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Minarcik robbins 2013_ch11-vessels

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  • IMHO, one of the most logical and clear, of all chapters!
  • Aorta (elastic artery), artery, vein, capillary: Know all the differentiating histologic features
  • Two types of vascular diseases:
    Atherosclerosis
    Everything else
  • Please note that the “NONSPECIFIC” reactions to injury, are very closely paralleling the process we call “atherosclerosis”, also note that these processes seem to be more typical of arteries rather than veins.
  • Prostacyclin INHIBITS platelet activation, Thrombomodulin inhibits thrombin, Heparin is body’s main anticoagulant, Plasminogen, precursor of plasmin dissolves fibrin!
  • Because of the simple geometric fact that smooth muscle cells are arranges axially (opposite) to the axis of the blood vessel, constriction of the smooth muscle cell results in constriction of the vessel.
    PDGF plays a role in embryonic development, cell proliferation, cell migration, and angiogenesis
    Endothelins are 21-amino acid vasoconstricting peptides produced primarily in the endothelium having a key role in vascular homeostasis. 
    HS binds to a variety of protein ligands and regulates a wide variety of biological activities, including developmental processes, angiogenesis, blood coagulation and tumor metastasis.
    Nitric oxide, known as the 'endothelium-derived relaxing factor', or 'EDRF‘
  • Intimal thickening is a NON-specific response to vascular (chiefly arterial) injury, and is they KEY feature in atherosclerosis as well.
    This is logical because almost all of the vessel injuring factors come from the LUMEN of the vessel.
  • A-V fistulas are also called A-V malformations.
  • CT Angiogram
  • Atherosclerosis and arteriosclerosis are often used so interchangeably, it is hardly worth differentiating them anymore, other than to know they are different!
  • Classical features of all diseases as defined in chapter 1.
  • Note that there is nothing listed as “CAUSE”
  • In this case, the “Natural History” is very similar, if not identical, to the concept of “Pathogenesis”.
  • Atherosclerosis is a LIFELONG, even childhood, process. This chart is worth knowing.
  • Fatty STREAKS can be SEEN as YELLOW, but NOT palpated, ATHEROMAS can be palpated, thrombi are symptomatic often.
    A rule of thumb is that stenosis is symptomatic if > 90%.
  • These are also, generally, in order of severity.
    * Do you think an ACUTELY or FIBROTICALLY(CHRONIC) inflamed arterial wall would be most likely to develop an aneurysm?
  • The streaks are more noticeable at the ostia of the aorta because that is where PRESSURE is the greatest. This simple observation makes it easier to understand the relationship between hypertension and atherosclerosis
  • Cholerterol (really cholesterol esters) makes macrophages “foamy” and cause “clefts” extracellularly.
  • These should all be household words in your vocabulary.
  • Also very closely related! When you cant identify a specific CAUSE, you talk about “risk factors”.
  • “Framingham” data. Please remember that these are the ONLY four MAJOR risk factors. If somebody tells you there is anything else which is a MAJOR risk factor, nominate that joker for a Nobel prize.
    Notice how many of the MAJOR risk factors are controllable?
  • Needle shaped washed out spaces in arteries, are cholesterol clefts, and can be nothing else, and like all other fat, yellow grossly, white microscopically.
  • Risk factors vs. ischemic heart disease
  • It is easy for a smoker to FORGET that cigarettes cause atherosclerosis. i.e., MAJOR risk factor. I hope YOU do not forget.
  • A major challenge is suggested here!
  • Homocystinuria, also known as cystathionine beta synthase deficiency or CBS deficiency, is an inherited disorder of the metabolism of the amino acid methionine, often involving cystathionine beta synthase. It is an inherited autosomal recessive disorder
    High levels of Lp(a) is associated with increased risk of atherosclerosis. It should be < 14 mg/dL (< 35 nmol/l)
  • Like the sequence of events described in acute inflammation, atherosclerosis is its own Cecil B. DeMille saga! Not only should you all be familiar with these processes, but their ORDER as well.
    * This may be the first (i.e., earliest) microscopic and gross finding.
  • A very well constructed graphic understanding of the pathogenesis of atherosclerosis. Please be expected to not only KNOW these five items, but their correct ORDER too.
