2 Flashcards
(442 cards)
1
Q
What is the pathophysiology of thromboembolism?
A
Mediating factor is endothelial injury from traumatic delivery or cesarean. Postpartum risk is increased fivefold. Coagulability is increased in pregnancy. Risk is more elevated in coagulation protein deficiencies.
2
Q
What are the clinical signs of superficial thrombophlebitis?
A
Symptoms include localized pain and sensitivity. Signs include erythema, tenderness, and swelling. Diagnosis is one of exclusion after ruling out DVT. Treatment is conservative: bed rest, local heat, NSAIDs.
3
Q
What is the usual location of deep venous thrombosis?
A
The site of thrombosis is typically in the lower half of the body. Half of cases occur in the pelvic veins and half occur in the lower extremities.
4
Q
What are the clinical signs of deep venous thrombosis?
A
Pain, skin sensitivity, or asymptomatic; calf pain on dorsiflexion (Homan), although these findings are not highly sensitive or specific. Diagnosis is by duplex Doppler (above knee) or venography (below knee).
5
Q
What is the management of deep venous thrombosis?
A
Anticoagulation with IV heparin to increase PTT to 1.5–2.5. SQ heparin is used once therapeutic levels are achieved. Warfarin contraindiated because of teratogenicity. Thrombophilia workup should be performed.
6
Q
What is pulmonary embolus?
A
This is a potentially fatal result of DVT in which emboli travel through the venous system to the lungs. The source of the emboli is most commonly in the lower extremities or pelvis.
7
Q
What are the clinical signs of pulmonary embolus?
A
Chest pain and dyspnea (80%), tachypnea (90%), chest x–ray often normal; low pO2, ECG may show tachycardia, right axis deviation (usually normal). Spiral CT is the best initial test. Pulmonary angiography is most definitive diagnostic method.
8
Q
What is the management of pulmonary embolus?
A
Treatment is full anticoagulation (IV, SQ) heparin to increase PTT by 1.5 to 2.5 times the control value. No warfarin is used antepartum due to teratogenic concerns. Thrombophilia workup should be performed.
9
Q
What is intrauterine growth restriction?
A
Fetus with estimated fetal weight (EFW)
10
Q
What are the fetal causes of intrauterine growth restriction?
A
Trisomies; infection (TORCH), congenital heart disease, neural tube defects, ventral wall defects. These causes typically lead to symmetric IUGR.
11
Q
What are the placental causes of intrauterine growth restriction?
A
Infarction, abruption, twin–twin transfusion syndrome, velamentous cord insertion. Placental causes lead to asymmetric IUGR.
12
Q
What are the maternal causes of intrauterine growth restriction?
A
Hypertension (e.g., chronic, preeclampsia), SLE, long–standing type 1 diabetes), malnutrition, tobacco, alcohol, street drugs. These causes typically lead to asymmetric IUGR.
13
Q
What is symmetrical IUGR?
A
All ultrasound parameters (HC, BPD, AC, FL) are smaller than expected. Etiology is decreased growth potential, i.e., aneuploidy, early intrauterine infection, gross anatomic anomaly. Workup: sonogram, karyotype, and screen for fetal infections.
14
Q
What is asymmetrical IUGR?
A
Ultrasound parameters show head sparing, but abdomen is small. Causes include decreased placental perfusion due to chronic maternal diseases (HTN, diabetes, SLE, cardiovascular disease) or abnormal placentation (circumvallate, infarction). AFI decreased.
15
Q
What is the antepartum fetal monitoring for intrauterine growth restriction?
A
Monitoring is with serial sonograms, non–stress test, amniotic fluid index, biophysical profile, and umbilical artery Dopplers.
16
Q
What is macrosomia?
A
Fetus with estimated fetal weight (EFW) >90–95th percentile for gestational age.
17
Q
Birth weight
A
Accuracy of ultrasound in estimating birth weight is poor. Errors in prediction of EFW at term are ±400 grams.
18
Q
What are the risk factors for ?
A
Gestational diabetes mellitus, overt diabetes, prolonged gestation, obesity, excessive pregnancy weight gain, multiparity, male fetus.
19
Q
What are the maternal hazards of macrosomia?
A
Operative vaginal delivery, perineal lacerations, postpartum hemorrhage (uterine atony), emergency cesarean section, pelvic floor injury.
20
Q
What are the fetal hazards of macrosomia?
A
Shoulder dystocia, birth injury, asphyxia. Neonatal hazards are neonatal intensive care admission, hypoglycemia, Erb palsy.
21
Q
What is the management of macrosomia?
A
Consider elective cesarean (if EFW >4,500 g in diabetic mother or >5,000 g in nondiabetic mother) or early induction.
22
Q
What are the most common indications for antepartum fetal testing?
A
Decreased fetal movements, diabetes, post dates, chronic hypertension, and IUGR.
23
Q
What is the non–stress test?
A
Assesses frequency of accelerations, which are abrupt increases in FHR above baseline lasting 10 bpm, lasting >10 s; after 30 wks, increase should be >15 bpm, >15 s.
24
Q
What is the cause of fetal heart rate accelerations?
A
Mediated by the sympathetic nervous system and always occur in response to fetal movements. Interpretation: Accelerations are always reassuring.
25
What is the criteria for a reactive non–stress test?
Presence of two accelerations in a 20–min window of time >15 beats/min and lasting >15 sec. This is reassuring and highly predictive for fetal well–being. Management is to repeat the NST weekly.
26
What is the criteria for a nonreactive nonstress test?
27
What is the management of nonreactive nonstress test?
Perform fetal vibroacoustic stimulation to provoke reactivity. If the NST is persistently nonreactive, then perform a biophysical profile.
28
What is the amniotic fluid index?
Assesses the deepest vertical amniotic fluid pocket in each of the four quadrants of the uterus. The sum of the pockets is the amniotic fluid index. 25 cm is polyhydramnios
29
What is the biophysical profile?
BPP measures five components of fetal well–being: NST, amniotic fluid volume, fetal gross body movements, fetal extremity tone, and fetal breathing movements. Scores given for each component are 0 or 2, with max score of 10 and min of 0.
30
What is a modified biophysical profile?
A modified BPP includes only the NST and amniotic fluid volume. Its predictive value is almost as high as a complete BPP.
31
What is a contraction stress test?
Assesses fetal tolerance to contractions. Based on presence of late decelerations, which are gradual decreases with onset–to–nadir time of >30 s. Deceleration onset and end is delayed in relation to contractions. Rarely performed.
32
What is a negative contraction stress test?
Absence of any late decelerations with contractions. This is reassuring and highly reassuring for fetal well–being. Management is to repeat the CST weekly.
33
What is a positive contraction stress test?
Late decelerations associated with 50% of contractions. 50% of positive CSTs are false positive and are associated with good FHR variability. 50% of true positives have absent variability. Management of positive CST is delivery.
34
What are the contraindications for contraction stress testing?
Conditions in which contractions would be hazardous to the mother or fetus, such as previous classical uterine incision, previous myomectomy, placenta previa, incompetent cervix, preterm membrane rupture, preterm labor.
35
What is the umbilical artery Doppler test?
Measures ratio of systolic and diastolic blood flow in umbilical artery. This test is predictive of poor perinatal outcome only in IUGR fetuses. Nonreassuring findings are absent diastolic flow and reversed diastolic flow.
36
What are the bones that comprise the pelvis?
The pelvis is constructed of four bones: ileum superior–laterally, ischium inferior–laterally, pubis anteriorly, and the sacrum and coccyx posteriorly.
37
What is labor?
Process whereby regular uterine contractions cause progressive effacement and dilation of the cervix, resulting in delivery of the fetus and expulsion of the placenta. Contractions normally occur at least every 5 min and last 30 s.
38
What is the normal physiologic mechanism that causes the frequency of contractions?
Increased contractions are caused by formation of gap junctions between uterine myometrial cells, which is caused by increasing levels of oxytocin and prostaglandins and multiplication of specific receptors.
39
What is cervical effacement?
Cervical softening and thinning occur as increasing levels of oxytocin and prostaglandins lead to breakage of disulfide linkages of collagen fibers, resulting in increasing water content. Uneffaced (0%) cervix is 2 cm long, 2 cm wide.
40
What is complete cervical dilation?
In early labor (latent phase), the rate of dilation is slow, but at 3–4 cm of dilation, the rate accelerates to a maximum rate in the active phase of labor. Complete dilation is 10 cm.
41
What are the cardinal movements of labor?
Engagement of presenting part below pelvic inlet. Descent presenting part down. Flexion of chin. Internal rotation of head from transverse to anterior–posterior. Extension of chin. External rotation of head. Expulsion of body.
42
What is stage one labor?
Begins with onset of regular uterine contractions and ends with complete cervical dilation at 10 cm. It is divided into a latent and an active phase.
43
What is the latent phase of stage one labor?
Begins with onset of regular contractions and ends with acceleration of cervical dilation at 3–4 cm of dilation. Average duration of the latent phase is 6.4 hours in a primipara and 4.8 hours in a multipara.
44
What is the active phase of stage one labor?
Begins at 3–4 cm of dilation, ending with complete cervical dilation. Cervical dilation is rapid. The cardinal movements of labor occur, with beginning descent of the fetus. Rate of dilation is 1.2 cm/h in a primipara and 1.5 cm/h in multipara.
45
What is stage two labor?
Begins with complete cervical dilation and ends with delivery of the fetus. Descent of the fetus through the birth canal occurs as maternal pushing efforts augment uterine contractions. Duration up to 2 h in a primipara and 1 h in multipara.
46
What is stage three labor?
Begins with delivery of fetus and ends with placental expulsion. Placental separation occurs as contractions shear off villi; augmented with oxytocin. Gush of blood, uterus changes to globular, lengthening cord. Duration up to 30 min.
47
What is stage four labor?
2–h period of close observation of the parturient immediately after delivery when vital signs and vaginal bleeding are monitored for onset of preeclampsia and postpartum hemorrhage.
48
What are the causes of prolonged latent phase?
Latent–phase abnormalities are most commonly caused by excessive analgesia. Other causes are hypotonic contractions or hypertonic contractions (high intensity but inadequate duration or frequency). Treatment: rest, sedation.
49
What is prolonged active phase of labor?
After cervical dilation is >2 cm, prolongation is diagnosed if cervical dilation is 2h.
50
What are the causes of prolonged active phase of labor?
Active–phase abnormalities may be caused by abnormalities of the passenger (excessive fetal size or abnormal fetal orientation in the uterus), abnormalities of the pelvis (bony pelvis size), or abnormalities of powers (inadequate contractions).
51
What is the management of prolonged or arrested active phase of labor?
Contractions should occur q2–3min, last 45–60 s with 50 mm Hg intensity. If contractions are hypotonic, administer oxytocin. If contractions hypertonic, give morphine. If labor is arrested despite adequate contractions, proceed to cesarean.
52
What is prolonged second stage of labor?
Cervical dilation at 10 cm, +1 station and failure to deliver the baby in 2 hours (primipara) or 1 hour (multipara). With epidural analgesia, add additional 1 hour.
53
What is the management of prolonged second stage of labor?
IV oxytocin. If the head is not engaged, proceed to cesarean section. If the head is engaged, consider a trial of either obstetric forceps or a vacuum extraction.
54
What is prolonged third stage of labor?
