Cervical Disease and STIs -> Flashcards

1
Q

What happens at the transformation zone of a normal cervix?

A

Physiologic replacement of columnar epithelium with squamous cell epithelium

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2
Q

The squamocolumnar junction in the cervix changes with _____.

A

age

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3
Q

Where is the squamocolumnar junction in younger women?

A

on the ectocervix

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4
Q

With age, how does the squamocolumnar junction move?

A

Toward the external os through process of squamous metaplasia

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5
Q

What is squamous metaplasia?

A

Columnar epithelium gradually converts to squamous epithelium

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6
Q

By age 50, where has the squamocolumnar junction receded to?

A

Endocervical canal (ectocervix is completely covered in squamous epithelium)

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7
Q

How may squamous metaplasia cause nabothian cysts?

A

Crypts/clefts of columnar epithelium are bridged over/may block glands –> mucous secretions may build up

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8
Q

How common are nabothian cysts?

A

very common

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9
Q

How would nabothian cysts appear on PE?

A

Yellow/translucent cysts on cervix that range from 2mm-3cm

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10
Q

Treatment for nabothian cysts?

A

None required

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11
Q

What are cervical polyps?

A

Small (<3 cm) pedunculated neoplasms of the cervix

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12
Q

Are cervical polyps common?

A

Yes

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13
Q

Are cervical polyps concerning for malignancy?

A

Most benign (<1% malignant)

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14
Q

S/sx of cervical polyps?

A

Typically asx, but if sx:
intermenstrual/post-coital bleeding MC, leukorrhea (white/yellow secretions), menorrhagia

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15
Q

How do cervical polyps appear on speculum exam?

A

Smooth, red, fingerlike projections from cervical canal

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16
Q

Can cervical polyps be felt bimanually?

A

Not usually (too soft)

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17
Q

Ddx of cervical polyps?

A

Endometrial cancer, endometrial polyp

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18
Q

Treatment for cervical polyps?

A

Polypectomy: office if small, OR if large w/ testing of cervical discharge if present

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19
Q

What is cervical stenosis?

A

Narrowing of cervical canal

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20
Q

Complications of cervical stenosis?

A

Hematometra (accumulation of blood in uterus), pain, dysmenorrhea, endometriosis

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21
Q

Causes of cervical stenosis?

A

Congenital, secondary to surgery/trauma, radiation, cervical cancer, menopause

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22
Q

How to dx cervical stenosis?

A

Clinical dx w/ inability to pass small cervical dilator

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23
Q

Treatment for cervical stenosis?

A

Dilation w/ small dilators followed by large dilators progressively

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24
Q

What is DES?

A

Synthetic, non-steroidal estrogen (used in 1940-71 for prevention of premature birth, miscarriage, or OB complications)

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25
Q

How can DES exposure affect the fetus?

A

Passes placenta –> affects reproductive tract differentiation –> structural abnormalities of cervix/uterus

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26
Q

What may be a cause of vaginal clear cell carcinoma in female offspring?

A

DES exposure

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27
Q

Women who were exposed to DES in the womb/develop cervical abnormalities are more at risk for what?

A

Infertility, pregnancy complications (miscarriage, ectopic, premature delivery), vaginal clear cell carcinoma, CIN (cervical neoplasia cell changes)

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28
Q

What are the screening guidelines for females affected by DES in utero?

A

Annual pelvic exam & pap, no stopping age for exams determined

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29
Q

What is CIN?

A

Cervical intraepithelial neoplasia

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30
Q

Screening method for CIN and cervical cancer?

A

Pap smear

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31
Q

What Bethesda system (cervical cytology classification) is ASC-US?

A

Atypical squamous cells of undetermined significance

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32
Q

What Bethesda system (cervical cytology classification) is ASC-H?

A

Atypical squamous cells - high grade lesion cannot be excluded

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33
Q

What Bethesda system (cervical cytology classification) is LSIL?

A

Low grade squamous intraepithelial lesion (consistent w/ CIN I)

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34
Q

What Bethesda system (cervical cytology classification) is HSIL?

A

High grade squamous intraepithelial lesion (consistent w/ CIN II/III)

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35
Q

First and last Bethesda System cervical cytology classifications?

A

First: normal
Last: invasive carcinoma

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36
Q

Normal histologic classification (biopsy results)?

A

No abnormal cells

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37
Q

CIN I histologic classification (biopsy results)?

A

Mild dysplasia (disordered growth of lower 1/3 epithelial lining)

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38
Q

CIN II histologic classification (biopsy results)?

A

Moderate dysplasia (disordered growth of lower 2/3 epithelial lining)

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39
Q

CIN III histologic classification (biopsy results)?

A

Severe dysplasia (disordered growth >2/3 or full thickness epithelial lining)

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40
Q

What is full thickness dysplasia?