  • A simplified (nothing is TOO or OVERLY simplified, imho) concept of atherosclerosis.
  • This is the VERY VERY best diagram of atherosclerosis you will ever see. The nice thing about diagrams is that you really do not have to memorize them, but just visually “recall” the concepts!
  • Degeneration/Neoplasm/Inflammation link! Isn’t atherosclerosis wonderful? Here we have all 3 classifications of disease in one entity----atherosclerosis!
  • In all honesty the correct answer is “NO”, however it can be slowed down by knowing the treatable or preventable risk factors. No doubt you will occasionally hear of AMAZING BREAKTHROUGHS, which are all claims by scammers and lunatics.
  • Note that classically topics of arterial diseases are divided into 1) atherosclerosis and 2) everything else.
  • When you think hypertension, think essential, then renal, then endocrine, then other!
  • Always know that hypertension can be understood best by remembering the simple BP=COxPR equation.
  • Sometimes this is called RAAS
    Renin
    Angiotensin (but angiotensis does SO MUCH MORE than just activate aldosterone)
    Aldosterone
    Sodium
  • Know ALL the ways angiotensin II increases blood pressure!
    Be familiar with the FIVE ways angiotensin II can INCREASE blood pressure: 1) increase sympathetic activity 2) tubular reabsorption of Na+ 3) Aldosterone secretion 4) arteriolar vasoconstriction 5) ADH secretion
    Chances are, every free dinner you attend with have a drug rep showing you some kind of RAAS diagram like this.
  • A little more thorough diagram of RAAS pathology---- genetic and acquired.
  • Often, benign or “malignant” hypertension is described as two different types of changes in arterioles, usually renal.
    Benign: Hyalization of arteriole wall
    Malignant: Fibrinoid necrosis and “onion skinning” of arteriole wall
  • Does it look like you’ve seen this somewhere before, i.e., the discussion of atherosclerosis?
  • Know the difference between a TRUE (endothelial expansion) and FALSE (NO endothelial expansion) aneurysm
  • Of course any artery with this abundance of elastic fibers would HAVE to be an aorta or an elastic artery!
    Imagine the wavy elastic fibers as being little rubber bands!
  • All logical?
  • Specifics of thoracic aneurysms.
  • Dissection (i.e., blood or hemorrhage disrupting the wall of a large artery) can be both a cause or an effect of an aneurysm.
    Would the continued dissection of that acute hemorrhage result in, more likely, a TRUE or FALSE aneurysm?
  • Why are arteritides highly linked to autoimmune diseases? Answer: Because there are rarely any known causative external (i.e., infectious) pathogens, and many are associated with known auto-antibodies.
  • Note the disruption of the internal elastic lamina. Why?
  • See my clipped pic, or go to the microscope directly by clicking on the link!
  • Pulseless is the buzzword in this case. Why?
  • Poly? Peri-?
  • Nuclear “dust” from neutrophils, i.e., leukocyto”clasia” is the hallmark.
  • Mortality has improved significantly, but flare-ups, i.e., recurrences, are still the main concern.
  • Why is the “necrosis” of Wegener’s not called “caseating”? Ans: Because, by tradition, rather than objectivity or logic, “caseation” has been attributed to tuberculosis. Yes, we know this is not fair.
    Wegener’s is PRIMARILLY a disease of the UPPER and LOWER respiratory tracts, however, eye involvement is frequent and may range from a mild conjunctivitis to dacryocystitis, episcleritis, scleritis, granulomatous sclerouveitis, ciliary vessel vasculitis and retro‐orbital mass lesions.
  • Hideous Buerger’s pics: https://www.google.ca/search?q=buerger%27s+smoking+no+arms+no+legs&hl=en&lr=&source=lnms&tbm=isch&sa=X&ei=7yEsUc3fOoO7ygGd94GABg&ved=0CAoQ_AUoAQ&biw=1173&bih=811#hl=en&lr=&tbm=isch&sa=1&q=buerger%27s+smoking+&oq=buerger%27s+smoking+&gs_l=img.3...48652.48652.2.48889.1.1.0.0.0.0.64.64.1.1.0...0.0...1c.1.4.img.XItLwh06TY8&bav=on.2,or.r_gc.r_pw.r_cp.r_qf.&bvm=bv.42965579,d.aWc&fp=afb17b9b024efed2&biw=1173&bih=811&imgrc=qgYMmGYN9XE04M%3A%3BF_gkVNI6-_0baM%3Bhttp%253A%252F%252Fsmokinggotme.com%252Fimages%252Flg%252Fpicture-11-_-Brandon%27s-Struggle-_-SmokingGotMe-lg.gif%3Bhttp%253A%252F%252Fsmokinggotme.com%252Fbrandon%27s%252520struggle%252Fpicture11.html%3B477%3B741
  • What is the most unforgettable picture I remember from medical school?