Failure to deliver the placenta within 30 minutes because of inadequate uterine contractions or abnormal placental implantation (accreta, increta, percreta). May require manual placental removal.
55
What are the types of prolapsed umbilical cord?
Prolapse can be occult (cord has not come through cervix but is being compressed), partial (cord is between head and the dilated cervical os but has not protruded into vagina), or complete (cord has protruded into vagina).
56
What are the risk factors for prolapsed umbilical cord?
Rupture of membranes with the presenting fetal part not applied firmly to the cervix and malpresentation. Amniotomy at –2 station. Severe variable decelerations.
57
What is the management of prolapsed umbilical cord?
Place patient in knee–chest position, elevate the presenting part, avoid palpating the cord, and perform immediate cesarean delivery.
58
What is shoulder dystocia?
Delivery of shoulders is delayed after delivery of head. Usually associated with fetal shoulders in anterior–posterior plane, with anterior shoulder impacted behind pubic symphysis. 1% of deliveries; neonatal neurologic damage in 2%.
59
What are the risk factors for shoulder dystocia?
Maternal diabetes, obesity, and postdates pregnancy, fetal macrosomia.
60
What is the management of shoulder dystocia?
Suprapubic pressure, maternal thigh flexion (McRobert's), internal rotation of the fetal shoulders to the oblique plane (Wood's corkscrew), manual delivery of the posterior arm, Zavanelli (cephalic replacement, then cesarean).
61
What is a first degree perineal laceration?
Involve only the vaginal mucosa. Suture repair is often not needed.
62
What is a second degree perineal laceration?
Involve the vagina and the muscles of the perineal body, but not involving the anal sphincter. Suturing is necessary.
63
What is a third degree perineal laceration?
Involve the vagina, the perineal body, and the anal sphincter but not the rectal mucosa. Suturing is necessary to avoid anal incontinence. 4th degree lacerations extend the vagina through rectal mucosa.
64
What are the indications for an episiotomy?
Not done routinely because of more pain; longer return to sexual activity; more extensions into anus. Possible indications include shoulder dystocia, non–reassuring tracing, forceps/vacuum delivery, breech delivery, narrow canal.
65
What is an epidural block?
Injection of local anesthetic into the epidural space to block the lumbosacral nerve roots during both stages 1 and 2 of labor. Used for either vaginal delivery or cesarean.
66
What are the complications of epidural block?
Hypotension from peripheral vascular dilation because of sympathetic blockade, spinal headache from inadvertent dural puncture, and CNS bleeding or infection. Hypotension treated fluids, ephedrine. Spinal headache.
67
What is the treatment of spinal headache after epidural block?
Hydration and blood patch.
68
What is the normal fetal heart rate at term?
Normal values are between 110 and 160 beats/min.
69
What are the causes of fetal bradycardia?
FHR is
70
What is the fetal tachycardia?
FHR is >160 beats/min. Hypoxia. Beta–adrenergic agonists (terbutaline, ritodrine), fever, thyrotoxicosis. Fetal arrhythmia, prematurity. Unexplained tachycardia is nonreassuring.
71
What are fetal heart rate accelerations?
Abrupt increases in FHR lasting 10 beats/min lasting >10 s; >32 weeks the increase should be >15 beats/min lasting >15 s. Accelerations are reassuring.
72
What are early decelerations of fetal heart rate?
Gradual decreases in FHR beginning and ending simultaneously with contractions. Early decelerations are mediated by vagal stimulation and occur in response to fetal head compression. Early decelerations have no impact on outcome.
73
What are variable decelerations of fetal heart rate?
Abrupt decreases of at least 15 bpm with onset–to–nadir time of 60 bpm or >60 s.
74
What is the significance of mild to moderate variable decelerations?
Mild to moderate variables have no impact on clinical outcome. Severe variables are nonreassuring and may be associated with fetal acidosis.
75
What are late decelerations of fetal heart rate?
Gradual decreases in FHR below baseline with onset–to–nadir time of >30 s. Deceleration onset and end is delayed in relation to contractions. Myocardial depression in response to uteroplacental insufficiency. Lates are nonreassuring; acidosis.
76
What is the triad of early decelerations?
Gradual drop of FHR. Gradual return of FHR. Mirror image of contraction.
77
What is the criteria for a reassuring fetal heart rate tracing?
Baseline rate is between 110 and 160 beats/min. Accelerations are present. Decelerations are absent. Variability is present.
78
What is the criteria for nonreassuring fetal heart rate tracing?
Baseline rate shows tachycardia or bradycardia without explanation. Accelerations are absent. Repetitive variable decelerations are severe. Repetitive late decelerations. Variability is absent.
79
What are the steps in intrauterine resuscitation?
Stop oxytocin, give terbutaline 0.25 mg SQ. 500 mL NS to enhance uteroplacental perfusion. O2 mask. Amnioinfusion. Left–lateral. Turn to other side to relieve cord compression. Exam for prolapsed cord. Digital scalp stimulation to cause accelerations.
80
What is the indication for intrapartum fetal scalp blood pH?
Used in labor if the EFM strip is equivocal. Prerequisites include cervical dilation, ruptured membranes, and adequate descent of the fetal head. Contraindicated in fetal blood dyscrasia. Normal fetal pH is 7.20.
81
What is the normal postpartum umbilical artery blood pH?
Used to confirm fetal status at delivery and involves obtaining samples of umbilical cord venous and arterial blood. Arterial pH, Pco2, and HCO3 values are higher than venous, but Po2 is lower. Normal fetal pH is 7.20.
82
What are the indications for forceps delivery?
Prolonged second stage because of dysfunctional labor or suboptimal fetal head orientation. Nonreassuring strip. To avoid maternal pushing when pushing may be hazardous. Breech presentation.
83
What are the prerequisites for forceps delivery?
Clinically adequate pelvic dimensions. Full cervical dilation. Engaged fetal head. Orientation of fetal head is certain.
84
What is vacuum extraction?
Cuplike instrument that is held against the fetal head with suction. Traction is applied to the fetal scalp, which along with maternal pushing efforts, results in descent of the head, leading to vaginal delivery.
85
What are the advantages of vacuum extraction over forceps?
Precise knowledge of fetal head position and attitude is not essential. The vacuum extractor does not occupy space adjacent to the fetal head. Third– and fourth–degree lacerations are fewer. Fetal head rotation occurs spontaneously.
86
What are the indications for primary cesarean section?
Cephalopelvic disproportion is the most common indication for cesarean delivery. Failure of the adequate progress in labor. Fetal malpresentation. Nonreassuring EFM strip.
87
What is the criteria for vaginal birth after cesarean?
Successful vaginal delivery after cesarean occurs at a rate of 80%. Criteria for trial of labor include previous low segment transverse uterine incision and clinically adequate pelvis.
88
What is external cephalic version?
Manipulating the gravid abdomen to turn the fetus from transverse lie or breech presentation at 37 weeks' gestation. and success rate is 60–70%. Potential hazards are umbilical cord compression or placental abruption requiring emergency cesarean.
89
What is postpartum lochia?
Superficial layers of endometrial decidua are shed through vagina during first 3 postpartum weeks. First few days red (lochia rubra), changing to pinkish (lochia serosa), ending with a whitish (lochia alba) by end of 2nd week.
90
What type of concentration is contraindicated in breast–feeding women?
Estrogen–progestin should not be used because estrogen will decrease milk. In nonlactating women, combination pills should be started after 3 weeks, after reversal of hypercoagulable state to decrease the risk of DVT.
91
What type of hormonal contraception can be used in breast–feeding women?
Progestin contraceptives (e.g., mini–pill, Depo–Provera, Implanon) do not diminish milk production so can safely be used during lactation. They can be started immediately after delivery.
92
What are the postpartum indications for RhoGAM?
If the mother is Rh(D) negative and her baby is Rh(D) positive, she should receive 300 µg of RhoGAM IM within 72 hours of delivery.
93
What is the postpartum treatment of rubella negative mothers?
If the mother is rubella IgG antibody negative, she should be administered active immunization with live–attenuated rubella virus. She should avoid pregnancy for 1 month to avoid potential fetal infection.
94
What is the most common cause of excessive postpartum bleeding?
Uterine Atony (50%). Retained placenta causes 10%.
95
What are the risk factors for uterine atony?
Rapid or protracted labor (most common), chorioamnionitis, MgSO4, beta–adrenergic agonists, and overdistended uterus.
96
What are the clinical findings of uterine atony?
A soft, doughy uterus (feels like dough) palpable above the umbilicus.
97
What is the management of uterine atony?
Uterine massage and uterotonic agents (e.g., oxytocin, methylergonovine, or carboprost). Lacerations of the cervix, vagina or perineum cause 20% of postpartum hemorrhage.
98
What are the risk factors for postpartum disseminated intravascular coagulation?
Abruptio placenta (most common), severe preeclampsia, amniotic fluid embolism, and prolonged retention of a dead fetus. Presents as generalized oozing or bleeding from IV sites or lacerations in presence of a contracted uterus.
99
What is the management of postpartum disseminated intravascular coagulation?
Removal of pregnancy tissues from the uterus, intensive care unit support, and selective blood–product replacement.
100
What is the management of uterine inversion?
Uterine replacement by elevating the vaginal fornices and lifting the uterus back into its normal anatomic position, followed by IV oxytocin.
101
What is the most common cause of postpartum fever on days 1–2?
Urinary tract infection. Risk factors include multiple intrapartum catheterizations and vaginal examinations due to prolonged labor.
102
What is the most common cause of postpartum fever on post partum day 2–3?
Endometritis is the most common cause of postpartum fever. Risk factors include emergency cesarean section prolonged labor. Prolonged membrane rupture and with uterine tenderness.
103
What is the most common cause of postpartum fever on post partum day 4–5?
Wound infection. Risk factors include emergency cesarean section after prolonged membrane rupture and prolonged labor. There is persistent spiking fever despite antibiotics, along with wound erythema, fluctuance, or drainage.
104
What is the most common cause of postpartum fever on day 5–6?
Thrombophlebitis. Risk factors include emergency cesarean section after prolonged membrane rupture and prolonged labor.
105
What are the clinical findings in septic thrombophlebitis?
Persistent wide fever swings despite broad–spectrum antibiotics with normal pelvic and physical examination. Management is intravenous heparin for 7–10 days to increase the PTT values at 1.5 to 2.0 times baseline.
106
What is the most common cause of postpartum fever on day 7–21?
Infectious mastitis. Risk factors include lactational nipple trauma leading to nipple cracking and allowing Staphylococcus aureus bacteria to enter breast ducts and lobes. Management is oral dicloxacillin. Breast feeding should be continued.
107
What is loop electrosurgical excision procedure?
LEEP is a technique used for diagnosing and treating cervical dysplasia. It uses an electric current passed through a thin wire loop to remove abnormal cervical tissues.
108
What are the American Cancer Society recommendations for mammography screening?
Initial study age 34 if there are risk factors (e.g., breast cancer in first–degree relative, family history of BRCA gene). Start annual routine screening at age 40 in women without risk factors.
109
What is the management of pelvic relaxation?
Kegels. Estrogen replacement in postmenopausal women. Pessaries inserted into vagina. Vaginal hysterectomy with an anterior and posterior vaginal repair. The anterior and posterior colporrhaphy uses endopelvic fascia plication.
110
What is sensory irritative incontinence?
