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GI/Endo/Repro > Assessment 5 > Flashcards

Assessment 5 Flashcards

1
Q

Boundaries of Pelvic inlet: Pelvic Brim

A

Pubic crest
Pectineal line
Arcuate line
Ala and promontory of sacrum

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2
Q

Boundaries of pelvic outlet

A 
Inferior end of pubic symphysis
Ischiopubic ramus
Ischial tuberosity
Sacrotuberous ligament
Tip of coccyx
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3
Q

Pelvis Major

A

False pelvis, above pelvic aperture

Part of abdominal cavity, abdominal viscera

Lateral: Iliac fossa
Posterior: L5 and S1
Anterior: Abdominal wall

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4
Q

Pelvis Minor

A

True pelvis, inferior to pelvic inlet

Inferior limit: inferior pelvic aperture/Pelvic brim

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5
Q

Conjugate diameter

A

Distance between sacral promontory and thickest portion of pubic symphysis

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6
Q

Greater sciatic foramen

A

Created by greater sciatic notch and sacrospinous ligament

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7
Q

Lesser sciatic foramen

A

Lesser sciatic notch
Sacrospinous ligament
Sacrotuberous ligament

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8
Q

Anterolateral wall of pelvis

A

Pubic bones
Portion of ischia
Obturator internus muscle
Lesser sciatic foramina

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9
Q

Posterolateral wall of pelvis

A

Pelvic surface of sacrum
Grater sciatic foramina
Priformis muscle

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10
Q

Structures originating from posterolateral wall exit…

A

Greater sciatic foramen

Piriformis muscle
Nerves of lumbosacral plexus
Arteris

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11
Q

Structures originating from anterolateral wall exit…

A

Lesser sciatic foramen

Obturator internus tendon

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12
Q

Pelvic diaphragm components

A

Levator ani

Coccygeus

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13
Q

Levator ani components

A

Pubocorectalis
Pubococcygeus
Iliococcygeus

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14
Q

Pubocorectalis

A

Puborectal swing, involved with incontinence

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15
Q

Origin of iliococcygeus

A

Arises from tendinous arch which comes from fascia of obturator internus

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16
Q

Coccygeus origin and insertion

A

Ischial spine to coccyx

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17
Q

Pelvic diaphragm - male

A

Urogenital diaphragm

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18
Q

Ureters: 3 constrictions

A

Ureteropelvic junction

Pelvic brim

Ureterovesical junction (bladder)

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19
Q

Parts of bladder

A

Detrusor muscle
Internal sphincter
Ureteric orifices
Interureteric fold

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20
Q

Rectosigmoid junction

A

Level of S3

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21
Q

Rectal ampulla

A

Dilation superior to pelvic diaphragm - stores feces before expulsion

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22
Q

Anorectal ring - pectinate line

A

Termination of puborectalis muscle

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23
Q

Blood supply to rectum: 3

A

Superior rectal artery
Middle rectal artery
Inferior rectal artery

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24
Q

Superior rectal artery origin

A

IMA

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25
Q

Middle rectal artery origin

A

Internal iliac artery

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26
Q

Inferior rectal artery origin

A

Internal pudendal artery

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27
Q

Superior rectal vein drains into..

A

IMV - portal system

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28
Q

Middle rectal vein drains into..

A

Internal iliac vein - caval

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29
Q

Inferior rectal vein drains into..

A

Internal pudendal then internal iliac - caval

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30
Q

Internal/External hemorrhoids

A

Internal: Dilation of veins of internal rectal plexus

External: Dilation of external veins of rectal plexus

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31
Q

Superior gluteal artery

A

Passes between lumbosacral trunk and S1

Exits greater sciatic foramen superior to piriformis muscle

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32
Q

Posterior division of male pelvis

A

Superior gluteal artery
Iliolumbar artery
Lateral sacral artery

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33
Q

Anterior division of male pelvic blood supply

A 
Umbilical artery
Obturator
Middle rectal
Inferior gluteal
Internal pudendal
Inferior vesical
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34
Q

Endopelvic fascia and spaces (ligaments)

A

Transverse cervical - cardinal
Uterosacral
Uterovesical

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35
Q

Rectouterine pouch

A

Adjacent to posterior fornix of vagina

Between vagina and rectum

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36
Q

Corpora cavernosa

A

Ventral portion of erectile tissue

Deep penile artery central within each tissue mass

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37
Q

Corpus spongiosum

A

Central tissue, attaches to glans

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38
Q

Crura of penis

A

Continuation of corpora cavernosa

Covered by ischiocavernosus muscle

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39
Q

Bulb of penis

A

Expanded portion at base of spongiosum

Covered by bulbospongiosus

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40
Q

Parts of urethra

A

Spongy
Intermediate (membranous)
Prostatic urethra
Intramural urethra

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41
Q

Parts of vagina

A 
Mons pubis
Glans clitoris
Labium majus
Labium minus
Vestibule - space between labia minora
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42
Q

Scrotum female equivalent

A

Labia majora

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43
Q

Ventral surface of penis female equivalent

A

Labia minora

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44
Q

Main innervation of perineum

A

Pudendal nerve and branches:

