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185 Cards in this Set
- Front
- Back
Where is FSH produced in males?
|
F[S]H = [S]ertoli cells -> [S]perm production
|
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Where is LH produced in males?
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[L]H = [L]eydig cells
|
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What are the three androgens?
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In order of potency:
[1] Dihydrotestosterone (DHT) [2] Testosterone [3] Androstenedione (They make a great band!) |
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Where are each of the androgens produced?
|
DHT & Testosterone -> Testis
Androstenedione -> Adrenal |
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How do you get DHT from Testosterone?
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5alpha-reductase converts DHT to testosterone. It is inhibited by finasteride.
|
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What are the targets for androgens?
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[] skin
[] prostate [] seminal vesicles [] epididymis [] liver [] muscle [] brain |
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What is the function of androgens?
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[A hairy wolf with a low voice and lots of muscles wants to swim and have sex]
[] Differentiation of wolffian duct system into internal gonadal structure [] Secondary sexual characteristics & pubertal growth spurt [] Spermatogenesis [] Anabolism [+]muscle size [+] RBC production [] [+] Libido |
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How do you get estrogens from androgens?
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Aromatase found in adipose tissue converts testosterone & androstenedione into estrogen.
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What are the different potencies of various estrogens?
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Estradiol > Estrone > Estriol
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What is the sources of estrogens?
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Ovary -> estradiol
Placenta -> Estriol Blood -> Aromatization |
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What are the functions of estrogens?
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[Things that change with puberty: 'Hair', 'Skin', Genitals, Breast, Fat, Liver, Hormones (FSH&LH), Excitement, Cholesterol]
[] Growth of follicle [] Endometrial proliferation [] Development of genitalia [] Stromal development of breast [] Female fat distribution [] Hepatic synthesis of transport proteins [] Feedback inhibition of FSH [] LH surge (feedback changes from negative -> positive just before surge) [] [+] myometrial excitability [] [+] HDL, [-] LDL |
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What's the deal with estrogen hormone replacement therapy?
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After menopause, estrogen -> [-] hot flashes, [-] bone loss BUT [+]endometrial cancer unless opposed by progesterone
|
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What can lead to increased risk of endometrial cancer?
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unopposed estrogen:
[] ERT [] Early Menarche [] Late Menopause |
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What enzyme in which cell does LH act upon?
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Desmolase in the Theca cell converts Cholesterol to Androstenedione.
|
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What enzyme in which cell does FSH act upon?
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Aromatase in the Granulosa cell converts Androstenedione to Estrogen.
|
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What is the pathway from Cholesterol to Estrogen?
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Cholesterol -> Androstenedione (via Desmolase in Theca cell)
... Androstenedione -> Estrogen (via Aromatase in Granulosa cell) |
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What is the source of progresterone?
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[] Corpus luteum
[] placenta [] adrenal cortex [] testes |
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What is indicated by elevation of progesterone?
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ovulation
|
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What are the functions of progesterone?
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[What happens when you're pregnant: secretions, varicosities (arteries), less sex (excitability), more mucus, feel hot, don't eat FiSH and then you try to relax)
[] Maintenance of pregnancy [] Stimulate endometrial glandular secretions [] Stimulate spiral artery development [] [-] myometrial excitability [] Production of thick cervical mucus [] [+] body temp [] Inhibits gonadotropins [LH, FSH] [] Relax uterine smooth muscles |
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What are the two phases of the menstrual cycle called?
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[] Proliferative phase
[] Secretory phase |
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During what part of the menstrual cycle is follicular growth fastest?
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second week of proliferative phase
|
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What stimulates endometrial proliferation?
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Estrogen
|
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What maintains endometrium to support implantation?
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Progesterone
|
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What happens with decreased progesterone?
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decreased fertility
|
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What is Mittelschmerz?
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blood from ruptured follicle causes peritoneal irritation ('feeling' ovulation)
|
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What are the steps that cause ovulation?
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[1] Estrogen surge day before ovulation
[2] Stimulates LH, inhibits FSH [3] LH surge causes ovulation [4] Progesterone induces temp increase [5] Ferning of cervical mucosa |
|
How do oral contraceptives work?
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They prevent estrogen surge so no LH surge so no ovulation.
|
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What stage would you find oocytes during childhood?
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Meiosis I is arrested in pr[O]phase until [O]vulation
|
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What stage would you find oocytes in the fallopian tubes?
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Meiosis II is arrested in [MET]aphase until the egg [MEETS] a sperm.
