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pathology > female Pathology > Flashcards

female Pathology Flashcards

1
Q

infections that cause vulvitis

A

HPV, HSV, gonococcal, syphilis, candida

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2
Q

candida vulvitis, risk factor

A

pregnant ladies, diabetes mellitus

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3
Q

most common vulvitis infectious agent

A

HPV

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4
Q

HSV vulvitis presentation

A

vesicular eruption could be perioral or paranasal

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5
Q

valvulitis complications

A

Bartholin glands ducts obstruction
cyst and abscess
Unilateral & painful dilation of the glands

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6
Q

Lichen Sclerosis:

A

Fibrotic disorder & Presents as leukoplakia

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7
Q

Lichen Sclerosis etiology

A

20% family history of AIDS or lichen sclerosis

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8
Q

Lichen Sclerosis association

A

40% vulvar carcinoma
1%-5% SCC

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9
Q

Lichen Sclerosis presention

A

pruritus, introital stenosis

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10
Q

Lichen Sclerosis pathology

A

loss of rete ridges, thin epithelium, ecchymosis

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11
Q

Lichen Sclerosis therapy

A

tropical testosterone or progesterone

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12
Q

Lichen Simplex Chronicus

A

Thickening of the epithelium, Presents also as leukoplakia.

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13
Q

Lichen Simplex Chronicus clinical presentation

A

pruritus, Thick gray white skin

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14
Q

Lichen Simplex Chronicus pathology

A

Acanthosis & hyperkeratosis

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15
Q

Lichen Simplex Chronicus treatment

A

Topical corticosteroids

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16
Q

Leukopenia etiology

A

Nneds, vitiligo, inflammatory dermansses, cis, pager disease, invasive carcinoma

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17
Q

HPV related to which cancers

A

Vulvar, vagina, cervical, head, neck & laryngeal

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18
Q

HPV pathoognomonic

A

Koilocyres

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19
Q

HPV low-risk

A

6 & 11

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20
Q

HPV low risk association

A

Dm, pregnancy & immunosuppression

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21
Q

HPV high risk

A

16, 18, 31, 45

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22
Q

HPV high risk proteins

A

E6 & E7

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23
Q

Low risk HPV may involve

A

Perineum, vulva, vagina, cervix, gnus

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24
Q

VIN1

A

limited to the lower 1/3 of the epithelium

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25
Q

VIN2

A

limited to the lower 2/3, Mitoses are often seen

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26
Q

VIN3

A

beyond the lower 2/3 (whole thickness: CIS)

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27
Q

Vulvar malignant tumors incidence

A

Very rare: less than 1% of all tumors & 3% of FGT tumors

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28
Q

Vulvar malignant tumors median age

A

older than 60
high grade VIN if younger

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29
Q

Vulvar malignant tumors cancers

A

95%: SCC, 2% melanoma (Pigments), AdenoCA, Basal CC

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30
Q

Vulvar malignant tumor’s symptoms

A

pruritis, infections, bleeding, masses

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31
Q

frequent SCC type

A

older women (77), no HPV, well differentiated

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32
Q

frequent SCC associations

A

NNED (lichen Sclerosis), cigarette smoking & DM

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33
Q

less frequent SCC

A

younger (55), poorly differentiated, HPV

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34
Q

less frequent SCC associations

A

HPV 16, CIN, VIN & cigarette smoking.

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35
Q

SCC survival

A

less than 2cm 90% 5 years
larger 20% 10 years

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36
Q

Extra-mammary Paget’s disease

A

Intraepidermal adeno CA in vulva

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37
Q

Extra-mammary Paget’s disease association

A

underlying adeno CA in 1/3 of cases

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38
Q

Extra-mammary Paget’s disease origin

A

multipotential epidermal cells.

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39
Q

Extra-mammary Paget’s disease manifestion

A

red scaly crusted plaque, may mimic appearance of inflammatory dermatitis.

