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The patient is confused and scores 22/30 on the Folstein Mini-Mental State Examination generic cialis soft 20mg visa. Mild meningismus and a left cranial nerve VI palsy are noted generic 20 mg cialis soft amex. Chest x-ray is negative except for an old Ghon complex cialis soft 20mg low cost. Results of cere- brospinal fluid examination are as follows: opening pressure buy cheap cialis soft 20 mg, 160 mm Hg discount 20 mg cialis soft with visa; glucose, 45 mg/dl; protein, 140 mg/dl; 250 cells/mm3 (75% lymphocytes). Gram stain and rapid tests for fungal and bacterial anti- gens are negative. Which of the following is the most likely diagnosis for this patient? Tuberculous meningitis Key Concept/Objective: To be able to recognize tuberculous meningitis Although uncommon in HIV-seronegative patients, this is one of the most serious and rapidly progressive forms of tuberculosis. Adults characteristically experience an indo- 12 BOARD REVIEW lent phase of headache, malaise, low-grade fever, and personality changes. After sever- al weeks, more characteristic CNS signs and symptoms develop, including meningis- mus, cranial nerve palsies, seizures, and signs of increased intracranial pressure (vomit- ing, altered consciousness, severe headache). Some patients present with a rapidly pro- gressive picture resembling bacterial meningitis. Only a minority will have a clinical history of prior tuberculosis. An early CSF examination is critical to accurate diagnosis. Characteristic findings include lowered CSF glucose (hypoglycorrhachia), elevated CSF protein, and a lymphocytic pleocytosis. A high index of suspicion is needed to make the diagnosis, because mycobacterial CSF cultures are positive in no more than 75% of cases, and acid-fast smears are positive in only 25% of cases. A number of biochemical, immunologic, and molecular biologic tests are currently available, but none has yet emerged as the gold standard. At times, a clinical diagnosis depends on response to anti- tuberculous therapy. A 32-year-old resident of the state penitentiary is found to test positive on a purified protein derivative skin test (PPD), with 10 mm of induration. He is asymptomatic, and his chest x-ray is negative. Which of the following would you recommend at this time? Induced sputum cultures; treat only if positive C. HIV-seropositive patients with a PPD of 5 mm or greater should receive 9 to 12 months of INH chemoprophylaxis. Patients younger than 35 years with a recent PPD conversion of 10 mm or greater and patients older than 35 years with a 15 mm PPD conversion are candidates for chemoprophy- laxis. Several other factors lower the threshold for chemoprophylaxis, including recent exposure, an abnormal chest x-ray consistent with old TB, and membership in high- incidence population groups (e. INH chemoprophylaxis is no longer administered for 1 year; therapy for 6 to 9 months achieves the best balance between reducing the risk of active TB and minimiz- ing the risk of hepatitis. Rifampin and pyrazinamide for 2 months can be substituted for INH chemoprophylaxis in patients who are unable to take INH or in whom INH resistance is suspected. A 48-year-old physician from New York City develops fever, night sweats, cough, weight loss, and malaise. Chest x-ray reveals an infiltrate in the posterior-apical segment of the right upper lobe. Which of the following treatment options would you institute for this patient at this time? Await cultures and sensitivity testing before instituting therapy B. INH, rifampin, ethambutol, pyrazinamide, and streptomycin Key Concept/Objective: To understand the treatment of active tuberculosis 7 INFECTIOUS DISEASE 13 This patient has a clinical syndrome very suggestive of tuberculosis. He is smear-posi- tive, and treatment should be initiated immediately, pending the results of mycobacte- rial culture and antimicrobial sensitivity. He should be hospitalized and placed in a neg- ative-pressure isolation room for induction of chemotherapy until his symptoms improve and he becomes smear-negative. The United States Public Health Service rec- ommends initiation of therapy with INH, rifampin, ethambutol, and pyrazinamide unless the INH-resistance rate in the community is low (< 4%), in which case ethamb- utol can be withheld.

