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FirstAID > Reproductive > Flashcards

Reproductive Flashcards

1
Q

Venous drainage of Left and Right Ovaries/Testes:

A

Left Ovary/Testis –> L gonadal vein –> L renal vein –> IVC

R ovary/testis –> R gonadal vein –> IVC

***this is the same as with the adrenals: Left adrenal drains to L renal vein before draining into IVC (but, Right adrenal drains into Right adrenal vein, which drains straight into IVC)

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2
Q

Lymphatic drainage of Ovaries/Testes:

A

Para-aortic lymph nodes

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3
Q

Lymphatic drainage of distal 1/3 of vagina, vulva, scrotum:

A

superficial inguinal nodes

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4
Q

Lymphatic drainage of proximal 2/3 of vagina, uterus

A

Obturator, external iliac, and hypogastric nodes

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5
Q

On which side is a varicocele more common to occur? Why?

A

Varicoceles are more common on the the left; b/c flow is less continuous on the left (left testis –> left spermatic vein –> left renal vein –> IVC)

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6
Q

Cell type in the Ovaries:

A

Simple cuboidal epithelium

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7
Q

Cell type in Fallopian Tubes?

A

Simple columnar epithelium

–> Ciliated!

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8
Q

Cell type in Uterus?

A

Simple columnar epithelium

–>pseduostratified, tubular glands

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9
Q

Cell type in Endocervix? Ectocervix?

A
  • Endocervix–> Simple columnar epithelium

* Ectocervix –> Stratified squamous epithelium

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10
Q

Cell type in Vagina:

A

stratified squamous epithelium

–>non-keratinized

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11
Q

Which female reproductive ligament is a derivative of the gubernaculum?

A

Round ligament of uterus

  • ->connects uterine fundus to labia majora
  • ->does not contain any structures!
  • ->Travels through the round inguinal canal
  • ->Gubernaculum involved in descent of ovaries/testes during development
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12
Q

Pathway of sperm during ejaculation:

A

“SEVEN UP”

*Seminiferous tubules –> Epididymis –> Vas deferens –> Ejaculatory ducts –> (Nothing) –> Urethra –> Penis

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13
Q

Which nerve is involved in male Erection? Emission? Ejaculation?

A

*First: Point and Shoot (Erection = PSNS; Emission = SNS)

  • Nerves involved:
  • Erection –> pelvic nerve (PSNS)
  • Emission –> hypogastric nerve (SNS)
  • Ejaculation –> pudendal nerve (visceral and somatic nerves)
  • Emission = sperm and seminal fluid travel from scrotum into prostatic urethra
  • Ejaculation = from prostatic urethra to outside world
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14
Q

Sildenafil and Vardenafil mechanism:

A

–> both inhibit cGMP breakdown. So: increased amounts of cGMP –> smooth muscle relaxation –> vasodilation –> proerectile

*NO also stimulates increased cGMP
*This is in opposed to Norepinephrine:
NE–>increases intracellular Calcium –> smooth muscle contraction –> vasoconstriction –> antierectile

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15
Q

What type of cell produce primary spermatocytes? Where are these cells located?

A
  • ->Spermatogonia = Germ cells –> produce primary spermatocytes
  • ->line seminiferous tubules
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16
Q

Sertoli cells:

  • Where are they located?
  • Functions?
A
  • ->line seminiferous tubules
  • ->overall: support sperm synthesis
  • Functions:
  • secrete inhibin (inhibits FSH)
  • secrete ABP (Androgen-Binding Protein)
  • produce anti-mullerian hormone (mullerian-inhibiting factor)
  • form blood-testis barrier (tight jxns b/w adjacent Sertoli cells)
  • support and nourish developing spermatozoa
  • regulate spermatogenesis

***note: sertoli cells are temperature sensitive: if increase temperature (like with a varicocele or cryptochordism (undescended testes)) –> get decreased sperm production and decreased inhibin

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17
Q

Leydig cells:

  • Where are they located?
  • Functions?
A
  • Located in interstitium of seminiferous tubules
  • Functions:
  • secrete Testosterone!
  • -> this is unaffected by temperature! (unlike Sertoli cells, which are affected by temperature)
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18
Q

Where does spermatogenesis occur? When does it occur?

A
  • -> occurs in seminiferous tubules

- -> begins at puberty

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19
Q

Spermiogenesis:

A

part of spermatogenesis: spermatids loss cytoplasmic contents, gain acrosomal cap to form mature spermatozoon

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20
Q

Testosterone vs DHT (Dihydrotestosterone) vs Androstenedione:

A

Potency: DHT > Testosterone > Androstenedione

*DHT and Testosterone are produced in testes:
Testosterone –> DHT (by 5-alpha-reductase)
*Androstenedione is produced in adrenals

***both Testosterone and Androstenedione are converted to Estrogen in adipose tissue and Sertoli cells by Aromatase!

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21
Q

Testosterone is involved in the differentiation of all internal genitalia, except?

