BIOL 460 1st Edition Lecture 21 Outline of Last Lecture I. Blood Vessels (Start of Final Material)a. Arteriesb. Veins c. Capillaries II. Lymphatic SystemOutline of Current Lecture I. Lymph VesselsII. Lymph NodesIII. Atherosclerosis IV. Blood Clotting a. Formationb. Anticoagulants Current Lecturea. Lymph Vesselsi. Connected to lymph capillariesii. Similar to veins, including valvesb. Lymph Nodesi. Afferent lymphatics – into the nodeii. Efferent lymphatics – out of nodeiii. More afferent than efferentiv. Lymph goes through node slowlyv. Contains B and T lymphocytes, macrophagesvi. Like a filtervii. Site of metastasis (cancer cells enter lymphatic system, get stuck, and divide) – biopsy near lymph nodes near cancer site to see if cancer has metastasized yetc. Thoracic Duct: carries most lymph in body to the left subclavian vein (returns most to blood)d. Right Lymphatic Duct: to R subclavian veinThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.e. Cisternae Chyli: from small intestine, transports chylomicronsAtherosclerosis1. Disease of arteries2. Responsible for ½ of deaths in America every year3. Formation of plaques in arteries (atheromas)a. Fatb. Crystals of cholesterol/calcium/bone4. Restricts blood supply to tissue downstream5. Often has roughened edge, causing stationary blood clot (thrombus)6. If the thrombus breaks loose and moves – embolus7. Injury hypothesisa. Atheromas: result of damage to endothelium of arteryb. Damage  inflammation  atheromac. How to damage: cigarette smoking, hypertension bacterial or viral infection (periodontal disease)8. Related to cholesterol and saturated fat in dieta. Familial Hypercholesteremab. Caused by autosomal dominant (AA=DEATH)c. Transported by LDLs (low density lipoproteins)i. Cholesterol and triglycerides in centerii. On membrane  apolipoproteinsd. Other cells have receptor for apolipoproteins, causing LDL to adhere to receptors,stimulating receptor-mediated endocytosise. Cell uses cholesterol and triglyceridesf. Liver makes LDLs then use the majority of themg. In Familial Hypercholesteremia – liver doesn’t have many apolipoprotein receptors, most LDLs taken up in blood streamh. Liver downregulates receptors when there is too much cholesterol consumed (bad diet)i. HDLs are “good cholesterol” – transports unused cholesterol to liverj. Liver cells are the only cells with HDL receptors, takes up and dispose of HDL in bilek. Ratio of HDL:LDL is important in determining risk factorIschemic Heart Disease1. Inschemia: lack of blood flow (and oxygen) to as tissue2. Atherosclerosis  myocardial ischemia  fermentation  lactic acid build up  anginapectoris  bad enough, heart muscle will die  myocardial infarction (heart attack)Blood Clotting1. Hemostasis – cessation of bleeding2. 3 stepsa. Vasoconstrictionb. Platelet plug – petechiae (red spots where platelets aren’t being properly produced)c. Clot3. Figure 13.7a. Endothelium of intact vessel produces NO (vasodilator) and prostacyclin (a prostaglandin that keeps platelets from sticking together and acts as a vasodilator)b. CD39 – ADPAP + P; ADP allows platelets to stick, so CD39 prevents ADP from building up when clotting is not needed4. Damaged Vessela. Rupture in endotheliumb. Underlying tissues exposed (lots of collagen)c. Platelets have proteins that stick to collagend. Von Willibrands Factor (VWF, pitchfork structure) – protein produced by endothelial cells, help platelets adhere to collagen (one type of hemophilia caused by a deficiency in this)e. Causes Platelet Release Reactioni. Degranulation (vesicles in platelet look like granules)ii. Vesicles undergo exocytosis, fusing with PMiii. Thromboxin A2 (prostaglandin) and ADP are released1. TXA2 helps platelets stick, also a vasoconstrictor2. ADP makes platelets sticky3. Growth factors released (speed repair of connective tissues)4. Tissue Factor released (important in clotting)5. Formation of a Clota. Fibrin – network/mesh of fibersb. Can contractc. Fibrinogen (soluble plasma proteins) [throbrin]  polymer of fibrind. Prothrombin  Thrombini. Intrinsic Mechanism1. Slower2. Blood only3. Clots by itselfii. Extrinsic Mechanism1. Involves chemicals from tissues2. Tissue Factorse. Clotting Factorsi. Mostly plasma proteins in bloodii. Work together to form clotiii. Ca2+ needed6. Dissolution of Clotsa. Prekallikrein  [XII]  kallikreinb. Plasminogen  [kallikrein, thrombin, or tissue plasminogen activator]  Plasmin(enzyme that digests fibrin)c. Same steps that form clot also aid in dissolution of clot (thrombin, XII)d. TPA  used to dissolve clots in stroke and myocardial infarctions, produced by endothelial cellse. Also use streptokinase (produced by streptococcus) to dissolve fibrin7. Anticoagulantsa. Aspirin  inhibits COX-1, inhibits platelet release reactionb. Coumarin (warfarin)  inhibits activation of vitamin K, no Ca2+ binding to clotting factorsc. Heparin  inhibits thrombin (what blood-storing glassware is coated with )d. Citrate  binds Ca2+, making it unavailablee. EDTA  binds Ca2+, making it