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What is the source of hCG?
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Syncytiotrophoblast of placenta?
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What does the syncytiotrophoblast produce?
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hCG
|
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What is the function of hCG?
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[] Maintains corpus luteum for 1st trimester by acting like LH. Placenta takes over in 2nd trimester
[] Detects pregnancy in urine 8 days after fertilization [] Elevated hCG also occurs in hydatidiform moles or choriocarcinoma |
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What hormonal changes occur in menopause?
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[-] estrogen
[++] FSH [+] LH (no surge) [+] GnRH |
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What is the average age of onset of menopause?
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51 y/o. Earlier in smokers
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What havoc does menopause cause?
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[HAVOC]
[H]ot flashes [A]trophy of the [V]agina [O]steoporosis [C]AD |
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What is a bicornuate uterus?
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"Two horned" uterus.
Results from incomplete fusion of the paramesonephric ducts. Associated with urinary tract abnormalities and infertility. |
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What are the two types of congenital penile abnormalities?
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Hypo[s]padias (pee on your [s]hoes; ventral side; more common)
[E]pispadias (pee on in your [e]ye; dorsal side) |
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What causes hypospadias?
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failure of urethral folds ot close. Associated with UTIs.
|
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What causes epispadias?
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Faulty positioning of genital tubercle. Associated with exstrophy of bladder.
|
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What are the different kinds of sex chromosome disorders?
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[XXY] Klinefelter Syndrome (male) 1:850
[XO] Turner Syndrome (female) 1:3000 [XYY] Double Y males (male) 1:1000 |
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What are the clinical findings associated with Klinefelter Syndrome?
|
[] Testicular atrophy
[] eunuchoid body shape [] long extremities [] gynecomastia [] female hair distribution [] barr body [] hypogonadism and infertility |
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<Male with Barr body>
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Klinefelter Syndrome
|
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What are the clinical findings associated with Turner Syndrome?
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[] Short stature
[] Menopause before menarche (streak ovary) [] Webbing of neck [] Coarctation of aorta [] common cause of primary amenorrhea [] no barr body [] "nuckle, nuckle, dimple, nuckle" |
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<Female with no barr body>
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Turner syndrome
|
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What is the clinical findings of Double Y males?
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[Why] are so many seen as inmates of penal institutions?
[] Phenotypically normal [] Very Tall [] Severe Acne [] Antisocial behavior |
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What is pseudohermaphroditism?
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Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.
|
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What are the clinical findings in female pseudohermaphroditism?
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Ovaries present but external genitalia are virilized or ambiguous. 46, XX
|
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What causes female pseudohermaphroditism?
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Excessive or inappropriate exposure to androgenic steroids during early gestation:
[] Congenital adrenal hyperplasia [] Exogenous administration of androgens during pregnancy |
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What is the clinical presentation of male pseudohermaphroditism?
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Testes present, but external genitalia are female or ambiguous.
Most common form is androgen insensitivity syndrome. 46, XY |
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What is the clinical presentation of a true hermaphrodite?
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Both ovary and testicular tissue is present; ambiguous genitalia. Very rare. (46,XX or 47,XXY)
|
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What is the clinical presentation of a person with Androgen insensitivity syndrome?
|
[] Normal appearing female with defect in androgen receptor.
[] Female external genitalia with rudimentary vagina [] Uterus and uterine tubes absent [] Develops testes (often found in labia majora) [] High levels of testosterone, estrogen & LH [] 46,XY |
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What is the clinical presentation of a person with 5alpha-reductase deficiency?
|
Unable to convert testosterone to DHT.
[] Ambiguous genitalia until puberty [] At puberty, [+] testosterone causes masculinization of genitalia [] Testosterone/Estrogen levels normal [] LH may be high. |
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What causes benign prostatic hyperplasia?
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Men > 50 years of age.
Age-related increase in estradiol sensitizes prostate to growth-promoting effects of DHT. |
|
What are the clinical findings associated with benign prostatic hyperplasia?
|
[] Men > 50 years of age.
[] Nodular enlargement of periurethral (lateral & middle) lobess of prostate [] Compression of urethra into a verticla slit [] [+] frequency of urination, nocturia, dysuria & difficulty stopping & starting stream of urine. |
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What are the complications associated with benign prostatic hyperplasia?
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[] distention and hypertrophy of the bladder
[] hydronephrosis [] UTI |
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What are the clinical presentations of prostatic adenocarcinoma?