A

Carcinoma in situ (CIS) confined to surface of cervix

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41
Q

When is dysplasia considered invasive cervical cancer?

A

When it spreads to local tissues

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42
Q

What will a pap report show (Bethesda system reporting process)?

A

Specimen type, specimen adequacy, interpretation/result

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43
Q

Specimen types for pap smear report?

A

Conventional or liquid based thin prep

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44
Q

Specimen adequacy for pap smear report?

A

Satisfactory or unsatisfactory for evaluation

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45
Q

Interpretations/results for pap smear report?

A

Negative for intraepithelial lesion/malignancy or epithelial cell abnormalities (squamous cell or glandular cells)

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46
Q

Squamous cell abnormalities that can be detected by pap?

A

ASC-U, ASC-H, LSIL (CIN I), HSIL (CIN II/III, moderate and severe dysplasia), SCC

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47
Q

Glandular cell abnormalities that can be detected by pap?

A

Atypical, endocervical adenocarcinoma in situ (CIS), adenocarcinoma

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48
Q

When is an annual pap recommended?

A

HIV pts (twice 1st year, then anually), hx of HSIL (CIN II/III), cancer (for 20yrs post-dx), DES exposure in utero, immunosuppressed

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49
Q

How common is cervical cancer?

A

3rd most common GYN cancer in the US

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50
Q

Prevalence of cervical cancer depends on what?

A

Socioeconomic factors

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51
Q

High grade lesions are typically diagnosed in women of what age?

A

25-35

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52
Q

Cervical cancer is more common after what age?

A

40, typically 8-13 yrs after high grade lesion dx

Avg age = 50

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53
Q

Causes of CIN/Cancer?

A

HPV (16&18) MC, 70-75% squamous cell carcinoma (HPV 16), 20-25% are different kinds of adenocarcinoma

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54
Q

Risk factors for CIN/Cervical cancer?

A

HPV***, smoking, multiple partners, early onset of sexual activity, high risk partner, STI hx, HIV/AIDS, immunosuppression, multiparity

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55
Q

Low risk types of HPV?

A

6, 11, 42, 43, 44

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56
Q

High risk types of HPV?

A

16, 18

57
Q

Most new HPV infections clear within what time?

A

6-12 mos

58
Q

S/sx of CIN?

A

Asx, usually found on abnormal pap

59
Q

S/sx of cervical cancer?

A

Abnormal bleeding MC, leukorrhea (may be blood stained, odorous, prurulent), post-coital bleeding
Advanced disease: pelvic pain (unilateral, radiating to hip)
Late disease: weakness, weight loss, anemia

60
Q

PE for CIN?

A

+/- obvious cervical lesion (if noticed must have bx)

61
Q

PE for cervical cancer?

A

Enlarged/irregular/firm cervix, deep necrotic ulcerations as advances

62
Q

90% of cervical cancer lesions occur where?

A

within 1 cm of the squamocolumnar junction (SCJ)

63
Q

How to diagnose CIN?

A

Pap & HPV testing, confirmed by colposcopy or endocervical sampling

64
Q

How to diagnose cervical cancer?

A

Bx aided by colposcopy

65
Q

Characteristics of colposcopy procedure?

A

Acetic acid brings out areas of dysplasia, magnified view of cervix, visualizes extent/location of CIN, directed biopsy

66
Q

Cervical cancer stage IB?

A

Cancer tissue within cervix

67
Q

Cervical cancer stage IIB?

A

Cancer spreads outside of cervix

68
Q

Treatment of CIN?

A

Destroy abnormal cells (prevent progression): electrocautery, cryotherapy, laser therapy, conization, LLEP or large-loop excision of transitional zone

69
Q

Treatment of cervical cancer?

A

Depends on stage: possible surgery (radical hysterectomy w/ pelvic lymph node resection), radiation, chemo

70
Q

Prognosis of cervical cancer?

A

35% will be recurrent/persistent post-tx, 50% of deaths 1st year after tx –> 25% after 2nd year –> 15% in third year

***POST TX FOLLOW UP RECOMMENDED FREQUENTLY INITIALLY AFTER TX

71
Q

Most common causes of cervicitis?

A

Neisseria gonorrhea, Chlamydia trachomatis, Herpes simplex, Trichomoniasis, BV

72
Q

S/sx of cervicitis?

A

Often asx, MC vaginal discharge
*discharge appearance depends on organism

73
Q

Screening for cervicitis is more important in which patients?

A

High risk

74
Q

Complications of cervicitis?

A

PID, infertility, ectopic pregnancy, chronic pelvic pain mostly w/ gonorrhea/chlamydia infection

75
Q

Most cases of genital herpes are caused by which virus?

A

HSV-2 (HSV-1 less common)

76
Q

S/sx of herpes simplex?

