@kimmi Communication between your brain and back changes over time when you have chronic lower back pain, leading the brain to interpret signals from the back differently and change how you move. It is thought that these neural changes make recovery from pain slower and more complicated, according to the Neuroscience Research Australia (NeuRA), a nonprofit research institute in Sydney, Australia.
@manish-sharma I think you should get seen by your Dr because you are obviously in pain. I'm not a Dr sometimes eyes can look a bit jaundice in the corners where there are lots of blood vessels, it doesn't necessarily mean you actually have jaundice. The only way to tell would be to see your Dr and get a liver profile blood test to check your bilirubin and general liver function. Its possible that you have an infection that's causing your stomach issues, a friend of mine had yellow loose stool and she had diverticulitis. I'm not saying that's the case with you, but I think you should make an appointment to get things checked. I hope you feel better really soon,
@bushith Hey, it seems you are in the prediabetic stage as this does not happen with a normal healthy person. It is really strange that your meter shows this reading after having a drink. It is a matter of concern and should go for a diagnosis. Apart from this, are you having an active lifestyle or passive lifestyle? If you have an active lifestyle then this is pretty good but if passive then you should be more cautious about your health. Try to adopt a healthy lifestyle by adding a few aerobic exercises and diabetic food meals. One other reason for the imbalance in glucose levels is stress, try to manage that by taking proper sleep, taking sleep for around 8 hours.
@moon Results from the new randomized, open-label, two-period crossover study comparing the two insulins were presented by Thomas Pieber, MD, on June 5 at the American Diabetes Association (ADA) 82nd Scientific Sessions. In the study, insulin icodec once weekly for 6 weeks was compared with glargine U100 once daily for 11 days, with single evaluations of doubling and tripling the doses during those periods. There were no differences in hypoglycemia between the two insulins, although some differences were found in other hormonal responses, said Pieber, who is head of the division of endocrinology and metabolism at the Medical University of Graz, Austria.
@somraj Faster action and a higher rate of resolution may, in part, explain the high level of satisfaction with dasiglucagon by patients in the study. When the researchers asked participants at the end of the open-label study how likely they were to use dasiglucagon as part of their diabetes management, 88% said they would be very likely to continue using the agent, with an additional 8% saying that they would likely use it,
@koushin Adults with type 1 diabetes and IAH have a reduced ability to perceive hypoglycemic symptoms and are at risk of severe hypoglycemic events because they are unable to take immediate corrective action. This is the first study to identify protective factors and risk factors of IAH in Japanese adults with type 1 diabetes. People with IAH may plan to loosen tight glucose management and intentionally omit insulin injection to prevent severe hypoglycemia. The information in this report may help improve the management of people with problematic hypoglycemia, the authors suggested. Treatment with an insulin pump and structured education aimed at improving problem-solving skills may be useful interventions for adults with type 1 diabetes and IAH, they suggested.
@titumir Based on these findings, doctors might counsel patients to prefer cooking at home [and] choosing fresher ingredients instead of buying ready-made meals and snacks.UPFs are highly manipulated, are packed with added ingredients, including sugar, fat, and salt, and are low in protein and fiber. Examples of UPFs include soft drinks, chips, chocolate, candy, ice cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hotdogs, fries, and many more.
@vetri The most characteristic histologic lesion of LCDD is nodular glomerulosclerosis (see the first image shown below) that is virtually indistinguishable from diabetic glomerulosclerosis when using light microscopy. Routine immunofluorescence findings are negative because the antibodies used to identify the immunoglobulins are directed at the heavy chains of immunoglobulins. Therefore, as the name suggests, special stains for light chains must be used to identify this using electron microscopy. Dense granular deposits on the endothelial side of the glomerular basement membrane, on the outer aspect of the tubular basement membrane, or on both may be seen with electron microscopy in persons with LCDD. Classic ultrastructure examination findings include amorphous, noncongophilic, and nonfibrillar deposits. Most of these deposits are of kappa light chains (see the fourth image shown below). At times, the histologic changes are minimal, and occasionally glomeruli may have mesangial deposits. Rarely, glomerular crescents can also be seen in patients with LCDD.
