FRS PATHOLOGY Flashcards
(161 cards)
1
Q
Q: What are the most common disorders affecting the fallopian tube?
A
A: Infections and inflammatory conditionsectopic pregnancy
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
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.
4
Q
Q: What is the most common benign tumor of the fallopian tube?
A
A: Adenomatoid tumors.
5
Q
Q: What are the four major tissue types that give rise to ovarian tumors?
A
A: Surface epithelium germ cells
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.
7
Q
Q: What are the key features of polycystic ovarian syndrome (PCOS)?
A
A: Hyperandrogenism menstrual abnormalities
8
Q
Q: What are the major classifications of ovarian tumors based on origin?
A
A: Surface epithelial tumors germ cell tumors
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
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.
11
Q
Q: What is a Brenner tumor?
A
A: An uncommon usually benign ovarian tumor composed of fibroblastic stroma and transitional epithelium.
12
Q
Q: What are granulosa cell tumors associated with?
A
A: Excess estrogen production precocious puberty
13
Q
Q: What are the key features of dysgerminomas?
A
A: Malignant radiosensitive germ cell tumors occurring in younger individuals
14
Q
Q: What is a Krukenberg tumor?
A
A: A metastatic ovarian tumor often from stomach or intestinal adenocarcinomas
15
Q
Q: What are the causes of dysfunctional uterine bleeding (DUB)?
A
A: Anovulatory cycles and inadequate luteal phase due to hormonal disturbances.
16
Q
Q: What is endometriosis?
A
A: The presence of ectopic endometrial tissue outside the uterus causing infertility
17
Q
Q: What is adenomyosis?
A
A: Endometrial tissue in the myometrium causing menorrhagia dysmenorrhea
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.
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).
20
Q
Q: What are the common types of myometrial tumors?
A
A: Leiomyomas (benign) and leiomyosarcomas (malignant).
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.
22
Q
Q: What are the major complications of tubal inflammation?
A
A: Tuboovarian abscess adhesions
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.
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
25
Q: What are the two major regions of ovarian stroma?
A: Cortical and medullary regions.
26
Q: What is the cause of functional follicular and luteal ovarian cysts?
A: They originate from unruptured graafian follicles or ruptured follicles that immediately seal.
27
Q: What are the common endocrine abnormalities in PCOS?
A: Hyperandrogenism chronic anovulation
28
Q: What are psammoma bodies and in which ovarian tumor are they found?
A: Concentric laminated calcified concretions commonly found in serous tumors of the ovary.
29
Q: How can mucinous ovarian tumors be distinguished from Krukenberg tumors?
A: Mucinous tumors are usually unilateral while Krukenberg tumors are bilateral and metastatic from the gastrointestinal tract.
30
Q: What are Exner bodies and which tumor are they associated with?
A: Small
31
Q: What is the clinical significance of thecoma tumors?
A: They produce estrogen causing symptoms like precocious puberty
32
Q: What are the two main types of teratomas?
A: Cystic teratomas (dermoid cysts) and solid teratomas.
33
Q: What is a struma ovarii?
A: A monophyletic teratoma composed entirely of thyroid tissue.
34
Q: What is Meigs syndrome?
A: A condition associated with ovarian fibromas peritoneal effusions
35
Q: What is the difference between adenomyosis and endometriosis?
A: Adenomyosis involves endometrial tissue within the myometrium while endometriosis involves ectopic endometrial tissue outside the uterus.
36
Q: What genetic mutation is commonly associated with endometrial hyperplasia and carcinoma?
A: Inactivation of the PTEN tumor suppressor gene.
37
Q: What is serous endometrial intraepithelial carcinoma (SEIC)?
A: A precursor lesion to serous endometrial carcinoma often associated with TP53 mutations.
38
Q: What are the three histologic grades of endometrioid carcinoma?
A: Well-differentiated (grade 1) moderately differentiated (grade 2)
39
Q: How does serous endometrial carcinoma typically spread?
A: By extrauterine lymphatic or transtubal dissemination even when confined to the endometrium.
