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Pathology Term 5 > Week 5 - FGS > Flashcards

Week 5 - FGS Flashcards

STIs, Cervical Cancer, PAP Test, Uterine Disorders

1
Q

What is post-coital bleeding suggestive of?

A

cervical cancer

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2
Q

What is the most common cause of post-menopausal bleeding?

A

endometrial cancer

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3
Q

What is the commonest cause of pre-pubertal vaginal bleeding?

A

trauma
also:
-foreign body
-rare malignancy (sarcoma botryoides)

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4
Q

What is the commonest cause of vaginal bleeding in pregnancy?

A
  • placenta praevia
  • miscarriage
  • ectopic pregnancy
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5
Q

What is the commonest cause of abnormal menstruation?

A

DUB - dysfunctional uterine bleeding

  • psychological, hormonal, hemostasis disorders
  • local –> fibroids, polyps, endometriosis
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6
Q

What is the cause of white cheesy discharge?

A

candida

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7
Q

What is the cause of clear/watery discharge?

A
  • trichomonas
  • gardnarella
  • chlamydia
  • eczema
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8
Q

What is the cause of pus/purulent discharge?

A

gonococcal, bacteria

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9
Q

What is the cause of bloody discharge?

A
  • infections
  • trauma
  • malignancy
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10
Q

What are the 2 embryonic ducts and what do they give rise to?

A

Mullerian duct

  • fallopian tubes
  • uterus
  • cervix
  • vagina

Mesonephric duct
-ovaries

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11
Q

What is the site of cervical cancer?

A

transformation zone

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12
Q

What happens to the cervix during puberty?

A
  • endocervix comes out (pre-pubertay –> endocervix is inside)
  • columnar cells are exposed (v. sensitive cells)
  • sexual activity can increase risk of infection
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13
Q

What is the transformation zone?

A
  • post-puberty, the exposed columnar cells of the endocervix undergo squamous metaplasia
  • site of cervical cancer
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14
Q

What type of epithelium is endocervix vs. ectocervix?

A 
endocervix = columnar
ectocervix = stratified squamous
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15
Q

What is sarcoma botryoides?

A

high grade connective tissue sarcoma in young children (1-5yrs)

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16
Q

What is bartholin cyst?

A

-reasonably common cysts that occur due to obstruction and infection of vaginal glands

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17
Q

What is vaginal adenosis?

A

-chronic inflammation of vagina leading to increased mucous glands

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18
Q

How does vulvo-vaginitis present?

A

vaginal discharge

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19
Q

What are causes of vulvo-vaginitis?

A

Contact dermatitis
-urine, soaps, antiseptics, deodorants, creams, foreign body, etc –> oozing + crusting papules (children common)

Infections
-chlamydia, herpes, candida, trichomonas, syphillis, HPV –> common in sexually reproductive ppl

Inflammations + Atrophy
-lichen sclerosis –> atrophic, hyperplastic

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20
Q

What are the investigations for STIs?

A
  • tested for multiple STI organisms
  • endocervical + high vaginal swab (males urethral swab)
  • first pass urine
  • nucleic acid amplification test (NAAT)
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21
Q

What is the standard test for STIs?

A

NAAT

  • nucleic acid amplification test
  • standard molecular genetic technique (PCR, RT-PCR, etc)
  • detects pathogen earlier than antibody tests –> because Abs take time to develop (window period)
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22
Q

What is contained in the transport media for STI swabs?

A

sucrose phosphate

-UTM-RT (universal transport media)

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23
Q

What is cervicitis secondary to?

A

common - secondary to vaginal infections

  • STIs –> gardnerella, chlamydia, trichomonas, candida, etc
  • *plenty of inflammatory cells on PAP smear
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24
Q

What does chronic cervical inflammation lead to?

A 
endocervical polyps (benign)
-plenty of inflammatory cells in PAP smear
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25
Q

What % of chlamydia in females is asymptomatic?

A

80%

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26
Q

What long term complications can arise from chlamydiasis in females?

A

PID, infertility, ectopic pregnancy, etc

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27
Q

Why is mycoplasma genitalium resistant to penicillin and what does this lead to?

A
  • organisms have NO cell wall

* *leads to recurrent + chronic STIs

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28
Q

True or False?

you can use antibiotics to treat trichomonas vaginalis

A

False

-it is a flagellate protozoa (NOT a bacteria)

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29
Q

What would you suspect if there was clear watery to white/yellow BUBBLY discharge?

A

trichomonas vaginalis

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30
Q

What is strawberry cervix?

A
  • commonly seen in trichomonas vaginalis infections

- inflammation of cervix leads to multiple erythematous spots (looks like a strawberry)

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31
Q

Why is there increased risk of HIV and other STIs in trichomonas vaginalis?

