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113 Cards in this Set

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Placenta Previa
**Attachment of the placenta to the lower uterine segment--often over the cervical os

**PAINLESS vaginal bleeding
Placenta Accreta
**Defective decidual layer allows the placenta to attach directly to the MYOMETRIUM

**May have MASSIVE hemorrhage after delivery
Predisposing Factors to Placenta Accreta?
=Prior C-section
=Inflammation
Abruptio Placentae
**Premature detachment of the placenta from the implantation site due to the formation of a RETROPLACENTAL CLOT

=causes PAINFUL uterine bleeding --> usually in the 3rd trimester

**Can cause FETAL DEATH and DIC

**
Risk Factors?
=HTN
=Smoking cigarettes
=Cocaine addiction
=Advanced maternal age
Ectopic Pregnancy
**Most often in the fallopian tubes

SUSPECT w/ an increased B-hCG and SUDDEN lower abdominal pain.
=confirm w/ ultrasound

**Often mistaken clinically for appendicitis.
=i.e. always do a B-hCG pregnancy test to rule out ectopic pregnancy!
Predisposition?
**Predisposed by SALPINGITIS (PID)
Preeclampsia
**TRIAD of:
=HTN
=Proteinuria
=Edema

**Eclampsia = addition of SEIZURES to the triad

**Affects 7% of pregnancy women from 20 weeks - 6 weeks postpartum
=i.e. usually occurs in the 3rd trimester
Who has an increased risk of eclampsia?
**women > 35 y.o.
=patients w/ preexisting HTN
=diabetes
=chronic renal disease
=autoimmune disorders
Etiology??
Placental hypoperfusion

=mechanical/functional occlusion of spiral arteries
=decreased vasodilators (PGE and NO)
=vasoconstrictors increased (TXA2, AngII)
What if we saw preeclampsia in the FIRST trimester?
Would signal a potential MOLAR PREGNANCY
What syndrome can preeclampsia/eclampsia be associated with?
HELLP Syndrome

=Hemolysis
=Elevated LFTs
=Low Platelets

**i.e. hemolytic anemia + DIC
Gestational Trophoblastic Neoplasms
1) Hydatidiform Moles

2) Choriocarcinoma
Hydatidiform Moles
**Benign tumors of the chorionic villus

**Can be:
1) Complete
2) Partial
Complete Mole
**Most common type

=the ENTIRE placenta is neoplastic
=you see dilated, swollen villi

NO EMBRYO IS PRESENT
=46XX --> BOTH chromosomes are of MALE origin
=i.e. the egg is fertilized by 2 haploid spermatozoa w/ X chromosomes

**INCREASED RISK OF developing CHORIOCARCINOMA
So what would be the clinical findings in a complete mole?
**Enlarged uterus
="honey-combed" or "cluster of grapes" appearance

**HIGH B-hCG

**Preeclampsia in the FIRST trimester
Partial Mole
**NOT all villi are neoplastic or dilated

**Embryo IS present --> TRIPLOID 69XXY
=i.e. egg w/ 23X is fertilized by a 23X and 23Y sperm

NO INCREASED RISK of developing choriocarcinoma!
Choriocarcinoma
**Malignant tumor composed of syncytiotrophoblast + cytotrophoblast

**chorionic villi ARE NOT PRESENT
Risk Factors:
1) Complete Mole (50% of cases)

2) Spontaneous Abortion (25%)

3) Normal pregnancy (25%)
Common Sites of Metastasis:
**Lungs and vagina

BUT, has good response to chemotherapy (=ONLY this gestational version, NOT the non-gestationally dervied version)
=evevn can make metastasis go away!
Amniotic Fluid Abnormalities
1) Polyhydraminos
2) Oligohydraminos
Polyhydraminos
**>1.5-2.0 L of amniotic fluid

**Associated w/ esophageal/duodenal atresia --> causes INABILITY to SWALLOW fluid

**Also associated w/ ANENCEPHALY
Oligohydraminos
**<.5 L of amniotic fluid

**Associated with:
=Bilateral renal agenesis
=Posterior urethral valves (in males) --> and thus an inability to excrete urine
Dysplasia and Carcinoma in Situ (CIN)
**Disordered epithelial growth
=begins at the BASAL layer and exends outward

