Week 3a + 3b Flashcards
(224 cards)
1
Q
- What are the screening methods for breast cancer?
- What about diagnositc?
- What about biopsy?
A
- mamogram
- ultrasound, special mammogram views, breast MRI, CT imaging
- FNA (cyst aspiration), ultrasound biopsy (with needle), stereotactic biopsy
seed localization - radioactive releasing seed - used as management
2
Q
TORCHeS infections
1. T =
2. O =
3. R =
4. C =
5. H =
6. S =
A
- Toxoplasma
- Other (HIV, Zika, Hep B, Parvo)
- Rubella
- CMV
- Herpes Simplex
- Syphilis
3
Q
- What are TORCHeS infections?
A
- TORCH Syndrome refers to infection of a developing fetus or newborn by any of a group of infectious agents
4
Q
Toxoplasma
1. How does mother get this?
2. How does this get transferred to baby
3. Triad of symptoms
4. When happens when infections occurs in 1st, 2nd, or 3rd trimester?
A
- mom can get from cat feces or undercooked meat
- transplacental
- Chorioretinitis, Hydrocephalus, Intracranial calcifications
- 1st trimester leads to spontaneous abortion - 2nd and 3rd trimester lead to transfer to baby and sx at birth
5
Q
HIV
1. How does mother get this?
2. How does this get transferred to baby
3. Symptoms in baby
A
- Mom can get from sexual contact, needlestick
- Transplacentally
- recurrent infections, chronic diarrhea
6
Q
Parvovirus B19
1. What happens when mother gets infected during pregnancy
2. How does this get transferred to baby
3. Triad of symptoms
A
- 80% of women are already exposed so reinfection at pregnancy is not bad + those who have never been exposed if exposed during second can have a high risk of fetal death
- Transplacentally
- Kills RBC –> leads to hydrops fetalis: abnormal accumulation of fluids and death is possible. Also see slapped cheek rash, aplastic crisis
7
Q
Rubella
1. How does mother get this?
2. How does this get transferred to baby
3. Triad of Symptoms
A
- Respiratory Droplets (humans are only resevoir)
- Transplacental
- Think I (eye) heart Ruby (rubella) (ear)rings: Eye cataracts, ear deafness, congenital heart disease + can also see microcephaly, neonatal purpura, cognitive deficits, celery stalking (bones), salt and pepper retinoapthy, congenital glaucoma
8
Q
CMV
1. How does mother get this?
2. How does this get transferred to baby
3. Symptoms
A
- sexual contact or just close contact. 40-90% of adults are CMV positive already
- transplacental
- hearing loss, seizures, periventricular calcifications in brain, petechial rash
9
Q
Herpes Simplex
1. How does this get transferred to baby
2. Symptoms
A
- Perinatal - baby gets this via skin or mucous membrane contact at birth
- Meningoencephalitis, vesicular skin lesiosn, etc
10
Q
Syphilis
1. How does this get transferred to baby
2. Symptoms
A
- transplacentally
- stillbirth, hydrops fetalis, notched teeth, nasal discharge (”snuffles”) - infectious, Saddle nose, Saber shins, Deafness
11
Q
Dilation and Evacuation
1. At what point of pregnancy can this occur?
2. What is the process
3. How is this different than D&C (AKA vacuum aspiration or urterine aspiration)
A
- after 12 weeks
- cervical dilation followed by removal of uterine contents using a combination of vacuum aspiration and instruments
- D&C is done before 12 weeks in first trimester.
12
Q
- Define abortifacient
A
- substance intended to cause termination of a pregnancy so that it does not result in live birth
13
Q
D&C vs D&E
1. sedation levels
2. levels of invasiveness
A
- D&C can be done while patient is awake but pt is still given analgesics. D&E requires IV sedation
- D&E is more invasive and requires more cervical prep
14
Q
- When can medical abortion be done?
A
- in 2nd trimester of pregnancy
15
Q
What is considered (in weeks)
1. First trimester
2. 2nd trimester
3. 3rd trimester
4. How many weeks is considered full term?
A
- first 12 weeks
- 13-26 weeks
- 27 weeks to full term
- 37-40 weeks
16
Q
Oxytocin
1. Therapeutic use (2)
2. MOA
3. What other hormone can stimulate oxytocin levels
A
- promotes milk ejection, stimulates uterine smooth muscle to induce labor, also given as adjunct after PGE to shorten abortion time
- Released from posterior pituitary and go to receptors in mammary glands and uterus to induce effect
- estrogen increases oxytocin
17
Q
Prostaglandins
1. MOA
2. Therapeutic use
A
- longer duration of action than that of oxytocin (given parenteral)
- Can induce labor more effectively (contractions) than oxytocin and can soften cervic for labor. This is often given to start labor before it naturally occurs for various reasons. Given via the vagina.
18
Q
Ergot Alkaloids
1. Drug of choice
2. MOA
3. Therapeutic use
A
- Ergonovine (rapid onset and prolonged duration)
- Actions on alpha adrenergic and serotonergic receptors -> cause more uterine contractions
- Stimulates smooth muscle postpartum to prevent bleeding and maintain uterine muscle tone
19
Q
Oxytocin vs PGE
1. Which is more effective in 2nd trimester
2. Which is more effective in 3rd trimester
A
- 2nd trimester- PGE
- 3rd trimester - oxytocin
20
Q
Terbutaline (for pregnancy usage)
1. type of drug
2. MOA
3. therapeutic use
A
- Beta 2 agonists
- Autonomic innervation of uterus
- Used to delay/prevent premature delivery. This decreases frequency, duration, and intensity of contractions.
21
Q
Indomethacin (NSAID)
1. Therapeutic use in pregnant women?
2. MOA
A
- inhibits uterine contractions
- blocks prostaglandin synthesis (remember PGE induces labor)
22
Q
MgSO4
1. Therapeutic use in pregnancy?
2. MOA
A
- inhibits contractions by direct effect on myometrium
- Excitation and contraction of smooth muscles are uncoupled. Repeated dosing can inhibit labor for more than a week at times.
23
Q
Nifedipine
1. Therapeutic use in pregnancy?
2. MOA/type of drug
A
- inhibit uterine contractions
- inhibit Ca2+ influx into myometrial cells to stop muscle activity/contraction
24
Q
- What key microbe is responsible for regulating the pH and protecting from infection in female genital tract?
- Which areas of the GI tract are free of microbes?
A
- Lactobacillus
- Kidney, ureter, urinary bladder are sterile
25
Bacterial Vaginosis
1. What organism causes?
2. Examination findings (discharge description, odor, inflammation?)
3. Treatment
4. What other organism can be seen on top of the main one?
1. gardnerella vaginalis
2. think off-white watery discharge, vaginal malodor-fishy, no inflammation
3. metronidazole
4. Mobiluncus curtisii or mulieris (more sickle shaped looking organism)
26
Bacterial Vaginosis
1. What type of cells are found?
2. Histology findings
3. pH changes
- this is gardnerella vaginalis
1. clue cells
2. shows clue cells (blurry borders) embedded with rod shaped bacteria
3. pH > 4.5
27
Trichomoniasis/Protozoan Vaginosis
1. What organism causes?
2. Examination findings (discharge description, odor, inflammation?)
3. Treatment
1. Trochomonas vaginalis
2. thin, yellow, green froty discharge, malodorous, vaginal inflammation
3. Metronidazole + tx partner too
28
Trichomoniasis/Protozoan Vaginosis
1. pH changes
2. Microscopic findings
1. pH >4.5
2. image
29
Candida Vaginitis/Fungal Vaginosis
1. What organism causes?
2. Examination findings (discharge description, odor, inflammation?)
3. Treatment
1. Candida albicans
2. Bright white thick cottage cheese discharge, vaginal inflammation
3. Fluconazole
30
Candida Vaginitis/Fungal Vaginosis
1. pH changes
2. what is seen on staining
1. normal pH
2. yeast seen on staining with pseudo hyphae
31
HSV (1 and 2) (one of the common STIs)
1. common hosts
2. Symptoms
3. How is it transmitted
4. Describe the latency, reactivation, and resolution phase of this
1. only humans
2. HSV1 is what causes cold sores, HSV2 is what causes genital herpes
3. direct contact
4. -> Latency - genetic material migrates to nucleus of sensory nerve and then its transcription stops. Latency sites are in neurons. (HSV-1 is in trigeminal root ganglia, HSV-2 is in sacral nerve ganglia)
-> Reactivation - occurs with stress, trauama, immune system failure
-> resolution - rarely occurs
32
1. What is the test to dx HSV1 and HSV2 (2)
2. Presentation of primary infection vs non-primary infection symptoms?
3. Tx of HSV1 or HSV2?
1. Tzanck smear (giemsa stain), PCR or direct florescent antibody
2. Primary infection is severe painful genital ulcers, Non-primary infection: pt has pre-existing antibodies - fewer, less severe and less painful lesions
3. Acyclovir
33
N. Gonorrhea
1. Dx tests (3)
2. Presentation if localized, localized invasive, and systemic
1. NAAT test, Microscopy, Culture on thayer-martin agar
2. Localized: urethritis with "the drip", anorectal infection --- Localized invasive: PID, Bartholin's gland abscess, prostatitis --- systemic: joint infections and disseminated gonococcal infection
34
Chlamydia Trachomatis
1. Types?
2. Which type causes Lymphogranuloma venereum (LGV)
3. What is LGV? (describe its sx and stages)
1. D-K and L1,L2,L3
2. L1,L2,L3
3. first stage (after organism gains acces through small abrasions or lacerations) is small, painless, vesicular lesion at site of infection. 2nd stage is 1-4 wks after primary lesion: enlarged LN that become painful buboes [ PLUS: fever, headache, myalgias occuring in both stages]
35
Chlamydia Trachomatis
1. what type causes urogenital disease, conjunctivits, infant pneumo, and proctitis?
