Atherosclerosis - Pathophysiology

armando has to drag on biology and medicine videos please make sure to subscribe to on the Forman group for the latest videos please visit Facebook Armando has pseudonym in this video we're going to talk about atherosclerosis which is hardening of the arteries actually it's in the narrowing of the arteries due to plot formation a plaque in this case is basically a waxy substance made of predominantly lipids and atherosclerosis is different to arteriosclerosis arteriosclerosis is just hardening of the arteries now arthrosclerosis is a common cause of heart attacks so if here I'm drawing the heart we have blood vessels called these coronary arteries that supply the heart with oxygen so let's take a look at two different scenarios here are vessels and here are cardiac muscle cells normally the vessels the blood vessels are carrying blood full of oxygen to the cardiac muscle cells thus allowing the cardiac muscle cells to function normally which means the heart will function normally however if we look at an authoress if we look at an authoress sclerosis scenario there is a plaque formation blood can't be delivered properly to the heart or there is reduced like blood flow to the heart and as a consequence the cardiac muscle cells are deprived of oxygen symptoms of otosclerosis in the coronary arteries include vomiting anxiety angina which is pain in the heart in the chest area coughing and feeling faint so again if the authoress grossest in the coronary artery here is so severe it can actually block everything it can block the blood supply all together and we get a schema of the cardiac muscle cells and so as a consequence them the these cells will die and you get a heart attack or heart failure so atherosclerosis formation of the coronary arteries can lead to myocardial ischemia but there can also be authoress corrosives formation in the carotid arteries this can cause symptoms such as weakness dis via head make facial numbness and paralysis and this is because the carotid artery is the blood supply to your brain so if you don't get any blood to your brain you get stroke as well as these symptoms atherosclerosis cure disease now peripheral vascular disease is the reduced circulation of blood to body pot other than the brain or hot so you know for example the liver or or something else like your reproductive organs and this is bad in every respect in peripheral vascular disease you can have hair loss erectile dysfunction and weakening of the associated area another important site where atherosclerosis can occur is the renal arteries this can cause a reduction in appetite swelling of the hands and and most importantly it can trigger a randomly release which will significantly increase the blood pressure okay so there were some common sites where authoress chlorotic plaques can occur but let's see how severe an autoscroller clot can become so here is the increase in severity the first blood vessel here is normal with normal blood flow as you can see a plaque can form within the layer of the blood vessel firstly will be growing downwards so pushing sort of the vessel down when more platforms the plot become begins growing upwards so it will actually narrow the blood vessel if the plot keeps growing severity increases and the blood vessel really begins to narrow the massive plaque at the end can actually then rupture forming a thrombus forming a clot which will stop or impede blood flow when an authoress chaotic plot ruptures it is serious now that we get the overall picture let's look at the mechanism of plaque formation in a bit more detail so let us zoom first into this blood vessel and look different layers and what they contain so here is our endothelial cells and here is the lumen where we have red blood cells and also lipo proteins such as LDLs which are low-density lipoproteins surrounding the endothelium we have the Tunica intima and then the tunica media in the tunica media we have smooth muscle cells that are important in contraction of vessels surrounding the media we have the adventitia which is essentially connective tissue there are a few theories of how otosclerosis begins one theory baguette suggests that there is endothelial dysfunction and when there is high amounts of circulating LDLs because there are high concentrations or high circulating low-density lipoproteins lower LDL s these LDLs can deposit in the Tunica intima and then become oxidized oxidized LDL activates endothelial cells causing the endothelial cells to express receptors are for white blood cells on their surface so to summarize here I wrote increase in LDL s deposits in Tunica intima and becomes oxidized which will activate endothelial cells so here I'm drawing the same layers of the blood vessel and we can see there is accumulation of oxidized LDL s which will activate endothelial cells which will begin expressing adhesion molecules for white blood cells adhesion of white blood cells adhesion of blood leukocytes to activated endothelial cells will allow monocytes and T helper cells to move into the Tunica intima layer of the blood vessel when monocytes move into the Tunica intima they will become macrophages and macrophages will then take up these oxidized LDLs and then become foam cells the foam cells are key in atherosclerosis foam cells do many things one of which is it promotes migration of smooth muscle cells SMC from the tunica media into the Tunica intima and also promotes smooth muscle cell proliferation an increase in smooth muscle cell proliferation heightens or increases synthesis