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Flashcards in Pathology - Nichols Deck (62)
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1
Q

Mucosa

A

lining (membrane) of body passages and cavities that communicate directly or indirectly with the exterior (commonly containing mucin-secreting glands)

2
Q

Serosa

A

outermost layer (covering) of an organ in a serosal cavity (peritoneal, pleura or pericardial) consisting of fibroelastic tissue covering by mesothelium continuous with the lining of the cavity

3
Q

Basement Membrane

A

acellular fibrous (collagenous) membrane separating the organized cellular elements of a tissue from the interstitium (space b/w organized cellular element of a tissue)

4
Q

Epithelium

A

purely cellular avascular layer covering and lining all the external and internal surfaces of the body and associated glands

5
Q

Stroma

A

supportive connective tissue around the parenchyma

6
Q

Parenchyma

A

-functional tissue of an organ, which performs the function of the organ

7
Q

Menstrual Endometrium

A

-fragmented glands and stroma, and degenerating blood

8
Q

Why does menstruation occur?

A

to slough infection

9
Q

What role does estrogen play in menstruation?

A

lack of it allows it to occure

10
Q

What role does progesterone play in menstruation?

A

being insufficent

11
Q

What role do the arteries play?

A

vasoconstrict, vasospasm, cut off blood supply causing ischemic necrosis

12
Q

Proliferative Endometrium (early)

A

-straight glands lined with pseudostratified epithelium and stroma with spindle-shaped cells

13
Q

Early Secretory Endometrium

A

-prominent basal cytoplasmic vaculoes (begin 36-48 hrs post-ovulation and are evidence that it has occurred)

14
Q

Secretory Endometrium

A

-tortuous dilated glands containing secretions

15
Q

Granulasa cells produce?

A

growth factors

16
Q

FSH stimulates?

A

-themselves to convert androgens from thecal cells to estradiol by aromatase during the proliferative phase

17
Q

What happens to granulosa cells after ovulation?

A

-the turn into granulosa lutein cells that produce progesterone

18
Q

How would a granulosa cell tumor manifest clinically in a child?

A

percuosis puberty

19
Q

How would a granulosa cell tumor manifest clinically in an adult?

A

abnormal uterine bleeding

-hirscitism

20
Q

Would a granulosa cell tumor manifest differently after menopause?

A

new bleeding

21
Q

What happens to the corpus luteum if fertilization of the ovum occurs?

A
  • gets big

- keeps producing hormones, progesterone is key

22
Q

What happens to corpus luteum if NO fertilization of the egg occurs?

A

it involutes

23
Q

Ovary Serosa

A

-single cell layer of modified peritoneal mesothelial cells, overlying stroma of spindle-shaped cells

24
Q

of ovarian tumors from serosal surface?

A
  • 70%

- 90% of malignant ones

25
Q

Histology of Fallopian Tube

A
  • papillary epithelium and muscular wall

- lined by ciliated epithelium

26
Q

Histology of Uterus

A
  • endometrium

- myometrium composed of smooth muscle

27
Q

Uterine Cervix

A

-transition from stratified squamous epithelium (exocervix) to columnar epithelium of cells with abundant cytoplasmic mucin (endocervix)

28
Q

Metaplastic squamous cells

A
  • in cervical transformation zone
  • prone to infection with HPV, which can progress to squamous cell carcinoma
  • prevented by Pap smear to detect dysplasia before it becomes carcinoma
29
Q

Breast Duct lining?

A

-two-cell layer of inner epithelial and outer myoepithelial cells, surrounded by basement membrane

30
Q

Breast Duct?

A
  • epithelial cells
  • myoepithelial cells
  • stromal cells
  • wavy collagen
  • blood vessel
31
Q

90% or breast cancers are?

A
  • ductal
  • in situ before they are invasive, and in situ carcinoma can look very much like hyperplasia, but hyperplasia will leave the layer of myoepithelia cells in place
32
Q

What do prolonged high levels of progesterone do?

A
  • produced by corpus luteum
  • transform spindle-shaped stromal cells of proliferative endometrial stroma into enlarged rounded cells with abundant smooth pink cytoplasm in a process called decidualization
33
Q

Decidualized Endometrium

A
  • large, rounded stromal cells

- abundant smooth eosinophilic cytoplasm

34
Q

Diseases of Vulva?

A

-inflammation, non-noeplastic epithelial disorders, dysplasia, tumors

35
Q

Diseases of Vagina?

A

-inflammation, dysplasia, tumors

36
Q

Diseases of Cervix?

A

-inflammation, dysplasia, tumors

37
Q

Diseases fo Corpus?

A

-menstrual cycle, inflammation, adenomyosis, abnormal bleeding, endometrial hyperplasia, tumors

38
Q

Diseases of Tubes?

