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Burns
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Brian Brisebois, Joyce McIntyre
Burn wounds produce a wide array of systemic effects including massive inflammation and a hypermetabolic state that can persist for years (Lundy). In a large case series of 242 children with severe burns, all patients experienced significant hypermetabolism, muscle loss, bone mineral content loss, serum protein abnormalities, cardiac abnormalities, and insulin resistance (Jeschke). The destruction of natural barriers, inflammation, and subsequent leaking of protein into the extravascular space results in rapid fluid shifts capable of causing severe edema and hypovolemic shock (Liu). In the United States, 67% of burns are small (<10% total surface body area, or TBSA) (Greenhalgh).
Heart disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
Following delivery, there is an immediate rise in cardiac output due to the relief of IVC obstruction and contraction of the uterus that empties blood into the systemic circulation. Cardiac output increases by 60%–80% followed by a rapid decline to prelabour values within about 1 hour of delivery. Transfer of fluid from the extravascular space increases venous return and stroke volume further.
Extrahepatic Synthesis of Acute Phase Proteins
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Gerhard Schreiber, Angela R. Aldred
A precursor-product relationship was indicated by structural13-15 and kinetic16-19 studies for an albumin-like protein synthesized in liver and albumin secreted into the medium of cell cultures (Figure 4) or into the bloodstream of living animals (Figure 5). From the bloodstream, plasma proteins migrate into the extracellular compartments of the body. For most plasma proteins, the amount found in the extravascular space is larger than in the intravascular space (see, e.g., References 4 and 20). Usually, the rates of migration of proteins from the vascular to the extravascular compartment are in the same range (see Reference 20 for rates of migration of albumin, transferrin, thiostatin, and α1-acid glycoprotein in healthy rats and in rats suffering from an acute inflammation).
Does cabergoline administration affect endometrial VEGFR-2 expression in a rat model of ovarian hyperstimulation syndrome?
Published in Gynecological Endocrinology, 2023
Nafiye Yilmaz, Pinar Gulsen Coban, Saynur Yilmaz, Hasan Ali Inal, Hakan Timur, Hacer Haltas
Ovarian hyperstimulation syndrome (OHSS) is one of the most severe and life-threatening iatrogenic complications of controlled ovarian hyperstimulation. OHSS is observed at a rate of 0.3% to 5% and can lead to severe morbidities, such as pleural effusion, acute renal insufficiency, and venous thromboembolism [1]. Various vasoactive-angiogenic substances have been implicated in the etiology of OHSS, including vascular endothelial growth factor (VEGF), prostaglandins, cytokines, renin-angiotensin-aldosterone, estradiol, progesterone, kinin-kallikrein, and nitric oxide. VEGF is attributed to be the leading factor in the shift of fluid into the extravascular space due to increased vascular permeability by activating VEGF receptor-2 (VEGFR-2) [2–6]. VEGF also plays a critical role in the stimulation of angiogenesis and endothelial cell mitosis [7–10].
Myopic Shift in a Patient with Dengue Fever
Published in Ocular Immunology and Inflammation, 2023
Helen Mi Fang, Oon Tek Ng, Rupesh Agrawal
Suprachoroidal effusion arises from a disturbance of the fluid equilibrium across the layers of the choroid. This condition can be classified into various pathophysiologic categories, including hydrodynamic, inflammatory, neoplastic or associated abnormal sclera.8 In our particular case, we postulate that an inflammatory mechanism is the most likely underlying cause, which can compromise vascular competence, resulting in an increased capillary protein permeability and accumulation of protein in the extravascular space. Another possible mechanism for the suprachoroidal effusion can be related to his acute transient hyponatremia, resulting in disturbances in the hydrodynamics of the suprachoroidal space. Hyponatremia is a known complication in patients with dengue fever,9 and this was previously described in a separate case report.10
Diuretic therapy in congestive heart failure
Published in Acta Cardiologica, 2022
Patrick Kennelly, Rajju Sapkota, Maimoona Azhar, Faisal Habib Cheema, Claire Conway, Aamir Hameed
Since mid-1990, the survival rates of those with HF have increased, leading to an increased prevalence of the disease. Our ability to increase survival time in those with HF can be partially attributed to a better and more appropriate use of pharmacological interventions [13]. These interventions also include the utilisation of diuretics such as spironolactone or eplerenone which have been found to reduce all-cause mortality, sudden death and hospitalisations in HF patients with impaired left ventricular dysfunction [14]. The influence of diuretics on the pathophysiology of heart failure as a chronic disease process is associated with the resulting fluid losses. Diuretic therapy decreases fluid volume of the intra-vascular space, allowing the mobilisation of oedema from the extravascular space. The primary mechanism underlying the action of diuretics is the creation of an environment of negative sodium (Na+) balance through increased Na + secretion. This is achieved by loop diuretics through inhibition of the sodium-potassium-chloride (Na+/K+/2Cl-) carrier, thiazide diuretics by inhibiting the Na+/Cl- cotransporter, and finally by potassium sparing diuretics, such as spironolactone, that act on the distal and collecting tubules by inhibiting Na + reabsorption along with K + and H + secretion [15].