A
  • -> Testosterone is NOT involved in differentiation of prostate!
  • -> DHT is! (DHT is also involved in differentiation of penis and scrotum –> external genitalia)
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22
Q

Which forms of Androgens are converted to Estrogen?

A

Testosterone and Androstenedione

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23
Q

17-beta-estradiol

A

Form of estrogen that is formed in the ovaries

–>predominant form of estrogen during reproductive years

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24
Q

Estriol

A
  • ->form of estrogen that is formed in placenta

- ->predominant type of estrogen in serum during pregnancy

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25
Q

Estrone

A
  • ->form of estrogen formed in blood via aromatization

- -> predominant form of estrogen during menopause

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26
Q

Which form of estrogen is most potent?

A

Highest potency: Estradiol > Estrione > Estriol

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27
Q

Affect of estrogen on Prolactin?

A

Estrogen stimulated prolactin secretion, BUT it inhibits prolactin’s action on the breast! (so, don’t give OCPs to breast-feeding women!)

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28
Q

Where on cell are estrogen receptors found?

A

–>receptors are in nucleus; translocate to nucleus when bound by ligand (cytosolic steroid receptor)

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29
Q

Effect of estrogen on HDL and LDL?

A

*increased HDL, decreases LDL!

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30
Q

Theca cells:

A

Stimulated by LH

*convert cholesterol –> Androstenedione, by the enzyme desmolase (17-alpha-hydroxylase!)

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31
Q

Granulosa cells:

A
  • stimulated by FSH

* get Andostenedione from Theca cells and convert: Androstenedione –> Estrogen, via Aromatase!

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32
Q

Desmolase

A

Enzyme that converts cholesterol –> Androstenedione in Theca cells of ovary
–>Desmolase = 17-alpha-hydorxylase

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33
Q

3 sources of Estrogens:

A
  • Ovaries (Estradiol)
  • Blood/Aromatization (Estrone)
  • Placenta (Estriol)
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34
Q

Sources of Progesterone:

A
  • Corpus luteum
  • Placenta
  • Adrenal Cortex
  • Testes
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35
Q

Progesterone functions:

A
  • -> it’s “Pro-gestation!”
  • stimulates endometrial gland secretions
  • maintains pregnancy
  • decreases myometrial excitability (vs estrogen, which increases it; but, want to maintain pregnancy, so not excite myometrium!)
  • produces thick cervical mucus (so sperm won’t enter)
  • increases body temp
  • INHIBITS FSH and LH
  • relaxes uterine smooth muscle (prevents contractions)
  • decreases estrogen receptor expressivity
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36
Q

Which phase of the menstrual cycle is variable length? Which is a constant length and how long?

A

Follicular phase = Proliferative phase –> phase from menstruation to ovulation = variable

Luteal phase = Secretory phase –> phase between ovulation and menstruation = constant 14 days.

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37
Q

Definition of:

  • oligomenorrhea?
  • polymenorrhea?
  • metrorrhagia?
  • menometrorrhagia?
A
  • oligomenorrhea: >35 days
  • polymenorrhea <21 days
  • metrorrhagia = frequent but irregular menstruation
  • menometrorrhagia = heavy, irregular menstruation at irregular intervals
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38
Q

Mittelschmerz

A

–>ovulation may mimic appendicitis: blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis

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39
Q

What happens during ovulation?

A

Estrogen surge and increased GnRH receptors on ant pit–> stimulates LH surge/release –> rupture of follicle (ovulation) –> increased progesterone (which causes an increased temperature)

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40
Q

Oogenesis:

  • phase at birth?
  • phase at ovulation?
A
  • Arrested in Prophase of Meiosis 1 until ovulation
  • Arrested in Metaphase of Meiosis 2 until fertilization

***If fertilization does not occur, secondary oocyte degenerates

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41
Q

Where does fertilization usually occur?

A
  • -> Ampulla of fallopian tube

- occurs within 1 day after ovulation

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42
Q

How long after fertilization does implantation within uterus wall occur?

A

6 days after fertilization

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43
Q

How long after fertilization/conception does hCG appear in blood? in urine?

A
  • ->in blood 1 week after conception/fertilization

- ->in urine (ie home pregnancy test) 2 weeks after conception/fertilization

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44
Q

Source of hCG?

A

Syncytiotrophoblast of placenta

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45
Q

Function of hCG?

