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The same disorder may be seen under conditions of severe dietary deprivation (Strachan syndrome blood pressure varies greatly purchase discount betapace line, page 992) and in patients with vitamin B12 deficiency (page 994) blood pressure under stress order 40mg betapace with mastercard. Another cause is Leber hereditary optic atrophy blood pressure form purchase betapace overnight delivery, an inherited disorder of mitochondria blood pressure juice betapace 40mg low cost, a subject that is reviewed by Newman and discussed in Chap. Subacute optic neuropathy of possible toxic origin has been described in Jamaican natives. It is characterized by a bilaterally symmetrical central visual loss and may have additional features of nerve deafness, ataxia, and spasticity. A similar condition has been described in other Caribbean countries, most recently in Cuba, where an optic neuropathy of epidemic proportions was associated with a sensory polyneuropathy. A nutritional etiology, rather than tobacco use (putatively, cigars in the Cuban epidemic), is likely but has not been proved conclusively (see Sadun et al and the Cuba Neuropathy Field Investigation report). Impairment of vision due to methyl alcohol intoxication (methanol) is abrupt in onset and characterized by large symmetrical central scotomas as well as symptoms of systemic disease and acidosis. The subacute development of central field defects has also been attributed to other toxins and to the chronic administration of certain therapeutic agents: halogenated hydroxyquinolines (clioquinol), chloramphenicol, ethambutol, isoniazid, streptomycin, chlorpropamide (Diabinese), inflixamab, and various ergot preparations. The main drugs reported to have a toxic effect on the optic nerves are listed in Table 13-3 and have been catalogued by Grant. Developmental Abnormalities Congenital cavitary defects due to defective closure of the optic fissure may be a cause of impaired vision because of failure of development of the papillomacular bundle. Usually the optic pit or a larger coloboma is unilateral and unassociated with developmental abnormalities of the brain (optic disc dysplasia and dysplastic coloboma). Vision may also be impaired as a result of developmental anomalies of the optic nerves; the discs are of small diameter (hypoplasia of the optic disc or micropapilla). Toxins and drugs Methanol Ethambutol Chloroquine Streptomycin Chlorpropamide Chloramphenicol Infliximab Ergot compounds, etc. Radiation-induced optic neuropathy Other Optic Neuropathies Optic nerve and chiasmal involvement by gliomas, meningiomas, craniopharyngiomas, and metastatic tumors (most often from lung or breast) may cause scotomas and optic atrophy (Chap. Pituitary tumors characteristically cause bitemporal hemianopia, but very large adenomas, in particular if there is pituitary apoplexy, can cause blindness in one or both eyes (see page 577). Of particular importance is the optic nerve glioma that occurs in 15 percent of patients with type I von Recklinghausen neurofibromatosis. Usually it develops in children, often before the fourth year, causing a mass within the orbit and progressive loss of vision. If the eye is blind, the recommended therapy is surgical removal to prevent extension into the optic chiasm and hypothalamus. If vision is retained, radiation and chemotherapy are the recommended forms of treatment. Thyroid ophthalmopathy with orbital edema, exophthalmos, and usually a swelling of extraocular muscles is an occasional cause of optic nerve compression. Anderson Cancer Center who received radiotherapy for carcinomas of the nasal or paranasal region, retinopathy occurred in 7, optic neuropathy with blindness in 8, and chiasmatic damage with bilateral visual impairment in 1. These complications followed the use of more than 50 Gy (5000 rad) of radiation (see Jiang et al). Finally, it should be mentioned again that long-standing papilledema from any cause may eventually lead to optic atrophy and blindness. In the case of pseudotumor cerebri, the visual loss may be unexpectedly abrupt, appearing in a day or less and even sequentially in both eyes. This seems to happen most often in patients with constitutionally small optic nerves, no optic cup of the nerve head, and, presumably, a small aperture of the lamina cribrosa. Thus the visual cortex receives a spatial pattern of stimulation that corresponds with the retinal image of the visual field. Visual impairments due to lesions of the central pathways usually involve only a part of the visual fields, and a plotting of the fields provides fairly specific information as to the site of the lesion. For purposes of description of the visual fields, each retina and macula are divided into a temporal and nasal half by a vertical line passing through the fovea centralis. A horizontal line represented roughly by the junction of the superior and inferior retinal vascular arcades also passes through the fovea and divides each half of the retina and macula into upper and lower quadrants. The retinal image of an object in the visual field is inverted and reversed from right to left, like the image on the film of a camera. Thus the left visual field of each eye is represented in the opposite half of each retina, with the upper part of the field represented in the lower part of the retina (see.
