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Rxn to Injury Theory.docx

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Nursing
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NURS 203
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All

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Rxn to Injury Theory Cells involved- platelets, monocytes, macrophages, cytotoxic t cells with cytokines (neutrophils not involved) Atherosclerosis in an aorta – rxn to injury theory = injury to endothelial cells lining the elastic arteries and muscular arteries – what is injuring it? Ammonia in cig smoke, CO in cig smoke; so, poisons damage the endothelial cells; LDL damages it, and if its oxidized, it damages it worse; nd viral infections damage it, too. Chlamydia pneumoniae (2 MCC atypical pneumoniae); pts with MI – most had Ab’s against Chlamydia pneumonia, homocysteine – all these things damage endothelial cells What happens when you damage endothelial cells? Platelets stick to it and PDGF is released into the artery and PDGF causes smooth muscle cells within the media to proliferate and they undergo hyperplasia and then, they chemotactically migrate to the subintimal level. They have all these smooth muscle cells migrating to the intima of the vessel. Monocytes have access into the vessel b/c it has been injured and monocytes also have GFs. As the LDL increases, the macrophages phagocytose them. Macrophages and smooth cells have LDL w/in them; the LDL becomes oxidized and a fatty streak is produced. Over time, a fibrofatty plaque develops, which is pathognomonic of atherosclerosis. It can be complicated by dystrophic calcification, fissuring, thrombosis and a complicated atherosclerosis. Atherosclerosis is a primary factor for certain dz’s – CAD; atherosclerotic stroke relates to plaques; abdominal aneurysm due to weakening of the vessel; nontraumatic amputation of lower extremity (peripheral vascular dz); mesenteric angina, small bowel infarction, renovascular atherosclerosis of the renal arteries. Atherosclerosis only involves muscular arteries and elastic arteries. Can small vessel, such as arterioles get hardened? Yes. Example: look at the spleen – hyaline arteriolar sclerosis and hyperplastic arteriolar sclerosis (onion skinning). Hyaline arteriosclerosis is a small vessel dz; lumen is narrow; whenever there is a lot of pink staining stuff, this is hyaline. Example: small vessel dz of diabetes and HTN – two major dz’s that produces a small vessel dz with different mechanisms: Diabetes: nonenzymatic glycoslyzation – aka HbA1c; glycoslyzation is glucose attaching to aa and protein. For HbA, its glucose attaching to aa and HbA, and the HbA is glycosylated. HbA1c levels correlate with the blood glucose levels of the last 6-8 weeks, so this is the best way of looking at long term glucose levels. All the damage seen in diabetes is due to glucose. For a diabetic, you should be under 6%, meaning that you are in a normal glucose range. There is nothing unique about diabetes except for a large glucose level, you keep that normal, and it’s as if you don’t have diabetes. The only two pathologic processes are this: nonenzymatic glycosylation of small BV’s including capillaries in the kidney, and osmotic damage. Those tissues that contain aldose reductase – lens, pericytes in the retina, schwann cells – all have aldose reductase and can convert glucose into sorbitol and sorbitol is osmotically active sucks water into it and those cells die, leading to cataracts, microaneurysms in the eye b/c the pericytes are destroyed and weakened and the retinal vessels get aneurysms, and you get peripheral neuropathy b/c schwann cells are destroyed. They all related to excess glucose. So, tight glucose control = normal life. What does nonenzymatic glycosylation to do the basement membrane of small vessels? Its renders them permeable to protein, so the protein in the plasma leaks through the BM and goes into the vessel wall, produces a hyaline change and narrows the lumen. What if there is nonenzymatic glycosylation of the GBM? It will render it permeable to protein – called microalbuminuria. This is the first change to be seen in diabetic nephropathy. So, what is the mechanism? Nonenzymatic glycosylation. Hypertension Does not use nonenzymatic glycosylation. It just uses bruit force and drives (b/c of increase in diastolic pressure) the proteins through the BM and produces the effect. When we look at a kidney in HTN, it is shrunken, has a cobblestone appearance – this is b/c there is hyaline arteriolosclerosis of the arterioles in the cortex, ischemia, and is wasting away with fibrosis and atrophy of tissue. Lacunaer strokes (tiny areas of infarction that occur in the internal capsule) are a hyaline arteriosclerosis problem related to HTN. Hyperplastic arteriosclerosis Seen in malignant HTN; more common in blacks then whites, mainly b/c HTN is more common in blacks than whites. Mainly see this vessel dz in malignant HTN (ie when pt has BP of 240/160). Aneurysm Definition: area of outpouching of a vessel due to weakening of the vessel wall. Atherosclerosis can cause weakening of the abdominal aorta leading to an aneurysm. What would be the analogous lesion in the lungs with weakening and outpouching? Bronchiectasis – due to cystic fibrosis with infection, destruction of elastic tissue leading to outpouching and dilatation of the bronchi. Example: what is the GI aneurysm? Diverticular dz – have a weakening and outpouching of mucosa and submucosa Law of Laplace – the wall stress increases as radius increases. In terms of this, once you start dilating it, it doesn’t stop b/c as you dilate something, you increase the wall stress and eventually it ruptures. So, in other words, all aneurysms will rupture – it’s just a matter of when. Abdominal Aorta Aneurysm: Why is the abdominal aorta the MC area of aneurysm? B/c there is no vasa vasorum or blood supply to the aorta below the renal arteries. So, the only way abd. aorta gets O2 and nutrients is from the blood that’s in the lumen. So, part furthest from it mgets screwed. Therefore, apart from the part that is not getting much O2 and nutrients, it will be m
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