OB/GYN IV Flashcards

1
Q

When is a pelvic exam indicated in an adolescent patient

A

Abnormal symptoms

sexually active

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2
Q

What are the common vulvovaginal lesions

A
  1. Lichen sclerosus et atrophicus
  2. Trauma
  3. Labial agglutinations
  4. Prolapsed Urethra
  5. Vaginal discharge
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3
Q

What is the treatment of lichen sclerosus

A

improved personal hygeine is the first step

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4
Q

What is labial agglutination

A

result from vulvat inflammation or skin disease, and the hypoestrogentic state. It is the adhesion of the labia minora in the midline

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5
Q

What is the most often malignant vaginal tumor

A

Sarcoma botryoides

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6
Q

How will sarcoma botryoides present

A

arises from mesenchymal tissue of the cervix or vagina, usually on the anterior wall of the upper vagina. Grows rapidly, fills the vagina, and then protrudes through the introitus

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7
Q

What are the 2 groups of ovarian tumors

A
Non germ cell (40%)
Germ cell (60%)
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8
Q

What are the non germ cell origins tumors

A

lipoid cell tumors (estrogen producing)

Granulosa-theca cell tumor (Estrogen producing)

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9
Q

What are the germ cell origin tumors

A
  1. benign cystic teratomas
  2. benign cysts
  3. Arrhenoblastomas (androgen producing)
  4. Dysgerminomas and gonadoblastomas
  5. Endodermal sinus tumors
  6. Embyonal carcinomas (hCG secreting tumros)
  7. Immature teratomas
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10
Q

What is MRKH syndrome

A

Vaginal and uterine agenesis. Represents a failure of the caudal mullerian duct to fuse with the urogential sinus

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11
Q

What are some causes of amibiguous genitalia

A
  1. Congenital Adrenal Hyperplasia (CAH)
  2. Adrenal Tumors
  3. Maternal ingestion of androgenic substances
  4. Childhood ingestion of androgens
  5. Androgen insensitivity syndrome (AIS)
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12
Q

What is the average age of onset of puberty

A

9 years

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13
Q

What is responsible for initiation of puberty

A

Increased production of LH and FSH

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14
Q

When is the peak growth velocity

A

11 - 12 years, usually 1 year before menarche

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15
Q

When does thelarche begin

A

9-11

It is usually completed over a 3 year period

It is a sign of ovarian estrogen production

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16
Q

What is adrenarche

A

refers to the production of androgens from the adrenal gland

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17
Q

What is pubarache

A

the development of axillary and pubic hair that results from the adrenal and gonadal androgens.

Usually follows thelarche

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18
Q

What is the average age of onset of menses

A

12-13

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19
Q

What is precoious puberty

A

secondary sexual characteristics before 8 years of age in caucasion girls and 7 years in african americans

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20
Q

What is delayed puberty

A

characterized by the absence of breast development by age 13 or the absence of menses by age 16

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21
Q

what is swyner syndrome

A

(46, XY)

characterized by a female phenotype with amenorrhea and lack of secondary sex characteristics

Inherited as X linked recessive

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22
Q

At what age will menses cease to occur spontaneously

A

40-58

90% between 45 and 55

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23
Q

What is premature menopause

A

permanent cessation of menses ocurring before age 40

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24
Q

What is the hallmark of reproductive aging

A

elevation of FSH to greater than 10 IU/mL in the early follicular phase (between day and day 5 of the menstrual cycle)

When menses have been absent for 1 year, FSH levels are persistently greater than 30 IU/mL

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25
Q

Discuss the physiology of menopause

A

FSH receptors are absent on a cellular level which causes a decrease in estradiol levels. Estrone is also reduced, but to a lesser degree because of its ability to be converted in the periphery from androstenedione

Ovarian stromal cells still posses LH receptors and they will respond with the production of ovarian androgens

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26
Q

How does obesity effect levels of estrogen

A

Adipose tissue contains aromatase enzymes.

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27
Q

What is the function of the aromatase enzymes

A

convert androgens to estrone

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28
Q

What are the circulating levels of testosterone in the menopausal state.

A

Free and unbound circulating testosterone is increased because of a 40% reduction in the SHBG. SHBG production is stimulated by estrodiol.

