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<ul><li> 1. Diseases of BLOOD VESSELS</li></ul><p> 2. COMPONENTS Intima, Media, Adventitia, M&gt;A or A&gt;M ENDOTHELIUM INTERNAL ELASTIC LAMINA ECM: Elastin (~aging), collagen,mucopolysaccharides Smooth Muscle Connective Tissue Fat 3. 1) Blockage(preceded by narrowing)2) RupturePreceded by weakening) 4. TOPICS Vascular wallresponses CongenitalAnomalies Atherosclerosis Arteriosclerosis Hypertension Aneurysms Vasculitides Raynaudphenomenon Veins Lymphatics Tumors Interventions 5. DEFINITIONS ARTERIO-sclerosis ATHERO-sclerosis Aneurysm Dissection Thrombus Hypertension Vasculitis/Vasculitides, infectious/NON-infectious(often-autoimmune) Varicosity DVT/Thrombo-phlebitis/Phlebo-thrombosis 6. DEFINITIONS Lymphangitis Lymphedema Angioma/Hemangioma (generic) Lymphangioma Angiosarcoma (generic) Lymphangiosarcoma 7. NON-Specific Vascular WallResponse to Injury Endothelial activation Smooth Muscle cell roles Development, Growth,Remodeling Intimal thickening 8. ENDOTHELIAL CELLS Recall Jeckyl/Hyde concept: maintainhemostasis/cause thrombosis Maintenance of Permeability Barrier Elaboration of Anticoagulant, Antithrombotic,Fibrinolytic Regulators Elaboration of Prothrombotic Molecules Extracellular Matrix Production (collagen,proteoglycans) Modulation of Blood Flow and Vascular Reactivity Regulation of Inflammation and Immunity Regulation of Cell Growth Oxidation of LDL 9. ENDOTHELIAL CELLACTIVATORS (?) Cytokines Bacterial Products Hemodynamic Forces Lipid Products Viruses Complement Hypoxia 10. VASCULAR SMOOTH MUSCLE Vasoconstriction Vasodilatation Make ECM: Collagen Elastin Proteoglycans Regulated by: PROMOTORS: PDGF, endothelin, thrombin, etc. INHIBITORS: Heparan SO4, NO, TGF- 11. Vessel Growth&amp; Remodeling The sum total of all the factors andprocesses involved in tissue injuryand the bodys ability to growvessels, develop new pathways,and re-perfuse areas in responseto tissue and/or blood vesselinjury. 12. CONGENITAL ANOMALIES Arteriovenous fistulas Also called ArterioVenous Malformation(AVM) Common factor is abnormal communicationbetween high pressure arteries and lowpressure veins Usually congenital, but can be acquired bytrauma or inflammation Most often described in the brain as an AVM Asymptomatic or with hemorrhage orpressure effects 13. ARTERIO-SCLEROSIS GENERIC term for ANYTHINGwhich HARDENS arteries Atherosclerosis (99%) Mnckeberg medial calcificsclerosis (1%) Arteriolosclerosis, involving smallarteries and arterioles, generallyregarded as NOT strictly being partof atherosclerosis, but more relatedto hypertension and/or diabetes 14. ATHEROSCLEROSIS(classical) Etiology/Risk Factors Pathogenesis Morphology Clinical Expression 15. ATHEROSCLEROSIS(ala Robbins) *Natural History *Epidemiology *Risk Factors *Pathogenesis *Other Factors *Effects *Prevention 16. *NATURAL HISTORY 17. 1) FATTYSTREAK2) ATHEROMA(plaque)3) THROMBUS 18. MORPHOLOGIC CONCEPTS Intimal Thickening Lipid Accumulation Streak Atheroma Smooth Muscle Hyperplasia and Migration Fibrosis Calcification Aneurysm Thrombosis 19. FATTYSTREAKS 20. PLAQUE 21. MILD ADVANCED 22. ADVANCED FEATURES RUPTURE ULCERATION EROSION ATHEROEMBOLI HEMORRHAGE THROMBOSIS ANEURYSM 23. FUN THINGS TO FIND:Lumen, Fibrous cap (fibrous plaque), Lipid core,External Elastic Membrane thinning/destruction,Calcification, Neovascularization 24. *EPIDEMIOLOGY&amp; RISK FACTORS 25. Epid./RiskFactors Related to development of nation US highest 50-70% DECREASE 19632000.Why? AGE SEX, M&gt;F until menopause,estrogen protection GENETICS 26. MAJORfactors Hyperlipidemia Hypertension Cigarette Smoking Diabetes Milletus 27. Risk Factors for AtherosclerosisMajor