Internal Medicine
Board Review

Educational Objective:

Differentiate condylomata lata from condylomata acuminata.

Key Point:

Secondary syphilis causes condylomata lata. Human papillomavirus types 6 and 11 (HPV), which is also sexually transmitted, causes condylomata acuminata, or anogenital warts.

Explanation:

Anogenital warts are caused by human papillomavirus (HPV), and more than 30 types of HPV can infect the genital tract. HPV is sexually transmitted, and most cases of infection are asymptomatic, with only 1% resulting in clinically apparent warts. Most visible genital warts are caused by HPV types 6 and 11. Warts may be single or multiple and, depending on their size and location, may be asymptomatic, painful, friable, or pruritic. Diagnosis is made clinically, and a speculum exam is indicated to evaluate the patient for intravaginal and cervical lesions. Biopsy is indicated for warts that are indurated, fixed, ulcerated, or darkly pigmented, or when the diagnosis is questionable.

Treatment for warts is best administered by the patient’s primary care physician and not through the emergency department. Treatment regimens can be patient applied (up to 4 cycles of Podofilox 0.5% BID for 3 days followed by 4 days off for up to four cycles, no therapy, imiquimod 5% cream at HS 3 times/week for up to 16 weeks) or provider applied (cryotherapy, podophyllin resin, trichloroacetic acid, surgical removal).

If left untreated, warts may resolve spontaneously, remain unchanged, or increase in number. The differential diagnosis includes condylomata lata - the lesions of secondary syphilis. They are flatter, paler, and smoother than condylomata acuminata. Anal squamous cell carcinoma is generally painful and may be tender and ulcerated where condylomata are not tender or ulcerated. The condylomata lata of secondary syphilis are occasionally misdiagnosed as HPV infection. Patients presenting with genital warts should be screened for other sexually transmitted infections.

References:

Birnbaumer DM. Sexually Transmitted Diseases. in Rosen's Emergency Medicine. 2014; 98: 1312-1325.

Educational Objective:

Identify the source of amaurosis fugax.

Key Point:

Amaurosis fugax or transient monocular blindness is a manifestation of emboli to the central retinal artery, usually originating from the same side carotid artery.

Explanation:

In this case, the right carotid artery is the most likely origin of an embolus in this patient.

Transient monocular blindness, or amaurosis fugax, is a specific symptom of transient ischemic attack (TIA). It is a result of emboli to the central retinal artery of one eye. The carotid artery on the same side as the symptoms is often at fault. Stroke or TIA in the distribution of the posterior circulation would not produce monocular symptoms, but it would produce gaze palsies and nystagmus. Anterior cerebral artery occlusion is not typically associated with visual symptoms.

References:

Ahmed R, Foroozan R. Transient monocular visual loss. Neurol Clin. 2010;28(3):619-629

Wu TC. Amaurosis Fugax: Physical Findings and Clinical Presentation. Ferri’s Clinical Advisor. 2017: 60-60.e1

Educational Objective:

Recognize pulsus paradoxus in cardiac tamponade.

Key Point:

Pulsus paradoxus, a drop in blood pressure with inspiration, can be found in cardiac tamponade.

Explanation:

A few clues demonstrate that this is cardiac tamponade. The chest pain is sharp and worse upon deep inspiration. The patient has lung cancer, which predisposes him to a large, pericardial effusion (see Figure). He also has pulsus paradoxus, meaning he has a systolic blood pressure that decreases more than 10 mm Hg during inspiration. Pulsus paradoxus can occur with other conditions, such as chronic obstructive pulmonary disease, acute pericarditis, and sleep apnea, but the entire constellation points toward tamponade. Neither pulmonary effusions nor acute MI usually cause pulsus paradoxus. Bacterial pneumonia usually does not cause cardiac effusions.

Figure. A very large, hemorrhagic pericardial effusion due to malignancy can be seen on ultrasonography. Closed arrow: heart; open arrow: effusion.

References:

Longo D, et al. Harrison’s Principles of Internal Medicine. 18th ed., 2012.

Sloane PD, et al. Essentials of Family Medicine. 6th ed., 2012.

Educational Objective:

Describe the risks of pregnancy in patients with PCOS.

Key Point:

Patients with PCOS who become pregnant are at risk for hypertension and pre-eclampsia.

Explanation:

Women with PCOS are at risk for gestational diabetes. They also have a 4-fold increase in the risk of hypertension and pre-eclampsia and are at risk for small for gestational age children (SGA).

References:

ACOG Committee on Practice Bulletins--Gynecology. ACOG practice bulletin no. 108: polycystic ovary syndrome. Obstet Gynecol. 2009;114:936-949.

Palomba S, de Wilde MA, et al. Pregnancy complications in women with polycystic ovary syndrome. Hum.Reprod.Update. 2015; 21: 575-592

Educational Objective:

Manage UTI during pregnancy.

Key Point:

Treatment is required for pregnant women with either UTIs or asymptomatic bacteriuria.

Explanation:

UTI in pregnancy is a common condition and has an overall incidence of about 8%. Hormonal differences coupled with stasis and mild urinary tract dilation secondary to pressure from the gravid uterus increase the likelihood of this condition. Complications of untreated UTI can be serious and include prematurity, low birth weight, and increased perinatal mortality. Maternal complications include preterm labor, increased incidence of hypertension, and chorio-amnionitis.

References:

McCormick T, Ashe RG, Kearney PM. Urinary tract infection in pregnancy. Obstet Gynaecol. 2008;10(3):156-162. 

Mazor-Dray E, Levy A, Schlaeffer F, Sheiner E. Maternal urinary tract infection: is it independently associated with adverse pregnancy outcome? J Matern Fetal Neonatal Med. 2009;22(2):124-128.

Easter SR, Cantonwine DE, Zera CA, Urinary Tract Infection During Pregnancy;  angiogenic factor profiles and risk of preeclampsia. American Journal of Obstetrics and Gynecology. 2016; 214: 381. e1-381. e7