40
Q: What are the two major categories of endometrial hyperplasia?
A: Non-atypical hyperplasia and atypical hyperplasia (endometrial intraepithelial neoplasia).
41
Q: What are the key features of endometrial polyps?
A: Exophytic masses projecting into the endometrial cavity often causing abnormal bleeding.
42
Q: What are the main risk factors for endometrioid carcinoma?
A: Obesity diabetes
43
Q: What is the common presentation of leiomyomas?
A: Benign smooth muscle tumors causing menorrhagia pelvic pain
44
Q: How do leiomyosarcomas differ from leiomyomas?
A: Leiomyosarcomas are malignant and show cytologic atypia high mitotic index
45
Q: What is the clinical significance of dysfunctional uterine bleeding (DUB)?
A: It often indicates anovulatory cycles or inadequate luteal phase without structural abnormalities.
46
Q: What is the most common primary lesion of the fallopian tube?
A: Paratubal cysts including hydatids of Morgagni.
47
Q: What are the main features of polycystic ovaries in PCOS?
A: Ovaries are twice the normal size gray-white with a smooth outer cortex
48
Q: What is the significance of the fimbriated end of the fallopian tube in cancer spread?
A: It allows fallopian tube carcinomas to frequently involve the ovary omentum
49
Q: What are the four types of surface epithelial ovarian tumors?
A: Serous mucinous
50
Q: What is pseudomyxoma peritonei typically caused by?
A: Metastatic mucinous adenocarcinomasn often from the gastrointestinal tract
51
Q: What are the three categories of mucinous ovarian neoplasms?
A: Benign borderline
52
Q: What are the hormonal effects of granulosa cell tumors?
A: Excess estrogen production leading to endometrial hyperplasia or precocious puberty.
53
Q: What is the most common ovarian tumor in young populations?
A: Germ cell tumors particularly benign cystic teratomas.
54
Q: What are the histological features of dysgerminomas?
A: Large round cells with prominent nuclei arranged in alveoli with lymphocyte infiltration.
55
Q: How do Krukenberg tumors present histologically?
A: Bilateral mucin-secreting tumors with signet-ring cells.
56
Q: What are the common symptoms of endometriosis?
A: Infertility dysmenorrhea
57
Q: What are the two major pathologic types of endometrial carcinoma?
A: Endometrioid carcinoma and serous carcinoma.
58
Q: How is atypical endometrial hyperplasia (endometrial intraepithelial neoplasia) characterized?
A: Proliferating glands with nuclear atypiaback-to-back gland arrangement
59
Q: What distinguishes serous endometrial carcinoma from endometrioid carcinoma?
A: Serous carcinoma is more aggressive
arises in older women
60
Q: What are the features of leiomyomas?
A: Benign smooth muscle tumors that may cause menorrhagia pelvic pain
61
Q: What are the common secondary tumors of the ovary?
A: Metastatic tumors from breast gastrointestinal tract
62
Q: What is adenomyosis and how does it differ from endometriosis?
A: Adenomyosis involves endometrial tissue in the myometrium
63
Q: What genetic mutation is common in endometrial carcinoma and hyperplasia?
A: PTEN tumor suppressor gene inactivation.
64
Q: What is Meigs syndrome associated with?
A: Ovarian fibromas peritoneal effusions
65
Q: What is the main difference between benign and malignant serous ovarian tumors?
A: Benign tumors are predominantly cystic while malignant ones are solid and invasive.
66
Q: What is the pathogenesis of dysfunctional uterine bleeding (DUB)?
A: Hormonal imbalance affecting the normal cyclical changes in the endometrium.
67
Q: What is the significance of Exner bodies in ovarian tumors?
A: They are characteristic microfollicles seen in granulosa cell tumors.
68
Q: What type of tissue is found in struma ovarii?
A: Thyroid tissue as part of a monophyletic teratoma.
69
Q: What is a characteristic histological feature of psammoma bodies?
A: Concentric laminated calcified concretions.