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29
Q

What is the most common cause of premature menopause

A

women have undergone premature oocyte atresia and follicular depletion from 1 of 3 mechanisms:

  1. decreased initial germ cell number at birth
  2. Accelerated oocyte atresia after birth
  3. Postnatal germ cell destruction
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30
Q

What are the manifestation of estrogen excess

A
  1. AUB
    a. Anovulatory cycles
    b. Obesity
    c. tumors
    d. other causes not related to hormones
  2. Endometrial hyperplasia
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31
Q

What should be suspected in all perimenopausal women who present with abnormal bleeding

A

Endometrial cancer

10% of bleeding postmenopausal is related to endometrial cancer

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32
Q

What are the symptoms traditionally attributed to menopause

A
Hot flashes
Headaches
Sleep disturbances
Mood disturbances
Sexual function changes
Weight gain
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33
Q

What are the treatment options for menopause

A

Progestin supplementation for estrogen excess

Combination hormone contraception therapy for women who are normotensive nonsmokers without other risk factors

Hormone therapy in a subcontraceptive dose. Progestin is added to the dose in all women that still have their uterus

NSAIDs to reduce menstrual bleeding

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34
Q

What are the progestin supplementation options available for treatment of menopause

A

MPA (medroxyprogesterone acetate)
Norethindrone acetate
Oral micronized progesterone
Progestin containing intrauterine system

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35
Q

What are the target organ responses to decreased estrogen

A
  1. urogenital atrophy: vagina, urethra, bladder and pelvic floor are estrogen responsive tissue
  2. Uterine changes
  3. Breast changes
  4. Skin changes
  5. Hair changes
  6. CNS changes
  7. Cardiovascular changes
  8. VMSs Vasomotor symptoms
  9. Altered menstrual function
  10. osteoporosis
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36
Q

What is the mechanism behind VMS

A

the result of inappropriate stimulation of the body’s heat releasing mechanisms by the thermoregulator centers in the hypothalamus.

Characterized by progressive vasodilation of the skin over the head, neck and chest

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37
Q

When estrogen is contraindicated, what treatment options are available for VMS

A
progestogen
clonidine
gabapentin
herbal remedies
SSRI's in low dose
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38
Q

What is the gold standard for monitoring bone loss

A

Dual energy x ray absorptiometry (DEXA) scan

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39
Q

What is the definition of osteoporosis

A

DEXA scan score T of -2.5 or less

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40
Q

What is the definition of osteopenia

A

DEXA scan score T of -1 to -2.5

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41
Q

What can be done to help prevent osteoporosis

A
adequate calcium intake
vitamin D
weight bearing exercise
reducing the risk of falling
decrease smoking and alcohol consumption
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42
Q

What amount of calcium is recommended daily after the age of 50

A

1500 mg of elemental calcium daily through diet or supplements

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43
Q

What amount of vitamin D is recomended daily for prevention of osteoporosis in postmenopausal women

A

600-800 daily. Up to 2000 IU/day is considered safe

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44
Q

What medications are available to limit bone loss

A
  1. Bisposphonates
  2. SERMs (selective estrogen receptor modulators)
  3. Calitonin
  4. HT and ET
  5. Teriparatide
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45
Q

What is teriparatide

A

daily injection for up to 18-24 months. It has an anabolic bone effect and decreases vertebral and nonvertebral fractures

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46
Q

What are the risks to HT (hormone therapy)

A

Endometrial cancer if using estrogen only in women with a uterus. Add progestin to women with a uterus

Abnormal bleeding

Increased risk of breast cancer with progestin and estrogen combination therapy

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47
Q

What are the absolute contraindications to HT

A
  1. undiagnosed abnormal genital bleeding
  2. known or suspected breast cancer or estrogen dependent neoplasia
  3. active or history of thrombosis
  4. history of stroke or MI in the previous year
  5. known or suspected pregnancy
  6. known hypersensitivity to HT/ET
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48
Q

What are the common scheduling of HT

A

Cyclic therapy: Continuous estrogen therapy is given with progestin added for 12-14 days each month.

