OB/GYN Shelf Exam
CLINICAL PRESENTATION: 25 y/o F c/o 8 week postpartum with excessive fatigue, weaker
and unsteady over past week. PE: b/l decrease leg weak spot, left side extra than right.
Hyperreflexia of knees b/l.
1. What is the dx?
2 How is this related to being pregnant?
3. Symptoms?
Four. Next step?
MULTIPLE SCLEROSIS: immune mediated inflammatory demyelinating ailment of CNS
-being pregnant is defensive of MS BUT elevated hazard in early postpartum length.
Three. Symptoms: motor weak spot, diplopia, gait distrubance, balance problems, sensory
signs and symptoms in limbs, u/l imaginative and prescient loss, vertigo, bladder disorder
(sclerotic plaques in cerebral cortex = impair UMN that exert inhibition of spinal nerves -->
LMN overactivity --> hyperreflexia, gait disturbance, overactivity if detrusor muscle)
4. Next step: MRI of brain = demyelinating plaques disseminated in area and time
-Also LP: oligoclonal bands and visible evoked potentials
CLNICAL PRESENTATION: 29 y/o F 20 week gestation with prior c-segment has U/S shows
unmarried cephalic fetus at fortieth percentile. Cervical length is four.4 cm and posterior
placenta extends over cervix. What is the dx?
1. What is the dx?
2. Risk factors?
3. Presentation?
4. How to diagnose?
Five. Management?
COMPLETE PLACENTA PREVIA: placenta extends and cowl the cervix
2. Risk elements:
a. Previous placenta previa
,b. Multiple gestation (multiplied placental surface location)
c. Superior maternal age (>35)
d. Prior c-section (uterine scare and exchange in vascularity alters pregnancy implantation)
three. Presentation: maximum are asymptomatic, painless vaginal bleeding > 20 weeks
gestation
four. Dx: Transabdominal U/S --> Transvaginal U/S.
5. Management: habitual OB care (repeat U/S in 3rd trimester) + no intercourse (potential
cervical contact) , no digital cervical examination, inpatient admission if bleeding
-Most resolve spontaneously because of lower uterine phase lengthening or placental
growth toward fundus
-Asymptomatic with continual previa can do schedules csection at 36-37 weeks
-Doppler U/S of umbilical artery to surveillance fetal growth restriction (fetal weight <10th
percentile) --> have excessive hazard of intrauterine fetal demise --> pressing delivery
-Cerclage: treats cervical insufficiency by using reinforcing cervix with suture or artificial tape
(hx of 2d trimester deliveries or short cervix <2.Five cm)
CLINICAL PRESENTATION: 34 y/o F c/o at 38 weeks has SOB. PE: S3. 3/five holosystolic
murmur at apex. Pittting edema over lower extremities. U/A: trace protein. EKG: sinus
tachycardia
1. What is the dx?
2. Presentation?
Three. Risk elements?
4. Diagnosis?
PERIPARTUM CARDIOMYOPATHY: dilated cardiomyopathy in last month of being pregnant
or within 5 months after delivery.
2. Presentation: LVEF <45%, SOB on exertion, secondary mitral regurg, S3
3. Risk factors: maternal age >30, a couple of gestation, eclampsia
four. Diagnosis: transthoracic echo = dilated LT ventricular hollow space with glocal systolic
disorder and EF <45%
,5. Management:
-Diuretics, beta blockers
-If hemodynamically unstable: urgent delivery
CLINICAL PRESENTATION: 24 y/o F c/o with seizure 10 days after NSVD. Had worsening
headache worse when waking up, vomiting, tonic-clonic seizure. Family hx of DVT. PE:
somnolent. B/l papilledema. Noncontrast CT scan: no intracranial hemorrhage or mass
lesions.
1. What is the dx?
2. Presentation?
3. Diagnosis?
4. Treatment?
CEREBRAL VENOUS THROMBOSIS: blood clot in dural sinuses --> obstructs dural venous
drainage from mind --> venous congestions, decreased cerebral perfusion, disrupt BBB,
impair CSF reabsorption --> multiplied ICP
-related to prothrombotic events (postpartum preg, DVT hx)
2. Presentation: headache, accelerated ICP (vomiting, papilledema), seizures,
encephalopathy
3. Diagnosis: head MRI venography (cerebral angiography more invasive and danger of
complications)
4. Treatment: anticoagulation (heparin acutely)
CLINICAL PRESENTATION: 24 y/o F has progestin-conintaing IUD positioned 2 years ago
