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PATHOMA Flashcards

1
Q

describe the anatomy of the vulva

A

skin and mucosa outside hymen
1- labias
2- mons pubis
3- vestibule

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2
Q

describe the histology of the vulva, vagina, cervix (lining)

A

vulva: lined by keratinized squamous epithelium
vagina: lined by NONkeratinized squamous epithelium
exocervix: lined by NONkeratinized squamous epithelium
endocervix: lined by SINGLE layer of columnar cells
(note: junction is the TRANSFORMATION ZONE SOS)

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3
Q

women in reproductive age
presents with
unilateral pain and cystic dilatation on the vulva
what is it?
where do you expect to see the dilatation?
pathogenesis?

A

bartholyn cyst
in the LOWER vestibule adjacent to the vaginal canal
d/t inflammation, the duct gets obstructed —> leading to dilatation of the bartholin gland —> cyst maybe abscess too

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4
Q

what is condyloma

A

painless genital warts

warty neoplasm of squamous epithelium

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5
Q

how to differentiate between high risk and low risk HPV?

A

based on DNA sequencing

low: 6,11 (leads to condyloma)
high: 16,18,31,33 (leads to dysplasia then ca)

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6
Q

what is the HALLMARK of HPV infected cells?

A

KOLIOCYTES ! (nucleus look WRINKLED)

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7
Q

where do we see :
condyloma acuminatum
condyloma latum:

A

acuminatum: HPV
latum: syphilis

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8
Q

differentiate between lichen sclerosis and lichen simplex chronicus in terms of:

  • women age
  • presentation and cause
  • benign vs malignant
  • risk of SCC
A

-women age
lichen sclerosis: POSTMENOPAUSAL
lichen simplex chronicus: any age, usually young

-presentation and cause
lichen sclerosis: LEUKOPLAKIA (PARCHMENT-LIKE VULVAR SKIN)
note: EPIDERMIS thins and DERMIS fibrosis (sclerosis) —AU usually
lichen simplex chronicus: LEUKOPLAKIA (THICK LEATHERY VULVAR SKIN
HYPERPLASIA)
note: hyperplasia d/t chronic irritation and scratching

-benign vs malignant
lichen sclerosis: BENIGN
lichen simplex chronicus: BENIGN

-risk of SCC
lichen sclerosis: INCREASED RISK
lichen simplex chronicus: NO RISK

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9
Q

2 causes of vulvar carcinoma with age

A

1- HPV 16, 18 (40-50 usually)

2- Non-HPV (long-standing lichen sclerosis) - age >70 yrs

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10
Q

leukoplakia DD 3

A

1- lichen sclerosis
2- lichen simplex chronicus
3- vulvar carcinoma (need biopsy)

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11
Q

pathophysi of HPV cases vulvar carcinoma

A 
arises from vulvar intraepithelial neoplasia (VIN) 
-neoplasia limited to epithelium 
-dysplasia characterised by:
1- koliocytic change 
2- disordered cellular maturation
3- nuclear atypia
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12
Q

presence of malignant epithelial cells in epidermis of vulva (carcinoma in situ)

A

extramammary paget disease

usually no underlying malignancy

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13
Q

extramammary paget dx vs paget dx of the nipple, which one has underlying malignancy?

A

paget dx of nipple

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14
Q

diagnose

erythematous, pruritic, ulcerated vulvar skin

A

extramammary paget dx

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15
Q

DD b/w paget cells (extamammary paget dx) and melanoma (similar there is malignant cells in the epidermis)
1- KERATIN
2- S100
3- PAS

A

paget cells
1- KERATIN +ve (epithelial)
2- S100 -ve
3- PAS + ve

melanoma
1- KERATIN -ve
2- S100 +ve
3- PAS -ve

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16
Q

reminder embryological origin of the vagina

A

upper 2/3: mullerian duct

lower 1/3: urogenital sinus

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17
Q

what is vaginal adenosis? and pathophys

A

persistence of COLUMNAR epithelial cells in UPPER VAGINA
-During development, squamous epithelium from lower 1/3rd of vagina (derived
from urogenital sinus) grows up to replace columnar cells (derived from
Mullerian ducts)

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18
Q

cause of vaginal adenosis?

