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Rezidentiat 2021 > Gine & Obstretica Step up 2 > Flashcards

Gine & Obstretica Step up 2 Flashcards

1
Q

Fetal to 4 yrs - Hormone Levels and Characteristics

A

High intrauterine FSH and LH that peak at 20-wk gestation and decrease until birth
FSH and LH increase again from birth until 6 mo of age then gradually decrease to low levels by age 4 yrs
Ch
All oocytes formed and partially matured by 20-wk gestation Tanner stage 1 characteristics

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2
Q

4–8 yrs - Hormone Levels and Characteristics

A

Low FSH, LH, and androgen levels caused by GnRH
suppression
Ch
Tanner stage 1 characteristics
Any sexual development considered precocious

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3
Q

11–17 yrs - Hormone Levels and Characteristics

A

Further increase of LH, FSH, and androgens to baseline mature levels
Hormones secreted in pulsatile fashion (higher at night) caused by sleep-associated increase in GnRH secretion
Ch
Puberty
Progression through Tanner stages
Development of secondary sexual characteristics and growth spurt
Menarche in females (beginning of menstrual cycles) and further oocyte maturation

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4
Q

17–50 yrs (females) - Hormone Levels and Characteristics

A 
LH and FSH follow menstrual cycle
Gradual increase in FSH and LH with ovarian insensitivity
Ch
Menstrual cycles
Mature sexual characteristics
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5
Q

≥50 yrs (females) - Hormone Levels and Characteristics

A

LH and FSH levels increase with onset of ovarian failure
Ch
Perimenopause: menstrual cycles become inconsistent
(oligomenorrhea)
Menopause: menstrual cycles cease (amenorrhea)

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6
Q

Which is the mean age of menarche? Are there differences between races?

A

The mean age of menarche is 13 years in the United States and tends to occur earlier in blacks than in whites

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7
Q

Which is the order of events in female puberty

A

Order of events of normal female puberty: adrenarche (adrenal androgen production), gonadarche (activation of gonads by FSH and LH), thelarche (appearance of breast tissue), pubarche (appearance of pubic hair), growth spurt, menarche (onset of menses).

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8
Q

Tanner Stage 1

A

Breast Development
Prepubertal: raised papilla (nipple) only
Pubic Hair Development
Prepubertal: no hair growth

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9
Q

Tanner Stage 2

A

Breast Development
Breast budding, areolar enlargement
Pubic Hair Development
Slight growth of fine labial hair

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10
Q

Tanner Stage 3

A

Breast Development
Further breast and areolar enlargement
Pubic Hair Development
Further growth of hair

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11
Q

Tanner Stage 4

A

Breast Development
Further breast enlargement: areola and papilla form secondary growth above the level of breast
Pubic Hair Development
Hair becomes coarser and spreads over much of pubic region

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12
Q

Tanner Stage 5

A

Breast Development
Mature breast: areola recedes to the level of the breast while papilla remains extended
Pubic Hair Development
Coarse hair extends from the pubic region to the medial thighs

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13
Q

Types of Precocious Puberty and Meaning

A

Isosexual

  1. Premature sexual development appropriate for the gender
  2. Can be complete (i.e., all sexual characteristics develop prematurely) or incomplete (i.e., only one sexual characteristic develops prematurely)

Heterosexual

  1. Virilization/masculinization of girls or feminization of boys
  2. In girls, most commonly results from congenital adrenal hyperplasia (CAH), exposure to exogenous androgens, or androgen-secreting neoplasm
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14
Q

Difference between Complete and Incomplete Isosexual Precocious Puberty

A

Complete isosexual: normal pubertal changes take place but at earlier-than-normal age
Incomplete isosexual: premature breast budding (i.e., thelarche), axillary hair growth, or pubic hair growth (i.e., pubarche) may take place

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15
Q

Precocious puberty in boys age and most common cause

A

Precocious puberty in boys occurs <9 years and is most commonly caused by adrenal hyperplasia.

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16
Q

Isosexual precocious puberty - most common cause

A

Central nervous system lesions or traumas are causes of isosexual precocious puberty in approximately 10% of cases.

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17
Q

Labs for Precocious Puberty - All cases

A

Increased LH and FSH with an additional release following administration of gonadotropin-releasing hormone (GnRH) suggest central precocious puberty; low LH and FSH with no response to GnRH suggest pseudo precocious puberty

Increased estrogen in the presence of low LH and FSH suggests ectopic hormone production (neoplasm) or
consumption of exogenous estrogen; significantly high levels of adrenal steroids may be seen with neoplasm or CAH.