A
  • it produces proteolytic enzymes, complement, neutrophils which breaks down mucosal defence
  • PID, preterm birth = longterm complications
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32
Q

What is the microscopy of trichomonas vaginalis?

A

-flagellate leaf-shaped cells (motile)

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33
Q

What populations are more affected by candida albicans?

A

candida vulvovaginitis (thrush)

  • pregnancy
  • diabetes
  • immunodeficiency
  • HIV
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34
Q

What are the features of candida vulvovaginitis (thrush)?

A
  • itchy, sore, burning, bright red rash

- thick, white cheesy discharge

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35
Q

How is candida vulvovaginitis diagnosed?

A

vaginal swab/PAP smear

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36
Q

What is characteristic microscopy of candida vulvovaginitis?

A

branching hyphae + budding yeast forms

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37
Q

Where would you see cowdry A inclusions on microscopy?

A

genital herpes

-large intranuclear inclusions (cowdry A) + multinucleated giant cells

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38
Q

What is the common clinical presentation of genital herpes?

A

asymptomatic in majority

*clusters of multiple, painful vesicles –> ulcers

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39
Q

What are Tzanck smears?

A

-simple smears of genital herpes lesions for testing (do NOT distinguish between VZV + HSV infections) –> NAAT for Dx confirmation

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40
Q

What is condyloma accuminatum?

A
  • soft, moist, papillomatous/warty lesions

- STI - HPV serotypes 6 + 11 (low malig. risk)

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41
Q

What are the microscopic features of HPV?

A
  • koilocytosis (perinuclear halo)
  • hyperkaratosis
  • parakeratosis
  • papillomatosis
  • dyskeratosis + dysplasia
  • intact basement membrane (benign)
42
Q

Which HPV serotype is responsible for vulval carcinoma?

A

HPV 16

43
Q

What is paget’s disease of vulva?

A
  • same as breast*

- eczematous lesion due to malignant cells spreading to skin

44
Q

Compare lichen sclerosus et. atrophicus and lichen simplex chronicus

A

Lichen sclerosus et. atrophicus

  • immune, T cell mediated
  • atrophy/thinning of epidermis

Lichen simplex chronicus

  • AKA squamous hyperplasia - chronic irritation
  • excess proliferation of skin (opposite)

*BOTH present as whitish scar-like patches

45
Q

What is the pathogenesis of pelvic inflammatory disease (PID)?

A
  • chronic complication of many STDs (esp. chlamydia/mycoplasma)
  • organism enters uterus and spreads through fallopian tube to peritoneal cavity –> chronic inflammation –> spreads to pelvic organs with chronic inflammation –> pain, fever, mass, fallopian tube obstruction (INFERTILITY) + interorganal adhesions (due to chronic inflamm. and scarring –> pelvic organs become one inflammatory mass)
46
Q

What is the first cancer to get a vaccine?

A

cervical ca.

47
Q

What type of cancer is cervical cancer?

A

squamous cell carcinoma

-STD due to HPV (16 + 18)

48
Q

What is the etiology of cervical cancer?

A
  1. HPV (initiator) - DNA virus
    - multiple partners - STI; mucosal contact
    - high risk (16 + 18) - bind to cell DNA
  2. estrogens (promoter)
    - early menarche, late menopause, lack of pregnancy, HRT, obesity, hyperestrogenemia (endometrial polyps, hyperplasia, etc)
  3. other factors
    - FHx, smoking/other carcinogens
49
Q

What is CIN?

A

cervical intraepithelial neoplasia –> prolonged pre-cancer dysplsia (10yrs)

  • dysplastic cells can be seen in PAP smear 2yrs prior to cancer
  • NOT all CIN progress to cancer
50
Q

What is 5yr survival of cervical cancer?

A

stage 1 –> 80%
stage 4 –> 10%

*early detection saves lives!

51
Q

How many genes does HPV have and which ones are the ones that lead to cancer?

A

8 genes in total (categorised as late (L) or early (E))

  • E6 - binds p53
  • E7 - binds Rb
  • -> tumour suppressor genes
52
Q

What cancers can HPV cause (other than cervical)?

A

-oropharynx, vulva, vaginal, penis, scrotum, rectum, perineum

53
Q

What does the Gardasil vaccine target against?

A
  • quadrivalent vaccine

- against HPV strains 6+11 (warts - benign) and strains 16+18 )cancer)

54
Q

What % of high grade vs low grade lesions lead to cervical cancer?

A

LSIL <5%

HSIL >70%

55
Q

What is the pathogenesis of HPV causing cervical cancer?