A

use of DES !! (diethylstilbestrol) in utero

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19
Q

complication of vaginal adenosis? sos

A

progression to clear cell adenocarcinoma of vagina

-> MALIGNANT proliferation of glands with clear cytoplasm

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20
Q

bleeding with grape like mass protruding from vagina OR penis (seen <5 yrs)

  • diagnosis?
  • what is the mass called?
A

-embryonal rhabdomyosarcoma
(rare cancer)
- SARCOMA BOTRYOIDES !!!

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21
Q

what does a biopsy of embryonal rhabdomyosarcoma show (2)

A

1- rhabdomyoblast (malignant proliferation of immature skeletal muscles) sos: cytoplasm shows CROSS STRIATIONS similar to muscle fibers
2-POSITIVE IMMUNOHISTOCHEMISTRY for DESMIN and MYOGENIN !!

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22
Q

what is vaginal carcinoma?

A

malignant proliferation of SQUAMOUS epithelium lining vaginal canal

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23
Q

cause of vaginal carcinoma?

what is the precursor lesion called?

A

HPV 16 18 31 33

VAIN (vaginal intraepithelial neoplasia)-dysplasia in epithelium

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24
Q

lymph spread of vaginal carcinoma 2

A

1- upper 2/3 (from MD) spread to ILIAC NODES

2- lower 1/3 (from UGS) spread to INGUINAL LYMPH NODES

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25
Q

3 characteristics of CIN

A

1- koliocytic change
2- nuclear atypia
3- increased mitotic activity

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26
Q

CIN grades of dysplasia 4 then develops into …..

what stages are reversible ?

A 
CIN I (1/3 epithelium thickness)
CIN II (2/3 epithelium thickness)
CIN III (almost complete thickness)
CIS (carcinoma in situ): (entire thickness) NO INVASION OF BM

into invasive SCC (and not ADENOCARCINOMA —> cells of the endocervix)
CIN I II III are REVERSIBLE , CIS is IRREVERSIBLE

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27
Q

main difference b/w dysplasia and carcinoma

A

reversibility

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28
Q

what region in the lower genital tract is especially infected with HPV ?

A

transformation zone of the cervix

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29
Q

remember

A
  • Infection usually eradicated by acute inflammation

- PERSISTENT !! infection can lead to cervical dysplasia and cervical intraepithelial neoplasia (CIN)

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30
Q

most common cause of SCC of genitourinal tract

A

HPV

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31
Q

SOSOSOOSOS

pathophysio of HPV infection leading to cancer 2

A

produces proteins:
1- E6 (inactivates p53)
tumor suppressor gene regulate G1 to S phase (looks at damaged DNA), if little damage fix it by repair enzymes. if too much damage: induce apoptosis calls BAX (bcla-2 decrease) thus loss of mitoch membrane stability, cytochrome C leaks leading to apoptosis

2- E7 (inactivates Rb)
Rb holds ETF another tumor suppressor gene essential for cell cycle

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32
Q 
HPV vaccination (QUADRIVALENT)
each type prevents what?
protects for how long? 
is it necessary to do a pap smear after?
A

-HPV 6 11 prevents against condylamata accuminata
HPV 16 18 prevents against CIN and cervical cancer

  • 5years
  • necessarily incase of infection from other subtypes 31 33
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33
Q

HPV can lead to what types of cancers (esp in cervix)?

A

SCC

ADENOCARCINOMA

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34
Q

middle aged women 40-50 yrs
present with postcoital bleeding and vaginal bleeding
what to think of?

A

cervical carcinoma

probably got infected with HPV 25 years ago :) and didnt perform any pap smears

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35
Q

sos 3 main risk factors for cervical carcinoma:

A

1- HPV infection
2- IMMUNOSUPPRESSION (it is an AIDS defining illness)
3- SMOKING

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36
Q

smoking leads to what 2 cancers that are not directly affected (i.e lungs pharynx etc,,,) ?