Inferior rectal
Perineal nerve
Dorsal nerve of penis/clitoris

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45
Q

Perineal nerve branches

A

Superficial perineal - posterior scrotal/labial

Deep perineal - muscles of superficial and deep pouches

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46
Q

Ilioinguinal nerve

A

Anterior scrotal/labial

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47
Q

Genitofemoral nerve

A

Genital branch - overlap anterior scrotal/labial

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48
Q

Inferior cluneal nerve

A

Inferior buttock and gluteal fold

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49
Q

Path of pudendal nerve

A

From S2-S4 –> through greater sciatic foramina and lesser sciatic foramina

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50
Q

Superficial perineal pouch boundaries

A

Superior: Perineal membrane

Inferior: Perineal fascia

Lateral: Ischiopubic rami

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51
Q

Deep perineal pouch boundaries

A

Superior: Inferior fascia of pelvic diaphragm

Inferior: Perineal membrane

Lateral : Obturator fascia

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52
Q

Epistiotomy

A

Controlled incision of perineum to aid passage of infant: Median and mediolateral incision

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53
Q

Primordial germ cells

A

Arise in yolk sack, migrate through umbilical cord to GI tract

Lie in intermediate mesoderm

Epithelial cells proliferate and surround PMG’s –> sex cords

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54
Q

Sex cords: Male and female

A

Early gonad has both so it is called indifferent gonad

Male sex cords develop first = primary. Located in inner region = medullary sex cords

Female sex cords develop second = secondary. Located in outer region = cortical sex cords

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55
Q

Medullary sex cords + TDF

A

Pre Sertoli cells –> Sertoli cells

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56
Q

Sertoli cells

A

Produce Anti Mullerian hormone

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57
Q

Leydig cells

A

Produce Testosterone when stimulated by LH

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58
Q

Anti mullerian hormone

A

Produced by Sertoli cells

Degenerate Mullerian duct = no uterus, cervix, superior vagina

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59
Q

Testes determining factor

A

Encoded by SRY

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60
Q

Female cortical sex cords development

A

Develop into follicle cells

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61
Q

Testosterone and development

A

Protect Wolffian duct = vas deferens, epididymis

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62
Q

Female development of Mullerian/Wolffian ducts

A

No TDF or AMH = no degeneration of Mullerian duct

No testosterone = Degeneration of Wolffian duct

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63
Q

Remodeling of female anatomy: Paramesonephric ducts

A

Paramesonephric ducts fuse caudally at pelvic urethra and thicken = Uterus, uterine tubes, cervix, fornix, superior vagina

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64
Q

Remodeling of female anatomy: Pelvic urethra

A

Endoderm, proliferates to form sinovaginal bulb

Elongates to form hymen and inferior portion of vagina

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65
Q

Incomplete fusion of paramesonephric ducts

A

Uterus bicornis: 2 uterine horns

Uterus didelphys: Double uterus

Uterus didelphys with double vagina

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66
Q

Incomplete formation of urorectal septum

A

Rectocloacal canal: Common outlet for urethra, vagina, rectum

Rectovaginal fistula: Common outlet for rectum and vagina

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67
Q

Androgen insensitivity sundrome

A

XY male with mutation of testosterone receptor

Testosterone normal/high –> converted to estrogen

Testes but no sperm, no male accessory organs

Anti mullerian hormone present = no internal female genitalia

Estrogen = female external genitalia, blind ended vagina, breasts

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68
Q

Formation of broad ligament

A

Fusion of mullerian ducts and break away from mesenchyme

Pouches anterior and posterior to broad ligament

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69
Q

Gubernaculum

A

Connects ovaries to labia majora, passes behind uterine tubes

When paramesonephric ducts fold, pulled medially

Superior: ovarian ligament
Inferior: round ligament of uterus

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70
Q

Kiss1 neurons

A

Part of HPG axis

Positive feedbak to GnRH neurons

Sex steroids inhibit Kiss1 = inhibition of GnRH

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71
Q

Excess and minimal GnRH and LH/FSH

A

Both can cause reduced LH/FSH release

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72
Q

HyperPRL and HPG

A

Decrease activity of entire axis

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73
Q

HyperTSH and HPG

A

Can activate FSH

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74
Q

Leptin and HPG axis

A

Lack of body fat can decrease HPG axis

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75
Q

HPG for males

A

FSH - sertoli cell function and spermatogenesis

LH - Leydig cell function –> testosterone

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76
Q

Inhibin

A

Released by sertoli cell, can inhibit FSH

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77
Q

Testicular Androgen binding protein

A

Need local androgen for spermatogenesis

ABP binds androgens from leydig cell to increase concentration of androgens

Exogenous androgen thus does not help with spermatogenesis

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78
Q

Developmental actions of testosterone

A

Differentiation of Wolffian ducts (DHT)

Descent of testes

Male brain

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79
Q

Adolescent and testosterone

A

Secondary sex characteristics: Voice, hair, penis size

Aggression

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80
Q

HP(ovarian) Axis

A

Requires pulsating GnRH

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81
Q

Developmental actions of estrogen/progesterone

A

Female sexual differentiation (no need for hormones)

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82
Q

Adolescent and estrogen/progesterone

A

E: Secondary sex characteristics - ovary/vagina/uterus/breast size increase

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83
Q

Overall process of male gonadal development

Gonads –> penis

A

Gonad + SRY = Testes

Mullerian ducts + AMH = degeneration

Wolffian ducts + Testosterone = Vas deferens, epidiymis, seminal vesical

DHT androgenizes external male genitalia

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84
Q

Critical in utero time for sex development

A

7-13 weeks

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85
Q

3 categories of DSD

A
  1. Sex chromosome DSD
  2. 46, XY DSD
  3. 46, XX DSD
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86
Q

Sex chromosome DSD (3)

A
  1. Turners - 45 X
  2. Klinefelters - 47 XXY
  3. Mixed gonadal dysgenesis - 45,X/46,XY
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87
Q

46, XY DSD etiology

A

Disorders of gonadal development

Disorders of androgen synthesis/action

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88
Q

46, XX DSD etiology

A

Disorders of gonadal development

Androgen excess - maternal and fetal

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89
Q

Palpable gonads in child = ?

