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Clinical Director, Western Michigan University Homer Stryker M.D. School of Medicine

Of interest, losartan did not have an incremental effect beyond that of the -blocker in preventing myocardial infarction, probably reflecting robust cardioprotective effects of the -blocker class. Losartan had a minimal effect on blood pressure, and its favorable renal effects seemed to be independent of blood pressure. Irbesartan treatment slowed the progression of renal disease compared with both placebo and amlodipine despite equivalent blood pressure reductions with amlodipine. The primary composite end point was reduced by 25% in the losartan group compared with the atenolol group. The reduction in heart failure was 41% greater in the losartan group than in the atenolol group. These findings are consistent with a renal mechanism as the "final common pathway" in the pathogenesis of clinical hypertension. Activation of these mineralocorticoid receptors is thought to stimulate intra- and perivascular fibrosis and interstitial fibrosis in the heart. The nonselective aldosterone antagonist spironolactone and the novel selective aldosterone receptor antagonist eplerenone are effective in preventing or reversing vascular and cardiac collagen deposition in experimental animals. Spironolactone and the better-tolerated selective aldosterone receptor antagonist eplerenone are being used to treat patients with hypertension, heart failure, and acute myocardial infarction complicated by left ventricular dysfunction or heart failure because of their unique tissue protective effects (106, 107). Evidence is accumulating that aldosterone excess may be a more common cause of or contributing factor to hypertension than previously thought. Hypokalemia was thought to be a prerequisite of primary hyperaldosteronism, but it is now recognized that many patients with primary hyperaldosteronism may not manifest low serum potassium levels. Accordingly, screening hypertensive patients for hyperaldosteronism has expanded and a higher prevalence of the disorder has been revealed. Prevalence rates between 8% and 32% have been reported on the basis of the patient population being screened (higher in referral practices, where the patient mix tends to be enriched with refractory hypertension and lower in family practices or community databases) (108). In our own referral practice, which includes a high proportion of patients with treatment-resistant hypertension, the prevalence of aldosterone excess is 24% (109). Endothelial function in the normal vasculature and in the hypertensive vasculature. Large conductance vessels (left), for example, epicardial coronary arteries, and resistance arterioles (right), are shown. At the level of the small arterioles, reduced vascular tone is maintained by constant release of nitric oxide. At the level of conductance arteries, a similar imbalance in the activity of endothelial factors leads to a proatherosclerotic milieu that is conducive to the oxidation of low-density lipoprotein, the adhesion and migration of monocytes, and the formation of foam cells. These activities ultimately lead to the development of atherosclerotic plaques, the rupture of which, in conjunction with enhanced platelet aggregation and impaired fibrinolysis, results in acute intravascular thrombosis, thus explaining the increased risk for cardiovascular events in patients with hypertension. These mechanisms may be operative in patients with high normal blood pressure and may contribute to their increased cardiovascular risk. Nitric 772 4 November 2003 Annals of Internal Medicine Volume 139 · Number 9 oxide is released by normal endothelial cells in response to various stimuli, including changes in blood pressure, shear stress, and pulsatile stretch, and plays an important role in blood pressure regulation, thrombosis, and atherosclerosis Increased oxidant stress and endothelial dysfunction may thus predispose to hypertension. Current treatment guidelines generally recommend a generic approach to treating hypertension, with little emphasis on selecting therapy on the basis of the underlying pathophysiology of the elevated blood pressure (100 ­102). With increased recognition of specific causes, it may be possible to develop therapies selective for distinct pathophysiologic mechanisms with fewer adverse effects, resulting in more effective blood pressure reduction. Use of powerful new techniques of genetics, genomics, and proteomics, integrated with systems physiology and population studies, will make possible more selective and effective approaches to treating and even preventing hypertension in the coming decades. Oparil (Abbott Laboratories, AstraZeneca, Aventis, Boehringer Ingelheim, Bristol MyersSquibb, Eli Lilly, Forest Laboratories, GlaxoSmithKline, King, Novartis (Ciba), Merck & Co. Circulating endothelin levels are increased in some hypertensive patients, particularly African Americans and persons with transplant hypertension, endothelial tumors, and vasculitis (114). Endothelin is secreted in an abluminal direction by endothelial cells and acts in a paracine fashion on underlying smooth-muscle cells to cause vasoconstriction and elevate blood pressure without necessarily reaching increased levels in the systemic circulation. Endothelin receptor antagonists reduce blood pressure and peripheral vascular resistance in both normotensive persons and patients with mild to moderate essential hypertension (115), supporting the interpretation that endothelin plays a role in the pathogenesis of hypertension. Development of this drug class for the indication of systemic hypertension has been discontinued because of toxicity (teratogenecity, testicular atrophy, and hepatotoxicity). However, endothelin antagonists are indicated for treating pulmonary hypertension (116) and may prove to be clinically useful in the therapy for other forms of vascular disease.