A

1- cervix

2- pancreas

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37
Q

sos

complication of cervical cancer

A

if the tumor invades through anterior uterine wall to the bladder and blocks the ureters: leads to HYDRONEPHROSIS and post RENAL FAILURE (common cause of death)

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38
Q

gold standard screening for cervical cancer, to screen for what type?

A 
pap smear
(note only for SCC type)
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39
Q

how long it takes CIN to develop to carcinoma?

A

10-20 years

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40
Q

how frequent should women do pap smear?

cells are scraped using the brusher from where?

A
  • every 3 years >21 yrs

- transformation zone

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41
Q

what is the confirmatory test after positive screening test (pap smear) foor cervical ca?

A

Colposcopy + biopsy !!

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42
Q

2 limitations of pap smear ?

A

1- ONLY for SCC (not for adenocarcinoma)

2- FALSE -ve if transformation zone is not sampled :)

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43
Q

review histology of abnormal pap smear

and comment on 3 abnorma findings

A

features of dysplasia
1- hyperchromatic dark nucleus
2- large nucleus
3- high nucleus to cytoplasm ratio

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44
Q

hormone cycle of the endometrium 3 (phase name, hormone, physio)

A

1- proliferative phase, estrogen, endo grows
2-secretory phase, progesterone, endo prepares for implantation
3- menstrual phase, loss of progesterone, endo falls

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45
Q

secondary amenorrhea
d/t loss of BASALIS (stem cell) and scarring
diagnose

A

asherman syndrome

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46
Q

overagressive dilatation and curettage (D&C) can cause ..

A

asherman syndrome

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47
Q

what is a common cause of dysfunctional uterine bleeding during MENARCHE and MENOPAUSE ?explain how?

A 
anovulatory cycle (lack of ovulation) 
b/c of no ovulation, corpus luteum doesn’t develop thus no progesterone is made. 
endo develops by estrogen  but not maintained by proges, so falls off
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48
Q 
after delivery or miscrriage: 
fever 
abnormal uterine bleeding 
pelvic pain 
diagnose? how?
A

acute endometriris

-retained products of conception serves as the nidus of infection

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49
Q 
abnormal uterine bleeding 
pain 
INFERTILITY 
w/ (retained products of infection, IUD, TB, PID (gonorrhea, CHLAMYDIA) 
diagnose:
A

chronic endometritis

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50
Q

acute vs chronic endometritis

type of inflammation?

A
  • acute: BACTERIAL infection of endo

- chronic: PLASMA CELLS (and lymphocytes) in biopsy sos

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51
Q

MoA of TAMOXIFEN?

can lead to?

A
  • ANTI-estrogenic effect on BREAST
  • PRO-estrogenic effect on endome

thus can lead to ENDOMETRIAL POLYP

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52
Q

abnormal uterine bleeding after the use of tamoxifen (for breast ca), what is it???

A

endometrial polyp (d/t HYPERPLASTIC protrusion of endometrium)

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53
Q

what is endometriosis ? definition

A

GLANDS and STROMA !!outside uterine endometrial lining (note that the glands follow normal menstruation cycle)

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54
Q

what are the 3 theories in order for the causes of endometriosis?

A

1- RETROGRADE menstruation with implantation at an ectopic site
2-Mullerian ducts lead to endometrial METAPLASIA
3- LYMPHATIC dissemination

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55
Q

what is the most common site of endometriosis?

A

OVARY (makes hemorrhagic- chocolate cyst !!!!)

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56
Q

remember: common sites of endometriosis and symptoms

A

-Ovary (most common) - makes hemorrhagic (aka chocolate) cyst
-Uterine ligament - cause pelvic pain
-Pouch of douglas - pain with defecation
-Bladder wall - pain with urination
-Bowel serosa - abdominal pain and adhesions
-Fallopian tube mucosa - scarring increases risk for ectopic tubal pregnancy
-Adenomyosis - if endometriosis occurs in myometrium of uterus
when soft tissue is involved: Sites classically appear as yellow-brown ‘gun powder’ nodules

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57
Q

if endometriosis occurs in the myometrium. what is it called?