Increased thyroid-stimulating hormone (TSH) with low thyroxine (T4) and triiodothyronine (T3) suggests precocious puberty in response to chronic hypothyroidism.

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18
Q

The role of Radiology in Precocious Puberty

A

magnetic resonance imaging (MRI) or computed tomography (CT) with contrast may detect cerebral or adrenal lesions

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19
Q

Treatment of Precocious Puberty

A

GnRH analogs are useful for LH and FSH suppression in central precocious puberty
Precocious puberty secondary to ectopic hormone secretion should be treated by locating and removing the source of the hormone.
Precocious puberty caused by CAH should be treated with cortisol replacement
Complete precocious puberty with an onset close to the expected start of puberty may not require treatment
Incomplete precocious puberty requires only observation to make sure that it does not become complete precocity

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20
Q

Complications of Precocious Puberty

A

short stature (bones fuse at early age); social and emotional adjustment issues

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21
Q

The follicular phase of the Normal Menstrual Cycle

A

Begins at the first day of menses (i.e., menstruation

FSH stimulates the growth of ovarian follicles (granulosa cells), which in turn secretes estradiol.

Estradiol induces endometrial proliferation and further increases FSH and LH secretion from the positive feedback of the pituitary.

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22
Q

The luteal phase of the Normal Menstrual Cycle

A

LH surge induces ovulation. Ovulation is the transition from the follicular phase of the menstrual cycle to the luteal phase. Cervical mucus immediately before ovulation is copious, thick, and clear, which is an indication of LH surge.

Residual follicle (i.e., corpus luteum) secretes estradiol and progesterone to maintain endometrium and induce the development of secretory ducts.

High estradiol levels inhibit FSH and LH.

If the egg is not fertilized, corpus luteum degrades, progesterone and estradiol levels decrease, and the endometrial lining degrades (i.e., menses).

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23
Q

Luteinizing hormone (LH) effects

A

Midcycle surge induces ovulation

Regulates cholesterol conversion to pregnenolone in ovarian theca cells as initial step in estrogen synthesis

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24
Q

Follicle-stimulating hormone (FSH) effects

A

Stimulates development of ovarian follicle

Regulates ovarian granulosa cell activity to control estrogen synthesis

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25
Q

Estrogens (estradiol, estriol) effects

A 
Stimulates endometrial proliferation
Aids in follicle growth
Induces LH surge
High levels inhibit FSH secretion
The principal role in sexual development
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26
Q

Progesterone effects

A

Stimulates endometrial gland development
Inhibits uterine contraction
Increases thickness of cervical mucus
Increases basal body temperature
Inhibits LH and FSH secretion; maintains pregnancy
The decrease in levels leads to menstruation

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27
Q

Human chorionic gonadotropin (hCG) effects

A

Acts like LH after implantation of fertilized egg

Maintains corpus luteum viability and progesterone secretion

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28
Q

What does the endometrial tissue secrets in order to maintain the corpus luteum

A

hCG

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29
Q

After which period of amenorrhea, a diagnosis of menopause can be achieved

A

One year of amenorrhea is required for a diagnosis of menopause.

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30
Q

Types of Menopause and Meaning

A
  1. Permanent end of menstruation because of ceasing of ovarian function in later middle age (∼51.5 years)
  2. Premature menopause is defined as an ovarian failure before age 40 years (more likely with a history of tobacco use, radiation therapy, chemotherapy, autoimmune disorders, or abdominal or pelvic surgery)
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31
Q

Menopause - Symptoms

A

H/P = hot flashes (secondary to thermoregulatory dysfunction), breast pain, sweating, menstrual irregularity with eventual amenorrhea, possible menorrhagia, fatigue, anxiety, irritability, depression, dyspareunia (caused by vaginal wall atrophy and decreased lubrication), urinary frequency, dysuria, change in bowel habits, sleep disturbances, decreased libido, cognitive decline; examination detects vaginal atrophy

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32
Q

Menopause - Labs

A

increased FSH, increased LH, decreased estradiol

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33
Q

Menopause - Treatment

A

a. Lubricating agents to treat dyspareunia (i.e., painful intercourse); short-term topical vaginal estrogen used in cases of significant vaginal symptoms
b. The first-line treatment for hot flashes is weight loss
c. Calcium, vitamin D, bisphosphonates, and exercise to prevent osteoporosis
d. Selective estrogen receptor modulators, such as raloxifene and tamoxifen, may serve a role in reducing osteoporosis and cardiovascular risks
e. Hormone replacement therapy poses an increased risk for breast cancer and deep vein thrombosis

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34
Q

Menopause - Complications

A

osteoporosis, coronary artery disease, dementia

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35
Q

Contraindication for Topical estrogen

A

Topical estrogen use is contraindicated in any patient with a history of breast cancer

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36
Q

Why is there an increased risk of osteoporosis?