A

–>maintains corpus luteum (and progesterone) during 1st trimester by secreting LH. During 2nd and 3rd trimesters, placenta synthesizes its own estriol and progesterone, so corpus luteum degenerates

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46
Q

Pathologic states with increased hCG?

A
  • hydatidiform mole

- choriocarcinoma (ovarian germ cell tumor)

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47
Q

Hormonal changes in menopause (estrogen, FSH, LH, GnRH):

A
  • decreased estrogen (primary source of estrogen = peripheral conversion of androgens –> estrone)
  • increased FSH
  • increased LH (but not as much as FSH)
  • increased GnRH
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48
Q

Hormone findings in Klinefelter’s: (LH, FSH, Testosterone, Estrogen)

A
  • decreased inhibin (d/t testicular atrophy, dysgenesis of seminiferous tubules) –> increased FSH
  • decreased testosterone (d/t abnormal Leydig cell fxn) –> increased LH –> increased Estrogen
  • So:
  • increased FSH
  • increased LH
  • decreased testosterone
  • increased estrogen
  • decreased sperm
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49
Q

Hormonal and other findings in Turner’s:

A
  • Atrophy of ovaries = “streak ovaries” –> infertility
  • horseshoe kidding
  • webbing of neck
  • short stature
  • preductal coarctation of aorta
  • bicuspid aortic valve
  • hormones:
  • decreased estrogen
  • increased LH and FSH

-No Barr body in neutrophils (b/c only have 1 X, so all X’s are active!)

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50
Q

Causes of female pseudohermaphroditism (XX, ovaries, but virilized or ambiguous external genitalia):

A
  • ->d/t excessive androgen exposure early in gestation:
  • Congenital Adrenal Hyperplasia (21-hydroxylase or 11-beta-hydroxylase deficiency)
  • Exogenous steroids during pregnancy
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51
Q

Causes of male pseduohermaphroditism (XY, tests, but female or ambiguous external genitalia):

A

–>Androgen Insensitivity Syndrome = Testes feminization

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52
Q

Androgen Insensitivity Syndrome:

  • Genotype
  • Defect
  • Presentation
  • Hormones (Testosterone, Estrogen, LH, FSH)
A
  • XY
  • Defect in androgen receptor
  • Presentation:
  • normal appearing female (b/c no response to androgens)
  • female external genitalia with rudimentary vagina (b/c still have lower 2/3rds of vagina, b/c lower 2/3rds develop from urogenital sinus; whereas upper 1/3rd develops from mullerian duct, but no mullerian duct in this case)
  • no uterus or uterine tubes
  • no sexual hair
  • develops testes (see 2 lumps in labia majora; must be removed to prevent cancer)
  • Hormones:
  • Elevated Testosterone
  • Elevated Estrogen
  • Elevated LH
  • Normal FSH
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53
Q

5-alpha-reductase deficiency:

  • presentation?
  • Hormones?
A
  • autosomal recessive, in XY males:
  • ->can’t convert testosterone to DHT
  • ambiguous genitalia until puberty, then masculinization/male external genitalia at puberty, b/c of increased testosterone secretion –> “penis at 12”
  • Normal internal genitalia
  • Hormones:
  • Normal testosterone, Estrogen
  • Normal or elevated LH
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54
Q

Anosmia, lack of secondary sex characteristics –> ?

-hormones in this condition (GnRH, FSH, LH, Testosterone…)?

A
  • ->Kallman syndrome
  • defective development of GnRH cells and olfactory –> so, decreased synthesis of GnRH in hypothalamus
  • autosomal dominant condition
  • Hormones:
  • decreased GnRH
  • decreased FSH and LH
  • decreased testosterone
  • decreased sperm count
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55
Q

“honeycombed uterus” or “cluster of grapes” appearance of uterus?

A

–>hydatidiform mole

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56
Q

“snowstorm” appearance at 1st sonogram?

A

–>Hydatidiform mole

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57
Q

Most common precursor of choriocarcinoma?

A

–>Hydatidiform mole

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58
Q

Treatment for hydatidiform mole?

A

–>D and C, and Methotrexate

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59
Q

Karyotype of Complete vs Partial Hydatidiform mole:

A
  • Complete: 46XX or 46XY

* Partial: 69XXX, 69XXY, 69XYY

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60
Q

Components (sperm, egg) of Complete vs Partial moles?

A
  • Complete: 2 sperm, no/empty egg

* Partial: 2 sperm + 1 egg

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61
Q

What is preeclampsia? eclampsia?

A
  • Preeclampsia = HTN + Proteinuria (and commonly edema too)

* Eclampsia = Preeclampsia + seizures

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62
Q

Preeclampsia timing? if before 20 weeks?