Involuntary increases in bladder pressure because of detrusor contractions stimulated by irritation from infection, stone, tumor, or a foreign body. Loss of urine occurs with urgency, frequency, and dysuria day or night.
111
What is stress incontinence?
Most common form of urinary incontinence. Increases in bladder pressure because of intraabdominal pressure increases (coughing and sneezing). Loss of urine in small spurts with coughing or sneezing. Proximal urethra is not supported.
112
What are the signs of stress incontinence?
Pelvic examination may reveal a cystocele. Neurologic examination is normal. The Q–tip test is positive (cotton–tip applicator is placed in urethra and the patient increases intraabdominal pressure, Q–tip will rotate). Cystometric studies normal.
113
What is the management of stress incontinence?
Kegels. Estrogen in postmenopausal. Surgical therapy elevates the urethral sphincter by attachment of the sphincter to the symphysis pubis (Burch, MarshallMarchetti–Kranz). Tension–free vaginal tape procedure.
114
What is motor urge incontinence?
Involuntary increases in bladder pressure caused by idiopathic detrusor contractions that cannot be voluntarily suppressed. Loss of urine occurs in large amounts without warning day and night. The most common symptom is urgency.
115
What are the signs of urge incontinence?
Pelvic and neurologic examination are normal. Urinalysis and culture are normal. Cystometric studies show normal residual volume, but involuntary detrusor contractions are present even with small volumes of urine in the bladder.
116
What is the management of urge incontinence?
Anticholinergic medications (e.g., oxybutynin [Ditropan]); NSAIDs to inhibit detrusor contractions; tricyclic antidepressants; calcium–channel blockers.
117
What is overflow incontinence?
Increased bladder pressure, overdistended, hypotonic bladder, causing involuntary urine loss because of diabetic neuropathy, multiple sclerosis, ganglionic blockers, anticholinergics. Loss of urine occurs intermittently in small amounts, day and night.
118
What is the triad of stress incontinence?
Involuntary loss of urine with coughing and sneezing. No urine lost at night.
119
What is the triad of hypertonic bladder?
Involuntary loss of urine. Inability to suppress urge to void. Urine loss day and night.
120
What is the triad of hypotonic bladder?
Involuntary loss of urine. Detrusor muscle not contracted. Urine loss day and night.
121
What are the signs of overflow incontinence?
Neurologic examination will show decreased pudendal nerve sensation. Cystometric studies show markedly increased residual volume, but without involuntary detrusor contractions.
122
What is the management of overflow incontinence?
Intermittent self–catheterization. Discontinue anticholinergics. Cholinergic medications to stimulate bladder contractions and alpha–adrenergic blocker to relax the bladder neck.
123
What medications are used as bladder relaxants?
Antispasmodics: oxybutynin (Ditropan), flavoxate (Urispas). Anticholinergics: Probanthine. Tricyclics: imipramine (Tofranil).
124
What medications are used to increase vesical neck contraction?
Ephedrine, imipramine, estrogen.
125
What is the normal vaginal pH?
The vagina is normally acidic
126
What is the bacterial vaginosis?
Most common (50%) cause of vaginal complaints. Normal lactobacilli are replaced by anaerobes and facultative aerobes. Frequently postmenopausal; not sexually transmitted, but associated with sexual activity.
127
What are the symptoms of bacterial vaginosis?
The most common patient complaint is a fishy odor. Itching and burning are not present.
128
What are the speculum examination abnormalities in bacterial vaginosis?
Vaginal discharge is thin, grayish–white. No vaginal inflammation. The vaginal pH is >5.0. A positive whiff" test is elicited when KOH is placed on the discharge."
129
What is the triad of bacterial vaginosis?
Vaginal discharge pH >4.5. Fishy odor. Clue" cells."
130
What is the management of bacterial vaginosis?
Metronidazole or clindamycin orally or vaginally. Metronidazole is safe in pregnancy, including the first trimester.
131
What is the triad of Trichomonas vaginitis?
Vaginal discharge pH
132
What is the Trichomonas vaginitis?
Most common cause of vaginal complaints worldwide and the second most common sexually transmitted disease in the United States. Caused by a flagellated pear–shaped protozoan that can be asymptomatic in male semen.
133
What are the symptoms of Trichomonas vaginitis?
Itching, burning, and pain with intercourse.
134
What are the speculum examination abnormalities of Trichomonas vaginitis?
Vaginal discharge is frothy and green. Vaginal epithelium is edematous and inflamed. Erythematous cervix with strawberry" appearance. The vaginal pH is elevated >5.0."
135
What are wet mount findings in Trichomonas vaginitis?
Motile trichomonads" on a saline preparation. WBCs are seen."
136
What is the management of Trichomonas vaginitis?
Oral metronidazole for the patient and sexual partner. Vaginal metronidazole gel has a 50% failure rate. Metronidazole is safe in pregnancy, including the first trimester.
137
What is the Candida vaginitis?
Second most common vaginal complaint in the United States. The most common organism is Candida albicans. It is not transmitted sexually.
138
What are the risk factors for Candida vaginitis?
Diabetes mellitus, systemic antibiotics, pregnancy, obesity, and decreased immunity.
139
What are the symptoms of candida vaginitis?
Itching, burning, and pain with intercourse.
140
What are the speculum examination abnormalities in Candida vaginitis?
Vaginal discharge is curdy and white. Vaginal epithelium is edematous and inflamed. Vaginal pH is normal
141
What are the wet mount abnormalities in Candida vaginitis?
Pseudohyphae on a KOH prep. WBCs.
142
What is the management of Candida vaginitis?
Single oral dose of fluconazole or vaginal azole" creams. Asymptomatic sexual partners do not need treatment."
143
What is normal psychologic vaginal discharge?
Thin, watery cervical mucus discharge seen with estrogen dominance.
144
What is the management of excessive physiologic vaginal discharge?
Steroid contraception with progestins.
145
What is the triad of yeast vaginitis?
Vaginal discharge with pH
146
65–year–old woman with vulvar itching. 1–cm white lesion of labia minora. Enlarged inguinal node. What is the diagnosis?
Vulvar cancer.
147
What are vulvar dystrophies?
Benign lesions without malignant predisposition vulvar itching, including squamous hyperplasia and lichen sclerosis.
148
What is vulvar squamous hyperplasia?
Whitish focal or diffuse areas that are firm and cartilaginous on palpation. Thickened keratin and epithelial proliferation. Management is fluorinated corticosteroid cream.
149
What is vulvar lichen sclerosis?
Bluish–white papula that can coalesce into white plaques. Thin and parchment–like. Epithelial thinning. Management is Clobetasol cream.
150
What is vulvar squamous dysplasia?
White, red, or pigmented, often multifocal. Cellular atypia is restricted to the epithelium without breaking through the basement membrane. Dysplasia. Management is surgical excision.
151
What is vulvar carcinoma in situ?
The appearance is indistinguishable from vulvar dysplasia. Cellular atypia is full thickness but does not penetrate the basement membrane. Management is laser vaporization.
152
What is vulvar squamous cell cancer?
The most common type of invasive vulvar cancer is squamous cell carcinoma, which has been associated with HPV.
153
What is vulvar melanoma?
The second most common histologic type of vulvar cancer is melanoma of the vulva. The most important prognostic factor is the depth of invasion. Dark or black lesion.
154
What is vulvar Paget disease?
Malignant red lesion, which is most common in postmenopausal white women. In 18–20% of cases there is invasion of basement membrane. Patients with Paget disease of the vulva have a higher association of other cancers from GI tract, GU, breast.
155
What is the management of vulvar squamous cell cancer?
Modified radical vulvectomy without lymphadenectomy. Any patient with vulvar cancer with invasion >1 mm should be treated with a lymphadenectomy.
156
What is molluscum contagiosum?
Common, benign, viral skin infection in children, sexually active adults, and immunodeficient patients. The molluscipox virus causes umbilicated tumors of the skin. Transmitted by skin contact. Management includes curettage and cryotherapy.
157
What is vulvar Condylomata acuminata?
Benign cauliflower– like vulvar lesions caused by HPV types 6 & 11. No malignant predisposition. Treat clinical lesions only.
158
What is a Bartholin cyst?
Obstruction of the Bartholin gland duct may occur due to infection (GC). The duct often remains obstructed, resulting in cystic dilation of the gland. Management is conservative unless there are pressure symptoms.
159
What are cervical polyps?
Fingerlike growths on cervix or endocervix. Relatively common in older multiparous women. Vaginal bleeding after intercourse. Bleeding occurs between normal menstrual periods. Biopsy reveals mildly atypical cells, infection.
160
What is the management of cervical polyps?
Polyps can be removed by gentle twisting followed by electrocautery or laser. An antibiotic may be given after the removal. Most cervical polyps are benign.
161
What are nabothian cysts?
Mucus–filled cyst on surface of cervix. Cyst appears as a small, white, pimple–like elevation. Singly or in groups. More common in women of reproductive age. Optional treatment is electrocautery or cryotherapy.
162
What are the signs of cervicitis?
Mucopurulent cervical discharge. No pelvic tenderness is noted. Cervical cultures are positive for chlamydia or gonorrhea. WBC and ESR are normal.
163
What is the management of cervicitis?
Oral azithromycin in a single dose or oral doxycycline BID for 7 days.
164
What is the etiology of cervical cancer?
Human papilloma virus 16, 18, 31, 33, and 35 are associated with cancer of the cervix. HPV 6 and 11 are associated with benign condyloma acuminata.
165
What are the risk factors for cervical cancer?
Early age of intercourse, multiple sexual partners, cigarette smoking, and immunosuppression.
166
When should Pap smears be started?
3 yrs after sexual activity or age 21 years, whichever occurs first. If under 30 years old, screen annually if using conventional methods or every 2 years if using liquid–based methods. If >30 years, screen every 2–3 years.
167
When should Pap smear screening be discontinued?
At age 70 if patient has had >3 consecutive normal Pap smears, and after total hysterectomy, if the procedure was performed for benign disease.
168
What is the management of abnormal HPV DNA testing?
HPV 16, 18, 31,33, 35 are associated with premalignant and invasive cervical cancer. If cells are reported with ASCUS with HPV 6 or 11, then repeat Pap smear in 1 year; however, if it is HPV DNA 16 or 18, evaluate by colposcopy, biopsy.
169
What are the causes of atypical squamous cells of undetermined significance?
ASCUS Pap smears can result from inflammatory and atrophic lesions, or may be caused by the initial stages of HPV infection. 10–15% of ASCUS Pap smears can have a premalignant lesion, small percentage have invasive carcinoma.
170
What are the diagnostic options for atypical squamous cells of undetermined significance?
A patient with an ASCUS Pap smear can be managed with any of 3 options: repeat cytology in 3–6 months, HPV DNA typing, or colposcopic evaluation and biopsy.
171
What is the management of atypical squamous cells of undetermined significance?
Accelerated repeat Paps. Repeat Pap at 4– to 6–month intervals until 2 consecutive, negative Paps. If a repeat Pap is ASC–US or worse, do colposcopy. HPV DNA testing is also an option for ASC–US. Colposcopy only if high–risk HPV DNA.
172
What is the indication for Colposcopy?
Patients with abnormal Pap should be evaluated by colposcopy. Nonpregnant patients undergoing colposcopy also undergo endocervical curettage. Lesions on ectocervix (mosaicism, punctation, white lesions, abnormal vessels) are biopsied.
173
What are the indications for cone biopsy?