A
  • HPV strains 16+18 infect immature squamous cells of transformation zone
  • HPV proteins E6 (bind p53) and E7 (bind Rb) which are both tumour suppressor genes –> loss of growth suppression –> low grade dysplasia –> high grade dysplasia –> cancer
56
Q

What are cervical cancer investigations?

A
  1. colposcopy
    - metaplastic cells of transformation zone lack epithelial maturation –> therefore cells don’t have glycogen
  2. PAP smear
    - nuclear shape and irregularity
  3. biopsy
    - tissue infiltration/depth of cancer
57
Q

Outline colposcopy method + principles

A
  1. saline
    - observe BV pattern - mosaic = abnormal
  2. acetic acid
    - whitening of dysplastic + columnar area (acetowhite = dysplastic)
  3. iodine
    - dark brown = normal
    - unstained = dysplastic (same region that appeared white after adding acetic acid) –> due to lack of glycogen
58
Q

Outline PAP smear appearance of normal and CIN 1-3

A

normal –> small and pyknotic nuclei
LSIL (1) –> bigger nucleus, smooth border
HSIL (2/3) –> very large irregular nucleus with chromatin clumping

59
Q

What is the first step in microscopy of HPV infections causing dysplasia?

A

koilocytes –> epithelial cells loaded with HPV viral particles + perinuclear halo

60
Q

Outline cervical cancer staging/progression

A
  • CIN (stage 0) –> dysplasia with intact basement membrane
  • stage 1 –> limited to cervix
  • 1a-1 –> <3mm
  • 1a-2 –> 3-5mm
  • 1b –> >5mm (still confined to cervix)
  • stage 2 –> beyond cervix (upper 1/3 vagina)
  • stage 3 –> to pelvic wall/lower 1/3 vagina
  • stage 4a –> bladder/rectum involvement
  • stage 4b –> beyond pelvis (metastases)
61
Q

What are the microscopic features of cervical cancer?

A
  • squamous cell carcinoma*
  • pleomorphic squamous cells
  • keratin pearls
62
Q

True or False?

PAP smear can Dx cervical cancer

A

False

-only suspect

63
Q

What cells are seen on a normal PAP smear?

A
  • superficial, mature pink cells (estrogen effect)
  • intermediate, blue cells (progesterone effect)
  • basal cells/metaplastic cells
  • smooth small to pyknotic nuclei
  • few bacilli/neutrophils in background
  • increase neutrophils/basal cells –> inflammation
  • pleomorphic/hyperchromatic cells –> ?cancer
64
Q

What smears are involved in a PAP smear?

A
  1. high vaginal smear
    - from the fornix
    - to detect infections
  2. cervical smear
    - from transformation zone
    - to detect carcinoma
65
Q

When is optimal PAP smear timing and why?

A
  • soon after menstrual period when estrogen effect is maximal to ensure ample superficial pink mature cells (small nuclei) present to increase likelihood of detecting any early dysplasia (bigger nuclei)
  • later in the cycle, nuclei are normally bigger anyway –> progesterone effect - intermediate blue cells (therefore difficult to detect dysplasia)
66
Q

What are clue cells?

A

-vaginal squamous epithelial cells coated with bacteria causing bacterial vaginosis
N.B. - can be normal

67
Q

When do you refer a patient for a colposcopy?

A
  • suspicion of cervical ca. (post-coital bleeding) –> do NOT do a PAP smear (it is only a screening tool for normal patients)
  • abnormal PAP smear:
  • any glandular abnormality
  • HSIL definite/possible
  • LSIL definite/possible + >30 with no Hx. of negative cytology in previous 2-3yrs (colposcopy or repeat PAP smear in 6mths)
  • LSIL definite/possible + <30yrs –> repeat PAP at 12mths –> if still LSIL definite/possible –> colposcopy
68
Q

What do you do if there are fluctuating repeat smear results?

A

-refer for colposcopy women with >/= 2 low grade smear reports (at least 12mths apart) within a 3yr time frame

69
Q

What is the myometrium and endometrium composed of?

A

myometrium –> smooth muscle

endometrium –> glands in stroma

70
Q

What happens to endometrium glands in proliferative vs secretory phase?

A

proliferative phase –> glands are small and round with plenty of stroma

secretory phase –> larger glands with secretions and less stroma

71
Q

What are the disorders of the myometrium?

A

ONLY tumours

  • benign –> leiomyoma (fibroid) –> submucosal, intramural, subserosal
  • malignant –> leiomyosarcoma
72
Q

What is the cause of endometrial hyperplasia?

A

hormone-induced (estrogen)

-polypoid + diffuse

73
Q

What is endometriosis?