  • Most classical systemic auto-immune diseases have an element of vasculitis. Remember the THREE magnets for Ag-Ab complexes: GBM, Synovia, and BLOOD VESSELS!!!!!
  • A “mycotic” aneurysm is any aneurysm that has become secondarily infected, usually by bacteria. Hence the name “mycotic” is a misnomer.
    Also note that aspergillis and mucormycosis were also previously mentioned as the two classic “mold” diseases of immunocompromised patients.
  • WHITEBLUERED is the proper order of color change.
  • Knowing the correct ORDER of color change, will help you diagnose it properly! WHITEBLUERED
  • The plural of varix is varices. Varices are generally the same as varicosities. Hemorrhoids are also varices or varicosities, but are not usually called that.
  • SEVERE VARICOSITIES
  • Thrombophlebitis = Phlebothrombosis
  • Is “dusky cyanosis” a redundant term? Probably.
  • All of these factors should make sense anatomically!
  • Recall the childhood warning.
  • Note the relative LACK of cellulitis, although in most cases cellulitis is present, and in the presence of cellulitis, the diagnosis of lymphangitis would usually not be hazarded.
  • Any imaginable type of damage to lymphatics could cause lymphedema.
  • Peau d’orange is classically described in INFLAMMATORY carcinoma of the breast in which dermal lymphatics are extensively plugged up by tumor nests
  • Blockage of the thoracic duct is the usual cause of chylothorax.
    If you ever aspirate white milky fluid from a chest, pericardial, or abdominal tap, I really do not think it can be anything but chyle.
    Whiteness is due to FFA’s.
  • Vascular tumors generally follow the same diagnostic patterns of other mesenchymal (i.e., “soft” tissue) tumors. Often the KEY difference is that “endothelium” lined blood filled spaces, or identification of endothelial cells by antigenic markers, such as factor VIII, is usually present.
  • The presence of the NUMBER of mitotic figures is a KEY feature in determining the benignity or malignancy of ANY connective tissue tumor.
    Most pathologists are terrified of soft tissue tumors with mitoses and/or atypia and ALWAYS seek expert opinions.
  • Small spaces = often small people, i.e., kids
    Large spaces = often large people, i.e., adults
  • Would a stain for Factor VIII help identify a tumor as being of vascular origin? Answer: YES
    Why? Because, if you remember, the coagulation Factor VIII is present in endothelial cells.
    Is “blanching” a most important clinical test to determine if a tumor is of blood vessel origin? Ans: YES
  • Almost all vascular tumors show endothelial lined spaces. If they are not apparent, a specific stain for endothelial cells, like Factor VIII is commonly ordered.
  • “-ectasia” is a generic term meaning dilation and is primarily used with regard to veins rather than arteries.
    Osler-Weber-Rendu syndrome, or hereditary hemorrhagic telangiectasia (HHT), is a rare genetically determined disorder that affects blood vessels throughout the body and results in a tendency for bleeding. HHT is an autosomal dominant disorder characterized by vascular dysplasia and hemorrhage. The prognosis for patients with the disease is good as long as bleeding is promptly recognized and adequately controlled.
  • Note the LACK of a malignant sounding name.
    Almost all malignant, or potentially metastasizable vascular tumors look alike so there is no need to try to differentiate them here microscopically.
  • KS
  • Almost all malignant, or potentially metastasizable vascular tumors look alike so there is no need to try to differentiate them here microscopically.
  • *Note ALSO the lack of a malignant sounding name.
    Almost all malignant, or potentially metastasizable vascular tumors look alike so there is no need to try to differentiate them here microscopically.
    Almost all malignant, or potentially metastasizable vascular tumors look alike so there is no need to try to differentiate them here microscopically.