Intermediate uveitis-The inflammation of the pars plana part of the ciliary body. Anatomical classification-The International Uveitis Study Group has recommended the classification based on anatomical location of uveal tract. Anterior uveitis-It can be divided as follows: · Iritis-The inflammation mainly affects the iris. Intermediate uveitis-There is inflammation of pars plana part of the ciliary body and peripheral retina and underlying choroid. There is associated inflammation of adjacent retina and hence the term "chorioretinitis" is used. Clinical classification-Uveitis can also be categorized by the clinical courses as: i. Pathological classification-Uveitis can be further divided according to the pathological lesions which can be of two types: i. Inflammation is insidious in onset, chronic in nature with minimum clinical features. Non-granulomatous uveitis-It is usually due to allergic or immune related reaction. Endogenous infection-Organisms lodged in some other organ of the body reach the eye through the bloodstream. Bacterial · Septicaemia due to Streptococcus, Staphylococcus, Meningococcus, Pneumococcus, etc. Allergic inflammation-It occurs in a sensitized ocular tissue which comes in contact again with the same organism or its protein (antigen-antibody reaction). Hypersensitivity reaction-It occurs due to hypersensitivity reaction to autologous tissue components (autoimmune reaction). Allergic (exudative or non-granulomatous)-It is of acute onset and short duration. It is characterized by the presence of fine keratic precipitates which are composed of lymphoid cells and polymorphs. Keratic precipitate Aqueous flare Iris nodule Posterior synechiae Posterior segment Slow and insidious Chronic course with remissions and exacerbations Features of low grade inflammation Mutton fat kp Mild with few cells Common Marked and organised Commonly involved 1. There is severe neuralgic pain referred to forehead, scalp, cheek, malar bone, nose and teeth (as the iris is richly supplied by sensory nerves from the ophthalmic division of 5th nerve). Lacrimation and photophobia may be present (without any mucopurulent discharge) due to associated keratitis. Impaired vision-It is mainly due to hazy plasmoid aqueous and opacity in the media. Photophobia is due to pain induced by pupillary constriction and ciliary spasm because of inflammation. Circumciliary congestion-There is hyperaemia around the limbus which is dull purple-red in colour. There is plasmoid aqueous containing leucocytes, minute flakes of coagulated proteins and fibrinous network. Aqueous flare grading +1 Faint +2 Moderate +3 Marked +4 Intense Slit-lamp examination in acute iridocyclitis - - - - Just detectable Iris details clear Iris details hazy With severe fibrinous exudate b. Keratic precipitates (kp)-The exudate tends to stick to the damaged endothelium in the lower part of cornea in a triangular pattern due to the convection currents in anterior chamber and effect of gravity. They are characteristic of granulomatous uveitis with predominance of macrophages. Hypopyon-In severe cases of iritis polymorphonuclear leucocytes are poured out which sink to the bottom of the anterior chamber forming hypopyon. Hyphaema-Blood in the anterior chamber rarely occurs due to spontaneous haemorrhage. It reacts sluggishly to light due to irritation of the third nerve endings in iris. Ectropion of uveal pigment is due to the contraction of exudates upon the iris so that the posterior surface of iris folds anteriorly. Anterior peripheral synechiae-The iris gets attached to the periphery of the cornea.