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[] Men > 50 y/o
[] Posterior lobe of prostate gland [] diagnosed as hard nodule on digital rectal exam [] elevated prostatic acid phosphate and PSA |
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What tumor markers are available for prostatic adenocarcinoma?
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PSA & Prostatic acid phosphatase
|
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<Elevated serum alkaline phosphatase & PSA>
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Osteoblastic metastases on prostatic adenocarcinoma
|
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<Honeycombed uterus>
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Hydatidiform mole
|
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What is a Hydatidiform mole?
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A pathologic ovum ("empty egg") resulting in cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).
|
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What is the clinical findings of a Hydatidiform mole?
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[] "Honeycombed uterus" or "cluster of grapes" appearance.
[] High Beta-hCG [] Common precursor of choriocarcinoma |
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What is a common precursor of choriocarcinoma?
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hydatidiform mole
|
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What is the difference between a complete and a partial hydatidiform mole?
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Genotype of [complete] mole is 46,XX and is [completely] paternal in origin with no associated fetus.
[Part]ial mole is made up of 3 or more [Parts] (triploid/tetraploid) with fetal [Parts] |
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What is the difference between preeclampsia and eclampsia?
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preeclampsia is a triad of findings:
[] hypertension [] proteinuria [] edema eclampsia adds: [] seizures |
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When does preeclampsia/eclampsia manifest itself?
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7% of pregnant women from 20 weeks' gestation to 6 weeks postpartum.
|
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What factors increase the risk of preeclampsia/eclampsia?
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[] preexisting hypertension
[] diabetes [] chronic renal disease [] autoimmune disorders |
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What is teh HELLP syndrome?
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Associated with preeclampsia/eclampsia:
[H]emolysis [E]levated [L]FTs [L]ow [P]latelets |
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What are the clinical features of preeclampsia/eclampsia?
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[] Headache
[] Blurred vision [] abdominal pain [] edema of face and extremities [] altered mentation [] hyperrelexia [] thrombocytopenia [] hyperuricemia |
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What is the treatment for preeclampsia?
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Delivery of fetus as soon as viable. Otherwise bed rest, salt restriction and monitering and treatment of hypertension.
For eclampsia, a medical emergency, IV magnesium sulfate & diazepam. |
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What is abruptio placentae?
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Premature separation of placenta. PAINFUL uterine bleeding (3rd trimester). Fetal death.
|
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What factors increase the risk of abruptio placentae?
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[] DIC
[] smoking [] hypertension [] cocaine use |
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What is placenta accreta?
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Defective decidual layer allows placenta to attach directly to myometrium. Massive hemorrhage after delivery.
|
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What factors increase the risk of placenta accreta?
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[] prior C-section
[] inflammation |
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What is placenta previa?
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Attachment of placenta to lower uterine segment. May occluse cervical os.
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What are the clinical findings assocaited with placenta previa?
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PAINLESS bleeding in any trimester
|
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What is an ectopic pregnancy?
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A fertalized egg outside the uterus. Most often in fallopian tubes.
|
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What are the clinical findings associated with ectopic pregnancy?
|
[] Salpingitis (PID)
[] [+] hCG w/ lower abdominal pain |
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What are the two types of amniotic fluid abnormalities?
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Polyhydramnios > 1.5-2 L amniotic fluid
Oligohydramnios < 0.5 L amniotic fluid |
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What causes polyhydramnios?
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An inability to swallow amniotic fluid due to esophageal/dudoenal atresia. Also associated with anencephaly.
|
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What causes oligohydramnios?
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An inability to exrete urine due to bilateral renal agenesis or posterior urethral valves in males.
|
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What different kinds of cervical pathology are found?
|
[] Dysplasia & CIS = Disordered epithelial growth associated with HPV 16,18. May progress to invasive carcinoma.
[] Invasive carcinoma = Often squamous cell carcinoma. |
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How can you prevent invasive cervical carcinoma?
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Pap smear can catch cervical dysplasia before it progresses to invasive carcinoma.
|
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What complications can arise from invasive cervical carcinoma?
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Lateral invasion can block uereters casuing renal failure.
|
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What are six different types of uterine pathology?
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[1] Endometriosis
[2] Adenomyosis [3] Endometrial hyperplasia [4] Endometrial carcinoma [5] Leiomyoma [6] Leiomyosarcoma |
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What is endometriosis?
|
Non-neoplastic endometrial glands/stroma in abnormal locations OUTSIDE the uterus.
|
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<"Chocolate cysts">
|
blood-filled ovarian cysts indicative of endometriosis of ovaries.
|
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What are the clinical manifestations of endometriosis?
|
[] cyclic bleeding from ectopic endometrial tissue.