  • If you know a patient who has had an angioplasty, chances are he has had more than one.
  • Transcript

    • 1. Diseases of BLOOD VESSELS
    • 2. COMPONENTS • • • • Intima, Media, Adventitia, M>A or A>M ENDOTHELIUM INTERNAL ELASTIC LAMINA ECM: Elastin (~aging) αS/D, collagen, mucopolysaccharides • Smooth Muscle • Connective Tissue • Fat
    • 3. 1) Blockage (preceded by narrowing) 2) Rupture Preceded by weakening)
    • 4. TOPICS • Vascular wall responses • Congenital Anomalies • Atherosclerosis • Arteriosclerosis • Hypertension • Aneurysms • Vasculitides • Raynaud “phenomenon” • Veins • Lymphatics • Tumors • Interventions
    • 5. • • • • • • • DEFINITIONS ARTERIO-sclerosis ATHERO-sclerosis Aneurysm Dissection Thrombus Hypertension Vasculitis/Vasculitides, infectious/NONinfectious (often-autoimmune) • Varicosity • DVT/Thrombo-phlebitis/Phlebo-thrombosis
    • 6. • • • • • • DEFINITIONS Lymphangitis Lymphedema Angioma/Hemangioma (generic) Lymphangioma Angiosarcoma (generic) Lymphangiosarcoma
    • 7. NON-Specific Vascular Wall Response to Injury • Endothelial “activation” • Smooth Muscle cell roles • Development, Growth, Remodeling • Intimal “thickening”
    • 8. ENDOTHELIAL CELLS • Recall Jeckyl/Hyde concept: maintain hemostasis/cause thrombosis • Maintenance of Permeability Barrier • Elaboration of Anticoagulant, Antithrombotic, Fibrinolytic Regulators J: Prostacyclin, Thrombomodulin, Heparin, Plasminogen • Elaboration of Prothrombotic Molecules H: vWF, TF, Plasminogen activator inhibitor • Extracellular Matrix Production (collagen, proteoglycans) • Modulation of Blood Flow and Vascular Reactivity – Vasoconstrictors: endothelin, ACE – Vasodilators: NO, Prostacyclin • Regulation of Inflammation and Immunity • Regulation of Cell Growth • Oxidation of LDL
    • 9. ENDOTHELIAL CELL “ACTIVATORS” • • • • • • • • Cytokines, GFs Bacterial Products Hemodynamic Forces Lipid Products Viruses Complement Hypoxia Cigarette smoke
    • 10. VASCULAR SMOOTH MUSCLE • Vasoconstriction • Vasodilatation • Make ECM: – Collagen – Elastin – Proteoglycans • Regulated by: – PROMOTORS: PDGF, endothelin, thrombin, FGF, etc. – INHIBITORS: Heparan SO4, NO, TGF-β
    • 11. Vessel Growth & Remodeling • The sum total of all the factors and processes involved in tissue injury and the body’s ability to grow vessels, develop new pathways, and re-perfuse areas in response to tissue and/or blood vessel injury.