and amenorrheic for past yr. Pap test: more than one Actinomycin organism
1. Explain pap smear locating
2. Next step?
ACTINOMYCES: gram + facultative anaerobe in GI --> near vagina and anus so can
colonize genital tract in ladies --> can purpose PID in particular in long term IUD use
, 2. Next step: If asymptomatic, have minimal threat of infection 00> keep IU and no further
control
-If pelvic pain, atypical vaginal discharge: IU removal and empiric extensive spec antibiotics
CLINICAL PRESENTATION: 22 y/o F c/o 36 wks gestation with hx of HSV. Non vulvar ache,
pruritic or lesions.
1. What is the following step?
2. Complications?
3. Why?
Four. What could have came about if mother had lively HSV contamination?
HSV infection: management at 36 weeks need antiviral prophylaxis (acyclovir, valacyclovir)
even though they dont have signs
2. Complication: meningoencephalitis, sepsis --> blindness, neurocognitive disability,
seizures
3. Prophylaxis reduces asymptomatic viral dropping and outbreak recurrences + can
nevertheless do vaginal delivery
four. If active infection (painful vesicles on pink base): viral debris shed from infection so do c
segment (can be vertical transmission OR from passage thru birth canal0
CLINICAL PRESENTATION: 15 y/o F c/p with intermittent sharp LLQ pain that radiates to
decrease again. Had nausea, vomiting. Pelvic U/S: 5 cm LT ovarian mass with everyday
ovarian arterial and venous flow. Now in acute distress and sever, regular tenderness to
palpation in LLQ.
1. What is the dx?
2. Presentation?
Three. Management?
PARTIAL OVARIAN TORSION: due to intermittent adnexal rotation round infundibulopelvic
ligament (has ovarian vessels) --> brief ovarian vessel occlusion + pelvic pain from ovarian
ischemia
2. Presentation: nausea, vomiting, intermittent ache that self-resolves (spontaneous
untwisting permits blood waft to go back) --> can end up COMPLETE TORSION: caused by
using physical hobby and extended hazard with ovarian mass which makes untwisting less
in all likelihood. -> gives with sever steady unilateral pelvic pain = ongoing ovarian ischemia
CLINICAL PRESENTATION: 25 y/o F c/o 8 week postpartum with excessive fatigue, weaker
and unsteady over past week. PE: b/l decrease leg weak spot, left side extra than right.
Hyperreflexia of knees b/l.
1. What is the dx?
2 How is this related to being pregnant?
3. Symptoms?
Four. Next step?
MULTIPLE SCLEROSIS: immune mediated inflammatory demyelinating ailment of CNS
-being pregnant is defensive of MS BUT elevated hazard in early postpartum length.
Three. Symptoms: motor weak spot, diplopia, gait distrubance, balance problems, sensory
signs and symptoms in limbs, u/l imaginative and prescient loss, vertigo, bladder disorder
(sclerotic plaques in cerebral cortex = impair UMN that exert inhibition of spinal nerves -->
LMN overactivity --> hyperreflexia, gait disturbance, overactivity if detrusor muscle)
4. Next step: MRI of brain = demyelinating plaques disseminated in area and time
-Also LP: oligoclonal bands and visible evoked potentials
CLNICAL PRESENTATION: 29 y/o F 20 week gestation with prior c-segment has U/S shows
unmarried cephalic fetus at fortieth percentile. Cervical length is four.4 cm and posterior
placenta extends over cervix. What is the dx?
1. What is the dx?
2. Risk factors?
3. Presentation?
4. How to diagnose?
Five. Management?
COMPLETE PLACENTA PREVIA: placenta extends and cowl the cervix
2. Risk elements:
a. Previous placenta previa
,b. Multiple gestation (multiplied placental surface location)
c. Superior maternal age (>35)
d. Prior c-section (uterine scare and exchange in vascularity alters pregnancy implantation)
three. Presentation: maximum are asymptomatic, painless vaginal bleeding > 20 weeks
gestation
four. Dx: Transabdominal U/S --> Transvaginal U/S.