A

ADENOMYOSIS

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58
Q
  • pain before/after/during menstruation
  • pain during sex, urinating or bowel movements
  • severe disabling pain or chronic pain
A

endometriosis

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59
Q

IMPORTANT complication of endometriosis? special location?

A

increased risk of carcinoma at site of endometriosis !!!

esp in ovary: ENDOMETOID TUMOR

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60
Q

postmenopausal uterine bleeding could indicate: … which is …

A

endometrial HYPERPLASIA , hyperplasia of endometrial GLANDS! relative to STROMA

or endometrial carcinoma (if theres cellular atypia)

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61
Q

what is the cause of endometrial hyperplasia

A

UNOPPOSED ESTROGEN
1- obesity
2- PCOS
3- estrogen replacement

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62
Q

most important predictor for progression from hyperplasia to carcinoma?

A

CELLULAR ATYPIA !

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63
Q

what is the most common incasive carcinoma of female genital tract?

A

endometrial carcinoma (malignant proliferation of endometrial GLANDS!)

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64
Q

endometrial carcinoma 2 causes

A

1- hyperplasia 75%

2- sporadic 25%

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65
Q

differentiate b/w hyperplasia vs sporadic pathways leading to endometrial cancer:
1- age
2- histology
3- risk factors/cause

A

1- age:

  • hyperplasia: 50-60 yrs
  • sporadic: 70 yrs

2-histology

  • hyperplasia: endometrOID (normal)
  • sporadic: SEROUS (characterized by PAPILLARY structures with psammoma bodies)

3-RF/cause

  • hyperplasia: increased estrogen exposure
  • sporadic: P53 mutation -aggressive
66
Q

list 4 causes for increased estrogen exposure

A

1- early menarche/late menopause
2- nulliparity (no babies)
3- inferitility with anovulatory cycle
4- obesity

67
Q

DD for psammoma bodies 4

sos sos sos

A

1- papillary ca of the thyroid
2- meningioma
3- papillary serous ca of the endometrium/ovary
4- mesothelioma (ca of the pleura)-related to asbestos

68
Q

most common tumor in females

is it benign or malignant

A

leiomyoma/ fibroma

benign (prolifeation of SM in myometrium)

69
Q

what is the cause for leiomyoma (fibroma)

A

estrogen exposure

70
Q 
differentiate between leiomyoma (fibroma) and leimyosarcoma in terms of:
1-age
2-size  
3-characteristics 
4- cause
A

1-age:

leiomyoma: premenopausal
leiomyosarcoma: postmenopausal

2- size

leiomyoma: multiple lesions
leiomyosarcoma: single lesion

3- characteristics:

leiomyoma: well defined WHITE whorled masses
leiomyosarcoma: areas of necrosis and hemorrhage

4- cause:

leiomyoma: estrogen exposure
leiomyosarcoma: DE NOVO

71
Q

how does leiomyoma/fibroma usually present

A

asymptomatic!!!!

or abnormal uterine bleeding, infertility, pelvic mass

72
Q

how does leiomyoma size change over time?

A

enlarges during pregnancy

shrinks after menopause

73
Q

can leiomyoma progress to leimyosarcoma

74
Q

functional unit of the ovary

75
Q

follicle consists of 3 parts

A

oocyte
granulosa
theca cells

76
Q

describe the follicle process of maturation starting from theca cells until end of secretory phase

A
  • theca cells produces androgen (stimulated by LH)
  • granulosa cells convert androgen to estrogen (estradiol) (stimulated by FSH)
  • then estrogen leads to the estadiol surge —> LH surge leading to ovulation
  • after ovulation, follicle become corpus luteum (very big and yellow) secretes progesterone and prepares endometrium for possible conception
77
Q

what are the 2 cysts that can occir in the follicle

A

1- hemorrhagic corpus luteal cyst

2- follicular cyst

78
Q

how is hemorrhagic corpus luteal cyst caused ?

when is it common?

A

formed when the CL fails to disintegrate and instead persist
-commonly found during early phase of pregnancy

79
Q

how follicular cysts are caused?

is it dangerous?