**Classified as CIN1, CIN2, CIN3 depending on the extent of dysplasia

=associated w/ HPV 16, 18 --> may progress slowly to invasive carcinoma
Invasive Cervical Carcinoma
**Now the LEAST COMMON gynecologic malignancy --> due to early detection of CIN w/ Pap Smears
=i.e. Pap Smear can catch cervical dysplasia (KOILOCYTES) BEFORE it progresses

**Majority are Squamous Cell Carcinoma
Risk Factors
**Same as for CIN

=early age of onset of sex
=multiple, high risk partners
=high-risk types of HPV in the biopsy
=smoking
=oral contraceptive pills
=immunodeficiency
Complications
**Can extend down into the vagina

**Can extend laterally to block the ureters
=i.e. postrenal azotemia leading to RENAL FAILURE is the #1 cause of death!
Uterine Disorders
=Adenomyosis

=Endometriosis

=Endometrial hyperplasia

=Endometrial Carcinoma

=Leiomyoma/Leiomyosarcoma
Adenomyosis
**GLANDS AND STROMA IN THE MYOMETRIUM

=i.e. glands and stroma THICKEN myometrial tissue --> produces uterine enlargement

**does NOT predispose to cancer!
Endometriosis
**Functioning glands and stroma OUTSIDE the confines of the uterus
Pathogenesis?
#1 --> REVERSE menses through the fallopian tubes

Also:
=coelomic metaplasia
=vascular or lymphatic spread
Common Sites?
#1 --> OVARIES

Others:
=Rectal pouch of Douglas
=Fallopian tubes
=Intestine
Recall: What is the Rectal Pouch of Douglas?
**the MOST DEPENDENT part of the female pelvis
=anterior to the rectum and posterior to the uterus
=can be palpated by DRE

**It is a common site to COLLECT things:
=blood --> ruptured ectopic pregnancy
=malignant cells --> seeding by ovarian cancer
=endometrial implants
=pus --> PID
Example:

=Woman comes in and complains that when she is on her period and she is going to the bathroom it really hurts when she defecates. DX?
**endometriosis in the pouch of douglas!
Clinical Findings:
**Women still have cyclic bleeding (=menstrual type) and so have these blood-filled "chocolate cysts"

=Dysmenorrhea
=Painful stools during menses (rectal pouch)
=enlargement of the ovaries
Risks?
**Infertility

**Increased risk of ectopic pregnancy
Endometrial Hyperplasia
**ABNORMAL endometrial gland proliferation --> Due to prolonged, UNOPPOSED estrogen stimulation
=NO progesterone effects!

**Usually manifests as VAGINAL BLEEDING

**Will INCREASED risk for endometrial carcinoma
Risk Factors:
=Early menarche or late menopause

=Nullparity

=Obesity (i.e. increased aromatization of androgens --> estrogens)
Example:

Woman who has been postmenopausal for >1 year and then has breakthrough bleeding.
**Endometrial cancer until proven otherwise

#1 step --> endometrial biopsy
Endometrial Carcinoma
**MOST COMMON GYN MALIGNANCY!
=AND best prognosis!

**Peaks at 55-60 y.o.

**Typically presents as VAGINAL BLEEDING --> usually preceded by endometrial hyperplasia
Review:

Most common GYN cancers overall?
#1 --> endometrial

#2 --> ovarian

#3 --> cervical
Most common GYN cancers by AGE BRACKET?
45 --> cervical cancer

55 --> endometrial

65 --> ovarian
Leiomyoma
**Most common of all tumors in females --> BENIGN smooth muscle tumor

**More common in BLACKS

=often presents as MULTIPLE tumors w/ well demarcated borders
=does NOT TRANSORM INTO LEIOMYOSARCOMA!
Cyclic Changes in Leiomyomas
**Estogen-sensitive tumors:
=i.e. tumor size INCRASES w/ pregnancy and DECREASES w/ menopause

**note: leiomyomas are sometimes referred to as "fibroids"
Leiomyosarcoma
**Bulky, irregular tumor w/ areas of necrosis + hemorrhage
=HIGHLY aggressive tumor w/ tendency to recur --> may protrude from the cervix and bleed!