A

Painful genital ulcers w/ prodromal sx (burning, parasthesia, numbeness), dysuria, +/- fever

77
Q

PE for herpes simplex?

A

Multiple, shallow, tender ulcers in grouped vesicles on an erythematous base, inguinal lymphadenopathy

78
Q

Are recurrent infections w/ herpes simplex as severe as the first?

A

No, often less severe

79
Q

How to diagnose herpes simplex?

A

PCR (test of choice), viral cultures

80
Q

Treatment for herpes siimplex?

A

PO antivirals (Acyclovir, Valacyclovir, Famciclovir), IV for severe dz

81
Q

Pregnant women with herpes simplex may require what?

A

Suppressive therapy at 36 wks

82
Q

What causes chancroid?

A

Haemophilus ducreyi (highly infectious gram neg rod bacteria)

83
Q

Incubation period of Haemophilus ducreyi (chancroid)?

A

4-10 days

84
Q

Is chancroid a reportable disease?

A

Yes

85
Q

How is chancroid transmitted?

A

sexually, but cutaneous transmission reported

86
Q

Development of chancroid?

A

Begins as erythematous papule –> pustule –> ulcer (~1-2cm)

87
Q

S/sx of chancroid?

A

ulcer w/ erythematous base & gray/yellow purulent exudate/bleeds when scraped, painful, heavy/foul smelling discharge that is contagious, painful inguinal lymphadenopathy more common in men

88
Q

How to diagnose chancroid?

A

Special media culture (has limitations) –> if unavailable: clinical dx (adenopathy w/ negative tests for other ulcer lesions like syphilis/HSV)

89
Q

Treatment for probable or confirmed cases of chancroid?

A

Antimicrobial: Azithromycin PO x1, Ceftriaxone IM x1, Cipro BID x3d, or Erythromycin TID x7d

*Tx all partners w/in 10 days of sx onset

90
Q

Screening for those with chancroid?

A

HIV screen

91
Q

Re-examine cases of chancroid how many days?

A

3-7 days

92
Q

What causes lymphogranuloma venereum (LGV)?

A

Aggressive serotype of chlamydia trachomatis

93
Q

Where is LGV most common?

A

Tropical/subtropical nations, Southeastern US

94
Q

Is LGV most common in men or women?

A

Men > women 6:1

95
Q

What is LGV strongly associated with?

A

HIV infection

96
Q

Is LGV a reportable disease?

A

Yes

97
Q

S/sx of LGV?

A

MC: tender, unilateral inguinal/femoral lymphadenopathy
Primary infection –> mild, painless blister that resolves @ site of inoculation
Secondary stage (2-6wks) –> tender, unilateral inguinal lymphadenopathy & hard tender masses (buboes) +/- fould smelling discharge

98
Q

How to diagnose LGV?

A

Clinical suspicion/exclusion of other etiologies, culture of lesions/lymph nodes (direct immunofluorescence or nucleic acid detection)

99
Q

Tx for LGV?

A

Abx: Doxy BID x21d or Erythromycin QID x21 days
Surgical: buboes may need aspiration to prevent inguinal/femoral ulcers

100
Q

Test those w/ LGV for what?

A

Other STIs

101
Q

When should sexual partners of those w/ LGV be examined/tested/treated?

A

w/in 60 days

102
Q

What is PID comprised of?

A

Spectrum inflammatory disorders of the upper female tract: any combo of endometriosis, salpingitis, tubo-ovarian abscess, pelvic peritonitis

103
Q

Causes of PID?

A

N. gonorrhoea and C. trachomatis MC, other vaginal flors microorganisms
In the setting of IUD: Actinomyces israelii

104
Q

Prevention measures for PID?

A

Screening/tx of pts and sexual partners for chlamydia/gonorrhea reduces risk, early dx/tx to prevent complications

105
Q

S/Sx of PID?

A

Subtle/mild (delays dx), lower abdominal/pelvic/back pain/pressure, purulent vaginal discharge, abnormal bleeding, dyspareunia, nausea, +/- vomiting, fever, general malaise

106
Q

PE for PID?

A

Abdominal tenderness in lower quadrants, distended abdomen, hypoactive/absent bowel sounds
Pelvic exam: +/- purulent d/c, chandelier sign, tenderness on palpation of ovaries/uterus

107
Q

What is chandelier sign?

A

Extreme cervical motion tenderness

108
Q

DDx for PID?

A

Anything causing R/L lower quadrant pain

109
Q

Complications of PID?

A

Peritonitis, prolonged ileus, septic pelvic thrombophlebitis, abscess, infertility/scarring, intestinal adhesions, obstructions
RARE: bacteremia/shock

110
Q

Labs for PID?