The brain edema is the result of active exocytosis of water rather than simply a passive leak from vessels subjected to high pressures pre hypertension emedicine buy 40mg betapace with mastercard. Treatment Lowering of the blood pressure with antihypertensive drugs may reverse the picture in a day or two hypertension 8 weeks pregnant order betapace online from canada. In the past pulse pressure is quizlet purchase betapace 40 mg with amex, when effective antihypertensive drugs were not available blood pressure chart blank purchase generic betapace online, the outcome was often fatal. The same can be accomplished by administering magnesium sulfate in the eclamptic woman. Treatment consists of measures that promptly reduce arterial blood pressure, but antihypertensive drugs must be used cautiously; a safe target is a pressure of 150/100 mmHg. Most of the vascular changes and edema are situated in the cortical watershed distributions between the middle and an anterior cerebral arteries. These imaging findings were transient, as was mild signal change in the occipital subcortical regions, the latter being typical of hypertensive encephalopathy, as in. These are discussed below, under "Arteritis Symptomatic of Underlying Systemic Disease and Sympathomimetic Drug Reactions. Diffuse and Focal Cerebral Vasospasm A focal reduction in the caliber of the basal vessels and their proximal branches is a well-known complication of subarachnoid hemorrhage, as described on page 718. Some degree of attenuation of large cerebral vessels is observed in hypertensive encephalopathy, in eclampsia, and with adrenergic drug use. A related condition of cerebral vasculitis caused by sympathomimetic drugs is discussed further on, with other vasculitides. The problem of stroke with migraine, which has a complex and uncertain relationship to vasospasm, is discussed on page 151. The middle cerebral artery and its branches are mainly affected; the angiographic appearance may be mistaken for arteritis. A number of similar cases have been described, and we have seen several that resulted in a small stroke. There may be a posterior leukoencephalopathy that is similar to the imaging appearance in hypertensive encephalopathy. A relationship to hypertensive encephalopathy or to delayed postpartum eclampsia has been suggested, because of the aforementioned white matter changes and the observation of widespread vasospasm in eclamptic women. The patients we have seen with this process, after several weeks of dramatically fluctuating focal neurologic symptoms and disabling headache, have recovered completely or nearly so. Calcium channel blockers or corticosteroids have been prescribed, but their effectiveness cannot be determined. It has recently been brought to attention- by Singhal and colleagues and others- that the use of serotonergic drugs may produce a similar syndrome of reversible multifocal vasospasm, severe headache, and stroke. One of their three patients was using the antimigraine medicine sumatriptan; the other two were using serotonin reuptake inhibitor antidepressants and, in addition, had taken over-the-counter cold remedies that included pseudophedrine and dextromethorphan; we are aware of other similar cases. These authors proposed that in these cases a "serotonin syndrome" had occurred, similar to what has been seen with overdoses of this class of antidepressants. There it was pointed out that meningovascular syphilis, tuberculous meningitis, fungal meningitis, and the subacute (untreated or partially treated) forms of bacterial meningitis may be accompanied by inflammatory changes and occlusion of the cerebral arteries or veins. Occasionally, in syphilitic, cryptococcal, and tuberculous meningitis, a stroke may be the first clinical sign of meningitis, but more often it develops well after the meningeal symptoms are established. Typhus, schistosomiasis, mucormycosis, malaria, and trichinosis are rare causes of inflammatory arterial disease, which, unlike the above, is not secondary to meningeal infections. In typhus and other rickettsial diseases, capillary and arteriolar changes and perivascular inflammatory cells are found in the brain; presumably they are responsible for the seizures, acute psychoses, cerebellar syndromes, and coma characterizing the neurologic disorder in these diseases. The internal carotid artery may be occluded in diabetic patients as part of the orbital and cavernous sinus infections with mucormycosis. Parasites have been found in the brain; in one of our patients the cerebral lesions were produced by bland emboli arising in the heart and related to a severe myocarditis. In cerebral malaria, convulsions, coma, and sometimes focal symptoms appear to be due to the blockage of capillaries and precapillaries by masses of parasitized red blood corpuscles. Noninfectious Inflammatory Diseases of Cranial Arteries Included under this heading is a diverse group of arteritides that have little in common except their tendency to involve the cerebral vasculature.