Continuous combined therapy

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49
Q

What are the availble routes of administration for HT

A
Systemic:
transdermal patches
percutaneous gel or emulsion
vaginal ring
oral estrogen or estrogen + progestin

Local:
topical estrogen
progestin containing intrauterine device

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50
Q

What are the age risk appropriate screening for post menopausal women

A

lipid profile: every 5 years beginning at 45
fasting blood sugar: every 3 years at 45
TSH: every 5 years at 50
Mamography: every 1-2 years at 40 then every year at 50
cervical cytology: every 1-3 years hx dependent
Osteoporosis: at age 65
Colon cancer: start at 50 with yearly fecal occult blood, 5 years for flexible sigmoid or 10 years for colonoscopy

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51
Q

What will latex condoms protect against

A
Herpes simplex
Neisseria gonorrhoeae
chlamydia trachomatis
Ureaplasma urelyticium
mycoplasma hominis
Trichomonas vaginalis
Treponema pallidum
HIV

NOT HPV

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52
Q

Do natural or non latex condoms protect against most STD’s

A

no

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53
Q

What are the time constraints with using a female condom

A

can be inserted up to 8 hours in advance, but must be removed immediately after each act of intercourse

DO NOT USE WITH A MALE CONDOM

54
Q

Is there a benefit of using a spermicide in addition to condom alone

A

no change in effectiveness

55
Q

What are the types of barrier methods

A
condoms
spermicides
vaginal sponges
diaphragms
cervical caps
56
Q

What is problem with prolonged or repetitive use of spermicide

A

damgages the vaginal epithelium and increases the risk of an HIV infection

57
Q

What is the time constraint with using a diaphragm

A

must be left in place at least 6 hours after intercourse

58
Q

What is an advantage of a cervical cap

A

can be left in place up to 48 hours after intercourse

59
Q

What are the types of IUD

A

Paragard: Copper - good for 10 years

Mirena: Levonorgestrel 20 - good for 5 years

60
Q

What is the mechanism of action for paragard

A

copper itself acts as a spermicide

IUD causes a local, sterile inflammatory reaction in the uterus and the intrauterine environment becomes spermicidal

61
Q

What is the mechanism for mirena

A

exerts its contraceptive effect locally on the endometrium and the cervix. Progestin alters the endometrium, rendering it unfacvorable from implantation.

Thickening of the cervical mucosa makes the passage of sperm more difficult. Uterine and tubal motility are impaired

62
Q

When can the types of IUD be implanted

A

Paragard (copper) any time in menstrual cycle

Mirena (levonorgestrel) inserted with in the first 7 days of the menstrual cycle

63
Q

What is the mechanism of progestin only contraception

A
  1. diminishing and thickening cervical mucus, preventing sperm penetration
  2. Produces a thin, atrophic endometrium, precluding implantation
  3. Reduces the ciliary action of the fallopian tube, preventing sperm and egg transport
  4. Diminishing the function of the corpus luteum
  5. Occasional inhibition of ovulation by suppressing the midcycle peaks of LH and FSH
64
Q

What is a benefit for a post partum progestin only contraception

A

no alteration of milk production and nearly 100% effectiveness in breast feeding women

65
Q

What is the injectable progestin

A

Depo-provera: medroxyprogesterone

Deep IM injection every 12 weeks

Efficacy is less than 1 in 100

66
Q

What are the implantable progestin

A

Implanon: 3-keto-desogestrel

serum hormone remains adequate for 3 years

Higher frequency of oligo and amenorrhea

67
Q

What is the mechanism of combination oral contraceptive pills

A

Primary mechanism is inhibition of the LH surge

  1. Suppresses ovulation
  2. Thickening of the cervical mucus
  3. Alteration of tubal motility
  4. Alteration of endometrium to make it thin and inactive, thus hampering implantation
68
Q

What specific effects does estrogen have on clotting factors

A

increase in serum levels of several clotting factors, especially factor VII.