2. Dual infection with what other organism is common?
3. Dx test most often used?
1. D-K
2. Neisseria gonorrhea
3. NAAT test
36
1. what are the two forms of chlamydia trachomatis
2. What is tx?
1. elementary body - infectious form
2. reticulate body - intracellular replicative form (replicates in cell by fission) and then eventually reorganizes into elementary bodies
3. Tx with azithromycin or doxycycline for 7 days
37
1. Oral papillomas can be caused by what infection?
2. What is and what causes condyloma acuminata (anogenital warts)
1. HPV 6 and 11 types: can be life threatening in children because of closure of larynx
2. HPV 6 and 11 - these are warts that happen almost exclusively on the external genitalia and perianal area (rarely becomes malignant)
38
1. What hallmarker does HPV cytology usually show?
2. How are warts from HPV treated?
1. koilocytic cells
2. These do not regress they have to get surgical cryotherapy, electrocautery, etc
39
Haemophilus Ducreyi
1. What is it?
2. Where and in who is this more common?
3. What is the common treatment
1. genital ulcers, soft painful chancre that is slow to heal without treatment
2. More common where HIV >8% and more commonly in men
3. Azithromycin
40
Klebsiella granulomatis (Donovanosis)
1. What is the presentation?
2. Where (location) does this occur?
3. Histology?
4. tx
1. beefy red painless lesions
2. caribbean and new guinea
3. image
4. Tetracylcines, erythromycin, and SXT
41
1. What is in the cortex of the ovary
2. What is in the medulla of the ovary?
1. follicles at diff stages of development [black bracket]
2. connective tissue (stroma) with blood vessels, nerves, and lymphatics [blue bracket]
42
1. What is the role of germinal epithelium around the ovary?
2. Where is the tunica albuginea of the ovary found?
1. simple cuboidal epithelium - releases mature ooctye (arrowhead)
2. irregular connective tissue behind germinal epithelium - no follicles present (bracket)
43
1. What is a primodial follicle?
2. What are follciular cells?
3. How do follicular cells change while follicle prepares to relase oocyte?
1. Small follicle in the cortex that contains a primary oocyte surrounded by a single layer of flat follicular cells. Eventually it gives rise to oocyte.
2. support cells in a follicle - when follicular cells become cuboidal and proliferate they form gap junctions with each other. (then they are called granulosa cells) - as follicle develops more layers of granulosa cells ocurrs
44
1. What is the zona pellucida in ovary?
2. What is its purpose?
1. thick extracellular matrix (ECM) that surrounds oocytes (arrowhead).
2. Zona pellucida supports communication between oocytes and follicle cells during oogenesis; protects oocytes, eggs, and embryos during development, and regulates interactions between ovulated eggs and free-swimming sperm during and following fertilization.
45
Secondary follicle
1. A (antrum) - what is its purpose?
2. TI (theca interna) - what is it/its purpose?
3. TE (theca externa) - what is it/its purpose?
4. GC (granulosa cell layer) - what is its purpose?
1. made from the liquor folliculi secreted from granulosa cells - an important mediator in bathing and carrying nutrients to the oocyte
2. organized stromal cells that are highly vascular, respond to LH to make androstenedione
3. organized stromal cells - connective tissue and smooth muscle
4. for support
46
1. What is the cumulus oophorus in women?
2. What is corona radiata of the oocyte?
1. granulosa cells surrounding oocyte and that form the stalk
2. granulosa cells surroudning oocyte that touch zona pellucida
47
1. What are the phases the follicle goes through in development starting with primordial and ending in corpus luteum (5)
2. Which phases are gonadotropin independent, gonadotropin responsive, gonadotropin dependent
1. primordial follicle -
2. primary, secondary follicle
3. antral follicle
4. mature graffian follicle
5. corpus luteum
6. independent is primordial to secondary (pre-antral);;; responsive is from antral to early mature graafian follicle;;; dependent is mature graafian follicle to corpus luteum
48
1. What is an atretic follicle
2. What cells differentiate and reorganize to form corpus luteum?
1. follicles that stop developing and die, this occurs in ovary and they are replaced by connective tissue
2. thecal cells
49
1. What happens in the antral phases of the follicle development?
2. What causes antrum to stop growing?
1. growth of granulosa cells (to multiple layers)
2. once follicle protrudes from ovary surface inhibin begins to be released and stops follicle development. (this is still before ovulation) - no longer responsive to FSH and LH
50
1. In the corpus luteum what cells develop?
2. what do these cells (2) produce?
1. granulosa lutein cells and theca lutein cells - these develop from granulosa and thecal cells respectively
2. Granulosa lutein cells (estrogen, progesterone, and inhibin) [arrow] +++ Theca lutein cells (progesterone and androgens) [arrowhead]
51
1. What is the corpus albicans?
2. when does it appear?
3. What does it cause in ovary?
1. degenerated corpus luteum
2. after pregnancy or if fertilization does not occur/fail
3. forms hyaline scar tissue in ovary
52
What is the purpose of these cells in the epithelium of the fallopian tubes?
1. Ciliated Cells
2. Peg Cells
1. wave oocyte (or zygote if fertilization has occured) toward uterus
2. secrete fluid for ovum/zygote
53
Endometrium vs myometrium
1. Which is black bracket vs blue bracket
2. which is site of embryo implantation
3. Which changes with menstrual cycle
4. Which undergoes hypertrophy during pregnancy
1. black = endometrium,, blue = myometrium
2. endometrium
3. endometrium
4. myometrium (also has many blood vessels, thick bands of smooth muscle, and no distinct layers)
54
Uterine epithelia of endometrium
1. Which part is stratum functionale
2. Which part is stratum basale
3. What is the function of the stratum functionale
4. What is the function of the stratum basale
5. Wha tis the function of the uterine glands (arrow)
1. black bracket - bottom 2/3 of endometrium
2. blue bracket - upper 1/3 of endometrium
3. sheds during menstruation
4. retained during menstruation but regenerates functionale layer
5. secretes fluid to support embryo if it implants
55
1. Describe what happens to endometrium in days 1-4 of menstrual cycle
2. Describe days 4-14
3. Describe days 15-28
1. functional layer breaks down, large amounts of blood excreted
2. endometrium thickness is minimal - uterine gland is straight and thin
3. endometrium thickness is max, now uterine glands have saw tooth appearance and are wide - ready for implantation in this stage
56
1. What are arcuate arteries of endometrium?
2. What are radial/straight arteries?
3. What are spiral arteries?
*this is all blood supply to the endometrium*
1. branch off uterine artery, winds through the myometrium
2. branch off of arcuate arteries, travel towards endometrium. Straight arteries supply the basal layer of endometrium.
3. Highly coiled arteries that supply functional layer. These grown during menstrual cycle and then constrict and breakdown during menstruation.
57
1. What is swabbed during pap smear?
1. the point where ectocervix transitions to endocervix because this change in cells can be dangerous and similar to cancer.
58
This is the surface of a part of the woman's reproductive tract. What is it?