70
Q: What are the basic principles of the endometrium and myometrium?
A: The endometrium is the hormonally sensitive mucosal lining of the uterine cavity while the myometrium is the underlying smooth muscle wall.
71
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72
Q: What is Asherman syndrome?
A: Secondary amenorrhea caused by loss of the basalis and scarring often due to overaggressive dilation and curettage (D&C).
73
Q: What causes an anovulatory cycle?
A: Lack of ovulation leads to an estrogen-driven proliferative phase without a progesterone-driven secretory phase causing dysfunctional uterine bleeding.
74
Q: What are the key causes and presentation of acute endometritis?
A: Bacterial infection due to retained products of conception presenting as fever
75
Q: What is required for a diagnosis of chronic endometritis?
A: Presence of plasma cells in the endometrium alongside lymphocytes.
76
Q: What is a common cause of endometrial polyps?
A: Tamoxifen due to its weak pro-estrogenic effects on the endometrium.
77
Q: What is the typical presentation of endometriosis?
A: Dysmenorrhea
pelvic pain
78
Q: What is adenomyosis?
A: Presence of endometrial tissue within the myometrium causing menorrhagia dysmenorrhea
79
Q: What are the risks of endometriosis?
A: Scarring
infertility
80
Q: What is endometrial hyperplasia and what is its major complication?
A: Hyperplasia of endometrial glands due to unopposed estrogen
81
Q: What are the two pathways of endometrial carcinoma development?
A: Hyperplasia pathway (estrogen-driven) and sporadic pathway (p53 mutations in atrophic endometrium).
82
Q: What are the distinguishing features of leiomyomas (fibroids)?
A: Benign smooth muscle tumors estrogen-sensitive
83
Q: What are leiomyosarcomas and how do they differ from leiomyomas?
A: Malignant smooth muscle tumors arising de novo
84
Q: What is the functional unit of the ovary?
A: The follicle composed of an oocyte surrounded by granulosa and theca cells.
85
Q: What causes polycystic ovarian disease (PCOD)?
A: Hormonal imbalance with increased LH:FSH ratio leading to androgen excess and cystic degeneration of follicles.
86
Q: What is the classic presentation of PCOD?
A: Obese young woman with infertility oligomenorrhea
87
Q: What are the three major types of ovarian tumors based on cell origin?
A: Surface epithelial tumors germ cell tumors
88
Q: What are the common subtypes of surface epithelial ovarian tumors?
A: Serous mucinous endometriod clear brenner
89
Q: What is the significance of BRCA1 mutation in ovarian cancer?
A: Increased risk of serous carcinoma of the ovary and fallopian tube; prophylactic surgery is often recommended.
90
Q: What are the key features of germ cell tumors?
A: Mimic fetal oocyte
91
Q: What are Schiller-Duval bodies and in which tumor are they found?
A: Glomerulus-like structures found in endodermal sinus tumors.
92
Q: What is a Krukenberg tumor?
Bilateral metastatic mucinous tumor of the ovaries typically from gastric carcinoma.
93
Q: What is Meigs syndrome?
A: Ovarian fibroma associated with pleural effusions and ascites which resolve upon tumor removal.
94
Q: What is pseudomyxoma peritonei?
A: Massive mucus accumulation in the peritoneum often due to a mucinous tumor of the appendix with ovarian metastasis.
95
Q: What is the role of CA-125 in ovarian cancer?
A: A serum marker used to monitor treatment response and screen for recurrence.
96
Q: What are the characteristics of a choriocarcinoma?
A: Malignant tumor of trophoblasts and syncytiotrophoblasts with high β-hCG early hematogenous spread
97
Q: What are the components of the cervix?
A: Exocervix (lined by nonkeratinizing squamous epithelium) and endocervix (lined by columnar cells). The transformation zone lies between them.
98
Q: What is HPV and how does it affect the cervix?
A: HPV is a sexually transmitted DNA virus that infects the transformation zone of the cervix
99
Q: Which HPV types are considered high-risk for cervical dysplasia?