MinorNON-modifiable ModifiableIncreasing age ObesityMale gender Physical inactivityFamily history Stress ("type A" personality)Genetic abnormalities Postmenopausal estrogen deficiencyHigh carbohydrate intakeModifiableHyperlipidemia AlcoholHypertension Lipoprotein Lp(a)Cigarette smoking Hardened (trans)unsaturated fat intakeDiabetes Chlamydia pneumoniae 28. MAJORfactors Hyperlipidemia Hypertension Cigarette Smoking Diabetes Milletus 29. HYPERLIPIDEMIA Chiefly CHOLESTEROL,LDL&gt;&gt;&gt;&gt;HDL HDL mobilizes cholesterol FROMatheromas to liver LOW CHOLESTEROL diet is GOOD UNSATURATED fatty acids GOOD Omega-3 fatty acids GOOD Exercise GOOD 30. CHOLESTEROL CLEFTS 31. HYPERTENSION HYPERTENSION causesATHEROSCLEROSIS. Why? ATHEROSCLEROSIS causesHYPERTENSION. Why? 32. CIGARETTES What more needs to be said? 33. DIABETES If there was one diseasewhich I could challenge youto, as a dare, to PROVE tome that was NOT EXACTLYTHE SAME asatherosclerosis, it would beDIABETES! Any takers? 34. NON major factors Homocysteinuria/homocysteinemia, relatedto low B6 and folate intake Coagulation defects Lipoprotein Lp(a), independent ofcholesterol. Lp(a) is an altered form of LDL Inadequate exercise, Type A personality,obesity (independent of diabetes) Protective effect of moderate alcohol? LIE! 35. PATHOGENESIS atherosclerosis is a chronicinflammatory response ofthe arterial wall initiated byinjury to the endothelium 36. PATHOGENESIS SAGA Chronic endothelial injury LDL, Cholesterol in arterial WALL OXIDATION of lipoproteins Monocytes migrate endothelium Platelet adhesion and activation Migration of SMOOTH MUSCLE from media tointima to activate macrophages (foam cells) Proliferation of SMOOTH MUSCLE and ECM Accumulation of lipids in cells and ECM 37. Main FOUR STARS ofPATHOGENESIS SAGA 1) Endothelial Injury 2) Inflammation 3) Lipids 4) Smooth Muscle Cells, SMCs 38. Other PathogenesisConsiderations Oligoclonality of cells inplaque Chlamydia, CMV asendothelial injurers 39. PREVENTION PRINCIPLES Know what is preventable Know what is MAJOR (vs. minor) Know PRIMARY vs. SECONDARYprinciples Understand atherosclerosis begins inCHILDHOOD Risk factors in CHILDREN predict theADULT profile Understand SEX, ETHNIC differences 40. NON ATHEROSCLEROSISVASCULAR DISEASESHYPERTENSIONANEURYSMSVASCULITIDES VEIN DISORDERS NEOPLASMS 41. HYPERTENSION ESSENTIAL 95% SECONDARY 5% 42. SECONDARY Renal Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis Renal artery fibromuscular dysplasia Renal vasculitis Renin-producing tumors Endocrine Adrenocortical hyperfunction (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion) Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oralcontraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidaseinhibitors) Pheochromocytoma, Acromegaly, Hypothyroidism (myxedema), Hyperthyroidism Pregnancy-induced Cardiovascular: Coarctation of aorta, Polyarteritis nodosa (or other vasculitis) Increased intravascular volume MISC: Increased cardiac output, Rigidity of the aorta, Neurologic, Psychogenic,Increased intracranial pressure, Sleep apnea, Acute stress, including, surgery 43. DEFINITION 140/90 SUSTAINED diastolic &gt;90 SUSTAINED systolic &gt;140 44. ALL HypertensionBP = CO x PR 45. ReninAngiotensinAldosteroneAXIS If the perfusion of the juxtaglomerularapparatus in the kidneys decreases, then thejuxtaglomerular cells release the enzymerenin. Renin cleaves an inactive peptide calledangiotensinogen, converting it intoangiotensin I. Angiotensin I is then converted to angiotensinII by angiotensin-converting enzyme (ACE),which is found mainly in lung capillaries. Angiotensin II is the major bioactive product ofthe renin-angiotensin system. Angiotensin IIacts as an endocrine, autocrine/ paracrine, andintracrine hormone. 