A

Testicles = Y chromosome

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90
Q

Uterus present/absent

A 
Absent = AMH = testicles
Present = No AMH = no testes = ovaries/abnormal testes
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91
Q

Normal puberty - males

First and second occurrences

A
  1. Testicular enlargement - 11.5yrs
  2. Pubic/axillary hair

Testicular enlargement before 9 is early

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92
Q

Spermarche

A

~13.5 yrs

Tanner 3-4 gonads

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93
Q

Growth spurt - males

A

Later than females

Tanner 3-4

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94
Q

Normal puberty females - first and second sign

A
  1. Thelarche - 10.7yrs, can be pubarche though
  2. Pubarche ~12yrs

Breast development before 8yrs is early

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95
Q

Menarche

A

Usually 2-2.5yrs after thelarche

Mean age - 12.7

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96
Q

Central precocious puberty

A

Gonadotropin dependent

Sexual development before: 9 in boys, 8 in girls - testes/breasts

Pubertal levels of FSH/LH

More in females

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97
Q

Central precocious puberty causes

A

Harmatomas (GnRH)

Pineal masses

Optic glioma

Abcess, encepalitis, trauma

MOST cases idiopathic

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98
Q

How does puberty start?

A

Mean LH/FSH rise - larger LH rise

Enhanced GnRH episodic secretion

Kiss1 and leptin = positve regulation

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99
Q

Mini puberty

A

Peak at 2-3 months, gone by 1yr

Males: Elevated testosterone = genitalia, sperm for later

Females: Still not sure, follicle development?

Understand HPG axis

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100
Q

Peripheral puberty

A

Gonadotropin independent

Estrogen/testosterone elevated but LH/FHS low

Gonadal causes: ovarian tumor, leydig tumor, familial testotoxicosis

Adrenal causes: CAH, tumor

HCG tumor (boys)

Exogenous exposure

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101
Q

Severe hypothyroidism

A

Precocious puberty (increase in GnRH release)

Spillover effect of TSH on FSH receptor maybe?

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102
Q

McCune Albright Syndrome clinical presentation

A

Triad of:

  1. Precocious puberty
  2. Cafe au lait pigmentation (coast of Maine
  3. Polyostotic fibrous dysplasia
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103
Q

McCune Albright Syndrome cause

A

Somatic activating mutation of Galpha protein

Pituitary adenomas with excess LH, FSH, GH, PRL

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104
Q

Bone age

A

Sex steroids determine ossification within epiphyses

Bone age = True physical development age

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105
Q

Estrogen recetor and aromatase enzyme mutations and bones?

A

Growth plates don’t fuse, become very tall

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106
Q

Constitutional delay of puberty

A

Delayed growth spurt but normal pre pubertal growth

Genetic

Bone age will be delayed

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107
Q

Hypogonadotropin hypogonadism

A

Isolated or part of other pituitary deficiency

Complete pituitary workup, head MRI

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108
Q

Kallman syndrome

A

Kallman 1 codes anosmin (other genes can be involved)

Gene mutation affect migration of GnRH neurons and creation/migration of olfactory neurons

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109
Q

Hypogonadotropin hypogonadism examples

A 
Functional
Anorexia (leptin)
Prader-Willi
HyperPRL
Hypothyroid
Cushings
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110
Q

Gonadal failure (boys) - common causes

A

Testicular failure (high gonadotropins)

Klinefelter syndrome

Mumps orchitis

Trauma/radiation

Vanishing testes

Noonan syndrome

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111
Q

Klinefelter syndrome

A

47, XXY

Most common cause of gonadal failure

Small testes, talls tature, gynecomastia, developmental delay

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112
Q

Noonan syndrome

A

Normal karyotype

Short stature, cubitis valgus, triangular fascies, mild MR

Cardiac defects

1/2 have testosterone/sperm production dysfunctions - delayed puberty

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113
Q

Gonadal failure (girls)

A

Ovarian failure (high gonadotropins)

Turners syndrome

Trisomy 21

Physical/medical injury

Autoimmune oophoritis

114
Q

PCOS

A

Polycystic Ovarian hyperandrogenism

Amenorrhea/chronic anovulation

Elevated LH

Numerous antral follicles - LH/FSH increases resulting in immature follicles

Insulin resistance - hyperpigmentation

Overweight/obese, metabolic syndrome

Elevated androgen levels - hirsutism

115
Q

Menstrual cycle overall

A

Ovarian cycle: Follicular genesis, Oogenesis

Uterine (endometrial cycle)