A

Preeclampsia: from 20 weeks gestation to 6 weeks postpartum

*If preeclampsia before 20 weeks –> Molar pregnancy

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63
Q

HELLP syndrome:

A
  • ->associated with preeclampsia/eclampsia:
  • Hemolysis
  • Elevated LFTs
  • Low Platelets

–>anemia + bruising/gum bleeding + jaundice + elevated BP

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64
Q

Treatment of Preeclampsia/Eclampsia?

A
  • ->Deliver fetus if possible, safe
  • ->Monitor, supportive, bed rest, salt restriction
  • -> IV magnesium sulfate (1st choice) or Diazepam for seizures in eclampsia
65
Q

Placental abruption:

  • what is it?
  • presentation?
  • risk factors?
A
  • ->premature detachment of placenta from implantation site
  • ->PAINFUL bleeding during 3rd trimester, fetal death; if abrupt, can be fatal
  • ->may lead to DIC
  • Risk factors: (anything that causes vasoconstriction)
  • smoking
  • HTN
  • cocaine use
66
Q

Placenta accreta:

  • what is it?
  • presentation?
  • risk factors?
A

–>placenta attaches to myometrium (instead of endometrium) so no separation of placenta after birth

–>Massive bleeding AFTER delivery

  • Risk factors:
  • prior C-section
  • inflammation
  • placenta previa
67
Q

Placenta previa:

  • what is it?
  • presentation?
  • risk factors?
A

–>attachment of placenta to lower uterine segment; placenta may cover/block the internal os (so don’t stick finger in to check/dx, b/c may tear and bleed)

–>PAINLESS bleeding in ANY trimester

  • Risk factors:
  • multiparity
  • prior C-section
68
Q

Endometrial biopsy of an ectopic pregnancy:

A

–>Decidualized endometrium, but no chorionic villi

69
Q

Ectopic Pregnancy:

  • most common location?
  • Presentation?
  • Risk factors?
A

–>usually in fallopian tubes

  • Presentation:
  • elevated hCG (to normal pregnancy levels)
  • sudden abdominal pain (may look like appendicitis)
  • may or may not have bleeding
  • decidualized endometrium, but no chorionic villi on biopsy
  • Risk factors: (anything that causes tubal scarring)
  • hx of PID
  • ruptured appendix
  • prior tubal surgery
70
Q

Painless bleeding any trimester of pregnancy?

A

–>Placenta previa (placenta attaching to lower part of uterine, ie cover the internal os)

71
Q

Painful bleeding during 3rd trimester?

A

–> placenta accreta (detachment of placenta from implantation site)

72
Q

bleeding after birth/delivery?

A
  • ->Placenta accreta (placenta doesn’t separate after birth)
  • ->can also get postpartum hemorrhage from any retained placental tissue
73
Q

Polyhdramnios - conditions?

A
  • Esophageal/Duodenal atresia (can’t swallow fluid)

- Anencephaly (can’t swallow fluid…)

74
Q

Oligohydramnios - conditions?

A
  • placental insufficiency
  • bilateral renal agenesis (can’t pee) (Potter’s)
  • posterior urethral valves in males (can’t pee)
75
Q

Cervical Carcinoma in situs (CIN):

  • what is it? where does it start?
  • cause?
  • risk factors?
A
  • ->begins at squamo-columnar jxn of cervix and extends out
  • Associated with HPV 16 and 18
  • may progress (slowly) to invasive carcinoma if untreated
  • Main risk factors:
  • ->multiple sex partners
  • ->smoking
76
Q

Which HPV strains are associated with cervical cancer? And, what is the MECHANISM?

A
  • ->HPV 16 and 18
  • HPV 16:
  • E6 gene inhibits p53 suppressor gene
  • HPV 18:
  • E7 gene inhibits Rb suppressor gene
77
Q

Koilocytes:

A
  • ->cells look kind of like fried eggs (wrinkled nuceli with perinuclear halo)
  • ->associated with cervical dysplasia; HPV
78
Q

Endometritis:

  • cause/what is it?
  • trtmnt?
A

–>inflammation of endometrium d/t retained products in the uterus (like after delivery, miscarriage, abortion, IUD/foreign body)

  • Treat:
  • cefoxitin (2nd gen cephalosporin)
  • ticarcillin-clavulanate (anti-pseudomonal + beta-lactamase inhibitor)
  • ampicillin-sulbactam (aminopenicillin + beta-lactamase inhibitor)
79
Q

Endometriosis:

  • what is it?
  • presentation?
  • treatment?
A

–>endometrial glands outside the uterus (in ovaries, peritoneum…)

  • Presentation:
  • cyclic bleeding from ectopic endometrial tissue
  • “chocolate cysts” = blood-filled areas from ectopic endometrial tissue bleeding
  • severe menstrual related pain
  • dyspareunia
  • menorrhagia
  • infertility
  • normal-sized uterus!

