Vascular Diseases & Section Review
| previous topic | next topic | syllabus | home page | BME Home Page | search the web | e-mail Doug |
This is what happened in class today (12-5-97).
As usual, all of this is in outline format with hypertext, so if you want to review the specifics, or if you have any questions on a specific topic, click the hypertext for that topic.
Today's topic:
Many of these topics are incomplete.
They should be completed when the
extra credit projects are turned in.
These are Dr. Schechtman's very own notes for this lecture.
I hope you find them helpful.
15 Vascular Disease Hypertension--factor in stroke, CHF, MI, peripheral vascular disease, renal failure Essential Hypertension--no apparent cause, more common, runs in families, more common in men and in blacks Secondary Hypertension--only ~5%. Usually if you correct the underlying medical condition, it fixes itself. problems-- causes heart to work harder, damages inner layer of blood vessels, a factor in atherosclerotic buildup By definition > 90 diastolic or 150 systolic Lack of patient compliance with diet and drug schedules is problem because patients feel fine. So physician has to “sell” the patient on the importance of treating high BP. Treatment of Hypertension Intensive sodium restriction can get good results, but poor patient compliance because must be very restrictive, which is expensive (buy special bread, etc.), time-consuming, and unpleasant. Always look for a primary cause of secondary hypertension before implementing therapy. Step 1. A diuretic lowers BP by reducing plasma volume. Well-tolerated and sufficient treatment for some hypertensives. Step 2. Beta-blocker (contraindicated in CHF) reduces cardiac output and vascular resistance. Step 3. Arteriolar vasodilator If none works, reevaluate possibilities for secondary hypertension. Stroke Thrombosis--clotting blocks already narrow artery Embolism--a bit of arterial wall, plaque, or small blood clot is carried in the bloodstream until it becomes wedged in a place where it obstructs blood flow Hemorrhage-- Aneurysm--a dilation of a segment of blood vessel Potential Problems-- can burst and cause loss of blood flow to an area and/or hemorrhaging can press on neighboring organs or nerves can cause turbulent flow leading to clot formation Effects and prognosis depend on brain location size of area damaged by ischemia extent of damage exerted by increased cranial pressure TPA Transient Ischemic Attack--temporary obstruction of an artery Causes transient loss of vision, paralysis, confusion, etc. depending on location; may forebode a major stroke Anticoagulant therapy used to prevent subsequent events and/or a major stroke Hemorrhage and Shock-- Compensatory mechanisms for blood loss are so fast and so effective, that in all but rare instances, donating half a liter of blood has no noticeable effect. Provide time for restoration of fluid over a few hours and the somewhat slower regeneration of proteins and blood cells. Acute Compensatory responses to blood loss Increased peripheral resistance includes reduced blood flow to kidneys and thus reduced urine output Symptoms: cool skin from cutaneous vasoconstriction rapid pulse and sweating are direct effects increased sympathetic activity sunken features result of tissue dehydration secondary to absorption of extracellular fluid intense thirst, dry mouth, and scanty urine reflect attempt to replenish lost fluid increased respiratory activity may occur, when oxygen supply drops and chemoreceptors kick in Irreversible Shock-- Caused by metabolic effects and anoxia Products of tissue damage are released including histamine and adenosine, which cause vasodilation (positive feedback loop) The reduction in tissue blood flow that follows an intense vasoconstriction leads, with time, to tissue hypoxia and local accumulation of metabolic end products (including histamine and adenosine). The vasoactive metabolites eventually reach a level where they override the vasoconstrictor effect of sympathetic stimulation. This permits capillary beds to fill with blood at the expense of arterial blood volume. Finally lack of tissue perfusion, cell damage, and death follow.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
| previous topic | next topic | syllabus | home | BME | search the web | e-mail Doug |
| 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | Exam #1 |
| 17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | Exam #2 |
| 28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39 | 40 | 41 | 42 | Exam #3 |