A

Increased risk of osteoporosis in menopausal women is caused by decreased estrogen production by the ovaries.

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37
Q

Risk factors for osteoporosis

A

Risk factors for osteoporosis are advanced age, postmenopausal, low body weight, white or Asian, smoking, ETOH, and vitamin D deficiency

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38
Q

Contraception - Method Choice

A
  1. Should consider likelihood of patient compliance.
  2. Side effects must be tolerated by patient.
  3. Certain methods may be contraindicated for comorbid medical conditions
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39
Q

Hormonal Methods for Contraception

A

Hormonal Methods

  • Oral contraceptive pills - combined formulation
  • Oral contraceptive pills - progestin formulation
  • Medroxyprogesterone acetate
  • Progestin implant
  • Transdermal contraceptive patch
  • Intravaginal ring
  • Emergency contraception
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40
Q

Barrier Methods for Contraception

A
  • Condom
  • Diaphragm or cervical cap
  • Contraceptive sponge
  • Spermicide alone
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41
Q

Sexual Practice Methods for Contraception

A
  • Abstinence
  • Rhythm method
  • Withdrawal method
  • Lactation
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42
Q

Intrauterine Devices and Surgical Method for Contraception

A
  • Copper IUD
  • Progestin-releasing IUD

Surgical: Sterilization

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43
Q

Types of Amenorrhea

A

Primary: the absence of menses (never has happened) with normal secondary sexual characteristics by a 16-year-old or absence of both menses and secondary sexual characteristics by a 13-year-old
Secondary: the absence of menses for 6 months or for >3 cycles in a patient with prior history of menses

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44
Q

Etiology of Amenorrhea

A

a. Primary: hypothalamic or pituitary dysfunction, anatomic abnormalities (e.g., absent uterus, vaginal septa), chromosome abnormalities with gonadal dysgenesis
b. Secondary: pregnancy, ovarian failure, hypothalamic or pituitary disease, uterine abnormalities (e.g., Asherman syndrome), polycystic ovary syndrome (PCOS), anorexia nervosa, malnutrition, thyroid disease, medications (hormonal contraception, dopamine antagonists)
c. Primary ovarian insufficiency (hypergonadotropic hypogonadism): cessation of ovarian function before 40 years old

45
Q

History and Symptoms of Amenorrhea

A

a. History should address occurrence of any previous menstruation periods (e.g., primary or secondary amenorrhea), exercise and eating habits (e.g., substantial exercise or inadequate eating), family history, medications, androgenous symptoms (e.g., facial hair, voice deepening), and known comorbidity.
b. Examination should note Tanner stages and should check for normal sexual anatomy.

46
Q

Amenorrhea athlete’s triad

A

Amenorrhea athlete’s triad is amenorrhea, osteoporosis, eating disorder

47
Q

Asherman syndrome (uterine synechiae)

A

Asherman syndrome (uterine synechiae) is intrauterine adhesions resulting from a surgical procedure or possibly infection.

48
Q

Amenorrhea - Labs

A

a. β-hCG test used to rule out pregnancy
b. TSH, LH, FSH, and PRL
c. Increased prolactin suggests prolactin-secreting tumor
d. FSH and LH levels measure hypothalamic-pituitary activity
e. Increased androgens (e.g., testosterone, dehydroepiandrosterone [DHEA]) suggest PCOS
f. Progestin challenge (i.e., the patient is observed for bleeding after a 5-day administration of progesterone) and estrogen-progesterone challenge (i.e., the patient is observed for bleeding after administration of estrogen and progesterone) can help detect anatomic abnormalities (bleeding indicates normal outflow tract), hormonal abnormalities, or hypothalamic-pituitary activity

49
Q

The first step in the workup of any type of amenorrhea

A

β-hCG pregnancy test is always the first step in the workup of any type of amenorrhea.

