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Final FA review > 3/17 repro > Flashcards

3/17 repro Flashcards

1
Q

renal cell carcinoma

-most common location of metastasis?

A

lungs

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2
Q

Where do primary brain neoplasms often metastasize to?

A

inside the CNS

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3
Q

link btwn hypothyroidism & amenorrhea/galactorrhea

A

inc. TRH can stimulate PRL prod.

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4
Q

Most common cause of spont. nipple discharge?

A

intraductal papilloma

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5
Q

polythelia

-what is it?

A

accessory nipple

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6
Q

ephelide

-what is it?

A

freckle

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7
Q

ANP & BNP

-which messenger system do they use?

A

inc. cGMP.

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8
Q

vitamin D

-wheres its receptor?

A

cytoplasm

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9
Q

AFP:

  • what normally produces it?
  • marker for which tumors?
A
  • fetal liver & yolk sac = normal

- HCC, nonseminomatous testicular carcinomas, ovarian carcinomas.

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10
Q

CA-125

-marker for what?

A

ovarian cancer

  • not good for screening: highly nonspecific.
  • use it to monitor progression.
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11
Q

Gross hematuria in a sickle cell pt/DM pt/tylenol abuser

  • which disease?
  • dont confuse w/what?
A

renal papillary necrosis

-dont confuse w/acute tubular necrosis which presents in a severely ill hospitalized pt w/oliguria.

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12
Q

choriocarcinoma

-most common distant metastasis?

A

lungs

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13
Q

choriocarcinoma

  • cancer of which cells?
  • villi? cytotropho? syncytiotropho?
A
  • neoplasm of trophoblast = which includes both cyto & syncytio.
  • NOT of villi.
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14
Q

klinefelters:

-abnormal hormone levels?

A
  • dec. testosterone
  • inc. FSH (bc dec inhibin)
  • inc. LH => inc. estrogen

*i dont understand why estrogen is inc.

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15
Q

CEA

-marker for what?

A

-colorectal & pancreatic cancer

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16
Q

Where do most ovarian malignancies arise from?

A

90% = surface epithelium derived

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17
Q

Case control study

-odds ratio or relative risk?

A

-odds ratio

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18
Q

Cohort study

-odds ratio or relative risk?

A

-relative risk

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19
Q

Most important chemical mediator of sepsis?

A

TNF-alpha

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20
Q

Suckling increases which hormone production?

A

oxytocin & PRL

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21
Q

Risks for child thats not breast-fed:

A

-Asthma, allergies, diabetes mellitus, and obesity.

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22
Q

hPL

-inc or dec. in hypoglycemia?

A
  • elevated to shunt what little glucose there is to the fetus.
  • inc. the moms resistance to insulin.
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23
Q

Which is a better diagnostic test for menopause, LH or FSH?

A

FSH.

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24
Q

Why do post menopausal woman have inc. risk of CAD?

A

bc estrogen inc. HDL and dec. LDL.

-and now you have way less estrogen!

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25
Q

spermiogenesis

A
  • loss of cytoplasmic contents, gain of acrosomal cap = forms mature spermatozoon.
  • dont confuse w/spermatogenesis.
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26
Q

Which hormone responsible for growth of penis?

A

Testosterone

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27
Q

Which hormone responsible for differentiation of penis?

A

DHT

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28
Q

Klinefelter vs Turner

-which one has a barr body, which one doesn’t?

A
  • Klinefelter (47 XXY) has a barr body

- Turner (45 XO) does NOT.

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29
Q

Genetics of Turners syndrome:

A

-Can be complete monosomy (45,XO) or mosaicism (e.g., 45,XO/46,XX).