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40
Q

Congenital vaginal anomalies

A

uncommon
Total absence of vagina (vaginal agenesis)
Septate or double vagina

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41
Q

Vaginitis

A

common, transit

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42
Q

atrophic Vaginitis

A

postmenopausal women

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43
Q

vaginitis infectious agents

A

Gonorrhoeal, candida albicans, trichomonas vaginalis, STD

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44
Q

Vaginal tumors

A

Adenocarcinoma, melanoma, sarcoma & SCC (95%)

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45
Q

Most common vaginal tumor

A

SCC

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46
Q

Highly malignant vaginal tumor

A

Sarcoma

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47
Q

Comments vaginal childhood umm

A

Sarcoma, (below 5 average 3)

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48
Q

Embryonal rhabdomyosarcoma is seen in

A

sarcoma

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49
Q

Embryonal rhabdomyosarcoma

A

mimics skeletal MC rhabdomyoblasts

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50
Q

cambium

A

condensation of malignant cells under mucosal surface

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51
Q

Sarcoma grossly

A

polypoid grape like mass protrude out of the vagina.

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52
Q

Exocervix epithelium

A

Non kertanized stratified squamous

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53
Q

Endocervix epithelium

A

Columnar

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54
Q

Cervicitis

A

Common condition with purulent vaginal discharge

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55
Q

Pop smear reduced mortality by

A

99 %

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56
Q

LSIL

A

Koiolocytosis

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57
Q

CIN 1

A

Mild dysplasia, (lower1/3 of epithelium): LSIL

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58
Q

CIN2

A

Moder dysplasia (lower2/3):HSIL

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59
Q

CIN3

A

more than 2/3 or totally involved, sever dysplasia or carcinoma, HSIL

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60
Q

can be detected in ____ of precancerous lesions & invasive malignancies.

A

85-90%

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61
Q

pathogensis of latent HPV

A

Integrates its DNA → Intranuclear replication or episomal

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62
Q

pathogensis of chromosomal HPV

A

E6 inhibits P53
E7 inhibirs RB

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63
Q

endocervix CA it is an ____ CA unlike the Exocervix Which is _____ ca.

A

adeno, sc

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64
Q

most effective method of cancer prevention

A

Detection of precursor lesions by cytological examination & their eradication

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65
Q

(?) of the population might be exposed to HPV

A

75%

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66
Q

(?) exposed to high risk HPV

A

50%

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67
Q

(?) exposed to HPV-induced CIN

A

10%

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68
Q

microinvasive Cervical Carcinoma

A

<3mm

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69
Q

invasive Cervical Carcinoma

A

exophytic (papillary), ulcerative (infiltrative),, nodular

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70
Q

cervical carcinoma SCC: ___ Adenoca: ___

A

80%, 10%

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71
Q

cervical carcinoma complications

A

Hydronephrosis (causes obstruction), pyelonephritis
Renal failure.
Lymphatic spread to regional pelvic nodes.
Vascular to lungs and liver

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72
Q

Endometritis

A

inflammation of the uterus endometrium

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73
Q

acute Endometritis etiology

A

N. gonorrhea or C. trachomatis after delivery or miscarriages.

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74
Q

acute Endometritis symptoms

A

Higher grade fever, intense abdominal pain, menstrual abnormalities, ectopic pregnancy, infertility

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75
Q

Chronic endometritis etiology

A

Chronic gonorrheal pelvic disease
 Tuberculosis
 Postpartal or postabortal endometrial cavities
 IUCDs: considered foreign bodies producing infection  Spontaneously in 15% of patients.

76
Q

Chronic endometritis symptoms

A

Lower grade fever & vague abdominal or pelvic pain

77
Q

Chronic endometritis pathognomonic

A

plasma cells

78
Q

Adenomyosis

A

Growth of basal cell layer of endometrium down into the myometrium (No cyclical bleeding).

79
Q

Adenomyosis symptoms

A

Menorrhagia (interfere with vascularity), dysmenorrhea, pelvic pain before onset of menstruation

80
Q

Adenomyosis complications

A

Reactive hypertrophy of myometriumm leading to thickened uterine wall (detected by US image).