50
Q

What do you do with the testicles of a XY patient with androgen insensitivity syndrome

A

If testicles are present in an XY patient with androgen insensitivity syndrome, they should be removed at an early age
because of increased risk of testicular cancer

51
Q

Treatment of Amenorrhea

A

a. Modify behaviors (e.g., eating disorders, exercise) to allow menstruation.
b. Anatomic abnormalities require surgical correction.
c. Hypothalamic–pituitary dysfunction may be treatable by GnRH or gonadotropin replacement.
d. Prolactinoma may be treated with dopamine agonists.
e. Hormone replacement therapy may be considered in ovarian failure.
f. Lysis of adhesions and estrogen administration performed for Asherman syndrome.
g. Thyroid dysfunction and Cushing syndrome treated according to specific pathology.
h. In some untreatable patients with appropriate anatomy, pregnancy may be accomplished through egg donation, in vitro fertilization, and hormone modulation.

52
Q

Complications of Amenorrhea

A

patients with genetic disorders or ovarian failure may be unable to achieve normal menstrual cycles

53
Q

Difference between Primary and Secondary dysmenorrhea symptoms

A

Primary dysmenorrhea symptoms occur in the beginning of menstruation and resolve over several days; secondary dysmenorrhea symptoms often begin midcycle before the onset of menstruation and increase in severity until the conclusion of menstruation.

54
Q

Dysmenorrhea definition and types

A

Periodic pain associated with menses that may be primary (without pelvic pathology) or secondary (caused by endometriosis, pelvic inflammatory disease [PID], uterine fibroids, ovarian cysts, or adenomyosis)

55
Q

Dysmenorrhea Risk factors

A

Risk factors = menorrhagia, menarche <12 years, body mass index <20, PID, sexual assault, smoking, premenstrual syndrome (PMS)

56
Q

Dysmenorrhea symptoms

A

H/P = crampy lower abdominal pain associated with menstruation, nausea, vomiting, headache, diarrhea; mild abdominal tenderness

57
Q

Dysmenorrhea Labs

A

β-hCG and blood and vaginal cultures are helpful to rule out pregnancy and infection

58
Q

Dysmenorrhea Radiology

A

Radiology = ultrasound (US) may be used to detect ovarian and uterine lesions; hysteroscopy or laparoscopy may be needed to detect intrauterine pathology, intra-abdominal pathology, or endometriosis

59
Q

Dysmenorrhea Treatment

A

Treatment = nonsteroidal anti-inflammatory drugs (NSAIDs) or oral contraceptive pills (OCPs) for primary disorders; treat the underlying infection or uterine disease

60
Q

What is Mittelschmerz?

A

Mittelschmerz is recurrent mild and unilateral mid cycle pain prior to ovulation. These episodes of pain last hours to days.

61
Q

Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD) Definition

A

Syndromes seen in women with normal functioning ovaries that precede menses (luteal phase) and are characterized by multiple pain, mood, and autonomic symptoms; mood symptoms are more severe in PMDD

62
Q

Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD) Risk factors

A

(for severe symptoms) = family history

63
Q

Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD) Symptoms

A

H/P = weight gain, headache, abdominal or pelvic pain, abdominal bloating, change in bowel habits, food cravings, mood lability, depression, fatigue, irritability; breast tenderness, edema, abdominal tenderness, acne

64
Q

Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD) Treatment

A

Treatment = exercise, vitamin B6, NSAIDs, OCPs, progestins; SSRIs ± alprazolam may improve mood symptoms in both PMS and PMDD

65
Q

Woman of childbearing age with abdominal pain - What’s the first thing you do?

A

Any woman of childbearing age with abdominal pain must be given a β-hCG pregnancy test to rule out ectopic pregnancy

66
Q

Endometriosis - Causes

A

Retrograde menstruation, vascular/lymphatic spread of endometrial tissue from uterus to pelvic cavity, or iatrogenic spread of endometrial tissue (e.g., during cesarean section) are most plausible causes of condition

67
Q

Endometriosis - Risk factors

A

Risk factors = family history, infertility, nulliparity (i.e., no history of childbirth), low body mass index

68
Q

Endometriosis - Symptoms

A

H/P = dysmenorrhea, dyspareunia, painful bowel movements (i.e., dyschezia), pelvic pain that peaks 1to 2 weeks before menses, possible infertility; uterine or adnexal tenderness; palpable adhesions on uterus or ovaries

69
Q

Endometriosis - Labs

A

Labs = biopsy of lesions shows endometrial tissue; β-hCG and urinalysis are helpful to rule out pregnancy and urinary tract infection; CA-125 marker frequently increases but is not a highly sensitive test

70
Q

Endometriosis - Radiology

A

Radiology = laparoscopy will show “powder-burn” lesions and cysts on involved areas and is an optimal diagnostic tool

71
Q

Endometriosis - Treatment

A

Treatment

a. Recording a journal of symptoms is useful for defining treatment.
b. OCPs, progestins, danazol, or GnRH agonists may supply symptomatic relief.
c. Laparoscopic ablation may successfully remove lesions while maintaining fertility potential.
d. Hysterectomy, lysis of adhesions, or salpingo-oophorectomy may be required in severe cases. Surgical pathology after hysterectomy provides the definitive diagnosis.