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30
Q

Double Y males [male] (XYY)

-Sxs:

A

Phenotypically normal

  • very tall, severe acne.
  • antisocial behavior.
  • Normal fertility.
  • Small % diagnosed with autism spectrum disorders.
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31
Q

True hermaphroditism

  • genetics?
  • aka?
A
  • 46,XX or 47,XXY
  • ovotesticular disorder
  • both ovary and testicular tissue present.
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32
Q

Female pseudo-hermaphrodite

  • genetics?
  • what is it?
A
  • XX
  • Ovaries present, but external genitalia are virilized or ambiguous.
  • Due to excessive and inappropriate exposure to androgenic steroids during early gestation (e.g., CAH or exogenous admin. of androgens during pregnancy)
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33
Q

Male pseudo-hermaphrodite

  • genetics?
  • what is it?
A
  • XY
  • Testes present, but external genitalia are female or ambiguous.
  • Most common form is androgen insensitivity syndrome (testicular feminization).
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34
Q

Maternal virilization during pregnancy

-possible cause?

A

-Aromatase deficiency: fetal androgens cross placenta.

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35
Q

Androgen insensitivity syndrome

  • genetics?
  • presentation?
A
  • 46,XY

- testes present, female external genitalia.

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36
Q

Androgen insensitivity syndrome (46,XY)

-hormone levels?

A
  • inc. test.
  • inc. estrogen
  • inc. LH
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37
Q

5α-reductase deficiency

  • inheritance pattern?
  • who gets this disease?
A
  • Autosomal recessive (like most enzyme deficiencies).

- genetic males 46 XY

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38
Q

5α-reductase deficiency

-Sxs:

A

ambiguous genitalia until puberty, then male.

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39
Q

“penis at 12” phenomenon

-aka?

A

5α-reductase deficiency

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40
Q

5α-reductase deficiency

-testosterone levels?

A

normal

  • you may think increased bc you’re not converting any to DHT, but thats not the case.
  • that is the case if you use 5α-reductase inhibitors.
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41
Q

hydatidiform mole

  • swelling of what?
  • proliferation of what?
A

-Cystic swelling of chorionic villi and proliferation of chorionic epithelium (only trophoblast).

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42
Q

hydatidiform mole

  • Tx:
  • monitor levels of what?
A
  • D&C and methotrexate

- b-HCG

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43
Q

Is uterine size inc. in partial mole?

A

no

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44
Q

Genetic components of a complete mole.

A
  • Enucleated egg + single sperm (subsequently duplicates paternal DNA)
  • empty egg + 2 sperm is rare
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45
Q

Genetic components of a partial mole.

A

2 sperm + 1 egg

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46
Q

Sxs of complete mole?

A
  • vaginal bleeding
  • enlarged uterus
  • hyperemesis
  • pre-eclampsia
  • hyperthyroidism
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47
Q

Sxs of preeclampsia before 20 wks gestation =

A

Molar pregnancy!

-most likely complete mole.

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48
Q

Mittelschmerz

A
  • transient mid-cycle ovulatory pain
  • classically associated with peritoneal irritation (e.g., follicular swelling/rupture, fallopian tube contraction).
  • Can mimic appendicitis.
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49
Q

potential cause of pre-eclampsia

A

placental ischemia

50
Q

Time frame for pre-eclampsia

A

20 wks gestation => 6 weeks post-partum

51
Q

Elevated liver enzymes and thrombocytopenia during pregnancy?

A

These are potential Sxs of pre-eclampsia.

52
Q

Eclampsia

-maternal death usually due to:

A

-stroke (intracranial hemorrhage) or ARDS.

53
Q

Eclampsia

-Tx:

A

-antihypertensives, IV magnesium sulfate, immediate delivery.

54
Q

Anti-HTN meds for pregnancy

A

α-methyldopa, labetalol, hydralazine, nifedipine

55
Q

Pre-eclampsia

-Tx:

A
  • antihypertensives
  • deliver at 34 weeks (severe) or 37 weeks (mild)
  • IV magnesium sulfate to prevent seizure.
56
Q

HELLP syndrome

  • what is it?
  • Tx:
A

Hemolysis, Elevated Liver enzymes, Low Platelets.
- A manifestation of severe preeclampsia, although may occur without hypertension.

-thrombotic microangiopathy in liver
-RBCs get sheared as they pass by these micro-clots
in the liver -> schistocytes.
-some liver tissue will infarct
-platelets being used up to form all these little thrombi.

-Tx: delivery immediately.