A: HPV types 16 18
100
Q: What are the functions of HPV E6 and E7 proteins?
A: E6 increases p53 destruction and E7 increases Rb destruction
101
Q: What are the grades of cervical intraepithelial neoplasia (CIN)?
A: CIN I (<1/3 epithelium thickness) CIN II (<2/3 thickness)
102
Q: What characterizes high-grade dysplasia in a Pap smear?
A: Hyperchromatic nuclei and high nuclear-to-cytoplasmic ratio.
103
Q: What are the two most common subtypes of cervical carcinoma?
A: Squamous cell carcinoma (80%) and adenocarcinoma (15%).
104
Q: What are the key risk factors for cervical carcinoma?
A: High-risk HPV infection smoking
105
Q: What is a common cause of death in advanced cervical carcinoma?
A: Hydronephrosis with postrenal failure due to tumor invasion blocking the ureters.
106
Q: What is the purpose of Pap smear screening?
A: To detect cervical dysplasia (CIN) before progression to carcinoma.
107
Q: At what age should Pap smear screening begin?
A: Screening starts at age 21.
108
Q: What is the most effective way to confirm an abnormal Pap smear?
A: Colposcopy and biopsy.
109
Q: What are the limitations of the Pap smear?
A: Inadequate sampling of the transformation zone and limited efficacy in detecting adenocarcinoma.
110
Q: What does the quadrivalent HPV vaccine cover?
A: HPV types 6 11
111
Q: How does the HPV vaccine protect against cervical cancer?
A: Antibodies against HPV types 16 and 18 protect against CIN and carcinoma while types 6 and 11 protect against condylomas.
112
Q: Why are Pap smears still necessary after HPV vaccination?
A: The vaccine covers only a limited number of HPV types so regular screening is essential.
113
Q: What is the second most common cancer in women worldwide?
A: Cancer of the cervix.
114
Q: What is the most common cancer in women in the developing world?
A: Cancer of the cervix (second only to breast cancer in Nigeria).
115
Q: What are the risk factors for cervical cancer?
A: High-risk HPV infection HIV
116
Q: Which HPV types are considered high-risk for cervical cancer?
A: HPV types 16 and 18 (account for ~70% of SIL and cervical carcinoma cases).
117
Q: Where do most cervical tumors arise?
A: The transformation zone where the squamous and columnar epithelia meet.
118
Q: How do HPV E6 and E7 oncoproteins contribute to cervical cancer?
A: E6 inhibits p53 and E7 inhibits Rb
119
Q: What are the stages of cervical cancer according to FIGO staging?
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: What are the methods of screening for cervical cancer?
A: Conventional Pap smear
Liquid-Based Cytology
121
Q: What are the characteristics of cervical intraepithelial neoplasia (CIN)?
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: What is adenocarcinoma in situ (AIS)?
A: A precursor lesion from columnar epithelium characterized by abnormal cells with hyperchromatic nuclei
123
Q: What distinguishes CIN I from CIN II and CIN III?
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: What is the mean interval for progression from CIN to invasive cancer?
A: 10 to 20 years.
125
Q: What is the main cause of HPV-related cervical carcinogenesis?
A: Persistent HPV infection leading to squamous intraepithelial lesions (SILs) which are precursors to invasive carcinoma.
126
Q: What are the hallmark cellular changes in CIN?
A: Enlarged nuclei
hyperchromasia
127
Q: What role does the host immune response play in HPV infections?
A: Most HPV infections are transient and eliminated by the immune system but persistent infections may lead to SILs and cervical carcinoma.
128
Q: What is an ectopic pregnancy?
A: Implantation of a fertilized ovum at a site other than the uterine wall most commonly in the fallopian tube.
129
Q: What is the classic presentation of ectopic pregnancy?
A: Lower quadrant abdominal pain a few weeks after a missed period.
130
Q: What are the major complications of ectopic pregnancy?
A: Hematosalpinx (bleeding into the fallopian tube) and tubal rupture.
131
Q: What is a spontaneous abortion?