If Pap smear is worse than histology, then cone biopsy. Other indications for conization of the cervix include abnormal ECC histology, a lesion seen entering endocervical canal, and a biopsy showing microinvasive carcinoma of cervix.
174
What is the management of cervical intraepithelial neoplasia1?
Observation and follow–up without treatment is appropriate for CIN 1 and includes any of the following: repeat Pap in 6 and 12 months; colposcopy and repeat Pap in 12 months; or HPV DNA testing in 12 months.
175
What are the indications for cervical ablative modalities?
Ablation used for CIN 1, 2, and 3. Cryotherapy, laser, electrofulguration. Excisional procedures include loop electrosurgical excision procedure or cold–knife conization. Hysterectomy only acceptable with recurrent CIN 2 or 3.
176
What is invasive cervical cancer?
Cervical neoplasia that has penetrated through the basement membrane.
177
What is the presentation of invasive cervical cancer?
Postcoital or irregular vaginal bleeding, lower extremity pain, edema. Cervical carcinoma is third most common gyn malignancy with a mean age of 45 years. Initial test is biopsy, most common diagnosis is squamous cell carcinoma.
178
What is the management of cervical cancer?
Treated surgically. Patients with risk factors for metastatic disease and tumor recurrence are offered adjuvant therapy (radiation therapy and chemotherapy).
179
What is the prevention of cervical cancer?
Quadrivalent HPV recombinant vaccine (Gardasil) is recommended for females 8–26 yrs, with a target age of 11–12.
180
What are the components of the quadrivalent HPV recombinant vaccine?
Gardasil uses noninfectious particles to protect against HPV (6, 11, 16, 18) that cause 70% of cervical cancer and 90% of genital warts. 3 doses: initial, 2 mths later, then 6 mths later.
181
What is the most common congenital uterine anomaly?
Bicornuate uterus 45%; results from failure of fusion of Mullerian ducts. Complete failure results in two separate single–horn uterine bodies sharing one cervix. Preterm delivery and malpresentation are common with pregnancy.
182
What is leiomyoma uteri?
Benign smooth muscle growth of myometrium; most common benign uterine tumor. Five times more prevalent in black women. Intermenstrual bleeding is the most common symptom of a submucosal myoma and can result in anemia.
183
What is the management of leiomyoma uteri?
Most leiomyomas can be managed conservatively and followed expectantly with regular pelvic examinations. GnRH analogs can be used adjuvunctively before surgical therapy.
184
What is adenomyosis?
Ectopic endometrial glands and stroma are located within myometrium of uterine wall. Most common presentation is diffuse involvement of the myometrium. If involvement is focal, surrounded by a pseudocapsule, the lesion is adenomyoma .
185
What are the symptoms of adenomyosis?
Majority asymptomatic. Dysmenorrhea, menorrhagia. Uterus is globular and 2–3 times normal size. Tenderness before and during menses. Ultrasound shows enlarged uterus with cystic areas within the myometrial wall.
186
What is the management of adenomyosis?
Levonorgestrel intrauterine system (IUS) may decrease heavy menstrual bleeding. Hysterectomy is the definitive treatment.
187
What is menopause?
A patient is considered to be in menopause after 3 continuous months of cessation of menses and elevated gonadotropins. Menopause usually occurs at 52 years of age.
188
What is the most common gynecologic malignancy?
Endometrial carcinoma is the most common gynecologic malignancy, occurring in 1% of women. The mean age at diagnosis is 61 years.
189
What is the differential diagnosis of post menopausal bleeding?
Endometrial carcinoma, vaginal or endometrial atrophy, and postmenopausal hormonal replacement therapy. The most common cause of postmenopausal bleeding is vaginal or endometrial atrophy. Most important is to rule out is endometrial carcinoma.
190
What is the etiology of endometrial cancer?
Unopposed estrogen causes excessive stimulation of the endometrium without the stabilizing effect of progesterone.
191
What are the risk factors for endometrial cancer?
Obesity, hypertension, and diabetes mellitus. Other risk factors include nulliparity, late menopause, and chronic anovulation conditions, such as polycystic ovarian disease.
192
What is the evaluation of postmenopausal bleeding?
Patients with postmenopausal bleeding must be evaluated with endometrial sampling. If postmenopausal cervical stenosis is present, and these patients should be evaluated with a dilatation and curettage.
193
What is the management of postmenopausal bleeding with a negative cancer histology?
If the endometrial sampling reveals atrophy and no evidence of cancer, then the patient can be assumed to be bleeding from atrophy and can be treated with estrogen and progesterone replacement. Estrogen given alone increases risk of endometrial cancer.
194
What is the treatment of endometrial adenocarcinoma?
Hysterectomy and bilateral salpingo–oophorectomy, lymphadenectomy, and peritoneal washings. Radiation if metastasis to lymph nodes, >50% myometrial invasion, positive margins, poorly differentiated. Chemotherapy for metastates.
195
What is the prevention of endometrial cancer?
Postmenopausal patients taking estrogen must be also treated with progestins to prevent unopposed estrogen stimulation, which may lead to endometrial cancer. Reproductive age women with anovulation should also be treated with progestins.
196
What are functional cysts?
The most common cause of a simple cystic mass in the reproductive age years is a physiologic cyst (luteal or follicular cyst).
197
What is the most common complex adnexal mass in young women?
Dermoid cyst or benign cystic teratoma. Other causes include endometrioma, tubo–ovarian abscess, and ovarian cancer.
198
What is the evaluation of an adnexal mass in a reproductive age woman?
Qualitative beta–human chorionic gonadotropin (beta–hCG) test will rule out pregnancy. Sonogram: a complex mass on ultrasound appearance will rule out a functional cyst.
199
What is the triad of functional ovarian cyst?
Pelvic mass in reproductive years. Beta–hCG (–). Sonogram: fluid–filled ovarian simple cyst.
200
What is the management of functional ovarian cysts
Observation: follow–up examination should be in 6–8 weeks, at which time the functional cyst should have spontaneously resolved. Oral contraceptive medication can be used to help prevent further functional cysts.
201
What is the management of ovarian cysts >7cm?
Laparoscopy. Surgical evaluation if: cyst >7 cm or prior steroid contraception. Functional cysts should not form if the patient has been on oral contraception for at least 2 months because gonadotropins should have been suppressed.
202
What is polycystic ovarian syndrome?
Ovaries bilaterally enlarged with multiple peripheral cysts (20 in each ovary) because of high circulating androgens and high circulating insulin levels cause arrest of follicular development. PCOS is associated with valproic acid.
203
What is ovarian hyperthecosis?
Nests of luteinized theca cells in the ovarian stroma that may be steroidogenically active, resulting is greater production of androgens and causing increased estrogen and endometrial hyperplasia and increased risk of endometrial carcinoma.
204
What are the clinical features of hyperthecosis?
Obesity, hirsutism. Virilization with clitoral enlargement, temporal balding, deepening of the voice, and male habitus. Most patients have amenorrhea, and remainder have irregular and anovulatory cycles.
205
What is the management of hyperthecosis?
Oral contraceptive pills to suppress androgen production (by reducing LH stimulation of the theca cells).
206
What is luteoma of pregnancy?
Rare, non–neoplastic mass of the ovary that appears during pregnancy and regresses after delivery. Usually asymptomatic. It can be hormonally active and produce androgens resulting in maternal and fetal hirsutism and virilization.
207
What are theca lutein cysts?
Benign neoplasms stimulated by high levels of FSH and beta–hCG. Associated with twins and molar pregnancies, but only rarely associated with a normal singleton pregnancy. Postpartum spontaneous regression.
208
What is the evaluation of prepubertal adnexal masses?
Adnexal mass in the prepubertal age group is abnormal. Therefore any ovarian enlargement is suspicious for neoplasm.
209
What is the evaluation of complex adnexal masses in girls and teenagers?
If sonography shows a complex adnexal mass in a girl or teenager, the possibility of germ cell tumors of the ovary should be considered. Obtain serum tumor markers: lactate dehydrogenase, beta–hCG, and alpha–fetoprotein.
210
What is the presentation of germ cell tumors of the ovary?
Sudden onset of acute abdominal pain. These tumors characteristically grow rapidly and give early symptomatology.
211
What is the triad of dysgerminoma?
Solid pelvic mass in reproductive years. Beta–hCG (–). Increased LDH level.
212
What is the management of germ cell ovarian tumors?
Unilateral salpingo–oophorectomy and surgical staging (peritoneal and diaphragmatic biopsies, peritoneal cytology, pelvic and para–aortic lymphadenectomy, and omentectomy) postoperative chemotherapy.
213
What is the most common complex adnexal mass in young women?
Dermoid cyst or benign cystic teratoma. Other diagnoses include endometrioma, tuboovarian abscess, and ovarian cancer.
214
What is the evaluation of complex adrenal masses in young women?
Qualitative beta–human chorionic gonadotropin (beta–hCG) test to rule out pregnancy. The appearance of a complex mass on ultrasound will rule out a functional cyst.
215
What is the management of patients in the reproductive age group with a complex adnexal mass?
Laparoscopic ovarian cystectomy to preserve ovarian function in reproductive age. If an ovarian cystectomy cannot be done because of the size of the dermoid cyst, then an oophorectomy is performed.
216
What is the triad of benign cystic teratoma?
Pelvic mass: reproductive years. Beta–hCG (–). Sonogram: complex mass, calcific.
217
What is benign cystic teratoma?
Dermoid cysts are benign tumors. Can contain cellular tissue from all three germ layers. Most common histology is ectodermal skin appendages (hair, sebaceous). Gastrointestinal histology and carcinoid syndrome have been described.
218
What is the presentation of ovarian torsion?
Sudden onset of severe lower abdominal pain in the presence of an adnexal mass is presumptive evidence of ovarian torsion.
219
What is the management of ovarian torsion caused by a cyst?
Laparoscopy to untwist ovary, then observe ovary for a few minutes to assure revitalization. If revitalization occurs, then an cystectomy can be performed with preservation of the ovary. If ovary necrotic, then a unilateral salpingo–oophorectomy.
220
What is the presentation of ovarian cancer?
Pelvic mass identified after menopause. Ovaries in the postmenopausal age group should be atrophic.
221
What is the triad of ovarian torsion?
Abrupt unilateral pelvic pain. Beta–hCG (–). 12–cm adnexal mass an ultrasound.
222
What is the evaluation of a postmenopausal adnexal mass?
Abdominal pelvic CT scan or a pelvic ultrasound. GI studies (barium enema) should also be done to rule out any intestinal pathology such as diverticular disease. IV pyelography to identify any impingement of the urinary tract.
223
What is the screening test for ovarian cancer?
Bimanual pelvic examination.
224
What is the most common fatal gynecologic cancer?
Ovarian carcinoma is the second most common gynecologic malignancy, with a mean age of 69 years. One percent of women die of ovarian cancer. It is the most common gynecologic cancer leading to death.
225
What are the risk factors for ovarian cancer?
BRCA 1 gene, positive family history, high number of lifetime ovulations, infertility, perineal talc powder.
226
What are protective factors for ovarian cancer?
Conditions that decrease the total number of lifetime ovulations, such as oral contraceptive pills, chronic anovulation, breast–feeding, and short reproductive life.
227
What is the most common type of ovarian cancer?
