Pathology Review Flash Cards for Revision Vascular, Cardiology, Pulmonary, Hematology

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Dish (polyarteritis nodosa). Medium estimated solid arteriesSpares lungsYoung adults30% HBV Ag , not connected with ANCAType III fibrinoid necrosistwo stages found at the same timeAcute-transmural neutrophil, eosinophils, and mononuclear cellsChronic-stringy vessel thickening, mononuclear cellsLeads to aneurysmal knobs in skin and organ dead tissue (renal disappointment, intense MI, bleeding looseness of the bowels, ulce

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Pathology Review Flash Cards for Revision Vascular, Cardiology, Pulmonary, Hematology Spring 2009

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PAN (polyarteritis nodosa) Medium measured strong supply routes Spares lungs Young grown-ups 30% HBV Ag+, not related with ANCA Type III fibrinoid rot two phases found in the meantime Acute-transmural neutrophil, eosinophils, and mononuclear cells Chronic-sinewy vessel thickening, mononuclear cells Leads to aneurysmal knobs in skin and organ dead tissue (renal disappointment, intense MI, ridiculous the runs, ulcers) Kidney infection significant reason for death yet NO glomerulonepthritis included

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Leukoclastic vasculitis (smaller scale PAN) Necrotizing vasculitis of little vessels: arterioles, vessels, venules Micropolyangitis=leukocytoclastic vasculitis all sores same stage (ACUTE), not at all like PAN divided PMNs in vessel dividers w/fibrinoid putrefaction p-ANCA (+) yet no insusceptible edifices discovered ("pauci-invulnerable") necrotizing glomerulonephritis , hemoptysis, discernable purpura Immune rxn. to medication, contamination, tumor. Settle on expulsion of causative specialist

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Takayasu's Arteritis Fibrosis, sporadic thickening and narrowing of aortic curve & awesome vessels Involvement of foundation of aorta may - dilatation with aortic valve inadequacy; association of coronary ostia may prompt to MI Affects Asian ladies < 40 y.o. Granulomatous aggravation w/mononuclear invade & mammoth cells "Pulseless malady" with powerless furthest point beats Ocular unsettling influences, hypertension Fever, joint inflammation, myalgia, night sweats

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Temporal (Giant Cell) Arteritis Involves conduits of the head: fleeting >> opthalmic, vertebral, aorta ?resistant reaction to elastin Granulomatous irritation w/goliath cells, lymphocytes, eosinophils, and neutrophils Nodular divider thickenings w/diminishment in lumen measure Affects elderly patients > 50 Headache, visual unsettling influence, visual deficiency, jaw claudication, discernable transient course Fever, exhaustion, weight reduction Associated w/polymyalgia rheumatica Treat with corticosteroids to forestall visual impairment

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Wegener's Vasculitis of little supply routes & veins of moderately aged men c-ANCA + Mostly includes Lungs and Upper Airways intense necrotizing granulomas→ central necrotizing vasculitis focal range of corruption encompassed by lymphs, plasma cells, macros, monster cells Also includes Kidneys intense central proliferative or diffuse crescentic necrotizing glomerulonephritis ulcerative sores of nose, sense of taste, pharynx; related with nosebleeds and hemoptysis ; endless sinusitis, pneumonitis Hematuria, proteinuria, renal disappointment Very poor guess

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Kawasaki's/Buerger's Kawasaki's Syndrome influences kids <4yo Disease of youthful youngsters (most <4 years); Epidemic in Japan, Hawaii Acute segmental putrefaction with articulated irritation and rot looking like PAN Vasculitis of expansive & medium corridors, esp. c oronary conduits ?irresistible process prompting to hostile to endothelial cell antibodies ; hereditary pre-air Lymphocyte/PMN penetrate with putrefaction, thrombosis Mostly self-constrained however may bring about intense MI/sudden passing Fever, skin rash (erythema of palms and soles, rash with desquamation) , cervical adenopathy, oral/conjunctival erythema ("strawberry tongue") (mucocutaneous lymph hub disorder) TX: IV IgG & Aspirin

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Other Buerger's Disease influences overwhelming smokers <age 35 Idiopathic segmental thromosing vasculitis of little & medium fringe corridors = " thromboangiitis obliterans " Involves tibial and spiral courses Intermittent claudication, shallow nodular phlebitis, cool affectability, autoamputation of digits Raynaud's ailment - Not related with natural injuries Raynaud's marvel - Vascular deficiency auxiliary to thromgoangiitis obliterans, SLE, and systemic sclerosis

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Churg-Strauss Churg - Strauss Small vessels : skin, lung, heart Eosinophil - rich granulomatous response Affects atopic individuals Associated with unfavorably susceptible rhinitis, asthma and blood eosinophilia P-ANCA in 70% Coronary arteritis and myocarditis Most regular reason for dreariness and mortality Pulmonary necrotizing vasculitis Henoch Schonlein Purpura: influences kids segmental fibrinoid corruption with IgA statement sequela to upper respiratory contamination (perhaps post-strep) discernable purpura, arthralgia , stomach torment w/intestinal drain, renal harm, fever

