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Which of the following statements regarding essential thrombocytosis (ET) is false? In patients with ET purchase 50mg avanafil free shipping laptop causes erectile dysfunction, an elevation in the platelet count is caused by increased production by megakaryocytes in conjunction with normal platelet survival B. To diagnose ET, you must exclude iron deficiency, malignancies, inflammatory conditions, and infections C. The platelets in patients with ET are functional, and hemorrhage rarely occurs D. Unlike PV, ET rarely progresses; leukemia develops in only 3% to 4% of patients Key Concept/Objective: To understand the clinical presentation, diagnosis, and treatment of ET The elevated platelet count in patients with ET is caused by increased production by megakaryocytes in conjunction with normal platelet survival. ET is diagnosed after sec- ondary causes of elevated platelet counts (e. Major thrombotic complications occur in 20% to 30% of patients. Thrombotic complications frequently manifest as DVT and pul- monary embolism. Thrombosis of hepatic veins leads to Budd-Chiari syndrome; throm- bosis of renal veins can cause nephrotic syndrome. Erythromelalgia and digital ischemia constitute microvascular forms of arterial thrombosis in ET. Hemorrhagic events occur in up to 40% of patients, with the gastrointestinal tract, urinary tract, skin, eyes, and brain being possible bleeding sites. Individual patients can suffer from both thrombotic and hemorrhagic episodes. Unlike PV, ET rarely progresses, and leukemia develops in only 3% to 4% of patients. The correlation between the degree of thrombocytosis and the risk of thrombosis is poor. Untreated asymptomatic patients and those who are at low risk for 44 BOARD REVIEW thrombohemorrhagic complications (i. The indications for therapeutic intervention have to be considered care- fully with regard to the risk of vascular complications. In general, treatment should be considered only in patients at high risk for thrombohemorrhagic events. He reports increasing fatigue over the past 3 months, accompanied by a 10 lb weight loss and a sense of abdominal fullness. On examination, he is slightly pale, with dullness to percussion in the left upper quadrant of his abdomen. The remainder of his exam is normal, with no bruising or lymphadenopathy. A CBC reveals a WBC count of 117,000, predomi- nantly neutrophils in all stages of maturation. Which of the following other findings would you expect to see in this patient upon further evaluation? A decreased leukocyte alkaline phosphatase (LAP) score E. All of the above Key Concept/Objective: To know the common laboratory findings in a patient with chronic myelogenous leukemia (CML) CML is an acquired clonal stem cell disorder in which more than 90% of patients express the Philadelphia chromosome (a translocation between chromosomes 9 and 22) on cyto- genetic analysis. Genetic material is exchanged between the BCR and ABL genes. Other common laboratory findings include a WBC count over 100,000, with a neutrophilic pre- dominance, anemia, thrombocytosis, basophilia, and a decreased LAP score. An active, otherwise healthy 32-year-old man with type 1 diabetes is found to have a hematocrit of 60%, a platelet count of 556,000, and a WBC count of 8,050 on routine blood work. These values were con- firmed on three separate occasions. His examination is unremarkable except for a mildly elevated blood pressure, at 148/92 mm Hg. Which of the following would you expect to find in this patient on further evaluation?
The anterior The blood supply to the spinal cord is shown in Figure portion of the temporal lobe has been removed on the left 2B and is discussed with Figure 68 discount avanafil 50mg trazodone causes erectile dysfunction. Within the fissure, small arter- CLINICAL ASPECT ies are given off to the basal ganglia, called the striate arteries (not labeled; see Figure 62). The artery emerges The vascular territories of the various cerebral blood ves- at the surface (see Figure 14A) and courses upward, divid- sels are shown in color in this diagram. The most common ing into branches that are distributed onto the dorsolateral clinical lesion involving the cerebral blood vessels is surface of the hemispheres (see Figure 60). This artery heads into the inter- deficits will be described with each of the major branches hemispheric fissure (see Figure 16) and will be followed to the cerebral cortex (with Figure 60 and Figure 61). A very short artery connects the ACAs major blood vessels of the circle, sometimes one of the of the two sides, the anterior communicating artery. One of the vascular syndromes of the The two vertebral arteries unite at the lower border of brainstem, the lateral medullary syndrome (of Wallenberg) the pons to form the midline basilar artery, which courses is discussed with Figure 67B. The basilar artery terminates at the © 2006 by Taylor & Francis Group, LLC Neurological Neuroanatomy 159 Anterior communicating F a. T Oculomotor Posterior nerve (CN III) communicating a. F = Frontal lobe T = Temporal lobe Areas supplied by: Anterior cerebral a. FIGURE 58: Blood Supply 1 — Arterial Circle of Willis (photograph with overlay) © 2006 by Taylor & Francis