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Because this patient has diabetes order cialis soft 20mg overnight delivery, microalbuminuria is predictive of progression of renal disease D generic cialis soft 20 mg mastercard. Smoking is a risk factor for microalbuminuria because of its associa- tion with hypertension E discount cialis soft 20 mg with mastercard. Although not clearly of benefit 20mg cialis soft with visa, a low-protein diet can be prescribed with little concern about deleterious effects Key Concept/Objective: To understand the risk factors for renal disease progression Evidence clearly shows that aggressive control of hyperglycemia in patients with type 1 diabetes mellitus will reduce the occurrence of microalbuminuria and macroalbu- minuria and will slow the progression of nephropathy buy cialis soft 20mg low cost. Control of hyperglycemia in patients with type 2 diabetes mellitus is more controversial, as there are conflicting results of this approach in the literature. This may be related to the fact that renal lesions resulting from type 2 diabetes are more heterogeneous than the typical lesion from type 1 diabetes. Because uncontrolled hypertension can contribute to the pro- gression of renal disease, target blood pressure values have been established. These val- ues vary slightly, depending on the source of the recommendation, but in general, a blood pressure of 130/80 mm Hg or less should be sought. Microalbuminuria is a risk factor for progression to end-stage renal disease in diabetic and nondiabetic patients with renal disease. Smoking is an independent risk factor for microalbuminuria in both hypertensive and normotensive patients. Finally, a low-protein diet can easily lead to malnutrition and calorie deficiency and therefore must be closely monitored. A previously healthy 54-year-old woman presents with a 3-week history of arthralgias and edema. Her examination is remarkable for a blood pressure of 170/106 mm Hg, bibasilar pulmonary crackles, and lower extremity edema. A freshly voided urine reveals red blood cells and red cell casts. Her serology is positive for antineutrophil cytoplasmic antibody (ANCA). For this patient, a renal biopsy with immunofluorescent staining would be expected to show which of the following? Positive staining for immune deposits IgG and C3 C. Positive staining for linear deposition of IgG and C3 E. Negative staining for antibody or C3 12 BOARD REVIEW Key Concept/Objective: To understand that ANCA–associated glomerulonephritis is not asso- ciated with staining for immunoglobulin, complement, or immune deposits ANCA-associated glomerulonephritis involves a vasculitic process of the small- and medium-sized blood vessels that usually presents as a focal segmental necrotizing glomerulonephritis. Renal involvement is usually acute, severe, and progressive, and glomeruli contain crescents. ANCA-associated glomerulonephritis is one of the causes of rapidly progressive glomerulonephritis, which many authors consider a medical emergency. ANCA-associated glomerulonephritis can be limited to the kidney or coex- ist with systemic illness such as Wegener granulomatosis. In contrast to many other kinds of glomerulonephritis, immunofluorescent staining fails to reveal the presence of antibody, complement, or immune complexes. This type of glomerulonephritis is also referred to as pauci-immune glomerulonephritis. If the disease is left untreated, the prognosis is poor. Initial treatment consists of corticosteroids and immunosuppressive therapy. A 45-year-old man presents for a routine examination. His history is remarkable for a bleeding peptic ulcer at age 30 that required transfusion of several units of packed red blood cells. His physical examination reveals a blood pres- sure of 154/98 mm Hg, confirmed on several occasions, but is otherwise not remarkable. His laboratory evaluation was remarkable for ALT and AST levels that were 2. Serum antibody testing for hepatitis C Key Concept/Objective: To understand the pathogenic link between chronic hepatitis C infec- tion and glomerulonephritis Membranoproliferative glomerulonephritis can present with either the nephrotic syn- drome or the nephritic syndrome. Type 1 membranoproliferative glomerulonephritis is caused by immune complex deposition in the subendothelium, most commonly im- mune deposits from hepatitis C virus (HCV) antigens and cryoglobulins. Approximately one third of patients present with microscopic hematuria and nonnephrotic protein- uria, and another third presents with nephrotic-range proteinuria with a mild decrease in renal function.