1. this is the vagina
2. It has mucosa highly folded with paipllae
59
Mammary glands
1. What is the terminal duct lobular unit?
2. What is the stroma of a lobule vs interlobular stroma
3. Where are alveoli found and their purpose?
1. in image - lobule plus its stalk
2. stroma within a lobule vs stroma between enclosed lobules
3. They are found in the ductule and they product milk
60
1. What is merocrine secretion
2. What is apocrine secretion
3. What is colustrum
1. release of proteins and sugar by exocytosis
2. release of lipid droplets with membrane
3. yellow fluid secreted righta after birth (high protein, lower fat, contains IgA from plasma cells - overtime fat and sugars rise to better feed baby)
61
1. Describe how breast milk moves through lobule/mammary gland to secrete milk?
1. Milk is made in alevoli
2. Go into ductule and then intralobular collecting duct
3. Then move through extralobular terminal duct
4. Then finally along with many other glands -> milk is secreted into lactiferous duct and then nipple
62
1. What do umbilical arteries carry and where does it take this blood?
2. What does umbilical vein carry and where does it take this blood?
1. deoxygenated blood and takes it to the placent to pick up oxygen
2. carries oxygenated blood to fetus
63
1. What is wharton's jelly?
2. Where is it found
3. what is its purpose?
1. connective loose tissue with fribroblasts and stem cells - found in the umbilical cord
2. provide cushion, protection, and structural support to umbilical vessels by preventing their compression, torsion, and bending
64
1. What is the amnion of the embryo?
2. What is chorionic villi?
3. What is basal plate?
1. the amnion contains a thin, transparent fluid in which the embryo is suspended, thus providing a cushion against mechanical injury. (blue bracket)
2. chorionic villi (black bracket) - make up a significant portion of the placenta and serve primarily to increase the surface area by which products from the maternal blood are made available to the fetus
3. basal plate (arrowhead) - holds maternal blood vessels that supply placenta. Used to be endometrium.
65
1. What are decidual cells?
2. What are they formed from?
3. What is their purpose?
1. Decidual cells are responsible for the secretion of hormonal factors for successful blastocyst implantation and for development of the utero-placental interface.
2. With placenta formation - the endometrium changes and stromal cells become decidual cells to form decidua
3. Create the decidua which is the maternal side of the placenta + lacunae expand into the decidua as well.
66
1. What are the syncytiotrophoblast made from?
2. What are their purpose?
1. This is made from outer layer of cells of embryo when it has implanted into uterus. This is different than decidual cells because decidual cells come from endometrium.
2. The syncytiotrophoblast, the outermost layer of the human placenta, is the main site of exchange for drugs and metabolites, nutrients, waste products, and gases between the maternal and fetal circulations.
## Footnote
Syncytiotrophoblast form inner fetal part of placenta while decidual cells form outer part of placenta from mother
67
1. Where is testosterone made in females
2. What about in males?
1. some in the ovaries, some in the adrenals, and some in peripheral tissues
2. Mostly in leydig cells of testes
68
1. What is the difference between testosterone and DHT?
2. How is DHT made and where?
1. DHT is a much more potent androgen than testosterone
2. DHT is made from testosterone via the 5α reductase enzyme. It is made in peripheral tissues.
## Footnote
DHT helps lead to penis, scrotum, prostate development
69
1. What are the three major forms of estrogen in females?
2. Which is the most potent estrogen
1. estradiol, estrone, estriol
2. estradiol
70
1. What is the mullerian inhibitor factory (AMH) meant for?
2. How is it related to the SRY gene?
1. This is something that males have and it stops the generation of the mullerian duct which normally would form the female genital tract and external genitalia
2. SRY gene codes for the AMH factor that stops female genitalia from forming
71
Tanner stages for female sexual development (pelvis and breast)
1. stage 1
2. stage 2
3. stage 3
4. stage 4
5. stage 5
1. preadolescent- no pubic hair and no changes in breast
2. sparse, pigmented hair mainly along labia with some breast budding
3. Darker, coarser curlier hair and continued enlargement of breast
4. adult, but decreased distribution of hair, areola and papilla from secondary mound
5. adult in quantity and type with spread to medial thighs _ mature female breast
72
1. Where in ovary is estrogen mainly made?
2. Where is estrogen degraded and excreted?
1. follicle
2. degraded in liver to inactive metabolites - excreted in urine
73
Estrogen
1. explain the synthesis of estrogen in ovary (including theca and granulosa cells)
2. Include how LH and FSH help these steps?
1. Theca cells - start with cholesterol which converts into pregnenolone via desmolase enzyme. Then with more changes you end up with androstenedione (an androgen) [THIS IS INDUCED BY LH]
2. Granulosa cells - takes androstenedione and converts it to testosterone. Then converted to estradiol via aromatase [THIS IS INDUCED BY FSH]
74
Progesterone
1. Where is it synthesized?
2. Where is it degraded?
3. What is its purpose? (7)
1. corpus luteum (but if pregnant - placenta too), adrenal glands, and testes if male
2. Degraded in liver
3. Opposes proliferative effects of estradiol, establishes and maintains pregnancy, inhibits LH and FSH, increases secretion and contraction of fallopian tubes, increases endometrial secretion and cervical mucus, in puberty along with estrogen - increases duct growth and branching in breast, in pregnancy along with estrogen, extensive ductal growth but inhibits milk production, increases thermoregulatory set point in hypothalamus to elevate temperature.
75
1. What are SHBGs?
2. What do they do?
3. Where are they made?
1.sex hormone binding globulins
2.they carry sex steroid hormones. Bind androgens more than estrogen.
3. the liver
76
# Estradiol effects on
1. Brain
2. Liver
3. Bones
4. Adipose tissue
5. Cardiovascular
6. Skin
1. inhibits neuronal cell death, helps hypothalamic maturation
2. Increase LDL receptor to clear circulatin HDL, produce transport proteins of hormones
3. promotes osteoblasts activity and inhibits osteoclasts. Required for epiphyseal plates closure.
4. Increases lipolysis
5. promotes vasodilation (increased NO production)
6. maintain healthy smooth skin
77
# Effects of estradiol on
1. Breast
2. Female reproductive tract (vagina, uterus, fallopian tubes, external genitalia)
3. Ovaries
1. development of ducts and stroma - deposition of fat
2. growth and maturation of reproductive tract, shifts vaginal epithelium from cuboidal to stratified to increase resistance to trauama and infection. thickens the endometrium during menstrual cycle.
3. stimulates maturation of follicles and synergizes with FSH to allow oocyte release
78
# OVARIAN CYCLE PHASES
Follicular Phase (day 1-13)
1. Changes in GnRH
2. changes in FSH
3. changes in LH
4. Changes in estrogen
5. changes in progesterone
6. changes to follicle
1. Increased GnRH pulse frequency leads to increased FSH and LH
2. Increased FSH
3. Increase in LH
4. Increase in FSH causes follicle to excrete estrogen so this increases. This is also doing negative feedback to diminish FSH and LH release.
5. Not much increase - barely any
6. follicle grows until its almost about to relase oocyte
| days 1-13
79
# OVARIAN CYCLE PHASES
Ovulation Phase (Day 14)
1. Changes in estrogen
2. Changes in GnRH
3. changes in FSH
4. changes in LH
5. changes in progesterone
6. changes to follicle
1. Mid cycle surge of estradiol - there is a switch of negative feedback to positive feedback
2. increase of estrogen triggers increase of GnRH pulses
3. surge in FSH
4. surge in LH (much more than FSH -this leads to ovulation)
5. no significant changes yet
6. release of follicle and begining to form corpus luteum
80
# OVARIAN CYCLE PHASES
Luteal phase (day 15-28)
1. Changes in estrogen
2. Changes in Progesterone
3. changes in FSH and LH
4. changes in GnRH
5. changes to follicle
1. corpus luteum produces some estradiiol but levels not same as in follicular phase (lower levels lead to eventual degradation of endometrium)
2. large amounts of progesterone made by corpus luteum
3. FSH and LH are very low because progesterone and estradiol do negative feedback on hypothalamus
4. GnRH is low because negative feedback
5. follicle is now corpus luteum - it will eventually degrade unless fertilization occurs and the hCG from embryo starts to maintain corpus luteum and thus progesterone production
81
# UTERINE CYCLE (due to ovarian cycles)
Proliferative Phase (Days 5- 14)
1. What is happening to endometrium
2. What is happening to glands, stroma, blood vessels
3. What ovarian cycle is this tied to?
1. endometrium is growing due to increase of estrogen release
2. growth of all
3. follicular phase
82
# UTERINE CYCLE (due to ovarian cycles)
Secretory Phase (Days 14-28)
1. What is happening to endometrium
2. What is happening to glands, stroma, blood vessels
3. What ovarian cycle is this tied to?
1. with progesterone - proliferation of endometrium is inhibited
2. numerous secretions to prepare for embryo. changes in blood vessels to support embryo like growth of spiral arteries.