Antithrombin III levels fall with in 10 days of starting OCPs

These risks are still lower than the coagulative state of pregnancy

69
Q

Name the 3rd generation OCPs

A

gestodene

desogesterol

70
Q

Name the 2nd generation OCPs

A

norethindrone

Levonorgesterel

71
Q

What is the difference of clotting factor between the 2nd and 3rd generation OCPs

A

3rd generation has a greater risk

72
Q

What is the problem with using OCPs in women with inherited thrombophilias

A

Antithrombin III, or protein C or S defects have a 6 times greater risk

Factor V leiden has a 10 times greater risk

Prothrombin mutation has a 7 times greater risk

73
Q

How is hypertension affected with use of OCPs

A

Plasma renin activity, angiotensin levels, aldosterone section, and renal retention of sodium are all increased in OCP users

Normotensive levels return in almost all women who developed hypertension while taking OCPs when the contraception is stopped

74
Q

Smoking and OCPs….

A

synergistic effect in the CV system, do not do it

75
Q

How is the liver effected with OCP usage

A

greater than 5 years increases the risk of hepatocellular adenoma

76
Q

What effect does progestin have on breast tissue

A

antagonizes the stimulating effects of estrogen

There is no increase in risk even in patients with family history of breast cancer

77
Q

What effect does progestin have on the endometrium

A

protective effect and decreases risk of cancer by 50% up to 15 years after taking them

78
Q

What effect do OCPs have on the ovaries

A

suppress ovarian activity and inhibit ovulation; the interuption of a significant number of ovulatory cycles in oral contraceptive users may lead to a decreased incidence of ovarian cancer.

Users of OCPs are less likely to develop ovarian cancer up to 15 years after taking them

79
Q

How does OCP effect hirsutism and acne

A

decreasing production of androgens by the ovary and adrenal and increasing sex hormone binding globulin production by the liver

80
Q

What is the NuvaRing

A

contraceptive device consists of a 5.4 cm flexible ring made of ethylene vinyl acetate copolymer containing ethinyl estradiol and etonogesterel. The ring is inserted into the vagina and the hormone is absorbed systemically

The ring is worn for 3 weeks and 1 week off.

81
Q

What is ortho Evra

A

Transdermal patch. Once weekly contraceptive patch releases norelgestromin, the active metabolite of norgestimate, and ethinyl estradiol daily to systemic circulation.

3 weeks on and 1 week off

May be associated with greater risk of VTE than OCPs

82
Q

What are the options for emergency contraception

A

Morning after pill:

  1. Yuzpe method (combination of ethinyl estradiol 100 microgram and 1 mg norgestrel)
  2. Progestin only (more effective) 1.5 mg single dose; less effective 0.75 mg 2 doses over 12 hours
  3. Plan B (OTC for over 18)

Copper IUD

Mifepristone: Single oral dose of 600 mg has 100% efficacy

83
Q

What is the basis of natural family planning to prevent conception

A

must restrict sexual intercourse from the end of menses to 1-2 days after the in increase of basal body temperature of 0.4 to 1.0 degrees

84
Q

What are the markers used in natural family planning

A

Fertility awareness
Basal body temperature
Menstrual calendar
Cervical secretions

85
Q

Based on cervical secretions when is a woman most fertile

A

secretions are abundant, clear or white, slippery and stretchy

86
Q

What are the bacterial sexually transmitted diseases

A
Gonorrhea
chlamydia
chancroid
Granuloma inguinale
Bacterial vaginosis
Lymphogranuloma venereum
87
Q

Where does neisseria gonorrhoeae have a predilection for

A

columnar and transitional epithelium

Women:
cervicitis
urethritis
PID
acute pharyngitis

Men:
urethritis
prostatis
epididymitis

88
Q

What is the problem with gonorrhea effecting newborns at birth

A

blindness
infection of the joints
sepsis

89
Q

Are men or women typically more symptomatic with a gonorrhea infection

A

men

90
Q

When will symptoms present with a gonorrhea infection

A

2-5 days after exposure, but may not be evident for 30 days.

