Playlist

Atherosclerosis: Pathophysiology (Nursing)

by Rhonda Lawes

My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides Atherosclerosis.pdf
    • PDF
      Download Lecture Overview
    Report mistake
    Transcript

    00:01 Alright, so we've given you the overview, we fast forward you through that.

    00:05 Now this is the slow motion replay, okay.

    00:09 I want you to be very clear how this happens so you understand the medications we use, the dietary recommendations that we make the patients.

    00:17 This is all part of you having a whole complete picture so you're better equipped to help your patients make healthier choices.

    00:24 So here we go with slow motion.

    00:29 So you know that first, the artery lining is injured - we got that.

    00:34 Now the response to the injuries, we're going to talk about next.

    00:37 So these fatty materials, let me give you a list of those: LDL, cholesterol, triglycerides - these are fatty materials.

    00:45 They're good things, I know they have a bad reputation in some areas however, we need them and they do do good things in the body but in this case, when there's too much of them, it can cause damage, injury, then you have a response to the injury with the fatty materials plus the inflammatory mediators.

    01:05 Now that's the combination when in excess, when there's too much inflammatory responses, now we've got a problem.

    01:13 So the fatty materials then we've got the inflammatory mediators, right - you know those, the microphages, the white cells, they all infiltrate the lining of the damaged artery.

    01:23 Damage - response so what are the two groups that respond? the fatty materials right and inflammatory mediators and they infiltrate into the lining of the damaged artery.

    01:36 Now what happens is the platelets release growth factor at the site.

    01:40 Okay, so when platelets release growth factor, things happen and that smooth muscle that we talked about earlier - that is stimulated to proliferate.

    01:50 Proliferate just measns it's gonna get bigger and bigger and bigger.

    01:53 So you've had that damaged area, we had the responders and the platelets release this growth factor right at the site so the smooth muscle is stimulated to proliferate.

    02:03 Now the lipids, eccetera are trapped in the wall so you got a great drawing for you there.

    02:09 Look you've got the epithelial lining, you saw where the damage was, we saw the responders.

    02:15 Now because of that proliferation, all that is trapped right in the wall.

    02:20 So the lipids and everything else are trapped in the wall of the artery and it's getting thicker When the wall get thicker, the area for blood flow gets smaller so becomes increasingly smaller and the opening becomes that much smaller so as this process is going on, we've got more and more and more impeding blood flow.

    02:44 So that's how you go from fatty deposits to plaque, right we've got this process started Now we're looking at over time those fatty deposits that are trapped in there, right? Proliferated, they're trapped in there, now they've become hard - that's what becomes the tough and fibrous plaque.

    03:02 So that was a lot of information.

    03:04 Before we finished on this slide, I want you to pause and go back and review, what you know from how do we move from damage to the endothelial lining till we get to this point? Okay, so pause the video, walk through that in your own mind, jot some quick notes so you're just up to speed with us again, great place to review.

    03:28 Alright, thanks for taking the time to do that.

    03:30 The reason we give you those study breaks, is that we know this is a lot of information.

    03:35 This is really important stuff but you can't process it as fast as we think we can so we'd encourage you to teach you as you're studying on your own, that you would pause, take those breaks and reflect.

    03:48 That'll supercharge your study habits and help you retain and recall important information Now we're talking about how do you go from these fatty deposits, remember they're trapped in there, how we go from fatty deposits to plaque? and why is plaque such a bad thing? Well because it's really tough and fibrous and it's a pretty significant blockage so that's why it's a problem, it's making that area of blood supply smaller.

    04:17 So let's look at these deposits.

    04:19 They can be there just on one side or they can be all the way around the lumen of the artery.

    04:23 There's not always a rhyme or reason as to why it happens.

    04:26 It just depends on the extent of the injury, where it occurred and how the body responded.

    04:32 But as the blood flow decreases, the arteries just can't supply enough enough oxygen-rich blood to meet the demands of the heart muscle.

    04:40 There's the problem or do we say, "Aye,there's the rub right there" Because we don't get enough oxygen to the heart, that's the source chest pain, ischemia and the worst case scenario - myocardial infarctions.

    04:56 So the patient usually will start to experiencing ischemia or chest pain and they have an increased risk of myocardial infarction.

    05:04 As this progresses, as it becomes worse, see ischemia is a sign to let us know not all is well with that patient's blood supply.

    05:13 We can intervene as early as possible and try and turn that situation around because our goal is to minimize ischemia, because we don't want ischemia or chest pain to progress to myocardial infarction, because that's dead tissue.

    05:29 So hopefully this helps you start to understand why in some patients, chest pain symptoms are so kind of intermittent.

    05:35 They start, they stop, why we see them, what the causes are - all this requires you to understand the process that's actually going on in their arteries.


    About the Lecture

    The lecture Atherosclerosis: Pathophysiology (Nursing) by Rhonda Lawes is from the course Coronary Artery Disease: Atherosclerosis (Nursing) .


    Included Quiz Questions

    1. Fatty materials, inflammatory mediators, macrophages, and WBCs
    2. Fatty materials, antioxidants, and neutrophils
    3. HDL, triglycerides, inflammatory mediators, and leukocytes
    4. Platelets, inflammatory mediators, WBCs, and RBCs
    1. Growth factor released by the platelets at the site of arterial damage
    2. Growth factor released by the fatty materials and inflammatory mediators
    3. Muscle hypertrophy, which is an idiopathic process
    4. Increased blood flow to the area from collateral circulation
    1. The narrowed arteries will not supply enough blood to the heart muscle.
    2. The fatty deposits become soft and pliable plaque.
    3. The fatty deposits become tough and fibrous, but only on 1 side of the arterial lumen.
    4. A myocardial infarction will occur immediately.

    Author of lecture Atherosclerosis: Pathophysiology (Nursing)

     Rhonda Lawes

    Rhonda Lawes


    Customer reviews

    (1)
    5,0 of 5 stars
    5 Stars
    5
    4 Stars
    0
    3 Stars
    0
    2 Stars
    0
    1  Star
    0