Search

Bladder cancer is the most frequent kind of urinary tract cancer. We will look at the most recent breakthroughs in the diagnosis and treatment of this illness in this review. The most significant tools in the diagnosis and follow-up of bladder cancer are cystoscopy and urine cytology. Several options have been examined, either to minimise the frequency of cystoscopy or to increase its sensitivity for tumour identification. Urine-based markers and point-of-care testing are examples of this. When compared to routine resection under white light, narrow-band imaging and photodynamic diagnosis/blue-light cystoscopy have showed promise in improving identification and minimising recurrence of bladder tumours by enhancing bladder resection completeness. The majority of individuals diagnosed with bladder cancer for the first time have non-muscle-invasive disease, which necessitates adjuvant intravesical chemotherapy and/or immunotherapy. The latest advancements in intravesical post-resection regimens are presented. Both laparoscopic radical cystectomy and robot-assisted radical cystectomy have been proven to minimise peri-operative morbidity while being oncologically equal to open radical cystectomy in the medium term for patients with muscle-invasive bladder cancer. Bladder-preserving methods include resection and chemoradiation, and in certain cases, they are as effective as surgery. These novel techniques are also examined in terms of their development, benefits, and drawbacks.

In clinical practice, heart failure (HF) and renal impairment are coexisting illness which is linked with one another. Heart and kidney have bidirectional inter-relationships, and it has been suggested that the kidney is the most significant organ involved in acute HF. The "cardio-renal syndrome" (CRS) is defined as acute or chronic malfunction of one organ causing acute or chronic dysfunction of the other [1, 2]. Furthermore, renal failure in HF can lead to decreased diuretic efficacy, diuretic resistance, congestion worsening, and further deterioration of renal function, creating a vicious cycle. In patients with acute HF, renal impairment is also a powerful independent predictor of short-term and long-term prognosis [3 - 9]. Renal hypoperfusion caused by inadequate cardiac output and over diuresis has long been thought to be the etiology of CRS. However, research has progressively shown a relationship between venous congestion and CRS, rather than inadequate cardiac output, correlating the failing right heart to CRS in recent decades. Indeed, both RHF and CRS have complicated and intertwined pathophysiologies that may affect several organs and systems in addition to isolated heart and kidney disease. This study focuses on the pathophysiology of RHF and cardio-centric phenotypes of CRS ("Type 1" and "Type 2"), as well as treatment options.

Malignant hyperthermia (MH) is a skeletal muscle pharmacogenetic disorder that manifests as a hypermetabolic response to powerful volatile anaesthetic gases like halothane, sevoflurane, desflurane, isoflurane, and the depolarizing muscle relaxant succinylcholine, as well as stressors like vigorous exercise and heat in human body. Anesthetics with an MH reaction rate vary from 1:10,000 to 1:250,000. On the other hand, the incidence of genetic anomalies might be as high as one in 400 people. Humans, specific pig breeds, dogs, and horses are all affected by MH. Hyperthermia, tachycardia, tachypnea, increased carbon dioxide generation, increased oxygen demand, acidosis, hyperkalaemia, muscular stiffness, and rhabdomyolysis are all typical indications of MH, all of which are associated with a hypermetabolic response. The condition is likely to be fatal if untreated. An early diagnostic indication is a rise in end-tidal carbon dioxide despite enhanced minute ventilation. Humans inherit the condition in an autosomal dominant form, whereas pigs inherit it in an autosomal recessive form. The pathophysiologic alterations are caused by an uncontrolled surge in myoplasmic calcium, which triggers biochemical pathways associated to muscle activation. A deficiency in the ryanodine receptor is the most common cause of the condition. The RYR1 gene, which is found on chromosome 19q13.1, has over 400 variations, at least 34 of which are linked to MH. In CACNA1S, less than 1% of variations have been discovered, although not all of them are causative. The in vitro contracture response of biopsied muscle to halothane, caffeine, and in certain centres, ryanodine and 4-chloro-m-cresol is used in diagnostic testing. The discovery of the genetic alterations has led to the development of DNA testing for MH susceptibility. Dantrolene sodium is a particular antagonist that should be provided in every setting where general anaesthesia is used. Because of a better knowledge of the clinical manifestations and pathophysiology of the disease, mortality has decreased from 80% thirty years ago to less than 5% in 2006.

Nutrients, foods, and dietary components have a significant role in the development and maintenance of depressive disorders as well as the intensity of depression symptoms. Nutritional elements may alter the biomarkers linked to depression and may also influence the onset of depression, obesity, and diabetes. Recent research has identified novel mediators of mood fluctuations and energy balance that operate the gut-brain networks. In this context, a number of healthy foods including olive oil, fish, fruits, vegetables, nuts, legumes, poultry, dairy, and unprocessed meat, have been shown to have a negative correlation with the risk of depression and may even help with the symptoms of depression. The use of sweetened beverages, processed foods, fried foods, processed meat, refined grains, high-fat dairy products, biscuits, snacks, and pastries, on the other hand, has been linked in longitudinal studies to an elevated risk of depression. Nevertheless, it is usually challenging to draw a firm conclusion about a true prospective causal association from this primarily retrospective research since depressed people may also alter their eating habits incidentally as a result of their sadness. Additionally, it has been suggested that some dietary substances, including as calcium, chromium, folate, PUFAs, vitamin D, B12, zinc, magnesium, and D-serine, might be utilised as add-on treatments with antidepressants. In this situation, food and lifestyle changes may be a desired, practical, effective, and non-stigmatizing depression preventive and treatment option. In early randomized controlled clinical studies, a number of drugs that have historically been used to treat metabolic disorders—including pioglitazone, metformin, exenatide, atorvastatin, and gram-negative antibiotics showed some promise for treating depression.