The changes in small arterioles include hyaline arteriolosclerosis (deposition of hyaline, collagenous material), which causes glomerular collapse (wrinkling and thickening of capillary basement membranes and collapse of capillary lumen) and solidification (glomeruli exhibit sclerosis and increase in mesangial matrix). The degree of scarring correlates with the degree of glomerular filtration deficit. Malignant nephrosclerosis is where hypertensive nephrosclerosis occurs in presence of malignant hypertension (when DBP > 130mmHg). Vessels feature intimal thickening, fibrinoid necrosis, red blood cell fragmentation, extravasation, thrombosis. These changes create an exaggerated layered appearance (onion skinning). Urine test
Microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. The majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. In the case of glomerular damage occurring in HN, hematuria can occur as well. Definitive diagnosis
The definitive diagnosis of HN requires morphological examination. Common histological features can be identified in the renal and glomerular vasculature. Glomerulosclerosis is often present, either focally or globally, which is characterized by hardening of the vessel walls. Also, luminal narrowing of the arteries and arterioles of the kidney system. However, this type of procedure is likely to be preceded by a provisional diagnosis based on laboratory investigations. Future diagnostic approaches
Increasing access to, and use of, genome profiling may provide opportunity for diagnosis based on presentation and genetic risk factors, by identifying ApoL1 gene variants on chromosome 22.
Nasal administration: Oxytocin is effectively distributed to the brain when administered intranasally via a nasal spray, after which it reliably crosses the blood–brain barrier and exhibits psychoactive effects in humans. No serious adverse effects with short-term application of oxytocin with 18~40 IU (36–80 mcg) have been recorded. Intranasal oxytocin has a central duration of at least 2.25 hours and as long as 4 hours. Oral: Oxytocin is destroyed in the gastrointestinal tract, so it is not active orally. History
Oxytocins uterine-contracting properties were discovered by British pharmacologist Henry Hallett Dale in 1906. Oxytocins milk ejection property was described by Ott and Scott in 1910 and by Schafer and Mackenzie in 1911.Oxytocin was the first polypeptide hormone to be sequenced or synthesized. Du Vigneaud was awarded the Nobel Prize in 1955 for his work. Etymology
The word oxytocin was coined from the term oxytocic. Greek ὀξύς, oxys, and τόκος, tokos, meaning "quick birth". Society and culture
Counterfeits
In African countries, some oxytocin products were found to be counterfeit medications. Other uses
The trust-inducing property of oxytocin might help those with social anxiety and depression, anxiety, fear, and social dysfunctions, such as generalized anxiety disorder, post-traumatic stress disorder, and social anxiety disorder, as well as autism and schizophrenia, among others. However, in one meta-analysis only autism spectrum disorder showed a significant combined effect size.People using oxytocin show improved recognition for positive social cues over threatening social cues and improved recognition of fear. Autism: Oxytocin may play a role in autism and may be an effective treatment for autisms repetitive and affiliative behaviors.