Epithelial tumors, 80%. The most common type of ovarian carcinoma is epithelial cancer; predominantly postmenopause. Epithelial tumors include serous, mucinous, Brenner, endometrioid, and clear cell tumors.
228
What age group is most affected by germ cell tumors?
Germ cell tumors are 15% of ovarian cancer; predominantly teenagers. Germ cell tumors are dysgerminoma, endodermal sinus tumors, teratomas, choriocarcinoma.
229
What type of ovarian cancer is functionally active?
Stromal tumors comprise 5% of ovarian cancers and are functionally active. Include granulosa–theca cell tumors, which secrete estrogen and can cause bleeding from endometrial hyperplasia. Sertoli–Leydig tumors secrete testosterone.
230
What are the most common sources of metastatic tumor?
The most common sources are the endometrium, GI tract, and breast. Krukenberg tumors are mucin–producing tumors from the stomach, which are metastatic to the ovary.
231
What is the triad of serous carcinoma?
Postmenopausal woman. Pelvic mass. Increased CEA or CA–125 level.
232
What is the triad of choriocarcinoma?
Postmenopausal woman. Pelvic mass. Increased hCG level.
233
What is the triad of Sertoli–Leydig tumor?
Postmenopausal pelvic mass. Masculinization. Increased testosterone.
234
What is the management of ovarian cancer?
If CT does not show evidence of ascites or spread to abdominal cavity, evaluation could be performed laparoscopically. Unilateral salpingo–oophorectomy is done and sent for a frozen section. If carcinoma, then follow–up with CA–125.
235
What is the triad of ovarian carcinoma with peritoneal metastasis?
Postmenopausal bilateral pelvic masses. Weight gain, anorexia. Abdominal shifting dullness"."
236
22–year–old Thai woman 15 weeks gestation by dates with vaginal bleeding, nausea, vomiting. Uterus extends to umbilicus but no fetal heart tones. Blood pressure is 150/90. Dipstick 2+ proteinuria. What is the diagnosis?
Gestational trophoblastic neoplasia.
237
What is gestational trophoblastic neoplasia?
Abnormal proliferation of placental tissue involving both the cytotrophoblast and/or syncytiotrophoblast. Benign or malignant. Malignant GTN can be localized or metastatic.
238
What are the types of benign gestational trophoblastic neoplasia?
Complete hydatidiform mole and incomplete mole. Incidence is 1:1200 in the US, but 1:120 in the Far East.
239
What is a complete hydatiform mole?
Most common benign GTN. Results from fertilization of an empty egg by single X sperm, resulting in paternally derived 46, XX karyotype. No fetus, cord, or amniotic fluid. Grape–like vesicles of edematous villi. Progression to malignancy 20%.
240
What is an incomplete hydatiform mole?
Less common benign GTN. Results from fertilization of a normal egg with 2 sperm, resulting in triploid 69, XXY karyotype. A fetus, cord and amniotic fluid is seen, but in fetal demise eventually occurs. Progression to malignancy is 10%.
241
What are the types of malignant gestational trophoblastic neoplasia?
This is the gestational trophoblastic tumor, which can be non metastatic, good prognosis metastatic, and poor prognosis metastatic. Non–metastatic disease is localized only to the uterus.
242
What is the triad of molar pregnancy?
Pregnancy
243
What are the risk factors for gestational trophoblastic neoplasia?
Increased prevalence in Taiwan and the Philippines. Other risk factors are maternal age extremes (35 years old) and folate deficiency.
244
What are the symptoms of gestational trophoblastic neoplasia?
Bleeding prior to 16 weeks' gestation and passage of vesicles from the vagina. Other symptoms of a molar pregnancy include hypertension, hyperthyroidism, and hyperemesis gravidarum, and no fetal heart tones.
245
What is the clinical presentation of gestational trophoblastic neoplasia?
Most common sign is fundus larger than dates, absence of fetal heart tones, bilateral cystic enlargements of the ovary known as theca –lutein cysts. Most common site of distant metastasis is the lungs.
246
How is gestational trophoblastic neoplasia diagnosed?
Snowstorm" ultrasound. The diagnosis is confirmed with sonogram showing homogenous intrauterine echoes without a gestational sac or fetal parts."
247
What is the management of benign gestational trophoblastic neoplasia?
Obtain baseline quantitative beta–hCG, chest X–ray to rule out lung metastasis. Suction D&C. Place patient on oral contraceptive to ensure no confusion between rising beta–hCG titers from recurrent disease and normal pregnancy.
248
What is the follow–up of benign gestational trophoblastic neoplasia?
Serial beta–hCG until neg for 3 wks, then monthly until neg for 1 yr. If beta–hCGs plateau or rise, persistent gestational trophoblastic disease is diagnosed; metastatic workup (CT brain, thorax, abdomen, pelvis) and chemotherapy are indicated.
249
What is the treatment of non–metastatic or Good Prognosis metastatic disease?
Administer single agent (methotrexate or actinomycin D) until weekly beta–hCG titers become negative for three weeks, then monthly titers until negative for 12 months.
250
17–year–old with bilateral pelvic pain after menstrual period. Sexually active, but no contraception. Mucopurulent cervical discharge. Bilateral adnexal tenderness, cervical motion tenderness. Beta–hCG neg. What is the diagnosis?
Pelvic inflammatory disease.
251
What is the bacteriology of pelvic inflammatory disease?
The most common initial organisms are chlamydia and gonorrhea. With persistent infection, secondary bacterial invaders include anaerobes and gram–negative organisms.
252
What are the signs of cervicitis?
Vaginal discharge. Mucopurulent cervical discharge. No pelvic tenderness. Afebrile. WBC and ESR are normal.
253
What is the management of cervicitis?
Single dose orally of cefixime and azithromycin.
254
What are the symptoms of acute salpingo–oophoritis?
Bilateral lower abdominal–pelvic pain. Gradual to sudden, often after menses. Nausea and vomiting may be if abdominal involvement is present.
255
What are the signs of salpigno–oophoritis?
Mucopurulent cervical discharge, cervical–motion tenderness, and bilateral adnexal tenderness. Fever, tachycardia, abdominal tenderness, peritoneal signs, and guarding. WBC is elevated. Cervical cultures positive for chlamydia or gonorrhea.
256
What is the differential diagnosis of pelvic inflammatory disease?
Adnexal torsion, ectopic pregnancy, endometriosis, appendicitis, diverticulitis, Crohn disease, and ulcerative colitis.
257
How is salpingo–oophoritis diagnosed?
Bilateral lower abdominal–pelvic tenderness, mucopurulent cervical discharge, cervical–motion tenderness, and elevated WBC and ESR.
258
What is the outpatient treatment of pelvic inflammatory disease?
Ofloxacin bid with metronidazole bid, both for 14 days.
259
What is the inpatient treatment of pelvic inflammatory disease?
IV cefoxitin or cefotetan plus IV doxycycline or IV clindamycin plus gentamicin.
260
What is the triad of acute salpingo–oophoritis?
Bilateral abdominal/pelvic pain. Mucopurulent cervical discharge. Cervical motion tenderness.
261
What are the symptoms of tubo–ovarian abscess?
Septic appearance. Severe lower abdominal–pelvic pain. Back pain, rectal pain, and pain with bowel movements. Nausea and vomiting.
262
What are the signs of tubo–ovarian abscess?
High fever with tachycardia. Septic shock with hypotension. Peritoneal signs, guarding, and rigidity. Bilateral adnexal masses.
263
What are the laboratory findings in tubo–ovarian abscess?
Cervical cultures are positive for chlamydia or gonorrhea. Blood cultures may be positive for gram–negative bacteria and anaerobic organisms such as Bacteroides fragilis. WBC elevated. Sonography: bilateral complex masses.
264
What is the differential diagnosis of tubo–ovarian abscess?
Septic abortion, diverticular abscess, appendiceal abscess, and adnexal torsion.
265
What is the management of tubo–ovarian abscess?
IV clindamycin and gentamicin. If the patient does not respond or if there is rupture of the abscess, perform exploratory laparotomy with possible TAH and BSO or percutaneous drainage.
266
What are the symptoms of chronic pelvic inflammatory disease?
Chronic bilateral lower abdominal–pelvic pain, from minimal to severe. Infertility, dyspareunia, ectopic pregnancy, and abnormal vaginal bleeding. Nausea and vomiting are absent.
267
What is the triad of chronic salpingo–oophoritis?
Bilateral abdominal/pelvic pain. No cervical discharge. Cervical motion tenderness.
268
What are the signs of chronic PID?
Bilateral adnexal tenderness and cervical–motion tenderness, but mucopurulent cervical discharge is absent. Fever and tachycardia are absent. Cervical cultures are negative. WBC and ESR are normal Sonography: bilateral cystic masses.
269
What is primary dysmenorrhea?
Recurrent, crampy lower abdominal pain, along with nausea, vomiting, diarrhea, that occurs during menstruation in the absence of pelvic pathology. The most common gynecologic complaint among adolescent females.
270
What is the presentation of primary dysmenorrhea?
Onset of pain after ovulatory menstrual cycles are established. The symptoms typically begin several hours prior to the onset of menstruation and continue for 1 to 3 days.
271
What is the pathogenesis of primary dysmenorrhea?
Excess production of endometrial prostaglandin Fla. Spiral artery constriction and necrosis follow progesterone withdrawal as corpus luteum involutes. Prostaglandins cause contractions, hypercontractility, increased uterine tone, ischemia.
272
What is the management of primary dysmenorrhea?
Suppression of prostaglandins with nonsteroidal antiinflammatory drugs (NSAIDs) are the first choice in treatment. Continuous combination estrogen–progesterone steroid agents (e.g., oral contraceptives).
273
32–year–old woman with dysmenorrhea, dyspareunia, infertility. Tender, 4–cm cul–de–sac mass, tenderness and nodularity of uterosacral ligaments. What is the diagnosis?
Endometriosis.
274
What is endometriosis?
Endometrial glands and stroma occur outside the uterus. Retrograde menstruation. The most common site is the ovary, endometrial implants bleed monthly and can create adnexal enlargements known as endometriomas or chocolate cysts.
275
What are the symptoms of endometriosis?
Pelvic–abdominal pain, dyspareunia, painful bowel movements (dyschezia). Infertility.
276
What are the signs of endometriosis?
Pelvic tenderness. A fixed, retroverted uterus is often caused by cul–de–sac adhesions. Uterosacral ligament nodularity. Enlarged adnexa. WBC is normal. CA– 125 may be elevated. Sonogram may show an endometrioma.
277
How is endometriosis diagnosed?
Laparoscopic identification of endometriotic nodules or endometriomas.
278
What is the triad of endometriosis?
Chronic pelvic pain. Painful intercourse. Painful bowel movements.
279
What is the medical treatment of endometriosis?
Pregnancy is helpful. Pseudopregnancy prevents progesterone withdrawal bleeding. Continuous oral medroxyprogesterone (Provera), IM medroxyprogesterone , or combination oral contraceptive pills. Danazol and a gonadotropin–releasing hormone analog.
280
What is the surgical management of endometriosis?
Laparoscopic lysis of paratubal adhesions may allow pregnancy. Ovarian cystectomies as well as oophorectomies. Laser vaporization. If severe pain is present, total abdominal hysterectomy and bilateral salpingo–oophorectomy.
281
What is the ,chancroid?
Caused by Haemophilus ducreyi, a Gram–negative bacterium. Uncommon in the United States. Presents with a painful ulcer.