72
Q

Endometriosis - Complications

A

Complications = fertility may not be achieved despite pharmacologic or laparoscopic intervention

73
Q

If a patient suspected of having PMS or PMDD has mood symptoms throughout her menstrual cycle - What do you do?

A

If a patient suspected of having PMS or PMDD has mood symptoms throughout her menstrual cycle, initiate a psychiatric workup for a mood disorder. Evaluate by asking the patient to keep a symptom/menstrual diary for 2 to 3 menstrual cycles. Menstrual-related symptoms should only occur in the second half of the cycle.

74
Q

Which is the most common cause of female infertility?

A

Endometriosis is the most common cause of female infertility and may be responsible for up to 50% of cases.

75
Q

Abnormal Uterine Bleeding - Definition

A

Irregular menstruation, excessive menses (i.e., menorrhagia), or increased duration of menses that may be the result of a variety of causes (e.g., uterine fibroids, endometrial cancer or hyperplasia, hypothalamic-pituitary dysfunction, bleeding diathesis [e.g., von Willebrand disease–impaired platelet aggregation], threatened abortion, molar pregnancy,
ectopic pregnancy)

76
Q

Abnormal Uterine Bleeding - Symptoms H/P

A

H/P = Uterine bleeding that does not follow the usual menstrual cycle or occurs in postmenopausal women. Menses with <24-day or >35-day intervals, lasting >7 days, or blood loss >80 mL (more than one menstrual pad every 2 hours), or irregular frequency are considered abnormal

77
Q

Abnormal Uterine Bleeding - Labs

A

Labs = β-hCG, complete blood count (CBC), coagulation studies, TSH, FSH, and LH; Papanicolaou (Pap) smear and endometrial biopsy (obtained during dilation and curettage [D&C]) used to rule out cancer; STI testing

78
Q

Abnormal Uterine Bleeding - Radiology

A

Radiology = US may detect uterine lesions; hysteroscopy frequently indicated to visualize lesions and perform D&C

79
Q

Abnormal Uterine Bleeding -Treatment

A

Treatment = treat underlying disorder (e.g., coagulopathies, thyroid disease, infection). OCPs can be used for cycle irregularity. Endometrial ablation for severe or recurrent bleeding

80
Q

What is Adenomyosis?

A

Adenomyosis is endometrial tissue that invades the myometrium, causing symmetric uterine enlargement, uterine tenderness, cyclical pelvic pain, heavy menses. Often presents as chronic pelvic pain in a woman over 40 years old.

81
Q

What is Polycystic Ovary Syndrome (PCOS)?

A

Hypothalamic–pituitary disease characterized by anovulation or oligoovulation (manifested as
amenorrhea/oligomenorrhea), androgen excess, and polycystic ovaries.
Excess LH secretion induces overproduction of androgens by ovaries
Excess androgens produced by ovaries and adrenals are converted to estrogen, which induces further ovarian
androgen production.

82
Q

Polycystic Ovary Syndrome (PCOS) - Insulin - is there any relation between the 2?

A

Some patients with PCOS may have hyperinsulinemia, which induces androgen production and increases risk of insulin resistance.

83
Q

Polycystic Ovary Syndrome (PCOS) - H/P

A

H/P = metabolic syndrome (obesity, diabetes mellitus, hypertension), hirsutism, acne, menstrual dysfunction,
infertility, bilateral ovarian enlargement on bimanual examination.

84
Q

Polycystic Ovary Syndrome (PCOS) - Labs

A

Labs = increased LH, LH:FSH ratio >2, increased DHEA, increased total testosterone; positive progestin challenge

85
Q

Polycystic Ovary Syndrome (PCOS) - Radiology

A

Radiology = US shows enlarged ovaries with multiple cysts.

86
Q

Polycystic Ovary Syndrome (PCOS) - Treatment

A

Treatment = exercise and weight loss, OCPs, metformin, spironolactone, clomiphene (for fertility).