*Treatment = Danazol (synthetic androgen that acts as partial agonist at androgen receptors)

80
Q

Adenomyosis:

  • what is it?
  • presentation?
  • treatment?
A

–>endometrial tissue within myometrium (so, like endometriosis, but still within uterus - in the myometrium)

  • Presentation:
  • menorrhagia (heavy bleeding)
  • dysmenorrhea
  • pelvic pain
  • Enlarged uterus (vs normal uterus in endometriosis)

*Treatment = hysterectomy

81
Q

Most common gynecological malignancy?

A
  • ->Endometrial carcinoma

- vaginal bleeding, post-menopause; usually preceded by endometrial hyperplasia (from elevated estrogens…)

82
Q

Most common tumor in females?

A

–>Leiomyoma = fibroid
=benign, smooth muscle tumor in uterus, well-demarcated, rare malignant transformation (does not progress to leiomyosarcoma)
-tumors are estrogen-sensitive (bigger during pregnancy; smaller during menopause)
-may cause uterine bleeding (leading to anemia)
-whorled pattern of smooth muscle bundles

83
Q

Gynecological tumors:

  • 3 highest incidence:
  • 3 with worst prognosis:
A

Incidence: Endometrial > Ovarian > Cervical
(Cervical is most common worldwide, but not in US)

Worst prognosis: Ovarian > Cervical > Endometrial
*so, ovarian has worst prognosis…

84
Q

Age of menopause in premature ovarian failure:

A

–>before 40 yo

85
Q

Hormone levels in PCOS: (LH, FSH, Testosterone, Estrogen):

-what is the primary cause?

A
  • elevated LH (primary cause)
  • decreased FSH
  • elevated testosterone
  • elevated estrogen (from testosterone aromatization)
86
Q

Increased risk of what cancer in PCOS pts?

A

–>increased risk of endometrial cancer (d/t elevated estrogens, from aromatization of androgens in fat cells)

87
Q

Treatment for PCOS:

A
  • Weight loss
  • OCPs
  • Medroxyprogesterone (decreases LH and adrogenesis)
  • Spirinolactone (treats acne and hirsutism; think: spirinolactone causes gynecomastia! so, has anti-androgen side effects)
  • Clomiphene (SERM; for women who want to get pregnant)
88
Q

most common ovarian mass in young women?

A

Follicular cyst = unrupture graafian follicle (so, fails to become corpus luteum); follicle distends…

89
Q

corpus luteum cyst:

A

–>ovarian cyst that arises d/t hemorrhage into a persistent corpus luteum; resolves spontaneously

90
Q

Dermoid cyst:

A

–>an ovarian cyst - a mature teratoma (benign)

91
Q

Endometroid cyst:

A

=”chocolate cyst” –> an ovarian cyst from endometriosis within ovary
–>varies with menstrual cycle (when filled with blood = chocolate cyst)

92
Q

ovarian germ cell tumor with elevated hCG and LDH?

A
  • ->Dysgerminoma (malignant, equivalent to male seminoma, but rarer)
  • ->associated with Turner’s
93
Q

ovarian germ cell tumor with elevated hCG?

A
  • ->Choriocarcinoma
  • NO chorionic villi
  • develop during pregnancy in baby or mother
  • may spread hematogenously to lungs
94
Q

ovarian germ cell tumor with elevated AFP (alpha-feto-protein)?

A
  • ->Yok sac/Endometrial sinus tumor
  • aggressive malignancy
  • yellow solid mass
  • 50% have Schiller-Duval bodies (look like glomeruli)
95
Q

Most common ovarian germ cell tumor (90% of them)?

A
  • ->Teratomas (most of which are benign, mature dematoid cysts)
  • Teratomas = contain cells from 2 or 3 germ cell layers
  • immature teratoma= malignant
  • struma ovarri = contains thyroid cells; may present as hyperthyroidism
96
Q

Schiller-Duval bodies:

A
  • -> look like glomeruli

- -> found in 50% of yolk sac tumors (both male and female)

97
Q

Struma Ovarii:

A
  • -> ovarian teratoma that contains thyroid tissue

- may present as hyperthyroidism

98
Q

CA-125:

A
  • ->tumor marker for ovarian cancer

- not very specific; so, good for monitoring progression, but not for screening

99
Q

Most important risk factor for ovarian non-germ cell tumors?