A

-spread of endometrium outside of the uterus

74
Q

What is adenomyosis?

A

-spread of endometrium into the uterus in the myocardium

75
Q

True or False?

Leiomyoma (fibroid uterus) are estrogen responsive

A

TRUE

76
Q

What gene mutation is commonly seen in fibroid uterus (leiomyoma)?

A

MED12 gene mutations in 70% cases

77
Q

What is microscopy of leiomyoma?

A

bundles of smooth muscle, well demarcated (benign)

78
Q

What are the clinical features of leiomyoma?

A
  • usually asymptomatic**

- DUB, abortion, malpresentation, post-partum haemorrhage, torsion/strangulation, etc

79
Q

What are the differences between leiomyoma and leiomyosarcoma?

A

Leiomyoma:

  • small, well-demarcated, slow growing
  • non-invasive, non-metastatic, well differentiated

Leiomyosarcoma:

  • large, poorly demarcated, rapidly growing with haemorrhage and necrosis
  • locally invasive, metastatic, poorly differentiated
80
Q

What is the common cause of acute endometritis?

A

STIs - neutrophilic

  • chlamydia = 1
  • gonorrhea = 2
81
Q

What is the common cause of chronic endometritis?

A
  • TB
  • PID
  • lymphocytic
82
Q

What are the complications of endometritis?

A

-DUB, infertility, ectopic pregnancy

83
Q

What are the 3 types of endometrial hyperplasia + polyp?

A
  1. simple
    - simple and cystic galnds
  2. complex
    - branching glands
  3. atypical/dysplastic
    - irregular glands –> incr. risk of malignancy
84
Q

How does endometrium spread beyond uterus in endometriosis?

A
  1. regurgitation –> via fallopian tube into pelvic cavity

2. vascular/lymphatic spread

85
Q

What are the causes of endometriosis?

A
  • hyperoestrogenemia

- increased PGE2

86
Q

What is chocolate cyst?

A

-result of endometriosis where endometrium spreads to ovary with resultant bleeding and increasing tumour

87
Q

What are the clinical features of endometriosis?

A
  • severe cyclic pain
  • pelvic inflammation –> fibrosis

*PID, infertility = complications

88
Q

What is Tx for endometriosis?

A

COX2 inhibitors

89
Q

What is adenomyosis caused by and what are the Sx?

A

-myometrial invasian by endometrium (internal endometriosis) –> hyperplasia
-etiology = hyperestrogenemia (+/- polyps)
Sx –> cyclic pain, DUB, uterine hypertrophy

90
Q

What type of cancer is endometrial cancer?

A

adenocarcinoma (estrogen related) –> pleomorphic cells forming closely packed irregular endometrial glands with scanty stroma

91
Q

Why is there early detection of endometrial cancer?

A

common cause of post-menopausal bleeding

92
Q

What are the 2 types of endometrial cancer?

A

type 1: - 80% (most common)
-assoc. with excess estrogens, obesity, DM, HTN

type 2: - 15%

  • thin, atrophic uterus, serous ca.
  • familial type
93
Q

When is dysfunctional uterine bleeding diagnosed?

A

-after excluding any other lesion (infection, inflamm., polyps, cancer)

94
Q

What is menorrhagia and metorrhagia?

A

menorrhagia = increased blood during cycle

metorrhagia = irregular bleeding between periods

95
Q

What is etiology of DUB?

A

ovulation failure** commonest **
-ends of reproductive period, early menarche, increased estrogen, endocrine disorders, nutrition, obesity, psychological, stress, etc

luteal phase failure; contraceptive-induced bleeding, etc

96
Q

What is microscopy of DUB?

A
  • proliferative, abnormal cystic glands
  • no secretory phase
  • scanty stroma –> breakdown of endometrial tissue –> bleeding
97
Q

What is Mx of DUB?

A
  • rule out any pathology

- then D+C (dilatation + curettage) –> cervix is dilated and a special instrument is used to scrape the uterine lining

98
Q

What is microscopy of LSIL?

A
  1. dysplastic (blue) cells in lower 1/2 sq. epithelium (dysplastic cells >1/3)
  2. mature (pink) cells in superficial area
  3. endocervical mucous gland in submucosa
  4. stroma shows inflammatory infiltrate
99
Q

What is microscopy of HDIL?

A
  1. full thickness dysplasia (blue cells) of epithelium
  2. no mature (pink cells)
  3. endocervical mucous gland in submucosa
  4. stroma shows inflammatory infiltrate
100
Q

What is microscopy of endometrial carcinoma type 1?

A
  1. pleomorphic cells forming irregular glands (adenoca.)

2. scanty stroma (closely packed cells)

Pathology Term 5 (6 decks)

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