3. Luteal phase
83
# UTERINE CYCLE (due to ovarian cycles)
Menses
1. What causes the occurence of menses?
2. What happens to the endometrium?
1. during days 1-5 - there is loss of corpus luteum so this period has no/low progesterone or estrogen. This state cannot maintain endometrium so it sloughs off and this is the menses.
84
Estrogen Priming
1. what is it?
1. estrogen secretion precedes progesterone secretion
2. estradiol upregulates progesterone receptor expression in some tissues preparing them to response to preogesterone.
85
1. why are obese menopausal women at risk for endometrial carcinoma?
1. adipose tissue is able to release estrogen. Menopausal women will have unopposed (bc no progesterone available) estrogen levels higher after menopause -> this leads to increased risk of abnormal endometrial growth
86
1. What leads to menopause?
2. What sx occur?
3. What changes to FSH and LH
1. ovarian reserve (follicles) are gone - so no follicles left to release oocyte or create corpus luteum. This leads to decreased estradiol (follicle) and progesterone (corpus luteum).
2. atrophy of vaginal epithelium, decrease vaginal secretions, bone loss, hot flashes
3. Still have increased FSH and LH - because body is trying to stimulate the process that before made it raise estrogen and progesterone levels
87
# Oogenesis
1. oogonium is 2n and then undergoes (Blank A) to form..
2. primary oocyte (2n) - then begins meiosis I but before birth this process arrests in (Blank B)
3. After puberty meiosis I resumes but then arrests at (Blank C) before sperm penetration
4. After sperm menetration - oocyte meiosis completes immediately after sperm penetrates the oocyte
1. Blank A - mitosis
2. Blank B - prophoase I
3. Blank C - metaphoase II
88
1. What is the process of capacitation in reproductive system? (2)
2. How long does it take?
3. What prevents other sperm from fertilizing same egg.
1. The change sperm undergo in the reproductive path in order to be able to penetrate the female egg. Destabilisation of the acrosomal sperm head membrane which allows it to penetrate the outer layer of the egg, and chemical changes in the tail that allow a greater mobility in the sperm.
2. Takes about 10 hours.
3. Once undergoing capacitation, sperm are able to get through zona pellucida - this triggers zona pellucida to become impermeable by other sperm at the very point that the first sperm gets through zona pellucida
89
1. What are the different names of a developing organism in a human - (start with zygote)
1. zygote (first 4 days)
2. morula
3. blastocyst (5-6 days after fertilization) - this still occurs in ampulla of fallopian tube
4. embryo (until 8 weeks)
5. fetus (after 8 eeks)
90
1. How are trophoblasts, syncyntiotrophoblasts, and cytotrophoblasts related?
2. What hCG released from?
1. trophoblasts are outer cells of the blastocyst.
2. As the blastocyst embeds itself in the endrometrium it differentiates into two layers: the cytotrophoblast (inner) and syncytiotrophoblast (outer).
3. released by the syncyntiotrophoblasts
91
1. What do syncyntiotrophoblast release?
2. What do they do?
1. hCG, estrogen, progesterone, HPL
2. hcg maintains corpus luteum functioning, estrogen increases blood flow in uterus, progesterone - suppresses ovulation and menstraution/inhibits uterine motility to maintain pregnancy, and more (remember placenta takes over progesterone secretion at weeks 8-10), HPL is in other card
92
HPL (human placental lactogen)
1. When is this released
2. what does it do?
1. increases release 2nd part of pregnancy
2. Insulin resistance - to increase glucose available for fetus.
*produced by syncyntiotrophoblasts*
93
Relaxin sex steroid
1. what produces it
2. what is its function?
1. corpus luteum, uterus, placenta, and mammary glands
2. relaxes the pubic symphysis and other pelvic joints - to soften and dilate the uterine cervix. Makes delivery easier and inhibits uterine contractions [PREPARES FOR DELIVERY]
94
1. Why do pregnant women not lactate but they do after delivering baby?
1. during pregnancy estrogen and progesterone levels are high and active. Both inhibit the secretion of prolactin
2. Without placenta providing estrogen and progesterone once baby is delivered - then prolactin cannot be inhibited and allows for lactation to occur.
3. BUT estrogen and progesterone do develop the breast properly during pregnancy to be able to lactate eventually
95
Ovaries
1. Blood supply
2. Innervation
1. abdominal aorta
2. aortic plexus (autonomic nerves)
96
Uterine tubes/fallopian tubes
1. Blood supply
2. parts
1. uterine artery (from internal iliac artery), ovarian artery (from abdominal aorta)
2. infundibulum (attached to ovary), ampulla (middle part-thick), isthmus (most narrow part connecting to uterus
97
Uterus
1. blood supply
2. innervation
3. changes in position - is it dangerous?
1. uterine artery
2. pelvic plexus
3. can be retroverted - this can at times cause painful intercourse but other times normal
98
Vagina
1. Blood supply
2. location (between what two things)
3. What is the vaginal fornix
1. vaginal artery, uterine artery (these anastomose)
2. between bladder and rectum
3. the recess between the cervix and vaginal wall
99
1. What is the recto-uterine pouch of douglas?
2. Why is it clinically important?
1. region/pouch situated between the rectum and uterus
2. This can be site of infection since fluid typically collects here - can be drained through vagina or rectum
100
1. What is the recto-vesicle pouch in men?
1. This is the equivalent as recto-uterine pouch of douglas in women. Lowest lying space in peritoneal cavity and infection can settle here too.
101
1. What are the most important support ligaments of the uterus?
2. What muscle forms the pelvic diaphragm and also helps support the uterus
1. cardinal ligament
2. levator ani
102
1. What three ligaments hold up the ovary?
1. suspensory ligament of the ovary (fold in the peritoneum), round ligament of the ovary (remnant of gubernaculum), broad ligament (specifically the mesovarium part)
103
Broad ligament
1. Extends from where to where in females?
2. Parts? (3)
3. Contents of broad ligament
1. uterus to the lateral pelvic walls
2. mesosalpinx (drapes over uterine tube), mesovarium (drapes over the ovary and ovarian ligament) , mesometrium (rest of broad ligament) (in image)
3. made up of layers of peritoneum, uterine tube, round ligament of uterus, round ligament of ovary, uterine and ovarian vessels, lymphatics, and more
104
1. What does water under the bridge mean for female anatomy
1. It means that the uterine artery (bridge) passes over the uretur (water) - something to note in surgeries
105
1. What are the two division of the perinum
1. urogenital triangle, anal triangle
106
Dermatomes of the perineum
1. What spinal cord sections are responsible for the perineum dermatomes?
2. Much of the somatic and sensory innervation of the perineum is provided by what nerve?
1. S3-S5
2. Pudendal nerve (S2-S4)
107
1. What does the vulva consist of? (3)
1. labia majora, labia minora, clitoris - external genitalia
108
1. Where is the pubic arch?
2. What structure fills the gap here?
3. Where is this structure in relation to the pelvic diaphragm??
1. found underneath the pubic symphysis
2. the urogential diaphragm (perineal membrane)- a dense fibrotic layer situated over the urogenital triangle
3. urogenital diaphragm is next to but more ventral than the pelivc diaphragm (image)
109
1. Where is the deep perineal space?
2. Where is the superficial perineal space?
1. Deep perineal space/pouch - space more internal from the perineal membrane/urogenital diaphragm. It is a pouch because it is between perineal membrane and the pelvic diaphragm (muscles of pelvic floor)
2. Superficial - space between exterior of the perineal membrane and superficial fascia of muscles on top of perineal membrane
110
1. What structures in the female body are in the deep perineal space?
2. What about superficial perineal space?
1. urethra, external urethral sphincter, arteries of clitoris, dorsal nerve of clitoris, vagina, nerve supply of muscles, and more
2. bulb of vestible, crura of clitoris (attached to pubic arch), bulbospongiosus, ischiocavernosus, perineal body, Bartholin's glands, and more
111
# In female body
1. What is bulb of vestibule?
2. What is crura of clitoris?
3. What is bulbospongiosus?
4. What is ischiocavernosus?
5. What are the Bartholin's glands?
1. bulb of vestibule during sexual arousal become engorged with blood
2. legs of clitoris that go along the pubic arch
3. contributes to clitoral erection and the contractions of orgasm, and closes the vagina.
4. assists with clitoral erection
5. lubricates vagina
112
1. What are the structures in the deep perineal space of the male body?
2. What about superficial?
1. membranous urethra, external urethral sphincter, arteries of penis, Cowper's gland, etc
2. bulb of penis, crura of penis, bulbospongiosus, ischiocavernosus, perineal body, etc
113
Ischioanal (ischiorectal) fossa
1. Where is this found?
2. What important structures (2) does it contain?
1. a space filled with fat lateral to the anal canal and just below the pelvic diaphragm (image)
2. pudendal nerve, internal pudendal vessels
114
1. What is the path of the pudendal nerve once it leaves the vertebral column (S2-S4)?
1. exits through the greater sciatic foramen
2. Passes around the ischial spine
3. goes to its target destinations
*image is from back side of the spine*
115
Urinary bladder - nerves or areas of spinal cord?
