40-year-old woman is brought to the emergency department due to difficulty breathing and muscle weakness. She was one of several people who developed symptoms in a movie theater. Temperature is 36.7 C (98.1 F), blood pressure is 112/62 mm Hg, pulse is 51/min, and respirations are 24/min. On physical examination, the patient is diaphoretic. The pupils are pinpoint and unreactive, and significant tearing is noted. Diffuse rhonchi and wheezing are present in the lungs bilaterally. Muscle strength is diminished throughout, and fasciculations are noted in the extremities. First-line therapy is administered, but the patient remains weak.
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This patient with bradycardia, miosis, diaphoresis, excessive secretions (eg, bronchonhea, tearing), and weakness with fasciculations has signs of cholinergic toxicity. Most cases of cholinergic toxicity are due to organophosphate pesticides. However, the occurrence in multiple patients in a city setting suggests intentional organophosphate exposure, possibly due to a chemical weapon (eg, sarin, soman).

Organophosphates inhibit acetylcholinesterase in the muscarinic and nicotinic cholinergic synapses, leading to decreased acetylcholine degradation and overstimulation of the corresponding receptors. In addition to widespread increased visceral smooth muscle tone and glandular secretions due to muscarinic hyperactivity (mnemonic: DUMBELLS), nicotinic hyperactivity causes muscle weakness and paralysis that can lead to rapid respiratory depression and death.

Initial management of organophosphate toxicity includes atropine, a competitive inhibitor of acetylcholine at the muscarinic receptor, which relieves muscarinic hyperstimulation. However, atropine does not have activity at the nicotinic receptors and cannot treat neuromuscular dysfunction. Therefore, pralidoxime, a cholinesterase- reactivating agent that works at both nicotinic and muscarinic sites, should be administered to any patient with neuromuscular dysfunction (eg, weakness, fasciculations). It should be given only after atropine because

pralidoxime can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms

(Choice A) Diphenhydramine is an inverse agonist of the histamine H1 receptor, which allows it to function as an antihistamine. Because the H1 receptor is similar to the muscannic receptor, diphenhydramine has some antimuscarinic effects (eg, urinary retention). However, it is less potent than atropine, and it would not reverse nicotinic dysfunction (weakness).

(Choice B) Hemodialysis is sometimes used to treat toxic alcohol poisoning, which usually presents with altered mental status, as well as vision changes (methanol) or flank pain and hematuria (ethylene glycol) It is not Indicated in cholinergic toxicity

Choice C) Hyperbaric oxygen is used to treat severe carbon monoxide poisoning, which presents with nausea, dizziness, and altered mental status. Patients typically have cherry-red cheeks and lips.

(Choice D) Physostigmine is an acetylcholinesterase inhibitor that is sometimes used to treat anticholinergic toxicity (le, flushing, mydriasis, anhidrosis, fever, urinary retention). It would worsen this patient's symptoms.

Educational objective:

Organophosphates inhibit acetylcholinesterase, leading to symptoms of muscarinic (mnemonic: DUMBELLS) and nicotinic (neuromuscular dysfunction) cholinergic hyperstimulation. Management includes atropine, a competitive inhibitor of acetylcholine at the muscarinic receptor (reverses muscarinic symptoms), followed by pralidoxime, a cholinesterase-reactivating agent that treats both nicotinic and muscarinic symptoms

A 27-year-old man comes to the office due to a 2-week history of genital papules that are not painful or pruritic. Over this period, he has also had fatigue and mild, generalized arthralgia but no urethral discharge or dysuria. The patient had gonococcal urethritis 3 months ago, which was adequately treated, and tests for other sexually transmitted infections at that time were negative. He is sexually active with several male and female partners and reports using condoms consistently after the episode of gonorrhea. Temperature is 37.6 C (99.6 F). Physical examination shows a faint, diffuse maculopapular skin rash involving the trunk, extremities, palms, and soles. There are several enlarged, nontender inguinal lymph nodes. Genital examination reveals multiple, raised, wart-like skin lesions on the scrotum and perineal region.
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Syphilis manifestations

Primary- Painless genital ulcer (chancre)

secondary- Diffuse rash (palms & soles) ,Lymphadenopathy (epitrochlear),
Condyloma latum,Oral lesions,Hepatitis

Latent-Asymptomatic

Tertiary-CNS (tabes dorsalis, dementia)
• Cardiovascular (aortic aneurysm/insufficiency)
Cutaneous (gummas)

Secondary syphilis is characterized by the spread of the causative spirochete, Treponema pallidum, through the blood to the skin and mucosal surfaces. Patients usually have a diffuse maculopapular skin rash that includes the palms and soles. They may also develop condylomata lata, which are painless, wart-like, elevated plaques, on moist areas of the skin such as the scrotum and perineum. Lymphadenopathy, fatigue, arthralgias, and mild fever are also common. Histopathologic examination of syphilitic lesions (at all stages) classically demonstrates proliferative endarteritis of small vessels with a surrounding plasma cell-rich infiltrate.