A

d/t degeneration of follicles

normal in women (if few)

80
Q

main cause of polycystic ovarian disease (PCOD)

sosoosso

A

hormonal imbalance
LH:FSH >2
sosososos

81
Q

what is PCOD

A

presence of multiple ovarian FOLLICULAR cysts

-affects 5% of women of reproductive age

82
Q

explain the pathophysiology of PCOD starting with the main finding

A

main finding: LH:FSH ratio >2

  • high LH stimulates theca cells to produce LOTS of androgen
    imp: when androgen goes to blood leads to hirsuitism
  • androgen is converted to estrone in adipose tissue (thus gives NEGATIVE feedback for FSH secretion)
  • thus granulosa cells and eventually follicle degenerates making a cyst :)
83
Q

obese young women with: -infertility
-oligomenorrhea
-hirsuitism
and explain the symptoms

A

PCOD

  • infertility d/t degenerated follicles
  • hirsuitism d/t excess androgen
84
Q

pt with PCOD is at risk of what cancer and why

A

ENDOMETRIAL cancer (d/t high estrone) unopposed effect

85
Q

what is a v impo complication for a women with PCOD after 10-15 yrs?

A

insulin resistance and T2D

86
Q

what are the 3 types of ovarian tumors? and 4- metastasis

A

1- surface epithelium
2- germ cells (from oocyte)
3- sex-cord stroma (granulos,theca,fibroblast)

87
Q

most common ovarian tumors types (2 in order)

A

1- surface epithelium 70%

2- germ cells 15%

88
Q

surface epithelium ovarian tumors is divided into 22 and 22

A 
1- common (with cyst)
a- serous tumor (filled with water) 
b- mucinos tumor (filled with mucin) 
2- less common (metaplasia) 
a-endometroid tumor
b- brenner tumor
89
Q

what is the worst prognosis of all female genital tract cancer

A

surface epithelium ovarian cancer!! its the most common as well!!

90
Q

what is the surface epithelium of the ovary?

A

coelomic epithelium (has the ability to produce multiple cell types)

91
Q

which ovarian tumor is detected LATE (thus has poor prognosis):
presents as:
-vague abdominal discomfort
-urinary frequency (compress on the bladder)

A

surface epithelium

92
Q

How are serous and mucinous tumor (surface epithelial tumors of the ovary) classified into benign, borderline, and malignant?

  • name
  • describe the cyst (since serous and mucinous are common and have cysts)
  • age
A 
1- name
benign: cystadenoma
borderline: -
malignant: cystadenocarcinoma 
2- description 
benign: SINGLE cyst with SIMPLE FLAT lining 
borderline: has malignant potential 
malignant: COMPLEX cyst with THICK SHAGGY lining 
3- age 
benign: premenopausal 30-40
borderline: —
malignant: postmenopausal 60-70
93
Q

What ovarian cancer is BRCA1 mutation associated with?
BRCA1 associated with increased risk of cancer where?
what is done prophylactically?

A
  • Serous carcinoma (serous cystadenocarcinoma)
  • breast and ovary
  • salpingo-oophroectomy (fallopian tube has risk as well!!) along with bilateral mastectomy
94
Q

what are the 2 surface epithelial tumors of the ovary with NO CYST? are they mostly malignant or benign?
remember: tumors with cyst: cystadenoma, borderline, cystoadenocarcimoa
sos

A

1- endometroid tumor mostly malignant

2- brennor tumor mostly benign

95
Q

women with ENDOMETRIOSIS may develop what type of ovarian tumor? sos

A 
surface epithelium (ENDOMETROID tumor) 
made of endometrial like gland
96
Q

women with an ovarian tumor that contains cells resembling UROTHELIUM (bladder like epithelium) sos

A 
BRENNOR TUMOR (surface epithelial tumor) 
remmeber: Bladder Brennor Benign
97
Q

if a women presents with endometroid carcinoma tumor of the ovary, it is imp to check what?

A

check for ENDOMETRIAL CARCINOMA !!! (15% have independent ca)

98
Q

what is the distant metastasis of SURFACE epithelial tumors of the ovary?

