Daiquiris and Dermatology: Recent Episodes
Habib Olapade
This episode covers plantar fasciitis!
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This episode covers osteochondritis dissecans!
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This episode covers ankle sprains!
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This episode covers osgood schlatter disease!
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This episode covers ACL injuries!
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This episode covers PCL injuries!
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This episode covers meniscal tears!
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This episode covers medial tibial stress syndrome!
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This episode covers patellar tendinopathy!
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This episode covers nail bed injuries!
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This episode covers lateral and medial epicondylitis!
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This episode covers kienbock's disease!
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This episode covers rotator cuff impingement!
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This episode covers bicep long head ruptures!
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This episode covers de Quervain's tenosynovitis!
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This episode covers clavicle fractures!
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This episode covers scabies!
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This episode covers pruritus!
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This episode covers pediculosis!
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This episode covers corticosteroids!
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This episode covers thallium poisoning!
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This episode covers antimony poisoning!
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This episode covers mercury poisoning!
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This episode covers aluminum poisoning!
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This episode covers chloromethyl ether poisoning!
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This episode covers zinc poisoning!
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This episode covers vanadium poisoning!
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This episode covers dibromochloropropane poisoning!
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This episode covers hepatitis A!
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This episode covers metacarpal head fractures!
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This episode covers hepatitis B!
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This episode covers distal phalanx fractures!
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This episode covers arsine poisoning!
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This episode covers selenium and tellurium poisoning!
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This episode covers nickel poisoning!
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This episode covers cadmium poisoning!
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This episode covers injuries caused by ultraviolet radiation!
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This episode covers injuries caused by ionizing radiation!
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This episode covers alkaline phosphatase tests for liver disease!
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This episode covers ulnar neuropathy!
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This episode covers reproductive assessments!
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This episode covers hexacarbons!
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This episode covers heat syncope!
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This episode covers heat exhaustion!
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This episode covers frontal sinus fractures!
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This episode covers nasoethmoidal complex fractures!
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This episode covers high pressure injection injuries!
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This episode covers cardiovascular abnormalities caused by organic nitrates!
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This episode covers beryllium poisoning!
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This episode covers osteochondral lesions of the talar bone!
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This episode covers heat cramps!
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This episode covers tests of ocular motility!
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This episode covers retina injuries!
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This episode covers occlusion of the central retinal vein!
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This episode covers iris injuries!
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This episode covers sickle thalassemia!
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This episode covers epidermal inclusion cysts!
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This episode covers postmenopausal vaginal bleeding!
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This episode covers granuloma inguinale!
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This episode covers infections caused by moraxella catarrhalis!
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This episode covers erysipelas!
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This episode covers seafood poisoning!
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This episode covers hives and angioedema!
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This episode covers erythema multiforme and stevens johnson syndrome!
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This episode covers mycetoma!
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This episode covers pigmentary disorders!
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This episode covers pulmonary alveolar proteinosis!
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This episode covers hyperventilation syndrome!
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This episode covers bronchial carcinoid tumors!
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This episode covers pulmonary infiltrates in immunocompromised patients!
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This episode covers colorado tick fever!
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This episode covers cholera!
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This episode covers pinguecula and pterygium!
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This episode covers corneal ulcers!
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This episode covers mucocutaneous candidiasis!
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This episode covers rosacea!
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This episode covers herpes zoster!
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This episode covers cellulitis!
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This episode covers olfactory dysfunction!
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This episode covers chlamydophila psittaci and psittacosis!
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This episode covers lichen planus!
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This episode covers alopecia!
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Hemolytic anemias are a group of disorders where red blood cell survival is reduced either continuously or episodically. Because a patient’s bone marrow has the ability to increase erythroid production up to eighteen times in response to reduced red blood cell survival, a patient will only present with anemia when the patient’s bone marrow production is outstripped. This will occur when red blood cell survival is extremely short or when the bone marrow’s ability to compensate is impaired. Hemolytic disorders are generally classified based on whether the defect is intrinsic to the red blood cell or due to some external factor. Certain laboratory features are common to all hemolytic anemias. To take just a few examples, Haptoglobin, a normal plasma protein that binds and clears free hemoglobin released into plasma, may be depressed in hemolytic disorders. Haptoglobin levels, though, are influenced by many factors and may not be a reliable indicator of hemolysis – particularly in end-stage liver disease. When intravascular hemolysis occurs, transient hemoglobinemia ensues. Here, hemoglobin is filtered through the renal glomerulus and is usually reabsorbed by tubular cells. Hemoglobinuria will be present only when the patient’s capacity for reabsorption of hemoglobin by renal tubular cells is exceeded, In the absence of hemoglobinuria, evidence for prior intravascular hemolysis is the presence of hemosiderin in shed tubular cells. With severe intravascular hemolysis, hemoglobinemia and methemsalbuminemia may be present. Hemolysis increases indirect bilirubin levels and the total bilirubin may rise to 4mg/dL or more. Bilirubin levels higher than this may indicate some degree of hepatic dysfunction.
