen -> increased conversion => increased oestrogen levels * young girls: **precocious** puberty (= EARLY puberty) * reproductive-age women: menstrual irregularities, infertility * post-menopausal women: abnormal uterine **bleeding**, increased risk of **endometrial hyperplasia and CA** ## Footnote these are the core symptoms of unopposed oestrogen! which could be due to increased oestrogen lvls (this case) or just a low progesterone relative to oestrogen
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symptoms of Sertoli-Leydig cell tumour
**stromal** cells **differentiate** into sertoli and leydig cells => overall increased **testosterone** AND **oestrogen** levels * masculinisation (e.g. menstrual irregularities, amenorrhoea, hirsutism, acne, deepening of voice clitomegaly) * some uterine bleeding and endometrial hyperplasia
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inflammatory mastitis: * usually occurs during (...) * pathogenesis: (...) -> (...) enter through **cracked** nipples and proliferate in (...) => infection and inflammation * treatment * complication
* usually occurs during **breastfeeding** early postpartum * pathogenesis: abundant **milk** in secretory units -> bacteria (esp **S. aureus**) enter through **cracked** nipples and proliferate in **stagnant milk** => infection and inflammation * treatment: **CONTINUE breastfeeding** * complication: **abscess**
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most common benign non-proliferative epithelial lesions
fibrocystic change
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pathophysiology (and thus symptoms) of fibrocystic change
* relative excess of oestrogen -> **epithelial hyperplasia** -> ducts become blocked and start ballooning out => formation of **cysts** * cells lining cyst also undergo **apocrine metaplasia** * chronic inflammation caused by trapped fluid => **fibrosis** (of STROMA)
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what could increase risk of fibrocystic change resulting in malignancy
* **EPITHELIAL HYPERPLASIA** * even more if w/ **atypia**
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fibroadenoma: * benign lesion in (...) * present as a (...), well-defined (...) lump * pathophysiology: proliferation of (...) => compressed (...) surrounded by (...)
* benign lesion in **intraLOBULAR stroma** * present as a **FIRM**, well-defined **MOBILE** lump * pathophysiology: proliferation of **glandular** AND **stromal** elements => **compressed ducts** surrounded by pink fibrous stroma ## Footnote * if the breast is a tree, lobule = "leaves" (where milk is actually made) duct = "branches" (the pipes that carry the milk to the trunk/nipple) * both are still lined by double layer of cells (luminal, myoepithelial)
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intraductal papilloma: * benign lesion in (...) * present with (...), (...) * pathophysiology: proliferation of (...) => formation of (...)
* benign lesion in **ducts** * present with **dilated** ducts, **bloody** nipple **discharge** * pathophysiology: proliferation of epithelial cells lining duct => formation of **papillae** w/ fibrovascular core and epithelial lining ## Footnote epithelial includes both luminal epithelial AND myoepithelial
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what condition is associated with **greenish** discharge
ductal ectasia: benign condition where milk **ducts** beneath nipple **dilate** and often fill w/ fluid
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what infectious agents can cross the placenta and cause congenital infection | hint: TORCHeS VPZ
* **T**oxoplasmosis * **O**thers (hep B, listeria, coxsackie virus) * **R**ubella * **C**MV * **H**IV * **H**erpes virus (HSV) **2** * **S**yphilis * **V**ZV * **P**arvovirus B19 * **Z**ika
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what infectious agents are detected during routine antenatal screening tests for pregnant women
* **R**ubella antibody * **H**IV antibody * **S**yphilis antibody * Hep *B* surface **ANTIGEN** & Grp *B* strep (pathogen itself via **vaginal swab**) ## Footnote * method most commonly used is Enzyme ImmunoAssay (EIA), esp for syphilis * Hep B and Grp B are only ones not rlly in TORCHHeS and thus are different
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which types of antibodies give a neonate immunity | from MGAE
* transported from maternal blood -> fetal circulation via **placenta** = Ig**G** * secreted in **milk** = Ig**A** ## Footnote thus if child has Ig**M** against a pathogen = active **infection**
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vaginal discharge: * bacterial (gonorrhoea, chlamydia) * bacterial vaginosis * fungal * protozoa * trichomoniasis
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types of pre-invasive malignant neoplasms
* ductal carcinoma in-situ (DCIS) * lobular carcinoma (LCIS) | where proliferating tumour cels **fill up** ducts or lobules
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DCIS: * features (2) * pattern * ipsilateral/bilateral subsequent cancer?
