Gine & Obstretica Step up 2

Question 1

Fetal to 4 yrs - Hormone Levels and Characteristics

Answer 1

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

Question 2

4–8 yrs - Hormone Levels and Characteristics

Answer 2

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

Question 3

11–17 yrs - Hormone Levels and Characteristics

Answer 3

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

Question 4

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

Answer 4

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

Question 5

≥50 yrs (females) - Hormone Levels and Characteristics

Answer 5

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

Question 6

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

Answer 6

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

Question 7

Which is the order of events in female puberty

Answer 7

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).

Question 8

Tanner Stage 1

Answer 8

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

Question 9

Tanner Stage 2

Answer 9

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

Question 10

Tanner Stage 3

Answer 10

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

Question 11

Tanner Stage 4

Answer 11

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

Question 12

Tanner Stage 5

Answer 12

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

Question 13

Types of Precocious Puberty and Meaning

Answer 13

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

Question 14

Difference between Complete and Incomplete Isosexual Precocious Puberty

Answer 14

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

Question 15

Precocious puberty in boys age and most common cause

Answer 15

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

Question 16

Isosexual precocious puberty - most common cause

Answer 16

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

Question 17

Labs for Precocious Puberty - All cases

Answer 17

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.

Question 18

The role of Radiology in Precocious Puberty

Answer 18

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

Question 19

Treatment of Precocious Puberty

Answer 19

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

Question 20

Complications of Precocious Puberty

Answer 20

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

Question 21

The follicular phase of the Normal Menstrual Cycle

Answer 21

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.

Question 22

The luteal phase of the Normal Menstrual Cycle

Answer 22

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).

Question 23

Luteinizing hormone (LH) effects

Answer 23

Midcycle surge induces ovulation

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

Question 24

Follicle-stimulating hormone (FSH) effects

Answer 24

Stimulates development of ovarian follicle

Regulates ovarian granulosa cell activity to control estrogen synthesis

Question 25

Estrogens (estradiol, estriol) effects

Answer 25

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

Question 26

Progesterone effects

Answer 26

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

Question 27

Human chorionic gonadotropin (hCG) effects

Answer 27

Acts like LH after implantation of fertilized egg | Maintains corpus luteum viability and progesterone secretion

Question 28

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

Answer 28

hCG

Question 29

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

Answer 29

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

Question 30

Types of Menopause and Meaning

Answer 30

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)

Question 31

Menopause - Symptoms

Answer 31

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

Question 32

Menopause - Labs

Answer 32

increased FSH, increased LH, decreased estradiol

Question 33

Menopause - Treatment

Answer 33

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

Question 34

Menopause - Complications

Answer 34

osteoporosis, coronary artery disease, dementia

Question 35

Contraindication for Topical estrogen

Answer 35

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

Question 36

Why is there an increased risk of osteoporosis?

Answer 36

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

Question 37

Risk factors for osteoporosis

Answer 37

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

Question 38

Contraception - Method Choice

Answer 38

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

Question 39

Hormonal Methods for Contraception

Answer 39

Hormonal Methods - Oral contraceptive pills - combined formulation - Oral contraceptive pills - progestin formulation - Medroxyprogesterone acetate - Progestin implant - Transdermal contraceptive patch - Intravaginal ring - Emergency contraception

Question 40

Barrier Methods for Contraception

Answer 40

- Condom - Diaphragm or cervical cap - Contraceptive sponge - Spermicide alone

Question 41

Sexual Practice Methods for Contraception

Answer 41

- Abstinence - Rhythm method - Withdrawal method - Lactation

Question 42

Intrauterine Devices and Surgical Method for Contraception

Answer 42

- Copper IUD - Progestin-releasing IUD Surgical: Sterilization

Question 43

Types of Amenorrhea

Answer 43

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

Question 44

Etiology of Amenorrhea

Answer 44

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

Question 45

History and Symptoms of Amenorrhea

Answer 45

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.

Question 46

Amenorrhea athlete’s triad

Answer 46

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

Question 47

Asherman syndrome (uterine synechiae)

Answer 47

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

Question 48

Amenorrhea - Labs

Answer 48

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

Question 49

The first step in the workup of any type of amenorrhea

Answer 49

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

Question 50

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

Answer 50

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

Question 51

Treatment of Amenorrhea

Answer 51

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.