282
What is the schedule for the progestin–only injectable contraceptive?
Depo–Provera is an IM injection of depo–medroxyprogesterone acetate (DMPA) given every 3 months. Frequent break–through bleeding. Failure rate is
283
What is the schedule for the progestin–only subcutaneous implant?
Implanon uses etonogestrel. Continuous release continues for 3 years. Frequent break–through bleeding. Failure rate is
284
What are the risks and benefits of low–dose contraceptive pills?
Do not significantly increase the risk of cancer, heart disease, or thromboembolic events in women with no risk factors (HTN, diabetes, smoking). Combination pill reduces menstrual flow and dysmenorrhea, regulates menses.
285
What is the mechanism of action of intrauterine contraception?
Inhibition of sperm transport; inhibition of implantation because of endometrial inflammation; phagocytic destruction of sperm and the blastocyst; and alteration of cervical mucus (progesterone IUS).
286
What are the absolute contraindications to intrauterine contraception?
Confirmed or suspected pregnancy; pelvic malignancy; undiagnosed vaginal bleeding; and salpingitis.
287
What are the relative contraindications to the intrauterine system?
Abnormal uterine size or shape; corticosteroid therapy, valvular heart disease, any immune suppression increasing the risk of infection; nulligravidity; abnormal Pap smears; and a history of ectopic pregnancy.
288
What are the side effects of intrauterine contraception?
Menstrual bleeding and menstrual pain may be increased with the copper IUS, but not with the progesterone intrauterine systems. The IUS does not increase ectopic pregnancies. Pregnancy from failed IUS increases ectopic risk.
289
What is Mirena"?"
Levonorgestrel–impregnated intra uterine system that releases the hormone gradually over the period of 5 years. Bleeding and cramping may be decreased. Failure rate is
290
What are the natural family planning methods?
Prediction or identification of ovulation by menstrual records, basal body temperature charting (temperature rise from progesterone), change in cervical mucus from thin and watery to thick and sticky.
291
What are the causes of sexual desire disorders?
Decreased sexual desire is the most common female sexual complaint. It may be organic (e.g., low androgens), medication related (e.g., selective serotonin reuptake inhibitors), or psychological (e.g., poor relationship).
292
What is the most common cause of sexual excitement disorders?
The most common cause is estrogen deficiency. Results in difficulty in vaginal lubrication.
293
What is the treatment of vaginismus?
Painful reflex spasm of the paravaginal thigh adductor muscles. Can be diagnosed on physical examination. Treatment is vaginal dilators.
294
What prophylaxis is indicated after sexual assault?
Antibiotics prophylactically for gonorrhea (ceftriaxone), chlamydia (doxycycline), trichomoniasis (metronidazole). Antiviral HIV prophylaxis administered within 24 hours after exposure. Active and passive immunization for hepatits B.
295
What hormones control the menstrual cycle?
Gonadotropin–releasing hormone (GnRH) from the hypothalamus, which stimulates FSH and luteinizing hormone from the anterior pituitary, which stimulate estrogen and progesterone from the ovarian follicle.
296
What is the menstrual phase of endometrium?
First 4 days of the menstrual cycle with the first day of menses as day 1. Disintegration of endometrial glands and stroma, leukocyte infiltration, and red blood cell extravasation. Sloughing of the functionalis and compression of basalis.
297
What is the proliferative phase of the endometrium?
Follows the menstrual phase. Endometrial growth secondary to estrogen stimulation, including division of stem cells that form new epithelial lining of the endometrium and new endometrial glands. The length of the spiral arteries increases.
298
What are the steps of the secretory phase of the endometrium if no pregnancy occurs?
Endometrium becomes edematous, spiral arteries become convoluted. Regression of corpus luteum on day 23 if no pregnancy. Decreased progesterone and estradiol cause endometrial involution.
299
What endometrial change causes menstruation?
Constriction of spiral arteries occurs one day before menstruation, causing ischemia, prostaglandins, RBC extravasation.
300
What are the steps of the secretory phase when pregnancy occurs?
When a pregnancy occurs, the beta–human chorionic gonadotropin becomes positive on day 22–23. The beta–hCG becomes positive when the zygote implants into the endometrium, usually 7–8 days after ovulation. beta–hCG becomes positive before missed period.
301
What is the role of follicle stimulating hormone?
FSH stimulates the growth of granulosa cells and induces the aromatase enzyme that converts androgens to estrogens. FSH increases its own receptors on granulosa cells. Stimulates the secretion of inhibin from granulosa cells and is suppressed by inhibin.
302
What is the role of luteinizing hormone?
LH stimulates androgens by theca cells, which is converted to estrogens by granulosa cell. Estrogen increases its receptors in granulosa cells. LH surge stimulates follicle rupture, ovulation. LH surge luteinizes granulosa cells, resulting in progesterone
303
What is the role of estrogen in the menstrual cycle?
E produced in granulosa cell stimulates endometrium. Neg feedback to FSH, but pos feedback to increase GnRH receptors. At low E there is neg inhibitory feedback for LH, but E for 50 hrs causes transition to a pos feedback, causing LH surge.
304
What is premenarchal bleeding?
Bleeding that occurs before menarche. The average age at menarche is 12 years of age.
305
What are the causes of premenarchal bleeding?
Ingestion of estrogen, foreign bodies, cancer of vagina or cervix (sarcoma botryoides), tumor of pituitary or adrenal gland, ovarian tumor, sexual abuse, idiopathic precocious puberty. Most common cause of premenarchal bleeding is a foreign body.
306
How is premenarcheal bleeding diagnosed?
Pelvic exam under sedation for foreign body, sexual abuse, tumor. Sarcoma botryoides looks like grapes from vaginal lining or from the cervix. CT or MRI of pituitary, abdomen, pelvis for pituitary, ovarian, adrenal tumor, which may secrete estrogen.
307
What are the causes of irregular vaginal bleeding in the reproductive age?
A patient with irregular bleeding during the reproductive age group should be considered for pregnancy or complications of pregnancy, anatomic causes of bleeding, or anovulation.
308
How is abnormal vaginal bleeding diagnosed?
If reproductive age, pregnancy or a complication of pregnancy must be ruled out. Complications of early pregnancy that are associated with bleeding include incomplete abortion, threatened abortion, ectopic pregnancy, and hydatidiform mole.
309
What are the anatomic causes of abnormal vaginal bleeding?
Vaginal lacerations, tumors, cervical polyps, cervicitis, tumors, submucous leiomyomas, polyps, hyperplasia, cancer, or adenomyosis.
310
What is dysfunctional uterine bleeding?
If the pregnancy test is negative and there are no anatomic causes of abnormal vaginal bleeding, then hormonal imbalance (DUB) is a probable cause.
311
What are the causes of dysfunctional uterine bleeding?
The most common cause of DUB is anovulation. Anovulation results in unopposed estrogen. With unopposed estrogen, there is continuous stimulation of the endometrium with no secretory phase.
312
How is anovulation diagnosed?
History of irregular, unpredictable menstrual bleeding without cramping. Cervical mucus will be clear, thin, and watery. Basal–body temperature chart will not show midcycle temperature rise. Endometrial biopsy will show proliferative.
313
What is the management of dysfunctional uterine bleeding?
Cyclic progestin from day 14 to 25 of each cycle or daily combination oral contraceptive pills. Progesterone (or progestins) stabilize the endometrium in the latter half of the cycle and prevent random breakdown. Check TSH and prolactin.
314
What is primary amenorrhea?
Menstrual bleeding has never occurred. Primary amenorrhea is diagnosed with absence of menses at age 14 without secondary sexual development or absence of menses at age 16 with secondary sexual development.
315
What is the triad of imperforate hymen?
Primary amenorrhea. Normal breasts and uterus. Normal height and weight.
316
What are the causes of primary amenorrhea?
The two main categories are anatomic (e.g., vaginal agenesis/septum, imperforate hymen, or Mullerian agenesis) or hormonal (e.g., complete androgen insensitivity, gonadal dysgenesis [Turner syndrome], or hypothalamic–pituitary insufficiency).
317
What is the clinical evaluation of a amenorrhea?
Presence of breasts indicates adequate estrogen production. Absence of breasts indicates inadequate estrogen exposure. An ultrasound of pelvis should be performed to assess presence of a normal uterus.
318
What is the differential diagnosis of amenorrhea if breasts are present and uterus present?
If breasts present, uterus present, the differential diagnosis includes imperforate hymen, a vaginal septum, anorexia nervosa, excessive exercise, the possibility of pregnancy before the first menses.
319
What is the differential diagnosis of amenorrhea if breasts are present and uterus is absent?
If breasts present, uterus absent, the differential diagnosis is Mullerian agenesis and complete androgen insensitivity (testicular feminization). Testosterone levels and karyotype make the diagnosis.
320
What is Mullerian agenesis?
Genetically normal females (46,XX) with absence of fallopian, uterus, cervix, upper vagina. Lower vagina is normal. Normal secondary sexual characteristics because ovarian function is intact. Normal pubic hair. T levels are normal female.
321
What is the management of Mullerian agenesis?
Treated with surgical elongation of the vagina.
322
What is androgen insensitivity syndrome?
Genetic male (46,XY) with lack of androgen receptor function. Genitalia differentiate female. Patients are brought up as girls. Primary amenorrhea at puberty. Female secondary sexual characteristics because testes secrete estrogens.
323
What are the pubic hair and axillary hair characteristics in androgen insensitivity syndrome?
No pubic or axillary hair. Testosterone level is normal male.
324
What is the management of androgen insensitivity syndrome?
These women should have their testes removed at the age of 20 because the higher temperatures associated with the intraabdominal position of the testes may lead to testicular cancer. Estrogen replacement is then needed.
325
What are the causes primary amenorrhea with breasts absent, uterus present?
Differential diagnosis is gonadal dysgenesis (Turner syndrome) and hypothalamic–pituitary failure. FSH level and karyotype make the diagnosis.
326
What is gonadal dysgenesis?
Turner syndrome (45,X) is caused by the lack of one X chromosome, develop streak gonads. FSH levels are elevated because of lack of estrogen feedback to the hypothalamus and pituitary. No secondary sexual characteristics.
327
What is the management of Turner syndrome?
Estrogen and progesterone replacement for development of the secondary sexual characteristics.
328
What is hypothalamic–pituitary failure?
Amenorrhea from stress, anxiety, anorexia nervosa, excessive exercise. Low FSH. Absence of secondary sexual characteristics but uterus present. Kallmann is inability of hypothalamus to produce GnRH and anosmia. Imaging will rule out a brain tumor.
329
What is the management of hypothalamic–pituitary failure?
Estrogen and progesterone replacement for development of the secondary sexual characteristics.
330
What is the triad of Müllerian agenesis?
Primary amenorrhea. Breasts present but uterus absent. Absence of pubic and axillary hair.
331
What is the triad of androgen insensitivity?
Primary amenorrhea. Breasts present but uterus absent. Absence of pubic and axillary hair.
332
What is the triad of gonadal dysgenesis?
Primary amenorrhea. Breasts absent but uterus present. Increased FSH levels.
333
What is the triad of hypothalamic–pituitary failure?
Primary amenorrhea. Breasts absent but uterus present. Decreased FSH levels.
334
What is the triad of Kallmann syndrome?
Primary amenorrhea. Breasts absent but uterus present. Anosmia.
335
What is secondary amenorrhea?