* features: 1. central **necrosis** 2. **CALCIFICATIONS** * pattern: comedo or cribiform <- INTACT E-cadherin * subsequent cancer is **ipsilateral** only <- INTACT E-cadherin ## Footnote * comedo: cells grow rapidly → central necrosis → debris in duct lumen * cribiform: cells grow around punched-out spaces
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LCIS: * pattern * ipsilateral/bilateral subsequent cancer?
* pattern: solid (uniform, loosely-packed) <- **LOSS** of **E-cadherin** * subsequent cancer can be ipsilateral or **bilateral** <- LOSS of E-cadherin
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which pre-invasive malignant neoplasm, DCIS or LCIS, results in greater risk of subsequent invasive neoplasm?
**D**CIS | it's **D**angerous!
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features of breast cancer
* palpable, hard **mass** (**upper outer** > subareolar) * nipple changes: nipple **retraction**, nipple **discharge** ## Footnote **peau d'orange** skin can occur but rarely
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how do features of **inflammatory** breast cancer differ from the usual (non-inflammatory)
* hallmark sign: **"PEAU D'ORANGE"** skin * breast appears **red, swollen and warm** * NO discrete mass ## Footnote * IBC is due to **lymphatics** being blocked by **tumour emboli** * and is significantly **more aggressive**
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risk factors for breast cancer
* peri**menopausal** age * **obese** * **ovarian** activity: early menarche/late menopause * **previous** breast disease * positive **family** history
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what does triple test in screening of breast cancer involve
* **clinical** assessment: HX, PE * **imaging**: **mammogram**, **US** * pathology: **biopsy**
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how often should screening for breast cancer happen
* **40**-49: every **year** * >**50**: every **2 years**
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tumour staging for breast cancer * at which T (T1-T4) does tumour **extend to skin or chest wall**? * N1, N2 and N3 involve which LNs respectively? ## Footnote recall **TNM**: **T** = **T**umour size **N** = lymph **N**ode metastases **M** = distant **M**etastases
* T**4** * N1: **axillary** N2: A OR **internal mammary** N3: A and IM OR **supraclavicular**
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# breast cancer compare gross appearance of the different types of invasive ductal carcinoma
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# breast cancer compare histological features of the different types of invasive ductal carcinoma
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# breast cancer which type of invasive ductal carcinoma is associated with **BRCA-1** gene
medullary
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what is the most common type (and subtype) of breast cancer
invasive **ductal** carcinoma * most common subtype: **no special type**
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# breast cancer which type of invasive ductal carcinoma has the tendency to metastasise to **axillary** LNs
all invasive breast neoplasms can, but very likely to is **no special type**
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invasive **lobular** carcinoma * common? * gross * histo * pathophysio
* 2nd most common breast cancer * gross: **no palpable mass**, instead just vague skin thickening or "fullness" * histo: **diffuse** infiltration, **SINGE-FILE** OR **"BULL'S EYE"** pattern, minimal desmoplasia * pathophysio: **LOSS** of **E-cadherin** ## Footnote desmoplasia = stroma proliferation around tumour to trap it
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Paget's disease of the nipple: * pathophysio * gross * histo
* **underlying malignancy** (e.g. DCIS, IDC) -> malignant tumour cells **migrate** from original site **through the ducts** and into the **epidermis** of the **nipple and areola** W/O breaching BM * gross: red, scaly/crusty patch on nipple => LOOKS like **eczema** * histo: **large** atypical cells with **clear cytoplasm** ## Footnote differentiate from eczema by the fact that eczema usually involves areola first and spares the nipple
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hormone therapy for breast cancer: * when can it be used * drugs
* when patient is either **Estrogen** Receptor positive (**ER+**), **Progesterone** REceptor positive (**PR+**) or **HER2+** * for ER+ and /or PR+ patients: 1) pre-menopausal: **SERM** (e.g. tamoxifen) => recall: acts as **estrogen antagonist** in **breast** tissue 2) post-menopausal: **aromatase inhibitors** (e.g. anastrozole, letrozole, exemestane) => prevent **conversion of androgens to estrogen** in fat and muscle * for HER2+ patients: HER2 inhibitors (e.g. humanized monoclonal antibody **trastuzumab (aka herceptin)**) => for breast cancers which overexpress **HER2 protein**, which drives **aggressive growth** ## Footnote goal of homone therapy for ER+ and PR+ patients is to** deprive cancer of estrogen**!