116
Q

Ovarian cycle overall

A

Day 0-14: Follicular phase

Day 14-28: Luteal phase

117
Q

Endometrial cycle overall

A

Day 0-4: Menses

Day 4-14: Proliferative phase

Day 14-28: Secretory phase

118
Q

Atresia

A

Degeneration of follicles

Can happen at any stage of development

119
Q

Peak oogenia

A

~20 weeks fetal development

6-7 million follicles

120
Q

Oogonia to primary oocyte

A

20 weeks fetus –> birth

Oogonia enters Meiosis I and arrests at Prophase I

Many become atretic but ~400k survive to puberty and surrounded by pregranulosa cells = primordial follicles

121
Q

Folliculogenesis overall

A 
Primary oocyte
Primordial follicle
Primary follicle
Secondary follicle 
Tertiary follicle
122
Q

Primordial –> Primary follicle

A

Granulosa cells develop and connected via gap junctions

Enlarges

123
Q

Primary –> Secondary follicle

A

Granulosa divides to form layers

Stromal cells differentiate into theca cells

Vascular supply forms

124
Q

Early tertiary follicles

A

Granulosa cells increase

Mucopolysaccharides secreted = zona pelucida

Antrum appears

125
Q

Graafian follicles

A

Dominant follicle

Second antral stage, much larger antrum

Antrum surrounds oocyte

126
Q

Pre antral stages of folliclulogenesis

A

Primordial

Primary

Secondary

127
Q

Antral stages of folliculogenesis

A

Early tertiary

Late tertiary

128
Q

Follicular phase dominant hormone

A

FSH

129
Q

Later follicular phase and luteal phase hormone

A

LH

130
Q

Domination of dominant (Graafian follicle)

A

Follicle with most FSH receptors and best blood supply will supply

Low FSH means others will die out - atresia

Dominant follicle will release oocyte during ovulation

131
Q

LH surge

A

Primary signal to rupture follicle (induce ovulation)

Proteolytic enzymes weaken follicular wall

Contraction of theca externa + prostaglandins = total rupture

Primary oocyte completes meiosis I, arrested in metaphase II

1st polar body formed

132
Q

Significance of 1st polar body

A

Can be used for genetic screening

Disease alleles can completely segregate into first polar body

133
Q

Corpus luteum

A

Non dominant follicle cells form corpus luteum after ovulation

Secrete mainly progesterone and some estrogen

134
Q

Corpus luteum and fertilization

A

If corpus luteum interacts with hCG due to implantation, remains

No hCG = degeneration to corpus albicans

135
Q

Endometrium layers

A

Functionalis - shed during menstruation

Basalis - not shed, regenerates functionalis layer

136
Q

Menstrual stages and hormone dominance

A

Menses

Proliferative - Unopposed estrogen driven

Secretory - Progesterone + estrogen driven (opposed estrogen)

137
Q

Time and location of fertilization

A

Usually in ampulla of uterine tube

Within 24hrs of ovulation

138
Q

Initiation of menstruation?

A

Degeneration of corpus luteum = lack of progesterone = hemorrhage of endometrium and menses

139
Q

Bartholin glands

A

Produce lubrication during sexual arousal

Not all lubrication

140
Q

Female sexual innervation

A

Parasympathetic: Sexual response
Sympathetic: Muscle contraction

S2-4 innervate clitoris erectile tissue

Very sensitive

141
Q

Female sexual response and sperm transport

A

Sperm do not travel all the way only by swimming

Oxytocin release during orgasm initates muscle contraction

Contraction drives sperm to uterine ampulla

142
Q

Two cell two gonadotropin model

A

Model by which androstedione and estradiol are produces

Theca cell produces androstedione from cholesterol –> travels to granulosa cell

Granulosa cell converts androstedione to estradiol (aromatase) - stimulated by FSH

143
Q

Total Menstrual cycle

A
  1. No fertilization = no hCG so progesterone decreases and endometrium hemorrhages
  2. End of luteal phase and decrease in hormones = no negative GnRH feedback –> FSH increases
  3. FSH rise = antral follicle growth, some estrogen produced
  4. Decrease FSH and increase estrogen = increase GnRH pulsation and LH rise
  5. Declining FSH means dominant follicle arises
  6. Dominant follicle increases estrogen levels over 200pg/mL for 36-48hrs –> positive feedback to GnRH and subsequent LH surge, increased sensitivity to GnRH receptors
  7. LH surge results in meiotic maturation, ovulation, corpus luteum formation
  8. Rise of progesterone and estrogen (opposed) results in negative feedback to GnRH, FSH/LH decline
  9. Basal LH required for corpus luteum function but becomes insensitive unless there is hCG. No hCG = luteolysis and menses
144
Q

Orally active steroidal estrogens

A

17 beta estradiol

conjugated equine estrogens

Ethinyl estradiol

Mestranol

DES

145
Q

17 B estradiol

A

Low bioavailability but most potent

Requires high doses but thats risky, only use low dose therapy

146
Q

Conjugated equine estrogens

A

From horse urine

Higher bioavailability but less potent

Estrone and estrone sulfate

147
Q

Ethinyl estrogen

A

Synthetic steroidal estrogen

Decreased first pass metabolism because of ethinyl group, higher bioavailability

Can be administered in low doses but still get good therapeutic effect

Administer with progestin as contraceptive

148
Q

Mestranol

A

First gen used in OCP

Combined with norethynodrel

149
Q

Diethylstilbestrol (DES)

