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By E. Kerth. Bethany College, Scotts Valley, CA. 2018.

A 58-year-old man presents to your office complaining of fever cheap 400 mg levitra plus mastercard, chills generic levitra plus 400mg with amex, muscle aches, and diarrhea of 3 days’ duration. He returned from an East African safari about 3 weeks ago. During his trip, he took doxycycline for prophylaxis against malaria; he took his last pill 2 weeks after arriving back in the United States. The patient thinks he probably has a viral illness, but he asks you if it is possible that he has malaria. For this patient, which of the following statements is true? It is unlikely that the patient has malaria because his symptoms are too nonspecific B. It is unlikely that the patient has malaria because he was taking prophylactic antimalarial medication C. It is very likely that the patient has malaria because he was taking a medicine that is inappropriate for prophylaxis against malaria D. It is possible that the patient has malaria because he took his pro- phylactic medication for an inadequate duration Key Concept/Objective: To understand malaria prophylaxis for persons traveling to areas endemic for malaria Persons infected with malaria remain asymptomatic during the time between the infecting mosquito bite and the erythrocytic stage of infection, a period that may range from about 1 to 4 weeks for Plasmodium falciparum infection. Because malaria chemo- prophylaxis does not actually prevent malaria but rather treats erythrocytic-stage infec- tion, chemoprophylactic medication must be continued for a full 4 weeks after a per- son returns from a malarious area. Failure to do so permits the development of malari- al infection. An exception to this is with so-called causal prophylactic medications, such as atovaquone-proguanil, which also kills liver-stage parasites. This form of pro- phylaxis can be discontinued a week after leaving a malarious area. The appropriate choice of prophylactic medication depends on the travel destination and includes chloroquine, mefloquine, doxycycline, atovaquone-proguanil, and primaquine. It is important to note that in someone at risk for malaria, the constellations of symptoms are nonspecific and may suggest diagnoses other than malaria; however, in a patient with fever who has recently returned from a trip to a known malarious area, this diag- nosis should be considered carefully in spite of the nonspecific nature of the symptoms. A 46-year-old white man with AIDS (CD4+ T cell count, 42 cells/µl) presents to the emergency depart- ment after having a seizure. He reports that for the past 3 weeks, he has been experiencing worsening tremor, visual disturbances, and headaches. CT scan of the brain with contrast reveals a single rounded lesion with ring enhancement. Which of the following statements regarding cerebral toxoplasmosis in AIDS patients is true? Reactivation of latent Toxoplasma infection is unlikely to occur until the CD4+ T cell count falls below 50 cells/µl B. Antibodies against Toxoplasma are rarely present in the cere- brospinal fluid of AIDS patients, because of their level of immuno- suppression C. During treatment for cerebral toxoplasmosis, clinical and radiologic improvement is often observed within 2 weeks after initiating therapy D. After acute treatment of cerebral toxoplasmosis, patients must remain on lifelong suppressive therapy, independent of CD4+ T cell count 104 BOARD REVIEW Key Concept/Objective: To understand the diagnosis and treatment of cerebral toxoplasmosis in AIDS patients Most cases of toxoplasmosis in patients with AIDS result from reactivation of latent Toxoplasma cysts acquired before infection with HIV; reactivation is particularly likely when the CD4+ T cell count falls below 100 cells/µl. Serum antibody tests cannot be relied on in the diagnosis of primary toxoplasmosis in patients with AIDS; antibody titers do not reach the high levels typical of immunocompetent patients with toxo- plasmosis, nor are IgM antibodies present in patients with AIDS. However, antibodies against Toxoplasma are present in the CSF in nearly two thirds of AIDS patients with cerebral toxoplasmosis, and their detection may assist in the diagnosis. With appropri- ate therapy, clinical and radiologic improvement is often observed within 1 to 2 weeks. If patients respond poorly to treatment and are seronegative or belong to population groups at high risk for tuberculosis, biopsy should be strongly considered. Patients with AIDS who have been treated for toxoplasmosis require prolonged suppressive therapy. If the CD4+ T cell count rises above 200 cells/µl for 3 months, secondary prophylaxis for toxoplasmosis can be stopped. A 37-year-old woman presents with complaints of foul-smelling, greasy diarrhea; nausea; and excessive flatulence. She states that she returned from a camping trip about 2 weeks ago. Immunologic assay detects giardial antigen in the stool. Which of the following statements about treatment and prevention of giardiasis is true?