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Tuberculous meningitis can be caused either by miliary spread or by a rupture of the meningeal tuberculoma that results from an earlier hematogenous seeding of tubercle bacilli from a pulmonary focus. The onset of the malady is usually gradual with the patient presenting with fever, anorexia, irritability, and listlessness followed by coma, convulsions, vomiting, and headache. In older patients, behavioral changes and headache are prominent early symptoms. Cranial nerve palsies and nuchal rigidity also occur as the meningitis progresses. A prior history of tuberculosis or evidence of active tuberculosis is present in about three out of four patients. In diagnosing the patient, the spinal fluid is often yellowish with increased pressure, contains more protein than usual and less glucose than usual, and has a lymphocyte cell count around 100-500 cells/mcL. In treating the disease, presumptive diagnosis followed by early, empiric antituberculosis is critical to ensure the patient’s survival. Even if the patient’s cultures are not positive, a full course of therapy is warranted if the clinical setting is suggestive of tuberculous meningitis. Regimes that are effective for pulmonary tuberculosis are also effective for tuberculous meningitis. Many authorities, though, recommend the addition of corticosteroids for patients with focal deficits or altered mental status. The drug of choice here is Dexamethasone (.15 mg/kg administered intravenously or orally five times a day for one to two weeks).
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This episode covers vitamin c deficiency!
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This episode covers folliculitis!
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Thyroglossal duct cysts occur along the embryologic course of the thyroid’s descent from the tuberculum impar of the tongue base to its usual position in the lower neck. Although they may occur at any age, they are most common before age 20. They present as a midline neck mass which is often just below the hyoid bone. Surgical excision is recommended to prevent recurrent infection. This requires removal of the entire fistulous tract along with the middle portion of the hyoid bone through which many of the fistulas pass. Preoperative evaluation should include a thyroid ultrasound to confirm the anatomic position of the thyroid.
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Branchial cleft cysts usually present as a soft cystic mass along the anterior border of the sternocleidomastoid muscle. These lesions are usually recognized in the second or third decade of the patient’s life when they suddenly swell or become infected. To prevent recurrent infection and possible carcinoma, they should be completely excised with their fistulous tracts. First branchial cleft cysts present high in the neck, sometimes just below the ear. A fistulous connection with the floor of the external auditory canal may be present. Second branchial cleft cysts, which are more common, may communicate with the tonsillar fossa. Finally, third branchial cleft cysts, which may communicate with the piriform sinus, are also rare and present low in the neck.
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Granulomatous neck masses are rather common. The differential diagnosis here includes mycobacterial adenitis, sarcoidosis, and cat-scratch disease due to Bartonella henselae. The incidence of mycobacterial lymphadenitis, however, is on the rise among both immunocompromised and immunocompetent individuals. The usual presentation of granulomatous disease in the neck is simply single or matted nodes. Although mycobacterial adenitis can extend to the skin and drain externally, this presentation is rather rare. FNA biopsy is usually the best initial diagnostic approach. Here, cytology, a smear for acid-fast bacilli, a mycobacterial culture, and a sensitivity test can all be done. PCR from FNA is the most sensitive test and is particularly useful when conventional methods have not been diagnostic but the practitioner’s clinical impression remains consistent for tuberculosis infection. While FNA has a high sensitivity (about 88%), its specificity is low (49%) and an excisional biopsy is often required to confirm the diagnosis. For atypical lymphadenopathy, treatment depends on the sensitivity results of the culture. Antibiotics, however, such as isoniazid (six months standard dosage) and rifampin (two months of the standard dosage) tend to be effective.