of collagen which can lead to hardening of the ostlers cleric clock during this whole process foam cells will also die releasing its lipid content this drives the growth of the plaque as the plot grows it builds in pressure which can cause rupturing of the block itself which is where things can become serious so here again we have the Tunica intima in tunica media of the blood vessel here are the smooth muscle cells which have accumulated in the Tunica intima layer as well as collagen foam cells are here and they die together with other cells in the area so here we have dead foam cells with lipid content spilt out the growth of the plaque is this area here now the plaque can then rupture which can lead to thrombosis thrombosis is when the plot ruptures and where coagulation happens to stop to stop the plot from spilling its content into the lumen this forms a thrombus a clot which can impede blood flow and cause serious complications so okay that was really tailed of how arthrospira platforms and how it ruptures but let us go a step further and look at it in a bit more detail and I guess a better diagram may be so here is we have the endothelial cell the Tunica intima layer and then we have the tunica media layer containing smooth muscle cells and here is our lumen the inside of the blood vessel we can where we can find red blood cells and we can find circulating low-density lipoproteins this black dot here of the LDL is called a is the protein part anyway let's just say we have dysfunction a dysfunctional endothelial cells dysfunction endothelial cells here this allows the you know a lot of LDLs to basically move into the Tunica intima layer when it moves in the Tunica intima layer the dysfunctional endothelial cells release reactive oxygen species and other enzymes such as metalloproteases which will oxidize the LDL so when the LDL is oxidized it cannot actually leave the Tunica intima it's trapped okay the dysfunctional endothelium and the ox subsequently oxidized LDL are triggers the endothelial cells to remember Express adhesion molecules for white blood cells so here we have monocytes circulating around it attaches to these receptors and then it will move in when it moves into the Tunica intima when monocytes move into tissues they become macrophages so here we have a macrophage 3 the macrophage has a receptor a scavenger receptor that will basically eat up but they will take in this ox of oxidized LDL the macrophage engulfs this oxidized LDL and then it will become a foam cell now foam cells they're basically macrophages containing lipids and they have many many functions one of which is that it will release chemokines to attract more macrophages foam cells can also do step four here I'm drawing it can release our igf-1 which is basically a growth factor and this growth factor will cause smooth muscle cells to migrate and cause smooth muscle cell proliferation in the Tunica intima so here we have the smooth muscle cells in the tunica media layer and they will migrate into the Tunica intima layer and they will proliferate and here because we have a lot of smooth muscle cells step 5 they make more collagen for foam cells in six can also die and they will die releasing their lipid content including DNA materials this DNA material will actually attract neutrophils because it's sort of it's it's actually inflammatory in this respect foam cells can also release pro-inflammatory cytokines and reactive oxygen species and and this together with neutrophils will increase inflammation in the area and this area is actually now the plot because it's got foam cells it's got dead dead foam cells it's got collagen it's got smooth muscle cells it's got all this stuff and this makes up the plot another interesting thing that occurs is we there is an increase in blood supply to the layer of the Tunica intima to the vessel so it's if you didn't know vessel blood vessels have its own vessel supply and this vessel these vessels are known as Vaes of Zoram anyways these T sub T cells also have a role in atherosclerosis so these T cells they can bind unto adhesion receptors which are expressed on endothelial cells they then enter the area the end of the plaque area they can be activated by macrophages and they can begin releasing other substances such as interferon gamma interferon gamma essentially promotes inflammation and it activates endothelial cells to attract more white blood cells and everything else so this plaque essentially will just keep growing it will cause it causes foam cells to die it's it's increase in lipid content there's inflammation and then all this as it grows it can rupture and this is when thrombosis occurs rupturing and when it ruptures a thrombus can form a clot can form and the clot forms when there's heaps of platelets heaps of clotting factors that all aggregate to the area and all this can impede blood flow ah so that was a video on atherosclerosis I hope you enjoyed it thank you you

Channel: Armando Hasudungan

Views: 560,409

Rating: 4.9529085 out of 5

Keywords: Pathophysiology (Field Of Study), artherosclerosis, arteriosclerosis, Atherosclerosis (Disease Or Medical Condition), pathogenesis, heart attack, anatomy and physiology, lecture, animation, cardiovascular disease, renal stenosis, periperhal vascular disease, foam cells, tunica intima, plaque formation, low density lipoproteins, LDLs, ischemia, thrombosis, thrombus formation, rupturing of a plaque, armando, tutorial, Health (Industry), medicine

Id: R6QTiBfzULE

Length: 14min 36sec (876 seconds)

Published: Thu Nov 20 2014