1. what is damaged if person is unable to relax detrusor muscle, constrict internal sphincter, and it is hard for bladder to fill completely?
2. What is damaged if person is unable to contract detrusor muscle, relax internal sphincter, and it is hard to empty the bladder?
3. What is damaged if person is unable to voluntarily control micturition
1. sympathethic nerves (T11-L2)
2. parasympathethic (S2-S4)
3. pudendal nerve (somatic nerves)
116
# Medications
Estrogens
1. indication
2. MOA
3. adverse effects
1. used in combined oral contraceptives
2. Inhibits ovulation by decreasing FSH and LH via negative feedback
3. nausea, breast tenderness, HTN, weight gain, thrombosis
117
# Medications
Progestins
1. indication
2. MOA
3. adverse effects
1. Used in combined oral contraceptives, progestin only pill, hormone replacement, emergency contraceptive, long-acting reversible contraception
2. inhibit ovulation by decreasing FSH and LH via negative feedback. Also thickens cervical mucus and decreases sperm penetration
3. HA, fatigue, change in mood, weight gain, etc
118
# Medications
Mifepristone
1. Indication
2. MOA
3. Adverse effect
1. used in medical abortion in first trimester + **used along with prostaglandins to promote uterine contraction and soften cervix**
2. inhibit progesterone receptor and cause termination
3. vaginal bleeding, cramps, diarrhea
119
Misoprostol
1. Indication
2. MOA
3. Adverse effect
1. **Combined with mifepristone** (an analogue for prostaglandin 1) for medical abortion
2. Increases uterine tonicity and contractility by stimulating prostaglandin receptors
3. diarrhea, abdominal pain
120
Tamoxifen, raloxifene
1. Indication
2. MOA
3. Adverse effect
1. ER+ breast cancer
2. selective estrogen receptor modulator -blocks estrogen from connecting to the cancer cells and telling them to grow and divide
3. Hot flashes, HA, mood swing
121
Anastrozole
1. Indication
2. MOA
3. Adverse effect
1. ER+ HER2- breat cancer
2. inhibits aromatase to reduce estrogenic hormone
3. hot flashes, edema, bone/back pain
122
Clomiphene
1. indication
2. MOA
3. Adverse Effects
1. Infertility
2. stimulates release of FSH and LH
3. hot flashes, headache, mood swing
123
Follitropins
1. indication
2. MOA
3. Adverse Effects
1. infertility
2. Increases folliculogenesis
3. HA, abdominal pain, ovarian cyst
124
1. What is the pill normally made up of?
2. how is it metabolized and eliminated?
3. Types?
4. Contraindications?
1. estrogen and progestin
2. metabolized in liver and excreted via kidney
3. Monophasic (same amount of estrogen and progestin), multiphasic (different amounts in the pill each week)
4. history of DVT, CV if older than 35, smoker, excess estrogen, current breast cancer
125
1. For those who cannot take estrogen what are their options?
2. What contraceptive option can make fertility take up to 1 year to return after stopping this conctraceptive
1. progestin only shot or pill - this still inhibits ovulation, thickens cervical mucus, thins endometrial lining
2. The progestin only shot. For progestin only pill fertility returns within one cycle of stopping mini pill.
126
# LARC
IUD
1. Mechanism of action
2. Types
1. IUD caus an inflammatory reaction to occur in uterus due to foreign object. This is toxic to sperm and ova and thus impairs implantation.
2. Hormonal and copper. Hormonal has additional levonorgestrel (estrogen analogue) hormone that also thickens cervical mucus and thins endometrium to make it even more harder for sperm to fertilize egg.
127
1. The implant in arm release what as a form of LARC
1. slowly releases etonogestrel (a progestin) into circulation.
128
1. what are the two options for emergency contraceptives?
1. placing copper IUD <120 hours after unprotected sex
2. Morning after pill (levonorgestrel or ulipristal) that should be taken <72 hours after unprotected sex. Ulipristal (ella) is Rx only. levonorgestrel is plan B
129
Anovulatory Cycles
1. Pathology
2. Sx
3. How does this affect ovulation?
4. When does this usually occur?
1. no progesterone secretion - leads to excessive endometrial growth from unopposed estrogen.
2. Irregular bleeding due to estrogen alone not being able to support the endometrium alone but also unopposed estrogen leads to thicker endometrium.
3. Ovulation does not occur - with no ovulation then corpus luteum cannot form and produce progesterone.
4. Usually at menarche bc HPA axis is underdeveloped or when approaching menopause bc loss of ovulation is starting to occur.
130
Chronic Endometritis
1. pathology
2. Histology hallmark
3. What causes this?
4. Sx?
1. Inflammation of endometrium
2. Plasma cell (A type of immune cell that makes large amounts of a specific antibody. Plasma cells develop from B cells that have been activated.) - image
3. IUDs, pelvic inflammatory disease, TB (rare)
4. infertility
131
Endometrial Polyps
1. pathology
2. Sx
3. When does this usually occur?
4. Histology of polyps
1. Hyperplastic growth of the GLANDS and STROMA of the endometrium that they project out.
2. Painless uterine bleeding
3. Common near menopause - bc estrogen is still produced and unopposed
4. polyps show stroma and glands
132
Endometrial Hyperplasia
1. pathology
2. sources of estrogen
3. when does it often occur?
4. sx?
5. Histology
1. Hyperplasia of endometrium due to unopposed estrogen and absence of progesterone. This is considered pre-malignant condition of uterus. Can develop endometrial carcinoma
2. Adipose tissue can release estrogen, hormone replacement therapy, ovarian granulosa cell tumor can secrete estrogen
3. peri/postmenopausal women since there may be no more ovulation (no progesterone)
4. abnormal uterine bleeding
5. hyperplasia, more bigger glands, more stroma
133
Asherman Syndrome
1. pathology
2. causes
3. sx
1. uterine adhesions that can involve endometrium and this can disrupt menstruation
2. 90% of cases is from uterine curettage (D&C) - uterus is scraped with a curette and then this damages the regenerative layer (basalis) of endometrium
3. Infertile, amenorrrhea (no menses) due to anatomical changes
134
Endometriosis
1. What is it?
2. symptoms
3. histology
4. malignancy risk?
1. presence of "ectopic" endometrial tissue at a site outside the uterus
2. Infertility, menstrual irregularities, severe dysmenorrhea (painful menses), pelvic pain, possible pain with defecation and dysuria
3. endometrial tissue found outside uterus has glands and stroma, chocolate cysts in ovary (ovarian cyst with old blood)
4. can co-exist with ovarian endometroid carcinoma
135
Adenomyosis
1. What is it?
2. symptoms
3. histology
1. when the tissue that normally lines the uterus (endometrial tissue) grows into the muscular wall of the uterus
2. menometrorrhagia (excessive and prolonged uterine bleeding occurring at irregular and/or frequent intervals), colicky dysmenorrhea, pelvic pain
3. irregular nests of endometrial stroma and glands present deep in myometrium. Hyperplasia of basal endometrium.
136
Endometriosis
1. common patient type
2. Etiology (possible theories - 4)
1. women in reproductive age, improves in menopause and in pregnancy
2. Retrograde flow (movement of menstrual tissue through fallopian tubes), metastasis (spread through venous or lymphatic system), Metaplasia (tissue in coelomic epithelium turn into endometrium in development), stem cells (develop into endometrial tissue in places they shouldnt)
137
Endometrial Carcinoma
1. types
2. mutations for each type
3. commmon ages for each?
4. which is more common
1. Type I (endometrioid) and type II (serous)
2. Endometrioid (PTEN or MLH1 mutation);; Serous (TP53 mutation)
3. Endometrioid (55-65);; serous (65-75 older)
4. Type 1
138
Endometrial carcinoma
1. Which type is estrogen dependent and independent
2. common clinical features of a pt with each type?
3. what are the differences seen in endometrium in each type
4. which is more aggressive?
1. Type I (endometrioid) is dependent on estrogen. Type II (serous) is independent
2. type I (obese, HTN, DM, h/o infertility);;; type II (thin physical condition)
3. Type I (unopposed estrogen so dysplastic growth of endometrium);; Type II (shows atrophy of endometrium - which is still dysplastic)
4. Type II (serous)
139
Carcinosarcoma (malignant mixed mullerian tumor)
1. What is this?
1. A malignant tumor that is a mixture of carcinoma (cancer of epithelial tissue [adenocarcinoma-glands], which is skin and tissue that lines or covers the internal organs) and sarcoma (cancer of connective tissue, such as bone, cartilage, and fat).