5. Management: habitual OB care (repeat U/S in 3rd trimester) + no intercourse (potential
cervical contact) , no digital cervical examination, inpatient admission if bleeding
-Most resolve spontaneously because of lower uterine phase lengthening or placental
growth toward fundus
-Asymptomatic with continual previa can do schedules csection at 36-37 weeks
-Doppler U/S of umbilical artery to surveillance fetal growth restriction (fetal weight <10th
percentile) --> have excessive hazard of intrauterine fetal demise --> pressing delivery
-Cerclage: treats cervical insufficiency by using reinforcing cervix with suture or artificial tape
(hx of 2d trimester deliveries or short cervix <2.Five cm)
CLINICAL PRESENTATION: 34 y/o F c/o at 38 weeks has SOB. PE: S3. 3/five holosystolic
murmur at apex. Pittting edema over lower extremities. U/A: trace protein. EKG: sinus
tachycardia
1. What is the dx?
2. Presentation?
Three. Risk elements?
4. Diagnosis?
PERIPARTUM CARDIOMYOPATHY: dilated cardiomyopathy in last month of being pregnant
or within 5 months after delivery.
2. Presentation: LVEF <45%, SOB on exertion, secondary mitral regurg, S3
3. Risk factors: maternal age >30, a couple of gestation, eclampsia
four. Diagnosis: transthoracic echo = dilated LT ventricular hollow space with glocal systolic
disorder and EF <45%
,5. Management:
-Diuretics, beta blockers
-If hemodynamically unstable: urgent delivery
CLINICAL PRESENTATION: 24 y/o F c/o with seizure 10 days after NSVD. Had worsening
headache worse when waking up, vomiting, tonic-clonic seizure. Family hx of DVT. PE:
somnolent. B/l papilledema. Noncontrast CT scan: no intracranial hemorrhage or mass
lesions.
1. What is the dx?
2. Presentation?
3. Diagnosis?
4. Treatment?
CEREBRAL VENOUS THROMBOSIS: blood clot in dural sinuses --> obstructs dural venous
drainage from mind --> venous congestions, decreased cerebral perfusion, disrupt BBB,
impair CSF reabsorption --> multiplied ICP
-related to prothrombotic events (postpartum preg, DVT hx)
2. Presentation: headache, accelerated ICP (vomiting, papilledema), seizures,
encephalopathy
3. Diagnosis: head MRI venography (cerebral angiography more invasive and danger of
complications)
4. Treatment: anticoagulation (heparin acutely)
CLINICAL PRESENTATION: 24 y/o F has progestin-conintaing IUD positioned 2 years ago
and amenorrheic for past yr. Pap test: more than one Actinomycin organism
1. Explain pap smear locating
2. Next step?
ACTINOMYCES: gram + facultative anaerobe in GI --> near vagina and anus so can
colonize genital tract in ladies --> can purpose PID in particular in long term IUD use
, 2. Next step: If asymptomatic, have minimal threat of infection 00> keep IU and no further
control
-If pelvic pain, atypical vaginal discharge: IU removal and empiric extensive spec antibiotics
CLINICAL PRESENTATION: 22 y/o F c/o 36 wks gestation with hx of HSV. Non vulvar ache,
pruritic or lesions.
1. What is the following step?
2. Complications?
3. Why?
Four. What could have came about if mother had lively HSV contamination?
HSV infection: management at 36 weeks need antiviral prophylaxis (acyclovir, valacyclovir)
even though they dont have signs
2. Complication: meningoencephalitis, sepsis --> blindness, neurocognitive disability,
seizures
3. Prophylaxis reduces asymptomatic viral dropping and outbreak recurrences + can
nevertheless do vaginal delivery
four. If active infection (painful vesicles on pink base): viral debris shed from infection so do c
segment (can be vertical transmission OR from passage thru birth canal0
CLINICAL PRESENTATION: 15 y/o F c/p with intermittent sharp LLQ pain that radiates to
decrease again. Had nausea, vomiting. Pelvic U/S: 5 cm LT ovarian mass with everyday
ovarian arterial and venous flow. Now in acute distress and sever, regular tenderness to
palpation in LLQ.
1. What is the dx?
2. Presentation?
Three. Management?
PARTIAL OVARIAN TORSION: due to intermittent adnexal rotation round infundibulopelvic
ligament (has ovarian vessels) --> brief ovarian vessel occlusion + pelvic pain from ovarian
ischemia
2. Presentation: nausea, vomiting, intermittent ache that self-resolves (spontaneous
untwisting permits blood waft to go back) --> can end up COMPLETE TORSION: caused by
using physical hobby and extended hazard with ovarian mass which makes untwisting less
in all likelihood. -> gives with sever steady unilateral pelvic pain = ongoing ovarian ischemia