A

Synthetic estrogen

Increased breast cancer risk for mother and cervical cancer in fetus

150
Q

Uses of therapeutic estrogens

A

Hormonal replacement

Contraception combined with progestin

Primary hypogonadism treatment

151
Q

Estrogen adverse effects

A 
Breast tenderness
Edema
Nausea/vomiting
Hyperpigmentation
Migration
Mid cycle breakthrough bleeding
152
Q

Estrogen SAE

A

Cancer risk: Decrease colorectal, uterine, ovarion

Increase benign hepatic adenomas, cervical, CNS

Increase gall stones

Increase cardiovascular risks: DVT, HTN, MI

153
Q

Estrogen Contraindications

A

Estrogen dependent neoplasm

Vaginal bleeding

Thromboembolic disorder

Cerebrovascular or CAD

Heavy smoking

Congenital hyperlididemia, liver disease

PREGNANCY

154
Q

Progestin physiological action

A

Thickened mucus

Decrease estrogen receptor, promote cell differentiation in endometrium

Decrease fallopian tube motility

Contraceptive actions

155
Q

Synthetic progestin ADME

A

Good absorption and distribution

CYP3A4

156
Q

Oral Progestin categories

A

C21 progestins - progesterone derivatives

C19 progestins - 19 nortestosterone derivatives

C17 progestin: Spironolactone analog

157
Q

C21 progestins

A

Progesterone derivative

MPA

DMPA

158
Q

C19 progestins

A

19-nortestosterone derivatives

1st gen: Northindrone acetate

2nd gen: Levonorgestrel

3rd gen: Desogestrel, Norgestimate

159
Q

C17 progestin

A

Spironolactone analog

Drospirenone (Yaz, Yasmin)

PR activity, Anti AR activity, Anti MR activity

Increased DVT

160
Q

Clinical use of progestins

A

Contraception: Alone or combination

Menstrual disorders

Hormone therapy

161
Q

Clomiphene

A

1st line drug for inducing ovulation

Partial agonist of estrogen receptor

Blocks ER –> Body senses as low estrogen –> increase GnRH –> Large rise in LH/FSH –> Follicle maturation and ovulation

Ovarian enlargement and risk of multiple births

162
Q

Raloxifine

A

2nd line for prevention of post menopausal osteoporosis

Estrogen agonist in bone - Prevents bone resorption

Estrogen antagonist in breast - Can reduce breast cancer risk

Hot flashes/DVT

163
Q

Tamoxifen

A

Use for prevention of breast cancer

Estrogen receptor competative antagonist in breast - prevent estrogen driven genetic transcription

Estrogen agonist in endometrium so risk for uterine neoplasia

DVT

164
Q

hMGs

A

Human Menopausal Gonadotropins

Ovulation induction when unresponsive to clomiphene

IVF

Hypothalmic/Pituitary amenorrhea

Ovarian enlargement/hyperactivity

165
Q

Mifepristone

A

Progesterone antagonist - Morning after pill

Prevents blastocyst implantation

Induces luteolysis of early pregnancy

Vaginal bleeding, infections, ectopic pregnancy rupture

166
Q

Leuprolide

A

GnRH analog - treatment of endometriosis, uterine fibrosis

Down regulation of GnRH receptors and reduction of hormones - LH/FSH/estrogen/Progesterone

Reversible osteoporosis

167
Q

Premature ovarian failure/primary ovarian insufficiency

A

Amenorrhea, hypoestrogen, elevated gonadotropins

Menopause like symptoms

Issue with ovaries, do not produce necessary hormones for proper uterine function

Low inhibin = higher FSH

Can be autoimmune, chromosome issue, genetic condition, damage to ovaries

168
Q

Causes of missed periods

A 
Secondary amenorrhea
Eating disorder
Pregnancy
Hypothyroidism
Medication
Exercise
Stress
169
Q

Functional cysts: Cystic follicle vs follicular cyst

A

Originate in graafian follicle

Pelvic pain

> 3cm - Follicular cyst

170
Q

Luteal cyst

A

Form in corpus luteum

Bright yellow on gross exam

Due to preovulatory LH surge or ovulatory stimulus

May rupture and cause peritoneal reaction

171
Q

Non functional cyst types and difference from functional cysts

A

Non functional cysts DO NOT resolve over time

  1. Endometriotic cyst
  2. Teratoma (younger)
  3. Cystadenoma (older)
172
Q

Pathophysiology of androgen excess in PCOD

A

Androstedione produced in adipocytes and converted to estrone –> Estrone stimulates LH release –> LH stimulates more androstedione production –> Can travel to adipocytes OR converted to testosterone

173
Q

Types of ovarian tumors

A

Surface epithelial tumors

Germ cell

Sex cord stroma

Metastatic (other)