140
Leiomyoma
1. occurs in what pt type/age
2. pathogenesis
3. sx
1. pre-menopausal women - common
2. Benign tumor of myometrium (smooth muscle of uterus) - usually multiple and growth is stimulated by estrogen. White masses within the myometrium.
3. usually asymptomatic and can be found as pelvic mass on exam or US. May cause irregular bleeding, infertility, pelvic pain, bladder issues.
141
Leiomyoma
1. Histology/morphology
1. these can grow very large
2. typically uniform cell structure, few or no mitotic figures.
142
Leiomyosarcoma
1. pathogenesis
2. sx and in what patient type
3. Morphologic features
1. arise de novo - malignant smooth muscle tumor of uterus (myometrium)
2. abnormal uterine bleeding - occurs in post-menopausal women
3. single large mass with ill defined borders - solitary, soft, hemorrhagic, necrotic mass
143
Leiomyosarcoma
1. What 3 things indicate malignancy in the tumor
1. Atypia
2. increased mitotic figures 10 or more
3. tumor necrosis
144
Benign Stromal Nodule
1. morphology
2. sx
3. Histology
1. benign well circumscribed **stromal** nodule in the myometrium. Typically looks yellow
2. abnormal uterine bleeding
3. uniform, small oval cells resembling those of endometrial stroma (but it is found in myometrium)
145
Endometrial Stromal Sarcoma
1. morphology
2. sx
3.Histology
1. yellow ropy or ball like masses filling dilated channels of the myometrium
2. abnormal uterine bleeding
3. infiltrative margin. Low grade resembles stromal nodules but high grade shows clear atypia.
146
1. what are the most common organisms to cause fallopian tube infections?
1. chlamydia trachomatis
2. but also gonorrhea
147
# OVARIAN TUMORS
1. What are the three main categories of ovarian tumors
1. tumors of surface epithelium of ovary
2. Germ cell tumors
3. Sex cord-stromal tumors
148
PCOS
1. pathogenesis/what is wrong
2. clinical sx
3. relationship to testosterone
4. relationship to insulin
1. Multiple follicular cysts in the ovary. Follicular cells are formed in follicles (cells that surround egg) and follicle grows but never releases an egg. These follicles are able to still release estrogen. + additional sx make up PCOS. Need to have additional sx bc you can have cysts without having PCOS.
2. amenorrhea, infertility, persistant anovulation, insulin resistance, obesity, premature menarche, excess body hair, acne, thinning hair
3. High levels of insulin causes the ovaries to produce too much testosterone, which interferes with the development of the follicles (the sacs in the ovaries where eggs develop) and prevents normal ovulation.
4. High insulin is associated with PCOS. It is a major driver of PCOS not just a sx. These patients can experience hyperinsulinemia.
149
Ovarian Tumors (general)
1. common patient age
2. sx
3. genetic predisposition
4. increased risk with
5. decreased risk with
1. females >55 years old
2. abdominal distention, bowel obstruction, pleural effusion
3. BRCA1 BRCA2 mutations, Lynch syndrome, strong family history
4. Advanced aged, infertility, endometriosis, PCOS, genetics
5. previous pregnancy, history of breastfeeding, oral contraceptives, tubal ligation
150
Epithelial Ovarian Tumors - Serous type
1. What are the two types (one benign, one malignant)
2. unilateral or bilateral?
3. pathology/what is wrong?
4. Histology for malignant type?
| Most common ovarian neoplasm
1. serous cystadenoma (benign) and serous cystadenocarcinoma (malignant)
2. bilateral both
3. serous means the tumor on epithelium secretes serum (water). Serous cystadenoma is thin walled cyst filled with watery fluid. S. cystadenocarcinoma has cells similar to fallopian tube cells and their growth has irregular bodies
4. psammoma bodies (these are laminated calcifications)
151
Epithelial Ovarian Tumors - Mucinous type
1. What are the two types (one benign, one malignant)
2. unilateral or bilateral? or special gross characteristics?
3. pathology/what is wrong?
4. genetic mutation in malignant type?
1. mucinous cystadenoma and mucinous cystadenocarcinoma
2. malignant ones are unilateral - benign ones are often multiloculated (divided into many segments)
3. Benign one is tumor lined by mucus-secreting epithelium that can lead to accumulation of mucinous material in peritoneum
4. KRAS mutation in about 50% of them
152
Epithelial Ovarian Tumors - Endometrioid type
1. Histology - what do the cells look like?
2. genetic mutaiton?
1. Tubular glands that look like endometrium but they are not from endometrial cells. Often seen in patients with endometriosis though.
2. PTEN mutation
153
Epithelial OVarian Tumor: Brenner Tumor
1. benign or malignant?
2. Gross findings
3. From what is it thought to arise from? (epithelial cells or...?)
4. Histology findings
1. benign
2. solid, unilateral pale, yellow-tan tumor that appears encapsulated.
3. surface epithelium or from urogenital epithelium (bladder transitional cells)
3. Coffee bean nuclei on H&E stain
154
# most common sex cord stromal ovarian tumor
Sex cord stromal ovarian tumor: Granulosa cell tumor
1. pathology/what is wrong
2. sx
3. Histology hallmark findings
4. Tumor marker
1. this tumor produces large amounts of estrogens (and/or progesterone). All are potentially malignant (uterine endometrial adenocarcinoma) but chances are low
2. postmenopausal bleeding, endometrial hyperplasia, sexual precocity, breast tenderness
3. Call-Exner bodies (granulosa cells arranged around collection of eosinophilic fluid) (image)
4. inhibin positive
## Footnote
cam be a yellow mass too
155
Sex cord stromal ovarian tumor: Thecoma
1. pathology/what is wrong
2. sx
3. benign or malignant
1. benign - stromal tumors that resemble thecal cells of the developing follicle and that are composed of a minimum (less than 10%) of cells with granulosa cell differentiation -> may produce estrogen
2. abnormal uterine bleeding
3. benign
156
Sex cord stromal ovarian tumor: Fibroma
1. benign or malignant - unilateral or bilateral
2. pathology/what is wrong
3. Sx - explain Meig's syndrome
1. benign - unilateral
2. tumors of fibroblasts within ovarian stroma- solid, white tumor
3. Meig's syndrome (triad: ovarian fibroma, ascites, pleural effusion) + sx of pulling sensation on groin
157
Sex cord stromal ovarian tumor: Sertoli-Leydig Cell tumor
1. benign or malignant?
2. gross findings
3. hormone findings
4. sx
1. benign
2. yellow-brown mass. Resembles testicular histology - with tubules/cords lined by pink sertoli cells
3. may produce androgens
4. Virlization (hirsutism, male pattern baldness, clitoral enlargement)
158
Germ Cell Ovarian Tumors: mature teratoma (dermatoid cyst)
1. what is it made of?
2. sx?
3. when does it commonly occur?
4. complications
1. all three germ layers - contains hair, sebaceous oily material, etc
2. usually asymptomatic and found randomly but if big enough it can cause pain secondary to ovarian enlargement or torsion.
3. seen in first 2 decades of life
4. Monodermal form with thyroid tissue can form and present with hyperthyroidism (this is a rare specialized mature teratoma called **struma ovarii**) and can also become squamous cell carcinoma
159
Germ Cell Ovarian Tumors: immature teratoma
1. what is it made of?
2. when does it commonly occur?
3. benign or malignant?
1. contains fetal tissue, neuroectoderm,
2. before 20 years old
3. malignant
| malignant
160
Germ Cell Ovarian Tumors: Dysgerminoma
1. malignant or benign;;; bilateral or unilateral
2. most common in what age group
3. tumor markers
4. Histology findings
1. malignant and usually unilateral
2. adolescents
3. increased hCG and LDH
4. undifferentiated germ cells that look like nests of large cells with clear cytoplasm, fried egg appearance
161
Germ Cell Ovarian Tumors: Choriocarcinoma - embryonal
1. malignant or benign
2. tumor markers
4. pathophysiology
1. malignant - often fatal but rare
2. beta hCG
3. presence of trophoblastic malignant cells in the absence of an ongoing pregnancy. Choriocarcinoma tends to be invasive and to metastasize early and widely through both the venous and lymphatic systems.
162
Germ Cell Ovarian Tumors: Yolk Sac -embryonal
1. malignant or benign
2. gross findings
3. tumor markers
4. Histology findings
5. age group
1. malignant
2. large yellow, friable hemorrhagic solid mass
3. increased AFP
4. 50% have Schiller Duval bodies (resemble glomeruli)
5. children and young adult females
163
1. what cancers most commonly metastasize to ovary?