    • 12. CONGENITAL ANOMALIES • Arteriovenous fistulas • Also called ArterioVenous Malformation (AVM) • Common factor is abnormal communication between high pressure arteries and low pressure veins • Usually congenital (malformation), but can be acquired by trauma or inflammation • Most often described in the brain as an AVM • Often asymptomatic or with hemorrhage or pressure effects
    • 13. ARTERIO-SCLEROSIS • GENERIC term for ANYTHING which HARDENS arteries – Atherosclerosis (99%) – Mönckeberg medial calcific sclerosis (1%) – Arteriolosclerosis, involving small arteries and arterioles, generally regarded as NOT strictly being part of atherosclerosis, but more related to 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) FATTY STREAK (nonpalpable, but a visible YELLOW streak) 2) ATHEROMA (plaque) (palpable) 3) THROMBUS (nonfunctional, symptomati c)
    • 18. MORPHOLOGIC CONCEPTS • • • • • • • • Macrophages (really monocytes) infiltrate Intimal “Thickening” Lipid Accumulation Streak Atheroma Smooth Muscle Hyperplasia and Migration Fibrosis Calcification • Aneurysm* • Thrombosis
    • 19. FATTY STREAKS
    • 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 & RISK FACTORS
    • 25. Epid./RiskFactors • Related to “development” of nation • US highest • 50-70% DECREASE 19632000. Why? “awareness”, dietary restrictions • AGE • SEX, M>F until menopause, estrogen “protection” • GENETICS (multigenic)
    • 26. MAJOR factors • Hyperlipidemia • Hypertension • Cigarette Smoking • Diabetes Milletus
    • 27. Risk Factors for Atherosclerosis Major NON-modifiable Minor Modifiable Increasing age Obesity Male gender Physical inactivity Family history Stress ("type A" personality) Genetic abnormalities Postmenopausal estrogen deficiency   High carbohydrate intake Modifiable Hyperlipidemia Hypertension Cigarette smoking Diabetes Alcohol Lipoprotein Lp(a) Hardened (trans)unsaturated fat intake Chlamydia pneumoniae
    • 28. MAJOR factors • Hyperlipidemia • Hypertension • Cigarette Smoking • Diabetes Milletus
    • 29. HYPERLIPIDEMIA • Chiefly CHOLESTEROL, LDL>>>>HDL • HDL mobilizes cholesterol FROM atheromas to liver • LOW CHOLESTEROL diet is GOOD • UNSATURATED fatty acids GOOD • Omega-3 fatty acids GOOD • Exercise GOOD
    • 30. “Foamy” MACROPHAGES
    • 31. CHOLESTEROL* CLEFTS * Really cholesterol esters
    • 32. HYPERTENSION • HYPERTENSION causes ATHEROSCLEROSIS. Why? • ATHEROSCLEROSIS causes HYPERTENSION. Why?
    • 33. CIGARETTES • What more needs to be said?
    • 34. DIABETES • If there was one disease which I could challenge you to, as a dare, to PROVE to me that was NOT EXACTLY as atherosclerosis, it would be DIABETES! Any takers? THE SAME
    • 35. NON major factors • Homocysteinuria/homocysteinemia, related to low B6 and folate intake • Coagulation defects • Lipoprotein Lp(a), independent of cholesterol. Lp(a) is an altered form of LDL • Inadequate exercise, Type “A” personality, obesity (independent of diabetes) • Protective effect of moderate alcohol? Medical LIE, sponsored by the booze industry and alcoholic physicians!
    • 36. PATHOGENESIS • “atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium” 
    • 37. 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 to intima to activate macrophages (foam cells) • Proliferation of SMOOTH MUSCLE and ECM • Accumulation of lipids in cells and ECM
    • 38. Main FOUR STARS of PATHOGENESIS SAGA • 1) Endothelial Injury • 2) Inflammation • 3) Lipids • 4) Smooth Muscle Cells, SMCs
    • 39. Other Pathogenesis Considerations • Oligoclonality of cells in plaque • Chlamydia, CMV as endothelial injurers
    • 40. PREVENTION PRINCIPLES • Know what is preventable • Know what is MAJOR (vs. minor) • Know PRIMARY vs. SECONDARY principles • Understand atherosclerosis begins in CHILDHOOD • Risk factors in CHILDREN predict the ADULT profile • Understand SEX, ETHNIC differences
    • 41. Can atherosclerosis be REVERSED? ?
    • 42. NON ATHEROSCLEROSIS VASCULAR DISEASES • HYPERTENSION • ANEURYSMS • VASCULITIDES • VEIN DISORDERS • NEOPLASMS
    • 43. HYPERTENSION • “ESSENTIAL” 95% • “SECONDARY” 5%
    • 44. • Renal   SECONDARY • • • • • • • Acute glomerulonephritis     Chronic renal disease     Polycystic disease     Renal artery stenosis     Renal artery fibromuscular dysplasia Renal vasculitis     Renin-producing tumors     • • • • • Adrenocortical hyperfunction  (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion) Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oral  contraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidase  inhibitors) Pheochromocytoma, acromegaly, HYPO-thyroidism (myxedema), HYPER-thyroidism pregnancy-induced     • Increased intravascular volume • Endocrine   • Cardiovascular: Coarctation of aorta, polyarteritis nodosa (or other vasculitis) • MISC: Increased cardiac output, Rigidity of the aorta, neurologic, Psychogenic,   Increased intracranial pressure, sleep apnea, acute stress, including, surgery
    • 45. DEFINITION • 140/90 • SUSTAINED diastolic >90 • SUSTAINED systolic >140
    • 46. ALL Hypertension BP = CO x PR
    • 47. E.F.
