Diabetes Complication and Pathophysiology of the complication

in this video we're going to look at diabetes mellitus - or diabetes type 2 diabetes type 2 is a progressive disorder defined by deficits in insulin secretion and action what I mean by deficit insulin action is insulin resistance for example here we have a blood vessel and here a cell with an insulin receptor in diabetes type 2 we have a decrease in insulin in the plasma and also insulin resistance where the effect of insulin on the cell does not take place as a result of a decrease in insulin secretion and insulin resistance we get hyperglycemia or high blood glucose persistent high blood glucose results in diabetes before we delve into the signs and symptoms and the pathology pacifism diabetes let us learn a bit more about insulin let us zoom into this area of the abdomen where we can find the pancreas the pancreas is tucked under the stomach and connects to the small intestine the pancreas contains glands and ducts let us zoom into this area of the pancreas here I'm drawing the pancreatic ducts and glands these clusters here are known as pancreatic Isana these Isana contains exocrine cells which release enzymes for digestion which then go essentially to the small intestine around the pancreatic Isana are clusters of cells known as islets of langerhans these cells are endocrine cells it is from these cells where the hormone insulin is secreted into the blood insulin ISM is an important hormone that has many effects on on our body the main site insulin target our skeletal muscles liver and adipose tissue or fat in general the main function of insulin is to store energy in skeletal muscle and adipose tissue insulin increases glucose uptake and glycolysis for energy storage insulin has a big effect on the liver including increasing glycolysis increasing protein synthesis increasing lipogenesis insulin also decreases gluconeogenesis lipolysis glycogenolysis and protein breakdown all in all insulin promotes glucose uptake and energy storage and inhibits the release of glucose to blood let us take a closer look at the islets of langerhans where insulin is produced so here are the Asuna cells which are your exocrine cells next to them we have islets of langerhans which are the cluster of endocrine cells which produce hormones the majority of endocrine cells within one islets of langerhans are beta cells which are the cells that actually produce insulin as well as amylin there are also other cells here the alpha cells which produce glucagon and Delta cells which produce somatostatin it is important to know that glucagon is another hormone that does essentially the opposite function of insulin now let us learn a bit more about how and when beta cells release insulin into the blood so here I am drawing a b2 cell of the pancreas the cell contains mitochondria and on the cell membrane we find many channels including glute - not for a glute - volt a calcium voltage-gated channel and potassium passive channel so let us look at the steps involved in insulin secretion by the beta cells after a meal there is an increase in blood glucose an increase in blood glucose result in glucose entering the B the cells through the glue to transporter the glucose in the cell is then metabolized through glycolysis and Krebs cycle in the cytoplasm and the mitochondria producing many ATP ATP is energy normally in the beta cell potassium flows out creating a negative gradient within the cell however the increase in ATP actually inhibits this process so step 4 increase in ATP triggers depolarization cascade within the cell resulting in insulin release so drawing it out the increase in cellular potassium causes depolarization resulting in opening of calcium voltage-gated channels this causes an influx of positively charged calcium the calcium then triggers insulin release from via the vesicles when insulin is secreted into the blood it then targets cells and binds to the insulin cell receptor telling the cell to increase the uptake of glucose and to store it this is a normal process and results in a decrease in blood glucose level however in diabetes type 2 this whole process gets messy in diabetes you do not have enough insulin secretion and you develop insulin resistance as a result this result in a blood glucose staying high persistent high blood glucose results in a click in the clinical manifestations we see in a patient who has diabetes a person with diabetes can can be asymptomatic for some time but common signs and symptoms include infections regular infections fatigue blurred vision and the 4ps paresthesia polydipsia polyuria and polyphagia the risk factors for diabetes include older age obese having a family history having other cardiovascular disease risk factors gestational diabetes and polycystic ovarian syndrome so we learnt about the signs and symptoms and the risk factors for diabetes but what happens when diabetes progresses and is untreated as diabetes progresses is undiagnosed or untreated several complications can actually occur these can be divided into micro vascular and macro vascular complications so micro vascular complications include retinopathy neuropathy and nephropathy macro vascular complications include coronary heart complications cerebral vascular complications and peripheral vascular complications let's focus on micro vascular complications beginning with retinopathy the eyes of a person with diabetes should be examined regularly internal changes such as cotton-wool spots microhemorrhages microaneurysms and macular thickening may occur eye conditions such as glaucoma and cataracts can may result neuropathy complications can be divided into peripheral and autonomic neuropathy peripheral neuropathy includes a decrease or increase in pain sensation painless injuries and decrease in reflex autonomic neuropathy include resting tachycardia urinary frequency and erectile dysfunction in men nephropathy complications include glomerular sclerosis and pyelonephritis pyelonephritis is infection of the kidney so that was micro vascular complications due to diabetes now we are looking at the macro vascular complications which include coronary heart complications and this can be chest pain congestive heart failure and Disney rebo vascular complications can result in hemorrhages cerebral infarcts and memory problems peripheral vascular disease complications include arthrosclerosis gangrene and alterations it isn't very important to have regular foot checks in a patient with diabetes as