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BLOCK POSTING 3 > FRS PATHOLOGY > Flashcards

FRS PATHOLOGY Flashcards

1
Q

Q: What are the most common disorders affecting the fallopian tube?

A

A: Infections and inflammatory conditionsectopic pregnancy

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2
Q

Q: What is salpingitis and its major complications?

A

A: Salpingitis is inflammation of the fallopian tubeoften due to Gonococcus or Chlamydiae. Major complications include infertility

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3
Q

Q: What are paratubal cysts and where are they found?

A

A: Paratubal cysts are the most common primary lesions of the fallopian tube. Larger varieties like hydatids of Morgagni are found near the fimbriated end or broad ligaments.

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4
Q

Q: What is the most common benign tumor of the fallopian tube?

A

A: Adenomatoid tumors.

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5
Q

Q: What are the four major tissue types that give rise to ovarian tumors?

A

A: Surface epithelium germ cells

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6
Q

Q: What are the common non-neoplastic cysts of the ovary?

A

A: Follicle cysts and luteal cysts often from unruptured or sealed follicles.

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7
Q

Q: What are the key features of polycystic ovarian syndrome (PCOS)?

A

A: Hyperandrogenism menstrual abnormalities

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8
Q

Q: What are the major classifications of ovarian tumors based on origin?

A

A: Surface epithelial tumors germ cell tumors

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9
Q

Q: What is a serous ovarian tumor and what are its subtypes?

A

A: A tumor resembling the fallopian tube lining; subtypes include benign

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10
Q

Q: What is pseudomyxoma peritonei and what causes it?

A

A: A condition caused by mucinous tumor cells from the appendix or gastrointestinal tract producing excessive mucin in the peritoneum.

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11
Q

Q: What is a Brenner tumor?

A

A: An uncommon usually benign ovarian tumor composed of fibroblastic stroma and transitional epithelium.

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12
Q

Q: What are granulosa cell tumors associated with?

A

A: Excess estrogen production precocious puberty

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13
Q

Q: What are the key features of dysgerminomas?

A

A: Malignant radiosensitive germ cell tumors occurring in younger individuals

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14
Q

Q: What is a Krukenberg tumor?

A

A: A metastatic ovarian tumor often from stomach or intestinal adenocarcinomas

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15
Q

Q: What are the causes of dysfunctional uterine bleeding (DUB)?

A

A: Anovulatory cycles and inadequate luteal phase due to hormonal disturbances.

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16
Q

Q: What is endometriosis?

A

A: The presence of ectopic endometrial tissue outside the uterus causing infertility

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17
Q

Q: What is adenomyosis?

A

A: Endometrial tissue in the myometrium causing menorrhagia dysmenorrhea

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18
Q

Q: What is the significance of endometrial hyperplasia?

A

A: Excess estrogen causes proliferation of endometrial glands increasing the risk of endometrial carcinoma.

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19
Q

Q: What are the two types of endometrial carcinoma?

A

A: Endometrioid carcinoma (associated with estrogen and hyperplasia) and serous carcinoma (aggressive associated with atrophy).

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20
Q

Q: What are the common types of myometrial tumors?

A

A: Leiomyomas (benign) and leiomyosarcomas (malignant).

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21
Q

Q: What are the common causes of fallopian tube infections (salpingitis)?

A

A: Gonococcus and Chlamydiae are the most common causes. Tuberculous and chronic infections are also significant in certain environments.

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22
Q

Q: What are the major complications of tubal inflammation?

A

A: Tuboovarian abscess adhesions

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23
Q

Q: What are hydatids of Morgagni?

A

A: Larger paratubal cysts found near the fimbriated end of the fallopian tube or in the broad ligament arising from remnants of the müllerian duct.

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24
Q

Q: What is the typical presentation of primary fallopian tube adenocarcinoma?

A

A: A dominant tubal mass that may be detected during pelvic examination often involving the ovary

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25
Q

Q: What are the two major regions of ovarian stroma?

A

A: Cortical and medullary regions.

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26
Q

Q: What is the cause of functional follicular and luteal ovarian cysts?

A

A: They originate from unruptured graafian follicles or ruptured follicles that immediately seal.