Group, LLC 160 Atlas of Functional Neutoanatomy FIGURE 59A artery; it is not uncommon to see the asymmetry in these vessels. The posterior inferior cerebellar artery (PICA) can BLOOD SUPPLY 2 be seen, a branch of the vertebral (it is also labeled in the upper radiograph), but not the anterior inferior cerebellar artery, a branch of the basilar (see Figure 58). The basilar MR ANGIOGRAM — MRA artery gives off the superior cerebellar arteries and then ends by dividing into the posterior cerebral arteries. The Recent advances in technology have allowed for a visual- ization of the major blood vessels supplying the brain, internal carotid artery can be followed through its curva- ture in the petrous temporal bone of the skull, before notably the arterial circle of Willis. This investigation does dividing into the anterior and middle cerebral arteries. Although the quality of such images One of the characteristic vascular lesions in the arteries cannot match the detail seen after an angiogram of select that make up the arterial circle of Willis is a type of blood vessels (shown in the next illustration), the nonin- aneurysm, called a Berry aneurysm. This is caused by a vasive nature of this procedure, and the fact that the patient weakness of part of the wall of the artery, causing a local is not exposed to any risk, clearly establishes this inves- ballooning of the artery. Often these aneurysms rupture tigation as desirable to provide some information about spontaneously, particularly if there is accompanying the state of the cerebral vasculature. This sudden rupture occurs into the sub- arachnoid space and may also involve nervous tissue of UPPER RADIOGRAPH the base of the brain. The whole event is known as a subarachnoid hemorrhage, and this diagnosis must be This arteriogram shows the circle of Willis as seen as if looking at the brain from below (as in the previous illus- considered when one is faced clinically with an acute major cerebrovascular event, without trauma, accompa- tration). The internal carotid artery goes through the cav- nied by intensely severe headache and often a loss of ernous (venous) sinus of the skull, forming a loop that is called the carotid siphon. Sometimes these aneurysms leak a little blood, which cerebral artery, which goes anteriorly, and the middle cere- bral artery, which goes laterally. The basilar artery is seen causes an irritation of the meninges and accompanying at its termination, as it divides into the posterior cerebral symptoms of headache. The anterior communicating artery is present, and visualize whether there is an aneurysm on one of the vessels of the circle, and whether the major blood vessels there are two posterior communicating arteries completing the circle, joining the internal carotid with the posterior are patent. Note to the Learner: One of the best ways of learning cerebral on each side. The blood supply to the brain- entation, as though you are looking at the patient “face- stem and the most common vascular lesions affecting this on,’ but, wtih his/her head tilted forward slightly. The two area will be discussed with the illustrations to follow. The lenticulostriate (striate) arteries given off en route supply the interior structures of the hemisphere (to CEREBRAL ANGIOGRAM be discussed with Figure 62). This radiograph shows the profuseness of the blood This radiograph was done by injecting a radiopaque dye supply to the brain, the hemispheres, and is presented to into the left internal carotid artery.
Certain drugs generic avanafil 50 mg overnight delivery impotence kit, such as chloramphenicol, produce marrow aplasia that is not dose dependent. Gold therapy and the inhalation of organic solvent vapors (e. In 2% to 10% of hepatitis patients, severe aplasia occurs 2 to 3 months after a seemingly typical case of acute disease. Often, the hepatitis has no obvious cause, and tests for hepatitis A, B, and C are negative. Aplasia can also be part of a prodrome to hairy-cell leukemia, acute lym- phoblastic leukemia, or, in rare cases, acute myeloid leukemia, or it can develop in the course of myelodysplasia. Parvovirus infection is the cause of the transient aplastic crises that occur in patients who have severe hemolytic disorders. The marrow in patients with such disorders must compensate for the peripheral hemolysis by increasing its production up to sevenfold. Although parvovirus can affect all precursor cells, the red cell precursors are the most profoundly affected. Anemia causes fatigue and shortness of breath; throm- bocytopenia causes petechiae, oral blood blisters, gingival bleeding, and hematuria, depending on the level of the platelet count. By far the major problem is the recurrent bac- terial infections caused by the profound neutropenia. The diagnosis of aplastic anemia requires a marrow aspirate and biopsy, as well as a thorough history of drug exposures, infections, and especially symptoms suggesting viral illnesses and serologic test results for hepatitis, infectious mononucleosis, HIV, and parvovirus. Measurement of red cell CD59 is helpful in the diagnosis of paroxysmal nocturnal hemoglobinuria. A 43-year-old white man presents to your clinic complaining of fatigue and paresthesias. He is a vegetar- ian and does not