81
Q

Endometriosis

A

Presence of endo. tissue (functional: respond to cyclical changes) in remote sites:

82
Q

where does Endometriosis occur

A

Ovaries (More common), Ovarian cyst might appear
Douglas pouch, uterine ligaments
tubes, peritoneal cavity, umbilicus
Uncommonly in LN, lungs, heart, & bone

83
Q

Endometriosis: clinical symptoms

A

Pain on defecation / Infertility / Dyspareunia & Dysuria (pain induced by cyclical changes), severe dysmenorrhea, pelvic pain (In almost all cases) & Abdominal discomfort.

84
Q

The favored theory

A

regurgitation of menstrual blood flow to fallopian tubes and ovaries.

85
Q

Benign mets theory

A

that endometrium spread to different sites via blood vessels of lymphatics

86
Q

Metaplastic theory

A

endometrium differentiation of coelomic epithelium is the real source

87
Q

Extrautarine, extrapelvic theory

A

circulating stem cells from BM, differentiate into endometrial tissue.

88
Q

Endometriosis grossly

A

Red blue to yellow brown implants, discoloration.
Variability in size & Chocolate cyst, as the blood ages, it turns brown.
Fibrosis, leading to adherence of pelvic structures, sealing of tubal fimbiriated ends (Infertility)

89
Q

The most common problem for which women seek medical attention

A

Dysfunctional uterine bleeding:

90
Q

Menorrhagia

A

profuse or prolonged bleeding at time of period

91
Q

Metrorrhagia

A

irregular bleeding between the periods.

92
Q

abnormal uterine bleeding common causes

A

polyps, leiomyomas, endometrial carcinoma, endometrial hyperplasia, and endometritis.

93
Q

abnormal bleeding in the absence of organic uterine lesion

94
Q

DUB causes

A

Anovulatory cycles (failure to ovulate) → excess of estrogen.
Inadequate luteal phase → delayed or underdevelopment of secretory phase.
Endomyometrial disorders; chronic endometritis, endometrial polyps, submucosal fibroids.
OCP

95
Q

DUB causes in Prepuberty

A

Precocious puberty (hypothalamic, pituitary, or ovarian origin)

96
Q

DUB causes in Adolescence

A

Abnormality within hormones – Anovulatory cycle

97
Q

DUB causes in Postmenopause

A

Endometrial atrophy (hormone loss), but should role
out Organic lesions first (carcinoma, hyperplasia, polyps).

98
Q

DUB causes in Reproductive age

A

Complications of pregnancy (abortion, trophoblastic disease, ectopic pregnancy)
Organic lesions (leiomyoma, adenomyosis, polyps, endometrial hyperplasia, carcinoma)
Anovulatory cycles and Ovulatory dysfunctional bleeding (inadequate luteal phase)

99
Q

you must role out _____ first to consider DUB in Reproductive age group

100
Q

DUB causes in Perimenopause

A

might have Anovulatory cycle, irregular shedding or organic (CA, HP, polyps).

101
Q

Endometrial hyperplasia etiology

A

Excess unopposed estrogen

102
Q

Excess unopposed estrogen seen in

A

Anovulatory cycles, Polycystic ovarian disease
Prolonged administration of estrogenic steroids.
Estrogen producing tumors (granulosa-theca cell
tumors, cortical stromal hyperplasia)
Obesity.

103
Q

Endometrial hyperplasia classified according to what

A

presence of atypia

104
Q

incident of Endometrial hyperplasia with atypia

105
Q

The most frequent CA of FGT

A

Endometrial adenocarcinoma

106
Q

Endometrial adenocarcinoma median age

A

55-65 (menopausal and postmenopausal women)

107
Q

Endometrial adenocarcinoma predisposing factors

A

estrogen stimulation due
endometrial hyperplasia, obesity, Infertility (single & nulliparous), late menopause, diabetes, HTN.