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27
Q

Q: What are the common endocrine abnormalities in PCOS?

A

A: Hyperandrogenism chronic anovulation

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28
Q

Q: What are psammoma bodies and in which ovarian tumor are they found?

A

A: Concentric laminated calcified concretions commonly found in serous tumors of the ovary.

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29
Q

Q: How can mucinous ovarian tumors be distinguished from Krukenberg tumors?

A

A: Mucinous tumors are usually unilateral while Krukenberg tumors are bilateral and metastatic from the gastrointestinal tract.

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30
Q

Q: What are Exner bodies and which tumor are they associated with?

A

A: Small

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31
Q

Q: What is the clinical significance of thecoma tumors?

A

A: They produce estrogen causing symptoms like precocious puberty

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32
Q

Q: What are the two main types of teratomas?

A

A: Cystic teratomas (dermoid cysts) and solid teratomas.

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33
Q

Q: What is a struma ovarii?

A

A: A monophyletic teratoma composed entirely of thyroid tissue.

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34
Q

Q: What is Meigs syndrome?

A

A: A condition associated with ovarian fibromas peritoneal effusions

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35
Q

Q: What is the difference between adenomyosis and endometriosis?

A

A: Adenomyosis involves endometrial tissue within the myometrium while endometriosis involves ectopic endometrial tissue outside the uterus.

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36
Q

Q: What genetic mutation is commonly associated with endometrial hyperplasia and carcinoma?

A

A: Inactivation of the PTEN tumor suppressor gene.

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37
Q

Q: What is serous endometrial intraepithelial carcinoma (SEIC)?

A

A: A precursor lesion to serous endometrial carcinoma often associated with TP53 mutations.

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38
Q

Q: What are the three histologic grades of endometrioid carcinoma?

A

A: Well-differentiated (grade 1) moderately differentiated (grade 2)

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39
Q

Q: How does serous endometrial carcinoma typically spread?

A

A: By extrauterine lymphatic or transtubal dissemination even when confined to the endometrium.

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40
Q

Q: What are the two major categories of endometrial hyperplasia?

A

A: Non-atypical hyperplasia and atypical hyperplasia (endometrial intraepithelial neoplasia).

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41
Q

Q: What are the key features of endometrial polyps?

A

A: Exophytic masses projecting into the endometrial cavity often causing abnormal bleeding.

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42
Q

Q: What are the main risk factors for endometrioid carcinoma?

A

A: Obesity diabetes

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43
Q

Q: What is the common presentation of leiomyomas?

A

A: Benign smooth muscle tumors causing menorrhagia pelvic pain

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44
Q

Q: How do leiomyosarcomas differ from leiomyomas?

A

A: Leiomyosarcomas are malignant and show cytologic atypia high mitotic index

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45
Q

Q: What is the clinical significance of dysfunctional uterine bleeding (DUB)?

A

A: It often indicates anovulatory cycles or inadequate luteal phase without structural abnormalities.

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46
Q

Q: What is the most common primary lesion of the fallopian tube?

A

A: Paratubal cysts including hydatids of Morgagni.

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47
Q

Q: What are the main features of polycystic ovaries in PCOS?

A

A: Ovaries are twice the normal size gray-white with a smooth outer cortex

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48
Q

Q: What is the significance of the fimbriated end of the fallopian tube in cancer spread?

A

A: It allows fallopian tube carcinomas to frequently involve the ovary omentum

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49
Q

Q: What are the four types of surface epithelial ovarian tumors?

A

A: Serous mucinous

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50
Q

Q: What is pseudomyxoma peritonei typically caused by?

A

A: Metastatic mucinous adenocarcinomasn often from the gastrointestinal tract

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51
Q

Q: What are the three categories of mucinous ovarian neoplasms?

A

A: Benign borderline

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52
Q

Q: What are the hormonal effects of granulosa cell tumors?

A

A: Excess estrogen production leading to endometrial hyperplasia or precocious puberty.

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53
Q

Q: What is the most common ovarian tumor in young populations?

A

A: Germ cell tumors particularly benign cystic teratomas.

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54
Q

Q: What are the histological features of dysgerminomas?

A

A: Large round cells with prominent nuclei arranged in alveoli with lymphocyte infiltration.