91
Q

what culture medium is selective for N. gonorrhoeae

A

Thayer-Martin culture medium

92
Q

What are the diagnostic testing options available for diagnosing N. gonorrhoeae

A

Thayer-Martin culture medium
gram stain
(NAAT) Nucleic acid amplification test

93
Q

What should be considered when choosing a treatment option for gonorrhea

A

it is often with a coinfection of chlamydia trachomatis. Consider using a treatment plan that covers both options

94
Q

What are the treatment options for gonorrhea

A
  1. Cephalosporins:
    a. cefixime 400 mg PO
    b. ceftriaxone 125 mg IM (pharyngeal infection)
  2. Quinolones (No prego or under 18)
    a. Ciporfloxacin 500 mg PO
    b. Ofloxacin 400 mg PO
    c. levofloxacin 500 mg PO
  3. Spectinomycin 2g IM
  4. Azithromycin 2g PO single dose
95
Q

What treatment options are recomended for coinfection of gonorrhea and chlamydia

A

add either:
azithromycin 1g PO or
doxycycline 100 mg PO BID for 7 days

96
Q

What is the problem with using NAAT to follow up on treatment success

A

can remain positive for up to 3 weeks post treatment

97
Q

What is chlamydia

A

a genus of obligatory gram negative intracellular bacteria

most commonly reported STD

98
Q

Are women typically symptomatic with a chlamydia infection

A

no

99
Q

What is the clinical presentation of a woman with a chlamydia infection

A
mucopurulent cervicitis 
urethritis 
pyuria
negative urine culture
Fever and lower abdominal pain (PID)
100
Q

How is chlamydia diagnosed

A

culture from endocervix in women an urethral swab in men (gold standard)
NAAT: PCR or LCR

101
Q

What are the treatment options for chlamydia

A
  1. doxycycline 100 mg PO BID for 7 days
  2. Azithromycin 1 g PO
  3. Ofoxacin 400 mg PO BID for 7 days
  4. Erythromycin base 500 mg PO QD 7 days
  5. Levofloxacin 500 mg PO 7 days
102
Q

What causes chancroid

A

Haemophilus ducreyi

103
Q

What is chancroid

A

a known cofactor in HIV transmission

lesions begin as small papules and progress to painful genital ulcers in 2-3 days.

104
Q

What is the incubation time for chancroid

A

3-5 days

105
Q

How is the diagnosis of chancroid determined

A

Probable diagnosis is made when painful genital ulcers are present without eveidence of herpes (culture) or syphilis (darkfield examination and serologic study)

106
Q

What is the treatment of chancroid

A
  1. Azithromycin 1 g PO
  2. Ceftriaxone 250 mg IM
  3. Ciprofloxacin 500 mg PO BID for 3 days
  4. Erthromycin base 500 mg PO TID 7 days
107
Q

What is granuloma inguinale

A

genital ulcerative disease, which is also known as donovanosis, is caused by klebsiella granulomatis, a gram negative intracellular bacterium

108
Q

What is the clinical presentation of granuloma inguinale

A

affected individuals present with a painless, beefy red, friable ulcerative lesion without regional lymphadenopathy, but with accompanying inguinal join swelling caused by subcutaneous spread of granuloma

109
Q

What are the treatment options for granuloma inguinale

A
  1. Doxycycline 100 mg PO BID 21 days
  2. TMP-SMX 160mg/800mg PO BID 21 days
  3. Ciprofloxacin 750 mg PO BID 21 days
  4. Erythromycin base 500 mg PO QD 21 days
  5. Azithromycin 1 g PO 21 days
110
Q

What causes Bacterial Vaginosis

A

the replacement of the normal H202 producing lactobacillus with high concentrations of other bacteria, such as Garnerella vainalis, mobiluncus, Bacteroides, and mycoplasma.

111
Q

How is the clinical diagnosis of BV determined

A

3 of the following criteria

  1. Homogenous, grayish, noninflammatory discharge that adheres to vaginal walls
  2. saline preparation of vaginal secretions that reveals squamous cells whose borders are obscured by coccobacillary forms, known as clue cells.
  3. pH of secretions greater than 4.5
  4. fishy odor after addition of 10% KOH (whiff test)
  5. DNA probe test
112
Q

What is the treatment for BV

A
  1. Metronidazole 500 mg BID 7days
  2. Metronidalzole gel one applicator intravaginally per day for 7 days
  3. Clindamycin cream one applicator intravaginally QHS
113
Q

What is lympgranuloma venereum (LGV)

A

rare in US

requires a 21-34 day incubation period and primary genital ulcers appear at the site of inoculation

diagnosis made by exclusion

114
Q

What is the treatment for LGV

A
  1. doxycycline 100 mg BID for 21 days

2. Erythromycin 500 mg QD for 21 days

115
Q

What is the cause of syphilis

A

Treponema pallidum

116
Q

What are the signs and symptoms of primary syphilis

A

THE GREAT IMITATOR

Initial lesion of primary syphilis is a painless, ulcerated, hard chancre, usually on the external genitalia.