For those with renal dysfunction blood pressure chart while pregnant purchase discount betapace line, only ~25% are expected to demonstrate renal improvement arteria hepatica comun cheap betapace 40 mg online, with deterioration in renal function in another 25% and stable function in ~50% hypertensive emergency buy 40 mg betapace. Small kidneys (<8 cm by ultrasound) are much less likely to respond favorably to revascularization arrhythmia treatments buy betapace cheap online. Renal biopsy will also demonstrate glomerulosclerosis and interstitial nephritis; pts will typically exhibit moderate proteinuria, i. Malignant nephrosclerosis may be seen in association with cocaine use, which also increases the risk of renal progression in pts with "benign" arteriolar nephrosclerosis. Aggressive control of bp can usually but not always halt or reverse the deterioration of renal function, and some pts have a return of renal function to near normal. Risk factors for progressive renal injury include a history of severe, longstanding hypertension; however, African Americans are at particularly high risk of progressive renal injury. Laboratory evaluation will usually reveal evidence of a microangiopathic hemolytic anemia, although this may be absent in certain causes. The reticulocyte count should be elevated, along with an increase in the red cell distribution width. Examination of the peripheral smear is key, since the presence of schistocytes will help establish the diagnosis. Treatment consists of bed rest, sedation, control of neurologic manifestations with magnesium sulfate, control of hypertension with vasodilators and other antihypertensive agents proven safe in pregnancy, and delivery of the infant. Stone formation begins when urine becomes supersaturated with insoluble components due to (1) low urinary volume, (2) excessive or insufficient excretion of selected compounds, or (3) other factors. Approximately 75% of stones are Ca-based (the majority Ca oxalate; also Ca phosphate and other mixed stones), 15% struvite (magnesium-ammonium-phosphate), 5% uric acid, and 1% cystine, reflecting the metabolic disturbance(s) from which they arise. Obstruction related to the passing of a stone leads to severe pain, often radiating to the groin, sometimes accompanied by intense visceral symptoms. Hyperoxaluria may be seen with intestinal (especially ileal) malabsorption syndromes. Ca oxalate stones may also form due to (1) a deficiency of urinary citrate, an inhibitor of stone formation that is underexcreted with metabolic acidosis; and (2) hyperuricosuria (see below). Uric acid stones develop when the urine is saturated with uric acid in the presence of an acid urine pH; pts typically have underlying metabolic syndrome and insulin resistance, associated with a relative defect in ammoniagenesis and urine pH that is <5. Hyperuricosuria without hyperuricemia may be seen in association with certain drugs. Cystine stones are the result of a rare inherited defect in renal and intestinal transport of several dibasic amino acids; the overexcretion of cystine (cysteine disulfide), which is relatively insoluble, leads to nephrolithiasis. Stones begin in childhood and are a rare cause of staghorn calculi; they occasionally lead to endstage renal disease. Table 154-1 outlines a reasonable workup for an outpatient with an uncomplicated kidney stone. Careful medical history and physical examination, focusing on systemic diseases 3. Nephrolithiasis Treatment of renal calculi is often empirical, based on odds (Ca oxalate stones most common), clinical Hx, and/or the metabolic workup. In contrast to prior assumptions, dietary calcium intake does not contribute to stone risk; rather, dietary calcium may help to reduce oxalate absorption and reduce stone risk. Table 154-2 outlines stone-specific therapies for pts with complex or recurrent nephrolithiasis. It is preponderant in women (pelvic tumors), elderly men (prostatic disease), diabetic pts (papillary necrosis), pts with neurologic diseases (spinal cord injury or multiple sclerosis, with neurogenic bladder), and individuals with retroperitoneal lymphadenopathy or fibrosis, vesicoureteral reflux, nephrolithiasis, or other causes of functional urinary retention. Physical exam may reveal an enlarged bladder by percussion over the lower abdominal wall. Laboratory studies may show marked elevations of blood urea nitrogen and creatinine; if the obstruction has been of sufficient duration, there may be evidence of tubulointerstitial disease. Urinalysis is most often benign or with a small number of cells; heavy proteinuria is rare.