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The bran- chial motor branch lies beneath the ganglion and exits via the foramen rotun- dum order cialis soft 20 mg amex. The sensory ganglion is located in the trigeminal (Meckle’s) cave in the floor of the middle cranial fossa cheap cialis soft 20 mg mastercard. The three major divisions of the trigeminal nerve buy 20mg cialis soft amex, ophthalmic nerve (V1) buy cialis soft 20mg free shipping, maxillary nerve (V2) buy cialis soft 20mg lowest price, and mandibular nerve (V3), exit the skull through the superior orbital fissure, the foramen rotundum and the foramen ovale, respectively. V1 (and in rare instances, V2) passes through the cavernous sinus (see Fig. Some features of trigem- inal neuropathy: A Motor lesion of the right trigeminal nerve. The jaw deviates to the ipsilater- al side upon opening the mouth. Note the unshav- ed patch, that corresponds to the area, where the attack is elicited 49 The extracranial pathway has three major divisions: 1. V1, the ophthalmic nerve: The ophthalmic nerve is positioned on the lateral side of the cavernous sinus, and enters the orbit through the superior orbital fissure. It has three major branches, the frontal, lacrimal, and nasociliary nerves. Intracranially, V1 sends a sensory branch to the tentorium cerebelli. The frontal nerve and its branches can be damaged during surgery and fractures. V2, the maxillary nerve: The maxillary nerve has three branches: the infraorbital, zygomatic, and pterygopalatinal nerves. It passes below the cavernous sinus and gives off some meningeal branches. V3, the mandibular nerve: The mandibular nerve’s major branches are the auriculotemporal, inferior alveolar, and lingual nerves. A separate motor division innervates the mas- seteric muscles and the tensor tympani and veli palatini muscles. Lesions of the V3 may result from dentistry, implantation, mandible resec- tion, hematoma of lower lip, or bites. The symptoms of trigeminal nerve lesions are predominantly sensory and rarely Symptoms motor. Pain in the distribution of the trigeminal nerve can vary widely from symptomatic pain to neuralgia. Sensory loss can be demonstrated by sensory examination of all qualities. Complete sensory loss, or loss of pain and temperature, may lead to ulcers on the skin, mucous membranes and the cornea. Sensory lesions in trigeminal nerve distribution may be also caused by central lesions and follow an “onion skin” pattern (Fig. Some neuralgic trigeminal pain syndromes may be associated with redness of the eye or abnormal tearing during the attack. Motor lesions are rarely symptomatic and could cause a mono- or diplegia masticatoria. When the patient’s mouth is opened widely, the jaw will deviate to the affected side (Fig. Toxic: Pathogenesis Trichloroethylene (TCE) Vascular: Medullary infarction may cause trigeminal sensory deficits (e. Infectious: Herpes zoster ophthalmicus: may rarely be associated with corneal ulcer, iridocyclitis, retinal and arterial occlusions, optic nerve lesions, and oculo- motor nerve lesions. Characterized by abrupt onset, usually affecting one or two branches unilaterally, numbness (may disturb motor coordination of speech), and pain. Compressive: Compressive lesion of the trigeminal nerve in the intracranial portion by vascular loops (posterior inferior cerebellar artery, superior cerebellar artery, arteriovenous malformation) is considered to be a major cause of trigeminal neuralgia. Trauma: Cranial fractures often cause local lesions of the supratrochlear, supraorbital and infraorbital nerves (e. Trigeminal injury caused by fractures of the base of the skull is usually combined with injury to the abducens and facial nerves. Injury to the maxillary and ophthalmic divisions results in facial numbness, and involvement of the mandibular branch causes weakness of the mastication muscles.

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