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113 Cards in this Set
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- Back
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Placenta Previa
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**Attachment of the placenta to the lower uterine segment--often over the cervical os
**PAINLESS vaginal bleeding |
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Placenta Accreta
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**Defective decidual layer allows the placenta to attach directly to the MYOMETRIUM
**May have MASSIVE hemorrhage after delivery |
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Predisposing Factors to Placenta Accreta?
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=Prior C-section
=Inflammation |
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Abruptio Placentae
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**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 ** |
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Risk Factors?
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=HTN
=Smoking cigarettes =Cocaine addiction =Advanced maternal age |
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Ectopic Pregnancy
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**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! |
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Predisposition?
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**Predisposed by SALPINGITIS (PID)
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Preeclampsia
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**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 |
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Who has an increased risk of eclampsia?
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**women > 35 y.o.
=patients w/ preexisting HTN =diabetes =chronic renal disease =autoimmune disorders |
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Etiology??
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Placental hypoperfusion
=mechanical/functional occlusion of spiral arteries =decreased vasodilators (PGE and NO) =vasoconstrictors increased (TXA2, AngII) |
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What if we saw preeclampsia in the FIRST trimester?
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Would signal a potential MOLAR PREGNANCY
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What syndrome can preeclampsia/eclampsia be associated with?
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HELLP Syndrome
=Hemolysis =Elevated LFTs =Low Platelets **i.e. hemolytic anemia + DIC |
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Gestational Trophoblastic Neoplasms
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1) Hydatidiform Moles
2) Choriocarcinoma |
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Hydatidiform Moles
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**Benign tumors of the chorionic villus
**Can be: 1) Complete 2) Partial |
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Complete Mole
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**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 |
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So what would be the clinical findings in a complete mole?
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**Enlarged uterus
="honey-combed" or "cluster of grapes" appearance **HIGH B-hCG **Preeclampsia in the FIRST trimester |
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Partial Mole
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**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! |
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Choriocarcinoma
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**Malignant tumor composed of syncytiotrophoblast + cytotrophoblast
**chorionic villi ARE NOT PRESENT |
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Risk Factors:
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1) Complete Mole (50% of cases)
2) Spontaneous Abortion (25%) 3) Normal pregnancy (25%) |
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Common Sites of Metastasis:
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**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! |
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Amniotic Fluid Abnormalities
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1) Polyhydraminos
2) Oligohydraminos |
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Polyhydraminos
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**>1.5-2.0 L of amniotic fluid
**Associated w/ esophageal/duodenal atresia --> causes INABILITY to SWALLOW fluid **Also associated w/ ANENCEPHALY |
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Oligohydraminos
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**<.5 L of amniotic fluid
**Associated with: =Bilateral renal agenesis =Posterior urethral valves (in males) --> and thus an inability to excrete urine |
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Dysplasia and Carcinoma in Situ (CIN)
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**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 |
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Invasive Cervical Carcinoma
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**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 |
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Risk Factors
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**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 |
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Complications
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**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! |
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Uterine Disorders
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=Adenomyosis
=Endometriosis =Endometrial hyperplasia =Endometrial Carcinoma =Leiomyoma/Leiomyosarcoma |
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Adenomyosis
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**GLANDS AND STROMA IN THE MYOMETRIUM
=i.e. glands and stroma THICKEN myometrial tissue --> produces uterine enlargement **does NOT predispose to cancer! |
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Endometriosis
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**Functioning glands and stroma OUTSIDE the confines of the uterus
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Pathogenesis?
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#1 --> REVERSE menses through the fallopian tubes
Also: =coelomic metaplasia =vascular or lymphatic spread |
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Common Sites?
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#1 --> OVARIES
Others: =Rectal pouch of Douglas =Fallopian tubes =Intestine |
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Recall: What is the Rectal Pouch of Douglas?
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**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 |
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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!
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Clinical Findings:
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**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 |
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Risks?
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**Infertility
**Increased risk of ectopic pregnancy |
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Endometrial Hyperplasia
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**ABNORMAL endometrial gland proliferation --> Due to prolonged, UNOPPOSED estrogen stimulation
=NO progesterone effects! **Usually manifests as VAGINAL BLEEDING **Will INCREASED risk for endometrial carcinoma |
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Risk Factors:
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=Early menarche or late menopause
=Nullparity =Obesity (i.e. increased aromatization of androgens --> estrogens) |
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Example:
Woman who has been postmenopausal for >1 year and then has breakthrough bleeding. |
**Endometrial cancer until proven otherwise
#1 step --> endometrial biopsy |
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Endometrial Carcinoma
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**MOST COMMON GYN MALIGNANCY!