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Normal lymph nodes in the neck are usually less than 1 cm in length. Infections involving the pharynx, salivary glands, and scalp often cause tender enlargement of neck nodes. Indeed, enlarged nodes are common in HIV-infected persons. Except for the occasional node that suppurates and requires incision and drainage, treatment is directed against the underlying infection. An enlarged node (larger than 1.5 cm) or node with a necrotic center that is not associated with an obvious infection should be evaluated further especially if the patient has a history of prior cancer, alcohol use, or smoking. Other common indicators for FNA biopsy of a node include its persistence or continued enlargement. On the other hand, common causes of cervical adenopathy include squamous cell carcinoma, lymphoma, occasional metastases from non-head and neck sites, and infection. While rare, adenopathy can also be caused by Kikuchi disease and autoimmune adenopathy.
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Miliaria can typically be found on the patient’s intertriginous areas and trunk. The malady is usually caused by prolonged exposure to a moist, hot environment. Risk of contraction can also be increased by occlusive clothing. Here, the sweat ducts’ ostia are plugged leading to the ultimate rupture of the sweat duct and a stinging, irritating reaction. The typical symptoms are itching and burning. The sweat gland obstruction’s histologic depth determines the clinical presentation. Obstruction in the superficial epidermis, deep epidermis, and dermis is referred to as miliaria crystallina, miliaria rubra, and miliaria profunda respectively. The lesions from this disease are usually non-follicular and between 1 to 3 millimeters in diameter. Miliaria can be prevented with topical antibacterial cream such as chlorhexidine and, if the patient has been hospitalized, miliaria on her back can be reduced by turning her over frequently. For treatment, the patient should be kept cool and wear light clothing. Triamcinolone acetonide, 0.1% in Sarna lotion, or mid-potency corticosteroid lotion or cream can be prescribed for application twice or four times each day. Secondary infections are treated with antistaphylococcal antibiotics (anticholinergic medication can be ordered in severe cases).
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Erythema nodosum is a symptom complex characterized by tender erythematous nodules that typically appear on the extensor surfaces of the lower legs (but can appear on the arms, face, and trunk). The lesions should range in color from pink to red and be between 1-10 centimeters in diameter. The malady usually lasts for six weeks and can be associated with pregnancy, oral contraceptive use, primary coccidioidomycosis, streptococcosis, tuberculosis, syphilis, diverticulitis, Y enterocolitica, Yersinia pseudotuberculosis, and other deep fungal infections. Erythema nodosum can also be accompanied by inflammatory bowel disease, Behcet disease, or sarcoidosis. The tender erythematous nodules can be preceded by arthralgia, malaise, and fever. The practitioner should evaluate the patient’s medication exposure history, and conduct a physical examination for a chest radiograph, a PPD, two consecutive ASO/DNAse B titers at 2 to 4 week intervals, diarrheal illness, symptoms of any deep fungal infection specific to the area, and prior upper respiratory infection. In its late stages, erythema nodosum must be distinguished from simple contusions and bruises. The patient can be treated with NSAIDs which typically takes the form of potassium iodide (5-15 drops three times daily), corticosteroid therapy, dapsone, colchicine, or hydroxychloroquine. Complete bed rest should be ordered if the lesions are painful. The reader should note that erythema nodosum differs from other forms of panniculitis in that it does not ulcerate. Erythema induratum from tuberculosis, though, does create lesions on the posterior surface of the legs and can ulcerate.
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Acute otitis media is a bacterial infection of the temporal bone’s mucosally lined air storage spaces typically caused by Streptococcus pneumoniae, Haemophilus influenzae, or Streptococcus pyogenes. The disease is often accompanied by mastoid tenderness caused by the presence of pus in the mastoid air cells. Here, material forms within the middle ear cleft and the pneumatized mastoid air cells and petrous apex. This disease is usually precipitated by a viral upper respiratory tract infection that obstructs the eustachian tube and results in the accumulation of infected fluid and mucous. Key symptoms include fever, decreased hearing, aural pressure, and otalgia accompanied by a physical finding of erythema and decreased tympanic membrane mobility. With appropriate counseling, spontaneous healing of the tympanic membrane occurs in most cases. If, however, the perforation continues for a prolonged period of time, the patient may develop chronic otitis media. Swelling over the mastoid bone or the association of cranial neuropathies or central findings indicates severe illness requiring urgent care. Acute otitis media can often be treated successfully with a combination of antibiotics and nasal decongestants. The antibiotics of choice are frequently amoxicillin (80-90 mg/kg/day divided twice daily), erythromycin with sulfonamide (50 mg/kg/day and 150 mg/kg/day respectively), cefaclor (20-40 mg/kg/day), and amoxicillin-clavulanate (20-40 mg/kg/day). The practitioner should only resort to surgical drainage of the middle ear when the patient suffers from severe otalgia or otitis complications. Reoccurring acute otitis media can be managed with long-term antibiotic prophylaxis (typically single daily doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) over 1 to 3 months). On the other hand, if the otitis media is recurring but the patient is immunocompromised, tympanocentesis can be resorted to.
