This episode covers olfactory dysfunction!

This episode covers chlamydophila psittaci and psittacosis!

This episode covers lichen planus! 

This episode covers alopecia!

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.

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).

This episode covers vitamin c deficiency!

This episode covers folliculitis!

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.

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.