174
Q

Types of surface epithelial tumors

A

Each has benign, borderline, malignant

Serous

Mucinous

Endometroid

Clear cell

Transition cell

175
Q

Types of germ cell tumors

A

Teratoma - Mature, immature, monodermal

Dysgerminoma - rapid growth, good prognosis

Yolk sac tumor - Elevated AFP

176
Q

Sex cord tumors

A

Granulosa cell tumor

Sertoli-Leydig tumor

177
Q

Metastatic tumors

A

Krukenberg

Psuedomyoxma peritonei

178
Q

Atresia in aging woman

A

Atresia accelerates around 35-38yrs

179
Q

Menopause

A

12 months without menses

Loss of follicular function

Mean age 51-52yo

180
Q

Premature menopause

A

Loss of menses before 40 yrs old

1% POI

Usually because of medication/therapy

181
Q

Perimenopause

A

Transitionary period between normal function and menopause

Mid/late 40s for 4-6yrs

182
Q

Ovarian function in perimenopause

A

Decrease ovary size

Decrease in # of follicles

Inhibin decrease –> FSH increase

Poor response to LH/FSH elevation

Erratic ovulation and irregular menses

183
Q

Perimenopause treatment

A

Oral contraceptives

Improve menstrual irregularities

Decrease ovarian cancer risk, no breast cancer risk

184
Q

Menopause vasomotor symptoms

A

Hot flashes and night sweats

Due to altered thermoregulatory function via estrogen withdrawal

Vasodilation –> increase blood flow –> Sweating –> Shivering

185
Q

Vasomotor symptom treatments

A

Lifestyle changes: Relaxation, cool down activity

Non hormonal: SSRI, SNRI, anti-epileptic, antiHTN

Soy isoflavanoids

Hormone therapy: Estrogen (no uterus), E+P (uterus) - Low breast cancer risk in younger women

186
Q

Menopause urogenital symptoms

A

Vaginal atrophy

Dryness/itchiness

Pain during sex

UTI’s and incontinence

187
Q

Menopause urogential pathophysiology and treatment

A

Lack of estrogen

Loss of glycogen rich superficial cells = No lactobacillus = alkaline vagina

More pathogen colonization

Treatment: Behavioral, moisturizers/lubrication

Local estrogen therapy

188
Q

HSDD

A

Hypoactive sexual desire disorder

Decreased libido

Low testosterone

189
Q

HSDD treatment

A

Filabanserin

Premenopausal women only

Dopamine and serotonin levels

190
Q

Where do tumors arise from in cervix?

A

Transition zone between endocervix and ectocervix

191
Q

Cancer associated with ectocervix

A

Squamous cell carcinoma

192
Q

Cancer associated with endocervix

A

Adenocarcinoma

193
Q

Lower genital tract infectious agents

A 
HSV
Candida
Trichomonas vaginalis
Gardnerella vaginalis
HPV
194
Q

Lower and upper genital tract infectious agents

A

Neisseria gonorrhea

Chlamydia

195
Q

Herpes Simplex Virus

A

DNA STD virus

Can be asymptomatic

Latent phase - trigger is immunosuppression or stress

196
Q

Active HSV presentation/test

A

TEst: TZank test

Vesicles and punched out ulcers - Require C section

197
Q

Congenital herpes

A

Baby born to active HSV mother transvaginally

Conjunctivitis, GI bleeds, jaundice, seizures

67% mortality

198
Q

Candida

A

Fungus

10% females are carriers

White curd like discharge

Pseudohyphae and yeast

No fetus damage/sequelae

199
Q

Trichomonas vaginalis

A

Purulent vaginal discharge

Strawberry cervix - petechial hemorrhages

Pear shaped flagellate organisms

200
Q

Gardnerella Vaginalis

A

Most common bacterial vaginosis

Fishy oder, low viscosity discharge

Bacteria adhere to “clue cells”

201
Q

Actinomyces

A

Associated with intrauterine device (IUD)