A

Normal or abnormal (supportive evidence only): leukocytosis w/ L shift, elevated ESR/CRP, endocervical swabs +/- gonorrhea/chlamydia, endometrial biopsy (endometriosis), HCG

111
Q

Imaging for PID?

A

Transvaginal US/MRI: thickened fluid filled tubes +/- free pelvic fluid/tubo -ovarian complex, Doppler studies, Laparoscopy: adjunct only when dx in question

*imaging may be normal in early dz

112
Q

How to diagnose PID?

A

Can be clinical/empiric tx started if:
-Pt has lower abdominal/pelvic pain
-No cause of illness other than PID
-1 or more present: cervical motion tenderness, uterine tenderness, adnexal tenderness

113
Q

Empiric tx for PID?

A

Broad spectrum Abx covering most likely pathogens ASAP) gonorrhea & chlamydia –> neg screenings don’t r/o upper infection)

114
Q

Admit patients w/ PID if…?

A

Severely ill, pregnant, surgical emergency not r/o, no response to outpt tx, non-compliance/unable to follow through w/ tx, tubo-ovarian abscess

115
Q

Abx for PID (outpt)?

A

Ceftriaxone 500mg or 1G (weight dependent) IM + x1 & Doxy 100mg PO BID x14d + Metro 500mg PO BID x 14d
If no response in 72 hrs: re-eval/admit

116
Q

Inpatient tx for PID?

A

IV Abx

117
Q

What are tubo-ovarian abscesses (TOA) preceded by?

A

PID, or one acute episode of salpingitis (but often seen w/ recurrent infection)

118
Q

What occurs in TOA?

A

Fallopian tube necrosis/epithelial damage by bacterial pathogens –> anaerobic invasion/growth (polymicrobial)

119
Q

Is TOA primarily unilateral or bilateral?

A

Unilateral

120
Q

When is TOA most common?

A

Young age (females) but can occur at any age

121
Q

TOA in a postmenopausal female is highly indicative of what?

A

Concurrent malignancy

122
Q

S/Sx of TOA?

A

Ranges from asx -> shock
Usually pelvic/abdominal pain, fever, N/V over a week

123
Q

PE for TOA?

A

Abd tenderness/guarding, pelvic exam limited d/t tenderness - adnexal mass may be present, if rupture: acute surgical abdomen/may develop septic shock sx

124
Q

Labs for TOA?

A

CBC varies (leukopenia -> leukocytosis), UA +/-abnormal, elevated ESR or CRP
* all suggestive of TOA if adnexal mass

125
Q

Imaging for TOA?

A

Pelvic US modality of choice: usually complex adnexal mass obscuring normal structures
CT: recommended if r/o appendicitis/diverticulitis

126
Q

Tx for unruptured TOA?

A

Similar to inpt tx for PID w/ longer duration depending on abscess size/response to tx
-24 hr inpatient obs
-If no improvement: surgical management (extent of resection depends on extent of dz) - laparoscopy, drainage, oophrectomy, hysterectomy

127
Q

Tx for ruptures TOA?

A

Life threatening emergency!!!
Immediate surgery w/ abx: total hysterectomy & bilateral bilat salpingo-oophrectomy (TAH-BSO)
-Post-op SICU obs of VS and UO

128
Q

Complications of unruptured TOA?

A

May rupture, sepsis, re-infection, bowel obstruction, infertility, ectopic preg d/t adhesions

129
Q

Complications of ruptured TOA?

A

Septic shock, intra-abd abscess, septic emboli w/ renal, lung, brain abscess

130
Q

Prognosis of unruptured TOA?

A

Excellent (yet inc. risk of infertility/ectopic preg)

131
Q

Prognosis of ruptured TOA?

A

Mortality <2% w/ medical/surgical therapy

132
Q

What bacteria causes toxic shock syndrome?

A

S. aureus

133
Q

Who does TSS commonly affect?

A

Menstrual females (use of tampons, diaphragm, post-delivery)

134
Q

Risk factors for TSS?

A

High absorbent tampons, continuous tampon use for more days than cycle, single tampon in place for long period of time

135
Q

S/Sx of TSS?

A

Rapid: fever, hypotension, tachycardia, skin manifestations, chills, malaise, HA, myalgia, fatigue, N/V/D, abd pain, orthostasis/syncope

136
Q

PE for TSS?

A

If tampon present -> remove
+/-mucosal/skin involvement

137
Q

How to diagnose TSS?

A

Culture for S. aureus (not required for dx though), clinical s/sx + organ dysfunction on lab w/u in abence of other cause

138
Q

Labs for TSS may reveal what?

A

Shock/organ failure

139
Q

Tx for TSS?

A

-Admit to ICU
-Supportive tx mainstay: fluids, vasopressors, packed RBCs, coagulation factors, mechanical vent, hemodialysis
-Abx: Vanco IV + Clindamycin IV + Cefepime IV and then tailor to culture results