87
Q

Polycystic Ovary Syndrome (PCOS) - Complications

A

Complications = infertility; increased risk for DM, hypertension, ischemic heart disease, ovarian torsion, and endometrial cancer.

88
Q

Which is the most common cause if androgen excess in women?

A

PCOS is the most common cause of androgen excess in women.

89
Q

Are ovarian cysts the cause if PCOS?

A

Ovarian cysts are not the cause of disease in PCOS but are a result of androgen hypersecretion.

90
Q

PCOS - does it increase the risk of any other disease?

A

Patients with PCOS are at an increased risk for endometrial cancer secondary to chronically high estrogen levels.

91
Q

Vaginitis - risk factors

A

Risk factors = DM, human immunodeficiency virus (HIV), unprotected sex, multiple partners, young age at first
intercourse, douching, intrauterine device (IUD) use, smoking

92
Q

Vaginitis - H/P

A

H/P = vaginal irritation or pruritus, vaginal discharge; examination detects vaginal inflammation with characteristic findings depending on cause
= Tabel carte pg 310

93
Q

Vaginitis - Labs

A

Labs = wet mount (i.e., smear of vaginal fluid examined under microscope) with saline or potassium hydroxide (KOH) and vaginal pH testing useful to distinguish cause; smell a fishy odor when KOH is added to the vaginal discharge on a slide (“whiff test”)

94
Q

Vaginitis - Treatment

A

Treatment = metronidazole (G. vaginalis or Trichomonas), clindamycin (G. vaginalis), or fluconazole (C. albicans)

95
Q

What are Lactobacilli?

A

Lactobacilli are a common normal bacteria whose presence on a wet mount does not suggest infection.

96
Q

Treatment of partners? Yes/No, What?

A

Treatment of partners is unnecessary for G. vaginalis or C. albicans but is required with Trichomonas infection
(metronidazole).

97
Q

What is Toxic Shock Syndrome?

A

Severe systemic reaction to Staphylococcus aureus exotoxin associated with prolonged tampon use, prolonged intravaginal contraception use, or postpartum or postabortion infection

98
Q

Toxic Shock Syndrome - H/P

A

H/P = vomiting, diarrhea, sore throat, headache; high fever, generalized macular rash; severe cases develop
hypotension, shock, respiratory distress, and desquamation of palms and soles

99
Q

Toxic Shock Syndrome - Labs

A 
Labs = vaginal fluid culture shows S. aureus; decreased platelets, increased alanine aminotransferase (ALT) and
aspartate aminotransferase (AST), and increased blood urea nitrogen (BUN) and creatinine in progressing cases
100
Q

Toxic Shock Syndrome - Treatment

A

a. Remove tampon or other intravaginal objects.
b. Supportive care for hypotension; pressors may be required.
c. Clindamycin or penicillinase-resistant β-lactam antibiotics (e.g., oxacillin, nafcillin); vancomycin required for methicillin-resistant strains.

101
Q

Cervicitis - what is it?

A

Infection of cervical columnar epithelium caused by Neisseria gonorrhoeae or Chlamydia trachomatis.
The urethra, oral cavity, or rectal area can also become infected through sexual contact

102
Q

Cervicitis - H/P

A

H/P = dyspareunia, dysuria, bleeding after intercourse, purulent vaginal discharge (milder for Chlamydia), dysuria; disseminated gonorrhea presents as pustular dermatitis, migratory asymmetric polyarthralgia, and tenosynovitis.

103
Q

Cervicitis - Labs

A

a. Gram stain of cervical scraping shows gram-negative diplococci with N. gonorrhoeae (usually nothing seen with Chlamydia infection).
b. Culture on Thayer-Martin agar detects N. gonorrhoeae.

104
Q

Which is the most common reportable STD?

A

Chlamydia infection is the most common reportable STD because it can be asymptomatic (especially in men) and frequently goes unrecognized

105
Q

Highly sensitive tests for STD?

A

DNA probes (NAAT) and DNA amplification testing of cervical fluid (i.e., PCR) are highly sensitive.

106
Q

Treatment of STDs

A

Treatment = ceftriaxone for N. gonorrhoeae, doxycycline (not in pregnancy) or azithromycin for Chlamydia; both antibiotics often given together because of frequent dual infection; sexual partners must be treated to reduce risk of reinfection

107
Q

Complication of STDs

A

Complication = PID, septic arthritis

108
Q

Clinical cervicitis with negative Gram stain and cultures - most likely diagnosis?

A

Clinical cervicitis with negative Gram stain and cultures

Rezidentiat 2021 (4 decks)

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