    • 48. ReninAngiotensinAldosteron e AXIS (RAAS) • • • • If the perfusion of the juxtaglomerular apparatus in the kidneys decreases, then the juxtaglomerular cells release the enzyme renin. Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries. Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as an endocrine, autocrine/ paracrine, and intracrine hormone. 
    • 49. GENETIC ACQUIRED
    • 50. HISTOPATHOLOGY of ESSENTIAL HYPERTENSION “HYALINE” = BENIGN HTN. 1) ONION SKIN “HYPERPLASTIC” = MALIGNANT HTN. SYS>200 2) “FIBRINOID” NECR.
    • 51. GENETIC vs. ENVIRONMENTAL • GENETIC UN-CONTROLLABLE • ENVIRONMENTAL CONTROLLABLE – STRESS – OBESITY – SMOKING – PHYSICAL ACTIVITY – NaCl INTAKE
    • 52. 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
    • 53. ANEURYSMS • 2 CAUSES: –1) ATHEROSCLEROSIS – 2) CYSTIC MEDIAL DEGENERATION (NECROSIS), can be familial NORMAL elastic fibers DISRUPTED, FRAGMENTED elastic fibers
    • 54. Most abdominal aortic aneurysms (AAA) occur between the renal arteries and the bifurcation of the aorta
    • 55. ANEURYSMS (sequelae) – RUPTURE – OBSTRUCTION – EMBOLISM – COMPRESSION • URETER • SPINE – MASS EFFECT
    • 56. THORACIC ANEURYSMS – Encroachment – Respiratory difficulties – Hoarseness? – Dysphagia – Cough – Pain – Aortic valve dilatation – Rupture
    • 57. DISSECTION
    • 58. ANEURYSMS (luetic) – Chiefly thoracic – Follows an AORTITIS • PLASMA CELLS predominate
    • 59. VASCULITIDES • • • • • • TEMPORAL “GIANT CELL” ARTERITIS TAKAYASU ARTERITIS POLY (PERI) ARTERITIS NODOSA KAWASAKI DISEASE WEGENER’s GRANULOMATOSIS THROMBOANGI(i)TIS OBLITERANS (BUERGER[‘s] DISEASE) • OTHER • INFECTIOUS
    • 60. VASCULITIDES • Chiefly arterial • Infectious (5%) vs. Non-infectious (95%) • NON-infectious are generally “AUTO”IMMUNE. Why? • Persistent findings: – Immune complexes – ANTI-NEUTROPHIL AB’s (Wegener’s, “Temporal”) – ANTI-ENDOTHELIAL CELL AB’s (Kawasaki) • Often DRUG related (Hypersensitivity, e.g.), especially small blood vessels.
    • 61. “TEMPORAL” ARTERITIS aka, Giant Cell Arteritis, GCA • ADULTS, older • Mainly arteries of the head and temporal arteries are the most visibly, palpably, and surgically accessible • BLINDNESS most feared sequelae • GRANULOMATOUS WALL inflammation diagnostic • OFTEN associated with marked ESR elevation to be then known as POLYMYALGIA RHEUMATICA • Anti-NEUTROPHIL AB’s often POSITIVE
    • 62. TEMPORAL ARTERITIS http://www.path. uiowa.edu/cgibinpub/vs/fpx_gen.c gi? slide=623&viewe r=java&view=0&l ay=iowa
    • 63. TAKAYASU ARTERITIS • Involves aortic arch and other heavilly elastic arteries, i.e., chief thoracic aorta branches, most commonly young Asian women • FEMALES <40 • “PULSELESS” disease • NECROSIS, Giant Cells also
    • 64. POLY-(Peri-) ARTERITIS NODOSA (PAN) • • • • • ANY MEDIUM or SMALL artery OFTEN visceral arteries Infarcts, aneurysms, ischemia CLASSICAL AUTOIMMUNE disease SEGMENTAL, TRANSMURAL, NECROTIZING (fibrinoid) inflammation • Sometimes anti-neutrophil antibodies, especially in the smaller vessel diseases • One of the CLASSICAL systemic autoimmune diseases, like SLE, RA, or SS