loss of sensation together with a compromised vascular supply can lead to some serious problems in the peripheral tissue so here is a foot if you have authoress chlorosis occurring gangrene can occur infections can occur and at times amputations are necessary ulcerations can also occur in the foot of a person without the person knowing it common sights are on the sole of the foot commonly around where most of the pressure is exerted now we are going to look at the pathophysiology of these complications that are current diabetes and in order to understand this we have to look at the vascular changes that occurs these vascular changes are essentially what leads to the micro vascular and macro vascular changes we see in diabetes three things happen in the vessels of patients with diabetes are atherosclerosis arteriosclerosis and inflammation atherosclerosis remember is the Plott buildup in the vessel the alteration in vascular homeostasis due to endothelial and smooth muscle cell dysfunction are the main features of diabetic vascular petha okay let us zoom into the layer of the vessel this is the lumen endothelium Tunica intima and tunica media tunica media is where the smooth muscle layer is within the lumen we have red blood cells and other proteins this is also where glucose you know travels in diabetes we have high blood glucose when there is high blood glucose the endothelial cells will eventually take most of it up the interesting thing here is that the endothelial cells of the vessels do not need insulin to take up glucose it just does it with so much glucose being taken inside the endothelial cells the cells produce a lot of energy and as a by-product reactive oxygen species or ro s the increase in reactive oxygen species ro s leads to a number of things one formation of advanced glycol aided glass elated protein product reactive oxygen species stimulates protein kinase II eight activity which sort of forms a sort of a continuous stimulate stimulatory cycle activation of protein kinase C leads to also a number of things including increased production of VEGF and other growth factors resulting in angiogenesis and cell growth protein kinase C also increases production of endothelium which stimulates platelet aggregation protein kinase C also results in increase in nuclear factor Kappa B within the cell nuclear factor Kappa B is an inflammatory transcription factor that promotes the inflammatory process the end result include increased expression of receptors for inflammatory cells as well as increasing the vascular permeability through produced stimulating cytokine production essentially the increase in vascular permeability and receptor expression allows monocytes you are circulating the blood to pass through to pass through the endothelial layer and enter the Tunica intima the increase in vascular permeability also allows LDLs to pass through LDLs are low-density lipoproteins so now we have LDLs within the Tunica intima and monocytes the monocytes have become macrophages monocytes become macrophages as they enter the tissue what happens next is what we see in atherosclerosis the macrophages engulfs the LDL becoming what is known as a foam cell during this process the macro fat the macrophage and foam cell release inflammatory cytokines such as TNF alpha interleukin 1 which causes further inflammation the foam cells also secrete some growth factors causing smooth muscle proliferation and migration into the Tunica intima the foam cells which contain a lot of lipids eventually cluster together and rupture within the Tunica intima the lipids are released inflammatory cytokines are released and growth factors within the foam cells are released when the cell ruptures and this all essentially will create a plot this whole process we just saw right from the beginning from reactive oxygen species protein kinase II to foam cells all are what lead to the vascular changes the vascular changes are you know there's increase in metabolic toxins the vascular changes are we see an increase in metabolic toxins and also a thorough thrombosis so to summarize the whole process starting from diabetes so we have genetics and obesity and other risk factors increase in age leads to insulin resistance insulin resistance leads to the B cell the beta cell failure the beta cell failure with impaired glucose tolerance leads to insulin deficiency insulin deficiency results in hyperglycemia or high blood glucose with high blood glucose the glucose enters the endothelial cells of the vessels resulting in the formation of or stimulating the function of protein kinase II reactive oxygen species a GP and VEGF and other growth factors all this causes toxic diabetic metabolism endothelial dysfunction and vascular inflammation this also leads to our throw a thorough thrombosis together they eventually lead to the macro micro vascular and macro vascular changes we see in diabetes which if you remember micro vascular include retinopathy neuropathy and nephropathy macro vascular changes include cardiovascular coronary heart disease cerebral vascular disease and peripheral vascular complications a note to make is that insulin deficiency can lead to some serious outcomes and these include diabetic ketoacidosis a hyperosmolar state as well as a hypoglycemic State now all these are different however they're interconnected so diabetic ketoacidosis occurs because insulin doesn't work and because of that fatty acids are broken down and ketone bodies are released into the blood increasing the acidity of the blood in in the hyperosmolar state what happens is that because you have so much glucose in the blood it gets urinated out and thus dragging water with it and this leads to an hyperosmolar state essentially a dehydrated state and then you have the hyperglycemic state which is essentially high blood glucose levels in the blood so I hope you enjoyed this video on diabetes as well as the pathophysiology of the complications associated with diabetes thank you for watching you

Channel: Armando Hasudungan

Views: 480,494

Rating: 4.9158363 out of 5

Keywords: Diabetes, diabetes mellitus, type 2 diabetes, complications, microvascular, macrovascular, nephropathy, diabetic retinopathy, pathophysiology, neuropathy, pathogenesis, mino and major complication, endocrinology, summary, overview, physiology of insulin, what is insulin and diabetes, signs and symptoms of diabetes, clinical presentation, medicine

Id: ZnnVUq1P5Yo

Length: 17min 54sec (1074 seconds)

Published: Tue May 31 2016