202
Q

HPV

A

Human papilloma virus

Benign and malignant lesions

203
Q

Low risk HPV serotypes

A

6/11

Most common

Spontaneously regress

Koliocytosis - Nuclear enlargement, darker nuclear stain

204
Q

High risk HPV serotypes

A

16, 18, 31-33, 35

Kolicytosis and dysplastic changes in epithelium starting at basal layer

205
Q

High Risk HPV pathogenesis

A

Increase E6 activity = Decrease p53

Increase E7 = Decrease RB

206
Q

Pelvic Inflammatory disease

A

Ab pain, fever, vaginal discharge, adnexal mass

Major cause of infertility and ectopic pregnancy

207
Q

Neisseria gonorrhea

A

Most common cause of PID and ascending bacterial infection

Acute infections: Cervicitis, urethritis, scarring of tubes

NO dysplasia or carcinoma risk

Neutrophilic disease, organisms in neutrophils

208
Q

Chlamydia trachomatis

A

Most common STD worldwide

Follicular cervicitis

No dysplasia/carcinoma

209
Q

Vulvar disease

A

Vulvar intraepithelial neoplasia

Invasive squamous cell carcinoma

Extramammary paget disease

210
Q

VIN

A

Vulvar intraepithelial neoplasia

Abnormal maturation confined to epithelium

HPV 16/18 (90%) - younger, multicentric leasions, VAIN/CIN

HPV negative (10%) - Older women, p53 mutation

211
Q

VIN staging

A

VIN I - Mild dysplasia, bottom 1/3 squamous epithelium

VIN II - Moderate, bottom 2/3 epithelium

VIN III - Severe, Full thickness abnormality

Invasion of basal layer - Squamous cell carcinoma

Non invasive can spontanouesly regress in YOUNGER WOMEN

212
Q

Vulvar squamous cell carcinoma

A

Association with HPV

Most common vulvar malignancy

Invasion through basement membrane

213
Q

Squamous cell carcinoma prognosis

A

Depends on: Tumor size, tumor invasion depth, lymphatic invasion

Less than 2cm = good prognosis with vulvectomy and lymphadectomy

214
Q

Extramammary paget disease of vulva

A

Occurs in late reproductive age group

White over black

Pruritis, ulcerated skin lesions in labia majora/minora

Affect epidermis layer

NOT associated with carcinoma

215
Q

Rhabdomyosarcoma

A

Sarcoma Botryoides

Malignant tumor of skeletal muscle cells

Grape like growths and hemorrhages

Under 5yrs old

Surgery + adjuvant chemo

216
Q

Cervical Intraepithelial Neoplasia

A

Disease of young women

Sex early and often is risk factor

Pap smear diagnosis

Koliocytes, multinucleated cells

217
Q

CIN staging

A

Same as VIN

Mild, moderate, severe

218
Q

Cervical squamous cell carcinoma

A

Most common cervical cancer, 8th highest mortality

Treat with partial hysterectomy, remove cervix

219
Q

Uterus layers

A

Endometrium - Glands & Stroma

Myometrium - Smooth muscle

220
Q

Menstrual phase and spiral arteries

A

Spiral arteries become ischemic and rupture

Functionalis shed

221
Q

Secretory phase histology

A

Piano key like structures

Glands irregularly shaped with subnuclear vacuoles

222
Q

Ch5ronic endometritis

A

Etiology - PID, IUD, TB, idiopathic, post partum

Symptoms - Bleeding, pain, infertility

Histology - 1 or more plasma cells

Endometrial scarring

223
Q

Endometriosis

A

Functioning endometrial tissue growing in places that aren’t endometrium: Ovary, uterine ligaments, fallopian tubes, lungs, pelvic peritoneum

Dysmenorrhea, infertility, ab pain

Hemisodern

224
Q

Ovarian endometriosis

A

Ovarian Chocolate cyst

225
Q

Pathogenesis of endometriosis

A

Congenital

Endometrial tissue travels back towards ovary

Shed tissue reaches blood supply and travels to other areas

226
Q

Adenomyosis

A

Endometrial glands within myometrium

Menorrhagia, colicky dysmenorrhea, pelvic pain, bleeding

Symmetrically enlarged, boggy uterus

FUNCTIONAL ENDOMETRIAL TISSUE

227
Q

Endometrial hyperplasia

A

Proliferation of glands

Increase gland/stroma

Precursor to endometrial carcinoma

Risk: Nulliparous, obesity, ovarian and stromal

PTEN mutation because of excess estrogen

228
Q

Simple hyperplasia

A

No atypia: Proliferative endometrium, increase in glands, bland morphology, less than 5% carcinoma

Atypia: Proliferative endometrium + loss of polarity/prominent nuclei, 8% carcinoma

229
Q

Complex hyperplasia

A

No atypia - Gland crowding no morphological change, 3% carcinoma

Atypia: Above with nuclear hyperchromasia, stratification, nucleoli, mitosis

230
Q

Endometrial adenocarcinoma

A

Most common malignancy of uterus

Most common female genital tract cancer

PM women

Risk: Nulliparity, obesity, diabetes, unopposed estrogen stimulation

231
Q

Two types of endometrial carcinoma

A
  1. Excess unopposed estrogen stimulation and endometrial hyperplasia
  2. Older individuals, p53 mutation, poor prognosis, poorly differentiated
232
Q

Grading system for adenocarcinoma

A

Grade I: Well differentiated, Less than 5% solid growth pattern

Grade II: Moderate differentiation, 6-50% of solid growth pattern

Grade III: Poor differentiation, >50% solid growth pattern

Atypia raises grade by 1 level

233
Q

Myometrium neoplasm types

A

Benign

Uncertain malignant potential

Malignant

234
Q

Diagnosis/behavior of smooth muscle neoplasms

A

Necrosis

MItotic count

Borders

235
Q

Leiomyoma

A

Most common benign smooth muscle tumor

Usually in uterine corpus

Pelvis

GI tract

Round whorled lesions, non infiltrating borders, fascicles

Cigar shaped nuclei

236
Q

Leiomyosarcoma

A

Rare malignant smooth muscle tumor

Peri/Post menopausal woman

Enlarged pelvic mass, vaginal bleeding

Infiltrative borders, increased mitotic activity, cellular atypia

Recurring

10-40% 5 yr survival

Hysterectomy

CHEMO DOES NOTHING

237
Q

Malignant neoplasms of fallopian tubes

A

Usually come from metastatic source from other area: Ovary, uterus, GI

Primary tumors very rare

238
Q

Serous/mucinous tumors

A

Most common types of surface epithelial cells tumors

Cystic

Benign, borderline, malignant

239
Q

Benign vs malignant serous/mucinous tumors

A

Benign: Cystadenoma
Single cyst, simple/flat lining, premenopasal women

Malignant: cystadenocarcinoma, multiple, large with complex lining, post menopausal women