In the medullary collecting ducts and papillary ducts, urea follows its concentration gradient and passively diffuses out of the filtrate and into the interstitial fluid, further concentrating the medullary interstitial fluid. Note that the urea diffusing out of the medullary collecting duct constitutes only a small amount of the total urea; much of the urea remains in the filtrate and is excreted in the urine. The Vasa Recta and the Countercurrent Exchanger the steep medullary osmotic gradient created by the countercurrent multiplier and urea recycling is maintained by the vasa recta, the capillaries surrounding the nephron loops of juxtamedullary nephrons. The vasa recta act as a special kind of vascular system called a countercurrent exchanger. Like the limbs of the nephron loop, the vasa recta descend into the renal medulla, and then, following a hairpin turn, ascend toward the renal cortex. This arrangement of countercurrent flow, the blood flowing in the opposite direction from the filtrate, enables them to exchange substances. First notice that the blood within the vasa recta has a concentration of about 300 mOsm as it enters the renal medulla (to the right of the nephron, as shown in the figure). This means that 1 as the blood descends into the medulla it is hypo-osmotic to the interstitial fluid. As we saw earlier, this situation causes water to leave the blood and enter the interstitial fluid by osmosis. In addition, more NaCl is present in the interstitial fluid than in the blood, which causes NaCl to diffuse from the interstitial fluid into the blood. The blood in the vasa recta continues to pick up NaCl and lose water as it descends deeper into the renal medulla. By the time the blood reaches the deepest part of the medulla, it has a concentration of about 1200 mOsm. However, 2 as the vasa recta ascend through the medulla, the gradient is reversed-the blood is now hyperosmotic to the interstitial fluid, and the opposite process occurs. NaCl now diffuses out of the blood and back into the interstitial fluid, and water moves by osmosis from the interstitial fluid into the blood. Notice what has happened here: All of the NaCl that was removed from the interstitial fluid by the blood in the descending limb of the vasa recta was "exchanged," or put back into the interstitial fluid by the blood in the ascending limb of the vasa recta. By the time the vasa recta exit the renal medulla, the blood has approximately the same concentration (about 300 mOsm) it had upon entering the renal medulla. The return of the blood to its initial osmolarity is critical, because it allows the vasa recta to deliver oxygen and nutrients to the cells of the medulla without depleting the medullary osmotic gradient necessary for water reabsorption and the production of concentrated urine. First, keep in mind that the entire homeostatic function of this system is to conserve water for the body when needed. Continued solute reabsorption, including urea recycling, from the filtrate in the medullary collecting duct adds to the gradient. The countercurrent exchanger of the vasa recta allows perfusion of the inner medulla while maintaining the medullary interstitial gradient. Filtrate from early distal tubule Late distal tubule 200 Cortical collecting duct 1 When filtrate enters the cortical collecting duct in the renal medulla, there is no osmotic gradient between the filtrate and the interstitial fluid, so no water is reabsorbed. Filtrate entering the renal medulla has the same concentration as the interstitial fluid, so no gradient is present to drive water reabsorption. The interstitial fluid in the renal medulla is more concentrated than the filtrate. Deeper into the medulla, interstitial fluid is more concentrated, so water reabsorption continues from the medullary collecting duct. The process continues because the interstitial fluid becomes progressively more concentrated in the deep renal medulla, allowing continued water reabsorption. We cannot make more concentrated urine, because after this point there is no longer a gradient to drive osmosis. Regardless of the cause, the result is the same: excessive fluid retention leading to a decreased plasma osmolarity and a high urine osmolarity. Glomerulonephritis, or inflammation of the glomerulus, results in excessively leaky glomerular capillaries and damaged glomeruli. Which compensatory mechanisms would you expect to be triggered, and what effects would they have? What three factors allow the kidney to produce and maintain the medullary osmotic gradient?