108
Q

Endometrial adenocarcinoma types

A

Endometroid, Serous, clear cell, adenosquamous

109
Q

common Endometrial adenocarcinoma

A

Endometroid

110
Q

Endometrial adenocarcinoma Estrogen related, Associated with hyperplasia

A

endometroid

111
Q

endometroid younger or older women

A

younger perimenpause

112
Q

Microsatellite instability & PTEN gene mutations

A

endometroid

113
Q

Endometrial adenocarcinoma Unrelated to estrogen, not associated with hyperplasia

A

Serous, clear cell, adenosquamous

114
Q

Serous, clear cell, adenosquamous younger or older women

115
Q

Endometrial adenocarcinoma mutation TP53

116
Q

Endometrial adenocarcinoma most aggressive type

A

adenosquamos

117
Q

syndromes have increased risk to develop endometrium CANCERS

A

Cowden’s syndrome, HNPCC

118
Q

HNPCC

A

Inherited genetic defect in DNA mismatch repair gene

119
Q

Clinical course of endometrial adenocarcinoma

A

Irregular bleeding & marked leukorrhea (vaginal secretion) , Enlarged uterus & palpable, fixation to surroundings.

120
Q

endometrial adenocarcinoma survival rate

A

stage 1 carcinoma has 90% 5 YSR
Stage 3 & 4 have less than 20% 5 YSR.

121
Q

Most common benign tumor arising from uterine smooth muscle in females

122
Q

Found in 30%-50% of women of reproductive age

123
Q

Leiomyoma common in which race

124
Q

Leiomyoma grossly

A

Well circumscribed, round, often multiple, firm to hard, gray-white.

125
Q

Monoclonal T with nonrandom chromosomal abnormalities in 40% of tumors

126
Q

leiomyoma symptoms

A

asymptomatic, menorrhagia &infertility

127
Q

Leiomyoma shape

A

Sharply demarcated, Whorled cut surfaces (wrinkled), Single or multiple, Variably sized.

128
Q

Leiomyosarcoma etilogy

129
Q

Smooth muscle tumors of uncertain malignant potential

A

Leiomyosarcoma

130
Q

Leiomyosarcoma features

A

tumor necrosis, cytologic atypia, mitotic activity.

131
Q

Leiomyosarcoma survival rate

A

40% 5 years

132
Q

most common disease; component of PID.

A

Salpingitis

133
Q

Salpingitis symptoms

A

Fever, lower abdominal pain, or pelvic pain.
Pelvic mass, adherence leading to tubo-ovarian abscess.

134
Q

Salpingitis complications

A

Increase risk of tubal pregnancy (Permanent sterility) – Dysfunctional cilia.

135
Q

Acute Salpingitis etiology

A

MO: NG, C.trachomatis, Mycoplasma hominis, U.urealyticum
Sources of infections: VTD from the LGT.
Puerperal or post abortive, especially after IU instrumentation.
Intra-abdominal infections following peritonitis.
Hematogenous as in TB.

136
Q

Primary adenocarcinoma origin

A

Papillary serous (derived from epithelium), or endometrioid (Mimic Endometrial Gland)

137
Q

Primary adenocarcinoma common site

138
Q

Primary adenocarcinoma mutation

139
Q

Primary adenocarcinoma presention

A

advanced stage, with involvement of the peritoneal cavity.

140
Q

Ovarian cysts origin

A

unruptured graffian follicles

141
Q

Ovarian cysts placement

A

immediately subjacent to serosal covering

142
Q

Ovarian cyst’s symptoms

A

Small, clear serous fluid, Pelvic pain, acute abdominal symptoms

143
Q

Polycystic ovaries etiology

A

Oligomenorrhea, hirsutism, infertility, obesity.

144
Q

Polycystic ovaries presention

A

Excessive estrogens & andorgens & some insulin resistant (Ovary twice the normal size).
 Thickened fibrotic outer tunica, numerous cysts lined by granulosa
cells with hypertrophic and hyperplastic lutenized theca interna.

145
Q

Absence of corpora lutea.

A

Polycystic ovaries

146
Q

5th common CA in US & 5th leading cause of CA death in women.