A

–> Family hx (genetics –> BRCA-1, BRCA-2, HNPCC)

100
Q

Krukenberg tumor:

A
  • -> Ovarian tumor that is d/t metastasis from GI (gastric adenocarcinoma)
  • ->have mucin-secreting signet cells
101
Q

Call-Exner bodies:

A
  • ->found in Granulosa cell tumors (ovarian tumor)

- ->fluid-filled spaces b/w granulosa cells

102
Q

Ovarian tumor that looks like bladder?

A
  • ->Brenner tumor
  • benign and unilateral
  • “coffee bean” nuclei
103
Q

Ovarian tumor that secretes estrogen?

A
  • ->Granulosa cell tumor
  • may have uterine bleeding (from elevated estrogen)
  • have Call-Exner bodies (small follicles filled with eosinophilic secretions; fluid-filled spaces b/w granulosa cells)
104
Q

Benign ovarian tumor with intestine-like tissue/mucus-secreting epithelium?

A

–>Mucinous cystadenoma (On histology, looks like intestines!)

105
Q

Ovarian tumor with psammoma bodies:

A
  • Serous Cystadenocarcinoma
  • malignant, often bilateral
  • accounts for 45% of ovarian tumors

(PSMM:

  • Papillary thyroid
  • Serous ovary
  • Meningioma
  • Mesothelioma)
106
Q

Benign tumor that accounts for 20% of non-germ cell ovarian tumors?

A

–>serous cystadenoma

***note: serous cystadenocarcinoma (malignant version) accounts for 45% of non-germ cell ovarian tumors

107
Q

Meig’s syndrome:

A

Triad:
Ovarian fibroma + Ascites + Hydrothorax
–>pulling sensation in groin

108
Q

Clear Cell Adenocarcinoma of Vagina: Main risk factor?

A

–> DES exposure to women when they were in-utero

109
Q

Sarcoma Botyroides:

A
  • ->a type of rhabdomyosarcoma
  • affects girls under 4 yo!
  • desmin positive tumor cells (desmin stains muscle…)
110
Q

Fibroadenoma:

A
  • ->most common breast tumor in women <35 yo
  • small, mobile, firm mass; benign
  • NOT precursor to breast cancer
110
Q

Intraductal Papilloma:

A
  • BENIGN breast tumor
  • tumor is in lactiferous ducts, so secretes serous of bloody nipple discharge
  • very slight risk for carcinoma
111
Q

Phyllodes tumor:

A
  • Benign breast tumor; may become malignant

- Large bulky mass of connective tissue and cystys; usually in women in their 60’s

111
Q

Most important prognostic factor in breast cancer?

A

–>Axillary lymph node involvement

112
Q

Noninvasive (ie no BM involvement) ductal breast cancer (type of ductal carcinoma in situ) with casesous necrosis (central necrosis surrounded by cancer cells)?

A

–>Comedocarcinoma

112
Q

Most common type of malignant breast cancer? Prognosis?

A
  • ->Invasive ductal breast cancer
  • ->most invasive; poorest prognosis
  • ->Precursor = DCIS (ductal carcinoma in situ)
  • firm, fibrous, rock-hard mass; classic “stellate” morphology
113
Q

Breast cancer in which breast skin looks like orange peel (“peau d’orange”)?

A
  • ->Inflammatory invasive breast cancer

- neoplastic cells block lymph drainage, so get edema, and the orange-peel-like breast skin.

114
Q

Paget’s disease of breast:

A
  • ->eczema-like patches on the nipple
  • Paget cells are large cells in epidermis with clear halo
  • may see on vulva too
115
Q

Acute Mastitis:

A
  • ->breast abscess associated with breast feeding
  • results b/c get increased cracks in nipple from breast feeding, so increased risk of bacterial infection through cracks
  • ->usually caused by S. aureus
116
Q

Gynecomastia: Causes?

A
  • Causes:
  • hyperestrogenism
  • Klinefelter’s
  • Drugs: “Some Drugs Create Awesome Knockers”
  • ->Spirinolactone
  • ->Digitalis
  • ->Cimetidine
  • ->Alcohol
  • ->Ketoconazole
  • Other drugs: marijuana, estrogen, heroin, psychoactive drugs
117
Q

BPH:

  • what is it?
  • serum marker?
  • treatment?
A

Benign Prostatic Hyperplasia (NOT hypertrophy!) –> Hyperplasia of prostate gland
-associated with elevated PSA (free Prostate-Specific Antigen)

  • Treatment:
  • Finasteride (anti-androgen; decreases size of prostate)
  • Tamsulosin or Terazosin (alpha-1-blockers) –> relax smooth muscle
118
Q

Elevated PSA (Prostate-Specific Antigen)?

A
  • Prostitis
  • BPH
  • Prostatic adenocarcinoma (have increased total PSA, but DECREASED fraction of Free PSA)
119
Q

Prostatic adenocarcinoma: May metastasize to?

