ESSAY: ATHEROSCLEROSIS ASSIGNMENT
Based on your readings, write a 2-page essay on the biochemical basis and clinical implications
of atherosclerosis. Your essay must be rich in molecular and mechanistic detail.
Materials for this assignment
Glew & Rosenthal: Chapters 17 — 19 (I don’t have access to this book, but if you can please get
a reference from here)
Below is the transcript for this assignment
Today we’ll be looking at a beta lipo. Nemea ABI lipo put anemia is a disorder of lipo protein
metabolism. Dot particularly affects the April be containing lipo proteins. It, it’s a disordered our
results from a genetic defect in the empty TP gene, which codes for the Microsoft mod transfer
protein, the micro zoomable trust WE, our protein is critical in the synthesis of these. It will be
continued lipo proteins because it serves to lipid dates the EPUB protons. While I thought what I
do is it will be pretend they are, it will be 100, which is found in the hepatocytes on, it will be 48,
which is formed in the end terrorist sites. It will be 40. It helps with the formation of your
chylomicrons, whereas it will be 100 is an integral protein in the synthesis of the V LDL’s very
low density lipoproteins. The intermediate density lipoproteins, we gotta ideals and a very low
under, low density lipoproteins. So the three would be very low density lipoproteins.
Intermediate density lipoproteins are low density lipoproteins, which, which all three contain
April BY 100, whereas it will be 48, is contained in the chylomicrons. Chylomicrons c, If you
remember, are responsible for the transport of dietary lipids. So your dietary cholesterol, dietary
triglycerides, even your dietary fat soluble vitamins, especially vitamins a, D, E, and K, they are
particularly transport that in the bloodstream by the chylomicrons. So back to the Microsoft will
transfer a proton in the synthesis of these lipoproteins, MDP plays a critical role in the LDP
Dacian of these proteins. In other words, it helps to pick up the lipids and then transfer the lipids
onto these newly formed it will be containing lipo proteins. And so what this means is that
without the Microsoft all transport protein, you will not be able to synthesize chylomicrons and
intestines. You will not be able to synthesize V LDL’s ideals. Ldl’s. Alright, so what this means is
that MCP is critical to the ability to form these. It will be continued lipoproteins WeChat, a major
carriers of cholesterol and triglycerides in the circulation. Generally speaking, the patients with
EBITDA lipo Nemea tend to present with stead to re-ask that urea is a ball key smelly, fatty stool
that results from impaired fought absorption or what we call fat malabsorption. Fat
malabsorption results because the patients are not able to synthesize chylomicrons, Indian
terrorist sites. You can synthesisers Carlo microbes and parasites, then you will not be able to
absorb anymore lipids, right? Anymore cholesterol anymore, vitamin a animal, vitamin K, you
will not be able to absorb those because the enterocytes are already Lu, dead. Well we those
lipids that have not been packaged into chylomicrons, and so that becomes a problem. So fat
malabsorption is a big problem in these patients. And for babies that are being breastfed or bottle
fed, whatever fats they have or whatever lipids or whatever fat-soluble vitamins they have in the
formula in the breast milk will likewise not be absorbed. So because of that, the patients can also
present with failure to thrive. The babies do not just grew as they should. Usually they out there
at about a day or less than the five percentile range for the age, sex, and weight. The patients also
experience neurologic problems like cerebellar conditions like ataraxia. They have decreased
proprioception. The peripheral neuropathy, they have loss of deep tendon reflexes. And in cases
that develop vitamin a deficiency, they can actually developed mind night blindness or does the
laboratory picture look like just based on what I described to you previously, it would make
sense that these patients would have low plasma cholesterol levels, right? Because they are not
able to transport endogenously synthesized cholesterol in the VLDB has on LDL’s, neither are
they able to transport dietary cholesterol from the chylomicrons and so are the patients will have
low plasma levels of cholesterol chylomicrons, VL deals, LDL’s would virtually be absent in
these patients. The patients would also have vitamin a deficiency. The patients will have my
blindness because of that, patients are vitamin E deficiency because the transport of vitamin E is
also dependent on these April be containing lipoproteins. And so even I’m even the delivery of
vitamin E, say from the liver to tissues that need vitamin E would also be compromise. And
particularly vitamin a deficiency affects cerebellar function. And so that’s what accounts for the
loss of proprioception. It accounts for the taxi at the patient’s experience because of low levels of
because of the low levels of cholesterol in the bloodstream, the red blood cells of the patients
tend to have abnormal Sparty shaped. Our parents, we call a canto side ptosis. Abnormally
shaped red blood cells all over the place. And so that again is because cholesterol is a critical
component of the cell membrane in our ability to transport endogenously synthesized cholesterol
generally leads to an accumulation of cholesterol and triglycerides in the liver, resulting in
hepatic stat ptosis, which is what we call a fatty, fatty liver. Which in the long term, if, if, if, if it’s
left unchecked can also result in chronic liver disease. And then when you look at the intestines
of the patients, it appears whitish. Okay. And that is because in the end terrorist sites I
accumulate so much lipids that are not able to be transported into the bloodstream. And so the
accumulation of those lipids Indian terrorist sides, gives the enterocytes a whitish appearance as
well. So malabsorption, I’ve diarrhea are key features in these patients. Just like I said, the
patients have low levels of cholesterol, which causes a canto site ptosis, which can then result in
excessive him or lysis and consequently anemia in the patients.