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55
Q

Q: How do Krukenberg tumors present histologically?

A

A: Bilateral mucin-secreting tumors with signet-ring cells.

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56
Q

Q: What are the common symptoms of endometriosis?

A

A: Infertility dysmenorrhea

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57
Q

Q: What are the two major pathologic types of endometrial carcinoma?

A

A: Endometrioid carcinoma and serous carcinoma.

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58
Q

Q: How is atypical endometrial hyperplasia (endometrial intraepithelial neoplasia) characterized?

A

A: Proliferating glands with nuclear atypiaback-to-back gland arrangement

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59
Q

Q: What distinguishes serous endometrial carcinoma from endometrioid carcinoma?

A

A: Serous carcinoma is more aggressive
arises in older women

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60
Q

Q: What are the features of leiomyomas?

A

A: Benign smooth muscle tumors that may cause menorrhagia pelvic pain

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61
Q

Q: What are the common secondary tumors of the ovary?

A

A: Metastatic tumors from breast gastrointestinal tract

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62
Q

Q: What is adenomyosis and how does it differ from endometriosis?

A

A: Adenomyosis involves endometrial tissue in the myometrium

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63
Q

Q: What genetic mutation is common in endometrial carcinoma and hyperplasia?

A

A: PTEN tumor suppressor gene inactivation.

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64
Q

Q: What is Meigs syndrome associated with?

A

A: Ovarian fibromas peritoneal effusions

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65
Q

Q: What is the main difference between benign and malignant serous ovarian tumors?

A

A: Benign tumors are predominantly cystic while malignant ones are solid and invasive.

66
Q

Q: What is the pathogenesis of dysfunctional uterine bleeding (DUB)?

A

A: Hormonal imbalance affecting the normal cyclical changes in the endometrium.

67
Q

Q: What is the significance of Exner bodies in ovarian tumors?

A

A: They are characteristic microfollicles seen in granulosa cell tumors.

68
Q

Q: What type of tissue is found in struma ovarii?

A

A: Thyroid tissue as part of a monophyletic teratoma.

69
Q

Q: What is a characteristic histological feature of psammoma bodies?

A

A: Concentric laminated calcified concretions.

70
Q

Q: What are the basic principles of the endometrium and myometrium?

A

A: The endometrium is the hormonally sensitive mucosal lining of the uterine cavity while the myometrium is the underlying smooth muscle wall.

71
Q

.

A

.

72
Q

Q: What is Asherman syndrome?

A

A: Secondary amenorrhea caused by loss of the basalis and scarring often due to overaggressive dilation and curettage (D&C).

73
Q

Q: What causes an anovulatory cycle?

A

A: Lack of ovulation leads to an estrogen-driven proliferative phase without a progesterone-driven secretory phase causing dysfunctional uterine bleeding.

74
Q

Q: What are the key causes and presentation of acute endometritis?

A

A: Bacterial infection due to retained products of conception presenting as fever

75
Q

Q: What is required for a diagnosis of chronic endometritis?

A

A: Presence of plasma cells in the endometrium alongside lymphocytes.

76
Q

Q: What is a common cause of endometrial polyps?

A

A: Tamoxifen due to its weak pro-estrogenic effects on the endometrium.

77
Q

Q: What is the typical presentation of endometriosis?

A

A: Dysmenorrhea
pelvic pain

78
Q

Q: What is adenomyosis?

A

A: Presence of endometrial tissue within the myometrium causing menorrhagia dysmenorrhea

79
Q

Q: What are the risks of endometriosis?

A

A: Scarring
infertility

80
Q

Q: What is endometrial hyperplasia and what is its major complication?

A

A: Hyperplasia of endometrial glands due to unopposed estrogen

81
Q

Q: What are the two pathways of endometrial carcinoma development?

A

A: Hyperplasia pathway (estrogen-driven) and sporadic pathway (p53 mutations in atrophic endometrium).

82
Q

Q: What are the distinguishing features of leiomyomas (fibroids)?

A

A: Benign smooth muscle tumors estrogen-sensitive

83
Q

Q: What are leiomyosarcomas and how do they differ from leiomyomas?

A

A: Malignant smooth muscle tumors arising de novo

84
Q

Q: What is the functional unit of the ovary?