A: Miscarriage of a fetus before 20 weeks gestation usually during the first trimester.
132
Q: What are common causes of spontaneous abortion?
A: Chromosomal anomalies (e.g. trisomy 16)
133
Q: What are the teratogenic effects of alcohol?
A: Mental retardation facial abnormalities
134
Q: How does cigarette smoke affect pregnancy?
A: Causes intrauterine growth retardation.
135
Q: What is placenta previa?
A: Implantation of the placenta in the lower uterine segment overlying the cervical os
136
Q: What is placental abruption?
A: Premature separation of the placenta from the uterine wall a common cause of stillbirth.
137
Q: What is placenta accreta?
A: Improper implantation of the placenta into the myometrium causing postpartum bleeding and difficulty delivering the placenta.
138
Q: What is preeclampsia?
A:
Pregnancy-induced hypertension
proteinuria
oedema
139
Q: What is eclampsia?
A: Preeclampsia with seizures.
140
Q: What is HELLP syndrome?
A: Preeclampsia with hemolysis elevated liver enzymes
141
Q: What are risk factors for sudden infant death syndrome (SIDS)?
A:
Sleeping on the stomach
cigarette
smoke exposure
142
Q: What is a hydatidiform mole?
A: Abnormal conception characterized by swollen villi and trophoblast proliferation.
143
Q: How is a complete mole different from a partial mole?
A: A complete mole has no fetal tissue all villi are hydropic
144
Q: What is the classic presentation of a hydatidiform mole?
A: Passage of grape-like masses through the vaginal canal and a uterus larger than expected for gestational age.
145
Q: How is a hydatidiform mole diagnosed?
A: Ultrasound showing a snowstorm appearance and absence of fetal heart sounds.
146
Q: What is the treatment for a hydatidiform mole?
A: Dilatation and curettage followed by β-hCG monitoring to detect choriocarcinoma.
147
Q: How do choriocarcinomas from gestational pathways respond to treatment?
A: They respond well to chemotherapy unlike those arising from germ cell pathways.
148
Q: What does Gestational Trophoblastic Disease (GTD) encompass?
A: A spectrum of tumors and tumor-like conditions characterized by the proliferation of placental tissue, either villous or trophoblastic.
149
Q: How does the WHO classify Gestational Trophoblastic Disease?
A: Into molar lesions (partial, complete, and invasive hydatidiform moles) and nonmolar lesions (choriocarcinoma and other trophoblast-derived malignancies).
150
Q: What hormone is elevated in all forms of Gestational Trophoblastic Disease?
A: Human chorionic gonadotropin (hCG).
151
Q: What characterizes a hydatidiform mole?
A: Cystic swelling of chorionic villi with variable trophoblastic proliferation.
152
Q: How does a complete mole differ genetically from a partial mole?
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: What is the histological difference between complete and partial moles?
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: What is an invasive mole?
A: A mole that invades or perforates the uterine wall, often associated with persistently elevated hCG levels.
155
Q: What are the complications of an invasive mole?
A: It can invade parametrial tissues and blood vessels, embolize to distant sites (lungs, brain), and may cause uterine rupture requiring hysterectomy.
156
Q: What is choriocarcinoma?
A: A malignant neoplasm of trophoblastic cells, often following hydatidiform moles, abortions, normal pregnancies, or ectopic pregnancies.
157
Q: How does choriocarcinoma appear grossly and histologically?
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: What are common clinical features of choriocarcinoma?
A: Irregular vaginal bleeding with bloody, brown fluid and extremely elevated hCG levels.
159
Q: How does choriocarcinoma typically spread?
A: It has a high propensity for hematogenous spread, commonly metastasizing to the lungs and bones.
160
Q: What conditions commonly precede choriocarcinoma?
A: 50% arise from complete moles, 25% from abortions, 22% from normal pregnancies, and others from ectopic pregnancies.
161
Q: How does choriocarcinoma respond to treatment?
A: It responds well to chemotherapy despite its invasive and metastatic potential.