Absence of menstrual bleeding after menstrual bleeding previously occurred.
336
What is the diagnostic criteria for secondary amenorrhea?
Diagnosed absence of menses for 3 months if previously regular menses or 6 months if previously irregular menses.
337
What are the causes of secondary amenorrhea?
Hypogonadotropic (suggesting hypothalamic or pituitary dysfunction), hypergonadotropic (ovarian follicular failure), and eugonadotropic (pregnancy, anovulation, or uterine or outflow tract pathology).
338
What is the first step in the evaluation of secondary amenorrhea?
Rule–out pregnancy. The first step in the evaluation of a patient with amenorrhea is a beta–hCG to diagnose pregnancy, which is the most common cause of secondary amenorrhea.
339
What are the signs of anovulation?
If no corpus luteum produces progesterone, progesterone–withdrawal bleeding will not occur. Anovulation is associated with unopposed estrogen stimulation of endometrium. Initially amenorrhea, but as endometrial hyperplasia develops, irregular bleeding.
340
What are the causes of anovulation?
Polycystic ovary syndrome, hypothyroidism, pituitary adenoma, elevated prolactin, and medications (e.g., antipsychotics, antidepressants).
341
What is the triad of anovulatory bleeding?
Irregular, unpredictable vaginal bleeding. Adolescent. Normal height and weight.
342
What are the causes of estrogen deficiency?
Without adequate estrogen priming the endometrium will be atrophic. The causes of hypoestrogenic states are absence of functional ovarian follicles or hypothalamic–pituitary insufficiency.
343
What are the causes of outflow tract obstruction?
Even with adequate estrogen stimulation and progesterone withdrawal, menstrual flow will not occur if the endometrial cavity is obliterated or stenosis of thelower reproductive tract is present.
344
What is the evaluation of secondary amenorrhea?
First step is qualitative beta–hCG test to rule out pregnancy. If beta–hCG is negative, hypothyroidism and hyperprolactinemia should be ruled out with TSH and prolactin.
345
What medications may cause amenorrhea?
An elevated prolactin level may be caused by antipsychotic medications or antidepressants, which have an anti–dopamine side effect (the hypothalamic prolactin–inhibiting factor is dopamine).
346
What test should be done if the prolactin level is elevated?
Pituitary tumor should be ruled out with MRI. If a pituitary tumor is 1 cm, surgery is indicated. If hyperprolactinemia is idiopathic, treatment is bromocriptine.
347
What is the next step in the evaluation of secondary amenorrhea if the beta–hCG is negative, and the TSH and prolactin levels are normal?
Progesterone Challenge Test administers either a single IM dose of progesterone or 7 days of oral medroxyprogesterone acetate . Positive PCT is any withdrawal bleeding and is diagnostic of anovulation.
348
What is the treatment of anovulation?
Cyclic MPA is required to prevent endometrial hyperplasia. Clomiphene ovulation induction will be required if pregnancy is desired.
349
What are the possible causes of secondary amenorrhea if the progesterone challenge test is negative?
Negative PCT: absence of withdrawal bleeding is caused by either inadequate estrogen priming of the endometrium or outflow tract obstruction.
350
What is the evaluation of secondary amenorrhea if the progesterone challenge test is negative?
Estrogen–Progesterone Challenge Test (EPCT). If the PCT is negative, then administer 21 days of oral estrogen followed by 7 days of medroxyprogesterone acetate.
351
What is the cause of a positive estrogen–progesterone challenge test?
Positive EPCT is any degree of withdrawal bleeding and is diagnostic of inadequate estrogen. An FSH level will help identify the etiology.
352
What are the causes of an elevated follicle stimulating hormone?
Elevated FSH suggests ovarian failure. If before 25 years, the cause could be Y chromosome mosaicism; therefore, order a karyotype. Resistant ovary syndrome: follicles in ovary by sonogram, but follicles do not respond to gonadotropins.
353
What are the causes of a low FSH?
A low FSH suggests hypothalamic–pituitary insufficiency. CNS imaging should be performed to rule out a brain tumor. Women with a positive EPCT will need estrogen–replacement therapy to prevent osteoporosis.
354
What are the causes of a negative estrogen–progesterone challenge test?
Absence of withdrawal bleeding is diagnostic of either an outflow tract obstruction or endometrial scarring. Hysterosalpingogram shows lesion. Asherman results from curettage or adhesions caused by infection (treated hysteroscopic lysis).
355
What is the diagnostic criteria for precocious puberty?
Female secondary sexual characteristics and accelerated growth before age 8 in girls and before age 9 in boys. Precocious puberty is more common in girls than boys.
356
What is the most common initial pubertal change in girls?
The most common initial change is thelarche (breast development at 9–10 years of age). This is followed by adrenarche (pubic and axillary hair at 10–11 years).
357
What age is associated with the maximal growth rate in girls?
Maximal growth rate occurs between ages 11 and 12 years.
358
What is the usual age of menarche?
The last change of puberty is menarche, which is onset of menses at age 12–13 years.
359
What is the triad of McCune–Albright syndrome?
Precocious complete isosexual puberty. 6–year–old girl. Cafe–au–lait skin lesions.
360
What is the triad of granulosa cell ovarian tumor?
Precocious complete isosexual puberty. 6–year–old girl. Pelvic mass.
361
What is incomplete isosexual precocious puberty?
Only one change of puberty occurs early – either thelarche, adrenarche, or menarche. This condition is the result of a transient hormone elevation or unusual end–organ sensitivity. Management is conservative.
362
What is complete isosexual precocious puberty?
All changes of puberty occur early, including breasts, growth spurt, menstrual bleeding. Premature closure of epiphyses causes short stature. Fertility and sexual response not impaired. Premature release of gonadotropins.
363
What is the most common cause of precocious puberty?
Constitutional without pathology, 80%. The patient is 6 or 7 years. The diagnosis is one of exclusion after CNS imaging is normal. Management is GnRH agonist suppression (leuprolide or Lupron) of gonadotropins until appropriate maturity or height.
364
What are the CNS pathologies that may cause precocious puberty?
Rare CNS pathologic processes that stimulate hypothalamic release of GnRH include hydrocephalus, von Recklinghausen disease, meningitis, sarcoid, and encephalitis. CNS imaging is abnormal. Patient is usually
365
What is McCune–Albright syndrome?
Characterized by autonomous stimulation of aromatase production of estrogen by ovaries. Multiple cystic bone lesions and café au lait skin spots. Accounts for 5% of precocious puberty. Management is aromatase inhibitor.
366
What type of ovarian tumor is associated with precocious puberty?
Granulosa cell tumor is rare cause of precocious puberty that autonomously produces estrogen. Management is surgical removal of the tumor.
367
What are the symptoms of premenstrual syndrome?
Fluid retention (bloating, edema, breast tenderness), autonomic changes (insomnia, fatigue, heart pounding), crying, anxiety, depression, mood swings, headache, muscle aches, joint aches.
368
What is criteria for premenstrual dysphoric disorder?
Last week of luteal: depression, hopelessness, anxiety, affective lability, irritability, decreased interest. Difficulty concentrating, fatigability, appetite change, insomnia. Breast tenderness/ swelling, headaches, joint/muscle pain, bloating, wt gain.
369
What is the treatment of premenstrual syndrome?
Selective serotonin reuptake inhibitors. Fluoxetine (Prozac); alprazolam, GnRH agonists, buspirone (BuSpar). Yaz (drospirenone/ethinyl estradiol), with the progestin, drospirenone. Yaz is combination OCP with 24 hormone days. 4 hormone–free days.
370
What is hirsutism?
Excessive male–pattern hair growth in a woman on the upper lip, chin, chest, abdomen, back, and proximal extremities.
371
What is virilization?
Excessive male–pattern hair growth in a woman plus clitorimegaly, baldness, lowering of voice, increasing muscle mass, or loss of female body contours.
372
What is the pathophysiology of hirsutism?
Vellus hair (fine, nonpigmented hair) converts to terminal hair (coarse, dark hair) because of androgens. In women, androgens are produced in the ovaries, the adrenal glands, and within the hair follicle.
373
What is the laboratory evaluation of hirsutism?
Dehydroepiandrosterone, 17 hydroxy progesterone, testosterone.
374
What is dehydroepiandrosterone sulfate?
DHEAS is produced only in the adrenal glands and an elevation is consistent with an adrenal tumor.
375
What is17–hydroxy progesterone?
Precursor of cortisol. Elevated in late–onset congenital adrenal hyperplasia (CAH), with 21 –hydroxylase deficiency. Converted peripherally into androgens.
376
What disorder is associated with a mildly elevated testosterone level in a female?
Testosterone is produced by both the ovary and the adrenal glands. A mildly elevated level is suggestive of polycystic ovary syndrome. A markedly elevated level indicates an ovarian tumor.
377
What is the presentation of adrenal tumors?
Rapid onset of virilization without a positive family history. Pelvic examination is unremarkable. DHEAS level is markedly elevated. CT scan will show an abdominal–flank mass. Treatment is removal of tumor.
378
What is the triad of adrenal tumor?
Abrupt–onset of virilization. Abdominal/flank mass. Increased DHEAS levels.
379
What is the presentation of ovarian tumor?
Rapid onset of virilization without positive family history with an adnexal mass. Testosterone is markedly elevated. Pelvic ultrasound will show an adnexal mass. Management is removal of the mass.
380
What is the presentation of congenital adrenal hyperplasia?
21–hydroxylase deficiency has a gradual onset in the second or early third decade with menstrual irregularities and anovulation. Precocious puberty with short stature. Family history may be positive. Late–onset CAH is a common autosomal recessive.
381
What are the signs of congenital adrenal hyperplasia?
Hirsutism without virilization. Pelvic examination is unremarkable. Serum 17–OH progesterone level is markedly elevated.
382
What is the management of congenital adrenal hyperplasia?
Continuous corticosteroid replacement, which will arrest the signs of androgenicity and restore ovulatory cycles.
383
What is the triad of Sertoli–Leydig tumor?
Abrupt–onset of virilization. Pelvic mass. Increased testosterone.
384
What is the triad of congenital adrenal hyperplasia 21–hydroxylase deficiency?
Gradual–onset hirsutism. Normal exam. Increased 17–OH progesterone.
385
What is the presentation of polycystic ovarian syndrome?
Gradual onset of hirsutism, frequently with a positive family history. Irregular bleeding and infertility. Obesity and increased acne. Bilaterally enlarged, smooth, mobile ovaries on pelvic examination. Acanthosis nigricans may be seen.
386
What are the laboratory abnormalities of polycystic ovarian syndrome?
Testosterone is mildly elevated. LH to FSH ratio is elevated (3:1). Sex hormone binding globulin (SHBG) is decreased. Pelvic ultrasound will show bilaterally enlarged ovaries with multiple subcapsular cystic follicles.
387
What is the management of polycystic ovarian syndrome?
Combination OCPs will lower free testosterone levels by suppressing LH stimulation of the ovarian follicle theca cells. Metformin can decrease insulin resistance and lower testosterone levels.
388
What is the presentation of idiopathic hirsutism?
Gradual onset of hirsutism, frequently with a positive family history. Menses and fertility are normal. Idiopathic hirsutism is the most common cause of androgen excess in women.
389
What are the laboratory findings in idiopathic hirsutism?
Normal levels of testosterone, DHEAS, and 17–OH progesterone.