57
Q

Thrombotic microangiopathy in liver during pregnancy?

A

HELLP syndrome

58
Q

Placental abruption

  • painful?
  • causes:
A
  • yes
  • trauma, smoking, HTN, preeclampsia, cocaine.

*life threatening for mother & fetus.

59
Q

Placenta previa

-painful?

A

no

60
Q

Placental abruption

-will mother have bleeding?

A

depends if bleeding is concealed or not.

61
Q

Placenta accreta

A
  • placenta attaches to myometrium without penetrating it

- most common type.

62
Q

Placenta increta

A

-placenta penetrates into myometrium.

63
Q

Placenta percreta

A
  • placenta penetrates (“perforates”) through the myometrium and into uterine serosa (invades entire uterine wall)
  • can result in placental attachment to rectum or bladder.
64
Q

decidua =

A

Endometrium under the effects of progesterone.

-aka during a pregnancy

65
Q

Placenta accreta/increta/percreta

  • due to defective what?
  • is it serious?
A
  • decidual layer (endometrium during pregnancy)

- life threatening for mother. no separation of placenta following birth => massive bleeding.

66
Q

Placenta accreta/increta/percreta

-risk factors:

A

prior C-section, inflammation, placenta previa.

67
Q

Placenta previa

  • risk factors?
  • Sxs:
A
  • prior C-section, multiparity.
  • may cause painless bleeding.
  • will require C-section to deliver.
68
Q

Ectopic pregnancy

-b-HCG levels:

A

lower than expected rise in b-HCG

-should be doubling every 2 days up until 7th week.

69
Q

Polyhydramnios

-associated w/what common disease the mother could have?

A

DM

70
Q

What types of cell does HPV infect?

A

Squamous cells

-thats why it only causes SCC.

71
Q

HPV 16 & 18

-E6 gene product: inhibits what?

A

p53

72
Q

HPV 16 & 18

-E7 gene product: inhibits what?

A

RB

73
Q

Invasive cervical SCC

-can it affect kidneys?

A

-Lateral invasion can block ureters, causing renal
failure.
-may present as hydronephrosis.
-post-renal failure is one of most common causes of death in pt. w/invasive cervical carcinoma.

74
Q

HPV infected cell histology

A

koilocytic change

-nucleus looks like a raisin.

75
Q

What age does cervical SCC present?

A

Takes about 20-25 years from HPV infection until
cervical carcinoma. So carcinoma usually presents
around 40-50 yr old females.

76
Q

Does pap smear detect adenocarcinoma well?

A

no

77
Q

HPV vaccine protects against which strains of HPV?

A

HPV 6, 11, 16, 18 (not 31 or 33)

-thats why u still need to get pap smear.

78
Q

Endometritis

-Tx:

A

gentamicin + clindamycin with or without ampicillin.

79
Q

How does endometriosis happen? How does it spread?

A

-Can be due to retrograde flow, metaplastic

transformation of multipotent cells, or transportation of endometrial tissue via the lymphatic system.

80
Q

endoemetriosis vs adenomyosis

-size of uterus?

A 
endometriosis = normal size uterus
adenomyosis = uniformly enlarged uterus
81
Q

Asherman Syndrome

A
  • Loss of basalis leading to secondary amennorhea.

- Caused by over aggressive D&C.

82
Q

Adenomyosis

-Tx:

A

hysterectomy

83
Q

Most common gynecologic malignancy?

A

endometrial carcinoma

84
Q

endometrial carcinoma

-what age does it present?

A

-55-65, postmenopausal.

85
Q

most common tumor in females?

-what race gets them the most?

A

leiomyoma

-blacks

86
Q

leiomyoma

  • hormone sensitive?
  • usually singular or multiple?
A
  • yes, estrogen sensitive

- multiple

87
Q

leiomyoma

-histology?

A

Whorled pattern of smooth muscle bundles w/well-demarcated borders.

88
Q

leiomyoma

-what age?

A

20-40, pre-menopausal.

89
Q

Between cervical, endometrial, and ovarian cancer:

-incidence rate?