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Since it is well beyond the scope of the nonspe- for example generic levitra plus 400 mg online, Figure 65A) will be shown with cialist to know all the details purchase levitra plus 400mg with amex, certain salient points have each cross-sectional level with the plane of the been selected, namely: cross-section indicated. These cross-sectional levels are the ones shown • The cranial nerve nuclei alongside the pathways in Section B (Func- • The ascending and descending tracts tional Systems) of this atlas (see Figure 31). Wherever one sees a cranial nerve attached to antibody markers, often tagged with fluorescent dyes. In the brainstem, one knows that its nucleus (or one of its general, the stains include those for: nuclei) will be located at that level (see Figure 8A and Figure 8B). Therefore, if one visually recalls or “memo- • Cellular components, the cell bodies of neurons rizes” the attachment of the cranial nerves, one has a key and glia (and cells lining blood vessels); these to understanding the brainstem. In the clinical setting, are general stains such as Hematoxylin & Eosin knowledge of which cranial nerve is involved is usually (H & E). This dia- the best known of these is the Golgi stain. The lines indicate the sections that will be depicted in The stain used for the histological sections in this atlas the series to follow. The cellular neuronal areas are usually lightly stained as the cells are more • Two through the midbrain dispersed, but the cell bodies can be visualized at higher • CN III, upper midbrain (superior colliculus magnification. Penetrat- this level) ing branches from the basilar artery supply nuclei and • CN V mid-pons (through the principal sen- tracts that are adjacent to the midline; these are called the sory and motor nuclei) paramedian branches. The lateral territory of the brain- • CN VI, VII, and part of VIII, the lower pons stem, both tracts and nuclei, is supplied by one of the • Three through the medulla cerebellar circumferential arteries, posterior inferior, • CN VIII (some parts), the upper medulla anterior inferior, and superior (see Figure 58). The fourth ventricle separates the pons and medulla This is a schematic drawing of the brainstem seen in a midsagittal view (see Figure 17 and Figure 18). The upper part of the roof is being presented because it is one that is commonly used of the fourth ventricle is called the superior medullary velum (see Figure 10 and Figure to portray the brainstem. This schematic also will be shown in each of the cross-section diagrams, with the exact level indicated, in CLINICAL ASPECT order to orient the learner to the plane of section through The information that is being presented in this series the brainstem. Such nucleus in the upper midbrain, the pontine nuclei that form lesions would also interrupt the ascending or descending the “bulging” of the pons, and the inferior olivary nucleus tracts, and this information would assist in localizing the of the medulla (not illustrated). Specific lesions will be discussed with the cross- attachments are shown as well but are not labeled. Using this orientation, one can approach the descrip- tion of the eight cross-sections in a systematic manner. PLAN OF STUDY: This is sometimes referred to as the floor plan of the brainstem: • A schematic of each section is presented in the upper figure, and the corresponding histological • Ventral or basal: The most anterior portion of section of the human brainstem is presented each area of the brainstem contains some rep- below. In the midbrain, the cerebral pedun- This visual cataloging is maintained uniformly cles include all these axon systems. The cortico- throughout the brainstem cross-sections (see bulbar fibers are given off to the various brain- page xviii). In the pons, the cortico-pontine fibers terminate in the pontine The brainstem is being described starting from the nuclei, which form the bulge known as the pons midbrain downward through to the medulla for two rea- proper; the cortico-spinal fibers are dispersed sons: among the pontine nuclei. In the medulla, the cortico-spinal fibers regroup to form the pyra- 1. This order follows the numbering of the cranial mids. The medulla ends at the point where these nerves, from midbrain downward fibers decussate (see Figure 7). This is the sequence that has been described for • Central: The central portion of the brainstem the fibers descending from the cortex is called the tegmentum. The reticular forma- tion occupies the core region of the tegmentum Others may prefer to start the description of the cross- (see Figure 42A and Figure 42B). It is suggested that the learner review these out the brainstem (see Figure 20A, Figure 20B, cross-sections using the text together with the CD-ROM. The brainstem level can often The histological images of the brainstem will be more be identified according to the ventricular system understandable after this combined approach. FIGURE 65, FIGURE 65A, AND The aqueduct of the midbrain helps to identify this cross-section as the midbrain area (see Figure 21). Poste- FIGURE 65B rior to the aqueduct are the two pairs of colliculi, which can also be seen on the dorsal view of the isolated brain- The midbrain is the smallest of the three parts of the stem (see Figure 9A and Figure 10). The temporal lobes of the hemispheres usually together form the tectal plate, or tectum, also called the obscure its presence on an inferior view of the brain (see quadrigeminal plate. The pretectal region, located in front of and some- The midbrain area is easily recognizable from the what above the superior colliculus, is