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Pemphigus is an uncommon intraepidermal blistering disease occurring on the skin and mucous membranes. It is caused by autoantibodies to adhesion molecules expressed in the skin and mucous membranes. The cause is unknown. The bullae appear spontaneously and are tender and painful when they rupture. Drug induced pemphigus from penicillamine, captopril, and others have been reported. There are several forms of pemphigus: pemphigus vulgaris and its variant, pemphigus vegetans; and the more superficially blistering pemphigus foliaceus and its variant, pemphigus erythematosus. All forms may occur at any age, but most present in middle age. The foliaceus form is especially apt to be associated with other autoimmune diseases, or it may be drug induced. Paraneoplastic pemphigus, a unique form of the disorder, is associated with numerous types of benign and malignant neoplasms (typically non-Hodgkin lymphoma). Pemphigus is characterized by an insidious onset of flaccid bullae, crusts, and erosions in crops or waves. In pemphigus vulgaris, lesions often appear first on the oral mucous membranes. These quickly become erosive. The scalp is another site of early involvement. Practitioners can rub a cotton swab or finger laterally on the surface of uninvolved skin which may cause easy separation of the epidermis (this is Nikolsky’s sign). The diagnosis is made with light microscopy and by direct and indirect immunofluorescence (IIF) microscopy. Autoantibodies to intercellular adhesion molecules can be detected with ELISA assays and have replaced the use of IIF in some centers. When the condition is severe, patients should be hospitalized at bed rest and given antibiotics/intravenous feedings. Anesthetic troches used before eating ease painful oral lesions. While pemphigus requires systemic therapy as early as possible, ironically, the main morbidity here is side effects from treatment. Initial therapy with systemic corticosteroids can consist of prednisone (60-80 mg daily). In most cases, a steroid sparing agent is added at the beginning at treatment (ex. azathioprine 100-200 mg daily, mycophenolate mofetil 1-1.5 twice daily). Treatment courses can be repeated in patients who do not achieve complete remission or relapse (ex. monthly IVIG at 2 g/kg intravenously over 3-4 days). In refractory cases, cyclophosphamide plus intravenous corticosteroids and plasmapheresis are also used. In patients who have a limited form of the disease, skin and mucous membrane lesions should be treated with topical corticosteroids. Complicating infection requires appropriate systemic and local antibiotic therapy. As far as complications are concerned, secondary infection can occur. This is a major cause of morbidity and mortality. Disturbances of fluid, electrolyte, and nutritional intake can occur as a result of painful oral ulcers. One in three patients will experience remission and, infection from S. aureus is the most frequent fatality cause.
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Tinea versicolor is a mild, superficial Malassezia infection of the skin. The condition has a high reoccurrence rate after treatment. Patients often report the malady after discovering an area of their skin that will not tan and, mistaken the disease as well as the resulting hypopigmentation for vitiligo. A few patients will also present with itching and velvety, tan, pink, or white macules or thin papules. Large, blunt hyphae, and thin walled budding spores will appear on the KOH. The patient can be treated with selenium sulfide lotion (applied from neck to waist every day and left on for five to fifteen minutes for seven days). This treatment is repeated weekly for a month and then monthly for maintenance. Ketoconazole shampoo (1% or 2%) lathered on the chest and back and left on for five minutes can also be used for treatment. Two doses of oral fluconazole (300 mg) fourteen days apart is the first-line treatment. Imidazole creams, solutions, and lotions are quite effective for localized areas but are too expensive for use over large areas such as the chest and back.