take a multivitamin. His examination reveals pallor, an absence of hepatosplenomegaly, normal muscle strength throughout, and loss of position sensation and vibratory sensation distally. A CBC reveals anemia, with a mean corpuscular volume (MCV) of 106 fl. His WBC, platelet count, and serum chemistries are normal. He has had no toxic exposures and is taking no medications. Which of the following statements about megaloblastic anemia is false? Absorption of cobalamin in the small intestine is dependent on pro- teins produced in the mouth and stomach B. Megaloblastic erythropoiesis is characterized by defective DNA synthe- sis and arrest at the G2 phase, with impaired maturation and a buildup of cells that do not synthesize DNA and that contain anom- alous DNA C. In most patients with severe cobalamin deficiency, the neurologic examination is normal D. Cobalamin deficiency is treated with parenteral cobalamin therapy Key Concept/Objective: To understand the etiology, diagnosis, and treatment of pernicious anemia Megaloblastic erythropoiesis is characterized by defective DNA synthesis and arrest at the G2 phase, with impaired maturation and a buildup of cells that do not synthesize DNA and that contain anomalous DNA. This condition leads to asynchronous maturation between the nucleus and cytoplasm. RNA production and protein synthesis continue; thus, larger cells, or megaloblasts, are produced. In addition to macrocytic and megaloblastic anemia, the patient with cobalamin deficiency may have weakness, lethargy, or dementia, as well as atrophy of the lingual papillae and glossitis. Neuropathy is the presenting fea- ture in about 12% of patients with cobalamin (vitamin B12) deficiency without concomi- tant anemia. Patients with severe cobalamin deficiency initially complain of paresthesia. The sense of touch and temperature sensitivity may be minimally impaired. The disease may progress, involving the dorsal columns, causing ataxia and weakness.
Teased fibers from a pa- tient with hereditary neuropa- thy and pressure palsy (HNPP) showing a large sausage shaped myelin enlargment (tomacula) Peripheral nerves in HNPP exhibit segmental demyelination and tomacula Anatomy/distribution (Fig generic 50 mg avanafil with visa erectile dysfunction pump as seen on tv. Patients appear to have recurrent mononeuropathies that cause weakness and Symptoms numbness, often following mild compression or trauma. Some cases present in childhood, Clinical syndrome/ while others can be delayed by several decades. Common sites for pressure signs palsies include the elbow and the neck of the fibula. In some cases, the neuropathies are progressive and can lead to a picture similar to CMT, with pes cavus, absent ankle reflexes, and distal weakness. One copy of the PMP-22 gene is missing, leading to a decrease in expression of this myelin protein. HNPP is inherited as an autosomal dominant event, although sporadic cases thought to arise from mistakes in meiosis can occur. EMG shows a demyelinating condition with distal motor latencies very pro- Diagnosis longed in comparison to the NCV findings. Entrapment neuropathies can be identified at common sites of pressure palsy (elbow, fibula). Genetic testing can be done to identify the chromosomal deletion. Differential diagnosis HNPP may resemble CMT, but the occurrence of pressure palsies and the EMG findings make HNPP distinctive. Inflammatory neuropathies like CIDP and multifocal motor neuropathy (MMN) with conduction block should also be considered. MMN does not usually show signs of sensory impairment with electrodiagnostic studies. The electrodiagnostic findings in CIDP are symmetri- cal. Surgical intervention for entrapment is controversial, as manipulations frequently cause nerve injury. Genetic counseling can be provided to family members. References Andersson PB, Yuen E, Parko K, et al (2000) Electrodiagnostic features of hereditary neuropathy with liability to pressure palsies. Neurology 54: 40–44 Chance PF (1999) Overview of hereditary neuropathy with liability to pressure palsies. Ann NY Acad Sci 883: 14–21 De Jonghe P, Timmerman V, Nelis E, et al (1997) Charcot-Marie-Tooth disease and related peripheral neuropathies. J Peripher Nerv Syst 2: 370–387 Pareyson D, Taroni F (1996) Deletion of the PMP22 gene and hereditary neuropathy with liability to pressure palsies. Curr Opin Neurol 9: 348–354 331 Porphyria Genetic testing NCV/EMG Laboratory Imaging Biopsy ++ ++ Porphyria causes axonal degeneration with some regions of demyelination. Anatomy/distribution Patients typically present with debilitating abdominal pain, changes in urine Symptoms color, constipation, and vomiting. Neuropathy usually follows the abdominal signs by several days, and resembles AIDP, with pain and potentially asymmet- ric weakness. CNS disturbances can precede neuropathy, including agitation, psychosis, Clinical syndrome/ seizures, and eventually coma. Weakness can involve the face and respiratory signs muscles. In some forms of porphyria, skin blisters can accompany an acute attack. Attacks can be precipitated by drugs that stress liver function, fasting, stress, and alcohol. Porphyria is rare and caused by disruption of heme biosynthesis.
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