**Usually arise de novo--NOT from leiomyomas

**Increased incidence in blacks
Hirsutism vs. Virilization
Hirsutism:
=excess hair in normal hair-bearing areas

Virilization:
=hirsutism + male secondary sex characteristics (=increased muscle mass, acne, CLITOROMEGALY)
What is the cause of hirsutism and virilization?
**BOTH conditions are due to INCREASED ANDROGENS of either ovarian OR adrenal origin

1) Ovarian origin (=most common)
=TESTOSTERONE is primarily increased

2) Adrenal origin
=DHEA-sulfate is primarily increased

**SO, if someone has hirsutism, get a testosterone level and a DHEA level = tells you where the probelm is!
Polycystic Ovarian Syndrome
**Increased pituitary synthesis of LH and decreased synthesis of FSH
Pathogenesis:
NOW, recall what happens during the proliferative phase:
=LH is responsible for stimulating the THECA INTERNA to synthesize DHEA + androstendione --> converted via oxidoreductase --> TESTOSTERONE

THUS, INCREASED LH leads to an INCREASE in androgen synthesis = HIRSUTISM!

BUT...testosterone will enter GRANULOSA cells of the follicle where there is AROMATASE and be converted into ESTROGENS
What will this increase in estrogens do?
**Increased estrogen has a POSITIVE feedback on LH and a NEGATIVE feedback on FSH
=NOW, suppression of FSH causes follicle degeneration --> FLUID ACCUMULATION produces abnormal cysts that ENLARGE the ovaries

AND THUS our findings in PCOS:
1) increased LH
2) decreased FSH

**Usually have an LH:FSH of >2!
Summary of Clinical Findings in PCOS:
#1 complaint = oligomenorrhea

Also:
=hirsutism, infertility, obesity
=polycystic ovaries

1) Increased LH, Decreased FSH
2) Increased testosterone and androstenedione
3) Increased estrogen
=increases your risk of developing endometrial hyperplasia/cancer
How could you break the cycle in PCOS?
**give a BC pill --> progestins in it will BLOCK LH

Also could treat with:
=weight loss
=gonadotropin analogs
=surgery
Dysmenorrhea
**Painful menses

**Can be primary or secondary:

1) Primary
=usually due to INCREASED PGF --> increases uterine contractions

2) Secondary Type
=usually due to endometriosis
Dysfunctional Uterine Bleeding (DUB)
**Bleeding that is UNRELATED to an anatomic cause
=i.e. NOT from endometrial polyp or cancer

**CAUSED BY A HORMONAL IMBALANCE

**Most common type of DUB = Anovulatory DUB
Anovulatory DUB
**Occurs at the extremes of reproductive life

**What happens is that you have EXCESSIVE estrogen stimulation of your mucosa and not enough progesterone stimulation --> results in:

=hyperplasia of the endometrium --> when it outgrows its space, it will SLOUGH --> can often have SIGNIFICANT BLEEDING
Primary Amenorrhea
**Absence of menses by 16 y.o.

**Usually due to a CONSTITUTIONAL DELAY
=i.e. FH of delayed menses
Secondary Amenorrhea
**Absence of menses for 3 months --> usually due to a PREGNANCY

i.e. the FIRST step in management of a woman w/ amenorrhea?
=pregnancy test
Pathogenesis of Amenorrhea
**Ask --> is it a...

1) Hypothalamic/Pituitary Problem
=GnRH, FSH/LH

2) Ovarian Problem

3) End organ defect
Hypothalamic/Pituitary Problem
Examples:
=Hypopituitarism
=Prolactinoma
=Anorexia
Ovarian Disorder
Examples:
=Turner's Syndrome

i.e. Primary amenorrhea + poor female secondary sex characteristics = probable Turner's Syndrome
End Organ Defect
**Prevents the normal egress of blood = an ANATOMIC problem

1) Imperforate Hymen
2) Rokitansky-Kuster-Hauser
3) Ashermann Syndrome
=removal of stratum basalis owing to repeated currettage (i.e. repeated D+C's)

**Will have NORMAL levels of FSH, LH, estrogen, and progesterone.
SO, you can really seperate out the causes of amenorrhea by looking at FSH/LH...
Hypothalamic Pituitary
=DECRASED FSH/LH

Ovarian Disorder
=INCREASED FSH/LH

End Organ Defect/Consitutional Delay
=NORMAL FSH, LH
Follicular Cyst
**MOST COMMON ovarian mass
=i.e. most common cause of a mass in a young woman

**Non-neoplastic cyst
=accumulation of fluid in a follicle or previously rupture follicle

**RUPTURE produces sterile peritonitis w/ PAIN
=if it occurs on the RIGHT side --> can mimic appendicitis!
What can follicular cysts be associated with?
=hyperestrinism