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Patients with pompholyx, or vesiculobullous dermatitis of the palms and soles, will typically present with small clear vesicles resembling grains of tapioca on the skin at the side of the fingers and the palms. The vesicles may be associated with intense itching and then become dry, scaly and fissured. The patient can be treated with topical and systemic corticosteroids. Typically, the practitioner will order a topical corticosteroid to ameliorate the flare and avoid pruritus. The patient should also avoid any skin irritants and wear cotton gloves when performing wet chores. Some patients have responded to PUVA therapy.
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Tinea pedis (commonly known as athlete’s foot) is an acute or chronic dermatosis. Most infections are caused by the Trichophyton species. The patient will present with itching, burning, or stinging. Pain here may indicate secondary infection with complicating cellulitis. Interdigital tinea pedis is the most common predisposing cause of lower extremity cellulitis in healthy individuals. On the sole and heel, tinea may appear as chronic noninflammatory scaling occasionally with thickening or fissuring. This may extend over the sides of the feet in a moccasin distribution. The KOH preparation is usually positive. Tinea pedis can also present as scaling or fissuring in the toe webs with maceration. As the web spaces become more macerated, the KOH preparation and fungal culture have a lower tendency to return positive results because bacterial species begin to dominate. The malady can be treated with aluminum subacetate solution soaks for 20 minutes twice daily. Broad spectrum antifungal creams and solutions will help combat dipheriods and other gram-positive organisms. If topical imidazoles fail, one week of topical allylamine treatment will often result in clearing. Itraconazole (200 mg daily for two weeks or 400 mg daily for one week) can be used in refractory cases.
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The primary symptoms of herpes simplex are burning and stinging. Neuralgia may precede or accompany attacks. The lesions consist of small, grouped vesicles on an erythematous base that can occur anywhere. Most cases occur on the patient’s vermillion lip border, the penile shaft, labia, perianal skin, and the rear end. The regional lymph nodes may be swollen and tender. The lesions usually crust and heal in one week. Immunosuppressed patients may also present with verrucous or nodular herpes lesions at the aforementioned sites of involvement. Herpes simplex lesions must be distinguished from chancroid, syphilis, pyoderma, and trauma. Direct fluorescent antibody slide tests offer a rapid means of diagnosis. The malady can be treated with acyclovir, valacyclovir, and famciclovir. Only the first drug is available for intravenous administration. For the initial clinical episode of herpes simplex, the patient is provided with acyclovir (400 mg orally, five times a day), valacyclovir (1000 mg orally twice every day), and famciclovir (250 mg orally three times every day). The duration of treatment is for seven to ten days typically.
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Chancroid is a sexually transmitted disease caused by the short gram negative bacillus Haemophilus ducreyi. The incubation period ranges from three to five days. At the location of inoculation, a vesicopustule develops that breaks down to form a painful, soft ulcer with a necrotic base, surrounding erythema, and undermined edges. There may be multiple lesions due to autoinoculation. The adenitis is usually unilateral and is composed of tender, matted nodules of moderate size with overlying erythema. The patient may also present with lymph node involvement, chills, malaise, and fever. While women typically have no external signs of infection, balanitis and phimosis are frequent complications in men. The diagnosis is established by culturing a swab of the lesion onto a special medium. To treat the disease, a single dose of azithromycin (1g orally) or ceftriaxone (250 mg intramuscularly) is effective as is erythromycin (500 mg orally four times a day for seven days) or ciprofloxacin (500 mg orally twice a day for three days).
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Yaws is a contagious disease that is limited to tropical regions and is caused by the T pallidum subspecies pertenue. The malady is characterized by granulomatous skin lesions, mucous membranes, and bone. While Yaws is rarely fatal, it can lead to chronic disfigurement and disability if left untreated. Yaws is acquired by direct non-sexual contact (usually in childhood) although it can occur at any age. The first papule (which later ulcerates) appears three to four weeks after exposure. There is usually associated regional lymphadenopathy. Six to twelve weeks later, secondary lesions that are raised papillomas and papules that seep highly infectious material appear and last for several months or years. Late gummatous lesions may occur with associated tissue destruction involving large areas of skin and subcutaneous tissues.