This patient was likely infected with syphilis at the same time he was infected with gonorrhea (coinfection is common). Serologic testing for syphilis (eg, rapid plasma reagin) is often falsely negative in early infection due to lag time between acquisition of T pallidum and the development of a measurable humoral antibody response. Patients who do not notice or ignore the genital chancre of primary syphilis often develop secondary syphilis 2-10 weeks later.

Secondary syphilis is characterized by the spread of the causative spirochete, Treponema pallidum, through the blood to the skin and mucosal surfaces. Patients usually have a diffuse maculopapular skin rash that includes the palms and soles. They may also develop condylomata lata, which are painless, wart-like, elevated plaques, on moist areas of the skin such as the scrotum and perineum. Lymphadenopathy, fatigue, arthralgias, and mild fever are also common. Histopathologic examination of syphilitic lesions (at all stages) classically demonstrates proliferative endarteritis of small vessels with a surrounding plasma cell-rich infiltrate.

This patient was likely infected with syphilis at the same time he was infected with gonorrhea (coinfection is common). Serologic testing for syphilis (eg, rapid plasma reagin) is often falsely negative in early infection due to lag time between acquisition of T pallidum and the development of a measurable humoral antibody response. Patients who do not notice or ignore the genital chancre of primary syphilis often develop secondary syphilis 2-10 weeks later.

(Choice A) Pemphigus vulgaris is characterized by autoantibodies against epithelial cell surface antigens, leading to the formation of mucous membrane blisters that quickly erode; histopathology usually shows acantholysis (detached keratinocytes) with superficial dermal infiltrate.

(Choice B) Kaposi sarcoma (KS) lesions appear as whirls of dysplastic spindle-shaped cells surrounding areas of angioproliferation. KS is due to human herpesvirus 8 infection and most commonly occurs in the setting of advanced AIDS. Lesions typically appear as purplish or dark brown plaques and nodules on the lower extremities.

(Choice D) Biopsy of erythema nodosum lesions usually reveals septal panniculitis with multinucleated giant cells. Erythema nodosum is a delayed-type hypersensitivity reaction that can occur due to drugs or other antigenic stimuli. Patients usually present with tender nodules on the bilateral shins.

(Choice E) Biopsy of anogenital warts will demonstrate papillomatous epidermal hyperplasia with cytoplasmic vacuolization. Anogenital warts are caused by specific serotypes of human papillomavirus (eg, HPV-6, HPV-11). Anogenital warts are not typically associated with diffuse maculopapular rash or systemic symptoms.
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A 39-year-old woman, gravida 1 para 1, comes to the office due to breast pain. She had an uncomplicated vaginal delivery a week ago and is breastfeeding her infant. Four days ago, the patient began to have bilateral nipple soreness with breastfeeding. However, for the past few days, the pain has worsened, is present between feeds, and has prevented breastfeeding. She has also developed bloody nipple discharge. The patient's pregnancy was complicated by gestational diabetes mellitus, but otherwise, she has no chronic medical conditions. Temperature is 37.5 C (99.5 F). Bilateral nipples and areolae have open, bloody, linear abrasions. The breasts are diffusely engorged and mildly tender to palpation, but there are no palpable masses or lymphadenopathy. The remainder of the examination is unremarkable.
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Proper breastfeeding technique promotes maternal comfort, ensures adequate infant nutritional intake, and facilitates long-term breastfeeding.

Most breastfeeding patients experience nipple pain in the immediate postpartum period as they become accustomed to nursing 8-12 times/day or more, but this typically resolves after a few weeks. Nipple pain that worsens and persists between feedings is commonly due to nipple injury caused by poor infant positioning and improper latch-on technique. On examination, patients can have open, linear areolar abrasions that cause a bloody-appearing nipple discharge, bruising, cracking, and blistering may also be present. Breast engorgement, as seen in this patient with bilateral, diffusely tender, and engorged breasts, can also develop because nipple pain limits breastfeeding.