Eventually spores are passed out with the feces and are ready to infect another host (3). Depending on the age and immune status of the host, the number of spores or oocysts ingested, and the pathogenicity of the parasites, these protozoa can cause asymptomatic infections, a self-limited diarrhea (usually lasting about 2 or 3 weeks), or a prolonged, severe diarrheal illness which may persist for months. It has been hypothesized that invasion of the intestinal cells stimulates the release of cytokines which activate phagocytes. These cells then release soluble factors which increase intestinal secretions of chloride and water, thereby causing symptoms of diarrhea. Cryptosporidium is the best studied of this group of parasites, but some fundamental questions concerning its pathogenicity remain, such as the possible production of an enterotoxin. Although the small intestine is the main site of infection, in some heavily parasitized patients, especially in the immunocompromised, the colon and liver may be also be affected. Dissemination to other parts of the body has only been observed regularly with Septata. Surveys to determine the prevalence of oocysts in stool samples generally report a higher incidence of infection in persons from Asia, Latin America, and Africa than in those from Europe and North America. Although only a small number of adults in developed countries have detectable oocysts in their stool specimens, antibodies to Cryptosporidium have been detected in 32­58% of population samples in Western countries (1). Therefore, many people in these countries have been exposed to this parasite during their lifetime. The other protozoa have been reported to cause diarrhea, at a lower frequency, in the same groups of people. In such patients with chronic diarrhea, 10­ 20% are infected with Cryptosporidium and 6­50% are infected with Septata or Enterocytozoon. Since the infective stages of these protozoa are present (at concentrations as high as 1,000,000/gram) in feces, some type of fecal contamination is responsible for new cases of diarrhea. Person-to-person transfer may occur in families and institutional settings such as daycare facilities. Although the infant was asymptomatic and the woman had washed her hands before preparing the salad, enough oocysts were transferred to the food to cause illness in more than half of the estimated 50 persons attending a social function (10). Water contaminated with oocysts (probably originating from animals) was responsible for the massive outbreak of cryptosporidiosis in Milwaukee (5) and for smaller outbreaks affecting 70­100 people in Nevada (6) and Florida (7) and for an outbreak of cyclosporiasis in Chicago (11). Cryptosporidium oocysts have also been isolated from cider made from apples which had fallen on the ground in a cow pasture (9) and from raw vegetables in Costa Rica (12). However, current methodology was not sensitive enough to detect oocysts on fresh fruit associated with these outbreaks. Efforts are underway to modify these assays so that low concentrations of Cryptosporidium and Cyclospora oocysts can be detected in foods. Cryptosporidium is notorious for its lack of host specificity, with most isolates from mammals capable of infecting many different mammalian species. In fact, a number of waterborne outbreaks of cryptosporidiosis in developed countries have resulted from contamination of drinking water sources with runoff from agricultural lands where infected cattle have grazed. Cyclospora oocysts, identical to those observed in human samples, have been isolated from fecal samples from baboons and chimpanzees in Africa (17). In addition, the investigation of the Chicago Cyclospora outbreak indicated that rodent or bird feces may have contaminated the drinking water supply for a dormitory. No cross connections between water and sewage pipes in the building were detected. But the drinking water, stored in a rooftop tank, was not adequately protected from the environment, and animal feces were observed on the rim of the tank. Cyclospora has also been isolated from stool specimens from members of a Peruvian family with diarrhea and from ducks bred by the family (18). High temperatures are known to be lethal to these protozoa and therefore boiled water and adequately heat-processed foods should be safe to consume. Recent experiments evaluating the efficacy of high-temperature­short-time pasteurization treatments demonstrated that heating to 71. Oocysts suspended in water retained their infectivity after 168 hours storage at +5°C and at ­10°C. At colder temperatures, infectivity was destroyed: at ­15, ­20, and ­70°C, no infective cells remained after 168, 24, and 1 hour of storage, respectively.