A

-inflammation & ectopic pregnancy

39
Q

Diseases of Ovary

A

-cysts, tumors

40
Q

HSV

A

STD, commonly affects vulva

  • sexually transmitted (HSV I or II)
  • common in young age
  • painful papules progressing to vesicles & ulcers on vulva, vagina, cervix
  • nuclear inclusions, multi-nucleation
  • transmitted during neonate delivery
41
Q

Molluscum contagiosum

A

STD, vulva

42
Q

HPV

A

STD, gential wart, intraepithelial dysplasia, invasive carcinoma

43
Q

Clamydia Trachomatis

A

STD, cervicitis, endometritis, salpingo-oophoritis

44
Q

Neisseria gonorrhoeae

A

STD, Skene gland adenitis, cervicitis, endometritis, salpingitis

45
Q

Candidia

A

endogenous, vulvovaginitis

  • about 10% of women
  • predisposition: DM, pregnancy, oral contraceptives
  • white mucosal surface w/curdy white vaginal discharge, discomfort, itching
46
Q

Trichomonas

A

STD, cervivovaginitis

  • caused by flagellated protozoa
  • sexually transmitted (must treat partner)
  • 15% of women
  • heavy, foamy, gray-green vaginal discharge, mucosal irritation & itching
  • “strawberry” cervix
  • feed on squamous cells
47
Q

Pelvic Inflammatory Disease (PID)

A
  • caused by Gonococcus, Chlamydia, Mycoplasm, enteric bacteria (in postpartum)-streptococci, staphlococci
  • presents with vaginal discharge, pelvic pain, fever, adnexal tenderness
  • vulva, vagina, cervix, endometrium, & adnexa re involved
48
Q

Pathology of Gonorrheal PID

A
  • spread: ascending from vestibular glands to vagina-cervix-corpus & adnexa
  • acute suppurative salpingitis
  • salpingo-oophoritis
  • tubo-ovarian abscess
  • pyosalpinx (resolved: hydrosalpinx)
49
Q

Complications of Gonorrheal PID

A
  • infertility (from tube closure)
  • sepsis (endocarditis, bacteria in blood)
  • peritonitis
  • suppurative arthritis
50
Q

Ectopic Pregnancy

A
  • abnormal implantation site of the fetus
  • most common: fallopian tubes
  • sudden abdominal pain, acute abdomen, shock-like presentation about six to twelve weeks following a previous menstrual period
  • early diagnosis is critical
51
Q

Endometrial Histology: Proliferative Phase

A
  • estrogen effect
  • straight glands with pseudo-stratified epithelium
  • negative for mucin production
  • stroma is composed of spindle cells with scant cytoplasm, high mitotic rate
52
Q

Endometrial Histology: Secretory Phase

A
  • progesterone effect
  • postovulation: basal secretory vacuoles decreasing mitotic activity, simple epithelial layer
  • late phase: tortuous, dilated glands, prominent secretory activity, prominent stromal spiral arteries, decidulization
53
Q

Endometrial Histology: Menstrual Phase

A
  • progressively decreasing estrogen and progesterone levels
  • extravasation of red blood cells into the stroma
  • leukocytic infiltration of stroma
  • fibrin thrombi
  • disintegrating glands & stroma
54
Q

Postmenopausal (atrophic) Endometrium

A

-inactive, simple or cystic glands
-no evidence of proliferation or secretion
-dense, inactive stroma
-can be reversed by exogenous hormones/or tumor producing hormones
“swiss cheese”

55
Q

Endometrial Hyperplasia Etiology

A

-prolonged, abnormally high estrogenic stimulation without progesterone effect

56
Q

Endometrial Hyperplasia Conditions

A
  • Stein-Leventhal syndrome
  • Perimenopause
  • Estrogen producing tumors
  • Obestiy
57
Q

Endometrial Hyperplasia Foms

A
  • simple with/without atypia

- complex with/without atypia

58
Q

Molecular Pathology of Hyperplasia & Carcinoma

A
  • inactivation of PTEN tumor suppressor gene through deletion and/or inactivation
  • normally unopposed estrogen increases PTEN production
  • PTEN inactivation increases the gland sensitivity to estrogen
59
Q

Simple Endometrial Hyperplasia

A

-glandular crowing, irregularly shaped glands with stroma

60
Q

Complex Endometrial Hyperplasia

A

-complex glandular architecture with stroma

61
Q

Complex Endometrial Atypical Hyperplasia

A
  • glands are crowded with almost total exclusions of stroma b/w them
  • cytological atypia is present
62
Q

Simple Endometrial Atypical Hyperplasia

A

-nuclei are rounded with prominent nucleoli