A

A: The follicle composed of an oocyte surrounded by granulosa and theca cells.

85
Q

Q: What causes polycystic ovarian disease (PCOD)?

A

A: Hormonal imbalance with increased LH:FSH ratio leading to androgen excess and cystic degeneration of follicles.

86
Q

Q: What is the classic presentation of PCOD?

A

A: Obese young woman with infertility oligomenorrhea

87
Q

Q: What are the three major types of ovarian tumors based on cell origin?

A

A: Surface epithelial tumors germ cell tumors

88
Q

Q: What are the common subtypes of surface epithelial ovarian tumors?

A

A: Serous mucinous endometriod clear brenner

89
Q

Q: What is the significance of BRCA1 mutation in ovarian cancer?

A

A: Increased risk of serous carcinoma of the ovary and fallopian tube; prophylactic surgery is often recommended.

90
Q

Q: What are the key features of germ cell tumors?

A

A: Mimic fetal oocyte

91
Q

Q: What are Schiller-Duval bodies and in which tumor are they found?

A

A: Glomerulus-like structures found in endodermal sinus tumors.

92
Q

Q: What is a Krukenberg tumor?

A

Bilateral metastatic mucinous tumor of the ovaries typically from gastric carcinoma.

93
Q

Q: What is Meigs syndrome?

A

A: Ovarian fibroma associated with pleural effusions and ascites which resolve upon tumor removal.

94
Q

Q: What is pseudomyxoma peritonei?

A

A: Massive mucus accumulation in the peritoneum often due to a mucinous tumor of the appendix with ovarian metastasis.

95
Q

Q: What is the role of CA-125 in ovarian cancer?

A

A: A serum marker used to monitor treatment response and screen for recurrence.

96
Q

Q: What are the characteristics of a choriocarcinoma?

A

A: Malignant tumor of trophoblasts and syncytiotrophoblasts with high β-hCG early hematogenous spread

97
Q

Q: What are the components of the cervix?

A

A: Exocervix (lined by nonkeratinizing squamous epithelium) and endocervix (lined by columnar cells). The transformation zone lies between them.

98
Q

Q: What is HPV and how does it affect the cervix?

A

A: HPV is a sexually transmitted DNA virus that infects the transformation zone of the cervix

99
Q

Q: Which HPV types are considered high-risk for cervical dysplasia?

A

A: HPV types 16 18

100
Q

Q: What are the functions of HPV E6 and E7 proteins?

A

A: E6 increases p53 destruction and E7 increases Rb destruction

101
Q

Q: What are the grades of cervical intraepithelial neoplasia (CIN)?

A

A: CIN I (<1/3 epithelium thickness) CIN II (<2/3 thickness)

102
Q

Q: What characterizes high-grade dysplasia in a Pap smear?

A

A: Hyperchromatic nuclei and high nuclear-to-cytoplasmic ratio.

103
Q

Q: What are the two most common subtypes of cervical carcinoma?

A

A: Squamous cell carcinoma (80%) and adenocarcinoma (15%).

104
Q

Q: What are the key risk factors for cervical carcinoma?

A

A: High-risk HPV infection smoking

105
Q

Q: What is a common cause of death in advanced cervical carcinoma?

A

A: Hydronephrosis with postrenal failure due to tumor invasion blocking the ureters.

106
Q

Q: What is the purpose of Pap smear screening?

A

A: To detect cervical dysplasia (CIN) before progression to carcinoma.

107
Q

Q: At what age should Pap smear screening begin?

A

A: Screening starts at age 21.

108
Q

Q: What is the most effective way to confirm an abnormal Pap smear?

A

A: Colposcopy and biopsy.

109
Q

Q: What are the limitations of the Pap smear?

A

A: Inadequate sampling of the transformation zone and limited efficacy in detecting adenocarcinoma.

110
Q

Q: What does the quadrivalent HPV vaccine cover?

A

A: HPV types 6 11

111
Q

Q: How does the HPV vaccine protect against cervical cancer?

A

A: Antibodies against HPV types 16 and 18 protect against CIN and carcinoma while types 6 and 11 protect against condylomas.

112
Q

Q: Why are Pap smears still necessary after HPV vaccination?