@hwyfar Tumor lysis syndrome
Uric acid released following chemotherapy may precipitate in the tubules and may precipitate acute kidney injury. Hence, pretreating patients undergoing chemotherapy with allopurinol and diuresis is important
@arghyadeep Maintain adequate fluid intake (2-3 L/d), especially before initiating chemotherapy, to prevent dehydration. Dehydration and aciduria favors precipitation of light chains. This is important in the precipitation of acute renal failure in a significant number (up to 95%) of patients.
Avoid nephrotoxic agents. NSAIDs, often used to relieve bone pain, are the most prominent offenders.
Ensure early and effective treatment of infections with nonnephrotoxic antibiotics. Intravenous immunoglobulin has been found to be safe when used as prophylaxis against infection in the so-called plateau phase.
Early recognition and treatment of hypercalcemia are important. Excessive calcium is an important cause of acute renal failure in patients with myeloma and may be present in up to 30% of patients. Hypercalcemia impairs renal concentrating ability, thus leading to dehydration and promoting precipitation of light-chain proteins in renal tubules. Nausea, vomiting, and altered mental state associated with hypercalcemia further increase the likelihood of dehydration. Hypercalciuria also exerts a direct nephrotoxic effect and thus causes tubular degeneration and necrosis. Implement aggressive treatment of hypercalcemia, with saline diuresis, steroids, calcitonin, and diphosphonate.
Perform contrast studies judiciously in patients with multiple myeloma because of the possibility of contrast-induced renal failure. However, McCarthy and Becker reviewed 7 retrospective studies of patients with myeloma who were receiving contrast media and noted that the incidence rate of acute renal failure was only 0.6-1.25%, compared to 0.15% in the general population
@nowelle Urinalysis results may indicate low-grade proteinuria. A discrepancy between the results of a urine dipstick test for protein and the findings from a test for 24-hour urine protein excretion should suggest the possibility of light-chain proteinuria. Light-chain proteins in the urine cannot be detected using Albustix or other dipstick methods.
Perform the Putnam heat test or the sulfosalicylic acid (SSA) test (with Exton reagent) to help detect urinary light-chain proteins. The results from either test are insensitive. The Putnam heat test can help detect urinary light chains only when the concentration exceeds 150 mg/dL. False-negative results are common with the SSA test if the specific gravity of urine is less than 1.01.
If a patient has a negative result from the Albustix test (which detects albumin) and a positive result from the SSA test, consider the possibility of light-chain proteinuria.
@roopendra Imaging Studies
Renal ultrasound images can help assess renal echogenicity and renal size in patients presenting with renal failure. Findings can also help to rule out renal calcification or stones. One third of the patients may have enlarged kidneys.
Results may show lytic bone lesions, osteoporosis, or compression fracture(s) in patients with possible multiple myeloma
@tamir Various glomerular abnormalities that are caused by the deposition of these monoclonal immunoglobulins (or their heavy-chain or light-chain subunits) and are broadly classified into 2 categories, organized or nonorganized, depending on the pattern of deposition.
Organized deposits include the following:
Microtubular (cryoglobulinemia, immunotactoid glomerulonephritis)
Nonorganized, granular deposits include the following:
Monoclonal immunoglobulin deposition disease (MIDD)
Light-chain, heavy-chain, and light- and heavy-chain deposition disease
@son Light chains (molecular weight 22,000 d) are polypeptides that are synthesized by plasma cells and form part of immunoglobulins. Plasma cells normally produce a slight excess of light chains that are either excreted or catabolized by the kidney, and only a minute amount of light-chain protein normally appears in the urine. Light-chain proteins appear in urine in high concentration either when the production of light-chain proteins is markedly increased or when the ability of the proximal tubules to reabsorb all the filtered protein is diminished.
The most characteristic histologic lesion of light chain deposition disease (LCDD) is nodular glomerulosclerosis, which must be distinguished from diabetic glomerulosclerosis by using electron microscopy. The term Bence Jones protein has been used to designate a urinary protein that leaves solution at approximately 56°C under certain conditions of pH and ionic strength and returns to the solution upon further heating to 100°C. The Bence Jones protein represents a homogeneous population of immunoglobulin light chains of either kappa type or lambda type and is the product of a presumed single clone of plasma cells. The presence of light-chain proteins in the urine is associated with a number of systemic diseases
@md-shafiq-khan Pseudocholinesterase deficiency is a clinically silent condition in individuals who are not exposed to exogenous sources of choline esters.