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Botulism is a paralytic disease caused by botulism toxin, which is produced by C botulinum, an anaerobic spore-forming bacillus found in soil. Four toxin types – F, E, B, and A cause disease in humans. Naturally occurring botulism comes in three forms: wound botulism, infant botulism, and food borne botulism. Food borne botulism is caused by ingestion of preformed toxin present in vacuum packed, canned, or smoked foods. Infant and wound botulism are both caused by the presence of organisms in the gut or wound that secrete toxins. Symptoms include diplopia and loss of accommodation, fixed dilated pupils, cranial never palsies with extraocular muscle impairment, dry mouth, dysphonia, dysphagia, and ptosis. Paralysis that develops into respiratory failure and death may occur unless assistance is provided. To test for the disease, the practitioner should use mouse inoculation and specific antiserum. If the practitioner suspects that her patient is suffering from botulism, she should contact State health authorities or the |Centers for Disease Control for assistance in procuring the equine serum heptavalent botulism antitoxin and the assays for toxin in serum, stool, or food. Skin testing is also recommended to remove hypersensitivity to the antitoxin preparation. Antitoxin should be administered within twenty-four hours of the onset of symptoms and parenteral fluids should be provided while the patient has difficulty swallowing.
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Human herpes virus 8 (HHV-8) or Kaposi sarcoma associated herpes virus is the cause of all forms of Kaposi sarcoma. Kaposi sarcoma occurs primarily in homosexual men with HIV infection as an AIDS defining illness and can complicate immunosuppressive therapy. Improvement is often seen after the immunosuppression is stopped. The patient will typically present with red or purple plaques or nodules on cutaneous or mucosal surfaces. Marked edema can occur with few or no skin lesions. Kaposi sarcoma commonly involves the GI tract and can be screened with fecal occult blood testing. In asymptomatic patients, these lesions are not sought or treated. Pulmonary Kaposi sarcoma, which can be asymptomatic and appear only on chest radiography, can present with shortness of breath, cough, hemoptysis, or chest pain. Chronic Kaposi sarcoma can develop in patients with HIV infection, high CD4 counts, and low viral loads. Here, the Kaposi sarcoma is in its endemic form and is indolent as well as localized. The sarcoma can be clinically aggressive, though. The presence of Kaposi sarcoma at the time of antiretroviral initiation is associated with Kaposi sarcoma-immune reconstitution inflammatory syndrome which has an especially aggressive course in patients with visceral disease. As far as treatment is concerned, in more seasoned patients, palliative local therapy with intralesional chemotherapy or radiation is usually all that is required. If the patient has iatrogenic immunosuppression, treatment consists of reduced doses of immunosuppressive medications. On the other hand, if the patient has AIDS associated Kaposi sarcoma, she or he should be given ART. Other therapeutic options include cryotherapy or intralesional vinblastine (0.1-0.5 mg/mL) for cosmetically objectionable lesions; radiation therapy for accessible and space occupying lesions; and laser surgery for certain intraoral and pharyngeal lesions. Systemic therapy is indicated in patients with rapidly progressive skin disease, edema or pain, and symptomatic visceral disease or pulmonary disease. Liposomal doxorubicin is highly effective in severe cases and may be used alone or in combination with bleomycin and vincristine. Paclitaxel and other taxanes can be effective even in patients who do not respond to anthracycline treatment.
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Patients with anorexia nervosa may present with severe emaciation and complain of cold intolerance or constipation. Amenorrhea is almost always present and may be accompanied by bradycardia, hypotension, and hypothermia. An examination will reveal loss of body fat, dry and scaly skin, and increased lanugo body hair. Parotid enlargement and edema may also occur. Patients may have elevated serum cholesterol levels, depressed levels of luteinizing and follicle stimulating hormones, and an impaired response of luteinizing hormone to luteinizing hormone-releasing hormone. In a few instances, medications such as tricyclic antidepressants, selected serotonin reuptake inhibitors (SSRIs), and lithium carbonate are effective. All cases should be co-managed with a psychiatrist and, a patient should be admitted if she presents with hypovolemia or major electrolyte disorders.