=endometrial hyperplasia
Best screening test?
Ultrasound
Corpus Luteum Cyst
=hemorrhage into persistent corpus luteum

**Causes menstrual irregularity
Theca-Lutein Cyst
**Often bilateral/multiple

**Due to gonadotropin stimulation

**ASsociated w/:
=choriocarcinoma
=moles
Ovarian Tumors:
Can be:

1) Surface-Derived Tumors
=account for 65-70% of all tumors

2) Germ Cell Tumors

3) Sex-Cord Stromal Tumors
Surface-Derived Tumors
**Most common group of ovarian tumors

=Serous Cystadenoma (benign)
=Serous Cystadenocarcinoma (malignant)

=Mucinous cystadenoma (benign)
=Mucinous cystadenocarcinoma (malignant)

=Brenner Tumor
Serous Tumors
**Key Facts:
=Frequently BILATERAL
=Lined w/ ciliated cells--like fallopian tube epithelium

**Serous cystadenocarcinomas have PSAMMOMA BODIES
=basically apoptosis of tumor cells + replacement w/ dystrophic calcification
Example:

65 y.o. woman w/ BILATERAL ovarian enlargement.
Odds:

=serous cystadenocarcinoma

Note: ANY woman >55 that you can feel their ovaries has CANCER until proven otherwise (i.e. they should ATROPHY w/ menopause)
Mucinous Cystadenoma
=multilocular cyst lined by MUCOUS-secreting epithelium

**Benign
Mucinous Cystadenocarcinoma
**Malignant

**Can cause PSEUDOMYXOMA PERITONEI
=intraperitoneal accumulation of mucinous material from ovarian or appendicecal tumor
Brenner Tumor
**Benign tumor that resembles BLADDER EPITHELIUM
Germ Cell Tumors
1) Dysgerminoma
2) Yolk Sac
3) Cystic Teratoma
Dysgerminoma
**Malignant
=equivalent to male seminoma
=associated w/ streak ovaries in Turners

**Sheet of uniform cells

**Increased hCG
Yolk Sac (Endodermal Sinus) Tumor
**Aggressive malignancy in OVARIES (testes in boys) and sacrococcygeal area of YOUNG children

**Increased AFP
Cystic Teratoma
**90% of ovarian germ cell tumors
=cells containn 2 or 3 germ layers

**MATURE teratoma = benign
**IMMATURE teratoma = aggressively malignant
Struma Ovarii
=teratoma looks like thyroid gland --> has FUNCTIONING THYROID TISSUE.
Sex-Cord Stromal Tumors
1) Thecoma-Fibroma

2) Granulosa-Thecal Cell Tumor

3) Sertoli-Leydig Cell Tumor
Ovarian Fibroma
**Bundles of spindle-shaped fibroblasts
=commonly CALCIFY

**Can lead to Meig's Syndrome
1) Ovarian fibroma
2) Ascites
3) Right-sided pleural effusion

=effusion regresses following removal of tumor!
Granulosa Cell Tumor
**Secretes ESTROGEN = feminizing tumor

**Contains Call-Exner Bodies
=small follicles filled w/ eosinophilic secretions
Produces:
**Precious puberty in kids

**Endometrial hyperplasia or carcinoma in adults
Sertoli-Leydig Cell Tumor
**Benign masculizing tumor = produces ANDROGENS
Krukenberg Tumor
**Affects BOTH ovaries
=contains signet-ring cells from hematogenous spread of a GASTRIC cancer
Breast Disorders
**HIGHEST Density of Breast Tissue = i.e. where cancer is usually found

#1 --> Upper outer quadrant
#2 --> Beneath the nipple
Most Common Cause of Bloody Nipple Discharge in a woman <50 y.o.
INTRADUCTAL PAPILLOMA

**In an older woman = Ductal Cancer
Purulent Nipple Discharge?
=Acute mastitis due to S. aureus (i.e. a breast absess)

**Usually occurs during lactation or breast feeding
Most Common Breast Mass in a Woman <50 y.o.
**Fibrocystic Change

=might have a "lumpy-bumpy" feel on exam
How does Fibrocystic Disease Present?
**Diffuse breast pain and multiple lesions--often bilateral

**Usually does NOT indicate an incrased risk of cancer
Histologic Types:
1) Fibrosis
=hyperplasia of breast stroma
=NO malignant potential

2) Cystic
=fluid-filled --> vary in size w/ menstrual cycle
=NO malignant potential

3) Sclerosing
=Proliferation of small ductules/acini in the lobule
=Often confused w/ infiltrating ductal carcinoma

4) Ductal (epithelial) hyperplasia
=increased number of epithelial cell layers in the terminal duct lobule
=usually occurs >30 y.o.
=INCREASED RISK OF CANCER IF ATYPICAL
Fat Necrosis
**A benign, painless lump.

