Patient portals

Fig.9.11a-c. Focal nodular hyperplasia associated with hemangioma. a Contrast-enhanced arterial phase shows typical FNH nodule which appears as hyperdense lesion with a small hypodense central scar. b,c In segment Vll of the same patient portal (b) and equilibrium phase (c) CT scans show a hyperdense small nodule whose imaging pattern is consistent with that of hemangioma (arrows)... 

They also are important portals for systemic therapy. However, many variables can influence dmg dissolution and absorption ia these areas, including rate of gastric emptying, intestinal motility, mass and pH of intestinal contents, and condition of the absorbiag surfaces (15—17). These variables, ia turn, can be affected by the patient s disease, posture, and eating habits, and even by such aspects of the treatment as the timing of doses (11). 

Garcea, G. et al.. Detection of curcumin and its metabolites in hepatic tissue and portal blood of patients following oral administration, Br. J. Cancer, 90, 1011, 2004. 

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

List the treatment goals for a patient with portal hypertension and its complications. 

Increased intrahepatic resistance to portal flow increases pressure on the entire splanchnic bed an enlarged spleen (splenomegaly) is a common finding in cirrhotic patient and can result in thrombocytopenia due to splenic sequestration of the platelets. Portal hypertension mediates systemic and splanchnic arterial vasodilation through production of nitric oxide and other vasodilators in an attempt to counteract the increased pressure gradient. Nitric oxide causes a fall in systemic arterial pressure unfortunately, this activates both the renin-angiotensin-aldosterone and sympathetic nervous systems and... 

Patients with ascites or known varices must be assumed to have portal hypertension and are treated as such, even if direct measurements of portal pressure have not been made.29... 

Non-selective fi-blockers such as propranolol and nadolol are first-line treatments to reduce portal hypertension. This effect reduces bleeding and decreases mortality in patients with known varices. Use of (1-blockers to prevent variceal formation is controversial. 

Only non-selective p-blockers reduce bleeding complications in patients with known varices. Blockade of P, receptors reduces cardiac output and splanchnic blood flow. 02-Adrenergic blockade prevents p2-receptor-mediated splanchnic vasodilation while allowing unopposed a-adrenergic effects this enhances vasoconstriction of both the systemic and splanchnic vascular beds. The combination of P, and P2 effects makes the non-selective p-blockers preferable to car-dioselective agents in treating portal hypertension.1,36,41... 

Nitrates have been suggested in patients who do not achieve therapeutic goals (heart rate reduction) with P-blocker therapy alone. Trials to evaluate the effects of nitrates (e.g., isosorbide mononitrate) on portal pressure, both alone and in combination with P-blockers, show enhanced reduction of portal pressure however, there is an increase in mortality when nitrates are used alone. Adverse effects are significantly higher in patients treated with the combination of non-selective P-blockers and nitrates as opposed to P-blocker monotherapy.42,43 Unfortunately,... 

About 10% of infected patients develop reactivation TB, with half occurring in the first 2 years after infection.2 6 12 Upper lobe pulmonary disease is the most common (85% of cases).2 Caseating granulomas result from the vigorous immune response, and liquefaction leads to local spread. Eventually, a pulmonary cavity results, and this provides a portal to the outside that allows for person-to-person spread. Bacterial counts in the cavities can be as high 1011 per liter of cavitary fluid (108 per milliliter).2,15 Prior to the chemotherapy era, pulmonary TB usually was associated with hypoxia, respiratory acidosis, and eventually death. 

The most important sequelae of portal hypertension are the development of varices and alternative routes of blood flow. Patients with cirrhosis are at risk for varices when portal pressures exceed the vena cava pressure by greater than or equal to 12 mm Hg. 

All patients with cirrhosis and portal hypertension should be considered for endoscopic screening, and patients with large varices should receive primary prophylaxis with /J-adrenergic blockers. 

Vasoactive drug therapy (somatostatin, octreotide, or terlipressin) to stop or slow bleeding is routinely employed early in patient management to allow stabilization of the patient and to permit endoscopy to proceed under more favorable conditions. These agents decrease splanchnic blood flow and reduce portal and variceal pressures, without significant adverse effects. 

For patients who fail to achieve sufficient reductions in portal pressure with /3-blocker therapy alone, combination therapy with isosorbide mononitrate may more effectively lower portal pressures. 

For patients with ascites, a serum-ascites albumin gradient should be determined. If the serum-ascites albumin gradient is greater than 1.1, portal hypertension is present with 97% accuracy. 

Approximately 20% of patients with chronic HBV infection develop complications of decompensated cirrhosis, including hepatic insufficiency and portal hypertension. HBV is a risk factor for development of hepatocellular carcinoma. 

Sookoian, S. etal., A1166C angiotensin II type 1 receptor gene polymorphism may predict hemodynamic response to losartan in patients with cirrhosis and portal hypertension, Am. J. Gastroenterol., 100, 636, 2005. 

The portals of entry for the smallpox virus are the mucous membranes of the upper respiratory tract. Smallpox is transmitted by large or small respiratory droplets and by contact with skin lesions or secretions. Patients are considered more infectious if they are actively coughing. Incubation period ranges from 10 to 14 days, but most... 

A wide spectrum of hepatic lesions has been reported in AIDS (H4), but it is not known whether the changes are related to the presence of HIV-1. Therefore, sections from livers of autopsied patients with AIDS were examined for the presence of HIV-1 antigen p 24 (core) and gp 41 (envelope) by the avidin-biotin-peroxidase complex methods using monoclonal antibodies. The most common histologic abnormalities were steatosis, portal inflammation, Kupffer cell hyperplasia, and focal hepatocellular and bile duct damage. Immunoreactivity for HIV-1 antigens was demonstrated in 80% of cases. 

The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are health topic pages which hst links to available materials relevant to isobutyryl-CoA dehydrogenase deficiency. Log on to httpvywww.nlm.nih.gov/medlineplus/healthtopics.html To access this system. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus hsted the following when searched for isobutyryl-CoA dehydrogenase deficiency ... 

Rectal Administer to adults during impending coma or coma stage of portal-systemic encephalopathy when the danger of aspiration exists or when endoscopic or intubation procedures interfere with oral administration. The goal of treatment is reversal of the coma stage so the patient can take oral medication. Reversal of coma may occur within 2 hours of the first enema. Start recommended oral doses before enema is stopped entirely. 

Hepatic function impairment Exercise caution when administering saquinavir to patients with hepatic insufficiency. Exacerbation of chronic liver dysfunction, including portal hypertension, in patients with underlying hepatitis B or C, cirrhosis or other underlying liver abnormalities have been reported. 

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