A

A: The vaccine covers only a limited number of HPV types so regular screening is essential.

113
Q

Q: What is the second most common cancer in women worldwide?

A

A: Cancer of the cervix.

114
Q

Q: What is the most common cancer in women in the developing world?

A

A: Cancer of the cervix (second only to breast cancer in Nigeria).

115
Q

Q: What are the risk factors for cervical cancer?

A

A: High-risk HPV infection HIV

116
Q

Q: Which HPV types are considered high-risk for cervical cancer?

A

A: HPV types 16 and 18 (account for ~70% of SIL and cervical carcinoma cases).

117
Q

Q: Where do most cervical tumors arise?

A

A: The transformation zone where the squamous and columnar epithelia meet.

118
Q

Q: How do HPV E6 and E7 oncoproteins contribute to cervical cancer?

A

A: E6 inhibits p53 and E7 inhibits Rb

119
Q

Q: What are the stages of cervical cancer according to FIGO staging?

A

A: Stage 0: CIN III (carcinoma in situ)
Stage I: Confined to the cervix
Stage II—Carcinoma extends beyond the cervix but not
to the pelvic wall. Carcinoma involves the vagina but
not the lower third.
• Stage III—Carcinoma has extended to the pelvic wall.
On rectal examination there is no cancer-free space
between the tumor and the pelvic wall. The tumor
involves the lower third of the vagina.
• Stage IV—Carcinoma has extended beyond the true
pelvis or has involved the mucosa of the bladder or
rectum. This stage also includes cancers with metastatic
dissemination

120
Q

Q: What are the methods of screening for cervical cancer?

A

A: Conventional Pap smear
Liquid-Based Cytology

121
Q

Q: What are the characteristics of cervical intraepithelial neoplasia (CIN)?

A

A: CIN is graded based on the proportion of undifferentiated cells in the epithelium: CIN I (<1/3 thickness) CIN II (<2/3 thickness)

122
Q

Q: What is adenocarcinoma in situ (AIS)?

A

A: A precursor lesion from columnar epithelium characterized by abnormal cells with hyperchromatic nuclei

123
Q

Q: What distinguishes CIN I from CIN II and CIN III?

A

A: CIN I: Undifferentiated cells in the lower third of the epithelium; CIN II: Dysplastic changes in the lower two-thirds; CIN III: Differentiation absent or limited to the superficial layer.

124
Q

Q: What is the mean interval for progression from CIN to invasive cancer?

A

A: 10 to 20 years.

125
Q

Q: What is the main cause of HPV-related cervical carcinogenesis?

A

A: Persistent HPV infection leading to squamous intraepithelial lesions (SILs) which are precursors to invasive carcinoma.

126
Q

Q: What are the hallmark cellular changes in CIN?

A

A: Enlarged nuclei
hyperchromasia

127
Q

Q: What role does the host immune response play in HPV infections?

A

A: Most HPV infections are transient and eliminated by the immune system but persistent infections may lead to SILs and cervical carcinoma.

128
Q

Q: What is an ectopic pregnancy?

A

A: Implantation of a fertilized ovum at a site other than the uterine wall most commonly in the fallopian tube.

129
Q

Q: What is the classic presentation of ectopic pregnancy?

A

A: Lower quadrant abdominal pain a few weeks after a missed period.

130
Q

Q: What are the major complications of ectopic pregnancy?

A

A: Hematosalpinx (bleeding into the fallopian tube) and tubal rupture.

131
Q

Q: What is a spontaneous abortion?

A

A: Miscarriage of a fetus before 20 weeks gestation usually during the first trimester.

132
Q

Q: What are common causes of spontaneous abortion?

A

A: Chromosomal anomalies (e.g. trisomy 16)

133
Q

Q: What are the teratogenic effects of alcohol?

A

A: Mental retardation facial abnormalities

134
Q

Q: How does cigarette smoke affect pregnancy?

A

A: Causes intrauterine growth retardation.

135
Q

Q: What is placenta previa?

A

A: Implantation of the placenta in the lower uterine segment overlying the cervical os

136
Q

Q: What is placental abruption?

A

A: Premature separation of the placenta from the uterine wall a common cause of stillbirth.