=due to injury to breast tissue
Gynecomastia--Causes?
**Results from:

1) Hyperestrogenism
=cirrhosis
=testicular tumor
=puberty
=old age

2) Klinefelter's

3) Drug-Induced
=cimetidine
=alcohol, marijuana, heroin
=digitalis
BENIGN BREAST TUMORS
1) Fibroadeoma
2) Intraductal papilloma
3) Phyllodes Tumor
Fibroadenoma
**Benign tumor derived from STROMA
=small, mobile, firm mass w/ sharp edges
=w/ proliferation of the stroma/tumor, it will compress the ducts = "slit-like spaces"

**Will have an INCREASE in size and tenderness w/ pregnancy

**NOT a precursor to breast cancer
=momst common tumor in women <25 y.o.
Intraductal Papilloma
**Tumor of lactiferous ducts

=often presents w/ serous or bloody nipple discharge

NO increased risk of cancer
Phyllodes Tumor
**Large, bulky mass of CT and cysts

=tumor may have "leaf-like" projections

**SOME may be malignant
Malignant Tumors
**Common postmenopause

=arise from mammary duct epithelium or lobular glands
#1 Prognostic Factor
LYMPH NODE INVOLVEMENT

Others:
1) Estrogen/Progesterone Receptor Status
=confers BETTER prognosis
=candidate for antiestrogen therapy w/ tamoxifen

2) ERBB2/HER-2 Oncogene Status
=poor prognosis if amplification is present
Side Effects of Tamoxifen
**Tamoxifen = a weak estrogen

SO, you have:
=postmenopausal symptoms
=risk of endometrial cancer
=prevents osteoporosis
Risk Factors for Developing Cancer:
1) Early 1st menarche (<12)OR late menopause (>50)
2) Delayed first pregnancy (>30)
3) FH in 1st degree relative

RISK IS NOT increased by:
=fibroadenoma
=nonhyperplastic cysts
Histologic Types:
1) DCIS
2) Invasive Ductal--no specific type
3) Comedocarcinoma
4) Inflammatory
5) Invasive Lobular
6) Medullary
7) Paget's Disease of the Breast
Ductal Carcinoma in Situ (DCIS)
**Early malignancy w/o basement membrane penetration
Invasive Ductal--no specific type
**WORST and MOST INVASIVE

=firm, fibrous mass

1/3 express ERBB2
Comedocarcinonma
**Ductal, w/ CHEESY CONSISENTCY due to central necrosis
Inflammatory
**Erythematous breast w/ dimpling like an orange--"peau d'orange"
=caused by PLUGS OF TUMOR blocking dermal lymphatics --> localized edema

VERY POOR PROGNOSIS
Invasive Lobular
**Often multiple, BILATERAL!
Medullary
**Big bulky soft tumor w/ LYMPHOCYTIC infiltrate

ASSOCIATED w/ BRCA 1 mutations

GOOD prognosis.
Paget's Disease of the Breast
**Eczematous patches on the nipple
=i.e. if you seen an older woman w/ a rash on her nipple

**SUGGESTS an underlying carcinoma--i.e. it has spread to the skin and produced a rash

**Paget Cells:
=large cells w/ a clear halo

**Also can be seen on the VULVA
Breast Cancer in Men
**RISK FACTORS:
=BRCA2 suppressor gene
=Klinefelter's Syndrome

POOR PROGNOSIS
Modified Radical Mastectomy
**Removal of nipple/areolar complex, breast tissue, pectoralis minor, and axillary nodes
What is there a potential damage of?
**WINGED SCAPULA
=due to damage of the long-thoracic nerve

(also a danger of developing lymphedema)
Breast Conservation Therapy
**Lumpectomy w/ microscopically free margins

**Removal of level I and II (lower) axillary nodes --> for staging

**BREAST RADIATION