A

spread LOCALLY to the PERITONEUM (via direct contact)

sosososos: OMENTAL CAKING !!!!!!

99
Q

CA-125 marker in what type of ovarian tumors? used to do what?

A

surface epithelial tumors

mostly to: 1- monitor tx response 2- screen for RECURRENCE 3-not so useful in screening

100
Q

what 4 tissues are made by germ cells, thus leading to what tumors 5?

A

1-Oocyte —> dysgerminoma
2- Placental tissue —> choriocarcinoma
3- Fetal tissue —> Embryonal ca, Cystic teratoma
4- Yolk sac —> endometril sinus (yolk sac) tumor

101
Q

all germ cells are MALIGNANT except —— is BENIGN?

A

cystic teratoma

102
Q
  • what is the most common MALIGNANT germ cell tumor?
  • what is the most common germ cell tumor? also, it is BEINGN!
  • what is the most common germ cell tumor in KIDS? is it benign or malignant?
A
  • dysgerminoma
  • cystic teratoma
  • yolk sac tumor (endodermal sinus tumor)-malignant
103
Q

schiller-duval bodies are seen in what tumor ?

A

endodermal sinus (yolk sac) tumor

104
Q

DD women presents with an ovarian tumor, if age is — what is the most likely diagnosis?
15-30
35-40
60-70

A

15-30: germ cell tumor
35-40: BENIGN surface epithelial tumor
60-70: MALIGNANT surface epithelial tumor

105
Q 
malignant tumor with cells that resemble oocytes: 
-large cells 
-clear cytoplasm 
-central nuclei 
—> FRIED egg appearance
A

Dysgerminoma

106
Q

what is the male counterpart of dysgerminoma? how do we distinguish histologically?

A

seminoma (histologically indistinguishable)

107
Q

serum LDL is elevated in what OVARIAN tumor?
prognosis?
response to radiotherapy?

A

dysgerminoma

  • good prognosis
  • responds to radiotherapy
108
Q

malignant tumor composed of cytotrophoblast and sycytiotrophoblast is called? does it spread?

A

choriocarcinoma - trophoblasts are VERY invasive

SPREADS HEMATOGENEOUSLY EARLY !!! it is small and hemorrhagic

109
Q

remember:

A

villi (fxnl unit of placenta) are absent in choriocarcinoma

110
Q

ovarian tumor with HIGH BETA HCG ?

response to chemotherapy?

A

choriocarcinoma

poor response to chemotherapy

111
Q

choriocarcinoma may lead to —- cysts in ovary

112
Q

embryonal carcinoma are malignant aggressive germ cell tumors that are composed of what type of cells?

A

LARGE PRIMITIVE CELLS (almost embryo-like)

113
Q

what is cystic teratoma?

A

tumor made up of fetal tissue derived from >2 embryonic layers (skin, hair, cartilage, thyroid, etc… )

114
Q

20 years old female presents with hyperthyroidism and mass in her ovary

A

STRAUMA OVARII (TERATOMA mainly composed of thyroid tissue !!!)

115
Q

cystic teratoma is mostly BENIGN but have malignant potential if what is present?
soso

A

1- immature tissue (esp neural ectoderm !!!)

2- somatic malignancy (SCC!!! of the skin of the TERATOMA)

116
Q

a female kid with serum AFP elevated and the biopsy shows glumeruloid structures on ovarian mass biopsy ?
-what are these glumeruloid strctures known as?

A 
endodermal sinus (yolk sac) tumor 
-schiller-duval bodies
117
Q

what are the 3 sex cord stroma tumors?

A

1- granulosa-theca tumor
2- sertoli-leydig cell tumor
3- fibroma

118
Q

Fibroma is a tumor of what cells? and what type of ovarian tumor is it?

A
  • fibroblast

- sex-cord stromal tumors

119
Q 
female presents with:
-ovarian tumor (what is it? benign or malignant?
-pleural effusion
-ascites
sosososososososo diagnose?
A

MEIGS syndrome

-ovarian tumor: fibroma !!!!!!! BENIGN

120
Q

granulosa-theca tumor is presented based on excess —— production? and presentation varies with age (how?)
1- prior to puberty
2 reproductive age
3- postmenopause

malignant or benign ?