46. GENETICACQUIRED 47. HISTOPATHOLOGY ofESSENTIAL HYPERTENSIONHYALINE = BENIGN HTN. HYPERPLASTIC = MALIGNANT HTN. SYS&gt;2001) ONION SKIN 2) FIBRINOID NECR. 48. GENETICvs.ENVIRONMENTAL GENETIC UN-CONTROLABLE ENVIRONMENTAL CONTROLABLE STRESS OBESITY SMOKING PHYSICAL ACTIVITY NaCl INTAKE 49. ANEURYSMS TRUE vs. FALSE ATHEROSCLEROTIC NON-ATHEROSCLEROTIC CONGENITAL LUETIC (SYPHILITIC) TRAUMATIC MYCOTIC (MIS-leading term) 2 to VASCULITIS SACCULAR (i.e., Berry) vs. FUSIFORM DISSECTION vs.NON-DISSECTION 50. ANEURYSMS 2 CAUSES:1) ATHEROSCLEROSIS2) CYSTIC MEDIAL DEGENERATIONNORMAL elastic fibers DISRUPTED, FRAGMENTED elastic fibers 51. Most abdominal aortic aneurysms (AAA) occur betweenthe renal arteries and the bifurcation of the aorta 52. ANEURYSMS(sequelae)RUPTUREOBSTRUCTIONEMBOLISMCOMPRESSION URETER SPINEMASS EFFECT 53. THORACICANEURYSMSEncroachmentRespiratory difficultiesDysphagiaCoughPainAortic valve dilatationRupture 54. DISSECTION 55. ANEURYSMS(luetic)Chiefly thoracicFollows an AORTITIS PLASMA CELLS predominate 56. VASCULITIDES TEMPORAL GIANT CELL ARTERITIS TAKAYASU ARTERITIS POLY (PERI) ARTERITIS NODOSA KAWASAKI DISEASE WEGENERs GRANULOMATOSIS THROMBOANGI(i)TIS OBLITERANS(BUERGER DISEASE) OTHER INFECTIOUS 57. VASCULITIDES Chiefly arterial Infectious (5%) vs. Non-infectious (95%) NON-infectious are generally AUTO-IMMUNE. Why? Persistent findings: Immune complexes ANTI-NEUTROPHIL ABs (Wegeners) ANTI-ENDOTHELIAL CELL ABs (Kawasaki) Often DRUG related (Hypersensitivity, e.g.) 58. TEMPORAL ARTERITISaka, Giant Cell Arteritis, GCA ADULTS Mainly arteries of the head andtemporal arteries are the most visibly,palpably, and surgically accessible BLINDNESS most feared sequelae GRANULOMATOUS WALLinflammation diagnostic OFTEN associated with marked ESRelevation to be then known asPOLYMYALGIA RHEUMATICA Anti-NEUTROPHIL ABs often POSITIVE 59. TEMPORAL ARTERITIShttp://www.path.uiowa.edu/cgi-bin-pub/vs/fpx_gen.cgi?slide=623&amp;viewer=java&amp;view=0&amp;lay=iowa 60. TAKAYASU ARTERITIS Involves aortic arch and other heavillyelastic arteries, i.e., chief thoracic aortabranches FEMALES &gt;&gt;F, 30s, 40s Often arteries are 100% obliterated,hence the name obliterans EXTREMITIES most often involved 69. http://www.path.uiowa.edu/cgi-bin-pub/vs/fpx_gen.cgi?slide=704&amp;viewer=java&amp;view=0&amp;lay=iowa 70. OTHER VASCULITIDES SLE RHEUMATOID ARTHRITIS 71. INFECTIOUS ARTERITIDES ASPERGILLIS MUCORMYCOSIS MYCOTIC ANEURYSMS 72. NON ATHEROSCLEROSISVASCULAR DISEASES HYPERTENSION ANEURYSMS VASCULITIDES VEIN DISORDERSNEOPLASMS 73. FINAL TOPICS Raynaud Phenomenon Veins and Lymphatics Varicosities Thrombophlebitis/Phlebothrombosis SVC/IVC syndromes Lymphangitis Lymphedema Tumors: Benign, Intermediate(Borderline), Malignant Vascular Interventions: Angioplasty,Stents, Grafts 74. Raynaud Phenomenon PRIMARY: (formerly Raynaud DISEASE) Digital PALLORCYANOSISHYPEREMIA (WHITE) (BLUE) (RED) Vasoconstriction usually triggered by COLD, emotion Can be tip of nose, not only digits Self Limited, Gangrene UN-common SECONDARY: (formerly Raynaud Phenomen.) Atherosclerosos SLE Buerger Disease 75. WHITEBLUERED 76. Varicose Veins 20% of population, F&gt;M Related to increased venous pressure,age, valve dysfunction Superficial veins of lower extremities mostcommon PATH: 1) DILATED, 2) TORTUOUS,3) ELONGATED, 4) SCARRED(phlebosclerosis), 5) CALCIFICATIONS,6) NON-UNIFORM SMOOTH MUSCLE Conceptually like varices or hemorrhoids 77. THROMBOPHLEBITIS 90% DEEP veins of the legs IDENTICAL to PHLEBOTHROMBOSIS Factors: CHF, Neoplasia (esp. GI, panc.Lung adenocarcinomas migratorythrombophlebitis), pregnancy, obesity,post-op, immobilization, or