Patients with prolonged paralysis following administration of succinylcholine can be treated in the following ways:
Prophylactic transfusion of fresh frozen plasma can augment the patient's endogenous plasma pseudocholinesterase activity. This practice is not recommended because of the risk of iatrogenic viral infectious complications. However, perioperative transfusion of fresh frozen plasma administered to correct a coagulopathy may mask an underlying pseudocholinesterase deficiency.
Mechanical ventilatory support is the mainstay of treatment until respiratory muscle paralysis spontaneously resolves. Recovery eventually occurs as a result of passive diffusion of succinylcholine away from the neuromuscular junction.
Administration of cholinesterase inhibitors, such as neostigmine, is controversial for reversing succinylcholine-related apnea in patients who are pseudocholinesterase deficient. The effects may be transient, possibly followed by intensified neuromuscular blockade.
Consultation with a geneticist may help to identify the specific atypical genotype alleles contributing to pseudocholinesterase deficiency.
Because the DNA sequence of the pseudocholinesterase gene and its amino acid structure is known, atypical alleles now can be identified by PCR amplification studies using DNA extracted from leukocytes in a blood sample.
@caitlin Diagnosis of pseudocholinesterase deficiency is made by plasma assays of pseudocholinesterase enzyme activity. A sample of the patient's plasma is incubated with the substrate butyrylthiocholine along with the indicator chemical 5,5'-dithiobis-(2-nitrobenzoic acid), which will produce a colored product that is assayed using spectrophotometry. The resulting amount of spectrophotometric absorption is proportionate to the pseudocholinesterase enzyme activity that is present in the patient's plasma sample. [9, 13]
Because succinylcholine metabolites can interfere with this assay, plasma samples should be collected after muscle paralysis has completely resolved. The dibucaine and fluoride numbers can be determined by repeating this assay in the presence of standard aliquots of either dibucaine (0.03 mmol/L) or fluoride (4 mmol/L) in the reaction mixture to determine the percent inhibition of enzyme activity caused by these agents.
A simplified screening test of pseudocholinesterase enzyme activity can be performed using the Acholest Test Paper (See Table 2, below). When a drop of the patient's plasma is applied to the substrate-impregnated test paper, a colorimetric reaction occurs. The time it takes the exposed Acholest Test Paper to turn from green to yellow is inversely proportional to the pseudocholinesterase enzyme activity in the plasma sample.
The complete DNA sequence and amino acid structure of both the normal pseudocholinesterase protein and most of its abnormal variants have now been identified. However, molecular genetic techniques such as polymerase chain reaction (PCR) amplification with allele-specific oligonucleotide probes for identifying abnormal pseudocholinesterase genotypes are currently available only in a limited number of research laboratories and are not in routine clinical use.
@visha A personal or family history of an adverse drug reaction to one of the choline ester compounds, such as succinylcholine, mivacurium, or cocaine, may be the only clue suggesting pseudocholinesterase deficiency. Most clinically significant causes of pseudocholinesterase deficiency are due to one or more inherited abnormal alleles that code for the synthesis of the enzyme. These abnormal alleles may result in a failure to produce normal amounts of the enzyme or in production of abnormal forms of pseudocholinesterase with altered structure and lacking full enzymatic function.
Patients with only partial deficiencies of inherited pseudocholinesterase enzyme activity often do not manifest clinically significant prolongation of paralysis following administration of succinylcholine unless a concomitant acquired cause of pseudocholinesterase deficiency is present. The acquired causes of pseudocholinesterase deficiency include a variety of physiologic conditions, pathologic states, and medications listed below.
The gene that codes for the pseudocholinesterase enzyme is located at the E1 locus on the long arm of chromosome 3, and 96% of the population is homozygous for the normal pseudocholinesterase genotype, which is designated as EuEu. The remaining 4% of the population carry one or more of atypical gene alleles for the pseudocholinesterase gene in either a heterozygous or homozygous fashion.