A

EXCESS ESTROGEN PRODUCTION
1- precious puberty
2- menorrhagia and metrorrhagia
3- postmenopausal uterine bleeding with endometrial hyperplasia

malignant (min risk metastasis)

121
Q

young girl present with precious puberty and ovarian tumor? what is it?

A

granulosa-theca cell tumor (excess estrogen production)

122
Q

what ovarian tumor leads to hirsuitism and virilization (more masculine) and high androgens!!???
what is an SOS histological characteristic?

A

sertoli-leydig cell tumor (sex cord stromal tumors)

-intracytoplasmic REINKE CRYSTALS !!!!!!!!!

123
Q

2 common tumor metastasis to ovary

A

1- krukenberg tumor

2- pseudomyxoma peritonei

124
Q

a female with gastric carcinoma (what type?why?) is at risk of metastasis to what part of the genital tract? what is the tumor called?

A 
DIFFUSE type (not intestinal) since it has MUCUS:::
remember: diffuse type has signet ring cell (nucleus is pushed to side and cell is filled with mucus) 
METASTASIS to OVARY: KRUKENBERG tumor-MUCINOUS TUMOR!!!

thus note: metastasis could come from breast, colon, anywhere with MUCUS!!!!

125
Q
  • bilateral ovarian mucinous carcinoma we think of?

- unilateral / / / / ?

A 
BILATERAL !! 
krukenberg tumor (metastasis of mucus ca (e.g diffuse gastric ca) leading to mucinous carcinoma in the ovary)

UNILATERAL: primary mucinous carcinoma of ovary

126
Q

what is jelly belly ?

it is found with what tumor?

A

huge amount of mucus in peritoneum

-mucinous tumor of APPENDIX metastasizing to the OVARY: leading to PSEUDOMYXOMA PERITONEI

127
Q

primary source of pseudomyxoma peritonei (metastasis tumor to the ovary) ?

A

mucinous tumor of appendix

-REMEMBER: jelly belly :)

128
Q

key risk of ectopic pregnancy

A

tube scarring (secondary to pelvic inflammatory disease or endometriosis)

129
Q

lower quadrant pain a few wks after a missed period

A

ectopic pregnancy

130
Q

tx of ectopic pregnancy

A

surgical emergency

131
Q

spontaneous abortion is :

A

<20 weeks of gestation (usually 1st trimester)

132
Q

vaginal bleeding with passage of fetal tissue

cramp like pain

A

spontaneous abortion

133
Q

most common cause of spontaneous abortion 4

A
  • chromosomal abnormalities (e.g trisomy 16) !!!
  • hypercoaguable states (antiphospholipid syndrome)
  • congenital infection
  • exposure to teratogens )first 2 wks)
134
Q

timewise effect of teratogen exposure

A

0-2 wks spontaneous abortion
3-8 wks organ malformation
3-9 mo organ hypoplasia

135
Q

effect of alcohol as a teratogen?

A

MOST COMMON CAUSE OF MENTAL RETARDATION… FACIAL ABORMALّّITIES, MICROCCEPHALY

136
Q

limb defects is caused by what teratogen

A

thalidomide

137
Q

discolored teeth caused by what teratogen

A

tetracycline

138
Q

effect of warfarin as a teratogen?

A

fetal bleeding

139
Q

DIGIT HYPOPLASIA AND CLEُFT LIP/PALATE cause by what teratogen ?? sos

140
Q

-hearing and visual impairment
-spontaneous abortion
is caused by what teratogen ?

A

isotretinoin

141
Q

cocaine and cig smoking if taken during pregnancy can lead to ..

