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Stroke
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The perfusion of an area of the brain with ischemia may require high BP since autoregulation is lost. Therefore, the BP is not decreased except if there are signs of other end-organ damage, or the use of recombinant tissue plasminogen activator (tPA) with or without mechanical thrombectomy is likely needed. Signs of other end-organ damage include acute MI, aortic dissection, hypertensive encephalopathy, pulmonary edema, acute renal failure, and retinal hemorrhages. Lowering the BP by 15% within 24 hours after the onset of stroke is done if the BP is 220/120 mm Hg or higher on 2 readings taken 15 minutes apart. If the patient is a good candidate for acute reperfusion therapy, but the BP is higher than 185/110 mm Hg, the BP can be treated to lower it to less than this level with labetalol, nicardipine, or clevidipine. Nicardipine is given via IV infusion at first, increasing doses every 5–15 minutes. Labetalol is given in an IV bolus over 1–2 minutes and can be repeated one time. Clevidipine is given via the same method but the dose is titrated, doubling every 2–5 minutes to reach the desired BP.
Emergency Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Alastair Brookes, Yiu-Che Chan, Rebecca Fish, Fung Joon Foo, Aisling Hogan, Thomas Konig, Aoife Lowery, Chelliah R Selvasekar, Choon Sheong Seow, Vishal G Shelat, Paul Sutton, Colin Walsh, John Wang, Ting Hway Wong
What complications can SIRS lead to?End-organ damage: Acute lung injuryAcute kidney injuryMultiorgan dysfunction syndromeShock
Metabolic Diseases
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Stephanie Grünewald, Alex Broomfield, Callum Wilson
Fabry disease is a lysosomal storage disease and accumulation of α-D-galactosyl moieties, particularly of globotriaosylceramide (Gb3) appears to be the initiation factor of the pathological cascades. While these include features suggestive of a classic vasculopathy, the overall pathological process is still poorly understood. Once significant end-organ damage has occurred, it is largely irreversible. The gene for Fabry disease, GLA, is on the X chromosome. Males tend to have more severe and earlier disease many females are also affected. There is a degree of genotype–phenotype correlation but no particular common mutation.
Real-world effectiveness of voxelotor for treating sickle cell disease in the US: a large claims data analysis
Published in Expert Review of Hematology, 2022
Nirmish Shah, Thokozeni Lipato, Ofelia Alvarez, Thomas Delea, Alexander Lonshteyn, Derek Weycker, Andy Nguyen, Anne Beaubrun, Irene Agodoa
Sickle cell disease (SCD) is a systemic, inherited disorder affecting approximately 100,000 people in the United States [1]. It predominantly occurs in ethnic groups of African, Middle Eastern, South Mediterranean, and Indian descent [2]. Mutations in the gene encoding hemoglobin (Hb) subunit β lead to sickle Hb (HbS), which then polymerizes under deoxygenated conditions and thereby disturbs red blood cell (RBC) shape. The consequences include the chronic destruction of RBCs, anemia, and limited oxygen delivery. This, in turn, can affect the function of various organs and increase the risk of morbidity, including disease progression and end-organ damage that can substantially impact quality of life [1–4]. Although mortality in children has decreased over time, mortality rates in adults have remained high over the past few decades [5]. Characteristic effects of SCD are chronic anemia, hemolysis, and painful vaso-occlusive crises (VOCs) [2–4]. VOCs cause reoccurring episodes of severe pain and are often the main reason for patient hospitalizations [6–9].
Management of asymptomatic severe hypertriglyceridemia
Published in Baylor University Medical Center Proceedings, 2022
Nathalie V. Scherer, Dipesh Bista
Patients presenting with hypertriglyceridemia of this severity are rare. When these patients do present, the highest priority is to lower TG as fast as possible to prevent morbidity and mortality that results from end-organ damage, which is associated with the increased viscosity of TG-rich plasma. This end-organ damage includes acute pancreatitis, acute kidney injury, acute respiratory failure, and myocardial infarction.3 Intravenous insulin, fibrates, and omega-3 fatty acids decrease serum TG breakdown by upregulating lipoprotein lipase activity and reducing the production of new TG.5 In patients with severe hypertriglyceridemia, information on the success of treatments has come primarily from case reports and retrospective chart reviews that have shown efficacy with the use of plasmapheresis.6 TPE was indicated in our patient and was successful in reducing her severe hypertriglyceridemia.7
Antioxidant and vasorelaxant effects of aqueous extract of large cardamom in L-NAME induced hypertensive rats
Published in Clinical and Experimental Hypertension, 2020
S K Kanthlal, Jipnomon Joseph, Bindhu Paul, Vijayakumar M, Uma Devi P
Hypertension, a global public health problem, is a major cause of morbidity and cardiovascular mortality. If not treated appropriately, it can lead to end-organ damage manifested as stroke, coronary heart disease, renal failure, etc. Optimal antihypertensive drug treatment can decrease the end-organ damage and hence reduce the incidence of cardiovascular events (1–4). Endothelial dysfunction resulting due to loss of balance between relaxing and constricting factors has been implicated in the pathogenesis of hypertension. This can lead to decreased nitric oxide (NO) bioavailability and impairment of vascular tone. In hypertension, there is excess production of reactive oxygen species (ROS) that is not counterbalanced by the body’s endogenous defense mechanisms. Angiotensin II has also been reported to stimulate ROS production through the activation of vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (5–10).