=AND best prognosis! **Peaks at 55-60 y.o. **Typically presents as VAGINAL BLEEDING --> usually preceded by endometrial hyperplasia |
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Review:
Most common GYN cancers overall? |
#1 --> endometrial
#2 --> ovarian #3 --> cervical |
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Most common GYN cancers by AGE BRACKET?
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45 --> cervical cancer
55 --> endometrial 65 --> ovarian |
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Leiomyoma
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**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! |
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Cyclic Changes in Leiomyomas
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**Estogen-sensitive tumors:
=i.e. tumor size INCRASES w/ pregnancy and DECREASES w/ menopause **note: leiomyomas are sometimes referred to as "fibroids" |
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Leiomyosarcoma
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**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 |
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Hirsutism vs. Virilization
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Hirsutism:
=excess hair in normal hair-bearing areas Virilization: =hirsutism + male secondary sex characteristics (=increased muscle mass, acne, CLITOROMEGALY) |
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What is the cause of hirsutism and virilization?
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**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! |
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Polycystic Ovarian Syndrome
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**Increased pituitary synthesis of LH and decreased synthesis of FSH
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Pathogenesis:
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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 |
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What will this increase in estrogens do?
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**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! |
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Summary of Clinical Findings in PCOS:
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#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 |
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How could you break the cycle in PCOS?
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**give a BC pill --> progestins in it will BLOCK LH
Also could treat with: =weight loss =gonadotropin analogs =surgery |
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Dysmenorrhea
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**Painful menses
**Can be primary or secondary: 1) Primary =usually due to INCREASED PGF --> increases uterine contractions 2) Secondary Type =usually due to endometriosis |
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Dysfunctional Uterine Bleeding (DUB)
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**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 |
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Anovulatory DUB
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**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 |
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Primary Amenorrhea
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**Absence of menses by 16 y.o.
**Usually due to a CONSTITUTIONAL DELAY =i.e. FH of delayed menses |
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Secondary Amenorrhea
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**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 |
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Pathogenesis of Amenorrhea
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**Ask --> is it a...
1) Hypothalamic/Pituitary Problem =GnRH, FSH/LH 2) Ovarian Problem 3) End organ defect |
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Hypothalamic/Pituitary Problem
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Examples:
=Hypopituitarism =Prolactinoma =Anorexia |
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Ovarian Disorder
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Examples:
=Turner's Syndrome i.e. Primary amenorrhea + poor female secondary sex characteristics = probable Turner's Syndrome |
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End Organ Defect
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**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. |
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SO, you can really seperate out the causes of amenorrhea by looking at FSH/LH...
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Hypothalamic Pituitary
=DECRASED FSH/LH Ovarian Disorder =INCREASED FSH/LH End Organ Defect/Consitutional Delay =NORMAL FSH, LH |
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Follicular Cyst
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**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! |
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What can follicular cysts be associated with?
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=hyperestrinism
=endometrial hyperplasia |
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Best screening test?
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Ultrasound
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Corpus Luteum Cyst
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=hemorrhage into persistent corpus luteum
**Causes menstrual irregularity |
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Theca-Lutein Cyst
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**Often bilateral/multiple
**Due to gonadotropin stimulation **ASsociated w/: =choriocarcinoma =moles |
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Ovarian Tumors:
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Can be:
1) Surface-Derived Tumors =account for 65-70% of all tumors 2) Germ Cell Tumors 3) Sex-Cord Stromal Tumors |
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Surface-Derived Tumors
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**Most common group of ovarian tumors
=Serous Cystadenoma (benign) =Serous Cystadenocarcinoma (malignant) =Mucinous cystadenoma (benign) =Mucinous cystadenocarcinoma (malignant) =Brenner Tumor |
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Serous Tumors
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**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 |
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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) |
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Mucinous Cystadenoma
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=multilocular cyst lined by MUCOUS-secreting epithelium
**Benign |
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Mucinous Cystadenocarcinoma
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**Malignant
**Can cause PSEUDOMYXOMA PERITONEI =intraperitoneal accumulation of mucinous material from ovarian or appendicecal tumor |
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Brenner Tumor
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**Benign tumor that resembles BLADDER EPITHELIUM
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Germ Cell Tumors
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1) Dysgerminoma
2) Yolk Sac 3) Cystic Teratoma |
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Dysgerminoma
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**Malignant
=equivalent to male seminoma =associated w/ streak ovaries in Turners **Sheet of uniform cells **Increased hCG |
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Yolk Sac (Endodermal Sinus) Tumor
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**Aggressive malignancy in OVARIES (testes in boys) and sacrococcygeal area of YOUNG children
**Increased AFP |
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Cystic Teratoma
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**90% of ovarian germ cell tumors
=cells containn 2 or 3 germ layers **MATURE teratoma = benign **IMMATURE teratoma = aggressively malignant |
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Struma Ovarii
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=teratoma looks like thyroid gland --> has FUNCTIONING THYROID TISSUE.