[] found in ovary & on peritoneum [] severe menstrual-related pain [] results in infertility |
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What is adenomyosis?
|
endometriosis within the myometrium
|
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What causes endometrial hyperplasia?
|
Excess estrogen stimulation causes endometrial gland proliferation.
|
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What are the clinical presentations of endometrial hyperplasia?
|
[] vaginal bleeding
[] [+] risk of endometrial carcinoma |
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What is the most common gynecological malignancy?
|
endometrial carcinoma
|
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What is the peak age for endometrial carcinoma?
|
55-65 years old
|
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What are the clinical manifestations of endometrial carcinoma?
|
[] vaginal bleeding
[] often preceeded by endometrial hyperplasia |
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What risk factors contribute to a greater risk of endometrial carcinoma?
|
[] prolonged estrogen use
[] obesity [] hypertension |
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What is the most common of all tumors in females?
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Leiomyoma = fibroid of myometrium.
|
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Does leiomyoma progress to leiomyosarcoma?
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Nope. Separate processes.
|
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What factors increase or decrease the size of a leiomyoma?
|
Estrogen size -> [+] pregnancy, [-] menopause
|
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Who is at an increased risk for developing leiomyoma and leiomyosarcoma?
|
[+] African americans
|
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What are the clinical findings of a leiomyosarcoma?
|
[] Bulky tumor with areas of necrosis & hemorrhage.
[] Agressive (recurs) [] May protrude from cervix and bleed |
|
<a single recurrant leiomyoma>
|
It's probably not a leiomyoma, but rather a leiomyosarcoma
|
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What causes polycystic ovarian syndrome?
|
[+] LH production leads to anovulation and hyperandrogenism due to deranged steroid synthesis. (aka high estrogens & high androgens)
|
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What are the clinical features of polycystic ovarian syndrome?
|
[] amenorrhea
[] infertility [] obesity [] hirsutism |
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What is the treatment for polycystic ovarian syndrome?
|
[] Weight loss
[] OCPs [] Gonadotropin analogs [] Surgery |
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What are four different types of ovarian cysts?
|
[1] Follicular cyst
[2] Corpus luteum cyst [3] Theca-lutein cyst [4] Chocolate cyst |
|
What is a follicular cyst?
|
Distention of unruptured graafian follicle. Associated with hyperestrinism & endometrial hyperplasia.
|
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What is a corpus luteum cyst?
|
Hemorrhage into persistent corpus luteum. Presents with menstrual irregularity.
|
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What is a theca-lutein cyst?
|
Often bilateral/multiple. Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.
|
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What is a "chocolate cyst"?
|
blood containing cyst from ovarian endometriosis. Varies with menstrual cycle.
|
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What kind of ovarian cyst is associated with hyperestrinism and endometrial hyperplasia?
|
Follicular cyst
|
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What kind of ovarian cyst is associated with choriocarcinoma and moles?
|
Theca-lutein cyst
|
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What kind of ovarian cyst varies with menstrual cycle?
|
"Chocolate cyst"
|
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What kind of ovarian cyst is associated with menstrual irregularity?
|
Corpus luteum cyst
|
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What are the five types of germ cell tumors?
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[1] Germinomas
[2] Yolk sac tumors [3] Choriocarcinoma [4] Embryonal carcinoma [5] Teratomoa |
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What is the most common malignant germ cell tumor of the ovaries and testes?
|
Germinomoa. Dysgerminoma in ovaries, Seminoma in testes
|
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What is the clinical presentation of a dysgerminoma?
|
Common malignant germ cell tumor of the ovary. Sheets of uniform cells with [+] hCG
|
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What is the clinical presentation of a seminoma?
|
Common malignant germ cell tumor of the testes. Presents with painless testicular enlargement. Increased risk with cryptorchidism.
|
|
What factors increase the risk for seminoma?
|
cryptorchidism
|
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Where are yolk sac tumors found?
|
Aggressive malignancy in ovaries, testes & sacrococcygeal area of young children.
|
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What are the clinical findings associated with yolk sac tumors?
|
Schiller-Duval bodies with primitive glomeruli and [+] AFP.
|
|
<Schiller-Duval bodies>
|
yolk-sac tumor
|
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What is a choriocarcinoma?
|
[] rare but malignant
[] large hyperchromatic syncytiotrophoblastic cells. [] develops during pregnancy in mother or baby. [] [+] hCG |
|
<hyperchromatic syncytiotrophoblastic cells>
|
choriocarcinoma
|
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What is the second most common testicular germ cell tumor?
|
embryonal carcinoma
|
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What is the clinical presentation of an embryonal carcinoma?
|
[] painful testicular mass
[] glandular with papillary convolutions |
|
How do teratomas present in females?
|
[] contain cells from 3 germ layers.
