Medical management
Neeraj Parakh, Ravi S. Math, Vivek Chaturvedi in Mitral Stenosis, 2018
The patient may be asked to decrease his/her salt intake if pulmonary vascular congestion is severe. In general, current diuretics have enough potency to take care of the excess sodium load incurred in normal diets and, hence, strict dietary restriction of salt is not required. In most patients with MS, recommendations for exercise are symptom-limited. Patients should be encouraged to pursue a low-level aerobic exercise program for maintenance of cardiovascular fitness.4 Many patients with mild MS will remain symptom-free even with strenuous exercise. Those with very severe MS may have sudden, marked exercise-induced elevations in left-atrial pressure precipitating pulmonary edema. The long-term sequelae of repeated exercise-induced elevation in left-atrial pressure and pulmonary venous hypertension are well characterized in terms of pulmonary interstitial changes and, in extreme cases, alveolar edema and hemorrhage. Subsequent elevation of pulmonary arterial pressure (that is in general always reversible, unlike severe precapillary hypertension) often leads to right-ventricular hypertrophy and functional tricuspid regurgitation, which gradually resolve after a successful mitral valve dilatation.7,8
Small Bowel Injury by Ethanol
Victor R. Preedy, Ronald R. Watson in Alcohol and the Gastrointestinal Tract, 2017
The morphological studies suggested that ethanol caused mucosal vascular congestion and hemoconcentration. To confirm and quantitate this by physiological means, we determined simultaneously the effect of ethanol on mucosal arterial blood flow, mucosal red blood cell volume, and mucosal plasma volume.69 Three percent ethanol to some extent and 6% considerably increased mucosal arteriolar blood flow and mucosal red blood cell volume without an equivalent increase in the mucosal plasma volume, indicating that hemoconcentration occurred which was more severe with 6% alcohol than with 3% (Figure 10.10). The mucosal microvascular stasis was accompanied by an intraluminal loss of plasma protein (Table 10.2), which was barely significant with 3% ethanol but was disproportionally greater with 6%. A biphasic response of protein leakage was observed with a peak at 20 to 30 min, followed by a decline in spite of continued perfusion with ethanol for 90 min. Similar biphasic leakage of albumin into the gut lumen was observed during acute administration of ethanol in the rabbit, 19,20'58,62'87-90) but the peak of the curve occurred later and the protein loss was greater in this species (Figure 10.11). A similar biphasic curve was observed in humans by Lavo and co-workers.91
Diseases of the Nervous System
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Snake venoms contain a complex mixture of toxic proteins which act on several organs with ensuing neurotoxicity or hemolysis.589 Snake neurotoxins are rapidly absorbed from subcutaneous tissues and distributed throughout the body, with high concentration at the motor end plates, where the primary action manifests. Scorpion venoms or scorpamines are lethal neurotoxins. They contain small basic proteins and hyaluronidase which increase capillary permeability. The mechanism of action of these toxins resides in the presence of disulfide bridges and lysine residues.71,168,411 Certain spider’s bites cause a variety of signs, ranging from local pain and necrosis to systemic hemolysis and nervous system dysfunction. Tarantulas secrete occasionally toxic venom, but the most toxic is the black widow spider, Lactrodectus mactans, which causes frequent and severe neurologic dysfunction.,71,589 Bee stings can exert nervous system actions. Severe anaphylactic reactions are accompanied by cerebral edema and vascular congestion. Widespread demyelination can exert effects on the peripheral and central nervous system. A relationship has been reported between the action of bee stings and local mononeuropathies.508
CardioMEMSTM System in the Daily Management of Heart Failure: Review of Current Data and Technique of Implantation
Published in Expert Review of Medical Devices, 2020
Muhammad Asif Mangi, Zeid Nesheiwat, Rehan Kahloon, George V. Moukarbel
Heart failure (HF) affects more than 26 million people worldwide and carries significant morbidity and mortality burden [1]. Despite advanced pharmacologic and device therapy, the rate of HF rehospitalization remains around 20 and 50% at 1 and 6 months, respectively [2]. The majority of patients have evidence of vascular congestion on hospitalization [3]. Concomitantly, extra-cardiac organs are also affected due to hypoperfusion from low cardiac output that leads to worsening renal function, bowel edema, and mortality [4]. Several strategies were applied in the past to decrease the incidence of HF hospitalization. However, these were limited by their low sensitivity to detect volume overload [5]. Cardiac rhythm management devices with ability to indirectly estimate volume status have not shown promising result in reducing HF hospitalization [6–8]. Given the shortcomings of other approaches, the Cardio Microelectromechanical System (CardioMEMSTM) has emerged as a tool for effective hemodynamic monitoring in HF patients.
Investigating the fate and toxicity of green synthesized gold nanoparticles in albino mice
Published in Drug Development and Industrial Pharmacy, 2023
Nosaibah Akkam, Alaa A. A. Aljabali, Yazan Akkam, Osama Abo Alrob, Bahaa Al-Trad, Hiba Alzoubi, Murtaza M. Tambuwala, Khalid M. Al-Batayneh
Histological examinations were performed on mouse tissue to investigate the effects of AuNPs. Figures 10–12 display histological images of mouse tissue after intraperitoneal administration of 50 nm AuNPs, as a single dose and daily dose. The following tissue changes were observed: Spleen: in the single-dose group, the architecture remained intact with mild congestion in the red pulp and mild white pulp follicular hyperplasia (Figure 11(A)). In the daily dose group, the architecture appeared mildly distorted with marked follicular hyperplasia in the white pulp (Figure 12(A)). Liver: the liver architecture was preserved in both the single and daily dose groups (Figures 11(B) and 12(B)). Scattered inflammatory foci containing lymphocytes were observed in the daily dose group (Figure 12(B)). Kidney: mild vascular congestion and tubular cell swelling were observed in the single-dose group (Figure 11(C)). The daily dose group exhibited moderate vascular congestion, interstitial chronic inflammatory foci, and proximal tubular atrophy (Figure 12(C)). Heart: the general architecture of the heart appeared similar in all groups (Figures 11(D) and 12(D)). Moderate vascular congestion was observed in the daily dose group (Figure 12(D)). These findings provide insights into the histological changes induced by AuNPs in the examined organs.
Mechanisms of COVID-19-induced cerebellitis
Published in Current Medical Research and Opinion, 2022
Mohammad Banazadeh, Sepehr Olangian-Tehrani, Melika Sharifi, Mohammadreza Malek-Ahmadi, Farhad Nikzad, Nooria Doozandeh-Nargesi, Alireza Mohammadi, Gary J. Stephens, Mohammad Shabani
COVID-19 affects the function and morphology of many organs and body tissues, including lungs, kidneys, heart, liver, and brain62. Several studies have reported hypoxic alterations and neuronal loss in the hippocampus, cerebral cortex, and cerebellar Purkinje cell layer, despite no signs of major thrombi or acute stroke63–65. However, some studies reported atherosclerosis and microhemorrhages in brain specimens62,66,67. Other histopathological findings include progressed myelin loss, terminal hypoxic-ischemic injury typified by necrotic neurons in the hippocampus and cerebellum, perivascular cellular infiltrates, with differing levels of axonal damage being observed62,64. The study of Bryce and coworkers66 reported that only one patient showed signs of a remarkably large cerebral artery territory infarct, and three patients demonstrated minor and sparse peripheral and deep parenchymal ischemic infarcts, while others were hemorrhagic. In addition to these microhemorrhages, some vascular congestion that worsens vascular damage and reperfusion injury has been reported62,65.