A

IUGR

+cocaine: placental abruption

142
Q

most common cause of spontaneous abortion 4

A
  • chromosomal abnormalities (e.g trisomy 16) !!!
  • hypercoaguable states (antiphospholipid syndrome)
  • congenital infection
  • exposure to teratogens )first 2 wks)
143
Q

DD:
1- painless 3rd trimester bleeding
2- painful 3rd trimester bleeding (and fetal insufficiency)
3- postpartum bleeding and difficulty to deliver the placenta

A

1- placenta previa
2- placenta abruption
3- placenta accreta

144
Q

what is placenta previa? tx?

A

placenta implants and closes cervical os

tx: requires C-section delivery

145
Q

what is placenta abruption? tx?

A

separation of placenta from decidua, prior to delivery of fetus

146
Q

what placental dx is a common cause of stillbirth

A

placental abruption

147
Q

when placenta implants to myometrium (with little or no decidua) it is called : differentiate based on the extent of invasion:
if superficially implanted/grows into/completely through (invade bladder/bowel) myometrium is called?

tx?

A

placenta accreta , increta, percreta

HYSTERECTOMY

148
Q

what is eclampsia

A

preeclampsia + seizures

149
Q

what is HELLP ?

A

preeclampsia + thrombotic MAHA (in liver)
Hemolysis
Elevated Liver enzyme
Low Platelets

150
Q

HELLP and Eclampsia require what tx ???

A

IMMEDIATE DELIVERY

151
Q

preeclampsia characteristics

A

-pregnancy induced HTN (headache, visual abnormality)
-proteinuria
-edema
usually arise in 3rd trimester

152
Q

what is the cause of preeclampsia ? tx?

A

caused due to abnormality in maternal-fetal vascular interface in placenta
resolves with delivery

remember: increased BP: fibrinoid necrosis)

153
Q

SIDS is ….., infants often expire during ….

A

death of infant (1mo - 1yr) with NO obvious cause

during sleep

154
Q

RF for SIDS 3 sos

A

1- EXPOSURE TO CIG smoking
2- sleeping on stomach
3- prematurity

155
Q

what is hydatidiform mole (molar pregnancy) ?

A 
abnormal conception (grow of abnormal placental tissue) 
; benign tumor, d/t genetic error (abnormal fertilized egg)
156
Q

what is hydatidiform mole (molar pregnancy) ?

A 
abnormal conception (grow of abnormal placental tissue) 
; benign tumor, d/t genetic error (abnormal fertilized egg)
157
Q

how is molar pregnancy detected?

A

if prenatal care present:

  • routine US (early 1st trimester)
  • no fetal heart sounds
  • ‘SNOW-STORM’ appearance (grape like masses filled w/ fluid)

if no prenatal care:
-pass of grapes-like masses (LARGE VILLI pass through vagina in 2nd trimester)

158
Q

-> uterus is much larger and
-> B-HCG is much higher
(than expected for date of gestation)

A

hydatidiform mole (molar pregnancy)

159
Q

tx of hydatidiform mole ? how is it monitored after?

A

D&C

monitor B-HCG to ensure mole is completely removed and CHECK for CHORIOCARCINOMA

160
Q

how can choriocarcinom arise?4

SOSOSOS how to differentiate between the major 2 types?

A
  • after spontaneous abortion
  • normal pregnancy
  • hydatidiform mole
  • spontaneous germ cell tumor

Choriocarcinoma that arise from gestational pathway respond well to
chemotherapy; those from germ cell pathway don’t.

161
Q

how to differentiate between partial and complete mole?

  • genetics
  • fetal tissue
  • villous edema
  • trophoblastic proliferation
  • risk for choriocarcinoma
A
  • genetics
    partial: normal ovum + 2 sperms = 69 chromosome
    complete: empty ovum + 2 sperms =46 chromosome
  • fetal tissue
    partial: present
    complete: absent
  • villous edema
    partial: some villi are hydropic, some normal
    complete: most villi are hydropic
  • trophoblastic proliferation
    partial: focal proliferation present around hydropic villi
    complete: diffuse proliferation around hydropic villi
  • risk for choriocarcinoma
    partial: minimal risk
    complete: 2-3%
162
Q

spontaneous abortion is :

A

<20 weeks of gestation (usually 1st trimester)

FEMALE reproductive (6 decks)

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