117
Q

What is the incubation period for primary syphilis

A

10-90 days for the lesion

lesions usually resolve in 2-6 weeks

118
Q

What is secondary syphilis

A

Untreated patients, the chancre is followed in 6 weeks to 6 months by a secondary or bacteremic stage in which the skin and mucous membranes are affected.

A maculopapular rash of the palms, soles and mucus membranes occur. Condyloma latum and generalized lymphadenopathy are seen as well. Lesions usually resolve with in 2-6 weeks.

119
Q

What is tertiary syphilis

A

33% of untreated patients develop tertiary syphilis with multiple organ involvement.

Endarteritis leads to aortic aneurysm and aortic insufficiency, tabes dorsal is, optic atrophy and meningovascular syphilis as well as granulamotous lesions.

120
Q

What is tabes dorsalis

A

slow degeneration (specifically, demyelination) of the sensory neurons that carry afferent information. The degenerating nerves are in the dorsal columns (posterior columns) of the spinal cord (the portion closest to the back of the body) and carry information that help maintain a person’s sense of position (proprioception), vibration, and discriminative touch.

121
Q

What is the problem with congenital syphilis

A

stillbirth, nonimmune hydrops, jaundice, infant hepatosplenomegal and skin rash and pseudoparalysis of an arm or leg

122
Q

How is syphilis diagnosed

A

Darkfield examination detects spirchetes in the primary and secondary stage

Serologic testing

  1. Nontreponemal:
    a. RPR (rapid plasma reagin)
    b. VDRL (Venereal Disease Research Lab)
  2. Treponemal antibody tests
    a. can remain positive for life
    b. FTS-ABS (fluorescent treponemal antibody absorption)
    c. TP-PA (T. Pallidum Particle agglutination)
123
Q

What is Jarisch-Herxheimer reaction

A

an acute febrile reaction that may be accompanied by myalgias, headache, and other systemic symptoms, can occur within 24 hours after treatment of syphilis at any stage, especially early disease

124
Q

What is the treatment of early syphilis

A
  1. Benazthine penicillin G 2.4 million units IM
  2. Doxycycline 100 mg BID 14 days
  3. Tetracycline 500 mg PO QD 14 days in nonpregnant penicillin allergic patients
125
Q

What should be used in pregnant patients with syphilis and a penicilin allergy

A

Skin testing following penicillin desensitization. All other medications are contraindicated

126
Q

What is the clinical presentation of HIV

A

80-90% are asymptomatic

Initial exposure of HIV results in a retroviral syndrome in 70%

  1. febrile phayngitis
  2. fever
  3. sweats
  4. myalgia
  5. arthralgia
  6. headache
  7. photophobia
127
Q

Hos is HIV diagnosied

A

ELISA
enzyme linked immunosorbent assay

Positive ELISA followed by a western blot analysis

Viral load for acute retroviral syndrome cases

128
Q

When should a patient be referred for treatment with HIV

A

asymptomatic: CD4 counts less than 300
symptomatic: CD4 counts less than 500

129
Q

What is the incubation period for HPV

A

6 weeks to 18 months with a mean of 3 months

130
Q

What types of HPV are strongly associated with CIN

A

16, 18, 31, 33, and 35

131
Q

On colposcopy, what will the lesions look like for HPV

A

flat, small and acetowhite, with a vascular punctuation or mosaicism.

Histologically, these lesions reveal koilocytosis, acanthuses, ad variable nuclear atypia

132
Q

What is the treatment of HPV warts

A

Patient applied methods

  1. Podofilox solution or gel
  2. Imiquimod cream

Provider applied methods

  1. Cyrotherapy
  2. Podophyllin resin
  3. Bicholor or tricholoracetic acid
  4. Surgical excision or ablation