240
Q

BRCA mutation and ovary

A

Risk of breast and ovarian cancer

Risk of serous malignant carcinoma or ovary and fallopian tube

241
Q

Endometrioid tumor

A

Endometrial tissue tumor, associated with endometriosis

Usually malignant

Check for endometrium endometrioid carcinoma

242
Q

Brenner tumor

A

Transitional cell tumor

Usually benign

Urothelial cells

243
Q

Germ cell tumors

A

2nd most common

Occur at reproductive age

Teratoma
Dysgerminoma
Endodermal sinus

244
Q

Cystic Teratoma

A

Cystic, bilateral, tissue from 2+ embryological tissues

Cysts contain numerous tissue types: Teeth, hair, bone, gut, skin etc

Mature = benign

Immature = malignant

245
Q

Immature cystic teratoma

A

Mainly contains neuroectodermal tissue

Malignant

246
Q

Somatic malignancy

A

Teratomal tissue has squamous cell carcinoma within

Bad

247
Q

Dysgerminoma

A

Germ cell mass

Increase LDH

Good prognosis

248
Q

Yolk sac tumor

A

Endodermal sinus tumor

Form from yolk sac

Elevated AFP

Schiller Duval bodies

249
Q

Granulosa cell tumors

A

Excess estrogen production

250
Q

Sertoli leydig cell tumor

A

Androgen production

251
Q

Choriosarcoma

A

Placental tumor

Elevated bhCG

Highly aggressive, no chemo response

252
Q

Meigs syndrome

A

Ovarian tumor

Right sided pleural effusion

Ascites

253
Q

Pseudomyoxma peritonei

A

Mucin deposition in peritoneum

Associated with appendix

254
Q

Krukenberg tumor

A

Metastatic tumor usually from GI tract

Signet ring

Bilateral

255
Q

Inflammatory conditions of breast

A

Acute mastitis

Periductal mastitis

Fat necrosis

Ductal ectasia

256
Q

Acute mastitis

A

Infection of breast usually via S. Aureus

Associated with breast feeding

Inflammation, warm erythematous breast

Treat with drainage and doxicilin

257
Q

Periductal mastitis

A

Associate with smoking - lack of Vit D so metaplasia of columnar epithelium to squamous

Subsequent block of subareolar duct and inflammation

Subareolar mass and nipple retraction

258
Q

Fat necrosis

A

Associated with trauma

Necrotic fat cells and giant cells

Presents as mass or calcification on mammogram

259
Q

Ductal Ectasia

A

Inflammation of subareolar ductal wall and dilation of duct

Inflammation

Multiparous post menopausal women

Green brown discharge

260
Q

Fibocystic breast changes

A

Cystic growth of fibrous tissue in breast

Hormone sensitive

BENIGN

261
Q

Fibrosis + cyst + Apocrine metaplasia

A

No increased risk for invasive carcinoma even though metaplasia

262
Q

Ductal hyperplasia

A

Increase in cells of duct

2x risk for invasive carcinoma

263
Q

Atypical hyperplasia

A

Atypical cells in duct or lobule

5x increase risk for invasive carcinoma

264
Q

Sclerosing adenosis

A

Development of mass due to glandular increase and stretching of tissue - associated fibrosis

2x increase risk invasive carcinoma

265
Q

Granulomatous mastitis

A

Rare

Sarcoidosis

Infections: Mycobacteria, fungal

Dense granulomatous infection

Scattered lymphocytes, giant cells

266
Q

Intraductal papilloma

A

Papillary finger like ductal growth surrounded by both types of epithelium

Bloody nipple discharge

267
Q

Fibroadenoma

A

Most common benign growth in pre menopausal women

Fibrous and glands

Estrogen sensitive

No invasive cancer risk

268
Q

Ductal vs Lobular carcinoma in situ

A

Ductal: 70-90% incidence, E cadherin (+), calcification, less frequently bilateral

Lobular: 10-30% incidence, e cadherin (-), less common calcifications, bilateral, no paget’s disease

269
Q

DCIS grading

A

Nuclear grading

Grade 1 - nucleus same size as normal ductal epithelial cell

Grade 2: Neither NG 1 or NG3

Grade 3: Pleomorphic nuclei, 2-3x size of normal ductal epithelial cells

270
Q

Invasive ductal carcinoma NOS - Luminal A

A

40-55% incidence

Post menopausal

ER+
Her2/Neu - Negative

271
Q

Invasive ductal carcinoma NOS - Luminal B

A

15-20%

Non specific pt characteristics

ER/PR +
Her2+

272
Q

Invasive ductal carcinoma NOS - Basal Like

A

13-25%

Young women, BRCA-1

Triple negative

Very bad

273
Q

Invasive ductal carcinoma NOS - Her 2 positive

A

7-12%

Brain metastases

ER/PR negative

Her 2 +

high proliferation and 3/3 tumor grade

274
Q

Axillary node management

A

Positive nodes: Axillary dissection

Negative: Sentinal lymph node biopsy

  • Positive = axillary dissection
  • Negative = No dissection
275
Q

Aromatase inhibitors

A

Anastrazole
Letrozole
Exemestane

Post menopausal women only

Inhibit androgen conversion to estrogen

276
Q

Trastuzumab

A

Targeted therapy

Monoclonal antibody that binds to extracellular Her 2 domain

277
Q

Pertuzumab

A

Monoclonal antibody that prevent Her2/3 dimerization

278
Q

Lapatinib

A

Intracellular domain action

Inhibits tyrosine kinase of Her2

279
Q

Denosumab

A

RANK ligand inhibitor

Prevents bone destruction

Use if metastatic at presentation

280
Q

Everolimus

A

mTOR inhibitor

Reverses endocrine resistance

GI/Endo/Repro (8 decks)

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