the nuclear area for anterior view in a dissected specimen of the isolated brain- the pupillary light reflex (see Figure 41C). The massive cerebral peduncles are located most anteriorly. These peduncles contain axons FIGURE 65: UPPER MIDBRAIN that are a direct continuation of the fiber systems of the (PHOTOGRAPHIC VIEW) internal capsule (see Figure 26). Within them are found the pathways descending from the cerebral cortex to the This is a photographic image, enlarged, of the sectioned brainstem (cortico-bulbar, see Figure 46 and Figure 48), midbrain. As shown in the upper left image, the brainstem to the cerebellum via the pons (cortico-pontine, see Figure was sectioned at the level of the cerebral peduncles; the 48 and Figure 55), and to the spinal cord (cortico-spinal corresponding level is shown on a medial view of the tracts, see Figure 45 and Figure 48). Many of the structures visible on this “gross” midbrain region — the substantia nigra and the red specimen will be seen in more detail on the histological nucleus, both involved in motor control.

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The results from these studies show both in vitro and in vivo function of PEG-encapsulated islets and the ability of PEG matrices to prevent immune rejection in allograft and xenograft models buy levitra plus 400mg low cost. Tissue Repair Since macromers can be prepared from bioactive polymers buy levitra plus 400mg mastercard, and solutions of these macromers can be applied to the sites of tissue defects and subsequently solidified into durable, bioresorbable matrices by the application of visible light, their use in tissue repair applications is logical. There are many tissue repair applications amenable to therapeutic intervention involving in situ matrix formation. Chronic cutaneous wounds are skin wounds that either will not heal or are very slow to heal as a result of an underlying disease state or other physiologic insufficiency. The three major types of chronic cutaneous wounds are decubitus ulcers, diabetic ulcers, and venous stasis ulcers. As the median age of the American population increases, the incidence of all three types of chronic skin ulcers increase as well. There are several approaches currently being investigated for the treatment of chronic cutaneous wounds. These approaches range from traditional wound dressings to gene therapy approaches to total artificial skin. An approach that utilizes in situ formation of a bioactive matrix directly in the wound bed offers many potential advantages. The dressing material is applied to the wound bed as a liquid that conforms completely and intimately to the wound surface. The solution is subsequently solidified by a brief illumination. The resulting ‘‘bandage’’ is composed of bioactive materials that are in intimate contact with the wound. The bioactivity of the matrix material is maximized, and bacteria are prevented from infiltrating into the wound. In addition, bioactive compounds can be added to the dressing formulation and slowly released into the wound. Wound healing formulations have been prepared from collagen, hyaluronic acid, and syn- thetic macromer solutions and evaluated in both partial and full thickness cutaneous wounds using a pig model. Results from these evaluations show no increased inflammatory or other host response of any formulation over controls covered with standard occlusive dressings. Some formulations showed enhanced reepithelization over controls receiving standard occlusive dress- ings. Cartilage is a unique tissue, strong and durable, but once damaged is unable to heal itself. This is particularly true for articular, or hyaline, cartilage, the material that lines the articulating joints. Defects caused by overuse or trauma, common in athletes and other physically active people, will not heal. Until recently, the only treatment for this condition was joint replacement. Currently, there are some therapies being evaluated that show great promise. Filling the defect with autologous chondrocytes (cartilage cells), matrices containing gene therapy agents, growth factors, bone morphogenetic proteins (BMPs), or combinations of these materials are some of the approaches being evaluated. One of the issues unique to hyaline cartilage repair is the tendency of the repaired tissue to form fibrocartilage instead of hyaline cartilage. Fibrocartilage is not as durable as hyaline cartilage and eventually deteriorates, forming a new defect. One way to direct the formation of hyaline cartilage instead of fibrocartilage is to deliver the bioactive substance to the defect in a hyaluronic acid matrix. A hyaluronic acid–rich environment favors the formation of hyaline cartilage. Cells, growth factors, and other bioactive substances can be added to a solution of hyaluro- nic acid macromer, applied to the defect as a viscous liquid and solidified by a brief illumination thereby fixing the matrix in place. The matrix is resorbed as new hyaline cartilage is formed. Prevention of Adhesions The formation of postsurgical adhesions is a common cause of surgical complications. Adhesions formed after abdominal surgeries are the leading cause of bowel obstruction in the United States. Likewise, the leading cause of infertility in women is the formation of adhesions following pelvic surgery. In addition, the formation of adhesions is a cause of complication in many types of surgeries including spinal and cardiovascular. For many years, the use of barriers and adjuvants has been evaluated. These materials essentially prevent tissues from interacting until the tissue healing response is complete, and then, ideally, they go away.

