9 Matching Annotations
  1. Apr 2026
    1. The most common cause of ascites is portal hypertension secondary to chronic liver disease, which accounts for over 80% of patients with ascites

      injection drug use, a history of viral hepatitis or jaundice, and birth in an area endemic for hepatitis. A history of cancer or marked weight loss arouses suspicion of malignant ascites. Fevers may suggest

      nonportal hypertensive ascites include infections (tuberculous peritonitis), intra-abdominal malignancy, inflammatory disorders of the peritoneum, and ductal disruptions (chylous, pancreatic, biliary

      pericarditis. A large tender liver is characteristic of acute alcoholic hepatitis or Budd-Chiari syndrome (thrombosis of the hepatic veins). Large abdominal wall veins with cephalad flow suggest portal hypertension; inferiorly directed flow implies hepatic vein obstruction The physical examination is relatively insensitive for detecting ascitic fluid. In general, patients must have at least 1500 mL of fluid to be detected reliably by this method

      A PMN count of > 250/mcL (0.25 × 109/L) (neutrocytic ascites) with a PMN percentage of > 75% of all white cells is highly suggestive of bacterial peritonitis, either spontaneous primary peritonitis or secondary peritonitis (due to an intra-abdominal source of infection, eg, a perforated viscus or appendicitis

  2. Jul 2024
  3. Oct 2023
  4. Apr 2022
    1. The pathogenesis of hypertension is multifactorial and complex, being related to differing concentrations of sodium and potassium in the body, obesity, insulin resistance, high alcohol intake, low calcium intake, stress and ageing diseases. The three main factors that determine blood pressure are renal sodium excretion (and the resultant impact on plasma and total body volume), vascular tone and cardiac performance and these factors control the cardiac output, the intravascular volume and the systemic vascular resistance [3,6].

      Hypertension's pathogenesis and factors

  5. Sep 2020
  6. Apr 2020
    1. Richardson, S., Hirsch, J. S., Narasimhan, M., Crawford, J. M., McGinn, T., Davidson, K. W., Barnaby, D. P., Becker, L. B., Chelico, J. D., Cohen, S. L., Cookingham, J., Coppa, K., Diefenbach, M. A., Dominello, A. J., Duer-Hefele, J., Falzon, L., Gitlin, J., Hajizadeh, N., Harvin, T. G., … Zanos, T. P. (2020). Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. JAMA. https://doi.org/10.1001/jama.2020.6775

  7. Dec 2018
    1. Alzheimer's disease (AD) is not normally diagnosed until later in life, although evidence suggests that the disease starts at a much earlier age. Risk factors for AD, such as diabetes, hypertension and obesity, are known to have their affects during mid-life, though events very early in life, including maternal over-nutrition, can predispose offspring to develop these conditions. This study tested whether over-nutrition during pregnancy and lactation affected the development of AD in offspring, using a transgenic AD mouse model. Female triple-transgenic AD dam mice (3xTgAD) were exposed to a high-fat (60% energy from fat) or control diet during pregnancy and lactation. After weaning (at 3 weeks of age), female offspring were placed on a control diet and monitored up until 12 months of age during which time behavioural tests were performed. A transient increase in body weight was observed in 4-week-old offspring 3xTgAD mice from dams fed a high-fat diet. However, by 5 weeks of age the body weight of 3xTgAD mice from the maternal high-fat fed group was no different when compared to control-fed mice. A maternal high-fat diet led to a significant impairment in memory in 2- and 12-month-old 3xTgAD offspring mice when compared to offspring from control fed dams. These effects of a maternal high-fat diet on memory were accompanied by a significant increase (50%) in the number of tau positive neurones in the hippocampus. These data demonstrate that a high-fat diet during pregnancy and lactation increases memory impairments in female 3xTgAD mice and suggest that early life events during development might influence the onset and progression of AD later in life.
  8. Oct 2017
    1. Beta blockers have long been associated with sleep disturbances such as difficulty falling asleep, staying asleep, and insomnia. They have been shown to reduce the production of melatonin via specific inhibition of beta-1 adrenergic receptors. Melatonin is a hormone secreted by the pineal gland in the brain, and helps in maintaining normal circadian rhythms.6,20-21 People with hypertension already have a lower melatonin production rate than those with normal blood pressure.22

      The question becomes, then, do beta blockers impair sleep when exogenous melatonin is administered concurrently?