    • 65. http://www .path.uiow a.edu/cgibinpub/vs/fpx _gen.cgi? slide=584 &viewer=j ava&view= 0&lay=iow a
    • 66. KAWASAKI DISEASE • CHILDREN <4 • CORONARY ARTERIES • LEADING cause of ACQUIRED heart disease in children • USA and JAPAN • Fatal in only 1% • Red tongue, adenopathy • Anti-endothelial cell ABs
    • 67. MICROSCOPIC POLYANGIITIS HYPERSENSITIVITY VASCULITIS LEUKOCYTOCLASTIC VASCULITIS • SMALL VESSELS OF ALL TYPES, e.g., capillaries and veins too • FRAGMENTED NEUTROPHILS • aka, LEUKOCYTOCLASIA • aka, NUCLEAR “DUST” • Most are ALLERGIC reactions to allergens like penicillin or strep • DERMATOLOGIST’s DISEASE
    • 68. http://ww w.path.ui owa.edu/ cgi-binpub/vs/fp x_gen.cg i? slide=63 4&viewer =java&vi ew=0&la y=iowa
    • 69. WEGENER GRANULOMATOSIS • M>F, often in 40’s • ACUTE NECROTIZING GRANULOMAS OF UPPER an LOWER respiratory tract • NECROTIZING GRANULOMATOUS VASCULITIS of SMALL vessels of ALL types • Often renal involvement, “crescentic” glomerulonephritis • ANTI-NEUTROPHIL-CYTOPLASMIC-AB’s (ANCA) usually present
    • 70. necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas necrosis granulomas
    • 71. THROMBOANGIITIS OBLITERANS BUERGER(‘s) Disease • 100% caused by cigarette smoking • MEN>>>F, 30’s, 40’s • Often arteries are 100% obliterated, hence the name “obliterans” • EXTREMITIES most often involved
    • 72. http://www.path.uio wa.edu/cgi-binpub/vs/fpx_gen.cgi ? slide=704&viewer= java&view=0&lay=i owa
    • 73. OTHER VASCULITIDES • SLE • RHEUMATOID ARTHRITIS
    • 74. INFECTIOUS ARTERITIDES • ASPERGILLIS • MUCORMYCOSIS • “MYCOTIC” ANEURYSMS are generally MISNOMERS
    • 75. NON ATHEROSCLEROSIS VASCULAR DISEASES • HYPERTENSION • ANEURYSMS • VASCULITIDES • VEIN DISORDERS • NEOPLASMS
    • 76. 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
    • 77. Raynaud “Phenomenon” • PRIMARY: (formerly Raynaud “DISEASE”) – – – – – – Digital PALLORCYANOSISHYPEREMIA (WHITE) (BLUE) (RED) Vasoconstriction usually triggered by COLD, emotion Can be tip of nose, not only digits Self Limited, Gangrene UN-common Arteries often do NOT show diagnostic pathology • SECONDARY: (formerly Raynaud “Phenomen.”) – Atherosclerosos – SLE – Buerger Disease
    • 78. WHITE BLUE RED
    • 79. “Varicose” Veins • 20% of population, F>M • Related to increased venous pressure, age, valve dysfunction • Superficial veins of lower extremities most common • PATH: 1) DILATED, 2) TORTUOUS, 3) ELONGATED, 4) SCARRED (phlebosclerosis), 5) CALCIFICATIONS, 6) NON-UNIFORM SMOOTH MUSCLE • Conceptually like varices or hemorrhoids • “Phlebosclerosis” is what your pathologist will call it
    • 80. THROMBOPHLEBITIS • 90% DEEP veins of the legs • IDENTICAL to PHLEBOTHROMBOSIS • Factors: CHF, Neoplasia (esp. GI, panc. Lung adenocarcinomas “migratory” thrombophlebitis), pregnancy, obesity, post-op, immobilization, or any of the parts of Virchow’s triangle • Sequelae: PE most feared • Symptoms: edema, cyanosis, heat, pain, tenderness, but usually……..NONE!!!