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A 32-year-old man presents to your clinic for a routine follow-up visit trusted levitra plus 400 mg. He complains of intermittent episodes of shaking generic levitra plus 400mg line, palpitations, sweating, and anxiety. He has a friend who is a hypoglycemic and is on a special diet, and he wonders if he too may have low blood sugar. While in the waiting room, he develops symptoms, and your nurse obtains a blood glucose level. What is the most appropriate step to take next in the workup of this patient? Admit the patient to the hospital for a prolonged fast B. Send the patient for an endoscopic ultrasound, looking for insulinoma C. Measure the insulin and C-peptide levels, assess for insulin antibodies, and have the patient follow up in 1 month D. Refer the patient directly to surgery for resection of presumed insulinoma E. No further workup for hypoglycemic disorder is necessary at this time Key Concept/Objective: To understand that a normal serum glucose concentration in a sympto- matic patient rules out hypoglycemic disorders A normal serum glucose concentration, reliably obtained during the occurrence of spon- taneous symptoms, eliminates the possibility of a hypoglycemic disorder; no further eval- uation for hypoglycemia is required. Glucometer measurements made by the patient dur- ing the occurrence of symptoms often are unreliable, because nondiabetic patients usual- ly are not experienced in this technique and the measurements are obtained under adverse circumstances. However, a reliably measured capillary glucose level that is in the normal range eliminates the possibility of hypoglycemia as the cause of symptoms. Normoglycemia during symptoms cannot be ascribed to spontaneous recovery from pre- vious hypoglycemia. In fact, the reverse is true; symptoms ease before the serum glucose achieves a normal level. A 53-year-old woman presents to your clinic complaining of transient episodes of diaphoresis, asthenia, near syncope, and clouding of thought process; she has had these symptoms for several months. These episodes most commonly occur several hours after she eats. She has no other significant medical histo- ry and takes no medications. A prolonged fast is begun, during which the patient becomes symptomatic. Her serum glucose concentration at the time is 43 mg/dl. The insulin level is elevated, and no insulin antibodies are present. The C-peptide level is high, and tests for the use of sulfonylureas and meglitinides are negative. Observe the patient and schedule a follow-up fast 2 to 3 months from now B. Obtain a transabdominal ultrasound and refer the patient to surgery for resection D. Begin phenytoin and octreotide and have the patient appear for a fol- low-up visit in 3 months Key Concept/Objective: To understand the diagnosis and treatment of insulinoma Insulinoma is characterized by hypoglycemia caused by elevated levels of endogenous insulin. Confirmation of the diagnosis requires exclusion of hypoglycemia from exoge- nous sources. Once a biochemical diagnosis of insulinoma is made, the next step is local- ization. The effective modalities are center dependent and include abdominal ultrasound, triple-phase spiral computed tomography, magnetic resonance imaging, and octreotide scan. After localization, the treatment of choice for insulinomas is surgical removal. Depending on the lesion, surgery may range from enucleation of the insulinoma to total pancreatectomy. Medical therapy is less effective than tumor resection but can be used in patients who are not candidates for surgery. The most effective medication for controlling symptomatic hypoglycemia is diazoxide, which lowers insulin production. Other medica- tions for insulinomas include verapamil, phenytoin, and octreotide. A 31-year-old woman presents to the emergency department complaining of episodes of dizziness, light- headedness, palpitations, sweats, anxiety, and confusion. On the morning of admission, she reports that she almost passed out. Her husband, who is a diabetic patient who requires insulin, checked her blood sugar level and noted it to be low. Her symptoms resolved after drinking some orange juice. She is admit- ted to the hospital for a prolonged fast.