Diabetes mellitus continues to be a disease that affects a good percentage of our population. The majority affected need insulin on a day-to-day basis. Before the invention of the first manufactured insulin in 1978, dealing with diabetes took a significant toll on patient's lives. As technology and human innovation prevail, significant advancements have taken place in managing this chronic disease. Patients have an option to decide their mode of insulin delivery. Intranasal insulin, one such form, has a rapid mode of action while effectively controlling postprandial hyperglycemia. It has also been proven to reduce hypoglycemia and insulin resistance problems, which seem to be the main adverse effects of using conventional insulin regularly. However, due to the large dosages needed and high incurring costs, Intranasal Insulin is currently being used as adjunctive therapy along with conventional insulin.We conducted a literature search in PubMed indexed journals using the medical terms "Intranasal insulin," "diabetes," and "cognitive impairment" to provide an overview of the mechanism of action of Intranasal Insulin, its distinctive cognitive benefits, and how it can be compared to the standard parenteral insulin therapy. One unique feature of intranasal insulin is its ability to directly affect the central nervous system, bypassing the blood-brain barrier. Not only does this help in reducing the peripheral side effects of insulin, but it has also proven to play a role in improving the cognitive function of diabetics, especially those who have Alzheimer's or mild cognitive impairment, as decreased levels of insulin in the brain has been shown to impact cognitive function negatively. However, it does come with its limitations of poor absorption through the nasal mucosa due to mucociliary clearance and proteolytic enzymes, our body's natural defence mechanisms. This review focuses on the efficacy of intranasal insulin, its potential benefits, limitations, and role in cognitive improvement in people with diabetes with pre-existing cognitive impairment.

The prevalence of intravenous drug use has increased in the past decade and it represents an important risk factor for deep vein thrombosis. Intravenous drug use is a global problem, with the main culprit being heroin. Peer pressure and poverty in high-risk groups such as sex workers, females, and young adults raise the risk of intravenous drug use, which expresses itself in the form of venous thromboembolism eventually. Deep vein thrombosis typically manifests itself eight years after the initial intravenous drug administration, rendering it a silent killer.Aiming to review and summarize existing articles in this context, we performed an exhaustive literature search online on PubMed and Google Scholar indexes using the keywords "Deep Venous Thrombosis (DVT)" and "Intravenous Drug Users (IVDU)." English articles that addressed epidemiology, pathogenesis, clinical manifestations, diagnosis, differential diagnosis, management, and outcomes of DVT, including those in IVDU, were selected and analyzed.The pathogenesis of DVT development in IVDU is mainly attributed to the interplay of trauma to the vessel by repeated injection and the injected drug itself. The right-sided femoral vein is the most common vein affected. Prevalent clinical presentations include local pain, swelling, and redness with typical systemic symptoms including fever, cough, dyspnea, and chest pain on top of addiction features. There appeared to be a delay in reporting symptoms, which was most likely due to the social stigma attached to IVDU.There are over 50 conditions that present with swollen and painful limbs comparable to DVT in IVDU, making precise diagnosis critical for timely treatment. Venous ultrasound is the method of choice for diagnosing DVT. Extended anticoagulant therapy with low-molecular-weight heparin combined with warfarin is the recommended treatment. Intravenous drug abusers having DVT are affected by multiple complications and poorer outcomes such as slower recovery, recurrent venous thromboembolism (VTE), and a longer hospital stay, which put them at higher risk of morbidity, mortality, reduced productivity, and economic burden.

Multiple sclerosis (MS) is an autoimmune disease affecting a large number of people every year. The exact causal factor for this disease is unclear, but it commonly affects middle-aged women, with known triggers like stress, childbirth, infections, poor diet, lack of sleep, etc.Many epidemiological studies have indicated that various genetic abnormalities are also critical drivers of the onset of MS. The major risk factors of MS identified include hypovitaminosis D while environmental protective factors include allele HLA DRB1 1501, obesity, Epstein-Barr virus infection, sexual hormones, and smoking.Our article explores the correlation between the deficiency of vitamin D and the onset and progression of MS. The study uses a systematic review methodology by researching and reviewing scholarly articles exploring the topic. We conducted online searches of literature on Google Scholar and PubMed using the keywords "vitamin D deficiency" and "multiple sclerosis" and accessed the relevant secondary literature sources for review. The variables under study included vitamin D insufficiency as the dependent variable while MS was the independent variable. Causal variables included environmental, genetic, and protective factors.We hypothesized that there is indeed a correlation between vitamin D deficiency and MS. The findings from our review indicate a strong correlation between the insufficiency of vitamin D and the onset and progression of MS. These results are essential in devising interventions to accomplish primary and secondary prevention of MS, as well as integrating vitamin D supplementation in current treatment protocols for MS.