1. breast and GI
164
Vaginal Intraepithelial Neoplasia
1. age
2. precancerous?
3. appearance
4. histology changes?
1. reproductive age
2. yes - but can also regress
3. white or raised lesion
4. epidermal thickening with hyperkeratosis, nuclear enlargement, basaloid cells extend to surface
165
Vaginal intraepithelial carcinoma
1. causes by what virus?
2. Histology?
1. HPV 16 and 18 (this also can cause vulvar intraepithelial carcinoma)
2. Nests and cords of basaloid cells (basaloid describes conglomerated cells with hyperchromatic nuclei and sparse cytoplasm). May have area of central necrosis
166
Warty carcinoma in female body
1. caused by what virus?
2. Where is found?
3. histology?
4. precursor?
1. HPV 16 and 18
2. an infiltrating tumor that can be found in vulva and uterine cervix and perineum including anus
3. exophytic, papillary architecture with koilocytic atypica
4. VIN
5. in pre-menopausal women
167
Keratinizng carcinoma of the vulva
1. pathophysiology?
2. difference from cause of warty carcinoma
3. more or less common than warty carcinoma
1. uncontrolled growth of the outer squamous cells of the epidermis,
2. NOT CAUSED BY HPV
3. more common than warty carcinoma. Keratnizing carcinoma of the vulva is the most common type of the vulvar SCC
168
Bartholin cyst
1. pathogenesis
2. histology of cyst
3. sx
1. obstruction of bartholin gland duct by inflammatory process
2. cyst is lined by transitional or squamous epithelium
3. mass lesion with or without tenderness
169
Lichen Sclerosus of lower female repro tract
1. patient age
2. histology findings
3. sx
1. postmenopausal women
2. thinning of epidermis, degeneration of basal cells, hyperkeratois, sclerotic changes in dermis, band like lymphocytic infiltrate
3. itchy, burning, and pain affecting the vulva. Smooth white plaques or leukoplakic. Sometimes it is asymptomatic though.
170
Extramammary paget disease of female lower repro tract
1. what is it?
2. what does it look like?
3. what sx occur?
1. skin cancer that arises from glandular cells (sweat glands)
2. This disease appears as a red, velvety area with white islands of tissue on the vulva. At times it may be pink, and occasionally there are moist, oozing ulcerations that bleed easily.
3. itching and soreness
171
Vaginal adenosis
1. risk factor that can cause this
2. What is this?
1. DES exposure in utero
2. originally while a developing fetus, vagina was columnar epithelium and then transitioned into squamous epithelium - but if there is left over columnar epithelium in outer cervix/vagina this is known as adenosis
172
Gartner Duct cyst
1. What is this?
2. what does it look like?
1. a cyst found along walls of vagina and it is derived from wolffian duct residuals.
2. fluid filled, submucosal cyst
173
Squamous cell carcinoma of vagina
1. caused by what virus
2. most commonly an extension of what?
3. What is typical histology for SCC?
1. HPV 16 and 18
2. cervical carcinoma
3. keratin pearls, papillary growth pattern
174
Embryonal Rhabdomyosarcoma
1. what is it?
2. age of presentation
3. sx
1. a tumor that derives from embryonal rhabdomyoblasts (immature msucle cells)
2. <5 years old
3. clear, grape like mass growing from vagina (botryoid)
175
Cervicitis
1. Infectious causes
2. non-infectious causes
1. C. Trachomatis, N. Gonorrhoeae, T. vaginalis, and HSV-2
2. mechanical irritation from tampon, condom, etc or chemical irritation like from vaginal douching
176
Endocervical polyps
1. Histology
2. Sx
1. loose fibromyxoid stroma covered by endocervical epithelium - a polyp. Often with inflammation
2. abnormal vaginal bleeding
177
Cervical Intraepithelial neoplasia
1. where does it occur
2. What are the types of cells involved?
1. occurs at the squamocolumnar junction - this is what splits endocervix and ectocervix
2. Includes columnar (endocervix) and ectocervix (squamous epithelium) cells
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cervical squamous cell carcinoma
1. Risk factors
2. sx
3. If it invades where does it do it?
| Most commom cervical cancer
1. HPV 16 and 18, immunodeficiency, cigarette smoking, set at a young age or multiple sex partners
2. asymptomatic often or can have abnormal vaginal bleeding
3. invades locally like bladder or rectum
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Endocervical Adenocarcinoma
1. risk factors
2. where in the cervix does it usually occur?
## Footnote
2nd most common cervical cancer type
1. HPV 16 and 18
2. endocervix (columnar epithelium)
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Pap smear screening for cervical cancer
1. what is this trying to detect? (cell type)
2. Limitations?
3. when should these begin and how often?
1. koilocytes (large darkened nuclei)
2. best at detecting SCC but not adenocarcinoma, cannot be done during menses, need to correlate results with hx
3. at 21 and then q 3 years
181
Acute Mastitis
1. typical in what type of patient
2. pathogenesis
3. sx
1. women who are breast feeding
2. Acute mastitis is usually a bacterial infection and is seen most commonly in the postpartum period. Bacteria invade the breast through the small erosions in the nipple of a lactating woman, and an abscess can result. (s. aureus)
3. breast erythema, tenderness, fever, malaise
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Periductal mastitis
1. typical patient/risk factors
2. pathogenesis
3. sx
1. female smokers and also women with vitamin A deficiency (non lactating women)
2. inflammation of subareolar ducts - this leads to squamous metaplasia such that duct epithelium changes from cuboidal to squamous - this obstructs duct
3. periareolar mass with redness, tenderness, warmth - often get infection
183
Fat necrosis
1. what causes this?
2. What is seen in histology?
3. sx
1. caused from trauma - this leads to a benign inflammatory process
2. fat necrosis with inflammatory cells. Breast does have fat but not as much or prevalent as is seen in fat necrosis.
3. painless mass, asymptomatic, calcifications on mammogram.
184
Mammary duct ectasia
1. typical patient?
2. pathogenesis?
3. morphology/histology?
4. Sx
1. older women around 50 - typically women who have had multiple children
2. a benign (non-cancerous) breast condition that occurs when a milk duct in the breast widens and its walls thicken. This can cause the duct to become blocked and lead to fluid build-up
3. Mishappen duct with inflammatory cells nearby
4. dirty white, green, or black nipple discharge - usually no pain
185
Lymphocytic Mastopathy
1. pathogenesis
2. sx?
3. associated with what disease?
1. keloid-like fibrosis and with lymphocytic infiltration. The pathogenesis is unknown, but it may represent an autoimmune reaction
2. palpable mass - usually painless
3. autoimmune disease - diabetes often
186
# Benign Breast Changes
Non-proliferative (fibrocytic) changes - **simple cysts**
1. clinical presentation?
2. Where do these often occur?
1. lumpy or bumpy breasts in premenopausal women - if cysts burst it can lead to inflammation
2. majorioty of cysts occur in TDLU - Most cysts are lined by flattened epithelium
187
# Benign Breast changes
Non-proliferative (fibrocytic) changes - **fibrosis**
1. How does this occur?
1. If cysts in TDLU burst they can lead to inflammation and then fibrosis. Fibrotic material exchanges the epithelial lining of the cysts
188
# Benign Breast changes
Non-proliferative (fibrocytic) changes - **apocrine metaplasia**
1. What is this?
1. Alterations to lobular epithelial cells - such athat they take on appearance of an apocrine gland
189
# Breast changes
Proliferative Changes without atypia: **Epithelial hyperplasia**
1. What occurs in this?
1. The ducts of breast have increased luminal and myoepithelial cells. Distended ducts or lobules can occur with lumen filled with cluster of cells.
190
Proliferative Changes without atypia: **Sclerosing Adenosis**
1. What occurs in this?
1. increased number of compressed acini with dense stroma
2. A benign (not cancerous) condition in which scar-like fibrous tissue is found in the breast lobules (the glands that make milk). In sclerosing adenosis, the lobules are larger than normal.
191
Proliferative Changes without atypia: **Radial Scar**
1. What is this?
1. stellate architecture - central nidus of elastic/fibrotic tissue with radiating glands and ducts
2. This is idiopathic
192
Proliferative Changes with atypia: **Atypical Ductal Hyperplasia**
1. What is this?
2. Is this cancer?
1. Atypical hyperplasia is a precancerous condition that affects cells in the breast. Atypical hyperplasia describes an accumulation of abnormal epithelial cells in the milk ducts of the breast. Atypical hyperplasia isn't cancer, but it increases the risk of breast cancer.