[] mature teratoma is benign while immature form is aggressively malignant |
|
How do teratomas present in males?
|
[M]en, [M]ature teratomas are [M]alignant and painful. Can present with gynecomastia.
|
|
What is struma ovarii?
|
ovarian teratoma containing thyroid tissue
|
|
What are the seven types of ovarian non-germ cell tumors?
|
[1] Serous cystadenoma
[2] Serous cystadenocarcinoma [3] Mucinous cystadenoma [4] Mucinous cystadenocarcinoma [5] Brenner tumor [6] Ovarian fibroma [7] Granulosa cell tumor |
|
What are the two most common non-germ cell tumors of the ovary? (Hint: They often present bilaterally)
|
[1] Serous cystadenoma (20%) Benign.
[2] Serous cystadenocarcinoma (50%) Malignant. |
|
What two types of non-germ cell ovarian tumors are lined by mucous-secreting epithelium?
|
[1] Mucinous cystadenoma
[2] Mucinous cystadenocarcinoma |
|
What is pseudomyxoma peritonei?
|
Intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor
|
|
What is a Brenner tumor?
|
benign non-germ cell tumor of the ovary that resembles [B]ladder epithelium
|
|
What is Meigs' syndrome?
|
Triad of: Ovarian fibroma, ascites & hydrothorax
|
|
<Ovarian fibroma, ascites & hydrothorax>
|
Meigs' syndrome
|
|
What are Call-Exner bodies?
|
small follicles filled with eosinophilic secretions
|
|
What does granulosa cell tumors secrete?
|
Estrogen (Granulosa cell!) -> precocious puberty in kids.
|
|
What are the three types of testicular non-germ cell tumors?
|
[1] Leydig cell
[2] Sertoli cell [3] Testicular lymphoma |
|
What is a Leydig cell tumor?
|
Benign non-germ cell testicular tumor containing Reinke crystals. Produces androgens -> gynecomastia / precocious puberty in boys
|
|
What tumors are associated with precocious puberty?
|
Girls: Granulosa cell tumors -> Estrogen
Boys: Leydig cell tumors -> Androgens |
|
What is a sertoli cell tumor?
|
Benign non-germ cell testicular tumor from sex cord stroma.
|
|
What is a the most common testicular cancer in older men?
|
testicular lymphoma
|
|
What type of breast disease is often bilateral?
|
Fibrocystic disease
|
|
What are the four histologic types of fibrocystic disease?
|
[1] Fibrosis = stromal hyperplasia
[2] Cystic = fluid filled [3] Sclerosing = [+]acini [4] Epithelial hyperplasia = [+] # epithelial cell layers in terminal duct lobule. [+] carcinoma risk with atypical cells. > 30y/o |
|
What are the three types of benign breast tumors?
|
[1] Fibroadenoma
[2] Cystosarcoma phyllodes [3] Intraductal papilloma |
|
What is the most common breast tumor in women under 25?
|
Fibroadenoma
|
|
What is the clinical presentation of a fibroadenoma of the breast?
|
Benign. Small, mobile, firm mass with sharp edges. [+] size and tenderness with period/pregnancy. <25 y/o
|
|
What is the clinical presentation of cystosarcoma phyllodes?
|
Benign tumor of the breast. Large, bulky mass of connective tissue and cysts. Tumor may have "leaflike" projections.
|
|
<Tumor with "leaflike" projections>
|
Cystosarcoma phyllodes of the breast
|
|
What is the clinical presentation of an intraductal papilloma?
|
Benign breast tumor of lactiferous ducts. Presents with nipple discharge.
|
|
<Bleeding from single hole when pressing on nipple>
|
Intraductal papilloma
|
|
Where does breast carcinoma arise from?
|
mammary duct epithelium or lobular glands
|
|
What receptors are frequently overexpressed in breast carcinoma?