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Bulimia nervosa is the episodic uncontrolled ingestion of large quantities of food followed by recurrent inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting, diuretic or cathartic use, or a regime that calls for strict dieting or overly vigorous exercise. Gastric dilatation and pancreatitis have been reported after binges. Moreover, vomiting can result in poor dentition, pharyngitis, esophagitis, aspiration, and electrolyte abnormalities. Treatment requires supportive care and psychotherapy. Individual, group, family, and behavioral therapy have all been used. On occasion, prescription of fluoxetine hydrochloride and other SSRIs may be helpful. All cases should be co-managed with a psychiatrist.
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Patients with very high levels of serum triglycerides (greater than 1000 mg/dL) are at risk for pancreatitis. Most patients with congenital abnormalities in triglyceride metabolism present in childhood. By way of contrast, hypertriglyceridemia-induced pancreatitis in adults is often due to an acquired lipid metabolism problem. Although, there are no clear triglyceride levels that predict pancreatitis, most clinicians treat fasting levels above 500 mg/dL. The risk of pancreatitis here may be more related to the triglyceride level following consumption of a fatty meal. Thus, because postprandial increases in triglyceride are inevitable if fat-containing foods are eaten, fasting triglyceride levels in persons prone to pancreatitis should be kept below that level. The primary treatment for high triglyceride levels is dietary and calls for reduced consumption of alcohol, simple sugars, and refined starches as well as saturated and trans fatty acids. In patients with fasting triglycerides greater than or equal to 500 mg/dL despite adequate dietary compliance, a triglyceride lowering drug such as niacin, a fibric acid derivative, an omega-3-acid ethyl ester, or an HMG-CoA reductase inhibitor may be helpful.
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Most patients with high cholesterol levels have no specific symptoms or signs. Indeed, the vast majority of patients with lipid abnormalities are detected with a lab test either as part of a preventative screening program or patient workup. Extremely high levels of chylomicrons or VLDL particles (triglyceride levels above 1000 mg/dL or 10 mmol/L) result in the formation of eruptive xanthomas (red-yellow papules typically on the rear end). High LDL concentrations result in tendinous xanthomas on certain tendons (usually the back of the hand and the patella). Finally, a patient presenting with lipemia retinalis (cream-colored blood vessels in the fundus) may have extremely high triglyceride levels.
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Riboflavin deficiency almost always occurs in connection with other vitamin deficiencies. The most common causes are alcoholism, interactions with a variety of medications, dietary inadequacy, and the other causes of protein-calorie undernutrition. Symptoms include anemia, corneal vascularization, weakness, seborrheic dermatitis, glossitis, angular stomatitis, and cheilosis. A riboflavin deficiency diagnosis can be confirmed by measurement of the riboflavin-dependent enzyme erythrocyte glutathione reductase. Readers should note that activity coefficients greater than 1.2-1.3 are suggestive of riboflavin deficiency. Patients can be treated by consuming the vitamin itself (5-515 mg/day) or foods such as fish or dairy products. While riboflavin can be provided parenterally, practitioners should note that the vitamin does not dissolve well in aqueous solutions.
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Vitamin A deficiency is one of the most common vitamin deficiency syndromes and is most prevalent in developing States. The malady is a leading cause of blindness. In the United States, vitamin A deficiency is usually due to fat malabsorption syndromes or mineral oil laxative abuse and is typically exhibited by older adults and individuals living in urban areas. The earliest symptom here is night blindness, which is followed by xerosis, and the development of Bitot spots on the conjunctiva. Ulceration and necrosis of the cornea, endophthalmitis, perforation, and blindness are late manifestations. Hyperkeratinization of the skin may also occur. Dark adaptation abnormalities are strongly suggestive of vitamin A deficiency as are serum levels below the normal range of 30-65 mg/dL. The most common treatment, of course, is vitamin A (30,000 international units daily for one week orally). Advanced deficiency with corneal damage calls for 20,000 international units/kg for at least five days. The potential antioxidant effects of beta-carotene can be achieved with supplements of 25,000-50,000 international units of beta-carotene. Excess intake of beta-carotene, however, can result in a staining of the skin in a yellowish-orange color. The change should be most apparent on the patient’s palms and soles. Practitioners, on the other hand, should also note that vitamin A can be quite toxic. Chronic toxicity often occurs after ingestion of daily doses of over 50,000 international units per day for more than three months. Symptoms here include vomiting, anorexia, mouth sores, hair loss, dry skin, lethargy, headache, and painful hyperostosis. Excessive vitamin A intake can also predispose patients for a hip fracture.
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