A

Ovarian Tumors

147
Q

Familial cases of ovarian tumors

A

Breast ovary syndrome related to BRCA 1
Ovary, endometrium and colon (Lynch II): DNA mismatch repair gene mutation

148
Q

overian tumor rf

A

 ↑ risk: Nulliparity (1.5-3.2 folds), Drugs (induce ovulation but have not become pregnant)
 OCP ↓ risk by 1/2

149
Q

Surface epithelial stromal tumors origin

A

multipotential coelomic covering epithelium

150
Q

Surface epithelial stromal tumors malignant or benign

A

90% malignant

151
Q

recapitulate the components of the Mullerian ducts.

A

Surface epithelial stromal tumors

152
Q

Serous Tumors median age

153
Q

Serous Tumors incident

A

60% benign (25% are bilateral), 15% malignant, 25% LMP.
LMP & M serous account for 60% of all ovarian CAs.

154
Q

most common malignant & bilateral tumour of the ovary

A

Serous cystadenocarcinoma

155
Q

Psammoma bodies

A

Serous Tumors

156
Q

Serous Tumors growth pattern

157
Q

Serous Tumors size

A

large, 30-40cm

158
Q

Serous Tumors borderline

A

Delicate papillary projections, Milder atypia, No or little stromal invasion.

159
Q

Serous Tumors carcinoma

A

Large bulky tumor mass, Anaplasia & stromal invasion.

160
Q

Mucinous Tumors median age

161
Q

Mucinous Tumors incident

A

80% benign (5% bilateral), 10% malignant (20% bilateral), 10% LMP.

162
Q

pseudomyxoma peritonei

A

Mucinous Tumors met to git

163
Q

Mucinous Tumors met or rupture

A

pseudomyxoma peritonei

164
Q

Krukenberg

A

mets of mucinous T of GIT

165
Q

Krukenberg presention

A

bilateral, glands infiltrating ovarian stroma, dirty necrosis.

166
Q

Teratomas incidence of ovarian tumors

167
Q

Teratomas age group

A

first two decades

168
Q

Teratomas incidence

A

> 90% benign
90% unilateral

169
Q

Commonest germ cell tumor in women

A

Mature cystic teratoma

170
Q

Mature cystic teratoma differentiation

171
Q

dermoid cysts found in

A

Mature cystic teratoma

172
Q

placental infections predisposing conditions

A

Premature rupture of membranes (>18 hours),

173
Q

placental infections mo

A

Mycoplasma, candida, vaginal flora

174
Q

placental infection’s complications

A

congenital pneumonia, gastroenteritis, otitis media, meningitis.

175
Q

placental infection’s pathogensis

A

ascending and hematogenous

176
Q

Acute villitis etiology

A

maternal sepsis, Syphilis, TB, listeriosis, toxoplasmosis., viruses.

177
Q

where does Ectopic pregnancy occure

A

ovaries (90%) , abdominal cavity, IU portion of the oviduct (interstitial pregnancy).

178
Q

Ectopic pregnancy etiology

A

chronic inflammatory changes, IU tumors, or endometriosis.
50%; no anatomic cause identified.

179
Q

Ectopic pregnancy complications

A

Hematosalpinx; intratubal hematoma.
Intense abdominal pain, can lead to shock.

180
Q

trophoblastic diseases etiology

A

Empty (NO M.dna) ovum fertilized by either 2 sperms or one diploid sperm.

181
Q

trophoblastic diseases histology

A

Large avascular villi with central edema & circumferential trophoblasts proliferation.

182
Q

mass of grape like vesicles.

A

trophoblastic diseases

183
Q

Choriocarcinoma age group

184
Q

Choriocarcinoma etiology

A

50% follow complete mole, 25% follow abortions.
24% follow normal pregnancy, 1% follow ectopic pregnanc

185
Q

Choriocarcinoma clinical

A

Very high titers of bhCG, Vaginal bleeding and discharge.
Hemorrhagic tumor with anaplasic sycytio and cytotrophoblasts, NO chorionic villi seen.

186
Q

Choriocarcinoma met

A

lungs (50%), vagina (30-40%), brain, liver, kidneys.

pathology (5 decks)

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