Initial management is with the observation of breastfeeding and patient education. Nipple injury is a significant risk factor for multiple adverse outcomes (eg, plugged milk ducts, mastitis, breast abscess), which often lead to premature cessation of breastfeeding.

(Choice A) Lactational mastitis is caused by bacterial overgrowth of stagnant milk in blocked ducts; it is a common cause of breast pain in breastfeeding patients. In contrast to this patient, those with lactational mastitis typically have fever and localized warmth or erythema over a single breast.

(Choice B) Candida mastitis can be caused by spread from infant oral flora. Patients typically have nipple pain that radiates across the breast with latching; however, the pain is described as sharp and shooting and is usually out of proportion to the examination. In addition, it is typically unilateral, and the affected breast often has flaky, scaling skin over the nipple.

(Choice C) Inflammatory breast cancer can cause unilateral, not bilateral, breast pain and tenderness. Patients typically have a breast mass with associated skin thickening and erythema (peau d'orange appearance) with axillary lymphadenopathy, which is not seen in this patient.

(Choice D) An intraductal papilloma, a papillary tumor involving the breast duct, typically presents with bloody nipple discharge but no associated breast pain.

TAKE HOME POINT

Persistent nipple pain with breastfeeding is typically due to nipple injury, which can present with bilateral nipple abrasions and bloody nipple discharge. The most common underlying causes are poor infant positioning and improper latch-on technique.

A 35-year-old man comes to the office due to a progressive increase in breast size over the past 6 months. He is sexually active, has no chronic medical conditions, and takes no medications. The patient does not use tobacco, alcohol, or illicit drugs. Vital signs are normal. BMI is 28 kg/m². Gynecomastia with mild bilateral breast tenderness is present. Genitourinary examination reveals a 1-cm nodule in the right testis. The examination is otherwise normal. Laboratory results are as follows:
LH: 3 U/L (normal: 6–23 U/L)
FSH: 2 U/L (normal: 4–25 U/L)
Testosterone: 270 ng/dL (normal: 300–1,000 ng/dL)
Estradiol: 115 pg/mL (normal: 20–60 pg/mL)
β-hCG: undetectable
Alpha-fetoprotein: undetectable

Malignant testicular neoplasms
Type Features Germ cell (95%)Seminoma• Retain features of spermatogenesis
• β-hCG, AFP usually negative
Nonseminoma• ≥1 partially differentiated cells: yolk sac, embryonal carcinoma, teratoma, and/or choriocarcinoma
• β-hCG, AFP usually positive Stromal (5%)Leydig• Often produces excessive estrogen (gynecomastia) or testosterone (acne)
• Can cause precocious puberty
Sertoli• Rare
• Occasionally associated with excessive estrogen secretion (eg, gynecomastia)
AFP = alpha-fetoprotein.
This patient with a testicular mass, gynecomastia, and elevated estrogen levels likely has a Leydig cell tumor, the most common type of testicular sex cord stromal tumor. These tumors arise from supporting cells of the testis such as Leydig, Sertoli, and granulosa cells; they account for approximately 5% of testicular tumors (germ cell tumors account for ~95%), arise in a wide range of ages, and have no clearly defined risk factors.
Leydig cells are the primary source of testicular testosterone but are also capable of generating estrogen. Therefore, Leydig cell tumors often present with endocrine manifestations due to excessive estrogen (eg, gynecomastia, loss of libido, erectile dysfunction) or testosterone (eg, acne, hirsutism). Examination frequently reveals a testicular mass, which is typically confirmed by bilateral scrotal ultrasound. In contrast to many germ cell tumors, Leydig cells do not generally produce serum tumor markers such as β-hCG or alpha-fetoprotein (AFP). However, the generation of estrogen or testosterone often leads to FSH and LH suppression.
(Choices A, D, and E) Choriocarcinoma, teratoma, and yolk sac tumors are nonseminomatous germ cell tumors. They typically present with a painless, firm testicular mass. However, they often produce β-hCG (particularly choriocarcinoma) or AFP (particularly yolk sac tumors) in addition; estrogen production is rare, so feminization is uncommon.
(Choice C) Seminoma is a germ cell tumor that does not usually produce β-hCG, AFP, or estrogen. Therefore, feminization would be atypical. Most seminomas present with a painless, unilateral testicular mass or swelling.


TAKE HOME MESSAGE
Leydig cell testicular tumors often cause feminization (eg, gynecomastia) due to the production of estrogen by tumor cells. This frequently causes secondary inhibition of FSH and LH. Serum tumor markers (eg, β-hCG, AFP) are not usually elevated.