1. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 17 Disorders of Blood Flow and Blood Pressure

2. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Artery Structure Tunica intima: endothelium Tunica media: smooth muscle Tunica adventitia: collagen and elastic fibers

3. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which vessel layer can expand to accommodate pressure changes? a.Tunica intima b.Tunica media c.Tunica adventitia d.Tunica externa

4. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer b.Tunica media Rationale: The tunica media is composed of smooth muscle, which can stretch/expand to accommodate changes in blood pressure.

5. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Vascular Endothelium Food and O 2 pass into tissues Wastes and CO 2 pass from tissues into blood Creates compounds that cause vasodilation or vasoconstriction Creates growth factors that can stimulate smooth muscle Forms a smooth lining of the blood vessels that resists clot formation Creates compounds to promote clot formation in injured areas

6. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Atherosclerosis Lipids get into the vascular endothelium White blood cells try to clear them away  foam cells WBCs and vascular endothelium release growth factors that promote plaque formation Plaques block the arteries

7. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Lipoproteins The more protein, the higher the density The more lipid, the lower the density

8. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Tell whether the following statement is true or false. LDL is considered to be “good” cholesterol.

9. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer False Rationale: LDL (low-density lipoprotein, which has more lipids and less protein) is the “bad” cholesterol. HDL (high-density lipoprotein) has more protein and less fat, and is considered “good” cholesterol.

10. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Lipid Transport in the Body Dietary lipids absorbed as chylomicrons Adipose and muscle cells take up lipids from chylomicrons Chylomicron remnants are intermediate-density lipoproteins

11. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Lipid Transport in the Body (cont.) IDLs become low- density lipoproteins (“bad cholesterol”) These can deliver fat to the liver and by other tissues LDL receptors are necessary for the liver to take them up Some LDLs are taken up by scavenger cells like macrophages

12. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Fatty Streaks and Atherosclerotic Plaques

13. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Atherosclerosis Atherosclerosis develops because scavenger cells encounter the fatty deposits in the artery lining and –Try to destroy the fats by oxidizing them ºOxidized fats injure the endothelium ºClots form and release growth factors ºSmooth muscle grows over the fatty core –Try to remove the fats by eating them Become “foam cells” in the core of the plaque

14. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Atherosclerotic Plaque CAP CORE Macrophages Smooth muscle cells Endothelial cell Lymphocytes Lipid-laden macrophage (foam cell)

15. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Lipid Transport in the Body High-density lipoproteins (“good cholesterol”) are made in the liver They go out to the peripheral tissues and pick up lipid Then they carry it back to the liver

16. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario A man has several genetic defects in his lipoprotein receptors. His liver lacks LDL receptors His muscle cells lack receptors for the apoproteins on chylomicrons His scavenger cells have extra LDL receptors Question: Why might he develop atherosclerosis?

17. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Stable Plaques Have thick fibrous caps Partially block vessels Do not tend to form clots or emboli

18. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Unstable Plaques Have thin fibrous caps Plaque can rupture and cause a clot to form May completely block the artery The clot may break free and become an embolus

19. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question What immediate threat do unstable plaques present? a.Clot formation will increase pressure in the vessel. b.Plaque may lead to angina (chest pain). c.Clots may break loose and block blood flow to key organs. d.All of the above constitute immediate threats.

20. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer c.Clots may break loose and block blood flow to key organs. Rationale: If a clot breaks loose, becoming an embolus, it may lodge in a blood vessel to the brain, heart, or lungs. When blood flow is significantly decreased or blocked altogether, the result is tissue death—in the examples here, stroke, heart attack, or pulmonary embolus. The other choices represent more long- term/chronic problems.

21. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario A woman complains of pain in her left leg. Her foot is cool and pale She reports that it is often red and warm when she is sitting down The pain occurs when she is walking to church on Sundays The skin on her left leg is shinier than on her right leg Question: What could have caused all this? How?

22. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Aneurysms Wall of artery weakens and stretches Risk of rupture and hemorrhage Risk of clot formation

23. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Discussion How would each of the following affect blood pressure? Vasodilation Decreased stretching of baroreceptors Hypoxemia Inhibiting angiotensin-converting enzyme Beta blockers Alpha-2 agonists Calcium-channel blockers