Question 52

Complications of Amenorrhea

Answer 52

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

Question 53

Difference between Primary and Secondary dysmenorrhea symptoms

Answer 53

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.

Question 54

Dysmenorrhea definition and types

Answer 54

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)

Question 55

Dysmenorrhea Risk factors

Answer 55

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

Question 56

Dysmenorrhea symptoms

Answer 56

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

Question 57

Dysmenorrhea Labs

Answer 57

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

Question 58

Dysmenorrhea Radiology

Answer 58

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

Question 59

Dysmenorrhea Treatment

Answer 59

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

Question 60

What is Mittelschmerz?

Answer 60

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

Question 61

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

Answer 61

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

Question 62

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

Answer 62

(for severe symptoms) = family history

Question 63

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

Answer 63

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

Question 64

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

Answer 64

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

Question 65

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

Answer 65

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

Question 66

Endometriosis - Causes

Answer 66

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

Question 67

Endometriosis - Risk factors

Answer 67

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

Question 68

Endometriosis - Symptoms

Answer 68

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

Question 69

Endometriosis - Labs

Answer 69

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

Question 70

Endometriosis - Radiology

Answer 70

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

Question 71

Endometriosis - Treatment

Answer 71

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.

Question 72

Endometriosis - Complications

Answer 72

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

Question 73

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

Answer 73

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.

Question 74

Which is the most common cause of female infertility?

Answer 74

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

Question 75

Abnormal Uterine Bleeding - Definition

Answer 75

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)

Question 76

Abnormal Uterine Bleeding - Symptoms H/P

Answer 76

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

Question 77

Abnormal Uterine Bleeding - Labs

Answer 77

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

Question 78

Abnormal Uterine Bleeding - Radiology

Answer 78

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

Question 79

Abnormal Uterine Bleeding -Treatment

Answer 79

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

Question 80

What is Adenomyosis?

Answer 80

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.

Question 81

What is Polycystic Ovary Syndrome (PCOS)?

Answer 81

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.

Question 82

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

Answer 82

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

Question 83

Polycystic Ovary Syndrome (PCOS) - H/P

Answer 83

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

Question 84

Polycystic Ovary Syndrome (PCOS) - Labs

Answer 84

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

Question 85

Polycystic Ovary Syndrome (PCOS) - Radiology

Answer 85

Radiology = US shows enlarged ovaries with multiple cysts.

Question 86

Polycystic Ovary Syndrome (PCOS) - Treatment

Answer 86

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

Question 87

Polycystic Ovary Syndrome (PCOS) - Complications

Answer 87

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

Question 88

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

Answer 88

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

Question 89

Are ovarian cysts the cause if PCOS?

Answer 89

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

Question 90

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

Answer 90

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

Question 91

Vaginitis - risk factors

Answer 91

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

Question 92

Vaginitis - H/P

Answer 92

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

Question 93

Vaginitis - Labs

Answer 93

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”)

Question 94

Vaginitis - Treatment

Answer 94

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

Question 95

What are Lactobacilli?

Answer 95

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

Question 96

Treatment of partners? Yes/No, What?

Answer 96

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

Question 97

What is Toxic Shock Syndrome?

Answer 97

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

Question 98

Toxic Shock Syndrome - H/P

Answer 98

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

Question 99

Toxic Shock Syndrome - Labs

Answer 99

``` 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 ```

Question 100

Toxic Shock Syndrome - Treatment

Answer 100

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.

Question 101

Cervicitis - what is it?

Answer 101

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

Question 102

Cervicitis - H/P

Answer 102

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.

Question 103

Cervicitis - Labs

Answer 103

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.

Question 104

Which is the most common reportable STD?

Answer 104

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

Question 105

Highly sensitive tests for STD?

Answer 105

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

Question 106

Treatment of STDs

Answer 106

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

Question 107

Complication of STDs

Answer 107

Complication = PID, septic arthritis

Question 108

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

Answer 108

Clinical cervicitis with negative Gram stain and cultures