Other viruses will involve particular classes of neurons of the brain or spinal cord blood pressure medication kills buy betapace 40 mg low price, giving rise to the more serious disorders such as encephalitis and poliomyelitis blood pressure chart generator discount 40 mg betapace with mastercard, respectively arteria iliolumbalis effective 40 mg betapace. In some viral infections hypertension over 60 order betapace uk, the susceptibility of particular cell groups is even more specific. In poliomyelitis, for example, motor neurons of cranial and spinal nerves are particularly vulnerable; in rabies, there is an affinity for neurons of the trigeminal ganglia, cerebellum, and lim631 Pathways of Infection Viruses gain entrance to the body by one of several pathways. Other viruses are acquired by inoculation, as a result of the bites of animals. Following entry into the body, the virus multiplies locally and in secondary sites and usually gives rise to a viremia. The virus or its nucleocapsid must be capable of penetrating the cell, mainly by the process of endocytosis, and of releasing its protective nucleoprotein coating. In acute encephalitis, susceptible neurons are invaded directly by virus and the cells undergo lysis. Neuronophagia (phagocytosis of affected neurons and their degenerative products by microglia) is a mark of this phenomenon. With other viral infections, zones of tissue necrosis of gray and white matter occur, and these changes may localize in particular regions. Only then will the inflammatory reaction to viral replication create symptoms (pain, weakness, sensory loss). Differentiating cells of the fetal brain have particular vulnerabilities, and viral incorporation may give rise to malformations and to hydrocephalus. In still other circumstances, a viral infection may exist in the nervous system for a long period before exciting an inflammatory reaction. There is no need, however, to consider these viruses individually, since there are only a limited number of ways in which they express themselves clinically. Seven syndromes occur with regularity and should be familiar to neurologists: (1) acute aseptic ("lymphocytic") meningitis; (2) chronic meningitis; (3) acute encephalitis or meningoencephalitis, which may be generalized or focal; (4) herpes zoster ganglionitis; (5) chronic invasion of nervous tissue by retroviruses, i. The last group is presently distinguished from infections with the unique prion agents, which are discussed later in the chapter. The term is now applied to a symptom complex that is produced by any one of numerous infective agents, the majority of which are viral (but a few of which are bacterial- mycoplasma, Q fever, other rickettsial infections, etc. Since aseptic meningitis is rarely fatal, the precise pathologic changes are uncertain but are presumably limited to the meninges. Headache, perhaps more severe than that associated with other febrile states, is the most frequent symptom. A variable degree of lethargy, irritability, and drowsiness may occur; confusion, stupor, and coma mark the case as an encephalitis rather than a meningitis. Stiffness of the neck and spine on forward bending attests to the presence of meningeal irritation (meningismus), but at first it may be so slight as to pass unnoticed. Here the Kernig and Brudzinski signs help very little, for they are often absent in the presence of manifest viral meningitis. When there are accompanying neurologic signs, they too tend to be mild or fleeting: paresthesias in an extremity, isolated strabismus and diplopia, a slight inequality of reflexes, or wavering Babinski signs. Other symptoms and signs are infrequent and depend mainly on the systemic effects of the invading virus; these include sore throat, nausea and vomiting, vague weakness, pain in the back and neck, conjunctivitis, cough, diarrhea, vomiting, rash, adenopathy, etc. The childhood exanthems associated with meningitis and encephalitis (varicella, rubella, mumps) produce well-known eruptions and other characteristic signs. An erythematous papulomacular, nonpruritic rash, confined to the head and neck or generalized, may also be a prominent feature (particularly in children) of certain echoviruses and Coxsackie viruses. An enanthem (herpangina), taking the form of a vesiculoulcerative eruption of the buccal mucosa, may also occur with these viral infections. In milder cases, in the first hours or day of the illness, there may be no abnormalities of the spinal fluid, and the patient may erroneously be thought to have migraine or a headache induced by a systemic infectious illness. Micro-organisms cannot be demonstrated by conventional smear or bacterial culture. Of these, the most common are the enteroviral infections- echovirus and Coxsackie virus.