A
  • ->may get osteoblastic metastases in bone, in late stages:

- have lower back pain + elevated serum alkaline phosphatase + elevated PSA

120
Q

Cryptochordism:

  • what is it?
  • Presentation?
  • Hormones: (FSH, LH, Testosterone)
  • increasd risk of what cancer?
A
  • -> undescended testes
  • ->decreased spermatogenesis (b/c testes are too warm; must be lower/cooler for spermatogenesis to occur)
  • Hormones:
  • Normal testosterone (b/c Leydig cells are unaffected by temperature; even though they’re in the testes)
  • Decreased inhibin (b/c secreted from Sertoli cells) –> Increased FSH
  • Normal LH

*Increased risk of germ cell tumors

–>increased risk of cryptochordism in preemies

120
Q

Varicocele:

  • what is it?
  • most common side?
A
  • ->dilated veins in pampiniform plexus d/t increased venous pressure
  • ->causes scrotal enlargement
  • ->usually on Left; because increased resistance to venous flow, b/c longer path than right side
  • ->may cause infertility
  • ->”bag of worms” appearance
121
Q

Testicular germ cell tumor with “fried egg” appearing cells?

A
  • ->Seminoma
  • malignant, painless tumor; testicular enlargement
  • most common testicular tumor
  • affects males 15-35
  • good prognosis (b/c late mestastasis)
121
Q

Malignant, PAINFUL testicular germ cell tumor with elevated hCG and elevated or normal AFP:

A

–>Embryonal carcinoma

122
Q

testicular germ cell tumor with elevated AFP?

A
  • ->yolk sac tumor (Schiller-duval bodies)

- ->also may see elevated (or normal) AFP in embryonal carcinoma and teratomas

122
Q

testicular germ cell tumor with elevated hCG:

A
  • ->Choriocarcinoma
  • ->Embryonal carcinoma (may also have normal or elevated AFP)
  • ->Teratoma (may also have normal/elevated AFP)
123
Q

Reinke crystals:

A

–>seen in Leydig cell tumors (non-germ cell testicular tumor; benign)

123
Q

Most common testicular cancer in older men? cause?

A
  • ->Testicular lymphoma

- d/t metastasis from lymphoma to testes

124
Q

Testicular Masses that can Transilluminate vs those that cannot transilluminate:

A
  • No transillumination–> think testicular cancer

* Transillumination –> think tunica vaginalis lesions (Hydrocele, Spermatocele)

125
Q

Hydrocele:

A
  • ->increased fluid in the tunica vaginalis; d/t incomplete fusion of the processus vaginalis (tunica vaginalis stays in communication with the peritoneum)
  • ->usually seen in newborns; resolves on own
126
Q

Most common cause of penile squamous cell carcinoma?

A

–> HPV (usally in Asia, Africa, S. America)

127
Q

Peyronie’s disease:

A

–>Bent penis (from fibrous tissue formation)

128
Q

Causes of Priapism:

A
  • Spinal cord trauma
  • Sickle cell disease (sickled RBCs get trapped i vascular channels)
  • Meds:
  • ->Trazadone
  • ->Cocaine
  • ->prostaglandin inhibitors
  • ->etc…
129
Q

Leuprolide:

  • what is it?
  • clinical uses?
A
  • GnRH analog:
  • ->agonist when pulsatile (increases LH/FSH)
  • ->antagonist when constant (decreased GnRH receptor in pituitary –> decreased FSH/LH)
  • Uses:
  • infertility (when pulsatile)
  • prostate cancer (when continuous); use together with Flutamide (anti-androgen) to treat prostate cancer
  • uterine fibroids
130
Q

Exemestane:

A

–>Testosterone drug that can be used to treat estrogen-responsive breast cancer (b/c inhibits aromatase –> decreased estrogen)

131
Q

Finasteride:

  • mechanism?
  • uses?
A

-antiandrogen: inhibits 5-alpha-reductase (so can’t convert testosterone –> DHT)

  • Treats:
  • BPH
  • Male baldness
132
Q

Flutamide:

  • mechanism?
  • use?
A

–>anti-androgen: non-steroid, competitively inhibits androgens at testosterone receptor

-treatment of prostate cancer (can give it with leuprolide (GnRH agonist, given continuously to treat prostate cancer)

133
Q

Ketoconazole:

  • mechanism?
  • use?
A

–>anti-fungal drug! But, can be used for non-fungal treatments: inhibits desmolase (17-alpha-hydroxylase) –> so inhibits steroid synthesis

  • Prevents hirsutism in PCOS
  • side effects = gynecomastia and amenorrhea
134
Q