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Sex-Cord Stromal Tumors
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1) Thecoma-Fibroma
2) Granulosa-Thecal Cell Tumor 3) Sertoli-Leydig Cell Tumor |
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Ovarian Fibroma
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**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! |
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Granulosa Cell Tumor
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**Secretes ESTROGEN = feminizing tumor
**Contains Call-Exner Bodies =small follicles filled w/ eosinophilic secretions |
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Produces:
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**Precious puberty in kids
**Endometrial hyperplasia or carcinoma in adults |
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Sertoli-Leydig Cell Tumor
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**Benign masculizing tumor = produces ANDROGENS
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Krukenberg Tumor
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**Affects BOTH ovaries
=contains signet-ring cells from hematogenous spread of a GASTRIC cancer |
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Breast Disorders
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**HIGHEST Density of Breast Tissue = i.e. where cancer is usually found
#1 --> Upper outer quadrant #2 --> Beneath the nipple |
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Most Common Cause of Bloody Nipple Discharge in a woman <50 y.o.
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INTRADUCTAL PAPILLOMA
**In an older woman = Ductal Cancer |
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Purulent Nipple Discharge?
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=Acute mastitis due to S. aureus (i.e. a breast absess)
**Usually occurs during lactation or breast feeding |
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Most Common Breast Mass in a Woman <50 y.o.
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**Fibrocystic Change
=might have a "lumpy-bumpy" feel on exam |
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How does Fibrocystic Disease Present?
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**Diffuse breast pain and multiple lesions--often bilateral
**Usually does NOT indicate an incrased risk of cancer |
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Histologic Types:
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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 |
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Fat Necrosis
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**A benign, painless lump.
=due to injury to breast tissue |
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Gynecomastia--Causes?
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**Results from:
1) Hyperestrogenism =cirrhosis =testicular tumor =puberty =old age 2) Klinefelter's 3) Drug-Induced =cimetidine =alcohol, marijuana, heroin =digitalis |
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BENIGN BREAST TUMORS
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1) Fibroadeoma
2) Intraductal papilloma 3) Phyllodes Tumor |
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Fibroadenoma
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**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. |
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Intraductal Papilloma
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**Tumor of lactiferous ducts
=often presents w/ serous or bloody nipple discharge NO increased risk of cancer |
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Phyllodes Tumor
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**Large, bulky mass of CT and cysts
=tumor may have "leaf-like" projections **SOME may be malignant |
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Malignant Tumors
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**Common postmenopause
=arise from mammary duct epithelium or lobular glands |
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#1 Prognostic Factor
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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 |
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Side Effects of Tamoxifen
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**Tamoxifen = a weak estrogen
SO, you have: =postmenopausal symptoms =risk of endometrial cancer =prevents osteoporosis |
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Risk Factors for Developing Cancer:
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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 |
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Histologic Types:
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1) DCIS
2) Invasive Ductal--no specific type 3) Comedocarcinoma 4) Inflammatory 5) Invasive Lobular 6) Medullary 7) Paget's Disease of the Breast |
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Ductal Carcinoma in Situ (DCIS)
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**Early malignancy w/o basement membrane penetration
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Invasive Ductal--no specific type
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**WORST and MOST INVASIVE
=firm, fibrous mass 1/3 express ERBB2 |
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Comedocarcinonma
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**Ductal, w/ CHEESY CONSISENTCY due to central necrosis
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Inflammatory
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**Erythematous breast w/ dimpling like an orange--"peau d'orange"
=caused by PLUGS OF TUMOR blocking dermal lymphatics --> localized edema VERY POOR PROGNOSIS |
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Invasive Lobular
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**Often multiple, BILATERAL!
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Medullary
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**Big bulky soft tumor w/ LYMPHOCYTIC infiltrate
ASSOCIATED w/ BRCA 1 mutations GOOD prognosis. |
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Paget's Disease of the Breast
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**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 |
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Breast Cancer in Men
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**RISK FACTORS:
=BRCA2 suppressor gene =Klinefelter's Syndrome POOR PROGNOSIS |
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Modified Radical Mastectomy
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**Removal of nipple/areolar complex, breast tissue, pectoralis minor, and axillary nodes
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What is there a potential damage of?
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**WINGED SCAPULA
=due to damage of the long-thoracic nerve (also a danger of developing lymphedema) |
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Breast Conservation Therapy
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**Lumpectomy w/ microscopically free margins
**Removal of level I and II (lower) axillary nodes --> for staging **BREAST RADIATION |