137
Q

Q: What is placenta accreta?

A

A: Improper implantation of the placenta into the myometrium causing postpartum bleeding and difficulty delivering the placenta.

138
Q

Q: What is preeclampsia?

A

A:
Pregnancy-induced hypertension
proteinuria
oedema

139
Q

Q: What is eclampsia?

A

A: Preeclampsia with seizures.

140
Q

Q: What is HELLP syndrome?

A

A: Preeclampsia with hemolysis elevated liver enzymes

141
Q

Q: What are risk factors for sudden infant death syndrome (SIDS)?

A

A:
Sleeping on the stomach
cigarette
smoke exposure

142
Q

Q: What is a hydatidiform mole?

A

A: Abnormal conception characterized by swollen villi and trophoblast proliferation.

143
Q

Q: How is a complete mole different from a partial mole?

A

A: A complete mole has no fetal tissue all villi are hydropic

144
Q

Q: What is the classic presentation of a hydatidiform mole?

A

A: Passage of grape-like masses through the vaginal canal and a uterus larger than expected for gestational age.

145
Q

Q: How is a hydatidiform mole diagnosed?

A

A: Ultrasound showing a snowstorm appearance and absence of fetal heart sounds.

146
Q

Q: What is the treatment for a hydatidiform mole?

A

A: Dilatation and curettage followed by β-hCG monitoring to detect choriocarcinoma.

147
Q

Q: How do choriocarcinomas from gestational pathways respond to treatment?

A

A: They respond well to chemotherapy unlike those arising from germ cell pathways.

148
Q

Q: What does Gestational Trophoblastic Disease (GTD) encompass?

A

A: A spectrum of tumors and tumor-like conditions characterized by the proliferation of placental tissue, either villous or trophoblastic.

149
Q

Q: How does the WHO classify Gestational Trophoblastic Disease?

A

A: Into molar lesions (partial, complete, and invasive hydatidiform moles) and nonmolar lesions (choriocarcinoma and other trophoblast-derived malignancies).

150
Q

Q: What hormone is elevated in all forms of Gestational Trophoblastic Disease?

A

A: Human chorionic gonadotropin (hCG).

151
Q

Q: What characterizes a hydatidiform mole?

A

A: Cystic swelling of chorionic villi with variable trophoblastic proliferation.

152
Q

Q: How does a complete mole differ genetically from a partial mole?

A

A: A complete mole has only paternal chromosomes (diploid) due to fertilization of an empty egg by two sperm. A partial mole is triploid with one maternal and two paternal chromosome sets.

153
Q

Q: What is the histological difference between complete and partial moles?

A

A: In a complete mole, most or all villi are hydropic, whereas in a partial mole, only some villi are enlarged and edematous.

154
Q

Q: What is an invasive mole?

A

A: A mole that invades or perforates the uterine wall, often associated with persistently elevated hCG levels.

155
Q

Q: What are the complications of an invasive mole?

A

A: It can invade parametrial tissues and blood vessels, embolize to distant sites (lungs, brain), and may cause uterine rupture requiring hysterectomy.

156
Q

Q: What is choriocarcinoma?

A

A: A malignant neoplasm of trophoblastic cells, often following hydatidiform moles, abortions, normal pregnancies, or ectopic pregnancies.

157
Q

Q: How does choriocarcinoma appear grossly and histologically?

A

A: Grossly as a soft, fleshy, yellow-white tumor with necrosis and hemorrhage. Histologically, it consists of proliferating syncytiotrophoblasts and cytotrophoblasts without chorionic villi.

158
Q

Q: What are common clinical features of choriocarcinoma?

A

A: Irregular vaginal bleeding with bloody, brown fluid and extremely elevated hCG levels.

159
Q

Q: How does choriocarcinoma typically spread?

A

A: It has a high propensity for hematogenous spread, commonly metastasizing to the lungs and bones.

160
Q

Q: What conditions commonly precede choriocarcinoma?

A

A: 50% arise from complete moles, 25% from abortions, 22% from normal pregnancies, and others from ectopic pregnancies.

161
Q

Q: How does choriocarcinoma respond to treatment?

A

A: It responds well to chemotherapy despite its invasive and metastatic potential.

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