A
  • endometrial > ovarian > cervical
  • USA
  • cervical is most common worldwide.
90
Q

Between cervical, endometrial, and ovarian cancer:

-worst prognosis?

A

Worst prognosis—ovarian > cervical > endometrial.

91
Q

Dermoid cyst

-what is it?

A

mature teratoma

92
Q

Endometrioid cyst

  • where?
  • aka?
A
  • endometriosis w/in ovary w/cyst formation.

- chocolate cyst (when filled w/blood)

93
Q

sex cord stroma =

A

-Granulosa cells + theca cells + fibroblasts

94
Q

tubal ligation

-inc or dec chances of ovarian cancer?

A
  • dec.

- if it increased ur chances then no one would get it.

95
Q

Ovarian neoplasms

  • how can they present?
  • how do you Dx?
A
  • presents with adnexal mass, abdominal distension, bowel obstruction, pleural effusion.
  • diagnose surgically
96
Q

Ovarian neoplasms

-whats one reason why they have a poor prognosis?

A

They present late.

97
Q

Serous cystadenoma

-unilateral or bilateral?

A

often bilateral

98
Q

most common ovarian tumor in women 20–30 years old.

A

mature cystic teratoma

-aka dermoid cyst

99
Q

Mature cystic teratoma (dermoid cyst)

-whats it called if it has functional thyroid tissue?

A

struma ovarii

100
Q

Ovarian cyst + hyperthyroidism

A

struma ovarii

-type of mature cystic teratoma (aka dermoid cyst).

101
Q

Brenner tumor

  • whats it look like?
  • whats its nuclei look like?
A
  • Looks like bladder, looks like transitional epi.

- “coffee bean” nuclei

102
Q

Meigs syndrome

A

Triad of ovarian fibroma, ascites, and

hydrothorax. Pulling sensation in groin.

103
Q

ovarian fibroma, ascites, and hydrothorax. Pulling sensation in groin.

A

Meigs syndrome

104
Q

Age 15-30:

-what is the ovarian mass?

A

germ cell tumor

105
Q

Age 35-40

-what is the ovarian mass?

A

benign surface epithelial tumor

106
Q

Age 60-70

-what is the ovarian mass?

A

malignant surface epi tumor.

107
Q

Thecoma

-may produce what hormone?

A

Estrogen

-My guess would be androgens, but answer is estrogen.

108
Q

BRCA-1: most common ovarian/fallopian tube neoplasm =

A

serous cystadenocarcinoma

109
Q

gene mutation leading to primary pulm. HTN.

A
  • BMPR2 mutation (normally inhibits vascular smooth muscle prolif.)
  • auto dom, variable penetrance
110
Q

Osteoporosis

-serum chemistry?

A

NORMAL serum chemistry!

111
Q

Osteoporosis

  • affects which type of bone?
  • example?
A

Trabecular

-distal radius, vertebral bodies, neck of femur.

112
Q

Mosaic pattern of lamellar and woven bone.

-which disease?

A

Paget’s disease of bone.

113
Q

Spongiosa filling medullary canals

-which bone disease?

A

Osteopetrosis

114
Q

What exits the jugular foramen?

A

CN 9, 10, 11 & jugular vein.

115
Q

Negative charges in basement membrane of glomerulus provides by what?

A

heparan sulfate

116
Q

acanthosis

-what is it?

A
  • inc. thickness of stratum spinosum

- psoriasis has this.

117
Q

Duchenne muscular dystrophy

-what kind of mutation?

A

frameshift

118
Q

Becker muscular dystrophy

-what kind of mutation?

A

point

-x-linked

119
Q

Rapid relief for RA - give what?

A

corticosteroids

120
Q

Vimentin

  • found where?
  • marker to Dx what?
A
  • Int. filament found in cells of mesenchymal origin.

- used ti Dx sarcomas

121
Q

Where do brain metastases usually occur?

A

Junction btwn white and grey matter.

122
Q

most commonly injured nerve in leg?

-location?

A 
common peroneal (fibular)
-due to its superficial location around the neck of the fibula.

Final FA review (52 decks)

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