    • 81. SVC SYNDROME • Usually from bronchogenic CA or mediastinal lymphoma • “DUSKY CYANOSIS” of: – Head – Neck – Arms
    • 82. IVC SYNDROME • Secondary to: – NEOPLASMS (external compression) – ASCENDING THROMBOSIS from FEMORALS, ILIACS – AAA, Gravid uterus • Bilateral leg edema • Massive proteinuria if renal veins involved (like nephrotic syndrome)
    • 83. LYMPHANGITIS • From regional infections • Group-A beta-hemolytic strep most common • Lymphatics dilated, filled with WBCs • Cellulitis usually present too • Lymphadenitis also usually follows • If lymph nodes cannot filter (process) antigens enough septicemia
    • 84. LYMPHEDEMA • Lymphatic channels blocked or scarred or absent: – Post surgical – Post radiation – Filaria – Congenital – Tumoral (peau d’orange- breast)
    • 85. CHYLE • CHYLOUS ASCITES • CHYLOTHORAX • CHYLOPERICARDIUM
    • 86. Vascular TUMORS • BENIGN (NEVER metastasize, in fact some are not even TRUE neoplasms, but hamartomas) • INTERMEDIATE (rarely metastasize) • MALIGNANT (FREQUENT and EARLY metastases, like any other sarcoma lung)
    • 87. BENIGN---------------------------------------MALIGNANT Rare mitosis--------------------------Common mitosis Mild, rare atypia------------Frequent, severe atypia NO mets----------------------------Early, frequent mets via BLOODSTREAM
    • 88. HEMANGIOMA • Often a generic term for ANY benign blood vessel tumor • CAPILLARY (small vascular spaces) – Also called “juvenile”, often called “birth marks” – Usually regress with age • CAVERNOUS (LARGE vascular spaces) – Also called “adult” – Usually do NOT regress
    • 89. PYOGENIC GRANULOMA • ORAL CAVITY MOST COMMON • Histology like capillary hemangioma • Regress • Indistinguishable from normal granulation tissue
    • 90. LYMPHANGIOMA • • • • Small 1-2 mm 90% Head and neck region in kids <2 Generally……RARE When large size and/or spaces present often called “CYSTIC HYGROMA”
    • 91. GLOMUS TUMOR GLOMANGIOMA • 1 cm • Most commonly under nail • Painful
    • 92. MISC. “BENIGN” TUMORS • -ectasias, telangiectasias • Nevus Flammeus, aka, port wine stain---- • Spiders (spider telangiectasias), ass. W. pregnancy, cirrhosis------------------------- • Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia)------------- • Bacillary Angiomatosis, in HIV patients, caused by bacilli of Bartinella species
    • 93. 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 PLAQUENODULE • HEMANGIOENDOTHELIOMA* (HETEROGENEOUS GROUP OF NEOPLASMS)
    • 94. Diagnosis of vascular neoplasms may require the use of endothelial cell markers such as Factor VIII or CD-31, especially if clear cut vascular spaces are difficult to see, especially if the tumor is UNDIFFERENTIATED enough to the degree that endothelial lined spaces are NOT clearly seen.
    • 95. MALIGNANT VASCULAR TUMORS • ANGIOSARCOMA – – – – May not look “vascular” at all Severe atypia Frequent and often bizarre mitoses Behave as any sarcoma might, i.e., early pulmonary metastases • HEMANGIOPERICYTOMA* – HETEROGENOUS group of disorders – Most commonly arising in pelvic retroperitoneum
    • 96. VASCULAR INTERVENTIONS • ANGIOPLASTY • STENTS • GRAFTS – Autologous (saphenous v., internal mammary a.) – Synthetic (Teflon)
    • 97. ANGIOPLASTIES • • • • Plaque fracture (crackling sound) Dissection Arterial dilatation initially Restenosis ~ 6 months
    • 98. STENTS • Metallic mesh • Permanently placed • Stays patent longer than angioplasty • OFTEN DRUG COATED • Goals: – Prevent thrombosis – Prevent spasm – Delay RE-stenosis
    • 99. GRAFTS • 400,000 CABG grafts per year in USA • Saphenous v. vs. Internal mammary a. (internal thoracic a.) • 50% patent after 10 years, for saphenous v. • 90% patent after 10 years, for mammary a. • Endothelial and smooth muscle migration and proliferation are key factors for success