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Atherosclerosis incendiary/recuperating response of the endothelium of expansive & medium estimated supply routes bringing about central intimal sores NO essential sores in media/adventitia 2 Main Features: Accumulation of cholesterol because of take-up of oxidized LDL by macrophages and smooth muscle cells  framing " froth cells " Healing stage with fibroblast multiplication  arrangement of stringy top & affidavit of ECM segments Lesions = "fibrofatty plaques"

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Atherosclerosis Pathogenesis Local cell damage  aggregation and oxidation of lipid (LDLs)  endothelial cell actuation & expanded vascular porousness  attachment/convergence of platelets & monocytes into intima  emission of cytokines  encourage inundation of fiery cells→migration/initiation of smooth muscle cells & fibroblasts →secretion of collagen & ECM segments Oxidized lipid seems to assume a focal part – they are chemotactic for monocytes,  provocative cytokines,  macrophage motility and are dangerous to endothelial cells/smooth muscle

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Atherosclerosis Fatty streaks (soonest sores) contain froth cells with variable measures of proteoglycans, extracellular lipid and T cells – can be found in babies Lesions advance with age  get to be distinctly raised  combine into plaques Over time, fibrotic plaque gets to be distinctly shaky  "break"  introduction of collagen advances platelet grip and neighborhood thrombus development Fissuring or burst of a plaque can deliver emboli and intense areas of dead tissue at removed destinations (e.g MI) Lipid/cholesterol emboli a specific issue in the kidney

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Atherosclerosis Distribution = stomach aorta > coronary supply routes > popliteal supply routes > diving thoracic aorta > inner carotids > hover of willis  happens at fanning focuses, ostia of vessels Major Risk Factors = hypertension, smoking, hyperlipidemia/hypercholesterolemia(**), diabetes Key segments sinewy top center of cell garbage, froth cells, cholesterol gems "shoulders" with enacted cells, froth cells, moving/multiplying smooth muscle cells ** NOTE  : hypothyroidism assoc with hypercholesterolemia**

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Varicosities Varicose veins are strangely extended, stretched and convoluted veins Most generally situated at the shallow saphenous vein, they can likewise be found in the distal throat (entryway HTN), anorectal district (hemorrhoids), or scrotum (varicocele) Caused by inadequacy of the venous valves which can be exacerbated by pregnancy, delayed standing, stoutness, oral contraceptives, and age There is a familial affiliation They can create optional to DVTs which cause enlargement of the veins

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Deep Venous Thrombosis Typically brought on by Virchow's Triad: 1. Stasis (causes the arrival of procoagulants, for example, thromboplastin from endothelium prompting to restricted coagulation) 2. Hypercoagulable state (Factor V leiden, growth) 3. Injury bring down furthest point beneath the knee; additionally regularly found in the shallow saphenous, hepatic and renal veins In the lower limits they normally stretch out toward the heart. can debilitate and sever normally prompting to embolization to a pneumonic supply route. Counteract with anticoagulant treatment (heparin, warfarin)

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Atherosclerosis Clinical Features  Blood stream = end organ ischemia  in diabetics, related with gangrene of the furthest points Intermittent ischemia of lower limits, " claudication "= cramping of muscles not getting enough oxygen (particularly w/effort)  Blood stream in renal flow  salt and water maintenance by means of renin-angiotension framework Compromised coronary course = effort ischemia and angina ( not MI) Ischemia of media  debilitating of divider  aneurysm

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Aneurysms and Dissections Berry/saccular Aneurysm Congenital shortcoming in divider Usually around Circle of Willis (Acomm is #1) Rupture in youthful grown-ups Subarachnoid discharge Associated with Ehlers Danlos, polycystic kidneys, Marfan's

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Aneurysms and Dissections Aortic Aneurysm (fusiform, tube shaped) Caused by serious atherosclerosis with hypertension Most normal amongst renal and iliac conduits Complications: crack, embolism (from atheroma, wall painting thrombus), impediment of vertebral vessels Other aortic aneuyrisms Mycotic - contamination (Salmonella): media devastation Luetic - syphilis: aortic curve aneurysm (from harm to media) with tree-yelping (intima harm), expansion of aortic valve  deficiency/cor bovinum

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Aneurysms and Dissections Aortic Dissection Follows tear in tunica intima Occurs inside tunica media Result of hypertension, connective tissue illness Most regular reason for death: hemopericardium Also causes aortic valve inadequacy; bargain of coronary, renal, mesenteric, as well as iliac veins Sudden onset front trunk torment that moves

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Aneurysms and Dissections Cystic average rot No putrefaction show (terrible phrasing) Associated with fusiform aneurysms, aortic dismemberments Changes: tissue discontinuity, little cystic spaces with undefined material, no irritation See in patients with Marfan's, Ehlers-Danlos

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Syphilitic Heart/Aortic Disease Seen in tertiary syphilis Most ordinarily includes proximal aortic root Mechanism : little vessel vasculitis Infiltration of lymphocytes and plasma cells in vasa vasorum, pulverization of vascular supply prompts to loss of media layer Loss of elastici