|
estrogen/progesterone receptors or erb-B2 / HER-2
|
|
What are the seven histologic types of breast carcinomas?
|
[1] Ductal carcinoma in situ (DCIS)
[2] Invasive ductal [3] Comedocarcinoma [4] Inflammatory [5] Invasive lubular [6] Medullary [7] Paget's disease of the breast |
|
<breast tumor with cheesy consistency>
|
Comedocarcinoma (think popping a zit)
|
|
<bilateral breast carcinoma>
|
Invasive lobular
|
|
<Large cells with clear halo>
|
Paget cells suggestive of underlying carcinoma
|
|
What is DCIS?
|
Ductal carcinoma in situ an early malignancy without basement membrane penetration.
|
|
What does DCIS grow up to become?
|
Invasive ductal carcinoma (that's why you need to catch DCIS fast)
|
|
What is the breast carcinoma with the worst prognosis?
|
Inflammatory = lymphatic involvement.
|
|
What is unique about the presentation of invasive lobular carcinoma?
|
It is often multiple and bilateral
|
|
<Eczematous patches on nipple>
|
Paget's disease
|
|
What are the risk factors for breast disease?
|
[] Gender
[] Age [] Early menarche <12 y/o [] Late menopause >50 y/o [] delayed 1st pregnancy > 30 y/o [] family history of 1st-degree relative with breast cancer at a young age [] NOT fibroadenoma or nonhyperplastic cysts |
|
What is the clinical use of Finasteride?
|
[Fin]asteride = [Five]alpha reductase inhibitor
[-] conversion of testosterone to DHT [] treat BPH [] treat Male pattern baldness |
|
What is the clinical use of Flutamide?
|
Nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma
|
|
What is the clinical use of Ketoconazole & spironolactone?
|
[] Inhibit steroid synthesis
[] Treat polycystic ovarian syndrome |
|
What is the clinical use for sildenafil/vardenafil?
|
[Fill] the penis (Erectile dysfunction)
|
|
What is the mechanism of sildenafil/vardenafil action?
|
[1] Inhibit cGMP phosphodiesterase,
[2] [+] cGMP [3] smooth muscle relaxation in the corpus cavernosum [4] [+] blood flow & penile erection |
|
What is the toxicity of sildenafil/vardenafil?
|
[!] Life threatening hypotension if takin nitrates.
[] Headache [] flushing [] dyspepsia [] blue-green color vision |
|
What is the clinical use of Leuprolide?
|
Pulsatile - Infertility
Continuous w/ flutamide - prostate cancer / uterine fibroids |
|
What is the mechanism of action of Leuprolide?
|
GnRH analog acts as agonist when used pulsatile, but antagonist when used continuously.
|
|
What is the toxicity of Leuprolide?
|
[] antiandrogen
[] nausea [] vomiting |
|
{BPH or Male Pattern Baldness}
|
Finasteride
|
|
{Prostate carcinoma}
|
Flutamide + continuous Leuprolide
|
|
{Polycystic ovarian syndrome}
|
Ketoconazole + Spironolactone
|
|
{Erectile Dysfunction}
|
Sildenafil / Vardenafil (Fill the penis)
|
|
{Infertility}
|
Pulsatile use of Leuprolide
-or- Clomiphene |
|
{Uterine fibroids}
|
continuous Leuprolide
|
|
{Abortifacient}
|
Mifepristone (RU-486)
|
|
What is the clinical use of Clomiphene?
|
Treatment of infertility
|
|
What is the mechanism of action for Clomiphene?
|
[+] LH/FSH via partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition.
|
|
What are the toxicities associated with Clomiphene?
|
Think estrogen toxicity:
[] Hot flashes [] Ovarian enlargement [] multiple pregnancies [] visual disturbances |
|
What is the clinical use for Mifepristone?
|
aka RU-486
[] Abortifacient (prevents implantation) |
|
What is the mechanism of action for Mifepristone?
|
Competitive inhibitor of progestins at progesterone receptors.
|
|
What is the toxicities associated with Mifepristone?
|
[] Heavy bleeding
[] GI effects (nausea, vomiting, anorexia) [] abdominal pain |
|
What are the advantages & disadvantages of oral contreception use?
|
Advantages:
[] Reliable [-] endometrial/ovarian cancer risk [-] ectopic pregnancy risk [-] pelvic infections [] regulation of menses Disadvantages: [] Taken daily [] No STD protection [+] triglycerides [] Depression, weight gain, nausea, hypertension [] hypercoagulable state |