Spirinolactone:

  • mechanism?
  • uses?
A
  • ->aldosterone-antagonist; K-sparing diuretic
  • by blocking aldosterone = inhibits steroid synthesis
  • prevents hirsutism in PCOS
  • side effects = gynecomastia and amenorrhea
135
Q

Clomiphene:

  • mechanism?
  • uses?
A
  • SERM (Selective Estrogen Receptor Modulator)
  • ->partial agonist at estrogen receptors in hypothalamus => prevents normal feedback inhibition; so increases LH and FSH release from pituitary –> stimulates ovulation
  • Treats:
  • Infertility
  • PCOS

*side effects: hot flashes, multiple simultaneous pregnancies, ovarian enlargement…

136
Q

Tamoxifen:

  • mechanism?
  • use>
A
  • SERM
  • ->breast-tissue antagonist (though, endometrial-agonist)

-treats Estrogen-positive breast cancer

137
Q

Raloxifene:

  • mechanism?
  • use?
A
  • ->SERM
  • agonist on bone; reduces bone resorption

-treats osteoporosis

138
Q

Anastrozole:

A
  • Aromatase inhibitor

- ->treats postmenopausal women with breast cancer (b/c inhibits estrogen production)

139
Q

Mifepristone (RU-486):

  • mechanism?
  • use?
A

–>competitive inhibitor of progestins at progesterone receptors

  • Uses:
  • abortions/termination of pregnancy
  • ->administor with Misopristol (PGE1) to induce contractions
140
Q

Ritodrine:

  • mechanism?
  • use?
A
  • ->Beta-2-agonist –> relaxes the uterus
  • ->used to reduce premature uterine contractions (prevents early delivery)

(beta-2 –> decreases uterine tone)

141
Q

Terbutaline:

  • mechanism?
  • use?
A
  • ->Beta-2-agonist

- ->Relaxes uterus; prevents premature contractions (prevents early delivery)

142
Q

Tamsulosin:

  • mechanism?
  • use?
A

–>alpha-1-blocker, selective for receptors on prostate (so does not lower BP, etc…; only affects prostate)

–>inhibits smooth muscle contraction, so used to treat BPH

143
Q

Danazol:

  • mechanism?
  • use?
A

–>synthetic androgen; acts as partial agonist at androgen receptors

  • Uses:
  • endometriosis
  • hereditary angioedema
144
Q

Sildenafil, Vardenafil:

  • ->mechanism?
  • ->Toxicity?
  • ->Contraindicated with what other drug?
A

-Inhibits cGMP phosphodiesterase (so increase cGMP –> smooth muscle relaxation –> vasodilation –> penile erection)

  • Toxicities:
  • impaired blue-green vision (it’s also a little blue pill!)
  • headache and flushing (d/t vasodilation)
  • dyspepsia (heartburn)
  • life-threatening hypotension if given with NITRATES!
145
Q

Anastrozole:

A
  • Aromatase inhibitor

- ->treats postmenopausal women with breast cancer (b/c inhibits estrogen production)

146
Q

Mifepristone (RU-486):

  • mechanism?
  • use?
A

–>competitive inhibitor of progestins at progesterone receptors

  • Uses:
  • abortions/termination of pregnancy
  • ->administor with Misopristol (PGE1) to induce contractions
147
Q

Ritodrine:

  • mechanism?
  • use?
A
  • ->Beta-2-agonist –> relaxes the uterus
  • ->used to reduce premature uterine contractions (prevents early delivery)

(beta-2 –> decreases uterine tone)

148
Q

Terbutaline:

  • mechanism?
  • use?
A
  • ->Beta-2-agonist

- ->Relaxes uterus; prevents premature contractions (prevents early delivery)

149
Q

Tamsulosin:

  • mechanism?
  • use?
A

–>alpha-1-blocker, selective for receptors on prostate (so does not lower BP, etc…; only affects prostate)

–>inhibits smooth muscle contraction, so used to treat BPH

150
Q

Danazol:

  • mechanism?
  • use?
A

–>synthetic androgen; acts as partial agonist at androgen receptors

  • Uses:
  • endometriosis
  • hereditary angioedema
151
Q

Sildenafil, Vardenafil:

  • ->mechanism?
  • ->Toxicity?
  • ->Contraindicated with what other drug?
A

-Inhibits cGMP phosphodiesterase (so increase cGMP –> smooth muscle relaxation –> vasodilation –> penile erection)

  • Toxicities:
  • impaired blue-green vision (it’s also a little blue pill!)
  • headache and flushing (d/t vasodilation)
  • dyspepsia (heartburn)
  • life-threatening hypotension if given with NITRATES!

FirstAID (24 decks)

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