390
What is the management of idiopathic hirsutism?
Spironolactone, an androgen–receptor blocker. Eflornithine (Vaniqa) is a topical drug for unwanted facial hair. It blocks ornithine decarboxylase, which slows the growth of the cells within the hair follicles.
391
What is the triad of idiopathic hirsutism?
Gradual–onset hirsutism. Normal exam. Normal DHEAS, testosterone, 17–OH progesterone.
392
A 30–year–old woman with vaginal bleeding, excessive facial hair, obesity, and enlarged bilateral ovaries. What is the diagnosis?
Polycystic ovarian syndrome.
393
What is polycystic ovarian syndrome (PCOS)?
Chronic anovulation with infertility. Irregular vaginal bleeding, obesity, and hirsutism.
394
What is the pathophysiology of polycystic ovary syndrome?
Chronic anovulation. There is no corpus luteum to produce progesterone. Endometrium is chronically stimulated by estrogen, without progesterone maturation. Endometrium is hyperplastic with irregular bleeding; can progress to cancer.
395
What hormonal abnormalities are associated with polycystic ovary syndrome?
Increased T. Increased LH causes increased ovarian follicular theca cell androgens. Increased androstenedione and T. PCOS is a common cause of hirsutism in women. Increased androgens prevent normal follicular development. Multiple cystic follicles.
396
How is polycystic ovarian syndrome diagnosed?
LH to FSH ratio is in the range of 3:1. The normal LH to FSH ratio in ovulatory patients is 1.5:1.
397
What is infertility?
Inability to achieve pregnancy after 12 months of unprotected and frequent intercourse. Both male and female factors should be evaluated in the patient with infertility. Fifteen percent of American couples have infertility.
398
What is fecundability?
Likelihood of conception occurring with one cycle of appropriately timed midcycle intercourse. A female age 20 years has a fecundity rate of 20%. By age 35 years, the rate drops to 10%.
399
What are the normal semen analysis values?
Volume >2 ml; pH 7.2–7.8; sperm density >20 million/ml; sperm motility >50%; and sperm morphology >50% normal. If values are abnormal, repeat the semen analysis in 4–6 weeks because semen quality varies with time.
400
What is the first step in the infertility evaluation?
Semen analysis, which should be obtained after 2–3 days of abstinence and examined within 2 h.
401
What is the management of minimally abnormal semen?
If sperm density is low, intrauterine insemination may be used. Washed sperm are directly injected into uterus. Idiopathic oligozoospermia is most common male infertility. Intracytoplasmic sperm injection, in vitro fertilization, embryo transfer.
402
What is the presentation of anovulation?
Irregular, menstrual bleeding with minimal or no uterine cramping. Basal body temperature will not show the normal mid–cycle temperature elevation. Progesterone will be low. Endometrial biopsy shows proliferative histology.
403
What are the correctable causes of anovulation?
Hypothyroidism or hyperprolactinemia are causes of anovulation that can be treated.
404
What is the treatment of anovulatory infertility?
Clomiphene administered orally for 5 days beginning on day 5 of the menstrual cycle. Clomiphene blocks estrogen receptors at pituitary, stimulating the pituitary to produce high levels of gonadotropins. HMG induces ovulation.
405
What is the next step in the fertility evaluation if semen analysis and ovulation are normal?
If semen is normal and ovulation is confirmed, assess fallopian tube abnormalities with hysterosalpingogram. Contrast should spill into peritoneal cavity. Scheduled during the week after end of menses after prophylactic antibiotics.
406
What is unexplained infertility?
Couples in which the semen analysis is normal, ovulation is confirmed, and patent oviducts are noted.
407
What is the management of unexplained infertility?
Ovarian hyperstimulation with clomiphene, and appropriately timed preovulatory intrauterine insemination. Fecundity rates for 6 months are comparable with IVF with a significantly lower cost and risk.
408
What is menopause?
3 months of amenorrhea with elevation of gonadotropins (FSH and LH). The mean age of 51 years. Smokers experience menopause up to 2 years earlier.
409
What is premature menopause?
Menopause occurs between 30 and 40 yrs. Mostly idiopathic, but can also occur after radiation. Premature ovarian failure occurs before age 30 years and may be associated with autoimmune disease or Y chromosome mosaicism.
410
What are the clinical findings in menopause?
Amenorrhea. Menses become anovulatory perimenopause. Hot flashes. Decreased vaginal lubrication, increased pH, vaginal infections. Urgency, frequency, nocturia, urge incontinence. Sleep disorders, depression. CVS disease, osteoporosis.
411
What are the most common sites of osteoporosis?
The most common anatomic site is in the vertebral bodies, leading to crush fractures, kyphosis, and decreased height. Hip and wrist fractures are the next most frequent sites.
412
How is osteoporosis diagnosed?
The most common method of assessing bone density is with a DEXA scan (dual–energy x–ray absorptiometry). The most common method of assessing calcium loss is 24–h urine hydroxyproline or N–telopeptide.
413
What are the risk factors for osteoporosis?
The most common risk factor is positive family history in a thin, white female. Other risk factors are steroid use, low calcium intake, sedentary lifestyle, smoking, and alcohol.
414
What is the prevention of osteoporosis?
Ca, vitamin D, exercise, eliminate cigarettes/alcohol. Bisphosphates inhibit osteoclasts. Selective estrogen receptor modulators (raloxifene) increase bone density. Estrogen is effective, but not primarily used.
415
What are the contraindications to estrogen replacement therapy?
A personal history of an estrogen–sensitive cancer (breast or endometrium), active liver disease, active thrombosis, unexplained vaginal bleeding.
416
What are the modes of estrogen replacement therapy?
Oral, transdermal, vaginal, or parenteral routes. Women without a uterus can be given continuous estrogen. All women with a uterus should also be given progestin therapy to prevent endometrial hyperplasia. Oral estrogen/ progestin continuously.
417
What are the recommendations for postmenopausal hormone therapy?
The only indication for hormone therapy is vasomotor symptoms. Although HT is effective for prevention of postmenopausal osteoporosis, consider nonestrogen medications first if osteoporosis prevention is the sole reason for using HT.
418
What is the duration of hormone therapy for menopausal symptoms?
Do not exceed 4 years. The increase in breast cancer risk with HT was not found prior to 4 years.
419
What are the alternatives to estrogen for menopausal symptoms?
In patients with contraindications to estrogen, selective estrogen receptor modulators can be used. Tamoxifen is a SERM with endometrial and bone agonist effects, but breast antagonist effects. Raloxifene has bone agonist effects.
420
What hormones cause breast development?
With the beginning of female puberty, release of estrogen–at first alone, and then in combination with progesterone causes breasts to fully mature. This process, on average, takes 3 to 4 years and is usually complete by age 16.
421
What is the composition of the female breast?
About 80–85% of normal breast tissue is fat during the reproductive years. 15 to 20 lobes are divided into lobules containing alveoli of secretory cells with ducts; reservoir under nipple. In nonpregnant, nonlactating breast, alveoli are small.
422
What are be breast changes associated with pregnancy?
During pregnancy, the alveoli enlarge. During lactation, the cells secrete milk substances (proteins and lipids). With the release of oxytocin, the muscular cells surrounding the alveoli contract to express the milk during lactation.
423
What hormones affect the breasts?
E promotes duct growth. Progesterone from corpus luteum, stimulates development of milk–producing alveolar cells. Prolactin, from anterior pit, stimulates milk production. Oxytocin, from posterior pit in response to suckling, causes milk ejection.
424
How is a cystic breast mass diagnosed?
Fine–needle aspiration of the palpable macrocyst can be performed in an office setting. Preaspiration mammography should be obtained. If the cyst disappears and the cytology is benign, no further workup is required.
425
26–year–old woman with bilateral breast tenderness, which fluctuates with menstrual cycle. Breast feels lumpy. Fine–needle aspiration reveals clear fluid followed by resolutions of cysts. What is the diagnosis?
Fibrocystic breast changes
426
How are fibrocystic breast changes diagnosed?
Breast discomfort accompanied by a palpable mass. Fine–needle aspiration can distinguish whether a mass is solid or cystic.
427
What is the management of breast cysts if the mass disappears after aspiration?
If cyst fluid is clear, it may be discarded. If cyst fluid is bloody, fluid should be sent for cytology. If there is no residual mass, the patient may be reexamined in 4–6 weeks for reaccumulation of fluid. If fluid reaccumulates, it should be aspirated.
428
What is the management of breast cysts if the mass persists after aspiration?
A mass that persists requires mammography and excision.
429
How is breast fibroadenoma diagnosed?
Fibroadenomas are the most common breast tumor in adolescence and young women. 15% multiple. Discrete, smooth, rubbery, nontender, freely moveable masses in upper outer quadrant. Association of fibroadenomas with cancer has not been established.
430
What is the management of fibroadenoma of the breast?
The lesion is shelled out" with a surrounding thin rim of breast tissue to avoid the necessity of reexcision in the rare instances when the tumor proves to be a phyllodes tumor."
431
What are mammographic microcalcifications?
Most of these lesions are benign, but 15–20% represent early cancer. An occult lesion requires stereotactic needle localization and biopsy under mammographic guidance.
432
What is the management of a persistent breast mass?
An excisional biopsy is usually recommended in following circumstances: Cellular, bloody cyst fluid. Failure of a suspicious mass to disappear upon fluid aspiration. Bloody nipple discharge. Edema and erythema.
433
How is bloody nipple discharge diagnosed?
Bloody nipple discharge usually results from an intraductal papilloma. The treatment is total excision of the duct and papilloma through a circumareolar incision.
434
What is the epidemiology of breast cancer?
Breast cancer is the most common cancer diagnosed in women. The incidence of breast cancer incidence is 110 cases per 100,000 women.
435
What is the management of breast cancer?
Treatment for most patients with stage I or II breast cancer is breast–conserving therapy with a wide excision, axillary lymph node dissection or sentinel lymph node biopsy, and radiotherapy.
436
What is the most important prognostic factor in breast cancer?
Axillary lymph node status is the most important factor in the prognosis of patients with breast cancer.
437
What is the most common type of breast cancer?
Infiltrating ductal carcinoma: 80% of breast cancers. Unilateral and start as atypical ductal hyperplasia, which may progress to ductal carcinoma in situ, which then may break through basement membrane and progress to invasive ductal carcinoma.
438
What is the second most common breast malignancy?
Infiltrating lobular carcinoma which accounts for 10% of breast cancers. Most are unilateral and start as lobular carcinoma in situ, which then may break through the basement membrane and progress to invasive lobular carcinoma.
439
What is inflammatory breast cancer?
Uncommon breast malignancy characterized by rapid growth with early metastasis. As the lymphatics get blocked, the breast becomes erythematous, swollen and warm to examination. The edematous skin of the breast appears peau d'orange.
440
What is Paget disease of the breast/nipple?
Uncommon breast malignancy. The lesion is pruritic and appears red and scaly, often located in the nipple spreading to the areola. Skin like eczema or psoriasis. Nipple may become inverted and discharge.
441
What are the risk factors for breast cancer risk factors?
BRCA 1 or 2 gene mutation. Ductal or lobular CIS. Atypical hyperplasia. Breast irradiation age
442
What is the management of node–positive early breast cancer?
In patients at moderate or high risk of developing systemic metastasis, it is preferable to give adjuvant therapy, beginning with chemotherapy followed with radiation therapy.