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In the latter instances arrhythmia flashcards cheap betapace 40 mg, spontaneous discharges may occur from an instability of axon polarization; hence a single nerve impulse may initiate a train of action potentials in nerve and muscle blood pressure 13080 discount 40 mg betapace, as in the tetany of hypocalcemia and in hemifacial spasm arrhythmia university order betapace line. The common cramps of calf and foot muscles (painful blood pressure chart hypotension cheap betapace 40 mg with visa, sustained contractions with motor unit discharges at frequencies up to 200 per second) may be due to increased excitability (or unstable polarization) of the motor axons. Quinine, procainamide, diphenhydramine, and warmth reduce the irritability of nerve and muscle fiber membranes, as do a number of anticonvulsant drugs that act by blocking sodium channels and thereby limiting spontaneous membrane discharges. To summarize, the muscle fiber, which is wholly dependent on the nerve for its stimulus to contract, may be physiologically activated or paralyzed in a number of ways. Similarly, the mechanisms involved in fasciculations, cramps, and muscle spasms may be traced to a number of different loci in the neuromuscular apparatus. There may be an unstable polarization of the nerve fibers, as in tetany and in dehydration with salt depletion, or unexplained hyperirritability of the motor unit, as in amyotrophic lateral sclerosis. The threshold of mechanical activation or electrical reactivation of the sarcolemmal membrane may be reduced, as in myotonia, or impairment of an energy mechanism within the fiber may slow the contractile process, as in hypothyroidism; or a deficiency of phosphorylase, which deprives muscle of its carbohydrate energy source, may prevent relaxation, as in the contracture of McArdle disease. Lesions of the most peripheral branches of nerves, which allow nerve regeneration, may give rise to continuous activity of motor units. This is expressed clinically as a rippling of muscle, or myokymia (see pages 1104 and 1278). In recent years, new technologies have made it possible to isolate each of the proteins and channels involved in neuromuscular transmission and the excitation-contraction-relaxation of muscle fibers. This information is being increasingly applied to the analysis of gene products in the normal state and under conditions of disease. Pertinent comments and references to this subject are found in the chapters that follow. Hypercalcemia above 12 mg/dL (as occurs in vitamin D intoxication, hyperparathyroidism, carcinomatosis, sarcoid, and multiple myeloma) causes weakness and lethargy, perhaps on a central basis. Extreme hypophosphatemia, observed most often with intravenous hyperalimentation or bone tumor, can cause acute areflexic paralysis with nerve conduction abnormalities. Reduction in the plasma concentration of magnesium also results in tremor, muscle weakness, tetanic muscle spasms, and convulsions; a considerable increase in magnesium levels leads to muscle weakness and depression of central nervous function. Since high concentrations of this enzyme are found in heart muscle and brain, raised serum values may be due to myocardial or cerebral infarction as well as to the necrotizing diseases of striated muscle (polymyositis, muscle trauma, muscle infarction, paroxysmal myoglobinuria, and the more rapidly advancing muscular dystrophies). Even more interesting is the rise in serum enzyme concentration in some children with progressive muscular dystrophy before there is enough destruction of fibers for the disease to be clinically manifest, at least as judged by the relatively crude tests of muscle strength. These disorders reflect the concentrations of electrolytes in the intra- and extracellular fluids. The normal reaction of muscle to direct percussion is also reduced or abolished, suggesting impairment of transmission along the sarcolemmal membranes themselves. Hypocalcemia of 7 mg/dL or less (as in rickets or hypoparathyroidism) or relative reduction in the proportion of ionized calcium (as in hyperventilation) causes increased muscle irritability and spontaneous discharge of sensory and motor nerve fibers. It would ґ be expected that the values would always be normal in denervation paralysis with muscular atrophy, but elevations are sometimes observed in patients with progressive spinal muscular atrophy and amyotrophic lateral sclerosis particularly if there is relatively rapid progression of muscle denervation. Detailed examination will usually reveal slight proximal weakness and perhaps minimal calf enlargement characteristic of the mildest forms of Becker dystrophy. In these latter instances, muscle biopsy shows a mosaic pattern of dystrophin immunostaining; i. Measurement in the serum of various transaminases or lactate dehydrogenase is not particularly useful for the diagnosis of muscle disease because of their ubiquitous distribution in many mammalian tissues. Destruction of striated muscle, regardless of the process- whether trauma, ischemia, or metabolic disease- liberates myoglobin, and because of its relatively small size, the molecule filters through the glomeruli and appears in the urine, imparting to it a burgundy red color. Because of the low renal threshold for myoglobin, excretion of this pigment is so rapid that the serum remains uncolored. In contrast, because of the high renal threshold for hemoglobin, destruction of red blood corpuscles colors both the serum and the urine. Myoglobinuria should thus be suspected when the urine is deep red and the serum is normal in color. It is estimated that 200 g of muscle must be destroyed to color the urine visibly (Rowland). As in hemoglobinuria, the guaiac and benzidine tests of urine are positive if myoglobin is present. On spectroscopic analysis, myoglobin shows an absorption band at 581 nm, but the most sensitive method for measuring myoglobin in the urine and serum is by radioimmunoassay (Rosano and Kenny). Hyperkalemia, hyperphosphatemia, and hypercalcemia may complicate massive rhabdomyolysis.