193
Proliferative Changes with atypia: **Atypical Lobular Hyperplasia**
1. What is this?
2. Is this cancer?
3. lack expression of what
1. Atypical hyperplasia is a precancerous condition that affects cells in the breast. Atypical hyperplasia describes an accumulation of abnormal epithelial cells in the lobules of the breast. Atypical hyperplasia isn't cancer, but it increases the risk of breast cancer.
2. loses e-cadherin expression
194
Intraductal papilloma
1. what is it?
2. sx?
3. benign or malignant?
1. proliferation of normal ductal epithelial cells. Cells grow in finger like projections
2. bloody/serous discharge or small mass near nipple
3. benign - but should monitor
195
Ductal Carcinoma In Situ (DCIS)
1. malignant growth of what?
2. what is seen on mammogram?
3. Histology pattern
4. What is comedo DCIS?
5. Risk of cancer is same or both breast?
1. epithelial cells of duct
2. microcalcifications
3. central necrossi, large tumor cells, and plemorphic nuclei
4. cribiform pattern (glands within glands)
5. same breast, same quadrant
196
Lobular Carcinoma In Situ (LCIS)
1. malignant growth of what?
2. what is seen on mammogram?
3. Histology pattern
4. Marker?
5. Risk of cancer is same or both breast?
1. epithelial cells of lobule
2. not detected in mammogram bc it doesn't make micro-calcifications
3. loose intercellular connections. Round cells clumped together
4. loss of e-cadherin marker - this causes the loose connections
5. increase risk of cancer in either breast
197
Paget Disease of breast
1. invsive or noninvasive?
2. What is it?
3. sx/presentation?
1. noninvasive
2. extension of underlying DCIS breast cancer up the lactiferous ducts and into the contiguous skin of nipple.
3. Eczematous patches over nipple and areolar skin.
198
Invasive Ductal Carcinoma
1. presentation of mass? (description)
2. Where in bresat is it more often occuring?
3. Histology patterns
1. firm, fibrous, rock hard palpable mass with sharp margins
2. outer lateral quadrant bc more breast tissue
3. Histology shows duct like cells appearing in stroma indicating they have invaded base basement membrane of ducts
199
Invasive Ductal Carcinoma vs invasive lobular carcinoma
1. mammography results
1. invasive ductal shows mass due to calcifications but lobular does not. Lobular can even be difficult to palpate
200
Invasive Lobular Carcinoma
1. Histology hallmark
2. marker?
3. ER, PR, HER2 positive/negative?
1. cancer cells grow in single file
2. lack e-cadherin so cells can't stick together
3. ER positive
201
# Breast cancers
Inflammatory Carcinoma
1. invasive or non-invasive?
2. sx
3. prognosis?
1. invasive - invades skin lymphatic vesses and causes skin to swell
2. breast pain, warm, swollen, erythematous skin around hair follicles (peau d'orange - looks like orange skin), skin dimpling
3. poor prognosis - often mistaken for mastitis or paget and lacks a palpable mass
202
# Breast cancers
Mucinous Carcinoma
1. what does lesion in breast appear like?
2. ER, PR, HER2 pos/neg?
3. Histology presentation
4. prognosis?
1. soft, rubbery lesion inside breast
2. often ER positive
3. clusters of cells floating in large lakes of mucin
4. good prognosis
203
# Breast cancers
Tubular Carcinoma
1. ER, PR, HER2 pos/neg?
2. Histology presentation
3. invasive or noninvasive
1. many are ER positive
2. well formed tubules
3. invasvie
204
# Breast cancer
Medullary carcinoma
1. tumor and histology description?
2. ER, PR, HER2 pos/neg?
3. genetic mutation?
4. What is this?
1. Tumor is well circumscribed ---- large, anaplastic cells growing in sheets with associated lymphocytes and plasma cells
2. triple negative
3. BRCA1 mutation
4. a rare form of invasive ductal carcinoma that begins in the breast's milk duct and spreads from there
205
Fetal Loss/Miscarriage
1. Why does this occur?
2. when does this occur?
3. What are the two types of fetal loss
1. random chromosomal erroes, infection, uterine structural abnormalities, truama, etc
2. before 20 weeks gestation
3. Embryonic/fetal demise (can't find fetal heart tones in US) -- anembryonic pregnancy (gestational sac but no development of embryo/fetus)
206
Fetal Loss/Miscarriage -> Threatened miscarriage
1. what is it?
2. sx?
3. management
1. possibility of losing embryo
2. vaginal bleeding before 20 weeks, lower abdominal pain, closed cervix
2. reassurance, pelvic rest (no sex), follow up
207
Fetal Loss/Miscarriage -> Inevitable miscarriage
1. sx?
2. management
1. vaginal bleeding, abdominal pain, open cervical loss
2. observation and analgesics
208
Fetal Loss/Miscarriage -> Complete miscarriage
1. sx?
2. management
3. PE findings
1. History of pain and passage of fleshy tan/pink tissue. Resolution of pain and improvement in bleeding.
2. follow beta HCG to see if it was truly a complete miscarriage
3. closed cervical os, empty uterine cavity, size of uterus smaller than gestational age
209
(Hydatidiform Mole) Molar Pregnancy
1. What is this?
2. What are the two types
3. Tx
1. Abnormal proliferation of trophoblasts
2. Complete and partial
3. surgical removal
210
1. What is a partial hydatidiform mole/molar pregnancy?
2. Karyotype?
1. when two sperm fertilize an egg. Fetal tissue is possibly present and uterine size is consistent with gestational age.
2. 69 XXX, 69 XXY, 69 XYY
211
1. What is a complete hydatidiform mole/molar pregnancy?
2. Karyotype?
3. What does this look like on US?
1. when sperm fertilize an egg with no genetic information. Has no fetal tissue and uterus size is larger than gestational age.
2. 46 XX or 46 XY
3. Snow storm uterus - due to the placental tissue swelling up and forming filled cysts
212
Invasive Mole
1. Is this benign or malignant?
2. risk factors?
3. What is it?
1. malignant
2. complete mole pregnancy
3. hydatidiform mole grows into the muscle wall of the uterus (myometrium). Invasive moles are cancerous but they usually do not spread outside of the uterus.
213
Placental Site Trophoblastic Tumor
1. What is it?
1. a rare, potentially malignant neoplasm originating from extravillous (intermediate) trophoblast cells.
2. They can occur months to years after a pregnancy. PSTTs most commonly develop after a term gestation, but also occur after a molar pregnancy
214
Pelvic Inflammatory Disease
1. What is this?
2. What can cause it often?
3. Dx criteria
1. a clinical dx that includes a spectrum of infectious and inflammatory diseases of upper female genital tract.
2. Think ascending infection - chlamydia and gonorrhea are more common but other things too
3. pelvic or lower abdominal pain AND uterine tenderness/adnexal tenderness/cervical motion tenderness
215
What are some complications if gonorrhea is left untreated?
1. local tissue damage/adhesions
2. chronic pelvic pain - due to inflammation and adhesions ---> adhesions like fitz-hugh curtis syndrome (violin strings) - between different organs. These adhesions are tight, very painful and dangerous
3. ectopic pregnancy (bc fallopian tube can lose cilia with PID)
4. tuboovarian abscess
216
1. >95% of breast cancers are (cancer pattern)?
1. adenocarcinoma
217
For each identify if it is found in benign breast lesion or malignant or both?
218
Identify if infiltrating ductal carcinoma, infiltrating lobular carcinoma, or both
219
What are some risk factors for breast cancer?
1. menarche age
2. menopause age
3. estrogen exposure
4. pregnancy
1. menarche at age younger than 12 increases risk of breast cancer
2. late menopause (after 55 years) increases risk
3. Menopausal therapy (estrogen exposure) - increases risk
4. Full term pregnancy before age of 20 decreases risk of breast cancer compared to nulliparous women or women who are >35 at the time of first pregnancy
220
stage vs grade
1. stage is how far a tumor has spread
2. grade is the histology of a tumor (undifferentiated vs differentiated and all that)
221
Nottingham score evalutaes what three things and gives them a score of 1-3
| This helps assign grade
1. tubule formation
2. nuclear pleomorphism
3. mitotic rate
222
1. ER positive, HER2 negative - name?
2. mutation with this?
3. types of medications for tx
1. luminal type
2. BRCA2 (increased risk for luminal type B)
3. Tamoxifen and Exemestane
223
HER2 positive
1. mutation
2. therapy for tx?
1. TP53 mutations
2. Trastuzumab
224
Triple negative breast cancer
1. name
2. germline mutation
1. basal type
2. Germline BRCA1 mutation