any of theparts of Virchows triangle Sequelae: PE most feared Symptoms: edema, cyanosis, heat, pain,tenderness, but usually..NONE!!! 78. SVC SYNDROME Usually from bronchogenic CAor mediastinal lymphoma DUSKY CYANOSIS of:HeadNeckArms 79. IVC SYNDROME Secondary to: NEOPLASMS (external compression) ASCENDING THROMBOSIS fromFEMORALS, ILIACS AAA, Gravid uterus Bilateral leg edema Massive proteinuria if renal veinsinvolved (like nephrotic syndrome) 80. LYMPHANGITIS From regional infections Group-A beta-hemolytic strep mostcommon Lymphatics dilated, filled with WBCs Cellulitis usually present too Lymphadenitis also usually follows If lymph nodes cannot filter (process)antigens enough septicemia 81. LYMPHEDEMA Lymphatic channels blocked orscarred or absent: Post surgicalPost radiation Filaria Congenital Tumoral (peau dorange) 82. CHYLE CHYLOUS ASCITES CHYLOTHORAX CHYLOPERICARDIUM 83. Vascular TUMORS BENIGN (NEVER metastasize, in factsome are not even TRUE neoplasms,but hamartomas) INTERMEDIATE (rarely metastasize) MALIGNANT (FREQUENT and EARLYmetastases, like any other sarcomalung) 84. BENIGN---------------------------------------MALIGNANTRare mitosis--------------------------Common mitosisMild, rare atypia------------Frequent, severe atypiaNO mets----------------------------Early, frequent metsvia BLOODSTREAM 85. HEMANGIOMA Often a generic term for ANY benign bloodvessel tumor CAPILLARY (small vascular spaces) Also called juvenile, often called birth marks Usually regress with age CAVERNOUS (LARGE vascularspaces) Also called adult Usually do NOT regress 86. PYOGENIC GRANULOMA ORAL CAVITY MOST COMMON Histology like capillaryhemangioma Regress Indistinguishable from normalgranulation tissue 87. LYMPHANGIOMA Small 1-2 mm Head and neck region GenerallyRARE When large size and/or spacespresent often called CYSTICHYGROMA 88. GLOMUS TUMORGLOMANGIOMA 1 cm Most commonly under nail Painful 89. MISC. BENIGN TUMORS -ectasias, telangiectasias Nevus Flammeus, aka, port wine stain Spiders (spider telangiectasias), ass. W.pregnancy, cirrhosis Osler-Weber-Rendu Disease (HereditaryHemorrhagic Telangiectasia) Bacillary Angiomatosis, in HIV patients, causedby bacilli of Bartinella species 90. INTERMEDIATE (BORDERLINE)VASCULAR NEOPLASMS Kaposi Sarcoma, KS 1) Classic European, described 1872, NON-HIV 2) African, pre-HIV, now HIV- and HIV+ 3) Transplant associated, HIV- 4) AIDS KS, caused by HHV-8, aka KSHV PATCH PLAQUENODULE HEMANGIOENDOTHELIOMA(HETEROGENEOUS GROUP OFNEOPLASMS) 91. Diagnosis of vascular neoplasms may requirethe use of endothelial cell markers such asFactor VIII or CD-31, especially if clear cutvascular spaces are difficult to see, especially ifthe tumor is UNDIFFERENTIATED enough to thedegree that endothelial lined spaces are NOTclearly seen. 92. MALIGNANT VASCULARTUMORS ANGIOSARCOMA May not look vascular at all Severe atypia Frequent and often bizarre mitoses Behave as any sarcoma might, i.e., earlypulmonary metastases HEMANGIOPERICYTOMA HETEROGENOUS group of disorders Most commonly arising in pelvic retroperitoneum 93. VASCULAR INTERVENTIONS ANGIOPLASTY STENTS GRAFTS Autologous (saphenous v., internalmammary a.) Synthetic (Teflon) 94. ANGIOPLASTIES Plaque fracture (crackling sound) Dissection Arterial dilatation initially Restenosis ~ 6 months 95. STENTS Metallic mesh Permanently placed Stays patent longerthan angioplasty OFTEN DRUG COATED Goals: Prevent thrombosis Prevent spasm Delay RE-stenosis 96. GRAFTS 400,000 CABG grafts per year in USA Saphenous v. vs. Internal mammary a. (internalthoracic a.) 50% patent after 10 years, for saphenous v. 90% patent after 10 years, for mammary a. Endothelial and smooth m...</p>